Endocrine Abstracts

The importance of thyroid hormones in neurological development has been well documented in both animals and humans. Thyroid hormones deficit during fetal development can have irreversible adverse effects on an individual’s neurological function; including mental retardation, deafness, and spasticity. The only source of thyroid hormones for the developing brain in early pregnancy is from the mother. There is a growing body of epidemiological and experimental evidence to suggest that even mild maternal hypothyroxinemia may lead to abnormalities in fetal neurological development. The fetal thyroid gland reaches maturity by about week 10–12 gestation and begins to produce thyroid hormones at around the 16th week of gestation. Fetal production of thyroid hormones becomes increasingly important in the second half of pregnancy. The molecular and cellular mechanisms by which thyroid hormones affect fetal neurological development are still not well understood. Evidence of the interaction between thyroid hormones and brain development so far has primarily come from animal experiments. Thyroid hormones play an important role in regulating gene expression of myelination and cell differentiation in rats. Severe iodine deficiency (median urinary iodine concentration <20 μg/l), which causes both maternal and fetal hypothyroidism, is the most common cause of mental retardation. Moderate iodine deficiency (median urinary iodine concentration 20–49 μg/l) may also be associated with increased risk of impaired fetal neurological development. Future studies are needed to improve the understanding of human iodine nutrition during pregnancy, maternal and fetal thyroid function and mechanisms of fetal neurological development.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.