Selenium nutritional status and thyroid dysfunction

Selenium (Se) is an essential micronutrient for several immune and regulatory functions in the body. In thyroid tissue, Se contributes to the antioxidant system and is a crucial component of deiodinases, which are selenoproteins that participate in thyroid hormone metabolism. Additionally, this micronutrient exerts a significant impact on thyroid pathophysiology, as low levels of Se lead to reduced activity of glutathione peroxidase, a selenoprotein involved in antioxidative processes, thereby resulting in increased oxidative stress and damage to thyroid tissue. Selenium deficiency (SeD) can cause growth retardation and reproductive failure; in women and children, it may result in Keshan's disease and Kashin-Beck's disease. Research has shown an inverse correlation between Se serum levels and autoimmune thyroiditis in areas with mild SeD. In Graves' disease, Se supplementation has been linked to faster achievement of euthyroidism as well as improvements in quality of life, lessened orbital involvement, and slower ocular progression of the disease. Furthermore, several studies suggest an association between serum SeD and the development of thyroid cancer. Maintaining physiological Se concentrations appears to be related to the prevention of thyroid disease, although current data are insufficient to conclusively support or refute the efficacy of supplementation. Through this narrative review, we aim to present the latest information on the role of selenium in thyroid pathophysiology. To identify relevant literature, specific search strategies were employed in the electronic databases PubMed, Lilacs, and SciELO.