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The implications of iodine and its supplementation during pregnancy in fetal brain development

机译:怀孕期间碘及其补充对胎儿脑发育的影响

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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.
机译:碘是生命必不可少的微量元素。它的生物学效应是其掺入甲状腺激素的结果,甲状腺激素在胎儿器官发生,特别是大脑发育中起关键作用。这发生在妊娠早期,涉及整个中枢神经系统的精细靶向,包括在不同部位的适当神经元生长,迁移和髓鞘化,例如大脑皮层和新皮层,视觉和听觉皮层,海马和小脑。怀孕的特征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要求。直到第20周,胎儿甲状腺仍未完全活跃,因此完全取决于母体甲状腺素的供应。因此,孕妇甲状腺必须通过产生约1.5倍以上的甲状腺素来适应这种情况。这就要求酶促腺体机能正常工作,同时要有足够的碘摄入量,而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通过临床和流行病学证据,与碘有关的母亲低甲状腺素血症的生物学后果都是众所周知的。相关的疾病与母亲甲状腺素缺乏症的程度平行,从新生儿死亡率上升和严重的精神障碍到活动过度,注意力障碍和母亲在怀孕期间缺乏碘的后代中不可逆性的智商大大降低。 。结果,碘缺乏症是世界上导致精神障碍的主要可预防因素,影响了多达20亿人(占总人口的35.2%)。预防胎儿碘缺乏症(大流行比例问题)是可行的,只要确保在妊娠之前,整个妊娠期间以及哺乳期间向母亲提供200-300μg/天的碘。

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