In presenting a review of current concepts of thyroid physiology, we have examined iodide metabolism, hormonogenesis, hormone secretion and peripheral metabolism, and finally homeostatic regulation. Iodide (I) is actively taken up by thyroid cells. As an essential constituent of thyroid homeostatically maintained at about 80 μg/day by the regulatory action of TSH on the trapping process. In large doses, I temporarily inhibits binding of I to tyrosine and the release of thyroid hormone by the gland. Trapped I is oxidized by peroxidase to a free radical, which then combines covalently with a tyrosyl free radical in preformed thyroglobulin to form MIT. Iodotyrosine residues within thyroglobulin combine to from T 4 or T 3 , which is stored in the follicular lumen. Secretion of thyroid hormone into the bloodstream involves the endocytosis of colloid material by the thyroid cell, fusion with lysosomes containing proteolytic enzymes, and subsequent proteolysis of thyroglobulin. TSH stimulates secretion by a process involving the activation of adenyl cyclase, so raising the intracellular content of cyclic AMP. The cyclic AMP may in turn activate a mechanism involving cyclic-nucleotide-dependent-protein kinase, contractile proteins, and Ca ++ . Thyroid hormone circulates in blood mostly bound to specific circulating proteins; only 0.05% is free. The free hormone level is homeostatically maintained at a constant level, and is in equilibrium with an intracellular pool of thyroid hormone. The peripheral action of thyroxine may involve its conversion in the tissues to T 3 , or its binding to specific receptor proteins within the cell. Pituitary secretion of TSH is subject to a negative feedback by circulating free thyroid hormone, and the sensitivity of the feedback system is modulated by TRF released by the hypothalamus.