Puig-Domingo Manel, Vila Lluis
Servei de Endocrinologia i Nutricio, Hospital Germans Trias i Pujol, Dpt de Medicina, Universitat Autonoma de Medicina, Barcelona, Spain.
Curr Clin Pharmacol. 2013 May;8(2):97-109. doi: 10.2174/1574884711308020002.
Iodine is an essential trace element for life. Its biological effects are a consequence of its incorporation to the thyroid hormones, which play a crucial role in fetal organogenesis, and in particular in brain development. This takes place during early gestation and involves delicate targeting throughout the central nervous system, including adequate neuronal growth, migration and myelinization at different sites, such as the cerebral cortex and neocortex, visual and auditory cortex, hippocampus and cerebellum. Pregnancy is characterized by an increased demand of thyroid hormones by the feto-placental unit in order to fulfill the necessary requirements of thyroid hormone action for normal fetal development. Up until week 20, the fetal thyroid is not fully active and therefore is completely dependent on the maternal thyroxine supply. Thus, the maternal thyroid has to adapt to this situation by producing about 1.5 fold more thyroxine. This requires that enzymatic gland machinery works normally as well as an adequate iodine intake, the principal substrate for thyroid hormone synthesis. Biological consequences of iodine related maternal hypothyroxinemia are currently very well known, by both experimental models and by clinical and epidemiological evidences. The associated disturbances parallel the degree of maternal thyroxine deficiency, ranging from increased neonatal morbi-mortality and severe mental dysfunction, to hyperactivity, attention disorders and a substantial decrease of IQ of an irreversible nature in the progeny of mothers suffering a deprivation of iodine during pregnancy. As a consequence, iodine deficiency is the leading preventable cause of mental impaired function in the world, affecting as many as 2 billion people (35.2% of the entire population). Prevention of fetal iodine deficiency - a problem of pandemic proportions- is feasible, provided that an iodine supply of 200-300 μg/day to the mother is ensured, before and throughout gestation as well as during the lactating period.
碘是生命必需的微量元素。其生物学效应是由于它参与合成甲状腺激素，而甲状腺激素在胎儿器官形成，尤其是大脑发育过程中起着至关重要的作用。这一过程发生在妊娠早期，涉及整个中枢神经系统的精细靶向作用，包括不同部位如大脑皮层和新皮层、视觉和听觉皮层、海马体和小脑的神经元充分生长、迁移和髓鞘形成。妊娠的特点是胎儿 - 胎盘单位对甲状腺激素的需求增加，以满足正常胎儿发育对甲状腺激素作用的必要需求。直到妊娠20周，胎儿甲状腺尚未完全活跃，因此完全依赖母体甲状腺素供应。因此，母体甲状腺必须通过产生约1.5倍的甲状腺素来适应这种情况。这需要甲状腺腺体制备机制正常运作以及充足的碘摄入，碘是甲状腺激素合成的主要底物。目前，无论是通过实验模型还是临床及流行病学证据，碘相关的母体甲状腺功能减退血症的生物学后果都已广为人知。相关干扰与母体甲状腺素缺乏程度平行，范围从新生儿发病率和死亡率增加以及严重的精神功能障碍，到母亲在孕期缺碘的后代出现多动、注意力障碍以及智商大幅下降且不可逆转。因此，碘缺乏是世界上可预防的导致智力功能受损的主要原因，影响多达20亿人（占全球总人口的35.2%）。只要在妊娠前、妊娠期间及哺乳期确保母亲每天摄入200 - 300μg碘，预防胎儿碘缺乏这一全球性问题是可行的。
