Department of Human Nutrition, University of Otago, Dunedin 9054, New Zealand.
Nutrients. 2011 Feb;3(2):265-73. doi: 10.3390/nu3020265. Epub 2011 Feb 18.
Iodine is an integral part of the thyroid hormones, thyroxine (T(4)) and tri-iodothyronine (T(3)), necessary for normal growth and development. An adequate supply of cerebral T(3), generated in the fetal brain from maternal free T(4) (fT(4)), 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 fT(4)) 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, characterised 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 randomised 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.
碘是甲状腺激素，即甲状腺素（T(4)）和三碘甲状腺原氨酸（T(3)）的组成部分，对正常生长和发育是必需的。胎儿的甲状腺激素依赖型神经发育需要足够的脑 T(3)，而脑 T(3)是由母体游离 T(4)（fT(4)）在胎儿大脑中生成的。这种神经发育始于妊娠第一 trimester 的后半期。大约在第二 trimester 开始时，胎儿的甲状腺也开始产生激素，但胎儿甲状腺的储备量很低，因此母体甲状腺激素对胎儿总甲状腺激素浓度的贡献持续到出生。为了使孕妇产生足够的甲状腺激素来满足她自己和她的宝宝的需求，建议增加 50%的碘摄入量。饮食中缺乏碘可能导致母亲和随后的胎儿碘缺乏。在碘缺乏的情况下，甲状腺素血症（即母体 fT(4)低）会导致发育中的大脑受损，而胎儿的甲状腺功能减退会进一步加重这种损伤。碘缺乏最严重的后果是呆小病，其特征是严重的智力迟钝。有明确的证据表明，妊娠期间严重的碘缺乏会损害儿童的大脑发育。然而，只有两项干预试验评估了中度碘缺乏母亲的儿童的神经发育，发现母亲在妊娠早期而不是晚期补充时，儿童的神经发育得到改善；这两项研究都不是随机的，也没有对照。因此，需要进行精心设计的试验来确定在中度至轻度碘缺乏的孕妇中补充碘对儿童神经发育的影响。
