Objective: This study investigates the influence of exposure to intimate partner violence (IPV) during pregnancy on offspring depressive problems during childhood, examining HPA axis dysregulation (via stress-induced levels of salivary cortisol) as a mediating mechanism. This research is guided by the "fetal programming" theory, which proposes that the environmental conditions during pregnancy can exert long-term neural adaptations and influence later physiological and psychological functioning. In addition, trauma theory supports the role of IPV as a particularly deleterious influence, due to its interpersonal and chronic nature, and well-established associated neuroregulatory deficits. Finally, consistent with developmental psychopathology, a number of factors at the individual and family levels were examined, and interactions between different levels of risk and protection were explored. Previous empirical studies support the proposed pathway: prenatal stress predicts child temperamental difficulties, internalizing symptoms, and HPA axis dysregulation. However, only one study to date has reported a link between prenatal stress, HPA axis functioning, and depression. No study to date has evaluated the distinct effect of prenatal IPV on long-term offspring neuroendocrine and psychological outcomes. Method: Participants were 119 children followed longitudinally since pregnancy, who were about 10 years old for the present assessment. Questionnaires assessed IPV, maternal mental health, maternal early parenting, family history of depression, and income. A coded laboratory task measured maternal warmth towards their child during infancy. HPA axis dysregulation was assessed via salivary cortisol levels before, 20 minutes after and 40 minutes after the Trier Social Stress Task for Children. Child depressive symptoms were assessed through maternal and child reports, using questionnaires and a semi-structured clinical interview (K-SADS-PL). Results: Structural Equation Modeling, Latent Class Analysis, Logistic Regression, and MANCOVA were used for hypothesis testing. Exposure to IPV during pregnancy and current exposure to IPV predicted higher salivary cortisol output. Depression during childhood was predicted by IPV during pregnancy, maternal mental health during pregnancy, early parenting, current exposure to IPV, current maternal mental health, gender, and cortisol levels; however, different predictors were significant for mother-reported and child-reported depressive symptoms. Gender and family history of depression moderated the relationships between child depressive symptoms and prenatal, postnatal, and familial risk. Discussion: Findings support the "programming hypothesis" and the role of prenatal IPV as a unique risk factor associated with HPA axis functioning and childhood depression, over and above the effects of other prenatal stressors and postnatal adversity. Results support the multi-determined nature of child depressive symptoms, as prenatal and postnatal factors at the individual and family levels significantly influenced outcomes. This is the first study to link prenatal IPV exposure with HPA axis dysregulation and depressive symptoms. Future research should replicate the present findings, using multiple indices of HPA axis functioning and examine whether this mechanism differentiates distinct subgroups of depressed children.
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