Perinatal depressive symptoms and infant self-regulation: Pathways through infant autonomic regulation and postnatal maternal sensitivity - PROJECT ABSTRACT/SUMMARY Offspring of mothers with depression are at threefold risk of developing depression themselves, known as the intergenerational transmission of depression (IGTD). Self-regulation (SR) impairments are conceptualized as a vulnerability linking maternal and offspring depression. In infancy, SR develops in the context of infant- caregiver interactions requiring both infant and caregiver contributions. However, elevated maternal perinatal depressive symptoms—which affect one in five mothers—may hinder infant SR development. Specifically, prenatal symptoms may undermine infant physiological regulation while postnatal symptoms may undermine sensitive parenting, both of which are critical for infant-caregiver interactions that support SR. Thus, infants exposed to different timing patterns of perinatal depressive symptoms (prenatal, postnatal, or both) may experience different mechanisms of risk (i.e., prenatal symptoms may affect SR through impaired infant physiological regulation while postnatal symptoms may affect SR through reduced sensitive parenting). Importantly, these pathways likely interact to produce particularly heightened risk in the case of perinatal symptoms occurring across both the pre- and postnatal periods. The present study uses a leading-edge analytical approach to examine 1) the specific timing effects of prenatal only, postnatal only, or both pre- and postnatal depressive symptoms on infant SR and 2) the two potentially interacting pathways linking maternal perinatal symptoms to infant SR. In a longitudinal sample of 168 pregnant women, prenatal maternal depressive symptoms are assessed at 34-35 weeks gestation; postnatal maternal depressive symptoms, infant autonomic regulation, and maternal sensitivity at 2 months postpartum; and infant SR at 6 months postpartum to address my specific aims. With the support of the NRSA fellowship and my mentoring team, I will complete the proposed research and my training goals, which are to 1) integrate my existing knowledge of the perinatal and infancy periods and infant SR into models of the IGTD; 2) develop expertise in processing and interpretation of cardiorespiratory indices of autonomic functioning; 3) gain experience in behavioral coding of infant SR; 4) advance my expertise in quasi-experimental approaches for strengthening causal inference by integrating concerns about developmental timing and causal mediation; and 5) engage in professional development and ethics training. By identifying which dyads are most at risk for SR difficulties and how that risk is transmitted, the proposed project will inform targeted prevention and intervention efforts that reduce difficulties in SR during infancy and thus interrupt the IGTD, addressing a clear public health need. The training I will receive with the support of this NRSA fellowship will also prepare me to achieve my career goal of becoming a professor at an R1 research institution and continuing to pursue a research program aimed at understanding and interrupting the IGTD and reducing the substantial burden of depressive symptoms on individuals and our broader society.
