Introduction

Clinical nutrition is a vast dynamic diverse field which encompasses

pathogenesis of deficiency diseases, aetiology, prevalence, clinical signs
and symptoms, clinical manifestations and nutrients involved in management of
diseases.

Clinical nutrition is gaining pace today as mounting scientific evidence regarding

the key role of nutrients in the and prevention of diseases is being put forth.
Under nutrition and over nutrition in the form of obesity and chronic
degenerative diseases seems to be prevalent in the society posing dual burden
in management of health and nutritional status of populations.

Both undernutrition and over nutrition are strongly associated with faulty and
unhealthy eating habits. Thus, Clinical Nutrition involves application of research
based evidence to aid in the care of individuals at risk for diet related diseases.

Nutritional status and disease

Individuals together with environmental factors are responsible for ensuring

good nutritional status of population. The individual is at the central position
and health or disease is governed by his environment. Identifying defects at each
level from household, community and at the physical level with allocation of
resources would help ensuring nutritional welfare of the population.

Diseases may in turn affect nutritional status by:

1. Decreasing the intake of nutrients

2. Altering the metabolism of nutrients (or unusual losses)
3. Altering energy expenditure.

Common deficiency diseases

Diseases in humans that are directly or indirectly caused by a lack of essential

nutrients in the diet are called nutritional diseases.

Deficiency diseases may result from a person's abnormally high metabolic needs
for a nutrient or from some imbalance in the nutrients ingested Nutritional
diseases are commonly associated with chronic malnutrition.

Nutritional deficiency diseases are of two types namely

Macronutrient deficiency diseases

These diseases are caused due to improper intake and metabolism of proteins,
carbohydrates and fats. A proper proportion of proteins, carbohydrates and fats
are very essential to maintain healthy life and to be free from lifestyle diseases.

Macrominerals include calcium, chloride, magnesium, phosphorus, potassium,

sodium, sulphur and magnesium.

micronutrient deficiency diseases

These diseases are caused by improper intake of micronutrients that the human
body needs in minute amounts so that it can function properly. Although,
micronutrients are needed only in small amounts, their deficiency leads to
critical health problems. Micronutrients include vitamins and mineral deficiency
diseases. Following below is a list of macronutrient and
micronutrient deficiency disorders along with clinical signs.

Micronutrient deficiency diseases

Micronutrient deficiency Signs

1. Night Blindness
2. Bitots spot
3. Conjuctival Xerosis
4. Corneal Xerosis
5. Corneal Ulcer
Vitamin A
6. Keratomalacia
7. Xerophthalmic fundus
8. Skin changes like
xerosis of skin and
follicular hyperkeratosis

Thiamin or Beri Beri

1. Loss of appetite
2. Tingling hands and legs
3. Numbness, aches and
pain
4. Polyneurits
Vitamin B1
5. Either odema or
emaciation of body
tissues
6. Wernicke’s Korsakoff
Syndrome
 Riboflavin or Ariboflavinosis

1. Glossitis (magenta
tongue)
2. Cheilosis
3. Angular stomatitis
4. Nasolabial dyssebacea
5. Angular blepharitis
Vitamin B2 deficiency
6. Lingual papillae
7. Scrotal or vulval
dermatosis
8. Eye lesions like corneal
vascularisation
9. Pharyngitis

1. Sunburn
2. Irritability
Niacin deficiency 3. Diarrhoea
4. Dementia
Pellagra 5. Swollen tongue
(The 4 Ds: dermatitis, diarrhea, 6. Mental confusion
dementia, and death). 7. Dermatitis
8. Insomnia
9. Weakness
10. Extreme cases death

1. Acne
2. Paresthesia
Pantothenic acid ( also called
3. Carpal tunnel syndrome
pantothenate)
4. Fatigue
5. Insomnia

1. Microcytic anemia
2. Depression,
3. Dermatitis, high blood
pressure (hypertension),
Pyridoxine or vitamin B6 water retention
4. Elevated levels of
homocysteine
5. Weakened immune
system

Micronutrient deficiency diseases

Micronutrient deficiency diseases

Micronutrient deficien
Signs
cy

1. Initial hair loss and rash

2. Convulsions and other
neurological disorders
3. Delayed growth and
Biotin or Vitamin H development
4. If not treated,
biotin deficiency causes ch
anges in blood pH that can
lead to coma and death

Megaloblastic Anaemia
(Pernicious anaemia)

1. Weakness and pallor

2. Degeneration of surface
mucosal tissues resulting
in ulceration
3. Secondary manifestations
Folic Acid or vitamin like sore tongue
B9 4. Gastrointestinal
disturbances like
diarrhoea and poor fat
absorption
5. During pregnant low
intake of folic acids may
result in neural tube
defects

Megaloblastic Anaemia
(Pernicious anaemia)

1. Anorexia
2. Nausea
3. Vomiting
4. Fatigue
Cyanocobalamin or 5. Abdominal pain
Vitamin B12 deficiency 6. Weight loss
7. Weakness
8. Dyspenoea
9. Palpitation
10. Pale skin
11. Liver and spleen may
enlarge
12. Spinal cord degeneration

Scurvy
Vitamin C
 1. Spongy bleeding gums
2. Folicular hyperkeratosis
3. Petechiae
4. Ecchymoses
5. Painful epiphysial
enlargement
6. Haematoma in muscles

Vitamin D

1. Epiphysial enlargement
2. Beading of ribs( Rachitoc
rosary)
Active rickets 3. Open fontanelles
4. Craniotabes
5. Muscular hypotonia

1. Bossing of skull
2. Deformation of thorax
Healed rickets 3. Harrisons sulcus
4. Bow legs
5. Knock knees

Local or generalised skeletal

Osteomalacia in adults deformities with tender
bones

1. Faulty absorption of
vitamins and liver
disorder that interfere
with the synthesis of
Vitamin K prothrombin
2. Prolonged clotting time of
blood
3. Bleeding tendency
developed

Deficiency Signs

Iron 1. Weakness
2. Pallid appearance
3. Frequent headaches
4. Hypochromic microcytic
anaemia
5. Low oxygen carrying
capacity
6. Fatigue
7. Pale conjunctivae (inner
eyelid), nail beds, gums,
tongue, lips and skin
 8. Atrophic lingual papillae
9. Koilonychia

1. Simple goitre
( enlargement of the
thyroid gland)
2. Myxoedema (progressive
destruction of epithelial
elements in thyroid )
3. Endemic cretinism and
deafness, spastic paralysis
of legs
Iodine
4. Hypothyroidism ( coarse
and dry skin, husky voice,
delayed tendon,
epiphyseal dysgenesis)
5. Psychomotor defects(poor
motor coordination)
6. Impaired mental function
7. Low intelligence level
8. High degree of apathy

Mineral Deficiency Diseases

Mineral Deficiency Diseases

Deficienc
Signs
y

Calcium

1. Decreased rate of growth

In 2. Hyperirritability and tetanyae
children leading to death
3. Loss of calcium from bone

In adults 1. Osteoporosis
2. Fracture of brittle bones even after
small accidents
3. Pain due to fracture
4. Hypocalcemia
5. Motor nerves become over-
susceptible to stimuli affecting face,
hands and feet producing clinical
features of tetanyae
6. Loose muscle tone and become
 flabby

1. Severe dehydration
2. Decrease in blood volume and blood
Sodium pressure
3. Circulatory failure
4. Chronic renal disease with acidosis

1. Muscular weakness
2. Irritability
Potassiu
3. Paralysis
m
4. Tachycardia
5. Dilation of heart with gallop rhythm

1. Mottled dental enamel

Fluorine 2. Genuvalgum ( adult form of knock
knees)

Lesson 2: Protein calorie malnutrition

Introduction

A nutritional deficiency disease ultimately develops when inadequate

amounts of essential nutrienvts are provided to the cells for their normal
metabolic functions. The nutritional deficiency may be of two types as per origin
namely primary and secondary nutritional inadequacy.

A primary nutritional inadequacy is caused by a faulty diet one that lacks

essential nutrients either in kind or amount or provides an imbalance of
nutrients.

Secondary or conditioned nutritional inadequacy results from factors

that interfere with ingestion, absorption, or utilization of nutrients as well as
from metabolic or functional conditions that increase the requirement for cause
unusual destruction or abnormal excretion of nutrients.

Pathogenesis of Nutritional deficiency diseases

The pathogenesis of nutritional deficiency diseases is outlined in brief in.

1. A nutritional inadequacy
2. Nutrient reserves
3. Release of nutrients
4. Tissue depletion
5. Biochemical lesions
 6. Functional changes
7. Anatomic lesions

A nutritional inadequacy

May be traced to either a primary (dietary) inadequacy or to a secondary

(conditioned) inadequacy. The mere presence of a nutritional inadequacy,
however, does not necessarily indicate either malnutrition or deficiency disease,
for the human body has interposed an important safety factor between the
occurrence of a nutritional inadequacy and the development
of deficiency disease.

Nutrient reserves

The safety factor upon which the occurrence of a nutritional inadequacy and the
development of deficiency disease depend is the nutrient reserves upon which
the tissues may draw during temporary lapses in the supply of nutrients. There is
a time lapse between initial exposure to a nutritional inadequacy, either primary
or conditioned, and the onset of a nutritional disease. This time period may be
short or long depending on the initial level of nutrient reserves and the degree of
nutritional inadequacy. The function of these reserves is to supply a metabolic
pool or a relatively constant level of nutrients. The reserves may be

 Very large, as is the case with vitamin A

 May also be relatively small, as is true of a labile protein or thiamine

Release of nutrients

 If the supply from the gut is temporarily inadequate, the reserves release
nutrients to the tissues via the blood.

 If the supply from the gut is temporarily greater than the tissue
requirements, nutrients reserves are filled first; and if the supply is still in
excess, the balance piles up temporarily in the blood, to be eliminated in
most instances in the urine. This accounts for the large urinary excretion
of nutrients following test doses if the nutrient reserves are filled and the
low urinary excretion of test doses if the reserves are low or depleted.

 The nutrient reserves of the body continue to supply essential nutrients to

the tissues for reasonable periods of time.
  If however, the nutrient supply continues to be less than the tissue
requirements, the reserves will eventually be depleted, and the tissues will
be dependent on the daily food supply

Tissue depletion

The exhaustion of nutrient reserves is manifested by tissue depletion. It may

occur rapidly or slowly, depending upon various factors:

1. The degree of nutritional inadequacy

2. The amount of nutrient reserves
3. The requirements of the body for essential nutrients.
Tissue depletion of nutrients results in gradually increasing alterations in the
efficient
operation of the enzyme systems which spark metabolic reactions.

Biochemical lesions

When tissue depletion has reached a critical level, biochemical “lesions” result.
These lesions are not too well known, although the biochemist is beginning to be
familiar with the changes in enzyme systems induced by tissue depletion of
several of the nutrients. Enzyme systems involved in the release of energy and
other metabolic reactions are dependent on vitamins such as thiamine,
riboflavin, niacin, pyridoxine, and pantothenic acid. As a result biochemical
lesions develop. In some instances, these are measurable by the fact that there is
an abnormal diversion of metabolites, such as:

 The accumulation of pyruvic acid in vitamin B1 deficiency

 The abnormal excretion of xanthurenic acid after a test load of tryptophan

in vitamin B6 inadequacy

 As deficiency proceeds, functional changes develop; for example,

impaired dark adaptation in vitamin A deficiency.

Functional chang

When a deficiency of these essential nutrients exists, biochemical alterations

develop which result in the “piling up” of certain metabolites and in the altered
metabolism of others. Following biochemical lesions, various functional changes
occur. These functional changes are manifested clinically by symptoms. They
include such common complaints as excessive fatigability, disturbances in sleep,
 inability to concentrate, “gas”, heart consciousness, and various queer bodily
sensations. Although these symptoms are definitely nonspecific in that they may
be caused by many factors other than malnutrition, their occurrence as a
manifestation of tissue depletion of certain nutrients is indisputable.

Anatomic lesion

Following functional changes, anatomic lesions become manifest. At first, they

are “subgross”, that is, microscopic in nature. Hence, early investigation of
tissues readily available for examination with the bio-microscope such as the
conjunctiva, the cornea, the tongue is entirely reasonable. Since these tissues are
known eventually to develop gross lesions as a result of tissue depletion.

 The conjuctiva develop Bitot’s spots in advanced vitamin ‘A’ deficiency.

 The cornea may develop increased and nutritional and abnormal

vascularity in riboflavin deficiency.

 The tongue shows glossitis in several vitamin ‘B’ deficiency diseases.

Progression of subgross lesions leads to gross manifestation becoming evident.
These are described collectively as the clinical signs.

Diagnosis of nutritional deficiency

Diagnosis can be done in three ways

 General evidence of deficiency in terms of inadequate diet, defective

absorption and increased utilization is very important
 Specific evidence of deficiency includes laboratory tests and clinical
tests for specific deficiency.
 Cause of condition: This can be based as from evidence from animals
or from human beings.
 Treatment: This is an important step to cure nutritional deficiencies.
Primary step is the identification of specific nutritional deficiencies
followed by identification of underlying conditions. Treatment of
underlying conditions along with dietary modification is very important.
Supplementation as required for specific conditions should be provided.

Lesson 3: Protein calorie malnutrition

Introduction
Protein energy malnutrition is a problem that includes two distinctly different
disease processes – kwashiorkor and marasmus. Protein energy malnutrition is
defined as a range of pathological conditions arising from coincident lack of
varying proportions of protein and calorie, occurring most frequently in infants
and young children and often associated with infection. (WHO, 1973)

Previously it was considered a problem of the poorer populations, but now it is

recognised that nearly 25 – 50 % of patients admitted into hospitals, who require
hospitalization for two weeks or longer, suffer from PEM. Therefore it is
important to identify and treat this problem.

Classification

 Marasmus
 Kwashiorkor
 Marasmic kwashiorkor

Marasmus

The weight is 60% of normal or lesser and the subject has a ‘skin and bones’
appearance. The skin is dry and wrinkles easily. Heart rate, blood pressure and
body temperature are low. Hair is sparse, thin and dry and it is easily pulled out
without pain. The patient has an apathetic and anxious expression. Most often
abdominal distention is present.

Kwashiorkor

Unlike marasmus, kwashiorkor is diagnosed based on laboratory indices. In

children kwashiorkor is often the result of a low protein, starchy diet during
stress periods of growth. In a hospitalized patient under stress and being
supported by 50% dextrose solution, kwashiorkor is often seen within as short a
period as two weeks. Fat reserves and muscle mass tend to be normal giving a
deceptive appearance of adequate nutrition. Signs which help in the diagnosis of
kwashiorkor are -

 Easily pluckable hair,

 Edema,
 Delayed wound healing.
Laboratory indices which changes are –

1. Severely depressed levels of serum proteins

1. Albumin < 2.8g/100ml
2. Transferrin < 150mg/dl
3. TIBC < 250mg
2. Depression in cellular immune function
1. Lymphopenia
2. Lyphocytes < 1200/ cu mm in adults & older children.
Lymphopenia: an abnormally small number
of lymphocytes in the circulating blood.

Lymphocyte: a type of white blood cell in the

vertebrate immune system.
Full blown kwashiorkor in adults requires aggressive nutritional support. In such
patients, surgical wounds do not heal, host defences are compromised and often
death may occur from infections despite antibiotic therapy. Kwashiorkor is
prevented much more easily than treated.

Marasmic kwashiorkor

The combined form of protein calorie malnutrition develops when the acute
stress of illness or surgery is experienced by the chronically starved patient

Characteristic features of marasmus and kwashiorkor

Marasmus Kwashiorkor
Clinical
setting Decreased
Decreased calories
protein + stress

Time
taken to Months, years Weeks
develop

Clinical  Starved  Well nourished

Features appearance appearance
 Weight/  Hair –easily
Height < 80% pluckable
of standard  Flag sign in
 Triceps skin children.
fold < 3mm  Edema
 Midarm  Hepatomegaly
muscle  Hyper pigmentation
 circumference
< 15cm
 Creatinine of skin
Height index <
60%

 Serum albumin <

2.8g/100 ml
 Serum transferring
Laborator < 150mg /100ml
No changes
y findings  Lymphocytes <1200
cells / cu mm
 Non reactive skin
tests.

 Wound healing.
Reasonably
 Immunocompetence
Clinical preserved
.
course responsiveness to
 Infections and other
short term stress.
complications.

Low(unless there is
Mortality High
underlying disease)

Hepatomegaly is swelling of the liver

beyond its normal size.

Cardiovascular and renal functions in PEM

 There is lowering of blood pressure, heart rate and cardiac output in PEM.
A diminished venous return and postural hypotension along with
tachycardia are observed.

 There is a decrease in renal glomerular filteration rate.

 Total body potassium decreases in PEM due to a reduction in muscle

protein. Total intracellular sodium increases leading to overhydration.
Changes in these electrolytes tend to increase the fatigueability of skeletal
muscles and decrease their strength.

 Atrophy of cells with greater cell turnover rates occurs as seen in the
intestinal mucosa where villi are flattened. Red bone marrow, testicular
epithetical cells and skeletal muscles also get atrophied due to lack of
proteins.

 Severe protein deficiency leads to a decreased production of gastric juice,

pancreatic secretions and bile. Gastric enzymes are low and there is
 lowering in intestinal absorption of lipids and disaccharides. Irregular
intestinal motility leads to diarrhoea.

Nutritional support

Marasmus should be treated gradually to reverse the loss in body reserves.

Overly aggressive repletion can result in severe, even life threatening, metabolic
imbalance. Enteral feeding is preferred. Treatment should be started slowly to
allow readaptation of metabolic and intestinal functions.

Kwashiorkor requires aggressive nutritional support through parenteral route.

Nutritional homeostasis should be attained rapidly.

Lesson 5: Vitamin A deficiency

Introduction

In 1915, Mc Collum and Davis described “Fat soluble A” as a growth promoting f

Vitamin A is an essential nutrient needed only in small amounts but is necessary
for the normal functioning of a large number of regulatory and other
physiological processes of the human body. Vitamin A deficiency disorders occur
when the body reserves are depleted to the limit at which
physiological functions are impaired.

Vitamin A is stored mainly in the liver as retinyl esters and these stores are
depleted due to inadequate dietary intake, sometimes associated with infection.
Relatively constant levels are maintained in the blood until body stores become
depleted below a critical point.

Vitamin A deficiency

The effects of vitamin A deficiency are seen in different body tissues and systems
which are affected by this deficiency. The main impact is on the integrity of the
epithelial tissues; however the enzyme system, auto immune, gene regulation
and vision systems are also affected.

Clinical and pathological effects

 The clinical effects of vitamin A deficiency that are best recognised are those
affecting the eye. However vitamin A deficiency affects all mucous membranes of
the body and the impact on the eye is later than that on some other organs. The
effects are seen most markedly in periods of greatest need; early growth,
pregnancy and lactation.

 Xerophthalmia and Keratomalacia: Xerophthalmia represents the

ocular consequences of vitamin A deficiency and includes
 Night blindness (XN)
 Conjuctival xeroses (X1A)
 Bitot’s spots (X1B)
 Corneal xerosis (X2)
 Ulceration (X3A)
 Necrosis/ Keratomalacia (X3b)
 Night blindness: is the earliest specific clinical symptom of vitamin A
deficiency.
Opsin, a protein binds covalently with 11- cis- retinal to form rhodopsin or
visual purple. Light exposure even at low levels bleaches rhodopsin. This
sends electrochemical impulses along the optic nerve to the brain that
results in vision. The vitamin A aldehyde is returned to the rods to form
rhodopsin once again and thus the visual cycle is completed. Due to a lack
of vitamin A, this cycle is disabled resulting in poor vision in dim light
followed by night blindness. This is commonly seen among preschool
children and pregnant women.
 Conjunctival xerosis with Bitot’s spots: Bitot’s spots are grey to
yellowish white foamy patches of keratinized cells present usually on the
temporal conjuctival surface. They respond to high potency vitamin A and
disappear within two weeks. In some cases they may persist for many
months despite overcoming vitamin A deficiency. Thus they may
represent past rather than present deficiency.
 Corneal xerosis, ulceration and necrosis: Corneal xerophthalmia
represents an acute decompensation of the corneal epithelium and is a
sight threatening emergency. It responds to vitamin A therapy if treated
immediately. If untreated it leads to blindness. Small ulcers in the cornea
also heal with a minimum damage if treated promptly. If it is not treated
it will result in meltdown of the eye with irreversible blindness in the eye.

Lesson 7:Anemia
Introduction

Iron deficiency anemia is the most prevalent micro nutrient deficiency in the
world. It affects more than 2000 million people in both developing and
developed countries. Young children and pregnant women are the most affected
group with a global prevalence of 40% and 50% respectively. Indian studies
show over 65% prevalence among preschool children (Seshadri, 1994). Anemia is
a public health problem in India with up to 70% of pregnant women being
anemic. Nutritional anemia is most commonly caused by a deficiency of iron.

Causes

Anemia is caused by several factors that often occur together. The

principal causes are -

 Negative iron balance due to inadequate dietary intake.

 Low dietary bioavailability.
 Iron loss from the body
During periods of rapid growth as in infancy, early childhood, adolescence and
pregnancy, the blood volume expands and extra iron is required to maintain the
concentration of blood components like hemoglobin. When the requirements are
not met, anemia could occur.
Foods which supply

Non heme
Heme iron
iron

 Green
leafy
Liver
vegetabl
es

 Rice
Mutton
flakes

 Gingelly
Fish
seeds

Crab  Soybean

 Bengal
gram
roasted
Prawns
 Dates
(dried)
 Bajra
The quality of iron supplied to the body – heme and non heme iron, the presence
of iron absorption inhibitors and promoters – also affect the iron made available
to the body.

Iron loss mainly occurs during menstruation, iron transfer to the fetus during
pregnancy, blood loss during child birth, helminth infestation and malaria. It can
also occur in accidental hemorrhages, and in bleeding ulcers and hemorrhoids.
 Inhibitors and Enhancers of iron absorption

Inhibitors Enhancers

 Low gastric
Increased acidity
acidity

 Phytates and
Ascorbic acid
oxalates

 Polyphenols
Presence of
 Minerals
meatBody’s need
 Infection

Screening for Iron deficiency

Iron deficiency is the point at which iron stores are completely exhausted and
any deficiency of functional iron is associated with liabilities.

*Ser
um Hemogl
Diagnosis
Ferri obin
tin

Norm No
Normal
al iron deficiency

Storage
Low Normal
depletion

Iron deficiency a
Low Low
nemia

Norm Other causes of

Low
al anemia
*Ferritin is the storage form of iron in the body.

Consequences of iron deficiency anemia

 Pregnancy outcome Anemia during pregnancy is associated with an

 increased risk to the fetus and the mother. The incidence of low birth
weight, premature births and perinatal mortality is higher when the
mother is even slightly anemic. Anemia is also a cause of maternal deaths.
Changes in neurotransmitter levels of fetal brain are seen if mother is
anemic.
 Mental and motor development
Anemia, even mild anemia, affects the psychomotor and cognitive
function of infants. Iron deficiency anemia at a critical period of brain
growth may produce irreversible abnormalities. Lack of sufficient iron can
affect attention, concentration and memory among school aged children.
 Effect on growth
Anemic children have a poor growth status as indicated by their weight
and height. During adolescence iron deficiency slows down the tempo of
growth and the ‘catch up’ growth may not be optimum. Low iron stores in
girls may contribute to a delayed age at menarche.

Work performance

In adults, impaired physical work performance is the most well documented

manifestation of iron deficiency. This affects productivity and therefore has
economic implications. Reduced hemoglobin in anemia is associated with
reduced blood oxygen content and this reduces the cytochrome mediated ATP
production and reduced energy for physical work performance.

 Plasma Ferritin levels give an idea of

iron stores.
 Transferrin saturation gauges iron
supply to tissues.
 Hemoglobin and Hematocrit
measurements can indicate anemia.
 Ratio of zinc protoporphyrin to heme
indicates iron supply to developing
RBCs.

Clinical Features

 The structure and function of epithelial cells is affected by

iron deficiency anemia.
 The tongue, mouth, stomach and nails are affected. The skin becomes pale
and the inside of lower eyelid is also pale Finger nails became thin and flat
and koilonychia develops (spoon shaped nails). Achlorhydria is also seen.
 There is atrophy of the lingual papillae and the tongue look smooth and
waxy. Angular stomatitis and dysphagia may be present.
 Lassitude, fatigue, breathlessness on exertion, palpitations, dizziness,
 headache, insomnia are some common features.

The normal Hb level for males is 14 to 18 g/dl; that for females is 12

to 16 g/dl.( NCBI)

Hemoglobin cut off points used to define anemia

Hemoglobi
Group Hematocrit
n (g/dl )

Children 6 months
11.0 33
to 5 yrs

5 – 11 yrs 11.5 34

12-13 yrs 12.0 36

Non pregnant
12.0 36
women

Pregnant women 11.0 33

Men 13 39

Source: WHO/UNICEF, 1998

Lesson 8: Iodine deficiency disorders

Introduction

Iodine deficiency is recognized as a major international public health problem

and nearly 13% of the world’s population is affected by
iodine deficiency disorders (IDD). As per the national IDD survey carried out in
40 districts all over India by NNMB in 2003, the prevalence of total goiter (%)
ranges between 7.2 to 39.6%. Higher prevalence is seen in most eastern Indian
states and some of the northern states. Nearly 197 districts all over India were
found to be endemic for IDD.

Iodine Deficiency Disorders refer to the wide spectrum of effects of

iodine deficiency on growth and development.

Functions
Iodine functions as an integral part of the thyroid hormones which regulate the
key processes in various cells of the body. The thyroid hormones are required for
the normal growth and development of individual tissues, for maturation of the
whole body, for energy production, oxygen consumption in cells and for
maintaining the body’s metabolic rate. If thyroid hormone secretion is not
adequate, the basal metabolic rate is reduced and the level of activity of the
individual is decreased (hypothyroidism)

The function of iodine in the body is to help synthesise thyroid hormones –

thyroxin (T4) and triiodothyronine (T3). The synthesis, release and action of
these hormones is regulated very finely as either excess or deficiency of these
hormones will be detrimental to normal body functioning. The thyroid gland has
to receive around 60µg of iodine per day to maintain an adequate supply of
thyroxin.

Deficiency

The spectrum of Iodine Deficiency disorders (IDD) are seen in Table

Goiter, a swelling of the thyroid gland is the most obvious and common feature
of iodine deficiency. (Figs 1, 2, 3). In iodine deficiency, the thyroid gland
attempts to increase production of thyroid hormones. Hyperplasia of the thyroid
cells occurs and thyroid gland increases in size. Goiter serves as a biological
marker for the potential existence of other IDD.

Spectrum of Iodine Deficiency Disorders (IDD)

 Abortions
 Still births
 Congenital anomalies
 Increased perinatal
mortality
 Increased infant
mortality
 Neurological cretinism:
Fetus
mental deficiency, deaf
mutism, spastic diplegia,
squirts.
 Myxoedematous
cretinism: mental
deficiency dwarfism,
hypothyroidism.
 Psychomotor defects
 Neonate  Neonatal hypothyroidism

Child and  Retarded mental and

adolescent physical development

 Goiter and its

complications
Adult
 Iodine induced
hyperthyroidism

 Goiter
 Hypothyroidism
All ages  Impaired mental function
 Increased susceptibility
to nuclear radiation.

During puberty and pregnancy, along with increased activity of estrogens,

thyroxin activity also increases, thereby increasing the demand for iodine during
these periods. Delayed onset of puberty and decreased fertility result due to
iodine deficiency during these phases of life. The most damaging consequences
of iodine deficiency are on fetal and infant development. Thyroid hormones and
therefore iodine are essential for normal development of the brain and
insufficient levels may lead to mental retardation of fetus or new born child.
Endemic cretinism is the most severe effect of fetal iodine deficiency- cretins are
mentally defective with physical abnormalities. In myxoedematous cretinism,
hypothyroidism is present during fetal and early postnatal development and it
leads to mental deficiency and stunted growth. In neurological cretinism, mental
retardation along with hearing and speech defects and disorders of gait are
present but hypothyroidism is absent. This syndrome is the result of low intake
of iodine by a pregnant woman.

Iodine deficiency in school children has a effect on their mental performance. A

difference of 13.5 points in IQ of iodine deficient and sufficient children has been
found in studies conducted. This indicates the effect of iodine deficiency on
neuropsychological development

Less severe iodine deficiency has been reported to cause elevated hearing
thresholds in children.

Gradation of iodine deficiency disorders (WHO/UNICEF, 1992)

Grading is also done based on the urinary excretion of iodine.

Category Urinary
Iodine
 level
mg/dl

Mild IDD 5.0 – 9.99

Moderat
2.0 – 4.99
e IDD

Severe
≤ 2.0
IDD
Cretinism in the visible but small component of IDD, whereas the other
components, through large are generally invisible.

Reasons Requirement and recommended dietary intakes

Approximately 1µg/kg body weight per day is necessary to prevent goiter.

However a large safety margin is given and the RDA is about 100 µg/day. For
pregnant and lactating women the requirements are higher, being 200-230
µg/day during pregnancy and 200-290 µg/day during lactation. The
requirements increase if the diet contains goitrogens as they interfere with the
biosynthesis of the thyroid hormones.