Humans maternal thyroid hormones

Although for years it has been published that the human fetus develops in the absence of thyroid hormones, there is increasing evidence of the active transfer of maternal thyroid hormones from the mother to the human fetus. 

Adverse reproductive effects have been observed in animals fed PCB in the diet. Fetal resorptions were common, and dose-related incidences of terata were found in pups and piglets when females were fed Arochlor 1254 at Img/kg/day or more. Long-term low-level maternal exposure of rats before breeding and throughout gestation and lactation caused permanent hearing deficits, decreased serum thyroid hormones, and reproductive effects. PCBs have been observed in human cord blood and in tissues of newborn humans and animals. ... 

Iodine and thyroid hormones affect all stages of human development, from in utero life to adulthood. Iodine deficiency leads to insufficient production of thyroid hormones, which play a vital role in the process of early growth and development of many organs. During pregnancy, both maternal and fetal thyroid hormones are required for normal fetal brain development. Of them, maternal hormones constitute the main source in the first and the second trimesters, whereas the contribution of fetal hormones becomes more important in the third trimester (de Escobar et aL, 1985 Vulsma et ai, 1989). Many studies indicate that iodine deficiency and iodine-induced maternal-fetal hypothyroxinemia result in impairment of central nervous system (CNS) development during fetal and early postnatal life. 

The importance of the transfer of thyroid hormones from the mother to the fetus during the second half of pregnancy in humans has received increasing attention (Burrow et ai, 1994). Recently, it has become evident that maternal hypothyroxinemia results not only in the birth of children with neurological cretinism, but also in decreased mental and psychomotor development of the rest of the population without cretinism (Beichrodt and Born, 1994). 

Adequate iodine intake is indispensable to the production of thyroid hormone (TH), which is essential for growth, development and cell differentiation. Iodine excess, as well as iodine deficiency, has adverse effects on health. One of the aims of the present review is to summarize the previous evidence and present the major advances in our knowledge of developmental toxic effects induced by excess iodine in animals and humans. Fetal and maternal thyroid systems interact mainly by means of the placenta. When a mother is exposed to excess iodine, alterations in maternal-fetal TH metabolism occur. Another aim of this review is to discuss the pathway of maternal-fetal TH metabolism influenced by excess iodine. Finally, the present review provides new insights into the molecular mechanism of TH action in skeletal development and highlights the potential regulation of the developmental genes, Hox genes (especially HoxcS), by TH in skeletal development. 

Thyroid hormones, T3 and T4, have been i cwn to play significant but poorly understood roles in development and differentiation of rodent and human brain (1-7). In the human, disorders of maternal and fetal thyroid function include maternal and secondary fetal iodine deficiency, maternal hypothyroidism or hyperthyroidism, as well eis disorders related to deficient fetal autcxiomous thyroid hormcaie secretion, i.e., goiter or i radic oongenitel hypothyroidism. These disorders are identifiable causes of mental retardation (4, 8, 9, 10), cer ral peilsy (11, 12), and other significant neurological abnormalities (5, 6, 11) ... 

The data suggesting the direct role of elemental iodine on brain development is the observation that correction of iodine deficiency in mothers prevents the emergence of neurological cretinism only if correction takes place before or during early gestation, thus before the onset of fetal thyroid function (83). What we would like to know in greater detail is which parameter is corrected in the human fetus when maternal iodine deficiency is corrected before the onset of fetal thyroid function Is it the fetal deficiency in iodine, in thyroid hormones or in both ... 

Motil KJ, Thotathuchery M, Montandon CM, Hachey DL, Boutton TW, Klein PD, Garza C. Insulin, cortisol and thyroid hormones modulate maternal protein status and milk production and composition in humans. J Nutr 1994 124 1248-1257. 

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