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Women possess significant power in determining whether a pregnancy will be desired, maintained, and terminated. The
hypothalamic-pituitary-ovarian-adrenal axis is the common pathway through which stress in pregnancy is delivered to the fetus.
Indeed, because of the crucial nature of the adrenal response to stressors during pregnancy, it is estimated that, on a daily basis,
as many as 10% of pregnant women experience a life-threatening exacerbation of physiologic stress that typically requires
medical intervention. During the first trimester of human pregnancy, placental corticotropin-releasing hormone (CRH) isexpressed and secreted into the maternal circulation. Moreover, up to 40% of the CRH produced in the fetus comes from thematernal placenta. As the placenta develops, a local glucocorticoid environment emerges, and the CRH regulatory feedback loop
becomes active. Once established, this feedback loop mediates the dynamic and reciprocal actions of the fetomaternal
hypothalamic-pituitary-adrenal-placental axis. In the fetal brain, placental CRH exerts a plethora of actions that include
neurogenesis and neuroplasticity, glucocorticoid negative feedback, the regulation of hypothalamic neuropeptides, and thepromotion of a pro-inflammatory environment. Evidence suggests that the fetal brain responds to increased stress by activating
CRH release. In turn, CRH acts as a secondary messenger to inhibit fetal hypothalamic appetite-regulating neurons. From anevolutionary perspective, these events may be responsible for the plethora of fetomaternal metabolic interactions that arealready present in the primitive fetus. In the first three trimesters of pregnancy, fetal adrenocortical function is suppressed byplacental CRH. After the CRH negative feedback loop is established, fetal HPA-axis activity is suppressed by glucocorticoids.
Because of this potent suppressor effect, research has suggested that fetal cortisol exposure to maternal stress may be
responsible for fetal brain development. Fetal neurogenesis, a process of neuronal differentiation, takes place as early as 15weeks of gestation. There is sufficient evidence to suggest that glucocorticoids accelerate fetal brain cell differentiation andmaturation. Conversely, CRH suppresses neurogenesis, which is a process wherein neurons are produced in the brain. During
the first trimester, an excess of cortisol can increase proliferation and inhibit differentiation of fetal brain cells. In the last
trimester of pregnancy,
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