Selenium and the thyroid — can selenium deficiency damage the thyroid?

Aim of the study: Apart from the essential trace element iodine, which is the central constituent of thyroid hormones, a second essential trace element, selenium, is required for appropriate thyroid hormone synthesis, activation and metabolism. The human thyroid gland has the highest selenium content per gram of tissue among all organs.

Results: Combined iodide and selenium deficiency such as in central Zaire is thought to cause the myxedematous form of endemic cretinism. Inadequate selenium supply and prediagnostically low serum selenium levels are significantly correlated with the development of thyroid carcinoma and other tumors. Though selenium supply controls expression and translation of selenocysteine-containing proteins no direct correlation is found between selenium tissue content and expression of various thyroidal selenoproteins, indicating that other regulatory factors contribute to or override selenium-dependent expression control, e.g., in thyroid adenoma, carcinoma or autoimmune disease. As both trace elements, iodine and selenium, were washed out from the upper layers of the soil during and after the ice ages in many regions of the world adequate supply with these essential compounds needs to be provided either by a balanced diet or supplementation.

Aim of the study: 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.

Results: 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.

Aim of the study: Inadequate supply of the essential trace element selenium (Se) has been associated with predisposition for, or manifestation of, various human diseases such as Keshan and Kashin-Beck disease, cancer, impaired immune function, neurodegenerative and age-related disorders and disturbances of the thyroid hormone axis. Se deficiency in combination with inadequate iodine contributes to the pathogenesis of myxedematous cretinism.

Results: The thyroid gland is among the human tissues with the highest Se content per mass unit similar to other endocrine organs and the brain. Selenoproteins involved in cellular antioxidative defence systems and redox control, such as the glutathione peroxidase (GPx) and the thioredoxin reductase (TxnRd) family, are involved in protection of the thyroid gland from excess hydrogen peroxide and reactive oxygen species produced by the follicles for biosynthesis of thyroid hormones. In addition, the three key enzymes involved in activation and inactivation of thyroid hormones, the iodothyronine deiodinases (DIO1,2,3), are selenoproteins with development, cell- and pathology-related expression patterns.

Aim of the study: Much research into the functions of selenium in the cell has concentrated on its role in selenium-containing glutathione peroxidases. However, selenium was recently shown to be an essential component of type I iodothyronine 5'-deiodinase in rats, which converts thyroxin to the more biologically active hormone 3,5,3'-triiodothyronine.

Results: Much research into the functions of selenium in the cell has concentrated on its role in selenium-containing glutathione peroxidases. However, selenium was recently shown to be an essential component of type I iodothyronine 5'-deiodinase in rats, which converts thyroxin to the more biologically active hormone 3,5,3'-triiodothyronine. Thus, selenium-deficient rats have low tissue deiodinase activities and abnormal thyroid hormone metabolism. The discovery of this function for selenium in thyroid hormone metabolism has important implications for the interpretation of the effects of selenium deficiency, especially in individuals with an adequate vitamin E status.

Aim of the study: The adequate availability and metabolism of three essential trace elements, iodine, selenium and iron, provide the basic requirements for the function and action of the thyroid hormone system in humans, vertebrate animals and their evolutionary precursors.

Results: The latter is generated by the dual oxidase system organized as 'thyroxisome' at the surface of the apical membrane facing the colloidal lumen of the thyroid follicles. Various selenoproteins expressed in thyrocytes defend the follicular structure and function against life-long exposure to H2O2 and reactive oxygen species derived therefrom. The pituitary hormone thyrotropin (TSH) stimulates all processes required for thyroid hormone synthesis and secretion and regulates thyrocyte growth, differentiation and function. Worldwide deficiencies of nutritional iodine, selenium and iron supply and the resulting endemic diseases are preventable with educational, societal and political measures.

Aim of the study: The trace element selenium is an essential micronutrient that is required for the biosynthesis of selenocysteine-containing selenoproteins. Most of the known selenoproteins are expressed in the thyroid gland, including some with still unknown functions.

Results: However, low selenium status correlates with risk of goiter and multiple nodules in European women. Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined. The baseline selenium status of an individual could constitute the most important parameter modifying the outcome of selenium supplementation, which might primarily disrupt self-amplifying cycles of the endocrine-immune system interface rectifying the interaction of lymphocytes with thyroid autoantigens. Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interaction.

Aim of the study: Several hypotheses concerning consequences of selenium deficiency on iodine metabolism can be proposed on the basis of experimental studies in rats and from epidemiological and experimental studies in humans. By decreasing intracellular GSH peroxidase activity, selenium deficiency may increase hydrogen peroxide (H2O2) supply and lead over several weeks to the thyroid atrophy observed in myxoedematous cretins.

Results: Several hypotheses concerning consequences of selenium deficiency on iodine metabolism can be proposed on the basis of experimental studies in rats and from epidemiological and experimental studies in humans. By decreasing intracellular GSH peroxidase activity, selenium deficiency may increase hydrogen peroxide (H2O2) supply and lead over several weeks to the thyroid atrophy observed in myxoedematous cretins. By improving thyroid hormone synthesis and by decreasing peripheral thyroxin (T4) deiodination, selenium deficiency could protect fetal brain T4 supply and thus prevent neurologic cretinism. Selenium deficiency may protect against iodine deficiency by decreasing T4 metabolism--and thus iodide leakage and--perhaps also by increasing H2O2 supply and thyroid hormone synthesis and thus thyroid efficiency.

Aim of the study: The incidence of papillary thyroid carcinoma (PTC) is constantly increasing in the global population, with no systematic screening. The current challenge is to define relevant risk factors contributing to this increase and to facilitate an early diagnosis.

Results: All plasma biomarkers showed significant positive correlations, supporting sample integrity, analytical quality and insufficient Se status. A predictive model was deduced, indicating a significant association between low plasma Se and PTC (OR=5.02, 95%; CI:1.51-16.73; P = 0.009). The results support the hypothesis that Se status is affected by thyroid cancer, that thyroid cancer risk increases in case of Se deficiency, or that the interrelationship is interconnected. As Se deficiency is an addressable health risk, longitudinal studies are required to elucidate the direction of interaction and for testing protective measures.