Exposure to Prenatal Psychobiological Stress Exerts Programming Influences on the Mother and Her Fetus
Accumulating evidence from a relatively small number of prospective studies indicates that exposure to prenatal stress profoundly influences the developing human fetus with consequences that persist into childhood and very likely forever.
Maternal/fetal dyads are assessed at ∼20, ∼25, ∼31 and ∼36 weeks of gestation. Infant assessments begin 24 h after delivery with the collection of cortisol and behavioral responses to the painful stress of the heel-stick procedure and measures of neonatal neuromuscular maturity. Infant cognitive, neuromotor development, stress and emotional regulation are evaluated at 3, 6 12 and 24 months of age. Maternal psychosocial stress and demographic information is collected in parallel with infant assessments. Child neurodevelopment is assessed with cognitive tests, measures of adjustment and brain imaging between 5 and 8 years of age.
Psychobiological markers of stress during pregnancy, especially early in gestation, result in delayed fetal maturation, disrupted emotional regulation and impaired cognitive performance during infancy and decreased brain volume in areas associated with learning and memory in 6- to 8-year-old children. We review findings from our projects that maternal endocrine alterations that accompany pregnancy and influence fetal/infant/child development are associated with decreased affective responses to stress, altered memory function and increased risk for postpartum depression.
Our findings indicate that the mother and her fetus both are influenced by exposure to psychosocial and biological stress. The findings that fetal and maternal programming occur in parallel may have important implications for long-term child development and mother/child interactions.
Sandman, C. A., Davis, E. P., Buss, C., & Glynn, L. M. (2012). Exposure to prenatal psychobiological stress exerts programming influences on the mother and her fetus. Neuroendocrinology, 95(1), 7–21. https://doi.org/10.1159/000327017
S. Karger AG, Basel
This is a pre-copy-editing, author-produced PDF of an article accepted for publication in Neuroendocrinology, volume 95, issue 1, in 2012 following peer review. The definitive publisher-authenticated version is available online at https://doi.org/10.1159/000327017.