Research
I integrate epidemiological and sociological perspectives with epigenetic and physiological data to investigate how social environments and psychosocial stressors impact biological functioning and chronic disease risk, ultimately shaping population health. A primary objective of my work is to contribute evidence that informs structural and policy-level interventions aimed to advance health equity.
My research centers on two interconnected areas: the first focuses on childhood and adolescent experiences and their lasting impacts on biological functioning, while the second area focuses on experiences in adulthood and how they shape chronic disease progression.
The first area of my research examines the biological risks associated with childhood and adolescent social contexts and psychosocial stressors. Using datasets like the Future of Families and Child Wellbeing Study, I explore how early-life social contexts shape patterns in DNA methylation, a specific epigenetic alteration that plays an important role in premature physiological deterioration and later-life susceptibility to chronic disease. In one paper, published in Social Science and Medicine, I found that Black youth who attended segregated and highly disadvantaged schools experienced accelerated biological aging, as measured by epigenetic clocks. I’ve also shown how interpersonal psychosocial stress, such as chronic bullying victimization, may impose lasting biological risks for youth. In a working paper focused on neighborhood contexts, I identified a dose-response relationship between residential proximity to deadly gun violence and accelerated biological aging during adolescence. The significance of this research lies in the utility of epigenetic data to predict future age-related morbidities and diverging health trajectories, highlighting opportunities to intervene before chronic disease onset and the manifestation of health inequities.
The second area of my research investigates how adult social contexts and psychosocial stressors influence racial inequities in chronic disease. I was awarded a competitive Ruth L. Kirschstein Predoctoral Individual National Research Service Award (F31) from the NIH to conduct this research, resulting in four first-authored papers that identified risk factors for racial inequities in disease progression among Black women with lupus. In a paper published in Brain, Behavior and Immunity, I was among the first to document a longitudinal association between incident experiences of racial discrimination and temporal increases in the inflammatory biomarker, C-reactive protein. I also moved the field forward by showing that beyond direct experiences of discrimination, vicarious or indirect exposure to racism-related stress contributes to racial inequities in lupus progression. Another paper, published in Health & Place, documented how residential segregation shapes exposure to neighborhood stressors and subsequent mental health comorbidities. In a fourth paper, I identified distinct sociodemographic profiles of organ damage accrual, providing useful information for clinicians in their assessment of subgroups at greatest risk of lupus progression. Collectively, these studies advance research on racial inequities in lupus by providing evidence—in a field dominated by biomedical approaches—on how social inequities accelerate disease progression for Black women.
My future research will build upon these areas by investigating mechanisms that link specific school and neighborhood contextual factors with age-related morbidities across the life course, offering critical insight into how social environments influence trajectories of health and aging.
Connor Martz, PhD 