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Mastorakos
The Iodine Deficiency Disorders, Chapter 20.Mastorakos G, Nezi M, Papadopoulos C
“Brain growth is characterized by two periods of maximal growth velocity (17). The first one occurs during the first and second trimesters between the third and the fifth months of gestation. This phase corresponds to neuronal multiplication, migration and organization. The second phase takes place from the third trimester onwards up to the second and third years postnatally. It corresponds to glial cell multiplication, migration and myelinisation. The first phase occurs before fetal thyroid has reached its functional capacity. It is now largely agreed that during this phase, the supply of thyroid hormones to the growing fetus is almost exclusively of maternal origin while during the second phase, the supply of thyroid hormones to the fetus is essentially of fetal origin.
“As a matter of fact, an important recent issue on thyroid function and regulation in the fetus is the concept that thyroid hormones are transferred from mother to fetus both before and probably after the onset of fetal thyroid function, contrasting with the previous dogma that this transfer is minimal or does not exist (19, 20). In humans, T4 can be found in the first trimester coelomic fluid from 6 weeks of gestational age, long time before the onset of secretion of T4 by the fetal thyroid, which occurs at the 24th week of gestation (21). Nuclear T3 receptors and the amount of T3 bound to these receptors increase about six to tenfold between 10 and 16 weeks, also before the secretion of hormones by the fetal thyroid (22). The T4 and T3 found in early human fetuses up to mid gestation are likely to be entirely or mostly of maternal origin. As a consequence, as recently confirmed and clarified (22 bis), infants born to women with hypothyroxinemia at 12 weeks gestation (fT4 concentrations <10th percentile) have significantly lower scores at the Neonatal Behavioural Assessment Scale than controls. These anomalies are already detectable at the age of 3 weeks of age. The transfer of thyroid hormones is decreasing but persists during later gestation as Vulsma et al (23) suggested that up to 30 % of serum T4 in cord blood at birth could be of maternal origin, although a much lower percentage has been reported by Delange et al. (24).
“Other mechanisms involved in the action of thyroid hormones in the brain working to deliver a proper amount of T3 to the target cells involve the deiodinases, especially the deiodinase D3 found in the uterine implementation site and in the placenta, producing rT3 from T4 and 3’,5’-T2 from T3 and having a protective effect to avoid an excess of thyroid hormone reaching the fetus. The membrane transporters for thyroid hormones physiologically relevant in the flux of thyroid hormones through the blood stream barrier, the choroid plexus and the cellular membranes of the astrocytes and neurons are also involved (24 bis).”
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