Cortisol is type of hormone called a glucocorticoid, which glucose usage in the body and tends to be activated during a fight-or-flight response. Cortisol is produced in the adrenal gland, whose activity is mediated by the hypothalamus and pituitary glands of the brain. Together, the collective signaling of the hypothalamus, pituitary gland, and adrenal gland is known as the hypothalamo-pituitary-adrenal (HPA) axis. During a period of psychosocial<unk> , cortisol is released, leading to physiological manifestations of<unk>  such as increased maternal blood pressure (MBP) and maternal heart rate (MHR). In the case of a pregnant woman, the release of cortisol from the adrenal glands also has an effect on the fetus being carried in the womb. Cortisol is a steroid hormone, and, like all steroid hormones, the receptors for cortisol are located intracellularly. In other words, cortisol does not need an extracellular receptor in order to enter the nucleus of cells and affect their gene expression. Because of this feature of steroid hormones, cortisol diffuses directly across the placenta, the barrier that separates the fetus from the mother. Luckily, the fetus has a protective mechanism against the inundation of cortisol from a<unk> ed mother. There is an enzyme in the placenta called 11beta-hydroxysteroid dehydrogenase type 2 that is capable of inactivating the vast majority of the cortisol passing through the placental barrier to the fetus. In cases of very high levels of maternal cortisol, this placental enzyme’s expression and activity are greatly reduced, thus buffering the fetus less from the mother’s high cortisol levels. There are detrimental effects to this loss of placental enzymatic activity. One such effect is a change in the set point for the HPA axis. Myriad studies in animal models indicate that, if fetal cortisol levels are high, then the HPA axis will be more active postnatally. High levels of fetal cortisol induce higher CRH expression in the paraventricular nucleus of the hypothalamus (PVN) and the central nucleus of the amygdala. In other words, excessive cortisol crossing the placental barrier causes the hypothalamus and amygdala to increase transcription of CRH, which in turn stimulates HPA axis activity early in postnatal life. With such an overactive HPA axis, glucocorticoid receptor expression in the brain increases, making it so that the release of minimal levels of cortisol elicit a substantial response at developing synapses. It is speculated that the HPA axis will more rapidly develop its neural circuitry as a result.
Maternal fetal stress transfer
Foetal cerebral redistribution
Maternal-fetal conflict
Neonatal sepsis
Intrauterine hypoxia
Traumatic asphyxia
Fetal-maternal haemorrhage
Perinatal asphyxia