Lee

"Dietary iodine is taken up readily through the gut in the form of iodide. From the circulation, it is concentrated in the thyroid gland by means of an energy-dependent sodium-iodate symporter. In the follicle cells of the thyroid gland, 4 atoms of iodine are incorporated into each molecule of thyroxine (T₄) and 3 atoms into each molecule of triiodothyronine (T₃). These hormones are essential for neuronal development, sexual development, and growth and for regulating the metabolic rate, body heat, and energy.

"When dietary iodine intake is inadequate for thyroid hormone synthesis, the serum T₄ level initially falls and a number of processes ensue to restore adequate thyroid hormone production. The pituitary gland senses low levels of circulating T₄ and releases more TSH. TSH stimulates the growth and metabolic activity of thyroid follicular cells. TSH stimulates each cell to increase iodine uptake and thyroid hormone synthesis and secretion. Increased TSH levels and reduction of iodine stores within the thyroid result in increased T₃ production relative to T₄ production. T₃ is 20-100 times more biologically active than T₄ and requires fewer atoms of iodine for biosynthesis.

"These processes tend to conserve iodine stores and help maintain normal thyroid function. In addition, thyroid hormones are deiodinated in the liver, and the iodine is released back into the circulation for reuptake and reuse by the thyroid gland. Even under these circumstances, iodine is passively lost in the urine, with additional small (10%) losses from biliary secretion into the gut.  

"Therefore, enlargement of the thyroid gland begins as an adaptive process to low iodine intake. Iodine deficiency is the most common cause of goiter in the world. The goiter initially is diffuse but eventually becomes nodular. Some nodules may become autonomous and secrete thyroid hormone regardless of the TSH level. These autonomous nodules have been demonstrated to frequently contain TSH-activating mutations. Initially, thyroid hormone output by the normal thyroid surrounding the autonomous nodules is reduced to maintain euthyroidism. Autonomous nodules may cause hyperthyroidism.

"High levels of iodine, such as those found in radiographic contrast dyes or amiodarone, may cause hyperthyroidism in the setting of nodular goiter with “hot” or autonomous nodules or hypothyroidism in the setting of autoimmune thyroid disease. If the total output of thyroid hormone by the autonomous nodules exceeds that of the normal thyroid gland, the patient becomes biochemically hyperthyroid. This condition is known as a toxic multinodular goiter.

"When iodine deficiency is more severe, thyroid hormone production falls and the patient experiences a hypothyroid condition. Adults have the usual signs and symptoms of hypothyroidism..., while hypothyroidism in the fetus and in young children prevents central nervous system development and maturation, with permanent mental retardation, neurological defects, and growth abnormalities known as cretinism."