Browsing by Subject "F"

Maternal prenatal depression is associated with increased prevalence of mental disorders in the offspring, but the underlying mechanisms are yet to be discovered. It has been proposed that prenatal stress could cause changes in the hypothalamus-pituitary-adrenal-axis (HPA) function and glucocorticoid secretion of the fetus. Animal models have shown that an adverse early life environment is associated with glucocorticoid receptor gene (GR) methylation and increased stress reactivity in adulthood through decreased negative feedback. Decreased negative feedback is thought to increase the concentration of glucocorticoids, which influence amongst other things central nervous system development. This bachelor thesis aims to clarify the role of glucocorticoids in fetal programming. To outline the subject the thesis seeks to answer two questions; first, whether maternal prenatal depression is linked to GR-gene methylation and second, if maternal prenatal synthetic glucocorticoid treatment is associated with increased psychiatric symptoms in the offspring. Based on the literature review, maternal prenatal depression and GR-gene methylation are not strongly associated. This interpretation could partly be due to small sample sizes and variability of depressive symptoms. Prenatal synthetic glucocorticoids and HPA-axis dysfunction seem to be associated with increased prevalence of mental health disorders. This highlights the importance of discretion in glucocorticoid treatments associated with pre-term birth. Glucocorticoid treatments can affect the epigenome and it is likely that future research should focus more on the epigenetic changes of GR responsive genes. Glucocorticoids are likely involved in mediating the effects of adverse prenatal environment on the fetus. More research combining data from longitudinal studies and experimental laboratory research is needed to discover the possible causal mechanisms.