Fetal brain development

Zoeller RT, Crofton RM. 2000. Thyroid hormone action in fetal brain development and potential for distribution by environmental chemicals. Neurotoxicology 21(6) 935-946. 

Creatures of the sea present a real conundrum for pregnant women. Fish is so good for you. We read it over and over again in the newspaper s science section. Unfortunately, it is also one of the most contaminated foods out there—the biggest source of exposure to mercury, which can cross the placenta and mess with fetal brain development. 

OH-PCBs can also influence thyroxine metabolism. Some of the OH-PCBs that are retained in blood were shown to strongly inhibit sulfation of thyroxine in vitro [204-206]. As sulfation is a major regulation pathway of thyroxine in the fetus, the OH-PCBs may negatively influence the development of the fetus, and in particular fetal brain development [44]. Diodinase mediation is another pathway for thyroxine metabolism e.g., to the active hormone triiodothyronine. Hydroxylated metabolites of CB-77 were shown to inhibit triiodothyronine formation in an in vitro assay using rat hepatic microsomes [207],... 

With this tool, the investigators were able to establish a relationship between maternal methylmercury exposure and indices of child development. Statistical analyses of the correlation between maternal hair levels and delayed walking, for example, suggested that even slightly elevated methylmercury consumption by a pregnant woman might pose a risk for fetal brain development. 

Gn Pig (Hartley) once Gd 21,28, 35, 42 (GW) 11.5 (retarded fetal brain development) Inouye and Kajiwara 1988b MMC... 

Fetal brain development is a vast subject, the focus of hundreds of research laboratories and clinical groups around the world. In this chapter I highlight some of this research to illustrate how the fetal environment can interact with brain development and to identify broadly the points at which that development is most vulnerable to environmental effects that may alter it in some way, whether divergently or disruptively. 

In general, prenatal exposure to infection apparendy increases the risk of later schizophrenia and other neurodevelopmental disorders. As discussed previously, the release of proinflamma-tory cytokines during maternal infection may have a damaging impact on fetal brain development.34... 

The expression of many of the genes identified to be related in some way to the appearance of adult schizophrenia is known to be changed by hypoxia. This suggests that hypoxia during fetal brain development may be somehow involved in the etiology of schizophrenia.36... 

Maternal psychological stress during pregnancy most certainly results in transient or enduring physiological and hormonal changes that may affect fetal brain development. So... 

The major problem concerning the impact of environmental neurotoxins on fetal brain development is not the absence of evidence but the absence of research on the many new chemicals in our midst. Regardless, the evidence that we do have tells us that simplistic genetic-determinist arguments about IQ are dubious. 

Three mechanisms have been suggested for the effect of iodine deficiency on fetal brain development. 

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 above-mentioned facts form the basis of a new concept of the adverse effects of not only maternal hypothyroidism, but also maternal hypothyroxinemia without overt hypothyroidism, on fetal brain development. This concept focuses on the necessity for therapeutic correction of maternal hypothyroxinemia detected in pregnancy. MRS, a quantitative laboratory and imaging technique, may be used to show the effects of hypothyroxinemia due to iodine deficiency and its correction in the human brain in an objective manner. 

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. 

Iodine supplementation probably begins late in many pregnant women (at the first prenatal care visit), missing the critical period of fetal brain development. However, there is no clinical data so far that supports the effect of iodine supplementation on neural development in pregnant women from mild iodine-deficient areas in both the short- and long-term. These data indicate that continued efforts for USI remain a public health priority. 

Before birth, immune system abnormalities of the mother may contribute to autism by interfering with the timing of fetal brain development. There is evidence of a link between autism and viral infection of the mother during pregnancy (see Section 5.22.8). Because autistic children exhibit extremely male brain characteristics, others are focusing on prenatal testosterone exposure. 

The fetotoxic effects of ethanol in humans first appeared in modem literature almost 40 years ago (Lemoine et al, 1968 Jones et al, 1973). Subsequently, a myriad of reports have linked maternal consumption of ethanol to alterations in fetal brain development, both in the human setting and in a variety of animal models (Schenker et al, 1990 Streissguth et al, 1990). The former is often reflected in a variety of behavioral and performance deficits (Streissguth et al, 1990 Wass et al, 2002 Wozniak et al, 2004) which range widely in severity. The most severe presentation... 

Fat is needed in pregnancy to snpply sufficient energy as well as precursors for essential fatty acids needed for fetal brain development. In pregnancy, about 30-35 % of calories should come from fat. For a 2,400-cal diet, this translates to 93 g of fat, the equivalent to approximately six tablespoons of fat. For expectant mothers on a fat-free or low-fat medical food, special attention must be paid to providing other sources of dietary fat. 

It is of interest that PA is detected in the tela choroidea, the precursor of the choroid plexus in the 11-day rat fetus, and thus could have a role in fetal brain development. Anatomical studies on sheep, pig and human fetuses show that epithelial tight junctions develop early in cerebral endothelium and choroid plexus epithelium. At the 50 to 70-days gestation period in the sheep, and the late fetal and early newborn period in the rat, there is development of the blood-brain barrier mechanisms that decrease penetration of hydrophyllic molecules. At the same time the protein concentration in the CSF decreases. 

Iodine Deficiency Disorders (IDD) are a major international public health problem (1). The effects of iodine deficiency occur at all ages, but are particularly important during the period of fetal development. The available epidemiological evidence has been complemented by experimental studies of fetal development in animal models. These have focussed particularly on fetal brain development because of its obvious importance Definite effects have been observed in a variety of animal models - the rat, the marmoset and the sheep. In addition studies of the mechanisms involved have been carried out which have revealed the importance of maternal thyroid function for fetal brain development. 

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