Connor D. Martz, PhD

Research Approach & Focus

My research takes a cells to society approach to understanding how structural inequities and social environments shape population health. I integrate sociological and life course perspectives with epigenetic and physiological data to investigate the biosocial pathways through which structural factors and chronic psychosocial stress “get under the skin” to influence chronic disease risk and accelerate biological aging. A primary objective of this work is to generate evidence that informs structural and policy-level interventions to mitigate health disparities before chronic disease onset.

Focal Area 1

Early-Life Environments and Biological Aging

The primary focus of my research program examines how school and neighborhood contexts during childhood and adolescence become biologically embedded to influence trajectories of aging and chronic disease risk later in adulthood and old age. Childhood and adolescence represent sensitive developmental periods during which social environments exert lasting influence on physiological functioning, making early-life exposures a critical leverage point for understanding and ultimately reducing population-level health disparities.

Much of this work uses DNA methylation-based biomarkers that capture the pace of biological aging (i.e., epigenetic clocks) as a molecular window into how social and structural disadvantage accumulate in the body over time. Using national longitudinal cohort data, I have shown that manifestations of structural racism in primary school contexts are associated with accelerated epigenetic aging among Black and White youth, and that residential proximity to deadly gun violence predicts similar patterns of accelerated biological aging during adolescence as well as respiratory health outcomes in early adulthood. Collectively, this work highlights how inequities embedded in the institutions and environments children navigate daily generate measurable biological consequences and identifiable opportunities for intervention.

My ongoing and future research in this area extends these findings in several directions: tracing the epigenome-wide signatures of early-life exposures, examining their downstream associations with chronic disease across distinct stages of adulthood, and identifying structural and policy-level risk and protective factors.

Focal Area 2

Social Determinants of Chronic Disease

A parallel and foundational line of my research investigates how chronic psychosocial stress and structural inequities drive racial disparities in chronic disease progression and outcomes. This work was initially developed through my NIH-funded (F31) dissertation research using longitudinal data from the Black Women’s Experiences Living with Lupus (BeWELL) Study, which provided a unique opportunity to examine the social and structural drivers of accelerated disease progression in a population that bears a disproportionate burden of systemic lupus erythematosus.

Across multiple papers, I have documented how direct and vicarious experiences of racial discrimination, exposure to neighborhood stressors, and residential segregation contribute to inflammation, organ damage, and mental health comorbidities among Black women with lupus. This body of work helped shift the field’s attention toward structural and psychosocial explanations for disease inequities and generated novel longitudinal evidence linking racism-related stress with changes in inflammatory biomarkers over time.

Looking forward, I aim to extend this work into the study of cognitive aging and neurodegeneration, examining how cumulative exposure to structural inequities and chronic stress across the life course shapes risk for cognitive decline and Alzheimer’s disease and related dementias (AD/ADRD). This emerging direction represents a natural convergence with Focal Area 1 by integrating early-life biological embedding and late-life chronic disease outcomes, and reflects a broader commitment to understanding how biological risk accumulates across the life course to generate health disparities in aging populations.