Introduction to Clinical Nutrition

Lesson 9
Diabetes Mellitus

Content
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Course Name Introduction to Clinical Nutrition

Lesson 9 Diabetes Mellitus

Content Creator Name Shalini Vaswani

U.P. Pt. Deen Dayal Upadhyaya Pashu Chikitsa Vigyan

University/College Name Vishwa Vidhyalaya Evem Go Anusandhan
Sansthan,Mathura

Course Reviewer Name Dr Sonika Sharma

University/College Name Punjab Agricultural University, Ludhiana

 Introduction to Clinical Nutrition

Objectives:

This lecture will help to learn about:

1. Coronary heart disease (CHD)

 Etiology: cardiovascular risk factors
 Pathophysiology of CHD

2. Common disorders of coronary heart disease and their management

 Dyslipidemia
 Atherosclerosis: A coronary artery disease
 Hypertension (HT)
 Angina pectoris
 Myocardial infarction (MI)
 Congestive cardiac failure
 Rheumatic heart disease

3. Prevention of coronary artery disease

Glossary
 Angina: Chest pain resulting from impaired blood flow to the
heart.

 Atherosclerosis: Sclerosis (hardening) and thickening of the

arterial wall, with loss of elasticity.

 Coronary Artery Disease: Disease involving the network of

blood vessels surrounding and serving the heart.

 Plaque: Part of lessons seen in atherosclerosis, composed of

lipid, calcium, cholesterol and fibrin.
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1. Coronary Heart Disease (Chd)

Coronary heart disease is a broad term comprising of a spectrum of
diseases associated with disorders of the circulation, heart muscles or the
vessels of the heart in particular. Coronary heart disease results from a lack
of blood flow to the network of blood vessels surrounding the heart and
serving the myocardium. The major underlying cause of CHD is
atherosclerosis, which involves structural and compositional changes in
the innermost or intimal layer of the large arteries. Atherosclerosis is thus
the main cause of heart attack, stroke, and gangrene of the extremities.
Hence, the arteries most often affected are the abdominal aorta and the
coronary and cerebral arteries.

1.1 Common Disorders and Complications of Coronary Heart Disease

(Chd)

Disorders/Complications Of Cld Definition

Dyslipidemia Abnormal lipid levels in blood
Atherosclerosis A thickening and narrowing of the
walls of the large and medium
sized blood vessels caused due to
elevated lipids and cholestrol
Angina pectoris A characteristic pain and
discomfort in the chest
Myocardial infarction An area of necrosis (dying/dead
cells of the myocardium) in a
tissue.
Congestive cardiac failure A clinical syndrome caused by
heart disease characterized by
breathlessness , chest pain and
abnormal sodium and water
retention

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Rheumatoid Heart Disease (RHD) A complication of rheumatic fever

and occurs after attacks of this
fever.
Hypertension Higher than normal blood pressure

1.2 Etiology: Cardiovascular Risk Factors

RISK FACTORS

MODIFIABLE NON-
RISK FACTORS MODIFIABLE
RISK FACTORS

1) Behavioral 1. AGE
 Smoking 2. Sex
 Sedentary Lifestyle Habits 3. Heredity
 Dietary Errors 4. Endomorphic
 Body Build
2) Physiological
 Hyperlipidemia
 Hypertension
 Obesity
 Diabetes Mellitus
 Hyperuricaemia And Gout
 Fibrinogen
 PLATELET AGGREGATION

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 LIPOPROTEIN
 HOMOCYSTIENE LEVEL
 LOW BIRTH WEIGHT
3) Psychological
 STRESS
 LOW SOCIO ECONOMIC STARTA
 TYPE A PERSONALITY
4) Geographic
 SOFT DRINKING WATER
 COLD WEATHER

1.3 Pathophysiology Of Cvd

We all know that heart attack i.e. myocardial infarction is not the beginning
but a last stage representing acute clinical manifestation of CHD. Several
clinical trials and autopsy studies have indicated that the process of
developing atherosclerotic lesions can begin as early as during infancy and
that it may take several decades for the lesions to develop into fatty streaks
and fibrous plaques that ultimately cause stenosis (complete blockage) of
the arteries. Diffuse intimal thickening during infancy which is considered
to be a normal physiological and not a pathological process can result in
the initialization of early clinical manifestations which may appear in the
smooth muscle cell layer between the endothelium and the internal elastic
lamina. These lesions may progress and develop into fatty streaks to reach
their maximum extent in the aortas over a period of two decades among
individuals having elevated cholesterol and/or triglyceride levels. There is
also focal proliferation of smooth muscle cells which are termed as
gelatinous lesions because they have a low lipid but high water content.
Some of these lesions may become large and develop a grayish opaque
center while remaining soft and translucent around the edges. These are
referred to as the transitional lesions. These lesions at times develop a

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fibrous cap with atheromatous lipids in the center and are known as fibrous
plaques. Such fibrous plaques may coalesce together resulting in blockage
of the arteries and hence reduced flow of blood to the tissues. The irritating
presence of plaques may cause injury to the intima of the arteries which
may result in thrombosis. Myocardial infarction/cerebral stroke is the
ultimate result of stenosis in the arteries.

2. Common Disorders Of Coronary Heart Disease And Their Management

2.1 Dyslipidemia

Dyslipidemia is frequently seen in the form of increased concentration of

either cholesterol or the triglycerides or frequently the both. There are
several types of blood lipid disorders, which hold different risks and require
somewhat different treatment methods. The proportions and total
amounts of specific lipoproteins present in the blood are used in
diagnosing hyperlipidemia.

Blood lipids (cholesterol, triglycerides and phospholipids) being insoluble

in blood need a ship to travel in our body; it therefore usually gets bound
to proteins and form complex particles called lipoproteins which vary in
size, composition and density. There are five classes of lipoproteins in the
blood. These include:

1. Chylomicrons: These are formed in the intestines when a Fatty meal is

taken. These pass into the blood through the lymphatics. It contains nearly
90% of triglycerides and 5% cholesterol.

2. Very Low Density Lipoproteins (VLDL): These are produced by the liver
and are the main transporters of triglycerides. VLDL generates most of the
LDL in the plasma. It contains about 60% of triglycerides and 10%
cholesterol.

3. Intermediary Density Lipoproteins (IDL): This is rich in cholesterol and

triglyceride. It contains about 40% of triglycerides and 10% cholesterol.

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4. Low Density Lipoproteins (LDL): This type of lipoprotein is most

artherogenic of all the lipoproteins and is responsible for the
atherosclerosis in the vessels. It has 10% of triglycerides and 45% of
cholesterol.

5. High Density Lipoprotein (HDL): The high HDL content is associated with
decrease in the risk of atherosclerosis. It contains about 3% triglycerides
and 20% cholesterol. Besides these lipoproteins, the other parameters,
which are of interest in CHD, include:

 Total Cholesterol: Serum total cholesterol equals the sum of HDL-

cholesterol (HDL-c), VLDL-cholesterol (VLDL-c) and LDL-cholesterol
(LDL-c). High level of cholesterol is associated with a high risk of
atherosclerosis.
 Triglycerides: The triglyceride-rich lipoproteins include
chylomicrons, VLDL and intermediate density lipoproteins (DL).
Their levels increase by many dietary factors such as excess calories,
fat, carbohydrates and alcohol. Indians are genetically more
susceptible to developing hypertriglyceridemia as compared to
Europeans primarily due to our cereal based diets.
 Apo proteins: Apo proteins are closely related to lipids as they
maintain the solution of lipoprotein lipids in plasma. Measurement
of Apo protein levels aids in diagnosing disorders of lipids and
preventing the risk of cardiovascular disease. The Apo proteins
include AI, AII, B100, B48, CI, CII, CIII, D and E. The Apo proteins AI and
A11 are associated with HDL (the good lipoprotein) and the rest are
associated with not so good lipoproteins.

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2.1.1 Etiology

The causative factors of dyslipidemia/hyperlipidemia may be

environmental (dietary/ lifestyle), genetic or secondary to certain
disease conditions or drugs.
1) Environmental factors: These include diets high in saturated
fats, excessive calorie intake, and alcohol intake and
sedentary lifestyle. A change in diet and lifestyle can help to
normalize elevated blood lipid levels.
2) Genetic defects: These lead to familial hyperlipidemia. In
such cases, the lipid levels may be alarmingly high and risk of
CHD very high. Myocardial infarction can occur within the
first two decades of life. Dietary modifications along with
drug therapy are beneficial.
3) Hyperlipidemia secondary to other conditions: The disorders
that upset lipid metabolism include poorly controlled
diabetes mellitus, kidney disease (nephrosis and end-stage
renal disease), liver disease, hypothyroidism and use of drugs
like oral contraceptives, thiazide diuretics, and
corticosteroids could be a cause of the lipid imbalances.

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2.1.2. Symptoms

The main symptom is presence of xanthoma: This is a yellowish

swelling, nodule or plaque in the skin resulting from deposits of fat.
There are various types of xanthoma for example, in type 2b, the
xanthoma may be on the hand, buttocks, knees, upper eyelids. In type
3, the planar xanthomas may be seen ia the creases of the palms of
hands and fingers. In type 5, the xanthoma may be present on the back
of the neck or buttocks.

2.1.3. Complications
The complications include:

 Pancreatitis
 Progressive atherosclerosis or asymptomatic coronary
disease.
Excess of triglycerides (hypertriglyceridemia) and
cholesterol (hypercholesterolemia) are the usual
problems for increase in very low-density lipoprotein
cholestrol (VLDLc), low-density lipoprotein cholesterol
(LDLc) levels. The following are possible causes of
elevated triglycerides and cholesterol and reduced HDLc
levels
Possible causes of elevated triglycerides:
o Obesity
o Uncontrolled diabetes
o Drugs
o Alcohol
o Genetic
o Hypothyroidism
o Liver disease

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Possible causes of elevated cholesterol:

o Excess fat in the diet

o Overweight/obesity
Possible causes of reduced serum/ HDL levels:

o Cigarette smoking
o Obesity
o Lack of exercise
o Uncontrolled diabetes
o Hypothyroidism
o Hypertriglyceridemia
o Genetic factors
o Drugs
o Liver disease
2.1.4 Goals of Dietary Treatment:

The goals of dietary management (alone or conjunction with exercise or with

lipid lowering drugs) are to reduce the total fat, saturated fat and
cholesterol intake. This is an attempt to reduce total cholesterol, LDL and
triglyceride levels, thus also reducing the risk of atherosclerosis and
modifying its progression in subjects with the disease.

o Cholesterol: It is a natural component of foods such as mutton, pork,

ham, sausages, lamb, chicken, eggs (yellow), whole milk, cheese, ice-
cream, butter and desi ghee. Cholesterol is present only in animal
kingdom and does not exist in vegetable kingdom. Increased
cholesterol in blood is called hypercholesterolemia, which leads to
atherosclerosis. Foods rich in cholesterol Mutton, pork, ham,
sausages, lamb, chicken, egg (yellow), glandular meat (brain, liver
and kidneys), whole milk, cheese, ice-cream, butter, desi ghee.
o Saturated Fatty Acids (SFA): These are found mostly in animal fats as
white marble-like solid at room temperature. Red meats are rich in

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it. Others sources of saturated fats are milk fat, butler, ghee, coconut
oil, palm oil, margarine and hydrogenated fats (vanaspati). These
saturated fats in the diet also give rise to high LDL, thus leading to
atherosclerosis. The three saturated fatty acids lauric acid, myristic
acid and palmitic acids increase cholesterol levels. The energy
provided from saturated fats should always be <10 % of the total
calories.Foods rich in saturated fatty acids (SFA) Milk fat, butter, pure
ghee, coconut oil, palm oil, margarine, vanaspati, red meats
(mutton).
o Monounsaturated fat (MUFA): These are liquid at room
temperature, the highest food source being olive oil, canola oil,
rapeseed oil, to some extent mustard oil. MUFA is an excellent fat as
it reduces the LDL levels and increases the good HDL levels and
cholesterol, thus preventing atherosclerosis. Oleic acid is a
monounsaturated fatty acid of great clinical relevance. Foods rich in
saturated fatty acids (SFA) Milk fat, butter, pure ghee, coconut oil,
palm oil, margarine, vanaspati, red meats (mutton) Oils high in
monounsaturated fatty Acid (MUFA) - Canola oil, olive oil and
rapeseed oil.
o Polyunsaturated Fatty Acids (PUFA): These are also liquid at room
temperature. There are two main types of dietary PUFA's of
significance:
a) linoleic acids (LAJn-6) present in good amounts in safflower,
sunflower, corn and sesame oil. b) Alpha linolenic (ALNA/n-3) fish
oils, to some extent olive oil, mustard and rapeseed oil.

The ratio of n-6: n-3 between 5-10 is considered healthy. This can be
obtained by using a mixture of two oils. Combination of safflower,
corn, sunflower or sesame oil (rich in n-6) with equal portions of
mustard oil or rapeseed oil (rich source of 11-3) can give a ratio
between 5-10. This is not artherogenic and hence healthy for the

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heart. Fish oils and fish also contain n-3 and are beneficial for the
heart as they decrease plasma triglycerides
o Hydrogenqted Fat: All vanaspati preparations are the result of
hydrogenation of oils, where unsaturated fat is converted to
saturated fat for its flavour and long shelf life. This is often preferred
by housewives, as it is an imitation of pure ghee. However; it is
saturated in nature and contains trans fatty acids. Trans fatty acids,
are known to raise LDL in blood thus enhancing atherosclerosis. This
is the reason why hydrogenated fats are harmful to the heart
o Carbohydrates: carbohydrates provide 4 Kcal/g of energy in our
diets. Since we take large amounts of carbohydrates, these provide
60-70% of our total calorie needs of the body. If taken in excess, it is
converted to fat in the body. The dietary sources of carbohydrates
are as follows:
a. Monosaccharides: Monosaccharides exist mainly as
glucose and fructose in our diets. Fruits, vegetable,
honey, jaggery are good sources of monosaccharides.
b. Disaccharides: Sucrose (common known as sugar) is the
commonest of them all and present in table sugar.
Lactose is found naturally in milk and milk products,
Maltose is the product of hydrolysis of starch and is
found in sprouted wheat and barley.
c. Oligosaccharides: These are found in plant seeds mainly
legumes, beans and peas.
d. Polysaccharides: Starch is one of the main
carbohydrates found in our diets and comes from
cereals, potato, bananas etc.
o Proteins: While the quantity of protein does not impose any
significant impact on the serum lipoproteins, it is the quality of
protein, which may be of significance. Patients should be advised to
consume plant origin proteins over those of animal origin. This is in

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view of the fact that plant origin foods, which are good sources of
protein, are generally rich sources of dietary fibre, have low amounts
of saturated Eat and are devoid of cholesterol, Egg white and lean
meats (meat without fat) should be the preferred options in case of
animal foods.

o Vitamins: Antioxidants and flavonoids, natural vitamin E, vitamins C

and A are nutrients (vitamins) that scavenge cell-damaging free
radicals and act as antioxidants .It is important to know this in view
of the fact that damage through free radicals is quite pronounced
among patients with Syndrome X -a risk factor for cardiovascular
disease. Vitamin A is present in good amounts in green and yellow
fruits and vegetables and lycopene in tomatoes and anthocyanin in
grapes and berries. Vitamin E rich foods include buck wheat (7.9 µg),
corn (5.8 µg), almonds (24.4 µg), sunflower seeds (52.1 µg), spinach
(3.0 µg) and soyabean (93.7 µg). Hence, vitamins (E,C and A)
containing foods, bright yellow fruits and vegetables like papaya,
orange, mango, strawberry, tomato, carrots and green leafy
vegetables like methi and spinach, cabbage, red wines, tea and
soyabean are excellent foods because of their antioxidant
properties.

o Minerals: The three most important minerals are chromium, zinc and
magnesium. These minerals play a critical role in maintaining proper
insulin function. Deficiency of these minerals increase the risk of
Syndrome X - ;I risk factor for cardiovascular disease. Excess of
sodium intake and lack of potassium have been seen to play an
important role in hypertension. Low intakes of calcium can also be a
risk for cardiac disorder. Sodium added to the food or sodium-rich
foods need to be restricted in cardiovascular diseases.
o Antioxidants and flavonoids :. The body makes use of a great variety
of antioxidants and free radical scavengers for different purposes

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and to protect tissues with different needs. Vitamins A, C and E have

important antioxidant functions as you have already studied above.
The B vitamins, although not technically antioxidants often acts as a
co-factor with antioxidants. Flavonoids are naturally occurring in
fruits, vegetables, Lea and wine.

2.2. Atherosclerosis: A Coronary Artery Disease

Atherosclerosis is an arterial lesion characterized by patchy thickening of
the intima (innermost coal of artery) comprising of fat and layers of
collagen like fibres. This is a slow or progressive disease, degenerative in
nature affecting small and large arteries and weaken them leading to
proliferation. This leads to problems in smooth flow of blood. These
deposits are referred to as plaque. The plaque reduces the size of the
lumen of the artery and consequently, the amount of blood flow. The
reduced blood flow causes an inadequate nutrient and oxygen supply and
water removal from the tissues, leading to a condition referred to as
ischemia. These condition causes pain in the chest which is referred to as
angina pectoris and it radiates down the left arm. When the lumen narrows
so much so that a blood clot occurs in a coronary artery and blood flow is
cut off, heart attack can result. The dead tissue that results is called an
infarct, The heart muscle that receives the blood is the myocardium. Thus,
such an attack is referred to as an acute myocardial infarction (MI).

Atherosclerosis is thus categorized as a continuum of as fatty streaks,

intermediate lesions, fibrous plaques and complicated lesions. There are 5
phases to atherosclerosis:

Phase I: Asymptomatic phase consists of fatly streaks, which are non-

obstructive, lipid-filled cells.

Phase 2: Consists of plaque with high lipid content and prone to rupture
usually the type of lipid is LDLc.

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Phase 3: Acute complicated phase with rupture and non-occlusive

thrombus.

Phase 4: Acute complicated lesions with occlusive thrombus, which are

associated I with angina/mycordial infarction and even sudden death.

Phase 5: Fibrotic or occlusive lesion. Large thrombi can cause serious acute
defects.

2.2.1 Etiology

Various factors are responsible for atherosclerosis. These include:

1. Hyperlipidemia: Excess circulating fats in blood especially the low-

density lipoproteins (LDL) and low levels of high-density lipoprotein (HDL)
can predispose to atherosclerosis.

2. Hypertension: HT can accelerate atherosclerosis and cause

complications.

3. Diabetes mellitus: An important risk factor commonly associated with

hypertension, due to abnormalities of coagulation, platelet adhesion and
aggregation, increased oxidative stress, and abnormalities in vessel
vasomotion can be a high risk for atherosclerosis.

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4. Obesity: Excessive triglycerides (hyperglyceridemia) and LDLc levels ore

commonly present in obese and lower HDL levels are a great independent
risk factors 'for atherosclerosis.

5. Lifestyle: Low physical activity, cigarette smoking could affect the rate
of atherosclerosis, increased CAD risk, On the other hand, regular exercise
is seen lo be protective.

6. Factors causing endothelial damage: Elevated blood homocysteine a

(genetically determined) and viral infections of lungs could damage the
endothelial and cause injury and hence lead to atherosclerosis.

2.2.2 Symptoms

Excessive weight, hypertension, high levels of cholesterol and triglycerides.

2.2.3 Complications:

Myocardial infarction, systolic and diastolic dysfunction, inflammatory

problems (pericarditis), stroke, gangrene (death and decay of body tissue)
and aneurism (blood filled dilation of a blood vessel).

2.2.4. Nutritional Management Goals:

The nutritional management goals include:

 Reduction of weight if overweight or obese.

 Reduction in the intake of total fat, saturated fat and cholesterol .
 Medication if required for treating lipid disorders and controlling BP
 Lifestyle changes-increase in physical exercise, moderation in
alcohol intake. No smoking, restricting coffee .
 Consuming a balanced adequate diet, rich in calcium, chromium,
iron and zinc.
 Medical management is through various lipid lowering drugs

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2.3. Hypertension
The first sound lup, is the systolic sound, which occurs when the heart
contracts and pushes out the blood into the various parts of the body. This
denotes the higher range of pressure called systolic blood pressure (SBP)
which is measured as millimeters of mercury (mm Hg). The sound clup is
the relaxation period of the heart when the blood enters the heart
chambers. This is the diastolic blood pressure (DBP) and denotes the lower
blood pressure.

Classification Of Blood Pressure And Stages Of Hypertension In Adults

Blood pressure range SBP/DBP Classification

120/80 Normal (optimal)
120-129/80-84 Prehypertension (optimal)
130-139/85-89 Prehypertension (borderline HT)
>140/90 Hypertension
Stage I 140-159/90-99 Hypertension stage I
Stage II 160-179/100-109 Hypertension stage II
Stage II >180/110 Hypertension stage III

2.3.1. COMPLICATIONS

Major complications of hypertension includes:

 Angina
 Heart attack
 Left ventricular hypertrophy Heart failure
 Left-side heart failure
 Stroke
 Cerebrovascular disease

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 Eye complications
 Cerebral haemorrhage
 Retinal damage haired vision
 Death

2.3.2. Classification of Hypertension

 Primary Hypertension
 Secondary Hypertension

Primary Hypertension: High blood pressure in the absence of any

underlying disease.
 Benign hypertension
 Malignant hypertension.
Secondary Hypertension: elevated blood pressure due to some
underlying disease.
 Cardiovascular hypertension
 Endocrine hypertension
 Renal hypertension
 Neurogenic hypertension
 Pregnancy induced hypertension

2.3.3. Etiology
i. Genetic factors: Currently it is be1ieved that there is polygenic
inheritance and when environmental factors are not healthy,
hypertension is precipitated.
ii. Body weight and height: Hypertension increases with increase in the
weight and height. Hence, those who are obese have higher blood
pressure values. Increase in BMI increases hypertension.
iii. Age: Increases steeply with age. Now scientists have found shifts in
BP. It is found in adolescents and the young as well.

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iv. Gender: Rise is greater in men than women but after menopause, the
difference decreases
v. Changes in rennin-angiotensin: Aldosterone system and excretion of
adrenocorticoids and prolactin may affect blood pressure.
vi. Hyperinsulinemia of obese may influence blood pressure
susceptibility through renal sodium reabsorption and transport.
vii. Dietary factors: Excess calories, fats especially saturated fat and
cholesterol in large quantities can increase blood pressure. Refined
carbohydrates (sugars) could have an effect but studies in humans are
inconclusive. High fibre intakes are beneficial (soluble fibre). Possible
role of chloride, low potassium (K) and high sodium diets is a suspect.
Less calcium and magnesium in diet could cause hypertension.
viii. Modern lifestyle: Sedentary life devoid of exercise, stress, smoking,
tobacco intake, alcohol are pointing towards increases in blood
pressure.

2.3.4. Objectives Of Nutritional Management:

The objective of nutritional management of hypertension includes:
 To achieve gradual weight loss in overweight and obese
individuals and maintain weight slightly below the normal
levels,
 To reduce sodium intake and maintain fluid and electrolyte
balance,
 To maintain adequate nutrition
 To lead a healthy lifestyle (no smoking, alcohol consumption
but a high physical activily), and
 To slow down the onset of complications.

 Energy: Calorie requirement should be based on the concept

of maintaining an ideal body weight. Excess calories through

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fats and carbohydrates have to be reduced so that the

weight is maintained.
 Proteins: Abnormal protein intake is recommended. Protein
should contribute 15-20% of the total energy needs. Excess
non-vegetarian foods especially red meat and egg yolks
could be avoided as it has greater proportion of saturated
fatty acids.
 Fats: The fats incorporated in the diet should be rich in
unsaturated fatty acids and should not provide more than
20% of the total .
 Carbohydrates: About 60-65% energy should be provided
from carbohydrates which are polysaccharides (complex
carbohydrates) rather than simple sugars (monosaccharides
and disaccharides).
 Minerals and Electrolytes:
Calcium (Ca): Adequate calcium intake is an essential part of
the treatment and this could be ensured through intakes of
milk and milk products and green vegetable as well as
adequate cereals and pulse intakes.
Sodium: Studies have shown that sodium restriction along
with weight reduction is effective in controlling mild to
moderate hypertension (1-2 &day) along with diuretics
recommended. Depending on the severity of hypertension,
different levels of sodium intake can be recommended.
These include:
 Mild Sodium restriction: 2-3 g sodium (2000-3000
mg). Salt may be used lightly in cooking, but no salt
at the table is allowed. There is no restriction on
naturally occurring fresh foods but processed
foods should be avoided.

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 Moderate Sodium restriction: 1 g sodium (1000

mg). In addition to the above restrictions, some
control in naturally occurring fresh foods and no
salt in cooking is added. Vegetables with high
sodium content are limited in use, canned
vegetables and baked products are avoided. Meat
and milk products are used in moderate amounts.
 Strict Sodium restriction: 0.5 g sodium (500 mg).
Apart from the restrictions stated above, meat,
milk and eggs are allowed in small portions and
vegetables with higher sodium content are
avoided.
 Severe Sodium restriction: 0.25 g sodium (250 mg).
This level is too restrictive and nutritionally
inadequate and realistic to be used practically. In
this, restricted quantities of meat and eggs are
used only occasionally.
Potassium: Increasing the potassium content in the diet lowers the blood
pressure and improves hypertension. This could be done by increasing
fruits and vegetables in the diet, which are rich in both potassium and fibre
content.
 Fluids: Fluid restriction is necessary only if oedema is present.
Dehydration may be observed in some patients on diuretics. Thus,
normal amount of fluids especially in the form of plain drinking water
can be taken.
Thus, remember the following points while chalking out a patient care plan
for hypertensives.
- Lifestyle changes: Avoiding smoking, use of tobacco, and excess alcohol
intake. , Physical activity like walking, 4 times a week for 40 minutes, is
beneficial.

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- Medications: Diuretics, calcium channel blockers and others should be

consumed regularly.
- Nutritious balanced diet: The diet of a hypertensive should be nutritious
.It should be low in calories (if required) and fat with a normal protein
content. It should be low in sodium but rich in potassium, calcium,
magnesium and fibre. Currently the DASH diets are recommended, These
are rich in fruits and vegetables, non-fat dairy products and low in total as
well as saturated fats

2.4. Angina Pectoris

Chest discomfort is often reported by most patients especially those which

are chronic cases of dyslipidemia and/or hypertension. Like diarrhoea and
fever, angina pectoris is a symptom and can appear in any cardiovascular
disease condition. It is a tight choking feeling in the chest brought about by
effort or less often by excitement. It is worse in cold weather or after heavy
meals and is due to lack of blood to heart muscles.
Most common causes associated with angina pectoris are enumerated
herewith:
o The usual cause of angina is the narrowing of the major coronary
artery due to atherosclerosis.
o Systemic hypertension increases myocardial demand and if the
supply of blood to the heart muscles is less, it can cause angina. .
o Heart disease: In late stages of aortic stenosis (narrowing of aorta)
it can precipitate an anginal attack.
o Anaemia: The heart gets less oxygen due to lack of haemoglobin in
anaemia.
o Thyroid disease: Thyroid disease is associated with angina.

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2.4.1 Symptoms
The pain of angina is usually over the center of the chest (below the
sternum) but can be felt from epigastrum to the jaw andarms. It is brought
about by exertion sometimes by stress and is relieved by rest. The duration
of angina is short and can be relieved in three minutes on rest.

2.4.2. Complications
It is a symptom giving a warning of impending myocardial infarction,
sudden cardiac death or even ischemic necrosis of the brain leading to
cerebral stroke.

2.4.3 Treatment And Dietary Management

Proper and careful treatment of the underlying cause (usually
dyslipidemia, advanced atherosclerosis or sever chronic hypertension) is
imperative to prevent the occurrence of any acute ischemic event namely
myocardial infarction /stroke. Dietary management is the key component
in preventing the progression of underlying disease condition. The most
vital objectives of dietary and life style management include:
 To maintain ideal weight for age
 To lower blood pressure through drugs and diet control
 To avoid exertion and unnecessary stress
 To follow a prudent diet /DASH diet


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2.5. Myocardial Infarction (Mi)

It is an initial acute phase of cardiovascular disease caused by the blockage

of a coronary artery supplying blood to the heart .Myocardial infarction
generally occurs when fibrous plaques coalesce together with blood clots
to result in complete blockage or stenosis in artery supplying oxygen and
nutrients through blood to the heart.

2.5.1. Dietary Management

Patients who suffer from an attack of myocardial infarction are
hospitalized and are usually kept under strict medical supervision. During
the initial 24 to 48 hours most patients are on intravenous support and if
needed on an artificial ventilator to meet their oxygen requirements.
Initially oral rood intake is restricted and not recommended as the ailing
heart cannot support the oxygen and absorption of food. Oral food intake
is resumed based on several cardiac function tests which likely in assessing
the residual functional capacity of the heart after injury. Alow fat soft diet
is generally recommended and during the initial stages foods may be
introduced in very small quantities every hour or after every two hours.
Observation of the patient during consumption of rood and at least till ½
to 1 hour after eating is essential to rule out the elicitation of angina
pectoris or another attack of myocardial infarction.
2.5.2. Objectives

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The objectives of dietary management of myocardial infarction patients

are as follows:
o to provide rest to the injured heart
o to maintain an optimum nutritional status
o to achieve and maintain a desirable body weight
o to prevent the development of another attack of MI

Energy: The diet should provide enough calories to meet the basal
requirements, hence a low-calorie diet is recommended. Other benefits of
providing a low calorie diet incIude: reduction in the adipose tissue mass
particularly among obese patients and hence reduced oxygen
requirements of the body (tissues); reduction in the requirement of oxygen
associated with ingestion, digestion and assimilation of food. The energy
intake may initially begin with 800 Kcal, which can be slowly progressed to
a 1200 Kcal diet till the patient is discharged. Thereafter, the patient's
energy intake should be governed on the

Maintenance of body weight, which is preferably 1 to 2 kg below IBW.

Protein, carbohydrates and Fat: The protein intake generally remains the
same as per the RDI i.e. 1.0 gm protein per kg body weight per day.
Adequate amount of proteins are necessary to promote regeneration of
the necrotic tissues in the myocardium, Majority of MI patients are also
hyperlipidemic and have elevated serum triglyceride levels. In such cases,
the calorie contribution from fat should not be above 20% and the dietary
cholesterol intake should remain below 200 mg per day.

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 Introduction to Clinical Nutrition

Carbohydrates should provide 60% of the total energy. However, emphasis

should be laid on the inclusion of easy-to-digest simple carbohydrates,
which are low in fibre. Low fibre cereals, roots and tubers should be served
in a soft well cooked/ blended form (purees etc.).

Vitamins and Minerals: The requirement of vitamins and minerals is largely

governed by the existing nutritional status and the clinical parameters of
the patient. Mild to moderate sodium restriction is generally
recommended if the patient is hypertensive or is at risk of developing
oedema due to congestive cardiac failure. Inclusion of low fibre, low
sodium fruits and vegetables can help in providing good amounts of iron
and B-group vitamins particularly folic acid and vitamin B12.
2.6. Congestive Cardiac Failure

Congestive cardiac failure is a form of chronic decompensated disease as

the condition may develop over a period of time. It results from an injury
to the heart muscle due to atherosclerosis, hypertension or rheumatic
fever resulting in progressive weakening of the heart muscle. This leads to
inadequate blood circulation and hence insufficient supply of nutrients and
oxygen to the tissues. This leads to malnutrition and underweight. If
oedema is present, it masks the state of malnutrition. Mostly
hemodynamic derangements are present. Congestive cardiac failure
causes left ventricular systolic dysfunction over a period of time. The heart
muscle -myocardium gets weakened progressively and is not able to
maintain normal cardiac blood output or blood circulation. Firstly, it can
cause pulmonary oedema causing breathing problems of pumping out
blood fast enough resulting in blood accumulation on the right side of the
heart, affecting normal circulation. This affects the normal flow of fluid
between tissue space and blood vessel, which thus starts accumulating in
the tissue causing oedema. The two hormones in the body that control
water balance also fail. (Antidiuretic hormone and the aldosterone). The
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 Introduction to Clinical Nutrition

aldosterone conserves sodium and water and worsens the oedema.

Reduced blood circulation effects the metabolism of tissues resulting in
increased cells breakdown and potassium is released. Increased potassium
in the cell increases the osmotic pressure and sodium tries to replace
potassium causing more water retention. Congestive heart failure
develops over a period of time when the necrotic tissues are not replaced
by functional connective cells thereby affecting the contraction and
relaxation capacity of the heart.

2.6.1 Etiology
The causes of this disorder can be numerous. The risk factors, which are
known, are
 Chronic hypertension
 Left ventricular hypertrophy
 Coronary heart disease (recurrent episodes of IHD particularly
myocardial infarction)
 Diabetes
 Advancing age
 Viral damage
 Alcohol abuse
 Injury
2.6.2. Symptoms
Congestive cardiac failure is a progressive form of cardiomyopathy. The
most classical symptom is fluid imbalance due to inadequate cardiac
output which results in cardiac/ pulmonary oedema, which may latter

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 Introduction to Clinical Nutrition

involve other organs in the abdomen. The most common symptoms seen
are :
 Fatigue, faintness and weakness
 Swelling of feet and ankles
 Shortness of breath even after lying down, loss of appetite,
indigestion, nausea and vomiting
 Congestion
 Inadequate cardiac output
 Altered fluid balance (oedema)
 Cardiac cachexia (severe malnutrition)
 Decreased urine production

Impaired cardiac function could also lead to cardiomegaly (enlargement of

heart), tachycardia (rapid pulse rate), heart rhythm problems, and growth
retardation in children. Poor peripheral perfusion results in cold
extremities, weak pulse, and low blood pressure. If pulmonary oedema is
present, it can cause wheezing and problems in breathing.

2.6.3. Treatment
A judicious and careful co-ordination between oxygen support, drug
therapy and nutrient intake can help in alleviating majority of the
symptoms associated with congestive cardiac failure thereby reducing the
frequency of morbiditics and mortalities associated with this disease. ACE
inhibitors, diuretics, beta-blockers and digitalis drugs are generally used in
conjunction with dietary management and oxygen support (severe
category hospitalized patients). Surgical management involves heart

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 Introduction to Clinical Nutrition

transplantation, cardiomyoplasty, mechanical support and dialysis. Most

of these are conducted as life-saving strategies. Whatever may be the
choice of treatment, it generally revolves around the following objectives.
 To provide relief from the symptoms
 To improve the quality of life
 Prolong life by reducing, stopping or reversing left ventricular
dysfunction
 To maintain adequate nutritional status.
2.6.4. Dietray Management
The objectives of dietary management include:
- to minimize stress workload on the heart
- To correct and maintain fluid and electrolyte imbalance
- To maintain a desirable body weight, and
- To maintain an optimum nutritional status.

2.7. Rheumatic Heart Disease (Rhd)

Rheumatic Heart Disease (RHD) is a very common cause of cardiovascular
disorder in children and adolescents in India. This disease involves damage
to the entire heart and its membranes. It is a complication of rheumatic
fever (resulting from an untreated Streptococcus throat injection) and
usually occurs after attacks of rheumatic fever. Rheumatic fever can
damage the heart valves. If the heart valves are damaged, they will fail to
open and close properly, when this damage is permanent, the condition is
called Rheumatic Heart Disease.

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2.7.1. Symptoms
Symptoms generally appear after 1 to 6 weeks of the fever and sometimes
the infection may have been too mild to have been recognized. The
symptoms are fever, fatigue, shortness of breath, fainting, palpitation and
chest pain. Swollen, tender, red, painful nodules or small protuberances
may appear. There could be red, raised, lattice-like sash and uncontrolled
movements of arms, legs and facial muscles.
2.7.2. Complications
Inflammation of lining of heart (pericarditis), anemia, heart, enlargement,
valve deformities (mitral and tricuspid valves), embolism, arrhythmia,
abdominal pain, fever, arthritis etc.
The diet should be nutritious and without restrictions except in those
patient with congestive heart failure, whose fluid and, sodium intake
should be restricted. Potassium supplementation may be necessary
because of the mineralocorticoid effect of corticosteroid and the diuretics
(if used).
3. Prevention Of Coronary Heart Diseases
Dietary Recommendations for the Prevention of Coronary Heart Disease
(Who) Year
Calories Sufficient To Maintain Ideal Body
Weight For Height
Total Fat 15-30% Of Calories
Cholesterol <300 Mg /Day
SFA <10% Of Total Calories
PUFA <8 % Of Total Calories
P/S Ratio 0.8-1.0

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 Introduction to Clinical Nutrition

Lionoleic Acid (LA/N6) 3-7% Of Total Calories

Alpha Linolenic Acid (ALNA/N3) <1 % Of Total Calories
LA/ALNA Ratio 5-10
Proteins 10-15% Of Total Calories
Carbohydrates 55-65 %
Sugars ≤10 % Of Total Calories
Salt 5-7 G/ Day
Dietary Fibre 40 G/Day

References
Krause’s (2000) Food, Nutrition and Diet Therapy, W.B Saunders Company,
tenth edition.pp:558-589
Srilakshmi B (2014) Dietetics, New Age International Private Limited,
seventh edition.pp:257-286.
Egyankosh (2018).website: egyankosh.ac.in

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