Selenium and Hypothyroidism
Hashimoto’s thyroiditis is the most common cause of hypothyroidism. Hypothyroidism is an under-active thyroid whereby the thyroid gland secretes below the normal level of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). Hashimoto’s is caused by an autoimmune response whereby the lymphocytes of the immune system differentiate into plasma cells and secrete antibodies which attack the thyroid causing a gradual swelling and inflammation. It is unclear as to what initiates the autoimmune response, it could be due to a genetic pre-disposition, exposure to radiation or an infection by a pathogenic species. Another factor that is thought to lead to the onset of the autoimmune response is a reduction in Selenium, Se, levels. It is thought that the absence of Selenium leads to a abnormally high level of antibodies within the lymphatic and blood system. Selenium is used as a cofactor for the enzymes involved in thyroid hormone synthesis and secretion. One of the enzymes involved is known as glutathione peroxidase, this enzyme protects the epithelial/follicle cells of the thyroid from potential damage caused by hydrogen peroxide which is key to oxidising iodide ions during the organification of iodide. If Selenium isn’t present the epithelial cells become damaged, these are rendered as foreign/harmful activating the specific immune response.
The activation of the immune system leads to increased levels of anti-thyroid peroxidase (anti-TPO) antibodies; these bind to the enzyme/autoantigen (polypeptide complex) known as thyroid peroxidase. Thyroid peroxidase catalyzes the organification of iodine and the formation of T3 and T4 thyroid hormones via coupling. During binding of anti-TPOs the enzyme undergoes an conformational change meaning thyroid peroxidase cannot catalyze the two main reactions to produce the thyroid hormones consequently leading to the initiation of hypothyroidism.