Concepts of Chemical Dependency PDF

Concepts of Chemical Dependency
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SEVENTH EDITION
Harold E. Doweiko
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Conepts of Chemical Dependency, © 2009, 2006 Brooks/Cole, Cengage Learning
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1 2 3 4 5 6 7 12 11 10 09 08
In loving memory of my wife, Jan
CONTENTS
Preface xvii
1 Why Worry About Recreational Chemical Abuse? 1

Who “Treats” Those Who Abuse or Are Addicted to Chemicals? 2
The Scope of the Problem of Chemical Abuse/Addiction 3
The Cost of Chemical Abuse/Addiction in the United States 4
Why Is It So Difficult to Understand the Drug Abuse Problem in the United States? 6
Summary 6
2 Statement of the Problem of Substance Use Disorders 7

The Continuum of Chemical Use 8
Why Do People Abuse Chemicals? 9
What Do We Mean When We Say That Someone Is “Addicted” to Chemicals? 12
Definitions of Terms Used in This Text 13
The Growth of New “Addictions” 15
What Do We Really Know About the Addictive Disorders? 15
The State of the Art: Unanswered Questions, Uncertain Answers 16
Summary 16
3 The Medical Model of Chemical Addiction 17

The Medical Model 17
Reaction Against the Disease Model of Addiction 22
Summary 27
4 Psychosocial Models of the Substance Abuse Disorders 28

Disturbing Questions 28
Multiple Models 29
The Personality Predisposition Theories of Substance Abuse 30
Real Versus Pseudo Personality Issues 32
The Final Common Pathway Theory of Addiction 33
Summary 35
5 Addiction as a Disease of the Human Spirit 36

The Rise of Western Civilization, or How the Spirit Was Lost 36
Diseases of the Mind—Diseases of the Spirit: The Mind-Body Question 38
The Growth of Addiction: The Circle Narrows 38
The Circle of Addiction: Addicted Priorities 39
Some Games of Addiction 39
A Thought on Playing the Games of Addiction 40
vii
viii Contents
Recovery Rests on a Foundation of Honesty 41

False Pride: The Disease of the Spirit 41
Denial, Projection, Rationalization, and Minimization: The Four Horsemen of Addiction 43
Summary 45
6 An Introduction to Pharmacology 46
The Prime Effect and Side Effects of Chemicals 46
Drug Forms and How Drugs Are Administered 47
Bioavailability 49
The Drug Half-Life 53
The Effective Dose 54
The Lethal Dose Index 54
The Therapeutic Index 55
Peak Effects 55
The Site of Action 55
The Blood-Brain Barrier 58
Summary 59
7 Introduction to Alcohol: The Oldest Recreational Chemical 60

A Brief History of Alcohol 60
How Alcohol Is Produced 61
Alcohol Today 62
Scope of the Problem of Alcohol Use 62
The Pharmacology of Alcohol 63
The Blood Alcohol Level 65
Subjective Effects of Alcohol on the Individual at Normal Doses in the Average Drinker 66
Effects of Alcohol at Intoxicating Doses for the Average Drinker 67
Medical Complications of Alcohol Use in the Normal Drinker 68
Alcohol Use and Accidental Injury or Death 70
Summary 71
8 Chronic Alcohol Abuse and Addiction 72

Scope of the Problem 72
Is There a “Typical” Alcohol-Dependent Person? 73
Alcohol Tolerance, Dependency, and Craving: Signposts of Alcoholism 73
Complications of Chronic Alcohol Use 75
Summary 88
9 Abuse of and Addiction to the Barbiturates and Barbiturate-like Drugs 89

Early Pharmacological Therapy of Anxiety Disorders and Insomnia 89
History and Current Medical Uses of the Barbiturates 90
Pharmacology of the Barbiturates 91
Subjective Effects of Barbiturates at Normal Dosage Levels 93
Complications of the Barbiturates at Normal Dosage Levels 93
Effects of the Barbiturates at Above-Normal Dosage Levels 95
Neuroadaptation, Tolerance to, and Dependence on the Barbiturates 96
Barbiturate-like Drugs 96
Summary 98
Contents ix
10 Abuse of and Addiction to Benzodiazepines and Similar Agents 99

Medical Uses of the Benzodiazepines 99
Pharmacology of the Benzodiazepines 100
Side Effects of the Benzodiazepines When Used at Normal Dosage Levels 102
Neuroadaptation to Benzodiazepines: Abuse of and Addiction to These Agents 102
Complications Caused by Benzodiazepine Use at Normal Dosage Levels 104
Subjective Experience of Benzodiazepine Use 106
Long-Term Consequences of Chronic Benzodiazepine Use 107
Buspirone 108
Zolpidem 110
Zaleplon 111
Rozerem 111
Rohypnol 112
Summary 113
11 Abuse of and Addiction to Amphetamines and CNS Stimulants 114

I. THE CNS STIMULANTS AS USED IN MEDICAL PRACTICE 114
The Amphetamine-like Drugs 114
The Amphetamines 117
II. CNS STIMULANT ABUSE 121
Scope of the Problem of Central Nervous System Stimulant Abuse and Addiction 121
Effects of the Central Nervous System Stimulants When Abused 122
Summary 130
12 Cocaine 131
A Brief Overview of Cocaine 131
Cocaine in Recent U.S. History 132
Cocaine Today 133
Current Medical Uses of Cocaine 133
Scope of the Problem of Cocaine Abuse and Addiction 133
Pharmacology of Cocaine 133
How Illicit Cocaine Is Produced 135
How Cocaine Is Abused 136
Subjective Effects of Cocaine When It Is Abused 138
Complications of Cocaine Abuse/Addiction 138
Summary 143
13 Marijuana Abuse and Addiction 145

History of Marijuana Use in the United States 145
A Question of Potency 147
A Technical Point 147
Scope of the Problem of Marijuana Abuse 148
Pharmacology of Marijuana 149
Methods of Administration 151
Subjective Effects of Marijuana 152
Adverse Effects of Occasional Marijuana Use 152
Consequences of Chronic Marijuana Abuse 154
The Addiction Potential of Marijuana 156
Summary 157
x Contents
14 Opioid Abuse and Addiction 158

I. THE MEDICAL USES OF NARCOTIC ANALGESICS 158
A Short History of the Narcotic Analgesics 158
The Classification of Narcotic Analgesics 160
The Problem of Pain 160
Where Opium Is Produced 160
Current Medical Uses of the Narcotic Analgesics 160
Pharmacology of the Narcotic Analgesics 161
Neuroadaptation to Narcotic Analgesics 164
Subjective Effects of Narcotic Analgesics When Used in Medical Practice 165
Complications Caused by Narcotic Analgesics When Used in Medical Practice 166
Fentanyl 167
Buprenorphine 168
II. OPIATES AS DRUGS OF ABUSE 169
The Mystique of Heroin 169
Other Narcotic Analgesics That Might Be Abused 171
Methods of Opiate Abuse 172
Scope of the Problem of Opiate Abuse and Addiction 173
Complications Caused by Chronic Opiate Abuse 175
Medical Complications of Opiate Addiction 176
Overdose of Illicit Opiates 177
Summary 178
15 Hallucinogen Abuse and Addiction 179

History of Hallucinogens in the United States 179
Pharmacology of the Hallucinogens 181
Subjective Effects of LSD 183
Phencyclidine (PCP) 185
Ecstasy (MDMA) 188
Summary 193
16 Abuse of and Addiction to the Inhalants and Aerosols 194

The History of Inhalant Abuse 194
The Pharmacology of the Inhalants 194
Why Are Inhalants So Popular? 196
Method of Administration 197
Subjective Effects of Inhalants 197
Complications From Inhalant Abuse 198
Anesthetic Misuse 199
Abuse of Nitrites 200
Summary 200
17 The Unrecognized Problem of Steroid Abuse and Addiction 201

An Introduction to the Anabolic-Androgenic Steroids 201
Medical Uses of Anabolic Steroids 201
Why Steroids Are Abused 202
Contents xi
The Legal Status of Anabolic Steroids 202

Scope of the Problem of Steroid Abuse 202
Pharmacology of Anabolic-Androgenic Steroids 203
Sources and Methods of Steroid Abuse 203
Understanding the Risks of Anabolic Steroid Abuse 204
Complications of Steroid Abuse 205
Are Anabolic Steroids Addictive? 207
Summary 208
18 The Over-the-Counter Analgesics: Unexpected Agents of Abuse 209

A Short History of the OTC Analgesics 209
Medical Uses of the OTC Analgesics 210
Pharmacology of the OTC Analgesics 212
Normal Dosage Levels of the OTC Analgesics 214
Complications Caused by Use of the OTC Analgesics 215
Overdose of OTC Analgesics 219
Summary 221
19 Tobacco Products and Nicotine Addiction 222

History of Tobacco Use in the United States 222
Pharmacology of Cigarette Smoking 223
The Effects of Nicotine Use 226
Nicotine Addiction 227
Complications of the Chronic Use of Tobacco 228
Smoking Cessation 233
Summary 235
20 Chemicals and the Neonate: The Consequences of Drug Abuse During Pregnancy 236
The Fetal Alcohol Spectrum Disorder 237
Cocaine Use During Pregnancy 239
Amphetamine Use During Pregnancy 242
Opiate Abuse During Pregnancy 242
Marijuana Use During Pregnancy 244
Benzodiazepine Use During Pregnancy 245
Hallucinogen Use During Pregnancy 245
Over-the-Counter Analgesic Use During Pregnancy 247
Inhalant Abuse During Pregnancy 248
Summary 248
21 Gender and Substance Use Disorders 249

Gender and Addiction: An Evolving Problem 249
How Does Gender Affect the Rehabilitation Process? 250
Differing Effects of Common Drugs of Abuse on Men and Women 252
A Positive Note 253
Summary 254
xii Contents
22 Hidden Faces of Chemical Dependency 255

Addiction and the Homeless 255
Substance Use Problems and the Elderly 255
Homosexuality and Substance Abuse 258
Substance Abuse and the Disabled 259
Substance Abuse and Ethnic Minorities 260
Summary 262
23 Chemical Abuse by Children and Adolescents 263

The Importance of Childhood and Adolescence in the Evolution of Substance Use Problems 263
Tobacco Abuse by Children/Adolescents 268
Why Do Adolescents Abuse Chemicals? 269
The Adolescent Abuse/Addiction Dilemma: How Much Is Too Much? 272
Possible Diagnostic Criteria for Adolescent Drug/Alcohol Problems 275
The Special Needs of the Adolescent in a Substance Abuse Rehabilitation Program 277
Summary 277
24 The Dual Diagnosis Client: Chemical Addiction and Mental Illness 279
Definitions 279
Dual Diagnosis Clients: A Diagnostic Challenge 279
Why Worry About the Dual Diagnosis Client? 280
The Scope of the Problem 281
Psychopathology and Drug of Choice 281
Problems in Working With Dual Diagnosis Clients 287
Treatment Approaches 288
Summary 290
25 Codependency and Enabling 291

Enabling 291
Codependency 292
Reactions to the Concept of Codependency 296
Summary 299
26 Addiction and the Family 300

Addiction and Marriage 300
Addiction and the Family 302
The Adult Children of Alcoholics (ACOA) Movement 304
Summary 308
27 The Evaluation of Substance Use Problems 309

The Theory Behind Alcohol and Drug Use Evaluations 309
Screening 310
Assessment 311
Diagnosis 313
Contents xiii
The Assessor and Data Privacy 314

Diagnostic Rules 315
The Assessment Format 316
Other Sources of Information 319
The Outcome of the Evaluation Process 321
Summary 322
28 The Process of Intervention 323

A Definition of Intervention 323
Characteristics of the Intervention Process 324
The Mechanics of Intervention 324
An Example of a Family Intervention Session 326
Intervention and Other Forms of Chemical Addiction 327
The Ethics of Intervention 328
Intervention via the Court System 328
Other Forms of Intervention 330
Summary 331
29 The Treatment of Chemical Dependency 332

A Cautionary Note 332
Characteristics of the Substance Abuse Rehabilitation Professional 332
The Minnesota Model of Chemical Dependency Treatment 334
Other Treatment Formats for Chemical Dependency 335
The Treatment Plan 339
Aftercare Programs 339
Summary 340
30 The Process of Recovery 341

The Decision to Seek Treatment 341
The Stages of Recovery 341
Specific Points to Address in the Treatment of Addiction to Common Drugs of Abuse 345
Summary 350
31 Treatment Formats for Chemical Dependency Rehabilitation 351

Outpatient Treatment Programs 351
Inpatient Treatment Programs 353
Inpatient or Outpatient Treatment? 357
Partial Hospitalization Options 359
Summary 361
32 Relapse and Other Problems Frequently Encountered in Treatment 362

Limit Testing by Clients in Treatment 362
Treatment Noncompliance 362
Relapse and Relapse Prevention 363
Cravings and Urges 367
The “Using” Dream 369
xiv Contents
Controlled Drinking 369

The Uncooperative Client 370
Toxicology Testing 371
The Addicted Person and Sexual Activity 378
The Addicted Patient With Chronic Pain Issues 378
Insurance Reimbursement Policies 379
D.A.R.E. and Psychoeducational Intervention Programs 381
Summary 381
33 Pharmacological Intervention Tactics and Substance Abuse 383

Pharmacological Treatment of Alcohol Use Disorders 383
Pharmacological Treatment of Opiate Addiction 388
Methadone Maintenance 389
Buprenorphine 392
Pharmacological Treatment of Cocaine Addiction 395
Pharmacological Treatment of Marijuana Addiction 395
Pharmacological Treatment of Amphetamine Abuse/Dependence 396
Pharmacological Treatment of Nicotine Dependence 396
Summary 398
34 Substance Abuse/Addiction and Infectious Disease 399

Why Is Infectious Disease Such a Common Complication of Alcohol/Drug Abuse? 399
The Pneumonias 400
Acquired Immune Deficiency Syndrome (AIDS) 401
Tuberculosis 407
Viral Hepatitis 408
Summary 411
35 Self-Help Groups 412

The Twelve Steps of Alcoholics Anonymous 412
The History of Alcoholics Anonymous 412
Elements of AA 413
AA and Religion 414
One “A” Is for Anonymous 415
AA and Outside Organizations 416
The Primary Purpose of AA 416
Of AA and Recovery 418
Sponsorship 418
AA and Psychological Theory 418
How Does AA Work? 419
Outcome Studies: The Effectiveness of AA 419
Narcotics Anonymous 421
Al-Anon and Alateen 422
Support Groups Other Than AA 422
Criticism of the AA/12-Step Movement 425
Summary 426
Contents xv
36 Crime and Drug Use 428

Criminal Activity and Drug Use: Partners in a Dance? 428
Urine Toxicology Testing in the Workplace 430
Unseen Victims of Street Drug Chemistry 431
Drug Analogs: The “Designer” Drugs 432
Some Existing Drug Analogs 433
Adulterants 439
Drug Use and Violence: The Unseen Connection 440
Summary 441
37 The Debate Around Legalization 442

The Debate Over Medicalization 442
The “War on Drugs”: The Making of a National Disaster 443
Summary 451
Appendix One Sample Assessment: Alcohol Abuse Situation 452
Appendix Two Sample Assessment: Chemical Dependency Situation 454
Appendix Three The “Jellinek” Chart for Alcoholism 457
Appendix Four Drug Classification Schedules 458
Appendix Five Modified Centers for Disease Control HIV/AIDS Classification Chart 459
Glossary 460
References 469
Index 537
PREFACE
The world of substance abuse and rehabilitation is al- emerging drugs of abuse, have been added to the ap-
ways evolving. This is often frustrating to students, who propriate chapters. Three new chapters have been in-
wish to find a simple answer that they might regurgitate cluded to the text in recent years. The first explores the
to an examiner, thus earning a passing grade. Unfortu- debate over the relationship between substance abuse
nately, because the world of substance abuse is dy- and criminal behavior, while the second addresses the
namic, many of the “right” answers have yet to be growing debate over the question of legalization. In
discovered. To further complicate matters, there are this chapter, issues such as the difference between
various social, religious, and legal forces that interplay medicalization and full legalization are explored, and
to shape society’s perception of what is, and is not, an questions are raised about how the Constitution has
acceptable drug for social use. This is perhaps most been reinterpreted in light of the “war on drugs.” The
clearly seen in the ongoing debate over marijuana, a issue of how the drugs of abuse affect women has
compound so frightening to society that its use is openly caused a new chapter to evolve specifically to address
discouraged while privately accepted. the question of gender and the addictions.
Change is perhaps the only constant in the world, In the field of addictions, there are few generally ac-
and this is certainly true in the field of addiction treat- cepted answers, a multitude of unanswered questions,
ment. Compounds that were viewed as emerging drugs and compared to the other branches of science, few in-
of abuse just 5 or 6 years ago have faded into obscurity, terdisciplinary boundaries to limit one’s exploration of
while new chemicals emerge that appear to hold the the field. This text has tried to capture the excitement
potential to become the latest trend. Methampheta- of this process while providing an overview of the field
mine is a fine example of this process, for the number of of substance abuse and its rehabilitation.
domestic illicit “labs” involved in the process of pro-
ducing methamphetamine has declined in the past 2
years. In their place are “superlabs” located in Mexico,
Disclaimer
with amphetamine being smuggled into this country to This text was written in an attempt to share the knowl-
replace the supply previously produced in smaller, edge and experience of the author with others inter-
local, illicit laboratories. ested in the field of substance abuse. While every effort
Access to inpatient rehabilitation centers has been has been made to ensure that the information is accu-
further curtailed in the time since the sixth edition of rate, this book is not designed for, nor should it be used
this text appeared. These conditions, plus a virtual ex- as, a guide to patient care. Further, this text provides a
plosion of research into the addictions, their causes, great deal of information about the current drugs of
and their treatment made a new edition of this text im- abuse, their dosage levels, and their effects. This infor-
perative. To keep pace with the world of addictions, mation is reviewed to inform the reader of current
more than 600 changes have been made to this text. trends in the field of drug abuse/addiction and is not in-
New references have been added in every chapter, tended to advocate or encourage the use or abuse of
many of which have been extensively rewritten, while chemicals. Neither the author nor the publisher as-
older, obsolete material has been deleted. New infor- sumes any responsibility for individuals who attempt to
mation on the tryptamines and the phenethylamines, use this text as a guide for the administration of drugs to
families of chemicals that include many potential or themselves, others, or as a guide to treatment.
xvii
xviii Preface
Acknowledgments Kohier, Missouri Baptist University; Paul J. Kowatch,

University of Pittsburgh; Vergel L. Lattimore, Methodist
It would not be possible to mention every person who Theological School in Ohio; Mike Lythgoe, Virginia
has helped to make this book a reality. However, I must Polytechnic Institute and State University; Kate
mention the library staff at Lutheran Medical Center in Mahoney, Kendall College; Jennifer F. Manner, The
La Crosse, Wisconsin, for their continued assistance in College of St. Joseph; J. Barry Mascari, Kean Univer-
tracking down many obscure references, many of sity; A. Zaidy MohdZain, Southeast Missouri State
which have been utilized in this edition of Concepts of University; Frederick A. Newton, California State Uni-
Dependency. versity, San Bernardino; John M. O’Brien, University of
I also thank the following reviewers who offered com- Maine at Augusta; Cynthia J. Osborn, Kent State Uni-
ments and advice on this edition: Louis F. Garzarelli, versity; Susan H. Packard, Edinboro University of
Mount Aloysius College; Debra Harris, California State Pennsylvania; Diane Powers, Colorado School of Pro-
University, Fresno; Robert Hayes, Lewis-Clark State fessional Psychology; Jerome P. Puma, Erie Commu-
College; A. Zaidy MohdZain, Southeast Missouri State nity College; Paul A. Rhoads, Williams College; Rick
University; Susan H. Packard, Edinboro University of Robinson, Southwest Minnesota State University;
Pennsylvania; Billy Slaton, Mercer University; Riley Helen Rosenberg, University of Wisconsin-Parkside;
Venable, Texas Southern University; and Deborah John M. Schibik, Barry University; Laurence Segall,
Wilson, Troy University. Housatonic Community College; Paul Sharpe, Mt. San
In addition, I appreciate the following people who Antonio College; Billy Slaton, Mercer University; Shon
contributed to the Web survey, which provided valu- Smith, Edinboro University of Pennsylvania; Nancy P.
able information: Hubert J. Alvarez, Fresno Pacific Taylor, John Carroll University; Riley H. Venable, Texas
University; Jody Bechtold, University of Pittsburgh; Southern University; and Keeley Weber, Rochester
Lisa Blanchfield, SUNY Institute of Technology; Rob College, Crittenton Hospital.
Castillo, Chicago School of Professional Psychology; Finally, I would also like to again thank my late wife,
Linda Chamberlain, Pasco/Hernando Community Jan, for her patience and her assistance. Until her un-
College; Thomas E. Davis, Ohio University; Perry M. timely death, she happily read each revision of each
Duncan, Old Dominion University; Madeleine A. chapter of each edition.1 She corrected my spelling
Dupre, James Madison University; Cass Dykeman, (many, many times over) and encouraged me when I
Oregon State University; Martha Early, East Carolina was up against the brick wall of writer’s block. Her feed-
University; Julie Ehrhardt, Des Moines Area Commu- back was received with the same openness that any
nity College; Mariellen Fidrych, Boston University, author receives “constructive criticism” about a
Endicott College; Abbe Finn, Florida Gulf Coast Uni- manuscript. But in spite of that fact she persisted with
versity; Louis F. Garzarelli, Mount Aloysius College; her feedback about each edition, and more often than
Westley M. Gillard, Lehman College; Charles Hanna, not she was right. She was indeed my best friend and,
Duquesne University; Debra Harris, California State my “editor in chief.” Hopefully, she would approve of
University, Fresno; Mehrnoosh Hashemzadeh, Whittier this edition of Concepts of Chemical Dependency. Most
College; Bob Hayes, Lewis-Clark State College; Jennifer certainly, I do miss her input.
H. Haywood, Columbus State Community College;
Leeann Jorgensen, St. Cloud State University; Marnie 1
Well, she told me that she was happy to do this for me. . . .
CHAPTER ONE
Why Worry About Recreational

Chemical Abuse?
History suggests that substance abuse has been a social • Between 24% and 31% of patients seen in the emer-
problem for thousands of years (Kilts, 2004). At the be- gency room, and possibly as many as 50% of those
ginning of the 21st century, the substance use disorders patients who suffer severe injuries that require hospi-
are collectively still the most prevalent mental health talization, have an alcohol use disorder (D’Onofrio &
problem facing the United States (Vuchinich, 2002). Degutis, 2004).
But in spite of an ongoing “war” on drug abuse, people • Substance abuse is the number one cause of pre-
still insist on abusing chemicals that change their con- ventable death in the United States, killing more
scious perception of the world (Phillips & Lawton, people each year than any other preventable cause
2004). The face of substance abuse takes many forms: of death (Gold & Jacobs, 2005).
the various alcohol use disorders (AUDs), abuse of pre- • Alcohol use disorders are the third leading cause of
scription medications, and the abuse of various illicit premature death in the United States (Freiberg &
compounds such as marijuana, cocaine, opioids, and Samet, 2005).
the hallucinogens.
The pattern of substance abuse waxes and wanes Recreational drug use is not simply a drain on the
over time. Proponents of the “war on drugs” point to general medical resources of the United States but is a
these trends as evidence that attacking the problem of significant contributing factor to psychiatric problems
substance misuse as a form of criminal behavior is that people experience. For example:
working. Detractors of this policy point to these same
trends as evidence that the “war on drugs” is a dismal • Alcohol or illicit drug abuse is a factor in 50%–75%
failure, and that other approaches to the problem of of all psychiatric admissions (Miller, 2004).
alcohol/drug abuse must be tried. They defend this posi- • Alcohol dependence is the second most common
tion with the observation that in spite of the best efforts psychiatric disorder in the United States (Mariani &
of law enforcement agencies, drugs are freely available Levin, 2004).
throughout this country at levels of purity far above • Between 40% and 60% of those who commit suicide
those seen a half century ago. were intoxicated at the time (Greenfield, 2007).
In this first decade of the 21st century, recreational One-third of suicide victims tested had evidence of
substance abuse is a deeply ingrained aspect of life in alcohol and 10% had evidence of other drugs in
the United States that is intertwined with every other as- their body at the time of their death (Karch, Cosby, &
pect of life. For example, although health care is a so- Simon, 2006).
cial priority, providing health care for the citizens of • Approximately 10% of those individuals with a sub-
this country is complicated by the ongoing problem of stance use disorder eventually commit suicide
chemical abuse: (Getzfeld, 2006).
• Approximately 25% of patients seen by primary care The problem of interpersonal violence has con-
physicians have an alcohol or drug problem (Jones, tributed to untold suffering in the United States for
Knutson, & Haines, 2004). generations. Fully 56% of all assaults are alcohol re-
• Between 20% and 50% of all hospital admissions are lated (Dyehouse & Sommers, 1998). Further, research
related to the effects of alcohol abuse/addiction has found that adults with a substance use disorder
(Greenfield & Hennessy, 2004; McKay, Koranda, & (SUD) were 2.7 times as likely to report having en-
Axen, 2004; Miller, 2004). gaged in the physical abuse of a child and 4.2 times as
1
2 Chapter One
likely to report child neglect as nonusing control sub- and brokering a consultative recommendation when
jects (Ireland, 2001). Approximately 50% of perpetra- alcoholism is the diagnosis” (Westermeyer, 2001, p. 458).
tors of violent crimes in the United States were using An example of the outcome of this neglect is that fewer
alcohol at the time of the offense (Parrott & Giancola, than 50% of patients who go to a physician for alcohol-
2006). Estimates of the percentage of homicide offend- related problems are actually asked about their alcohol
ers who were under the influence of alcohol at the use (Pagano, Graham, Frost-Pineda, & Gold, 2005).
time of the murder range from 28% to 86%1 (Parrott & Further, in spite of the known relationship between sub-
Giancola, 2006). The authors found that illicit drug stance abuse and traumatic injury, alcoholism remains
use in the home increased a woman’s chances of being undetected or undiagnosed by physicians (Greenfield &
murdered by a significant other by 28-fold even if she Hennessy, 2004). In the defense of physicians, note that
was not herself using drugs. a 60-year-old law in many regions allows insurance
The impact of alcohol/drug abuse on the health care companies to deny payment for treatment for trauma
crisis facing the United States in the early years of the patients who are found to have alcohol in their systems,
21st century is not limited to the problem of interper- and knowledge of this causes many physicians not to
sonal violence. For example, the alcohol-related disor- test for alcohol or drugs of abuse in patients who are
ders are, collectively, the third-largest health problems treated for traumatic injuries (Haugh, 2006).
in the United States (Biju et al., 2005). The alcohol/drug Although the benefits of professional treatment of
use disorders are the largest contributing factor to trau- alcohol abuse/addiction have been demonstrated time
matic brain injuries (TBI) in the United States (Miller & and again, many physicians continue to consider alco-
Adams, 2006). Researchers estimate that 29% to 52% of hol and illicit drug use problems to be virtually untreat-
all patients admitted to the hospital for TBI have alco- able, and they ignore research findings suggesting
hol in their systems at the time of admission (Miller & otherwise (Renner, 2004b). Indeed, “more often than
Adams, 2006). Collectively, the substance use disorders not, [the physician will] view the addicted patient as
will touch every individual in the United States either challenging at best and not worthy of customary com-
directly or indirectly. passion” (R. Brown, 2006, p. 5). While postgraduate
training programs for physicians have devoted instruc-
tional time to the treatment of substance use disorders,
Who “Treats” Those Who Abuse the average amount of time devoted to this training was
or Are Addicted to Chemicals? only 8 hours (Renner, 2004b).
In spite of the damage done by alcohol/drug abuse Nor is this diagnostic blindness limited only to
or addiction, only four cents of every dollar spent by physicians. Although nursing professionals frequently
the 50 states is devoted to prevention and treatment of have more contact with patients than do physicians,
substance use problems (Grinfeld, 2001). Nor are the “the majority of nursing schools . . . required only 1 to
various state governments alone in not addressing the 5 clock hours of instruction on alcohol and drug abuse
issue of substance abuse. Nationally, less than one-fifth content during their entire undergraduate curricula”
of the physicians surveyed considered themselves pre- (Stevenson & Sommers, 2005, p. 15). Thus, as a general
pared to deal with alcohol-dependent patients, while rule, nurses are also ill-prepared to work with patients
less than 17% thought they had the skills necessary to with substance use disorders. Marriage/family therapists
deal with prescription drug abusers (National Center also share this lack of preparation in recognizing and
on Addiction and Substance Abuse at Columbia dealing with the substance use disorders. When a sub-
University, 2000). Indeed, at the end of their training, stance use problem within a marriage or family is not
most physicians have a more negative attitude toward uncovered, therapy proceeds in a haphazard fashion.
patients with substance use disorders than they did at Vital clues to a very real illness within the family are
the beginning of their graduate training (Renner, missed, and the attempt at family or marital therapy is
2004b). ineffective unless the addictive disorder is identified and
As a result of this professional pessimism, physicians addressed.
tend to “resist being involved in negotiating a referral In spite of the obvious relationship between substance
abuse and the various forms of psychopathology, “most
1The different estimates reflect different methodologies utilized by the
clinical psychologists are not well prepared to deal with is-
researchers, different sample groups, different definitions of “recent” sues involving substance use or abuse” (Sobell & Sobell,
alcohol use, etc. 2007, p. 2). Fully 74% of the psychologists surveyed
Why Worry About Recreational Chemical Abuse? 3
admitted that they had no formal education in the iden- Estimates of the problem of alcohol use, abuse, and
tification or treatment of the addictions and rate their addiction. Alcohol is popular in the United States, with
graduate school training in the area of drug addiction as an estimated 119 million alcohol users (Office of Na-
inadequate (Aanavi, Taube, Ja, & Duran, 2000). In a tional Drug Control Policy, 2004). For most of these
very real sense, mental health professions have re- people, alcohol is a recreational chemical ingested on
sponded to the problem of substance use disorders with occasion. But between 8 million (Bankole & Ait-Daoud,
a marked lack of attention or professional training. 2005) and 16.27 million (Office of National Drug Con-
trol Policy, 2004) drinkers in the United States are phys-
ically dependent on it, while another 5.6 million abuse
it on a regular basis (Bankole & Ait-Daoud, 2005).
The Scope of the Problem
The discrepancy in the amount of alcohol con-
of Chemical Abuse/Addiction sumed by casual drinkers as compared to problem
Globally, it is estimated that 200 million people, or 5% drinkers might best be seen in the observation that only
of the world’s population, have abused an illicit sub- 34% of the population in this country consumes 62% of
stance at least once (United Nations, 2006a). This is in all of the alcohol produced (Kotz & Covington, 1995).
addition to those who have abused alcohol, which is Approximately 10% of those who drink alcohol on a
legal in most countries. The retail cost of the world’s il- regular basis will become alcohol dependent (Kotz &
licit drug market is estimated at $457 billion, a figure Covington, 1995). The majority of individuals with an
that is larger than the gross domestic product figures of alcohol use disorder (AUD) in the United States are
90% of the world’s countries (United Nations, 2005b). male, with the ratio of male to females with an AUD
Although the population of the United States makes falling between 2:1 and 3:1 (Blume, 1994; Cyr &
up under 5% of the world’s population, by some esti- Moulton, 1993; Hill, 1995; Kranzler & Ciraulo, 2005).
mates we consume 60% of the world’s illicit drugs These figures suggest that significant numbers of
(“Drug War Success Claims Challenged,” 2006). It is women have also developed an AUD. Because alcohol
thought that 35% of men and 18% of women will de- can be legally purchased by adults over the age of 21,
velop some kind of substance use disorder at some many people tend to forget that it is also a drug. How-
point during their lives (Rhee et al., 2003). However, ever, the grim reality is that this “legal” chemical makes
the greater proportion of this number are those who up the greatest part of the drug abuse/addiction prob-
will develop an alcohol use disorder, and only 10.3% of lem in this country.
adults will develop a drug use disorder (Comptom, Estimates of the problem of narcotics abuse and ad-
Thomas, Conway, & Colliver, 2005). Only 2.6% of diction. When many people hear the term “narcotics
adults will become dependent on a drug other than al- addiction,” they immediately think of the heroin use
cohol in their lives (Compton et al., 2005). disorders. Globally, it is estimated that around 10 million
Some of the confusion about substance use disor- people abuse or are addicted to heroin (Milne, 2003).
ders might be seen by the scope of the “war” on drugs. It In the United States, approximately 3 million people
is difficult to justify such an expenditure when the total have probably abused or are addicted to narcotics, and
number of intravenous drug abusers and intravenous currently an estimated 810,000 to 1 million people are
drug addicts in the United States is only an estimated dependent on opiates (Kleber, quoted in Grinfeld,
1.5 million people, or less than 1% of the population of 2001; Jaffe & Strain, 2005). The opiate use disorders
this country (Work Group on HIV/AIDS, 2000). But cost the United States an estimated $21 billion annually
depending on the research study being cited, substance (Fiellin, Rosenheck, & Kosten, 2001).
abuse is/is not a serious problem, is/is not getting worse The states with the greatest concentration of heroin
(or better), will/will not be resolved in the next decade, abusers are (in descending order) California, New York,
and is something that parents should/should not worry Massachusetts, and New Jersey, although this problem is
about. The truth is that large numbers of people use found in every state in the Union (Jaffe & Strain, 2005).
one or more recreational chemicals but that only a Approximately 20% of those who are addicted to opiates
small percentage of people who use them will ulti- are women (Krambeer, von McKnelly, Gabrielli, &
mately become addicted to the chemical(s) being Penick, 2001). Given an estimate of 800,000 heroin-
abused (Peele, Brodsky, & Arnold, 1991). The next sec- dependent persons in the United States, this would
tion provides an overview of the problem of substance mean that there are approximately 160,000 women who
abuse in this country. are addicted to opiates in the United States.
4 Chapter One
In addition to heroin addicts, there is a very large this text speaks of the “problem of hallucinogenic
hidden population of people with an opiate use disor- abuse.” Perhaps 10% of the entire population of the
der in this country: individuals who have regular jobs, United States has abused hallucinogenics at least once
possibly have private health care insurance, and have (Sadock & Sadock, 2003). However, hallucinogenic
opiate use disorder. Fully 76% of illicit drug abusers are use is actually quite rare, and of those young adults who
employed, as are 81% of the binge drinkers and 81% of have used hallucinogenic drugs, only 1% or 2% will
the heavy drinkers in the United States (Lowe, 2004). have done so in the past 30 days, according to the au-
Very little is known about these individuals, who often thors. This suggests that the problem of addiction to
go to great lengths to avoid being identified as having a hallucinogenics is exceedingly rare.
substance use disorder. Some of these individuals Estimates of the problem of tobacco addiction. To-
abuse heroin, while others abuse pharmaceutical opi- bacco is a special product. Like alcohol, it is legally sold
oids obtained/diverted from medical sources. An esti- to adults. Unfortunately, tobacco products are also
mated 2 million episodes of medication misuse in the readily obtained by adolescents, who make up a signifi-
United States occurred in the year 2003 (Miller & cant proportion of those who use tobacco. Researchers
Brady, 2004). An unknown percentage of the individu- estimate that approximately 25% of Americans are cur-
als involved have an opiate use disorder, and many have rent smokers, 25% are former smokers, and the other
never been identified as opiate abusers by authorities. 50% never smoked (Sadock & Sadock, 2003). An esti-
Thus, the estimated 810,000 to 1 million intravenous mated 24 million smokers in the United States are
heroin addicts must be accepted only as a minimal esti- male, and 22.3 million are female.
mate of the narcotics abuse/addiction problem in the
United States.
Estimates of the problem of cocaine abuse and addic-
tion. Cocaine abuse in the United States peaked in the
The Cost of Chemical Abuse/Addiction
mid-1980s, but cocaine still remains a popular drug of
in the United States
abuse. Globally, an estimated 15 million people abuse Although the total number of people in this country
or are addicted to cocaine, the vast majority of whom who abuse or are addicted to recreational chemicals is
are thought to live in North America (Milne, 2003). In limited, recreational substance use still extracts a
contrast to this estimate, Grinfeld (2001) estimated that terrible toll from society. The combined annual cost of
there were 2.5 million cocaine addicts in the United alcohol and drug use disorders in the United States
States. alone is estimated to be at least $375 billion2 (Falco,
Surprisingly, in spite of its reputation as an addictive 2005). Cigarette smoking is the primary cause of death
substance, only a fraction of those who use cocaine ever for 420,000 to 440,000 people each year in the United
actually become addicted to it. Researchers now be- States, while an additional 35,000 to 56,000 nonsmokers
lieve that only between 3% to 20% of those who have die each year as a result of their exposure to secondhand
used cocaine will go on to become addicted to this sub- cigarette smoke (Benson & Sacco, 2000; Bialous &
stance (Musto, 1991). Other researchers have suggested Sarna, 2004; Mokdad, Marks, Stroup, & Gerberding,
that only 1 cocaine user in 6 (Peele, Brodsky, & Arnold, 2004). Each year, an estimated 100,000 (Fleming,
1991) to 1 in 12 (Peluso & Peluso, 1988) was actually Mihic, & Harris, 2001; Naimi et al., 2003; Small, 2002)
addicted to the drug. to 200,000 (Biju et al., 2005) die from alcohol-related
Estimates of the problem of marijuana abuse/addiction. illness or accidents. But this figure is misleading, as al-
Marijuana is the most commonly abused illegal drug cohol contributes to some 60 different diseases (Room,
in the United States (Kaufman & McNaul, 1992) as Babor, & Rehm, 2005). When these additional deaths
well as Canada (Russell, Newman, & Bland, 1994). It are correctly attributed to the individual’s alcohol use
is estimated that approximately 25% of the entire popu- problem, it becomes clear that each year on this planet,
lation of the United States, or more than 70 million alcohol causes as many deaths or disabilities as does to-
people, have used marijuana at least once. Of this bacco (Room et al., 2005).
number, approximately 3 million are thought to be ad-
dicted to marijuana (Grinfeld, 2001). 2The various statistics concerning the cost of alcohol/drug use disor-
Estimates of the problem of hallucinogenic abuse. As ders will vary, depending on the methodology utilized in each study.
with marijuana, there are questions as to whether one Thus, different research might arrive at very different conclusions
may become addicted to hallucinogenics. For this reason, about the scope and cost of the same problem.
Why Worry About Recreational Chemical Abuse? 5
There are many contradictions in the field of addic- whose alcohol use has contributed at least in part to
tions treatment. For example, the annual drug-related their need for placement in a nursing home (Schuckit,
death toll including drug-related infant deaths, overdose- 2006). Many of these nursing home beds are supported,
related deaths, suicides, homicides, motor vehicle acci- at least in part, by public funds, making chronic alcohol
dent deaths, and the various diseases associated with abuse a major factor in the growing cost of nursing
drug abuse in the United States is estimated to be be- home care for the elderly.
tween 12,000 (Miller & Brady, 2004) and 17,000 people It was estimated that alcohol-related vehicle and
a year (Donovan, 2005; Mokdad et al., 2004). However, property destruction costs total $24.7 billion a year in
even this number is still just one-sixteenth as many the United States (Craig, 2004), with alcohol being a
people as are thought to die as a result of just tobacco factor in approximately 40% of all fatal motor vehicle
use each year in this country, yet tobacco remains legal accidents. Alcohol abuse is thought to be a factor in
for individuals over the age of 21 to purchase. 25% to 60% of all accidents resulting in traumatic in-
There are many hidden facets to the annual impact juries (Dyehouse & Sommers, 1998). The individuals
of SUDs in the United States. Between 20% and 40% of involved will require medical treatment. Ultimately,
patients being treated at the average urban hospital, for this medical treatment is paid for by the public in the
example, are being treated for diseases caused/exacer- form of higher insurance costs and higher taxes. In-
bated by their alcohol use disorder (Greenfield, 2007; deed, alcohol use disorders are thought to account for
Mersey, 2003). Over 70% of patients admitted to a 15% of the money spent for health care in the United
major trauma center had evidence of alcohol/illicit States each year (Schuckit, 2000). Yet in spite of the
drugs in their bodies at the time of hospitalization pain and suffering that alcohol causes each year, only
(Cornwell et al., 1998). Yet the role of alcohol/drugs in 5% (Prater, Miller & Zylstra, 1999) to 10% of alcohol-
causing or helping to cause these injuries is often not dependent individuals are ever identified and referred
included in estimates of the financial cost of SUDs to a treatment program (Wing, 1995).
each year in this country. The cost of tobacco use. Although it is legally pro-
The cost of alcohol abuse. Globally, alcohol use is a duced and might be consumed by adults without legal
factor in 10% to 11% of all diseases or deaths each year problems, tobacco use extracts a terrible cost. Globally,
(Stevenson & Sommers, 2005). In the United States, it more than 3 million people die each year as a result of
is estimated that 85,000 to 140,000 people lose their smoking-related illness; 435,000 of these live in the
lives annually because of alcohol use/abuse/addiction United States (Mokdad et al., 2004; Patkar, Vergare,
(Mokdad et al., 2004). In the United States alone, the Batka, Weinstein, & Leone, 2003). In this country
annual economic cost of alcohol abuse/addiction is tobacco-related illness acounts for 60% of direct health
thought to cost society $185 billion a year, of which care costs, and one in every five deaths can be traced to
$26 billion is for direct health care costs and an esti- smoking-related disease (Sadock & Sadock, 2003).
mated annual economic loss of $37 billion as a result of The cost of illicit substance abuse. A number of fac-
alcohol-related premature death (Belenko, Patapis, & tors must be included in any estimate of recreational
French, 2005; Petrakis, Gonzalez, Rosenheck, & Krystal, drug use in the United States, including the estimated
2002; Smothers, Yahr, & Ruhl, 2004). On a more per- financial impact of premature death or illness caused
sonal level, alcohol use disorders are estimated to cost by substance abuse, lost wages from those who lose
every man, woman, and child in the United States $638 their jobs as a result of substance abuse, the financial
each year (Grant et al., 2006). losses incurred by victims of drug-related crimes, and
The annual cost of alcohol-related lost productivity the expected costs of drug-related law enforcement ac-
in the United States alone is estimated at between tivities, among others. With this in mind, researchers
$67.7 billion a year (Craig, 2004) and $138 billion a have suggested that the annual economic cost of recre-
year (Brink, 2004). Collectively, the alcohol use disor- ational chemical use in the United States is approxi-
ders consume 15% to 25% of the total annual health mately $383 per person (Swan, 1998). The total annual
care expenditure in the United States (Anton, 2005; economic impact of illicit chemical use/abuse in the
Swift, 2005). Although only 5% to 10% of the general United States is estimated at between $168 billion
population has an alcohol use problem, they use a dis- (Belenko, Patapis, & French, 2005) and $276 billion a
porportionate amount of health care resources in this year (Stein, Orlando, & Sturm, 2000). No matter which
country. Further, between 15% and 30% of the nursing of these estimates you accept as being the most accu-
home beds in this country are occupied by individuals rate, it is clear that drug abuse is an expensive luxury.
6 Chapter One
Drug use as an American way of life. Notice that in failed to point out that only 5.5 million Americans (or
the last paragraph drug abuse was identified as a “lux- about 2% of the then-current population of approxi-
ury.” To illustrate how we have, as a nation, come to mately 260 million) was addicted to illegal drugs
value recreational chemical use, consider that money (Holloway, 1991).
spent on illicit recreational chemicals is not used to buy It is not the goal of this text to advocate substance use,
medical care, food, shelter, or clothing for people in the but there are wide discrepancies between the scope of
United States, but simply on illegal chemicals that are recreational drug use as reported in the mass media and
used for personal pleasure. that reported in the scientific research. For example,
In conclusion, there is no possible way to fully esti- Wilens (2004a) suggested that between 10% and 30% of
mate the personal, economic, or social impact that these the adults in the United States have a substance use dis-
various forms of chemical addiction have had on soci- order of some kind. In contrast to this estimate, other re-
ety. The cumulative economic impact of medical costs, searchers have suggested that only a small percentage of
lost productivity, and the indirect costs of “hidden” the U.S. population is using illicit chemicals. Given
drug abuse and addiction make the SUDs a significant these wide discrepancies, it is difficult to reach any con-
contributing factor to the cost of health care in the clusion but that much of what has been said about the
United States. drug abuse “crisis” in the United States has been tainted
by misinformation, or disinformation. To understand the
problem of recreational chemical use/abuse, it is neces-
sary to look beyond the “sound bytes” or the “factoids” of
Why Is It So Difficult to Understand the the mass media and the politicians.
Drug Abuse Problem in the United States?
For the past two generations, politicians have spoken
Summary
about society’s war on drug use/abuse. One of the basic
strategies of this ongoing war has been the exaggeration It has been estimated that at any time, between 2% and
of the dangers associated with chemical use (King, 10% of American adults either abuse or are addicted to
2006). This technique is known as disinformation, and illegal drugs. While this percentage would suggest that
it seems to have been almost an unofficial policy of the large numbers of people are using illicit chemicals in
government’s antidrug efforts to distort and exaggerate this society, it also implies that the drugs of abuse are not
the scope of the problem and the dangers associated universally addictive. It was also suggested in this chap-
with recreational drug use. As Szalavitz (2005) ob- ter that the various forms of chemical abuse/addiction
served: “[e]ntire government bureaucracies—from the reflect different manifestations of a unitary disorder:
U.S. Drug Enforcement Administration and the drug chemical abuse/addiction. Finally, although drug ad-
tsar to state police and prosecutors” have invested a diction is classified as a “disease,” most physicians are
great deal of time and energy to convince us that “expo- ill-prepared to treat substance-abusing patients.
sure to corrupting substances inevitably causes addic- In this chapter we have examined the problem of
tion and death” (p. 19). recreational drug use and its impact on society. In later
For generations, the media have presented drugs in sections of this book we will find detailed information
such a negative light that “anyone reading or hearing of on the various drugs of abuse, their effects on the user,
them would not be tempted to experiment with the the consequences of their use, and information on the
substances” (Musto, 1991, p. 46). Unfortunately, such rehabilitation process for those who are abusing or ad-
scare tactics have not been found to work. For example, dicted to chemicals. This information should help you
in the mid-1980s, the media presented report after regain a better understanding of the problem of recre-
port of the dangers of chemical addiction yet consistently ational substance use in this country.
CHAPTER TWO
Statement of the Problem

of Substance Use Disorders
Why do people abuse chemicals? This question can be tic society, the person fails to receive clear guidance
examined from a number of different perspectives. on how to cope with the temptations inherent in
Biologists now believe that at least some mammals these chemically induced pleasures. On some levels,
seem to have a inborn predisposition to seek out com- people are even encouraged to seek out socially sanc-
pounds, such as apples that have fallen to the ground tioned chemicals to alter their perspective of reality.2
and fermented, that can alter the user’s perception of For a variety of reasons, drugs of abuse have become
the world. Anybody who has ever seen a flock of birds part of our environment. The prevailing atmosphere of
that have raided an apple orchard to ingest partially chemical use or abuse then forces each of us to make a
fermented apples in the late fall, or a cat seek out decision to use or not use recreational chemicals every
“catnip,” can attest to this. It is now thought that hu- day. Admittedly, for most of us, this choice is relatively
mans share this urge with other mammals: We are simple and probably did not even require conscious
driven to find ways to alter our perspective of the real- thought. But regardless of whether the individual ac-
ity around us. knowledges the need to make a decision, he or she is
Behavioral scientists now understand that various faced with the opportunity to use recreational chemi-
chemicals play different roles within the social context, cals each day and the decision of whether to engage in
such as facilitating bonding activities, heightening reli- recreational drug abuse.
gious services, or serving as a means of rebellion. On Although some people might challenge the impli-
the individual level, chemicals might to allow the in- cation that substance use disorders reflect an element
dividual to express forbidden impulses, to cope with of personal choice, there is a grim logic to the state-
overwhelming pain or anxiety, to experience eupho- ment made in the last paragraph. Stop for an instant,
ria and pleasure, or to escape from negative affective and think: Where is the nearest liquor store? If you
states such as depression, physical pain, or posttrau- wanted to do so, where could you buy some marijuana?
matic stress disorder. In some cases, individuals are If you are above the age of about 15, the odds are very
able to concentrate better after abusing a compound; good that you could answer either of these questions.
in other cases, they seek to escape from themselves But why didn’t you buy any of these chemicals on
for awhile, as when attempting to avoid intrusive your way in to work or to school this morning? Why did
memories from the past. you, or didn’t you, buy a recreational drug or two on
On the individual level, which is to say within the your way home last night? The answer is that you (we
realm of psychology or the medical sciences, some- hope) made a decision not to do so. It is a matter of
one is viewed as abusing a drug because the com- choice.
pound in question is able to induce a sense of One arena in which individual choice is evalu-
pleasure or perhaps even intense euphoria that is im- ated and poor choices punished is the legal system.
portant to the person. Through the process of behav- From the perspective of the legal system, the individ-
ioral conditioning, the individual comes to desire this ual is viewed as abusing a drug because she or he is a
experience again and again. When the seeds of the
addiction are planted, motivation for abusing that 1Or dysphoria.
chemical might switch from the desire for euphoria 2Before you argue against this statement, consider the case of caf-
to the attempt to avoid the opposite1 induced by the feine: How many of us would care to face life’s trials and tribulations
withdrawal from that compound. Living in a hedonis- without that first cup or two of coffee in our system?
7
8 Chapter Two
criminal. Since the use of these compounds outside of thus becomes a behavior with a number of possible inter-
strictly defined limits3 is, by definition, illegal, the individ- mediate steps between the two extreme points of total ab-
ual who elects to abuse a drug is choosing to engage in a stinence and physical addiction, not a “condition” that
criminal act. It is a matter of choice for which the individ- either is or is not present. For the purpose of this text,
ual is held accountable by the standards of that society. we will view the phenomenon of recreational alcohol/
Thus, the answer to the question of why people drug use along the continuum in Figure 2.1.
abuse certain chemicals depends on the perspective of This continuum, like all such tools, is an artificial
the person viewing the problem. In the next three chap- construct. The points along this scale are the following:
ters the problem of the SUDs will be examined from Level 0: Total abstinence: Individuals whose substance
the perspective of the medical sciences and the behav- use falls in this category abstain from all alcohol/drug
ioral sciences, and as a manifestation of a spiritual disor- abuse and would present no immediate risk for sub-
der. In this chapter, the parameters of the problem of stance use problems (Isaacson & Schorling, 1999).
SUDs are examined, and some of the factors that sup- Level 1: Rare/social use: This level would include ex-
port such disorders in spite of social and medical prohi- perimental use of a chemical, and individuals whose sub-
bitions are explored. stance use falls in this category would present a low risk
for the development of an SUD (Isaacson & Schorling,
1999). They would not experience any of the social,
The Continuum of Chemical Use financial, interpersonal, medical, or legal problems that
It is surprising how often people confuse chemical use are the hallmark of the pathological use of chemicals.
with abuse and addiction. Indeed, these terms are often Further, such individuals would not demonstrate the
mistakenly used as if they were synonymous, even in loss of control over their chemical use that is found at
clinical research studies (Minkoff, 1997). In reality, any higher levels of the continuum, and their chemical use
definition of addiction must take into account the fact would not result in any danger to their lives.
that “drug use is considered a normal learned behavior Level 2: Heavy social use/early problem drug use: In-
that falls along a continuum ranging from patterns of dividuals whose substance use falls in this category are
little use and few problems to excessive use and depend- in the “gray area” between social use and clear-cut
ence” (Budney, Sigmon, & Higgins, 2003, p. 249). problem use. This is because there is no clear consen-
Cattarello, Clayton, and Leukefeld (1995) have iden- sus on what constitutes normal use as opposed to abuse
tified five different patterns of recreational chemical use: of even our oldest recreational chemical: alcohol
(a) total abstinence; (b) a brief period of experimentation (Cooney, Kadden, & Steinberg, 2005). People whose
followed by a return to abstinence; (c) irregular, or occa- chemical use falls at this point in the continuum would
sional, use of illicit chemicals; (d) regular use of chemi- use chemicals in such a way as to (a) be clearly above
cals, and (e) the pathological or addictive pattern of use the norm for society, and/or (b) begin to experience var-
that is the hallmark of the substance use disorders. Unfor- ious combinations of legal, social, financial, occupa-
tunately, there are no firm boundaries between the points tional, and personal problems associated with chemical
on a substance use continuum (Sellers et al., 1993). Only use. They could be classified as being “at risk” for a sub-
the end points, total abstinence and the active physical stance use disorder (Isaacson & Schorling, 1999) or of
addiction to a chemical(s), remain relatively fixed. becoming “problem drinkers.”
One very real advantage of a drug use continuum is Individuals in this category are more numerous than
that it allows for the classification of various intensities those who are clearly addicted to chemicals. For example,
and patterns of substance use. Drug use/abuse/addiction Comptom, Thomas, Conway, and Colliver (2005)
concluded that while 10.3% of adults will develop a
3As when a physician prescribes a controlled substance to a patient for drug use disorder at some point in their lives, only 2.6%
the control of pain, for example. The prescription provides an exemp- of all adults will become dependent on a drug other
tion to the legal sanction that the use of the narcotic is against the law, than alcohol. Thus, not everybody whose substance use
and thus punishable. might fall within this category would automatically
The use of alcohol is sanctioned within certain limits as well: progress to an addictive disorder. Still, at this level, one
Drinkers must be above a certain age, and if they elect to use alcohol,
they must do so in a controlled manner to avoid legal sanctions for be-
begins to see signs that the individual attempts to hide
haviors under the influence of alcohol such as driving a motor vehicle or deny the problems that develop as a result of his or
with a blood alcohol level greater than a certain level. her substance abuse.
Statement of the Problem of Substance Use Disorders 9
0 1 2 3 4
Total abstinence Rare/social use Heavy social Heavy problem Clear addiction to drugs
from drug use of drugs use/early problem use/early addiction
use of drugs to drugs
FIGURE 2.1 The Continuum of Recreational Chemical Use
Level 3: Heavy problem use/early addiction: Here, associated with his or her alcohol or drug use. More
alcohol or chemical use has reached the point that than one elderly alcoholic, for example, has tried to ex-
there clearly is a problem. Indeed, people at this stage plain away an abnormal liver function as being the af-
may have become physically addicted to chemicals, termath of a childhood illness. However, to an impartial
although they may argue this point.4 Individuals outside observer, the person at this level clearly is ad-
whose chemical abuse falls at this level have started to dicted to alcohol or drugs.
experience medical complications associated with Admittedly, this classification system, like all others,
their chemical use, as well as classic withdrawal symp- is imperfect. The criteria used to determine where on
toms when they are deprived of drugs/alcohol. Isaac- the continuum an individual might fall are arbitrary
son and Schorling (1999) classified individuals at this and subject to discussion. Further, there are no clear
level as engaging in “problem use.” They are often points of demarcation between, for example, heavy sub-
preoccupied with their drug of choice and have lost stance abuse and the addictive use of that same chemi-
control over their chemical use (Brown, 1995; Gordis, cal (Jaffe & Anthony, 2005). Physical addiction to a
1995). They are in the early stages of an addiction to a chemical is just one point on a continuum of drug use
compound. Categories 3 and 4 would include the 40 styles that ranges from total abstinence through the var-
million alcohol abusers in the United States identified ious forms of occasional substance use, to the extreme
by Shute and Tangley (1997), for example. of physical dependence on that substance to avoid
Level 4: Middle to late stage addiction: At this point withdrawal symptoms.
on the continuum, people demonstrate all the symp-
toms of the classic addiction syndrome, in combination
Why Do People Abuse Chemicals?5
with multiple social, medical, legal, financial, occupa-
tional, and personal problems that are the hallmark of At first, this question might seem rather simplistic.
an alcohol/drug dependency. People whose chemical People use drugs because the drugs of abuse make
use falls at this point in the continuum would clearly them feel good; and because they do, some people wish
have the physical disorder of alcohol/drug dependency to repeat the experience. As a result of this continual
(Minkoff, 1997). search for drug-induced pleasure, the drugs of abuse
Surprisingly, even at this level on the continuum, have become part of our environment. The prevailing
an individual might try to rationalize or deny problems atmosphere of chemical use or abuse then forces each
4“I can quit any time I want to!” is a common statement heard by 5
This question is a reference not to those people who are addicted
health care professionals and chemical dependency counselors when to chemicals but to those who abuse chemicals for recreational
they meet a client whose substance use is at this level. purposes.
10 Chapter Two
of us to make a decision to use or not use recreational this context, it should not be surprising to learn that
chemicals every day. Admittedly, for most of us, this since many people find the effects of the drugs of
choice is relatively simple. Usually the decision not to abuse6 to be pleasurable, they will be tempted to use
use chemicals did not even require conscious thought. them again and again. But the reward potential of a
But regardless of whether the individual acknowledges chemical substance, while a powerful incentive for its
the need to make a decision, each person is faced with repeated use, is not sufficient in itself to cause addiction
the opportunity to use recreational chemicals each day (Kalivas, 2003).
and the decision of whether to engage in recreational The social learning component of drug use. Individu-
drug abuse. So, in one sense, the answer to the question als do not start life expecting to abuse chemicals.
of why people use the drugs of abuse is because they Rather, the alcohol/drug abuser must (a) be taught that
choose to do so. But there are a number of factors that substance use is acceptable, (b) recognize the effects of
influence the individual’s decision to use or not use the chemical, and (c) interpret them as desirable. All of
recreational chemicals. these tasks are accomplished through the process of so-
cial learning, which takes place through peer groups,
Factors That Influence Recreational mass media, familial feedback, and other ways (Cape,
Drug Use 2003). Marijuana abuse provides a good illustration of
The pharmacological reward potential. One factor that this process. First-time marijuana users must be taught
influences the individual’s decision to use alcohol/drugs by their drug-using peers (a) how to obtain and smoke
is anticipation that the drug will have pleasurable effects. marijuana, (b) how to recognize the effects of the drug,
Researchers call this the “pharmacological reward and (c) why marijuana intoxication is so pleasurable
potential” of the compound being abused (Budney, (Kandel & Raveis, 1989).
Sigmon, & Higgins, 2003; Kalivas, 2003; Monti, Kad- The same learning process takes place with the
den, Rohsenow, Cooney, & Abrams, 2002; O’Brien, other drugs of abuse such as alcohol (Monti et al.,
2006). The reward potential of different chemicals 2002). It is not uncommon for a novice drinker to be-
varies in response to differences in their chemical struc- come so ill after a night’s drinking that she or he will
ture and route of administration. Not surprisingly, those swear never to drink again. However, more experienced
compounds that lend themselves to rapid onset of action drinkers will help the novice learn such things as how
have the highest reward potential, and thus the greatest to drink, what effects to look for, and why these alcohol-
potential for abuse (O’Brien, 2006). Since the most induced physical sensations are so pleasurable. This
popular drugs of abuse share the characteristic of rapid feedback is often informal and comes through a variety
onset of action, it is possible to understand how the of sources such as a “drinking buddy,” newspaper
principles of operant conditioning might apply to the articles, advertisements, television programs, conversa-
phenomenon of drug abuse/addiction (Budney et al., tions with friends and co-workers, casual observations
2003). of others who are drinking, and so on. The outcome of
The basic laws of behavioral psychology hold that if this social learning process is that the novice drinker is
something (a) increases the individual’s sense of pleas- taught how to drink and how to enjoy the alcohol he or
ure or (b) decreases his or her discomfort, then she or she consumes.
he is likely to repeat that behavior. This process is Individual expectations as a component of drug use.
called reward process. In contrast to the reward process, The individual’s expectations for a drug have been found
if a certain behavior (c) increases the individual’s sense to be a strong influence on how that person interprets the
of discomfort or (d) reduces the person’s sense of pleas- effects of that chemical. These expectations evolve in
ure, he or she is unlikely to repeat that behavior. This childhood or early adolescence as a result of multiple
is called the punishment potential of the behavior in factors, such as peer group influences, the child’s expo-
question. Further, immediate consequence (either sure to advertising, parental substance use behaviors,
reward or punishment) has a stronger impact on behav- and mass media (Cape, 2003; Monti et al., 2002). To il-
ior than delayed consequence. When these rules of be- lustrate this process, consider the individual’s expections
havior are applied to the problem of the SUDs, one
discovers that the immediate consequences of chemical 6Obviously, the OTC analgesics are exceptions to this rule since they
use (that is, the immediate pleasure) has a stronger im- do not cause the user to experience “pleasure.” However, they are in-
pact on behavior than the delayed consequences (i.e., cluded in this text because of their significant potential to cause
possible disease at an unspecified later date). Within harm.
for alcohol. Research has shown that these are most influences, and (e) the context within which alcohol/
strongly influenced by the context in which the individ- drugs are used. At each of these levels, factors such as
ual uses alcohol and by his or her cultural traditions, the availability of recreational substances, combined
rather than the pharmacological effects of the alcohol with prevailing attitudes and feelings, govern the indi-
consumed (Lindman, Sjoholm, & Lang, 2000; Sher, vidual’s use of mood-altering chemicals (Kadushin,
Wood, Richardson, & Jackson, 2005). Reber, Saxe, & Livert, 1998; Westermeyer, 1995).
The individual’s expectations about the effects of a Given the impact of these social forces on the indi-
drug play a powerful role in shaping the person’s vidual’s substance use behavior, it is not surprising to
drug/alcohol use behavior (Blume, 2005). For example, learn that in “cultures where use of a substance is com-
it has been found that those individuals who were most fortable, familiar, and socially regulated both as to style
likely to abuse MDMA (ecstasy) at dances were more of use and appropriate time and place for such use, ad-
likely to anticipate gaining self-knowledge and less likely diction is less likely and may be practically unknown”
to expect negative consequences from the abuse of this (Peele, 1985, p. 106). Unfortunately, in contrast to the
compound (Engels & ter Bogt, 2004). In the case of rapid rate at which new drug use trends develop, cul-
LSD, the individual’s negative expectations are a signifi- tural guidelines concerning chemical use might require
cant factor in the development of a “bad trip.” Novice generations or centuries to develop (Westermeyer,
LSD users are more likely to anticipate negative conse- 1995).
quences from the drug than are more experienced users. An interesting transition is emerging from the Jewish
This anxiety seems to help set the stage for the negative subculture, especially in the ultraorthodox sects. Only
drug experience known as the “bad trip.” certain forms of alcohol are blessed by the local rabbi as
For the most part, an individual’s expectations about having been prepared in accordance to Jewish tradition
the effects of alcohol/drugs are not static or unchang- and thus are considered “kosher.” Recreational drugs,
ing. Admittedly, in some cases the individual’s expecta- on the other hand, are not considered “kosher” and
tions about the use of a specific drug are so extremely are forbidden (Roane, 2000). Yet younger generations
negative that she or he will not even contemplate the explore new behaviors and come into contact with
use of that compound. This is often seen in cases where outside cultures, many of them are turning toward ex-
a person grew up with a violent, abusive alcoholic parent perimental use of the “unclean” chemicals. Signifi-
and subsequently made a vow never to use alcohol. This cant numbers of these individuals are becoming
is an extreme adaptation to the problem of personal alco- addicted to recreational chemicals in spite of reli-
hol use, but it is not uncommon. But in the typical case, gious sanctions against their use, in large part be-
individual expectations about alcohol/drugs can be cause their culture and education failed to warn them
modified by both personal experience and social feed- of the addictive powers of these compounds (Roane,
back systems. For example, if an adolescent with initial 2000).
misgivings about drinking found alcohol’s effects to be In the Italian-American subculture, drinking is lim-
pleasurable or was rewarded with a degree of social ac- ited mainly to religious or family celebrations, and ex-
ceptance, she or he would be more likely to continue to cessive drinking is strongly discouraged. The “proper”
use alcohol (Smith, 1994). Thus, after his or her first (i.e., socially acceptable) drinking behavior is modeled
use of a recreational chemical, the individual’s precon- by the adults during religious or family activities, and
ceptions are reassessed in light of personal experience there are strong familial and social sanctions against
and social feedback. those individuals who do not follow these rules. As a re-
Cultural/social influences on chemical use patterns. sult of this process of social instruction, the Italian-
Human beings are social animals. A given individual’s American subculture has a relatively low rate of
decision to use or not use a recreational chemical is alcoholism.
made within the context of his or her community and Another example of the impact of social group affili-
the social group or groups to which she or he belongs ation on substance use patterns might be seen in the
(Monti et al., 2002; Rosenbloom, 2000). use of alcohol by various Native American tribes. As a
There are five ways in which the individual’s cultural group, Native Americans have a rate of alcohol use dis-
heritage might impact his or her chemical use (Pihl, orders (AUDs) that is 2.4 times that seen in the general
1999): (a) the general cultural environment, (b) the spe- population (Cook & Wall, 2005). But under the um-
cific community in which the individual lives, (c) sub- brella of the term Native Americans are various tribes
cultures within the specific community, (d) family/peer that significantly differ in the prevalence of AUDs
12 Chapter Two
(Cook & Wall, 2005). Two different tribal groups from

different cultures might inhabit the same general geo- Culture
graphic area but have vastly different patterns of alcohol
use/abuse.
The reader will notice that for the most part, the dis- Individual social groups
within parent culture
cussion has been limited to the use of alcohol in this
section. This is because alcohol is the most common
recreational drug used in the United States. However,
this is not always true for other cultural groups. For
example, the American Indians of the Southwest fre-
quently will ingest mushrooms with hallucinogenic po-
tential as part of their religious ceremonies. In many
cultures in the Middle East alcohol is prohibited, but FIGURE 2.2 The Relationship Between Different
the use of hashish is either quite acceptable, or at least Subgroups and the Parent Culture
tolerated. In both cultures, strict social rules dictate
when these substances might be used, the conditions
under which they might be used, and the penalties for
change. A flow chart of the decision-making process
unacceptable substance use.
to use or not use alcohol or drugs might look some-
The point to remember is that cultural rules pro-
thing like Figure 2.3.
vide the individual with a degree of guidance about
Note, however, that we are discussing the individ-
acceptable/unacceptable substance use. But within
ual’s decision to use alcohol or drugs on a recreational
each culture, there are various social groups that may
basis. People do not plan to become addicted to alcohol
adopt the standards of the parent culture to only a
or drugs. It is now accepted that the factors that initiate
limited degree. The relationship between different
chemical use are not the same factors that maintain
social groups and the parent culture is shown in
chemical abuse (Zucker & Gomberg, 1986). For
Figure 2.2.
example, a person might begin to abuse narcotic anal-
Individual life goals as helping shape chemical use.
gesics because these chemicals help him or her deal
Another factor that influences the individual’s decision
with painful memories. However, after that individual
to either begin or continue the use of chemicals is
has become physically addicted to the narcotics, fear of
whether the use of a specific drug or drugs is consistent
withdrawal may be one reason for continuing to use the
with his or her long-term goals or values. This is rarely a
drugs.
problem with socially approved drugs, such as alcohol,
and, to a smaller degree, tobacco. But consider the
example of a junior executive who smokes and has just
What Do We Mean When We Say
won a much hoped for promotion, only to find that the
new position is with a division of the company with a
Someone Is “Addicted” to Chemicals?
strong “no smoking” policy. Surprisingly, there is no single definition of addiction to
In this hypothetical example, the executive might alcohol/drugs. The definitions of such terms as sub-
find that giving up the habit of smoking is not as seri- stance abuse or addiction are quite arbitrary (O’Brien,
ous a problem as she or he had once thought, if this 2006). A generation ago, George Vaillant (1983) sug-
was part of the price for the promotion. In such a gested that “it is not who is drinking but who is watch-
case, the individual has evaluated the issue of ing” (p. 22, italics added for emphasis) that defines
whether further use of that drug (tobacco) is consis- whether a given person is alcohol dependent. The
tent with his or her life goal of a major administrative same is true for the use of the other drugs of abuse. In
position with a large company. However, there are the final analysis, a diagnosis of a SUD reflects a profes-
also many cases when the individual in question has sional opinion of one individual.
elected to search for a new position rather than to ac- Such a professional opinion might be aided by a list of
cept the restriction on his or her cigarette use. In such standardized diagnostic criteria, such as those outlined in
a case, the individual would have considered the pro- the American Psychiatric Association’s (2000) Diagnostic
motion and weighed the cost of giving up cigarettes and Statistical Manual of Mental Disorders—TR (4th
against the benefits of not making a major lifestyle edition—Text Revision, or DSM-IV-TR). According to the
Does person choose to use drugs at this time?
No
Yes
Was chemical Person decides not to use

use rewarding? No drug again in near future
Yes
Is there social reinforcement Person decides not to use

for further drug use? No drug again in near future
Yes
Is drug use consistent Person decides not to use

with life goals? No drug again in near future
Yes
Person abstains from use of drug
in question. Must make daily
Continued drug use decision to use or to not use.
FIGURE 2.3 The Chemical Use Decision-Making Process
DSM-IV-TR, these are some of the signs of alcohol/drug Any combination of four or more of these signs is used
addiction: to identify the individual who is said to suffer from the
“disease” of addiction.
1. Preoccupation with use of the chemical between pe-
riods of use.
2. Using more of the chemical than had been antici- Definitions of Terms Used in This Text
pated.
Social use: Currently, only alcohol use is acceptable in a
3. The development of tolerance to the chemical in
social setting as long as the use of the compound in ques-
question.
tion is limited to that social setting, and within the limits
4. A characteristic withdrawal syndrome from the
established by the culture in which the individual lives.7
chemical.
Substance abuse: Takes place when an individual is
5. Use of the chemical to avoid or control withdrawal
using a drug with no legitimate medical need to do so
symptoms.
or in excess of accepted social standards (Schuckit,
6. Repeated efforts to cut back or stop the drug use.
2006). Thus, the definition of substance abuse is based
7. Intoxication at inappropriate times (such as at work)
on current social standards. One who abuses a chemi-
or when withdrawal interferes with daily functioning
cal might be said to have made poor choices regarding
(hangover makes a person too sick to go to work, for
use of that substance, but she or he is not addicted to
example).
the chemical (Minkoff, 1997).
8. A reduction in social, occupational, or recreational
activities in favor of further substance use. 7
The social standards for that culture usually prohibit the abuse or ex-
9. Continuing chemical use even though the individ- cessive use of a compound and limit it to infrequent use. Since mari-
ual suffers social, emotional, or physical problems juana or other drugs are illegal, their use is abusive by definition and
related to drug use. thus one could argue that they are not “social” drugs.
14 Chapter Two
Drug of choice: Clinicians once spoke about the indi- text, we limit our discussion to just two subforms: (a)
vidual’s drug of choice as an important component of the metabolic tolerance and (b) pharmacodynamic tolerance.
addictive process. In theory, it was assumed that the drug Metabolic tolerance develops when the body becomes
a person would use if he or she had the choice was an im- more effective in biotransforming a chemical into a
portant clue to the nature of the person’s addiction. Since form that can be easily eliminated from the body. (The
the mid-1990s clinicians have placed much less emphasis process of biotransformation is discussed in more detail
on the concept of the individual’s drug of choice (Walters, in Chapter 3.) The liver is the main organ in which the
1994). One reason for this change is polypharmacology.8 process of biotransformation is carried out. In some cases,
It is rare for a person to be addicted to just one chemical the constant exposure to a chemical causes the liver to be-
now. Rather, most drug abusers have used a wide variety come more efficient at breaking down the drug, making a
of substances. Many stimulant users will also drink alco- given dose less effective over time.
hol or use benzodiazepines to control the side effects of Pharmacodynamic tolerance is a term applied to the
cocaine or amphetamines, for example. increasing insensitivity of the central nervous system
Addiction/dependence: Technically, addiction is a (CNS) to the drug’s effects. When the cells of the cen-
term that is poorly defined, and most scientists prefer tral nervous system are continuously exposed to a
the more precise term dependence (Shaffer, 2001). In chemical, they will often try to maintain normal func-
this text, these terms are used interchangeably. Physical tion by making minute changes in their cell structure to
dependence on alcohol or drugs might be classified as compensate for the drug’s effects. The cells of the cen-
tral nervous system then become less sensitive to the ef-
a primary, chronic, disease with genetic, psychoso- fects of that chemical, and the person must use more of
cial and environmental factors influencing its devel- the drug to achieve the initial effect.
opment and manifestations. The disease is often Withdrawal syndromes: If abused for an extended pe-
progressive and fatal. It is characterized by impaired riod of time,9 recreational chemicals will bring about a
control over drinking, preoccupation with the drug characteristic withdrawal syndrome. A rule of thumb is
alcohol, use of alcohol despite adverse consequences, that the withdrawal effects will be the opposite of the
and distortions in thinking. (Morse & Flavin, 1992, drug’s effects on the individual. Thus, one of the with-
p. 1013) drawal symptoms from the CNS stimulants will be a
feeling of fatigue, and possibly extended sleep. The
In this definition, one finds all of the core concepts exact nature of the withdrawal syndrome will vary de-
used to define drug addiction. Each form of drug addic- pending on the class of drugs being used, the period of
tion is viewed as (a) a primary disease, (b) with multiple time the person has abused that chemical, and the indi-
manifestations in the person’s social, psychological, spir- vidual’s state of health.
itual, and economic life; (c) it is often progressive, (d) In clinical practice, the existence of a withdrawal
potentially fatal, and (e) marked by the person’s inability syndrome is evidence that pharmacodynamic tolerance
to control the use of that drug and (f) preoccupation has developed, since the withdrawal syndrome is caused
with chemical use. In spite of the many consequences by the absence of the chemical that the central nervous
inherent in the use of that chemical, (g) the individual system had previously adapted to. When the drug is dis-
develops a distorted way of looking at the world that continued, the central nervous system will go through a
supports his or her continued use of that chemical. In period of readaptation as it learns to function normally
addition, dependence on a chemical is marked by (a) without the drug being present. During this period of
the development of tolerance to the effects of that time, the individual will experience the physical signs
chemical and (b) a characteristic withdrawal syndrome of withdrawal.
when the drug is discontinued (Schuckit, 2000). Each This process is clearly seen during alcohol with-
of these symptoms of addiction to a chemical are dis- drawal. Alcohol functions very much like a chemical
cussed below. “brake” on the cells of the central nervous system,
Tolerance develops over time, as the individual’s body much like the brakes on your car. If you attempt to
struggles to maintain normal function in spite of the drive while the brakes are engaged, it might be possible
presence of one or more foreign chemicals. Technically, to eventually force the car to go fast enough to meet the
there are several different subforms of tolerance. For this
9Defined by the pharmacological characteristics of the drug as well as
8
See Glossary. the abuser’s biochemistry and psychosocial adjustment.
posted speed limits. But if you were then to release the on a distorted sample of people: those who are in treat-
pressure on the brakes, the car would suddenly leap ment for substance abuse problems (Gazzaniga, 1988).
ahead because the brakes were no longer fighting the for- Virtually nothing is known about people who use chem-
ward motion of the car. You would have ease up on the icals on a social basis but who never become addicted,
gas pedal, so that the engine would slow down enough or those individuals who are addicted to chemicals but
to keep you within the posted speed limit. who recover from their chemical use problems without
During that period of readjustment, the car would, in formal intervention or treatment. A serious question that
a sense, be going through a withdrawal phase. Much the must be asked is whether individuals in treatment are
same thing happens in the body, when the individual representative of all drug/alcohol-addicted persons.
stops using drugs. The body must adjust to the absence of For example, individuals who seek treatment for a
a chemical that previously it had learned would always substance use disorder are quite different from those
be there. This withdrawal syndrome, like the presence of who do not (Carroll & Rounsaville, 1992). As a group,
tolerance to the drug’s effects, provides strong evidence those alcohol/drug-addicted persons who do not seek
that the individual is addicted to one or more chemicals. treatment seem to be better able to control their sub-
stance use and have shorter drug use histories than
people who seek treatment for their substance use prob-
The Growth of New “Addictions” lem. This may be why the majority of those who abuse
In addition to the tendency for the popular press to exag- chemicals either stop or significantly reduce their chem-
gerate the dangers associated with chemical abuse, there ical use without professional intervention (Carroll &
is a disturbing trend within society to speak of “addictions” Rousaville, 1992; Humphreys, Moos, & Finney, 1995;
to a wide range of behaviors/substances, including food, Tucker & Sobell, 1992). It appears that only a minority
sex, gambling, men, women, play, television, shopping, of those who begin to use recreational chemicals lose
credit cards, making money, carbohydrates, shoplifting, control over their substance use and require profes-
unhappy relationships, french fries, lip balm, and a sional intervention. Yet it is on this minority that much
multitude of other “nondrug” behaviors or substances of the research into the recognition and treatment of
(Jaffe & Anthony, 2005; Shaffer, 2001). This expansion substance abuse problems is based.
of the definition of the term addiction does not appear Consider for a moment the people known as “chip-
to have an end in sight, and may have reached its zenith pers.” They make up a subpopulation of drug users
of idiocy with the formation of “Lip Balm Anonymous” about which virtually nothing is known. They seem to
(Shaffer, 2001). be able to use a chemical, even one supposedly quite
Fortunately, there is little evidence that nondrug addictive, only when they want to, and then seem to dis-
centered behaviors can result in physical addiction as is continue the use of the drug when they wish to do so.
the case in alcohol/drugs. In this text, the term addic- Researchers are not able to make even an educated
tion will be limited to the physical dependence on alco- guess as to their number. It is thought that chippers use
hol and chemical agents commonly known as the chemicals in response to social pressure and then dis-
“drugs of abuse.” continue the use of drugs when the social need for
them to do so has passed. But this is only a theory, and it
might not account for the phenomenon of “chipping.”
What Do We Really Know About
Yet another reason that much of the research in sub-
the Addictive Disorders? stance abuse rehabilitation is flawed is that a significant
If you were to watch television talk shows or read a proportion of this research is carried out either in Veter-
small sample of the self-help books currently on the ans Administration (VA) hospitals or public facilities
market, you would be left with the impression that re- such as state hospitals. However, individuals in these fa-
searchers fully understand the causes and treatment of cilities are not automatically representative of the “typi-
drug abuse. Nothing could be further from the truth! cal” alcohol/drug-dependent person. For example, to
Much of what is “known” about addiction is based on be admitted to a VA hospital, the individual must have
mistaken assumptions, clinical myths, theory, or, at successfully completed a tour of duty in the military.
best, incomplete data. The simple fact that the individual was able to com-
An excellent example of how incomplete data might plete a term of military service means that she or he is
influence the evolution of treatment theory is the fact quite different from those people who either never en-
that much of the research on substance abuse is based listed in the military or who enlisted but were unable to
16 Chapter Two
complete a tour of duty. The alcohol/drug addict who is (blackout, legal problem, etc.) at some point in their
employed and able to afford treatment in a private treat- lives (Sadock & Sadock, 2003). Yet this does not mean
ment center might be far different from the indigent that 30% to 45% of the adult population is alcohol de-
alcohol/drug-dependent person who must be treated in pendent! Rather, this fact underscores the need for re-
a publicly funded treatment program. searchers to more clearly identify the features that
Only a small proportion of the available literature on might identify the potential alcoholic.
the subject of drug addiction addresses forms of addic- There are three elements necessary to the diagnosis
tion other than alcoholism. An even smaller proportion of alcoholism or drug addiction (Shaffer, 2001):
addresses the impact of recreational chemical use in
women (Cohen, 2000). Much of the research con- 1. Craving/compulsion to use the chemical, during
ducted to date has assumed that alcohol/drug use is the which the individual’s thoughts become fixated on
same for men and women, overlooking possible differ- the possibility of obtaining and using the chemical
ences in how men and women come to use chemicals, she or he has become dependent upon.
the effects that recreational chemicals might have on 2. Loss of control when the person will use more of the
men and women, and the differing impact that addic- chemical than she or he intended, is unable to cut
tion to alcohol/drugs might have on the two groups. back on the amount used, or is unable to stop using
Further, although it has long been known that chil- the chemical.
dren/adolescents abuse chemicals, there still is virtually 3. Continued use despite consequences brought on by
no research on the subject of drug abuse/addiction in the individual’s use of that chemical. Such conse-
children or adolescents. Yet, as will be discussed in the quences might include impairment in the person’s
Chapter 23, the problem of child and adolescent drug social, vocational, or physical well-being as well as
and alcohol abuse is a serious one. Children and adoles- possible legal or financial problems.
cents who abuse chemicals are not simply small adults. What is the relationship between substance abuse
It is thus not possible to automatically generalize from and addiction? The abuse of a chemical such as alco-
research done on adults to the effects of substance hol, while problematic, does not automatically progress
abuse on children or adolescents. into physical addiction to that compound (Swift, 2005).
Thus, much of what we think we know about addic- Do the same treatment methods developed for people
tion is based on research that is quite limited at best, and addicted to alcohol work for those people who abuse it
many important questions remain to be answered. Yet but who are not actually addicted to it? Are there spe-
this is the foundation on which an entire “industry” of cial forms of alcohol abuse that predict a progression to
treament has evolved. It is not the purpose of this text to alcohol dependence? The answers to these questions
deny that large numbers of people abuse drugs or that would be of great help to mental health and substance
such drug abuse carries with it a terrible cost in personal abuse rehabilitation professionals who deal with pa-
suffering. It is also not the purpose of this text to deny that tients who struggle with alcohol use problems.
many people are harmed by drug abuse. Admittedly,
people become addicted to chemicals. The purpose of
this section is to make the reader aware of the shortcom- Summary
ings of the current body of research on substance abuse.
In this chapter, the concept of a continuum of drug use
was introduced. Research studies outlining the extent of
the problem of the abuse of various drugs were reviewed,
The State of the Art: Unanswered
along with studies that identified the extent of the prob-
Questions, Uncertain Answers
lem of addiction to different chemicals. The issues of ac-
As the reader has discovered by now, there is much con- tual and hidden costs of chemical use/abuse were
fusion in the professional community over the prob- explored. Often, this is reflected solely in financial or eco-
lems of substance abuse/addiction. Even in the case of nomic terms. However, it is important that society not
alcoholism, which is perhaps the most common of the lose sight of the “hidden” impact that substance abuse
drug addictions, there is an element of confusion, or has on the individual’s spouse, family members, and the
uncertainty, over what the essential features of alco- entire community. Unanswered questions about chemi-
holism might be. For example, 30% to 45% of all adults cal abuse were raised, and the media’s role in the evolu-
will have at least one transient alcohol-related problem tion of the substance abuse problem were discussed.
CHAPTER THREE
The Medical Model

of Chemical Addiction
Society has long struggled to understand (a) why people Medical Association’s decision to classify alcoholism as
begin to abuse chemicals, (b) why they continue to use a formal “disease” in 1956, it was viewed as a moral dis-
recreational chemicals, and (c) why they become ad- order both by society in general and by the majority of
dicted to them. In an attempt to find answers to these physicians.2 In contrast to this, Jellinek (1952, 1960)
questions, various professions have examined the sub- argued that alcoholism was a disease, like cancer or
stance use disorders (SUDs) from within the framework pneumonia. As with these other disease states, alco-
of their respective worldview. In this chapter, the an- holism presented certain characteristics, Jellinek argued,
swers to these questions will be examined from the per- including (a) the individual’s loss of control over his or
spective of what has come to be known as the “medical,” her drinking, (b) a specific progression of symptoms,
“biomedical,” or “disease” model of addiction. and (c) the fact that if it was left untreated, alcoholism
would result in the individual’s death.
In an early work on alcoholism, Jellinek (1952) sug-
The Medical Model gested that the addiction to alcohol progressed through
four different stages. The first of these stages, which he
The medical model accepts as one of its basic tenets the called the Prealcoholic phase, was marked by the individ-
belief that much of behavior is based on the individual’s ual’s use of alcohol for relief from social tensions en-
biological predisposition. Based on this assumption, it countered during the day. In the prealcoholic stage, one
is logical to believe that if the individual’s behavior is sees the roots of the individual’s loss of control over his or
inappropriate, there must be a biological dysfunction her drinking in that the individual is no longer drinking
that causes this “pathology.” But as is true for much of on a social basis, but has started to drink for relief from
medicine, there is no single, universally accepted “dis- stress and anxiety. As the individual continues to engage
ease model” that explains alcohol/drug use problems. in “relief drinking” for an extended period of time, she or
Rather, there is a group of loosely related theories that he enters the second phase of alcoholism: the Prodromal
state alcohol/drug abuse/addiction is the outcome of an stage (Jellinek, 1952). This second stage of alcoholism
unproven biomedical or psychobiological process and was marked by the development of memory blackouts,
thus can be called a “disease” state. secret drinking (also known as hidden drinking), a preoc-
For decades the treatment of those who suffered cupation with alcohol use, and feelings of guilt over the
from an SUD rested not with physicians but with sub- person’s behavior while intoxicated.
stance abuse counselors and mental health profession- With the continued use of alcohol, the individual
als (Stein, & Friedmann 2001). It was only in the latter would eventually become physically dependent on it, a
part of the 20th century that physicians started to claim hallmark of what Jellinek (1952) called the Crucial
that patients with addictive disorders suffer from a phase. Other symptoms of this third stage of drinking
chronic, relapsing illness that falls in their purview were a loss of self-esteem, a loss of control over one’s
(Stein, & Friedmann 2001). One reason physicians drinking, social withdrawal in favor of alcohol use, self-
make this claim is the work of E. M. Jellinek. pity, and a neglect of proper nutrition while drinking.
Jellinek’s work. Jellinek (1952, 1960) has had a pro- During this phase, the individual would attempt to re-
found impact on how alcoholism1 was viewed by physi- assert his or her control over alcohol by entering periods
cians in the United States. Prior to the American
2Unfortunately,there are still those in the field of medicine who view
1One point that is often overlooked is that Jellinek’s work addressed the addictions as a “shameful problem of personality rather than
only alcohol dependence. physiology” (Henderson, Morton, & Little, 2005, p. 1).
17
18 Chapter Three
the Greek alphabet to identify the most common forms

Prealcoholic Phase Prodromal Phase
of alcoholism found in the United States. Table 3.1 pro-
First blackouts; vides a brief overview of Jellinek’s theoretical system to
Alcohol used for preoccupation with use illustrate his theory:
relief from social of alcohol; development
tension of guilt feelings Advanced in an era when the majority of physicians
viewed alcohol dependence as being caused by a moral
weakness, Jellinek’s (1960) model of alcoholism offered
a new paradigm to physicians. First, it provided a diag-
nostic framework within which physicians could clas-
Crucial Phase Chronic Phase sify different patterns of drinking, as opposed to the
restrictive dichotomous view in which the patient was
Loss of control over Loss of tolerance
alcohol; withdrawal for alcohol; obsessive either alcoholic or not, that had previously prevailed.
symptoms; preoccu- drinking; alcoholic Second, Jellinek’s (1960) model of alcoholism as a
pation with drinking tremors physical disease made it worthy of study and the person
with this disorder worthy of “unprejudiced access”
FIGURE 3.1 Jellinek’s Four Stages of Alcoholism (Vaillant, 1990, p. 5) to medical treatment. Finally, the
Jellinek model attributed the individual’s use of alcohol
not to a lack of willpower but to the fact that the drinker
suffered from a medical disorder (Brown, 1995).
of abstinence, only to return to the use of alcohol after Since the Jellinek (1960) model was introduced, re-
short periods of time. Finally, with continued alcohol searchers have struggled to determine whether it is
use, Jellinek (1952) thought that the alcoholic would valid or not. A generation ago, the team of Sobell and
enter the Chronic phase. The symptoms of the chronic Sobell (1993) found that there was a clear-cut progres-
phase included a deterioration of one’s morals, drinking sion in the severity of the individual’s drinking in only
with social inferiors, the development of motor tremors, 30% of the cases. In the same year, Schuckit, Smith,
an obsession with drinking, and for some, the use of Anthenelli, and Irwin (1993) argued that there was clear
“substitutes” when alcohol was not available (i.e., drink- evidence of a progression in the severity of problems
ing rubbing alcohol, etc.). A graphic representation of experienced by the alcohol-dependent men in their
these four stages of alcoholism might look like the chart research sample. But the authors concluded that there
in Figure 3.1. was remarkable variation in the specific problems en-
In 1960, Jellinek presented a theoretical model of al- countered by their subjects, suggesting that alcohol-
coholism that was both an extension and a revision of dependent individuals do not follow a single progressive
his earlier work. According to Jellinek (1960), the alco- pattern. Thus, the research data supporting the Jellinek
holic was unable to consistently predict in advance how model continues to be mixed.
much he or she would drink at any given time. Alco- The genetic inheritance theories. The average person
holism, like other diseases, was viewed by Jellinek as on the street seems to share two popular misconcep-
having specific symptoms, which included the physical, tions about genetic inheritance: (a) the belief that ge-
social, vocational, and emotional complications often netic evolution stopped with the onset of human
experienced by the compulsive drinker. Further, Jellinek culture, and (b) the belief that genetic predisposition is
continued to view alcoholism as having a progressive the same as genetic predestination (Wade, 2006). The
course that, if not arrested, would ultimately result in former misconception is clearly mistaken, although the
the individual’s death. pace of genetic change is much too slow for the individ-
However, in his 1960 book, Jellinek went further ual to appreciate in the course of his or her lifetime
than he had previously by attempting to classify differ- (Wade, 2006). The latter is also easily disproven: The
ent patterns of addictive drinking. Like Dr. William person whose genetic predisposition says that she or he
Carpenter did in 1850, Jellinek came to view alco- will be 6′4″ tall might not reach that height if raised in
holism as a disease that might be expressed in a number an impoverished environment that does not provide ad-
of different forms, or styles, of drinking (Lender, 1981). equate food intake, for example.
Unlike Dr. Carpenter, who thought that there were Thus, genetic inheritance does not mean inexorable
three types of alcoholics, Jellinek identified five sub- outcome. Rather, genetic predisposition means just that:
forms of alcoholism. Jellinek used the first five letters of The individual is predisposed toward certain outcomes,
The Medical Model of Chemical Addiction 19
TABLE 3.1 Comparison of Jellinek’s Drinking Styles
Type of alcoholism Alpha Beta Delta Gamma Epsilon
Psychological Yes Yes Yes Yes Possibly but

dependence on not automatically
alcohol?
Do physical No Yes Minimal to Multiple and Possibly, but rare
complications no physical serious physical because of binge
develop? complications problems from pattern of alcohol
drinking use
Tolerance to the No No Yes. Person will Yes. Person will Possibly, but rare
effects of alcohol? “crave” alcohol if “crave” alcohol if because of binge
forced to abstain forced to abstain pattern of alcohol
from use. from use. use
Can the individual For short periods For short periods No. Person has No. Person has Yes. Person is able
abstain from of time, if of time, if lost control over lost control over to abstain during
alcohol use? necessary necessary his or her alchohol his or her alcohol periods between
use. use. binges.
Is this pattern Yes Yes Yes Yes Unknown*
of drinking stable?
Is this pattern In rare cases, but Possibly, but not Strong chance of No. This is an Unknown*
of drinking not automatically automatically progression to end-point style of
progressive? gamma, but not drinking.
automatic
If so, to what Gamma Gamma Gamma Not applicable Unknown*
pattern will this
style of drinking
progress?
*According to Jellinek (1960), the epsilon style of drinking was the least common in the United States and only limited information about this
style of drinking was available to him.
depending on his or her life experiences.3 Still, the av- Early evidence suggested that a gene called slo-1, which
erage person tends to view genetic predisposition as controls the activity of a certain protein known as the
being predestination, and that his or her genetic inheri- BK channel, seemed to mediate the individual’s sensi-
tance is not just influential but inescapable. This is tivity to alcohol’s effects (Lehrman, 2004). The BK
often seen at case reviews where it is mentioned that channel protein usually controls the flow of ions out of
one/both of the patient’s parents were physically depen- the neuron during the normal cycle of neural “firing.”
dent on a substance. Upon hearing this, staff members at When alcohol binds at this protein complex, it holds
the rehabilition center might share a look or nod know- the ion channel open for far longer than is normal, thus
ingly. “There is the genetic predisposition” one might say, slowing the rate at which that neuron can prepare for
as if having a parent who was addicted to chemicals was the next firing cycle (Lehrman, 2004). This line of re-
proof that the patient had inherited the disorder from search suggests that the slo-1 gene might be involved in
that parent.4
4This is not to deny that the person might have inherited such a ge-
In the last 20 years of the 20th century, researchers
netic predisposition toward an SUD. But until scientists can identify
began to identify genetic patterns that seemed to predis-
which genes are the basis of such a predisposition and proper tests are
pose the individual to develop alcohol use patterns. carried out to determine whether a given patient actually has inher-
ited those genes, it is improper to engage in what might be called
3 guilt-by-genetic-association.
Which is a fancy way of saying “environmental influences,” right?
20 Chapter Three
the development of an alcohol use disorder, although team of Gruber and Pope (2002) found that unspeci-
the picture of how this occurs is far from clear. fied “genetic factors” (p. 392) accounted for 44% of the
Another neurochemical that seems to be associated risk for marijuana abuse, while “family environmental
with the SUDs is known as ΔFosB.5 Technically, ΔFosB factors” (p. 392) accounted for an additional 21% of the
is a protein, which is produced in many neurons each risk for this disorder. The impact of cultural factors on
time it is exposed to many of the compounds that gen- the genetic predisposition for an SUD might be seen in
erate addiction (Doidge, 2007). A little ΔFosB is pro- the ongoing cultural experiment taking place in Sweden.
duced each time the neuron is exposed to an addictive As social restrictions against the use of tobacco products
substance. At some point, it is hypothesized, the accu- by women slowly relax, a greater number of women are
mulated ΔFosB triggers the activation (or possibly de- beginning to indulge in the use of tobacco products
activation) of a gene, altering the organism’s response to (Kendler, Thornton, & Pedersen, 2000). There is no
the neurotransmitter dopamine, which is involved in reason to suspect that the impact of the individual’s
the reward process, thus making the individual more familial and cultural environment should have less of
prone to addiction to that substance (Doidge, 2007). an impact on whether she or he abuses any of the other
On the basis of research conducted on monkeys, the drugs of abuse.
team of Barr et al. (2007) concluded that a variant of One of the earliest explorations of the genetics of
the mu receptor site in the brain6 seemed to make alco- alcohol use disorders was carried out by Cloninger,
hol’s effects more rewarding to the test animals. The ob- Gohman, and Sigvardsson (1981). The authors utilized
served variant of the μ-receptor site in the monkeys was a comprensive set of adoption records of some 3,000
very similar to one found in humans, suggesting that children who were adopted shortly after birth, and con-
humans with this genetic variation might be more vul- cluded that the children who later developed an AUD
nerable to the euphoric effects of alcohol, and thus “at essentially fell into two groups. The first subgroup was
risk” for developing an alcohol use disorder. This study made up of three-fourths of the children whose parents
does strongly suggest that there is a genetic component had an AUD and who themselves went on to develop
to the AUDs. an AUD. During young adulthood these individuals
In contrast to those simplistic studies for “the alco- used alcohol only in moderation but later in life devel-
hol gene,” the team of Tsuang et al. (1998) concluded oped an AUD. Throughout their adult lives, these indi-
that both genetic and environmental factors predis- viduals were productive and only rarely were involved
posed their subjects toward the abuse of classes of in antisocial behaviors. They were classified as “Type I”
chemicals. This makes clinical sense, in that rehabilita- (or “Type A” or “late onset”) alcoholics (Gastfriend &
tion professionals have long observed that patients with McLellan, 1997; Goodwin & Warnock, 1991).
SUDs tend to prefer one compound over the others. Pa- A second, smaller group of alcoholics was identified
tients who are addicted to heroin, for example, often by Cloninger, Gohman, and Sigvardsson (1981). These
speak of how they had tried stimulants such as metham- individuals were men who were more violent, involved
phetamine, but that “it didn’t do anything for me” or in criminal activity, and who also demonstrated an AUD.
that the stimulant did not feel “right” to them. It was They were classified as having “Type II” (or “male lim-
suggested that each class of drug had a unique genetic ited,” “Type B,” or “early onset”) alcoholism (Gastfriend &
predisposition, according to the authors, possibly ex- McLellan, 1997; Goodwin & Warnock, 1991). A male
plaining why different individuals seem “drawn” to very child born into such a family ran almost a 20% chance
specific drugs of abuse. Thus, there might be a separate of himself growing up to become alcohol dependent,
gene that predisposes the individual to the abuse of no matter what the social status of his adoptive parents.
each class of substances. The authors concluded that this was evidence for a
Doidge (2007) observed that the human brain is strong genetic influence in the development of AUDs
constantly rewiring itself in response to the demands of for this subgroup of children.
the environment. The individual’s family and his or her In 1996, the team of Sigvardsson, Gohman, and
culture are both factors that helps to shape that environ- Cloninger (1996) successfully replicated this earlier study
ment. Thus, it should not be surprising to learn that the on the inheritability of alcoholism. The authors exam-
ined the adoption records of 557 men and 600 women
5
The symbol “Δ” is the Greek letter “delta” from the Greek alphabet. who were born in Gothenburg, Sweden, and who were
Thus, the name of this neuroprotein is pronounced “delta Fos B.” adopted at an early age by nonrelatives. The authors con-
6Discussed in Chapter 14. firmed their earlier identification of two distinct subtypes
of alcoholism for men. Further, the authors found These findings were supported by an independent
that the “Type I” and “Type II” subtypes appear to be study conducted by Bierut et al. (1998). The authors
independent but possibly related forms of alcoholism. suggested that there was “a general addictive tendency”
Where one would expect 2% to 3% of their sample to (p. 987) that was transmitted within the family unit.
have alcohol use problems on the basis of population However, the authors could not be more specific about
statistics, the authors found that 11.4% of their male the nature of this genetic predisposition toward alcohol/
sample fit the criteria for Type I alcoholism and 10.3% substance abuse. Other researchers have concluded
fit the criteria for Type II alcoholism. But in contrast that at least for males, 48% to 58% of the risk for alco-
to the original studies that suggested Type II alcoholism is based on the individual’s genetic inheritance
holism was limited to males, there is now evidence that (Prescott & Kendler, 1999). Further, researchers have
a small percentage of alcohol-dependent women might found evidence that within each family, forces are at
also be classified as Type II alcoholics (Cloninger, work that seem to help shape the individual’s choice of
Sigvardsson, & Gohman, 1996; Del Boca & Hesselbrock, recreational chemicals to abuse (Bierut et al., 1998;
1996). Merikangas et al., 1998).
The distinction between Type I and Type II alco- The biological differences theories. In the latter half
holics has lent itself to a series of research studies de- of the 20th century, a number of researchers suggested
signed to identify possible personality traits unique to that there were biological differences between individ-
each group of alcohol dependents. Researchers have uals who were alcohol dependent, and those who were
found that, as a group, Type I alcoholics tend to engage not. This theory has stimulated a great deal of research
in harm-avoidance activities, while Type II alcoholics in the hope of finding such differences, the full scope of
tend to be high in the novelty-seeking trait7 (Cloninger which is beyond this chapter section. But the general
et al., 1996). Other researchers have found differences theme of this research is that alcohol-dependent indi-
in brainwave activity between the Type I and Type II al- viduals seem to metabolize alcohol differently from
coholics on the electroencephalograph (EEG). Fur- nondependent drinkers, that the site/speed/mechanism
ther, as a group, Type I alcoholics tend to have higher of alcohol biotransformation is different for the alcohol-
levels of the enzyme monoamine oxidase (MAO) than dependent persons as compared to the nonalcoholic, or
Type II alcoholics do. It was hypothesized that this that the alcohol-dependent person seems to react differ-
lower MAO level in Type II alcoholics might account ently to the effects of that chemical than do those who
for their tendency to be more violent than Type I alco- are not dependent on it.
holics (Cloninger et al., 1996). Thus, the Type I–Type II One such study was conducted by Ciraulo et al.
typology seems to have some validity as a way of classify- (1996). The authors selected a sample of 12 adult
ing different patterns of alcohol use/abuse. women who had alcohol-dependent parents and 11
Using a different methodology and a research sample women whose parents were not alcohol dependent.
of 231 substance abusers, 61 control subjects, and 1,267 The authors then administered either a 1 mg dose of
adult first-degree relatives of these individuals, the team the benzodiazepine alprazolam or a placebo to their
of Merikangas et al. (1998) found evidence of “an 8-fold subjects and found that the women who had alcoholic
increased risk of drug [use] disorders among relatives of parents and who had received alprazolam found it to be
probands with drug disorders” (p. 977). According to more enjoyable than did those women whose parents
the authors, there was evidence of familial predisposi- were not alcohol dependent. This finding was consis-
tion toward the abuse of specific substances, although tent with the findings of Tsaung et al. (1998), who sug-
they did admit that the observed familial “clustering of gested on the basis of their research that people
drug abuse could be attributable to either common ge- developed vulnerabilities to classes of drugs rather than
netic or environmental factors” (p. 977). Such environ- to a specific substance. In this case, the class of drugs
mental factors might include impaired parenting skills, was the CNS depressants, which includes both alcohol
marital discord, stress within the family unit, and/or and the benzodiazepines.
physical/emotional/sexual abuse, as well as exposure to One area of inquiry that appears to hold some prom-
parental chemical abuse at an early age, according to ise is the P300 response cycle (Nurnberger & Bierut,
the authors. 2007). When an individual has electrodes connected
to the scalp to measure brain wave activity, and then is
7Which would mean that they are more likely to engage in high-risk exposed to a standard stimulus (a strobe light, for
behaviors. example), there is a short spike in electrical activity in
22 Chapter Three
the brain between 300 and 500 milliseconds after the would make them less sensitive to natural reinforcers
stimulus begins. As a group, both alcoholic men and such as food and sex (Ivanov et al., 2006). It is theorized
their children tend to have a weaker response to the that this provides a biological vulnerability to any sub-
stimulus than do nonalcoholic men or their children stance that might force the release of more dopamine
(Nurnberger & Bierut, 2007). This altered electrical re- into the appropriate receptor sites. Such a theory is sup-
sponse pattern seems to reflect a reduced level of activ- ported by studies that find a 400% to 500% increase in
ity in those neurons responsible for inhibition, allowing dopamine levels in the nucleus accumbens following
the excitatory neurons to overwhelm those whose func- the administration of a dose of cocaine, and a reduction
tion is to inhibit neural activity. The theory is that alcohol in dopamine levels in this same region of the brain dur-
functions as an external agent to enhance the inhibitory ing acute withdrawal from cocaine (Ivanov et al., 2006).
activities of gamma-aminobutryric acid (GABA),8 as the The dopamine D2 receptor sites are most numerous
individual seeks to restore the balance between neural in the nucleus accumbens.9 This reduction in dopamine
inhibition and excitation (Nurnberger & Bierut, 2007). D2 receptor sites is thought to predate the development
However, it is not known whether this same (or a simi- of the substance use disorder (Commission on Ado-
lar) latency in P300 response intensity might be found lescent Substance and Alcohol Abuse, 2005). But the
in those who abuse drugs other than alcohol, or the development of a comprehensive biomedical model of
relationship between such a hypothetical finding and how the dopamine D2 receptor level might contribute
other SUDs. to vulnerability of substance use disorders is still being
The team of Goldstein and Volkow (2002) utilized developed.
neuro-imaging technology to explore which areas of
the brain become active during the experience of “crav-
ing” and intoxication. The authors noted that some of
the same regions of the brain activated during these Reaction Against the Disease
drug-use experiences, such as the orbiotofrontal cortex Model of Addiction
and the anterior cingulate gyrus, are interconnected It is tempting to speak of the “disease model” of alcohol/
with the limbic system. These regions of the brain are drug abuse as if there were a single, universally accepted
thought to be involved in the process of cognitive- definition of the substance use disorders (SUDs), but
behavioral integration activities such as motivation this is not true. There are actually a number of different
and goal-directed behavior. The authors suggest that subforms of the “disease model” of addiction. This re-
through repeated exposure to a compound, the individ- flects the fact that there are often subtle, and, on occa-
ual comes to expect certain effects from that chemical, sion, not so subtle, philosophical differences between
and as a result of the repeated drug-induced episodes of how physicians view the same disease. This is clearly
pleasure, she or he becomes less sensitive to normal re- demonstrated by the treatment protocols for a condi-
ward experiences. Through both a cognitive and neu- tion such as a myocardial infarction that are found in
robehavioral process the individual also learns to health care facilities.
overvalue the reinforcing effects of alcohol/drugs and to Advocates for the disease model of alcoholism point
focus more and more cognitive energy on obtaining the out that alcohol dependence (and, by extension, the
drug of choice so that she or he might experience the other SUDs) have strong similarities to other chronic
drug’s effects again. This theory, although still in its relapsing disorders such as asthma, hypertension, or di-
formative stages, would seem to account for many of abetes, and that because of the genetic predisposition
the facets of alcohol/drug use disorders. for SUDs and the similarity to the other forms of illness,
The dopamine D2 hypothesis. There are five known the addictions are medical disorders (Marlowe &
subtypes of dopamine receptors in the human brain DeMatteo, 2003). In contrast, it is also argued that the
(Ivanov, Schulz, Palmero, & Newcorn, 2006). One of SUDs are forms of reckless misconduct such as speed-
these receptor subtypes, the dopamine D2 receptor site, ing, and that as such individuals who engage in these
has come to be viewed as especially important to the behaviors should best be treated as criminals by the
development of an SUD (Hurd, 2006). Research has court system (Marlowe & DeMatteo, 2003).
shown that individuals with an SUD have a reduced
number of dopamine D2 receptor sites, which in theory 9Which, as discussed in the Glossary, is a part of the brain involved in
the reward system and also the process of integrating sensory stimuli
8See Glossary. with conscious behavior.
Critics of the disease model often center their attack of alcoholism suggested by Jellinek develops only in a
on how disease is defined. In the United States, “dis- minority (25%–30%) of the cases (Sobell & Sobell,
ease” is defined as reflecting a biophysical dysfunction 1993; Toneatto, Sobell, Sobell & Leo, 1991). The ma-
that interferes with the normal function of the body. In jority of individuals with an AUD alternate between pe-
an infectious process, a bacterium, virus, or fungus in- riods of abusive and nonabusive drinking or even total
vading the host organism would be classified as a “dis- abstinence. Illicit drug use also tends to follow a variable
ease” by this criterion. Another class of diseases is those course for drug abusers (Toneatto, Sobell, Sobell, &
resulting from a genetic disorder that causes abnormal Rubel, 1999).
growth or functioning of the individual’s body. A third The concept of loss of control over alcohol use, a cen-
class of diseases is those in which the optimum function tral feature of Jellinek’s theory, has been repeatedly chal-
of the organism is disrupted by acquired trauma. lenged (Schaler, 2000). Research suggests that chronic
As noted, there is a consensus among behavioral sci- alcohol abusers drink to achieve and maintain a desired
entists that there is a genetic “loading” for SUDs that in- level of intoxication, suggesting that the alcohol abuser
creases the individual’s risk for developing this disorder has significant control over his alcohol intake (Schaler,
(Ivanov et al., 2006). If there is a genetic predisposition 2000). Rather than speak of loss of control, clinicians
for addictive behaviors, then chemical dependency is now speak of alcohol-dependent individuals as having
very much like the other physical disorders in which inconsistent control over their alcohol intake (Toneatto
there is a genetic predisposition. In this sense, sub- et al., 1991; Vaillant, 1990, 1995).
stance abuse might be said to be a “disease,” which is The genetic inheritance theories. In the latter part of
what E. M. Jellinek proposed in 1960. But Jellinek’s the 20th century, medical practitioners began to think
model has itself been challenged. of the addictions as reflecting a genetic disorder. In-
Reaction to the Jellinek model.10 In the time since it deed, there is an impressive body of evidence suggest-
was introduced, researchers have concluded that the ing a strong role for the individual’s genetic inheritance
Jellinek (1960) model is seriously flawed. First, Jellinek’s in the development of substance use disorders. How-
(1960) research methodology was inappropriate for ever, much to the dismay of many clinicians, re-
such a sweeping model. Remember that Jellinek (1960) searchers have failed to identify a single “alcohol gene.”
based his work on surveys that were mailed out to 1,600 Scientists now speak of SUDs as being “polygenetic”
members of Alcoholics Anonymous (AA). But of the rather than monogenetic in nature and acknowledge
1,600 copies of the surveys mailed out, only 98 were re- that genetic inheritance is not the sole cause of alco-
turned (a return rate of just 6%). Such a low return rate holism (Nurnberger & Bierut, 2007).
is rarely accepted as the foundation for a research study. The theory that the genetic foundation for the SUDs
Further, Jellinek (1960) assumed that (a) AA members is polygenetic is supported by the work of Rosemarie
were the same as nonmembers and (b) those people Kryger and Peter Wilce (discussed in Young, 2006).
who returned the survey were the same as those who did The authors concluded that 772 different genes were af-
not return the survey. These assumptions are incorrect fected by alcohol ingestion in their subjects, with two-
and undermine the validity of his research. thirds of these genes being expressed at lower levels
Further, Jellinek utilized a cross-sectional research than found in normal subjects. While suggestive, these
design. While this does not violate any rule of statistical findings did not identify genes that increased the
research, one must keep in mind that cross-sectional re- chances that the individual would ingest alcohol, as op-
search might not yield the same results as a lifespan posed to genes that were unable to express themselves
(longitudinal) research design. Given this weak re- normally because of the individual’s alcohol ingestion.
search design, it should come as no surprise that the The polygenetic nature of AUDs would seem to
Jellinek model begins to break down when it is used to have been identified in the research study by the rather
examine the alcohol use patterns of individuals over the large research team of Mulligan et al. (2006), who ex-
course of their lifetimes (Vaillant, 1995). For example, amined the genetic structure of research mice bred for
one of the core assumptions of the Jellinek model is either high or low alcohol preference. They concluded
that alcohol use disorders (AUDs) are automatically that more than 4,000 individual genes were affected by
progressive. But this has been challenged (Skog & alcohol consumption, with perhaps 75 of these appar-
Duckert, 1993). At best, the progression in the severity ently being most actively involved in the development
of alcohol dependence for the animals in their study.
10
See also Appendix Three. This would suggest that the expression of most of the
24 Chapter Three
genes identified in this study was affected by the inges- are alcohol dependent in different cultures around the
tion of alcohol, but was not causal to that act. world. In the United States, the male to female ratio for
Finally, the team of Johnson et al. (2006) examined alcohol use disorders is about 5.4:1. In Israel, this same
the genetics of AUDs and concluded that 51 different ratio is approximately 14:1, while in Puerto Rico, it is
regions of genes, including many involved in the 9.8:1, and 29:1 in Taiwan. In South Korea, the male to
process of intercell signaling, regulation of gene expres- female ratio for alcohol use disorders is 20:1, and it is
sion, and cellular development, were involved in the 115:1 in the Yanbian region of China (Hill, 1995). One
development of alcohol use disorders in humans. Many would expect that if alcoholism were simply a matter of
of these regions of genes seem to have included the spe- genetic inheritance, there would not be a significant
cific genes identified by earlier studies. variation in the male to female ratio. For example, ap-
Different researchers may have concluded that vastly proximately 1% of the population has schizophrenia in
different numbers of genes are affected by and influence every culture studied, and the male to female ratio for
the use of alcohol or drugs because different genes are in- schizophrenia is approximately the same around the
volved in the process of initiating and maintaining SUDs globe.
(“Addiction and the problem of relapse,” 2007). Further, Thus, on the basis of research to date, it is clear that
while there is strong evidence of a genetic predisposition both a biological predisposition toward alcohol addic-
toward the SUDs, researchers have found that environ- tion and strong environmental influences help to shape
mental forces can do much to mitigate the impact of the the individual’s alcohol/drug use pattern. But there is
individual’s biological heritage (Jacob et al., 2003). After still a great deal to be discovered about the evolution of
examining the histories of over 1,200 pair of monozy- substance use disorders: For reasons that are not under-
gotic and dizygotic twins born in the United States stood, up to 60% of known alcoholics come from fami-
between 1939 and 1957 and conducting structured lies with no prior evidence of alcohol dependence
psychiatric interviews with these individuals, the authors (Cattarello, Clayton, & Leukefeld, 1995).
concluded that the individual’s “genetic risk [for alco- Do genetics rule? Throughout much of the world,
holism] in many cases becomes actualized only if there is people view the individual’s genetic heritage as inalter-
some significant environmental sequela to the genetic able fate (Watters, 2006). This belief is identified as
vulnerability” (Jacob et al., 2003, p. 1270, italics added “neurogenetic determinism,” which sees humans as
for emphasis). In other words, the environment must ac- nothing more than “slaves to their genes or their neuro-
tivate this genetic predisposition by providing opportu- transmitters, and with no more free will than a child’s
nity for the individual to engage in alcohol abuse. radio-controlled car” (Begley, 2007, p. 252). If one ac-
The role of the environment might best be seen in the cepts this stance, as the author points out, then the whole
study conducted by Cloninger, Gohman, and Sigvards- concept of personal responsibility comes crashing down
son (1981). On the basis of their research, the authors around your ears. If people are not responsible for their
classified some individuals as having “Type I” alco- addictions because they had an inherited predisposition
holism, also known as milieu-limited alcoholism. In con- for the disorder, then how can they be held accountable
trast to the Type I alcoholics identified by Cloninger et al. for developing that condition?
(1981) were the “Type II” or male-limited alcoholics. Fortunately, to a scientist, genetic inheritance is
These individuals tend to be both alcoholic and involved viewed as only reflecting the impact of earlier environ-
in criminal behaviors. The male offspring of a “violent” ments upon the gene pool of past generations
alcoholic adopted in infancy ran almost a 20% chance of (Moalem & Prince, 2007). The individual’s genetic in-
becoming alcohol dependent regardless of the social sta- heritance reflects the impact of plagues, predation,
tus of the child’s adoptive parents. However, here again parasitic infestation, and geological upheavals on the
the statistics are misleading: While almost 20% of the gene pool of past generations, with genetic combina-
boys born to a “violent alcoholic” themselves eventually tions that offered a survival advantage being retained
became alcoholic, more than 80% of boys born to these and passed on to subsequent generations while those
fathers do not follow this pattern. This would suggest that that failed to offer a survival advantage were culled
environmental forces may play a role in the evolution of from the population (Moalem & Prince, 2007). Such
alcoholism for Type II alcoholics. modifications are not achieved easily, and genetic
Perhaps the strongest evidence of an environmental changes that provided an adaptation to one condition
impact on the development of alcoholism is the signifi- often cause an increased risk for other conditions
cant variations in the male:female ratio of those who (Moalem & Prince, 2007). For example, the authors
postulated that hemochromatosis11 in persons of Euro- doses of alcohol to the rats under rigidly controlled con-
pean descent might have given them an increased ditions. Rather than responding to the alcohol in a uni-
chance of surviving the bubonic plague of the 12th and form manner, the rats in the various laboratories had a
13th centuries. But this genetic adaptation brought with variety of responses. If the rats’ reaction to alcohol was
it the danger of significant organ damage in later life as determined by their genetic heritage alone, since they
the accumulated iron stores in the body caused destruc- were genetically identical, it would have been logical to
tion of various body tissues.12 expect a uniform outcome to this experiment. But the
The danger with our knowledge of genetics is not environment in each laboratory differed from the others
what we know, but what we think we know. Rather in significant ways.13 This study supports the contention
than simply being the expression of a genetic predispo- that cultural, social, and environmental forces play an
sition, the addictions are the end stage of a complex equally strong role in the evolution of SUDs as does the
process involving genetic heritage, exposure, social genetic inheritance.
feedback, and other factors. For example, nonfamilial The role of the dopamine D2 receptor sites. At this
alcoholism accounts for 51% of all alcohol-dependent time, the dopamine D2 receptor site theory appears to
persons, a finding that raises questions about the ge- be the most promising aspect of the medical model of
netic foundation of addictions since the individual’s ge- the addictions. But it is easy to forget that this is a hy-
netic heritage is passed on to him or her from the pothesis that may or may not be proven correct upon
previous generation (Renner, 2004a). This finding rein- further inquiry. For example, it is possible that the ob-
forces the truism that “genes confer vulnerability to but served findings reflect not a preexisting condition but
not the certainty of developing a mental disorder” the brain’s protective downregulation of receptor sites
(Hyman & Nestler, 2000, p. 96). in response to the repeated substance-induced release
Unfortunately, this does not prevent counselors of large amounts of dopamine (O’Brien, 2004).14 But
from speaking knowlingly of the patient’s “genetic load- the idea that a deficit in the dopamine D2 receptor
ing” for an addictive disorder. There are no genetic tests might predate the development of a SUD has received
that will identify such a genetic predisposition, but it is only limited support, something that advocates of the
assumed to be present if the patient has an SUD, espe- dopamine D2 receptor site theory tend to overlook
cially if another family member also has an addiction. (Krishnan-Sarin, 2000).
This ignores the fact that a genetic predisposition or Other biological vulnerability studies. Earlier in this
“loading” for an SUD does not guarantee that it will de- chapter, a study by Marc Schuckit (1994) was pre-
velop (Weinberger, 2005). It is not possible to predict sented as evidence of a biological predisposition toward
who will or will not develop a substance use disorder on substance use disorders in certain men. The author
the basis of genetic predisposition at this time (Madras, based this study on one conducted in the early 1980s
2002). The individual’s genetic predisposition should involving 223 men who were found to have an abnor-
be viewed only as a rough measure of his or her degree mally low physical response to a standard dose of alco-
of risk, not an inalterable outcome (Weinberger, 2005). hol. At the time of his earlier study, Schuckit had found
Significant evidence is emerging to suggest that that fully 40% of the men who had been raised by alco-
while the individual’s genetic heritage does set the holic parents but only 10% of the control group demon-
stage for his or her life, environmental experiences help strated this unusual response. A decade later, in the
determine which genes are activated or inactivated early 1990s, the author found that 56% of the men who
throughout the individual’s life span (Begley, 2007). had the abnormally low physiological response to alco-
One experiment that demonstrated this was discussed hol had progressed to the point of alcohol dependence.
by Tabakoff and Hoffman (2004). A series of genetically The author interpreted this finding as evidence that the
identical rats were sent to researchers in a number of
different laboratories, who then administered standard 13For example, how much time did the researchers spend touching or
petting the rats? Were they housed individually or in small groups?
What was the ambient noise level in the laboratory where the rats
11
See Glossary. were living? What was the room temperature in each laboratory? And
12
The manner in which a genetic adaptation to one condition might so on.
influence the expression of another, unrelated, disorder is far too 14One interesting study would be for researchers to identify young
complex to discuss further in this chapter. The reader is referred to children who had a dopamine D2 receptor deficit and then follow
Moalem and Prince (2007) for a more comprehensive discussion of them over the next 30–40 years to see what percentage developed a
this topic. substance use disorder and what percentage did not.
26 Chapter Three
abnormally low physical response to a standard dose of an The medical model and individual responsibility. For
alcoholic beverage might identify a biological “marker” some unknown reason we exempt addiction from our
for the later development of alcoholism. beliefs about change. In both popular and scientific
But an often overlooked point is that only a minority models, addiction is seen as locking you into an in-
of the men raised by an alcoholic parent demonstrated escapable pattern of behavior (Peele, 2004a, p. 36).
this abnormally low physiological response to the alco- One of the reasons for this therapeutic myth is the mis-
hol challenge test utilized by Schuckit (1994). Only 91 perception that a person’s biology always provides an
men of the experimental group of 227 had this abnor- excuse for unacceptable behavior. As Steven Pinker
mal response. Further, a full decade later, only 56% of (2002) observed, some point to biological research as
these 91 men (or just 62 men) appeared to have be- “the perfect alibi, the get-out-of-jail-free card, the ulti-
come dependent on alcohol. While this study is sugges- mate doctor’s excuse” (p. 49), a perspective that totally
tive of possible biochemical mechanisms that might absolves the individual of responsibility for choices she
predispose the individual toward alcoholism, it also il- or he made.
lustrates quite clearly that biological predisposition Proponents of the medical model usually point to
does not predestine the individual to develop an alcohol dramatic brain scan pictures from procedures such as
use disorder. the PET scan process, which shows the brains of addic-
Other challenges to the disease model of addiction. tive persons becoming very active when they are shown
Addictionologists are quick to raise the concept of neu- drug-use cues as evidence that the addictions are brain
roplasticity15 to support their belief that exposure to the disorders. Yet, as Sommers and Satel (2005) point out,
various drugs of abuse causes permanent changes in “it is easy to read too much into brain scans . . . they al-
how the individual’s brain is “wired.” The possibility most never permit scientists to predict whether a person
that the individual’s brain might also rewire itself, with a desire-activated brain will act on that desire. Nor
changing the synaptic connections between neurons can they distinguish between an impulse that is irre-
in response to experiential changes over time (such as sistible and an impulse that is not resisted” (p. 103).
abstinence/recovery), is quietly overlooked. The truth is Further, as the authors point out, the brain scans of ad-
that scientists know very little about the factors that fa- dicted persons who are experiencing a craving but who
cilitate or inhibit neuroplasticity, and thus it is unrealis- are resisting it show activation in the same regions of
tic to cite such evidence as supporting the belief that the brain, with indications that there is more activity in
the addictions cause permanent changes in the way the these regions of the brain than in the brains of those
patient’s brain responds to the presence or absence of who give in to the craving to use drugs. But this latter
drugs of abuse. observation is never pointed out by proponents of the
No matter how you look at it, addiction remains a addiction-as-a-brain-disease school of thought.
most curious “disease.” George Vaillant (1983) sug- There is an inherent conflict between those who be-
gested that to make alcoholism fit the disease model, it lieve in free will and those who advocate biological de-
had to be “shoehorned” (p. 4). Even if alcoholism was a terminism. To bridge this gap, proponents of the
disease, he said, “both its etiology and its treatment are medical model suggest that
largely social” (Vaillant, 1983, p. 4). Further, he sug-
gested that while genetics appear to determine the indi- in the gradation between determinism and free will,
vidual’s biological vulnerability to alcoholism, the the initiation of substance use may occur toward the
social environment determined whether or when this free-will end of the spectrum, whereas continued
transition might occur. abuse may fall more toward the deterministic end,
The alcohol “industry” spends an estimated $1 bil- after certain neurochemical changes have taken
lion a year to promote their product. If alcohol abuse/ place in the brain. Once the addictive process be-
dependence is indeed a “disease,” then why is the use of gins, neurobiological mechanisms make it increas-
the offending agent, alcohol, promoted through com- ingly difficult for the individual to abstain from the
mercial advertising? The answers raise some interesting drug. (Committee on Addictions of the Group for
questions about the role of alcohol in this society and the Advancement of Psychiatry, 2002, p. 706)
the classification of excessive alcohol use as a “disease.”
Thus, the individual is viewed as having freely cho-
sen to initiate the substance use, but that once entan-
15See Glossary. gled, he or she increasingly becomes a helpless victim of
his or her biology. From this perspective, the individual dependent persons successfully resist the desire to drink
essentially ceases to exist except as a genetically prepro- (or use illicit drugs) for weeks, months, years, or decades,
grammed disease process who is absolved of responsi- casting doubt on the concept of an “irresistible” craving
bility for his or her behavior. Consider, for example, the for alcohol/drugs of abuse. Could a hypothetical person
following case summary: The afflicted individual is an resist the ravages of breast cancer, or a brain tumor,
adolescent. One parent is a physician, while the other is without medical assistance?
a pharmacist. The parents, identified as the “Lowells” One central feature of the medical model of illness
were “well-versed in the clinical aspects of substance is that once a person has been diagnosed as having a
abuse, [but were] . . . outmaneuvered by the cunning certain “disease,” she or he is expected to take certain
that so often accompanies addiction” (Comerci, Fuller & steps toward recovery. According to the medical model,
Morrison, 1997, p. 64). In this clinical summary, the the “proper way to do this is through following the ad-
child is totally absolved of any responsibility for his or vice of experts (e.g., doctors) in solving the problem”
her manipulative behavior toward the parents.16 In- (Mais-to & Connors, 1988, p. 425). Unfortunately, as
deed, the case summary suggests that the disease was discussed in Chapter 1, physicians are not required
process brought with it the “cunning” necessary to out- to be trained in either the identification or the treat-
wit the parents, not that the parents were ill-equipped to ment of the addictions. The medical model of addic-
deal with their child’s behavior. tion thus lacks internal consistency: While medicine
Another challenge to the genetic predisposition claims that addiction is a “disease,” it does not routinely
model of the addictions is the phemonenon in which train its practitioners in how to treat this ailment.
the majority of those persons with a substance use disorder Finally, it should be pointed out that Jellinek (1960)
come to terms with it on their own, without any form of proposed a theoretical model of alcohol dependence,
professional or paraprofessional assistance (Peele, 2004a). not all substance use disorders. In spite of this fact, his
This is in stark contrast to the other medical disorders model has been applied to virtually every other form of
that require professional assistance or intervention to addiction without anybody doing the research to see if
control or cure, such as heart disorders, cancer, and his (1960) model did indeed apply to other drug use
others. If the addictions are true medical disorders, then disorders.
should they not follow the same treatment pattern as
the other diseases?
Summary
Proponents of the disease model often will state that
substance use disorders are “a brain disease. The behav- This chapter has explored some of the leading theories
ioral state of compulsive, uncontrollable drug craving, that attempt to answer the question of why people
seeking, and abuse comes about as a result of funda- use/abuse alcohol and drugs from the perspective of
mental and long-lasting changes in brain structure and what has come to be called the “medical” or “disease”
function” (Leshner, 1997a, p. 691). Yet when one model. Factors that modify the individual’s predisposi-
speaks with persons with an SUD, they usually admit tion toward or away from substance use disorders were
that they can resist the craving for their drug of choice, explored. The controversy surrounding the degree to
if the reward for doing so is high enough. Many alcohol- which the individual’s genetic inheritance also con-
tributes to or detracts from the individual’s predisposi-
tion to abuse chemicals was also discussed. Although
16Sommers and Satel (2005) refer to this process as the “doctrine of
E. M. Jellinek’s (1960) work has been the center of the
the ‘real me,’” in which it is assumed that the “real” me would never
do anything so detestable as attempt to manipulate the parents, and medical model of the addictions for more than 45 years,
the responsibility is shifted to the medical disorder rather than placed it was found to be flawed, and its applicability to the
on the individual. other substance use disorders has been challenged.
CHAPTER FOUR
Psychosocial Models of
the Substance Use Disorders
Treat the person with the disease, not the disease in ongoing debate over whether the substance use disorders
the person. are or are not an actual form of mental illness (Kaiser,
1996; Schaler, 2000; Szasz, 1988).
—Sir William Osler (1910) At what point does a trait that is just atypical or un-
usual become evidence of a “disease”? This debate is
Although the disease model has come to dominate contaminated by the intrusion of the pharmaceutical
the way that the substance use disorders (SUDs) are industry into the medical field. The shy person of a gen-
viewed, it has not met with universal acceptance. Many eration ago is now said to have “social phobia,” and by
health care professionals and scientists maintain that coincidence the pharmaceutical industry has a drug
there are no biological or personality traits that auto- that will treat this condition (“Don’t Buy It,” 2006). Last
matically predispose the individual to substance use dis- generation’s occasional impotence is this generation’s
orders (SUDs). Even today, “lively debate still abounds “erectile dysfunction,” and the pharmaceuticals indus-
about whether addiction is truly a disease at all or under try again has a family of compounds that will provide
what circumstances it may be conceptualized in that temporary relief. Both are examples of “disease mon-
manner” especially in the area of forensic psychiatry gering”1 (Healy, 2006, pp. 38, 5). But are they true dis-
(Gendel, 2006, p. 650). Some researchers suggest that ease states or industry-generated illusions of a “disease”
certain environmental forces are needed to activate the to boost sales of pharmaceutical agents?
biological predisposition toward addiction. In this chap- This question of whether addictions are true disease
ter, some of the psychosocial models of substance abuse states has become so muddled that
are examined.
today any socially-unacceptable behavior is likely to
be diagnosed as an “addiction.” So we have shopping
Disturbing Questions addiction, videogame addiction, sex addiction, Dun-
geons and Dragons addiction, running addiction,
Proponents of the disease model often point out that
chocolate addiction, Internet addiction, addiction to
Dr. Benjamin Rush first suggested that alcoholism was
abusive relationships, and so forth. . . . [A]ll of these
a disease more than 250 years ago. In his day, a “dis-
new “addictions” are now claimed to be medical ill-
ease” was anything classified as being able to cause an
nesses, characterized by self-destructiveness, compul-
imbalance in the nervous system (Meyer, 1996a). Most
sion, loss of coontrol, and some mysterious, as-yet-
certainly, alcohol appears capable of causing such an
unidentified physiological component. (Schaler,
“imbalance” or disruption in the normal function of
2000, p. 18, italics added for emphasis)
the CNS; and by the standards used by Benjamin Rush
in the 1700s, alcoholism could be classified as a dis- Through this process of blurring the distinction be-
ease. But those who point to Dr. Rush’s work overlook tween unacceptable behavior and actual disease states
the change that has occurred in the definition of “dis- we have “become a nation of blamers, whiners, and vic-
ease” since the 18th century. At the start of the 21st cen- tims, all too happy, when we get the chance, to pass the
tury the question of whether the addictions are true buck to someone else for our troubles” (Gilliam, 1998,
“disease states” is hardly clear. The branch of medicine p. 154), including the possibility that we have a “disease.”
charged with the treatment of the addictions, psychia-
try, is still defining what is and is not a manifestation of 1Defined by Healy as “selling a disease so you can sell treatments
mental illness (Bloch & Pargiter, 2002), and there is an for it” (p. 38).
28
Psychosocial Models of the Substance Use Disorders 29
One point that is often misunderstood by those both the same sense that an infection does. Alcohol or drugs
outside and within the medical field is that the concept do not magically appear in the individual’s body.
of a “disease” and its treatment are fluid, and that they Rather, the “victim” of this disorder must go through
change in response to new information. Stomach ulcers, several steps to introduce the chemical into his or her
once thought to be the consequence of stress-induced body.
overproduction of gastric acids, are now viewed as the Consider the case of heroin addiction: First, the ad-
site of a bacterial infection in the stomach wall and are dicted individual must perceive the need for it, and
treated with antibiotics rather than tranquilizers, for then obtain the money to buy it. Then, he or she must
example. The very nature of the concept of “disease” find somebody who is selling heroin, and complete the
makes it vulnerable to misinterpretation, and a small transaction to buy heroin for personal use (in a manner
but vocal minority both within and outside the field of that will not bring about the attention of the legal sys-
psychiatry question whether the medical model should tem). Next, the “victim” must find a safe place and pre-
be applied at all to behavioral disorders. pare the heroin for injection. This involves mixing the
To complicate the issue of how to define the addic- powder with water, heating the mixture, and then at a
tions is the fact that neither alcohol nor drugs are inher- predetermined point pouring it into a syringe. The indi-
ently evil (Shenk, 1999; T. Szasz, 1997; T. S. Szasz, vidual must then find a vein to inject the drug into, and
1988, 1996). Rather, it is the manner in which they are insert the needle into the vein. Finally, after all these
used by the individual that determines whether they are steps, the individual must actively inject the heroin into
helpful or harmful. Is cocaine “good” or “bad”? As a his or her own body. This is a rather complicated chain
topical anesthetic, cocaine might provide welcome re- of events, each of which involves the active participa-
lief from injury, while the same cocaine, if abused, tion of the individual, who is now said to be a “victim”
might lead the individual down the road to addiction. of a disease process. If it took as much time and energy
But society has made a series of arbitrary decisions to to catch a cold, pneumonia, or cancer, it is doubtful
classify some drugs as “dangerous” and others as being that any of us would ever be sick a day in our lives!
acceptable for social use. The antidepressant medica- Thus, the first question—What is a “disease” state?—
tion Prozac (fluoxetine) and the hallucinogen MDMA is still rather ambiguous and undefined. Then, there is
both cause select neurons in the brain to release the the question of how the behavioral sciences should ad-
neurotransmitter serotonin, and then block its reabsorp- dress the addictive disorders. It is any wonder that there
tion. Surprisingly, although fluoxetine is an antidepres- is such a lack of consensus as to which behavioral
sant, a small but significant percentage of patients who model best fits the addictions?
started taking it did so for its mood-enhancing effects
rather than because they needed an antidepressant
Multiple Models
(“Better Than Well,” 1996).2 This raises a dilemma: If a
pharmaceutical is being used by a person only because Although the medical model predominates the field of
she or he enjoys its effects, where is the line between substance abuse rehabilitation in the United States,
the legitimate need for that medication and its abuse? there are a number of theoretical models within the be-
The basis for making this distinction is often not in sci- havioral sciences that also address the problem of the
entific studies, but in “religious or political (ritual, so- SUDs. One of the less credible models is known as the
cial) considerations” (Szasz, 1988, p. 316). moral model. In spite of the scientific research that sug-
The unique nature of addictive disorders. In spite of all gests there is a genetic predisposition toward addictions,
that has been written about the problem of alcohol/drug as well as body of psychological data that suggests spe-
use/abuse over the years, researchers continue to over- cific personality traits that predispose the individual
look a very important fact. Unlike the other diseases, toward addictive behaviors, a significant percentage
the substance use disorders require the active participa- of the population still believes the SUDs, especially
tion of the “victim” in order to exist. The addictive dis- alcoholism, are self-inflicted disorders (Schomerus,
orders do not force themselves on the individual in Matschinger, & Angermeyer, 2006). Schomerus and
colleagues concluded after telephone interviews with
2
The same point might be made about the drugs used to treat “erec- 1,012 adults living in Germany that 85% thought that
tile dysfunction”: A small, but significant percentage of those taking
alcohol dependence was a self-inflicted disorder, while
this medication do so not because they need to do so, but because
they find it enhances sexual performance. Is this appropriate, or is it only 30% of the sample thought that it could be treated
medication abuse? effectively. The results of this study underscore the rigid
30 Chapter Four
TABLE 4.1 Theoretical Models of Alcohol/Drug Abuse
Moral model Temperance model Spiritual model Dispositional disease model
Core The individual is viewed This model advocates Drunkenness is a sign that The person who becomes
Element as choosing to use the use of alcohol in the individual has slipped addicted to alcohol is somehow
alcohol in problematic moderate manner. from his or her intended different from the nonalcoholic.
manner. path in life. The alcoholic might be said to
be allergic to alcohol.
Educational model Characterological model General systems model Medical model
Core Alcohol problems are Problems with alcohol People’s behavior must be The individual’s use of
Element caused by a lack of use are based on viewed within context of alcohol is based on biological
adequate knowledge abnormalities in the social system in which predispositions, such as his or
about harmful effects personality structure they live. her genetic heritage, brain
of this chemical. of the individual. physiology, and so on.
Source: Chart based on material presented by Miller & Hester (1995).
dichotomy between the scientific world, where the ad- There are a number of variations on this “predisposing
dictions are viewed as the outcome of biological or so- personality” theme, but as a group they all are strongly
cial forces, and the belief system of the general public, deterministic in the sense that the individual is viewed as
which holds that the addictions are a reflection of an being powerless to avoid the development of an addictive
unspecified moral weakness. disorder if she or he is exposed to certain conditions. This
In contrast to the moral model, the psychosocial is clearly seen in the “very word addict [that] confers an
models of addictions maintain that the individual has identity that admits no other possibilities” (Peele, 2004a,
come to rely on alcohol or drugs because of a complex p. 43, italics in original). For example, a number of re-
process of learning. Some of the more important psy- searchers have suggested that the personality traits of im-
chosocial models of the SUDs are reviewed in Table 4.1. pulsiveness, thrill seeking, rebelliousness, aggression, and
It should be noted that although each of these theoreti- nonconformity were “robust predictors of alcoholism”
cal models has achieved some degree of acceptance in (Slutske et al., 2002, p. 124).
the field of substance abuse rehabilitation, no single However, these conditions can also be viewed as dif-
model has come to dominate the field as has the disease ferent manifestations of a common genetic disfunction
model. (Slutske et al., 2002). Personality traits of nonconfor-
mity, risk taking, and rebelliousness are thought to re-
flect disturbances in the dopamine utilization system in
The Personality Predisposition Theories
the brains of individuals who would develop an alcohol
of Substance Abuse use disorder (AUD). To test this hypothesis, the team of
Personality factors have long been suspected to play a Heinz et al. (1996) examined the clinical progress of 64
role in the development of the substance use disorders, alcohol-dependent individuals and attempted to assess
but research has failed to isolate a prealcoholic person- their sensitivity to dopamine through various biochemi-
ality (Renner, 2004a). In spite of this fact, many clinical tests. In spite of the expected association between
cians argue that certain personality types seem to be depression, anxiety, disturbances in dopamine utiliza-
associated with alcoholism more often than one would tion, and alcohol use problems, the authors found little
expect by chance. Further, it is often argued by some evidence to support the popular beliefs that alcoholism
types of psychopathology seem to be more common for is associated with depression, high novelty seeking, or
certain personality types than for others. Type II alco- anxiety.
holic males, for example, were found by Cloninger, Sig- The researcher C. R. Cloninger proposed what he
vardsson, and Bohman (1996) to be three times more called a “unified biosocial” model of personality, in
likely to be depressed, and four times as likely to have which certain individuals who were predisposed to
attempted suicide, as Type I alcoholic males. exhibit a given personality characteristic (such as risk
taking) could have that trait reinforced by social/envi- (Ziedonis & Brady, 1997) and 90% of individuals with
ronmental factors. In other words, Cloninger attempted ASPD will have an alcohol/drug use problem at some
to identify the interaction between genes and environ- point in their lives (Preuss & Wong, 2000). This is not
ment (Howard, Kivlahan, & Walker, 1997). He then to suggest that the antisocial personality disorder caused
applied his theory of personality to the evolution of al- the substance use. Rather, ASPD and the addiction are
cohol use disorders, on the theory that individuals who postulated to be two separate disorders, which might co-
were high on the traits of Harm Avoidance (HA), Nov- exist in the same individual (Schuckit, Klein, Twitchell, &
elty Seeking (NS) and Reward Dependence (RD) Smith, 1994; Stetter, 2000).4
would be “at risk” for developing an AUD. Many point An alternate theory about how people began to be-
to this research to support their contention that there is lieve that there was an “addictive personality” might be
an “alcoholic personality” or an “addictive personality” traced to the impact of psychoanalytic thought in the
that predisposes the individual to develop an SUD. first half of the 20th century. While there is no standard
Howard, Kivlahan, and Walker (1997) examined a definition or form of psychoanalysis, as a group the psy-
series of research studies that attempted to relate choanalytic schools postulated that substance abuse is a
Cloninger’s theory of personality to the development of symptom of an underlying disorder that motivates the
alcohol abuse/addiction. The authors found that even individual to abuse chemicals in an attempt to calm
when a test specifically designed to assess Cloninger’s these inner fires (Leeds & Morgenstern, 2003). Various
theory of personality was used, the results did not psychoanalytic theorists offered competing theories as
clearly support his theory that individuals high on the to the role of substance misuse in the personality of the
traits of HA and RD were likely have an alcohol use dis- addicted person, but essentially all major psychoana-
order. Indeed, it has been suggested that the “alcoholic lytic theories suggest that there is an “addictive person-
personality” is nothing more than a clinical myth within ality” that suffers from an internal conflict that paves
the field of substance abuse rehabilitation (Gendel, the ground for addictive behavior. While theoretically
2006; Stetter, 2000). According to this theory, clinicians appealing, psychoanalytic inquiry has failed to agree on
are trained to expect certain characteristics and then the nature of this conflict or how it might be addressed
identify individuals who meet those expectations, selec- (Leeds & Morgenstern, 2003). But psychoanalytic the-
tively recalling those cases that most closely meet the ories have continued to influence how addictive behav-
characteristics that they were trained to expect3 and for- iors are viewed in spite of the identified failings of these
getting those that did not. schools of thought.
But in spite of the limited evidence supporting these An example of this was offered by Khantzian (2003b),
beliefs, clinicians continue to operate on the assump- who suggested that individuals with anxiety disorders
tions (a) that alcohol-dependent individuals are devel- might be drawn to the use of compounds such as alco-
opmentally immature, (b) that the experience of hol, benzodiazepines, opioids, or the increasingly rare
growing up in a disturbed family helps to shape the per- barbiturates because such compounds offer individuals
sonality of the future alcoholic, and (c) that alcohol- temporary relief from their defensiveness and help
dependent individuals tend to overuse ego defense them to feel less isolated, lonely, anxious, and empty.
mechanisms such as denial. Unfortunately, much of Along similar lines, Karen Horney (1964) suggested
what is called “treatment” in the United States rests on that individuals used alcohol to numb themselves to
such assumptions about the nature of addicted people emotional pain.
that have not been supported by clinical research. Another perspective on the AUDs is offered by
Traits identified in one research study as being central Reich and Goldman (2005), who found that high-risk
to the personality of addicted people are found to be of and low-risk alcohol users seemed to have different ex-
peripheral importance in subsequent studies. pectations for their alcohol use. High-risk alcohol
In the face of this evidence, then, one must ask how users, as a group, tended to expect positive effects from
the myth of the “alcoholic personality” evolved. One their alcohol use, especially in the realm of social in-
possibility is that researchers became confused by the teractions and general arousal. In contrast, low-risk al-
high comorbidity levels between alcohol/drug use dis- cohol users tended to expect more negative outcomes
orders and antisocial personality disorder (ASPD). This from alcohol use, such as expecting alcohol to be more
is understandable considering that between 84%
4The antisocial personality disordered client is discussed in more de-
3Which is called the “illusion of correlation.” tail in Chapter 24.
32 Chapter Four
sedating and to negatively impact their social interaction search into the subject it remains unclear whether
skills, according to the authors. Thus, one factor that must there is a relationship between the individual’s person-
be assessed in understanding the individual’s alcohol use ality style and the specific drugs that she or he abuses
is his or her expectations for the impact of drinking on his (Grekin, Sher, & Wood, 2006). The strongest associa-
or her life. tion between personality style and substance use is the
A different and some would say more mechanical view one between antisocial personality disorder5 and the
of the addictions is offered by those who view human be- SUDs, according to the authors. Thus, the issue of
havior as following certain rules of reinforcement/punish- whether certain pesonality styles predispose the individ-
ment: The behavior modification perspective suggests ual to SUDs is not clear at this time.
that humans, like all animals, work to either (a) in-
crease personal pleasure or (b) decrease discomfort. Be- Real Versus Pseudo Personality Issues
haviors that allow the individual to accomplish one of
Having established that what is or is not a true “disease”
these goals is said to be “reinforcing” while those behav-
state is still ill-defined and that the behavioral sciences
iors that achieve the opposite are said to be “punish-
still do not understand how the individual’s personality
ing.” From this perspective, the various drugs of abuse
interacts with the addictions, it is time to complicate
might be said to offer the individual both social support
the issue even further.6 The addictions, by virtue of
and recognition (usually a positive outcome), escape
from perceived emotonal or physical pain, while offer- their very existence, require individuals to make certain
ing escape from unpleasant affect states (such as pain, adaptations in how they face the demands of daily life,
depression, shame, etc.). Eventually, as the addiction in order to allow the addiction to continue to exist. In
takes hold of the individual, she or he begins to use other words, at least some of the association between
chemicals not so much for the original benefits but to the SUDs and personality types might be explained by
avoid the distress of the withdrawal process. Thus, from the impact that the substance use disorder has on the
this perspective, the addictive disorders might be viewed growth of the individual’s personality (Grekin, Sher, &
as following the rules of behavioral learning and behavior Wood, 2006). While someone is in a rehabilitation pro-
modification. gram, for example, it is not uncommon for the addicted
A cautionary note about the “addictive personality” person to say, “I never thought that I would do _____, but,
was offered by Pihl (1999). The author, drawing upon well, I did do it.” In Alcoholics Anonymous,7 this is called
earlier research, pointed out that 93% of the early re- “hitting bottom,” a process in which addicted individuals
search studies that attempted to isolate the so-called ad- come to accept that they have engaged in various unac-
ceptable behaviors8 in the service of their addiction.9
dictive personality were based on samples drawn from
It is thus important to keep in mind that the impact
treatment centers. While research on such samples
of the drugs of abuse on the individual’s brain might
often does reveal important information about the
alter his or her behavior in such a manner as to simu-
SUDs that are useful in treatment, such studies also ig-
late various forms of psychopathology.10 Under normal
nore the major differences between those who do or do
not enter treatment for a substance use problem. The
5
person with an SUD who enters treatment because she Discussed in Chapter 24.
6
or he recognizes the need is far different from the one At this point, the reader is welcome to groan in frustration or despair.
7Discussed in Chapters 5 and 35.
who does so because of external forces such as family or
8Such as steal from family members, lie to trusted friends/family
legal pressures. Both groups of people are potentially
members, commit crimes, engage in prostitution and/or promiscuous
far different from the person who refuses to enter treat-
sex, spend money intended for support of the family on their drug of
ment under any circumstances. There is a very real choice, etc.
possibility that the early studies cited by Pihl (1999) 9An interesting question that might be debated either way is whether
might have isolated a “treatment personality” more the person who engaged in such behaviors did so because of the pres-
than an “addictive” personality, with those who enter ence of the addiction or because she or he had the potential to engage
formal rehabilitation programs having common per- in such behaviors and they were simply activated by the addiction.
Which came first: the chicken or the egg?
sonality traits, compared with those who do not enter 10For example, amphetamine or cocaine-induced paranoia. If the in-
treatment.
dividual should become violent while under the influence of a chem-
While researchers have found that certain traits, ical, is this because she or he is a violent person or because she or he
such as neuroticism and disinhibition, seem to predis- was under the influence of the chemical? The issue of co-existing
pose the individual to SUDs, in spite of decades of re- mental illness and the SUDs will be discussed in Chapter 24.
conditions, such behaviors are often interpreted as The Final Common Pathway Theory
signs of a personality disorder or of a mental illness. of Addiction
As will be discussed in Chapter 24, distinguishing
true personality disorders from substance-induced As should be evident by now, most practitioners in the
pseudo-personality disorders is difficult and often re- field view the addictions as a multimodal process, rest-
quires extended observation of the now substance- ing on a foundation of genetic predisposition, and a
free client. But for the sake of this chapter, it is process of social learning (Monti, Kadden, Rohsenow,
sufficient to say that the behavioral sciences must at- Cooney, & Abrams, 2002). But to date both the biologi-
tempt to identify treatment methods for a disorder that cal and the psychosocial theories of addiction have
might or might not be a true disease, which holds the failed to explain all the phenomena found in the sub-
potential to distort the individual’s behavior pattern stance use disorders, and a grand unifying theory of ad-
from his or her personal norm. diction has yet to emerge.
Thus, one reason there are so many different per- But there is another viewpoint to consider, one called
spectives on the nature of the addictive disorders in the final common pathway (FCP) theory of chemical de-
the behavioral sciences is that the nature of the beast pendency. In a very real sense, FCP is a nontheory: It is
itself—the addictions—is so poorly defined. Further, not supported by any single group or profession. How-
the understanding of personality growth and develop- ever, the final common pathway perspective holds that
ment with all of its subtle variations, not to mention addiction to chemicals is an end stage disease, or a com-
the study of those forces that initially shape and later mon end point (Sommer, 2005). In their discussion of
maintain addiction, are still so poorly defined that it the genetics of alcohol dependency, Nurnberger and
is quite impossible to say with any degree of certainty Bierut (2007) observed that “there are different paths to
that there are specific personality patterns that may alcoholism and different pathways underlying them”
precede the development of substance use disorders, (p. 51). The authors also point out that individuals in
or how the behavioral sciences might best view the the early stages of alcohol dependence demonstrate a
addictions. For the immediate and foreseeable future remarkable variation in their specific symptoms, al-
there are going to be many different, conflicting theo- though by the latter stages of the disorder there is less
ries about the application of the behavioral sciences variation in how the disease manifests itself in different
to the addictions. individuals.
O’Brien and McLellan (1996) offered a modified According to the FCP theory, a multitude of different
challenge to the disease model of the addictions as it factors contribute to or detract from the individual’s risk
now stands. The authors accepted that drug/alcohol of developing an SUD. In this way, the FCP model
addiction are forms of chronic “disease.” But they might be viewed as similar to the biopsychosocial model,
state that while the addictive disorders are chronic which holds that the “addictive behaviors are complex
diseases like adult-onset diabetes or hypertension, disorders multiply determined through biological, psy-
there also are behavioral factors that help to shape the chological and sociocultural processes” (Donovan,
evolution of these disorders. Thus, according to the 2005, p. 2). Proponents of this position acknowledge a
authors, “Although a diabetic, hypertensive or asth- possible genetic predisposition toward substance abuse.
matic patient may have been genetically predisposed But the FCP theory also suggests that it is possible for a
and may have been raised in a high-risk environment, person who lacks this genetic predisposition for drug
it is also true that behavioral choices . . . also play a part dependency to become addicted to chemicals, if she or
in the onset and severity of their disorder” (p. 237). It is he has the proper life experiences (including extended
the individual’s behavioral choices that will help to exposure to the drugs of abuse).
shape the evolution of the addictive disorders. For Strong support for the final common pathway model
example, if an obese person were to lose 10% of his or of addiction might be found in the latest neurobiological
her body weight after being diagnosed with type 2 dia- research findings. It is now the general consensus that
betes and start a steady program of exercise, he or she the same dopamine-based motivational and reward sys-
would be making behavioral choices that impacted tems that evolved to help the species survive are also ei-
the disease state. The individual retains responsibility ther directly or indirectly implicated in the development
for correcting his or her behavior, even if he or she of addictions (Ivanov, Schulz, Palmero, & Newcorn,
has a “disease” such as addiction (Vaillant, 1983, 2006). Rewarding experiences (either natural or drug-
1990). induced) increase the concentration of a neurochemical
34 Chapter Four
involved in memory formation known as 6FosB,11 in in the nucleus accumbens will inform the cortex that
the nucleus accumbens. This makes clinical sense: In whatever the individual just did (in the example cited
the wild, it would be to the individual’s advantage to be here, drink water when hot and thirsty) was good for
able to recall cues that identified natural rewards such him or her. This information is carried to the amygdala
as food, water, or sex. and hippocampus regions of the brain to establish a mem-
Unfortunately, when compared to the natural rein- ory of the event that triggered the reward circuits for future
forcers that the individual is likely to encounter in life reference. At the same time, the cortical control/decision-
(i.e., food, water, sex) the drugs of abuse cause the making regions of the brain use the information to es-
pleasure center to react so strongly that it can be said to tablish a hierarchy of rewards, which then help to
“short circuit” the entire system. This is clearly seen in shape future behavioral decisions.12
the observation that the drugs of abuse cause a transi- Admittedly, factors such as drug availability, the re-
tory fivefold to tenfold increase in the dopamine levels inforcing potential of the drug being used, and the avail-
in the nucleus accumbens region of the brain, far more ability of drug-free alternative activities interact with the
than the levels observed when the individual encoun- individual’s biological potential for addiction and exist-
ters a natural reinforcer. Further, repeated episodes of ing social supports to contribute to or reduce the possi-
alcohol/drug-induced pleasure induce a process of be- bility of the user’s developing an SUD. But the
havioral overlearning, in which the individual becomes important point is that all of the drugs of abuse (includ-
very sensitive to environmental cues associated with the ing alcohol) activate the same nerve pathways involved
substance-induced pleasure response and comes to atin the process of learning/memory formation in addition
tach great importance to repeating the experience to the reward circuitry in the brain (Correia, 2005;
(“Addiction and the Problem of Relapse,” 2007; Wolf, 2006). They share this final common pathway in
Hyman, 2005). At the same time, those brain regions in- spite of differences in their route of administration or
volved in behavioral inhibition (especially the insula re- chemical structure. From this perspective, the disorder
gion of the brain) become less active, enhancing the of addiction might be viewed as one with multiple
drive to abuse the drugs of choice again (Bechara, 2006; forms (activating chemicals) but a common etiology
Gendel, 2006; Volkow, 2006a). (Shaffer et al., 2004).
This ability to activate the brain’s reward system is As a side effect of the process of drug-centered mem-
called the “pharmacological reward potential” of a ory formation, the individual’s environment becomes
compound. The various drugs of abuse create an in- flooded with behavioral cues associated with substance
tense, but false, signal in the brain that is interpreted as use (sights, smells, locations, specific sounds, people,
indicating the arrival of something with a huge fitness/ etc.). These cues trigger the release of small amounts of
survival benefit (Nesse & Berridge, 1998; Reynolds & dopamine within the reward system, and the cortex,
Bada, 2003). Repeated exposure to the drugs of abuse having “learned” to interpret these cues as a reminder
initiates a process of “restructuring” in the brain’s re- of past drug-induced pleasure, motivates the individual
ward system, memory centers, and the higher cortical to seek out alcohol/drugs once more (Viamontes &
functions that control reward-seeking behaviors. Strong Beitman, 2006). The subjective experience is one of
drug-centered memories are formed, helping to guide “craving” for the drug or alcohol until the desired sen-
the individual to select behavioral choices that lead sation is once again experienced (Anthony, Arria, &
to further drug-induced rewards (D. Brown, 2006; Johnson, 1995; Nutt, 1996; O’Brien, 1997). This sensa-
Bruijnzeel, Repetto, & Gold, 2004; Gardner, 1997; tion of “craving,” while admittedly quite strong, is not
Gendel, 2006; Kilts, 2004; Reynolds & Bada, 2003; overpowering.
Volkow, 2006). Essentially, a normal biological process If the individual establishes and maintains abstinence,
that evolved to help early humans survive in the wild these memory traces between past episodes of substance-
has been subverted by the reward potential of the com- induced pleasure and behavioral cues will eventually be-
pounds that they have invented. come weaker. This takes an extended period of time,
This process is clearly seen in the neuropharmacol- many months, or even years, but the result is that the indi-
ogy of the drugs of abuse: Initially the nucleus accum- vidual will experience fewer and less intense periods of
bens is involved in the initial reinforcing effects of a “craving” over time. To treat the addiction, the chemical
compound, releasing significant amounts of dopamine
12For example, “Getting some water to drink would be nice right now,
in response to drug exposure. The release of dopamine
but I am really starving, and so having something to eat from the re-
11Also known as “delta FosB.” See Glossary. frigerator sounds even better at the moment!”
dependency counselor must identify the forces that fail to document such a difference. For each study that
brought about and support each individual’s drug ad- claims to have isolated personality characteristics that
diction. Further, it is necessary to help the individual seem to predispose one toward addiction, other studies
identify the internal and external cues that trigger fail to find that these characteristics have predictive
thoughts and urges to engage in further drug abuse. On value, or find that the personality characteristic in
the basis of this understanding, the chemical depend- question is brought about by the addiction and does
ency counselor might then establish a treatment pro- not predate it.
gram that will help the individual abstain from further It was suggested that the medical model of addiction
chemical abuse. is a metaphor through which people might better un-
derstand their problem behavior. However, the medical
model of addiction is a theoretical model, one that has
Summary not been proven, and one that does not easily fit into
Although the medical model of drug dependency has the concept of disease as medicine in this country un-
dominated the treatment industry in the United derstands the term. Indeed, it was suggested that drugs
States, this model is not without its critics. For each were themselves valueless, and that it was the use to
study that purports to identify a biophysical basis for which people put the chemicals that was the problem,
alcoholism or other forms of addiction, other studies not the drugs themselves.
CHAPTER FIVE
Addiction as a Disease
of the Human Spirit
Primack and Abrams (2006) argue convincingly that this measurement, or replication under controlled condi-
culture “is probably the first major culture in human his- tions or experimental verification were worthy of belief
tory with no shared picture of reality” (p. 4). It is through (Cahill, 2006). This emphasis on what would be called
this shared view of reality that the individual member of the scientific method forced a growing schism between
a society gains a sense of perspective on his or her place those who espoused this position and those who held to
in the universe. This perspective, in turn, provides the traditional religious belief, since by definition God, who
individual with a sense of being “grounded” in the real- stands above and outside of His creation, cannot be sub-
ity in which he or she exists. Lacking this sense of being jected to experimental verification (Cahill, 2006). By
grounded, the person is at risk of developing a discon- the start of the 21st century, science and spirituality had
nection syndrome in which she or he is blinded to his moved so far apart that many doubted that they might
or her place in reality. ever be reconciled.
Groundedness requires the individual to place the Spirituality might be viewed as one of the factors that
“self” into a direct relationship with something greater, helps to define, give structure to, and provide a framework
be it the whole of creation or a “higher power” that within which to interpret human existence (Mueller,
transcends the self. The converse of this, the lack of a Plevak, & Rummans, 2001; Primack & Abrams, 2006). It
direct relationship with something greater than oneself, provides what Primack and Abrams (2006) call the “big
might be said to reflect a disease of the spirit, or the self. picture” (p. 16), or worldview, within which the individ-
Within this context, the addictions might be viewed as a ual interprets the meaning of his or her existence. “This
spiritual disorder, in that rather than establish a work- picture of reality was constructed through a lifetime of
ing relationship with something greater than the self, hearing such stories and witnessing or performing ritu-
the individual settles for the false promise of a sense of als . . . [t]hat made sense of the world” (Primack &
meaning offered by recreational chemicals (Alter, 2001). Abrams, 2006, p. 16).
It thus follows that the concept of alcoholism as a spiri- Such rituals include the religious system in which
tual disorder is the basis of the Alcoholics Anonymous the individual lives. But in the Western world, so great
(AA) 12-Step program (Miller & Hester, 1995; Miller & has the schism between science and spirituality be-
Kurtz, 1994). To understand the reality of addiction is, come that many “physicians question the appropriate-
ultimately, to understand something of human nature ness of addressing religious or spiritual issues within a
itself. In this chapter, the spiritual foundation for the medical setting” (Koenig, 2001, p. 1189). This is an ex-
addictions is explored. tension of the “Cartesian bargain” (Primack & Abrams,
2006, p. 78) by which the Church and the emerging sci-
ences established “turf” for each: If it concerned physi-
The Rise of Western Civilization, cal matter, it was in the realm of science, and spiritual
or How the Spirit Was Lost matters fell into the purview of the Church (Primack &
One could convincingly argue that the roots of the Abrams, 2006). Today’s physicians turn away from the
schism between the natural sciences and spirituality in need to discuss “spiritual” matters. The “spirit” is viewed
the Western world can be traced back to the Middle Ages, as a remnant of man’s primitive past, just like spears or
when philosophers such as Roger Bacon1 argued that clothing made of animal skins. But while science has
only those facts that can lend themselves to observation, effectively eliminated the worldview of the Middle
Ages, it has yet to replace the values once held dear by
1See Glossary. so many.
36
Addiction as a Disease of the Human Spirit 37
The ghost in the machine. The word spirit is derived The reader might question what relevance this ma-
from the Latin word spiritus. On one level this word terial has to a text on chemical dependency. The an-
simply means “breath” (Mueller et al., 2001). On a swer is found in the observation that the early members
deeper meaning, however, spiritus refers to the divine, of Alcoholics Anonymous (AA) came to view alco-
living life force within each of us. Human beings hold a holism (and by extension, the other forms of addiction)
unique position in the circle of life, for in humans, life, as a “disease” of the spirit. In so doing, they transformed
spiritus, has become aware of itself. Further, in addition themselves from helpless victims of alcoholism into ac-
to an awareness that we are no longer a part of nature, tive participants in the healing process of recovery.
each person is aware of his or her isolation from others Out of this struggle, the early members of AA shared
(Fromm, 1956). But the awareness of “self” carries a their intimate knowledge of the nature of addiction not
price: the painful understanding that each of us is for- as a phenomenon to be dispassionately studied but as
ever isolated from his fellows. Fromm termed this an elusive enemy that held each member’s life in its
awareness of one’s basic isolation as being an “unbear- hands. The early members of AA struggled not to find
able prison” (1956, p. 7), in which are found the roots the smallest common element that might “cause” ad-
of anxiety and shame. “The awareness of human sepa- diction but to understand and share in the healing
ration,” wrote Fromm, “without reunion by love—is process of recovery. In so doing, the early pioneers of
the source of shame. It is at the same time the source of AA came to understand that recovery was a spiritual
guilt and anxiety” (p. 8). process through which the individual recovered the
While the individual’s awareness of “selfhood” al- spiritual unity that she or he tried to achieve but could
lows him or her to determine what he or she will be- never find through chemicals.
come to a greater or lesser degree, it also places on the Self-help groups, such as Alcoholics Anonymous
individual the responsibility for the choices the person and Narcotics Anonymous,2 do not postulate any spe-
makes. A flower, bird, or tree cannot help but be what cific theory of how chemical addiction comes about
its nature ordains. A bird does not think about “being” a (Herman, 1988). Rather, it is simply assumed that any
bird or what kind of a bird it might become. The tree does person whose chemical use interferes with his or her
not think about “being” a tree. Each behaves according to life has a substance use disorder. The need to attend AA
its gifts to become a specific kind of bird or tree, living the was, to its founders, self-evident to the individual in that
life allotted to that tree or bird. But man possesses the twin either you were addicted to alcohol or you were not.
gifts of self-awareness and self-determination. Fromm The addiction was viewed as resting upon a spiritual
(1956, 1968) viewed the individual’s awareness of her or flaw within the individual, who was viewed as being
his fundamental isolation as being the price that she or
he has to pay for the power of self-determination. on a spiritual search. They really are looking for
Through self-determination, the individual learns that something akin to the great hereafter, and they flirt
she or he is different from the animal world by virtue of with death to find it. Misguided, romantic, foolish,
self-awareness. But only through the giving of “self” to needful, they think they can escape from the world
another through love does Fromm (1956, 1968) envi- by artificial means. And they shoot, snort, drink, pop
sion the individual as transcending his or her isolation or smoke those means as they have to leave their
to become part of a greater whole. pain and find their refuge. At first, it works. But,
The 20th-century philosopher Thomas Merton then it doesn’t. (Baber, 1998, p. 29)
(1978) took a similar view on the nature of human exis-
tence. Yet Merton clearly understood that one could In a very real sense, the drugs do not bring about addic-
not seek happiness through compulsive behavior, in- tion; rather, the individual abuses or becomes addicted
cluding the use of chemicals. Rather, happiness may be to drugs because of what he or she believes to be impor-
achieved through the love that is shared openly and tant (Peele, 1989). Such spiritual flaws are not uncom-
honestly with others. Martin Buber (1970) took an even mon and usually pass unnoticed in the average person.
more extreme view, holding that it is only through our But in the person with a substance use disorder, the
relationships that our life has definition. Each individ- spiritual flaw is expressed in part by the individual’s
ual stands “in relation” to others, with the degree of re-
lation, the relationship, being defined by how much of 2
Although there are many similarities between AA and NA, these are
the “self” one offers to the other and that which is re- separate programs. On occasion, they might cooperate on certain
ceived in return. matters, but each is independent of the other.
38 Chapter Five
affirmation of chemical abuse as acceptable, appropri- challenged the prevailing model of reality that was evi-
ate, and desirable as a means to reach a goal that is ill- dent in the 14th century. But what is the true nature of the
defined, at best. addictions? They are not totally a physical illness, nor are
Another expression of this spiritual flaw is the indi- they exclusively a mind disorder. Rather, the addictions
vidual’s hesitation to take responsibility for the “self” rest on a triad of interlocking forces: the individual’s psy-
(Peele, 1989). Personal suffering is, in a sense, a way of chological makeup, his or her biological inheritance/state
owning responsibility for one’s life. Most certainly, suf- of health, and the individual’s spirituality.
fering is an inescapable fact of life. We are, thus,
granted endless opportunities to take personal responsi-
bility for our lives. Unfortunately, modern society looks The Growth of Addiction:
down on the process of individual growth and the pain The Circle Narrows
inherent in growth. With its emphasis on individual
As the disease of alcoholism progresses, the individual
happiness, any pain is viewed as unnecessary, if not dys-
comes to center his or her life around the use of alco-
functional. Further, modern society advocates that pain
hol. Indeed, one might view the drugs of abuse as being
automatically be eradicated through the use of medica-
the axis (Brown, 1985; Hyman, 2005) around which
tions, as long as the pills are prescribed by a physician
the addicted person’s life revolves. Chemicals assume a
(Wiseman, 1997).
role of “central importance” (Brown, 1985, p. 78) for
both the addicted person and the family. It is difficult
A reflection of this modern neurosis is that many
for those who have never been addicted to chemicals to
people are willing to go to quite extraordinary lengths
understand this fact. The addicted person often will
to avoid our problems and the suffering they cause,
demonstrate a preoccupation with continued chemical
proceeding far afield from all that is clearly good and
use and will protect his or her source of chemicals. To
sensible in order to find an easy way out, building the
illustrate this point, it is not uncommon for cocaine ad-
most elaborate fantasies in which to live, sometimes
dicts to admit that if it came down to a choice, they
to the total exclusion of reality. (Peck, 1978, p. 17)
would choose cocaine over friends, lovers, or even fam-
ily. In many cases, the drug-dependent person has al-
Thus, individuals in a 12-Step program such as that
ready made this choice in favor of the chemicals.
of Alcoholics Anonymous will often speak of the ad-
Individuals with substance use disorders (SUDs)
dicted person as being “spiritually blind” and believe
often present with a level of self-centeredness that puz-
that recovery requires the individual to learn to sur-
zles, if not offends, others. This might be viewed as a
mount his or her spiritual flaws.
form of “moral insanity” that allows a chemical to take
on a role of central importance in the individual’s life.
Other people, other commitments, assume secondary or
Diseases of the Mind—Diseases of the
no importance. Addicted people might be said to “never
Spirit: The Mind-Body Question seem to outgrow the self-centeredness of the child” (Nar-
The question of whether the addictions are a brain disor- cotics Anonymous World Service Office, 1983, p. 1). As
der, as is suggested by the medical model (discussed in a result of this process
Chapter 3), or a spiritual disorder (the premise of this
chapter) has implications beyond that of the nature of we could not manage our own lives. We could not
the substance use disorders alone. The final answer to live and enjoy life as other people do. We had to
this question will rest on the foundation provided by so- have something different and we thought we found
ciety’s answer to the question of the nature of man. it in drugs. We placed their use ahead of the welfare
Twelve-step groups such as AA and NA view the addic- of our families, our wives, husbands, and our chil-
tions as being a spiritual illness. Their success in helping dren. We had to have drugs at all costs. (Narcotics
people to achieve and maintain abstinence would argue Anonymous, 1982, p. 11; italics in original deleted)
that there is some validity to this claim. Indeed, there is
an emerging body of evidence suggesting that strong There are many people whose all-consuming inter-
spiritual beliefs are positively correlated with recovery est is themselves. They are often presented as objects of
from substance use disorders (Sterling et al., 2006). ridicule in popular television shows, for example. They
However, society struggles to adhere to the artificial care for nothing outside of that little portion of the uni-
mind-body dichotomy that came about when science verse known as “self.” Their only love seems to be the
“self,” which they view as being worthy of adoration; they “nothing should come between me and my drug use!”
see themselves as superior to the average person. Just as No price is too high nor is any behavior so unthinkable
this personality type epitomizes the perversion of self- if it allows for further drug use. People will be forced to
love, so also might the substance use disorders be viewed lie, cheat, and steal to support their addiction and yet
as a perversion of self-love. It is through the use of chemi- will seldom if ever count the cost, as long as they can
cals that the individual seeks to cheat his or her self of the obtain the alcohol/drugs they crave.
experience of reality, replacing it with the distorted de- While many addicts have examined the cost de-
sires of the “self.” manded of their drug use and turned away from chemi-
To say that the addicted person demonstrates an on- cals with or without formal treatment, there are those
going preoccupation with chemical use is something of who accept this cost willingly. These individuals will go
an understatement. The addicted person may also through great pains to hide the evidence of their drug
demonstrate an exaggerated concern about maintain- addiction so that they are not forced to look at the grim
ing his or her supply of the drug, and he or she may reality that they are addicted.
avoid those who might prevent further drug use. For Although those who are alcohol/drug dependent are
example, consider an alcoholic who, with six or seven active participants in this process, they are also blinded
cases of beer in storage in the basement, goes out to buy to its existence. If you were to ask the alcohol-dependent
six more cases “just in case.” This behavior demon- person why she or he uses alcohol, you would be un-
strates the individual’s preoccupation with maintaining likely to learn the real reason. As one individual said, at
an “adequate” supply. Other people, when their exis- the age of 73, “You have to understand, the reason why
tence is recognized at all, are viewed by the addict ei- I drink now is because I had pneumonia when I was
ther as being useful in the further use of chemicals or as 3 years old.” For her to say otherwise would be for her to
being impediments to drug use. But nothing is allowed run the risk of admitting that she had a problem with al-
to come between the individual and his or her drug, if cohol, an admission that she had struggled very hard to
at all possible. It is for this reason that recovering ad- avoid for most of her adult life.
dicted persons speak of their still addicted counterparts As the addiction comes to control more and more of
as being morally insane. their lives, greater and greater effort must be expended
by addicts to maintain the illusion that they are living
normal lives. Gallagher (1986) told of one physician,
The Circle of Addition: addicted to a synthetic narcotic known as fentanyl, who
Addicted Priorities ultimately would buy drugs from the street because it
was no longer possible to divert enough drugs from hos-
The authors of the book Narcotics Anonymous con-
pital sources to maintain his drug habit. When the tell-
cluded that addiction was a disease composed of three
tale scars from repeated injections of street drugs began
elements: (a) a compulsive use of chemicals, (b) an ob-
to form, this same physician intentionally burned him-
session with further chemical use, and (c) a spiritual dis-
self on the arm with a spoon to hide the scars.
ease that is expressed through a total self-centeredness
Those who are addicted find that as the drug comes
on the part of the individual. It is this total self-centered-
to control more and more of their lives, they must invest
ness, the spiritual illness, that causes the person to de-
significant effort in maintaining the addiction itself.
mand “what I want when I want it!” and makes the
More than one cocaine or heroin addict has had to en-
individual vulnerable to addiction. But for the person
gage in prostitution (homosexual or heterosexual) to
who holds this philosophy to admit to it would be for
earn enough money to buy more alcohol or drugs.
that person to have to face the need for change. So
Everything is sacrificed to obtain and maintain an “ad-
those who are addicted to chemicals will begin to use
equate” supply of the chemicals.
the defense mechanisms of denial, rationalization, pro-
jection, and/or minimization to justify their increas-
ingly narrow range of interests both to themselves and
Some Games of Addiction
to significant others.
To support the addiction, individuals must come to One major problem in working with those who are ad-
renounce more and more of the “self” in favor of new dicted to chemicals is that these individuals will often
beliefs and behaviors that make it possible to continue seek out sources of legitimate pharmaceuticals either to
to use chemicals. This is the spiritual illness that is supplement their drug supply or as their primary source
found in addiction, for people come to believe that of chemicals. There are many reasons for this. First, as
40 Chapter Five
Goldman (1991) observed, pharmaceuticals may be sample on demand.5 The object of such “games” is to
legally purchased if there is a legitimate medical need for obtain a prescription for narcotics from a sympathetic
the medication. The drug user does not need to fear arrest doctor who wants to treat the patient’s obvious “kidney
if he or she has a legitimate prescription for a medication stone.” Patients with real injuries have been known to
signed by a physician. visit a multitude of hospital emergency rooms to have
Second, for the drug-addicted person who is able the same condition treated over and over again, just to
to obtain pharmaceuticals, the medication is of a obtain a prescription for a narcotic analgesic from each
known product at a known potency level. The drug treatment facility. In a large city, this process might be
user does not have to worry about low-potency “street” repeated 10 times or more (Goldman, 1991). Individu-
drugs, impurities that may be part of the drugs pur- als who utilize such manipulative games often study
chased on the street (as when PCP is mixed with low- medical textbooks to better simulate their “disease” for
potency marijuana), or misrepresentation (as when the attending physician.
PCP is sold as “LSD”). Also, the pharmaceuticals are
usually much less expensive than street drugs. For
example, the pharmaceutical analgesic hydromorphone A Thought on Playing the Games
costs about $1 per tablet at a pharmacy. On the street, of Addiction
each tablet might sell for as much as $45 to $100
(Goldman, 1991). A man, who worked in a maximum security penitentiary
In order to manipulate physicians into prescribing for men, was warned by older, more experienced correc-
desired medications, addicts are likely to “use ploys tions workers not to try to “outcon a con”—which is to
such as outrage, tears, accusations of abandonment, say that a person should not try to outmanipulate the in-
abject pleading, promises of cooperation, and seduc- dividual whose entire life centers on manipulating
tion” (Jenike, 1991, p. 7). The physician who works others. “You should remember that, while you are
with an addicted person must keep in mind that she home, watching the evening news, or going out to see a
or he cares little for the physician’s feelings. For the movie, these people have been working on perfecting
alcohol/drug-dependent person, the goal is to obtain their ‘game.’ It is their game, their rules, and in a sense
more drugs at virtually any cost. One favorite manipula- their whole life.” This is also a good rule to keep in
tive “scam” is for the addict (or accomplice) to visit a mind at all times when working with the addicted per-
hospital emergency room or the physician’s office in son. For addiction is a lifestyle, one that involves to a
an attempt to obtain desired medications through real large degree the manipulation of others into supporting
or feigned displays of suffering. Some individuals have the addiction. This is not to say that the addict cannot,
gone so far as to have false back surgery scars tattooed if necessary, “change his spots,” at least for a short time.
on to their backs to support their claim of having back This is especially true early in the addiction process or
pain due to trauma and/or failed surgery. Physicians during the early stages of treatment.
hear stories such as (a) “nobody else has been able Often, addicts will go “on the wagon” for a few days
to help me (except you),” (b) “my dog/cat/horse ate or perhaps even a few weeks to prove both to them-
the pain medication you gave me,”3 or (c) the ever- selves and to others that they can “still control it.” Un-
popular “I lost my pain medication and need another fortunately, whose who “go on the wagon” overlook the
prescription.”4 fact that by attempting to “prove” their control, they ac-
Patients being seen for reported “kidney stones,” tually demonstrate their lack of control over the chemi-
when asked to produce a urine sample for testing, have cals. However, as the addiction progresses, it takes more
been discovered adding a drop of blood to the sample and more to motivate addicts to give up their drug, even
from a pinprick to a finger to support their claim that for a short time. Eventually, even “a short time” be-
they were passing a kidney stone. Others have inserted comes too long.
foreign objects into the urethra to irritate the urethral There is no limit to the manipulations the addicted
lining so that they might provide a “bloody” urine person will use to support his or her addition. Vernon
Johnson (1980) spoke at length of how the addicted
3
Why does the dog/cat/horse never eat amoxicillin or antidepressant person will even use compliance as a defense against
medications, for example?
4 5Such patients run the risk of rupturing the urethra, with all the in-
These patients have earned such nicknames as frequent flyers, drug-
seekers, manipulators, repeaters, emergency department groupies, herent dangers of that problem, but this is viewed as a minor risk
fabricators, etc. when compared with the possibility of obtaining the desired drugs.
treatment. Overt compliance may be, and is often uti- addiction is the center of the universe. Addicts might go
lized as, a defense against acceptance of one’s own spir- without food for days on end, but very few would will-
itual, emotional, and physical deficits (Johnson, 1980). ingly go without using chemicals for even a short pe-
riod of time. Cocaine addicts have spoken about how
they would avoid sexual relations with their spouse or
Recovery Rests on a Foundation significant other in order to continue using cocaine.
of Honesty Just as the alcoholic will often sleep with an “eye
opener” (i.e., an alcoholic drink) already mixed by
One of the core features of the physical addiction to a
the side of the bed, some intravenous drug addicts have
chemical is “a fundamental inability to be honest . . .
been known to sleep with a “rig” (i.e., a hypodermic
with the self ” (Knapp, 1996, p. 83, italics in original).
needle) loaded and ready for use next to the bed so they
Honesty is the way to break through this deception, to
could inject the drug as soon as they woke up in the
bring the person face to face with the reality of the ad-
morning.
diction. The authors of the book Narcotics Anonymous
There is an old joke in Alcoholics Anonymous that
(1982) warned that the progression toward the under-
starts out: “How can you tell if an alcoholic is telling a
standing that one was addicted was not easy. Indeed,
lie?” The jokester then pauses for dramatic effect before
self-deception was part of the price that the addict paid
the punch line is delivered: “His (her) lips are moving!”
for addiction; according to the NA “big book,” it was
This grim “joke” underscores a painful reality: Ad-
“only in desperation did we ask ourselves, ‘Could it be
dicted people often lie to protect their addiction. They
the drugs?’” (pp. 1–2).
lie to family members, spouses, children, probation or
Addicted persons will often speak with pride about
parole officers, therapists, and physicians.
how they have been more or less “drug free” for various
The person in a relationship who forgets this dour
periods of time. An examination of the individual’s mo-
reality risks being manipulated by the addicted person
tivation for remaining drug free is often revealing: One
who seeks to protect his or her addiction. Because of
person, for example, might abstain from alcohol/drugs
the addiction, (a) for the person who is addicted, the
because of a fear of incarceration, while another might
chemical comes first, and (b) the addicted person cen-
abstain because she or he has been threatened with di-
ters his or her life around the chemical. To lose sight of
vorce should she or he relapse again. In each instance,
this reality is to run the danger of being trapped in the
the person is drug free only because of an external
addict’s web of lies, half truths, manipulations, or out-
threat that, when removed, opens the door to a re-
right fabrications.
lapse. It is simply impossible for one person to provide
Recovering addicts will speak of how manipulative
the motivation for another person to remain drug free
they were and will often admit that they were their own
forever. Many an addicted person has admitted, often
worst enemy. As they move along the road to recovery,
only after repeated and strong confrontation, that he or
addicts will realize that they would also deceive them-
she had simply switched addictions to give the appear-
selves as part of the addiction process. One inmate said,
ance of being “drug free.” It is not uncommon for an
“Before I can run a game on somebody else, I have to
opiate addict in a methadone maintenance program to
believe it myself.” As the addiction progresses, the ad-
use alcohol, marijuana, or cocaine. The methadone
dict does not question his or her perception but comes
does not block the euphoric effects of these drugs as it
to believe what he or she needs to believe to maintain
does the euphoria of narcotics. Thus, the addicted per-
the addiction.
son can maintain the appearance of complete coopera-
tion, appearing each day to take his or her methadone
without protest, while still using cocaine, marijuana, or False Pride: The Disease of the Spirit
alcohol at will.
In a very real sense, the addicted person has lost Every addiction is, in the final analysis, a disease of the
touch with reality. Over time, those who are addicted to spirit. Edmeades (1987) told of Carl Jung, who was
chemicals come to share many common personality treating an American, Rowland H., for alcoholism in
traits. There is some question whether this personality 1931. Immediately after treatment, Rowland H. re-
type, the so-called addicted personality, predates addic- lapsed, but Jung refused to take him back into analysis.
tion or evolves as a result of the addiction (Bean-Bayog, Rather, Jung said, Rowland’s only hope of recovery lay
1988; Nathan, 1988). However, this chicken-or-the-egg in his having a spiritual awakening, which he later
question does not alter the fact that for the addict, the found through a religious group in America. Thus,
42 Chapter Five
Carl Jung identified alcoholism as a disease of the spirit true place in the universe and the pain and suffering
(Peluso & Peluso, 1988). The Twelve Steps and Twelve that life might offer is one capable of any degree of spiri-
Traditions of Alcoholics Anonymous (1981) speaks of ad- tual growth (Peck, 1978). But many choose to turn away
diction as being a sickness of the soul. In support of this from reality, for it does not offer them what they think
perspective, Kandel and Raveis (1989) found that a they are entitled to. In so doing, these people become
“lack of religiosity” (p. 113) was a significant predictor of grandiose and exhibit the characteristic false pride or
continued use of cocaine and/or marijuana for young pathological narcissism so frequently encountered in
adults with previous experience with these drugs. For addiction (Nace, 2005a).
each addicted individual, a spiritual awakening appears One cannot accomplish the illusion of being more
to be an essential element of recovery. than what one is without an increasingly large invest-
In speaking with addicted persons, one is impressed ment of time, energy, and emotional resources. This
by how often the individual has suffered in his or her lack of humility, the denial of what one is in order to
lifetime. It is almost as if one could trace a path from give an illusion of being better than this, plants the
the emotional trauma to the addiction. Yet the addict’s seeds of despair (Merton, 1961). Humility implies an
spirit is not crushed at birth, nor does the trauma that honest, realistic view of self-worth. Despair rests on a
precedes addiction come about overnight. The individ- distorted view of one’s place in the universe. This de-
ual’s spirit comes to be diseased over time, as the addict- spair grows with each passing day, as reality threatens
to-be loses his or her way in life. Where we “all start out time and again to force on the individual an awareness
with hope, faith and fortitude” (Fromm, 1968, p. 20), of the ultimate measure of his or her existence.
the assorted insults of life often join forces to bring In time, external supports are necessary to maintain
about disappointment and the destruction of the indi- this false pride. Brown (1985) identified one character-
vidual’s spirit. The individual comes to feel an empty istic of alcohol as being its ability to offer the individual
void within. It is at this point that if something is not an illusion of control over his or her feelings. This is a
found to fill the addict’s “empty heart, he will fill his stom- common characteristic of every drug of abuse. If life
ach with artificial stimulants and sedatives” (Graham, does not provide the pleasure one feels entitled to, at
1988, p. 14). least one might find this comfort and pleasure in a
Few of us escape events that challenge us spiritually, drug, or combination of drugs, that free one from life’s
and we all face moments of supreme disappointment or pain and misery—at least for awhile.
ultimate awareness (Fromm, 1968). It is at this moment When faced with this unwanted awareness of their
that we are faced with a choice. People at this point may true place in the universe, addicted individuals must in-
come to “reduce their demands to what they can get and creasingly distort their perceptions to maintain the illu-
. . . not dream of that which seems to be out of their sion of superiority. Into this fight to avoid the painful
reach” (Fromm, 1968, p. 21). The danger develops reality of what is, the chemical injects the ability to
when the individual refuses to examine, or reduce, these seemingly choose one’s feelings at will. There is no sub-
demands but continues to assert that “I want what I want stance to the self-selected feelings brought about by the
when I want it.” The Narcotics Anonymous (1983) pam- chemical, only a mockery of peace. The deeper feel-
phlet The Triangle of Self Obsession noted that addicted ings made possible through the acceptance of one’s lot
persons tend to “refuse to accept that we will not be in life (which is humility) seem to be a mystery to the ad-
given everything. We become self-obsessed; our wants dicted person. The individual develops an ego-centered
and needs become demands. We reach a point where personality that is the antithesis of healthy spirituality
contentment and fulfillment are impossible” (p. 1). (Reading, 2007). This ego-centeredness might be seen
It is at this point that the individual encounters de- in the melancholy cry of what many recovering addicts
spair at the experience of being powerless. Existential- call “terminal uniqueness”: the supreme manifestation
ists speak of the realization of ultimate powerlessness as of the ego known as “false pride,” the antithesis of
an awareness of one’s nonexistence. In this sense, the humility.
individual feels the utter futility of existence. When Humility is the honest acceptance of one’s place in
people face the ultimate experience of powerlessness, the universe (Merton, 1961). Included in this is the
they have a choice. They may either accept their true candid and open acceptance of one’s strengths and
place in the universe, or they may continue to distort one’s weaknesses. At the moment when people become
their perceptions and thoughts to maintain the illusion aware of the reality of their existence, they may come to
of self-importance. Only when one accepts his or her accept their lot in life, or they may choose to struggle
against existence itself. Alcoholics Anonymous views ical addiction reflects a misguided attempt to achieve
false pride, or pathological narcissism, as a sickness of complete control over one’s life. The drugs of abuse
the soul (Nace, 2005b). In this light, chemical abuse also give an illusion of control to users, a dangerous il-
might be viewed as a reaction against the ultimate de- lusion that allows them to believe that they are asserting
spair of encountering one’s lot in life. The false sense of their own appetites on the external world while in real-
being that says “not as it is, but as I want it!” in response ity losing their will to the chemical.
to one’s discovery of personal powerlessness. Another manifestation of false pride is often found
Surprisingly, in light of this self-centered approach to in “euphoric recall,” a process in which the addicted
life, various authors have come to view the substance- person selectively recalls mainly the pleasant aspects of
abusing person as essentially seeking to join with a drug use while selectively forgetting the pain and suf-
higher power. But in place of the spiritual struggle neces- fering experienced as a consequence (Gorski, 1993). In
sary to achieve inner peace, the addicted person seems to listening to alcohol/drug-addicted people, one is almost
take a shortcut through the use of chemicals (Chopra, left with the impression that they are speaking about
1997; Gilliam, 1998; Peck, 1978, 1993, 1997b). Thus, the joys of a valued friendship instead of a drug of abuse
May (1988) was able to view alcohol/drug addiction as (Byington, 1997). More than one addicted person, for
sidetracking “our deepest, truest desire for love and example, has spoken at length of the quasi-sexual thrill
goodness” (p. 14). But this shortcut comes to dominate he or she achieved through cocaine or heroin, dismiss-
the life of addicts and they center more and more of ing the fact that abuse of this same drug cost him or her
their existence around the chemical, until at last they a spouse, family, or perhaps several tens of thousand of
believe that they cannot live without it. Further spiri- dollars. There is a name for this distorted view of one’s
tual growth is impossible when people view chemical self and one’s world that comes about with chronic
use as their first priority. chemical use: It is called the insanity of addiction.
As one expression of sidetracking the drive for truth
and spiritual growth, the addict comes to develop a sense Denial, Projection, Rationalization,
of false pride. This false pride expresses itself almost as a and Minimization:
form of narcissism. The clinical phenomenon of narcis-
The Four Horsemen of Addiction
sism is itself a reaction against perceived worthlessness
and loss of control (Millon, 1981). To cope, individuals The traditional view of addiction is that all human be-
become so self-centered that they “place few restraints on havior, including the addictive use of chemicals, rests
either their fantasies or rationalizations . . . their imagina- on a foundation of characteristic psychological defenses.
tion is left to run free” (Millon, 1981, p. 167). In the case of chemical dependency, the defense mech-
While drug-dependent persons are not usually nar- anisms that are thought to be involved are denial, pro-
cissistic personalities in the pure sense of the word, jection, rationalization, and minimization. Like all
there are significant narcissistic traits present in addic- psychological defenses, these defense mechanisms are
tion. One finds that false pride, which is based on the thought to operate unconsciously. While it is not clear
lack of humility, causes individuals to distort not only whether they predate the individual’s drug addiction or
their perceptions of “self,” but also of “other,” in the evolve in response to the personality changes forced by
service of their pride and their chemical use (Merton, the addiction, it is known that they exist to protect the in-
1961). In speaking of the normal division that takes dividual from the conscious awareness of anxiety. One
place within man’s soul, one must keep in mind that very real anxiety-provoking situation is the danger that
there are people whose entire life centers on the “self.” the individual’s SUD might be brought into the light of
Such people “imagine that they can only find them- day.
selves by asserting their own desires and ambitions and Denial. Clinical lore among substance abuse reha-
appetites in a struggle with the rest of the world” (Merton, bilitation professionals suggests that the individual’s
1961, p. 47). SUD hides behind a wall of denial (Croft, 2006). Es-
In this quote are found hints of the seeds of addic- sentially, denial occurs when the individual disregards
tion. For the chemical of choice allows the individual or ignores a disturbing reality (Sadock & Sadock,
to assert his or her own desires and ambitions on the 2003). It is a form of unconscious self-deception, classi-
rest of the world. Brown (1985) speaks at length of the fied as one of the more primitive, narcissistic defenses
illusion of control over one’s feelings that alcohol gives by Sadock and Sadock (2003). It is used by the individ-
to the individual. May (1988) also speaks of how chem- ual, usually unconsciously, to help him or her avoid
44 Chapter Five
anxiety and emotional distress (Sadock & Sadock, 2003). to having “only three drinks a night!” (overlooking the
This is accomplished through a process of selective per- fact that each drink is equal to three regular-sized
ception of the past and present so that painful and fright- drinks). Those with a substance use problem might
ening elements of reality are not recognized or minimize their chemical use by claiming to drink “only
accepted. This has been called “tunnel vision” by the four nights a week,” and hope that the interviewer does
Alcoholics Anonymous program (to be discussed in a not think to ask whether a “week” means a 5-day work
later section). week or the full 7-day week. They minimize their drink-
Projection is an unconscious defense mechanism, ing by not mentioning the weekend, as they assume you
through which material that is emotionally unaccept- know that they are intoxicated from Friday night until
able in oneself is unconsciously rejected and attributed Monday morning. In such cases, it is not uncommon to
to others (Sadock & Sadock, 2003). Johnson (1980) de- find that the client drinks four nights out of five during
fined projection differently, noting that the act of pro- the work week, and that she or he is intoxicated from
jection is the act of “unloading self-hatred onto others” Friday evening until she or he goes to bed on Sunday
(p. 31, italics in original deleted). evening, with the final result being that the individual
At times, the defense mechanism of projection will drinks 6 nights out of each full week. Another expres-
express itself when the individual attributes to others sion of rationalization occurs when individuals claim
motives, behavior, or intentions that he or she finds un- time when they were in treatment, in jail, or hospital-
acceptable (Sadock & Sadock, 2003). This is usually ized as “straight time” (i.e., time they were not using
done unconsciously. Young children will often cry out, chemicals), overlooking the fact that they were unable
“See what you made me do!” when they have misbe- to get alcohol/drugs because they were incarcerated.6
haved, in order to project responsibility for their action Marijuana abusers/addicts often rationalize their use of
onto others. Individuals with substance use problems marijuana as reflecting the use of a natural substance
will often do this as well, blaming their addiction or un- and thus they are not like the alcohol or methampheta-
acceptable aspects of their behavior on others: “She mine users, who inject or ingest an artificial chemical.
made me so angry I had to have a few drinks to calm Another popular rationalization is that it is “better to be
down!” an alcoholic than a needle freak . . . after all, alcohol is
Rationalization/intellectualization is classified by legal!”
Sadock and Sadock as one of the “neurotic” defenses Reactions to the spiritual disorder theory of addiction.
through which the individual attempts to justify otherwise Although the traditional view of substance abuse in the
unacceptable attitudes, beliefs, or behaviors through the United States has been that the defense mechanisms of
use of cognitive rationalizations. Examples of rationaliza- denial, projection, rationalization, and minimization
tion used by addicted individuals include blaming their are traditionally found in cases of chemical dependency,
spouse or family (“if you were married to _______ , you this view is not universally accepted. A small, increas-
would drink, too!”), or medical problems (a 72-year-old ingly vocal minority has offered alternative frameworks
alcoholic might blame his drinking on his chronic med- within which substance abuse professionals might view
ical problems). The individual who injects a drug for the the defense mechanisms that they encounter in their
first time might rationalize this as being necessary be- work with addicted individuals.
cause of his or her inability to obtain enough to ingest For example, Foote (2006) challenged the concept
orally, as he or she usually did. that failure in treatment is automatically the patient’s
Minimization operates in a different manner from fault, noting that the therapeutic failure might be
the defensive operations discussed so far. In a sense, viewed as a reflection of an unsuccessful match be-
minimization operates like the defense mechanism of tween client and therapist. Further, the author pointed
rationalization, but it is more specific than rationaliza- out, confrontation is powerful predictor of negative out-
tion. The addicted individual who uses minimization as come, with the client becoming more resistive the
a defense will actively reduce the amount of chemicals more he or she is confronted about the lack of
that he or she admits to using, or the impact that the “progress.”
chemical use has had on his or her life, by a variety of It has been suggested that believing that individuals
mechanisms. with SUDs automatically utilize denial might actually
Alcohol-dependent individuals, for example, might
pour their drinks into an oversized container, perhaps 6Often referred to as “situational abstinence” rather than “recovery”
the size of three or four regular glasses, and then claim by professionals.
do more harm than good (Foote, 2006; Peele, 1989). In Rollnick, 2002). From this perspective, defense mecha-
some cases, the individual’s refusal to admit to an SUD nisms such as “denial” are not a reflection of a patho-
might not be denial at all and may mean that she or he logical condition on the part of the client but the result
does not have a substance use disorder (Peele, 1989). of the wrong intervention being utilized by the profes-
This possibility underscores the need for an accurate as- sional. These theories offer challenging alternatives to
sessment of the client’s substance use patterns (dis- the traditional model of the addicted person having
cussed later in this text) to determine whether there is characteristic defense mechanisms such as discussed in
or is not a need for active intervention or treatment. this chapter.
Miller and Rollnick (2002) offered a theory that rad-
ically departs from the belief that addicts typically uti-
Summary
lize denial as a major defense against the admission of
being “sick.” The authors suggest that alcoholics, as a Many human service professionals who have had lim-
group, do not utilize denial more frequently than any ited contact with addiction tend to have a distorted view
other average group. Rather, a combination of two fac- of the nature of drug addiction. Having heard the term
tors has made it appear that addicts frequently utilize disease applied to chemical dependency, the inexperi-
defense mechanisms such as denial, rationalization, enced human service worker may think in terms of
and projection in the service of their dependency. more traditional illnesses and may be rudely surprised at
First, the process of selective perception on the part of the deception that is inherent in drug addiction. While
treatment center staff makes it appear that substance- chemical dependency is a disease, it is a disease like no
dependent persons frequently use the defense mecha- other. It is, as noted in an earlier chapter, a disease that
nisms discussed earlier. The authors point to the phe- requires the active participation of the “victim.” Further,
nomenon known as the “illusion of correlation” to self-help groups such as Alcoholics Anonymous or Nar-
support this theory. According to the illusion of correla- cotics Anonymous view addiction as a disease of the
tion, human beings tend to remember information that spirit and offer spiritual programs to help their members
confirms their preconceptions and to forget or overlook achieve and maintain their recovery.
information that fails to meet their conceptual model. Addiction is, in a sense, a form of insanity. The insan-
Substance abuse professionals would be more likely to ity of addiction rests on a foundation of psychological de-
remember clients who did use the defense mechanisms fense mechanisms such as rationalization, minimization,
of denial, rationalization, projection, or minimization, denial, and projection. These defense mechanisms, plus
according to the authors, because that is what they were self-deception, keep the person from becoming aware of
trained to expect. the reality of his or her addiction until the disease has pro-
It has also been suggested that when substance gressed quite far. To combat self-deception, Alcoholics
abuse rehabilitation professionals utilize the wrong Anonymous places emphasis on honesty, opennness,
treatment approach for the client’s unique stage of and a willingness to try to live without alcohol. Honesty,
growth, they interpret the resulting conflict as evidence both with self and with others, is the central feature of
of the client’s defensive refusal to accept the staff’s per- the AA program, which offers a program designed to fos-
ception that the client has an SUD; they seldom see it as ter spiritual growth to help the individual overcome his
a therapeutic mismatch (Berg & Miller, 1992; Miller & or her spiritual weaknesses.
CHAPTER SIX
An Introduction to Pharmacology
It is virtually impossible to discuss the effects of the vari- of factors such as the specific chemical being used, the
ous drugs of abuse without touching upon a number individual’s state of health, and so on. The treatment of
basic pharmacological concepts. In this chapter, some of a localized infection caused by the fungus on the skin
the basic principles of pharmacology will be reviewed, presents us with a localized site of action, that is, on
which will help the reader better understand the impact the surface of the body. This makes it easy to limit the
that the different drugs of abuse may have on the user’s impact that a medication used to treat the “athlete’s
body.1 foot” infection might have on the organism as a whole.
There are numerous misconceptions about recre- The patient is unlikely to need more than a topical
ational chemicals. For example, many people believe that medication that can be applied directly to the infected
recreational chemicals are somehow unique. This is not region.
true; they work in the same manner that other pharma- But consider, for a moment, the drugs of abuse; as
ceuticals do. Alcohol and the drugs of abuse act by chang- mentioned in the last section, the site of action for each
ing (strengthening/weakening) a potential that already of the recreational chemicals lies deep within the cen-
exists within the cells of the body (Ciancio & Bourgault, tral nervous system (CNS). There is increasing evi-
1989; Williams & Baer, 1994). In the case of the drugs of dence that each of the various drugs of abuse ultimately
abuse, all of which exert their desired effects in the brain, will impact the limbic system of the brain. However,
they modify the normal function of the neurons of the the drugs of abuse are very much like a blast of shotgun
brain. pellets: They will have an impact not only on the brain
Another common misconception about the drugs but also on many other organ systems in the body.
of abuse is that they are somehow different from legiti- For example, as we will discuss in the chapter on co-
mate pharmaceuticals. This is also not incorrect. caine, this drug causes the user to experience a sense of
Many of the drugs of abuse are—or were—once phar- well-being or euphoria. The euphoria and sense of
maceutical compounds used by physicians to treat dis- well-being that might result from cocaine abuse are
ease. Thus, the drugs of abuse obey the same laws of called the primary effects of the cocaine abuse. But the
pharmacology that apply to the other medications in chemical has a number of side effects; one of these
use today. causes the coronary arteries of the user’s heart to con-
strict. Coronary artery constriction is hardly a desired
effect, and, as discussed in Chapter 12, it might be the
The Prime Effect and Side Effects cause of heart attacks in cocaine users.2 Such un-
of Chemicals wanted effects of a chemical are often called secondary
One rule of pharmacology is that whenever a chemical effects, or side effects. The side effects of a chemical
is introduced into the body, there is an element of risk might range from simply making the patient feel un-
(Laurence & Bennett, 1992). Every chemical agent comfortable to a life-threatening event.
presents the potential to cause harm to the individual,
although the degree of risk varies as a result of a number 2Wilson, Shannon, and Stang (2007) refer to a chemical’s primary ef-
fects as the drug’s therapeutic effects (p. 21). However, their text is de-
1 voted to medication and its uses, not to the drugs of abuse. In order to
This chapter is designed to provide the reader with a brief overview
of some of the more important principles of pharmacology. It is not keep the differentiation between the use of a medication in the treat-
intended to serve as, nor should it be used for, a guide to patient care. ment of disease and the abuse of chemicals for recreational purposes,
Individuals interested in reading more on pharmacology might find this text will use the term primary effects in reference to any com-
several good selections in any medical or nursing school bookstore. pound introduced into the body.
46
An Introduction to Pharmacology 47
A second example is aspirin, which inhibits the designed to be swallowed whole, although in some
production of chemicals known as prostaglandins at cases it might be broken up to allow the patient to in-
the site of an injury. This helps to reduce the individ- gest a smaller dose than would be possible if she or he
ual’s pain from an injury. But the body also produces had ingested the entire tablet. A number of compounds
prostaglandins within the kidneys and stomach, where are administered in tablet form, including both legiti-
these chemicals help control the function of these or- mate pharmaceuticals such as aspirin and illicit drugs
gans. Since aspirin tends to nonselectively block such as the hallucinogens and some amphetamine
prostaglandin production throughout the body, in- compounds. Another common form that oral medica-
cluding the stomach and kidneys, this unwanted ef- tion might take is the capsule. Capsules are modified
fect of aspirin may put the user’s life at risk as the tablets, with the medication being surrounded by a gel-
aspirin interferes with the normal function of these atin capsule. The capsule is designed to be swallowed
organs. whole, and once it reaches the stomach the gelatin cap-
A third example of the therapeutic effect/side effect sule breaks down, allowing the medication to be re-
phenomenon might be seen when a person with a bac- leased into the gastrointestinal tract for absorption into
terial infection of the middle ear (a condition known as the body.
otitis media) takes an antibiotic such as penicillin. The Medications can take other forms, although they are
desired outcome is for the antibiotic to destroy the bac- less often the preferred route of administration. For
teria causing the infection in the middle ear. However, example, some medications are administered orally in
a side effect might be drug-induced diarrhea as the an- liquid form, such as certain antibiotics and over-the-
tibiotic suppresses normal bacteria growth patterns in counter analgesics designed for use by very young chil-
the intestinal tract. Thus, one needs to keep in mind dren. Liquid forms of a drug make it possible to tailor
that all pharmaceuticals, and the drugs of abuse, have each dose to the patient’s weight and are ideal for pa-
both desired effects and numerous, possibly undesir- tients who have trouble taking pills or capsules by
able, side effects. mouth. Of the drugs of abuse, alcohol is perhaps the
best example of a chemical that is administered in liq-
uid form.
Drug Forms and How Drugs Some medications, and a small number of the drugs
Are Administered of abuse, might be absorbed through the blood-rich tis-
A drug is essentially a foreign chemical that is intro- sues under the tongue. A chemical that enters the body
duced into the individual’s body to bring about a spe- by this method is said to be administered sublingually.
cific desired response. Antihypertensive medications The sublingual method of drug administration is consid-
are used to control excessively high blood pressure; ered a variation on the oral form of drug administration.
antibiotics are used to eliminate unwanted bacterial Certain compounds, like nitroglycerin and fentanyl, are
infections. The recreational drugs are introduced well absorbed by the sublingual method of drug admin-
into the body, as a general rule, to bring about feel- istration. Because of the characteristics of the circula-
ings of euphoria, relaxation, and relief from stress. tory system, sublingual administration of drugs avoids
The specific form in which a drug is administered will the danger of the “first-pass metabolism” effect (dis-
have a major effect on (a) the speed with which that cussed later in this chapter), which is also a desirable
chemical is able to work and (b) the way the chemical feature for some medications (Jenkins, 2007). In spite of
is distributed throughout the body. In general, the this advantage, most compounds are not administered
drugs of abuse are administered by either the enteral through sublingual means.
or parenteral route.
Parenteral Forms of Drug Administration
Enteral Forms of Drug Administration The parenteral method of drug administration involves
Medications that are administered by the enteral route injecting the medication directly into the body. There
are taken orally, sublingually, or rectally (Jenkins, 2007; are several forms of parenteral administration that are
Williams & Baer, 1994). The most common form for commonly used in both the world of medicine and the
an orally administered medication is the tablet. A tablet world of drug abuse. First, there is the subcutaneous
is a given dose of a select medication mixed with a bind- method of drug administration. In this process, a chem-
ing agent that gives the tablet shape and holds its form ical is injected just under the skin. This allows the drug
until it is administered. For the most part, the tablet is to avoid the dangers of passing through the digestive
48 Chapter Six
tract, where the various digestive juices might break advantage of the potential offered by transdermal drug
down at least some of the compound before it is ab- administration to provide the patient with a low, steady
sorbed. However, drugs that are administered in a subcu- blood level of a chemical. A drawback of transdermal
taneous injection are absorbed more slowly than are drug administration is that it is a very slow way to intro-
chemicals injected either into muscle tissue or into a duce a drug into the body. But for certain agents, it is
vein. As we will see in the chapter on narcotics addiction, useful. An example is the “skin patch” used to adminis-
heroin addicts will often use subcutaneous injections, a ter nicotine to patients who are attempting to quit
process that they call “skin popping.” smoking. Some antihistamines are administered trans-
A second method of parenteral administration in- dermally, especially when used for motion sickness.
volves the intramuscular injection of a medication. There also is a transdermal “patch” available for the
Muscle tissues have a good supply of blood, and med- narcotic analgesic fentanyl, although its success as a
ications injected into muscle tissue will be absorbed means of providing analgesia has been quite limited.
into the general circulation more rapidly than when in- Occasionally, chemicals might be administered in-
jected just under the skin. As we will discuss in the tranasally. The intranasal administration of a chemical
chapter on anabolic steroid abuse, it is quite common involves “snorting” the material in question so that it is
for individuals abusing anabolic steroids to inject the deposited on the blood-rich tissues of the sinuses. From
chemicals into the muscle tissue. But some com- that point, many chemicals can be absorbed into the
pounds, such as chlordiazepoxide, are poorly absorbed general circulation. For example, both cocaine and
from the muscle tissue and thus are rarely, if ever, ad- heroin powders might be—and frequently are—
ministered by this route (DeVane, 2004). “snorted.”
The third method of parenteral administration is the The process of “snorting” is similar to the process of
intravenous (IV) injection. In the intravenous method, inhalation, which is used by both physicians and illicit
the chemical is injected directly into a vein. When a drug users. Inhalation of a compound takes advantage of
chemical is injected into a vein, it is deposited directly the fact that the blood is separated from exposure to the
into the general circulation (DeVane, 2004). Heroin, air in the lungs by a layer of tissue that is less than
cocaine, and some forms of amphetamine compounds 1/100,000ths of an inch (or 0.64 microns) thick (Garrett,
are examples of illicit drugs that might be administered 1994). Many chemical molecules are small enough to
by the intravenous route. But the speed with which the pass through the lungs into the general circulation, as is
chemical reaches the general circulation when admin- the case with surgical anesthetics. Some of the drugs of
istered by intravenous injection does not allow the body abuse, such as heroin and cocaine, might also be
time to adapt to the arrival of the foreign chemical abused by inhalation when they are smoked. In another
(Ciancio & Bourgault, 1989). This is one reason users of form of inhalation, the particles being inhaled are sus-
intravenously administered chemicals, such as heroin, pended in the smoke. These particles are small enough
frequently experience a wide range of adverse effects in to reach the deep tissues of the lungs, where they are
addition to the desired effects. then deposited. In a brief period of time, the particles
Just because a parenteral method of drug administra- are broken down into smaller units until they are small
tion was utilized, the chemical in question will not enough to pass through the walls of the lungs and reach
have an instantaneous effect. The speed at which all the general circulation. This is the process that takes
forms of drugs administered by parenteral administra- place when tobacco products are smoked.
tion begin to work are influenced by a number of fac- Each subform of inhalation takes advantage of the
tors, discussed in the section on drug distribution later blood-rich, extremely large surface area of the lungs
in this chapter. through which chemical agents might be absorbed
(Benet, Kroetz, & Sheiner, 1995; Jenkins, 2007). Fur-
Other Forms of Drug Administration ther, depending on how quickly the chemical being in-
A number of additional methods of drug administra- haled can cross over into the general circulation, it is
tion need to be identified at least briefly. Some chem- possible to introduce chemicals into the body relatively
icals might be absorbed through the skin, a process rapidly. But researchers have found that the actual
that involves a transdermal method of drug adminis- amount of a chemical absorbed through inhalation
tration. Eventually, chemicals absorbed transdermally tends to be quite variable for a number of reasons. First,
reach the general circulation and are then distrib- the individual must inhale at just the right time to allow
uted throughout the body. Physicians will often take the chemical to reach the desired region of the lungs.
Second, some chemicals pass through the tissues of the that are weak bases are usually absorbed through the
lung only very poorly and thus are not well absorbed by small intestine (DeVane, 2004; Jenkins, 2007).
inhalation. A good example of this is smoked marijuana: The human body is composed of layers of special-
The smoker must use a different technique from the ized cells, which are organized into specific patterns to
one used for smoking tobacco to get the maximum ef- carry out certain functions. For example, the cells of
fect from the chemicals that are inhaled, with many of the bladder are organized to form a muscular reservoir
the compounds in marijuana smoke passing through in which waste products can be stored and from which
the tissues of the lungs only very poorly. Variability in excretion can take place. The cells of the circulatory
the amount of chemical absorbed through the lungs system are organized to form tubes (blood vessels) that
limits the utility of inhalation as a means of medication contain the cells and fluids of the circulatory system.
administration. However, for some of the drugs of abuse, Each layer of cells that a compound must pass through
inhalation is the preferred method. to reach the general circulation will slow down the ab-
There are other methods through which pharmaceu- sorption. For example, just one layer of cells separates
ticals might be introduced into the body. For example, the air in our lungs from the general circulation. Drugs
the chemical might be prepared to be administered rec- that are able to pass across this boundary may reach the
tally or through enteral tubes. However, because the circulation in just a few seconds. In contrast, a drug that
drugs of abuse are generally introduced into the body is ingested orally must pass through several layers of
by injection, orally, intranasally, or through smoking, cells lining the gastrointestinal tract before reaching
we will not need to discuss these obscure methods of the general circulation. Thus, the oral method of drug
drug administration any further. administration is generally recognized as one of the
slowest methods by which a drug can be admitted into
the body. The process of drug absorption is shown in
Bioavailability Figure 6.1.
In order to work, the drugs being abused must enter the Drug molecules can take advantage of several spe-
body in sufficient strength to achieve the desired effect. cialized cellular transport mechanisms to pass through
Pharmacists refer to this as the bioavailability of the the walls of the cells at the point of entry. These trans-
chemical. Bioavailability is the concentration of the un- port mechanisms are quite complex and function at the
changed chemical at the site of action (Loebl, Spratto, & cellular level. Without going into too much detail, we
Woods, 1994; Sands, Knapp, & Ciraulo, 1993). The can classify these methods of transportation as either ac-
bioavailability of a chemical in the body is influenced, tive or passive methods (Jenkins, 2007).
in turn, by the factors of (a) absorption, (b) distribution, Some drug molecules simply diffuse through the
(c) biotransformation, and (d) elimination (Benet et al., cell membrane, a process that is known as passive diffu-
1995; Jenkins, 2007). To better understand the process sion, or passive transport, across the cell boundary. This
of bioavailability, we will consider each of the factors is the most common method of drug transport into the
that might influence the bioavailability of a chemical in body’s cells and operates on the principle that chemi-
more detail. cals tend to diffuse from areas of high concentration to
areas of lower concentration. Other compounds take
advantage of one of several cellular transport mecha-
Absorption nisms that move various essential molecules into or out
Except for topical agents, which are deposited directly of cells. Collectively, these different molecular trans-
to the site of action, chemicals must be absorbed into port mechanisms provide a system of active transport
the body. The concentration of a chemical in the across cell boundaries and into the interior of the body.
serum, and at the site of action, is usually influenced by A number of specialized absorption-modification
the process of absorption (Jenkins, 2007).3 This process variables can influence the speed at which a drug might
involves the movement of drug molecules from the site be absorbed from the site of entry. For example, there is
of entry, through various cell boundaries, to the site of the rate of blood flow at the site of entry and the molecu-
action. Compounds that are weak acids are usually ab- lar characteristics of the drug molecule being admitted
sorbed through the stomach lining, while compounds to the body. Another factor that influences the absorp-
tion of a drug is whether it is consumed with food or on
3An exception is when a compound is applied directly to the site of an empty stomach (DeVane, 2004). As a general rule,
action, as when an ointment is applied directly to the skin. the best absorption of a drug occurs when it is taken on
50 Chapter Six
Blood vessel collecting waste

products and returning to liver
Drug molecules at site

of entry, being absorbed
Drug molecules being transferred

from cell bodies to blood vessels
Cells lining wall of

gastrointestinal tract
FIGURE 6.1 The Process of Drug Absorption
an empty stomach; however, there are exceptions to own natural chemical distribution system to move from
this rule as well (DeVane, 2004). It is important simply the point of entry to the site of action. A chemical can
to remember that the process of absorption refers to the use the circulatory system in several different ways to
movement of drug molecules from the site of entry to reach the site of action. Some chemicals are able to mix
the site of action. In the next section, we discuss the sec- freely with the blood plasma. Such chemicals are classi-
ond factor that influences how a chemical acts in the fied as water-soluble drugs. Because water is such a
body: its distribution. large part of the human body, the drug molecules from
water-soluble chemicals are rapidly and easily distrib-
Distribution uted throughout the fluid in the body. Alcohol, for
The process of distribution refers to how the chemical example, is a water-soluble chemical that is rapidly dis-
molecules are moved about in the body. This includes tributed throughout the body to all blood-rich organs,
both the process of drug transport and the pattern of including the brain.
drug accumulation within the body at normal dosage A different approach is utilized by other drugs. Their
levels. As a general rule, very little is known about drug chemical structure allows them to “bind” to fat mole-
distribution patterns in the overdose victim (Jenkins, cules known as lipids that are found floating in the gen-
2007). Although this would seem to be a relatively eral circulation. Chemicals that bind to these fat
straightforward process, because of such factors as the molecules are often called lipid soluble. Because fat
individual’s sex, muscle/adipose tissue ratio, blood flow molecules are used to build cell walls within the body,
patterns to various body organs, the amount of water in lipids have the ability to rapidly move out of the circula-
different parts of the body, the individual’s genetic her- tory system into the body tissues. Indeed, one character-
itage, state of hydration, and his or her age, there are istic of blood lipids is that they are constantly passing
significant interindividual differences in the distribu- out of the circulatory system and into the body tissues.
tion pattern of various compounds (DeVane, 2004; Chemicals that are lipid soluble will be distributed
Jenkins & Cone, 1998). throughout the body, especially to organs with a high
Drug transport. Once a chemical has reached the concentration of lipids.
general circulation, it can then be transported to the In comparison to the other organ systems in the
site of action. But the main purpose of the circulatory body, which are made up of between 6% and 20%
system is not to provide a distribution system for drugs! lipid molecules, fully 50% of the weight of the brain is
In reality, a drug molecule is a foreign substance in the made up of lipids (Cooper, Bloom, & Roth, 1986).
circulatory system that takes advantage of the body’s Thus, chemicals that are highly lipid soluble will tend
to concentrate rapidly within the brain. Thus, it should be Fortunately, although a chemical might be strongly
no surprise to learn that most psychoactive compounds protein bound, a certain percentage of the drug mole-
are highly lipophilic (DeVane, 2004). The ultrashort- cules will always be unbound. For example, if 75% of a
and short-acting barbiturates are good examples of drugs given drug’s molecules are protein bound, then 25% of
that are lipid soluble. Although all the barbiturates are that drug’s molecules are unbound, or free. It is this un-
lipid soluble, there is a great deal of variability in the bound fraction of drug molecules that is able to have an
speed with which various barbiturates can bind to lipids. effect on the bodily function (to be “biologically active”)
The speed at which a given barbiturate will begin to (Jenkins, 2007). Protein-bound molecules are unable to
have an effect will depend, in part, upon its ability to have any effect at the site of action and are biologically
form bonds with lipid molecules. For the ultrashort- inactive while bound (Rasymas, 1992). Various com-
acting barbiturates, which are extremely lipid soluble, pounds differ as to their degree of protein binding. The
the effects might be felt within seconds of the time antidepressant amitriptyline is 95% protein bound, for
they are injected into a vein. This is one reason the example, while nicotine is only 5% protein bound
ultrashort-duration barbiturates are so useful as surgical (Jenkins, 2007). The sedative effects of diazepam (see
anesthetics. Chapter 10) are actually caused by the small fraction
Because drug molecules are foreign substances in (approximately 1%) of the diazepam molecules that re-
the body, their presence is tolerated only until the mained unbound after the drug reaches the circu-
body’s natural defenses against chemical intruders are lation.
able to eliminate the foreign compound. The body will As noted earlier, unbound drug molecules may eas-
thus be working to detoxify (biotransform) and/or elimi- ily be biotransformed and/or excreted (the process of
nate the foreign chemical molecules in the body almost drug biotransformation and excretion of chemicals will
from the moment they arrive. One way that drugs are be discussed in a later section of this chapter). Thus,
able to avoid the danger of biotransformation and/or one advantage of protein binding is that the protein-
elimination before they have an effect is to join with pro- bound drug molecules form a “reservoir” of drug mole-
tein molecules in the blood. These protein molecules cules that have not yet been biotransformed. These drug
are normally present in human blood for reasons that molecules are gradually released back into the general
need not be discussed further here. It is sufficient to un- circulation as the chemical bond between the drug and
derstand that some protein molecules are normally the protein molecules weakens or as other molecules
present in the blood. compete with the drug for the binding site. The drug
By coincidence, the chemical structures of many molecules that are gradually released back into the gen-
drug molecules allow them to bind with protein mole- eral circulation then replace those molecules that have
cules in the general circulation. This most often in- been biotransformed and/or excreted.
volves a protein known as albumin. Such compounds It is the proportion of unbound to bound molecules
are said to become “protein bound” (or if they bind to that remains approximately the same. Thus, if 75% of the
albumin, “albumin bound”).4 The advantage of protein drug was protein bound and 25% was unbound when
binding is that while a drug molecule is protein bound, the drug was at its greatest concentration in the blood,
it is difficult for the body to either biotransform or ex- then after some of that drug had been eliminated from
crete it. The strength of the chemical bond that forms the body the proportion of bound to unbound drug
between the chemical and the protein molecules will would continue to be approximately 75 to 25. Although
vary, with some drugs forming stronger chemical bonds at first glance the last sentence might seem to be in error,
with protein molecules than others. The strength of this remember that as some drug molecules are being re-
chemical bond then determines how long the drug will moved from the general circulation, some of the protein-
remain in the body before elimination. The dilemma is bound molecules are also breaking the chemical bonds
that while they are protein bound, drug molecules are that held them to the protein molecule to once again be-
also unable to have any biological effect. Thus, to have come unbound. Thus, while the amount of chemical in
an effect, the molecule must be free of chemical bonds the general circulation will gradually diminish as the
(“unbound”). body biotransforms or eliminates the unbound drug mol-
ecules, the proportion of bound:unbound drug mole-
cules will remain essentially unchanged for an extended
4In general, acidic drugs tend to bind to albumin while basic drugs
tend to bind to alpha1-acid glycoprotein (Ciancio & Bourgault, period of time. This allows the compound to have an ex-
1989). tended duration of effect and is related to the concept of
52 Chapter Six
the biological half-life of a compound, which will be dis- Although it is easier to speak of drug biotransforma-
cussed later in this chapter. tion as if it were a single process, in reality there are four
different subforms of this procedure, known as (a) oxi-
Biotransformation dation, (b) reduction, (c) hydrolysis, and (d) conjuga-
Because drugs are foreign substances, the natural de- tion (Ciraulo, Shader, Greenblatt, & Creelman, 2006).
fenses of the body try to eliminate the drug almost im- The specifics of each form of drug biotransformation
mediately. In some cases, the body is able to eliminate are quite complex and are best reserved for pharmacol-
the drug without the need to modify its chemical struc- ogy texts. It is enough for the reader to remember that
ture. Penicillin is an example of a drug that is excreted there are four different processes collectively called
unchanged from the body. Many of the inhalants as drug metabolism, or biotransformation. Many chemi-
well as many of the surgical anesthetics are also elimi- cals must go through more than one step in the bio-
nated from the body without being metabolized to any transformation process before that agent is ready for the
significant degree. But as a general rule, the chemical next step: elimination.
structure of most chemicals must be modified before The process of drug biotransformation changes a
they can be eliminated from the body. foreign chemical into a form that can be rapidly elimi-
This is accomplished through what was once re- nated from the body (Clark, Bratler, & Johnson, 1991;
ferred to as detoxification. However, as researchers have Jenkins, 2007). But this process does not take place in-
come to understand how the body prepares a drug mol- stantly. Rather, the process of biotransformation is ac-
ecule for elimination, that term has been replaced with complished through chemical reactions facilitated by
the term biotransformation.5 Drug biotransformation enzymes produced in the body (especially in the liver).
usually is carried out in the liver, although on occasion It is carried out over a period of time and depending on
this process might involve tissues of the body. The mi- the drug involved may require a number of intermedi-
crosomal endoplasmic reticulum of the liver produces a ate steps before the chemical is ready for elimination
number of enzymes6 that transform toxic molecules from the body. This is especially true for compounds
into a form that might be more easily eliminated from that are very lipid soluble; their chemical structure
the body. Technically, the new compound that emerges must be altered so that the compound becomes less
from each step of the process of drug biotransformation lipid soluble and thus more easily eliminated from the
is known as a metabolite of the chemical that was intro- body (Jenkins, 2007).
duced into the body. The original chemical is occasion- There are two major forms of drug biotransforma-
ally called the parent compound of the metabolite that tion. In the first subtype, a constant fraction of the drug
emerges from the process of biotransformation. is biotransformed in a given period of time, such as a
In general, metabolites are less biologically active than single hour. This is called a first-order biotransformation
the parent compound, but there are exceptions to this process. Certain antibiotics are metabolized in this
rule. Depending on the substance being biotransformed, manner, with a set percentage of the medication in the
the metabolite might actually have a psychoactive effect body being biotransformed each hour. Other chemicals
of its own. On rare occasions, a drug might have a are eliminated from the body by what is known as a
metabolite that is actually more biologically active than zero-order biotransformation process. Drugs that are bio-
the parent compound.7 It is for this reason that pharma- transformed through a zero-order biotransformation
cologists have come to use the term biotransformation process are metabolized at a set rate, no matter how
rather than the older terms detoxification or metabolism high the concentration of that chemical in the blood.
for the process of drug breakdown in the body. Alcohol is a good example of a chemical that is bio-
transformed through a zero-order biotransformation
5This process is inaccurately referred to as “metabolism” of a drug. process.
Technically, the term drug metabolism refers to the total ordeal of a First-pass metabolism effect. Chemicals that are
drug molecule in the body, including its absorption, distribution, bio- administered orally are absorbed either through the
transformation, and excretion.
6The most common of which is the P-450 metabolic pathway, or the
stomach or the small intestine. However, the human
microsomal P-450 pathway. circulatory system is designed in such a way that chemi-
7For example, after gamma-hydroxybutyrate (GHB) was banned by cals absorbed through the gastrointestinal system are
the Food and Drug Administration, illicit users switched to gamma- carried first to the liver. This makes sense, in that the
butyrolactone, a compound with reported health benefits such as im-
proved sleep patterns, which is biotransformed into the banned liver is given the task of protecting the body from toxins.
substance GHB in the user’s body. By taking chemicals absorbed from the gastrointestinal
tract to the liver, the body is able to begin to break down takes for 50% of a single dose to be eliminated from the
any toxins in the substance that was introduced into the body.
body before those toxins might damage other organ For example, different chemicals might rapidly mi-
systems. grate from the general circulation into adipose or muscle
Unfortunately, one effect of this process is that the tissues, so the compound would have a short distribu-
liver is often able to biotransform many medications tion half-life. THC, the active agent in marijuana, is
that are administered orally before they have had a one example of such a compound. However, for heavy
chance to reach the site of action. This is called first- users, a reservoir of unmetabolized THC forms in the
pass metabolism (DeVane, 2004). First-pass metabolism adipose tissue and is gradually released back into the
is one reason it is so hard to control pain through the user’s circulation when he or she stops using mari-
use of orally administered narcotic analgesics. When juana. This gives THC a long elimination half-life in
these are taken by mouth, a significant part of the dose the chronic user, although the therapeutic half-life of a
of an orally administered narcotic analgesic such as single dose is quite short.
morphine will be metabolized by the liver into inactive In this text, all of these different measures of half-
forms before reaching the site of action. life are lumped together under the term biological
half-life (or half-life) of that chemical. Sometimes the
Elimination half-life is abbreviated by the symbol t1/2. The half-life
In the human body, biotransformation and elimination of a chemical is the time needed for the individual’s
are closely intertwined. Indeed, some authorities on body to reduce the amount of active drug in the circu-
pharmacology consider these to be a single process, lation by one-half (Benet et al., 1995). The concept of
since one goal of the process of drug biotransformation t1/2 is based on the assumption that the individual in-
is to change the foreign chemical into a water-soluble gested only one dose of the drug, and the reader should
metabolite that can be easily removed from the circula- keep in mind that the dynamics of a drug following a
tion (Clark, Bratler, & Johnson, 1991). single dose are often far different from those for the
The most common method of drug elimination in- same drug when it is used on a steady basis. Thus,
volves the kidneys (Benet et al., 1995). However, the bil- while the t1/2 concept is often a source of confusion
iary tract, lungs, and sweat glands may also play a role even among health professionals, it does allow health
(Wilson, Shannon, & Stang, 2007). For example, a care workers to roughly estimate how long a drug’s ef-
small percentage of the alcohol that a person has infects will last when that chemical is used at normal
gested will be excreted when that person exhales. A dosage levels.
small percentage of the alcohol in the system is also One popular misconception is that it only takes two
eliminated through the sweat glands. These character- half-lives for the body to totally eliminate a drug. In re-
istics of alcohol contribute to the characteristic smell of ality, 25% of the original dose remains at the end of the
the intoxicated individual. second half-life period, and 12% of the original dose
still is in the body at the end of three half-life periods.
As a general rule, it takes five half-life periods before the
The Drug Half-Life body is able to eliminate virtually all of a single dose of
There are several different measures of drug half-life, a chemical (Williams & Baer, 1994), as illustrated in
which all provide a rough estimate of the period of time Figure 6.2.
that a drug remains active in the human body. The dis- Generally, drugs with long half-life periods tend to re-
tribution half-life is the time it takes for a drug to work main biologically active for longer periods of time. The
its way from the general circulation into body tissues reverse is also true: Chemicals with a short biological
such as muscle and fat (Reiman, 1997). This is impor- half-life tend to be active for shorter periods of time. This
tant information in overdose situations, for example, is where the process of protein binding comes into play:
when the physician treating the patient has to estimate Drugs with longer half-lives tend to become protein
the amount of a compound in the patient’s circulation. bound. As stated earlier, the process of protein binding
Another measure of drug activity in the body is the ther- allows a reservoir of an unmetabolized drug to gradually
apeutic half-life, or the period of time it takes for the be released back into the general circulation as the drug
body to inactivate 50% of a single dose of a compound. molecules become unbound. This allows a chemical to
The therapeutic half-life is intertwined with the concept remain in the circulation at a sufficient concentration to
of the elimination half-life. This is the period of time it have an effect for an extended period of time.
54 Chapter Six
100
90
Percentage of drug in body tissues
80
70
60
50
40
30
20
10
0
0 1 2 3 4 5
Half-life periods
FIGURE 6.2 Drug Elimination in Half-Life Stages
The Effective Dose point that they can no longer function normally. At its ex-
treme, chemicals may disrupt the body’s activities to the
The concept of the effective dose (ED) is based on dose- point of putting the individual’s life in danger.
response calculations, in which pharmacologists calcu- Scientists express this continuum as a form of modi-
late the percentage of a population that will respond to fied dose-response curve. In the typical dose-response
a given dose of a chemical. Scientists usually estimate curve scientists calculate the percentage of the popula-
the percentage of the population that is expected to ex- tion that would be expected to benefit from a certain
perience an effect by a chemical at different dosage exposure to a chemical; the calculation for a fatal expo-
levels. For example, the ED10 is the dosage level for sure level is slightly different. In such a dose-response
which 10% of the population will achieve the desired curve, scientists calculate the percentage of the general
effects from the chemical being ingested. population that would, in theory, die as a result of being
The ED50 is the dosage level for which 50% of the exposed to a certain dose of a chemical or toxin.
population would be expected to respond to the drug’s This figure is then expressed in terms of a “lethal
effects. Obviously, for medications, the goal is to find a dose” (LD) ratio. The percentage of the population that
dosage level for which the largest percentage of the would die as a result of exposure to that chemical/toxin
population will respond to the medication. However, source is identified as a subscript to the LD heading.
you cannot keep increasing the dose of a medication Thus, if a certain level of exposure to a chemical or toxin
forever: Sooner or later you will raise the dosage to the resulted in a 25% death rate, this would be abbreviated as
point that people will start to become toxic and quite the LD25 for that chemical or toxin. A level of exposure to
possibly die from the effects of the chemical. a toxin or chemical that resulted in a 50% death rate
would be abbreviated as the LD50 for that substance.
The Lethal Dose Index For example, as we will discuss in the next chapter, a
Drugs, by their very nature, are foreign to the body. By person with a blood alcohol level of .350 mg/mL would
definition, drugs that are introduced into the body will stand a 1% chance of death without medical interven-
disrupt the body’s function in one way or another. Indeed, tion. Thus, for alcohol, a blood alcohol level of .350
one common characteristic of both legitimate pharma- mg/mL is the LD01 for alcohol. It is possible to calcu-
ceuticals and the drugs of abuse is that the person who late the potential lethal exposure level for virtually
administered that chemical hopes to alter the body’s every chemical. These figures provide scientists with a
function to bring about a desired effect. But chemicals way to calculate the relative safety of different levels of
that are introduced into the body hold the potential to exposure to chemicals or radiation and to determine
disrupt the function of one or more organ systems to the when medical intervention is necessary.
The Therapeutic Index centration of a specific chemical in the body allows it to

begin to have the desired effect on the user. The chemi-
In addition to their potential to benefit the user, all drugs cal’s effects continue to become stronger and stronger
also hold the potential for harm. Since they are foreign until finally the strongest possible effects are reached.
substances being introduced into the body, there is a dan- This is the period of peak effects. Then, gradually, the im-
ger that if used in too large an amount, the drug might ac- pact of the drug becomes less and less pronounced as the
tually harm the individual rather than help him or her. chemical is eliminated/biotransformed over a period of
Scientists have devised what is known as the thera- time. Eventually, the concentration of the chemical in
peutic index (TI) as a way to measure the relative safety the body falls below the therapeutic level. Scientists have
of a chemical. Essentially, the TI is the ratio between learned to calculate dose-response curves in order to esti-
the ED50 and the LD50. In other words, the TI is a ratio mate the potential for a chemical to have an effect at any
between the effectiveness of a chemical and its poten- given point after it was administered. A hypothetical dose-
tial for harm. A smaller TI means that there is only a response curve is shown in Figure 6.3.
small margin between the dosage level needed to The period of peak effects following a single dose of a
achieve the therapeutic effects and the dosage level at drug varies from one chemical to another. For example,
which the drug becomes toxic. A large TI suggests that the peak effects of an ultrashort-acting barbiturate
there is a great deal of latitude between the normal might be achieved in a matter of seconds following a
therapeutic dosage range and the dosage level at which single dose, while the long-term barbiturate phenobar-
that chemical might become toxic to the user. bital might take hours to achieve its strongest effects.
Unfortunately, many of the drugs of abuse have a small Thus, clinicians must remember that the period of peak
TI. These chemicals are potentially quite toxic to the user. effects following a single dose of a chemical will vary for
For example, as we will discuss in the chapter on barbitu- each chemical.
rate abuse, the ratio between the normal dosage range and
the toxic dosage range for the barbiturates is only about
The Site of Action
1:3. In contrast, the ratio between the normal dosage
range and the toxic dosage level for the benzodiazepines is To illustrate the concept of the site of action, consider a
estimated to be about 1:200. Thus, relatively speaking, the person with an “athlete’s foot” infection. This condition
benzodiazepines are much safer than the barbiturates. is caused by a fungus that attacks the skin. Obviously,
the individual who has such an infection will want it
cured, and there are several excellent over-the-counter
Peak Effects antifungal compounds available. In most cases, the in-
The effects of a chemical within the body develop over a dividual need only select one and then apply it to the
period of time until the drug reaches what is known as the proper area on his or her body to be cured of the
therapeutic threshold. This is the point at which the con- infection.
Peak effect
Response
Minimum effective dose
Therapeutic
threshold
Time
FIGURE 6.3 Hypothetical Dose-Response Curve

56 Chapter Six
At about this point, somebody is asking what antifun- stand how receptor sites work, consider the analogy of a
gal compounds have to do with drug abuse. Admittedly, key slipping into the slot of a lock. The structure of the
it is not the purpose of this chapter to sell antifungal transmitter molecule fits into the receptor site in much
compounds. But the example of the athlete’s foot infec- the same way as a lock into a key, although on a greatly
tion helps to illustrate the concept of the site of action. reduced scale. The receptor site is usually a pattern of
This is where the drug being used will have its prime ef- molecules that allows a single molecule to attach itself
fect. In the medication for the athlete’s foot infection, to the target portion of the cell at that point. Under nor-
the site of action is the infected skin on the person’s mal circumstances, receptor sites allow the molecules
foot. For the drugs of abuse, the central nervous system of naturally occurring compounds to attach to the cell
(CNS) will be the primary site of action. walls to carry out normal biological functions.
By coincidence, however, many chemicals may be in-
The Central Nervous System (CNS) troduced into the body that also have the potential to
The CNS, without question, is the most complex organ bind to these receptor sites and possibly alter the normal
system in the human body. At its most fundamental level, biological function of the cell in a desirable way. Those
the CNS comprises perhaps 100 billion neurons. These bacteria susceptible to the antibiotic penicillin, for
cells are designed to both send and receive messages from example, have a characteristic “receptor site,” in this case
other neurons in a process known as information process- the enzyme transpeptidase. This enzyme carries out an
ing. To accomplish this task, each neuron may communi- essential role in bacterial reproduction. By blocking the
cate with tens, hundreds, or thousands of its fellows action of transpeptidase, penicillin prevents the bacte-
through a system of perhaps 100 trillion synaptic junc- ria cells from reproducing. As the bacteria continue to
tions (Stahl, 2000).8 To put this number into perspective, grow, the pressure within the cell increases until the
it has been estimated that the average human brain has cell wall is no longer able to contain it, and the cell
more synaptic junctions than there are individual grains ruptures.
of sand on all of the beaches of the planet Earth. Neurotransmitter receptor sites are a specialized
Although most of the CNS is squeezed into the conform of receptor site found in the walls of neurons at the
fines of the skull, the individual neurons do not actually synaptic junction. Their function is to receive the chem-
touch. Rather, they are separated by microscopic spaces ical messages from the presynaptic neuron in the form
called synapses. To communicate across the synaptic of the neurotransmitter molecules, discussed earlier, at
void, one neuron will release a cloud of chemical mole- specific receptor sites. To prevent premature firing, a
cules that function as neurotransmitters. When a suffi- number of receptor sites must be occupied at the same
cient number of these molecules contact a corresponding instant before the electrical potential of the receiving
receptor site in the cell wall of the next neuron, a profound (postsynpatic) neuron is changed, allowing it to pass the
change is triggered in the postsynaptic neuron. Such message on to the next cell in the nerve pathway. Essen-
changes may include the postsynaptic neuron “making, tially, all of the known chemicals that function as neuro-
strengthening, or destroying synapses; urging axons to transmitters within the CNS might be said to fall into
sprout; and synthesizing various proteins, enzymes, and two groups: those that stimulate the neuron to release a
receptors that regulate neurotransmission in the target chemical “message” to the next cell and those that in-
cell” (Stahl, 2000, p. 21). Another change may be to force hibit the release of neurotransmitters. By altering the
the postsynaptic neuron to release a cloud of neurotrans- flow of these two classes of neurotransmitters, the drugs
mitter molecules in turn, passing the message that it just of abuse alter the way the CNS functions.
received on to the next neuron in that neural pathway. Co-transmission. When neurotransmitters were first
identified, scientists thought that each neuron utilized
The Receptor Site just one form of neurotransmitter molecule. In recent
The receptor site is the exact spot either on the cell wall years, it has been discovered that in addition to one
or within the cell itself where the chemical molecule “main” neurotransmitter, neurons often both receive and
carries out its main effects (Olson, 1992). To under- release “secondary” neurotransmitter molecules that are
quite different from the main neurotransmitter (Stahl,
8Although the CNS is, by itself, worthy of a lifetime of study, for the 2000). The process of releasing secondary neurotrans-
purpose of this text the beauty and complexities of the CNS must be mitters is known as co-transmission, with opiate peptides
compressed into just a few short paragraphs. The reader who wishes
to learn more about the CNS should consult a good textbook on most commonly being utilized as secondary neurotrans-
neuropsychology or neuroanatomy. mitters (Stahl, 2000). The process of co-transmission
Presynaptic neuron Postsynaptic neuron
Direction
of nerve
impulse
Postsynaptic neuron
Neurotransmitter molecules
Synaptic vesicles
Axon of presynaptic neuron

Molecule-sized receptor
sites in cell wall
Neurotransmitter molecules
being passed from first
neuron to second
FIGURE 6.4 Neurotransmitter Diagram
may explain why many drugs that affect the CNS have creasing or decreasing the number of neurotransmitter
such wide-reaching secondary or side effects. receptor sites on the cell wall. If a neuron is subjected
Neurotransmitter reuptake/destruction. In many to low levels of a given neurotransmitter, that nerve cell
cases, neurotransmitter molecules are recycled. This will respond by increasing (upregulating) the number
does not always happen, however, and in some cases of possible receptor sites in the cell wall to give the neu-
once a neurotransmitter is released it is destroyed by an rotransmitter molecules a greater number of potential
enzyme designed to carry out this function. But some- receptor sites. An anology might be a person using a di-
times a neuron will activate a molecular “pump” that rectional microphone to enhance faint sounds.
absorbs as many of the specific neurotransmitter mole- But if a neuron is exposed to a large number of neu-
cules from the synaptic junction as possible for reuse. rotransmitter molecules, it will decrease the total num-
This process is known as “reuptake.” In both cases, the ber of possible receptor sites by absorbing/inactivating
neuron will also work to manufacture more of that neu- some of the receptor sites in the cell wall. This is down-
rotransmitter for future use, storing both the reabsorbed regulation, a process by which a neuron decreases the
and newly manufactured neurotransmitter molecules total number of receptor sites where the neurotransmit-
in special sacks within the nerve cell until needed (see ter (or drug) molecule can bind to that neuron. Again,
Figure 6.4). an analogy would be a person who turns down the vol-
Upregulation and downregulation. The individual ume of a sound amplification system so that it becomes
neurons of the CNS are not passive participants in the less sensitive to distant sound sources.
process of information transfer. Rather, each individual Tolerance and cross-tolerance. The concept of drug
neuron is constantly adapting its sensitivity by either in- “tolerance” was introduced in the last chapter. In brief,
58 Chapter Six
tolerance is a reflection of the body’s ongoing struggle to existing neurotransmitters, they either enhance or re-
maintain normal function. Because a drug is a foreign tard the frequency with which the neurons of the brain
substance, the body will attempt to continue its normal “fire” (Ciancio & Bourgault, 1989). The constant use of
function in spite of the presence of the chemical. Part any of the drugs of abuse force the neurons to go through
of the process of adaptation in the CNS is the upregula- the process of neuroadaptation as they struggle to main-
tion/downregulation of receptor sites, as the neurons at- tain normal function in spite of the artificial stimula-
tempt to maintain a normal level of firing. tion/inhibition caused by the drugs of abuse. In other
As the body adapts to the effects of the chemical, the words, depending on whether the drugs of abuse cause a
individual will find that he or she no longer achieves the surplus/deficit of neurotransmitter molecules, the neu-
same effect from the original dose and must use larger rons in many regions of the brain will upregulate/down-
and larger doses to maintain the original effect. When a regulate the number of receptor sites in an attempt to
chemical is used as a neuropharmaceutical—a drug in- maintain normal function. This will cause the individ-
tentionally introduced into the body by a physician to ual’s responsiveness to that drug to be different over
alter the function of the CNS in a desired manner— time, a process that is part of the process of tolerance.
tolerance is often referred to as the process of neuroad- When the body begins to adapt to the presence of
aptation. If the drug being used is a recreational one chemical, it will often also become tolerant to the
substance, the same process is usually called tolerance. effects of other drugs that use the same mechanism of
However, neuroadaptation and tolerance are essentially action. This is the process of cross-tolerance. For
the same biological adaptation. The only difference is example, a chronic alcohol user will often require
that one involves a pharmaceutical while the other in- higher doses of CNS depressants than a nondrinker to
volves a recreational chemical. achieve a given level of sedation. Physicians have often
The concepts of a drug agonist and antagonist. To noticed this effect in the surgical theater: Chronic alco-
understand how the drugs of abuse work, it is necessary hol users will require larger doses of anesthetics than
to introduce the twin concepts of a drug agonist and the nondrinkers to achieve a given level of unconscious-
antagonist. These may be difficult concepts for students ness. Anesthetics and alcohol are both classified as
of drug abuse to understand. Essentially, a drug agonist CNS depressants. The individual’s tolerance to the ef-
mimics the effects of a chemical that is naturally found fects of alcohol will, through the development of cross-
in the body (Wilson et al., 2007). The agonist either tolerance, cause him or her to require a larger dose of
tricks the body into reacting as if the endogeneous many anesthetics to allow the surgery to proceed.
chemical were present, or it enhances the effects of the
naturally occurring chemical. For example, as we will
The Blood-Brain Barrier
discuss in the chapter on the abuse of opiates, there are
morphine-like chemicals found in the human brain The blood-brain barrier (BBB) is a unique structure in
that help to control the level of pain that the individual the human body. It functions as a “gateway” to the brain.
is experiencing. Heroin, morphine, and the other nar- In this role, the BBB will admit only certain molecules
cotic analgesics mimic the actions of these chemicals needed by the brain to pass through. For example, oxy-
and for this reason might be classified as agonists of the gen and glucose, both essential to life, will pass easily
naturally occurring pain-killing chemicals. through the BBB (Angier, 1990). But the BBB exists to
The antagonist essentially blocks the effects of a chem- protect the brain from toxins or infectious organisms.
ical already working within the body. In a sense, aspirin To this end, endothelial cells that form the lining of
might be classified as a prostaglandin antagonist because the BBB have established tight seals with overlapping
aspirin blocks the normal actions of the prostaglandins. cells.
Antagonists may also block the effects of certain chemi- Initially, students of neuroanatomy may be confused
cals introduced into the body for one reason or another. by the term blood-brain barrier; when we speak of a
For example, the drug Narcan blocks the receptor sites “barrier,” we usually mean a single structure. But the
in the CNS that opiates normally bind to in order to BBB actually is the result of a unique feature of the cells
have their effect. Narcan thus is an antagonist for opi- that form the capillaries through which cerebral blood
ates and is of value in reversing the effects of an opiate flows. Unlike capillary walls throughout the rest of the
overdose. body, those of the cerebral circulatory system are securely
Because the drugs of abuse either simulate the ef- joined together. Each endothelial cell is tightly joined to
fects of actual neurotransmitters or alter the action of its neighbors, forming a tight tube-like structure that
protects the brain from direct contact with the general into the interior of the endothelial cell. Later it will also
circulation. Thus, many chemicals in the general circu- pass through the lining of the far side of the endothelial
lation are blocked from entering the CNS. However, the cell to reach the neurons beyond the lining of the BBB.
individual cells of the brain require nutritional support,
and some of the very substances needed by the brain are
Summary
those blocked by the endothelial cell boundary. Thus,
water-soluble substances like glucose or iron, needed by In this chapter, we have examined some of the basic
the neurons of the brain for proper function, are blocked components of pharmacology. It is not necessary for
by the lining of the endothelial cells. students in the field of substance abuse to have the
To overcome this problem, specialized transport sys- same depth of knowledge possessed by pharmacists to
tems have evolved in the endothelial cells in the cerebral begin to understand how the recreational chemicals
circulatory system. These transport systems selectively achieve their effects. However, it is important for the
allow needed nutrients to pass through the BBB to reach reader to understand at least some of the basic concepts
the brain (Angier, 1990). Each of these transport systems of pharmacology to understand the ways that the drugs
will selectively allow one specific type of water-soluble of abuse achieve their primary and secondary effects.
molecule, such as a glucose, to pass through the lining of Basic information regarding drug forms, methods of
the endothelial cell to reach the brain. drug administration, and biotransformation/elimina-
But lipids also pass through the lining of the endothe- tion were discussed in this chapter.
lial cells and are able to reach the central nervous sys- Other concepts discussed include drug bioavailabil-
tem beyond. Lipids are essentially molecules of fat. ity, the therapeutic half-life of a chemical, the effective
They are essential elements of cell walls, which are dose and lethal dose ratios, the therapeutic dose ratio,
made up of lipids, carbohydrates, and protein mole- and how drugs use receptor sites to work. The student
cules, arranged in a specific order. As the lipid molecule should have at least a basic understanding of these con-
reaches the endothelial cell wall, it gradually merges cepts before starting to review the different drugs of
with the molecules of the cell wall and passes through abuse discussed in the next chapters.
CHAPTER SEVEN
Introduction to Alcohol
The Oldest Recreational Chemical
Klatsky (2002) noted that fermentation occurs naturally ing and consumption of beer was a matter of consider-
and that early humans discovered, but did not invent, able importance to the inhabitants of Sumer.1 Many
alcohol-containing beverages such as wine and beer. clay tablets devoted to the process of brewing beer have
Most certainly, this discovery occurred well before the been found in what was ancient Sumeria (Cahill, 1998).
development of writing, and scientists believe that man’s If this theory is correct, it would seem that human civi-
use of alcohol dates back at least 10,000–15,000 years lization owes much to ethanol, or ethyl alcohol,2 or as it
(Potter, 1997). Prehistoric humans probably learned is more commonly called, alcohol.
about the intoxicating effects of fermented fruit by
watching animals eat such fruit from the forest floor
and then act strangely. Curiosity may have compelled A Brief History of Alcohol
one or two brave souls to try some of the fermented fruits The use of fermented beverages dates back before the
that the animals seemed to enjoy, introducing prehistoric invention of writing, but it is clear that early humans
humans to the intoxicating effects of alcohol (R. Siegel, viewed alcohol as a powerful chemical. The Bible, for
1986). Having discovered alcohol’s intoxicating action example, refers to alcohol as nothing less than a gift
and desiring to repeat the use of fermented fruits, pre- from God (Genesis 27:28). Historical evidence suggests
historic humans started to experiment and eventually that mead, a form of beer made from fermented honey,
discovered how to produce alcohol-containing bever- was used during the late paleolithic3 era. Historical evi-
ages at will. dence suggests that forms of beer made from other in-
It is not unrealistic to say that “alcohol and the privi- gredients might date back to around the year 9000
lege of drinking have always been important to human B.C.E.4,5 (Gallagher, 2005). Such forms of beer were
beings” (Brown, 1995, p. 4). Indeed, it has been sug- thick and quite nutritious, providing the drinker with
gested that humans have an innate drive to alter their both vitamins and amino acids. By comparison, mod-
awareness through the use of chemical compounds, and ern beer is very thin and appears almost anemic.6 Both
one of the reasons early hominids may have climbed out beer and wine are mentioned in Homer’s epic stories
of the trees of Africa was to gain better access to hallu- The Iliad and The Odyssey, legends that are thought to
cinogenic mushrooms that grew in the dung of savanna- date back thousands of years. Given the casual manner
dwelling grazing animals (Walton, 2002). Although this in which these substances are mentioned in these
theory remains controversial, (a) virtually every known
culture discovered or developed a form of alcohol pro- 1
See Glossary.
duction, and (b) every substance that could be fer- 2
The designation ethyl alcohol is important to a chemist, as there are
mented has been made into a beverage at one time or 45 other compounds that might be classified as a form of alcohol and
another (Klatsky, 2002; Levin, 2002). Virtually every it is important to identify which form is under discussion. But ethyl
culture discovered by anthropologists has advocated the alcohol is the one consumed by humans, and thus these other com-
pounds will not be discussed further in this chapter.
use of certain compounds to alter the individual’s per- 3
What is commonly called the latter part of the Stone Age.
ception of reality (Glennon, 2004; Walton, 2002). In this 4
Which stands for Before the Common Era.
context, alcohol is the prototype intoxicant. 5
Remember, it is the 21st century. The year 9000 B.C.E. was thus
Some anthropologists now believe that early civiliza- 11,000 years ago.
tion came about in response to the need for a stable 6
Globally, the United States ranked 11th in per capita beer con-
home base from which to ferment a form of beer sumption, consuming 82.8 liters per person in 2005 (Carroll,
known as mead (Stone, 1991). Most certainly, the brew- 2006).
60
Introduction to Alcohol 61
epics, it is clear that their use was commonplace for an was seen not as a sign of religious ecstasy as it had been
unknown period before the stories were developed. in the pre-Christian Roman empire, but as a public
Scientists have discovered that ethyl alcohol is an ex- disgrace. This perception still exists in many quarters
traordinary source of energy. The human body is able today.
to obtain almost as much energy from alcohol as it can
from fat, and far more energy gram for gram than it can
obtain from carbohydrates or proteins (Lieber, 1998). How Alcohol Is Produced
Although ancient people did not understand these
facts, they did recognize that alcohol-containing bever- As discussed in the last section, at some point before the
ages such as wine and beer were an essential part of the invention of writing, people discovered that if you
individual’s diet, a belief that persisted until well into crush certain forms of fruit and allow it to stand for a
modern times.7 period of time in a container, alcohol will sometimes
The earliest written record of wine making is found appear. We now know that unseen microorganisms
in an Egyptian tomb that dates back to around 3000 called yeast settle on the crushed fruit, find that it is a
B.C.E. (“A Very Venerable Vintage,” 1996), although
suitable food source, and begin to digest the sugars in
scientists have uncovered evidence suggesting that an- the fruit through a chemical process called fermenta-
cient Sumerians might have used wine made from fer- tion. The yeast breaks down for food the carbon, hydro-
mented grapes around 5400 B.C.E. (“A Very Venerable gen, and oxygen atoms it finds in the sugar and in the
Vintage,” 1996). The earliest written records of how process produces molecules of ethyl alcohol and car-
beer is made are approximately 3,800 years old (Stone, bon dioxide as waste. Waste products are often toxic to
1991). These findings suggest that alcohol played an the organism that produces them, and so it is with alco-
important role in the daily life of early people, since hol. When the concentration of alcohol in a container
only the most important information was recorded after reaches about 15%, it becomes toxic to the yeast, and
the development of writing.8 fermentation stops. Thus, the highest alcohol concen-
Ethyl alcohol, especially in the form of wine, was tration that one might achieve by natural fermentation
central to daily life in both ancient Greece and is about 15%.
Rome9 (Walton, 2002). Indeed, ancient Greek prayers Several thousand years elapsed before humans
for warriors suggested that they would enjoy contin- learned to obtain alcohol concentrations above this
ual intoxication in the afterlife, and in pre-Christian 15% limit. Although Plato had noted that a “strange
Rome intoxication was seen as a religious experience water” would form when one boiled wine (Walton,
(Walton, 2002). When the Christian church began to 2002), it was not until around the year 800 C.E. that an
play a major role in the Roman Empire in the fourth unknown person thought to collect this fluid and explore
century C.E., it began to stamp out excessive drinking its uses. This is the process of distillation, which histori-
at religious celebrations as reflecting pagan religions cal evidence suggests was developed in the Middle East,
and began to force its own morality on to the inhabi- and which had reached Europe by around 1100 C.E.
tants of the Empire10 (Walton, 2002). The Puritan (Walton, 2002). Since ethyl alcohol boils at a much
ethic that evolved in England in the 14th and 15th lower temperature than water, when wine is boiled
centuries placed further restrictions on drinking, and some of the alcohol content boils off as a vapor, or
by the start of the 19th century public intoxication steam. This steam contains more ethyl alcohol than
water vapor. If it is collected and allowed to cool down,
7When the Puritans set sail for the New World, for example, they car- the resulting liquid will have a higher concentration of
ried 14 tons of water and 42 tons of beer (Freeborn, 1996). One of the alcohol and a lower concentration of water than the
reasons they elected to settle where they did was because they had ex- original mixture. Over time, it was discovered that the
hausted their supply of beer (McAnnalley, 1996). cooling process could take place in a metal coil, allow-
8I leave it to the reader to decide whether this text is consistent with
ing the liquid to drip from the end of the coil into a
this dictum or not.
container of some kind. This device is the famous
9For example, the Roman proverb “Bathing, wine, and Venus exhaust
“still” of lore and legend.
the body, but that is what life is about.”
10Just 300 years later, around 700 C.E., the Qur’an was written, which
Around the year 1000 C.E. , Italian wine growers had
included an injunction against the use of alcohol by adherents of started using the distillation process to produce differ-
Islam, with recommended punishment for the drinker as public ent beverages by mixing the obtained “spirits” that re-
thrashing (Walton, 2002). sulted from distillation with various herbs and spices.
62 Chapter Seven
This produced various combinations of flavors for the there are exceptions to this rule, and some beverages
resulting beverage, and physicians of the era were quick contain 80% or higher alcohol concentrations, such as
to draw upon these new alcohol-containing fluids as po- the famous Everclear distilled in the southern United
tent medicines. These flavorful beverages also became States. As evidence of the popularity of alcohol as a
popular for recreational consumption. Unfortunately, recreational intoxicant, scientists are attempting to find
as a result of the process of distillation, many of the vita- medications that might take away the negative conse-
mins and minerals found in the original wine and beer quences of alcohol use, allowing the drinker either to re-
are lost. For this reason, many dietitians refer to alcohol cover from intoxication in a matter of minutes or not to
as a source of “empty” calories. Over time, the chronic in- even experience many of the negative consequences of
gestion of alcohol-containing beverages can contribute to acute alcohol use at all (Motluk, 2006).
a state of vitamin depletion called avitaminosis, which
will be discussed in the next chapter.
Scope of the Problem of Alcohol Use
Beverages that contain alcohol are moderately popular
Alcohol Today drinks. It has been estimated that 90% of the adults in the
Over the 900 years since the development of the distil- United States have consumed alcohol at one point in
lation process, various forms of fermented wines using their lives, 70% engage in some level of alcohol use each
numerous ingredients, different forms of beer, and dis- year, and 51% of the population above the age of 12 con-
tilled spirits combined with flavorings have emerged. sume alcohol at least once each month (Kranzler &
The widespread use of alcohol has resulted in multiple Ciraulo, 2005; O’Brien, 2006). For much of the last
attempts to control or eliminate its use over the years, quarter of the 20th century there was a gradual decline
but these programs have had little success. Given the in the per capita amount of alcohol consumed in the
widespread, ongoing debate over the proper role of al- United States. This continued until 1996, and since
cohol in society, it is surprising to learn that there is no then the annual per capita consumption of alcohol has
definition of what constitutes a “standard” drink or the gradually increased each year (Naimi et al., 2003). Cur-
alcohol concentrations that might be found in different rently, the average adult in the United States consumes
alcoholic beverages (Duvour, 1999). 8.29 liters (or 2.189 gallons) of pure alcohol a year, as
At this time in the United States, most beer has an compared to 12.34 liters a year for Greenland, 9.44
alcohol content of between 3.5% and 5% (Dufour, liters a year for the average adult in Finland, and 16.01
1999; Herman, 1993). However, some brands of “light” liters a year for the average adult in the Republic of Ire-
beer might have less than 3% alcohol content, and land (Schmid et al., 2003).
“speciality” beers or malt liquors might contain up to These figures are averages, and there is a significant
9% alcohol (Duvour, 1999). In the United States, wine interindividual variation in the amount of alcohol con-
continues to be made by allowing fermentation to take sumed. For example, it has been estimated that just
place in vats containing various grapes or other fruits. 10% of those who drink alcohol in the United States
Occasionally, especially in other countries, the fermen- consume 60% of all the alcohol ingested, while the top
tation involves products other than grapes, such as the 30% of drinkers consume 90% of all the alcohol in-
famous “rice wine” from Japan called sake. In the gested (Kilbourne, 2002). Beer is the most common
United States, wine usually has an alcohol content of form of alcohol-containing beverage utilized in the
approximately 8% to 17% (Herman, 1993), although United States (Naimi et al., 2003). Unfortunately, as
what are classified as “light” wines might be about 7% the individual’s frequency of alcohol use and the
alcohol by content, and wine “coolers” contain 5% to amount of alcohol ingested increase, she or he be-
7% alcohol as a general rule (Duvour, 1999). comes more likely to develop some of the complica-
In addition to wine, there are the “fortified” wines. tions induced by excessive alcohol use. In the United
These are produced by mixing distilled wine with fer- States it is estimated that 8% of those who consume al-
mented wine, to raise the total alcohol content to about cohol will go on to become alcohol dependent (Sterling
20% to 24% (Duvour, 1999). Examples of fortified wines et al., 2006). But even a surprisingly small amount of al-
include various brands of sherry and port (Herman, cohol can cause serious harm to the drinker (Motluk,
1993). Finally, there are the “hard liquors,” the distilled 2004). The impact of excess alcohol use will be dis-
spirits whose alcohol content generally contains 40% to cussed in more detail in the next chapter. In this chap-
50% alcohol by volume (Duvour, 1999). However, ter, we will focus on the casual, nonabusive drinker.
The Pharmacology of Alcohol gastric alcohol dehydrogenase, which begins the process of
alcohol biotransformation in the stomach (Frezza et al.,
Ethyl alcohol might be introduced into the body intra- 1990). The levels of gastric alcohol dehydrogenase are
venously or inhaled as a vapor,11 but the most common highest in rare social drinkers and are significantly lower
means by which alcohol gains admission into the body in regular/chronic drinkers or those who ingested an as-
is by oral ingestion as a liquid. The alcohol molecule is pirin tablet before drinking (Roine, Gentry, Hernandez-
quite small and is soluble in both water and lipids, al- Munoz, Baraona, & Lieber, 1990).
though it shows a preference for the former (Jones, Researchers have long known that men tend to have
1996). Alcohol molecules are rapidly distributed to all lower blood alcohol levels than do women after con-
blood-rich tissues in the body, which obviously in- suming a given amount of alcohol. There are several
cludes the brain. Because alcohol is so easily soluble in reasons for this observed discrepancy. First, males tend
lipids, the concentration of alcohol in the brain quickly to produce more gastric alcohol dehydrogenase than do
surpasses that of the level in the blood (Kranzler & women, as the production of this enzyme is dependent
Ciraulo, 2005). Although alcohol does diffuse into adi- on the level of testosterone in the blood (Swift, 2005).
pose12 and muscle tissues, it does not enter these as eas- Also, women tend to have lower body weights, lower
ily as it does water-rich tissues such as those of the muscle-to-body-mass ratios, and 10% less water volume
brain. But the effect is strong enough that a very obese in their bodies than do men (Zealberg & Brady, 1999).
or very muscular person will achieve a slightly lower Individuals consume alcohol for its effects on the
blood alcohol level than would a leaner person after brain. However, even though it has been used for at
consuming the same amount of alcohol. least 4,000 years, its effects on the human brain are still
The main route of alcohol absorption is through the not completely understood, and different theories have
small intestine (Baselt, 1996; Swift, 2005). A number of been advanced over the years to attempt to explain its
factors will affect the speed with which the drinker’s acute effects (Motluk, 2006). In the early 20th century,
body absorbs the alcohol ingested. For example, certain it was suggested that this effect might be caused by the
compounds such as carbonated beverages or seltzer in- disruption of the structure and the function of lipids in
crease the speed with which it is moved into the small the cell wall of neurons (Tabakoff & Hoffman, 1992).
intestine and then absorbed into the body (Sher et al., This theory was known as the membrane fluidization
2005). On the other hand, when ingested with food, es- theory, or the membrane hypothesis. This theory sug-
pecially high-fat foods, the absorption of much of the gested that since alcohol was known to disrupt the
ingested alcohol is slowed (Sher, Wood, Richardson, & structure of lipids, this might make it more difficult for
Jackson, 2005). Depending on which study you read, neurons in the brain to maintain normal function.
10% (Kaplan, Sadock, & Grebb, 1994) to 20%–25% However this theory has gradually fallen into disfavor.
(Baselt, 1996; Levin, 2002) of the alcohol is immedi- Scientists now believe that the alcohol molecule is a
ately absorbed through the stomach lining, with the “dirty” drug, binding at a number of neurotransmitter
first molecules of alcohol appearing in the drinker’s receptor sites in the brain. This will either enhance or
blood in as little as 1 minute (Rose, 1988). Thus, when block the effects of the neurotransmitter that normally
alcohol is consumed on an empty stomach, the drinker uses that receptor site. Further, alcohol is thought to in-
will experience the peak blood levels of alcohol in 30 to terfere with the action of messenger molecules within
120 minutes following a single drink (Baselt, 1996). the neuron (Tabakoff & Hoffman, 2004).13
When consumed with food, peak alcohol blood levels One neurotransmitter that is strongly affected by al-
are not be achieved until 1 to 6 hours after a single drink cohol is gamma-amino-butyric acid (GABA). GABA is
was ingested (Baselt, 1996). However, all of the alcohol the main inhibitory neurotransmitter in the brain, and
consumed will eventually be absorbed into the drinker’s approximately 20% of all neurotransmitter receptors in
circulation. the brain utilize GABA, including neurons in the cor-
Although the liver is the primary organ where alco- tex,14 the cerebellum, the hippocampus, the superior
hol is biotransformed in the human body, people pro-
duce an enzyme in the gastrointestinal tract known as
13To show how little is known about the effects of ethyl alcohol, it is
11Although devices have been introduced to take advantage of this thought that this compound will impact on the norepinephrine re-
method of alcohol administration, many states have already banned ceptor sites in the brain, although the outcome of this process is still
them, and the rest are expected to do so soon. unknown.
12See 14
Glossary. See Glossary.
64 Chapter Seven
and inferior colliculi regions of the brain, the amygdala, the release of the neurotransmitter dopamine. This the-
and the nucleus accumbens (Mosier, 1999). But there ory is supported by evidence suggesting that alcohol in-
is not just one type of GABA receptor in the brain. gestion forces the neurons to empty their stores of
Rather, there are several subtypes of GABA, and these dopamine back into the synaptic junction (Heinz et al.,
different subtypes of GABA receptors seem to account 1998). When dopamine is released in the nucleus ac-
for many of the effects of alcohol on the drinker cumbens region of the brain, the individual experi-
(Motluk, 2006). When alcohol molecules bind at the ences a sense of pleasure, or euphoria.
GABAa1 receptor subtype site, it enhances the influx of A third possibility is that alcohol’s ability to potenti-
chloride atoms into the neuron, altering its normal fir- ate the effects of the neurotransmitter serotonin at the 5-
ing rate (Tabakoff & Hoffman, 2004). The subjective HT3 receptor site plays a role in the euphoric and
effect is one of feeling sedated, or “woozy” (Motluk, intoxicating effects of alcohol (Hobbs et al., 1995;
2006). When alcohol binds to the GABAa2 receptor Tabakoff & Hoffman, 2004). This receptor site is lo-
site, it tends to have a calming effect on the drinker, and cated on certain neurons that inhibit behavioral im-
when it binds to the GABAa5 receptor site, it causes pulses, and it is this action that seems to account at least
memory loss, motor impairment, and the feeling of eu- in part for alcohol’s disinhibitory effects. As this mate-
phoria that makes the drinker want to repeat the experi- rial suggests, there is still a great deal to learn about how
ence (Motluk, 2006). alcohol affects the brain of the drinker.
Another neurotransmitter affected by alcohol is the Technically, alcohol intoxication is an acute con-
amino acid N-methyl-D-aspartate (NMDA) (Nace, 2005). fusional state reflecting the dysfunction of the cortex
NMDA fulfills an excitatory function within the brain of the brain (Filley, 2004). If pressed to its extreme,
(Hobbs, Rall, & Verdoorn, 1995; Valenzuela & Harris, this drug-induced neurological dysfunction can be
1997). Alcohol blocks the influx of calcium atoms fatal.
through the ion channels normally activated when
NMDA binds at those sites, slowing down the rate at The Biotransformation of Alcohol
which that neuron can “fire.” It is for this reason that In spite of its popularity as a recreational drink, ethyl al-
ethyl alcohol might be said to be an NMDA antagonist cohol is essentially a toxin, and after it has been ingested
(Tsai, Gastfriend, & Coyle, 1995). By blocking the effects the body works to remove it from the circulation before
of the excitatory amino acid NMDA, while facilitating it can cause widespread damage. Depending on the in-
the inhibitory neurotransmitter GABA in these various re- dividual’s blood alcohol level, between 2% and 10% of
gions of the brain, alcohol is able to depress the normal the alcohol ingested will be excreted unchanged through
function of the central nervous system. the lungs, skin, and urine, with higher percentages of al-
The main reason people ingest alcohol is that it is cohol being excreted unchanged in those individuals
able to induce a sense of pleasure in the drinker. Scien- with greater blood alcohol levels (Sadock & Sadock,
tists still disagree as to the exact mechanism by which 2003; Schuckit, 1998).
alcohol produces this sense of euphoria. On the cellu- But the liver is the primary site where foreign chem-
lar level, it is thought that alcohol affects the function icals such as ethyl alcohol are broken down and re-
of both primary neurotransmitters and various “second- moved from the blood (Brennan, Betzelos, Reed, &
ary” messengers within neurons affected by ethyl alco- Falk, 1995). Alcohol biotransformation is accomplished
hol. At moderate to high blood levels, alcohol is known in two steps. First, the liver produces an enzyme known
to promote the binding of opiate agonists15 to the mu as alcohol dehydrogenase (or ADH), which breaks the al-
opioid receptor site16 (Modesto-Lowe & Fritz, 2005; cohol down into acetaldehyde. It has been suggested
Tabakoff & Hoffman, 2004). This theory is supported that evolution equipped our ancestors with ADH to en-
by the observation that opioid blocking agents like nal- able them to biotransform fermented fruits that might be
trexone reduce alcohol intake in chronic alcohol users. ingested, or the small amount of alcohol produced en-
However, other researchers believe that alcohol’s eu- dogenously (Jones, 1996).
phoric effects are brought on by its ability to stimulate However, this is where even casual or social drinking
may prove to be more damaging to the body than origi-
15
See Glossary nally suspected. Scientists have learned that acetalde-
16
The various subtypes of opioid receptor sites are discussed in hyde is so toxic to the human body that there is virtually
Chapter 14. no safe level of exposure (Melton, 2007). In the normal
individual, this is not a problem, since many different mal individuals who had consumed the same amount
parts of the body produce aldehyde dehydrogenase, a of alcohol. Acetaldehyde is a toxin, and the person with
family of enzymes.17 The form of aldehyde dehydro- a significant amount of this chemical in his or her blood
genase #218 is the form that is mainly responsible for will become quite ill. This phenomenon is thought to
the rapid biotransformation of acetaldehyde down into be one reason that heavy drinking is so rare in persons
acetic acid,19 which can be burned by the muscles as of Asian descent.
fuel Melton, 2007). Ultimately, alcohol is biotransformed
into carbon dioxide, water, and fatty acids (carbohy-
The Blood Alcohol Level
drates).
The speed of alcohol biotransformation. There is Because it is not yet possible to measure the alcohol
some individual variation in the speed at which alcohol level in the brain of a living person, physicians have to
is biotransformed in the body (Garriott, 1996). How- settle for a measurement of the amount of alcohol in a
ever, a rule of thumb is that the liver may biotransform person’s body known as the blood alcohol level
about one mixed drink of 80-proof alcohol, 4 ounces of (BAL).20 The BAL is essentially a measure of the level
wine, or one 12-ounce can of beer, every 60–90 minutes of alcohol actually in a given person’s bloodstream. It
(Fleming, Mihic, & Harris, 2001; Nace, 2005a; Renner, is reported in terms of milligrams of alcohol per 100
2004a). As was discussed in the last chapter, alcohol is milliliters of blood (or mg/mL). A BAL of 0.10 is thus
biotransformed through a zero-order biotransformation one-tenth of a milligram of alcohol per 100 milliliters
process, and the rate at which alcohol is biotransformd of blood.
by the liver is relatively independent of the concentra- The BAL provides a rough approximation of the in-
tion of alcohol in the blood (Levin, 2002). Thus, if the dividual’s subjective level of intoxication. For reasons
person consumes more than one standard drink per that are still not clear, the individual’s subjective level
hour, the alcohol concentration in the blood would in- of intoxication, and euphoria, is highest when the BAL
crease, possibly to the point that the drinker would be- is still rising, a phenomenon known as the Mellanby ef-
come intoxicated. fect (Drummer & Odell, 2001; Sher et al., 2005). Fur-
The alcohol-flush reaction. After drinking even a small ther, individuals who drink on a chronic basis become
amount of alcohol, between 3% and 29% of people of Eu- somewhat tolerant to the intoxicating effects of alcohol.
ropean descent, and between 47% and 85% of people of For these reasons a person who is tolerant to the effects
Asian descent experience what is known as the alcohol- of alcohol might have a rather high BAL while appear-
flush reaction (Collins & McNair, 2002; Sher & Wood, ing relatively normal.
2005). This is caused by a genetic mutation that is The BAL that will be achieved by two people who
found predominantly in persons of Asian descent. Be- consume a similar amount of alcohol will vary as a re-
cause of this genetic mutation, the liver is unable to sult of a number of different factors such as the individ-
manufacture sufficient aldehyde dehydrogenase, which ual’s body size (or volume). To illustrate this confusing
prevents it from rapidly producing the acetaldehyde that characteristic of alcohol, consider the hypothetical
is normally manufactured in the first stage of alcohol example of a person who weighs 100 pounds, who con-
biotransformation. sumed two regular drinks in one hour’s time. Blood
Because of the high levels of aldehyde in their tests would reveal that this individual had a BAL of 0.09
blood, individuals with the alcohol-flush syndrome will mg/mL (slightly above legal intoxication in most states)
experience symptoms such as facial flushing, heart pal- (Maguire, 1990). But an individual who weighs 200
pitations, dizziness, and nausea as the blood levels of pounds would, after consuming the same amount of al-
acetaldehyde climb to 20 times the level seen in nor- cohol, have a measured BAL of only 0.04 mg/mL. Each
person would have consumed the same amount of alco-
17Sometimes abbreviated as the ALDHs. hol, but it would be more concentrated in the smaller
18
Or, ALDH2. individual, resulting in a higher BAL.
19
The medication Antabuse (disulfiram) works by blocking aldehyde Other factors also influence the speed with which al-
dehydrogenase, thus allowing the aldehyde to build up in the
cohol enters the blood and the individual’s blood alcohol
drinker’s blood, forcing him or her to become ill from the toxic effects
of this compound. But recent discoveries about the toxicity of alde-
20Occasionally, the term blood alcohol concentration (BAC) will be
hyde raise questions in the minds of some researchers about the safety
of disulfiram. used in place of blood alcohol level.
66 Chapter Seven
Weight (pounds)
100 120 140 160 180 200 220
2 0.07 0.06 0.05 0.05* 0.04 0.04* 0.03
3 0.10 0.09 0.07 0.07* 0.06 0.05 0.05*

Number of drinks in 1 hour
4 0.14 0.11 0.10 0.08 0.08* 0.07 0.06

Level of legal intoxication with
5 0.18 0.14 0.12 0.11 0.10 0.08 0.08* measured blood alcohol level
of 0.08 mg/dl. Individuals at
or below this line are legally
6 0.20 0.18 0.14 0.12 0.12* 0.10 0.09 too intoxicated to drive.
7 0.25 0.20 0.18 0.16 0.12 0.12* 0.11
8 0.30 0.25 0.20 0.18 0.16 0.14 0.12
*Rounded off.
FIGURE 7.1 Approximate Blood Alcohol Levels

Note: The chart is provided only as an illustration and is not sufficiently accurate to be used as legal evidence or as a guide to
“safe” drinking. Individual blood alcohol levels from the same dose of alcohol vary widely, and these figures provide an average
blood alcohol level for an individual of a given body weight.
level. However, Figure 7.1 provides a rough estimate of At low to moderate dosage levels, the individual’s
the blood alcohol levels that might be achieved expectations play a role in both how a person inter-
through the consumption of different amounts of alco- prets the effects of alcohol and his or her drinking be-
hol. This chart is based on the assumption that one havior (Sher et al., 2005). These expectations about
“drink” is either one can of standard beer or one regular alcohol’s effects begin to form early in life, perhaps as
mixed drink. It should be noted that although the BAL early as 3 years of age, and such expectations solidify
provides an estimate of the individual’s current level of between the ages of 3 and 7 (Jones & McMahon,
intoxication, it is of little value in screening individuals 1998). This is clearly seen in the observation that ado-
for alcohol abuse problems (Chung et al., 2000). lescents who abused alcohol were more likely to antici-
pate a positive experience when they drank than did
their nondrinking counterparts (Brown, Creamer, &
Subjective Effects of Alcohol on the Stetson, 1987).
Individual at Normal Doses After one or two drinks, alcohol causes a second ef-
in the Average Drinker fect, known as the disinhibition effect, on the individ-
Both as a toxin and as a psychoactive agent, alcohol is ual. Researchers now believe that the disinhibition
quite weak. To compare the relative potency of alcohol effect is caused when alcohol interferes with the nor-
and morphine, to achieve the same effects of a 10 mg mal function of inhibitory neurons in the cortex. This is
intravenous dose of morphine, the individual must the part of the brain most responsible for “higher” func-
ingest 15,000–20,000 mg of alcohol (Jones, 1996).21 tions, such as abstract thinking, speech, and so on. The
However, when it is consumed in sufficient quanti- cortex is also the part of the brain where much of our
ties, alcohol does have an effect on the user, and it is voluntary behavior is planned. As the alcohol interferes
for its psychoactive effects that most people consume with cortical nerve function, one tends to temporarily
alcohol. “forget” social inhibitions (Elliott, 1992; Julien, 2005).
During periods of alcohol-induced disinhibition, the
21
This is the approximate amount of alcohol found in one standard individual may engage in some behavior that under
drink. normal conditions he or she would never carry out. It is
this disinhibition effect that may contribute to the rela- BAL of 0.30 mg/mL would be stuporous and con-
tionship between alcohol use and aggressive behavior. fused (Renner, 2004a). With a BAL of 0.35 mg/mL, the
For example, approximately 50% of those who commit stage of surgical anesthesia is achieved (Matuschka,
homicide (Parrott & Giancola, 2006) and up to two-thirds 1985). At higher concentrations, alcohol’s effects are
of those who engage in self-injurious acts (McClosky & analogous to those seen with the anesthetic ether
Berman, 2003) used alcohol prior to or during the act (Maguire, 1990).
itself. Individuals with either developmental or ac- Unfortunately, the amount of alcohol in the blood
quired brain damage are especially at risk for the disin- necessary to bring about a state of unconsciousness is
hibition effects of alcohol (Elliott, 1992). This is not to only a little less than the level necessary to bring about a
say, however, that the disinhibition effect is seen only in fatal overdose. This is because alcohol has a therapeu-
individuals with some form of neurological trauma. In- tic index (TI) of between 1:4 and 1:10 (Grinspoon &
dividuals without any known form of brain damage may Bakalar, 1993). In other words, the minimal effective
also experience alcohol-induced disinhibition. dose of alcohol (i.e., the dose at which the user be-
comes intoxicated) is a significant fraction of the lethal
dose. Thus, when a person drinks to the point of losing
Effects of Alcohol at Intoxicating Doses consciousness, she or he is dangerously close to over-
for the Average Drinker dosing on alcohol. Because of alcohol’s low TI, it is very
easy to die from an alcohol overdose, or acute alcohol
For a 160-pound person, two drinks in an hour’s time poisoning, something that happens 200 to 400 times a
would result in a BAL of 0.05mg/mL. At this BAL, the year in the United States (Garrett, 2000). Even experi-
individual’s reaction time and depth perception be- enced drinkers have been known to die from an over-
come impaired (Hartman, 1995). The individual will dose of alcohol. The exact blood alcohol level (BAL)
feel a sense of exhilaration and a loss of inhibitions necessary to cause death varies from person to person,
(Renner, 2004a). Four drinks in an hour’s time will with death occurring with BALs as low as 0.180
cause a 160-pound person to have a BAL of 0.10 (Oehmichen et al., 2005). About 1% of drinkers with
mg/mL or higher (Maguire, 1990). At about this level of BAL of 0.35 mg/mL will die without medical treatment
intoxication, the individual’s reaction time is approxi- (Ray & Ksir, 1993).23,24 However, the majority of those
mately 200% longer than it is for the nondrinker (Garriott, who succumb to an alcohol overdose have measured
1996), and she or he will demonstrate ataxia.22 The BALs between 0.450 and 0.500 (Oehmichen et al.,
drinker’s speech will be slurred, and she or he will stag- 2005). At these BALs, alcohol interferes with the brain’s
ger rather than walk (Renner, 2004a). ability to control respiration, and thus respiratory arrest
If our hypothetical 160-pound drinker were to drink is the most common cause of death in an alcohol over-
more than four drinks in an hour’s time, his or her blood dose (Oehmichen et al., 2005). For these reasons all
alcohol level would be even higher. Research has shown cases of known/suspected alcohol overdose should be im-
that individuals with a BAL between 0.10 and 0.14 mediately treated by a physician. A BAL of 0.40 mg/mL
mg/mL are 48 times as likely as the nondrinker to be in- will cause the drinker to fall into a coma and has about
volved in a fatal car accident (“Drinking and Driving,” a 50% death rate without medical intervention (Bohn,
1996). A person with a BAL of 0.15 mg/mL would be 1993). The LD50 is thus around 0.40 mg/mL. In the-
above the level of legal intoxication in every state and ory, the LD100 is reached when the drinker has a BAL
would definitely be experiencing some alcohol-induced between 0.5 and 0.8 mg/mL for the nontolerant
physical problems. Also, because of alcohol’s effects on drinker. However, there is a case on record of an alco-
reaction time, individuals with a BAL of 0.15 mg/mL hol-tolerant person who was still conscious and able to
are between 25 times (Hobbs, Rall, & Verdoorn, 1995) talk with a BAL as high as 0.78 mg/mL (Bohn, 1993;
and 380 times (Alcohol Alert, 1996) as likely as a non- Schuckit, 2000). The effects of alcohol on the rare
drinker to be involved in a fatal car accident. The per- drinker are summarized in Table 7.1.
son who has a BAL of 0.20 mg/mL will experience At high doses of alcohol, the stomach will begin to
marked ataxia (Garriott, 1996; Renner, 2004a). The per- excrete higher levels of mucus than is normal and will
son with a BAL of 0.25 mg/mL would stagger around also close the pyloric valve between the stomach and
and have difficulty making sense out of sensory data
(Garriott, 1996; Kaminski, 1992). The person with a 23
Thus, the LD01 for alcohol is approximately 0.35.
24As the individual’s BAL increases above this point, she or he is more
22 likely to die.
See Glossary.
68 Chapter Seven
TABLE 7.1 Effects of Alcohol on the Infrequent Drinker hangover is still unknown (Swift & Davidson, 1998).
Indeed, researchers are still divided over whether the
Blood alcohol
hangover is caused by the alcohol ingested by the
level (BAL) Behavioral and physical effects
drinker, a metabolite of alcohol (such as acetaldehyde),
0.02 Feeling of warmth, relaxation. or some of the compounds found in the alcoholic bev-
erage that give it flavor, aroma, and taste (called con-
0.05–0.09 Skin becomes flushed. Drinker is more geners) (Swift & Davidson, 1998). Some researchers
talkative, feels euphoria. At this level,
believe that the hangover is a symptom of an early alco-
psychomotor skills are slightly to moderately
hol withdrawal syndrome (Ray & Ksir, 1993; Swift &
impaired, and ataxia develops. Loss of
inhibitions, increased reaction time, Davidson, 1998). Other researchers suggest that the
and visual field disturbances. alcohol-induced hangover is caused by the lower levels of
ß-endorphin that result during alcohol withdrawal
0.10–0.19 Slurred speech, severe ataxia, mood
(Mosier, 1999).
instability, drowsiness, nausea
What is known about the alcohol-induced hangover
and vomiting, staggering gait, confusion.
is that 75% of those individuals who drink to excess will
0.20–0.29 Lethargy, combativeness, stupor, experience a hangover at some point in their lives, al-
severe ataxia, incoherent speech, amnesia, though there is evidence that some drinkers are more
unconsciousness.
prone to experience this alcohol-use after effect than
0.30–0.39 Coma, respiratory depression, anesthesia, are others (Swift & Davidson, 1998). Some of the phys-
respiratory failure. ical manifestations of the alcohol hangover include fa-
Above 0.40 Death. tigue, malaise, sensitivity to light, thirst, tremor and
nausea, dizziness, depression, and anxiety (Sher et al.,
Sources: Based on Baselt (1996); Brown & Stoudemire (1998); Brust 2005; Swift & Davidson, 1998). While the hangover
(2004); Lehman, Pilich, & Andrews (1994); Morrison, Rogers, &
Thomas (1995).
may, at least in severe cases, make the victim wish for
death (O’Donnell, 1986), there usually is little physi-
cal risk for the individual, and in general the symp-
the small intestine to try to slow down the absorption of toms resolve in 8 to 24 hours (Swift & Davidson,
the alcohol that is still in the stomach (Kaplan et al., 1998). Conservative treatment such as antacids, bed
1994). These actions contribute to feelings of nausea, rest, solid foods, fruit juice, and over-the-counter
which will reduce the drinker’s desire to consume more analgesics are usually all that is required to treat an al-
alcohol and might also contribute to the urge to vomit cohol-induced hangover (Kaminski, 1992; Swift &
that many drinkers report they experience at the higher Davidson, 1998).
levels of intoxication. Vomiting will allow the body to The effects of alcohol on sleep. While alcohol, like the
rid itself of the alcohol the drinker has ingested, but al- other CNS depressants, may induce a form of sleep, it
cohol interferes with the normal vomit reflex; this does not allow for a normal dream cycle. Alcohol-in-
might even cause the drinker to attempt to vomit when duced sleep disruption is strongest in the chronic
she or he is unconscious, causing the drinker to run the drinker, but alcohol can disrupt the sleep of even the rare
risk of aspirating some of the material being regurgi- social drinker. The impact of chronic alcohol use on the
tated. This can contribute to the condition known as as- normal sleep cycle is discussed in the next chapter.
pirative pneumonia,25 or can cause death by blocking Even moderate amounts of alcohol consumed within
the airway with stomach contents. 2 hours of going to sleep can contribute to episodes of
sleep apnea.26 The use of alcohol prior to going to sleep
Medical Complications of Alcohol can weaken pharyngeal muscle tone, increasing the
chances that the sleeper will experience increased
Use in the Normal Drinker
snoring, and sleep breathing problems (Qureshi & Lee-
The hangover. There is evidence suggesting that hu- Chiong, 2004). Thus, people with a respiratory disor-
mans have experienced alcohol-induced “hangovers” der, especially sleep apnea, should discuss their use of
for thousands of years. However, the exact mechanism alcohol with their physician to avoid alcohol-related
by which alcohol is able to cause the drinker to suffer a sleep breathing problems.
25See 26
Glossary. See Glossary.
Alcohol use and cerebrovascular accidents. There is drink, as moderate to heavy alcohol use can cause the
mixed evidence that alcohol use increases the individ- user’s body to biotransform the warfarin more quickly
ual’s risk of a cerebrovascular accident (CVA, or stroke). than normal (“Alcohol-Medication Interactions,” 1995;
D. Smith (1997) concluded that even light alcohol use, Graedon & Graedon, 1995).
defined as ingesting 1–14 ounces of pure alcohol per There is some evidence that the antidepressant
month, more than doubled an individual’s risk for hem- amitriptyline might enhance alcohol-induced euphoria
orrhagic stroke. It should be noted that the lower limit of (Ciraulo, Shader, Greenblatt, & Creelman, 2006). The
this range of alcohol use, 1 ounce of pure alcohol per mixture of alcohol and certain antidepressant medica-
month, is less than the amount of alcohol found in a tions such as amitriptyline, desimipramine, or doxepin
single can of beer. Yet Jackson, Sesso, Buring, and might also cause the user to experience problems con-
Gaziano (2003) concluded that moderate alcohol use centrating, since alcohol will potentiate the sedation
(defined as no more than 1 standard drink in 24 hours) caused by these medications, and the interaction be-
reduced the individual’s risk of both ischemic and hem- tween alcohol and the antidepressant might contribute
orrhagic strokes in a sample of male physicians who had to rapid blood pressure changes (Weathermon &
already suffered one CVA. The reason for these appar- Crabb, 1999). A person who drinks while under the in-
ently contradictory findings is not known at this time. fluence of one of the selective serotonin reuptake in-
Other consequences of rare alcohol use. Researchers hibitors (SSRIs) may experience the serotonin syndrome
have long known that even occasional alcohol use in- as a result of the alcohol-induced release of serotonin
terferes with the body’s ability to cope with uric acid within the brain and the blockade effect of the SSRIs
crystals in the blood, a matter of some concern for (Brown & Stoudemire, 1998).
drinkers who suffer from gout. Zhang et al. (2006) com- Surprisingly, there is some animal research to suggest
pared the level of alcohol intake with the occurrence of that individuals who take beta carotene and who drink
acute gout attacks and found that even occasional alco- to excess on a chronic basis might experience a greater
hol use increased the individual’s risk of an acute gout degree of liver damage than the heavy drinker who did
attack if she or he were predisposed to this condition, not take this vitamin supplement (Graedon & Graedon,
usually within 24 hours of the alcohol intake. 1995). When combined with aspirin, alcohol might
Drug interactions involving alcohol.27 There has contribute to bleeding in the stomach because the gas-
been little research into the effects of moderate alcohol tric irritation effects of alcohol are multiplied by aspirin
use (defined as 1–2 standard drinks per day) on the ac- (Sands, Knapp & Ciraulo, 1993). While acetamino-
tion of pharmaceutical agents (Weathermon & Crabb, phen does not irritate the stomach lining, the chronic
1999). It is known that alcohol functions as a CNS de- use of alcohol causes the liver to release enzymes that
pressant and thus it may potentiate the action of other transform the acetaminophen into a poison, even if the
CNS depressants such as antihistamines, opiates, barbi- latter compound is used at recommended dosage levels
turates, anesthetic agents, and benzodiazepines, and (Ciraulo et al., 2006; Zernig & Battista, 2000).
thus should not be used by patients using these agents Patients taking certain oral medications for diabetes
(Weathermon & Crabb, 1999; Zernig & Battista, 2000). should not drink, as the antidiabetic medication may
Patients who take nitroglycerin, a medication often interfere with the body’s ability to biotransform alcohol.
used in the treatment of heart conditions, frequently de- This may possibly result in acute alcohol poisoning
velop significantly reduced blood pressure levels, possibly from even moderate amounts of alcohol for the individ-
to the point of dizziness and loss of consciousness, if they ual who combines alcohol and oral antidiabetic medica-
drink while using this medication (Zernig & Battista, tions. Further, because the antidiabetic medication
2000). Patients taking the antihypertensive medication prevents the body from being able to biotransform alco-
propranolol should not drink, as the alcohol will de- hol, the individual will remain intoxicated far longer
crease the effectiveness of this antihypertensive medica- than he or she would normally. In such a case, the indi-
tion (Zernig & Battista, 2000). Further, patients taking vidual might underestimate the time before which it
the anticoagulant medication warfarin should not would be safe for him or her to drive a motor vehicle.
Patients who are on the antidepressant medications
27The list of potential alcohol-drug interactions is quite extensive. Pa- known as monoamine oxidase inhibitors (MAO in-
tients who are taking either a prescription or over-the-counter med-
ication should not consume alcohol without first checking with a
hibitors, or MAOIs) should not consume alcohol under
physician or pharmacist to determine if there is a danger for an inter- any circumstances. The fermentation process produces
action between the two substances. an amino acid, tyramine, along with the alcohol.
70 Chapter Seven
Normally, this is not a problem. Indeed, tyramine is Alcohol Use and Accidental
found in certain foods, and it is a necessary nutrient. Injury or Death
But tyramine interacts with the MAO inhibitors, caus-
ing dangerously high, and possibly fatal, blood pressure Advertisements in the media proclaim the benefits of
levels (Brown & Stoudemire, 1998). Patients who take recreational alcohol use at parties, social encounters, or
MAO inhibitors are provided a list of foods they should celebrations of good news; they rarely mention alco-
avoid while they are taking their medication, which hol’s role in accidental injury or violence. The grim re-
usually includes alcohol. ality is that there is a known relationship between
Researchers have found that the calcium channel alcohol use and accidental injury. For example, in
blocker Verapamil inhibits the process of alcohol bio- 2002, 17,970 people were killed on U.S. roads in alco-
transformation, increasing the period of time in which hol-related motor vehicle accidents (41% of the total
alcohol might cause the user to be intoxicated (Brown number of traffic-related deaths that year) (“National
& Stoudemire, 1998). Although early research studies Traffic Death Total,” 2003). A BAL between 0.05 and
suggested that the medications Zantac (ranitidine)28 0.079, which is below the legal limit of 0.08, still in-
and Tagamet (cimetidine) interfered with the biotrans- creases the individual’s risk of being involved in a motor
formation of alcohol, subsequent research failed to sup- vehicle accident by 546%, while a BAL above 0.08 in-
port this hypothesis (Jones, 1996). creases his or her risk at least 1,500% above that of a
Patients who are taking the antibiotic medications nondrinking driver (Movig et al., 2004).
chloramphenicol, furazolidone, and metronidazole or In addition to its role in motor vehicle deaths, alco-
the antimalarial medication quinacrine should not hol use has been found as a factor in 51% of all boating
drink alcohol. The combination of these antibiotics fatalities (Smith, Keyl, Hadley, Bartley, Foss, Tolbert, &
with alcohol may produce a painful reaction very simi- McKnight, 2001), and an estimated 70% of the motor-
lar to that seen when the patient on disulfiram (to be dis- cycle drivers who are killed in an accident are thought
cussed in a later chapter) consumes alcohol (Meyers, to have been drinking prior to the accident (Colburn,
1992). Individuals taking the antibiotic erythromycin Meyer, Wrigley, & Bradley, 1993). Alcohol use is a fac-
should not consume alcohol, as this medication can tor in 17% to 53% of all falls, and 40% to 64% of all fa-
contribute to abnormally high blood alcohol levels due talities associated with fires (Lewis, 1997). Thirty-two
to enhanced gastric emptying (Zernig & Battista, 2000). percent of the adults who die in bicycling accidents
Persons taking the antibiotic doxycycline should not were found to have alcohol in their systems (Li, Baker,
drink, since alcohol can decrease the blood levels of Smialek, & Soderstrom, 2001). Indeed, 52% of individ-
this medication, possibly to the point that it will no uals treated at one major trauma center had alcohol in
longer be effective (Brown & Stoudemire, 1998). Any- their blood at the time of admission (Cornwell et al.,
one taking the antitubercular drug isoniazid (or INH as 1998). No matter how you look at it, even casual alco-
it is often called) should also avoid the use of alcohol. hol use carries with it a significantly increased risk of
The combination of these two chemicals will reduce accidental injury or death. Indeed, the recommenda-
the effectiveness of the isoniazid and may increase the tion has been made that any patient involved in an
individual’s chances of developing hepatitis. alcohol-related accident or who suffered an injury
Although there has been little research into the pos- while under the influence of alcohol be examined to
sible interaction between alcohol and marijuana, since determine whether she or he has an alcohol use disorder
the latter substance is illegal, preliminary evidence (Reynaud, Schwan, Loiseaux-Meunier, Albuisson, &
does suggest that alcohol’s depressant effects might exac- Deteix, 2001).
erbate the CNS depressant effects of marijuana (Garriott, Although the majority of those who drink to intoxica-
1996). Alcohol is a very potent chemical, and it is not tion do not become violent, research has shown that in
possible to list all of the potential interactions between approximately 50% of cases of interpersonal violence the
alcohol and the various medications currently in use. perpetrator had been using alcohol immediately prior to
Thus, before mixing alcohol with any medication, an the offense (Parrott & Giancola, 2006). Statistically, up
individual should consult a physician or pharmacist to to 86% of those who commit murder, 60% of sex offend-
avoid potentially dangerous interactions between phar- ers, 37% of those who commit physical assault, and 30%
maceutical agents and alcohol. of child abuse offenders are under the influence of alco-
hol at the time of the offense (Greenfield, 2007; Parrott &
28The most common brand name is given first, with the generic Giancola, 2006). When one considers the possibility
name in parenthesis. that the victim had been using alcohol as well, these
percentages are significantly increased. Thus, while are obtained from wine. The use of distillation to
there is a public perception of alcohol as a social bever- achieve concentrations of alcohol above 15% was re-
age, the reality is somewhat different. viewed, and questions surrounding the use of alcohol
were discussed. The effects of alcohol on the rare social
drinker were reviewed, and some of the more signifi-
Summary cant interactions between alcohol and pharmaceutical
This chapter has briefly explored the history of alcohol, agents were examined. The history of alcohol con-
including its early history as man’s first recreational sumption in the United States was briefly discussed, as
chemical. In this chapter, the process of distillation was was the pattern of alcohol use in the United States at
discussed, as was the manner in which distilled spirits this time.
CHAPTER EIGHT
Chronic Alcohol Abuse and Addiction
The focus of the last chapter was on the acute effects of entirely from alcohol, or drink only on rare occasions. A
alcohol on the “average” or rare social drinker. But a sig- small percentage of the population consumes a dispro-
nificant percentage of drinkers do not limit themselves portionate amount of the ethanol that is produced, as
to rare or occasional alcohol ingestion, which places evidenced by the fact that 10% of those adults who con-
them at increased risk for premature death from a vari- sume alcohol drink 50% of the ethanol that is produced
ety of alcohol-related conditions (Timko, DeDenedetti, (Sommer, 2005).
Moos, & Moos, 2006). Collectively, the alcohol use dis- Depending on the criteria used to define the term
orders (AUDs) are the third leading preventable cause alcohol use disorder (AUD), it has been estimated that
of death in the United States, causing between 85,000 between 10% (Fleming, Mihic, & Harris, 2001) and
and 175,000 premature deaths each year (Mokdad, 20% (Kranzler & Ciraulo, 2005) of those adults who
Marks, Stroup, & Gerberding, 2004; Schuckit & consume alcohol will meet the criteria for a diagnosis
Tapert, 2004). The AUDs can also cause or exacer- of an AUD at some point in their lives.2 But this still
bate a wide range of physical, social, financial, and means that the AUDs are the most common psychiatric
emotional problems for the individual and/or the disorder encountered by mental health professionals
drinker’s family. Yet they are all too often undiag- (Gold & Miller, 1997b; Schuckit, 2005a, 2005b,
nosed and thus untreated (Brady, Tolliver, & Verduin, 2006). Drawing on the results of the National Epi-
2007). Indeed, given its potential for harm, one could demiologic Survey on Alcohol and Related Condi-
argue that if alcohol were to be discovered only today, tions, Grant et al. (2006) estimated that there was an
its use might never be legalized (Miller & Hester, increase in the percentage of adults in the United
1995). In this chapter, some of the manifestations, States who had abused alcohol in the past year. Fully
and consequences, of alcohol use disorders will be 4.65% of adults in the this country had abused alcohol
discussed. in the preceding 12-months, according to the authors.
However, the percentage of adults who could be said
to be actively addicted to alcohol dropped from 4.38%
Scope of the Problem to 3.81% in the same 12-month period, according to
At the start of the 21st century, Europeans have the du- the authors.
bious distinction of being the heaviest drinkers in the Using a different methodology, Gold (2005) and
world, with 5% of the men and 1% of the women meet- Bankole and Ait-Daoud (2005) estimated that 8 million
ing the criteria for a diagnosis of alcohol dependence adults in the United States were physically dependent
(“Europeans Heaviest Drinkers in the World,” 2006). on alcohol and that another 5.6 million people abused
In the United States, 90% of all adults are thought to use it. Statistically, AUDs affect predominantly men, with
alcohol at some point in their lives (Schuckit & Tapert, women making up only 20% to 25% of the individuals
2004), and 65% of adults are current alcohol users with an AUD (Anton, 2005; Schuckit, 2005a, 2005b).
(Nace, 2005a). The per capita consumption of alcohol But whether the heavy drinker is a man or a woman,
in the United States is estimated at 2.2 gallons of pure the individual’s alcohol use disorder will impact his or
ethanol1 each year (Schuckit, 2005a, 2005b, 2006). But her social life, interpersonal relationships, educational
this statistic is misleading in that many people abstain or vocational activities, and health, and will cause or
contribute to any of a wide range of legal problems.
1
Remember that this the average amount of pure ethanol per capita.
2
That ethanol is then mixed with various compounds to produce beer, This figure includes those who are addicted to alcohol as well as
wine, etc. those who abuse alcohol at some point in their lives.
72
Chronic Alcohol Abuse and Addiction 73
Many heavy drinkers will deny being alcohol depen- son with an alcohol use problem is that she or he has
dent on the grounds that they are “only problem drinkers.” nothing in common with the stereotypical “skid row”
Unfortunately, there is little evidence to suggest that derelict. In reality, only about 5% of those who are de-
“problem drinkers” are different from alcohol-dependent pendent on alcohol fit the image of the skid row alco-
individuals (Prescott & Kendler, 1999; Schuckit, Zisook, holic (Knapp, 1996). The majority of those with alcohol
& Mortola, 1985). At best, research data suggest that the use problems might best be described as “high-
so-called problem drinker will have a smaller number of functioning” (Knapp, 1996, p. 12) individuals, with
or less severe consequences from his or her AUD. Fur- jobs, responsibilities, families, and public images to pro-
ther, the problem drinker is well on his or her way to be- tect. In many cases, the individual’s growing dependence
coming alcohol dependent. This dependence on alcohol on alcohol is hidden from virtually everybody, including
usually develops after 10 (Meyer, 1996b) to 20 years the drinker. It is only in secret moments of introspection
(Alexander & Gwyther, 1995) of heavy drinking. Once that these people will wonder why they seem unable to
established, alcohol dependence can have lifelong im- drink “like a normal person.”
plications for the individual. For example, once alcohol
dependence has developed, it is always there, lurking in
the shadows. If the individual should return to the use of Alcohol Tolerance, Dependence, and
alcohol, the physical addiction can reassert itself “in a Craving: Signposts of Alcoholism
matter of days to weeks” (Meyer, 1996b, p. 165). In a
Certain symptoms, when present, suggest that the
sense, a person with alcohol dependence is similar to
drinker has moved past the point of simple social drink-
one with a severe allergy: After it develops, the individual
ing or even heavy drinking and has become physically
cannot be exposed to the offending agent without risking
dependent on alcohol and its effects. The first of these
a severe reaction. If, after the disorder develops, the indi-
signs is tolerance.
vidual did not experience a severe reaction, this does not
As the individual repeatedly consumes alcohol, his
guarantee that she or he won’t have a catastrophic reac-
or her body will begin to make certain adaptations to try
tion the next time.
to maintain normal function in spite of the continual
use of alcohol, a process known as tolerance. The de-
velopment of tolerance to alcohol depends on many
Is There a “Typical”
factors, including the individual’s drinking history and
Alcohol-Dependent Person?
genetic inheritance (Swift, 2005). It is important to re-
A “binge” is defined as consumption of five or more member that there are several different forms of toler-
cans of beer or regular mixed drinks during a single ance, including metabolic tolerance. Metabolic tolerance
episode of alcohol consumption by a person who is not is seen when the individual’s liver becomes more effi-
a daily drinker (Naimi et al., 2003). The authors used cient in biotransforming alcohol over time. As meta-
this definition to determine that 15% of the adults in bolic tolerance to alcohol develops, the drinker notices
the United States had engaged in at least one period of that she or he must consume more alcohol to achieve a
binge drinking in any given 30 day period, and 15% re- desired level of intoxication (Nelson, 2000). In clinical
ported having done so on 12 or more days in the pre- interviews, the drinker might admit that when she or
ceding year (Freiberg & Samet, 2005). It was estimated he was 21, it took “only” six to eight beers before she or
that 1.5 billion episodes of binge drinking take place an- he became intoxicated; now it takes 12 to 15 beers con-
nually in the United States (Freiberg & Samet, 2005). sumed over the same period of time before she or he is
Not surprisingly, heavy drinkers were more likely to en- drunk.
gage in binge drinking and were more likely to con- Another form of tolerance to alcohol’s effects is be-
sume more alcohol during a binge than were light to havioral tolerance. Where a novice drinker might ap-
moderate drinkers. pear quite intoxicated after five or six beers, the
Alcohol abusers/addicts are frequently “masters of de- experienced drinker might show few outward signs of
nial” (Knapp, 1996, p. 19), able to offer a thousand and intoxication even after consuming far more alcohol
one rationalizations as to why they cannot possibly have than this. On occasion, even skilled law enforcement or
an alcohol use problem: They always go to work; never health care professionals are shocked to learn that the
go to the bar to drink; know 10 people who drink as apparently sober person in their care has a BAL well
much as, if not more, than they do; and on and on. One into the range of legal intoxication; this is why objective
of the most common rationalizations offered by the per- test data are used to determine whether an individual is or
74 Chapter Eight
TABLE 8.1 Effects of Alcohol on the Chronic Drinker Individuals with an AUD become dependent on it
in both a psychological and a physical sense. Psycholog-
Blood alcohol
ical dependence reflects a state of mind in which the
level (BAL) Behavioral and physical effects
drinker comes to believe that alcohol is necessary to
0.05–0.09 None to minimal effect help him or her socialize, relax, sleep better, and so on.
observed. This individual uses alcohol as a “crutch,” believing
that he or she is unable to be sexual, sleep, cope with
0.10–0.19 Mild ataxia, euphoria.
strong negative emotions, or socialize without alcohol
0.20–0.29 Mild emotional changes. being involved in the process somehow. In contrast to
Ataxia is more severe. this, the physical dependence on alcohol manifests it-
0.30–0.39 Drowsiness, lethargy, stupor. self through the physical adaptations the drinker’s body
has made in trying to maintain normal function. When
0.40–0.49 Coma. Death is possible.
alcohol is suddenly removed from the body, there will
0.50–0.60 Respiratory paralysis that may be a period of readjustment, known as a withdrawal
result in drinker’s death.a syndrome.
aBrust(2004) discussed how, on rare occasions, a patient with a The alcohol withdrawal syndrome (AWS) involves
measured BAL of up to 0.80 might be alert or conscious, although not only some degree of subjective discomfort for the
such exceptions are rare, and usually a BAL of 0.50 is fatal. individual but is also potentially life threatening.3 The
Sources: Based on information in Baselt (1996); Lehman, Pilich, & alcohol withdrawal dyndrome (AWS) is influenced by
Andrews (1994); Morrison, Rogers, & Thomas (1995); Renner (2004a). several factors, including (a) the frequency and amount
of alcohol use and (b) the individual’s general state of
health. The longer the period of alcohol use and the
is not legally intoxicated at the time of being stopped by greater the amount ingested, the more severe the AWS
the police. will be. The symptoms of alcohol withdrawal for the
Pharmacodynamic tolerance is another form of toler- chronic alcoholic will be discussed in more detail in a
ance. As the cells of the central nervous system attempt later section of this chapter.
to carry out their normal function in spite of the contin- Often the recovering alcoholic will speak of a crav-
ual presence of alcohol, they become less and less sen- ing for alcohol that continues long after he or she has
sitive to the intoxicating effects of the chemical. Over stopped drinking. Some individuals experience this as
time, the individual has to consume more and more al- being “thirsty,” or find themselves preoccupied with the
cohol to achieve the same effect on the CNS. As phar- possibility of drinking. Whichever, preoccupation with
macodynamic tolerance develops, the individual might or craving for alcohol is a diagnostic sign indicating that
switch from beer to “hard” liquor or increase the the drinker is physically dependent on alcohol.
amount of alcohol consumed to achieve a desired state The TIQ hypothesis. In the late 1980s Trachtenberg
of intoxication. and Blum (1987) suggested that chronic alcohol use
If either of these forms of tolerance has developed, significantly reduces the brain’s production of the en-
the patient is said to be “tolerant” to the effects of alco- dorphins, the enkephalins, and the dynorphins. These
hol. Compare the effects of alcohol for the chronic neurotransmitters function in the brain’s pleasure cen-
drinker in Table 8.1 (above) with those in Table 7.1 (in ter to help moderate an individual’s emotions and be-
the previous chapter). havior. It was also suggested that a by-product of alcohol
Tolerance requires great effort from the individual’s metabolism and neurotransmitters normally found
body, and eventually the different organs prove unequal within the brain combined to form the compound
to the continual task of maintaining normal function in tetrahydroisoquinoline (or TIQ) (Blum, 1988). The TIQ
spite of the individual’s drinking. When this happens, is thought to be capable of binding to opiate-like recep-
the person actually becomes less tolerant to alcohol’s ef- tor sites within the brain’s pleasure center, causing the
fects. It is not uncommon for chronic drinkers to admit individual to experience a sense of well-being (Blum &
that in contrast to the past, they now can become intox- Payne, 1991; Blum & Trachtenberg, 1988). However,
icated on just a few beers or mixed drinks. An assessor
would say that this individual’s tolerance is “on the 3All known or suspected cases of alcohol withdrawal should be as-
downswing,” a sign that the drinker has entered the sessed by a physician so that the proper precautions and treatment
later stages of alcohol dependence. might be initiated to minimize the risk to the individual’s life.
TIQ’s effects were thought to be short-lived, forcing the These observations remain true today. However, the
individual to drink more alcohol to regain or maintain chronic use of alcohol will have an impact on virtually
the initial feeling of euphoria achieved through the use every body system. We briefly discuss the effects of
of alcohol. chronic alcohol use on various organ systems below.
Over time, it was thought that the individual’s The effects of chronic alcoholism on the digestive sys-
chronic use of alcohol would cause his or her brain to tem. As discussed in the last chapter, during distilla-
reduce its production of enkephalins, as the ever- tion many of the vitamins and minerals that were in
present TIQ was substituted for these naturally pro- the original wine are lost. Thus, where the original
duced opiate-like neurotransmitters (Blum & Payne, might have contributed something to the nutritional
1991; Blum & Trachtenberg, 1988). The cessation of requirements of the individual, even this modest con-
alcohol intake was thought to result in a neurochemi- tribution is lost through the distillation process. Fur-
cal deficit, which the individual would then attempt ther, when the body biotransforms alcohol, it finds
to relieve through further chemical use (Blum, & “empty calories” in the form of carbohydrates from
Payne, 1991; Blum & Trachtenberg, 1988). Subjec- the alcohol, without the protein, vitamins, calcium,
tively, this deficit was experienced as the craving for and other minerals needed by the body. Also, the fre-
alcohol commonly reported by recovering alcoholics, quent use of alcohol interferes with the absorption of
according to the authors. While the TIQ theory had a needed nutrients from the gastrointestinal tract and
number of strong adherents in the late 1980s and early may cause the drinker to experience chronic diarrhea
1990s, it has gradually fallen into disfavor. A number (Fleming, Mihic, & Harris, 2001). These factors may
of research studies have failed to find evidence to sup- contribute to a state of vitamin depletion called
port the TIQ hypothesis, and currently few re- avitaminosis.
searchers in the field of alcohol addiction believe that Although alcohol does not appear to directly cause
TIQ plays a major role in the phenomenon of alcohol cancer, it does seem to facilitate the development of
craving. some forms of it (Bagnardi, Blangiardo, La Vecchia, &
Corrao, 2001). Indeed, alcohol has been identified as a
Complications of Chronic Alcohol Use leading risk factor for the development of cancer
(Danaei, Vander Hoorn, Lopez, Murry, & Ezzadi,
Because alcohol is a mild toxin, its chronic use will 2006). Chronic alcohol use is associated with higher
often result in damage to one or more organ systems. rates of cancer of the upper digestive tract, the respira-
Such organ damage is often the direct cause of death, tory system, the mouth, pharynx, larynx, esophagus,
although alcohol’s role in causing this organ failure is and liver (Bagnardi et al., 2001; Schuckit, 2006). Alco-
frequently overlooked. The risk of premature death for hol use is associated with 75% of all deaths due to
chronic drinkers has been estimated as 2.5 to 4 times cancer of the esophagus (Rice, 1993). Further, although
higher than for nondrinkers—strong evidence that the the exact mechanism is not known, there is an apparent
chronic use of alcohol carries with it significant dangers relationship between chronic alcohol use and cancer of
(Oehmichen, Auer, & Konig, 2005). It is important to the large bowel in both sexes, and cancer of the breast in
recognize that chronic alcohol abuse includes both women (Bagnardi et al., 2001; Room, Babor, & Rehm,
“weekend”/“binge” drinking and more regular alcohol 2005; Zhang et al., 2007).
abuse. Episodic alcohol abuse may, over time, bring The combination of cigarettes and alcohol is espe-
about many of the same effects seen with chronic alco- cially dangerous. Chronic alcoholics experience almost
hol use. Unfortunately, there is no simple formula by a sixfold increase in their risk of developing cancer of the
which to calculate the risk of alcohol-related organ dam- mouth or pharynx (Pagano, Graham, Frost-Pineda, &
age or to predict which organs will be affected (Segal & Gold, 2005). For comparison, consider that cigarette
Sisson, 1985). As the authors noted two decades ago, smokers have slightly over a sevenfold increased risk of
developing cancer of the mouth or pharynx. Surpris-
Some heavy drinkers of many years’ duration appear ingly, however, alcoholics who also smoke have a 38-fold
to go relatively unscathed, while others develop increased risk of cancer in these regions, according to
complications early (e.g., after five years) in their the authors.4
drinking careers. Some develop brain damage; others
liver disease; still others, both. The reasons for this are 4Therelationship between tobacco use and drinking is discussed in
simply not known. (p. 145) Chapter 19.
76 Chapter Eight
The body organ most heavily involved in alcohol preted as being caused by other conditions such as ap-
biotransformation is the liver, which often bears the pendicitis, pancreatitis, or an inflammation of the gall
brunt of alcohol-induced organ damage (Sadock & bladder. If the physician were to attempt surgical inter-
Sadock, 2003). Unfortunately, scientists do not know ventions, the patient’s life might be placed at increased
how to determine the level of exposure necessary to risk because of the complications caused by the undiag-
cause liver damage for any given individual, but it is nosed alcoholism.
known that chronic exposure to even limited amounts Between 10% and 20% of individuals with alcohol-
of alcohol may result in liver damage (Frezza et al., induced hepatitis go on to develop cirrhosis of the liver
1990; Lieber, 1996; Schenker & Speeg, 1990). Indeed, (Bankole & Ait-Daoud, 2005; Karsan, Rojter, & Saab,
chronic alcohol use is the most common cause of liver 2004; Nace, 2005a). At this stage, the chronic exposure
disease in both the United States (Hill & Kugelmas, to alcohol has caused liver cells to die, and these cells
1998) and the United Kingdom (Walsh & Alexander, are replaced by scar tissue. Unfortunately, scar tissue is
2000). Approximately 80% to 90% of heavy drinkers essentially nonfunctional. As more and more liver cells
will develop an early manifestation of alcohol-related die, the liver becomes unable to effectively cleanse the
liver problems: a “fatty liver” (also called steatosis) blood, allowing various toxins to accumulate in the cir-
(Nace, 2005a; Walsh & Alexander, 2000). In this condi- culation. Some toxins, like ammonia, are thought then
tion the liver becomes enlarged and does not function to damage the cells of the CNS (Butterworth, 1995). A
at full efficiency (Bankole & Ait-Daoud, 2005). There physical examination of the patient with cirrhosis of the
are few indications of a fatty liver that would be noticed liver will reveal a hard, nodular liver; an enlarged
without a physical examination, but blood tests would spleen; “spider” angiomas on the skin; tremor; jaun-
detect characteristic abnormalities in the patient’s liver dice; mental confusion; signs of liver disease on various
enzymes (Schuckit, 2000). This condition will usually blood tests; and possibly testicular atrophy in males
reverse itself with abstinence (Walsh & Alexander, (Nace, 2005a).
2000). Although some researchers believe that alcoholic
Between 10% and 35% of individuals with alcohol- hepatitis precedes the development of cirrhosis of the
induced fatty liver and who continue to drink go on to liver, this has not been proven. Indeed, “alcoholics may
develop a more advanced form of liver disease: alco- progress to cirrhosis without passing through any visible
holic hepatitis (Nace, 2005a). In alcohol-induced stage resembling hepatitis” (“Alcohol and the Liver,”
hepatitis, the cells of the liver become inflamed as a 1993, p. 1). Cirrhosis can develop in people who con-
result of the body’s continual exposure to alcohol, and sume as little as two to four drinks a day for just 10 years
the individual develops symptoms such as a low-grade (Karsan et al., 2004). A number of different theories
fever; malaise; jaundice; an enlarged, tender liver; have been advanced to explain alcohol-induced liver
and dark urine (Nace, 1987). Blood tests would also disease. One theory suggests that “free radicals” that are
reveal characteristic changes in the blood chemistry generated during the process of alcohol biotransforma-
(Schuckit, 2005a), and the patient might complain of tion might contribute to the death of individual liver
abdominal pain (Hill & Kugelmas, 1998). Even with cells, initiating the development of alcohol-induced
the best of medical care, 20% to 65% of the individuals cirrhosis (Walsh & Alexander, 2000).
with alcohol-induced hepatitis will die (Bondesson & There is exciting evidence suggesting that the con-
Sapperston, 1996). sumption of coffee might actually reduce the individ-
Doctors do not know why some chronic drinkers de- ual’s risk of alcohol-induced cirrhosis (Klatsky, Morton,
velop alcohol-induced hepatitis and others do not, al- Udaltsova, & Friedman, 2006). The authors found that
though the individual’s genetic inheritance is thought the individual’s risk of developing alcohol-induced cir-
to play a role in this process. For those whose genetic rhosis seemed to be reduced by 22% for each cup con-
history puts them at risk for this condition, it usually de- sumed, although the exact mechanism by which coffee
velops after 15–20 years of heavy drinking (Walsh & consumption might reduce the individual’s cirrhosis
Alexander, 2000). Individuals who have alcohol-induced risk is still not clear.
hepatitis should avoid having surgery, if possible, as At one point, it was thought that malnutrition was a
they are poor surgical risks. Unfortunately, if the patient factor in the development of alcohol-induced liver dis-
were to be examined by a physician who was not aware ease. However, research has found that the individual’s
of the individual’s history of an alcohol use disorder, dietary habits do not seem to influence the develop-
symptoms such as abdominal pain might be misinter- ment of alcohol-induced liver disease (Achord, 1995).
Recently, scientists have developed blood tests capable Bode, 1996), and there is evidence that beverages con-
of detecting one of the viruses known to infect the liver. taining just 5% to 10% alcohol can damage the lining
The virus is known as the hepatitis virus type C (or of the stomach (Bode et al., 1996). This process seems
hepatitis-C, or HVC).5 Normally this virus is found in to be why about 30% of chronic drinkers develop gas-
about 1.6% of the general population. But between tritis7 as well as bleeding from the stomach lining and
25% and 60% of chronic alcohol users are thought to be the formation of gastric ulcers (Mc Analley, 1996;
infected with HVC (Achord, 1995), suggesting that Willoughby, 1984). If an ulcer forms over a major
there may be a relationship between HVC infection, blood vessel, the stomach acid will eat through the
chronic alcohol use, and the development of liver stomach lining and blood vessel walls, causing a bleed-
disease. ing ulcer. This is a severe medical emergency, which
Whatever its cause, cirrhosis can bring about severe may be fatal. Physicians will try to seal a bleeding ulcer
complications, including liver cancer, and sodium and through the use of laser beams, but in extreme cases
water retention (Nace, 1987; Schuckit, 2000). As the conventional surgery is necessary to save the patient’s
liver becomes enlarged, it begins to squeeze the blood life. The surgeon may remove of part of the stomach to
vessels that pass through it, which in turn causes blood stop the bleeding. This, in turn, will contribute to the
pressure to build up within the vessels, adding to the body’s difficulties in absorbing suitable amounts of vita-
stress on the drinker’s heart. This condition is known as mins from food that is ingested (Willoughby, 1984).
portal hypertension, which can cause the blood vessels This, either by itself or in combination with further al-
in the esophagus to swell from the back pressure. Weak cohol use, helps to bring about a chronic state of mal-
spots form on the walls of the vessels much like weak nutrition in the individual.
spots form on an inner tube of a tire. These weak spots Unfortunately, the vitamin malabsorption syndrome
in the walls of the blood vessels of the esophagus are that develops following the surgical removal of the ma-
called esophageal varices,6 which may rupture. Rup- jority of the individual’s stomach will, in turn, make the
tured esophageal varices is a medical emergency that, drinker a prime candidate for the development of tu-
even with the most advanced forms of medical treat- berculosis (or TB) if she or he continues to drink
ment, results in death for 20% to 30% of those who de- (Willoughby, 1984). The topic of TB is discussed in
velop this disorder (Hegab & Luketic, 2001). Between more detail in Chapter 34. However, upward of 95% of
50% and 60% of those who survive will develop a sec- alcohol-dependent individuals who had a portion of
ond episode of bleeding, resulting in an additional 30% their stomach removed secondary to bleeding ulcers
death rate. Ultimately, 60% of those afflicted with and who continued to drink ultimately developed TB
esophageal varices will die as a result of blood loss from (Willoughby, 1984).
a ruptured varix (Giacchino & Houdek, 1998). The chronic use of alcohol can cause or contribute to
As if that were not enough, alcohol has been identi- a number of vitamin malabsorption syndromes, in which
fied as the most common cause of a painful inflamma- the individual’s body is no longer able to absorb needed
tion of the pancreas, known as pancreatitis (Fleming, vitamins or minerals from food. Some of the minerals
Mihic, & Harris, 2001). While pancreatitis can be that chronic drinkers have trouble absorbing include
caused by other things—such as exposure to a number zinc (Marsano, 1994), sodium, calcium, phosphorus,
of toxic agents including the venom of scorpions or cer- and magnesium (Lehman, Pilich, & Andrews, 1994).
tain insecticides—chronic exposure to ethyl alcohol is Chronic use of alcohol also interferes with the body’s
the most common cause of toxin-induced pancreatitis ability to absorb or properly utilize vitamin A, vitamin D,
in this country, accounting for 66% to 75% of the cases vitamin B-6, thiamine, and folic acid (Marsano, 1994).
of pancreatitis (McCrady & Langenbucher, 1996; Chronic drinking is a known cause of a condition
Steinberg & Tenner, 1994). Pancreatitis develops known as glossitis8 as well as possible stricture of the
slowly, usually after “10 to 15 years of heavy drinking” esophagus (Marsano, 1994). Each of these conditions
(Nace, 1987, p. 26). can indirectly contribute to failure on the part of the
Even low concentrations of alcohol appear to inhibit individual to ingest an adequate diet, further contribut-
the stomach’s ability to produce the prostaglandins nec- ing to alcohol-related dietary deficiencies within the
essary to protect it from digestive fluids (Bode, Maute, & drinker’s body. As noted, alcohol-containing beverages
5 7See
Discussed in Chapter 34. Glossary.
6 8See
Varix is the singular form of varicies. Glossary.
78 Chapter Eight
are a source of empty calories, and many chronic 2003).10 For reasons that are not well understood, the
drinkers obtain up to one-half of their daily caloric in- moderate use of alcohol-containing beverages has been
take from alcoholic beverages rather than from more found to bring about a 10% to 40% reduction in the in-
traditional food sources (Suter, Schultz, & Jequier, dividual’s risk of developing coronary heart disease
1992). Alcohol-related dietary problems can con- (CHD) (Fleming et al., 2001; Klatsky, 2002, 2003).
tribute to a decline in the immune system’s ability to Mukamal et al. (2003) suggested that the actual form of
protect the individual from various infectious diseases the alcohol-containing beverage was not as important
such as pneumonia and tuberculosis (TB). Alcohol- as the regular use of a moderate amount,11 although
dependent individuals, for example, are three to seven there is no consensus on this issue (Klatsky, 2002).
times as likely to die from pneumonia as are non- However, this effect was moderated by the individual’s
drinkers (Schirmer, Wiedermann, & Konwalinka, genetic heritage, with some drinkers gaining more
2000). benefit from moderate alcohol use than others (Hines
The chronic use of alcohol is a known risk factor in et al., 2001).
the development of a number of different metabolic One theory for the reduced risk of CHD is that alco-
disorders. For example, although there is mixed evi- hol may function as an anticoagulant. Within the body,
dence to suggest that limited alcohol use9 might serve alcohol inhibits the ability of blood platelets to bind to-
a protective function against the development of type gether (Klatsky, 2003; Renaud & DeLorgeril, 1992).
2 diabetes in women, heavy chronic alcohol use is a This may be a result of alcohol’s ability to facilitate the
known risk factor for the development of type 2 dia- production of prostacyclin and to reduce the fibrogen
betes (Wannamethee, Camargo, Manson, Willett, & levels in the body when it is used at moderate levels
Rimm, 2003). Between 45% and 70% of alcoholics (Klatsky, 2002, 2003). By inhibiting the action of blood
with liver disease are also either glucose intolerant (a platelets to start the clotting process, the moderate use
condition that suggests that the body is having trouble of alcohol may result in a lower risk of heart attack by
dealing with sugar in the blood) or diabetic (“Alcohol 30% to 40% (Stoschitzky, 2000). It is theorized that
and Hormones,” 1994). Many chronic drinkers expe- moderate alcohol consumption also “significantly and
rience episodes of abnormally high (hyperglycemic) or consistently raises the plasma levels of the antiathero-
abnormally low (hypoglycemic) blood sugar levels. genic HDL cholesterol” (Klatsky, 2002, p. ix), making it
These conditions are caused by alcohol-induced in- more difficult for atherosclerotic plaque to build up.
terference with the secretion of digestive enzymes However, physicians still hesitate to recommend
from the pancreas (“Alcohol and Nutrition,” 1993, that nondrinkers turn to alcohol as a way of reducing
1994). their risk of heart disease because alcohol offers a
Chronic alcohol use may interfere with the way the “double-edged sword” (Goldberg, 2003; Klatsky, 2002,
drinker’s body utilizes fats. When the individual reaches p. ix). Although the moderate use of alcohol might pro-
the point that he or she obtains 10% or more of daily en- vide a limited degree of protection against coronary ar-
ergy requirements from alcohol rather than more tradi- tery disease, it also increases the individual’s risk of
tional foods, the person’s body will go through a series of developing alcohol-related brain damage (Karhunen,
changes (Suter et al., 1992). First, the chronic use of al- Erkinjuntti, & Laippala, 1994). Further, heavy alcohol
cohol will slow down the body’s energy expenditure use increases the individual’s chances of coronary heart
(metabolism), which in turn causes the body to store the disease by 600% (Schuckit, 2006).
unused lipids as fatty tissue. This is the mechanism that When used to excess, alcohol not only loses its pro-
produces the so-called beer belly commonly seen in the tective action but may actually harm the cardiovascular
heavy drinker. system. Excessive alcohol use causes the suppression
Effects of chronic alcohol use on the cardiopul- of normal red blood cell formation, and both blood
monary system. Researchers have long been aware of
10Advocates of the moderate use of alcohol point to the lower inci-
what is known as the “French paradox,” a lower-than-
expected rate of heart disease in the French in spite of dence of heart disease experienced by the French, who consume
wine on a regular basis. But they overlook the significantly higher in-
a diet rich in the foods that supposedly are associated cidence of alcohol-related liver disease experienced by the French
with an increased risk of heart disease (Goldberg, (Walton, 2002).
11“Moderate” alcohol use is defined as no more than two 12-ounce
9
Defined as 1 standard drink, 12 ounces of beer, or 4 ounces of wine cans of beer, two 5-ounce glasses of wine, or 1.5 ounces of vodka, gin,
in a 24-hour period. or other “hard” liquor in a 24-hour period (Klatsky, 2003).
clotting problems and anemia are common complica- result in a condition known as the “holiday heart syn-
tions of alcoholism (Brust, 2004). Chronic alcohol use drome” (Bankole & Ait-Daoud, 2005; Klatsky, 2003;
has been identified as one cause of essential hyperten- Raghavan, Decker, & Meloy, 2005; Stoschitzky, 2000).
sion, and abnormal blood pressure levels might be one When used on an episodic basis, such as when the indi-
reason that alcohol abuse is a factor in the development vidual consumes larger-than-normal quantities of alco-
of cerebral vascular accidents (strokes or CVAs). Light hol during a holiday break from work, alcohol can
drinkers (2–3 drinks a day) are estimated to have a interfere with the normal flow of electrical signals
twofold higher risk of a stroke, while heavy drinkers (4+ within the heart. This might then contribute to an ir-
drinks a day) have almost a threefold higher risk of a regular heartbeat known as atrial fibrillation, which
CVA (Ordorica & Nace, 1998). Nationally, alcohol is can be fatal if not diagnosed and properly treated.
thought to be the cause factor in 23,500 strokes each Thus, even episodic alcohol abuse is not without some
year (Sacco, 1995). degree of risk.
In large amounts, defined as more than one to two The effects of chronic alcoholism on the central nerv-
drinks a day, alcohol is known to be cardiotoxic. Animal ous system (CNS). Alcohol is a neurotoxin: At least half
research has shown that the chronic use of alcohol in- of heavy drinkers show evidence of cognitive deficits
hibits the process of muscle protein synthesis, especially (Roehers & Roth, 1995; Schuckit & Tapert, 2004). The
the myobibrillar protein necessary for normal cardiac exact mechanism by which chronic alcohol use causes
function (Ponnappa & Rubin, 2000). In humans, chronic neurological damage remains unclear, but without
alcohol use is considered the most common cause of question, chronic alcohol use is associated with neuro-
heart muscle disease (Rubin & Doria, 1990). Alcohol has logical damage (Harper & Matsumoto, 2005).
been identified as a toxin that will destroy striated muscle One of the more common forms of alcohol-induced
tissues, including those of the heart itself (Schuckit, neurological dysfunction is the effect of chronic drink-
2005a, 2005b). Prolonged exposure to alcohol—six ing on memory. Alcohol-induced deficits in memory
beers a day or a pint of whiskey a day for 10 years—may are seen after as little as one drink. Fortunately, one nor-
result in permanent damage to the heart muscle tissue, mally needs to consume more than five standard drinks
inflammation of the heart muscle, and a general weak- in an hour’s time before alcohol is able to significantly
ening of the heart muscle known as alcohol-induced impact the process of memory formation (Browning,
cardiomyopathy (Figueredo, 1997; Schuckit, 2005a, Hoffer, & Dunwiddie, 1993). This is a level of alcohol
2005b, 2006). use rarely seen in the social drinker. But when the
Alcohol-induced cardiomyopathy accounts for 40% blood alcohol level (BAL) reaches 0.14–0.20, the indi-
to 50% of all cases of cardiomyopathy in the United vidual becomes vulnerable to an alcohol-induced
States (Wadland & Ferenchick, 2004; Zakhari, 1997). blackout.13 This is a period of alcohol-induced amne-
There is a dose-dependent relationship between alcohol sia, which may last from less than an hour to several
intake levels and the development of this condition days depending on the amount of alcohol ingested
(Lee & Regan, 2002). Clinical cardiomyopathy12 devel- (White, 2003). During a blackout, the individual may
ops in 25% to 40% of chronic alcoholic users (Figueredo, appear to others to be conscious, be able to carry on a
1997; Lee & Regan, 2002), although it is thought that vir- coherent conversation, and be able to carry out many
tually all alcohol-dependent persons have some degree of complex tasks. However, after recovering from the
alcohol-induced damage to the heart muscle. This dam- acute effects of alcohol, the drinker will not have any
age might not be evident unless special tests were carried memory of what she or he did during the blackout.
out to detect it, but it is still present (Figueredo, 1997; Such alcohol-induced blackouts are viewed as “an early
Rubin & Doria, 1990). Between 40% and 50% of those and serious indicator of the development of alco-
with alcohol-induced cardiomyopathy will die within holism” (Rubino, 1992, p. 360).
4 years if they continue to drink (Figueredo, 1997; In a sense, the alcohol-induced blackout is similar to
Stoschitzky, 2000). another condition known as transient global amnesia
Although many individuals take comfort in knowing (Ropper & Brown, 2005). During the blackout period,
that they drink to excess only occasionally, even binge
drinking is not without its dangers. Binge drinking may 13White (2003) suggested that alcohol-induced blackouts might be
experienced by social drinkers as well as alcohol-dependent persons.

12Which is to say, cardiomyopathy so severe as to cause symptoms for However, heavy drinkers are most prone to alcohol-induced black-
the drinker. outs due to the blood alcohol levels necessary to cause this effect.
80 Chapter Eight
the individual’s brain does not seem to encode memory possible. If the individual should return to the use of al-
traces, causing the loss of memory for that period of cohol after a period of abstinence, even this limited de-
time (Ropper & Brown, 2005). The mechanism by gree of recovery will be lost, and the progression of
which this occurs seems to reflect alcohol-induced dis- alcohol-induced brain damage will continue.
ruption of the neurotransmitters gamma-amiobutyric The chronic use of alcohol is thought to be a cause
acid (GABA), and N-methyl-D-aspartate (NMDA) of cerebellar atrophy, a condition in which the cerebel-
(Nelson et al., 2004). The individual’s vulnerability to lum withers away as individual cells in this region of the
alcohol-induced blackouts reflects the manner in brain die from constant alcohol exposure. Fully 30% to
which the drinker consumed alcohol and his or her ge- 40% of alcohol-dependent individuals eventually develop
netic vulnerability for this effect (Nelson et al., 2004). this condition, marked by characteristic psychomotor
Not all alcohol-dependent persons will experience dysfunction, gait disturbance, and loss of muscle con-
blackouts, but a majority of heavy drinkers will admit to trol (Berger, 2000; Oehmichen et al., 2005). Another
having them if they are asked about this experience central nervous system complication seen as a result of
(Schuckit, Smith, Anthenelli, & Irwin, 1993). chronic alcohol abuse is vitamin deficiency amblyopia.
Although most people would assume that the liver This condition will cause blurred vision, a loss of visual
bears the brunt of alcohol-induced damage, in about perception in the center of the visual field known as
15% of heavy drinkers brain damage becomes apparent central scotomata, and in extreme cases, atrophy of the
well before there is evidence of alcohol-induced liver optic nerve (Mirin, Weiss, & Greenfield, 1991). The
damage (Berg, Franzen, & Wedding, 1994; Bowden, alcohol-induced damage to the visual system may be
1994; Volkow et al., 1992). The most extreme form of permanent.
alcohol-induced brain damage is the development of Wernicke-Korsakoff syndrome. In 1881, Carl Wer-
alcohol-induced dementia. The exact mechanism by nicke first described a brain disorder that subsequently
which chronic alcohol use causes or contributes to the came to bear his name. Wernicke’s encephalopathy is
development of dementia remains unclear at this time, recognized as the most serious complication of chronic
although the association between chronic alcohol use alcohol use (Day, Bentham, Callaghan, Kuruvilla, &
and dementia is beyond dispute (Filley, 2004). Alcohol- George, 2004). About 20% of chronic drinkers can be
induced dementia is the single most preventable cause expected to develop Wernicke’s encephalopathy. The
of dementia in the United States (Beasley, 1987) and is causal mechanism appears to be alcohol-induced avita-
the “second most common adult dementia after minosis, which causes depletion of the B family of vita-
Alzheimer’s disease” (Nace & Isbell, 1991, p. 56). Up to mins from the drinker’s body after just 7–8 weeks of
75% of chronic drinkers show evidence of alcohol- abusive drinking (Harper & Matsumoto, 2005; Ropper &
induced cognitive impairment following detoxification Brown, 2005). This theory is supported by studies show-
(Butterworth, 1995; Hartman, 1995; Tarter, Ott, & ing that between 30% and 80% of chronic drinkers dis-
Mezzich, 1991). This alcohol-induced brain damage play evidence of clinical/subclinical thiamine14 defi-
might become so severe that institutionalization will be ciency (Day et al., 2004). Wernicke’s encephalopathy
necessary when the drinker is no longer able to care for can result in death for up to 20% of individuals who de-
himself or herself. It is estimated that between 15% and velop this disorder (Day et al., 2004; Shader, 2003). So
30% of all nursing home patients are there because of important is thiamine replacement that Ropper and
permanent alcohol-induced brain damage (Schuckit, Brown (2005) recommend automatic intravenous in-
2006). jections of thiamine even if the physician only suspects
A limited degree of improvement in cognitive func- the possibility that the patient has Wernicke’s disease.
tion is possible in some alcohol-dependent persons who Behaviorally, the patient who is suffering from Wer-
remain abstinent from alcohol (Filley, 2004; Grant, nicke’s encephalopathy will often appear confused,
1987). After chronic drinkers have achieved just 2 possibly to the point of being delirious and disoriented.
months of abstinence, scientists have found evidence of She or he often appears apathetic and unable to sustain
a 1.85% increase in brain volume and an improvement physical or mental activities (Day et al., 2004; Victor,
in communications efficiency on the order of 20% 1993). A physical examination would reveal a charac-
(Bartsch et al., 2007). Not every alcohol-dependent per- teristic pattern of abnormal eye movements known as
son will regain all lost cognitive function with absti- nystagmus and such symptoms of organic brain damage
nence, but these findings do suggest that some degree
of recovery from alcohol-induced brain dysfunction is 14Thiamine is one of the B family of vitamins.
as gait disturbances and ataxia (Aminoff, Greenberg, & In rare cases, people will lose virtually all memories
Simon, 2005; Ropper & Brown, 2005). after a certain period of their lives and be almost
Before physicians developed a method to treat Wer- “frozen in time.” For example, Sacks (1970) offered an
nicke’s encephalophy, up to 80% of the patients who example of a man who, when examined, was unable to
developed this condition went on to develop a condi- recall anything that happened after the late 1940s. The
tion known as Korsakoff’s psychosis. Another name for patient was examined in the 1960s but when asked,
Korsakoff’s syndrome is alcohol amnestic disorder would answer questions as if he were still living in the
(Charness, Simon, & Greenberg, 1989; Day et al., 1940s. This example of confabulation, while extremely
2004; Victor, 1993). The standard treatment for Wer- rare, can result from chronic alcoholism. More fre-
nicke’s disease is aggressive replacement of thiamine. quent are the less pronounced cases, where significant
But even when Wernicke’s encephalophy is properly portions of the memory are lost but the individual re-
treated through the most aggressive thiamine replace- tains some ability to recall the past. Unfortunately, the
ment procedures known to modern medicine, fully exact mechanism of Wernicke-Korsakoff syndrome is
25% of the patients who develop Wernicke’s disease still unknown at this time. The characteristic nystagmus
go on to develop Korsakoff’s syndrome (Sagar, 1991). seems to respond to massive doses of thiamine.15 It is
For many years, scientists thought that Wernicke’s en- possible that victims of Wernicke-Korsakoff syndrome
cephalopathy and Korsakoff’s syndrome were separate possess a genetic susceptibility to the effects of the
disorders. It is now known that Wernicke’s encephalopa- alcohol-induced thiamine deficiency (Parsons &
thy is the acute phase of the Wernicke-Korsakoff syn- Nixon, 1993). While this is an attractive theory, it does
drome. One of the most prominent symptoms of the not explain why some chronic drinkers develop
Korsakoff phase of this syndrome is a memory distur- Wernicke-Korsakoff syndrome and others do not.
bance, when the patient is unable to remember the past There is an emerging body of evidence suggesting
accurately. The individual will also have difficulty that chronic alcohol use causes a disconnection syndrome
learning new information. This should not be surpris- between neurons in the brain (Harper & Matsumoto,
ing, as magnetic resonance imaging (MRI) reveals sig- 2005; Jensen & Pakkenberg, 1993). Such a disconnec-
nificant areas of atrophy in the brain (Bjork, Grant, & tion syndrome prevents the nerve pathways involving
Hommer, 2003). The observed loss of brain tissue is those neurons from being activated. Since neurons re-
most conspicuous in the anterior superior temporal cor- quire regular stimulation, the unstimulated nerve cells
tex region of the brain, which seems to correspond to begin to wither and eventually die. Another theory was
the behavioral deficits observed in the Wernicke- offered by Pfefferbaum, Rosenbloom, Serventi, and
Korsakoff syndrome (Pfefferbaum, Sullivan, Rosen- Sullivan (2004), who suggested that the liver dysfunc-
bloom, Mathalon, & Kim, 1998). However, there are tion found in chronic alcohol abusers, combined with
subtle differences between the pattern of brain damage the poor nutrition and chronic exposure to alcohol it-
seen in male and female alcohol abusers (Hommer, self, all combined to cause the characteristic pattern of
Momenan, Kaiser, & Rawlings, 2001; Pfefferbaum, brain damage seen in alcohol-dependent individuals.
Rosenbloom, Deshmukh, & Sullivan, 2001). But these theories remain unproven. It is known that
Frequently, in spite of clear evidence of cognitive once Wernicke-Korsakoff syndrome has developed,
impairment, the patient appears indifferent to his or her only a minority of its victims will escape without lifelong
memory loss (Ropper & Brown, 2005). In the past, it neurological damage. By some estimates, at least 10% of
was thought that patients with Korsakoff’s syndrome the patients with this disorder will be left with a perma-
would confabulate answers to cover up their inability to nent memory impairment (Vik, Cellucci, Jarchow, &
remember information, and confabulation was viewed Hedt, 2004).
as a diagnostic sign for this disorder. However, Ropper There is evidence that chronic alcohol abuse/addic-
and Brown (2005) suggested that confabulation might tion is a risk factor in the development of a movement
not automatically be present and challenged the utility disorder known as tardive dyskinesia (TD) (Lopez &
of this diagnostic sign in the identification of patients Jeste, 1997). This condition may result from alcohol’s
with Korsakoff’s disease. Confabulation is most com- neurotoxic effect, according to Lopez and Jeste. Al-
mon in the earlier stages of Korsakoff’s syndrome when though TD is a common complication in patients who
it is present, and as the individual adjusts to the mem- have used neuroleptic drugs for the control of psychotic
ory loss, he or she will not be as likely to resort to con-
fabulation (Ropper & Brown, 2005). 15See Glossary.
82 Chapter Eight
conditions for long periods of time, some alcohol- following the initiation of abstinence, chronic drinkers
dependent individuals have developed TD even though have been found to spend an abnormal amount of time
they had no prior exposure to neuroleptic agents in REM sleep, a phenomenon known as REM re-
(Lopez & Jeste, 1997). The exact mechanism by which bound. During REM rebound the individual will spend
alcohol causes the development of tardive dyskinesia more time in REM sleep and will report vivid, intense
remains to be identified, and scientists have no idea dreams that are often difficult for the individual to sepa-
why some alcohol-abusers develop TD while others do rate from reality (Ropper & Brown, 2005). These dreams
not. But TD usually emerges in chronic alcohol users might be so frightening that the individual is tempted to
who have a history of drinking for 10–20 years, accord- return to the use of alcohol to “get a decent night’s
ing to the authors. sleep.” REM rebound can last for up to 6 months
Alcohol’s effects on the sleep cycle. Although alcohol after the person has stopped drinking (Brower, 2001;
might induce a form of sleep, the chronic use of alcohol Schuckit & Tapert, 2004). Further, scientists have dis-
interferes with the normal sleep cycle (Karam-Hage, covered that the chronic use of alcohol interferes with
2004). But there is still a great deal to learn about how the normal sleep process for 1–2 years after detoxifica-
alcohol impacts the normal sleep cycle. Karam-Hage tion (Brower, 2001; Karam-Hage, 2004).
(2004) suggested, for example, that chronic drinkers Chronic alcohol use has been identified as a cause of
tend to require more time to fall asleep,16 and as a sleep apnea17 episodes both during the period of acute
group, they report that their sleep is both less sound and intoxication and for a number of weeks after the indi-
less restful than that of nondrinkers (Karam-Hage, 2004). vidual’s last drink (Berger, 2000; Brower, 2001; Le Bon
In contrast to this, Milne (2007) suggested that chronic et al., 1997). Such apnea episodes interfere with the in-
alcohol users tended to overestimate the amount of time dividual’s sleep and can cause problems such as hyper-
necessary for them to fall asleep and the length of time tension, depression, poor concentration, daytime fatigue,
that they were asleep. It is known that the chronic use of and other symptoms.
alcohol suppresses melatonin production in the brain, The effects of chronic alcohol use on the peripheral
which in turn interferes with the normal sleep cycle nervous system. The human nervous system is usually
(Karam-Hage, 2004; Pettit, 2000). However, it is also viewed as two interconnected systems. The brain and
possible that the chronic use of alcohol interferes with spinal cord make up the central nervous system; the
the individual’s ability to accurately access his or her nerves found in the outer regions of the body are
sleep pattern or its effectiveness. classified as the “peripheral” nervous system. Unfortu-
Unfortunately, clinicians often encounter patients nately, the effects of alcohol-induced avitaminosis are
who complain of sleep problems without revealing sufficiently widespread to affect the peripheral nerves,
their alcohol abuse. Where 17% to 30% of the general especially those in the hands and feet. This is a condi-
population might suffer from insomnia at least occa- tion known as peripheral neuropathy and is found in
sionally, fully 60% of alcohol-dependent persons will 10% (Schuckit, 2005a, 2005b) to 33% (Monforte et al.,
experience symptoms of insomnia (Brower, Aldrich, 1995) of chronic alcohol abusers. Symptoms of a pe-
Robinson, Zucker, & Greden, 2001). The importance ripheral neuropathy include feelings of weakness,
of these data is that extended periods of insomnia might pain, and a burning sensation in the afflicted region of
serve as a relapse trigger during early recovery unless the body (Lehman et al., 1994). Eventually, the person
this problem is addressed. Karam-Hage (2004) suggested will lose all feeling in the affected region of his or her
that gabapentin (sold under the brand name of Neuron- body.
tin) is quite useful as a hypnotic agent in alcohol- At this time, the exact cause of alcohol-induced pe-
dependent persons. ripheral neuropathies is not known. Some researchers
Alcohol is a powerful suppressant of rapid eye move- believe that peripheral neuropathy is the result of a
ment (REM) sleep (Hobson, 2005). Neuroscientists chronic deficiency of the B family of vitamins (Charness
have demonstrated that REM sleep is associated with et al., 1989; Levin, 2002; Nace, 1987). In contrast to
dreaming and that we need to dream. Further, it has this theory, Monforte et al. (1995) suggested that pe-
been proven that anything that reduces the amount of ripheral neuropathies might be the result of chronic ex-
time spent in REM sleep will interfere with normal posure to either alcohol itself or its metabolites. As
waking cognitive function. During the first few nights discussed in the last chapter, some of the metabolites of
16Known as sleep latency. 17See Glossary.

alcohol are quite toxic to the body. The researchers that 10% to 40% of individuals who are alcohol depen-
failed to find evidence of a nutritional deficit for those dent also have an anxiety disorder of some kind. Be-
hospitalized alcoholics who had developed peripheral tween 10% to 20% of patients being treated for some
neuropathies, but they did find a dose-related relation- form of an anxiety disorder also have an alcohol use dis-
ship between the use of alcohol and the development order (Cox & Taylor, 1999). For these individuals, the
of peripheral neuropathies. anxiety co-exists with their alcohol use disorder and
Surprisingly, in light of alcohol’s known neurotoxic does not reflect alcohol withdrawal as is often the case.
effects, some research findings suggest that at certain The diagnostic dilemma for the clinician is determin-
doses it might suppress some of the involuntary move- ing which patients have withdrawal-induced anxiety
ments of Huntington’s disease (Lopez & Jeste, 1997). and which have a legitimate anxiety disorder in addi-
This is not to suggest that alcohol is an acceptable treat- tion to their substance use problem. To make this deter-
ment for Huntington’s, but this effect of alcohol might mination more difficult, chronic alcohol use can cause
explain why patients with movement disorders such as drinkers to experience feelings of anxiety for many
essential tremor, or Huntington’s disease, tend to abuse months after they have stopped drinking (Schuckit,
alcohol more often than close relatives who do not have 1998, 2005a).
a movement disorder, according to the authors. The differentiation between “true” anxiety disorders
The effects of chronic alcohol use on the person’s emo- and alcohol-related anxiety-like disorders is quite diffi-
tional state. The chronic use of alcohol can simulate cult, and it is complicated by the fact that some
the symptoms of virtually every form of neurosis, and alcohol-withdrawal symptoms are virtually the same
even those seen in psychotic conditions. These symp- as those seen in panic attacks and generalized anxiety
toms are thought to be secondary to the individual’s disorder (Schuckit, 2005a). One diagnostic clue is
malnutrition and the toxic effects of chronic alcohol the observation that, in general, problems such as
use (Beasley, 1987). These symptoms might include de- agoraphobia and social phobias usually predate alcohol
pressive reactions, generalized anxiety disorders, and use (Kushner, Sher, & Beitman, 1990). Victims of
panic attacks (Blondell, Frierson, & Lippmann, 1996; these disorders usually attempt self-medication through
Schuckit, 2005a, 2005b). the use of alcohol and only later develop alcohol use
There is a complex relationship between anxiety problems.
symptoms and alcohol use disorders. For example, with- Another form of phobia that frequently co-exists
out medical intervention, almost 80% of alcohol- with alcoholism is the social phobia (Marshall, 1994).
dependent individuals will experience panic episodes Individuals with social phobias fear situations in which
during the acute phase of alcohol withdrawal (Schuckit, they are exposed to other people; they are twice as likely
2000). The chronic use of alcohol causes a paradoxical to have alcohol-use problems as people from the gen-
stimulation of the autonomic nervous system (ANS), eral population. However, social phobia usually pre-
which the drinker might interpret as a sign of anxiety. cedes the development of alcohol abuse/addiction.
At this point the drinker turns either to further alcohol Unfortunately, it is not uncommon for alcohol-
abuse or to antianxiety medications to control this sub- dependent individuals to complain of anxiety symptoms
jective anxiety. A cycle is then started in which the when they see their physician, who may then prescribe a
chronic use of alcohol actually sets the stage for further benzodiazepine to control the anxiety. Because of the
anxiety-like symptoms, resulting in the perceived need similarity in the subjective effects of these two com-
for more alcohol or medication. Stockwell and Town pounds, the physician is placed in the position of replac-
(1989) discussed this aspect of chronic alcohol use and ing the individual’s dependence on alcohol with a
concluded: “Many clients who drink heavily or abuse dependence on prescribed benzodiazepines (McGuiness
other anxiolytic drugs will experience substantial or & Fogger, 2006). So similar are the effects of the benzo-
complete recovery from extreme anxiety following suc- diazepines to those of alcohol that they have been called
cessful detoxification” (p. 223). The authors recom- alcohol in pill form (Longo, 2005) or “freeze-dried alco-
mend a drug-free period of at least 2 weeks in which to hol” (McGuinness & Fogger, 2006, p. 25).
assess the need for pharmacological intervention for It has been estimated that 25% to 50% of persons
anxiety. who are addicted to alcohol are also addicted to ben-
But this is not to discount the possibility that the in- zodiazepines (Sattar & Bhatia, 2003). If the physician
dividual has a concurrent anxiety disorder and an alco- fails to obtain an adequate history and physical (or if
hol use disorder. Indeed, researchers have discovered the patient lies about his or her alcohol use), there is
84 Chapter Eight
also a risk that the alcohol-dependent person might Further, even limited alcohol use will exacerbate
combine the use of antianxiety medication, which is feelings of depression for the drinker who suffers from a
a CNS depressant, with alcohol (which is also a CNS depressive disorder (Schuckit, 2005a, 2005b). It is often
depressant). There is a significant potential for an quite difficult to differentiate between a primary depres-
overdose when two different classes of CNS depressive disorder and an alcohol-induced depression, but
sants are combined. the latter will usually clear after 2–5 weeks of absti-
The interaction between benzodiazepines and alco- nence. Some researchers do not recommend formal
hol has been implicated as one cause of the condition treatment other than abstinence and recommend that
known as the paradoxical rage reaction (Beasley, 1987). antidepressant medication be used only if the symp-
This is a hypothetical drug-induced reaction in which a toms of depression continue after that period of time
CNS depressant brings about an unexpected period of (Decker & Ries, 1993; Miller, 1994; Satel, Kosten,
rage in the individual. During the paradoxical rage reac- Schuckit, & Fischman, 1993). However Charney (2004)
tion, individuals might engage in assaultive or destruc- recommended that depressive disorders be aggressively
tive behavior toward either themselves or others—and treated with the appropriate medication as soon as they
later have no conscious memory of what they did during are detected.
the paradoxical rage reaction (Lehman et al., 1994). At least one-third of those who end their own lives
If antianxiety medication is needed for long-term have an alcohol use disorder (Connor et al., 2006).
anxiety control in recovering drinkers, buspirone Since alcohol-dependent persons are vulnerable to
should be used first (Kranzler et al., 1994). Buspirone is the development of depression as a consequence of
not a benzodiazepine and thus does not present the po- their drinking, it is logical that as a group they are at
tential for abuse seen with the benzodiazepines. Kranzler high risk for suicide. Indeed, research has demon-
and colleagues found that alcoholic participants in strated that alcohol-dependent persons are 58 to 85
their study who suffered from anxiety symptoms and times more likely to commit suicide as individuals
who received buspirone were more likely to remain in who are not alcohol dependent (Frierson, Melikian, &
treatment and to consume less alcohol than anxious Wadman, 2002). Various researchers have suggested
participants who did not receive buspirone. This sug- that the suicide rate for alcohol-dependent persons is
gests that buspirone might be an effective medication 5% (Preuss et al., 2003), 7% (Connor, Li, Meldrum,
in treating alcohol-dependent people with concurrent Duberstein, & Conwell, 2003), or even as high as 18%
anxiety disorders. (Bongar, 1997; Preuss & Wong, 2000). It has been sug-
Chronic alcohol use has been known to interfere with gested that alcohol-related suicide is most likely to
sexual performance for both men and women (Jersild, occur late in middle adulthood, when the effects of the
2001; Schiavi, Stimmel, Mandeli, & White, 1995). Al- chronic use of alcohol begin to manifest as cirrhosis of
though the chronic use of alcohol has been shown to in- the liver and other disorders (Nisbet, 2000).
terfere with the erectile process for men, Schiavi et al. Preuss et al. (2003) followed a cohort of 1,237
(1995) found that once the individual stopped drinking, alcohol-dependent persons for 5 years and found that in
the erectile dysfunction usually resolved itself. However, the course of the study, individuals in their sample were
there is evidence that disulfiram (often used in the treat- more than twice as likely to commit suicide as were
ment of chronic alcoholism) may interfere with a man’s nonalcoholic individuals. These findings were consis-
ability to achieve an erection. tent with those of Dumais et al. (2005), who concluded
Although researchers once thought that primary de- that alcohol’s disinhibition effect, combined with the
pression was rare in chronic drinkers, they now believe impulsiveness demonstrated by many personality disor-
that there is a relationship between alcohol use disorder types and the presence of major depression, were
ders and depression. Hasin and Grant (2002) examined significant risk factors for suicide in chronic male
the histories of 6,050 recovering alcohol abusers and drinkers. But when Preuss et al. (2003) conducted an
found that former drinkers had a fourfold increased in- extensive evaluation of their subjects prior to the start of
cidence of depression compared to nondrinkers. Fur- their study in an attempt to identify potential predictors
ther, depression was found to have a negative impact on of suicide, they failed to identify such a pattern of risk
the individual’s ability to benefit from alcohol rehabili- factors. The authors concluded that there was only a
tation programs and might contribute to higher dropout modest correlation between the identified risk factors
rates from substance use treatment (Charney, 2004; and completed suicide, and that factors with the great-
Mueller et al., 1994). est impact on suicide potential had not been identified.
Roy (1993) did suggest that the following were po- discontinued or the individual significantly cuts back
tential indicators for an increased risk of suicide for the on his or her alcohol use, the neurons in the drinker’s
adult alcoholic: brain begin to work erratically because the delicate bal-
ance of excitatory/inhibitory neurotransmitters has been
1. Gender: Men tend to commit suicide more often upset, initiating the onset of the alcohol withdrawal syn-
than women, and the ratio of male:female suicides drome (AWS) (Heinz, 2006).
for alcoholics may be about 4:1. In the United States, up to 2 million people go
2. Marital status: Single/divorced/widowed adults are through the alcohol withdrawal syndrome each year. In
significantly more likely to attempt suicide than are most cases the symptoms of withdrawal usually subside
married adults. quickly without the need for medical intervention and
3. Co-existing depressive disorder: Depression is associ- the withdrawal symptoms might not even be attributed
ated with an increased risk of suicide. by the individual to his or her use of alcohol. Only 10%
4. Adverse life events: The individual who has suffered to 20% of the cases of AWS will require hospitalization
an adverse life event such as the loss of a loved one, a (Bayard, McIntyre, Hill, & Woodside, 2004). This is be-
major illness, or legal problems is at increased risk cause the AWS is potentially life threatening, and even
for suicide. with the best of medical care carries with it a significant
5. Recent discharge from treatment for alcoholism: The risk of death.
first 4 years following treatment were associated with For reasons that are not known, chronic drinkers
a significantly higher risk for suicide, although the vary in their risk for developing AWS (Saitz, 1998).
reason for this was not clear. However, some evidence suggests that repeated cycles
6. A history of previous suicide attempts: Approximately of alcohol dependence and withdrawal might con-
one-third of alcoholic suicide victims had attempted tribute to AWS becoming progressively worse each
suicide at some point in the past. time (Kelley & Saucier, 2004; Littleton, 2001). In 90%
7. Biological factors: Decreased levels of serotonin in of cases, the symptoms of AWS develop within 4–12
the brain and other biological factors are thought to hours after the individual’s last drink, although in some
be associated with increased risk for violent behav- cases withdrawal develops simply because a chronic
ior, including suicide. drinker significantly reduces his or her alcohol intake
(McKay, Koranda, & Axen, 2004; Saitz, 1998). In a
One possible mechanism through which chronic small percentage of cases AWS symptoms do not ap-
drinking might cause or contribute to depressive disor- pear until 96 hours after the last drink or reduction in
ders is the increase in dopamine turnover in the brain alcohol intake (Lehman et al., 1994; Weiss & Mirin,
caused by chronic alcohol use; this forces the brain to 1988), and in extreme cases they might not appear for
reduce the number of dopamine binding sites to pro- 10 days after the individual’s last drink (Slaby, Lieb, &
tect itself from the massive amounts of dopamine being Tancredi, 1981).
released (Heinz, 2006). Alcohol withdrawal symptom is an acute brain syn-
The chronic use of alcohol has also been associated drome that might at first be mistaken for such condi-
with reduced serotonin turnover, with a 30% reductions as a subdural hematoma, pneumonia, meningitis,
tion in serotonin transporters being found in the or an infection involving the CNS (Saitz, 1998). The
brains of chronic drinkers (Heinz et al., 1998). Low severity of AWS depends on the (a) intensity with which
levels of both dopamine and serotonin have been im- that individual used alcohol, (b) the length of time the
plicated by researchers as causing depression, so this individual drank, (c) the individual’s overall state of
mechanism might explain how chronic alcohol use health, and (d) concurrent withdrawal from other com-
contributes to increased levels of depression in heavy pounds. For example, concurrent nicotine withdrawal18
drinkers. may result in a more intense AWS than withdrawal from
Alcohol withdrawal for the chronic alcoholic. The alcohol alone (Littleton, 2001). For this reason, the au-
chronic use of alcohol causes the individual’s brain to thor recommends that patients’ nicotine addiction be
increase the number of NMDA receptors in an attempt controlled through the use of transdermal nicotine
to compensate for alcohol’s ability to block the effects patches until after they have completed the withdrawal
of this neurotransmitter. At the same time, the individ- process from alcohol.
ual’s brain has learned to become relatively insensitive
to GABA (Heinz, 2006). When the alcohol is suddenly 18
Discussed in Chapter 19.
86 Chapter Eight
In the hospital setting, the Clinical Institute With- escape from the hallucinations (Soyka, 2000; Tekin &
drawal Assessment for Alcohol Scale-Revised (CIWA- Cummings, 2003).
Ar) is the most common assessment tool used to In extreme cases of alcohol withdrawal, the symp-
determine the severity of the AWS (Kelley & Saucier, toms will continue to increase in intensity for the next
2004; McKay et al., 2004). This noncopyrighted tool 24–48 hours after the individual has stopped drinking,
measures 15 symptoms of alcohol withdrawal such as and by the third day she or he will start to experience
anxiety, nausea, and visual hallucinations among fever, incontinence, and/or tremors in addition to the
others. It takes 3–5 minutes to administer and has a above noted symptoms.19 Approximately 10%–16% of
maximum score of 67 points, with each symptoms heavy drinkers will experience a seizure as part of the
being weighted in terms of severity. A score of 0–4 withdrawal syndrome (Berger, 2000; D’Onofrio, Rath-
points indicates minimal withdrawal discomfort, 5–12 lev, Ulrich, Fish, & Freedland, 1999; McRae, Brady, &
points indicates mild alcohol withdrawal, 13–19 points Sonne, 2001). In 90% of such cases, the first seizure
suggests moderately severe alcohol withdrawal, and takes place within 48 hours after the last drink, al-
20+ points is indicative of severe alcohol withdrawal. though in 2%–3% of the cases it might occur as late as
The CIWA-Ar can be administered repeatedly over 5–20 days after the last drink (Renner, 2004a; Trevisan,
time to provide a baseline measure of the patient’s Boutros, Petrakis, & Krystal, 1998). Approximately 60%
recovery from the acute effects of alcohol intoxication. of adults who experience alcohol withdrawal seizures
Symptoms of mild intensity AWS include agitation, will have multiple seizures (Aminoff et al., 2005;
anxiety, tremor, diarrhea, abdominal discomfort, exag- D’Onofrio et al., 1999). Alcohol-withdrawal seizures
gerated reflexes, insomnia, vivid dreams/nightmares, are seen in individuals who do and do not experience
nausea, vomiting, abdominal discomfort, anorexia, rest- alcoholic hallucinosis, but 28% of patients who experi-
lessness, sweating, tachycardia, headache, memory ence withdrawal seizures go on to develop delirium
impairment, difficulty concentrating, hallucinations, tremens (DTs).
seizures, and vertigo (Kelley & Saucier, 2004; Saitz, Alcohol-dependent persons who experience the most
1998; Shader, 2003). Depending on the individual’s severe complication associated with drinking, the delir-
drinking history, these symptoms may become more ium tremens (DTs), are estimated at 1% (McRae et al.,
intense over the first 6–24 hours following the individ- 2001) to 10% (Weiss & Mirin, 1988) of chronic drinkers.
ual’s last use of alcohol. The patient may also begin to Once the DTs develop, they are extremely difficult
experience alcoholic hallucinosis. Alcoholic hallucinosis to control (Palmstierna, 2001), and up to 15% of pa-
occurs in up to 10% of patients experiencing the AWS tients who developed the DTs will die without ade-
and usually begins 1–2 days after the individual’s last quate medical intervention, usually as a result of
drink or major reduction in alcohol intake (Olmedo & co-occuring medical problems (Filley, 2004). Some of
Hoffman, 2000). The hallucinations may be visual, tac- the medical and behavioral symptoms of the DTs in-
tile, or auditory and occur when the patient is conclude delirium, hallucinations, delusions, fever, hy-
scious (Kelley & Saucier, 2004; Ropper & Brown, potension, and tachycardia (Aminoff et al., 2005; Filley,
2005). 2004). While the individual is going through the DTs,
These hallucinations usually resolve a few days after he or she is vulnerable to developing rhabdomyolsis20 as
the individual’s last drink, although in rare cases they a result of alcohol-induced muscle damage (Richards,
have continued for a period of months (Tekin & Cum- 2000; Sauret, Marinides, & Wang, 2002).
mings, 2003). The exact mechanism of alcoholic hallu- Drawing upon the experiences of 334 patients in
cinosis is not understood at this time but in 10% to 20% Stockholm, Palmstierna (2001) identified five symptoms
of the cases, the individual enters a chronic psychotic that seemed to identify patients “at risk” for the develop-
stage (Soyka, 2000). Alcoholic hallucinosis can be quite ment of the DTs: (a) concurrent infections such as pneu-
frightening to the individual, who frequently does not monia, (b) tachycardia, (c) signs of autonomic nervous
recognize the episodes as hallucinations and responds system overactivity in spite of an alcohol concentration at
to them as if they were real experiences (Ropper & or above 1 gram per liter of body fluid, (d) previous
Brown, 2005). This contributes to anxiety on the part of epileptic seizure, and (e) a history of a previous delirious
the individual, and cases are on record where the episode. The author suggested that such patients receive
patient has called the police for protection against the
unseen speakers (Ropper & Brown, 2005). Some drinkers 19
Called the “rum fits” in some quarters (Ropper & Brown, 2005).
have attempted suicide or become violent trying to 20
See Glossary.
aggressive treatment with benzodiazepines to minimize ment of three different bone disorders: (a) osteoporosis
the risk of developing the full DTs. (loss of bone mass), (b) osteomalacia (a condition in
In some cases of DTs, the individual will experience which new bone tissue fails to absorb minerals appropri-
a disruption of normal fluid levels in the brain (Trabert, ately), and (c) secondary hyperparathyroidism21 (Griffiths,
Caspari, Bernhard, & Biro, 1992). This results when Parantainen, & Olson, 1994). Even limited regular al-
the mechanism in the drinker’s body that regulates nor- cohol use can double the speed at which the body ex-
mal fluid levels is disrupted by the alcohol withdrawal cretes calcium (Jersild, 2001). These bone disorders
process. The individual might become dehydrated or, in contribute to the higher than expected level of injury
other cases, might retain too much fluid. During alcohol and death that occur when alcoholics fall or when they
withdrawal, some individuals become hypersensitive to are involved in automobile accidents.
the antidiuretic hormone (ADH). This hormone is nor- Alcohol is also a factor in traumatic brain injury
mally secreted by the body to slow the rate of fluid (TBI), with between 29% and 52% of patients who live
loss through the kidneys when the person is some- long enough to reach the hospital testing positive for al-
what dehydrated. This excess fluid may contribute to cohol at the time of admission (Miller & Adams, 2006).
the damage the alcohol has caused to the brain, possi- Further, alcohol (or drug) use disorders will both medi-
bly by bringing about a state of cerebral edema (Trabert ate and complicate the patient’s recovery from TBI
et al., 1992). Researchers have found that only patients (Miller & Adams, 2006). While the popular myth is
going through the DTs have the combination of higher that the individual might have turned to alcohol in an
levels of ADH and low body fluid levels. This finding attempt to self-medicate frustation, pain, and other con-
suggests that a body fluid dysregulation process might sequences of the TBI, research data suggest that the in-
somehow be involved in the development of the DTs dividual’s substance use disorder usually will predate
(Trabert et al., 1992). the TBI (Miller & Adams, 2006).
In the past, between 5% and 25% of those individu- Chronic alcohol use is thought to be the cause of
als who developed the DTs died from exhaustion 40% to 50% of deaths in motor vehicle accidents, up to
(McKay et al., Schuckit, 2000). However, improved 67% of home injuries, and 3% to 5% of cancer-related
medical care has decreased the mortality from DTs to deaths (Miller, 1999). Chronic alcohol users are 10
about 1% (Enoch & Goldman, 2002) to 5% (Kelly & times more likely to develop cancer than nondrinkers,
Saucier, 2004; Ropper & Brown, 2005; Weaver, Jarvis, & and it is estimated that 4% of all cases of cancer in men
Schnoll, 1999). The main causes of death for persons and 1% in women are alcohol-related (Ordorica & Nace,
going through the DTs include sepsis, cardiac and/or 1998; Schuckit, 1998). There also is mixed evidence
respiratory arrest, cardiac arrhythmias, hyperthermia, and suggesting that up to 5% of all cases of breast cancer are
cardiac and/or circulatory collapse (Aminoff et al., 2005; caused by alcohol use. Acetaldehyde exposure even
Kelly & Saucier, 2004). Persons who are going through years before the development of such cancers is hypoth-
the DTs are also a high-risk group for suicide, as they esized to play a role in the development of breast
struggle with the emotional pain and terror associated cancer (Melton, 2007). In addition, women who drink
with this condition (Hirschfield & Davidson, 1988). while pregnant run the risk of causing alcohol-induced
Although a number of different compounds have birth defects, a condition known as the fetal alcohol syn-
been suggested to control the AWS, currently the ben- drome.22
zodiazepines, especially chlordiazepoxide or diazepam, Chronic alcoholism has been associated with a pre-
are considered the drugs of choice for treatment mature aging syndrome, when the chronic use of alco-
(McKay et al., 2004). The use of pharmaceutical agents hol contributes to the individual’s appearing much older
to control the alcohol withdrawal symptoms is dis- than he or she is (Brandt & Butters, 1986). In many
cussed in more detail in Chapter 33. cases, the overall physical and intellectual condition of
Other complications from chronic alcohol use. Either these people is more like that of a person 15 to 20 years
directly or indirectly, alcohol contributes to more than older than the individual’s chronological age. One per-
half of the 500,000 head injuries that occur each year son, a man in his 50s, was told by his physician that he
in the United States (Ashe & Mason, 2001). It is not was in good health . . . for a man about to turn 70! Ad-
uncommon for the intoxicated individual to fall and mittedly, not every alcohol-dependent person will suffer
strike his or her head on coffee tables, magazine stands,
or whatever happens to be in the way. Unfortunately, 21See Glossary.
the chronic use of alcohol contributes to the develop- 22Discussed in Chapter 22.
88 Chapter Eight
from every consequence reviewed in this chapter. Some then becomes less intense over the next few days, some
chronic alcohol users will never suffer from stomach symptoms of alcohol withdrawal, such as anxiety and
problems, for example, but they may develop advanced sleep problems, might persist for 4–6 months after the
heart disease as a result of their drinking. individual’s last drink (Schuckit, 2005a, 2005b).
Research has demonstrated that in most cases the
first alcohol-related problems are experienced when
Summary
the person is in the late 20s or early 30s. Schuckit et al.
(1993) outlined a progressive course for alcoholism, This chapter explored the many facets of alcoholism.
based on their study of 636 male alcoholics. The au- The scope of alcohol abuse/addiction in this country
thors admitted that their subjects experienced wide dif- was reviewed, as was the fact that the alcohol use disor-
ferences in the specific problems caused by their ders are the most common form of substance abuse in
drinking, but as a group, the alcoholics began to experi- the United States at this time. In this chapter, the dif-
ence severe alcohol-related problems in their late 20s. ferent types of tolerance and the ways the chronic use
By their mid-30s, they were likely to have recognized of alcohol can affect the body were discussed. The im-
that they had a drinking problem and to experience pact of chronic alcohol use on the central nervous sys-
more severe problems as a result of continued drinking. tem, the cardiopulmonary system, the digestive system,
However, as the authors pointed out, there is wide vari- and the skeletal bone structure were reviewed. In addi-
ation in this pattern, and some subgroups of alcoholics tion, the relationship between chronic alcohol use and
might fail to follow it. physical injuries, and premature aging and death from
Extended alcohol-withdrawal: Although the alcohol chronic alcohol use were examined. Finally, the process
withdrawal syndrome usually begins within 8 hours of of alcohol withdrawal for the alcohol-dependent person
abstinence, peaks on about the fourth or fifth day, and was discussed.
CHAPTER NINE
Abuse of and Addiction to the Barbiturates

and Barbiturate-like Drugs
The anxiety disorders are, collectively, the most com- In 18703 chloral hydrate was introduced as a hyp-
mon form of mental illness found in the United States; notic. Chloral hydrate was rapidly absorbed from the
they will affect approximately 14% of the general popu- digestive tract, and an oral dose of 1–2 grams would
lation (Getzfeld, 2006). Over the course of their lives, cause the typical person to fall asleep in less than an
approximately one-third of all adults will experience at hour. The effects of chloral hydrate usually lasted 8–11
least transient periods of anxiety intense enough to in- hours, making it appear to be ideal for use as a hyp-
terfere with their daily lives (Spiegel, 1996). Further, notic. However, physicians quickly discovered that
each year at least 35% of the adults in the United States chloral hydrate had several major drawbacks. One, it is
will experience at least transitory insomnia (Brower, quite irritating to the stomach lining, which can be sig-
Aldrich, Robinson, Zucker, & Greden, 2001; Lacks & nificantly damaged by chronic use. In addition, chloral
Morin, 1992). hydrate is quite addictive; at high doses it exacerbates
For thousands of years, alcohol was the only agent preexisting cardiac problems (Pagliaro & Pigliaro,
that could reduce people’s anxiety level or help them 1998).
fall asleep. However, as discussed in the last chapter, Further, as physicians became familiar with its phar-
the effectiveness of alcohol as an antianxiety1 agent is macological properities, they discovered that chloral
quite limited. Thus, for many hundreds of years, there hydrate had a narrow therapeutic window of perhaps
has been a very real demand for effective antianxiety or 1:2 or 1:3 (Brown & Stoudemire, 1998; Ciraulo &
hypnotic2 medications. In this chapter, we review the Sarid-Segal, 2005), making it quite toxic to the user. Fi-
various medications that were used to control anxiety or nally, after it had been in use for awhile, physicians dis-
promote sleep prior to the introduction of the benzodi- covered that withdrawal from chloral hydrate after
azepines in the early 1960s. In the next chapter, we extended periods of use could result in life-threatening
focus on the benzodiazepine family of drugs and on seizures.
medications that have emerged since the benzodi- Technically, chloral hydrate is a prodrug.4 After inges-
azepines first appeared. tion, it is rapidly biotransformed into trichloroethanol, the
metabolite of chloral hydrate that actually causes it to
function as a hypnotic. In spite of the dangers associated
Early Pharmacological Therapy
with its use, chloral hydrate continues to have a limited
of Anxiety Disorders and Insomnia role in modern medicine. Its relatively short biological
Prior to the introduction of the benzodiazepines (BZs), half-life makes it of value in treating some elderly patients
the early anxiolytic/hypnotic agents produced a dose- who suffer from insomnia. Thus, even with all the newer
dependent increase in effects ranging from sedation to medications available to physicians, there are still patients
sleep, profound unconsciousness, a state of surgical anes- who will receive chloral hydrate to help them sleep.
thesia, coma, and ultimately death (Charney, Mihic, & Paraldehyde was isolated in 1829 and first used as a
Harris, 2006). Thus, depending on the dosage level uti- hypnotic in 1882. As a hypnotic, paraldehyde is quite
lized, the same compound might be used as a sedative or effective. It produces little respiratory or cardiac depres-
a hypnotic. sion, making it a relatively safe drug for patients who
have some forms of pulmonary or cardiac disease. How-
1Occasionally, mental health professionals will use the term anxi- ever, it tends to produce a very noxious taste, and users
olytic rather than antianxiety. For the purpose of this section, how-
ever, the term antianxiety is utilized. 3
Pagliaro and Pagliaro (1998) said that this happened in 1869, not 1870.
2See Glossary. 4
See Glossary.
89
90 Chapter Nine
Death
Level of
intoxication: Mild Moderate Severe
Observed Sedation Coma, but person Deep coma

symptoms: Slurred speech may be aroused Gag reflex absent
Disorientation by pain Apnea episodes
Ataxia Hypoventilation (may progress to
Nystagmus Depression of deep respiratory arrest)
tendon reflexes Hypotension
Shock
Hypothermia
FIGURE 9.1 Spectrum of Barbituate Intoxication
develop a strong odor on their breath after use. Paralde- of other CNS depressants. Another shared characteris-
hyde is quite irritating to the mucous membranes of the tic is a significant potential for abuse. Still, in spite of
mouth and throat, and must be diluted in a liquid be- these shortcomings, these agents were the treatment of
fore use. choice for anxiety and insomnia until the barbiturates
The half-life of paraldehyde ranges from 3.4 to 9.8 were introduced.
hours, and about 70% to 80% of a single dose is bio-
transformed by the liver prior to excretion. Between
History and Current Medical Uses
11% and 28% of a single dose leaves the body un-
changed, usually by being exhaled, causing the charac-
of the Barbiturates
teristic odor on the user’s breath. Paraldehyde has an In 1864 the German chemist Aldolph von Baeyer dis-
abuse/addiction potential similar to that of alcohol, and covered barbituric acid, the parent compound from
intoxication on this drug resembles alcohol-induced in- which all the barbiturates are derived (Numeroff &
toxication. After the barbiturates were introduced, par- Putnam, 2005). Barbituric acid by itself does not have
aldehyde gradually fell into disfavor, and at the start of any sedative-hypnotic properties, but modifications of
the 21st century it has virtually disappeared (Doble, this core compound yielded a large family of com-
Martin, & Nutt, 2004). pounds that could be used as sedatives or, at higher
The bromide salts were first used for the treatment dosage levels, hypnotic agents. The first of the family,
of insomnia in the mid-1800s. They were available barbital, was introduced in 1903, after which these
without a prescription and were used well into the compounds so dominated the sedative-hypnotic market
20th century. While bromides are indeed capable of during the first half of the 20th century that no other
causing the user to fall asleep, they tend to accumulate sedative-hypnotics appeared during that era (Nelson,
in the chronic user’s body, causing a drug-induced de- 2000; Numeroff & Putnam, 2005).
pression after as little as just a few days of continuous Since the time of their introduction, some 2,500 dif-
use. The bromide salts have been totally replaced by ferent barbiturates have been developed, although most
newer compounds. were never marketed and have remained only labora-
Despite superficial differences in their chemical tory curiosities. Of these, perhaps 50 barbiturates were
structure, all these compounds are central nervous sys- eventually marketed in the United States, 20 of which
tem (CNS) depressants. The relative potency of the are still in use (Nishino, Mishima, Mignot, & Dement,
barbiturate-like drugs is reviewed in Figure 9.1. 2004). The relative potency of the most common barbi-
These compounds share many common characteris- turates is shown in Table 9.1.
tics, in spite of the superficial differences in their chem- The barbiturates were originally thought to be non-
ical structure, such as the ability potentiate the effects addicting, although clinical experience with these
Abuse of and Addiction to the Barbiturates and Barbiturate-like Drugs 91
TABLE 9.1 Dosage Equivalency for Barbiturate-like Drugs in the popularity of the barbiturates as drugs of abuse
(Doble et al., 2004). A number of older people, usually
Generic name Dose equivalent to 30 mg
over the age of 50, who became addicted to the barbitu-
of drug of phenobarbital
rates when they were younger continue to abuse these
Chloral hydrate 500 mg compounds. Also, a small number of physicians have
turned back to the barbiturates as anxiolytic and hypnotic
Ethchlorvynol 350 mg agents to avoid the extra paperwork imposed by some
Meprobamate 400 mg state regulatory agencies, refueling the problem of bar-
Methyprylon 300 mg biturate abuse/addiction in some cases.
Glutethimide 250 mg
Pharmacology of the Barbiturates
All the barbiturates are variations of the parent com-
compounds soon showed otherwise (Ivanov, Schulz,
pound barbituric acid. The small chemical differences
Palmero, & Newcorn, 2006). Currently, barbiturates
among the various barbiturates cause them to vary in
are classified as Category II controlled substances5 and
the time the body needs to absorb, distribute, biotrans-
are available only by prescription. After the introduc-
form, and then excrete the specific compound in-
tion of the benzodiazepines in the 1960s, the barbitu-
gested. The various chemical derivatives of barbituric
rates gradually fell into disfavor. But in spite of the
acid differ in terms of lipid solubility; variations that
pharmacological revolution that took place in the latter
have greater lipid solubility are more potent and have a
half of the 20th century, there are still some areas of
more rapid onset of action, although their effects tend
medicine where barbiturates remain the pharmaceuti-
to be briefer than those barbiturates with less lipid solu-
cal of choice (Ciraulo, Ciraulo, Sands, Knapp, & Sarid-
bility (Levin, 2002; Ropper & Brown, 2005). Thus,
Segal, 2005). Some examples of these specialized uses
when a single dose of pentobarbital is ingested, its high
for a barbiturate include certain surgical procedures,
level of lipid solubility means it will have an effect in
possible control of brain swelling after traumatic brain
10–15 minutes whereas phenobarbital, which is poorly
injuries, treatment of migraine headaches, emergency
lipid soluble, does not begin to have an effect until 60
treatment of seizures, and control of epilepsy (Charney
minutes or longer after it was ingested.
et al., 2006; Nemeroff & Putnam, 2005; Ropper &
Because they are all variations of the same parent
Brown, 2005).
molecule, the barbiturates share a similar mechanism
With newer drugs having all but replaced the barbi-
of action (Nemeroff & Putnam, 2005). They inhibit the
turates in modern medicine, it is surprising to learn that
ability of the GABAA chloride channel to close, thus
controversy still rages around the appropriate use of
slowing the rate at which the cell can “fire” (Ciraulo &
many of these chemicals. For example, although barbi-
Sarid-Segal, 2005; Doble et al., 2004; Nishino et al.,
turates have long been considered valuable in controlling
2004; Numeroff & Putnam, 2005). This is accom-
trauma-induced brain swelling (Nemeroff & Putnam,
plished even in the absence of the GABA molecule it-
2005), their value in this role has been challenged
self, making the compound effective even without the
(Lund & Papadakos, 1995). Another area of controversy is
inhibitory effects of GABAA (Carvey, 1998; Doble et al.,
the use of one barbiturate as the “lethal injection” to exe-
2004; Parrott, Morinan, Moss, & Scholey, 2004).
cute criminals (Truog, Berde, Mitchell, & Brier, 1992).
Barbiturates can be classified on the basis of their
Equally controversial is the use of barbiturates to help se-
duration of action.6 The ultrashort barbiturates are
date terminally ill cancer patients in extreme pain (Truog
the first group; when injected, their effects begin in a
et al., 1992).
matter of seconds and last for less than half an hour.
The abuse potential of barbiturates. The barbiturates
Such compounds include Pentothal and Brevital.
have a considerable abuse potential. In the period be-
These ultrashort-acting barbiturates are exceptionally
tween 1950 and 1970, the barbiturates were second
only to alcohol as drugs of abuse (Reinisch, Sanders, 6Other researchers might use different classification systems than the
Mortensen, & Rubin, 1995). Remarkably, the first years one in this text. For example, some researchers use the chemical
of the 21st century have witnessed a minor resurgence structure of the different forms of barbiturate as the defining criteria
for classification. This text follows the classification system suggested
5
See Appendix Four. by Zevin and Benowitz (1998).
92 Chapter Nine
lipid soluble and thus can pass through the blood-brain of only 3–6 hours and virtually all of it is biotransformed
barrier quickly. This group of compounds is useful in by the liver before it is excreted from the body (American
dental/surgical procedures where a rapid onset of effect Society of Health System Pharmacists, 2002). Another
and a short duration of action are desirable. difference between the different barbiturates is the de-
The short-acting barbiturates usually begin to act gree to which the compound becomes protein bound.
quickly, and their effects last for between 3 and 4 hours As a general rule, the longer the drug’s half-life, the
(Zevin & Benowitz, 1998). An example is Nembutal, stronger the degree of protein binding for that form of
which has an elimination half-life of 10 to 50 hours; it barbiturate.
begins to have an effect on the user in 10–15 minutes, Although they might be injected into muscle tissue or
and the effects last 3–4 hours (Numeroff & Putnam, directly into a vein in a medical setting, the barbiturates
2005). In terms of lipid solubility, the short-acting bar- are usually administered orally. On rare occasions, ad-
biturates fall between the ultrashort-acting barbitu- ministration is rectally through suppositories. When
rates and the next group, the intermediate duration taken orally, the compound is rapidly and completely ab-
barbiturates. sorbed from the small intestine (Levin, 2002; Nemeroff &
This third group of compounds is moderately lipid Putnam, 2005). Once it reaches the blood, it is distrib-
soluble; the effects begin within an hour when the drug uted throughout the body, with the highest concentra-
is ingested orally, and they generally last some 6–8 hours tions in the liver and the brain (American Society of
(Meyer & Quenzer, 2005; Zevin & Benowitz, 1998). In- Health System Pharmacists, 2002). The behavioral ef-
cluded in this group are Amytal (amobarbital) and Buti- fects of the barbiturates are very similar to those of alco-
sol (butabarbital) (Schuckit, 2006). Finally, there are hol (Nishino et al., 2004). Just like alcohol, the
the long-acting barbiturates. These are absorbed slowly, barbiturates will depress not only the brain activity but
and their effects last for 6–12 hours (Meyer & Quenzer, also to a lesser degree the activity of the muscle tissues,
2005; Zevin & Benowitz, 1998). Phenobarbital is per- the heart, and respiration (Ciraulo et al., 2005). Al-
haps the most commonly encountered drug in this though high concentrations of barbiturates are quickly
class. achieved in the brain, the drug is rapidly redistributed
One point of confusion that must be addressed is to other body organs (Levin, 2002). The speed at which
that the short-acting barbiturates do not have extremely this redistribution occurs varies from one barbiturate to
short elimination half-lives. As discussed in Chapter 3, another; thus different barbiturates have different thera-
the biological half-life of a drug provides only a rough peutic half-lives. Following the redistribution process,
estimate of the time a specific chemical will remain in the barbiturate is metabolized by the liver and eventu-
the body. The shorter-acting barbiturates might have an ally excreted by the kidneys.
effect on the user for only a few hours and still have an The impact of barbiturates on the various subunits
elimination half-life of 8–12 hours or even longer. This of the brain depends on the degree to which they uti-
is because their effects are limited not by the speed at lize GABA as a neurotransmitter. At the regional level,
which they are biotransformed by the liver but by the the barbiturates have their greatest impact on the cortex
speed with which they are removed from the blood and and the reticular activating system (RAS),7 and the
redistributed to various body organs. Significant amounts medulla oblongata8 (American Society of Health Sys-
of some shorter-acting barbiturates are stored in differ- tem Pharmacists, 2002). At low dosage levels, the barbi-
ent body tissues and then released back into the general turates will reduce the function of the nerve cells in
circulation after the individual has stopped taking the these regions of the brain, bringing on a state of relax-
drug, contributing to the barbiturate “hangover” effect ation and, at slightly higher doses, a form of sleep. How-
(Uhde & Trancer, 1995). ever, because of their effects on the respiratory center of
As a general rule, the shorter-term barbiturates are the brain, it is recommended that patients with breathing
almost fully biotransformed by the liver before being disorders such as sleep apnea not use the barbiturates ex-
excreted from the body (Nishino, Mignot, & Dement, cept under a physician’s supervision (Nishino et al.,
1995). In contrast, a significant proportion of the 2004). At extremely high dosage levels, the barbiturates
longer-term barbiturates are eliminated from the body have such a strong effect on the neurons of the CNS
essentially unchanged. Thus, for phenobarbital, which that death is possible.
may have a half-life of 2–6 days, between 25% and 50%
of the drug will be excreted by the kidneys virtually un- 7
See Glossary.
changed. The barbiturate methohexital has a half-life 8
See Glossary.
Barbiturate-induced death either by accident or as a progression of sleep from one stage to another and also
result of suicide is not uncommon (Filley, 2004). Some suppress the sleep stage known as rapid eye movement
barbiturates have a therapeutic dosage to lethal dosage (or REM) sleep (Nemeroff & Putnam, 2005). Scientists
level ratio of only 1:3 to 1:10 (Ciraulo et al., 2005; who study sleep believe that people need to experience
Meyer & Quenzer, 2005), reflecting the narrow thera- REM sleep for emotional well-being. Barbiturate-
peutic window of these agents. In the past, when barbi- assisted sleep reduces the total time that the individual
turate use was more common, a pattern of 118 deaths spends in REM sleep (Nishino et al., 2004). Through
per 1 million prescriptions was noted for these drugs this interference in normal sleep patterns, barbiturate-
(Drummer & Odell, 2001). This low safety margin and induced sleep may impact a person’s emotional and
the significantly higher safety margin offered by the physical health.
benzodiazepines are reasons the barbiturates have for When a barbiturate is discontinued after an ex-
the most part been replaced by newer medications in tended period of use as a hypnotic, the user will experi-
the treatment of anxiety and for inducing sleep. ence “REM rebound” (Charney et al., 2006). In this
condition, the person will dream more intensely and
more vividly for a period of time, as the body tries to
Subjective Effects of Barbiturates
catch up on lost REM sleep time. These dreams have
at Normal Dosage Levels been described as nightmares that were strong enough
At low doses, the barbiturates reduce feelings of anxiety to tempt the individual to return to the use of drugs in
or even bring on a sense of euphoria (Ciraulo et al., order to get a “good night’s sleep again.” The rebound
2005). Some users also report a feeling of sedation or fa- effect might last for 1 to 3 weeks, and in rare cases for
tigue, possibly to the point of drowsiness, and a de- up to 2 months (Tyrer, 1993).
crease in motor activity. This means a person’s reaction Barbiturates can cause a drug-induced “hangover”
time increases, and he or she might have trouble coor- the day after use (Wilson, Shannon, Shields, & Stang,
dinating muscle movements, similar to someone intoxi- 2007). Subjectively, the individual who is going
cated with alcohol (Filley, 2004; Nishino et al., 2004). through a barbiturate hangover simply feels that he or
This is to be expected, since both alcohol and the barbi- she is “unable to get going” the next day. This is be-
turates affect the cortex of the brain through similar cause barbiturates often require an extended period of
pharmacological mechanisms. The disinhibition ef- time for the body to completely biotransform and ex-
fects of the barbiturates, like alcohol, may cause a state crete the drug. As discussed in Chapter 3, in general, it
of “paradoxical” excitement or even a paradoxical rage takes five half-life periods to completely eliminate a
reaction (Ciraulo et al., 2005). Patients who have re- single dose of a chemical from the blood. Because
ceived barbiturates for medical reasons have reported many of the barbiturates have extended biological half-
unpleasant side effects such as nausea, dizziness, and a life periods, some small amounts of a barbiturate might
feeling of mental slowness. Anxious patients report that remain in the person’s bloodstream for hours, or even
their anxiety is no longer as intense, while patients who days, after just a single dose. For example, although the
are unable to sleep report that they are able to slip into a therapeutic effects of a single dose of secobarbital might
state of drug-induced sleep quickly. last 6–8 hours, the medication might continue to impair
motor coordination for 10–22 hours (Charney et al.,
Complications of the Barbiturates 2006).
When people continually add to this reservoir of un-
at Normal Dosage Levels metabolized drug by ingesting additional doses of the
For almost 60 years, the barbiturates were the treat- barbiturate, there is a greater chance that they will ex-
ment of choice for insomnia. As they were so exten- perience a drug hangover. However, whether from one
sively prescribed to help people sleep, it is surprising or repeated doses, the drug hangover is caused by the
that research has shown tolerance developing rapidly same mechanism: traces of unmetabolized barbiturates
to their hypnotic effects. Indeed, research suggests remaining in the individual’s bloodstream for extended
that they are not effective as hypnotics after just a few periods of time after the medication is discontinued.
days of regular use (Drummer & Odell, 2001; Rall, Subjectively, the individual might feel “not quite
1990). In spite of their traditional use as a treatment awake,” or “drugged,” the next day. The elderly or
for insomnia, barbiturate-induced sleep is not the same people with impaired liver function are especially likely
as normal sleep. Barbiturates interfere with the normal to have difficulty with the barbiturates. This is because
94 Chapter Nine
the liver’s ability to metabolize many drugs, such as the medication that further reduces the effectiveness of this
barbiturates, declines with age. In light of this fact, neurological system will contribute to the development
Sheridan, Patterson, and Gustafson (1982) have ad- of ADHD symptoms.
vised that older individuals who receive barbiturates be Drug interactions between the barbiturates and other
started at one-half the usual adult dosage, and that the medications. Research has found that the barbiturates
dosage level gradually be increased until the medica- are capable of interacting with numerous other chemi-
tion is having the desired effect. cals, increasing or decreasing the amount of these
One side effect of long-term phenobarbital use is a drugs in the blood through various mechanisms. Be-
possible loss in intelligence. Researchers have docu- cause of the potentiation effect, patients should not use
mented a drop of approximately 8 IQ points in patients barbiturates if they are using other CNS depressants
who have been receiving phenobarbital for control of such as alcohol, narcotic analgesics, phenothiazines, or
seizures for extended periods of time, although it is not benzodiazepines unless under a physician’s supervision
clear whether this reflects a research artifact, a drug ef- (Barnhill, Ciraulo, Ciraulo, & Greene, 1995). Another
fect, or the cumulative impact of the seizure disorder class of CNS depressants that might unexpectedly cause
(Breggin, 1998). It is also not clear whether this ob- a potentiation effect with barbiturates are the antihista-
served loss of 8 IQ points might be reversed or if a simi- mines (Rall, 1990). Since many antihistamines are
lar reduction in measured IQ develops as a result of the available without a prescription, there is a very real dan-
chronic use of other barbiturates. However, this obser- ger of an unintentional interaction between these two
vation does point out that the barbiturates are potential medications.
CNS agents that will affect the normal function of the Patients who are taking barbiturates should not use
brain. antidepressants known as monoamine oxidase inhibitors
Another consequence of barbiturate use, even in a (MAOIs, or MAO inhibitors) as the MAOI may inhibit
medical setting, is that this class of pharmaceuticals the biotransformation of the barbiturates and thus pro-
can cause sexual performance problems such as de- long barbiturate-induced sedation (Ciraulo, Shader,
creased desire for the user, as well as erectile problems Greenblatt, & Creelman, 2006). Patients using a barbi-
and delayed ejaculation for the male (Finger, Lund, & turate should not take the antibiotic doxycycline except
Slagel, 1997). Also, hypersensitivity reactions have under a physician’s supervision as barbiturates reduce
been reported with the barbiturates. These are most the effectiveness of this antibiotic, an action that may
common in individuals with asthma. Other complica- have serious consequences for the patient (Ciraulo et al.,
tions occasionally seen at normal dosage levels include 2006). Because of drug-drug interactions, patients
nausea, vomiting, diarrhea, and in some cases, consti- should not take barbiturates and any of the tricyclic an-
pation. Some patients have developed skin rashes tidepressants except under a physician’s supervision as
while receiving barbiturates, although the reason for they speed up the process of antidepressant biotransfor-
this is not clear. Finally, some who take barbiturates mation, thus reducing their effectiveness (Ciraulo et al.,
develop an extreme sensitivity to sunlight known as 2006).
photosensitivity. Thus, patients who receive barbitu- This is the same process through which the barbitu-
rates must take special precautions to avoid sunburn, rates will speed up the metabolism of many oral contra-
or even limit exposure to the sun’s rays. Because of ceptives, corticosteroids, and the antibiotic Flagyl
these problems and because medications are now (metronidazole) (Kaminski, 1992). Thus, when used
available that do not share the dangers associated with concurrently, barbiturates will reduce the effectiveness
barbiturate use, this class of drugs is not considered to of these medications, according to Kaminski. Women
have any role in the treatment of anxiety or insomnia who are taking both oral contraceptives and barbitu-
(Tyrer, 1993). rates should be aware that the barbiturates may reduce
Children who suffer from attention deficit-hyperac- the effectiveness of the oral contraceptives (Graedon &
tivity disorder (ADHD, or what was once called “hyper- Graedon, 1995, 1996).
activity”) who also receive phenobarbital are likely to Individuals who are taking the anticoagulant med-
experience a resurgence of their ADHD symptoms. ication warfarin should not use a barbiturate except
This effect would seem to reflect the ability of the bar- under a physician’s supervision. Barbiturate use can in-
biturates to suppress the action of the reticula activating terfere with the normal biotransformation of warfarin,
system (RAS) in the brain. Currently, it is thought that resulting in abnormally low blood levels of this anti-
the RAS of children with ADHD is underactive, so any coagulant medication (Graedon & Graedon, 1995).
Further, if the patient should stop taking barbiturates TABLE 9.2 Normal Dosage Levels
while on warfarin, it is possible for the individual’s war- of Commonly Used Barbiturates
farin levels to rebound to dangerous levels. Thus, these
Barbiturate Sedative dose* Hypnotic dose**
two medications should not be mixed except under a
physician’s supervision. Amobarbital 50–150 mg/day 65–200 mg
When the barbiturates are biotransformed by the
liver, they activate a region of the liver that also is in- Aprobarbital 120 mg/day 40–60 mg
volved in the biotransformation of the asthma drug Butabarbital 45–120 mg/day 50–100 mg
theophylline (sold under a variety of brand names). Pa- Mephobarbital 96–400 mg/day Not used as
tients who concurrently use a barbiturate and theo- hypnotic
phylline might experience abnormally low blood levels
Pentobarbital 60–80 mg/day 100 mg
of the latter drug, a condition that might result in less
than optimal control of the asthma. Thus, these two Phenobarbital 30–120 mg/day 100–320 mg
medications should not be used by the same patient at Secobarbital 90–200 mg/day 50–200 mg
the same time except under a physician’s supervision
Talbutal 30–120 mg/day 120 mg
(Graedon & Graedon, 1995).
As is obvious from this list of potential interactions *Administered in divided doses.
between barbiturates and other pharmaceuticals, the **Administered as a single dose at bedtime.
barbiturates are a powerful family of drugs. As in every Source: Based on information provided in Uhde & Trancer (1995).
case when a person is using two different chemicals
concurrently, he or she should always consult a physi-
cian or pharmacist.
problem in such cases, as the barbiturates have a small
“therapeutic window.” The barbiturates cause a dose-
dependent reduction in respiration as the increasing
Effects of the Barbiturates at
drug blood levels interfere with the normal function of
Above-Normal Dosage Levels the medulla oblongata.10 Hypothermia is another barbi-
When barbiturates are used at above-normal dosage turate-induced side effect seen either when these drugs
levels, they can cause a state of intoxication similar to are ingested at above-normal doses or when mixed with
alcohol intoxication (Ciraulo & Sarid-Segal, 2005). other CNS depressants (Ciraulo et al., 2005; Pagliaro &
Patients who are intoxicated by barbiturates will Pagliaro, 1998). Other complications of larger-than-
demonstrate such behaviors as slurred speech and un- normal doses include a progressive loss of reflex activity,
steady gait, without the characteristic smell of alcohol respiratory depression, tachycardia, hypotension, low-
(Jenike, 1991). When they discontinue their use of ered body temperature, and, if the dose is large enough,
barbiturates, they might also experience a withdrawal coma and ultimately death (Nemeroff & Putnam,
syndrome similar to the delirium tremens (DTs) seen 2005).
in chronic alcohol abusers (Ciraulo & Sarid-Segal, In past decades, prior to the introduction of the
2005). Chronic abusers are at risk for the develop- benzodiazepines, the barbiturates accounted for up-
ment of bronchitis and/or pneumonia, as these med- ward of three-fourths of all drug-related deaths in the
ications interfere with the normal cough reflex. United States (Peluso & Peluso, 1988). Even now, in-
Individuals under the influence of a barbiturate will tentional or unintentional barbiturate overdoses are
not test positive for alcohol on blood or urine toxicol- not unheard of. Fortunately, the barbiturates do not
ogy tests.9 Specific blood or urine toxicology screens directly cause any damage to the central nervous sys-
must be carried out to detect or rule out barbiturate tem. If overdose victims reach medical support before
intoxication. they develop shock or hypoxia, they may recover com-
Because barbiturates can cause a state of intoxica- pletely from a barbiturate overdose (Nishino et al.,
tion similar to that induced by alcohol, some abusers 2005). For this and other reasons any suspected barbi-
will ingest above-normal normal doses of these com- turate overdose should be immediately be treated by a
pounds. The danger of unintentional overdose is a physician.
9Unless 10See Glossary.

they have also ingested alcohol along with the barbiturate.
96 Chapter Nine
Neuroadaptation, Tolerance to, and cross-tolerance between the barbiturates and the opiates,
Dependence on the Barbiturates and barbiturates and the hallucinogen PCP (Kaplan
et al., 1994).
With continual use, people will experience a process of The United States went through a wave of barbitu-
neuroadaptation, becoming tolerant to many of the bar- rate abuse and addiction in the 1950s, so physicians
biturate’s effects. The process of barbiturate-induced have long been aware that once the person is addicted,
neuroadaptation is not uniform, however. When they withdrawal from barbiturates is potentially life threaten-
are used for the control of seizures, tolerance may not ing and should be attempted only under medical super-
be a significant problem. A patient who is taking phe- vision (Meyer & Quenzer, 2005). The barbiturates
nobarbital for the control of seizures will eventually be- should never be abruptly withdrawn, as to do so might
come somewhat tolerant to the sedative effect of the bring about an organic brain syndrome that might in-
medication, but he or she will not develop a significant clude confusion, seizures, possible brain damage, and
tolerance to the drug’s anticonvulsant effect; but a per- even death.
son taking a barbiturate for its hypnotic effects might A high percentage of barbiturate abusers who
become habituated to the medication’s effects in just a abruptly discontinue the use of these compounds will
couple of weeks of continuous use (Nemeroff & Putnam, experience withdrawal symptoms. Unfortunately, it is
2005). difficult to estimate the danger period for barbiturate
Some patients try to overcome neuroadaptation to the withdrawal problems. As a general rule, however, the
barbiturates by increasing their dosage of the drug with- longer-lasting forms of barbiturates tend to have longer
out consulting their physician. Unfortunately, while the withdrawal periods. Some of the symptoms of barbitu-
individual might become tolerant to the sedating effect rate withdrawal include rebound anxiety, agitation,
of the barbiturates, he or she does not develop any sig- trembling, and possibly seizures. Other symptoms that
nificant degree of tolerance to the respiratory depressant the patient will experience during withdrawal include
effect of these compounds (Meyer & Quenzer, 2005). muscle weakness, anorexia, muscle twitches, and a pos-
This is why barbiturates have a history of involvement in sible state of delirium very similar to the delirium
a large number of unintentional overdoses, some of tremens seen in the chronic alcohol drinker. When an
which have been fatal. In spite of the individual’s level individual abruptly stops taking a short-acting to inter-
of neuroadaptation, the lethal dose of the barbiturates mediate-acting barbiturate, withdrawal seizures will
remains relatively unchanged (Charney et al., 2006; normally begin on the 2nd or 3rd day. Barbiturate with-
Meyer & Quenzer, 2005). Thus, patients who increase drawal seizures are rare after the 12th day following ces-
their dose without consulting a physician will run the sation of the drug. When the individual was abusing
risk of crossing the threshold between an effective and a one of the longer-acting barbiturates, he or she might
lethal dose. not have a withdrawal seizure until as late as the 7th day
This process contributes to the unintentional death after the last dose of the drug (Tyrer, 1993). All of these
of many barbiturate abusers. Where first-time barbitu- symptoms will pass after 3–14 days, depending on the
rate abusers report that they experience a feeling of eu- individual. Physicians are able to utilize many other
phoria when they use these compounds, they will, over medications to minimize these withdrawal symptoms;
time, become tolerant to the euphoric effects. The however, the patient should be warned that there is no
abuser might try to recapture that effect by increasing such thing as a symptom-free withdrawal.
the dosage level. Unfortunately, the lethal dose of bar-
biturates remains relatively stable in spite of the indi-
vidual’s growing tolerance or neuroadaptation to the Barbiturate-like Drugs
drug. As barbiturate abusers increase their daily dosage Because of the many adverse side effects of the barbitu-
level to continue experiencing the drug-induced eu- rates, pharmaceutical companies have long searched for
phoria, they will come closer and closer to the lethal substitutes that were effective but safe. During the
dose. 1950s, a number of new drugs were introduced to treat
In addition to the phenomenon of tolerance, cross- anxiety and insomnia in place of the barbiturates. These
tolerance11 is also possible between barbiturates and drugs included Miltown (meprobamate), Quaalude and
similar compounds. Cross-tolerance between alcohol Sopor (both brand names of methaqualone), Doriden
and the barbiturates is common, as is some degree of (glutethimide), Placidyl (ethchlorvynol), and Noludar
11See Glossary. (methyprylon).
Although these drugs were thought to be nonaddicting ing to Cole and Yonkers (1995). Physical dependence
when they were first introduced, research has shown that on meprobamae is common when patients reach a
barbiturate-like drugs are very similar to the barbiturates dosage level of 3,200 mg/day or more.
in their abuse potential. This should not be surprising Methaqualone. This drug was introduced as a safe,
since the chemical structure of some of the barbiturate- nonaddicting barbiturate substitute (Neubauer, 2005,
like drugs such as glutethimide and methyprylon are very p. 62) in 1965 and quickly achieved popularity among
similar to that of the barbiturates themselves (Julien, illicit drug abusers in the late 1960s and early 1970s. Il-
2005). Like the barbiturates, glutethimide and methypry- licit drug users soon discovered that when they resisted
lon are metabolized mainly in the liver. the sedative/hypnotic effects of methaqualone, they
Both Placidyl (ethchlorvynol) and Doriden (glute- would experience a sense of euphoria.
thimide) are considered especially dangerous, and nei- Depending on the dosage level being used, physi-
ther drug should be used except in rare, special circum- cians prescribed it both as a sedative and as a hypnotic
stances (Schuckit, 2000). The prolonged use of (Lingeman, 1974). The effects are very similar to those
ethchlorvynol may result in a drug-induced loss of vision of the barbiturates. Following oral administration,
known as amblyopia. Fortunately, this drug-induced methaqualone is rapidly absorbed from the gastroin-
amblyopia is not permanent, but will gradually clear testinal tract and begins to take effect in 15–20 minutes.
when the drug is discontinued (Michelson, Carroll, When prescribed as an anxiolytic, the usual dose of
McLane, & Robin, 1988). Since its introduction, the methaqualone was 75 mg and the hypnotic dose was
drug glutethimide has become “notorious for its high between 150 and 300 mg. Tolerance to the sedating
mortality associated with overdose” (Sagar, 1991, p. 304) and the hypnotic effects of methaqualone developed
as a result of the drug’s narrow therapeutic range. The rapidly. Many abusers gradually increased their daily
lethal dose of glutethimide is only 10 grams, only dosage levels in an attempt to reachieve the initial ef-
slightly above the normal dosage level (Sagar, 1991). fect, and some methaqualone abusers were known to
Meprobamate was a popular sedative in the 1950s, use up to 2,000 mg in a single day (Mirin, Weiss, &
when it was sold under at least 32 different brand Greenfield, 1991). Methaqualone has a narrow thera-
names, including Miltown and Equanil (Lingeman, peutic window, and its estimated lethal dose is approxi-
1974). However it is considered obsolete by current mately 8,000 mg for a 150-pound person (Lingeman,
standards (Rosenthal, 1992). Surprisingly, this med- 1974).
ication is still quite popular in older patients, and Shortly after methaqualone was introduced, reports
older physicians often continue to prescribe it. An began to appear suggesting that it was being abused. It
over-the-counter prodrug, Soma (carisoprodol), that is was purported to have aphrodisiac properties (which
sold in many states is biotransformed in part into has never been proven) and to provide a mild sense of
meprobamate after being ingested, and there have euphoria for the user (Mirin et al., 1991). People who
been reports of physical dependence on Soma, just as have used methaqualone report feelings of euphoria,
there were on Meprobamate in the 1950s and 1960s well-being, and behavioral disinhibition. As for the bar-
(Gitlow, 2007). biturates, while tolerance to the drug’s effects develops
Fortunately, although meprobamate is quite addic- quickly, the lethal dosage of methaqualone remains the
tive, it has generally not been in use since the early same. Death from methaqualone overdose was com-
1970s, but on occasion an older patient who has been mon, especially when the drug was taken with alcohol.
using this medication since that period will surface. The typical cause of death was heart failure, according
Also, in spite of its reputation and history, meprobamate to Lingeman (1974).
still has a minor role in medicine, especially for patients In the United States, methaqualone was classified as
who are unable to take benzodiazepines (Cole & a Schedule I12 compound in 1984 and was withdrawn
Yonkers, 1995). The peak blood levels of meprobamate from the market. It is still manufactured by pharmaceu-
following an oral dose are seen in 1–3 hours, and the tical companies in other countries and is either smuggled
drug’s half-life is 6–17 hours following a single dose. into this country or manufactured in illicit laboratories
The chronic use of meprobamate may result in the and sold on the street (Shader, 2003). Thus, the sub-
half-life being extended to 24–48 hours (Cole & stance abuse counselor must have a working knowledge
Yonkers, 1995). The LD50 of meprobamate is estimated of methaqualone and its effects.
to be about 28,000 mg. However, some deaths have
been noted following overdoses of 12,000 mg, accord- 12See Appendix Four.
98 Chapter Nine
Summary However, like alcohol, the barbiturates also have a

significant potential for addiction. This resulted in a
For thousands of years, alcohol was the only chemical search for nonaddictive medications that could replace
even marginally effective as an antianxiety or hyp- them. In the post–World War II era, a number of syn-
notic agent. Although a number of chemicals with thetic drugs with chemical structures very similar to the
hypnotic action were introduced in the mid-1800s, barbiturates were introduced, often with the claim that
each was of limited value in the treatment of insom- these drugs were “nonaddicting.” However, they were
nia. Then, in the early 1900s, the barbiturates were ultimately found to have an addiction potential similar
introduced. These drugs, which have a mechanism of to that of the barbiturates. Since the introduction of the
action very similar to that of alcohol, were found to benzodiazepines (to be discussed in the next chapter),
have an antianxiety and a hypnotic effect. The barbi- the barbiturates and similar drugs have fallen into disfa-
turates rapidly became popular and were widely used vor. However, the barbiturates do continue to play a
both for the control of anxiety and to help people fall minor role in medicine and are still occasionally en-
asleep. countered by the mental health or medical professional.
CHAPTER TEN
Abuse of and Addiction to Benzodiazepines

and Similar Agents
In 1960, the first of a new class of antianxiety1 drugs, tonin reuptake inhibitors (SSRIs) have become the
chlordiazepoxide, was introduced in the United States. “mainstay of drug treatment for anxiety disorders”
Chlordiazepoxide is a member of a family of chemicals (Shear, 2003, p. 28). The BZs remain the treatment of
known as the benzodiazepines (BZs). Since their intro- choice for acute anxiety (such as panic attacks or short-
duction, some 3,000 different BZs have been devel- term anxiety resulting from a specific stressor) and con-
oped, of which about 50 have been marketed around tinue to have a role in the treatment of such conditions as
the world, and roughly 12 are used in the United States generalized anxiety disorder (GAD) (Stevens & Pollack,
(Dupont & Dupont, 1998). BZs have been found effec- 2005). Because the mechanism of action of the BZs is
tive in the treatment of a wide range of disorders, such more selective than in the barbiturates, they are able to
as the control of anxiety symptoms, insomnia, muscle reduce anxiety without causing the same degree of seda-
strains, and the control of seizures. Because they are far tion and fatigue seen with the barbiturates. The most fre-
safer than the barbiturates, they have collectively be- quently prescribed BZs for the control of anxiety are
come the most frequently prescribed psychotropic shown in Table 10.1.
medications in the world (Gitlow, 2007). Each year, ap- In addition to the control of anxiety, some BZs have
proximately 10% to 15% of the adults in the Western been found useful in the treatment of other medical
world will use a BZ at least once (Dubovsky, 2005; problems such as seizure control and helping muscles
Jenkins, 2007). Legally, BZs are Category II com- recover from strains (Ashton, 1994; Raj & Sheehan,
pounds.2 2004). The benzodiazepine clonazepam is especially
The BZs were initially introduced as nonaddicting effective in the long-term control of seizures and is in-
substitutes for the barbiturates or barbiturate-like drugs. creasingly being used as an antianxiety agent (Raj &
In the time since their introduction, however, it has be- Sheehan, 2004).
come clear that the benzodiazepines have a very signifi- Researchers estimate that 25%–35% of adults in
cant abuse potential both when abused in isolation, or the United States suffer from at least occasional insom-
when abused along with other compounds. Each year nia, while 10%–15% suffer from chronic insomnia
in the United States, the use and abuse of BZs results in (Neubauer, 2005). In the 1970s and 1980s, BZs such as
hundreds of millions of dollars in unnecessary medical temazepam (Restoril), triazolam (Halcion), flurazepam
costs (Benzer, 1995). In this chapter, the history of the (Dalmane), and quazepam (Doral) were used as hyp-
BZs, their medical applications, and the problem of notics.3 However, since the last years of the 20th century
abuse/addiction to the benzodiazepine and similar a new class of medications known as the benzodiazepine
agents in the United States will be examined. receptor agonists (BRAs) have been introduced; they
have a lower potential for abuse, are more selective
than the benzodiazepines, and are now the primary drugs
Medical Uses of the Benzodiazepines
of choice for the treatment of insomnia (“Insomnia in
Although the BZs were originally introduced as an- Later Life,” 2006).
tianxiety agents, and they remain valuable aids in the Two different BZs, alprazolam (Xanax) and adinazo-
control of specific anxiety disorders, the selective sero- lam (Deracyn) are reportedly of value in the treatment
of depression. Alprazolam has minor antidepressant ef-
1Technically,
these compounds are called anxiolytics, but the fects but is most useful in controlling anxiety that often
term antianxiety is used in this text.
2See 3
Appendix Four. A hypnotic is a compound that will induce sleep.
99
100 Chapter Ten
TABLE 10.1 Selected Pharmacological Characteristics While the LD50 for humans is not known, these figures
of Some Benzodiazepines do suggest that diazepam is an exceptionally safe drug.
However, other benzidoazepines have smaller thera-
Average half-life
peutic indexes than diazepam. Many physicians recom-
Generic name Equivalent dose (hours)
mend that the benzodiazepine Serax (oxazepam) be
Alprazolam 0.5 mg 6–20 used in cases when the patient is at risk for an overdose
because of its greater margin of safety (Buckley, Dawson,
Chlordiazepoxide 25 mg 30–100
Whyte, & O’Connell, 1995).
Clonazepam 0.25 mg 20–40 Note, however, that the benzodiazepine margin of
Clorazepate 7.5 mg 30–100 safety is drastically reduced when an individual ingests
one or more additional CNS depressants in an attempt
Diazepam 5 mg 30–100
to end his or her life. This is because of the synergistic4
Flurazepam 30 mg 50–100 effect that develops when different CNS depressants
Halazepam 20 mg 30–100 are mixed and is one reason any known or suspected
overdose should be evaluated and treated by medical
Lorazepam 1 mg 10–20
professionals. In cases of benzodiazepine overdoses, the
Oxazepam 15 mg 5–21 medication flumazenil has been found to counteract
Prazepam 10 mg 30–100 the effects of the BZs, by binding to and blocking the
receptor sites where the benzodiazepine molecules
Temazepam 30 mg 9.5–12.4
normally bind (O’Brien, 2006). Unfortunately, it is ef-
Triazolam 0.25 mg 1.7–3.0 fective only for 20–45 minutes, making continuous in-
fusion of flumazenil necessary, and it is specific only to
Sources: Based on Hyman (1988) and Reiman (1997).
BZs (Brust, 1998).
Pharmacology of the Benzodiazepines

accompanies depression (Dubovsky, 2005). It is also
The BZs are very similar in their effects, differing
used to treat panic disorder, although there are rare case
mainly in their duration of action (Dubovsky, 2005).
reports of alprazolam-induced panic attacks (Bashir &
Table 10.1 reviews the relative potency and biological
Swartz, 2002). Unlike the other BZs, adinazolam
half-lives of some of the BZs currently in use in the
(Deracyn) does seem to have a direct antidepressant
United States. Like many pharmaceuticals, BZs can be
effect. Researchers believe that adinazolam (Deracyn)
classified on the basis of their pharmacological charac-
works by increasing the sensitivity of certain neurons
teristics and are often classified on the basis of their
within the brain to serotonin (Cardoni, 1990). A deficit
therapeutic half-lives (Charney, Mihic & Harris,
of, or insensitivity to, serotonin is thought to be the
2006):5
cause of at least some forms of depression. Thus, by
increasing the sensitivity of the neurons of the brain
1. ultrashort acting (< 4 hours or less)
to serotonin, Deracyn (adinazolam) would seem to
2. short acting (< 6 hours)
have a direct antidepressant effect that is lacking in
3. intermediate acting (6–24 hours)
most BZs.
4. long acting (24+ hours)
BZs and suicide attempts. The possibility of suicide
through a drug overdose is a very real concern for the
The various BZs currently in use range from moder-
physician, especially when the patient is depressed. Be-
ately to highly lipid soluble (Ciraulo, Ciraulo, Sands,
cause of their high therapeutic index (discussed in
Knapp, & Sarid-Segal, 2005; Raj & Sheehan, 2004).
Chapter 3), the BZs have traditionally held the reputa-
Lipid solubility is important because the more lipid sol-
tion of being “safe” drugs to use with patients who are
uble a chemical is, the faster it is absorbed through the
potentially suicidal. Unlike the barbiturates, the thera-
peutic index of the BZs has been estimated to be above
4See Glossary.
1:200 (Kaplan & Sadock, 1996) and possibly as high as
5Remember: there are differences between therapeutic half-life, distri-
1:1,000 (Carvey, 1998). In terms of overdose potential,
bution half-life, and the elimination half-life of various compounds,
animal research suggests that the LD50 for diazepam is even in the same family of chemicals. Charney et al. (2006) base their
around 720 mg per kilogram of body weight for mice, classification system on the therapeutic half-life of the different ben-
and 1240 mg/kg for rats (Thompson PDR, 2004). zodiazepines being considered.
Abuse of and Addiction to Benzodiazepines and Similar Agents 101
small intestine after being taken orally (Roberts & this benzodiazepine might continue to have an effect on
Tafure, 1990). Highly lipid soluble BZs pass through the the user for as long as 280 hours after a single dose. Fortu-
blood-brain barrier to enter the brain more rapidly than nately, the BZs lorazepam, oxazepam, and temazepam
less lipid-soluble compounds (Raj & Sheehan, 2004). are either eliminated without biotransformation or pro-
Once in the general circulation, the BZs are all produce meta-bolites that have minimal physical effects on
tein bound, with between 70% and 99% of the specific the user. These are often preferred for older patients,
BZ being utilized becoming protein bound (Dubovsky, who may experience oversedation as a result of the long
2005). Diazepam has the greatest degree of protein half-lives of some benzodiazepine metabolites.
binding, with more than 99% of the drug molecules be- Although the BZs are often compared with the bar-
coming protein bound (American Psychiatric Associa- biturates, they are more selective in their action and
tion, 1990), whereas 92% to 97% of chlordiazepoxide is have a larger safety margin than barbiturates. In the
protein bound (Ayd, Janicak, Davis, & Preskorn, 1996) brain, benzodiazepine molecules bind to a gated chlo-
and 80% of the alprazolam molecules are protein ride channel in the neuron wall that normally is activated
bound (Thompson PDR, 2004). This variability in pro- by gamma aminobutyric acid (GABA). But where the
tein binding is one factor that influences the duration barbiturates will activate this channel even in the absence
of effect for each benzodiazepine after a single dose of GABA, the BZs have no effect on the rate at which the
(American Medical Association, 1994). Another factor channel gate opens or closes unless GABAA receptor site6
that influences the therapeutic effects of a benzodi- is occupied by GABA molecules (Charney et al., 2006).
azepine is the degree to which the drug molecules are But when a benzodiazepine molecule is present and
distributed throughout the body (Raj & Sheehan, GABA binds to the appropriate receptor site, the effects
2004). Benzodiazepine molecules might be sequestered of the GABA are enhanced, causing the chloride chan-
in body tissues, such as fat cells, only to be released nel to remain open far longer than it would normally
slowly back into the general circulation, providing an (Raj & Sheehan, 2004; Ramadan, Werder, & Preskorn,
extended therapeutic half-life for that benzodiazepine 2006). But the BZs have no effect on the neuron in the
compared with compounds that are not distributed so absence of GABA (Charney et al., 2006; Hobbs, Rall, &
extensively through the body. Verdoorn, 1995; Pagliaro & Pagliaro, 1998).
For the most part, the BZs are poorly absorbed from Neurons that utilize GABA are especially common
intramuscular or subcutaneous injection sites (Ameri- in the locus ceruleus7 region of the brain (Cardoni,
can Medical Association, 1994). The limited absorp- 1990; Johnson & Lydiard, 1995). Nerve fibers from
tion from injection sites makes it difficult to predict in the locus ceruleus connect with other parts of the
advance the degree of drug bioavailability when a ben- brain thought to be involved in fear and panic reactions.
zodiazepine is injected. For this reason these medica- By enhancing the effects of GABA, the BZs reduce the
tions are usually administered orally. One exception is level of neurological activity in the locus ceruleus, re-
when the patient is experiencing uncontrolled seizures. ducing the individual’s anxiety level. Unfortunately,
In such cases, intravenous injections of diazepam or a this theory does not provide any insight into the ability
similar benzodiazepine might be used to help control of the BZs to help muscle tissue relax or to stop
the seizures. Another exception is the benzodiazepine seizures (Hobbs et al., 1995). Thus, there is still a lot
Versed (midazolam) that is often used as a short-term that remains to be discovered about how these drugs
pre-anesthetic agent for medical procedures. work.
Most BZs must be biotransformed before elimination As these medications have been in use for almost a half
can proceed, and in the process of biotransformation century, it is surprising that there is disagreement about
some BZs will produce metabolites that are biologically their long-term effectiveness as anxiolytic medications.
active for extended periods of time. Thus, the duration Some researchers believe that the antianxiety effects of
of effect of many BZs is far different from the elimina- the BZs last only about 1–2 months and that they are not
tion half-life of the parent compound, a factor that useful in treating anxiety continuously over a long period
physicians must keep in mind when prescribing these of time (Ashton, 1994; Ayd et al., 1996). For this reason
medications (Dubovsky, 2005). For example, during
6At this time, neuropharmacologists have identified 16 possible
the process of biotransformation, the benzodiazepine
subtypes of the GABAA receptor site, suggesting that the different
flurazepam will produce five different metabolites, each subtypes play different roles in the process of neurotransmission in
of which has its own psychoactive effect. Because of nor- various regions of the brain, or on the basis of which neurotransmitter
mal variation with which the individual’s body can bio- molecules were in each specific receptor subtype.
transform or eliminate flurazepam and its metabolites, 7See Glossary.
102 Chapter Ten
the concurrent use of both BZs and selective serotonin re- than diazepam and similar BZs (Ashton, 1994; Graedon
uptake inhibitors (SSRIs) is recommended for the long- & Graedon, 1991).
term treatment of anxiety, with BZs then being slowly Patients who receive Deracyn (adinazolam) and
withdrawn after 6–8 weeks (Raj & Sheehan, 2004). This Doral (quazepam) are very likely to experience seda-
treatment paradigm avoids such dangers as benzodi- tion as a result of their medication use. Up to two-thirds
azepine-related rebound anxiety, or the benzodiazepine of those who receive this medication at normal dosage
plateau effect seen when the medication becomes less ef- levels might initially experience some degree of drowsi-
fective as an anxiolytic over time. ness (Cardoni, 1990). Thus sedation in response to one
But this medication paradigm is not universally ac- of these medications is not automatically a sign that too
cepted, and some physicians view the BZs as being ef- large a dose is being prescribed for the patient. Further,
fective in the long-term control of anxiety. There is since the active metabolites of Doral (quazepam) have
little evidence to suggest that the patient becomes toler- a half-life of 72 hours or more, there is a strong possibil-
ant to the anxiolytic effects of BZs, although they might ity that the user will experience a drug-induced hang-
reach therapeutic plateaus in which the patient reports over the next day (Hartmann, 1995).
that the medication does not “work as it used to” Drug-induced hangovers are possible with benzodi-
(Ciraulo et al., 2005; Raj & Sheehan, 2004). Raj and azepine use, especially with some of the longer-lasting
Sheehan (2004) recommend that the medication BZs (Ashton, 1992, 1994). The data in Table 10.1 sug-
dosage be adjusted after one or possibly two therapeutic gest that for some individuals, the half-life of some BZs
plateaus have been reached, but they warn of the dan- might be as long as 100 hours. Further, it usually re-
ger of ever-increasing dosage levels as the patient seeks quires five half-life periods before virtually all of a drug is
the initial sense of relaxation and relief once achieved biotransformed and eliminated from the body. If that
through the use of BZs. Thus, even within the medical patient were to take a second or third dose of the medica-
community there is disagreement as to the optimal use tion before the first dose had been fully biotransformed,
of the BZs or their potential for misuse. he or she would begin to accumulate unmetabolized
medication in body tissues. The unmetabolized medica-
tion would continue to have an effect on the individual’s
Side Effects of the Benzodiazepines
function well past the time that he or she thought the
When Used at Normal Dosage Levels
drug’s effects had ended.
Between 4% and 9% of patients prescribed a benzodi- Even a single 10 mg dose of diazepam can result in
azepine will experience some degree of sedation fol- visual motor disturbances for up to 7 hours after the
lowing the initial period of BZ use, but this sedation medication was ingested (Gitlow, 2007), a finding that
will pass as the individual’s body adjusts to the medica- might account for the observation that younger adults
tion (Ballenger, 1995; Stevens & Pollack, 2005). Exces- who use a benzodiazepine are at increased risk for
sive sedation is uncommon unless the patient received motor vehicle accidents (Barbone et al., 1998). Fur-
a dose that was too large for him or her (Ayd et al., ther, even therapeutic doses of diazepam contribute to
1996). Advancing age is one factor that may make the prolonged reaction times in the user, increasing his
individual more susceptible to the phenomenon of or her risk for motor vehicle accidents by up to 500%
benzodiazepine-induced oversedation (Ashton, 1994; (Gitlow, 2007).
Ayd, 1994). Because of an age-related decline in blood
flow to the liver and kidneys, elderly patients often re- Neuroadaptation to Benzodiazepines:
quire more time to biotransform and/or excrete many
Abuse of and Addiction to These Agents
drugs than do younger adults (Bleidt & Moss, 1989).
This might contribute to oversedation or in some cases, Within a few years of the time benzodiazepines were
a state of paradoxical excitement in older patients. To il- introduced, reports of abuse and addiction began to sur-
lustrate this process, consider that an elderly patient face. Although they were introduced as nonaddicting
might require three times as long to fully biotransform a agents, clinical evidence suggests that most patients will
dose of diazepam or chlordiazepoxide as would a young experience a discontinuance syndrome after using these
adult (Cohen, 1989). If a benzodiazepine is required in medications at recommended dosage levels for just a
an older individual, physicians tend to rely on lo- few months (O’Brien, 2005; Smith & Wesson, 2004).
razepam or oxazepam because these compounds have This is because continual use at recommended dosage
a shorter “half-life” and are more easily biotransformed levels will cause the patient’s nervous system to go
through a process of neuroadaptation8 (O’Brien, 2005, At best, there is only limited evidence that BZs
2006; Sellers et al., 1993). might be used safely with individuals with substance
Thus, when the patient abruptly discontinues a ben- use problems (Sattar & Bhatia, 2003). Clark, Xie, and
zodiazepine after an extended period of use, he or she Brunette (2004) found, for example, that while BZs are
will experience a rebound or “discontinuance” syn- often used as an adjunct to the treatment of severe men-
drome. The period of time necessary to trigger a BZ distal illness, their use did not improve clinical outcomes
continuance syndrome varies from person to person but and persons with a substance use disorder were likely to
might develop after just days to weeks of regular use abuse them. For this reason these medications should
(Miller & Gold, 1991b). By itself, the rebound or dis- be used with individuals recovering from a substance
continuance syndrome “is not sufficient to define drug- use disorder only as a last resort, after alternative treat-
taking behavior as dependent” (Sellers et al., 1993, p. 65). ments have proven ineffective (Ciraulo & Nace, 2000;
Rather, it is simply a natural process by which the body Seppala, 2004; Sommer, 2005). Further, it is recom-
adjusts to the sudden absence of the benzodiazepine, as mended that if BZs must be used, physicians use
happens whenever any medication is discontinued Clonopin, which has a lower abuse potential than
(O’Brien, 2005). short-acting BZs and that they place special controls on
It is not clear how many patients will develop a dis- the amount of drug dispensed to the patient at any time
continuation syndrome. Ashton (1994) suggested that (Seppala, 2004).
approximately 35% of patients who take a benzodi- Fully 80% of benzodiazepine abuse is seen in
azepine continuously for 4 or more weeks will experi- people with a pattern of polydrug abuse (Longo, Parran,
ence this syndrome. In most cases when the BZs are Johnson, & Kinsey, 2000; Sattar & Bhatia, 2003). Poly-
used at normal dosage levels for less than 4 months, the drug abuse seems to take place to (a) enhance the
risk of a patient’s becoming habituated to a benzodi- effects of other compounds, (b) control some of the un-
azepine and thus being at risk for a discontinuance syn- wanted side effects of the primary drug of abuse, or (c)
drome are virtually nonexistent (Blair & Ramones, help the individual withdraw from the primary drug of
1996). Even so, the Royal College of Psychiatrists in abuse (Longo et al., 2000). Only a small percentage of
Great Britain now recommends that the BZs not be abusers report experiencing a sense of BZ-induced eu-
used continuously for longer than 4 weeks (Gitlow, phoria, which is consistent with the observation that
2007). the abuse potential of BZs is quite low. The exact
Patients taking high doses of benzodiazepines, or mechanism by which BZs induce a sense of euphoria
those individuals who abuse the BZs at high dosage in these people is not known (Ciraulo et al., 2005).
levels, are at risk for developing a sedative-hypnotic Abusers seem to prefer the shorter-acting BZs such as
withdrawal syndrome when they discontinue the drug lorazepam or alprazolam (Dubovsky, 2005; Longo &
(Smith & Wesson, 2004). This is an extreme form of the Johnson, 2000; Walker, 1996), although there is evidence
discontinuance syndrome noted in the last paragraphs, that the long-acting benzodiazepine clonazepam also
and without timely medical intervention it might in- has some abuse potential that is exploited by illicit drug
clude such symptoms as anxiety, tremors, anorexia, users (Longo & Johnson, 2000).
nightmares, insomnia, nausea, vomiting, postural hy- Even when the medications were used as prescribed,
potension, fatigue, seizures, delirium, and possibly death withdrawal from the BZs after extended use can be quite
(Ciraulo et al., 2005; Smith & Wesson, 2004). difficult. In such cases, a gradual “taper” in the individ-
The abuse potential of the BZs is viewed as being ual’s daily dosage over 8–12 weeks, if not longer, might
quite low. But 5%–10% of those who do abuse the med- be necessary to minimize withdrawal distress (Miller &
ication will become dependent on it (Schuckit, 2006). Gold, 1998). To complicate the withdrawal process,
Patients who are recovering from any substance use dis- many patients experience rebound anxiety symptoms
order are at increased risk for the reactivation of their when their daily dosage levels reach 10%–25% of their
addiction if they receive a benzodiazepine for medical original daily dose (Wesson & Smith, 2005). To combat
reasons, as evidenced by the observation that approxi- these anxiety symptoms and increase the individual’s
mately 25% of recovering alcoholics relapse after receiv- chances of success, Wesson and Smith recommended
ing a prescription for a benzodiazepine (Fricchione, the use of mood stabilizing agents such as carba-
2004; Gitlow, 2007; Sattar & Bhatia, 2003). mazepine or valproic acid during the withdrawal
process. Winegarden (2001) suggested that Seroquel
8See Glossary. (quetiapine fumarate) might provide adequate control
104 Chapter Ten
of the patient’s anxiety while he or she is being with- chemicals is thought to lower the individual’s inhibi-
drawn from BZs. tions to the point that he or she is unable to control
Factors influencing the benzodiazepine withdrawal anger that would have otherwise been repressed.
process. The severity of BZ withdrawal was dependent Although the BZs are very good at the short-term
on five different “drug treatment” factors plus several control of anxiety, antidepressant medications such as
“patient factors” (Rickels, Schweizer, Case, & Greenblatt imipramine or paroxetine are more effective than BZs
1990): (a) the total daily dose of BZs being used, (b) the after 8 weeks of continual use (Fricchione, 2004). One
time span over which BZs were used, (c) the half-life of benzodiazepine, alprazolam, is marketed as an antianx-
the benzodiazepine being used (short half-life BZs tend iety agent, but there is evidence to suggest that its dura-
to produce more withdrawal symptoms than do long tion of effect is too short to provide optimal control of
half-life BZs), (d) the potency of the benzodiazepine anxiety (Bashir & Swartz, 2002). Further, some patients
being used, and (e) the rate of withdrawal (gradual, ta- may develop alprazolam-induced anxiety according to
pered withdrawal, or abruptly stopped). Bashir and Swartz, a previously unreported side effect
Some of the patient factors that influence the with- that might contribute to long-term dependence on al-
drawal from BZs include (a) the patient’s premorbid per- prazolam as the patient takes more and more medication
sonality structure, (b) expectations for the withdrawal in an attempt to avoid what is, in effect, drug-induced
process, and (c) individual differences in the neurobio- anxiety.
logical structures within the brain thought to be involved The benzodiazepine Dalmane (flurazepam) fre-
in the withdrawal process. Interactions between these quently causes confusion and oversedation, especially in
two sets of factors probably determine the severity of the the elderly. Dalmane (flurazepam) was developed as a
withdrawal process, according to Rickels et al. (1990). treatment for insomnia. One of its metabolites of flu-
Thus, for the person who is addicted to these medica- razepam, desalkyflurazepam, might have a half-life of be-
tions, withdrawal can be a complex, difficult process. tween 40 and 280 hours depending on the individual’s
biochemistry (Doghramji, 2003). Thus, the effects of a
single dose might last for up to 12 days in some patients.
Complications Caused by Benzodiazepine
Obviously, with such an extended half-life, if the person
Use at Normal Dosage Levels
used flurazepam for even a few days he or she might de-
The BZs are not perfect drugs. For example, the process velop a reservoir of unmetabolized medication that
of neuroadaptation limits the applicability of the BZs would result in significant levels of CNS depression for
for controlling seizures to short-term seizure control some time after the last dose of the drug. Further, if the
(Morton & Santos, 1989). BZs may cause excessive user should ingest alcohol or possibly even an over-the-
sedation even at normal dosage levels, especially counter cold remedy before the flurazepam was fully
early in the treatment process, with older patient(s), biotransformed, the unmetabolized drug could combine
or in persons with significant levels of liver damage. It with the depressant effects of the alcohol or cold remedy
is unfortunate that the elderly are most likely to expe- to produce serious levels of CNS depression.
rience excessive sedation because two-thirds of those Because alcohol is a CNS depressant that impacts
who receive prescriptions for BZs are above the age of the action of a calcium channel in the wall of a neuron
60 (Ayd, 1994). also affected by BZs, cross-tolerance between the BZs
Some of the known side effects of the BZs include and alcohol is common (O’Brien, 2006). When used
hallucinations, a feeling of euphoria, irritability, tachy- concurrently, the BZs will potentiate the effects of
cardia, sweating, and disinhibition (Hobbs et al., 1995). other CNS depressants such as antihistamines, alcohol,
Even when used at normal dosage levels, BZs may oc- or narcotic analgesics, presenting a danger of overseda-
casionally bring about a degree of irritability, hostility, tion or even death9 (Ciraulo, Shader, Greenblatt &
rage, or outright aggression, called a paradoxical rage Creelman, 2006). At normal dosage levels, many of the
reaction (Drummer & Odell, 2001; Hobbs et al., 1995; benzodazepines have been found to interfere with nor-
Walker, 1996). This paradoxical rage reaction appears mal sexual function (Finger, Lund, & Slagel, 1997).
to be the result of the BZ-induced cortical disinhibi-
tion. A similar effect is often seen in persons who drink 9Before taking two or more medications at the same time, the patient
alcohol, thus the combination of alcohol and BZs should consult a physician, local poison control center, or pharmacist
might also cause a paradoxical rage reaction in some in- to rule out the possibility of a drug interaction among the compounds
dividuals (Beasley, 1987). The combination of the two being used.
When used at night, the BZs reduce the amount of depression (Charney et al., 2006; Drummer & Odell,
time spent in rapid eye movement (REM) sleep and 2001). Also, BZs should not be used by patients who
may cause rebound insomnia when discontinued after suffer from Alzheimer’s disease or partial obstruction
extended periods of use (Qureshi & Lee-Chiong, of the airway while asleep as they might potentiate
2004). The phenomenon of rebound insomnia follow- preexisting sleep breathing problems (Charney et al.,
ing treatment with a benzodiazepine has not been stud- 2006).
ied in detail (Doghramji, 2003). In theory, discontinuing In rare cases, therapeutic doses of a benzodi-
a benzodiazepine following an extended period of use azepine can cause a depressive reaction in the patient
might produce symptoms that mimic the anxiety or (Drummer & Odell, 2001; Miller & Adams, 2006). The
sleep disorder for which the patient originally started to exact mechanism is not clear at this time. To further
use the medication (Gitlow, 2007; Miller & Gold, complicate matters, benzodiazepine use might actually
1991b). The danger is that the patient might begin to contribute to thoughts of suicide in the user (Ashton,
take BZs again in the mistaken belief that the with- 1994; Drummer & Odell, 2001; Juergens, 1993). Al-
drawal symptoms indicated that the original problem though it is not possible to list every reported side effect
still existed. of the BZs, the above list should clearly illustrate that
Although the change might be so slight as to escape these medications are both extremely potent and have a
notice by the patient, when used at normal dosage significant potential to cause harm to the user.
levels BZs interfere with normal memory function Drug interactions involving the BZs. The absorption
(Ciraulo et al., 2005; Gitlow, 2007). This drug-induced of an oral benzodiazepine is slowed by the concurrent
anterograde amnesia10 is more pronounced at higher use of over-the-counter antacids, thus reducing its anxi-
dosage levels of a BZ or when the benzodiazepine is olytic effect (Raj & Sheehan, 2004). There have been a
used by an older person. Indeed, fully 10% of older pa- “few ancedotal case reports” (Ciraulo et al., 2006,
tients referred for evaluation of a memory impairment p. 267) of patients who have suffered adverse effects from
suffer from drug-induced memory problems, with BZs the use of BZs while taking lithium. Ciraulo et al. re-
being the most common cause of such problems in the viewed a single case report of a patient who suffered
older person (Curran et al., 2003). Benzodiazepine- profound hypothermia from the combined use of
related memory problems appear to be similar to the lithium and diazepam. In this case, lithium was impli-
alcohol-induced blackout (Juergens, 1993) and last for cated as the agent that caused the individual to suffer a
the duration of the drug’s effects on the user (Drummer & progressive loss of body temperature. Further, the au-
Odell, 2001). thors noted that diazepam and oxazepam appear to
Even at recommended dosage levels, and most cer- cause increased levels of depression in patients who are
tainly at above-normal dosages, the BZs might impair also taking lithium. The reason for this increased level
the psychomotor skills necessary to safely operate me- of depression in patients taking BZs and lithium is not
chanical devices such as power tools or motor known at this time.
vehicles. For example, the individual’s risk of being in- Patients who are on Antabuse (disulfiram) should
volved in a motor vehicle accident was found to be use BZs with caution since disulfiram reduces the
50% higher after a single dose of diazepam (Drummer speed at which the body can metabolize benzodi-
& Odell, 2001). These drug-induced psychomotor co- azepines such as diazepam and chlordiazepoxide
ordination problems might persist for several days and (DeVane & Nemeroff, 2002). When a patient must use
are more common after the initial use of a benzodi- both medications concurrently, Zito (1994) recom-
azepine (Drummer & Odell, 2001; Woods, Katz, & mended that oxazepam or lorazepam be used as these
Winger 1988). Further, rare cases of benzodiazepine- do not produce any biologically active metabolites.
induced respiratory depression have been identified at Surprisingly, grapefruit juice has been found the alter
normal therapeutic dosage levels. Patients with pul- the P-450 metabolic pathway in the liver, slowing the
monary disease appear especially vulnerable to this ef- rate of benzodiazepine biotransformation (Charney,
fect, and for this reason patients who suffer from sleep Mihis, & Harris, 2001).
apnea, chronic lung disease, or other sleep-related In some patients taking Halcion (triazolam), the
breathing disorders should not use this class of medica- levels of this drug in their blood might be almost
tions in order to avoid serious, possibly fatal, respiratory double when they are also taking the antibiotic erythro-
mycin (sold under a variety of brand names) (DeVane &
10See Glossary. Nemeroff, 2002; Graedon & Graedon, 1995). Further,
106 Chapter Ten
probenecid might slow the biotransformation of the out the possibility of an adverse interaction between the
benzodiazepine lorazepam, thus causing excess seda- medications being used.
tion in some patients (Sands, Creelman, Ciraulo,
Greenblatt, & Shader, 1995).
The issue of benzodiazepine interactions with many
Subjective Experience
antipsychotic medications has been well documented, of Benzodiazepine Use
with the BZs causing an increase in the blood plasma When used as an antianxiety agent at normal dosage
levels of antipsychotic medications such as haloperidol levels, BZs induce a gentle state of relaxation in the
and fluphenazine by competing with these compounds user. In addition to their effects on the cortex, the BZs
for access to the liver’s biotransformation enzymes have an effect on the spinal cord, which contributes to
(Ciraulo et al., 2006). Because the concurrent use of BZs muscle relaxation through some unknown mechanism
and digoxin can cause blood levels of the latter drug to (Ballenger, 1995). When used in the treatment of in-
rise, possibly to dangerous levels, patients with heart con- somnia, these drugs initially reduce the sleep latency
ditions who are taking both medications should have fre- period, and users report a sense of deep and refreshing
quent blood tests to check their digoxin levels (Graedon & sleep. However, they interfere with the normal sleep
Graedon, 1995). Further, the use of BZs with medica- cycle, almost suppressing stages III and IV/REM sleep
tions such as anticonvulsants (e.g., phenytoin, mepheny- for reasons that are not clear (Ballenger, 1995). When
toin, and ethotoin), the antidepressant fluoxetine, or they are used for extended periods of time as hypnotics,
medications for the control of blood pressure such as pro- the user is prone to experience REM rebound after
pranolol, and metopropolol might cause higher than stopping their use (Hobbs et al., 1995; Qureshi & Lee-
normal blood levels of such BZs as diazepam (DeVane & Chiong, 2004).11 In some cases REM rebound was ex-
Nemeroff, 2002; Graedon & Graedon, 1995). Patients perienced after as little as 1–2 weeks (“Sleeping Pills
using St. John’s wort may experience more anxiety, as and Antianxiety Drugs,” 1988; Tyrer, 1993). To help the
this herbal medication lowers the blood level of alprazo- individual return to normal sleep, melatonin might be
lam (DeVane & Nemeroff, 2002). Thus, it is unwise for a used to mitigate the symptoms of benzodiazepine with-
patient to use these medications at the same time except drawal (Garfinkel, Zisapel, Wainstein, & Laudon, 1999;
under a physician’s supervision. Pettit, 2000).
Women who are using oral contraceptives should In addition to possibly experiencing REM rebound,
discuss their use of a BZ with a physician prior to taking patients who have used a benzodiazepine for daytime
one of these medications. Zito (1994) noted that oral relief from anxiety have reported symptoms such as
contraceptives will reduce the rate at which the body anxiety, agitation, tremor, fatigue, difficulty concentrat-
metabolizes some BZs, thus making it necessary to re- ing, headache, nausea, gastrointestinal upset, a sense of
duce the dose of these medications. Patients who are paranoia, depersonalization, and impaired memory
taking antitubercular medications such as isoniazid after stopping the drug (Graedon & Graedon, 1991).
might need to adjust their benzodiazepine dosage Some people have experienced rebound insomnia
(Zito, 1994). for as long as 3–21 days after the last benzodiazepine
Because of the possibility of excessive sedation, the use (Graedon & Graedon, 1991). The BZs with shorter
BZs should never be intermixed with other compounds half-lives are most likely to cause rebound symptoms
classified as CNS depressants except under the supervi- (Ayd, 1994; O’Donovan & McGuffin, 1993; Rosenbaum,
sion of a physician. One medication that is potentially 1990). Such rebound symptoms might be common
dangerous when mixed with a benzodiazepine is when the patient experiences an abrupt drop in med-
buprenorphine, a CNS depressant (Smith & Wesson, ication blood levels. For example, alprazolam has a
2004). Individuals taking a benzodiazepine should dis- short half-life, and the blood levels drop rather rapidly just
continue their use of the herbal medicine kava (Cupp, before it is time for the next dose. It is during this period of
1999). The combined effects of these two classes of time that the individual is most likely to experience an in-
compounds may result in excessive, if not dangerous, crease in anxiety levels. This process results in a phenom-
levels of sedation. While this list is not exhaustive, it enon known as “clock watching” (Raj & Sheehan, 2004)
does illustrate the potential for an interaction between by the patient, who waits with increasing anxiety until
the BZs and a number of other medications. A physi- the time comes for his or her next dose.
cian or pharmacist should always be consulted prior to
taking two or more medications at the same time to rule 11See Glossary.
To combat rebound anxiety, it has been suggested possible drug-induced withdrawal psychosis, paranoid
that a long-acting benzodiazepine such as clonazepam delusions, depression, agitation/manic behaviors, feelings
be substituted for the shorter-acting drug (Rosenbaum, of depersonalization/derealization, formication, halluci-
1990). The transition between alprazolam and clon- nations, abdominal pain, constipation, chest pain, incon-
azepam takes about 1 week, after which time the tinence, and loss of libido (Miller & Adams, 2006; Brown
patient should be taking only clonazepam. This med- & Stoudemire, 1998).
ication may then be gradually withdrawn, resulting in a As hypnotics, BZs are useful for short periods of
slower decline in blood levels. However, the patient time. However, the process of neuroadaptation limits
still should be warned that there will be some rebound the effectiveness of the BZs as sleep-inducing (or hyp-
anxiety symptoms. Although the patient might believe notic) medications to just a few days (Ashton, 1994) to a
otherwise, these symptoms are not a sign that the origi- week (Carvey, 1998) to 2–4 weeks (American Psychi-
nal anxiety is still present. Rather, they are an indica- atric Association, 1990; Ayd, 1994) of continual use.
tion that the body is adjusting to the gradual reduction Knowing this, physicians should prescribe the BZs
in clonazepam blood levels. only for the short-term treatment of insomnia (Taylor,
McCracken, Wilson, & Copeland, 1998). Surprisingly,
many users continue to use BZs for anxiety control or as
Long-Term Consequences of Chronic a sleep aid for months or even years. In the latter case
Benzodiazepine Use the person might be taking these medications as part of
Although the benzodiazepines were originally intro- the psychological ritual he or she follows to ensure
duced as safe and nonaddicting substitutes for the bar- proper sleep more than for a pharmacological effect
biturates in the 1960s, physicians in the 21st century from the medication (Carvey, 1998).
have realized that the benefits of the BZs must be Some benzodiazepine abusers have been known
weighed against their potential dangers. For example, it to increase their daily intake to dangerous levels in an
is now generally accepted that the BZs present an abuse attempt to overcome their growing tolerance of the
potential, although this varies from one compound in drug. For example, although 5–10 mg of diazepam
this class to the next. BZs such as diazepam, lorazepam, might cause sedation in initial users, some abusers
alprazolam, and triazolam appear to have a higher gradually build their daily intake level up to 1,000
abuse potential than other compounds in this class, mg/day as their tolerance to the BZs develops
but all BZs have some abuse potential (Ciraulo & (O’Brien, 2006). Such dosage levels would be dan-
Sarid-Segal, 2005). gerous, possibly fatal, in the drug-naive user and re-
Benzodiazepine abusers fall into one of two groups quire gradual detoxification to slowly wean the abuser
(O’Brien, 2005, 2001): (1) individuals who abuse these from the medication safely.
compounds to bring about a sense of euphoria or con- All the CNS depressants, including the BZs, are ca-
trol the withdrawal experience brought on by abuse of pable of producing a toxic psychosis, especially in overdose
other compounds, and (2) those who are prescribed a situations. This condition might also be called an organic
benzodiazepine and then begin to abuse their prescrip- brain syndrome by some professionals. Some of the symp-
tion by taking the medication for longer and/or at a toms seen with a benzodiazepine-related toxic psychosis
higher dosage level than originally prescribed. Individ- include visual and auditory hallucinations, paranoid delu-
uals who fall in the first group are usually polydrug sions, as well as hyperthermia, delirium, convulsions, and
abusers; for this reason, these medications should rarely possible death (Ciraulo & Sarid-Segal, 2005). With proper
if ever be administered on a chronic basis to patients treatment, this drug-induced psychosis will usually resolve
with chemical use disorders (Jones, Knutson, & Haines, in 2 to 14 days (Miller & Gold, 1991b). Because of the
2003; O’Brien, 2001). potential for seizures during benzodiazepine withdrawal,
Following long-term use/abuse, the BZs are capable of medical supervision is imperative.
bringing about a state of pharmacological dependence There is a small and controversial body of evidence
and a characteristic withdrawal syndrome (O’Brien, suggesting that individuals who use BZs for extended
2005). The benzodiazepine withdrawal process closely re- periods of time might experience transient changes in
sembles the alcohol withdrawal syndrome (Filley, 2004) cognition, which may not resolve with abstinence
and will include symptoms such as anxiety, insomnia, (Stewart, 2005). Thus, the benefits of benzodiazepine
dizziness, nausea, vomiting, muscle weakness, tremor, treatment should be weighed against their potential for
confusion, convulsions (seizures), irritability, sweating, a harm to the user.
108 Chapter Ten
BZs as a substitute for other drugs of abuse. Just as buspirone was quite limited, researchers found that it
physicians use BZs to control the symptoms of alcohol was approximately as effective in controlling anxiety
withdrawal, so alcohol abusers often abuse these med- as were the BZs (Drummer & Odell, 2001). In addi-
ications to control their alcohol withdrawal distress. For tion, buspirone was found to cause sedation or fatigue
example, several alcohol-dependent patients have re- for the user only rarely (Rosenbaum & Gelenberg,
ported to the author of this text that 10 mg of diazepam 1991; Sussman, 1994), and there was no evidence of po-
has the same subjective effect for them as 3–4 stiff tentiation between buspirone and select BZs, or alcohol
drinks. Further, some alcohol-dependent persons are and buspirone (Drummer & Odell, 2001; Feighner,
able to hide their alcohol use from co-workers by substi- 1987; Manfredi et al., 1991).12
tuting diazepam for alcohol during the workday. Di- The advantages of buspirone over the BZs are more
azepam, often taken for an anxiety disorder (which is to than outweighed by the fact that the patient must take
say a misdiagnosed alcohol-withdrawal syndrome symp- this medication for up to 2 weeks before it becomes ef-
tom), prevents the individual from demonstrating the fective (Doble, Martin, & Nutt, 2004). Some of the
symptoms of the alcohol withdrawal process during the more common side effects of buspirone include gas-
workday, so co-workers don’t smell alcohol on the user’s trointestinal problems, drowsiness, decreased concen-
breath or see him or her drink. tration, dizziness, agitation, headache, feelings of light-
Finally, research has shown that up to 90% of pa- headedness, nervousness, diarrhea, excitement, sweating/
tients in methadone maintenance programs will abuse clamminess, nausea, depression, nasal congestion, and
BZs, often at high dosage levels (Sattel & Bhatia, 2003). rarely, feelings of fatigue (Cole & Yonkers, 1995;
Patients will take a single, massive dose of a benzodi- Graedon & Graedon, 1991; Hudziak & Waterman,
azepine (the equivalent of 100–300 mg of diazepam) be- 2005; Manfredi et al., 1991; Pagliaro & Pagliaro, 1998).
tween 30–120 minutes after ingesting their methadone in Buspirone has also been found to cause decreased
order to “boost” the effect of the latter drug (Drummer & sexual desire in some users, as well as sexual perfor-
Odell, 2001; O’Brien, 2005, 2006). There is evidence mance problems in some men (Finger et al., 1997).
that the narcotic buprenorphine may, when mixed with In contrast to the benzodiazepine family of drugs,
BZs, offer the user less of a high, thus reducing the in- buspirone has no significant anticonvulsant action. It
centive for the narcotics user to try to mix medications also lacks the muscle relaxant effects of the benzodi-
(Sellers et al., 1993). azepines (Eison & Temple, 1987). Indeed, buspirone
has been found to have little value in cases of anxiety
that involve insomnia, which is a significant proportion
Buspirone of anxiety cases (Manfredi et al., 1991). It has some
In 1986, a new medication, BuSpar (buspirone), was in- value in controlling the symptoms of general anxiety
troduced as an antianxiety agent. Buspirone is a member disorder but does not seem to control the discomfort of
of a new class of medications known as the azapirones, acute anxiety/panic attacks (Hudziak & Waterman,
which are chemically different from the BZs. Buspirone 2005).
was found during a search by pharmaceutical companies On the positive side, buspirone is effective in the
for antipsychotic drugs that did not have the harsh side treatment of many patients who suffer from an anxiety
effects of the phenothiazines or similar chemicals disorder with a depressive component (Cohn, Wilcox,
(Sussman, 1994). While the antipsychotic effect of Bowden, Fisher, & Rodos, 1992). At high doses, bus-
pirone functions as an antidepressant in some cases,
and it can also enhance the effects of other antidepres-
TABLE 10.2 Novel Anxiolytic and Hypnotic Compounds sant medications (Hudziak & Waterman, 2005). In ad-
dition, buspirone has been of value in the treatment of
Average half-life
obsessive-compulsive disorder and social phobias, and
Generic name (hours)
as an adjunct to the treatment of posttraumatic stress
Buspirone 1.0–10.0 disorder (Sussman, 1994). It does not appear useful in
treating alcohol or benzodiazepine withdrawal distress
Ramelteon 1.0–2.6
Zaleplon 1.0 12
This is not, however, a suggestion that the user try to use alcohol
Zolpidem 1.5–2.4 and buspirone at the same time. The author does not recommend the
use of alcohol with any prescription medication.
(Hudziak & Waterman, 2005; Rickels, Schweizer, each day, where the half-life of BZs like diazepam allow
Csanalosi, Case, & Chung, 1988). Physicians who treat the drug to be used only 1–2 times a day (Schweizer &
geriatric patients have found that buspirone is effective Rickels, 1994). Finally, unlike many other sedating
in controlling aggression in anxious, confused older chemicals, there does not appear to be any degree of
adults without exacerbating psychomotor stability prob- cross-tolerance between buspirone and the BZs, alco-
lems that can contribute to the patient’s falling (Ayd hol, the barbiturates, or meprobamate (Sussman,
et al., 1996). However, when used with older adults it 1994).
should be given in smaller doses because of age-related Buspirone’s abuse potential is quite limited (Smith
changes in how fast the drug is removed from the circu- & Wesson, 2004). There is no evidence of a significant
lation (Drummer & Odell, 2001). It has also been withdrawal syndrome similar to that seen after pro-
found to reduce the frequency of self-abusive behaviors tracted periods of benzodiazepine use/abuse (Anton,
(SAB) in mentally retarded subjects (Ayd et al., 1996). 1994; Sussman, 1994). Further, unlike BZs, there is no
There also is limited evidence that buspirone might evidence that buspirone has an adverse impact on
be useful as an adjunct to cigarette cessation for smok- memory (Rickels, Giesecke, & Geller, 1987). There is
ers who have some form of an anxiety disorder (Covey evidence that patients currently taking a benzodi-
et al., 2000). azepine might be slightly less responsive to buspirone
while they are taking both medications (Hudziak &
The Pharmacology of Buspirone Waterman, 2005). But unlike the BZs, there is no evi-
The mechanism of action for buspirone is different dence of tolerance to buspirone’s effects, nor any
from that of the BZs (Eison & Temple, 1987). Where evidence of physical dependence or a withdrawal
the BZs tend to bind to receptor sites that utilize the syndrome from buspirone when the medication is used
neurotransmitter GABA, buspirone functions as a par- as directed for short periods of time (Rickels et al.,
tial agonist at one of the subtypes of the serotonin fam- 1988).
ily of receptor sites known as the 5-HT1A site (Ramadan One very rare complication of buspirone use is the
et al., 2006). These receptor sites are located in the hip- development of a drug-induced neurological condi-
pocampus region of the brain, a different area from tion known as the serotonin syndrome, especially when
where the BZs exert their effect (Manfredi et al., buspirone is used with the antidepressants bloxetine or
1991). fluvoxamine (Sternbach, 2003). Although the sero-
Buspirone has the effect of balancing serotonin tonin syndrome might develop as long as 24 hours after
levels in the brain. If there is a deficit of serotonin, as the patient ingests a medication that affects the sero-
there is in depressive disorders, buspirone seems to tonin neurotransmitter system, in 50% of the cases the
stimulate its production (Anton, 1994; Sussman, 1994). patient developed the syndrome within 2 hours of start-
If there is an excess of serotonin, as there appears to be ing the medication (Mills, 1995).
in many forms of anxiety states, buspirone seems to Drug interactions involving buspirone. Buspirone is
lower the serotonin level. Unfortunately it may require known to interact with a class of antidepressant medica-
3–4 weeks before any significant improvement in the tions known as the monoamine oxidase inhibitors
patient’s status is noticed, and the user might have to (MAOIs, or MAO inhibitors). It is recommended that
take high doses of buspirone before achieving any relief patients discontinue the use of MAOIs 2 weeks prior to
from anxiety (Renner, 2001). Patients with addictive initiating therapy with buspirone to avoid the danger of
disorders tend to want instant solutions to their prob- hypertensive episodes brought on by the combination
lems, and thus dislike buspirone because it takes so of these two compounds (Ramadan et al., 2006). Bus-
long to become effective. pirone should also not be used in patients who are
Depending on the individual’s biochemistry, the taking medications such as diltiazem, verapamil, or
peak blood levels of buspirone are achieved in 60–90 intraconazole, as these medications will block the bio-
minutes, and the half-life is 2–11 hours (Cole & transformation of buspirone and cause the buspirone
Yonkers, 1995; Hudziak & Waterman, 2005). The ab- blood levels to rise (Ramadan et al., 2006). Patients who
sorption of buspirone is delayed if the individual takes it are taking buspirone should not use antibiotics such as
with food. Further, the compound is extensively bio- erythromycin or clarithromycin without consulting their
transformed as a result of “first-pass metabolism” physician, as these medications can cause abnormally
(Hudziak & Waterman, 2005). The short half-life re- high blood levels of buspirone by blocking its biotransfor-
quires that the individual take 3–4 doses of buspirone mation (Venkatakrishnan, Shader, & Greenblatt, 2006).
110 Chapter Ten
While this list does not include all possible drug/drug in- single dose of zolpidem is biotransformed by the liver
teractions involving buspirone, it does illustrate that the into inactive metabolites before excretion by the kid-
user should consult a physician or pharmacist before tak- neys. There is little evidence of neuroadaptation to
ing two or more medications at the same time to avoid zolpidem’s hypnotic effects when the drug is used at
the danger of drug interactions. normal dosage levels, even after it has been used for as
It is unfortunate, but the manufacturer’s claim that long as 1 year (Folks & Burke, 1998; Holm & Goa,
buspirone offers many advantages over the BZs in the 2000). However, Schuckit (2006) suggested that at least
treatment of anxiety states has not been totally fulfilled. a limited degree of neuroadaptation does develop to the
Indeed, Rosenbaum and Gelenberg (1991) cautioned effects of this medication if it is used each night for ap-
that “many clinicians and patients have found bus- proximately 2 weeks, and there are rare reports of pa-
pirone to be a generally disappointing alternative to tients who have become tolerant to the hypnotic effects
BZs” (p. 200). In spite of this note, Rosenbaum and of zolpidem after using this medication at very high
Gelenberg recommended a trial of buspirone for “per- dosage levels for a period of several years (Holm & Goa,
sistently anxious patients” (p. 200). Further, at this 2000).
time, Buspirone would seem to be the drug of choice in Unlike the BZs or barbiturates, zolpidem causes
the treatment of anxiety states in the addiction-prone only a minor reduction in REM sleep patterns at nor-
individual. mal dosage levels (Hobbs et al., 1995; Schuckit, 2006).
Further, it does not interfere with the other stages of
sleep, allowing for a more natural and restful night’s
Zolpidem sleep by the patient (Doble et al., 2004; Hartmann,
Zolpidem is a member of the benzodiazepine receptor 1995). When used as prescribed, the most common ad-
agonist (BRA)13 class of medications and was approved verse effects include nightmares, headaches, gastroin-
for use in the United States in 1993 (Hobbs et al., 1995; testinal upset, agitation, and some daytime drowsiness
“Insomnia in Later Life,” 2006). In the United States, it (Hartmann, 1995). There have also been a few isolated
is sold as an orally administered hypnotic under the cases of a zolpidem-induced hallucinations/psychosis
brand name of Ambien, and is marketed as a short-term (Ayd, 1994; Ayd et al., 1996) and rebound insomnia
(defined as less than 4 weeks) treatment of insomnia, when the medication is discontinued after extended pe-
available only by a physician’s prescription. riods of use (Gitlow, 2007; Schuckit, 2006). Side effects
Pharmacology of zolpidem. Technically, zolpidem is are more often encountered at higher dosage levels,
classified as a member of the imidazopryidine family of and for this reason the recommended dosage level of
compounds. As discussed earlier, the BZs bind to re- zolpidem should not exceed 10 mg/day (Hold & Goa,
ceptor sites at numerous places in the brain. Zolpidem 2000; Merlotti et al., 1989).
is more selective, binding to only a subset of the BZ re- Zolpidem has been found to cause some cognitive
ceptor sites. For this reason, it is also classified as a ben- performance problems similar to those seen with the
zodiazepine receptor agonist (BRA). It is more selective BZs, although this medication appears less likely to
than the BZs in terms of binding sites and has only a cause memory impairment than the older hypnotics
minor anticonvulsant effect because of this. Indeed, re- (Ayd et al., 1996). Further, alcohol enhances the effects
search has demonstrated that zolpidem’s anticonvul- of zolpidem and thus should not be used by patients on
sant action is seen only at doses significantly above this medication because of the potentiation effect
those that bring about sleep in the user (Doble et al., (Folks & Burke, 1998). Zolpidem is contraindicated in
2004). The selective method of action is also why zolpi- patients with obstructive sleep apnea as it increases the
dem has minimal to no effect on muscle injuries. duration and frequency of apnea episodes (Holm &
Following a single oral dose, peak blood levels of Goa, 2000).
zolpidem are achieved in 2–3 hours (Dubovsky, 2005; Effects of zolpidem at above-normal dosage levels. At
Schuckit, 2006). The elimination half-life is between dosage levels of 20 mg/day or above, zolpidem has been
2–3 hours in the normal adult (Dubovsky, 2005) and found to significantly reduce REM sleep, and there are
slightly longer in geriatric patients (Charney et al., reports of REM rebound after long-term use (Ciraulo
2006; Doble et al., 2004; Folks & Burke, 1998; Kryger, et al., 2005). At dosage levels of 50 mg/day, volunteers
Steljes, Pouliot, Neufeld, & Odynski, 1991). Most of a who received zolpidem reported such symptoms as vi-
sual perceptual disturbances, ataxia, dizziness, nau-
13See Glossary. sea, and/or vomiting. Patients who have ingested up to
40 times the maximum recommended dosage have re- feces. The time required for biotransformation is pro-
covered without significant aftereffects. It should be longed in individuals with significant levels of liver dis-
noted, however, that the effects of zolpidem will com- ease (Charney et al., 2006). In humans, the half-life of
bine with those of other CNS depressants if the patient zaleplon is estimated to be between 1 hour (Doble et al.,
has ingested more than one medication in an overdose 2004) to 1.5 hours (Dubovsky, 2005) to a high of 2 hours
attempt, and such multiple-drug overdoses might prove (Charney et al., 2006).
fatal.14 Zaleplon binds at the same brain receptor site as
Abuse potential of zolpidem. Since the time that it zolepidem (Charney et al., 2006; Walsh, Pollak, Scharf,
was introduced, evidence has emerged suggesting that Schweitzer, & Vogel, 2000). There is little evidence of
the abuse potential of zolpidem might be higher than a drug hangover effect, although it is recommended
originally thought. Ciraulo and Sarid-Segal (2005) pre- that the patient not attempt to operate machinery for
sented a summary of one case in which the individual 4 hours after taking the last dose (Danjou et al., 1999;
increased his daily dose from 5–10 mg/day to over 800 Doble et al., 2004; Walsh et al., 2000).
mg/day over time, for example. Reports of zolpidem This medication is intended for the short-term treat-
abuse appear for the most part to be limited to individu- ment of insomnia, in part because of the rapid develop-
als who have histories of sedative-hypnotic abuse ment of tolerance to its effects. Individuals who have
(Gitlow, 2007; Holm & Goa, 2000), and the abuse po- used zaleplon nightly for extended periods have re-
tential of this compound is rated at about the same level ported rebound insomnia upon its discontinuation, al-
as the benzodiazepine family of drugs (Charney et al., though this might be more common when the drug is
2001). Thus, the prescribing physician must balance the used at higher dosage levels (Dubovsky, 2005). Because
potential for abuse against the potential benefit that this of the rapid onset of sleep, users are advised to take this
medication would bring to the patient. Because of zolpi- medication just before going to sleep or after being un-
dem’s sedating effects, this drug should not be used in able to go to sleep naturally. Patients using zaleplon
persons with substance use problems, as its sedating ef- have reported such side effects as headache, rhinitis,
fects may trigger thoughts about returning to active nausea, myalgia, periods of amnesia while under the ef-
chemical use again (Jones, Knutson, & Haines, 2003). fects of this medication, dizziness, depersonalization,
drug-induced hangover, constipation, dry mouth, gout,
Zaleplon bronchitis, asthma attacks, nervousness, depression,
problems in concentration, ataxia, and insomnia.
Zaleplon is sold in the United States under the brand The abuse potential of zaleplon is similar to that of
name of Sonata. It is a member of the pyrazolpyrimi- the BZs, especially triazolam (Smith & Wesson, 2004).
dine class of pharmaceuticals, and is also a BRA (“In- When used on a regular basis for 2 weeks or more, zale-
somnia in Later Life,” 2006). It is intended for plon has been implicated as causing withdrawal symp-
short-term symptomatic treatment of insomnia. Animal toms such as muscle cramps, tremor, vomiting, and in
research suggests that zaleplon has some sedative and rare occasions seizures. Because zaleplon is a sedating
anticonvulsant effects, although it is approved only for agent, Jones, Knutson, and Haines (2003) do not rec-
use as a hypnotic in the United States (Danjou et al., ommend it for persons with substance use problems, as
1999). Zaleplon is administered orally in capsules con- its effects may trigger thoughts about returning to active
taining 5 mg, 10 mg, or 20 mg of the drug. In most cases, chemical use.
the 10 mg dose was thought to be sufficient to induce
sleep, although for individuals with low body weight, 5
mg might be more appropriate (Danjou et al., 1999). Rozerem
Once in the body, approximately 30% of the dose of Rozerem (ramelteon) was recently introduced as a hyp-
zaleplon is biotransformed by the liver, through the notic agent in the United States. It does not bind at any
first-pass metabolism process. Less than 1% of the total of the benzodiazepine or barbiturate receptors but
dose is excreted in the urine unchanged, with the ma- binds at the receptor site used by a naturally occurring
jority of the medication being biotransformed by the neurotransmitter known as melatonin (Winkelman,
liver into less active compounds that are eventually 2006). Melatonin is thought to be involved in the main-
eliminated from the body either in the urine or the tenance of the normal sleep/wake cycle of the individ-
14
As stated before, any suspected drug overdose should immediately ual, with higher levels of melatonin being found in the
be assessed and treated by a physician. early phases of normal sleep.
112 Chapter Ten
Ramelteon is rapidly absorbed from the gastrointesti- Because it is not manufactured as a pharmaceutical
nal tract, with peak blood levels occurring approxi- in the United States, there was little abuse of fluni-
mately 45 minutes after the dose was administered trazepam by U.S. citizens prior to the mid-1990s. Sub-
(Neubauer, 2005; Winkelman, 2006). But the majority stance abuse rehabilitation professionals in this country
of the drug that is absorbed is subject to the first-pass had virtually no experience with Rohypnol (fluni-
metabolism process, with only about 1.8% of the dose trazepam) when people first began to bring it into this
administered actually reaching the brain (Neubauer, country. It was classified as an illegal substance by the
2005; Winkelman, 2006). The drug is biotransformed United States government in October of 1996, and in-
in the liver, and about 85% of the metabolites are ex- dividuals convicted of trafficking or distributing this
creted in the urine (Neubauer, 2005). The elimination drug may be incarcerated for up to 20 years (“Rohypnol
half-life of ramelteon is between 1–2.6 hours, and virtu- and Date Rape,” 1997).
ally all of the drug is eliminated from the body within Although it is used for medicinal purposes around
96 hours of a single dose (Neubauer, 2005). There is no the world, in the United States, Rohypnol has gained a
apparent interaction between ramelteon and the ben- reputation as a “date rape” drug (Gahlinger, 2004;
zodiazepines, according to Neubauer. Saum & Inciardi, 1997). This was because the pharma-
Because ramelteon is biotransformed in the liver, cological characteristics of flunitrazepam, especially
blood levels of the drug are somewhat higher in pa- when mixed with alcohol, could cause a state of drug-
tients who have mild to moderate liver impairment, induced amnesia that lasts 8–24 hours. To combat its
and repeated use in such patients might cause 10-fold use as a date-rape drug, the manufacturer now includes
higher blood levels after a week’s use than those a harmless compound in the tablet that will turn the
found in patients with normal liver function drink blue if added to a liquid such as alcohol (Klein &
(Neubauer, 2005). It does not seem to exacerbate Kramer, 2004). Because of this history of abuse and the
apnea problems in patients with respiratory disorders, fact that flunitrazepam is not detected on standard
although patients with severe sleep apnea and/or urine toxicology tests, the company that manufactures
chronic obstructive pulmonary disease (COPD) are Rohypnol, Hoffmann-La Roche pharmaceuticals, has
not advised to use this medication (Neubauer, 2005). instituted a program of free urine drug testing to pro-
Ramelteon appears to result in a very small hangover vide law enforcement officials with a means to detect
effect in normal subjects, according to Neubauer. fluintrazepam in the urine of suspected victims of a
Concurrent use with alcohol results in a limited po- date rape (Palmer & Edmunds, 2003).
tentiation effect15 and there has been no abuse poten- In addition to its use in date-rape situations, some
tial identified as of this time. Thus, ramelteon would drug abusers will mix Rohypnol (flunitrazepam) with
appear to be safe for patients who have SUDs, al- other compounds to enhance the effect of these com-
though the danger that its use might serve as a relapse pounds. Illicit users may also use flunitrazepam while
trigger has not been ruled out. smoking marijuana and while using alcohol (Lively,
1996). The combination of Rohypnol (flunitrazepam)
and marijuana is said to produce a sense of “floating”
Rohypnol ion the user. There are reports of abusers inhaling fluni-
Rohypnol (flunitrazepam) was first identified as being trazepam powder and of physical addiction developing
abused in the United States in the mid-1990s. It is a mem- to this substance following periods of continuous use.
ber of the benzodiazepine family of parmaceuticals, used Adolescents have also been reported to abuse fluni-
in more than 60 other countries around the world as a trazepam as an alternative to marijuana and/or LSD or
presurgical medication, a muscle relaxant, and a hyp- to achieve a state of intoxication during classes without
notic, but it is not manufactured or used as a pharmaceu- the smell of alcohol on their person (Greydanus &
tical in the United States and is classified as a Schedule IV Patel, 2003; Wesson & Smith, 2005).
compound under the Controlled Substances Act of Chemically, flunitrazepam is a derivative of the ben-
197016 (Gahlinger, 2004; Gwinnell & Adamec, 2006; zodiazepine chlordiazepoxide (Eidelberg, Neer, &
Klein & Kramer, 2004; Palmer & Edmunds, 2003). Miller, 1965) and is reportedly 10 times as powerful as
diazepam (Gahlinger, 2004; Klein & Kramer, 2004).
15This is not to suggest that ramelteon, or any other medication, When it is used as a medication, the usual method of
should be used concurrently with alcohol. administration is by mouth, in doses of 0.5–2 mg. Flu-
16See Appendix Four. nitrazepam is well absorbed from the gastrointestinal
tract, with between 80% and 90% of a single 2 mg dose Kramer, 2004). Flunitrazepam has an anticonvulsant ef-
being absorbed by the user’s body (Mattila & Larni, fect (Eidelberg et al., 1965) and is capable of bringing
1980). Following a single oral dose, the peak blood about a state of pharmacological dependence. Although
levels are reached in 30 minutes (Klein & Kramer, flunitrazepam has a wide safety margin, concurrent use
2004) to 1–2 hours (Saum & Inciardi, 1997). Once in with alcohol or other CNS depressants may increase the
the blood, 80%–90% of the flunitrazepam is briefly danger of overdose. Withdrawal from flunitrazepam is
bound to plasma proteins, but the drug is rapidly trans- potentially serious for the chronic abuser, and there
ferred from the plasma to body tissues. Because of this have been reports of withdrawal seizures taking place as
characteristic, flunitrazepam has an elimination half- late as 7 days after the last use of the drug (“Rohypnol
life that is significantly longer than its duration of effect. Use Spreading,” 1995). For this reason, patients with a
Indeed, depending upon the individual’s metabolism, history of flunitrazepam abuse should be withdrawn from
the elimination half-life can range from 15 to 66 hours this compound only under the supervision of a physician.
(Woods & Winger, 1997) while the effects last only
8–10 hours (Klein & Kramer, 2004).
Summary
During the process of biotransformation, fluni-
trazepam produces a number of different metabolites, Since their introduction in the 1960s, the benzodi-
some of which are themselves biologically active azepines have become one of the most frequently pre-
(Mattila & Larni, 1980). Less than 1% of the drug is ex- scribed medications. As a class, these drugs are the
creted unchanged. About 90% of a single dose is elimi- treatment of choice for the control of anxiety and insom-
nated by the kidneys after biotransformation, while nia as well as many other conditions. They have also be-
about 10% is eliminated in the feces. Because of this come a significant part of the drug abuse problem. Even
characteristic elimination pattern, patients in countries though many of the BZs were first introduced as “non-
where flunitrazepam is legal who have kidney disease addicting and safe” substitutes for the barbiturates, there
require modification of their dosage level, since the is evidence that they have an abuse potential similar to
main route of elimination is through the kidneys. Al- that of the barbiturate family of drugs.
though the usual pharmaceutical dose of Rohypnol A new series of pharmaceuticals, including bus-
(flunitrazepam) is less than 2 mg, illicit users will often pirone, which is sold under the brand name BuSpar, and
take 4 mg of the drug in one dose, which will begin to zolpidem were introduced in the last years of the 20th
produce sedation in 20–30 minutes. The drug’s effects century. Buspirone is the first of a new class of antianxi-
normally last for 8–12 hours. ety agents that works through a different mechanism
The effects of flunitrazepam are similar to the other than the BZs. While buspirone was introduced as nonad-
BZs, including sedation, dizziness, memory problems dicting, this claim has been challenged by at least one
and/or amnesia, ataxia, slurred speech, impaired judg- team of researchers. Zolpidem has an admitted potential
ment, mood swings, headaches, tremor, nausea, sleep, for abuse; however, research at this time suggests that this
and loss of consciousness (Calhoun, Wesson, Galloway, & abuse potential is less than the benzodiazepine most
Smith, 1996; Klein & Kramer, 2004). Like the BZs used commonly used as a hypnotic: triazolam. Researchers
in the United States, flunitrazepam is capable of caus- are actively discussing the potential benefits and liabili-
ing paradoxical rage reactions in the user (Klein & ties of these new medications at this time.
CHAPTER ELEVEN
Abuse of and Addiction to Amphetamines

and CNS Stimulants
The use of central nervous system (CNS) stimulants than a curiosity until 1930. Then, a report appeared in
dates back several thousand years. There is historical a medical journal suggesting that ephedrine was useful
evidence that gladiators in ancient Rome used CNS in treating asthma (Karch, 2002) and it quickly became
stimulants at least 2,000 years ago to help them over- the treatment of choice for this condition. The intense
come the effects of fatigue so they could fight longer demand for ephedrine soon raised concern as to
(Wadler, 1994). People still use chemicals that act as whether the demand might exceed the supply of plants
CNS stimulants to counter the effects of fatigue so they in the 1930s. The importance of this fear is discussed
can work or, in times of conflict, fight longer. later in “History of the Amphetamines.” In the United
Currently, several different families of chemicals are States, ephedrine was sold as an over-the-counter agent
classified as CNS stimulants, including cocaine, the marketed as a treatment for asthma, sinus problems,
amphetamines, amphetamine-like drugs such as Ritalin and headaches as well as a “food supplement” used to
(methylphenidate), and ephedrine. The behavioral ef- assist weight-loss programs and as an aid to athletic per-
fects of these drugs are remarkably similar (Gawin & formance. In February 2004 the Food and Drug Ad-
Ellinwood, 1988). For this reason, the amphetamine- ministration (FDA) issued a ban on the over-the-counter
like drugs will be discussed only briefly, while the am- sale of ephedrine that took effect on April 12, 2004
phetamines will be reviewed in greater detail in this (Neergaard, 2004). After that time, ephedrine could be
chapter. Cocaine is discussed in the next chapter. How- prescribed only by a physician.
ever, because the CNS stimulants are controversial and Medical uses of ephedrine. Ephedrine is used in
the source of much confusion, this chapter is subdivided the treatment of bronchial asthma and respiratory
into two sections. The first discusses the medical uses of problems associated with bronchitis, emphysema, or
the CNS stimulants, their effects, and complications chronic obstructive pulmonary disease (American Soci-
from their use. The second section explores the compli- ety of Health-System Pharmacists, 2002). Although
cations of CNS stimulant abuse. ephedrine was once considered a valid treatment for
nasal congestion, it is no longer used for this purpose
after questions were raised as to its effectiveness. In hos-
I. THE CNS STIMULANTS AS USED pitals it might also be used to control the symptoms of
IN MEDICAL PRACTICE shock and in some surgical procedures when low blood
The Amphetamine-like Drugs pressure is a problem (Karch, 2002). Ephedrine might
modify the cardiac rate; however, with the introduction
Ephedrine of newer, more effective medications, it is rarely used in
Scientists have found Ephreda plants at Neanderthal cardiac emergencies now (American Society of Health
burial sites in Europe that are thought to be 60,000 System Pharmacists, 2002). Ephedrine may, in some
years old (Karch, 2002). Whether the plants were used situations, be used as an adjunct to the treatment of
for medicinal purposes in the Paleolithic era is not myasthenia gravis (Wilson, Shannon, Shields, & Stang,
clear, but it is known that by 5,000 years ago, Chinese 2007).
physicians were using Ephedra plants for medicinal Pharmacology of ephedrine. In the human body,
purposes (Ross & Chappel, 1998). The active agent of ephedrine’s primary effects are strongest in the periph-
these plants, ephedrine, was not isolated by chemists eral regions rather than the central nervous system,
until 1897 (Mann, 1992), and it remained nothing more and ephedrine is known to stimulate the sympathetic
114
Abuse of and Addiction to Amphetamines and CNS Stimulants 115
nervous system in a manner similar to that of adrena- Side effects of ephedrine at normal dosage levels. The
line (Laurence & Bennett, 1992; Mann, 1992). This therapeutic index of ephedrine is quite small, which
makes sense, since ephedrine blocks the reuptake of suggests that this chemical may cause toxic effects at
norepinephrine at the receptor sites in the body. relatively low doses. A meta-analysis of the efficacy and
When used in the treatment of asthma, ephedrine safety of ephedrine suggests that even users who take
improves pulmonary function by causing the smooth ephedrine at recommended doses are 200% to 300%
muscles surrounding the bronchial passages to relax more likely to experience psychiatric problems, auto-
(American Society of Health-System Pharmacists, 2002). nomic nervous system problems, upper gastrointestinal
It also alters the constriction and dilation of blood ves- irritation, and heart palpitations (Shekelle et al., 2003).
sels by binding at the alpha-2 receptor sites in the body, Some of the side effects of ephedrine include anxiety,
which modulate blood vessel constriction and dilation feelings of apprehension, insomnia, and urinary reten-
(Rothman et al., 2003). When blood vessels constrict, tion (Graedon & Graedon, 1991). The drug may also
the blood pressure increases as the heart compensates cause a throbbing headache, confusion, hallucinations,
for the increased resistance by pumping with more tremor, seizures, cardiac arrhythmias, stroke, euphoria,
force. hypertension, coronary artery spasm, angina, intracra-
Depending on the patient’s condition, ephedrine nial hemorrhage, and death (American Society of Health-
might be taken orally or be injected, and it might System Pharmacists, 2002; Karch, 2002; Samenuk et al.,
be smoked. Smoking was the preferred method of 2002; Zevin, & Benowitz, 2007).
ephedrine abuse in the Philippines for many years, but Complications of ephedrine use at above-normal dosage
this practice is gradually declining (Karch, 2002). Oral, levels. Used at greater than normal levels, ephedrine
intramuscular, or subcutaneous doses are completely can cause the side effects noted earlier as well as coro-
absorbed. Peak blood levels from a single oral dose are nary artery vasoconstriction, myocardial infarction, cere-
achieved in about 1 hour (Drummer & Odell, 2001). bral vascular accidents (CVAs, or strokes), and death
Surprisingly, as it has been in use for more than three- (Samenuk et al., 2002). Over-the-counter ephedrine
quarters of a century, there is very little research into use/abuse was linked to at least 155 deaths and “dozens of
the way that ephedrine is distributed within the body. heart attacks and strokes” at the time its sale was restricted
The serum half-life has been estimated at between 2.7 in February 2004 (Neergaard, 2004, p. 3A).
and 3.6 hours (Samenuk et al., 2002). The drug is elim- Medication interactions involving ephedrine. It is rec-
inated from the body virtually unchanged, with only a ommended that patients using ephedrine avoid any of
small percentage being biotransformed before elimina- the “tricyclic” antidepressants, as these medications will
tion by the kidneys. The exact percentage that is elimi- add to the stimulant effect of the ephedrine (DeVane &
nated unchanged depends on how acidic the urine is, Nemeroff, 2002). Patients using ephedrine should check
with a greater percentage being eliminated without bio- with a physician or pharmacist before the concurrent
transformation when the urine is more acidic (Ameri- use of different medications.
can Society of Health-System Pharmacists, 2002).
Tolerance to its bronchodilator action develops rap-
idly, so physicians recommend that ephedrine be used Ritalin (Methylphenidate)
as a treatment of asthma for only short periods of time. Ritalin (methylphenidate) is a controversial pharma-
The chronic use of ephedrine may contribute to car- ceutical agent, frequently prescribed for children who
diac or respiratory problems in the user, and for this have been diagnosed with attention-deficit hyperactiv-
reason the medication is recommended only for short- ity disorder (ADHD) (Breggin, 1998; Sinha, 2001). Al-
term use except under a physician’s supervision. As an though one would assume that ADHD would be a
over-the-counter diet aid, ephedrine appears to have a worldwide problem, fully 80% of the methylphenidate
modest, short-term effect. Shekelle et al. (2003) found produced globally is consumed in the United States
in their meta-analysis of the medical literature that (Diller, quoted in Marsa, 2005). Thus this medication
ephedrine can help the user lose about 0.9 kilograms of is quite popular and is not without its critics. Indeed,
weight for short periods of time. There is no informa- the challenge has been made that parents “medicate
tion on its long-term effectiveness as an aid to weight our kids more, and for more trivial reasons, than any
loss, and there is no evidence that it is able to enhance other culture. We’d rather give them a pill than disci-
athletic ability (Shekelle et al., 2003). pline them” (Diller, quoted in Marsa, 2005, p. 164).
116 Chapter Eleven
Serious questions have been raised about whether phenidate’s effects are stronger at higher dosage levels.
children are being turned into chemical “zombies” At normal therapeutic doses, methylphenidate is able
through the use of methylphenidate or similar agents in to block 50% or more of the dopamine transporters
the name of behavioral control (Aldhous, 2006). Most within 60–90 minutes of the time the drug is adminis-
certainly, the use of methylphenidate does not repre- tered (Jaffe, Ling, & Rawson, 2005).
sent the best possible control of ADHD symptoms, as Side effects of methylphenidate. Even though
evidenced by the fact that about half of the prescrip- methylphenidate is identified as the treatment of choice
tions for this medication are never renewed (Breggin, for ADHD, very little is known about its long-term eff-
1998). Given the strident arguments for and against the ects as most follow-up studies designed to identify its
use of methylphenidate, it is safe to say that this com- side effects have continued for only a few weeks
pound will remain quite controversial for many decades (Schachter, Pham, King, Langford, & Moher, 2002;
to come. Sinha, 2001). There have been rare reports of drug-
Medical uses of methylphenidate. Methylphenidate induced cardiac problems, and up to 5% of the chil-
has been found to function as a CNS stimulant and has dren taking the medication will experience visual
value in the treatment of a rare neurological condition hallucinations (Aldhous, 2006). When used at therapeu-
known as narcolepsy. Methylphenidate is used in treat- tic dosage levels, methylphenidate can cause anorexia,
ing ADHD although not without criticism. It also used insomnia, weight loss, failure to gain weight, nausea,
occasionally as an adjunct to the treatment of depres- heart palpitations, angina, anxiety, liver problems,
sion (Fuller & Sajatovic, 1999). dry mouth, hypertension, headache, upset stomach,
Pharmacology of methylphenidate. Methylphenidate enuresis, skin rashes, dizziness, or exacerbation of the
was originally developed by pharmaceutical companies symptoms of Tourette’s syndrome (Fuller & Sajatovic,
looking for a nonaddicting substitute for the ampheta- 1999). Other side effects of methylphenidate range
mines (Diller, 1998). Chemically, it is a close cousin to from stomach pain, blurred vision, leukopenia, possible
the amphetamines, and some pharmacologists classify cerebral hemorrhages, hypersensitivity reactions, anemia,
methyphenidate as a true amphetamine. In this text, it and preseveration (Breggin, 1998).1
is considered an amphetamine-like drug. Methylphenidate has been implicated as a cause of
When methylphenidate is used in the treatment of liver damage in some patients (Karch, 2002). It has the
attention-deficit/hyperactivity disorder, patients will potential to lower the seizure threshold in patients with
take between 15 and 90 mg per day, in divided doses a seizure disorder, and the manufacturer recommends
(Wender, 1995). Oral doses of methylphenidate are rap- that if the patient should have a seizure, the drug be dis-
idly absorbed from the gastrointestinal tract (Greenhill, continued immediately. Some reports suggest that
2006). Peak blood levels are achieved in 1.9 hours methylphenidate can damage heart tissue, a frightening
following a single dose, although in sustained release possibility considering the frequency with which it is
forms this will not occur until 4–7 hours after the dose prescribed to children (Henderson & Fischer, 1994).
was ingested (Wilson et al., 2007). Methylphenidate is There are also reports that methylphenidate induces a
estimated to have a 1:100 therapeutic window—that is, reduction in cerebral blood flow when used at thera-
the individual dose is about 1/100th the estimated peutic doses, an effect that may have long-term conse-
lethal dose (Greenhill, 2006). The half-life of methyl- quences for the individual taking this medication
phenidate is from 1 to 3 hours, and the effects of a (Breggin, 1998). These findings suggest a need for fur-
single oral dose last for 3 to 6 hours. The effects of a single ther research into the long-term consequences of
dose of an extended-release form of methylphenidate methylphenidate use/abuse.
might continue for 8 hours. In the intestinal tract, Children who are taking methylphenidate at recom-
about 80% of a single oral dose is biotransformed to ri- mended dosage levels have experienced a “zombie” ef-
tanic acid that is then excreted by the kidneys (Karch, fect in which the drug dampens the user’s personal
2002). initative (Breggin, 1998). This seems to be a common
Within the brain, methylphenidate blocks the ac- effect of methylphenidate, even when it is used by nor-
tion of a molecular dopamine transporter system by mal individuals, although in students with ADHD this
which free dopamine molecules are shunted back into effects is claimed to be beneficial (Diller, 1998). The
the neuron from the synapse. This allows the dopamine
to remain in the synapse longer, enhancing its effect 1A condition in which the individual continues to engage in the same
(Volkow & Swanson, 2003; Volkow et al., 1998). Methyl- task long after it ceases to be a useful activity.
“zombie” effect reported by Breggin (1998) and Diller Unlike many medical conditions, the diagnosis of
(1998) was challenged by Pliszka (1998), who cited re- ADHD is descriptive and without biological markers
search to support his conclusion that the drug did not that might clearly identify the patient with this disorder
cause this effect. Thus, whether methylphenidate causes (Zuvekas, Vitiello, & Norquist, 2006). This is one rea-
a “zombie” effect in children has yet to be determined. son the concept of ADHD has been controversial, and
On rare occasions, methylphenidate has been impli- therapists such as Breggin (1998) have been vocal crit-
cated in the development of a drug-induced depression, ics of the whole concept of this disorder.
which might reach the level of suicide attempts (Breggin, Many clinicians dismiss Breggin’s comments as
1998). being too extreme, but some of his observations appear
Medication interactions involving methylphenidate. to have merit. For example, although the long-term
Individuals on methylphenidate should not use “tri- benefits of methylphenidate use have never been
cyclic” antidepressants, as these medications can com- demonstrated, the American Medical Association sup-
bine with the methylphenidate to cause potentially toxic ports the long-term use of this medication to control the
blood levels of the antidepressant medications (DeVane manifestations of ADHD. Research has also demon-
& Nemeroff, 2002). Patients should not use any of the strated that the child’s ability to learn new material im-
MAOI family of antidepressants while taking methyl- proves at a significantly lower dose of methylphenidate
phenidate because of possible toxicity (DeVane & than is necessary to eliminate behaviors that are not ac-
Nemeroff, 2002). The mixture of mythylphenidate and cepted in the classroom (Pagliaro & Pagliaro, 1998).
the selective serotonin reuptake inhibitor family of anti- When the student is drugged to the point that these be-
depressants has been identified as a cause of seizures haviors are eliminated or controlled, learning suffers,
and thus should not be used (DeVane & Nemeroff, according to the authors.
2002). Patients who are using antihypertensive medica- Further, a pair of ongoing research studies into the
tions while taking methylphenidate may find that their long-term effects of methylphenidate have found evi-
blood pressure control is less than adequate, as the lat- dence of a progressive deterioration in the student’s
ter drug interferes with the effectiveness of the antihy- performance on standardized psychological tests, com-
pertensives (DeVane & Nemeroff, 2002). pared to the performance of age-matched peers on
Challenges to the use of methylphenidate as a treat- these same tests (Sinha, 2001). There is also data from
ment for ADHD. A small but vocal group of clinicians animal research suggesting a connection between
has started to express concern about the use of methylphenidate use and the later development of
methylphenidate as a treatment for ADHD (Breggin, Parkinson’s disease, although this connection has not
1998; Diller, 1998). Most certainly, it is recommended been demonstrated in humans (Rothenberger &
that medications not be the sole treatment for ADHD, Banaschewski, 2004). These arguements present thought-
that behavior therapy be the initial treatment modality provoking challenges to the current forms of pharma-
utilized, and that medications be used only in severe cological treatment of ADHD and suggest a need for
cases (Rothenberger & Banaschewski, 2004). Further, further research in this area.
CNS stimulants such as methylphenidate should not
be used to treat ADHD in patients with concurrent sub- The Amphetamines
stance use disorders except in very rare occasions be-
cause of the abuse potential that these medications History of the Amphetamines
present (Croft, 2006). Chemically, the amphetamines are analogs2 of
Although short-term outcome studies have found ephedrine (Lit, Wiviott-Tishler, Wong, & Hyman 1996).
that methylphenidate does reduce target behaviors by The amphetamines were first discovered in 1887, but it
70% to 90%, its long-term efficacy has never been was not until 1927 that one of these compounds was
demonstrated in the clinical literature (Schachter et al., found to have medicinal value, and 1932 before the
2002). In contrast to this pattern of reports in the clini- first amphetamine compound was introduced for med-
cal literature, parents (and teachers) are assured that ical use (Jaffe & Anthony, 2005; Kaplan & Sadock,
methylphenidate is the treatment of choice for ADHD, 1996). One factor behind the decision to develop the
mainly because the “material on [methylphenidate’s] amphetamines was the possibility that the demand for
lack of efficacy, while readily available in the profes- ephedrine might exceed the supply. In 1932 the first
sional literature, is not presented to the public” (Breggin,
1998, p. 111). 2See Glossary and Chapter 35.
118 Chapter Eleven
amphetamine compound was introduced as a treat- feel good. Many of the pills prescribed by physicians for
ment for asthma and rhinitis under the brand name patients were diverted to illicit markets, and there is no
Benzedrine (Karch, 2002; Derlet & Heischober, 1990). way of knowing how many of the 10 billion ampheta-
The drug was contained in an inhaler similar to mine tablets manufactured in the United States in the
“smelling salts.” The ampule, which could be pur- year 1970 were actually used as prescribed.
chased without a prescription until 1951, would be bro- The amphetamines occupy a unique position in his-
ken, releasing the concentrated amphetamine liquid tory, for medical historians now believe that it was the
into the surrounding cloth (Ling, Rawson, & Shoptaw, arrival of large amounts of amphetamines, especially
2006). The Benzedrine ampule would then be held methamphetamine, that contributed to an outbreak of
under the nose and the fumes inhaled to reduce the drug-related violence that ended San Francisco’s “sum-
symptoms of asthma. mer of love” of 1967 (D. Smith, 1997, 2001). Ampheta-
Soon, however, abusers discovered that the Ben- mine abusers had also discovered that when used at
zedrine ampules could be unwrapped, carefully broken high dosage levels, the amphetamines would cause agi-
open, and the concentrated Benzedrine injected,3 caus- tation and could induce death from cardiovascular col-
ing effects similar to those of cocaine. The dangers of lapse. They had also discovered that these compounds
cocaine were well known to drug abusers/addicts of the could induce a severe depressive state that might reach
era, but since the long-term effects of the ampheta- suicidal proportions and could last for days or weeks
mines were not known, they were viewed as a safe sub- after the drug was discontinued. By the mid-1970s am-
stitute for cocaine. Shortly afterward, the world was phetamine abusers had come to understand that chronic
plunged into World War II, and amphetamines were amphetamine use would dominate users’ existence,
used by personnel in the American, British, German, slowly squeezing the life out of them. In San Francisco,
and Japanese armed forces to counteract fatigue and physicians at the Haight-Ashbury free clinic coined the
heighten endurance (King & Ellinwood, 2005). U.S. slogan that “speed kills” by way of warning the general
Army Air Corps crew members stationed in England public of the dangers of amphetamine abuse (Smith,
took an estimated 180 million Benzedrine pills during 1997, 2001).
World War II (Lovett, 1994), while British troops con- By this same time, physicians had discovered that
sumed an additional 72 million doses (Walton, 2002) the amphetamines were not as effective as once
to help them function longer in combat. It is rumored thought in the treatment of depressive states or obesity.
that Adolf Hitler was addicted to amphetamines This fact, plus the development of new medications de-
(Witkin, 1995). veloped for the treatment of depression, reduced the
The use of amphetamines during World War II or frequency with which physicians prescribed ampheta-
Operation Desert Storm might possibly be excused as mines. The amphetamines were classified as Schedule
necessary to meet the demands of the war. But for rea- II substances in the Controlled Substances Act of 1970
sons that are not well understood, there were waves of and as such are considered compounds with a high po-
amphetamine abuse in both Sweden and Japan imme- tential for abuse. However, they continue to have a lim-
diately following World War II (King & Ellinwood, ited role in the control of human suffering. Further,
2005). The amphetamines were frequently prescribed although the dangers of amphetamine use are well
to patients in the United States in the 1950s and 1960s, known, during the Desert Storm campaign of 1991
and President John F. Kennedy is rumored to have used some 65% of United States pilots in the combat theater
methamphetamine, another member of the ampheta- admitted to having used an amphetamine compound at
mines, during his term in office in the early 1960s least once during combat operations (Emonson & Van-
(Witkin, 1995). The amphetamines continued to gain derbeek, 1995). Thus, the amphetamines have never
popularity as drugs of abuse, and by the year 1970 entirely disappeared either from the illicit drug world or
their use had reached “epidemic proportions” (Kaplan & from the world of medicine.
Sadock, 1996, p. 305) in the United States. Physicians Medical uses of the amphetamines. The ampheta-
would prescribe amphetamines for patients who wished mines improve the action of the smooth muscles of
to lose weight or were depressed, while illicit ampheta- the body (Hoffman & Lefkowitz, 1990) and thus have
mine users would take the drug because it helped them a potential for improving athletic performance at least
to some degree. However, these effects are not uniform,
3Needless to say, amphetamines are no longer sold over the counter and the overuse of the CNS stimulants can actually
without a prescription. bring about a decrease in athletic abilities in some
users. Because of their use as athletic enhancement quite controversial, and while these drugs are recog-
agents, sports regulatory agencies routinely test for evi- nized as being of value in the control of ADHD symp-
dence of amphetamine use among athletes, and am- toms, there is a need for research into their long-
phetamine abuse among athletes is limited. term effects, and some suggest that these medications
The amphetamines have an anorexic4 side effect, and may do more harm than good (Breggin, 1998; Spencer
at one time this was thought to be useful in the treat- et al., 2001).
ment of obesity. Unfortunately, subsequent research has
demonstrated that the amphetamines are only mini-
mally effective as a weight control agent. Tolerance of Pharmacology of the Amphetamines
the appetite-suppressing side effect of the ampheta- The amphetamine family of chemicals consists of sev-
mines develops in only 4 weeks (Snyder, 1986). After eral different variations of the parent compound. Each
users have become tolerant to the anorexic effect of am- of these variations yields a molecule that is simi-
phetamines, it is not uncommon for them to regain the lar to the others except for minor variations in potency
weight they initially lost. Research has demonstrated and pharmacological characteristics. The most com-
that after a 6-month period, there is no significant differ- mon forms of amphetamine are dextroamphetamine
ence between the amount of weight lost by patients (d-amphetamine sulfate), which is considered twice
using amphetamines and by patients who simply dieted as potent as the other common form of ampheta-
to lose weight (Maxmen & Ward, 1995). mine (Lingeman, 1974), and methamphetamine (or, d-
Prior to the 1970s, the amphetamines were thought desoxyephedrine hydrochloride). Because of its longer
to be antidepressants and were widely prescribed for the half-life and ability to cross the blood-brain-barrier,
treatment of depression. However, research revealed illicit amphetamine abusers seem to prefer metham-
that the antidepressant effect of the amphetamines was phetamine to dextroamphetamine (Albertson, Derlet, &
short-lived at best. With the introduction of more effec- Van Hoozen, 1999).
tive antidepressant agents the amphetamines fell into Methods of administration in medical practice.
disfavor and are now used only rarely as an adjunct to the Physicians can administer an amphetamine to a patient
treatment of depression (Potter, Rudorfer, & Goodwin, in several ways. The drug molecule tends to be basic
1987). They are the treatment of choice for a rare and when taken orally is easily absorbed through the
neurological condition known as narcolepsy.5 Re- lining of the small intestine (Laurence & Bennett,
searchers believe that narcolepsy is caused by a chemi- 1992). However, even though the amphetamines have
cal imbalance within the brain in which the neuro- been used in medical practice for generations, very
transmitted dopamine is not released in sufficient little is known about their absorption from the gastroin-
amounts to maintain wakefulness. By forcing the neu- testinal tract in humans (Jenkins & Cone, 1998). A
rons in the brain to release their stores of dopamine, single oral dose of amphetamine will begin to have an
the amphetamines are thought to at least partially cor- effect on the user in 20 (Siegel, 1991) to 30 minutes
rect the dopamine imbalance that causes narcolepsy (Mirin, Weiss, & Greenfield, 1991). The amphetamine
(Doghramji, 1989). molecule is also easily absorbed into the body when in-
The first reported use of an amphetamine, Ben- jected into either muscle tissue or a vein.
zedrine, for the control of hyperactive children oc- In the normal patient who has received a single oral
curred in 1938 (Pliszka, 1998). Surprisingly, although dose of an amphetamine, the peak plasma levels are
the amphetamines are CNS stimulants, they appear to achieved in 1–3 hours (Drummer & Odell, 2001). The
have a calming effect on individuals who have attention- biological half-life of the different forms of ampheta-
deficit hyperactivity disorder. Research has revealed that mine vary, as a result of their different chemical struc-
the amphetamines are as effective in controlling the tures. For example, the biological half-life of a single
symptoms of ADHD as methylphenidate in about oral dose of dextroamphetamine is between 10 and 34
50% of patients with this disorder and that 25% of the hours hours, while that of a single oral dose of metham-
patients will experience better symptom control through phetamine is only 4 to 5 hours (Fuller & Sajatovic,
the use of an amphetamine (Spencer et al., 2001). 1999; Wilson et al., 2007). However, when injected,
However, the use of amphetamines to treat ADHD is the half-life of methamphetamine can be as long as
12.2 hours (Karch, 2002).
4See Glossary. The chemical structure of the basic amphetamine
5See Glossary. molecule is similar to that of norepinephrine and
120 Chapter Eleven
dopamine and thus might be classified as an agonist of creted unchanged when the individual‘s urine is more
these neurotransmitters (King & Ellinwood, 2005). acidic (Karch, 2002). When the user’s blood is extremely
The effects of amphetamines in the peripheral regions alkaline, perhaps as little as 5% of the dose of ampheta-
of the body are caused by its ability to stimulate norepi- mine will be filtered out of the blood by the kidneys and
nephrine release, while its CNS effects are the result of excreted unchanged (Karch, 2002). This is because
its impact on the dopamine-using regions of the brain amphetamine molecules tend to be reabsorbed by the
(Lit et al., 1996). Once in the brain, the amphetamine kidneys when the urine is more alkaline. That propor-
molecule is absorbed into those neurons that use tion of the dose that is not excreted unchanged will un-
dopamine as a neurotransmitter and both stimulates dergo biotransformation in the liver. A number of
those neurons to release their dopamine stores and si- different amphetamine metabolites are formed as the
multaneously blocks the reuptake pump that normally biotransformation process progresses from one step to
would remove the dopamine from the synapse (Haney, the next, with the exact number of metabolites formed
2004). The mesolimbic region of the brain is especially depending on the specific form of amphetamine being
rich in dopamine-containing neurons and is thought to used. For example, during the process of methamphet-
be part of the “pleasure center” of the brain. This seems amine biotransformation, seven different metabolites
to account for the ability of the amphetamines to cause are formed at various stages in the process of biotrans-
a sense of euphoria in the user. Another region in the formation before the drug is finally eliminated from
brain where the amphetamines have an effect is the the body.
medulla (which is involved in the control of respira- At one point, physicians were trained to try to make
tion), causing the individual to breathe more deeply a patient’s urine more acidic to speed up the excretion
and more rapidly. At normal dosage levels, the cortex is of the amphetamine molecules following an overdose.
also stimulated, resulting in reduced feelings of fatigue However, this treatment method has been found to in-
and possibly increased concentration (Sadock & crease the chances that the patient will develop car-
Sadock, 2003). diac arrhythmias and/or seizures, and it is no longer
There is considerable variation in the level of indi- recommended (Venkatakrishnan, Shader, & Greenblatt,
vidual sensitivity to the effects of the amphetamines. 2006).
The estimated lethal dose of amphetamines for a non- Neuroadaptation/tolerance to amphetamines. The
tolerant individual is 20–25 mg/kg (Chan, Chen, Lee, & steady use of an amphetamine by a patient will result in
Deng, 1994), shown in one clinical report of a person an incomplete state of neuroadaptation. For example,
ingesting only 1.5 mg/kg, and rare reports of toxic reac- when a physician prescribes an amphetamine to treat
tions at dosage levels as low as 2 mg (Hoffman & narcolepsy, it is possible for the patient to be main-
Lefkowitz, 1990). There are also case reports of tained on the same dose for years without any loss of ef-
amphetamine-naive individuals6 surviving a single dose ficacy (Jaffe, Ling, et al., 2005). However, patients
of 400–500 mg (or 7.5 mg/kg body weight for a 160 become tolerant to the anorexic effects of the ampheta-
pound person). However, the patients who ingested mines after only a few weeks, and the initial drug-
these dosage levels required medical support to over- induced sense of well-being does not last beyond the
come their toxic effects. Individuals who are tolerant to first few doses when used at therapeutic dosage levels.
the effects of the amphetamines may use massive doses Interactions between the amphetamines and other
“without apparent ill effect” (Hoffman & Lefkowitz, medications. Patients on amphetamines should avoid
1990, p. 212). taking them with fruit juices or ascorbic acid as these
A part of each dose of amphetamine will be biotrans- substances will decrease the absorption of the ampheta-
formed by the liver, but a significant percentage of the mine dose (Maxmen & Ward, 1995). Patients should
amphetamines will be excreted from the body essen- avoid mixing amphetamines with opiates as the am-
tially unchanged. Under normal conditions 45% to phetamines will increase the anorexic and analgesic ef-
70% of a single dose of methamphetamine will be ex- fects of narcotic analgesics. Further, patients should not
creted by the body unchanged within 24 hours (Jenkins, mix amphetamines with the antidepressants known as
2007; Karch, 2002). The exact percentage that is monoamine oxidase inhibitors (MAOIs, or MAO inhibi-
excreted unchanged depends on the acid level of the tors) as the combination can result in dangerous eleva-
individual’s urine, with more amphetamine being ex- tions in the blood pressure (Barnhill, Ciraulo, Ciraulo, &
Greene, 1995). You should always consult a physician or
6See Glossary. pharmacist before taking two or more medications at the
same time, to make sure that there is no danger of a harm- take an amphetamine as prescribed will experience
ful interactions between the chemicals being used. an amphetamine-induced tachycardia (Breggin, 1998;
Fuller & Sajatovic, 1999). Amphetamine use, even at
therapeutic dosage levels, has been known to cause or
Subjective Experience of Amphetamine Use
exacerbate the symptoms of Tourette’s syndrome in
The effects of the amphetamines on any given individ- some ptients (Breggin, 1998; Fuller & Sajatovic, 1999).
ual will depend upon that individual’s mental state, the Other potential side effects at normal dosage levels in-
dosage level utilized, the relatively potency of the spe- clude dizziness, agitation, a feeling of apprehension,
cific form of amphetamine, and the manner in which flushing, pallor, muscle pains, excessive sweating, and
the drug is used. The subjective effects of a single dose delirium (Fawcett & Busch, 1995). Rarely, a patient
of amphetamines is to a large degree very similar to that will experience a drug-induced psychotic reaction when
seen with cocaine or adrenaline (Kaminski, 1992). taking an amphetamine at recommended dosage levels
However, there are some major differences between (Breggin, 1998; Fuller & Sajatovic, 1999).
the effects of cocaine and of the amphetamines: (1) Surprisingly, although the amphetamines are CNS
Whereas the effects of cocaine might last from a few stimulants, almost 40% of patients on amphetamines
minutes to an hour at most, the effects of the ampheta- experience drug-induced feelings of depression, which
mines last many hours. (2) Unlike cocaine, the amphet- might become so severe that the individual attempts
amines are effective when used orally. (3) Unlike cocaine, suicide (Breggin, 1998). Feelings of depression and a
the amphetamines have only a very small anesthetic sense of fatigue or lethargy that last for a few hours or
effect (Ritz, 1999). days are common when the amphetamines are discon-
When used in medical practice, the usual oral tinued by the patient.
dosage level is between 5–60 mg per day for ampheta-
mine and 5–20 mg/day for methamphetamine (Jenkins,
2007). At low to moderate oral dosage levels, the indi- II. CNS STIMULANT ABUSE
vidual will experience feelings of increased alertness,
an elevation of mood, a feeling of mild euphoria, less
Scope of the Problem of Central Nervous
mental fatigue, and an improved level of concentration System Stimulant Abuse and Addiction
(Sadock & Sadock, 2003). Like many drugs of abuse, Globally, abuse of the amphetamines and amphetamine-
the amphetamines will stimulate the “pleasure center” in like compounds is quite common. An estimated 35 mil-
the brain. Thus, both the amphetamines and cocaine lion abusers around the world are thought to have
produce “a neurochemical magnification of the pleasure abused just one compound—methamphetamine—at
experienced in most activities” (Gawin & Ellinwood, some point in their lives (Rawson, Sodano, & Hillhouse,
1988, p. 1174) when initially used. Sadock and Sadock 2005). Three-quarters of this number live in Asia or
noted that the initial use of amphetamines or cocaine Southeast Asia (Ling et al., 2006). In the United States,
would “produce alertness and a sense of well-being . . . methamphetamine is the second most commonly
lower anxiety and social inhibitions, and heighten energy, abused illicit compound after marijuana. An estimated
self-esteem, and the emotions aroused by interpersonal 12 million people in the United States have abused
experiences. Although they magnify pleasure, they do methamphetamine at least once, and 1.5 million people
not distort it; hallucinations are usually absent” (2003, are regular users (“America’s Most Dangerous Drug,”
p. 1174). 2005). Approximately 12% of high school seniors sur-
veyed admit to having abused an amphetamine at least
once (Johnston, O’Malley, Bachman, & Schulenberg,
Side Effects of Amphetamine Use 2006a).
at Normal Dosage Levels Methamphetamine abusers typically use com-
Patients who are taking amphetamines under a physi- pounds produced in clandestine laboratories. A single
cian’s supervision may experience such side effects as ounce of methamphetamine manufactured in an illicit
dryness of the mouth, nausea, anorexia, headache, in- laboratory by some estimates can provide about 110
somnia, and periods of confusion (Fawcett & Busch, doses of the drug. Another major source of illicit am-
1995). The patient’s systolic and diastolic blood pres- phetamines is Mexican drug dealers, who manufacture
sure will both increase, and the heart rate may reflex- the compound in that country and then smuggle it into
ively slow down. More than 10% of the patients who the United States (Lovett, 1994; Witkin, 1995).
122 Chapter Eleven
Effects of the Central Nervous System Theoretically, at high levels ephedrine can increase the
Stimulants When Abused workload of the cardiac muscle and cause the muscle
tissue to utilize higher levels of oxygen. This is poten-
Ephedrine tially dangerous if the user should have some form of
Because ephedrine was sold over the counter as a diet coronary artery disease.
aid and as a treatment for asthma, the true scope of Other complications from ephedrine abuse might
ephedrine abuse in the United States was not known include necrosis (death) of the tissues of the intestinal
(Karch, 2002). The drug was thought to be abused by tract, potentially fatal arrhythmias, urinary retention, ir-
cross-country truckers, college students, and others who ritation of heart muscle tissue (especially in patients
wanted to ward off the effects of fatigue. It was occasion- with damaged hearts), nausea, vomiting, stroke, drug-
ally sold in combination with other herbs as “herbal ec- induced psychosis, formation of ephedrine kidney
stasy” (Schwartz & Miller, 1997); it was sold alone or in stones in rare cases, and possibly death (American Soci-
combination with other chemicals as a “nutritional sup- ety of Health-System Pharmacists, 2002; Antonio, 1997;
plement” to enhance athletic performance or aid Karch, 2002; Solotaroff, 2002).
weight-loss programs (Solotaroff, 2002). Also, ephedrine
is used in the manufacture of illicit amphetamine com- Ritalin (Methylphenidate)
pounds. The over-the-counter sale of ephedrine in the Effects of methylphenidate when abused. In the early years
United States was outlawed in 2004, but this ban was of the 21st century, researchers were surprised to discover
overturned by a federal judge a year later (“Utah Judge that the Internet offered access to “pharmacies” that
Strikes Down,” 2005). would supply CNS stimulants such as methylphenidate
Effects of ephedrine when abused. Ephedrine’s ef- to buyers without documentation of the medical need
fects when the drug is abused are essentially the same as for the individual to use this medication (Aldhous,
when it is used in medical practice, although higher 2006). It is suspected that some of those who are abusing
doses of ephedrine increase chances of adverse effects. the medication do so to get high, while others use it to
Alcohol abusers often will ingest ephedrine so they can help them study longer, and still others abuse the drug to
drink longer, using the ephedrine to conteract the seda- stay awake longer at parties or to drink longer (Aldhous,
tive effects of the alcohol. At very high doses, ephedrine 2006; Arria & Wish, 2006; Diller, 1998).
can cause the user to experience a sense of euphoria. Unfortunately, methylphenidate abusers do not fol-
Methods of ephedrine abuse. The most common low recommended dosing patterns. While it is rare
method of ephedrine abuse is for the user to ingest for orally administered methylphenidate to be abused
ephedrine pills purchased over the counter. On rare oc- (Volkow & Swanson, 2003), these medications are often
casions, the pills will be crushed and the powder either abused by those who wish to enchance academic or voca-
“snorted” or even more infrequently injected. Ephedrine tional performance (Vedantam, 2006). Some users crush
and its chemical cousin pseudoephedrine are also used methylphenidate tablets and either inhale the powder or
in the illicit production of methamphetamine, a fact inject it into a vein (Karch, 2002; Volkow & Swanson,
that may have contributed to the Food and Drug Ad- 2003). The strongest effects of methylphenidate abuse
ministration’s decision to outlaw the use of pseu- are thought to be achieved when it is injected intra-
doephedrine in 2004 (Office of National Drug Control venously. In contrast to the effects of methylphenidate
Policy, 2004). Unfortunately, this ban was overturned when used at therapeutic doses, intravenously adminis-
by a federal judge a year later, leaving the status of tered methylphenidate doses are able to bring about the
ephedra uncertain at this time (“Utah Judge Strikes blockage of more than 50% the dopamine transporter
Down,” 2005). system within a matter of seconds, causing the user to
Consequences of ephedrine abuse. Consequences are feel “high” (Volkow & Swanson, 2003; Volkow et al.,
essentially an exaggeration of the side effects of 1998).
ephedrine seen at normal dosage levels. Although ad- Consequences of methylphenidate abuse. The conse-
verse effects are possible at very low doses, the higher quences of methylphenidate abuse are similar to those
the dosage level being used, the more likely the user is to seen when its chemical cousin, the amphetamines, are
experience an adverse effect from ephedrine (Antonio, abused. Even when used according to a physician’s in-
1997). There is mixed evidence that ephedrine can structions, methylphenidate will occasionally trigger a
contribute to cardiac dysfunctions, including arrhyth- toxic psychosis in the patient that is similar to paranoid
mias, when used at high dosage levels (Karch, 2002). schizophrenia (Aldhous, 2006; Karch, 2002). A small
percentage of abusers will experience a drug-induced pound. With repeated use, the sense of gentle euphoria
stroke or cardiac problems associated with methylphen- often turns into a harsh, abrasive sensation that is said to
idate abuse (Karch, 2002). be quite unpleasant by amphetamine abusers. The
When drug abusers crush methylphenidate tablets abusers will attempt to control these unpleasant effects
then mix the resulting powder with water for intra- through the concurrent use of alcohol, benzodiazepines,
venous use (Volkow et al., 1998), “fillers” in the tablet or other CNS depressants.
are injected directly into the circulation. These fillers Chronic amphetamine abuse at high dosage levels
are used to give the tablet bulk and form, and when the has been identified causing a sensitization effect8 in
medication is used according to instructions they pass abusers, making them more susceptible to drug-
harmlessly through the digestive tract. When a tablet is induced adverse effects such as seizures. Amphetamine
crushed and injected, these fillers gain admission to the abuse may cause violent outbursts, possibly resulting
bloodstream and may accumulate in the retina of the in the death of bystanders (King & Ellinwood, 2005).
eye, causing damage to that tissue (Karch, 2002). Between 5% and 12% of abusers report episodes of
suicidal ideation, hallucinations, and/or confusion,
The Amphetamines while about 3% experience a seizure (Zevin & Benowitz,
Effects of the amphetamines when abused. Scientists are 2007).
only now starting to understand how an amphetamine Animal research suggests that following periods of
such as methamphetamine affects the brain (Rawson, chronic abuse at high dosage levels, norepinephrine
Gonzales, & Brethen, 2002). When the amphetamines levels are depleted throughout the brain and these
are abused, the effects vary as a result of such factors as levels might not return to normal even after 6 months
(a) the specific form of amphetamine being abused, (b) of abstinence (King & Ellinwood, 2005). Chronic
the dose, (c) concurrent abuse of other compounds, abuse of amphetamines also causes a depletion of
and (d) and the route by which it was administered. To dopamine levels, especially in the caudate putamen re-
illustrate the last point, the effects of orally ingested am- gion of the brain. Animal research suggests that the
phetamine compounds are usually experienced in dopamine levels in the caudate putamen also might not
about 20 minutes.7 When the drug is abused in- return to normal even after 6 months of abstinence
tranasally (“snorted”), the effects are felt in about 5 (King & Ellinwood, 2005).
minutes, and the effects of injected or smoked There is strong evidence that the chronic adminis-
methamphetamine are felt within a matter of seconds tration of high doses of methamphetamine can cause
(Gwinnell & Adamec, 2006). some parts of the brain such as the parietal cortex and
The intensity of the amphetamine-induced mood caudate nucleus to increase in size compared to the
changes also varies, depending on the method by which size of these brain regions in nonabusing individuals of
the drug is abused. The strongest effects are achieved the same age (Jernigan et al., 2005). Jernigan et al. spec-
when the compound is smoked or injected into a vein. ulated that this might reflect the effects of localized
Abusers of smoked or injected methamphetamine expe- trauma to the brain induced by the chronic use of
rience an intense sense of euphoria, which has been methamphetamine. These findings are also consistent
called a “rush” or a “flash,” described as “instant eupho- with the observation that the chronic administration of
ria” by the author Truman Capote (quoted in Siegel, amphetamines at high dosage levels is toxic to the
1991, p. 72). Other users have compared the “flash” to brain, possibly through amphetamine-induced release
sexual orgasm. The “rush” appears to last for only a short of large amounts of the neurotransmitter glutamate
period of time, perhaps only seconds (Acosta, Haller, & (Batki, 2001; Haney, 2004; King & Ellinwood, 2005).
Schnoll, 2005; Jaffe, Ling, et al., 2005). Finally, there have been documented changes in the
Following the initial “rush,” the intravenous am- vasculature of the brain in chronic amphetamine
phetamine abuser may experience a warm glow or abusers, although it is not clear whether these changes
gentle euphoria that may last for several hours. Oral or are permanent or how these blood flow changes are
intranasal users usually do not experience the “rush” caused (Breggin, 1998).
but do have a sense of gentle euphoria at first that will Scope of amphetamine abuse. Globally, the abuse of
last for a number of hours after they ingest the com- amphetamine or amphetamine-like compounds is esti-
mated to be a $65 billion/year industry (United Nations,
7
This assumes that the individual is abusing only an amphetamine
8
compound. See Glossary.
124 Chapter Eleven
2003). There are regional variations in the pattern of Dangerous Drug,” 2005). The Drug Enforcement Ad-
CNS stimulant abuse around the globe, but in the ministration reported that some 8,063 illegal metham-
United States, methamphetamine is the most commonly phetamine labs were discoved around the United States
abused amphetamine compound (United Nations, in 2003, and some 10,063 such facilities were discov-
2003). It has been estimated that 1 in every 25 people ered by law enforcement officials in 2004 (“Drug Tests
in this country has abused methamphetamine at least Say,” 2005).
once (Acosta et al., 2005; Miller, 2005). However, only One method of methamphetamine production is
583,000 people in the United States were thought to known as “Nazi Meth,” so named for the Nazi symbols
be regular users of methamphetamine (King, 2006), decorating the paper that had the formula on it when it
and 257,000 people are thought to be addicted to it was discovered by police officials (“Nazi Meth,” 2003).
(Substance Abuse and Mental Health Services Admin- This method does not rely on the use of red phosphorus
istration, 2005). but uses compounds easily obtained from lithium bat-
To put the methamphetamine “crisis” into perspec- teries, ammonia, and other sources (“Nazi Meth,”
tive, remember that four times this number of people 2003). A $200 investment in the required materials will
are thought to use cocaine at least once a month, 30 yield methamphetamine that might sell for $2,500 on
times this number are thought to use cannabis at least the street, although there is a danger that some of the
once a month, and 90 times this number engage in contaminants contained in the compound might prove
binge drinking at least once a month (King, 2006). toxic to the user (apparently a matter of little concern to
This is not to deny the danger of amphetamine abuse, the abuser).
especially methamphetamine. The total number of Methods of amphetamine abuse. The amphetamines
methamphetamine abusers around the globe is now are well absorbed when taken orally. They are also well
estimated to outnumber the total combined number absorbed when injected into muscle tissue or a vein,
of cocaine and heroin abusers (“U.S. Warns,” 2006). when the powder is “snorted,” and when the substance
In the United States, an estimated 300,000 people is smoked. Illicit drug chemists developed a smokable
use methamphetamine for the first time each year, a form of methamphetamine in the 1950s sold under the
number that has remained stable since 1999 (King, name of “Ice.” When amphetamine is smoked, the am-
2006). Information on how to manufacture methamphetamine molecule is absorbed through the lining of
phetamine is available on the Internet, and there is the lungs and the molecules reach the brain in just a
evidence that organized crime cartels have started to matter of seconds. In the United States, methampheta-
manufacture and distribute methamphetamine in mine is commonly abused through smoking or intra-
large quantities (Milne, 2003; United Nations, 2003). venous injection (Rollo, Sane, & Ewin, 2007).
Unfortunately, there are about as many formulas for However, the amphetamine molecule is also easily ab-
producing methampetamine as there are “chemists” sorbed through the tissues of the nasopharynx, and thus
who try to make it—so understanding the toxicology amphetamine powder might be “snorted” (Rollo, Sane, &
of illicit forms of methamphetamine is quite difficult. Ewen, 2007).
The news media have paid special attention to the Subjective effects of amphetamine abuse. Because the
number of illegal laboratories manufacturing this sub- amphetamines have a reputation for enhancing normal
stance that have been uncovered by law enforcement offi- body functions (alertness, concentration, etc.), users as-
cials in the past few years. Most illicit amphetamine labs sume that they are less dangerous than other illicit com-
are “mom and pop” operations that produce relatively pounds (United Nations, 2003). The subjective effects
small amounts of amphetamine (usually methamphet- of the amphetamines is dependent upon (1) whether
amine) for local consumption.9 In Iowa, for example, tolerance to the drug has developed and (2) the method
only two small amphetamine production laboratories by which the drug was used. Amphetamine abusers
were uncovered in 1994, compared to 803 in 1999 who are not tolerant to the drug’s effects and who use
(Milne, 2003) and 1,325 in 2004 (“America’s Most oral forms of the drug or who snort it report a sense of
euphoria that may last for several hours. Individuals
9
It has been estimated that for every pound of methamphetamine who are not tolerant to the drug’s effects and who inject
produced in such “labs,” 5–7 pounds of toxic waste are produced,
amphetamines report an intense feeling of euphoria,
which then becomes a hazardous waste cleanup problem for the
community where the lab was located and a hazardous waste expo- followed by a less intense feeling of well-being that
sure problem for those who first investigate the laboratory site (Rollo might last for several hours. The “high” produced by
et al., 2007). methamphetamine might last 8–24 hours, a feature
that seems to make the drug more addictive than co- likely to experience some of the negative consequences
caine (Castro, Barrington, Walton, & Rawson, 2000; associated with the abuse of these compounds.
Rawson et al., 2005). Central nervous system. Researchers have discovered
Tolerance to the amphetamines. Amphetamine that amphetamine abuse can cause damage on both a
abusers quickly become tolerant to some of the eu- cellular and a regional level of the brain. At the cellular
phoric effects of the drug (Haney, 2004). In an at- level, up to 50% of the dopamine-producing cells in the
tempt to recapture the initial drug-induced euphoria, brain might be damaged after prolonged exposure to even
amphetamine abusers try to overcome their tolerance low levels of methamphetamine (Rawson et al., 2005).
to the drug in one of three ways: First, amphetamine High doses of amphetamines, especially metham-
abusers will try to limit their exposure to the drug to phetamine, are thought to enhance the production of
isolated periods of time, allowing their bodies to re- free radicals10 by cellular mitochondria (Acosta et al.,
turn to normal before the next exposure. The develop- 2005; Ballas, Evans, & Dinges, 2004; Jeng, Ramkissoon,
ment of tolerance requires constant exposure to the Parman, & Wells, 2006).
compound; otherwise the neuroadaptive changes that Methamphetamine-induced neurological damage
cause tolerance are reversed and the body returns to a might be more widespread than the dopamine-producing
normal state. Some individuals are able to abuse am- neurons. For example, Thompson et al. (2004) utilized
phetamines for years by following a pattern of inter- high resolution magnetic resonance imaging (MRI)
mittent abuse followed by periods of abstinence studies to find a significant reduction in the gray matter
(possibly by switching to other compounds that are in the brains of methamphetamine addicts as com-
then abused). pared to normal subjects. However, research has
Another method by which amphetamine abusers at- demonstrated that at least a limited degree of recovery
tempt to recapture the initial feeling of euphoria in- is possible with long-term abstinence from the amphet-
duced by the drug and to overcome tolerance is to amines (Nordahl et al., 2005).
embark on a cycle of using higher and higher doses When abused at high levels, methamphetamine
(Peluso & Peluso, 1988). Other abusers “graduate” causes the release of free radicals, peroxides, and hy-
from oral or intranasal methods of amphetamine abuse droxyquinones—compounds that are quite toxic to the
to intravenous injections to provide a more concen- nerve terminals in the synapse (Ling et al., 2006). These
trated dose. Finally, when this fails to provide abusers toxins might be the mechanism by which methamphet-
with sufficient pleasure, they might try a “speed run,” amine abuse causes damage to and even the death of
injecting more amphetamine every few minutes to try serotonin-producing neurons (Jaffe, Ling, et al., 2005;
to overcome their tolerance to the drug. Some amphet- King & Ellinwood, 2005). There is also evidence that
amine addicts might inject a cumulative dose of methamphetamine-induced cellular damage might re-
5,000–15,000 mg in a 24-hour time span while on a flect the release of large amounts of glutamate within
“speed run” (Chan et al., 1994; Derlet & Heischober, the brain, although the mechanism by which this hap-
1990). Such dosage levels would be fatal to the “naive” pens is not clear. Large amounts of glutamate are toxic
(inexperienced) drug user and are well within the to neurons, causing neuronal damage or even death
dosage range found to be neurotoxic in animal studies. (Fischman & Haney, 1999).
Speed runs might last for hours or days and are a sign Another mechanism by which amphetamine
that the individual has progressed from amphetamine abuse might cause brain damage is the ability of these
abuse to addiction to these compounds. compounds to bring about both temporary and perma-
nent changes in cerebral blood flow patterns. Some of
the more dangerous temporary changes in cerebral
Consequences of Amphetamine Abuse blood flow include the development of hypertensive
There is wide variation in what might be considered a episodes, cerebral vasculitis, and vasospasm in the
toxic dose of amphetamine (Julien, 2005). However, a blood vessels in the brain. There have been isolated
general rule is that the higher the concentration of am- cases of carotid artery dissection in methamphetamine
phetamines in the blood, the more likely the individual abusers (McIntosh, Hungs, Kostanian, & Yu, 2006). All
is to experience one or more adverse effects. Since am- these amphetamine-induced changes in cerebral blood
phetamine abusers typically utilize dosage levels far in flow can cause or contribute to either a hemorrhagic or
excess of those recommended by physicians when these
chemicals are used for medical purposes, they are more 10See Glossary.
126 Chapter Eleven
an ischemic stroke that might be fatal, depending on drug-induced hallucinations, and/or a drug-induced
its location (King & Ellinwood, 2005; Miller, 2005; delusional state (Julien, 2005; King & Ellinwood, 2005;
Oehmichen, Auer, & Konig, 2005; Rawson et al., 2005; Miller, 2005).
Wadland & Ferenchick, 2004). Further, reductions in Other possible consequences of amphetamine abuse
cerebral blood flow were found in 76% of ampheta- include agitation, assaultiveness, tremor, headache, irri-
mine abusers, changes that persisted for years after the tability, weakness, and suicidal and homicidal tenden-
individual had discontinued the use of these drugs cies (Albertson et al., 1999; Ballas et al., 2004; Rawson
(Buffenstein, Heaster, & Ko, 1999). et al., 2005). Physicians have found that haloperidol
Chronic amphetamine abusers might experience and diazepam are effective in helping the individual
sleep disturbances for up to 4 weeks after their last use calm down from an amphetamine-induced agitation
of the drug (Satel, Kosten, Schuckit, & Fischman, (Albertson et al., 1999). All amphetamine compounds
1993). The chronic amphetamine abusers might also are capable of inducing a toxic psychosis, although evi-
have abnormal EEG tracings (a measure of the electri- dence suggests that methamphetamine is more likely to
cal activity in the brain) for up to 3 months after their be involved in a drug-induced psychotic episode than
last drug use (Schuckit, 2006). Another very rare com- other forms of amphetamine, in part because of its
plication of amphetamine use/abuse is the develop- extensive availability (Ballas et al., 2004; Batki, 2001;
ment of the neurological condition known as the Kosten & Sofuoglu, 2004). Using positron emission to-
serotonin syndrome (Mills, 1995).11 mography (PET) scan data, Sekine et al. (2001) were
Consequences of amphetamine abuse on the person’s able to document long-lasting reductions in the num-
emotions. Clinicians have long been aware that am- ber of dopamine transporter sites in methamphetamine
phetamine abusers experience a period of depression abusers. They suggested that this reduction might be
after the drug’s effects wear off, and this can, in extreme associated with the onset of the methamphetamine-
cases, reach suicidal proportions (Rawson et al., 2005). induced psychosis in users who develop this complica-
Also, the amphetamines are capable of causing both tion of methamphetamine abuse.
new and chronic users to experience increased anxiety In its early stages, this drug-induced psychosis is often
levels (Ballas et al., 2004). Three-quarters of ampheta- indistinguishable from schizophrenia and might include
mine abusers report significant degrees of anxiety when such symptoms as confusion, suspiciousness, paranoia,
they started using amphetamines, and in some cases auditory and visual hallucinations, delusional thinking
the amphetamine-related anxiety might reach the level (including delusions of being persecuted), anxiety, and
of panic attacks (Breggin, 1998). These drug-induced periods of aggression (Beebe & Walley, 1995; Kaplan &
anxiety episodies have been known to persist for months Sadock, 1996; King & Ellinwood, 2005; United Nations,
or even years after the last use of amphetamines (Satel 2003). There is evidence that for methamphetamine the
et al., 1993). Researchers have found that methamphet- drug-induced aggression might appear both during peri-
amine abusers demonstrate an altered metabolism of ods of acute intoxication and during the withdrawal
brain structures thought to be involved in the genera- (Sekine et al., 2006). Chronic methamphetamine
tion of anxiety and depression, which is consistent with abusers often have methamphetamine-induced reduc-
the report of drug-induced anxiety by these abusers tion in the serotonin transporter systems within the
(London et al., 2004). neurons of multiple regions of the brain, and aggressive
It is not uncommon for illicit amphetamine users to episodes seem to reflect this condition; these aggressive
try to counteract the drug-induced anxiety and tension episodes can persist at least as long as 1 year following
through the use of other agents—alcohol, marijuana, the last methamphetamine abuse and they might be
or benzodiazepines. They will attempt to control the permanent (Sekine et al., 2006). Less common symptoms
side effects of the amphetamines by using CNS depres- of an amphetamine-induced psychotic episode include
sants such as the benzodiazepines or alcohol.12 Am- psychomotor retardation, incoherent speech, inappropri-
phetamine abusers also might experience periods of ate or flattened affect, and depression (Srisurapanont,
drug-induced confusion, irritability, fear, suspicion, Marsden, Sunga, Wada, & Monterio, 2003). Nearly two-
11See
thirds of chronic methamphetamine abusers report at
Glossary.
12The
least some symptoms of a drug-induced psychosis when
reverse has also been observed: Some heavy drinkers have been
known to ingest amphetamine compounds to counteract the sedation asked (Rawson et al., 2005). But where Kaplan and
inherent in heavy alcohol use, to allow them to continue to drink Sadock (1996) suggested that amphetamine-induced hal-
longer. lucinations tend to be mainly visual, which is not typical
of a true schizophrenic condition, Srisurapanont et al. mouth” (Davey, 2005; Rawson et al., 2005). Individuals
(2003) suggested that auditory hallucinations were more who suffer from this condition rapidly develop so much
common in the amphetamine- induced psychosis. tooth decay and damage that extensive dental repairs or
Under normal conditions, this drug-induced psy- extractions are often necessary. It is not known whether
chosis clears up within days to weeks after the drug is this is a direct effect of the methamphetamine, which
discontinued (Haney, 2004). However, in some cases, reduces the user’s saliva production to about one-fourth
it may continue for several months (Rawson et al., the normal levels, or a consequence of the abuser’s ten-
2005). Researchers in Japan following World War II dency to ingest sugar-sweetened foods to satisify the
noted that in 15% of cases of amphetamine-induced body’s hunger (Rawson et al., 2005). A third possibility
psychosis, it took up to 5 years following the last am- is that some of the compounds utilized in the manufac-
phetamine use before the drug-induced psychotic con- ture of illicit methamphetamine might cause or exacer-
dition eased (Flaum & Schultz, 1996). Occasionally, the bate the tooth decay (Davey, 2005; Rollo et al., 2007).
amphetamine-induced psychosis does not remit and the In many cases the individual’s tooth decay is so exten-
individual develops a chronic psychosis. It was once sive that the only treatment is complete removal of the
thought that the amphetamine-induced psychosis re- affected teeth, with dental prosthetics then being
flected the activation of a latent schizophrenia in a per- necessary.
son who was vulnerable to this condition. Chen et al. The cardiovascular system. As clinicians have gained
(2003) assessed 445 amphetamine abusers in Taipei experience with methamphetamine abusers, they have
(Taiwan) and found a tendency for those individuals come to understand that the abuse of this compound
who subsequently developed a methamphetamine- can cause severe cardiovascular damage. Ampheta-
induced psychosis to have been younger at the time of mine abuse, especially methamphetamine abuse, has
their first drug use, to have used larger amounts of been implicated as the cause of accelerated develop-
methamphetamine, and to have premorbid schizoid or ment of plaques in the coronary arteries, thus contribut-
schizotypal personalities. Further, the authors found a ing to the development of coronary artery disease
positive relationship between the degree of personality (CAD) in users (Karch, 2002). Amphetamine abuse
dysfunction and the length of the methamphetamine- can also result in hypertensive episodes, tachycardia, ar-
induced psychotic reaction. rhythmias, and sudden cardiac death, especially when
Prolonged use of the amphetamines may also produce the drug is used at high dosage levels (Ballas et al.,
a condition known as formication (Tekin & Cummings, 2004; Gitlow, 2007; Karch, 2002; Rawson et al., 2005).
2003). Victims have been known to scratch or burn their Amphetamine abusers have been known to suffer a
skin in an attempt to rid themselves of these unseen bugs. number of serious, potentially fatal cardiac problems, in-
Further, when the abuser discontinues the use of amphet- cluding myocardial ischemia (Derlet & Heischober,
amines, he or she will experience profound feelings of fa- 1990), chest pain (angina), congestive heart failure
tigue and depression, the latter possibly reaching the level (Derlet & Horowitz, 1995), myocardial infarction (Acosta
of suicidal proportions (Schuckit, 2006). et al., 2005; Karch, 2002; Wadland & Ferenchick, 2004),
The digestive system. Amphetamine abuse may cause and cardiomyopathy (Greenberg & Barnard, 2005;
such digestive system problems as anorexia, diarrhea or Oehmichen et al., 2005). Yeo et al. (2007) considered
constipation, nausea, vomiting, and ischemic colitis young methamphetamine abusers to have a risk of de-
(Albertson et al., 1999; Rawson et al., 2005; Sadock & veloping cardiomyopathy that was 350% higher than
Sadock, 2003). There have been isolated reports of that of their non–drug-abusing peers.
amphetamine-induced liver damage, although the exact The mechanism of an amphetamine-induced my-
mechanisms by which illicit amphetamines are able to ocardial infarction is thought to be similar to that seen
cause damage to the liver are still not clear (Jones, in cocaine-induced myocardial infarctions (Wijetunga
Jarvie, McDermid, & Proudfoot, 1994). The conse- et al., 2004). Amphetamine abuse has been identified
quences of prolonged amphetamine use, like those of as causing rhabodmyolysis in some users, although the
cocaine, include the various complications seen in exact mechanism by which the amphetamines might
users who have neglected their dietary requirements. cause this disorder remains unclear (Ballas et al., 2004;
Vitamin deficiencies are a common consequence of Oehmichen et al., 2005; Richards, 2000).
chronic amphetamine abuse (Gold & Verebey, 1984). The pulmonary system. Amphetamine abuse has
One emerging consequence of methamphetamine been identified as a cause in such respiratory problems
abuse is a poorly understood condition known as “meth as sinusitis, pulmonary infiltrates, pulmonary edema,
128 Chapter Eleven
exacerbation of asthma, pulmonary hypertension, and to experience pleasure—feelings of apathy—for months,

pulmonary hemorrhage/infarct (Acosta et al., 2005; or even years after their last use of amphetamines
Rawson et al., 2005). (Miller, 2005; Schuckit, 2006). Other symptoms noted
Other consequences of amphetamine abuse. One un- in the first few days following cessation include muscu-
intended consequence of any form of amphetamine loskeletal pain, depression, anorexia-impaired social
abuse is that the amphetamine being abused might functioning, and sleep disturbance. These symptoms
interact with surgical anesthetics if the abuser should gradually wane in intensity over the first 2 weeks follow-
be injured and require emergency surgery (Klein & ing methamphetamine cessation.
Kramer, 2004). Further, there is evidence that amphet-
amine use/abuse might exacerbate some medical disor-
ders such as Tourette’s syndrome or tardive dyskinesia “Ice”
(Lopez & Jeste, 1997). In the late 1970s a smokable form of methampheta-
Amphetamine abuse has been implicated as a cause mine called “Ice” was introduced to the U.S. mainland
of sexual performance problems for both men and (“Ice Overdose,” 1989). Although it differs in appear-
women (Albertson et al., 1999; Finger, Lund, & Slagel, ance from methamphetamine tablets, on a molecular
1997). High doses or chronic use of amphetamines can level it is simply methamphetamine (Wijentunga et al.,
cause an inhibition of orgasm in the user, according to 2004). Historical evidence suggests that this form of
Albertson et al., as well as delayed or inhibited ejaculation methamphetamine was brought to Hawaii from Japan
in men. The practice of smoking methamphetamine by U.S. Army troops following World War II; it has be-
has resulted in the formation of ulcers on the cornea of come the most commonly abused drug among those
the eyes of some users (Chuck, Williams, Goldberg, & seeking help for a substance use problem in Hawaii
Lubniewski, 1996). Methamphetamine abusers have (Tominaga, Garcia, Dzierba, & Wong, 2004). Smoking
been identified as being at increased risk for seizures methamphetamine is also endemic in Asia, where it is
and for elevated body temperature,13 which itself might known as “shabu” (United Nations, 2003). The prac-
be a risk factor for rhabdomyolsis (Ballas et al., 2004). tice has slowly spread across the United States, but by
The addictive potential of amphetamines. There is no 2004 only 4% of the high school seniors surveyed ad-
test that will identify those who are most “at risk” for mitted to having used Ice at least once (Johnston, O’-
amphetamine addiction—just another in the long list Malley, Bachman, & Schulenberg, 2004a).
of reasons that the abuse of these chemicals is not rec- How Ice is used. Ice is a colorless, odorless form of
ommended. When abused, these compounds stimulate concentrated crystal methamphetamine that resembles
the brain’s “reward system,” possibly with greater effect a chip of ice, or clear rock candy. Although injection or
than natural reinforcers such as food or sex (Haney, inhalation of methamphetamine is common, smoking
2004). This effect helps create “vivid, long-term memo- Ice is also quite popular in some regions of the United
ries” (Gawin & Ellinwood, 1988, p. 1175) of the drug States (Karch, 2002). Ice is smoked in a manner similar
experience for the user. These memories help sensitize to “crack” cocaine, crossing into the blood through the
the individual to drug use cues, which cause the abuser lungs and reaching the brain in a matter of seconds.
to “crave” the drug when exposed to these cues. Subjective effects of Ice abuse. In contrast to cocaine,
Methamphetamine abstinence syndrome.14 Evidence which induces a sense of euphoria that lasts perhaps
is emerging of a constellation of symptoms that appear 20 minutes, the high from Ice lasts for a significantly
in the first few days following a protracted period of longer period of time. Estimates of the duration of its
methamphetamine abuse. In the first 72 hours, the effects vary from 8 hours (“Raw Data,” 1990) to 12
symptoms of anhedonia,15 irritability, and poor concen- (“Drug Problems in Perspective,” 1990; “New Drug
tration are the most prominent (Miller, 2005; Newton, ‘Ice’ Grips Hawaii,” 1989), to 14 (“Ice Overdose,” 1989)
Kalechstein, Duran, Vansulis, & Ling, 2004). Chronic or 18 (McEnroe, 1990), up to 24 hours (Evanko, 1991).
amphetamine abusers have reported a reduced ability Kaminski (1992) suggested that the effects of Ice might
last as long as 30 hours. The long duration of its effect,
13Or hyperthermia. while obviously in some dispute, is consistent with the
14This assumes that the individual was abusing only amphetamines. If pharmacological properties of the amphetamines com-
the individual was a polydrug abuser, then the withdrawal picture will pared with those of cocaine. The stimulant effects of the
be complicated by the effects of these other compounds. amphetamines in general last for hours, where cocaine’s
15See Glossary.
stimulant effects usually last for a shorter period of time.
The effects of Ice. Users have found that Ice has sev- “Kat”
eral advantages over “crack” cocaine. First, although it In the late 1990s it appeared that methcathinone, or
is more expensive than crack, dose for dose, Ice is about “Kat” (sometimes spelled “Cat,” “qat,” “Khat,” and also
25% as expensive as crack (Rawson et al., 2005). Sec- known as “miraa”) might become a popular drug of
ond, because of its duration of effect, it seems to be abuse in the United States. Kat leaves contain
more potent than crack. Third, since Ice melts at a norephedrine and cathinone, which is biotransformed
lower temperature than crack, it does not require as into norephedrine by the body. Kat is found naturally in
much heat to use. This means that Ice may be smoked several species of evergreen plants that grow in east
without the elaborate equipment needed for crack Africa and southern Arabia (Community Anti-Drug
smoking. Because it is odorless, Ice may be smoked Coalitions of America, 1997; Haroz & Greenberg,
in public without any characteristic smell alerting 2005). The plant grows to 10–20 feet in height, and the
passersby that it is being used. Finally, another advan- leaves produce the alkaloids cathinone and cathine. Il-
tage of Ice is that if the user decides to stop smoking Ice licit producers began to produce an analog of cathi-
for a moment or two, it will cool and reform as a crystal. none, known as methcathinone, which has a chemical
This makes it highly transportable and offers an advan- structure similar to that of the amphetamines and
tage over crack cocaine; the individual can use only a ephedrine (Karch, 2002).
part of the piece of Ice at any given time rather than The legal status of Kat. Kat was classified a Category
having to use it all at once, as necessary with crack. I16 controlled substance in 1992, and because of this
Complications of Ice abuse. Essentially, the compli- classification the manufacture of this drug or its distri-
cations of Ice use are the same as those of other forms of bution is illegal (Monroe, 1994).
amphetamine abuse. This is understandable, since Ice How Kat is produced. Kat is easily synthesized in il-
is simply a different form of methamphetamine than the licit laboratories, using ephedrine and such compounds
powder or pills sold on the street for oral or intravenous as drain cleaner, epsom salts, battery acid, acetone, tou-
use. However, in contrast to the dosage level achieved lene, various dyes, and hydrochloric acid to alter the
when methamphetamine is used by a patient under a basic ephedrine molecule. These chemicals are mixed
physician’s care, the typical amount of methampheta- in such a way as to add an oxygen molecule to the origi-
mine admitted into the body when the user smokes Ice nal ephedrine molecule (“Other AAFS Highlights,”
is between 150 and 1,000 times the maximum recom- 1995) to produce a compound with the chemical struc-
mended therapeutic dosage for methamphetamine ture 2-methylamino-1-pheylpropan-1-one.
(Hong, Matsuyama, & Nur, 1991). At such high dosage The scope of Kat use. After the introduction of Kat to
levels, it is common for the abuser to experience one or the United States, it could be purchased in virtually any
more adverse effects from the drug. major city by the mid-1990s (Finkelstein, 1997). How-
In addition to the adverse effects of any ampheta- ever, by the start of the 21st century, methcathinone
mine abuse, which are also experienced by Ice users, has virtually disappeared from the drug scene, except
there are many problems specifically associated with for sub-Saharan immigrants who continue the practice
the use of Ice. Methamphetamine is a vasoconstrictor, of chewing the leaves even after arriving in the United
which might be why some Ice users develop potentially States (Karch, 2002; “Khat Calls,” 2004).
dangerous elevations in body temperature (Beebe & The effects of Kat. Users typically either inhale or
Walley, 1995). When the body temperature passes smoke Kat, although it can be injected (Monroe, 1994).
above 104°F, the prognosis for recovery is quite poor. On rare occasions, the leaves are chewed (Haroz &
There have also been reports that female patients who Greenberg, 2005). The drug’s effects are similar to
have had anesthesia to prepare them for caesarean sec- those of the amphetamines (Haroz & Greenberg,
tions have suffered cardiovascular collapse because of 2005). Users report that the drug can cause a sense of
the interaction between the anesthesia and Ice. Some euphoria (Community Anti-Drug Coalitions of Amer-
Ice abusers have reported having myocardial infarc- ica, 1997) as well as a more intense “high” than does
tions or developing a pulmonary edema up to 36 hours cocaine (“Cat Poses National Threat,” 1993). In con-
after their last use of the drug, although the mecha- trast to cocaine, the effects of Kat can last from 24 hours
nism by which smoked methamphetamine might (Community Anti-Drug Coalitions of America, 1997)
cause these potentially lethal problems is not clear up to 6 days (Goldstone, 1993; Monroe, 1994). Once in
(Tominaga et al., 2004). As these findings suggest, Ice is
hardly safe. 16
See Appendix Four.
130 Chapter Eleven
the body, Kat is biotransformed into ephedrine, nor- was discovered that the ampules were a source of con-
pseudoephedrine, and other compounds (Haroz & centrated amphetamine, which could be injected. The
Greenberg, 2005). The compound is abused for its resulting “high” was found to be similar to that of co-
amphetamine-like euphoric effects. caine—which had gained a reputation as being a dan-
Adverse effects of Kat abuse. There has been little re- gerous drug to use—but with the added benefit lasting
search into the pharmacology of Kat or its adverse ef- much longer.
fects, and much of what is known about this compound The amphetamines were used extensively both dur-
is based on clinical data drawn from cases seen by ing and after World War II. Following the war, Ameri-
physicians. Known side effects of Kat include vasocon- can physicians prescribed amphetamines for the
striction, hyperthermia, increased blood pressure, in- treatment of depression and as an aid for weight loss. By
somnia, anorexia, and constipation as well as a drug- the year 1970, amphetamines accounted for 8% of all
induced psychosis, hallucinations, paranoia, anxiety, prescriptions written. However, since then physicians
depression, and mood swings (Haroz & Greenberg, have come to understand that the amphetamines pres-
2005). Following the period of drug use, it is not uncom- ent a serious potential for abuse. The amphetamines
mon for Kat users to fall into a deep sleep that might last have come under increasingly strict controls, which
for as long as several days (Monroe, 1994). limit the amount of amphetamine manufactured and
Scope of the problem of Kat abuse. The scope of the reasons an amphetamine might be prescribed.
Kat abuse remains unknown. It is rarely abused by ca- Unfortunately, the amphetamines are easily manufac-
sual drug abusers, but hard-core stimulant abusers will tured and there has always been an underground manu-
occasionally become Kat abusers (O’Brien, 2001). facture and distribution system for these drugs. In the late
1970s and early 1980s street drug users drifted away from
the amphetamines to the supposedly safe stimulant of
Summary the early 1900s: cocaine. In the late 1990s, the pendu-
Although they were discovered in the 1880s, the am- lum began to swing the other way, and illicit drug users
phetamines were first introduced as a treatment for began to use the amphetamines, especially metham-
asthma some 50 years later, in the 1930s. The early phetamine, more and more frequently. This new genera-
forms of amphetamine were sold over the counter in tion of amphetamine addicts has not learned the dangers
cloth-covered ampules that were used much like of amphetamine abuse so painfully discovered by am-
smelling salts today. Within a short time, however, it phetamine users of the late 1960s: “Speed” kills.
CHAPTER TWELVE
Cocaine
Historically, the United States experienced a resurgence (White, 1989). The lime works with saliva to release the
of interest in and abuse of cocaine in the early to mid- cocaine from the leaves and also helps to reduce the
1980s. This wave of cocaine abuse peaked around 1986, bitter taste of the coca leaf. Chewing coca leaves is
gradually declined in the middle to late 1990s, and by the thought to actually help the chewer absorb some of the
early years of the 21st century cocaine abuse levels in the phosphorus, vitamins, and calcium contained in the
United States were significantly lower than those seen 15 mixture (White, 1989). Thus, although its primary use
years earlier. However, after declining in popularity, co- is to help the natives work more efficiently at high alti-
caine abuse is once again becoming popular, at least in tudes, there might also be some small nutritional bene-
some age groups (Acosta, Haller, & Schnoll, 2005). This fit obtained from the practice of chewing coca leaves.
chapter examines cocaine abuse and addiction. As European scientists began to explore the bios-
phere of South America, they took a passing interest in
the coca plant and attempted to isolate the compounds
A Brief Overview of Cocaine
that made it so effective in warding off hunger and fa-
At some point in the distant past, a member of the plant tigue. In 18591 a chemist by the name of Albert Neiman
species Erythroxylon coca began to produce a neuro- isolated a compound that was later named cocaine
toxin in its leaves that would destroy the nervous system (Scaros, Westra, & Barone, 1990). This accomplishment
of bugs that might try to ingest its leaves (Breiter, 1999). allowed researchers to first produce large amounts of
This neurotoxin, cocaine, was able to ward off most of relatively pure cocaine for research. One of these exper-
the insects that would otherwise strip the coca plant of iments involved the injection of concentrated co-
its leaves, allowing the plant to thrive in the higher ele- caine directly into the bloodstream with another new
vations of Peru, Bolivia, and Java (DiGregorio, 1990). invention: the hypodermic needle.
At least 5,000 years ago, someone discovered that chew- Before long researchers discovered that even orally
ing the leaves of the plant could ease feelings of fatigue, administered cocaine made the user feel good. Extracts
thirst, and hunger, enabling one to work for longer peri- from the coca leaf were used to make a wide range of
ods of time in the thin mountain air (Levis & Garmel, popular drinks, wines, and elixirs (Martensen, 1996).
2005). By the time the first European explorers arrived, Physicians of the era, lacking effective pharmaceuticals
the Inca empire was at its height, and the coca plant for most human ills, experimented with cocaine con-
was used extensively within the Incan empire. centrate as a possible agent to treat disease. No less a fig-
Prior to the arrivial of the first European explorers, ure than Sigmund Freud experimented with cocaine,
the coca plant’s use was generally reserved for the upper at first thinking it a cure for depression (Rome, 1984),2
classes of society (Mann, 1994). However, European and later as a possible “cure” for narcotic withdrawal
explorers soon found that when native workers were symptoms (Byck, 1987; Lingeman, 1974). However,
given coca leaves to chew on, they were more produc- Freud soon discovered cocaine’s previously unsus-
tive. The coca plant became associated with the expected dangers, although his warnings received little at-
ploitation of South America by European settlers, who tention from scientists of the era (Gold & Jacobs, 2005).
encouraged its widespread use. Even today, the prac-
tice of chewing coca leaves or drinking a form of tea 1Schuckit (2006) reported that cocaine was isolated in 1857, rather
brewed from the leaves has continued. Modern natives than 1859.
of the mountain regions of Peru chew coca leaves 2Surprisingly, recent research (Post, Weiss, Pert, & Uhde, 1987) has
mixed with lime, which is obtained from sea shells cast doubt on the antidepressant properties of cocaine.
131
132 Chapter Twelve
Cocaine in Recent U.S. History mid-1960s. The amphetamines had acquired a reputa-
tion as known killers. Drug users would warn each
After the city of Atlanta prohibited alcohol, John Stith- other that “speed kills,” a reference to the amphet-
Pemberton developed a new product that he thought mines’ ability to kill the user in a number of different
would serve as a “temperance drink” (Martensen, 1996, ways. Cocaine had the reputation of inducing many of
p. 1615), and until 1903 it contained 60 mg of cocaine the same sensations caused by amphetamine use with-
per 8-ounce serving (Gold, 1997). In time, the world out the dangers associated with the abuse of other CNS
would come to know Stith-Pemberton’s product by an- stimulants. Cocaine’s reputation as a special, glam-
other name: “Coca-cola.” Although modern readers orous drug, combined with increasing government re-
may be surprised to learn its original ingredients, restrictions on amphetamine production by legitimate
member that consumer protection laws were virtually pharmaceutical companies, all helped focus drug
nonexistent when this product was first introduced, and abusers’ attention on cocaine as a substitute by the late
chemicals such as cocaine and morphine were readily 1960s.
available without a prescription. These compounds were By the middle of the 1980s, cocaine had again be-
widely used in a variety of products and medicines, usu- come a popular drug of abuse in a number of countries
ally as a hidden ingredient. This practice contributed around the world. The United States did not always
to epidemics of cocaine abuse in Europe between the lead in the area of cocaine abuse. For example, by the
years 1886 and 1891, and in both Europe and the mid-1970s, the practice of smoking coca paste was pop-
United States between 1894 and 1899 and again in ular in parts of South America but had only started to
the United States between 1921 and 1929. gain popularity in the United States. But as cocaine be-
These waves of cocaine abuse/addiction, the use of came more popular in this country, it attracted the at-
cocaine in so many patent medicines, fears over its sup- tention of what is loosely called organized crime. At the
posed narcotic qualities, and concern that cocaine was same time, cocaine dealers were eager to find new mar-
corrupting Southern blacks prompted both the passage kets for their “product” in the United States, where the
of the Pure Food and Drug Act of 1906 (Mann, 1994) primary method of cocaine abuse was intranasal inhala-
and the classification of cocaine as a narcotic in 1914 tion of the cocaine powder. After a period of ex-
(Martensen, 1996). The Pure Food and Drug Act of periementation, illicit drug manufacturers developed
1906 required makers to list the ingredients of a patent “crack,” a form of cocaine that could be smoked without
medicine or elixir on the label. As a result of this law, elaborate preparation or equipment, and crack started to
cocaine was removed from many patent medicines. become the preferred form of cocaine in this country in
With the passage of the Harrison Narcotics Act of 1914, the early 1980s. Approximately 50% of the illicit co-
nonmedical cocaine use in the United States was procaine in the United States is crack (Greydanus & Patel,
hibited (Derlet, 1989). 2005).
These regulations, the isolation of the United States The epidemic of cocaine use/abuse that swept the
during the First and Second World Wars, and the am- United States in the 1980s and 1990s will not be dis-
phetamines in the 1930s helped to virtually eliminate cussed here; this topic is worthy of a book in its own
cocaine abuse in this country. Cocaine did not resur- right. But by the start of the 21st century, drug abusers
face as a major drug of abuse until the late 1960s. By had come full circle: The dangers of cocaine abuse
then, it had the reputation in the United States of being were well known, and drug users were eager for an al-
the “champagne of drugs” (White, 1989, p. 34) for ternative to cocaine. Just as the then-new ampheta-
those who could afford it. It again became popular here mines replaced cocaine as the preferred stimulant of
as a drug of abuse in the 1970s and early 1980s. There choice in the 1930s, the amphetamines, especially
are many reasons for this resurgence in cocaine’s popu- methamphetamine, are again replacing cocaine as the
larity. First, cocaine had been all but forgotten since CNS stimulant of choice for drug abusers. Cocaine
the Harrison Narcotics Act of 1914. Stories of cocaine use/abuse appears to have peaked sometime around
abusers sneezing out long tubes of damaged or dead 1986 in the United States, and casual cocaine abuse
cartilage in the latter years of the 19th and early years of reached its lowest levels in the late 1990s (Gold & Jacobs,
the 20th centuries were either forgotten or dismissed as 2005). However, cocaine has by no means disappeared,
“moralistic exaggerations” (Gawin & Ellinwood, 1988, and recreational cocaine use is slowly increasing in
p. 1173; Walton, 2002). popularity in the United States (Acosta et al., 2005;
Also, there had been a growing disillusionment with Gold & Jacobs, 2005).
the amphetamines as drugs of abuse that started in the
Cocaine 133
Cocaine Today 1 minute, and its effects would last as long as 2 hours
(Wilson, Shannon, Sheilds, & Stang, 2007). Cocaine was
At the start of the 21st century, Erythroxylon coca contin- also included in a mixture called Brompton’s cocktail,
ues to thrive in the high mountain regions of South which was used to control the pain of cancer. However,
America, and the majority of the coca plants grown in this mixture has fallen out of favor and is rarely, if ever,
South America are harvested for the international co- used today (Scaros et al., 1990). At the start of the 21st
caine trade and not for local use (Mann, 1994). But century, cocaine’s role in medicine is so limited that it is
people who live in the high mountain plateaus continue remarkable when a physician orders it for a patient.
to chew coca leaves to help them work and live. Some
researchers have pointed to this practice as evidence
that cocaine is not as addictive as drug enforcement offi- Scope of the Problem of Cocaine
cials claim, possibly because chewing the leaves is a Abuse and Addiction
rather inefficient method of abusing cocaine. Much of In 2004 an estimated 687 metric tons of cocaine was
the cocaine that is released by this method is destroyed produced around the globe and consumed by an esti-
by the acids of the digestive tract. As a result of these mated 13.4 million cocaine abusers (United Nations,
forces, the native who chews cocaine is not thought to 2006). Approximately 6.5 million of these cocaine
obtain a significant level of cocaine in the blood. abusers are thought to live in North America,5 while an
Other researchers have suggested that the natives of estimated 3.5 million cocaine abusers are found in Eu-
South America who chew coca leaves do indeed be- rope, and 2.3 million in South America (United Nations,
come addicted to the stimulant effect of the cocaine. 2006). The remaining 1.8 million cocaine abusers live in
These scientists point to studies revealing that the blood areas of the globe where cocaine abuse is not a major so-
level of cocaine achieved when coca leaves are chewed cial problem.
barely enters the lower range of blood levels achieved In the United States, cocaine abusers consume 250
by those who “snort” cocaine in the United States, with metric tons of the cocaine produced around the world
a significant proportion of the cocaine absorbed from each year (Office of National Drug Control Policy,
the gastrointestinal tract being subjected to the first-pass 2004). The cocaine abusers in New York City alone con-
biotransformation effect.3 The amount of cocaine that sume probably 16.4 tons of cocaine (172 grams/person)
reaches the individual’s brain is barely enough to have a each year (“New York Remains Cocaine Capital,”
psychoactive effect, but it is still a large enough dose to 2007). In the San Francisco area, the annual per capita
be addicting, in the opinion of some scientists (Karch, cocaine consumption is approximately 40 grams/year,
2002). Thus, the answer to the question of whether na- while in the Washington, D.C., area it is 73 grams/year
tives who chew coca leaves are or are not addicted to (“New York Remains Cocaine Capital,” 2007). More
the cocaine that they might absorb has not been re- than 30 million people in the United States have proba-
solved. Legally, cocaine is classified as a Schedule II4 bly used cocaine at least once (Hahn & Hoffman,
substance in the United States. 2001), and between 1.7 and 2 million of those are regu-
lar users (Acosta et al., 2005; Carroll & Ball, 2005). The
Current Medical Uses of Cocaine annual consumption statistics would suggest that those
who engage in cocaine abuse do so with great abandon,
Cocaine was once a popular pharmaceutical agent, spending approximately $35 billion each year to pur-
used in the treatment of a wide range of conditions. By chase the illicit drug (Levis & Garmel, 2005). On a pos-
the 1880s, physicians had discovered that it was an ef- itive note, this amount is half the estimated amount
fective local anesthetic (Byck, 1987; Mann, 1994). It spent by cocaine abusers in the United States in 1990
was found to block the movement of sodium ions into (Levis & Garmel, 2005).
the neuron, thus altering its ability to carry pain signals
to the brain (Drummer & Odell, 2001). Because of this
effect, cocaine was once commonly used by physicians Pharmacology of Cocaine
as a topical analgesic for procedures involving the ear, Cocaine is best absorbed into the body when it is ad-
nose, throat, rectum, and vagina. When used as a local ministered as cocaine hydrochloride, a water-soluble
anesthetic, cocaine would begin to be effective in about compound. After entering the body, it quickly diffuses
3
See Glossary. 5TheUnited Nations classifies North America as being composed of
4
See Appendix Four. Canada, Mexico, and the United States.
134 Chapter Twelve
into the general circulation and is rapidly transported to Cocaine also alters the function of a protein known
the brain and other blood-rich organs, such as the as postsynaptic density-95 (Sanna & Koob, 2004). Long-
heart. It spite of its rapid distribution, the level of co- term changes in this protein, which is involved in the
caine in the brain is usually higher than it is in the process of helping the neuron adapt the synapse to
blood plasma, especially in the first 2 hours following changing neurotransmitter mixtures, are thought to be
use of the drug (“Cocaine in the Brain,” 1994). involved in learning and memory formation; this possi-
In the brain, cocaine produces a buildup of dopa- bly accounts in part for cocaine’s ability to cause the
mine in several interconnected regions of the brain user to form strong memories of the drug’s effects and
known as the limbic system such as the nucleus accum- help explain the high relapse rate seen in newly absti-
bens, the amygdala, and the anterior cingulate (Haney, nent abusers (Acosta et al., 2005; Sanna & Koob, 2004).
2004; Nestler, 2005). It does this by blocking the action After periods of prolonged abuse, the neurons within
of a protein molecule in the wall of some neurons the brain will have released virtually all their stores of
known as the dopamine transporter, whose function is the neurotransmitter dopamine without being able to
to absorb some of the dopamine found in the extracel- reabsorb virtually any of the free dopamine found in the
lular space for reuse (Haney, 2004; Jaffe, Rawson, & synapse. Low levels of dopamine are thought to be one
Ling, 2005; Nestler, 2005). This allows greater concen- cause of depression. This pharmacological effect of co-
trations of dopamine than normal to build up in the caine might explain the observed relationship between
limbic system, enhancing its effects on the neurons of cocaine abuse and depression, which has been known
the limbic system to the point that cocaine’s reward po- to reach suicidal proportions in some cocaine abusers.
tential might be stronger than that of natural reinforcers Tolerance to cocaine’s euphoric effect develops very
such as food or sexual activity (Haney, 2004). Perhaps rapidly (Schuckit, 2006). As tolerance develops, the in-
for this reason cocaine addicts refer to their drug as the dividual will require more and more cocaine to achieve
“white lady” and speak of it almost as if it were a human a euphoric effect. This urge to increase the dosage and
lover. continue using the drug can reach the point that it
There are at least five different subtypes of dopamine “may become a way of life and users become totally
receptors in the brain, and the reinforcing effects of co- preoccupied with drug-seeking and drug taking behav-
caine seem to reflect its ability to stimulate some of iors” (Siegel, 1982, p. 731). Unfortunately, as the indi-
these receptor subtypes more strongly than others. For vidual’s cocaine abuse becomes more frequent and
example, Romach et al. (1999) found that when the prolonged, the normal function of the diencephalon7 is
dopamine D1 receptor was blocked, their volunteers disrupted. This will result in a higher than normal body
failed to experience the pleasure that cocaine usually temperature for the user. At the same time, the cocaine
induces when it is injected into the circulation. On the will cause the constriction of surface blood vessels. This
basis of this finding, the authors concluded that the combination of effects results in hyperthermia.8 The
dopamine D1 receptor site was involved in the experi- cocaine abuser’s body will conserve body heat at just
ence of euphoria reported by cocaine abusers. It thus is the time it needs to release the excess thermal energy
not surprising to learn that in the human brain, the caused by the cocaine-induced dysregulation of body
dopamine D1 receptors are concentrated in the limbic temperature, possibly with fatal results (Gold & Jacobs,
system of the brain. 2005; Jaffe, Rawson, et al., 2005).
Cocaine also seems to activate the mu and kappa Cocaine’s effects on the user are very short-lived.
opioid receptors and cause long-term changes in the Peak plasma levels following an intravenous injection of
function of compounds such as 6FosB6 (Nestler, 2005; cocaine are reached in just 5 minutes, and after 20–40
Unterwald, 2001). These findings help to explain the minutes the effects begin to diminish (Weddington,
intensity of the craving that cocaine-dependent people 1993). The half-life of injected cocaine is estimated to
report experiencing when they abstain from the drug. be between 30 and 90 minutes (Jaffe, Rawson, et al.,
In addition to blocking the reuptake of dopamine, co- 2005; Mendelson & Mello, 1996). In spite of the half-
caine also blocks the reuptake of the neurotransmitters life period, evidence suggests that the cocaine abuser
serotonin and norepinephrine, although the signifi- will begin to crave further cocaine 10–30 minutes after
cance of this effect is not known at the present time
(Acosta et al., 2005; Reynolds & Bada, 2003). 7A region of the brain responsible for temperature regulation, among
other things.
6 8See
See Glossary. Glossary.
Cocaine 135
he or she smoked or injected cocaine, possibly as the sudden cardiac death from the combination of alcohol
blood plasma levels begin to drop (O’Brien, 2006). and cocaine 18-fold over that of cocaine abuse alone
The organ most involved in the elimination of co- (Acosta et al., 2005; Hahn & Hoffman, 2001; Repetto &
caine from the body is the liver, which produces about Gold, 2005). Research also has suggested a possible re-
a dozen metabolites of cocaine during the process of lationship between the concurrent use of cocaine and
biotransformation (Karch, 2002). About 80% of a dose alcohol in the development of a fatal pulmonary edema
of intravenously administered cocaine is biotrans- (Barnhill, Ciraulo, Ciraulo, & Greene, 1995). Unfor-
formed into one of two primary metabolites: benzoylec- tunately, cocaethylene may lengthen the period of
gonine (BEG), and ecogonine methyl ester (Levis & cocaine-induced euphoria, possibly by blocking dopa-
Garmel, 2005). The other metabolites are of minor im- mine reuptake, making it more likely that the person
portance and need not be considered further in this will continue to coadminister these two compounds in
text. Only about 5% to 10% of a single dose of cocaine spite of the danger associated with this practice.
is excreted from the body unchanged. Neither of the Some abusers will inject a combination of cocaine
major metabolites of cocaine has any known biological and an opiate, a process known as “speedballing.” How-
activity in the body. BEG has a half-life of 7.5 hours ever, for reasons that are not well understood, cocaine
(Marzuk et al., 1995). Because the half-life of BEG is will actually enhance the respiratory depressive effect
longer than that of the parent compound, and because of the opiates, possibly resulting in episodes of respira-
it is stable in urine samples that have been frozen, this tory arrest in extreme cases (Kerfoot, Sakoulas, &
is the chemical that laboratories usually test for when Hyman, 1996). As discussed later in this chapter, cocaine
they test a urine sample for evidence of cocaine use.9 abuse often results in a feeling of irritation or anxiety.
Drug interactions involving cocaine. Cocaine interacts To control the cocaine-induced agitation and anxiety,
with a wide range of chemicals, but there has been sur- users often ingest alcohol, tranquilizers, or marijuana.
prisingly little research into cocaine-drug interactions The combination of marijuana and cocaine appears
(Karch, 2002). Cross-addiction is a common complica- capable of increasing the heart rate by almost 50 beats
tion of chronic cocaine use. For example, more than per minute in individuals who are using both substances
62%–90% of cocaine abusers have a concurrent alcohol (Barnhill et al., 1995).
use disorder (Gold & Jacobs, 2005), and 21% of adults There is one case report of a patient who was abus-
with ADHD are thought to have a cocaine use disorder ing cocaine and took an over-the-counter cold medica-
(Acosta et al., 2005). tion that contained phenylpropanolamine. This person
As scientists have come to better understand the in- developed what seems to have been a drug-induced psy-
teraction between alcohol and cocaine, they have dis- chosis that included homicidal thoughts (Barnhill et al.,
covered that when a person uses cocaine while 1995). It is not clear whether this was an isolated inci-
intoxicated there is a 30% increase in the cocaine blood dent or if the interaction between cocaine and phenyl-
plasma levels due to alcohol-induced reduction in the propanolamine might precipitate a psychotic reaction,
liver’s ability to biotransform the cocaine (Acosta et al., but the concurrent use of these chemicals is not
2005). Unfortunately, a small amount (less than 10%) recommended.
of the cocaine is biotransformed into cocaethylene
(Gold & Miller, 1997a; Karch, 2002; Repetto & Gold,
How Illicit Cocaine Is Produced
2005). Cocaethylene is extremely toxic to the user’s
body and is thought to be 25–30 times as likely to in- Cocaine production has changed little in the past gen-
duce death as cocaine itself (Karan, Haller, & Schnoll, eration. First, the cocaine leaves are harvested. In
1998). Cocaethylene functions as a powerful calcium some parts of Bolivia, this may be done as often as
channel blocker in the heart and has a biological half- once every 3 months, as the climate is well suited for
life that is five times longer than that of cocaine alone, the plant to grow. Second, the leaves are dried, usually
factors that are thought to raise the individual’s risk of by letting them sit in the open sunlight for a few hours
or days, and although this process is illegal in many
9The estimation of blood cocaine levels following death is quite diffi- parts of South America, the local authorities are quite
cult because cocaine will auto-metabolize following death. This tolerant and do little to interfere with the drying of
means that the body will continue to biotransform cocaine in the
blood even after the user’s death, thus making is very difficult to deter-
coca leaves.
mine how much cocaine was in the individual’s system at the time of In the next step, the dried leaves are put in a plastic
his or her death. lined pit and mixed with water and sulfuric acid
136 Chapter Twelve
(White, 1989). The mixture is crushed by workers who 2005). One gram of illicit cocaine usually will yield
wade into the pit in their bare feet. After the mixture about 30 such “lines” (Acosta et al., 2005; Karan et al.,
has been crushed, diesel fuel and bicarbonate are 1998). The powder is diced up, usually with a razor
added to the mixture. After a period of time, during blade on the glass or mirror, to make the particles as
which workers reenter the pit several times to continue small as possible and enhance absorption. The powder
stomping through the mixture, the liquids are drained is then inhaled through a drinking straw or rolled
off. Lime is then mixed with the residue, forming a paper.
paste (Byrne, 1989) known as cocaine base. It takes 500 When it reaches the nasal passages, which are richly
kilograms of leaves to produce one kilogram of cocaine supplied with blood vessels, about 60% of the available
base (White, 1989). cocaine is absorbed in short order. This allows some of
In step four, water, gasoline, acid, potassium per- the cocaine to gain rapid access to the bloodstream,
manganate, and ammonia are added to the cocaine usually in 30–90 seconds (House, 1990). Once in the
paste. This forms a reddish brown liquid, which is then blood, the cocaine molecules are rapidly transported to
filtered. A few drops of ammonia added to the mixture the brain. The peak effects of cocaine when it is
produces a milky solid that is filtered and dried. Then snorted are reached within 15–30 minutes, and the
the dried cocaine base is dissolved in a solution of hy- effects wear off in about 45–60 minutes after a single
drochloric acid and acetone. A white solid forms and dose (Kosten & Sofuoglu, 2004; Weiss, Greenfield, &
settles to the bottom of the tank (Byrne, 1989; White, Mirin, 1994) and between 2–3 hours for chronic use
1989). This solid material is the compound cocaine hy- (Hoffman & Hollander, 1997).
drochloride. Eventually, the cocaine hydrochloride is Researchers believe that 70% to 80% of the cocaine
filtered and dried under heating lights. This will cause absorbed through the nasal passages is biotransformed
the mixture to form a white, crystalline powder that is by the liver before it reaches the brain, limiting the
gathered up, packed, and shipped, usually in kilogram amount of cocaine that can induce euphoria in the
packages. Before sale to the individual cocaine user, user (Gold & Jacobs, 2005). Further, because cocaine
each kilogram is adulterated, and the resulting com- is a vasoconstrictor, it tends to limit its own absorption
pound is packaged in one gram units and sold to indi- through the nasal mucosa. Thus, inhalation of cocaine
vidual users. powder is not the most effective means of introducing
cocaine into the body.
Intravenous cocaine abuse. Cocaine can be intro-
How Cocaine Is Abused duced directly into the body through intravenous injec-
Cocaine may be used in several ways. First, cocaine hy- tion. Cocaine hydrochloride powder is mixed with
drocloride powder might be inhaled through the nose water then injected into a vein. This method of cocaine
(intranasal use, also known as “snorting,” or, more ap- abuse is actually the least common one. Intravenously
propriately, insufflation). Second, it may be injected di- administered cocaine will reach the brain almost im-
rectly into a vein (an intravenous injection). Cocaine mediately: in 3–5 seconds (Restak, 1994) or 30 seconds
hydrochloride is a water soluble form of cocaine and (Kosten & Sofuoglu, 2004). In contrast to the limited
thus is well adapted to either intranasal or intravenous amount of cocaine that is absorbed when it is snorted,
use (Sbriglio & Millman, 1987). Third, cocaine base intravenous administration allows virtually all the co-
might be smoked. Fourth, cocaine may be used orally caine to be absorbed into the user’s circulatory system
(sublingually). We examine each of these methods of (Acosta et al., 2005).
cocaine abuse in detail. It should be noted that each Intravenous cocaine abusers often report experienc-
method of cocaine administration can result in toxic ing a rapid, intense feeling of euphoria called the
levels of cocaine building up in the user’s blood “rush” or “flash.” This is similar to a sexual orgasm but
(Repetto & Gold, 2005). feels different from the rush reported by opiate abusers
Insufflation. Historical evidence suggests that the (Brust, 1998; Meyer & Quenzer, 2005). Researchers
practice of “snorting” cocaine began around 1903, the believe it is the subjective experience of cocaine-
year that case reports of septal perforation began to ap- induced changes in the ventral tegmentum and the
pear in medical journals (Karch, 2002). When snorted, basal forebrain regions of the user’s brain. Following
cocaine powder is usually arranged on a piece of glass the rush, the user will experience a feeling of euphoria
such as a pocket mirror, in thin lines one-half to two that lasts 10–15 minutes. During this time, the individ-
inches long and one-eighth of an inch wide (Acosta et al., ual might also experience a sense of invulnerability,
Cocaine 137
which often contributes to the abuser’s denial that he or of the obtained powder. Unfortunately, the process of
she has a cocaine use disorder (Gitlow, 2007). filtration does not remove all the impurities from the
Sublingual cocaine use. Abusing cocaine sublin- powdered cocaine (Siegel, 1982).
gually, the third method of administration discussed The cocaine powder obtained through this process
thus far, is becoming increasingly popular, especially might then be smoked, but the process of transforming
when the hydrochloride salt of cocaine is utilized (Jones, cocaine hydrochloride into smokable cocaine involves
1987). The tissues in the mouth, especially under the the use of volitile compounds and a significant risk of
tongue, are richly supplied with blood, allowing large fire, or even an explosion—so smoking cocaine freebase
amounts of the drug to enter the bloodstream quickly. never became popular in the United States. But when
The cocaine is rapidly transported to the brain, with re- cocaine freebase was smoked, the fumes would reach
sults similar to those in the intranasal administration of the brain in just 7 seconds (Beebe, & Walley, 1991;
cocaine. Hahn & Hoffman, 2001), with between 60% and 90%
Rectal cocaine use. Male homosexuals are increas- of the cocaine crossing over into the general circulation
ingly using cocaine rectally (Karch, 2002). Cocaine’s from the lungs (Beebe & Walley, 1991; Hatsukami &
local anesthetic properties provide the desired effects for Fischman, 1996). Indeed, there is evidence that when
the user, allowing for participation in otherwise painful it is smoked, cocaine reaches the brain more quickly
forms of sexual activity. Unfortunately, the anesthetic than when it is injected (Hatsukami & Fischman, 1996)
properties of cocaine might mask signs of physical and has been called “the most addictive substance used
trauma to the tissues in the rectal area, increasing the by humankind” (Wright, 1999, p. 47).
individual’s risk of death from these activities (Karch, This characteristic suggested to illicit drug produc-
2002). ers that there would be a strong market for a form of co-
Cocaine smoking. Historically, the practice of burn- caine that could easily be smoked, and by the mid-
ing or smoking different parts of the coca plant dates 1980s such a product had reached U.S. streets. Called
back to at least 3,000 B.C., when the Incas would burn “crack,” it was essentially a solid chunk of cocaine base
coca leaves at religious festivals (Hahn & Hoffman, that was prepared for smoking before it was delivered
2001). The practice of smoking cocaine resurfaced in for sale at the local level. This is done in illicit factories
the late 1800s, when coca cigarettes were used to treat or laboratories where cocaine hydrochloride is mixed
hay fever and opiate addiction. By the year 1890, co- with baking soda and water and then heated until the
caine smoke was being used in the United States for the cocaine crystals begin to precipitate at the bottom of
treatment of whooping cough, bronchitis, asthma, and the container (Warner, 1995). The cocaine is then pre-
a range of other conditions (Siegel, 1982). But in spite pared for sale to individual abusers.
of this history of cocaine smoking for medicinal rea- The crack produced in illicit factories is sold in small,
sons, recreational cocaine smoking in the United States ready-to-use pellets that are packaged in containers that
did not become popular until the early to mid-1980s. allow the user one or two inhalations for a relatively low
This is because the medicinal uses of cocaine have price (Beebe & Walley, 1991). Although at first glance
gradually been reduced as other, more effective, agents crack seems less expensive than other forms of cocaine, it
have been introduced for the control of various ill- is actually about as expensive as cocaine used for intra-
nesses. When cocaine hydrochloride became a popular venous injection (Karch, 2002). But since it is sold in
drug of abuse in the 1970s, users quickly discovered smaller quantities, it is attractive to the under-18 crowd
that it is not easily smoked. The high temperatures and in low-income neighborhoods (Bales, 1988; Taylor &
needed to vaporize cocaine hydrochloride also destroy Gold, 1990). Since the introduction of crack, the prac-
much of the available cocaine, making it of limited tice of smoking cocaine has arguably become the most
value to those who wish to smoke it. To transform co- widely recognized method of cocaine abuse.
caine hydrochloride into an alkaloid base, cocaine Sometimes intraveneous cocaine addicts will at-
powder had to be mixed with a solvent such as ether, tempt to dissolve pellets of crack in alcohol, lemon
and then a base compound such as ammonia (Warner, juice, vinegar, or water and then inject it into their bod-
1995). The cocaine will then form an alkaloid base that ies through large-bore needles (Acosta et al., 2005). Ap-
might be smoked. This form of cocaine is called “free- parently, intravenous cocaine abusers were resorting to
base” (or, simply, “base”). Then the precipitated co- this practice when their traditional sources of cocaine hy-
caine freebase is passed through a filter, which removes drochloride were unable to provide them with the pow-
some of the impurities and increases the concentration der used for injection. This practice has not become
138 Chapter Twelve
widespread but does occasionally take place. A more Tolerance of the euphoric effects of cocaine develop
disturbing trend is for cocaine addicts in England, quickly. To overcome their tolerance many users en-
Wales, and Scotland to increasingly prefer crack co- gage in a cycle of continuous cocaine use known as
caine over other forms of the drug, suggesting that the “coke runs.” The usual cocaine run lasts about 12
practice of smoking crack has become common in these hours, although some have lasted up to 7 days (Gawin,
countries (Jaffe, Rawson, et al., 2005). Khalsa, & Ellinwood, 1994). During this time, the user
is smoking or injecting additional cocaine every few
minutes, until the total cumulative dose might reach
Subjective Effects of Cocaine
levels that would kill the inexperienced user. The coke
When It Is Abused run phenomenon is similar to the behavior when ani-
Several factors influence the subjective experience of mals are given unlimited access to cocaine. Rats who
cocaine. First, people’s expectations play a role in how are given intravenous cocaine for pushing a bar set in
they interpret the drug’s effects and serve to trigger fur- the wall of their cage will do so repeatedly, ignoring
ther episodes of drug use by users. The experience of food or even sex, until they die from convulsions or in-
cocaine abuse creates “vivid, long-term memories” in fection (Hall, Talbert, & Ereshefsky, 1990).
the abuser (Gold & Jacobs, 2005, p. 227). These mem-
ories then serve as relapse triggers between episodes of
Complications of Cocaine
cocaine abuse, triggering additional cocaine abuse.
Abuse/Addiction
In addition to the individual’s expectations, there is
the dose being abused, a factor that is difficult to quan- Cocaine is a factor in approximately 40% to 50% of
tify since different samples vary in terms of purity. Also, deaths associated with illicit drug abuse (Karch, 2002).
there are the actual physiological effects of the drug that In some cases death occurs so rapidly from a cocaine
must be considered. These factors interact to shape the overdose that “the victim never receives medical atten-
individual’s experience from cocaine and to a lesser de- tion other than from the coroner” (Estroff, 1987, p. 25).
gree how it is abused. Experienced cocaine users expe- In addition, cocaine abuse might cause a wide range of
rience both positive (e.g., euphoria) and negative (e.g., other problems, including the following.
depression) effects from the drug (Schafer & Brown, Addiction. In the 1960s and early 1970s some
1991). Low doses of cocaine cause an increase in li- people believed that cocaine was not addictive, prob-
bido, a feeling of increased energy, and a generalized ably because few users in the late 1960s could afford to
feeling of arousal. Intravenous or smoked cocaine can use cocaine long enough to become addicted. At the
cause the user to experience a feeling of intense eupho- start of the 21st century, scientists have concluded
ria or rush or within seconds of using the drug (Jaffe, that cocaine addiction develops more rapidly than
Rawson, et al., 2005). The rush is often so intense and the addiction to compounds such as alcohol or
of such a sexual nature for some users that “it alone can cannabis, with 6% of those who begin to abuse it
replace the sex partner of either sex” (Gold & Verebey, being addicted within the first year (Carroll & Ball,
1984, p. 719). Some male abusers have reported having 2005). As users continue to abuse cocaine, their
a spontaneous ejaculation without direct genital stimu- chances of becoming addicted increase, with about
lation after either injecting or smoking cocaine. Within 15% ultimately becoming addicted (Carroll & Ball,
seconds, the initial rush is replaced by a period of exci- 2005; Jaffe, Rawson, et al., 2005). The median period
tation or euphoria that lasts for 10 (Strang, Johns, & for the development of cocaine addiction is about 10
Caan, 1993) to 20 minutes (Weiss et al., 1994). years (Jaffe, Rawson, et al., 2005).
Higher blood levels of cocaine cause users to feel a There appears to be a progression in the methods by
sense of importance or grandiosity as well as impulsive- which cocaine abusers utilize the drug, as their addic-
ness, anxiety, agitation, irritability, confusion, and some tion to cocaine grows in intensity. With the develop-
suspiciousness or outright paranoia; they also experience ment of tolerance, the individual switches from the
hallucinations, tachycardia, and increased blood pres- intranasal method of cocaine use to those methods that
sure (Acosta et al., 2005). Toxic blood levels of cocaine introduce greater concentrations of the drug into the
might cause cardiac arrhythmias, rhabadomyolysis, con- body. For example, 79% to 90% of those who admitted
vulsions, strokes, and possible death from cardiorespi- to the use of crack cocaine started to use the drug in-
ratory arrest (Acosta et al., 2005; Zevin & Benowitz, tranasally and then progressed to other methods of co-
2007). caine abuse (Hatsukami & Fischman, 1996).
Cocaine 139
Respiratory system dysfunctions. The cocaine smoker invading microorganisms. This process causes protein
may experience chest pain, cough, and damage to the molecules to form on the cell walls of invading micro-
bronchioles of the lungs (Gold & Jacobs, 2005). In some organisms, eventually making them burst from internal
cases, the alveloli of the user’s lungs have ruptured, allow- pressure. The damaged cells are then attacked by the
ing the escape of air (and bacteria) into the surrounding body’s “scavenger” cells, the microphages. Some re-
tissues. This establishes the potential for infection to searchers believe that the microphages are also involved
develop, while the escaping gas may contribute to the in the process of atherosclerotic plaque formation. They
inability of the lung to fully inflate (a pneumothorax). suggest that atherosclerotic plaque is formed when the
Approximately one-third of chronic crack users develop microphages mistakenly attack cholesterol molecules cir-
wheezing sounds when they breathe, for reasons that culating in the blood and attach these molecules to the
are still not clear (Tashkin, Kleerup, Koyal, Marques, & endothelial cells of the coronary arteries, thus providing a
Goldman, 1996). Other potential complications of co- possible avenue through which cocaine abuse might re-
caine smoking include the development of an asthma- sult in the development of atherosclerotic plaques in the
like condition known as chronic bronchiolitis (also coronary arteries of the user.
known as crack lung), hemorrhage, pneumonia, and This piece of clinical wisdom has been challenged
chronic inflammation of the throat (Albertson, Walby, in a recent study by Pletcher et al. (2005). The authors
& Derlet, 1995; House, 1990; Taylor & Gold, 1990). drew on the results of a 15-year longitudinal study of
There is evidence that cocaine-induced lung damage cardiovascular risk factors known as the “Coronary
may be irreversible. Artery Risk Development in Young Adults” (CARDIA)
At least some of the observed increase in the incidence Project. One-third of the 5,000 study participants ad-
of fatal asthma cases might be caused by unsuspected co- mitted to having abused cocaine at some point in their
caine abuse (“Asthma Deaths,” 1997). While cocaine lives. Yet, after factoring in the effects of the partici-
abuse might not be the cause of all asthma-induced pant’s age, sex, ethnicity, family medical history, and al-
deaths, it is known that smoking crack cocaine can cause cohol and tobacco use patterns, the authors were
irritation to the air passages in the lungs, contributing to unable to identify any impact caused by the individual’s
both fatal and nonfatal asthma attacks (Tashkin et al., cocaine abuse on his or her coronary artery health sta-
1996). The chronic intranasal use of cocaine can also tus. Those factors that were most strongly associated
cause sore throats, inflamed sinuses, hoarseness, and on with coronary artery disease, according to the authors,
occasion, a breakdown of the cartilage of the nose were being male, alcohol abuse, and cigarette smoking
(Karch, 2002). Damage to the cartilage of the nose may (the majority of those who abuse cocaine are polydrug
develop after as little as 3 weeks of intranasal cocaine abusers). While the authors did not rule out the possibil-
use (O’Connor, Chang, & Shi, 1992). Other medical ity that cocaine abuse might contribute to cardiovascu-
problems caused by intranasal cocaine use might include lar problems, the mechanism for such cocaine-induced
bleeding from the nasal passages and the formation of ul- heart problems was probably “nonatherogenic”10
cers in these passages, according to the authors. (Pletcher et al., 2005, p. 925) in nature. Obviously, there
Cardiovascular system damage. For decades, cocaine is a need for more research into whether cocaine abuse
abuse has been viewed as a major risk factor for the can or cannot contribute to the buildup of cholesterol
buildup of plaque in the coronary arteries of individuals plaque in the coronary arteries, and if so under what
between the age of 18 and 45 (Karch, 2002; Lai et al., conditions.
2005; Levis & Garmel, 2005). This process is enhanced But this does not change the fact that cocaine abuse is
in cocaine abusers who are infected with HIV-1 (Lai et al., associated with such cardiovascular problems as severe
2005). Researchers still do not understand the exact hypertension, sudden dissection of the coronary arteries,
mechanism by which cocaine abuse can cause the de- cardiac ischemia, tachycardia, myocarditis, cardiomy-
velopment of atherosclerotic plaque in the abuser’s opathy, and sudden death (Gold & Jacobs, 2005;
coronary arteries, but animal research has revealed that Greenberg & Barnard, 2005; Jaffe, Rawson, et al., 2005;
cocaine abuse can trick the body’s immune system into Karch, 2002; Levis & Garmel, 2005; Repetto & Gold,
attacking the tissue of the heart and endothelial cells 2005; Zevin & Benowitz, 2007). At one time, researchers
that line the coronary arteries (Tanhehco, Yasojima,
McGeer, & Lucchesi, 2000). Cocaine accomplishes 10Which, in plain English, means that cardiac problems in cocaine
this feat by triggering what is known as the “comple- abusers do not seem to be caused by cocaine-induced plaque buildup
ment cascade,” part of the immune system’s response to in the coronary arteries of the abuser.
140 Chapter Twelve
believed that cocaine abuse could cause increased In the 1990s cocaine abuse was believed to alter the
platelet aggregation, causing the user’s blood cells to normal action of the catecholamines12 in the heart
form blood clots more easily. This possible side effect of (Beitner-Johnson & Nestler, 1992). This was thought to
cocaine seemed to account for clinical reports in which be the mechanism by which cocaine abuse caused car-
cocaine abusers were found to be at risk for many of the diac stress and distress in the abuser (Karch, 2002).
cardiovascular problems noted in the last paragraphs. However, Tuncel et al. (2002) challenged these theo-
However, research has failed to find support for this hy- ries, noting that in rare cocaine abusers, a normal phys-
pothesis (Heesch et al., 1996). iological response known as the baroreflex would block
For many years, clinical wisdom held that the cocaine- the release of excess norepinephrine, reducing the
induced coronary artery spasm was the mechanism by stress on the heart. Thus, the theory that the chronic
which cocaine was able to induce so many heart attacks use of cocaine causes increased levels of norepineph-
in abusers. While such spasms do take place, they seem rine in the blood, placing an increased workload on the
to play a minor role in the cocaine-induced heart attack heart, especially the left ventricle, and thus placing the
(Patrizi et al., 2006). This is consistent with the conclu- individual at risk for sudden death remains only a
sions of Hahn and Hoffman (2001), who suggested that theory.
cocaine causes the coronary arteries to constrict at In addition to being a known cause of all the above
points where the endothelium is already damaged and conditions, cocaine abuse might also cause “microin-
the blood flow is already reduced by the buildup of farcts,” or microscopic areas of damage to the heart
plaque. Patrizi et al. (2006) concluded that cocaine- muscle (Gold & Jacobs, 2005). These microinfarcts ul-
induced coronary artery disease was the most important timately will reduce the heart’s ability to function effec-
cause of myocardial infarctions (MI) in abusers, and tively and may lead to further heart problems later. It is
that cocaine abusers had significantly greater levels of not known whether these microinfarcts are the cause of
atherosclerosis in the coronary arteries than non- chest pain reported by some cocaine abusers, but co-
abusers. caine abuse can induce areas of ischemia in body or-
Cocaine abusers and researchers alike point out that gans, especially the heart and the brain (Oehmichen,
cocaine use can cause a significant increase the heart Auer, & Konig, 2005). Cocaine abuse is also associated
rate, and it is not uncommon for abusers to state that with sudden death, according to Oehmichen et al.
their hearts were beating so fast they thought they were Researchers have since found that in some settings
about to die (Karch, 2002; Levis & Garmel, 2005). This fully 17% of the patients under the age of 60 seen in
is another reason the risk of an MI is 23.7 times higher in hospital emergency rooms for chest pain had cocaine
the first hour after the individual begins to use cocaine metabolites in their urine (Hollander et al., 1995).
(Karch, 2002; Wadland & Ferenchick, 2004). Further, There seems to be no pattern to cocaine-induced car-
the individual may experience symptoms of cardiac is- diovascular problems, and both first-time and long-term
chemia up to 18 hours after the last use of cocaine be- cocaine users have suffered cocaine-related cardiovascu-
cause of the length of time it takes for the rupture of lar problems. In a hospital setting, between 56% and
atherosclerotic plaque to manifest as a coronary artery 84% of patients with cocaine-induced chest pain have
blockage (Karch, 2002; Kerfoot, Sakoulas, & Hyman, abnormal electrocardiograms (Hollander, 1995). Un-
1996). There is also evidence that younger women tend fortunately, for cocaine users who experience chest
to be at greater risk for cocaine-induced cardiac compli- pain but do not seek medical help, there is a very real
cations than their male counterparts, although cocaine danger that these symptoms of potentially fatal cocaine-
can cause such problems in either sex (Lukas, 2006). related cardiac problems might be ignored by the indi-
Cocaine abuse has been implicated as the cause of a vidual. It is important for physicians to be aware of
number of different cardiac arrhythmias, such as atrial possible cocaine abuse by the patient since physicians
fibrillation, sinus tachycardia, and ventricular tachycar- use drugs known as beta-adrenergic antagonists to treat
dia, although the exact mechanism by which cocaine myocardial ischemia on many occasions. If the patient
interferes with normal heart rhythm is not known had recently used cocaine, these drugs can contribute
(Gold & Jacobs, 2005; Hahn & Hoffman, 2001). It ap- to cocaine-induced constriction of the blood vessels
pears to be a contributing factor in the development of surrounding the heart, making his or her condition
torsade de pointes.11 worse (Thompson, 2004).
11See Glossary. 12See Glossary.

Cocaine 141
A rare but potentially fatal complication of cocaine In severe cases, cocaine-induced reduction in cere-
abuse is a condition known as acute aortic dissection bral blood flow might reach the level of cerebral is-
(Gold & Jacobs, 2005; Karch, 2002; O’Brien, 2006; chemia,13 and if this state continues for too long, the
Repetto & Gold, 2005). This condition develops when neurons that are deprived of blood will begin to die, a
the main artery of the body, the aorta, suddenly devel- condition also called a stroke (Kaufman et al., 1998). Co-
ops a weak spot in its wall. The exact mechanism by caine abuse has been found to double the user’s risk for
which cocaine might cause an acute aortic dissection is both an ischemic and hemorrhagic stroke compared to
not known, and it does occasionally develop in persons that of a nonuser (Vega, Kwoon, & Lavine, 2002; West-
other than cocaine abusers. Acute aortic dissection is a over, McBride, & Haley, 2007). In the hemorrhagic
medical emergency that may require immediate sur- cerebral vascular accident (CVA), a weakened section of
gery to save the patient’s life. Another side effect of co- an artery in the brain ruptures, depriving the neurons de-
caine abuse can affect male cocaine abusers, who may pendent on that blood vessel of blood and placing the
develop erectile dysfunctions, including a painful, po- patient’s life at risk from the uncontrolled hemorrhage.
tentially dangerous condition known as priapism (Karch, Cocaine-induced strokes might be microscopic in size
2002; Finger, Lund, & Slagel, 1997). (micro-strokes), or they might involve major regions of
In contrast to abusers of opiates who inject them in- the brain. Scientists have estimated that cocaine abusers
travenously, intravenous cocaine abusers do not usually are 14 times more likely to suffer a stroke than are
develop scar tissue at the injection site. This is because nonabusers (Johnson, Devous, Ruiz, & Ait-Daoud, 2001),
the adulterants commonly found in powdered cocaine and cocaine-induced strokes have reached “epidemic pro-
are mainly water soluble and are less irritating to the portions” (Kaufman et al., 1998, p. 376) in recent years.
body than the adulterants found in opiates and thus less The risk for a cocaine-induced CVA appears to be cumu-
likely to cause scarring (Karch, 2002). lative, with long-term users being at greater risk than
Cocaine abuse as a cause of liver damage. There is ev- newer users. However, a cocaine-induced CVA is possible
idence that cocaine metabolites, especially cocaethyl- even in a first-time user.
ene, are toxic to the liver; even so, the possibility that One possible mechanism by which cocaine might
cocaine abuse can cause or contribute to liver disease re- cause CVAs, especially in users without preexisting vas-
mains controversial (Karch, 2002). However, medical cular disease, is through drug-induced periods of va-
research has discovered that a small percentage of the sospasm and reperfusion14 between periods of drug use
population simply cannot biotransform cocaine, no (Johnson et al., 2001; Karch, 2002). This cycle can in-
matter how small the dose. In the condition known as duce damage to the blood vessels within the brain, con-
pseudocholinesterase deficiency (Gold, 1989), the liver is tributing to the development of a CVA in the user.
unable to produce an essential enzyme necessary to break Cocaine-induced strokes have been documented to
down cocaine. For people with this condition, the use of occur in the brain, retina, and spinal cord (Brust, 1997;
even a small amount of cocaine could be fatal. Derlet, 1989; Derlet & Horowitz, 1995; Jaffe, Rawson, et
Cocaine abuse as a cause of central nervous system al., 2005; Mendoza & Miller, 1992). Cocaine abusers
damage. Cocaine abuse causes a reduction in cerebral may also experience transient ischemic attacks (TIAs) as a
blood flow patterns in at least 50% of chronic cocaine result of their cocaine use, a phenomenon that could very
abusers (Balamuthusamy & Desai, 2006). MRI studies well be caused by the cocaine-induced vasoconstriction
have revealed evidence of toxic changes to the brain’s identified by Kafuman et al. (1998).
structure that continue to persist for at least 6 months Another very rare complication of cocaine abuse is a
after the individual’s last use of cocaine. Given these drug-induced neurological condition known as the
changes in the physical strcture of the brain, it is not serotonin syndrome15 (Mills, 1995). Further, cocaine
surprising that chronic cocaine abusers also demon- has been known to induce seizures in some abusers, al-
strate cognitive deficits in verbal learning, memory, and though the mechanism by which it does so remains un-
attention (Kosten & Sofuoglu, 2004). This neurological known (Gold & Jacobs, 2005). The individual’s potential
damage has been classified as “moderate to severe” in for a cocaine-induced seizure appears to be significantly
intensity (Kaufman et al., 1998, p. 376). Cocaine’s vaso- higher for the first 12 hours after the active abuse of
constrictive effects on the blood vessels in the brain are
thought to be the mechanism by which chronic co- 13
See Glossary.
caine use might cause these changes in brain structure 14
See Glossary.
and function (Brust, 1997; Pearlson et al., 1993). 15
See Glossary.
142 Chapter Twelve
cocaine (O’Connor et al., 1992). The development of psychobiological interaction between the effects of the
seizures does not appear to be dose-dependent, and drug and their traumatic experiences.
seizures have been noted in first-time as well as long- Cocaine abusers are at higher risk for death from ei-
term cocaine abusers (Gold, 1997; Post et al., 1987). ther homicide or suicide (Oehmichen et al., 2005).
There is strong evidence that cocaine abuse might initi- Oehmichen et al. reported that in cases where the
ate a process of “kindling” through some unknown abuser died, homicide was the cause of death in approx-
mechanism, causing or exacerbating seizure disorders imately 20% of the cases, while suicide was the cause of
(Karch, 2002; Post et al., 1987). death in approximately 10% of the cases. Further, co-
Although cocaine itself might have a short half-life, caine abuse can exacerbate symptoms of disorders such
the sensitization or kindling effects are long lasting. as Tourette’s syndrome and tardive dyskinesia (Lopez &
Further, “Repeated administration of a given dose of Jeste, 1997). After periods of extended use some co-
cocaine without resulting seizures would in no way as- caine abusers have experienced the so-called cocaine
sure the continued safety of this drug even for that given bugs, a hallucinatory experience in which the person
individual” (Post et al., 1987, p. 159) (italics and under- feels as if bugs were crawling on, or just under, the skin.
lining added for emphasis). This is known as formication (Gold & Jacobs, 2005). Pa-
The amygdala is known to be especially vulnerable tients have been known to burn their arms or legs with
to the kindling phemonenon (Taylor, 1993). Thus, co- matches or cigarettes or to scratch themselves repeat-
caine’s effects can make this region of the brain hypersen- edly in trying to rid themselves of these unseen bugs
sitive, causing the user to experience cocaine-induced (Lingeman, 1974).
seizures. The relationship between cocaine abuse and Cocaine has also been implicated as one cause of
seizures in children was so strong that Mott, Packer, drug-induced anxiety, or panic reactions (DiGregorio,
and Soldin (1994) recommended that all children and 1990). One study found that in the early 1990s one-
adolescents brought to the hospital for a previously un- quarter of the patients seen at one panic disorder clinic
diagnosed seizure disorder be tested for cocaine abuse eventually admitted to using cocaine (Louie, 1990). Up
at the time of admission. In addition, there is evidence to 64% of cocaine users experience some degree of anxi-
that chronic cocaine abuse can cause or at least signifi- ety as a side effect of the drug, according to DiGregorio.
cantly contribute to a disruption in body temperature There is a tendency for cocaine users to try to self-
regulation known as malignant hyperthermia (Karch, medicate this side effect through the use of marijuana.
2002). Individuals who develop this condition suffer ex- Other chemicals often used by cocaine abusers in an at-
tremely high, possibly fatal, body temperatures, and tempt to control the drug-induced anxiety include the
this condition can cause extensive damage to the CNS. benzodiazepines, narcotics, barbiturates, and alcohol.
An emerging body of evidence suggests that chronic These cocaine-induced anxiety and panic attacks might
cocaine abuse might cause alterations in the brain at continue for months after the individual’s last cocaine
the cellular level (Tannu, Mash, & Hemby, 2006). The use (Gold & Miller, 1997a; Schuckit, 2006).
authors compared brain samples from 10 people who Between 53% (Decker & Ries, 1993) and 65%
had died of a cocaine overdose with those of a similar (Beebe & Walley, 1991) of chronic cocaine abusers will
number of people who had died of other, nondrug develop a drug-induced psychosis very similar in ap-
causes. They found alterations in the expression of 50 pearance to paranoid schizophrenia, sometimes called
different proteins associated with the process of neural “coke paranoia” by illicit cocaine users. Although the
connection or communication in the nucleus accum- symptoms are very similar to those of paranoid schizo-
bens region of the brain in the brain samples of patients phrenia, a cocaine-induced psychosis tends to include
who had died of a cocaine overdose. These results sup- more suspiciousness and a strong fear of being discovered
port other evidence suggesting that there are long-term or of being harmed while under the influence of cocaine
changes in brain function in chronic cocaine abusers. (Rosse et al., 1994). Further, the cocaine-induced psy-
Cocaine’s effects on the user’s emotional state and chosis is usually of relatively short duration, possibly
perceptions. Cocaine abuse may exacerbate the symp- only a few hours (Haney, 2004; Karch, 2002) to a few
toms of posttraumatic stress disorders (PTSD) (Hamner, days (Kerfoot et al., 1996; Schuckit, 2006) after the person
1993). The exact mechanism by which cocaine adds to stops using cocaine.
the emotional distress of PTSD is not clear at this time. The mechanism by which chronic cocaine abuse
However, it seems that individuals who suffer from might contribute to the development of a drug-
PTSD might find that their distress made worse by the induced psychosis remains unknown. Gawin et al. (1994)
Cocaine 143
suggested that the delusions found in a cocaine- (c) sleep disorders (insomnia/hypersomnia), (d) anorexia,
induced psychotic reaction usually clear after the indi- and (e) psychomotor agitation/retardation (Carroll &
vidual’s sleep pattern has returned to normal, suggesting Ball, 2005). Two of these five symptoms are necessary
that cocaine-induced sleep disturbances might be one for a formal diagnosis of cocaine withdrawal. These
factor in the evolution of this drug-induced psychosis. symptoms will vary in intensity, and experts disagree as
Another theory suggests that individuals who develop a to their significance (Carroll & Ball, 2005).
cocaine-induced paranoia might posess a biological vul- Cocaine use as an indirect cause of death. In addition
nerability for schizophrenia, which is then activated by to its very real potential to cause death by a variety of
chronic cocaine abuse (Satel & Edell, 1991). Kosten mechanisms, cocaine use may indirectly cause, or at
and Sofuoglu (2004) disputed this theory, however, stat- least contribute to, premature death of the user. For
ing there was little evidence that cocaine-induced psy- example, cocaine abuse is a known cause of rhabdomy-
chotic episodes are found mainly in those predisposed olsis.16 This is a result of cocaine’s toxic effects on
to these disorders. muscle tissue, and its vasoconstrictive effects, which
Approximately 20% of the chronic users of crack co- can cause muscle ischemia (Karch, 2002; Repetto &
caine in one study were reported to have experienced Gold, 2005; Richards, 2000). There is also evidence
drug-induced periods of rage, or outbursts of anger and that cocaine abuse may alter the blood-brain barrier,
violent assaultive behavior (Beebe & Walley, 1991), facilitating the entry of the human immunodefi-
which may be part of a cocaine-induced delirium that ciency virus (HIV) into the brain.17 This may be why
precedes death (Karch, 2002). This cocaine-induced cocaine abusers are at increased risk of infection from
delirium might reflect the effects of cocaine on the various bacterial, fungal, or viral contaminants found
synuclein family of proteins within the neuron. Under in some samples of illicit cocaine as well (Acosta et al.,
normal conditions, these protein molecules are thought 2005).
to help regulate the transportation of dopamine within
the neuron. But recent evidence suggests that cocaine
can alter synuclein production within the cell, causing
Summary
or contributing to the death of the affected neurons, if Cocaine has a long history, which predates the present
not the individual (Mash et al., 2003). by hundreds if not thousands of years. The active agent
Cocaine withdrawal. A few hours after the individual of the coca leaf, cocaine, was isolated only about 160
last snorted cocaine, or within 15 minutes when the per- years ago, but people were using the coca leaf long be-
son last injected it, he or she will slide into a state of de- fore that. Coincidentally, at just about the time cocaine
pression. After prolonged cocaine use, post-cocaine was isolated, the hypodermic needle was developed,
depression might reach suicidal proportions (Gold & Ja- and this allowed users to inject large amounts of the rel-
cobs, 2005). Cocaine-induced depression is thought to atively pure cocaine directly into the circulatory system,
be the result of cocaine’s depleting the brain’s nerve cells where it was rapidly transported to the brain. Users
of the neurotransmitters norepinephrine and dopamine. quickly discovered that intravenously administered co-
After a period of abstinence, the neurotransmitter levels caine brought on a sense of euphoria, which immedi-
usually recover and the individual’s emotions return to ately made it a rather popular drug of abuse.
normal. But there is a very real danger that the cocaine At the start of the 20th century, government regula-
abuser might attempt or complete suicide while in a tions in the United States limited the availability of co-
drug-induced depressive state. One recent study in caine, which was mistakenly classified as a narcotic at that
New York City found that one-fifth of all suicides in- time. The development of the amphetamine family of
volving a victim under the age of 60 were cocaine re- drugs in the 1930s, along with increasingly strict enforce-
lated (Roy, 2001). Further, the individual’s cocaine ment of the laws against cocaine use, allowed drug-
abuse might have masked a concurrent depressive dis- addicted individuals to substitute amphetamines for the
order, which becomes apparent only after the drug is increasingly rare cocaine. In time, the dangers of cocaine
discontinued. In such cases antidepressant medications use were forgotten by all but a few medical historians. But
such as desimpramine or buproprion might be better in the 1980s, cocaine again surfaced as a major drug of
for individuals with cocaine use disorders than other abuse in the United States, as government regulations
agents (Rounsaville, 2004).
Chronic abusers who stop abusing cocaine will report 16See Glossary.
symptoms such as (a) fatigue, (b) vivid, intense dreams, 17Discussed in Chapter 34.
144 Chapter Twelve
made it difficult for users to obtain amphetamines. To peaked around the year 1986 and that fewer and fewer
entice users, new forms of cocaine were introduced, in- people are becoming addicted to this drug. Because of
cluding concentrated “rocks” of cocaine, known as crack. the threat of HIV-1 infection from using contami-
To the cocaine user of the 1980s, cocaine seemed to nated needles for injecting the drug (see Chapter 34)
be a harmless drug, although historical evidence sug- and the increased popularity of heroin in the United
gested otherwise. Cocaine has been a major drug of States, many cocaine abusers are smoking a combina-
abuse ever since. tion of crack cocaine and heroin. When cocaine is
In the 1980s, users rediscovered the dangers associ- smoked, either alone or in combination with heroin
ated with cocaine abuse, and the drug gradually has prepared for smoking, the danger of HIV transmission
fallen into disfavor. At this time, it seems that the most is effectively avoided, since intravenous needles are
recent wave of cocaine addiction in the United States not involved.
CHAPTER THIRTEEN
Marijuana Abuse and Addiction
For many generations, marijuana has been a most con- History of Marijuana Use
troversial substance of abuse and the subject of many in the United States
misunderandings. People talk about marijuana as if it
were a chemical in its own right, when in reality mari- Almost 5,000 years ago cannabis was in use by Chinese
juana is not a chemical or a drug; it is a plant, a mem- physicians as a treatment for malaria, constipation, the
ber of the Cannabis sativa family of plants. The name, pain of childbirth, and, when used with wine, as a surgi-
Cannabis sativa, is Latin for “cultivated hemp” (Green, cal anesthetic (Robson, 2001). Cannabis continued to
2002). History shows that some strains of cannabis have be used for medicinal purposes throughout much of
been cultivated for the hemp fiber it produces, which recorded history. As recently as the 19th century, physi-
are used to manufacture a number of products,1 for cians in the United States and Europe used marijuana
over 12,000 years (Welch, 2005). as an analgesic, hypnotic, a treatment for migraine
Unfortunately, in the United States, the hysteria headaches, and as an anticonvulsant (Grinspoon &
surrounding the use/abuse of Cannabis sativa have Bakalar, 1993, 1995). The anticonvulsant properties of
reached the point that any member of this plant family cannabis were illustrated by an incident that took place
is automatically assumed to have an abuse potential in 1838, when physicians were able to completely con-
(Williams, 2000). To differentiate between forms of trol the terror and “excitement” (Elliott, 1992, p. 600)
Cannabis sativa with abuse potential and those that of a patient who had contracted rabies through the use
have low levels of the abusable compounds and are of hashish.
useful plants for manufacturing and industry, Williams In the early years of the 20th century, cannabis came
(2000) suggested that the term hemp be used for the to be viewed with disfavor as a side effect of the hue-
latter. Marijuana, he suggested, should refer to only and-cry against opiate abuse (Walton, 2002). At the
those strains of Cannabis sativa that have an abuse po- same time, researchers concluded that the chemicals in
tential. This is the pattern that will be followed in this the marijuana plant were either ineffective or at least
text. less effective than pharmaceuticals being introduced as
Unlike other substances such as alcohol, cocaine, or part of the fight against disease. These two factors caused
the amphetamines, marijuana is not in itself a drug of it to fall into disfavor as a pharmaceutical (Grinspoon &
abuse. It is a plant that happens to contain some chem- Bakalar, 1995, 1993), and by the 1930s, marijuana was
icals that, when admitted to the body, alter the individ- removed from the doctor’s pharmacopoeia. By a histori-
ual’s perception of reality in a way that some people cal coincidence, during the same period when medici-
find pleasurable. In this sense, marijuana is similar to nal marijuana use was being viewed with suspicion,
the tobacco plant: They both contain compounds that recreational marijuana smoking was being introduced
when introduced into the body cause the user to experi- into the United States by immigrants and itinerant
ence certain effects that the individual deems desirable. workers from Mexico who had come north to find work
In this chapter, the uses and abuses of marijuana are (Mann, 1994; Nicoll & Alger, 2004). Recreational mar-
discussed. ijuana smoking was quickly adopted by others, espe-
cially jazz musicians (Musto, 1991). With the start of
Prohibition in 1920, many members of the working
1The Gutenberg and King James Bibles were first printed on paper
class turned to growing or importing marijuana as a
manufactured from hemp. Both Rembrandt and Van Gogh painted
on “canvas” made from hemp (Williams, 2000). While George substitute for alcohol (Gazzaniga, 1988).
Washington cultivated cannabis to obtain hemp, there is no direct ev- Recreational cannabis use declined with the end of
idence that he smoked marijauana (Talty, 2003). Prohibition, when alcohol use once more became legal
145
146 Chapter Thirteen
in the United States. But a small minority of the popu- and identify the mechanism by which marijuana might
lation continued to smoke marijuana, and this alarmed bring about this effect is necessary.
government officials. Various laws were passed in an at- Sparked by reports about its antinausea effects, the
tempt to eliminate the abuse of cannabis, including the drug Marinol (dronabinol) was introduced as a syn-
Marijuana Tax Act of 1937.2 But the “problem” of mar- thetic version of THC to control severe nausea. Mari-
ijuana abuse in the United States never entirely disap- nol has met with mixed success, possibly because
peared, and by the 1960s it again became popular. By marijuana’s antinausea effects are caused by a chemical
the start of the 21st century, marijuana was the most other than THC found in marijuana (D. Smith, 1997).
commonly abused illicit drug in the United States Preliminary research conducted in the 1980s suggested
(Martin, 2004), with more than 50% of the entire popu- that the practice of smoking marijuana might help con-
lation having used it at least once (Gold, Frost-Pineda, & trol certain forms of otherwise unmanageable glaucoma
Jacobs, 2004; Gruber & Pope, 2002). (Green, 2002; Grinspoon & Bakalar, 1993). Unfortu-
Medicinal marijuana. Since the 1970s, a growing nately, the initial promise of marijuana in the control
number of physicians in the United States have won- of glaucoma was not supported by follow-up studies
dered whether a chemical found in marijuana might (Watson, Benson, & Joy, 2000). Although marijuana
continue to be of value in the fight against disease and smoking does cause a temporary reduction in the fluid
suffering in spite of its legal status as a controlled sub- pressure within the eye, only 60% to 65% of patients
stance. This interest was sparked by reports from mari- who smoke marijuana experience this effect (Green,
juana smokers receiving chemotherapy for cancer that 1998). Further, to achieve and maintain an adequate
they experienced less nausea if they smoked marijuana reduction in eye pressure levels, the individual would
after receiving chemotherapy treatments (Robson, have to smoke 9–10 marijuana cigarettes per day
2001). In Canada, the compound Sativex, made from (Green, 1998). Research into the possible use of mari-
cannabis and designed to be sprayed under the tongue, juana in the treatment of glaucoma continues at this
is being considered for use in treating multiple sclero- time, usually outside the United States.
sis (MS) (Wilson, 2005). In the Netherlands, early re- Marijuana may be able to relieve at least some of the
search has suggested that marijuana use can ease the symptoms of amyotrophic lateral sclerosis (ALS) at least
symptoms of neurological disorders and pain, and help for short periods of time (Amtmann, Weydt, Johnson,
reverse the wasting syndrome often associated with Jensen, & Carter, 2004). Smoking marijuana also
cancer (Gorter, Butorac, Coblan, & van der Sluis, seems to help patients with multiple sclerosis, rheuma-
2005). toid arthritis, and chronic pain conditions (Green,
There is even evidence that (Δ-9-tetrahydro-cannabi- 2002; Grinspoon & Bakalar, 1997b; Robson, 2001;
nol (THC)3 might offer promise in the treatment of Watson et al., 2000). An example is the work of Karst
Alzheimer’s disease (Eubanks et al., 2006). The exact et al. (2003), who utilized a synthetic analog of THC4
mechanism by which THC might prevent plaque for- known as CT-35 to treat neuropathic pain. The authors
mation in the brain of Alzheimer’s disease victims re- found that CT-3 was not only effective in controlling
mains unclear, but initial research findings are quite neuropathic pain but did not seem to have any adverse
promising. Further research to confirm the early results effects in the experimental subjects. Preliminary evi-
dence suggests that it might help control the weight loss
2This act was passed by Congress against the advice of the American often seen in patients with late-stage AIDS or cancer
Medical Association (Nicoll & Alger, 2004). Contrary to popular be- (Green, 2002; Watson et al., 2000). Further, a body of
lief, the Marijuana Stamp Act did not make possession of marijuana evidence suggests that one or more compounds in mar-
illegal, but did impose a small tax on it. People who paid the tax ijuana might help control HIV-related neuropathic
would receive a stamp to show that they had paid the tax. Obviously,
pain (Abrams et al., 2007).
since the stamps would also alert authorities that the owners either
had marijuana in their possession or planned to buy it, illegal users Using research animals, scientists have found that a
did not apply for the proper forms to pay the tax. The stamps are of in- compound found in marijuana might function as a po-
terest to stamp collectors, however, and a few collectors have actually tent antioxidant, possibly limiting the amount of dam-
paid the tax in order to obtain the stamp for their collection. The Fed- age caused by cerebral vascular accidents (CVAs, or
eral Marijuana Stamp Act was found to be unconstitutional by the
United States Supreme Court in 1992. However, 17 states still have
similar laws on the books (“Stamp Out Drugs,” 2003). 4See “Pharmacology of Marijuana” section later in this chapter.
3The compound thought to give marijuana its psychoactive effects. 5Chemical shorthand for: 1′ 1′Dimethylheptyl-Δ8-tetrahydro-cannabinol-
Discussed later in this chapter. 11-oic acid.

Marijuana Abuse and Addiction 147
strokes) (Hampson et al., 2002), and this is being actively plant by adding other substances to the marijuana be-
explored by scientists eager to find a new tool to treat fore smoking it or by using strains with the highest pos-
stroke victims. There is also limited evidence suggest- sible concentrations of the compounds thought to
ing that marijuana might be useful in controlling the cause marijuana’s effects. To this end, users have begun
symptoms of asthma, Crohn’s disease, and anorexia as growing strains of marijuana that have high concentra-
well as emphysema, epilepsy, and possibly hyperten- tions of the compounds most often associated with
sion (Green, 2002). There may also be a compound in pleasurable effects, and marijuana might be said to be
marijuana that inhibits tumor growth (Martin, 2004). the biggest cash crop in the United States at this time8
Given all of these claims, one would naturally expect (“Grass Is Greener,” 2007).
marijuana to be the subject of intense research. Unfortu- Researchers generally agree that the marijuana cur-
nately, the Food and Drug Administration and the Drug rently sold on the streets is more potent than the mari-
Enforcement Administration (DEA) dismiss all these juana sold in the 1960s, although there are exceptions.
claims on the grounds that they are only anecodotal in Grinspoon, Bakalar, and Russo (2005), for example,
nature (Marmor, 1998). Admittedly, the Institute of stated that on “average, street cannabis is not much
Medicine concluded that there was enough evidence to more potent than it was in the 1960s” (p. 264). In con-
warrant an in-depth study of the claims that marijuana trast to this assessment, however, the Commission on
has medicinal value (Watson et al., 2000). But the Adolescent Substance and Alcohol Abuse (2005) sug-
United States Food and Drug Administration (FDA) dis- gested that where the typical marijuana cigarette in the
missed this conclusion in 2006 on the grounds that since 1960s yielded a dose of about 10 mg of THC, the cur-
there is no scientific evidence to support these claims— rent marijuana cigarette will yield an effective dose of
evidence that would require controlled research with re- 150–200 mg. The average marijuana sample seized by
sults published in scientific journals—there is no the police in the year 1992 had 3.08% THC, which had
legitimate medical application for marijuana (“No Dope increased to 5.11% THC in the year 2002 (Compton,
on Dope,” 2006). Without research funding, and with Grant, Colliver, Glantz, & Stinson, 2004).9 It has been
the numerous regulatory obstacles in place, it unlikely suggested that the potency of the marijuana currently
that such research might be carried out in the United available is as much as 15 times as potent as the mari-
States (“No Dope on Dope,” 2006). juana sold in the 1960s (Parekh, 2006). One strain de-
In spite of evidence that at least some of the chemi- veloped in British Columbia, Canada, reportedly has a
cals in marijuana might have medicinal value, all at- THC content of 30% (Shannon, 2000). But there is so
tempts at careful, systematic research into this area much variation in the potency of different batches of
have been blocked by various U.S. government agen- marijuana that the only definitive answer to the ques-
cies (“No Dope on Dope,” 2006; Stimmel, 1997b).6 tion of potency will depend on the toxicology report
However, in response to citizen initiatives, 11 different rendered by a properly trained chemist who has as-
states have legalized the medical use of marijuana as of sessed each sample.
2006.7 Thus, it would appear that marijuana will con-
tinue to remain a controversial substance for many A Technical Point
years to come.
THC is found throughout the marijuana plant, but the
highest concentrations are in the small upper leaves
A Question of Potency and flowering tops of the plant (Hall & Solowij, 1998).
Historically, the term marijuana is used to identify
Ever since the 1960s, marijuana abusers have sought preparations of the cannabis plant that are used for
ways to enhance the effects of the chemicals in the
8The estimated value of all of the marijuana grown in the United
6A great example of how the federal government blocks research into States is $35.4 billion, easily more than the estimated value of the
possible benefits from compounds in marijuana is seen in the 1988 next two cash crops: corn ($23.3 billion) and soybeans ($17.6 billion)
ruling by an administrative law judge that marijuana should be reclas- (“Grass Is Greener,” 2007).
sified as a Schedule II substance (see Appendix Four). The Drug 9Schlosser (2003) and Earlywine (2005) argued that the higher po-
Enforcement Administration immediately overruled its own ad- tency of the marijuana currently being sold through illicit sources ac-
ministrative law judge and left marijuana a Schedule I compound tually made it safer to use. The authors argued that since it would take
(Kassirer, 1997). less to reach a desired state of intoxication, this increased the safety
7However, possession of marijuana is still a federal crime and thus margin of the marijuana being used. A counter-argument has not
might be punished under existing federal laws. been advanced, to date.
smoking or eating. The term hashish is used to identify In the United States, marijuana is the most fre-
the thick resin that is obtained from the flowers of the quently abused illicit substance, a status it has held for a
marijuana plant. This resin is dried, forming a brown or number of decades (Comptom et al., 2004; Hall &
black substance that has a high concentration of THC. Degenhardt, 2005; Sussman & Westreich, 2003). Fig-
This is either ingested orally (often mixed with some ure 13.1 shows the percentage of high school seniors
sweet substance) or smoked. Hash oil is a liquid ex- who have engaged in marijuana use. It is estimated that
tracted from the plant, which is 25%–60% THC, that is more than 50% of the entire population of this country
added to marijuana or hashish to enhance its effect. In has used marijuana at least once (Gold et al., 2004). An
this chapter, the generic term marijuana is used for any estimated 15 million people are thought to be current
part of the plant that is to be smoked or ingested, except marijuana abusers, with 7 million using it at least once
when the term hashish is specifically used. Unfortu- a week (Brust, 2004; Sabbag, 2005). The scope of mari-
nately, there is evidence that hashish is growing in pop- juana abuse in the United States has been stable since
ularity as a form of cannabis abuse (United Nations, 1991, although some subgroups have shown an in-
2006). crease in the frequency of marijuana abuse and the per-
centage of abusers who are addicted has increased in
that period (Comptom et al., 2004).
Scope of the Problem of Marijuana Abuse It is rare for individuals under the age of 13 to abuse
The abuse of cannabis is found around the world marijuana. Most individuals who use marijuana began
(United Nations, 2006). It has been estimated that 162 after the age of 13, with the peak age of initiation falling
million people worldwide have abused marijuana at one around 18–19 years of age (Ellickson, Martino &
point in their lives, and the number is growing each year Collins, 2004; Hubbard, Franco, & Onaivi, 1999). This
(United Nations, 2006). Hall and Degenhardt (2005) is supported by observations such as the one by Johnston,
gave a slightly lower estimate of 150 million. Fully O’Malley, Bachman, and Schulenberg (2006a) that only
30% of all marijuana abusers live in Asia, while North 16.1% of eighth graders surveyed admitted to having
America (Mexico, Canada, and the United States) and ever used marijuana, while by the 12th grade this per-
Africa each have about 24% of the world’s marijuana centage had increased to 42.3% of students surveyed. If
abusers. Another 20% are found in Europe (United the individual has not started to abuse marijuana by the
Nations, 2004). age of 20, he or she is unlikely to do so (Ellickson et al.,
50
40
Percentage
30
20
10
0
2001 2002 2003 2004 2005 2006
Year
FIGURE 13.1 Percentage of High School Seniors Admitting to the Use

of Marijuana at Some Time in Their Lives, 2001–2006
Source: Data from Johnston, O’Malley, Bachman, & Schulenberg (2006a).
2004). Marijuna abuse peaks in early adulthood and utes, and blood THC levels drop to 10% of the peak
usually is discontinued by the late 20s or early 30s levels within 1 hour (Hall & Degenhardt, 2005).
(Ellickson et al., 2004; Gruber & Pope, 2002). Once in the brain, THC mimics the action of two
As is true for alcohol, a small percentage of those naturally occurring neurotransmitters, now classified
who consume marijuana use a disporportionate amount as endocannabinoids (Kraft, 2006). The first of these
of this substance. Approximately 14% of those who use endocannabinoids has been named anandamide and
marijuana do so daily, consuming 95% of the cannabis the second is called sn-2 arachidonylglycerol (2-AG)11
found on the illicit market (United Nations, 2006). (Martin, 2004). Scientists suspect that anandamide is
Only a small percentage of marijuana abusers use more involved in such activities as mood, memory, cogni-
than 10 grams a month (about enough for 25–35 mari- tion, perception, muscle coordination, sleep, regula-
juana cigarettes) (Mac Coun & Reuter, 2001). Mari- tion of body temperature, and appetite and possibly
juana is addictive, and it is estimated that 10%–20% of helps to regulate the immune system (Gruber & Pope,
marijuana abusers will ultimately become addicted to it 2002; Nowak, 2004; Parrott, Morinan, Moss, & Scholey,
(Lynskey & Lukas, 2005). 2004; Robson, 2001). Receptor sites for endocannabi-
Because of its popularity, the legal and social sanc- noids have been found in various regions of the brain
tions against marijuana use have repeatedly changed in including the hippocampus, cerebral cortex, basal gan-
the past 30 years. In some states, possession of a small glia, and cerebellum (Gruber & Pope, 2002; Martin,
amount of marijuana was decriminalized, only to be 2004; Nicoll & Alger, 2004; Watson et al., 2000; Zajicek
recriminalized just a few years later (Macfadden & et al., 2003 ). There is evidence that endocannabinoid
Woody, 2000). Further, there is a growing trend to receptors also are found in peripheral tissues that help
allow the medicinal use of marijuana in a number of mediate the body’s immune response (Martin, 2004;
states. Currently, the legal status of marijuana varies Reynolds & Bada, 2003), which might explain why
from one state to another. cannabis seems to have a mild immunosuppressant
effect.
Thus, THC mimics the actions of naturally occur-
Pharmacology of Marijuana ring neurotransmitters, although evidence suggests that
it is 4 to 20 times as potent as anandamide and has a far
In spite of its popularity as a drug of abuse, the mecha-
stronger effect than this natural neurotransmitter (Martin,
nisms by which marijuana affects normal brain func-
2004). In general, the endocannabinoids function as
tion remain poorly understood (Sussman & Westreich,
retrograde transmitters, allowing one neuron to inform
2003). It is known that the Cannabis sativa plant con-
another that the message was received, and thus to stop
tains at least 400 different compounds, of which an esti-
sending additional excitatory neurotransmitter mole-
mated 61 have some psychoactive effect (Gold et al.,
cules (Kraft, 2006). Researchers have found that by
2004; McDowell, 2005; Sadock & Sadock, 2003). The
blocking endocannabinoid receptors with experimen-
majority of marijuana’s psychoactive effects are appar-
tal compounds it is possible to reduce drug-seeking be-
ently the result of a single compound, Δ-9-tetrahydro-
havior not only for marijuana but also for nicotine,
cannabinol10 (THC), which was first identified in 1964
food, and possibly other drugs of abuse as well. These
(Nicoll & Alger, 2004; Sadock & Sadock, 2003). A sec-
findings suggest new avenues of possible treatment for
ond compound, cannabidiol (CBD), is also inhaled
the eating disorders as well as the substance use disor-
when marijuana is smoked, but researchers are not sure
ders (Kraft, 2006; Le Foll & Goldberg, 2005).
whether this compound has a psychoactive effect on
One of the endocannabinoids identified thus far,
humans (Nelson, 2000).
sn-2 arachidonylglycerol, is even more of a mystery to
Once in the body, THC is biotransformed into the
neuroscientists than is anandamide. It is thought to be
chemical 11-hydroxy-Δ9THC, a metabolite that is
manufactured in the hippocampus, a region of the
thought to cause its central nervous system effects
brain known to be involved in the formation of memo-
(Sadock & Sadock, 2003). Between 97% and 99% of
ries (Parrott et al., 2004; Watson et al., 2000). Animal
the THC in the blood is protein bound, with the result
research would suggest that the brain uses these
that the observed effects are caused by the 1%–3% of
cannabinoid-type chemicals to help eliminate aver-
THC that remains unbound (Jenkins, 2007). When
sive memories (Marsicano et al., 2002; Martin, 2004).
smoked, the peak THC levels are seen within 10 min-
11
There is preliminary evidence of a possible third endogenous
10“Δ” is the Greek symbol for the letter known as “delta.” cannabinoid, but its role and chemical structure remain unclear.
Evidence suggests that THC disregulates the firing se- whether metabolic tolerance has developed. However,
quence of subunits in the hippocampus, disrupting the the liver is not able to biotransform THC very quickly,
synchrony between the hippoocampi subunits neces- and in experienced users THC has a half-life of 24–96
sary for normal memory function (Robbe et al., 2006). hours (Oehmichen, Auer, & Konig, 2005) to a week for
In addition to its impact on memory function, mari- the rare, casual abuser (Gruber & Pope, 2002). About
juana has been found to affect the synthesis and acetyl- 65% of the metabolites of THC are excreted in the
choline12 turnover in the limbic system and the feces, and the rest are excreted in the urine (Hubbard
cerebellum (Fortgang, 1999; Hartman, 1995). This et al., 1999; Schwartz, 1987).
might be the mechanism by which marijuana causes Tolerance for the subjective effects of THC will de-
the user to feel sedated and relaxed. Marijuana has a velop rapidly (O’Brien, 2006). Once tolerance has de-
mild analgesic effect and is known to potentiate the veloped, the user must either wait a few days until his or
analgesia induced by morphine (Martin, 2004; Welch, her tolerance for marijuana begins to diminish or alter
2005). These effects appear to be caused by marijuana- the manner in which he or she uses it. For example,
induced inhibition of the enzyme adenylate cyclase, after tolerance to marijuana has developed, the chronic
which is involved in the transmission of pain messages, marijuana smoker must use “more potent cannabis,
although the exact mechanism by which this is accom- deeper, more sustained inhalations, or larger amounts
plished remains to be identified. Marijuana is also able of the crude drug” (Schwartz, 1987, p. 307) to over-
to inhibit the production of cyclooxygenase,13 which come his or her tolerance to marijuana.
may also play a role in its analgesic effects (Carvey, Interactions between marijuana and other chemicals.
1998). The analgesic effects of marijuana seem to peak There has been relatively little research into the pos-
around 5 hours after it was used, and evidence suggests sible interaction beween marijuana and other com-
that marijuana is about as potent an analgesic as pounds. It was suggested that the concurrent use of
codeine (Karst et al., 2003; Robson, 2001; Welch, 2005). marijuana and lithium could cause serum lithium
Once in the circulation, THC is rapidly distributed levels to rise, possibly to dangerous levels (Ciraulo,
to blood-rich organs such as the heart, lungs, and brain. Shader, Greenblatt, & Creelman, 2006). As lithium
It then slowly works its way into tissues that receive less has only a narrow “therapeutic window,” this interac-
blood, such as the fat tissues of the body, where unme- tion between marijuana and lithium is potentially dan-
tabolized THC will be stored. Repeated episodes of gerous to the person who uses both substances.
marijuana use over a short period of time allow signifi- There also has been one case report of a patient who
cant amounts of THC to be stored in the body’s fat re- smoked marijuana while taking Antabuse (disulfiram).
serves. Between periods of active marijuana abuse, the The patient developed a hypomanic episode that sub-
fat-bound THC is slowly released into the blood, proba- sided when he stopped using marijuana (Barnhill,
bly in amounts too small to have any psychoactive ef- Ciraulo, Ciraulo, & Greene, 1995). When the patient
fect on the user (McDowell, 2005). In rare cases, this again resumed the use of marijuana while taking
process results in heavy marijuana users testing positive Antabuse, he again became hypomanic, suggesting that
for THC in urine toxicology screens for 30 days after the episode of mania was due to some unknown inter-
their last use of marijuana (Stephens & Roffman, action between these two chemicals. For reasons that
2005). However, this happens only with very heavy mar- are not clear, adolescents who use marijuana while tak-
ijuana users, and casual users will usually have metabo- ing an antidepressant medication such as Elavil (amitri-
lites of THC in their urine for only about 3 days after ptyline) run the risk of developing a drug-induced
the last use of marijuana.14 delirium. Thus, individuals who are taking antidepres-
The primary site of THC biotransformation is in the sants should not use marijuana.
liver, and more than 100 metabolites are produced dur- Cocaine users will often smoke marijuana while
ing the process of THC biotransformation (Hart, 1997). using cocaine because they believe the sedating effects
The half-life of THC appears to vary depending on of marijuana will counteract the excessive stimulation
12See
caused by the cocaine. Unfortunately, cocaine is
Glossary.
13See
known to have a negative impact on cardiac function
Glossary.
14Some individuals claim that their urine toxicology test was
when it is abused. There has been no research into the
“positive” for THS because they had consumed a form of beer made
combined effects of marijuana and cocaine on cardiac
from hemp. While creative, there is little evidence supporting this function in either healthy volunteers or patients with
claim. some form of preexisting cardiovascular disease.
Although there is evidence that the concurrent use Marijuana is smoked alone or mixed with other sub-
of marijuana and alcohol results in a greater sense of stances. Most commonly, the marijuana is smoked by
subjective pleasure for the marijuana abuser, Craig itself in the form of cigarettes, commonly called
(2004) warned against the concurrent use of these two “joints.” The typical marijuana cigarette usually con-
compounds. One of the body’s natural defenses against tains 500–750 mg of marijuana and provides an effec-
poisons such as alcohol is vomiting. But marijuana in- tive dose of approximately 2.5 to 20 mg of THC per
hibits nausea and vomiting. If users were to ingest too cigarette (depending on potency). The amount of mari-
much alcohol while also using marijuana, their bodies juana in the average “joint” weighs about 0.014 ounces
would less likely be able to expell some of the alcohol (Abt Associates, Inc., 1995a). A variation on the mari-
through vomiting, raising their chances of an overdose juana cigarette is the “blunt.” Blunts are made by re-
on alcohol. There has been no research to test this hy- moving one of the outer leaves of a cigar, unrolling it,
pothesis, but the concurrent use of alcohol and cannabis filling the core with high-potency marijuana mixed
should be avoided on general principles. with chopped cigar tobacco, and then rerolling the
mixture into the cigar’s outer leaves so that the mixture
assumes the shape of the original cigar (Gruber &
Methods of Administration Pope, 2002). Users report some degree of stimulation,
In the United States, marijuana is occasionally ingested possibly from the nicotine in the cigar tobacco entering
by mouth, usually after it has been baked into a product the lungs along with the marijuana smoke.
such as cookies or brownies. This process allows the The technique by which marijuana is smoked is
user to absorb 4%–12% of the available THC, with a somewhat different from the normal smoking tech-
large part of the THC being destroyed in the digestive nique used for cigarettes or cigars (Schwartz, 1987).
tract (Drummer & Odell, 2001; Gold et al., 2004; Users must inhale the smoke deeply into their lungs,
Stimmel, 1997b). In contrast to smoked marijuana, oral then hold their breath for 20–30 seconds to get as much
ingestion results in a slower absorption into the general THC into the blood as possible (Schwartz, 1987). Be-
circulation so that the user does not feel the effects of cause THC crosses through the lungs into the circula-
THC until 30–60 minutes (Mirin et al., 1991) to per- tion very slowly, only 25%–50% of the THC that is
haps 2 hours (Schwartz, 1987) after ingesting it. The inhaled will actually be absorbed through the lungs
peak blood concentration of THC is usually seen 60–90 (McDowell, 2005).
minutes after the person has ingested the cookie or But the effects of this limited amount of THC begin
brownie, although in rare cases this might be delayed within seconds (Weiss & Mirin, 1988) to perhaps 10
for as long as 1–5 hours (Drummer & Odell, 2001). Es- minutes (Bloodworth, 1987). To produce a sense of eu-
timates of the duration of marijuana’s effects when in- phoria, the user must inhale approximately 25–50 mi-
gested orally range from 3 to 5 hours (Mirin, Weiss, & crograms per kilogram of body weight when marijuana
Greenfield, 1991; Weiss & Mirin, 1988) to 8 to 24 hours is smoked, and between 50–200 micrograms per kilo-
(Gruber & Pope, 2002). gram of body weight when ingested orally (Mann,
The most popular means by which marijuana is 1994). Doses of 200–250 micrograms per kilogram by
abused is by smoking (Gruber & Pope, 2002), a prac- smoking or 300–500 micrograms when taken orally
tice that can be traced back at least 5,000 years (Walton, may cause the user to hallucinate, according to Mann
2002). Health professionals disagree as to the amount of (1994), indicating that it takes an extremely large dose
THC admitted to the body when marijuana is smoked. of THC to produce hallucinations. Marijuana users in
It has been suggested that almost 60% of the available other countries often have access to high-potency
THC is admitted into the body by smoking (Drummer & sources of THC and thus may achieve hallucinatory
Odell, 2001; Gold et al., 2004). In contrast, Stephens doses. But it is extremely rare for marijuana users in this
and Roffman (2005) suggested that 30% to 80% of the country to have access to such potent forms of the
available THC was either destroyed by the smoking plant. Thus, for the most part, the marijuana being
process or lost through “sidestream” smoke. Of the re- smoked in the United States will not cause the individ-
mainder, the authors suggested that only 5% to 24% ual to hallucinate. Even so, marijuana is often classified
was actually absorbed into the user’s body. There is a as a hallucinogenic by law enforcement officials.
great deal of interindividual variability in the absorp- The effects of smoked marijuana reach peak inten-
tion rates, however, and there is a need for research into sity within 20–30 minutes and begin to decline in an
this subject. hour (McDowell, 2005; Nelson, 2000). Estimates of the
duration of the subjective effects of smoked marijuana physical effects of marijuana, which cause a transient
range from 2–3 (O’Brien, 2006; Zevin & Benowitz, release of dopamine, a neurochemical thought to be in-
2007) to 4 hours (Grinspoon et al., 2005; Sadock & volved in the experience of euphoria.
Sadock, 2003) after a single dose. The individual might At exceptionally high doses, some abusers have re-
suffer some cognitive and psychomotor problems for ported a synesthesia16-like experience in which they
as long as 5–12 hours after a single dose, however, sug- have a visual sensation in response to sounds (Early-
gesting that the effects of marijuana on motor skills last wine, 2005). Over half of abusers report enhanced tac-
longer than the euphoria (O’Brien, 2006; Sadock, & tile sensations while under the influence of marijuana,
Saodck, 2003). according to Earlywine. While taste is not improved,
Proponents of the legalization of marijuana point the user often reports enjoying taste sensations more,
out that in terms of immediate lethality, marijuana and some abusers report enhanced sexual orgasm while
appears to be a “safe” drug. Various researchers have under the influence of marijuana (Earlywine, 2006).
estimated that the effective dose is 1/10,000th (Sci- The individual’s expectations influence how he or
ence and Technology Committee Publications, 1998) she interprets the effects of marijuana. Marijuana users
to 1/20,000th, or even 1/40,000th the lethal dose tend to anticipate that the drug will (a) impair cognitive
(Grinspoon & Bakalar, 1993, 1995; Kaplan, Sadock, & function as well as the user’s behavior, (b) help the user
Grebb, 1994). It was reported that a 160-pound person relax, (c) help the user to interact socially and experience
would have to smoke 900 marijuana cigarettes simulta- enhanced sexual function, (d) enhance creative abili-
neously to achieve a fatal overdose (Cloud, 2002). An ties and alter perception, (e) bring with it some negative
even higher estimate was offered by Schlosser (2003), effects, and (f) bring about a sense of craving (Schafer
who suggested that the average person would need to & Brown, 1991). Individuals who are intoxicated on
smoke 100 pounds of marijuana a minute for 15 min- marijuana frequently report an altered sense of time as
utes to overdose on it.15 In contrast to the estimated well as mood swings (Sadock & Sadock, 2003).
434,000 deaths each year in this country from tobacco Marijuana users have often reported a sense of being
use and the 125,000 yearly fatalities from alcohol use, on the threshold of a significant personal insight but are
only an estimated 75 marijuana-related deaths occur unable to put this insight into words. These reported
each year; these are usually accidents that take place drug-related insights seem to come about during the
while the individual is under the influence of this sub- first phase of the marijuana reaction. The second phase
stance rather than as a direct result of its toxic effects of the marijuana experience begins when the individ-
(Crowley, 1988). As these data would suggest, there has ual becomes sleepy, which takes place following the
never been a documented case of a marijuana overdose acute intoxication caused by marijuana (Brophy,
(Gruber & Pope, 2002; Schlosser, 2003). In terms of its 1993).
immediate toxicity, marijuana appears to be “among
the least toxic drugs known to modern medicine” (Weil,
1986, p. 47).
Adverse Effects of Occasional
Marijuana Use
Research into the effects of marijuana on the brains of
Subjective Effects of Marijuana users or on their behavior has been “surprisingly
At moderate dosage levels, marijuana will bring about a scarce” (Aharonovich et al., 2005, p. 1507). Until the
two-phase reaction (Brophy, 1993). The first phase be- mid-1990s, few researchers accepted that marijuana
gins shortly after the drug enters the bloodstream when abuse had any significant negative consquences for the
the individual will experience a period of mild anxiety; user (Aharonovich et al., 2005). But with more than
altered sense of time; a calm, gentle, euphoria; and a 2,000 separate metabolites of the 400 chemicals found
sense of relaxation and friendliness (Grinspoon et al., in the marijuana plant finding their way into the body
2005; Hall & Degenhardt, 2005). Other abusers report of the user, it would be unusual for there to be no ad-
enhanced perception or appreciation of colors and verse effects (Jenike, 1991). Many of the metabolites of
sounds (Earlywine, 2005; Zevin & Benowitz, 2007). these chemicals remain in the body for weeks after a
These subjective effects are consistent with the known single exposure to marijuana, and scientists have not
addressed the issue of long-term effects of exposure to
15Itshould be noted that some abusers have made valiant efforts to
reach this level of intoxication, although with little success. 16See Glossary.
these compounds, although there is little evidence of accident by 300% to 700% (Lamon, Gadegbeku, Martin,
neurological impairment following 24 hours of absti- Biecheler, & the SAM Group, 2005; Ramaekers,
nence (Filley, 2004; Zevin & Benowitz, 2007). Berghaus, van Laar, & Drummer, 2004).
Further, if the marijuana is adulterated (as it fre- A more serious but quite rare adverse reaction is the
quently is), the various adulterants add their own con- development of a marijuana-induced psychotic reac-
tribution to the flood of chemicals admitted to the body tion, often called a toxic or drug-induced psychosis. The
when the person uses marijuana. Although marijuana effects of a marijuana-induced toxic psychosis are usu-
advocates point to its safety record, it is not a benign ally short-lived and usually will clear up in a few days to
substance. Approximately 40%–60% of users will expe- a week (Johns, 2001). Psychotic reactions that last
rience at least one other adverse drug-induced effect longer than this seem to suggest that the individual had
beyond the famous “bloodshot eyes” seen in marijuana a preexisting psychotic condition. For more than 150
smokers (Hubbard et al., 1999). This argues that there years, scientists have questioned whether there is a link
is a definite need for research into marijuana’s effects between cannabis abuse and psychotic reactions, and
on the user’s body. while there is no evidence of a causal link, research
The famous “bloodshot eyes” effect of marijuana is does suggest that marijuana use can exacerbate preex-
caused by the small blood vessels in the eyes dilating in isting psychotic disorders, or initiate a psychotic reac-
response to a chemical found in marijuana, thus allow- tion in patients predisposed to this condition (Johns,
ing them to be more easily seen. Further, many mari- 2001; Lawton, 2005; Linszen, Dingemans, & Lenior,
juana abusers report feelings of anxiety after using this 1994; O’Brien, 2001; Zerrin, 2004).
substance (Johns, 2001; McDowell, 2005). Between One study conducted in Sweden found that recruits
50% and 60% of abusers report at least one period of into the Swedish army who had used marijuana more
marijuana-induced anxiety at some point in their mari- than 50 times in their lifetimes had a 670% higher inci-
juana use (O’Brien, 2006). Factors that seem to influ- dence of schizophrenia than their nonsmoking peers
ence the development of marijuana-induced anxiety or (Iverson, 2005). This is strong evidence that marijuana
panic are the use of more potent forms of marijuana, can exacerbate schizophrenia or contribute to the
the individual’s prior experience with marijuana, ex- emergence of a psychotic disorder in biologically pre-
pectations for its effects, the dosage level being used, disposed individuals (Hall & Degenhardt, 2005). Other
and the setting in it is abused. Marijuana-induced research has found that individuals who abused mari-
panic reactions are most often seen in the inexperi- juana in adolescence, especially prior to the age of 15,
enced marijuana user (Grinspoon et al., 2005; Gruber & had a significantly higher risk of schizophrenia than
Pope, 2002). Usually the only treatment needed is those individuals who did not (Lawton, 2005). The
simple reassurance that the drug-induced effects will causal mechanism remains unclear, and there are
soon pass (Millman & Beeder, 1994; Kaplan, Sadock, & many confounding variables that make it difficult to at-
Grebb, 1994). Because smokers are able to titrate the tribute the observed effect to marijuana abuse alone
amount used more easily than oral users, there is a ten- (Iverson, 2005). But the ability of marijuana to affect
dency for panic reactions to occur more often after mar- the dopamine neurotransmitter system, which is impli-
ijuana is ingested orally as opposed to being smoked cated in the psychotic disorders, might be one avenue
(Gold et al., 2004). by which cannabis abuse contributes to this mental
Marijuana also seems to bring about a splitting of health problem (Linszen et al., 1994).
consciousness, in which the user will possibly experience Even limited marijuana use is known to reduce sex-
depersonalization and/or derealization while under ual desire in the user, and for male users, it may con-
its influence (Earlywine, 2005; Johns, 2001). Medical tribute to erectile problems, lower testosterone levels,
professionals have described one case of marijuana- lowered sperm count, and delayed ejaculation (Finger,
induced transient global amnesia in a child acciden- Lund, & Slagel, 1997; Greydanus & Patel, 2005; Hall &
tally exposed to this compound, which spontaneously Degenhardt, 2005). Finally, there is a relationship be-
resolved after a period of several hours (Prem & Uzoma, tween cannabis abuse and depression, although re-
2004). Marijuana use also contributes to impaired researchers are not sure whether the depression is a
flexes for at least 24 hours after the individual’s last use result of the cannabis use (Freimuth, 2005; Grinspoon
of this substance (Gruber & Pope, 2002; Hubbard et al., et al., 2005). This marijuana-related depression is most
1999). Even occasional marijuana use increases the common in the inexperienced user and may reflect the
individual’s risk of being involved in a motor vehicle activation of an undetected depression in the abuser.
Such depressive episode are usually mild and short- as much tar as cigarette smokers (Tashkin, 1993). In
lived, and only rarely require professional intervention addition, the marijuana smoker will absorb five times
(Grinspoon et al., 2005). as much carbon monoxide per joint as would a ciga-
rette smoker who smoked a single regular cigarette
(Oliwenstein, 1988; Polen, Sidney, Tekawa, Sadler, &
Consequences of Chronic Friedman, 1993; University of California, Berkeley,
Marijuana Abuse 1990b). Smoking just four marijuana “joints” appears
Although long touted as a “safe” recreational drug, the re- to have the same negative impact on lung function as
ality is that the neurocognitive and physiological effects smoking 20 regular cigarettes (Tashkin, 1990).
of chronic marijuana use remain to be identified (Sneider Marijuana smoke has been found to contain 5–15
et al., 2006). Thus, until scientists have a better under- times the amount of a known carcinogen, benzpyrene,
standing of the long-term effects of chronic marijuana as does tobacco smoke (Bloodworth, 1987; Tashkin,
abuse, the claim that it is “safe” remains an unsupported 1993). Indeed, the heavy use of marijuana was sug-
one that might be proven wrong in the years to come. gested as a cause of cancer of the respiratory tract and
Researchers have found that chronic marijuana the mouth (tongue, tonsils, etc.) in a number of
abuse is associated with a range of physical and emo- younger individuals who would not be expected to have
tional consequences for the user. For example, chronic cancer (Gruber & Pope, 2002; Hall & Solowij, 1998;
marijuana use appears to suppress REM-stage sleep, al- Tashkin, 1993). There are several reasons for the ob-
though it is not clear whether isolated episodes of mari- served relationship between heavy marijuana use and
juana abuse have any significant impact on REM sleep lung disease. In terms of absolute numbers, marijuana
(McDowell, 2005). Researchers have also found pre- smokers tend to smoke fewer joints than cigarette smok-
cancerous changes in the cells of the respiratory tract of ers do cigarettes. However, they also smoke unfiltered
chronic marijuana abusers similar to those seen in ciga- joints, a practice that allows more of the particles from
rette smokers (Gold et al., 2004; Tashkin, 2005; Tetrault smoked marijuana into the lungs than is the case for
et al., 2007). However, Hashibe et al. (2005) concluded cigarette smokers. Marijuana smokers also smoke more
that the apparent relationship between marijuana of the joint than cigarette smokers do cigarettes. This
smoking and cancer was an artifact caused by the high increases the smoker’s exposure to microscopic con-
incidence of concurrent tobacco use by marijuana taminants in the marijuana. Finally, marijuana smok-
abusers. The authors found that the marijuana smokers ers inhale more deeply than cigarette smokers and
who were at highest risk for cancer were also the heavi- retain the smoke in the lungs for a longer period of time
est cigarette smokers, suggesting that the increased risk (Polen et al., 1993). Again, this increases the individ-
for cancer was induced by the individual’s tobacco use ual’s exposure to the potential carcinogenic agents in
and not the marijuana smoking. marijuana smoke. These facts seem to explain why mar-
Chronic exposure to THC has been found to reduce ijuana smokers, like tobacco smokers, have an increased
the effectiveness of the respiratory system’s defenses frequency of bronchitis and other upper respiratory in-
against infection (Gruber & Pope, 2002; Hubbard et al., fections (Hall & Solowij, 1998). The chronic use of mari-
1999). Tetrault et al. (2007) found that chronic marijuana also may contribute to the development of chronic
juana smokers had increased incidence of cough and obstructive pulmonary disease (COPD), similar to what is
wheezing, and that marijuana smoking had much the seen in cigarette smokers (Gruber & Pope, 2002).
same impact on the lungs as did cigarette smoking. Animal research also suggests the possibility of a
With the exception of nicotine, which is not found drug-induced suppression of the immune system as a
in the cannabis plant, marijuana smokers are exposed whole, although it is not clear whether this effect is
to virtually all the toxic compounds found in cigarettes, found in humans (Abrams et al., 2003; Gold et al.,
and if they smoke a “blunt,”17 their exposure to these 2004). But given the relationship between HIV-1 virus
compounds is even higher (Gruber & Pope, 2002). The infection and immune system impairment,18 it would
typical marijuana cigarette has between 10 and 20 seem that marijuana abuse by patients with HIV-1 in-
times as much “tar” as tobacco cigarettes (Nelson, 2000), fection is potentially dangerous.
and marijuana smokers are thought to absorb four times Marijuana abuse has been implicated as the cause of
a number of reproductive system dysfunctions. For
17Discussed earlier in this chapter. Essentially a cigarette/cigar where
18Discussed
most of the tobacco was replaced with marijuana, then smoked. in Chapter 34.
example, there is evidence that marijuana use con- More frightening are studies that found changes in
tributes to reduced sperm counts as well as a reduction the electrical activity of the brain, as measured by elec-
in testicular size in men (Hubbard et al., 1999; troencephalographic (EEG) studies, in chronic mari-
Schuckit, 2006). Further, chronic marijuana abuse has juana abusers. It is not known at this time whether
been implicated as the cause of reduced testosterone these EEG changes predate the abuse of marijuana, are
levels in men, although this condition might reverse it- caused by the abuse of cannabis, or result from the
self with abstinence (Schuckit, 2006). Chronic female abuse of other recreational chemicals (Grant, Gonzalez,
marijuana smokers may experience menstrual abnor- Carey, Natarajan, & Wolfson, 2003). Neuropsychologi-
malities and/or a failure to ovulate (Gold, Frost-Pineda, & cal testing of chronic marijuana users in countries such
Jacobs, 2004; Hubbard, Franco, & Onaivi, 1999). as Greece, Jamaica, and Costa Rica has failed to uncover
These problems are of clinical importance, and women evidence of permanent brain damage (Grinspoon &
who wish to conceive are advised to abstain from mari- Bakalar, 1997b). However, there is evidence that chronic
juana use prior to the initiation of pregnancy. cannabis use might cause changes in regional blood
People who have previously used hallucinogenics flow patterns in the brain of the user that continue at
may also experience marijuana-related “flashback” ex- least for the first few weeks following abstinence
periences (Jenike, 1991). Such flashbacks are usually (Sneider et al., 2006).
limited to the 6-month period following the last mari- Along similar lines, Hernig, Better, Tate, and Cadet
juana use (Jeinke, 1991) and will eventually stop if the (2001) used a technique known as transcranial Doppler
person does not use any further mood-altering chemi- sonography to determine the blood flow rates in the
cals (Weiss & Mirin, 1988). The flashback experience brains of 16 long-term marijuana abusers and 19
is discussed in more detail in the chapter on the hallu- nonusers. The authors found evidence of increased
cinogenic drugs, as there is little evidence that cannabis blood flow resistance in the cerebral arteries of the mar-
alone can induce flashbacks (Sadock & Sadock, 2003). ijuana abusers, suggesting that chronic marijuana
There is a small but growing body of evidence sug- abuse might increase the individual’s risk of a cerebral
gesting that chronic marijuana use results in brain vascular accident (stroke). Within 4 weeks of their last
damage and/or permanent cognitive dysfunction (Vik, use of cannabis, the blood flow patterns of young mari-
Cellucci, Jarchow, & Hedt, 2004). The research team juana abusers was comparable to that seen in normal
of Matochik, Eldreth, Cadet, and Bolla (2005) found 60-year-old adults, according to the authors. It was not
evidence of significant levels of brain tissue loss in the possible to predict whether the brain blood flow pat-
right parahippocampal gyrus and the left parietal lobe terns would return to normal with continued absti-
regions of the brain on neuroimaging tests conducted nence from marijuana. This places cannabis in the
on 11 heavy marijuana abusers. The authors concluded paradoxical position of possibly contributing to the in-
that there was a positive correlation between duration dividual’s risk for stroke and as possibly containing a
of marijuana abuse and the level of brain tissue loss, compound that might limit the damage caused by a
suggesting that marijuana abuse might cause at least a cerebrovascular accident after it occurs.
temporary loss of neurons in the affected regions of the The “amotivational syndrome.” Scientists have found
brain. conflicting evidence as to whether chronic marijuana
Further, chronic marijuana abusers have been found use might bring about an “amotivational syndrome.”
to demonstrate long-term deficits in cognitive function The amotivational syndrome is thought to consist of de-
(Messinis, Kyprianidou, Malefaki, & Papathanasoupoulos, creased drive and ambition, short attention span, easy
2006; Sussman & Westreich, 2003). It is possible to detect distractibility, and a tendency not to make plans beyond
evidence of cognitive deficits in the chronic cannabis the present day (Mirin et al., 1991). Indirect evidence
abuser for up to 7 days after the last use of marijuana suggesting that the amotivational syndrome might exist
(Pope, Gruber, Hudson, Huestis, & Yurgelun-Todd, was provided by Gruber et al. (2003). The authors com-
2001; Pope & Yurgelun-Todd, 1996). The identified pared psychological and demographic measures of 108
memory deficits associated with cannabis abuse appear individuals who had smoked cannabis at least 5,000 times
to be progressively worse in chronic users (Gruber, Pope, and 72 age-matched control subjects who admitted to
Hudson & Yurgelun-Todd, 2003; Lundqvist, 2005; having abused marijuana no more than 50 times. The
Solowij et al., 2002). But these cognitive changes seem authors found that the heavier marijuana users reported
to reverse after 2 weeks of abstinence from marijuana significantly lower incomes and educational achieve-
(Vik et al., 2004). ment than did the control group even though the two
groups came from similar families of origin. While sug- Husak, 2004). However, the chronic abuser who is
gestive, this study does not answer the question of more tolerant of the effects will experience less of the
whether these findings reflect the effects of marijuana or sedating effects and be more capable of violence than a
if individuals prone to marijuana abuse tend to have less rare user (Walton, 2002). Currently, few clinicians now
drive and initiative and are drawn to marijuana because believe that marijuana, by itself, is associated with an
its effects are similar to their personalities. increased tendency for violent acting out.
The “amotivational syndrome” has been challenged
by many researchers in the field. Even chronic mari-
The Addiction Potential of Marijuana
juana abusers demonstrate “remarkable energy and en-
thusiasm in the pursuit of their goals” (Weiss & Because marijuana does not cause the same dramatic
Millman, 1998, p. 211). It has been suggested that the withdrawal syndromes seen with alcohol or narcotic ad-
amotivational syndrome might reflect nothing more diction, people tend to underestimate the addiction po-
than the effects of marijuana intoxication in chronic tential of cannabis. But tolerance, one of the hallmarks
users (Johns, 2001), and there is little evidence of “a of addiction, does slowly develop to cannabis (Stephens &
specific and unique ‘amotivational syndrome’” (Iverson, Roffman, 2005). Researchers believe that smoking as
2005; Mendelson & Mello, 1998, p. 2514; Sadock & few as three marijuana cigarettes a week may result in
Sadock, 2003). some degree of tolerance to the effects of marijuana
Marijuana abuse as a cause of death. Although mar- (Bloodworth, 1987). Further, it is estimated that between
ijuana is, in terms of immediate lethality, quite safe, 8% (Zevin & Benowitz, 2007) and 20% (Lynskey &
there is significant evidence that chronic marijuana use Lukas, 2005) of chronic cannabis abusers will become
can contribute to or is the primary cause of a number of addicted to marjuana. In contrast to this figure, Gruber
potentially serious medical problems. For example, and Pope (2002) suggested that one-third of the adoles-
there is evidence that some of the chemicals in mari- cents who abuse marijuana daily are addicted to it.
juana might function as “dysregulators of cellular regu- Although at first Gruber and Pope’s (2002) assertion
lation” (Hart, 1997, p. 60) by slowing the process of might seem at odds with the other estimates of mari-
cellular renewal within the body. juana addiction offered in the last paragraph, it is im-
Marijuana abusers experience a 30% to 50% in- portant to remember that the addiction to cannabis in a
crease in heart rate that begins within a few minutes of 15-year-old might manifest itself differently and follow a
the time of use and can last for up to 3 hours (Craig, different path from a similar addiction in an adult
2004; Hall & Degenhardt, 2005; Hall & Solowij, (Ellickson et al., 2004). This makes the identification
1998). For reasons that are unknown, marijuana also of cannabis addiction difficult since there are different
causes a reduction in the strength of the heart contrac- pathways to the end point of addiction (Ellickson et al.,
tions and the amount of oxygen reaching the heart 2004). One characteristic that seems to identify individ-
muscle, changes that are potentially serious for pa- uals who are at risk for becoming addicted to marijuana
tients with heart disease (Barnhill et al., 1995; Schuckit, is a positive experience with it early in life (prior to age 16)
2006). Although these changes are apparently in- (Fergusson, Horwood, Lynskey, & Madden, 2003).
significant for younger cannabis users, they may be the The withdrawal syndrome from cannabis has not
reason older users are at increased risk for heart attacks been examined in detail (Budney, Moore, Bandrey, &
in the first hours following their use of marijuana Hughes, 2003). A popular misconception is that there
(“Marijuana-Related Deaths?” 2002; Mittleman, Lewis, is no withdrawal syndrome with marijuana; however,
Maclure, Sherwood, & Muller, 2001). research has found that chronic marijuana abusers ex-
The myth of marijuana-induced violence. In the perience a withdrawal syndrome that includes irritabil-
1930s and 1940s, it was widely believed that marijuana ity, aggressive behaviors, anxiety, insomnia, sweating,
would cause the user to become violent. Researchers nausea, anorexia, and vomiting (Budney, Hughes,
no longer believe that marijuana is likely to induce vio- Moore, & Vandrey, 2004; Gruber & Pope, 2002;
lence. Indeed, “only the unsophisticated continue to Lynskey & Lukas, 2005; Stephens & Roffman, 2005).
believe that cannabis leads to violence and crime” These withdrawal symptoms begin 1–3 days after the
(Grinspoon et al., 2005, p. 267). The sedating and eu- last use of cannabis, peak between the second and tenth
phoric effects of marijuana are thought to reduce the day, and can last up to 28 days or more (Budney,
tendency toward violence while the user is intoxicated Moore, et al., 2003; Sussman & Westreich, 2003). The
rather than to bring it about (Grinspoon et al., 2005; cannabis withdrawal syndrome has been classified as
flu-like in intensity (Martin, 2004). It would thus ap- differ as to the potential for marijuana to cause harm.
pear that, despite claims to the contrary, marijuana For example, in contrast to Weil’s (1986) assertion that
meets the criteria necessary to be classified as an addic- marijuana was one of the safest drugs known, Oliwen-
tive compound. stein (1988) classified it as a dangerous drug. In reality,
the available evidence at this time would suggest that
marijuana is not as benign as it was once thought. Ei-
Summary ther alone or in combination with cocaine, marijuana
Marijuana has been the subject of controversy for the will increase heart rate, a matter of some significance to
past several generations. In spite of its popularity as a those with cardiac disease. There is evidence that
drug of abuse, surprisingly little is actually known about chronic use of marijuana will cause physical changes in
marijuana. Indeed, after a 25-year search, researchers the brain, and the smoke from marijuana cigarettes has
have identified what appears to be the specific receptor been found to be even more harmful than tobacco
site the THC molecule uses to cause at least some of its smoke. Marijuana remains such a controversial drug
effects on perception and memory. that the United States government refuses to sanction
Although very little is known about this drug, some research into its effects, claiming that they do not want
groups have called for its complete decriminalization. to risk researchers’ finding something about marijuana
Other groups maintain that marijuana is a serious drug that proponents of its legalization might use to justify
of abuse with a high potential for harm. Even the experts their demands (D. Smith, 1997).
CHAPTER FOURTEEN
Opioid Abuse and Addiction
Pain is the oldest problem known to medicine (Meldrum, as many as 73% of people in moderate to severe distress
2003). It is also one of the most common complaints receive less than adequate doses of narcotic analgesics
by patients. Each year in the United States, more because of this fear (Gunderson & Stimmel, 2004;
than 70% of adults will experience at least one episode Stimmel, 1997a).
of acute pain (Williams, 2004). The history of pain and To further complicate matters, regulatory policies of
its treatment is virtually synonymous with the use of the Drug Enforcement Administration (DEA) aimed at
opioids such as morphine or codeine. More recently, discouraging the diversion of prescribed narcotic anal-
semisynthetic and synthetic narcotic analgesics have gesics1 often intimidate or confuse physicians who wish
been introduced to provide options for the physician to prescribe these medications for patients in pain. Ad-
treating the patient in pain. But the problem of pain mittedly, the narcotic analgesics do have a significant
persists. abuse potential. But they are also potent and extremely
In spite of all of the advances made by medical sci- useful medications. To clear up some of the confusion
ence, there is no objective way to measure pain, and the that surrounds the legitimate use of narcotic analgesics,
physician must rely almost exclusively on the patient’s this chapter is split into two sections. The first section
subjective assessment of his or her pain (Cheatle & examines the role and applications of narcotic anal-
Gallagher, 2006; Williams, 2004). Even now, scientists gesics as pharmaceutical agents; the second looks at the
do not fully understand the complex neurophysiological opiates as drugs of abuse.
processes involved in the sensation of pain (Chapman &
Okifuji, 2004). Given the fact that scientists have only
an imperfect understanding of the problem of pain, it
I. THE MEDICAL USES
should not be surprising to learn that the medications OF NARCOTIC ANALGESICS
used to control severe pain, narcotic analgesics, are also A Short History of
a source of confusion both for physicians and the gen- the Narcotic Analgesics
eral public. Because of their potential for abuse, both
the general public and physicians view these medica- Anthropological evidence suggests that opium was used
tions with distrust (Herrera, 1997; Vourakis, 1998). Over in religious rituals and was being cultivated as a crop as
the years, myths and mistaken beliefs about narcotic early as 10,000 years ago (Booth, 1996; Spindler, 1994;
analgesics and pain management have been repeated so Walton, 2002). At some point before the development
often that they ultimately become incorperated into proof written words, it had been discovered that if you
fessional journals and textbooks as medical “fact,” shap- made an incision at the top of the Papaver somniferum
ing patient care and further complicating pain control plant during a brief period in its life cycle, the plant
(Vourakis, 1998). would extrude a thick resin that was “an elaborate cock-
For example, because of the widespread problem of tail containing sugars, proteins, ammonia, latex, gums,
opioid addiction, many physicians hesitate to prescribe plant wax, tats, sulphuric and lactic acids, water,
large doses of narcotic analgesics for patients out of fear meconic acid, and a wide range of alkaloids” (Booth,
that they would cause or contribute to a substance use 1996, p. 4). The exact composition of this resin would
disorder (SUD) (Antoin & Beasley, 2004). This leads 1For many years, the problem of drug diversion was thought to be
many physicians to underprescribe narcotic analgesics quite insignificant. However, since the middle 1990s it has become
for patients in pain, causing them to suffer needlessly apparent that the diversion of compounds such as OxyContin is a
(Carvey, 1998; Kuhl, 2002). It has been estimated that very real problem (Meier, 2003).
158
Opioid Abuse and Addiction 159
not be determined for thousands of years. But even so, field hospitals, and the recently invented intravenous
early human beings had discovered that it could be needle all combined to produce widespread epidemics
used for ritual and medicinal purposes. Eventually, it of morphine addiction both in the United States and
was called opium (Jenkins, 2007). Europe in the last half of the 19th century.
The English word opium can be traced to the Greek The “patent medicine” phenonemon of the 19th
word opion, which means “poppy juice” (Stimmel, century played a major role in the morphine addiction
1997a). In a document known as the Ebers Papyri, that developed in the United States and Europe in the
which dates back to approximately 7,000 B.C.E., there is latter years of the 19th century. At that time, the average
a reference to the use of opium as a treatment for chil- person had little confidence in medical science. Physi-
dren who suffer from colic (Darton & Dilts, 1998). His- cians were often referred to as “croakers,” a grim testi-
torical evidence suggests that by around 4,200 B.C.E., monial to their skill in treating disease. It was not
the use of opium was quite common (Walton, 2002). It unusual for the patient to rely on time-honored folk
was used by healers for thousands of years and was remedies and patent medicines rather than see a physi-
viewed as a gift from the gods because it could treat cian (Norris, 1994). Unfortunately, both cocaine and
such diverse conditions as pain and severe diarrhea, morphine were common ingredients in many of the
especially massive diarrhea such as that of dysentery.2 patent medicines that were sold throughout the United
By the 18th century, physicians had discovered that States without any form of regulation. Even if users of a
opium could control anxiety, and its limited antipsy- patent medicine were aware of the contents of the bottle,
chotic potential made it marginally effective in control- they were unlikely to believe this “medicine” could
ling the symptoms of psychotic disorders, important hurt them. The concept of addiction was totally foreign
discoveries when physicians had no other effective treat- to the average person of the era, especially since the
ment for these conditions (Beeder & Millman, 1995; concept of “drug abuse” did not emerge until the latter
Woody, McLellan, & Bedrick, 1995). years of the 19th century (Walton, 2002). As a result,
In 18033 a chemist named Friedrich W. A. Serturner large numbers of people unknowingly became addicted
first isolated a pure alkaloid base from opium that was to one or more chemicals in the patent medicine they
recognized as being the substance’s active agent. This took in good faith to treat real or perceived illness.
chemical was later called morphine after the Greek god In other cases, the individual had started using either
of dreams, Morpheus. Surprisingly, morphine is a “ni- opium or morphine for the control of pain or to treat di-
trogenous waste product” (Hart, 1997, p. 59) produced arrhea only to become physically dependent on it. When
by the opium poppy and not the reason for the plant’s the user tried to stop using the patent medicine, he or she
existence. But by happy coincidence this waste product would begin to experience withdrawal symptoms from
happens to control many of the manifestations of pain the narcotics or cocaine in the bottle. Like magic, an-
in humans. As chemists explored the various chemical other dose of the medicine would make the withdrawal
compounds found in the sap of the opium poppy, they symptoms disappear, bringing relief for a time.
discovered a total of 20 distinct alkaloids in addition to During this same period in United States history,
morphine that could be obtained from that plant, in- Chinese immigrants (many of whom had come to this
cluding codeine (Gutstein & Akil, 2006). After these al- country to work in railroad construction) introduced
kaloids were isolated, medical science found a use for the practice of smoking opium to the United States.
many of them. Unfortunately, many also can be abused. Opium smoking became popular especially on the Pa-
About a half century after morphine was first iso- cific coast, and many opium smokers became addicted
lated, in the year 1857, Alexander Wood invented the to the drug. By the year 1900 fully a quarter of the
hypodermic needle. This device made it possible to opium imported into the United States was used not for
quickly and relatively painlessly inject compounds medicine but for smoking (Jonnes, 1995; Ray & Ksir,
such as morphine into the body. The availability of rel- 1993). As a result of all of these different forces, by the
atively pure morphine, its unregulated use in patent year 1900 more than 1% of the entire population of the
medications, the common use of morphine in military United States was addicted to opium or narcotics
(Restak, 1994). It is estimated that between two-thirds
2SeeGlossary. and three-fourths of those individuals were women
3Restak (1994) suggested that morphine was isolated in 1805, not (Kandall, Doberczak, Tantunen, & Stein, 1999).
1803, while Antoin and Beasley (2004) and Jaffe and Strain (2005) Faced with an epidemic of unrestrained opiate use,
suggested that this event took place in 1806. the U.S. Congress passed the Pure Food and Drug Act
160 Chapter Fourteen
of 1906. This law required manufacturers to list the in- Acute pain is short and intense, and it resolves when
gredients of their product on the label, revealing for the the cause of the pain (incision, broken bone, etc.)
first time that many a trusted remedy contained nar- heals. Non-cancer chronic pain5 is associated with a
cotics. Other laws, especially the Harrison Narcotics nonmalignant pathological condition in the body,
Act of 1914, prohibited the use of narcotics without a while cancer pain is the result of the tumor’s growth or
prescription signed by a health care provider such as a expansion (Holleran, 2002).
physician or dentist. These early attempts at controlling In general, three different groups of compounds are
the problem of narcotics addiction through regulation used to control acute pain in humans. The first are gen-
were limited in their success, and the battle against nar- eral anesthetic agents, which cause the individual to
cotic abuse/addiction has waxed and waned over the lose consciousness and thus block his or her awareness
decades since then without ever disappearing entirely. of the pain. Then there are the local anesthetics, which
block the transmission of nerve impulses from the site
of the injury to the brain and thus prevent the brain
The Classification
from receiving the nerve impulses that transmit the
of Narcotic Analgesics pain message from the site of the injury to the brain.
Since morphine was first isolated, medical researchers Cocaine was once used in this capacity.
have developed a wide variety of natural, semisynthetic The third group of compounds used to control pain
or synthetic compounds that, in spite of differences in is those that reduce or block the individual’s awareness
their chemical structure, have pharmacological effects of pain within the central nervous system without caus-
similar to that of morphine. These compounds are clas- ing a general loss of consciousness. The opioids fall in
sified into three groups (Segal & Duffy, 1999): this category, and are “unsurpassed analgesic agents”
(Bailey & Connor, 2005, p. 60) when used to control
1. Natural opiates obtained directly from the opium, of moderate to severe levels of pain. Another group of
which morphine and codeine are examples. compounds in this group are the over-the-counter anal-
2. Semisynthetic opiates, which are chemically altered gesics such as aspirin, acetaminophen, and ibuprofen,
derivatives of natural opiates. Dihydromorphine and which will be discussed in Chapter 18.
heroin are examples of this group of compounds.
3. Synthetic opiates, which are synthesized in laborato-
ries and are not derived from natural opiates at all. Where Opium Is Produced
Methadone and propoxyphene are examples of these
At the start of the 21st century, morphine remains the
compounds.
gold standard for narcotic analgesics. While it is pos-
sible to synthesize morphine in the laboratory, this
Admittedly, there are significant differences in the chem-
process is extremely difficult, and morphine is usually
ical structures of these different compounds. However,
derived from opium poppies (Gutstein & Akil, 2006).
in this chapter they are grouped together under the
Virtually the entire planet’s need for legitimate opium
generic terms opioids, opiates, or narcotic analgesics for
might be met by the opium produced by just India. All
the sake of simplification, since all have similar phar-
the opium raised in other countries, such as Afghanistan
macological properties.
(which itself produces 87% of the opium produced on
the planet) is produced for illicit markets (United
The Problem of Pain Nations, 2005a).
We tend to view pain as something to be avoided if pos-
sible. The very word pain comes from the Latin word Current Medical Uses of
poena, which means a punishment or penalty (Cheatle & the Narcotic Analgesics
Gallagher, 2006; Stimmel, 1997a). There are three
basic types of pain: acute, chronic, and cancer-induced Since the introduction of aspirin, narcotics are no
pain (Gunderson & Stimmel, 2004; Holleran, 2002).4 longer utilized to control mild levels of pain. As a gen-
eral rule, the opiates are most commonly used for se-
4Other classification systems also exist. Costigan, Scholz, Samad, and vere, acute pain (O’Brien, 2001) and some forms of
Wolf (2006), for example, identified just two types of pain: inflamma-
tory pain (associated with tissue injury) and neuropathic pain (caused 5Thetreatment of the patient with concurrent chronic pain and
by a lesion in, trauma to, or a disease of the nervous system). SUDs is discussed in Chapter 32.
TABLE 14.1 Some Common Narcotic Analgesics*
Generic name Brand name Approximate equianalgesic parenteral dose
Morphine — 10 mg every 3–4 hours

Hydromorphone Dilaudid 1.5 mg every 3–4 hours
Meperidine Demerol 100 mg every 3 hours
Methadone Dolophine 10 mg every 6–8 hours
Oxymorphone Numorphan 1 mg every 3–4 hours
Fentanyl Sublimaze 0.1 mg every 1–2 hours
Pentazocine Talwin 60 mg every 3–4 hours
Buprenorphine Buprenex 0.3–0.4 mg every 6–8 hours
Codeine — 75–130 mg every 3–4 hours**
Oxycodone Perdocet, Tylox Not available in parenteral dosage forms
Source: Based on information contained in Thomson PDR (2006) and Cherny & Foley (1996).
*This chart is for comparison purposes only. It is not intended to serve as, nor should it be used as, a guide to
patient care.
**It is not recommended that doses of codeine above 65 mg be used because doses above this level do not
produce significantly increased analgesia and may result in increased risk of unwanted side effects.
chronic pain6 (Belgrade, 1999; Marcus, 2003; Savage, enkephalins, endorphins, and dynorphins (Gutstein &
1999). In addition, they are of value in the control of se- Akil, 2006). These opioid peptides function as neuro-
vere diarrhea and the cough reflex in some forms of dis- transmitters in the brain and spinal cord, although there
ease. A number of different opiate-based analgesics have is much that remains to be discovered about their func-
been developed over the years, with minor variations in tion and mechanisms of action (Gutstein & Akil, 2001;
potency, absorption characteristics, and duration of Hirsch, Paley, & Renner, 1996). These neurotransmitters
effects. The generic and brand names of some of the are known to carry out a wide range of regulatory activities
more commonly used narcotic analgesics are provided in the CNS including the perception of pain, moderation
in Table 14.1. of emotions, the perception of anxiety, sedation, appetite
suppression, and possibly an anticonvulsant function. In
Pharmacology of the Narcotic Analgesics the body, the opioid peptides are involved in such activi-
ties as smooth muscle motility and regulation of such
The resin collected from the Papaver somniferum plant body functions as temperature, heart rate, respiration,
contains 10%–17% morphine (Jenkins, 2007; Jenkins blood pressure, and even possibly the perception of pleas-
& Cone, 1998). Chemists isolated the compound mor- ure (Hawkes, 1992; Restak, 1994; Simon, 1997).
phine from this resin almost 200 years ago and quickly In 1994, scientists identified a new compound in the
concluded that it was the active agent of opium. In spite brain that shares many of the characteristics of the
of the time that has passed since then, it is still the stan- known opioid peptides; they named it nociceptin/
dard against which other analgesics are measured orphanin FQ (N/OFQ). The role of N/OFQ in the body
(D’Arcy, 2005; Nelson, 2000). or how narcotic analgesics impact the binding sites used
Researchers have come to understand that narcotic by this compound remains unknown at this time.
analgesics such as morphine mimic the actions of a sev- As this list suggests, the opioid peptides are powerful
eral families of endogenous opioid peptides, including neurochemicals. In contrast, morphine and its chemi-
cal cousins are only crude copies of the opioid peptides.
6The use of narcotic analgesics for the control of chronic pain is rather
For example, the opioid peptide known as beta endor-
controversial, sparking fierce debate among health care providers
(Antoin & Beasley, 2004). Martell et al. (2007) suggested after their phin (ß-endorphin) is thought to be 200 times as potent
review of the literature that the efficacy of opioids in the treatment of an analgesic as morphine. Currently, researchers be-
chronic pain for longer than 16 weeks has not been proven. lieve that the narcotic analgesics function as opioid
TABLE 14.2 Brain Receptor Sites Utilized cotic analgesics in the ventral tegmental region of the
by Narcotic Analgesics brain (Schuckit, 2006). This area of the brain is rich in
dopamine receptor sites and connects the cortex of the
Biological activity associated
brain with the limbic system. The chronic administra-
Opioid receptor with opioid receptor
tion of morphine to rats caused these same dopamine-
Mu1 Analgesia utilizing neurons to shrink in volume by approximately
25% (Sklair-Tavron et al., 1996). This is consistent
Mu2 Gastrointestinal motility, bradycardia,
with the theory that dopamine serves an alerting func-
respiratory depression
tion to novel stimuli, priming the brain to attend to a
Delta Analgesia (at level of spinal cord), new, novel stimulus that is either a positive or a nega-
endocrine effects, psychomotor tive reinforcer. The chronic administration of opioids
functions, feelings of euphoria would make their effects ordinary rather than novel,
Kappa Analgesia (at level of spinal cord), reducing the need for a neurotransmitter whose primary
miosis, sedation, respiratory activity function is to alert the nervous system to something new.
Sigma Dysphoria, hallucinations, increased One region of the brain rich in opioid peptide recep-
psychomotor activity, respiratory tors is the amygdalae (singular: amygdala) (Reeves &
activity Wedding, 1994). The amygdalae function as halfway
points between the senses and the hypothalamus—the
Epsilon Function is unknown at this time
“emotion center” of the brain, according to Reeves and
Lambda Function is unknown at this time Wedding. It is thought that the amygdalae will release
Source: Based on information provided in Barnett (2001); Katz opioid peptides in response to sensory data, thus influ-
(2000); Knapp et al. (2005); Jaffe & Jaffe (2004); Zevin & Benowitz encing the formation of emotionally laden memories
(1998). (Jaffe & Strain, 2005). The sense of joy or pleasure that
someone feels on solving an intricate mathematics
problem is caused by the amygdala’s release of opioid
peptide agonists, occupying the receptor sites in the peptides. This pleasure will make it more likely that the
CNS normally utilized by the opioid peptides to simu- person will remember the solution to that problem if
late or enhance the action of these naturally occurring she or he should encounter it again.
neurotransmitters. Opioid molecules tend to bind preferentially to one
Researchers have identified a number of opioid pep- of several receptor subtypes in the brain. When the mu
tide receptor sites within the brain; these are identified receptor site is occupied by opioid molecules, the indi-
by letters from the Greek alphabet: the mu, kappa, and vidual will experience a reduction in pain awareness,
delta receptor sites (Jenkins, 2007). Each site has at least and if not in pain, he or she will have a sense of well-
two subtypes: There are two subtypes of the mu receptor, being that lasts for 30–60 minutes after a single injec-
three subtypes of the kappa receptor, and two subtypes of tion (Giannini, 2000; Jaffe & Strain, 2005; Schuckit,
the delta receptor (Jenkins, 2007). A fourth receptor, the 2006). When the kappa receptor sites are occupied,
sigma receptor, has been identified, but virtually nothing the individual will feel somewhat sedated, and the size
is known about its distribution or function. of the individual’s pupils will be affected (Schuckit,
There is strong evidence that opioids will alter the 2006).
blood flow pattern within the human brain, although The drowsiness the individual feels when the kappa
the significance of this in the reduction of pain is still receptor sites are occupied by morphine seems to ex-
not clear. With single photon emission computed to- plain the ability of narcotic analgesics to cause the indi-
mography (SPECT) scans it is possible to visualize vidual to relax, or even fall asleep, in spite of the
changes in regional blood flow patterns in the brain in experience of intense pain (Gutstein & Akil, 2006; Jaffe
response to opioids, especially in the limbic region of et al., 1997). This effect seems to reflect the impact of
the brain (Schlaepfer et al., 1998; Schuckit, 2006). the morphine molecule on the locus ceruleus region of
When administered to volunteers who are not in the brain (Gold, 1993; Jaffe, Knapp, & Ciraulo, 1997).
pain, narcotic analgesics usually produce an unpleas- Further, when these receptor sites are occupied, the
ant sensation known as dysphoria. Few of these volun- individual will also feel a sense of dysphoria7 and his or
teers report experiencing any degree of pleasure, but
when they do, it seems to result from the effects of nar- 7
See Glossary.
her appetite will be affected. When the kappa receptor The peak effects of a single dose of morphine are
sites in the medulla are activated by opioid molescules, seen in about 60 minutes after an oral dose and in
the individual’s vomiting reflex is activated, which seems 30–60 minutes after an intravenous injection (Wilson,
to account for the ability of these drugs to cause nausea Shannon, Shields, & Stang, 2007). After absorption
and vomiting in patients (Jenkins, 2007). into the circulation, morphine will go through a two-
Codeine. Codeine is also an alkaloid found in the phase process of distribution throughout the body
same milky sap of the Papaver somnifeum plant from (Karch, 2002). In the first phase, which lasts only a few
which opium is obtained. It was first isolated in 1832 minutes, morphine is distributed to various blood-rich
(Gutstein & Akil, 2006; Jaffe, 2000). Like its chemical tissues, including muscle tissue, the kidneys, liver,
cousin morphine, codeine is able to suppress the cough lungs, spleen, and the brain. In the second phase,
reflex, and it has a mild analgesic potential, being about which proceeds quite rapidly, the majority of the mor-
one-fifth as potent as morphine (Dilts & Dilts, 2005). phine is biotransformed into a metabolite known as
About 10% of a dose of codeine is biotransformed into morphine-3-glucuronide (M3G), with a smaller amount
morphine (Gutstein & Akil, 2006; Karch, 2002). As an being transformed into the metabolite morphine-6-
interesting side note, about 10% of people of European glucuronide (M6G), or one of a small number of addi-
descent have a genetic mutation that prevents their tional metabolites (Karch, 2002).
body from producing an enzyme that transforms codeine The process of morphine biotransformation takes
into morphine, and thus they do not obtain any sig- place in the liver, and within 6 minutes of an intravenous
nificant pain relief from this compound (Goldstein, injection, the majority of a single dose of morphine has
2005; Zevin & Benowitz, 2007). been biotransformed into one of the two metabolites dis-
Following a single oral dose of codeine, peak blood cussed in the last paragraph. Scientists have only re-
levels are seen in 1–2 hours, and the half-life of codeine cently discovered that M6G is biologically active, and it
is between 2.4 and 3.6 hours (Gutstein & Akil, 2006; has been suggested that this metabolite might even be
Karch, 2002). The analgesic potential of codeine is more potent than the parent compound, morphine
enhanced by over-the-counter analgesics such as as- (Karch, 2002). About 90% of morphine metabolites are
pirin or acetaminophen, which is why it is commonly eventually eliminated from the body by the kidneys,
mixed with these compounds (Cherny & Foley, 1996; while the other 7%–10% are excreted in the bile (Wilson
Gutstein & Akil, 2006). Another advantage of codeine et al., 2007). Eighty-seven percent of the metabolites
is that it is not as vulnerable to the first-pass metabolism produced by a single dose of morphine are eliminated
effect as is morphine, allowing patients to obtain a from the body within 72 hours (Jenkins, 2007).
steady level of analgesia for mild to moderate pain relief The biological half-life of morphine ranges from 1
when the drug is administered in oral doses (Gutstein & to 8 hours, depending on the individual’s biochemistry,
Akil, 2006). with most textbooks giving an average figure of 2–3
Codeine, like many narcotic analgesics, is also quite hours (Drummer & Odell, 2001). Following a single
effective in the control of cough. This is accomplished dose, approximately one-third of the morphine be-
through codeine’s ability to suppress the action of a por- comes protein bound (Karch, 1996). The analgesic ef-
tion of the brain known as the medulla that is respon- fects of a single dose of morphine last for approximately
sible for maintaining the body’s internal state (Gutstein & 4 hours (Gutstein & Akil, 2006). Although it is well ab-
Akil, 2006; Jaffe et al., 1997). Except in extreme sorbed when administered through intramuscular or in-
cases, codeine is the drug of choice for cough control travenous injection, morphine takes 20–30 minutes to
(American Medical Association, 1994). cross over the blood-brain barrier to reach the appropri-
Morphine. Morphine is well absorbed from the gas- ate receptor sites in the brain (Angier, 1990). Thus,
trointestinal tract but for reasons discussed later in this there is a delay between the time that the narcotic anal-
chapter, orally administered morphine has only limited gesic is injected and when the patient begins to experi-
value in the control of pain. Morphine is easily ab- ence some relief from pain.
sorbed from injection sites, and because of this charac- Methadone. Methadone binds at the mu receptor
teristic it is often administered through intramuscular site, and has been found to be quite useful in the con-
or intravenous injections. Finally, morphine is easily trol of severe, chronic pain (Toombs & Kral, 2005).
absorbed through the mucous membranes of the body, When used as an analgesic, methadone begins to work
and it is occasionally administered in the form of rectal within 30–60 minutes, its effects peak about 4 hours,
suppositories. and it may remain effective for 6–12 hours depending
on the individual’s biochemistry (Chau, Shull, & agent in other countries and is used to treat severe
Mason, 2005; Jenkins, 2007). The elimination half-life levels of pain. Historically, it is the opioid that comes to
of methadone is estimated to be 15–40 hours following mind first when people think of the problem of nar-
a single dose, a characteristic that makes it ideal for the cotics abuse. Surprisingly, both animal studies and
control of opioid withdrawal smptoms when used in autopsy-based human data suggest that heroin has a
opioid agonist treatment programs8 (Gutstein & Akil, cardioprotective potential during periods of cardiac is-
2006; Jenkins, 2007). chemia, although the exact mechanism for this is not
There is some confusion about methadone when clear at present (Gutstein & Akil, 2006; Mamer, Penn,
used as an analgesic, and when it is used as an opioid Wildmer, Levin, & Maslansky, 2003; Peart & Gross,
agonist to block withdrawal symptoms resulting from 2004).
narcotics addiction. The latter dose is far smaller than
an effective analgesic dose of methadone, and patients
Neuroadaptation to Narcotic Analgesics
on opioid agonist programs will require larger than nor-
mal doses of narcotic analgestics to achieve appropriate Analgesia is not a static process but one influenced by a
levels of analgesia following surgery or injury (Toombs & host of factors such as disease progression, an increase in
Kral, 2005). physical activity, lack of compliance in taking the med-
In terms of pharmacokinetics, methadone is a very ication, and medication interaction effects (Pappagallo,
versatile compound. When used as an analgesic, it 1998). Another factor that influences the effectiveness
might be administered orally, as it is well absorbed from of a narcotic analgesic is the process of neuroadapta-
the gastrointestinal tract. But it also might be injected tion,10 which is occasionally misinterpreted as evidence
into muscle tissue, subcutaneously, or intravenously that the patient is addicted to the narcotic analgesic
(Toombs & Kral, 2005). Initially, methadone-induced being used in medical practice.
analgesia usually lasts 3–6 hours, but with repeated dos- The development of neuroadaptation is incomplete
ing this increases to 8–12 hours as methadone tends to and uneven (Jaffe & Jaffe, 2004). Animal research has
accumulate in body tissues with repeated doses. This al- demonstrated that there are changes on the cellular
lows a reservoir of unmetabolized methadone to gradu- level in the brain that alter the neuron’s responsiveness
ally be released back into the general circulation to opioids after just a single dose (Bailey & Connor,
between doses to maintain a relatively steady plasma 2005). But there is wide variation between individuals
level (Toombs & Kral, 2005). Scientists are unsure why in the speed at which the body adapts to the presence of
the analgesic effect is so short-lived in light of its ex- an opioid. Some patients might become tolerant to
tended elimination half-life (Toombs & Kral, 2005). opioid-induced analgesia after just a few days of contin-
OxyContin. Introduced in December 1995 as a time- uous use (Ivanov, Schulz, Palmero, & Newcorn, 2006).
release form of oxycodone, this drug was designed for use In contrast, this same hypothetical patient might never
by patients whose long-term pain could be controlled become fully tolerant of the ability of narcotics to affect
through the use of oral medications rather than intra- the size of the pupil of the eyes or to drug-induced con-
venously administered narcotic analgesics (Thompson stipation (Gutstein & Akil, 2006; McNicol et al., 2003).
PDR, 2006). The time-release feature of OxyContin As a result of the process of neuroadaptation, the indi-
allowed the patient to achieve relatively stable blood vidual’s daily medication requirements might reach levels
levels of the medication after 24–36 hours of use, pro- that would literally have killed that patient in the begin-
viding a better level of analgesia than could be achieved ning of treatment. For exmple, a single intravenous
with shorter-acting agents. In theory, this feature would dose of 60 mg of morphine is potentially fatal to the
provide for fewer episodes of break-through pain, al- opiate-naive person while terminal cancer patients might
lowing the patient to experience better pain control. require 500 mg/hour of intravemous morphine to
The abuse of OxyContin is discussed later in this achieve adequate pain control (Kaplan, Sadock & Grebb,
chapter. 1994; Knapp, Ciraulo & Jaffe, 2005). Such changes in
Heroin. Heroin has no recognized medical use in dosage requirements usually result from the progres-
the United States and is classified as a Schedule I sub- sion of the disorder causing the pain (Savage, 1999).
stance9 under the Controlled Substances Act of 1970 Only a minority of cases involve neuroadaptation to the
(Jenkins, 2007). It is a recognized pharmaceutical analgesic effects of the opiate being prescribed. Clinical
8Discussed
research has found that the concurrent administration
in Chapter 33.
9See 10
Appendix Four. See Glossary.
of dextromethorphan, an NMDA receptor antagonist, between the methadone and the antibiotic (Barnhill,
slows the development of neuroadaptation and im- Ciraulo, Ciraulo, & Greene, 1995). Barnhill et al.
proves analgesia without the need for an increase in the noted that the withdrawal symptoms did not manifest
morphine dose (O’Brien, 2001). It has also been found themselves until approximately the fifth day of Rifampin
that the concurrent use of NSAIDs such as aspirin or therapy, suggesting that the interaction between these
acetaminophen may potentiate the analgesic effect of two medications might require some time before the
narcotic analgesics through an unknown mechanism withdrawal symptoms develop.
(Gutstein & Akil, 2006). Thus physicians may attempt While this list does not include every possible inter-
to offset the development of neuroadaptation to the action between opiates and other chemical agents, it
analgesia effects of narcotic analgesics or enhance their does underscore the potential for harm that might re-
analgesic potential through the concurrent use of sult if narcotic analgesics are mixed with the wrong
NSAID compounds. medications.
Unfortunately, many physicians mistakenly interpret
the process of neuroadaptation to an opiate as evidence
of addiction. This misperception results in the under- Subjective Effects of Narcotic Analgesics
utilization of opiates in patients experiencing severe When Used in Medical Practice
pain (Herrera, 1997). Cherny (1996) termed the patient’s
The primary use of narcotic analgesics is to reduce the
repeated requests for additional narcotic analgesics in
distress caused by pain (Darton & Dilts, 1998). To un-
such cases pseudoaddiction, noting that in contrast to
derstand how this is achieved, one must understand
true addiction the patient ceases to request additional
that pain
drugs once the pain is adequately controlled.
Drug interactions involving narcotic analgesics.11
may be simplistically classified as acute or chronic.
Even a partial list of potential medication interactions
Acute pain implies sudden onset, often within min-
clearly underscores the potential for narcotic analgesics
utes or hours. Usually, there is a clear-cut etiology,
to cause harm to the individual if he or she should mix
and the intensity of acute pain is severe, often re-
them with the wrong medications. Narcotic analgesics
flecting the degree of pathology. Chronic pain is on-
should not be used by patients who are taking or have
going for weeks, months, or years; the original
recently used monoamine oxidase inhibitors (MAOIs, or
source of pain, if ever known, is often no longer ap-
MAO inhibitors) (Pies, 2005). The effects of these two
parent. This is particularly true of nonmalignant
classes of medications might prove fatal to the patient
pain. (Katz, 2000, pp. 1–2)
who has used a MAO inhibitor within the past 14 days
(Peterson, 1997). Patients who are taking narcotic anal-
Acute pain serves a warning function, forcing the in-
gesics should not use any other chemical classified as a
dividual to rest until recovery from an injury can take
CNS depressant, including over-the-counter antihista-
place. Morphine is usually prescribed for the control of
mines or alcohol, except under a physician’s supervi-
severe, acute forms of pain, although it can help control
sion. Since narcotic analgesics are CNS depressants,
severe levels of chronic pain as well (Knapp, Ciraulo, &
the combination of any of these medications with other
Jaffe, 2005).
CNS depressants carries with it a danger of excessive se-
Many factors affect the degree of analgesia achieved
dation or even death (Ciraulo, Shader, Greenblatt, &
through the use of morphine including (a) the route by
Creelman, 1995).
which the medication was administered, (b) the interval
There is evidence that the use of a selective sero-
between doses, (c) the dosage level being used, and (d) the
tonin reuptake inhibitor such as fluvoxamine might re-
half-life of the specific medication being used (Fishman &
sult in significantly increased blood levels of methadone,
Carr, 1992). Other factors that influence the individual’s
possibly to the point that the individual’s methadone
experience of pain include (a) the person’s anxiety level,
blood level reaches toxic levels (Drummer & Odell,
(b) his or her expectations for the narcotic, (c) the length
2001). Further, 21 of 30 methadone maintenance pa-
of time that he or she has been receiving narcotic anal-
tients who started a course of antibiotic therapy with
gesics, and (d) the individual’s biochemistry. The more
Rifampin experienced opiate withdrawal symptoms
tense, frightened, and anxious a person is, the more likely
that were apparently caused by an unknown interaction
he or she is to experience pain in response to a given
11The reader is advised always to consult a physician or pharmacist stimulus. Between 80% and 95% of patients who receive
before taking two different medications. a dose of morphine experience a reduction in their level
of fear, anxiety, and/or tension (Brown & Stoudemire, Gastrointestinal side effects. When used at therapeu-
1998), and they report that their pain becomes less in- tic dosage levels, narcotic analgesics can cause nausea
tense or less discomforting, or perhaps disappears entirely and vomiting, especially within the first 48 hours of the
(Jaffe et al., 1997; Knapp et al., 2005). initial dose of medication or after a major dose increase
(Barnett, 2001; Dilts & Dilts, 2005). At normal dosage
levels, 10%–40% of ambulatory patients will experi-
Complications Caused ence some degree of nausea, and approximately 15%
by Narcotic Analgesics When Used will actually vomit as a result of having received a narcotic
in Medical Practice analgesic (McNicol et al., 2003; Swegle, & Logemann,
2006). Ambulatory patients seem most likely to expe-
Constriction of the pupils. When used at therapeutic
rience nausea or vomiting, and patients should rest
dosage levels, the opiates will cause some degree of
for a period of time after receiving their medication to
constriction of the pupils (miosis). Some patients will
minimize this side effect. Opiate-induced nausea is a
experience this even in total darkness (Wilson et al.,
dose-related side effect; some individuals are quite sen-
2007). Although this is a diagnostic sign that physicians
sitive to the opiates and experience drug-induced nau-
often use to identify the opioid abuser (discussed later
sea and vomiting even at low dosage levels. This may
in this chapter), it is not automatically a sign that the
reflect the individual’s genetic predisposition toward
patient is abusing his or her medication. Rather, this is
sensitivity to opiate-induced side effects (Melzack,
a side effect of opioids that the physician expects in the
1990). There is experimental evidence that ultra-low
patient who is using a narcotic analgesic for legitimate
doses of the narcotic blocker naloxone might provide
medical reasons, and which is unexpected in the
some relief from morphine-induced nausea in postsur-
patient who is not prescribed such a medication.
gical patients without blocking the desired analgesic
Respiratory depression. Another side effect seen at
effect of the morphine (Cepeda, Alvarez, Morales, &
therapeutic dosage levels is some degree of respiratory
Carr, 2004).
depression. The degree of respiratory depression is not
At therapeutic dosage levels, morphine and similar
significant when narcotics are given to a patient in
drugs have been found to affect the gastrointestinal
pain. But even following a single therapeutic dose of
tract in a number of ways. All of the narcotic analgesics
morphine (or a similar agent), respiration might be af-
decrease the secretion of hydrochloric acid in the stom-
fected for up to 24 hours (Brown & Stoudemire, 1998).
ach and slow the muscle contractions of peristalsis
There is an ongoing debate in the field of medicine
(which push food along the intestines) (Dilts & Dilts,
as to whether narcotic analgesics can be safely used in
2005; Gutstein & Akil, 2006). In extreme cases, nar-
cases where the patient has a respiratory disorder. Sev-
cotic analgesics may actually cause spasm in the
eral research studies have examined this issue and
muscles involved in peristalsis and possibly even consti-
found that if the attending physician were to increase
pation (Jaffe & Jaffe, 2004; Swegle, & Logemann,
the patient’s dose in a timely and appropriate manner,
2006). This is the side effect makes morphine ex-
there was little danger for the patient whose respiratory
tremely useful in the treatment of dysentery and severe
system had been compromised (Barnett, 2001; Estfan
diarrhea. But when the narcotic analgesics are used for
et al., 2007; Peterson, 1997). George and Regnard
the control of pain, this side effect might prove bother-
(2007) went even further, stating that it was the physi-
some if not unhealthy. Further, there is little evidence
cian who was prescribing the narcotic analgesics who
that tolerance to this side effect develops over time
was more dangerous than the medications being used.
(Swegle & Logemann, 2006). This problem can usually
They observed that because of the therapeutic myth
can be corrected by over-the-counter laxatives (Barnett,
that opioids adversely affect respiration, most cancer-
2001; Herrera, 1997).
related pain was under-medicated, leaving the patient
Blood pressure effects. Narcotic analgesics are used
in needless pain. Still, in spite of such studies, many
with extreme caution in patients who have experienced
physicians feel uncomfortable prescribing opioids for a
a head injury. Edema12 is common, and if the narcotic
patient with a respiratory disorder (McNicol et al.,
analgesic should reduce respiration, the body will
2003). Even so, the evidence suggests that these med-
pump even more blood to the brain in an attempt to
ications might be used in respiratory problems such as
compensate for increased carbon dioxide levels in the
asthma, emphysema, chronic bronchitis, and pulmonary/
heart disorders if the benefits outweigh the risks (McNicol
et al., 2003). 12See Glossary.
blood. This will compound the problem of cerebral tion to the analgesic effects of opioids over time is a nor-
edema, if it is present. mal phenomenon and should not automatically be in-
Other side effects. Narcotic analgesics stimulate the terpreted as a sign that the patient is becoming addicted
smooth muscles surrounding the bladder while simulta- to these medications (Knapp et al., 2005).
neously reducing the voiding reflex. These factors result Routes of administration for narcotic analgesics in
in a tendency for the patient to experience some degree of medical practice. Although the narcotic analgesics are
urinary retention (Dilts & Dilts, 2005). Between 20% and well absorbed from the gastrointestinal tract, the first-
60% of patients who are started on a narcotic analgesic or pass metabolism effect severely limits the amount of
whose dosage level is significantly increased will experi- the drug that is able to reach the brain. For example,
ence some degree of sedation (Swegle & Logemann, the liver biotransforms 70%–80% of the morphine that
2006). Further, there are reports of transient changes in is absorbed through the gastrointestinal tract before it
cognition following the initial administration of a nar- reaches the brain (Drummer & Odell, 2001). Thus,
cotic analgesic, which may compound cognitive orally administered narcotics are of limited value in the
changes seen in infection, dehydration, metabolic dyscontrol of severe pain. A standard conversion formula
functions, or late-stage cancer (Swegle & Logemann, suggests that 60 mg of orally administered morphine
2006). Between 4% and 35% of patients on a narcotic provides the same level of analgesia as 10 mg of in-
analgesic such as morphine will experience some drug- jected morphine (Cherny & Foley 1996).
induced irritability, and 4% to 25% will experience The intravenous administration of narcotics actually
some degree of depression as a side effect. An unknown allows for the greatest degree of control over the amount
percentage will experience morphine-induced night- of drug that actually reaches the brain. For this reason
mares. In extremely high doses, narcotic analgesics have the primary method of administration for narcotic anal-
been known to induce seizures, although this side effect gesics is intramuscular or intravenous injection (Jaffe &
is most commonly seen when narcotic analgesics are Martin, 1990). However, there are exceptions. For
abused (Gutstein & Akil, 2006). example, there is a new transdermal patch, developed
One rarely discussed but very real danger with nar- for the narcotic fentanyl. This is discussed in more
cotic analgesics is that they might contribute to dizzi- detail in the section on fentanyl.
ness, loss of balance, and falls and in this manner cause Withdrawal from narcotic analgesics when used in
bone fractures in the person receiving these medica- medical practice. Most patients who receive narcotic
tions (Vestergaard, Rejnmark, & Mosekilde, 2006). analgesics for the control of pain, even when they do so
Since advancing age is an independent risk factor for for extended periods of time, are able to discontinue the
falls and bone fractures, the risk of narcotic-induced medication without problems. A small number of pa-
falls with subsequent bone fractures is naturally higher tients will develop a “discontinuance syndrome.” This
in older patients. However, even young adults are at risk condition can be seen in patients who use as little as
for this possible complication of narcotic analgesic use. 15 mg of morphine (or the equivalent amount of other
On rare occasions, opioids can induce memory loss narcotic analgesics) three times a day for 3 days (Ropper
and/or an acute confusional state in the patient, condi- & Brown, 2005). The effects of the opioid discontinu-
tions that will reverse on abstinence (Filley, 2004). ance syndrome is usually mild but may require that the
The danger of addiction. Many health care workers patient gradually taper the total daily dosage level of the
admit to being afraid they will cause the patient to be- offending medication rather than just discontinue it.
come addicted to narcotic analgesics by giving the
patient too much medication.13 In reality, the odds are
probably only 1 in 14,000 cases that a patient with no Fentanyl
prior history of alcohol or drug addiction will become
Fentanyl is a synthetic narcotic analgesic introduced in
addicted to narcotic analgesics when these medications
the United States in 1968. Because of its short duration
are used for the short-term control of severe pain
of action, fentanyl has become an especially popular
(Roberts & Bush, 1996). Most patients who develop a
analgesic during and immediately after surgery (Wilson
psychological dependence on opiates after receiving
et al., 2007). It is well absorbed from muscle tissue, and
them for the control of pain seem to have a preexisting
a common method of administration is intramuscular
addictive disorder (Paris, 1996). Further, neuroadapta-
(IM) injection. Unlike morphine, it does not stimulate
13
This would technically be an iatrogenic addiction, as opposed to the the release of histamine, which is an important consid-
usual form of addiction to narcotics discussed later in this chapter. eration in some cases (Gutstein & Akil, 2006).
Fentanyl is well absorbed through the skin, allowing it The effects of fentanyl on the individual’s respira-
to be administered by a transdermal patch that allows the tion might last longer than the analgesia produced by
body to absorb small amounts of the drug through the the drug (Wilson et al., 2007). This is a characteristic
skin over extended periods of time. Unfortunately, thera- that must be kept in mind when the patient requires
peutic levels of fentanyl are not achieved for up to 12 long-term analgesia. But the analgesic effects of fen-
hours when a transdermal patch is used, making short- tanyl are often seen in just minutes after injection, a de-
term pain control via this method difficult or even impos- cided advantage for the physician who seeks to control
sible (Tyler, 1994). the pain of surgery or immediately after surgery.
In the 1990s, a new dosage form was introduced— Side effects of fentanyl. About 10% of patients who
fentanyl-laced candy, which is used as a premedication receive a dose of fentanyl experience somnolence
for children about to undergo surgery (“Take Time to and/or confusion, while 3%–10% experience dizziness,
Smell the Fentanyl,” 1994). It is interesting to note that drug-induced anxiety, hallucinations, and/or feelings of
opium was once used in Rome to calm infants who depression (Brown & Stoudemire, 1998). Approxi-
were crying (Ray & Ksir, 1993). After thousands of years mately 1% of the patients who receive a dose of fentanyl
of medical progress, we have returned to the starting experience agitation and/or a drug-induced state of am-
point of using opiates to calm the fears of children—in nesia, and about 1% experience a drug-induced state of
this case, those about to undergo surgery. paranoia. Other side effects include blurred vision, a
Pharmacology and subjective effects of fentanyl. Fen- sense of euphoria, nausea, vomiting, dizziness, delir-
tanyl is extremely potent, but there is some controversy ium, lowered blood pressure, constipation, possible res-
over exactly how potent it is. Some researchers have es- piratory difficulty, and in extreme cases, respiratory
timated that fentanyl is 10 (Greydanus & Patel, 2005) and/or cardiac arrest (Wilson et al., 2007). At high
to 50–100 times as potent as morphine (Gutstein & dosage levels, muscle rigidity is possible (Foley, 1993).
Akil, 2006; Zevin & Benowitz, 2007). Ashton (1992) When fentanyl is administered, the patient’s blood
suggested that fentanyl was 1,000 times as potent as pressure might drop by as much as 20% and heart rate
morphine, while Kirsch (1986) concluded that it is “ap- might drop by as much as 25% (Beebe & Walley, 1991).
proximately 3,000 times stronger than morphine (and) Thus, the physician must balance the potential benefits
1,000 times stronger than heroin” (p. 18). While there to be gained by against fentanyl’s potential to cause ad-
is some controversy about how potent this medication verse effects. Unfortunately, although fentanyl is an ex-
is, it has been determined that the active dose of fen- tremely useful pharmaceutical, it is also a popular drug
tanyl in man is 1 microgram or 1/60,000th the weight of of abuse. This aspect of fentanyl is discussed in the next
the typical postage stamp. section.
Fentanyl is highly lipid soluble and reaches the
brain quickly after it is administered. It is also highly
Buprenorphine
lipophilic, with 80% of a single dose binding to blood
lipids (Jenkins, 2007). The biological half-life of a Buprenorphine is a synthetic analgesic introduced in
single intravenous dose of fentanyl is ranges from 1 to 6 the 1960s that is estimated to be 25–50 times as potent
hours depending on the individual’s biochemistry14 as morphine (Karch, 2002). Medical researchers quickly
(Drummer & Odell, 2001). Laurence and Bennett discovered that orally administered doses of buprenor-
(1992) offered a middle-of-the-road figure of 3 hours, phine are extremely useful in treating postoperative
which is the average therapeutic half-life of fentanyl. and cancer pain. Further, researchers have discovered
Fentanyl’s primary site of action is the mu opioid recep- that when administered orally, buprenorphine appears
tor site in the brain (Brown & Stoudemire, 1998), and to be at least as effective as methadone in blocking the
the duration of fentanyl’s analgesic effect persists only effects of illicit narcotics and opioid withdrawal.
for 30–120 minutes. The drug is rapidly biotransformed Buprenorphine has a rather unique absorption pat-
by the liver and excreted from the body in the urine tern. The drug is well absorbed from intravenous and
(Karch, 2002). intramuscular injection sites as well as when adminis-
tered sublingually (Lewis, 1995). However, these meth-
14Because of differences between individuals, different people bio- ods of drug administration offer the advantage of rapid
transform and/or eliminate drugs at different rates. Depending on the
specific compound, there might be a difference of several orders of
access to the general circulation without the danger of
magnitude between those who are “fast metabolizers” of a specific first-pass metabolism. Unfortunately, when ingested,
drug and those whose bodies make them “slow metabolizers.” buprenorphine suffers extensive first-pass metabolism,
a characteristic that makes oral doses of this compound II. OPIATES AS DRUGS OF ABUSE
difficult to use for analgesia. Thus, when physicians use
buprenorphine for analgesia, it is usually injected into Many people are surprised to learn that after mari-
the patient’s body. juana, prescription opioids are the most commonly
Upon reaching the general circulation, approxi- abused class of chemicals (Blume, 2005; International
mately 95% of buprenorphine becomes protein bound Narcotics Control Board, 2005). In this part of the
(Walter & Inturrisi, 1995). The drug is biotransformed chapter, the opiates as agents of abuse/addiction are
by the liver, with 79% of the metabolites being excreted discussed.
in the feces and only 3.9% being excreted in the urine Why do people abuse opiates? Simply put, opioids
(Walter & Inturrisi, 1995). Surprisingly, animal research are popular drugs of abuse because they make the user
suggests that the various buprenorphine metabolites feel good. The exact mechanism by which narcotics
are unable to cross the blood-brain barrier, according to can induce a sense of pleasure remains unknown
Walter and Inturrisi. This suggests that the drug’s anal- (Gutstein & Akil, 2006). But when they are adminis-
gesic effects are achieved by the buprenorphine mole- tered to individuals who are not in pain, many report a
cules that cross the barrier to reach the brain rather than sense of euphoria or well-being that is assumed to re-
any of its metabolites. flect the effect of these compounds on the brain’s re-
Once in the brain, buprenorphine binds to three of ward system (Kosten & George, 2002). Depending on
the same receptor sites in the brain utilized by mor- such factors as the specific compound being abused,
phine. Buprenorphine binds most strongly to the mu and the method by which it is abused, and the individual’s
kappa receptor sites, where other narcotic analgesics also drug use history, intravenous drug abusers report expe-
act to reduce the individual’s perception of pain. How- riencing a “rush” or “flash” similar to sexual orgasm
ever, buprenorphine does not cause the same degree of (Bushnell & Justins, 1993; Hawkes, 1992; Jaffe, 1992,
activation at the mu receptor site that morphine causes. 2000; Jaffe & Martin, 1990) but different from the rush
For reasons that are still not clear, buprenorphine is able reported by CNS stimulant abusers (Brust, 1998). Fol-
to cause clinically significant levels of analgesia with a lowing the rush, the user will experience a sense of eu-
lower level of activation of the mu receptor site than mor- phoria that usually lasts for 1–2 minutes (Jaffe, 2000).
phine requires (Negus & Woods, 1995). Finally, the user often experiences a prolonged period of
Buprenorphine also tends to form weak bonds with blissful drowsiness that may last several hours (Scarlos,
the sigma receptor site, without activating the rece- Westra, & Barone, 1990).
ptor (Lewis, 1995; Negus & Woods, 1995). Buprenor- Narcotic analgesics seem to mimic the action of nat-
pine has been found to function as a kappa receptor urally occurring, opiate-like neurotransmitters, especially
site antagonist at the same dosage level necessary to in the nucleus accumbens and the ventral tegmentum
provide significant activation of the mu receptor sites in regions of the brain. These areas seem to be associated
the brain, thus bringing about analgesia (Negus & with the pleasurable response that many users report
Woods, 1995). Finally, buprenorphine molecules only when they use opioids (Kosten & George, 2002). When
slowly “disconnect” from their receptor sites, thus block- abused, opioids trigger the release of massive amounts
ing other buprenorphine molecules from reaching of dopamine in the nucleus accumbens, which is experi-
those same receptor sites. Thus, at high dosage levels, enced by the person as pleasure.
buprenorphine seems to act as its own antagonist,
limiting its own effects.
The Mystique of Heroin
Buprenorphine causes significant degrees of seda-
tion for 40%–70% of the patients who receive a dose of There is widespread abuse of synthetic and semisyn-
this medication. Between 5% and 40% will experience thetic narcotic analgesics such as Vicodin and Oxy-
dizziness, and in rare instances (less than 1%) patients Contin in the United States, with more than 1.5
have reported drug-induced feelings of anxiety, eupho- million people abusing these drugs for the first time
ria, hallucinations, or feelings of depression (Brown & each year (Kalb et al., 2001). But it is heroin that people
Stoudemire, 1998). As is obvious from this brief review think of when the topic of opioid abuse/addiction is
of buprenorphine’s pharmacology, it is a unique nar- raised, an image sustained by the fact that heroin
cotic analgesic that is more selective and more power- abuse accounts for 71% of the opiate abuse problem
ful than morphine. However, it is slowly becoming around the world (United Nations, 2007). Globally,
more popular as a drug of abuse. 9 million people are thought to be addicted to heroin
(diacetylmorphine) (United Nations, 2007), and approx- heroin molecule does not bind to known opiate receptor
imately 1 million people in the United States are heroin sites in the brain, and researchers have suggested that it
addicts (Kranzler, Amin, Modesto-Lowe, & Oncken, might more accurately be described as a prodrug15 than
1999; O’Brien, 2001). Olmedo and Hoffman (2000) sug- as a biologically active compound in its own right
gested an even higher number of 1.5 million “chronic” (Jenkins & Cone, 1998). In the body, heroin is biotrans-
heroin users in the United States but did not identify formed into morphine, a process that gives heroin its
what percentage of these people were addicted. Each analgesic potential (Drummer & Odell, 2001; Karch,
year, heroin-related deaths account for about half of all 2002; Thompson, 2004). But because of differences in
illicit drug-use deaths in the country (Epstein & Gfroerer, its chemical structure, heroin is much more lipid solu-
1997; Karch, 1996). ble than morphine. The difference in chemical struc-
A short history of heroin. Like aspirin, heroin was first ture allows heroin to cross the blood-brain barrier 100
developed by chemists at the Bayer pharmaceutical com- times faster than morphine (Angier, 1990), a character-
pany of Germany and was first introduced in 1898. Also, istic that makes it especially attractive as a drug of abuse.
like its chemical cousin morphine, heroin is obtained Subjective effects of heroin when abused. Two factors
from raw opium. One ton of raw opium will, after pro- that influence the subjective effects of heroin are (a)
cessing, produce approximately 100 kilograms of heroin the individual’s expectations for the drug and (b) the
(“South American Drug Production Increases,” 1997). method of heroin abuse. When it is used intranasally,
The chemists who developed diacetylmorphine first only about 25% of the available heroin is absorbed by
tried it on themselves and they found that the drug made the user’s body, and the rate of absorption is slower than
them feel “heroic.” Thus, the drug was given the brand if the drug is directly injected into the circulation. In
name of “Heroin” (Mann & Plummer, 1991, p. 26). contrast to the slower rate of absorption and the limited
During the Civil War in the United States, large amount of drug that reaches the brain, virtually 100%
numbers of men became addicted to morphine as a re- of intravenously administered heroin reaches the circu-
sult of its widespread use to treat battlefield wounds or lation. This seems to explain why intranasal users re-
illness. Because heroin was found to suppress the with- port a sense of gentle euphoria while intravenous
drawal symptoms of morphine addicts at low doses, abusers report that the drug causes rush or a flash that is
physicians of the era thought it was nonaddicting, and it very similar to a sexual orgasm lasting about 1 minute.
was initially sold as a cure for morphine addiction Other sensations include a feeling of warmth under the
(Walton, 2002). Physicians were also impressed by the skin, dry mouth, nausea, and a feeling of heaviness in
ability of morphine, and its chemical cousin heroin, to the extremities. Users also report a sense of nasal con-
suppress the severe coughs seen in tuberculosis or pneu- gestion and itchy skin, both the result of heroin’s ability
monia, both leading causes of death in the 19th century, to stimulate the release of histamine. After the flash,
and thus to comfort the patient. It was not until 12 years heroin abusers report experiencing a sense of floating,
after it was introduced, long after many morphine ad- or light sleep, that will last for about 2 hours, accompa-
dicts had become addicted to heroin, that its true addic- nied by clouded mental function.
tion potential was finally recognized. However, by that In contrast to alcohol, narcotic analgesics do not in-
time heroin abuse/addiction had become a fixture in the duce slurred speech, ataxia, or emotional lability when
United States. During the 1920s, the term junkie was abused in high doses (Gutstein & Akil, 2006).
coined for the heroin addict who supported his or her Heroin in the United States today. In many countries
drug use by collecting scrap metal from industrial diacetylmorphine is a recognized therapeutic agent
dumps, for resale to junk collectors (Scott, 1998). used to treat severe levels of pain. But heroin is not a
Pharmacology of heroin. Chemically, the heroin mol- recognized pharmaceutical in the United States, and
ecule is best visualized as a pair of morphine molecules its possession or manufacture is illegal. Even so, heroin
that have been joined chemically. The result is an anal- use has been viewed by many as a sign of rebellion, per-
gesic that is more potent than morphine, and a standard haps reaching its pinnacle with the rise of the “heroin
conversion formula is that 4 milligrams (mg) of heroin is chic” culture in the late 1990s (Jonnes, 2002). It is esti-
as powerful as 10 mg of morphine (Brent, 1995). The mated that heroin abusers in the United States con-
half-life of intravenous heroin is between 2 minutes sume between 13 and 18 metric tons of heroin each
(Drummer & Odell, 2001) and 3 minutes (Kreek, year (Office of National Drug Control Policy, 2004).
1997), although Karch (2002) gave a higher estimate of
36 minutes. Surprisingly, research has shown that the 15
See Glossary.
The average age of the individual’s first use of heroin and inject the material into a vein. Other abusers will
dropped from 27 in 1988 to 19 by the middle of the simply ingest a larger than prescribed dose for the eu-
1990s (Cohen et al., 1996; Hopfer, Mikulich, & Crowley, phoric effect. In part because of a number of media re-
2000). Adolescents (12–17 years of age) make up just ports, OxyContin quickly gained a reputation as a
under 22% of those who admit to the use of heroin in “killer” drug. However, clinical research has suggested
the United States (Hopfer et al., 2000). One major rea- that the vast majority of those who died from drug over-
son for this increase in popularity among younger drug doses had ingested multiple agents such as benzodi-
abusers in the late 1990s was the availability of increas- azepines, alcohol, cocaine, or other narcotic analgesics
ingly high potency heroin for relatively low prices. In along with OxyContin (Cone et al., 2003). The authors
the mid-1980s, the average sample of heroin from the found that only about 3% of the drug-induced deaths
street was 5%–6% pure (Sabbag, 1994). By the start of reported oxycodone alone as the cause of death.
the 21st century heroin that was produced in South Still, OxyContin was heavily marketed by the phar-
America and sold in the United States averaged 46% maceutical company that produced it, which also
pure, while heroin produced in Mexico averaged 27% downplayed its abuse potential (Meier, 2003). But
pure (Office of National Drug Control Policy, 2004).
Heroin produced in Asia usually averaged about 29% while prescription-drug abusers may differ in their
pure when sold on the streets in the United States (Of- pharmaceutical choices, the dynamic of abuse shares
fice of National Drug Control Policy, 2004). a common theme: whatever a manufacturer’s claims
In spite, or possibly because of, the best efforts of the about a drug’s “abuse liability,” both hardcore
federal government’s “war on drugs,” there is a glut of addicts and recreational users will quickly find ways
heroin available to illicit users in the United States. Al- to make a drug their own. (Meier, 2003, p. 89, quotes
though the entire world’s need for pharmaceutical di- in original)
acetylmorphine16 could be met by cultivation of 50
square miles of opium poppies, it is estimated that over It is estimated that OxyContin is involved in approxi-
1,000 square miles of poppies are under cultivation at mately half of the estimated 4 million episodes of non-
this time (Walton, 2002). The high purity of the heroin prescribed narcotic analgesic abuse that occurs each
being sold, combined with its relatively low cost and year in the United States (Office of National Drug
the misperception that insufflated (“snorted”) heroin Control Policy, 2004). Indeed, there is evidence that
was nonaddicting, all contributed to an increase in this medication may have unique dosing characteristics
heroin use in the United States in the early 1990s that make it especially attractive to drug abusers, which
(Ehrman, 1995). clouds the issue of whether it is a valuable tool in the
fight against pain.
Buprenorphine. Buprenorphine is another drug that
Other Narcotic Analgesics is growing in popularity as an opiate of abuse. This
That Might Be Abused compound is an effective narcotic analgesic and in sub-
Codeine. Surprisingly, codeine has emerged to become lingal form is also used as an alternative to methadone
a popular opiate of abuse, involved in 12% of all drug- as an opioid agonist. Unfortunately, street addicts have
related deaths (Karch, 2002). There is little information discovered that intravenously administered buprenor-
available on codeine abuse, although it is possible that phine has a significant abuse potential, although this is
some of the codeine-related deaths are the result of not common in the United States at this time (Horgan,
heroin addicts miscalculating the amount of codeine 1989; Ling, Wesson, & Smith, 2005; Moore, 1995).
they will need to block their withdrawal discomfort When this drug is abused, the user will inject either
when they are unable to obtain their primary drug of buprenorphine alone or a mixture of buprenorphine
choice. and diazepam, cyclizine, or temazepam.
OxyContin. OxyContin has emerged as a drug of Fentanyl. With fentanyl, abusers have been known
abuse since its introduction in 1995. A generic form of to inject it, smoke it, and use it intranasally; also, trans-
this substance is to be released in 2004. Abusers will dermal skin patches may be heated and the fumes in-
often crush the time-release spheres within the capsule haled (Karch, 2002). Some abusers also drain the
transdermal patches by poking holes in the patch mate-
16Which is to say the medicinal use of heroin in countries where it is rial and consuming the reservoir. The drug that is ob-
an accepted, pharmaceutical agent. tained in this manner is either used orally or injected,
or possibly smoked. Because standard urine toxicology One method by which heroin might be smoked is
screens do not detect fentanyl, it is not clear how wide- known as “chasing the dragon” (Karch, 2002). In this
spread the abuse of this pharmaceutical actually is at process, the user heats heroin powder in a piece of
this time. However, anecdotal information suggests that aluminum foil, using a cigarette lighter or match as
it is a significant part of the opioid use disorders. the heat source. The resulting fumes are then inhaled,
allowing the individual to get “high” without exposure
to contaminated needles (Karch, 2002). Another prac-
Methods of Opiate Abuse tice is to smoke a combination of heroin and crack
When opiates are abused, they might be injected under cocaine pellets. This combination of chemicals re-
the skin (a subcutaneous injection, or “skin popping”), portedly results in a longer high and a less severe post-
injected directly into a vein (“mainlining”), smoked, or cocaine use depression (Levy & Rutter, 1992). However,
used intranasally (technically, insufflation). As the po- there is evidence that cocaine might exacerbate the res-
tency of heroin sold on the streets has increased, skin piratory depression produced by opiates when they are
popping has become less and less popular while insuf- abused.
flation and smoking it have increased in popularity The most common method of heroin abuse is the
(Karch, 2002). Prescription opioids are usually taken intravenous injection. In this process, the abuser/addict
orally, although some are crushed and then injected.
Historically, the practice of smoking opium has not mixes heroin in the spoon with water, or glucose
been common in the United States since the start of the and water, in order to dissolve it. Lemon juice, citric
20th century. Supplies of opium are quite limited in acid or vitamin C may be added to aid dissolving.
the United States, and opium smoking wastes a great This cocktail is heated until it boils, drawn into the
deal of the chemical. However, in parts of the world syringe through a piece of cotton wool or cigarette
where supplies of opium are more plentiful, the prac- filter to remove solid impurities, and injected whilst
tice of smoking opium remains quite common. still warm. (Booth, 1996, p 14)
Snorting heroin powder and smoking heroin have
become commonplace in the United States, fueled by Where do opioid addicts obtain their drugs? Opiate
a popular myth that you cannot become addicted unless abusers obtain their daily supply of the drug from many
you inject heroin into your body (Drummer & Odell, sources. The usual practice for the street addict is for
2001; Greydanus & Patel, 2005; Gwinnell & Adamec, the individual to buy street opiates unless he or she has
2006; Smith, 2001). In reality, at least one-third of those access to a “pharmaceutical.”17 Pharmaceuticals are ob-
who smoke heroin will go on to become addicted to it tained by either “making” a doctor18 or by diversion of
(Greydanus & Patel, 2005). Heroin is snorted much medication from a patient with a legitimate need for it
the same way that cocaine powder is inhaled. The user to illicit abusers. For example, some opioid addicts have
will dice the powder with a razor blade or knife until it been known to befriend a person with a terminal ill-
is a fine, talcum-like consistency. The powder then is ness, such as cancer, in order to steal narcotic anal-
arranged in a small pile, or a line, and inhaled through a gesics from the suffering patient for their own use. This
straw. The effects are felt in 10–15 minutes and include is how most users obtain their supplies of pharmaceuti-
a sense of gentle relaxation or euphoria, plus a flushing cals such Vicodin and OxyContin.
of the skin. Unwanted effects include severe itching, Heroin is smuggled into the United States from
nausea, and vomiting (Gwinnell & Adamec, 2006). other parts of the world. The bulk heroin has already
In the 1990s, the availability of high potency heroin been mixed with adulterants to increase its bulk and
allowed the practice of smoking heroin to become pop- thus the profits for the supplier. At each level of the dis-
ular in the United States. Heroin is well absorbed tribution network, the heroin is mixed with other adul-
through the lungs when it is smoked. The user begins terants, increasing the bulk (and reducing the potency)
to experience the effects of smoked heroin in 10–15 still further, to increase the profits for the supplier at
minutes, while the effects of injected heroin are felt in that level of the distribution network. Eventually, it
about 8 seconds (Grinnell & Adamec, 2006). Because reaches the local supplier, where it is distributed for
up to 80% of smoked heroin is destroyed in the heat sale on the local level. The opiates are usually sold in a
produced by smoking it, the blood levels achieved by
smoking heroin are only 50% that of injected heroin at 17See Glossary.
best (Drummer & Odell, 2001). 18See Glossary.
powder form in small individual packets. The powder is eign compounds can cause extensive scarring at injec-
mixed with water, then heated in a small container tion site. These scars form the famous “tracks” caused by
(usually a spoon) over a flame from a cigarette lighter or repeated injections of illicit opiates.20
candle, and then injected by the user. The development of tolerance. Over time, opiate
If the users are health care professionals, with ac- abusers develop significant tolerance to the analgesic,
cess to pharmaceutical supplies, they might divert respiratory, and sedating effects of opiates while they
medications to themselves. Because of the strict con- develop a lower degree of tolerance to the miotic and
trols over narcotic analgesics, this is quite difficult for constipating effects of this class of drugs (Jaffe &
health care professionals. The health care provider Jaffe, 2004; Jaffe & Strain, 2005; Zevin & Benowitz,
will then either ingest or inject the pharmaceutical. 1998). For this reason the chronic abuse of narcotics
Since health care professionals have access to forms of can (and often does) cause significant constipation
narcotic analgesics prepared for injection, they do not problems for the illicit user (Karch, 2002; Reisine &
need to crush the tablet or capsule intended for oral Pasternak, 1995). Opiate abusers also never develop tol-
use until it is a fine powder, as illicit drug users must erance to the pupillary constriction induced by this
do, to inject the contents. The method of injection class of medications (Nestler, Human, & Malenka,
utilized by intravenous opiate abusers will differ from 2001).
the manner in which a physician or nurse will inject Intravenous opiate abusers develop some degree of
medication into a vein. The process has changed little tolerance to the euphoric effects of narcotics and do not
in the past 60 years, and Lingeman’s (1974) descrip- experience the intense rush from opiates that they did
tion of the technique called “booting” remains as when they first started to use these drugs (Jaffe & Strain,
valid today as when it was first set to paper a quarter of 2005). They will, however, experience a sense of gentle
a century ago. As the individual “boots” the drug, he euphoria; while not as reinforcing as the rush, it is still
or she injects it an incentive for further opiate abuse (Jaffe & Strain,
2005). In an attempt to reacquire the rush experience,
a little at a time, letting it back up into the eye drop- narcotics addicts will often increase the dosage of the
per, injecting a little more, letting the blood-heroin drugs being abused, possibly to phenomenonal levels.
mixture back up, and so on. The addict believes that For example, heroin addicts have been known to in-
this technique prolongs the initial pleasurable sen- crease their daily dosage level 100-fold over extended
sation of the heroin as it first takes effect—a feeling periods of time in their attempt to overcome their de-
of warmth in the abdomen, euphoria, and some- veloping tolerance to the euphoric effects of the drug
times a sensation similar to an orgasm. (p. 32) (O’Brien, 2006). Eventually, the individual might
reach the point that he or she is no longer using opioids
Through this process, the hypodermic needle and the for the pleasure that the drugs induce but simply to
syringe will be contaminated with the individual’s “maintain” their intoxicated state and avoid opioid
blood. If other intravenous drug abusers share the same withdrawal.
needle, a common practice among illicit drug abusers,
contaminated blood from one individual is passed to
the next, and the next, and the next. Scope of the Problem of Opiate
Some illicit narcotic abusers will attempt to inject a Abuse and Addiction
narcotic analgesic intended for oral use. Such tablets or
capsules contain “fillers”19 intended to give them bulk Addiction. Physical dependence on narcotics can de-
so they are more easily handled by the patient. Injecting velop in a very short time, possibly as short as a few days
the crushed tablet or the contents of a capsule intended of continuous use (Ivanov et al., 2006).
for oral use inserts starch or other substances not in- Opiate abuse around the world. It is estimated that
tended for intravenous use directly into the bloodstream there are 16 million opioid abusers around the world, of
(Wetli, 1987). These fillers, or the adulterants mixed whom 1.6 million live in North America (both Canada
with illicit heroin, damage the blood vessel and might and the United States) (United Nations, 2007). Glob-
either form an embolus or cause blood clot formation at ally, an estimated 5,000 metric tons of illicit opium
the site of injection. The repeated exposure to such for-
20
Which the IV heroin abuser might attempt to hide through the use
19
See Glossary. of strategically placed tattoos (Greydanus & Patel, 2005).
were produced in 2005, of which approximately 4,260 a narcotic analgesic. Finally, patients with actual disor-
metric tons were channeled into the illicit drug market ders have been known to exaggerate their distress in the
(United Nations, 2007). hope of being able to obtain a prescription for a nar-
The abuse of prescribed narcotic analgesics. Surpris- cotic analgesic from an overworked physician. Thus,
ingly, although heroin is the stereotypical opiate of one of the warning signs a physician will look for in a
abuse in the United States, addiction to prescribed opi- medication-seeking patient is multiple consultations
oids appears to be more frequent than heroin addiction for the same problem.
(Hasemyer, 2006). The abuse of prescription narcotic Heroin abuse/addiction. The reputation of heroin is
analgesics is now the second most common form of il- that it is the most potent and most commonly abused
licit drug abuse in the United States, with an estimated narcotic analgesic. It is “often billed as being irrestibly
2.4 million people over the age of 12 starting to abuse seductive and addictive” (Szalavitz, 2005, p. 19). How-
prescription narcotics in the preceeding 12 months, ever, much of its reputation is exaggerated or wildly in-
compared with only 2.1 million new marijuana abusers accurate. Clinical research suggests that as an analgesic
and 1 million new cocaine abusers (National Survey on it is no more potent than hydromorphone, and only a
Drug Use and Health, 2006). fraction of those who briefly abuse opiates, perhaps one
Not all of those people who abuse prescribed nar- in four people, will become addicted (O’Brien, 2006;
cotics go on to become addicted to them. Rather, as is Sommer, 2005).21 But one should keep in mind that
true for the other recreational drugs, the phenomenon heroin, like the other narcotic analgesics, is potentially
of prescription narcotic abuse is a fluid, dynamic addictive (O’Brien, 2006).
process, with many individuals abusing a prescription It has been estimated that there are about 1 million
medication out of curiosity, then either avoiding that heroin-dependent persons in the United States
class of medications or using them only intermittently. (Hasemyer, 2006; Tinsley, 2005). Addiction to heroin
At the same time, an unknown number of current does not develop instantly; the period between the initi-
abusers discontinue the abuse of these medications ation of heroin abuse and the development of physical
every year and thus could be classified as “previous dependence is approximately 2 years (Hoegerman &
users” or “recovering abusers/addicts.” But the scope of Schnoll, 1991). Further, there is a wide variation in in-
narcotic prescription abuse is frightening. dividual opiate abuse patterns. This is clearly seen in a
Nationally, an estimated 31.8 million people over subpopulation of opioid abusers who engage in occa-
the age of 12 have abused a prescribed narcotic anal- sional abuse of heroin or narcotic analgesics without
gesic opioid medication at some point in their lives becoming addicted (Shiffman, Fischer, Zettler-Segal, &
(National Survey on Drug Use and Health, 2006). Pre- Benowitz, 1990). These people are called “chippers.”
scription drug abuse might take many different forms. Chippers seem to use opiates in response to social stim-
For example, a man who had received a prescription for uli (the “set”) or because of transient states of internal
a narcotic analgesic after breaking a bone might share a distress, but they apparently have no trouble abstaining
leftover pill or two with a family member who had the from opiates when they wish to do so. But because re-
misfortune to sprain an ankle and be in severe pain. search in this area is prohibited, scientists know virtu-
With the best of intent, this person has provided an- ally nothing about heroin chipping or what percentage
other with medications that are, technically, being of those who start out as chippers progress to a more ad-
abused, in the sense that the second person did not re- dictive pattern of heroin use.
ceive a prescription for the narcotic analgesic that he or Researchers generally agree that as with alcohol ad-
she ingested. diction, males tend to outnumber females who are ad-
It is important to remember that most people who dicted to heroin by a ratio of about 3 to 1. Thus, of the
abuse narcotic analgesics on a regular basis try to avoid estimated 900,000 heroin addicts in the United States,
being identified as a medication abuser, a drug addict, perhaps 675,000 are males, and 225,000 are female. If
or someone engaging in “drug seeking.” It is not un- the higher estimate of 1 million active heroin addicts is
common for some patients to visit different physicians used, then some 250,000 women are addicted to heroin
or different hospital emergency rooms to obtain mul- in the United States.
tiple prescriptions for the same disorder. Patients have
also been known to manufacture symptoms (after doing 21However, because it is not possible to predict in advance who will
a bit of research) so they can simulate the signs of a dis- become addicted and who will not, the abuse of narcotic analgesics is
order virtually guaranteed to result in a prescription for not recommended.
Complications Caused cause of incarceration, might have no personal invest-

by Chronic Opiate Abuse ment in the success of the withdrawal program and thus
respond to every withdrawal symptom as if it were
Narcotics withdrawal syndrome. The narcotics with- major trauma. In contrast, highly motivated clients
drawal syndrome is often portrayed as a dramatic, possi- might cope with many or all of the withdrawal symp-
bly life-threatening condition. In reality, withdrawal toms through the use of hypnotic suggestion (Erlich,
distress has been compared to the distress of a severe 2001). In extreme cases, however, the individual’s fear
case of influenza (Kosten & O’ Connor, 2003). The of the withdrawal proceess might almost reach phobic
opioid withdrawal process might be said to involve two proportions, contributing to the urge to continue to
stages: (a) acute withdrawal symptoms and (b) extended abuse opioids (Collins & Kleber, 2004; Kenny, Chen,
withdrawal symptoms. Both the acute and the extended Kitamura, Markou, & Koob, 2006).
withdrawal symptoms are influenced by a number of A complicating factor during withdrawal from opi-
different factors, including (a) the specific compounds ates is that the withdrawal process can increase the indi-
being abused, (b) the length of time the person has vidual’s sensitivity to pain, both through increased
abused this compounds,22 (c) the speed with which with- muscle activity and the stimulation of the sympathetic
drawal is attempted (Jaffe & Jaffe, 2004), (d) the half-life nervous system that occurs during the withdrawal
of the opioid being abused (Jaffe & Jaffe, 2004; Kosten & process (Gunderson & Stimmel, 2004).24 Further, opi-
O’Connor, 2003), and (e) the individual’s cognitive ate withdrawal can induce anxiety and craving for opi-
“set.” ates, conditions that also lower the pain threshold and
Obviously, the specific compounds being abused increase the individual’s pain sensitivity.
influence the narcotics withdrawal syndrome.23 Heroin Acute withdrawal. The withdrawal phemonemon is a
withdrawal symptoms, for example, peak 36–72 hours dynamic process. Depending on the dose and the spe-
after the last dose of this compound, and the acute cific compounds being abused, the acute withdrawal
withdrawal discomfort lasts for 7–10 days. In contrast, symptoms of opioid withdrawal include a craving for
the acute phase of methadone withdrawal peaks 4–6 more narcotics, tearing of the eyes, running nose, re-
days after the last dose and continues for approxi- peated yawning, sweating, restless sleep, dilated pupils,
mately 14–21 days (Collins & Kleber, 2004; Kosten & anxiety, anorexia, irritability, insomnia, weakness, ab-
O’Connor, 2003). The acute withdrawal symptoms of dominal pain, nausea, vomiting, gastrointestinal upset,
other opioids are specific to each compound but usually chills, diarrhea, muscle spasms, muscle aches, irritabil-
follow the same pattern seen for heroin or methadone ity, increased sensitivity to pain, and in males, possible
withdrawal. ejaculation (Collins & Kleber, 2004; Gold, 1993;
The speed at which the individual is tapered from Gunderson & Stimmel, 2004; Hoegerman & Schnoll,
narcotic analgesics also influences the withdrawal syn- 1991; Kosten & O’Connor, 2003). It has been suggested
drome. The opiate-dependent person who is placed on that 600–800 mg of ibuprofen every 4–6 hours can pro-
a drug taper will have fewer and less intense withdrawal vide significant relief from the muscle pain experienced
symptoms than the individual who just suddenly in opiate withdrawal (Collins & Kleber, 2004). The etiol-
stopped using the drug (cold turkey). But his or her ogy of the pain must first be identified, however, to avoid
withdrawal discomfort might be prolonged by the taper the danger that a real medical problem might remain
program. Thus physicians try to balance the individ- untreated because it was assumed to be withdrawal-
ual’s withdrawal discomfort with the speed of the with- related pain (Gunderson & Stimmel, 2004).
drawal process. Constipation is a potential complication of narcotic
The individual’s cognitive set also influences the abuse/addiction and in rare cases can result in fecal im-
withdrawal process. This set reflects such factors as the paction and intestinal obstruction (Jaffe, 1990; Jaffe &
individual’s knowledge, attention, motivation, and de- Jaffe, 2004). During withdrawal, the individual will
gree of suggestibility. The person who is forced to go often experience bouts of diarrhea as the body returns
through opiate withdrawal by the courts, possibly be- to a normal state. On very rare occasions, withdrawal
22However,
can cause or contribute to seizures, especially if the
after 2–3 months of continuous use, there is no increase
in the severity of the opiate withdrawal distress.
23This assumes that the individual is abusing only opioids. If he or she 24A medical examination will reveal whether the withdrawal distress is
is a polydrug addict, then the withdrawal syndrome will be more caused by a concurrent medical illness that needs to be addressed
complicated. (Gundersen & Stimmel, 2004).
opiate being abused was one that could precipitate drugs. The typical opiate addict must inject drugs pur-
seizures (Collins & Kleber, 2004). Anxiety is a common chased from illicit sources of questionable purity. In ad-
withdrawal-induced emotion, which might make the dition to this, the lifestyle of the opioid addict carries
person so uncomfortable as to reinforce the tendency with it serious health risks beyond those of the drug
toward continued drug use (Bauman, 1988; Collins & being abused. Common health complications found in
Kleber, 2004). Rather than a benzodiazepine, Seroquel heroin abusers include cerebral vascular accidents
(quetiapine fumarate) has been suggested as a means to (CVA, or stroke), cerebral vasospasms, infectious endo-
control opiate-withdrawal related anxiety (Winegarden, carditis, botulinism, tetanus, peptic ulcer disease, liver
2001). failure, disorders of the body’s blood clot formation
A cautionary note. Opiate-dependent people will mechanisms, malignant hypertension, heroin-related
often emphasize their physical distress during with- nephropathy, and uremia (Brust, 1993, 1997; Karch,
drawal, especially in a medical setting, in an attempt to 2002; Greydanus & Patel, 2005).
obtain additional drugs. Such displays are often quite Heroin addicts have been known to die from pul-
dramatic but are hardly a reflection of reality. With- monary edema, but the etiology of this possible compli-
drawal from narcotics may be uncomfortable, but it is cation of heroin addiction is not clear at this time
not fatal if the patient is in good health; it is rarely if (Karch, 2002). Chronic opiate abuse can reduce the ef-
ever a medical emergency in the healthy adult (O’Brien, fectiveness of the immune system, although the exact
2001). mechanism by which this occurs is also not known
Extended withdrawal symptoms. During this phase, (Karch, 2002). Chronic opiate abusers occasionally de-
which might last for several months after the individ- velop renal disease and rhabdomyolysis25 but it is not
ual’s last dose, the individual may experience symptoms clear whether this is because of the opiate being
such as fatigue, heart palpitations, and a general feeling abused, the individual’s lifestyle, abuse of other com-
of restlessness as well as strong urges to use opioids pounds, or the adulterants found in illicit narcotics
again (Jaffe & Strain, 2005). During this stage of pro- (Karch, 2002). For reasons that are not clear, oxy-
tracted abstinence, the physical functioning of the indi- codone abusers are especially vulnerable to a drug-
vidual slowly returns to normal over a period of weeks induced autoimmune syndrome that affects the kidneys
to months. and can cause significant damage to these organs (Hill,
Dwyer, Kay, & Murphy, 2002).
One complication of intravenous heroin abuse/
Medical Complications addiction that occasionally is encountered is cotton fever
of Opiate Addiction (Brent, 1995; Karch, 2002). The heroin abuser/addict
Organ damage. Some patients in extreme pain (such as will try to “purify” the heroin by using wads of cotton or
in some forms of cancer) who receive massive doses of even the filter from a cigarette to try to filter out impuri-
narcotic analgesics for extended periods of time fail to ties in the heroin. During times of hardship, when
show evidence of opiate-induced damage to any of the heroin supplies are scarce, some users will try to use the
body’s organ systems. This is consistent with historical residual heroin found in old cotton “filters.” When they
evidence from early in the 20th century, before the inject the material that results from this process, they
strict safeguards imposed by the government were insti- will inject microscopic cotton particles as well as the
tuted. Occasionally, a case would come to light in impurities filtered out by the cotton, causing such con-
which a physician (or less often a nurse) had been ad- ditions as pulmonary arteritis.26
dicted to morphine for years or even decades. The There is much debate in the medical community as
health care professional involved would take care to uti- to whether prolonged exposure to narcotic analgesics
lize proper sterile technique, thus avoiding the danger alters the function of the neurvous system. Studies in-
of infections inherent in using contaminated needles. volving rats, for example, have found that the chronic
With the exception of his or her opiate addiction, the use of heroin seems to cause the shrinkage of
addicted physician or nurse would appear to be in good dopamine-utilizing neurons in the brain’s “reward sys-
health. For example, the famed surgeon William Halsted tem” (Nestler, 1997). This seems to reflect, at least in
was addicted to morphine for 50 years without suffering part, an adaptive response by the brain to the constant
any apparent physical problems (Smith, 1994).
However, health care professionals have access to 25See Glossary.
pharmaceutical quality narcotic analgesics, not street 26See Glossary.
presence of heroin in the body, and it appears to reverse abusers may cause injury to peripheral nerves near the
with continued abstinence (Nestler, 1997). point of injection, which is most likely caused by adul-
Generally, the complications seen when narcotics terants or the conditions under which the opioid is in-
are abused at above-normal dosage levels are an exag- jected (Ropper & Brown, 2005). There also has been
geration of the side effects of these medications when one case report of a possible heroin-induced inflamma-
used in medical practice. Thus, whereas morphine can tion of the nerves in the spinal cord in a man from Hol-
cause constipation in patients when it is prescribed by land who resumed the practice of smoking heroin after
physicians, morphine abusers/addicts experience pro- 2 months of abstinence (Nyffeler, Stabba, & Sturzeneg-
nounced constipation that can reach the levels of intes- ger, 2003). However, the etiology of the inflammatory
tinal obstruction. Further, when abused at high dosage process in this patient’s spinal cord was not clear, and it
levels, many narcotics are capable of causing seizures is possible that heroin was not a factor in the develop-
(Gutstein & Akil, 2006). This rare complication of nar- ment of this disorder.
cotics use is apparently caused by the high dosage level
of the opioid being abused and usually responds to the
effects of a narcotics blocker such as Narcan (nalox- Overdose of Illicit Opiates
one), according to Gutstein and Akil (2006). One ex-
Ropper and Brown (2005) identified four reasons why
ception to this rule are seizures caused by the drug
the individual might overdose on opioids:28 (a) suicide
meperidine. If nalaxone is administeed to the patient to
attempt, (b) the use of substitute or contaminated illicit
treat the meperidine overdose, it will reduce the
drugs, (c) unusual sensitivity on the part of the individ-
patient’s seizure threshold, making it more likely that
ual to narcotics,29 or (d) errors in calculating the proper
he or she will continue to experience meperidine-
dosage level. It is estimated that at least 50% of heroin
induced seizures (Foley, 1993). Thus, the physician
abusers and an unknown percentage of those who
must identify the specific narcotics being abused to ini-
abuse other narcotics will experience at least one over-
tiate the proper intervention for seizures in the patient
dose (Schuckit, 2006). Often, illicit abusers overesti-
with an opiate use disorder.
mate their tolerance for opioids and take too much of
Illicit heroin abuse, especially the practice of smok-
the compound, initiating an overdose. This is espe-
ing heroin, might cause neurological damage in iso-
cially common when the abuser has restarted the use of
lated cases. In rare cases, this practice has resulted in a
illicit drugs after being incarcerated or in treatment for
progressive spongiform leukoencephalophy, a condi-
a period of time.
tion similar to “mad cow” disease seen in English cattle
Many overdose victims die before they reach the
in the mid-1990s (Zevin & Benowitz, 2007). It is not
hospital, some so quickly that they are found with the
known whether this effect is caused by the heroin itself
needle still in their arm. The most common cause of
or by one or more adulterants27 found in the illicit
death in such cases is respiratory depression (Gutstein &
heroin (Ropper & Brown, 2005). There was an outbreak
Akil, 2006). Even if the overdose victim survives long
of heroin-induced progressive spongiform leukoen-
enough to reach the hospital for emergency medical
cephalophy in the Netherlands in the 1990s, with the
care, death from the overdose is not unusual. Death
first cases in the United States being identified in 1996.
from a narcotics overdose follows a characteristic pat-
This complication of illicit drug use is quite rare but is
tern of reduced consciousness, pinpoint pupils,30 respi-
not unheard of here in the United States.
ratory depression, and cerebral edema, possibly resulting
Indirectly, intravenous opioid abuse has been identi-
in the user’s death (Carvey, 1998; Drummer & Odell,
fied as the cause of damage to peripheral nerves. As the
2001; Henry, 1996; Schuckit, 2006). Even when the
abuser slips into a state of drug-induced stupor, he or
she might come to rest in a position that pinches off 28This assumes that the individual has used only opiates. Any sus-
blood flow to peripheral nerves. If the individual should pected overdose is a medical emergency and requires immediate
remain in this position for an extended period of time, medical care by trained professionals. This section is not intended as
as is common during the drug-induced stupor, the a guide to the treatment of a drug overdose.
29Many medical conditions, such as concurrent liver disease, Addi-
nerve fibers will die for lack of oxygenated blood. How-
son’s disease, or pneumonia, may increase the individual’s risk for an
ever, the opioid itself is not clearly the cause of the
opioid overdose (Ropper & Brown, 2005).
nerve damage in such cases. But intravenous opioid 30Unless the individual has suffered some form of brain damage, in
which case the pupil responses will reflect the brain damage rather
27
Discussed in Chapter 36. than the drug’s effects (Schuckit, 2006).
individual survives the overdose, he or she might suffer peutic half-life of only 60–90 minutes, which might
partial paralysis, peripheral neuropathy, and partial or require that the patient receive several doses before he
complete blindness as a result of anoxia-induced nerv- or she recovers from the opiate overdose (Roberts,
ous system damage (Dilts & Dilts, 2005). Without med- 1995). Further, the naloxone hydrochloride might in-
ical intervention, death from an opioid overdose usually duce unanticipated side effects, although this is quite
occurs 5–10 minutes following an intravenous injec- rare (Henry, 1996).
tion, and 30–90 minutes following an intramuscular in-
jection of the narcotic (Hirsch et al., 1996). However,
Summary
these data apply only for cases of overdose with pharma-
ceutical compounds. Polydrug use and the various adul- The narcotic family of drugs has been effectively uti-
terants31 contribute to the individual’s risk of death in a lized by healers for several thousand years. Indeed, after
multitude of (mostly unknown) ways. For example, alcohol, the narcotics might be thought of as man’s old-
there is evidence that the concurrent use of heroin and est drug. Various members of the narcotic family of
cannabis might increase the individual’s risk of an over- drugs have been found to be effective in the control of
dose, although the exact mechanism for this is not severe pain, cough, and diarrhea. The only factor that
known (Drummer & Odell, 2001). limits their application in the control of less grave con-
Street myths and narcotics overdose. The treatment ditions is the addiction potential that this family of
of any real or suspected drug overdose is a complicated drugs represents. The addiction potential of narcotics
matter, requiring careful assessment and treatment of has been known for hundreds if not thousands of years.
the patient by a licensed physician. Even in the best For example, opiate addiction was a common compli-
equipped hospital, an alcohol or drug overdose may re- cation of military service in the last century, and was
sult in death. The current treatment of choice for a nar- called the “soldier’s disease.”
cotics overdose is a combination of respiratory and But it was not until the advent of the chemical revo-
cardiac support as well as the intravenous administra- lution, when synthetic narcotics were first developed,
tion of Narcan (naloxone hydrochloride) (Ropper & that new forms of narcotic analgesics became available
Brown, 2005). This compound binds at the opioid re- to drug users. Fentanyl and its chemical cousins are
ceptor sites in the brain displacing the drug molecules products of the pharmacological revolution that began
from those receptors. If administered in time, this will in the late 1800s and which continues to this day. This
reverse the opioids that caused or contributed to the chemical is estimated to be several hundred to several
drug overdose. But naloxone hydrochloride has a thera- thousand times as powerful as morphine and promises
to remain a part of the drug abuse problem for genera-
31Discussed in Chapter 36. tions to come.
CHAPTER FIFTEEN
Hallucinogen Abuse and Addiction
About 6,000 different species of plants contain com- One family of organic compounds that has been
pounds that might alter normal consciousness (Brophy, subjected to the greatest level of scientific scrutiny is
1993). This list contains several species of mushrooms those produced by ergot fungus, which grows on vari-
that when ingested will produce sensory distortions and ous forms of grain. Historical evidence long suggested
possibly outright hallucinations (Commission on Ado- that this fungus could produce exceptionally strong
lescent Substance and Alcohol Abuse, 2005; Rold, 1993). compounds. For example, the ingestion of grain prod-
Such plants have been used for thousands of years in reli- ucts infected by ergot fungus can cause vasoconstric-
gious ceremonies and healing rituals, and for predicting tion so severe that entire limbs have been known to
the future (Metzner, 2002; Sessa, 2005). Anthropologi- auto-amputate or affected individuals have died from
cal data suggest that peyote has been used for its hallu- gangrene (Walton, 2002). History has recorded mass
cinogenic properties for at least 5,000 years (Nichols, outbreaks of ergot-induced illness, such at that seen in
2006). On occasion these plants were also used to pre- the French district of Aquitaine around the year 1000
pare warriors for battle (Rold, 1993). Even today, certain C.E.1 Scientists believe that ergot fungus–infected bread
religious groups use mushrooms with hallucinogenic caused the death of some 40,000 people who ate it dur-
properties as part of their worship. ing that epidemic (Walton, 2002).
Scientific interest in hallucinogenic compounds has Compounds produced by the ergot fungus were of
waxed and waned over the years. Currently, scientists interest to scientists eager to isolate chemicals that
are actively investigating whether at least some of these might help in the fight against disease. In 1943, during
compounds might have medicinal value (Horgan, 2005; a clinical research project exploring the characteristics
Karch, 2002). In addition to this renewed scientific in- of one compound obtained from the rye ergot fungus
terest in hallucinogens, there are those who advocate Claviceps purpurea (Lingeman, 1974), lysergic acid
their use as a way to explore alernative realities or gain diethylamide-25 (LSD-25, or simply, LSD), was identi-
self-knowledge (Metzner, 2002). They are also drugs of fied as a hallucinogen. Actually, this discovery was
abuse whose popularity has come and gone over time. made by accident, as the purpose of the research was to
In this chapter, the hallucinogens are examined. find a cure for headaches (Monroe, 1994). But Albert
Hoffman, a scientist involved in that research project,
accidentally ingested a small amount of LSD-25 while
History of Hallucinogens
conducting an experiment, and later that day he began
in the United States to experience LSD-induced hallucinations. After he re-
Over the years, researchers have identified approxi- covered, he correctly concluded that the source of the
mately 100 different hallucinogenic compounds in var- hallucinations was the specimen of Claviceps purpurea
ious plants or mushrooms. In some cases, the active on which he had been working. He again ingested a
agent has been isolated and studied by scientists. Psilo- small amount of the fungus and experienced hallucina-
cybin is an example of such a compound; it was isolated tions for the second time, confirming his original con-
from certain mushrooms that are found in the south- clusion.
western region of the United States and the northern Following World War II, there was a great deal of sci-
part of Mexico. However, many potential hallucino- entific interest in the various hallucinogenics, espe-
genic compounds have not been subjected to systematic cially in light of the similarities between the subjective
research, and much remains to be discovered about
their mechanism of action in humans (Glennon, 2004). 1
Common Era.
179
180 Chapter Fifteen
effects of these chemicals and various forms of mental ported that they had used it within the past year
illness. Further, because these compounds were so po- (Markel, 2000), only 3.3% of the class of 2006 reported
tent, certain agencies of the United States government, having ever used LSD (Johnston, O’Malley, Bachman, &
such as the Department of Defense and the Central In- Schulenberg, 2006a). The incidence of reported LSD
telligence Agency, experimented with various chemical abuse by young adults in recent years is depicted in
agents, including LSD, as possible chemical warfare Figure 15.1.
weapons (Budiansky, Goode, & Gest, 1994). There is The compound phencyclidine (PCP) deserves spe-
strong evidence that the United States Army adminis- cial mention. Because of its toxicity, PCP fell into dis-
tered doses of LSD to soldiers without their knowledge favor in the early 1970s (Jaffe, 1989). But in the 1980s,
or permission between 1955 and 1975 as part of its re- a form of PCP that could be smoked was introduced,
search into possible uses for the compound (Talty, and it again became popular with illicit drug users in
2003). part because the smoker could more closely control
In the 1950s, the term psychedelic was coined how much of the drug she or he used. PCP remained a
to identify this class of compounds (Callaway & common drug of abuse until the middle to late 1990s,
McKenna, 1998). By the 1960s these chemicals had when it began to decline in popularity (Karch, 2002).
moved from the laboratory into the streets where they PCP is still occasionally seen, especially in the big
quickly became popular drugs of abuse (Brown & cities on the East and West coasts (Drummer &
Braden, 1987). The popularity and widespread abuse of Odell, 2001), and is often sold to unsuspecting users
LSD in the 1960s prompted the classification of this in the guise of other, more desired, substances. It is
chemical as a controlled substance in 1970 (Jaffe, also part of the compound sold under the name of
1990). But this did not solve the problem of its abuse. “dip dope” or “dip,” in which cigarettes or marijuana
Over the years, LSD abuse has waxed and waned, cigarettes are dipped into a mixture of PCP, formalde-
reaching a low point in the late 1970s and then increas- hyde, and methanol before being smoked (Mendyk &
ing until it was again popular in the early 1990s. The Fields, 2002). Another drug, N,alpha-dimethyl-1,3-
abuse of LSD in the United States peaked in 1996, and benzodioxole-5-ethanamine (MDMA) has been a
it has gradually been declining since then (Markel, popular drug of abuse since the 1990s and the first
2000). Where 12% of high school seniors in the class of part of the 21st century. Both PCP and MDMA are
2000 admitted to having used LSD once and 8% re- discussed later in this chapter.
13
12
11
10
9
8
Percentage
7
6
5
4
3
2
1
0
1999 2000 2001 2002 2003 2004 2005 2006
Year
FIGURE 15.1 Percentage of High School Seniors Admitting to the Use of LSD, 1999–2006
Source: Data from Johnston et al. (2006a).
Hallucinogen Abuse and Addiction 181
Scope of the Problem Odell, 2001; Glennon, 2004). In spite of the chemical
differences between hallucinogens and differences in
Perhaps 1 million people in the United States have potency, illicit drug abusers tend to adjust their intake
abused a hallucinogen at least once (Kilmer, Palmer, & of the drugs being abused to produce similar effects
Cronce, 2005). Approximately 8.3% of 12th graders sur- (Schuckit, 2006).
veyed admitted to the use of a hallucinogen at least once In spite of their classification as hallucinogenics,
(Johnston et al., 2006a). While some hallucinogens these compounds do not produce frank hallucinations
have been falling in popularity, others have been grow- except at very high doses (Jones, 2005). As a group, they
ing. For example, LSD is relatively unpopular in the might be said to alter the individual’s perceptions, or
United States at this time (Gwinnell & Adamec, 2006), cause illusions, but for the most part they do not cause
partly because in the middle of the first decade of the actual hallucinations (Jones, 2005). By altering the nor-
21st century, law enforcement authorities arrested two mal function of serotonin in the raphe nuclei of the
men who were responsible for the production of virtu- brain, these compounds allow acetylcholine neurons
ally all of the LSD consumed in the United States that normally are most active during dream states to ex-
(Boyer, 2005). It is still too early to determine whether press themselves during the waking state. In other
this will shift interest away from LSD or if other suppli- words, users begin to dream while they remain in an al-
ers will appear to fill this void in the production and dis- tered state of waking, a condition interpreted as halluci-
tribution networks. nations by the users (Hobson, 2001).
Ecstasy (MDMA), another popular hallucinogen, It is common for a person under the influence of
has a mixed history. There is preliminary evidence that one of the hallucinogens to believe that he or she has a
adolescent drug abusers are avoiding MDMA because new insight into reality. But these drugs do not generate
of the dangers associated with the abuse of this com- new thoughts so much as alter the user’s perception of
pound (Parekh, 2006). But other evidence suggests that existing sensory stimuli (Tacke & Ebert, 2005). The
in some regions of the country MDMA abuse is becom- waking-dreams called hallucinations are usually recog-
ing more popular. nized by the user as being drug-induced (Lingeman,
1974). Thus, the terms hallucinogen or hallucinogenic
Pharmacology of the Hallucinogens are usually applied to this class of drugs. Since LSD is
still the prototypical hallucinogen, this chapter focuses
To comprehend how the hallucinogenic compounds on LSD, with other drugs in this class discussed only as
affect the user, it is necessary to understand that normal needed.
consciousness rests on a delicate balance of neurologi-
cal functions. Compounds such as serotonin and dopa-
The Pharmacology of LSD
mine, while classified as neurotransmitters, might better
be viewed as neuromodulators that shift the balance of LSD is one of the most potent chemicals known to sci-
brain function from normal waking states through to ence, but much remains to be discovered about how
the pattern of neurological activity seen in sleep or vari- LSD affects the human brain (Sadock & Sadock,
ous abnormal brain states (Hobson, 2001). 2003). Researchers have compared LSD to hallucino-
The commonly abused hallucinogenics can be di- genic chemicals naturally found in plants such as psilo-
vided into four major groups (Glennon, 2004; Jones, cybin and peyote, and found that LSD is 100–1000
2005):2 the ergot alkaloid derivatives (of which LSD is times as powerful as these “natural” hallucinogens
the most common example), the phenylalkylamines (Schwartz, 1995). It has been estimated to be 3,000
(mescaline and MDMA, for example), the indoleal- times as potent as mescaline (O’Brien, 2006) but is also
kyamines (which include psilocybin and DMT), and weaker than synthetic chemicals such as the hallucino-
atypical hallucinogenic compounds such as Ibogaine, genic DOM/STP (Schuckit, 2000).
which are of minor interest to drug abusers. The “clas- It is usually administered orally but can be adminis-
sic” hallucinogens such as LSD seem to act as agonists to tered intranasally, intravenously, and by inhalation
the 5-HT serotonin receptor site, and their effects are (Klein & Kramer, 2004; Tacke & Ebert, 2005). For the
blocked by experimental 5-HT antagonists (Drummer & casual user, LSD might be effective at doses as low as
50 micrograms, although the classic LSD “trip” usually
2
Jones (2005) identified phencyclidine (PCP) as a “dissociative anes- requires that the user ingest twice that amount of the
thetic” rather than a hallucinogen. drug (Schwartz, 1995). Where LSD users in the 1960s
182 Chapter Fifteen
might ingest a single 100–200 microgram dose, current fects of LSD, increasing the dosage level will have little
LSD doses on the street seem to fall in the 20–80 mi- if any effect (Henderson, 1994a). However, the individ-
crogram range, possibly to make it more appealing to ual’s tolerance will also abate after 2–4 days of absti-
first-time users (Gold & Miller, 1997c). This requires nence (Henderson, 1994a; Jones, 2005). Cross-tolerance
the user to ingest two or three doses to obtain a suffi- between the different hallucinogens is also common
cient level of the drug to be effective, with the result (Callaway & McKenna, 1998). Thus, most abusers alter-
that the abuser has ingested more than was typically nate between periods of active hallucinogen use and
used in the 1960s, when much of the research into spells during which they abstain from further hallucino-
LSD’s effects was conducted. gen abuse.
The LSD molecule is water-soluble. Following in- In terms of direct physical mortality, LSD is perhaps
gestion, it is completely and rapidly absorbed from the the safest compound known to modern medicine, and
gastrointestinal tract, then distributed to all blood-rich scientists have yet to identify a lethal LSD dosage level
organs in the body (Tacke & Ebert, 2005). Because of (Pechnick & Ungerleider, 2004). Some abusers have
this characteristic, only about 0.01% of the original survived doses up to 100 times those normally used
dose actually reaches the brain (Lingeman, 1974). The without apparent ill effect (Pechnick & Ungerleider,
chemical structure of LSD is very similar to the neuro- 2004). Reports of LSD-induced death are exceptionally
transmitter serotonin, and it functions as a serotonin ag- rare and usually reflect accidental death caused by the
onist (Jenkins, 2007; Klein & Kramer, 2004). In the individual’s misperception of sensory data than the di-
brain, LSD seems to bind most strongly to the 5-HT2a rect effects of the compound (Drummer & Odell,
receptor site, although it might have other binding sites 2001; Pechnick & Ungerleider, 2004). But this is not to
in the brain that have not been identified (Glennon, say that LSD is entirely safe. There are reports that LSD
2004). is capable of inducing seizures in the user for more
As the highest brain concentrations of LSD are than 60 days after it was last used (Klein & Kramer,
found in the regions associated with vision as well as the 2004).
limbic system and the reticular activating system The biological half-life of LSD is estimated to be ap-
(RAS), it is not surprising that LSD impacts the way proximately 2.5 to 3 hours (Jenkins, 2007; Oehmichen,
the individual perceives external reality (Jenkins, Auer & Konig, 2005). It is rapidly biotransformed by the
2007). Although classified as a hallucinogen, LSD ac- liver, and then eliminated from the body. Only about
tually causes the individual to misinterpret reality in a 1%–3% of a single dose of LSD is excreted unchanged,
manner better classified as illusions, with actual hallu- with the rest being biotransformed by the liver and ex-
cinations being seen only when very high doses of LSD creted in the bile (Drummer & Odell, 2001; Tacke &
are utilized (Jones, 2005; Pechnick & Ungerleider, Ebert, 2005). So rapid is the process of LSD biotrans-
2004). formation and elimination that traces of the major
In the RAS, which has a high concentration of sero- metabolite of LSD, 2-oxy-LSD, will remain in the
tonin neuroreceptors, the highest concentrations of user’s urine for only 12–36 hours after the last use of the
LSD are found in the region known as the midbrain drug (Schwartz, 1995). Although illicit drug abusers
raphe nuclei, also known as the dorsal midbrain raphe will often claim that the LSD found in urine toxicology
(Hobson, 2001; Jenkins, 2007). Evidence emerging tests was the result of passive absorption through the
from sleep research suggests that one function of the skin, there is little evidence to suggest that this is
raphe nuclei of the brain is to suppress those neurons possible.
most active during rapid eye movement (REM) sleep. The subjective effects of a single dose of LSD appear
By blocking the action of this region of the brain, LSD to last 8–12 hours (Jenkins, 2007; Klein & Kramer,
appears to cause acetylcholine-induced REM sleep to 2004), although Mendelson and Mello (1998) sug-
slip over into the waking state, causing perceptual and gested that the drug’s effects might last 18 hours. The
emotional changes normally seen only when the indi- duration of this LSD-induced trip is apparently dose
vidual is asleep (Henderson, 1994a; Hobson, 2001; related, with larger doses having a longer effect on the
Lemonick, Lafferty, Nash, Park, & Thompson, 1997). person’s perception (Drummer & Odell, 2001). Thus,
Tolerance of the effects of LSD develop quickly, the discrepancy in the estimates of LSD’s duration of
often within 2 to 4 days of continual use (Commission effect might be an artifact caused by the different
on Adolescent Substance and Alcohol Abuse, 2005; doses ingested by abusers in different regions of the
Jones, 2005). If the user has become tolerant to the ef- country.
Subjective Effects of LSD also experience marked mood swings and a feeling of
ego disintegration. Feelings of panic are often experi-
Subjectively, the user will begin to feel the first effects enced during this phase, as are occasional feelings of
of a dose of LSD in about 5–10 minutes. These initial depression (Lingeman, 1974). It is during the third
effects include such symptoms as anxiety, gastric distress, stage of the LSD trip that one often sees individuals ex-
and tachycardia (Schwartz, 1995). In addition, the user press a belief that they possess quasi-magical powers or
might also experience increased blood pressure, in- they are magically in control of events around them
creased body temperature, dilation of the pupils, nau- (Tacke & Ebert, 2005). This loss of contact with reality
sea, and muscle weakness following the ingestion of is potentially fatal, and people have been known to
the drug (Tacke & Ebert, 2005). Other side effects of jump from windows or attempt to drive motor vehicles
LSD include an exaggeration of normal reflexes (a con- during this phase of the LSD trip. On rare occasions
dition known as “hyperreflexia”), dizziness, and some LSD might induce suicidal thoughts or acts (Shea,
degree of muscle tremor (Tacke & Ebert, 2005). These 2002; Tacke & Ebert, 2005).
changes are usually easily tolerated, although the inex- The effects of LSD normally start to wane 4–12
perienced user might react to them with some degree of hours after ingestion (Pechnick & Ungerleider, 2004).
anxiety. As the individual begins to recover, he or she will expe-
The hallucinogenic effects of LSD usually begin 30 rience “waves of normalcy” (Mirin, Weiss, & Greenfield,
minutes to an hour after the user first ingested the drug, 1991, p. 290; Schwartz, 1995) that gradually blend into
peak 2–4 hours later, and gradually wane after 8–12 the waking state of awareness. Within 12 hours, the
hours (O’Brien, 2006; Pechnick & Ungerleider, 2004). acute effects of LSD have cleared, although the person
Scientists believe that the effects of a hallucinogen such might experience a “sense of psychic numbness [that]
as LSD will vary depending on a range of factors, in- may last for days” (Mirin et al., 1991, p. 290).
cluding (a) the individual’s personality makeup, (b) ex- The LSD “bad trip.” It is not uncommon for people
pectations for the drug, (c) the environment in which who have ingested LSD to experience significant anxi-
the drugs are used, and (d) the dose of the compounds ety, which may reach the levels of panic reactions. This
used (Callaway & McKenna, 1998; Tacke & Ebert, is known as a “bad trip” or a “bummer.” Scientists used
2005). to believe the bad trip was more likely with inexperi-
Users often refer to the effects of LSD as a “trip” dur- enced users, but now it is known that even experienced
ing which they experience such effects as a loss of psy- LSD abusers can have one. The likelihood of a bad trip
chological boundaries, a feeling of enhanced insight, a seems determined by three factors: (a) the individual’s
hightened awareness of sensory data, enhanced recall expectations for the drug (known as the “set”), (b) the
of past events, a feeling of contentment, and, a sense of setting in which the drug is used, and (c) the psycholog-
being “one” with the universe (Callaway & McKenna, ical health of the user (Strassman, 2005). If the person
1998). The LSD trip is made up of several distinct does develop a panic reaction to the LSD experience,
phases (Brophy, 1993). The first phase, which begins she or he will often respond to calm, gentle reminders
within a few minutes of taking LSD, involves a release from others that these feelings are caused by the drug
of inner tension. During this phase, the individual will and that they will pass. This is known as “talking down”
often laugh or cry and feel a sense of euphoria (Tacke & the LSD user.
Ebert, 2005). The second stage usually begins 30–90 In extreme cases, the individual might require phar-
minutes (Brown & Braden, 1987) to 2–3 hours (Brophy, macological intervention for the LSD-induced panic
1993) following the ingestion of the drug. During this attack. There is some evidence that the newer, “atypi-
portion of the LSD experience, the individual will ex- cal” antipsychotic medications clozapine and risperi-
perience the perceptual distortions such as visual illu- done bind to the same receptor sites as LSD and that
sions and synesthesia3 that are the hallmark of the they can abort the LSD trip within about 30 minutes of
hallucinogenic experience (Pechnick & Ungerleider, the time the medication was administered (Walton,
2004; Tacke & Ebert, 2005). 2002). This recommendation has not been replicated
The third phase of the hallucinogenic experience by researchers, however, and it is somewhat controver-
will begin 3–4 hours after the drug is ingested (Brophy, sial. At the same time, the use of diazepam to control
1993). During this phase of the LSD trip, users will ex- anxiety and haloperidol to treat psychotic symptoms
perience a distortion of the sense of time. They may has been suggested by some physicians (Jenike, 1991;
3See Glossary. Kaplan & Sadock, 1996; Schwartz, 1995), while others
184 Chapter Fifteen
(Jenike, 1991) have advised against the use of diazepam The LSD flashback. Between 15% and 77% of LSD
in controlling LSD-induced anxiety. In the latter case abusers will probably experience at least one flashback
the theory is that diazepam distorts the individual’s (Tacke & Ebert, 2005). In brief, the flashback is a spon-
perception, which might contribute to even more anxi- taneous recurrence of the LSD experience that is now
ety. Normally, this distortion is so slight as to be unno- classified as the hallucinogen persisting perceptual dis-
ticed, but when combined with the effects of LSD, the order by the American Psychiatric Association (2000)
benzodiazepine-induced sensory distortion may cause (Pechnick & Ungerleider, 2004). The exact mecha-
the patient to have even more anxiety than before (Jenike, nism by which flashbacks occur remains unknown
1991).4 (Drummer & Odell, 2001). They might develop days,
The LSD-induced “bad trip” normally lasts only weeks, or months after the individual’s last use of LSD,
6–12 hours and typically will resolve as the drug’s ef- and even first-time abusers have been known to have
fects wear off (Jone, 2005). However, in rare cases LSD them (Batzer, Ditzler & Brown, 1999; Commission
is capable of activating a latent psychosis (Tacke & on Adolescent Substance and Alcohol Abuse, 2005;
Ebert, 2005). Support for this position is offered by Pechnick & Ungerleider, 2004). Flashbacks have been
Carvey (1998), who noted that various Indian tribes classified as being (a) perceptual, (b) somatic, or (c)
who have used the hallucinogen mescaline for centuries emotional (Weiss & Millman, 1998). The majority in-
fail to have significantly higher rates of psychosis than volve visual sensory distortion, according to Weiss and
the general population, suggesting that the psychosis Millman. Somatic flashbacks consist of feelings of de-
seen in the occasional LSD user is not a drug effect. personalization, and in emotional flashbacks the indi-
However, the final answer to this question has not been vidual reexperiences distressing emotions felt during
identified as of this time. the period of active LSD use (Weiss & Millman, 1998).
One reason it is so difficult to identify LSD’s rela- Flashbacks might be triggered by stress, fatigue, mar-
tionship to the development of psychiatric disorders ijuana use, emerging from a dark room, illness, the use
such as a psychosis is that the “LSD experience is so ex- of certain forms of antidepressant medications, and oc-
ceptional that there is a tendency for observers to at- casionally by intentional effort on the part of the indi-
tribute any later psychiatric illness to the use of LSD” vidual. The use of sedating agents such as alcohol
(Henderson, 1994b, p. 65, italics added for emphasis). might also trigger LSD-induced flashbacks for reasons
Thus, as Henderson points out, psychotic reactions that that are not understood (Batzer et al., 1999). Flashbacks
develop weeks, months, or even years after the last use usually last a few seconds to a few minutes, although oc-
of LSD have on occasion been attributed to the individ- casionally they last hours or even longer (Sadock &
ual’s use of this hallucinogen rather than other factors. Sadock, 2003). Approximately 50% of people who have
The ability of LSD to induce a psychosis is not clear at them will do so in the first 6 months following their last
the present time. use of LSD. In about 50% of the cases, the individual
LSD overdose is rare under normal circumstances will continue to experience flashbacks for longer than
but is not unknown. Some symptoms of an LSD over- 6 months and possibly for as long as 5 years after the last
dose include convulsions and hyperthermia. Medical LSD use (Schwartz, 1995; Weiss, Greenfield, & Mirin,
care is necessary in any suspected drug overdose to re- 1994).
duce the risk of death. In a hospital setting, the physi- Flashback experiences often are occasionally fright-
cian can take appropriate steps to monitor the patient’s ening to the inexperienced user; for the most part, how-
cardiac status and to counter drug-induced elevation ever, they seem to be accepted by seasoned LSD users
in body temperature, cardiac arrhythmias, seizures, and in much the same way that chronic alcohol users ac-
other symptoms. cept some physical discomfort as being part of the price
4On
they must pay for their chemical use. LSD abusers
occasion, the LSD (or other hallucinogens) are adulterated with
belladonna or other anticholinergic compounds (Henderson,
might not report flashbacks unless specifically ques-
1994a). If the physician were to attempt to control the patient’s anxi- tioned about them (Batzer et al., 1999). Reactions to
ety and or agitation through the use of a phenothiazine, the combina- LSD flashbacks vary from one individual to another.
tion of these compounds might induce a coma and possibly even Some LSD abusers enjoy the visual hallucinations,
cause the patient’s death through cardiorespiratory failure. It is for “flashes” of color, halos around different objects, per-
this reason that the attending physician needs to know what drugs
have been ingested, and even provided with a sample of the com-
ception that things are growing smaller or larger, and
pounds ingested if possible, to determine what medication is best for feelings of depersonalization that are common in an
the patient and which medications should be avoided. LSD flashback (Pechnick & Ungerleider, 2004). Others
have been known to become depressed, develop a 2006). PCP continues to be used as a veterinary anes-
panic disorder, or even become suicidal in response to thetic in other parts of the world and is legally manufac-
the perceived onset of insanity and loss of control over tured by pharmaceutical companies outside the United
one’s feelings. The only treatment needed for the typi- States (Kaplan, Sadock, & Grebb, 1994). As a drug of
cal patient having an LSD flashback is reassurance abuse in the United States, PCP’s popularity has waxed
that it will end. On rare occasions an anxiolytic med- and waned, and currently it is not in vogue with illicit
ication might be used to control any flashback-induced drug abusers here.
anxiety. Scope of PCP abuse. Approximately 6 million people
Post hallucinogen perceptual disorder. Following the (0.02% of the population) aged 12 or older in the
individual’s use of LSD, he or she might experience vi- United States have used PCP at least once (Gwinnell &
sual field disturbances, afterimages, or distorted “trails” Adamec, 2006). At this time, intentional PCP use is
following behind objects in the environment for ex- rare, but unintentional PCP use remains a very real
tended periods after the last use of LSD (Hartman, problem. PCP is easily manufactured in illicit laborato-
1995). It has been suggested that LSD might be a selec- ries by people with minimal training in chemistry. It is
tive neurotoxin that destroys the neurons that inhibit often mixed into other street drugs to enhance the ef-
stimulation of the visual cortex, allowing a form of vi- fects of low-quality illicit substances. Further, misrepre-
sual perseveration to develop (Gitlow, 2007). This vi- sentation is common, with PCP being substituted for
sual field disturbance gradually remits in some former other compounds that are not as easily obtained (Zukin,
LSD users, but seems to remain a permanent aftereffect Sloboda, & Javitt, 2005).
for others (Gitlow, 2007).
Although LSD has been studied by researchers for Methods of PCP Administration
the past 70 years, in many ways it remains a mystery. PCP can be smoked, used intranasally, taken by mouth,
For example, there is one case report of a patient who injected into muscle tissue, or injected intravenously
developed grand mal seizures after taking LSD while (Karch, 2002; Weaver, Jarvis, & Schnoll, 1999). It is
taking the antidepressant fluoxetine (Ciraulo, Shader, most commonly abused by smoking, either alone or
Greenblatt, & Creelman, 2006). It is not known whether mixed with other compounds. This allows the abuser to
this was a coincidence or the result of an unknown drug titrate the dose to suit his or her taste or needs. Thus, if
interaction. Unfortunately there is little clinical research the individual finds the drug experience too harsh and
into the pharmacology or neurochemistry of LSD. aversive, he or she can simply stop smoking PCP for a
few minutes, hours, or days.
Phencyclidine (PCP) Subjective Experience of PCP Abuse
The drug phencyclidine (PCP) was first introduced in Phencyclidine’s effects might last for several days, dur-
1957 as an experimental intravenously administered ing which the user will experience rapid fluctuations in
surgical anesthetic (Tacke & Ebert, 2005). By the mid- his or her level of consciousness (Weaver et al., 1999).
1960s, researchers had discovered that 10%–20% of the The main experience for the user is a sense of dissocia-
patients who had received PCP experienced a drug- tion in which reality appears distorted or distant. Parts
induced delirium and/or psychotic reaction that in of the user’s body might feel numb or as if they were no
some cases lasted up to 10 days, and the use of phency- longer attached. These experiences might prove fright-
clidine in human patients was discontinued (Jenkins, ening, especially to an inexperienced user, resulting in
2007; McDowell, 2004). Unfortunately, at about this panic reactions. Some of the other desired effects of
same time illicit drug abusers began to experiment with PCP intoxication include a sense of euphoria, de-
PCP, with the first reports of PCP abuse dating to creased inhibitions, a feeling of immense power, a re-
around 1965. duction in the level of pain, and altered perception of
Even after its use as a surgical anesthetic in humans time, space, and the user’s body image (Milhorn,
was discontinued in the United States, phencyclidine 1991).
continued to be used in veterinary medicine until 1978, Not all the drug’s effects are desired by the user. In-
when all legal production of PCP in the United States deed, “most regular users report unwanted effects”
was discontinued. It was classified as a Schedule II sub- (Mirin, Weiss, et al., 1991, p. 295) caused by PCP.
stance under the Comprehensive Drug Abuse Preven- Some of the more common negative effects include
tion and Control Act of 1970 (Grinnell & Adamec, feelings of anxiety, restlessness, and disorientation. In
186 Chapter Fifteen
some cases, the user retains no memory of the period of Weaver, 2004). The level of PCP in the brain might be
intoxication, a reflection of the anesthetic action of the 10–113 times as high as blood plasma levels (Zukin et al.,
drug (Ashton, 1992). Other negative effects of PCP in- 2005; Shepherd & Jagoda, 1990). Further, animal re-
clude disorientation, mental confusion, assaultiveness, search data suggest that PCP remains in the brain for up
anxiety, irritability, and paranoia (Weiss & Mirin, 1988). to 48 hours after it is no longer detectable in the blood
Indeed, so many people have experienced so many (Hartman, 1995). Once in the brain, PCP tends to act at
different undesired effects from PCP that researchers a number of different receptor sites, including blocking
remain at a loss to explain why the drug was ever a those utilized by a neurotransmitter known as N-methyl-
popular drug of abuse (Newell & Cosgrove, 1988). D-aspartic acid (NMDA) (Drummer & Odell, 2001;
PCP can cause the user to experience a drug-induced Zukin et al., 2005). PCP functions as an NMDA chan-
depressive state; in extreme cases, this can reach suicidal nel blocker, preventing NMDA from being able to carry
proportions (Jenike, 1991; Weiss & Mirin, 1988). This out its normal function (Jenkins, 2007; Zukin et al.,
is consistent with the observations of Berger and Dunn 2005). PCP also binds to the sigma opioid receptor site,
(1982), who, drawing on the wave of PCP abuse that which is how it causes many of its less pleasant effects
took place in the 1970s, reported that the drug would (Daghestani & Schnoll, 1994; Drummer & Odell, 2001),
bring the user either to “the heights, or the depths” and its hallucinogenic effects may be traced to its finding
(p. 100) of emotional experience. some of the same cannabinoid receptor sites occupied by
THC (Glennon, 2004).
Pharmacology of PCP The effects of PCP on the brain vary, depending on
There have not been any systematic studies of PCP the concentration of the compound in the brain and the
abuse, dependence, or the withdrawal syndrome that individual’s prior experience with the compound
emerges following chronic use (Zukin, Sloboda, & (Jenkins, 2007). At 10 times the minimal effective dose,
Javitt, 2005). Much of what is known about the effects PCP begins to function as a monoamine reuptake
of PCP on the individual are based on case studies of blocker, blocking the normal action of this group of neu-
drug abusers or clinical experience with patients who rotransmitters. Thus, PCP might function as an anes-
were given phencyclidine as an anesthetic. thetic, a stimulant, a depressant, or a hallucinogenic,
Chemically, phencyclidine is a weak base, soluble in depending on the dose utilized (Brown & Braden, 1987;
both water and lipids. When ingested orally, because it Weiss & Mirin, 1988). PCP is biotransformed by the
is a weak base it will be absorbed mainly through the liver into a number of inactive metabolites that are then
small intestine rather than the stomach lining (Javitt et al., excreted mainly by the kidneys (Zukin et al., 2005;
2005). This will slow the absorption of the drug into the Zukin & Zukin, 1992). Following a single dose of PCP,
body, for the drug molecules must pass through the only about 10% (Karch, 2002) to 20% (Crowley, 1995)
stomach to reach the small intestine. But the effects of of the drug will be excreted unchanged. The effects of
an oral dose of PCP are still generally seen in just 20–30 smoked PCP peak in 15–30 minutes and continue for
minutes. There is a great deal of intraindividual variabil- about 4–6 hours after a single dose (Jenkins, 2007).
ity in how long PCP remains in the body but the pri- Unfortunately, one characteristic of PCP is that it
mary effects of an oral dose usually last 3–4 hours. takes the body an extended period of time to biotrans-
When smoked, PCP is rapidly absorbed through the form and excrete it. This time period is extended even
lungs. The user will begin to experience symptoms of further in overdose situations, and the half-life of PCP
PCP intoxication within about 2–3 minutes after smok- following an overdose may be as long as 20 (Kaplan et al.,
ing the drug (Schnoll & Weaver, 2004). When smoked, 1994) to 72 hours (Jaffe, 1989), and in extreme cases
much of the PCP will be converted into the chemical might be several weeks (Grinspoon & Bakalar, 1990).
phenylcyclohexene by the heat of the smoking process One reason for the extended half-life of PCP is that it
(Shepherd & Jagoda, 1990) and only about 30%–50% tends to accumulate in the body’s adipose (fat) tissues
of the PCP in the cigarette will actually be absorbed where in chronic use it can remain for days or even
(Crowley, 1995). When injected or ingested orally, weeks following the last dose of the drug. There have
70%–75% of the available PCP will reach the circula- even been cases of a chronic PCP user losing weight,
tion (Crowley, 1995). The effects of injected PCP last either through trying to lose weight or because of
for about 3–5 hours. trauma, and unmetabolized PCP still in the person’s
PCP is very lipid-soluble and thus tends to accumu- adipose tissue was released back into the general circula-
late in fatty tissues and tissues of the brain (Schnoll & tion, causing the user to have flashback-type experiences
long after the last use of the drug (Zukin & Zukin, ited drug-induced fever, an excess of salivation, drug-
1992). induced psychosis, and violence.
In the past, physicians believed it was possible to re- Symptoms of severe levels of PCP intoxication. As the
duce the half-life of PCP in the body by making the dosage level reaches the 10–25 mg level or higher, the
urine more acidic. This was done by having the patient individual’s life is in extreme danger. At this dosage
ingest large amounts of ascorbic acid or cranberry juice level users might experience vomiting, seizures, and if
(Grinspoon & Bakalar, 1990; Kaplan & Sadock, 1996). still conscious, seriously impaired reaction times.
However, it was discovered that patients were vulner- There are reports of PCP abusers entering a comatose
able to developing a condition known as myoglobin- state at this dosage, although with their eyes open
uria, which may cause the kidneys to fail (Brust, 1993). (Zevin & Benowitz, 2007). Other symptoms include se-
Because of this potential complication, many physi- vere hypertension, rhabdomyolysis, renal failure, tachy-
cians do not recommend the acidification of the patient’s cardia, and severe psychotic reactions similar to those of
urine for any reason. schizophrenia (Grinspoon & Bakalar, 1990; Zevin &
Tolerance of PCP’s euphoric effects develops rapidly Benowitz, 2007; Zukin et al., 2005;). The PCP-induced
(Zukin et al., 2005). Clinical evidence with burn pa- coma might last from 10 days (Mirin et al., 1991) to sev-
tients who have received repeated doses of the anes- eral weeks (Zevin & Benowitz, 1998). Further, because
thetic agent ketamine, which is similar in chemical of the absorption and distribution characteristics of the
structure to PCP, suggests that some degree of toler- drug, the individual might slip into and apparently re-
ance to its effects are possible (Zukin et al., 2005). cover from a PCP-induced coma several times before
Symptoms of mild levels of PCP intoxication. Small the drug is fully eliminated from the body (Carvey,
doses of PCP, usually less than 1 mg, do not seem to 1998). Other symptoms of severe PCP intoxication are
have an effect on the user (Crowley, 1995). The typical cardiac arrhythmias, encopresis, visual and tactile hal-
dose is about 5 mg, at which point the individual will ex- lucinations, and a drug-induced paranoid state. PCP
perience a state similar to alcohol intoxication (Zukin overdoses have caused death from respiratory arrest,
et al., 2005). The abuser will also experience symptoms convulsions, and hypertension (Zukin et al., 2005).
such as confusion, agitation, aggression, nystagmus, There would appear to be some minor withdrawal
ataxia, and hypertensive episodes (Zevin & Benowitz, symptoms following prolonged periods of hallucinogen
2007). Other effects at this dosage level include agita- use. Chronic PCP users have reported memory prob-
tion, some feelings of anxiety, flushing, visual hallucina- lems, which seem to clear when they stopped using the
tions, irritability, possible sudden outbursts of rage, drug (Jaffe, 1990; Newell & Cosgrove, 1988). Recent
feelings of euphoria, and changes in the body image evidence suggests that chronic PCP use can cause neu-
(Beebe & Walley, 1991; Crowley, 1995; Zukin et al., ronal necrosis5 especially in the hippocampus and lim-
2005; Milhorn, 1991). The acute effects of a small dose bic system (Zukin et al., 2005). These findings are
of about 5 mg of PCP last 4–6 hours. Following the pe- consistent with early studies, which found the same pat-
riod of acute effects is a post-PCP recovery period that tern of neuropsychological deficits as in other forms of
can last 24–48 hours (Beebe & Walley, 1991; Milhorn, chronic drug use, suggesting that PCP might cause
1991). During the post-PCP recovery period the user chronic brain damage (Grinspoon & Bakalar, 1990;
will gradually “come down,” or return to normal. Jentsch et al., 1997).
Symptoms of moderate levels of PCP intoxication. As The PCP-induced psychosis. The PCP psychosis usu-
the dosage level increases to the 5–10 mg range, many ally will progress through three different stages, each of
users will experience a number of of symptoms, includ- which lasts approximately 5 days (Mirin et al., 1991;
ing a disturbance of body image, where different parts Weiss & Mirin, 1988). The first stage is usually the most
of their bodies will no longer seem “real” (Brophy, severe and is characterized by paranoid delusions,
1993). Users may also experience slurred speech, nys- anorexia, insomnia, and unpredictable assaultiveness.
tagmus, dizziness, ataxia, tachycardia, and an increase During this phase, the individual is extremely sensitive
in muscle tone (Brophy, 1993; Weiss & Mirin, 1988). to external stimuli (Jaffe, 1989; Mirin et al., 1991), and
Other symptoms of moderate levels of PCP intoxica- the “talking down” techniques that might work with an
tion might include paranoia, severe anxiety, belliger- LSD bad trip are generally not effective with PCP
ence, and assaultiveness (Grinspoon & Bakalar, 1990) (Brust, 1993; Jaffe, 1990).
as well as unusual feats of strength (Brophy, 1993; Jaffe,
1989) and extreme salivation. Some people have exhib- 5See Glossary.
188 Chapter Fifteen
The middle phase is marked by continued paranoia not cause the nausea or vomiting often experienced by
and restlessness, but the individual is usually calmer and MDMA users. The compound was considered unwor-
in intermittent control of his or her behavior (Mirin thy of classification as an illegal substance when the
et al., 1991; Weiss & Mirin, 1988). This phase will again drug classification system currently in use was set up in
usually last 5 days and will gradually blend into the final the early 1970s.
phase of the PCP psychosis recovery process. The final Partially because it was not considered an illicit sub-
phase is marked by a gradual recovery over 7 to 14 days; stance, illicit drug producers became interested in
however, in some patients the psychosis may last for MDMA in the mid-1970s. The marketing process be-
months or even years (Filley, 2004; Mirin et al., 1991; hind the drug was impressive: Possible product names
Slaby, Lieb, & Tancredi, 1981; Weiss & Mirin, 1988). were discussed before “Ecstasy” was selected (Kirsch,
Social withdrawal and severe depression are also com- 1986; McDowell, 2004), a demand for the “product”
mon following chronic use of PCP (Jaffe, 1990). was generated, and supply and distribution networks
PCP abuse as an indirect cause of death. PCP- evolved to meet this demand. The original samples of
induced hypertensive episodes, typically seen when PCP ecstasy included a “package insert” (Kirsch, 1986, p. 81)
is abused at high dosage levels, might last as long as that “included unverified scientific research and an
3 days after the drug was ingested (Weiss & Millman, abundance of 1960s mumbo-jumbo” (p. 81) about how
1998). These periods of unusually high blood pressure the drug should be used and its purported benefits. The
may contribute to the development of a cerebral vascular package inserts also warned the user not to mix ecstasy
accident (CVA, or stroke) in the individual’s brain (Brust, with alcohol or other chemicals, to use it only occasion-
1993; Daghestani & Schnoll, 1994; Zukin et al., 2005). ally, and to take care to ensure a proper “set” in which
PCP abuse is also a factor in homicide, as many users to use MDMA.
end up as the victim or perpetrator of a homicide while Within a few years, MDMA became a popular drug
under the drug’s effects (Ashton, 1992). Finally, the dis- of abuse in both the United States and Europe. The
sociative and anesthetic effects of PCP place the abuser Drug Enforcement Administration (DEA) classified
at risk for traumatic injuries, which may result in death MDMA as a Schedule I compound7 (McDowell, 2004,
(“Consequences of PCP Abuse,” 1994). Given its effects 2005). In spite of this, MDMA has remained a popular
on the user, researchers are mystified as to why anybody drug of abuse, as indicated by the worldwide produc-
would wish to use PCP. Still, at the start of the 21st cen- tion of MDMA, which is thought to exceed 8 metric
tury PCP continues to lurk in the shadows, and it may tons a year (United Nations, 2006). Another measure of
again become a popular drug of abuse just as it has been MDMA’s popularity is the more than 150 street names
in the past. for various preparations of the compound (Kilmer et al.,
2005). Currently, MDMA is the most commonly abused
stimulant in dance clubs (Gahlinger, 2004). There is a
Ecstasy (MDMA) growing trend for MDMA powder to be abused rather
History of ecstacy. The hallucinogen N, alpha-dimethyl- than tablets, as producing the powder is far easier than
1,3 benzodioxole-5-ethanamine (MDMA) was first iso- molding the compound into tablet form (Boyer, 2005).
lated in 1914.6 Initially it was thought that MDMA
would function as an appetite suppressant, but subse- Scope of MDMA Abuse
quent research failed to support this expectation and re- In the United States, an estimated 8 million people are
searchers quickly lost interest in it. In the mid-1960s thought to have used MDMA at least once in their lives
some psychiatrists suggested that MDMA might be use- (Gwinnell & Adamec, 2006). In Europe MDMA is
ful as an aid in psychotherapy (Batki, 2001; Gahlinger, thought to be the second most common illicit drug of
2004; Rochester & Kirchner, 1999). MDMA also abuse, surpassed only by marijuana (Morton, 2005).
briefly surfaced as a drug of abuse during the 1960s but Globally, the number of MDMA abusers probably sur-
was eclipsed by LSD, which was more potent and did passes the cocaine and heroin abusers combined
(United Nations, 2003, 2004). The total worldwide an-
6Cook (1995) said that MDMA was patented in 1913, and Rochester nual production of MDMA is estimated to be about
& Kirchner (1999) suggested that the patent was issued in 1912 in 113 tons, and there is evidence that MDMA abuse is in-
Germany. Schuckit (2006) suggested that MDMA was first synthe-
sized in 1912, and that the patent was for this compound issued in
creasing globally (United Nations, 2003, 2004).
1914. There obviously is some disagreement over the exact date that
7See
the patent for this chemical was issued. Appendix Four.
Initially, MDMA was widely believed to be harmless 2004, 2005). It first forces the release of and then in-
(Ramcharan et al., 1998). It found wide acceptance in a hibits the reabsorption of serotonin, with a smaller ef-
subculture devoted to loud music and parties centered fect on norepinephrine and dopamine (Gahlinger,
around the use of MDMA and dancing, similar to the 2004; Parrott, Morinan, Moss, & Scholey, 2004).
LSD parties of the 1960s (Randall, 1992). Such parties, While scientists think that MDMA’s main effects in-
known as “raves,” began in Spain, spread to England in volve the serotonin neurotransmitter system, there is
the early 1980s, and from there to the United States very little objective research into its effects on users,
(McDowell, 2004; Rochester & Kirchner, 1999). While and virtually all that is known about the drug’s effects
these parties have become less common, MDMA has is based on studies done on illicit drug abusers or in-
moved into more mainstream nightclubs and is popular dividual case reports.
among older adolescents (Morton, 2005).
Patterns of MDMA Abuse
Pharmacology of MDMA MDMA abusers will typically ingest 60–120 mg of the
drug10 although binge abusers might take 5–25 tablets
Technically, MDMA is classified as a member of the
at one time to enhance the euphoria found at lower
phenethylamine8 family of compounds, but its chemi-
doses (Outslay, 2006). Unlike abusers of other drugs,
cal structure is also so similar to that of the ampheta-
ecstasy abusers tend to use their drug of choice on an
mines that it was classified as a “semisynthetic hallu-
episodic basis, interspaced with periods of abstaining
cinogenic amphetamine” by Klein and Kramer (2004,
from further MDMA use to recover from the drug’s ef-
p. 61). In this text it will be identified as a hallucinogenic
compound, since this is the context in which it is most fects (although polydrug abusers might continue to use
commonly abused. other compounds during this period of time) (Commis-
Because MDMA is well absorbed from the gastroin- sion on Adolescent Substance and Alcohol Abuse,
testinal tract, the most common method of use is 2005; Gouzoulis-Mayfrank et al., 2000).
through oral ingestion (McDowell, 2004). The effects This pattern of MDMA abuse reflects the pharma-
of a dose of MDMA usually begin in about 20 minutes cology of this compound in the brain. Since the drug
and peak within an hour (Gahlinger, 2004; McDowell, functions as a serotonin reuptake blocker, the MDMA
2004, 2005) to an hour and a half (Schwartz & Miller, abuser is less likely to experience euphoria through
1997). Peak blood levels are usually seen in 1–3 hours the use of a large dose or frequent abuse of this com-
after a single dose is ingested (de la Torre et al., 2005). pound. There is a “plateau effect” beyond which point
Maximum blood levels of MDMA are achieved about the individual is only more likely to experience nega-
2–4 hours following a single dose, and the estimated tive effects of the drug rather than euphoria (Bravo,
half-life of a single dose is estimated at 4–7 (Karch, 2001). Thus, the typical abuser will demonstrate peri-
2002) to 8–9 hours (de la Torre et al., 2004; Gahlinger, ods of active MDMA abuse, interspaced with periods
2004; Klein & Kramer, 2004; Schwartz & Miller, of abstaining from all drugs of abuse, or at least
1997). MDMA.
MDMA is biotransformed in the liver, and its elimi- Subjective and Objective Effects
nation half-life9 is estimated to be approximately 8 of MDMA Abuse
hours (Tacke & Ebert, 2005). About 9% of a single dose
Currently, at least six different methods of making
of MDMA is biotransformed into a metabolite that is it-
MDMA are known, and specific instructions on how to
self a hallucinogen: MDA (de la Torre et al., 2004).
make MDMA are available on the Internet (Rochester &
However one study, which used a single volunteer sub-
Kirchner, 1999). Specialized equipment and training in
ject, found that almost three-fourths of the MDMA in-
organic chemistry are required to avoid the danger of
gested was excreted unchanged in the urine within
contamination of the MDMA by toxins, but beyond
72 hours of the time the drug was ingested.
these requirements the drug is easily synthesized. In past
Because it is so highly lipid soluble, MDMA can
decades, MDMA was usually produced in Europe and
cross the blood-brain barrier into the brain itself with-
then shipped to the United States; now it is increasingly
out significant delay. Within the brain, MDMA func-
being produced in this country. Much of what is known
tions as an indirect serotonin agonist (McDowell,
10Although it is common for other compounds to be substituted
8Discussedin Chapter 36. for the MDMA that the individual thought she or he was buying
9See Chapter 3 and Glossary. (Gwinnell & Adamec, 2006).
190 Chapter Fifteen
about MDMA’s effects are based on observations made include fatigue, dry mouth, anorexia, insomnia, irri-
of illicit drug users, although there are now a limited tability, drowsiness, difficulty concentrating, depres-
number of studies in which volunteers have ingested a sion, and headache (de la Torre et al., 2004; McDowell,
measured dose of MDMA to help scientists better un- 2005; Morgan, 2005).
derstand the drug’s effects (Outslay, 2006). Some of the symptoms of the chronic phase, which
The subjective effects of MDMA can be divided into begins as the subacute phase tapers into the final phase,
three phases: (a) acute, (b) subacute, and (c) chronic include anxiety, depression, confusion and cognitive
(Outslay, 2006). The subjective effects of MDMA dur- dysfunction, insomnia, irritability, low energy, and sus-
ing the acute phase are to a large degree dependent on piciousness and paranoia (Outslay, 2006). It is not
the setting in which it is used, the dose ingested, and known how long these effects last, if they are induced
the individual’s expectations for the drug (Bravo, 2001; by ecstasy, or if they are co-existing conditions that were
Engels & ter Bogt, 2004; Outslay, 2006). At dosage exacerbated by the ingestion of this compound.
levels of 75–100 mg, users report initially experiencing Many abusers will attempt to control the MDMA-
a sense of euphoria, a sense of closeness to others, in- related bruxism by using baby pacifiers or candy to suck
creased energy, mild perceptional disturbances such as on after ingesting MDMA (Gahlinger, 2004; Klein &
enhanced color and sound perception, a sense of well- Kramer, 2004). MDMA abuse has been implicated as
being, a lowering of interpersonal defenses, and im- the cause of decreased sexual desire as well as—in
proved self-esteem (Bravo, 2001; de la Torre et al., men—inhibition of the ejaculatory reflex and erectile
2004; Outslay, 2006). problems following drug ingestion (Finger, Lund &
The feeling of self-esteem might reflect MDMA’s Slagel, 1997; McDowell, 2004). Paradoxically, male
ability to stimulate the release of the neurochemical users often report feeling sexually aroused when the ef-
prolactin, which is normally released after the individ- fects of MDMA begin to wear off during the subacute
ual has reached sexual orgasm (Passie, Hartmann, phase (Buia et al., 2000).
Schneider, Emrich, & Kruger, 2005). At this dosage
level, the user might also possibly experience mild vi- Complications of MDMA Use
sual hallucinations (Evanko, 1991), although these Unfortunately, MDMA has an unfounded reputation
are altered perception than actual hallucinations. The for safety in spite of the fact that there is a significant
effects of MDMA usually start 30–60 minutes after in- overlap between the therapeutic and toxic levels of
gestion of the drug, peak at about 75–120 minutes MDMA (Karch, 2002;Outslay, 2006; Ropper & Brown,
after ingestion, and last for 6–12 hours (Outslay, 2005). Animal research suggests that the lethal level of
2006). MDMA is about 6,000 mg in humans (Rosenthal &
Some of the side effects of a single dose of MDMA Solhkhah, 2005). In the early 1950s, the United States
that might occur during the acute phase include loss of Army conducted a series of secret research projects to
appetite, clenching of the jaw muscles or grinding of the explore MDMA’s possible military applications, and
teeth (bruxism), dry mouth, thirst, restlessness, heart the data from these studies suggest that just 14 of the
palpitations, ataxia, dizziness, drowsiness, nystagmus, more potent MDMA pills being produced in illicit lab-
weakness, muscle tension, insomnia, confusion, feelings oratories might prove fatal to the user if ingested to-
of depersonalization and derealization, anxiety or panic gether (Buia et al., 2000).
attacks, and tremor (Bravo, 2001; Buia, Fulton, Park, Some of the symptoms induced by MDMA toxicity
Shannon, & Thompson, 2000; de la Torre et al., 2004; include nausea, vomiting, dry mouth, dehydration,
Grob & Poland, 2005; McDowell, 2005). Higher dosage sweating, restlessness, tremor, exaggerated reflexes, irri-
levels are more likely to cause an adverse effect than are tability, bruxism, heart palpitations and arrhythmias,
low doses, although unpleasant effects are possible even confusion, aggression, panic attacks, drug-induced psy-
at very low doses (Grob & Poland, 2005). chosis, hypertension, extreme (possibly fatal) elevations
The subacute phase begins 6–12 hours after the in body temperature, delirum, coma, hypotension,
drug was ingested and continues for up to 1 month, al- rhabdomyolysis, and possible renal failure (de la Torre
though in most cases it lasts only 1–7 days (Outslay, et al., 2004; Jaffe, 2000; McDowell, 2005; Morton,
2006). This phase is also called coming down or the 2005; Parrott, 2004; Rosenthal & Solhkhah, 2005;
hangover phase by drug abusers, according to Outslay. Williams, Dratcu, Taylor, Roberts, & Oyefeso, 1998;
Some of the symptoms experienced during this time Zevin & Benowitz, 2007).
MDMA-related cardiac problems. It is now known MDMA-related neurological problems. There is pre-
that MDMA causes an increase in the heart rate and liminary evidence that for reasons not understood,
blood pressure while also increasing the rate at which women might be more vulnerable to MDMA-induced
cardiac tissues use oxygen (Grob & Poland, 2005). brain damage than men (Greenfield, 2003). There are
These effects may exacerbate preexisting cardiac prob- reports of intracranial hemorrhage in some abusers as
lems, even when the individual has not actually experi- well as nonhemorrhagic cerebral vascular accidents.13 At
enced any symptoms of a possible heart problem high doses, MDMA has been known to induce seizures
(Grob & Poland, 2005). This is one reason MDMA (Thompson, 2004). Further, animal research has demon-
abuse is associated with such heart problems as cardiac strated that MDMA causes the body to secrete abnor-
arrhythmias such as ventricular tachycardia (Beebe & mal amounts of the antidiuretic hormone (ADH)
Walley, 1991; Gahlinger, 2004; Grob & Poland, 2005; (Gahlinger, 2004; Henry & Rella, 2001; Tacke & Ebert,
Karch, 2002; Klein & Kramer, 2004; Schwartz & 2005). This hormone then promotes water reabsorption
Miller, 1997). One study of the hospital records of 48 by the kidneys, reducing urine production and forcing
patients admitted to a hospital accident and trauma the water back into the body. If users ingest a great deal of
center following MDMA use showed that two-thirds of water in an attempt to avoid dehydration, they might
the patients had heart rates above 100 beats per minute then develop abnormally low blood sodium levels (hy-
(Williams et al., 1998). It was recommended that ponatemia), which could cause or contribute to arrhyth-
MDMA overdoses be treated with the same protocols mias, seizures, or other problems (Grob & Poland, 2005;
used to treat amphetamine overdoses, with special em- Henry & Rella, 2001; McDowell, 2005; Parrott et al.,
phasis placed on assessing and protecting cardiac func- 2004). Thus, the problem of how to deal with MDMA-
tion (Gahlinger, 2004; Rochester & Kirchner, 1999). related dehydration is far more complex than simply hav-
Further, there is experimental evidence that MDMA ing the user ingest fluids prior to exercise or dancing.
functions as a cardiotoxin11 causing inflammation of A growing body of evidence from both animal and
the heart muscle (Badon et al., 2002). Patel et al. (2005) human studies suggests that MDMA can induce memory
compared heart tissue samples from one group of de- problems that may persist for weeks or even months after
ceased MDMA abusers (as confirmed by blood toxi- the individual’s last use of this compound (McDowell,
cology tests) with those of deceased persons whose blood 2005; Morton, 2005). Researchers have found a dose-
did not reveal signs of MDMA abuse at the time of related relationship between MDMA use and reduced
death. The authors found that the deceased MDMA abilities in such cognitive areas as coding information into
abusers had heart weights that were 14% heavier than long-term memory, impaired verbal learning, increased
those of nonabusers. This weight gain seems to reflect distractability, and a general loss of efficiency that did not
the development of fibrous tissue within the cardiac resolve over long periods of time (Lundqvist, 2005; Qued-
muscle, which interferes with the electrical impulses now et al., 2006). Zakzanis and Campbell (2006) com-
within the heart necessary for normal heart rhythm. pared psychological test scores of former MDMA
This seems to be the mechanism by which many abusers with those of continued abusers and found that
chronic MDMA abusers develop a drug-induced car- the test results of the latter group demonstrated serious
diomyopathy (Klein & Kramer, 2004). There is also ev- deterioration in memory function compared to the test
idence that the chronic use of MDMA can damage the performance of their former drug-abusing companions. It
valves of the heart (Setola et al., 2003). The authors exis not clear whether this MDMA-induced memory dys-
amined the impact of MDMA on tissue samples in lab- function might be reversed with abstinence, but there is
oratories and found many of the same changes to the the possibility that the observed loss of memory function
heart valves caused by the now-banned weight-loss might become permanent in heavy MDMA abusers.
medication fenfluramine.12 Given the widespread popu- MDMA has also been implicated as the cause of the
larity of MDMA, these research findings hint at a possible serotonin syndrome14 (Henry & Rella, 2001; Karch,
future epidemic of MDMA-induced cardiac problems in 2002; Sternbach, 2003). Since temperature dysregulation
chronic abusers. is one effect of the serotonin syndrome, this process might
11See Glossary.
explain why some abusers develop severe hyperthermia
12Also known as “phen-fen.” After it was introduced, scientists discovered
13See Glossary.
evidence of increased degeneration of the tissue of heart valves in some
14See Glossary.
users, prompting the manufacturer to withdraw it from the market.
192 Chapter Fifteen
following MDMA ingestion (Klein & Kramer, 2004). damage occurs at dosage levels most frequently utilized
Animal research suggests that MDMA’s ability to cause by human abusers (Ricaurte, Yuan, Hatzidimitriou,
the release of serotonin and dopamine within the brain Branden, & McCann, 2002). Further, MDMA-induced
might be a temperature-sensitive effect, with higher brain damage is possible even on the first occasion that
ambient temperatures being associated with higher the drug is ingested (McDowell, 2005). Researchers dis-
levels of serotonin and dopamine release in the brains agree as to whether this MDMA-induced brain damage
of experimental rats (O’Shea et al., 2005). Unfortu- is permanent (Walton, 2002) or if some limited degree of
nately, these same neurotransmitters are also involved recovery is possible (Buchert et al., 2003; Buchert et al.,
in the sensation of pleasure that many MDMA abusers 2004; Gouzoulis-Mayfrank et al., 2000; Reneman et al.,
experience, with the result that MDMA abuse in areas 2000; Ritz, 1999). But whether it is a temporary or per-
of high ambient temperatures might cause the user to manent aftereffect of MDMA abuse, the brain damage
feel greater levels of pleasure even while his or her life does appear to be real.
is at greater risk from increased body temperature At one point it was suspected that the neurotoxic ef-
(O’Shea et al., 2005). fects of MDMA were possibly due to contaminants in
For reasons that are not well understood, MDMA the MDMA rather than the drug itself (Rochester &
seems to lower the seizure threshold in users (Karch, Kirchner, 1999). Positive emission tomographic (PET)
2002). Such MDMA-related seizures can be fatal studies have uncovered significant evidence suggesting
(Henry, 1996; Henry & Rella, 2001). Further, the avail- global, dose-related decreases in brain 5-HT trans-
able evidence suggests that MDMA is a selective neuro- porter, a structural element of neurons that utilize sero-
toxin15 both in humans and animals. Genetic research tonin (Buchert et al., 2004; McCann, Szabo, Scheffel,
indicates that individuals who possess two copies of the Dannals & Ricaurte, 1998). Even limited MDMA use
“short” serotonin transporter gene may be most vulner- has been found to be associated with a 35% reduction in
able to MDMA-induced neurotoxicity (Roiser, Cook, 5-HT metabolism (an indirect measure of serotonin ac-
Cooper, Rubinsztein, & Sahakian, 2005). This may be tivity in the brain) for men, and almost a 50% reduction
the mechanism by which MDMA functions as a neuro- in 5-HT metabolism in women (Hartman, 1995), find-
toxin, and provides an interesting interface between beings that are highly suggestive of organic brain damage
havioral genetics and toxicology. Most certainly, the at a cellular level. However, there is preliminary evi-
results of the study by Roiser et al. (2005) support ear- dence that a single dose of the selective serotonin reup-
lier observations that MDMA functions as a selective take inhibitor Prozac (fluoxotine) might protect neurons
neurotoxin in humans that destroys serotonergic neu- from MDMA-induced damage if it is ingested within 24
rons (Batki, 2001; Gouzoulis-Mayfrank et al., 2000; hours of the MDMA dose (Walton, 2002).
McDowell, 2005; Reneman, Booij, Schmand, van den MDMA-related emotional problems. The MDMA
Brink & Gunning, 2000; Vik, Cellucci, Jarchow, & user might experience flashbacks very similar to those
Hedt, 2004; Wareing, Risk, & Murphy, 2000). seen with LSD use (Creighton, Black, & Hyde, 1991).
MDMA abuse might place the user at higher risk These MDMA flashbacks usually develop in the first
for developing Parkinson’s disease in later life few days following the use of the drug (Cook, 1995).
(Gahlinger, 2004). However, the exact relationship be- Another interesting drug effect is seen at normal dosage
tween MDMA abuse and Parkinson’s disease remains levels, when the user will occasionally relive past memo-
unclear at this time. In contrast, Morton (2005) dis- ries. The new memories are often those that were sup-
agreed, suggesting that it was unlikely that society pressed because of the pain associated with the earlier
would be forced to deal with a generation of former experience (Hayner & McKinney, 1986). Thus, users
MDMA abusers who had developed premature Parkin- might find themselves reliving experiences they did not
son’s disease, raising questions as to the exact relation- want to remember. This effect, which many psychother-
ship between MDMA abuse and Parkinson’s disease in apists thought might be beneficial in the confines of the
later life. therapeutic relationship, may seem so frightening as to
MDMA-induced brain damage seems to be dose- be “detrimental to the the individual’s mental health”
related, with higher levels of impairment found in those (Hayner & McKinney, 1986, p. 343). Long-time use has
individuals who had ingested greater amounts of contributed to episodes of violence and on occasion to
MDMA. But animal evidence suggests that neurological suicide (“The Agony of ‘Ecstasy,’” 1994).
MDMA abuse might also result in such residual ef-
15See Glossary. fects as anxiety attacks, persistent insomnia, irritability,
rage reactions, and a drug-induced psychosis (Commis- Wirshing, & Friedman, 1993). Rochester and Kirchner
sion on Adolescent Substance and Alcohol Abuse, (1999) advised against using these agents as they might
2005; Gahlinger, 2004; Karch, 2002; McDowell, 2005). make control of blood pressure more difficult since the
The exact mechanism by which MDMA might cause a alpha-adrenergic system would remain unaffected. At
paranoid psychosis is not clear at this time (Karch, this time, the best treatment of MDMA-induced toxic-
2002). It is theorized that MDMA is able to activate a ity is thought to be supportive maintenance of normal
psychotic reaction in a person who has a biological pre- body temperature, airway, and cardiac function, and if
disposition for this disorder (McGuire & Fahy, 1991). necessary the judicious use of a benzodiazepine to con-
As the effects wane, users typically experience a depres- trol anxiety (Schuckit, 2006).
sive reaction that varies from mild to quite severe, last- Drug interactions involving MDMA. Little research
ing 48 hours or more (Gahlinger, 2004). has been done on the possible interactions between illicit
MDMA-related gastrointestinal problems. In Europe, drugs such as MDMA and pharmaceuticals (Concar,
where MDMA abuse is common, liver toxicity and 1997). There have been case reports of interactions
hepatitis have been reported in MDMA abusers. The between the antiviral agent Ritonavir18 and MDMA
exact relationship between the MDMA abuse and the (Concar, 1997; Harrington, Woodward, Hooton, &
development of liver problems is not clear, and it is pos- Horn, 1999). Each agent affects the serotonin level in
sible that these were idiosyncratic reactions in isolated the blood, and the combination of these two chemicals
individuals (Karch, 2002). Another possibility is that results in a threefold higher level of MDMA than nor-
the liver problems were induced by one or more con- mal, and some fatalities have been reported in users
taminants in the MDMA dose consumed by the user who have mixed these compounds (Concar, 1997).
(Cook, 1995; Grob & Poland, 2005; Henry, Jeffreys, &
Dawling, 1992; Henry & Rella, 2001; Jones, Jarvie,
McDermid, & Proudfoot, 1994).
Summary
Other MDMA-related physical problems. MDMA Weil (1986) suggested that people initially use chemicals
abuse can cause rhabdomyolysis,16 which appears to be to alter the normal state of consciousness. Hallucinogen
a consequence of the motor activity induced by or asso- use in this country, at least in the last generation, has fol-
ciated with the abuse of this compound (Gahlinger, lowed a series of waves, as first one drug and then an-
2004; Grob & Poland, 2005; Karch, 2002; Klein & other becomes the current drug of choice for achieving
Kramer, 2004; Sauret, Marinides, & Wang, 2002). this altered state of consciousness. In the 1960s, LSD was
MDMA abuse as cause of death. While fatalities in- the major hallucinogen, and in the 1970s and early
volving MDMA alone are rare, the potential danger for 1980s, it was PCP. Currently, MDMA seems to be gain-
abusers is increased if multiple agents are ingested ing in popularity as the hallucinogen of choice, although
(McDowell, 2004, 2005). This is not to say that MDMA research suggests that MDMA may cause permanent
abuse by itself is not without its dangers, and The Econo- brain damage, especially to those portions of the brain
mist (“Better than Well,” 1996) estimated that MDMA that utilize serotonin as a primary neurotransmitter.
causes one death for each 3 million doses ingested. One If we accept Weil’s (1986) hypothesis as correct, it is
such case was discussed by Kalantar-Zaden, Nguyen, logical to expect that other hallucinogens will emerge
Chang, and Kurtz, (2006); the authors summarized the over the years, as people look for a more effective way to
treatment of an otherwise healthy 20-year-old female alter their consciousness. One might expect that these
college student, who was found upon arrival in the hos- drugs will, in turn, slowly fade as they are replaced by
pital to have abnormally low sodium levels in her newer hallucinogenics. Just as cocaine faded from the
blood.17 In spite of aggressive medical care, the patient drug scene in the 1930s and was replaced for a time by
died about 12 hours after being admitted to the hospital. the amphetamines, so one might expect wave after
Physicians were once taught that ß-blocking agents wave of hallucinogen abuse, as new drugs become
(Beta blockers, ß-blockers, or Beta adrenergic block- available. Thus, chemical dependency counselors will
ers) were helpful in treating MDMA toxicity (Ames, have to maintain a working knowledge of an ever-
growing range of hallucinogens in the years to come.
16See Glossary.
17A 18Used in the treatment of HIV infections.
condition known as hyponatremia.
CHAPTER SIXTEEN
Abuse of and Addiction to

the Inhalants and Aerosols
The inhalants are unlike the other chemicals of abuse. practice of “glue sniffing” (Morton, 1987; Westermeyer,
They are toxic substances that include various cleaning 1987) in which the individual uses model airplane glue
agents, herbicides, pesticides, gasoline, kerosene, cer- as an inhalant. The active agent of model glue in the
tain forms of glue, lacquer thinner, and chemicals used 1950s was often toluene. Nobody knows how the prac-
in felt-tipped pens. These agents are not primarily in- tice of “glue sniffing” first started, but there is evidence
tended to function as recreational substances, but that it began in California when teenagers accidentally
when inhaled, many of the chemicals in these com- discovered the intoxicating powers of toluene-containing
pounds will alter the manner in which the user’s brain model glue (Berger & Dunn 1982). The first known
functions, possibly causing a sense of euphoria. reference to glue sniffing appeared in 1959, in the mag-
It is often possible for adolescents, and even children, azine section of a Denver newspaper (Brecher, 1972;
to purchase many agents that have the potential to be Sharp & Rosenberg, 2005). Local newspapers soon
abused by inhalation. For these reasons, children, adoles- began to carry stories on the dangers of inhalant abuse,
cents, or even the rare adult will occasionally abuse in the process explaining just how to use airplane glue
chemical fumes. Because these chemicals are inhaled, to become intoxicated and what effects to expect. Within
they are often called inhalants, or volatile substances a short time, a “Nationwide Drug Menace” (Brecher,
(Esmail, Meyer, Pottier, & Wright, 1993). In this text, 1972, p. 321) emerged in the consciousness of parents
the term inhalants will be used. The inhalation of volatile in the United States. Currently, inhalant abuse is
substances, or inhalants, has become a major concern in thought to be a worldwide problem (Brust, 1993) and
the European Union, where one in every seven adoles- is especially common in Japan and Europe (Karch,
cents in the 15- to 16-year age group abuses inhalants 2002).
(“Solvent Abuse Puts Teens at Risk,” 2003). Because
inhalants are so easily accessible to children and adoles-
cents, their abuse continues to be a major form of chemi-
The Pharmacology of the Inhalants
cal abuse for adolescents in the United States as well. Inhalation is one of the most effecient ways of introduc-
This chapter examines the problem of inhalant abuse. ing many compounds into the general circulation.
Physicians often utilize this characteristic to introduce
certain chemicals into the patient’s body for a specific
The History of Inhalant Abuse
purpose, such as the use of anesthetic gases during sur-
The use of inhaled substances to alter the user’s percep- gery. Unfortunately, inhalation is also popular for abus-
tion of reality might be traced back to ancient Greece ing many compounds for recreational purposes. In this
and the oracle at Delphi (Hernandez-Avila & Pierucci- context, inhalation is perhaps the most poorly re-
Lagha, 2005). More recently, the use of anesthetic searched area of medicine (McGuinness, 2006).
gasses for recreational purposes was popular in the 19th When a chemical is inhaled, it is able to enter the
century, and the modern era of inhalant abuse started in bloodstream without its chemical structure being al-
the 1920s when various industrial solvents became avail- tered in any way by the liver (Bruckner & Warren,
able (Commission on Adolescent Substance and Alcohol 2003). Once in the blood, the speed with which these
Abuse, 2005; Hernandez-Avila & Pierucci-Lagha, 2005; compounds reach the brain is determined by whether
Sharp & Rosenberg, 2005). the molecules can form chemical bonds with the lipids
By the mid-1950s and early 1960s, attention was in the blood. As a general rule, inhalants are quite lipid-
being paid by the media in the United States to the soluble (Bruckner & Warren, 2003; Crowley & Sakai,
194
Abuse of and Addiction to the Inhalants and Aerosols 195
2004; Hernandez-Avila & Pierucci-Lagha, 2005). Be- Even where there has been research into the effects
cause of this characteristic, inhalants can rapidly cross of a specific compound on the human body, it has only
the blood-brain barrier to reach the brain in an ex- rarely involved the concentrations of these agents at the
tremely short period of time, usually within seconds levels commonly used by inhalant abusers (Bruckner &
(Commission on Adolescent Substance and Alcohol Warren, 2003; Fornazzazri, 1988; Morton, 1987). For
Abuse, 2005; Crowley & Sakai, 2004; Hartman, 1995). example, the maximum permitted exposure to toluene
Crowley and Sakai (2005) grouped the inhalants fumes in the workplace is 50–100 parts per million (ppm)
into four categories: (1) solvents, (2) propellants for (Crowley & Sakai, 2005). But when abused, it is not
spray cans, (3) paint thinners, and (4) fuels. In contrast, uncommon for the individual to willingly use levels
Espeland (1997)1 suggested four different classes of in- 100 times as high as the maximum permitted industrial
halants: (1) volatile organic solvents such as those exposure level.
found in paint and fuel;2 (2) aerosols, such as hair To further complicate matters, abusers might use a
sprays, spray paints, and deodorants; (3) volatile nitrites compound in which the desired substance is a second-
(such as amyl nitrite or its close chemical cousin, butyl ary ingredient, thus exposing themselves to various
nitrite); and (4) general anesthetic agents such as ni- chemicals, including potential toxins, in addition to the
trous oxide. desired inhalant3 (Hernandez-Avila & Pierucci-Lagha,
It has been estimated that there are over 1,000 com- 2005). Although there is no single “pharmacology” of
mon household products that might be abused if the inhalants, many of these compounds do share common
fumes are inhaled (McGuinness, 2006). Feuillet, Mallet, toxicological characteristics. For example, many of the
and Spadari (2006) presented a case history of twin more common inhalants must be biotransformed by
sisters who were inhaling fumes produced by mothballs the liver before being elimated from the circulation by
after classmates encouraged them to do so for the the kidneys (Bruckner & Warren, 2003; Sharp &
“high.” Both girls suffered skin lesions, which at first Rosenberg, 2005). Other inhalants, such as the general
puzzled physicians until their abuse of the mothballs anesthetic gases, are exhaled without extensive biotrans-
was identified by staff, providing a rare example of the formation taking place (Brooks, Leung, & Shannon,
abuse of such substances through inhalation. Of the 1996; Crowley & Sakai, 2004).
four categories of inhalants identified above, children Scientists do not fully understand the mechanism by
and adolescents will most often abuse the first two which the inhalants alter the user’s brain function
classes of chemicals. They have limited access to the (Commission on Adolescent Substance and Alcohol
third category of inhalants, while the abuse of anesthet- Abuse, 2005; McGuinness, 2006), but they are thought
ics is usually limited to health care professionals who to alter the normal function of the membranes of the
have access to these compounds (Hernandez-Avila & neurons. There is preliminary evidence that the in-
Pierucci-Lagha, 2005). halants affect the gamma-amino-butyric acid (GABA)
Virtually no information is available about the ef- and/or the N-methyl-D-aspartate (NMDA) neurotrans-
fects of the inhalants at the cellular level (McGuinness, mitter systems (Crowley & Sakai, 2004). However, the
2006). Indeed, most of the compounds abused were effect of a specific inhalant on neuron function is de-
never intended for inhalation, so there was little incen- pendent on the exact compound being abused. Conse-
tive for the manufacturer to conduct research into these quently, there is no standard formula by which to
effects. And while information about the toxicology of estimate the biological or elimination half-lives of a spe-
inhalants in adults is limited, there is virtually no infor- cific inhalant since so many different chemicals are
mation available about the toxic effects of many of the abused. However, the half-life of most solvents tends to
commonly abuse compounds in children (Bruckner & be longer in obese abusers (Hartman, 1995). The elim-
Warren, 2003). ination half-life of the various compounds commonly
abused through inhalation might range from hours to
1Children and adolescents have only limited access to volatile ni-
days, depending on the exact chemicals being abused
trites, although butyl nitrite is sometimes sold without a prescription
in some states. Except in rare cases, the abuse of surgical anesthetics (Brooks et al., 1996).
is usually limited to a small percentage of health care workers, be- Either directly or indirectly, the compounds inhaled
cause access to anesthetic gases is carefully controlled. for recreational purposes are all toxic to the human
2Technically, alcohol might be classified as a solvent. However, since
3Forexample, nitrous oxide, the desired inhalant, is often used as a
the most common method of alcohol use/abuse is through oral inges-
tion, ethyl alcohol will not be discussed in this chapter. propellant for other compounds that are stored in a can.
196 Chapter Sixteen
body to one degree or another (Blum, 1984; Fornazzazri, abusing inhalants (Henretig, 1996). Physical depend-
1988; Morton, 1987). Behavioral observations of ani- ence on inhalants is quite rare, but it does occur, with
mals who have been exposed to inhalants suggest that about 4% of those who abuse inhalants becoming de-
many inhalants act like alcohol or barbiturates on the pendent on them (Crowley & Sakai, 2004). The prac-
brain (Commission on Adolescent Substance and Alco- tice of abusing inhalants appears to involve boys more
hol Abuse, 2005; Hernandez-Avila & Pierucci-Lagha, often than girls by a ratio of about 3:1 (Crowley &
2005). Indeed, alcohol and the benzodiazepines have Sakai, 2005). The most commonly abused compounds
been found to potentiate the effects of many inhalants appear to be spray paint and gasoline, which collec-
such as toluene. tively accounted for 61% of the compounds abused by
subjects in a study by Spiller and Krenzelok (1997).
Scope of the Problem Hernandez-Avila and Pierucci-Lagha (2005) identi-
fied four patterns of inhalant abuse:
Although the mass media in this country most often
focus on inhalant abuse in the United States, it is a
1. Transient social use: use for a brief period of time in
worldwide problem (Spiller & Krenzelok, 1997). In-
response to social situations where inhalant abuse is
halant abuse is growing in popularity, increasing by
accepted. Usually involves individuals 10 to 16 years
44% in sixth graders in recent years (“Huffing Can Kill
of age.
Your Child,” 2004). In the United States, there is evi-
2. Chronic social use: daily inhalant abuse for 5 or
dence that approximately equal numbers of boys and
more years. Usually involves individuals 20 to 30
girls are abusing inhalants, with roughly 4.5% of the
years of age who demonstrate evidence of brain
children/adolescents reporting the use of inhalants at
damage and who usually have minor legal problems.
some time in their lives (“Patterns and Trends in In-
3. Transient isolated use: a short history of inhalant use
halant Use,” 2007).
in isolation, usually involving individuals 10 to 16
More than 2 million people in the United States
years of age.
are thought to have abused an inhalant in the past
4. Chronic isolated use: a history of continuous solo
12 months, of whom 1.1 million are between 12 and
abuse of inhalants for 5 or more years. Usually found
17 years of age (“Agency: More Teens Abusing Inhalants,”
in persons 20 to 29 years of age with poor social
2005). Sixteen percent of the eighth graders and 11% of
skills, a history of serious legal problems, and possi-
high school seniors surveyed in 2006 admitted to having
bly evidence of brain damage.
abused an inhalant at least once (Anderson & Loomis,
2003; Johnston, O’Malley, Bachman, & Schulenberg,
Unfortunately, for a minority of those who abuse
2006a). This pattern of abuse suggests that inhalants are
them, the inhalants appear to function as a “gateway”
becoming increasingly popular with younger teens
chemical, the use of which seems to set the stage for
(“Agency: More Teens Abusing Inhalants,” 2005;
further drug use in later years. It has been found, for
Hernandez-Avila & Pierucci-Lagha, 2005).
example, that 23% of the children/adolescents who
Most adolescents who abuse inhalants will do so
abuse cocaine, alcohol, or marijuana began by abusing
only a few times and then stop without going on to de-
inhalants first (Worcester, 2006). Compared to the gen-
velop other drug use problems (Crowley & Sakai,
eral population, people who admitted to using in-
2005). Of the more than 2 million individuals who
halants were found to be 45 times as likely to have used
abused an inhalant in the past year, more than 1 mil-
self-injected drugs while those who admitted to both
lion did so for the very first time (“Agency: More Teens
the use of inhalants and marijuana were 89 times as
Abusing Inhalants,” 2005). The mean age of first time
likely to have injected drugs (Crowley & Sakai, 2005).
inhalant abuse is about 13 years (Anderson & Loomis,
2003), and the mean age of inhalant abusers is about
16.6 years (with a standard deviation of 7.3 years)
Why Are Inhalants So Popular?
(Spiller & Krenzelok, 1997). These statistics demon- The inhalants are utilized by children/adolescents for
strate that inhalant abuse is most popular in the 11– to several reasons. First, these chemicals have a rapid onset
15-year-old age group, after which it becomes less and of action, usually in a few seconds. Second, inhalant
less common (Commission on Adolescent Substance users report pleasurable effects, including a sense of
and Alcohol Abuse, 2005). However, while inhalant euphoria, disinhibition, and visual hallucinations in
abuse tends to be most common in adolescence, there response to these compounds (McGuinness, 2006).
are reports of children as young as 7 or 8 years of age Third, and perhaps most important, the inhalants are
relatively inexpensive and are easily available to chil- lucinations (Hernandez-Avila & Pierucci-Lagha, 2005;
dren or adolescents (Cohen, 1977). They offer a quick, Sharp & Rosenberg, 2005; Schuckit, 2000; Tekin &
cheap way to achieve a form of intoxication that is Cummings, 2003). Occasionally, the individual will
very similar to that of alcohol intoxication (Sharp & feel as if he or she is omnipotent, and episodes of agitation
Rosenberg, 2005). Virtually all of the commonly used and violence have been reported (Hernandez-Avila &
inhalants may be easily purchased, without legal re- Pierucci-Lagha, 2005).
strictions being placed on their sale to teenagers. An After the initial euphoria, central nervous system
additional advantage for the user is that the inhalant is (CNS) depression develops. The stages of inhalant abuse
usually available in small, easily hidden packages. are summarized in Figure 16.1. Many inhalant abusers
Unfortunately, many of the inhalants are capable of experience an inhalant-induced hangover lasting from a
causing harm to the user, and sometimes death. In- few minutes to a few hours (Sharp & Rosenberg, 2005),
halant abusers thus run a serious risk whenever they although in rare cases it might last for several days
begin to “huff.”4 (Heath, 1994). Abusers also report a residual sense of
drowsiness and/or stupor, which will last for several hours
Method of Administration after the last use of inhalants (Commission on Adoles-
cent Substance and Alcohol Abuse, 2005; Kaplan,
Inhalants can be abused in several ways depending on
Sadock & Grebb, 1994; Sharp & Rosenberg, 2005).
the specific chemical involved. Some compounds may
be inhaled directly from the container, a practice called
“sniffing” or “snorting” (Anderson & Loomis, 2003).
Others, such as glue and adhesives, may be poured into Stage 1
a plastic bag, which is then placed over the mouth and
nose so that the individual can inhale the fumes, a prac- Sense of euphoria,
visual and/or auditory
tice called “bagging” (Anderson & Loomis, 2003; Esmail hallucinations, and
et al., 1993; Nelson, 2000). Sometimes, the compound excitement
is poured into a rag that is then placed over the individ-
ual’s mouth and nose, a practice is called “huffing”
(Anderson & Loomis, 2003; Nelson, 2000).
Fumes from aerosol cans may also be directly in- Stage 2
haled or sprayed straight into the mouth, according
Esmail et al. (1993). Finally, there have been reports of Confusion, disorientation,
loss of self-control,
users attempting to boil the substance to be abused so blurred vision, tinnitus,
they could inhale the fumes (Nelson, 2000). Obviously, mental dullness
if the substance being boiled is flammable, there is a
significant risk of fire if the compounds should ignite.
Subjective Effects of Inhalants Stage 3
The initial action of an inhalant begins within seconds Sleepiness, ataxia,

to minutes and lasts for up to 45 minutes (Schuckit, diminished reflexes,
nystagmus
2000; Zevin & Benowitz, 2007). The desired effects in-
clude a sense of hazy euphoria somewhat like the feel-
ing of intoxication caused by alcohol (Anderson &
Loomis, 2003; Crowley & Sakai, 2005; Henretig, 1996;
Sharp & Rosenberg, 2005). As is true with alcohol in-
toxication, inhalant abusers also experience behavioral Stage 4
disinhibition, although it is not clear whether this is a Seizures, EEG changes
desired effect (Zevin & Benowitz, 2007). noted on examination,
Some of the undesirable effects of inhalant abuse in- paranoia, bizarre behavior,
tinnitus; possible death of
clude nausea and vomiting, amnesia, slurred speech, inhalant user
excitement, double vision, ringing in the ears, and hal-
4
See Glossary. FIGURE 16.1 The Stages of Inhalant Intoxication
198 Chapter Sixteen
Complications From Inhalant Abuse The impact of the inhalants on the central nervous
system (CNS) is perhaps the most profound effect, if
When the practice of abusing inhalants first surfaced, only because inhalant abusers are usually so young.
most health care professionals did not think it had Many of the inhalants have been shown to cause dam-
many serious complications. However, in the last quar- age to this system, producing such problems as cerebel-
ter of the 20th century, researchers uncovered evidence lar ataxia,7 nystagmus, tremor, peripheral neuropathies,
that inhalant abuse might cause a wide range of physi- memory problems, coma, optic neuropathy, and deaf-
cal problems. Depending on the concentration and the ness (Anderson & Loomis, 2003; Brooks et al., 1996;
compound being abused, even a single episode of abuse Crowley & Sakai, 2005; Maas, Ashe, Spiegel, Zee, &
might result in the user’s developing symptoms of solvent Leigh, 1991; Sharp & Rosenberg, 2005). There is a re-
toxicity or death (Worcester, 2006). lationship between inhalant abuse and the develop-
Below is a partial list of the possible consequences of ment of a condition similar to Parkinson’s disease
inhalant abuse: (Zevin & Benowitz, 2007). One study found that 44%
of chronic inhalant abusers had abnormal magnetic
Liver damage resonance imaging (MRI) results, compared with just
Cardiac arrhythmias5 25% of chronic cocaine abusers (Mathias, 2002). In-
Kidney damage/failure, which may become perma- halants can also cause a dementia-like process, even in
nent the very young child (Filley, 2004).
Inhalant abuse can lead to death after the first use of
Transient changes in lung function one of these compounds, or the 200th time it is abused
Anoxia and/or respiratory depression possibly to the (“Huffing Can Kill Your Child,” 2004). Some of the
point of respiratory arrest mechanisms by which inhalant abuse can immedi-
Reduction in blood cell production possibly to the ately kill the abuser include sudden cardiac death and
point of aplastic anemia suffocation/asphyxiation (Worcester, 2006). Approxi-
mately 50% of inhalant-related deaths are the result
Possible permanent organic brain damage (includ- of ventricular fibrillation, or sniffing death syndrome
ing dementia and inhalant-induced organic psy- (McGuinness, 2006).
chosis) Depending on the compounds being abused, there
Permanent muscle damage secondary to the devel- is a very real danger that the abuser might be exposed to
opment of rhabdomyolysis6 toxic levels of various heavy metals such as copper or
Vomiting, with the possibility of the user aspirating lead, which can have lifelong consequences for the in-
some of the material being vomited, resulting in his dividual (Crowley & Sakai, 2005). Prior to the intro-
or her death (Crowley & Sakai, 2004, 2005; Filley, duction of unleaded gasoline, the practice of using
2004; Sharp & Rosenberg, 2005; Anderson & gasoline as an inhalant was a significant source of
Loomis, 2003; Karch, 2002; Zevin & Benowitz, childhood exposure to lead, and while this compound
2007) is no longer included in gasoline in the United States,
it is still a leading source of lead poisoning in other
In addition to these, inhalant abuse might also cause countries.
damage to the bone marrow, sinusitis (irritation of the Further, although the standard neurological exami-
sinus membranes), erosion of the nasal mucosal tissues, nation is often unable to detect signs of solvent-induced
and laryngitis (Crowley & Sakai, 2004; Henretig, 1996; organic brain damage until it is quite advanced, sensitive
Westermeyer, 1987). The user might develop a cough neuropsychological tests often find evidence of signifi-
or wheezing, and those prone to asthma may experi- cant neurological dysfunction in workers who are ex-
ence an exacerbation of this condition (Anderson & posed to solvent fumes on a regular basis (Hartman,
Loomis, 2003). Inhalant abuse can also produce chem- 1995). Toluene is found in many forms of glue and is the
ical burns and frostbite on the skin, depending on the solvent that is most commonly abused (Hernandez-Avila
exact compound being abused (Anderson & Loomis, & Pierucci-Lasha, 2005). Researchers have found that
2003; Hernandez-Avila & Pierucci-Lagha, 2005). chronic toluene exposure might result in intellectual
impairment (Crowley & Sakai, 2004; Maas et al., 1991).
5See Glossary.
6See 7See Glossary.
Glossary.
Finally, researchers have identified what appears (Hernandez-Avila & Peirucci-Lagha, 2005). There is a
to be an inhalant withdrawal syndrome that is very dose-related range of effects from the anesthetic rang-
similar to the alcohol-induced delirium tremens ing from an initial period of sedation and relief from
(DTs) (Hernandez-Avila & Pierucci-Lasha, 2005; Mirin, anxiety on through sleep and analgesia. At extremely
Weiss, & Greenfield, 1991). This withdrawal syndrome high dosage levels, the anesthetic gases can cause death.
depends on the specific chemicals being abused, the du- Nitrous oxide. One of the most commonly abused
ration of inhalant abuse, and the dosage levels being uti- anesthetic gases is nitrous oxide. It presents a special
lized (Miller & Gold, 1991b). Some symptoms of danger as special precautions must be observed to
inhalant withdrawal include muscle tremors, irritability, maintain a proper oxygen supply to the individual’s
anxiety, insomnia, muscle cramps, hallucinations, sweat- brain. Room air alone will not provide sufficient oxy-
ing, nausea, foul odor on the user’s breath, loss of vision, gen to the brain when nitrous oxide is used (Sharp &
and possible seizures (Crowley & Sakai, 2005; Worcester, Rosenberg, 2005), and oxygen must be supplied under
2006). pressure to avoid the danger of hypoxia (a decreased
Inhalant abuse and suicide. Inhalant abuse is oxygen level in the blood that can result in permanent
correlated with depression and suicidal behavior brain damage if not corrected immediately). In surgery,
(McGuinness, 2006). Espeland (1997) found a disturb- the anesthesiologist takes special precautions to ensure
ing relationship between inhalant abuse and adoles- that the patient has an adequate oxygen supply. How-
cent suicide. The author suggested that some suicidal ever, few nitrous oxide abusers have access to supple-
adolescents might actually put an inhalant into a plastic mental oxygen sources, and thus they run the risk of
bag and then put their heads into the bag. When the serious injury or even death when they abuse this
plastic bag is closed around the head/neck area, the in- compound.
halant causes the individual to lose consciousness and It is possible to achieve a state of hypoxia from virtu-
quickly suffocate, as the oxygen in the bag is used up; ally any of the inhalants, including nitrous oxide
unless the person is found quickly, he or she will die. In (McHugh, 1987). Nitrous oxide abusers report that the
such cases, it is quite difficult to determine whether the gas is able to bring about feelings of euphoria, giddi-
individual intended to end his or her own life or if the ness, hallucinations, and a loss of inhibitions (Lingeman,
death was an unintended side effect of the method by 1974). Dental students, dentists, medical school stu-
which the inhalant was abused. dents, and anesthesiologists, all of whom have access to
surgical anesthetics through their professions, will oc-
casionally abuse agents such as nitrous oxide as well as
Anesthetic Misuse ether, chloroform, trichlorothylene, and halothane.
Nitrous oxide and ether, the first two anesthetic gases to Also, children and adolescents will occasionally abuse
be used, were first introduced as recreational drugs prior nitrous oxide used as a propellant in certain commer-
to their introduction as surgical anesthetics (Hernandez- cial products by finding ways to release the gas from the
Avila & Pierucci-Lasha, 2005). Horace Wells, who intro- container. In rare cases, the nitrous oxide abuser might
duced medicine to nitrous oxide, noted the pain-killing even make his or her own nitrous oxide, risking possible
properties of this gas when he observed a person under death from impurities in the compound produced
its influence trip and gash his leg without any apparent (Brooks et al., 1996).
pain (Brecher, 1972). As medical historians know, the The volatile anesthetics are not biotransformed to
first planned demonstration of nitrous oxide as an anes- any significant degree but enter and leave the body es-
thetic was something less than a success. Because ni- sentially unchanged (Glowa, 1986). Once the source of
trous oxide has a duration of effect of about 2 minutes the gas is removed, the concentration of the gas in the
following a single dose and thus must be continuously brain begins to drop and the circulation brings the
administered, the patient returned to consciousness in brain to a normal state of consciousness within mo-
the middle of the operation, and started to scream in ments. While the person is under the influence of the
pain. However, in spite of this rather frightening begin- anesthetic gas, however, the ability of the brain cells to
ning, physicians began to understand how to use nitrous react to painful stimuli seems to be reduced.
oxide properly to bring about surgical anesthesia, and it The medicinal use of nitrous oxide, chloroform, and
is now an important anesthetic agent (Brecher, 1972). ether are confined, for the most part, to dental or gen-
The pharmacological effects of the general anes- eral surgery. Very rarely, however, one will encounter a
thetics are very similar to those of the barbiturates person who has abused or is currently abusing these
200 Chapter Sixteen
agents. There is little information available concerning headache; increased pressure of the fluid in the eyes (a
the dangers of this practice, nor is there much informa- danger for those with glaucoma); possible weakness;
tion as to the side effects of prolonged use. nausea; and possible cerebral hemorrhage (Schwartz,
1989).
When abused, both amyl nitrite and butyl nitrite
Abuse of Nitrites will cause a brief (90-second) “rush,” that includes
Two different forms of nitrites are commonly abused: dizziness, giddiness, and the rapid dilation of blood ves-
amyl nitrite, and its close chemical cousins butyl nitrite sels in the head (Schwartz, 1989), which in turn causes
and isabutyl nitrite. When inhaled, these substances an increase in intracranial pressure (“Research on Ni-
function as coronary vasodilators, allowing more blood trites Suggests,” 1989). It is this increase in intracranial
to flow to the heart. This effect made amyl nitrite useful pressure that may, on occasion, contribute to the rup-
in the control of angina pectoris. The drug was admin- ture of unsuspected aneurysms, causing the individual
istered in small glass containers, embedded in cloth to suffer a cerebral hemorrhage (a CVA, or stroke).
layers. The user would “snap” or “pop” the container The nitrites suppress the activity of the body’s im-
with his or her fingers and inhale the fumes to control mune system, especially the natural killer cells, increas-
the chest pain of angina pectoris.8 ing the individual’s vulnerability to various infections
With the introduction of nitroglycerine prepara- (Hernandez-Avila & Pierucci-Lagha, 2005). Given the
tions, which are as effective as amyl nitrite but lack multitude of adverse effects associated with inhalant
many of its disadvantages, amyl nitrite fell into disfavor abuse, one is left with the question as to why it is popular.
and few people now use it for medical purposes
(Hernandez-Avila & Pierucci-Lasha, 2005). It does con- Summary
tinue to have a limited role in diagnostic medicine and
the medical treatment of cyanide poisoning. For many individuals, the inhalants are the first chemi-
While amyl nitrite is available only by prescription, cals abused. Inhalant abuse seems to involve mainly
butyl nitrite and isabutyl nitrite are often sold legally by teenagers, although occasionally children will abuse an
mail-order houses or in speciality stores, depending on inhalant. Inhalant use appears to be a phase and the in-
specific state regulations. In many areas, butyl nitrite is dividuals will generally abuse them on an episodic
sold as a room deodorizer, being packaged in small basis.
bottles that may be purchased for under $10. Both Individuals who use these inhalants usually do so for
chemicals are thought to cause the user to experience a no more than 1 or 2 years, but a few continue to inhale
prolonged, more intense orgasm when they are inhaled the fumes of gasoline, solvents, certain forms of glue, or
just before the individual reaches orgasm. However, other compounds for many years. The effects of these
amyl nitrite is also known to be a cause of delayed or- chemicals seem to be rather short-lived. There is evi-
gasm and ejaculation in the male user (Finger, Lund, & dence, however, that prolonged use of certain agents
Slagel, 1997). Aftereffects include an intense, sudden can result in permanent damage to the kidneys, brain,
and liver. Death, either through hypoxia or through
8
It was from the distinctive sound of the glass breaking within the cloth
prolonged exposure to inhalants, is possible. Very little
ampule that both amyl nitrite and butyl nitrite have come to be known is known about the the effects of prolonged use of this
as “poppers” or “snappers” by those who abuse these chemicals. class of chemicals.
CHAPTER SEVENTEEN
The Unrecognized Problem

of Steroid Abuse and Addiction
The anabolic steroids, which are also classified as their physical appearance. To this end, a whole industry
anabolic-androgenic steroids, are members of a group of has evolved to help people modify their physical appear-
compounds that share a basic element in their chemical ance so they might better approximate the social ideal of
structure.1 Members of this group of compounds include size, shape, and appearance deemed acceptable by their
progesterone, adrenocortical hormones,2 bile acids, culture. Both subgroups abuse the same compounds, the
some poisons produced by toads, and some carcino- steroids, in the hopes of achieving their desired goals.
genic3 compounds. The abuse potential of some of these In response to an ever-growing number of adverse re-
compounds, such as poisons produced by certain species actions to these compounds, federal and state officials
of toads, is virtually nonexistent. However, it has been placed rigid controls on their use in the 1990s.5 How-
discovered that the anabolic-androgenic steroids can ever, the rumors of and abuse of these compounds con-
affect the development of muscle mass, a feature that tinue. Some of the reasons for the continued abuse of
made these compounds attractive to certain subcultures. steroids are discussed later in this chapter. But given the
They have become part of a poorly understood phenom- scope of the problem and the potential for these com-
enon: the abuse of certain compounds not to produce pounds to harm the user, it is important for the coun-
euphoria but to improve athletic performance. selor to have a working knowledge of steroid abuse.
Because of this potential, the anabolic-androgenic
steroids4 have become a manifestation of a social dis- An Introduction to the
ease. Society places so much emphasis on appearances Anabolic-Androgenic Steroids
and winning that many people, including athletes, look
for something—anything—that will give them an edge The term anabolic refers to the action of this family of
over the competition. This might include the use of drugs to increase the speed of growth of body tissues
certain coaching techniques, special equipment, diets, (Redman, 1990), or to the ability of this group of chem-
or the use of a chemical substance designed to enhance icals to force body cells to retain nitrogen (and thus in-
performace. For decades persistent rumors have circu- directly enhance tissue growth) (Bagatell & Bremner,
lated that the anabolic steroids are able to significantly 1996). The term androgenic indicates that these com-
enhance athletic performance or physical appearance pounds are chemically similar to testosterone, the male
(Dickensheets, 2001). These rumors are fueled by real sex hormone. Because of the chemical similarity with
or suspected use of a steroid by different athletes or teams. testosterone, steroids have a masculinizing (androgenic)
An “arms race mentality” (Joyner, 2004, p. 81) emerged, effect upon the user (Pope & Brower, 2004). Thus the
in which nonabusing athletes came to believe that their term anabolic-androgenic steroids.
only hope of success lay in the use of the same chemi-
cals they thought their competitors were abusing: ana- Medical Uses of Anabolic Steroids
bolic steroids.
Although the anabolic steroids have been in use since
Other people use these steroids not to improve athletic
the mid-1950s, there still is no clear consensus on how
performance but to change real or perceived deficits in
5In response to these controls, a $4 billion a year industry has devel-
1Technicallya hydrogenated cyclopentophenanthrine ring.
2Also known as corticosteroids.
oped in what are known as “nutritional” supplements; these are com-
posed of various combinations of amino acids, vitamins, proteins, and
3
See the term carcinogen in the Glossary. naturally occurring simulants such as ephedrine (Solotaroff, 2002).
4Inthis chapter, these compounds will be referred to as steroids or an- As is true of the anabolic steroids, the consequences of long-term use
abolic steroids. of many of these compounds at high dosage levels are not known.
201
202 Chapter Seventeen
they work (Wadler, 1994). There are few approved uses this observation, it should not be surprising that many
for these compounds (Dobs, 1999; Pope & Brower, 2005; nonathletic steroid abusers believe that these drugs will
Sturmi & Diorio, 1998). Physicians prescribe some help them look more physically attractive (Kanayama
members of the steroid family6 of compounds to pro- et al., 2006; Pope & Brower, 2004, 2005).
mote tissue growth and help damaged tissue recover In addition, there is a subgroup of people, especially
from injury (Wilson, Shannon, Shields, & Stang, 2007). some law enforcement/security officers, who will abuse
Physicians also prescribe certain steroids to treat specific anabolic steroids because of their belief that the drugs
forms of anemia, help patients regain weight after peri- will increase their strength and aggressiveness (Corrigan,
ods of severe illness, and treat endometriosis. 1996; Eisenberg & Galloway, 2005; Galloway, 1997).
Physicians also utilize some members of the steroid Another subgroup of steroid abusers uses these com-
family of compounds to treat delayed puberty in adoles- pounds in the belief that they will improve their physi-
cents and as an adjunct to the treatment of certain cal appearance. One such group is composed of adoles-
forms of breast cancer in women (Bagatell & Bremner, cent girls who abuse these compounds in the mistaken
1996; Congeni & Miller, 2002). The steroids may also belief that they will help them reduce body fat and look
promote the growth of bone tissue following injuries to more “toned” or attractive (“Girls Are Abusing Steroids,
the bone in certain cases and might be useful in the Too,” 2005).
treatment of specific forms of osteoporosis (Congeni &
Miller, 2002). There is evidence that steroid compounds
The Legal Status of Anabolic Steroids
might be of value in treating AIDS-related weight loss
(the so-called wasting syndrome) and certain forms of Since 1990, anabolic steroids have been classified as a
chronic kidney failure (Dobs, 1999). As this list suggests, Category III controlled substance.7 Some 28 different
these compounds are quite powerful and useful in the chemical compounds in the anabolic steroid group
treatment of disease. have been classified as being illegal substances, and
their use for nonmedical purposes and their sale by in-
dividuals who are not licensed to sell medications was
Why Steroids Are Abused made a crime punishable by a prison term of up to 5 years
Repeated, heavy physical exercise can actually result in (10 years if the steroids are sold to minors) (Fultz, 1991).
damage to muscle tissues. Athletes abuse steroids be-
cause they are thought to (a) increase lean muscle Scope of the Problem of Steroid Abuse
mass, (b) increase muscle strength, and (c) reduce the
period of time necessary for recovery between exercise Anabolic steroid abuse is a silent epidemic, and even
periods (Karch, 2002). On occasion, they may be abused the true scope of the problem in the United States is
because of their ability to bring about a sense of eu- not known (Eisenberg & Galloway, 2005; Karch, 2002).
phoria (Eisenberg & Galloway, 2005; Hildebrandt, It is thought that males are more likely to abuse steroids
Langenbucher, Carr, Sanjuan, & Park, 2006; Johnson, than females, possibly by as much as a 13:1 ratio, in part
1990; Kashkin, 1992; Schrof, 1992). However, this is because few adolescent girls are interested in adding
not the primary reason that most people abuse the ana- muscle mass (Kenayama et al., 2006; Pope & Brower,
bolic steroids. 2004). Another disturbing trend is that of younger adoles-
Many anabolic steroid abusers develop a condition cent athletes turning to these compounds to both im-
identified as a “reverse anorexia nervosa” (Kanayama, prove appearance and improve athletic ability (Calfee &
Barry, Hudson, & Pope, 2006, p. 697), in which they Fadale, 2006).
become preoccupied with body image, and express a It is estimated that there are 400,000 current abusers
fear that they might look “small” to others. It is not clear of anabolic steroids in the United States, and that at least
whether the individual’s abuse of anabolic steroids 1 million people have abused a steroid at some time in
caused this condition, or whether body image problems their lives (Kanayama et al., 2006; Pope & Brower,
predated (and possibly contributed to) the abuse of the 2005). An estimated 3% to 11% of high school students
steroids, but body image disorders are common to ana- in the United States are thought to have abused steroids
bolic steroid abusers (Kanayama et al., 2006). Given at some point in their lives (Kanayama et al., 2006) and
in some parts of the United States between 5% and 7%
6Remember, the anabolic steroids are members of a large family of
related compounds. 7See Appendix Four.
The Unrecognized Problem of Steroid Abuse and Addiction 203
of high school or middle school girls admit to the use of without their steroid abuse being detected or even sus-
steroids at least once (“Girls Are Abusing Steroids, pected (Mahoney, 2006). Even the team physician
Too,” 2005). In contrast to the other recreational chem- might not suspect the steroid abuse by the team’s star
icals, steroids do not seem to become popular as drugs players. This is because most physicians receive little
of abuse until early adulthood. The median age for ana- training in the recognition or treatment of anabolic
bolic steroid abusers is 18 (Karch, 2002). Most college- steroid abuse (Pope & Brower, 2005). Some physicians
aged steroid users did not begin to use these compounds will attempt to limit their patient’s use of anabolic
until just before or just after they entered college (Brower, steroids, promising to prescribe medications for the in-
1993; Dickensheets, 2001). dividual if he or she will promise only to use the med-
ications prescribed by the physician (Breo, 1990). This
Pharmacology of Anabolic-Androgenic misguided attempt at “harm reduction”8 is made by the
physician in the belief that he or she would then be
Steroids
able to monitor and control the individual’s steroid use.
Steroids are thought to force the body to increase protein However, in most cases the user supplements the pre-
synthesis as well as inhibit the action of chemicals known scribed medications with steroids from other sources.
as the glucocorticoids, which cause tissue to break down. Thus, this method of harm reduction is not recom-
These compounds fall into two classes: (a) those that are mended for physicians (Breo, 1990).
active when used orally, and (b) those that are active only Rarely, users will obtain their steroids by diverting9
when injected into muscle tissue. Anabolic steroids in- prescribed medications or by obtaining multiple pre-
tended for oral use tend to be more easily administered scriptions for steroids from different physicians. But be-
but have a shorter half-life and are also more toxic to the tween 80% (Bahrke, 1990) and 90% (Tanner, 1995) of
liver than parenteral (see Chapter 6) forms of steroids the steroids used by athletes comes from the “black
(Bagatell & Bremner, 1996; Tanner, 1995). market,”10 with many of the steroids smuggled into the
The anabolic steroids have been found to stimulate United States coming from the former Soviet Union
protein synthesis, a process that indirectly will help (Karch, 2002). Various estimates of the scope of the il-
muscle tissue development, possibly increase muscle licit steroid market in the United States range from
strength, and limit the amount of damage done to muscle $100 million (DuRant, Rickert, Ashworth, Newman, &
tissues through heavy physical exercise (Congeni & Slavens, 1993; Middleman & DuRant, 1996) to $300–
Miller, 2002; Gottesman, 1992; Pettine, 1991; Pope & $500 million (Fultz, 1991; Wadler, 1994) to $1 billion a
Katz, 1990). year (Hoberman & Yesalis, 1995).
There are more than 1,000 known derivatives of the
Sources and Methods of Steroid Abuse testosterone molecule (Sturmi & Diorio, 1998). Be-
cause performance-enhancing drugs are prohibited in
Because of their illegal status and strict controls on many sports, chemists will attempt to alter the basic
their being prescribed by physicians, most anabolic testosterone molecule to develop a designer steroid that
steroids are obtained from illicit sources (Eisenberg & might not be found with the current tests used to detect
Galloway, 2005; Galloway, 1997). These sources in- such compounds. An example of such a designer steroid
clude drugs smuggled into the United States and legiti- is tetrahydrogestrinone (THG). This compound appears
mate pharmaceuticals that are diverted to the black to have “all the hallmarks of an anabolic steroid, crafted
market. There is also a thriving market for what are to escape detection in urinanalysis tests” (Kondro, 2003,
known as designer steroids (Knight, 2003, p. 114), p. 1466). THG was undetectable by standard urine
which are not detected by standard laboratory tests uti- tests until late 2003. Acting on an anonymous tip and a
lized by sports regulatory agencies. Another common syringe, the Olympic Analytical Laboratory in Los An-
source of steroids is veterinary products, which are then geles developed a test that would detect this steroid in
sold on the street for use by humans. These compounds the urine of athletes. Armed with the new test, various
are distributed through an informal network that fre- regulatory agencies have conducted urine toxicology
quently is centered around health clubs or gyms and
are relatively easy to obtain (Eisenberg & Galloway, 8See Glossary.
2005; Mahoney, 2006; Schrof, 1992). 9See Glossary.
In contrast to alcohol/drug abusers, anabolic steroid 10
As used here, black market is any illicit source from which a steroid
abusers are often rewarded for their physical performance is obtained and then sold for human consumption.
tests on samples provided by athletes in various fields, 2004; Porcerelli, & Sandler, 1998). Some steroid abusers
prompting a flurry of reports that various athletes had who engage in the pyramiding are, at the midpoint of
tested positive for this performance-enhancing com- the cycle, using massive doses of one or more com-
pound, were suspected of having abused it, or were about pounds. Episodes of pyramiding are interspaced with
to be suspended for having submitted a urine sample periods of abstinence from anabolic steroid use that may
that had traces of THG in it (“Athletes Caught Using,” last several weeks or months (Landry & Primos, 1990),
2003; Knight, 2003). or perhaps even as long as a year (Kashkin, 1992). Un-
Anabolic steroids may be injected into muscle tissue fortunately, during the periods of abstinence, much of the
or taken orally; sometimes both intramuscular and oral muscle mass gained by the use of steroids will be lost,
doses of the medication are used at the same time. Ana- sometimes quite rapidly. When this happens, anabolic
bolic steroid abusers have developed a vocabulary of steroid abusers often become frightened into prema-
their own to describe many aspects of steroid abuse, the turely starting another cycle of steroid abuse to recap-
most common of which are summarized in Table 17.1. ture the muscle mass that has disappeared (Corrigan,
Many of the practices discussed in Table 17.1 are 1996; Schrof, 1992; Tanner, 1995).
quite common among steroid abusers. For example,
fully 61% of steroid-abusing weight lifters were found to
have engaged in the practice of “stacking” steroids Understanding the Risks
(Brower, Blow, Young, & Hill, 1991; Pope & Brower, of Anabolic Steroid Abuse
Numerous adverse effects of members of the steroid
TABLE 17.1 Some Terms Associated With Steroid Abuse family of compounds have been documented at the rel-
atively low dosage levels utilized when these medica-
Term Definition tions are used to treat medical conditions for short
periods of time (Hough & Kovan, 1990). The potential
Blending Mixing different compounds for use at
consequences of long-term steroid abuse are not known
the same time.
(Porcerelli, & Sandler, 1998; Wadler, 1994). At recom-
Bulking up Increasing muscle mass through steroid mended dosage levels, steroids can cause sore throat or
use. Nonusers also use the term to fever, vomiting (with or without blood being mixed into
refer to the process of eating special the vomit), dark-colored urine, bone pain, nausea, un-
diets and exercising to add muscle
usual weight gain, headache, and a range of other side
mass before a sporting event such as a
effects (Congeni & Miller, 2002).
football game or race.
Unfortunately, many steroid abusers utilize dosage
Cycling Taking multiple doses of a steroids over levels that are 10 (Hough & Kovan, 1990), 40–100
a period of time, according to a (Congeni & Miller, 2002), 200 (Eisenberg & Galloway,
schedule, with drug holidays built into
2005), or even 1,000 times (Council on Scientific Affairs,
the schedule.
1990; Wadler, 1994) the maximum recommended
Doping Using drugs to improve performance. therapeutic dosage level for these compounds. There is
Injectables Steroids that are designed for injection. very little information available on the effects of the
anabolic steroids on the user at these dosage levels
Megadosing Taking massive amounts of steroids,
(Johnson, 1990; Kashkin, 1992).
usually by injection or a combination
of injection and oral administration. The effects of the anabolic steroids on muscle tissue
are known to last for several weeks after the drugs are
Orals Steroids designed for oral use. discontinued (Pope & Katz, 1991). This characteristic
Pyramiding Taking anabolic steroids according to a is known to muscle builders, who often discontinue
schedule that calls for larger and larger their use of steroids shortly before competition to avoid
doses each day for a period of time, the danger of having their steroid use detected by urine
followed by a pattern of smaller doses toxicological screens, or who attempt to find a
each day. performance-enhancing drug that cannot be detected
Shotgunning Taking steroids on an inconsistent basis. by standard blood/urine tests (Knight, 2003). This re-
Tapering Slowly decreasing the dosage level of a flects the ongoing “arms race” between steroid abusers
steroid being abused. and regulatory agencies. The former search for anabolic
steroids or similar compounds that cannot be detected
by testing, while the latter search for new methods by permanent (Volkow, 2006b). Unfortunately, many of the
which unauthorized steroid use might be detected. A other masculinization effects of steroids on women do
good example is the controversy over tetrahydrogestri- not reverse themselves when these compounds are dis-
none (THG) that erupted in late 2003 (discussed ear- continued (Pope & Brower, 2005; Volkow, 2006b). Thus,
lier in this chapter). Thus, a “clean” urine sample does the woman who abuses an anabolic steroid might expe-
not rule out steroid use in modern sporting events, or rience permanent male-pattern baldness that is irre-
the possibility that the individual is at risk for any of a versible (Tanner, 1995).
wide range of complications. Effects on the liver, kidneys, and digestive systems.
In general, the adverse effects of anabolic steroids Steroid abusers may experience altered liver function,
depend on the (a) route of administration used, (b) the which may be detected through blood tests such as the
specific compounds utilized, (c) the dosage levels, (d) serum glautamic-oxaloacetic transaminase (SGOT)
the frequency of use, (e) the health of the individual, and the serum glautamic-pyruvic transaminase (SGPT)
and (f) the age of the individual (Johnson, 1990). Un- (Johnson, 1990; Karch, 2002; Sturmi & Diorio, 1998).
fortunately, many steroid abusers view themselves as Oral forms of anabolic steroids might be more likely to
being at least the equal of—if not more knowledgeable result in liver problems than injected forms (Tanner,
than—physicians about the adverse effects of steroids 1995). Anabolic steroid abuse has been implicated as a
and will attempt to control the adverse effects of their cause of hepatoxicity12 (Kanayama et al., 2006; Pope &
steroid abuse without seeking medical treatment Brower, 2004, 2005; Stimac, Milic, Dintinjana, Kovac, &
(Hildebrandt et al., 2006). Ristic, 2002). In addition, there is evidence that when
used for periods of time at excessive doses, steroids
might contribute to the formation of both cancerous
Complications of Steroid Abuse and benign liver tumors (Eisenberg & Galloway, 2005;
Karch, 1996; Pope and Brower, 2005; Sturmi & Diorio,
Effects on the reproductive system. Males who utilize 1998; Tanner, 1995).
steroids at the recommended dosage levels might experi- Effects on the cardiovascular system. Anabolic steroids
ence enlargement of breasts11 (to the point that breast tis- are abused mainly by those who wish to increase
sue formation similar to that seen in adolescent girls muscle size. Unfortunately, the heart is itself a muscle,
takes place). The male steroid abuser might also experi- and it is affected by steroid use (“Steroids and Growth
ence increased frequency of erections or continual erec- Hormones,” 2003). Anabolic steroid abuse may cause
tions (a condition known as priapism, which is a medical hypertension, cardiomyopathy, myocardial infarction,
emergency), unnatural hair growth or loss, reduced or chronic heart disease (Eisenberg & Galloway, 2005).
sperm production, and a frequent urge to urinate. Male One mechanism for these effects is a steroid-induced
steroid abusers might experience a degeneration of the reduction in high-density lipoprotein levels and a con-
testicles, enlargement of the prostate gland, difficulty in current increase in the low-density lipoprotein levels by
urination, impotence, and sterility (Blue & Lombardo, up to 36%, contributing to accelerated atherosclerosis
1999; Eisenberg & Galloway, 2005; Galloway, 1997; of the heart and its surrounding blood vessels (Blue &
Pope & Brower, 2004, 2005; Schuckit, 2006; Sturmi & Lombardo, 1999; Kanayama et al., 2006; Pope & Brower,
Diorio, 1998). On rare occasions steroid abuse has re- 2005; Tanner, 1995).
sulted in carcinoma (cancer) of the prostate (Pope & Anabolic steroid abuse might also result in the user’s
Brower, 2005; Tanner, 1995). Both men and women experiencing a thrombotic stroke—a stroke caused by a
might experience infertility and changes in libido as a re- blood clot in the brain (Karch, 2002; Tanner, 1995).
sult of steroid abuse (Sturmi & Diorio, 1998). Such strokes are a side effect of high doses of the ana-
Women who use steroids at recommended dosage bolic steroids, which cause blood platelets to clump to-
levels may experience an abnormal enlargement of the gether, forming clots. Researchers have also found that
clitoris, irregular menstrual periods, unnatural hair steroids have a direct, dose-related, cardiotoxic effect
growth and/or unusual hair loss, a deepening of the (Slovut, 1992). There are physical changes in the heart
voice, and a possible reduction in the size of the breasts structure of some steroid users, although how steroids
(Galloway, 1997; Pope & Brower, 2004; Schuckit, 2006; cause this effect is not known (Milddleman & DuRant,
Tanner, 1995; Volkow, 2006b). The menstrual irregu- 1996). Also, for unknown reasons, anabolic steroid
larities caused by steroid use may or may not become abusers are at increased risk for sudden cardiac death
11Technically, 12
this is called gynecomastia. See Glossary.
(Fineschi et al., 2005). Chronic use of anabolic steroids steroids might do so because of criminal thinking that
at large doses causes edema in the hands and/or feet predates their steroid abuse (Klotz, Garle, Granath, &
(Schuckit, 2006). Some steroid abusers might take Thiblin, 2006). Klotz et al. suggested that some crimi-
large doses of diuretics to counteract this effect, and annals might find the steroid-enhanced muscle mass ad-
tibiotics to control steroid-induced acne (Eisenberg & vantageous for their criminal activities. Also, their violent
Galloway, 2005). behavior could be attributed to their steroid abuse rather
Effects on the central nervous system. Although it than possible criminal thinking or antisocial behaviors.
was disputed in the latter part of the 20th century, re- While this is an interesting hypothesis, it has not been
searchers now accept the fact that anabolic steroids proven and thus is but one possibility for the apparent
cause behavioral changes in the user. The massive doses connection between steroid abuse and violence.
of steroids utilized by some athletes have been identi- In the early 1990s a number of researchers challenged
fied as the trigger of a drug-induced psychosis in some the suspected relationship between anabolic steroid
cases (Johnson, 1990; Kashkin, 1992; Pope & Brower, abuse and increased violent tendencies. Yesalis, Kennedy,
2004, 2005; Pope & Katz, 1994). Kopstein, and Bahrke (1993) suggested that for some un-
Although most abusers reported minimal impact on known reason, anabolic steroid abusers might have exag-
measured aggression levels, Pope, Kouri, and Hudson gerated their self-report of violent behavior in earlier
(2000) found that 2% to 10% of male abusers became studies. Thus, the evidence suggesting a relationship
manic and/or developed other neuropsychiatric prob- between aggressive behavior and steroid abuse for at
lems after abusing steroids. The authors found no sig- least a minority of steroid abusers appears to be strong,
nificant premorbid sign that might identify those but whether it is a causal relationship remains unproven
steroid abusers who would develop such problems as a (Pope, Kouri, et al., 2000; Pope, Phillips, et al., 2000).
result of their steroid use, raising questions as to why Steroids have been identified as causing depression,
they responded so strongly to the chemicals they in- especially during the withdrawal phase (Pope & Brower,
jected. Other responses noted in steroid abusers in- 2004, 2005; Schuckit, 2006). Such depressive reactions
cluded depressive reactions or drug-induced psychotic seem to respond well to simple discontinuation of the
reactions (Eisenberg & Galloway, 2005; Pope & Brower, offending substances (Schuckit, 2006) or the use of se-
2004, 2005). Sometimes, the individual becomes vio- lective serotonin reuptake inhibitors (SSRIs) (Pope &
lent after using steroids, a condition called “roid rage” Brower, 2004). On occasion, steroid abusers have devel-
(Eisenberg & Galloway, 2005; Galloway, 1997; Pope & oped a form of body dysmorphic disorder, especially fol-
Brower, 2005). In rare cases, steroid-induced violence lowing their decision to discontinue steroid use (Kilmer,
has resulted in the death of the user or a victim who be- Palmer, & Cronce, 2005; Pope & Brower, 2004). Again,
came the target of the abuser’s anger (Pope, Phillips, & this condition responds well to psychotherapy combined
Olivardia, 2000), and it has been recommended that with the appropriate SSRI, according to Pope and Brower.
large, muscular, perpetrators of interpersonal violence Other complications. Patients with medical condi-
be screened for steroid abuse (Pope & Brower, 2004). tions such as certain forms of breast cancer; diabetes
One excellent example of roid rage is the incident mellitus; diseases of the blood vessels; kidney, liver, or
when one anabolic steroid abuser reportedly started to heart disease; or prostate problems in males should not
smash three different automobiles out of frustration utilize steroids unless the physician is aware that the
over a traffic delay (Pope & Katz, 1994). Another indi- patient has these problems (Eisenberg & Galloway,
vidual was implicated in a murder plot, while yet a 2005). The anabolic steroids are thought to be possibly
third beat his dog to death, according to Pope and Katz carcinogenic (Johnson, 1990), and their use is not rec-
(1994). Another individual rammed his head through a ommended for patients with either active tumors or a his-
wooden door, and several others were expelled from tory of tumors except under a physician’s supervision.
their homes because of their threatening behavior Other side effects caused by steroid use include severe
(Back Letter, 1994). Other psychiatric effects of ana- acne (especially across the back) and possibly a foul odor
bolic steroid abuse include loss of inhibition, lack of on the breath (Redman, 1990). There has been one iso-
judgment, irritability, a “strange edgy feeling” (Corrigan, lated case of unnatural bone degeneration that was at-
1996, p. 222), impulsiveness, and antisocial behavior tributed to the long-term use of steroids by a weight lifter
(Corrigan, 1996). (Pettine, 1991). Also, animal research suggests that ana-
One possible factor overlooked thus far is that indi- bolic steroids may contribute to the degeneration of ten-
viduals who become violent while taking anabolic dons, a finding that is consistent with clinical case reports
of athletes using anabolic steroids who have tendons rup- on steroids (“I need to use steroids”), (2) the individual’s
ture under stress (Eisenberg & Galloway, 2005). perceived benefit from past steroid abuse, and (3) ulti-
There is evidence that anabolic steroid abuse mately, the physical dependence on further steroid use
might prove to be a gateway to the abuse of other com- to avoid withdrawal symptoms. The psychological de-
pounds such as narcotic analgesics (Kanayama, Cohane, pendence on steroids often rests on a fear that the indi-
Weiss, & Pope, 2003). Kanayama et al. suggested that the vidual will become less imposing unless he or she
abuse of anabolic steroids might be one avenue through continues to abuse illicit steroids, setting the stage for
which some individuals began to abuse opiates, consid- the possible addiction to steroids.
ering that eight of their subjects first purchased opiates The second factor, perceived benefit, rests on exter-
from the same source that sold them anabolic steroids. nal feedback (“you look good” or “you can lift a lot
A history of anabolic steroid abuse might be an under- more weight now than you could 6 months ago!”), as
recognized problem among those admitted to treatment well as from possible feelings of euphoria induced by
for more traditional substance use problems. steroids. These compounds have been known to bring
Growth patterns in the adolescent. Adolescents who about a sense of euphoria both when used for medical
use steroids run the risk of stunted growth, as these drugs purposes and when abused (Fultz, 1991; Middleman &
may prematurely and permanently stop bone growth DuRant, 1996). This may reflect the ability of these
(Volkow, 2006b). A further complication of steroid compounds to affect the opioid and dopamine neuro-
abuse by adolescents is that the tendons do not grow at transmission systems in the brain, especially the
the same accelerated rate as the bone tissues, producing mesolimbic system (Pope & Brower, 2005; Wood, 2004).
increased strain on the tendons in adolescent steroid Because their use is rewarding to the individual, they
abusers and thus a higher risk of injury to these tissues also have an addictive potential, which seems to be sim-
(Galloway, 1997; Johnson, 1990). ilar to that of caffeine, nicotine, or possibly the benzodi-
Anabolic steroid abuse and blood infections. In addi- azepines (Wood, 2004).
tion to the complications of steroid abuse itself, individ- The withdrawal syndrome from steroid addiction
uals who abuse steroids through intramuscular or seems very similar to that of cocaine withdrawal and in-
intravenous injection often share needles. These indi- cludes such symptoms as depressive reactions, possibly
viduals run the same risk of infections being transmit- to the point of suicide attempts (Pope & Brower, 2005),
ted by contaminated needles seen in heroin or cocaine as well as insomnia, fatigue, dysphoria, restlessness,
addicts. There have been numerous cases of athletes anorexia, headaches, and lowered libido (Brower et al.,
contracting AIDS when they used a needle that had been 1991; Kilmer, Palmer, et al., 2005). Some 14% to 69%
used by another athlete who was infected (Eisenberg & of abusers will ultimately become addicted to anabolic
Galloway, 2005). steroids (Pope & Brower, 2005). Further, when steroid
Drug interactions between steroids and other chemi- abusers turn to illicit opiates to self-medicate pain in-
cals. The anabolic steroids interact with a wide range of duced by overwork, they become vulnerable to an opiate
medications, including several drugs of abuse. Poten- addiction as well.
tially serious drug interactions have been noted when Like their drug-using counterparts, many steroid
the individual has utilized acetaminophen in high abusers require gradual detoxification from the drugs
doses while on steroids. The combination of these two over time as well as intensive psychiatric support to limit
drugs—steroids and acetaminophen—should be avoided the impact of withdrawal and to try to prevent a return
except when the individual is being supervised by a to steroid use (Bower, 1991; Hough & Kovan, 1990;
physician. Patients who take Antabuse (disulfiram) Kashkin & Kleber, 1989). According to Robert Dimeff,
should not take steroids, nor should individuals who Donald Malone, and John Lombardo (cited in Bower,
are taking Trexan (naltrexone), anticonvulsant med- 1991), some of the symptoms of steroid addiction are
ications such as Dilantin (phenytoin), Depakene (val- (a) the use of higher doses than originally intended, (b)
proic acid), or any of the phenothiazines (United States a loss of control over the amount of steroids used, (c) a
Pharmacopeial Convention, 1990). preoccupation with further steroid use, (d) the contin-
ued use of steroids in spite of the individual’s awareness
of the problems caused by their use, (e) the develop-
Are Anabolic Steroids Addictive?
ment of tolerance to steroids and the need for larger
The development of steroid addiction appears to reflect doses to achieve the same effects as once brought on by
three factors: (1) the individual’s psychological reliance lower doses, (f) the disruption of normal daily activities
by steroid use, and (g) the continued use of steroids to drugs of abuse rests on different dynamics from those
control or avoid withdrawal symptoms. The authors sug- of the more traditional recreational substances. Ado-
gested that three or more of these symptoms would iden- lescents and young adults abuse steroids because
tify those individuals who were dependent on steroids. they believe these substances will increase aggressive-
Kashkin (1992) suggested that anyone who had gone ness and athletic ability and improve personal appear-
through five or more “cycles” of steroid use was very likely ance. Little is known about the effects of these drugs at
to be a “heavy” steroid user. the dosage levels utilized by individuals who abuse
steroids. The identification and treatment of steroid
abusers is primarily a medical issue, but substance
Summary abuse counselors should have a working knowledge of
The anabolic steroids emerged as drugs of abuse in the the effects of steroid abuse and the complications it
latter part of the 20th century, but their popularity as causes.
CHAPTER EIGHTEEN
The Over-the-Counter Analgesics

Unexpected Agents of Abuse
At first glance the reader might wonder why the com- amounts of this compound for commercial use. As-
pounds discussed in this chapter, the over-the-counter or pirin, or acetylsalicylic acid, was first developed from
OTC analgesics, are included in this text. These com- salicin, which is found in the bark of certain willow
pounds do not induce a sense of euphoria in the user trees. In the 1800s, chemists learned to produce a
and are virtually never used as recreational compounds. chemical cousin of salicin known as salicylic acid that
Yet they are ubiquitous: 70% of adults over the age of 65 had the same properties as salicin but was easier to pro-
take an over-the-counter analgesic at least once a week duce. However, salicylic acid, like salicin, was found to
(Stillman & Stillman, 2007). Further, each of the cause a great deal of gastric distress when ingested. So
compounds discussed in this chapter presents unique chemists continued to search for a compound with the
advantages and potential dangers for the user, inde- advantages of salicin but less intense side effects. In
pendent of whether he or she has a concurrent sub- 1898 Bayer Pharmaceuticals introduced the com-
stance use disorder (SUD). To illustrate, each year in pound acetylsalicylic acid under the brand name “As-
the United States, an estimated 103,000 people are hos- pirin.”1 Like its chemical cousin salicin, aspirin was
pitalized for complications induced by OTC analgesics, found to be effective in controlling mild to moderate
and some 16,500 of these people die as a result of levels of pain without the danger of addiction inherent
OTC analgesic-related complications (Stillman & with narcotic analgesics. Further, aspirin was found to
Stillman, 2007). For these reasons it is important for control inflammation and reduce fever while produc-
the reader to have a working knowledge of the OTC ing less gastric distress than its chemical cousins sali-
analgesics. cylic acid and salicin. Because of its multiple uses,
aspirin has become the most frequently used drug in
A Short History of the OTC Analgesics the world (Mann & Plummer, 1991). An estimated 50
billion doses of aspirin2 are consumed around the
Plants that contain chemical cousins of aspirin have world each year (Begley, 1997), of which 12.5 billion
long been used to control pain and fever. For example, doses (or approximately 25% of the total amount con-
willow bark, which contains salicin (from Salix, the sumed) are ingested in the United States alone (Page,
Latin name for willow) has been recommended for the 2001).
relief of pain and fever for 2,000 years or more (Jeffreys, Although aspirin’s side effects are less intense than
2004; Stimmel, 1997a). Around the year 400 B.C.E., the those of salicylic acid or salicin, it still has a significant
Greek physician Hippocrates recommended that pa- potential to cause harm to the user. This was one of
tients chew the bark of the willow tree for such condi- the reasons that companies embarked on a search for
tions as headache, fever, and labor pain. But although pharmaceuticals with the analgesic, antipyretic,3 and
willow bark was recognized as an herbal remedy for anti-inflammatory actions of aspirin but safer to use.
pain, the bitter taste, limited availability of the bark, This search resulted in the discovery of a class of
and inconsistent effect forced physicians to utilize nar-
1Aspirin is a member of a family of closely related compounds, many
cotic analgesics for even mild levels of pain. Narcotic
of which have some analgesic, anti-inflammatory, and antipyretic
analgesics, however, are both addictive and have a de-
action. However, since none of these compounds is as potent (nor
pressant effect on the central nervous system, so they as widely used) as aspirin, they will not be discussed further in this
are a poor choice for the control of anything less than chapter.
severe pain (Giacona, Dahl, & Hare, 1987). 2
Technically, the word aspirin is a historical accident, which is dis-
Then, in the 1880s, the active agent of willow bark cussed in detail in Mann and Plummer (1991).
was isolated, and ways were found to synthesize large 3See Glossary.
209
210 Chapter Eighteen
chemicals known as the propionic acids, from which the prescription, are also classified as NSAIDs (Jackson &
pharmaceutical agents now known as naproxen, keto- Hawkey, 2000).
profen, and ibuprofen were developed (Yost & Morgan,
1994).
Medical Uses of the OTC Analgesics
Acetaminophen was introduced as an OTC anal-
gesic in this country in the 1950s. The term acetamino- Aspirin. Aspirin was first introduced in 1897, and in
phen is based on a form of chemical shorthand. The spite of its age scientists are still discovering new uses
true name of this chemical is N-acetyl-para-aminophenol, for it. The most common application for aspirin is the
from which the term acetaminophen is obtained. This control of mild to moderate levels of pain from such
compound was first isolated in 1878, and its ability to conditions as common headaches, neuralgia, the pain
reduce fever was identified shortly after its discovery. associated with oral surgery, toothache, dysmenorrhea,
But at the time it was thought that acetaminophen and various forms of musculosketal pain (Giacona et al.,
would share the dangerous side effects found in a close 1987; Supernaw, 1991). Further, just one aspirin tablet
chemical cousin, para-aminophenol. So it was set aside, every other day has been found to reduce the frequency
and chemists did not pay much attention to it until the of migraines by 20% in a small subgroup of patients who
early 1950s (Mann & Plummer, 1991). By that time suffer migraine headaches (Gilman, 1992; Graedon &
sufficient evidence had accumulated to show that acet- Ferguson, 1993; Graedon & Graedon, 1991).
aminophen was much safer than para-aminophenol Aspirin continues to be a popular treatment for the
and that it did not have the same potential for harm found control of fever (Payan & Katzung, 1995). This is brought
in aspirin. A massive advertising campaign followed the on, in part, by aspirin’s ability to cause peripheral vasodi-
introduction of acetaminophen, stressing that while as- lation and sweating in the patient, as well as its ability to
pirin might irritate the stomach, acetaminophen does interfere with prostaglandin production in the hypo-
not. This advertising campaign was successful, and by thalamus4 (Wilson, Shannon, Shields, & Stang, 2007).
the start of the 21st century acetaminophen was the These effects help to reduce fever but do not lower the
most common compound used for the control of fever body temperature below normal.
on this planet (Sharma, 2003). In the closing decade of the 20th century regular
However, aspirin still remains a popular OTC anal- low-dose aspirin use was discovered to reduce the inci-
gesic (Jeffreys, 2004). Aspirin has been called “the most dence of myocardial infarctions in both men and women
cost-effective drug available today” (Elwood, Hughes, & (Berger et al., 2006; Buring & Ferrari, 2006; Chan et al.,
O’Brien, 1998, p. 587). It is such a potent drug that 2007; Eidelman, Hebert, Weisman, & Henneckens,
were it to be discovered today rather than over a century 2003), and aspirin is of value in the treatment of a
ago, its use would be closely regulated and it would be myocardial infarction once it develops (Dajer, 2005;
available only by prescription (Graedon & Ferguson, Hung, 2003). Paradoxically, extended periods of use at
1993). Indeed, since the early 1990s physicians have high dosage levels have been found to increase the indi-
discovered that even at recommended dosage levels, vidual’s risk of a cardiovascular problem, especially if the
the OTC analgesics such as aspirin are far more toxic to patient has one or more other risk factors for cardiovas-
the user than had been thought earlier (“Strong Medi- cular disease (D’Arcy, 2007).5
cine,” 1995). There are several mechanisms by which low-dose as-
The origin of the term NSAID. Aspirin and the propi- pirin use is able to reduce the risk of myocardial infarc-
onic acid derivatives have an anti-inflammatory effect. tion. One is aspirin’s ability to reduce the blood levels
Another class of chemicals with this effect are the adreno- of the C-reactive protein (Berger et al., 2006; Ridker,
cortical steroids, potent agents whose function lies be- Cushman, Stampfer, Tracy, & Hennekens 1997). Higher
yond the scope of this text. However, because aspirin and levels of C-reactive protein in the individual’s blood are
the propionic acid derivatives have a different chemical
structure from that of the adrenocortical steroids, they 4See Glossary.
are often called non-steroidal anti-inflammatory drugs 5This side effect of the NSAIDs was first identified with the COX-2
(or NSAIDs). There are approximately 20 NSAIDs inhibitors, and several lawsuits were filed after patients taking COX-2
currently in use in the United States, although most are inhibitors developed cardiovascular problems. Scientists later discov-
ered that this effect was not specific to the COX-2 inhibitors, al-
available only by prescription. The exceptions are aspirin though it might have been more pronounced with this class of
and the propionic acid derivatives ibuprofen, ketoprofen, medication, but that all NSAIDs had this side effect through an un-
and naproxen. The COX-2 inhibitors, available only by known mechanism.
The Over-the-Counter Analgesics 211
associated with a greater risk of either a myocardial in- 80% or more and ovarian cancer by 25% (Page, 2001).
farction, an occlusive stroke (CVA),6 and a blood clot Regular use of aspirin or another NSAID might reduce
that might block a vein (a venous thrombosis). However, a man’s risk of prostate cancer and improve blood flow
this beneficial effect of aspirin was noted only for indi- to capillaries that feed the retina, inhibiting the devel-
viduals older than 50 years of age, and for reasons that opment of diabetic retinopathy7 (Adler & Underwood,
are not known are strongest in those with lower blood 2002; Roberts et al., 2002); also, low-dose aspirin use
cholesterol levels. might slow the development of cataracts (Payan &
Aspirin has also been found to inhibit the action of a Katzung, 1995) and protect the sensitive structures of
form of prostaglandin known as thromboxane A2, which the inner ear from damage during the normal aging
is found in blood platelets and is involved in the forma- process and damage caused by certain medications
tion of blood clots (Hutchison, 2004; Jeffreys, 2004; (Coghlan, 2006a). Aspirin may interfere with the forma-
Page, 2001). This is the mechanism by which regular tion of gallstones (Elwood et al., 1998), and some data
low-dose aspirin use reduces the individual’s risk for even suggest that aspirin might interfere with the ability
heart attacks. However, there is a great deal of variation of the virus that causes AIDS to replicate to some degree
people’s sensitivity to aspirin’s ability to destroy throm- (Stolberg, 1994).
boxane A2, and each individual’s daily aspirin require- Acetaminophen. Because acetaminophen has no
ment needs to be assessed by the physician. Further, significant anti-inflammatory effect, it is not usually
since platelets have a normal lifetime of 8–10 days, the classified as an NSAID (Supernaw, 1991). However,
body is constantly replacing old blood platelets with acetaminophen is not without its uses. It has been found
new ones. These new blood platelets will have unal- as effective in the control of fever as aspirin (American
tered thromboxane A2, incrementally restoring blood Society of Health System Pharmacists, 2002). Further,
clot formation proficiency. To avoid this danger, the as an OTC analgesic, acetaminophen is as potent as
patient must take a dose of aspirin every day, or at least aspirin and might be used for pain control in virtually
every other day, to provide optimal inhibition of clot the same situations as aspirin.
formation. Although it was initially thought that some The propionic acids. This class of medications in-
patients might be resistant to the anti-thrombotic ef- cludes ibuprofen, naproxen, and ketoprofen. As a group,
fects of aspirin (Halushka & Halushka, 2002), simple the propionic acids are used to control fever, inflamma-
patient noncompliance in taking the recommended tion, and mild to moderate levels of pain. The anti-
doses of aspirin appears to be the more likely explana- inflammatory effect of these compounds make them
tion for why some patients do not seem to benefit as useful in treating such condtions as rheumatoid arthri-
much as expected from low-dose aspirin therapy (Dalen, tis, dysmenorrhea, gout, tendinitis, and bursitis as well
2007). as headaches, the aches of the common cold, backache
Physicians have found that low doses of aspirin are and muscle aches, arthritis, and the the discomfort of
one form of treatment for a rare neurological disorder menstrual cramps (Gannon, 1994). Physicians have
known as the transient ischemic attack (TIA). At higher found that when used in combination with narcotic
dosage levels, it is also an effective anti-inflammmatory analgesics, some NSAIDs are of value in controlling
agent, thus making it of value in the treatment of such the pain associated with certain forms of cancer. There
disorders as rheumatoid arthritis and osteoarthritis is mixed evidence suggesting that the regular use of
(Graedon & Graedon, 1991; Jeffreys, 2004; McGuire, NSAIDs (including aspirin) might slow the develop-
1990). There is an impressive body of evidence suggest- ment of Alzheimer’s disease (Launer, 2003). There is
ing that regular low-dose aspirin use interferes with the no evidence suggesting that any of the NSAIDs are able
development of some forms of cancer (Page, 2001; to slow the development of what is known as vascular
Terry et al., 2004; Wright, 2001). dementia (Adler & Underwood, 2002; Veld et al., 2001).
In women, regular low-dose aspirin use is associated In addition to these general applications, researchers
with a reduced risk of breast cancer, especially the sub- have identified specific applications for each of these
type of breast cancer known as hormone receptor- compounds.
positive cancers (Terry et al., 2004). There is also While the risk of NSAID-related cardiovascular com-
preliminary evidence that regular low-dose aspirin use plications is lower with ibuprofen and naproxen, these
might reduce the incidence of esophageal cancer by compounds still carry the potential to cause or exacerbate
6See 7See Glossary.

Glossary.
cardiovascular disorders such as myocardial infarction prostaglandins. The inflammation and pain that result
and/or stroke when used for extended periods of time when these chemicals are released serves both to warn
(D’Arcy, 2007). the individual that he or she has been injured and to ac-
tivate the body’s repair mechanisms. Aspirin’s analgesic
effect at the site of the injury is attributed to its power to
Pharmacology of the OTC Analgesics inhibit the production of prostaglandins (Jeffreys, 2004).
Aspirin. Aspirin is usually administered by mouth. In It inhibits the production of two known subtypes of the
the body, acetylsalicylic acid is biotransformed into sali- enzyme cyclooxygenase, known as COX-1 and COX-2,
cylic acid, which is the active agent for aspirin’s effects which were discovered in the early 1990s. In 2002
(Peterson, 1997). In contrast to the 15-minute half-life scientists discovered a third subform, which has been
of aspirin, the half-life of its primary metabolite, sali- designated COX-3 (Greener, 2003).
cylic acid, is between 2 and 3 hours (Katz, 2000), ac- COX-1 is predominantly involved in essential
counting for its duration of effect. It is rapidly absorbed, prostaglandin production in body organs, where the
and when it is taken on an empty stomach, aspirin be- prostaglandins carry out a protective function. COX-2
gins to reach the bloodstream in as little as 1 minute on the other hand is produced mainly by body tissues
(Rose, 1988). However, its primary site of absorption is when they are damaged, contributing to the inflamma-
the small intestine, so that while it is possible to detect tion response (Pairet et al., 1998; Rehman & Sack, 1999).
the first atoms of aspirin in the blood in approximately On a molecular level, COX-1 and COX-2 share about
1 minute, it usually takes about 1 hour before aspirin is 60% of their chemical structure, and it is through the
able to bring about any significant degree of analgesia shared elements that NSAIDs interfere with the produc-
(Stimmel, 1997a). tion of both COX-1 and COX-2 (Rehman & Sack, 1999).
After a single dose, peak blood levels of aspirin are In other words, aspirin (and the other NSAIDs) func-
achieved in 15 (Wilson et al., 2007) to 60–120 minutes tion as nonselective cyclooxygenase inhibitors to block
(McGuire, 1990; Stimmel, 1997a). In the blood, 80% injury-induced COX-2 prostaglandin production, lower
to 90% of aspirin is bound to plasma proteins (Stimmel, pain levels, and reduce inflammation, at the cost of in-
1997a). Aspirin is rapidly biotransformed by the liver hibiting COX-1 levels in the body (Stillman & Stillman,
into water-soluble metabolites, which are then promptly 2007).
removed from the blood by the kidneys (Payan & The ability of aspirin to inhibit COX-2 production
Katzung, 1995). Only about 1% of a single dose of as- also seems to be the mechanism by which it affects the
pirin is excreted unchanged from the body. In contrast development of colorectal cancer (Adler & Underwood,
to its 2- to 3-hour half-life following a single dose, when 2002; Baron et al., 2003; DuBois, Sheng, Shao,
aspirin is used at high dosage levels for longer than a Williams, & Beauchamp, 1998; Kreeger, 2003). Taking
week, its half-life might be extended to between 8 one 325 mg tablet of aspirin a day for an extended period
(Kacso & Terezhalmy, 1994) and 15 (Payan & Katzung, of time seemed to provide a modest degree of protection
1995) hours. It is rare for tolerance to the analgesic ef- against colorectal, prostate, and breast cancer in one
fects of aspirin to develop (Stimmel, 1997a). study (Jacobs et al., 2007). While this would suggest that
Unlike the narcotic analgesics, which seem to work everybody should use aspirin to limit the risk of colorectal
mainly within the brain, aspirin seems to have a different cancers, Dube et al. (2007) warned against this. The au-
mechanism of action. First, aspirin does not seem to work thors suggested that the risks associated with the use of an
within the cortex of the brain (Kacso & Terezhalmy, NSAID such as aspirin8 outweighed any benefit from its
1994). Rather, it appears to work at the site of the injury, use in preventing colorectal cancer in the average person.
in the hypothalamic region of the brain, and, although Acetaminophen. Acetaminophen is usually adminis-
scientists are not sure how, through unidentified sites in tered orally—in tablet, capsule, or liquid form. It may
the spinal cord (Fishman & Carr, 1992; Graedon & also be administered as a rectal suppository. After oral
Ferguson, 1993; Kacso & Terezhalmy, 1994). administration, virtually 100% of the medication is ab-
To understand how aspirin works at the site of the in- sorbed through the gastrointestinal tract (Wilson et al.,
jury, it is necessary to investigate the body’s response to 2007). The peak effects are seen in 30 minutes to 2 hours
injury. Each cell in the human body contains several after a single dose. Acetaminophen is metabolized in
chemicals that are released when that cell is damaged.
Some of these chemicals include histamine, bradykinin, 8Discussed in the section “Complications Caused by Use of the OTC
and a group of chemicals collectively known as the Analgesics.”
the liver, and virtually 100% of the drug is eliminated in dosage level of 2,400 mg/day,9 ibuprofen is as effective
the urine, although small amounts might also be found an anti-inflammatory agent as aspirin in the average
in breast milk of nursing mothers. adult. But it might take 2–4 weeks of continuous use
In terms of its analgesic and fever-reducing potential, before the anti-inflammatory effect is seen (Fischer,
acetaminophen is thought to be as powerful as aspirin 1989). The patient should not mix ibuprofen with other
and might be substituted for aspirin on a milligram-for- NSAIDs, unless directed to do so by a physician, as
milligram basis (Supernaw, 1991). When used above there is strong evidence to suggest that when ibuprofen
recommended doses, there is a danger of acetaminophen is taken concurrently with aspirin these two chemicals
toxicity. However, liver toxicity or damage from aceta- interfere with the anti-inflammatory action of the other
minophen is rare as long as the user does not ingest more (Payan & Katzung, 1995).
than 4,000 mg of acetaminophen per day (Cherny & Ibuprofen has been found to be about one-fifth to
Foley, 1996) or use the drug for more than 10 days one-half as irritating to the stomach as aspirin (Giacona,
(Peterson, 1997). et al., 1987). But, while ibuprofen is less irritating to the
Scientists speculate that acetaminophen might stomach, it has been estimated that 4% to 14% of those
block the synthesis of the only recently discovered COX- who use ibuprofen still experience some degree of gas-
3 enzyme, which may account for its ability to reduce trointestinal irritation (Graedon & Graedon, 1996).
fever and pain without interfering with inflammation Approximately 3 out of every 1,000 chronic ibuprofen
(Greener, 2003). COX-3 synthesis is limited to the cen- users will experience drug-induced gastrointestinal bleed-
tral nervous system (CNS), which is where acetamino- ing (Carlson et al., 1987). Further, 27% of a sample of
phen seems to have its main effect. Unlike aspirin, patients who had used ibuprofen for an extended period
acetaminophen does not interfere with the normal clot- of time had evidence of gastric ulcer formation (Taha,
ting mechanisms of the blood (Wilson et al., 2007). Fi- Dahill, Sturrock, Lee, & Russell, 1994).
nally, individuals who are allergic to aspirin do not Naproxen may be more effective than aspirin as an
usually suffer from adverse reactions when they take anti-inflammatory agent (American Medical Associa-
acetaminophen according to label instructions. These tion, 1994; American Society of Health-System Phar-
are features that often make acetaminophen an ideal macists, 2002; Graedon & Graedon, 1991). Like aspirin,
substitute for individuals who are unable to take aspirin naproxen has an antipyretic effect. Researchers are not
due to any of the following conditions: They are aller- sure of the exact mechanism through which naproxen
gic to it, they are prone to bleeding disorders, or the as- reduces fever; however, it is thought that naproxen is
pirin might interfere with another medication they are able to suppress the synthesis of prostaglandins in the
using. hypothalamus (American Society of Health System Phar-
Ibuprofen. Ibuprofen is most commonly adminis- macists, 2002). Researchers have found that naproxen
tered orally. About 80% of a single dose of ibuprofen is has only a limited antiplatelet effect and thus has only
absorbed from the gastrointestinal tract. The primary limited value in the treatment of cardiovascular disease
site of biotransformation is the liver, and its half-life is (Hutchison, 2004; Solomon, Glynn, Levin, & Avorn,
between 2 and 4 hours (Wilson et al., 2007). About 2002).
99% of ibuprofen molecules becomes protein bound When used as an analgesic, naproxen will begin to
following absorption into the general circulation (Olson, have an effect in 1 hour, and its effects will last for 7–8
1992). Peak plasma levels following a single oral dose hours (American Medical Association, 1994). The bi-
are achieved in 30 minutes to 1.5 hours, and the thera- ological half-life of naproxen in the healthy adult is
peutic half-life of a single dose of ibuprofen is between approximately 10–20 hours. About 30% of a given
1.8 and 2.6 hours (American Medical Association, 1994). dose of naproxen is metabolized by the liver into the in-
Ibuprofen and its metabolites are excreted mainly by active metabolite 6-desmethylnaproxen (American So-
the kidneys, although a small amount of ibuprofen is ciety of Health System Pharmacists, 2002), and only
eliminated through the bile. 5% (American Medical Association, 1994) to 10%
Although ibuprofen inhibits the action of the en- (American Society of Health System Pharmacists,
zyme cyclooxygenase, this does not mean that ibupro- 2002) of a standard dose of naproxen is excreted un-
fen might automatically be substituted for aspirin to changed. The majority of the drug is excreted in the
control inflammation. There is disagreement as to urine as either metabolized or unmetabolized drug.
ibuprofen’s effectiveness as an anti-inflammatory agent.
Payan and Katzung (1995) stated that when used at a 9Taken in divided doses, as per label instructions.
Naproxen binds to proteins in the blood plasma, which level of aspirin of 325 to 650 mg every 4 hours as
can absorb only so much of the medication before needed for the control of pain. Furthermore, this text
reaching a saturation point. Research suggests that the warns that aspirin should not be used continuously for
concentration of naproxen reaches a plateau if the longer than 10 days by an adult, and longer than 5 days
patient takes 500 mg twice daily for 2–3 days (American for a child under the age of 12, except under a doctor’s
Society of Health System Pharmacists, 2002).10 orders.11
Although all of the OTC analgesics are usful in the When taken by mouth, aspirin is rapidly and com-
control of mild to moderate levels of pain or fever, a completely absorbed from the gastrointestinal tract and is
mon danger inherent in the use of these agents is that distributed by the blood to virtually every body tissue
they might mask the development of a serious medical and fluid. The actual speed at which aspirin is ab-
condition. For example, although the OTC analgesics sorbed depends on a number of factors such as (a) the
are effective in controlling fever, the cause of the fever acidity of the stomach contents (Sheridan, Patterson, &
must still be identified, and treated to ensure adequate Gustafson, 1982) and (b) whether the individual has in-
medical care for the patient (Fishman & Carr, 1992). gested aspirin on an empty stomach or after eating.
When taken on an empty stomach, the rate at which as-
Normal Dosage Levels pirin is absorbed depends on how quickly the tablet
of the OTC Analgesics may crumble after reaching the stomach (Rose, 1988).
After the tablet disintegrates, the individual aspirin mol-
Aspirin. McGuire (1990) reported that 650 mg of as- ecules will pass through the gastrointestinal tract lining
pirin or acetaminophen, a standard dose of two regular into the general circulatory system.
strength tablets of either medication, provided an anal- Taken with food, aspirin may take 5–10 times longer
gesic effect equal to that of 50 mg of the narcotic to reach the individual’s bloodstream (Pappas, 1990).
painkiller meperidine (Demerol). It has been estimated Ultimately, however, all of the aspirin will be absorbed
that 325–650 mg of aspirin has the same analgesic from the gastrointestinal tract. This is useful knowl-
potential as 32 mg of codeine, 65 mg of Darvon edge, since Rodman (1993) suggested that the patient
(propoxyphene), or a 50 mg oral dose of Talwin (penta- take aspirin with meals or at least a snack to limit
zocine) (Gutstein & Akil, 2001). Thus, although it is an aspirin-induced irritation to the stomach lining. How-
“just” an OTC analgesic, aspirin is a very potent com- ever, in some cases, it is desirable to achieve as high a
pound. blood level of aspirin as possible. The patient should
Even after more than a century of use, physicians discuss with his or her physician or pharmacist whether
still debate the optimum dosage level for aspirin use. to take aspirin on an empty stomach or with a meal be-
Kacso and Terezhalmy (1994) reported that a single fore attempting to use this technique to limit stomach
1,300 mg dose of aspirin seemed to provide a greater irritation.
degree of relief from pain than did a single 600 mg Aspirin is sold both alone and in combination with
dose. However, dosage levels above 1,300 mg in a various agents designed to reduce the irritation that it
single dose did not provide a greater degree of analgesia might cause to the stomach. In theory, timed-released
and actually put the user at risk for a toxic reaction from and enteric coated tablets have the potential for reduc-
the aspirin, according to the authors. These findings ing the irritation to the gastrointestinal tract. However,
were consistent with the conclusions of Aronoff, Wagner, both forms of aspirin have been known to bring about
and Spangler (1986), who found a “ceiling effect” of erratic absorption rates, making it harder to achieve the
“approximately 1,000 mg every 4 hr” (p. 769) for aspirin. desired effect (Wilson et al., 2007). Some patients will
Dosage levels higher than this did not provide greater take aspirin with antacids to reduce the irritation to the
pain relief and would “only increases the threat of a stomach caused by aspirin. When antacids are mixed
toxic reaction” (McGuire, 1990, p. 30). with aspirin, the patient’s blood level of aspirin will be
The American Society of Health System Pharma- 30% to 70% lower than when aspirin is used alone
cists (2002) recommends a normal adult oral dosage (Graedon & Graedon, 1996; Rodman, 1993). This is a
10This is the recommended prescription dose. When sold as an over- 11On occasion, the physician might recommend that the patient take
the-counter analgesic, the recommended dosage level is much lower above-normal doses of aspirin, such as when the medication is being
than this. As always, it is recommended that the user follow the dos- used as an adjunct to the treatment of arthritis. This is a specialized
ing instructions provided by the manufacturer or on the prescription application of aspirin carried out under a physician’s supervision, and
bottle. such doses are not discussed further in this chapter.
matter of some concern for individuals who are taking oral dose is absorbed from the intestinal tract. Follow-
the drug for the control of inflammation or pain, since ing a single oral dose, peak blood plasma levels are
lower blood levels of aspirin mean that less of the drug achieved in 1–2 hours (American Society of Health
is available to help control the pain. System Pharmacists, 2002). The drug’s half-life is be-
Acetaminophen. The usual adult dose of acetamino- tween 1.8 and 2.6 hours, and the effects of a single dose
phen is also 325 to 650 mg every 4 hours as needed for of ibuprofen last for about 6–8 hours following a single
the control of pain (American Society of Health System oral dose (Wilson et al., 2007).
Pharmacists, 2002). In many ways, dosage recommen- Naproxen. Naproxen is well absorbed from the intes-
dations for aspirin and acetaminophen are very similar. tinal tract, with 100% of a single dose being absorbed.
For example, Aronoff et al. (1986) observed that aceta- Absorption is somewhat delayed when naproxen is in-
minophen’s antipyretic and analgesic effects are equal gested with food, but eventually, all of the medication
to those of aspirin, and that the ceiling level of aceta- will be absorbed. Peak blood concentrations are found
minophen is the same for these two drugs. 2–4 hours after a single dose, and 99% of the medica-
Peak blood concentrations are achieved in 30 min- tion is bound to proteins in the blood after absorption.
utes to 2 hours after an oral dose of acetaminophen Although this compound will cross the placenta, it does
(Wilson et al., 2007). The half-life of an oral dose of so with difficulty, and fetal plasma levels will be approx-
acetaminophen normally ranges from 1 to 4 hours. imately 1% of those in the mother’s blood (American
However, since this chemical is biotransformed in the Society of Health-System Pharmacists, 2002).
liver, people with significant liver damage might experi- About 30% of a single dose of naproxen is biotrans-
ence a longer acetaminophen half-life than is normally formed by the liver into the inactive metabolite 6-
the case and should avoid the use of acetaminophen ex- desmethylnaproxen (American Society of Health-System
cept under the supervision of a physician. Pharmacists, 2002). The rest is biotransformed into other
Ibuprofen. When used as an OTC analgesic, the rec- metabolites, and less than 1% is excreted unchanged
ommended dose of ibuprofen is 200–400 mg every by the kidneys. Only 5% of the drug is excreted in the
4 hours (Dionne & Gordon, 1994). At these dosage feces, and 95% is excreted in the urine, mainly as one
levels, ibuprofen is about as potent an analgesic as ther- of the many metabolites formed when naproxen is
apeutic doses of aspirin or acetaminophen (Jeffreys, biotransformed by the liver.
2004). As a prescription medication, individual dosage
levels of 400–800 mg three or four times a day are often
Complications Caused by Use
utilized, depending on the specific condition being
of the OTC Analgesics
treated (Wilson et al., 2007). The authors suggest that
400 mg every 4–6 hours be utilized in the control of The OTC analgesics are hardly “safe” medications, ac-
mild to moderate pain. However, there is some dis- counting for nearly 25% of the adverse drug reactions
agreement as to the analgesic potential of ibuprofen. reported to the Food and Drug Administration (FDA)
Dionne and Gordon (1994) noted that the greatest de- each year (Noble, King, & Olutade, 2000). As a group,
gree of relief from pain is achieved with doses of the OTC analgesics cause 103,000 hospitalizations
400–600 mg, and that additional ibuprofen above this and 16,500 deaths yearly in the United States alone
level is unlikely to result in greater levels of analgesia. (Graumlich, 2001). Further, there is strong evidence
In contrast, however, Rosenblum (1992) stated that of a dose-related increased risk of hypertension associ-
800 mg of ibuprofen provided greater control of postop- ated with all of the OTC analgesics, including aspirin
erative pain than did therapeutic doses of the narcotic (Forman, Rimm, & Curhan, 2007). Thus, although these
fentanyl in a small sample of women who had laparo- medications are available without a prescription, the
scopic surgery. OTC analgesics pose a significant potential for harm, a
It is necessary to keep in mind that the OTC dosage fact that many people tend to forget.
levels of ibuprofen are limited to 200–400 mg every Aspirin. Aspirin is the most commonly used drug in
4 hours. Even when used as a prescription medication, the United States, with an estimated 35,000 kilograms
it is recommended that the total daily dosage level not of aspirin being consumed each day in the United
exceed 3,200 mg per day, in divided doses (Dionne & States, and 6,000 kilograms are consumed each day in
Gordon, 1994; Wilson et al., 2007). Ibuprofen is rap- the United Kingdom (Halushka & Halushka, 2002).
idly absorbed when used orally, and the drug is rapidly Steele and Morton (1986) gave another measure of as-
distributed throughout the body. About 80% of a single pirin use in this country, stating that between 30 and 74
million pounds of aspirin are consumed in the United common (Fischer, 1989; Wilson et al., 2007). Symp-
States each year. toms of an allergic reaction to aspirin might include
With even occasional use of aspirin at recom- rash and breathing problems (Zuger, 1994). Patients with
mended doses, up to 15% of the users will have at least a history of nasal polyps, asthma, and sensitivity to as-
one significant, potentially fatal, adverse side effect pirin12 should not use any NSAID except under the su-
(Rapoport, 1993). For example, even a single dose of as- pervision of a physician (Craig, 1996; Schuckit, 2006).
pirin can reduce the level of melatonin in the brain by Aspirin can trigger spasms in the bronchial passages
as much as 75%, possibly contributing to insomnia in between 4% and 11% of individuals who have asthma
(Pettit, 2000). At recommended dosage levels, aspirin (Barr, Kurth, et al., 2007). Paradoxically, frequent as-
will cause a minor amount of bleeding in the gastroin- pirin use has been identified as slightly reducing the
testinal tract. The chronic use of aspirin can cause the individual’s odds of developing asthma as an adult, pos-
patient to become anemic (Pappas, 1990; Talley, 1993), sibly through inhibition of COX enzymes (Barr, Kurth,
and between 500 and 1,000 people die each year in the et al., 2007). This is surprising as all the NSAIDs in-
United States from massive aspirin-induced hemor- cluding aspirin are capable of exacerbating asthma as a
rhage (Grinspoon & Bakalar, 1993). result of their ability to inhibit prostaglandin production
Of patients who use an NSAID for an extended pe- (Craig, 1996; McFadden & Hejal, 2000).
riod of time, 4% will develop gastric ulcers, and up to People with a history of chronic rhinitis should not use
40% who use aspirin at recommended doses on a aspirin except under a physician’s supervision (Wilson
chronic basis will experience an erosion in their stom- et al., 2007). These conditions are warning signals for
ach lining (Marcus, 2003). Researchers believe aspirin individuals at risk for an allergic reaction to aspirin or
is a factor in the formation of between 20% (Talley, similar agents. About 5% to 15% of those who suffer
1993) and 41% (Wilcox, Shalek, & Cotsonis, 1994) of from asthma will experience an adverse reaction if they
all cases of “bleeding” ulcers. Even dosage levels as low use an NSAID (Craig, 1996). If the asthma patient also
as 75 mg/day have been found to significantly increase has a history of nasal polyps, the possibility of an ad-
the individual’s risk for damage to the lining of the gas- verse reaction to a NSAID might be as high as 40%, ac-
trointestinal system (Guslandi, 1997). Many of the gas- cording to the authors.
trointestinal ulcers that form as a result of aspirin use Surprisingly, aspirin (and the other COX-2 in-
fail to produce the major warning symptoms usually as- hibitors) might block the immune response following
sociated with ulcer formation (Taha et al., 1994). an innoculation such as the one for influenza (Ryan,
Aspirin’s ability to cause gastric irritation is thought Malboeuf, Bernard, Rose, & Phipps, 2006). Ryan et al.
to be a side effect of its nonselective ability to interfere found a reduced immune response from individuals
with production of both the COX-1 and COX-2 sub- who utilized aspirin (or other COX-2 inhibitors) com-
types of cyclooxygenase. This may also be why, when pared with those who did not normally utilize OTC
used at recommended dosage levels for extended peri- analgesics such as aspirin. Further research is necessary
ods of time, aspirin can cause breathing problems in up to confirm this finding, but it does seem to suggest why
to 33% of the users (Kitridou, 1993). For these reasons, older patiens (who are often on COX-2 inhibitors for a
aspirin should not be used by people with a history of variety of problems) do not seem to respond as well to
ulcers, bleeding disorders, or other gastrointestinal dis- innoculations as do younger subjects.
orders (American Society of Health System Pharma- Aspirin can cause a number of other side effects, in-
cists, 2002). Further, people should not mix aspirin cluding anorexia, nausea, and vomiting (Sheridan et al.,
with acidic foods such as coffee, fruit juices, or alcohol, 1982). Due to their effects on blood clotting, aspirin,
which might further irritate the gastrointestinal system naproxen, or ibuprofen should not be utilized by any-
(Pappas, 1990). one with a bleeding disorder such as hemophilia
Aspirin can also cause allergic reactions in some users. (American Society of Health System Pharmacists,
Approximately 0.2% of the general population is aller- 2002; Wilson et al., 2007). People who are undergoing
gic to aspirin. However, of those individuals with a his- anticoagulant therapy involving such drugs as heparin
tory of any kind of allergic disorder, approximately 20% or warfarin should not use aspirin except when directed
will be allergic to aspirin. Patients who are sensitive to by a physician (Rodman, 1993). The combined effects
aspirin are likely also to be sensitive to ibuprofen or
naproxen, as cross-sensitivity between these drugs is 12Known as the “aspirin triad” of warning signs.
of aspirin and the anticoagulant may result in signifi- effectiveness of intrauterine devices, which normally
cant, unintended blood loss for the patient, especially if act to prevent pregnancy. Aspirin has also been impli-
he or she were to have an accident. Further, the antico- cated in fertility problems for couples who wish to have
agulant effect of aspirin can contribute to the develop- children. The use of aspirin at therapeutic dosage levels
ment of a hemorrhagic stroke (He, Whelton, Vu, & Klag, may reduce the ability of sperm to move (sperm motil-
1998). Thus, the physician must weigh the advantages ity) by up to 50%, thus reducing the chances of success-
of aspirin use in treating heart disease against its poten- ful conception in some cases. This is not to say that
tial to cause or contribute to a potentially fatal hemor- aspirin might serve as a method of birth control. But
rhagic stroke. aspirin-induced reduction in sperm motility might in-
Patients should not use different OTC analgesics si- terfere with the couple’s ability to conceive when they
multaneously, except under the supervision of physi- wish to do so.
cian. Aspirin, naproxen, and ibuprofen may all cause Medication interactions involving aspirin.14 Individ-
tinnitus (loss of hearing and a persistent ringing in the uals being treated for hyperuricemia (a buildup of uric
ears). The patient’s hearing will usually return to nor- acid in the blood) should not use aspirin except under a
mal when the offending medication is immediately dis- physician’s direction. When used at normal dosage
continued. Also, aspirin use may result in a very rare levels, aspirin reduces the body’s ability to excrete uric
side effect known as hepatotoxicity13 (Gay, 1990). In such acid, contributing to the problem of uric acid buildup.
cases, aspirin prevents the liver from being able to filter Further, aspirin blocks the action of the prescription
the blood effectively (Gay, 1990). Further, in rare cases, medication probenecid, one of the drugs used to treat
aspirin use can induce a state of depression in the user hyperuricemia. Acetaminophen has been advanced as
(Mortensen & Rennebohm, 1989). a suitable substitute for patients who suffer from hyper-
Because of age-related changes in blood flow and uricemia and need a mild analgesic (Wilson et al., 2007).
liver function, the elderly are especially susceptible to Aspirin also should not be used in patients who are
toxic reactions from aspirin and similar agents. These receiving medications for the control of their blood
age-related changes make it more difficult for older pressure, or anticoagulants such as warfarin, except
NSAID users to biotransform and excrete many com- under a physician’s supervision. It has been found that
pounds, including aspirin. About 1% of patients who aspirin or the other NSAIDs might interfere with some
use NSAIDs for extended periods of time experience antihypertensive medications (Fischer, 1989). The exact
drug-induced kidney failure (Marcus, 2003). There is mechanism by which this happens is unclear; however,
also preliminary evidence that regular aspirin use is as- it may reflect the impact of aspirin use on prostaglandin
sociated with an increased risk for end stage renal dis- production within the kidneys, resulting in fluid reten-
ease (ESRD) (Fored et al., 2001). tion (“Strong Medicine,” 1995). Individuals who are
Another complication of aspirin use in the elderly taking aspirin for its anticoagulation effect should avoid
is the development of drug-induced anxiety states the use of vitamin E, which also has an anticoagulation
(Sussman, 1988). Aspirin or related compounds should effect, except under a physician’s direction, since the
not be used with children who are suffering from a viral combination of these two compounds increases the
infection, except when directed by a physician. Research individual’s risk of abnormal bleeding (Harkness &
strongly suggests that aspirin might increase the possibil- Bratman, 2003).
ity of the child’s developing Reye’s syndrome as a com- Patients using any of the NSAIDs should be aware
plication of the viral infection (Graedon & Graedon, that these compounds can interfere with folate metabo-
1996; Jeffreys, 2004; Stimmel, 1997a). Although aspirin is lism (Harkness & Bratman, 2003). High folate levels
commonly used to treat the symptoms of a common cold, pose a health risk for the individual, and the concurrent
it may actually suppress the body’s immune response to use of these compounds should be avoided except
the invading virus to a small degree (Bartlett, 1999). under a physician’s direction, according to Harkness
Surprisingly, aspirin has been implicated in the fail- and Bratman. There is also a danger that patients using
ure of intrauterine devices (or IUD) to prevent preg- aspirin and the prescription medication valproate will
nancy. The anti-inflammatory action of aspirin is 14Itis not possible to list in this text every possible interaction between
thought to be the cause of its ability to interfere with the aspirin and other compounds. If you are in doubt about the possibil-
ity of an interaction between two or more compounds, consult a
13
See Glossary. physician or pharmacist.
experience higher-than-normal blood levels of the lat- supervision. Ibuprofen has been identified as the cause
ter drug, because the aspirin molecules will bind to the of aseptic meningitis in patients with SLE. On very rare
albumin sites that valproate normally binds to (DeVane & occasions, patients with no known autoimmune disor-
Nemeroff, 2002). Patients on valproate should discuss der will also develop aseptic meningitis after taking
their use of aspirin with their physician before mixing ibuprofen (Rodriguez, Olguin, Miralles, & Viladrich,
these two medications. 2006).
Individuals who plan to consume alcohol should not The compound lithium is often used to control some
use aspirin immediately prior to or while they are actively psychiatric disorders. When a patient taking lithium
drinking. There is evidence that the use of aspirin prior also ingests ibuprofen, the blood levels of lithium can
to the ingestion of alcohol decreases the activity of gastric increase by 25% to 60% (DeVane & Nemeroff, 2002;
alcohol dehydrogenase, an enzyme produced by the Rodman, 1993). This effect is most pronounced in the
stomach that starts to metabolize alcohol even before it older individual and may, given lithium’s narrow thera-
reaches the bloodstream (Roine, Gentry, Hernandez- peutic window, contribute to lithium toxicity (Pies,
Munoz, Baraona, & Lieber, 1990). Finally, patients who 2005). Close monitoring of blood lithium levels would
are using aspirin should not use the herbal medicine be necessary in patients who use both lithium and
ginkgo biloba because this combination of compounds ibuprofen to avoid the danger of lithium toxicity. Patients
might contribute to excessive bleeding (Cupp, 1999). who are on lithium should discuss with their physician
Ibuprofen. Ibuprofen has been implicated as the their use of ibuprofen and other OTC compounds to
cause of blurred vision in patients (Nicastro, 1989). Be- avoid the danger of lithium toxicity.
cause it has also been associated with the formation of Patients taking the prescription medication methotrex-
cataracts, it should be used by patients with cataracts ate should not use ibuprofen except under a physician’s
only under a physician’s supervision. Patients who ex- supervision, since this drug reduces the rate at which
perience a change in vision while taking ibuprofen methotrexate is excreted from the body (Rodman, 1993).
should contact their physician immediately (Graedon & Reduced excretion rates may result in toxic levels of
Graedon, 1996). methotrexate building up in the patient, according to
When ibuprofen was first introduced as a prescrip- the author. If an OTC analgesic should be required,
tion medication in 1974, it was manufactured by the Rodman (1993) recommended the use of acetamino-
Upjohn Company and sold under the brand name phen. The combined effects of NSAIDs may result in
Motrin. The manufacturer warned that ibuprofen can excessive irritation to the gastrointestinal tract and pos-
cause a number of side effects including heartburn, sibly severe bleeding. Further, the use of ibuprofen has
nausea, diarrhea, vomiting, nervousness, hearing loss, been found to block the antiplatelet effects of aspirin, a
congestive heart failure in persons who had marginal matter of some concern for patients who use aspirin for
cardiac function, changes in vision, and elevation of its effect on blood clot formation (Catella-Lawson et al.,
blood pressure (Thompson PDR, 2006). 2001; Hutchison, 2004). Concurrent use of NSAIDs
Recent research has also suggested that ibuprofen can should be avoided except under a physician’s supervi-
cause or contribute to kidney failure in persons with high sion (Rodman, 1993).
blood pressure, kidney disease, or other health problems Acetaminophen. Although acetaminophen has been
(Squires, 1990). This may be a side effect of ibuprofen’s called “the safest of all analgesics” when used as di-
ability to block the production of prostaglandins. By rected (Katz, 2000, p. 100), there are more than 100,000
blocking the body’s production of prostaglandins, ibupro- cases of acetaminophen overdoses each year in the
fen reduces the blood flow throughout the body, espe- United States, of which approximately 57% reflect acci-
cially to the kidneys. If the individual is already dental rather than intentional overdoses (Russo, 2006).
suffering from a reduction in blood flow to the kidneys In the United States, acetaminophen overdose has been
for any reason, including “normal aging, liver or car- identified as the leading cause of liver failure resulting
diovascular disease or simply dehydration from vomit- in the need for liver transplant surgery (Russo, 2006).
ing, diarrhea and fever accompanying the flu” (Squires, Thus, while this medication is considered safe when used
1990, p. 4E), ibuprofen might either cause or contri- as directed, it also carries a very real potential for harm.
bute to acute kidney failure in the patient. Individuals who have alcohol-related liver damage
Patients who are suffering from autoimmune disor- or are actively drinking should not use acetaminophen
ders such as systemic lupus erythematosus (lupus or SLE) except under a physician’s supervision (Draganov,
should not use ibuprofen except under a physician’s Durrence, Cox, & Reuben, 2000; Johnston & Pelletier,
1997; Peterson, 1997; Sands, Knapp, & Ciraulo, 1993). of peptic ulcers and gastrointestinal bleeding. Men have
Even when used as directed, acetaminophen com- occasionally experienced naproxen-induced erectile
bined with alcohol can rise to toxic levels in the problems and/or loss of the ability to ejaculate (Finger,
drinker’s body. When acetaminophen is ingested, about Lund, & Slagel, 1997).
4% to 5% of the drug is biotransformed into a toxic Known side effects of naproxen include drowsiness,
metabolite known as N-acetyl-p-benzoquinoneimine dizziness, feelings of depression, diarrhea, heartburn,
(Peterson, 1997). Normally, this metabolite poses no constipation, abdominal pain/vomiting, and vertigo
danger to the healthy user and it is rapidly biotransformed (Qureshi & Lee-Chiong, 2004). On rare occasions, pa-
into other substances by the liver enzyme glutathione. tients taking naproxen have experienced side effects
However, chronic drinkers, people who suffer from mal- such as skin rash, headache, insomnia/sleep problems,
nutrition, those who are fasting for extended periods of hearing problems, and/or tinnitis. The team of Taha
time, and those with alcohol-induced liver damage rap- et al. (1994) found that 44% of their sample who had
idly experience glutathione depletion even when the used naproxen for extended periods of time had evidence
acetaminophen is used at recommended dosage levels, of gastrointestinal ulcers. Because of this, it was recom-
and thus they are vulnerable to acetaminophen toxicity. mended that naproxen not be utilized by patients with
Individuals who ingest very large doses of vitamin C a history of peptic ulcer disease unless under the super-
should not use acetaminophen except under a doctor’s vision of a physician (Dionne & Gordon, 1994).
supervision (Harkness & Bratman, 2003). Very high Many of the NSAIDs, including naproxen, have
doses of vitamin C15 appear to interfere with acetamin- been implicated as a cause of ESRD (Perneger et al.,
ophen biotransformation, increasing the risk that the 1994). There have also been reports of potentially fatal
individual’s blood level of the latter chemical might liver dysfunctions that seem to have been caused by
reach toxic levels, according to Harkness and Bratman. naproxen. Animal research has suggested the possibility
The potential for cumulative dose toxicity induced of damage to the eyes as a result of naproxen use, al-
by the chronic use of acetaminophen is possible, but re- though it is not clear at this time whether this medica-
searchers know very little about this phenomenon tion may cause damage to the visual system of a human
(Smith, 2007). But because of acetaminophen’s cumu- being. On rare occasions, naproxen has been identified
lative toxic effects on the liver, it should not be used for as the cause of aseptic meningitis in patients using this
longer than 10 days except as directed by a physician medication (Rodriguez et al., 2006). While this list
(Kacso & Terezhalmy, 1994). In rare cases, acetamino- does not identify every possible adverse reaction to
phen has been implicated as the cause of anaphylactic naproxen, it does suggest that it is a very potent chemi-
reactions in patients. Acetaminophen has also been cal that should be used only when the benefits are
found to be nephrotoxic—that is, if used too often or at thought to outweigh the possible consequences.
too high a dosage level, it may be toxic to the cells of the
kidneys. A controversial research finding is that aceta-
minophen use is associated with end state renal disease Overdose of OTC Analgesics
(ESRD) (Perneger, Whelton, & Klag, 1994). However, Acetaminophen. Unfortunately, in spite of its value as
these results have been challenged (Fored et al., 2001; an OTC analgesic, acetaminophen is also the drug
Rexrode et al., 2001). Thus, until a definitive conclu- most commonly ingested in an overdose attempt, ac-
sion is reached, it must be assumed that acetamino- counting for 5% to 10% of all hospital admissions and
phen should be used only when the advantages outweigh 94% of all intentional drug overdoses (Sharma, 2003).
the potential for harm from this OTC analgesic. The fact that the mortality from acetaminophen over-
Naproxen. Much of the information available on doses is only 0.03% overall, and < 2% for those patients
naproxen and its effects is based on experience ob- admitted to the hospital (Sharma, 2003), is a reflection
tained with the prescription-strength preparation of this of the skill with which physicians have been able to
chemical. Naproxen has been found to be a factor in treat acetaminophen overdoses.16 However, it should
potentially fatal allergic reactions in some users, and be noted that some of those who survived an acetamin-
patients with the “aspirin triad” (discussed earlier) should ophen overdose required a liver transplant in order to
not use naproxen except under a physician’s supervision. live (Cetaruk, Dart, Horowitz, & Hurlbut, 1996).
This medication may also contribute to the formation
16
The reader is reminded that any real, or suspected, overdose should
15
Defined as 3 grams/day or more. be assessed and treated by a physician immediately.
Acetaminophen is often ingested by individuals, es- The mechanism by which acetaminophen overdoses
pecially adolescents, who want to make a suicide ges- induce liver damage and possibly death is through the
ture. While the individual who makes this gesture destruction of the liver enzyme glutathione. Glutathione
rarely intends to complete the suicide attempt, aceta- is a chemical produced by the liver to protect itself from
minophen’s narrow therapeutic window makes it a poor various toxins (Smith, 2007). This enzyme is exquisitely
choice for a suicide gesture. The first objective evi- sensitive to large doses of acetaminophen, however, and
dence of acetaminophen toxicity might not appear can be depleted or even totally destroyed if the individ-
until 12–24 hours after the overdose was ingested, giv- ual takes more than 4,000 mg/day (just 8 “extra strength”
ing the individual a false sense of security after his or tablets), or even less if the person is also drinking alcohol
her overdose. Because of this, the individual might not (“Scientists Call for Stronger Warnings,” 2002). A dose of
seek medical assistance until hours or even days after just 7.5–15 grams of acetaminophen (just 15–30 “extra-
the overdose was ingested, well past the time for effec- strength” tablets) in a single dose, or 5–8 grains (650–975
tive treatment of the overdose. The compound known mg) per day for several weeks is enough to cause a toxic
as N-acetylcysteine (NAC) is an effective counteragent reaction in the healthy adult (McDonough, 1998;
if an acetaminophen overdose has been ingested, but it Supernaw, 1991; Whitcomb & Block, 1994).
must be administered within 12 hours of the overdose to One factor that seems to contribute to liver damage
be fully effective (Smith, 2007). If the individual waits in at least some cases is whether the individual ingested
until the symptoms of acetaminophen toxicity develop the acetaminophen on an empty stomach (Schiødt,
before seeking help, it may be too late to prevent per- Rochling, Casey, & Lee 1997; Whitcomb & Block,
manent liver damage, or even death. 1994). Even otherwise normal patients who were at-
The untreated acetaminophen overdose will progress tempting to control their weight through semi-starvation
through four different stages: First, within 30 minutes or fasting seem to be especially at risk for an uninten-
to 24 hours of the time the overdose was ingested, the tional toxic acetaminophen reaction (Schiødt et al.,
individual will experience symptoms such as anorexia, 1997). The authors pointed out that the enzyme glu-
nausea, diaphoresis,17 and vomiting in response to the tathione is depleted by starvation diets, placing the indi-
effects of the acetaminophen on the digestive system vidual at risk for a toxic reaction to even normal dosage
(McDonough, 1998; Smith, 2007). Phase 2 starts 24– levels of acetaminophen. Thus, the individual’s diet is
72 hours after the overdose was ingested and is marked an important factor to consider when he or she is using
by symptoms such as abdominal pain, oliguria,18 and acetaminophen for the control of mild to moderate
pain over the liver (McDonough, 1998; Smith, 2007). levels of pain. These studies suggest that at least for cer-
During this phase, blood tests will reveal abnormal liver tain individuals, acetaminophen has the potential to
function and it is possible for the kidneys to show signs cause toxic reactions at dosage levels just above the nor-
of distress. In phase 3 (72–96 hours after the overdose mal therapeutic dosage range.
was ingested) the individual will begin to experience Aspirin. Aspirin is often ingested in suicide gestures
nausea, vomiting, jaundice, and symptoms of liver fail- or attempts (Sporer & Khayam-Bashi, 1996). The aver-
ure (McDonough, 1998; Smith, 2007). Other possible age dosage level necessary to produce a toxic reaction
complications that might emerge during the third to aspirin is about 10 grams for an adult and about
phase include hemorrhage, hypoglycemia, renal fail- 150 mg for every kilogram of body weight for children.
ure, and hypotensive episodes. It is during this phase A dose of 500 mg of aspirin per kilogram of body weight
that death might occur from an acetaminophen over- is potentially fatal to the individual. Symptoms of as-
dose unless the person (a) did not ingest a fatal overdose pirin toxicity include headache, dizziness, tinnitus,
or (b) was treated for the overdose in time. If the indi- mental confusion/delirium, hallucinations, increased
vidual survives phase 3, he or she will move into the sweating, thirst, dimming of sight, and hearing impair-
fourth and final phase, which begins 4 days to 2 weeks ment. Other symptoms of aspirin toxicity include rest-
after the overdose was ingested (Smith, 2007). During lessness, excitement, apprehension, tremor, convulsions,
this time, the liver begins to repair itself, a process that stupor, coma, hypotension, and at higher dosage levels,
might require 3 months or more following the overdose possible death (Sporer & Khayam-Bashi, 1996; Wilson
(Smith, 2007). et al., 2007). While these symptoms are most often seen
in the person who has ingested a large dose of aspirin,
17
See Glossary. even small doses might result in toxicity for the individ-
18
See Glossary. ual who is aspirin-sensitive.
Ibuprofen. Symptoms of an ibuprofen overdose in- Aspirin, acetaminophen, naproxen, and ibuprofen
clude seizures, acute renal failure, abdominal pain, are all quite effective in the control of mild to moder-
nausea, vomiting, drowsiness, and metabolic acidosis ate levels of pain without exposing the patient to the
(Lipscomb, 1989). There is no specific antidote for a toxic side effects found with narcotic analgesics. Some of
dose of ibuprofen, and medical care is often aimed at the OTC analgesics are also useful in controlling the
supportive treatment only. inflammation of autoimmune disorders and in help-
Naproxen. The life-threatening dose of naproxen in ing to control postsurgical pain. Researchers have dis-
humans is not known (Thompson PDR, 2006). No spe- covered that the OTC analgesics are of value in
cific antidote is known for an overdose of naproxen, and controlling the pain associated with cancer. Surpris-
medical care is limited to supportive treatment only. ingly, research has suggested that aspirin might even
There are no symptoms specific to a naproxen over- contribute to the early detection of some forms of
dose. Symptoms of an NSAID overdose include lethargy, cancer: it thins blood, causing cancerous tumors to
drowsiness, nausea, vomiting, epigastric pain, respira- begin to bleed at an earlier stage than they would nor-
tory depression, coma, and convulsions. The NSAIDs mally do, allowing earlier detection. Although aspirin is
are capable of causing gastrointestinal bleeding in over- the oldest OTC analgesic, introduced more than a cen-
dose situations and may cause either hypotension or hy- tury ago, medical researchers are still discovering new
pertension (Thompson PDR, 2006). applications for this potent medication and its chemical
cousins.
But in spite of the fact that they are available over the
Summary counter, the OTC analgesics do carry significant poten-
Over-the-counter analgesics are often discounted by tial for harm. Acetaminophen in near-normal dosage
many as not being “real” medications. However, al- levels has been implicated in toxic reactions in chronic
though it is often discounted by the average user as alcohol users. It also has been implicated as the cause of
being something less than a real pharmaceutical, aspirin death in people who have taken overdoses of it. Aspirin
is America’s most popular “drug.” Each year, more than and ibuprofen have been implicated in fatal allergic
20,000 tons of aspirin are manufactured and consumed reactions, especially in those who suffer from asthma.
in this country alone, and aspirin accouts for only about The use of aspirin in children with viral infections is
28% of the OTC analgesic sales. not recommended.
CHAPTER NINETEEN
Tobacco Products and Nicotine Addiction
Historians believe that the natives of the New World was interpreted as a mark of sophistication both in
were familiar with tobacco at least 16,000 years B.C.E.1 Europe and North America, but in the last half of the
and that natives living in what is modern-day Peru and 20th century tobacco use came under fire as its addic-
Equador have been actively cultivating it since 5000 tive properties and the long-term consequences of its
B.C.E. (Burns, 2007). Tobacco was used in religious and use became clear. In the first years of the 21st century,
social ceremonies of the era, and when the smoke of tobacco use is both widespread and the subject of much
the tobacco plant was delivered rectally it was thought controversy. In this chapter, the history of tobacco use
to be a useful medicine (Burns, 2007).2 The first writ- and the complications caused by using tobacco are
ten record of tobacco use in the New World is found in reviewed.
Mayan carvings that date back to approximately 600
B.C.E. (Schuckit, 2006). Then the first European ex-
plorers arrived in what would one day be called the
History of Tobacco Use
Americas. The art of smoking was carried back across in the United States
the Atlantic to Europe by these early explorers, many of Anthropological evidence suggests that a form of to-
whom had themselves adopted the habit of smoking tobacco was cultivated in South America as early as 8,000
bacco during their time in the New World. years ago (Burns, 2007; Walton, 2002). But today’s to-
In Europe, the use of tobacco for smoking was re- bacco is much different from the tobacco used cen-
ceived with some skepticism if not outright hostility. In turies ago in the New World. The original strain of the
Germany, public smoking was once punishable by tobacco plant used by the natives of the New World was
death, while in Russia, castration was the sentence for possibly more potent and may have contained halluci-
the same crime (Hymowitz, 2005). In Asia, the use or natory substances not found in the form of tobacco now
distribution of tobacco was deemed a crime punishable in general use (Schuckit, 2006; Walton, 2002). This is
by death, and smokers were executed as infidels in because European tobacco users preferred the milder
Turkey. In spite of these rather harsh measures, the prac- Nicotiana tabacum as opposed to the more potent
tice of smoking became quite popular in Europe, and Nicotina rustica used by the native peoples of what would
within a few decades of its introduction the use of tobacco come to be called the New World by early European ex-
had spread across Europe and moved into Asia (Schuckit, plorers (Burns, 2007; Hilts, 1996).
2000). Tobacco use was quite common in England in the
Because of tobacco’s ability to impact how the body 15th and 16th centuries, and it can be argued that the
functioned, European physicians in the 14th and 15th English demand for tobacco fueled the early English
centuries viewed tobacco as a medicine, and like their settlement of what would become the thirteen original
New World counterparts saw it as a cure for numerous colonies and later the United States (Burns, 2007). To-
conditions. By the 19th and early 20th centuries, smoking bacco use was also popular in the colonies, usually in
the form of pipe or cigar smoking, although the tobacco
1Which stands for Before Common Era. leaf was also used as a form of currency in some
2
Although, as the author suggests, it is hard to imagine that practition- colonies. In spite of the prevalence of tobacco smoking
ers of the era were enthusiastic about the use of this folk medicine in the colonies, a small number of nonconformists pre-
(Burns, 2007). Burns also presented evidence that at least some tribal
warriors in the New World would chew tobacco leaves so they might
ferred to chew the leaf, either spitting out the expecto-
attempt to spit the expectorant into the eyes of their opponent, thus rant, or, if they were of the upper classes, swallowing it
blinding him in the heat of battle. (Burns, 2007). No less a person than John Hancock was
222
Tobacco Products and Nicotine Addiction 223
one of those who chose to chew the leaf, and he went man, woman, and child on earth, with 15 billion ciga-
on to prove that he was indeed a nonconformist when rettes being smoked each day on this planet (Sundaram,
he became the first person to sign the Declaration of In- Shulman, & Fein, 2004). In the United States, the esti-
dependence in 1776. mated 45 million active cigarette smokers consumed an
By the 19th century, tobacco was well entrenched in estimated 378.6 billion cigarettes in 2005 (Kaufman,
American culture, but by mid-century several different 2006). Although this figure is impressive, it is actually
forces combined to change the shape of tobacco use. the lowest number of cigarettes consumed in this coun-
First, new varieties of tobacco were planted, allowing try in the past 21 years, according to Kaufman (2006).
for greater yields, while new methods of curing the leaf Approximately 20.9% of adults in the United States
of the tobacco plant were found, speeding up the smoke cigarettes at this time (“Cigarette Smoking Among
process by which the leaf might be prepared for use. Adults,” 2004).
Also, the advent of the industrial age brought with it While only a small minority of cigarette smokers
machinery capable of manufacturing the cigarette, a abuse other chemicals, it is not uncommon for sub-
smaller, less expensive, neater way to smoke than hand- stance abusers to be heavy smokers. The prevalence
made cigars. Just one machine invented by James A. rates for cigarette smoking among alcohol- and drug-
Bonsack could produce 120,000 mini-cigars, or ciga- dependent persons range from 71% to 100% (el- Guebaly,
rettes, a day. The development of such machines greatly Cathcart, Currie, Brown, & Gloster, 2002). These figures
increased the number of cigarettes that could be pro- suggest that cigarette use is a significant problem for
duced while reducing the price. This made it possible those who are addicted to other chemicals.
for less affluent groups to afford tobacco products, and Although children are not often viewed as a major
cigarettes soon became a favorite of the poor (Tate, 1989). part of the smoking problem, researchers have found
By 1890, the price of domestic cigarettes had fallen to a that they actually begin to form pro-smoking attitudes
nickel for a pack of 20 (Tate, 1989), making them af- early in life, and then experiment with the use of ciga-
fordable to all but the poorest smoker. But this rapid rettes either in late childhood or early adolescence.
acceptance of cigarettes was not always welcomed; by One-third of 9-year-olds in the United States have
1909, no less than 10 different states had laws that pro- taken at least one experimental “puff” on a cigarette
hibited the use of cigarettes, with little effect on the (Hymowitz, 2005). The median age at which individuals
practice of smoking them. begin to experiement with regular cigarette use is thought
The most common method of tobacco use in the to be around 15 (Patkar, Vergare, Batra, Weinstein, &
18th and 19th centuries was chewing. The practice of Leone, 2003). The fact that the roots of adult smoking
chewing tobacco, then spitting into the ever-present are found in the childhood years has apparently not
cuspidor, was found to contribute to the spread of tu- been lost on some cigarette manufacturers, who have
berculosis and other diseases at the start of the 20th cen- developed flavored cigarettes that are apparently most
tury (Brecher, 1972). Public health officials began to attractive to younger individuals.
campaign against chewing tobacco after 1910, and in
many cases they suggested cigarettes as a more sanitary Pharmacology of Cigarette Smoking
and relatively inexpensive alternative to chewing to-
bacco. Unlike cigar or pipe smokers, cigarette smokers The primary method by which tobacco is used is by
soon discovered that the cigarette smoke was also so smoking cigarettes (Schuckit, 2006), although chewing
mild that it could be inhaled (Burns, 1991). Cigarette tobacco and cigar smoking are again becoming popular
smoking became the preferred method through which in some quarters. Chemically, cigar smoke is very simi-
their nicotine addiction might be serviced, and the lar to cigarette smoke, although it does contain a higher
world has never been the same since. concentration of ammonia (Jacobs, Thun, & Apicella,
1999). For these reasons, the terms smoking, cigarette,
and tobacco will be used interchangeably in this chap-
Scope of the Problem ter, except when other forms of tobacco (such as to-
At the start of the 21st century, approximately 1 billion bacco prepared for chewing) are discussed.
men and 250 million women around the world were The chemistry of tobacco smoke is influenced by a
smoking on a daily basis (Levitz, Bradley, & Golden, number of variables, including (a) the exact composition
2004; Rose et al., 2003). The global per capita cigarette of the tobacco, (b) how densely the tobacco is packed,
consumption is estimated at 1,000 cigarettes for every (c) the length of the column of tobacco (for cigarette
224 Chapter Nineteen
or cigar smokers), (d) the characteristics of the filter through machines used in the manufacturing process)
being used (if any), (e) the paper being used (for ciga- (Glantz, Slade, Bero, Hanauer & Barnes, 1996). Al-
rette smokers), and (f) the temperature at which the though the smoker inhales these products when he or
tobacco is burned (Jaffe, 1990). To further complicate she smokes a cigarette, there has been virtually no re-
matters, the cigarette of today is far different from the search into the effects of these chemicals on the human
cigarette of 1900, or even the cigarette of 1950, with up body when they are smoked.
to 40% of the typical cigarette being composed of “left- In an effort to combat the negative image of cigarette
over stems, scraps and dust” (Hilts, 1996, p. 44). In 1955, smoking, many tobacco companies introduced “light”
it took 2.6 pounds of tobacco leaves to produce a thou- or “ultra-light” brands of cigarettes in the 1960s. Unfor-
sand cigarettes; today, the use of these fillers has re- tunately, research suggests that these brands do not
duced the amount of tobacco needed to produce a bring about a significant reduction in the exposure to
thousand cigarettes to 1.7 pounds (Hilts, 1996). This the toxins found in regular cigarettes, and they are just
practice seems to account for why a pack of Marlboro cig- as addictive as regular cigarettes (“Light Cigarettes Just
arettes that sells for $3.15 yields a profit of $1.40 for the as Addictive,”2006; Hymowitz, 2005).
manufacturer, the Phillip Morris Tobacco Company— The concentrations of many of the chemicals found
a profit margin of 44% per pack (Fonda, 2001). While in cigarette smoke, such as carbon monoxide, are such
the price of cigarettes might be higher, the profit mar- that “uninterrupted exposure” (Burns, 1991, p. 633)
gin is still the same. would result in death. For example, Burns noted that the
Some 4,700 chemical compounds have been identi- concentration of carbon monoxide found in cigarettes
fied in cigarette smoke, of which some 2,550 come from is “similar to that found in automobile exhaust” (p. 633),
the unprocessed tobacco itself (Fiore, 2006; Schmitz & a known source of potentially dangerous concentra-
Delaune, 2005; Stitzer, 2003). It has been estimated that tions of this chemical. There are at least 60 compounds
perhaps as many as 100,000 other chemical compounds found in cigarette smoke that are known carcinogens3
might also remain to be discovered in cigarette smoke (Levitz et al., 2004). When the individual smokes,
(Schmitz & Delaune, 2005). Many of the compounds radioactive compounds absorbed from the soil by the
in cigarette smoke come from additives, pesticides, and tobacco plant are also carried into the lungs along with
a range of other organic or metallic compounds that the smoke. Over a year, the cumulative radiation expo-
either intentionally or unintentionally find their way sure for a two-pack-a-day smoker is equal to what a per-
into the cigarette tobacco. A partial list of the com- son would receive if he or she had 250–300 chest x-rays
pounds found in tobacco smoke would include these: (Evans, 1993). Further, cigarette smoke is known to
acetaldehyde, acetone, aceturitrile, acrolein, acrolein, contain a small amount of arsenic, a known poison
acrylonitrile, ammonia, arsenic, benzeye, butylamine, (Banerjee, 1990).
carbon monoxide, carbon dioxide, cresols, crotononitrile, Nicotine. Nicotine was first isolated in 1828, and
DDT, dimethylamine, endrin, ethylamine, formalde- while this substance was known as early as 1889 to have
hyde, furfural hydroquinone, hydrogen cyanide (used in an effect on nervous tissue, not until almost a century
the gas chamber), hydrogen sulfide, lead, methacrolein, later was the mechanism by which nicotine affected
methyl alcohol, methylamine, nickel compounds, nico- neurons identified (Stitzer, 2003). As a result of legal ac-
tine, nitric oxide, nitrogen dioxide, phenol, polonium- tion against tobacco companies, documents have come
210 (radioactive), pyridine, “tar” (burned plant resins) to light revealing that these companies knew for decades
(Shipley & Rose, 2003, p. 83, heavy print in original that nicotine was the major psychoactive agent in ciga-
deleted). rettes, and that they view cigarettes as little more than a
In addition to all of these compounds, various per- single-dose nicotine administration system (Benowitz &
fumes are added to the tobacco leaves to give the ciga- Henningfield, 1994; Glantz, Barnes, Bero, Hanauer, &
rette a distinctive aroma (Hilts, 1996). Dane, Havey, Slade, 1995; Glantz et al., 1996; Hilts, 1996). Further,
and Voohees (2006) found dangerous levels of pesti- there is strong evidence that cigarette manufacturers in-
cides classified as human carcinogens in the cigarettes creased the nicotine content of most major brands of ciga-
that they tested. Other compounds found in cigarettes rettes by almost 10% from 1998 to 2004 (R. Brown, 2006).
or the paper wrapper include various forms of sugar, Although nicotine is well absorbed through the gas-
herbicides, fungicides, rodenticides, and manufactur- trointestinal tract, much of orally administered nicotine
ing machine lubricants (which come into contact with
the tobacco leaves and paper as these products move 3See Glossary.
is rapidly biotransformed by the liver as a result of the to feel stimulated or aroused (Gwinnell & Adamec,
“first-pass metabolism” effect, limiting its effect on the 2006). It also stimulates the release of the neurotrans-
body (see Chapter 3). Cigarette smoking avoids this dan- mitters acetylcholine and dopamine in the brain, the
ger and is the ideal method of introducing nicotine into latter activating the brain’s pleasure center and making
the body. Each “puff” on a cigarette introduces a small the smoker feel relaxed (Gwinnell & Adamec, 2006).
dose of nicotine into the circulation that reaches the The impact of the dopamine that is released is en-
brain in less than 10 seconds (Gwinnell & Adamec, hanced by nicotine’s ability to reduce the levels of
2006). Through this process, the typical two-pack-a-day monoamine oxidase β in the brain, which breaks down
smoker self-administers approximately 400 doses of nico- dopamine molecules after their release into the synapse.
tine each day without the problem of first-pass metabo- At the same time, nicotine stimulates the release of ni-
lism (Gwinnell & Adamec, 2006; Jorenby, 1997; Parrott, tric oxide in the brain, which has the effect of slowing
1999). The smoker “over-learns” the process of nicotine the process of dopamine reuptake (Fogarty, 2003).
self-administration through hundreds of thousands or Other neurochemical changes included in the
even millions of repetitions over his or her lifespan nicotine-induced cascade include vasopressin, GABA,
(Hughes, 2005). glutamate, beta endorphine (β-endorphin), and sero-
The lethal dose of nicotine for the average adult is tonin (Fogarty, 2003; Hymowitz, 2005; Schmitz &
estimated to be approximately 60 mg (Stitzer, 2003). Delaune, 2005). Nicotine causes virtually a complete
Atlhough the average cigarette contains approximately saturation of at least one subtype of acetylcholine recep-
10 milligrams (mg) of nicotine (Greydanus & Patel, tor in the brain5 (Brody et al., 2006). Long-term binding
2005), only about 25% of this actually enters the of nicotine to this acetylcholine receptor subtype causes
smoker’s bloodstream (Sadock & Sadock, 2003). Nico- these receptors to become desensitized, and when they
tine is not able to cross from the lungs to the blood are not occupied by nicotine molecules this might cause
very easily, and so the typical smoker actually absorbs or exacerbate nicotine withdrawal symptoms, according
only 1–3 mg of the available nicotine in each cigarette to the authors.
(Oncken & George, 2005; Stitzer, 2003). In terms of ab- Peak nicotine concentrations are reached in the first
solute toxicity, the typical smoker will receive between minutes after the cigarette is smoked, and then drop as
1/60th and 1/24th of the estimated lethal dose of the nicotine is redistributed to various body tissues. The
nicotine with each cigarette. Over the course of the biological half-life of nicotine is approximately 2 hours
typical day, the average smoker absorbs a cumulative (J. R. Hughes, 2005; Stitzer, 2003). Since only 50%
dose of 20–40 mg of nicotine, a dosage level that, if not of the nicotine from one cigarette is biotransformed
lethal to the smoker, is still quite toxic to his or her body during the first half-life period, over the course of a
(Henningfield, 1995). day a reservoir of unmetabolized nicotine is estab-
Once in the body, nicotine is rapidly distributed to lished in the smoker’s body. A limited degree of tolerance
virtually every blood-rich tissue including the lungs, to nicotine’s effects develops each day, but this ac-
spleen, and especially the brain (Hymowitz, 2005). quired tolerance is lost just as rapidly during the night
Nicotine is both water-soluble and lipid-soluble, and its hours when the typical smoker abstains from cigarette
lipid solubility allows it to cross over the blood-brain use (J. R. Hughes, 2005). This is why many smokers
barrier into the brain very rapidly. This allows nicotine find that the first cigarette of the day has such a strong
to accumulate, and the level of nicotine in the brain effect.
will be approximately twice as high as the level found Only 5% to 10% of the nicotine that enters the body is
in the blood (Fiore, Jorenby, Baker, & Kenford, 1992). excreted unchanged (Hymowitz, 2005). The rest is bio-
Very little nicotine becomes protein bound in the blood transformed by the liver, with about 90% of the nicotine
(Hymowitz, 2005). being biotransformed into cotinine, a metabolite of nico-
The nicotine molecule has a shape similar to that tine that in recent years has been shown to possibly have
of the neurotransmitter acetylcholine, and it rapidly psychoactive effects of its own (Schmitz & Delaune,
causes a cascade of neurochemical changes in the 2005). The other 10% of the nicotine is biotransformed
brain (Schmitz, & Delaune, 2005). One of the earliest into nicotine-N-oxide. These chemicals are then ex-
of these changes involves the nicotine-induced release creted from the body in the urine. Although it was once
of the neurotransmitter epinephrine,4 causing the smoker thought that cigarette smokers were able to biotransform
4Also known as adrenaline. 5

It is known as the α4β2 nicotinic acetylcholine receptor subtype.
nicotine more rapidly than nonsmokers, research has Dore, & Clark, 2002). It has also been found to increase
failed to support this belief (Benowitz & Jacob, 1993). the blood levels of medications such as clomipramine,
Acetaldehyde. In addition to nicotine, tobacco smoke and antidepressant medications such as desipramine,
also includes a small amount of acetaldehyde. By coin- doxepin, and nortriptyline (American Psychiatric Asso-
cidence, this is also the first metabolite produced by the ciation, 1996).
liver when the body biotransforms alcohol. Researchers Scientists have discovered that between 70% (Enoch &
now know that the acetaldehyde that forms as a result of Goldman, 2002) and 95% (Hughes, Rose, & Callas,
cigarette smoking bonds with the saliva, which then al- 2000) of heavy drinkers also smoke, possibly because
lows the toxin a longer period of contact with oral tis- nicotine is more reinforcing for alcohol users than for
sues than the smoke allows, increasing the individual’s nondrinkers.6 There is also an emerging body of evi-
risk of oral cancer (Melton, 2007). dence based on animal research that suggests that nico-
Drug interactions between nicotine and other chemi- tine addiction is mediated by many of the same genes
cals. Drug interactions between nicotine and various that trigger alcohol dependence (Le et al., 2006). Ciga-
other therapeutic agents are well documented. Ciga- rettes slow the process of gastric emptying, and thus the
rette smokers, for example, will require more morphine process of alcohol absorption, and this reinforces the
for the control of pain (Bond, 1989; Jaffe, 1990). Smok- tendency for the drinker to also smoke (Nelson, 2000).
ers also achieve a lower blood plasma concentration of Further, the nicotine absorbed by the smoker seems to
such compounds as propranolol, haloperidol, and dox- counteract some of the sedation seen with alcohol use.
epin at a given dosage level than do nonsmokers (J. R. While the list of potential interactions between nico-
Hughes, 2005). Tobacco smokers may experience less tine and various pharmaceuticals reviewed in the last
sedation from benzodiazepines than do nonsmokers few paragraphs does not list every possible chemical
(Barnhill, Ciraulo, Ciraulo, & Greene, 1995). Surpris- that might interact with nicotine, it does highlight nico-
ingly, cigarette smokers appear to biotransform THC tine’s very strong effect on the way other chemicals
faster than nonsmokers, and thus the effects of mari- work in the body.7
juana do not last quite as long in the cigarette smoker as
in the nonsmoker (Nelson, 2000). The Effects of Nicotine Use
Tobacco also interacts with many anticoagulants as
well as the beta blocker propranol and caffeine (Bond, Nicotine causes a dose-dependent, biphasic response at
1989). Women who use oral contraceptives and who the level of the individual neuron, especially those that
smoke are more likely to experience strokes, myocardial utilize the neurotransmitter acetylcholine (Oncken &
infarction, and thromboembolism than their nonsmok- George, 2005; Ritz, 1999; Rose et al., 2003). The
ing counterparts, according to Bond. There is an inter- chemical structure of nicotine is very similar to that of
action between cigarette smoking and theophylline, acetylcholine, and nicotine initially stimulates these
and after the smoker stops smoking, he or she will expe- neurons, possibly contributing to the smoker’s feeling
rience a 36% rise in theophylline blood levels over the of increased alertness. However, over longer periods of
first week of abstinence. This seems to be caused by the time nicotine blocks the acetylcholine receptor sites,
effects of such chemicals as benzopyrene in the to- reducing the rate at which those neurons “fire.” This
bacco smoke (Henningfield, 1995). Also, the concen- might be the mechanism by which cigarette smoking
tration of caffeine in the blood might increase by as makes the individual feel relaxed. Further, the chronic
much as 250% following smoking cessation, causing use of nicotine results in an increase in the total num-
caffeine-induced anxiety symptoms. Anxiety is an early ber of nicotine receptors in the wall of the neurons,
symptom of nicotine withdrawal, and smokers quickly which might explain at least part of the craving that
learn to avoid this unpleasant experience by smoking smokers experience initially after they stop smoking.
another cigarette (Little, 2000). The result of this process Nicotine is quite toxic, and the estimated lethal oral
is that the former smoker might interpret caffeine-related dose is thought to be between 40 and 60 mg (Hymowitz,
anxiety symptoms as a sign that he or she should have
6The author has met a number of alcohol abusers, for example, who
a cigarette.
report that they smoke only when they are drinking. The author has
Nicotine use has been found to decrease the blood never met somebody who has claimed the opposite, however.
levels of clozapine and the antipsychotic medication 7To avoid potentially dangerous interactions between medications
haloperidol by as much as 30% to 50% (American Psychi- and cigarettes, the individual is advised to consult a physician or phar-
atric Association, 1996; Kavanagh, McGrath, Saunders, macist before using a pharmaceutical and then smoking.
2005). Symptoms of nicotine toxicity include nausea, sues of the lungs and pulmonary system. The process of
vomiting, diarrhea, abdominal pain, headache, sweat- smoking deposits potentially harmful chemicals in the
ing, and pallor (Hymowitz, 2005).8 These symptoms lungs and causes a decrease in the motion of the cilia10
seem to account for reports that first-time smokers often in the lungs. These features of cigarette smoking are
experience a sense of nausea and may possibly even thought to contribute to the development of pulmonary
vomit (Restak, 1991). However, if the individual persists problems in long-term smokers.
in his or her attempts to smoke, the stimulation of the
neurotransmitter systems outlined above will eventu- Nicotine Addiction
ally result in an association between smoking and the
nicotine-induced pleasurable sensations, as the smoker Sometime in the early 1960s, researchers for various to-
“over-learns” the association between smoking and the bacco companies discovered that nicotine, which is the
drug-induced subjective experience of pleasure as the chemical in cigarettes that makes smoking rewarding, was
neurotransmitters norepinephrine and dopamine are also highly addictive. This research was apparently sup-
released within the brain. pressed by the tobacco industry for many years (Hurt &
For much of the latter part of the 20th century, to- Robertson, 1998; Slade, Bero, Hanauer, Barnes, &
bacco companies argued that since nicotine does not Glantz, 1995). Indeed, one memo from 1963, cited by
produce the pattern of intoxication seen with alcohol or Slade et al., illustrates that the tobacco industry knew it
barbiturate abuse, it was not addicting in the traditional was “in the business of selling nicotine, an addictive
sense of the word (Stitzer, 2003).9 However, as the drug” (p. 228), to smokers. However, not until 1997 did
brain mechanisms involved in addiction have become a major tobacco company in the United States, the
more clearly defined, it has become evident that nico- Liggett Group, admit in court that tobacco was addic-
tine is indeed an addictive substance in every sense of tive (Solomon, Rogers, Katel, & Lach 1997).
the word (Stitzer, 2003). Unfortunately, scientists still Nicotine, like other addictive compounds, is able to
do not fully understand the mechanism by which nico- activate the mesolimbic dopaminergic pathways that
tine causes the smoker to become addicted (Rose et al., make up part of the reward system in the brain (Zubieta
2003). et al., 2005). The addictive potential of cigarettes would
Outside of the brain, nicotine stimulates the release seem to be significantly greater than that of cocaine:
of acetylcholine, which is involved in controlling many Only 3% to 20% of those who try cocaine once go on to
of the body’s muscle functions. Nicotine-induced become addicted to it (Musto, 1991), but 33% to 50% of
acetylcholine release in the body seems to account, at those who experiment with smoking will become ad-
least in part, for nicotine’s immediate effects on the car- dicted (Henningfield, 1995; Oncken & George, 2005;
diovascular system, such as an increase in heart rate and Pomerleau, Collins, Shiffman, & Pomerleau, 1993).
blood pressure, as well as an increase in the strength of Further, like the other drugs of abuse, the greater the
heart contractions (Jorenby, 1997). At the same time, individual’s level of exposure to cigarette smoking, the
the heart rate is increased, as nicotine causes the blood greater are his or her chances of becoming addicted.
vessels in the outer regions of the body to constrict, As another reflection of the strength of nicotine
causing a reduction in peripheral blood flow (Schuckit, addiction, scientists have discovered neurochemical
2000). In addition, nicotine causes a decrease in the changes in the brain after even a few cigarettes, suggest-
strength of stomach contractions (Schuckit, 2000), ing that even a limited exposure to nicotine may initiate
while the cigarette smoke can cause irritation of the tis- the addiction process (Mansvelder, Keath, & McGehee,
2002). This might explain why children who smoke
just four or more cigarettes stand a 94% chance of con-
8In extreme cases, oral doses of nicotine might also cause dizziness, tinuing to smoke (Walker, 1993).
weakness, confusion, coma, and possible death from respiratory
Given its addictive potential, it is surprising that a small
paralysis. Unfortunately small children who ingest tobacco are excep-
tionally vulnerable to a nicotine overdose, which might result in minority (perhaps 5%–10%) of those who smoke ciga-
death for the child. rettes are not addicted to nicotine (Jarvik & Schneider,
9In an intesting twist, the tobacco industry has also switched tactics 1992; Shiffman, Fischer, Zettler-Segal, & Benowitz,
from a blanket denial that smoking is bad for your health to blaming 1990). These individuals, who demonstrate an episodic
the victims of tobacco-related illness, pointing to the federally man- pattern of nicotine use, are classified as “chippers.” As a
dated warnings on cigarette packages as evidence that they had
warned consumers about the dangers of cigarette use (“Tobacco
10
Company Tactics,” 2007). See Glossary.
group, chippers do not appear to smoke in response to many cigarette smokers report that the act of smoking a
social pressures, and they do not seem to smoke to avoid cigarette helps to calm them down, evidence now sug-
the symptoms of withdrawal (Shiffman, Fischer, Zettler- gests that nicotine can induce or exacerbate anxiety
Segal, & Benowitz, 1990). Unfortunately, very little is symptoms in individuals who suffer from a panic disor-
known about the phenomenon of tobacco “chipping,” der (Isensee, Hans-Ulrich, Stein, Hofler, & Lieb, 2003;
and researchers still do not understand what personality Parrott, 1999; West & Hajek, 1997). The subjective dis-
or biological characteristics separate those who “chip” tress caused by the cigarette withdrawal syndrome will
from those who go on to become addicted to cigarette gradually decrease over the first 2 weeks after the indi-
smoking. vidual’s last cigarette. However, some withdrawal dis-
But 90% to 95% of those who smoke are addicted to comfort and craving for cigarettes will continue for at least
nicotine and demonstrate all of the characteristics typi- 6 months after the last cigarette (Hughes, Gust, Skoog,
cally seen in necessary drug addiction: (a) tolerance, (b) Keenan, & Fenwick, 1991).
a withdrawal syndrome, and (c) drug-seeking behaviors
(Rustin, 1988, 1992). Further, like drug abusers, to- Complications of the Chronic
bacco users develop highly individual drug-using ritu-
Use of Tobacco
als that seem to provide the individual with a sense of
security and contribute to the person’s tendency to en- Tobacco use is associated with increased mortality; this
gage in smoking behaviors when he or she is anxious. It has now been established beyond question. Globally,
has been observed that cigarette smokers tend to smoke the smoking of tobacco products is thought to cause
in such a way as to regulate the nicotine level in their 21% of all cancer deaths, while in areas with a long tra-
blood (Oncken & George, 2005). When given ciga- dition of smoking this figure increases to 40% of deaths
rettes of a high nicotine content, smokers will use fewer caused by cancer (Ezzati, Henley, Lopez, & Thun,
cigarettes; the reverse is true when a smoker is given 2005). In the United States, 87% of all cases of cancer
low-nicotine cigarettes (Benowitz, 1992; Djordjevic, of the lung, 75% of all cases of esophageal cancer, 30%
Hoffmann, & Hoffmann, 1997; Jaffe, 1990). Smokers to 40% of all bladder cancers, and 30% of the cases of
using “low tar” brands have been found to inhale more cancer of the pancreas are thought to be attributable to
deeply and to hold the smoke in their lungs longer than cigarette smoking (World Health Organization, 2006;
do smokers of traditional cigarettes (Djordjevic et al., Hymowitz, 2005; Sherman 1991).
1997). This difference in smoking pattern may account In the United States, the average male smoker is
for the increased incidence of certain forms of cancer thought to lose 13.2 years of his life because of
found in the lungs of some smokers. Obviously, there is smoking-related illness, and the average female smoker
a need for more research into how the “tar” content of a is thought to lose 14.5 years of potential life (Carmona,
cigarette affects the way a smoker smokes. 2004; Sundaram et al., 2004). Scientists believe that to-
Nicotine withdrawal. Withdrawal symptoms usually bacco use is the cause of 19% of the annual deaths in
begin within 2 hours of the last use of tobacco, peak the United States, or an estimated 440,000 premature
within 24 hours (Oncken & George, 2005), then gradu- deaths (Fiore, 2006; Hymowitz, 2005). This number in-
ally decline over the next 10 days to several weeks cludes 15,000 nonsmokers who are estimated to die
(Hughes, 1992; Jaffe, 1989). The exact nature of the each year in the United States from what is known as
withdrawal symptoms varies from person to person. passive, environmental tobacco smoke (ETS) or sec-
Surprisingly, in light of the horror stories often heard ondhand smoke (which will be discussed, below).
about the agony of giving up cigarette smoking, re- It is difficult to state the risks associated with cigarette
search has found that approximately one-quarter of smoking strongly enough. Wadland and Ferenchick
those who quit cigarettes report no significant with- (2004) estimated that one of every six deaths in the
drawal symptoms at all (Benowitz, 1992). United States might be traced to cigarette smoking.
Some symptoms of nicotine withdrawal include Table 19.1 identifies the various causes of death associ-
sleep disturbance, irritability, impatience, difficulties ated with cigarette smoking.
in concentration, lightheadedness, restlessness, fatigue One of the mechanisms by which cigarette smoking
and/or drowsiness, strong craving for tobacco, hunger, is thought to cause death is by exacerbating, if not caus-
gastrointestinal upset and/or constiptation, headache, ing, the development of cancer in the smoker’s body.
and increased coughing (Fiore et al., 1992; Jarvik & The carcinogenic potential is clearly seen in the fact
Schneider, 1992; Oncken & George, 2005). Although that researchers have found abnormal bronchial cells
TABLE 19.1 Tobacco-Related Causes of Death
Percentage of If annual death toll from If annual death toll from

smoking-related smoking is 430,000 people smoking is 450,000 people
Condition deaths a year in the U.S. a year in the U.S.
Smoking-induced 28% 120,000 126,000

lung cancer
Smoking-induced coronary 23% 98,900 103,500
heart disease
Smoking-induced chronic 17% 73,100 76,500
lung diseases other than
lung cancer
Other forms of smoking- 7% 30,100 31,500
induced cancer
Smoking-related strokes 6% 25,800 27,000
All other forms of smoking- 19% 81,700 85,500
induced illness
in 98% of current smokers, as opposed to just 26% of million in property damage each year in the United
nonsmokers (Wadland & Ferenchick, 2004). In addi- States alone (Bhandari, Sylvester, & Rigotti, 1996).
tion to the cancer-related deaths, each year in the There is hardly a body system that is not affected by
United States, cigarette smoking is thought to cause cigarette smoking. What follows is just a short list of the
(J. R. Hughes, 2005; Miller, 1999) various conditions known or strongly suspected to be a
result of cigarette smoking.
• 17%–30% of the deaths caused by cardiovascular The mouth, throat, and pulmonary system. Chronic
disease smokers are at increased risk for sleep-related respira-
• 24% of deaths caused by pneumonia and/or influenza tory problems (Wetter, Young, Bidwell, Badr, & Palta,
• 10% of infant deaths 1994). The authors examined data from 811 adults who
were observed at the sleep disorders program at the Uni-
versity of Wisconsin-Madison medical center and
The direct annual cost of health care problems
found that current smokers were at greater risk than
caused by cigarette smoking is estimated at $75 billion
nonsmokers for such sleep breathing disorders as snor-
in the United States alone, with an additional $82 bil-
ing and sleep apnea. The relationship between smok-
lion a year in lost productivity from smoking-related ill-
ing and sleep disorders is so strong that Wetter et al.
ness (Carmona, 2004). For each person who dies from
(1994) recommended that smoking cessation be con-
smoking-related illness, 20 people are thought to be liv-
sidered one of the treatment interventions for a patient
ing with a tobacco-related disorder (Carmona, 2004).
with a sleep-related breathing disorder.
The cost of cigarette smoking to society (in terms of lost
In spite of the tobacco industry’s refusal to admit to
productivity, medical care, and premature death) is esti-
the evidence, the research data strongly support a firm
mated at $3,000 per smoker per year (Centers for Disease
link between smoking and lung cancer (Carmona,
Control, 2004).11 Smoking is a known risk factor for res-
2004). Researchers believe that cigarette smokers are
idential fires, causing an estimated 187,000 smoking-
10–15 times (1,000%–1,500%) more likely to develop
related fires that result in an estimated loss of $550
lung cancer than are nonsmokers (Kuper et al., 2002).
Fully 24% of male cigarette smokers in the United
11Many smokers argue that since they are forced to pay taxes on the States can expect to develop lung cancer (World
cigarettes that they purchase, they are contributing their fair share to
the government’s income. However, even the most dedicated smoker
Health Organization, 2006). Cigarette smokers are also
does not pay $3,000 per year in taxes for the amount of cigarettes he 10–15 times (Kuper, Boffetta & Adami, 2002) to 27
or she consumed, and thus this argument is not valid. times (World Health Organization, 2006) more likely
to develop laryngeal cancer than nonsmokers, with the has been identified as the “single most important pre-
degree of risk increasing with greater cigarette con- ventable risk factor for cardiovascular disease” (Tresch &
sumption. In addition to the increased risk for cancer, Aronow, 1996, p. 24). Smoking is thought to be the
cigarette smokers have higher rates for chronic bronchi- cause of 30% of the annual death toll from coronary
tis, pneumonia, and chronic obstructive pulmonary heart disease deaths in the United States, with smokers
disease (COPD) such as emphysema, compared to being at greater risk for such problems as hypertension,
nonsmokers (Carmona, 2004). Indeed, it has been esti- aortic aneurysms, and atherosclerotic peripheral vascu-
mated that 90% of all deaths from COPD might be lar disease than nonsmokers.
traced to cigarette smoking (Anczak & Nogler, 2003). Smoking is also a known risk factor for leukemia
One often forgotten aspect of the problem of cigarette (Carmona, 2004), with approximately 14% of all cases
smoking is that approximately 10% of individuals over of adult-onset leukemia in the United States thought to
the age of 65 continue to smoke cigarettes (Gwinnell & be caused by cigarette smoking (Brownson, Novotony, &
Adamec, 2006). Many of these people mistakenly be- Perry, 1993). Cigarette smokers are at increased risk for
lieve that since they have been smoking for so long, the cerebrovascular diseases such as cerebral infarction or a
damage to their bodies is already irrevocable and so cerebral hemorrhage (a stroke or CVA) (Carmona,
there is no sense in quitting at their age. In reality there 2004; Robbins, Manson, Lee, Satterfield, & Hennekens,
are benefits to quitting even for the elderly. For example, 1994; Sherman, 1991). Cigarette smoking is thought to
3 months after giving up cigarettes, lung function im- be the cause of 60,000 strokes a year in the United
proves by about one-third, an issue of some importance States alone (Sacco, 1995), of which an estimated
for many older individuals with chronic obstructive pul- 26,000 are fatal (Carpenter, 2001).
monary disease (COPD) (Gwinnell & Adamec, 2006). One way that cigarette smoking impacts the cardio-
Thus, smoking cessation has benefits even for older vascular system is by causing the coronary arteries to
smokers. constrict briefly. Fifteen years ago, Moliterno et al.
The digestive tract. Cigarette smoking is the cause of (1994) measured the diameters of the coronary arteries
approximately half of all cases of tooth loss and gum dis- of 42 cigarette smokers who were being evaluated for
ease (Centers for Disease Control, 2004). Smokers are complaints of chest pain. The authors found a tempo-
also at greater risk for oral cancers than nonsmokers rary 7% decrease in coronary artery diameter for those
(Carmona, 2004). This risk is compounded by the ef- without identified coronary artery disease who had re-
fects of alcohol, if the smoker is also an alcohol abuser cently smoked a cigarette. Since the coronary arteries
(Garro, Espin, & Lieber, 1992). Heavy drinkers have al- are the primary source of blood for the heart, anything
most a sixfold greater chance of developing cancer that causes a reduction in the amount of blood flow
in the mouth and pharynx than nondrinkers, while through the coronary arteries, even if for a short period
cigarette smokers have a sevenfold increased risk of of time, holds the potential to cause damage to the
mouth or pharynx cancer over nonsmokers. However, heart itself. Thus, the short-term reduction in coronary
alcoholics who also smoke have a 38-fold greater risk artery diameter brought on by cigarette smoking may
for cancer of the mouth or pharynx than do nonsmok- ultimately contribute to cardiovascular problems for
ing nondrinkers (“Alcohol and Tobacco,” 1998). the smoker.
For reasons that are not entirely clear, the use of to- In addition to causing a reduction in coronary artery
bacco products is thought to contribute to the forma- diameter, cigarette smoking introduces large amounts
tion of peptic ulcers (Carmona, 2004; Jarvik & of carbon monoxide into the circulation. The blood of
Schneider, 1992; Lee & D’Alonzo, 1993) and cancer of a cigarette smoker might lose as much as 15% of its
the stomach (Carmona, 2004), and contributes to the oxygen-carrying capacity, as the carbon monoxide
development of cancer of the pancreas (Carmona, binds to the hemoglobin in the blood and blocks the
2004). For reasons that are not clear, regular smoking transportation of oxygen to the body’s cells (Parrott,
also places the smoker at increased risk for developing Morinan, Moss, & Scholey, 2004; Tresch & Aronow,
diabetes (Rimm, Chan, Stampfer, Colditz, & Willett, 1996).
1995). The skin. Smoking contributes to the well-
The cardiovascular system. The negative impact of documented process of premature aging of the skin
cigarettes is so great that even a single cigarette has noted in chronic cigarette smokers (Parrott et al., 2004).
been shown to cause the heart to alter its regular Drawing on the results of a study involving 82 subjects
rhythm (McClain, 2006). Chronic cigarette smoking aged 22–91 years of age, Hefrich et al. (2007) attempted
to develop an objective scale to assess skin aging in prostate, although they suffer from a higher mortality
adults and in the process observed that cigarette smok- rate than nonsmokers when this form of cancer devel-
ing does seem to be associated with changes in the skin ops (Carmona, 2004).
normally seen with simple aging. Further, the authors Other complications caused by cigarette smoking. For
identified evidence that these changes were not just reasons that remain unclear, cigarette smoking is
limited to the facial regions or to body parts normally thought to be a risk factor for the development of psori-
exposed to sunlight, but that they occurred across the asis (Baughman, 1993). Cigarette smokers are known to
entire skin surface, which scientists had not suspected. suffer from higher rates of cancer of the kidneys than
Further, the authors found that there was a strong cor- nonsmokers, and there appears to be a relationship be-
relation between the amount of cigarette smoking by tween cigarette smoking and a thyroid condition known
the research subjects and the level of changes in the as Graves’ disease (Carmona, 2004). There is a relation-
skin. ship between cigarette smoking and bone density re-
The visual system. In addition to cigarette-induced duction in postmenopausal women (Carmona, 2004).
cancer, smokers may experience other, nonfatal forms Further, as a group, older women who smoke were
of illness as well. Cigarette smoking appears to be asso- found to be physically weaker and had less coordination
ciated with a higher risk of cataract formation (Centers than did nonsmoking women of the same age (Nelson,
for Disease Control, 2004; Christensen et al., 1992; Nevitt, Scott, Stone, & Cummings, 1994). The mecha-
Hankinson et al., 1992). Although the exact mechanism by which cigarette smoking might interfere with
nism for cataract formation was not clear, male smokers neuromuscular performance in women smokers is not
who used 20 or more cigarettes a day were twice as likely known.
to form cataracts as were nonsmokers (Christensen et al., Finally, there is evidence that smoking can alter
1992). Former female smokers were found to be at in- brain function, possibly for many years after the individ-
creased risk for cataract formation, even if they had quit ual stops (Sherman, 1994). There is a measurable de-
smoking a decade earlier (Hankinson et al., 1992). The cline in mental abilities that begins about 4 hours after
findings from these two studies reveal that cigarette- the last cigarette, and many former smokers report that
induced disease is far more extensive than previously they have never felt “right” for as long as 9 years after
believed, and that at least some of the physical damage their last cigarette. While there has been no research
caused by cigarette smoking does not reverse itself if the into the long-term effects of cigarette abstinence on
smoker quits. cognitive function (Sherman, 1994), these reports are
The reproductive system. The chemicals introduced quite suggestive.
into the body by smoking reach every body system, in- The degrees of risk. There is no such thing as a “safe”
cluding the reproductive system. Smoking has been cigarette, and smoking cessation is the only proven way
identified as a cause of reduced fertility in women and to reduce or avoid these known smoking-related prob-
as a causal factor for fetal death/stillbirth (Carmona, lems (Carmona, 2004). “Low tar” cigarettes were found
2004; Reichert et al., 2005). Cigarette smoking has been to present the same degree of risk as regular cigarettes
identified as a risk factor for the development of cervi- (Carmona, 2004).
cal cancer (Carmona, 2004; Reichert, Selzer, Efferen, & The passive smoker. Many nonsmokers are exposed to
Kohn, 2005; World Health Organization, 2006). Fortu- the toxins found in cigarette smoke by inhaling cigarette
nately when a woman stops smoking, her risk of cervi- smoke exhaled by others. This is called “environmental
cal cancer slowly declines; and in many cases stopping tobacco smoke,” “secondhand smoke,” or “passive smok-
smoking might even contribute to a reduction in the ing,” and it would appear to be a common problem. For
size of a cancerous growth that has already developed example, research has shown that more than almost 88%
(Szarewski et al., 1996). of nonsmokers have cotinine12 in their blood, suggesting
Male smokers are also at increased risk for reproduc- that passive exposure to cigarette smoke in the United
tive system dysfunctions as a result of cigarette smoking. States is quite common (Pirkle et al., 1996).
There is a significant body of evidence that cigarette In light of all of the toxins found in cigarettes, it
smoking is a cause of erectile dysfunction for men, pos- would be natural to expect that nonsmokers would also
sibly through smoking-induced circulatory damage to suffer from the toxic effects of cigarette smoke. After all,
blood vessels involved in the erectile response (Bach, these toxins do not disappear when the smoker exhales.
Wincze, & Barlow, 2001). Surprisingly, men who smoke
do not appear to be at increased risk for cancer of the 12A metabolite of nicotine.
This is supported by studies that suggest that 3,000–8,000 chance of developing lung cancer than nonsmokers
people die from lung cancer each year as a result of ex- who do not live with a smoker (Fontham et al., 1994).
posure to environmental tobacco smoke (Fiore, 2006). Nonsmoking women who are exposed to cigarette
It is also thought that secondhand smoke causes 22,700 smoke have also been found to have a higher incidence
to 69,000 cases of fatal heart disease in nonsmokers in of breast cancer (Morabia, Bernstein, Heritier, &
the United States each year (Fiore, 2006). The coro- Khatchatrian, 1996), and there is evidence of a relation-
nary arteries of nonsmokers who are exposed to second- ship between secondhand smoke and sudden infant
hand smoke become constricted, just as happens in death syndrome (SIDS) (Klonoff-Cohen et al., 1995).
cigarette smokers, reducing the blood flow to the heart In response to these studies and the EPA’s decision
(Otsuka et al., 2001). Exposure to ETS is now thought to classify environmental smoke as a carcinogen, sev-
to increase the speed at which atherosclerotic plaque eral scientists were paid by the tobacco industry to write
forms by 20%, as compared to 50% faster for the smoker letters or papers questioning these conclusions (Hanners,
(Howard et al., 1998). 1998). The tobacco industry paid some $156,000 to
Children are especially vulnerable to secondhand 13 scientists to write challenges to the EPA’s ruling and
tobacco smoke. Mannino, Moorman, Kingsley, Rose, reviewed their work before it was submitted for edito-
and Repace (2001) found that 85% of the children stud- rial review for possible publication. In some cases the
ied were exposed to tobacco smoke at least once in the letters or articles were actually written by the staff of law
6 days preceeding their study. Environmental tobacco firms that represented the tobacco industry and only
smoke exposure has been identified as the cause of ap- signed by the scientists in question (Hanners, 1998). Most
proximately 6,100 childhood deaths per year in the certainly, these actions underscore the length that the to-
United States and thousands of nonfatal bouts of such bacco industry is willing to go to in order to keep their
conditions as acute otitis media (Aligne & Stoddard, product on the market with as few restrictions as possible.
1997) or respiratory disease in the United States alone Complications caused by chewing tobacco. There are
(Bartecchi, MacKenzie, & Schrier, 1994a). Children three types of “smokeless” tobacco: moist snuff, dry snuff,
who are exposed to secondhand tobacco smoke are at and chewing tobacco (Westman, 1995). Chewing to-
increased risk for asthma (Guilbert & Krawiec, 2003), bacco is also known as “spit tobacco” (Bell, Spangler, &
and it has been estimated that secondhand smoke Quandt, 2000). Of these three forms of smokeless to-
causes 202,000 childhood asthma attacks and 789,000 bacco, chewing tobacco is the most common, although
middle ear infections in children each year in this even then it is quite rare. Only 5.6% of men, and 0.6%
country (Fiore, 2006). Finally, there is emerging evi- of the adult women in the United States use smokeless
dence that children exposed to environmental tobacco tobacco, although there are regional variations in the
smoke are significantly more likely to begin to smoke frequency with which people use chewing tobacco (Bell,
themselves than are children who are not exposed to Spangler, & Quandt, 2000).
secondhand smoke (Becklake, Ghezzo, & Ernst, 2005). Many of those who use chewing tobacco mistakenly
By the start of the 21st century, ETS remains the believe that the use of oral tobacco is safer than ciga-
third most common preventable cause of death in the rette smoking, or that it will expose them to lower levels
United States, and only active smoking and alcohol use of nicotine. Research has shown that using smokeless
result in a greater number of preventable deaths in this tobacco 8–10 times a day will expose the user to as
country (Werner & Pearson, 1998). However, in spite of much nicotine as if he or she had smoked 30–40 ciga-
these facts, what is loosely called “the tobacco industry” rettes (Shipley & Rose, 2003). Further, at least three
(Glantz & Parmley, 2001, p. 462) attempts to dispute compounds in smokeless tobacco are capable of causing
research findings suggesting that secondhand cigarette hypertension: nicotine, sodium, and licorice (Westman,
smoke is dangerous (Glantz & Parmley, 2001), possibly 1995). Research has also shown that there are 16 known
to limit the movement to allow cigarette smoking only carcinogens in the typical sample of chewing tobacco,
in designated areas. placing individuals who use oral forms of tobacco at
The initiative to limit cigarette smoking to specific increased risk for cancer of the mouth and throat
areas is supported by research findings such as the ap- (Hecht & Hatsukami, 2005). Research has demonstrated
parent precancerous changes in the lung tissue of non- that 60%–78% of those who use smokeless tobacco
smokers who live with smokers (Trichopoulos et al., products on a regular basis were found to have some
1992) and the finding that nonsmoking women who kind of oral lesion (Sundaram et al., 2004). Other pos-
were exposed to secondhand smoke have a 30% greater sible consequences that seem to be caused by the use of
smokeless tobacco include damage to the tissues of the ual had engaged in over the course of his or her lifetime
gums, staining of the teeth, and damage to the teeth and the stiffness of the walls of the body’s arteries. This
(Spangler & Salisbury, 1995). Surprisingly, former smok- in turn affects the workload imposed on the individual’s
ers who switched to chewing tobacco were found to suf- heart, with the greater workload being associated with
fer a 46% higher incidence of lung cancer than their the highest degree of arterial wall stiffness. However, the
nonusing peers, suggesting that chewed tobacco is still authors also found that smoking cessation was associated
associated with an increased incidence of lung cancers with a linear improvement in arterial wall flexibility
(Henley et al., 2007). over the first decade after the individual’s last cigarette.
It is not clear whether tobacco chewers experience Other improvements in the ex-smoker’s health status
the same degree of risk for coronary artery disease as include a slowing of peripheral vascular disease and an
cigarette smokers, but they are known to have a greater improved sense of taste and smell, according to Lee and
incidence of coronary artery disease than individuals D’Alonzo (1993). In addition, Grover, Gray-Donald,
who do not use tobacco. Further, smokeless tobacco Joseph, Abrahamowicz, and Coupal (1994) found that
can contribute to problems with the control of the indi- former cigarette smokers as a group added between 2.5
vidual’s blood pressure (Westman, 1995). Thus, while and 4.5 years to their life expectancy when they stopped
smokeless tobacco is often viewed as “the lesser of two smoking. The authors found that cessation of cigarette
evils,” it is certainly not without an element of risk. use was several times as powerful a force in prolonging
Recovery from risk. When a cigarette smoker stops the life as was changing one’s dietary habits. Finally, as a
use of all tobacco products, his or her body will begin the group, former smokers show less cardiac impairment
process of recovery from smoking-related damage. It has and lower rates of reinfarction than do smokers who
been estimated, for example, that the impact of smoking continue to smoke after having a heart attack. As these
cessation is at least as powerful a treatment for coronary findings suggest, there are very real benefits to giving up
artery disease as are the effects of the cholesterol-lowering cigarette smoking.
agents, aspirin, and angiotensin-converting enzyme in-
hibitors (ACE) combined (Critchley & Capewell, 2003).
The Centers for Disease Control (2004) identified some
Smoking Cessation
of the benefits of quitting smoking: In spite of the health advantages noted in the last sec-
Stroke/CVA: Within 5–15 years of the last cigarette, tion, it is difficult to quit smoking. J. R. Hughes (2005)
the former smoker’s risk of a CVA is about that of a per- suggested that only 19% of cigarette smokers have never
son who never smoked. tried to quit, which means that more than 80% of ciga-
Cancer of mouth, throat, and esophagus: These are rette smokers will try to quit smoking at least once. The
50% less likely to develop after 5 years of abstinence success rate for smoking cessation is quite low, with
from smoking. only 30% of those who try to quit remaining smoke-free
Coronary artery disease (CAD): The former smoker’s for as long as 48 hours, and only 5%–10% achieving
risk of CAD is cut in half after 1 year of abstinence, and long-term abstinence (J. R. Hughes, 2005). The typical
is virtually the same as a person who never smoked after smoker requires 5–10 attempts before being able to stop
15 years of abstinence. smoking, although 50% of smokers will eventually be
Lung cancer: This is 50% less likely to develop in the able to stop (J. R. Hughes, 2005). In the United States,
former smoker who abstains for 10 years. the number of former smokers is now larger than the
A recent findings by Jatoi, Jerrard-Dunne, Feely, and number of current smokers (Fiore, Hatsukami, & Baker,
Mahmud (2007) found that there was a relationship be- 2002). There is cause for optimism, but it is difficult for
tween the amount of cigarette smoking that the individ- the smoker to stop smoking cigarettes. (See Table 19.2.)
TABLE 19.2 The Stages of Smoking Cessation
Precontemplation phase Contemplation phase Action phase Maintenance phase
Smoker is not considering Smoker is now seriously thinking Day to stop smoking is selected. Having been smoke free
an attempt to stop smoking. about trying to give up smoking The individual initiates his or for 6 months, the ex-smoker
Smoker is still actively in the next 6 months. her program to stop smoking. works to remain smoke free.
smoking.
The process of smoking cessation is quite complex In addition to depression, some cigarette smokers
and surprisingly includes the smoker’s dietary choices have come to rely on cigarette smoking as a way to deal
(McClemon, Westman, Rose, & Lutz, 2007). The au- with such negative emotional states as anxiety, bore-
thors found that cigarette smokers as a group said that dom, and sadness (Sherman, 1994). Because nicotine
foods such as meat, coffee, and alcohol tended to en- is an easily administered, quick method for coping with
hance their pleasure from cigarettes, while diary prod- these feelings, the smoker soon learns that he or she can
ucts and some vegetables such as celery tended to control such negative emotional states through the use
reduce the subjective pleasure from cigarette use. of cigarettes. Unless the smoker learns alternative meth-
Thus, individuals who wish to quit smoking need to re- ods for coping with these painful emotional states, he
view their dietary habits and change their food intake or she is unlikely to be able to give up reliance on ciga-
patterns at least on a temporary basis to enhance their rette smoking as a way to deal with the emotional
chances of quitting cigarettes. stresses of everyday life.
The most common and least effective method of Cigarette smoking and Alzheimer’s disease? In the
smoking cessation is going “cold turkey” (Patkar et al., early 1990s, researchers found a “negative association”
2003). The sudden discontinuation of cigarettes tends (Brenner et al., 1993, p. 293) between cigarette smok-
to result in the highest relapse rates; those methods that ing and the later development of Alzheimer’s disease.
utilize a nicotine replacement therapy combined with However, subsequent research failed to support the the-
psychosocial support have higher success rates (Patkar ory that cigarette smoking somehow protected the indi-
et al., 2003). The various methods of nicotine replace- vidual from Alzheimer’s. Indeed, later studies found
ment are discussed in Chapter 33. that cigarette smokers were13 at increased risk for devel-
Former smokers are vulnerable to relapse “triggers,” oping some form of dementia in later life (Ott et al.,
the most important of which is being around people 1998; Sundram et al., 1998).
who are still smoking. Watching others smoke ciga- Cigarette smoking cessation and weight gain. Many
rettes, going through their smoking rituals, and express- cigarette smokers justify their continued use of ciga-
ing satisfaction at being able to smoke obviously would rettes because of stories they have heard about former
make it difficult for the individual to quit, while the smokers gaining weight after they quit smoking. Admit-
smell of cigarette smoke from other people would add tedly, about 80% of former smokers will gain some
an olfactory relapse trigger to the individual at a time of weight after they quit, but this statistic is misleading:
vulnerability. Such situations appear to be factors in 57% of cigarette smokers also gain weight during the
more than 50% of the cases when a former smoker re- same period of life (Centers for Disease Control, 2004).
lapses (Ciraulo, Piechniczek-Buczek, & Iscan, 2003). Still, it is known that following smoking cessation, the
As with other forms of drug addiction, smokers who average smoker increases his or her daily caloric intake
want to quit will have to avoid contact with friends who by 200 calories a day, a factor that over time will con-
continue to use cigarettes. tribute to weight gain (Stitzer, 2003).
There is a poorly understood relationship between Another factor that contributes to weight gain fol-
cigarette smoking and depression. Evidence suggests lowing smoking cessation is the impact of nicotine on
that individuals who are depressed experience more re- the smoker’s metabolism. Regular use of nicotine raises
inforcement from cigarette smoking than nondepressed the individual’s metabolism by about 10%, which
individuals, while persons with a history of depression means that he or she burns off weight faster when
seem vulnerable to a recurrence of this disorder after smoking (Stitzer, 2003). Finally, most smokers are
giving up cigarette use (Patkar et al., 2003). Cigarette underweight for their sex/age/body frame so that post-
smoking seems to precede the development of depres- cessation weight gain tends to reflect the body’s at-
sion in teenagers (Goodman & Capitman, 2000). tempt to “catch up” to its normal weight level (Stitzer,
These findings suggest that cigarette smoking and de- 2003). But a smoker also tends to retain less fluid com-
pression are separate conditions that may be influenced pared to a nonsmoker, and some of the weight gain
by the same genetic factors (Breslau, Kilbey, & Andreski,
13The initial research finding was apparently the result of flawed
1993; Glassman, 1993). For this reason, individuals
who wish to quit smoking and who have experienced methodology, which failed to take into account the many complica-
tions of cigarette smoking that would have caused the death of many
past depressive episodes should be warned about the of those individuals who had the potential to develop a neurodegen-
possibility that depression might trigger thoughts of re- erative disease like Alzheimer’s before they could actually develop
turning to cigarette smoking. symptoms of the disease.
noted after a person stops smoking might reflect fluid those from cigarette smoking (Brunton, Henningfield, &
weight gain. Solberg, 1994).
Following smoking cessation, the average individual
gains about 5 pounds (Centers for Disease Control,
Summary
2004). Ten percent of men and 13% of women who stop
smoking experience a larger weight gain of 13 kilograms Tobacco use, once limited to the New World, was first
(28.6 pounds) following their last cigarette. On the posi- introduced to Europe by Columbus’s men. Once the
tive side, those who gain weight following smoking ces- practice of smoking or chewing tobacco reached Europe,
sation seem more likely to remain abstinent from tobacco use rapidly spread. Following the introduction
cigarettes (Hughes et al., 1991; Shipley & Rose, 2003). of the cigarette around the turn of the century, smoking
Klesges et al. (1997) found that former smokers who re- became more common, rapidly replacing tobacco chew-
mained abstinent for an entire year averaged a 13-pound ing as the accepted method of tobacco use.
(5.90-kg) weight gain, while smokers who had “slipped” The active psychoactive agent of tobacco, nicotine,
during the initial year had a smaller average weight gain has an addiction potential similar to that of cocaine or
of 6.7 pounds (3.04 kg). Also, although the initial weight narcotics. Each year, 34% of people who smoke at-
gain is often distressing to the former smoker, there is tempt to quit, but only 2.5% are ultimately successful in
strong evidence that the individual’s weight will return this endeavor (McRae, Brady, & Sonne, 2001). More
“to precessation levels at 6 months [following his or her comprehensive treatment programs have been sug-
last cigarette]” (Hughes et al., 1991, p. 57). gested for nicotine addiction/smoking cessation. These
Although obesity is a known risk factor for cardio- comprehensive programs are patterned after alcohol
vascular disease, the health benefits obtained by giving addiction treatment programs but have not demon-
up cigarette use far outweigh the potential risks associ- strated a significantly improved cure rate for cigarette
ated with post-smoking weight gain (Eisen, Lyons, smoking. It has been suggested that such formal treat-
Goldberg, & True, 1993). A former smoker would ment programs might be of value for those individuals
have to gain 50–100 pounds after giving up cigarettes whose tobacco use has placed them at risk for tobacco-
before the health risks of the extra weight came close to related illness.
CHAPTER TWENTY
Chemicals and the Neonate

The Consequences of Drug Abuse During Pregnancy
Scientists have long known that the drug molecules of fetus and possibly the mother. Fetal vulnerability is ele-
many pharmaceuticals and most of the drugs of abuse vated by the fact only 60% of the blood that the fetus re-
are able to cross from the mother’s blood into that of the ceives from the umbilical cord is processed by the liver
fetus, usually in just a matter of minutes (Bolnick & before it proceeds on to the rest of the body. The other
Rayburn, 2003). Unfortunately, recreational drug abuse 40% of the fetal venous blood, and any toxins found in
is most prevalent in the same age group that is actively that blood, directly enters the general circulation (Barki
involved in reproduction (Bolnick & Rayburn, 2003). et al., 1998). Further, the fetal liver and excretatory sys-
Even so, very limited research has been done on the tems are still quite immature, so compounds that are
impact of maternal chemical abuse on fetal growth and routed to the liver by the fetal circulation are not bio-
development, or to determine which biological or envi- transformed at the same rate as in the mother’s body.
ronmental forces might intervene to mitigate against This can contribute to the buildup of potential toxins
this potential damage (Kandall, 1999). In this chapter, within the fetal circulatory system.
the topic of prenatal exposure to the drugs of abuse is To further compound the problem, the blood-brain
explored. barrier of the fetus is still immature, allowing many
compounds to enter the fetal central nervous system
more easily than that same compound would be able to
Scope of the Problem do later in life (Barki et al., 1998). Finally, the fetal cir-
A period of special vulnerability. Women who have culatory system has lower blood protein levels than an
abused alcohol or illicit drugs during pregnancy should adult’s blood, allowing a greater concentration of un-
be classified as having a high-risk pregnancy (Finnegan & bound drug molecules to circulate in fetal blood system
Kandall, 2004). The very nature of prenatal growth makes than would be possible in an adult’s blood system. All of
the period of pregnancy, especially the first trimester, these factors combine to magnify the effects of a toxin
one of special vulnerability for the rapidly developing on the body of the fetus, possibly with lifelong conse-
fetus (Barki, Kravitz, & Berki, 1998). Unfortunately, many quences. The perinatal “effects [of drugs] may . . . reflect
women will not even attempt to alter their chemical pharmacological effects of individual agents or the com-
abuse pattern until their pregnancy has been con- bined effects of multiple drugs” (Finnegan & Kandall,
firmed or until relatively late in the pregnancy (Bolnick & 2004, p. 547). In an era of polydrug abuse and addic-
Rayburn, 2003). Research has shown that the majority tion, it is very difficult to isolate the effects of one spe-
of women who knowingly continue to abuse alcohol/ cific compound. Further, perinatal drug exposure has
drugs during pregnancy were themselves raised by parents been found to be just one of the risk factors that collec-
who had a substance use disorder (SUD) (Gwinnell & tively would then alter normal fetal/infant development
Adamec, 2006). to a greater or lesser degree (Moe & Slinning, 2001).
Prenatal exposure to alcohol or drugs has the poten- Other potential risk factors include the quality of prena-
tial for profound consequences for the developing fetus. tal medical care, poor postnatal caregiving, malnutri-
For example, the process of organ differentiation takes tion, and an adverse social environment. It is difficult, if
place during the third to eighth week following concep- not impossible, to separate the effects of these other risk
tion, often before the mother-to-be is even aware that factors from those of prenatal drug exposure.
she is pregnant. Maternal exposure to certain agents Each year an estimated 140,000 pregnant women in
that might interfere with normal fetal development dur- the United States alone drink potentially dangerous
ing this period could prove disastrous for the developing levels of alcohol (Cohen, 2000); an estimated 221,000
236
Chemicals and the Neonate 237
infants are born each year in this country who are thought of women who consume alcohol during pregnancy
to have been exposed to an illicit compound at least might be much higher than this, since there is a ten-
once during gestation (Chasnoff et al., 1998; Kandall, dency for pregnant women to underreport their alco-
1999). Another measure of the scope of the problem of hol use during pregnancy (Chang, 2006). This is
prenatal alcohol and drug exposure was provided by important because alcohol quickly crosses the pla-
Pichini et al. (2005), who tested the neonatal muco- centa into the fetal bloodstream, reaching the same
nium following birth for evidence of drug exposure in level as the mother’s in only 15 minutes (Rose, 1988). In
the immediate period prior to birth. The authors found effect, the fetus becomes an unwilling participant in
that 8.7% of the samples were positive for opioids, 4.4% the mother’s alcohol use. If the mother has been drink-
were positive for cocaine, and 2.2% of the samples tested ing shortly prior to childbirth, the smell of alcohol
revealed the presence of multiple substances. Further, might be detected on the breath of the infant following
the authors found a strong relationship between the birth (Rose, 1988). If the mother is alcohol dependent,
abuse of opiates and/or cocaine, and maternal cigarette the infant will also be alcohol dependent, and he or
smoking, which resulted in a lower average birth weight she will begin to go through alcohol withdrawal 3–12
for the infants than was generally seen for infants exposed hours after delivery (American Academy of Pediatrics,
to opiates or cocaine alone. 1998).
The effects of the drugs of abuse on neonatal growth In the early 1970s, maternal alcohol use during
are not limited to the prenatal period. Maternal preoc- pregnancy was identified as a major contributing factor
cupation with drug use, the effects of poverty, the impact to the problem of birth defects in children. The most
of maternal depression on the parent-child relation- severe of the problems brought on by maternal alcohol
ship, and/or competing demands for the mother’s at- use during pregnancy was the fetal alcohol syndrome
tention by siblings, combined with the intense needs (FAS) that was first described in a medical journal in
of the drug-exposed infant, can result in a “serious mis- 1973 (Sokol, Delaney-Black, & Nordstrom, 2003). FAS
match between the mother’s limited emotional resources is the third most common cause of birth defects in the
and the infant’s intense caregiving needs” (Johnson, United States and the most common preventable cause
Nusbaum, Bejarano, & Rosen, 1999, p. 450). Indeed, of mental retardation in developed countries (Cunniff,
Werner (1989b) concluded that the impact of such ad- 2003; Getzfeld, 2006; Glasser, 2002; Krulewitch, 2005;
verse social factors were 10 times as likely as perinatal Sadock & Sadock, 2003; Swift, 2005).
complications to cause poor development in childhood, But FAS is actually the most extreme outcome
adolescence, and young adulthood. brought on by maternal alcohol use during pregnancy.
Because all these forces impact fetal growth and de- Physicians now recognize that many children who were
velopment, scientists have consistently failed to find a exposed to alcohol in utero will have some but not nec-
pattern or syndrome unique to prenatal drug exposure. essarily all of the symptoms of FAS (Cunniff, 2003;
Many of the consequences attributed to maternal drug Sokol et al., 2003). In the 1990s these children were
use are similar to those reported in the literature for said to have fetal alcohol effects (or FAE) (Charness,
such conditions as maternal depression, stress, poverty, Simon, & Greenberg, 1989; Streissguth et al., 1991).
and limited social support, all conditions commonly Although FAS and FAE are still used in clinical re-
found in both normal and drug-abusing homes (Johnson ports, physicians are increasingly using the term fetal
et al., 1999). Yet in spite of the large number of vari- alcohol spectrum disorder (FASD) to identify children
ables that can impact fetal growth, scientists have been whose prenatal growth was affected in any way by ma-
able to determine that the drugs of abuse have the po- ternal alcohol use during pregnancy (Sokol et al., 2003).
tential to deflect normal development in a number of However, FASD is still not a recognized medical diag-
ways. The definitive example of this is the impact of nosis and it remains a theoretical construct (P. Brown,
maternal alcohol use on prenatal growth and devel- 2006).
opment. Scope of the problem of prenatal alcohol exposure. It
is estimated that one in every eight pregnant women
consumes alcohol at least once during her pregnancy
The Fetal Alcohol Spectrum Disorder
(Krulewitch, 2005). While even a single exposure to al-
It has been estimated that 13% of pregnant women use cohol increases the risk to the fetus, research suggests
alcohol during pregnancy, and 10% do so on a regular that several factors interact to caus or contribute to
basis (Chang, 2006; Cunniff, 2003). The actual number FASD. First, there is the degree of fetal exposure to
238 Chapter Twenty
alcohol as a result of the mother’s drinking. Many 2003; Krulewitch, 2005; Sokol et al., 2003). Although
health care professionals now recommend that women few heavy drinkers would consider 4–6 drinks a day a
avoid the use of alcohol even when they are attempting significant level of alcohol intake, research has shown
to become pregnant to minimize the risk of alcohol- that this amount of alcohol use during pregnancy will
related conceptional problems and possible prenatal result in 66% of the children having some form of
exposure before the pregnancy is confirmed (Gwinnell & FASD (Raut, Stephen, & Kosopsky 1996).
Adamec, 2006). Since scientists identified the fetal alcohol syn-
Second, there is the genetic inheritance of the fetus, drome, it has become clear that maternal alcohol use
which can either enhance vulnerability or provide some during pregnancy affects more than just the developing
degree of protection against the effects of prenatal alco- fetal nervous system. There is evidence that any alco-
hol exposure. But this is only a theory, and it is believed hol use during pregnancy increases the child’s risk of
that the longer and the more severe the fetal exposure to developing acute lymphoid leukemia in later life
alcohol might be, the greater the odds that the child will (Menegaux et al., 2006). There is also evidence that
develop alcohol-induced problems that will manifest maternal alcohol use can contribute to, if not cause,
after birth, increasing the chances that he or she would the later development of attention deficit disorder in
require special support later in life (Autti-Ramo, 2000). the child (Peters, 2007). Finally, maternal alcohol use
Finally, the effects of alcohol on fetal development are during pregnancy increases the odds that the child will
stage specific, and so the manifestations of the disorder also develop an alcohol use disorder before the age of
might vary depending on the exact stage of fetal devel- 21 (Alati et al., 2006). While these findings need to be
opment in which the alcohol use occurred (Chang, replicated in future research, they do reinforce the
2006). basic message that any alcohol use by the mother dur-
Current estimates suggest that each day in the ing pregnancy is dangerous.
United States 24 children are born with the full FAS Characteristics of severe fetal alcohol spectrum disor-
and an unknown number are born with some degree of der children. Infants who develop severe FASD usually
FASD (P. Brown, 2006; Finnegan & Kandall, 2005; have a lower than normal birth weight, a characteristic
Peters, 2007; Sokol et al., 2003; Wattendorf & Muenke, pattern of facial abnormalities, and often a smaller
2005). In South Africa, the nation with the highest rate brain size at birth. Noninvasive neurodiagnostic imag-
of FAS in the world, 6.66% of the children, or 1 in every ing of the brains of children who experienced neonatal
15 live births, is a child with fetal alcohol syndrome exposure to alcohol reveals damage to such structures
(Glasser, 2002). of the infant’s brain as the cerebral cortex, cerebellum,
How does maternal alcohol use impact fetal develop- basal ganglia, hippocampus, and the corpus callosum
ment? Maternal alcohol use during pregnancy is thought (Cunniff, 2003; Mattson & Riley, 1995). In later life
to inhibit the production (biosynthesis) of chemicals these children often demonstrate behavioral problems
known as gangliosides within the developing fetal such as hyperactivity, a short attention span, impul-
brain (Rosenberg, 1996). These chemicals play a role siveness, poor coordination, and numerous other de-
in brain development, especially in the earlier stages velopmental delays (Gwinnell & Adamec, 2006; Peters,
of development. Because gangliosides are thought to 2007).
be most active during the first trimester of pregnancy, al- Seventeen percent of the infants with fetal alcohol
cohol’s effects on fetal neural development can be espe- syndrome are stillborn or die shortly after birth (Renner,
cially disruptive during this phase of growth (Pirozzolo & 2004a). Of those who survive, one in five will have a
Bonnefil, 1995). Unfortunately, the woman might not demonstrable birth defect (Renner, 2004a). Less than
even know that she is pregnant until well into the first 6% of the FAS infants who begin school are able to
trimester, if not even later, and by then the damage has function without special support, and many are mildly
been done. to moderately retarded. Indeed, the average IQ of 61
Pregnant women who ingest greater amounts of al-
cohol or who drink more frequently are thought to put 1Some women who had been informed that they should ingest no
the fetus at increased risk, since the more frequent and more than one “standard” drink in a 24-hour period have formed the
intense the fetal exposure to alcohol the greater its im- mistaken belief that they could “save up” each day’s acceptable drink-
ing level and consume it all at one time, such as on the weekends.
pact on fetal ganglioside biosynthesis. But at this time, This would constitute a “binge,” and even one episode of binge drink-
research suggests that there is no “safe” level of alcohol ing has been found to place the child at risk for FAS/FASD (P. Brown,
exposure during pregnancy1 (Chang, 2006; Cunniff, 2006).
children with FAS was found to be 682 (Chasnoff, fant, with higher levels of maternal alcohol consump-
1988; Renner, 2004a; Streissguth et al., 1991). Further, tion resulting in greater developmental delays for the
72% of FAS children were found to suffer from a major infant (Little, Anderson, Ervin, Worthington-Roberts, &
psychiatric disorder of some kind later in life (Renner, Clarren, 1989). In addition to this direct effect on in-
2004a). fant growth, maternal alcohol use may well interfere
Because there are no disease-specific biological with the development of the child’s immune system
markers that physicians can use to identify the child (Gilbertson & Weinberg, 1992). These results would
who was exposed to alcohol in utero, it is possible that strongly suggest that alcohol use by the mother who is
many children with mild FASD remain undiagnosed breast-feeding is a risk factor for the infant, and should
(Cunniff, 2003; Sokol et al., 2003). But Green, Munoz, be avoided.
Nikkel, and Reynolds (2007) suggested that children
with FASD tend to have significantly slower reaction
Cocaine Use During Pregnancy
times to a simple eye movement control test, offering
promise of a diagnostic test that might help identify Prior to the start of the cocaine abuse epidemic in the
these special-needs students. This is important because latter part of the 20th century, some medical textbooks
in many cases FASD-related cognitive deficits do not claimed that maternal cocaine use did not have a harm-
fully manifest until the child enters school or even later ful effect on the fetus (Revkin, 1989). But when the last
in life (P. Brown, 2006; Peters, 2007; Wattendorf & wave of cocaine abuse in the United States began in the
Muenke, 2005). last quarter of the 20th century, questions were raised as
FAS/FASD-related deficits are usually lifelong. Only to the possibility that maternal cocaine abuse might af-
6% of students with full FAS were found to be able to fect the growth and development of the fetus. A series of
function in regular school classes without special help research studies were carried out, which warned of im-
and “major psychosocial problems and lifelong adjust- paired children born to cocaine-abusing mothers. The
ment problems were characteristic of most of these mass media seized upon this first generation of studies,
patients” (Streissguth et al., 1991, pp. 1965–1966). Sur- and based on this research provided the general public
prisingly, the low birth weight characteristic of FAS with ever-larger estimates of the number of infants
seemed to at least partially resolve itself by adolescence, whose lives were supposedly forever damaged by mater-
so that children with FAS/FASD often fall within the nal cocaine abuse during pregnancy.
normal range for height and weight in adolescence or A wave of near hysteria developed in the 1980s and
adulthood (Peters, 2007). But the other effects of mater- 1990s and Draconian steps were adopted on the grounds
nal alcohol use during pregnancy can have lifelong that these steps were necessary to protect the unborn
consequences for the child. child from the mother’s cocaine abuse. An example of
Breast-feeding and alcohol use. Alcohol in the these steps were the laws enacted to allow legal sanctions
mother’s circulation passes freely into her breast milk in to be brought gainst a cocaine-abusing pregnant woman
concentrations similar to the alcohol level in her blood for child abuse. In response, many cocaine-abusing
(BAL) (Heil & Subramanian, 1998). Fortunately, even women began to avoid medical care until the onset of
if the infant were to nurse while the mother was quite labor to avoid prosecution under these new laws (Lester
intoxicated, the amount of alcohol ingested by the in- et al., 2001).
fant along with the mother’s milk would be diluted In retrospect, it appears that society overreacted to
throughout his or her system, resulting in a lower BAL the anticipated wave of “crack babies” (Garrett, 2000;
for the infant (Heil & Subramanian, 1998). But even King, 2006; Stanwood & Levitt, 2007). The question of
this limited exposure to alcohol has been shown to whether maternal cocaine abuse causes harm to the
cause abnormal gross motor development for the in- fetus remans open to interpretation for reasons dis-
cussed later in this section. This is not to say that mater-
2The average IQ is 100, with a standard deviation of 15 points. IQs nal prenatal cocaine use is entirely safe. Indeed,
lower than 70 or lower fall two or more standard deviations below the Stanwood and Levitt (2007) found evidence to suggest
mean. The significance of this is that the IQ of 70 is usually taken as permanent changes in the brains of animals exposed to
the definition of mental retardation. Unfortunately, there is only a cocaine during gestation. But much remains to be dis-
weak correlation between IQ and functional performance (Peters,
2007). This means that even those children whose IQ falls above the
covered about the mechanism through which cocaine
mandated cut-off of 70 points might still experience significant func- might be able to harm the fetus, the degree of risk, the
tional performance problems later in life. implications of such exposure, and whether there are
240 Chapter Twenty
protective factors that might aid the fetus in recovering just 45,000 women, having abused cocaine during their
from prenatal cocaine exposure. pregnancy (Chasnoff et al., 1998; Kandall, 1999).
Clinical research has provided contradictory results as What do we really know about the effects of maternal
to whether prenatal cocaine exposure causes behavioral cocaine use? Not much. Unlike the fetal alcohol syn-
changes following the birth of the child (“Prenatal Co- drome, a consistent pattern of cocaine-specific deficits
caine Exposure,” 2006). Virtually every prenatal compli- has not been identified in the infants who were exposed
cation initially attributed to prenatal cocaine abuse was to cocaine prenatally (Frank et al., 2001; Keller &
later found to have been caused by such factors as a lack Snyder-Keller, 2000). For example, Myers et al. (2003)
of prenatal care, the effects of maternal polydrug abuse, attempted to identify whether prenatal cocaine expo-
instability within the family unit, poor maternal nutrition, sure might be detected through the use of the Brazelton
and maternal depression (Finnegan & Kandall, 2005; Neonatal Behavioral Assessment Scale after birth and
Frank, Augustyn, Knight, Pell, & Zuckerman, 2001; failed to find significant differences between cocaine-
Juliana & Goodman, 2005; “Prenatal Cocaine Expo- exposed and non-exposed babies.
sure,” 2006). Where researchers have found differences between
For example, researchers initially concluded that infants who were and were not exposed to cocaine pre-
maternal cocaine abuse caused placentia previa. But natally, such findings have been small in magnitude.
since most cocaine abusers smoke cigarettes, and ciga- For example, Butz et al. (2005) examined the head cir-
rette smokers have a 2.3 times greater incidence of pla- cumference of infants exposed to cocaine and heroin
centia previa than nonsmokers, the role of maternal prior to birth with those of infants whose mothers did
cocaine abuse in the development of placentia previa is not abuse drugs. A follow-up examination by the au-
not clear at this time (Karch, 2002). Research has also thors included IQ testing and measurement of head cir-
found that half of the women who abused cocaine dur- cumference at age 3 years. The 204 infants who had
ing pregnancy also consumed alcohol, a known toxin, been exposed to cocaine and/or heroin prior to birth
during their pregnancy. This makes it difficult to iden- had significantly smaller head circumference at birth
tify whether cocaine played a causal role in the ob- than non-exposed infants. However, by age 3 both groups
served developmental problems (Sexson, 1994). But this had similar head circumference and IQ scores, accord-
did not prevent the mass media from presenting the pub- ing to the authors. These findings mirror those of Singer
lic with a picture of cocaine-damaged children who were et al. (2004) who found that the minor difference in
“inevitably and permanently damaged” (Zuckerman, measured IQ levels in drug exposed infants was not ap-
Frank, & Mayes, 2002, p. 1991). parent in subsequent studies.
Many pregnant women avoided prenatal care in The current theories. There has been surprisingly
order to avoid legal prosecution for child endanger- little empirical research into the long-term effects of
ment. An unintended consequence of this law was that prenatal cocaine exposure on the infant (Finnegan &
for many women the first “prenatal care” that many Kandall, 2004; Tronick & Beeghly, 1999). But at this
cocaine-abusing pregnant women received was when time limited evidence suggests that prenatal cocaine
they arrived at a hospital emergency room in labor use can result in developmental delays for the infant in
(Sexson, 1994). Since limited prenatal care has been the areas of psychomotor skills (Zickler, 1999), language
found to significantly reduce the possibility of abnor- use skills (Lewis et al., 2004), and mental development
mal fetal growth and improve the chances of a healthy (Singer et al., 2002).
baby at birth, it is difficult to identify the role that ma- One empirical research study examined brain me-
ternal cocaine abuse might play in neonatal growth tabolism of children who had been exposed to cocaine
problems (Racine, Joyce, & Anderson, 1993). through maternal cocaine abuse 8 years earlier and
The scope of the problem of maternal cocaine abuse found evidence of altered function in the frontal cortex
during pregnancy. Even now, the prevalence of maternal of these children (J. M. Smith et al., 2001). These find-
cocaine abuse during pregnancy is simply not known ings were similar to those showing evidence of altered
(Karch, 2002). Maternal self-report, a popular method by frontal cortex function in men who were abstinent
which substance abusers are identified, tends to underes- from cocaine use, although it is not clear if the same
timate the prevalence of prenatal cocaine abuse (Lester mechanism was responsible for the similarity between
et al., 2001), but the National Institute on Drug Abuse the observed effects of cocaine on children and adults.
(NIDA) provided a working estimate of about 1.1% of Remember that fetal exposure to cocaine might
the 4 million pregnant women in the United States, or have a far different impact on the fetus than on the
mother. Biologists have found, for example, that the time. This cocaine-induced reduction in uterine blood
concentration of cocaine in the amniotic fluid might be flow is postulated to be a possible cause of poor in-
higher than that in the maternal blood system (Woods, trauterine growth for the infant exposed to cocaine pre-
1998). This is important when one considers that the natally. The same mechanism has been suggested as the
skin of the fetus does not develop an ability to block pas- cause of premature labor and birth in pregnant cocaine-
sive absorption of cocaine from the amniotic fluid until abusing women (Behnke & Eyler, 1993; Chasnoff,
the 24th week of pregnancy (Woods, 1998), and the 1991b; Glantz & Woods, 1993; Plessinger & Woods,
long-term consequences of fetal cocaine exposure are 1993). However, there has not been any research to de-
simply not known (Keller & Snyder-Keller, 2000). termine whether this is indeed the case with human in-
At this time, maternal cocaine abuse during preg- fants born to cocaine-abusing mothers.
nancy is thought to cause spontaneous abortion, abrupto Cocaine’s vasoconstrictive effects may also be the
placentae, low birth weight, microcephaly,3 premature mechanism by which maternal cocaine abuse may result
labor or birth, strokes in the developing fetus, disrup- in injury to the developing bowel of the fetus (Cotton,
tion in normal uterine blood flow patterns, and vitamin 1994; Plessinger & Woods, 1993). Animal research sug-
deficiencies for both the mother and fetus, increased gests that maternal cocaine use can cause damage to
frequency of respiratory distress syndrome following the fetal mesenteric artery, which provides blood to the
birth, malformations of the genitourinary tract, and in- intestines. An alternative hypothesis is that cocaine is
farction of the bowels (Acosta, Haller & Schnoll, 2005; able to cause a reduction in blood flow to nonvital organ
Finnegan & Kandall, 2005; Gold & Jacobs, 2005; systems of the developing fetus, including the bowel and
Karch, 2002; Keller & Keller-Snyder, 2000; Moffett, kidneys. This would explain why Mitra, Ganesh, and
2006). Women who abuse cocaine during pregancy are Apuzzio (1994) found evidence that the renal artery in
at increased risk for hypertensive crises, cardiac prob- the fetus did not function normally, reducing the blood
lems, cerebrovascular accidents (CVA), and possible flow to the kidneys for extended periods of time.
death for both the mother and fetus (Acosta et al., 2005; There is also evidence that infants born to mothers
Finnegan & Kandall, 2004, 2005). Although the exact who use cocaine during pregnancy might suffer from
mechanism is not known, scientists suspect that mater- one or more small strokes prior to birth (Oehmichen,
nal cocaine abuse during pregnancy is associated with Auer, & Konig, 2005). One research study found that
an increased risk for sudden infant death syndrome 6% of cocaine-exposed infants had at least one cerebral
(SIDS) following birth (Finnegan & Kandall, 2005). infarction (stroke, or CVA) (Volpe, 1995). Another
However, this possibility has been challenged by other study found evidence of CVAs in 35% of infants ex-
researchers (Karch, 2002; Ostrea, Ostrea, & Simpson, posed to cocaine or amphetamines in utero (Kandall,
1997; Plessinger & Woods, 1993; Weathers, Crane, 1999). These strokes are thought to be a result of the
Sauvian, & Blackhurst, 1993). Thus, the possible rela- rapid changes in the mother’s blood pressure brought
tionship between SIDS and prenatal cocaine exposure on by cocaine abuse. Such strokes appear to be similar
remains unknown. in nature to those occasionally seen in adults who use
Unanswered questions. Animal research has revealed cocaine. There is also evidence that cocaine use during
that at least some of the cocaine in the mother’s blood pregnancy may result in cardiac and central nervous
will cross the placenta and enter the fetal circulation. system abnormalities in the fetus as well (Chasnoff,
However, it is still not clear whether the fetal cocaine 1988).
levels are the same as or significantly different from Cocaine and breast-feeding. Because cocaine is
those found in the maternal blood. In some animal highly lipid soluble, it may be stored in breast milk, and
species the placenta appears to biotransform limited some of the drug may be passed on to the infant by the
amounts of cocaine before it enters the fetal circulatory mother through breast-feeding (Peters & Theorell,
system, but this may or may not be true for humans 1991; Revkin, 1989). But the level of cocaine exposure
(Plessinger & Woods, 1993). for the infant might be far higher than it was for the
Animal research has also demonstrated that mater- mother. Research has shown that cocaine levels in the
nal cocaine use during pregnancy can cause constric- maternal milk might be eight times as high as the level
tion of the blood vessels in the placenta and uterine of cocaine in the mother’s blood (Revkin, 1989). If the
bed, reducing the blood flow to the fetus for a period of cocaine-using mother were to breast-feed her infant,
that child might be exposed to extremely high levels of
3See Glossary. cocaine through the mother’s breast milk. For this
242 Chapter Twenty
reason, maternal cocaine use during the time when the placental hemorrhage, and neonatal anemia (Beebe &
mother breast-feeds her infant should be discouraged. Walley, 1995). Following birth, infants exposed to am-
phetamines in utero are thought to be vulnerable to ab-
normal psychosocial development (Bell & Lau, 1995)
Amphetamine Use During Pregnancy or frontal lobe dysfunction (Beebe & Walley, 1995).
Surprisingly, research into the effects of amphetamine However, most normal developmental milestones are
abuse during pregnancy is scanty (Finnegan & Kandall, achieved on time, and there is little firm evidence of
2005, p. 830). Since the behavioral effects of ampheta- long-term damage to the fetus or neonate (Pirozzolo &
mines are so similar to those of cocaine, it is assumed Bonnefil 1995).4 Thus, it is difficult to predict what
that the effects of maternal amphetamine abuse will be long-term effects maternal amphetamine use during
similar as well (Finnegan & Kandall, 2005). pregnancy will have on the child following birth.
Women who abuse amphetamines during preg-
nancy, especially methamphetamine, will frequently
deny CNS stimulant abuse even when confronted with Opiate Abuse During Pregnancy
urine toxicology test results to the contrary (Catanzarite Each year, it is estimated that 1% to 21% of expectant
& Stein, 1995). Researchers have found that infants mothers will use a narcotic analgesic at least once dur-
who were exposed to amphetamines during pregnancy ing their pregnancy (Behnke & Eyler, 1993). Most of
tend to be born with a decreased head circumference, these women are using narcotic pharmaceuticals under
length, and body weight (Bell & Lau, 1995). The au- a physician’s supervision for medically necessary rea-
thors also suggested that maternal amphetamine use sons, and their use is limited to periods of their medical
during pregnancy was associated with a higher rate of need. But an estimated 700,000 women in the United
premature births and congenital brain lesions. There is States have used heroin at least once even though it is
a possibility that maternal amphetamine abuse during illegal (Kieser, 2005). Most of these women are of
pregnancy might increase the mother’s risk for fatal childbearing age, and a significant percentage who use
complications in the pregnancy, although there is heroin on a regular basis will do so while they are
a lack of definitive research in this area that would pregnant.
identify the potential risks to the mother who abused Unfortunately, many of the early symptoms of preg-
amphetamines while pregnant (Catanzarite & Stein, nancy—feelings of fatigue, nausea, vomiting, pelvic
1995). cramps, and hot sweats—might be interpreted by the
Researchers have found that infants who were ex- narcotics-addicted woman as early withdrawal symp-
posed to methamphetamine prior to birth seem to have toms rather than signs of possible pregnancy (Kieser,
altered neurological function in the frontal cortex, as 2005). Even physicians experienced in the treatment of
evidenced by creatine levels in this region of the brain narcotics addiction find it quite difficult to diagnose
(L. M. Smith et al., 2001). This would suggest possible pregnancy in narcotics-addicted women (Levy & Rutter,
damage to the neurons in this critical brain area, al- 1992). All too often, rather than seek prenatal care for
though the significance of these findings has not been her unborn child, the woman will initally try to self-
determined. Research studies using animal subjects medicate what she believes are withdrawal symptoms
suggest that prenatal exposure to methamphetamine by using even higher doses of narcotics. This results in
seems to predispose the fetus to the neurotoxic effects of fetal exposure to significant opioid levels (as well as the
this compound later in life through some unknown chemicals used to adulterate street narcotics) by a
mechanism (Heller, Bubula, Lew, Heller, & Won, 2001). woman who is not yet aware that she is pregnant.
It is not known if humans also experience this vulnera- Maternal narcotics abuse during pregnancy carries a
bility to the neurotoxic effects of methamphetamine number of serious consequences for both the mother
following prenatal exposure to this drug. and the developing fetus. Pregnant women who abuse
There is also evidence that maternal use of opiates are at risk for such problems as anemia, still-
methamphetamine during pregnancy is associated with birth, breech presentation during childbirth, placen-
problems such as premature birth, poor intrauterine tal insufficiency, spontaneous abortions, premature
growth, and a tendency for the placenta to separate
from the wall of the uterus (Catanzarite & Stein, 1995). 4
Of course, there also is no evidence that amphetamine use during
Other possible complications of maternal amphetamine pregnancy is safe, either. If only for this reason, amphetamine abuse
use during pregnancy include meconium aspiration, by the pregnant woman should be discouraged.
delivery, neonatal meconium aspiration syndrome mother be withdrawn from opioids during pregnancy if
(which may be fatal), amenorrhea, postpartum hemor- she is addicted. Except in special cases, the danger to
rhage, placental insufficiency, spontaneous abortion, the fetus seems higher if the mother is withdrawn from
neonatal infections acquired through the mother (sepsis, narcotic analgesics during the gestation period (Kieser,
sexually transmitted diseases, etc.), lower birth weight, 2005). Rather, the use of an opioid agonist such as
neonatal narcotic addiction, and diabetes (Finnegan methadone is recommended, to normalize the in-
& Kandall, 2004, 2005; Glantz & Woods, 1993; trauterine environment (Finnegan & Kandall, 2005;
Hoegerman & Schnoll, 1991; Kieser, 2005; Levy & Vincenzo et al., 2003). When stabilized on an appro-
Rutter, 1992). priate dose of methadone, women are less likely to
In addition to all of these potential complications to abuse illicit drugs (Vincenzo et al., 2003). Further,
pregnancy, children born to women who are addicted children born to mothers whose opiate addiction has
to narcotics have a risk of suffering from SIDS that is been stabilized on methadone tend to have longer ges-
two to three times higher than for children whose tation periods and to weigh more at birth than children
mothers never used illicit chemicals (Finnegan & whose drug-abusing mothers are not using methadone
Kandall, 2004, 2005; Pirozzolo & Bonnefil, 1995). Volpe (Finnegan & Kandall, 2005; Kaltenbach, 1997). Also, it
(1995) suggested that the risk of SIDS increased with is better for the fetus if the mother’s methadone dose is
the severity of the infant’s withdrawal from narcotics. administered in two, or even three, small units—in the
Chronic use of narcotics during pregnancy results in morning and in the early evening (Kandall, Doberczak,
a state of chronic exposure to opiates for the fetus. Such Jantunen, & Stein, 1999). This split dosing schedule re-
infants are physicially dependent on narcotics at birth sults in lower daily dosage levels of methadone for the
because of their passive exposure to the drug. Following mother and seems to lower the danger of drug-induced
birth, the infant will no longer be able to absorb drugs suppression of fetal activity (Kandall et al., 1999). Fol-
from the mother’s blood and will go through drug with- lowing delivery, both the mother and child can then be
drawal starting within 24–72 hours of birth. Depending detoxified from opioids through the use of the appropri-
on the specific narcotic being abused by the mother, ate medications. For the infant, morphine is a better
the withdrawal process may last for weeks or even choice for detoxification than methadone, although
months in the newborn (Finnegan & Kandall, 2005; some physicians like to use barbiturates as well in order
Hoegerman & Schnoll, 1991; Levy & Rutter, 1992; to help avoid possible withdrawal-related seizures in the
Volpe, 1995). An infant going through opioid with- infant (Kieser, 2005).
drawal will demonstrate such symptoms as yawning, There is no evidence that opioids contribute to birth
wakefulness, watery eyes, fever, shrill or high-pitched defects (Kieser, 2005). After following a sample of 330
cry, stuffy/runny nose, salivation, hiccups, vomiting, di- children children, 120 of whom were raised by heroin-
arrhea, poor weight gain, apnea, sneezing, tremors, and dependent parents, researchers at the Hebrew Univer-
seizures (American Academy of Pediatrics, 1998; Kieser, sity Medical School in Israel concluded that except for
2005). The acute phase of the neonatal opioid withdrawal a small percentage of infants with neurological prob-
process might last 3–6 weeks (Pirozzolo & Bonnefil, lems, the developmental delays noted in children born
1995). Following the acute phase, opiate-dependent in- to heroin-dependent mothers were more the result of
fants will experinence a subacute stage marked by such environmental deprivation than prenatal heroin expo-
symptoms as restlessness, agitation, tremors, and sleep sure (Fishman, 1996). Thus, with the proper childhood
disturbance; these might continue for 4–6 months environment, it appears possible for the child to out-
after the acute stage of withdrawal ends (Pirozzolo & grow most if not all of the negative effects of prenatal
Bonnefil, 1995) exposure to narcotic analgesics.
In years past, neonatal narcotics withdrawal re- Narcotics and breast-feeding. The woman who is
sulted in almost a 90% mortality rate (Mirin, Weiss, & using narcotics and is breast-feeding her child will pass
Greenfield, 1991). The mortality rate has dropped signifi- some of the drug on to the infant through the milk
cantly in recent years in response to increased medical (Lourwood & Riedlinger, 1989). In theory, prolonged
awareness of the special needs of the addicted infant use of narcotics by a breast-feeding mother might cause
and improved withdrawal programs for such children the child to become sleepy, eat poorly, and possibly de-
(Mirin et al., 1991). velop respiratory depression. Because of the infant’s
Surprisingly, in light of the dangers of maternal nar- “immature liver metabolizing functions” (Lourwood &
cotics abuse to the fetus, it is not recommended that the Riedlinger, 1989, p. 85), there is a danger that narcotics
244 Chapter Twenty
will accumulate in the child’s body if the mother is juana smoke the user inhaled. It is thus not surprising
using a narcotic analgesic during breast-feeding. that research into the possible effects of maternal mari-
Research has shown, however, that breast-feeding juana use on fetal growth and development has re-
mothers who are taking morphine can do so safely sulted in conflicting or inconclusive results. There are
under a physician’s supervision, since only minimal simply too many variables to allow for an easy answer.
levels of morphine are found in breast milk and only a One study that attempted to isolate the effects of ma-
small portion of that actually reaches the infant’s circu- ternal marijuana abuse during pregnancy found that
lation (Hale, 2003). A similar situation exists for women the children who were exposed to marijuana in utero
who on codeine or methadone maintenance programs had lower than average reading comprehension skills at
and who are breast-feeding an infant. The methadone the age of 10 (Goldschmidt, Richardson, Cornelius, &
levels in the mother’s milk are usually less than 5% of Day, 2004). The role of the mother’s marijuana use in
the maternal dosage level, while only minimal levels of this academic performance problem was not clearly
codeine are ingested through maternal milk by the in- identified, and it is possible that other factors might also
fant if the mother is on a low to moderate dosage (Hale, play a role. Other studies, summarized by Eyler and
2003; Kaltenbach, 1997). Less than 1% of the methadone Behnke (1999), have uncovered abnormal tremors, star-
used by the mother will be found in breast milk, which tle reflexes, and eye problems in children exposed to
is far too low a level of exposure to have an effect on the marijuana in utero. Women who used marijuana at least
infant (Kieser, 2005). Physicians do, however, recom- once a month during pregnancy were also found to have
mend against the use of the narcotic meperidine during a higher risk of premature delivery, infants with lower
breast-feeding, as this medication causes the infant to birth weights, and children who were smaller than nor-
become sedated (Hale, 2003). mal for their gestational age (Bays, 1992).
A contrast to the studies that identified a clear effect
of maternal marijuana use on fetal growth and develop-
Marijuana Use During Pregnancy ment is the study conducted by Dreher et al. (1994).
After more than a quarter century of study, the effects of The authors examined 24 babies born in rural Jamaica
THC on fetal growth and development are still unclear where heavy marijuana use is common; the infants
(Finnegan & Kandall, 2004). This is surprising, since were known to have been exposed to marijuana in
some researchers believe that marijuana is the most utero. The development of these infants was contrasted
commonly abused illicit substance by women of child- with that of 20 other infants known not to have been ex-
bearing years (Kandall, 1999). Nationally, between 2.9% posed to marijuana. The authors failed to find any de-
(Kandall, 1999) and 12% (Pirozzolo & Bonnefil, 1995) velopmental differences in the two groups that could be
of the women who are pregnant in non-ghetto urban attributed to maternal marijuana use. Where signifi-
areas are estimated to use marijuana at least once during cant differences between the two groups of infants were
their pregnancy. found, the authors were able to attribute them to the
Scientists have discovered that the placenta is able to mother’s social status. Marijuana-using mothers were
provide the fetus with some protection from marijuana also found to have a greater number of adults living
smoke, with fetal blood levels of THC reaching only within the household and to have fewer children
one-sixth those of the mother (Nelson, 2000). But there within the home. These factors allowed for more care
remains a great deal to discover about the effects of to be given to the newborn than was the case in the
marijuana use on either the pregnant mother or the homes where the mother did not use marijuana, ac-
fetus (Dreher, Nugent, & Hudgins, 1994). For example, cording to the authors. While these findings are sugges-
Hurd et al. (2005) concluded that infants exposed to tive, there is too little known about either the short-term
marijuana in utero weighed less and were shorter than or long-term effects of maternal marijuana use during
average infants at birth. But it is difficult to isolate the pregnancy to allow researchers to reach any definite
effects of maternal marijuana use from confounding vari- conclusions (Day & Richardson, 1991).
ables such as the effects of poor nutrition, cigarette smok- One possibility that has been overlooked in the re-
ing, other drug abuse, poor prenatal care, or maternal search efforts to date is that it might take several years
health. Other variables that would affect such research for the effects of maternal marijuana use to manifest
include the frequency of marijuana use, the potency of in the child. Fried (1995) examined this possibility
the marijuana being used, and the amount of mari- and found that older children whose mothers used
marijuana during pregnancy showed subtle neuropsy- benzodiazepines should be used only when the antici-
chological deficits in the “executive functioning” re- pated benefits to the mother outweigh the potential dan-
gions of the brain (Fried, 1995, p. 2159). Fried found ger to the fetus (Barki et al., 1998; Iqbal et al., 2002).
evidence of problems in prefrontal lobe brain function Benzodiazepine use during breast-feeding. All the
in these children when they were 6–9 years of age. benzodiazepines will cross from the nursing mother’s
Admittedly, there are many variables that might con- circulation to her milk. Even so, Hale (2003) concluded
found the conclusions reached by Fried (1995) includ- that the short-term use of a benzodiazepine by a breast-
ing the quality of the child’s environment, parental feeding mother (i.e., 1–2 weeks) was “not problematic”
interactions with the child, and other factors. While (p. 344). However, long-term use of a benzodiazepine
there is little conclusive evidence that marijuana use such as diazepam has been identified as the cause of in-
during pregnancy has an adverse effect on fetal growth fant sedation and lethargy (Iqbal et al., 2002), and this
and development (Science and Technology Commit- is one reason that nursing mothers have been advised
tee Publications, 1998), given the lifelong consequences not use benzodiazepines (Graedon & Graedon 1996).
for the child if it should be so, marijuana use during Since these drugs are metabolized mainly by the liver,
pregnancy should be discouraged. an organ not fully developed in the infant, nursing
Marijuana and breast-feeding. THC, the active mothers should not use any of the benzodiazepines un-
agent of marijuana, will be concentrated in human less the potential benefits to the mother outweigh the
milk and passed on to the infant during breast-feeding. risk to the baby in the opinion of the attending physi-
The THC level in breast milk has been found to be six cian (Lourwood & Riedlinger 1989).
(Nelson, 2000) to eight times (Hartman, 1995) as high
as the mother’s blood plasma level. This would suggest
that maternal marijuana use might have some impact
Hallucinogen Use During Pregnancy
on the infant if the mother breast-feeds her child. Breast- There is only limited research into the effects of maternal
feeding by mothers who smoke marijuana is thought to hallucinogen abuse on fetal growth and development
result in slower motor development for the child in the (Kandall, 1999). Because of the lack of information on
first year of life (Frank, Bauchner, Zuckerman, & Fried, the pharmacokinitics of the hallucinogens in the breast-
1992; “Marijuana and Breast Feeding,” 1990). Admit- feeding mother, the use of these medication is not rec-
tedly, this is based on a preliminary study of the effects ommended (Hale, 2003).
of the mother’s use of marijuana on the infant’s devel- PCP abuse during pregnancy. Tabor, Smith-Wallace,
opment, but it does suggest a potential hazard that and Yonekura (1990) compared information on 37 chil-
should be avoided, if at all possible. dren born between 1982 and 1987 whose medical
records indicated that their mothers had used PCP dur-
ing pregnancy. The authors then compared the birth
Benzodiazepine Use During Pregnancy records against those of infants born to mothers who
Early studies suggested that the use of benzodiazepines had abused cocaine during pregnancy. They con-
during the first trimester of pregnancy was associated cluded that the majority of the women in both groups
with an increased risk of facial abnormalities such as cleft had minimal prenatal care, a factor that might influ-
palate, congenital heart defects, inguinal hernia, and py- ence the growth and development of the fetus, and
loric stenosis. Subsequent studies often failed to find most of the women in the study were polydrug users.
such a relationship (Barki et al., 1998; Iqbal, Sobhan, & However, on the basis of their study, the authors con-
Ryals, 2002). Thus, the teratogenic5 potential of benzodi- cluded that infants who were exposed to PCP in utero
azepines remains unclear at this time (Raj & Sheehan, had a high incidence of intrauterine growth retarda-
2004). It is recommended that expectant mothers be tion, premature birth, and often required extended hos-
weaned off benzodiazepines; if absolutely necessary, pitalization following birth. Infants born to women
they should be used at the lowest possible dose for the who had used PCP during pregnancy also seemed to
shortest possible period of time during pregnancy experience abrupt changes in the level of conscious-
(Iqbal et al., 2002; Raj & Sheehan, 2004). Further, the ness, fine tremors, sweating, and irritability, according
to Tabor et al. (1990).
5Which is to say the potential of these compounds to cause or con- MDMA/ecstasy use in pregnancy. Since widespread
tribute to birth defects. abuse of ecstasy is a relatively recent phenomenon,
246 Chapter Twenty
there has been little time in which to conduct systematic the fetus throughout pregnancy (Buka, Shenassa, &
research into the effects of this compound on fetal Niaura, 2003). In terms of fetal development, maternal
growth and development. Preliminary research suggests, cigarette use during pregnancy might be worse than
however, that congenital growth problems are five times maternal cocaine use (Cotton, 1994). The nicotine that
more prevalent than normal for children of women the mother inhales when she smokes causes the blood
who used MDMA during pregnancy (McElhatton, vessels in the placenta to constrict for a period of time,
Bateman, Evans, Pughe, & Thomas, 1999). The authors reducing maternal blood flow to the fetus (Lee &
reported on the outcome of 136 pregnancies in the D’Alonzo, 1993). This contributes to a tendency for ba-
United Kingdom, 74 of which involved women who bies of cigarette smokers to have lower than normal
had abused only MDMA during their pregnancy, and birth weights (Centers for Disease Control, 2004). Ma-
found that 15% of the infants born to the drug-abusing ternal cigarette use is thought to account for 20% of the
women had a congenital abnormality, a rate five times problem of low birth weight children as well as 8% of
higher than the normal rate of 2%–3%. the cases of premature labor and 5% of the instances of
Buspirone use during pregnancy. Buspirone has not perinatal death (Higgins, 2006).
been studied in sufficient detail to determine whether it Pregnant women who smoke have a 30% higher risk
has a potential for harming the human fetus (Barki of stillbirth (Bell & Lau, 1995). Women who smoke (or
et al., 1998). Animal research involving rats found an who are exposed to cigarette smoke) during pregnancy
increased risk for stillbirth when the mother used bus- are more likely to suffer spontaneous abortion and an
pirone at high dosage levels, but there did not appear to increased chance of vaginal bleeding (Centers for Dis-
be any effect on the speed with which newborn rats ease Control, 2004; Lee & D’Alonzo, 1993). Women
were able to learn, their level of motor activity, or their who smoke during pregnancy are also at risk for a pre-
emotional development (Miller, 1994). mature rupture of uterine membranes as well as de-
Bupropion use during pregnancy. The effects of layed crying time in the infant and decreased fetal
bupropion on the developing fetus have not been stud- breathing time following birth (Graedon & Graedon,
ied in detail (Miller, 1994). 1996).
Disulfiram use during pregnancy. Disulfiram is not There is a strong association between maternal ciga-
recommended for use in pregnant women (Miller, rette use during pregnancy and the later development
1994). Animal research suggests that the combination of asthma in the young child (Guilbert & Krawiec,
of alcohol and disulfiram is potentially dangerous for 2003). There is also evidence that maternal cigarette
the fetus, according to Miller. Further, there is evi- smoking during pregnancy may contribute to neurolog-
dence, based on animal research, that a metabolite of ical problems for the developing fetus and following
disulfiram, diethyldithiocarbamate, may bind to lead, birth, for cognitive developmental problems for the
allowing this metal to cross the blood-brain barrier and child (Olds, Henderson, & Tatelbaum, 1994). Olds et
reach the central nervous system. Lead is a known toxin al. found that children born to mothers who smoked 10
that may cause neurological disorders and mental retar- or more cigarettes a day during pregnancy scored an av-
dation. There is a need for further research into this po- erage of 4.35 points lower on a standardized intelli-
tential danger, to determine whether disulfiram use gence test at 3–4 years of age than did children born to
may contribute to higher lead levels in humans. nonsmoking mothers. The authors concluded that the
Cigarette use during pregnancy. Approximately observed effects were due to maternal cigarette use dur-
820,000 women, or about 20% of the estimated 4 mil- ing pregnancy.
lion women who give birth in this country each year, There is also a growing body of literature suggesting
smoke during their pregnancy (Finnegan & Kandal, that maternal cigarette use during pregnancy is one
2004). Byrd and Howard (1995) give an even higher es- risk factor for the development of attention deficit-
timate of 29% of the infants born in the United States hyperactivity disorder (ADHD) (Milberger, Biederman,
each year, or 1 million infants each year who are exposed Faraone, Chen, & Jones, 1996). Maternal cigarette use
to cigarette smoke prenatally. An additional 22% of all in- during pregnancy has also been linked to such neu-
fants are exposed to secondhand or environmental ciga- rodevelopmental problems as impulsiveness, although
rette smoke after birth, even if their mothers did not it is not clear what role cigarette smoking plays in the
themselves smoke cigarettes (Byrd & Howard, 1995). development of these problems (Day & Richardson,
Many of the compounds in cigarette smoke, including 1994). Finally, after examining the records of some
nicotine, are able to cross the placental barrier and reach 1.57 million births in Hungary over a 10-year period,
Czeizel, Kodaj, and Lenz (1994) concluded that mater- supervision of a physician (Black & Hill, 2003; Wilson,
nal cigarette smoking was a risk factor for the condition Shannon, Shields, & Stang, 2007). Aspirin has been im-
known as congenital limb deficiency (a failure for the plicated as a cause of decreased birth weight in children
limbs of the fetus to develop properly). The authors hy- born to women who used it during pregnancy. Aspirin
pothesized that nicotine’s ability to disrupt blood flow also may be a cause of stillbirth and increased perinatal
patterns to the uterus might be the cause of this devel- mortality (United States Pharmacopeial Convention,
opmental abnormality. 1990).
Infants born to smoking mothers appear to suffer from Briggs, Freeman, and Yaffe (1986) explored the im-
reduced lung capacity, with such infants experiencing on pact of maternal aspirin use on the fetus and concluded
average a 10% reduction in lung function (Byrd & that it might produce “anemia, antepartum and/or post-
Howard, 1995). Infants born to women who smoke a partum hemorrhage, prolonged gestation and pro-
pack a day or more were found to be twice as likely to longed labor” (p. 26a). Aspirin has also been implicated
grow up to become cigarette smokers as children born to in significantly higher perinatal mortality and retarda-
nonsmokers (Buka et al., 2003). Finally, infants who are tion of intrauterine growth when used at high doses by
exposed to cigarette smoke suffer a significantly higher pregnant women (Briggs et al., 1986). The authors
rate of SIDS than infants who are not exposed to this envi- noted that maternal use of aspirin in the week before
ronmental hazard. Research suggests that the risk of a delivery might interfere with the infant’s ability to form
newborn infant dying from SIDS increases 300% to blood clots following birth. The United States Pharma-
400% if the mother smokes (Centers for Disease Control, copeial Convention (1990a) went further, warning that
2004). Thus, maternal cigarette use during pregnancy women should not use aspirin in the last 2 weeks of
carries with it a number of risks for the developing fetus. pregnancy. Aspirin can cross the placenta, and research
Cigarette smoking during breast-feeding. Medical re- has suggested that maternal aspirin use during preg-
search suggests that the mother abstain from cigarette use nancy might result in higher levels of aspirin in the
during the period that she is breast-feeding the infant. fetus than in the mother (Briggs et al., 1986).
Nicotine tends to concentrate in breast milk, with a half- Acetaminophen. Acetaminophen is viewed as the
life in breast milk of 1.5 hours (Byrd & Howard, 1995). OTC analgesic of choice for women who are pregnant
The total concentration of nicotine in the woman’s breast (Black & Hill, 2003). There have been no reports of se-
milk is dependent on the number of cigarettes she smokes rious problems in women who have used acetamino-
and the time between the last cigarette and the time she phen during pregnancy. The reported death of one
breast-feeds the infant, according to the authors. Nicotine infant from kidney disease shortly after birth was later
has been shown to interfere with the process of breast- attributed to the mother’s continuous use of acetamino-
feeding, reducing the amount of milk produced and the phen at high dosage levels during pregnancy (Briggs
process of milk ejection (the “let down” reflex) (Byrd & et al., 1986). However, there are no reports of harmful
Howard, 1995). Infants who are breast-fed by cigarette- effects on the fetus if the drug is used as directed.
smoking mothers tend to put on weight more slowly than Although acetaminophen is excreted in low concen-
breast-fed infants whose mothers do not smoke. trations in the mother’s breast milk, Briggs et al. (1986)
Nicotine replacement therapy during pregnancy. As found no evidence suggesting that this had an adverse
nicotine and its primary metabolite, cotinine, are thought effect on the infant. Lourwood and Riedlinger (1989)
to be harmful to the fetus, one would expect that nicotine suggested, however, that since acetaminophen is me-
replacement therapies would be contraindicated for the tabolized mainly by the liver, which is still quite imma-
pregnant woman. However, the other 4,000 chemicals in ture in the newborn child, the mother who breast-feeds
cigarette smoke are also at least potentially harmful to the during the immediate postpartum period should not
fetus, so the use of nicotine replacement devices is appro- use this drug. The authors did not warn against the oc-
priate if, in the physician’s opinion, the potential benefits casional use of acetaminophen in women who are
outweigh the risks (Black & Hill, 2003). breast-feeding their children after the immediate post-
partum period.
Ibuprofen. There has been limited research into the
Over-the-Counter Analgesic
effects of maternal ibuprofen use during pregnancy on
Use During Pregnancy the fetus (Black & Hill, 2003). However, similar drugs
Aspirin. Women who are or suspect that they might have been known to inhibit labor, prolong pregnancy,
be pregnant should not use aspirin except under the and potentially cause other problems for the developing
248 Chapter Twenty
child. Because of the limited research into the potential problems including premature birth, craniofacial ab-
dangers of using ibuprofen during pregnancy, it is rec- normalities (abnormal ears, thin upper lip, small nose,
ommended to be used only under a doctor’s supervi- etc.), abnormal muscle tone, renal abnormalities, de-
sion (Black & Hill, 2003). velopmental delays, abnormal scalp hair patterns, and
Research suggests that ibuprofen does not enter retarded physical growth.
human milk in significant quantities when used at nor- To explain the similarity between the effects of
mal dosage levels (Briggs et al., 1986; Hale, 2003) and it toluene abuse and alcohol abuse on the developing
is considered “compatible with breast feeding” (p. 217i). fetus, the authors hypothesized that toluene and alco-
Indeed, Lourwood and Riedlinger (1989) reported that hol might both result in a state of maternal toxicity.
ibuprofen was “felt to be the safest” of the nonsteroidal This state of maternal toxicity would, in turn, contribute
anti-inflammatory drugs for the woman who was breast- to the fetal malformations seen in cases of toluene and
feeding her child. alcohol exposure during pregnancy (Pearson et al., 1994).
These findings were consistent with those of Bowen,
Batis, Mohammadi, and Hannigan (2005), who exam-
Inhalant Abuse During Pregnancy
ined the impact of toluene exposure on pregnant rats
Virtually nothing is known about the effects of the vari- and found that prenatal exposure to toluene fumes
ous inhalants on the developing fetus. It is thought that caused growth restriction, physical abnormalities, and
only a small percentage of those who experiment with impaired development in the rat pups. While these stud-
inhalants go on to abuse these chemicals on a chronic ies are only preliminary, it would appear that toluene
basis, but more than 50% of those persons who chroni- exposure during pregnancy may have lifelong conse-
cally abuse inhalants are women “in their prime child- quences for the developing fetus. Until proven otherwise,
bearing years” (Pearson, Hoyme, Seaver, & Rimsza, 1994, it would be safe to assume that maternal abuse of the
p. 211). It is thus safe to assume that some children are other inhalants would have similar destructive effects
being exposed to one or more of the inhalants during on the growing fetus.
gestation.
There is very little information available about the
Summary
toxicology of inhalants on the human fetus. Prelimi-
nary evidence does suggest that maternal inhalant If a substance-abusing woman becomes pregnant, the
abuse can cause a fatal neonatal syndrome and growth fetus that she carries will become an unwilling partici-
retardation if the fetus is carried to term (Sharp & pant in the mother’s chemical use/abuse. However, the
Rosenberg, 2005). Maternal inhalant abuse has also impact of the chemical use is often much greater on the
been identified as a possible cause of microcephaly as growing fetus than it is on the mother. Because of this,
well as infant tremors and ataxia (Sharp & Rosenberg, infants born to women who have used chemicals of
2005). One of the most common inhalants, toluene, is abuse during pregnancy represent a special subpopula-
known to cross the placenta into the fetal circulation tion of alcohol/drug users. The child who was exposed
when the mother inhales toluene fumes. In adults, to recreational chemicals did not willingly participate
about 50% of the toluene inhaled is biotransformed in the process of chemical use, yet his or her life might
into hippuric acid and the remainder is excreted un- be profoundly affected by the effects of alcohol or
changed (Pearson et al., 1994). But neither the fetus drugs.
nor the newborn child has the ability to biotransform An extreme example of the unwilling participation
toluene. There is thus some question as to whether the of infants in maternal alcohol or drug use is the child
effects of toluene exposure for the fetus or newborn born already addicted to the chemicals the mother used
would be the same as it would be for the adult who in- during pregnancy. Other fetal complications of mater-
haled toluene fumes. nal chemical abuse might include stroke, retardation,
To attempt to answer this question, Pearson et al. or lower weight at birth as well as a number of other drug-
(1994) examined 18 infants who were exposed to specific complications. The over-the-counter analgesics
toluene through maternal paint sniffing during preg- present a special area of risk, for the effects of these med-
nancy. They found several similarities between the ef- ications on fetal growth and development are not well
fects of toluene on the developing fetus and the effects understood. However, available research suggests that
of alcohol on the fetus. Like alcohol exposure, toluene the OTC analgesics should be used with caution by
exposure during pregnancy may cause a wide range of pregnant or nursing women.
CHAPTER TWENTY-ONE
Gender and Substance

Use Disorders
There is an interesting conundrum in society at this For example, during the epidemic of chemical abuse
time. By the last quarter of the 20th century, many of that took place in the last years of the 19th century, the
the traditional social values that limited the exposure of ratio of men to women who were addicted to chemicals
women to alcohol/drug abuse had significantly weak- was only 1:2 (Lawson, 1994). Significant numbers of
ened or entirely disappeared (Blume & Zilberman, women were addicted to one or more of the various
2004). An example is the media shift that took place in mail-order medicines that were freely available without
the 1980s and 1990s, targeting women to make alcohol prescription in that era. Then a series of laws were
use more acceptable to them (Blume, 1994). At the same passed that limited the availability of such compounds,
time, the popular stereotype of the woman with a sub- and the epidemic of drug addiction for both men and
stance use disorder is that of a “fallen” woman: immoral, women gradually waned.
a poor parent, and most certainly nothing like “us.” For much of the 20th century, most medical re-
These popular stereotypes are both quite persistent search focused on males. For example, while the bene-
and grossly inaccurate (Schneiderman, 1990).1 As pop- fits of daily aspirin use for men with cardiovascular
ular as they are, few people recognize that they serve disease have long been established, research into the
only to limit our vision. If the addicted person deviates utilization of daily aspirin doses for women with cardio-
from our expectation, we might not recognize the vascular disease has been limited (Chan et al., 2007).
chemical dependency hiding behind the polished so- Using males as the focus of research was true also in
cial facade. Drug addiction that has an atypical appear- studies of the substance use disorders. Only in the last
ance often confuses the lay person, and when a quarter of the 20th century did a small group of re-
substance use disorder (SUD) is identified in a woman, searchers begin to call attention to the problem of
society is often quick to pass judgment on her or place women with addictive disorders (Green, 2006). Unfor-
barriers in the way of her access to treatment. It is the tunately, during the 20th century, a double standard for
goal of this chapter to help to dispell these misconcep- treatment of persons with SUDs evolved. Women who
tions and to shed light on the problem of substance use abused or were addicted to chemicals were subjected to
disorders in women in the early 21st century. greater levels of social condemnation than were men
(Chang, 2001). Further, women’s substance use disor-
ders were often viewed as being less important than those
Gender and Addiction: of men (Cohen, 2000; Jersild, 2001; Ramlow, White,
An Evolving Problem Watson, & Leukefeld, 1997).
All too often, the lessons of history are discovered Statement of the problem. Society’s response to the
through hindsight: Only rarely is a lesson from history ac- issue of women with SUDs has been to hide the prob-
knowledged before a crisis develops so that the problem lem, to protect the individual or she might be totally
might be circumvented or addressed in its early stages. abandoned by traditional sources of social/familial sup-
port (Cohen, 2000; Blume & Zilberman, 2005a). While
1In previous editions of this book, the topic of substance use disorders this continues in many places, society as a whole is slowly
and gender was included in the chapter titled “Hidden Faces of becoming more accepting of the fact that women suf-
Chemical Dependency.” But the subject of women and substance fer from SUDs as well as men. This is fortunate because
use disorders has gradually emerged from the shadows to the point at the start of the 21st century it is believed that one of
that it has become the focus of a small but growing field of literature
(Green, 2006). For this reason, the decision was made to devote an
every three individuals with an alcohol use disorder
entire chapter to this one issue rather than to include it in a multifac- (AUD) is a woman (Sinha, 2000). Statistically, this
eted chapter that addressed a number of different issues. means that approximately 4.4 million women in the
249
250 Chapter Twenty-One
United States either abuse or are addicted to alcohol as a general rule, the woman with an SUD is more
(Greenfield, 2003). Further, an additional 2 million likely to be referred to treatment through a social worker,
women in this country have an SUD other than alcohol a mental health professional, or a family service worker
abuse/addiction. Such disorders extract a terrible price than is the man with an SUD (Green, 2006).
from their victims: Women with an AUD are up to 23 As a general rule, men tend to externalize responsibil-
times as likely to commit suicide as their nondrinking ity for their SUD whereas women tend to internalize
counterparts (Markarian & Franklin, 1998). blame for their disorder (Lala & Straussner, 1997). Thus
Yet in spite of the growing awareness of the problem, the emotional mind-set of women in treatment is often
research into the need for, or the effectiveness of, gender- quite different from that of men in a rehabilitation set-
specific treatment programs has been slow to develop ting; note that women with an AUD tend to suffer from
(Brady & Randall, 1999; Greenfield, 2003; Han & poor self-esteem more often than men with an alcohol
Evans, 2005). It is acknowledged that different dynam- use disorder (Alexander, 1996; Cohen, 2000; Coughey
ics might be at work for adolescent girls with SUDs et al., 1998; North, 1996; Sinha, 2000). Evidence suggests
compared with adolescent boys, but there is virtually no that substance abuse might reflect the woman’s attempt
research into the specific dynamics at work or the most to medicate feelings of low self-worth (Alexander, 1996).
effective treatment methods. Even for women who Women, both those with and without SUDs, experi-
have SUDs, there is a “paucity of female-only support ence different demands on their time than do men
groups” (Coughey, Feighan, Cheney, & Klein, 1998, (Kauffman, Dore, & Nelson-Zlupko, 1995; O’Dell,
p. 929). The situation in many parts of the country is so Turner, & Weaver, 1998; Sinha, 2000). For example, it
dismal that the development of gender-specific treat- is not uncommon for the woman to be granted custody
ment programs is still said to be in its infancy, even of the children following divorce on the grounds that
though the need for such programs has been known for the children should live with their mother. Child cus-
a generation (Sinha, 2000). tody obviously requires a greater commitment to par-
The “convergence” theory. In brief, the “convergence” enting than is required from the parent who does not
theory is based on the assumption that substance use dis- have custody. But few treatment programs accept a
orders were relatively rare in the population of women woman who is pregnant or who has custody of children
during the 20th century, but that such problems be- (Blume & Zilberman, 2004; Ringwald, 2002). Thus,
came more common during the last quarter of the 20th child custody often becomes a barrier to treatment ac-
century and the early years of the 21st century. This the- cess for women with SUDs (Blume & Zilberman, 2004,
ory is supported by research findings that there are 1.6 2005a, 2005b; Kauffman et al., 1995).
men with an SUD for every woman with an SUD As a group, women with an SUD appear to be less
(Zilberman & Blume, 2005). However, this theory rests likely to seek help with alcohol or drug use problems
on the assumption that we have accurate data on the than a man with a chemical use problem of the same
scope of addiction in women during the 20th century. severity (Green, 2006). When women do seek assis-
Even today, the woman with an alcohol use disorder is tance for their SUD, they are more likely to utilize the
less likely to be identified than the man with a similar resources of a health care professional, clergy member,
SUD (Brady, Tolliver, & Verduin, 2007). As the veil of or mental health professional than a substance abuse
secrecy is slowly removed, we may learn that the con- rehabilition professional (Blume & Zilberman, 2005a;
vergence theory is an illusion, one that evolved not be- Freimuth, 2005; Green, 2006). The tendency for women
cause there were more women who had SUDs but with SUDs to seek assistance from mental health pro-
because they were more likely to be identified. fessionals might be explained, in part, by their tendency
to suffer from depression or anxiety disorders more
How Does Gender Affect often than men with similar substance use problems
(Blume & Zilberman, 2005a, 2005b; Dixit & Crum,
the Rehabilition Process? 2000; Green, 2006). Unfortunately, such “indirect” treat-
Having established that a significant percentage of ment often is less effective than treatment in a formal sub-
women develop an SUD at some point in their lives, it stance abuse rehabilition program (Green, 2006).
is natural to question whether the traditional rehabilita- Also, the dynamics of depression are different for
tion process, developed mainly for males, is effective for men and women with SUDs. For the woman with an
women with SUDs. Not surprisingly, gender impacts SUD, the symptoms of depression are likely to serve as
the process of rehabilitation in a number of ways. First, a cue for further substance use as the woman attempts
Gender and Substance Use Disorders 251
to self-medicate her depression. When a man with an disorder have been exposed to some form of physical or
SUD becomes depressed, he is more likely to reduce sexual violence, as opposed to just 20% of the men with
his substance use in an attempt to reduce his level of an SUD (Mignon, 2006). These women will have to
depression (Schutte, Moos, & Brennan, 1995). While come to terms with these victimization issues as part of
not dismissing the need to treat depression in male their recovery program (Byington, 1997; Cohen, 2000;
substance-abusing clients, this does point to the need Del Boca & Hesselbrock, 1996; Mignon, 2006; Sinha,
for rehabilition programs treating women with SUDs to 2000). However, the treatment setting might lack the
see that the women have access to psychiatric care so resources, time, or the treatment staff with training to
that their anxiety or depression can be aggressively con- address such issues,2 even though a history of victimiza-
trolled through the use of the appropriate medication. tion is a significant complicating factor for the rehabilita-
Women with SUDs also present unique needs when tion program (Alexander, 1996; Blume, 1998; Cohen &
admitted to treatment. Many women with SUDs have Hien, 2006).
supported their addiction through prostitution, for Work, gender, and chemical abuse. There is a com-
example, while men are more likely to have engaged in plex relationship between work status and SUDs in
such activities as illicit drug sales to support their addic- women. For example, women who are less satisified
tion (Lala & Straussner, 1997). Further, when admitted with their work status tend to abuse alcohol more often
to a rehabilitation program, women typically present a than satisfied women (Jersild, 2001), a significant prob-
different constellation of interpersonal support re- lem when one stops to consider that many women in
sources than do substance-abusing men who are admit- the workforce are working below their potential capac-
ted to treatment. As an example, while marriage is a ity, often in low status-high frustration positions. For
protective factor against relapse following treatment for some women, the increased social status, social support,
men, it is a possible risk factor for women, especially if and improved self-esteem that go along with full-time
the relationship is not supportive or if the marital part- paid employment seems to help reduce the chances that
ner also has an SUD (Sinha, 2000). she will develop an SUD (Brady & Randall, 1999;
The problem of substance-abusing partners is hardly Wilsnack & Wilsnack, 1995; Wilsnack, Wilsnack, &
irrelevant. Women with an AUD are four times more Hiller-Sturmhoffel, 1994). Yet for reasons that are not
likely than males to be living with a partner who also well understood, employment can also facilitate the de-
has an AUD (Blume & Zilberman, 2005a; Miller & velopment of an SUD for women (Brady & Randall,
Cerbantes, 1997). This is partly because men whose 1999), as evidenced by the fact that women working in
partner has an AUD are more likely to turn to divorce as nontraditional, male-dominated professions3 tend to re-
a way of coping than are women in a similar position port higher levels of alcohol use problems (Wilsnack &
(Byington, 1997). Further, many women are initially Wilsnack, 1995; Wilsnack et al., 1994).
introduced to illicit drugs by their male partner, who Working women with SUDs are less likely to be mar-
then serves as their source of supply (Blume, 1998; ried than are their male counterparts (Green, 2006). Also,
Blume & Zilberman, 2005a, 2005b). In this manner the detection of an SUD in working women is often
the woman’s SUD is rendered “invisible” by the male quite difficult (Jersild, 2001). Being underemployed,
partner, making the detection of her SUD less likely their chemical use is less likely to cause unacceptable job
and thus reducing the chances of a referral to treat- performance than it is for a man (Blume & Zilberman,
ment. It should not be surprising to learn that women 2004). The low-paying jobs that many women hold
with SUDs report receiving less support from their part- usually do not allow for easy access to employee assis-
ners in their recovery efforts than do recovering men tance program counselors, thus making the referral
(Green, 2006; Kauffman et al., 1995; O’Dell et al., process more difficult for the woman than for many
1998). men. Also, the threat of loss of employment if the ad-
Dual diagnosis/victimization issues for women. There dicted woman does not seek treatment is not as effective
is a significant overlap between identified psychiatric
2Treatment for PTSD issues is often prolonged and difficult, and the
problems in women with SUDs and a history of physi-
limited treatment stays allowed by insurance companies rarely permit
cal or sexual victimization. The majority of women
staff to do more than identify the problem, help the client understand
who present with a history of posttraumatic stress disor- that PTSD is a possible “relapse” trigger, and perhaps refer her to a
der (PTSD) and a history of an SUD, for example, were therapist as part of the SUD aftercare program.
abused as children (Cohen & Hein, 2006). It has been 3Defined as one in which more than 50% of their co-workers are
estimated that 50% of women with a substance use male.

as it is for men, since the majority work only to supple- to opioids in humans” (Han & Evans, 2005, p. 205). As
ment their husband’s income. It is often easier for such a group, women tend to begin abusing narcotics at an
a woman to simply quit her job when threatened with older age than do male opioid abusers, although they
the loss of employment if she did not seek treatment. also tend to enter treatment at about the same age
Victimization histories and substance use patterns. as males (Hernandez-Avila, Rounsaville, & Kranzler,
Women with SUDs often report a history of victimiza- 2004). Their substance use history is thus “telescoped”
tion, but it is a mistake to think that women’s SUDs are into a shorter time frame than is typical for male opioid
automatically a result of having been abused by a signif- abusers.
icant other (Holloway, 1998; Jersild, 2001). The assump- There is also some evidence that there are differ-
tion that such an abuse history will result in an SUD is ences in how male and female opioid abusers use their
“not only damaging but also antitherapeutic and disem- drug of choice. In England, Gossop, Battersby, and
powering” (Jersild, 2001, p. 35) to women in treatment. Strang (1991) found that male narcotics addicts were
Staff must carefully assess whether the substance use more likely to inject their drug while female narcotics
disorder might have been caused or exacerbated by vic- addicts were more likely to inhale narcotic powder. Fe-
timization, or whether the SUD might have been the male addicts were also more likely to be involved in a
result of forces other than the victimization itself. sexual relationship with another drug user than were
Although the woman with a substance use problem male narcotics addicts. Finally, just under half the fe-
is often referred to a mixed-sex group as part of her treat- male narcotics addicts studied by the authors had re-
ment program, research has found that many women ceived drugs as a present from a sexual partner, according
fail to benefit from a mixed-group format (Greenfield, to the authors.
2003; Lala & Straussner, 1997). Many women feel in- Cocaine abuse and gender. Female gonadal hor-
hibited in mixed groups, especially if they have been mones might influence the individual’s subjective re-
victimized by a male at some point in life (Alexander, sponse to cocaine, with higher levels of progesterone
1996; Lala & Straussner, 1997). Often, the language blocking some cocaine-induced euphoria (Han & Evans,
used by many men in the therapeutic setting is intimi- 2005; Lukas, 2006). Thus, one variable that must be as-
dating to women and in some cases may even revictim- sessed in future research into the subjective effects of
ize them as memories of past abuse surface. This con- cocaine on the female user is her blood progesterone
tributes to the increased dropout rate for women from level, which varies depending on where the woman is
mixed groups as opposed to unisex groups. in her monthly menstrual cycle. Such research has not,
Gender and substance use patterns. Within the past to date, been carried out.
generation researchers have discovered that women But based on the limited data available at this time,
usually obtain their drug of choice in different ways than there are subtle differences between male and female
men. Unlike male substance abusers, women with SUDs cocaine abusers in their response to this compound
often obtain their drugs from a physician. In the last (McCance-Katz, Hart, Boyarsky, Kosten, & Jatlow, 2005).
quarter of the 20th century, it was suggested that sedatives McCance-Katz et al. found that female cocaine abusers
and “diet pills” had become “women’s drugs” (Peluso & rated their subjective sense of well-being significantly
Peluso, 1988, p. 10), a distinction that continues to be higher than men. This would suggest that female co-
true. Because women so often obtain their drugs of caine abusers might be at greater risk for a cocaine over-
choice by prescription, their drug abuse problem is vir- dose as they ignore internal warning signs of distress in
tually invisible to society. favor of seeking a continued sense of drug-induced
well-being (McCance-Katz et al., 2005).
As a group, female cocaine abusers are known to
Differing Effects of Common Drugs
start their drug use at an earlier age and seem to reach
of Abuse on Men and Women the stage of addiction more rapidly than do male co-
As medical researchers learn more about the effects of caine abusers (Kender & Prescott, 1998; Zilberman &
various drugs on men and women, they are starting to Blume, 2005). Cocaine-addicted women are likely to
uncover significant differences in how each gender re- be significantly younger at the time of their first admis-
sponds to different chemicals. Not surprisingly, there sion to a drug treatment program than their male coun-
are also differences in how men and women react when terparts, and to have followed a different pathway to
they use one or more of the popular drugs of abuse. cocaine addiction (Griffin, Weiss, Mirin & Lang, 1989;
Narcotics abuse and gender. To date “only a handful Hernandez-Avila et al., 2004). Yet in spite of this grow-
of studies [have] investigated sex differences in response ing awareness that the dynamics of cocaine addiction
Gender and Substance Use Disorders 253
might differ between the genders, little research has AUDs (or other substance use disorders) in their female
been conducted into how treatment programs should patients (Blume & Zilberman, 2005b; North, 1996).
be modified to be more effective with cocaine abusers Women can be grouped into two subtypes of alcohol
of either sex. use disorders (Hill, 1995). The first group, composed
Alcohol use disorders and gender. Because of differ- only of a minority of women drinkers, appears to include
ences in body mass, fluid content, and lower levels of those whose alcoholism finds full expression between
gastric alcohol dehydrogenase found in the woman’s the ages of 18 and 24 years of age. These women might
body, women require up to 40% less alcohol than men be said to have “early-onset” (Hill, 1995, p. 11) alcohol
to achieve the same blood alcohol level (Blume, 1998; dependence, and their drinking pattern tends to be
Blume & Zilberman, 2005a; Collins & McNair, 2002). atypical. In contrast to this group, however, is the larger
Further, the monthly variations in estrogen levels can group of alcohol-dependent women. These women are
affect the speed with which the woman’s body absorbs classified as the “later-onset” (Hill, 1995, p. 11) drinkers,
alcohol, while oral contraceptive medications used by whose drinking seems to reach its peak between the
women can slow the biotransformation of the alcohol ages of 35 and 49 years of age. However, the relation-
already in the body (Reynolds & Bada, 2003; North, ship between the two subtypes of female alcoholics
1996). identified by Hill, and the Type I/Type II typology of al-
Women also tend to experience alcohol-related phys- coholism in males (discussed elsewhere in this text), is
ical complications at an earlier point in life than do still not clear.
men who drink abusively (Blume & Zilberman, 2005a, Current research (Graham, Massak, Demers, &
2005b). Women who drink abusively seem to develop Rehm, 2007) suggests that women who engage in “binge”
alcohol-related health problems at about one-third the drinking5 were significantly more likely to suffer from
alcohol intake level seen in men who develop similar major depression than were women who did not. The
health problems (North, 1996). Further, women ap- authors found that 24.5% of those women who engaged
pear to be more sensitive to the toxic effects of alcohol in binge drinking behavior met the diagnostic criteria
on striated muscle tissues such as the heart than are for depression, as opposed to only 8.2% of the general
male alcohol users (Blume & Zilberman, 2005a, population. The authors based their conclusion on data
2005b). As a group, women who enter rehabilitation generated from telephone interviews conducted on a
programs have more severe medical consequences than representative sample of 6,009 men and 8,054 women
those seen in the typical male who enters treatment for between the ages of 18 and 76 and living in Canada.
an alcohol use disorder (Green, 2006; Sinha, 2000). They found that depressed women tended to consume
The typical alcoholic woman will develop cirrhosis of larger amounts of alcohol per drinking episode, sug-
the liver after about 13 years of addictive drinking, as op- gesting that the depressed women were using alcohol to
posed to 22 years for the typical male alcoholic (Blume, self-medicate their depression.
1994; Hennessey, 1992). In a sense, the woman’s expe-
riences of alcohol-related consequences are often tele-
scoped into a shorter time frame than that of the typical A Positive Note
male alcoholic (Blume & Zilberman, 2004; Greenfield, Although a great deal remains to be discovered about
2003; Schuckit, Daeppen, Tipp, Hellelbrock, & Bucholz, the impact of gender on the substance use disorders
1998).4 and their treatment, there are also hopeful signs emerg-
There is a known association between AUDs and re- ing from the research that has been conducted to date.
productive problems such as infertility, miscarriage, For example, Miller and Cervantes (1997) found that
amenorrhea, uterine bleeding, dysmenorhea, and abnor- women with AUDs were more likely to respond posi-
mal menstruation. Women who drink heavily are also at tively to minimal interventions. One reason for this is
increased risk for osteoporosis and possibly breast cancer that as a group women “are often first to recognize their
(Emanuele, Wezeman, & Emanuele, 2002; Kovalesky, drinking problem, while men are more likely to have
2004; Sampson, 2002). Unfortunately, in spite of this confrontations, especially with authorities, that bring
known association between alcohol abuse/addiction them involuntarily into contact with treatment care-
and illness, physicians are very poor at recognizing givers” (Beckman, 1993, p. 236). Women also appear
4Chen, Yoon, Yi, and Lucas (2007) found that women with hepatitis to be more accepting of the need for treatment and
type C infection who were heavy alcohol drinkers died on average 10
5
years earlier than women who were infected but who were not heavy Defined by the authors of this study as 7 or more standard drinks on
alcohol users. one occasion.
receptive to its benefits, largely because these women Nicotine use disorders. An emerging body of evidence
generally have responsibility for children (Kline, 1996). suggests that adolescent girls are more likely to initiate
Treatment outcomes for women with SUDs appear to the practice of cigarette smoking and that they are less
be as good as if not better than those obtained by men likely to quit smoking than adolescent boys (Wunsch,
who enter treatment (Green, 2006). Women who 2007). There is also significant evidence that nicotine’s
complete treatment were found to be nine times as effects on the smoker’s brain are influenced by the
likely to abstain from chemicals than women who do smoker’s gender (Fallon, Keator, Mbogori, Taylor, &
not complete treatment, while men who complete Potkin, 2005). Using positron emission tomography
treatment are only three times as likely to abstain as (PET) technology, Fallon et al. examined the impact of
those men who fail to graduate from rehabilitation nicotine on the brains of men and women (both smok-
(Green, 2006). ers and nonsmokers) who were involved in a vigilance
A cautionary note. Although Alcoholics Anonymous task. The authors found a decrease in brain metabolism
(AA) is often suggested as an adjunct to the woman’s ef- in the brains of female smokers who were using a trans-
forts to recover from an SUD, there is often a “subtle dermal nicotine patch, while their male counterparts
but significant form of sexism” in such meetings (Coker, demonstrated an increase in brain metabolism while
1997, p. 268). For example, the AA program “which performing the same task. The authors interpreted their
confronts the false pride of the alcoholic, may not be results as reflecting a gender effect on nicotine’s impact
helpful to a woman who needs to build her self-esteem on brain metabolism, a result that will certainly stimu-
from the ground up” (Jersild, 2001, p. 6). late further research into the impact of gender on the
As a group, women tend to feel higher levels of effects of cigarette smoking.
shame than do men who enter AA. It is for this reason
that women are more like to to be solitary drinkers than
men with AUDs. AA’s heavy emphasis on uncovering
Summary
sources of shame might make women feel unwanted or In the late 20th century, medical researchers began to
unwelcome in AA (Blume & Zilberman, 2004; Coker, identify variations in the ways that many commonly
1997; Jersild, 2001). To complicate matters, there is prescribed medications affected women compared to
strong evidence that the face of alcoholism in women is men. They also began to notice that the course of many
changing. Women are apparently starting to drink alco- disease states differed between men and women, and a
hol at an earlier age and in far greater quantities than growing body of researchers began to question whether
did their older counterparts (Greenfield, 2003; Sinha, much of the existing research, done primarily with
2000). Thus, the challenge that faces AA is the need to males, was applicable to female patients. In a parallel
both eliminate the subtle sexism inherent in its 12-Step process, addictionologists began to discover that men
program while making the program relevant to all age and women often differed in the course their addiction
cohorts of women. followed and in their reactions to the often standard-
Marijuana use disorders in women. There has been ized treatment protocols that were used in an attempt to
virtually no research into the possibility that women help them overcome their substance use disorders. Fur-
who smoke marijuana might react differently to it than ther, often subtle and occasionally not so subtle differ-
men, or the possible interaction between gonadal hor- ences were discovered in how the sexes reacted to the
mones and the woman’s reaction to marijuana (Han & various drugs of abuse. In this chapter, the topic of sub-
Evans, 2005). stance use disorders in women was reviewed.
CHAPTER TWENTY-TWO
Hidden Faces of Chemical Dependency
There are many faces to chemical dependency. Many (Luggen, 2006). But in spite of this fact, research into
of these images are familiar. For example, there is the the identification and treatment of substance use dis-
stereotype of the “typical” “skid row” alcoholic, drink- orders (SUDs) in the elderly has progressed very
ing a bottle of cheap wine wrapped in a plain brown slowly (Zimberg, 2005; Zisserson & Oslin, 2004). One
paper bag. Another popular image is the young male reason might have been the myth that alcoholism was
heroin addict with a belt wrapped around his or her a self-limiting disorder, in the sense that alcohol-
arm, pushing a needle into a vein. If the addicted per- dependent individuals rarely lived long enough to
son deviates from our expectation, we might not recog- reach old age (Zimberg, 2005). In reality, as the cohort
nize the chemical dependency right before us. For of the population born between 1950 and 1960—and
example, how many of us would expect to meet a white, raised in the permissive atmosphere of the 1960s,
middle-class, well-groomed heroin addict at work? How 1970s, and the early 1980s—is approaching middle
many people would recognize the benzodiazepine- age, the problem of AUDs/SUDs in older age groups
dependency behind the smiling face of a day care worker? is of increasing concern, a trend that is expected to
It is the purpose of this chapter to explore some of continue well into the 21st century (Colliver, Compton,
the hidden faces of chemical dependency, so that the Gfroerer, & Condon, 2006; Gomberg, 2004; Zisserson &
reader might be more sensitive to the many forms that Oslin, 2004).
substance abuse might take. Scope of the problem. The elderly make up approxi-
mately 12% of the population of the United States,
using approximately one-third of all prescription med-
Addiction and the Homeless ications and one-half of all over-the-counter medi-
There has been a limited amount of research into sub- cations (Gomberg, 2004; Reid & Anderson, 1997).
stance use problems among the homeless. Researchers Approximately 2% to 4% of the elderly are thought to
have found that 45% to 78% of those who are homeless have a substance use disorder (SUD) involving alcohol,
have a substance use disorder (Arehart-Treichel, 2004; drugs, or both. SUDs other than alcohol are expected
Smith, Meyers, & Delaney, 1998). Surprisingly, the in- to become more common as the “baby boomer” gener-
cidence of substance abuse does not seem to increase ation ages, and researchers expect that the total number
after the person becomes homeless, and in some cases of drug abusers in the elderly age cohort might be as
losing one’s home seems to serve as an incentive for the high as 2.5 to 5 million persons by the year 2020 (“U.S.
individual to stop using alcohol/drugs (Arehart-Treichel, Face of Drug Abuse,” 2006). Even now, researchers be-
2004). The role of the individual’s substance use in the lieve that 1% of the elderly have used an illicit drug in
loss of his or her home is not always clear, and there is the past 30 days, and that 13% of the men and 9% of the
not always a causal relationship. Rather, substance abuse women over the age of 60 have an alcohol use disorder
and loss of housing may reflect co-existing issues that (AUD) (Gwinnell & Adamec, 2006). Because of age-
reflect a third factor, such as loss of employment or men- related changes in the body, older individuals are more
tal illness. vulnerable to the negative effects of alcohol, even if
the amount of alcohol consumed is not significant by
the standards of younger drinkers (J. W. Smith, 1997;
Substance Use Problems and the Elderly Stevenson, 2005).
The alcohol use disorders (AUDs) are the third most Nor is the problem of recreational drug use among
common psychiatric problem found in older persons the elderly limited to alcohol. It has been estimated that
255
256 Chapter Twenty-Two
15% of the elderly patients with an AUD also have an alcohol use on the part of their patients (Stevenson,
SUD (Greenfield, 2007). One study found that of 2005). These factors combine to make the differen-
3,700 drug-related deaths in California in the year tial diagnosis of an AUD/SUD in an older person quite
2003, only 51 involved people under the age of 20 difficult.
(Sherer, 2006). Further, data drawn from 30 metropoli- Another factor that can hinder the identification of
tan areas across the United States revealed that more an AUD/SUD in older people is the social myth that
than half of those who died from drug overdoses in the the older person deserves to use alcohol as a reward for a
year 2003 were between the ages of 35 and 54 (Sherer, lifetime of hard work (Stevenson, 2005; Zimberg,
2006). 2005). Social isolation, especially in the nonworking/
To further complicate matters, older people often retired older drinker, or the social belief that older
receive prescriptions for age-related medical problems drinkers do not respond to treatment interventions so
such as arthritis or heart disease and are frequent users treating them is a waste of time also contribute to the
of over-the-counter medications to self-medicate con- nondetection or underreporting of SUDs in older indi-
ditions such as arthritis, constipation, and others. The viduals.
mixture of prescription and over-the-counter medica- Older individuals do not demonstrate such tradi-
tions raises the individual’s risk of an adverse drug in- tional symptoms of an AUD/SUD as consuming large
teraction (Stevenson, 2005; Zimberg, 2005). If the amounts of alcohol/drugs or missing work, indicators so
individual were to also have an alcohol/drug use often seen in younger patients with such disorders. Be-
disorder, the danger for an adverse outcome is even cause older individuals are more vulnerable to the neg-
higher (Gwinell & Adamec, 2006; Stevenson, 2005; ative effects of alcohol or drugs of abuse, they tend to
Zimberg, 2005). experience negative consequences of their chemical
As a group, the elderly are frequent users of the abuse at levels that do not raise suspicion in family
health care system. Older persons with an AUD are members or outsiders (Baselt, 1996; Gomberg, 2004;
overrepresented among those seeking health care be- Zisserson & Oslin, 2004). For example, as a result of
cause alcohol abuse exacerbates or causes many med- normal, age-related bodily changes, older drinkers
ical disorders for which older persons seek medical achieve higher blood alcohol levels than younger
treatment (Stevenson, 2005). Alcohol use disorders adults after consuming a given amount of alcohol
have been identified in 25% to 30% of men and 5% to (Lieber, 1998; Zimberg, 1996). Just three beers or
12% of women hospitalized for medical treatment of mixed drinks consumed by a 60-year-old may have the
conditions other than the AUDs (Stevenson, 2005). same effect on the drinker as 12 beers or mixed drinks
A definition of abusive alcohol use in the elderly. consumed by someone who is 21 (Anderson, 1989).
Medical researchers now believe that one standard al- Also, since a large percentage of older adults are re-
cohol-containing beverage per day is the upper limit of tired, there probably is not a concerned employer who
“moderate” alcohol use for those over the age of 60 could detect the individual’s SUD and use the threat of
(Rigler, 2000; Zisserson & Oslin, 2004). Anything job loss to encourage the person to enter treatment, as
above this level might be classified as an abusive level in the case of a younger adult with a problem (Stevenson,
of alcohol use. As was noted earlier, the consequences 2005).
for older individuals who consume more than the rec- Alcohol/drug use disorders in older persons are often
ommended one drink a day limit are all too evident, hidden from family and friends because either they or
since AUDs can create medical problems in older those close to them are ashamed of the problem. This
drinkers. sets up a cycle of avoidance among family and friends
Why is the detection of substance use disorders in who avoid confronting the suspicion that an older indi-
the elderly so difficult? One reason is that older adults vidual might have an AUD/SUD or ignore the evi-
tend naturally to have more medical problems than do dence that such a disorder exists (Goldstein, Pataki, &
younger adults. In the early stages, an AUD/SUD Webb, 1996; Gomberg, 2004).
often mimics symptoms of other disorders commonly What are the consequences of AUDs/SUDs in the eld-
found in the elderly, making the differential diagnosis erly? The older drinker or substance abuser is subject to
very difficult for the attending physician. Older drinkers all of the dangers associated with the abuse of alcohol
tend to attribute physical complications caused by or drugs, a risk that is compounded by age-related
their drinking to the aging process rather than to bodily changes. Older individuals with an AUD are at
their alcohol use, and physicians rarely inquire about higher risk for accidental falls, bone fractures, depression,
Hidden Faces of Chemical Dependency 257
memory problems, liver disease, cardiovascular disor- tent problem drinking over the years but developed a
ders, and sleep problems (Council on Scientific Affairs, more chronic alcohol problem only in late adulthood.
1996; Luggen, 2006; Rigler, 2000; Zisserson & Oslin, This group has late-onset exacerbation drinking, accord-
2004). Older drinkers also seem to have an increased ing to Zimberg (1995). Finally, those whose alcohol
risk for motor vehicle accidents. Higgins, Wright, and problems started in young adulthood and continued
Wrenn (1996) found that 14% of elderly patients seen into later life have early-onset alcoholism (Mundle,
for injuries suffered in motor vehicle accidents had evi- 2000; Zimberg, 1995). About two-thirds of those indi-
dendence of alcohol in their bodies at the time of the viduals with an AUD are thought to fall into the early-
accident. onset group (Stevenson, 2005).
Researchers disagree as to whether dementia is a Compared with nondrinkers, people with early-
normal consequence of aging. However, it is a feared onset AUDs are usually from lower socioeconomic
disorder for older individuals. Thus the “high associa- levels, have less education, smoke more, socialized
tion between alcoholism and dementia” (Goldstein with individuals who abused alcohol more often, or
et al., 1996, p. 941; J. W. Smith, 1997) should make the came from families in which alcohol use was tolerated
detection and treatment of AUDs in older persons of or encouraged, and more often come from estranged
special importance. Alcohol’s contribution to such families or are single or divorced (Stevenson, 2005). In
medical problems as myopathy, cerebrovascular dis- contrast, individuals with late-onset AUDs generally
ease, gastritis, diarrhea, pancreatitis, cardiomyopathy, come from higher socioeconomic levels, enjoy a
various sleep disorders, hypertension, diminished resis- higher income level, and have stronger familial/social
tance to infections, peripheral muscle weakness, elec- support systems on which to call (Stevenson, 2005). In-
trolyte and metabolic disturbances, and orthostatic dividuals with late-onset AUDs tended to report more
hypotension (Liberto, Oslin & Ruskin, 1992; Luggen, negative life events such as retirement, illness or death
2006; Szwabo, 1993) should further underscore the im- of a spouse, geographic relocation, loss of lifelong
portance of detection and treatment of AUDs in older friends, deteriorating health, and depression (Stevenson,
persons. 2005).
Although few people stop to consider the possible Misuse of prescription medication is another prob-
impact of alcohol/drug abuse problems on the mental lem area for the elderly. Campbell (1992) estimated
health of older individuals, substance abuse extracts a that 10% of the elderly misuse prescription medica-
terrible toll on peace of mind. Depression is a common tions. Drug misuse takes several forms including (a) in-
problem in old age, and it is also a common conse- tentional overuse of a medication, (b) underuse of a
quence of alcohol/drug abuse. An estimated 25% to medication, (c) erratic use of a prescribed medication,
50% of all elderly suicide victims have used alcohol or (d) the failure of the physician to obtain a complete
prior to their suicide attempt (Abrams & Alexopoulos, drug history, including use of over-the-counter medica-
1998). For reasons that are not clear, there seems to be a tions, resulting in dangerous medication combinations
relationship between alcohol abuse problems in early (Abrams & Alexopoulos, 1998). The intentional misuse
or middle adulthood and the development of depres- of prescribed medications is the largest category of drug
sion in the older years, even if the alcohol use is not abuse in the elderly, but within that, the largest cate-
problematic in those later years (Abrams & Alexopoulos, gory of medication misuse involves the underutilization
1998). Unrecognized substance-induced depressive of prescribed medications rather than overuse of these
episodes can result in both misdiagnosis and mistreat- compounds, usually because of financial problems
ment of mental health problems (Council on Scien- (Abrams & Alexopoulos 1987, 1998; Piette, Heisler, &
tific Affairs, 1990), adding urgency to the need for an Wagner, 2004).
accurate diagnosis of the causes of depression in the The treatment of the older alcohol/drug abuser. There
elderly. are few outcome studies involving older individuals with
Different patterns of alcohol/drug abuse in the eld- addictive disorders (Satre, Mertens, Arean, & Weisner,
erly. There seem to be three subgroups of older persons 2004; Zimberg, 2005). Even when the older alco-
with an AUD. The first is individuals who had no drink- holic/drug abusing patient is referred to treatment, he or
ing problem in young or middle adulthood but devel- she will present special treatment needs rarely found in
oped an AUD later in life. This is called late-onset younger addicts, which few treatment centers are
alcoholism (Mundle, 2000; Rigler, 2000). The second prepared to meet (Goldstein et al., 1996). To address
subgroup of older alcoholics had a history of intermit- these special treatment needs, Dunlop, Manghelli, and
Tolson (1989) recommended that treatment programs that in addition to the drinking problem, older alco-
for the elderly include several different components: holics are also experiencing age-specific stressors such
as retirement, bereavement, loneliness, and the effects
1. A primary prevention program to warn about the of physical illness (Dunlop et al., 1989; Zimberg, 1996,
dangers of using alcohol as a coping mechanism for 2005). On a positive note, there is evidence that late-
life’s problems onset drinkers respond better to treatment than younger
2. An outreach program to identify and serve older al- alcohol abusers (Brennan & Moos, 1996; Mundle, 2000;
coholics who might be overlooked by more tradi- Satre et al., 2004). Compared to younger clients, older
tional treatment services individuals remained in treatment longer, responded
3. Detoxification services with counselors trained and better to psychosocial interventions such as Alcoholics
experienced in working with the elderly, who fre- Anonymous, and were less likely to relapse following
quently require longer detoxification periods than treatment (Satre et al., 2004).
younger addicted persons
4. Protective environments for the elderly—that is,
structured living environments that allow the indi-
Homosexuality and Substance Abuse
vidual to take part in treatment while being pro- With the advent of the AIDS epidemic, a great deal of re-
tected from the temptation of further alcohol use search has addressed the issue of substance use disorders
5. Primary treatment programs for those who could (SUDS) among men who prefer sex with other men
benefit from either inpatient or outpatient short- (Hughes et al., 2006). In contrast, alcohol/drug misuse
term primary treatment programs among women whose sexual preference is directed
6. Aftercare programs to help the older alcoholic with toward other women has received comparatively little at-
the transition between primary care and indepen- tention (Hughes et al., 2006). Currently, it is thought
dent living, that homosexual males and lesbians tend to abuse chem-
7. Long-term residental care for those with severe icals more often than the general public (Hughes &
medical and/or psychiatric complications from Wilsnack, 1997; King et al., 1997; Rathbone-McCuan &
alcoholism Stokke, 1997; Warn, 1997). This is clearly seen in the
8. Access to social work support services levels of methamphetamine abuse within the gay com-
munity (Ling, Rawson, & Shoptaw, 2006). These indi-
In working with the older alcoholic or drug-abusing viduals constitute a “special needs” population that many
patient, remember that he or she might require an ex- substance abuse rehabilitation professionals do not
tended period of time just to fully detoxify from alcohol understand or feel qualified to work with (Cabaj, 1997,
or drugs (Gomberg, 2004; Mundle, 2000; Stevenson, 2005; Rathbone-McCuan & Stokke, 1997).
2005). The 21- to 28-day inpatient treatment program, Statement of the problem. There is a high instance
itself quite rare in this age of “managed care,” often fails of SUDS among homosexual men and women: For
to meet the needs of elderly clients as they would example, 28% to 35% of homosexual individuals have
hardly have completed the detoxification process be- engaged in noninjection recreational drug abuse, com-
fore being discharged as “cured.” Further, older adults pared to 10% to 12% of the heterosexual population
might require more help than younger clients to build a (Cabaj, 2005; Ungvarski & Grossman, 1999). This vul-
nonalcoholic support structure (Anderson, 1989). Older nerability for SUDS is enhanced by the central role
clients often have a slower physical and mental pace than that substances play in the social lives of gay/lesbian/
younger individuals, present a range of sensory deficits bisexual individuals (Cabaj, 2005). Living on the fringes
rarely found in younger clients, and very often dislike the of a society that does not tolerate homoerotic activities
profanity commonly encountered with younger indi- and interests, opportunities for socialization within the
viduals in treatment (Dunlop et al., 1989). gay community are limited. It is for this reason that the
Unless these special needs are addressed, the older gay bar assumes a role of central importance in the lives
individual is unlikely to be motivated to participate in of many homosexual males and lesbians. It is a place
treatment and might even resist admission to a treat- where one might socialize without fear of ridicule,
ment facility if referred to one (Zimberg, 2005). Treat- meet potential partners, or simply escape from society
ment professionals must help older addicts deal with in general (Paul, Stall, & Bloomfield, 1991).
more than the direct effects of their chemical addiction. Further, the gay bar often plays a role of central impor-
For example, health care professionals need to be aware tance in learning about one’s sexuality for homosexual
men and women. Within this context, recreational treatment for substance abuse problems live a nontradi-
chemicals might also provide an excuse for engaging in tional lifestyle.
otherwise unacceptable behaviors for the conflicted in- Unfortunately, the development of specialized treat-
dividual who can then blame the state of intoxication ment services for gay/lesbian clients has been “slow”
for the sexual experiences (Cabaj, 2005). Finally, some (Hughes & Wilsnack, 1997, p. 31). There are few treat-
researchers have suggested that alcohol/drugs might espe- ment programs dedicated to working with homosexual
cially be abused by male homosexuals to deaden the pain adults, and such programs are usually located in major
of receptive anal intercourse (Ungvarski & Grossman, cities where there is a significant homosexual popula-
1999). tion. There is no program known that is devoted en-
Some research data report that more than half of all tirely to the treatment of lesbians (Rathbone-McCuan
lesbians have alcohol use problems, a rate 5–7 times & Stokke, 1997). A significant percentage of substance
higher than in nongay women (Blume, 1998; North, abuse professionals were deficient in their ability to
1996). But the research methodology on which these work with the homosexual client, and in almost 40% of
estimates are based has been challenged (Cabaj, 2005). the cases substance abuse counselors received no for-
It would also appear that substance use rates and pat- mal training at all in how to work effectively with the
terns differ for older age cohorts of gay men and women gay/lesbian client (Hellman, Stanton, Lee, Tytun, &
as opposed to younger age cohorts (Hughes, 2005). Vachon, 1989).
Other research claims that 15% of lesbians will seek In the last decade of the 20th century, there was a
treatment for an SUD, as opposed to only 1.6% of het- movement to establish special AA groups oriented
erosexual women (Hughes et al., 2006). toward the specific needs of bisexual/gay/lesbian com-
Thus, there is ample evidence that SUDs might be munity (Paul et al., 1991), but such groups are usually
more common in the homosexual community than in located in the same major metropolitan areas where
the heterosexual population. Unfortunately, many of there are significant numbers of gay/lesbian persons.
the early studies into the scope of SUDs in the homo- Further, because formal religions often persecute or re-
sexual population were based on research samples ject gay/lesbian members, the heavy emphasis of AA
drawn from gay bars. Such studies might inflate the esti- groups on spirituality often causes homosexual mem-
mate of SUDs disorders among the bisexual/gay/lesbian bers to feel uncomfortable or to even reject the idea of
population (Cabaj, 1997; Friedman & Downey, 1994). joining them entirely (Hughes, 2005). In spite of the
Statistically, those most likely to frequent these bars are progress that society has made toward accepting homo-
the people who are more likely to have alcohol/drug sexual/lesbian persons, there remains a significant need
use problems, and because many research samples for substance abuse counselors to become aware of the
were drawn from volunteers recruited in gay bars, a nat- unique needs presented by these clients, and for the
ural selection bias against individuals who did not have treatment professional to arrange for the specialized
an SUD was established. training necessary to effectively meet these needs.
In contrast, Hughes and Wilsnack (1997) concluded
that lesbians may indeed have higher rates of alcohol
Substance Abuse and the Disabled
use problems than their heterosexual counterparts.
However, there is a lack of adequate research studies, There is a very limited body of information about the
and many of the estimates of alcohol use problems scope or consequences of substance use by individuals
among lesbians are extrapolated from studies done on with physical disabilities. Substance abuse is known to
male homosexuals; therefore, the authors call for more be more common among persons with disabilities than
research into alcohol/drug abuse patterns among ho- it is in the general population (Corrigan, Bogner,
mosexual women. There also is little research into the Lamb-Hart, Heinemann, & Moore, 2005). By some es-
special health care needs of the bisexual/gay/lesbian timates, up to 62% of individuals who are disabled have
client, and virtually no research into what treatment an alcohol use disorder (AUD) (Heinemann & Rawal,
methods are effective for the substance abusing gay/ 2005).
lesbian client (Cabaj, 1997, 2005). However, with some To further complicate matters, treatment resources
estimates stating that gay/lesbian individuals make up for working with substance-abusing clients with a phys-
10% to 15% of the population (Fassinger, 1991) and ical disability are quite limited. For example, coun-
that approximately one-third of these abuse chemicals, selors working with hearing-impaired clients often must
it would appear that a significant percentage of those in rely not on professional interpreters but on friends and
family members to translate the spoken word into sign Thus, the physically disabled form an invisable sub-
language (Heinemann & Rawal, 2005). Although many group of those who abuse or are addicted to chemicals
treatment programs have videotapes of lectures with in the United States. As such, they are hidden victims
closed captions and might even utilize sign language of the world of drug abuse/addiction.
interpreters during group therapy sessions for the hearing-
impaired client, few programs have sign language in-
Substance Abuse and Ethnic Minorities
terpreters outside of these sessions (Cavaliere, 1995).
This prevents the hearing-impaired client from partici- As a group, ethnic minorities are underserved in terms
pating in the informal give-and-take discussions outside of access to general health and substance abuse treat-
of group that are so much a part of the rehabilitation ment services even though there is strong evidence that
program. Thus, within the treatment setting, the hearing- substance abuse treatment is equally as effective for
impaired client continues to be isolated and treated as members of ethnic minority groups as it is for other
if she or he were “different.” Americans (Blume & de la Cruz, 2005). But the issue
Patients who have suffered a traumatic brain injury of substance abuse rehabilitation in minority groups is
(TBI) also present treatment staff with special needs for quite complex. One factor that must be addressed in
which they have rarely been trained (Corrigan et al., considering substance use patterns among minority
2005). Research guidelines for working with the subgroups is whether the individual is a native-born Ameri-
stance-abusing patient who has suffered a TBI are lack- can and if not, the length of time the person has been
ing, although there is evidence that duration of treatment living in this country (Collins & McNair, 2002).
is one predictor of a positive outcome for these special As each successive generation moves closer to the
needs patients (Corrigan et al., 2005). According to social norms of this country and further away from the
Corrigan et al., financial incentives appeared to be of cultural identity of the previous generation, they be-
value when working with clients who have suffered a come more vulnerable to SUDs (Collins & McNair,
TBI and who have a substance use disorder. 2002). There are thus intergenerational variations in
In a very real sense, rather than being identified as a the development of substance use disorders in different
special needs subgroup, the disabled are often “per- minority groups. There are also significant intragroup
ceived as isolated occasional cases, only remembered differences among the various ethnic groups. The next
because of the difficulty and frustration they present to section is a brief summary of the substance abuse pat-
the professionals trying to serve them” (Nelipovich & terns of some of the larger ethnic groups found in the
Buss, 1991, p. 344). Nelipovich and Buss call for “cre- United States.
ativity” (p. 345) on the part of rehabilitation staff who Native Americans. Approximately 2 million individ-
are attempting to meet the needs of the disabled, sub- uals in the United States can be classified as Native
stance-abusing client, especially since only a minority Americans (Beauvais, 1998). They are members of the
of treatment programs have the special resources nec- estimated 200 (Franklin & Markarian, 2005) or 500
essary for working with the disabled (wheelchair (Caetano, Clark & Tam, 1998; Collins & McNair,
ramps, etc.). 2002) individual tribes in the United States, and these
Many programs would rather not serve this subpop- groups speak more than 200 distinct languages and
ulation (Tyas & Rush, 1993). In contrast, drug dealers have different cultural and social histories. Only about
are only too happy to offer their services to the disabled. one-third live on identified reservations; the majority
To further complicate the problem, family members live in traditional residential areas outside of estab-
often come to believe that the disabled person is “enti- lished reservation lands (Beauvais, 1998).
tled” to use recreational chemicals, even if he or she Collectively, these individuals are called Native
does so to excess. A common attitude among family Americans or (less politically correct) Indians, or Ameri-
members of a hearing-impaired person is that he or she can Indians. They are often viewed as if they form a single
should be allowed to use chemicals because of the dis- group, although as the statistics in the last paragraph
ability (Cavaliere, 1995). Family and friends often ra- demonstrate, Native Americans are a heterogeneous
tionalize the substance abuse by the hearing-impaired group. To further complicate matters, some studies
individual on the grounds that “I’d drink too if I were have grouped “American Indians” with “Alaska natives”
deaf!” In this manner, the significant others of hearing- (“Alcohol and Minorities,” 2002, p. 1) as if these diverse
impaired individuals might overlook signs that their groups might share similar cultural or social traditions.
substance use was starting to interfere with their lives. Such groupings create difficulty in understanding the
alcohol use patterns of these diverse, geographically evidence to suggest that Native Americans are espe-
widespread groups. cially vulnerable to alcohol’s effects for either physical
Collectively, alcohol use is thought to be quite wide- or psychological reasons (Caetano et al., 1998). Fur-
spread among the Native American population. The al- ther, although popular belief is that European traders
cohol-related death rate for Native Americans is 440% introduced the Native American population to alcohol,
higher than for the general population, and alcohol is a there is historical evidence that at least some Native
factor in just under one-fifth of all Native American American tribes used alcohol for religious purposes,
deaths (Ringwald, 2002). But drug/alcohol use patterns as a medicine, or as part of the preparation for warfare
and expectations for recreational chemical use vary prior to the arrival of European settlers (Collins &
from tribe to tribe (Beauvais, 1998; Caetano et al., 1998; McNair, 2002).
Collins & McNair, 2002). This is clearly seen in the There is little information about the treatment
drinking patterns of the Navaho and Hopi tribes of modalities that might work best for Native Americans,
the Southwest. Both the Navaho and Hopi tribes live in and the data that do exist suggest that individuals with
the same geographic region of Nevada, yet the Navaho substance use disorders have better treatment outcomes
tolerate alcohol use while the Hopi view drinking as a if they are referred to a program that specializes in work
sign of irresponsibility (Caetano et al., 1998). with these clients (Schmidt et al., 2006). However,
As a general rule, alcohol use problems are about these preliminary findings have not been subjected to
twice as common among the males as the women appropriate research to confirm the initial results, and
members of different tribes (“Alcohol and Minorities,” there is still a great deal to learn about working with the
2002; Beauvais, 1998). But there are exceptions to this substance-abusing Native American client.
rule. For example, the rate of heavy drinking is about Hispanics. In the United States, approximately 11% of
the same for male and female members of the Sioux na- the entire population is Hispanic American (Randolph,
tion (Collins & McNair, 2002). There is also signifi- Stroup-Benham, Black, & Markides, 1998). Although
cant variation in alcohol use patterns between different sociologists tend to speak of the Hispanic subgroup as if
tribal units, with 111 of every 1,000 members of some it were a single entity, in reality a multitude of cultures
tribes in the northern United States being diagnosed as fall under the heading of Hispanic, each with different
having alcohol use problems while some tribes in the attitudes and expectations for alcohol/drugs (Caetano
southwestern United States have alcohol use problems et al., 1998; Franklin & Markarian, 2005). About 60%
diagnosed in only 11 people per 1,000 (Beauvais, 1998). of Hispanic Americans in the United States trace their
There is also evidence of marked intergenerational national heritage through Mexico, another 15% origi-
differences in alcohol use rates within tribal units, with nally were from Puerto Rico, 5% trace their roots to
the younger individuals tending to use alcohol more Cuba, and the remainder are from other Spanish-
often than their elders (Beauvais, 1998). speaking nations in this hemisphere (Randolph et al.,
While Native Americans with substance use disor- 1998). As these statistics suggest, the different cultures
ders might follow different paths to this condition than lumped together under the classification of Hispanic
more traditional clients (Schmidt, Greenfield, & often have different social beliefs, expectations, and
Mulia, 2006), less than 20% of alcohol/drug rehabili- patterns of alcohol/drug use (Franklin & Markarian,
tion programs offer specialized treatment for this popu- 2005).
lation (Schmidt et al., 2006). Markarian and Franklin In general, within Hispanic cultures in the United
(1998) suggested that Native American clients in sub- States, drinking, especially heavy drinking, tends to be
stance abuse rehabilitation programs might withdraw a male activity. Women tend to be light drinkers or to
into themselves if exposed to high levels of confronta- abstain from alcohol use entirely (Collins & McNair,
tion similar to those found in many traditional treat- 2002; Randolph et al., 1998). But there are significant
ment programs, reinforcing the observation that in- variations within the Hispanic community, depending
dividuals working with these subpopulations must be on the nation of origin. For example, 18% of Mexican
sensitive to the cultural differences and beliefs of their American males were considered heavy drinkers, while
clients. only 5% of Cuban American males met the criteria for
Although one popular misconception is that Native heavy alcohol use. In each culture, 2% or less of the
Americans are more sensitive to the effects of alcohol, women met the criteria for heavy drinking, and 10% to
there is little evidence to support this belief (Garcia- 11% were light drinkers, compared with 4% of the
Andrade, Wall, & Ehlers, 1997). There has been little Mexican American and 38% of the Cuban American
males (Randolph et al., 1998). In each Hispanic sub- than males whose heritage is from Europe (Franklin &
group, only a small minority of women drink alcohol, and Markarian, 2005).
an even smaller minority abuse it (Collins & McNair, There is preliminary evidence that suggests that
2002). Unfortunately, only about one-third of substance African Americans with chemical use disorders tend to re-
use rehabilitation programs offer specialized compo- ceive a different quality of treatment than do whites with
nents for Hispanic clients (Schmidt et al., 2006). Thus, the same disorders (Schmidt et al., 2006). For example,
there is a need for substance abuse rehabilitation pro- black women are 10 times more likely to be reported to
grams to develop a sensitivity toward and treatment the authorities for court intervention in cases of substance
methods to work with Hispanic Americans. abuse/addiction than are white women (Schmidt et al.,
Asian Americans. The term Asian American is quite 2006). Further research is needed to identify whether this
misleading as it includes Chinese Americans, Filipino perceived treatment disparity does indeed exist, and
Americans, Asian Indians, Korean Americans, Japanese methods by which it might be corrected.
Americans, and Vietnamese Americans as well as a Treatment implications. Overall, very little is known
multitude of other, diverse cultures from other nations about what forces bring about remission in minor-
in Asia (Franklin & Markarian, 2005). To complicate ity members, especially women (Warner, Alegria, &
matters, some researchers also include persons from the Canino, 2004). All too often, research studies that have
various island groups of the Pacific island in the sub- included minority group members with substance use
group of Asian Americans (“Alcohol and Minorities,” disorders have utilized exclusively male samples.
2002).
In general, women from Asian American cultures
are more likely to abstain, or drink only on social occa-
Summary
sions, than are their male partners (Caetano et al., We all have, within our minds, a picture of what the
1998). But even this generalization must be tempered “typical” addict looks like. For some, this is the picture
with the observation that women in different Asian of the “skid row” alcoholic, while for others the picture
American subgroups have widely disparate alcohol use associated with addiction is that of a heroin addict, hid-
patterns. For example, only 20% of Korean American den in the ruins of an abandoned building with a belt
women reported that they consumed alcohol, while around his or her arm, ready to inject the drug into his
67% of Japanese American women admitted to using or her vein. These images of addiction are correct, yet
alcohol (Caetano et al., 1998). each fails to accurately reflect the many hidden faces of
African Americans. Franklin (1989), for example, addiction.
found that of 16,000 articles on alcoholism published There is a grandfather who is quietly drinking him-
between 1934 and 1974, only 11 “were specifically self to death, or the mother who exposes her unborn
studies of blacks” (p. 1120). In the decade since child to staggering amounts of cocaine, heroin, or alco-
Franklin’s original study, a small number of research hol. There is the working woman whose chemical ad-
studies have addressed the issue of alcohol use prob- diction is hidden behind a veil of productivity, or who is
lems among African Americans. One such study was an addict whose drug use is sanctioned by the unsus-
conducted by Markarian and Franklin (1998), who pecting physicians trying to help her cope with feelings
found that African American males are more likely to of depression or anxiety. There are faces of addiction so
initiate heavy drinking later in life than European well hidden that even today they are not recognized. As
males, but they experience alcohol-related health prob- professionals, we must learn to look, and recognize, the
lems at about the same age, or perhaps even earlier, hidden forms of addiction.
CHAPTER TWENTY-THREE
Chemical Abuse by Children

and Adolescents
Scientists have long known that the childhood and ado- developmental demands for the child as he or she
lescent years are critical developmental periods for the matures. Wunsch (2007) identified three separate sub-
individual as they build the foundation for the transi- phases of adolescence known as the (a) early, (b) middle,
tion into the early adult years (“Young Adult Drinking,” and (c) late stages. Early adolescence starts at about the
2006). Unfortunately, research has demonstrated that age of 10, and during this phase children address physi-
(a) mid-adolescence is the most common period in life cal development issues while their central nervous sys-
when individuals begin to use recreational chemicals tems continue the pattern of development started in
(Flanagan & Kokotailo, 1999) and (b) substance use childhood. During middle adolescence, which Wunsch
disorders are most prevalent during the period from 18 (2007) identified as starting at the age of 15 and lasting
to 25 years of age (Substance Abuse and Mental Health for approximately 2 years, teenagers’ cognitive develop-
Services Administration, 2005). Between 7% and 10% ment continues while they struggle with self-acceptance
of adolescents will meet the diagnostic criteria for a issues. Finally, during the stage of late adolescence, the
substance use disorder at some point, although only a focus shifts to the psychosocial realm as teenagers explore
fraction will ever be referred to a treatment program adult roles and their relationship with the larger society
(Kaminer & Bukstein, 2005). around them (Wunsch, 2007).
Adolescent substance abuse is not a recent phemo- As would appear obvious given this breakdown, the
nenon. During the early 19th century, alcoholism was impact of drug use on the individual’s development
rampant among the youth of England (Wheeler & would be far different if it were to occur in late adoles-
Malmquist, 1987), giving impetus to the child welfare cence as opposed to the early or middle phase. Unfortu-
movement of the 19th century. These social reforms nately, there is strong evidence that for a significant
helped to drive child/adolescent recreational chemical percentage of adolescents, their normal development is
abuse underground, but the problem never disappeared. potentially being altered by exposure to alcohol and/or
Over the decades it has waxed and waned in intensity illicit drugs at various points during these critical peri-
and assumed different forms as new compounds of abuse ods of development.
have emerged, but it has never disappeared. But in the By the age of 18 years, 66% of adolescents have tried
21st century a significant body of evidence has emerged cigarettes, and 13% smoke at least half a pack per day
suggesting that the consequences of child/adolescent (Kaminer & Tarter, 2004). Eight percent of 18-year-
substance abuse might last for the rest of the individual’s olds have used cocaine at least once, while 15% have
life. For these reasons substance abuse rehabilitation used an inhalant, hallucinogen, or stimulant at least
professionals should have a working knowledge of the once (Kaminer & Tarter, 2004). Further, 4.3% of the
manifestations of substance use disorders (SUDs) in high school seniors surveyed admitted to having abused
childhood and adolescence, and how they are treated. OxyContin at least once, while 9.7% admitted to the
unauthorized use of Vicodin at least once (Wunsch,
The Importance of Childhood 2007). All of this illicit drug use, in addition to the 75%
of high school seniors who admit to the use of alcohol
and Adolescence in the Evolution
at least once during adolescence, is taking place during
of Substance Use Problems a period of special vulnerability.
Although the average person speaks of “childhood” and Developmental neurologists have discovered that
“adolescence” as if they were single phases of life, in re- adolescence is a dynamic period of brain growth and
ality both are made up of substages, each with specific development that continues into early adulthood
263
264 Chapter Twenty-Three
(Parekh, 2006).1 Unfortunately, there has been virtually period of significant development in the CNS, and
no research into the long-term effects of alcohol or drug there is no information on the impact of even limited
exposure (either to therapeutics or illicit compounds) substance abuse on the neurological, social, or cognitive
on the growth and development of the central nervous development of the child or adolescent.
system (Ling, Rawson, & Shoptaw, 2006). Thus, sub- Child and adolescent drug use patterns: What do we
stance abuse during this period of life holds the poten- know? Substance abuse in childhood and adolescence
tial to alter normal brain growth, possibly with lifelong is quite controversial, and distinctions between adoles-
consequences for the child/adolescent. cent substance use, abuse, and dependence are blurred
Substance abuse, especially in early adolescence, is and arbitrary. Some believe that any recreational sub-
associated with a higher risk of alcohol/drug addiction stance use in the childhood or adolescent years is a sign
later in life combined with a lower rate of treatment- of a serious problem; others argue that experimental use
seeking (Rosenbloom, 2005). For example, 15% of indi- might be just one aspect of adolescence (Bell, 1996;
viduals who become alcohol dependent do so before the Kaminer & Tarter, 2004). Indeed, at the start of the 21st
age of 18, while another 32% develop their addiction be- century “the question is not whether most teenagers will
tween the ages of 18 and 20 (Nelson, 2007). Thus, al- use drugs, but which one(s) will they try” (Greydanus &
most half of those who become alcohol dependent meet Patel, 2005, p. 392), how often, and when?
the diagnostic criteria for a diagnosis of alcoholism be- The answers to these questions have proven quite
fore they are legal adults (Nelson, 2007). In contrast, difficult to uncover, because research into childhood/
only about 20% who become dependent on alcohol will adolescent substance use behavior is very limited (Com-
do so after the age of 30, according to Nelson. mittee on Child Health Care Financing and Committee
By definition, any alcohol use by individuals under on Substance Abuse, 2001; Evans & Sullivan, 2001;
the age of 21 years is illegal, but adolescents are thought Parekh, 2006). Many of the estimates of childhood/
to purchase 17% to 20% of all alcohol-containing bev- adolescent SUDs are little more than watered-down ver-
erages sold in the United States (Commission on Ado- sions of the assumptions made for adults (Knight, 2000;
lescent Substance and Alcohol Abuse, 2005; Kaminer, Wu & Ringwalt, 2006). Other estimates are based on
2001).2 Yet, as discussed in Chapter 7, alcohol is a neu- studies that use school students as research subjects.
rotoxin. There is little information available on the con- Unfortunately, many high-risk adolescents do not attend
sequences of even limited alcohol abuse on the school on a regular basis, if at all, and thus are unlikely
developing central nervous system (CNS) of the child to participate in a study based on students (Committee
or adolescent at this time, but the potential is obviously on Child Health Care Financing and Committee on
there for at least some impact on the CNS, which Substance Abuse, 2001). Further, childhood/adolescent
might have lifelong consequences. drug use patterns may exhibit regional variation, as the
Little is known about the scope of illicit drug addic- percentage of adolescents thought to have a substance
tion in the population of children or adolescents. It is es- use problem ranges from 3% to 10% (Kaminer & Tarter,
timated that 2.19 million adolescents reported abusing 2004). Childhood/adolescent substance abuse patterns
an illicit drug other than alcohol for the first time in the are affected by a wide range of variables, including the
year 20053 (Wunsch, 2007). While this statistic is fright- individual’s geographic location, peer group, the cur-
ening, substance abuse, although a risk factor for later rent drug use “trends,” and drug availability. The phe-
addiction, does not automatically lead to the addictive nomenon of inhalant abuse is one such drug use “fad,”
use of chemicals (Hogan, 2000; Kaminer & Bukstein, which rapidly waxes and wanes in a given geographic
2005; Kaminer & Tarter, 2004). Many of the adoles- area over time as individuals embrace and then aban-
cents who initiate the use of an illicit compound do so don the practice. Other regional variations in the abuse
out of curiosity and discontinue the use of that drug after patterns of different compounds also exist, making it
a few episodes of abuse. Unfortunately, adolescence is a virtually impossible to develop a comprehensive picture
of the problem of child/adolescent substance abuse.
1
The topic of developmental neurology lies beyond the scope of this
chapter. There are many excellent textbooks on the subject available,
and the reader is referred to books on this topic for further information. Scope of the Problem
2
Since alcohol use by adolescents is, by definition, illegal, why is “the
alcohol industry” allowed to make nearly 20% of its profits from the Childhood chemical abuse patterns. Alcohol use during
illegal sale of alcohol to adolescents? childhood/adolescence is more common than most
3The last year for which such data are available at this time. parents are willing to admit, as evidenced by the finding
Chemical Abuse by Children and Adolescents 265
that just under half of the 11- to 14-year-old students in far the most popular chemical of choice for adolescents
their sample admitted to the use of alcohol, with half of (Hogan, 2000; Komro & Toomey, 2002). The most
these students doing so before the age of 9 years (Fetro, common pattern of adolescent alcohol use is binge
Coyle, & Pham, 2001). Research suggests that boys drinking (Mller, Naimi, Brewer, & Jones, 2007). Seventy-
tend to begin drinking earlier than girls, with an aver- two percent of 12th graders surveyed admitted using
age age for the first drink of alcohol being 11.9 years for alcohol at some point in their lives, while 5%–8% of
boys, compared with 12.7 years for girls (Alexander & these students meet the diagnostic criteria for a for-
Gwyther, 1995; Morrison, Rogers, & Thomas, 1995). mal diagnosis of alcohol use disorder (AUD) (Johnston
This observed age difference may reflect different pat- et al., 2006a; Parekh, 2006; “Young Adult Drinking,”
terns of alcohol availability (Van Etten, Neumark, & 2006). As a group, adolescents are estimated to make
Anthony, 1999). The authors found evidence that boys up 12%–20% of the entire alcohol market in the United
and girls are equally likely to abuse chemicals if their States, with an estimated 4.3 million adolescents con-
access to recreational substances is equal, but that boys suming alcohol each year in just the United States
are more likely than girls to have access to alcohol/ (Pumariega & Kilgus, 2005; Rosenbloom, 2005; Wu &
drugs. Ringwalt, 2006). The most popular alcohol-containing
Adolescent chemical abuse patterns. In the last quar- beverage ingested by adolescents is beer (Rosenbloom,
ter of the 20th century adolescent substance abuse 2005). Although there was a time when few adolescents
peaked sometime around the year 1981, and then it were drawn to “hard” liquor, there is now evidence that
slowly declined for about a decade until it reached a it is growing in popularity with teens, in part because it
plateau in the early 1990s. After years of relative stabil- is more easily hidden by mixing it with soft drinks (Cen-
ity, there were modest declines in the level of adoles- ters for Disease Control and Prevention, 2007).
cent substance abuse in the early years of the 21st In spite of their often-expressed concern about pos-
century (Doyle, 2001b; Johnston, O’Malley, Bachman, & sible substance abuse by their children, especially dur-
Schulenberg, 2006a) (see Figure 23.1). However, an es- ing adolescence, parents are poor sources of information
timated that 7% to 10% of older adolescents in the about their children’s possible substance abuse. As a
United States still appear to meet the diagnostic criteria group parents tend to underestimate their teenager’s
for an SUD severe enough to warrant treatment alcohol use by a factor of at least 4:1, illicit drug use
(Kaminer & Bukstein, 2005). consumption by at least 2:1 (Center for Substance
In a society where alcohol is the most popular recre- Abuse Research, 2006), and inhalants by a factor of 4:1
ational chemical, it should not be surprising that it is by (Worcester, 2006). Fisher (2006) found that parents
90
80
70
60
Percentage
50
40
30
20
10
0
2000 2001 2002 2003 2004 2005 2006
Year
FIGURE 23.1 Reported Alcohol Use by High School Seniors, 2000–2006

Source: Johnston, O’Malley, Bachman, & Schulenberg (2006a).
were essentially clueless about their child’s substance Currently, adolescents are classified as adults at the
use behavior. While 80% of parents expressed a belief age of 18, although every state has placed restrictions
that alcohol and marijuana were not available at the on their ability to purchase alcohol until they reach the
parties their adolescent children attended, 50% of the age of 21. In spite of this, more than 90% of college stu-
teens surveyed admitted that both alcohol and illicit dents view drinking as a central part of their social lives,
drugs were freely available at such parties (Sheff, and 44% engage in binge drinking (Saffer, 2002; Wu,
Warren, Ketcham, & Eban, 2007). Pilowsky, Schlenger, & Hasin, 2007). As a group, col-
In spite of its popularity, alcohol is not the only lege students “spend more on alcohol than they spend
recreational chemical used by adolescents. By the time on books, soda, coffee, juice and milk combined”
of graduation, 52% of 12th graders surveyed admitting (Jersild, 2001, p. 99). Unfortunately, the developmen-
to the use of an illicit chemical at least once (Johnston tal immaturity of the student’s brain during the early
et al., 2006a). Marijuana was the most commonly college years might actually predispose individuals in
abused illicit substance, with 42% of high school sen- this age group to alcohol’s reinforcing effects in spite of
iors surveyed admitting to the use of marijuana at least its potential for causing neurological damage (Spear,
once, according to Johnson et al. Other compounds 2002).
abused by adolescents include inhalants and increas- Because colleges provide a high concentration of
ingly the benzodiazepines as well as opioids diverted or consumers, advertisers tend to invest heavily in promot-
stolen from legitimate sources (Wunsch, 2007). ing alcohol-containing products in college newspapers,
Many adolescents begin “snorting” heroin or pre- at college athletic events, and other college sites (Saffer,
scribed narcotic analgesics, and over time “graduate” to 2002). This might account for the research finding that
the injection of these compounds (Marsch et al., 2005). college students, especially women, tend to drink more
Hallucinogens are unpopular, with only 8.3% of the heavily than their noncollege peers (Coombs, 1997;
high school seniors surveyed admitting to the use of any Demers-Gendreau, 1998; Slutske, 2005; Slutske et al.,
hallucinogen, and 7.8% admitting to the use of a hallu- 2004). Another reason many college students abuse al-
cinogen other than LSD (Johnston et al., 2006a). Of cohol might be their misperception of the amount of al-
those entering treatment, 23% have abused a CNS cohol ingested by their peers. As a group, college
stimulant such as methylphenidate or one of the am- students tend to overestimate both acceptance of the in-
phetamine compounds, while 6% have abused one or dividual’s drunken behavior by their peer group and the
more to a “significant extent” (Croft, 2006, p. 557). number of their peers who are actually drinking heavily
These stimulants are usually chewed and swallowed, or (White & Jackson, 2004/2005). This is unfortunate,
crushed and snorted intranasally. The intravenous use since by the time the student arrives at college, the in-
of any compound is so rare during adolescence that it is fluence of his or her peer group is one of the strongest
automatically a sign of a serious SUD. factors to shape individual drinking patterns (Marlatt
College students form a unique subpopulation. Tra- et al., 1998).
ditionally, the college experience is viewed as spanning College students typically binge drink rather than
the period from late adolescence to early adulthood, a drink daily (Weingardt et al., 1998).4 Further, when col-
period in life when risk-taking behaviors reach their lege students do drink it is most often with the goal of
peak (Arnett, 2000). Neurologically, the individual’s becoming intoxicated, following an alcohol use pattern
brain is in a state of transition during the college years first established in high school (Demers-Gendreau,
as the individual matures. It is also a period of life when 1998; Wechsler, 2002). Unfortunately, there is a growing
alcohol/drug abuse is at least tolerated if not supported body of evidence that such alcohol use in adolescence or
by the college subculture. early adulthood might facilitate the development of
The compound most frequently associated with a compound known as C-reactive protein,5 which is
college life is alcohol. The problem of excessive alco- thought to be associated with the development of
hol use by college students is hardly a new one. In heart disease in later life. Thus the individual’s abuse
1354 in England, Oxford University students and towns- of alcohol during the college years might have lifelong
people became engaged in a drunken brawl after a period consequences. Fortunately, binge drinking becomes less
of heavy drinking, leaving 63 students dead (Boyd,
McCabe, & Morales, 2005). Other examples of the ex- 4
Defined as the individual consuming five or more 12-ounce cans of
cessive use of alcohol by college students are found beer or standard drinks at one time.
throughout the pages of history. 5See Glossary.
common after the age of 23 as the student begins to face drink, a consequence that far outweighs the estimated
the demands of adult life (Boyd et al., 2005; Marlatt 10¢ each drink generates in tax revenue for society
et al., 1998; Wechsler, 2002). Only a minority (5%–19% (Miller et al., 2006). This figure is based on the esti-
of those students surveyed) were found to continue drink- mated impact of alcohol-related rape, homicide, as-
ing abusively over an extended period of time (Weingardt sault, other violent crime, larceny, burglary, motor
et al., 1998). vehicle theft, loss of employment, and medical care ne-
While this would suggest that alcohol/drug abuse by cessitated by underaged drinking. Alcohol-related vio-
the majority of college students is only part of a phase, it lence alone accounted for more than half the estimated
does not negate the fact that for some college students cost of underaged drinking, according to Miller et al.
their alcohol/drug use is indicative of an SUD that will A growing body of evidence suggests that because
be present in later life. Unfortunately, researchers have the brain is still developing in childhood/adolescence,
not isolated the diagnostic signs that can distinguish in- SUDs can have a lifelong impact on subsequent neuro-
dividuals who are at risk for a substance use disorder logical development. The adolescent brain seems to be
later in adulthood from those for whom alcohol use is four to five times as vulnerable to alcohol-induced
only a phase of life. But this phase-specific alcohol abuse brain damage as adult brains (Tapert, Caldwell, &
by college students carries with it a terrible price: Each Burke, 2004/2005; Wuethrich, 2001). One region of
year in the United States alone, alcohol use is a factor the brain that is especially vulnerable to alcohol-related
in the death of 1,400 college students as well as 500,000 brain damage during this phase of life is the hippocam-
injuries, 600,000 physical assaults, and 70,000 sexual pus, which is still maturing throughout adolescence
assaults in this age group (Hingson, 2003; Rimsza & (DeBellis et al., 2000; Tapert et al., 2004/2005). This
Moses, 2005; Slutske, 2005; Slutske et al., 2004). brain damage might not become evident until after the
Drug abuse by college students. Marijuana is the individual has stopped drinking, as evidenced by a
most frequently abused illicit compound on college small (7%–10%) but marked decline in psychological
campuses, just as it is in society. But college students test performance found in recovering adolescent
have been found to abuse compounds such as the pre- drinkers (Strauch, 2003). This decline in cognitive abil-
scription medications methylphenidate and Adderall ities appears to be permanent, again suggesting that
(Center for Substance Abuse Research, 2006). Indeed, adolescent alcohol abuse can have lifelong conse-
there is a subculture of college students who abuse pre- quences.
scription stimulants to help them study because the ef- Understanding the impact of adolescent drinking is
fects of such medications are more consistent that those not just a matter of comparing the adolescent to the
of caffeine, last longer, and do not place them at risk for adult drinker. The adolescent brain reacts differently to
ingestion of unwanted calories (Center for Substance alcohol than does the brain of the adult. Adolescents
Abuse Research, 2006). There is also evidence that at who drink do not seem to develop the same sense of se-
least some college students abuse the prescription med- dation that adults do after consuming a similar amount
icaton Provigil6 to help them stay awake longer to study of alcohol (Strauch, 2003; Varlinskaya & Spear, 2006).
for tests. This lack of sedation might contribute to the individ-
Why worry about child/adolescent substance abuse? ual’s decision to engage in risky behaviors such as
There are a number of reasons substance use disorders driving motor vehicles while intoxicated, and also to
(SUDs) are of particular importance. First, SUDs are consume more alcohol than perhaps intended, both
one of the leading causes of mortality for adolescents, behaviors that will put his or her life at increased risk for
contributing to deaths from suicide, drownings, inter- injury or legal problems.
personal violence, and motor vehicle accidents; they For many children/adolescents, inhalants are the
also contribute to adolescents having unprotected sex first mood-altering chemical they experiment with
and thus being exposed to the risks of sexually transmit- (Hogan, 2000). But for a significant minority of children/
ted diseases and unwanted pregnancy (Kaminer & adolescents, inhalants are their compound of choice.
Bukstein, 2005; Miller, Levy, Spicer, & Taylor, 2006; Some 16.3% of the eighth graders surveyed in 2005
Shepard, Sutherland, & Newcombe, 2006). had used an inhalant at least once (Johnston et al.,
Of equal if not greater importance is the cumulative 2006a). Fortunately for most children/adolescents, in-
cost of underaged drinking, estimated at $3 per illegal halant abuse is usually only a transient process and
thus the potential for inhalant-induced brain damage
6Normally used to treat narcolepsy. is limited. Adolescent inhalant abusers typically engage
in rare, episodic inhalant abuse over a 1- to 2-year marijuana abusers (364 male and 304 females) who were
span of time, after which they will generally abandon followed from adolescence until the age of 34–35 years.
this practice. The authors found four subgroups of abusers: (1) early-
The “gateway” drug theory. For more than 60 years, onset/heavy use group, (2) early-onset/light use group,
clinicians have suggested that (a) there is a progression (3) midadolescence-onset/heavy use group, and (4) mid-
in substance use disorders in adolescence and (b) that adolescence-onset, light use group. By itself, the early
certain chemicals serve as “gateway” drugs that lead the use of marijuana was not found to be predictive of later
individual toward more severe forms of substance problems or to lead to the abuse of other chemicals.
abuse. Walker, Venner, Hill, Myers, and Miller (2004) This is not surprising, given that just under 50% of indi-
found that based on the responses of 52 subjects there viduals 13–24 will use cannabis at least once (Knight,
appeared to be a progression in adolescent substance 2002). However, Kandel and Chen (2000) found that
abuse from alcohol, to tobacco, and then to the in- the individual’s motivation for using marijuana and the
halants, marijuana, and finally to other drugs of abuse. presence of other dysfunctional behaviors were associ-
To test the gateway theory, Ellgren, Spano, and Hurd ated with later drug abuse/dependence problems, cast-
(2006) administered cannabis to adolescent rats, then ing doubt on the gateway theory as it applied to
offered their rats the opportunity to use heroin. The au- marijuana abuse. Thus, whether there are certain gate-
thors found that the marijuana-exposed rats were more way substances that predispose the individual to the
likely to self-administer heroin later in their lives and to abuse of other compounds remains a theory that has
administer more than non-exposed rats. This results of not been proven.
this study were interpreted as providing support for the
gateway theory by the authors. In contrast to this inter-
pretation of the experimental data, Rosenbloom (2005)
Tobacco Abuse by Children/Adolescents
suggested that marijuana’s role as a gateway chemical is Cigarettes and other tobacco products occupy a unique
simply an illusion, as most “drug users begin with alco- place within this society. These substances are known to
hol and nicotine before marijuana” (Watson, Benson, & be addictive, are terribly destructive, and yet may be
Joy, 2000, p. 551). Personality characteristics such as legally purchased by adults. While children/adolescents
conduct disorder in adolescence or the antisocial per- are forbidden by law to purchase tobacco products, to-
sonality disorder in late adolescence/early adulthood bacco use problems are a very real part of childhood and
might be more predictive of subsequent substance use adolescence. In the United States, the average age at
disorders than simple marijuana abuse, in the opinion which a smoker begins is about 12 years, and most of
of several authors (Clark, Vanyukrov, & Cornelius, 2002; those who begin to smoke at this stage of life are regular
Watson et al., 2000). smokers by the age of 14 (Hogan, 2000). This may be
More doubt about the gateway theory was gener- because the adolescent brain, which is still growing,
ated by Tarter, Vanyukov, Kirisci, Reynolds, and Clark seems especially vulnerable to the addictive effects of
(2006). These authors reported that about 25% of the tobacco (Strauch, 2003).
200 male subjects in their study admitted to the use of Each day in the United States an estimated 3,000 chil-
marijuana before trying alcohol or tobacco products, dren/adolescents become cigarette smokers (Pumariega
substances that were supposed to be gateway com- & Kilgus, 2005). In spite of the known dangers asso-
pounds that would open the door to the use of illicit ciated with smoking, cigarette smoking seems to be
drugs such as cannabis. Further, the authors concluded growing in popularity with 18- to 24-year-olds in this
that those subjects who did abuse cannabis were more country (Rimsza & Moses, 2005). For example, fully
likely to live in homes where there was less parental su- 95% of those who smoke cigarettes began to do so before
pervision and in neighborhoods where marijuana was 19 years of age (Falco, 2005). Unfortunately, there are
more easily obtained. The majority of those who very limited resources to help the adolescent smoker
abused marijuana did not progress to the use of other il- who wishes to quit smoking cigarettes (Blum, 2006).
licit drugs, the author noted, and they concluded that At least one major tobacco company has conducted
their results failed to support the marijuana-as-a-gate- research into the phases of adolescent cigarette smok-
way-drug theory. ing, apparently to better understand how to help the
Another challenge to the gateway theory came from individual make the transition to regular cigarette
Kandel and Chen (2000), who examined the mari- smoking (Hilts, 1996). Another major tobacco com-
juana use patterns of a community-based sample of 708 pany referred to adolescents in an internal memo as an
“up and coming new generation of smokers” (Phelps, a specific peer group; (4) to relax and feel good; and
1996, p. 1A). The R. J. Reynolds Tobacco Co., a major (5) to satisfy curiosity about the drug’s effects. Unfor-
cigarette producer, went so far as to refer to 12-year-old tunately, many adolescents do not perceive their
children as “younger adult” smokers (“Big Tobacco’s abuse of chemicals as a problem, and even if they do
Secret Kiddie Campaign,” 1998). recognize that they have an SUD, they rarely know how
The natural cognitive immaturity of adolescence to access help (Wu & Ringwalt, 2006). Further, some
makes it difficult for individuals in this age group to ac- adolescents view chemicals as an acceptable way to
curately estimate the risk associated with behaviors self-medicate negative feelings such as depression or in-
such as cigarette smoking (Pumariega & Kilgus, 2005; terpersonal stress (Cleary, & Shinar, 2001; Joshi & Scott,
Strauch, 2003). Also, the natural rebelliousness of ado- 1988; Morrison, Rogers, & Thomas, 1995). Some indi-
lescents makes them especially vulnerable to the image viduals view alcohol/drugs as a way to prove sexual
that cigarette smoking is a way to go against parental au- prowess (Barr, 1999; Morrison et al., 1995).
thority (Dickinson, 2000; Greydanus & Patel, 2005). As this list of potential contributing factors illus-
The image of cigarette smoking as a form of rebellion is trates, there is no simple reason as to why adolescents
encouraged by media advertising campaigns. So perva- use recreational chemicals. One factor that seems to be
sive is the influence of the mass media for this age related to the individual’s abstinence or use of recre-
group that the media might be viewed as a “superpeer” ational chemicals is his or her cognitive development.
(Hogan, 2000, p. 937). Because adolescents tend to view themselves as being
Parental smoking behavior also plays a major role in immortal, many have trouble assessing the risks inher-
helping to shape the adolescent’s decision to smoke or ent in such behaviors as substance abuse (Hogan, 2000;
not smoke, as evidenced by the observation that 75% of Pumariega & Kilgus, 2005). In the section that follows
all teenagers who smoke had parents who also smoked are specific elements that might influence adolescent
(Males, 1992). Parental cigarette smoking will expose substance use behaviors.
the child to passive cigarette smoke, and thus adoles- Adolescent affective disorders. Depression is one of
cent cigarette smoking might be viewed as “largely the the risk factors for adolescent SUDs that has been iden-
active continuation of a childhood of passive smoking” tified to date (Kriechbaum & Zernig, 2000). The dy-
(Males, 1992, p. 3282). namics of depression are often different for adolescent
The child/adolescent’s transition from nonsmoker to males than for adolescent females. Few adolescent boys
smoker is thought to pass through several distinct stages are able to recognize the existence of their depression
(Holland & Fitzsimons, 1991): (Mayeda & Sanders, 2007). For both sexes, chemical
abuse might reflect an attempt to self-medicate emo-
1. The preparatory phase (during which the individual tional distress (Jorgensen, 2001). However, the adoles-
will form attitudes accepting of cigarette smoking) cent girl might be more in touch with her depression
2. The initiation phase (in which he or she will smoke than the adolescent boy. For this reason, adolescents
for the first time) who suffer from an affective disorder such as anxiety or
3. The experimentation phase, in which the child or depression should be viewed as being at high risk
adolescent learns how to smoke (Burke, Burke, & Rae, 1994, p. 454) for a substance use
4. The transition to regular smoking disorder because of the association between emotional
distress and substance abuse.
In addition to the long-term health risks associated It is surprising for many people to learn that ex-
with teen smoking, research has found that individuals tremes of behavior (i.e., total abstinence or serious drug
who begin to smoke in adolescence are 50% more abuse) have actually been identified as signs of malad-
likely to go on to develop an alcohol use disorder later justment in adolescents (Lundeen, 2002; Shedler &
in life than are those adolescents who do not begin to Block, 1990). The crucal factor is not whether the ado-
smoke cigarettes (Grucza & Bierut, 2006). lescent has experimented with alcohol/drugs but the
state of his or her emotional health and interpersonal/
intrapersonal resources. Adolescents who frequently
Why Do Adolescents Abuse Chemicals? abuse drugs tend to have poor impulse control, be so-
Hogan (2000) suggested that there were five basic reasons cially alienated, and experience high levels of emotional
adolescents use/abuse chemicals: (1) to feel grownup; distress, all signs that these individuals lack the emo-
(2) to take risks or rebel against authority; (3) to fit into tional resources necessary to cope with life effectively.
Adolescents who totally abstain from chemical use tend potential of the compound being abused, at least at
to be anxious and emotionally constricted, lack self- first.
confidence, and lack social skills (Shedler & Block, There is a strong relationship between peer group
1990). Thus, the individual’s pattern of substance abuse membership and substance use patterns of the individ-
can be understood only within the context of his or her ual (Farrell & White, 1998; Kaminer & Bukstein, 1998;
emotional adjustment. Pumeriega & Kilgus, 2005; Simkin, 2002). For example,
Conduct disorder/oppositional defiant disorder. Con- exposure to alcohol-using social models such as peers is
duct disorder (CD) and oppositional defiant disorder one factor that predicts the development of positive ex-
(ODD) are two forms of mental illness that first appear pectations for alcohol in children/adolescents in the
in childhood and adolescence. The diagnostic criteria fifth to seventh grades (Cumsille, Sayer, & Graham,
for both conditions are outside of the scope of this text 2000). Surprisingly, peer group selection is the last step
but are listed in the American Psychiatric Association’s in the chain of events that ultimately results in the ado-
Diagnostic and Statistical Manual of Mental Disorders lescent’s use of alcohol/drugs (Kumpfer, 1997). Adoles-
(4th edition—text revision) (American Psychiatric Asso- cents actively seek out a peer group consistent with
ciation, 2000). These conditions both share the common their values, expectations, and demands, including the
characteristic of reflecting a behavioral control disorder area of substance use patterns (Oetting, Deffenbacher &
that first is apparent during childhood/adolescence, and Donnermeyer, 1999; Strauch, 2003). Thus, peer group
which increases the individual’s risk for subsequent de- selection often precedes active chemical use, as the
velopment of a substance use disorder (SUD) (Clark individual’s perception of approval from peers pre-
et al., 2002). These signposts of behavioral dyscontrol cedes his or her first use of marijuana. But the actual
seem to precede the development of SUDs, and it is use of a chemical is often the last step in a chain of
hypothesized that both the behavioral control disorders events that started with the selection of a specific peer
and the development of alcohol/drug use disorders might group, then moved to the anticipation of approval
reflect a common neurological or genetic basis (Clark from members of that group for chemical use behav-
et al., 2002). This theory is supported by the obser- ior, and which finally included the actual use of the
vation that 50%–80% of children with a diagnosis of substance itself.
CD will have a concurrent SUD (Kaminer & Bukstein, The peer-group influence model has been chal-
2005). lenged by other scientists, however (Bauman & Ennett,
Researchers have found evidence on neurological 1994; Novello & Shosky, 1992). Novello and Shosky
tests that the prefrontal cortex region of the brain is ac- (1992) noted, for example, that of the 10.6 million ado-
tively involved in the process of behavioral control. Pre- lescents who consume alcohol, almost one-third do so
liminary evidence suggests that individuals with severe when alone rather than in groups. The authors inter-
forms of antisocial behavior (including CD and ODD) preted these data as evidence that the theory that ado-
have abnormal brain function in this region, suggesting lescents use chemicals in response to peer pressure
that this might be one cause of the behavioral control must be accepted only as a theory and it may not be
disorders (Clark et al., 2002). Further, both CD and true in all cases.
ODD complicate the treatment process and reduce the A factor that might distort the apparent relationship
chances of success. For treatment to be at all effective, between substance use patterns and peer group mem-
it is necessary for the therapist to include a program de- bership was the possibility of projection on the part of
signed to aid in the development of behavioral control, the research subjects. When asked about their friends’
in addition to the treatment of the SUD (Clark et al., substance use, drug-using adolescents are more likely
2002). to respond on the basis of their own drug use behavior
Peer group influences on adolescent substance use rather than on the basis of what they know about their
patterns. For adolescents, peer groups may serve either friends’ chemical use. In support of this theory, Bauman
as a protective or a negative influence (Ross, 2002; and Ennett (1994) pointed out that adolescents who do
Simkin, 2002). Although genetic factors influence not use chemicals were more likely to be judged as
whether a substance use disorder is likely to develop, using recreational drugs by their drug-using friends than
peers were found to strongly influence the initiation of they were by their non–drug-using friends. On the basis
chemical abuse in adolescents (Rhee et al., 2003). In- of their research, Bauman and Ennett (1994) suggested
deed, for the adolescent, peer approval might be a more that the effect of adolescent peers on substance abuse
powerful reinforcer than the pharmacological reward patterns was “overestimated” (p. 820).
Personal values and their influence on adolescent supportive or who came from intact families were also
chemical use patterns. One factor that does seem to less likely to engage in alcohol/drug abuse (Farrell &
protect the child/adolescent from pressure to use White, 1998; Griffin et al., 2000).
alcohol/drugs are his or her personal values. There is a Parental control seems to be another factor that
negative correlation between such forces as scholastic shapes the individual’s chemical use pattern (Patock-
performance, church attendance, the individual’s be- Peckham & Morgan-Lopez, 2006). Adolescents who re-
liefs about the importance of academic achievement, ported the highest levels of parental monitoring and
and adolescent substance use behaviors (Kaminer & enforcement of house rules have lower levels of miscon-
Bukstein, 1998; van den Bree & Pickworth, 2005). duct, including delinquency and substance use disor-
However, it is not clear whether these forces help to ders (Burstein, Stanger, Kamon, & Dumenci, 2006;
protect the adolescent from becoming ensnared in sub- Griffin et al., 2000; Patock-Peckham & Morgan-Lopez,
stance use problems since correlation does not imply 2006). The reverse is also true: Parents who utilize fewer
causality. control practices provide greater opportunities for the
The impact of parent-child relationships on adoles- adolescent to associate with deviant peer groups, includ-
cent chemical use patterns. Children learn by observing ing those who abuse alcohol/drugs, and thus greater op-
parental behavior, especially the behavior of the same- portunities for alcohol/drug use by the adolescent.7
sex parent (Patock-Peckham & Morgan-Lopez, 2006). Victimization history. Another factor that consis-
Although parents often dismiss their ability to affect tently seems to identify adolescents who are at risk for
their child’s substance use behavior, research has substance use problems is whether the individual had
shown that parental behaviors such as consistently ever (a) been the victim of some form of physical/sexual
spending time with their children, parental substance abuse (Fuller & Cabanaugh, 1995) or (b) had wit-
use patterns, and the degree of parental emotional in- nessed violence within the family (Kilpatrick et al.,
volvement with or neglect of their children have all 2000). It is thought that adolescents might turn to
been found to influence childhood and adolescent sub- alcohol/drugs as a way of self-medicating their feelings
stance use patterns (Kaminer & Bukstein, 2005). Chil- of shame and fear as a result of their victimization. An-
dren who reported that their parents spend more time other group of adolescents who are vulnerable to the ef-
with them and who make greater efforts to communi- fects of recreational chemicals are those who become
cate with them have lower rates of alcohol/tobacco use aware of homosexual urges within themselves. Accord-
(Cohen, Richardson & LaBree, 1994; Griffin, Botvin, ing to Fuller and Cabanaugh (1995), the homosexual
Scheier, Diaz, & Miller, 2000). adolescent might use alcohol and/or drugs in an at-
Children/adolescents are also very aware of parental tempt to self-medicate feelings of guilt, inadequacy, or
modeling behaviors, especially those of the same-sex self-deprecation.
parent (Cohen et al., 1994; Patock-Peckham & Morgan- Rebellion. A number of researchers have suggested
Lopez, 2006; Shalala, 1997). This seems to be why that it is the very fact that adolescents are prohibited
there is a strong relationship between parental sub- from using alcohol that makes drinking a goal for many
stance use behaviors, expecially during childhood, and (Barr, 1999). Because any use of alcohol by the adoles-
those seen when the child enters adolescence. This has cent is considered illegal by authorities, individuals
been found to be true for adolescent alcohol/substance who indulge in heavy alcohol use are viewed as being
use patterns during adolescence (Chassin, Flora, & King, especially daring in the eyes of their peers (Barr, 1999).
2004) and for adolescent cigarette smoking (Hill, Section summary statement. Ultimately, the research
Hawkins, Catalano, Abbott, & Guo, 2005). data do not support a simplistic unidirectional model
Although parental leverage on the child’s behavior is such as the individual’s peer group membership as a
muted by social and peer influences as he or she enters cause of his or her chemical use pattern (Curran, Stice, &
adolescence, it does not entirely disappear. Parental be- Chassin, 1997). Rather, it is the interplay between such
havior impacts such emerging facets of the adolescent’s factors as the quality of parent-child relationships,
personality as his or her values, and the quality of the whether the adolescent is depressed, and his or her
family’s affectional interactions also help shape the in-
7This is not to say that strict parental rules will prevent the adoles-
dividual’s substance use decisions (Cohen et al., 1994).
cent from engaging in substance abuse. But high levels of parental
Children whose parents spent more time interacting monitoring and enforcement of established rules seem to be asso-
with them were less likely to abuse chemicals, and ado- ciated with lower levels of deviant behavior, including substance
lescents who felt that their parents were emotionally abuse.
age-specific struggle for autonomy that together health changes (anorexia, injuries in accidents, etc.),
might play a role in the development of substance (b) sudden failure in work/school/home tasks (failure
use/abstinence patterns in the teenager. The early ado- to do assigned chores, for example), (c) legal problems,
lescent years appear to be a time of special vulnerability and (d) deterioration in social relationships. Most cer-
for later drug use problems. tainly, if adolescents are abusing alcohol/drugs, their
chemical abuse must be considered in terms of their
psychosocial development (Bukstein, 1995; Cattarello,
The Adolescent Abuse/Addiction Clayton, & Leukefeld, 1995; Kriechbaum & Zernig,
Dilemma: How Much Is Too Much? 2000). Heavy use of alcohol to the point of intoxication
Adolescent substance use/abuse/addiction falls along a in early adolescence appears to identify adolescents
continuum with total abstinence on one end and severe who are at risk for later alcohol use disorders (Young,
dependency on the other. In between these two ex- Hansen, Bigson, & Ryan, 2006). The authors found
tremes are the conditions of experimental chemical that Marine Corps recruits who reported risky alcohol
use, occasional chemical use, and abuse of recreational use prior to enlistment were more likely to have come
chemicals (Tweed, 1998). Total abstinence from alco- from smaller towns and to have suffered emotional
hol and drugs during adolescence is rare, with only and/or sexual abuse in childhood, as well as to have
11% of those studied abstaining throughout adoles- grown up in a home where there was a mental health
cence (Chassin et al., 2004). Unfortunately, clinicians problem or SUD present. The significance of these
lack definitive criteria by which to identify adolescents findings are discussed in the section devoted to the diag-
with SUDs (Knight, 2000; Rohde, Lewinsohn, Kahler, nosis of adolescent SUDs.
Seeley, & Brown, 2001), how to measure the adoles- Problems in diagnosis and treatment of adolescent
cent’s motivation to participate in such treatment drug abuse. In spite of the attention that has been paid
(Melnick, De Leon, Hawke, Jainchill, & Kressel, 1997), to the problem of adolescent substance use/abuse since
or the effectiveness of adolescent treatment programs the mid-1980s, “the standards guiding diagnosis and
(Kaminer, 2001). These may be some of the reasons treatment decisions specifically related to adolescents
that 50% of adolescents who are admitted to substance are relatively primitive and often lack empirical sup-
abuse treatment programs return to the abuse of recre- port” (Bruner & Fishman, 1998, p. 598). For the most
ational chemicals within 90 days of their discharge part, diagnostic criteria used for adolescents are based
(Latimer, Newcomb, Winters, & Stinchfield, 2000). on standards developed for adults, and these may not be
There is a very real need for diagnostic criteria by applicable to this special population (Kaminer, 1999;
which to identify adolescents who are abusing alcohol/ Kaminer & Bukstein, 2005; Monti, 2003; Parekh, 2006;
drugs. One reason is that adolescents are at greater risk Pollock, & Martin, 1999; Rohde et al., 2001). Further,
for the development of a physical addiction to alcohol/ even when an SUD is correctly identified, there are few
drugs than adults (Freimuth, 2005). Where an adult re- treatment programs, including appropriate aftercare
quires 2–7 years of chronic abuse before he or she programs, for adolescents with SUDs (Ross, 2002;
might become addicted to a chemical, adolescents Scheinin, 2006; Zunz, Ferguson, & Senter, 2005).
seem to become addicted in as little as 12–18 months One way to improve the accuracy in assessing an ado-
(Freimuth, 2005). lescent’s chemical use pattern is to establish an extensive
The adolescent’s substance use status also impacts database about the individual and his or her substance
on his or her utilization of the health care system. For use patterns (Evans & Sullivan, 2001; Juhnke, 2002). For
example, chest pain is the third most common reason example, the occasional use of alcohol or marijuana at a
adolescents seek medical care, and research has found party, say once every 6 months, is not, automatically, a
that 17% of the adolescents tested in a hospital setting sign of a drug abuse problem but may reflect only curios-
had evidence of ephedrine in their urine, in spite of ity about the effects of these chemicals (Hogan, 2000).
their denial that they had used this compound (James Referrals for a chemical dependency evaluation on
et al., 1998). Thus, physicians need diagnostic tools to an adolescent will come from many potential sources.
rule out both cocaine and/or ephedrine abuse as a pos- The juvenile court system, especially the emerging
sible cause of chest pain in adolescents who are seen in “drug courts” will frequently refer an offender for an
the emergency room setting. evaluation, especially when that individual was under
Parekh (2006) suggested several signs of a possible the influence of chemicals at the time of his or her
adolescent alcohol/substance use problem: (a) physical arrest. School officials may request an evaluation on a
student suspected of abusing chemicals. Treatment Finally, it is not unusual for treatment center staff to
center admissions officers will frequently recommend interpret “acting-out” behaviors as a sign of rebellion, as
an evaluation, although this is usually referred to in- opposed to an attempt on the part of the adolescent to
house staff rather than to an independent professional. overcome emotional trauma (Jorgensen, 2001). A mul-
Some parents, especially those who are “religious [and] tidisciplinary team approach to assessment in cases of
restrictive” (Farrow, 1990, p. 1268), will also request an suspected adolescent substance abuse will allow the ac-
evaluation and/or treatment after the first known episode curate identification of the client’s strengths, weak-
of alcohol or drug use by their child. nesses, level of maturity, and adaptive style so that staff
As a group, adolescents tend to have a rather imma- can understand what role resistance and acting-out be-
ture view of life and the consequences of their decisions. haviors play in the individual’s coping style.
Unfortunately, this simplistic outlook and possible con- The stages of adolescent chemical use. For many ado-
tinued chemical use may mistakenly be interpreted by lescents who abuse chemicals, there is a progression that
treatment staff as a sign of denial or resistance rather leads, ultimately, to more serious substance use prob-
than emotional immaturity. Adolescents tend to view al- lems. Both Jones (1990) and Chatlos (1996) suggested
coholism (and by extension the other SUDs) as a sign of five-stage models of adolescent substance use/abuse.
moral weakness, a characteristic that might make it dif- These two different models are contrasted in Table 23.1.
ficult for a given individual to acknowledge that he or Greydanus and Patel (2005) also suggested a five-
she has an SUD (Corrigan et al., 2005). Further, adoles- stage model of adolescent substance use. According to
cents rarely understand that the beverage they are con- this model, in Stage 0 the adolescent has not actually
suming contains alcohol, or they view their “sipping” engaged in substance use, but he or she is curious
behavior as being different from “drinking” behavior about the drug’s effects, suffers from low self-esteem,
(Rosenbloom, 2005). Like their adult counterparts, ado- and is vulnerable to peer pressure, according to the au-
lescents frequently minimize their drinking. They might, thors. Stage 1 is a stage of experimentation, when the
for example, admit to drinking “one or two beers” with- individual first engages in substance abuse but does not
out revealing that they are referring to 40-ounce cans of suffer any serious consequences. In Stage 2 the adoles-
beer, not the 12-ounce cans of beer usually associated cent now actively seeks the drug-induced euphoria and
with the phrase “can of beer” (Rosenbloom, 2005). center his or her life more and more around continued
TABLE 23.1 Two Theories of the Stages of Adolescent Substance Abuse
Stages of adolescent substance use/abuse Stages of adolescent substance use/abuse

according to Jones (1990) according to Chatlos (1996)
Learning the mood swing: The adolescent is exposed Initiation: The adolescent begins to abuse a mood-
to the drugs of abuse and learns what to expect from altering chemical.
their use.
Learning the mood swing: The adolescent must learn
Seeking the mood swing: The adolescent’s life what effects to expect from a given chemical and
begins to revolve around the use of that chemical— why these effects are desirable.
for example, changing friends to those who
Regular use/seeking the mood swing: The adolescent
use chemicals.
continues to seek what she or he has come to view as
Preoccupied with the mood swing: The adolescent the positive effects of recreational chemical use.
ends relationships with nonusing friends; may lose job,
Abuse/harmful consequences: The negative effects of
be expelled from school, and begin to lie to friends and
recreational chemical use begin to manifest in the
family about chemical use.
user’s life (poor academic performance, etc.), but
Using just to feel “normal”: The adolescent’s chemical the adolescent continues to abuse chemicals.
abuse has reached the point that he or she must use
Substance dependency/compulsive use: The adolescent is
chemicals just to achieve a relatively normal level of
now physically addicted to chemicals and is trapped in a
functioning. The person may become suspicious of
cycle of compulsive use, in spite of the serious
others, have memory loss, experience flashbacks,
consequences of this behavior.
and so on.
substance abuse. In Stage 3 the adolescent has become development of physical tolerance to the effects of the
preoccupied with substance abuse, developing mood drug of choice (Martin & Winters, 1998). Hoffmann,
swings and demonstrating acting-out behaviors while Belille, and Harrison (1987) found, for example, that
suffering consequences from his or her substance use dis- more than three-fourths of their sample of 1,000 ado-
order. Finally, in Stage 4 the adolescent has started to lescents in treatment reported having developed toler-
need the chemical just to feel “normal.” The progression ance to alcohol or other drugs. But because adolescents
from Stage 0 to Stage 4 can be as short as a few months usually do not have an extensive history of substance
or as long as several years, according to Greydanus and abuse, they are less likely to have experienced any major
Patel (2005), and it is not automatic. Social forces and organ damage as a result of their alcohol/drug abuse
the natural developmental process during adolescence (Kriechbaum & Zernig, 2000). Thus, “physical health
can alter the individual’s path from one stage to another problems associated with substance abuse [are] infre-
or even block further substance abuse, according to the quent in adolescents” (Harrison, Fulkerson, & Beebe,
authors. 1998, p. 491), although they are found in rare cases
Each model suggests that the adolescent substance (Chassin & DeLucia, 1996).
user must first be exposed to the chemical he or she will A common misconception is that adolescents with a
abuse and learn what to expect from the use of that sub- substance use disorder will “mature out” of their chemi-
stance. Each model suggests that for those who con- cal use disorder. Unfortunately, adolescent heavy drinkers
tinue to engage in recreational chemical use there is a were frequently found to typically continue a pattern of
change in friendship patterns as the adolescent begins heavy alcohol use in the early adult years, suggesting that
to drift away from his or her former peer group toward a adolescent heavy drinkers do not quickly “mature out of”
new peer group that is more accepting of chemical use. their substance use disorder if they do so at all (Rohde
Other new behaviors that might develop during this et al., 2001; Wells, Horwood, & Fergusson, 2006).
stage include erratic school performance, unpre- Adolescent substance use: A cause for optimism?
dictable mood swings, and manipulative behaviors, all Even if the adolescent has developed an alcohol use
in the service of continued substance abuse. disorder, there is strong evidence that the prognosis is
If the individual’s SUD should progress, his or her better than it is for an adult (Kriechbaum & Zernig,
daily activities increasingly center around the contin- 2000). This is because the adolescent’s personality is
ued use of chemicals (Greydanus & Patel, 2005; Tweed, still evolving, allowing the potential for growth. In
1998). For some individuals, their SUD will reach the many cases, the trauma that prompted the adolescent
“burnout” stage by which time he or she is forced to to use chemicals is easier to access and address through
continue to abuse chemicals just to feel normal again. therapy than it is in older clients (Jorgensen, 2001).
During this stage the individual will experience physi- Also, only a minority of those adolescents who abuse
cal complications from his or her drug use as well as chemicals go on to develop a drug dependency problem
memory loss and/or flashbacks, paranoia, anger, and (Chatlos, 1996; Kaminer, 1994, 1999; Kriechbaum &
drug/alcohol overdoses. Feelings of guilt, shame, depres- Zernig, 2000; Larimer & Kilmer, 2000). Heavy alcohol/
sion, remorse, and possible suicidal thinking are all pos- drug use is often “adolescence limited” (Kaminer, 1999,
sible during this phase (Tweed, 1998). p. 277). Only a small percentage of adolescents continue
Adolescence and addiction to chemicals. The issue of to have problems with chemicals later in life.
whether adolescents might become physically addicted to The financial incentive for overdiagnosis. The admis-
a chemicals is quite controversial (Commission on Ado- sions officers of many treatment centers claim that the
lescent Substance and Alcohol Abuse, 2005). The signs use of chemicals by adolescents automatically means
of alcohol/ drug dependence as seen in adults are not al- that there is a drug abuse problem present. Such treat-
ways found in the adolescent substance abuser (Evans & ment professionals, perhaps with an eye more on the
Sullivan, 2001; Pumariega & Kilgus, 2005). A history of balance sheet than on the individual’s needs, frequently
alcohol withdrawal symptoms is one of the major land- recommend treatment at the first sign of drug abuse by
marks used to identify an adult with an alcohol use disor- an adolescent. This ignores the reality that an unknown
der, but only 23% of adolescents diagnosed as being percentage of intervention/treatment programs actually
dependent on alcohol had ever experienced any symp- harm the adolescent (Dishion, McCord & Poulin, 1999;
toms of alcohol withdrawal (Martin & Winters, 1998). Szalavitz, 2006) and assumes that any treatment exposure
One of the most frequently encountered symptoms for the adolescent would be a positive experience for
of alcohol/drug dependence in the adolescent is the that individual.
Because it is against the law for adolescents to crease in the rate of adolescent suicide, caused at least
buy/use alcohol or recreational chemicals, in many in part by adolescent drug/alcohol abuse (Bukstein,
treatment centers “the term substance ‘use’ has been 1995; Simkin, 2002; Weiner et al., 2001). The exact na-
largely abandoned in favor of substance ‘abuse,’ reflect- ture of this relationship is not clear, but researchers do
ing the ideology that any use among minors constitutes know that SUDs are a factor in a significant percentage
abuse, since it violates the law” (Harrison, Fulkerson & of adolescent suicides (Miller et al., 2006). Other risk
Beebe, 1998, p. 486). Unfortunately, financial consid- factors include the individual (a) suffering from a major
erations often influence the decision to admit an ado- depression, (b) having thoughts of suicide within the
lescent to a substance abuse treatment probram. Such past week, (c) having a family history of suicide and/or
programs became a “lucrative industry” (Bell, 1996 depression, (d) facing legal problems, and (e) having
p. 12) in the 1980s, and in order to maximize profits easy access to a handgun (Bukstein et al., 1993; Simkin,
many treatment centers blur the lines between use, 2002).
abuse, and addiction for adolescents, offering a “one Substance abuse is a common factor in accidental
size fits all” type of treatment (Weiner, Abraham, & injuries for adolescents (Miller et al., 2006). Erlich,
Lyons, 2001). Brown, and Drongowski (2006) found that 40% of the
Forcing the individual—even if this person is “only” adolescents tested in one hospital emergency room had
an adolescent—into treatment when he or she does not evidence of drugs and/or alcohol in their urine. How-
have a chemical addiction may have lifelong conse- ever, while this information was used to guide medical
quences (Peele, 1989). Such action may violate the intervention, the authors noted, it rarely resulted in a
rights of the individual, for in some states it is illegal to referral to treatment for a possible substance use disor-
force an adolescent into treatment against his or her der. Adolescent substance use might be a contributing
will, even with parental permission (Evans & Sullivan, factor in risk-taking behaviors that result in accidental
2001). Further, in spite of the fact that diagnostic crite- injury or possibly even death for the individual, and
ria to identify adolescents with substance use problems might be one of the first signs that the adolescent has a
have not been developed, many drug rehabilitation pro- serious SUD.
grams continue to try to convince the patient that he or Thus, the chemical dependency treatment profes-
she is permenently impaired because of problem alcohol/ sional who works with adolescents must attempt to
drug use in their adolescent years, and that they will find the middle ground between underdiagnosis, with
never be “whole” emotionally (Peele, 1989). Lamenta- all of the dangers associated with teenaged drug/alcohol
bly, there is no research into how this treatment ap- abuse, and overdiagnosis, which may leave the indi-
proach will affect the individual’s subsequent emotional vidual with a false lifelong diagnosis of chemical de-
growth. Nor is there research to determine if there pendency.
might be a negative consequence to telling the adoles-
cent that he or she is forever an addict at such a young
Possible Diagnostic Criteria for Adolescent
age, especially when the literature does not support this
extreme view.
Drug/Alcohol Problems
Statistically, the majority of adolescents identified Each adolescent will present the assessor with a com-
as having an SUD do not go on to become addicted to plex, constantly evolving pattern of strengths and needs
chemicals later in life (Kaminer & Bukstein, 2005). (Weiner et al., 2001). Problems such as preexisting mood/
Thus, one should not assume that the adolescent who anxiety disorders, conduct disorders, or an evolving per-
might have abused chemicals on a regular basis will sonality disorder may identify many adolescents who
automatically develop a problem with chemicals in are at high risk for a substance use problem (Clark et al.,
adulthood. 2002; Evans & Sullivan, 2001). Fortunately, a number
The risks of underdiagnosis. Although there are sig- of possible diagnostic criteria, listed below, are avail-
nificant risks associated with failing to treat adolescents able to help the clinician identify the child/adolescent
who have a serious drug use problem (Evans & Sullivan, with a possible substance use problem (Adger &
2001), there is evidence that health care providers Werner, 1994; Alexander & Gwyther, 1995; Fuller &
fail to identify the majority of adolescent substance Cabanaugh, 1995; Johnson, Hoffmann, & Gerstein,
abusers (Lee, Garnick, Miller, & Horgan, 2004). The 1996; Kirisci, Vanyukov, & Tarter, 2005; Kriechbaum &
implications of this failure are staggering. For example, Zernig, 2000; Miller, Davies, & Greenwald, 2000;
the last half of the 20th century saw a phenomenal in- Nunes & Parson, 1995; Simkin, 2002; Tweed, 1998;
Wills et al., 2001; Wills, McNamara, Vaccaro, & Hirky, McCabe, & Morales, 2005). Both the CAGE and the
1996): TWEAK8 were found to be relatively insensitive to ado-
lescents with alcohol use disorders, although the AUDIT
• Family history of alcoholism or drug abuse has been found to be more useful with this population
• Depression or other psychiatric illness (Boyd et al., 2005).
• A history of suicide attempts Age at the onset of alcohol use was found to be one
• Loss of a loved one significant factor, with the individual’s risk of develop-
• Low self-esteem ing a lifelong alcohol use problem declining 8%–14%
• High levels of stress per year for each year that the individual delayed the
• Poor social skills/maladaptive coping mechanisms initiation of alcohol abuse beyond the age of 12
• Problems in relationship with parents (parents are (Larimer & Kilmer, 2000). This conclusion is sup-
either too permissive or too authoritarian), resulting ported by the results of a study involving 43,000 adults
in lower levels of parental support in the United States conducted by Hingson, Heeren,
• Member of a single-parent/blended family and Winter (2006). The authors found that 47% of
• Feelings of alienation/running away from home those who began drinking before the age of 14 became
• School problems or limited commitment to school alcohol dependent by the time of their interview, as op-
• Low expectations for school posed to 9% of those who did not begin to drink until
• Family tolerance for deviant behavior the age of 21. This is consistent with the conclusion
• Peer tolerance for deviant behavior that adolescents who began to drink before the age of
• Accepting attitude toward drug use 15 were 4–6 times as likely to become alcohol-dependent
• Early cigarette use later in life as individuals who waited until after the
• High levels of engagement with drug-using peers age of 21 to begin to use alcohol (Commission on Ado-
• Antisocial behavior/poor self-control lescent Substance and Alcohol Abuse, 2005; Komro &
• Early sexual experience Toomey, 2002).
• Early experimental drug use However, even those who began to use alcohol at an
• Legal problems during adolescence early age were not doomed to remain alcohol-depen-
• Absence of strong religious beliefs dent. Research has found that only 40% of 12-year-old
• Tendency to seek novel experiences/take risks alcohol abusers would meet the diagnostic criteria for
• Unsuccessful attempts to cut back on frequency/ alcohol dependence for the rest of their lives (Larimer &
intensity of chemical abuse Kilmer, 2000).
• Experience with alcohol/drug withdrawal symptoms According to Martin and Winters (1998), the signs
• Continued alcohol/drug use in spite of social, physi- of an adolescent with an SUD include (a) use of alco-
cal, or legal consequences hol/drugs under hazardous conditions (driving while
• Experience with one or more alcohol-induced under the influence of chemicals, for example), (b) use
blackouts of alcohol/drugs in a manner that allows development
of tolerance to the effects of that chemical, (c) reduc-
The greater the number of the risk factors identified tion of activities that are not alcohol/drug related, (d)
above, the greater are the chances that the individual blackouts, (e) loss of consciousness due to chemical
has a substance use disorder. abuse, (f) engaging in risky sexual behavior while under
An instrument that has shown some promise as a the influence of chemicals, (g) the development of
screening tool is the CRAFFT (Knight, 2005; Parekh, “craving” for the drug of choice between periods of ac-
2006). A “yes” answer to two or more of the six ques- tive use, (h) unsuccessful attempts by the individual to
tions on this screening tool suggests a need for a more quit on his or her own, and (g) a drop in academic per-
complete substance abuse assessment (Knight, 2005). formance due to substance use.
Three “yes” answers were found to identify approxi- As the adolescent becomes more and more preoccu-
mately two-thirds of adolescent substance abusers pied with chemical use or demonstrates an interest in
(Knight, 2005). an expanding variety of chemicals, he or she might be
CAGE and AUDIT have become established tools said to have developed the adolescent equivalent to the
for screening adult alcohol abusers, but these instru- progression of chemical use often seen in adults (Evans &
ments are of limited effectiveness with an adolescent
population (Parekh, 2006) or college students (Boyd, 8See Chapter 27.
Sullivan, 2001). Loss of control for adolescent substance Next, the treatment process should also be of sufficient
abusers is expressed through the violation of personal duration to ensure a meaningful change in how the
rules about drug use (i.e., “I will not use marijuana, adolescent and his or her family cope with life’s prob-
tonight,” or “I will only drink on weekend parties,” or lems (Bukstein, 1995). Adolescents who had a signifi-
“I will only drink three beers at the party tonight”), ac- cant nonusing peer and who remained in treatment/
cording to the authors. aftercare for approximately a year were less likely to re-
Although these diagnostic suggestions offer promise lapse than those without this support (Latimer et al.,
in the identification of adolescents with SUDs, even 2000). These findings show that behavioral change
when the legitimate need for treatment is identified, takes time. Thus, the treatment process should be suffi-
several factors might interfere with the treatment ciently long and intense enough to allow these neces-
process, including (a) unrealistic parental expectations sary components of recovery to take place.
for treatment, (b) hidden agendas for treatment by both The next component of an adolescent treatment
the adolescent and the parents, (c) parental psy- program should be access to a wide range of specialized
chopathology, and (d) parental drug or alcohol abuse social service agencies by the treatment center staff. In
(Kaminer & Frances, 1991). A common problem is addition to their own work with the adolescent, treat-
parental refusal to provide consent for treatment even ment center staff might need to make referrals to juve-
after the child/adolescent has been identified as an nile justice, child welfare, and social support agencies
alcohol/drug abuser (Kaminer, 1994). (Bukstein, 1994, 1995). As part of the rehabilitation
process, involvement in AA/NA might be useful for the
adolescent, especially if there is a “young person’s”
The Special Needs of the Adolescent in a
group available. Al-Anon might be a valuable support
Substance Abuse Rehabilitation Program
for the family members who question their role in the
The adolescent who needs rehabilitation because of a adolescent’s substance use. Finally, the goal of the reha-
substance use problem presents special issues to treat- bilitation effort should be for the adolescent to achieve
ment staff. First, staff should be sufficiently aware of the a chemically free lifestyle (Bukstein, 1994, 1995).
developmental process that is taking place during ado- While adolescents offer treatment center staff unique
lescence to be able to understand the adolescent’s cog- challenges, there are also rewards that are earned through
nitive abilities, strengths, and defensive style. Second, effectively working with a younger substance abuser.
the treatment center should be able to offer a wide vari- Adolescents are less entrenched in their pathology and
ety of services, including the ability to work with the are thus more responsive to rehabilitation efforts in
student’s educational needs, recreational needs, and many cases. Thus, when substance abuse does become
possibly co-existing psychiatric disorders (Bukstein, 1994). an issue for the adolescent, rehabilitation offers the op-
The staff should also address peripheral issues to the portunity to help the individual turn his or her life
adolescent’s substance abuse, such as AIDS, birth con- around.
trol, and the individual’s vocational needs, according to
Bukstein.
Summary
Treatment center staff should be sensitive to the ado-
lescent’s cultural heritage and the social status of the Clearly, children and adolescents are often hidden
adolescent and his or her family (Bukstein, 1994, 1995; victims of drug addiction. Yet there is a serious lack of
Rosenbloom, 2005). A diverse staff helps to ensure that research into the problem of child or adolescent drug
the adolescent can identify with at least one member of use/abuse. Mental health professionals acknowledge
the staff while he or she is in treatment. Also, rehabilita- that peer pressure and family environment influence
tion center staff should attempt to engage family mem- the adolescent’s chemical use pattern, but the exact
bers in the treatment process (Bukstein, 1994). Some of role these forces (or the media) play in shaping the
the goals that might be addressed with family members adolescent’s behavior is still not known. There are
include improving communications between family many unanswered questions surrounding the issue of
members, the development of problem-resolution skills, child and adolescent drug use, and in the years to
resolution of discipline problems, and the identifica- come one might expect to see significant break-
tion of problems within the family unit that might un- throughs in our understanding of the forces that
dermine the efforts of the treatment center staff (such as shape chemical use beliefs and patterns of use in the
undiagnosed substance use by one or both parents). young. In the face of this dearth of clinical research,
the treatment professional must steer a cautious path range of emotional and physical problems that develop
between the underdiagnosis of chemical dependency during this phase of life, the diagnostic criteria needed
in the younger client and overdiagnosis. Just as sur- to identify adolescents at risk for subsequent problems
gery carried out on the individual during childhood as a result of their chemical use are still evolving. Treat-
or adolescence will have lifelong consequences, so ment professionals have no firm guidelines for what
will the traumatic experience of being forced into treat- symptoms might indicate the adolescent who is passing
ment for a problem that may or may not exist. The treat- through a phase of experimental chemical use or the
ment professional should carefully weigh the potential adolescent whose chemical use reflects a more serious
benefits from such a procedure against the potential problem.
for harm to the individual. The forces that predispose the child/adolescent to,
During adolescence, a young person might demon- or provide resilence from, substance use disorders have
strate repeated and regular use of one or more chemi- deep roots in early childhood. One such factor appears
cals only to settle down in young adulthood to a more to be the quality of the individual’s attachment bonds with
acceptable pattern of chemical use (Szalavitz, 2006). his or her parents (Bell, Forthun, & Sun, 2000; Flores,
Mental health professionals are well aware of the phe- 2004; Hogan, 2000). Infants with positive attachment
nomenon by which the troubled youth settles down in bonds tend to become adolescents who have positive
his or her middle 20s to lead a normal life. Thus, the relationships with their parents, have more positive peer
adolescent who abused chemicals on a regular basis relationships, are more socially competent, and exhibit
may or may not go on to develop and maintain an SUD better coping skills, all characteristics found in adoles-
in young adulthood. cents who abuse chemicals. This fact might also explain
Although treatment professionals understand that why antidrug programs developed for students in grade
chemical use during adolescence is a factor in a wide school have been found to be ineffective.
CHAPTER TWENTY-FOUR
The Dual Diagnosis Client

Chemical Addiction and Mental Illness
In spite of the growing awareness that alcohol/drug dependent) will be used to denote individuals with a
abuse frequently co-exists with various forms of mental co-existing psychiatric disorder and a substance use
illness, mental health professionals lack the knowledge disorder (SUD).
of what forces initiate or maintain substance abuse in SUDs can magnify preexisting psychiatric disorders
those who have a form of mental illness (Sharp & Getz, or bring about a drug-induced disorder that simulates
1998). Indeed, resarchers have yet to develop a univer- any of a wide range of psychiatric problems (Buckley,
sally accepted definition of the dual diagnosis client 2006; Schuckit & Tapert, 2004). But these drug-induced
(Patrick, 2003), and there has only been limited research complications will usually diminish or entirely disappear
into what treatment methods might work best with shortly after the patient stops abusing recreational drugs.
this population (Drake, Mueser, Brunette, & McHugo, These conditions are “substance induced.” Dual diagno-
2004; Petrakis, Gonzalez, Rosenheck, & Krystal, 2002). sis refers to disorders that are (a) equally important, (b) in-
Although psychiatric textbooks of even the mid-1970s dependent disorders that (c) co-exist in the same patient at
suggested that substance use problems among the men- the same time (Minkoff, 2001).
tally ill population were rare, mental health workers The concept of co-existing disorders is really not diffi-
now understand that patients with co-existing sub- cult to understand. Consider, for example, an alcohol-
stance use disorders (SUDs) and mental health issues dependent person who also suffers from a concurrent
are not just a small minority of the patients they see but medical problem. Perhaps the alcohol-dependent indi-
actually comprise the majority of individuals seen in vidual has a kidney dysfunction or a genetic disorder of
substance abuse rehabilitation settings (Buckley, 2006; some kind. The patient’s medical condition did not
Goldsmith & Garlapati, 2004; Minkoff, 2001; Seppala, cause him or her to become alcohol dependent, nor did
2004). In this chapter, the problem of substance abuse his or her SUD bring about the medical condition. Yet
in people with some form of mental illness is explored. each disorder, once it develops, is intertwined with the
other. In this hypothetical example, the physician would
Definitions need to consider how any proposed treatment for one
condition might impact the other.
Patients who suffer from a form of mental illness and In much the same way, MI/CD clients have separate
who also abuse chemicals are often said to be “dual di- disorders that are intertwined with and able to influ-
agnosis” clients. Unfortunately, the term dual diagnosis ence the progression of the other condition (Drake et al.,
has been applied to a wide range of co-existing1 prob- 2001; Woody, McLellan, & Bedrick, 1995).
lems, including combinations of substance use disorders
and (a) anorexia, (b) bulimia, (c) gambling, (d) spouse
abuse, (e) AIDS, and (f) any of a wide range of physical Dual Diagnosis Clients:
disorders. To further complicate matters, mental health A Diagnostic Challenge
professionals have used a wide variety of terms to de-
scribe just the substance-abusing psychiatric patient. In assessing the dual diagnosis client, the assessor must
Freimuth (2005) suggested the term MICA (mentally have “the ability to distinguish the signs and symptoms of
ill chemical abuser). For the purpose of this text, the the primary psychiatric illness from those caused or exac-
terms dual diagnosis or MI/CD (mentally ill/ chemically erbated by a primary SUD [substance use disorder]”
(Geppert & Minkoff, 2004, p. 105). This is a daunting
1Sometimes referred to as comorbid disorders. task. For example, up to two-thirds of patients admitted
279
280 Chapter Twenty-Four
to substance abuse treatment programs have symp- view their situation as being hopeless (Ziedonis & Brady,
toms of psychiatric problems at the time of admission 1997).
(Falls-Stewart & Lucente, 1994). But many of these
psychiatric problems are substance induced and remit Why Worry About the Dual
after a period of abstinence. To identify those with a
Diagnosis Client?
true dual diagnosis disorder, the assessor might have to
wait for as long as 8 weeks for the diagnostic picture to Perhaps the most eloquent answer to this question was
clear (Jones, Knutson, & Haines, 2004). However, this provided by Geppert and Minkoff (2004), who noted,
is a luxury that the psychiatist might not have and in se-
vere cases pharmacological treatment should be initi- As a whole, this population has worse treatment out-
ated as soon as a working diagnosis is formulated (Busch, comes; higher health care utilization; increased risk
Weiss, & Najavits, 2005; Watkins, Hunter, Burnam, of violence, trauma, suicide, child abuse and neg-
Pincus, & Nicholson, 2005). lect, and involvement in the criminal justice system;
There are three basic subgroups of alcohol-abusing more medical comorbidity, particularly of infec-
psychiatric patients (Shivani, Goldsmith, & Anthenelli, tious diseases; and higher health care costs than
2002): (a) individuals with alcohol-related psychiatric people with a single disorder. (p. 103)
symptoms, (b) individuals with alcohol-induced psychi-
atric syndromes, and (c) individuals with cormorbid The risk of suicide in alcohol-dependent persons has
alcohol and psychiatric disorders. In the first group, the been found to be 60–120 times higher in cases when
individual’s heavy use of alcohol results in a disruption the individual has a concurrent mental illness (Nielson
of normal brain function, causing him or her to experi- et al., 1998). As a group, dual diagnosis clients are at in-
ence symptoms of a psychiatric disorder. In the second creased risk of incarceration, are less likely to be able to
group, the individual suffers from any of a range of handle personal finances, and are more prone to de-
alcohol-induced psychiatric problems. Admittedly there pression and/or feelings of hopelessness (Drake et al.,
is a fine line between these two groups of people, and 1998). Further, they are more likely to function on the
the distinction between the two is made even more dif- fringes of social groups than fully participate in society
ficult as in each case the psychiatric symptoms clear (Todd et al., 2004).
after a period of abstinence. However, in the third The individual’s abuse of recreational chemicals can
group, there is clear evidence of a co-occurring psychi- contribute to or exacerbate feelings of hopelessness or
atric disorder and an alcohol use disorder, according to symptoms of virtually any other psychiatric disorder
Shivani et al. (Cohen & Levy, 1992; Evans & Sullivan, 2001; Ries &
Accurate diagnosis of either a substance use disorder Ellingson, 1990; Rubinstein, Campbell, & Daley, 1990;
or a form of mental illness is further complicated be- Sharp & Getz, 1998). Further, researchers have also
cause each condition is viewed as a stigmatizing disor- found that “patients with mental disorders have such
der in this culture (Pies, 2003). Just like their “normal” fragile brain chemistry that even ‘social’ use of alcohol
counterparts, dual diagnosis patients are motivated by or drugs can destabilise them and cause psychotic
the stigma associated with substance abuse problems to episodes” (Patrick, 2003, pp. 68–69). Thus, even low
utilize the defense mechanisms of denial and mini- levels of alcohol or drug use might exacerbate the indi-
mization to try to hide their chemical abuse problems vidual’s psychiatric condition (Prochaska, Gill, Hall, &
(Carey, Cocco, & Simons, 1996; Shivani et al., 2002). Hall, 2005; Spalletta, Bria, & Caltagirone, 2007). For
But these attempts to hide their addiction are com- patients who suffer from schizophrenia, even limited
plicated (a) by their ongoing psychiatric problems alcohol use at levels not abusive by traditional standards
(Kanwischer & Hundley, 1990), (b) because direct predicted which patients would require rehospitalization
questions about alcohol or drug use contribute to feel- within a year (Hopko, Lachar, Bailley & Varner, 2001;
ings of shame (Pristach & Smith, 1990), (c) because RachBeisel, Scott, & Dixon, 1999). Dual diagnosis
of a fear that by admitting to having a substance use clients are at significantly higher risk to be the victims
problem they will lose entitlements (such as Social of violent assault than their nondrinking counterparts
Security payments) or be denied access to psychi- (Brekke, Prindle, Woo Bae, & Long, 2001), and un-
atric treatment (Mueser, Bellack, & Blanchard, 1992). treated psychiatric problems can serve as a relapse trigger
Further, (d) many dual diagnosis patients have little for individuals with concurrent substance use disorders
motivation to stop using a drug of abuse because they (Jones, Knutson, & Haines, 2004).
The Dual Diagnosis Client 281
It is for these reasons that dual diagnosis clients tend TABLE 24.1 The Overlap Between Substance Use
to make less progress in therapy and suffer a greater Disorders and Various Psychiatric Disorders
number of problems while in treatment (Busch, Weiss, &
Lifetime prevalence of
Najavits, 2005; Drake et al., 1998; Goldsmith & Garlapati,
Psychiatric diagnosis substance-use disorder
2004; Laudet et al., 2004; Osher & Drake, 1996; Sharp &
Getz, 1998). The presence of an SUD in a mentally ill Depression 32%
client places an increased financial strain on the fam-
Bipolar affective disorder
ily’s resources (Clark, 1994). Further, when one in-
(or manic depression) 64%
cludes the emotional pain experienced by the mentally
ill; the cost of lost productivity; the cost of hospitaliza- Anxiety disorder 36%
tion and treatment; and the added financial, social, and Antisocial personality disorder 84%
personal cost brought on by substance abuse of men-
Attention deficit hyperactivity
tally ill clients, the need to address this problem be-
disorder (ADHD) 23%
comes undeniable.
Eating disorders 28%
The Scope of the Problem Schizophrenia 50%
Some 7–10 million individuals in the United States are Somatoform disorders Unknown, but suspected
estimated to have a concurrent substance use disorder to be related
and mental health disorder.2 Unfortunately, only 8% of Source: Based on Ziedonis & Brady (1997).
MI/CD patients received treatment for both disorders in
the preceding 12 months, and 72% received no treatment
at all (Prochaska et al., 2005). When treatment is offered atric condition to the exclusion of the SUD (Schanzer,
to the patient, it is usually for either the SUD or the men- First, Dominguez, Hasin, & Caton, 2006).3
tal illness, but not for both disorders (Buckley, 2006).
It was once thought that only a minority of patients
with a mental illness would abuse illicit drugs; now we Psychopathology and Drug of Choice
understand that the co-occurrence of these disorders is For many years, clinical lore has maintained that dual
common (Buckley, 2006). Indeed, if the individual has diagnosis clients abuse alcohol/drugs in an attempt to
any form of mental illness, he or she is 270% more self-medicate their emotional pain (Rubinstein et al.,
likely to have a substance use disorder than the average 1990). This hypothesis, although it remains popular, has
person (Volipcelli, 2005). Various estimates suggest that received only limited support from clinical research
30%–80% of people with a form of mental illness also studies (Drake & Mueser, 2002). While the substance
abuse alcohol or drugs (Appleby, Dyson, Luchins, & abuser might be using chemicals to self-medicate his or
Cohen, 1997; Leshner, 1997b; Patrick, 2003; Roberts, her emotional distress, different dynamics develop after
2004; Watkins, Burnam, Kung, & Paddock, 2001). the individual has moved from substance abuse to ad-
Table 24.1 summarizes the overlap between substance diction (R. D. Weiss, 2005). Thus, by the time the per-
use disorders and various psychiatric disorders. son comes to the attention of authorities, his or her
The relationship between mental illness and a con- self-medication has evolved into a complicated addic-
current substance use disorder is quite complex. There is tion, obscuring the original intent at self-treatment.
evidence, for example, that the more serious the psychi- Proponents of the self-medication hypothesis often
atric disorder, the more difficult it is for the individual to point to the relationship between SUDs and patients who
abstain from drugs of abuse (Ritsher, Moos, & Finney, have developed posttraumatic stress disorder (PTSD)
2000). Unfortunately, physicians or mental health pro- (Cross & Ashley, 2007; Khantzian, 2003b; Preuss &
fessionals are rarely trained in the detection and treat- Wong, 2000; Volpicelli, Balaraman, Hahn, Wallace, &
ment of SUDs in their client populations. Indeed, Bux, 1999). This is a complicated matter, for the natural
emergency room physicians will, when confronted
with a substance-abusing psychiatric patient, often at- 3In defense of emergency room physicians, they frequently have lim-
tribute the observed symptoms to the patient’s psychi- ited historical data on the client and thus find the differentiation
between psychiatric dysfunction and substance-induced problems
2This estimate includes both children as well as adults with dual difficult to make. However, a misdiagnosis could carry with lifelong
diagnosis issues. consequences for the client.
course of PTSD is variable and often involves different Thus, alcohol is one of the most commonly abused
stages over time. Initially, the individual will experi- substances by dual diagnosis clients simply because it is
ence a process known as emotional flooding, which legal and easily available. This hypothesis is supported
may threaten to overwhelm him or her. During such by Swartz et al. (2006) who found that the pattern of
times, the use of sedating substances might seem very substance abuse in the schizophrenic patients in their
attractive to the individual. But during periods of emo- study were similar to those of people in the surrounding
tional numbing, the person will struggle to feel “safe” community.
emotions while controlling those feelings that threaten At this point, there does not appear to be strong sup-
to reawaken memories of the original trauma. The indi- port for the self-medication hypothesis (Busch et al.,
vidual’s goal in self-medication will vary, depending on 2005; Miles et al., 2003). Miles et al. (2003) did find a
whether he or she is struggling with intrusive memories positive relationship between the abuse of CNS stimu-
of the trauma or the emptiness of emotional numbing lants and violence, but it was not clear on the basis of
(Khantzian, 2003b). To complicate matters, after a pe- their study whether the CNS stimulant abuse was the
riod of time early withdrawal symptoms might come to cause of or a marker for the violent tendencies of the in-
be associated with the return of PTSD symptoms by the dividuals in this subgroup of drug abusers. In the sec-
individual and thus become a relapse trigger. tions that follow, the literature exploring some specific
But the theory that MI/CD clients are attempting forms of mental illness and alcohol/ drug use problems
to self-medicate their emotional pain has been chal- are explored.
lenged (Dervaux et al., 2001). Some dual diagnosis Attention deficit hyperactivity disorder (ADHD).
clients may be drawn to recreational chemical use for ADHD has emerged from the depths of diagnostic
the same reason that other people are: because it is controversy to become an accepted diagnostic entity,
considered “cool” (Sharp & Getz, 1998, p. 642). Chem- although its existence is still occasionally challenged.
ical abuse is also thought to facilitate the development Clinical research suggests that ADHD is about as preva-
of a social network and even offers an identity of sorts lent as asthma, affecting about 4%–5% of the popula-
(Busch et al., 2005; Drake & Mueser, 2002). Also, the tion (Khurana & Schubiner, 2007).
pharmacological reward potential of the drugs must A relationship between ADHD and the substance
be considered. Finally the social stigma associated use disorders (SUDs) was first identified in the mid-
with substance use/abuse is far less severe than that of 1990s (Diller, 1998; Milin, Loh, Chow, & Wilson,
mental illness, motivating some dual diagnosis patients 1997; Renner, 2001; Smith, Molina, & Pelham, 2002).
to try to substitute the less severe stigma of an alcohol/ Researchers noted that ADHD preceded the develop-
drug abuser for that associated with their mental illness ment of substance use disorders, although it was not
(Sharp & Getz, 1998). clear whether the ADHD actually caused the develop-
It was also pointed out that substance-abusing schiz- ment of the substance use disorder, the ADHD predis-
ophrenic patients, like their drug-abusing counterparts posed the individual to the later development of an
in the general population, were more impulsive and SUD, both disorders reflected a third as yet unidenti-
interested in new sensations than nonabusing people fied disorder, or the finding was simply by chance and
(Dervaux et al., 2001). Thus, psychiatric patients and did not have any clinical significance. As scientists
those with SUDs might simply share the same desire came to better understand the forces that shape ADHD
to impulsively seek new sensations like the typical they realized that both ADHD and substance use disor-
substance abuser rather than be attempting to self- ders reflect a dysfunction in the dopamine neurotrans-
medicate anhedonia.4 Another factor that has been mission system of the medial forebrain region of the
overlooked by those who believe in the self-medication brain. Thus, it would appear that the ADHD sets the
hypotheisis is the impact of the availability of alcohol/ stage for possible later development of a substance use
drugs on the individual’s substance abuse pattern. For disorder.
years, research studies have attempted to identify a cor- At about the same time, a popular myth developed
relations between certain diagnoses and preferred drugs that adolescents with ADHD are at increased risk for
of abuse, with little success. This is possibly because the CNS stimulant abuse. There is little evidence to support
issue of drug availability is an overlooked variable. this belief, if the child’s ADHD is adequately controlled
(Wilens, 2004b; Zickler, 2001). The chances that the
4
See Glossary. individual will later develop a substance use problem
are as likely as those for the average individual without accurate tests to identify patients with ADHD might be
ADHD, if the disorder is well controlled (Kaminer & developed. However, even if such tests do become
Bukstein, 2005; Wilens, 2004a). Even so, a parent should available, it will be necessary for the individual to be al-
control the child’s access to his or her medication to cohol/drug-free before the ADHD can be assessed, just
minimize potential substance abuse problems (Knight, as is true now. Unfortunately, researchers do not agree
2005). as to how long the individual must be alcohol/drug-free
The exception to the above rule are children with before an evaluation for ADHD can be carried out.
one of the conduct disorders5 such as the oppositional Schizophrenia. Perhaps 40% (Kavanagh, McGrath,
defiant disorder. These chldren do appear to be at higher Saunders, Dore, & Clark, 2002) to 50% (Goldsmith &
risk for later developing an SUD (August et al., 2006; Garlapati, 2004; Roberts, 2004) of the patients with
Disney, Elkins, McGue, & Iacono, 1999; Lynskey & schizophrenia will have a comorbid SUD. Surprisingly,
Hall, 2001).6 The apparent relationship between ADHD research has found that higher-functioning patients
and SUDs later in life might underline that between with schizophrenia are more likely to engage in sub-
33% and 50% of children with ADHD also have a con- stance abuse, possibly because their level of function al-
duct disorder (Smucker & Hedayat, 2001). lows them to better interact with others (a skill necessary
Although much of the clinical research has ad- to find and purchase alcohol or drugs of abuse) (Swartz
dressed the issue of ADHD in children and adoles- et al., 2006).
cents, this condition does carry over into adulthood in There is no apparent relationship between the indi-
about 50%–85% of the cases (Khurana & Schubiner, vidual’s psychiatric diagnosis and his or her drug of
2007; Wilens, 2006). Researchers believe that 15%–25% choice, but there is an interesting interaction between
of adults with an SUD have a concurrent (usually undi- the dynamics of schizophrenia and the subjective expe-
agnosed and untreated) ADHD (Wilens, 2006). Such rience of cocaine withdrawal. Central to the disease
cases of ADHD might not demonstrate the usual pat- concept of schizophrenia is that this disorder reflects a
tern of childhood symptoms and are best classified as disruption of the normal function of neurotransmitters
“atypical” ADHD (Wilens, 2006).7 such as dopamine (especially the dopamine D2 recep-
The treatment of ADHD is complicated and contro- tor sites) and serotonin within the brain. Since co-
versial. Some have suggested that highly addictive sub- caine’s effects are heavily dependent on the dopamine
stances such as methylphenidate not be used with neurotransmitter systems, it is logical to assume that
patients who have concurrent ADHD and SUDs, espe- those individuals who suffer from schizophrenia might
cially since compounds such as bupropion, pemoline, have a different reaction to this drug than nonschizo-
and atomoxetine have been found to be both safe and phrenic patients who abuse cocaine (Carol, Smelson,
effective for use with adolescents with ADHD.8 These Losonczy, & Ziedonis, 2001). Carol et al. found that
compounds lack the high abuse potential of CNS stim- cocaine-abusing schizophrenic individuals seemed to
ulants such as methylphenidate or the amphetamines experience more intense craving for cocaine during the
(Riggs, 2003). first three months of abstinence than did nonschizo-
While physicians still lack standard guidelines for phrenic cocaine abusers, suggesting the need for more
the assessment of ADHD in either children or adults, intense treatment efforts for cocaine-abusing schizo-
cutting-edge research using functional magnetic reso- phrenic patients to help them achieve and maintain
nance imaging (fMRI) technology does hint at differ- abstinence.
ences in regional brain activation patterns between Anxiety disorders. The relationship between the SUDs
normal subjects and patients with ADHD, hinting that and the anxiety disorders is quite complicated. As a
general rule, the anxiety disorders will predate the de-
5See Glossary. velopment of alcohol use disorders (Cheng, Gau, Chen,
6Discussed in the next chapter. Chang, & Chang, 2004). But a case-by-case assessment
7It is important to note at this point that substance abuse rehabilita-
is necessary to determine the relationship between the
tion professionals are usually not trained to diagnose ADHD in either
individual’s anxiety disorder and his or her substance
adolescents or adults. Suspected cases of ADHD should be referred to
a psychologist or physician trained in the diagnosis of such disorders. use behavior. For example, the alcohol-dependent per-
8The physician should carry out periodic liver function blood tests son might experience anxiety during withdrawal and
when these medications are used, but they are generally safe when the first few weeks of recovery, but this is a withdrawal
used as directed. effect rather than a reflection of an anxiety disorder
(Driessen et al., 2001). Such anxiety usually subsides in more than one personality, a condition known as disso-
the first days and weeks following alcohol cessation. ciative personality disorder (DPD, once called “mul-
Only if the individual continues to experience moder- tiple personality disorder,” or MPD).
ate to severe levels of anxiety or depression after 3 weeks Although the diagnosis of a dissociative disorder is
of abstinence should the possibility be considered that quite complex, Kolodner and Frances (1993) found
he or she has a concurrent anxiety disorder (Driessen two diagnostic signs that might suggest that the patient
et al., 2001). being examined had a co-existing substance abuse and
The anxiety disorders, at least in theory, provide the dissociative disorder. First, the authors suggested that
clearest example of the self-medication hypothesis ad- unlike “regular” patients who were addicted to chemi-
vanced by psychoanalytic theorists such as Khantzian cals, patients with dissociative disorders did not feel
(2003b). According to this theory, individuals with anxi- better after completing the detoxification stage of
ety disorders are drawn to the use of alcohol, opioids, treatment. Rather, they tended to experience signifi-
benzoediazepines, or the increasingly rare barbiturates cant levels of emotional pain after detoxification from
because such compounds provide them with relief chemicals. Second, patients who suffer from dissocia-
from their ongoing anxiety states. This theory is sup- tive disorders tend to relapse at times of “relative com-
ported by research evidence that up to 20% of individu- fort and clinical stability” (p. 1042), in contrast to
als with a primary anxiety disorder will also have a “regular” substance-abusing patients who relapse
concurrent SUD (Preuss & Wong, 2000). About 15% of most often under stress (see Chapter 27). The authors
those in treatment for an alcohol use disorder have suggested that these situations might alert the clini-
social anxiety, while 20% of those individuals in treat- cian to the possibility that the patient suffered from a
ment for social anxiety also have an alcohol use disorder dissociative disorder, which might then be addressed
(Book & Randall, 2002). in treatment.
There are several effective pharmacological and The most serious form of a dissociative disorder is
psychological treatments for social anxiety as well as the dissociative personality disorder (DPD). Perhaps
some medications that are contraindicated for use with one-third of those who suffer from DPD are thought to
substance-abusing patients with anxiety disorders. For also abuse chemicals (Putnam, 1989). These individu-
example, although the monoamine oxidase inhibitors als tend to utilize CNS depressants and alcohol, al-
(MAOIs) have been found to be quite effective in control- though stimulants are also frequently abused by DPD
ling the symptoms of social anxiety disorder, these med- patients, according to Putnam. Hallucinogenics, possi-
ications are not recommended for use in alcohol-abusing bly because of the nature of DPD, did not seem to be a
social phobia patients because of the danger in mixing popular drug of abuse for this subgroup (Putnam,
MAOIs with alcohol (Book & Randall, 2002). Some of 1989). The exact reason that chemicals are so popular
the common chemicals in many alcoholic beverages with those who suffer from DPD is not clear. However,
can combine with MAOIs to cause a potentially fatal clients who suffer from dissociative disorders or DPD
hypertensive crisis. might be using chemicals in an attempt to medicate
Because of the “well known abuse potential” their internal distress (Putnam, 1989).
(Riggs, 2003, p. 24) of the benzodiazepines, these med- Obsessive-compulsive disorder (OCD). Falls-Stewart
ications should not be used in treating social phobia and Lucente (1994) reported that OCD is the fourth
in patients with concurrent alcohol use disorders (Book & most common psychiatric disorder found in the United
Randall, 2002; Jones, Knutson, & Haines, 2004; Riggs, States; it is 4–5 times as common among substance
2003). The selective serotonin reuptake inhibitors abusers as in the general population, although the rea-
(SSRIs) were seen as a more appropriate choice for son for this is not clear. It has been estimated that 36%
this subgroup of patients (Book & Randall, 2002; Jones of the individuals with OCD will have a comorbid sub-
et al., 2004). stance use disorder (Goldsmith & Garlapati, 2004).
Dissociative disorders. Dunn, Paolo, Ryan, and Van Bipolar affective disorders. Virtually all the drugs of
Fleet (1993) found evidence that over 41% of the pa- abuse can cause mania-like or depressive syndromes
tients in treatment settings for alcohol/drug use disor- either when the individual is under the influence of
ders might also experience some form of a dissociative these compounds or during the acute stage of with-
disorder. The dissociative disorders are marked by drawal (Quello, Brady, & Sonne, 2005; Sonne & Brady,
episodes in which the individual loses touch with reality. 1999; Suppes & Keck, 2005). Thus, it is imperative for
In the most extreme form, the individual might develop the physician to have an accurate substance abuse
history to accurately diagnose the reason for the self-medicate, with the drug-induced mood changes
patient’s observed mental status. For example, acute al- then becoming a secondary reinforcer that contributes
cohol intoxication can induce some of the symptoms of to further substance abuse by the patient (R. D. Weiss,
mania—such as elevated mood, grandiosity, irritability, 2005). There is still much to learn about treatment
and aggressiveness—that might otherwise be misdiag- interventions that would be most effective with the
nosed as a bipolar affective disorder (Sonne & Brady, substance-abusing patient with a concurrent bipolar
2002). affective disorder.
What is now called a bipolar affective disorder (or sim- Depression. The condition known as depression
ply, bipolar disorder) was once called manic-depression. spans a range of disorders, including dysthymia and the
Research has shown that individuals who suffer from various manifestations of major depression both with
bipolar disorder are at higher risk for a substance use and without psychotic features. There is a known rela-
disorder than the general public (Brown, 2005; Vornik & tionship between depression and SUDs; studies have
Brown, 2006). Between 40% and 70% of patients with a found that of those individuals who have suffered a de-
bipolar affective disorder will also have a substance use pressive episode in the past year, 21% also had an alco-
disorder at some point in their lives (Ostacher & Sachs, hol use disorder and 9% had a drug use disorder (Wells,
2006). Paddock, Zhang, & Wells, 2006). Over the individual’s
Because the drugs of abuse can exacerbate and sim- lifetime, 27% of patients with a major depressive disor-
ulate bipolar disorder, the physician might be forced to der and 31%–43% of those with dysthymia will also
wait 2–4 weeks after the patient’s last substance abuse to have a substance use disorder (Evans & Sullivan, 2001;
determine whether the observed depression was sub- Goldsmith & Garlapati, 2004; McIlveen, Mullaney,
stance related (Sonne & Brady, 1999). However, because Weiner, Diaz, & Horton, 2007; Sonne & Brady, 1999).
patients with concurrent substance use disorders and a Substance use disorders complicate the treatment of
bipolar disorder have higher rates of suicide, experience depression, and untreated depressive disorders compli-
longer episodes of either mania or depression, and re- cate the treatment of substance use disorders (Wells,
port lower qualities of life, it is imperative that an accu- Paddock, Zhang, & Wells, 2006). One study found that
rate diagnosis be made and appropriate treatment be the amount of money spent for treating patients with
initiated (Ostacher & Sachs, 2006). comorbid dysthymia and substance use disorders was
As with many cases where substance abuse co-exists almost five times as great as the amount of money
with psychiatric problems, substance abuse by patients spent on patients with only a substance use disorder
with an affective disorder complicates the treatment of (Westermeyer, Eames, & Nugent, 1998). Further, un-
their psychiatric illness, resulting in more frequent hos- treated depression is one factor that increases the patient’s
pitalizations and less effective symptom control for the risk of relapse following detoxification (Driessen et al.,
individual (Sonne & Brady, 1999, 2002). This process 2001; McIlveen, Mullaney, Weiner, Diaz, & Horton,
contributes to higher hospitalization costs for society 2007; Nunes & Levin, 2006).
and needless emotional suffering for the individual. To identify primary depressive disorders9 it is neces-
Unfortunately, the reasons patients with bipolar affec- sary to obtain a detailed and complete psychiatric his-
tive disorder also abuse recreational chemicals are not tory to determine whether the depression predated the
understood (Vornik & Brown, 2006). It is hypothesized individual’s use of alcohol/drugs or developed after the
that some patients with a bipolar affective disorder initiation of substance abuse (Nunes & Levin, 2006).
might actively abuse drugs to cause some of the symp- In cases when the individual has a long-standing SUD,
toms of this disorder. Behavioral health professionals this determination might be quite difficult if not impos-
now believe that some individuals with manic depres- sible. In all cases the SUD should be addressed imme-
sion might use cocaine to artifically induce or prolong diately while the clinician continues to explore the
the sense of power and invulnerability often experi- possibility that the patient has a primary depressive dis-
enced in the earlier stages of mania (Jamison, 1999). order as opposed to a substance-induced depression
Their theory is supported by evidence that individuals (Nunes & Levin, 2006).
with bipolar disorder tend to be most prone to alcohol/ Compulsive gambling. As a behavior, gambling is de-
drug use problems during the manic phase of their ill- fined as “placing something of value at risk with the
ness (Brown, 2005; Modesto-Lowe & Kranzler, 1999). hope of gaining something of greater value” (Potenza,
Another theory is that individuals with bipolar affective
disorders might abuse alcohol or drugs in an attempt at 9Defined here as conditions that predate the use of alcohol/drugs.
Kosten, & Rounsaville, 2001, p. 141). Such behavior is and obsessive-compulsive personality-disordered clients
unique as it is found only in humans. The act of (10% each).
gambling is not, in itself, a sign of mental illness, but The most common personality disorder encountered
about 2% of the general population will gamble com- in treatment settings, however, is the antisocial personal-
pulsively and in a manner inconsistent with the mainte- ity-disordered (ASPD) patient. Just under 6% of men
nance of proper health (Grant, Kushner, & Kim, 2002; and 1.2% of women will meet the diagnostic criteria for
Potenza, Fiellin, Heninger, Rounsaville, & Mazure, ASPD during their lifetimes (Daghestani, Dinwiddie, &
2002). Further, the individual who gambles in spite of Hardy, 2001). However, this one personality type ac-
past negative experiences gambling is at risk for redevel- counts for 23% of the association between personality
oping a compulsive gambling problem. types and the SUDs (Grekin, Sher, & Wood, 2006).
Pathological or compulsive10 gambling frequently co- People with ASPD do not, as the name would seem to
exists with alcohol and/or drug abuse. Researchers have suggest, dislike people. Rather, they have trouble living
found that up to 44% of individuals who have a compul- within society’s limits; they view their own needs/desires
sive gambling problem will also have an alcohol use dis- as being of supreme importance and the rights of others
order at some point in their lives (Grant et al., 2002). as insignificant. The presence of ASPD is viewed as a
Individuals with compulsive gambling problems are negative influence on the rehabilitation process, and
thought to be 2–4 times as likely to develop an alcohol individuals with ASPD tend to do poorly in and after
use disorder as are persons without the compulsion to treatment (Compton, Cottler, Jacobs, Ben-Abdallah, &
gamble (Grant et al., 2002). This shared vulnerability Spitznagel, 2003; Rounsaville, 2004). Unfortunately,
suggests that both behaviors activate the brain’s reward given the association between ASPD and negative treat-
circuitry. ment outcomes, individuals with ASPD are exceptionally
There is also a relationship between depression and vulnerable to SUDs. The person with ASPD is probably
gambling. In spite of popular belief, however, there is 21 times as likely to have an AUD as are similar individu-
little correlation between the amount of money lost als who do not have this personality pattern (Moeller, &
and the depth of the individual’s depression (Unwin, Dougherty, 2001). Between 15% and 50% (McCrady,
Davis, & De Leeuw, 2000). Suicidal thinking is pos- 2001) of alcohol-dependent males and 10% of alcohol-
sible, especially if the gambler is losing or has lost a sig- dependent females are thought to have ASPD (Shivani
nificant amount of money. Long-term rehabilitation et al., 2002). Other studies suggest that between 35%
involves confronting the individual’s irrational beliefs and 60% of individuals with an SUD also meet the diag-
and helping the compulsive gambler develop a coping nostic criteria for ASPD (Sadock & Sadock, 2003).
system to prevent him or her from gambling any more. The diagnostic category of ASPD is quite broad, and
Although self-help groups such as Gambler’s Anonymous there are various subtypes of this personality pattern.
(GA) are modeled after similar groups for alcohol and Alterman et al. (1998) found six subgroups of individuals
drug abuse problems, they are not associated with sub- in a research sample of 252 individuals in a methadone
stance-based self-help groups. Treatment for gambling maintenance program, all of whom met the criteria for
problems should specifically address gambling-related ASPD. The characteristics of these groups are shown in
issues, and the two disorders should be treated as co- Table 24.2.
existing but equally important disorders for the substance- In working with the substance-abusing, antisocial,
abusing compulsive gambler. personality-disordered person, it is imperative to remem-
Personality-disordered client. Many personality disor- ber that his or her apparent ASPD is probably an artifact
ders seem to be intertwined with SUDs (Gendel, of the substance use disorder rather than an actual
2006). Echeburua, de Medina, and Aizpiri (2005) ex- personality disorder (Evans & Sullivan, 2001). Chronic
plored the relationship between personality disorders alcohol/drug abuse can block normal personality devel-
and alcohol use disorders and concluded on the basis of opment, causing the development of an “acquired”
psychological test results that 40% of the alcohol- (Shea, 2002, p. 44) or substance-induced personality
dependent sample, but only 6% of their control sample, disorder. Thus, part of the assessment process should
had a personality disorder. The most common sub- include a determination of whether the personality dis-
group was those individuals with a dependent personal- order preceded or followed the onset of the substance
ity disorder (13% of the sample) followed by paranoid use disorder.11
10These 11
two terms are used interchangeably. The process of assessment is discussed in Chapter 27.
TABLE 24.2 Summary of Subgroups of Antisocial Personality-Disordered (ASPD) Clients
Percentage of Conduct disorder Characteristics of

Group research sample in childhood? members of this group
Early onset/strong ASPD features 10% Yes Meet DSM-IV criteria for formal
diagnosis of antisocial personality
disorder
Late onset/strong ASPD features 12% Yes, but not as often as Antisocial personality disorder
subgroup 1 behaviors do not appear until
adulthood, with minor conduct
problems as child or adolescent
Emotionally unstable ASPD subgroup 18% Moderately strong Hostility, guilt, dependency, and
history of conduct avoidant personality features are
disorder in childhood all part of clinical picture with this
subgroup when they become adults
Non-ASPD/drug-induced behaviors 17% Rarely had a formal Antisocial behaviors found in
diagnosis of conduct these people can be traced back
disorder in childhood to their substance abuse
Moderate substance abuse/ 15% Rarely had a formal Strong ASPD features, intermixed
moderate ASPD diagnosis of conduct with low levels of guilt/depression,
disorder in childhood and moderate levels of alcohol- or
drug-related distress
Low ASPD 28% Rare reports of conduct Rare reports of antisocial
disorder in childhood behavior in adulthood
Source: Alterman et al. (1998).
The concept of an “acquired” personality disorder ing with a dual diagnosis client is the medical model
might explain why individuals with ASPD and comor- (Patrick, 2003). Unfortunately, residental treatment
bid substance use disorders who are able to experience beds for substance abuse rehabilitation clients, espe-
psychiatric distress in the form of anxiety and/or depres- cially MI/CD clients, are “woefully scarce” (Pepper,
sion might be able to benefit from treatment for their 2004, p. 343). A further treatment complication is that
alcohol/drug use problem (Evans & Sullivan, 2001; dual diagnosis clients often have fragile support sys-
Modesto-Lowe & Kranzler, 1999). Their ability to ex- tems, and the 12-Step support groups most commonly
perience psychiatric distress might suggest that they used as an adjunct to traditional rehabilitation pro-
have an acquired rather than a primary personality dis- grams are often intolerant of the special needs of this
order, whereas individuals with histories of violence re- population. It is still not uncommon for older members
sulting in serious injury to a victim, who rationalize of the recovering community to view the use of pre-
away antisocial behavior, use fear to control others, and scribed medication for treating dual diagnosis clients as
are unable to form deep emotional attachments to an indication that the patient is substituting one addic-
others are poor candidates for traditional rehabilitation tion for another (Evans & Sullivan, 2001; Penick et al.,
programs because they have a more primary personality 1990; Riley, 1994). Mental health/substance abuse pro-
disorder. fessionals may also fall into this trap and should exam-
ine their attitude toward prescribed use of psychotropic
medications by substance abusers. If they are uncom-
Problems in Working With Dual
fortable with the idea, they should not work with MI/
Diagnosis Clients
CD clients.
The dual diagnosis client usually will enter treatment Dual diagnosis clients often demonstrate significant
as a result of a personal/family/legal crisis (Goldsmith & levels of denial. Co-existing “thought or affective disor-
Garlapati, 2004). The most effective approach to work- ders may exacerbate denial of substance abuse” in dual
diagnosis clients (Kofoed, Kania, Walsh, & Atkinson, Garlapati, 2004; Owen, Fischer, Booth, & Cuffel, 1996).
1986, p. 1209). Such denial might take different forms As a group, MI/CD patients are 8.1 times more likely
in the dual diagnosis client. For example, some clients not to take medications as prescribed as non–drug-
will focus almost exclusively on the psychiatric disorder abusing psychiatric patients (RachBeisel et al., 1999).
when talking to an alcohol/drug counselor, and focus Medication noncompliance might be expressed in a va-
entirely on the chemical abuse problem when talking riety of ways, such as (a) refusing to take prescribed
to a mental health professional. This is the process of medications or (b) continuing to use alcohol or illicit
“interchangable” or “free-floating” denial. In a sense, drugs even after admission to inpatient psychiatric treat-
the client is using one disorder as a shield against inter- ment (Alterman, Erdlen, La Porte, & Erdlen, 1982).
vention for the other disorder. In another example of Some MI/CD clients will even stop taking prescribed
this process, individuals who suffer from dissociative medication in anticipation of their recreational drug use
identity disorder attribute their loss of memory (experi- to avoid potentially dangerous chemical interactions
enced when one personality is forced out of conscious- (Ryglewicz & Pepper, 1996). The most common reason
ness and another takes over) to the use of chemicals for these behaviors is not to self-medicate psychiatric dis-
rather than to the process of dissociation. tress but simply to get “high” (Bellack & DiClemente,
Dual diagnosis patients are often viewed as being pri- 1999).
marily psychiatric patients by chemical dependency pro- Prescribed medications offer another avenue for
fessionals, whereas mental health professionals often view medication noncompliance. Many psychiatric medica-
the same clients as being primarily substance abuse cases. tions have a significant abuse potential of their own. For
The deplorable outcome of this refusal-to-treat philoso- example, anticholinergic medications, which are often
phy is that clients are bounced between psychiatric and prescribed to help control the side effects of antipsy-
chemical dependency treatment programs, much as a chotic agents, have been abused by patients for recre-
Ping-Pong ball is bounced between the different players ational purposes (Buhrich, Weller, & Kevans, 2000).
(Osher & Kofoed, 1989; Wallen & Weiner, 1989). This is The anticholinergics may potentiate the effects of alco-
a legacy of the federal drug treatment initiatives of the hol or the amphetamines (Land, Pinsky, & Salzman,
1970s and 1980s, which resulted in the establishment of a 1991). Even when used alone, the “buzz” that may be
number of agencies devoted to the identification and re- obtained from anticholinergic medications is often sub-
habilitation of the substance user (Osher & Drake, 1996). stituted for the effects of other chemicals when supplies
Responsibility for substance-abusing psychiatric patients run short. Thus, treatment center staff must remember
was assigned to a different series of federal agencies. Inter- that MI/CD clients might even resort to abusing psychi-
departmental communication/cooperation between these atric medications as part of their substance use disorder.
two groups was virtually nonexistent, even though they Urine toxicology testing is a useful tool to help deter-
were all funded by the same taxpayers. As a result of this mine whether patients are taking their antipsychotic
“political” (Layne, 1990, p. 176) atmosphere, the treat- medications as prescribed. Urine toxicology testing is
ment of substance abuse cases became separated from also valuable to detect illicit chemical use, since MI/CD
traditional psychiatric care. clients often test positive for recreational drugs even
Unfortunately, staff psychiatrists in traditional psychi- when they have openly denied the use of such agents
atric hospitals usually lack training and experience for (Drake et al., 1996). For individuals with a thought dis-
working with the addicted individual (Howland, 1990; order, there are long-acting injectable forms of some
Riley, 1994). They do not understand that the intense medications available that sidestep the danger of med-
emotions generated by psychiatric problems might serve ication noncompliance (Fariello & Scheidt, 1989).
as a trigger for a relapse back into substance abuse
(Goldsmith & Garlapati, 2004). Further, these clients
Treatment Approaches
might receive potentially addictive medication as part of
their psychiatric care, prescribed by the psychiatrist who Although treatment professionals have finally recog-
is more experienced in working with the “traditional” nized that dual diagnosis clients exist, many of the treat-
client (Drake, Mueser, Clark, & Wallach, 1996). ment recommendations rest not on a firm foundation
The MI/CD client and medication compliance. As with of clinical research but only on expert opinion (Watkins
traditional medical patients, medication compliance et al., 2005). There is a “dearth of empirically sound in-
is a major problem for dual diagnosis clients (Bellack & terventions” for dual diagnosis clients (Bellack, Bennett,
DiClemente, 1999; Drake et al., 1998; Goldsmith & Gearon, Brown, & Yang, 2006, p. 427). Further, there
is strong evidence that access to psychiatric care for The stages of treatment. The first goal in working with a
substance-abusing clients is becoming more difficult dual diagnosis client is to establish a firm therapeutic rela-
(Knudsen, Roman, & Ducharme, 2004). tionship (Drake & Mueser, 2002). This task might take a
The treatment standard for dual diagnosis clients at protracted period of time. The therapist must make every
this time is the “integrated” treatment program, in effort to remain nonconfrontational, optimistic, and em-
which both substance abuse and psychiatric care profes- pathetic; he or she should avoid making moralistic judg-
sionals work as a team to help the client. Unfortunately, ments about the client’s behavior and work on estab-
few treatment centers—perhaps less than 10% of the total lishing a therapeutic relationship (Patrick, 2003).
number—offer integrated treatment options for MI/CD During the second phase of treatment, that of per-
patients (Patrick, 2003; Renner, 2004b). In place of this suasion (Drake & Mueser, 2002), treatment staff focus
ideal approach is the more traditional serial treatment on helping clients understand the relationship between
model (Miller, 1994; Goldsmith & Garlapati, 2004). As their substance use and their psychiatric problems.
it is applied today, the most severe disorder is addressed This is done to break “the cycle of substance abuse,
first, and after that condition is stabilized, then the non-compliance, decompensation, and rehospitaliza-
patient is referred to another treatment setting so that tion once the patient is sober and psychiatrically stable”
the co-existing disorder can be addressed (Busch et al., (Fariello & Scheidt, 1989, p. 1066). It is during this stage
2005). Usually, psychiatric care professionals work with that treatment staff attempt to convince clients that
the client first to achieve a reduction in the patient’s psy- abstinence is a goal that is worth their efforts not only
chiatric symptoms, and then substance abuse rehabili- because substance use complicates their psychiatric
tation professionals address the client’s SUD. Further, condition but because substance use problems are de-
the “managed care” initiatives of the late 1990s have structive in their own right. Motivational interviewing
significantly complicated the treatment environment skills are of value in this process (Patrick, 2003).
(Evans & Sullivan, 2001; Patrick, 2003). This second stage of treatment has also been called en-
An alternative to the serial treatment model is the par- gagement (Minkoff, 1989) or motivational enhancement/
allel treatment model, in which both disorders are engagement (Geppert & Minkoff, 2004). It is during
treated concurrently (Busch et al., 2005). In the parallel this phase of treatment that staff attempt to break
treatment approach, the patient will address his or her through clients’ denial system that surrounds both their
mental health concerns on one unit and substance use mental illness and the SUD. This is the same process
issues on another unit. Unfortunately, while such treat- that Fariello and Scheidt (1989) identified as breaking
ment is the most common form of dual diagnosis treat- the cycle of addiction. Osher and Kofoed (1989) called
ment, it is also the least effective treatment model (Drake this phase of treatment persuasion. The therapeutic
et al., 2004). Communications between the staff on the goals of this phase of treatment are (a) to persuade
different programs is often poor, and the act of physically clients of the reality of their drug dependency and (b) to
moving from one facility to the next increases the indi- persuade clients to seek continued treatment for their
vidual’s level of stress during a time of vulnerability. An- substance abuse problems.
other drawback of this model is that while treatment The third stage of treatment, active treatment, involves
depends on the establishment of a firm therapeutic rela- teaching clients the skills and helping them find the
tionship between the therapist and the client (Drake & sources of support to manage their illness (Drake &
Mueser, 2002), this task is made more difficult when Mueser, 2002; Osher & Kofoed, 1989). The third stage
mental health and substance use disorders are addressed of treatment has been called the stage of prolonged sta-
on different treatment units by different staff members. bilization: active treatment/relapse prevention (Geppert &
The most effective treatment model for dual diagno- Minkoff, 2004), or continuing care (Director, 1995).
sis patients is the integrated model (Busch et al., 2005). During this phase group therapy might be the most ef-
In this model, the treatment team is composed of men- fective treatment modality for working with the dual di-
tal health and substance abuse professionals who work to agnosis client (Kofoed & Keys 1988). Because of the
address both the client’s substance use disorder and his stigma associated with mental illness, it is usually more
or her mental health concerns. Since the treatment staff effective for these groups to be held on the psychiatric
functions as a single team, communications between dif- unit rather than in the substance abuse unit (Kofoed &
ferent professionals is facilitated, allowing for an inte- Keys, 1988; Layne, 1990).
grated program designed to meet each patient’s needs to The final phase of treatment is relapse prevention
be developed and carried out. (Drake & Mueser, 2002). During this phase clients and
clinical team work together to identify potential prob- traditional support systems. All too often, dual diagnosis
lems that might cause or contribute to a relapse of either clients tend to feel out of place in 12-Step group meet-
the psychiatric or the substance use disorder and develop ings (Petrakis et al., 2002), especially in the earlier states
techniques to minimize the impact of these problems. of rehabilitation (Drake, Mueser, Clark, & Wallach,
During this stage of rehabilitation, staff might need to 1996). For this reason special 12-Step groups designed
teach clients specific life skills to help them learn how to work with dual diagnosis clients are a useful adjunct
to function in society without the use of alcohol/drugs to treatment for these patients (Laudet et al., 2004).
in spite of their ongoing psychiatric problems (Layne, In the therapeutic setting, groups provide an avenue
1990). One major factor in recovery, even for dual diag- through which clients may share their experiences with
nosis clients, has been the extent of their nonusing sup- even limited recreational drug abuse, discuss the need
port system (Swartz et al., 2006). for the support of a 12-Step group, and talk about the
Many of the techniques utilized in general drug ad- problems they have encountered in their individual re-
diction treatment groups are useful in working with dual covery programs (Fariello & Scheidt, 1989; Kofoed &
diagnosis clients. But there is no single intervention for Keys, 1988; Rado, 1988). When the group is effective,
MI/CD clients that is equally effective with each indi- dual diagnosis clients tend to achieve a lower rehospital-
vidual patient in this population (Geppert & Minkoff, ization rate (Kofoed & Keys, 1988) and function better
2004). Rather, the treatment team must tailor each in society. However, the few limited follow-up studies
treatment intervention to the individual patient’s phase suggest that MI/CD clients tend to continue to abuse al-
of recovery, stage of treatment, and stage of change cohol and/or drugs in spite of the best efforts of staff
(Geppert & Minkoff, 2004). As a general rule, the con- (Drake, Mueser, Clark, & Wallach, 1996). Thus, while
frontational model often used with traditional substance the therapeutic goal is complete abstinence from recre-
abusing clients is counterproductive with MI/CD ational drug use, the treatment professional must accept
clients, especially those with schizophrenia (Bellack & that a major reduction in substance abuse levels is still a
DiClemente, 1999). When confrontational approaches positive accomplishment for the dual diagnosis client.
are deemed to be appropriate, the confrontation should
be less intense than with more traditional SUD clients
(Carey, 1989; Penick et al., 1990; Riley, 1994).
Summary
Unfortunately, once the patient’s psychiatric condi- The dual diagnosis client presents a difficult challenge to
tion is controlled, the client’s drug-related defenses again mental health and chemical dependency professionals.
begin to operate (Kofoed & Keys, 1988). Dual diagnosis Many of the syndromes that may result from the chronic
clients will often believe that once their psychiatric use of chemicals are virtually indistinguishable from
symptoms are controlled, they are no longer in danger of organic or psychiatric problems. This makes it most dif-
being addicted to chemicals. These clients are often un- ficult to arrive at an accurate diagnosis. Further, MI/CD
able to see the relationship between their chemical clients often use defenses, such as an interchangeable
abuse and the psychiatric symptoms they experience. system of denial, that further complicate the diagnostic
This is a form of denial, but not one that is unique to the process.
MI/CD client. For example, the patient who has finan- Dual diagnosis clients are also difficult to work with
cial problems and an addictive disorder might express a in the rehabilitation setting. When they are in treat-
similar belief that once his or her financial problem is re- ment, they will often talk about their psychiatric prob-
solved he or she will no longer be in danger of relapse. lem with drug addiction counselors, while talking about
Another common form of denial is evident when the their drug abuse or addiction with mental health profes-
client informs the drug rehabilitation specialist that he or sionals. Because of these characteristics, it has been found
she has discontinued all drug/alcohol use and thus fur- necessary to modify some of the traditional treatment
ther treatment is not necessary. In effect, the client enters methods used when working with the chemically depen-
a period when he or she will try to “tell the counselor dent client. For example, the degree of confrontation use-
what he wants to hear” to avoid confrontation. ful in working with a personality-disordered client is far
Although 12-Step groups12 are traditionally a large too strong for working with a dual diagnosis client who
part of alcohol and other drug abuse rehabilitation pro- suffers from schizophrenia or other form of mental ill-
grams, MI/CD clients are often unable to utilize these ness. However, gentle confrontation will often work
with the mentally ill and drug-dependent client who is
12Discussed in Chapter 35. not personality disordered.
CHAPTER TWENTY-FIVE
Codependency and Enabling
Scientists who specialize in the behavioral sciences are the problem, not the solution. The enabler came to be
often faced with a bewildering array of behaviors that viewed as doing something that prevented the person
they must both categorize and try to understand. Be- with a chemical use problem from taking advantage of
havioral scientists utilize constructs as an aid in this the many opportunities to discover firsthand the cost
task, to help them express complex ideas to others more and consequences of his or her chemical abuse. The
easily. An example of a construct is the symbol of a spouse, for example, might call the partner’s workplace
weather front on a meteorological map: in reality there with the excuse that the substance-abusing partner was
are no lines between different weather cells or firm “sick” when he or she was actually under the influence
boundaries between different bodies of air. But by using of chemicals.
the analogy of battle lines from World War I, meteorol- A popular misconception is that only family mem-
ogists can quickly summarize data by the construct of bers can enable a substance abuser. The truth is that
warm/cold fronts, and communicate that information you do not have to be a family member to enable a per-
to others. son with a chemical use problem. An “enabler” might be
As substance abuse rehabilitation professionals began a parent, sibling, co-worker, neighbor, or even a supervi-
to explore the interpersonal dynamics within the family sor. Other potential enablers include a well-meaning
with a substance abuser, they developed a number of friend, a trusted advisor, a teacher, a therapist, or even a
new constructs to help them explain the impact of alco- drug rehabilitation worker. Any person who knowingly
holism or drug addiction on the family. Two of these acts in such a way as to protect the alcohol/drug abuser
constructs were codependency and enabling, topics that from the natural consequences of his or her behavior
were quite popular in the 1980s and early 1990s but might be said to be an enabler (Johnson Institute,
have drifted out of the public spotlight in the past few 1987). The same criteria might be applied to those who
years. In this chapter, the constructs of enabling and enable people who are addicted to other drugs of abuse:
codependency are examined. The enabler is any person who knowingly shields the
alcohol/drug-abusing person from the harmful conse-
quences of her or his behavior.
Enabling One does not need to be involved in an ongoing re-
To enable someone means to knowingly behave in such lationship with a person who abuses chemicals to be an
a way as to make it possible for another person to con- enabler. People who refuse to provide testimony about
tinue to use chemicals, without having to pay the natu- a crime they witnessed out of fear or because they don’t
ral consequences for his or her substance use disorder. want to become involved might be said to have enabled
This concept emerged in the early 1980s, when it was the perpetrator of that crime to escape. But the clinical
suggested that within some families there almost always theory suggests that the enabler is usually involved in
seemed to be a conspiracy in which at least some family an ongoing relationship with a person with a substance
members supported the continued use of chemicals by use problem.
the individual with a substance use problem. This belief The relationship between enabling and codependency.
rests in part on the observation that some family mem- The key concept to remember is that an enabler know-
bers confuse caretaking with the expression of love, and ingly behaves in such a manner as to protect the ad-
thus continue to foster the expression of dysfunctional dicted person from the consequences of his or her
behavior (Ruben, 2001). Through this process the be- behavior. We all behave in ways that, in retrospect, may
havior of at least some family members became part of have enabled someone to avoid some consequences
291
292 Chapter Twenty-Five
that he or she would otherwise have suffered as a result won out. There have even been challenges about
of his or her drug use. This is a point that is often quite whether codependency is a valid construct (Blume,
confusing to the student of addiction. Codependency 2005).
and enabling may be, and often are, found in the same In spite of such controversies, families have long
person. However, one may also enable an addicted talked about how they have suffered, and often con-
person without being codependent on that person. tinue to suffer, as a result of having “a relationship with
Enabling refers to specific behaviors, while codepen- a dysfunctional person” (Beattie, 1989, p. 7). In the
dency refers to a relationship pattern. Thus, one may en- next section of this chapter, we look at the concept of
able addiction without being codependent. But the codependency in more detail.
codependent individual, because he or she is in an on- Codependency defined. Codependency was viewed
going relationship with the addict, will also frequently by Gwinnell and Adamec (2006) as an “unhealthy rela-
enable the alcohol/drug abusing person. Enabling does tionship in which a person who is closely involved with
not require an ongoing relationship. A tourist who gives an alcoholic or addicted person . . . acts in such a way as
a street beggar a gift of money, knowing that the beggar to allow the addict to continue the addicted behavior”
is likely addicted and in need of drugs, might be said to (p. 68). This relationship usually exists between spouses,
have enabled the beggar, although he or she is hardly in lovers, or family members, according to the authors,
a meaningful relationship with the beggar. but might also exist between close friends.
The issues of codependency and enabling may be A different conceptualization of codependency sug-
thought of as overlapping issues that may or may not gests that it is a relationship in which
be found in the same individual. A diagram of this re-
lationship is shown in Figure 25.1. This diagram il- the needs of two people are met in dysfunctional
lustrates how these two forms of behavior might ways. The chemical dependent’s need for a care
overlap. But it is most important to keep in mind that taker, caused by an increasing inability to meet
enabling and codependency are two different patterns basic survival needs as the drug becomes increas-
of behavior that are not automatically found in the ingly intrusive . . . is met by the codependent’s need
same person. to control the behavior of others who have difficulty
caring for themselves. (O’Brien & Gaborit, 1992,
p. 129)
Codependency
The concept of codependency emerged in the latter In contrast, Blume (2005) suggested that codepen-
part of the 20th century to become one of the corner- dency might be viewed “loosely as emotional depend-
stones of rehabilitation. Surprisingly, codependency is ence upon the person with a drug problem” (p. 168).
only a theoretical construct, and in spite of its popularity But perhaps the most inclusive definition is offered by
in clinical circles it has no standard definition (Jaffe & Zelvin (1997), who suggested that “codependency [is a]
Anthony, 2005; Sadock & Sadock, 2003). Mental health problematic or maladaptive seeking of identity, self
professionals long disagreed on such a basic issue as worth, and fulfillment outside the self” (p. 50).
whether the word was hyphenated (i.e., co-dependency) All of these definitions seek to identify different core as-
(Beattie, 1989), although the closed spelling eventually pects of codependency: (a) the over-involvement with the
dysfunctional family member, (b) the obsessive attempts
on the part of the codependent person to control the
dysfunctional family member’s behavior, (c) the ex-
treme tendency to use external sources of self-worth (i.e.,
approval from others, including the dysfunctional per-
son in the relationship), and (d) the tendency to make
Codependent Enabling
personal sacrifices in an attempt to “cure” the dysfunc-
tional family member of his or her problem behavior.
The dynamics of codependency. In an early work on the
subject, Beattie (1987) spoke of codependency as a
process in which the individual’s life had become un-
FIGURE 25.1 The Relationship Between manageable because he or she is involved in a committed
Codependency and Enabling Behaviors relationship with a person who is addicted to chemicals
Codependency and Enabling 293
(Beattie, 1987). The codependent person interprets the suffer (and perhaps learn from) the consequences of his
commitment as prohibiting him or her from leaving own behavior. This woman had yet to learn how to detach
the addicted person or confronting the individual about from her son’s behavior. Detachment is one of the corner-
his or her behavior. In many cases, the codependent stones of the recovery process (Brown & Lewis, 1995).
person also comes to believe that somehow the ad- By learning to detach and separate from her dysfunc-
dicted person’s behavior is a reflection on him or her. tional son, this woman could learn to “let go” and cease
This process of extreme involvement in the life of an- in her attempt to control his life. But with the best of in-
other person illustrates the boundary violations often tentions, the woman in this example remains over-
seen in codependency and is called enmeshment. involved in her son’s life.
Enmeshment (or its opposite, fusion) is based on the The rules of codependency. Although the codepen-
individual’s unconscious fear of abandonment (Dayton, dent person often feels as if he or she is going crazy, an
2005). In this process identities become intertwined outside observer will notice certain patterns, or “rules”
and fused, until the codependent person believes that to codependent behavior. Beattie (1989) identified sev-
“your behavior is a reflection of me.” Inappropriate behav- eral of these unspoken rules: (a) it’s not OK for me to
ior on the part of the significant other is viewed as a feel; (b) it’s not OK for me to have problems; (c) it’s not
threat to the codependent’s self-esteem. To avoid the OK for me to have fun; (d) I’m not lovable; (e) I’m not
perceived danger of abandonment, which is a threat to good enough; and (f) if people act bad or crazy, I’m
the individual’s sense of self-worth, the codependent responsible. These rules are actively transmitted from
person often becomes obsessed with the need to control one partner in the relationship to the other, setting the
the behavior of the addicted person, assuming responsi- pattern for codependency. “If you weren’t so unreason-
bility for decisions or events not normally under his or able, I would never have gone out drinking last night!”
her control (Beattie, 1987). In an extreme example of is a common example of rule “f.” “You shouldn’t have
this process, the codependent person will assume re- tried in the first place!” might enforce rules “b,” “c,”
sponsibility for the significant other’s recreational chem- “d,” and “e.”
ical use, as when the codependent person takes the Are codependents born, or made? Proponents of the
blame for “causing” the alcoholic spouse to go out on a concept of codependency suggest that this is a learned
binge after having a fight. “It’s all my fault that he or she behavior, often as a result of the codependent individual’s
went out drinking” is a common belief of the codepen- having been physically or sexually abused in childhood
dent partner. (Knauer, 2002). In dysfunctional homes, caretaking be-
Thus, the codependent person becomes preoccupied haviors are often learned as a way to avoid conflict
(Wegscheider-Cruse, 1985) or obsessed (Beattie, 1989) (Ruben, 2001). As a result of childhood abuse experi-
with controlling the behavior of the significant other. ences, the codependent individual becomes exception-
This obsession with controlling another’s behavior ally tolerant of boundary violations, and he or she
might extend to the point that the codependent will try attempts to achieve a sense of control over his or her
to control the addicted person’s drug use, or even his or personal life by attempting to “fix” the dysfunctional
her life. For example, a staff psychologist at a maximum partner (Knauer, 2002; Ruben, 2001).
security penitentiary for men in the Midwest received a Zelvin (1997) identified three routes to codepen-
telephone call from the elderly mother of an inmate. dency: (a) being in a close relationship with an alcohol/
She asked the psychologist to “make sure that the man drug abuser; (b) growing up in a dysfunctional family;
who shares my son’s cell is a good influence” on her (c) being socialized into accepting a codependent
son, because “there are a lot of bad men in that prison, role. Each of these routes allows codependent behav-
and I don’t want him falling in with a bad crowd!” iors to be passed from one generation to another. The
The woman in this case overlooked the grim reality first two routes reflect the impact of a chaotic life on
that her son was not simply in prison for singing off-key the individual. A very good example of the third route
in choir practice and that he had been to prison on sev- might be seen in the parent who screams at a child
eral previous occasions for various crimes. Rather than who wants to go to college with the taunt: “You’re too
let him live his life and try to get on with hers, she con- dumb to go to college! The best that you can hope for
tinued to worry about how to “cure” him of his behavior is that somebody is stupid enough to marry you, and
problem. She continued to treat him as a child, was take care of you!” Through this and a multitude of
overly involved in his life, and was quite upset at the other boundary violations, the codependent individ-
suggestion that it might be time to let her son learn to ual comes to learn that he or she is “less than” others
and not worthy of ordinary levels of respect or achieve- substitute an external measure of personal worth for
ment (Knauer, 2002). their inability to generate self-worth.
Clinicians have long recognized that people fre- Another core characteristic of codependent persons
quently try to resolve “unfinished business” from their is their intense desire to control the behavior of the ad-
childhood by recreating significant early relationships dicted person (Craig, 2004). They have difficulty recog-
in their adult lives (Scarf, 1980). Feeling as if their lives nizing boundaries, often tolerating role reversals within
were “out of control,” with feelings of low self-esteem the relationship and accepting responsibility for issues
and worthlessness, the codependent person almost be- beyond their control (Craig, 2004). Codependent per-
comes “addicted” to a significant other. This pseudo- sons also utilize denial to avoid facing truths that
addiction may reflect the individual’s fear of aban- threaten their sense of security, and often are prone
donment, or other unresolved issues from childhood to depression as well as feelings of hopelessness and
(Knauer, 2002). As the dysfunctional elements of a re- helplessness (Craig, 2004). They often demonstrate
lationship develop, the codependent person may feel emotional constriction to avoid facing such negative
“imprisoned” in the relationship. The codependent emotions, living rigid, compulsive lifestyles that are ex-
person becomes obsessed with “fixing” what is wrong ternally focused on the other person’s behavior (Craig,
with the marriage or the family. Communication, if 2004).
this ever existed in the relationship, grinds to a stop. In It is surprising to see that in spite of all of their emo-
contrast to the healthy relationship, where partners tional pain, many codependent persons do not want to
confront unhealthy elements of their relationship and end their pain. Rather, they seem to be locked into their
work on resolving them, in the codependent relation- codependency, often resisting efforts by friends or mental
ship, this “working through” process is stalled. If one health professionals to help them escape from their un-
partner does express some concern over a possible happy lifestyles. For the codependent person, there is a
problem, the other partner will move to prevent the reward for enduring their pain! Many people feel a
problem from being clearly identified, or if it is identi- sense of moral victory through suffering at the hands of
fied, resolved. Stability is seen as being of critical another (Shapiro, 1981). By suffering at the hands of a
importance. dysfunctional spouse, the codependent individual is
One way that this drive to maintain stability might able to accuse “the offender by pointing at his victim; it
be seen is in the avoidance of any discussion of the dis- keeps alive in the mind’s record an injustice committed,
eased individual’s substance use problem. The code- a score unsettled” (p. 115). For some people, such suf-
pendent individual might become afraid to say the fering is “a necessity, a principled act of will, from which
“wrong” thing, talk to the “wrong people,” or even to ashe cannot release himself without losing his self-respect
sert self-hood in any way, lest he or she displease the ad- and feeling more deeply and finally defeated, humili-
dicted partner. The codependent person comes to feel ated, and powerless” (Shapiro, 1981, p. 115). Through
“trapped”: unable to leave the sick partner but also un- this process, the trials and suffering imposed on the
able to feel fulfilled in the relationship. codependent person become almost a badge of honor, a
Codependency and self-esteem. In an attempt to live defense against the admission of personal powerlessness
up to the unspoken rules of codependency, the code- or worthlessness. In such cases, it is not uncommon for
pendent experiences a great deal of emotional pain. the codependent person to affirm personal worth by
One core trait of codependent persons is low self- being willing to “carry the cross” of another person’s ad-
esteem (Craig, 2004). Unfortunately, “co-dependents diction or dysfunctional behavior.
frequently appear normal, which in our culture is asso- The cycle of codependency. Once the cycle of codepen-
ciated with a healthy ego. Nevertheless, they also de- dency has started, it takes on a life of its own. A graphic
scribe themselves as ‘dying on the inside,’ which is representation of the cycle of codependency might ap-
indicative of low self-worth or esteem” (Zerwekh & pear something like Figure 25.2. Notice that on the chart
Michaels, 1989, p. 111). Because of low self-esteem, outlining the steps involved in the growth of codepen-
the codependent person often comes to measure per- dency, there are two necessary components. First, one
sonal worth by how well he or she can take care of or partner, the codependent, suffers from low self-esteem. If
please or fix the dysfunctional partner. Another way one partner does not suffer from low self-esteem, he or she
that codependent individuals measure self-worth is would be able to affirm “self.” Such a person would back
through the sacrifices they make for significant others away from a dysfunctional partner or at the very least find
(Miller, 1988). In this way, codependent individuals a way to cope without depending on the dysfunctional
Person suffers
from poor self-
esteem: unable
to affirm “self”
Person feels External sources

powerless: self- of support and
esteem is lost affirmation are
substituted for
self-acceptance
Person tries to Significant other

avoid issues that proves to be
might threaten dysfunctional
relationship
Person believes
“self” to be un-
able to withstand
rejection by
partner
FIGURE 25.2 The Circle of Codependency
partner’s approval. In such a case, it is unlikely that a to maintain the pseudo-stability1 that the famly has
codependent relationship pattern would evolve. achieved (also called a joiner)
Second, the “significant other” must prove to be dys-
Controller: who engages in controlling behaviors in
functional. The dysfunctional significant other is neces-
an attempt to control every aspect of their lives,
sary, for if the partner were to be emotionally healthy, he
which the person feels (often with justification) are
or she would affirm the codependent, breaking the cycle.
out of control
Patterns of codependency. In the last quarter of the 20th
century, substance abuse rehabilitation professionals at- Martyr: who comes to measure self-worth by the sac-
tempted to identify common behavioral styles that might rifices that he or she makes in his or her life with the
identify the codependent person. There are a number of addicted individual
such roles, including the ones listed below (Capretto, Family mascot/clown: attempts to deflect attention
2007; Craig, 2004; Ellis, McInerney, DiGiuseppe, & from the family member’s SUD on to herself or
Yeager, 1988): himself
Apathetic person: who simply stopped caring (who Messiah: fights against the addict’s chemical use, but
might also be called a “silent sufferer”) does so in such a way that the addict is never forced
to experience the consequences of his or her behav-
Approval seeker: who constantly seeks the approval/ ior (also called the chief enabler)
acceptance of the partner
Persecutor: who blames everybody but the addicted
Caretaker: who devotes his or her life to taking care
person for the problems, expressing anger and bitter-
of the addicted person
ness that the martyr is unable to express
Coconspirator: who will undermine the efforts of the
addicted person to change his or her lifestyle, possibly 1Discussed in Chapter 26.
Mental health and substance abuse rehabilitation characteristics that define codependency are also found
professionals often encounter family members of an ad- in healthy human relationships. Only a few “saints and
dicted person who exhibit some or all of the behaviors hermits” (Tavris, 1990, p. 21A) fail to demonstrate at
of one of these behavioral patterns. A common example least some of the characteristics of the so-called code-
of a coconspirator is the woman who might seek marital pendent individual.
counseling because her husband would not limit his Even Wegscheder-Cruse and Cruse (1990), strong
cocaine use to the $100 a week that she set aside in the advocates of codependency, admitted that “codepen-
family budget for his drug use, or the couple who re- dency is an exaggeration of normal personality traits”
quest marital counseling for one partner’s angry out- (p. 28). But in some cases these traits become so pro-
bursts but who do not continue once the subject of nounced that the individual “becomes disabled (disease
substance abuse on the part of one or both partners is of codependency)” (p. 28). To further complicate mat-
broached. ters, because of the way that love is viewed within this
Another all too common example of the coconspirator society, there is a strong relationship between love rela-
is the spouse who drinks or who uses chemicals along tionships and codependency (Zelvin, 1997). This is be-
with the addicted person in the hope of somehow control- cause society places much emphasis upon the blending
ling the addict’s chemical use. Substance abuse rehabili- of identities or the loss of ego boundaries in love rela-
tation professionals know that it is quite common for a tionships, making the individual vulnerable to code-
spouse to go to a bar with the alcohol abusing/dependent pendency (Zelvin, 1997). This is in sharp contrast to
partner, hoping to teach the partner how to drink in a many personality patterns, where the individual’s ego
“responsible” manner. Such efforts to join the spouse boundaries are so intensely defended that he or she is
with the substance use problem and change the person virtually isolated from interpersonal feedback. In between
from within are usually doomed to failure. After all, if the these two extremes is an interdependency that is the
addicted spouse were capable of drinking or using chemi- hallmark of healthy relationships. The continuum that
cals in a responsible manner, would he or she be addicted includes the endpoints of codependency on one end
in the first place? and the total affirmation of the ego’s boundaries on the
A very good example of the messiah might be seen in other end would look like Figure 25.3.
the father of an opiate-dependent young adult woman There are degrees of codependency, just as there are
who was in a mixed group of family members and other degrees of ego affirmation and isolation from interper-
opiate-addicted patients during “family day” at a treat- sonal feedback. Few of us are at either extreme, and the
ment center. The father admitted tearfully that he had majority of people tend to fall somewhere in the middle:
taken out a personal loan several times to pay off his exhibiting both tendencies to behave in codependent
daughter’s drug debts, an act he viewed as a measure of ways and to be overly isolated from feedback from
how much he loved his daughter. Another group mem- others.
ber confronted the father for allowing his daughter to
continue to abuse drugs without having to pay for them
Reactions to the Concept
and suggested that she be forced to pay her own bills.
The father responded that if he did not pay, his daughter
of Codependency
“might leave us!” Several group members then sug- The roots of the concept of codependency might be
gested that this would not be a bad thing, since his traced to M. L. Lewis’s (1937) hypothesis that the spouse
daughter might need to suffer some consequences in of the alcohol-dependent person (usually the wife) had
order to “hit bottom” and accept the need to address her a disturbed personality in that she tried to resolve her
addiction to chemicals. The father was silent for a mo- own neurotic conflicts through marriage to an alcohol-
ment, then said, “Oh, I couldn’t do that! She’s not ready dependent partner. Through this work, the partner of
to assume responsibility for herself yet!” the alcohol-dependent person was now identified as
The relationship between codependency and emo- herself being dysfunctional. From that time until the
tional health. There is a very real tendency for some to present, mental health professionals have struggled to
over-identify with the codependency concept. As Beattie determine whether codependency is a legitimate form
(quoted in Tavris, 1992) pointed out, there are those of psychopathology. Further, codependency has been
who believe that codependency is “anything, and every- characterized as “an addiction, a personality disorder, a
one is codependent” (p. 194). This is an extreme posi- psychosocial condition, and an interpersponal style”
tion that overlooks the fact that many of the same (Hurcom, Copello, & Orford, 2000, p. 487). The wide
0 1 2 3 4
Codependent: Strong Interdependent: Strong Totally

totally codependent balances own tendency to discounts
dependent traits feelings with isolate self external
on external external from feed- feedback in
feedback for feedback back from favor of
self-worth others own desires
FIGURE 25.3 The Continuum Between Isolation and Dependency
range of conditions inherent in codependency suggests ries and presenting symptoms might be an artifact intro-
that it is not a very useful diagnostic category for mental duced into the therapeutic relationship by therapist ex-
health professionals. pectations, selective attention to symptoms that confirm
No less an organization than Hazelden (a world- rather than dispute the diagnosis, and self-fulfilling
famous alcohol and drug treatment center) has stated vague diagnostic criteria guaranteeing that virtually every-
that there is no evidence to suggest that this syndrome body will qualify for the condition of “codependency”
exists (Blume, 2005). Many professionals believe that (Randle et al., 1999). The very nature of the defining
codependency was a pseudo problem more than a legit- characteristics of the codependent person virtually guar-
imate mental health concern. This position would antees that any given individual will meet at least one of
seem to have been the correct one as research into the defining “criteria” (Tarvis, 1992; Walker, 1996).
codependency and enabling had all but disappeared One reason for the uniformity of codependency is
from the professional journals by the first few years of the basic assumption that up to 99% of all people are
the 21st century. If it were a legitimate problem in the raised in a dysfunctional home. Building upon this
1980s and the 1990s, like coronary artery or kidney dis- foundation, much of the codependency literature strives
ease, why has it disappeared from the professional liter- to convince the reader that he or she is “doomed to
ature in the early years of the 21st century? suffer as a result of the trauma of childhood travails”
Many mental health professionals are uncomfort- (Japenga, 1991, p. 174). Codependents are “encouraged
able with the concept of codependency because it dis- to see themselves as victims of family life rather than
empowers the individual and because it transforms self-determining participants” (Kaminer, 1992, p. 13).
relationship problems into a medical problem (Hurcom Those who challenge the concept of codependency
et al., 2000). In contrast to most effective forms of psy- note that the family is viewed as nothing more than an
chotherapy, codependency reduces the individual’s power “incubator of disease” (Kaminer, 1992, p. 12). Within
base. The concept of codependency is based on tradi- this incubator, the helpless child is infected with one or
tional 12-Step program beliefs that the “disease” of more dread conditions that he or she will have to struggle
codependency is progressive, and that the individual can with forever, unless salvation is achieved through the
come to terms with codependency only through the aid appropriate 12-Step group.
of the appropriate “self-help” group (Randle, Estes, & Yet there is little research evidence that a child
Cone, 1999). raised in a dysfunctional home is automatically
Proponents of the concept of codependency point doomed. The reality is that many, perhaps a majority, of
out that individuals diagnosed as having this disorder those who are exposed to extreme conditions in child-
tend to have similar life experiences and similar person- hood find a way to adjust, survive, and fulfill their life
ality traits. However, such uniformity in patient histo- goals (Garbarino, Dubrow, Kostelny, & Pardo, 1992).
Admittedly, some children will suffer deep emotional fired a rifle at family members, missing his intended tar-
scars as a result of childhood trauma, but the evidence gets while neighbors called the police. The impact that
does not suggest children are automatically doomed to each father would have on the family would be far dif-
suffer if their home life is less than perfect. One reason ferent. Yet in the literature on codependency, both
is that children are naturally resilient (Masten, 2001; events are treated as being of equal importance.
Wolin & Wolin, 1993, 1995). Far from being rare, re- Critics of the codependency movement have pointed
silience appears to be common in children (Bonanno, out that the theory of codependency seems to excuse
2004). This natural resilience helps them weather the the addicted individual from all responsibility for his
emotional storms not only of childhood but of later or her behavior (Roehling, Koelbel, & Rutgers, 1994;
adult life as well. Indeed, the very fact that the child’s Tavris, 1990). In effect, through the “disease” of code-
environment is dysfunctional might serve as an impetus pendency, blame is shifted from the individual with the
toward the development of positive emotional growth substance use problem to his or her significant other,
in many cases (Garbarino et al., 1992; Wolin & Wolin, who is said to “enable” the unhealthy behaviors of the
1993, 1995). Proponents of codependency do not ap- afflicted person to continue. Further, the codependency
pear to accept the possibility of individual resilience. model pathologizes the spouse for engaging in behav-
Rather, they suggest that all children raised in a dys- iors that might very well be role specific, simply because
functional environment have emotional scars that must his or her partner is addicted to alcohol (Hurcom et al.,
be addressed. 2000).
Another objection to the concept of codepencency The foundation of the codependency movement
is that self-help groups that are supposed to help the in- rests upon the family disease model of family therapy,
dividual actually tend to “promote dependency under which holds that “the solution is for each family mem-
the guise of recovery” (Katz & Liu, 1991, p. xii). To ber to recognize that he or she has a disease” (Fals-
maintain membership and the identity as a group Steward, O’Farrell, & Birchler, 2003, p. 148) either of
member, the individual is expected to produce material addiction or codependency. Within this model, family
that is consistent with the expectations of the group— members are judged not because of their own accom-
that is, to continue to behave (and think) in a “codepen- plishments but on whether the addicted family mem-
dent” manner (Randle et al., 1999). The codependency ber is able to abstain from chemicals. This is an apparent
model presents the individual with a subtle demand extension of Lewis’s (1937) research, cited earlier in
that he or she not grow and achieve a sense of auton- this chapter. Family members are thus guilty of “addic-
omy but conform to a standard recipe for salvation and tion by association” (Katz & Liu, 1991, p. 13). As an il-
grace (Kaminer, 1992). According to the codependency lustration of this concept, entire communities, states,
model, no matter how trivial or serious the trauma, and even nations might be described as codependent
there is just one model for recovery. If the individual re- (Hurcom et al., 2000). Through the application of the
sists the various “insights” offered by different books on concept of codependency, the problem becomes not one
codependency, that person is automatically viewed as parent’s alcohol dependence, or physical and/or sexual
being in “denial” (Kaminer, 1992; Katz & Liu, 1991). abuse of the family members, or emotional inappropri-
There is no room for individuality in the codependency ateness or absence. Rather, the problem is that the family
model, as it is applied to therapeutic situations. members suffer from the disease of codependency!
This position reflects the theory (frequently ad- Although Lewis’s (1937) work was advanced almost a
vanced in different books on the subject) that all suffer- century ago, it was recycled and reformulated as a theory
ing is relative. In reality, it is virtually impossible to (popular in the 1950s) that the spouse of the alcohol was
equate degrees of suffering (Kaminer, 1992). To illus- a “co-alcoholic” (Sher, 1991; Simmons, 1991). This the-
trate, consider two hypothetical children in two differ- ory assumed that the co-alcoholic was as much in need
ent families. Both were the oldest boys in a family of of treatment as the alcoholic, on the assumption that he
three children with an alcoholic father. In the first fam- or she (a) helped to bring about the other’s alcoholism,
ily, the father was a “happy” drunk who would drink (b) currently continued to support it, and (c) must, ac-
each evening after work, tell a few “funny” jokes, watch cordingly, be quite disturbed. These beliefs reflect the
television, and fall asleep in his favorite chair. In the historical fact that the spouse of the alcoholic has “been
second family, the father would drink each evening blamed and pathologized for the partner’s drinking”
after work and become violently angry. He would phys- (Hurcom et al., 2000, p. 473). This theory continues to
ically abuse his wife and children, and on one occasion survive even though researchers have failed to find any
evidence that the spouse of the alcoholic has any pre- In considering the construct of codependency, there
dictable form of psychopathology (Tavris, 1992). But the is a need for balance. Admittedly, there are those
discredited theory of co-alcoholism has been resurrected people who experience significant hardship because of
in the guise of “codependency.” their involvement in an ongoing relationship with an
Another challenge to the concept of codependence addict. But not every person who is in such a relation-
was offered by Jaffe and Anthony (2005), who observed ship is codependent. Indeed, there is little evidence to
that the term has become so watered down and has support the concept of codependency, according to its
been applied to such a variety of problems that it has detractors. Further, according to the codependency
lost any possible hint of diagnostic specificity. For model, the victim must somehow come to terms with his
example, O’Brien and Gaborit (1992) suggested that or her emotional pain, without blaming the substance
codependency is a separate condition, while Knauer abuser for virtually anything he or she might have done.
(2002) argued that it may even be an addiction in its In other words, “according to adherents of this theory,
own right. An additional example of the vagueness of families of alcoholics cannot . . . hold them responsible
codependency is M. Scott Peck’s definition of codepen- for the abuse. Somehow the victim must get well by dint
dency as “a relationship in which the partners cater of pure self-analysis, meditation and prayer, without ref-
to—and thereby encourage—each other’s weaknesses” erence to the social, economic, legal and psychological
(1997b, p. 180). This would certainly seem to be an apt forces that create dysfunctional families in the first
definition of virtually all relationships, not just those place” (University of California, Berkeley, 1990a, p. 7).
that are “codependent,” since we all tend to encourage For many people, this is an impossible task.
others to behave in unhealthy ways at least on occasion.
Many critics of the concept of codependency point Summary
out that it rests on little more than a foundation of “New
Age” rhetoric. For example, the husband and wife team In the late 1970s, substance abuse professionals were in-
of Wegecheder-Cruse and Cruse (1990) speak know- troduced to a new way of viewing the substance-abusing
ingly of how codependency results from the “interac- person and his or her support system. The constructs of
tion between one’s own manufactured ‘brain chemicals’ “codependency” and “enabling” were introduced to ex-
(having to do with our reinforcement center) and one’s plain the way members of the substance abuser’s sup-
behavior that stimulates the brain to establish compul- port system behaved. However, since these constructs
sive and addictive behavior processes” (p. 12). The au- were introduced, the fact that they are just theoretical
thors go on to conclude that codependency is a disease constructs has been forgotten. Proponents have seized
of the brain, on the grounds that “we have a brain that upon these theoretical entities and suggested that they
gives us an excessive rush, (and) we get into self- are real manifestations of a new “disease”—that of
defeating behaviors that keep the rush coming (co- “codependency.” In the last decade, a battle has raged
dependency)” (pp. 12–13). over whether these constructs are indeed real entities
What the authors overlook is that there is no scien- and the applicability of this new disorder to the problem
tific evidence to support this theory. Science has failed, of substance-related interpersonal dysfunctions.
to date, to find evidence of “an excessive rush.”2 Nor That the partner of the alcohol-dependent person
have scientists found evidence to suggest that people might play a role in the development and maintenance
tend to “get into self-defeating behaviors that keep the of the alcohol dependence was first suggested in 1937 by
rush coming.” Indeed, such a position tends to be a M. L. Lewis. Another version of this theory surfaced in
contradiction, in the sense that if human beings as a the 1950s, when it was suggested that the alcoholic
species engaged in self-defeating behaviors simply for spouse was a “co-alcoholic.” These theories were last dis-
the “rush,” how would homo sapiens ever have survived? credited in the 1960s, but they seem to have found new
life under the guise of codependency. Ultimately, these
2Out of curiosity, what would be a “sufficient” rush? If something exists constructs might be said to still be evolving, and the role
to excess, does this not imply that there is a middle ground where there that they will play in the understanding and rehabilita-
is a sufficient supply of this thing, without it being present in excess? tion of substance abusers remains to be determined.
CHAPTER TWENTY-SIX
Addiction and the Family
Outside of residence in a concentration camp, there Addiction and Marriage

are very few sustained human experiences that make
Unfortunately, the relationship between alcohol/drug
one the recipient of as much sadism as does being a
abuse and family dynamics is both extremely complex
close family member of an alcoholic.
and poorly understood. For example, it was found that
marriages in which there were wide discrepancies in
—Vaillant (1995, p. 22)
the alcohol use patterns of the partners tended to
demonstrate lower levels of intimacy than marriages in
A conservative estimate suggests that at least 4–5
which the alcohol use patterns of the partners are simi-
people are hurt for every person with a substance
lar (Roberts & Leonard, 1998). To further complicate
use disorder (SUD) (Capretto, 2007). Parental alco-
matters, it is virtually impossible to identify a specific
holism, the most common avenue by which children
area of a marriage/family that is affected only by the
are exposed to individuals with an addictive disorder,
alcohol abuse of one or both partners (McCrady &
is known to have a strong impact on familial dynam-
Epstein, 1995). Problems within the marital unit become
ics (Vaillant, 1995). Yet little is known about the im-
intertwined, with parental alcoholism impacting virtu-
pact of parental SUDs on the family, or how such
ally every other aspect of the family’s life. But while it is
families interact (Green, 2006; Leonard & Roberts,
almost impossible to determine which part of the prob-
1996; Merikangas, Dierker, & Szatmari, 1998). In
lem is due to the parental alcoholism, it is known that
this chapter, what is known and what is suspected
there is a reciprocal relationship between alcohol/drug
about the impact of chemical abuse on the family is
use and marital problems (O’Farrell, 1995).
explored.
Clinicians are often confronted by the spouse of the
addicted person, who wonders why the partner demon-
strates an SUD now when the person seemed so normal
Scope of the Problem during courtship. The answer to this dilemma is that
Researchers believe that 9.6 million children are liv- during the courtship phase and the first year of mar-
ing in a home where at least one parent is actively riage, alcohol abusers commonly reduce their alcohol
abusing alcohol/drugs (Capretto, 2007). Further, at intake (Leonard, & Mudar, 2003; Leonard & Roberts,
least twice this many children are estimated to live in 1996). There is also a shift in relationship patterns
a home where at least one parent has been actively following marriage, as husbands tend to drop friends
abusing alcohol/drugs in the past year (Capretto, whose alcohol use does not correspond with that of
2007). More than one-half of the adults in the United their own and spend less time in social activities (or
States probably live in families with at least one mem- more time with their partner, depending on how you
ber who has or has had an alcohol use disorder look at it) in the first year of marriage (Leonard, &
(AUD) (Grant et al., 2006).1 As these statistics sug- Mudar, 2003; Leonard & Roberts, 1996).
gest, the problem of SUDs within the family is hardly Either consciously or unconsciously, the individual’s
insignificant. drinking preference seems to play a role in the choice
of a marital partner. In many cases people select a part-
1The
ner whose alcohol use is very similar to their own.
differences between these two estimates reflect in part how
“family” is defined. For example, is a second cousin who lives When there is a discrepancy in the alcohol use pattern
1,000 miles away and with whom you never have contact but who is of the partners, there are several possible adjustments:
actively alcohol dependent a “family” member? First, in the pattern seen in the majority of cases, each
300
individual will adjust his or her alcohol use until it is the family system, since the children might learn that
more consistent with that of the partner. However, in a these “rules” are not universal. Faced with the threat
minority of cases, a wide discrepancy in the alcohol use of an independent child, the parents might become
pattern of the partners evolves, and there is a negative im- smothering, crushing the child’s independence under
pact on the marriage or the family (Roberts & Leonard, layer upon layer of parental control to ensure that the
1998). family environment does not change.
The family system’s perspective. As a general rule, The threat of abandonment is often used by the
people tend to marry those who have achieved similar parents to limit or destroy children’s natural desire to
levels of “differentiation of self” (Bowen, 1985, p. 263). explore, to become self-reliant and independent. Au-
The concept of differentiation is “roughly equivalent to tonomy becomes a source of shame for children as the
the concept of emotional maturity” (Bowen, 1985, parents instill the family “rules” in them. If this shame
p. 263). This primary developmental task calls for the is experienced for too long or too intensely, it becomes
individual to separate from the parents (individuate) and so painful for the children that they begin to detatch
to resolve the various emotional attachments to the themselves from an awareness of their feelings in order
parents that evolved during childhood. Through this to cope. They thus learn to cope through adherence
process, the relationship between the parent and the to the family rules: Don’t talk, don’t feel, and don’t
child should evolve, as the child becomes more and trust.
more independent. In the healthy family, this process is Through this process, children come to view their
encouraged. But in unhealthy families, the individual natural inclination to individuate not as a source of
is often encouraged to put the family’s needs before his pride but as a threat to familial stability. Instead of learn-
or her own (Knauer, 2002). Rather than progressing ing autonomy, they learn to view themselves as weak,
through the various stages of individuation (Bowen, incompetent, unable to stand alone, and as a source of
1985), the person must subvert his or her normal growth shame. This shame becomes a central feature of their
process to meet the needs of significant others. self-concept, and children come to believe that “I am
For the first few years following birth, children are not worthy . . . I am spoiled . . . damaged . . . unable to
almost totally dependent on their parents. As they ma- cope on my own.” Being unable to “nuture” the “self,”
ture, children become less and and less dependent on the individual becomes dependent upon external
their parents and communicate their growing inde- sources of feedback and support, which might be pro-
pendence by a variety of means to the parents. In vided either by continued dependence on the parents
healthy families, the parents gradually withdraw their or a parental substitute. Since we look for a marital
control as the children become more capable of inde- partner with a similar level of individuation as our own
pendent living. But just as parents may encourage chil- (Bowen, 1985), we then replace the emotionally dam-
dren’s emotional growth, they might also inhibit it. If aged parent with a partner who is also emotionally
the parents teach children that they must take care of damaged, allowing us to relive the same conflicts in our
others, the children may come to believe mistakenly marriage that we had with our parents. If neither part-
that if they cannot provide the service for which they ner has achieved a significant degree of individuation,
are valued (i.e., caretaking, being a sexual object, etc.), each would look to the partner to meet his or her
others will not care for them (Knauer, 2002). This is emotional needs (Bowen, 1985). Within this marriage,
often the outcome of the home where there is an further emotional growth of either partner is viewed as
alcohol-dependent parent. a threat to the stability of the marital unit, especially if
Because of parental psychopathology, communica- such growth threatens to break through the layers of de-
tion patterns within the family unit are often quite dis- nial that each partner has used to insulate the “self”
rupted. This is also true for families where there is from each one’s respective shame-based identities. In
parental substance abuse. In such families, three “rules” response, they turn away from the potential for growth
are developed: (a) Don’t talk, (b) don’t have feelings, and accept a form of pseudo-intimacy and the illusion
and (c) don’t trust anybody (Capretto, 2007). Within of control offered by alcohol or chemicals.
the framework of these rules, parents find themselves Characteristics of the alcohol abusing marriage.
unable to provide the proper guidance and support to Remember that the individual’s first priority is the
their children. Indeed, in many cases, children’s natu- service of his or her addiction, which is a destabiliz-
ral predilection to mature and become less and less de- ing factor in a marriage. Within the marriage where
pendent on the parents may be interpreted as a threat to one member is an alcohol abuser/addict, issues of
302 Chapter Twenty-Six
control become important as each person struggles to for every other member of the family. The circle of
achieve some sense of order within the unstable marital shame is then complete, insulating the alcoholic from
unit. Control often becomes a central theme within the responsibility for his or her addiction and behavior.
marriage, and conditional love becomes one of the av-
enues through which each tries to control the other. Con-
ditional love finds expression in a number of demands,
Addiction and the Family
such as (1) you must behave in a certain way if you want From the family system perspective, the treatment of an
to be (a) loved by me, (b) supported by me, and so on; (2) addictive disorder involves identifying and ultimately
if you don’t meet my demands, I will (a) leave you, modifying whatever dysfunctional family system al-
(b) withdraw my love from you, (c) not give you money, lowed the development and maintenance of the addic-
(d) go out and get drunk, or (e) abuse you physically. tion in the first place (Bowen, 1985). In the alcoholic
Within the SUD-centered family, the addicted marriage, for example, alcoholism becomes a “secret
members adopt the position that they should be exempt partner” first of the marriage and ultimately of the fam-
from scrutiny (Capretto, 2007). At the same time, they ily. Those who threaten to violate the “rules”—(a) don’t
strive to build a “support system” that will enable them talk, (b) don’t feel, and (c) don’t trust—run the risk of
to continue to abuse chemicals, possibly at the price of emotional expulsion from the famly (Dayton, 2005).
familial harmony (Brown, 1985; Capretto, 2007). The Such injunctions serve to transmit the “secret” to the
members of the family are then faced with the cruel children, allowing the dysfunctional family system to
choice of either (a) confronting the problem directly, be passed from one generation to the next. Further,
possibly at the cost of destroying the marriage, or (b) find- children are taught not to trust their own perception
ing some way to adjust or cope. Often, silence is seen as but that of the significant other, a situation that fosters
the least threatening alternative to total destruction of overdependence on others for guidance as to what is
the family. That such confrontation will destroy the “correct” thinking in a given situation (Linehan, 1993).
family is an impression that the substance-abusing One of the developmental tasks facing a new child is
member reinforces through the use of emotional with- to learn to adapt to the environment into which he or
drawal. Sometimes family members respond to the mem- she was born. In addition to the normal adaptations the
ber with the SUD with the threat or reality of emotional child faces, in the home where one or both parents is
withdrawal. Hurcom, Copello, and Orford (2000) alcohol dependent, the whole family must learn to
found, for example, that almost 50% of those married to cope with the parental alcoholism (Ackerman, 1983).
an alcohol-abusing spouse use this tactic to cope at least One way the family might come to terms with parental
occasionally. While the nonabusing spouse may with- alcoholism is to structure itself so that the alcoholic par-
draw from his or her partner in the hope that this will ent is allowed to continue drinking. Although this is
reduce or stop the substance abuse, more often than often surprising to an outside observer, there are rewards
not it has the opposite effect. for this behavior! Although alcoholism is demonized by
Emotional withdrawal reflects more a means of society, in some marriages it actually plays a stabilizing
control than the active process of detachment. Detach- influence, helping one partner cope (Heath & Stanton,
ment, as opposed to withdrawal, is an active process 1998; Hurcom et al., 2000).
that paradoxically reflects unconditional love. In effect, For the person with an alcohol use problem, mar-
the nondrinking spouse comes to affirm that “your be- riage provides an opportunity to form a “drinking part-
havior is not a reflection of me” and “I love you enough nership” (Leonard & Roberts, 1996, p. 194) with his or
to let you be an independent person.” Through the her partner. A reflection of this partnership is the “role
process of detachment, the individual learns appropri- reversal” (Ackerman, 1983) that develops in such fami-
ate interpersonal boundaries. Boundary violations are lies. The alcohol-dependent member of the marital
rife in the home with an alcohol-dependent member unit will give up some of the power and roles he or she
(Black, 2003). With the lack of boundaries, each family would normally hold within the family unit in return
member develops an unnatural involvement in the life for opportunities to drink. In time, this role reversal
of the other family members. Part of the natural growth might span two or even three generations as an un-
process that results in individuation lets children learn to healthy state of interlocking dependency patterns evolves
establish boundaries between themselves and others. In within that family unit. Often marital partners or family
the alcoholic home, however, children learn to become members find themselves holding unusually powerful
enmeshed in the lives of others, afraid to be independent positions within the new family constellation, as the
of the family and trained to believe they are responsible family adapts itself to the individual’s alcoholism.
Adapting to familial rules, values, and beliefs is a quo and even enable the individual’s dysfunctional
normal part of family life (Bradshaw, 1988b). However, behavior to continue.3
when the family’s rules, values, and beliefs are warped Because such states of familial pseudo-stability are
by a dysfunctional partner, the entire family must struggle accomplished in an atmosphere of real and unspoken
to adapt to the resulting unhealthy family themes. This fear and guilt, many professionals view addiction as a
adjustment to the addiction of one member takes place multigenerational, family-centered disorder in which
without external guidance or support. Family members parental SUDs become “a governing agent affecting
are left to their own devices as they struggle to come to the development of the family as a whole and the indi-
terms with the problems within the family and often viduals within” (Brown & Lewis, 1995, p. 281). Unless
come to use the same defense mechanisms so charac- there is a drastic change of some kind, such as profes-
teristic of addicted individuals: denial, rationalization, sional intervention, it is often difficult for individual
and projection.2 family members to learn how to detach from the mem-
As the other family members come to assume reber who has the SUD and allow the person to suffer the
sponsibilities formerly held by the addicted member of natural consequences of his or her behavior (Johnson
the family, the addicted individual becomes less and Institute, 1987). Rather, the life of the entire family
less responsible for his or her family duties, and less in- centers on the pathology of a single member, and the
volved in the family life. An older brother assumes re- family members live their lives in an attempt to some-
sponsibility for discipline of the children, or a daughter how “cure” that person of the SUD.
assumes responsibility for making sure that the children The cost of parental addiction. As scientists learn
are fed each night before they go to bed. In each case, more about how extreme abuse impacts the develop-
one of the children has assumed a parental responsibility mental process, they are gaining new insights into the
left vacant because of alcoholism. long-term impact of physical, sexual, and emotional
The parent with the SUD is hardly a passive partic- abuse on the child. Extreme abuse in childhood is of
ipant in this process, often using fear, guilt, and threats special importance because the child’s brain is still
(spoken or unspoken) to control family members. The growing (Sheff, Warren, Ketcham, & Eban, 2007;
logic used within the parental unit often changes on Teicher, 2002). The impact of parental alcoholism is
an hour-to-hour basis while chaos reigns supreme especially destructive at critical periods in the child’s
within the family (Brown & Lewis, 1995). In addition development, such as when he or she is developing
to the ever-present threat of violence or of substance “core beliefs about security and safety” (Sheff et al.,
use, there might even be the additional threat of 2007, p. 7). The impact of such events is enhanced if
incest as boundaries become blurred and unclear the parents neglect to meet the child’s needs for com-
(Brown & Lewis, 1995). It is within this atmosphere fort and security because of their preoccupation with
that the family as a unit, and each individual member, the parental SUD (Sheff et al., 2007). Extreme abuse or
must attempt to achieve some degree of stability, and neglect may predispose the child to depression, anxiety
grow. states, suicide attempts or thoughts, or the development
Where healthy families provide stability, in dysfunc- of posttraumatic stress disorder as well as impulse con-
tional families a form of pseudo-stability might become trol disorders and substance abuse (Teicher, 2002). In
the norm. Although uncomfortable with the ongoing studying the impact of parental alcoholism on 9,346
SUD, the family members are able to tolerate and even adults, Anda et al. (2002) found that parental alco-
become comfortable with the current distribution of holism was strongly associated with the later develop-
power and responsibility within the family unit. Peace ment of depression in children raised in these homes,
at any cost becomes the central theme of the family, although parental alcoholism was not thought to cause
and in service of this goal the family members turn a the depression.
blind eye toward the ongoing SUD. If the members of Another impact of parental alcoholism was found
the family lose sight of the origins of this pseudo- by Wyman et al. (2007): Chronic stress in the family
stability or that it evolved out of the family’s attempt to resulted in higher levels of illness for the children. The
accommodate itself to the dysfunctional behavior of Wyman study did not directly address parental alco-
one member, they might come to defend it as the status holism, but the finding that chronic stress from any
2The 3Capretto (2007) gave as an example a spouse of an addicted person

Johnson Institute (1987) called the process of “denial” simple
“avoidance.” In spite of the different words used, the process is still who would not discuss the partner’s SUD even 15 years after that
the same. person’s death because the addicted one would not want this to happen.
cause impacted the growing child’s health status was on the family than one who has been physically de-
suggestive of the effect of parental alcoholism on the pendent on alcohol for the child’s entire life.
child’s health. In a similar finding of such stress, Dube A third factor that influences the impact of parental
et al. (2001) identified growing up in a home where substance use problems on the individual child’s growth
there was substance abuse as one factor associated with and development is the sex of the child. A daughter will
later suicidal behavior on the part of the individual. be affected differently by an alcohol-dependent father
It has been suggested that some of the children than a son (Ackerman, 1983). Also, the specific family
raised in an alcoholic home would become “addicted” constellation will play a role in how parental alcoholism
to excitement (Ruben, 2001; Webb, 1989). According will impact each individual child. Consider two different
to this theory, the excitement-addicted child might en- families. In the first, the father has a 3-month relapse
gage in fire-setting behaviors or be attracted to a partner when the third boy in a family of six children is 9 years
who struggles with substance use problems in later life. old. Contrast this child’s experience with that of the oldest
Other coping responses to parental alcoholism might child in a family of six children whose father relapsed for
involve either over- or under-functioning by other 3 months when the child was 9 years old. Both of these
family members (Dayton, 2005). An example of over- children would experience a far different family constella-
functioning is the adolescent who stays awake while the tion than would the only child, a girl, whose father re-
alcoholic parent is out drinking, checks on the safety of lapsed for 3 months when she was 9 years old. All three
sleeping siblings, and develops elaborate fire escape children would have a far different experience in life than
plans that might involve thoughts of returning time and would the third boy in a family of six children whose
time again to the burning house to rescue siblings, pets, mother was constantly drinking until he turned 14.
and valuables (Webb, 1989). These adolescents might be- Finally, as Ackerman (1983) observed, it is possible
come overly mature, serious, and well organized; such for children to escape the major impact of parental al-
behaviors are likely to be viewed as signs of emotional coholism if they are able to find a parental surrogate. If
maturity and stability by others (Dayton, 2005; Ruben, children can find a parental substitute (uncle, neigh-
2001; Webb, 1989). bor, real or imagined hero, etc.), they may be able to
The adolescent raised in an alcoholic home is avoid the worst of their alcoholic parenting (Ackerman,
forced to spend so much time and energy meeting basic 1983). This is discussed later in the chapter.
survival needs that he or she is unlikely to have the
opportunity to establish a strong self-concept (Juliana & The Adult Children of Alcoholics
Goodman, 2005; Sheff et al., 2007). Because of the
(ACOA) Movement
atmosphere of “chronic trauma” (Brown & Lewis, 1995,
p. 285), a significant percentage of children raised in an In the latter part of the 20th century, a number of adults
alcoholic home were thought to develop long-lasting stepped forward to claim that they were suffering from
emotional injuries. These observations are consistent emotional dysfunctions that could be traced in large
with clinical experience suggesting that children raised part to the impact of their parents’ alcoholism. These
in an alcoholic home did indeed seem to suffer some individuals came to be known as “adult children” of
form of psychological harm. alcoholics (ACOA). At the height of this movement,
But since the 1980s, researchers have discovered the number of adult children of alcoholics (or ACOA)
that parental alcohol/drug use problems do not auto- in this country was thought to range from 22 million
matically result in problems for the growing child. A (Collette, 1990) to 34 million adults (Mathew, Wilson,
number of factors shape the impact of parental alco- Blazer, & George, 1993). Although the therapeutic focus
holism on the developing children (Ackerman, 1983). has since shifted away from the ACOA model, treat-
One such factor is the sex of the parent with the SUD. ment professionals and lay persons alike still hear the
Since each parent carries out a different role within occasional hint that the ACOA movement is still
the familial unit, an alcoholic mother will have a far alive. There was never a single definition of the “adult
different impact on the family than will an alcoholic child,” but Ruben (2001) suggested that the term adult
father. A second factor that influences the impact of children of alcoholics “carries a double meaning: an
parental substance abuse on the family is the length of adult who is trapped in the fears and reactions of a child,
time the parent has actively been abusing chemicals. and the child who was forced to be an adult without
For example, an alcoholic father who has used chemi- going through the natural stages that result in a healthy
cals for “only” 3 years will have a far different impact adult” (p. 8).
Proponents of the ACOA model suggested that the by extensive interviews. Their study produced these
alcoholic home was dysfunctional and that children findings:
raised in such a home were emotionally scarred for life
(Ruben, 2001). Because of the parent’s abusive drink- 1. College freshmen with an alcoholic father tended to
ing, these children would grow into adults who would drink more and to have more symptoms of alco-
holism than freshmen who were not raised by an al-
1. Have to “guess” at what normal adult behavior is. coholic father.
2. Have trouble in intimate relationships. 2. Women who were raised by an alcoholic parent or
3. Have difficulty following a project through from parents reported a greater number of alcohol-related
beginning to end. consequences than their nondrinking counterparts.
4. Have a tendency to lie in situations when it is just as 3. Children of alcoholic parents have an increased risk
easy to tell the truth. of using not only alcohol but other drugs of abuse as
5. Often be unable relax, but always be ready to judge well.
themselves harshly and feel the need to always keep 4. Adolescent children of alcoholic parents had more
busy. positive expectancies for alcohol than did adolescent
6. Tend not to feel comfortable with themselves and children of nonalcoholic parents.
constantly seek affirmation from significant others. 5. As adults, children raised by alcoholic parents
7. Try to avoid conflict situations or handle them poorly. tended to have higher scores on test items suggesting
8. Be loyal to others, even when that person has abused “behavioral under control” (p. 444), than did those
them or failed to respect their loyalty. (Ruben, 2001; individuals who were not raised by alcoholic
Woititz, 1983) parents.
6. As college students, children raised by alcoholic par-
The “adult child” might also have a tendency to self- ents tended to score lower on academic achieve-
sabotage (Ruben, 2001), experience symptoms of in- ment tests than did their non-ACOA counterparts.
ternalized behavioral problems (e.g., anxiety and de-
pression) and externalized behavioral problems (e.g., Although the findings were suggestive, the study failed
conduct disorder and alcohol use disorders) (Fals-Stewart, to answer many questions about the assumed relation-
O’Farrell, & Birchler, 2004). People raised in a home ship between the parental drinking pattern and the stu-
with an alcohol-abusing parent also tend to be more dent’s academic performance. However, it did suggest
self-critical and deprecate themselves more than adult that parental alcoholism had a strong impact on the sub-
children of nonalcoholic parents (Berkowitz & Perkins, sequent growth and adjustment of the children raised in
1988). There is a danger that they will not allow them- that family, providing support for the ACOA model.
selves to exceed their parents’ level of competence in Hart and Fiissel (2003) explored the impact of having
life (Ruben, 2001). an alcohol-dependent parent during childhood on the
Some argue that the traditional view of the adult later adjustment of the individual and found that the
child of alcoholic parents is too narrow (Hunter & children of an alcohol-dependent parent might be vul-
Kellogg, 1989; Ruben, 2001). In addition to the expected nerable to later illness as an adult for reasons that were
forms of psychopathology, the authors suggested that not entirely clear. These self-reported medical problems
ACOAs might also develop personality characteristics did not seem to reflect neuroticism so much as an in-
that are the opposite of those expected of a child raised in creased incidence of actual medical problems in the
a dysfunctional home. For example, one characteristic ACOA sample examined in this research study. Earlier
thought to apply to ACOAs is that they tend to have research has suggested that being raised in such an envi-
trouble following a project through from start to finish, ronment might predispose the child to later mental
but some ACOAs might actually be compulsive worka- health problems such as dysthymia, phobias, and anxi-
holics and come to assume great responsibility in their ety disorders (Mathew et al., 1993). These research
family (Ruben, 2001). studies suggest that being raised in a home with an
In the early 1990s, Sher, Walitzer, Wood, and Brent alcohol-dependent parent might predispose the child to
(1991) explored the differences between young adults later stress-related medical and psychiatric problems.
who had or had not been raised by alcoholic parents. There are other ways in which adult children of al-
The authors used a volunteer sample of college stu- coholic parents have suffered, beyond the development
dents whose parental drinking status was confirmed of psychiatric problems. They might learn to blame
themselves for their parent’s drinking (Collette, 1988, This trend was called “therapism” (Sommers & Satel,
1990; Freiberg, 1991), live in fear that their parents 2005, p. 6), and it has spawned an entire industry using a
might separate or divorce (Sanders, 1990), or learn not therapeutic model that negates the possibility of an indi-
to excel beyond the level that their parents achieved vidual coping with psychological trauma and asserting
(Ruben, 2001). Not surprisingly, a number of research that the best way is for the individual to first express it
studies have revealed higher levels of psychiatric prob- emotionally (with the assistance of a trained helper) and
lems in adult children of alcoholic parents, providing then banish it from consciousness. Proponents of this
some support for the ACOA model. perspective place a great deal of emphasis on anecdotal
The growth of ACOA groups. Obviously, in a survey evidence rather than scientific research, raising the pos-
text such as this book, it is not possible to examine the sibility that any “cures” achieved through this process
self-help movement Adult Children of Alcoholics in are probably due to “placebo” effects rather than skilled
great detail. However, the reader should be aware that therapeutic intervention.
the historical growth and later decline of ACOA groups The “therapism” movement has become big business,
was phenomenal. At one point, it was estimated that with research being conducted by publishing companies
40% of the adults in this country belonged to some kind to identify market trends so the next wave of self-help
of a 12-Step self-help group such as Adult Children of books might reach the largest number of people, without
Alcoholics (Garry, 1995). This number was viewed as a helping them do more than spend money on the latest
reflection of many different factors. First, it seemed to re- craze in the self-help book market (Salerno, 2005). Such
flect how many people had been hurt by a parent’s alco- “self-help” literature identifies traumatic events such as
holism. Second, the growth of the ACOA groups was childhood abuse or rape, perpetuating the victim status of
seen as the attempt of these hidden victims of parental ad- those who rush to buy such books rather than stressing the
diction to find peace by working through the shame and individual’s strengths and potential for further growth
guilt left over from their childhood years (Collette, 1990). (Salerno, 2005; Walker, 1996; Zur, 2005).
It has even been suggested that the ACOA move-
Criticism of the ACOA Movement ment is an artifact of the “baby boomer” generation’s
The ultimate goal of the ACOA movement was to pro- entry into middle and later adulthood (Blau, 1990). In
vide a self-help group for those who believed their emo- attaching the label “adult child” to themselves, the
tional growth had been hurt by being raised in a “baby boomers” were able to “perpetuate the process of
dysfunctional environment. However, the movement was blaming [the parents] in a new language” (Treadway,
short-lived, suffering a significant reduction in the num- 1990, p. 40). After all, it is “fashionable to be a victim”
ber of groups and members from its peak enrollment in (Zur, 2005, p. 49). This stance also keeps the focus on
the mid-1980s (Gillham, 2005). In some regions of the the perceived misdeeds of the previous generation, not
country there has been a 90% decline in the number of the coping skills of the present one (Peele, Brodsky, &
ACOA groups, and some once-thriving groups now boast Arnold, 1991; Salerno, 2005). While the ACOA group
memberships of just 10–20 members (Gillham, 2005). might be said to help meet the ever-present human
This decline is perhaps due to fundamental prob- need for “a sense of community, empowerment, and
lems with the ACOA theoretical foundation. First, it spiritual renewal” (Treadway, 1990, p. 40), this theory
has never been proven that being raised by a parent would seem to account for the observed phenomenon
with an alcohol use disorder is, by itself, sufficient to in which individuals became dependent on the ACOA
cause psychosocial disturbances for the children in that program, almost as if they were “addicted” to being in
home (Bijttebier, Goethals, & Ansoms, 2006; Kaminer & an ACOA recovery group (May, 1991; Salerno, 2005).
Bukstein, 1998). Further, the theory on which the Admittedly, some children are raised in terrible, abu-
ACOA rests was challenged on philosophical grounds sive environments. But the assumption that children
that it is “an enterprise wherein people holding the growing up in a home with an alcohol-dependent par-
thinnest of credentials diagnose in basically normal ent will have psychosocial disturbances later in life has
people symptoms of inflated or invented maladies, so never been proven (Bijttebier et al., 2006). Indeed, vir-
that they may then implement remedies that have never tually all children are raised in homes that are dysfunc-
been shown to work” (Salerno, 2005, p. 2). This process is tional in one way or another, since the “healthy,”
a natural reflection of American culture at the start of the conflict-free family is itself a therapeutic myth. Historians
21st century, in which there is a “popular assumption that “have been unable to identify a period in America’s past
. . . without professional help most people are incapable when family life was untroubled” (Furstenberg, 1990,
of dealing with adversity” (Sommers & Satel, 2005, p. 6). p. 148). Indeed, one could argue that one factor that
led to the westward expansion of the United States dur- challenge model (Wolin & Wolin, 1993). This takes
ing the 18th and 19th centuries was the desire of many into account the possibility of individual resiliency,
to escape their dysfunctional home environments by something the damage model automatically fails to do.
striking out on their own. Resilience does not mean that the individual is invul-
The assumption that growing up in a home where nerable to the trials and tribulations of life (Blum,
there is an alcohol-dependent parent automatically 1998). Rather, it acknowledges that individuals differer
causes damage to the child is what Wolin and Wolin in their ability to cope with stress, and that there is a nat-
(1993, 1995) term the damage model. Proponents of ural development of adaptive systems in childhood that
this position suggest, as did Claudia Black (1982), that help the typical child become resilient to life’s trials
all “children are affected” by parental alcoholism (Masten, 2001). It is only when these protective systems
(Black, 1982, p. 27; 2003). The damage model assumes are shattered by extreme stress that normal growth is
that people are simply “passive vessels whose dysfunc- threatened. But under normal circumstances the indi-
tional histories inhabit and control them like so many ma- vidual learns from life’s experiences without being over-
lignant spirits” (Garry, 1995, p. 10A). Yet in spite of this come by trauma (Masten, 2001). Some of the signs of
model’s often strident advocates, research studies have resilience include the ability to find surrogate parents to
generally failed to support the damage model. People replace natural parents who are unavailable due to acci-
tend to find ways to cope with trauma. For example, dent or illness during childhood, or the development of
Bijttebier et al. (2006) drew on data from a community support systems during adulthood to help the individual
sample of 10- to 14-year-old schoolchildren from the cope during times of trial (Blum, 1998). Other character-
Netherlands and Belgium. The children of parents with istics include a tendency to look for things to change in
an identified alcohol use disorder did not demonstrate the future and to set goals in the future as well as to rec-
higher levels of anxiety or depression than the control ognize personal strengths in spite of adverse situations.
group. While they did report lower levels of familial cohe- A close examination of the ACOA model suggests
sion, which could contribute to the observed low feelings that in spite of its often vocal supporters, the literature
of self-worth reported by the children in this study, the re- on which the movement is based rests on a foundation
searchers were unable to identify the direction of causal- of nothing more than “assertions, generalizations and
ity.4 Further, the authors found that parental support by anecdotes” (University of California, Berkeley, 1990a,
the nondrinking parent and peer group relationships p. 7). It is “long on rhetoric and short on empirical
helped to mediate the impact of parental alcoholism. data” (Levy & Rutter, 1992, p. 12). Although research
This latter conclusion might explain the findings into characteristics of the ACOA population was popu-
reported by Senchak, Leonard, Greene, and Carroll lar for a few years, little research has been conducted in
(1995), who examined a group of 82 adult children of this area for more than a decade.
alcoholic parents, 80 adult children of divorced parents, Another criticism of the ACOA movement is that the
and 82 control subjects whose parents were neither entire model reflects an oversimplification (Zweig &
divorced nor alcoholic. The authors concluded that Wolf, 1997). Simply naming a process, even one that is
“negative outcomes among adult children of alcoholics oversimplified, does not mean that the individual un-
are neither pervasive nor specific to paternal alcoholism” derstands it on all levels. Most certainly, parental behav-
(p. 152). Indeed, research to date has failed to find iors can impact the child’s development. But even if this
any significant form of psychopathology specific to the impact was a negative one, the oversimplified AOCA
adult children of alcohol-dependent parents (D’Andrea, movement often leaves the reconstructive process un-
Fisher, & Harrison, 1994; Giunta & Compas, 1994; finished because it did not proceed on to the deepest
Kelly & Myers, 1996). This may suggest that resilience levels of the victim’s personality (Zweig & Wolf, 1997).
has a genetic foundation involving a gene that is included Surprisingly, even though psychology as a science is
in the synthesis of serotonin (“Resilience,” 2006). more than a century old, very little is known about what
These findings cast doubt on the damage model, constitutes a “normal” family or the limits of those un-
which serves as the foundation of the ACOA move- healthy behaviors5 that might be tolerated in an otherwise
ment. Perhaps a more appropriate model might be the “normal” family. There has been even less valid scientific
research into the psychodynamics of families of alcohol-
4In
or drug-addicted individuals (D’Andrea et al., 1994;
other words, did parental alcohol use disorders result in lower
familial cohesion or did families with lower levels of cohesion con-
5Which, if the truth be told, we all have to some degree. Well, most of
tribute to the development of parental alcohol use disorders? This
study was unable to determine which came first. us, anyway.
Goodwin & Warnock, 1991; Sher, 1991, 1997; University Given these findings, one must wonder to what de-
of California, Berkeley, 1990a). On this exceptionally gree the characteristics identified by the proponents of
weak foundation, proponents of the ACOA model claim the ACOA movement reflect not some form of pathol-
that 96% of the population was raised in a “dysfunctional” ogy but simply common problems-in-living. But now,
family (Garry, 1995; Peele et al., 1991; Salerno, 2005). thanks to an overabundance of self-help books, we have
In reality, there has never been any research to the “language” with which to blame earlier generations
suggest that this 96% figure is accurate (Hughes, 1993). for all the problems-in-living we might encounter,
But proponents of the ACOA movement quote it as if it without taking steps to address them.
were gospel truth. They point to studies in which a high
percentage of the ACOA adults questioned claim to
Summary
have one or more of the characteristics often attributed
to ACOAs. However such studies are flawed because the This chapter explored the family of the addicted indi-
language used to describe the typical adult child of alco- vidual, and the impact that one individual’s addiction
holic parents is so vague that Sher (1997) suggested it to chemicals is thought to have on the rest of the family.
has “a little something in it for everybody” (p. 252). Both Unfortunately, few research studies actually explore the
ACOA and non-ACOA adults tend to agree that the impact of one member’s alcohol/drug addiction on the
common ACOA descriptors apply to them (Sher, 1997). other members of the family. Much of what is assumed
Other detractors of the ACOA movement note that to be true about the family in which one or more per-
where the ACOA movement places great emphasis on sons is addicted to alcohol or drugs is based on theory,
the so-called inner child, the inner child concept is not not established fact.
a part of any single therapeutic theory. Rather, the the- The theory of codependency assumes that the indi-
ory behind the ACOA concept of the inner child is a vidual who is codependent is “trained” by a series of ad-
complex blend of “[Carl] Jung, New Age mysticism, holy verse life events to become dependent on the feedback
child mythology, pop psychology, and psychoanalytic the- and support of others. Further, it is assumed that family
ories about narcissism and the creation of a false self” members come to assume new roles, as the addicted
(Kaminer, 1992, p. 17). At the start of the 21st century, person gives up the power and responsibility that he or
adults “ought to be figuring out where their Inner Adult she would normally hold within the family. In this
is, and how that disregarded oldster got buried under the manner, the family comes to “accommodate” or adapt
rubble of pop psychology and short-term gratification” to the individual’s chemical addiction.
(Hughes, 1993, p. 29, italics added for emphasis). But From the perspective of the codependency model,
the ACOA movement keeps the focus not on the prob- the individual’s substance abuse is viewed as a family-
lems of adulthood but on a hypothetical construct centered disorder, which is passed on from one genera-
called the inner child. Even if this elusive creature ex- tion to the next. The self-help group movement of adult
isted, the “inner child” reflects a phase of life when the children of alcoholics (ACOA) is viewed as a logical
individual was developmentally, socially, psychologi- response to the pain and suffering that the family mem-
cally, and neurologically immature. bers experienced because of their participation in a
Finally, the charge has been made that the ACOA “dysfunctional” family. However, the “adult child” con-
movement is a white, middle-class invention (Levy & cept has met with some criticism. Some health care
Rutter, 1992). It is not known whether this model applies professionals stress that the theory behind the “adult
to inner-city children or others. As the authors note, chil- children” movement places too much emphasis on past
dren of heroin and cocaine addicts are “primarily non- suffering, at the expense of possible resilience on the
white, minority members who live in poverty. They have part of the individual or his or her future growth.
no national movement . . . do not write books and make Another criticism of the “adult children” movement
the rounds of the talk shows” (Levy & Rutter, 1992, p. 5). is its automatic assumption that the individual has expe-
However, as the authors remind us, many children are rienced some lasting psychological trauma as a result of
raised by parents who are addicted to chemicals other parental alcoholism or drug addiction. This theory has
than alcohol, in environments other than the white, never been tested and thus much of the ACOA self-help
middle-class world. Where the literature that supports the movement rests on a a series of unproven assumptions.
ACOA model is limited, the body of research into the ef- Research is needed to begin to understand how chemi-
fects of parental drug addiction on the children is “far less cal addiction impacts the growth and development of
evolved” (Fals-Stewart et al., 2004, p. 38). both the individual family members and the family unit.
CHAPTER TWENTY-SEVEN
The Evaluation of Substance Use Problems
Assessment procedures and diagnostic categories are problems. Indeed, behavioral scientists have yet to de-
not helpful if merely used to label . . . while ignoring velop a universally accepted definition of addiction
the strengths, coping capacities and desire for growth (Erlich, 2001). Thus the assessor must use imperfect
and development inherent in most people. Rather, tools to determine whether the client/patient does or
systems of classification are useful in identifying does not have an SUD, a decision that might have life-
symptoms, challenges, and abilities, necessary for long implications for the person. For example, a per-
planning and implementing effective treatment and son’s eligibility for health care insurance at age 50
. . . interventions. might be affected by a diagnosis of alcohol dependence
—Levy and Orlans (1998, p. 81) made 30 years earlier when he or she was only 20 years
old.
In this era of managed care, program cutbacks, and in- The assessment process is quite complicated. Sim-
creased accountability, health care professionals are ply screening a patient (to determine whether indica-
being required to justify each procedure in advance to tions of a specific condition are present) is not the same
ensure the maximum return for each dollar spent on as making a formal diagnosis (Miller et al., 1995). The
health care. This is accomplished, in part, through the process of screening is carried out to identify those indi-
process of assessment. The assessment is the foundation viduals within a certain population who might have a
of the rehabilitation process, a gatekeeping procedure, certain disease or condition (Knight, 2005). Following
and serves the more traditional role of identifying those the screening process, a more through assessment should
individuals who require some form of professional in- be carried out to confirm the presence of the disorder,
tervention to help them deal with their substance use assess its severity, and guide treatment (Knight, 2005).
problems (Juhnke, 2002). This chapter examines the After the appropriate diagnosis has been made, the cri-
process of evaluating a client’s drug/alcohol use pattern teria supporting that diagnosis need to be indicated and
and how assessment is related to rehabilitation. the appropriate form of care identified. The assessor must
determine (a) whether there is or is not evidence of a
substance use disorder, (b) the severity of this disorder,
The Theory Behind Alcohol
and (c) the most appropriate form of treatment for each
and Drug Use Evaluations individual.
The use of a substance by itself, even an illegal sub- An aid to this process are the “four C’s” suggested by
stance, is not proof that a person has an SUD (Gitlow, Rustin (2000):
2007). It is through the substance use assessment that
the facts to support the diagnosis of an SUD are identi- 1. The individual has a Compulsion to use chemicals.
fied and tied together in a coherent manner. Further, 2. The individual has struggled to Control his or her
the assessment is “more than a one-time paperwork pro- chemical use (or can no longer control it).
cedure conducted at the onset of treatment to simply 3. The individual has tried to Cut down on his or her
gather minimal facts and secure a . . . diagnosis” chemical use.
(Juhnke, 2002, p. vii). It is the first step in the rehabilita- 4. The individual has suffered Consequences of his or
tion process (Miller, Westerberg, & Waldron, 1995). her alcohol or drug use.
Unfortunately, in spite of decades of effort, scien-
tists have yet to develop a “Holy Grail” (Fleming, If substance abusers were all alike, there would be
2001, p. 321) for the detection of alcohol or drug use no need for the assessment process to move beyond
309
310 Chapter Twenty-Seven
determining whether the individual does or does not drinking pattern (Smith, Touquet, Wright, & Das Gupta
have a chemical use problem. However, all substance 1996), and (e) it does not differentiate between current
abusers are not alike, and there is no “one size fits all” and past drinking (Schorling & Buchsbaum, 1997).
form of treatment for alcohol/drug dependence prob- Thus, although the MAST is suited to the detection of
lems (Leshner, 2001a, 2001b). Effective treatment individuals with severe alcohol dependence (Saunders,
must be (a) individualized, (b) continually evaluated as Aasland, Babor, de la Fuente, & Grant, 1993), it is of
to its effectiveness, and (c) modified when necessary limited value with a person who abuses other chemicals
(Leshner, 2001a, 2001b). On the basis of the informa- or with a patient who is a “problem” drinker but not
tion uncovered during a careful evaluation, the substance alcohol dependent.
abuse rehabilitation professional is able to identify the Another screening tool for alcoholism that is grow-
appropriate goals and treatment strategies for each client. ing in popularity is the CAGE questionnaire (Ewing,
The opposite is also true: Without a careful evaluation 1984). CAGE is an acronym for the four questions used
of the client’s strengths, experiences, and needs, it will in this test:
be difficult to identify appropriate goals or to intervene
effectively (Blume, 2005). The evaluation process con- Have you ever felt you ought to Cut down on your
sists of three interrelated phases: screening, assessment, drinking?
and diagnosis. Have people Annoyed you by being critical about
your drinking?
Screening Have you ever felt bad or Guilty about your
To aid in the screening process, researchers have de- drinking?
vised a number of paper-and-pencil tests, or question- Have you ever had a drink first thing in the morning
naires, to help detect individuals who might have a to steady your nerves or to get rid of a hangover (Eye-
substance use problem. Note that a test score by itself opener)?
does not establish whether the individual has a sub-
stance abuse problem (Vanable, King, & de Wit, 2000). A “yes” response to one of these four questions sug-
The test results are one part of the overall assessment gests the need for a more detailed inquiry by the assessor.
process, which is designed to provide an overview of Affirmative answers to two or more items suggests that
each individual’s substance use pattern. These instru- the client has an alcohol use problem. The CAGE ques-
ments are filled out by either the client (and as such are tionnaire has an accuracy rate of 80%–90% in detecting
known as self-report instruments) or by the assessor as alcoholism when the client answers “yes” to two or
he or she asks questions of the person being evaluated. more of these questions. But the CAGE does not ad-
Self-report instruments offer the advantages of being in- dress binge drinking, nor does it identify frequency or
expensive and may possibly be less threatening to the level of consumption (Cooney, Kadden, & Steinberg,
client than a face-to-face interview (Cooney, Zweben, & 2005). It also is most effective in detecting alcohol-
Fleming, 1995; Juhnke, 2002). dependent individuals rather than alcohol abusers or
One of the most popular self-report instruments for persons at risk for developing an alcohol use problem
alcohol use problems is the Michigan Alcoholism (Saunders et al., 1993; Vanable et al., 2000). It is of
Screening Test (MAST) (Selzer, 1971). The MAST is little value in working with adolescents (Knight, 2002),
composed of 24 questions that may be answered either women with alcohol use disorders, and minority popu-
“yes” or “no” by the respondent. Test items are lations (Bradley, Boyd-Wickizer, Powell, & Burman,
weighted with a value of 1, 2, or in some cases 5 points. 1998; “Screening for Alcohol Problems,” 2002). By some
A score of 7 or more suggests an alcohol use problem estimates, up to 50% of at risk drinkers (Fleming, 1997,
(Craig, 2004). The effectiveness of this screening in- p. 345) might be missed by the CAGE because of these
strument has been demonstrated in clinical literature flaws.
(Miller, 1976). But the MAST has some drawbacks: Another paper-and-pencil screening tool that has
(a) it can be used only in cases of alcohol dependence grown in popularity in the past decade is the Alcohol
(Vanable et al., 2000), (b) the MAST provides only a Use Disorders Identification Test (AUDIT) (Saunders
“crude general screen” (Miller et al., 1995, p. 62) for alco- et al., 1993). Research has suggested that the AUDIT is
hol use problems, (c) the MAST does not detect “binge” over 90% effective in detecting alcohol use disorders
drinking, (d) it does not shed light on the individual’s (Brown, Leonard, Saunders, & Papasoulioutis, 1997),
The Evaluation of Substance Use Problems 311
and it appears to be effective in detecting women with problems, might best be viewed as detecting personality
drinking problems (Bradley et al., 2003). However, the patterns commonly associated with substance use prob-
AUDIT tends to miss active drinkers over 65 (Isaacson & lems (Rouse, Butcher, & Miller, 1999). Clients who are
Schorling, 1999), and it is not appropriate for use with extroverted, exhibitionistic, experience “blackouts” for
adolescent drinkers (Knight, 2002). any reason (such as a seizure disorder), are assertive, or
Other instruments have been developed for the de- enjoy risk-taking behaviors tend to score higher on the
tection of alternate forms of chemical abuse. Brown et al. “Mac” scale even if they are not addicted to chemicals
(1997) suggested a simple, two-item question set to detect (Graham, 1990).
possible substance use disorders: In their work with the original MMPI, Otto, Lang,
Megargee, and Rosenblatt (1989) discovered that
1. In the last year, have you ever drunk or used drugs alcohol-dependent persons might be able to “conceal
more than you meant to? their drinking problems even when the relatively subtle
2. Have you felt you wanted or needed to cut down on special alcohol scales of the MMPI are applied” (p 7).
your drinking or drug use in the last year? This is because personality inventories such as the
MMPI/MMPI-2, are vulnerable to both conscious and
Despite the instrument’s brevity, the authors claimed unconscious attempts at denial, self-deception, and dis-
that a “yes” answer to one item indicated a 45% chance tortion (Isenhart & Silversmith, 1996). Thus, although
that the individual had a substance use disorder and a the MMPI “Mac” scale was designed as a subtle test for
“yes” response to both items indicated a 75% chance alcoholism, it can possibly yield either false positive or
(Brown, Leonard, Saunders, & Papasoulioutis, 1997). false negative results. Counselors should assume that
Although these results are promising, the authors also the revised “Mac” scale on the MMPI-2 shares this same
pointed out that their two-item test might result in false- weakness with the original “Mac” scale until proven
positive results in some cases and that their initial find- otherwise.
ings needed to be replicated in follow-up studies. Unlike many of the other assessment tools, the
However, this two-item test shows promise for health MMPI offers an advantage of having five “truth” scales
care workers as a screening tool. built into it. These scales offer insight into how truthful
One instrument that is often mistakenly considered the individual taking the test may have been, and they
a screening or assessment tool is the Minnesota Multi- are discussed in more detail by Graham (1990). A major
phasic Personality Inventory (MMPI). The original disadvantage is the length of time the typical client
MMPI was introduced almost 65 years ago. To aid in needs to complete the MMPI/MMPI-2 test items. This
the utility of the MMPI for identifying addicted per- makes it a test better employed in the diagnosis phase of
sons, the MacAndrew Alcoholism Scale (also known as assessment (discussed later in this chapter) than during
the “Mac” scale) was introduced in 1965 after an the screening phase.
MMPI item analysis suggested that alcohol-dependent
individuals tended to give answers to 49 of the 566 items
of the MMPI that were different from the answers of
Assessment
nonalcoholics. A cutoff score of 24 items out of 49 an-
swered in the “scorable” direction correctly identified As Browne (2003) observed in her work on the impact
82% of the alcohol-dependent clients in a sample of of terrorism on children, “Before therapists can decide
400 male psychiatric patients (Graham, 1990). In 1989 on appropriate treatment, they need to be clear about
an updated version of the MMPI, the Minnesota what it is that they are treating” (p. 206). The same
Multiphasic Personality Inventory-2 (MMPI-2) was in- might be said about the treatment of substance use dis-
troduced. The “Mac” scale was modified slightly, but orders. This is accomplished during the assessment
was retained in essentially its original form. Craig (2004) phase of the evaluation process. During this phase, the as-
suggested that the “Mac” scale is 85% accurate in the sessor attempts to measure the severity of the individual’s
detection of substance abuse. substance use problem identified in the screening phase.
While this is an impressive figure, the “Mac” scale is One of the most useful tools of the assessment phase is
not perfect. Black clients have been discovered, for the clinical interview, which forms the cornerstone of
example, to score higher on the “Mac” scale than do the drug/alcohol use evaluation.
White clients. Also, research has suggested that the Juhnke (2002) identified four benefits of the clinical
“Mac” scale, rather than being specific for alcohol use interview:
1. It is more flexible than paper-and-pencil or computer- client’s only source of income was an unemployment
based assessment procedures. check for $120 each week, this person is devoting fully
2. It allows the assessor or therapist to establish a basic 50% of his income to buy alcohol. This information re-
level of rapport with the client. veals more about the individual’s chemical use pattern,
3. The confused or distressed client might respond helping the evaluator better understand the client.
better to a living person than to a computer screen or In addition to the clinical interview, Juhnke (2002)
written test. suggests that the assessor use a standardized test to aid
4. The therapist or assessor can watch the client’s non- in the assessment process. The test results will then be-
verbal behaviors in response to questions, to identify come part of the database on which the assessor will
areas for further exploration. make his or her conclusions. There are several assess-
ment instruments available that aid the professional
Client information provides an important source of who is conducting an alcohol use evaluation.1 One
data about clients’ current and previous chemical use. popular instrument for individuals over the age of 16 is
Keep in mind, however, that clients may either con- the Alcohol Use Inventory (AUI). The AUI is a copy-
sciously or unconsciously distort the information they righted instrument made up of 228 items, and it takes
provide. This underscores the need for collateral infor- 30–60 minutes for the individual to complete. The
mation sources (discussed below). answers to the test items provide data for 24 subscales
The first part of the interview process is an introduc- that the assessor can use to better understand the
tion by the assessor who explains that he or she will be client’s alcohol use pattern. But the AUI is limited to
asking questions about the client’s possible chemical alcohol use problems.
use patterns and that specific responses are most help- A popular research instrument that is gaining popu-
ful. The assessor explains that many of these questions larity as an assessment tool is the Addiction Severity
may have been asked by others in the past, but this in- Index (ASI). The ASI is administered during a semi-
formation is important. The client is asked if he or she structured interview with adult clients. The fifth edition
has any questions, after which the interview will begin. contains 161 items and requires approximately an hour
The assessor should attempt to review the diagnostic to complete. The administrator asks the questions of the
criteria for chemical use problems utilized in the Diag- client and records the answers on the answer form. The
nostic and Statistical Manual of Mental Disorders (4th ASI is in the public domain, which means it is not
edition-Text Revision) (DSM-IV-TR) (American Psychi- copyrighted, and it provides a severity rating score
atric Association, 2000). This manual provides a frame- based on the impressions of the person who administers
work within which the diagnosis of chemical dependency the test. Unlike the AUI, the ASI can be used for evalu-
can be made and provides a standard language under- ating the severity of abuse of other drugs such as co-
stood by most treatment professionals. The DSM-IV- caine and opiates. In spite of its many advantages, the
TR criteria for alcohol/drug abuse problems is discussed ASI has limited effectiveness with dual diagnosis clients
in more detail in the next section. (see Chapter 24) (Monti, Kadden, Rohsenow, Cooney, &
Many of the questions in the clinical interview are Abrams, 2002).
designed to explore the same piece of information from Another pair of instruments that are gaining wide-
different perspectives. For example, at one point in the spread acceptance are the Substance Abuse Subtle
interview process the client might be asked, “In the Screening Inventory-3 (SASSI-3) and the version of the
average week, how often do you use drugs/alcohol?” At SASSI-3 designed for use with adolescents (Juhnke,
a later point in the interview, this same client might be 2002). This copyrighted instrument can be used with
asked “How much would you say, on the average, that individuals 16 years or older with a fourth-grade reading
you spend for drugs/alcohol in a week?” The purpose of level. It takes about 15 minutes for the client to com-
this redundancy is not to “trap” the client but to provide plete the SASSI-3, and it can be scored by computer or
different perspectives on the client’s chemical use pat-
tern. For example, it is often wise to consider the per- 1
There are many assessment instruments currently in use. It is not
centage of the client’s income spent on recreational possible to review them all, especially since new tools are constantly
chemicals (Washton, 1995). Consider the client who being introduced. This section discusses only some of the more popu-
lar instruments. Also, there is no single instrument for the assessment
claimed to use alcohol one or two nights a week, spend- of drug use that is widely accepted, nor is it expected that such a
ing $60 per week on beer. This person’s alcohol use screening tool will be developed (Connors, Donovan, & DiClemente,
would be seen as excessive in anybody’s eyes. But if the 2001).
by hand. The SASSI-3 provides the user with scores on 5. Use of the chemical to avoid or control withdrawal
10 different scales such as the Symptoms Scale, the symptoms
Obvious Attribute Scale, and so on. Some of the scales 6. Repeated efforts to cut back or stop the drug use
are face-valid measures of alcohol/drug use problems, 7. Intoxication at inappropriate times (such as at work)
whereas other scales measure the effects of the individ- or when withdrawal interferes with daily functioning
ual’s substance use through subtle questions that do not (for example, a hangover makes the person too sick
reveal their intent to the reader. The Defensiveness and to go to work)
Supplemental Addiction Measure scales attempt to 8. A reduction in social, occupational, or recreational
measure the degree to which the client attempted to activities in favor of further substance use
hide his or her addiction (Juhnke, 2002). 9. Chemical use continues even though the individual
has suffered social, emotional, or physical problems
related to drug use
Diagnosis
The final stage in the evaluation process is diagnosis. Any combination of three or more of these signs is used
Abel (1982) identified four elements as necessary to the to identify the individual who is said to suffer from an
diagnosis of alcohol/drug addiction. These were the in- addiction to one or more recreational chemicals.
terrelated elements of (a) a compulsion to continue use In Chapter 1 the concept of a substance use contin-
of the chemicals in question, (b) the development of uum was introduced. Figure 27.1 illustrates the con-
tolerance, (c) major withdrawal symptoms following tinuum of drug use/abuse, showing the different points
withdrawal from the drug, and (d) adverse effects of on the continuum ranging from total abstinence from
drug use for both the individual and society. A more chemicals to chronic addiction. If the DSM-IV-TR cri-
standardized conceptual model was presented by the teria are applied to this continuum, the individual who
American Psychiatric Association (2000). In its Diag- meets four or more might be viewed as falling in level
nostic and Statistical Manual of Mental Disorders (4th 3 or 4 of the continuum of drug use introduced in
edition-Text Revision) (DSM-IV-TR ) the American Psy- Chapter 1.
chiatric Association suggested that signs of alcohol/drug Of these various diagnostic systems, the one offered
addiction include these: by the American Psychiatric Association in its DSM-IV-
TR (2000) provides a standardized framework within
1. Preoccupation with use of the chemical between which a professional can make a diagnosis of substance
periods of use dependence. It is through the evaluation process that
2. Using more of the chemical than had been anticipated the professional gathers the data on which to make
3. Development of tolerance to the chemical in question such a diagnosis—that is, an opinion of where on any of
4. Characteristic withdrawal syndrome from the chem- the above continuums the individual being assessed
ical might fall. A second part of the evaluation process is to
0 1 2 3 4
Total abstinence Rare/social use Heavy social Heavy problem Clear addiction to drugs
from drug use of drugs use/early problem use/early addiction
use of drugs to drugs
FIGURE 27.1 The Continuum of Recreational Chemical Use

determine the client’s motivation to the degree pos- chemical use, and other pertinent data. The same is
sible. Willingness to enter treatment does not automati- true if any information is to be released to a designated
cally translate into willingness to change one’s chemical party. This written permission is recorded on a form
use pattern (Connors et al., 2001). Some clients enter known as a release-of-information authorization (ROI)
treatment mainly for the purposes of impression man- form. The ROI should identify what specific informa-
agement (Wild, Cunningham, & Hobdon (1998), not tion is being requested and released, the person or
for rehabilitation. This is the client who wants to “get agency from which this information is to be released,
into treatment so I will look good to the judge.” While the length of time the ROI remains valid, and the spe-
the vast majority of individuals who are abusing or are cific individual or agency who is to receive the desired
addicted to chemicals are unready or unwilling to pur- information.
sue abstinence (Miller et al., 1995), the client who enters When the client is referred for an evaluation by the
“treatment” for the sole purpose of attempting to manip- court system, the court will often provide referral infor-
ulate the courts wastes valuable treatment resources bet- mation about the client’s previous legal history. The
ter used to treat other patients. courts will often include a detailed social history of the
client, which was part of the presentence investigation.
If asked, the evaluator should acknowledge having read
The Assessor and Data Privacy this information but should not discuss the contents of
The issue of confidentiality has always been quite com- the referral information provided by the courts. Such
plicated, and recent changes in federal regulations that discussions are to be avoided because (a) the purpose of
govern data privacy2 have made matters even more the clinical interview is to assess the client’s chemical
confusing. When the clinician is not clear about his or use patterns. A discussion of what information was or
her responsibility under the various state and federal was not provided by the court does nothing to further
data privacy regulations, it is wise to consult an attor- this evaluation. Also, (b) the client has access to this
ney. However, as a general rule, information about the information through his or her attorney. Thus, if
client is always considered privileged information. the client wishes to review the information he or she
There are exceptions, however. For example, if a client may do so at another time through established legal
were to indicate that he or she were seriously thinking channels.
about suicide or committing a homicide, the assessor Clients will occasionally ask to see the records pro-
may need to break confidentiality to protect the client vided by the court during the clinical interview. Fre-
from the impulse to end his or her life or to protect an- quently, they are checking to see what information has
other person from the client’s anger.3 been provided to decide how much and what they
Because of data privacy regulations, the assessor should admit to during the interview. This often reflects
might not have immediate access to privileged informa- the philosophy of “let me know how much you know
tion from such sources as treatment centers that the about me, so that I will know how ‘honest’ I should be!”
client attended earlier or the client’s past medical/ The solution to this dilemma is a simple statement that
psychiatric history. Also, clients can refuse to provide a the client may obtain a copy of the court record
specific item of information or even to talk to the assessor through the established legal channels. Persistent
if they do not want to.4 If information is obtained from clients who demand to see their court records on the
persons other than the client, the professional must always grounds that “it is about me, anyway” are to be reminded
first obtain written permission from the client authoriz- that the purpose of this interview is to explore the client’s
ing him or her to contact specific individuals to obtain drug and alcohol use patterns, not to review court records.
the desired information about the client, his or her However, under no circumstances should the assessor
let the client read the referral records. To do so would
2Such as the Health Insurance Portability and Accountability Act be a violation of the data privacy laws, since the referral
(HIPAA), for example. Entire Web sites have been devoted to the information was released to the assessor, not to the
ramifications of HIPAA. Hippa.org is one such site that provides a client.
wealth of information about the scope of this law and consequences
for violations of its provisions.
When the final evaluation is written, the evaluator
3The reader is advised to become familiar with the data privacy should identify the source of the information summa-
and duty-to-report regulations that are applicable in his or her home rized in the final assessment. Collateral information
state. sources should be advised that the client, or the client’s
4
The problem of the uncooperative client is reviewed in Chapter 32. attorney, has a right to request a copy of the final report
before the interview. It is extremely rare for a client to tions imposed on the assessment process might prevent
request a copy of the final report, although technically the use of some of these collateral resources. If the assess-
the client does have the right to do so after the proper ment must be completed by the end of the week, and
release-of-information authorization forms have been the professional is unable to contact the client’s mother,
signed. it may be necessary to write the final report without
benefit of her input. In addition, the other people in-
volved may simply refuse to provide any information
Diagnostic Rules whatsoever. It is the assessor’s responsibility, however, to
Many clients will initially resist a diagnosis of chemical attempt to contact as many of these individuals as pos-
dependency (Washton, 1990). Because of this, there sible, and to include their views in the final evaluation
are two diagnostic rules that should be followed as report.
closely as feasible in the evaluation and diagnosis of a Rule 2: Always assume deception until proved other-
possible substance use disorder (SUD). Occasionally, wise. The patient being assessed might or might not
an assessor cannot adhere to each of these diagnostic consciously try to deceive the assessor. It is more likely
rules for one reason or another; however, he or she that clients will offer the assessor what they believe is
should always attempt to carefully evaluate each indi- the truth, based on their pattern of distorted thinking
vidual case in light of these guidelines, even in special (Ross, 2002). Thus, the individual who drinks eight
cases. Then, even if the rule is not followed, the profes- beers in a bar with friends 5 to 7 nights a week might say
sional making the diagnosis should identify why one that he or she was an “infrequent” drinker not because
guideline or another could not be met in a given situa- of a conscious attempt at deception but because he or
tion to avoid missing important information. she literally believes that 5–7 nights a week is “infre-
Rule 1: Gather collateral information.5 As a group, quent” alcohol consumption, when compared to the
alcohol-dependent individuals will, when sober, be rea- person who drinks a minimum of 12–15 beers every
sonably accurate as to the amount and frequency of night of the week, plus more at home.
their alcohol use. But there are exceptions, such as Even so, some individuals will attempt to deceive
when the individual is facing some kind of legal prob- the assessor. The wise assessor will simply remember
lem (Donovan, 1992; Gendel, 2006; McCrady, 1994). that even “cooperative” patients will answer questions
Further, individuals who have both a mental illness based on their beliefs and defense systems. For example,
and a substance use problem also tend to underreport one individual reported that he was spending “$20 a
the extent of their substance use problems (Carey, week” on alcohol consumed with friends. The assessor
Cocco, & Simons, 1996). To provide as accurate an simply multiplied the $20 per week times the number
overview of the client’s SUD as possible, the assessor of weeks in a year to arrive at the figure of $1,040 that
should utilize as many sources of information as avail- this individual spent on alcohol each year. Yet when
able rather than rely on just the client’s self-report the client was confronted with this figure, he became
(Evans & Sullivan, 2001; Juhnke, 2002; McCrady, slightly angry and repeated that, no, he was spending
1994). only $20 a week for alcohol. His denial system would
To illustrate the importance of collateral informa- not allow him to admit to the higher figure of more
tion, every assessor has encountered cases in which the than $1,000 a year.
individual being evaluated claimed to drink “once a It is not uncommon for a person who is addicted to
week . . . no more than a couple of beers after work.” alcohol to admit to drinking only “once or twice a
The spouse of the person often reports, however, that week” until reminded that his or her medical problems
the client was intoxicated “five to seven nights a week,” were unlikely to have been caused by such moderate
which is quite different from the client’s self-assessment. drinking levels. The individual might or might not be
Collateral information sources might include the attempting to deceive the assessor. He or she might also
patient’s family, friends, employer or co-workers, clergy literally not remember drinking more often than this.
members, local law enforcement authorities, primary However, even when confronted with such evidence of
care physician, and psychotherapist (if any) (Slaby, serious, continuous alcohol use, many alcoholics deny
Lieb, & Tancredi, 1981). Obviously, the time restric- the reality of their alcoholism. Clients have been
known to admit to “one” arrest for driving under the in-
5Morgan (2003) advises the assessor to obtain Release-of-Information fluence of alcohol or possession of a controlled sub-
authorizations before contacting collateral information sources. stance. Records provided by the court at the time of
admission into treatment have often revealed that the since the person’s last arrest for an alcohol-related
person in question had been arrested in two or three dif- offense.
ferent states for similar charges. When confronted, From time to time, one will encounter a person who
these clients might respond that they thought that the has proudly claimed not to have had a drink or to have
evaluator “only meant in this state,” or “since that hap- used chemicals in perhaps the last 6–12 months or even
pened outside of this state, it doesn’t apply.” Thus, to longer. This person may forget to report that he or she
avoid the danger of deception or distorted recall, the as- was locked up in the county jail awaiting trial during
sessor must utilize as many different sources of informa- that time or was under strict supervision after being re-
tion as possible. leased from jail on bail and had little or no access to
chemicals. This is a far different situation from the
client who reports that he or she has not had a drink or
The Assessment Format
used chemicals in the last year, is not on probation or
The assessor’s diagnosis is generally recorded on a stan- parole, and has no charges pending.
dardized form, which is often titled an “Alcohol and Thus, the evaluator should explore the client’s living
Drug Use Evaluation Summary.” Although each indi- situation to determine whether there were any environ-
vidual is unique, there is a general assessment format mental restrictions on the individual’s drug use. Obvi-
that professionals can use for record keeping. This for- ously, a person who is incarcerated, in treatment, or on
mat is modified as necessary to take into account the probation and required to have frequent and unan-
differences between individuals; it provides a useful nounced supervised urine screens to detect drug/alcohol
framework within which to evaluate the individual and use will be under environmental restrictions. In such a
his or her chemical use pattern. This format is utilized case, a report of having “not used drugs in 6 months”
for this chapter. may be the literal truth but fail to identify the situa-
tional constraints that prohibit substance misuse. Also,
Area 1: Circumstances of Referral the individual’s chemical use pattern and his or her
The first step in the diagnostic process is to examine the beliefs about his or her drug use should then be com-
circumstances under which the individual is seen. Per- pared with the circumstances surrounding referral. For
sons with a substance use disorder will rarely come in example, a client may have stated that he does not have
for help on a voluntary basis and are usually forced into a problem with chemicals. Earlier in the interview, he
the assessment process through external pressure (Craig, may also have admitted that he was recently arrested for
2004). possession of a controlled substance for the second
The manner in which the client responds to the time in 4 years. In this situation, the client has provided
question “what brings you here today?” can provide two important but quite discrepant, pieces of informa-
valuable information about how willing a participant tion to the evaluator.
the individual will be in the evaluation process. If the Several important areas should be explored at this
individual responds with words like “I don’t know, they point in the evaluation process. The evaluator needs to
told me to come here,” or “You should know, you’ve consider whether the client has ever been in a treat-
read the report” obviously is being less than fully coop- ment program for chemical dependency, whether the
erative. The rare client who responds “I think I have a individual’s drug or alcohol use has ever resulted in
drug problem” is demonstrating some degree of coop- legal, family, financial, social, or medical problems, and
erativeness with the assessor. In each case, the manner whether there is evidence of psychological dependence
in which the client identifies the circumstances sur- or physical addiction to drugs or alcohol.
rounding his or her referral for evaluation provides a To understand this point, contrast the case of two hy-
valuable piece of information to the assessor. pothetical clients who were seen following their recent
arrests for driving a motor vehicle while under the in-
Area 2: Drug and Alcohol Use Patterns fluence of alcohol/drugs. The first person might claim
The next step is for the evaluator to explore the individ- (and have collateral information sources to support her
ual’s drug and alcohol use patterns both past and present. claim) that she drank only in moderation once every
All too often, clients will claim to drink “only once a few weeks. Furthermore a background check con-
week, now,” or to have had “nothing to drink in the last ducted by the court might reveal that this client never
6 months.” Treatment center staff are not surprised to had any previous legal problems of any kind. The eval-
find that this drinking pattern has been the rule only uation might show that after receiving a long-awaited
promotion, the client celebrated with some friends. There are many cases on record where the individ-
The client was a rare drinker, who uncharacteristically ual was finally convicted of a misdemeanor charge for
drank heavily with friends to celebrate the promotion, possession of less than an ounce of marijuana. How-
and she apparently misjudged the amount of alcohol ever, all too often, a review of the client’s police record
that she had consumed. reveals that the individual was arrested for felony drug
In contrast is the client who also was seen following possession and that the charges were reduced through
his arrest for driving a motor vehicle under the influ- a “plea bargain” agreement. The assessor needs to be
ence of chemicals. This individual’s collateral informa- aware of both the initial charge and the ultimate disposi-
tion sources suggest a more extensive chemical use tion by the court of these charges. The assessor should
pattern than he admitted during the interview. A back- also inquire as to whether the client has had charges
ground check conducted by the police at the time of brought against him or her in other states or by federal
the individual’s arrest revealed several prior arrests for authorities. Individuals may admit to one charge for
the same offense. possession of a controlled substance, only for the staff to
In the first case, one might argue that the client sim- later find that this same client has had several arrests
ply made a mistake. Admittedly, the person in question and convictions for the same charge in other states. Or
was driving under the influence of alcohol. However, the client may have admitted to having been arrested
in this case, she had never done so in the past and does for possession charges in other states but may not men-
not fit the criteria necessary for a diagnosis of even tion that he or she had left the state before the charges
heavy social drinking. The report to the court would were brought to trial.
outline the sources of data examined and in this case Many clients will reason that since they were never
provide a firm foundation for the conclusion that this convicted of the charges, they will not have to mention
individual made a mistake in driving after drinking. them during the assessment. The fact that the charges
But in the second case, the individual’s drunk were never proven in court because the client was a
driving arrest was the tip of a larger problem, which was fugitive from justice (as well as the fact that interstate
outlined in the report to the court. The assessor would flight to avoid prosecution is a possible federal offense)
detail the sources of information that supported this may well be overlooked by the client.
conclusion, including information provided by family Past military record. One important and often over-
members, the individual’s physician, the patient, the looked source of information is the client’s military
county sheriff’s department, and friends of the client. history, if any. Many clients with military history will
The final report in this case would conclude that the report only on their civilian legal history unless specifi-
client has a significant addiction problem that requires cally asked about their military legal record. Clients
treatment in a chemical dependency treatment program. who may have denied any drug/alcohol legal charges
whatsoever may upon inquiry admit to having been
Area 3: Legal History reprimanded or brought before a superior officer on
Part of the assessment process should include an exami- charges because of chemical use while in the military.
nation of the client’s legal history. This information The assessor must specifically inquire whether the
might be based on the individual’s self-report or a re- individual has ever been in the service. If the client
view of the client’s police record as provided by the denies military service, it might be useful to inquire
court, the probation/parole officer, or other source. It is why the client has never been in the service. Often, this
important to identify the source of the information upon question will elicit a response to the effect that “I
which the report is based. The following questions wanted to join the Navy, but I had a felony arrest
should be answered: record,” or “I had a DWI (driving while under the influ-
ence of alcohol) on my record and couldn’t join.”
1. What charges have been brought against the client These responses provide valuable information to the as-
in the past by the local authorities, and what was sessor and open new areas for investigation. If the client
their disposition? has been in the military, was the client’s discharge sta-
2. What charges have been brought against the client tus honorable, a general discharge under honorable
in the past by authorities in other localities, and conditions, a general discharge under dishonorable con-
what was their disposition? ditions, or a dishonorable discharge? Was the client
3. What is the nature of the current charges (if any) ever brought up on charges while in the service? If so,
against the individual? what was the disposition of these charges? Was the
client ever referred for drug treatment while in the might be hinting that they are also uncomfortable with
service? Was the client ever denied a transfer or promo- the term alcoholic as it applies to themselves. But they
tion because of drug/alcohol use? Finally, was the may also have accepted the rationalization that they
client ever transferred because of his or her drug/alcohol are problem drinkers, just like their brother or sister.
use? Information about either parental or sibling chemical
The client’s legal history should be verified, if pos- use is important for another reason as well. There is
sible, by contacting the court or probation officer, espe- significant evidence suggesting a genetic predisposi-
cially if the client was referred for evaluation for an tion toward alcoholism. By extension, one might ex-
alcohol- or drug-related offense. The legal history will pect that future research will uncover a genetic link
often provide significant information about clients’ toward the other forms of drug addiction as well. Thus,
lifestyle and the extent to which their drug use has a sibling who is perceived as being addicted to alcohol/
resulted in conflict with social rules and expectations. drugs by the individual being assessed hints at the pos-
sibility of a familial predisposition toward substance use
Area 4: Educational/Vocational History disorders.
The next step in the assessment process is to determine In addition, the reviewer will be able to explore the
the individual’s educational and vocational history. client’s attitudes about parental alcohol/drug use in the
This information, which might be based on the individ- home while he or she was growing up. Did the client
ual’s self-report or school and employment records, pro- view this chemical use as normal? Was the client angry
vides information on the client’s level of function and or ashamed about his or her parents’ chemical use?
on whether chemical use has interfered with his or her Does the client view chemical use as being a problem
education or vocation. The evaluator should also iden- for the family? It is important for the assessor to exam-
tify the source of this information. For example, the ine the possibility of either parental or sibling chemical
client who says that she dropped out of school in the use either while the client was growing up or at the
10th grade “because I was into drugs” presents a differ- present time. Such information will offer insights into
ent picture from the client who completed a bachelor the client’s possible genetic inheritance, especially as to
of science degree from a well-known university. The in- whether he or she might be at risk for developing an ad-
dividual who has had five jobs in the last 2 years might diciton. An overview of the family environment pro-
present a far different picture from the individual who vides clues as to how the client views drug or alcohol
has held a series of responsible positions and received use.
regular promotions in the same company for the last Family environments differ. Clients whose parents
10 years. Thus, the assessor should attempt to determine were rare social drinkers would have been raised in a far
the client’s educational/vocational history to learn the different environment from that of clients whose par-
person’s educational level and potential, and the degree ents were drug addicts. Clients who reported that never
to which chemical use has started to interfere with his knowing their mother because she was a heroin addict
or her educational or work life. who put the children up for adoption when they were
young might view drugs far differently from clients who
Area 5: Developmental/Family History reported that they were raised to believe that hard work
The assessor can often uncover significant material would see a person through troubled times and whose
through an examination of the client’s developmental parents never consumed alcohol.
and family history. The client might reveal that his or her
father was “a problem drinker” in response to the ques- Area 6: Psychiatric History
tion, “Were either of your parents chemically depen- Often, chemical use will result in either outpatient or
dent?” but hesitate to call that parent an alcoholic. How inpatient psychiatric treatment. A natural part of the
the client describes parental or sibling chemical use assessment process should be to discuss with the client
might reveal how the client thinks about his or her own whether he or she has ever been treated for psychiatric
chemical use. problems on either an inpatient or an outpatient basis,
For example, the client who says that his or her including the possible role that his or her alcohol and
mother “had a problem with alcohol” might be far drug use patterns might have played in the need for
different from the client who says “My mother was an hospitalization (Beeder & Millman, 1995).
alcoholic.” Clients who hesitate to call a sibling an alco- For example, clients have been known to admit to
holic but are comfortable with the term problem drinker having been hospitalized for observation for a variety of
reasons, such as a psychotic reaction of unknown origin, Area 8: Previous Treatment History
a suicide attempt, treatment of injuries sustained in an In working with a person who may be addicted to
accident, or because they were violent or depressed. chemicals, it is helpful for the evaluator to determine
Upon admission to chemical dependency treatment, whether the client has ever been in a treatment pro-
perhaps months or years later, this same individual gram for chemical dependency. This information,
might reveal that he or she was using drugs immedi- which may be based on the client’s self-report or infor-
ately prior to or at the time of hospitalization for a “psy- mation provided by the court system, sheds light on the
chiatric” disorder. But the client might reveal that he or client’s past and potential to benefit from treatment.
she failed to mention the substance abuse to the staff of The person who has been hospitalized three times
the psychiatric hospital either because of outright decep- for a heart condition and who continues to deny having
tion or because the hospital staff did not ask the appropri- any heart problems is not facing the reality of the condi-
ate questions. For these reasons that the assessor should tion. The same is true for the client who says that she
always ask whether clients (a) have ever been hospital- does not think she has a problem with chemicals but
ized for psychiatric treatment, (b) have ever had outpa- has been in drug treatment three times; she may not
tient psychiatric treatment, and (c) if so, had revealed have accepted the reality of her drug problem. The
to the mental health professional the truth about their issue then is to make a recommendation for the client
drug use. in light of his or her previous treatment history and his
If possible, the assessor should obtain a release-of- or her current status.
information form from the client and request the treat- The assessor should pay attention to the discharge
ment records and the discharge summary from the status from previous treatment programs and to the
treatment center where the client was previously hospi- period of time after treatment that the person main-
talized. The possibility that drugs contributed to the tained abstinence. More than one client has pro-
psychiatric hospitalization or outpatient treatment should claimed that he or she was alcohol free for a given
be either confirmed or ruled out if possible. This infor- period, only to admit to having used marijuaua during
mation then will allow the assessor to determine whether that same time. Further, the client may admit that he
the client’s drug use has—or has not—resulted in psy- or she started to use drugs shortly after discharge if not
chiatric problems serious enough for professional help before. Deplorably, the case of the client who reports
to be necessary. using chemicals on the way home following treatment
Area 7: Medical History is familiar to chemical dependency treatment profes-
sionals. Clients who admit using chemicals throughout
The assessor needs to explore the client’s medical history, the time they were in treatment provide valuable infor-
especially as it relates to his or her chemical abuse mation about their possible attitude toward this treat-
history (Gendel, 2006). Questions such as whether the ment exposure as well. These clients would have a
client has ever been hospitalized and if so, for what different prognosis from clients who had maintained
reasons are of special relevance when working with total sobriety for 3 years following the last treatment ex-
alcohol- or drug-abusing clients. The client’s hospital- posure and then relapsed.
ization might have been for drug-related injuries—one The evaluator should pay attention to the individ-
client reported having been hospitalized many times ual’s past treatment history, the discharge status from
after rival drug dealers had tried to kill him—or for the these treatment programs, and the total period of time
treatment of an infection acquired through the intra- the individual was sober after completing treatment.
venous abuse of illicit chemicals. When in doubt, the Specific questions should be asked as to when clients
assessor should attempt to obtain copies of admission entered treatment, how long they were there, and when
and discharge summaries from the hospitals where the they started to use chemicals following treatment.
client was treated, after obtaining the proper written au-
thorization from the client. The assessor should also in-
quire about current medical problems, whether the Other Sources of Information
client is taking one or more prescription medications,
and possible over-the-counter medication use. An at- Medical Test Data
tempt should be made to identify the client’s regular Laboratory test data are of only limited value in the
physician and to learn whether the client has been assessment of a person who is suspected of being ad-
“doctor shopping” to try to obtain prescriptions. dicted to chemicals. There are no blood or urine tests
specific for alcohol/drug addiction that a physician might test conducted within an hour of the accident may reveal,
use for general screening purposes. It was suggested that however, that the client’s BAL was far higher than what
elevations in certain blood tests such as liver function would be achieved from “only” two beers. This informa-
tests might serve as “alerting factors” (Hoeksema & tion would suggest some distortion on the client’s part.
de Bock, 1993, p. 268) to the physician for possible al- Clients who tested negative for marijuana on one
cohol dependence. Thus, laboratory test data do provide occasion may very well test positive for this same chemi-
one important piece of information to the assessor: The cal only a few days later. Subsequent inquiry might reveal
results of blood or urine studies might provide impor- that they used drugs sometime after the first test, think-
tant hints about a person’s chemical use status. For ing that it was “safe.” Such deception might be detected
example, if a patient being assessed admitted that his or by frequent and unannounced urine tests that are closely
her personal physician had warned about alcohol- supervised to detect illicit drug use.6 It is for these rea-
related liver damage 3 years ago, this would suggest that sons that the assessor should always attempt to utilize
the problems caused by the patient’s alcohol use date medical test information where possible to establish a
back at least that long and provide strong evidence that foundation for the diagnosis of a chemical use problem.
the client is alcohol dependent.
Medical test data can often shed light on the client’s Psychological Test Data
chemical use pattern at the time of the evaluation by A number of psychological tests may directly or indi-
detecting actual traces of alcohol or illicit drugs in the rectly be of use in the diagnosis of chemical depend-
patient’s body. It is for this reason that Washton (1995) ency. A major disadvantage of paper-and-pencil tests is
recommended that urine toxicology testing be a rou- that they are best suited to situations in which the client
tine part of a drug or alcohol use assessment. Consider is unlikely to “fake” (the technical term is “positively
the client who claimed never to have used marijuana, dissimulate”) his or her answers on the test in order to
only to have a supervised blood or urine toxicology test appear less disturbed (Evans & Sullivan, 2001). A com-
be positive for THC. This would strongly suggest that mon problem, well known to chemical dependency
the patient was using marijuana, in addition to whatever rehabilitation professionals, is that these instruments
drugs of abuse he or she might also have been using. are subject to the same problems of denial, distortion, and
Medical tests can often outright misrepresentation often encountered in the
clinical interview setting.
1. Confirm the presence of certain chemicals in the A technique that may be useful in the detection of
client’s blood or urine samples. intentional dissimulation is to review the test results with
2. Identify the amount of certain chemicals present in a not only the client but the client’s spouse or significant
person’s blood or urine sample (example, the BAL). other also present. The assessor then reviews the test item
3. Determine whether the drug levels in the blood or by item, stating the client’s response. Often, the spouse
urine sample have increased (suggesting further drug or significant other will contradict the client’s response
use), remained the same (which also might suggest to one or more test items, providing valuable new data
further drug use), or declined (suggesting no further for the assessment process. For example, on the Michigan
drug use since the last test). Alcoholism Screening Test (MAST), clients often answer
4. Offer hints as to how long the patient has been using “no” to the question inquiring whether the client had
chemicals. ever been involved in an alcohol-related accident. The
client’s wife, if present, may speak up at this point, ask-
The detection of chemical use by laboratory testing is ing about “that time when you drove off the road into
very technical and is affected by many different vari- the ditch a couple of years ago.” When, in this hypothet-
ables. Although urine toxicology testing is less intrusive ical example, the client pointed out that the police had
than blood tests it still involves an element of intrusive- ruled the cause of the accident as ice on the road, the
ness (Cone, 1993). At the very least, urine toxicology wife may have responded, “But you told me that you
testing involves an invasion of privacy while the process had been drinking earlier that night.”
of obtaining a blood sample for toxicology screening is Another technique to detect dissimulation is to
physically invasive, according to Cone. However, med- administer the same test or ask the same questions twice
ical test data are often quite useful to the assessor. It is during the assessment process. For example, the MAST
not uncommon, for example, for a client who was in-
volved in an automobile accident to claim to have “only 6
The use of urine, hair, and saliva samples for toxicology testing is
had two beers” before driving. A blood alcohol (or BAL) discussed in more detail in Chapter 32.
may be administered during the initial interview and drug abusers has been disputed (“California Judges Get
again at the follow-up interview a week or so later. If there Tougher,” 1997). However, when used properly, psycho-
are significant discrepancies, this is explored with the logical test data can add an important dimension to the
client to determine why there are so many differences diagnostic process.
between the two sets of test data. Obviously, if a client
scored 13 points when he or she first took the MAST but
The Outcome of the Evaluation Process
only 9 points a week later, the assessor would have reason
to conduct further inquiry and might suspect some level At the end of the assessment (see Figure 27.2 for a flow-
of deception until this hypothesis is disproven. chart of the assessment process), the chemical depend-
Psychological test data can often provide valuable ency professional should be in a position to answer four
insights into the client’s personality pattern and chemi- interrelated questions (Connors et al., 2001; McCrady,
cal use. Many such tests require a trained professional to 1994): (a) Does the client seem to have a substance use
administer and interpret the test to the client. The accu- problem? (b) How severe is the problem? (c) What is the
racy of psychological test data in the detection of alcohol/ individual’s motivation to change? (d) What factors seem
Does initial screen suggest

that client has a alcohol/drug
use problem?
No Yes
Does evaluation suggest Does assessment phase

that the client has other of evaluation process
needs or problem areas? suggest that the client is
addicted to chemicals?
No Yesa No Yes
Assessor makes Treatment Client’s status Client’s drug or

determination recommenda- and concerns alcohol use
that client has tions are made are diagnosed problem is
no evidence of based on the according to diagnosed
ongoing drug, assessment of established according to
alcohol, or the client’s criteria. Referrals established
other problems needs and his/ are made as criteria.
at present time. her resources. necessary.b
Client’s level
of care is
a Example: Client was not found to have substance abuse problem, but might determined,
have medical problem that requires treatment. and referral to
b Example: Client might be referred to early-intervention program for alcohol appropriate
abusers before demonstrating evidence of alcohol addiction. level of
c Example: On the basis of standardized criteria such as those proposed by the treatment is
American Society of Addiction Medicine (ASAM), client might be referred to made.c
day outpatient treatment, inpatient program, or intensive evening program.
FIGURE 27.2 A Flowchart of the Assessment Process

to contribute to further substance use by the individual? the Addiction Severity Index, the Minnesota Multipha-
Based on the assessment, the professional should also be sic Personality Inventory (MMPI), and the Michigan
able to determine the level of care that appears neces- Alcoholism Screening Test (MAST) were discussed as
sary to help the client and make recommendations as to aids to the evaluation process. The goal of each phase
the disposition of the client’s case. of the evaluation process was examined, as was the
Obviously, if the client is found to be addicted to one need for a wide database to provide the most compre-
or more chemicals, a recommendation that he or she hensive picture possible of the client’s chemical use
enter treatment would be appropriate. The detection of a pattern. Data sources discussed include the client and
substance use problem is of little value if there is no rec- collateral information as well as the application of med-
ommendation for treatment (Appleby, Dyson, Luchins, ical test data as possibly providing information that
& Cohen, 1997; Paton, 1996). The form of treatment, would aid the evaluation process.
however, would be determined by the assessor’s opinion Information from medical personnel who would be
as to the appropriate level of care. Treatment programs in a position to evaluate the client’s physical status can
are ranked by the intensity of the treatment program. For often prove valuable in understanding a client and the
example, a medical inpatient treatment program is con- role that drugs have had on his or her life. Finally, psy-
sidered more intense than a day outpatient treatment chological test data may reveal much about the client’s
that meets 5 days a week, and both of these programs are personality profile and drug use pattern. However, psy-
considered more intense than an evening outpatient chological test data suffer from the drawback that it is eas-
treatment program that meets once a week. The decid- ily manipulated by a client who wishes to dissimulate.
ing factor is the client’s need for treatment. The outcome of the assessment process should be a
formal report in which the evidence supporting the
conclusion that the client is or is not abusing or depen-
Summary dent on chemicals is outlined. The recommendations
The evaluation process involves three phases: screen- that result from the evaluation process might include
ing, assessment, and diagnosis. Each of these phases suggestions for further treatment, even if the client is
was reviewed. The application of various tools such as found not to be addicted to chemicals.
CHAPTER TWENTY-EIGHT
The Process of Intervention
The most promising way—perhaps the only way—to of this country. Even so, individuals with alcohol use
put enough addicts into treatment for long enough to problems rarely perceive the need for treatment (Flora,
make a difference entails a considerable measure of 2005; Wu & Ringwalt, 2004). It must be assumed that
coercion. the same is true for individuals with other forms of sub-
—Satel and Farabee (2005, p. 690) stance use disorders. In this chapter, the process of in-
tervention in cases of a substance abuse disorder is
Many would challenge the quote from Satel and discussed.
Farabee (2005), but the benefits of treating individuals
who are abusing recreational chemicals are great: Each
dollar invested in treatment brings a return of $7 (Ettner
A Definition of Intervention
et al., 2006) to $10 (Lowe, 2004). Part of these savings It was once thought that for the addict to accept the
are in the reduced cost of health care. Researchers have need for help he or she had to “hit bottom,” as it is
found that following treatment for alcohol dependency, called in Alcoholics Anonymous. “Bottom” is the point
for those treated there is a 26% reduction in hospitaliza- where the individual has to admit absolute, total defeat.
tions for general health problems, a 25% reduction in When the alcohol- or drug-dependent individual reached
the length of hospitalizations, a 38% reduction in visits this point, he or she would have no question about the
to hospital emergency rooms, and a 14% reduction in need to stop using chemicals. But this passive approach
physician visits, all of which translates into savings for to treatment meant that many abusers died before
health care insurance providers (R. M. Weiss, 2005). reaching “bottom,” and many others never accepted
Nor are these savings limited to alcoholism. The aver- the need to stop abusing chemicals.
age monthly medical cost for a drug abuser is estimated In 1980, Vernon Johnson, a pioneer in the interven-
at $750 per month (Rosenbloom, 2000). Following treat- tion process, challenged the belief that it was necessary
ment, those same costs drop to $200 per month, com- for the addict to “hit bottom” before he or she could ac-
pared with the typical monthly medical care cost of cept help. He suggested that the alcohol-dependent
$100 a month for a person who never abused recre- person could learn to comprehend the reality of his
ational chemicals. These figures demonstrate that the or her addiction, if this information was presented in
attempt to rehabilitate substance abusers/addicts is cost language that he or she could understand. Even the
effective and could bring about a marked reduction in substance-abusing client who was functioning poorly
the annual expenditure for health care in this country if (McCrady, 2001) or the person who was “not in touch
adequate treatment could be provided for those who with reality” (Johnson, 1980, p. 49) because of his or
abuse or are addicted to recreational chemicals. her chemical abuse was “capable of accepting some
Surprisingly, considering that alcohol/drug use is a useful portion of reality, if that reality is presented in
factor in so many accidents and diseases, the cost of informs they can receive” (p. 49, italics in original). Fur-
surance benefits for substance abuse rehabilitation was ther, because of the physical and emotional damage
found to be only 13% of the total expenditure for behav- that uncontrolled addiction could cause, Johnson
ioral health care and less than 1% of the expenditure for (1980) did not recommend that concerned family or
overall health care (Schoenbaum, Zhang, & Strum, friends wait until the addicted person “hit bottom.”
1998). These data suggest that substance abuse/addiction Rather, he advocated early intervention in cases of
causes an inordinate drain on the health care resources addiction.
323
324 Chapter Twenty-Eight
In a later work, the Johnson Institute identified inter- dict’s social circle break the rule of silence surrounding
vention as a the person’s addiction. Effective intervention sessions
are planned in advance and are repeatedly rehearsed by
process by which the harmful, progressive and de- the participants to ensure that the information pre-
structive effects of chemical dependency are inter- sented is appropriate for an intervention session.
rupted and the chemically dependent person is Participants must agree in advance about the goal of
helped to stop using mood-altering chemicals, and to the intervention effort: to help the addicted person ac-
develop new, healthier ways of coping with his or her cept the need to immediately enter treatment. To do
needs and problems. (1987, p. 61) this, each person involved confronts the addicted per-
son with specific evidence that he or she has lost con-
In the eyes of Twerski (1983), an early advocate of trol of his or her drug use, in language that the individual
the intervention process, intervention was “a collective, can understand. The participants also express their de-
guided effort by the significant persons in the patient’s sire for the addict to seek professional help for the drug
environment to precipitate a crisis through confronta- problem (Flora, 2005; Williams, 1989). In the process,
tion, and thereby to remove the patient’s defensive ob- each member affirms his or her concern for the addict,
structions to recovery” (p. 1028). but each participant will offer hard data showing how
A final definition. Drawing on these three defini- the addicted person is no longer in control of his or her
tions, it is possible to define an intervention project as life.
being (a) an organized effort on the part of (b) signifi- The collective hope is that those involved will be
cant others in the addict’s environment to (c) break able to break through the addicted person’s system of
through the wall of denial, rationalization, and projec- denial. But addicted individuals rarely deny that they
tion by which the addict seeks to protect his or her ad- are addicted, at least by the time that family and friends
diction. The purpose of this collective effort, which is plan an intervention session, so much as they deny that
(d) usually supervised by a chemical dependency profes- their addiction has affected anybody besides themselves
sional, is to (e) secure an agreement to immediately seek (Flora, 2005). Thus, the participants seek to break
treatment. through the addicted person’s denial about how his or
A consequence of early intervention projects. Unfortu- her chemical use problem has affected others, in the
nately, substance abusers might not view their chemi- hope that he or she will come to understand the need
cal abuse as problematic (McCrady, 1994). Because for treatment.
they have not “hit bottom,” they might not have come Although the intervention process has been an ac-
to understand or accept the relationship between the cepted tool for more than a generation, there has been
problems they have encountered and their chemical little research into its effectiveness (Flora, 2005). Thus,
use. Thus, they might resist efforts by concerned others it is possible that some families and some types of client
to intervene in an area where they do not see a need for might benefit more or less from an intervention session
corrective action. There is real potential for a negative (Flora, 2005). The process of intervention is based on a
outcome from poorly planned or executed intervention clinical theory that has not been subjected to research
projects, especially if agreed-upon sanctions are im- studies designed to identify its utility or effectiveness,
posed on the individual (Fals-Stewart, O’Farrell, & or the optimum conditions under which it might be
Birchler, 2003). Thus, intervention techniques are not utilized.
to be utilized lightly or by inexperienced practitioners.
The Mechanics of Intervention
Characteristics of the Intervention Process The intervention process is planned and should be re-
Pressure on an individual from family or loved ones to hearsed beforehand by the participants. Usually, three
address his or her substance use problem is second only to four sessions are held prior to the formal intervention
to legal pressure as a way to force the person to seek session, so participants can learn about the process and
treatment (Fals-Stewart, O’Farrell, & Birchler, 2003). practice what they are going to say (O’Farrell, 1995).
Such pressure is applied without malice. This is not a The intervention process should involve every person in
session to allow people to vent their pent-up frustration the addicted person’s life who might possibly have
but rather a “profound act of caring” (Johnson Institute, something to add, including the spouse, siblings, chil-
1987, p. 65) through which significant others in the ad- dren, possibly friends, supervisor/employer, minister,
The Process of Intervention 325
co-workers, or others (Johnson Institute, 1987). Each she needs to state clearly that if the addicted individual
individual is advised to bring forward specific incidents does not seek treatment, his or her position will be ter-
when the addicted person’s behavior, especially the minated. Then, if the addicted person refuses treat-
chemical use, interfered with their lives in some ment, the employer should follow through with this
manner. action.
Individually confronting an addicted person is diffi- Family members should also have thought about
cult at best and in most cases is an exercise in futility and discussed possible options through which they
(Johnson Institute, 1987). Anyone who has tried to talk might begin to detach from the addict. This should be
to an addicted person knows that the addict will deny, done prior to the start of the intervention session, and if
rationalize, threaten, or simply try to avoid any con- the addicted person refuses treatment (possibly by leav-
frontation that threatens the continued drug use. If the ing the session before it ends) they should follow
spouse, individually, questions whether the alcoholic through with their alternative plan. The options should
was physically able to drive the car home last night, he be discussed with the other participants of the interven-
or she might be told, “No, but my friend Joe drove the tion project, and during the rehearsal each participant
car home for me, then walked home after he parked the should practice informing the addicted person what he
car in the driveway.” or she will do if the addicted person does not accept
However, if Joe also is present, he can confront the treatment.
alcohol-dependent person and say that he did not drive There is no malice in the intervention process.
the car home last night or any other night! His wife might There is a very real danger that without proper guid-
be surprised to hear this, as the excuse “Joe drove me ance, the intervention session might become little
home last night” could very well have been a common more than a weapon that is used by some family mem-
one. But quite likely, nobody ever asked Joe whether he bers to control the behavior of another (Claunch,
did or did not drive the family car home. Before every- 1994). The participants in the intervention process do
body was brought together for an intervention session, not engage in threats to force the addicted person into
it was likely that nobody checked out the isolated lies, treatment. Having the addicted person see and accept
rationalizations, or episodes of denial. The addicted in- the need for treatment is one goal of the intervention
dividual’s denial, projection, and rationalization will process, but it is not the only goal. An even more impor-
often crumble when confronted with all the significant tant goal is for participants to begin to break the con-
people in his or her environment. This is why a collec- spiracy of silence that surrounds the addicted person’s
tive intervention session is most powerful in working behavior.
with the alcohol/drug addicted person. In the intervention process, each participant will
Twerski (1983) observed that it is common for the learn that he or she has the right to choose how he or
person for whom the intervention session was called to she will respond, should the addicted person decide to
make promises to change his or her behavior. These continue using chemicals. The addicted person is still
promises might be made in good faith or they might be able to exercise his or her own freedom of choice, by ei-
simply a means of avoiding further confrontation. But ther accepting the need for treatment or not, as he or
the fact remains that since the disease of addiction “re- she sees fit. But now the involuntary “support system”
sponds to treatment and not to manipulation, it is un- of friends and family members will not be as secure:
likely that any of these promises will work, and the People will be talking to each other and drawing
counselor must recommend treatment as the optimum strength from each other. One goal of the intervention
course” (Twerski, 1983, p. 1029). session is to have the addicted person either accept the
If the alcohol/drug user refuses to acknowledge the need for treatment or have a clear understanding of the
addiction, or admits to the addiction but refuses to enter consequences of not going into treatment, but an
treatment, each participant in the intervention session equally important goal is for everybody in the family to
should be prepared to detach from the addict. This is be heard voicing his or her concern (Claunch, 1994).
not an attempt to manipulate the addict through empty Family intervention. Family intervention is a special-
threats. All those involved should be willing to follow ized intervention process by which every concerned
through with a specific action to help themselves begin family member will, under the supervision of a trained
to detach from the addicted person, should he or she re- professional, gather together and plan a joint confronta-
fuse to enter treatment. For example, if the individual’s tion of the individual. The family intervention session,
employer or supervisor has decided to participate, he or like all other forms of intervention, is carried out to
break through the addict’s denial, allow the family mem- One of Jim’s siblings, Sara, also lives at home with
bers to voice their concerns, and possibly obtain a com- their parents. She immediately pointed out how just
mitment from the addict to enter treatment. The focus 3 weeks earlier Jim had run out of vodka early in the
is on the individual’s drug-using behaviors and on the evening after having four or five mixed drinks. Sara said
concern the participants have for him or her. that Jim had driven to the liquor store to buy a new
An advantage of the intervention session is that bottle or two after having consumed the last of the
through confrontation family members of the addicted vodka in the house. Sara concluded that she was not
person may begin to “detach” from the addict. The calling Jim a liar, but that she knew he had driven a car
conspiracy of silence that existed within the family is after drinking, at least on this one occasion. She was
broken, and family members may begin to communi- concerned about the possibility that he might have had
cate more openly and more effectively. Meyer (1988) an accident, and still felt uncomfortable about this inci-
identified the intervention process as an “opportunity dent. She was afraid he might do it again and that the
for healing” (p. 7) for this reason. The participants in next time he might not be so lucky as to make it back
the intervention session can express their love and con- home again in one piece.
cern for the addicted person and at the same time reject Jim’s mother then spoke. She pointed out that she
his or her drug-induced behaviors. had found her son unconscious on the living room
It is often helpful during the stress of the moment for floor twice in the past month. She identified the exact
the participants in the intervention process to have writ- dates that this had happened and observed that she felt
ten notes they can refer to. These notes should include uncomfortable with his sleeping on the floor, surrounded
information about the specific episodes of drug use, by empty beer bottles. So she picked up the empty
dates, and the addict’s response to these episodes. bottles to keep them from being broken by accident and
Sometimes family members will bring a personal diary covered Jim with a blanket while he slept. But she also
to use as a reference in the intervention session. One was concerned and believed that her son was drinking
advantage of the written notes is that they help to focus more than he thought.
the participant on the specific information that he or As Jim’s mother finished, his other sister, Gloria,
she wishes to bring to the intervention session. began to present her information and concerns. She
During the rehearsal, the professional who will coor- had had to ask Jim to leave her house last week, which
dinate the intervention session decides who will present was news to the rest of the family. She took this step, she
information and in which order. As much as possible, explained, because Jim was intoxicated, loud, and abu-
this planned sequence is followed during the interven- sive toward his nephew. She said that everybody who
tion session itself. The participants do not threaten the was present, including her son’s friend who was visiting
addict. Rather, they present specific concerns and infor- at the time, smelled the alcohol on his breath and was
mation that highlight the need for the addicted person repulsed by his behavior. Gloria concluded by stating
to enter treatment. Johnson’s (1980) work provides a that Jim was no longer welcome in her home unless he
good overview of the intervention process. (a) went through treatment and (b) abstained from al-
cohol use in the future.
At this point, the chemical dependency counselor
An Example of a Family spoke, pointing out to Jim that his behavior was not so
Intervention Session different from that of many thousands of other addicted
In this hypothetical intervention session, the central persons. The counselor said that this was the point in
character is a patient named Jim. Also involved are his the intervention session when the addict begins to
parents as well as two sisters and a chemical depend- make promises to cut back or totally eliminate the drug
ency counselor. The intervention session was held at use, a prediction that caught Jim by surprise because it
his parents’ home where Jim had been living. During was true. His protests and promises died in his throat,
the early part of the session, Jim asserted that he had even before he opened his mouth.
never drank to the point of passing out. He also claimed Before he could think of something else to say, the
that he always drank at home so that he wouldn’t be out counselor pointed out that Jim gave every sign of hav-
on the roads while intoxicated. He did not believe that ing a significant alcohol problem. The counselor listed
his drinking was as bad as everybody said it was for these the symptoms of alcohol addiction one by one, and
reasons, and said that he could see no reason why every- noted that Jim’s family had identified different symp-
body was so concerned. toms of addiction in their presentations. “So now,” the
counselor concluded, “we have reached a point where of some family members from others (Blume, 2005;
you must make a decision. Will you accept help for Flora, 2005).
your alcohol problem?” If Jim says “Yes,” family mem- There are alternatives, such as “motivational inter-
bers will explain that they have contacted the admis- viewing” techniques that allow the therapist to effectively
sions officer of two or three nearby treatment centers work with the substance-abusing client (Flora, 2005).
that have agreed to hold a bed for him until after the in- While there are strong advocates of the family interven-
tervention session ends. Jim will be given a choice of tion model presented here, there is limited research into
which treatment center to enter and will be told that its effectiveness (Connors, Donovan, & DiClemente,
travel arrangements have been taken care of. His lug- 2001; Flora, 2005). The professional coordinating the
gage is packed in the car, waiting, and if he wishes, the intervention session should be familiar with alternative
family will escort him to the treatment center as a show models of intervention to best meet the client’s needs.
of support. Rather than utilizing a “one size fits all” approach, the
If Jim says “No,” the family members then will con- therapist should attempt to match a specific form of in-
front him about the steps they are prepared to take to tervention with the needs of the addicted person and
separate from his addiction. His parents may inform the family.
him that they have arranged for a restraining order from
the court and present him with papers from the court
informing Jim that if he should come within a quarter
Intervention and Other Forms
of a mile of their home he will be arrested. The other
of Chemical Addiction
family members might then inform Jim that until he The Johnson Institute (1987) addressed the issue of in-
seeks professional assistance for his drinking, he is not tervention when the person’s drug of choice was not al-
welcome to live with them either. If his employer is cohol but any of a wide range of other chemicals. The
present, Jim may be told that his job is no longer there same techniques used in alcoholism also apply to cases
for him if he does not enter treatment.1 when the individual’s drug of choice is cocaine, benzo-
Jim may be told that, no matter what he may think, diazepines, marijuana, amphetamines, or virtually any
these steps are not being taken as punishment. Each other drug of abuse. Significant others will gather, dis-
person will inform him that because of his drug addic- cuss the problem, and review their data about the ad-
tion, they find it necessary to detach from him until he dict’s behavior. Practice intervention sessions are held,
chooses to get his life in order. Each person there will and the problems are addressed during the practice ses-
affirm his or her concern for Jim but will also start the sions as they are uncovered.
process of no longer protecting Jim from his addiction Finally, when everything is ready, the formal inter-
to chemicals. These decisions have all been made in vention session is held with the addicted person. The
advance of the intervention session. Which option the addicted person might need to be tricked into attending
participants will take depends in large part on Jim’s re- the intervention session, but there is no malice in the
sponse to the question: “Will you accept help for your attempt to help him or her see how serious the drug
alcohol problem?” Through the process of interven- problem has become. Rather, there is a calm, caring re-
tion, the family members have been helped to identify view of the facts by person after person, until the indi-
boundaries, which are limits that they can enforce for vidual is unable to defend his or her chemical use and
their own well-being (Claunch, 1994). comes to recognize the need for professional help.
Criticism of the Johnson Institute Model. Many de- The goal of the intervention session is to secure an
tractors claim that the “Surprise Party Intervention” agreement from the individual to enter treatment im-
model is not the best way to intervene with people who mediately. During the pre-intervention practice ses-
have a substance use problem (Miller, 2003). Such sions, arrangements are made to find a time when the
“tough love” based interventions have been compared addicted person would be able to participate. A family
to “emotional powder kegs that can go horribly wrong” reunion might provide the opportunity to carry out an
(Flora, 2005, p. 41). Such negative outcomes include intervention session, for example. Although this might
families ripping themselves apart and lifelong alienation seem disruptive to a family holiday, would the interven-
1The
tion session be any more painful than the family’s un-
employee has certain legal rights, and it is necessary for the em-
ployer to consult with an attorney to ensure that he or she does not spoken anger and frustration at the addicted member’s
violate the employee’s rights by this process. See Kermani and behavior? Indeed, the intervention project might serve
Castaneda (1996) for a discussion of this issue. as a catalyst for change within the family constellation,
opening the door for changes in other areas. However, person. This is the grounds upon which pregnant sub-
the point being stressed here is that the timing of the instance abusers are remanded to treatment in many
tervention project must be such that the person who is parts of the country (Kleinig, 2004).
the focus of the effort can participate for as long as the Another issue that must be addressed in the inter-
intervention session might last. vention project is the issue of data privacy (Kleinig,
Arrangements are made in advance for the individ- 2004). Information can not be indiscriminately revealed
ual’s admission into treatment. This may be accom- to others, even if the goal is to help the client who is the
plished by a telephone call to the admissions officer of center of the intervention project. The individual’s sub-
the treatment center. The caller may then explain the stance use problems are viewed in many districts as
situation and ask if the center would be willing to ac- matters of private concern and thus protected by data
cept the target person as a client. Usually, the treatment privacy regulations. This is of particular concern in
center staff will want to carry out their own chemical teaching hospitals or professional training programs
dependency evaluation to confirm that the person is an where students might be exposed to information about
appropriate referral to treatment. But most treatment clients that clients would rather remain hidden.
centers should be more than willing to consider a refer- One of the more common ethical problems that
ral from a family intervention project. emerges in the intervention project is the potential for a
conflict of interest that might arise if substance abuse
counselors coordinating the intervention process should
The Ethics of Intervention refer the client only to themselves, or a facility where
Like the counselor who works with substance-abusing they work (Fals-Stewart et al., 2003). The counselor
clients, the process of intervention is fraught with ethi- who coordinates the intervention project should have
cal dilemmas (Scott, 2000). For example, the “judge- no vested economic interest in where the client goes for
ment that a person constitutes a sufficiently significant treatment. Ideally, the client who is the focus of the in-
danger to himself or others such that some intervention tervention project should be offered a number of treat-
is justified is often highly speculative” (Kleinig, 2004, ment options, although in reality economic and geo-
p. 381). Thus, the case for intervention needs to be graphic realities might limit the options available.
firmly established before the process is allowed to pro- Finally, other aspects of the intervention project,
ceed (Rothenberg, 1988). The process of intervention such as the counselor’s qualifications and adherence to
rests on the assumption that through treatment, the professional ethical codes, must also be considered
substance-abusing individual can be saved from the when planning the intervention project (Kleinig, 2004).
negative consequences of his or her behavior. However, Obviously, legal counsel is necessary to guide the
as Kleinig (2004) pointed out, the success rates of exist- chemical dependency professional through the legal
ing treatment modalities do not offer much of a guaran- quagmire that surrounds the intervention, and chemi-
tee that this assumption will be met. At the very least, a cal dependency professionals are advised to consult
thoughtful and honest assessment of the risks, benefits, with an attorney about specific laws that might apply to
and alternatives to treatment as the goal of the interven- the process of intervention in their state, as well as fed-
tion project should be carried out (Kleinig, 2004). eral guidelines that might supersede state laws (Scott,
Another concern is the patient’s informed consent is 2000).
a necessary component of the intervention project
(Kleinig, 2004). In the past, the authoritative assertion
Intervention via the Court System
of the health care professional that the intervention was
necessary was deemed sufficient; now, however, the It is unfortunate that court-mandated treatment is
legal environment holds that the patient must offer in- viewed not so much as an opportunity for intervention
formed consent before participating in any form of as a punitive response by the legal system to the prob-
treatment, including intervention (Kleinig, 2004). One lem of substance use disorders, such as driving under
of the tenets of informed consent is that the individual the influence of alcohol or drugs (Dill & Wells-Parker,
is free to refuse the proposed treatment at any point. 2006). In reality, court-ordered treatment reflects the
But to complicate matters, there are exceptions to this theory that while internal motivation appears to be nec-
rule. Kleinig (2004) suggested that one such exception essary for the individual to change his or her substance
is in such cases where harm will occur to one individ- use behavior, external motivation can promote absti-
ual because of the chemical abuse problem of a second nence during the critical early stages of recovery while
the individual possibly develops the internal motivation (Wells-Parker, 1994). Further, the author concluded
to sustain a recovery program (DiClemente, Bellino, & that DWI offenders who were mandated to treatment
Neavins, 1999; Satel, 2000; Satel & Farabee, 2005). In- had a 30% lower mortality rate than untreated offend-
dividuals who participate in court-mandated treatment ers, although the exact mechanism through which
arrive at this point through a variety of mechanisms. treatment might reduce mortality is still not clear at this
Some have been convicted of driving while under the time.
influence of alcohol or drugs (a DWI, as it is called in There are many problems with the concept of
some states), for possession of chemicals, or for some court-mandated treatment. First, by law, third-party
other drug-related offense. payers might refuse payment for such treatment (Dill &
Court-mandated treatment is often offered as an Wells-Parker, 2006). Further, individuals who are court-
“either/or” condition: either the client successfully com- ordered into treatment do only about as well as those who
pletes the selected treatment, or the client will be re- were self-referred into treatment (Kleber, 1997; Miller,
turned to incarceration for a specified period of time. 1995; Satel & Farabee, 2005). Court-mandated treat-
The threat of court-mandated consequences has been ment is not a guarantee of success for a number of rea-
viewed as providing an incentive for the client to re- sons. Three were identified by Howard and McCaughrin
main in treatment until he or she has started to inter- (1996). The authors examined 330 treatment programs
nalize the goals and philosophy of recovery (Satel & that accepted court-mandated treatment patients but
Farabee, 2005). Such either/or treatment admissions did not utilize methadone. The authors found that (a)
are often easier to work with than voluntary admissions treatment programs whose staff did not view the fact
to treatment. Court-sponsored intervention is a power- that the client was court-ordered into treatment as a
ful incentive for the individual to complete the treat- hindrance had better client outcomes; (b) programs with
ment program he or she selected, and research suggests more than 75% court-mandated referrals had poor
that those individuals in treatment at the invitation of client outcomes; and (c) treatment programs that al-
the court system do tend to work harder on treatment lowed the court-mandated client some input into his or
goals than individuals who volunteered to enter treat- her length of stay, whether the employer was to be noti-
ment (Moylan, 1990; Satel, 2000). fied that the individual was in treatment, the treatment
Further, the fact that there is a legal hold on the per- goals, and treatment methods seemed to have better
son means that there is less chance for the client to client outcomes than programs that did not grant these
leave treatment when he or she is confronted about the rights.
substance use problem. The circumstances surround- These findings, while suggestive, do not show uni-
ing the individual’s admission make it quite difficult for versal support among clinicians. For example, Jaffe and
him or her to deny that there is a chemical use prob- Anthony (2005) suggested that court referrals might be
lem, although this has been known to happen! said to “coerce” (p. 1152) people into treatment, and
Individuals who are “legally induced to seek treat- that the outcome of such a process is simply “coerced
ment” (Collins & Allison, 1983, p. 1145) have been abstinence” (p. 1152). Peele (1989) argued that treat-
found to present a less severe clinical profile at the time ment should never be substituted for legal sanctions,
of admission than clients who present for admission noting that court-ordered punishment is often as effec-
without court pressure (Kelly, Finney, & Moos, 2005). tive, or even more effective, than the treatment’s impact
They are also as likely to benefit from treatment as on the individual. In place of treatment, Peele (1989)
those who enter treatment on a voluntary basis (Kelly argued that drug/alcohol users be held responsible for
et al., 2005; Ouimette, Finney, & Moos, 1997; Satel & their actions, including the initial decision to use chemi-
Farabee, 2005). Further, there is evidence that those cals, and that chemical use or abuse did not excuse
who seek treatment at the invitation of the court system them from responsibility for their behavior. Thus the
might remain in treatment longer than patients who are final question of the efficacy of such legal sanctions in
in treatment on their own initiative, a finding that seems the treatment of chemical abuse has not been settled at
to mitigate some of the negative aspects of their pretreat- this time.
ment lifestyle (Satel & Farabee, 2005). Such individuals Drug court is a concept that was first tried in 1989
also appear to be slightly less likely to reoffend than (Taylor, 2004). Since then, at least 1,180 drug court
those who elect to accept incarceration for their crimes, programs have been established in at least 40 different
especially if the original offense was operating a motor states (Huddleston, Freeman-Wilson, & Boone, 2004;
vehicle while under the influence of alcohol or drugs Taylor, 2004). The drug court model will
quickly identify substance abusing offenders and motivation (Wild et al., 1998). According to the Johnson
place them under strict court monitoring and com- Institute (1987), this is unusual, although it does hap-
munity supervision, coupled with effective, long-term pen. It is more common, however, to learn that the
treatment services. . . . the drug court participant un- substance-abusing person would continue to use chem-
dergoes an intense regimen of substance abuse and icals if he or she could do so. It is for this reason that
mental health treatment, case management, drug external pressure of some kind, be it family, legal, med-
testing, and probation supervisionwhile reporting to ical, or professional penalties, is often necessary to help
regularly scheduled status hearings before a judge the addicted person see the need to enter treatment.
with specialized expertise in the drug court model.
(Huddleston et al., 2004, p. 1)
Other Forms of Intervention
Such programs are most effective with first-time of- Morgan (2003) suggested that contingency manage-
fenders (Goldkamp, White, & Robinson, 2002), breaking ment techniques are often effective in working with in-
the “revolving door” cycle of repeated offenses for those dividuals with substance use problems. Another way to
who might turn aside from their current life direction. view contingency management is that the client is con-
The drug court program includes frequent urine toxi- fronted with an either/or situation: “Either you stop
cology testing conducted at least weekly if not more drinking, or I will _____.” Clients who enter treatment
often. Consequences for “dirty” urines or failure to par- under such circumstances might be said to demon-
ticipate in agreed-upon treatment programs are immedi- strate controlled motivation (Wild et al., 1998). A com-
ate. But rewards for participation and progress are equally mon source of such external motivation is when a
swift. Such programs have a lower recidivism rate than physician threatens to file commitment papers on the
traditional legal sanctions and are quite cost effective individuals with a substance use problem unless he or
(Huddleston et al., 2004; Reuter & Pollack, 2006; Taylor, she enters treatment. Also, with the advent of worksite-
2004). New York State, for example, found that drug mandated urine toxicology testing, it is not uncommon
court saved $250 million in a year’s time, while St. Louis, for employees to be referred to a specific form of treat-
Missouri, found that every dollar invested in drug court ment after failing a worksite urine toxicology test. An-
resulted in a savings of $6.32 in welfare, medical, and other source of external motivation might be supplied
law enforcement expenses (Taylor, 2004). Further, drug by the spouse, in the form of a promise that “either you
court clients are more likely to successfully complete stop using chemicals or I will leave/seek a divorce!”
mandated treatment programs, thus reducing the risk of Employer-mandated treatment. With the advent of
recidivism in the future (Satel & Farabee, 2005). widespread urine toxicology testing at the job site and
Court-ordered involuntary commitment. In more increasing sensitivity of industry to the economic losses
than 30 states it is possible for people to be committed incurred from employee substance abuse, employer-
to treatment against their will if the courts have suffi- mandated treatment referrals are becoming more and
cient evidence to believe they are in imminent danger more common. But there is little research data to pro-
of harming themselves or others (Gendel, 2006; Olson vide hints as to which forms of intervention are most ef-
et al., 1997). The exact provisions of such a court- fective in the workplace (Roman & Blum, 1996). It has
ordered commitment vary from state to state but usu- been found that although employees who had to be co-
ally are imposed in cases where the individual has erced into treatment under threat of loss of employment
failed to respond to less intensive interventions (Olson tend to have more serious substance use problems, they
et al., 1997). In spite of the frequency with which these also tend to benefit more from treatment (Adelman &
laws are used to commit individuals to treatment for Weiss, 1989; Lawental, McLellan, Grissom, Brill, &
SUDs, there is little research into the effectiveness of O’Brien, 1996). Employer-mandated treatment has been
this form of intervention (Olson et al., 1997). Wild, justified from an economic standpoint. For example, a
Cunningham, and Hobdon (1998) suggested that clients company with just 500 employees will typically pay
who enter treatment because of such external motivation $132,881 in health care costs for alcohol-related prob-
might comply with treatment expectations for a short pe- lems each year (Brink, 2004). Further, individuals who
riod of time without making any permanent changes in are abusing or are dependent on alcohol typically use
attitude or behavior. twice as many “sick” days and are five times as likely to
Occasionally, the individual will enter treatment on file a “workman’s compensation” claim as nondrinkers
a voluntary basis, a client who demonstrates autonomous (Brink, 2004). Thus, “constructive coercion” (Adelman &
Weiss, 1989, p. 515) might actually provide a positive In this chapter, we discussed the mechanics of the
service to those employees with substance use prob- intervention project and some of the more common
lems. However, a great deal of research is needed to de- forms that intervention might take. It was pointed out
termine which forms of intervention are most effective that the individual retains the right to choose to enter
in the workplace (Roman & Blum, 1996). treatment or to refuse to enter treatment. Persons who
participate in the intervention project must be prepared
for either choice and to have alternate plans in hand in
Summary case the addicted individual does not accept the need
The intervention process is an organized effort by sig- for treatment.
nificant others in the addicted person’s social environ- Also in this chapter, we discussed the fact that the in-
ment to break through the wall of defenses that protect dividual retains certain rights, even during the inter-
the individual from the realization that his or her life is vention process. Indeed, the individual might not be
out of control. Intervention projects are usually super- detained if he or she expresses the wish to leave the in-
vised by a substance abuse rehabilitation professional tervention session. Finally, the question of when legal
and are held with the goal of securing an agreement sanctions should be imposed or when treatment might
from the individual to immediately enter treatment. be substituted for these legal sanctions was discussed.
CHAPTER TWENTY-NINE
The Treatment of Chemical Dependency
Questions about the effectiveness of substance abuse sanctions to solve the drug use problem. The most ap-
treatment no longer sparks fierce debate among health propriate answer to the problems of SUDs would seem
professionals. As these professionals have examined the to lie in a balance between treatment and criminal jus-
impact of chemical abuse and addiction on society, they tice sanctions. In this chapter, the benefits and disad-
have seen clearly that alcohol and drug use problems vantages of treatment are discussed.
constitute a serious drain on the health care resources
of this country. To illustrate: The cost of providing med-
A Cautionary Note
ical care for each drug-addicted person is $1,000 more
per year than for individuals who do not abuse chemicals In the United States, AODA1 treatment programs de-
(Laine et al., 2001). veloped in a haphazard manner. The evolution of treat-
Breithaupt (2001) estimated the cost of treating med- ment formats was not guided by scientific feedback or
ical problems caused or exacerbated by substance use guidance (Miller & Brown, 1997). Unfortunately, treat-
disorders (SUDs) in the United States each year at $300 ment methods that are least effective seem to be the
billion. In contrast, the estimated annual cost of treat- most deeply entrenched in the United States (Miller,
ment for SUDs in this country is just $16–18 billion a Andrews, Wilbourne, & Bennett, 1998; Miller & Brown,
year (Smith et al., 2006). Admittedly, substance abuse 1997). Fierce debates have raged in the professional lit-
rehabilitation is not perfect, but its success rate com- erature as to which form of treatment is most effective
pares very well with that of other chronic, relapsing dis- for individuals with substance use disorders, and the
eases such as diabetes, hypertension, or multiple sclerosis question is far from resolved.
(Frances & Miller, 1998; McLellan, 2001). The return
for every dollar invested in rehabilitation efforts is esti- Characteristics of the Substance
mated to range from $4 to $12 (Breithaupt, 2001; Dobbs,
Abuse Rehabilitation Professional
2007; Frances & Miller, 1998; Mee-Lee, 2002) to as
much as $50 (Garrett, 2000). In the late 1990s California The relationship between the client and the counselor is
conducted a research study that found that an invest- of such critical importance to the rehabilitation process
ment of $209 million for drug treatment resulted in a that it has been compared to the individual’s initial re-
savings of $1.5 billion in terms of reduced criminal ac- lationship with his or her parents (Bell, Montoya, &
tivity and health care costs (Craig, 2004). This reduc- Atkinson, 1997). To effectively help persons with sub-
tion in health care costs might be seen in the finding stance use disorders, the helper should have certain
that the typical alcohol-dependent individual requires characteristics. For example, individuals who are deal-
10 times the health care expenditure as the nonalco- ing with chemical dependency or psychological issues
holic, while family members of alcoholics utilize five of their own should be discouraged from actively work-
times the health care resources of normal family mem- ing with clients in treatment, at least until they have re-
bers (McLellan, 2001). solved their own problems. This injunction makes
These statistics would suggest that substance abuse sense: If the counselor is preoccupied with personal
treatment is the answer to the nation’s drug abuse prob- problems, including those of chemical addiction, he or
lem. Unfortunately, treatment by itself is unlikely to re- she would be unlikely to be able to help the client ad-
solve the problem of drug abuse in the United States vance further in terms of personal growth. “The therapist
(Reuter & Pollack, 2006). But, as will be discussed in
Chapter 37, it is also not possible for society to use legal 1Which stands for “alcohol or drugs of abuse.”
332
The Treatment of Chemical Dependency 333
who works with patients with substance use disorders TABLE 29.1 Factors That Facilitate or Inhibit Recovery
. . . possesses many characteristics, some of which in- From Substance-Use Problems
clude genuineness, empathy, modeling the desired
Factors that facilitate Factors that inhibit
behavior, and an appropriately humorous outlook”
abstinence abstinence
(Shea, 2006, p. 13). Further, the therapist should be
adapt at guiding clients toward recovery rather than Empowerment Disempowerment
telling them what they need to do, according to Shea.
Active interest in Hostility, disinterest
Most clients have the resources to solve their own prob-
client as person
lems if they are assisted in finding that solution within
themselves (Shea, 2006). Thus, it is the therapist’s job Empathy Confrontation
to assist and guide, not to demand or order clients in Making client feel Making client feel that she or
their search for the answers. These skills are especially responsible for change he is not responsible for
important during the early stages of treatment when change
the client’s commitment toward making a major life Advice about how to change Ordering client to change
change is still tentative and weak (Adelman & Weiss,
1989; Connors, Carroll, DiClemente, Longabaugh, & Helping client find a Hopelessness or powerlessness
sense of hope
Donovan, 1997; Joe, Simpson, Dansereau, & Rowan-
Szal, 2001; Simpson, 2004). Involving client in Giving client a passive role
Clients who enter a rehabilitation program do so change process
with different levels of motivation and problem severity Environment will support Environment does not support
(Simpson, 2004). In a sense, clients who enter a reha- recovery the client’s recovery
bilitation program are admitting that they have been
Source: Based on Miller (2003).
unable to change on their own (Bell et al., 1997). As the
client is unable to make the desired change without
professional assistance, it would make sense that the Confrontation has been a central feature of many reha-
therapist with the strongest interpersonal skills would bilitation programs and in theory is used to help the
be better equipped to help the client change. At the client begin to understand the impact that substance
same time, it is obvious that the client’s acceptance of use has had on his or her life. But there is little evidence
the therapist’s efforts is one of the most essential charac- that such confrontation actually helps to bring about
teristics of a successful therapeutic relationship (Bell behavior change (Hester, 1994; Miller, 1995; Miller &
et al., 1997). Such a therapeutic relationship would be Rollnick, 2002; Miller et al., 1993; Washton, 1995;
based on mutual trust, the client’s ability to depend on Zoldan, 2000).
the therapist and be open with him or her, and the indi- Harsh, confrontational treatment approaches are
vidual’s ability to accept external help (Bell et al., counterproductive when applied to substance abusers
1997). Miller (2003) identified several factors that seem (Miller, 2003; Miller et al., 1993; Miller et al., 1998).
to facilitate or inhibit recovery from a substance use This makes clinical sense, since one factor that predicts
problem (see Table 29.1). successful treatment outcomes is the client’s satis-
One common misperception of AODA treatment faction with the rehabilitation process (Hser, Evans,
professionals is that they are “bleeding hearts” who will Huang, & Anglin, 2004). Few people would enjoy the
excuse virtually any misdeed by the client because of levels of confrontation once thought necessary by sub-
his or her SUD. Indeed, many therapists in the early stance abuse rehabilitation professionals. Indeed, as the
stages of their careers attempt to “buy” client approval therapist’s level of confrontation increases, the client’s
through such permissiveness. Remember: Caring for a level of resistance increases proportionally (Miller et al.,
client does not mean protecting him or her from the natu- 1993).
ral consequences of his or her behavior. To counter this resistance, empathy combined with
Confrontation and other treatment techniques. For a a “supportive-reflective” (Miller et al., 1993, p. 455)
number of years, substance abuse rehabilitation in the style of therapy seems to be effective (Miller, 1998;
United States has used a “hard-hitting, directive, exhorta- Miller et al., 1998). Ramsay and Newman (2000) sug-
tional style” (Miller, Benefield, & Tonigan, 1993, p. 455) gested that when confrontation is necessary it be in-
designed to overwhelm the client’s defenses against his fused with caring and concern. Clients should not be
or her acceptance and understanding of the disease. “shamed” into conformity but should be allowed to save
334 Chapter Twenty-Nine
face, with the therapist initially placing emphasis on their This new treatment approach, since called the Min-
distress and slowly assisting them as they learn how the nesota Model of treatment, was designed to work with
chemical abuse contributed to those problems. Such a dependency on alcohol (“ONDCP Gives Rundown,”
therapeutic style places emphasis upon clients’ ability to, 1990). Since its introduction it has also been used to
and responsibility for, change, combined with therapist treat other forms of chemical addiction. The Minnesota
advice, the development of behavioral alternatives, and Model utilizes a treatment team comprised of chemical
attempts to help clients achieve a sense of self-efficacy. dependency counselors familiar with A. A., psychologists,
physicians, nurses, recreational therapists, and clergy, all
of whom work with the client during the treatment
The Minnesota Model of Chemical
program.
Dependency Treatment The Minnesota Model allows each professional to
To say that what has come to be called the Minnesota make recommendations for the client’s treatment plan.
Model of chemical dependency treatment has been a When treatment goals are established, the professionals
success is something of an understatement. Within a meet as a team to discuss the areas they feel should be
short time of its inception, it became and has remained the focus of treatment. The treatment team meeting is
the dominant model for rehabilitation programs in the chaired by the individual who is ultimately responsible
United States (Foote, 2006; Ringwald, 2002). With the for the execution of the treatment process, known as the
changes in insurance program reinbursement policies case manager. This is usually the chemical dependency
in the late 1990s, the basic model has been revised. But counselor. Interested persons such as the client, his or
it still remains a strong influence on both inpatient and her parole/probation officer, and family members are
outpatient rehabilitation program formats (Foote, 2006; all invited to participate in the treatment plan meeting.
Ringwald, 2002). As a result of this meeting, a formal treatment plan is
The Minnesota Model was designed in the 1950s by developed. The treatment plan will be multimodal and
Dr. Dan Anderson. In order to earn money to finish his offer a wide variety of goals and recommendations. It
college education, Dr. Anderson worked as an attendant will identify specific problem areas, behavioral objec-
at the state hospital in Willmar, Minnesota (Larson, tives, methods by which to measure progress toward
1982). Following graduation, Anderson returned to the these objectives, and a target date for each goal. The
state hospital as a recreational therapist. He was as- treatment plan is discussed in more detail in the next
signed to work with the alcoholics who were in treat- section of this chapter; a flowchart of the treatment
ment there, the least desirable position at that time. plan process is shown in Figure 29.1.
Anderson was himself influenced by the work of Mr. The strength of the Minnesota Model of treatment
Ralph Rossen, who was later to become the Minnesota lies in its redundancy and its multimember concept.
State Commissioner of Health. At the same time, the Thus, the chemical dependency counselor does not
growing influence of Alcoholics Anonymous was utilized need to be a “jack of all trades, master of none.” This
by Dan Anderson and a staff psychologist, Dr. Jean Rossi, feature helped to make the Minnesota Model one of
as a way to understand and work with the alcoholic. They the dominant treatment program models in the field of
were supported in this approach by the medical director chemical dependency rehabilitation for more than 40
of the hospital, Dr. Nelson Bradley (Larson, 1982). years, although under managed care it has been modi-
These individuals joined together in an effort to un- fied or replaced by other treatment formats.
derstand and treat the patients who were sent to the Reaction to the Minnesota Model. The Minnesota
state hospital for treatment of their alcoholism. Each Model has been challenged for a number of reasons.
profession contributed a different perspective on the pa- First, although the model was designed to work with
tients’ needs and issues that should be addressed to help alcohol-dependent clients, it has been utilized in the
these patients abstain from chemicals. Initially, the role treatment of virtually every known form of substance
of spiritual advisor was filled by the Reverend John abuse in spite of little evidence that it is effective in
Keller, who had been sent to Willmar State Hospital to such cases (“ONDCP Gives Rundown,” 1990).
learn about alcoholism in 1955. With his arrival, the The Minnesota Model draws heavily on the philoso-
staff had “knowledge of medicine, psychology, A. A. phy of Alcoholics Anonymous (AA), and participation
and theology together under one roof to develop a new in AA is often required. Yet AA itself is not a form of
and innovative alcohol treatment program” (Larson, treatment (C. M. Clark, 1995). Further, there is no
1982, p. 35). clear evidence that AA is effective in cases where the
Medical
Treatment
evaluation
plan
staffing
Psychological
evaluation (includes
case
Comprehensive
manager,
Social treatment plan
client,
evaluation (established in
interested
treatment plan
family
staff meeting)
members,
Recreational
and staff
evaluation
members)
Spiritual
evaluation
FIGURE 29.1 Flowchart of the Evolution of a Treatment Plan
individual is coerced into joining. Thus, there is an in- to each treatment philosophy, we briefly examine some
herent contradiction involved in the Minnesota Model of the more promising models that have emerged in the
in that one of its central tenets is mandatory participation past three decades.
in AA. Detoxification programs. Technically, the term detoxi-
Another challenge to the Minnesota Model involves fication refers to the process of removing toxins from
its length. When it was developed, the client’s length of the body. A second, related definition is the medical
stay at Willmar State Hospital was often arbitrarily set at management of the patient’s withdrawal from a drug of
28 days, but there is little research data supporting a need abuse (Haack, 1998). The process of detoxification from
for a 28-day inpatient treatment stay (Turbo, 1989). In- alcohol or drugs is not viewed as a form of treatment
deed, the optimal length of treatment for inpatient treat- in itself but as a prelude to the individual’s rehabilita-
ment programs has yet to be defined (McCusker, tion (Gerada, 2005; Leshner, 2001a, 2001b; Mattick &
Stoddard, Frost, & Zorn, 1996). Unfortunately, the 28-day Hall, 1996; Tinsley, Finlayson, & Morse, 1998). Research
treatment program became something of an industry has shown that up to 95% of people who complete
standard for Minnesota model programs for several “detox” will relapse without further treatment (Craig,
decades (Turbo, 1989) and at one time served as a guide 2004). Further, detox by itself will not address the em-
for insurance reimbursement (Berg & Dubin, 1990). In ployment, marital, or psychosocial problems that so
spite of its popularity, however, there is little evidence to often complicate recovery from addictions (Gerada,
suggest that the Minnesota Model is actually effective 2005).
(Hester & Squires, 2004; McCrady, 2001). Fortunately, it Thus detox is the first step in the process of rehabili-
has become almost extinct except at a few private treat- tation for individuals with substance abuse problems.
ment centers where clients can afford to pay for their The goal of the detoxification process is to offer the
own extended substance abuse rehabilitation programs patient a safe, humane, withdrawal from alcohol/drugs
(Monti, Kadden, Rohsenow, Cooney, & Abrams, 2002). of abuse (Mattick & Hall, 1996). The patient’s safety is
assured, to the degree that this is possible, by having the
detoxification process carried out under the supervision
Other Treatment Formats
of a physician who is both trained and has experience
for Chemical Dependency
in this area of medicine (Miller, Frances, & Holmes,
In the last years of the 20th century, rehabilitation pro- 1988). The physician will evaluate the patient’s needs
fessionals explored a number of treatment approaches and resources, and then recommend that the process of
to alcoholism rehabilitation that differed from the Min- detoxification be carried out either on an inpatient or
nesota Model. While it is not possible to do full justice an outpatient basis.
Although detoxification from alcohol/drugs has tra- to the patient but there is strong evidence that opiate-
ditionally been carried out in a hospital setting, only dependent patients who are detoxified on an inpatient
10%–15% of alcohol-dependent persons will require basis are more likely to complete the detoxification
hospitalization for detoxification from alcohol (Anton, process (Mattick & Hall, 1996).
2005; Blondell, 2005). Individuals who have a history There is some debate as to whether detoxification
of serious physical or psychiatric illness, who have been programs should function as a “funnel” for guiding pa-
unable to successfully complete outpatient detoxifica- tients into the rehabilitation process. When detoxifica-
tion in the past, who have a history of withdrawal tion is carried out at a free-standing clinic, many
seizures, or who are geographically isolated are among patients fail to go on to participate in rehabilitation pro-
those who should be hospitalized for detoxification grams (Miller & Rollnick, 2002). On the other hand,
(Anton, 2005). With careful screening, more than 90% the charge has been made that detoxification programs
of alcohol-dependent patients can be detoxified on an that are housed in treatment settings are often little
outpatient basis (Abbott, Quinn, & Knox, 1995; Blondell, more than recruitment centers for the treatment pro-
2005). gram. To counter this danger, the patient should be ad-
Patients who are selected for outpatient detoxifica- vised of his or her treatment options, including the
tion, called “ambulatory detox” (Blondell, 2005) or “so- possibility of seeking treatment elsewhere, in order to
cial detox” (Mattick & Hall, 1996), must first be evalu- avoid a possible conflict of interest.
ated by a physician. Then, depending on their medical Whether detoxification is carried out on an inpa-
status, the patient might be sent home with instructions tient or an outpatient basis, the patient being with-
on how to complete the detoxification process, or re- drawn from chemicals should be closely monitored by
ferred to a special detoxification setting. In either case, staff to detect signs of drug overdose or seizures, to
the patient’s progress after this point is monitored by a monitor medication compliance, and to ensure absti-
physician, nurses, or other trained personnel. When pa- nence from recreational chemical use (Miller et al.,
tients are sent home, they might have a nurse stop by to 1988). Unfortunately, it is not uncommon for patients
check on their progress once or twice a day or be in- who are addicted to chemicals to “help out” the with-
structed to see their physician on a daily basis (Anton, drawal process by taking additional drugs when they are
2005; Prater, Miller, & Zylstra, 1999). In the detoxifica- supposedly being withdrawn from chemicals.
tion center, the patient’s progress and vital signs are The process of detoxification is vulnerable to being
monitored as often as necessary. abused in other ways besides having the patient self-
Depending on how the individual fares during the administer alcohol or drugs. Some individuals who are
process of detoxification, a referral to an inpatient set- addicted to alcohol/drugs will go through detoxification
ting might be necessary (Anton, 2005). But if she or he dozens or hundreds of times just to get a place to live
is able to cope with the alcohol withdrawal syndrome (Whitman, Friedman, & Thomas, 1990). Others will
through the use of home medical care, a significant “check into detox” as a place to hide because of drug
cost savings can be achieved while the patient is safely debts or to try and escape from the police. Individuals
withdrawn from alcohol. who are addicted to opiates have been known to enter a
The individual’s drug abuse history plays an impor- detox program when they are unable to obtain drugs or
tant role in whether to refer the patient to an inpatient when they want to lower their daily drug requirement
or outpatient detoxification program. Some of the to more affordable levels. At other times, the authorities
drugs of abuse can, when the patient is addicted to might create a panic by arresting a major drug supplier
them, cause severe or even life-threatening problems or by breaking up a major drug supply source. In such
during the detoxification process. Further, polydrug ad- cases, it is not uncommon for large numbers of opiate-
diction is so common that the physician is advised to dependent patients to seek admission to detox to have a
obtain a urine sample for toxicology testing to rule out source of drugs while they wait for new supplies of opi-
abuse of compounds that require inpatient detoxifica- ates to become available through illicit sources. Thus,
tion (Blondell, 2005). Withdrawal from substances while detoxification programs provide a valuable service,
such as the barbiturates or benzodiazepines can result they are also vulnerable to abuses.
in life-threatening seizures for patients who are physi- Videotape/self-confrontation. The utilization of video-
cally dependent on these drugs. In the case of opiate tape to show people how they looked and behaved
withdrawal, there is little evidence that the detoxifica- while intoxicated, usually while in the emergency
tion process can cause any significant physical danger room/admissions unit, has long been viewed as a useful
means of demonstrating to clients their behavior while nonexistent within the dysfunctional family. These and
intoxicated. There are few data to support this form of a multitude of other issues can be addressed within the
confrontation, and some data suggest that it might con- context of family/marital therapy.
tribute to higher than anticipated client dropout from The effectiveness of marital therapy as a treatment
treatment (Hester & Squires, 2004). modality for chemical dependency has repeatedly been
Acupuncture. A form of “alternative medicine,” demonstrated in the clinical literature (Fals-Stewart et al.,
acupuncture is occasionally applied to the treatment of 2004). It is a specialized area of expertise with a vast,
the addictive disorders. Individual case reports have evolving literature of its own, requiring specialized train-
suggested that acupuncture may have a calming effect ing in the areas of substance abuse rehabilitation and
on some individuals and may reduce craving for chemi- marital therapy in order to be utilized effectively.
cals. The theory behind acupuncture is beyond the scope Group therapy approaches. The most common treat-
of this text. In brief, small sterile needles are inserted into ment modality for substance abuse treatment is group
specific locations on the individual’s body in an attempt therapy (Weiss, Jaffee, de Menil, & Cogley, 2004). Ad-
to liberate or block the body’s energy. vocates of group therapy approaches suggest that this
At this time, there is limited evidence that acupunc- modality offers a number of advantages over individual
ture is effective in the rehabilitation of substance abusers therapy (Connors, Donovan, & DiClemente, 2001;
(Hester & Squires, 2004). Margolin et al. (2002) con- Yalom, 1985). One of the most important of these ad-
cluded that acupuncture does not seem to be effective vantages is that therapy groups allow one professional to
by itself as a treatment for cocaine addiction. Ernst work with a number of different individuals at once.
(2002) concluded that the “complementary therapies” Second, in the therapy group, group members are able
(p. 1491) such as acupuncture were about as effective to learn from each other and to offer feedback to each
as placebos in treating the addictive disorders. other. Third, group members provide behavioral mod-
Family and marital therapy. Although once looked els for each other, and this is useful for those clients
upon with some measure of disdain, family and marital who do not trust the therapist. The group format pro-
therapy have been proven to be valuable components of vides an opportunity for clients to work on many of the
alcohol/drug rehabilitation programs and are now con- interpersonal deficits that contribute to their own addic-
sidered an integral part of treatment except in unusual tion within the safety of the group setting. Finally, be-
circumstances (Fals-Stewart, O’Farrell, & Birchler, 2003, cause of the nature of the therapy group, clients can
2004). The best known and most common form of fam- often find within the group members a reflection of
ily therapy is the family disease approach, which holds their family of origin, allowing them to work through
that substance misuse is an illness of the family, not just problems from earlier stages of growth.
the person with the substance use problem (Fals-Stewart While individual sessions might be utilized for spe-
et al., 2003, 2004). Within this framework, the therapist cial problems too sensitive to discuss in a therapy group
and family members work to identify the role that the situation, clients are usually encouraged to bring their
substance abuse plays within the family and to correct concerns to group, which may meet every other day,
dysfunctional interaction patterns such as communica- daily, or more often than once a day, depending on the
tions problems. In many marriages or families where pace of the program. Unfortunately, there is limited ev-
one partner has a substance use problem, communica- idence that group psychotherapy approaches are at all
tion patterns tend to be unhealthy, helping to support effective in the rehabilitation of substance abusers
the individual’s addiction (Alter, 2001). For this reason (Hester & Squires, 2004; Weiss et al., 2004). Group
marriage and family therapy approaches that stress therapy formats that utilize cognitive-behavioral ap-
communications skills training are four to five times as proachs to identify and help clients learn how to deal
effective as rehabilitation programs that focus on the in- with painful affective states that might contribute to the
dividual (Alexander & Gwyther, 1995). urge to use chemicals seem to be effective in working
Such therapy is quite difficult. It is not uncommon with personality-disordered substance abusers (Fisher &
for the defense systems of the addicted member and Bentley, 1996).
other family members to be inter-reinforcing (Williams, McCrady (2001) pointed out that women who have
1989). As a result of this pattern of interlocking defense substance use problems seem to be somewhat inhibited
systems, the family will, as a unit, resist any change in in group settings, possibly because of shame-based issues.
the addicted person’s behavior. Also, as discussed in the Further, the author suggested, the elderly might feel
chapter on codependency, boundaries are often fluid or overwhelmed by the complex pattern of interactions
within the group setting. In such cases the individual cant changes on standard psychological tests used to
might respond more favorably if seen on an individual measure the personality pattern of the respondent, and
basis. Thus, while group therapy approaches are a com- that these changes continued over an extended follow-
mon treatment modality, there is limited evidence at up period. It was suggested by the authors that
best as to their effectiveness. biofeedback training, especially alpha and theta brain
Assertiveness/social skills training. Many individuals wave training, might offer a new, possibly more effec-
with substance use problems began to abuse alcohol or tive treatment approach for working with the chronic
drugs while they were adolescents, and this interfered alcoholic.
with their developing the interpersonal skills necessary Ochs (1992) examined the application of biofeed-
for adulthood (Monti et al., 2002). There is evidence back training techniques to the treatment of addictive
assertiveness training is useful as an adjunct to rehabili- disorders. The author concluded that the term biofeed-
tation in such cases, helping to build clients’ self- back training for the addictions was a bit misleading as
esteem and self-confidence and aiding the development different clinicians employed a wide range of tech-
of interpersonal relationship skills (Monti et al., 2002). niques and a wide range of body functions for biofeed-
Such social skills programs might include training in back training. In spite of the variations in treatment
more effective communication and substance use re- techniques, the author found that biofeedback training
fusal skills, as well as helping the recovering individual for the treatment of addictive disorders did seem to have
learn to increase non-drug-related pleasant activities value, especially when biofeedback was integrated into
(Morgan, 2003). While social skills training is not the pri- a larger treatment format designed to address social,
mary focus of the rehabilitation program, it does seem to economic, vocational, psychological, and familial prob-
provide a useful tool for those who turn to alcohol/drugs lems. Thus, there is evidence that biofeedback training
as a way of coping with their perceived weak interpersonal might be a treatment method that will play an increas-
coping skills (Morgan, 2003). ing role in the treatment of addictive disorders.
Self-help groups. The topic of self-help or 12-Step Harm reduction model. The harm reduction (HR)
groups is discussed in Chapter 35. However, the reader model of substance abuse rehabilitation is quite differ-
should be aware that participation in these groups is ent from the Minnesota Model or the other models of
often a valuable adjunct to substance abuse rehabilita- treatment discussed in this chapter. It is based on the as-
tion programs. sumption that it is possible over time to change the be-
Biofeedback training. A number of treatment plans havior of individuals with SUDs, including the ways
advocate the use of biofeedback training as an aid to the they use chemicals so that they will gradually come to
treatment of addictive disorders. The technique of behave in ways that reduce the consequences of their
biofeedback involves monitoring select body functions, substance abuse (MacCoun, 1998). This model is in
such as skin temperature or muscle tension, and provid- sharp contrast to “zero tolerance” (Marlatt, 1994) or
ing information to the individual as to how his or her supply reduction (MacCoun & Reuter, 1998) models
body is doing. Depending on the parameter selected (i.e., of chemical use intervention.
muscle tension of a certain muscle group, skin temper- Methadone maintenance (discussed in Chapter 33)
ature, brain wave patterns) and the training provided, is a good example of HR, as it is thought to be better to
the individual is thought to be able to learn how to have the individual using opioids in a controlled man-
modify his or her body functions at will. This skill, in ner while working toward recovery than to be abusing
turn, is thought to allow the individual to learn how to illicit drugs. Another example of the HR philosophy is
change these body functions in a desired direction, the “needle exchange” programs in place in several
such as to relax without the use of drugs. cities around the country. Because the virus that causes
Peniston and Kulkosky (1990) attempted to teach a AIDS is often transmitted through contaminated intra-
small number of patients in an alcoholic treatment pro- venous needles, some cities allow intravenous drug
gram to change the frequency with which their brain abusers to exchange “dirty” needles for new, uncontami-
could produce two specific electrical patterns, known nated ones. It has been estimated that such programs will
as alpha and theta waves. These patterns of electrical pay for themselves if they prevent just one or two individ-
activity in the brain are thought to reflect the process of uals from contracting HIV-1 infection2 per year. Further,
relaxation and stress-coping responses by the individ-
ual. The authors found that their sample had signifi- 2Discussed in Chapter 34.
there is little evidence of an increase in drug use in com- The following example is a treatment goal for a
munities with needle exchange programs (MacCoun & 24-year-old male who is polydrug addicted (cocaine,
Reuter, 1998). Unfortunately, in spite of their apparent alcohol, marijuana, and occasionally benzodiazepines)
advantages, there is strong resistance toward the estab- and who has abused alcohol/drugs daily for the last
lishment of such programs in many communities. 27 months:
Problem: Client has used chemicals daily for at least

The Treatment Plan the past 2 years and has been unable to abstain from
No matter what treatment approach the therapist elects drug use on his own.
to utilize, he or she should develop a treatment plan to Long-Term Goal: That the client abstain from fur-
guide work with the client. The treatment plan is based ther chemical abuse.
on information obtained during the assessment process
and “serves as the plan of action for pursuing the identi- Short-Term Objective: That the client not use mood-
fied goals of treatment” (Connors et al., 2001, p. 82). It altering chemicals for 90 days.
is a highly specific form, which in some states might be Method of Measurement: Random supervised urine
viewed as a legal document. Different treatment cen- toxicology screens to detect possible drug use. Patient
ters tend to use different formats, depending upon the self-report.
specific treatment format being utilized and the licen- Methodology: Client to attend AA daily for 90 days
sure requirements in that state. and at least four times a week for the next 90 days
However, all treatment plans share several similari- after this time. Daily telephone contact with thera-
ties. First, the treatment plan should provide a brief pist at time designated. Individual psychotherapy ap-
summary of the problem that brought the client into pointments with therapist twice weekly, during first
treatment. Another section might provide a brief sum- 90 days, and once/week after that time. Also assigned
mary of the client’s physical and emotional state of readings to be completed during designated periods.
health. A third section might contain the individual’s Written assignments, as assigned. Urine toxicology
own input into the treatment process—what he or she testing, as designated.
thinks should be included in the treatment plan. The
section where the specific goals of treatment are identi- Target Date: Scheduled discharge date.
fied is the heart of the treatment plan. Following this
are discharge criteria, which list the steps that must be The typical treatment plan might identify as many as
accomplished in order to discharge the client from treat- five or six different problem areas, and the goals become
ment. Finally, there is a brief summary of those steps the heart of the treatment program. Each of these goals
that are to be made part of the client’s aftercare program. might be modified as the treatment program progresses,
Treatment goals should include (a) a problem state- and each provides a yardstick of the client’s progress.
ment, or brief statement of the problem; (b) long-term
goals; (c) short-term objectives; (d) measurement criteria;
Aftercare Programs
and (e) a target date. The problem statement is short,
usually a sentence or two in length, identifying a spe- Because of the chronic, relapsing nature of the SUDs,
cific problem that will be addressed in treatment. The participation in a continuing care or aftercare program sig-
long-term goal is the ultimate objective, a general state- nificantly contributes to client abstinence from alcohol/
ment of a hoped-for outcome. The long-term goal state- drugs (Ritsher, Moos, & Finney, 2002; Smith et al., 2006).
ment is usually also only one or two sentences in Such aftercare programs should focus on issues such as
length. Following the long-term goal is a short-term ob- the (a) maintenance of gains made in treatment, and
jective. The objective is a very specific behavior that can (b) helping to prevent relapse to active chemical use or
be measured. The objective statement is usually one to abuse (McKay et al., 1998). Included in the concept of
three sentences long and identifies the measurement aftercare programs are the identification and correc-
criteria by which both the client and staff will be able to tion of the client’s mistaken beliefs that might con-
assess whether progress toward this objective is being tribute to a possible relapse, as well as helping the client
made. Finally, there is the target date, or the specific establish and monitor “the habit of sobriety” (Downing,
date by which this goal will be achieved. 1990, p. 22).
Participation in self-help groups such as Alcoholics Summary

Anonymous or Narcotics Anonymous is often part of
the aftercare program, especially programs based on the This chapter reviewed the Minnesota Model of treat-
Minnesota Model of treatment (C. M. Clark, 1995). ment, one of the primary treatment models found in
Medical problems identified earlier in the rehabilita- this country. The concept of a comprehensive treatment
tion process are also addressed in the aftercare program, plan, which serves as the heart of the treatment process,
as are needs for such issues as transitional living facili- was also discussed. Various pharmacological supports
ties or special needs. The aftercare program is designed for persons who are in the early stages of sobriety and
and carried out on the assumption that treatment does for those going through detoxification from chemicals
not end with the individual’s discharge from a formal were explored in this chapter.
rehabilitation program. Rather, treatment is the first The role of assertiveness training, biofeedback, and
part of a recovery program that (hopefully) continues marital and family therapy as a component of a larger
for the rest of the individual’s life. The aftercare compo- treatment program were examined. The use of blood
nent of the treatment plan covers issues that should be and urine samples for toxicology screening to detect
addressed following discharge from the rehabilitation medication compliance and illicit drug use was also re-
program. viewed.
CHAPTER THIRTY
The Process of Recovery
It is common for substance abuse rehabilitation profes- Prochaska (Prochaska, 2002; Prochaska, DiClemente, &
sionals to speak of the process of recovering from a drug/ Norcross, 1992). This model of the change process is
alcohol use problem as if this were a single step. In real- based on the assumption that the person recovering from
ity the addictions “are often wrongly viewed as acute con- drug abuse/addiction passes through definite stages, and
ditions, like a broken leg or infection, that can be fixed that individuals at each different point have different char-
by brief episodes of treatment” (“Addiction Recovery,” acteristics (Connors, Donovan, & DiClemente, 2001;
2005, p. 1, italics added for emphasis). Thus, recovery Sadock & Sadock, 2003).
from this disorder is a process, which, like life itself, has The first stage of recovery is precontemplation (Blume,
a definite beginning, but no definite end point. In this 2005; Connors et al., 2001; DiClemente, Bellino, &
chapter, the process of recovering from an alcohol/drug Neavins, 1999; Prochaska, 1998, 2002). About 40% of the
abuse problem is discussed. population is thought to be in this stage (DiClemente &
Prochaska, 1998; Prochaska, 2002). During precontem-
plation the individual is actively abusing chemicals and
The Decision to Seek Treatment has no thought of trying to abstain from chemical use or
Researchers have discovered that several factors impact abuse. This phase can continue for years or decades. It is
the individual’s decision to seek treatment for a sub- during this phase that denial and rationalization are most
stance use disorder, including the severity of his or her prominent (Ramsay & Newman, 2000). Also, clients in
substance abuse problem (abuse versus dependence) this stage will overestimate the problems inherent in
and the severity of the consequences of that chemical quitting while underestimating their available resources
abuse on the individual (Kessler et al., 2001). Those for change (Prochaska, 2002). If they are in treatment
who seek formal treatment tend to be more impaired as a result of external pressure, they also might attempt
and to have more severe life problems than those who to use compliance as a defense against the pressure to
are able to abstain without formal intervention (Moos, change (Blume, 2005).
2003). On average, people with substance use disorders The challenge for the therapist who is faced with
seek professional treatment after about 5–8 years of de- clients in this phase is (a) to teach them the effects of
pendence on a chemical or 10–19 years of heavy abuse the drugs of abuse, (b) to teach them the dangers associ-
(Kessler et al., 2001). Substances that result in greater ated with continued substance use/abuse, (c) to help
levels of impairment (cocaine or heroin, for example) awaken within the clients a desire for a different lifestyle,
will generally cause a person to enter treatment earlier (d) to help them identify barriers to their recovery, and
than chemicals such as alcohol (Kessler et al., 2001). (e) to help them identify routes by which they might
enhance their self-esteem. Another goal for the therapist
working with clients in this stage of recovery is to address
The Stages of Recovery their ambivalence about change (Blume, 2005; Ramsay &
Clinicians have long known that clients enter treat- Newman, 2000; Rose, 2001). The stages in the process of
ment with different levels of motivation to change prob- recovery are shown in Figure 30.1.
lem behaviors such as alcohol or drug use (Cooney, Only during the contemplation phase does the client
Kadden, & Steinberg, 2005), but not until the last begin to entertain vague thoughts about possibly stop-
decade of the 20th century did the first theoretical mod- ping the alcohol/drug use “one of these days.” About
els of the change process begin to emerge. The most 40% of the population of alcohol/drug abusers might be
detailed of these models is the one suggested by James found in the contemplation phase at any given time
341
342 Chapter Thirty
Stage Behaviors Therapeutic challenge

Precontemplation Individual is still actively using chemicals Teach client about effects of drugs of
and has not thought of stopping the use abuse and risks associated with their use.
of recreational chemicals. Individual might Help client build self-esteem. Help client
not see use of chemicals as a problem. identify barriers to recovery.
Contemplation Individual is still actively using chemicals Teach client about effects of drugs of
but has ambivalence about whether she abuse and risks associated with their use.
or he wants to continue. Enhance motivation for change.
Relapse pathway
Determination Individual has decided to quit in the Enhance motivation for change. Help
immediate future. individual make behavioral plans to
support impending change.
Action Individual has started to try to avoid Identify relapse triggers. Help individual
further chemical use. recognize symptoms of impending
relapse.
Maintenance Individual has made behavior change and Ensure stability of change. Help individual
continues to work to learn behaviors that identify and deal with any personal issues
will support recovery from chemical use. that might be a threat to his or her
recovery program.
Termination stage: Patient

has made cognitive changes
that support abstinence.
FIGURE 30.1 The Stages of Recovery
Source: Based on Prochaska (1998) and Prochaska et al. (1992).
(DiClimente & Prochaska, 1998). During this phase, of the model suggested by Prochaska (DiClemente &
users remain ambivalent about the possibility of change Prochaska, 1998). Most clients fall in the earlier phases of
but have a growing sense of dissatisfaction with their the recovery model (Connors et al., 2001; DiClemente &
present (alcohol- or drug-centered) lifestyle. Users may Prochaska, 1998; Prochaska et al., 1992).
remain in this phase for months or even years while they It is a sad reality that few individuals reach the actual
continue to engage in active chemical use. For the ther- initiation of abstinence, which the Prochaska model
apist who is confronted with clients at this stage in the identified as the action phase (Brown, 1997; Connors
recovery process, the challenge is to (a) enhance the et al., 2001; DiClemente et al., 1999; Prochaska et al.,
motivation to change, (b) awaken within the clients a 1992). During this phase the individual actively en-
desire for spiritual growth (see Chapter 35), and (c) help gages in the process of changing his or her addictive
clients learn how chemical use has impacted their lives. behaviors. Therapeutic goals during this phase include
Brown (1997) suggested that this process takes place (a) optimizing opportunities for growth, (b) being alert
not in the contemplation phase of treatment, as advocated to signs that the client is unable to handle the per-
by Prochaska et al. (1992), but rather in the determination ceived level of stress, (c) encouraging the client to begin
phase of treatment. According to Brown (1997), it is dur- the process of building a substance-free support system,
ing the determination phase of treatment that the individ- (d) helping the client to handle the emotional “roller
ual begins to make the cognitive changes necessary to coaster” that he or she might experience, (e) helping the
support his or her recovery. It is the therapist’s goal to client to be realistic about his or her progress (for clients
nurture this process, offering encouragement, support, often overestimate their growth and progress), and (f) serv-
feedback, gentle confrontation, humor, and external vali- ing as a parent-substitute, mentor, cheering section, and
dation for the client’s struggles. But even with this sup- guide for the client.
port, the recovery process for the client is difficult, as only Relapse is a very real danger during this phase of recov-
20% of all addicted persons fall in the last three stages ery. In the past, this was viewed as a signal of treatment
The Process of Recovery 343
failure, although this view has been challenged (Burge & as periods of abstinence are mixed with periods of re-
Schneider, 1999). Recovery is a dynamic process that lapse. Rehabilitation professionals should not accept
will, with the possible exception of the “one-session continued chemical use/abuse as being unavoidable,
learning experience,”1 proceed through the various but they should recognize the process of recovery from
stages of change in a cyclical rather than a linear man- substance use disorders as a difficult, ongoing process
ner (DiClemente & Prochaska, 1998). An example is the in which relapse to active chemical use is a constant
struggle many people face in giving up cigarette smok- danger.
ing. In the first 3–4 weeks following cessation of ciga- One interesting observation was offered by Cun-
rette smoking, the individual is especially vulnerable to ningham, Sobell, Gavin, Sobell, and Breslin (1997).
smoking “cues,” such as being around other smokers These authors suggested that the individual with a
(Bliss, Garvey, Heinold, & Hitchcock, 1989). At such substance use problem would subjectively evaluate
times, the person is less likely to cope effectively with the benefit or cost of quitting far differently at each
the urge to smoke and is in danger of a relapse into ac- discrete stage in the recovery process. In other words,
tive cigarette smoking again. This is one reason smokers a person in the precontemplation stage would view
who want to quit typically require an average of three or the benefits/costs of stopping the use of alcohol far
four (Prochaska et al., 1992) to perhaps as many as five differently from someone in the maintenance stage
to seven “serious attempts” (Brunton, Henningfield, & of recovery. For the substance abuse rehabilitation pro-
Solberg, 1994, p. 105; Sherman, 1994) before being able fesional working with a client who wishes to stop using
to stop smoking cigarettes. Thus, one task that will face chemicals, it is necessary to help him or her reassess
the client during the action phase of recovery is to the potential benefits of abstinence and the discom-
learn about his or her relapse “triggers” (discussed in fort associated with gaining this state at each stage of
Chapter 35). recovery.
After clients have abstained from recreational chem- Surprisingly, the model suggested by Prochaska et al.
ical use for at least 6 months, they enter the mainte- (1992) seems to apply to those who recover from sub-
nance phase (Brown, 1997; Prochaska et al., 1992). stance use problems both with and without profes-
During this phase they work on learning the behaviors sional intervention. This makes sense, since “natural”
that will enable them to continue to abstain from recovery from substance use problems is the norm
chemical use, including possibly addressing employ- rather than the exception (DiClimente & Prochaska,
ment issues that have been ignored while they were ac- 1998; Walters, Rotgers, Saunders, Wilkinson, & Towers,
tively abusing chemicals. Also, during this phase clients 2003).
might have to confront personal issues that contributed Another model of recovery was suggested by Nowinski
to, or at least supported, their use of chemicals. The (2003). In this model the first stage of recovery from a
maintenance phase blends into the termination phase at chemical use problem is acceptance (Nowinski, 2003).
around 5 years (Prochaska, 2002). Only about 20% of But there appear to be several pathways to recovery for
clients who begin the recovery process will reach this users: (a) They could decide that the consequences of
phase, which is marked by cognitive changes that free further use of the chemical are not worth the antici-
them from such things as dreaming about using the pated benefits and cut back or discontinue its use on
drug of choice and preoccupation with chemical use their own. (b) They might turn to a self-help group such
(Prochaska, 2002). During these periods the therapist as Alcoholics Anonymous (AA) to help them learn how
must work to assure the stability of change and help to abstain from chemical use. (c) They might seek out-
clients identify then address issues that might threaten patient therapy to help them learn how to abstain from
their recovery. chemical use. Finally, (d) they might seek inpatient
One of the more frustrating aspects of substance treatment to help them learn how to abstain from fur-
abuse rehabilitation is that it does proceed in a cyclical ther chemical use.
rather than a linear manner. Because of this, relapse During this stage, individuals struggle to understand
must be acknowledged as a possible outcome for any why willpower alone is not sufficient to guarantee absti-
given attempt at abstinence. The process of smoking nence or recovery. Only after they have reached the sec-
cessation provides an excellent example of this process, ond stage, surrender, do they become willing to make
the lifestyle changes necessary to support their recovery,
1Acrisis point so profound that the individual changes his or her according to Nowinski (2003). As discussed in a later
behavior after just this single experience. section of this chapter, the goal of the substance abuse
344 Chapter Thirty
rehabilitation professional is to facilitate the individual’s Interpersonal relationships. People who drink more
movement through the different stages of recovery. have fewer interpersonal relationships to draw on as
Reactions against stage models of recovery. It is often sources of support. Those who drink less seem to
surprising to the student of substance abuse rehabilita- have stronger interpersonal support systems.
tion to learn that stage models of change are not univer- Cognitive reappraisals. Many former drinkers iden-
sally accepted. However, few theoretical models of tify reaching a point at which they realize that their
any kind are accepted without challenge, modifica- alcohol use was causing physical and emotional
tion, or extensive revision. In psychology, stage mod- damage as being critical to their recovery.
els tend to pass through several periods, starting with
the phase of uncritical acceptance that follows the in- Demographic variables. There is a tendency for
troduction of a new theoretical model (Davidson, 1998). those who drink more to come from lower socioeco-
After a period of time, the model is subjected to guarded nomic groups.
and sympathetic commentary, and cautious cricitism Severity of drinking problems. Alcohol-related prob-
is offered suggesting that the model might not be totally lems such as blackouts, job problems, and legal
accurate. The upswelling of criticism grows until the problems may serve as warning signs to some people
theoretical model is awash in a sea of downright hostil- that their drinking has started to reach problematic
ity, after which it is relegated to the archives as being levels.
good only for illustrative purposes since not every per- Health problems. Physical symptoms may serve as a
son follows each stage in the predicted order (Davidson, warning to users that their alcohol use has started to
1998). reach problematic levels.
In recovery from substance abuse problems, it is not
clear what percentage of clients do so by progressing Involvement in AA and/or religious groups. Atten-
from one stage to the next (Davidson, 1998). Further, dance in various groups may help individuals begin
interindividual variation might result in one person to realize that their drinking has started to cause
progressing rapidly from one stage to the next, while an- problems.
other person might remain in the same stage for up to Individual expectations and self-evaluation. Personal
2 years or more (Davidson, 1998). The author suggested examination serves to shape individuals’ beliefs about
that stage models of recovery such as those discussed in themselves and their behavior.
this text are “at best descriptive rather than explanatory”
(p. 32). Thus, such stage models illustrate a general Humphreys et al. (1995) followed a sample of 135
process and are not an outline of specific stages that individuals classified as “problem drinkers” who went
each individual must pass through. through an alcohol detoxification program or con-
Then what works in predicting substance abuse and tacted an alcoholism information and referral center to
recovery? Although there is a great deal to be discovered determine what steps these individuals went through in
about how recovery from substance use problems takes their recovery. Although these people did not enter for-
place, research suggests that “ongoing environmental mal treatment for their alcohol use problems, the au-
factors can augment or nullify the short-term influence thors found that there were still two “pathways” away
of an intervention” (Moos, 2003, p. 3). This is not to say from problem drinking. Further, the authors found that
that the treatment process is ineffective! Rather, “rela- these individuals fell into three subgroups at the end of
tively stable factors in people’s lives, such as informal a 3-year period. The first subgroup was made up of indi-
help and ongoing social resources, tend to play a more viduals who reported that they had achieved stable ab-
enduring role” (Moos, 2003, p. 3) than the effects of stinence and were apparently able to abstain from
formal treatment. The treatment process might best be further alcohol use during the 3-year follow-up period.
envisioned as the foundation of a recovery program, not In the second subgroup were those who had achieved a
an end in itself. moderate drinking pattern, consuming no more than
Research has also suggested that this foundation five beers or mixed drinks within any given 24-hour
might be most effective when psychosocial factors are time span during the 3-year follow-up period. The final
addressed as part of the individual’s recovery program. group was composed of those who continued to abuse
Humphreys, Moos, and Finney (1995) identified a alcohol in a problematic manner.
number of the most important factors, presented here, Humphreys et al. (1995) then examined the histories
that should be addressed: of the individuals in these three groups to determine
what factors seemed relevant to the observed outcome. the substance use disorders requires that the therapist
The authors found that problem drinkers who became address more than just the individual’s chemical use, as
controlled drinkers had consumed less alcohol at the such problems are best thought of as reflecting a prob-
start of the study and tended to be members of higher lem in living that allows alcohol/drugs to become part
socioeconomic groups for the most part. As a group, of the individual’s life. Some of the domains that must
they also viewed their drinking as less of a problem than be addressed by the treatment professional and the pos-
did other drinkers, had higher self-esteem, and were sible outcome of the treatment process are reviewed in
more confident that they could resist the temptation to Table 30.2.
return to abusive drinking. The authors found that indi-
viduals who adopted an alcohol-free lifestyle tended to
Specific Points to Address in the Treatment
be from lower socioeconomic groups. These people
tended to suffer a greater number of lost jobs and eco-
of Addiction to Common Drugs of Abuse
nomic problems related to their drinking. As a group, Although the process of recovering from any substance
the alcohol-free group members were less sure of their use problem tends to reflect the steps identified by Pro-
ability to control their drinking and they tended to turn chaska et al. (1992), specific issues must be considered
to social support groups such as church and/or AA in and addressed in working with individuals who have
their quest for recovery. been abusing or are addicted to the various chemicals
Overall, the model that is emerging from clinical ex- of abuse. In this section, some of the specific issues as-
perience and research is that recovery from an alcohol/ sociated with abstinence from different drugs of abuse
drug use problem is a dynamic process in which indi- are addressed.
viduals must proceed through a series of specific stages
before they can make any meaningful changes in their Opiate Addiction: Is Treatment Worthwhile?
chemical use patterns. Some of the variables that must The man on the street seems to believe that once an
be addressed for a successful attempt at alcohol/drug opiate addict, always an addict, and is quite pessimistic
rehabilitation are reviewed in Table 30.1. about treatment for narcotic addiction. Indeed, there
Should abstinence be the goal of treatment? This does seem to be some basis for this pessimism, since re-
question is fiercely debated. Should the goal of treat- search has found that 90% of opiate-dependent individ-
ment should be to help people learn to control their uals who successfully are withdrawn from narcotics will
chemical use or how to abstain from all recreational return to chemical use within 6 months (Schuckit,
chemicals? Although most treatment programs believe 2000).
that abstinence is the only viable goal of rehabilitation, A pair of research studies have provided a rather
the truth is that following treatment the majority of gloomy view of the evolution of narcotics addiction
those with alcohol use disorders continue to use alco- (Hser, Anglin, & Powers, 1993; Hser, Hoffman, Grella,
hol at least occasionally (Peele, 1985; Peele, Brodsky, & & Anglin, 2001). In 1986, 24 years after an original
Arnold, 1991). George Vaillant (1983, 1996) found in sample of 581 narcotics addicts was identified as opiate
his follow-up studies on identified alcohol-dependent addicts by the criminal justice system, only 22% were
individuals that over the course of their alcohol use, opiate free (Hser et al., 1993). Some 7% of the original
they tended to alternate between periods of more and sample was involved in a methadone maintenance pro-
less problematic drinking. gram, and 10% reported engaging in only occasional
This raises an interesting question, as treatment narcotics use. Almost 28% of the original sample had
centers advocate that the individual abstain from all died, with the main causes of death being homicide,
chemical use, an outcome that is achieved by only a suicide, and accidents, in that order.
very small minority of those who are “treated” for A decade later, in 1996–97, researchers contacted
alcohol/drug use problems. For example, in the treat- the original subjects and found that almost half of the
ment of marijuana addiction, total abstinence from all subjects (284 of the original 581) were dead. Almost
psychoactive drugs is considered essential if treatment 56% of those who were still alive were opiate free, as
is to be effective (Bloodworth, 1987). While the ulti- confirmed by urine toxicology testing, while another
mate answer to this problem has not been found, it does 10% refused to provide a urine sample for testing. Just
suggest that there is still a great deal to learn about the about the same percentage of opiate-dependent indi-
natural history of alcohol/drug use problems and their viduals had died than had achieved lasting abstinence
treatment. At the same time, successful intervention for (Hser et al., 2001). The authors concluded on the basis
346 Chapter Thirty
TABLE 30.1 Variables That Affect Rehabilitation
Variable Reason
Age Older clients are more likely to have a successful treatment outcome. Research suggests
that clients younger than 30 are more likely to become re-addicted to narcotics following
treatment, for example.
Employment Clients with a stable employment history seem to do better in treatment than those with
a history of employment problems.
Motivation Clients who acknowledge that their substance use is causing them problems and who
seek help on their own seem to be more likely to benefit from treatment.
Consequences or sanctions Clients who understand that continued substance use will result in sanctions of some
brought on by substance use/abuse kind (health problems, loss of employment, legal problems) seem to do better in
treatment and afterward.
Physical/social environment Clients who make a break with past associates and avoid going to places where they used
to use alcohol/drugs (bars, homes of friends who use drugs, etc.) are less likely to resume
using chemicals.
Legal status or peer criminal activity Clients with fewer arrests have a higher success rate than clients with a long legal history.
Clients who restrict or avoid contact with friends who are still using alcohol/drugs have
higher success rates.
Social support If clients’ interpersonal support systems are strained, they are more likely to relapse. For
example, if there is a lot of family conflict, the family will be unable to provide much
support for the recovering individual.
History of drug use Clients who use a greater variety of chemicals, who use chemicals more often, who
began to use at a younger age, and who have been addicted for longer periods of time
seem to relapse more often. Length of previous sobriety also seems to predict level of
success; clients with long periods of sobriety in their past are more likely to benefit from
treatment.
Treatment history Clients who are “treatment wise” as a result of having been enrolled in many treatment
programs in the past are more likely to return to the use of chemicals than are those
individuals who haven’t been in treatment before.
Concurrent psychiatric problems Clients with concurrent psychiatric diagnoses are more likely to return to the use of
chemicals. (Dual-diagnosis clients are discussed in Chapter 24.)
Anger Clients with a great deal of anger (a history of fighting, etc.) are more likely to have
trouble handling stress—and thus more likely to use chemicals to help them deal with
their frustration. They are less likely to be able to abstain without help in learning how
to deal with their anger and frustration.
History of victimization in Clients who have been physically, sexually, and/or emotionally abused in the past have
interpersonal relationships trouble dealing with the intense feelings of anger and shame that surface during
treatment and are at high risk for return to chemical use.
Chronic illness Clients who have concurrent chronic illness (chronic back pain, cancer, arthritis,
asthma, HIV infection, etc.) are at high risk for return to chemical use as a way of dealing
with the pain of their disease and/or the emotional frustration caused by their disorder.
Source: Based on Alemi, Stephens, Llorens, & Orris (1995).
of their data that heroin use patterns were “remarkably heroin addiction was a lifelong condition, with severe
stable” (p. 503) for the group as a whole, with returns to social and medical consequences for those who were
alcohol/drug use taking place even after some subjects addicted to this chemical. However, there are also some
had been drug free for 15 years. It was concluded that studies that have concluded that more than one-third of
TABLE 30.2 Summary of Possible Treatment Outcomes
Domain Possible outcome
Employment history • Increased chances of finding suitable work

• Increased job retention
• Improved job performance in present position
• Reduced number of potential accidents
• Reduced absenteeism
Criminal justice • Reduced involvement with criminal justice system
• Reduction in number of subsequent DWI or drug-related arrests
• Reduced involvement in number of criminal activities
• Reduced violent behavior
Relapse prevention • Reduced possibility of further substance use
• Learning how to cope with relapse situations
• Learning how to minimize adverse effects of relapse for self and family
Substance use • Abstinence
• Reduced consumption of chemicals
• Fewer days intoxicated by a chemical
• Substitution of illicit drug by authorized medication (such as opiate agonist agents for
those addicted to narcotics)
Medical/physical health • Increased likelihood of taking steps to meet basic needs (food, housing, clothing, etc.)
• Improved overall health, resulting in reduced use of health care system
• Fewer medical problems
• Reduced family stress level, thus reducing family’s stress-related illness and use of health
care system
• Reduced incidence of high-risk sexual behavior
• Reduced sharing of needles
Psychosocial functioning • Initiation into drug-free lifestyle
• Improved quality of interpersonal relationships
• Reduced level of conflict within family
• Improved access to psychiatric care
• Improved parenting skills
Source: Based on information provided in Landry (1997).
all opiate-dependent persons will ultimately be able to information into possible genetic “markers” that might
stop using drugs. For those individuals who survive identify the person who is vulnerable to cocaine or am-
their addiction to opiates and who establish a recovery phetamine addiction. The point here is that not all
program, abstinence from opiate use is finally achieved CNS stimulant users are or will become addicted to
in 6 (Smith, 1994) to 9 (Jaffe, 1989; Jenike, 1991) years that chemical. Only through the process of assessment
after their addiction to opiates first developed. (discussed in Chapter 27) is the individual’s need for
treatment for a cocaine use problem and the appro-
priate level of care for that person determined. For-
CNS Stimulant Abuse: Withdrawal tunately, people with only CNS stimulant abuse
and Recovery Issues
problems rarely require hospital-based detoxification
Unfortunately, there is virtually no research into the services (“Amphetamines,” 1990). This is because phys-
factors that contribute to the development of CNS ical withdrawal from the CNS stimulants is rarely life
stimulant addiction. In contrast to the research into the threatening.
genetics of alcoholism, “research on genetic factors in One major exception is the potential for CNS stimu-
stimulant abuse has not been pursued” (Gawin & lant abuse/addiction to result in suicidal thinking. For
Ellinwood, 1988, p. 1177). Thus, there is virtually no users suffering from a post-stimulant depression that
348 Chapter Thirty
has reached suicidal proportions, hospital-based obser- Hall, Havassy, and Wasserman (1991) concluded that
vation and treatment may be necessary to protect them approximately 80% of cocaine addicts who were able to
from self-destructive impulses. The decision to hospi- abstain from cocaine use for 12 weeks after treatment
talize a CNS stimulant abuser should be made on a were still drug free after 6 months. However, this does
case-by-case basis by qualified physicians. Some of the not mean that users have fully recovered from their
factors that must be considered include the individual’s CNS stimulant addiction. Cocaine and amphetamine
current state of mind, the person’s medical status, and addicts might suddenly experience craving for these drugs
whether he or she has adequate resources and social “months or years after its last appearance” (Gawin &
support to deal with the withdrawal process on an out- Ellinwood, 1988, p. 1176), and long after the last period
patient basis. of chemical use.
Although the physical withdrawal from CNS stimu- However, Satel et al. (1991) examined the cocaine
lants is achieved quite rapidly, protracted cocaine abuse withdrawal process and concluded that their data failed
may result in an extended withdrawal syndrome (Satel to support the model advanced by Gawin and Kleber
et al., 1991). Although cocaine withdrawal does not in- (1986). The authors found that for their sample, the co-
clude the severe physical withdrawal distress seen in caine withdrawal process was marked by mild with-
opiate withdrawal, it does include such symptoms as drawal symptoms that declined over the first 3 weeks
paranoia, depression, fatigue, craving for cocaine, agita- of inpatient treatment. However, the withdrawal symp-
tion, chills, insomnia, nausea, changes in the individ- toms they noted were much milder than had been
ual’s sleep patterns, ravenous hunger, muscle tremors, anticipated and failed to follow the triphasic model
headache, and vomiting (DiGregorio, 1990). These suggested by earlier research.
symptoms begin 24–48 hours after the last dose of co- The treatment of stimulant addiction involves more
caine and persist for 7–10 days, according to the author. than just helping the user discontinue drug use. One
A similar process seems to exist for amphetamine common complication of stimulant addiction is that
withdrawal. the individual has often forgotten what a drug-free life
Stages of recovery from CNS stimulant abuse/addic- is like (Siegel, 1982). Total abstinence from recreational
tion. A triphasic model for the post-cocaine binge re- chemicals is thought to be essential if the individual
covery process has been proposed by Gawin, Khalsa, wants to avoid further CNS stimulant use problems.
and Ellinwood (1994) and Gawin and Kleber (1986). Hall et al. (1991) found that cocaine-dependent people
In the early part of the first stage, which lasts 1–4 days, who made a commitment to full abstinence following
individuals experience feelings of agitation, depression treatment were more likely to avoid further cocaine use
and anorexia (loss of desire to eat), as well as a strong than were addicts who did not desire abstinence as a
craving for cocaine. As they progress through the sec- treatment goal. Follow-up treatment should include
ond half of the first phase, they lose the craving for behavior modification and psychotherapy to help
cocaine but experience insomnia and exhaustion, clients learn the skills they will need to continue ab-
combined with a strong desire for sleep. The authors staining from chemicals (Gold & Verebey, 1984). Social
also suggested that the second half of the first phase support and self-help group support in the form of Alco-
would last from the fourth until the seventh day of holics Anonymous (AA), Narcotics Anonymous (NA),
abstinence. or Cocaine Anonymous (CA) are often of great help. As
After the seventh day of abstinence, people return with the other forms of drug addiction, recovering indi-
to a normal sleep pattern but gradually experience viduals are at risk for cross-addiction to other chemicals
stronger cravings for cocaine or stimulants and higher and need to avoid other recreational drug use for the
levels of anxiety. Conditioned cues could exacerbate rest of their lives.
their craving for stimulants, drawing them back to
chemical abuse. If they can withstand the environmen- Issues Surrounding Recovery
tal and intrapersonal cues for further drug use, they can From Marijuana Abuse
move into the “extinction” phase, where they will grad- Although marijuana use has been popular in this coun-
ually return to a more normal level of functioning. try since the Prohibition era and most certainly after
The extinction phase begins after 10 weeks of absti- the “hippie” generation “discovered” marijuana in the
nence. If individuals relapse, the cycle repeats itself. 1960s, virtually nothing is known about the treatment of
But if they are able to withstand the craving, there is a marijuana abuse or dependence (“Treatment Protocols
good chance that they can achieve lasting recovery. for Marijuana Dependence,” 1995; Stevens, Roffman, &
Simpson, 1994). It is known that the short-term, acute (Benowitz & Henningfield, 1994; Henningfield, 1995;
reaction to marijuana does not require any special in- Sherman, 1994).
tervention (Brophy, 1993). Thus, marijuana-induced Although health care workers have tried for many
feelings of anxiety or panic reactions usually respond to years to identify which factors contribute to a person’s
“firm reassurance in a non-threatening environment” successful attempt to quit smoking, they have met with
(Mirin, Weiss, & Greenfield, 1991, p. 304). However, little success (Kenford et al., 1994). Thus, cigarette cessa-
these patients should be watched to ensure that they do tion programs are something of a hit-or-miss affair in
no harm to themselves or others. which neither the leaders nor the participants have little
There are several problems associated with working knowledge of what really works. Smoking cessation train-
with marijuana abusers, First, it is rare for a person to ing programs usually help 70%–80% of the participants
be abusing only marijuana. Thus, treatment usually to stop smoking on a short-term basis, but of those who
must focus on the abuse of a number of chemicals attempt to stop smoking, two-thirds may stop for a very
rather than just marijuana alone. Second, marijuana few days, but only 2%–3% will be tobacco free a year
users rarely present themselves for treatment unless later (Henningfield, 1995). The research team of Hughes,
there is some form of coercion. One reason is that mari- Gust, Skoog, Keenan, and Fenwick (1991) found that
juana abusers rarely view themselves as being addicted 65% of their experimental sample relapsed within the
to cannabis (“Treatment Protocols for Marijuana De- first month of quitting, suggesting that the first month is
pendence,” 1995). especially difficult for the recent ex-smoker.
Specific therapeutic methods for working with the There appears to be a relationship between the fre-
chronic marijuana user are not well developed (Mirin quency with which a given individual smokes and his
et al., 1991). Total abstinence from all recreational or her success in giving up tobacco use. Cohen et al.
chemical use is thought to be imperative (Smith, 2001). (1989) reviewed data from 10 different research projects
Since marijuana users often use it as a way to cope with that involved a total of 5,000 participants who were
negative feelings such as anger (“Treatment Protocols for attempting to stop smoking cigarettes.
Marijuana Dependence,” 1995), rehabilitation profes- The authors found that light smokers, defined as
sionals must help clients identify specific problem areas those who smoked fewer than 20 cigarettes each day,
in their lives and then find non-drug-related coping were significantly more likely to be able to stop smoking
mechanisms for these “trigger” situations. on their own than were heavy smokers. Cohen et al.
A treatment program that identifies clients’ reasons for (1989) also found that the number of previous attempts
continued drug use and helps them find alternatives to to quit smoking was not an indication of hopelessness.
further drug use is most effective. Auxiliary groups that Rather, the number of unsuccessful previous attempts
focus on vocational rehabilitation and socialization skills was unrelated to the question of whether the smoker
are also of value in the treatment of chronic marijuana would be able to quit this time. They concluded that
users (Mirin et al., 1991). Jenike (1991) reported that “most people who fail a single attempt [to quit smoking]
treatment efforts should focus on understanding abusers’ will try again and again and eventually quit” (p. 1361).
disturbed psychosocial relationships. Bloodworth (1987) Another factor that seems to be associated with the
concluded that “family therapy is almost a necessity” difficulty smokers experience when they attempt to quit
(p. 183). Group therapy as a means of dealing with peer is their expectancies for the nicotine withdrawal process.
pressure to use chemicals was necessary in this author’s Tate et al. (1994) formed four subgroups from their re-
opinion, and self-help support groups such as AA or NA2 search sample of 62 cigarette smokers. Former smokers
“cannot be overemphasized” (Bloodworth, 1987, p. 183). who were led to believe they would not experience any
significant distress during the nicotine withdrawal
Issues in the Treatment of Nicotine Addiction process reported significantly fewer physical or emo-
When one asks a cigarette smoker why he or she contin- tional complaints than did the other research groups. It
ues to smoke in spite of the dangers associated with this appeared to the authors that people’s expectations for
habit, the response is often “I can’t help myself. I’m ad- the nicotine withdrawal process might play a role in
dicted.” Indeed, it is believed that the addictive power how they interpret and respond to the symptoms they
of nicotine is why 90%–98% of those who attempt to experience during early abstinence.
quit smoking in any given year will ultimately fail There is other evidence to support the theory that
people’s expectations for recovery influence their expe-
2Discussed in detail in Chapter 35. rience of abstinence. Kviz, Clark, Crittenden, Warnecke,
350 Chapter Thirty
and Freels (1995) found that for smokers over the age of potential complications of steroid abuse is necessary.
50, the perceived degree of difficulty in quitting was The attending physician may need to consider a gradual
negatively associated with their actual attempts to quit detoxification program for the steroid abuser. Most med-
smoking. In other words, the authors found that espe- ical complications caused by steroid abuse will usually
cially for smokers over the age of 50, the harder smokers clear up after the individual stops the use of steroids
expected the task of quitting to be, the less likely they (Hough & Kovan, 1990); however, some of the compli-
were to try. Thus, people’s expectations for quitting cations caused by steroid abuse (i.e., heart tissue dam-
were found to play a significant role in whether they age) may be permanent. Surgical intervention may be
actually quit smoking cigarettes. possible to correct some of the side effects of steroid use
Thus, smokers who wish to quit should be warned (Hough & Kovan, 1990) but this is not always possible.
that the struggle against cigarette smoking is lifelong Following patients’ detoxification from anabolic
and that their mind-set will play a major role in whether steroids, staff members should work with them to iden-
they are successful. Further, former smokers should be tify why they started using steroids to begin with. Self-
warned that they will be vulnerable to relapsing back to concept problems should be identified and the proper
cigarette smoking for the rest of their lives. therapy initiated to help users learn to accept them-
Although there has been a great deal of emphasis on selves without leaning on an artificial underpinning
formal cigarette cessation treatment programs, perhaps such as chemicals. Proper nutritional counseling may
as many as 90% (Brunton et al., 1994; Fiore et al., be necessary to help athletes learn how to enhance
1990) to 95% (Hughes, 1992; Kozlowski, et al., 1989; body strength without using potentially harmful sub-
Peele, 1989) of cigarette smokers who quit do so with- stances such as anabolic steroids. Group and individual
out participating in a formal treatment program. Of support programs should also be considered as possible
those smokers who do quit, their motivation to quit treatment modalities, depending on clients’ needs.
smoking is most “critical” (Jaffe, 1989, p. 682) to the
success of their efforts. These conclusions raise serious
Summary
questions as to whether extensive treatment programs
are necessary for tobacco dependence. But formal treat- In this chapter, two different models of the recovery
ment programs might be of value to heavy smokers or process were discussed. The most popular model was
those at risk for tobacco-related illness. introduced by Prochaska et al. (1992). This model sug-
gested that clients who wish to make behavioral changes
Issues Associated With the Treatment proceed from a precontemplation period, in which no
of Anabolic Steroid Abusers specific change is being contemplated, through a phase
The first step in the treatment of the steroid abuser is in which they are thinking about possibly making some
identification of people who are indeed abusing ana- changes (contemplation), to a period in which they are
bolic steroids. The physician may, on the basis of clini- actively considering the possibility of change (determi-
cal history, blood, and/or urine tests, be the first person nation phase).
to suspect that a patient is abusing steroids, and he or Clients next enter the action phase, in which they at-
she is in the best position to confront the user. At this tempt to make the desired behavioral changes, and, if
point the addictions counselor is not thought to have a successful, they enter the maintenance phase, where
significant role to play, at least in the earliest stages, un- the new behavior becomes entrenched. Also discussed
less the person is abusing other chemicals also. in this chapter were specific points that should be ad-
Once the steroid abuser has been identified, close dressed in treating clients who are abusing some of the
medical supervision of the patient to identify and treat more popular drugs of abuse.
CHAPTER THIRTY-ONE
Treatment Formats for Chemical

Dependency Rehabilitation
For many years, researchers and clinicians have de- therapy in working with the addicted person. Most such
bated the relative merits of outpatient versus inpatient programs will follow a 12-Step philosophy, usually ei-
rehabilitation programs. This debate, which continued ther Alcoholics Anonymous or Narcotics Anonymous,
through much of the past 30 years, has been spirited. To and the individual is expected to attend regular self-
date, neither side has scored a decisive victory, and both help group meetings as part of the treatment format.
inpatient and outpatient treatment programs have vocal The individual’s treatment program is usually coordi-
proponents. In this chapter, some of the characteristics nated by a certified chemical dependency counselor
of an average outpatient treatment program, the typical (sometimes called an addictions, AODA, or substance
inpatient program, and some of the issues that have abuse counselor).
been raised about the relative advantages and disadvan- During the rehabilitation process, a formal treat-
tages of each are discussed. ment plan will be established, review sessions will be
scheduled on a regular basis, and the client’s progress
toward the agreed-on goals will be monitored by staff.
Outpatient Treatment Programs Individual and group therapy sessions are utilized to
Outpatient treatment: A working definition. Outpatient help clients work through their denial and identify and
chemical dependency treatment may best be defined as address the problems of daily living without the use of
a formal treatment program (a) involving one or more chemicals. Psychoeducational lectures might also be
professionals who are trained to work with individuals used to present clients with factual information about
who are addicted to a chemical, (b) designed specifi- the disease of chemical addiction and its treatment.
cally to work with the addicted person to help him or Referrals are made as necessary to vocational counsel-
her achieve and maintain a recovery program, (c) uti- ing centers or community mental health centers for indi-
lizing a number of different treatment modalities (e.g., vidual, family, or marital counseling. Some programs
psychoeducational approaches; family, marital, indi- provide a “family night” when family members are en-
vidual, and/or group therapies) to help the addicted couraged to participate once a week or once a month to
person come to terms with his or her chemical abuse discuss their concerns. Other programs feature a family
problem, and (d) working with the patient on an out- group orientation, when couples participate together on
patient basis. Such programs are extremely popular at a day-to-day basis as part of the program. In such a for-
the start of the 21st century, with an estimated 85% of mat, the spouse of the addicted person will sit in on the
all patients in substance abuse treatment receiving their group sessions and participate as an equal with the ad-
care in an outpatient rehabilitation program (Fuller & dicted person in the group therapy.
Hiller-Sturmhofel, 1999; Tinsley, Finlayson, & Morse, Whatever the general approach, the goal of any
1998). In spite of their popularity, however, the effective- outpatient treatment program is to enhance the high-
ness of outpatient treatment programs has not been est level of functioning while providing support for the
established. alcoholic. Some programs require the detoxification
phase of treatment, when the individual is withdrawn
Components of Outpatient Treatment Programs from chemicals, to be carried out either at a detoxifi-
Outpatient treatment programs will utilize many of the cation center or in a general hospital. However, the
components of treatment discussed in the last chapter. individual is generally expected to have stopped all
Such programs will usually have individual and group chemical use before starting any treatment program.
therapy formats as well as possibly marital and family Abstinence from alcohol or drug use is expected. Many
351
352 Chapter Thirty-One
treatment programs will require the use of Antabuse to require more intensive treatment. Such programs
(disulfiram) or will conduct random breath or urine are usually for patients with lower severity substance
tests to detect alcohol or drug use by the patient. One use problems. In spite of the promise of this level of
advantage of urine testing is that it allows the staff treatment for patients who have limited substance use
to check on the individual’s compliance in taking experience, short-term rehabilitation programs seem
Antabuse (disulfiram), if this is a part of the treatment to be ineffective for individuals who do not have ex-
program. tensive substance abuse problems (Shepard, Larson, &
Outpatient treatment programs allow clients to live Hoffmann, 1999). The reason for this apparent paradox
at home, continue to work, and participate in family ac- is not clear.
tivities while they are in a rehabilitation program de- Intensive short-term outpatient programs. Programs
signed to help them achieve and maintain abstinence at the intensive short-term outpatient level are aimed at
(Youngstrom, 1990b). Unfortunately, in spite of their patients with a moderate to severe substance use prob-
advantages, outpatient treatment programs experience lem. Participants are usually seen in both individual
high dropout rates. and group therapy sessions, for up to 5 nights a week.
Programs at this level are time limited, but treatment
Varieties of Outpatient Treatment Programs is more intense than treatment on the previous level
for Substance Abuse Rehabilitation (4–5 times a week versus 1–2 times a week) and usually
DWI school. Outpatient rehabilitation programs differ lasts longer (up to 6 months). Program participants are
mainly in the frequency with which clients meet with often required to attend self-help group meetings such
treatment professionals and the specific methods used as AA in addition to participating in scheduled treat-
by the staff in working with clients. For example, the ment activities. Additional sessions for family or marital
psychoeducational approach is often the mainstay of counseling are scheduled outside of regular treatment
the “DWI school” or DWI class. The DWI school is hours for those whose recovery requires additional
usually limited to first-time offenders who are assumed forms of intervention and support.
to have simply made a mistake by driving under the in- Patients assigned to this level of intervention usually
fluence of chemicals. Participants in the DWI school have middle severity substance use problems. The pro-
are not addicted to alcohol or drugs in the opinion of gram seeks to (a) break through clients’ denial about
the assessor. They are exposed to 8–12 hours of educa- their substance use, (b) achieve a commitment to absti-
tional lectures designed to help them better understand nence from those who are unlikely to benefit from less
the dangers inherent in driving while under the influ- intense forms of treatment, and (c) make appropriate
ence of chemicals. This is done in the hope that they referrals for clients who appear to require more inten-
will learn from their mistake. sive help. Shepard et al. (1999) concluded that pro-
Short-term outpatient programs (STOP). A short- grams at this level of intensity were most effective,
term program is usually time limited. Some STOP pro- especially when applied to the target population of in-
grams utilize only individual therapy sessions; others dividuals with mid-severity substance use problems.
combine individual and group therapy formats for Intensive long-term outpatient treatment. Programs at
people whose substance use problems is, in the opinion this level are usually open ended and designed for clients
of the assessor, mild to moderate in its severity. Clients whose substance use problems are moderate to severe
may be required to attend Alcoholics Anonymous (AA) in intensity but for whom less radical treatment would
or similar self-help group meetings in addition to ses- hold little chance of success. This level usually lasts for
sions with the therapist at least once a week. Clients in a minimum of 6 months and often for 12–18 months.
this level of treatment are often assigned material to Program participants are involved in a series of individ-
read between sessions with the therapist, and psychoed- ual and group therapy sessions for a specified number
ucational lectures can provide program participants of days each week, with the exact timing and sequence
with factual information about the effects of the drugs of of individual and/or group sessions determined by the
abuse. Clients participate in program activities 1–2 nights individual’s treatment plan.
a week usually for less than 2 months. Such programs were designed for patients with mod-
The goal of such rehabilitation programs is to (a) erate to severe substance use problems. As with less in-
break through clients’ denial about their substance use, tensive levels of treatment, these program seek to (a)
(b) achieve a commitment to abstinence from them, break through clients’ denial about their substance use,
and (c) make appropriate referrals for those who appear (b) achieve a commitment to abstinence from clients
Treatment Formats for Chemical Dependency Rehabilitation 353
who have not benefited from less intense forms of treat- substance abuse program by health insurance carriers.
ment, or whose substance use pattern suggests that less Although statistical research has found no significant
intense treatment is likely to fail, (c) support clients difference in the percentage of outpatient treatment
during the early stages of recovery from drug/alcohol program “graduates” who remains abstinent, as op-
use problems, and (d) to make appropriate referrals for posed to those who complete inpatient treatment pro-
those who appear to require even more intensive forms grams, this is not to say that outpatient treatment is as
of treatment. Surprisingly, such programs were found effective as inpatient treatment. Rather, inpatient treat-
to be less effective than short-term intervention pro- ment programs tend to deal more effectively with a dif-
grams for people with moderate to severe substance use ferent class of client from those in outpatient treatment
problems (Shepard et al., 1999). programs. This difference makes comparisons between
inpatient and outpatient treatment difficult.
Advantages of Outpatient Treatment Programs Outpatient treatment programs typically do not offer
Outpatient treatment programs are popular. Perhaps as the same degree of structure and support found in the
many as 88% of those who are treated for alcohol abuse or inpatient treatment setting. Further, outpatient treat-
addiction are treated on an outpatient basis (McCaul & ment programs offer less control over the client’s envi-
Furst, 1994). Outpatient treatment programs are signif- ronment, since he or she continues to live at home, and
icantly less expensive than inpatient treatment pro- thus is of limited value for some patients who require a
grams, with average weekly costs estimated at $77–$93 great deal of support during the early stages of recovery.
a week (Belenko, Patapis, & French, 2005). Outpatient While outpatient treatment of substance abuse seems
treatment programs also avoid the need to remove pa- to work for many clients, it does not seem to be the ulti-
tients from their environment. In many cases, they are mate answer to the problem of chemical dependency.
able to continue to work and thus remain self-supporting
during treatment. Unlike inpatient treatment programs,
there is no community reorientation period needed
Inpatient Treatment Programs
after outpatient treatment (Youngstrom, 1990b). In ad- Definition of inpatient treatment. The inpatient treat-
dition, outpatient treatment programs tend to last longer ment program might best be defined as a residential
than inpatient rehabilitation programs, and research treatment facility where clients live while in treatment.
consistently shows that the longer clients are involved These programs usually deal with the hard-core, the
with treatment, the better are their chances of long- seriously ill, or the “difficult” patient. These are indi-
term abstinence. viduals for whom outpatient treatment has either not
Outpatient treatment programs offer yet another ad- been successful or has been ruled out. Residential
vantage over inpatient rehabilitation programs: flexibil- treatment programs usually have a strong emphasis on
ity (Turbo, 1989). Program participation may be through a 12-Step philosophy and utilize individual and group
an outpatient day treatment program, with treatment therapy extensively. Clients’ length of stay in treatment
activities scheduled during normal working hours, or depends on such factors as their motivation, support
through an outpatient evening treatment program. An system, and a range of other variables that the treat-
evening program will utilize the evening hours for treatment team considers.
ment activities. Finally, outpatient treatment programs Residential treatment programs provide clients the
let clients practice recovery skills while still living in the greatest degree of support and help. Inpatient treatment
community. This is a significant advantage over tradi- also is “the most restrictive, structured, and protective
tional inpatient treatment programs, which remove of treatment settings” (Klar, 1987, p. 340). It combines
clients from their home communities for the duration the greatest potential for positive change with high fi-
of treatment. nancial cost and the possibility of branding the patient
for life (Klar, 1987). The decision to utilize inpatient
Disadvantages of Outpatient Treatment Programs treatment is one that should not be made lightly.
Surprisingly, although inpatient treatment might cost Many general hospitals offered inpatient rehabilita-
more, because of available insurance coverage, many tion programs for drug/alcohol abusers in the 1990s but
clients actually pay less for inpatient treatment than have since either scaled back the number of available
they would for outpatient treatment. This is because beds or closed their doors entirely. In the mid-1990s,
outpatient treatment programs traditionally are not reim- 21% of the hospitals surveyed offered inpatient treatment
bursed at the same rate as the more expensive inpatient for substance abuse (Bell, 1995). Other, non-hospital
programs such as therapeutic communities or halfway 2004). In general the “traditional” TC might be viewed
houses also were available in many geographic areas. But as a program that operates on the theory that drug abuse
by the first decade of the 21st century, many of these pro- is a deviant behavior reflecting impeded personality de-
grams had closed, victims of the economic realities and velopment or chronic deficits in social, educational,
shift in priorities that took place at the start of the new and economic skills (DeLeon, 2004; Satel & Farabee,
millennium. Not all inpatient/residental programs closed 2005). To correct the deficits, the TC attempts to help
their doors, however, and even at the start of the 21st the individual through a global lifestyle change, includ-
century there were many inpatient treatment programs ing abstinence from illicit drugs, elimination of antiso-
in the United States. cial activity, and the development of prosocial attitudes
and behaviors (DeLeon, 2004). In spite of differences
Varieties of Inpatient Treatment in treatment philosophies or methods, the effective TC
Hospital/program-based inpatient treatment. Traditional helps patients understand and cope with their specific
inpatient drug rehabilitation is often carried out either in life circumstances without the use of recreational
a center that specializes in chemical dependency treat- chemicals (Moos, 2003).
ment or in a traditional hospital setting as part of a spe- In length of stay, the “traditional” TC programs usu-
cialized drug treatment unit. Some of these programs ally require a commitment of 6 months to 3 years
utilize the Minnesota Model, which was explored in de- (DeLeon, 2004; Ringwald, 2002). This extended length
tail in the last chapter, although this is becoming less and of stay is thought to be necessary to help the individual
less common as managed care providers demand shorter learn to live without reliance on chemicals. The TC pro-
treatment stays for their clients. gram originated in the United States and was designed to
Inpatient rehabilitation programs, especially those work with people who were addicted to opiates. Now the
in a hospital setting, will often begin with detoxifica- format has evolved to the point that it is being integrated
tion. The process of detoxification, in addition to help- into some penal institutions to help substance-dependent
ing clients stop abusing chemicals, also sets the stage criminals (Ringwald, 2002) as well as those addicted to
for their entry into rehabilitation (Swift, 2005). In this other chemicals (DeLeon, 2004).
context, detoxification allows patients patient to begin All therapeutic communities share the characteristic
treatment while in the last stages of withdrawal from of a single treatment philosophy. One central tenet of
chemicals, aiding patient retention. Patients live on the the TC model is that the individual’s drug abuse is
treatment unit and participate in a program of daily lec- viewed as a whole person disorder (Satel & Farabee,
tures and individual and group therapy sessions. Each 2005). Further, the community is viewed as the healing
patient is assigned some form of “homework,” which modality by which the individual changes (DeLeon,
might include assignments to read certain material that 2004). This adherence to a single vision seems to con-
rehabilitation staff believe will support the individual’s tribute to the effectiveness of the TC. Other character-
recovery. In most programs, patients are also expected istics of the TC include social and physical isolation, a
to begin to follow the 12-Step program of AA or a simi- structured living environment, a firm system of rewards
lar self-help group, and attendance in self-help group and punishments, and an emphasis on self-examination
meetings is required. and the confession of past wrongdoing. Clients are ex-
Therapeutic communities. One controversial form of pected to work, either outside the TC in an approved
inpatient treatment is the therapeutic community (TC). job or within the TC itself as part of the housekeeping
At the start of the 21st century the TC movement has or kitchen staff.
evolved away from the harsh confrontational format Although many TCs will utilize the services of mental
that marked its inception in the post–World War II era, health professionals, much of the treatment is carried out
and although the original TC concept was quite resist- by paraprofessional staff members, often former residents
ant to the use of 12-Step groups, there is a growing of the TC. This is done on the theory that only a person
trend within the TC movement to integrate these into “who has been there” can understand and help the
the program (Ringwald, 2002). addicted person. Such paraprofessional counselors are
At the start of the 21st century, the TC concept has thought to be effective on the basis of personal experience
become a generic term for a wide variety of short- and in breaking through clients’ denial and manipulation.
long-term residental treatment programs as well as for The TC might offer an extended family for the indi-
some outpatient day programs that have evolved from vidual. Indeed, the original members of Synanon (one
the residental TCs of the 1960s and 1970s (DeLeon, of the early therapeutic communities) were expected to
remain there on a permanent basis as part of the “family” workforce (Berg, 2003). While these results do not re-
(Lewis, Dana, & Blevins, 1988). flect a panacea for the field of substance abuse rehabili-
About two-thirds of those admitted to TCs are under tation, they do suggest that TCs play a valuable role in
the supervision of a probation or parole agent and thus the rehabilitation of some chronic drug abusers.
are involved in the criminal justice system (Hiller,
Knight, Rao, & Simpson, 2002). This legal coercion is Is There a Legitimate Need for Inpatient Treatment?
viewed as providing an additional incentive for the indi- In the mid-1980s, a flurry of research studies con-
vidual to remain in the treatment setting until he or she cluded that “the relative merits of residential treatment
has started to internalize the philosophy and goals of re- are less than clear” (Miller & Hester, 1986, p. 794).
covery (Satel & Farabee, 2005). But in spite of the Many critics of inpatient treatment point to the Project
“family” orientation in TCs or the incentive of avoiding MATCH Research Group study of the mid-1990s as
incarceration by successfully completing treatment, providing evidence that inpatient treatment is not au-
these programs suffer from significant dropout rates tomatically superior to less intense methods of treat-
(Satel & Farabee, 2005). DeLeon (2004) suggested that ment. The Project MATCH Research Group tried to
30%–40% of those admitted to a TC will drop out in isolate the patient characteristics that predicted a bet-
the first 30 days and only 10%–15% complete the typi- ter response to inpatient versus outpatient treatment
cal 2-year program. A significant percentage of those for alcoholism. The project failed to find evidence that
who do not leave on their own are asked to leave or are matching patients to one form of treatment or another
discharged from treatment because of various rules in- yielded any additional benefit or that there were spe-
fractions (Gelman, Underwood, King, Hager, & Gordon, cific patient characteristics that suggested one treat-
1990). ment setting was more advantageous than the other
A great deal of controversy continues to surround the (Rychtarik et al., 2000). As a result of such studies, the
therapeutic community phenomenon. At the time of its “advantages of inpatient versus outpatient care . . .
inception, programs would routinely use methods such have been difficult to show” (Chick, 1993, p. 1374).
as ego stripping and unquestioned submission to the However, the Project MATCH Research Group study
rules of the program. However, some (DeLeon, 1989, also failed to provide for a control group in their exper-
1994; Peele, 1989; Yablonsky, 1967) argue that the TC iment, making comparisons between groups quite dif-
was effective where more traditional treatment meth- ficult (Moos, 2003).
ods had failed. Individuals who enter the TC typically The team of Miller and Hester (1986) were also
pass through three stages before successfully complet- quite critical of inpatient treatment programs. While
ing treatment (Satel & Farabee, 2005): (a) compliance, they did not advocate the complete abolition of inpa-
(b) conformity, and (c) commitment to change. Propo- tient treatment programs, they noted that “there may be
nents of the therapeutic community model note that subpopulations for whom more intensive treatment is
more than 90% of those who complete the program will justifiable. From the limited matching data available at
be drug free (Dekel, Benbenishty, & Amram, 2004), present, it appears that intensive treatment may be bet-
and that even 5 years after completion of the program ter for severely addicted and socially unstable individu-
70% of completers remain abstinent (Satel & Farabee, als” (Miller & Hester, 1986, p. 1246).
2005). Detractors of the TC concept point out that only In response to Miller and Hester’s original (1986)
10%–15% of those admitted to TCs actually graduate work, Adelman and Weiss (1989) conducted their own
(DeLeon, 2004). research into the merits of inpatient treatment. The au-
The picture is not quite so bright for those who fail thors found that 77% of those individuals treated for al-
to finish the therapeutic community program. Approxi- coholism eventually required some form of inpatient
mately 50% of those who remained in the program for treatment. Further, the authors concluded that there
1 year before dropping out were able to abstain from was a treatment duration effect, with those who were
drugs for at least 2 years, and 25% of those who re- discharged from shorter term programs having a higher
mained in the TC for less than 1 year were able to ab- relapse rate than persons who had remained in treat-
stain from drugs for at least 2 years following their ment longer.
decision to leave (DeLeon, 2004). However, 3 years fol- In 1991, Walsh et al. reported the results of a research
lowing discharge from a TC in Scandinavia, almost half project in which 227 workers at a large factory who
of those who were still alive were either working full were known to be abusing alcohol were randomly as-
time or were in training for eventual entry into the signed to one of three conditions: compulsory attendance
at Alcoholics Anonymous, compulsory inpatient treat- to be a cost-effective way to deal with individuals who
ment, or one of these two alternatives chosen by the in- are addicted to heroin.
dividual. The authors were surprised to find that while
the referral to compulsory AA meetings initially was The Advantages of Inpatient Treatment
more cost effective, in the long run inpatient treatment In some ways it is a mistake to compare patients who
resulted in higher abstinence rates. enter outpatient rehabilitation programs with those
How does one determine whether inpatient or out- who enter inpatient treatment programs. Inpatient sub-
patient rehabilitation was successful? One of the tradi- stance abuse treatment programs generally work with
tional measures was whether the former patient would individuals who have encountered a greater number
take part in follow-up care. However, Berg (2003) iden- and severity of problems than those referred to outpa-
tified a subgroup of former drug abusers who were tient treatment.
(a) stable at the time of follow-up but who (b) refused to Individuals need a residental treatment program be-
take part in follow-up studies or treatment because they cause they require more comprehensive treatment pro-
did not wish to reawaken memories of their past life as gramming than is possible in an outpatient treatment
an addicted person. This is not to say that every former setting (Klar, 1987). Because environmental factors play
patient who refuses to take part in follow-up care or a significant role in long-term recovery from substance
research is recovering, but it is possible that a percent- use problems (Moos, 2003), logically a well-designed
age of those who do not participitate in posttreatment residental treatment program would allow patients to
research (including effectiveness-of-treatment studies) assess and address those environmental forces that
might simply not wish to call attention to their former might contribute to their substance use problem. For
addiction. example, research has found that chemically depen-
In spite of the problems in determining which form dent individuals often live alone or lack close inter-
of treatment might be best, the emerging consensus personal supports. The inpatient “community” can func-
seems to be that individuals most likely to benefit from tion as a pseudo-family in the critical early stages of
inpatient rehabilitation programs are those with the recovery when patients are learning to “let go” of the
most severe alcohol/drug addiction problems or those support system that helped to sustain their chemical
with substance use and mental illness issues (Moos, use.
King, & Patterson, 1996; Rychtarik et al., 2000; Shepard Further, people who require inpatient treatment
et al., 1999). Some researchers have found evidence tend to have more medical problems than patients who
that there is a “threshold effect” for the treatment can be referred to an outpatient rehabilitation program.
process, with stronger results achieved after 14 days of Inpatient treatment settings allow for early identifica-
inpatient treatment for people who require inpatient tion and treatment of these ongoing medical problems.
treatment (Moos et al., 1996). Other researchers have Malnutrition is a common problem for people with a
found that lower-functioning alcohol abusers or addicts chronic substance use disorder, for example, and inpa-
appear to benefit more from inpatient than outpatient tient treatment settings allow medical professionals to
treatment (Rychtarik et al., 2000). address the effects of this and other substance-related
The benefits of inpatient treatment do not appear to health problems.
be limited to alcohol abusers; inpatient treatment also Inpatient rehabilitation provides for almost total
appears to be a cost-effective approach for rehabilitat- control over clients’ environment, so staff members can
ing heroin addicts. Swan (1994) noted that the cost of a help to discourage continued drug use in the early
6-month inpatient treatment program for a person ad- stages of recovery. It is not unknown for clients to at-
dicted to heroin would be about $8,250, while the cost tempt to “help out” the detoxification process by taking
to society for not treating the heroin-addicted person in a few additional drugs or drinks during detoxification.
terms of criminal activity, social support services, and When they are detected, these individuals often try to
health care services would be approximately $21,500 defend their continued substance use on the grounds
for the same period. Although a residential treatment that they were in distress and needed the drugs or alco-
program was four times as expensive as simply placing hol that they had ingested. In such cases, the medical
the heroin addict in a methadone maintenance pro- staff can address the clients’ continued substance use
gram, it still was only 40% as expensive as not providing and outstanding medical issues.
any form of treatment for the individual. Thus, one Another advantage offered by the inpatient reha-
could argue that residential treatment programs appear bilitation setting is the opportunity for a structured
environment in which individual and group therapy severity (especially the abuse of multiple substances),
sessions, meals, recreational opportunities, self-help (b) having a criminal history, (c) lack of social/psycho-
group meetings, and spiritual counseling are avail- logical resources, and (d) psychiatric problems prior to
able (Berg & Dubin, 1990). Many clients will attend or in treatment.
their first Alcoholics Anonymous meeting while in an Since their introduction, the patient placement cri-
inpatient setting. In some cases, clients will often af- teria suggested by the American Society of Addiction
firm that they would never have attended the meeting Medicine (ASAM) have been the most commonly used
of Alcoholics Anonymous or Narcotics Anonymous if guide for determining the level of care that will best
they had not been required to do so by treatment meet patient’s needs (American Society of Addiction
staff. Medicine, 2001; Gastfriend, 2004a). The original
The observation that outpatient treatment might be- ASAM placement criteria formed a grid on which each
come a “revolving door” (Nace, 1987, p. 130) is quite individual’s needs could be plotted, as shown in Table
old. Such charges reflect the treatment bias of many 31.1. The most recent revision of the ASAM patient
health care professionals who believe that unlike treat- placement criteria provides for six levels of care:
ment for cancer, heart disease, or diabetes, people
should require just one residental treatment program to 1. Level 0.5: Early intevention
address their substance use disorder. While there is a 2. Level I: Outpatient treatment
danger that inpatient treatment will become a revolv- 3. Level II: Intensive outpatient/partial hospitalization
ing door, an effective, well-designed treatment program 4. Level III: Residential/inpatient treatment
should offer patients the same chances of recovery as a 5. Level IV: Medically managed intensive inpatient
well-designed cancer or cardiac treatment center. treatment
6. Level OMT: Methadone maintenance programs
Disadvantages of Inpatient Treatment
The ASAM placement criteria system requires the
Residental inpatient treatment is quite expensive, with assessor to determine the patient’s strengths and needs
estimated average costs of $525–$792 per week (Belenko in each of six areas or dimensions, such as the individ-
et al., 2005). It is also very disruptive to the individual’s ual’s potential for serious medical problems during
social, vocational, and family life (Morey, 1996). Clients detoxification from drugs, the strength of the individ-
are forced to leave their normal environment to partici- ual’s abstinence support system, and so on. Depending
pate in the rehabilitation program, with no time to work, on the patient’s requirements in each area, he or she
participate in family life, or engage in activities outside might then be placed in one of above levels of care.
the treatment center. Inpatient treatment programs usu- Since its introduction, the ASAM placement crite-
ally address severe and chronic substance use problems ria have been found to be effective by research studies
and thus are generally unsuited for individuals with less designed to address criticism of this system raised by
intense chemical abuse issues (Larimer & Kilmer, 2000). managed care1 programs (Gastfriend, 2004). But the
Finally, the treatment center setting might be quite iso- original ASAM placement criteria were relatively inflex-
lated, preventing easy contact between the patient and ible, grouping treatment options together and forcing
family or friends. All of these factors are disadvantages restrictions on patient placement (Gastfriend, 2004b).
of the inpatient rehabilitation program. The latest revision added sublevels for different treat-
ment options as outpatient or evening/day treatment,
partial hospitalization, and halfway house placement.
Inpatient or Outpatient Treatment? In terms of total cost, outpatient treatment programs
Whether to use inpatient or outpatient treatment are usually less expensive than inpatient programs.
for a client is one of the most important decisions a Outpatient rehabilitation programs are best suited to
treatment professional will make (Washton, Stone, & clients without an extensive prior treatment history
Hendrickson, 1988). Fortunately, in the last decade sev- (Nace, 1987). Motivation for treatment and past treat-
eral organizations have published referral guidelines ment history both offer hints as to whether an inpatient
to assist in referring substance abusers to the proper re- or an outpatient program would be most effective in a
habilitation program. Simpson (2004) identified several person’s recovery. A sad and rarely discussed fact is that
client characteristics that suggested a need for the more
intensive inpatient treatment program: (a) addiction 1
TABLE 31.1 The ASAM Placement Criteria
Level I Level II Level III Level IV
Level of care Intensive outpatient Medically managed

treatment/partial Medically monitored inpatient treatment
hospitalization inpatient treatment (traditional medical
Dimension Outpatient treatment program (residential treatment) treatment)
Acute intoxication/ None Minimal Severe risk, but Severe risk that
withdrawal potential* does not require requires hospi-
hospitalization talization
Biomedical conditions None/stable Minimal: can Serious: requires Serious: requires
or complications* be managed in medical monitoring inpatient hospi-
outpatient setting talization
Emotional/behavioral None/stable Mild: but can Serious: requires Serious: requires
conditions or be managed in patient to be moni- inpatient psychi-
complications outpatient setting tored 24 hours/day atric care
Readiness to change Cooperative: needs Some resistance: Resistance is severe: N/A
guidance and intensive treatment requires intensive
monitoring needed treatment
Relapse/continued Minimal risk of High risk of relapse Patient is unable to N/A
chemical abuse/ relapse: needs without close moni- control use without
ongoing problem monitoring and toring and support being in inpatient
potential guidance only by staff setting
Recovery environment Patient has skills and Patient lacks envi- Environment is dan- N/A
support to abstain ronmental support gerous to patient, and
on own but has skills to she or he must be
cope, with some removed from it
structure
Note: This table is designed to illustrate the 2001 revision of the ASAM placement criteria and should not be used as a guide
to patient placement.
*As determined by a licensed physician.
the restrictions on funding will play a role in deciding Turbo (1989) identified several client classifications
which treatment options are available for the individ- suggesting that an inpatient treatment program might
ual. The person whose insurance will pay for only inpa- be better for the client than the outpatient setting.
tient chemical dependency treatment will have certain These criteria included (a) clients with repeated failure
financial restrictions placed on his or her treatment op- to maintain sobriety in outpatient treatment, (b) acutely
tions. Thus, availability of funding is one factor that in- suicidal clients, (c) clients with seriously disturbed home
fluences the decision of whether to seek inpatient or environments, (d) clients with serious medical prob-
outpatient treatment for substance abuse. Finally, the lems, and (e) clients with serious psychiatric problems.
individual’s psychiatric status and availability of social In addition, Allen and Phillips (1993) suggested that
support should be evaluated when considering outpa- the patient’s legal status also be considered in deciding
tient treatment as an option (Group for the Advance- whether to refer the patient to inpatient or outpatient
ment of Psychiatry, 1990; Nace, 1987). Obviously, a treatment. People who have been arrested for drug pos-
deeply depressed individual who is recovering from an session or for driving while under the influence of
extended period of cocaine use might benefit more chemicals might do better in an outpatient treatment
from the greater support offered by an inpatient treat- program, according to the authors. Patients who had
ment program, at least during the initial recovery pe- achieved periods of sobriety but had then relapsed
riod when the depression is most severe. might be treated briefly on an inpatient basis, according
to the authors. But following a brief “stabilization” stay Turbo (1989) discussed an interesting variation on
in the hospital, these patients might be switched to an the two by four program developed for the Schick
outpatient treatment program, according to Allen and Shadel chain of hospitals, located in California, Texas,
Phillips. and Washington. These programs admit the individual
The final decision about inpatient or outpatient for 10 days of inpatient treatment, followed by two addi-
treatment ultimately centers around this: Given the tional inpatient “reinforcement” days later. The first
client’s resources and needs, what is the least restrictive “reinforcement” day of hospitalization occurs 1 month
treatment alternative? (American Psychiatric Associa- after discharge, and another 2 days of inpatient treat-
tion, 1995). The treatment referral criteria advanced by ment are scheduled for 2 months following the initial
ASAM (Morey, 1996) are useful guides to the selection admission. One disadvantage of inpatient treatment is
of the least restrictive alternative that will meet the that admission to such a level of care, even for short pe-
client’s needs. Although some will argue that the inpa- riods of time, appeared to result in “a lower probability
tient treatment program sounds very similar to a con- of complying with outpatient after care” (Berg & Dubin,
centration camp experience, one must recall that the 1990, p. 1177) by the client. Berg and Dubin found a
dysfunction caused by drug addiction often requires 60% dropout rate for those who were initially hospital-
drastic forms of intervention. ized for a brief period of time and then were referred to
an intensive outpatient treatment program.
Day hospitalization. The day hospitalization format
Partial Hospitalization Options is also known as partial day hospitalization. Such pro-
In recent years, several new treatment formats have grams typically provide 3–12 hours a day of treatment,
been explored that combine elements of inpatient and for 3–7 days of the week. After detoxification has been
outpatient rehabilitation programs. In terms of effec- accomplished, the client is allowed to live at home. But
tiveness, partial hospitalization programs offer success the individual will come to the treatment center during
rates that are equal to or possibly even superior to inpa- scheduled treatment hours to participate in the rehabil-
tient treatment, yet are only one-third to one-half as ex- itation program.
pensive as inpatient treatment (Gastfriend & McLellan, There are several advantages to partial hospital pro-
1997). Each of these rehabilitation formats offers ad- grams for substance abuse rehabilitation, including the
vantages and disadvantages, yet each should be consid- fact that such programs provide “an intensive and struc-
ered as a viable treatment option for clients who present tured treatment experience for patients with substance
themselves for treatment. Depending upon the client’s dependence who require more services than those
needs, some of the new treatment formats might prove generally available in traditional outpatient settings”
to be quite beneficial. (American Psychiatric Association, 1995, p. 23). Fur-
Two by four programs. One proposed solution to the ther, day hospitalization programs tend to be less expen-
inpatient/outpatient treatment dilemma is the so-called sive than traditional inpatient treatment programs, with
two by four program. This program format borrows the cost of day treatment being approximately half that
from both inpatient and outpatient treatment programs of inpatient treatment (French, 1995). Such programs
to establish a biphasic rehabilitation system that seems provide a greater intensity of therapeutic intervention
to have some promise. The patient is first hospitalized than is available through traditional outpatient treatment
for a short period of time, usually 2 weeks, in order to while still avoiding the need for inpatient treatment
achieve total detoxification from chemicals. Depend- where possible (Guydish, Werdeger, Sorensen, Clark, &
ing on the individual’s needs, the initial period of hos- Acampora, 1998).
pitalization might be somewhat shorter or longer than An essential element of day hospitalization is that the
2 weeks. However, the goal is to help clients reach a client have a supportive, stable family. Obviously, if the
point that they can participate in outpatient treatment client’s spouse (or other family member) also has a
as soon as possible. If, as will occasionally happen, chemical abuse problem, day hospitalization may not be
clients are unable to function in the less restrictive out- a viable treatment option. If the client’s spouse is severely
patient rehabilitation program, they may be returned codependent and continues to enable the client’s chemi-
to the inpatient treatment format. Later, when addi- cal use, day hospitalization should not be the treatment
tional progress has been made, clients may again re- of choice. But if the client has a stable home environ-
turn to an outpatient setting to complete their treatment ment, day hospitalization offers the opportunity to com-
program. bine intensive programming with the opportunities for
growth possible by having the client spend the morning centers across the United States; these people had been
and evening hours at home. Such a program is of value referred to community residential living facilities fol-
for clients who need to rebuild family relationships lowing completion of their primary treatment program.
after a protracted period of chemical use, and they have The authors found that patients who had remained in
been found to be as effective as inpatient treatment pro- the community residential living facility were signifi-
grams in client rehabilitation (Guydish et al., 1998). cantly less likely to have been readmitted for substance
Halfway houses. The halfway house concept emerged use in the 4 years following discharge from the commu-
in the 1950s in response to the need for an an interme- nity living unit.
diate step between the inpatient treatment format and These findings were supported by Hitchcock, Stain-
independent living (Miller & Hester, 1980). For clients back, and Roque (1995), who compared the relapse
without a stable social support system, the period of rate of 82 patients who elected not to enter a halfway
time following treatment is often most difficult. Even if house with that of 42 patients who did. The authors
they are strongly motivated to remain sober, clients found that patients discharged to a community setting
must struggle against the urge to return to chemical use (i.e., home, to live in an apartment, or to live with friends
without the social support necessary to aid in this struggle. or relatives) were significantly more likely to drop out of
The halfway house provides a transitional living facility treatment in the first 60 days following discharge from
for such clients during the time immediately following an inpatient substance abuse rehabilitation program.
treatment. The authors concluded that halfway house placement
Miller and Hester (1980) identified several common can significantly enhance patient retention in aftercare
characteristics of halfway houses including (a) a small programs, thus improving treatment outcome.
patient population (usually fewer than 25 individuals), Two variables that seem to impact patient outcome
(b) a brief patient stay (less than a few months), (c) em- after placement in a halfway house setting were (a)
phasis on Alcoholics Anonymous or a similar 12-Step length of stay in the halfway house, and (b) the individ-
philosophy, (d) minimal rules, and (e) a small number ual’s continuing to be involved in a rehabilitation pro-
of professional staff members. Most halfway houses uti- gram (Moos, Moos, & Andrassy, 1999). Moos et al.
lize a 12-Step philosophy. Many hold in-house self-help (1999) examined the outcome of 2,376 cases of pa-
group meetings such as Alcoholics Anonymous while tients who were admitted to halfway house settings
others require a specified number of community self- after completing primary treatment in Veterans Ad-
help group meetings a week. Each individual is expected ministration hospital units. Patients who remained in
to find work within a specified period of time (usually the halfway house longer abstained from alcohol/drug
2–3 weeks) or is assigned a job within the halfway house. use longer than patients who stayed for a shorter time.
The degree of structure in the traditional halfway Further, those assigned to halfway houses that placed
house setting is somewhere between an inpatient treat- emphasis on continued rehabilitation—through the ex-
ment program setting and a traditional household. It pectation that clients would participate in programming
provides the client with enough support to function designed to help them abstain from chemicals—did bet-
during the transitional period between treatment and ter than those who were referred to “undifferentiated”
self-sufficiency, yet allows the client to make choices halfway houses where there was no attempt at contin-
about his or her life. As Miller and Hester (1980) ued treatment.
pointed out, halfway houses usually have fewer rules The findings of Moos et al. (1999) help to explain
than an inpatient treatment center. Halfway house par- the often contradictory findings of earlier researchers
ticipation is usually time-limited, usually 3–6 months, who examined the usefulness of halfway house place-
after which the client is ready to assume his or her re- ment. According to Moos et al., it is necessary to exam-
sponsibilities again. ine the treatment philosophy of the different halfway
Although Miller and Hester (1980) found little evi- houses utilized in previous research studies to deter-
dence that the halfway house concept was a useful ad- mine whether they attempted to involve the resident in
junct to treatment, a number of subsequent studies some form of aftercare. Thus, although early research
have failed to support this conclusion. For example, failed to support the halfway house concept, subse-
Moos and Moos (1995) followed a sample of 1,070 indi- quent investigations have revealed that halfway houses
viduals who had been treated for substance abuse prob- do indeed seem to be an effective adjunct to the reha-
lems at one of 77 Veterans Administration medical bilitation process of chemical abusers.
Summary from outpatient treatment programs, however, and much

remains to be learned about how to make outpatient
There is significant evidence that for some addicted in- addiction treatment more effective.
dividuals, outpatient treatment is an option that should Inpatient treatment is often viewed as a drastic step.
be considered by treatment professionals. For clients Yet, for a minority of those who are addicted to chemi-
with the proper social support, and for whom there is cals, such a drastic step is necessary if the client is ever
no co-existing psychiatric illness or need for inpatient to regain control of his or her life. The inpatient reha-
hospitalization, outpatient therapy for drug addiction bilitation program offers many advantages over less re-
may allow the individual to participate in treatment strictive treatment options, including a depth of support
while still living at home. This avoids the need for a services unavailable in outpatient treatment. For many
reorientation period following treatment, as is often of those in the advanced stages of addiction, inpatient
necessary for patients who have been hospitalized in an treatment offers the only realistic hope of recovery.
inpatient rehabilitation facility. In recent years, questions have been raised concerning
Outpatient treatment also allows for long-term ther- the need for inpatient treatment programs or halfway
apeutic support that is often not available from shorter house placement following treatment. It has been sug-
inpatient programs. Within an outpatient drug addic- gested that inpatient treatment does not offer any ad-
tion program, random urine toxicology screening may vantage over outpatient treatment or that a longer length
be used to check on medication compliance and to of stay was any more effective than short-term treat-
identify individuals who have engaged in illicit drug ment. However, others have concluded that length of
use. Research evidence suggests that for many patients, stay was inversely related to the probability of relapse
outpatient drug addiction treatment is as effective as in- following treatment.
patient programs. There is a significant drop-out rate
CHAPTER THIRTY-TWO
Relapse and Other Problems

Frequently Encountered in Treatment
Research has consistently demonstrated that treatment program director, or anyone else so the client won’t be
is more effective than criminal justice sanctions as a discharged from treatment.
way of dealing with substance use disorders (SUDs) For the chemical dependency professional to honor
(Scheer, 1994b). But no matter which treatment ap- the request not to tell other staff members would be to
proach therapists choose, they may experience a num- enter into collusion with the addicted person—a part-
ber of potential problems in working with the client. In nership which, because it was set up by the addicted
this chapter, we examine some of the more common person, will make the professional an “enabler.” In
and more serious problems encountered by treatment some situations, not to report this rule violation might
professionals working with clients with SUDs. make the professional vulnerable to later extortion by
the client, who would be in the position of reporting
the professional to his or her superiors for not passing
Limit Testing by Clients in Treatment on the information to staff as he or she should have
done.
Clients in therapeutic relationships, which include ad-
The proper response to this situation is to properly
dicted clients in a treatment setting, will often “test the
document the material discussed immediately, in writ-
limits.” They do this consciously or unconsciously to
ing, through proper channels. This might be a memo
determine whether the professional will be consistent
or an entry into the client’s progress notes as well as a
in his or her treatment of the client. This limit testing
discussion of the material revealed by the client with
can take a number of forms, from missed appointments
the professional’s immediate supervisor. This is done
to using chemicals while in treatment.
without malice to ensure both uniform enforcement of
The chemical dependency professional should be
the rules for all clients and to protect the professional’s
aware that “dependability” and “consistency” also apply
reputation.
to the enforcement of the rules of the program. McCarthy
and Borders (1985) found that clients in a methadone
maintenance program who were warned that four Treatment Noncompliance
“dirty”1 urine toxicology tests in a year would result in
involuntary termination from the program did better In no other sphere of medicine is the social stigma sur-
than individuals who had no such warning. rounding substance use as apparent as in the arguments
The counselor and treatment “secrets.” One common that because substance abuse rehabilitation programs
situation is for the client to ask for an individual confer- suffer from high dropout and relapse rates, they are not
ence with the staff member and then to confess to a effective. These assertions are not applied to the other
rules infraction. Often this admission of guilt is made to specialties in medicine, where patient noncompliance
a student or intern at the agency rather than to a regular is also a problem, but exclusively to the field of addic-
staff member. The confession might be an admission of tion medicine. To illustrate, consider how cancer
having used chemicals while in treatment or some treatment programs do not insist that the patient be in
other infraction. Then, after having made this admis- remission before he or she is admitted for treatment,
sion, the client will ask the staff member not to bring although this is the standard for care in the addictions
this information to the group, other staff members, the field (Blume, 2005). A patient who is repeatedly hos-
pitalized for diabetes-related problems might be
1A urine toxicology test is said to be “dirty” if it reveals evidence of termed a “brittle” diabetic by physicians, whereas the
illicit drug use. alcohol-dependent individual who is rehospitalized
362
Relapse and Other Problems Frequently Encountered in Treatment 363
TABLE 32.1 Approximate Rates with treatment recommendations (Cooney, Zweben, &
of Treatment Noncompliance Fleming, 1995).
Unfortunately, there are no specific personality traits
Percentage of patients
that are predictors of patient drop out (Miller, 2003). A
who fail to follow
Class of medications dosing instructions complicating factor is that the individual’s commitment
to treatment is not the same as making the commitment
Antiepileptics 30–50 to change (Connors, Donovan, & DiClemente, 2001).
People might agree to enter a rehabilitation program for
Antihypertensives 30–60
many different reasons and never make a commitment
Blood-lipid-lowering agents 25–30 to actually discontinue their substance abuse (Connors
Antiarrhythmics 20 et al., 2001). Others, usually those who have been man-
dated to treatment, may go through the motions of fol-
Antidepressants 30–40
lowing a treatment program without having any internal
Immunosuppressive agents 18 desire to stop or reduce their chemical abuse (Connors
Antidiabetics 30–50 et al., 2001).
As a general rule, substance abuse rehabilitation
Anticoagulants 30
programs experience significant levels of patient attri-
Antiasthmatics 20–60 tion. Researchers have found that up to 50% of those
Sources: Based on Lacombe, Bicente, Pages, & Morselli (1996);
admitted to substance abuse rehabilitation programs
McLellan, Lewis, O’Brien, & Kleber (2000). will drop out of treatment before the 90th day, and 66%
will drop out by the end of 6 months (McCusker,
Stoddard, Frost, & Zorn, 1996). In Israel, Rabinowitz
for alcohol-related problems is called “a treatment fail- and Marjefsky (1998) examined the issue of premature
ure.” Proponents of the public health model of addic- termination from treatment through a retrospective
tions point out that each of these patients has a chronic, analysis of the records of 764 male patients. The au-
relapsing disorder, yet only in the field of substance thors found that social isolation was a major predictor of
abuse rehabilitation is rehospitalization referred to as a patient dropout. Behaviors such as soliary drinking, not
treatment failure. being married, having no children, and being unem-
Patient noncompliance is a problem for each spe- ployed were associated with a greater chance of treat-
ciality in medicine, not just substance abuse rehabilita- ment failure, the authors concluded. These indicators
tion. For example, 40%–60% of patients with Type 1 could serve as possible warning signals for male patients
diabetes, hypertension, or asthma do not take the med- who are at risk for premature termination from treat-
ications prescribed for these conditions as instructed ment, possibly alerting staff to the need for special ef-
(Marlowe & DeMatteo, 2003).2 Even for mild bacterial forts to help these individuals remain in and benefit
infections, it is the rare patient who completes the pre- from treatment.
scribed 10-day course of antibiotics (Markel, 2004).
Table 32.1 provides a summary of different medical Relapse and Relapse Prevention
conditions and the percentage of patients who do not
follow treatment recommendations for that disorder. Technically, the term relapse is based on the medical
Thus, although treatment noncompliance is not model in which the individual falls into a disease state
limited to substance abuse rehabilitation programs, it after a period of remission (Marlatt & Witkiewitz, 2005).
is a significant problem. Even when the client has re- In the field of substance abuse rehabilitation, the term
quested detoxification from alcohol/drugs, he or she will is applied to situations in which the individual returns
often fail to complete the detox program because of con- to the active abuse of a chemical after a period of ab-
current medical problems, severity of withdrawal symp- stinence. Unfortunately, although 99% of substance
toms encountered, drug use “urges,” and other reasons abuse treatment programs aspire to the goal of total ab-
(Franken & Hendriks, 1999). Only 10%–30% of people stinence, only a minority of people who complete a re-
at risk for an alcohol use disorder actually follow through habilitation program will totally abstain from further
chemical abuse (Leavitt, 2003). Between 50% and 90%
2
Pirisi and Sims (1997) suggested that this percentage might be as of those treated for substance use disorders (SUDs) will
high as 86% for some conditions. relapse at least once within the first 90 days following
364 Chapter Thirty-Two
discharge, and 45%–50% will have returned to their 1. Self-efficacy: The individual’s confidence in his or
pretreatment drinking levels within a year (Polivy & her ability to cope with high risk situations/thoughts/
Herman, 2002). urges.
While these statistics would suggest a rather pes- 2. Outcome expectancies: The individual’s expectations
simistic view of the efficacy of treatment for substance about the effects of a substance if he or she should
use disorders, eventually 40% of individuals with an use it.
SUD learn to abstain either on their own or with profes- 3. Craving: Although craving itself is a poor predictor
sional assistance (Gitlow, 2007). An additional 20% ex- of relapse, it may be triggered by drug use cues
perience periods of greater or lesser abstinence and (smells, the sight of the drug, sounds, etc.) and trig-
within 3–5 years of the start of treatment begin to ab- ger moods and memories that predispose the indi-
stain from all alcohol/drug abuse (Gitlow, 2007). The vidual to substance use. For example, the sight of a
remaining 40% go on to develop a progressive addic- cigarette ashtray may reawaken memories of past
tion to alcohol/drugs that may ultimately prove fatal smoking, causing the individual to “crave” a cigarette
(Gitlow, 2007). These data reflect the grim reality that at that time.
the disease of addiction is one that at best can be arrested 4. Motivation: The individual’s motivation to change
but can never be cured. his or her behavior or to return to past behaviors has
Relapse prevention is defined as a self-management been found to play an important role in his or her
program to assist the individual in arresting his or her successful coping with drug use cues.
addiction to the best degree possible (Marlatt & Donovan, 5. Coping: This poorly understood determinant of re-
2005). Within this context, the individual’s relapse is lapse seems to reflect the individual’s ability to call
not a sign that rehabilitation has failed, and more than upon learned coping resources (behavioral, cogni-
the diabetic patient’s hospitalization for stabilization tive, etc.) when confronted with drug use cues.
is needed as a sign that the treatment program has 6. Emotional states: Research suggests a strong associa-
failed. tion between affect states and relapse, with negative
Relapse is the end product of one of three mecha- emotions being more often reflective of a full relapse
nisms: (a) drug exposure (either to the same compound while positive states seem to be associated with a be-
as abused before, a similar compound, or another drug havioral lapse.
of abuse), (b) stress exposure, or (c) cue reexposure (en- 7. Interpersonal support: The individual’s access to strong
vironmental cues previously associated with substance social support systems during times of craving seem to
use) (Boles, 2007). Unfortunately, these three pathways contribute to continued abstinence.
interact, providing an almost infinite number of indi-
vidual pathways to the return to active substance use. For either system, there are both proximal4 and distal5
For example, drug exposure in all its forms holds the forces that can move the individual closer to or further
potential to reactivate the reward pathways once stimu- away from the danger of relapse (Donovan, 2005). For
lated by the original drug of abuse, initiating a neuro- example, the individual’s biological heritage is an often
chemical cascade that can cause urges and a relapse overlooked distal factor in relapse, in that it might iden-
(Boles, 2007). Or exposure to stressors, including that of tify someone whose biological heritage contributes to
social isolation3 can contribute to strong cravings for urges to abuse chemicals (Donovan, 2005; Westphal,
chemicals, and thus to relapse (Boles, 2007). Finally, Wasserman, Masson, & Sorenson, 2005). A proximal sup-
through the process of associative learning, certain neu- portive factor might be the individual’s active involve-
rochemical states are associated with chemical abuse, ment in a 12-Step support group such as Narcotics
triggering thoughts and urges to use when these (or Anonymous (NA), while not being involved in such a
similar) neurochemical states are encountered again group could be a proximal factor contributing to relapse.
(Boles, 2007).
In contrast to this overview of the predictors of re- 4Proximal forces are those that are in close proximity to the event in
lapse, Marlatt and Wikiewitz (2005) identified a large question. For example, hitting a major pothole might have caused the
driver to lose control of the vehicle and thus is the proximal cause of a
number of factors that interacted to predict a possible
motor vehicle accident.
relapse to active chemical abuse: 5Distal forces are those that are more distant from the relapse event in
time. Using the example above, the winter’s freeze-thaw cycles that
3 weakened the road pavement and caused the pothole to form would
Hence the need for a substance-free support system, especially dur-
ing early recovery. be a distal cause of the accident that ultimately took place.
Factor analysis research has revealed three categories Cognitive errors play a significant role in relapse.
of proximal warning signs that suggest the individual is at One such error is a person’s tendency to take a very
higher risk for a relapse (Donovan, 2005): (a) cognitive short-term view of recovery. Researchers have found that
traits (such as “euphoric” recall, or a tendency to engage after people have abstained for 6 years they are unlikely
in cognitive errors), (b) emotional states, and (c) behav- to relapse to active drinking (Vaillant, 1996). Treatment
ioral characteristics. These groups of factors might inter- staff must thus help recovering patients learn not to let
act to bring about a relapse or help protect the individual down their guard before abstinence becomes a new
from relapsing. Cognitive factors that move the individ- lifestyle. During this interim period newly abstinent in-
ual closer to a relapse are also called maladaptive dividuals will continue to think in much the same way
thoughts6 (Beck, 2004; Daley & Marlatt, 2005; Keller, they did when actively addicted. They must learn not to
2003). Examples of maladaptive thoughts include “I can rush their recovery in the first months or years after that
control it now,” or “relapse won’t happen to me.” An- last drink or use of a drug.
other common maladaptive thought is the desire to Emotional states have long been suspected of con-
“test” one’s recovery, often rationalized as a desire to re- tributing to or protecting from the risk of relapse.
turn to the bar to see friends. Such maladaptive thoughts While clinical evidence has pointed to negative emo-
may allow the individual to (a) convert ordinary stress tional states as a possible relapse trigger, research has
into a source of excessive distress (e.g., “I can not stand suggested that positive emotional experiences can also
feeling this way!”), (b) transform distress into a craving be a relapse trigger when people begin to view chemi-
(e.g., “I need to use [have a drink, etc.] in order to cope cal abuse as a way to ensure that the positive feelings
with this!”), and (c) rationalize the individual’s relapse continue.
(e.g., “Surely I can handle just one”) (Beck, 2004). Spiritual issues can serve as a path away from sub-
Another category of maladaptive thoughts centers stance use disorders or contribute to relapse (Gitlow,
around the individual’s desire for indulgence (Blume, 2007). Such issues might include ongoing feelings of
2005). The person might come to believe that “I deserve shame as well as social and spiritual isolation.
a drink after what I’ve accomplished,” for example. He Psychological stressors can serve as relapse triggers.
or she might want to escape from negative life stressors, An often overlooked factor is that people’s substance
if only for awhile, by indulging in the use of alcohol or use might fill a need such as allowing them to associate
drugs. Planned or unplanned meetings with drug-using with others (even if these others are intoxicated or
friends offer one category of high-risk situation (Blume, under the influence). The core personality type, while
2005; Westphal et al., 2005). Finally, the individual best conceptualized as a distal relapse trigger because it
might be disappointed that abstinence does not bring is relatively fixed and unchanging, may predispose some
with it the immediate rewards of alcohol/drug use and persons to relapse (Chiauzzi, 1990, 1991; Donovan,
drift back to substance use as a consequence of this dis- 2005). Such relapse-prone personality traits include a
covery. Such maladaptive thoughts or cognitive distor- tendency toward compulsive behaviors, since such in-
tions need to be addressed if the person is to successfully dividuals do not adjust well to even minor changes in
abstain from alcohol/drugs. routine. Psychological dependency is another person-
Social pressure was found to play a significant role in ality trait that increases vulnerability to a relapse, since
the return to alcohol use by Zywiak et al. (2006). The such individuals have trouble asserting their wish to
authors based their conclusions on the data obtained maintain a recovery program when confronted with
from 592 patients enrolled in a larger research study drug use cues and opportunities (Chiauzzi, 1990,
known as “Project MATCH,” and found three classes of 1991). Passive-aggressive personality traits also place
relapses: (a) negative affect/family influences, (b) craving/ individuals at risk for relapse because of a tendency to
cued relapses, and (c) social pressure, with the last ac- blame others for their behavior. The narcissistic traits
counting for more than 58% of the identified relapse often found in addicted persons prevent many from
events. The authors also found that motivational inter- admitting to the need for help during a weak mo-
viewing seemed to provide greater protection against ment, while antisocial personality traits underscore a
social pressure–related relapses than the other interven- tendency toward impulsiveness and a desire not to
tions utilized in the Project MATCH study. follow the road taken by others (Chiauzzi, 1990,
1991).
6Members of Alcoholics Anonymous would call such cognitive errors Another emotional state that contributes to the
“stinking thinking” (Keller, 2003). risk of relapse is the tendency to substitute addictions
for the chemicals were once abused (Chiauzzi, 1990, people develop an awareness of their potential areas of
1991). Examples of such substitute addictions in- weakness so they can rehearse how to deal with the
clude compulsive work, relationships, food, or switch- identified high-risk situations. Some people carry a re-
ing from one drug of abuse to another. It is not minder card in the wallet or purse so they will have
uncommon for people who have relapsed to admit written instructions on the steps to take to limit the re-
that after they stopped abusing a specific chemical lapse. Through this process, they enhance their cop-
their use of another chemical increased or became ing skills and self-efficacy. But it is not possible to
problematic. The cocaine abuser might, upon achiev- identify every potential high-risk situation in advance
ing abstinence from cocaine, suddenly begin to drink (Daley & Marlatt, 2005). Further, people’s cognitive
alcohol abusively or switch to the compulsive use of assessment of their ability to cope with internal and
opioids. external substance use cues is a major factor in deter-
The relapse, if it occurs, does not suddenly appear. mining whether they are able to cope with the high-
Rather, it is preceded by a range of warning signals of risk situation.
the impending relapse. Unfortunately, the individual in It is important to remember that a process of condi-
the earlier stages of recovery is often insensitive to these tioned learning takes place while people are using
warning signs of potential danger (Daley & Marlatt, alcohol/drugs. Following cessation, sights, sounds, smells,
2005). Through a series of seemingly irrelevant decisions, and mood states associated with chemical use can trig-
newly recovered individuals will often place themselves ger thoughts, urges, and cravings to use chemicals. This
in a high-risk situation (discussed below) possibly with- process of associative learning is clearly seen in the ob-
out being aware of more than the last decision in a servation that 58% of recovering alcohol-dependent
chain of choices that ultimately resulted in the relapse persons say that they smoke cigarettes to cope with the
(Keller, 2003). urge to drink alcohol (Monti, Kadden, Rohsenow,
It is necessary to remind the reader that relapse is a Cooney, & Abrams, 2002). Given the strong association
process, not a single event (Daley & Marlatt, 2005). Indi- between alcohol use and cigarette smoking, resorting to
viduals who relapse do so after making a series of deci- cigarette use to cope with an urge to drink might be
sions of greater or lesser importance, which cumulatively viewed as engaging in a “half measure.” In another
contribute to the ultimate relapse. Such decisions do not view, by smoking, the individual is trying to cope with the
involve a choice to actively abuse chemicals until the urge to drink by engaging in a behavior associated with
very end of the chain of events that results in the relapse. drinking without actually using alcohol.
Examples of such a “mini-decision” might be for the re- Recovering opiate-dependent people can suddenly
covering person to reduce the frequency with which he experience a craving for narcotics after being drug free
or she attends a support group, or to maintain a relation- for months or even years if they return to the neigh-
ship with a person who is still actively abusing chemicals. borhood where they once used chemicals (Galanter,
The therapist is often able to reconstruct the decision 1993). The mechanism through which this takes place
chain that marked the individual’s step-by-step progres- could be based in the unconscious, for “most of a
sion toward the final decision to once again use alcohol/ person’s everyday life is determined not by their con-
drugs. scious intentions and deliberate choices but by men-
High-risk situations contribute to the possibility of tal processes that are put into motion by features of
relapse by exposing the individual to chemical use the environment and that operate outside of conscious
cues and opportunities. Such situations often arise awareness” (Bargh & Chartrand, 1999, p. 462). It is
without warning (Witkiewitz & Marlatt, 2004) and for this reason that clients learn relapse prevention
usually involve intra/interpersonal situations (Daley & skills through behavioral rehearsal procedures to help
Marlatt, 2005; Keller, 2003). Techniques that help the them recognize and avoid environmental triggers.
individual identify potential high-risk situations and Such behavioral training might be viewed also as fos-
develop appropriate coping skills will increase his or tering self-efficacy (Witkiewitz & Marlatt, 2004). It is
her chances of achieving long-term recovery (Donovan, not possible to identify every relapse trigger, but the
2005). Psychological tests such as the Inventory of more significant antecedents of relapse are summa-
Drinking Situations (IDS-100)7 are of value in helping rized in Table 32.2.
Successful relapse prevention training programs in-
7See Glossary. clude support in the earliest stages of recovery, when
TABLE 32.2 Common Relapse Situations
Description of situation that

Category of relapse contributed to or caused relapse Percentage of cases
Negative emotional states Feelings of frustration, anger, anxiety, depression, or boredom 35

Peer pressure Pressure from either a single person (such as a close friend) 20
or a group of people (co-workers, for example) to use
chemicals
Interpersonal conflict Conflict between patient and a friend, employer, employee, 16
family member, or dating partner
“Craving” for drugs/alcohol Person becoming preoccupied with use of alcohol and/or 9
drugs, in spite of abstinence
Testing personal control Person exposing self to high-risk situation to see whether 5
he or she is able to resist urges to use chemicals
Negative physical states Person experiencing a negative physical state such as 3
illness, postsurgical distress, or injury
Source: Based on material provided by Dimeff & Marlatt (1995) and Daley & Marlatt (2005).
individuals are most vulnerable to relapsing. The re- 2003; Merikle, 1999; Weiss et al., 2003). Different re-
search data suggest that those who remain in a relapse searchers have used each term in widely disparate ways,
prevention program tend to be the ones who achieve resulting in confusion about their meaning and defini-
long-term abstinenence. tion not only in the professional literature but also in
There is mixed evidence to support the concept of the popular media.
relapse prevention training (Hester & Squires, 2004; For this text, craving is viewed as an intense sub-
Irvin, Bowers, Dunn, & Wang, 1999). Such programs jective emotional and physical experience that varies
may very well combat the sense of demoralization, in intensity from one individual to another (Merikle,
anger, and depression that seem to identify those 1999). Because it is a subjective experience the same
most prone to relapse (Miller & Harris, 2000), and in- symptoms of craving might be interpreted as intense
volvement in an ongoing relapse prevention program by one individual and as quite weak by another
that has both individual and group sessions does seem (Weiss et al., 2003). It has been reported that the ex-
to increase the chances of long-term abstinence perience of craving will wax and wane in intensity
(McKay, 2006). Patients who remain in a relapse pre- during the first 12 months of recovery, with the
vention group for a year or more after primary treat- strongest craving for chemicals developing during the
ment show significantly higher rates of abstinence first 90 days (Carol, Smelson, Losonczy, & Ziedonis,
than patients who fail to do so (McKay, 2006). Such 2001).
ongoing relapse prevention program work in concert On the basis of animal research, scientists have
with 12-Step group programs and provide ongoing in- identified a reduction in the number of receptor sites
dividual and group support for the individual during for the neurotransmitter glutamate in the nucleus ac-
times of crisis. cumbens region of the brain, which seems to correlate
with drug craving (Kuehn, 2006). Symptoms of crav-
ing include obsessive thoughts about obtaining chemi-
Cravings and Urges cals, and physical symptoms of arousal such as sweating
Although researchers agree that craving and urges are palms, rapid heartbeat, and salivation (Anton, 1999;
important concepts in the treatment of substance use Merikle, 1999). In humans, researchers have found al-
disorders, there is no universally accepted definition of tered blood flow patterns during periods of craving in
either term, nor a way to measure these constructs those regions of the brain associated with pleasure and
(Anton, 1999; Ciraulo, Piechniczek-Buczek, & Iscan, reward, even in alcohol-abusing adolescents whose
past alcohol use history is limited (Tapert et al., 2003; withdrawal. As discussed earlier, many of the recre-
F. Weiss, 2005). The combination of human and ani- ational chemicals have a characteristic pattern of with-
mal research suggests that there are neurological com- drawal symptoms. To avoid this withdrawal syndrome,
ponents to the process of craving that contribute to the people will engage in additional substance use. For
subjective experience of wanting to use chemicals example, the nicotine-dependent individual will smoke
again. But keep in mind that there is a vast difference a cigarette or the alcohol-dependent individual will
between a hard choice to abstain from chemicals and have another drink when they experience the earliest
no choice but to engage in substance use (Gendel, symptoms of withdrawal.
2006). Next, there is the tendency for former users to want
Psychologically, the experience of craving might to use chemicals when they are unhappy or uncomfort-
best be understood as a “pathological motivational state” able (Beck et al., 1993). These chemical-use urges are
(Wexler et al., 2001, p. 86) in which the individual be- triggered by some of the “antecedents” of relapse iden-
comes fixated on the drug of choice. Such periods of tified by De-Jong (1994). These antecedent situations
craving might be triggered by internal mood states; en- then cause the individual to crave chemicals as a way of
vironmental cues such as smells, exposure to drugs, or coping with the negative situation. Over time, the indi-
drug use paraphernalia; and exposure to environments vidual gives in to these cravings by beginning to make
where the individual once engaged in substance use specific behavioral plans to use chemicals: the urge to
(Kilts, 2004). During this altered motivational state, the use alcohol/drugs.
individual experiences a strong compulsion to obtain The third source of drug use urges is external drug
and use that chemical. As part of the cognitive preoccu- use cues, including the perceived opportunity to en-
pation with the chemical of choice, the individual gage in drug use behaviors (Beck et al., 1993; Wertz &
might engage in euphoric recall about past chemical Sayette, 2001). Such chemical use cues might include
use experiences (Anton, 1999; Beck, Wright, Newman, cleaning out one’s apartment and finding a forgotten
& Liese, 1993). stash of alcohol or drugs. Other cues might be a chance
Euphoric recall takes place when former users re- (or intentional) encounter with a former using/drinking
member their drug use experience as being desirable partner, the return to the same environment where the
and pleasurable while they minimize the negative con- individual had once used chemicals, or unexpected ex-
sequences of the substance use (Blume, 2005). A pat- posure to the many sights, sounds, or smells associated
tern of activation in the brain develops after repeated with chemical use (Monti et al., 2002). For example,
periods of drug/alcohol use, and this pattern may be- some recovering heroin addicts will begin to think
come activated in response to drug use cues that the in- about using heroin again if they smell the smoke of a
dividual encounters in the environment and which act burning match.
as possible relapse triggers (Wexler et al., 2001). Finally, the fourth source of chemical use urges is
Urges are of less intensity than cravings and were the individual’s desire to enhance positive experiences
viewed as more of a cognitive experience than the (Donovan, 2005). Many recovering individuals find
whole-body episode of craving (Merikle, 1999). In a that they associated chemical use with feelings of pleas-
very real sense urges might be viewed as behavioral im- ure. When, especially in the earlier stages of recovery,
pulses to find and use one’s drug of choice (Beck et al., they find themselves starting to feel good, they begin to
1993). As behavioral scientists come to better under- fear losing this feeling. The urge is to return to the use
stand the forces that sustain human motivation, they of chemicals to extend or enhance the positive experi-
are discovering that many of the triggers for decision ence so that it might last longer. This category of urge
making are based on unconscious perceptions and mo- was discussed by DeJong (1994) under the heading of
tivations only later rationalized by the conscious mind “positive emotional states.”
(Bargh & Chartrand, 1999). These discoveries are open- Both urges and periods of craving are normal in the
ing up new avenues for uncovering the sources of urges early stages of abstinence, and existing psychosocial
and craving for chemicals, and why people respond to treatment modalities appear to help the individual deal
these sensations as they do. with these experiences (Monti et al., 2002; F. Weiss,
Beck et al. (1993) identified four different situations 2005). In spite of the frequency with which urges and
that contributed to urges to use chemicals. The first is cravings are encountered, however, behavioral scien-
the individual’s learned response to the discomfort of tists have yet to identify the mechanisms by which these
conditions are generated. Further, there is only limited Fortunately, anticipatory guidance8 and reassurance
evidence that urges and/or craving for chemicals are sig- seem to be the best tools to help clients through this
nificant predictors of relapse (Anton, 1999; Spanagel & stage. As the association between the dream state expe-
Hoelter, 2000). However, since most individuals in the rience and substance abuse becomes weaker with the
earliest stages of recovery experience craving and urges, passage of time, the using dream seems to become less
it is important for them to learn how to cope with these intense and less frequent. It is rare for clients to report a
experiences. The alternative is that the individual’s re- using dream after the first 3 months of abstinence.
covery will be threatened or destroyed in the earliest
stages of recovery by his or her urges to return to the use
of chemicals. Controlled Drinking
In contrast to England, where 75% of all alcohol reha-
The “Using” Dream bilitation programs offer patients training to help them
moderate their drinking (Barr, 1999), in the United States
A phenomenon frequently encountered and little un- the theory that the alcoholic might return to “social” or
derstood is the “using” dream. Such dream experiences “controlled” drinking has met with skepticism (Hester,
may be quite distressing to newly abstinent individuals, 1995; Vaillant, & Hiller-Sturmhofel, 1996). Unfortu-
who will awaken and (if asked) report that they had a nately, ever since the first preliminary reports stating
dream in which they had just used alcohol/drugs and that it might be possible to help a small number of people
that the experience was so intense and seemed so real with alcohol use problems to return to a state of con-
they actually thought they were under the influence of trolled drinking, many alcohol-dependent individuals
chemicals for the first few seconds after awakening. have seized on the concept as a justification for their con-
Such dreams then become relapse triggers because of tinued drinking.
the intensity of the dream imagery, especially if dream- The effectiveness of controlled drinking has been
ers were not informed that they would have such dreams challenged in the research literature. Miller, Walters,
in the early stages of recovery. and Bennett (2001) suggested that only 10% of test sub-
Research into the dream state is still in its infancy, jects were able to remain controlled drinkers during the
and there has been no research into the using dream. It first 12 months after treatment. Other studies have
is known that dreams taking place during rapid eye found that less than 2% of individuals who are depen-
movement (REM) sleep are noted for bizarre, intense dent on alcohol can engage in social drinking again
imagery (Doweiko, 2002). A second element of the (Helzer et al., 1985; Vaillant, 1996; Vaillant & Hiller-
dream state—a neuromuscular blockade that prevents Sturmhofel, 1996). Controlled drinking is a viable goal
the brain from acting on the movement commands only for people who are not addicted to alcohol and
generated by the motor cortex in the dream state—also who have not experienced significant problems associ-
seems to contribute to the using dream. The final piece ated with alcoholism (Hester, 1995). It might be pos-
to the puzzle is the brain’s formation of the dream sible to teach a large percentage of those who abuse
memory in the transitional stage between the dream alcohol to control their drinking, but research has
state and full waking. In these few moments, dreamers shown that “stable moderate drinking [is] a rare out-
must come to terms with trace memories of the dream come among treated alcoholics” (Wallace, 2003, p. 19).
experience and make sense out of what seemed like a Typically, individuals who are moderately to severely
bizarre, unusual situation in which the brain did not addicted to alcohol do not remain controlled drinkers
function normally. This is also a pretty good capsule but quickly return to the abusive drinking pattern of the
summary of the subjective experience of intoxication: past (Watson, Hancock, Malovrh, Gearhart, & Raden,
The brain experiences a bizarre, atypical state often 1996). Those who attempted to return to controlled al-
marked by intense, vivid imagery in which the individual cohol use following treatment were four times as likely
is unable to properly coordinate muscle activity because to return to abusive drinking as those who focused on
of substance-induced ataxia. Thus, the using dream seems abstinence (Watson et al., 1996).
to result from the mind’s attempting to make sense of the
recently terminated dream state by comparing it to a wak- 8A therapeutic technique in which the therapist warns the client what
ing experience of a similar state of being: when the indi- to expect in certain settings, so that he or she might anticipate these
vidual was under the influence of chemicals. feelings and thus not feel overwhelmed on encountering these feelings.
Unfortunately, many alcohol-dependent individuals he or she slurs words, or keeps slipping breath mints into
cling to the hope that they can somehow find their way his or her mouth, or is chewing a huge wad of gum9
into the 1%–10% who can be trained to engage in con- throughout the interview. In some cases, the staff mem-
trolled or social alcohol use. Levin (2002) warned that ber might actually smell marijuana or alcohol on the
the longer the individual has been drinking, the less client. For these or any number of other reasons, the
likely it is that he or she would be able to return to so- counselor might suspect that the client either (a) is under
cial drinking, and Morgan (2003) advised that con- the influence of chemicals, or (b) has recently abused
trolled drinking is not accepted as a viable treatment alcohol/drug(s). In such cases, the treatment profes-
goal for alcohol-dependent people. However, Hester sional might (a) confront the client with his or her suspi-
(1995) suggested that alcohol-dependent individuals cion that the client is under the influence of chemicals,
who wish to attempt to learn how to drink in a social and/or (b) request that the client provide a urine sample
manner be allowed to try. An attempt at controlled under appropriate supervision for toxicology testing. It
drinking may help the individual realize the need for should be explained that the addictions are diseases that
total abstinence (Hester, 1995). Further, many who often are both cunning and deceptive, and that the
start out working to become social drinkers switch to hard evidence of a breath analysis or urine toxicology
total abstinence as they encounter problems in control- test report would help to shed light on the counselor’s
ling their alcohol intake (Hester, 1995). Once people suspicion and the client’s possible chemical use. The
fail in this task, they may be more willing to accept al- counselor should not be deflected from the decision to
coholism as a disease “that can be arrested with absti- seek urine toxicology or breath testing, even if the client
nence but never cured in a way that will permit the swears on his mother’s grave that he or she has not
person to drink again” (Brown, 1995, p. 11). abused alcohol/drugs.
But the mental health or substance abuse profes- If the counselor’s suspicion is confirmed, either by
sional needs to weigh the potential benefits from this the test results or by an admission by the client, two dif-
trial against the potential risks. Alcohol-dependent people ferent issues are raised. First, there is a clinical issue of
who believe that they can learn and maintain a pattern the client’s abuse of chemicals prior to his or her ses-
of social drinking for the rest of their lives are taking a sion. This reflects a serious substance use problem and
bet with odds that are 49:1 if not 99:1 against them. Few interferes with the assessment or counseling process. It
of us would be willing to chance an operation where the is impossible to conduct a therapy session or complete
odds were 50 to 1 against us. Few would consent to a sur- an accurate assessment of the client’s substance use pat-
gical procedure with only a 1% or 2% chance of recov- tern when he or she is under the influence of recre-
ery. Yet many alcoholics have voiced the secret wish that ational chemicals (Washton, 1995).
they could win this bet and land in what more than one But the client’s use of recreational chemicals prior to
alcoholic has called “the lucky 2%.” the session raises a serious liability issue for the thera-
pist. If the counselor should allow the client to go
The Uncooperative Client home, he or she might be held liable if that person were
to be injured or to harm somebody else. Imagine, for
Clients who are being assessed or who are in treatment example, that a client appears for an appointment with
for an AODA problem often have little incentive to a strong odor of alcohol and is obviously intoxicated.
cooperate with treatment staff. There are many ways Breath analysis yields a blood alcohol level (BAL) of
that a client might be less than fully cooperative with the 0.19, well above the legal definition of impairment.10
assessor or the treatment staff. In this section, some of the The therapist takes no action other than to tell the
more common forms of client resistance are discussed. client to “go home and sleep it off ” and to call back for
Appearing for sessions under the influence of chemi- a new session time. If the client were to have a motor
cals. It is not uncommon for clients to appear for a ses- vehicle accident on the way home, the therapist might
sion under the influence of a chemicals, especially if be held liable on the grounds that he or she knew the
they are being assessed for forensic reasons such as the client had used alcohol/drugs but did not take steps to
determination of competency to stand trial (Gendel, ensure that the client had medical supervision while
2006). In such cases, the session should be rescheduled
(Gendel, 2006). 9
Breath mints or gum might possibly hide the smell of alcohol/cannabis
At other times, staff members might question whether on the client’s breath.
the client is under the influence of alcohol/drugs because 10Which, if you will remember from Chapter 7, is 0.08.
under the influence of chemicals, and thus the thera- having any significant others that the assessor might
pist might be at least partly to blame for the motor contact (Juhnke, 2002). This refusal in itself might say a
vehicle accident. To protect themselves from such lia- great deal about how open and honest the client has
bility, rehabilitation professionals should review with been with the assessor, especially if the evaluator has ex-
an attorney their state’s laws governing the limits of lia- plained to the client exactly what information will be
bility and the steps to deal with this possibility. Such requested. One possible solution to this problem, which
steps might include involuntary hospitalization for some professionals advocate, is to have the client sit in
such clients while they recover from the effects of the on the collateral interview. One drawback is that the
chemicals ingested. If clients refuse to stay, the authori- client’s presence might inhibit the collateral informa-
ties may be notified that they are attempting to drive tion source from being free to discuss his or her percep-
and that the staff member has reason to suspect that tion of the client. If this were to happen, a potentially
they are dangers to themselves and others because they valuable source of information about the client would be
are under the influence of chemicals. unavailable to the assessor. Thus, it is rarely productive to
The threatening client.11 On occasion, clients will behave the client or the client’s representative sit in on col-
have in a threatening manner. Therapists should not lateral interviews.
hesitate to call the police if they believe that such Another approach is to suggest to the client that
clients are a danger to themselves or others. It is recom- since the therapist must complete some kind of an as-
mended that therapists carefully document as soon as sessment, this is the client’s chance to tell his or her ver-
possible after calling the authorities the reasons they be- sion of the incident. Otherwise, the counselor will be
lieved a client was a danger. For example, the client forced to rely on the official version of the incident
who said during a session that he or she was “so mad I alone, and that might put the client in a negative light.
could have killed him” might just be venting anger and Reminding the client that the therapist is the one who
not present a real danger to another person. However, is in charge of the session and that he or she will deter-
the client who states during a session that “I want to mine what issues should or should not be included in
take my shotgun from the closet and shoot my ex-wife the report might help the client to become more coop-
and her boyfriend” has identified (a) specific victims erative. A skilled therapist might ask the client to help
(ex-wife and her current boyfriend), with a (b) specific him or her understand why the client does not wish to
method (shotgun blast) of harm. Careful assessment of cooperate in order to explore the source of the client’s
the client’s potential for harm and appropriate action to lack of cooperation.
reduce the danger to the client and others should be
taken. Documentation is also necessary to justify the steps
taken, and if necessary the authorities should be called Toxicology Testing
to intervene as necessary. Urine
On occasions, the client might begin to behave in a
threatening manner during the session. The therapist At the start of the 21st century, the testing of urine
must (a) not tolerate threats and (b) maintain control of samples for evidence of illict drug use is the most com-
the session. This might be accomplished by gently con- mon and cost effective method by which drug use is de-
fronting the client with the observation that he or she tected (Bolnick & Rayburn, 2003; Nordgren & Beck,
seems to be making a threat or by suggesting that the 2004).12 The assessor must understand, however, that a
client seems to be overly upset. If the client does not show positive urine toxicology screen is not sufficient to diag-
signs of becoming less agitated, the therapist should call nose an addictive disorder and cannot substitute for a
for assistance (including the police). A good rule of clinical interview and a medical evaluation (United
thumb is that if the thought occurs that you should call States Department of Health and Human Services,
for help, the time has come to immediately do so. 2004). The use of urine toxicology testing is an adjunct
The uncooperative client. It is not unusual for some to treatment. It is not a form of treatment in its own right.
clients to be less than cooperative. A client might deny
12
The information provided in this section is designed to illustrate the
known strengths and weaknesses of urine toxicology tests. It is not in-
11Prudent therapists will document in the client’s chart or appropriate dended to serve as a guide for prosecution of or for employee assess-
treatment log (a) the reason they came to believe the client was under ment of possible substance use disorders. A toxicologist should be
the influence of chemicals, (b) the steps taken, and (c) the time these consulted for the most recent findings about the strengths and weak-
steps were taken, in as much detail as possible. nesses of each urine test utilized.
Although a urine toxicology test is a powerful tool in when large numbers of urine samples must be screened
the treatment of addictions, remember that like all for illicit drugs (Craig, 2004). The results are often
medical tests, improperly conducted urine toxicology available in less than 2 hours. Unfortunately, these re-
tests can yield invalid results. If the collection process is sults are reported only in terms of positive or negative,
improperly carried out, the urine sample can (a) sug- and this test is best suited for initial screening of urine
gest drug use where none exists or (b) fail to identify a samples (Craig, 2004).
person who has actually abused an illicit substance Gas liquid chromotography (GC) is a more expen-
(Levy, Harris, Sherritt, Angulo, & Knight, 2006). Thus, sive and labor-intensive procedure that is often used to
rigid adherence to proper collection procedures is im- confirm positive TLC tests (Craig, 2004). The equip-
perative. Further, because of privacy concerns and the ment necessary for GC testing is quite expensive, and
intrusive nature of supervised urine toxicology testing, the technicians who carry out the tests must receive spe-
it is necessary to obtain the client’s written consent prior cial training. However, GC has fewer false positive re-
to the time such testing is initiated. Some programs insults than TLC testing and provides quantitive levels of
form clients at the time of admission that urine toxicol- chemicals detected in the individual’s urine (Craig,
ogy testing might be requested at any time and that if 2004; Woolf & Shannon, 1995).
they are not comfortable with this aspect of their treat- Another form of urine toxicology testing is the im-
ment program they are welcome to seek treatment at a munoassay family of tests. Such tests are sensitive and
facility that does not conduct such testing (Katz & can be used to test large numbers of urine samples for
Fanciullo, 2002). Acknowledgment of this aspect of initial screening (Craig, 2004; Woolf & Shannon, 1995).
their treatment is then included in the consent for treat- However, because of structural similarities between var-
ment form that patients sign at the time of admission to ious compounds, such tests might mistakenly identify a
the program. The written consent should contain the benign substance as an illicit drug (Katz & Fanciullo,
information that staff might collect a urine sample at 2002). For this reason confirmatory testing utilizing an-
their discretion as part of the treatment process and other technique such as the spectrometric tests (dis-
should identify the procedures that will be employed in cussed in the next paragraph) should be done when
this testing. immunoassay test results suggest illicit drug use.
One misconception about urine toxicology testing is Mass spectrometric procedure provides the greatest
that a positive urine sample is indicative of impairment level of sensitivity and specificity. The gold standard for
(“Predicting Drug-Related Impairment,” 2004). Insur- such tests is the gas chromatography/mass spectometry
ance companies and employers argue that even the procedure (Katz & Funciullo, 2002). But such tests are
smallest trace of a drug of abuse in an employee’s urine both labor intensive and expensive and can be used on
after an accident is evidence of impairment, an argu- only a small number of urine samples at a time (Craig,
ment that is both unfounded and widely believed (“Pre- 2004). The test is most often used to confirm drugs de-
dicting Drug-Related Impairment,” 2004). It is unfortu- tected by another, less expensive or labor-intensive pro-
nate that employers choose to judge employees on the cedure.
basis of this myth, without regard to the lives that might As a therapeutic tool, urine toxicology testing is not
be affected by inaccurate evidence of or by trace amounts perfect. There are “detection windows” for various re-
of a drug of abuse. creational chemicals after which urine toxicology tests
One of the advantages of urine toxicology testing is will probably not detect them. Also, most commercial
that it supplements the client’s self-report about his or drug screens do not test for every possible drug of abuse
her recent substance abuse (Katz & Fanciullo, 2002). (Verebey & Buchan, 1997). Compounds such as LSD,
The results of such toxicology testing are potentially Fentanyl, Dilaudid, MDMA, Rohypnol, and many of
valuable as a means to (a) check patient compliance the “designer drugs” are not routinely included in
with program expectations and (b) determine whether standard urine drug screens and may require special,
the individual is abstaining from illicit chemical use, very expensive tests to be detected (Verebey, Buchan, &
especially in the preceding 1–3 days (Dolan, Rouen, & Turner, 1998). Further, urine toxicology tests usually
Kimber, 2004; Verebey & Buchan, 1997). do not not detect illicit chemicals used in the last
Technically, urine toxicology testing is not a single, 6 hours, as the body needs to begin the biotransforma-
uniform procedure but a generic term for a number of tion and elimination process before urine toxicology
different testing procedures. Thin-layer chromatography testing can detect the presence of such drugs (Juhnke,
(TLC) is the most commonly used procedure, especially 2002).
False positive test results are a significant problem, occasionally effective, especially when the levels of il-
especially with the growing popularity of on-site testing licit chemicals in the user’s urine are close to the mini-
by employers, law enforcement officials, and others. mum level used by laboratories to detect drug abuse
On-site tests have a high false positive rate, possibly as (Coleman & Baselt, 1997).
high as 30%–35%, meaning that the test results fre- It is not uncommon for patients who anticipate a
quently indicate possible illicit drug use in cases where urine drug test to flush their bodies with large amounts
the individual has not abused any of these chemicals of fluid in the hours or days before giving the urine
(“Why Confirmatory Testing Is Always a Necessity,” sample for toxicology testing. Some illicit drug users in-
1997; Schuckit, 2006). Depending on the specific test gest up to a gallon of water at once either to (a) flush
equipment utilized, non-steroidal anti-inflammatory drug metabolites from their bodies or (b) at least dilute
drugs (NSAIDS) such as aspirin, ibuprofen, and Tol- them so much that they might not be detected by the
metin might interfere with some of the urine toxicology urine toxicology test procedure. Staff (or the laboratory
test procedures currently in use. The nonnarcotic cough conducting the toxicology test) should test the urine
suppressant dextromethorphan might register as a meta- sample’s specific gravity, acidity level, and creatinine
bolite of a narcotic or the hallucinogen PCP on some of levels as part of the test procedure. Abnormally low re-
the on-site urine toxicology tests currently in use. Also, sults should alert staff that the urine sample had been
the quinolone family of antibiotics might register as opi- altered in some way and is thus of questionable value
ate metabolites in the same way (Gwinnell & Adamec, (Coleman & Baselt, 1997).
2006). Many herbal products might cause false positive Another method by which illicit drug abusers might
results on some on-site tests, such as the false positive for attempt to manipulate the urine toxicology test results
methamphetamine abuse caused by ephedra (Levisky is through various urine substitution methods. This is
et al., 2003). For this reason, on-site test results should al- accomplished by having a “clean” (i.e., drug-free) urine
ways be confirmed by independent toxicology testing in a sample on hand, possibly hidden in a balloon or small
certified laboratory that will either confirm the on-site test bottle, that can be substituted for the individual’s own
result or rule it as a false positive. urine if necessary. This method is most effective (a) if
Because there are so many different urine toxicology the urine sample being substituted did not come from
test procedures currently in use, substance abuse reha- another drug abuser and (b) staff do not closely super-
bilitation professionals should request a written sum- vise the urine collection process.
mary from the manufcturer or laboratory concerning Clients asked to provide a urine sample for toxicol-
the (a) methods by which the laboratory attempts to de- ogy testing have also been known to “accidentally” dip
tect illicit chemical use, (b) the accuracy of this method, the bottle into the toilet water in the hope that the labo-
(c) the specific chemicals that can be detected by that ratory or staff do not detect the attempted deception.
laboratory, (d) the detection windows for various drugs This will dilute their urine so much that it is unlikely
of abuse, and (e) the other compounds (including over- that the laboratory could detect any urine, never mind
the-counter medications and antibiotics) that might possible chemical use. The specific gravity and level of
yield false positive results. This statement should be acidity of the urine sample will reveal this form of de-
updated on a regular basis to make sure that the treat- ception, since toilet water has a different specific gravity
ment center staff are familiar with the strengths and and acid level than does human urine. Also, toilet water
weaknesses of the test procedures being utilized by the is unlikely to be as warm as the human body. Urine is
laboratory. always within one to two degrees of the core body temper-
Client attempts at deception. It is not uncommon for ature if the temperature of the urine sample is meas-
clients to attempt to deceive urine toxicology test re- ured within 4 minutes of the time the sample was
sults. An extreme form of client deception is for clients produced (Katz & Fanciullo, 2002). Immediately test-
to simply not keep a scheduled appointment if they ing the temperature of the urine sample will detect ab-
anticipate being asked to submit to urine toxicology normally warm or cool “urine” samples and alert staff
testing (Gitlow, 2007). There are also a number of to possible deception. Some treatment centers color
products available through various sources that are pur- the toilet water with a dye so that it cannot be substi-
ported to remove toxins from the urine or correct any tuted for urine, but this procedure is not carried out at
apparent urinary imbalances caused by “flushing” one’s every test collection facility.
body with massive amounts of water (Coleman & Baselt, Another way clients attempt to defeat the urine toxi-
1997; Gwinnell & Adamec, 2006). Such products are cology screen is to substitute another substance for the
urine sample. The list of compounds submitted as deceive urine toxicology test results, extremely close su-
“urine” by various individuals includes (but is not lim- pervision of both male and female clients who are giving a
ited to) apple juice, citrus-flavored soda, dilute tea, gin- urine sample for detection of illicit drug use is necessary.
ger ale, lemonade, salt water, plain tap water, and This means that the person supervising the collection of
white grape juice (Winecker & Goldberger, 1998). the urine sample must actually see the urine enter the
Again, testing the temperature, specific gravity, and bottle and not just stand outside the men’s room or
acidity of the liquid submitted for testing will reveal ladies’ room or the toilet stall while the client is inside.
many of these substitutions. Other drug abusers believe Urine toxicology testing should not be routine or
the myth that it is possible to “hide” evidence of illicit predictable. Surprise is one way to avoid the problem of
drug use by adding a foreign substance to the urine adulterant use or substitution (Juhnke, 2002). Staff might
sample. There are also some commercial products that wait until clients are about to enter the lavatory, then
supposedly will eliminate evidence of illicit drug use inform them that they have been selected for urine
from urine samples. A partial list of adulterants used at drug testing. It is unlikely that clients will carry around
one time or another in attempts to disguise illicit drug a bottle of substitute urine all the time on the off
use includes the following (Schuckit, 2006; Winecker & chance that they will be asked for a urine sample. This
Goldberger, 1998): procedure is likely to force the client to give a sample of
his or her own urine, especially if the collection is super-
ammonia bleach blood vised. Another technique is for the counselor to an-
Drano ethanol gasoline nounce at the beginning of a group session or other
supervised activity that clients have 2 hours in which to
kerosene lemon juice liquid soap
provide a supervised urine sample for toxicology testing.
peroxide vinegar table salt Clients will then be unable to leave the group to pick up
sodium bicarbonate vitamin C a urine sample stored in their rooms without staff being
aware that they have left the group. Clients should have
The myth is that such substances will, when added to a access to fluids to stimulate the production of urine but
urine sample, disrupt the chemical reactions on the tox- not be allowed to leave the group room until they are es-
icology test being used, thus hiding evidence of recent corted to the bathroom or lab for collection of the urine
drug use. On rare occasions such procedures actually sample.
work (Schuckit, 2006). Depending on the test proce- With all the shortcomings and problems associated
dure utilized, bleach or table salt added to the urine with urine toxicology testing in mind, the following is a
sample might hide evidence of recent subtance use summary of the “detection window” for some of the
such as cocaine, while small amounts of table salt, liq- more popular recreational chemicals, if proper urine
uid soap, or the commercial drain cleaner Drano might toxicology test procedures are utilized.
alter the chemical properties of the urine sample so that Marijuana. Urine from a person who is an occasional
the test will not reveal evidence of illicit cannabis abuse cannabis abuser might test positive for THC for 5 days
(Jenkins, Tinsley, & Van Loon, 2001; Winecker & (Greydanus & Patel, 2005; Schuckit, 2006). However,
Goldberger, 1998). But the Drano also makes the urine because the body stores THC in various body tissues
more alkaline than would be possible if it were a real and gradually releases it back into the blood, chronic
urine sample (Jenkins, Tinsley, & Van Loon, 2001). marijuana users will test positive at the 20ng/ml level
While a small amount of the metal salt alum might for up to 20 days (Greydanus & Patel, 2005). However,
hide evidence of methamphetamine use, it will also Jenkins et al. (2001) suggested that THC could be de-
alter the acidity of the urine sample, a characteristic tected for 10–45 days following the last use of mari-
that can easily be detected if staff perform a simple juana, depending on the potency of the marijuana and
acidity test (“Tolmetin Foils EMIT Assay,” 1995d). the frequency with which it was used. Katz and Fanciullo
These pervasive myths among illicit drug abusers re- (2002) suggested that chronic cannabis abusers might
inforce the need to closely supervise individuals during continue to test positive for THC metabolites for 80 days
the urine collection process. But this is controversial. after the individual’s last cannabis abuse in extreme
Some rehabilitation professionals argue that as long as cases, although this figure has not been supported by
the temperature of the urine sample is above 90° F., the other researchers.
urine sample is probably valid. It is suggested here that To avoid controversy about whether the individual
given the various ways that patients might attempt to did or did not use marijuana recently, the journal
Forensic Drug Abuse Advisor (“Secondhand Crack would be necessary for that person to produce docu-
Smoke,” 1995) suggested daily urine toxicology tests mentation supporting this claim.13
until the user tested negative for 3 days in a row to en- The 72- to 96-hour detection window is an approxi-
sure that any residual THC had been eliminated from mate guide to the period of time in which cocaine
the chronic user’s body. Another possible confounding might be detected. There is evidence that very heavy
factor is that the synthetic THC compound Marinol, a cocaine abusers might store small amounts of cocaine
Schedule III compound, will register as evidence of in the body tissues, especially in body fat, which could
cannabis use on urine toxicology tests; the test report then be released back into the general circulation after
will show that the user has used THC (McWilliams, it was last used (Preston et al., 2002). Jaffe, Rawson, and
1999). To avoid this problem, it is necessary to deter- Ling (2005) cited one study, for example, that found
mine whether the individual being tested has been 20% of chronic cocaine abusers still tested positive for
placed on Marinol by a physician, and confirm this cocaine metabolites 105 hours after their last docu-
claim by examination of the original prescription or by mented use of the drug. Greydanus and Patel (2005)
consultation with the prescribing physician. suggested that chronic cocaine abusers might continue
Occasionally a person whose urine tested positive to test positive on urine toxicology tests for up to 2 weeks
for THC might claim to have passively inhaled mari- after their last use. Schuckit (2006) simply stated that
juana smoke because they were in a room or motor chronic abusers might test positive for “several days”
vehicle where other people were smoking it. Such pas- (p. 30) following their last use of cocaine.
sive inhalation of sufficient marijuana smoke is said to In such cases, serial quantitative urine toxicology
be “extraordinarily unlikely” under normal conditions tests should shed light on whether the cocaine being
(Ahrendt & Miller, 2005, p. 962). Under special condi- detected is residual or the result of new cocaine use, as
tions it is possible for a nonusing individual to be exposed it is believed that recent use will result in higher levels
to sufficient concentrations of secondhand marijuana of cocaine metabolites than residual cocaine in the
smoke to cause his or her urine to test positive for THC. body could produce.
To accomplish this feat, volunteers had to sit in a cham- LSD. This substance can be detected in a person’s
ber so filled with smoke from marijuana cigarettes that urine for up to 8 hours after it was ingested, if the labo-
they had to wear special eye covers to protect their eyes ratory conducts special tests for it (Craig, 2004).
from the smoke in the room (“Oral Fluid Drug Test- PCP. The hallucinogen PCP or its metabolites
ing,” 2005). With the exception of these extraordinary might be detected for 2–3 days following its use by a ca-
circumstances, it is unlikely that a person could pas- sual user (Jenkins et al., 2001). Craig (2004) offered a
sively absorb sufficient THC to test positive on a stan- detection window of 2–8 days for PCP, but chronic
dard toxicology test. abusers might continue to show evidence of PCP in
Cocaine. Depending on the route of administration, their urine for up to 21 days after the last use of this sub-
the frequency with which the individual abuses co- stance (Greydanus & Patel, 2005). Depending on the
caine, and the amount of cocaine utilized, testing can toxicology test utilized, it is possible for some over-
detect metabolites of cocaine in urine samples for the-counter medications to cause false positive results,
72–96 hours after the last drug use (Craig, 2004; Jenkins and thus supplementary testing using a different toxi-
et al., 2001; Schuckit, 2006). False positive urine toxicology test procedure is necessary to confirm the initial
cology tests are unlikely but are possible. If the patient results (Ahrendt & Miller, 2005). As discussed in Chap-
were prescribed a cocaine-containing topical agent by a ter 13, the speed at which PCP is excreted from the
physician, for example, he or she would have traces of body depends on the acidity of the urine, and thus there
cocaine metabolites in his or her urine if it were tested. will be significant variation in the speed at which PCP
Fortunately, such situations are very, very rare (Ahrendt is eliminated from the individual’s body.
& Miller, 2005). Physicians or other health care profes- MDMA. This substance might be detected for
sionals whose practice brings them into frequent con- 24–48 hours after it was used if the proper urine toxicol-
tact with cocaine might possibly absorb enough cocaine ogy test procedures are employed (Craig, 2004).
through their skin to have cocaine metabolites in their
13Such as patient notes demonstrating that cocaine was adminis-
urine for 72–96 hours after their last exposure to this
tered to that patient in a form that could be passively absorbed by
compound (Gitlow, 2007). Obviously, if the health the health care professional. Fortunately, such situations are excep-
care professional were to claim passive absorption as tionally rare, although it is possible for this to happen, according to
the excuse for his or her positive urine test results, it Gitlow (2007).
Alcohol. Although breath analysis or blood tests are chronic use of benzodiazepines, with chronic abusers
the gold standard by which recent alcohol use is de- testing positive for a longer period of time than the in-
tected, a recent urine test for a metabolite of alcohol dividual who ingested a single benzodiazepine dose.
known as ethyl glucuronide has been introduced. This Although Rohypnol (flunitrazepam) is technically a
metabolite is specific for ethyl alcohol and it remains in benzodiazepine, it is illegal in the United States. Rou-
the individual’s blood for about 5 days after the last expo- tine urine toxicology testing will not detect it, and spe-
sure to alcohol. Unfortunately, a growing body of evi- cial test procedures must be carried out to identify this
dence suggests that exposure to alcohol through such compound in urine samples within 60 hours of the time
things as using an alcohol-based hand sanitizer might it was ingested (Lively, 1996).
also cause this test to register positive for alcohol, lead-
ing to false positive test results (Kirn, 2006). At this time,
ethyl glucuronide does not appear to be specific for the Hair Samples
detection of alcohol use disorders and is not widely rec- When a person ingests a chemical, molecules of that
ognized as an acceptable test for this purpose. substance are circulated throughout the body. De-
Amphetamines. Amphetamines may be detected for pending on the pharmacokinetics of that chemical,
only 24–48 hours after the last use of this class of drugs molecules will enter various types of cells found in the
(Bolnick & Rayburn, 2003; Greydanus & Patel, 2005; body. If the cell were to die and be ejected from the
Schuckit, 2006). Because high doses of ephedrine or body before the drug molecule were to be released
pseudoephedrine might cause false positive urine test back into the general circulation, then the drug mole-
results, federal guidelines require that amphetamine cules would remain attached to the cell wall and thus
molecules be identified along with methampheta- could be detected through specific test procedures de-
mine to rule that urine sample positive for the latter signed to detect these molecules. This characteristic
substance. In the body, methamphetamine is biotrans- makes it possible to find evidence of illicit drug use in
formed into amphetamine, but ephedrine or pseu- hair samples of patients because the roots of hair re-
doephedrine do not produce amphetamine molecules main alive even though the hair itself is composed of
when biotransformed, allowing the presence or abs- long strands of dead cells pushed outward from the
cence of amphetamine to determine whether that root by the pressure of new hair cells forming at the
urine sample contains evidence of methamphetamine root.14
abuse. Scientists have developed the technology to detect
Opiates. The detection window for opiates depends metabolites of many illicit drugs in the hair of the
on the specific compound being abused, and the test user, and some people have suggested this as a less in-
procedures employed. Propoxyphene is a popular drug trusive alternative to urine or blood toxicology testing
of abuse, and its window of detection is just 8 hours if the (Brady, 1997). Hair samples also offer a detection win-
laboratory is testing for the drug itself. But metabolites of dow that usually is between 7–100 days (Dolan et al.,
this compound may be detectable for up to 48 hours fol- 2004; Gwinnell & Adamec, 2006). This detection
lowing use (Jenkins et al., 2001). window is far longer than the one offered by urine tox-
Other narcotic analgesics such as heroin, morphine, icology tests, thus eliminating the danger that a drug
codeine, or Dilaudid (hydromophone) might be de- abuser might abstain for a few days prior to a urine tox-
tected for 1–2 days following the last use of this class of icology test to hide his or her chemical abuse (Craig,
drugs (Jenkins et al., 2001). Special tests might be nec- 2004). There are no known methods by which hair
essary to detect some of the semisynthetic and synthetic samples can be adulterated or diluted to hide evi-
narcotic analgesics not included in the standard toxicol- dence of illicit drug use, and substitution is virtually
ogy tests (Ahrendt & Miller, 2005). Methadone may be impossible since the hair samples are removed from
detected for 96 hours following the last dose (Bolnick & the individual’s body by the technician collecting the
Rayburn, 2003). sample. Although some people think that if they shave
Benzodiazepines. Drugs in this family currently in their heads they can defeat the process of hair toxicol-
use in the United States might be detected by urine tox- ogy testing, any body hair can be used for such tests
icology tests for 1–4 weeks after their last use (Craig, (Brady, 1997).
2004). Schuckit (2006) suggested that such compounds
might be detected for only 3 or more days. This discrep- 14
This is why it is possible to have your hair cut without feeling pain:
ancy might reflect the difference between acute versus The hair is dead and thus does not have functional nerve endings.
Advocates of hair follicle testing point out that this hair toxicology tests do not detect substance abuse in
procedure is far less intrusive than urine toxicology the 7 days preceeding the test (Juhnke, 2002) and
testing. However, the test results are hardly conclusive. cannot be used to detect alcohol use (Gwinnell &
The Food and Drug Administration (FDA) has advised Adamec, 2006).
several companies that produce hair-testing kits to in- Even if there is evidence of alcohol/drug use de-
clude the warning that false positive results are possible tected, hair testing does not provide information on the
(“FDA Revised Guidelines,” 2004). Indeed, in 60 out level of impairment caused by the individual’s exposure
of 100 cases, the preliminary positive results for opiate to the chemicals (Juhnke, 2002). The fact that hair toxi-
abuse were found to be inaccurate when further testing cology testing requires the removal of hair from the
was carried out (“FDA Revised Guidelines,” 2004). body, as opposed to the collection of urine, a waste
Fully 50% of the preliminary positive results for am- product expelled from the body, makes it of limited
phetamine abuse, 10% of the preliminary positive re- value for serial toxicology tests such as those utilized in
sults for marijuana abuse, and 2% of the initial positive correctional or rehabilitation facilities (Craig, 2004).
results for cocaine abuse were found to be false posi- Thus, while toxicological testing of hair samples is of
tive15 on further testing. possible value, its applicability in the detection of illicit
In the case of hair testing for marijuana abuse, Uhl drug use remains uncertain at this time.
and Sachs (2004) suggested that researchers search for
metabolites other than THC such as 11-nor-delta-9-tetra- Saliva
hydrocannabinol-9-carboxylic acid (THCA) in order
Another emerging technology is the use of saliva to test
to differentiate between actual marijuana use and
for residual traces of alcohol (Wilson & Kunsman,
passive exposure to marijuana smoke. The authors
1997). Although laboratories have been able to use
pointed out that hair samples from nonsmokers ex-
saliva samples to test for alcohol traces since the 1950s,
posed to marijuana smoke failed to show evidence of
new techniques are making this procedure attractive for
THCA whereas hair samples from marijuana smokers
workplace screening programs, according to Wilson
had both THC and THCA in them. This discovery
and Kunsman. The individual will place a cotton swab
might allow researchers to identify actual marijuana
in his or her mouth, allowing it to become moistened
smokers and negate the defense that the hair sample
by saliva. The cotton swab is then tested by exposing it
was contaminated by marijuana smoke that was in the
to chemicals that will react to the presence of alcohol.
environment.
The use of saliva allows for a simple, short (less than
Detractors to hair testing point out that a number
20 minute) test that is just as accurate as breath testing
of hairs must be removed (Craig [2004] suggested
but can be carried out in the workplace. Saliva testing
40–60 strands). Further, it is virtually impossible to
offers a detection window of 1–36 hours (Dolan et al.,
determine when the individual indulged in illicit drug
2004). As with any screening procedure, there is a need
use by hair sample testing according to detractors. In
for follow-up testing to rule out false positive results.
theory, by measuring the distance that the drug mole-
cules are from the root, and then estimating the time
it would take for hair to grow that distance at a stan- Sweat
dard growth rate of 1 centimeter (cm) per month, one A number of companies offer transdermal patches im-
could estimate the time since the person had used an pregnated with compounds designed to react to and re-
illicit chemical. Unfortunately, the accuracy of hair veal evidence of illicit drugs in the individual’s body.
testing has not been proven in clinical practice Such detection programs are useful for continuous
(Harrell & Kleiman, 2002). There also are questions monitoring of the individual over a 1–14 day period of
as to whether there are racial differences in the absorp- time (Dolan et al., 2004). Clients will occasionally
tion rate at which the drug molecules are incorper- claim that their skin produces an oil that causes the
ated into body hair (Gitlow, 2007). Further, at any transdermal patch to fall off or that it fell off in the
given time 15% of the hairs are either in resting phase shower. Other detection methods (urine or hair) should
or are ready to fall out, factors that potentially influence be instituted to identify clients who might possibly have
the accuracy of hair samples in the detection of drug used an illicit compound after their transdermal patch
abuse (McPhillips, Strang, & Barnes, 1998). Finally, “fell off.” It is extremely unlikely that such test patches
will fall off on their own, and they are considered
15See Glossary. tamper proof (Ahrendt & Miller, 2005).
The Addicted Person and Sexual Activity some forms of chronic pain (Cheatle & Gallagher,
2006). But because of opiophobia, many physicians
Unfortunately, some individuals learn to associate their hesitate to utilize narcotic analgesics for pain control
use of compounds such as cocaine with involvement in for the patient with a substance use disorder and a
sexual activities and report finding that “normal” sex16 is chronic pain problem, as such medications are thought
not as rewarding (Gitlow, 2007). Some compounds have to increase the individual’s risk for relapse (Compton &
a reputation as aphrodisiacs, leading the individual to Athanasos, 2003). Most certainly there are those indi-
believe that their use prior to or during sexual activity viduals who will attempt to manipulate physicians into
enhances the subjective experience. Other individuals prescribing narcotic analgesics for personal profit or
find that the anxiolytic effect of compounds such as pleasure. But there are also patients who suffer legiti-
alcohol, marijuana, or other sedating agents help ward mate pain issues even if they do have a concurrent ad-
off anxiety induced or exacerbated by sexual activity. It dictive disorder. The diagnostic dilemma is whether a
is not unusual in such cases for individuals to indicate given individual is seeking narcotic analgesics to con-
that it is difficult if not totally impossible for them to be trol pain or to support his or her SUD. Compton and
sexually active without the use of such compounds. For Athanasos (2003) suggested that the latter group of pa-
these individuals, the opportunity to engage in sexual tients tend to use narcotic analgesics to self-medicate
activity will often serve as a relapse trigger, forcing them non-pain issues such as insomnia, depression, loneli-
to confront the possibility of engaging in sexual activity ness, and anxiety when they lack such supports as fam-
without their favorite sexual aid. After assessing the role ily and 12-Step groups. Addictive patients are also less
that the drugs play in the individual’s sexual activity, likely to respond to pain management programs, less
appropriate treatment referrals should be made (such likely to consider non-opioid based pain management
as to a licensed, experienced sex therapist or individual techniques (such as biofeedback, etc.), and more likely
psychotherapist). to present histories of chronic opioid therapy, according
to the authors.
In spite of clinical lore, patient requests for additional
The Addicted Patient medication are not automatically a sign of an SUD. Un-
With Chronic Pain Issues relieved or only partially controlled pain might result in
Between one-third and one-half of the adults in the patients’ requesting additional medications. To compli-
United States are estimated to suffer from some form of cate matters, patients with addictive disorders tend to
persistent or recurrent pain of greater or lesser intensity be less tolerant of pain than are nonaddicted patients
(Cheatle & Gallagher, 2006). Even in the best of cases, (Compton & Athanasos, 2003). While there is no evi-
the issue of chronic pain “has remained an enduring dence that withholding narcotic analgesics from pa-
and significant health care problem in spite of the ad- tients with concurrent SUDs and chronic pain is at all
vances in diagnostic imaging, pharmacotherapy, and ineffective, some physicians continue to believe this ther-
vasive procedures” (Cheatle & Gallagher, 2006, p. 371). apeutic myth. An essential question seems to be whether
Frequently intertwined with the chronic pain issues are the patient would require narcotic analgesics (or an in-
problems such as concurrent anxiety problems or decrease in medication dosage) to control his or her pain if
pressive disorders (Cheatle & Gallagher, 2006). When he or she were not addicted.
the patient has a concurrent substance use disorder, The treatment of a drug-addicted person with con-
health care professionals involved in the patient’s care current pain problems is a complex, demanding task
become even more concerned about the potential for that is best addressed by a treatment team that works to-
medication misuse or diversion, as well as the possibil- gether closely and utilizes intra-staff communication
ity that the physician’s use of certain medications might frequently. Many centers have utilized a treatment con-
cause or exacerbate an addictive disorder17 (Compton & tract that specifies that the patient will use only one
Athanasos, 2003). pharmacy and the services of only one physician (except
The narcotic analgesics18 have come to be accepted in emergencies). The treatment contract should also
as playing a major role in the treatment of acute and specify that the staff will utilize urine toxicology testing
both to check treatment compliance and to discourage
16That is to say, sexual activity without the use of such chemicals. the use of nonprescribed substances. Further, staff
17
Technically, the term for this fear is opiophobia. should utilize non-opioid treatments where indicated,
18
Discussed in Chapter 14. such as gabapentin, valproate, and carbanazepine—for
the control of diabetes-related neuropathic pain, for costs reflect inefficiency, not increased effectiveness.
example (Cheatle & Gallagher, 2006). Given this perception on the part of health care insur-
Unfortunately, while the utilization of an integrated ers, it was only natural that they would institute pro-
pain treatment team is the ideal, in many areas, such as grams designed to reduce costs. These programs,
rural communities, the issue of chronic pain control known as managed care (MC) initiatives, became pop-
falls on the shoulders of such people as the indepen- ular in the 1990s with the purported goal of controlling
dent physician, who is often poorly trained in the area the rising cost of providing for health care. In the time
of chronic pain control and who lacks resources such as since such programs were introduced, it has become
the referral to ancillary services or the support of an in- clear that MC is a system designed to ration health
tegrated pain management team. Thus, it is to the ad- care services for individuals covered by such health
vantage of substance abuse professionals to identify the care insurance programs (Sanchez & Turner, 2003).
proper ways to respond to the substance-abusing client Managed care has also been found to cut costs for the
with chronic pain, since these professionals will often insurance provider while doing little if anything to
be called on to advise the independent physician on change long-term health risks (Cassell, 1997; Ceren,
how to best proceed with these difficult-to-treat, refrac- 2003; Prochaska, 2002).
tory patients. In theory, MC is designed to provide the most appro-
priate care for the patient at the best possible price to
the insurance company. In reality, the MC system
Insurance Reimbursement Policies “wasn’t meant to care for sick people; it was meant to
Health care insurance providers hesitate to provide make and manage money” for the insurance company
reimbursement for mental health or substance abuse (Glasser, 1998, p. 36). The danger is that while many
treatments because of the mistaken beliefs that (a) there MC systems have a legitimate interest in helping people
are no effective treatments for substance abuse prob- find the appropriate medical care at an affordable
lems, and (b) to provide funds for such treatment price,
would require a major increase in premiums. In real-
ity, full parity for mental health and substance abuse there are great potential profits for the unscrupulous
treatment could be funded by an increase of just pen- managed care companies that will maximize their
nies per month (Goldman et al., 2006; Greenfield, profits without concern for the well-being of the
2005). Unfortunately, not only are health insurance patient. Ethics do not seem dependent on the size
benefits for such services rarely on a parity with other of the company and unethical companies appear
major medical treatments but many health care pro- from among the largest as well as the smallest com-
viders now provide funding for less than half the rec- panies. (Frances & Miller, 1998, p. 11)
ommended length of treatment for substance use
problems. Indeed, managed care is called by many health care
The issue of health care coverage and who is going providers “managed profits” because of the way this
to pay for it is quite controversial at this time. Some pro- process has come to limit the amount of care an insur-
ponents of health care insist that it is a right, while ance company is liable for under its policy with the in-
others hold that health care is a commodity (Kluge, dividual. For example, from 1989 to 1999 the value of
2000). To complicate the debate, medical advances re- benefits paid out by managed care companies fell by
sult in the need for greater expenditures for health care 54%, a process that has “translated into big money for
(Levant, 2000). For example, as treatment advances re- these largely for-profit companies” (“Magellan Slashes
duce the death rate from myocardial infarction, a pool Fees,” 1999, p. 5). During this same period, the cost of
of heart attack survivors requiring aggressive medical health care was increasing by approximately 8.3% per
management is established placing an unanticipated year (Teich, 2000).
drain on health care resouces. Thus, the increase in In the time since MC initiatives became wide-
health care costs over the past decades appears to re- spread in the 1990s, it has become clear that such pro-
flect, in part, the impact of successful medical interven- grams, “by refusing to recognize (and pay for) the
tions in earlier decades, not evidence of inefficiency on medical necessity of inpatient treatment for most cases
the part of health care providers. of drug and alcohol dependence, largely dismantled
But insurance companies have adopted the positions the ‘28 day’ inpatient alcohol and drug dependent pro-
that (a) health care is a commodity, and (b) increased grams” (Jaffe & Anthony, 2005, p. 1151). The impact
of MC on substance abuse treatment programs has A third way that insurance companies attempt to limit
been to restrict the emphasis of treatment to the short- their losses is to adopt a very conservative definition of
term needs of the client population while simultane- disease. Thus, it is uncommon for health insurance com-
ously reducing accessability to treatment (Ceren, 2003; panies to provide substantial benefits for substance abuse
Olmstead & Sindelar, 2005; Simpson, 2004). Unfortu- rehabilitation, in spite of the fact that the cost of provid-
nately, health care professionals know that “years of ing unlimited benefits for such programs was estimated
abuse cannot be reversed by days of treatment” to cost program members only about $5 a year per mem-
(Pagano, Graham, Frost-Pineda, & Gold, 2005, p. 479), ber (Breithaupt, 2001). Even when insurance companies
but this is exactly what the managed care system de- have provided benefits for substance abuse rehabilita-
mands. The treatment industry has been virtually tion, they have substituted symptom reduction for the
stripped of flexibility and forced to conform to a strict “treatment” or “cure” of the addictive disorder (Kaiser,
set of guidelines in order to earn limited reinburse- 1996; Sanchez & Turner, 2003). In the area of alcohol/
ment for treatment services provided (Marinelli-Casey, drug use problems, insurance companies utilize a very
Domier, & Rawson, 2002). conservative definition of “recovery” to determine when
A point that is often overlooked by health care benefits should be terminated. The outcome of this
providers is that insurance companies do not exist to process is that many health insurance providers now pro-
provide funding for health care procedures. They exist to vide coverage that funds less than half the recommended
make money for the owners of the company (stockhold- treatment period for substance use problems (Wu &
ers), and one method by which they do this is by selling Schlenger, 2004).
health insurance. A health insurance policy is, in effect, This is true even though a large number of studies
a gamble by the insurance company that the policy have found that the longer the individual is involved in
holder will not become ill for the period of time that a rehabilitation program, the better are the chance of
the policy is in effect. The company charges a “pre- a successful outcome (Brochu, Landry, Bergeron, &
mium,” which the company will then keep if the policy Chiocchio, 1997). For example, Sadock and Sadock
holder does not become ill with any of the conditions (2003) observed that treatment for addiction to sub-
identified by the company as reflecting “illness.” If the stances such as cocaine and heroin must last “at least
policy holder does become ill, the insurance company 3 months” (p. 389) for maximum effectiveness, and
is then required to provide a certain level of care, as Ringwald (2002) suggested that the typical alcoholic
identified in the policy, if it is “medically necessary” might require 30 days of abstinence to “clear” from the
(Ford, 2000). effects of chronic alcohol use. Unfortunately, few health
Needless to say, the insurance company will attempt care insurance policies would fund such an extended
to control costs to maximize profit. This is accom- period of “detox,” and all too often insurance benefits
plished, in part, through a process known as “prior au- are limited to just 5–7 days of inpatient treatment. Al-
thorization,” in which an insurance company repre- though such programs are more cost effective by some
sentative whose credentials are often “questionable and measures, one sad consequence of this process is that
whose role is to cut costs” (Ceren, 2003, p. 77) must be many clients are being referred to aftercare programs
consulted prior to the initiation of any but emergency without having completed treatment (Coughey, Feighan,
care. Depending on the company, up to half the individ- Cheney, & Klein, 1998).
ual’s insurance fee might be applied to administrative The apparent contradiction is easy to understand if
fees and company profit (Gottlieb, 1997). The money one accepts that insurance companies are able to pres-
that an insurance company spends providing health ent symptom resolution as a substitute for long-term
care coverage for those who purchase such a policy from treatment. In other words, health insurance companies
that company is considered a financial loss to the com- have come to view the stabilization of the immediate
pany. The insurance company thus attempts to maxi- crisis as an acceptable goal for inpatient treatment and,
mize the inflow of money while reducing or eliminating in the case of the addictive disorders, not long-term re-
the need to pay money to policyholders. Some ways to habilitation. Unfortunately, symptom reduction does
accomplish this include excluding as many conditions not automatically mean that the condition that caused
as possible from the health insurance coverage and ex- the symptoms has been resolved. For example, patients
cluding individuals with known medical problems from who suffer a ruptured appendix frequently report a sig-
participation in the policy on the grounds of a “preexist- nificant reduction in pain after their appendix has
ing condition.” burst, but if they do not undergo immediate surgery
and further treatment, they will probably die of infec- programs began to appeal for ever-increasing levels of
tion. The fact that a patient is no longer in imminent funding and larger amounts of student classroom time
danger of acute alcohol withdrawal does not mean that on the theory that the changes would somehow im-
his or her substance abuse or addiction has been ade- prove the effectiveness of these psychoeducational
quately resolved; it has just been temporarily halted. programs.
Thus the conflict between health care providers: Ade- Critics of D.A.R.E and similar programs suggest that
quate treatment of the addictive disorders requires time they consist of negative propaganda, an approach that
for meaningful change. has never been shown to work (Leavitt, 2003; Walton,
Few health care providers are willing to accept symp- 2002). At best, critics of the D.A.R.E. program note that
tom resolution, which in this case means the immediate “evidence suggests that, although knowledge can be in-
cessation of chemical use, as adequate “treatment.” In creased, and expressed attitudes may be changed, af-
contrast, the health care insurance companies interpret fecting drinking behavior through school programmes
“adequate” treatment as just that: the stabilization of the is a very difficult task” (Room, Babor, & Rehm, 2005,
immediate crisis. But managed care companies often p. 525). At worst, the critics of D.A.R.E. and similar
view substance abuse rehabilitation treatment as im- programs believe that such programs continue in spite
perfect at best, reflecting their “deep suspicion of any- of their proven lack of effectiveness simply because they
thing unquantifiable, unprovable, or lingering as give the illusion of doing something effective in the
probably being poor technique on the therapist’s part, face of childhood and adolescent substance use disor-
self-indulgence on the patient’s, and a waste of money ders (Leavitt, 2003).
by both” (Gottlieb, 1997, p. 47). The reality is that psychoeducational programs that
rely on providing vast amounts of information to adoles-
cents will, at best, result in a temporary modification of
D.A.R.E. and Psychoeducational behavior (Renya & Farley, 2006, 2007). They lack a
conceptual framework in which to appropriately assess
Intervention Programs
the risks associated with questionable behaviors (Reyna
Much enthusiastic support . . . little evidence of effec- & Farley, 2006, 2007). Further, the cognitive level of
tiveness. most adolescents is such that when they find that they
have successfully “dodged the bullet” by not suffering
Drug Abuse Resistance Education (D.A.R.E.) and sim- anticipated adverse consequences from a potentially
ilar programs were established on the theory that teach- dangerous behavior, they tend to underestimate the
ing children about the harmful effects of alcohol and risks associated with that behavior in the future (Reyna
drugs while helping them build self-esteem would & Farley, 2006, 2007). The implication of this finding
somehow inoculate them against the desire to abuse is that students will dismiss information provided by
chemicals later in life. The D.A.R.E. program is typi- psychoeducational programs such as D.A.R.E. when
cally coordinated by a local police officer and is taught they find that they did not experience a dreaded conse-
in the classroom setting. Similar programs are coordi- quence after engaging in a perceived dangerous behavior.
nated by a variety of mental health or school guidance In other words, the theoretical foundation for such pro-
professionals. There is a great deal of testimonial sup- grams is flawed.
port for such programs and virtually no evidence that
they are effective in reducing adolescent or young adult
substance abuse (Gorman, 2003; Lynam et al., 1999;
Summary
Rowe, 1998).
In terms of the continuum of care, such psychoedu- Even after a client has been identified as being in
cational programs are said to fall at the level of primary need of substance abuse rehabilitation services, the
prevention, and school systems all too often respond course of treatment is often a difficult one. Clients
that more intensive levels of treatment for substance- often test the limits imposed on them by the therapist
abusing adolescents are not an educational systems or the treatment center. Other clients will, with
issue (Zunz, Ferguson, & Senter, 2005). Proponents of greater or lesser degrees of justification, challenge the
D.A.R.E. or similar approaches admit that even as a pri- accuracy of urine toxicology test results. Clients will
mary prevention level of intervention, such programs occasionally come to treatment sessions under the
have not lived up to their promise. So in the 1990s such influence of chemicals. Virtually every client will
experience urges and craving to use chemicals after can be in an inpatient or an outpatient rehabilitation
he or she begins a recovery program. Some of these program.
individuals will relapse and return to active chemical While this chapter cannot possibly discuss every
abuse, especially if they fail to respond appropriately problem that a client might encounter while in a reha-
to relapse triggers that are encountered in everyday bilitation program, it does touch on some of the more
life. Finally, insurance company policies often place common situations that might interfere with a client’s
severe constraints on the length of time a given client recovery from alcohol/drug use problems.
CHAPTER THIRTY-THREE
Pharmacological Intervention
Tactics and Substance Abuse
Pharmacotherapy,1 the utilization of select pharmaceu- withdrawal syndrome (Bayard, McIntyre, Hill, &
ticals to treat a specific condition, often provides a use- Woodside, 2004; Daeppen et al., 2002; Mariani & Levin,
ful adjunct to the rehabilitation of a person with a sub- 2004; McKay, Koranda, & Axen, 2004). Long-acting or
stance use disorder (SUD) (Lukas, 2006; Rounsaville, intermediate-duration benzodiazepines are preferred
2006). Even so, pharmaceutical companies have not over shorter-acting compounds, as they reduce the risk
demonstrated any significant interest in developing of rebound withdrawal symptoms (Bayard et al., 2004).
agents that might be useful in the fight against drug The judicious use of chlordiazepoxide (20–100 mg
abuse, in part because they view this market as too lim- every 6 hours) or diazepam (5–20 mg every 6 hours) has
ited (Ciraulo, 2004). Thus, the pharmaceutical agents been found to control the tremor, hyperactivity, convul-
currently used to treat substance use problems are usually sions, and anxiety associated with alcohol withdrawal
those originally developed for other purposes and then (Milhorn, 1992; Miller, Frances, & Holmes, 1989; Yost,
found to be of value in treating drug abuse/addiction 1996). However, in very rare cases exceptionally high
(Ciraulo, 2004). doses of up to 2,000 mg/day of diazepam have been
Lukas (2006) identified several subgroups of medica- necessary to control these symptoms (Bayard et al.,
tions that can be useful adjuncts to the individual’s treat- 2004).
ment program. These are (a) medications that control For many years, physicians advocated the use of
withdrawal symptoms, (b) substances that control the “standing orders/fixed schedule” for the administration
individual’s craving for drugs, (c) aversive agents that of benzodiazepines to control AWS. In such a program
cause dysphoria when the individual engages in sub- the patient might receive an oral dose of 50–100 mg of
stance abuse, (d) pharmaceuticals used to treat concur- chlordiazepoxide every 6 hours, with an additional dose
rent psychiatric problems, (e) medications used in drug of 25–100 mg of chlordiazepoxide by mouth adminis-
maintenance programs, and (f) medications used to treat tered at 1-hour intervals, until the withdrawal symp-
drug overdoses. Each of the medications discussed in toms are controlled (Saitz & O’Malley, 1997). Then, the
this chapter falls in one or more of these categories. daily dosage level of benzodiazepines should be re-
duced by 10%–20% each day, until the medication is fi-
nally discontinued (Miller et al., 1989).
Physicians now advocate the use of a “symptom-
Pharmacological Treatment driven” approach to the AWS (McKay, Koranda, &
of Alcohol Use Disorders Axen, 2004). Depending on the patient’s withdrawal
Medications used in the treatment of the alcohol with- symptoms, a benzodiazepine such as chlordiazepoxide
drawal syndrome (AWS). The benzodiazepines are ac- or diazepam would be administered to control the
cepted as the treatment of choice for the alcohol symptoms. Symptom-driven alcohol withdrawal pro-
grams allow patients to be given significantly smaller
1The pharmacological support of alcohol or drug withdrawal, or as total dosage levels of benzodiazepines and to have
part of the treatment of an ongoing substance abuse problem, should shorter hospital stays (Bayard et al., 2004; Daeppen et al.,
be supervised by a licensed physician who is skilled and experienced 2002). If the patient should begin to experience signifi-
in working with substance abuse cases. The information provided in
cant levels of agitation or hallucinations, a low dose of
this chapter is provided for information purposes only. It is not in-
tended to encourage self-treatment of substance abuse problems, nor an antipsychotic medication such as haloperidol can be
should it be interpreted as a standard of care for patients who are added to the medication regimen as an adjunct to the
abusing/addicted to chemicals. benzodiazepines being used (Bayard et al., 2004).
383
384 Chapter Thirty-Three
One research study in the United States utilized an fortable effects of the alcohol-disulfiram interaction.
anticonvulsant medication, carbamazepine, as an alter- A veteranian, observing the interaction in co-workers,
native to benzodiazepines in mild to moderate AWS. suggested that this compound might be useful in the
This medication has frequently been used to control treatment of alcoholism (Bohn, 2001).
the symptoms of AWS in Europe, with great success Since the compound was first suggested as a way to
(Bayard et al., 2004). Dosage levels are usually 800 mg combat chronic alcoholism, researchers have discov-
on the first day of alcohol withdrawal and are gradually ered that disulfiram is potentially dangerous and should
reduced to 200 mg on the fifth day of treatment (Bayard not be used with patients who have serious medical dis-
et al., 2004). Carbamazepine is nonsedating and ap- orders such as diabetes, hypothyroidism, cerebral dam-
pears to reduce the individual’s craving for alcohol age, epilepsy, nephritis, or in women who are pregnant
following acute detoxification. (Gitlow, 2007). Prior to 1970, when dosage levels of
Medications used in the treatment of alcohol depend- 1–2 grams per dose were used, disulfiram was noted to
ence. A generation ago, Frances and Miller (1991) struck cause dilirium, depression, anxiety, and manic and psy-
a rather pessimistic note when they observed that even chotic reactions. However, it is not known whether these
after a century of searching for an antidipsotrophic2 med- same problems will be encountered now that the stan-
ication “at this writing there is no proven biological dard dose is only 250–500 mg/dose (Petrakis, Gonzalez,
treatment for alcoholism. Each promising drug that has Rosenheck, & Krystal, 2002). These reactions are much
been tested in the hope it would reduce relapse by inter- less common at lower doses, but still occur. Other known
vening in the basic disease process has failed” (p. 13). At or suspected side effects of disulfiram include skin rash,
the start of the 21st century, just four medications are fatigue, halitosis, a rare and potentially fatal form of
approved by the Food and Drug Administration (FDA) hepatitis, peripheral neuropathies, hallucinations, and
for the treatment of alcohol dependence (Pettinati & potential optic nerve damage (Schuckit, 1996a; Tekin &
Rabinowitz, 2006): (a) disulfiram, (b) oral naltrexone, Cummings, 2003).
(c) acamprosate, and (d) injected extended release nal- For many years, disulfiram has been commonly rec-
trexone. These medications are reviewed below. ommended by rehabilitation professionals as an essen-
Antabuse (disulfiram). At the 1949 annual meeting tial component in recovery. In reality there is only
of the American Psychiatric Association, Barrera, Osinski, limited evidence that it is effective as an antidipsotrophic
and Davidoff (1949/1994) presented a paper in which (Bohn, 2001; Carroll, 2003; Mariani & Levin, 2004;
they reported the outcome of their research into the Sofuoglu & Kosten, 2004). Research studies have re-
possible use of Antabuse (disulfiram) as an antidip- peatedly demonstrated that disulfiram is no more effec-
sotrophic3 medication. Antabuse reflects an attempt to tive than a placebo in supporting abstinence. Because of
apply aversive conditioning principles to the treatment its very limited effectivess and wide range of side effects,
of alcoholism, since the combination of alcohol and its use in the treatment of alcohol dependence has be-
Antabuse produces “unpleasant effects” for the drinker, come quite rare (Standridge & DeFranco, 2006).
thus reducing the reward value of the alcohol, accord- Disulfiram is not recommended for elderly patients
ing to the authors. because it might cause or contribute to hypotension,
These “unpleasant effects” were first discovered by myocardial infarction, and stroke in these individuals
workers in rubber factories, who had experimented (Goldstein, Pataki, & Webb, 1996). Further, some re-
with disulfiram to vulcanize rubber. After work, many ports suggest that disulfiram has exacerbated the symp-
of the workers stopped off for a drink or two, only to find toms of schizophrenia in patients with this disorder
themselves becoming ill from the interaction of the alco- (Fuller, 1995). Individual case reports suggest that
hol with the disulfiram that they had absorbed through disulfiram can interfere with male sexual performance
their skin (Bohn, 2001). A few years later, researchers (Schiavi, Stimmel, Mandeli, & White, 1995).
administered disulfiram to animals in an attempt to Disulfiram has been shown to interact with pheny-
cure worm infestations and at the end of the work day toin, warfarin, isoniazid,4 diazepam, chlordiazepoxide,
went out for a few drinks only to rediscover the uncom- and several commonly used antidepressants (Fuller,
1995). The combination of isoniazid (or INH as it is
2This term is a carry-over from the 19th century, when alcoholics also called) and disulfiram have been found to bring on
were said to suffer from “dipsomania.” A medication that was antidip- a toxic psychosis or cause neurological problems
sotrophic would thus be against dipsomania.
3See Glossary. 4See Glossary.
Pharmacological Intervention Tactics and Substance Abuse 385
(Meyer, 1992). Further, depending on the patient’s bio- in about 30 minutes. Typically, the interaction lasts for
chemistry, disulfiram might react to the small amounts 30–180 minutes. The strength of these side effects de-
of alcohol found in many over-the-counter medications pends on such factors as (a) how much alcohol has
or other products. The individual using disulfiram should been ingested, (b) the amount of disulfiram being used
be warned to avoid certain foods or commercial products each day, and (c) the length of time since the last dose
to keep from having an unintentional reaction caused by of disulfiram was ingested. The last point is important
the small amounts of alcohol found in these com- since the body begins biotransforming disulfiram almost
pounds. Most treatment centers or physicians who uti- immediately. The full effect of disulfiram last only about
lize disulfiram have lists of such products and foods and 24–48 hours, although there have been rare reports of
will provide a copy to patients on disulfiram. alcohol-disulfiram interactions up to 2 weeks after the
Physicians have found that medication compliance last dose of the drug. But in most cases, the individual’s
is a major problem for patients who have been pre- body ceases to react to alcohol on the sixth or seventh
scribed disulfiram, with only 20% taking the medica- day after the last dose of disulfiram. When disulfiram is
tion as prescribed (Rounsaville, 2006). To address this prescribed, most patients take it every day, or every other
problem, researchers have experimented with disulfi- day, for optimal effectiveness.
ram implants designed to release a steady supply of the To make sure users understand the consequences of
medication into the user’s circulatory system. However, mixing alcohol with disulfiram, they are repeatedly
subsequent research failed to demonstrate any signifi- warned about the danger of any alcohol exposure while
cant advantage in abstinence rates over the oral prepa- there is disulfiram in their blood. Some treatment cen-
rations of disulfiram currently in use (Bohn, 2001; ters advocate a learning process in which patients take
Tinsley, Finlayson, & Morse, 1998). disulfiram for a short period of time (usually a few days)
When used properly, disulfiram can provide an addi- after which they are allowed to drink a small amount of
tional source of support in a weak moment because alcohol under controlled conditions. The hope is that
people know they cannot drink alcohol without side ef- this experience will be so unpleasant as to make them
fects until the medication is entirely out of their sys- less likely to drink a large amount of alcohol later.
tems. This process can take as long as 10–14 days, On occasion, the spouse of an alcohol abuser will in-
providing time for the individual to have second quire about the possibility of obtaining disulfiram to
thoughts about drinking. But the patients need to be teach the drinker a “lesson.” Inquiry usually reveals that
warned that disulfiram does not reduce the frequency the spouse wants to put a sample of disulfiram in the al-
or intensity of their craving for alcohol. It can only in- coholic’s coffee or “eye opener.” With the best of inten-
terfere with the biotransformation of alcohol after it en- tions, the spouse wants the drinker to experience the
ters the individual’s body, not alter the patients’ desire alcohol-disulfiram interaction when he or she is not
for alcohol. expecting it in an effort to discourage further drinking.
Clinically, disulfiram interferes with the body’s ability Disulfiram should never be given to an individual without
to biotransform alcohol by destroying the enzyme alde- his or her knowledge and consent (American Psychiatric
hyde dehydrogenase. Without this enzyme, acetalde- Association, 1995).
hyde, a metabolite of alcohol that is about 30 times as As an aversive conditioning agent disulfiram leaves
toxic to the body as alcohol itself, is able to to build up in much to be desired. Theoretically, an effective behav-
the circulation (Moalem & Prince, 2007). The subjec- ior modification program for alcohol dependence
tive experience of acetaldehyde poisoning includes facial would involve an immediate negative consequence to
flushing, heart palpitations, a rapid heart rate, difficulty drinking to shape the alcohol use behavior. The delay
in breathing, nausea, vomiting, and possibly a serious between the ingestion of alcohol and the disulfiram-
drop in blood pressure (Schuckit, 2006; Sofuoglu & alcohol reaction (about 30 minutes after the start of alco-
Kosten, 2004). The disulfiram/alcohol reaction can be hol ingestion) is far too long for it to function as an
fatal and if someone should experience a reaction he or aversive conditioning agent. As an indication of disulfi-
she should be seen by a physician immediately. ram’s failure as an adversive conditioning agent, some
Under normal conditions, it takes 3–12 hours after alcohol-dependent individuals will drink in spite of the
the first dose of disulfiram to begin to interfere with the disulfiram in their system, a process known as “drinking
metabolism of alcohol. But the individual who has through” the disulfiram. Others will drink in spite of
been using disulfiram for several days and then ingests having ingested disulfiram in the recent past because
alcohol will experience the alcohol-disulfiram reaction they believe they know how to neutralize the drug while
it is in their body. Also, many individuals with an alco- site seems to reduce alcohol consumption in both ani-
hol use disorder will stop taking disulfiram several days mals and man (Mariani & Levin, 2004).
before a “spontaneous” relapse to prepare for their return In spite of its initial promise, naltrexone has not
to active drinking. proven to be the hoped-for magic bullet against alcohol
Although it was adopted as an aid to alcohol absti- dependence. Research into the effectiveness of naltrex-
nence, research has suggested that disulfiram interacts one in controlling craving for alcohol is mixed. One
with the neurotransmitter serotonin to boost brain study found that 50% of patients treated with naltrexone
levels of a byproduct of serotonin known as 5-hydrooxy- relapsed within 12 weeks (Kiefer et al., 2003), and at least
tryptophol (or, 5-HTOL) (Cowen, 1990). Animal re- one study failed to find any significant effect for naltrex-
search suggests that increased levels of 5-HTOL result one in preventing relapse (Mariani & Levin, 2004).
in greater alcohol consumption. While research with However, many who take 50 mg/day of naltrexone
human subjects has yet to be completed, preliminary report that they derive less pleasure from their use of al-
data suggest a need for alcohol-dependent persons to cohol and that they crave it less (Mason, Salvato,
avoid “serotonin rich” foods such as bananas and wal- Williams, Ritvo, & Cutler, 1999). Naltrexone does not
nuts, which theoretically might increase their craving seem to prevent alcohol-dependent individuals from
for alcohol when using disulfiram as an aid to their having the initial “slip,” but it does seem to prevent that
recovery. slip from turning into a full relapse (Volpicelli, 2005).
Lithium. In the late 1980s and early 1990s, there was Medication compliance is a significant problem, with
a great deal of interest in the possible use of lithium in 40% of the patients started on naltrexone discontinuing
the treatment of alcoholism. Lithium is an element that the medication within 30 days, and 60% within 90 days
has been found to be useful in the treatment of bipolar of being started on this agent (Carroll, 2003). To com-
affective disorders (formerly called the manic-depressive bat this, a time-released injectable form of naltrexone
disorder). Early research suggested that lithium reduced has been developed and sold under the brand name of
the number of relapses in chronic drinkers, lowering the Vivitrol (Prescribing Information, 2006). This once-a-
apparent level of intoxication and the desire of chronic month injectable form of naltrexone offers promise in
alcohol users to drink (Judd & Huey, 1984; Miller et al., helping to control the craving for alcohol over extended
1989). Unfortunately, subsequent research failed to periods of time (Garbutt et al., 2005).
support these early findings. An obvious exception is Naltrexone hydrochloride is thought to reduce alco-
when the patient has a bipolar affective disorder in ad- hol’s reward value by blocking the mu opioid receptors.
dition to alcohol abuse/dependence, for lithium is quite This limits the craving for alcohol that so often compli-
effective in controlling the mood swings in manic de- cates rehabilitation efforts (American Psychiatric Asso-
pression. ciation, 1995; Holloway, 1991; Meza & Kranzler, 1996;
Ondansetron. This substance has been used to treat Swift, Whelihan, Kuznetsov, Buongiorno, & Hsuing,
early-onset alcoholism with some success (Johnson et al., 1994). Unfortunately, this medication has a dose-
2000). Drawing on the knowledge that early-onset alco- dependent toxic effect on the liver, limiting its use to
holism might reflect a serotonergic system dysfunction, people who have not suffered significant liver damage
Johnson et al. utilized a serotonin blocking agent that (Mason et al., 1999).
focused its effects on the 5-HT3 receptor subtype, Acamprosate (calcium acetylhomotaurinate). This
which has been found to be involved in the subjective substance has been used by physicians in Europe to
experience of alcohol-induced pleasure for drinkers. treat alcohol use disorders since 1989 (Hunter &
Ondansetron reduced the individual’s desire to drink as Ochoa, 2006). It was finally approved for this purpose
well as the subjective experience of pleasure if he or she in the United States in 2004. In spite of its widespread
did consume alcohol. However, this medication is still acceptance in Europe and Asia as an adjunctive treat-
experimental, and research suggests that it works best ment for alcohol dependence, the exact mechanism by
when taken twice per day. Whether ondansetron has a which Acamprosate works remains unknown (Hunter &
role in the treatment of alcoholism remains to be seen. Ochoa, 2006). It is thought to work by influencing the
Naltrexone hydrochloride. When an individual con- GABA and gluamatergic neurotransmitter systems in
sumes alcohol, his or her brain is thought to release en- the brain, possibly by altering the responsiveness of
dogenous opioids. These neurotransmitters are involved calcium channels in neurons to stimulation (Carroll,
in the pleasure center of the brain. Researchers have dis- 2003; Hunter & Ochoa, 2006; Mariani & Levin, 2004;
covered that antagonists for the the mu opioid receptor Overman, Teter, & Guthrie, 2003).
Acamprosate is a relatively safe medication, with no Sofuoglu, & Kosten, 2004). Research suggests that
evidence of a “rebound” effect when it is discontinued when alcohol-dependent individuals take topiramate,
and no documented abuse potential (Hunter & Ochoa, they are 600% more likely to abstain than people who
2006). There are no reports of interactions with com- did not receive this medication, suggesting that it might
monly used pharmaceuticals, including disulfiram be at least as effective as other pharmaceuticals being
(Overman et al., 2003; Sherman, 2000a). The most se- examined as possible aids in the treatment of alco-
rious side effect of acamprosate is diarrhea, which is ex- holism (Johnson, Ait-Daoud, Akhtar, & Ma, 2004).
perienced by 10%–17% of patients and usually resolves The early studies will need to be replicated to confirm
in a few days (Hunter & Ochoa, 2006; Litten, 2001; the value of this medication in the fight against alcohol
Standridge & Defranco, 2006). Other rare side effects dependence.
include dizziness, insomnia, anxiety, depression, nau- Other pharmacological treatments for chronic alco-
sea, drowsiness, dry mouth, and increased sexual desire hol dependence. Scientists have considered a number of
(Hunter & Ochoa, 2006). compounds as potential antidipsotrophic medications.
Acamprosate has a chemical structure similar to that At one point in the 1970s, the antibiotic compound
of the neurotransmitter GABA. Unlike the disulfiram/ Flagyl (metronidazole) was examined as a possible ad-
alcohol interaction, acamprosate stimulates the pro- junct to the treatment of alcoholism, since it will cause
duction of GABA in the brain. This, in turn, inhibits discomfort when mixed with alcohol, but it was not
the effects of glutamate, a neurotransmitter that stimu- shown to be effective as a possible antidipsotrophic
lates the CNS (Whitworth et al., 1996). The apparent medication (Hester & Squires, 2004).
effect is that people feel less need to ingest alcohol and Another compound that was considered for possible
if they do so, they feel less of a reward from the alcohol use with alcohol-dependent individuals is nalmefene,
than before (Hunter & Ochoa, 2006). an opioid antagonist similar to naltrexone in its chemi-
Acamprosate is excreted unchanged by the kidneys cal structure (Mason et al., 1999). The medication has
(Overman et al., 2003; Sherman, 2000a). Like Antabuse, a longer half-life than naltrexone and binds more effec-
it is most effective with those who volunteer to take it tively at the mu, kappa, and sigma opioid receptor sites
as an aid in their recovery program (Sommer, 2005). (which are thought to be most involved in the pleasura-
Preliminary evidence suggests that this medication ble effects caused by drinking) than naltrexone, sug-
might help improve sleep patterns in the alcohol- gesting that nalmefene might be at least of equal value
dependent individual during acute withdrawal (Staner in the treatment of alcoholism. However, there has
et al., 2006). This makes intuitive sense, as this medica- been little interest in developing this compound for use
tion helps the newly abstinent individual crave alcohol with alcohol-dependent persons.
less, thus sleeping more easily. The clinical evidence Buspirone. Initial research suggested a role for bus-
supporting the efficacy of acamprosate is limited, with pirone in the treatment of alcohol dependence. In se-
some studies finding no significant difference in long- lect cases when the individual also had a concurrent
term recovery rates between those who do use this com- anxiety disorder, buspirone might be useful. However,
pound and those who do not (Gitlow, 2007). Most subsequent research suggested that it was effective only
studies have found acamprosate to be effective in the for drinkers with a preexisting anxiety disorder (Mariani &
treatment of chronic alcohol use disorders, but at least Levin, 2004).
one failed to find any significant effect from this med- Selective serotonin reuptake inhibitors (SSRIs). The
ication (Anton et al., 2006). Further research appears SSRIs, most commonly used in the treatment of depres-
necessary to identify the role that acamprosate might sion, were examined as possible aids to alcohol cessa-
play in the pharmacological treatment of alcohol use tion, but to date research has failed to find that they
disorders. reduce alcohol abuse/addiction, except in drinkers with
Topiramate. Originally introduced as an anticonvul- a concurrent depressive disorder (Bohn, 2001; Mariani &
sant medication, researchers have found that topira- Levin, 2004).
mate enhances GABA’s effects in the brain; this blocks Baclofen. This compound functions as a GABAB re-
the rewarding effects of alcohol and thus reduces the ceptor agonist. The team of Addolorato, Leggio, Agabio,
incentive for the individual to drink. Preliminary stud- Colombo, and Gasbarrini (2006) have suggested that it
ies have found that this medication does seem to re- is useful during the phase of acute alcohol withdrawal,
duce the frequency of alcohol use in chronic alcohol where it is about as effective as diazepam in suppress-
users (Johnson et al., 2003; Mariani & Levin, 2004; ing withdrawal distress, and as an agent to reduce the
individual’s craving for alcohol. Further research is nec- Naltrexone is not a form of treatment for the opioid
essary to determine whether this medication will prove of use disorders by itself. It is best utilized as part of a
value as a pharmacological treatment of the alcohol use comprehensive psychosocial treatment program. Jenike
disorders. (1991) reported that a 50 mg dose of naltrexone hy-
drochloride will block the euphoria of an injection of
narcotics for 24 hours, while a 100 mg dose will work for
Pharmacological Treatment
about 48 hours. Further, a 150 mg dose of naltrexone
of Opiate Addiction hydrochloride will block the euphoria from injected
Naltrexone hydrochloride. Although it has been found narcotics for 72 hours. According to Jenike, the usual
to be of value in the treatment of alcohol dependence, oral dosage schedule is three times per week, with 100
naltrexone hydrochloride is primarily used in the treat- mg being administered on Monday and Wednesday, and
ment of alcohol addiction. But since it affects the mu 150 mg being administered on Friday to provide a
opioid receptor, it is also of value in treating the addi- longer dose for the weekend.
tion to opoioids. Naltrexone is an opioid antagonist To date, no research demonstrates an unequivocal
with no significant agonist effect (Kranzler, Amin, benefit from this medication in the treatment of nar-
Modesto-Lowe, & Oncken, 1999). The drug is well ab- cotics addiction (Thompson PDR, 2004). Indeed, re-
sorbed when taken orally, and peak blood levels are search has revealed that orally administered naltrexone
achieved within an hour of ingestion, according to is most effective for that subgroup of opiate-dependent
Kranzler et al. (1999). In spite of its elimination half-life persons who are most likely to follow treatment recom-
of 3.9 to 10.3 hours, the drug has an extended action mendations (Carroll, 2003). One early study found that
within the brain, and depending on the dosage used only 2% of opiate-dependent patients continued to take
naltrexone can block the euphoric effects of injected this drug for 9 months (Youngstrom, 1990a). It is not
opiates for up to 72 hours. known if the long-term injectable form of naltrexone
In 2006 a time-released, injectable form of naltrex- will alter this statistic. To date, naltrexone hydrochlo-
one was introduced under the brand name of Vivitrol ride has not proven to be the “magic pill” for the treat-
(Prescribing Information, 2006). The applicability of ment of opiate addiction.
this form of naltrexone in the treatment of opioid de- Ibogaine. This is an alkaloid obtained from the
pendence has not been determined, but since this med- root bark of the shrub Tabernanthe iboga, which grows
ication was initially developed for the treatment of in some regions of Africa. It has some hallucino-
opioid dependence rather than alcoholism, it is logical genic properties (Abrams, 2003). In spite of this char-
to assume that it will be utilized in this capacity as well. acteristic, a growing number of researchers are study-
The theory behind the use of naltrexone hydrochlo- ing ibogaine, which seems to be able to eliminate the
ride is that if the person taking this medication does not individual’s craving for narcotics such as heroin in the
experience any feelings of euphoria from opiates, he or early phases of abstinence (Glick & Maisonneuve,
she is less likely to use opiates again. But naltrexone use 2000). Scientists uncomfortable with the use of ibo-
has several dangers. First, to avoid initiating an unde- gaine, since research has demonstrated that high doses
sired opiate withdrawal syndrome, this medication can result in cellular damage to certain regions of the
should be used only after the person is completely detoxi- brain, have limited its applicability in humans (Glick &
fied from narcotics. To avoid the danger of overdose, the Maisonneuve, 2000). Further, ibogaine has side effects
patient must also be warned not to attempt to “shoot that are unpleasant for many users, which also limits its
through” a narcotic antagonist such as naltrexone. This usefulness.
warning is necessary because on rare occasions individu- Researchers have found that the major metabolite
als have been known to attempt to inject a large enough of ibogaine is a compound called noribogaine. This
dose of narcotics to overcome the antagonist, in spite of metabolite has a biological half-life of several weeks; its
the risk of narcotic overdose (Callahan, 1980). Further, chemical structure lends itself to manipulation by scien-
when the individual stops using naltrexone, he or she tists who hope to find a chemical cousin to ibogaine that
will then begin to reexperience a craving for narcotics. is effective, yet lacking the potentially destructive side
There is no extinction of the craving for the drug during effects of the parent compound (Glick & Maisonneuve,
the period of time that the narcotics addict is usually 2000). They have developed a derivative of igobaine
maintained on a narcotics blocker, and the patient must known as 18-MC, which seems to block the craving for
be warned about this to minimize the danger of relapse. narcotics in animal test subjects without the harsh side
effects of the parent compound (Abrams, 2003). Unfor- methadone was found to be able to block the craving
tunately, there are still many misconceptions and gov- for opioids at dosage levels far below those necessary to
ernment bureaucratic hurdles that must be overcome induce analgesia. The ability of methadone to block
before a controversial compound such as 18-MC might opioid withdrawal symptoms was discovered in the
be approved for human use, even if subsequent studies 1960s. Researchers found that low doses of orally ad-
prove that it is effective in humans. ministered methadone would block the narcotic with-
drawal process and the individual’s craving for further
opioid use for at least 24 hours (Kreek, 2000). However,
Methadone Maintenance this line of research was considered illegal by the Drug
Methadone is a synthetic narcotic analgesic developed Enforcement Administration (DEA), which threatened
by German chemists during World War II. It is an effec- to prosecute Dr. Vincent Dole and Dr. Marie Nyswander
tive analgesic that is well absorbed after oral administra- for their research (“After 40 Years,” 2005). Eventually,
tion, intravenously, and from intramuscular injections the DEA allowed the researchers to continue their work.
(Toombs & Kral, 2005). In the United States, methadone In a methadone maintenance program (MMP), low
is used as an aid to the treatment of opioid dependence doses of orally administered methadone are utilized, as it
in two ways. First, it can help control the withdrawal has been found that when only 25%–35% of the opiate
discomfort that the patient might experience when he receptor sites in the brain are occupied by methadone
or she discontinues the use of opioids. Second, orally molecules, the development of withdrawal symptoms or
administered doses of methadone have been found to drug craving is blocked (Kreek, 2000). Further, the
block the craving for additional narcotics that opioid pharmacokinetics of methadone allowed it to be admin-
addicts report, allowing them to live a more normal life. istered orally just once daily for the control of opioid
When used in this manner, methadone is referred to as withdrawal symptoms. These factors made methadone
a maintenance agent, or an an opioid agonist. “corrective, but not curative” of the problem of opioid
There is a great deal of confusion about methadone. addiction (Dole, 1988, p. 3025).
Although it is often used with good effect as an analgesic In spite of their promise, opioid agonists such as
for chronic pain patients or individuals with cancer- methadone have no magical effect on the individual’s
related pain, patients often object to its use because they personality, vocational skills, or support system (Gerada,
associate the name methadone with drug addiction. In 2005), and following stabilization, the individual will
such cases, it is necessary to explain to the patient that still require psychosocial counseling (Dole, 1988). But
this medication has many applications, only one of which methadone maintenance programs are extremely cost
is the treatment of opioid use disorders. effective, with each dollar invested in such treatment
Dole and Nyswander (Dole, 1988; Dole & Nyswander, ultimately providing a return of $38 to society in terms
1965) had theorized that when certain individuals of reduced health care costs, reduced criminal activity,
abused an opiate, permanent changes in brain function increased employment, and other benefits (Zarkin,
would occur at the cellular level. They came to believe Dunlap, Hicks, & Mamo, 2005). In spite of these advan-
that even a single dose of an opioid would be sufficient tages, methadone maintenance is extremely controver-
to cause changes in the brain at a cellular level, subjec- sial (Khantzian, 2003b).
tively interpreted as a craving for further opioid use Pharmacokinetics of methadone.5 Methadone is highly
when the indivdual’s blood levels began to drop. This lipophilic6 and once in the blood it is rapidly distrib-
craving for opioids was hypothesized to continue for uted to blood-rich organs such as the brain, liver, lungs,
months or even years after the individual’s last dose of a and kidneys. The compound has a long elimination half-
narcotic, motivating him or her to continue to abuse life of around 22 hours (Toombs & Kral, 2005) with a
opioids again in order to feel “normal” and stop the range of 13 to 58 hours, depending on the individual’s
drug craving (Dole & Nyswander, 1965). biochemistry (Karch, 2002). One factor that signifi-
Based on this theory, it was assumed that if a com- cantly affects the half-life of methadone is the acidity of
pound could block the individual’s craving for opi- the individual’s urine. If the patient’s urine is very acidic,
oids, it would then be possible to begin a program of
psychosocial rehabilitation (Dole & Nyswander, 1965). 5
Since this section discusses the use of methadone in the treatment of
Methadone was found to be such an agent, and it was opioid addiction, the pharmacokinetics reviewed are those associated
soon suggested as a compound that might be used with methadone maintenance, not analgesia.
in the fight against narcotics addiction. Significantly, 6
See Glossary.
the half-life of methadone can be 50% shorter than if compounds involved, the methadone-drug interactions
the urine is not acidic (Drummer & Odell, 2001). might simply alter the pharmacokinetics of one or both
Because of variability in such factors as drug absorp- compounds, or they might be life threatening. Some
tion, distribution, biotransformation, and elimination, medications that interact with methadone include car-
there is a great deal of interindividual variability in the bamazepine, phenytoin, risperidone, Ritonavir, and the
blood levels achieved by a given dose of methadone. Scien- herbal medicine St. John’s Wort, all of which may re-
tists have found a 17-fold variation in blood methadone duce the blood levels of methadone (Scottenfeld, 2004).
levels between different patients receiving the same Other medications, such as fluoxetine, fluvoimine, san-
dosage of the drug (“Methadone Dose Debate Contin- quinavir, cimetidine, erythomycin, and ciprofloxacin,
ues,” 2003). For this reason, many clinics utilize blood may slow the rate of methadone biotransformation, in-
level analysis to help determine the individual’s medica- creasing the blood plasma levels of this medication
tion requirements. Once a steady dosage level has been possibly to fatal levels (Drummer & Odell, 2001;
achieved, blood studies usually reveal a peak methadone “Methadone-Cipro Interactions,” 2002; Scottenfeld,
blood level that is 2–4 times as high as the individual’s 2004). There is also evidence that methadone is able to
lowest blood level (the “trough”) (Scottenfeld, 2004). block the antithrombotic action of aspirin, allowing
Methadone’s safety record when used as an agonist the body to form blood clots more easily when the
agent is quite good, and even after extended periods of patient is taking aspirin and methadone concurrently, a
use there is no evidence of methadone-related damage reaction that is of some concern to patients using aspirin
to the heart, lungs, kidneys, liver, brain, or other body for antithrombotic purposes (Malinin, Callahan, &
organs (Schottenfeld, 2004). One common side effect Serebruany, 2001).
is excessive sweating (Jaffe & Jaffe, 2004). A rare but po- Methadone overdoses can be fatal. Doses as low as
tentially fatal complication of methadone treatment is 5–10 mg have proven deadly to children who acciden-
the possible development of a heart rhythm disturbance tally ingested this medication (Schottenfeld, 2004).
known as Torsade de Pointes (TdP) (Justo, Gal-Oz, The lethal dose is higher in adults, but even then
Paran, & Seltser, 2006; Roden, 2004; Sticherling, Schaer, adults should not be started on doses greater than
Ammann, Maeder, & Osswald, 2005). This is a form of 40–50 mg/day at the start of methadone agonist ther-
ventricular tachycardia in which the normal pattern of apy, and daily doses should be increased only slowly
electrical discharge/repolarization cycle of the heart is (Schottenfeld, 2004). If a methadone overdose is treated
disrupted, setting the stage for possible sudden cardiac with a narcotic blocker such as naloxone, it is necessary
death. It is estimated that 5%–10% of people who de- to continue the administration of the narcotic blocker
velop this disorder have a subclinical form of ventricu- for extended periods of time because of methadone’s
lar tachycardia that is exacerbated by medications such extended half-life, as death can occur up to 24 hours
as methadone (Roden, 2004; Sticherling et al., 2005). after the overdose was ingested or naloxone was discon-
Some of the risk factors for Torsades de Pointes in tinued (Schottenfeld, 2004).
methadone maintenance patients include (a) high dose Methadone maintenance. Following stabilization,
of methadone, (b) concurrent use of compounds that the individual’s methadone is usually administered in a
increase the methadone syrum levels, (c) HIV-1 infec- single dose, although some of the more progressive pro-
tion, (d) hypokalemia,7 (e) liver cirrhosis, (f) renal fail- grams allow split dosing in which the patient takes the
ure, or (g) preexisting heart disease (Justo et al., 2006). medication in two or three equal doses either at the
Although the exact percentage of methadone patients clinic or at home if he or she has earned “take home”
who are affected by Torsade de Pointes is not known, it is dosing privileges. Traditionally, methadone is adminis-
believed that less than 1% of patients on methadone de- tered in the morning, usually in liquid form to reduce
velop this potentially fatal disorder (Roden, 2004). the risk of diversion of the drug to the streets. Another
Physicians have found that methadone will interact advantage of this dosage form is that the methadone
with at least 100 different pharmaceuticals currently in can be mixed with a fruit juice to make it easier to
use in the United States (Scottenfeld, 2004; “Taming swallow.
Drug Interactions,” 2003).8 Depending on the specific Depending on program rules and patient compli-
ance to these rules, the individual might be permitted
7See Glossary. “take-home” dosing privileges, with federal guidelines
8Alwaysconsult a physician or pharmacist before mixing two or more allowing for up to 30 “take home” doses a month for in-
medications, including over-the-counter or herbal agents. dividuals who adhere to program rules. Methadone
maintenance has been used for the past 40 years (Marion, methadone maintenance (DeVane & Nemeroff, 2002;
2005). Research has repeatedly demonstrated that when Gunderson & Stimmel, 2004). This is apparent in the
sufficiently high dosage levels of methadone are com- confusion that arises when a patient in a methadone
bined with a range of psychosocial support services (i.e., maintenance program requires analgesia following sur-
psychotherapy, vocational counseling, social services, gery or traumatic injury. Health care providers typically
etc.) significantly larger numbers of opiate-dependent do not understand that the dosage level of methadone uti-
individuals are able to remain drug-free for longer lized in maintenance programs is usually not sufficient to
periods of time (Kauffman, 2003a, 2003b; McLellan, block significant levels of pain. Patients in methadone
Arndt, Metzger, Woody, & O’Brien, 1993). Indeed, once maintenance programs will often require higher than
a patient is stabilized on a sufficiently high dose, his or normal levels of narcotic analgesics to achieve adequate
her daily dosage requirement should remain stable for pain control following trauma (Gunderson & Stimmel,
years. The minimum recommended period of in- 2004). Thus, special provision for pain control must
volvement with a methadone maintenance program is be made for patients on methadone maintenance
12 months to allow the patient sufficient time to address (Krambeer, von McKnelly, Gabrielli, & Penick, 2001).
problems in living (Gerada, 2005; Kauffman, 2003a, Criticism of methadone maintenance. Dole utilized
2003b). a theoretical model of opioid addiction that assumed
The reality of methadone maintenance. In spite of the the opiate being abused played a role similar to that of
promise of methadone maintenance programs, fewer insulin in diabetes (Kleber, 2002). However, Marlowe
than 15% of known opioid-dependent persons are actu- and DeMatteo (2003, 2004) suggest that this analogy,
ally involved in such programs (Fiellin, Rosenheck, & while useful, does not make chemical dependency a
Kosten, 2001). In other words, fewer than 180,000 of true disease state. Their challenge to the disease model
the estimated 600,000–800,000 people in the United also is a challenge to the foundation of methadone
States who are thought to be dependent on heroin are maintenance programs.
enrolled in a methadone maintenance program (Kreek, Critics also argue that providing methadone for
2000). Further, because of political and philosophical narcotic-dependent persons is simply switching addic-
constraints, more than one-third of those patients in a tions (Joseph, 2004; Kauffman, 2003a, 2003b; Kleber,
methadone maintenance program receive less than 2002). That methadone is not the “magic bullet” for ad-
60 mg of the drug a day (D’Aunno & Pollack, 2002), diction is proven by the fact that 50%–90% of the pa-
even though Dole and Nyswander (1965) suggested that tients on methadone maintenance will abuse other
the lowest effective dose to help normalize the opiate- compounds (Glantz & Woods, 1993). Patients have also
dependent individual was 80 mg/day, leaving many found weak spots in the methadone maintenance con-
patients at risk for subclinical withdrawal symptoms cept. They are often well aware that compounds such
because they are being undertreated. as alcohol and cocaine will speed up the process of
Further, psychosocial support services, including psy- methadone biotransformation. This will cause the patient
chological/psychiatric care, have been found necessary to experience earlier withdrawal symptoms, which, if the
to effectively treat the patient in a methadone mainte- program staff did not detect the concurrent substance
nance program. Kraft, Rothbard, Hadley, McLellan, and abuse, might cause them to administer higher doses of
Asch (1997) concluded that a total of three counseling methadone to avoid opiate withdrawal (Karch, 2002;
sessions per week was the most cost effective in helping Kreek, 2000). Other patients on methadone will try to
clients abstain from heroin use. Such counseling ses- obtain propoxyphene, which enhances the effects of
sions are labor intensive, and few programs come close to the methadone and produces a sense of euphoria
providing this level of support for the individual on (DeMaria & Weinstein, 1995). These drug-seeking be-
methadone maintenance. The sad reality is that many haviors raise serious questions as to the individual’s
methadone maintenance clinics have become little motivation for using methadone in the eyes of some
more than drug distribution centers providing subthera- critics.
peutic doses of methadone to clients while making no Dole (1989) acknowledged that methadone is “highly
effort at actual rehabilitation (Kauffman, 2003a, 2003b). specific for the treatment of opiate addiction” (p. 1880),
Many physicians do not fully understand the phar- and that it will not block the euphoric effects of other
macokinetics9 of methadone or the theory behind drugs of abuse. Further, methadone diversion is a sig-
nificant problem (Dole, 1995), although the abuse poten-
9
See Glossary. tial of methadone is quite limited. There is anecdotal
evidence that some opioid-dependent persons will pur- When administered as an adjunct to the treatment
chase methadone diverted from legitimate programs to of an opioid addiction, buprenorphine is administered
carry out a methadone “taper” so they can reduce their sublingually, a method of administration providing a
daily opioid dosage requirement. Further, the dropout level of bioavability that is 30%–50% of an intravenous
rate from methadone maintenance programs is greater dose (Donaher & Welsh, 2006). The medication is ab-
than 50% in the first year (Schottenfeld, Pakes, Oliveto, sorbed through the blood-rich tissues at the base of the
Ziedonis, & Kosten, 1997), suggesting that such programs mouth, thus avoiding the first-pass metabolism10 effect
are not the final answer to the problem of narcotics that would inactivate the medication if it were absorbed
addiction. through the gastrointestinal tract. When administered
in this manner, buprenorphine functions much like
methadone in that it is able to block opioid withdrawal
Buprenorphine symptoms without causing a sense of euphoria.
Buprenorphine is a chemical cousin to morphine, and The ability of buprenorphine to block the mu recep-
when used as an analgesic it is thought to be 25–50 tor site for extended periods of time at relatively low
times as potent as morphine. A standard conversion is suiblingual doses allows physicians to prescribe it as an
that 0.3 mg of intravenously administered buprenorphine alternative to methadone for patients who might bene-
provides the same level of analgesia as 10 mg of intra- fit from opioid agonist therapy (Donaher & Welsh,
venous morphine (Fudala & O’Brien, 2005). However, 2006). Sublingual doses of 2–8 mg/day of buprenor-
the level of analgesia induced by buprenorphine is not phine are thought to be as effective as up to 65 mg/day
as high as that achieved with other narcotic analgesics, of methadone in blocking opioid withdrawal symptoms
and it is not a popular pain control medication for this (Donaher & Welsh, 2006). Some individuals require
reason (United States Department of Health and higher doses than 2–8 mg/day to block their opioid with-
Human Services, 2004). drawal symptoms, and up to 32 mg/day of buprenor-
Buprenorphine has the unique property of acting as phine might be prescribed in divided doses (Donaher &
either an opioid agonist or an opioid antagonist, depend- Welsh, 2006; Sofuoglu & Kosten, 2004).
ing on the dosage level. At low doses buprenorphine Buprenorphine has several advantages over
functions as an opioid agonist. But its effects quickly methadone. Where the latter drug must be administered
reach a plateau, after which additional buprenorphine each day, buprenorphine might be administered as infre-
will have no additional effect. At high doses buprenor- quently as three times a week if the patient has been sta-
phine functions as an opioid antagonist, limiting its bilized on this medication (United States Department
own analgesic potential (Jones, 2004; Kosten & George, of Health and Human Services, 2004). Another advan-
2002; United States Department of Health and Human tage of is that its withdrawal syndrome is not as long as
Services, 2004). If used in conjunction with other nar- nor as intense as that seen during the methadone with-
cotic analgesics or when abused at high doses through drawal syndrome (Glasper, de Wet, Bearn, & Gossop,
intravenous injections, buprenorphine can actually 2007; Jones, 2004; O’Connor, 2000).
precipitate an opiate withdrawal syndrome (O’Connor, Buprenorphine also is not the final answer to the prob-
2000; United States Department of Health and Human lem of opioid use disorders, and physicians have been
Services, 2004). slow to embrace it as a treatment option (Vastag, 2003). At
Buprenorphine functions as a partial mu opioid re- best, buprenorphine is only as effective as methadone, and
ceptor agonist, binding to but not fully activating the it is significantly more expensive (Donaher & Welsh,
mu opioid receptor sites (United States Department of 2006). Further, there is a significant abuse potential
Health and Human Services, 2004). Buprenorphine when sublingal tablets are diverted for intravenous use
molecules have a strong affinity for this receptor site (United States Department of Health and Human
and continue to occupy it long after activating it. This Services, 2004). Such diversion has been implicated
blocks other opioid molecules from being able to reach in a number of deaths of illicit drug abusers (Fudala &
the receptor site for an extended period of time and is O’ Brien, 2005; Kintz, 2002). For this reason, sublin-
the mechanism by which buprenorphine functions as gual buprenorphine used in treating narcotic-dependent
its own antagonist (Donaher & Welsh, 2006). Buprenor- patients has been modified to also contain naloxone.
phine also functions as a kappa receptor antagonist al- When injected, the nalaxone will cause the user to go
though the exact significance of this fact is not known
(Fudala & O’Brien, 2005). 10
into opiate withdrawal, but it will be harmless if the brand name of “Orlaam.” Like methadone, orally ad-
compound is used sublingually as intended (Leinwand, ministered LAAM is able to prevent opiate-addicted indi-
2000). viduals from going into withdrawal. LAAM’s biologi-
Opioid-dependent patients must be totally abstinent cal half-life of more than 48 hours (compared with
from opioids before buprenorphine maintenance is ini- methadone’s 24-hour half-life) allowed for a dosing
tiated in order to avoid drug-induced withdrawal (United schedule of once every 2–3 days for patients placed on
States Department of Health and Human Services, this compound (Leinwand, 2000). This dosing schedule
2004). Buprenorphine has also been found to interact virtually eliminated the need for take-home doses, vastly
with a wide range of other agents, including benzodi- reducing the problem of drug diversion to the illicit
azepines, alcohol, and other CNS depressants, which market.
may cause the patient to die from the combined effects Initial research suggested that LAAM was potentially
of the medications involved (Jones, 2004; United States useful against opiate dependence. Unfortunately, after
Department of Health and Human Services, 2004). it was introduced, research revealed that LAAM can
Buprenorphine has also been shown to interact with cause serious, potentially fatal cardiac arrhythmias, and
nifedipine, imipramine, and antiviral agents such as in the United States the production of LAAM was dis-
the protease inhibitors used to treat HIV-1 infection continued in late 2004 (Ivanov, Schulz, Palmero, &
(Fiellin et al., 2001; United States Department of Health Newcorn, 2006; Jones, 2004).
and Human Services, 2004). Opiate withdrawal. Physician-supervised withdrawal
Some of the side effects of buprenorphine include from narcotic analgesics can be done either on an in-
constipation, urinary retention, and sedation (Dunaher & patient or outpatient basis (Collins & Kleber, 2004).
Welsh, 2006). To date there have been no reports of an Research has found that only 17% of opiate-dependent
overdose involving buprenorphine alone, although there individuals will successfully complete an outpatient
have been a number of reports of intravenously adminis- withdrawal program, however, in contrast to the 80%
tered buprenorphine interacting with benzoidazepines retention rate seen in inpatient withdrawal programs
to bring about a drug overdose (Dunaher & Welsh, (Collins & Kleber, 2004). For both outpatient and inpa-
2006). In such cases, the treating physician must utilize tient programs, methadone is the drug of choice for opi-
very large doses of naloxone for an extended period of ate withdrawal (Karch, 2002), although other compounds
time to reverse buprenorphine-induced respiratory de- are occasionally utilized in addition to or in place of
pression. This is because of buprenorphine’s high affin- methadone.
ity for the kappa opioid receptor site and the extended Initially, the individual will receive 10 mg/hour of
period of time it takes to detatch from that receptor methadone until his or her withdrawal symptoms are
(Fudala & O’Brien, 2005). brought under control (Collins & Kleber, 2004). Once
An interesting application of a modified form of the withdrawal symptoms have been controlled, the total
buprenorphine was reported by Bai-Fang et al. (2004). dose of methadone administered becomes the start-
The authors utilized an experimental polymer mi- ing dose for withdrawal. On Day 2 of withdrawal, the
croencapsulated long-acting form of buprenorphine for patient receives this same dose as a single dose. From
intravenous injection in a small group of volunteers this point on, there are two variations on the methadone
who were opiate dependent. This new process allowed withdrawal process (Collins & Kleber, 2004). In the
for a single injection to gradually release small amounts most common variant, the individual’s daily dose of
of buprenorphine into the individual’s blood over a 4- to methadone is reduced by 5–10 mg/day until he or she
6-week period, gradually allowing the volunteer to with- is completely off narcotic analgesics. An alternative
draw from narcotics without significant distress. The program is to reduce the individual’s daily dose by
medication also appeared to block narcotic-induced eu- 5–10 mg/day until the daily dose reaches just 10 mg/day,
phoria while it was in the patient’s system, according to after which the daily dose is reduced by 2 mg/day until
the authors. It is too soon to determine whether this the patient is drug free (Collins & Kleber, 2004). There
process would be of more than experimental interest to are no data comparing the efficacy of these two methods,
researchers, but this application of a modified form of however.
buprenorphine does seem promising at this time. Patients should be warned that when their daily
LAAM. Another chemical that was initially ap- dosage levels drop to the 15 or 20 mg/day range they
proved for the treatment of opiate addicts was L-alpha- will experience some withdrawal distress (Mirin, Weiss, &
acetylmethadol, sold in the United States under the Greenfield, 1991). It is at this point that many individuals
drop out of detoxification programs. At one time it was the patch was in place. However, because of the delay
hoped that drawing out the withdrawal process over a in absorption, the author advocated the use of an oral
180-day span rather than the traditional 5- to 21-day pe- “loading” dose of 0.2 mg of clonidine, at the beginning
riod would improve the retention and abstinence rates. of the withdrawal process.
However, such programs have failed to demonstrate a Although clonidine has been proven to be an effective
significant improvement over the more traditional short- tool in controlling the withdrawal symptoms in opiate-
term withdrawal process (O’Connor, 2000). dependent individuals, some have learned to combine
Clonidine. This compound is an antihypertensive clonidine with methadone, alcohol, benzodiazepines,
that has value in controlling the symptoms of opiate or other drugs to experience a sense of euphoria (Jenike,
withdrawal. Narcotic analgesics suppress the action of 1991). Health care professionals must carefully monitor
the locus coeruleus region of the brain. During the the patient’s medication use to avoid medication misuse
withdrawal process, the locus coeruleus becomes hyper- through such patient-directed pharmacotherapy.
active, contributing to the individual’s subjective sense Experimental methods of opiate withdrawal. In the
of discomfort. Clonidine, which is technically an alpha- late 1990s, a new approach to opioid detoxification,
2 adrenergic agonist, helps to suppress the activity of the “ultra-rapid” method was introduced. Developed at
the locus coeruleus, easing the individual’s withdrawal- the Center for Investigation and Treatment of Addic-
related discomfort. tion (CITA) in Israel, ultra-rapid opiate detoxification
In contrast to methadone-based withdrawal, where was developed in the hope of avoiding the discomfort
patients tend to drop out of treatment when their daily induced by opiate withdrawal (Whitten, 2006). Ultra-
dose drops to lower levels, the highest dropout rate for rapid detoxifiction is carried out while the patient is in
clonidine-based withdrawal is usually seen at the start of a state of general anesthesia. Both clonidine and opiate
treatment (Collins & Kleber, 2004). The reasons for antagonists are administered to patients while they are
this phenomenon are not known. Some programs uti- unconscious, and the entire withdrawal process is com-
lize both clonidine and an opiate blocker such as nal- pleted within a single day (Rabinowitz, Cohen, &
trexone hydrochloride in a 4- to 5-day opiate withdrawal Kotler, 1998). The program has been found to be safe
program (Stein & Kosten, 1992). The combination of when proper procedures are followed, and it allows the
naltrexone hydrochloride and clonidine is not a stan- patient to avoid much of the discomfort associated with
dard treatment for narcotics withdrawal (Weiss, Green- opiate withdrawal (Kaye et al., 2003).
field, & Mirin, 1994). However, Weiss et al. noted that Proponents of this detoxification protocol suggest
this approach “holds promise” (p. 281) as a method of that following completion withdrawal, the individual
withdrawal from opiates. When used appropriately, the should participate in a 6-month follow-up course of
combination of clonidine and naltrexone hydrochlo- naltrexone and individual counseling. The former is to
ride appears to be as effective as a 20-day methadone block the euphoric effects of narcotics that the indi-
withdrawal program for opiate addicts (Stein & Kosten, vidual might attempt to use following detoxification,
1992). The combined effects of naltrexone hydrochlo- while the latter is to help identify and resolve issues
ride (which blocks the opiate receptors in the brain) that might contribute to the individual’s relapse. Pro-
and clonidine (which serves to control the individual’s ponents claim that up to 80% of clients remain absti-
craving for narcotics and the severity of the withdrawal nent for a 6-month period of time, although Rabinowitz
symptoms) thus allow for rapid detoxification from et al. (1998) found that only 57% of their sample of
opiates with minimal discomfort. 113 opiate-dependent males had not relapsed in the
The authors found that over 95% of their sample 6 months following ultra-rapid detoxification from
were completely withdrawn from narcotics at the end opiates.
of 5 days. While there is some degree of discomfort for Although there was a great deal of media attention to
the addicted person, Stein and Kosten (1992) suggested the process, ultra-rapid detoxification has proven only
that individuals report about the same level of discom- about as effective as more traditional detox programs
fort from withdrawal using a combination of clonidine using methadone or buprenorphine (Collins, Kleber,
and naltrexone hydrochloride as they experienced dur- Whittington, & Heitler, 2005; Whitten, 2006). There is
ing a methadone taper. Milhorn (1992) suggested that little evidence that the individual is more likely to
withdrawal discomfort might be further reduced achieve long-term abstinence after ultra-rapid detoxifi-
through the use of transdermal clonidine patches, cation (Collins & Kleber, 2004; Kosten & O’Connor,
which would provide a steady supply of the drug while 2003). Thus, the utility of this experimental method of
opiate withdrawal remains unproven at the present her feelings of anxiety and agitation and improving his
time, is quite expensive, and exposes the individual to or her responsiveness to psychosocial treatment programs
the significant risks of anesthesia (Whitten, 2006). (Kampman, 2005). Another medication that is being
investigated for the treatment of cocaine addiction is
Baclofen, which is a muscle relaxant that seems to reduce
Pharmacological Treatment the individual’s responsiveness to conditioned cues for
of Cocaine Addiction cocaine use (Kampman, 2005). The medication topira-
In spite of an extensive search for a pharmacological treat- mate also may help prevent the relapse to active cocaine
ment for cocaine addiction, researchers have failed to use following abstinence (Kampman, 2005).
identify a compound that effectively treats cocaine abuse Other researchers have tried to teach the body to use
or dependence (Carroll, 2003; Gerada, 2005; Kampman, the immune system against cocaine molecules (Wright,
2005; McRae, Brady, & Sonne, 2001; O’Brien, 2006; 1999). In theory, it is possible to develop a “vaccine”
Rounsaville, 2006; Sofuoghu & Kosten, 2004). But the against cocaine that would target an immune response
search continues (“Addiction Treatment,” 2004). against certain elements of the cocaine molecule so the
There have been many false alarms in the search for body would attack and destroy any molecule that had
a pharmacological treatment for cocaine addiction. At the same chemical structure (Wright, 1999). However,
one point researchers hoped that bromocriptine (sold researchers have not developed such a vaccine for gen-
in this country under the brand name Parlodel) might eral use. Even if such an anti-cocaine vaccine could be
control post-withdrawal craving for cocaine (DiGregorio, developed, it would only be specific to cocaine and
1990). However, subsequent research did not support thus not interfere with the use of other recreational
this theory (Kosten & O’Connor, 2003). Another com- drugs (Wright, 1999). The long-term consequences of
pound, flupenthixol, has not only demonstrated some such a vaccine are not known, and it is difficult to imag-
initial promise in the treatment of cocaine use prob- ine that cocaine abusers would volunteer to be injected
lems but has also continued to appear effective in with such a vaccine without strong external pressure.
controlling cocaine use and abuse by reducing post- There was experimental evidence that carbamazepine,
withdrawal craving (Mendelson & Mello, 1996). But it a compound used to control seizures in patients with
remains to be seen whether flupenthixol will live up to seizure disorders, might also be useful during the with-
its initial promise as a potential agent in the war against drawal phase of cocaine addiction treatment and the
cocaine use/abuse. earliest stages of abstinence (Sherman, 2000b). A med-
Surprisingly, disulfiram appears to reduce the craving ication used as an adjunct to the control of seizures,
for cocaine by increasing the dopamine levels while re- tiagabine (sold under the brand name of Gabitril),
ducing the norepinephrine levels in the brains of newly which is a GABA reuptake blocker, also seems to re-
abstinent individuals (el-Kashen, 2001; Sofuoghu & duce the frequency of cocaine abuse and increase the
Kosten, 2004). At therapeutic doses, disulfiram inhibits number of cocaine-free days for individuals in treat-
the enzyme dopamine beta hydroxylase in the patient’s ment (Heidbreder & Hagan, 2005). However, no single
body and functions indirectly as a dopamine agonist medication or combination of medications has been
(Kosten & Sofuoglu, 2004). When patients mix cocaine found to effectively treat cocaine addiction.
and disulfiram, they will experience a sense of dyspho- The medication Baclofen, originally introduced to
ria11 rather than cocaine-induced pleasure (el-Kashen, treat muscle spasms experienced by people with mul-
2001; Kampman, 2005; Leshner, 2001b; Rounsaville, tiple sclerosis, offers some promise in the treatment of
2006). While disulfiram does not eliminate the problem cocaine addiction. Baclofen interacts with the GABA
of cocaine abuse, it does appear to hold promise in the receptors in the brain and thus is able to inhibit the re-
treatment of cocaine addiction. lease of dopamine, reducing the rewarding effects of co-
There is preliminary evidence that the ß-blocker caine use.
propranolol might be of value in the treatment of severe
cocaine withdrawal (Kampman, 2005). Although its
Pharmacological Treatment
primary use is as an antihypertensive, propranolol
of Marijuana Addiction
might reduce the newly abstinent individual’s sensitiv-
ity to andrenalin and noradrenalin, thus reducing his or At this time there are no medications that specifically
treat marijuana use disorders (Sheff, Warren, Ketcham,
11See Glossary. & Eban, 2007). Behavioral therapies, combined with
pharmaceutical interventions for co-occurring disorders as high as that achieved through cigarette use, while a
such as depression, are the mainstay of treatment for piece of gum with 4 mg of nicotine brought about a
these disorders. blood level only about two-thirds that achieved through
smoking (American Psychiatric Association, 1996).
Further, nicotine-containing gum itself causes signifi-
Pharmacological Treatment cant side effects such as sore gums, excessive salivation,
of Amphetamine Abuse/Dependence nausea, anorexia, headache, and the formation of ulcers
There are no known, reliable pharmacological treat- on the gums (Lee & D’Alonzo, 1993). Beverages with a
ments for amphetamine abuse/dependence, although high acid content, such as orange juice or coffee, were
scientists are following a number of lines of research to found to block the absorption of the nicotine from the
identify such a compound (Ling, Rawson, & Shoptaw, gum, making it necessary for the user to monitor his or
2006). her beverage use to avoid such acidic compounds while
using nicotine-containing gum. At this point, nicotine-
containing gum does not appear to hold much promise
Pharmacological Treatment for helping smokers quit and remain abstinent from ciga-
of Nicotine Dependence rette use.
Nicotine replacement therapies. Because nicotine is the By 1991, several companies had introduced trans-
chemical thought to cause most, if not all, of the addic- dermal nicotine patches, designed to supply a con-
tion to smoking, one therapeutic approach has been stant blood level of nicotine to the user without the
to provide the individual with a steady blood level of need to smoke cigarettes. It was hypothesized that the
nicotine without the other 4,000 compounds found in smoker might find it easier to break the habit of smok-
cigarettes that seem to cause the undesired health con- ing if he or she did not actually have to smoke to obtain
sequences associated with smoking. In theory, after smok- a moderately high blood level of nicotine. Later (usually
ers had achieved a stable blood level of nicotine, they 2–8 weeks) after the individual no longer engaged in
could gradually be “tapered” from nicotine and be free the physical motions of smoking, the dosage levels of
of the addiction to cigarettes. nicotine in the patches would be reduced, providing a
Nicotine-containing gum was first introduced to gradual taper in blood nicotine levels.
U.S. consumers as a prescription-only medication in Since these nicotine replacement systems were de-
1984 and became available as an over-the-counter aid veloped, it has been determined that this approach is
to smoking cessation in 1996 (Anczak & Nogler, 2003). moderately effective. Ten to sixteen percent of those
The thinking was that the gum would provide a safe, who quit smoking while using transdermal nicotine
convenient nicotine replacement mechanism for smok- patches are still smoke free at the end of 6 months, as
ers who wished to quit. However, in spite of initial opposed to 6%–26% of those who used a placebo
promising results suggesting that up to 27% of patients (Okuyemi et al., 2006). The transdermal nicotine re-
who used this technique to quit smoking were still placement systems reduce some of the more trouble-
smoke free 6 months after they started treatment, gen- some side effects of cigarette cessation, such as the
eral medical practitioners believe that the 6-months insomnia many people report in the early days of absti-
abstinence rate for smokers who used the gum was no nence, but they also have serious drawbacks. First,
higher than that achieved through the use of a placebo transdermal nicotine patches do not provide the rapid
(Okuyemi, Nollen, & Ahluwalia, 2006). rise in blood nicotine levels achieved when the individ-
Smokers who use these products as an adjunct to ual smokes a cigarette. In contrast to the nearly instanta-
smoking cessation need to be trained in how to use the neous rise in blood nicotine levels from smoking a
gum, as the manner in which nicotine-containing gum cigarette, the transdermal nicotine patch requires approx-
is chewed differs from that normally used for traditional imately 1 hour for blood nicotine levels to reach their
chewing gum. With nicotine-containing gum, the indi- peak (Nelson, 2000). Another problem with transder-
vidual must adopt a “chew-park-chew-park” system mal nicotine patches is that individuals who smoke
(Fiore, Jorenby, Baker, & Kenford, 1992, p. 2691). while using the nicotine transdermal patch, or within
When the gum is used properly, about 90% of the nico- an hour of removing the patch, run the risk of nicotine
tine is released in the first 30 minutes. But the 2 mg toxicity and even possible cardiovascular problems.
form of nicotine-containing gum allows the individual Further, the nicotine blood levels achieved by transder-
to achieve a blood level of nicotine only about one-third mal patches often were lower than those achieved by
cigarette smoking, which can cause some degree of tion). This device is used in place of cigarettes, deliver-
craving for cigarettes (Henningfield, 1995).12 Also, the ing about 4 mg of nicotine to the user out of the 10 mg
transdermal patch was found to cause skin irritation in contained in the cartridge. The device is designed for
some users as well as abnormal or disturbing dreams, short-term use only, and the individual should not use
insomnia, diarrhea, and a burning sensation near where more than 16 cartridges per day, but 23% of smokers
the patch is resting on the skin. who used this system were able to remain smoke-free
The first month following smoking cessation is espe- for 6 months, as opposed to only 11% of those who used
cially difficult for the ex-smoker (Kenford et al., 1994). a placebo (Okuyemi et al., 2006).
Some smokers become dependent on the transdermal Pharmacological interventions for cigarette smoking.
nicotine patch, using it for years to abstain from ciga- The antidepressant bupropion has been found to have
rette use (Sherman, 1994). This approach makes sense a mild effect on the acetylcholine receptors, thus block-
from a harm reduction standpoint, since the potential ing some of the craving that smokers experience in the
for harm from the 4,000 compounds in cigarette smoke early stages of recovery. The exact mechanism by
are obviously much higher than the one compound, which this medication is able to achieve this result re-
nicotine, in the transdermal patch (Gitlow, 2007). mains unknown (Fogarty, 2003). Research has shown
A nicotine-containing nasal spray is available by pre- that 21%–30% of patients using this medication are
scription (Sofuloglu & Kosten, 2004). The user admin- able to abstain from cigarette use for 6 months, as op-
isters one spray in each nostril up to 40 times a day posed to only 10%–19% of those patients receiving a
(Pagliaro & Pagliaro, 1998). Within 10 minutes of placebo (Okuyemi et al., 2006). Bupropion should not
using the spray, the nicotine blood level will reach two- be used by patients with an identified seizure disorder,
thirds (Anczak & Nogler, 2003) to about the same level nor should it be mixed with alcohol (Gitlow, 2007).
(Pagliaro & Pagliaro, 1998) as achieved by smoking one Varenicline. When varenicline is used with bupro-
tobacco cigarette. It is suggested that this spray be used pion, the effects of these two medications increases the
for less than 6 months, but while there was initial con- smoker’s chances of abstaining from cigarettes in the
cern that the user might become addicted to the nico- first few weeks following smoking cessation. Varenicline
tine in the nasal spray, there is little evidence that this was introduced under the grand name of “Chantix” by
occurs (Anczak & Nogler, 2003). Pfizer Pharmaceuticals in 2006. The compound func-
Sutherland et al. (1992) found that the nasal spray uti- tions as a partial agonist at the nicotinic acetylcholine
lized in their investigation was rapidly absorbed through receptor sites in the brain, thus blocking nicotine
the nasal membranes, and that with the exception of from these receptor sites when the individual smokes
some sinus irritation, there are no serious side effects (“Chantix Prescribing Information,” 2006). When used
from this method of nicotine administration. According in combination with bupropion, the individual’s odds of
to the authors, only 2 people of the 116 in the treatment quitting smoking are approximately doubled. Maximum
group had to discontinue use of the nicotine nasal spray blood levels are achieved 3–4 hours after a single dose is
because of adverse side effects, suggesting that this ingested, and steady-state levels are achieved after 3–4
method of nicotine replacement therapy is quite safe. days of regular use (“Chantix Prescribing Information,”
Heavy smokers seemed to be the most likely to benefit 2006). Less than 20% of the compound is protein
from the use of the nasal spray (Sutherland et al., 1992). bound, and the elimination half-life of varenicline is ap-
Smokers who used the spray had less weight gain than proximately 24 hours, with 92% of the compound being
those who received a placebo nasal spray, and 31% of the eliminated unchanged in the urine (“Chantix Prescribing
smokers using nicotine-containing nasal spray remained Information,” 2006).
smoke free for 6 months as opposed to just 14% of those This medication should not be used in combination
taking a placebo (Okuyemi et al., 2006). with nicotine replacement therapies: Approximately
In 1998, McNeil Pharmaceuticals introduced a 36% of subjects who used varenicline in combination
nicotine inhalation system for use by smokers who were with nicotine replacement therapies discontinued the
trying to quit (Korberly, 1998, personal communica- use of this medication due to adverse side effects
(“Chantix Prescribing Information,” 2006). Known
12To try to eliminate this problem, the American Psychiatric Associa- side effects from this medication include nausea, ab-
tion (1996) recommended that the user try supplementary doses of
nicotine-containing gum if he or she should find that the transdermal
dominal pain, flatulence, insomnia, and in rare cases
skin patch did not provide sufficiently high levels of nicotine to block angina pectoris, arrhythmias, myocardial infarction, dry
this craving. eyes, blurred vision, and gingivitis; 30% of users reported
drug-induced nausea, anxiety, and depression. While ter acetylcholine by blocking the receptor site. This has
this medication is somewhat effective in helping people the advantage of diminishing the individual’s desire to
quit smoking, it is “not a panacea for smoking cessa- smoke cigarettes, since many of the acetylcholine re-
tion” (Klesges, Johnson, & Somes, 2006, p. 95). ceptor sites are also utilized by nicotine. This medica-
Clonidine. A number of researchers have attempted tion is moderately successful in helping the individual
to use an antihypertensive drug, clonidine, to control quit smoking cigarettes.
the craving for nicotine often reported by former ciga- Other agents. Other medications that have been uti-
rette smokers. Although the initial research studies lized in the treatment of nicotine withdrawal over the
were promising, subsequent research suggested that the years include the tricyclic antidepressants and lobeline
side effects of clonidine were so severe that it was not (a drug derived from a variety of tobacco) (Lee &
useful as an initial approach to cigarette cessation D’Alonzo, 1993) but none have proved to be extremely
(Anczak & Nogler, 2003). Scientists now believe that successful. Ultimately, the process of smoking cessation
clonidine might be most effective only in smokers who is difficult, and many smokers will have to make mul-
experience high levels of agitation when they try to quit tiple attempts before they finally discontinue the use of
smoking (Covey et al., 2000). The American Psychiatric tobacco products.
Association (1996) recommended that clonidine be Pharmacological interventions for marijuana use dis-
used only with smokers who had attempted other nico- orders. Scientists have failed to identify a single pharma-
tine replacement therapies without success. cological agent that would be helpful in the treatment
Silver acetate. When used by a cigarette smoker, silver of marijuana use disorders (Gitlow, 2007). Co-existing
acetate is a chemical that will produce a disulfiram-like medical or psychiatric disorders should be addressed
reaction (Hymowitz, Feuerman, Hollander, & Frances, with the appropriate medications in order to reduce the
1993). Chewing gum and lozenges containing silver ac- risk of relapse for the individual who engages in mari-
etate have been used in Europe for smoking cessation for juana use to self-medicate these disorders.
more than a decade, although this medication is not avail-
able in the United States. When the individual has re-
cently used the gum or lozenge and then attempts to
smoke, a “noxious metallic taste” results (Hymowitz et al.,
Summary
1993, p. 113). As the taste causes the smoker to discard The pharmacological treatment of substance abuse in-
the cigarette, this medication replaces the nicotine-based volves the use of selected chemicals to aid the recover-
pharmacological reward with an aversive experience. ing addict in his or her attempt to maintain sobriety.
Silver acetate is quite dangerous, and overuse may These agents might be classified into one of five differ-
result in permanent discoloration of the skin and body ent groups (Bailey, 2004): (a) agents that ameliorate
organs (Hymowitz et al., 1993). However, this side effect withdrawal-related distress; (b) agents that decrease the
of silver acetate is quite rare, and is usually seen only effect of a drug of abuse, thus reducing its reinforcing
after “massive overuse and abuse” (p. 113). Another effects; (c) agents that cause an aversive reaction when
drawback of silver acetate is that its effectiveness has not a drug of abuse is ingested; (d) drug agonists that pro-
been fully tested. However, preliminary research has mote abstinence from more dangerous drugs of abuse;
suggested a possible role for silver acetate lozenges and and (e) compounds used to treat comorbid medical/
gum as an aid in smoking cessation. psychiatric conditions.13 In addition, a number of ex-
Buspar (buspirone). This substance was initially perimental compounds are being examined to deter-
thought to be potentially useful in cigarette cessation mine whether they might be able to prevent the effects
programs because of its ability to conteract the agitation of various drugs of abuse possibly by activating the
and anxiety often experienced when the individual body’s immune system so that it will attack drug mole-
tried to quit smoking. However, subsequent research cules as foreign substances. However, to date, pharma-
failed to support its use unless the individual experi- cological treatment of the addictions has met with only
enced concurrent high levels of anxiety when he or she limited success.
tried to give up cigarettes (Covey et al., 2000).
Inversine (mecamylamine). Inversine is an antihyper- 13The last group of pharmaceuticals lies outside of the scope of this
tensive agent that stops the effects of the neurotransmit- book.
CHAPTER THIRTY-FOUR
Substance Abuse/Addiction
and Infectious Disease
As a group, illicit drug abusers are twice as likely as infection almost a guaranteed complication. Intra-
nonusers to require the services of a hospital emergency venous drug abusers rarely use proper sterile technique
room and seven times as likely to need hospitalization when injecting a chemical into their bodies. In a hos-
(Laine et al., 2001).1 Further, when they are hospital- pital setting, staff will sterilize the injection site with
ized, illicit drug users tend to require longer stays be- alcohol or an antiseptic solution and then inject a sterile
fore they are ready for discharge. One reason for their solution containing the pharmaceutical into the patient’s
greater need for inpatient medical treatment is the body. In contrast, intravenous drug addicts usually sim-
higher frequency of infection found among intra- ply find a vein and then insert the needle directly into
venous drug abusers. it without even attempting to wash the injection site
Infectious diseases are, collectively, one of the more with any kind of an antiseptic. In so doing, the intra-
serious medical complications of intravenous drug abuse venous drug addict will push microscopic organisms
(Mathew et al., 1995; Passaro, Hartmann, Schneider, on the surface of the skin directly into the vein, bypass-
Emrich, & Kruger, 1998). These infectious gain admis- ing the protective layers of skin that usually keep such
sion into the individual’s body in a variety of ways: by microorganisms from the blood-rich tissues inside the
being “punched through” the skin with needles in in- body.
traveneous drug use, by being inhaled when individuals Another reason that intravenous drug users are
smoke a drug of abuse, or by passive exposure in an en- prone to infections is that street drugs are often con-
vironment that predisposes the individual to infection. taminated with various microscopic pathogens. When
Some of the infections commonly found in intravenous users inject the compounds, they also inject whatever
drug addicts include peripheral cellulitis, skin ab- pathogens are in the mixture directly into their bodies
scesses, pneumonia, lung abscesses, and tetanus. In this as well. Also, intravenous drug abusers commonly share
chapter, we discuss some of the infections commonly needles. It is not uncommon for several people to use
associated with recreational chemical abuse. the same needle and syringe without stopping to steril-
ize it. This practice exposes each subsequent user of
that needle to infectious agents in the blood of previous
Why Is Infectious Disease Such a Common users (Garrett, 1994). Admittedly, some intravenous
Complication of Alcohol/Drug Abuse? drug users will try to clean the needle before use, per-
Chronic substance abuse is a prime cause of malnutri- haps by licking the needle clean before use. This will
tion, which in turn lowers the individual’s resistance to transfer microorganisms such as Neisseria sicca and
infection. Alcohol-related malnutrition or vitamin Streptococcus viridans, bacteria normally limited to the
malabsorption syndromes as well as alcohol use by itself mouth, to the intravenous needle that is about to be in-
can all compromise the effectiveness of the body’s im- serted under the user’s skin, contributing to infection
mune system (Szabo, 1997). Each of these factors con- (Dewitt & Paauw, 1996). Some IV drug abusers have
tributes to the higher rate of infectious disease seen in been known to wash the “rig”2 with water. But ordinary
alcohol abuser/addicts. tap water may also contain microorganisms that are
Sterile technique. The conditions under which in- harmless when the water is ingested but which can
travenous drug abusers inject the chemicals also make cause infection if injected into the user’s circulation
(Dewitt & Paauw, 1996).
1Theauthor would like to express his appreciation to John P. Doweiko,
M.D., for his kindness in reviewing this chapter for technical accuracy. 2See Glossary.
399
400 Chapter Thirty-Four
Among the infections that can be transmitted from development of pneumonia, including alcohol de-
one person to another through contaminated needles pendence, immune system disorders, cigarette smok-
are any of the viruses that cause hepatitis. Occasionally, ing, extreme age, vitamin malabsorption syndromes,
malaria is transmitted this way (Cherubin & Sapira, and exposure to infective agents. Alcohol/drug abuse
1993; Garrett, 1994) as well as bacterial infections such can predispose the individual to one or more forms of
as syphilis. Some of the more common forms of infec- pneumonia. Alcoholics have at least twice the rate of
tion are discussed below. bacterial pneumonia as nonalcoholics (Nace, 1987).
Endocarditis. A potentially life-threatening condi- Fungal pneumonia. Fungal pneumonia is a com-
tion that develops when bacteria infect the valves of the mon complication of HIV infection and of heroin
heart, endocarditis will be developed by approximately abuse/addiction (Karch, 1996). There are two primary
1 in every 20,000 people in the general population. reasons for this. First, chronic heroin abuse interferes
However, 1 in every 500 intravenous drug abusers will with the effectiveness of the immune system. Second,
eventually develop this disorder (Robinson, Lazo, many samples of street heroin are contaminated by
Davis, & Kufera, 2000). The chronic use of irritating fungi. When the user injects fungi-contaminated heroin,
chemicals such as those often used to adulterate illicit the fungi are able to evade the defensive barriers of the
narcotics is one cause of endocarditis (Mathew et al., skin or the respiratory tract. They are often deposited
1995). Another cause is thought to be the bacteria nor- within the lungs by the circulatory system, helping to
mally found on the skin, which are punched into the cause a fungal pneumonia.
subdermal tissues when an intravenous drug abuser Aspirative pneumonia. In addition to providing a
fails to sterilize the injection site. Finally, shared holding site for undigested food, the stomach allows
needles allow bacterial infections to be rapidly trans- bacteria essential to the digestive process access to the
mitted from one individual to another. food that has been ingested so they can begin their work
Necrotizing fascitis. An infection in which subcuta- in transforming essential nutrients into forms that can
neous tissues are attacked by bacteria normally found be absorbed by the body. By blocking the normal func-
on the surface of the skin (Karch, 1996), necrotizing tion of the upper digestive tract, especially the vomiting
fascitis is a special danger to cocaine users, but it can and gag reflexes, alcohol can cause the drinker to in-
develop in any intravenous drug abuser who fails to hale (aspirate) some of the stomach contents being
clean the skin before injection, thus pushing bacteria passed up the esophagus during the act of vomiting. As
on the skin into the blood-rich tissues of the body. As a result, bacteria normally found only in the digestive
the bacteria destroy the tissues under the skin, the in- tract are able to gain access to the respiratory tract,
fection can spread to internal organs or deeper tissues. which has few defenses specific to the bacteria found
The surface of the skin appears normal until late in the in the digestive system, and undigested food particles
course of the infection, making diagnosis difficult. This might also be aspirated into the lungs, where they
condition can be fatal. decay, fueling bacterial growth. The chronic use of al-
Skin abscesses. Abscesses of the skin are a common cohol also alters the normal pattern of bacterial
complication of intravenous drug abuse. It is thought growth in the mouth and throat. These factors, along
that adulterants mixed with heroin or cocaine can with alcohol’s ability to interfere with the normal
cause skin abscesses. Because the adulterants are usu- cough/gag reflex, combine to make it more likely that
ally not water soluble, they cause the body to react to chronic drinkers will aspirate in the process of vomit-
their presence at the injection site, which is rarely ing and expose themselves to bacteria not normally
cleaned before the drug is injected. The result of these found in the lungs, which then infect the lung tissues
factors is the formation of abscesses under the surface of (Mandell & Niederman, 1999; Marik, 2001; Saitz,
the skin, which may develop into a life-threatening in- Ghali, & Moskowitz, 1997).
fection. All of the factors reviewed in the last paragraph can
contribute to a condition known as aspiration pneu-
monia. The true incidence of aspiration pneumonia is
The Pneumonias not known, since many cases are misdiagnosed as ei-
Technically, the term pneumonia refers to an acute in- ther community-acquired or nosocomial pneumonias
fection of the lung tissue, usually caused by bacteria. (Johnson & Hirsch, 2003). When the amount of mate-
Pneumonia is generally diagnosed by x-ray examination rial is sufficient, the individual may develop hypoxemia
of the lungs. Numerous conditions contribute to the and may die if he or she is unable to reestablish adequate
Substance Abuse/Addiction and Infectious Disease 401
airflow to the respiratory tract (Johnson & Hirsch, seemed to be isolated to the homosexual male popula-
2003). Aspiration pneumonia is a serious medical con- tion. In afflicted persons, the immune system would
dition that can be caused by the abuse of alcohol or rapidly fail, leaving them vulnerable to rare opportunis-
other CNS depressants and has the potential to be fatal tic infections virtually never encountered in patients
if not treated adequately. with a normal immune system. Medical researchers
Community-acquired pneumonia. Intravenous he- termed this process the acquired immune deficiency
roin abusers, cigarette smokers, and alcohol-dependent syndrome (AIDS).
persons are all known to be at increased risk for a condi- Shortly after it was identified, physicians began to
tion known as community-acquired pneumonia (CAP) uncover cases of AIDS in some intravenous drug
(Karch, 1996).3 CAP affects an estimated 2–4 million abusers and in individuals whose only apparent risk fac-
people in the United States each year. There are 10 differ- tor was that they had received a blood transfusion in the
ent microorganisms that can cause a form of community- past. These facts suggested that AIDS was caused by
acquired pneumonia (Finch & Woodhead, 1998). While some kind of blood-borne infection, and within a short
mild cases might be treated on an outpatient basis, fully period of time researchers had isolated a virus they
20% of those individuals with CAP will eventually require named the human immunodeficiency virus (HIV)
hospitalization (Campbell, 1994; Rubins & Janoff, 1997). (McCutchan, 1990). As other members of the same
Those most likely to require hospitalization for CAP are virus family have been identified, it has become neces-
persons with cormorbid conditions in addition to the sary to identify each by a number. AIDS is now known
lung infection, a term that includes alcohol/drug abusers. to result from a viral infection with either the HIV or
Unfortunately, depending on the patient’s age and health HIV-2 viruses (Lashley, 2006).
status, approximately 45,000 people each year die of CAP What is AIDS? Technically, AIDS is not a disease in
in spite of the best possible medical care (Campbell, its own right but a constellation of symptoms, the most
1994; Finch & Woodhead, 1998; Leeper & Torres, 1995; important of which is the destruction of the individual’s
Mandell & Niederman, 1999). immune system (Welsby, 1997). AIDS is the end stage
As early as the 1890s, pneumonia was recognized as of a viral infection caused by one of the subtypes of
a significant cause of death for alcohol-dependent indi- HIV. As the HIV infection progresses, the untreated
viduals, although doctors did not know how alcohol con- patient eventually will die from an infection or neo-
tributed to the development of pneumonia (Leeper & plasm, or other condition that the immune system was
Torres, 1995). Since then, researchers have found that once able to easily control. By the start of the 21st cen-
chronic alcohol use interferes with the lung’s ability to tury, AIDS had become the fourth most common cause
defend itself against infectious microorganisms, thus con- of death around the world, with 95% of all new infec-
tributing to the possible development of CAP (Nelson, tions occurring in the developing nations (Lashley,
Mason, Kolls, & Summer, 1995). Researchers have also 2006; Markel, 2004, p. 176).
discovered that intravenous drug abuse can indirectly im- Where did HIV come from? Apparently, HIV and
pair the effectiveness of the immune system, contributing HIV-2 “jumped” between the original host species to
to the development of CAP in drug abusers. Finally, ciga- humans. When this happens, the new virus causes a far
rette smoking both reduces the effectiveness of the lung’s more serious illness in its new host (in this case hu-
defenses and causes changes within the lungs, making mans) than it did in the original animal host (David
smokers vulnerable to CAP, especially the form caused by Baltimore, quoted in Svatil, 2003). Some other examples
the bacteria H. influenzae (Finch & Woodhead, 1998; of viral infections that have jumped from animal species
Leeper & Torres, 1995; Rubins & Janoff, 1997). to humans include the West Nile Virus, hantavirus,
and Ebola (David Baltimore, quoted in Svatil, 2003).4
This is known as “a trans-species jump. The virus
Acquired Immune Deficiency changes during the course of a jump, adapting to its
Syndrome (AIDS) new host. The trans-species jump is the virus’s most im-
In 1981, medical researchers realized that a previously portant means of long-term survival. Species go extinct;
unknown disease had started to spread through the pop- 4Glasser (2004) stated that there are more than 1,400 known microor-
ulation of the United States. Initially, the disease ganisms that can infect humans, of which half initially caused dis-
eases in animals. As of this time, scientists have identified about 1%
3Asopposed to pneumonia acquired in a hospital setting, aspirative of the bacteria and 4% of the viruses on the earth, according to
pneumonia, or pneumonia secondary to some form of lung trauma. Glasser (2004).
viruses move on” (Preston, 1999, p. 54). Researchers Markel, 2004). This protein group functions as a “virus
believe that the HIV viruses originally made the jump receptor” site, a term that identifies where the virus first
to humans sometime in the 1930s, possibly when a gains entry into the cells that it ultimately infects. Un-
hunter with a cut on his hand was exposed to the blood fortunately, in the case of HIV, the receptor site is com-
of an infected animal (Cantor, 2001; Fauci, 1999; Park, monly found in the cells of the immune system,
2000). After making the jump to humans, the virus was especially the type of lymphocytes known as the CD4,
passed from individual to individual via sexual inter- or T4-helper cells (Covington, 2005; Markel, 2004).
course and blood transfusions. However, until the ad- These cells serve to “activate” the body’s immune re-
vent of modern transportation systems, HIV infection sponse. Between 93% and 99% of the HIV virus
remained isolated in remote Africa and was not a major particles in a person’s body might be found in the CD4
threat to the human population as a whole. There is cells (Pomerantz, 1998). Thus, in the infected individ-
little, if any, credible evidence that HIV was intention- ual, the greatest concentration of the virus will be hid-
ally released into the population to target homosexual ing in the very cells designed to destroy an invader such
males or other minority group members, or that it is dias HIV. Small concentrations of the virus invade other
vine retribution for past sins (Vaughn, 2006). regions of the body, such as the cells of the retina, the
How does AIDS kill? Every species of bacterium, brain, the testes, and other sites in the body providing
virus, or fungus has a characteristic pattern of protein reservoirs of virus particles that can reinfect a person
molecules in the wall of its cells. When the human whose body has been otherwise cleansed of the virus
body is invaded by a bacterium, fungus, or virus, the (Pomerantz, 1998, 2003).
immune system learns to recognize the specific pattern In the early 1980s, researchers believed that the
of proteins that make up the cell wall of the invader and virus passed through a period of “latency,” in which
attack those with foreign protein patterns. The first time there was little viral activity (Weiner, 1997). However, it
the body is exposed to a new organism, the body must is now known that the virus begins to replicate almost
rely on more generalized disease-fighting cells, which immediately after it gains admission to the human
are known as lymphocytes. These generalists roam body. The apparent latency period was actually an illu-
through the body, seeking out and attacking micro- sion caused by the fact that the earliest blood tests to de-
scopic invaders with a foreign protein pattern in the cell termine whether a person was infected were designed
wall. These generalist cells are the ones that mount the to detect the lymphocytes manufactured by the body in
initial attack against a new invader, while the body an attempt to fight off the virus. Since a given person’s
learns to produce disease-specific antibodies. Unfortu- body might need 9 months to begin to manufacture
nately, the process of producing the disease-specific lymphocytes specific to the AIDS virus, there were
cells necessary to fight off a new invader may take none of these lymphocytes to show up in a blood test,
hours, days, weeks, or in some cases, years. and scientists were left with the impression that the
After it has been exposed to a virus, fungus, or species virus was latent (Markel, 2004). But after the develop-
of bacterium, the body “tailor makes” some immune ment of special HIV viral load tests, scientists discov-
cells (antibodies) for each different form of microorgan- ered what was really occurring (Henry, Stiffman, &
ism that it encounters. These pathogen-specific anti- Feldman, 1997).
bodies are designed to recognize the individual protein Each time the HIV virus replicates in a person’s
pattern on the surface of each species of bacterium, body, it produces slightly different copies of itself. The
fungus or virus, and drift in the individual’s blood specific mechanism is quite technical and well beyond
searching for just one specific species of invader. This is the scope of a text such as this. However, in brief, HIV
the mechanism through which a person who once had tends to be “sloppy” during replication, allowing subtle
an infection becomes “immune” to that disease. After “mistakes” to slip into the genetic code of each new
recovering from the infection, the individual will have generation of virus particles. These new “daughter”
a number of white blood cells from the previous expo- virus particles are called mutations or variants (Forstein,
sure to the invader in reserve, patiently waiting until 2002). These HIV variations are eventually released
the next time the same microorganism might try to en- back into the general circulation. Because of the altered
ter his or her body. He or she is now “immune” to that genetic code of each new generation of HIV, the body
disease. responds to them as if they were new viral invaders
In the body, HIV is able to infect cells with the CD4 (Nowak & McMichael, 1995; Terwilliger, 1995). As a
protein group in the cell wall (Covington, 2005; result of this process, by the later stages of HIV infection
a single individual might have as many as 1 billion differ- 1:2 million chance of contracting an HIV infection
ent forms of the HIV virus in his or her body (Richardson, (Goodnough, Brecher, Kanter, & AuBuchon, 1999).
1995). Further, research suggests that up to 10 billion In the United States, approximately 70% of new
new virus particles will be produced each day in an in- cases of HIV infection occur in men (Work Group on
fected person’s body (Henry et al., 1997; Saag, 1997). HIV/AIDS, 2000). The avenue by which the individual
Toward the end of the infectious process, the individual’s becomes infected varies between men and women. For
body is host to and ultimately overwhelmed by a “swarm” men, 60% who contract HIV do so as a result of homo-
of viruses (Barre-Sinoussi, 1996, p. 32; Beardsley, 1994; sexual activity, 25% through sharing contaminated in-
Terwilliger, 1995). travenous needles, and 15% as a result of heterosexual
As the immune system becomes weaker, various op- activity (Lashley, 2006; Vaughn, 2006). In the United
portunistic infections caused by microorganisms that States, approximately 6% of previously uninfected homo-
were once easily controlled by the immune system sexual males contract HIV each year (Garrett, 2000). In
begin to develop. When the person develops AIDS, the contrast to this, 75% of the women who contract HIV
body’s weakened defenses are overwhelmed by these in- do so as a result of heterosexual activity with an infected
vading microbes and eventually the patient dies. partner, while 25% become infected because of intra-
The chain of HIV infection. In spite of its reputation, venous drug abuse involving the sharing of needles
HIV is actually a fragile virus that is not easily transmit- (Work Group on HIV/AIDS, 2000). Unfortunately, it
ted from one person to another (Langone, 1989). The has been estimated that up to 25% of those individuals
most common methods of HIV transmission are (a) sex- infected with HIV are not aware of this fact, which con-
ual contact (homosexual or heterosexual) with an in- tributes to the transmission of the virus through unsafe
fected partner, (b) exposure to HIV-infected blood by sex and sharing of needles.
direct inoculation (sharing needles, blood transfusion Research into the genetics of HIV has revealed that
from an infected donor, organ transplantation from an there are three basic families of HIV: the “M” (“Main”)
infected donor, etc.), and (c) transmission of the virus group, the “O” (“Outlier”) and the “N” (“New”).
from an infected mother to the infant during the birth Although there are no known subtypes of the “O” or the
process or breast-feeding (Lashley, 2006). “N” forms of HIV, there are 10 known subtypes of the
Sax (2003) estimated the odds of contracting HIV in- “M” form of HIV, identified by the letters A–H, J, and K
fection after sharing a contaminated needle with an (Kuiken, Thakallapalli, Eskild, & de Ronde, 2000).
HIV-infected person one time as 1:150. In contrast to Different substrains of HIV are found in different re-
this, the odds of contracting HIV infection after a single gions of the world, suggesting that the virus has been
episode of unprotected vaginal intercourse were esti- moving in waves as infected individuals have carried
mated at 1:500 to 1:1,250 (Sax, 2003). The odds of con- one strain of the virus or another to different part of the
tracting HIV infection after a single episode of receptive globe. At this time, the B is the most common strain of
anal intercourse with an infected male were estimated HIV in the United States, Europe, South America, and
at 1:300 to 1:1,000 (Sax, 2003). As these statistics Australia (Kuiken et al., 2000). The E subtype, which is
demonstrate, the most common means of HIV transmis- found mainly in Asia and Africa, is more easily passed
sion in the United States is the sharing of intravenous from an infected male to his female partner. This is the
needles. But there is a great deal of variation in terms of reason heterosexual transmission of HIV is the most
how HIV is transmitted both around the world and even common means by which the virus is passed on from
within different countries, with heterosexual and homo- one person to another in Asia and Africa. But the B sub-
sexual activities being the most common method of type of the HIV virus is not able to easily pass into the
HIV transmission in Africa and Asia (Steinbrook, 2004). mucous membranes of the woman, thus making het-
A rare method of HIV transmission is known as “ver- erosexual transmission of the B subtype more difficult
tical transmission,” in which an infected woman passes (Anderson, 1993).
the virus on to the fetus. Another rare method of HIV The scope of the problem. According to the United
transmission is through the use of contaminated blood Nations6 the number of people around the world estima-
products for blood transfusion. At this point, it is esti- ted to be infected with HIV is approximately 39.1 million
mated that the typical patient receiving a blood transfu- (Lashley, 2006). An estimated 4.1 million people a year
sion consisting of one unit of blood5 has an estimated are infected with the virus worldwide, while an estimated
5Usually 6
1,000 cubic centimeters, or just under one pint of blood. The only agency that tracks HIV infection on a worldwide basis.
3.1 million die from HIV infection annually (“Get Over Rich, 2001; Work Group on HIV/AIDS, 2000).
It,” 2006). Approximately 1.1% of all people around the While the individual’s body has not yet started to
world between 15 and 49 years of age are infected with a produce an immune response specific to HIV dur-
virus that 30 years ago was unknown to medical science. ing this state, the virus itself is actively replicating
Another 15,000 people are infected with HIV each day throughout the body and the individual can pass the
globally (Markel, 2004; Schmitt & Stuckey, 2004). By infection on to others during this stage.
the year 2012 it is possible that as many as 150 million 3. Seroconversion: Occurring within 6 months of the date
people will be infected with HIV globally (Forstein, of infection, this stage is the point when the individ-
2002), a number that might increase to 500 million ual’s body has started to mount an immune response
people by the year 2020 unless effective, inexpensive to the HIV virus and when HIV-specific antibodies
treatments are found before then (Garrett, 2000). can be detected in the individual’s blood. Such indi-
The continent of Africa has been especially hard hit; viduals are said to be seropositive or HIV-positive.
an estimated 28 million people there are currently in- Seronegative individuals are those whose blood test re-
fected with HIV and 20 million people have died from sults failed to detect evidence of HIV-specific antibod-
AIDS (Will, 2002). The rate of infection varies from ies. There are two possible explanations for a negative
country to country, but in some regions of Africa, 80% test result: (a) the individual in question has never
of the adults between 20 and 49 years of age are thought been exposed to the HIV, or (b) he or she has been ex-
to be infected with HIV (Bowers, 2000). In the United posed to the virus but it is still too early for the tests to
States, between 900,000 and 1 million people have detect the virus in the person’s blood. In either case,
been infected with HIV, of whom about 25% do not the individual should be tested again at a later date,
know that they are infected (Kenny, 2004). The num- usually 3 months after the initial blood test or last high-
ber of people infected with HIV in the United States in- risk behavior to rule out the second possibility.7
creases by an estimated 44,000 people each year If HIV-specific antibodies are detected in the
(Steinbrook, 2004). Unfortunately, HIV infection in patient’s blood through blood tests such as the
the United States is most often a disease of youth, with enzyme-linked immunosorbent assay (ELISA), con-
approximately half of those who contract the infection firmation through such blood tests as the Western
each year in the United States being under the age of blot test should be carried out (Kenny, 2004). The
25 (Khalsa, 2006). Western blot assay screens for three specific protein
The stages of HIV infection. Sax (2003) identified six markers indicative of HIV infection. Once the person
stages of HIV infection in humans: (1) viral transmission, is known to be infected, the more detailed viral load
(2) acute HIV infection, (3) seroconversion, (4) asympto- test can be performed; this test measures the approxi-
matic HIV infection, (5) symptomatic HIV infection, mate number of HIV virus particles per cubic milli-
and (6) acquired immune deficiency syndrome (AIDS). liter of the individual’s blood and is used to assess the
patient’s status once HIV infection has been diag-
1. Viral transmission: The point at which a previously nosed (Henry et al., 1997; Mylonakis et al., 2001).
noninfected individual becomes infected with the 4. Asymptomatic infection: Individuals in this stage
virus (see “Chain of HIV Infection,” above). might remain stable for many years, and the HIV
2. Acute HIV infection: Within 1–4 weeks 50%–90% of infection would be detectable only through the use
newly infected individuals develop a mild, flu-like of the appropriate blood tests. However, even though
syndrome that might be dismissed by the individual the individual is asymptomatic, he or she might pass
as inconsequential. Because the initial symptoms the infection on to other persons through needle
are so vague and nonspecific, HIV infection is often sharing or unprotected sex.
misdiagnosed at this stage (Khan & Walker, 1998; 5. Symptomatic HIV infection: In this stage, the victim’s
Yu & Daar, 2000). If the physician is suspicious, he immune system has been weakened to the point that
or she might order a viral load test that might detect opportunistic infections begin to develop. These are
the presence of HIV in the patient’s blood a few infections rarely seen except in patients whose im-
days after infection, although in most cases it takes mune system has been compromised in some manner.
2–6 weeks before such blood tests can detect HIV 7Itshould be noted that screening tests to detect exposure to HIV are
(Sax, 2003; Yu & Daar, 2000). The current viral load not perfect. Kleinman et al. (1998) found a false positive rate of 1 in
test procedures can detect as few as 20 virus particles every 379,000 samples of blood tested at one of five blood banks. An
in a cubic milliliter of blood (Mylonakis, Paliou, & initial positive screen should be verified through further testing.
TABLE 34.1 Antiviral Agents Currently Used to Treat HIV-1 Infection
Class of antiviral agent Mechanism of action
Nucleoside/nucleotide analogs Compounds act as DNA chain termination agents, inhibiting the
transcription of viral RNA into DNA in cells infected with HIV-1, thus
inhibiting viral replication.
Nonnucleoside reverse transcriptase inhibitors Chemicals that bind to and inhibit the actions of the enzyme reverse
transcriptase, which is essential for viral replication.
Protease inhibitors Chemicals that block the action of a protein known as viral protease, which is
necessary for viral replication.
Fusion inhibitors Chemicals that block the protein complex on the host cell that HIV-1 grabs
onto to bind to the cell wall. This is the first step by which HIV-1 then invades
the cell, forcing the cell to make copies of itself to go out and invade other
cells.
DNA: deoxyribonucleic acid; genetic code that governs development of cell, found in the nucleus of the cell.
RNA: ribonucleic acid; messenger molecule that carries instructions from cell nucleus to outer regions of the cell.
Such disorders include “thrush” infections, cervical The natural history of HIV infection. Untreated, it
dysplasia/carcinomas, constant low-grade fevers, unusually will take 9–11 years before HIV infection is able
explained weight loss, the development of peripheral to progress to AIDS in the patient (Steinbrook, 2004).8
neuropathy, and many others (Sax, 2003). Blood tests About 10% of those infected are thought to be “rapid
for the HIV antibody are positive, and viral load tests progressors” who develop AIDS within about 5 years of
show large numbers of virus particles per cubic milli- infection, while a similar proportion of those infected
liter of blood. do not seem to progress to the stage of AIDS (Hogan &
6. AIDS: Normally, there are between 1,000–1,200 Hammer, 2001; Sax, 2003). Without effective antiviral
CD4+ T cells for every cubic milliliter of blood treatment, HIV infection is “chronic and usually fatal”
(Khalsa, 2006; Lisanti & Zwolski, 1997). These cells (Sax, 2003, p. 227).
help the body fight off infections caused by micro- The treatment of HIV infection. Since HIV was first
scopic organisms. When the number of CD4+ T identified as the virus that causes AIDS, a number of an-
cells falls below 200 per cubic milliliter (mm3) of tiviral drugs have been developed to help fight the infec-
blood, the individual becomes vulnerable to one or tion. These antiviral agents have changed the clinical
more opportunistic infections, such as Pneumocystis picture of HIV infection in the United States from an au-
carinii pneumonia (or P. carinii, or PCP) as well as tomatic death sentence to a chronic condition, such as
various tumors, and bacterial and fungal infections. diabetes or heart disease (Kuhl, 2002). Unfortunately,
One bacterial infection that is commonly encoun- the high cost of providing effective treatment for HIV in-
tered in the HIV-positive patient is tuberculosis, fection limits the accessibility to treatment (Craig, 2004).
which is 100 times more common in individuals in- Currently, four classes of antiviral agents are used to
fected with HIV than in the general population fight HIV: nucleoside/nucleotide analogs, the protease
(Bartlett, 1999). Thus, if a physician were to en- inhibitors, the nonnucleoside reverse transcriptase in-
counter a patient who had recently developed tuber- hibitors, and the fusion inhibitors (Clavel & Hance, 2004;
culosis, he or she would automatically consider the Godwin, 2004). The method by which each class of drug
possibility that the patient had AIDS. interferes with viral replication is quite complex, but a
The median survival time is 1 year when the brief summary of the different classes of antiviral agents
CD4+ T cell count falls below 50 cells per cubic mil- and their mechanism of action appears in Table 34.1.
liliter, although some individuals have been known
to survive as long as 3 years with a CD4+ T cell 8
This estimate, however, assumes that the individual has been in-
count this low (Sax, 2003). Death usually occurs fected just once with HIV, as there is evidence suggesting that subse-
from one or more opportunistic infections easily quent exposure to the virus might accelerate the progression of the
controlled by an intact immune system. disorder (Smith et al., 2004).
Following the introduction of the protease in- copies of the HIV virus in the body of an infected per-
hibitors, AIDS-related deaths dropped from 29.4 per son. To further complicate matters, the virus can hide
100 patient-years9 in 1995 to just 8.8 per 100 patient- in the body for up to 10 years after antiviral treatment
years in 1997 (Palella et al., 1998). While these figures has been initiated (J. Doweiko, 2004, personal commu-
are impressive, it still means that almost 9 of every 100 nication). Scientists have no idea how to elimate every
individuals infected die of AIDS each year in spite of virus particle from the body of a living person, and the
the most aggressive treatment with the most advanced cost of antiviral therapy is so great that many infected
medications available. persons cannot afford the medications currently avail-
Unfortunately, HIV is adept at finding ways to resist able without government assistance. Given these facts,
the effects of these antiviral compounds, and as many as it is clear that the ultimate treatment for AIDS at this
80% of those being treated for HIV have a virus strain time is prevention.
that has become resistant to at least one antiviral com- AIDS and suicide. There is a great deal of controversy
pound they are taking (Coughlan, 2006b). The current about whether those who are infected with HIV are or
treatment methodology calls for the patient to take a are not prone to suicide. Research does suggest that indi-
complex mixture of two, three, or possibly even all four viduals who have been infected with the virus are be-
varieties of antiviral medications simultaneously, since tween 7 and 36 times as likely to end their own lives as
it is unlikely that the different strains of HIV are resist- are uninfected persons of the same age (Kalichman,
ant to all of the antiviral medications at once (Clavel & Heckman, Kochman, Sikkema, & Bergholte, 2000; Roy,
Hance, 2004). While these antiviral agents slow the 2003; Treisman, Angelino, & Hutton, 2001). The period
progression of HIV, they do not prevent the ultimate of greatest risk appears to be right after the individual
progression to AIDS (Garrett, 2000). learns that he or she is infected with HIV (Kalichman
A new class of antiviral agents that is currently under et al., 2000; Treisman et al., 2001). However, suicide risk
development is called maturation inhibitors (Coghlan, must be assessed on a case-by-case basis, as there are nu-
2006b). The maturation inhibitors interfere with the merous factors that can contribute to or inhibit a person’s
formation of a protein shell that normally surrounds desire to end his or her life.
and protects the RNA in the core of the virus, thus pre- AIDS and Kaposi’s sarcoma. When AIDS was first
venting the virus RNA from replicating to infect other identified in the early 1980s, physicians thought that a
cells. This new class of antiviral agents is still under de- rare form of cancer known as Kaposi’s sarcoma, was a
velopment and is not expected to reach the general manifestation of AIDS. This misunderstanding arose
market until 2009 at the earliest (Coghlan, 2006b). because 40% of people who had AIDS in 1981 also de-
While the antiviral agents in the current generation veloped Kaposi’s sarcoma and because doctors still had
are able to significantly slow the progression of HIV in- not isolated the cause of AIDS itself (Antman & Chang,
fection, thus far there has not been one proven cure of 2000). However, by the early 1990s researchers had
an HIV infection (Schmitt & Stuckey, 2004). The virus identified both the cause of AIDS and Kaposi’s sarcoma.
is known to persist in areas of the body not reached by Whereas AIDS was found to result from infection with
the current generation of antiviral agents, making erad- HIV-1, Kaposi’s sarcoma was caused by a member of the
ication of the virus in the individual’s body virtually herpes virus family known as the Kaposi’s sarcoma-asso-
impossible (Hayes, 2005). Further, the high cost of ciated herpesvirus (KSHV, or human herpesvirus 8)
treating HIV with the current generation of antiviral (Antman & Chang, 2000).
agents is a financial burden beyond the reach of most As researchers have come to better understand
patients in the developing world. Finally, the side ef- KSHV, they realized that Kaposi’s sarcoma was usually
fects of the current antiviral medications may be quite found in patients whose immune systems were compro-
debilitating, making it difficult for many patients who mised by HIV infection, had been deliberately sup-
can afford these medications to continue taking them pressed by physicians following organ transplant
(Farber, 2000). procedures (Antman & Chang, 2000), or had been ex-
Scientists remain hopeful that they can eventually posed to radiation (Miles, 1996). The virus was also
develop a treatment that will completely arrest the profound to be endemic in certain regions of Africa
gression of HIV, but to accomplish this goal, it will be (Antman & Chang, 2000) and is the most common
necessary to destroy every one of the estimated 1 trillion AIDS-related cancer in the United States. But it is a
separate disorder from HIV (Antman & Chang, 2000;
9See Glossary. Miles, 1996).
Tuberculosis ward sign that an individual is infected with HIV might

be when he or she develops TB (Karlen, 1995). It is for
Tuberculosis (TB) has been with us for a long time. this reason that alcohol/drug rehabilitation counselors
Between 1600 and 1900 TB is thought to have caused need to be aware of the relationship between substance
one in every five deaths in Europe and an unknown misuse and tuberculosis infections.
number of deaths in other parts of the world (MacKenzie, What is tuberculosis? Tuberculosis (TB) is an in-
2007). Even now, in the first decade of the 21st century, fectious disease, caused by the bacterium Mycobac-
TB is the most common cause of death from infectious terium tuberculosis (Markel, 2004). With the advent of
disease on the planet (Markel, 2004; Simon, 2007). effective antibiotic treatments for TB in the mid-20th
Globally, 2.4 billion people are thought to be in- century, public health officials and physicians in the
fected with this disease, with an additional 8.8 million United States became complacent, and treatment ef-
new cases, and 2 million deaths, occurring each year forts were scaled back or eliminated entirely. The late
(Schurr, 2007). In the United States, TB infection rates 1980s and 1990s saw a resurgence of new cases in this
began to decline around 1900, as physicians and public country, although the vast majority of these were later
health workers began to learn how to limit its spread determined to be reactivation of formerly latent infec-
and to treat those who were afflicted. The introduction tions rather than new infections (Markel, 2004). Several
of effective antibiotic treatments in the mid-20th cen- factors contributed to the return of TB, but the most
tury brought it to virtual extinction in the United States important of these was treatment noncompliance
(Simon, 2007). However, around 1984, U.S. public (Markel, 2004).
health officials were stunned to detect an increasing The lifestyle of the typical alcohol/drug abuser often
number of cases of TB in this country, in part because makes treatment compliance for TB very difficult.
of the phenomenon of homelessness and HIV-1 infec- Treatment noncompliance and professional noncha-
tion. More disturbing, new strains of TB emerged that lance plus the rise of AIDS all contributed to the emer-
were resistant to the traditional antibiotic treatments gence of the antibiotic-resistant strains of TB that began
(Simon, 2007). to be identified in the early 1990s. Fully 90% of antibi-
Tuberculosis is not just a bacterial infection of the otic-resistant TB infections occur in people whose im-
lungs. This infection requires certain environmental mune systems are compromised by HIV infection
factors such as intensity of exposure, poor health, mal- (Savitch, 1998; Telenti & Iseman, 2000). Such drug-
nutrition, and genetic predisposition to the disease be- resistant strains of TB can be fatal in 80%–90% of cases.
fore it can develop (Schurr, 2007).10 The more of these How does TB kill? TB most often invades the pul-
predisposing factors an individual has, the greater are monary system, although it can infect virtually every
the odds that he or she will develop TB.11 There is also organ system in the body. The bacteria seem to prefer
preliminary evidence that either dietary or metabolic oxygen-rich body tissues such as those found in the
conditions that limit the body’s absorption of vitamin D lungs, the central nervous system, and the kidneys
places the individual at increased risk for contracting (Markel, 2004). If the infection becomes established in
tuberculosis (Wilkinson et al., 2000). Since individuals the lungs, then whenever the infected person sings,
who abuse drugs/alcohol on a chronic basis tend to also talks, coughs, or sneezes, he or she will release micro-
be malnourished, the vitamin D hypothesis might help scopic droplets of moisture from the lungs that will re-
to explain why this subgroup of people tends to be at risk main suspended in the air for extended periods of time.
for TB infection. So strong is the relationship between These droplets can harbor Mycobacterium tuberculosis
chronic alcohol use and TB that Cunha (1998) recom- cells and carry the bacteria into the surrounding air
mended that the attending physician specifically rule out where another person can breathe them in and become
tuberculosis in alcohol-abusing patients who present infected (Markel, 2004).
with symptoms of pneumonia. Once the Mycobacterium tuberculosis cells gain ad-
Individuals whose immune systems are compro- mission into the victim’s body, his or her immune system
mised by infection, such as HIV, are also at high risk for begins to mount a counterattack against the invading
contracting TB (Garrett, 1994). Indeed, the first out- virus. The immune system’s initial response begins when
10Which is also true for the addictions, is it not? the macrophages engulf the invading bacteria, surround
11For example, if a person who has the genetic predisposition to TB them, and wall them inside little pockets known as granu-
infection is also malnourished but never exposed to TB, he or she lomas. This then prevents the infection from proceeding
would never acquire the infection. further. However, Mycobacterium tuberculosis is difficult
for the body to destroy, and the bacteria might continue to tract a virus that attacked the liver. This virus was iden-
survive in a dormant stage within the granulomas for tified as the hepatitis type A (HVA) virus.
years or decades. An estimated 200,000 new cases of HVA infection
If the individual’s immune system becomes weak- emerge each year in the United States (Shute, Licking, &
ened by conditions such as another infection, disease, or Schultz, 1998). Although the usual route of transmis-
malnutrition, the body loses its ability to isolate the TB sion is food or water that has become contaminated with
bacteria in the granulomas. Eventually, the TB bacteria fecal matter from a person infected with HVA, on occa-
might burst out and again invade the surrounding body sion HVA is passed between intravenous drug abusers.
tissue. This is known as reactivation TB, which accounts Although physicians have long been aware of HVA,
for virtually all new cases of TB in the United States they also knew that some patients who had received
(Markel, 2004). It is at this point that the body tries a dif- blood transfusions developed symptoms of liver disease
ferent approach to the invading bacteria. Another part of other than HVA. These patients were said to have de-
the immune system, the lymphocytes, attempt to destroy veloped serum hepatitis. In 1966, a virus later classified
the bacteria that cause TB. Unfortunately, during this as hepatitis type B (HVB) was identified (Lee, 1997).
process they release a toxin that destroys surrounding Unfortunately, scientists soon realized that the virus
lung tissue. Eventually, as less and less of the lung is that causes HVB was responsible for only 28% (Bondes-
able to properly function, the patient dies of pulmonary son & Saperston, 1996) to 43% (Vail, 1997) of all new
failure. cases of viral hepatitis in the United States (Hoffnagle &
The treatment of TB. Although a great deal has been Di Bisceglie, 1997). There was evidence of at least one
written about treatment-resistant TB in the past few years, other virus capable of causing hepatitis, which for many
physicians still have a wide range of medications they can years was classified simply as Non A–Non B hepatitis. In
call on to treat this infection. Unfortunately, these treat- 1988,13 Non A–Non B hepatitis was identified as result-
ment regimens can take as long as 12–24 months, with ing from an infection by one of five previously unidenti-
the patient being expected to take the proper medica- fied viral agents, which have since been classified as
tions as often as 3–4 times a day (Cohen, 2004; Markel, hepatitis virus type C (HVC), type D (HVD), type E
2004). Even this intensity of treatment is not always effec- (HVE), type F (HVF), and type G (HVG) (Sjogren,
tive, and with the best of medical care TB remains poten- 1996). Surprisingly, there is genetic evidence to suggest
tially fatal to those who are infected. While there are new that HVG is a distant cousin of HVC.
drugs under development that might cut the length of Relationship between viral hepatitis and intravenous
treatment down to just a single week-long course of an- drug abuse. Although exposure to food or water that was
tibiotics, these treatments are still years away from clinical contaminated with fecal material is the most common
use (Cohen, 2004). route of HVA infection, HVA might also be passed from
one person to another by sharing intravenous needles.
It is estimated that 40%–70% of intravenous drug
Viral Hepatitis abusers will contract HVA at some point in their drug-
There are at least seven different viruses that can infect abuse careers (Sorensen, Masson, & Perlman, 2002).
the liver. Each form of viral infection results in inflam- However, because the body usually overcomes HVA in-
mation of the liver, a condition known as hepatitis.12 fection without serious complications, this infection is
Physicians often refer to each different virus simply not discussed in detail.
by a letter, such as hepatitis A, B, and so on. At least The most common route of transmission for the
four different forms of viral hepatitis are known to affect other forms of viral hepatisis discussed here is by con-
alcohol/drug users. In this section these disorders are taminated intravenous needles shared by injection
discussed. drug abusers. Each IV drug abuser leaves a small
A brief orientation to viral hepatitis. Physicians have amount of fluid in the needle that he or she used. If an-
long known that if a person is exposed to water or food other person uses that same needle, he or she is exposed
contaminated by fecal matter he or she might become to whatever bacteria or viral agents were in the previous
ill. In the 20th century, researchers discovered that in user’s blood (Becherer, 1995; Vail, 1997). However, IV
addition to the various strains of bacteria that might be drug abusers rarely worry about possible exposure to
contracted in this manner it was possible to also con-
13
Pearlman (2004) stated that the virus that causes HVC was first iso-
12
See Glossary. lated in 1989, not 1988.
blood-borne infections in their haste to use the first in the United States (1.8% of the population) are be-
available needle to inject their drugs. In some commu- lieved to be infected with HVC (Karsan, Rojter, &
nities, 60%–90% of IV drug abusers contract HVB Saab, 2004; Patel & McHutchison, 2003), with approxi-
and/or HVC (Krambeer, von McKnelly, Gabrielli, & mately 30,000 new cases occurring each year (Dieperink,
Penick, 2001; Pearlman, 2004; Sorensen et al., 2002). Willenbring, & Ho, 2000).
In the late 1990s, a theory was advanced that snorting Prevalence of HVD and HVE. Fortunately, these
cocaine might be one way that people contracted HVC. viruses are rarely found in the United States (Shute et al.,
However, it is now thought that unreported intravenous 1998). There are an estimated 15 million people in-
cocaine use was the most likely reason that those who re- fected with HVD in the world, of whom 70,000 live in
ported that they snorted cocaine actually contracted this the United States (Najm, 1997). Each year in the United
viral infection (Willenbring, 2004). About 78% of new States an estimated 5,000 new cases of HVD are identi-
intravenous drug abusers will probably contract HVC fied (Karsan et al., 2004).
within a year, 83% within 5 years, and 94% after 10 years Routes of transmission for HVB. HVB is extremely
if they share needles (Parini, 2003). Sharing intravenous contagious, possibly 100 times as contagious as HIV.
needles has been estimated to raise the individual’s risk of Physicians have identified cases of individuals contract-
contracting HVC 150-fold (15,000%) (Dienstag, 2006). ing HVB by sharing a toothbrush or a razor, or even sim-
Prevalence of HVB. The virus that causes HVB is a ply by kissing an infected person (Brody, 1991). HVB
member of the Hepadnaviridae family of viruses, which may also be transmitted through blood transfusions—
show a preference for infecting liver cells (Ganem & and this has resulted in the development of new blood
Prince, 2004). Globally, 5% of the world’s population, tests to screen out blood donors who might carry the
or about 350 million (Lee, 1997) to 400–500 million virus. In the early 1970s, the rate of infection with the
people (Bondesson & Saperston, 1996), are thought to hepatitis B virus was 1 per 100 units of blood transfused
be infected with HVB. In the United States an esti- in the United States (Edelson, 1993). However new
mated 12.5 million people have been exposed to HVB blood tests for screening potential blood donors (and
(Krain, Wisnivesky, Garland, & McGinn, 2004). There ways of storing blood prior to use) have reduced the rate
are six known subforms of HVB at this time. It is not of transfusion-related HVB infection in the United States
known whether all of these subforms, or genotypes, carry to about 1 in 250,000 units of blood (Goodnough et al.,
the same potential for liver damage, or if some geno- 1999).
types are less likely to cause HVB-induced liver disease Intravenous drug abuse is a common method of
than others (Russo, 2004). HVB transmission in the United States. Research has
Prevalence of HVC. HVC was first isolated in 1988 shown that 75%–98% of intravenous drug abusers have
(Kirchner, 1999). Since it was first isolated, researchers been exposed to HVB in the United States (Michelson,
have discovered that up to 300 million people around Carroll, McLane, & Robin, 1988). However HVB in-
the globe are infected with this virus, a number five fection is also transmitted through sexual contact, and
times as large as the number of people infected with in the United States sexual transmission of HVB infec-
HIV (Hines, 2002; Woods & Herrera, 2002). There are tion is the most common cause of new cases (Russo,
six known subtypes of HVC (Bonkovsky & Mehta, 2004). Thus, like HIV, HVB is now classified both as a
2001; Karch, 2002; Parini, 2003; Seymour, 1997). But blood-borne and as a sexually transmitted disease (STD).
the prevalence of HVC infection varies from region to Routes of transmission for HVC: The Centers for
region around the globe. Between 9% and 14.6% of Disease Control estimate that 15% of those individuals
the population in north Africa has been exposed to infected with HVC in the United States contracted the
HVC, while elsewhere the percentage of the popula- infection through unprotected sex (Davies, 2005). Sixty
tion that is infected with HVC is much lower percent are thought to have become infected by sharing
(Dieperink, Willenbring, & Ho, 2000). intravenous needles, while 10% contracted the virus
In the United States, HVC has become the most through a blood transfusion conducted before wide-
common chronic blood-borne infection, and it is the spread testing of blood donations for HVC began in
most common cause for liver transplant surgery, a trend 1990 (Davies, 2005). Since the advent of these blood
that is likely to increase as more of those infected in the tests, the risk of contracting HVC from a blood transfu-
1970s and 1980s begin to develop long-term conse- sion has virtually disappeared (Dienstag, 2006).
quences of HVC infection (Grinnell & Adamec, 2006; In the United States, the most common method by
Pearlman, 2004; Willenbring, 2004). Four million people which a patient contracts HVC infection is through
contaminated intravenous needles (Pearlman, 2004). infections develop cirrhosis (Ganem & Prince, 2004),
Approximately 80% of intravenous drug addicts who and each year in the United States between 3,500 (Lee,
share needles will be exposed to HVC within a year of 1997) and 5,000 (Karlen, 1995) people die as a result of
their first injection (Miller & Brady, 2004). HVC is HVB-induced cirrhosis. However, hepatitis B may kill
found in almost every body fluid, although it is not in another way. For unknown reasons, the person who
thought to be active in bile acids and the stool, and it is has been infected with the hepatitis B virus is 10 to 390
most concentrated on the blood (Woods & Herrera, times more likely than a noninfected person to develop
2002). Because both HVC and HIV are transmitted liver cancer (Ganem & Prince, 2004; Gordon, 2000).
through contaminated intravenous needles, at least Liver cancer is quite difficult to detect or treat and is
33% of patients with HIV are also infected with HVC usually fatal. Each year, an estimated 1,200 cases of
(Parini, 2003). Other possible routes of HVC transmis- HVB-related liver cancer are identified in the United
sion include contaminated needles used in tattooing, States (Karlen, 1995).
an organ transplant from a donor infected with HVC, What are the consequences of HVC infection? In up to
and hemodialysis (Di Bisceglie & Bacon, 1999; Hager & 80% of the cases, people who are infected with HVC do
Reibstein, 1998; Sharara, Hunt, & Hamilton, 1996). not experience any significant symptoms of viral infec-
Routes of transmission for HVD. HVD is a blood- tion until years, possibly decades, after infection. These
borne virus that requires some of the enzymes pro- people will carry the virus in their bodies, but they will
duced by the HVB virus to replicate (Russo, 2004). For not feel sick until possibly 20 or 30 years after being in-
this reason HVD is sometimes referred to as being infected. By that time, the virus may have so damaged the
complete or defective (Sjogren, 1996, p. 948). By itself, individual’s liver that he or she will die without a liver
HVD is unable to replicate, and if the patient has not transplant (Davies, 2005). HVC-induced liver disease is
been exposed to HVB, HVD cannot infect the individ- thought to kill between 8,000 (Davies, 2005) and 12,000
ual. Researchers have discovered that 20%–80% of intra- (Coghlan, 2004; Parini, 2003; Schiff & Ozden, 2003)
venous drug abusers (Vail, 1997) and 10% of individuals people each year in the United States alone.
with chronic HVB infection also test positive for exposure Approximately 20% of people who become infected
to HVD (Di Bisceglie, 1995). will be able to fight off the infection, usually in the first
Routes of transmission for HVE. Although HVE 6 months after exposure to the virus (Davies, 2005;
might be transmitted by exposure to body fluids, the Dieperink et al., 2000; Hines, 2002; Lieber, 2001;
most common method of transmission is exposure to Woods & Herrera, 2002). But only a blood test will re-
water contaminated by humans who were infected veal whether the individual was able to fight off the in-
(Shute et al., 1998). fection since HVC is a silent killer that does not cause
What are the consequences of HVB infection? HVB any outward sign of infection until quite late in the dis-
infection is the most common cause of liver disease on ease process. It used to be thought that in 20%–25% of
the face of the earth (Vail, 1997). The vast majority of people infected with HVC, the body would be able to
HVB infections in normal, healthy adults are self-limited contain the infection and fight it to a standstill. Now it
and the immune system is able to eventually eliminate appears that the infectious process just proceeds more
the virus from the body (Ganem & Prince, 2004). slowly in these individuals, and that the infection will
However, in about 5%–10% of the cases the individual progress at markedly different rates for different people
develops a chronic HVB infection (Ganem & Prince, (Parini, 2003). In about 20% of HVC infection the virus
2004; Hines, 2002; Russo, 2004). causes progressive liver damage, cirrhosis, end-stage
Each year in the United States approximately 5,000 liver disease, cancer of the liver, or various combina-
people die as a result of HVB infection (Coghlan, tions of these conditions, usually after 20–40 years
2004). HVB can kill through a variety of mechanisms. (Patel & McHutchison, 2003). If a person with HVC
About 40% of individuals infected with HVB will expe- infection should also be a chronic alcohol user, the de-
rience HVB-induced liver problems, and a significant struction of the liver is significantly accelerated (Karsan
percentage will die (Purow & Jacobson, 2003). Although et al., 2004; Lieber, 2001; Parini, 2003; Schiff & Ozden,
it was once thought that the virus caused significant 2003; Willenbring, 2004). Chen, Yoon, Yi, and Lucas
damage to the liver, mounting evidence suggests that in (2007) found, for example, that a woman who had HVC
chronic HVB infection it is the body’s reaction to the and was a heavy drinker died approximately 10 years ear-
infection that causes damage to the liver (Ganem & lier than a nondrinking woman of the same age who also
Prince, 2004). About 20% of people with chronic HVB had HVC infection.
What are the consequences of HVD infection? Early ribavirin.14 This combination of drugs is effective in
evidence suggests that the combination of HVB and 50%–60% of the patients treated (Davies, 2005; Patel &
HBD infections results in a more severe syndrome than McHutchison, 2003). Patients’ adherence to the thera-
with HVB alone (Karsan et al., 2004). Approximately peutic program is a strong indicator of their response to
60%–70% of people infected with HVD will develop treatment, so they must be encouraged to complete the
cirrhosis of the liver, usually in 2 to 15 years after being full course of treatments in spite of such side effects
infected (Najm, 1997). such as fever, chills, headache, anxiety, and problems
What are the consequences of HVE infection? Scientists concentrating in the hours and days after the medica-
are still exploring the impact of HVE infection on the in- tions are injected.
dividual. The virus can cause loss of appitite, nausea, and The treatment of HVD. Preliminary evidence suggests
vomiting as a result of liver inflammation, as well as fever, that since co-infection with HVB is necessary for HVD
fatigue, and abdominal pain (Shute et al., 1998). Up to infection to develop, immunization against HVB will pro-
20% of pregnant women who contract HVE will die as a vide protection against HVD (Vail, 1997). Immunization
result of the infection (Gorbach, Mensa, & Gatell, 1997). against HVB blocks the chain of infection, preventing
The treatment of HVB. The most effective “treat- HVD co-infection if an individual should be exposed to
ment” for HVB is prevention. A vaccine against HVB this virus (Najm, 1997).
was developed in the early 1980s and it is recom- The treatment of HVE, HVF, and HVG. Very little is
mended that individuals who are likely to be exposed to know about how these viral infections might be treated.
the body fluids of an infected individual be vaccinated Like HVB, the most effective “treatment” for these viral
against possible HVB infection (Vail, 1997). In some infections is prevention by avoiding exposure to body
states, vaccination against HVB is required before a fluids of other individuals who are known or suspected
child is admitted to public school (Vail, 1997). Others to have a form of viral hepatitis.
who should be immunized against HVB include health
care workers, the spouse of an individual who is in-
fected, and children/adolescents.
Summary
There has been an ongoing search for effective phar- It is impossible to identify in advance every potential in-
macological treatments for HVB infection in the past fectious disease that substance abusers are exposed to as a
20 years, and this research is starting to produce results. result of their chemical use. In this chapter, a few of the
Interferon has been shown to suppress HVB viral replica- more common forms of infection that might arise as a re-
tion, and in many cases there has been no evidence of viral sult of alcohol/drug abuse have been reviewed. Although
activity for up to 8 years afterward (Purow & Jacobson, this chapter is not intended to serve as a guide for the
2003). Another medication, lamivudine, has been ap- treatment of these infections, it is important that sub-
proved by the Food and Drug Administration (FDA) stance abuse rehabilitation professionals understand
for the treatment of both HIV and HVB infections. In some of the risk factors associated with such infectious
September 2002 the FDA also approved adefovir to diseases found in alcohol- and drug-abusing individuals
treat HVB infection. To date, there have been no identi- as the hepatitis family of viral infections, HIV, and tuber-
fied resistant mutations of the HVB virus to this medica- culosis (TB), both to better understand the needs of their
tion, making it an important adjunct to the treatment of patients and to protect themselves from exposure as a re-
chronic HVB infection (Purow & Jacobson, 2003). sult of their work with infected patients.
The treatment of HVC. The current treatment for
HVC infection is a combination of interferon and 14A nucleoside analog compound that is taken orally.
CHAPTER THIRTY-FIVE
Self-Help Groups
The Twelve Steps Alcoholics Anonymous (AA)2 is the “most frequently con-
of Alcoholics Anonymous1 sulted source of help for drinking problems” (Miller &
McCrady, 1993, p. 3). Approximately 1 in every 10
Step One: We admitted that we were powerless over adults in the United States has attended an AA meeting
alcohol—that our lives had become unmanageable. at least once (Miller & McCrady, 1993; Tonigan &
Step Two: Came to believe that a Power greater than Toscova, 1998; Zweben, 1995). This is not to say that all
ourselves could restore us to sanity. of these people had alcohol use problems of their own,
Step Three: Made a decision to turn our will and our however. Perhaps two-thirds of those who have attended
lives over to the care of God as we understood Him. at least one AA meeting have done so out of a concern for
Step Four: Made a searching and fearless moral in- another person’s drinking (Zweben, 1995). However,
ventory of ourselves. this still means that one-third of those who have attended
Step Five: Admitted to God, to ourselves, and to an- AA, or 3.1% of the adults in the United States, have done
other human being the exact nature of our wrongs. so because they thought they might have an alcohol use
problem (Godlaski, Leukefeld, & Cloud, 1997).
Step Six: Were entirely ready to have God remove all
In spite of its popularity, however, AA is perhaps the
these defects of character.
least rigorously studied element in the spectrum of re-
Step Seven: Humbly asked Him to remove our habilitation programs (Meza & Kranzler, 1996). Even
shortcomings. though the organization has existed for over 60 years,
Step Eight: Made a list of all persons we had harmed, “the empirical research on the efficacy of Alcoholics
and became willing to make amends to them all. Anonymous is sparse and inconclusive” (Watson et al.,
Step Nine: Made direct amends to such people wher- 1997, p. 209). AA remains something of a mystery not
ever possible, except when to do so would injure them only to nonmembers but all too often even to active
or others. members, a fact that makes AA or similar self-help groups
Step Ten: Continued to take personal inventory and rather controversial. Supporters claim that AA is the
when we were wrong, promptly admitted it. most effective means of treating alcoholism. Critics of
Step Eleven: Sought through prayer and meditation AA, or similar programs, challenge this claim. In this
to improve our conscious contact with God as we un- chapter, the self-help group phenomenon patterned after
derstood Him, praying only for knowledge of His will the Alcoholics Anonymous program is examined.
for us, and the power to carry that out.
Step Twelve: Having had a spiritual awakening as The History of Alcoholics Anonymous
the result of these steps, we tried to carry this message
One of the diverse forces that were to blend together to
to alcoholics, and to practice these principles in all
form Alcoholics Anonymous (AA) was the American
our affairs.
temperance movement of the late 1800s (Peele, 1989).
The AA program was also strongly influenced by a non-
1Reprinted by permission of Alcoholics Anonymous World Services, denominational religious group known as the Oxford
Inc. Permission to reprint this material does not mean that AA has re- Group, popular in the 1930s (Bufe, 1998; Nace, 2005a),
viewed or approved the contents of this publication, nor that AA
agrees with the views expressed herein. AA is a program of recovery
from alcoholism—use of the Twelve Steps in connection with pro- 2The Web site for AA is www.alcoholics-anonymous.org. Every effort
grams and activities that are patterned after AA, but which address has been made to ensure that Internet Web site addresses are correct
other problems, does not imply otherwise. as of the time of publication.
412
Self-Help Groups 413
and the psychoanalysis of an American alcoholic by Carl 2. Education, not psychotherapy, is the primary goal of
Jung in the year 1931 (Edmeades, 1987). The Oxford AA membership.
Group was especially influential, imparting to the AA 3. Self-help groups are self-governing.
program a strong belief in free will and personal respon- 4. The group places emphasis on accepting responsibil-
sibility (Committee on Adddictions of the Group for ity for one’s behavior.
the Advancement of Psychiatry, 2002). 5. There is but a single purpose to the group.
Historically, AA was thought to have been founded 6. Membership is voluntary.
on June 10, 1935, the day an alcoholic physician had 7. The individual member must make a commitment to
his last drink (Nace, 2005a). Following a meeting personal change.
between the surgeon, Dr. Robert Holbrook Smith, and 8. The group places emphasis on anonymity and
a stockbroker, William Griffith Wilson, the foundation confidentiality.
of AA was set down. William “Bill” Wilson was strug-
gling to protect his newfound sobriety while on a
George Vaillant (2000) identified four factors that
business trip in a strange city. After making several tele-
were common to recovery programs from substance
phone calls to try to find support in his struggle, Wilson
use disorders: (a) compulsory supervision, (b) introduc-
was asked to talk to Dr. Smith, who was drinking at the
tion of and use of competing behavior to replace the
time Wilson called.
chemical use pattern, (c) new love relationships, and
Rather than looking out for his own needs, Wilson
(d) increased spirituality and religiosity. Many of these
choose a different approach. He carried a message of so-
elements are contained in the list of helpful elements
briety to another alcoholic, Dr. Smith. The self-help phi-
of AA advanced by Rootes and Aanes (1992).
losophy of AA was born from this moment. In the half-
Most researchers acknowledge the core characteris-
century since then, it has grown to a fellowship of 97,000
tics of AA as very much a product of society in the
“clubs” or AA groups that includes chapters in 150 coun-
United States in the late 1930s, especially the Oxford
tries, with a total membership estimated at more than
Group movement (Bufe, 1998). Americans have always
2 million persons (Humphreys, 1997; Nace, 2005a).
had a strong belief in the power of public confession,
During its early years, AA struggled to find a method
contrition, and salvation through spirituality, all ele-
that would support its members in their struggle to
ments in the AA program. Further, as the Twelve Steps
achieve and maintain sobriety. Within 3 years of its
and Twelve Traditions (1981) acknowledged, the early
founding, three different AA groups were in existence,
members of AA also freely borrowed from medicine and
but even with three groups, “it was hard to find two score
religion to establish a program that worked for them.
of sure recoveries” (Twelve Steps and Twelve Traditions,
The program that emerged is the famous “12 Steps” of
1981, p. 17). But the fledgling group continued to grow
AA, which form the core of the recovery program that
slowly until by the fourth year following its inception
AA offers.
there were about 100 members in isolated AA groups
A breakdown of the 12 Steps. The core of the recov-
(Nace, 2005b). In spite of this rather limited beginning,
ery program for AA is the 12 Steps, which are suggested
the early members decided to write of their struggle to
not as the only way to recovery, but as a way that might
achieve sobriety in order to share their discoveries with
work for the individual (Beazley, 1998). The 12 Steps
others. The book that was published as a result of this
fall into three groups. The first three steps are viewed as
process was the first edition of the book Alcoholics
necessary for the acceptance of one’s limitations.
Anonymous in 1939. The organization took its name
Through these steps, the individual is able to come to
from the title of this book, which has since come to be
accept that his or her own resources are insufficient for
known as the “Big Book” of AA (Twelve Steps and Twelve
dealing with the problems of life, especially his or her
Traditions, 1981).
addiction to alcohol. In the final step of this first group
the individual is called upon to make a profound
choice: to surrender and turn his or her life over to God
Elements of AA (Cole & Pargament, 1999).
Several factors help to shape an effective self-help Steps Four through Nine are a series of change-
group (Rootes & Aanes, 1992): oriented activities. These steps are designed to help the
individual identify, confront, and ultimately overcome
1. Members have shared experience, in this case their character shortcomings that were so much a part of his
inability to control their drug or alcohol use. or her addicted lifestyle. Through these steps, members
414 Chapter Thirty-Five
may work through the guilt associated with past behav- person. At the same time, if the individual is still
iors and learn to recognize the limits of personal re- “shaky,” he or she is encouraged to work with another
sponsibility. These steps allow them to learn the tools of member. Emphasis during this phase of recovery is on
non–alcohol-centered living, something which at first acceptance of responsibility and the resolution of the
is often alien to both alcohol-dependent people and anger and resentments upon which addiction is so
their families. often established. Finally, after the first year of recovery,
Finally, Steps Ten through Twelve challenge the in- the rehabilitation process has reached what Brown
dividual to continue to build on the foundation estab- (1985) termed “ongoing sobriety.” Alibrandi (1978)
lished in Steps Four through Nine. The person is asked identified the goal during this phase of recovery as the
to continue to search out personal shortcomings and to maintenance of a “spiritual condition.” The person is
confront them. He or she also is challenged to continue warned not to dwell on the shortcomings of others, to
the spiritual growth initiated during the earlier steps suspend judgment of self and others, and to beware of
and to carry the message of hope to others. the false pride that could bring him or her back to
In a sense, AA functions as a form of psychotherapy chemical use again.
that aids personal growth (Alibrandi, 1978; Peck, 1993; Although the AA program is designed to aid spiritual
Tobin, 1992), or a series of successive approximations growth, this process is not rapid. The process of correct-
toward a better way of life (McCrady & Delaney, 1995). ing the spiritual defects upon which alcoholism rests
The guiding philosophy behind AA is that while the in- takes many years. Beazley (1998), for example, suggested
dividual’s resources are inadequate for controlling his that the member must be actively involved in AA for at
or her addiction to alcohol, through a lifelong commit- least 5 years, before the process of spiritual growth might
ment to the group he or she is able to achieve some proceed. But once this process of spiritual renewal is
measure of control over the incurable disease of addic- initiated “there is no going back. You develop a knowl-
tion (Davison, Pennebaker, & Dickerson, 2000). As a edge that is so powerful that you will wonder how you
self-help growth program, the AA program has five dif- could have lived any other way. The awakened life begins
ferent phases (Alibrandi, 1978). The first stage starts on to own you, and then you simply know within that you
the first day of membership in AA and lasts for the next are on the right path” (Dyer, 1989, p. 17).
week. During this phase, the individual’s goal is simply Whether the the 12 Steps are effective, or why they
to stay away from his or her first drink (or episode of are effective, is often disputed. But within the AA com-
chemical use). munity, there are those who believe that the 12 Steps
The second phase of recovery starts at the end of the offer a program within which personality transformation
first week and lasts until the end of the second month of might be accomplished (DiClemente, 1993). Surpris-
AA membership (Alibrandi, 1978). Major steps during ingly, the steps are not required for AA membership. But
this part of the recovery process include the recovering they are viewed within AA as a proven method of behav-
addict’s acceptance of the disease concept of addiction ioral change that offers the individual a chance to re-
and willingness to accept help with his or her addiction. build his or her life. There are many who believe that
During this phase, the individual struggles to replace these steps were instrumental in saving their lives.
old drug-centered behavioral habits with new, sobriety-
oriented habits. The third stage of recovery spans the
AA and Religion
interval from the second through to the sixth month of
recovery, according to Alibrandi (1978). During this The discussion of spiritual matters in the United States
stage, the individual is to use the Twelve Steps as a is frequently complicated because the words faith, reli-
guide and try to let go of old ideas. Guilt feelings about gion, and spirituality are mistakenly used interchange-
past chemical use are to be replaced with gratitude for ably. But there are very real differences between them.
sobriety, wherever possible, and the member is to stand Religion is an organized set of beliefs that are encoded
available for service to other individuals who are ad- in certain texts (considered sacred by believers) and are
dicted to alcohol. viewed as providing some of the answers to life’s ques-
The fourth stage begins around the sixth month of tions for those who belong to that community of believ-
recovery and lasts until the end of the first year of absti- ers (Ameling & Povilonis, 2001). Through religious
nence (Alibrandi, 1978). During this stage, members belief the individual’s search for meaning is raised to
are encouraged to take a searching and fearless moral the level of the community of believers, where spiritual-
inventory of themselves and to share this with another ity is a reflection of the individual’s search for answers.
There is a strong positive relationship between spiri- forming the foundation for the addiction. In turning his
tuality and abstinence, with those individuals who have or her will over to a higher power, the individual comes
the strongest spiritual beliefs being least likely to abuse to accept that his or her own will is not enough to main-
alcohol (Nace, 2003). The difference between spiritu- tain recovery, and that the disease has affected his or
ality and religion was best summarized by McDargh her perception of reality. The individual learns how his
(2000), who observed that “religion is for those who are or her resentments from the past contribute to the spiri-
afraid of going to hell . . . spirituality is for those who tual sickness that is so essential to alcoholism and how
have already been there [as a result of their substance to resolve or renounce these resentments.
use problems].” Within this context, it is possible to To further the process of spiritual growth, the individ-
view the alcohol-dependent person as having a “higher ual is encouraged to carry out a daily self-examination
power”: alcohol. In effect, addicts have placed alcohol similar to that of the Examen or Conscious Examen pro-
(or drugs) in the role of being their “god” (Ringwald, posed by Ignatius as one of the rules of the Jesuit order.
2002). Twelve-step programs seek to help them switch This is done by members in order to better understand
from their addiction to a more benign higher power the will of their higher power and how it applies to their
(Wallace, 2003). It is through this process that AA pres- lives. In a similar manner, AA offers a spiritual program
ents itself as being a program for spiritual growth, but not that ties the individual’s will in to that of a “higher
as a religious movement (Berenson, 1987; McGowan, power,” without offering a specific religious dogma that
1998; Vaillant, 2000; Wallace, 2003). might offend members.
To better understand the distinction between spiritu-
ality and belief, it is helpful to view religion as the form
and spirituality as the content of belief (McGowan,
One “A” Is for Anonymous
1998). To counter the addiction, the newcomer is asked Anonymity is central to the AA program (Alcoholics
to “let go,” something that he or she might find impos- Anonymous World Services, 1981). This is one major
sible to understand. But “having faith is not a question reason most meetings are “closed.” There are three
of clinging to a particular set of beliefs, a particular set types of closed meetings. In the first, where there is a
of . . . practices or psychotherapeutic techniques. designated speaker, one individual will talk at length
Having faith . . . requires that we let go of what we are about his or her life and substance use, and how he or
clinging to” (Rosenbaum, 1999, p. xii). In order to re- she came to join AA and benefit from the program
cover, the individual is required by AA to be receptive to (Nowinski, 2003). In the second form of a closed AA
the possibility that there is more than “self” and to stop meeting, the “discussion” meeting, a theme or prob-
clinging to unhealthy doubts, resentments, demands, lem of interest to the members of the AA group is iden-
and eventually, alcohol. An example of this process is tified, and each member of the group is offered the
Step Three of the AA 12-Step program. This step chance to talk about how this problem affects him or
“doesn’t demand an immediate conversion experi- her. Finally, in the last type of closed meeting, the
ence . . . but . . . does call for a decision” (Jensen, “Step” meeting, the group will focus on one of the
1987b, p. 22) for alcohol-dependent individuals to make 12 Steps for a month at a time, with each member being
a conscious decision to turn their will over to their God. offered the chance to talk about his or her understand-
The emphasis on spiritual growth in the AA program ing of the step and how he or she attempts to put that
rests on the dual assumptions that (a) each individual step into practice in his or her recovery program. Closed
seems to desire a relationship with the infinite (higher meetings are limited to members of AA only. In con-
power), and (b) it is the individual’s distorted percep- trast to the closed meeting, there are also open AA
tion of “self” as the center of the universe rather than meetings. In the open meeting, which any interested
his or her higher power that helps to make him or her person can attend, one or two volunteers will speak, and
vulnerable to alcoholism (McCrady, 1994; McDargh, visitors are encouraged to ask questions about AA and
2000; Ringwald, 2002). how it works.
Note that the third step of the AA program does not Anonymity is a central concept of AA. It is for this rea-
name God or His “true” religion. It “simply assumes that son that many AA members believe that court-ordered
there is a God to understand and that we each have a or employer-mandated attendance at AA runs counter
God of our own understanding” (Jensen, 1987b, p. 23). to the central philosophy of anonymity: In order to verify
In this manner, AA sidesteps the question of religion his or her attendance, the individual must ask a member
while still addressing the spiritual disease that it views as of AA to break anonymity to confirm that the person
indeed did attend the meetings he or she was ordered to The Primary Purpose of AA
attend. The AA program places emphasis on anonymity
to protect the identities of members and to ensure that The primary purpose of AA is twofold. First, the mem-
no identified spokesperson emerges who claims to speak bers of AA strive to “carry the message to the addict who
for AA (Alcoholics Anonymous World Services, 1981). still suffers” (The Group, 1976, p. 1). Second, AA seeks
Through this policy, the members of AA strive for hu- to provide for its members a program for living. This is
mility, each knowing that he or she is equal to the other done not by preaching to the alcohol- or drug-addicted
members. The concept of anonymity is so important individual but by presenting a simple, truthful, realistic
that it is said to serve “as the spiritual foundation of the picture of the disease of addiction. The alcohol- or drug-
Fellowship” (Alcoholics Anonymous World Services, addicted person is confronted in language that he or she
1981, p. 5) of AA. can understand. The manner in which this confronta-
The concept of equality of the members underlies tion is carried out is somewhat different from the usual
the AA tradition that no directors are nominated or voted methods of confrontation. In AA, speakers share their
on. Rather, service boards or special committees are cre- own life stories, a public confession of sorts in which
ated from the membership as needed. These boards each individual tells of the lies, the distortions, the self-
always remain responsible to the group as a whole and deceptions, and the denial that supported his or her own
must answer to the entire AA group. As noted in Tradi- chemical use. In so doing, the speaker hopes to break
tion Two of AA: “our leaders are but trusted servants; through the defensiveness of the alcohol-addicted per-
they do not govern” (Twelve Steps and Twelve Traditions, son by showing that others have walked the same road
1981, p. 10). Because of this emphasis on equality, the and yet found a way to recovery.
structure of AA has evolved as one where the “interper- Helping others is a central theme of AA, in part
sonal conflicts and the petty jealousy, greed or self- because
importance that could create havoc among fellowship
members” (DiClemente, 1993, p. 85) is minimized, if even the newest of newcomers finds undreamed re-
not almost totally avoided. wards as he tries to help his brother alcoholic, the
one who is even blinder than he. . . . And then he
discovers that by the divine paradox of this kind of
AA and Outside Organizations giving he has found his own reward, whether his
Each Alcoholics Anonymous group is both self- brother has yet received anything or not. (Twelve
supporting and not-for-profit. Individual groups are au- Steps and Twelve Traditions, 1981, p. 109)
tonomous and must support themselves only through
the contributions of the members. Further, each indi- In this, one finds a therapeutic paradox (not the only
vidual member is prohibited from contributing more one!) in AA, for the speaker seeks first of all to help him-
than $1,000 per year to AA. Outside donations are dis- self or herself through the public admission of power-
couraged to avoid the problem of having to decide how lessness over chemicals. This is not to say that the
to deal with these gifts. Outside commitments are also individual is helpless but only that he or she is powerless
discouraged for AA groups. As stated in the text Twelve over the addiction (Wallace, 2003). Through the public
Steps and Twelve Traditions (1981), AA groups will not admission of weakness, the speaker seeks to gain strength
“endorse, finance, or lend the AA name to any related from the group. It is almost as if by owning the reality of
facility or outside enterprise, lest problems of money, his or her own addiction, the speaker says, “This is what
property and prestige divert us from our primary pur- my life was like, and by having shared it with you, I am
pose” (p. 11). reminded again of the reason I will not to return to
The relationship among different autonomous AA alcohol again.”
groups and between different AA groups and other This is the method pioneered by Bill Wilson in his
organizations are governed by the Twelve Traditions of first meeting with Bob Smith. In that meeting, Bill
AA. The Traditions are a set of guidelines or framework Wilson spoke at length of his own addiction to alcohol,
within which different groups may interact, and through of the pain and suffering he had caused others and that
which AA may work as a whole. They are not reviewed he had suffered in the service of his addiction. He did
in this chapter; however, interested readers might wish not preach but simply shared with Dr. Smith the history
to read The Twelve Steps and Twelve Traditions (1981) of his own alcoholism. Bill Wilson concluded with the
to learn more about the Traditions. statement: “So thanks a lot for hearing me out. I know
now that I’m not going to take a drink, and I’m grateful to do now that you are here,” as one member said to a
to you” (Kurtz, 1979, p. 29). newcomer. Neither is the member admonished for
Earlier, it was noted that the methods of AA present being unable to live without chemicals. Members of
a paradox in that it is by helping others that the speaker AA know from bitter experience that relapse is possible
comes to receive help for his or her own addiction to al- and common (McCrady & Irvine, 1989). Chemical ad-
cohol/drugs. At the same time, he or she confronts the diction is assumed in membership: “If chemicals were
defenses of the new member by saying, in effect, “I am not a problem for you, you would not be here!” In place
a mirror image of you, and just as you cannot look into of the chemical-centered lifestyle, the new member is
a mirror without seeing your own image, you cannot offered a step-by-step program for living that allows one
look at me without seeing a part of yourself.” Paradoxi- to achieve and maintain recovery.
cally, the helper benefits from giving this message as To take advantage of this program, the member need
much as the recipient (Zemore, Kaskutas, & Ammon, only accept the program. Admittedly, in doing so the in-
2004). dividual is asked to accept yet another therapeutic para-
As mentioned above, Alcoholics Anonymous is a dox, known as Step One. The first step, which is the only
spiritual program that is at the same time not religious. one that specifically mentions alcohol by name, asks that
Within the AA program, alcoholism is viewed as a “spir- the individual accept that he or she is powerless over this
itual illness, and drinking as a symptom of that illness. chemical. The individual is asked to do so not on the
The central spiritual ‘defect’ of alcoholics is described most superficial of levels necessary to speak the words “I
as an excessive preoccupation with self. . . . Treatment am powerless over chemicals,” but on the deepest level
of the preoccupation with self is at the core of AA’s ap- of his or her being. In so doing, the individual is forced
proach” (McCrady & Irvine, 1989, p. 153). Within this to accept a measure of humility and to cast doubt on his
framework, compulsive alcohol use is viewed as the dia- or her ability to face life alone (Norris, 1998). This is a
metric opposite of spiritual growth (Martin & Booth, difficult step. The individual must learn that he or she is
1999). Thus, by engaging in activities that enhance not God, a lesson that must be learned over and over
spiritual growth such as a 12-Step program like AA, the again (Yancey, 2000). The essence of the First Step is the
individual turns away from the temptation of alcohol acceptance in the deepest level of the individual’s soul
use (McCrady, 1994; Miller & Hester, 1995). that he or she is addicted to and totally powerless over
Proponents of 12-Step groups note that in alco- alcohol.
holism the individual lives a self-centered lifestyle. To At first, the newcomer might view alcohol as the
combat this excessive preoccupation with self, AA offers problem. But at some point he or she will be forced to
the 12 Steps as a guide for spiritual growth and for living. accept that “it is we ourselves, not the pills or alcohol,
But the individual is not required to follow the 12 Steps who cause most of our problems. Chemicals will not
to participate in AA. Rather, “the program does not issue bring destruction upon a person until that person learns
orders; it merely suggests Twelve Steps to recovery” how to justify continual use and abuse of those chemi-
(Jensen, 1987a, p. 15, italics in original). Thus, the indi- cals” (Springborn, 1987, p. 8). In other words, the indi-
vidual is offered a choice between the way of life that vidual is helped to see that while he or she is not
preceded AA or acceptance of a program that others have responsible for having the bio/psycho/spiritual/genetic
used to begin their journey toward recovery. But the indi- predisposition for alcoholism, he or she is responsible
vidual does not passively accept the 12 Steps. Rather, for working toward his or her recovery (Wallace, 2003).
the emphasis is on using the 12-Step program that the Hitting bottom. The process of “hitting bottom” has
person has joined, a process that requires active partici- been challenged by some theorists but remains a cen-
pation at meetings, not just passive attendance, and an tral component of the AA program. When people reach
intentional application of the lessons learned from the the point that they learn how completely alcohol/drugs
12-Step work to the individual’s problems in living have come to dominate their lives they are said to have
(Nowinski, 2003). “hit bottom.” At that moment, they accept the painful,
The 12 Steps offer the promise and the tools neces- bitter, frightening reality that their lives have been
sary for daily abstinence. One of these tools is that the spent in the service of the addiction. They recognize
member of AA is not encouraged to look for the “cause” that nothing they might do will allow them to control
of his or her addiction to alcohol. Rather, the individ- the chemical, for they are addicted to it. This is a mo-
ual’s alcoholism is accepted as a given fact. “It is not so ment of extreme despair, when the addicted person
much how you came to this place, as what you are going might turn to another, and say: “I need help.” It is at this
point that the individual becomes receptive to the pos- (Alibrandi, 1978; McCrady & Irvine, 1989). Each new
sibility of living without the chemicals. AA member is expected to have daily contact with his or
her sponsor either by telephone or in person, at least at
first (Nowinski, 2003). In spite of frequent communica-
Of AA and Recovery tions between the new member and the sponsor, the re-
Alcoholics Anonymous does not speak of a “cure” for the sponsibility for recovery remains with the individual. In a
disease of alcoholism. Rarely do members of AA speak of sense, the sponsor says to the client: “I can be concerned
themselves as having recovered, for the process of recov- for you, but I am not responsible for you.” In today’s
ery is viewed as a lifelong process of growth (Wallace, terminology, the sponsor is a living example of what
2003). This growth process is perhaps best seen in the might be called “tough love.” In a sense, the sponsor’s
lapse of several months that often occurs between the role is similar to that of a skilled folk psychotherapist
time a new member begins to attend AA and when he or (Peck, 1993).
she stops drinking. Research has shown that a new mem- Sponsors should be the same sex as the new AA mem-
ber might attend AA for 20 months before even admit- bers they are sponsoring; a sponsor should be aware of his
ting to being a member of AA, and 8 more months before or her own limitations and not try to be a “superman”
he or she stops drinking (Zweben, 1995). During this who does everything (McCrady & Delaney, 1995;
2-year period, the individual is taking the first steps of a Nowinski, 2003). The sponsor should also possess many
lifelong process of growth. of the characteristics of the healthy human services pro-
Alcoholics Anonymous also does not speak of itself as fessional identified by Rogers (1961).
an ultimate “cure” for alcoholism because it views the re- In a very real sense, the sponsor, acting as an exten-
covering person as being only a moment away from the sion of AA, is a tool, but it is up to the newcomer to
next “slip.” The 25-year veteran may, in a weak moment, grasp and use this tool to achieve sobriety. There are no
relapse and begin to drink again. Simple affiliation with guarantees, and the sponsor often struggles with many
AA does not guarantee abstinence from alcohol/drugs of the same issues that face the newcomer. The new-
(McCrady & Irvine, 1989). Each member faces a per- comer must assume the responsibility for reaching out
sonal struggle to abstain from alcohol/drugs, a struggle and using the tools that are offered. Sponsorship is, in
that members are advised to face “one day at a time.” If essence, an expression of the second mission of AA which
“today” is too long a period to think about, the individual is to “carry the message” to other addicts who are still
is encouraged to think about abstaining for the next actively using chemicals. This is a reflection of Step
hour, or the next minute, or just the next second. Twelve, and one will often hear the sponsor speak of
Once the addicted person accepts the program, he having participated in a Twelfth Step visit, or of having
or she finds a way of living that provides support for been involved in Twelfth Step work. The sponsor is a
recovery 24 hours a day, for the rest of his or her life guide, friend, peer-counselor, fellow traveler, con-
(DiClemente, 1993). In accepting the program, the science, and devil’s advocate all rolled into one.
addicted person may discover a second chance that he
or she thought was forever lost.
AA and Psychological Theory
The AA program does not provide motivation for
Sponsorship change. It provides a program for change, through a
To help members on the spiritual odyssey that will form of folk psychology (Peck, 1993). But the AA/NA
hopefully result in their sobriety, new members of AA 12-Step programs are different from other therapeutic
are encouraged to find a “sponsor.” Indeed, the sponsor programs that the addicted person might have been ex-
is seen as a key element to the AA program (McCrady & posed to in the past, in the sense that the steps are “re-
Delaney, 1995; Nace, 2005). The sponsor is a person ports of action taken rather than rules not to be broken”
who has worked his or her way through the step program (Alibrandi, 1978, p. 166). Each step is a public (or private)
and has achieved a basic understanding of his or her demonstration of action taken in the struggle to achieve
own addiction. The sponsor acts as a spiritual (but not a and maintain sobriety rather than a rule that might be
religious) guide, offering confrontation, insight, and sup- broken.
port in equal amounts to the new member. Brown (1985) speaks of the AA steps as serving another
It is the duty of the sponsor to take an interest in the purpose as well. For Brown (1985), the 12 Steps serve
newcomer’s progress, but not to take responsibility for it to keep recovering members focused on the addiction.
For just as the alcohol was an axis around which these time when he or she feels that there is nobody to turn to
individuals centered their lives while drinking, through (Bean-Bayog, 1993; Nace, 2005b).
the 12 Steps they continue to center their lives around Herman (1988) observed that 12-Step programs such
alcohol in a different way: a way without chemicals. as AA offer at least one more feature to the recovering ad-
During the period of active chemical use these individu- dict: predictability. Consistency was one of the character-
als learned to center their lives around their drugs of istics identified by Rogers (1961) as being of value in the
choice (Brown, 1985). To avoid the danger of being de- helping relationship, and one must wonder if the pre-
ceived, they need to learn a new way to openly relate to dictability of AA is not one of the curative forces of this
their addiction. But the addicts must learn to do so in a self-help group. However, this remains only a hypothesis.
way that allows them to achieve and maintain sobriety. The AA 12-Step program provides a format for “a
According to Brown (1985), the 12 Steps accomplish this planned spontaneous remission” (Berenson, 1987, p. 29)
by providing a structured program by which members that is “designed so that a person can stop drinking by
continue to relate to their addiction while still being either education, therapeutic change, or transformation”
able to draw on the group for support and strength. (p. 30). As part of the therapeutic transformation inher-
ent in AA participation, Berenson (1987) speculated that
people would “bond to the group and use it as a social
How Does AA Work? support and as a refuge to explore and release their sup-
One of the tenets on which AA rests is the belief that alco- pressed and repressed feelings” (p. 30). Most certainly,
hol dependence is a spiritual disorder. “What was once these things are possible in the typical AA meeting,
called ‘idolatry,’ enlightened Westerners call addictions” which is “generally characterized by warmth, openness,
(Yancey, 2003, p. 33). Within this context, the “idolater honesty, and humor” (Nace, 1987, p. 242)—attributes
chooses things that may be good in themselves and grant that may promote personal growth. AA is thought to be
to them a power they were never meant to have” (p. 33). “the treatment of choice” (Berenson, 1987, p. 27) for ac-
Eventually, however, the object of the idolatry—in this tive alcoholics, although Brodsky (1993) challenged this
case alcohol—takes control of the individual’s life. claim. Brodsky’s challenge to the AA 12-Step recovery
Although AA has been a social force in the United model is discussed later in this chapter.
States for three-quarters of a century, there has been sur-
prisingly little research into what elements of the 12-Step
Outcome Studies: The Effectiveness of AA
program are effective (Emrick, Tonigan, Montgomery, &
Little, 1993). Charles Bufe (1988) offered three reasons Many substance abuse rehabilitation professionals view
he thought AA was effective “at least for some people” AA as the single most important component of a person’s
(p. 55). First, AA provides a social outlet for its mem- recovery program. Surprisingly, there has been relatively
bers. “Loneliness,” as Bufe (1988) observed, “is a terrible little research into whether people referred to AA by
problem in our society, and people will flock to almost treatment professionals actually attend group meetings,
anything that relieves it—even AA meetings” (p. 55, or to the effectiveness of such meetings (Ferri, Amato, &
italics in original). In contrast, AA offers the opportu- Davoli, 2006; Watson et al., 1997). One study that did ad-
nity for the drinker to engage in a relationship with dress some of these issues was conducted by Kaskutas
others, possible the first honest relationship that he or et al. (2005), and it shed some light into the posttreatment
she has entered into (Gitlow, 2007). AA participation pattern of 349 people who entered for-
Second, AA allows its members to recognize that their mal treatment for alcohol use disorders. The posttreat-
problems are not unique (Alibrandi, 1978; Bufe, 1988). ment AA involvement of these subjects in the 5 years after
Through AA participation, the individual member is able their discharge from treatment fell into four subgroups:
to restore identity and self-esteem through the uncondi-
tional acceptance of the group members, all of whom suf- 1. Low AA involvement: Individuals in this group usu-
fer from the same disease (Nace, 1997). Through this ally attended AA just during the first year following
connection, each member of AA is able to discover a re- treatment.
latedness to others. Finally, AA can offer a proven path to 2. Medium AA involvement: Individuals in this group
follow that can “look awfully attractive when your world attended about 60 AA meetings in the first year and
has turned upside down and you no longer have your best slightly increased their AA involvement by year five.
friend—alcohol—to lean on” (Bufe, 1988, p. 55). Thus, 3. High initial AA involvement: Individuals in this
the AA program is able to offer the individual hope, at a group were attending 200 meetings a year in the first
year, with a slight decrease in AA involvement by the By definition, people who join AA are not a repre-
fifth year after discharge from treatment. sentative sample of everybody with an alcohol use dis-
4. Declining AA involvement: Individuals in this group order (AUD), if only because they decided to join AA4
initially attended about 200 or more AA meetings a (Galanter et al., 1991). Those who join AA but who
year but by the end of the fifth year this had declined drop out are different from those who remain active
to about six meetings a year. participants in the 12-Step group. At least half of those
who initially join stop going to meetings within 3 months,
Further, at the end of the fifth year, the authors found and at the end of 1 year 95% of the new members will
that 79% of the individuals in group 1 were abstinent3 have dropped out (Dorsman, 1996; Nace, 2003). Propo-
while 73% of those in group 2 were still abstinent from nents point out that 70% of those who abstain from alco-
alcohol at the end of the fifth year. Sixty-one percent of hol for 1 year will still be alcohol free at the end of their
those in group 3 were still abstaining from alcohol at second year, while 90% of those who abstained from
the end of the fifth year, while 43% of those in group alcohol for 2 full years were still alcohol free at the end of
4 were still alcohol free at the time of the follow-up their third year of AA participation.
study. But these statistics belie the fact that only 2% of
Another recent study into the effectiveness of 12-Step, those individuals who initially join AA will be alcohol
group-oriented rehabilitation programs was conducted free at the end of 2 years (Dorsman, 1996). However,
by Humphreys and Moos (2007). The authors found abstinence rates for those individuals who begin and
that treatment programs that included 12-Step group maintain their involvement in AA over an 8-year period
involvement was both 30% less expensive than cognitive- were found to be very similar to those obtained by a
behavioral treatment (CBT) programs, and that 30% sample of alcohol-dependent individuals who entered
more subjects were alcohol free after 2 years than those formal treatment programs (Timko, Moos, Finney, &
who went through a CBT program. Lesar, 2000). Nace (2003) pointed out that national sur-
Such research will do little to silence the criticism of veys have found the average AA member has 84 months
AA and might indeed fuel the controversy. Virtually of recovery, and that 18% have been alcohol free for more
everything about AA has been challenged and/or de- than 5 years while 30% have less than 1 year of recovery
fended. It has been suggested that 12-Step groups such to their credit.
as AA should be viewed only as an adjunct to treatment Paradoxically, one factor that seems to predict relapse
(Lewis, Dana, & Blevins, 1988), and as a form of treat- is not participating in 12-Step program meetings, with
ment in their own right (Tobin, 1992). While propo- those who are less active in meetings being most likely
nents advocate 12-Step group involvement as being to relapse (Chappel & DuPont, 1999; Gitlow, 2007).
critical for the individual’s recovery, the truth is that a Unfortunately, it is not uncommon to learn that although
majority of those referred to such groups either fail to a given individual claimed to have attended several
join or fail to consistently participate in the group 12-Step group meetings, he or she “sat in the back of the
process (Zemore et al., 2004). room, arrived late, left early, never spoke with anyone,
Unfortunately, there continues to be very little em- and didn’t have a sponsor” (Gitlow, 2007, pp. 226–227).
pirical research into effectiveness of AA or similar pro- Thus, involvement in AA meetings must be measured
grams, or for what types of people it might be most by a standard other than simple attendance.
useful (Galanter, Castaneda, & Franco, 1991; George & There is strong evidence that while continued involve-
Tucker, 1996; McCaul & Furst, 1994; Tonigan & ment with a 12-Step support group such as AA might not
Hiller-Sturmhofel, 1994). The very nature of AA makes change the individual’s beliefs about religion, over time
it virtually impossible to carry out a well-designed out- the person does grow spiritually (Robinson, Cranford,
come study that might help isolate the effective elements Webb, & Brower, 2007). Since spirituality is one of the
of the program (Gernstein, 2003). Rehabilitation profes- core elements of the AA program, it is not surprising that
sionals and patients often ask whether AA is necessary, 72% of the study subjects were able to reduce their alco-
but even critics of AA seem to accept the fact that it hol use or abstain entirely and that there was a positive
might be helpful at least to some, but not necessarily correlation between the degree of change in spirituality as
all, of those who have a problem with chemicals (Brod- measured by the authors and the individual’s abstinence.
sky, 1993; Ogborne & Glaser, 1985).
4
Yet, as the reader might recall, Jellinek’s (1960) research was
3Which the authors defined as no alcohol use in the past 30 days. conducted on members of AA.
One very real advantage of 12-Step/self-help groups Surprisingly, in light of how often individuals are re-
such as AA is that “alcohol self-help organizations may quired to attend AA meetings by the courts, there is little
promote positive outcomes in alcohol-dependent indi- evidence that this approach is effective (Clark, 1995;
viduals and may also take a significant burden off the Hester & Squires, 2004; Humphreys & Moos, 1996;
public and private health care sectors” (Humphreys & Miller, Andrews, Wilbourne, & Bennett, 1998). The
Moos, 1996, p. 712). Which is to say that the individ- practice of requiring the individual to attend AA meet-
ual’s involvement in 12-Step groups reduces the impact ings has been cited as one factor that has changed the AA
of the individual’s drinking on the cost of health care. movement itself (Humphreys & Moos, 1996).5 Further,
A very closely related factor that impacts the success of there is evidence that those individuals who face legal
12-Step groups such as AA is the frequency with which a consequences as a result of driving while intoxicated
person attends AA meetings (Watson et al., 1997). There (incarceration/probation) had better subsequent driving
is a positive relationship between AA attendance follow- records (i.e., fewer accidents or further arrests) than those
ing discharge from a rehabilitation program and contin- “sentenced” to treatment (Bufe, 1998; Peele, Brodsky, &
ued abstinence from chemicals (Brigham, 2003; Moos & Arnold, 1991). These findings raise questions about the
Moos, 2005; Nace, 2003; Watson et al., 1997). AA in- effectiveness of court-ordered participation in AA or
volvement appears to reflect some of the same forces that similar 12-Step groups for individuals who are convicted
predicted the individual’s efforts to make meaningful per- of driving while under the influence of alcohol.
sonality changes, such as attempting to learn more effec- Ultimately, the issue of whether AA is effective is far
tive ways to cope with stress (Morgenstern, Labouvie, too complex to be measured by a single research study
McCrady, Kahler, & Frey, 1997). (Glaser & Ogborne, 1982; Ogborne, 1993). The very
One popular belief is that life stressors trigger in- nature of AA ensures that there will be vast differences
creased alcohol use. Although suggestive, this theory between different AA groups, even though they all share
actually is misleading. Miller and Harris (2000) found the same name (Ogborne, 1993). There continues to be
that a sense of general depression and demoralization a need for a series of well-controlled research studies
seemed to be predictive of relapse in those individuals designed to identify all of the variables that might influ-
who had successfully completed treatment. If people ence the outcome of AA participation (McCrady &
feel overwhelmed by the stressors they face, they are Irvine, 1989). Thus, the very nature of the question “Is
more likely to engage in increased alcohol use/abuse. AA effective?” makes it unanswerable. For example,
Further, increased alcohol use seems to predate the would the chronic alcoholic who, as a result of partici-
development of many stressors, which then sets the stage pation in AA, stopped drinking on a daily basis but then
for even more alcohol use by the individual began a pattern of binge drinking, be measured as a
(Humphreys, Moos, & Finney, 1996). Active involve- successful outcome or as a failure? Would the chronic
ment in AA seems to allow members to begin to develop alcohol user who entered AA, stopped drinking, but
a support system that is both nondrinking and seeks to died of alcohol-induced liver disease 6 weeks or even
help them cope with their problems without encourag- 6 years later be a successful or unsuccessful outcome?
ing them to drink, thus breaking the cycle of drinking These examples illustrate how the question “Is AA effec-
and ineffectual coping, according to the authors. tive?” is unlikely to generate a meaningful answer
While the results of these studies are suggestive, there (Ogborne & Glaser, 1985). A more meaningful approach
still is insufficient evidence to conclude that AA is would be to attempt to identify which types of people are
effective in the treatment of alcoholism (Hester, 1994). most likely to benefit from 12-Step programs such as AA.
At best, it would appear that AA is most effective with a
subset of problem drinkers: those socially stable white
males, over 40 years of age, who are physically depen- Narcotics Anonymous
dent on alcohol, are prone to guilt, and are the firstborn In 1953, another self-help group patterned after AA was
or only child in their families. Research also suggests founded that called itself Narcotics Anonymous (NA).6
that individuals with stronger religious beliefs and/or Although this group honors its debt to Alcoholics
who are severely addicted to alcohol are more likely to
attend AA meetings (Weiss et al., 2000). The majority of 5Remember that one of the foundation stones of AA is voluntary at-
AA members are males, but approximately 35% of the tendance, which is not true if the individual is required to attend by
members are women, a figure that increases to 43% of the court, probation officer, or other authority.
those under the age of 30 (Coker, 1997). 6The Web site for Narcotics Anonymous is www.na.org.
Anonymous, the members of Narcotics Anonymous talk over their problems. At some point, the decision was
feel that made to try applying to their own lives the same 12 Steps
that their husbands had found so helpful, and the group
we follow the same path with only a single excep- known as Al-Anon was born. At the start of the 21st cen-
tion. Our identification as addicts is all-inclusive in tury there are an estimated 30,000 Al-Anon groups in
respect to any mood-changing, mind-altering sub- the United States with perhaps 390,000 members
stance. “Alcoholism” is too limited a term for us; (Gwinnell & Adamec, 2006; White, 2005).7
our problem is not a specific substance, it is a dis- In the beginning, each isolated group made whatever
ease called “addiction.” (Narcotics Anonymous, changes it felt necessary in the 12 Steps. However, by
1982, p. x) 1948 the wife of one of the co-founders of AA became in-
volved in the growing organization, and in time a uniform
To the members of NA the problem is the disease of ad- family support program emerged. This program, known
diction. This self-help group emerged for those whose as the Al-Anon Family Group borrowed and modified the
only “common denominator is that we failed to come Twelve Steps and Twelve Traditions of AA to make them
to terms with our addiction” (Narcotics Anonymous, applicable to the needs of families of alcoholics, as 86% of
1982, p. x). On the other hand, many outsiders view the members believed that their mental health had been
major difference between AA and NA as being one of adversely affected by another person’s drinking, most
emphasis. Alcoholics Anonymous addresses only alco- often a parent and/or a spouse (Gwinnell & Adamec,
holism, while NA addresses addiction to chemicals in 2006). Little is known about the characteristics of an ef-
addition to alcohol. fective Al-Anon group or the successful Al-Anon mem-
The growth of NA has been phenomenonal, with a ber. Thus, although Al-Anon is viewed as a resource for
600% increase in the number of NA groups from 1983 the spouse of the alcohol-abusing individual, its effective-
to 1988 (Coleman, 1989), and there are more than ness is still not proven.
25,000 chapters of NA meetings in the United States By 1957, in response to the recognition that teenagers
with about 250,000 active members (Ringwald, 2002). presented special needs and concerns, Al-Anon itself gave
Alcoholics Anonynous and Narcotics Anonymous are not birth to a modified Al-Anon group for teens known as
affiliated with each other, although there is an element Alateen. Currently, it is thought that there are 2,300
of cooperation between these organizations (M. Jordan, Alateen groups in the United States (Capretto, 2007;
personal communication, February 27, 1989). Each fol- Gwinnell & Adamec, 2006). Alateen members follow the
lows a similar 12-Step program that offers the addicted same 12 Steps outlined in the Al-Anon program. The goal
person a day-by-day program for recovery. This is under- of the Alateen program, however, is to provide the oppor-
standable, since NA is essentially an outgrowth of AA. tunity for teenagers to come together to share their experi-
One major difference is that AA speaks only about al- ences, discuss current problems, learn how to cope more
coholism, while NA speaks of “addiction” or “chemicals.” effectively with their various concerns, and provide en-
There are no inherent advantages of one program couragement to each other (Facts About Alateen, 1969).
over the other. The most important point is this: Which Through Alateen, teenagers learn that alcoholism is
group works best for the individual? Some people feel a disease, and they are helped to detach emotionally
quite comfortable going to AA for their addiction to al- from the alcoholic’s behavior while still loving the indi-
cohol. Other people feel that NA offers them what they vidual. The goal of Alateen is also to help the individual
need to deal with their addiction. The name of the learn that he or she did not “cause” the alcoholic to
group does not matter so much as the fact that it offers drink and to see that he or she can build a rewarding
the recovering person the support and understanding life in spite of the alcoholic’s continued drinking (Facts
that he or she needs to abstain for today. About Alateen, 1969).
Al-Anon and Alateen Support Groups Other Than AA

The book Al-Anon’s Twelve Steps and Twelve Traditions Criticism has been aimed against the AA program for
provides a short history of Al-Anon in its introduction. its emphasis on spiritual growth, its failure to empower
According to this history, while their husbands were at women, or its basic philosophy. Several new self-help
the early AA meetings, the wives would often meet to
wait for their husbands. As they waited, they would often 7The Al-Anon/Alateen Web site is www.al-anon.alateen.org.
groups have emerged since 1986 that offer alternatives out having a drink!” and “I should be able to drink, just
to AA. like everybody else” are examples of this kind of
Rational Recovery. This organization discontinued thinking.
the use of support groups in January of 2000, on the SMART groups assume that virtually any approach
grounds that such groups impede the individual’s to rehabilitation will be of some value to the individual
progress toward abstinence (Horvath, 2005). The orga- and thus encourages participation in traditional 12-Step
nization still maintains an Internet Web site, which rec- groups (Horvath, 2000). In a comparison of the effec-
ommends books that might aid the individual in his or tiveness of traditional 12-Step programs and cognitive-
her quest for abstinence. behavioral (CB) treatment approaches, Ouimette et al.
Self Management and Recovery Training (SMART).8 (1997) discussed the results of a multicenter experi-
This organization was founded in 1985 and initially ment involving 3,018 patients who were being treated
was part of the Rational Recovery movement. But for substance use problems at one of 15 selected Veterans
SMART is a splinter group that broke away from RR in Administration hospitals in the United States. The par-
1994 (Chappel & DuPont, 1999; Horvath, 2000, 2005). ticipants in this study were assigned to one of three
Currently, it is estimated that SMART has more than treatment conditions: “pure” 12-Step treatment, “pure”
350 groups around the United States each week, and it CB treatment, or a mixed CB/12-Step format. Partici-
offers 15 “online” meetings and a 24-hour-a-day online pants in this study were interviewed after 1 year’s time to
support group for members with access to the Internet determine their employment and substance use status.
(Bishop, 2002; Gernstein, 2003; Horvath, 2000). The authors concluded that “pure” cognitive-behavioral
The SMART program is an abstinence-oriented pro- and 12-Step programs were equally effective in helping
gram that draws heavily on the cognitive-behavioral people address substance use problems. This study thus
school of psychotherapy, stressing four points: (a) en- supported treatment approaches such as the SMART
hancing and maintaining the individual’s recovery to program for persons with substance use problems.
abstain, (b) coping with thoughts/cravings about chem- In terms of those people who seem to be best suited
icals, (c), solving old problem behaviors through to SMART groups, research suggests that they are
cognitive-behavioral techniques, and (d) developing a people with an internal locus of control (Gernstein,
balance in one’s lifestyle (Gernstein, 2003; Horvath, 2003). Such people tend to avoid passive recovery pro-
2000). Within this perspective, alcoholism (or other grams, although 10% of SMART program members
drug abuse) is viewed as reflecting the impact of nega- also attend more traditional 12-Step programs such as
tive, self-defeating thoughts (Ouimette, Finney, & AA (Gernstein, 2003). The program is not used for
Moos, 1997; Tonigan & Toscova, 1998). For example, treating adolescents but is intended mainly for work
members are encouraged to stop drinking as a sign of with adults, but there are efforts under way to deter-
self-respect, as opposed to drinking in order to feel good mine whether the SMART group approach might be
about themselves. Groups are advised by mental health used with adolescents with substance use problems either
professionals and strive to help individual addicts iden- in its current or a modified form.
tify and correct self-defeating ways of viewing them- Secular Organizations for Sobriety (SOS).9 This
selves and the world. group was founded in 1986. By the late 1990s there were
Gorski (1993) identified two general irrational an estimated 2,000 SOS groups that met each week, and
thought groups that contribute to the individual’s sub- total membership was about 100,000 people (Chappel &
stance use. The first of these was termed addictive DuPont, 1999; Ringwald, 2002). But the program was
thinking (p. 26), which was defined as the individual’s struggling in the eyes of some (Gernstein, 2003).
use of irrational thoughts to support a claim that he or SOS was founded as a self-help group established in
she has a “right” to use chemicals, and that his or her reaction to the heavy emphasis given to spirituality in
chemical use is not the cause of the problems facing AA and NA (Ringwald, 2002). SOS draws heavily from
the person. The second group of irrational thoughts cognitive-behavioral psychotherapies, and the guiding
used to support substance use were relapse justifications philosophy of SOS stresses personal responsibility, the
(p. 26), according to the author. These were specific role of critical thinking in recovery, and the identifica-
thoughts used by the individual to justify his or her re- tion of the individual’s specific “cycle of addiction”
turn to chemical use. “I can’t cope with the stress with-
9The current Web site for Secular Organizations for Sobriety is
8The current Web site for SMART is www.smartrecovery.org. www.cfiwest.org/sos/index.htm.
(Horvath, 2005; Tonigan & Toscova, 1998). The SOS MM evolved out of the frustration of its founder,
model suggests that addiction rests on three elements: Shirley Kishline, with traditional alcohol rehabilitation
(a) the physiological need for the chemical, (b) the programs. Kishline felt that although she was referred
learned habit of using the chemical as a coping mecha- to a traditional inpatient treatment program that placed
nism, and (c) the denial of both the need and the habit great emphasis on 12-Step program involvement, her
(Horvath, 2005). In contrast to the AA model, in which addiction to alcohol was apparently never firmly estab-
the individual must call on a higher power to achieve lished in her mind. Kishline initially recommended that
abstinence, SOS teaches that the individual has the po- moderation was the most appropriate goal for her, on the
tential within to learn how to live without alcohol grounds that she was a “problem drinker” (Kishline,
(Ringwald, 2002). The program is neutral toward tradi- 1996, p. 53), but not “alcoholic.” Ms. Kishline defined
tional 12-Step groups, and a significant portion of the a problem drinker as a person who consumes no more
members have attended a 12-Step group (or are currently than 35 drinks per week and who has experienced only
doing so). mild to moderate alcohol-related problems (Kishline,
Women for Sobriety (WFS).10 This group was founded 1996). She rationalized in her book Moderation
in 1976 by Jean Kirkpatrick, who passed away in June Management published in 1994 that the chronic drinker
of 2000 at the age of 77 (Chappel & DuPont, 1999; was a person who was physically dependent on alco-
Horvath, 2005). There are approximately 300 WFS hol and who would, in the majority of cases, experience
groups and about 5,000 active members in the United severe withdrawal symptoms when he or she stopped
States (Ringwald, 2002). It is an organization specifi- drinking (Shute & Tangley, 1997). The goal of MM
cally for women and was founded on the theory that the was to “provide a supportive environment in which
AA program failed to address the very real differences people who have made the decision to reduce their
between the recovery process from alcoholism for men drinking can come together to help each other change”
and women (Horvath, 2005). There are 13 core state- (p. 55).
ments or beliefs that are aimed at providing the mem- MM drew heavily on behavior modification prin-
ber with a new perspective on herself. There is a great ciples used by professionals to help people learn how to
deal of emphasis on self-esteem and on building self- change their behavior. MM members were encouraged
esteem for the member. Research suggests that about to accept personal responsibility for their alcohol use and
one-third of the members of WFS continue their in- to work toward limiting their drinking to no more than
volvement in AA, and that approximately the same per- four standard drinks in a 24-hour period (Horvath,
centage of members of WFS groups as AA groups learn 2005). The MM movement initially gained some ac-
to abstain from chemicals (Chappel & DuPont, 1999). ceptance in the United States, and eventually meetings
Unlike those in traditional 12-Step groups, WFS were held in 25 states. Critics of the MM movement sug-
members are encouraged to leave the group to live on gested that members with actual alcohol dependence
their own when they feel they have recovered from problems would use the group as an excuse to continue
their alcohol dependency (Ringwald, 2002). Thus, the trying to achieve “controlled” drinking. Ultimately, the
small number of active members does not do justice to founder of MM renounced her objections to traditional
this program, which claims that an additional 36,000 12-Step groups and accepted total abstinence as the treat-
individuals were members at one time or another. The ment method of choice for her alcohol use disorder
program attempts to address from women’s perspective (Vaillant, 2000). Shortly after taking this step, Ms. Kishline
the stumbling blocks to recovery such as guilt, shame, was involved in an alcohol-related motor vehicle acci-
powerlessness, and depression, and many members dent in which a father and his 12-year-old daughter
note that traditional 12-Step groups were designed to were killed when her truck struck theirs on an interstate
help male members or are male-oriented. highway (Noxon, 2002). Ms. Kishline’s measured BAL
Moderation Management (MM).11 This organiza- was 0.260, more than three times the legal limit for the
tion was founded in 1993 (Chappel & DuPont, 1999) state of Washington, and she was charged and convicted
and was been quite controversial ever since it started. of the crime of vehicular homicide.
Surprisingly, many of the goals of MM are consis-
10Thecurrent Web site Women for sobriety is www.womenforsobriety. tent with the teaching of Alcoholics Anonymous
org. (Humphreys, 2003). Further, research suggests that the
11Moderation Management maintains a Web site at www.moderation. vast majority of those who are drawn to MM tend to
org. have alcohol-related problems that are low severity,
strong social supports, and little interest in a program lates federal law (Peele, 2004b). Based on these rulings,
such as AA that adovcates total abstinence as its goal programs cannot require participants to attend AA
(Horvath, 2005; Humphreys, 2003). The program meetings.
seems to be of some value to those individuals who are It has also been suggested that the AA program is
indeed not dependent on alcohol, in the opinion of one based on fear, which demands conformity and
Humphreys. which fails to affirm the individual (Gilliam, 1998).
LifeRing. LifeRing12 is an alternative to traditional Although the AA 12-Step program has helped thou-
12-Step groups that originated in California and is sands of people, it was established in the 1930s. It
based in Oakland. Its foundation is the concepts of so- might not meet the needs of addicted people in the
briety, secularity, and self-help. One of the core prin- early 21st century because AA was founded on the ex-
ciples of LifeRing is that the individual’s spirituality is a periences of a limited sample (100 individuals) whose
private matter and thus not a focus of group or individ- worldview was formed during the Great Depression.
ual discussion if the individual wishes not to discuss it. The applicability of these life lessons to the individual
Each participant is encouraged to develop a recovery living in the early 21st century is open to debate. Further,
program that fits his or her individual needs, without a the AA program is a “one size fits all” program, in spite
prescribed program that each is forced to follow. of the fact that clinical research has demonstrated that
Currently there are meetings in about 20 states and the alcohol use disorders assume many forms. Indeed,
4 foreign countries. While this organization is indepen- Szalavitz (2006) takes this criticism even further, point-
dent of traditional 12-Step groups, it also does not dis- ing out that the AA 12-Step program has been adopted
courage members from attending such groups if their virtually unchanged to address a wide range of addic-
recovery program includes this. tions, including addictions to food, heroin, and other
substances.
Originally, the AA program was designed to “com-
Criticism of the AA/12-Step Movement pletely deflate the [individual’s] ego” on the assump-
Although the 12-Step movement has achieved an almost tion that this was a common characteristic of those who
irreproachable status in the addictions recovery com- were addicted to alcohol. But this core assumption
munity, it is not without a small, vocal group of critics. might make AA inappropriate for many of those who
For example, while it is an article of faith in 12-Step struggle with chemical use disorders at the start of the
groups that the alcohol-dependent person might be 21st century, since it is not clear to what degree individ-
recovering, he or she never fully recovers from alco- uals with substance use disorders now share this charac-
holism (Fletcher, 2003). In reality, the AA “Big Book” teristic with their forefathers of 80 years or more ago.
speaks of people having “recovered” from alcohol It has also been suggested that one of the pillars on
dependency several times. Indeed, the “Big Book” which AA stands—the spiritual “awakening” by one of
speaks of how the individual might reach a time when the founders of AA, William (“Bill”) Griffith Wilson—
he or she no longer needs to depend on AA (Fletcher, was possibly based on his having received belladonna
2003), a point that advocates of such groups rarely administered by his physician to help him recover from
mention. the acute effects of alcohol (Bufe, 1998; Lemanski,
Another criticism of the AA 12-Step program is that 1997; Peck, 1993). Others object to the heavy emphasis
it is potentially “damaging, violative and ineffective” of such programs on a “higher power” (Marvel, 1995;
(Brodsky, 1993, p. 21) for many individuals. Brodsky Wallace, 2003). Because it was an outgrowth of an early
bases his criticism of the 12-Step program on the as- 20th century religious movement, the 12-Step model
sumption that while it might be a useful tool for some, accepts the necessity of an external, supernatural “higher
it is based “a 19th century fundamentalist tradition” power” to which the individual must “surrender” if she
(p. 21) that is essentially conservative Protestant in na- or he is to learn how to abstain from drugs/alcohol
ture. When forced on participants, the program holds (Gernstein, 2003).
the potential to be more destructive than helpful (Brod- It is interesting that what might be viewed as one of
sky, 1993; Szalavitz, 2006). Further, the courts have ruled the more destructive elements of the 12-Step program,
that AA is a religious movement, and for this reason at- the need for spiritual desperation, is only rarely ac-
tendance can not be forced on the individual as this vio- knowledged as a possible problem (Gilliam, 1998;
Lemanski, 1997). Yet any other form of psychological/
12The current Web site for LifeRing is www.unhooked.com. psychiatric treatment that required the individual to
experience the depths of despair and defeat, as is re- and that recovering staff are quite uninterested in treat-
quired in the experience of “hitting bottom,” would be ment approaches that do not utilize such an approach
branded as abusive by the mental health community. (Brigham, 2003).
Indeed, the need to hit bottom has been challenged by Finally, many critics of AA have observed that the
Fletcher (2003), although it remains a pillar of the re- AA/12-Step model does not embrace the possibility of a
covery movement. cure (Fletcher, 2003; Gilliam, 1998; Lemanski, 1997).
Another criticism of the AA/12-Step movement is Indeed, the AA/ 12-Step model does not even incorpo-
that it is based not on scientific research but on testimo- rate the concept of health (Gilliam, 1998). The individ-
nials by its members, asserting that it was indeed essen- ual must, according to the 12-Step model, continue to
tial to their recovery (Szalavitz, 2006). The input from attend meetings forever, according to critics, although
mental health professionals is often dismissed because few people actually maintain their involvement in
they do not “understand” the disease of addiction, or AA/12-Step programs for extended periods of time. Nace
because they have not “been there,” while program par- (2005b) reported, for example, that only 50% of new
ticipants are elevated to the status of “experts” in the members remain in AA for more than 3 months. These
field of addictions because they were once actively criticisms of AA are rarely discussed, but they strongly
abusing a chemical (Szalavitz, 2006). suggest that the program is not a panacea for recovery.
A vocal critic of the 12-Step recovery movement,
Stanton Peele (1989, 1998) has pointed out that the
AA/12-Step model, as it is currently applied, is based on
Summary
an unproven theory about the cause of alcoholism first At the start of the 21st century, self-help groups such as
suggested by the physician Benjamin Rush in the Alcoholics Anonymous (AA) have become one of the
17th century. This theory has long since been discred- predominant forces in the field of drug abuse treat-
ited, but the 12-Step movement that rests in part on this ment. Drawing on the experience and knowledge of its
pillar, continues to exist. Further, according to Peele members, AA has developed a program for living that is
(1989, 1998), the AA/12-Step model points to those spiritual without being religious, confrontive without
individuals who were least successful in dealing with using confrontation in the traditional sense of the word,
their addiction, the members who were able to recover reliant on no outside support, and believed by many
only through the use of the 12-Step program, as role members to be effective in helping them stay sober on a
models for new members. Individuals who were able to daily basis.
recover from their substance use disorder on their own The program for living established by AA is based on
are not widely used as role models and certainly never those factors that early members believed were impor-
with the 12-Step community, whose role models for tant to their own sobriety. This program for living is
new members are those who have suffered through ex- known as the 12 Steps. The Steps are suggested as a
tended periods of failure and relapse before their ulti- guide to new members. Emphasis is placed on the
mate recovery. Finally, the goal of AA/12-Step programs, equality of all members, and there is no board of direc-
total abstinence, is only rarely achieved: Most alcohol- tors within the AA group. Questions continue to exist
dependent individuals merely cut back on the amount about whether AA is effective. Researchers agree that it
of their alcohol use, and only few achieve total abstinence seems to be effective for some people but not for every-
(Peele, 1998). body. Currently, the evidence suggests that spirituality
Critics point out that many of the basic tenets of AA, based programs such as AA might be more effective for
such as the twin beliefs that (a) alcoholism will always people with strong spiritual beliefs prior to the onset
grow worse without treatment and (b) individuals cannot of the substance use disorder (Cooney, Kadden, &
cut back or quit drinking on their own are not supported Steinberg, 2005).
by research data. Alcohol-dependent persons rarely fol- The AA/12-Step program has served as a model
low the downward spiral thought to be inescapable by for many other self-help groups, including Narcotics
AA. Also, the manner in which the AA program is im- Anonymous (NA). One of the central tenets of NA is
plemented has been characterized as a form of “indoc- that the alcohol focus of AA is too narrow for persons
trination” (Bufe, 1998, p. 6). This theory is supported who have become addicted to other chemicals, either
by the observation that up to 95% of inpatient treat- alone or in combination with alcohol. Narcotics
ment programs utilize some kind of 12-Step approach Anonymous expounds the belief that addiction is a
common disease that may express itself through many spouses of early AA members and strives to provide an
different forms of drug dependency. NA has estab- avenue for helping the families of those who are addicted
lished a 12-Step program based on the 12 Steps offered to alcohol. Alateen emerged from Al-Anon in response
by Alcoholics Anonymous, while reaching out to those to the recognition that adolescents have special needs.
whose addiction involves chemicals other than alcohol. Both groups strive to help the member learn how to be
Other self-help groups that have emerged as a result of supportive without being dependent on the alcoholic,
the AA experience have included Al-Anon and Alateen. and to learn how to detach from the alcoholic and his
Al-Anon emerged from informal encounters between the or her behavior.
CHAPTER THIRTY-SIX
Crime and Drug Use
Social scientists have long known that there is a strong the economic impact of drug-related criminal activity
correlation between substance misuse and criminal ac- in the United States alone is about $59.1 billion a year
tivity. But as statistics instructors repeat over and over (Craig, 2004). In spite of protracted efforts to reduce
again, correlation does not imply causality. Researchers drug abuse around the world in the last decade of the
continue to debate whether the drug use precedes 20th century, the supply and scope of drug abuse has
criminal activity or follows it, or if both criminal behavior increased rather than dropped (“Losing Tolerance,”
and substance misuse might not reflect a third, un- 2005).
known but common factor (McCollister & French, Depending on which facts one chooses to embrace, it
2002; Moore, 1991; Newcomb, Galaif, & Carmona, is possible to argue that substance use is or is not a causal
2001). The last idea suggests that individuals who are factor in criminal activity. For example, those who sug-
predisposed to crime might also be predisposed to use gest that substance abuse causes crime overlook certain
of alcohol and/or drugs. This position is supported by facts, such as longitudinal studies that have repeatedly
research findings that 60%–80% of those who break the found that deliquency usually precedes the development
law have abused recreational drugs at some point in of substance use problems, and that while the individual
their lives (Hartwell, 2004; McCollister & French, might outgrow deliquent behavior in the young adult
2002). Unfortunately, less than 15% of inmates with a years, he or she is less likely to outgrow the substance use
substance use disorder (SUD) receive some form of problems (Husak, 2004).
treatment for their SUD while incarcerated (Aldhous, However, a different perspective on the relationship
2006). The rest are returned to society when their sen- between criminal activity and chemical abuse was of-
tence expires, bringing their SUD (and other problems) fered by Elliott (1992). He suggested that chemical
with them. abuse and criminal activity both reflect the “decline in
The debate over the relationship between criminal the power of cultural restraints” (p. 599) taking place in
activity and substance abuse has been the subject of nu- this country. The author supported his argument with
merous books and learned essays on the subject. The the observation that Europe had experienced “tidal
debate over the degree to which substance misuse con- waves of crime” (Elliott, 1992, p. 599) every few
tributes to criminal behavior raged through much of decades since the 14th century. According to Elliott, a
the 20th century and shows no sign of being resolved as similar pattern has emerged in the United States over
we enter the 21st century. In this chapter, the relation- the past 200 years. A common thread connecting these
ship between these two social phenomena—drug use waves of crime, according to the author, is that in each
and criminal activity—is very briefly examined. successive period of social unrest, one could observe
“an erosion of personal integrity, widespread dehuman-
ization, a contempt for life, material greed, corruption
Criminal Activity and Drug Use:
in high places, sexual promiscuity, and increased
Partners in a Dance? recourse to drugs and alcohol” (p. 599, italics added for
The problems of substance misuse and criminal be- emphasis).
havior are hardly insignificant. Globally, an estimated In the present social climate, those most likely to ex-
200 million people are thought to take illegal drugs periment with new drugs of abuse are white, middle-
each year, and an estimated 4 million farmers are eco- class, suburban males (Boyer, 2005). These individuals
nomically dependent on the cultivation of illegal crops tend to be younger and thus less likely to believe that
(“Losing Tolerance,” 2005). It has been estimated that they can be harmed by a drug; also, they are bored and
428
Crime and Drug Use 429
have significant amounts of discretionary money at ability to think coherently. This is an extreme position
their command (Boyer, 2005). By the time the drug has that is based on the unproven assumption that sub-
reached the inner cities, it is well established as a drug stance abuse obliterates free choice (Husak, 2004). As
of abuse (Boyer, 2005). was observed two generations ago, any “perceived cor-
There are multiple pathways between substance relation between the use of a drug and the unwanted
abuse and criminal activity, with drug use problems consequences is attributed to the drug, removing the
both resulting from and predicting criminal behavior individual from any and all responsibility” (National
(Newcomb et al., 2001). Early drug abuse was found to Commission on Marihuana and Drug Abuse, 1973, p. 4).
predict later criminal activity in a community sample, This position was echoed by Walton (2002), who, in
while substance use was found to impair impulse control, speaking of alcohol, noted that “if intoxication is
contributing to the tendency for the individual to engage wrong, it is in large part these days because it is per-
in socially inappropriate behavior. Newcomb et al. found ceived to be guilty of inciting criminality and other
evidence that “a proneness toward criminality” (p. 190) anti-social activities in too many of those who regularly
was associated with substance use problems, while lim- take intoxicants” (p. 75).
ited evidence was found supporting the theory that both Both of these views reflect the “demon rum” philos-
drug use and criminal activity reflected the impact of a ophy commonly espoused in the United States during
third factor called “social conformity” (p. 191). Thus, the late 1800s (Peele, 1989; Walton, 2002). According
there seems to be no single pathway between substance to this belief, once the person ingests even one drink,
abuse and criminality. the alcohol totally overwhelms his or her self-control.
Unfortunately, alcohol is the substance most com- From this point on, according to this theory, that per-
monly involved in criminal activity (Husak, 2004). son’s behavior is controlled by the demon “alcohol.” It
Twenty-one percent of individuals incarcerated for vio- is generally believed that when a crime is committed by
lent crimes were under the influence of alcohol alone a person who is under the influence of chemicals, the
at the time they committed the crume whereas only 3% responsibility for the act is attributed not to the person
of those incarcerated for violent crimes were under the but to the chemicals being abused. But the law holds
influence of cocaine alone and 1% were under the in- that the individual remains responsible for the decision
fluence of heroin at the time of the offense (Husak, to initially abuse the drugs involved and thus indirectly
2004). This fact is overlooked by those who wish to use for his or her behavior while intoxicated, although in
the link between substance misuse and criminal be- some states a “diminished capacity” defense might be
havior as justification for the harsh prison sentences used to mitigate against the full weight of the charges
given to those convicted of substance-related criminal for some crimes (Gendel, 2006; Husak, 2004; Kermani &
activity. Castaneda 1996).
Criminal activity and personal responsibility. Con- The law and morality: Where to draw the line? In the
cerning the relationship between substance use and modern “war on drugs” federal and state authorities
criminal activity, over 50% of opiate-dependent persons have instituted legal sanctions against individuals with
have been arrested for criminal activity prior to their a substance use disorder, which many argue turns a
first use of opiates (Jaffe & Strain, 2005). Is their subse- medical issue into a legal problem. But the legal system
quent involvement in criminal activity a reflection of is selective: Only certain substances, and only certain
their SUD or an extension of their previous antisocial euphoric states, are deemed inappropriate and worthy
behavior? To further complicate this debate, to deter- of prosecution (Husak, 2004). For example, caffeine
mine the level of personal responsibility in cases where users achieve a certain drug-induced psychological
the individual might have been under the influence of state without fear of arrest or incarceration, and long-
chemicals at the time of the offense is difficult. Unfortu- distance runners still experience the “runner’s high”
nately this is a very real problem, as 51%–76% of adult without fear of legal concequences (Husak, 2004). But
males and 39%–85% of adult females who are arrested the use of certain other compounds are by definition
test positive for at least one illicit substance at the time criminal acts, and individuals using them become,
of their arrest (Farabee, Prendergast, & Cartier, 2002; again by definition, criminals. This general policy, in
Makkai, 2003). effect since the 1930s, has proven to be ineffective in
The issue of responsibility for criminal behavior is the battle against recreational chemical use, a fact that
often sidestepped through the use of the social fiction does not stop its application in the war on drugs (Gray,
that the drugs somehow interfered with the individual’s 1998; Husak, 2004).
430 Chapter Thirty-Six
The decision to bring the weight of the legal system use and abuse? The legal system tends to be extraordi-
to bear on substance abusers demands that clear deci- narily selective and fails to provide any rationale for its
sions be made about what is or is not acceptable behav- actions, all too often ruining the life of the individual
ior, a moral dilemma in that there are no clear for making the decision to seek a drug-induced mood
cut-standards of behavior. The state without the benefit of a prescription.
Manufactured criminals. The national prohibition
person to be blamed must have done something against certain compounds has essentially served only
wrongful; no one can merit blame for conduct that to prohibit access to certain chemicals except through
is permissible. But whether and to what extent illicit channels. Since access to these chemicals is
someone should be blamed is not simply a function under the control of those willing to break the law, they
of the wrongfulness of his conduct. We must also de- are not sold in a free market. Access is under the control
cide whether the wrongful act is fairly attributed to of those who have the drugs to sell, at the price charged
him, that is, whether he is responsible for it. (Husak, by the seller. Users must then raise the money de-
2004, p. 405) manded by the seller, even if they must engage in bur-
glary, theft, armed robbery, prostitution (heterosexual
To punish a person with a substance use disorder and homosexual), car theft, forgery, or the sale of drugs
simply because he or she has a substance use disorder is to obtain this money. In this manner, the individual’s
illegal, as it violates the Eighth Amendment to the U.S. consensual act is transformed into a crime, supported
Constitution (Gendel, 2006). But if a person has a sub- by crime, and treated by society as a criminal problem.
stance use disorder and acts in a manner entirely con- Further, users who support their drug habit through
sistent with the addiction, should he or she be theft will receive only a fraction of the stolen material’s
punished? The courts have ruled that interpreting the worth. Thus they must steal more and more so that the
law to mean that the individual should not be punished pittance they receive for the stolen property will pro-
for addictive behavior is inappropriate, and the person is vide a sufficient income to meet their drug needs. It
still held accountable for behaviors that are clearly part has been estimated that the typical heroin addict in an
of the addiction (Gendel, 2006). average city would need to steal $200,000 worth of
Made-to-order-mood states: The first steps toward mind goods annually to support a drug habit (Kreek, 1997).
control? In the early years of the 21st century the line Thus, it is possible to argue that the national prohibi-
between legitimate medical purposes, recreational drug tion against drugs of abuse contributed to the wave of
use, and the use of prescribed medications to achieve a crime that developed in the United States in the latter
desired mood state has become quite vague (Husak, half of the 20th century.
2004). It has been argued that personal, recreational,
drug use (as opposed to distribution of illicit chemicals to
others) is simply a consensual crime in the sense that the
Urine Toxicology Testing in the Workplace
individual who is using a recreational chemical had Estimates of drug-related lost productivity in the United
made the choice to do so in a manner that does not hurt States range from $14.2 billion (Craig, 2004) to $30 bil-
others (McWilliams, 1993). Are individual euphoric lion a year (May, 1999). In the mid-1980s, prior to the
states grounds for legal constraints? At what point does initiation of widespread urine toxicololgy testing for
medical necessity blend into recreational drug use? workers, it was thought that as many as 20% of workers
Nobody would fault a man for using a drug such as Viagra were abusing illicit drugs at work (Goldberg, 2002).
if he suffered from a clear case of erectile dysfunction. With the encouragement of the federal government
But what about the businessman who ingests Viagra only and insurance companies, an increasing number of
to enhance his sexual performance? Each individual employers now require urine toxicology testing at the
would have obtained the same drug from a physician, but time an employee is hired and on a random basis dur-
where is the line between legitimate medical use and ing the work week.
recreational use of that same chemical compound? The widespread testing of employees for signs of il-
Is the businessman who takes diazepam to help him licit drug use is controversial. Proponents of the con-
relax after a hard day’s work that different from the busi- cept of drug testing in the workplace point to research
nessman who drinks a martini or the individual who findings that during 1987–1994 the number of work-
smokes marijuana to relax after a hard day’s work? ers testing positive for an illicit drug dropped by 57%.
Where does society draw the line between substance Detractors of this movement point out that (a) urine
drug testing does not include testing for alcohol, which brew” (beverages containing alcohol) might contain
is thought to be consumed on the job site by 8% of the methanol, a form of alcohol that could blind or even kill,
hourly workers and 23% of the managers; (b) members rather than the desired ethanol. The number of victims
of Congress are exempt from the mandatory drug testing of methanol poisoning during prohibition was thought
laws that they have imposed on everybody else; (c) drug to number in the “tens of thousands” (Nadelmann,
testing does not tell when workers used the chemicals Kleiman, & Earls, 1990, p. 46). This was one reason that
detected, just that there were signs of an illicit chemical smuggled alcohol was so popular during Prohibition:
in their urine (Schlosser, 2003); and (d) a positive test People could trust that a legitimate alcoholic beverage
does not determine impairment (Husak, 2004). The last would not blind or kill them.
two points are illustrated by the case when a urine The problems associated with illegally manufac-
sample drawn on a Tuesday morning detected THC tured alcohol were not limited to just the Prohibition
in the worker’s urine. But what does that mean? It era. Even today, whiskey produced by illegal stills,
might suggest that the person had used marijuana known in many parts of the country as moonshine (or
prior to coming to or at work. But the same results might “shine”), is frequently contaminated with high levels of
be obtained if the individual had used marijuana the lead (Morgan, Barnes, Parramore, & Kaufmann, 2003).
preceding weekend in the privacy of his or her home The lead contamination is caused by the practice of
(Schlosser, 2003). many producers of filtering the brew through old auto-
Random toxicology testing in the workplace, schools, mobile radiators, according to Morgan et al., where it
and other places has been challenged on various legal comes into contact with lead from soldered joints. So
grounds, but the courts have supported the need for what common is this problem that illegal whiskey is “an im-
is viewed by many as an erosion of personal liberties portant and unappreciated source of lead poisoning”
brought on by this process. Critics of drug testing in the (p. 1501) in some parts of the country.
workplace point to the episode in the early 1990s where In today’s world, contaminants are commonly found
38 different federal agencies tested 29,000 employees at a in the drugs sold on the street. If the drug was manufac-
cost of $12 million, only to find just 155 individuals tured in an illegal laboratory, a simple mistake in the
whose urine samples were positive for illicit drugs (mostly production process might produce a dangerous or even
cannabis) (Leavitt, 2003; Petersen, 2000). This was ac- a lethal chemical combination. For example, the illicit
complished at a cost of $77,000 per positive sample, production of methamphetamine requires only a few
hardly a cost-effective approach to the problem of workers common chemicals and a basic knowledge of chemistry.
engaging in illicit drug use (Petersen, 2000). But the use of lead acetate in one of the more common
In the past, agencies such as the National Institute production processes for illicit methamphetamine can
on Drug Abuse (NIDA) have argued that if every worker contaminate the drug with high levels of lead if the
in the United States were to be tested for alcohol/drug “chemist” should make a mistake (Norton, Burton, &
use at once, 14%–25% would test positive for a con- McGirr, 1996).
trolled substance (Vereby, Buchan, & Turner, 1998). In the mid-1970s heroin addicts in California were
Such figures are used by proponents of urine toxicology sold a compound that was, they were told, synthetic
testings to justify the use of this procedure. However, heroin. These addicts injected the drug and quickly
Leavitt (2003) has challenged the foundation on which developed a drug-induced condition very similar to
this (and similar) estimates rests, pointing out that these advanced cases of Parkinson’s disease (Kirsch, 1986).
are assumptions, not research study results, and thus it Chemists discovered that as a result of a mistake in the
is possible that only a small proportion of those tested production process, what had been produced was not
would show evidence of illicit drug use in their urine. 1-methyl-4-4-phenyl-4-pro-pionoxy-piperidine (a syn-
thetic narcotic known as MPPP), but the chemical
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (known as
Unseen Victims of Street Drug Chemistry MPTP).1 Unfortunately, once in the body, the enzyme
Because their use is illegal, many of the drugs of abuse monoamine oxidase biotransforms MPTP into a neuro-
are produced in illicit laboratories. Product reliability is toxin known as 1-methyl-4-phenylpyridinium (MPP+),
hardly a strong emphasis in these clandestine, illegal which kills the dopamine-producing brain cells in the
drug laboratories, providing stark reminders of the
problems from the Prohibition era. During Prohibition, 1The very names of these chemicals gives the reader some idea as to how
a very real danger was that the “bathtub gin” or “home easy it would be for chemists to make mistake in their manufacture.
nigrostriatal region of the brain (Langston & Palfreman, each atom in relation to every other atom in the chemi-
1995; Lopez & Jeste, 1997). Subsequent research re- cal chain of that drug molecule. After review by the
vealed that the loss of these same neurons is implicated Food and Drug Administration, the pharmaceutical
in the development of Parkinson’s disease. Thus, in- company may then be granted a patent on that drug
directly, this mistake in the manufacture of illicit molecule for a specific period of time.
narcotics allowed researchers to make an important When law enforcement agencies wish to classify a
discovery in the cause of Parkinson’s disease. Unfortu- drug as an illicit substance, they must go through much
nately, because MPTP was sold on the street, many opi- the same process. Chemists must identify the chemical
ate abusers died as a result of a simple mistake in the structure of the new drug molecule and record the
process of making what was supposed to be heroin. exact location of each atom in relation to every other
Others developed a lifelong drug-induced disorder very atom in the chemical chain of that drug molecule. This
similar to that of Parkinson’s disease. process can take several months but will yield a chemi-
There is no way to determine how many people have cal formula that can then be used to identify that spe-
suffered or died because of other impurities in illicit cific compound as an illicit substance.
drugs, but such reports are quite common. In France, Because drug molecules are very complex, it is often
some samples of heroin were found to be contaminated possible to add, rearrange, or remove some atoms from
with the heavy metal thallium, resulting in the death of the “parent” drug molecule without having much impact
at least one individual (“Bald Is Not Beautiful,” 1996). on the original drug’s psychoactive effect. Depending on
Nor is the problem of contaminated drugs limited to the exact chemical structure of the parent drug, it is
narcotics or cocaine. Most of the drugs “intended for possible to develop dozens or even hundreds of varia-
popular recreational use are most often produced in tions of the original drug molecule. For example, there
clandestine laboratories with little or no quality control, are 184 known potential variations on the parent drug
so generally speaking users cannot be sure of the purity from which the hallucinogen MDMA was developed
of what they are ingesting” (Hayner & McKinney, 1986, (“Market Update,” 1993). These variations on the origi-
p. 341). Where illicit drugs are concerned, “misrepre- nal drug molecule are called analog drugs, or analogs.
sentation is the rule” (Brown & Braden, 1987, p. 341). Many of the drug analogs will have no psychoactive effect
For example, Kalasinksy, Hugel, and Kish (2004) found and thus are of little interest to the illicit chemists who
that what was being sold on the streets of Toronto as produce chemicals for sale on the street. Some drug
MDMA was often MDA (a related compound) or analogs will be abusable, and thus would be of interest
methamphetamine. Only 30% of the pills sold as to illicit drug producers. A drug analog might be less
MDMA in Europe and the United States were found to potent than the parent compound, equally potent, or
actually contain this compound, with other chemicals even in some cases more potent than the original
such as PCP, ketamine, paramethoxyamphetamine, chemical. For example, some of the analogs of the
methamphetamine, dog worm pills, and prescription pharmaceutical fentanyl are more powerful than the
meds also being found (“Dance Safe,” 2001; Walton, original drug.
2002). The average user cannot, without a detailed The main point is that if just one atom has been
chemical analysis, be sure what the substance pur- added or moved around on the chemical chain, the
chased actually is, whether it is contaminated, or how chemical structure of the drug analog will be different
potent it might be. Thus, one should not automatically from that of the parent drug. If the parent drug has been
assume that any illicit drugs are actually what they were classified as an illegal substance, by removing just one
reported to be. Indeed, without a chemical analysis one atom from the chemical chain of the original drug
should not even assume that the chemical is safe for chemists can create a “new” drug that has not been out-
human consumption. In the world of illicit drug use, it lawed. For the sake of discussion, assume that the sim-
is indeed a case of “let the buyer beware.” plified drug molecule in Figure 36.1 has been
outlawed as an illegal hallucinogen.2
Notice that in the simplified example, the parent
Drug Analogs: The “Designer” Drugs drug “molecule” has only four atoms, not the thousands
When a pharmaceutical company develops a new com- of atoms found in some actual chemical molecules.
pound for use in the fight against disease, the company
applies for a patent. To do so, the pharmaceutical com- 2
Simplified drawing: Real drug molecules are much more complex
pany must identify and record the exact location of than this.
A B C A B C
D D E
FIGURE 36.1 Parent Molecule FIGURE 36.3 Second Analog
E A B C
A B C E D
FIGURE 36.4 Third Analog
D Notice that there is a very subtle difference in the

chemical structure of the last two hypothetical drug
molecules. In each case, however, in the eyes of the
FIGURE 36.2 First Analog
law, they are “different” drugs. Technically, this is a new
drug, which is not covered by the law that prohibited
the parent drug. If this drug molecule were to be out-
However, a drug with the chemical structure in Figure lawed, the street chemist might again change the drug
36.2 would technically be a different drug, since its mo- into something like Figure 36.4.
lecular structure is not exactly the same as the first The drug “molecule” used in this example was a
chemical. very simple one, with only five “atoms.” However, even
This chemical would be a drug analog of the parent with this simplistic example, it was possible to produce
drug. There is an obvious difference in the chemical several different analogs of the original parent mole-
structure of the first and the second drug. The new cule. When you stop to consider that many of the psy-
atom that was added to the chemical structure might choactive drugs have drug molecules that contain
not make the analog more potent than the parent com- many hundreds or thousands of atoms, the number of
pound, but it will change the chemical structure of potential combinations is rather impressive.
that drug just enough that it is not covered by the law
that made the original parent drug illegal. For this ana-
log to be declared illegal, researchers would have to
Some Existing Drug Analogs
identify the location of every atom in the second com-
pound and the nature of the chemical bond that held It should be no surprise that street chemists manipulate
that atom in place. Then law enforcement officials the chemical structure of known drugs of abuse in the
would have to present their findings to the appropriate hopes of coming up with a new drug that has not yet
agency for the drug analog to be outlawed. This is a been outlawed. Some of the following drug analogs
process that might take months or even longer. When have been outlawed by government agencies, while
this happens, it would be a simple matter to again action against some of the other compounds is still
change the chemical structure a little bit, build a new pending.
analog, and start the whole cycle over again. For Analogs of the amphetamines. The amphetamine
example, the new analog might look like the one in molecule lends itself to experimentation, and several
Figure 36.3. analogs of the original molecule have been identified
by law enforcement agencies. Some known analogs of the (or PHP), (1-piperidinocyclohexanecarbonitrile) (or
amphetamines include 2,5-dimethoxy-4-methylamphet- PCC), and Eu4ia (pronounced “euphoria”), an
amine, or the hallucinogenic DOM (Scaros, Westra, & amphetamine-like drug synthesized from legally pur-
Barone, 1990). MDMA, also known as “ecstacy,” is itself chased, over-the-counter chemicals (Scaros et al.,
a drug analog of the amphetamine family of chemicals. 1990).
There are 184 identified analogs of the parent drug of Ketamine. The compound (2-o-chorophenyl)-2-
MDMA, some of which are known to have a psychoac- methylamine cyclohexanone) is a chemical cousin to
tive effect on the user. PCP. It was classified as a Schedule III3 compound in
The drug 3,4-methylenedioxyamphetamine, or 1999 (McDowell, 2005). Ketamine itself is a surgical
MDEA, is another drug analog of the amphetamine anesthetic which, because it does not cause respiratory
family. When the hallucinogen ecstacy (or MDMA) or cardiac depression, is of value when other anesthet-
was classified as a controlled substance in 1985, many ics cannot be used (McDowell, 2005; Walton, 2002).
street chemists simply started to produce MDEA. The Although it is possible to manufacture ketamine in
chemical structures of MDEA and MDMA are very illicit laboratories, it is quite difficult to do so and so
similar, and the effects of MDEA are much like those of most of the ketamine found on the streets is diverted
MDMA (Mirin, Weiss, & Greenfield, 1991). This sub- from human or veterinary supplies (Gahlinger, 2004;
stance is often sold under the name of Eve. There have McDowell, 2005).
been isolated reports of death associated with MDEA Neuropharmacologists believe that ketamine binds
use, and it is not known what role, if any, MDEA had in at an NMDA receptor on the neuron, forcing a calcium
these deaths. Further, the long-term effects of MDEA ion channel to close (McDowell, 2004, 2005). This
are still unknown. reduces the rate at which that neuron can fire, thus
A recent addition to the list of illicit stimulants being suppressing the action of that neuron. Ketamine has
produced by street chemists in this country is meth- a fairly large therapeutic window (McDowell, 2004,
cathinone, or Kat. However, Kat is also a designer drug. 2005). Because it does not suppress cardiac or respira-
Another derivative of the amphetamines is a compound tory function at recommended doses, ketamine is po-
known as Ya ba (“crazy medicine”), which is used in tentially useful in combat, post-earthquake, or other
southeast Asia, especially in Thailand where up to 5% situations where an emergency anesthetic is necessary
of the population is reported to use it (Hilditch, 2000; (Schultz, 2002). It also has been used as an experimen-
Kurutz, 2003). It has recently been imported into the tal drug for treatment-resistant major depression with
United States and is occasionally found on the West promising results (Szalavitz, 2007; Zarate et al., 2006).
Coast. This compound, which includes ephedrine, caf- When used as a surgical anesthetic, ketamine may
feine, methamphetamine, lithium (obtained from be introduced into the body by intravenous injection,
extended-use batteries), and some chemicals from intramuscular injection, or orally. Abusers may ingest
household cleaning products, among others, provides ketamine in oral form or use a powdered form of the
an extended (8- to 12-hour) “high.” The compound compound to mix with tobacco or marijuana for smok-
can be inhaled, smoked, or used transdermally in the ing (Gahlinger, 2004). On rare occasions the powder is
form of a skin patch, but it is usually taken orally. Long- also used intranasally, which abusers refer to as a
term use seems to contribute to suicidal/homicidal im- “bump” (Gahlinger, 2004).
pulses, and so most abusers follow a pattern of taking Ketamine is a colorless and odorless compound,
the drug for 2–3 days, followed by a day or two of sleep. qualities that in combination with its rapid onset of
Very little is known about the toxicology of Ya ba, which effects and its ability to interfere with normal memory
has not been subjected to controlled research by function makes it an attractive “date rape” drug to per-
physicians. sons inclined to use such compounds (Gwinnell &
Analogs of PCP. PCP is a popular “parent” drug mol- Adamec, 2006). When ingested by abusers, the effects
ecule for illicit chemists to experiment with. To date, at of ketamine begin in 30–45 minutes and are dose-
least 30 drug analogs of PCP have been identified, dependent (Freese, Miotto, & Reback, 2002; Gahlinger,
many of which are actually more potent than PCP itself 2004). Lower doses produce a feeling of euphoria, visual
(Crowley, 1995; Weiss, Greenfield, & Mirin, 1994). hallucinations, a sense of unreality, depersonalization,
These are the drugs N-ethyl-1-phenylcyclohexylamine and vivid dreams (Freese et al., 2002; Gahlinger, 2004).
(also known as PCE), (1-(1-2-thienylcyclohexyl) piperi-
dine) (or TCP), (1-(1-phenylcyclohexyl)-pyrrolidine) 3
See Appendix Four.
Higher doses will obviously cause anesthesia, since this window limited its usefulness, and further research into
is the major use of this compound. It is believed that its uses was discontinued. Currently, it is only rarely
the typical abuser will ingest a dose that is about half as used by physicians in Europe as a presurgical agent
strong as that needed to cause anesthesia, or about (Galloway et al., 1997).
1/60th the LD50 for this compound (McDowell, 2004, There was little interest in GHB by illicit drug
2005). abusers until the 1990s, when bodybuilders began to
The half-life of ketamine is 3–4 hours. The drug is use it as a legal alternative to the anabolic steroids.
extensively biotransformed prior to excretion from the Preliminary evidence that GHB might possibly stimu-
body, and only 3% of a single dose is excreted un- late the production of growth hormones, and the fact
changed in the urine. In abuse situations, standard that it was still legal to purchase in the United States fo-
urine toxicology testing might not detect ketamine, and cused attention on this compound. But in 2000 GHB
so it will be necessary to request a special assay to detect was classified as a Schedule I4 substance (Gahlinger,
metabolites of this compound in the urine. Long-term 2004; Ingels, Rangan, Bellezzo, & Clark, 2000). In re-
use, especially at high doses may result in drug-induced sponse to the government’s ban on GHB, users simply
memory problems (Gahlinger, 2004; Jansen, 1993). switched to any of a number of legal compounds that
Some of the side effects of ketamine abuse include a are biotransformed into GHB after ingestion or illicit
sense of psychological dissociation and/or a trance- sources of this compound. Instructions on how to man-
like state that appears similar to catatonia, panic states, ufacture GHB are also available over the Internet, allow-
and at higher doses hallucinations, hypertension, tachy- ing amateur chemists to produce their own stockpiles of
cardia, respiratory depression, paranoia, and apnea the drug if they should wish to do so (Gahlinger, 2004;
(Gahlinger, 2004; McDowell, 2004, 2005; Walton, Li, Stokes, & Woechener, 1998; Moore & Ginsberg,
2002). Some users report that they have experienced 1999; Smith, 2001). However, there are a number of
flashback-like experiences days or even weeks after their different formulas available on the Internet and the pu-
last use of this compound (Gahlinger, 2004; McDowell, rity and potency of the GHB produced will vary with
2005). the formula used making overdose a very real danger
Aminorex. For a number of years, the drug analog for the user; 26% of regular GHB abusers have over-
2-amino-4-methyl-5-phenyl-2-oxazoline has appeared on dosed on the compound at least once (Rosenthal &
the streets, from time to time, usually under the guise of Solhkhah, 2005).
methamphetamine (Karch, 2002). This compound is Small amounts of GHB are normally found in the
derived from a diet pill sold in Europe under the brand human kidney, heart, muscle tissue, and the brain
name of Aminorex in the 1980s, and it is easily synthe- where it is thought to function as a neurotransmitter
sized (Karch, 2002). Aminorex was classified as a Sched- (Drummer & Odell, 2001; McDowell, 2005). In the
ule I compound in April of 1989 (Karch, 2002). brain, GHB is thought to help mediate sleep cycles and
The effects of the drug are not well known at this body temperature, control cerebral glucose metabo-
time, but available evidence suggests that it is a CNS lism, and possibly play a role in memory formation
stimulant, with effects similar to those of the ampheta- (Gahlinger, 2004). When abused, GHB is usually in-
mines (Karch, 2002). Following a single oral dose of gested orally as it is well absorbed from the gastrointesti-
Aminorex, peak blood levels are seen in about 2 hours, nal tract, although it may also be directly injected into
and its half-life is approximately 7.7 hours (Karch, the venous system. GHB’s effects begin 10–30 minutes
2002). There is no clinical research into the effect of il- after ingestion (Gahlinger, 2004; Klein & Kramer,
licit forms of 2-amino-4-methyl-5-phenyl-2-oxazoline 2004). Peak plasma levels of GHB are seen within
on the human body, and the potential for harm from 20–40 minutes of a single oral dose, and it has a half-life
Aminorex-like compounds available on the street remains of about 20 minutes (Drummer & Odell, 2001; Karch,
unknown. 2002). If the drug has been mixed with food, its effects
Gamma hydroxybutyric acid (GHB). Neurochemists might take as long as 60 minutes to develop (Gahlinger,
first synthesized gamma hydroxybutyric acid (GHB) in 2004). Depending on the dose ingested, the effects will
1960 while conducting research on the neurotrans- last for 3–6 hours, with larger doses having a longer du-
mitter GABA. Initially, there was some interest in the ration of effect (Klein & Kramer, 2004; Rosenthal &
possible use of GHB as a pre-anesthetic agent, but the Solhkhah, 2005).
vomiting and seizures that occurred when patients re-
covered from its effects and its narrow therapeutic 4See Appendix Four.
The subjective effects of GHB are similar to those typical therapeutic dose, unintentional overdose with
experienced with alcohol (Freese et al., 2002; McDowell, GHB is common (Commission on Adolescent Sub-
2005). Users report a sense of euphoria, which at higher stance and Alcohol Abuse, 2005; McDowell, 2005). The
doses progresses to dizziness, hypersalivation, hypotonia, very small therapeutic window for GHB becomes even
and amnesia (Gahlinger, 2004). When GHB is mixed smaller when it is mixed with other CNS depressants
with alcohol, its sedating effects are enhanced, and such as alcohol (Commission on Adolescent Substance
because of this effect it has gained favor as a “date rape” and Alcohol Abuse, 2005; McDowell, 2004).
drug. Users who use it as a sleep aid report rebound in- Long-term abusers can become physically depen-
somnia and a period of reduced alertness that develops dent on GHB. Following periods of protracted use,
2–3 hours after the drug was ingested. This effect is withdrawal symptoms such as anxiety, tremor, insom-
thought to be caused by the drug’s rapid elimination nia, nausea, tachycardia, and hypertension have been
from the body (Freese et al., 2002). Unfortunately, many reported (Freese et al., 2002; Klein & Kramer, 2004;
law enforcement officials view the victim of a GHB- Rosenthal & Solhkhah, 2005). These symptoms usually
facilitated date rape as an unreliable witness because of start about 12 hours after the last dose and continue for
drug-induced changes in perception and anteriograde about 12 days following the last use of GHB (Olmedo &
amnesia (Abramowitz, 2004). Further, GHB cannot be Hoffman, 2000). In addition to these withdrawal symp-
detected by standard urine toxicology tests, although if toms, there have been reports of a delirium tremens–like
a urine sample is collected within 12 hours of the time withdrawal process that begins within 24 hours of the last
it was ingested and special tests are conducted, it might dose and continues for up to 15 days in heavy abusers
be found (Abramowitz, 2004; Grinnell & Adamec, who abruptly discontinue the drug (Freese et al., 2002;
2006). Rosenthal & Solhkhah, 2005).
Researchers are still not certain how GHB works in Conservative medical care is the best treatment for a
the body. The GHB molecule is known to be similar to GHB overdose or addiction, although intubation and
GABA, but in spite of this similarity it has limited effect physical restraints may be necessary in extreme cases
on the GABA receptors in the brain. At low dosage (Chin et al., 1998; Miro, Nogue, Espinoza, To-Figueras,
levels GHB is thought to inhibit the release of & Sanchez, 2002). During the process of biotransforma-
dopamine in the brain, while at high levels it has the tion, most of the drug is transformed into carbon dioxide
opposite effect of stimulating the release of dopamine. and only 2%–5% is excreted from the body in the urine
Clinical evidence suggests that at doses of 0.1–1.5 mg/kg (Drummer & Odell, 2001; Galloway et al., 1997). The
GHB is able to induce a sleep-like state in the user with elimination half-life of GHB is only 27 minutes (Li et al.,
both delta and REM sleep being initiated (Li et al., 1998). Following death, natural biochemical processes
1998). When used at doses of around 10 mg/kg,5 GHB produce significant amounts of GHB in the blood of the
can induce a sense of euphoria and amnesia, and can deceased, making the identification of GHB-related
lower inhibitions. Some abusers report experiencing death by toxicology testing very difficult (Drummer &
nausea, headaches, itching, and vomiting at this dosage Odell, 2001).
level as well (Rosenthal & Solhkhah, 2005). It is rare for GHB to be used alone, which is unfortu-
Doses of 20–30 mg/kg cause drowsiness and sleep in nate since GHB will interact with many other com-
addition to the effects seen at lower doses. When dosage pounds. Its effects are intensified by the concurrent use
levels of 40–50 mg/kg are used, the individual will expe- of other CNS depressants, such as alcohol, hydrocodone,
rience sleep. Dosage levels of 60–70 mg/kg cause deep or the benzodiazepines (Klein & Kramer, 2004). When
coma and possibly seizures (Chin, Sporer, Cullison, used concurrently with the methamphetamines, GHB
Dyer, & Wu, 1998; Koesters, Rogers, & Rajasingham, may cause seizures (Smith, 2001). Patients taking any
2002). Potential side effects of GHB abuse include nau- of the antiviral drugs known as protease inhibitors
sea, vomiting, cardiopulmonary depression, tunnel should not use GHB, for these antiviral compounds
vision, ataxia, confusion, agitation, hallucinations, alter the liver’s ability to biotransform many drugs, in-
seizures, and respiratory failure, symptoms that indicate cluding GHB (Drummer & Odell, 2001; Harrington,
a need for immediate medical attention (Commission Woodward, Hooton, & Horn, 1999).
on Adolescent Substance and Alcohol Abuse, 2005). Phenylethylamines. There are more than 250 mem-
Because the LD50 for GHB is only about five times the bers of this family of compounds, which include the
naturally occurring compound mescaline found in the
5
Which means 10 mg per kilogram of body weight. peyote cactus of the American southwest, MDA, and
MDMA (Haroz & Greenberg, 2005; Strassman, 2005). Sharma, 2005; Muller, 2005). Some compounds in this
Of the various synthetic phenylethylamines, a com- group are thought to be able to induce the “serotonin syn-
pound called Nexus is perhaps the best known (Boyer, drome” (Boyer, 2005). There may be a synergistic effect
2005). Nexus, or 2,5 dimethoxyphenethylamine, is usu- between Foxy and compounds such as GHB, ketamine,
ally ingested orally. A single oral dose of 10–20 mg of and marijuana, but little is known about its pharmacol-
2,5 dimethoxyphenethylamine will cause the user to ex- ogy or potential for harm. The best medical treatment is
perience intoxication, euphoria, and visual distor- supportive care, and there is little information about
tions/hallucinations for 6–8 hours. Side effects include how to block the drug’s effects or long-term conse-
nausea, abdominal cramps, pulmonary problems, and quences of tryptamine abuse.
cough. Nexus is not intended for human use and is ille- 2C-T-7. The chemical formula for this compound is
gal in the United States; virtually nothing is known 2,5-dimethoxy-4-(n)-propylthiophenethylamine and it
about its toxicology at this time (Karch, 2002). is sometimes called 7-Up or “Tripstasy” (Boal, 2002).
Another member of the phenethylamine family of Very little is known about this compound, which is a
compounds is 2C-T-7, known by the street name “Blue member of the phenethylamine family of compounds.
Mystic” (Boyer, 2005). In addition to the visual halluci- The compound is about 12 times as potent as mesca-
nations that are desired by the abuser, this compound line in terms of psychoactive potential. However, this
can cause vomiting, cramps, seizures, and possible compound has a narrow therapeutic window, and the
death from aspiration (Boyer, 2005). difference between an effective dose and a toxic dose is
Tryptamines.6 The tryptamines are a family of about only a matter of micrograms. It is slowly becoming pop-
200 different compounds with chemical structures simi- ular among those who attend “Rave” parties.
lar to psilocybin, psilocin, and bufotenine, hallucinogens Psilocybin. This compound is found in the mush-
that enjoyed varying degrees of popularity in the 1960s room Psilocybe mexicana found in northern Mexico
and 1970s and have since been classified as Schedule I7 and the southwestern United States. The Aztecs called
substances by the Drug Enforcement Administration psilocybin the “Flesh of the Gods,” suggesting that they
(DEA) (Haroz & Greenberg, 2005). One member of this were quite familiar with the ability of this compound to
family of drugs is the compound 5-MeO-DiPT (short for induce a mystical state of mind in the user (Griffiths,
5-methoxy-N,N-diisopropyltryptamine), known by abusers Richards, McCann, & Jesse, 2006). Research into the
by a variety of names, including “Foxy” (Meatherall & effects of psilocybin has been virtually nonexistent
Sharma, 2005) or “Foxy Methoxy” (Boyer, 2005; since the 1960s, and there is much to be discovered
Muller, 2005). This compound began to appear in the about how this compound brings about its effects.
late 1990s and was classified as a Schedule I substance Recent research has found that psilocybin does indeed
by the Drug Enforcement Administration (DEA) in facilitate a “mystical” experience for approximately
April of 2003 (Muller, 2005). Chemically, “Foxy” has a two-thirds of drug-naive test subjects (Griffiths et al.,
different chemical structure than MDMA, but it has 2006). Two-thirds of the subjects who had received psilo-
many of the same behavioral effects on the abuser, in- cybin under controlled conditions said that their drug-
cluding the risk for neurological damage (Muller, induced state was one of the five most meaningful
2005). experiences in their lives. High doses can induce
Little is known about the mechanism of action of seizures or confusional states, but fatalities that occur
the tryptamines (Haroz & Greenberg, 2005; Muller, after the ingestion of psilocybin usually are the result of
2005). It is known that because many of these com- accidents or suicide rather than direct effects of the
pounds are broken down by the first-pass metabolism drug on the user’s body (Filley, 2004).
effect, most of the tryptamines must either be snorted or Fentanyl. The fentanyl molecule is easy for chemists
smoked. The compound known as Foxy is an exception to manipulate, and it may be synthesized from a few
to this rule and can be ingested orally, with its effects ordinary industrial chemicals (Langston & Palfreman,
starting 20–30 minutes after it is ingested (Muller, 1995). By making just a minor change in the molecule
2005). It can cause sexual stimulation as well as mild of the parent drug, chemists can produce a fentanyl ana-
hallucinations, and side effects include restlessness, log that will extend the drug’s effects from the normal
anxiety, insomnia, and possibly seizures (Meatherall & 30–90 minutes up to 4–5 hours, or with the right modifi-
cations to the parent drug, even 4–5 days (Langston &
6Also known as indolealkylamines. Palfreman, 1995). Thus, it is a popular drug for illicit
7See Appendix Four. drug manufacturers to experiment with.
In the early 1980s, there was a series of fatal narcotic but is not understood by medicine. Some researchers
overdoses in California, as street chemists started to pro- attribute the rapid death to the narcotic itself, while
duce various “designer drugs” that were similar to the others have suggested that the user’s death is caused by
analgesic fentanyl (Hibbs, Perper, & Winek, 1991). the various chemicals added to the drug to cut or dilute
Kirsch (1986) identified nine different drug analogs of it on the street. For example, fentanyl is so potent that
fentanyl that are known or suspected to have been sold some illicit samples of the drug are made up of 0.01%
on the streets. These drug analogs range in potency fentanyl, and 99.9% “filler” (Langston & Palfreman,
from one-tenth that of morphine for the fentanyl ana- 1995).
log benzylfentanyl, to 1,000 times (Hibbs et al., 1991) It is difficult to understand the addictive potential of
to 3,000 times (Kirsch, 1986) the potency of morphine fentanyl. Dr. William Spiegelman (quoted in Gallagher,
for 3-methyl fentanyl. 1986) observed that “it can take years to become ad-
The drug 3-methyl fentanyl, also known to chemists dicted to alcohol, months for cocaine, and one shot for
as “TMF,” is thought to be about 6,000 times as potent fentanyl” (p. 26). Unfortunately, fentanyl and its analogs
as morphine (Morgan, 2005). The chemical structure continue to be a significant part of the drug abuse prob-
of fentanyl makes it possible for the drug molecule to lem in the United States, and there is no end in sight to
be snorted, much like cocaine. When used intranasally, this problem.
the drug will be deposited on the blood-rich tissues of Fry. This drug is found in limited areas in the United
the sinuses, where it will be absorbed into the general States. It is marijuana soaked in formaldehyde and
circulation. Fentanyl might also be smoked. Like co- laced with PCP (Klein & Kramer, 2004). These chemi-
caine, when fentanyl is smoked, the molecules easily cals can induce a toxic psychosis, hallucinations, delu-
cross into the general circulation through the lungs. sional thinking, panic, paranoia, reduced attention
Indeed, so rapidly is fentanyl absorbed through the span, and loss of consciousness. Brain and lung damage
lungs that it is possible for the user to overdose on the are also possible side effects of the embalming fluid
medication after just one inhalation (“Take Time to (Klein & Kramer, 2004).
Smell the Fentanyl,” 1994). Dextromethorphan. This synthetic compound, a
Obviously, given the characteristics of fentanyl, it is chemical cousin to opioids, was initially marketed in
safe to assume that analogs of this chemical will present the 1960s as an antitussive8 for mild to moderate in-
similar abuse profiles. Law enforcement officials have tensity coughs (Haroz & Greenberg, 2005). In this
struggled to deal with the problem of diversion of fen- context, patients will ingest around 30 mg of dex-
tanyl products to illicit users almost from the moment tromethorphan every 4–6 hours. Currently more than
the drug was introduced. But the drug is so powerful 140 compounds are sold in the United States with
that even small amounts have a value to illicit drug dextromethorphan (DXM) either as the primary or one
users. For example, some opiate abusers will scrape the of the primary ingredients (Bobo, Miller, & Martin,
residual medication from transdermal fentanyl patches 2005). In recent years, concentrated dextromethorphan
to obtain small amounts of fentanyl, which they then powder has become available through some Internet
smoke, inject, or use orally (Haroz & Greenberg, sources (“Escalating DXM Abuse,” 2007). Internet Web
2005). sites have also been identified that provide specific in-
Fentanyl is so potent a drug that extremely small structions as to doses and expected effects at different
doses are effective in humans. To be detected, a special dosage levels for anybody who desires this information,
test procedure to detect fentanyl in the blood or urine thus contributing to the wave of DXM abuse taking
sample must be carried out (Evanko, 1991). Routine place in this country.
drug toxicology screens easily miss the presence of such The peak ages during which DXM abuse takes
small amounts of fentanyl in the blood or urine of a sus- place is around 15–16 years of age (Bryner et al., 2006).
pected drug user (“Take Time to Smell the Fentanyl,” In contrast to the normal dosage levels identified ear-
1994). Thus, even a “clean” urine or blood drug toxi- lier, DXM abusers routinely ingest dosage levels of
cology test might not rule out fentanyl use on the part 150–2000 mg at once.
of an addict. In the brain, DXM functions as an NMDA9 channel
Some opiate abusers have been known to die so blocker. At higher than recommended doses, it can cause
rapidly after using fentanyl that they were found with the
needle still in their arms (Evanko, 1991). This phenom- 8An agent that suppresses the cough reflex.
enon is well documented in cases of narcotic overdoses, 9See Glossary.
visual, tactile, and auditory hallucinations, euphoria, and users, with the ultimate cost of that same kilogram of co-
an altered sense of time (Bobo et al., 2005; Haroz & caine being around $70,000 on the streets (Villalon,
Greenberg, 2005). At doses of 300–1,000 mg/kg of body 2004).
weight, the effects of dextromethorphan are similar to Another example of how the cost of illicit drugs is in-
those of PCP (Bobo et al., 2005). The psychoactive ef- flated at each step in the production process is the way
fects usually begin within 15–30 minutes and last for the price of illegal narcotics is determined. The farmer
2–6 hours after the drug is ingested (Haroz & Greenberg, in Pakistan who raises opium poppies might be paid
2005). Adverse consequences of dextromethorphan $90 for a kilogram of raw opium. The illicit opium is
abuse include disorientation; paranoia; auditory, tac- then cut (adulterated) at each stage of the production
tile, and visual hallucinations; slurred speech; ataxia; process that ultimately produces heroin for sale on the
tremor; nausea; nystagmus; and vomiting (Bobo et al., street. Currently in the United States, more than 25%
2005).10 A DXM overdose might produce such symp- of the contents of the typical heroin sample is made up
toms as lethargy, hyperexcitability, ataxia, slurred speech, of one or more adulterants added along the way. This is
tremor, rigidity, tachycardia, hypertension, nystagmus, usually done by mid-level or high-level drug suppliers
respiratory depression, acute psychosis, coma, and pos- to expand profits, possibly as much as 1,600 times12 the
sible death from cardiovascular collapse. original price of the opium (Coomber, 1997; Schuckit,
2006). Street samples of illicit heroin in the United
States have been found to range from 12% to 71% pure
Adulterants heroin (“How They Smack Up,” 2005).
It is important to keep in mind that product reliabil-
Another consequence of the prohibition against the ity or safety is hardly a priority for illicit drug manufac-
recreational chemicals is that most illicit drugs are rarely turers. Adulterants are simply sold to the individual
sold in their pure form to the user. The typical sample of intermixed with the desired drugs. For example, less
cocaine sold on the street, for example, ranges from than 50% of the MDMA tablets sold on the street actu-
10%–50% pure, with only rare samples reaching 70% ally contain that compound, and research has shown
potency (Gold & Jacobs, 2005). Intermixed with the co- that compounds such as caffeine, aspirin, cocaine,
caine are various compounds known as adulterants. PCP, LSD, opiates, GHB, ketamine, dextromethor-
Adulterants are mixed with the drugs being sold for a va- phan, and paramethoxyamphetamine (or PMA) have
riety of reasons. Some compounds are made in illicit been sold to unsuspecting drug abusers as MDMA
laboratories, and mistakes in “cooking” the batch of a (Grob & Poland, 2005).
drug can result in adulterants becoming intermixed Adulterants are important because of the damage
with the drug being manufactured. they do to the body. When a person injects an illicit
Most commonly, adulterants are added by middle- compound, the adulterants are introduced directly into
and upper-level drug dealers to increase their profits. the circulation, bypassing the defensive acids and en-
This process is known as cutting the drug (Coomber, zymes of the digestive tract (Leavitt, 2003). Fortunately,
1997). For example, by adding an ounce of an inert sub- in spite of persistent rumors, there is little evidence that
stance to an ounce of pure cocaine, the dealer obtains illicit drug distributors are adding substances such as
two ounces of 50% pure cocaine that he or she can then ground glass or dust from bricks to compounds being
sell. The adulterants added at each stage of the drug man- sold to drug abusers (Coomber, 1997). Intuitively, it
ufacture and distribution process inflate the price of the does not make much sense for a drug dealer to kill his
compound at each stage, increasing profits. For example, customers—at least not immediately—and such reports
the coca paste that brought the farmer in South America appear to be more urban legends than reflections of
$1,000 a kilogram11 will be adulterated time and time truth.
again, until it is about 45% pure when it is sold to illicit Identified adulterants seem to fall into one of five
categories: (a) various forms of sugar, (b) stimulants,
10Another possible adverse consequence is a toxic reaction to com- (c) local anesthetics, (d) toxins, and (e) any of a num-
pounds such as acetaminophen that are mixed with the dex- ber of inert compounds added to give the product
tromethorphan, as are commonly found on over-the-counter cold
and flu medications some adolescents ingest in their quest to obtain
bulk. Some of the compounds that have been found in
sufficient DXM to cause the effects outlined above. The dangers of samples of illicit cocaine include mannitol, lactose,
an acetaminophen overdose are discussed in Chapter 18.
11 12Or 1.6 million percent over the original cost of the opium.
Approximately 2.4 pounds.
glucose, caffeine, lidocaine, amphetamines, quinine, they cause micro-emboli that damage such organs as
and even heroin (Gold & Jacobs, 2005). the heart, eyes, and the lungs (Greenhill, 2006).
Marijuana, when purchased on the street, is also fre-
quently adulterated. It is not uncommon for up to half
Drug Use and Violence:
of the “marijuana” to be seeds and woody stems, which
must be removed before the marijuana can be smoked.
The Unseen Connection
Further, the marijuana may be laced with other com- Researchers have recently discovered what police officers
pounds ranging from PCP, cocaine paste, or opium to have long known: There is a relationship between sub-
toxic compounds such as insect spray (Scaros et al., stance abuse and violence. As a group, substance abusers
1990). Marijuana samples have also been adulterated are 12–16 times as likely to resort to violence as the gen-
with dried shredded cow manure (which may expose eral population (Marzuk, 1996). Approximately 50% of
the user to salmonella bacteria) as well as herbicide all sexual assaults are committed by men under the in-
sprays such as paraquat (Jenike, 1991). Other sub- fluence of alcohol (Abbey, Zawacki, Buck, Clinton, &
stances reportedly found in marijuana samples include McAuslan, 2001), while 26% of violent offenders were
alfalfa, apple leaves, catnip, cigarette tobacco, hay, under the influence of alcohol when they committed
licorice, mescaline, methamphetamine, opium, pipe their crime (Nace, 2005b).
tobacco, straw, wax, and wood shavings (Schauben, For a number of reasons, the amphetamines and co-
1990). caine tend to predispose the user toward violence. Gold
Some of the compunds that have been intermixed and Jacobs (2005) observed that cocaine abusers are at
with illicit cocaine samples include13 lidocaine, diphen- significantly higher risk for premature death from both
hydramine, ephedrine, phenylpropanolamine, aceta- homicide and suicide. There are a number of reasons
minophen, methaqualone, codeine, boric acid, heroin, for this: Cocaine users tend to associate with people
aspirin, mannitol, dextrose, starch, benzene, and ace- who are more likely to respond with violence and are
tone (Roth, Benowitz, & Olson, 2007). Identified adul- less likely to avoid situations where violence might
terants found in illicit PCP include14 benzocaine, occur. Further, individuals under the influence of co-
procaine, caffeine, ketamine, magnesium sulfate, am- caine might behave in ways that trigger others to re-
monium chloride, and toluene (Roth et al., 2007). The spond violently to them, resulting in what is known as a
list of adulterants identified in illicit samples of heroin victim-precipitated homicide.
includes15 thepaine, acetylcodeine, quinine, phenobar- The disinhibition effects of many recreational
bital, methaqualone, lidocaine, caffeine, diazepam, drugs may also account for some of the observed ten-
acetaminophen, fentanyl, Doxepin, arsenic, strychnine, dency toward violence among alcohol/drug abusers.
vitamin C, toluene, ethanol, and acetone (Roth et al., As discussed in Chapter 7, alcohol is a common factor
2007). in violent behaviors. For example, “more than half”
When a drug abuser uses a compound that has been (Kermani & Castaneda, 1996, p. 2) of those who com-
adulterated, some or all of the adulterants are intro- mit homicide were actively using chemicals at the time.
duced into his or her body, increasing the health risks But this does not automatically mean that alcohol
associated with chemical abuse. This is the primary rea- caused the homicide. Many homicides were planned in
son that “pharmaceuticals” are so highly prized among advance, and the murderer then drank to bolster his or
illicit drug users. Pharmaceuticals are of a known qual- her courage before committing an act that had already
ity and potency, and they are also unlikely to be con- been planned. In other cases, the murder was sponta-
taminated. But pharmaceuticals are not without their neous, brought on, at least in part, by the disinhibiting
own danger: When compounds intended for oral use, effect of alcohol. Thus, the relationship between alcohol
such as methylphenidate, are crushed and injected, the and interpersonal violence is more complex than a
talc particles are injected into the circulation, where simple cause-and-effect one.
13This
The world of illicit drug use/abuse is violent. Drug
is only a partial list. Each sample of an illicit drug would need
pushers have been known to attack customers to steal
to be analyzed by toxicologists to determine what adulterants are in-
termixed with that sample. their money, armed with the knowledge that the drug
14Same notation as above. user is unlikely to press charges. After all, when people
15This is only a partial list. To identify the adulterants in a specific engage in illegal acts (such as the use of illicit chemi-
sample of heroin, it would be necessary to submit it for chemical cals) or have obtained their money through illegal
analysis by trained professionals. channels (such as burglary), they are unlikely to report
being victimized by another criminal to the police! complex interaction between the individual’s personality,
Drug pushers have also been known to kill their cus- his or her use of chemicals, and the tendency to engage in
tomers for such unpaid drug debts and as a warning to illegal behaviors.
others who might be behind in their payments. There is strong evidence that at least some of the
At this time, there does not appear to be any end to the harm associated with chemical use/abuse is a direct result
drug-related violence. It has been suggested that if drug of society’s efforts at supply reduction (MacCaun, 1998).
use were legalized, there would be a significant decrease By making chemical use illegal, society has generated a
in the level of violence in this country. However, this is new class of criminals, and proponents have used this in-
only a theory. formation to call for the legalization of recreational
drugs. The sanctions against chemical use have resulted
in overburdened courts, overcrowded jails/prisons, and
Summary no apparent reduction in the level of illicit drug use in
The relationship between criminal activity and sub- the United States. Because of the way drugs are identi-
stance use/abuse is exceptionally complex, and in this fied and regulated in the United States, illicit drug pro-
chapter the relationship between alcohol/drug use and ducers are motivated to find new “designer” drugs; this
crime was briefly explored. Although some criminal ac- practice and the rewards reaped by sellers of recreational
tivity does seem to result from the use/abuse of recre- drugs for finding unregulated drug molecules were dis-
ational chemicals, many of those who engage in cussed. The role of adulterants in the production and dis-
criminal activity and substance use are the types of tribution of illicit drugs was reviewed and many of the
people who are prone to engage in illegal activities. more common adulterants were identified. The relation-
In such cases, the apparent relationship between sub- ship between people’s use of recreational chemicals and
stance use and criminal behavior is not causal but a their responsibility for their behavior was discussed.
CHAPTER THIRTY-SEVEN
The Debate Around Legalization
When the United States is not invading some sover- compounds that it deems inappropriate. In terms of the
eign nation—or setting it on fire from the air, which effectiveness of this policy, in the early 1950s, 60,000
is more fun for our simple-minded pilots—we’re usu- people were thought to be addicted to narcotics in the
ally busy “declaring war” on something here at home. United States (Ropper & Brown, 2005). Fifty years
Anything we don’t like about ourselves, we declare later, an estimated 1 million persons in the United
war on it. We don’t do anything about it, we just de- States are heroin dependent, and an unknown number
clare war. “Declaring war” is our only public are addicted to prescription opioids (Hasemyer, 2006;
metaphor for problem solving. We have a war on Tinsley, 2005). An estimated 8,000 people in the United
crime, a war on poverty, a war on hate, a war on litter, States begin to use illicit drugs each day, illicit drugs are
a war on cancer, a war on violence, and Ronald Rea- more plentiful than they have ever been, and people
gan’s ultimate joke, the war on drugs. More accu- are spending more for illicit drugs in this country than
rately, the war on the Constitution. they do for cigarettes (Debusmann, 2006; Dobbs, 2007;
—Carlin (2001, p. 109) Schlosser, 2003).
As future historians look back on this most curious
The comedian George Carlin, in the opinion of many, “war,” they will see that the face of the “enemy” is
is at his best when he is poking fun at social trends. shaped by religious, social, and political forces that are
However, in a very real sense, the observation quoted at only poorly understood; the war is fought with weapons
the beginning of this chapter is more of a joke on the proven to be ineffective, in which the rights of the major-
general public than most people realize for it is the ity have been trampled in order for society to impose its
truth. The “war” on drugs is almost 100 years old will on those who are, in reality, only a small minority
(Shenk, 1999). Currently, the United States is spending of the population. In terms of the cost to society, nico-
an estimated $200 billion a year on the war on drugs tine addiction is far more expensive than cocaine addic-
either directly through the criminal justice system or in- tion (Henderson, Morton, & Little, 2005), yet cigarettes
directly through such problms as drug-related health are legal whereas cocaine is illegal. The most destruc-
care expenses and lost productivity (Dobbs, 2007). At tive chemicals, alcohol and tobacco, are for the most
the end of the first century of this conflict the United part exempt from attack, while relatively benign chemi-
States, with just 4% of the world’s population, was con- cals with high social disapproval ratings are subjected to
suming two-thirds of the world’s illicit drugs (Dobbs, multipronged assaults. Entire books have been devoted
2007). Statistics such as these hardly reflect a resound- to the “war” on drugs and how it has manufactured
ing success, yet politicians continue to reaffirm their “criminals” in this country. In this chapter, the debate
commitment to following the same course year after over whether the time has come to legalize drugs is
year. discussed.
In terms of effectiveness, the war on drugs has been
compared to the Vietnam conflict of the 1960s and
The Debate Over Medicalization
1970s. In the Vietnam conflict, the observation was
made that to save a village from the enemy, one had to be Although opponents of the medicalization of certain
prepared to destroy it (Simon & Burns, 1997). In much recreational drugs speak of this suggestion as if it were
the same manner, the United States government seems the legalization of these substances, in reality medical-
to have adopted a policy of arresting and prosecuting its ization and legalization are two different concepts, as
own citizens to protect them from the scourge of using shown in Figure 37.1. For a physician to be allowed to
442
The Debate Around Legalization 443
All drugs
Legalization
remain 100%
of drug use
illegal
Medicalization
FIGURE 37.1 Medicalization and Legalization as Two Different Concepts
prescribe certain substances, such as marijuana, would moved in to take control of the emerging supply and
simply place that substance in the same status as other distribution network of alcohol to meet the demand of
prescription medications. It is not the full legalization those who desired it for personal recreational use (Gray,
of that substance but simply the use of a selected com- 1998). Their motive was personal profit; at its height
pound in the treatment of specific disease states. But the alcohol black market made up 5% of the entire
the federal government’s policy is that even conducting gross national product of the United States during the
basic scientific research into possible medical benefits Prohibition era (Schlosser, 2003). But business prac-
from compounds such as cannabis could be grounds tices were often difficult. Contract negotiations were
for arrest. In effect, the federal government has adopted often marked by gunfire, with those who resisted often
a policy affirming that (a) there are no proven uses for receiving the benefit of a decent burial. Other market-
cannabis, and (b) you cannot do research into possible ing techniques of these suppliers included bribing offi-
benefits from any compounds found in cannabis because cials to look the other way or to leave them alone, and
there are no proven uses for it. fighting with other distributors for control of various
But the issue has become more complex than this, markets.
for a federal judge has ruled that the Drug Enforce- One totally unanticipated change brought by Prohi-
ment Administration’s threat to suspend a physician’s bition was that it forced people to switch from drinking
license to write prescriptions was a violation of the beer to drinking hard liquor (Gray, 1998). In compari-
physician’s First Amendment rights under the U.S. son to the bulk, low alcohol content, and short shelf life
Constitution (“Medical Reprieve,” 2003). Thus, the issue of beer, hard liquor had a high alcohol content and less
of whether some substances might be medicalized has bulk, and it did not spoil. Before the start of Prohibition,
become rather complicated indeed. alcohol users would “sip” alcoholic beverages through-
out the day or drink beer without evidence of wide-
spread intoxication (Barr, 1999; Gray, 1998). Following
The “War on Drugs”: The Making the start of Prohibition, drinkers shifted to a “binge”
of a National Disaster pattern of alcohol use, with periods of heavy alcohol
use interspaced with periods of abstinence, with intoxi-
What history could teach us. In the 1930s, the United cation being the goal of drinking (Barr, 1999; Gray,
States carried out an experiement in social reform 1998). At the same time, alcohol users switched from
known as Prohibition in which the nonmedicinal use of beer to hard liquor, which produced the highest levels
alcohol was prohibited by law.1 Criminal elements of intoxication in the least amount of time (Gray, 1998).
In this manner, the “noble experiment” of Prohibition
1One must question this nation’s commitment to the experiment of helped to shape the drinking habits of people for gener-
Prohibition, as then-president Warren G. Harding and the U.S.
Senate both flouted the law by maintaining well-stocked supplies of
ations to come.
liquor that were continuously replaced by new shipments of liquor A similar process took place in the 1970s, although the
seized by customs agents (Walton, 2002). parallels with the Prohibition era were not discovered
444 Chapter Thirty-Seven
until much later. Researchers now believe that the in- However, in one of the great reversals of all time, just
terdiction efforts against marijuana may have caused 14 years later Congress again imposed mandatory
drug smugglers to switch from transporting marijuana prison sentences for drug-related offenses. The lessons
to cocaine (Scheer, 1994a). This theory is based on the of the past were again forgotten. Through the Sentencing
fact that pound for pound, cocaine is “less bulky, less Reform Act of 1984, Congress again mandated mini-
smelly, more compact, and more lucrative” than mari- mum prison terms. Even first-time offenders were sent
juana (Nadelmann, Kleinman, & Earls, 1990, p. 45). to prison for extended periods of time without the hope
The prohibition against recreational cocaine use has of parole. One result of the Sentencing Reform Act
also contributed to the wave of violence that spread of 1984 is that the prison system soon became filled
across the United States in the late 1980s as drug pushers with individuals serving lengthy mandatory sentences.
fought over potential markets very much like the gang In 1970, only 16% of all federal prisoners were incarcer-
members during the Prohibition era fought for the right ated because of drug-related convictions; by 1994 fully
to distribute alcohol in city after city (Hatsukami & 62% of those incarcerated in federal penitentiaries were
Fischman, 1996). there because of drug-related convictions (Nadelmann &
Yet another example of how the legal sanctions Wener, 1994; “The Drug Index,” 1995; Schlosser,
against illicit drug use have contributed to the very 1994).
problem that they were designed to solve is the current By 2001, the largest category of offenders, 21% of the
wave of methamphetamine use in this country. The estimated 1.32 million persons in state prisons, were
focus of law enforcement agencies on “mom and pop” there because of drug-related convictions, as opposed
laboratories that produced small amounts of metham- to the 13% of those incarcerated in various state prisons
phetamine for local consumption appears to have con- because of a conviction for murder or manslaughter
tributed to the development of “superlabs” producing (Doyle, 2001b). If we add in those persons arrested and
large amounts of relatively pure methamphetamine in awaiting trial, who are under the supervision of the
the form of “Ice,” which is designed to be smoked; this criminal justice system (CJS), the CJS now holds more
often replaced the less pure forms of methampheta- people with substance use problems than are found in
mine produced locally that were injected (Smith, all of the public and private treatment programs in the
2006). United States combined (DuPont, 2002). The total
Another lesson from history is from the aftermath of number of people arrested just for marijuana-related
the 1950s efforts to deal with the drug use problem. In crimes (possession, etc.) in 2001 exceeded the total
the 1950s, Congress passed a series of mandatory number of people arrested for murder, manslaughter,
minimum-sentence laws in the fight against narcotics forcible rape, robbery, and aggravated assault combined
abuse that were loosely called the “Boggs Act” (“Marijuana Arests,” 2003).
(Schlosser, 1994). These laws imposed minimum In retrospect, like the Boggs Act, the Sentencing
prison sentences for the illicit use of narcotics in this Reform Act of 1984 has been a dismal failure. Many of
country and met with almost universal acceptance. those incarcerated for drug-related crimes are first-time
In contrast to the general acceptance of the “Boggs offenders who have never had a prior conviction for any
Act” laws, the director of the United States Bureau of Pris- offense and who are sentenced to serve terms that are
ons at the time, James V. Bennett, expressed strong reser- not proportional to the offense. Consider that in spite of
vations about the act’s effectiveness. Although he had not the legal penalities in place against illicit drug abuse,
personally broken any laws in doing so, Mr. Bennett, “millions of people every year join the legions who
himself a federal employee, was subsequently followed have experimented with illegal substances” (Phillips &
by agents of the Federal Bureau of Narcotics, who sub- Lawton, 2004, p. 33). To place in perspective the fair-
mitted regular reports on the content of speeches that ness of the legal sanctions against drug abuse, consider
he gave to their superiors (Schlosser, 1994). By the late that an employee caught embezzling $10–$20 million
1960s, it was clear that Mr. Bennett was right: Mandatory from a bank would be sentenced to prison for 5 years.
sentencing did little to reduce the scope of narcotics This is the same sentence a person would receive for
use/abuse in this country. In 1970, the Boggs Act was re- possession of 5 grams of crack cocaine (Bovard, 1997).
placed by a more appropriate series of sentencing guide- If only we listened. Historians may very well con-
lines, through which a judge could assign appropriate clude that the reason for the war on drugs that has raged
sentences to defendants based on the merits of each for much of the 20th century lies not in the destructive
individual case. potential of the chemicals being abused but on the
irrational beliefs of those in command, which are often black market has evolved to ensure that these chemicals
blindly applied to the problems of society. In spite of are available to potential users, for a price (Buckley, 1996;
the lessons from the Prohibition era, the process of drug McWilliams, 1993; Nadelmann, 1989; Nadelmann &
interdiction has become one of the most enduring fea- Wenner, 1994; Walton, 2002). In a process quite simi-
tures of the war on drugs. The modern war on drugs lar to alcohol distribution in the Prohibition era, the
was shaped by President Richard Nixon in the early price for drugs is rigidly controlled by those who oper-
1970s and reflects his personal beliefs that (a) people ate the supply and distribution network—in return for
who drink do not consume alcohol for its intoxicating taking the risk of criminal prosecution for bringing the
effects but only for fun, and (b) people who used mari- drugs into this country, usually a major city, from where
juana were mainly those people who protested against they are funneled to outlying regions (Furst, Herrmann,
the then-current Vietnam conflict and thus were inter- Leung, Galea, & Hunt, 2004). For this, the modern
ested in the spread of communism (Zeese, 2002). There drug supplier at each level demands a significant profit.
were also covert racial undertones to the antidrug efforts In the mid-1990s, the supply and distribution network
of the Nixon administration, only recently discovered by was estimated to generate $50–$60 billion in profits
historians (Zeese, 2002). each year in the United States alone (Nadelmann &
But even this knowledge has not influenced the on- Wenner, 1994).
ward march toward stupidity. For example, a center- As an illustration of the profit available with illicit
piece of the current war on drugs is interdiction. The drugs, a patch of ground the size of a pool table might
possiblity that drug interdiction could be an effective yield $250,000 worth of cannabis in a year’s time at cur-
response to the problem of drug abuse/addiction over- rent market prices (Walton, 2002). Considering the
looks the fact that on a worldwide level the production effectiveness of the war on drugs in the latter part of the
and distribution of illicit drugs is a $400 billion a year 20th century, a coalition of lawyers, physicians, and
industry (United Nations, 2007). These criminal groups clergy from Washington, D.C., concluded that after
use both bribery and violence to make sure that their spending $45 billion in the last quarter of the 20th cen-
drugs reach those who are willing to pay for them (Gray, tury fighting the war on drugs “the Federal strategy has
1998). Only a very small percentage of the illicit drugs failed to curb drug use . . . drugs are cheaper and easier
sent to the United States are ever confiscated by law to get than ever” (“Drug War Is Lost,” 2005, p. 4).
enforcement officials, and drug interdiction results The war on drugs has been a dismal failure, given
only in short-term, local, reductions in the supply of that the price for heroin or cocaine in 2000 was only a
certain chemicals, which are rapidly corrected by market fraction of what it was 20 years earlier, while the po-
pressures. tency per gram of each substance was many orders of
The policy toward interdiction of drugs ignores the magnitude greater than it was in 1981. One conse-
fact that quence of this increase in potency at reduced cost is
that there were 66% more hard-core drug addicts at
the more “effective” police activity is, the more the start of the 21st century than there were at the start
[drug] prices rise, increasing the profits of smug- of the last decade of the 20th century (Falco, 2005).
gling, and the more likely it will be that drug purity Another admittedly unintended consequence of the
and concentration will also increase, to make im- prohibition against illicit drug use is that law enforce-
portation more cost-effective and detection more ment agencies have become “addicted” to the money
difficult. (Manderson, 1998, p. 589) invested in the war on drugs (Leavitt, 2003). Further,
the war contributes to the problem of police corruption.
This was a lesson that law enforcement officials could The forfeiture fiasco. During the administration of
have learned from the Prohibition era if only they had President Reagan in the 1980s, Congress enacted a law
bothered to study its history and effects. If drug interdic- that would allow authorities to confiscate property pur-
tion were to be effective, it would only increase the chased with money made from the illicit drug trade. It
profit margin of those who engage in providing recre- was not necessary for the authorities to prove that drug
ational chemicals for those who desire them. money had been used to purchase the property in ques-
As a result of the prohibition against recreational tion or that the money that had been confiscated was
drugs, their production, distribution, and sale are for the result of illicit drug trade activities. The authorities
the most part carried out by those who are by definition just had to voice their suspicion that the individual had
criminals. As with alcohol during the Prohibition era, a gained the money or property from illegal drug sales to
justify the seizure. The goal was to prevent drug dealers like Bristol-Meyers Squibb, Eli Lilly or Pfizer. And
from being able to profit from their illegal activities. it’s vital that we understand that these southern
In the time since taking effect, the “forfeiture” laws hemisphere plants and their cultivators are to blame
have been widely abused. Some police departments now because the alternative is to believe that our national
depend on money and property seized under these laws appetite for drugs is our own problem. And that’s
for at least part of their operating budget. As an illustra- just plan crazy talk. (Maher, 2002, p. 49)
tion of the level of abuse, up to 80% of the money seized
by federal authorities comes from people who are never So, rather than for politicians to admit that it is our
indicted for criminal acts, much less convicted (Leavitt, demand for drugs such as cocaine that is the problem,
2003). Police officials in at least two states (Florida and we spray defoliants on hundreds of thousands of acres
Louisiana) have been known to use minor traffic offenses of land in far-off Colombia, destroying entire eco-
as a pretense to confiscate money from motorists who spheres in the process. But the demand for cocaine is
had committed no illegal act other than the traffic rules still there, so the farmers just move over into the next
violation (Leavitt, 2003). They will claim that money in the valley to plant a new crop of coca for next year’s harvest.
driver’s wallet is “drug money” and confiscate it, forcing They are, after all, just trying to grow a cash crop that
the driver either to engage in an expensive lawsuit to re- they can sell to feed their children and buy the basic ne-
claim the money or to just accept the loss. Police cannot cessities of life—which obviously is a good reason to
be sued for damages as they are protected by the law. spray poisons on them, at least in the eyes of some.
The forfeiture laws do contain a provision that allows Manufacturing criminals. It has been argued that the
the citizen whose property was seized to seek its return, war on drugs reflects the tactics and philosophny of
but the process involves filing a lawsuit against the po- World War I era being applied to the issue of drug
lice agency that seized the money or property and then abuse in the 21st century (Walton, 2002). Just as the
proving in a court of law that the person did not obtain generals of that long-ago conflict kept sending wave
the seized items as a result of participation in some illegal after wave of soldiers into the killing fields created by
drug-related activities. This process is expensive and time- the recently invented machine gun, so do the modern
consuming, and the final cost might be several times generals of public order send greater and greater num-
greater than the property or money seized by the author- bers of citizens to jail or prison in the name of the pub-
ities. Further, the authorities are not required to pay any lic good. Indeed, the analogy is quite apt, for the
kind of interest to the owners if they can prove to the generals of public order often call their struggle a “war”
court that they were the rightful owners of the seized on drugs while sending not the drugs to prison but
property. Few people are willing to pay $4,000 in legal those who abuse them.
fees to prove that the $1,000 the police seized was right- Consider the controversy surrounding urine toxicol-
fully theirs, and thus many people who have had money ogy testing in the workplace. Employers often argue
taken by the authorities do not attempt to get it back. that even the smallest trace of a drug of abuse in an
The war on drugs as political nonsense. The war employee’s urine after an accident is evidence of drug-
against drug use is so irrational that politicians can now induced impairment, an argument that is both un-
score political points by simply making the claim that founded and widely believed (“Predicting Drug-Related
their opponent is “soft” on drugs (Maher, 2002). This Impairment,” 2004). For this reason, the employee would
claim does not have to be proven correct; one politician be blamed for the accident, not possible unsafe working
simply has to hint that his or her opponent is soft on conditions. But imagine a situation where two different
drugs to undermine that person’s campaign for office. employees had the same accident at work on successive
Another example of the irrational nature of the war days. One who is being treated for attention deficit-
on drugs is the federal government’s program to spray hyperactivity disorder (ADHD) had a prescription for an
defoliants on Colombian cropland where cocaine is amphetamine compound that was detected in his or
being grown. This is done with the blessing of the her urine, but this was not viewed as evidence of im-
Colombian government after appropriate bribes and pairment since it was a prescribed pharmaceutical. The
contributions to the ruling party. But second employee might have traces of the same am-
phetamine compound in his or her urine because of a
it’s got to be done, because some of the plants that false positive test result caused by the use of pseu-
grow in the southern hemisphere are just plain evil. doephedrine taken to control the symptoms of an
We know that because they’re not stamped with labels allergy.
The second employee might lose his or her job in this local law enforcement agencies are spending an esti-
hypothetical example because the initial positive test re- mated $68,000 per minute on drug enforcement activities
sult was not confirmed with more expensive follow-up (Sabbag, 2005). This sum of money is being spent to fight
testing, while the first employee might have no action our impulse to alter our state of consciousness, which
taken against him or her even though the urine test has been with us since prehistoric times (Phillips &
does not reveal that he or she was abusing the pre- Lawton, 2004). One very real result of the prohibition
scribed medication by taking more than the prescribed against recreational drug use is that it has served mainly
amount for the “buzz.” The war on drugs is thus quite to increase the price of the forbidden chemicals since
complicated. As the number and type of intoxicants they are under the control of a criminal element rather
available to the general public have grown, the “reper- than sold in a free market. To obtain the money neces-
toire of sanctions against them has grown more invasive sary to buy the drugs needed to feed their addiction,
and prohibitive” (Walton, 2002, p. 225). many people are forced to engage a range of crimes.
As a result of the “war,” those who engage in recre- The reason so many otherwise unremarkable citi-
ational drug use are classified as criminals, effectively zens have been classified as criminals is quite complex
turning what had been a medical problem into a legal and certainly does not reflect the pharmacological
issue. By making the use of these compounds illegal, potential for harm inherent in the recreational chemi-
individuals who indulge in their use become, by defini- cals. For example, in the 1980s, President Ronald Reagan
tion, criminals who face sanctions from the legal system. was quite frustrated with the apparent widespread
This general policy, in effect since the 1930s, has proven flouting of civil authority inherent in recreational drug
to be ineffective in the battle against recreational chem- use. Ignoring the lessons learned during the reign of the
ical use (Gray, 1998; Nadlemann, 2002; Walton, 2002), “Boggs age” (discussed earlier in this chapter), he called
yet it remains a centerpost of the government’s efforts to for a “zero tolerance” program in the early 1980s. Just a
eliminate drug use/abuse in 21st century. few years later, in 1988, Congress passed a resolution
Some political observers have suggested that per- calling for the goal of a “drug-free” America by 1995
sonal, recreational drug use (as opposed to the distribu- (Nadlemann, 2002). Legal sanctions and incarceration
tion of illicit chemicals to others) is simply a consensual were immediately imposed on those who were con-
crime, on the grounds that the individual who is using a victed of a drug-related criminal offense, even if the
recreational chemical has made a conscious choice to crime was only the possession of a single seed of a mari-
do so in a manner that does not hurt others (McWilliams, juana plant. Mandatory sentencing provisions were also
1993; Royko, 1990; Walton, 2002). By classifying indi- applied in cases where the individual had used a con-
vidual drug use as a consensual crime, it might be pos- trolled substance. The goal of such “zero tolerance”
sible to avoid the “gun battles, the corruption and the programs is to make substance use “as dreadful as pos-
wasted money and effort trying to save the brains and sible in order to discourage others from engaging in drug
noses of those who don’t want them saved” (Royko, experimentation” (Husak, 2004, p. 427). Unfortunately,
1990, p. 46). such programs have proven to be dismal failures, as by
One possible solution to the drug use problem is 1995 this nation enjoyed a greater quantity and quality
that recreational drug use be legalized, possibly with re- of illicit drugs than had existed at any point before the
strictions by the authorities as to who might dispense passage of the “zero tolerance” laws.
the compounds. This would allow some measure of But President Reagan’s stance on recreational drug
control over who has access to drugs and at what age abuse was not motivated by the potential for harm
they might be allowed to use them, in much the manner found in the compounds being abused. If this were
that access to alcohol is restricted by law. A benefit of true, alcohol and tobacco products would have been
this approach is that it would make the compounds the target of his wrath. These substances were noticably
available to anyone who wished to “sniff away his nose absent from his “zero tolerance” effort, and the pro-
or addle his brain” (Royko, 1990, p. 46) without classi- gram’s dismal failure has been quietly ignored by histo-
fying large numbers of citizens who engage in this con- rians. The statistics on heroin and cocaine in the last
sensual act as “criminals.” 20 years of the 20th century speak to this failure. In that
But such commonsense suggestions are drowned period of time, “imprisonment for drug dealing . . .
out by the strident cry that we must protect the public increased about tenfold, but the prices of cocaine and
from their own impulse to engage in recreational drug heroin [fell to] about 25% of 1980 levels” (Harrell &
use. To achieve this goal, the various federal, state, and Kleiman, 2002, p. 150). There is such a glut of cocaine
flowing into the United States at the start of the Cocaine hydrochloride, usually sold as a powder, is
21st century, compared with the amount smuggled abused mainly by middle-class users; crack is found most
into this country in the early 1980s, that even if law en- often in the ghetto areas. Federal sentencing guidelines
forcement officials were to suddenly find a way to in- require that a first-time offender with 5 grams of crack
terdict 50% of it, the price of illicit cocaine on the be sentenced to prison for 5 years whereas a first-time
street would increase by only about 5% (Reuter & offender would need to have 500 grams of cocaine
Pollack, 2006; Walton, 2002). This was demonstrated hydrochloride on his or her possession to receive a sim-
by the United States–funded coca plant eradication ilar sentence (Hatsukami & Fischman, 1996). This dis-
program in Colombia (discussed elsewhere in this tinction has contributed to inequities in prosecution
chapter), which by 2003 had resulted in a 38% reduc- and sentencing. It has been estimated that 90% of all
tion in the number of coca plants available for harvest. those incarcerated in state and federal prisons for
Yet the price of cocaine in the United States remained substance-related offenses during the administration of
unchanged (“Coca Leaf Production Decreases,” 2003). the first President Bush were either African American
The mandatory sentencing of drug offenders and the or Latino (Garrett, 2000).
whole war on drugs has become a prime example of The war on drugs as a drain on national resources. It
how the lessons of history are ignored to maintain the has been suggested that the attempt to “treat” individu-
illusion of doing something without addressing the als with substance use disorders through the courts and
causes of the problem. In the years following World criminal justice system carries with it a cost that is far
War II, some heroin dealers in the United States were out of proportion to the harm caused by the chemicals
actually executed in the government’s attempt to stem on either the individual or society (King, 2006). In 1972
the tide of narcotics abuse (Walton, 2002); the number there were an estimated 200,000 jail and prison cells in
of abusers continued to increase, and the harsh punish- the entire United States; at this time there are more
ment was soon discontinued. But by the 1980s lawmak- than 2 million jail and prison cells in this country
ers were again discussing the possibility of imposing the (Pepper, 2004). More than 400,000 people are incarcer-
death penalty for drug dealers as a deterrent, in spite of ated in state and federal prisons for violating one of the
its proven lack of effectiveness. antidrug laws—24% of the total number of people in-
Mandatory sentencing is based on the assumption that carcerated in this country (MacCoun & Reuter, 1998;
society can arrest its way out of the [drug abuse] problem Nadelmann, 2002). At the start of the 21st century,
(Correia, 2005; Simon & Burns, 1997). In spite of its many states are spending more for the construction of
widespread popularity, this policy ignores the truism that prison cells than they are for building college class-
it is impossible to punish an undesirable behavior out of rooms (Taylor, 2004).
existence (Husak, 2004; Lundeen, 2002). While treat- It is expensive to keep a person in prison. Erlich
ment for substance use problems is not the panacea (2001) offered an estimate of $93,000 per inmate per
suggested by the treatment community, mandatory sen- year in a state prison. If there are 400,000–800,000
tencing is certainly not the answer, either (Reuter & people in prison for drug-related offenses, then the
Pollack, 2006). Critics of the mandatory sentencing individual states are spending up to $74 billion a year
laws for possession of illegal substances point out that just to keep already convicted drug offenders incar-
the small-time user is usually the victim of lengthy cerated. This is in addition to money spent to fight
mandatory prison terms (Steinberg, 1994). In spite of the war on drugs. The benefits of this expenditure are
the intent of the law (which was intended to punish not clear. While substance abuse treatment programs
those involved in the process of drug distribution), mid- are required to demonstrate their effectiveness to
level and upper-level suppliers are frequently able to obtain funding, prisons are not required to do so
bargain their knowledge of who is buying drugs from (MacCoun & Reuter, 1998; Reuter & Pollack, 2006;
them for lighter prison sentences. Thus, in the United Smith, 2001). As one consequence of not requiring
States prison population, which reached a staggering prisons to demonstrate any form of effectiveness, al-
2.17 million people in 2003 as a result of mandatory though 80% of those who are incarcerated have some
sentencing requirements (Mailer, 2004), fully 52% are form of a chemical use problem, only 5% receive any
drug users or those who “deal” on the streets, while only substance abuse treatment while incarcerated (Smith,
11% are major suppliers (Dwyer 2000; Petersen, 1999). 2001).
Racial bias of the war on drugs. The Sentencing If it is such a failure, why does the war on drugs
Reform Act of 1984 had a racial/class bias built into it. continue? This is a very difficult question to answer. It has
been suggested that the “war” on drugs continues a greater variety and greater quantity of illicit drugs
“because it suits politicians to blame drug abusers for available now than at any time in history (Bovard,
many of the social problems that currently beset America; 2001; Nadlemann, 2002). As should be obvious by
by sounding tough on drugs they can sound tough on now, the social program to solve the drug abuse prob-
crime without having to address the real problems con- lem through law enforcement and interdiction has
fronting the urban poor” (Barr, 1999, p. 304). From this been a failure. However, this does not stop law enforce-
perspective, the “war” has continued as a form of polit- ment officials from trumpeting the successes of the
ical smokescreen, allowing those in power to use moral past year, or from hinting that for just a few billion dol-
insecurities and false images of what is right to fool the lars more it might be possible to eliminate the problem
population into spending money to protect itself from of drug abuse in the United States. For example, after a
mythical dangers while avoiding the real problems fac- 5-year, multibillion dollar program to try to eradicate
ing society (Barr, 1999; Gray, 1998; Leavitt, 2003). As cocaine in Colombia via airborne spraying of cocaine
support for this hypothesis, the original draft of the fields funded by the Bush administration, the purity
Federal Omnibus Crime Bill called for criticism of the and cost of cocaine in the United States remains unaf-
government’s antidrug policies to be classified as treason, fected (Chu, 2005). Yet those who are openly calling
which would then become grounds for criminal prose- the war on drugs a failure and who call for alternatives
cution (Leavitt, 2003). for this failed social policy are ignored or called
Another reason the federal government might not unrealistic.
really be interested in “winning” the war against drug The debate over legalization. For the reasons dis-
use is that it provides money to fund covert activities by cussed earlier, some citizens and political observers
government agencies. History has repeatedly demon- have suggested that perhaps at least some of the chemi-
strated that the Central Intelligence Agency (CIA) has cals now deemed illegal should be legalized. But it is
allowed, and in some cases actually encouraged and impossible to enter the debate over the legalization of
supported, the drug trade to finance insurrections or some or all of the drugs of abuse without becoming en-
armed conflict in various regions of the world (Leavitt, snared in the minefield of political agendas. The prob-
2003). The heroin and cocaine grown in such places as lem of drug abuse in the United States has reached the
Afghanistan and Central America eventually found point where the military has been recruited to help law
their way to the United States, sometimes on aircraft enforcement authorities stem the flow of illicit drugs
supplied by the CIA (Leavitt, 2003). That one agency that are being purchased by citizens of this country. In
of the federal government has taken such action should effect, the military is now at war with the citizens of this
not be surprising, since the United States government country (Walton, 2002), a sign that the issue of legaliza-
often holds itself exempt from laws passed to control the tion is exceptionally complex.
general population. During Prohibition both Congress It has been suggested, for example, that federal and
and the White House maintained their own bars, state law enforcement agencies need to keep marijuana
using supplies of alcohol seized by the Coast Guard to classified as an illicit substance, since marijuana
quench the thirst of its members (Walton, 2002). abusers make up the bulk of those classified as “drug
Summary section on the “war on drugs.” The “war on abusers” in the United States (Gray, 1998; Walton,
drugs” has continued through most of the 20th century, 2002). If this group of people were to be reclassified as
reaffirmed by every president, and while it has been a nonoffenders by the decision to legalize marijuana,
dismal failure it has cost each man, woman, and child then the number of illegal drug abusers in the United
in the United States about $133 each year (Buckley, States would instantly drop from 13 million to just 3 or
1997). A minimal estimate of $500 billion has been 4 million, a number that makes it difficult to justify
spent “fighting” the war on drugs at the federal, state, the expenditure of so many billions of dollars on enforce-
and local levels since 1980 (Falco, 2005). Yet, in spite of ment and interdiction (Dwyer, 2000; Gray, 1998; Walton,
this expenditure of time, energy, and resources, in 2002).
many regions of the country it is now easier for high Perhaps, as some federal and state law enforcement
school students to buy marijuana than it is to buy beer agencies justify their continued existence on the basis
(Bovard, 2001). of a drug “problem,” it should not be surprising to learn
In return for this investment, the past 20 years have that some of these same law enforcement agencies have
seen an erosion of traditional constitutional rights, and been known to simply manufacture data for their offi-
we are yet to become drug free (Elders, 1997). There is cial reports (Gray, 1998). In other instances, they have
utilized questionable statistical methods to prove the Portugal and Belgium, while in France, Spain, England,
need for their existence. In 1994, for example, “the Austria, and Italy an adolescent can legally purchase
Center on Addition and Substance Abuse at Columbia alcohol at the age of 16 (Barr, 1999; Peele, 1996). In
University made the shocking announcement that mar- these countries, it is felt that adolescents should learn to
ijuana smokers were eighty-five times more likely to go drink within the context of their families to learn mod-
on to cocaine than nonsmokers” (Gray, 1998, p. 177). erate, social drinking skills. In spite of this rather liberal
This figure has since been frequently cited as evidence pattern of alcohol use, these countries have rates of
that marijaua is a “gateway” drug, the use of which will child/adolescent alcohol abuse similar to those seen in
place the user on a “slippery slope” to further drug the United States.
abuse. Yet few people understand that this “fact” was One alternative to the free-market legalization pro-
uncovered by “taking the estimated number of cocaine gram so fearfully envisioned by Frances (1991) is for
users who had smoked reefer first, and dividing it by the recreational drugs to be made available through a physi-
estimated number who hadn’t (almost nobody)” (Gray, cian’s prescription (Lessard, 1989; Schmoke, 1997). This
1998, p. 177). Using such quasi-statistical methods, the is very similar to the approach adopted by England,
author pointed out, it would be possible to “prove” that where physicians who hold a special license may pre-
coffee, alcohol, tobacco, and apple pie were also “gate- scribe heroin to individuals proven to be addicted to it
way” chemicals placing the individual on a slippery (“Rx Drugs,” 1992). As a compromise for those who fear
slope to further drug abuse. the impact of legalized marijuana, the medical journal
Advocates of drug legalization point out that through The Lancet (1995) suggested the legalization of mari-
legalization an important source of revenue for orga- juana, with controls similar to those on the sale of to-
nized crime would be removed since the manufacture bacco, arguing that the criminal sanctions currently in
and transport of illicit drugs is an important source of place against marijuana only added a degree of glamor
income for criminal groups. Further, there is evidence to its use.
that drugs would lose their appeal to adolescents and Admittedly, chemical users might experience health
young adults, many of whom are drawn to substance problems. However, Curley (1995) suggested that in-
use as a form of rebellion (Barr, 1999). surance companies might be permitted to charge higher
The theory that decriminalization of a substance health insurance premiums for drug users, as they do
such as cannabis would reduce substance abuse is now for cigarette smokers. These higher health care
based on the idea that “if the appeal of drugs lies in premiums would be to cover the expense of health care
their prohibited status, then we must expect that to people who engage in such high-risk behaviors as
cannabis will soon be as fascinating as a new set of tax abusing recreational chemicals. In this way, access to
guidelines [if decriminalized]” (Walton, 2002, p. 137). the drugs could be limited while the profit incentive for
As partial evidence for this theory, in Holland, Spain, organized crime would be removed. What Lessard
and Italy, countries that have decriminalized mari- (1989) suggested, in other words, is that the problem of
juana, the cannabis abuse pattern is virtually the same drug abuse be approached from a health perspective, as
as in neighboring countries where it is prohibited it is in Holland and England.
(MacCoun & Reuter, 2001). The point is that although In contrast to these positions, however, Walton
a certain percentage of a population will want to use (2002) suggested that one immediate consequence of
marijuana regardless of its legal status, over time it will legalization would be that the number of drug abusers
become less attractive to social rebels. In 2001 Portugal might increase. The reduction in legal sanctions
decriminalized the possession of all drugs, while Canada might encourage greater numbers of individuals to en-
has decriminalized possession of small amounts of mar- gage in the abuse of chemicals now prohibited by
ijuana (Schlosser, 2003). Many other countries in the various laws. But even this price would not be unrea-
European Union are following the Dutch example of sonable since large segments of society currently being
allowing individuals to possess small amounts of mari- criminalized for nothing more than attempting to fulfill
juana for personal use (McAllister et al., 2001). their desire to become intoxicated would no longer run
Another example of what might happen if drugs afoul of the legal system, according to Walton (2002).
were legalized is New Zealand, where there are no laws Other consequences of the prohibition against drug
that prohibit minors from buying or consuming alcohol abuse. Medical sociologists have observed that because
in public if they are with their parents. There is no min- of the prohibition against drugs, users must use the
imum age requirement for the purchase of alcohol in limited supply of drugs under hazardous conditions.
Various researchers have suggested that between 1%–3% substance use/abuse should be developed with the
(Drummer & Odell, 2001) and 2%–4% (Anthony, lessons from the past kept in mind.
Arria, & Johnson, 1995) of heroin abusers die each year
from violence or infection. This death rate is 6–20 times
Summary
higher than for nonusers (Drummer & Odell, 2001).
The causes of death for intraveneous drug abusers Whether illicit drugs should be legalized and under what
include drug overdose, infections (including AIDS), conditions is a social issue, not a medical one (Brust,
malnutrition, accidents, and violence. 2004). Although legalization might not be the answer to
Section summary. Although legalization might not the problem of alcohol/drug abuse in this country, the
be the answer to the problem of alcohol/drug abuse in current policy of intradiction and punishment of those
this country, it is clear that the current policy of inter- who choose to violate U.S. substance use laws is clearly a
diction and punishment of those who violate the sub- failure. While there are no unambiguous answers for
stance use laws in the United States also has failed. addressing this problem, without question new social
There are no clear answers on how to address this prob- policies should be developed for substance use and abuse,
lem, but it is clear that new social policies addressing informed by the lessons from the past.
APPENDIX ONE
Sample Assessment
Alcohol Abuse Situation
History and Identifying Information

1 is a 35-year-old married white male from
Mr. John D County, Missouri. He is em-
ployed as an electrical engineer for the XXXXX company, where he has worked for the last
3 years. Prior to this, Mr. D was in the United States Navy, where he served for 4 years.
He was discharged under honorable conditions and reported that he only had “a few” minor
rules infractions. He was never brought before a court-martial, according to Mr. D .
Circumstances of Referral
Mr. D was seen after having been arrested for driving while under the influence of
alcohol. Mr. D reported that he had been drinking with co-workers to celebrate a pro-
motion at work. His measured blood alcohol level (or BAL) was .150, well above the legal
limit necessary for a charge of driving while under the influence. Mr. D reported that
he had “seven or eight” mixed drinks in approximately a 2-hour time span. By his report,
he was arrested within a quarter hour of the time that he left the bar. After his initial court
appearance, Mr. D was referred to this evaluator by the court to determine whether
Mr. D has a chemical dependency problem.
Drug and Alcohol Use History

Mr. D reports that he first began to drink at the age of 15, when he and a friend would
steal beer from his father’s supply in the basement. He would drink an occasional beer
from time to time after that and first became intoxicated when he was 17, by Mr. D ’s
report.
When he was 18, Mr. D enlisted in the United States Navy, and after basic train-
ing he was stationed in the San Diego area. Mr. D reported that he was first exposed
to chemicals while he was stationed in San Diego, and that he tried both marijuana and
cocaine while on weekend liberty. Mr. D reported that he did not like the effects of
cocaine and that he only used this chemical once or twice. He did like the effects of mari-
juana and reported that he would smoke one or two marijuana cigarettes obtained from
friends perhaps once a month.
During this portion of this life, Mr. D reports that he would drink about twice a
weekend, when on liberty. The amount that he would drink ranged from “one or two
beers” to 12 or 18 beers. Mr. D reported that he first had an alcohol-related blackout
while he was in the navy and that he “should” have been arrested for driving on base while
under the influence of alcohol on several different occasions but was never stopped by the
Shore Patrol.
1This case is entirely fictitious. No similarity between any person, living or dead, is intended, or should be inferred.
452
Sample Assessment: Alcohol Abuse Situation 453
Following his discharge from the navy under honorable conditions at the age of 22,
Mr. D enrolled in college. His chemical use declined to the weekend use of alcohol,
usually in moderation, but Mr. D reported that he did drink to the point of an alcohol-
related blackout “once or twice” in the 4 years that he was in college. There was no other
chemical use following his discharge from the navy, and Mr. D reports that he has not
used other chemicals since the age of 20 or 21.
Upon graduation, at the age of 26, Mr. D began to work for the XXXXX Com-
pany, where he is employed now. He met his wife shortly after he began work for the
XXXXX Company, and they were married after a courtship of 1 year. Mr. D ’s wife,
Pat, does not use chemicals other than an “occasional” social drink. Exploration of this
revealed that Mrs. D will drink a glass of wine with a meal about twice a month.
She denied other chemical use.
Mrs. D reported that her husband does not usually drink more than one or two
beers, and that he will drink only on weekends. She reported that the night he was arrested
was “unusual” for him, in the sense that he is not a drinker. His employer was not con-
tacted, but court records failed to reveal any other arrest records for Mr. D .
Mr. D admitted to several alcohol-related blackouts, but none since he was in
college. He denied seizures, DTs, or alcohol-related tremor. There was no evidence of
ulcers, gastritis, or cardiac problems noted. His last physical was “normal” according to
information provided by his personal physician. There were no abnormal blood chem-
istry findings, nor did his physician find any evidence suggesting alcoholism. Mr. D
denied having ever been hospitalized for an alcohol-related injury, and there was no evi-
dence suggesting that he has been involved in fights.
On the Michigan Alcoholism Screening Test, Mr. D ’s score of four (4) points
would not suggest alcoholism. This information was reviewed in the presence of his wife,
who did not suggest that there was any misrepresentation on his test scores. On this ad-
ministration of the MMPI, there was no evidence of psychopathology noted. Mr. D ’s
MacAndrew Alcoholism Scale score fell in the normal range, failing to suggest an addic-
tive disorder at this time.
Psychiatric History
Mr. D denied psychiatric treatment of any kind. He did admit to having seen a mar-
riage counselor “once” shortly after he married, but reported that overall he and his wife
are happy together. Apparently, they had a question about a marital communications issue
that was cleared up after one visit, which took place after 3 or 4 years of marriage.
Summary and Conclusions

At this time, there is little evidence to suggest an ongoing alcohol problem. Mr. D
would seem to be a well-adjusted young man, who drank to the point of excess after hav-
ing been offered a long-desired promotion at work. This would seem to be an unusual
occurrence for Mr. D , who usually limits his drinking to one or two beers on the
weekends. There was no evidence of alcohol-related injuries, accidents, or legal problems
noted.
Recommendations
Recommend light sentence, possibly a fine, limited probation, with no restrictions on
license. It is also recommended that Mr. D attend “DWI School” for 8 weeks to learn
more about the effects of alcohol on driving.
APPENDIX TWO
Sample Assessment
Chemical Dependency Situation
History and Identifying Features

1
Mr. Michael S is a 35-year-old divorced white male who is self-employed. He has
been a resident of County, Kansas, for the last 3 months. Prior to this, he apparently
was living in County, New York, according to information provided by Mr. S .
On the night of June 6 of this year, Mr. S was arrested for possession of a controlled
substance. In specific, Mr. S was found to be in possession of 2 grams of cocaine,
according to police records. This is his first arrest for a drug-related charge in Kansas,
although by history he has been arrested on two other occasions for similar charges in
New York State. A copy of his police record is attached to this report.
Circumstances of Referral
Mr. Michael S was referred to the undersigned for a chemical dependency evalua-
tion, which will be part of his presentence investigation (or PSI) for the charge of
felony possession of a controlled substance and the charge of sale of a controlled
substance.
Drug and Alcohol Use History

Mr. S reported that he began to use alcohol when he was 13 years of age, and that by
the age of 14 he was drinking on a regular basis. Exploration of this revealed that by the
time just prior to his 15th birthday, Mr. S was drinking on “weekends,” with friends.
He reported that he first became intoxicated on his 15th birthday, but projected responsi-
bility for this on to his friends, who by his report “kept on pouring more and more into the
glass until I was drunk.”
By the age of 16, Mr. S was using alcohol “four or five nights a week” and was
also using marijuana and hallucinogenics perhaps two or three times a week. He projected
responsibility for his expanded chemical use on to his environment, noting that “every-
body was selling the stuff, you couldn’t walk down the street without people stopping you
to ask if you wanted to buy some.”
Also, by the age of 16, Mr. S was supporting his chemical use through burglaries,
which he committed with his friends. He was never caught but volunteered this informa-
tion, informing the undersigned that since the statute of limitations has expired, he does
not have to fear being charged for these crimes anymore.
By the age of 21, Mr. S was using cocaine “once or twice a week.” He was
arrested for the first time when he was about 22 for possession of cocaine. This was when
1This case is entirely fictitious. Any similarity between any person in this report, and any person living or dead,
is entirely coincidental.
454
Sample Assessment: Chemical Dependency Situation 455
he was living in the state of . After being tried in court, he was convicted of felony
possession of cocaine and placed on probation for 5 years. When asked if he used chemi-
cals while he was on probation, Mr. S responded that “I don’t have to answer that.”
Mr. S reported that he first entered treatment for chemical dependency when he
was 27 years of age. At that time, he was found to be addicted to a number of drugs, in-
cluding alcohol, cocaine, and “downers.” Although in treatment for 2 months, at the
chemical dependency unit of Hospital, Mr. S reported that “I left as addicted
as when I arrived” and reported with some degree of apparent pride that he had found a
way to use chemicals even while in treatment. His chemical use apparently was the reason
for his ultimate discharge from this program. While Mr. S was somewhat vague about
the reasons he was discharged, he did report that “they did not like how I was doing” while
he was in treatment.
Since that time, Mr. S has been using cocaine, alcohol, various drugs obtained
from a series of physicians, and opiates. Mr. S was quite vague as to how he would
support his chemical use, but noted that “there are ways of getting money, if you really
want some.”
In the last year, Mr. S reported that he has been using cocaine “four or five times a
week,” although on occasion he did admit to having used cocaine “for a whole week
straight.” He has been sharing needles with other cocaine users from time to time but re-
ported that “I am careful.” In spite of this, however, he was diagnosed with hepatitis B in the
last year, according to Mr. S . He also reported that he had overdosed on cocaine “once
or twice,” but that he treated this overdose himself with benzodiazepines and alcohol.
In addition to the possible cocaine overdoses noted above, Mr. S admitted to hav-
ing experienced chest pain while using cocaine on at least two occasions and has used
alcohol or tranquilizers to combat the side effects of cocaine on a regular basis. He has
admitted to frequently using tranquilizers or alcohol to help him sleep after using cocaine
for extended periods of time. He also admits to having spent money on drugs that was
meant for other expenses (loan payments, etc.) and by his report has had at least one auto-
mobile reposessed for failure to make payments on the loan.
Mr. S has been unemployed for at least the last 2 years but is rather vague as to
how he supports himself. He apparently was engaged in selling cocaine at the time of his
arrest, this being one of the charges brought against him by the police.
Mr. S had not seen a physician for several years prior to this arrest. During this in-
terview, however, it was noted that he had scars on both arms strongly suggestive of intra-
venous needle use. When asked about these marks, he referred to them as “tracks,” a
street term for drug needle scars. This would suggest long-term intravenous drug use on
Mr. S ’s part. He denied the intravenous use of opiates, but a urine toxicology screen
detected narcotics. This would suggest that Mr. S has not been very open about his
narcotic drug use.
On this administration of the Michigan Alcoholism Screening Test (MAST)
Mr. S achieved a score of 17 points, a score that is strongly suggestive of alcoholism.
He reported that the longest period he has been able to go without using chemicals in the
last five years was only “hours.” His profile on this administration of the Minnesota Multi-
phasic Personality Inventory (MMPI) was suggestive of a very impulsive, immature indi-
vidual, who is likely to have a chemical dependency problem.
Psychiatric History
Mr. S reported that he has been hospitalized for psychiatric reasons only “once.” This
hospitalization took place several years ago, while Mr. S was living in the state of
XXXXX. Apparently, he was hospitalized for observation following a suicide attempt in
456 Appendix Two
which he slit his wrists with a razor blade. Mr. S was unable to recall whether he had
been using cocaine prior to this suicide attempt, but thought that it was “quite possible”
that he had experienced a cocaine-induced depression.
Medical History
As noted above, Mr. S had not seen a physician for several years prior to his arrest.
Since the time of his arrest, however, he has been examined by a physician for a cough
that he has had for some time. The physician (report enclosed) concluded that Mr. S
is “seropositive” for HIV and classified Mr. S as falling into category CDC1. While it
is not possible to determine if Mr. S contracted HIV through sharing needles, this is at
least a possibility.
Summary and Conclusions

Overall, it is quite apparent that Mr. S has a long-standing chemical dependency
problem. In spite of his evasiveness and denial, there was strong evidence of significant
chemical dependency problems. Mr. S seems to support his drug and alcohol use
through criminal activity, although he is rather vague about this. He has been convicted of
drug-related charges in the state of XXXXX and was on probation following this convic-
tion. One might suspect that Mr. S ’s motivation for treatment is quite low at this time,
as he has expressed the belief that his attorney will “make a deal for me” so he will not have
to spend time in prison.
Recommendations
1. Given the fact that Mr. S has contracted HIV and hepatitis B from infected
needles, it is strongly recommended that he be referred to the appropriate medical
facility for treatment.
2. It is the opinion of this reviewer that Mr. S ’s motivation for treatment is low at this
time. If he is referred to treatment, it is recommended that this be made part of his sen-
tencing agreement with the court. If he is incarcerated, chemical dependency treat-
ment might be made part of his treatment plan in prison.
3. Referral to a therapeutic community should be considered for Mr. S for long-term
residential treatment.
APPENDIX THREE
The “Jellinek” Chart for Alcoholism
Following the publication of earlier editions of Con- chart is actually the work of Dr. Maxwell Glatt, a British
cepts of Chemical Dependency, questions were raised physician who was so taken by Jellinek’s work that he
concerning my decision not to mention the so-called operationalized the gamma subtype of alcoholism
Jellinek chart in this text. This chart, which is viewed as in chart form. This chart, which addresses only the
gospel within the alcohol/drug rehabilitation industry, gamma subtype of alcoholism as suggested by Jellinek
purports to show the progression from social drinking to (1960), has mistakenly been accepted by countless
alcoholism, then on to recovery. Since the time of its alcohol/drug rehabilitation professionals as the chart
introduction, this chart has been used to illustrate the that identifies the progression of all forms of alco-
“unalterable” progression of alcoholism to countless holism. As a result of this mistake many patients in re-
patients who were in the earlier stages of alcohol use habilitation programs, whose symptoms of alcohol use
problems, as well as to browbeat reluctant individuals problems did not “fit” the progression of symptoms sug-
into accepting the need for help with their supposed gested in this chart, have been subjected countless
drinking problem. Variations of this chart have been de- hours of confrontation because they were “in denial.”
veloped for compulsive gambling, steroid abuse, com- Rather than perpetuate this misunderstanding, I de-
pulsive spending, both heroin and cocaine addiction, cided not make any reference to this chart in the text of
and countless other disorders. An example of this chart Concepts of Chemical Dependency.
is shown in Figure A3.1.
The problem is that Jellinek did not devise this
chart! Even though it is often attributed to him, this
Onset of relief drinking
Increasing frequency of alcohol use

Individual’s road
Blackouts to recovery
Increasing confidence in recovery

Family problems due
to drinking
Active involvement in self-help groups
Individual’s progression
along road to alcoholism Person admits he or she is powerless over alcohol
Person reaches out for help
Endless cycle of
addictive behaviors
FIGURE A3.1 Alcohol Progression Chart Often Mistakenly Called the “Jellinek” Chart
457
APPENDIX FOUR
Drug Classification Schedules
One of the most confusing aspects of drug rehabilita- the United States are lumped together by the Drug En-
tion work for both physicians and mental health profes- forcement Administration. (For example: heroin, which
sionals is that the legal classification of many of the is a narcotic analgesic, and MDMA, which is a hallu-
drugs of abuse is carried out not on the basis of the cinogenic substance that might also be neurotoxic, are
pharmacological properties of the compound in ques- both Schedule I compounds.) Table A4.1 should help
tion but by its perceived abuse potential. Thus, com- you to understand the drug classification schedule now
pounds perceived to have no accepted medical use in in use in the United States:
TABLE A4.1 Drug Classification Schedule
Schedule Definition Examples
Schedule I Compounds with no accepted medical use Marijuana, LSD, MDMA, heroin*
Schedule II Compounds with recognized medical use, Morphine, methadone, amphetamines
but with severe abuse potential
Schedule III Compounds with recognized medical use, Ketamine, acetaminophen with codeine compounds
but with moderate abuse potential
Schedule IV Compounds with recognized medical use, Phenobarbital, benzodiazepines
but with mild abuse potential
Schedule V Compounds with recognized medical use, Buprenorphine
but with low abuse potential
*Heroin has no recognized medical use in the United States. It is used in some other countries for control of acute pain.
458
APPENDIX FIVE
Modified Centers for Disease Control

HIV/AIDS Classification Chart
Number of CD4+ T-helper Symptomatic but not Patient has full-blown

cells per mm3 of blood* Asymptomatic full-blown AIDS** AIDS***
Greater than or equal to 500 cells A1 B1 C1

Between 499 and 200 T-helper cells A2 B2 C2
< 200 T-helper cells A3 B3 C3
*
The normal person has 800–1,200 CD4+ T-helper cells per cubic mm of blood.
**
Patients in this column would have developed infections such as bacterial endocarditis, meningitis, pneumonia, or sepsis, which are not specific
to AIDS patients alone. For example, it is not uncommon for individuals with normal immune systems to develop bacterial pneumonia. Contrast
this with the defining criteria for column C (see below).
***
Patients in this column have developed one or more infections rarely seen except in patients who have AIDS. For example, the patient might
have a Candidiasis infection of the esophagus or AIDS-induced diarrhea that lasts longer than 1 month.
Source: Based on Rubin (1993) and Work Group on HIV/AIDS (2000).
459
GLOSSARY
Abruptio placentae: A condition in which bleeding starts be- Amphetamine naive: Descriptive of a person who has never
tween the placenta and the wall of the uterus. As the blood ac- used the amphetamines and thus has no acquired tolerance
cumulates, it gradually separates the placenta from the wall of for this class of medications.
the uterus, cutting the fetus off from its supply of oxygen. The Amygdala: A region of the brain that is shaped like an almond,
result may be fatal for both the mother and the infant. found in the temporal lobe, which is part of the brain’s limbic
Absorption: The movement of drug molecules from the site system. It is thought to be concerned with the process of at-
of entry, through various cell boundaries, to the site of action. taching the emotional content to memory as well as modulat-
Acetaldehyde: The first intermediate chemical, or metabolite, ing emotional responses to external reality.
formed when the alcohol molecule is biotransformed. This Analgesic: A compound that will provide relief from pain
occurs through the process known as oxidation. Acetaldehyde without causing a major change in the individual’s level of
is quite toxic to the body. In low levels, it is also found in ciga- consciousness.
rette smoke. Analog of a drug: A compound that is a variation in the
Acetylcholine: One of the major neurotransmitters in the chemical structure of the original drug, producing a “new”
body. Acetylcholine is found mainly in the outer regions of drug. The original compound is known as the “parent”
the body, where the central nervous system interacts with the drug.
tissues of the body. Acetylcholine is involved in alerting the Anandamide: A compound produced in the brain, which
body to a potential danger, or in the communication between functions as a neurotransmitter in certain regions of the
the central nervous system and the muscles of the body. brain, especially those regions involved in pain perception.
Addiction: A disorder that is considered progressive, chronic, Anhedonia: Inability of a person to take pleasure in activities
primary, and relapsing that involves features such as a com- that she or he once enjoyed. This condition is a feature of
pulsion to use a chemical, loss of control over the use of a sub- some personality disorders, major depression, and schizo-
stance, and continued use of a drug in spite of adverse phrenia and is often seen during drug-withdrawal states.
consequences caused by its use.
Anorexia: Loss of desire to eat.
Adipose tissue: Fat tissue.
Anorexic: Descriptive of a state of anorexia.
Affinity: A term that refers to the strength with which drug
Antagonist: A compound that blocks or reverses the effect of
molecules bind to the receptor site in the cell wall.
an agonist.
Agonist: A chemical molecule that has the ability, because of
Anterograde amnesia: Inability to remember after a specific
its unique structure, to bind with a receptor molecule located
event, such as a blow to the head or the ingestion of a chemi-
in the cell wall. The degree of a “match” between the agonist
cal known to interfere with memory formation. Such drugs
and the receptor is called the affinity of the agonist molecule.
include the benzodiazepines or the barbituates, as well as al-
An agonist might be a natural substance or an artificial
cohol. See also Blackout.
compound.
Antidipsotrophic: Descriptive of a compound or behavioral
Albumin: One of the primary protein molecules found in the
treatment for dipsomania. This term was popular in the 19th
general circulation.
and early 20th centuries and is rarely used now.
Alcohol use disorder (AUD): A condition of individuals
Antisocial personality disorder (ASPD): A personality pat-
whose alcohol use is far beyond the normal level for their so-
tern marked by a pervasive disregard for the rights of others,
cial or cultural group. This term is gaining acceptance as a re-
repeated violations of the rights of others, impulsiveness, risk
placement for alcohol abuse, or alcoholism.
taking, disregard for the truth, and self-centeredness. Individ-
Allele: One of the variants of a gene. uals with ASPD may be very articulate and convincing, but
Amino acid: Chemical molecules that the body uses to form tend to be most interested in their own gratification even at
proteins, which have a variety of functions in the body. the expense of other people.
460
Glossary 461
Anxiety: An emotional state that can range from mild to severe who did not know if the tissue sample came from an alcoholic
in intensity; the individual feels that he is in some form of im- or a nonalcoholic person.
minent danger, although there is no identified threat. Botulism: An acute paralytic disease caused by the micro-
Anxiogenic: Descriptive of a compound or experience that scopic organism Clostridium botulinum. Usually seen when
increases the individual’s level of anxiety. the victim ingests food contaminated by the organism. The
Anxioyltic: Descriptive of a compound that decreases the in- toxin produced by the organism is one of the most potent neu-
dividual’s anxiety level. rotoxins known to man, and exposure to this agent is potentially
fatal.
Apnea: Cessation of normal respiration. If this occurs during
sleep, the condition is called sleep apnea. Carcinogen: A chemical that is known or strongly suspected
of being able to cause cancer in humans.
Arrhythmia, cardiac: Disturbance of the normal rhythm of
the heart. Depending on the etiology of the arrhythmia, this Cardiomyopathy: A disease of the heart muscle in which the
might prove fatal to the individual. muscle tissue becomes flabby and weaker than usual. One or
more of the ventricles of the heart might enlarge, and this
Arteritis: Inflammation of an artery. For example, pulmonary condition might progress to congestive heart failure.
arteritis involves the inflammation of the pulmonary arteries.
Cardiotoxin: Any compound that is toxic to the muscle tissue
Aspirative pneumonia: A type of pneumonia that has two of the heart.
components: (a) aspiration of gastric contents into the lungs
as a result of a breakdown of the normal body defenses that Catecholamines: A family of chemicals, including epinephrine,
are supposed to prevent this, and (b) damage to the tissues that normally is produced in the adrenal glands, and the neuro-
of the lungs from gastric fluids or bacterial infection transmitters norepinephrine and dopamine. Catecholamines
(Bartlett, 1999). help to regulate various body functions. For example, epineph-
rine functions as a vasoconstrictor, whereas norepinephrine
Ataxia: Inability to control muscle movement. and dopamine are neurotransmitters.
Atherosclerosis: A condition in which fatty plaques accumu- Central nervous system (CNS): The brain and spinal cord.
late in the inner walls of the arteries of the circulatory system.
If too much of the artery is obstructed, the blood flow through Cerebellar ataxia: Loss of motor coordination and balance
that artery is obstructed. caused by damage to this region of the brain.
AUD: See Alcohol use disorder. Cerebellum: A part of the brain, or CNS, located at the base
of the brain. This region is involved in coordination of muscle
Basal ganglia: A region of the brain involved in the exertion activity, balance, and some sensorimotor activity.
of the individual’s will on conscious movement—the area
where spontaneous movement is initiated. The basal ganglia Cerebrovascular accident (CVA): Once called “stroke.”
has indirect connections to the reticular activating system and There are two forms of CVA. The first is the “occlusive” form,
extensive connections to the cortex of the brain. in which a blood clot or other material clogs a blood vessel,
preventing blood from reaching the brain cells serviced by
Benzodiazepine receptor: Any of a number of compounds that vessel. The second form of CVA is the “hemorrhagic”
that bind to the benzodiazepine receptors in the brain, acti- form. In this form, a blood vessel ruptures, exposing sur-
vating that receptor site. rounding neurons to blood (which is toxic to nervous system
Blackout, alcohol-induced: Alcohol-induced memory dys- tissue) and disrupting the blood supply to those neurons serv-
function. Technically, a state of alcohol-induced anterograde iced by the vessel that has ruptured. Of the two, the occlusive
amnesia. form is by far the most common. See also Embolus;
Bioavailability: The degree and rate at which a substance is Embolism.
absorbed into a living system or is made available at the site of Cerebrum: The largest region of the brain, including the
physiological activity. cortex.
Biotransformation: The process, usually carried out in the Cilia: Microscopic, hairlike projections from cell walls. Cilia
liver, by which the body alters the chemical structure of a are found in many regions of the human body. In the lungs,
foreign molecule to a form that will allow it to be eliminated the motion of the cilia help to push mucus to the top of the
from the body, usually by excretion. The process of changing lungs, where it is expelled, helping to keep the lungs clean.
a foreign molecule into a form that might be excreted yields Conduct disorder: A condition seen in childhood or adoles-
intermediate metabolites, some of which might be biologi- cence, marked by behaviors that repeatedly violate the rights
cally active. of others or the age-appropriate norms and rules. Usually, the
Blind research study: One in which the data are examined with- violation of rules is quite serious, such as running away from
out the researcher knowing if any given piece of data is from the home two or more times when there is no physical or sexual
research sample or the control sample. For example, tissue abuse situation, violation of parental curfews before the age of
samples from subjects might be examined by a researcher 13, vandalism, arson, theft, and other deviations. Deceitfulness
462 Glossary
is commonly seen in conduct-disordered children and adoles- genes within that neuron. 6FosB is one of a family of com-
cents, and the child has little empathy for the feelings of pounds known as “genetic transcription factors,” which
others, including those that she or he has hurt. By definition, control when or if certain genes are activated within the
this condition is not due to any other form of mental illness, neuron.
such as intellectual impairment or schizophrenia. For a list of Dendrite: A thin, branched part of a nerve cell that extends
the diagnostic criteria for this condition, consult the Diagnos- from the body of the neuron toward other nerve cells and col-
tic and Statistical Manual of Mental Disorders, 4th edition lects information from those neurons through the receptor
(Text Revision) (American Psychiatric Association, 2000). sites located along the walls of the dendrite.
Congestive heart failure: Inadequate heart function, resulting Dependence: A state in which the body requires the contin-
in shortness of breath, fluid accumulation in the extremities, ued use of a compound to continue to function. See also
possible arrhythmias, formation of emboli, and sudden death. Neuroadaptation.
Conjugation: One of the four primary methods of biotrans- Depression: An emotional state marked by pervasive and in-
formation used by the liver. tense sadness, that may include disturbance of sleep pattern,
Cortex: The outermost layer of the human brain where the the individual’s sex drive, appetite, ability to concentrate, and
“higher functions” of thought are generated. This region of enthusiasm for daily activities. The depressed individual may
the brain is intricately folded in upon itself in the adult experience feelings of worthlessness, feel guilt about real or
human brain and contains specialized neurons devoted to imagined past mistakes, and may actively seek to terminate
such tasks as motor coordination, speech, language interpre- his or her life through the act of suicide.
tation, and processing of sensory information.
Diabetes mellitus: A metabolic disorder in which the body
COX-1: A subtype of cyclooxygenase found in the human loses the ability to regulate the blood sugar level, either
body. Researchers think that COX-1 is normally produced by through a deficiency in the production of insulin (known as
the body to help regulate the activity of different organs. Type 1 diabetes) or insensitivity to the insulin that is produced
COX-2: A subtype of cyclooxygenase found in the human (Type 2 diabetes).
body. Researchers think that COX-2 is produced mainly Diabetic retinopathy: A complication of diabetes that is the
when body tissues are damaged, helping to trigger the inflam- leading cause of blindness in persons 20–74 years of age.
matory response at the site of injury.
Diaphoresis: Excessive sweating.
C-reactive protein: A compound normally produced by the
body in response to infection or tissue damage. Some evi- Dipsomania: Obsolete term for alcohol dependence.
dence suggests that the level of C-reactive protein in the body Distribution: How the chemical molecules are moved about
is a rough measure of the individual’s cardiovascular risk, and in the body. This is usually accomplished by the circulatory
it might even contribute to the development of plaque in the system.
arteries that supply blood to the heart. Diversion of drugs: A process through which compounds
Cross tolerance: A phenomenon that exists when an individ- originally prescribed by a physician are used by people for
ual has become tolerant to the effects of one compound and whom those drugs were not prescribed. Sometimes, the med-
develops tolerance to other, similar compounds. For example, ications are stolen from drug stores or a person’s medicine
a person who is tolerant to the effects of the barbiturates will cabinet; on other occasions an individual with a legitimate
also be tolerant to the effects of benzodiazepines or alcohol, need for a desired medication will (for a fee) visit several dif-
both of which are also CNS depressants. ferent doctors in a short period of time to obtain prescriptions
CVA: See Cerebrovascular accident. from each physician for the same medication. The medica-
tions obtained from this process are then sold to other drug
Cyclooxygenase: An enzyme involved in the production of
abusers.
the prostaglandins in the human body. Since one type of
prostaglandin is involved in the inflammation response, this “Doctor making”: Slang term for manipulating a physician
enzyme might be said to be indirectly involved in the devel- into providing a prescription for a desired compound, such as
opment of inflammation at the site of injury. an amphetamine or opioid.
“Date rape”: Experience in which one partner in a dating Dopamine: One of the major neurotransmitters in the body.
relationship will initiate sexual activity with the partner, even Dopamine is used as a neurotransmitter by many different re-
if the partner has not expressed an interest in sexual activity. gions of the CNS. There are five known subtypes of dopamine
A common part of the date rape process is the use of drugs by found in the CNS.
the aggressor to overcome the victim’s resistance to the sexual Dopaminergic: Using dopamine. See also Dopamine.
advances.
Down-regulation: A process in which the number of neuro-
DeltaFosB: See 6FosB. transmitter receptors in a neuron is reduced, decreasing the
6FosB: A compound utilized within neurons to control the sensitivity of the cell to the neurotransmitter to avoid over-
manufacture of proteins and thus the expression of certain stimulation.
Glossary 463
Dysentery: A painful infection of the lower intestinal tract, corn starch or talc. The chemical properties of these com-
caused by the ingestion of contaminated water. The person pounds allow them usually to be destroyed by stomach acid
with dysentery will develop massive diarrhea that is often when the medication is taken orally or at least prevented from
mixed with blood and mucus. Unless the fluid loss caused by being absorbed into the body. In the latter case, the filler will
the diarrhea is rapidly controlled, dysentery can prove rapidly harmlessly pass through the body and ultimately be excreted
fatal. Dysentery was common in the crowded army camps of while the active agent in the tablet is absorbed through the
the 1700 and 1800s, as well as in many cities of that era. gastrointestinal tract.
Dysphoria: Acute, transient changes in mood, usually involv- First-order biotransformation process: A subform of bio-
ing such emotions as sadness, sorrow, and depression. transformation in which a set percentage of the medication is
Edema: Swelling caused by the accumulation of excess fluids biotransformed each hour.
in body tissues. First-pass metabolism: A process through which substances
Effective dose: Result of a calculation performed by pharma- absorbed into the body from the small intestine are routed
cologists to estimate the percentage of a population that will through the liver, allowing that organ to begin to neutralize
respond to a given dose of a chemical. Example: The effective poisons before they reach the general circulation. As a result
dose (ED) that 95% of the population will respond to is writ- of first-pass metabolism, the liver is often able to biotransform
ten by pharmacologists as the ED95. many medications that are administered orally before they
have had a chance to reach the site of action.
Elimination half-life: The period of time that the body re-
quires to eliminate 50% of a single dose of a drug. Contrast Fluoxetine: Generic name of an antidepressant of the selec-
this to the therapeutic half-life of a drug. tive serotonin reuptake inhibitor (SSRI) class.
Embolism: The blockage of a blood vessel by a foreign sub- Fluvoxamine: Generic name of an antidepressant of the se-
stance (a blood clot, fat droplet, talc, etc.) known as an embo- lective serotonin reuptake inhibitor (SSRI) class.
lus. The embolus is been transported by the blood from Formication: The sensation of having unseen bugs crawling
another part of the body and might lodge in any number of either on or just under the skin, possibly induced by medica-
different blood vessels of the body. If it lodges in a blood vessel tions such as the amphetamines or cocaine.
in the lung, it is called a pulmonary embolism, and if the em-
Free radical(s): Highly reactive molecules that can bond to
bolus lodges in the brain, it is said to cause an ischemic event,
unwanted areas of the body, causing damage to various tissues.
ischemic stroke, or CVA.
Frontal cortex: Region of the brain involved in such activities
Embolus (pl. emboli): An abnormal particle circulating in
as planning, anticipation of long-term consequences of be-
the blood, such as fat or a blood clot, or possibly a foreign sub-
havior, or focus of attention on a specific task.
stance, such as talc, introduced into the body when a drug
abuser injects a drug contaminated with this substance. The GABA: Shorthand for gamma-amino-butyric acid. GABA is
embolus will travel through the blood stream, propelled by the main inhibitory neurotransmitter in the brain. Neurons
the action of the heart until it lodges in a blood vessel too that utilize GABA are found in the cortex, cerebellum, the
small to allow it to move any farther. A cork or a plug would hippocampus, the superior and inferior colliculi regions of
be a good analogy. the brain, the amygdala, and the nucleus accumbens.
Enkephalins: Small molecules that belong to the neuropep- Gastritis: Inflammation of the lining of the stomach.
tide family of chemicals. The enkephalins bind to the opioid Glossitis: A very painful inflammation of the tongue.
receptor sites in the CNS, contributing to the control of Glutamate: A chemical that functions as an excitatory neuro-
mood, movement, behavior, and pain perception. transmitter within certain regions of the brain. Excessive
Excretion: A process by which the body removes waste prod- amounts of glutamate can be toxic to the neurons that it
ucts or foreign chemicals from the general circulation. This comes into contact with.
is usually accomplished by the kidneys, although some Half-life: The period of time that it takes for the concentra-
drugs are excreted from the body in the feces or through the tion of a drug in the blood plasma to be reduced by 50% fol-
lungs. lowing a single dose. This process depends, in part, on the
False negative: Result of a test that has failed to detect some- health of the individual’s liver and kidneys.
thing that it should—for example, a test that failed to detect Harm reduction: An approach to drug abuse that attempts to
evidence of drug abuse when it was known that the person limit the damage that the drug might cause to the individual’s
tested had indeed abused a controlled substance. body. This approach is based on the theory that by limiting
False positive: Result of a test that suggests something is true the amount of damage to the individual, the ultimate cost of
when it is not—for example, a test result that suggests the indi- that person’s chemical abuse to society will be reduced.
vidual used a controlled substance when she or he did not do so. HDL: Short-hand for “high density lipoproteins.” Sometimes
Fillers: Compounds added to a tablet intended for oral inges- called the “good” cholesterol as it helps to remove the more
tion, to give the tablet bulk and form. Some fillers include dangerous “low density lipoproteins” from the body.
464 Glossary
Hepatitis: Inflammation of the liver, characterized by jaun- Limbic system: Region of the brain thought to be involved in
dice, liver enlargement, possible abdominal and gastric dis- the development and expression of emotions.
comfort, abnormal liver function, and in extreme cases, Lipids: Fat molecules within the blood, used by the body for
scarring of the liver. various purposes, including formation of cell walls.
Hepatoxicity: Liver failure. Lipophilic: Descriptive of compounds that bind to fat mole-
Hippocampus: A portion of the brain that is thought to be in- cules, or lipids, in the blood.
volved in the processing of sensory information and the for- Liter: Unit of liquid measure in the metric system. A liter is
mation and retrieval of both verbal and emotional memories. 1.056 liquid quarts, or 33.792 liquid ounces.
Huff: Inhale (use) an inhalant. This is a slang term. Locus ceruleus: A region of the brain thought to be involved
Hydrolysis: One of the four primary methods of drug bio- in the perception of pain, alarm states, anxiety, and fear.
transformation used by the liver.
“Making a doctor.” See “Doctor making.”
Hypertension: Abnormally high blood pressure, usually de-
Mean corpuscular volume (MCV): A measure of the aver-
fined as blood pressure in excess of 140/90 in an adult.
age size of a sample of an individual’s red blood cells.
Hypertensive: Related to hypertension.
Medulla oblongata: Region of the brain (sometimes called
Hyperthermia: Excessive body heat. Opposite of hypother- the brain stem) involved in the control of respiration and
mia. body temperature, and which plays a role in arousal.
Hypnotic: A medication designed to help the user become Metabolite: One of the compounds that is formed, usually by
drowsy and fall asleep. the liver, during the process of drug biotransformation. Each
Hyponatremia: Low sodium levels in blood. May be fatal if of the metabolites is a variation of the original parent mole-
not corrected. cule that has been chemically altered so that the body can
Hypothalamus: A region of the brain that helps to regulate eventually remove it from the circulation through the process
body temperature. of elimination.
MI. See Myocardial infarction.
Iatrogenic disease: A disorder that arises as a complication of
the medical treatment of a separate disorder. Microcephaly: Reduced head circumference.
IDS-100. See Inventory of Drinking Situations. Myocardial infarction: Commonly called a “heart attack.” A
process in which the blood supply to a region of the heart is
Intramuscular: Within muscle tissue.
disrupted, possibly by coronary artery diseaseor an embolus
Intranasal method of drug administration: Depositing a that blocks a blood vessel leading to the heart. Heart muscle
compound on the blood-rich tissues of the sinuses where it cells that are deprived of blood may be damaged, or in ex-
can be absorbed into the circulation. treme cases, might die. This condition might kill the individ-
Intravenous: Within the veins of the circulatory system. ual if enough cardiac tissue is destroyed; it results in scar
Inventory of Drinking Situations: A 100-item questionnaire tissue formation in those patients who do survive. If patients
that, when scored, suggests situations where a person is most survive, their cardiac function might be impaired to the point
likely to drink. that they are at risk for later myocardial infarctions, congestive
heart failure, the formation of emboli, arrhythmias, and other
Ischemia: Local oxygen deprivation within tissue, usually heart conditions.
caused by a reduction in the amount of blood reaching that
Necrosis: Death or destruction of body tissues.
region of the body. In time, this might result in the destruc-
tion of the affected tissue. Narcolepsy: A very rare lifelong neurological condition in
which the patient will experience sudden attacks of sleep.
Ischemic stroke: Blockage of a blood vessel in the brain, leading
to ischemia in that region of the brain. If not corrected immedi- Neuroadaptation: A process that takes place within the CNS,
ately, those brain cells may be damaged or even die. in which the neurons make basic changes in how they per-
form regular functions to adapt to continued exposure to a
Isoniazid: Antibiotic compound, sometimes referred to as
chemical that affects the CNS. This same process was once
“INH,” which is used to treat tuberculosis infections.
called “tolerance” to the effects of the drug, although toler-
LDL: Shorthand for “low density lipoproteins.” Sometimes ance is now used primarily to describe the process of neuroad-
this is called “bad” cholesterol, as plaque tends to be made up aptation to drugs of abuse. It is seen with a multitude of
of low density lipoproteins. pharmaceuticals, including many anti-hypertensive medica-
Lethal dose level: Result of a calculation performed by scien- tions and anxiolytic medications. When the medication in
tists to determine the percentage of the general population question is abruptly discontinued, the nervous system must go
who will die from exposure to a toxin or chemical. The lethal through a refractory period in which it attempts to reverse the
dose (LD) at which 95% of the population would die without changes in function made to accommodate the presence of
medical intervention is written as LD95. the compound that has been withdrawn.
Glossary 465
Neuron: A nerve cell. Neurons are actually microscopic OTC medications by the Food and Drug Administration
chemical-electrical generators that produce a small electrical (Scheller, 1998).
“message” by actively moving sodium and calcium ions back Oxidation: One of the four primary methods of drug biotrans-
and forth across the cell boundary. Sodium and calcium ions formation used by the liver. In this process, a hydrogen atom
pass through the cell wall through special “channels” that are is removed from the molecule being biotransformed, or an
formed by protein molecules in the cell wall. By concentrat- oxygen atom is added to the molecule, changing its chemical
ing sodium ions inside the cell, a small electric potential is es- structure in a minor way. Ultimately, the atom in question is
tablished. When the neuron fires, calcium ions rush into the changed in such a way that the kidneys can then eliminate
cell, replacing the sodium ions, and the cell loses the electric the compound from the blood.
charge it had built up. The cell then repeats the cycle, pump-
ing calcium ions out and sodium ions back in to build up an- Panic attack: The experience of intense feelings of anxiety,
other electric charge so it can “fire” again. Any chemical that often with symptoms such as shortness of breath, rapid heart-
interacts with the protein molecules that form sodium or cal- beat, a feeling of impending doom, or a feeling that something
cium ion channels in the cell wall of the body’s tissues will af- terrible is about to happen. Panic attacks are usually very short
fect how those cells function. in duration (10–60 minutes), but can cause extreme distress.
Neuroplasticity: Ability of the brain to change in response to Parent compound: The original drug molecule, usually in
trauma and experience. The process of building memories is reference to the time before it is altered by biotransformation.
one example. During the formation of memories, new den- Patient year: A statistical concept; 100 patient years means
dritic connections are thought to form in the brain. 100 patients, all of whom have a common medical condition,
who are followed for 1 year.
Neurotoxin: A chemical that destroys nerve cells, or neurons.
Pharmaceuticals: Used as a street term to describe medica-
Neurotransmitter: Any molecule released by a neuron to
tions that have been diverted to illicit markets. For example,
cause a change in the function of a designated target cell.
narcotic analgesics stolen from a pharmacy during a burglary
After being released, the neurotransmitter molecules cross
and then sold on the street would be called “pharmaceuti-
the synapse to bind at a receptor site on the target cell. This
cals” to differentiate them from the drugs produced in illegal
then causes the target cell to respond to the chemical mes-
laboratories.
sage transmitted by the first cell’s neurotransmitter molecules.
Pharmacokinetics: Study of the time course of a drug and its
NMDA. See N-methyl-D-aspartate.
metabolites in the body after it is administered.
N-methyl-D-aspartate: An amino acid that functions as an ex-
Platelets: A part of the body’s circulatory system. The disk-
citatory neurotransmitter within some regions of the brain.
shaped platelets circulate in the blood until there is an injury,
Nucleus accumbens: At one time thought to be the reward at which time they help to form a blood clot to stop bleeding.
center in the brain. It has now been discovered that this re-
Polydrug abuse: Abusing more than one substance at the
gion of the brain is involved in integrating the individual’s
same time. Prior to the mid-1970s, individuals with substance
psychomotor activities with conscious motivation. As such,
use problems were usually abusing just one chemical, such as
this region of the brain is involved with the drug-induced feel-
alcohol or heroin. This pattern of substance abuse is rarely seen
ing of pleasure as well as helping shape the brain’s response to
today, except in older individuals whose substance use pattern
the need for food, water, and, sex. In other words it is part of
was established in the mid-1970s or early 1980s. Currently, it is
the reward system but not the entire reward system in the
more common for the individual who has a substance use
brain. The nucleus accumbens triggers the reward system
problem to be abusing several chemicals simultaneously.
mainly in response to unexpected pleasurable stimuli. But
other sections of the brain soon become involved in the re- Polypharmacology. See Polydrug abuse.
sponse to predictable stimuli, making the drug-induced re- Potentiate: Often, when similar compounds are ingested, the
ward cascade more complicated than originally thought. effects of the one drug will intensify that of the others, possi-
Oliguria: Significant reduction in the amount of urine pro- bly producing lethal results. See also Synergistic response.
duced by the kidneys. Prime effect of a drug: The intended effect of a drug. For
Opiophobia: Fear of inducing or contributing to the develop- example, a person with a fever might take some aspirin to
ment of an addictive disorder by prescribing too high a dose of lower his or her fever. This reduction in fever is thus the
narcotic analgesics or by prescribing narcotic analgesics for prime effect of the aspirin. Compare with side effects.
too long a period of time. Proband: An identified research subject who possesses a cer-
Over-the-counter (OTC) medication: A medication that can tain trait (such as a genetic disorder or substance use disorder)
be purchased without a prescription. These medications are and then, with similar subjects, becomes the primary focus of
sold in various outlets besides a pharmacy, such as a grocery the research study.
store. Over 600 medications that were once available in the Prodrug: A compound that is administered to the patient,
United States only by prescription have now been classified as which is then biotransformed by his or her liver into a
466 Glossary
compound that is biologically active. Technically, this Reye’s syndrome: A serious medical condition that usually
compound is a metabolite of the parent drug. The parent develops in children between the ages of 2 and 12. The con-
drug may or may not have a biological action of its own. dition usually follows a viral infection such as influenza or
But the metabolite has a stronger biological action that chickenpox and may have symptoms such as swelling of the
that of the parent compound and is the reason the patient brain, seizures, disturbance of consciousness, a fatty degener-
is using the drug. ation of the liver, coma, and in about 30% of the cases, death.
Prostaglandins: A family of compounds found in the body that Rhabdomyolysis: Destruction of skeletal muscle tissue on a
help to mediate the inflammatory response following an injury massive scale. When muscle cells die, they release a chemical
and also help to control body functions. The prostaglandins known as myoglobin, which helps to store oxygen in the
function like hormones in the body and are active in very low muscle cell. During rhabdomyolysis, massive amounts of
concentrations. myoglobin are released at once. The accumulated myoglobin
Pulmonary arteritis. See Arteritis. interferes with kidney function and in extreme cases can re-
sult in kidney failure, cardiac arrhythmias, and death.
Rapid eye movement sleep. See REM sleep.
Rhinitis: Inflammation of the nasal passages.
RAS. See Reticular activating system.
Rig: Slang for intravenous needle.
Receptor: A protein molecule or group of molecules an-
chored in the cell wall that allow the cell to receive chemicals Schizophrenia: A psychiatric disorder characterized by delu-
from the outside wall. If the chemical molecule transmits a sional thinking, hallucinations, and disorganized behavior.
form of information between cells, it is called a transmitter Secondary hyperparathyroidism: Hormonal disorder that de-
molecule. Examples of these include hormones, antigens, or velops when alcohol interferes with the body’s ability to regu-
peptides. If the transmitter molecule is from one of the neu- late calcium levels in the blood for extended periods of time.
rons of the CNS, it is referred to as a neurotransmitter. Neuro- The calcium in the bones is then reabsorbed into the blood,
transmitters pass information between neurons. and the bones become weakened through calcium loss.
Receptor site: The region in the cell wall of a neuron where a Sedative: A drug designed to decrease the individual’s activity
receptor is located. level, moderate excitement, and calm the patient taking the
Reduction: One of the four primary methods of drug bio- drug.
transformation used by the liver. Sensitization effect: Result of a process by which certain re-
REM rebound: REM rebound is a phenomenon in which gions of the brain become hypersensitive to the effects of a
the individual experiences an increase in the amount of sleep drug, such as cocaine or the amphetamines, so that certain ef-
time spent in REM sleep after stopping the use of a CNS defects (such as seizures) might be triggered by doses once easily
pressant, apparently to “catch up” on lost REM sleep. During tolerated by the abuser.
this period, he or she will experience vivid dreams, which Serotonergic: Using serotonin.
may be quite frightening to the dreamer; in some cases the Serotonin: One of the major neurotransmitters in the body.
nightmares are so disturbing that the patient will begin to use Serotonin is used as a neurotransmitter by many different re-
alcohol or drugs again to “get a good night’s sleep.” gions of the CNS. There are 15 known subtypes of serotonin
REM sleep: A stage of sleep usually associated with dream found in the CNS, each of which is assumed to control one or
states. Research suggests that the individual usually spends a more subfunctions within the CNS.
portion of each sleep cycle in REM sleep and if this stage of Serotonin syndrome: A rare, drug-induced neurological dis-
sleep is disrupted by drugs, a sleep disorder, or inability to order that can be life threatening. In spite of the best medical
sleep for more than a few nights, the disruption will have an care, approximately 11% of the persons afflicted with this con-
effect on the individual’s ability to function during the waking dition will die. Symptoms of the serotonin syndrome include
portion of his or her day. irritability, confusion, an increase in anxiety, drowsiness hy-
Reperfusion: The sudden restoration of blood flow to a re- perthermia (increased body temperature), sinus tachycardia,
gion of the body that has been deprived of oxygen for a period dilation of the pupils, nausea, muscle rigidity, and seizures.
of time, such as a region of the brain that was deprived of oxy- Although the serotonin syndrome might develop as long as
gen during a stroke. In addition to the damage caused by the 24 hours after the patient ingested a medication that affects
lack of oxygenated blood, the period of reperfusion may also the serotonin neurotransmitter system, in 50% of the cases the
cause damage to the affected tissue. patient will develop the syndrome within just 2 hours of start-
Reticular activating system: Portion of the brain that inte- ing the medication or illicit drug (Mills, 1995). This condition
grates sensory stimuli, screening out unnecessary sensory sig- constitutes a medical emergency and should be treated by a
nals and integrating others to coordinate awareness. Other physician.
functions of this part of the brain include respiration and car- Side effects of a drug: The unintended effects of a chemical
diac function modulation; this system also plays a role in the in the body. For example, if a person takes some aspirin to
control of muscle actions. control his or her fever, this is the prime effect of the aspirin.
Glossary 467
The ability of aspirin to contribute to gastrointestinal bleeding T-helper cell: A form of cell found in the body’s immune sys-
is an undesired side effect. tem that helps to activate the body’s immune response to a
“Silent” cardiac ischemia: Episode of cardiac ischemia that foreign cell.
is not accompanied by pain or shortness of breath, symptoms Therapeutic half-life: The period of time the body requires
that usually occur when the heart muscle is deprived of oxy- to reduce the effectiveness of a single dose of a drug by 50%.
gen. See also Ischemia. Therapeutic index (TI): The ratio between the ED50 (dose at
Single photon emission computed tomography: A diagnos- which 50% of the population will experience the desired effect
tic scanning process that allows scientists to study blood flow from a compound) and the LD50 (dose at which 50% of the
patterns in living tissues. population will die from the effects of a compound—or the
Site of action: Where a drug has its prime effect. level of radiation exposure that is estimated to kill 50% of
the unprotected population).
Sleep apnea: A breathing disorder in which the individual’s
ability to breathe is disrupted during sleep. Complications of Therapeutic threshold: The point at which the concentra-
sleep apnea can include high blood pressure, a disruption of tion of a specific chemical begins to have the desired effect on
the normal heart rate, and possibly death. the user.
Sleep latency: The period of time between when the individ- Therapeutic window: The dosage range in which the person
ual first goes to bed and when he or she finally falls asleep. is taking enough of a pharmaceutical agent to benefit from it
Subdural hematoma: Hemorrhage in the skull leading to the without taking so much that she or he would become toxic
collection of blood between the membranes surrounding the from that compound.
brain or spinal cord and the skull bones. This condition usually Thiamine: Also known as vitamin B-1. The body uses B-1 to
develops as a result of trauma. It puts pressure on the surround- maintain appropriate function of cells in the cardiovascular
ing tissues of the CNS and can lead to paralysis or even death. and nervous systems.
Sublingual method of drug administration: Method of drug Tolerance: Resistance to the drug’s effects developed over
administration in which a tablet, capsule, or liquid is placed time as the body adapts to the repeated administration of a
under the tongue where it can be absorbed quickly through chemical compound.
the blood-rich tissues into the blood. Some medications and a Transdermal: Literally, “across the skin.”
small number of the drugs of abuse are administered this way.
Type 2 diabetes mellitus: Also known as “adult onset” dia-
Substance use disorder: A condition in which a person’s betes. Condition in which the individual’s body becomes in-
chemical use has exceeded social or cultural norms, some- sensitive to the effects of the insulin being produced. This is
times to the point of the person’s being addicted to a the most common form of diabetes, accounting for 85% of all
chemical. cases of diabetes mellitus.
SUD. See Substance use disorder. Ulcer, “bleeding”: Created when a stomach ulcer forms
Suicide: The intentional self-termination of one’s life. over a blood vessel; the acid will destroy the walls of the
Sumer: The first city-state, located in what is now Iraq. The blood vessel, allowing blood to escape into the stomach.
city-state of Sumer gave rise to the Sumerian empire. It was in Bleeding ulcers are a life-threatening emergency. See also
Sumer that the art of writing was developed, initially as a sys- Ulcer, gastric.
tem for economic record-keeping. Shortly after writing was de- Ulcer, gastric: Condition occurring when stomach acid is
veloped, laws and important events were also recorded on clay brought into contact with the tissues of the stomach, gradu-
tablets. Many of the tablets are devoted to the process of brew- ally destroying an area of stomach lining. The condition is
ing beer, apparently a favorite beverage in this ancient empire. usually quite painful.
Synapse: A microscopic gap between two neurons, across Upregulation: The process by which a neuron will increase
which one neuron will release neurotransmitter molecules to the number of receptors in the cell wall, thus increasing the
receptor sites to transmit a message to the next neuron in that sensitivity of that neuron to a certain neurotransmitter. This is
nerve pathway. usually done to provide the neurotransmitter molecules more
Synergistic response: The result when two or more com- potential receptor sites at which they might “bind.”
pounds with the same or similar actions multiply the effects of Vasospasm: A phenomenon in which a blood vessel will go
each other. into spasms, which interferes with the ability of that vessel to
Synesthesia: A phenomenon in which information from one control blood flow. If the vasospasm continues long enough,
sense may “slip over” into another sensory system. A person blood clots might form, which then could cause an occlusion
who is experiencing synesthesia may report that they are able by blocking the blood flow through either an artery or vein.
to “taste” colors or “see” music. Ventricular fibrillation: A pattern of rapid and essentially un-
Temporal lobe: A region of the brain’s cortex involved in sen- coordinated contractions of the lower two chambers of the heart
sory function, language use, and some aspects of emotions. (the “ventricles”), disrupting the pumping action of the heart.
468 Glossary
Viral load test: A procedure using DNA technology designed Wound botulism: A form of botulism that develops when
to provide an estimate of the number of virus particles in a spores of the microscopic organism Clostridium botulinum
given unit of blood (usually cubic millimeter). This test is infect a wound and begin to produce the neurotoxin
used to estimate the progression of viral infections such as botulinum.
HIV/ AIDS and the various hepatitis viruses. Zero-order biotransformation process: A subform of the bio-
Withdrawal: The characteristic process of reverse adaptation transformation process in which a foreign chemical is metab-
that occurs when a drug that has been repeatedly used over a olized at a set rate, no matter how high the concentration of
short period of time is suddenly discontinued. See also that chemical is in the blood.
Tolerance.
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INDEX
(1-(1-2-thienylcyclohexyl) piperidine) ACOA (Adult Children of Alcoholics), agonist, defined, 58

(TCP), 434 304–308 AIDS, 401–406
(1-(1-phenylcyclohexyl)-pyrrolidine) acquired immune deficiency aspirin and, 211
(PHP), 434 syndrome. See AIDS how it kills, 402–403
(1-piperidinocyclohexanecarbonitrile) acupuncture, as treatment Kaposi’s sarcoma and, 406
(PCC), 434 technique, 337 suicide and, 406
2-amino-4-methyl-5-phenyl-2- addiction See also HIV
oxazoline, 435 addictive personality, source of belief Al-Anon, 422
2-methylamino-1-pheylpropan- in, 31–32 Alateen, 422
1-one, 129 biopsychosocial model, 33 alcohol
(2-o-chorophenyl-2-methylamine chronic pain and, 378–379 accidental injury, as factor in, 70–71
cyclohexanone), 434 as common end point, 33 acetaminophen and, 218–219, 220
2-oxy-LSD, 182 as a continuum, 8–9 addiction to, 17–18
2,5-dimethoxy-4-methylamphetamine current research, 15–16 alcohol content, modern, 62
(DOM), 434, 437 defined, 12–13, 14 alcoholic personality, myth of, 31
6-desmethylnaproxen, 213, 215 as disease, 26 alcoholism as disease, 2, 16, 17–18
elements of, 16 anxiety, relationship of abuse to, 83
AA. See Alcoholics Anonymous as end stage disease, 33 aspirative pneumonia, 68
absorption, of drugs into families and, 300–308 assessment of problem for
body, 49–50 as form of insanity, 45 rehabilitation, 309–322
Acamprosate (calcium acetylhomotau- growth of pseudoaddictions, 15 atrial fibrillation, 79
rinate), 386–387 honesty in recovery, 41 biotransformation of, 64–65
accidental injury infectious disease as result of, blackouts, alcohol-induced, 79–80
alcohol use as cause of, 70–71 399–411 blood alcohol level, 65–66, 68, 74
as sign of adolescent chemical manipulation by addicts, 39–41 breast-feeding and use of, 239
abuse, 275 medical model of, 17–27 cancer, and chronic use of, 75
acetaldehyde, as byproduct of tobacco psychosocial models of, 28–35 cardiomyopathy, alcohol-
use, 226 sexual activity and, 378 induced, 79
acetaminophen spiritual disorder theory, 36–45 as cardiotoxin, 79
alcohol use and, 220 theoretical models of, 30 cirrhosis of the liver, 77
as analgesic, 213 See also specific drugs consumption in Europe, 72
complications of use, 218–219 Addiction Severity Index, 312 consumption in United States,
dosage, normal, 219 ADH (antidiuretic hormone), 87 62, 72
dosage levels, normal, 215 ADHD. See attention deficit- controlled drinking, 369–370
end state renal disease and, 219 hyperactivity disorder (ADHD) cost of abuse, 5
history of, 210 adinazolam, 99–100, 102 cultural influences on, 11–12
liver damage and, 218–219, 220 adolescents. See children and death caused by abuse of, 87
medical uses of, 211 adolescents dementia, alcohol-induced, 80
overdose, 213, 219–220 Adult Children of Alcoholics (ACOA), depression, alcohol use and, 84–85
pharmacology of, 212–213 304–308 dietary deficiencies, 77–78
pregnancy, use during, 247 adulterants, added to illegal drugs, disinhibition effect, 66–67
suicide attempts and, 220 439–440 distillation, as production method
vitamin C and, 219 aerosols. See inhalants of, 61
acetylcholine, nicotine use and, 225, 227 African-Americans, substance abuse drug interactions, 69–70
acetylsalicylic acid, 209. See also and, 262 elderly people and, 255–258
aspirin aftercare treatment, 339–340 emotions, effect on, 83–5
537
538 Index
alcohol (continued) alcohol amnestic disorder, 81 amphetamine-like drugs, 114–117

esophageal varices caused by, 77 alcohol dehydrogenase, 63, 64, 218 analogs of, 433–434
expectations of use of, 10–11, 66 alcohol-flush reaction, 65 anorexia, caused by, 119
gastritis, alcohol-induced, 77 Alcohol or Drugs of Abuse cardiovascular system, effects on, 127
gender as issue in tolerance of, 63, (AODA), 332 central nervous system, effects on,
253, 254 alcohol use disorder (AUD) 123–125
glossitis, as result of chronic use, as cause of suicide and violent children and abuse of, 266
77–78 crime, 1–2 depression and, 119, 121
hallucinations, during withdrawal elderly people and, 255–258 digestive system, effects on, 127
phase, 86 gender and, 252 drug interactions, 120–121
hangovers, 68 impact on health care system, 2, 5 formication, as result of abuse of, 127
heart disease, 78–79 pharmacotherapy for, 383–388 history of, 117–119
hepatitis, 77 scope of problem, 72–73 medical uses of, 118–119
history of, 60–61 See also chemical abuse methods of administration, 119–120
intoxication, as result of use of, Alcohol Use Inventory (AUI), 312 narcolepsy and, 119
67–68 alcohol withdrawal syndrome neuroadaptation to, 120
Jellinek’s drinking styles (table), 19 (AWS), 74, 85–86, 88, 383–388 pharmacology, 119–121
Jellinek’s four stages of alcoholism, 18 alcoholic hallucinosis, 86 pharmacotherapy for addiction, 396
limited use, defined (footnote), 78 Alcoholics Anonymous, 32 pregnancy, use during, 242
liver damage, chronic use as cause “Big Book,” 425 psychosis, amphetamine-induced,
of, 76–77, 219 criticism of, 425–426 125–126
marijuana use and, 151 effectiveness of, 419–421 pulmonary system, effects on,
marriage and abuse of, 301–302 “hitting bottom,” 32 127–128
medical complications, 68–70, homosexuals and, 259 side effects at abused dosage, 123
75–84 organization, 412–421 side effects at normal dosage, 121
Mellanby effect, 65 role in recovery, 348 “speed run,” 125
moderate use, defined (footnote), 78 spiritual beliefs, 37–38, 43, 45, in sports, 119
pancreatitis caused by abuse, 77 414–415 strokes, as caused by, 125–126
pharmacology, 63–65 telling the truth, 41 subjective use of, 121
portal hypertension caused by Twelve Steps and Twelve Traditions testing for use, 376
abuse, 77 (book), 42, 416 tolerance to, 120, 125
pregnancy, use during, 237–239 women alcoholics and, 254 Tourette’s syndrome, aggravated by
production of, 61–62 aldehyde dehydrogenase, 65 use of, 116, 121
rare social drinker, effects on, 66–71 alpha alcoholic, 19 toxic dose, 125
relationship to substance abuse, 16 alprazolam, 99–100, 104 violence, caused by use of, 123
sleep, effects on, 68, 82 Alzheimer’s disease in weight control, 119
smoking and, 226 benzodiazepines and, 105 See also methamphetamines
social learning process, 10 smoking cigarettes and, 234 amygdala
strokes, as cause of, 69 Ambien. See zolpidem cocaine’s effects on, 134
subjective effects of, 66–67 amblyopia narcotic analgesics and, 162
suicide, as factor in, 84–85 alcohol-induced, 80 amyl nitrite, abuse of, 200
teenagers, use by, 265 (figure) drug-induced, 97 anabolic-androgenic steroids. See
testing for use, 376 See also vitamin deficiencies steroids
TIQ hypothesis, 74–75 American Society of Addiction anabolic steroids. See steroids
tolerance, as sign of alcoholism, Medicine (ASAM), 357 analgesics, over-the-counter
73–74 Aminorex, 435 See also aspirin; NSAIDs
as toxin, 64–65 amnesia complications of use, 209–221
ulcers, alcohol-induced, 77 alcohol-induced, 79 elderly people and toxic reactions
vitamin deficiencies, 62, 75, 77–78, benzodiazepine-induced, 105 from, 217
80–81 See also blackouts history of, 209–210
Wernicke-Korsakoff’s syndrome, amotivational syndrome, 155–156 medical uses of, 210–212
80–81 amphetamines overdose, 219–221
withdrawal from, by chronic drinker, abuse of, 121, 123–128 pharmacology of, 212–214
74, 85–88 addiction, scope and problem of, potential for abuse, 209–221
withdrawal syndrome, 14–15, 121–130 anandamide, 149
85–86, 88 addictive potential of, 128 anemia
women alcoholics, 254 ADHD, as treatment for, alcohol-induced, 79
See also alcohol use disorder (AUD) 115–117, 119 steroids as treatment for, 202
Index 539
angina pectoris, amyl nitrite in drug interactions, 217–218 BAL (blood alcohol level), 65–66,
treatment of, 200 elderly people and toxic reactions 68, 74
anorexia from, 217 barbiturates, 93–94
acetaminophen-induced, during hepatotoxicity, as side effect, 217 absorption into bloodstream, 51
overdose, 220 history of, 209 abuse of and addiction to, 89–98
alcohol withdrawal syndrome as IUDs, effects on, 217 abuse potential, 91
cause of, 86 medical uses of, 210–211 ADHD and use of, 94
amphetamine use and, 121, 127, 128 melatonin, effect on, 216 complications of, 93–95
aspirin and, 216 myocardial infarctions, as treatment death caused by, 93, 95
aspirin use, as side effect of, 216 for, 210–211 dosage levels (table), 95
barbiturate withdrawal and, 96 opioids used with, 165 drug interactions, 94–95
marijuana and, 147, 156 overdose, 220 history of, 90–91
MDMA abuse, side effect of, 190 pharmacology of, 212 intoxication caused by, 95
methylphenidate-induced, 116 pregnancy, use during, 247 IQ, as affected by chronic use of, 94
nicotine gum, as side effect of, 296 primary and side effects of, 47 lethal injection, used in, 91
opioid withdrawal, as symptom Reye’s syndrome and, 217 neuroadaptation to, 96
of, 175 sperm, effect on, 217 pharmacology, 91–93
PCP abuse and, 187 suicide attempts and, 220 photosensitivity, caused by use of, 94
steroid withdrawal and, 207 thromboxane A2, effects on, 211 REM sleep and, 93
Antabuse (disulfiram), 384–386 TIA, as treatment for, 211 spectrum of intoxication (figure), 90
antagonist, defined, 58 See also analgesics, over-the-counter subjective effects of, 93
antidiuretic hormone (ADH), 87 “aspirin triad,” as contraindications substitutes for, 91 (table), 96–97
antisocial personality disorder (ASPD), to NSAID use, 216 withdrawal syndrome, 95, 96
286–287 (footnote), 219 behavioral tolerance, to alcohol, 73
anxiety asthma belladonna, 184, 425
alcohol-related, 83 aspirin and, 216 Benzedrine
benzodiazepines, as treatment for, cocaine abuse as cause of, 139 ADHD, as treatment for, 119
89, 99, 101–102, 104, 107 ephedrine, as treatment for, 115 history of use, 118
buspirone, as treatment for, 110 inhalants as cause of, 198 benzodiazepine receptor agonists
dual diagnosis patients and, 283–284 secondhand smoke as cause of, 232 (BRAs), 99, 110
marijuana-induced, 153 ataxia benzodiazepines (BZs)
MDMA-induced, 190 alcohol use/abuse as cause of, 67 abuse of and addiction to, 99–113
morphine, as treatment for, 165–166 GHB-induced, 436 alcohol, as substitute for, 83–84
nicotine withdrawal, as symptom inhalants as cause of, 198 Alzheimer’s disease and, 105
of, 226 MDMA abuse as cause of, 190 amnesia, caused by use of, 105
PCP-induced, 186 PCP abuse as cause of, 187 anxiety, as treatment for, 89, 99,
AODA (Alcohol or Drugs of zaleplon-induced, 111 101–102, 107
Abuse), 332 atrial fibrillation children and abuse of, 266
arrhythmias. See cardiac arrhythmias alcohol-induced, 79 complications of use, 104–106
arthritis, aspirin use and, 211 cocaine-induced, 140 depression and, 105
ASAM (American Society of Addiction attention deficit-hyperactivity disorder discontinuance syndrome, 102
Medicine), 357 (ADHD) drug interactions, 105–106
aseptic meningitis, 218, 219 addiction in dual diagnosis patients, elderly people, side effects in,
Asian culture and alcohol abuse, 282–283 102, 104
65, 262 barbiturates and, 94 hallucinations, as side effect,
ASPD (antisocial personality disorder), Benzadrine and, 119 104, 107
286–287 cigarette smoking during pregnancy hangovers, 102
aspirative pneumonia, as result of and, 246–247 insomnia, taken for, 99, 107
alcohol consumption, 68 Ritalin and, 115–117 long-term consequences of abuse,
aspirin AUD. See alcohol use disorder (AUD) 107–108
AIDS virus and, 211 AUI (Alcohol Use Inventory), 312 LSD and, 184
alcohol and, 218 avitaminosis, 62, 75, 77 medical uses of, 99–100
allergic reaction to, 216 AWS. See alcohol withdrawal neuroadaptation to effects of,
asthma and, 216 syndrome (AWS) 103–104
cancer, as prevention of, 211, 212 azapirones, 108 paradoxical rage reaction and, 104
complications of use, 215–218 pharmacological characteristics of,
death caused by high dosage, 220 Baclofen, 387–388, 395 100 (table)
dosage levels, normal, 214–215 “bad trip,” LSD-induced, 11, 183–184 pharmacology, 100–102
540 Index
benzodiazepines (continued) bupropion, 246 steroid abuse and, 206

pregnancy, use during, 245 BuSpar. See buspirone See also CNS stimulants
rebound anxiety and, 107 buspirone, 108–110 cerebral infarction. See strokes
side effects of, 102 alcohol dependence and, 387 cerebral vascular accidents. See strokes
sleep apnea and, 105 anxiety, taken for, 110 “Challenge Model” of child’s
subjective effects of, 106–107 depression, taken for, 108 growth, 307
as substitute for other drugs of drug interactions, 109–110 chemical abuse. See substance abuse
abuse, 108 elderly people, effects on, 109 chemical dependency, decision-
suicide, as result of taking, 100 pharmacology, 109–110 making process, 13
testing for use, 376 pharmacotherapy, use in, 398 child abuse, as result of alcohol
tolerance to, 107 pregnancy, use during, 246 abuse, 70
toxic psychosis, as result of chronic serotonin syndrome, induced by, 109 children and adolescents
use, 107 side effects of, 108 abuse/addiction, how to define,
withdrawal syndrome, 103–104 tolerance to, 109 272–275
benzopyrene, 226 withdrawal syndrome, 109 age as factor in substance abuse,
benzoylecgonine, 135 butyl nitrite, 195, 200 263–264, 267
benzylfentanyl, as drug analog of BZs. See benzodiazepines (BZs) alcohol, use by, 265 (figure)
fentanyl, 438 amphetamines, abuse of, 266
beta alcoholic, 19 CAGE, 276, 310 benzodiazepines, abuse of, 266
beta endorphin, 161 calcium acetylhomotaurinate, cigarette smoking as addiction, 227
“Big Book” of AA, 425. See also 386–387 college students and substance
Alcoholics Anonymous cancer abuse, 266–267
“binge,” defined, 73 alcohol abuse as cause of, 75 deaths related to substance abuse, 267
bioavailability, 49–53 aspirin in prevention of, 211, 212 depression and, 269–270
biomedical model of addiction. marijuana as cause of, 154 diagnosis and treatment of abuse,
See medical model of steroid use as possible cause of, 272–275
addiction 205, 206 diagnostic criteria of abuse, 275–277
biopsychosocial model of addiction, 33 tobacco as suspected cause of, drug use patterns, 264
biotransformation, 52–53 228–230, 232 ephedrine, use of, 266
bipolar affective disorders, 284–285 carbon monoxide gateway drug theory and, 267
birth defects cigarette smoking and, 224, 230 hallucinogens, abuse of, 266
alcohol-induced, 87, 237–239 marijuana smoking and, 154 heroin, abuse of, 266
opiate abuse and, 243 cardiac arrhythmias inhalants, abuse of, 194, 195, 196,
blackouts, alcohol-induced, 79–80 amphetamine-induced, 127 266, 267–268
blood alcohol level (BAL), 65–66, cocaine-induced, 140 LSD, use by, 180 (figure), 266
68, 74 ephedrine-induced, 122 marijuana, use by, 148 (figure),
blood-brain barrier, 58–59 MDMA-induced, 190–191 266, 267
“blunts,” 151 cardiomyopathy methylphenidate, abuse of, 266, 267
Boggs Act, 444 alcohol-induced, 79 narcotic analgesics, abuse of, 266
“booting,” 173 MDMA as cause of, 191 parent relationship and substance
bradykinin, 212 methamphetamines as cause abuse, 271
brain damage of, 127 peer pressure and substance
alcohol abuse as cause of, 7, 75, 80, “Cat,” 129–130 abuse, 270
87, 267 cataracts rehabilitation, special needs
amphetamine abuse as cause of, 125 aspirin as inhibitor of, 211 during, 277
barbiturate abuse as cause of, 96 cigarette smoking as suspected cause secondhand smoke and, 232
inhalant abuse as cause of, 198, 199 of, 231 stages of abuse, 273–274
marijuana use as cause of, 155 ibuprofen as suspected cause of, 218 substance abuse, scope of problem,
MDMA use as cause of, 191–192 CD (conduct disorder), 270 264–268
PCP use as cause of, 187 CD4+ T cells, 405 substance abuse and, 263–278
substance use disorder as cause cellular transport mechanisms, 49 tobacco abuse, 268–269
of, 2 and drug distribution, 49 violence, drug-related, 267, 303
bromide salts, 90 central nervous system (CNS) why children abuse drugs, 269–272
bromocriptine, 395 alcohol and, 79–80 children of alcoholics. See Adult
Brompton’s cocktail, 133 benzodiazepines and, 104, 106 Children of Alcoholics (ACOA)
bruxism, 190 cocaine use and, 141–142 “chippers”
buprenorphine, 168–169, 171, inhalant abuse and, 197, 198 narcotics and, 174
392–395 narcotic analgesics and, 161–162 tobacco and, 227–228
Index 541
chloral hydrate, 89, 91 (table) snorting, as method of abuse, 136 alcohol abuse as cause of accidental,
chlordiazepoxide, 99 subjective effects of abuse, 138 70–71
chronic phase of alcoholism, 18 suicide, as result of use of, 142 alcohol addiction as cause,
cigarette smoking. See tobacco testing for use, 375 75, 85
“circle” of addiction, 38–39 tolerance to, 134 and aspirin, normal use of, 221
cirrhosis of the liver Tourette’s syndrome, aggravated by and aspirin overdose, 220
alcohol as cause of, 77 use of, 142 barbiturate-induced, 93, 96
in women versus men, 253 violence, caused by use of, 143 blood alcohol level, 67
CIWA-Ar, 86 withdrawal syndrome, 143 cigarette smoking as cause, 4
Claviceps purpurea, 179 Cocaine Anonymous, 348 cocaine-induced, 135, 138
Clinical Institute Withdrawal codeine, 163, 171 codeine-related, 171
Assessment for Alcohol Scale- codependency ephedrine-induced, 115, 122
Revised, 86 cycle of, 294–295 heroin-induced, 177
“clock watching,” 106 defined, 292, 297 inhalant abuse as cause of, 197
clonazepam, 99, 103, 107 dynamics of, 292–293 LSD-induced, 182
clonidine, 398 enabling and, 291–292 marijuana abuse as cause of, 156
Clonopin, 103 as learned behavior, 293–294 MDMA abuse as cause of, 193
CNS stimulants patterns of, 295–296 PCP abuse as cause of, 188
abuse of and addiction to, 114–130 reactions to, 296–299 secondhand smoke and, 232
chemicals classed as, 114 rules of, 293 substance abuse and preventable
recovery from abuse, 347–348 self-esteem in codependent death, 1
violence and, 282 relationships, 294 tobacco use as cause of,
co-alcoholic, 298 “coke paranoia,” 142 228–230
cocaine, 131–144 “coke runs,” 138 delirium tremens (DTs)
abuse, scope of, 133, 136–138 Comprehensive Drug Abuse alcohol and, 86–87
addiction to, 138 Prevention and Control Act of barbiturates and, 95, 96
adulterants added to, 440 1970, 185 inhalants and, 199
Benzedrine as substitute for, 118 conduct disorder (CD), 270 delta alcoholic, 19
cardiovascular system, effects on, controlled drinking, 369–370 delta FosB, 20, 34
139–141 convulsions. See seizures dementia
as center of addict’s life, 38 coronary heart disease, alcohol and, 78 alcohol-induced, 80, 257
central nervous system and, 141–142 “cotton fever,” 176 inhalant-induced, 198
complications caused by abuse of, “crack,” as form of cocaine, 132 “demon rum,” 429
138–143 “crack babies,” 239–240 denial, defined, 43–44
“crack” as form of, 132 “crack lung,” 139 dependence
death, as indirect cause of, 143 craving, 367–369 on alcohol, 74
dopamine receptors, impact on, 134 C-reactive protein, 210–211 on barbiturates, 96
drug interactions, 135 crime, drug use and, 428–441 defined, 14
formication, as result of abuse of, 142 cross-tolerance, between chemicals, depression
gender and abuse of, 252–253 96 alcohol abuse and, 84–85, 257
as “good” drug, 29 crucial phase of alcoholism, 17–18 amphetamines and, 119, 121
history of, 131–133 “crystal.” See methamphetamines benzodiazepines and, 104
human immunodeficiency virus culture buspirone and, 108
(HIV) and, 143 African-American, 262 children and, 269–270
liver damage, caused by, 141 Asian, 65 cigarette smoking, relationship
marijuana use and, 150 Asian-American, 262 to, 234
medical use of, 133 Hispanics, 261–262 dual diagnosis patients and, 285
pharmacology of, 133–135 Jewish, 11 marijuana as cause, 153–154
pharmacotherapy for addiction, 395 Native Americans, 11–12, 260–261 MDMA-induced, 190
pregnancy, use during, 239–242 CVA. See strokes methylphenidate and, 117
primary and side effects of, 46 naproxen and, 219
psychosis, induced by abuse of, 142 Dalmane, 99, 104 PCP as cause of, 186
recovery from addiction, 348 damage model of child’s growth, 307 steroids and, 206
respiratory system, effects on, 139 D.A.R.E., 381 Deracyn, 99–100, 102
scope of abuse, 4 DEA. See Drug Enforcement description of, 56
seizures, induced by, 142 Administration “designer” drugs, 432–433
serotonin syndrome, induced by, death detoxification, defined, 52
141–142 acetaminophen-induced, 220, 221 dextromethorphan, 438–439
542 Index
Diagnostic and Statistical Manual of DTs. See delirium tremens (DTs) Eu4ia, 434
Mental Disorders-TR (DSM- dual diagnosis client, 279–290 “euphoric” recall, 365
IV-TR), 12, 270, 312, 313, 462 defined, 279 expectations
diazepam, 101, 102 diagnostic challenge, 279–281 alcohol’s effects on user and, 66
dietary deficiencies, alcohol-induced, drug of choice for, 281–287 cocaine use and, 138
77–78 scope of problem, 281 drug effects and, 10–11
“dip dope,” 180 dual diagnosis patients
disabled people, substance abuse and, denial of substance abuse problems, false pride, 41–43
259–260 287–288 families
disconnection syndrome, 81 medication compliance as problem addiction and, 300–308
disease in, 288 adult children of alcoholics,
as defined in United States, 23, 35 treatment models, 288–289 304–308
fluctuating definitions, 28–29 treatment stages, 289–290 marriage, 300–302
disease model of addiction. See medical dysphoria, 162 parental addiction, 303–304
model of addiction scope of problem, 300
disinhibition effect Ecstasy. See MDMA FAS (fetal alcohol syndrome), 237
alcohol and, 66–67 effective dose, defined, 54 FASD (fetal alcohol spectrum
barbiturates and, 93 elderly people disorder), 237–239
recreational drugs and, 440 alcohol abuse, definition of, 256 “fatty liver,” 76
dissociative personality disorder, 284 analgesics, over-the-counter, toxic FCP. See final common pathway
distribution of drugs through body, reactions from, 217 (FCP)
50–52 aspirin, toxic reactions from, 217 FDA. See Food and Drug Administra-
disulfiram benzodiazepines, side effects from, tion (FDA)
alcoholism, in treatment of, 384–386 102, 104 fentanyl, 167–168, 171–172, 437–438
pregnancy, use during, 246 buspirone, effects on, 109 fetal alcohol effects, 237
DMT, 181 cigarette smoking and, 230 fetal alcohol spectrum disorder
DOM late-onset alcoholism, 257 (FASD), 237–239
as drug analog to amphetamines, 434 prescription medication, abuse fetal alcohol syndrome (FAS), 237
as weaker than LSD, 181 of, 257 final common pathway (FCP), 33–35
dopamine substance abuse and, 255–258 first-order biotransformation, 52
amphetamine use and, 123 elimination, of drugs from body, 53 first pass metabolism, 47, 52–53
cocaine use and, 134 enabling “flash.” See “rush”
nicotine use and, 225, 227 codependency and, 291–292 flashbacks
substance abuse and, 22 defined, 291 LSD as cause of, 184–185
dopamine D2 receptors, 22, 25 therapeutic professionals and, 362 marijuana and, 155
Doral, 99, 102 endocarditis, 400 MDMA as cause of, 192
Doriden, 96–97 endorphins, and narcotics, 161 flunitrazepam, 112–113
dose-response curve (figure), 55 enkephalins, and narcotics, 161 as “date rape” drug, 112
downregulation, defined, 57 enteral methods of drug history of, 112
dream, “using,” 369 administration, 47 legal status of, in United States, 112
drug absorption (figure), 50 ephedrine, 114–115 pharmacology, 113
drug abuse. See substance abuse abuse of, 122 withdrawal from, 113
Drug Enforcement Administration central nervous system, effects on, 122 fluoxetine, 29, 106, 185, 390
drug classification and, 458 children and use of, 272 flupenthixol, in cocaine abuse
marijuana use and, 147 complications of at high dosage, 115 treatment, 395
MDMA, status of, 437 drug interactions, 115 flurazepam, 99, 101, 104
medicalization and, 443 history of, 114 Food and Drug Administration (FDA)
methadone treatment and, 389 medical uses, 114 alcoholism, medications for
and war on drugs, 6 pharmacology, 114–115 approved by, 384
drug forms, 47–53 side effects of, 115 hair-testing kits, labeling of, 377
drug half-life, 53–54 epsilon alcoholic, 19 HIV treatments approved by, 411
drug of choice, defined, 14 ergot fungus, 179 marijuana and, 147
drugs, misconceptions of, 46 Erythroxylon coca, 131, 133 opiates and, 159
drug transport mechanisms, 50–52 esophageal varices, 77 OTC analgesics and, 215
DSM-IV-TR (Diagnostic and ethanol, 60 OTC ephedrine ban, 114
Statistical Manual of Mental ether, 67 pseudoephedrine outlawed, 122
Disorders-TR), 12, 270, 312, ethnic minorities, substance abuse and, formication, defined, 127
313, 462 260–262 “freebasing,” 137
Index 543
“French paradox,” 78 hashish, 148 overdose, 221

Freud, Sigmund, 131 health care insurance and rehabilita- pharmacology of, 213
“fry,” 438 tion, 379–381 pregnancy, use during, 247–248
heart attacks. See myocardial “Ice.” See methamphetamines
GABA infarctions IM method of drug administration, 48
alcohol and, 63–64, 80, 85 heart disease, alcohol and, 78–79 individuation, 301
barbiturates and, 92 hepatitis infectious disease, and substance abuse,
benzodiazepines and, 101 alcohol as cause of, 77 399–411
gabapentin, 82 viral, 408–411 inhalants, 194–196
gait disturbance, 80, 81 hepatoxicity abuse of and addiction to, 194–200
gambling, compulsive, 285–286 aspirin-induced, 217 anesthetics, abuse of, 199–200
“games” of addiction, 39–41 steroid abuse and, 205 categories of, 195
gamma alcoholic, 19 heroin children and abuse of, 194, 195, 196,
gamma aminobutryic acid. See GABA abuse, scope of, 3–4, 174 266, 267–268
gamma hydroxybutyric acid (GHB), addiction and personal choice, 29 complications induced by,
435–436 children and abuse of, 266 198–199
gangliosides, 238 death from abuse of, 176 deafness, as cause of, 198
gastric alcohol dehydrogenase, 63 history of, 170 death as result of abuse, 197, 198
gastritis, alcohol-induced, 77 medical use of, 164 as gateway drug, 196
gateway drug theory, discussed, 268 mystique of, 169–171 half-life of, 195
gender and substance abuse, 249–254 pharmacology of, 170 hangover induced by, 197
genetic inheritance theories, 18–22, smoking, complications of, 177 history of, 194
23–25 subjective effects of abuse, 170 intoxication, stages of, 197 (figure)
GHB (gamma hydroxybutyric acid), hippocampus nitrites, abuse of, 200
435–436 adolescent substance abuse and, 267 NMDA and, 195
glue sniffing. See inhalants fetal alcohol syndrome and, 238 pharmacology of, 194–196
glutamate marijuana abuse and, 149, 150 pregnancy, use during, 248
amphetamine, effects on, 123, 125 Hispanics, alcohol abuse and, 261–262 subjective effects of, 197
tobacco use and, 225 “hitting bottom,” 32, 417–418 toxicity of, 195–196
glutathione, 219, 220 HIV withdrawal syndrome, 199
glutethimide, 96, 97 cocaine and, 143 inhalation
Graves’ disease, 231 history of, 401–402 as method of abuse, 194
group therapy, 289, 337–338, 349, 351, impact on immune system, 402–403 as method of drug administration,
352, 353, 357 marijuana use and, 154 48–49, 194–195
scope of problem, 403–404 injectables, 204 (table)
Halcion, 99 stages of infection, 404 inpatient treatment, 353–357
halfway houses, 354 transmission of, 403 insomnia
hallucinations treatment of infection, 405–406 alcohol use and, 82
in alcoholic withdrawal, 86 “holiday heart syndrome,” 79 alcohol withdrawal and, 86
benzodiazepines, as side effect, homeless people, substance abuse amphetamine use and, 121
104, 107 and, 255 aspirin, as cause of, 216
See also delirium tremens (DTs) homosexuals, substance abuse and, benzodiazepines, taken for,
hallucinogenic drugs, scope of abuse, 4. 258–259 99, 106
See also MDMA honesty as part of recovery buspirone, taken for, 108
hallucinogens process, 41 cocaine, as cause of, 142–143
abuse of and addiction to, 179–193 Horney, Karen, 31 MDMA abuse and, 190
children and abuse of, 266 human immunodeficiency virus. opiate withdrawal and, 175
defined, 181 See HIV PCP abuse and, 187
history of, 179–180 Huntington’s disease, 83 zaleplon and, 111
pharmacology of, 181–182 hydromorphone, 174 zolpidem and, 110
pregnancy, use during, 245–247 hypothalamus, 162, 210, 213 intellectualization, defined, 44
See also LSD hypoxia, 95, 199, 200 intervention
hangovers characteristics of, 324
alcohol-induced, 68 ibogaine, 388–389 court system and, 328–330
drug-induced, 93–94, 102 ibuprofen, 210 defined, 323–324
inhalant-induced, 197 anti-inflammatory properties of, 213 detaching, 325, 326
MDMA-induced, 190 complications caused by, 218 ethical questions about, 328
Harrison Narcotics Act, 160 dosage levels, normal, 215 process of, 324–326
544 Index
intramuscular method of drug naproxen and, 219 history of, 145–147

administration, 48 PCP and, 186 legalization of, 149
intranasal method of drug administra- steroid use and, 205 medicinal, debate surrounding,
tion, 48 liver failure. See hepatoxicity 146–147
intravenous method of drug lorazepam, 101, 106 occasional use, adverse effects of,
administration, 48 loss of control, 23 152–154
Inversine (mecamylamine), 398 LSD pharmacology of, 149–151
IQ abuse, scope of, 181 pharmacotherapy for addiction,
cocaine abuse by mother and, 240 “bad trip,” 183–184 395–396, 398
fetal alcohol syndrome and, 238–239 benzodiazepines and, 184 pregnancy, use during, 244–245
phenobarbitol, effects on, 94 death caused by, 182 psychosis, drug-induced, 153
isabutyl nitrite, abuse of, 200 dosage, 181–182 recovery from abuse, 348–349
Italian-American culture and alcohol flashbacks induced by, 184–185 respiratory system and, 154
abuse, 11 half-life of, 182 social learning process, 10
IV method of drug administration, 48 hallucinations induced by, 183–185 subjective effects of, 152
history of, 179–180 teenagers, use by, 148 (figure),
Jellinek, E. M., 17–18, 19, 23, 27 liver as site of biotransformation, 182 266, 267
Jewish culture and drug abuse, 11 pharmacology of, 181–182 testing for use, 374–375
psychosis and, 184 violence, caused by, 156
Kaposi’s sarcoma, 406 seizures induced by, 182 women users and, 254
“Kat,” 129–130 subjective effects of, 182–185 MAST (Michigan Alcoholism
ketamine, 434–435 suicide induced by, 184–185 Screening Test), 310
ketoprofen, 210 teenagers, use by, 180 (figure) MATCH project, 365
“Khat,” 129–130 testing for use, 375 MDMA
“kindling,” 142 See also hallucinogens abuse, scope and patterns of, 181,
Korsakoff’s psychosis, 81 lungs, damage to 188–189
by amphetamines, 124 amphetamines, as similar to, 189
LAAM (L-alpha-acetylmethadol), 393 by cigarette smoking, 224, 227, 228 anxiety induced by, 190
late-onset alcoholism, 257 by cocaine, 139 complications of use, 190–193
lead, 198, 431 by inhalation, 48–49 death, caused by, 193
least restrictive alternative, 359 by marijuana, 438 drug interactions, 193
legalization lupus, 218 flashbacks induced by, 192
of drug use, 442–451 lysergic acid diethylamide-25. as “good” drug, 29
medicalization and, 442–443 See LSD hallucinations induced by, 190
lesbians, substance abuse and, heart damage caused by, 191
258–259 M3G, 163 history of, 180, 188
lethal dose index, 54 M6G, 163 insomnia, induced by, 190
LifeRing, 425 MacAndrew Alcoholism Scale, 311 legal status of, 188
limbic system, role in body’s reward male-limited alcoholics, 24 liver damage, relationship to, 193
system, 22 malnutrition neurotoxic effects of, 191–192
limit setting, in treatment, 362 alcoholism and, 76–77 pharmacology of, 189
lipid-soluble drugs, 50–51 substance abuse and, 356, 399 pregnancy, use during, 245–246
lithium MAO inhibitors psychosis, induced by, 193
alcoholism, in treatment of, 386 buspirone and, 109–110 rage induced by abuse, 192–192
ibuprofen and, 218 narcotic analgesics and, 165 serotonin, impact on, 189,
liver marijuana, 145–157 191–192
acetaminophen and, 218–219, 220 abuse, scope of, 4, 148–149 subjective effects of, 189–190
alcohol and, 76–77, 219 addiction potential of, 156–157 tachycardia induced by, 191
amphetamines and, 120, 127 adulterants added to, 440 testing for use, 375
aspirin and, 217 alcohol use and, 151 mecamylamine, 398
barbiturates and, 92, 95 amotivational syndrome, 155–156 medicalization, legalization and,
benzodiazepines and, 104, 106, 110, anxiety caused by, 153 442–443
111, 112 chronic abuse, consequences of, medical model of addiction, 17–27,
biotransformation and, 52–53 154–156 28–30
LSD and, 182 cocaine use and, 150 defined, 17
marijuana and, 150 death, as cause of, 156 and personal responsibility, 26–27
MDMA and, 189, 193 depression caused by, 153–154 reactions against, 22–27
methylphenidate use and, 116 drug interactions, 150–151 variation of, 33
Index 545
medulla mind-body question, 38 children and abuse of, 266

amphetamines and, 120 “mini-decision,” 366 classification of, 160
barbiturates and, 92, 95 minimization, defined, 44 complications from, 166–167,
codeine and, 163 Minnesota Model of chemical 176–177
melatonin, 106, 111 dependency treatment, 334–335 death from abuse, 176, 177–178
aspirin and, 216 Minnesota Multiphasic Personality drug interactions, 165
Mellanby effect, 65 Inventory, 311 gender and abuse of, 252
membrane fluidization theory, 63 MMPI, 311 history of, 158–160
memory MOA inhibitors, amphetamine use medical uses of, 158–169
alcohol abuse and loss of, 17, 79–80 and, 120–121 pharmacology of, 161–164
benzodiazepine, interference of, 105 Moderation Management, 424–425 pregnancy, use during, 242–244
cocaine abuse and, 134, 141 monoamine oxidase inhibitors. See pseudoaddiction, 165
marijuana use and, 149–150 MAO inhibitors subjective effects of in medical
mental illness. See dual diagnosis client moral insanity, 38, 44 practice, 165–166
meprobamate, 97 morphine testing for use, 376
Merton, Thomas, 37 anxiety, in treatment of, 165–166 tolerance of, 173
mescaline, 181, 184 compared to alcohol, 66 treatment, points to address during,
mesolimbic region of brain, role in history of, 159 345–347
body’s reward system, 22 pharmacology of, 163 withdrawal from, 167, 175–176
metabolic tolerance, defined, 14 morphine-3-glucuronide, 163 Narcotics Anonymous (book),
methadone morphine-6-glucuronide, 163 39, 41
as analgesic, 164 MPP+, 431 Narcotics Anonymous (organization)
as cover for addiction, 41 MPPP, 431 description of, 421–422
as maintenance for opioid addiction, MPTP, 431 role in recovery, 348
389–392 multiple personality disorder, 284 spiritual beliefs, 37–38, 45
pharmacology of, 163–164 myocardial infarctions The Triangle of Self Obsession
methamphetamines amphetamine-induced, 127 (pamphlet), 42
abstinence syndrome, 128 aspirin as treatment for, 210–211 Native Americans, alcohol abuse and,
abuse of, 121 cigarette smoking as contributing 11–12, 260–261
homosexuals and abuse of, 258 to, 230 nausea
“Ice,” 124, 128–129 cocaine-induced, 140 alcohol-induced, 65, 68
“meth mouth,” 127 NSAIDs and, 211–212 aspirin-induced, 216
“Nazi meth,” 124 steroid-induced, 205 fentanyl-induced, 168
scope of abuse, 123–124 myocardiopathy. See cardiomyopathy ibuprofen-induced, 218
methaqualone, 97 myoglobinuria, 187 inhalant abuse and, 197
methcathinone, 129–130 marijuana, antinausea effects of, 146
“meth mouth,” 127 N-acetylcysteine (NAC), 220 marijuana withdrawal and, 156
methylphenidate, 115–117 N-acetyl-para-aminophenol, 210 MDMA-induced, 188, 190
abuse of, 122–123 naloxone hydrochloride, 178 nicotine-induced, 227
ADHD and, 115–117 N alpha-dimethyl-1,3 benzo-dioxole- opiate-induced, 166
central nervous system, effects on, t-ethanamine (MDMA), 188. necrotizing fascitis, and injected drug
122–123 See also MDMA abuse, 400
challenges to use of for ADHD, 117 naltrexone hydrochloride, 386 Neisseria sicca, 399
children and abuse of, 266, 267 naproxen, 210 N-ethyl-1-phenylcyclohexylamine
drug interactions, 117 allergic reactions caused by, 219 (PCE), 434
impact on heart, 116 anti-inflammatory properties, neuroadaptation, 58
liver damage caused by use of, 116 213–214 neurogenetic determinism, 24
medical uses of, 116 complications of use, 219 Neurontin, 82
pharmacology, 116 dosage levels, normal, 215 neurotransmitters, 56–58
psychosis caused by use of, liver damage caused by, 219 nicotine
122–123 overdose, 221 acetylcholine, effect on, 225, 227
side effects, 116–117 pharmacology of, 213–214 addiction to, 227–228
“zombie” effect caused by, 116–117 Narcan (naloxone hydrochloride), 178 bioavailability of in cigarettes,
Michigan Alcoholism Screening Test narcolepsy, 119 224–225, 225–226
(MAST), 310 narcotic analgesics dopamine, effect on, 225, 227
midazolam, 101 addiction to, 159, 167, 173 drug interactions, 226
milieu-limited alcoholism, 24 brain receptor sites utilized by, gender as an issue in use of, 254
Miltown, 96–97 162 (table) lethal dose of, 225, 226–227
546 Index
nicotine (continued) benzodiazepines and alcohol community-acquired, 401

potential for addiction, 227 interaction, 84 fungal, 400
pregnancy, nicotine replacement use flunitrazepam and, 113 Pneumocystis carinii (PCP), 405
during, 247 paraldehyde, 89–90 portal hypertension, 77
recovery from abuse, 349–350 paranoia post hallucinogen perceptual
replacement therapies, 396–398 MDMA-induced, 190 disorder, 185
tolerance to, 225 PCP-induced, 186, 188 potentiation effect, 11, 94, 108, 112
transdermal patch, use of, 48, 85, parenteral methods of drug prealcoholic phase of alcoholism, 17, 18
254, 396–397 administration, 47–48 pregnancy
withdrawal from, 226, 228 passive diffusion, as cellular transport aspirin as birth control, 218
nicotine-n-oxide, 225 mechanism, 49 substance abuse during, 236–248
nitrous oxide, abuse of, 199–200 PCC, 434 prime effects of chemicals, 46–47
NMDA PCE, 434 “problem drinkers,” 73
alcohol’s effect on, 64, 80, 85 PCP (phencyclidine) prodromal phase of alcoholism, 17, 18
inhalants and, 195 abuse, scope of, 185 projection, defined, 44
opioids and, 164–165 analogs of, 434 proprionic acids, 210, 211–212
PCP and, 186 biotransformation of, 186 prostaglandins, 212, 218
Noludar, 96–97 death, as indirect cause of, 188 Provigil, 267
non-steroidal anti-inflammatory depression as result of abuse, 186 psilocybin, 437
drugs, 210 half-life of, 186–187 psychadelic compounds, 180.
norepinephrine history of, 10, 185 See also LSD
amphetamines and, 120, 123 intoxication induced by, 187 psychosis, drug-induced. See specific
cocaine abuse and, 134, 140, 143 memory problems induced by, drugs as cause of psychosis
nicotine use and, 227 186, 187 punishment potential, defined, 10
NSAIDs (non-steroidal anti- panic reaction as result of abuse, 185 Pure Food and Drug Act of 1906, 132,
inflammatory drugs), 210, pharmacology of, 186–188 159–160
211–212 pregnancy, abuse during, 245 pyramiding, 204
nucleus accumbens, 22, 34, 64, 134, psychosis as result of abuse, 187–188
142, 169, 367 subjective effects of, 185–186 “qat,” 129–130
nystagmus suicide, as result of abuse, 186, 188 Quaalude, 96–97
inhalant abuse and, 198 testing for use, 375 quazepam, 99, 102
MDMA abuse and, 190 tolerance of, 187
PCP abuse and, 187 withdrawal syndrome, 186, 187 ramelteon, 111–112
Wernicke-Korsakoff’s syndrome and, PCP (Pneumocystis carinii pneumo- rationalization, defined, 44
80–81 nia), 405 Rational Recovery, 423
peak effects of drugs, defined, 55 rebound anxiety and
obsessive-compulsive disorder, 284 peripheral neuropathy, 82–83 benzodiazepines, 107
ODD (oppositional defiance peristalsis, 166 receptor site, 56–58
disorder), 270 personality disorders, real versus recovery, stages of, 341–345
ondansetron, 386 pseudo, 32–33 rectal method of drug administration, 47
opiate abuse and addiction, 158–178 pharmacodynamic tolerance, defined, 14 rehabilitation, health care insurance
opium, meaning of, 159 pharmacological reward potential, 10 and, 379–381
oppositional defiance disorder pharmacology overview, 46–59 relapse prevention, 363–367
(ODD), 270 pharmacotherapy for substance abuse, REM rebound
oral method of drug 383–398 barbiturates and, 93
administration, 47 phencyclidine. See PCP (phencyclidine) benzodiazepines and, 106–107
Orlaam, 393 phenethylamine, 189 zolpidem and, 110
outpatient treatment, 351–353 phenylcyclohexene, 186 respiratory depression
over-the-counter medication, phenylethylamines, 436–437 benzodiazepine-induced, 105
defined, 209 photosensitivity, barbiturates, as side buprenorphine-induced, 393
oxazepam, 101 effect of, 94 cocaine and, 172
OxyContin, 164, 171 PHP, 434 narcotic analgesic related, 166
Placidyl, 96–97 opiate overdose and, 177
pain, forms of, 158, 160 Pneumocystis carinii pneumonia See also sleep apnea
pancreatitis, alcohol-induced, 77 (PCP), 405 Restoril, 99
panic, drug-induced. See anxiety pneumonia reticular activating system (RAS) and
paradoxical rage reaction alcohol abuse and, 400–401 barbiturates, 94
barbiturates and, 93 aspirative, in chronic alcohol use, reward process, defined, 10
benzodiazepines and, 104 400–401 Reye’s syndrome, 217
Index 547
Ritalin. See methylphenidate SMART, 423 cost of abuse (in United States), 4–6
Rohypnol. See flunitrazepam sn-2 arachidonyglycerol (2-AG), defined, 13
“roid rage,” 206 149–150 disabled people and, 259–260
Rozerem (ramelteon), 111–112 sniffing death syndrome, 198 dopamine and, 22
rules of codependency, 293 “snorting,” 48 genetic predisposition, 18–22
“rush” social learning and drug use, 10, homeless people and, 255
amphetamine-induced, 123 11–12 homosexuals and, 258–259
cocaine-induced, 136, 138 social use, defined, 13 pregnancy and, 236–248
opiate-induced, 169 Sonata, 111 reasons for abuse, 7–8, 9–12
Rush, Dr. Benjamin, 28 Sopor, 96–97 recreational, 1–6
SOS (Secular Organizations for relationship to addiction, 16
schizophrenia and dual diagnosis Sobriety), 423–424 scope of abuse, 3–4
patients, 283 “speed run,” 125 treatment, 2–3
“secrets,” treatment, 362 spiritual disorder theory of addiction, Substance Abuse Subtle Screening
Secular Organizations for Sobriety 36–45 Inventory-3 (SASSI-3), 312–313
(SOS), 423–424 spiritus, 37 substance use disorder (SUD)
sedative-hypnotic withdrawal SSRIs (selective serotonin reuptake as cause of brain injury, 2
syndrome, 103 inhibitors), 387 as cause of child abuse, 1–2
seizures “stacking” steroids, 204 elderly people, 255–258
alcohol withdrawal and, 86 steroids gender and, 249–254
barbiturates withdrawal, 89, 91, 96 abuse of and addiction to, 201–208 personal choice and, 29
benzodiazepines withdrawal, 103, addictive potential of, 207–208 psychosocial models of, 28–35
107, 113 adolescent growth pattern and, 207 self-centeredness, 38–39
cocaine-induced, 141–142 complications of abuse, 205–207 See also chemical abuse
ibuprofen overdose and, 221 death caused by abuse of, 205–206 SUD. See substance use disorder
inhalant-induced, 199 defined, 201 (SUD)
LSD-induced, 182, 184, 185 depression caused by, 206 sudden infant death syndrome (SIDS)
MDMA-induced, 192 drug interactions, 207 cocaine abuse as suspected cause
narcotics use and, 177 as gateway drug, 207 of, 241
opiate abuse and, 175–176 legal status of, 202 opiate abuse as suspected cause
PCP-induced, 187 medical uses of, 201–202 of, 243
selective serotonin reuptake inhibitors pharmacology of, 203 secondhand smoke as suspected
(SSRIs), 99, 387 psychosis, drug-induced, 206 cause of, 232
selfhood, 37 recovery from abuse, 350 suicide
Self-Management and Recovery “roid rage,” 206 acetaminophen in attempts of, 220
Training (SMART), 423 side effects, 204 AIDS and, 406
serotonin violence, caused by abuse of, 206 alcohol, as factor in, 84–85
alcohol and, 64 withdrawal syndrome, 207–208 aspirin in attempts of, 220
buspirone and, 109 STP. See DOM benzodiazepines, caused by use
LSD and, 181, 182 Streptococcus viridans, 399 of, 100
MDMA and, 189 strokes cocaine, as caused by use of, 142
serotonin syndrome alcohol use as cause of, 69, 78–79 inhalant abuse and, 199
buspirone, as cause of, 109 amphetamines, as cause of, 125–126 PCP abuse and, 186, 188
cocaine-induced, 141–142 aspirin and, 211, 217 as result of substance abuse, 1
MDMA-induced, 191–192 cigarette smoking and, 226, 230, 233 risk factors, 85
side effects of chemicals, 46–47 cocaine-induced, 141 synapse, defined, 56
SIDS. See sudden infant death ephedrine as cause of, 115, 122 synesthesia, 152, 183
syndrome (SIDS) NSAIDs and, 211–212 systemic lupus erythematosus, 218
silver acetate, 398 steroid use as cause of, 205
site of action, of chemical agent, 55–56 subcutaneous method of drug “talking down,” LSD use and,
“skin popping,” 48 administration, 47–48 183, 187
SLE (systemic lupus sublingual method of drug “tar”
erythematosus), 218 administration, 47 cigarette smoking and, 224, 228
sleep apnea substance abuse marijuana smoking and, 154
alcohol use and, 68, 82 as an American way of life, 6 tardive dyskinesia, 81–82
benzodiazepines and, 105 assessment of problem for TBI. See traumatic brain injuries (TBI)
Rozerem (ramelteon) and, 112 rehabilitation, 309–322 TCP, 434
tobacco use and, 229 children and, 263–278 teenagers. See children and adolescents
zolpidem and, 110 continuum of addiction, 8–9 temazepam, 99, 101
548 Index
testosterone toxicology testing, 371–377, 430–431 Veterans Administration (VA) hospitals,

in marijuana users, 153, 155 transdermal method of drug 15–16
steroids, similar to, 201 administration, 48 violence
tetrahydroisoquinoline (TIQ), 74–75 transdermal patches adolescents, and drug-related,
THC, 53, 149–150, 151 as drug detection, 377 267, 303
therapeutic communities, 354 fentanyl, 167–168, 171, 438 alcohol-related, 1–2, 70, 267
therapeutic index of a drug, 55 nicotine, 48, 85, 254, 396–397 amphetamine-related, 118, 123
thromboxane A2, 211 use in narcotic withdrawal, 394 CNS stimulants and, 282
TIA. See transient ischemic transient global amnesia, 79–80 cocaine use, as cause of, 143
attack (TIA) transient ischemic attack (TIA) drug-abusing lifestyle and, 440–441
TIQ hypothesis of alcoholism, 74–75 aspirin as treatment for, 211 inhalant-induced, 197
tobacco cocaine-induced, 141 marijuana-induced, 156
abuse, scope of, 4 transport mechanisms, cellular, 49 MDMA-induced, 192
addiction, 222–235 treatment PCP-induced, 187
alcohol use and smoking, 226 inpatient, 353–357 steroid-induced, 206
Alzheimer’s disease and smoking, 234 limit setting, 362 vitamin deficiencies
buspirone, help with withdrawal, 109 Minnesota Model, 334–335 alcohol, as cause of, 62, 75, 77–78,
cancer, suspected causal role in, noncompliance by patient, 362–363 80–81
228–230, 232 outpatient, 351–353 amblyopia, 80
carcinogenic qualities of outpatient versus inpatient, 357–359, amphetamine abuse, as cause of,
questioned, 232 361 127
cessation of smoking, 233–235 partial hospitalization, 359–360 vitamin deficiency amblyopia, 80
chewing, as method of use, 232–233 pharmacotherapy, 383–398 vitamin malabsorption syndrome,
children and, 227, 232, 268–269 plan, 335 (figure), 339 77–78
complications from use of, 228–233 points to address, 345–350 volatile substances. See inhalants
cost of abuse, 5 problems encountered, 362–382
deaths associated with use of, therapists, characteristics of, war on drugs
228–229 332–334 disinformation in United States and, 6
elderly people and smoking, 230 types of, 335–339 trends, 1
gender as issue in use of, 254 uncooperative client, 371 in United States, 442–451
Graves’ disease and, 231 Triangle of Self Obsession, The water-soluble drugs, defined, 50
health benefits of quitting, 233 (pamphlet), 42 Wells, Horace, 199
history of use, 222–223 triazolam, 99 Wernicke’s encephalopathy, 80–81
nicotine as psychoactive agent tryptamines, 437 western civilization, rise of, 36–38
in, 224 tuberculosis, 407–408 Willmar State Hospital
pharmacology of smoking, 223–226 Twelve Steps (Michigan), 334
pharmacotherapies for smoking, analysis of, 413–414 withdrawal syndrome
397–398 criticism of, 425–426 alcohol, 14, 85–86, 88, 383–388
pregnancy, cigarette smoking during, listed, 412 barbiturates, 95, 96
231, 246–247 Twelve Steps and Twelve Traditions buspirone and, 109
recovery from smoking, 349–350 (book), 42, 416 cocaine, 143
scope of problem, 223 Type I alcoholic, 21, 24 flunitrazepam and, 113
secondhand smoke, effects of, Type II alcoholic, 21, 24 inhalants and, 199
231–232 “typical” drinker, 73 opiates, when abused, 175–176
weight gain and quitting smoking, PCP and, 186, 187
234–235 ulcers steroids, 207–208
tolerance alcohol-induced, 77 women and substance abuse,
defined, 14, 58 ibuprofen and, 213 249–254
as sign of alcoholism, 73–74 naproxen and, 219 Women for Sobriety, 424
toluene, 194, 195, 196, 198, 248, 440 tobacco products, induced by, 230 Wood, Alexander, 159
topiramate, 387 upregulation, defined, 57
torsade de pointes, 140 “urges” to use chemicals, 367–369 Xanax, 99–100
Tourette’s syndrome “using” dream, 369
amphetamine use and, 121 zaleplon, 111
cocaine use and, 142 varenicline, 397–398 zero-order biotransformation, 52
methylphenidate and, 116 Versed, 101 zolpidem, 110–111

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Concepts of Chemical Dependency

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Concepts of Chemical Dependency

Proofreader: Mary Anne Shahidi

Cengage Learning products are represented in Canada by Nelson Education, Ltd.

For your course and learning solutions, visit academic.cengage.com.

1 Why Worry About Recreational Chemical Abuse? 1

2 Statement of the Problem of Substance Use Disorders 7

3 The Medical Model of Chemical Addiction 17

4 Psychosocial Models of the Substance Abuse Disorders 28

5 Addiction as a Disease of the Human Spirit 36

Recovery Rests on a Foundation of Honesty 41

7 Introduction to Alcohol: The Oldest Recreational Chemical 60

8 Chronic Alcohol Abuse and Addiction 72

9 Abuse of and Addiction to the Barbiturates and Barbiturate-like Drugs 89

10 Abuse of and Addiction to Benzodiazepines and Similar Agents 99

11 Abuse of and Addiction to Amphetamines and CNS Stimulants 114

13 Marijuana Abuse and Addiction 145

14 Opioid Abuse and Addiction 158

15 Hallucinogen Abuse and Addiction 179

16 Abuse of and Addiction to the Inhalants and Aerosols 194

17 The Unrecognized Problem of Steroid Abuse and Addiction 201

The Legal Status of Anabolic Steroids 202

18 The Over-the-Counter Analgesics: Unexpected Agents of Abuse 209

19 Tobacco Products and Nicotine Addiction 222

21 Gender and Substance Use Disorders 249

22 Hidden Faces of Chemical Dependency 255

23 Chemical Abuse by Children and Adolescents 263

25 Codependency and Enabling 291

26 Addiction and the Family 300

27 The Evaluation of Substance Use Problems 309

The Assessor and Data Privacy 314

28 The Process of Intervention 323

29 The Treatment of Chemical Dependency 332

30 The Process of Recovery 341

31 Treatment Formats for Chemical Dependency Rehabilitation 351

32 Relapse and Other Problems Frequently Encountered in Treatment 362

Controlled Drinking 369

33 Pharmacological Intervention Tactics and Substance Abuse 383

34 Substance Abuse/Addiction and Infectious Disease 399

35 Self-Help Groups 412

36 Crime and Drug Use 428

37 The Debate Around Legalization 442

Appendix One Sample Assessment: Alcohol Abuse Situation 452

Appendix Two Sample Assessment: Chemical Dependency Situation 454

Appendix Three The “Jellinek” Chart for Alcoholism 457

Appendix Four Drug Classiﬁcation Schedules 458

Acknowledgments Kohier, Missouri Baptist University; Paul J. Kowatch,

Why Worry About Recreational

Statement of the Problem

FIGURE 2.1 The Continuum of Recreational Chemical Use

(Cook & Wall, 2005). Two different tribal groups from

Does person choose to use drugs at this time?

Was chemical Person decides not to use

Is there social reinforcement Person decides not to use

Is drug use consistent Person decides not to use

FIGURE 2.3 The Chemical Use Decision-Making Process

The Medical Model

the Greek alphabet to identify the most common forms