Abstract
The human placenta expresses the genes for proopiomelanocortin and the major stress hormone, corticotropin-releasing hormone (CRH), profoundly altering the “fight or flight” stress system in mother and fetus. As pregnancy progresses, the levels of these stress hormones, including maternal cortisol, increase dramatically. These endocrine changes are important for fetal maturation, but if the levels are altered (e.g., in response to stress), they influence (program) the fetal nervous system with long-term consequences. The evidence indicates that fetal exposure to elevated levels of stress hormones (i) delays fetal nervous system maturation, (ii) restricts the neuromuscular development and alters the stress response of the neonate, (iii) impairs mental development and increases fearful behavior in the infant, and (iv) may result in diminished gray matter volume in children. The studies reviewed indicate that fetal exposure to stress peptides and hormones exerts profound programming influences on the nervous system and may increase the risk for emotional and cognitive impairment.
Highlights
The Developmental Origins of Disease or Fetal Programming model predicts that early exposures to threat or adverse conditions have lifelong consequences that result in poor health outcomes [1]
We have reported that fetuses of women with elevated placental CRH (pCRH) concentrations during the third trimester were less responsive to the presence of a novel stimulus [7] and that fetal heart rate (FHR) habituation was delayed when fetuses were exposed to overexpression of maternal endogenous opiates [56]
We found that low pCRH at 15 gestational weeks, but not later, predicted a more mature fetal heart rate pattern at 25 gestational weeks suggesting that the pattern of development was altered by these early exposures [58]
Summary
The Developmental Origins of Disease or Fetal Programming model predicts that early exposures to threat or adverse conditions have lifelong consequences that result in poor health outcomes [1]. The placenta expresses the genes for the major stress hormones, CRH (hCRHmRNA) and proopiomelanocortin, the precursor for ACTH and beta-endorphin (BE) All of these stress hormones increase as pregnancy advances, but the exponential increase in placental CRH (pCRH) in maternal plasma is especially dramatic, reaching levels observed only in the hypothalamic portal system during physiological stress [5]. If the CRH response is blocked during environmental desiccation, the rate of development is arrested and the tadpole’s survival is compromised This remarkable surveillance and response system has evolved and is conserved so that many species including the human fetus can detect threats to survival and adjust its developmental trajectory [8, 18,19,20]. Placental CRHmRNA is found only among some primates, and, even among nonhuman primates, the timing of synthesis and release of pCRH is different than for humans (and great apes)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
