Exposure to prenatal psychobiological stress exerts programming influences on the mother and her fetus

Abstract

Background/aims: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Fig. 1

Schematic representation of the psychobiological stress, fetal programming model that guides our research program. Fetal exposure to stress can influence infant/child development directly or indirectly (though fetal behavior, birth outcomes and neonatal functioning). The consequences of prenatal and very early development on later outcomes can be mediated or moderated by postnatal influences. Genetic and epigenetic influences interact at all stages of the model.

Fig. 2

As described in the text, our prospective, longitudinal assessment protocol is designed to follow fetuses at regular intervals from ∼15 weeks' gestation to birth and then to follow the child at regular intervals through 8 years of age. It is important to acknowledge that measures of maternal behavior and self-report also are collected at each child visit.

Fig. 3

Maternal reports of high levels of PSA throughout pregnancy are associated with maternal reports of elevated negative affectivity in the infant at 3 months of age independent of the effects of postpartum maternal psychological states.

Fig. 4

Areas of reduced gray matter volume in 6- to 8-year-old children in association with elevated PSA at ∼19–20 weeks' gestation. The primary effect is observed among girls. Voxels with p < 0.001 (uncorrected) are displayed.