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Dunn
Iodine Deficiency and Excess an Environmental GoitrogensDunn JT in Environmental Goitrogens by E Gaitan, 1989, pp 139-148.
"Iodine differs from the other goitrogens considered in this book in that its lack, as well as its excess, impairs thyroid function and produces goiter. While the other conditions described as environmental goitrogens result from direct toxic effects of the offending agents, the most significant goitrogenic stimulus of iodine comes with its deficiency. Indeed, iodine deficiency is by far the most important goitrogenic factor in the world today....
"Iodine excess also produces goiter and hypothyroidism by direct interference with thyroid hormone synthesis. Common sources are medicines, food additives, and industrial products. The average daily intake in the US is at least ten times the minimum requirement. While most people can tolerate large doses of iodine well, those with autoimmune thyroid disease may be particularly sensitive to its antithyroid effects. Some epidemiologic evidence suggests an association between higher iodine intakes and increasing incidences of autoimmune thyroid disease and of papillary carcinoma of the thyroid."
"In addition to its role as a constituent of the thyroid hormones, iodine also appears to participate in modifying the structure of thyroglobulin by cleaving peptide bonds, an action associated with the coupling of iodotyrosines to form iodothyronines. The glycosylation of thyroglobulin may also be related to iodine utilization by the thyroid."
"Endemic Goiter. Enlargement of the thyroid is the first and mildest manifestation of iodine deficiency. Inadequate iodine supply leads to inadequate thyroid hormone formation, to which the pituitary responds by increasing secretion of thyrotropin (TSH).... TSH has a number of effects, which together increase hormone production, but it also makes the gland hyperplastic and produces thyroid enlargement, or goiter. In the early stages, the thyroid enlargement is characterized by diffuse hyperplasia, but as the process progresses, the hyperplasia becomes increasingly focal, and nodules eventually develop. At this point the gland will present a variegated appearance consisting of cysts, areas of hemorrhage, necrosis, and adenomas, some hypofunctioning and some hyperfunctioning. When the goiter is at the diffuse hyperplastic stage, correction of iodine deficiency can return it to normal size, but when it has progressed to the nodular stage, complete regression is unlikely."
"Hypothyroidism. Goiter may be regarded as an adaptation to iodine deficiency. With increased TSH the subject may be able to compensate satisfactorily and maintain euthyroidism, with the only apparent damage being the goiter itself. With more severe iodine deficiency, these compensatory mechanisms will not be fully adequate to maintain euthyroidism, and hypothyroidism develops."
"The acute effects of iodine on the thyroid have been carefully studied over many decades. In rats, excessive iodine inhibits iodination of thyroglobulin and subsequent iodothyronine synthesis (the Wolff-Chaikoff effect). However, with continued iodine administration, the thyroid escapes from this effect through an autoregulatory inhibition of thyroid iodide transport. The thyroid attempts to adapt to chronic excess of iodine by decreasing the reutilization of iodide, resulting in iodide leakage from the gland. These experimental studies are parallel to clinical observations in man."
"The minimum daily requirement of iodine is in the range of 50 to 100 mcg/d. The upper limit of safety is uncertain. Short-term studies have shown that large doses, of the order of 100 mg/d, produce mild increases in serum TSH but no other adverse effects in normal subjects. In many other studies, chronic administration of large doses of iodine produced no obvious goitrogenic effects.
"Patients with autoimmune thyroid disease (Graves' disease and Hashimoto's thyroiditis) are particularly sensitive to iodine excess. Several epidemiologic studies have suggested an increase in autoimmune thyroid disease, particularly Hashimoto's thyroiditis, with increasing dietary consumption of iodine. Increased dietary iodine has also been associated with an apparent increase in the incidence of papillary carcinoma of the thyroid.
"In summary, large doses of iodine are goitrogenic by direct toxic effects on the thyroid. Smaller chronic doses of iodine are usually safe, but may be goitrogenic in susceptible individuals, particularly those with autoimmune thyroid disease."
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