Life-course sociogenomic analysis of social inequalities in aging
Summary
Life-course social science links early-life social disadvantage with adverse outcomes in aging, including earlier onset of disease and disability, reduced wellbeing, economic hardship, and earlier mortality. A gap in knowledge is how social disadvantage is biologically embedded, leading to social inequalities in aging. One hypothesis is that the burdens of social disadvantage actually hasten the aging process. Chronological age increases at the same rate for everyone. But the biological changes that occur with advancing chronological age may proceed faster for some and slower for others. These biological changes, including metabolic, inflammatory, and epigenetic modifications, are thought to be a root cause of disease and disability and a potential target for interventions to prevent or delay many different chronic diseases. A gap in knowledge is whether social disadvantage hastens these aging-related biological changes. If so, it would open a fertile opportunity to join forces between biomedical research developing so-called geroprotective interventions to slow aging and social science research to address social inequalities. Recent advances in genomics and bioinformatics have yielded several new methods to quantify biological aging using whole-genome DNA methylation, as well as combinations of clinical biomarkers. Proof-of-concept studies link these new biological aging measures with disease, disability, and death. But it is not known if new measures of biological aging are related to social disadvantage or how they are affected by social mobility. This research will implement these new measures in several existing biosocial datasets to conduct rigorous tests of the hypothesis that social disadvantage accelerates biological aging, contributing to social inequalities in aging.