Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Abstract

The purpose of the study was to determine the specific periods during pregnancy in which human fetal exposure to stress hormones affects newborn physical and neuromuscular maturation. Blood was collected from 158 women at 15, 19, 25, and 31 weeks' gestation. Levels of placental corticotropin-releasing hormone (CRH) and maternal cortisol were determined from plasma. Newborns were evaluated with the New Ballard Maturation Score. Results indicated that increases in maternal cortisol at 15, 19, and 25 weeks and increases in placental CRH at 31 weeks were significantly associated with decreases in infant maturation among males (even after controlling for length of gestation). Results also suggested that increases in maternal cortisol at 31 weeks were associated with increases in infant maturation among females, although these results were not significant after controlling for length of gestation. Findings suggest that stress hormones have effects on human fetal neurodevelopment that are independent of birth outcome.

Psychobiological Stress and Preterm Birth

“…One new area of research that we only briefly acknowledged was sex differences in birth and developmental outcomes. We have reported that (i) female fetuses displayed more mature responses than males at 31 and 36 gestational weeks (Buss et al, 2009a), (ii) delayed neuromotor development associated with fetal exposure to cortisol early in gestation and CRH late in gestation was confined to males (Ellman et al, 2008) and (iii) the reduction in brain volumes in children exposed to elevated PSA early in gestation primarily were observed in girls . These findings are consistent with findings of sex specific trajectories of fetal development and the sexually dimorphic risk of neurological impairment associated with neonatal complications (Kesler et al, 2008).…”

“…In a study from our group (Ellman et al, 2008) the New Ballard Maturation Score was used to assess physical and neuromuscular maturation of 158 newborns within 24 hours after birth. Specifically, the neuromuscular and physical characteristics of the newborn were rated and consisted of measures of muscle tone, distinct posture, and angles of resistance in key muscle groups.…”

Glucocorticoids: Biochemical Group That Play Key Role in Fetal Programming of Adult Disease

“…High P-CRH, as a marker of maternal stress, during third trimester associated with weak fetal responsiveness to noval stimuli (79). Postnataly, there is significant reduction in physical and neuromuscular development in neonates who exposed to higher maternal cortisol as well as P-CRH during second and third trimester respectively (80). Those neonates also express prolonged cortisol response to stress, which similar to the effect of synthetic prenatal GCs (81).…”

Effects of Maternal Stress during Different Periods of Pregnancy on the Early Neurobehavioral Response of Rats

“…A typical response in these situations is the elevation of stress hormone, cortisol and the activation of hypothalamic-pituitary-adrenal axis (HPAaxis). While we know that cortisol is transported through the placenta and it has a critical role in tissue and organ maturation, the exact mechanism how its excess level may cause alterations in fetal development has not been completely understood [2,5]. In normal pregnancy the level of cortisol in fetus is about 10-fold lower than in the mother because it is converted into inactive cortisone by placental 11β-hydroxysteroid-dehydrogenase-2 (11β-HSD2) enzyme.…”

“…In normal pregnancy the level of cortisol in fetus is about 10-fold lower than in the mother because it is converted into inactive cortisone by placental 11β-hydroxysteroid-dehydrogenase-2 (11β-HSD2) enzyme. Animal experiments suggest that maternal stress may lead to decreased functioning of 11β-HSD2 enzyme resulting in high amount of glucocorticoids affecting the developing brain [3,[5][6][7]. They might have detrimental effects on cell proliferation, differentiation and synapse formation, mainly in amygdala, hippocampus and limbic cortical areas leading to short-and long-term postnatal consequences [8][9][10][11][12].…”