Prenatal Maternal Depression Symptoms but Not Synthetic Glucocorticoids Predict Infant Cortisol Response: Exploring The Prenatal Determinants of Infant HPA Axis Functioning

• In Event: Intergenerational and Developmental Origins of Health: Maternal Prenatal Distress and Implications for Offspring Psychopathology

Abstract

Background: The hypothalamic pituitary adrenal (HPA) axis plays a critical role in regulating the body’s response to stress. There is growing evidence that the organization of the HPA axis is shaped by early life experiences and is even sensitive to perturbations in the uterine environment. However, more work is needed to elucidate the prenatal determinants of offspring HPA axis functioning and disentangle the effect of prenatal environment from postnatal factors. In the current study we investigate influence of two key prenatal factors that have been implicated in the HPA axis development: maternal depression and exposure to synthetic glucocorticoids. Utilizing a prospective, longitudinal design we test whether these prenatal risk factors independently or jointly predict infant HPA axis response amongst a sample of women with medically high-risk pregnancies, a population in which depression and synthetic glucocorticoid treatment more frequently occur. We also carefully consider alternative explanations in the postnatal period by testing whether study findings can be accounted for by maternal postpartum depression or sensitive parenting behaviors.

Method: Participants were recruited in southern California and include women who are predominantly Latina (72%), socioeconomically diverse, and high in obstetric risk factors. Infants were delivered at term and 61.6% were exposed to the synthetic glucocorticoid betamethasone in utero as part of their standard medical care. Maternal depression symptoms were assessed via self-report during pregnancy and at 6 months postpartum. Maternal sensitivity was coded from video recordings of semi-structured parent-child play interactions. Infant salivary cortisol concentrations were repeatedly assessed in response to a series of laboratory stressors (e.g., selected LabTAB tasks and the Still Face procedure) at 6 months.

Results: Hierarchical linear modeling revealed that synthetic glucocorticoid exposure did not relate to the baseline level (β = -0.81, SE = 4.60, t = -0.18, p = .862) or the trajectory (β = -0.19, SE = 0.18, t = -1.08, p = .286) of infant cortisol response. However, we found that prenatal maternal depression symptoms predicted the trajectory of infant salivary cortisol response (β = -0.06, SE = 0.03, t = -2.08, p = .041), in that higher maternal depression symptoms during pregnancy were associated with a greater infant cortisol response to laboratory challenge. This effect persisted after controlling for antenatal glucocorticoid exposure. Notably, neither postnatal maternal depression symptoms nor the quality of maternal care, predicted infant cortisol response (all p’s > .05), and the effect of prenatal maternal depression symptoms remained after accounting for these key postnatal risk factors.

Discussion: Findings suggest that maternal depression symptoms during pregnancy have robust and persisting consequences for offspring stress physiology. Results provide compelling evidence that the prenatal period is a sensitive window in which maternal depression can influence the developing HPA axis, as this effect persists even in the presence of other risk factors such as synthetic glucocorticoid exposure, postpartum depression, and low sensitivity caregiving behaviors. The offspring HPA axis is thus a plausible biological pathway by which maternal prenatal depression can impact the next generation.

Author

• Danielle Swales, University of North Carolina at Chapel Hill
  Presenting Author