Title: Iodine Deficiency

Key words: RDAs, goiterogenic substances, thyroxine, Foetal Iodine Deficiency Disorder, goitre, selenium, cretinism, fertility, perinatal and infant mortality, supplementation, pituitary TSH, oligomenorrhoea, hypothyroidism, myxoedema

Date: July 2000

Category: Micronutrients

Type: Article

Author: Dr M Draper

 

Iodine Deficiency

The clinical consequences of iodine deficiency

Iodine deficiency and iodine deficiency disorders (IDD)The RDAs for iodine are 100 microgms/day for adults and adolescents, 60-100 microgms for children aged 1-10years and 35-40microgms for infants (1). The presence of goiterogenic substances in the diet, such as cassava (which contains thiocyanates), can increase the adult RDA to 300 microgms/day. Levels of less than 25% normal in pregnancy result in low maternal thyroxine level and can affect the brain development of the foetus (2) (Foetal Iodine Deficiency Disorder FIDD). Levels of 50% RDA can cause goitre in adults and children . Cooking can reduce the iodine content (frying 20%, grilling 23%,and boiling upto 58%).

Iodine is readily absorbed from the gut and skin and excess intake is excreted in the urine. When the physiological requirements are not met a series of functional and developmental abnormalities occur including thyroid function abnormalities ( which can be compounded by coexistent Selenium deficiency eg in Zaire (3)) and in severe deficiency, endemic goitre, and cretinism, endemic mental retardation, decreased fertility, increased perinatal and infant mortality.

Mountainous areas of preindustrialised countries ( Asia, Africa and South America) are particularly at risk of IDD and potentially one billion people could be affected. However, it is worth noting that up to 50-100 million people in Europe may also be affected.

The most important target groups from a public health point of view are pregnant mothers, foetuses, neonates and young infants because of the irreversible mental retardation. Supplementation programs started in Switzerland started in the 1920s with iodised salt and this is still favoured for instance in Central and South America , China and Finland. Iodised oil injection has been used in Papua New Guinea and oral iodized oil in China and India ( cited in (2)). The pitfalls to avoid when confronting endemic iodine deficiency are discussed by Dunn (4). The assessments of status in these areas includes goitre rate ( palpable and visible), measurement of urinary iodine excretion and blood thyroxine (T4 ) and thyroid stimulating hormone ( pituitary TSH).

Borderline deficiency states lead to TSH stimulation resulting in compensatory thyroid enlargement (goitre) despite continuing iodine deficiency (5). Most people remain euthyroid or gradually progress into mild hypothyroidism. Milder deficiencies are associated with symptoms grouped as, iodine deficiency disorders (IDD)(6), including slow growth velocity (7), arrested pubertal development and intellectual & neuromuscular impairment(8), increased foetal, perinatal and infant mortality. The developing brain is especially vulnerable to iodine deficiencies, which is the most common preventable cause of mental retardation in the world (cretinism) (9).

Young women have oligomenorrhoea, amenorrhoea, menorrhagia, hyperprolactinaemia and infertility. Other symptoms include poor memory, depression, psychosis, arthralgia, myalgia and deafness. The classical picture of severe hypothyroidism is a slow, dry-haired, thick-skinned, deep-voiced patient with weight gain, cold intolerance, bradycardia, constipation and myxoedema (mucopolysaccharide accumulation in subcutaneous tissue).

Examination reveals numerous features such as ataxia, myotonia, muscular hypertrophy, proximal myopathy, slow reacting reflexes, carpal tunnel syndrome, periorbital oedema, large tongue, hypertension, hypothermia and heart failure.

References;

(1) Delange F ' The disorders induced by iodine deficiency '

Thyroid,1994 Spr, 4:1, 107-28

(2) ' Trace elements in human nutrition and health ' WHO

ISBN 92-4-156173-4.

(3) Vanderpas JB et al. ' Selenium deficiency mitigates hypothyroxinemia in iodine deficient subjects' Am J Clin Nutr,1993 Feb, 57:2 Suppl,271S-275S.

(4) Dunn JT ' Severn deadly sins in confronting endemic iodine deficiency, and how to avoid them '. J Clin Endocrinol Metab , 1996 Apr, 81:4, 1332-5.

(5). Kumar, P. & Clark, M.. Clinical Medicine. Third Edition. W.B. Saunders Company Ltd. 1996

 

(6) Delange, F. The disorders induced by iodine deficiency. Thyroid. 1994; 4:1, 107 128.

(7) Wan Nazaimoon, W.M. et al. Effects of iodine deficiency on insulin-like growth factor-I, insulin-like growth factor-binding protein-3 levels and height attainment in malnourished children. Clin. Endocrinol. (Oxf). 1996; 45:1, 79 83.

(8) Grantham McGregor, S.M. & Fernald, L.C. Nutritional deficiencies and subsequent effects on mental and behavioral development in children. Southeast Asian J. Trop. Med. Public Health. 1997; 28 (Suppl) 2: 50S 68S.

(9) Stanbury, J.B. Iodine Deficiency and the Iodine Deficiency Disorders. In: Ziegler E. & Filer L Present knowledge in Nutrition. Seventh Edition. ILSI Press. Washington. 1996; Chapter 36 pp 378 383.