Early Life Adversity and the Developmental Programming of Early Childhood Telomere Biology: A Longitudinal Study of Developmental Context and Behavioral Mediators

Project Summary 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. We propose to examine the early biological embedding of health and disease risk in young children’s telomeres, a biomarker of cellular aging. Telomeres naturally shorten with each cell replication (cellular aging) and erode most rapidly in the first years of life, reflecting a sensitive period of development. We propose 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. We also propose a novel examination of developmental context (i.e., parenting quality) and child behavioral (i.e., self-regulation) mediators in these pathways to elucidate potential mechanisms that may contribute to the early origins of health and disease risk. Participants (n = 200) will be drawn from a prospective longitudinal cohort study funded by NICHD (Brain and Early Experience Study; R01 HD091148-01A1). Early life adversity will be assessed via maternal report at prenatal (28 week’s gestation) and postnatal home visits (6 mo). Parenting quality (sensitivity and harsh intrusiveness) will be assessed via videotaped and coded mother- child interactions at the 6-month visit. Child self-regulation will be assessed via videotaped and coded child observations at the 27- and 36- month home visits, as well as maternal report. Biospecimens (i.e., saliva) will be collected from mothers and children at the 6-, 27-, and 36-month visits and assayed for telomere length at all three time points and DNAm conversion will be performed to provide epigenetic aging clocks at the 6- and 36- month time points. The proposed study will be the first to investigate potential linkages between early life adversity, parenting quality, child self-regulation, and biological aging during this critical period in early childhood when telomeres are eroding most rapidly and may be most susceptible to environmental input. Our long-term goal is to determine how early adversity becomes biologically embedded in early childhood in order to prevent or mitigate risk to later health and wellness. Findings will provide important information to help in the development and/or optimization of early risk-mitigating intervention and prevention efforts to improve the quality of life for children.