Grants and Contracts Details


Recent evidence has emerged of a shared molecular mechanism linking prenatal metal, nutritional, and psychosocial stress exposures to later infant and child adiposity, though this possibility has not been explicitly tested. The proposed study will examine whether prenatal metal, nutritional, and stress exposures jointly contribute to epigenetic alterations of HPA-related genes (NR3C1, HSD11B2, HSD11B1) and whether such alterations in turn impact adiposity in early infancy and childhood. To generate preliminary results and demonstrate proof of concept, I will perform a secondary data analysis of 1018 mother-child dyads from The Avon Longitudinal Study of Parents and Children and leverage a unique, existing birth cohort with unparalleled and extensive dietary, psychosocial stress, anthropometric, clinical, and epigenomic data. The internalization of environmental stressors or "epigenetic memory" is one potential pathway through which ongoing disparities in nutritional status, chemical exposures, and social experiences (discrimination, stress) become embedded within our biology and perpetuated. To reduce the burden of health disparities related to obesity in the US and implement appropriate interventions, it is crucial to understand the role of early life "programming."
Effective start/end date9/1/203/31/21


  • National Institute of Environmental Health Sciences


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