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The state of mild to severe iodine deficiency persisting in many European countries
has important public health consequences, including on the intellectual development
of infants and children. As an example, Table 5 summarizes the situation in Belgium
where the consequences of mild iodine deficiency on the main target groups, i.e.
pregnant and nursing women, neonates and young infants, have been extensively
investigated. More generally speaking, the consequences of iodine deficiency in Europe can be summarized as follows: In adults: the frequency of simple goiter is elevated in many countries and the cost of therapy of thyroid problems resulting from iodine deficiency in the adult population is enormous. For example, the cost for the diagnosis and treatment of goiter due to iodine deficiency in Germany for the year 1986 was estimated at 900 million DM (approximately 500 million $, or 8 $ per inhabitant per year)28 while prevention by iodized salt would cost only 2–8 US cents per inhabitant and per year29. Thyroidal uptake of radioiodine varies markedly from one European country to another and is inversely related to the iodine intake30. Elevated thyroidal uptake due to iodine deficiency aggravates the risk of thyroid irradiation and development of thyroid cancer in case of a nuclear accident31. The best prophylaxis of nuclear hazards in case of radioiodine fallout is to increase the basal intake of iodine of the population32. Thyroid function is usually normal in young adults in European countries with borderline or low iodine supply. By contrast, it is frequently altered during pregnancy, when three synergistic mechanisms stimulate the thyroid gland: a) direct stimulation by the human chorionic gonadotropin, b) stimulation by TSH which rises because the higher thyroxine-binding globulin concentration lowers the free thyroxine, and finally, c) the overall enhancing role of limited iodine availability33. At least under conditions of borderline iodine intake, pregnancy is accompanied by a progressive decrease of serum free T4 and consequently by an increase of serum TSH. This state of chronic TSH hyperstimulation results in the development of goiter in about 10 % of the pregnant women and in a progressive increase in the serum concentration of thyroglobulin. Goiter can persist after pregnancy in an important number of women34. Pregnancy, especially in conditions of borderline iodine intake, at least partly explains the higher frequency of thyroid problems in women than in men. The consequences of marginal iodine deficiency during pregnancy in Belgium on the thyroid function of the neonate include even more elevated serum levels of TSH and thyroglobulin in cord blood than in the mothers and a slight enlargement of the thyroid gland33. The role played by iodine deficiency in these changes is demonstrated by the fact that they are prevented by iodine supplementation of the mothers during pregnancy35 and that they do not occur in iodine replete areas in Europe such as The Netherlands36. Another consequence of longstanding iodine deficiency in the adult is the development of hyperthyroidism, especially in the elderly with multinodular goiters and autonomous nodules15,37-39. The mechanism involved is, as for iodine-induced hyperthyroidism, acceleration of thyrocytes proliferation which, in turn, triggers the development of cell clones harbouring activation mutations of the TSH receptors. It thus appears that both spontaneous and iodine-induced hyperthyroidism constitute additional aspects of the disorders induced by iodine deficiency. In adolescents and children: Euthyroid pubertal goiter is especially frequent in adolescents and occasionally requires substitutive therapy by T4 or iodide. Iodine metabolism is accelerated during this period of life40. A very important issue is that clinically euthyroid schoolchildren born and raised in moderately iodine deficient regions of Europe exhibit subtle or even overt neuropsychointellectual deficits when compared to iodine-sufficient controls living in otherwise identical ethnic, demographic, nutritional and socio-economic populations. These deficits are of the same nature, although less marked, than those found in schoolchildren in areas with severe iodine deficiency and endemic mental retardation41. As demonstrated in severe iodine deficiency, these deficits most probably result from transient thyroid failure occurring during foetal or early postnatal life, i.e. during the critical period of brain development. In neonates: The most important and frequent alterations of thyroid function due to iodine deficiency in Europe occur in neonates and young infants: 1) The frequency of transient primary hypothyroidism is almost 8 times higher in Europe than in North America42. This syndrome is characterized by postnatally acquired severe primary hypothyroidism lasting for a few weeks and requiring substitutive therapy43. The risk of transient hypothyroidism in the neonates increases with the degree of prematurity44. The specific role played by iodine deficiency in the etiology of this type of hypothyroidism is demonstrated by the disappearance of neonatal transient thyroid failure in Belgian preterms since they were systematically supplemented with 30 µg potassium iodide/day. 2) There is an inverse relationship between the urinary iodine concentrations in newborn populations in Europe and the frequency of serum TSH above 50 µU/ml at day 5, at the time of screening for congenital hypothyroidism45, when it constitutes the criterion for recalling the babies under suspicion of congenital hypothyroidism. Consequently, the recall rate of neonatal thyroid screening appears as a particularly sensitive index of the presence of goitrogenic stimuli in the environment and neonatal thyroid screening can be used for monitoring iodine prophylaxis at a population level46. The reason for the particular sensitivity of newborns to the effects of iodine deficiency is their low iodine content of the thyroid with an extremely fast turnover rate of intrathyroidal iodine. By contrast, in adults, iodine deficiency, unless severe, does not affect the iodine stores of the thyroid45. Therefore, thyroid failure is more likely to occur in neonates than in adults in conditions of iodine deficiency.
Table 5. Functional consequences of mild iodine deficiency in Belgium
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