Excessive iodine intake, on thyroid

The effect of excessive iodine intake on thyroid function, the role of iodine-containing pharmaceuticals, and clinical aspects of iodine-induced thyroid dysfunction are discussed in this review. 

Effects of Excessive Iodine Intake on Thyroid Hormone and Thyroid Function... 

Various effects of excessive iodine intake on thyroid function have been described, but the exact mechanism by which iodine overload induces thyroid dysfunction remains unclear. 

Teng et al. (2006) explored the effect of iodine intake on thyroid diseases in China. Baseline characteristics of three populations were estabfished in three communities in 1999 and then again 5 years later. The communities had different levels of iodine nutrition mild deficiency more than adequate and excessive intake. Salt iodization had been implemented in China in 1996. In the general population, median UI increased from 165 pg/1 in 1995 to approximately 300 pg/1 in 1999. The concern was with oversupplementation of iodine to a level that is more than adequate, in a region in which iodine intake was previously mildly deficient, which in turn may accelerate the development of subclinical hypothyroidism to overt hypothyroidism. High levels of iodine intake may increase the incidence and prevalence of autoimmune thyroiditis, making it imperative to tailor supplementation needs to each region. 

On the other hand, excess iodine intake may also inhibit thyroid function, by either inhibition of iodide organification (Wolff-Charkoff effect) or inhibition of Tg proteolysis with reduction in hormone secretion, and may manifest itself either as a goiter, as hypothyroidism with/without goiter, or as hyperthyroidism (0.01-0.6% in populations on iodine prophylaxis), the outcome depending on the initial and current iodine status and current thyroid dysfunction (European Commission, 2002). The comparison of iodine intake and concentrations of serum Tg at various physiological or pathophysiological conditions is shown in Table 6.1. 

Previously published reports have described both sub-clinical and overt thyroid dysfunction as a result of excess iodine ingestion. Moreover, iodine-induced hypothyroidism is not rare, at least in iodine-replete areas. The possible underlying mechanisms of this impairment consist of both the inhibition of thyroid function by excess iodine and the iodine-induced enhancement of thyroid autoimmunity. On the basis that an excess iodine intake may cause hypothyroidism, several study results support iodine restriction for the treatment of hypothyroidism. The success rate of dietary iodine restriction alone, without thyroid hormone replacement, is reported to be approximately 50-80% in patients with primary hypothyroidism due to Hashimotos thyroiditis and other causes. Relatively mild hypothyroidism, high radioactive iodine uptake and uptake, increased free plasma iodine and... 

On the basis that excess iodine intake may cause hypothyroidism, several study results support iodine restriction for the treatment of hypothyroidism. Thus, when we integrate these study results, it is clear that patients with primary hypothyroidism, including those diagnosed with Hashimoto s, may benefit from dietary iodine restriction in reducing a titer of anti-thyroidal antibody and recovering normal thyroid function. 

Iodine is an essential component of thyroid hormones, and iodine deficiency can lead to severe hypothyroidism. On the other hand, excessive iodine intake also results in thyroid dysfunction in certain persons. Coindent described the first case of iodine-induced hyperthyroidism in 1821 (Fradkin and Wolff, 1983), and Hurxthal (1945) reported the first case of iodine-induced hypothyroidism. Ingestion of iodine-rich foods, such as seaweed, can cause hyperthyroidism, and the incidence of hyperthyroidism showed an increase in regions of dietary iodine deficiency after prophylactic iodization of bread or salt. Iodine-containing pharmaceuticals, such as povidone-iodine (PVP-I), radiographic contrast media and amiodarone, are a major source of excessive iodine intake (Wolff, 1969 Fradkin and Wolff, 1983 Markou et aL, 2001 Roti and degli Uberti, 2001). 

Wolfi ChaikofF effect. Raben (1949) showed that this effect was dependent on the amount of iodine in the thyroid gland and not on the plasma concentration of iodine. The acute inhibitory effect of iodine overload is usually transient. Intrathyroidal iodine decreases within a few days despite a high plasma iodine concentration and thyroid hormone synthesis then returns to the previous level. This resumption of the organification of iodine is known as the escape phenomenon (Wolff, 1969), and it means that hypothyroidism will not develop in most individuals despite excessive iodine intake. 

Amiodarone also has intrinsic effects on the thyroid and thyroid hormone production besides those related to excessive iodine intake (Table 96.4), and this means that it induces thyroid dysfunction more frequently than any other iodine-containing pharmaceutical. 

Adequate iodine intake is indispensable to the production of thyroid hormone (TH), which is essential for growth, development and cell differentiation. Iodine excess, as well as iodine deficiency, has adverse effects on health. One of the aims of the present review is to summarize the previous evidence and present the major advances in our knowledge of developmental toxic effects induced by excess iodine in animals and humans. Fetal and maternal thyroid systems interact mainly by means of the placenta. When a mother is exposed to excess iodine, alterations in maternal-fetal TH metabolism occur. Another aim of this review is to discuss the pathway of maternal-fetal TH metabolism influenced by excess iodine. Finally, the present review provides new insights into the molecular mechanism of TH action in skeletal development and highlights the potential regulation of the developmental genes, Hox genes (especially HoxcS), by TH in skeletal development. 

Although several sporadic reports on the developmental toxic effects of excess iodine have been found in the literature, systematic study is rare. Developmental toxic effects of excess iodine in animals were mainly indicated by embryo-lethal effects and skeletal variations. Embryo-lethal effects were reported in animals exposed to high doses of iodine, which reached 500-1000 times the required minimal dietary level. Skeletal variations were found in mice exposed to 10 times the adequate iodine intake. No apparent developmental toxic effects has been reported in humans exposed to excess iodine. However, excess iodine ingestion during pregnancy causes maternal thyroid dysfunction, which may result in an adverse pregnancy outcome. The potential developmental toxic effects of excess iodine in humans also need consideration. 

The excessive consumption of soybean and its products has been considered goitrogenic in humans and animals. Several researchers have reported the induction of goitre in iodine-deficient rats maintained on a soybean diet [133, 134, 135], Tn some cases, the extreme intake of soybean has been correlated with cancer. Thus, Kimura et al reported an increase of up to 40% in thyroid carcinoma in rats fed on iodine-deficient defatted soybean [136],... 

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