Indmedica Home | About Indmedica | Medical Jobs | Advertise On Indmedica
Search Indmedica Web
Indmedica - India's premier medical portal

Indian Journal for the Practising Doctor

Health Consequences of Iodine Deficiency

Author(s): Kapil, U

Vol. 5, No. 6 (2009-01 - 2009-02)

ISSN: 0973-516X

Kapil, U

Dr Umesh Kapil, Professor, Department of Human Nutrition,
All India Institute of Medical Sciences, New Delhi. (Email: umeshkapil(at)yahoo.com)

Iodine is a trace metal of vital importance to human beings. Although a teaspoonful is sufficient for whole life, millions in the world suffer because they do not get it. Human beings need the mineral right from the stage of organogenesis till their death; however, the requirement is essential during the foetal life and the formative years of physical and mental development. The health consequences are beyond the long-perceived cosmetic goiter; foetal loss, still birth, severe mental retardation, deaf-mutism, and other physical and mental disorders can result from iodine deficiency. Here we discuss the health consequences of iodine disorder.

Key Words: Iodine, Cretinism, Mental Retardation, Functions of Iodine

Introduction

Iodine is a trace element essential for the synthesis of thyroid hormones, triodothyronine (T3) and thyroxine (T4). These hormones regulate the metabolic pattern of most cells and play a vital role in the process of early growth and development of most organs, especially the brain. In humans, the early development of the brain occurs during foetal and early postnatal life1. Inadequate intake of iodine leads to insufficient production of these hormones, adversely affecting the muscle, heart, liver, kidney and the developing brain and resulting in the disease states collectively known as Iodine Deficiency Disorders (IDD).

Magnitude of IDD

Iodine Deficiency Disorder is known to be a significant public health problem in 118 countries of the world. At least 1,572 million people worldwide are estimated to be at risk of IDD i.e. people who live in areas where iodine deficiency is prevalent (Total Goitre rates above 5%), and at least 655 million of them are believed to be affected by Goitre. Most of these live in developing countries of Africa, Asia, and Latin America, however, large parts of Europe are also vulnerable.2

Physiological Functions of Iodine

Iodine is an essential dietary element which is required for the synthesis of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). The T4 and T3, which are iodinated molecules of the essential amino acid tyrosine, regulate cellular oxidation and hence effect calorigenesis, thermoregulation, and intermediary metabolism. These hormones are necessary for protein synthesis, and they promote nitrogen retention, glycogenolysis, intestinal absorption of glucose and galactose, lipolysis, and uptake of glucose by adipocytes.3

The healthy human body contains 15-20 mg of iodine, of which about 70-80% is present in the thyroid gland. In a day, 60 mg of circulating iodine needs to be trapped by the thyroid for adequate supply of T3 and T4. To extract this amount of iodine from the circulation, the thyroid daily clears several hundred litres of plasma of its iodine. This work can increase further by several times in severely iodine deficient environments. To cope up with this increased workload the thyroid enlarges in size, under the influence of Thyroid Stimulating Hormone (TSH), secreted from the pituitary gland. This compensatory mechanism, triggered by the hypothalamus to increased TSH secretion from the pituitary, causes remarkable enlargement of the thyroid gland (goitre)4.

Failure to have an adequate dietary intake of iodine leads to insufficient production of thyroid hormones, which affect many parts of the body, particularly muscle, heart, liver, kidney, and the developing brain. Inadequate hormone production adversely affects these tissues, resulting in the disease states collectively known as the iodine deficiency disorders, or IDD. Dietary iodine deficiency stimulates TSH secretion which results in thyroid hypertrophy. The enlargement of the thyroid gland due to dietary iodine deficiency is called endemic goitre. Iodine intakes consistently lower than 50 μg /day usually result in goitre. Severe and prolonged iodine deficiency, may lead to a deficient supply of thyroid hormones. This condition is referred to as hypothyroidism (3).

Etiology of IDD

Iodine is one of the essential elements required for normal human growth and development. It’s daily per capita requirement is 150 micrograms. Soils from mountain ranges, such as the Himalayas, Alps, and Andes, and from areas with frequent flooding, are particularly likely to be iodine deficient. The problem is aggravated by accelerated deforestation and soil erosion. The food grown in iodine deficient regions can never provide enough iodine to the population and live-stock living there. Unlike nutrients such as iron, calcium or the vitamins, iodine does not occur naturally in specific foods; rather, it is present in the soil and is ingested through foods grown on that soil. Iodine deficiency results when there is lack of iodine on the earth’s crust. Living on the sea coast does not guarantee iodine sufficiency and significant pockets of iodine deficiency have been reported from Costal regions in different parts of the world.5

Iodine deficiency thus results mainly from geological rather than social and economic conditions. It cannot be eliminated by changing dietary habits or by eating specific kinds of foods grown in the same area. Besides nutritional iodine deficiency, a variety of other environmental, socio-cultural and economic factors operate to aggravate iodine deficiency and related thyroid dysfunctions. These include poverty- related protein-energy malnutrition, ingestion of goitrogens through unusual diets (particularly by the poor), bacteriologically contaminated drinking water, as well as bulky high residue diets which interfere with intestinal absorption of iodine.6

Several environmental and genetic factors interfere with the processes of thyroxin synthesis leading to goitre formation. The genetic factors, which are rare, mainly affect the enzymes involved in thyroxin synthesis.

Environmental factors are amongst the most common factors that interfere in thyroxin synthesis and lead to goitre formation. The most important environmental factors are (i) environmental iodine deficiency (ii) goitrogens. Undoubtedly, the most frequent cause of goitre in India and other countries is environmental iodine deficiency. However, there is emerging evidence in different countries of world that goitrogens may be playing a secondary role in several endemic foci. Goitrogens are chemical substances, that occur primarily in plant foods.

They can occasionally be present in contaminated drinking water. Goitrogens interfere in thyroxin synthesis by inhibiting the enzymes involved in the synthesis of thyroxin.

There is also evidence to believe that intensive cropping, resulting in large scale removal of biomass from the soil, as well as widespread use of alkaline fertilizers, rapidly deplete the soil of its iodine content. Since both these factors are widely practiced in almost all developing the countries, it is not surprising that nutritional iodine deficiency and endemic goitre are seen wherever they are looked for in these regions.3 The relationship between dietary iodine intake and severity of IDD is shown in Table-II.

Health Consequences of Iodine Deficiency

Iodine deficiency remains the single greatest cause of preventable brain damage and mental retardation worldwide. Eliminating iodine deficiency is recognized as one of the most achievable of the goals that the 1990 World Summit for Children had set for the year 2000.

The most important biological role played by thyroxin is in the early foetal life, when it ensures the growth, differentiation and maturation of different organs of the body, in particular the brain. Iodine deficiency has been identified as the world’s major cause of preventable mental retardation. Its severity can vary from mild intellectual blunting to frank cretinism, a condition that includes gross mental retardation, deaf mutism, short stature, and various other defects. In areas of severe iodine deficiency, the majority of individuals are at risk some degree of mental impairment. The damage to the developing brain results in individuals who are poorly equipped to fight disease, and to learn, work effectively, or reproduce satisfactorily. The spectrum of disorders caused due to iodine deficiency affects all the stages of life – from foetus to adult age (Table I).7

Table I: Spectrum of IDD Across the Stage of Life7

Stage in Life Health Effects
Foetus Abortions
Stillbirths
Congenital Anomalies
Increased Perinatal Mortality
Increased Infant Mortality
Neurological Cretinism:
Mental deficiency
Deaf-mutism
Spastic diplegia
Squint
Myxedematous Cretinism :
Mental deficiency
Dwarfism
Psychomotor Defects
Neonate Neonatal goiter Neonatal hypothyroidism
Child and Adolescent Goiter
Juvenile hypothyroidism
Impaired mental function
Retarded physical development
Adult Goiter with complications
Hypothyroidism
Impaired mental function

If a pregnant woman’s diet does not contain adequate iodine, the foetus cannot produce enough thyroxin and foetal growth is retarded. Hypothyroid fetuses often perish in the womb and many infants die within a week of birth. The current data on the embryology of the brain suggest that the critical time for the effect of iodine deficiency is the mid second trimester i.e. 14-18 weeks of pregnancy. At this time, neurons of the cerebral cortex and basal ganglia are formed. It is also the time of formation of the cochlea (10-18 weeks) which is also severely effected in endemic cretinism. A deficit in iodine or thyroid hormones occurring during this critical period results in the slowing down of the metabolic activities of all the cells of the foetus and irreversible alterations in the development of brain. The growth and differentiation of the central nervous system are closely related to the presence of iodine and thyroid hormones. Hypothyroidism may lead to cellular hypoplasia and reduced dendritic ramification gemmules and interneuronal connections. Hypothyroid children are intellectually subnormal and may also suffer physical impairment. They lack the aptitudes of normal children of similar age, and are often incapable of completing the school. Studies have documented that, in areas with an incidence of mild to moderate IDD, IQs of school children are, on average, 10 12 points below those of the children living in areas where there is no iodine deficiency.8

i) Endemic cretinism

Endemic cretinism is the extreme clinical manifestation of severe hypothyroidism during the foetal, neonatal and childhood stages of development. The condition is characterised by severe and irreversible mental retardation, short stature, deaf-mutism, spastic diplegia and squint. In early eighties, in many seriously endemic Tarai districts of north India, an average prevalence of 1-2% of cretinism was seen. The situation has improved significantly with the supply of iodized salt and the cretins are no more born.

Cretinism seen in severe endemic areas is predominantly of two types (a) Neurological cretinism, with only the neurological manifestations of thyroxin deficiency early in life, i.e. hypothyroidism confined to the in-utero or neonatal stages. (b) Myxedematous cretinism, where besides having mental retardation, the patient has has myxoedema and dwarfism. This variant of cretinism is presumably because of the continuing hypothyroidism through all the phases of life.

ii) Cretinoids

Besides the few children with manifest cretinism, in an endemic goiter area, a large number of individuals with lesser degrees of mental retardation, speech and hearing defects, psychomotor retardation, as well as gait defects may be seen. Such individuals are known as cretinoids. In a severely endemic region, the prevalence of cretinoids may be ten-fold or more than the fully manifested cretins.9

iii) Other syndromes due to foetal iodine deficiency

There is preliminary scientific evidence suggesting that severe iodine deficiency can lead to foetal wastage such as abortion, still births, and congenital abnormalities. However, hard evidence available in this regard is limited.3

iv) Neonatal and childhood hypothyroidism

Studies have documented that more than 30% the goitrous subjects in endemic areas are functionally decompensated and hypothyroid despite the `adaptive’ enlargement of the thyroid. Screening of the cord blood of over 20,000 newborns revealed that one out of every 10 newborns from the Tarai regions of Uttar Pradesh were hypothyroid at birth.10

iv) Adult Hypothyroidism

A large number of goitrous adults in an endemic region can have varying degrees of hypothyroidism leading to a variety of clinical features and complications related to hypometabolic states. This symptomatology can seriously hamper human energy and work capacity with resultant erosion of economic productivity of the endemic regions.10

Metabolism of iodine in thyroid

Iodine enters the body in the form of iodate or iodide in the water we drink or in the food we eat; the iodate is converted to iodide in the stomach. The thyroid gland traps and concentrates iodide and uses it in the synthesis and storage of thyroid hormones (Figure 1). The minimum daily iodine uptake needed to maintain normal thyroid function in adults is about 150 g/d. Iodide (I-) is rapidly absorbed from the Gastro-intestinal tract and distributed to extracellular fluids. But the concentration of I- in the extracellular fluid is usually low because of the rapid uptake by the thyroid gland and the renal clearance. It is estimated that 75% of the Itaken into the body each day enters the thyroid by active transport. About two-thirds of that is used in hormone synthesis, with the remaining amount is being released back into the extra cellular fluid. The thyroid gland contains the body’s largest pool of iodide, about 8 to 10 mg. Most of this iodide is associated with thyroglobulin, thyroid hormone precursor and source of the hormone and the iodinated tyrosines.

The thyroid produces thyroxine (T4) and triiodothyronine (T3). Iodine is an essential component of both T3 and T4. These hormones regulate the rate of metabolism and affect the physical and mental growth and rate of function of many other systems in the body. The thyroid is controlled by the hypothalamus and pituitary iodine. (The iodine content of common food items is given in table III). The rich sources are sea fish, green vegetables and leaves like spinach grown on iodine rich soil. The common sources are milk, meat, and cereals. Common salt fortified with small quantities of sodium or potassium iodate is now compulsorily made available in the market as Iodized Salt to control IDD. Certain vegetables like cabbage, cauliflower and radish contain glucosinolates. The production of thyroxine and triiodothyronine is regulated by thyroidstimulating hormone (TSH), released by the anterior pituitary. TSH production is suppressed when the T4 levels are high, and vice versa. The TSH production itself is modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus.

Table II: Relationship between Iodine intake and IDD

Nutritional Status Daily Iodine intake (μg)
Associated with cretinism 20 or less
Associated with goiter 20 – 50
Marginal 50 – 100
Normal 100 – 300
More than normal 300 and above

About 90% of the iodine intake is obtained from the food consumed, and the remainder from the water Iodine is available in traces in water, food, and common salts. It is very low in the foods grown in high mountains and altitudes. Iodine found in sea-water is 0.2 mg per liter. Sea weeds and spongy shells are rich in (thiogluosides) which are potential goitrogens. Eating too much of these foods inhibit the availability of iodine to the body from the food and thus lead to development of goitre.

Box: Daily Reference Intake of Iodine

Life Stage DRI (mcg)
Infants
0-6 months 110
7-12 months 130
Children
1-3 years 90
4-8 years 90
Males
9-13 years 120
14-18 years 150
19-30 years 150
31-50 years 150
51-70 years 150
> 70 years 150
Females
9-13 years 120
14-18 years 150
19-30 years 150
31-50 years 150
51-70 years 150
> 70years 50
Pregnancy
< 18 years 220
19-30 years 220
31-50 years 220
Lactation
< 18 years 290
19-30 years 290
31-50 years 290

The Daily Reference Intakes (DRI) for iodine are shown in the box above.

Sources of Dietary Iodine

Food Iodine(mcg)
Salt, iodized, 1 Tea Spoon full. 400
Haddock, 75 G. 104 – 145
Bread, regular process, One slice 35
Cheese, cottage, 2% fat, 1/2 cup 26 – 71
Shrimp, 75G. 21 – 37
Egg, 1 18 – 26
Cheese, cheddar, 30g. 5 – 23
Ground beef, 75 g, cooked 8

Conclusion

Today, iodine deficiency is claimed to be the world’s single most significant preventable cause of brain damage and mental retardation.

The detrimental effect of iodine deficiency on mental and physical development of children as well as productivity of adults has been recognized. The neurological sequelae of iodine deficiency are mediated by thyroid hormone deficiency. All the basic processes of neurogenesis: cellular proliferation, differentiation, migration and selective cell death are impaired during period of brain growth spurt, if sufficient iodine is provided.

There is probably no other mineral whose deficiency can have such devastating effects on mankind, and no other disease which could be prevented so easily and so economically.

References

  1. Bernal J, Nunez J. Thyroid hormone action and brain development. Trends Endocrinol Metab 2000; 133:390-398.
  2. Assessment of Iodine Deficiency Disorders and Monitoring their Elimination. A guide for programme managers. 2nd Edition. ICCIDD/UNCF/WHO. WHO, 2001.WHO Press Geneva; pp 7-9
  3. Hetzel BS. SOS for a billion – the nature and magnitude of iodine deficiency disorders. In: SOS for a billion- the conquest of iodine deficiency disorders. 2nd Edn. Eds. Hetzel BS and Pandav CV. Oxford University Press, New Delhi 1997; pp 1-29.
  4. Stanbury JB. The iodine deficiency disorders: Introduction and general aspects. In: The prevention and control of iodine deficiency disorders. Eds. Hetzel BS, Dunn JT and Stanbury JB. Elseiver Science publishers, 1987; pp 35-48.
  5. Indicators for assessing Iodine Deficiency Disorders and their control through salt iodization. WHO-UNICEF-ICCIDD. World
  6. Health Organization, Geneva WHO Press Geneva,1994, pp 12-16.
  7. Dunn JT. Endemic goitre and cretinism. An updated on iodine status. Pediatr Endocrinol Metab 2001; 14: 1469-1473.
  8. Markou K, Georgopolous N, Kyriazopoulou V, Vagenakis GA. Iodine induced hypothyroidism. Thyroid 2001; 11: 501-507.
  9. Delange FM, Fisher DA. Thyroid hormone and iodine requirements in man during brain development. In: Iodine in pregnancy. Eds Stannbury JB, Delange F, Dunn JT and Pandav CS. Delhi. Oxford University Press, 1998; pp 1-27.
  10. WHO. Iodine. In: Trace Elements in Human Nutrition and Health. Geneva, Macmillan, 1996; pp 49-71.
  11. Kochupillai N, Godbole MM, Pandav CS, Karmarkar MG and Ahuja MMS. Neonatal thyroid status in iodine deficient environments of the Sub-Himalayan region. Indian J Med Res, 1984; 80:293-299.
Access free medical resources from Wiley-Blackwell now!

About Indmedica - Conditions of Usage - Advertise On Indmedica - Contact Us

Copyright © 2005 Indmedica