Posted on 22nd Dec 2019 @ 9:32 AM

Iodine is an element that is needed for the production of thyroid hormone. The body does not make iodine, so it is an essential part of your diet. Iodine is found in various foods (see Table 1). If you do not have enough iodine in your body, you cannot make enough thyroid hormone. Thus, iodine deficiency can lead to enlargement of the thyroid (goiter – see Goiter brochure), hypothyroidism (see Hypothyroidism brochure) and to intellectual disabilities in infants and children whose mothers were iodine deficient during pregnancy.

Before the 1920s, iodine deficiency was common in the Great Lakes, Appalachian, and Northwestern U.S. regions and in most of Canada. Prevention of iodine deficiency by the introduction of iodized salt has virtually eliminated iodine deficiency and the so-called “goiter belt” in these areas. However, many other parts of the world do not have enough iodine available through their diet and iodine deficiency continues to be an important public health problem globally. Approximately 30% of the world’s population remains at risk for iodine deficiency.

Iodine is a requisite substrate for the synthesis of the thyroid hormones, the minimum daily requirement being about 50 micrograms. An autoregulatory mechanism within the thyroid serves as the first line of defense against fluctuations in the supply of iodine and also permits escape from the inhibition of hormone synthesis that a very large quantity of iodine induces (Wolff-Chaikoff effect and escape therefrom). Environmental iodine deficiency continues to be a significant public health problem worldwide, compounded in some geographic regions by the presence of other goitrogens in some staple foods. The pathologic consequences of severe iodine deficiency include endemic goiter, endemic cretinism, increased fetal and infant mortality, and an increased prevalence in the community of cognitive and neuromotor disabilities.

The implementation of an iodization program prevents endemic cretinism and reduces the frequency of the other pathologic consequences of iodine deficiency. Iodine excess results principally from the use of iodine-containing medicinal preparations or radiographic contrast media. The pathologic consequences of iodine excess will ensue only when thyroid autoregulation is defective, in that escape from the Wolff-Chaikoff effect cannot occur, or when autoregulation is absent. Defective autoregulation characterizes the fetal and neonatal thyroid, Hashimoto's thyroiditis, radioiodine or surgically treated Graves' hyperthyroidism, the thyroid of patients with cystic fibrosis, and the thyroid that has been exposed to weak inhibitors of the organic binding of iodine.

In these circumstances, the provision of excess iodine may lead to iodide goiter with or without hypothyroidism. Absent autoregulation may be a feature of longstanding multinodular goiter, and the provision of excess iodine in this circumstance may induce thyrotoxicosis (Jod-Basedow disease). The pathologic consequences of iodine excess will resolve when the source of iodine has been dissipated. In addition to its role in reversing iodine deficiency, iodine is used as adjunctive therapy for hyperthyroidism. By inhibiting the proteolytic release of iodothyronines from thyroglobulin, it induces a prompt slowing of thyroid hormone secretion. This effect is exploited in the treatment of thyrotoxic crisis or severe thyrocardiac disease. Iodine also reduces thyroid cellularity and vascularity and therefore is used in the preparation of the patient for thyroidectomy. Finally, by exploiting the failure of escape from the Wolff-Chaikoff effect, iodine may also be used in the early management of radioiodine-treated Graves' hyperthyroidism.