Consequences of excess iodine

Abstract

Iodine is a micronutrient that is essential for the production of thyroid hormones. The primary source of iodine is the diet via consumption of foods that have been fortified with iodine, including salt, dairy products and bread, or that are naturally abundant in the micronutrient, such as seafood. Recommended daily iodine intake is 150 µg in adults who are not pregnant or lactating. Ingestion of iodine or exposure above this threshold is generally well-tolerated. However, in certain susceptible individuals, including those with pre-existing thyroid disease, the elderly, fetuses and neonates, or patients with other risk factors, the risk of developing iodine-induced thyroid dysfunction might be increased. Hypothyroidism or hyperthyroidism as a result of supraphysiologic iodine exposure might be either subclinical or overt, and the source of the excess iodine might not be readily apparent.

Figure 1

The Wolff–Chaikoff effect. a | The proposed mechanism for the acute Wolff–Chaikoff effect. During initial iodine exposure, excess iodine is transported into the thyroid gland by the sodium–iodide symporter. This transport results in transient inhibition of TPO and a decrease in the synthesis of thyroid hormone. b | The mechanism by which adaptation to the acute Wolff–Chaikoff effect occurs. A decrease in the expression of the sodium–iodide symporter results in reduced iodine transport, which enables the synthesis of thyroid hormone to resume. Abbreviations: DIT, diiodotyrosine; I⁻, iodide; MIT, monoiodotyrosine; TPO, thyroid peroxidase. Permission obtained from Massachusetts Medical Society © Pramyothin, P. et al. N. Engl. J. Med. 365, 2123–2127 (2011).