Early life adversity is a potent predictor of health and disease burden during middle and late adulthood, as well as earlier, all-cause, and specific disease mortality. Even more disturbing, longitudinal studies suggest that experiences of early life adversity appear to be biologically embedded such that improved later life circumstances have only modest ameliorative effects. Thus, it is critical to investigate how adversity becomes biologically embedded at an early age. This study will examine the early biological embedding of health and disease risk in young children’s telomeres, a biomarker of cellular aging. We will conduct a novel longitudinal study to examine the effects of prenatal and postnatal early life adversity (i.e., poverty, parent conflict, maternal stress) on accelerated biological aging, including telomere erosion and epigenetic aging clocks, across the first three years of life.