Maternal fetal stress transfer

From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

Maternal fetal stress transfer describes the physiological phenomenon by which psychosocial stress experienced by a mother during her pregnancy can be transferred to the fetus. Psychosocial stress (or simply social stress) describes the brain's physiological response to perceived social threat. Because of a link in blood supply between a mother and fetus, it has been found that stress can leave lasting effects on a developing fetus, even before a child is born. According to recent studies, these effects are mainly the result of two particular stress biomarkers circulating in the maternal blood supply: cortisol and catecholamines.

Mechanism of action[edit]

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 stress, cortisol is released, leading to physiological manifestations of stress such as increased maternal blood pressure (MBP) and maternal heart rate (MHR).[1]

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 stressed 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.[2]

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.[1] Myriad studies in animal models indicate that, if fetal cortisol levels are high, then the HPA axis will be more active postnatally.[3]

High levels of fetal cortisol induce higher CRH expression in the paraventricular nucleus of the hypothalamus (PVN) and the central nucleus of the amygdala.[3] 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,[3] 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.

See also[edit]

References[edit]

  1. ^ a b Rakers, Florian; Bischoff, Sabine; Schiffner, Rene; Haase, Michelle; Rupprecht, Sven; Kiehntopf, Michael; Kühn-Velten, W. Nikolaus; Schubert, Harald; Witte, Otto W.; Nijland, Mark J.; Nathanielsz, Peter W.; Schwab, Matthias (November 2015). "Role of catecholamines in maternal-fetal stress transfer in sheep". American Journal of Obstetrics and Gynecology. 213 (5): 684.e1–684.e9. doi:10.1016/j.ajog.2015.07.020. PMID 26212181.
  2. ^ Duthie, Leanne; Reynolds, Rebecca M. (2013). "Changes in the Maternal Hypothalamic-Pituitary-Adrenal Axis in Pregnancy and Postpartum: Influences on Maternal and Fetal Outcomes". Neuroendocrinology. 98 (2): 106–115. doi:10.1159/000354702. PMID 23969897.
  3. ^ a b c Li, Yong; Gonzalez, Pablo; Zhang, Lubo (August 2012). "Fetal stress and programming of hypoxic/ischemic-sensitive phenotype in the neonatal brain: Mechanisms and possible interventions". Progress in Neurobiology. 98 (2): 145–165. doi:10.1016/j.pneurobio.2012.05.010. PMC 3404248. PMID 22627492.
  • Rakers, Florian, et al. “Transfer of Maternal Psychosocial Stress to the Fetus.” Neuroscience & Biobehavioral Reviews, 2017, doi:10.1016/j.neubiorev.2017.02.019.