Fetus 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. 

Altogether, these findings indicate not only that a transfer of maternal thyroid hormone, namely of T4, to the fetus is effective from early pregnancy, but also that the systems regulating the availability of T3 to the fetal brain are expressed and likely operating by that time. 

During pregnancy and breast-feeding, both fetus and neonate are dependent on maternal thyroid hormones, of which iodine is an essential component. Thyroid hormones regulate key biochemical reactions, are essential for... 

More information is needed on teratogenicity of PCDEs as well as the role of thyrotoxicity in the developmental toxicity of PCDEs [104], Teratogenicity caused by nitro-PCDEs has been suggested to involve alterations in thyroid hormone status [87] and transient alterations in maternal thyroid status might affect development of the fetus [143], Effects of PCDEs after prenatal exposure have been similar to those of PCBs [104]. 

Endemic cretinism has been a common finding in the mountains or isolated regions, such as the Alps or the Himalayas and has been described or depicted in drawings over the centuries. McCarrison (1917) studied this condition in the Himalayas, describing two types of cretinism the nervous and myxedematous types. He already suspected the influence of the maternal thyroid function on the fetus. Early observations in the Alps (Hunziker-Shild, 1915) already reported that the fetus could receive the hormone from the mother, and proposed the prophylactic administration of iodine from conception. 

After the initiation of fetal thyroxine synthesis, transfer of thyroid hormones from the mother to the fetus does not stop, but continues until birth. During that period, 20—50% of cord serum thyroxine is composed from maternal supply (de Escobar et aL, 1990 Vulsma et ai, 1989). Several clinical syndromes attributable to iodine deficiency vary according to the timing and the severity of the deficiency. It has been shown that neurodevelopmental disorders in... 

Iodine deficiency at any degree of severity causes maternal and fetal hypothyroxinemia. As thyroid hormones of the mother and the fetus must be kept at optimal levels, iodine prophylaxis should be provided, especially in iodine deficient areas. To establish normal fetal brain development, iodine supplementation must be started before pregnancy and should be continued during the gestational period. 

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). 

Although essential, the fetus does not make thyroid hormone until 12 weeks of gestation. Therefore, during the first trimester, the fetus is totally dependent on maternal supply of this hormone. The presence of adequate levels of thyroid hormone ensure normal formation of all organs, especially the brain and the thyroid gland in the fetus. Adequate levels depend on an adequate iodine supply to the mother. 

Bonet and Herrera and Esa ar et al have recently reported that thyroid hormones cross the placenta from dam to fetus and that maternal hypothyroidism does affect fetal growth and development and brain T3 cc itent. Further studies in the rat and other species, inclxiding man, will further clarify this question. 

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 ... 

The myxoedematous form of endemic cretinism, which is still prevalent in many parts of the world (CoNTEMPRE et al. 1991), is not only due to the lack of iodine, but also of selenium. The selenoprotein type 1 5 -deiodinase catalyses the deiodination of the prohormone L-thyroxine (3,3 ,5,5 -tetraiodo-L-thyronine, T4) to the biologically active form 3,3 ,5-triiodo-L-thyronine (L-T3). During fetal development the maternal organism contributes at least minimal amounts of thyroid hormone for the fetus. After birth, the baby then slowly reaches the condition of thyroid hormone deficiency, because contin-... 

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