Iodine is an essential component of thyroid hormones, and its deficiency
causes endemic goiter, cretinism, and a constellation of syndromes known as iodine
deficiency disorders. Although iodine deficiency still affects most of the world,
national or regional salt iodization programs have increased the number of countries
with adequate intake. Endemic cretins were classified as either predominantly
neurological or myxedematous (hypothyroid). Severe maternal iodine deficiency
causes fetal neurological damage during the first half of gestation, which is prevented
by administering iodine to mothers before or early in pregnancy. Myxedematous
cretins present thyroid atrophy, hypothyroidism, and growth arrest, and no neurological
involvement. Physiological adaptations to iodine deficiency include thyroid growth
(goiter) and thyroidal autoregulatory mechanisms leading to decreased serum T4 and
preserved serum T3. This situation is known as hypothyroxinemia, as described in
Chapter 4. The brain, which depends on the T3 generated locally, shows an increased
type 2 deiodinase activity and T3 formation from T4. When iodine intake is severe,
these mechanisms cannot maintain T3 concentrations in the brain, leading to brain
damage.
Keywords: Cretinism, Dehalogenase, Deiodinases, Goiter, Hypothyroidism, Hypothyroxinemia, Micronutrients, Pregnancy, Selenium.
