الفهرس 
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Abstract
Iodine is an integral part of the thyroid hormones, thyroxine (T4) and triiodothyronine
(T3), necessary for normal growth and development. An adequate
supply of cerebral T3, generated in the fetal brain from maternal free T4 (fT4), is
needed by the fetus for thyroid hormone dependent neurodevelopment, which begins
in the second half of the first trimester of pregnancy. Around the beginning of the
second trimester the fetal thyroid also begins to produce hormones but the reserves of
the fetal gland are low, thus maternal thyroid hormones contribute to total fetal
thyroid hormone concentrations until birth. In order for pregnant women to produce
enough thyroid hormones to meet both her own and her baby’s requirements, a 50%
increase in iodine intake is recommended. A lack of iodine in the diet may result in
the mother becoming iodine deficient, and subsequently the fetus. In iodine
deficiency, hypothyroxinemia (i.e., low maternal fT4) results in damage to the
developing brain, which is further aggravated by hypothyroidism in the fetus. The
most serious consequence of iodine deficiency is cretinism, characterized by profound
mental retardation. There is unequivocal evidence that severe iodine deficiency in
pregnancy impairs brain development in the child. However, only two intervention
trials have assessed neurodevelopment in children of moderately iodine deficient
mothers finding improved neurodevelopment in children of mothers supplemented
earlier rather than later in pregnancy; both studies were not randomized and were
uncontrolled. Thus, there is a need for well-designed trials to determine the effect of
iodine supplementation in moderate to mildly iodine deficient pregnant women on
neurodevelopment in the child.