The Intergenerational Transmission of Stress: Investigating Mediators and Moderators of the Association between Maternal Adverse Childhood Experiences and Child Development

Abstract

Objective: The intergenerational transmission of adverse childhood experiences (ACEs) has been observed, however the biological mechanisms underlying these associations have yet to be elucidated. Given the dearth of research examining prenatal biological mechanisms, the overall objective of this dissertation was to understand the role of the maternal hypothalamic-pituitary-adrenal (HPA) axis during pregnancy in transducing the effects of maternal ACEs to child developmental outcomes. A subsequent aim was to evaluate social support as a moderator that may buffer the intergenerational transmission of stress. Methods: Data were from 356 pregnant women and their children enrolled in the longitudinal Alberta Pregnancy Outcomes and Nutrition (APrON) study. Maternal HPA axis function was assessed via self-collected salivary cortisol samples collected over multiple days in early (6-22 weeks) and late (27-37 weeks) pregnancy. Maternal ACEs, mental health, and social support were assessed via self-report measures. At 6 months of age, infant HPA axis reactivity was assessed via salivary cortisol samples at baseline and 20 minutes after a standardized laboratory stressor. At 4 years, child behaviour problems were assessed via a standardized maternal report. Results: Maternal ACEs were associated with higher morning cortisol levels and a flattened diurnal slope, consistent with a pattern of cortisol hypersecretion. Maternal HPA axis alterations mediated the association between maternal ACEs and infant HPA axis reactivity to stress at 6 months. These mediated effects were moderated by social support indicating that social support may be a factor that buffers the intergenerational transmission of stress. Maternal ACEs were associated with higher child internalizing problems at 4 years of age, and there were multiple mediators of this association including maternal HPA axis function, prenatal depression, and gestational age at birth. Unexpectedly, the HPA axis pathway predicted lower child internalizing problems and may represent a biological resiliency pathway in an otherwise healthy low sociodemographic risk sample. Conclusions: These studies provide the first evidence that prenatal maternal HPA axis function is a biological mediator of the association between maternal ACEs and child outcomes, and offers some insights into potential avenues for preventing the intergenerational transmission of stress.