are released through proteolysis under the stimulus of thyrotropin from the anterior pituitary.
Iodine is absorbed with high efficiency after ingestion. Most iodine containing substances are deiodinated in the gut and the resulting iodine absorbed. It is captured by the thyroid from the blood at a rate dependent on the history of supply. Most appear in the urine in inorganic form in amounts that largely reflect recent rates of ingestion. The daily excretion is the amount absorbed and that derived from hormone degradation, but not taken up by the thyroid. Under normal circumstances, the thyroid takes about 20 percent of the available iodine.
There are limits: too little iodine over too long a time leads to serious consequences, as described below. When too much is ingested, the thyroid may shut down; under certain circumstances, it becomes overactive.
The anatomical response to chronic iodine deficiency is enlargement of the thyroid gland. Initially there is hypertrophy of the thyroid epithelial cells. With fluctuating iodine supply, involuntary changes occur; the epithelial cells flatten, follicles fuse to form nodules, degenerative changes occur, cysts form, and calcifications are seen. The changes may be highly irregular from one site to another within the gland. Iodine-deficiency goiter may appear in preadolescence and nodules may form when the deficiency is severe, but there is usually a modest enlargement in the young that progresses over the years to multinodular goiter (Kopp et al., 1994; Parma et al., 1994; Taylor, 1953). It is customarily more evident in the female; regression usually occurs in the postadolescent male. When deficiency is severe, goiter rates may approach 100 percent, even in the young.
Goiter is usually harmless, if unattractive. Nevertheless, nodules may cause tracheal obstruction or impair the function of the laryngeal nerves. When surgery is required or elected, the risks of surgery in the local setting must be considered, and these may not be negligible. Malignant degeneration is a much debated issue; there is probably a slightly increased risk in endemic goiter (Riccabona, 1972).
Neuromotor and cognitive impairments are the most important consequences of iodine deficiency. The endemic cretin is the classic example.