Early-Life School Contexts, Education Policy, and Biological Aging
Overview
A central question in population health research is how early-life social environments become durably encoded in biology to shape health trajectories long before chronic disease manifests. This project investigates school contexts during childhood and adolescence as a key structural site where inequities are reproduced and biologically inscribed. Schools are not merely educational institutions; they are policy-structured environments that concentrate or buffer risk across racial, economic, and geographic lines, and their structural features shape children’s daily experiences of stress, opportunity, and social belonging in ways that have potentially long-lasting physiological consequences for aging and chronic disease.
Current Work
The foundation of this project is a study published in Social Science & Medicine demonstrating that manifestations of structural racism in primary school contexts — including school-level racial segregation and concentrated disadvantage — are associated with changes in accelerated epigenetic age acceleration among Black and White youth in a national longitudinal cohort. Epigenetic clocks, DNA methylation-based biomarkers that capture the pace of biological aging, provide a molecular readout of cumulative physiological stress and predict future morbidity and mortality risk. This study was among the first to directly link school-level structural inequities with changes in epigenetic aging across childhood and adolescence, using data from the Future of Families and Child Wellbeing Study (FFCWS).
Complementary work has examined how interpersonal stressors experienced within school environments — such as bullying victimization and punitive disciplinary sanctions — contribute to accelerated epigenetic aging, and how the racial composition of school contexts moderates these associations. Together, this body of work identifies schools as a critical institutional site where structural inequities translate into biological risk during a developmentally sensitive period.
Future Directions
Ongoing work extends these findings in several directions. Using new waves of FFCWS data as the cohort ages into adulthood, I am examining whether the epigenetic risks documented in adolescence persist, attenuate, or accumulate into early adulthood, and whether they are associated with downstream chronic disease outcomes. A related line of inquiry moves upstream to examine specific structural drivers of these associations — particularly school finance systems and the distribution of educational resources across communities — as modifiable policy-level targets for intervention.
A longer-term direction examines how educational inequality shapes biological risk for cognitive aging and neurodegeneration across the life course. Educational attainment is among the strongest predictors of cognitive decline and dementia, yet the mechanisms connecting school contexts to late-life brain health remain poorly understood. By linking structural features of adolescent school environments to neurodegeneration biomarkers in midlife and older adulthood, this work aims to identify the early-life policy-level determinants of population brain health and AD/ADRD risk disparities.
Selected Publications
Martz CD, Benner AD, Goosby BJ, Mitchell C, Gaydosh L. (2024). Structural racism in primary schools and changes in epigenetic age acceleration among Black and White youth. Social Science & Medicine, 347(116724).
Del Toro J, Martz CD, Freilich CD, Rea-Sandin G, Markon K, Cole S, Krueger RF, Wilson S. (2024). Longitudinal changes in epigenetic age acceleration across childhood and adolescence. JAMA Pediatrics, 178(12):1298–1306.
Additional manuscripts under review and in preparation.
Connor Martz, PhD 