Impact of iodine intake on the pathogenesis of autoimmune thyroid disease in children and adults

Abstract

Thyroid hormone (TH) regulates the body's metabolism and iodine, a vital trace mineral, is vital for TH synthesis. As a TH biosynthesis catalyst, iodine has a substantial role in our health. When there is a modest iodine deficit, the thyroid gland grows autonomously, resulting in thyrotoxicosis. Those who consume excessive iodine risk developing hypothyroidism and thyroid autoimmunity. A transient hyperthyroid condition may rapidly increase iodine consumption. Iodine deficiency is common across the globe, and provision of supplementary iodine, in forms such as iodized salt or vegetable oil, has many benefits. Vegetarians, for instance, may not consume adequate amounts of iodine in some countries with high iodine content. Reduced dietary iodine intakes may be a consequence of efforts to reduce salt intakes to prevent hypertension. In addition, iodine consumption is decreasing in many countries, even among those where endemic goiter has previously been eradicated, leading to the re-emergence of iodine-deficiency-related disorders such as goiter. This review will discuss how iodine can contribute to the development of thyroid disease.

Keywords: Hormone synthesis; Iodine; Metabolism; Thyroid diseases.

Fig. 1.

Synthesis of thyroid hormone. DIT, diiodotyrosine; MIT, monoiodotyrosine; ER, endoplasmic reticulum.

Fig. 2.

Role of apoptosis in thyroid disease. FADD, Fas associated death domain; TNF, tumor necrosis factor; TRAIL, TNF related, apoptosis induced ligand. FADD, Fas associated death domain; TNF, tumor necrosis factor; TRAIL, TNF related, apoptosis induced ligand.