Doctoral Dissertation Research: Intergenerational Effects of Maternal Stress

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Research on the developmental origins of health and disease (DOHaD) has shown that the prenatal environment can be associated with long-term risks for chronic and metabolic disorders, including obesity, cardiovascular disease, hypertension, and diabetes. This biocultural doctoral dissertation project investigates how maternal stress during the perinatal period shapes the development of the central stress response system in infants, in a population undergoing rapid social and economic change. This work will contribute to our understanding of the factors shaping fetal development from an evolutionary life history perspective, and offer insights into the social and biological underpinnings of the rising rates of metabolic diseases around the world. The research findings may inform policy on maternal care during pregnancy. The project will also support graduate student training and international collaborations and research capacity. The fetal origins framework has shown that maternal psychosocial stress can modify fetal development, programming a fetus's HPA axis with permanent consequences on a variety of systems, leading to increased risk of metabolic disease. While previous research has examined isolated mechanisms linking maternal stress to infant HPA axis dysregulation, largely in wealthy, biomedical settings, the proposed research investigates how multiple pathways work in tandem from the second trimester through early infancy to shape HPA axis development in a middle-income, ecological setting. Through twelve months of mixed methods data collection, including semi-structured interviews, stress scales, and biomarker testing, this project seeks to contribute to anthropology not only as an important case study on maternal stress in a nation undergoing dramatic change, but also as an investigation that will add a critical component to the understanding of DOHaD as a larger phenomenon shaping health. Specifically, the researchers will investigate: the role of prenatal maternal stress, the role of placental 11ß-HSD2 expression, and the role of postnatal maternal stress in the development of the infant HPA axis. The proposed work emphasizes the continuum of early development from the prenatal into the postnatal period. In addition to investigating maternal stress at multiple time points during pregnancy, the work adds the examination of placental 11ß-HSD2 expression and of stress in the postnatal period as integrated pathways through which the HPA axis can be modified in offspring.