aromatase converts testosterone to estradiol. This process is called aromatization.

According to the aromatization hypothesis, perina- tal testosterone does not directly masculinize the brain; the
brain is masculinized by estradiol that has been aromatized from perinatal testosterone. Although the idea that
estradiol—the alleged female hormone—masculinizes the brain may seem counterintuitive, there is strong evi-
dence for it. Most of the evidence is of two types, both coming from experiments on rats and mice: (1) findings
demonstrating masculinizing effects on the brain of early estradiol injections, and (2) findings showing masculin-
ization of the brain does not occur in response to testos- terone administered with agents that block aromatization or
in response to androgens that cannot be aromatized (e.g., dihydrotestosterone).

How do genetic females of species whose brains are masculinized by estradiol keep from being masculin- ized by
their mothers’ estradiol, which circulates through the fetal blood supply? Alpha fetoprotein is the answer. Alpha
fetoprotein is present in the blood of rodents during the perinatal period, and it deactivates circulat- ing estradiol by
binding to it (see Yang & Shah, 2014). Although the role of alpha fetoprotein in deactivating estradiol is firmly
established in rodents, its function in humans remains controversial (see Koebele & Bimonte- Nelson, 2015).

How, then, does estradiol masculinize the brain of the male rodent fetus in the presence of the deactivating effects of
alpha fetoprotein? Because testosterone is immune to alpha fetoprotein, it can travel unaffected from the testes to the
brain cells where it is converted to estradiol. Estradiol is not broken down in the rodent brain because alpha feto-
protein does not readily penetrate the blood–brain barrier.

sex differences in tHe brAin: tHe Modern perspective. So far, our discussion of the development of sex differences has
focused on the reproductive organs, secondary sex characteristics, and the hypothalamus. You have learned from
this discussion that one theory accounts for the development of many sex differences: The default program of
development is the female program, which is overridden in genetic males by perinatal exposure to tes- tosterone.
The initial assumption was that this same mech- anism would prove to be the sole mechanism responsible for the
development of other differences between male and female brains. However, this has not proven to be the case (see
Lenz, Nugent, & McCarthy, 2012).

Before considering the mechanisms by which sex differences in the brain develop, it is important to under- stand the
nature of the differences. The vast majority of sex differences in the brain are not all-or-none, men-are- men-and-
women-are-women differences. Most of the sex differences in the brain that have been documented are

slight, variable, and statistical. In short, many differences exist between average male and female brains, but there is
usually plenty of overlap (see Lenroot & Giedd, 2010).

In thinking about the meaning of these statistical sex differences in the brain, it is important to understand that in no
case has the behavioral significance of such a difference been identified (see Hines, 2010; McCarthy et al., 2012). It
is unlikely that such sex differences in the brain would not be reflected in behavioral differences (see Cahill, 2014),
but so far no such brain–behavior links have been clearly identified.

Although research on the development of sex dif- ferences in the brain is still in its infancy, one important principle
has emerged. Brains are not masculinized or fem- inized as a whole: Sex differences develop independently in
different parts of the brain at different points in time and by different mechanisms. For example, aromatase is found
in only a few areas of the rat brain (e.g., the hypothala- mus), and it is only in these areas that aromatization is
critical for testosterone’s masculinizing effects (see Lentini et al., 2012; McCarthy & Arnold, 2011). Also, some sex
dif- ferences in the brain are not manifested until puberty, and these differences are unlikely to be the product of
perinatal hormones (see Ingalhalikar et al., 2014), which, as you have just learned, play a role in the development of
some sex differences in the brain.

Further complicating the study of the development of sex differences in the brain is the fact that two factors that
have proven to play little or no role in the sexual dif- ferentiation of the reproductive organs do play a role in the
sexual differentiation of the brain. First, sex chromo- somes have been found to influence brain development
independent of their effect on hormones (see Hines, 2011; Maekawa et al., 2014; Ngun et al., 2011); for exam- ple,
different patterns of gene expression exist in the brains of male and female mice even before the gonads become
functional (e.g., Wolstenholme, Rissman, & Bekiranov, 2013). Second, although the female program of reproductive
organ development proceeds typically in the absence of gonadal steroids, recent evidence sug- gests that estradiol
plays an active role; knockout mice without the gene that forms estradiol receptors do not display a typical female
pattern of brain development (see Maekawa et al., 2014).

Thus, although the conventional view that a female program of development is the default program does a good job
of explaining differentiation of the reproductive organs and hypothalamus, it falters badly when it comes to
differentiation of other parts of the brain.

The mechanisms of brain differentiation appear to be much more complex and selective. Complicating their study is
the fact that these complex mecha-
nisms are different in different mammalian
species (see Sekido, 2014); for example,

Hormones and Sex 367

368 Chapter 13

aromatization seems to play a less prominent role in pri- mates than in rats and mice (see Gillies & McArthur, 2010;
Zuloaga et al., 2008).

Development of Sex Differences in Behavior

LO 13.11 describe the results of studies of sex differences in behavior in humans

and nonhumans.

Because it is not ethical to conduct experiments on the devel- opment of sex differences in humans, most of the
research on this topic has focused on the development of reproductive behavior in laboratory animals. Until recently,
this research has focused on the effects of perinatal hormones.

developMent of reproductive beHAviors in lAborAtorY AniMAls. Phoenix and colleagues (1959) were among the first
to demonstrate that the perinatal injection of testosterone masculinizes and defeminizes a genetic female’s adult
reproductive behavior. First, they injected pregnant guinea pigs with testosterone. Then, when the litters were born,
the researchers ovariectomized the female offspring. Finally, when these ovariectomized female guinea pigs reached
maturity, the researchers

injected them with testosterone and assessed their copulatory behavior. Phoenix and his colleagues found that the
females exposed to

perinatal testosterone displayed more male-like mounting behavior in response to testosterone injections in adult-
hood than adult females who had not been exposed to perinatal testosterone. And when as adults the female guinea
pigs were injected with progesterone and estradiol and mounted by males, they displayed less lordosis (the
intromission-facilitating arched-back posture that signals female rodent receptivity).

In a study complementary to that of Phoenix and col- leagues, Grady, Phoenix, and Young (1965) found that the
lack of early exposure of male rats to testosterone both feminizes and demasculinizes their reproductive behavior as
adults. Male rats castrated shortly after birth failed to display the typical male copulatory pattern of mounting,
intromission (penis insertion), and ejaculation (ejection of sperm) when as adults they were treated with testoster-
one and given access to a sexually receptive female, and when they were injected with estrogen and progesterone as
adults, they exhibited more lordosis than uncastrated controls.

The aromatization of perinatal testosterone to estra- diol seems to be important for both the defeminization and the
masculinization of rodent copulatory behavior (see Goy & McEwen, 1980; Shapiro, Levine, & Adler, 1980). In
contrast, aromatization does not seem to be critical for these effects in monkeys (Wallen, 2005).

When it comes to the effects of perinatal testosterone on behavioral development, timing is critical. The ability of
single injections of testosterone to masculinize and defemi- nize rat reproductive behavior seems to be restricted to
the first 11 days after birth.

Because much of the research on hormones and the development of reproductive behavior has focused on the
copulatory act, we know less about the role of hormones in the development of proceptive behaviors (solicitation
behav- iors) and in the development of sex-related behaviors that are not directly related to reproduction. However,
perinatal testosterone has been found to disrupt the proceptive hopping, darting, and ear wiggling of receptive
female rats.

Before you finish this section, we want to clarify an important point. If you are like many of our students, you may
be wondering why biopsychologists who study the development of male–female behavioral differences always
measure masculinization separately from defeminization and feminization separately from demasculinization. If you
think that masculinization and defeminization are the same thing and that feminization and demasculinization are the
same thing, you have likely fallen into the trap of the men-are- men-and-women-are-women assumption—that is,
into the trap of thinking of maleness and femaleness as discrete, mutually exclusive, opposite categories. In
fact, male behaviors and female behaviors can
coexist in the same individual, and they do not
necessarily change in opposite directions if the individual receives physiological treatment such as hormones or
brain lesions. For example, “male” behaviors (e.g., mounting receptive females) have been observed in the females
of many different mammalian species, and “female” behaviors (e.g., lordosis) have been observed in males (see
Dulac & Kimchi, 2007). Furthermore, lesions in medial preoptic areas have been shown to abolish male
reproductive behaviors in both male and female rats without affecting female behav- iors (see Singer, 1968; Will,
Hull, & Dominguez, 2014). Think about this idea carefully; it plays an important role in later parts of the chapter.

developMent of sex differences in tHe beHAvior of HuMAns. There is much research on the develop- ment of
behavioral differences in human females and males. However, because experimental investigations of this process
are not ethical, virtually all of the research is based on case studies and correlational studies, which are difficult to
interpret (see Chapter 1). Still, three general conclusions have emerged.

First, some sex differences in human behavior appear to be sexual dimorphisms (see McCarthy et al., 2012; Rigby
& Kulathinal, 2015; Yang & Shaw, 2014). Sexual dimor- phisms are instances where a behavior (or a structure)
typi- cally comes in two distinctive classes (male or female) into which most individuals can be unambiguously
assigned.

In the case of humans, it appears to be only reproduction- related behaviors that clearly fall into this category. The
presence or absence of prenatal testosterone appears to be a major factor in the development of these behaviors (see
Balthazart, 2011; Kreukels & Cohen-Kettenis, 2012).

Second, most differences between the behavior of aver- age human males and average human females are small and
characterized by substantial overlap between individuals of the two groups (see Hines, 2011; McCarthy et al., 2012;
Miller & Halpern, 2014). For example, there are human behavioral sex differences of this type in play behavior,
social interac- tion, reaction to pain, language, cognition, emotionality, drug sensitivity, and responses to stress (see
Bale & Epperson, 2015; Eisenegger, Haushofer, & Fehr, 2011; Loyd & Murphy, 2014; Miller & Halpern, 2014;
Mogil, 2012). The presence or absence of prenatal testosterone exposure has been shown to contrib- ute to the
development of these kinds of sex differences, but in general they account for only a portion of each difference.

The third conclusion that has emerged from the study of human behavioral sex differences is that there are often
differences in the susceptibility of human males and

females to behavioral disorders (see McCarthy et al., 2012; ter Horst et al., 2012; Zhao, Woosy, & Chhibber, 2015).
For example, dyslexia (reading difficulties), early-onset schizo- phrenia, stuttering, and autism spectrum disorders
are each about three times more prevalent in males; and atten- tion deficit hyperactivity disorder is 10 times more
likely in males. In contrast, females are twice as likely to be diag- nosed with depression, anxiety disorders, and
Alzheimer’s disease; and about 10 times as many females are diag- nosed with certain eating disorders. The
mechanisms lead- ing to the development of any of these sex differences in susceptibility to behavioral disorders is
unclear (see Cahill, 2014; ter Horst et al., 2012).

Before leaving the topic of sex differences in brain and behavior, we want to emphasize that the frequent finding
that prenatal testosterone exposure influences the devel- opment of sex differences does not preclude other factors
(see Hines, 2011). For example, cultural factors have been shown to play a major role in the development of many
sex differences, perhaps by acting on the same brain mechanisms influenced by prenatal hormones.

Hormones and Sex 369

Scan Your Brain

Before you proceed to a consideration of three cases of exceptional human sexual development, scan your brain to see whether
you understand the basics of typical sexual development. Fill in the blanks in the following sentences. The correct answers are
provided at the end of the exercise. Review material related to your errors and omissions before proceeding.

1. Glands that release chemicals into ducts that carry them to targets mostly on the surface of the body are called
_____.
2. The ovaries and testes release steroid hormones called _____.
3. The pituitary gland is made up of two glands: _____.
4. Neurons that release hormones into general circulation are called _____ cells.

5. _____ is the anterior pituitary hormone that stimulates the release of hormones from the thyroid gland.

6. _____, calcium, and sodium levels in the blood influence the release of hormones.

7. A typical pattern of hormone release, where hormones are discharged several times per day in large surges, is _____.

8. Cells formed from the amalgamation of a sperm cell and an ovum are reformed as a _____.

9. The hormone that triggers the release of adrenal hormones from the adrenal cortices is called the _____.
Three Cases of Exceptional Human Sexual Development
This module discusses three cases of exceptional sexual development. We are sure you will be intrigued by these
three cases, but that is not the only reason we have cho- sen to present them. Our main reason is expressed by

a proverb: The exception proves the rule. Most people think this proverb means that the exception “proves” the rule
in the sense that it establishes its truth, but this is clearly wrong: The truth of a rule is challenged by, not confirmed
by, exceptions to it. The word proof comes from the Latin probare, which means “to test”—as in proving ground or
printer’s proof—and this is the sense in which it is used in the proverb. Hence, the proverb

Scan Your Brain answers: (1) exocrine glands, (2) progestin, (3) posterior and anterior, (4) neurosecretory, (5) Thyrotropin, (6) Glucose, (7)
pulsatile hormone release, (8) zygote,
(9) adrenocorticotropic hormone.
370 Chapter 13
means that the explanation of exceptional cases is a major

challenge for any theory.

Exceptional Cases of Human Sexual Development

LO 13.12 explain what androgen insensitivity syndrome, adrenogenital syndrome, and

ablatio penis have taught us about human sexual development.

So far in this chapter, you have learned the “rules” accord- ing to which hormones seem to influence typical sexual
development. Now, three exceptional cases are offered to prove (to test) these rules.

to them because of the mutation to her androgen receptor gene; thus, her development proceeded as if no andro-
gens had been released. Her external genitals, her brain, and her behavior developed along female lines, without the
effects of androgens to override the female program, and her testes could not descend from her body cavity with no
scrotum for them to descend into. Furthermore, Anne did not develop typical internal female reproductive ducts
because, like other genetic males, her testes released Müllerian-inhibiting substance; that is why her vagina was
short and her uterus underdeveloped. At puberty, Anne’s testes released enough estrogens to feminize her body in
the absence of the counteracting effects of androgens; how- ever, adrenal androstenedione was not able to stimulate
the growth of pubic and axillary hair.

Although the samples are small, patients with com- plete androgen insensitivity syndrome have been found to be
comparable to genetic females. All aspects of their behavior that have been studied—including gender iden- tity,
sexual orientation, interests, and cognitive abilities— have been found to be typical of many females (see Cohen-
Bendahan, van de Beek, & Berenbaum, 2005).

An interesting issue of medical ethics is raised by the androgen insensitivity syndrome. Many people believe that
physicians should always disclose all relevant findings to their patients. If you were Anne’s physician, would you
tell her that she is a genetic male? Would you tell her hus- band? Her doctor did not. Anne’s vagina was surgically
enlarged, she was counseled to consider adoption, and, as far as we know, she is still happily married and unaware
of her genetic sex. On the other hand, we have heard from several genetic females who have partial androgen
insensitivity, and they recommended full disclosure. They had faced a variety of sexual ambiguities throughout their
lives, and learning the cause helped them.

The Case of Anne S., the Woman Who Wasn’t

Anne S., an attractive 26-year-old female, sought treatment for two sex-related disorders: lack of menstruation and pain during
sexual intercourse (Jones & Park, 1971). She sought help because she and her husband of 4 years had been trying without
success to have children, and she correctly surmised

that her lack of a menstrual cycle was part of the problem. A physical examination revealed that Anne was a healthy young
female. Her

only readily apparent peculiarity was the sparseness and fineness of her pubic and axillary hair. Examination of her exter- nal
genitals revealed nothing atypical; however, there were some differences with her internal genitals. Her vagina was only 4
centimeters long, and her uterus was underdeveloped.
At the start of this chapter, we said that you would encounter some remarkable things, and the diagnosis of Anne’s
case certainly qualifies as one of them. Anne’s doc- tors concluded that her sex chromosomes were XY; they
concluded that Anne, the attractive young female, had the genes of a genetic male. Three lines of evidence supported
their diagnosis. First, analysis of cells scraped from the inside of Anne’s mouth revealed that they were of the XY
type. Second, a tiny incision in Anne’s abdomen, which enabled Anne’s physicians to look inside, revealed a pair of
internal- ized testes but no ovaries. Finally, hormone tests revealed that Anne’s hormone levels were those typical of
a male.

Anne suffers from complete androgen insensitivity syndrome; all her symptoms stem from a mutation to the
androgen receptor gene that rendered her androgen recep- tors totally unresponsive (see Chen et al., 2015; Mongan
et al., 2015). Complete androgen insensitivity syndrome is rare, occurring in about 1 of 100,000 genetic male births
(see Wang et al., 2014).

During development, Anne’s testes released male- typical levels of androgens, but her body could not respond

The Case of the Little Girl Who Grew into a Boy

The patient—let’s call her Elaine—sought treatment in 1972. Elaine was born with somewhat ambiguous external genitals, but
she was raised by her parents as a girl without incident until the onset of puberty, when she suddenly began to develop male
secondary sex characteristics. This was extremely distressing. Her treatment had two aspects: surgical and hor- monal. Surgical
treatment was used to increase

the size of her vagina and decrease the size of

her clitoris; hormonal treatment was used to
suppress androgen release so that her own estrogen could feminize her body. Following treatment, Elaine developed into an
attractive young female—narrow hips and a husky voice be- ing the only signs of her brush with masculinity (see Money &
Ehrhardt, 1972).

What treatment(s) do you think should be given to infants born with ambiguous external genitals? Why?

Elaine suffered from adrenogenital syndrome, which is the most common atypical form of sexual development,
affecting about 1 in 10,000. Adrenogenital syndrome is caused by congenital adrenal hyperplasia—a congeni-
tal deficiency in the release of the hormone cortisol from the adrenal cortex, which results in compensatory adrenal
hyperactivity and the excessive release of adrenal andro- gens. This produces an array of serious health problems
(see Turcu & Auchus, 2015), but its most widely studied effect is on sexual development. There is little effect on the
sexual development of males, other than accelerating the onset of puberty, but it has major effects on the devel-
opment of genetic females. Females who suffer from the adrenogenital syndrome are usually born with an enlarged
clitoris and partially fused labia. Their gonads and internal ducts are usually typical because the adrenal androgens
are released too late to stimulate the development of the Wolffian system.

Most female cases of adrenogenital syndrome are diagnosed at birth. In such cases, the external genitals are altered
to be more typically female, and cortisol is admin- istered to reduce the levels of circulating adrenal andro- gens.
Following early treatment, adrenogenital females grow up to be physically typical females except that the onset of
menstruation is likely to be later than for most females. This makes them good participants for studies of the effects
of fetal androgen exposure on psychosexual development.
Adrenogenital teenage girls who have received early treatment tend to display more tomboyishness, greater strength,
and more aggression than most teenage girls, and they tend to prefer boys’ clothes and toys, and play mainly with
boys (e.g., Matthews et al., 2009; Pasterski et al., 2011). However, it is important not to lose sight of the fact that
many teenage girls display similar char- acteristics—and why not? Accordingly, the behavior of treated
adrenogenital females, although tending toward the masculine, is usually within the range considered to be typical
female behavior by the current standards of our culture.

The most interesting questions about the develop- ment of females with adrenogenital syndrome concern their
romantic and sexual preferences as adults. They seem to lag behind typical females in dating and mar- riage—
perhaps because of the delayed onset of their menstrual cycle. Most are heterosexual, although a few studies have
found an increased tendency
for these females to express an interest in
other females and a tendency to be less
involved in heterosexual relationships (see Piaggio, 2014). Complicating the situation further is the fact that these
slight differences may not be direct consequences of early androgen exposure but may arise from the fact that some
adrenogenital girls have ambiguous genitalia and certain male characteristics (e.g., body hair), which may result in
different experiential influences (see Jordan-Young, 2012).

Prior to the development of cortisol therapy in 1950, genetic females with adrenogenital syndrome were left
untreated. Some were raised as boys and some as girls, but the direction of their pubertal development was unpre-
dictable. In some cases, adrenal androgens predominated and masculinized their bodies; in others, ovarian estrogens
predominated and feminized their bodies. Thus, some who were raised as boys were transformed at puberty into
females and some who were raised as girls were trans- formed into males—sometimes with devastating emotional
consequences.

One of the most famous cases in the litera-

ture on sexual development is David Reimer,
an identical twin whose penis was accidentally
destroyed during circumcision at the age of
7 months. Because there was no satisfactory way of surgi- cally replacing the lost penis, an expert in such matters, John Money,
recommended that he be castrated and raised as a girl, that an artificial vagina be created, and that estrogen be administered at
puberty to feminize the body. After a great deal of anguish, the parents followed Money’s advice.

Money’s (1975) report of this case of ablatio penis was influential. It was seen by some as the ultimate test of the nature–
nurture controversy (see Chapter 2) with respect to the development of gender identity and behavior. It seemed to pit the
masculinizing effects of male genes and male prenatal hormones against the effects of being reared as a girl. And the availability
of a genetically identical control, the twin brother, made the case all the more interesting. According to Money, the outcome
strongly supported the social-learning theory of

Hormones and Sex 371

The mere existence of...transsexualism is a challenge to the mamawawa.

The Case of the Twin Who Lost His Penis

372 Chapter 13

gender identity. Money reported in 1975, when the patient was 12, that “she” had developed as a typical female, thus confirm-
ing his prediction that being gonadectomized, having the geni- tals surgically altered, and being raised as a girl would override
the masculinizing effects of male genes and early androgens.

A long-term follow-up study published by impartial experts tells an entirely different story (see Diamond & Sigmundson, 1997).
Despite having female genitalia and being treated as a female, he/she developed along male lines. Apparently, the or- gan that
determines the course of psychosocial development is the brain, not the genitals (see Reiner, 1997). The following description
gives you a glimpse of her/his life:

From an early age, she tended to act in a masculine way, preferring boys’ activities and games and display- ing little interest in
dolls, sewing, or other conventional female activities. At the age of four, she refused to put on mother’s make-up, demanding
instead to shave like dad. And by seven, she felt like a boy. Despite the absence of a penis, she often tried to urinate while
standing and would sometimes go to the boys’ lavatory.

She was attractive as a girl, but when she moved or talked her masculinity became apparent. She was teased by the other girls,
and she often retaliated violently, which resulted in her expulsion from school. Put on an estrogen regimen at the age of 12, she
rebelled. She did not want to be feminized; she hated her developing breasts and re- fused to wear a bra.

At 14, she changed her name to David and decided to live as a male. At that time, David’s father revealed David’s entire early
history to him. All of a sudden every- thing clicked; for the first time, he understood who and what he was.

David requested androgen treatment, a mastectomy (surgical removal of breasts), and phalloplasty (surgical creation of a penis).
He became a handsome and popular young man (see Figure 13.10). He married at the age of 25 and adopted his wife’s children.
He was strictly heterosexual, and his ability to ejaculate and experi- ence orgasm returned following his androgen treatments.
However, his early castration permanently eliminated his reproductive capacity.
Figure 13.10 David Reimer, the twin whose penis was accidentally destroyed.

David remained bitter about his early treatment and his inability to produce offspring. To save others from his expe-
rience, he cooperated in writing his biography, As Nature Made Him (Colapinto, 2000). However, David never
recov- ered from his emotional scars, and he committed suicide. His case suggests that the clinical practice of
surgically modi- fying a person’s sex at birth should be curtailed—irrevocable treatments should await early puberty
and the emergence of the patient’s gender identity. At that stage, a compatible course of treatment can be selected.

do tHe exceptionAl cAses prove tHe rule? Do current theories of hormones and sexual development pass the test of the
three preceding cases of exceptional sexual development? In our view, the answer is “yes.” Although current
theories do not supply all of the answers, especially when it comes to brain and behavior, they have contributed
greatly to the understanding of exceptional patterns of sexual differentiation of the body.

Notice one more thing about the three cases: Each of the three was male in some respects and female in others.
Accordingly, each case is a serious challenge
to the men-are-men-and-women-are-women
assumption: Male and female are not oppo-
site, mutually exclusive categories (see Ainsworth, 2015; Carothers & Reis, 2013).

Effects of Gonadal Hormones on Adults

Once an individual reaches sexual maturity, gonadal hor- mones begin to play a role in activating reproductive
behavior. These activational effects are the focus of the first two sections of this module. They deal with the role of
hormones in activating the sexual behavior of males and females, respectively. The third section of this module
deals with anabolic steroids.

Male Sexual Behavior and Testosterone

LO 13.13 describe the role of testosterone in male sexual behavior.

The important role played by gonadal hormones in the activation of male sexual behavior is clearly demonstrated by
the asexualizing effects of orchidectomy. Bremer (1959) reviewed the cases of 215 orchidectomized Norwegians.
Many had committed sex-related offenses and had agreed to castration to reduce the length of their prison terms.

Two important generalizations can be drawn from Bremer’s study. The first is that orchidectomy leads to
a reduction in sexual interest and behavior; the second is that the rate and the degree of the loss are variable. About
half the males became completely asexual within a few weeks of the operation; others quickly lost their ability to
achieve an erection but continued to experience some sexual interest and pleasure; and a few continued to copulate
successfully, although somewhat less enthu- siastically, for the duration of the study. There were also body changes:
a reduction of hair on the torso, limbs, and face; the deposition of fat on the hips and chest; a soften- ing of the skin;
and a reduction in muscle mass.

Of the 102 sex offenders in Bremer’s study, only 3 were reconvicted of sex offenses. Accordingly, he recom-
mended castration as an effective treatment of last resort for male sex offenders.

Why do some males remain sexually active for months after orchidectomy, despite the fact that testicu- lar
hormones are cleared from their bodies within days? It has been suggested that adrenal androgens may play some
role in the maintenance of sexual activity in some castrated males, but there is no direct evidence for this hypothesis.

Orchidectomy removes, in one fell swoop—or, to put it more precisely, in two fell swoops—a pair of glands that
release many hormones. Because testoster- one is the major testicular hormone, the major symp- toms of
orchidectomy have been generally attributed to the loss of testosterone rather than to the loss of some other testicular
hormone or to some nonhormonal consequence of the surgery. The therapeutic effects of replacement injections of
testosterone have confirmed this assumption.
The very first case report of the effects of tes- tosterone replacement therapy concerned an unfortunate 38-year-old World War I
veteran,

who was castrated in 1918 at the age of 19 by a shell frag- ment that removed his testes but left his penis undamaged (de Kruif,
1945).

His body was soft, as if he had little muscle, and his hips had grown wider and his shoulders narrower.

He got married—though the doctors had told him he would surely be impotent (unable to achieve an erection). He made some
attempts at sexual intercourse for his wife’s sake, but he had been unable to satisfy her.

Dr. Foss began injections of testosterone into the mus- cles of his patient, and after the fifth injection, erections became rapid and
prolonged. Moreover, after 12 weeks of treatment he had gained 18 pounds, mainly of muscle, and all his clothes had become too
small. Testosterone had resur- rected a broken man to the ‘manhood’ that had been taken

from him by the shell fragment. Since this first clinical trial, tes- tosterone has breathed sexuality into the lives of many males.
Testosterone does not, however, eliminate the sterility (inability to reproduce) of males who lack functional testes.

The fact that testosterone is necessary for male sexual behavior has led to two widespread assumptions: (1) that the
level of a man’s sexuality is a function of the amount of testosterone he has in his blood, and (2) that a man’s sex
drive can be increased by increasing his testosterone levels. Both assumptions are incorrect. Sex drive and
testosterone levels are uncorrelated in healthy males, and testosterone injections do not increase sex drive.

It seems that each healthy male has far more testos- terone than required to activate the neural circuits that produce
his sexual behavior, and having more than the minimum is of no advantage in this respect. A classic experiment by
Grunt and Young (1952) clearly illustrates this point.

First, Grunt and Young rated the sexual behavior of each of the male guinea pigs in their experiment. Then, on the
basis of the ratings, the researchers divided the male guinea pigs into three experimental groups: low, medium, and
high sex drive. Following castration, the sexual behavior of all of the guinea pigs fell to
negligible levels within a few weeks (see
Figure 13.11), but it recovered after the initia-
tion of a series of testosterone replacement injections. The important point is that although each subject received the
same, very large replacement injections of testosterone, the injections simply returned each to its previous level of
copulatory activity. The conclusion is clear: With respect to the effects of testosterone on sexual behavior, more is
not necessarily better.

Dihydrotestosterone, a nonaromatizable androgen, restores the copulatory behavior of castrated male pri- mates;
however, it fails to restore the copulatory behavior of castrated male rodents (see Hull & Dominguez, 2007). These
findings indicate that the restoration of copulatory behavior by testosterone occurs by different mechanisms in
rodents and primates: It appears to be a direct effect of testosterone in primates, but it appears to be produced by
estradiol aromatized from testosterone in rodents.

Female Sexual Behavior and Gonadal Hormones

LO 13.14 describe the role of testosterone in female sexual behavior.

Sexually mature female rats and guinea pigs display 4-day cycles of gonadal hormone release. There is a gradual

Hormones and Sex 373

The Case of the Man Who Lost and Regained His ‘Manhood’

374 Chapter 13

(Ziegler, 2007). However, in one study, human females were more likely to engage in masturbation and other sexual
activity during periods of fertility, and they preferred masculine faces more on their fertile days than on their
nonfertile days (see Gangestad, Thornhill, & Garver- Apgar, 2005). Moreover, ovariectomy has been shown to
reduce sexual desire and frequency of sexual fantasies (see Cappalletti & Wallen, 2015).

So which particular ovarian hor- mone is responsible for sexual desire in females? Is it estradiol, progesterone, or
testosterone?

 Roney and Simons (2013) found that only high estradiol levels were related to human females’ sexual
desire.
 In experiments on nonhuman fe- male primates, replacement in- jections of testosterone, but not estradiol,
increased the proceptivity of ovariectomized and adrenalecto- mized rhesus monkeys (see Everitt &
Herbert, 1972).
 Some studies of postmenopausal human females found that estrogen therapy renewed sexual interest,
whereas other stud- ies did not. Likewise, some studies found that tes- tosterone renewed sexual interest,
whereas other studies did not (see Cappalletti & Wallen, 2015; Wylie

et al., 2010).

• Still other studies found that testosterone increased sexual desire in postmenopausal human females but only at
supraphysiological levels (i.e., levels above natu- ral levels)—see Cappalletti and Wallen (2015); Davis and
Braunstein (2012).

So, the jury is still out as to whether estradiol or testos- terone is responsible for a female’s sexual drive.

Anabolic Steroid Abuse

LO 13.15 describe the dangers associated with anabolic steroid use.

Anabolic steroids are steroids, such as testosterone, that have anabolic (growth-promoting) effects. Testosterone
itself is not very useful as an anabolic drug because it is broken down soon after injection and because it has unde-
sirable side effects. Chemists have managed to synthesize a number of potent anabolic steroids that are long-acting,
but they have not managed to synthesize one that does not have side effects.
Figure 13.11 The sexual behavior of male guinea pigs with low, medium, and high sex drive. Sexual behavior was disrupted
by castration and returned to its original level by very large replacement injections of testosterone.

(Based on Grunt, J. A., & Young, W. C. (1952). Differential reactivity of individuals and the response of the male guinea pig to testosterone propionate.
Endocrinology, 51, 237–248.)

increase in the secretion of estrogens by the developing follicle (ovarian structure in which eggs mature) in the 2
days prior to ovulation, followed by a sudden surge in progesterone as the egg is released. These surges of estro-
gens and progesterone initiate estrus—a period of 12 to 18 hours during which the female is fertile, receptive (likely
to assume the lordosis posture when mounted), procep- tive (likely to engage in behaviors that serve to attract the
male), and sexually attractive (smelling of chemicals that attract males).

The close relation between the cycle of hormone release and the estrous cycle—the cycle of sexual receptivity—in
female rats and guinea pigs and in many other mamma- lian species suggests that female sexual behavior in these
species is under hormonal control. The effects of ovariec- tomy confirm this conclusion: Ovariectomy of female rats
and guinea pigs produces a rapid decline of both procep- tive and receptive behaviors. Furthermore, estrus can be
induced in ovariectomized rats and guinea pigs by an injection of estradiol followed a day and a half later by an
injection of progesterone.

Female primates are different from female rats, guinea pigs, and other mammals when it comes to the hormonal
control of their sexual behavior: Female primates are the only female mammals moti- vated to copulate during
periods of nonfertility

Copulatory activity

We are currently in the midst of an epidemic of ana- bolic steroid abuse. Many competitive athletes and body-
builders are self-administering appallingly large doses, and many others use them for cosmetic purposes. Because
steroids are illegal, estimates of the numbers who use them are likely underestimates. Still, the results of numer- ous
surveys have been disturbing. Elite athletes began to use anabolic steroids in the 1950s to improve their athletic
performance, but by the 1980s they were in widespread use by the general population, often for cosmetic reasons
(see Figueiredo & Silva, 2014). Particularly troubling is the scale of anabolic steroid use: Global estimates of
lifetime prevalence rates for anabolic steroid are 6.4 percent for males and 1.6 percent for females (see Sagoe et al.,
2014).

Although it is about 40 years since anabolic steroids began to be used by the general public, we still do not fully
understand all the risks. This is because anabolic ste-

roid use is illegal, because there are more than 100 different testosterone derivatives (see Yavari, 2009), and because
users vary

greatly in their patterns and doses of administration. Hazardous effects, although well documented, typically occur
in only a small proportion of users (see van Amsterdam, Opperhuizen, & Hartgens, 2010).

Anabolic steroids have been shown to have a variety of cardiovascular effects, which have been linked to pre-
mature death (see Angell et al., 2012; Kanayama et al., 2010). Also, oral anabolic steroids have been shown to have

adverse effects on the liver, including liver tumors. Less dangerous, but still disturbing, are the muscle spasms,
muscle pains, blood in the urine, acne, general swelling from the retention of water, bleeding of the tongue, nausea,
vomiting, and fits of depression and anger (see Kanayama et al., 2008; Kraus et al., 2012).

The main question of relevance in the context of this chapter is the following: Do the outrageously large doses of
anabolic steroids routinely administered by many users enhance their sexual function? The answer is an emphatic
“no.” In fact, the effects appear to be uniformly disruptive.

In males, the negative feedback from high levels of anabolic steroids reduces gonadotropin release; this leads to a
reduction in testicular activity, which can result in testicular atrophy (wasting away of the testes) and steril- ity.
Gynecomastia (breast growth in males) can also occur, presumably as the result of the aromatization of anabolic
steroids to estrogens. In females, anabolic steroids can produce amenorrhea (cessation of menstruation), steril- ity,
hirsutism (excessive growth of body hair), growth of the clitoris, development of a masculine body shape, baldness,
shrinking of the breasts, and deepening and coarsening of the voice. Unfortunately, some of the mas- culinizing
effects of anabolic steroids on females appear to be irreversible.

There are two major points of concern about the adverse health consequences of anabolic steroids. First, the use of
anabolic steroids in puberty, before developmental programs of sexual differentiation are complete, is particu- larly
risky. Second, many of the adverse effects of anabolic steroids may take years to be manifested—steroid users who
experience few immediate adverse effects may pay the price later.

Hormones and Sex 375

What should be done about the current epidemic of anabolic steroid abuse? Would you make the same recommendation if a

safe anabolic steroid were developed?

Scan Your Brain

You encountered many forms of atypical sexual development 4. and also many clinical problems in the preceding two modules of
the chapter. Do you remember them? Write the 5. name of the appropriate condition or syndrome in each blank

based on the clues provided. The answers appear at the end 6. of the exercise. Before proceeding, review material related to 7.

Castrated males, gonadectomized males

Castrated females, gonadectomized females

Unable to achieve erection

your errors and omissions.

Enlargement of a male’s breasts

8. Cessation of menstruation
9. Excessive body hair in females

Name of condition 1.

2. 3.

Clues or syndrome

Genetic male, sparse pubic hair, short vagina

Congenital adrenal hyperplasia, elevated androgen levels
David Reimer, destruction of penis

Scan Your Brain answers: (1) androgen insensitivity syndrome, (2) adrenogenital syndrome, (3) abla penis, (4) orchidectomized,
(5) ovariectomized, (6) impotent, (7) gynecomastia, (8) amenorrhea, (9) hirsutism

376 Chapter 13
Brain Mechanisms of Sexual Behavior
Human sexual behavior is complex and varied. Sexual practices vary from culture to culture, and from person to
person within each culture. Furthermore, behavioral prefer- ences of individuals are often changed by experience
(see Hoffman, Peterson, & Garner, 2012). However, there are four brain structures whose role in sexual behavior
has been well established: cortex, hypothalamus, amygdala, and ven- tral striatum. This module focuses on these
four structures.

Four Brain Structures Associated with Sexual Activity

LO 13.16 describe the roles of the cortex, hypo- thalamus, amygdala, and ventral striatum in sexual activity.

Our current knowledge of the brain mechanisms of sexual behavior is based on the study of both human volunteers
and nonhuman subjects (see Georgiadis, Kringelbach, & Pfaus, 2012). Because functional brain imaging is the main
technology used to study the relation between brain activ- ity and sexual behavior in human volunteers, there are
some major limitations. Specifically, it is virtually impos- sible using current imaging technology to investigate the
neural activity associated with coitus (copulation) between a female and a male—given cultural constraints, the
require- ment to remain motionless during brain scans, and the difficulty of squeezing two active adults into a
conven- tional brain scanner. Consequently, research on humans has focused on sexual arousal, occasionally to
orgasm, triggered by sexually provocative visual images or masturbation.

The study of the brain mechanisms of sexual behavior in laboratory animals—most commonly rats—circumvents
the problems associated with studies of human volun- teers. First, it is possible to study brain mechanisms in more
detail by using invasive techniques. Second, it is possible to study natural patterns of copulatory activity.
Conversely, several important aspects of sexual activity are difficult or impossible to study in laboratory animals: for
example, sexual imagery, delayed orgasm, female orgasm, and feelings of love. The important point here is that both
humans and nonhumans have major weaknesses as subjects in the investigation of the brain mechanisms of sexual
behavior, but the weaknesses tend to be comple- mentary. Thus, knowledge in this area often depends on an
amalgamation of both lines of research (see Georgiadis et al., 2012).

cortex And sexuAl ActivitY. Because of its fun- damental role in reproduction, and thus the very survival
of our species, sexual behavior was once assumed to be regulated by archaic circuits in the brain stem of early
evolutionary origin. This assumption is no longer tenable. Widespread cortical activation has been routinely
recorded during functional brain imaging studies of volunteers exposed to sexually arousing stimuli (see Georgiadis,
2012; Stoléru et al., 2012). In both males and females, the following areas are often activated: occipitotemporal,
inferotemporal, parietal, orbitofrontal, medial prefrontal, insular, cingulate, and premotor cortices. Interestingly, the
activity in secondary visual cortex (occipitotemporal and inferotemporal cortices) occurs during sexual arousal even
when eyes are closed (see Georgiadis, 2012), and the activ- ity in prefrontal cortex is suppressed during orgasm (see
Stoléru et al., 2012).

Presumably cortical activation mediates the most complex aspects of sexual experience. These may include feelings
of release and loss of control, changes in self- awareness, disturbances of perceptions of space and time, and feelings
of love.

Interest in the role of the hypothalamus in sexual behavior was driven by the discovery of a specific structural
difference in the male and female hypothalamus. In 1978, Gorski and his col- leagues discovered a nucleus in the
medial preoptic area of the rat hypothalamus that was several times larger in males.

They called this nucleus the sexually dimorphic nucleus. At birth, the sexually dimorphic nuclei of male and
female rats are the same size. In the first few days after birth, the male sexually dimorphic nuclei grow at a high rate
and the female sexually dimorphic nuclei do not. The growth of the male sexually dimorphic nuclei is nor- mally
triggered by estradiol, which has been aromatized from testosterone (Gorski, 1980)—see Figure 13.12. Since the
discovery of the sexually dimorphic nuclei in rats, many other sex differences in hypothalamic anatomy have been
identified in rats and in other species. These sex differences in the hypothalamus include differences in volume of
various nuclei, cell number, connectivity, cell morphology, neural activity, and neurotransmitter type—all of which
are influenced by perinatal exposure

to estradiol (see Lenz & McCarthy, 2010).

The medial preoptic area (which includes the sexually

dimorphic nucleus) is one area of the hypothalamus that plays a key role in male sexual behavior (see
Will, Hull, & Dominguez, 2014). Destruction
of the entire area abolishes sexual behavior in

the males of all mammalian species that have been studied (see Hull et al., 1999). In contrast, medial preoptic area
lesions do not eliminate the female sexual behaviors of females, but they do eliminate the male sexual behaviors
(e.g., mounting) that are sometimes observed in females (see Singer, 1968). Conversely, electrical stimulation of the

HYpotHAlAMus And sexuAl ActivitY.

Figure 13.12 The effects of neonatal testosterone exposure on the size of the sexually dimorphic nuclei in male and female
adult rats, as reported by Gorski (1980).

VMN do not display lordosis, and they are likely to attack suitors who become too ardent.

The influence of the VMN on the sexual behavior of female rats appears to be mediated by a tract that descends to
the periaqueductal gray (PAG) of the tegmen- tum. Destruction of this tract eliminates female sexual behavior (see
Hennessey et al., 1990), as do lesions of the PAG itself (see Sakuma & Pfaff, 1979)—see Figure 13.13.

AMYGdAlA And sexuAl ActivitY. The amygdalas, located in the left and right medial temporal lobes, play a general
role in the experience of emotions and social cognition (see Olson et al., 2013; Rolls, 2015).
With respect to sexual behavior, they seem
to play a role in the identification of poten-
tial mating partners based on sensory social signals, which are primarily visual in humans and olfactory in rats.
Support for this view comes from three lines of research.

The first line of evidence involves the study of bilateral amygdala lesions in male and female primates, including
humans. Such lesions have a variety of effects on primate behavior, which together have been termed the Kluver-
Bucy syndrome (see Chapter 17). The effects on sexual behavior are particularly striking (see Baird et al., 2004). For
example, humans display flat affect, hypersexuality, and a complete inability to limit their sexual advances to
appropriate part- ners or locations (see Anson & Kuhlman, 1993).

The second line of research stems from Everitt’s (1990) classic study of bilateral amygdalar lesions in male rats. The
lesions disrupted copulatory behavior, but

Figure 13.13 The hypothalamus-tegmentum circuits that play a role in female and male sexual behavior in rats.

Hormones and Sex 377

100% 75% 50% 25%
0%

100% 75% 50% 25%

0%

Placebo Injection on Day 4

Testosterone Injection on Day 4

Female rats

Male rats

Castration on Day 1
Castration on Day 4

Normal Male Control

Periaqueductal gray

Medial preoptic area

Female sexual circuit Male sexual circuit

Lateral

tegmental Ventromedial field

nucleus
medial preoptic area elicits copulatory behavior in male rats (see Rodriguez-Manzo et al., 2000), and copulatory
behavior can be reinstated in castrated male rats by medial preoptic implants of testosterone (see Davidson, 1980).

The medial preoptic area appears to control

male sexual behavior via a tract that projects to
an area of the midbrain called the lateral tegmental
field. Destruction of this tract disrupts the sexual behavior of male rats (see Brackett & Edwards, 1984). Moreover,
the activity of individual neurons in the lateral tegmental field of male rats is often correlated with aspects of the
copulatory act (see Shimura & Shimokochi, 1990); for example, some neurons in the lateral tegmental field fire at a
high rate only during intromission.

The ventromedial nucleus (vMn) of the rat hypothal- amus contains circuits that appear to be critical for female
sexual behavior. Female rats with bilateral lesions of the

Relative Volume of the Sexually Relative Volume of the Sexually Dimorphic Nuclei in Adult Rats Dimorphic Nuclei in
Adult Rats

378 Chapter 13

this did not occur because the males had difficulty copulating. The defi- cit occurred because the males were
incapable of responding to the olfac- tory and visual cues from receptive females.

And the third line of evidence comes from the study of the reac- tions of human males and females to erotic images.
Males are more likely than females to be sexually aroused by erotic images (see Rupp & Wallen, 2008), and this
difference is reflected in differences in amygdalar activa- tion. In several studies, erotic images presented to male
and female vol- unteers undergoing functional brain scans produced greater amygdalar activation in males (see
Hamann, 2005; Stoléru, 2012).

Figure 13.14 The cortex, hypothalamus, amygdala, and ventral striatum: their putative roles in sexual activity. The amygdala
and ventral striatum are hidden
in this view.
Cortex

Ventral Striatum

Hypothalamus

Mediates the most complex aspects of sexual experience.

Associated with the anticipation and experience of sexual activity and other pleasurable activities.

The ventromedial nucleus plays a role in female sexual behavior; the medial preoptic area plays a role in male sexual behavior.

ventrAl striAtuM And sexuAl

ActivitY. Sexual activity is
clearly among the most pleasurable
human activities (see Georgiadis &
Kringelbach, 2012). Accordingly, it
is not surprising that sexual activity
can serve as a powerful reinforcer.
Indeed, Pfaus and colleagues (2012) have shown that both male and female rats learn to prefer partners, locations,
and odors associated with copulation.

Because orgasm is associated with pleasure, it comes as no surprise that the ventral striatum is activated in human
volunteers by sexually provocative visual images (see Stoléru et al., 2012). Research on rats has shown that the
activity in this area is associated with the anticipation and experience of sex and other forms of pleasure (see
Matsumoto et al., 2012; Pitchers et al., 2010).

Figure 13.14 summarizes this module. It illustrates the location of the four brain structures that were discussed and
summarizes their putative roles in sexual activity.

Sexual Orientation and Gender Identity

So far, this chapter has not systematically addressed the topics of sexual orientation and gender identity. As you
know, people differ in their sexual orientation: Some peo- ple are heterosexual (sexually attracted to members of
the other sex), some are gay (sexually attracted to members of the same sex), some are bisexual (sexually attracted
to both males and females), and some are asexual (not

Amygdala
Plays a role in the identification of potential mating partners.

sexually attracted to others). People also vary in their gender identity (the gender that a person most identi- fies
with: female, male, some combination of male and female, neither female or male, or some other gender category).
A discussion of sexual orientation and gender identity is a fitting conclusion to this chapter because it further
underscores its anti-mamawawa theme.

Sexual Orientation
LO 13.17 describe the results of the two studies on the genetics of sexual orientation by bailey and pillard
(1991, 1993), and describe the fraternal birth order effect and why it is thought to occur.

sexuAl orientAtion And Genes. Research has shown that differences in sexual orientation are influenced by genes. For
example, Bailey and Pillard (1991) studied a group of gay males who had twin brothers, and they found that 52
percent of the monozygotic twin brothers and 22 percent of the dizygotic twin brothers were gay. In a comparable
study of female twins by the same research group (Bailey et al., 1993), it was found that 48 percent of the
monozygotic twin sisters and 16 percent of the dizy- gotic twin sisters were gay.

sexuAl orientAtion And eArlY HorMones.

Many people mistakenly assume that gay persons have lower levels of sex hormones. They don’t: Heterosexuals and
gay persons do not differ in their levels of circulating hormones. Moreover, orchidectomy reduces the sexual
behavior of both heterosexual and gay males, but it does not redirect it; and replacement injections simply reacti-
vate the preferences that existed prior to surgery.

Many people also assume that sexual orientation is a matter of choice. It isn’t. People discover their sexual
orientation; they don’t choose it. Sexual orientation seems to develop very early, and a child’s first indication of
their sexual orientation usually does not change as they mature. Could perinatal hormone exposure be the early
event that shapes sexual orientation?

Because experiments involving levels of perinatal hormone exposure are not feasible with humans, efforts to
determine whether perinatal hormone levels influence the development of sexual orientation have focused on
nonhuman species. A consistent pattern of findings has

emerged. In those species whose exposure to early sex hormones has been modified (e.g., rats, hamsters, ferrets,
pigs, zebra

finches, and dogs), it has not been uncommon to see males engaging in female-typical sexual behavior such as being
mounted by other males. Nor has it been uncommon to see females engaging in male-typical sexual behavior such as
mounting other females. However, because the defining feature of sexual orienta- tion is sexual preference, the key
studies have examined the effect of early hormone exposure on the sex of preferred sexual partners. In general, the
perinatal cas- tration of males has increased their preference as adults for male sex partners; similarly, prenatal
testosterone exposure in females has increased their preference as adults for female sex partners (see Henley, Nunez,
& Clemens, 2011).

On the one hand, we need to exercise prudence in drawing conclusions about the development of sexual orientation
in humans based on the results of experiments on laboratory species; it would be a mistake to ignore the profound
cognitive and emotional components of human sexuality, which have no counterpart in laboratory ani- mals. On the
other hand, it would also be a mistake to think that a pattern of results that runs so consistently through so many
species has no relevance to humans.

There are some indications that perinatal hormones do influence sexual orientation in humans—although the
evidence is sparse (see Balthazart, 2011; Diamond, 2009). Support comes from the quasiexperimental study of
Ehrhardt and her colleagues (1985). They interviewed adult females whose mothers had been exposed to dieth-
ylstilbestrol (a synthetic estrogen) during pregnancy. The females’ responses indicated that they were significantly

more sexually attracted to females than was a group of matched controls. Ehrhardt and her colleagues con- cluded
that perinatal estrogen exposure does encourage lesbianism and bisexuality in females but that its effect is relatively
weak: The sexual behavior of all but 1 of the 30 participants in this study was primarily heterosexual.

One promising line of research on sexual orientation focuses on the fraternal birth order effect, the find- ing that
the probability of a male being gay increases as a function of the number of older brothers he has (see Alexander et
al., 2011; Blanchard & Lippa, 2007). A recent study of blended families (families in which biologically related
siblings were raised with adopted siblings or step-siblings) found that the effect is related to the number of males
previously born to the mother, not the number of older males one is reared with (see Bogaert, 2007). The effect is
relatively large: The probability of a male being gay increases by 33.3 per- cent for every older brother he has (see
Puts, Jordan, & Breedlove, 2006).

The maternal immune hypothesis has been pro- posed to explain the fraternal birth order effect. This hypothesis is
that some mothers become progressively more immune to masculinizing hormones in male fetuses (see Bogaert &
Skorska, 2011), and a mother’s immune system might deactivate masculinizing hormones in her younger sons.

What Triggers the Development of Sexual Attraction?

LO 13.18 describe the hypothesized role of adrenal cortex steroids in the emergence of sexual