Co-funded with the Ford Foundation
Childhood poverty is a risk factor for deleterious outcomes later in life. Both environmental and biological processes are associated with these outcomes, but the biological mechanisms that account for how socioeconomic status (SES) disadvantages affect long-term vulnerability are not well understood. Some biological research suggests that early disadvantage programs the epigenome through DNA methylation (DNAm) marks that affect gene expression, and that childhood adversity can induce lasting DNAm changes. DNAm profiles are associated not only with the risk for disease, but also outcomes such as adult socioeconomic status and educational attainment. Most research on these associations is based on cross-sectional analyses of a few candidate genes and is unable to evaluate the links between early socioeconomic adversity, epigenome-wide DNAm, and later-life outcomes. It is also not clear if there are specific ages when children are more vulnerable to the effects of adversity or if exposure to adversity differentially affects DNAm.
Working with an interdisciplinary team, Erin Dunn will address these gaps by integrating longitudinal data with insights from genetics, epigenetics and human development to characterize the causes and consequences of DNAm during childhood. She plans to test four hypotheses: First, does early exposure to SES disadvantage explain more variability in DNAm at age 7 than the duration or recency of disadvantage? Second, do adversity-induced DNAm changes correspond with genes that regulate sensitive periods? Third, do age 7 DNAm profiles predict adolescent academic and vocational outcomes? Last, do age 7 DNAm changes mediate the relationship between the timing of childhood disadvantage and adolescent outcomes?