Psychosocial Epidemiology

An area of some contention has been whether psychological stress is truly a mechanism by which social disparities influence health. Research has consistently demonstrated that social adversity is associated with greater likelihood of complex physical diseases (e.g., cancer, cardiovascular diseases). As a result, social disparities in health are often attributed to social adversity. Though we have long known about these relationships, why they persist, exactly how they occur, or how we might mitigate the effects remains unclear. Emotions and other psychological factors both shape and are shaped by social processes; thus, if they truly influence disease processes they provide a likely mechanism by which social processes (e.g., nurturing, adversity) influence physical health. Research on whether emotions influence disease development is often susceptible to concerns about reverse causality and the difficulty in detecting effects that accumulate slowly over long periods of time. Thus, a primary goal has been to provide rigorous and compelling evidence that social and emotional experiences influence chronic disease development.

My work in psychosocial epidemiology (along with that of others) has highlighted our limited understanding of how fundamental biological processes reflect social conditions. Studies directly evaluating molecular and cellular processes linking emotions with disease endpoints are rare. I have conducted research designed to fuse social epidemiologic and experimental studies and employing novel analytic techniques to elucidate causal mechanisms that explain how the social environment gets under the skin. This involves translating questions derived from population-based research into experimental studies, and then testing experimental findings more precisely in population-based studies. Studies in this line of work have integrated neurobiology with higher-order processes resulting in an enhanced understanding of the interplay between micro- (e.g., cellular), meso- (e.g., psychological) and macro-level (e.g., social structure) factors. This approach directly addresses concerns about causal inference and biological plausibility.

Sample Publications:

• Lee HH, Okuzono S, Trudel-Fitzgerald C, James P, Koga HK, Sims M, Grodstein F, Kubzansky LD. Social integration and risk of mortality among African-Americans: The Jackson Heart Study. Social Psychiatry and Psychiatric Epidemiology, 2023; 58:1317-1327. PMCID: PMC10423160.
• Shutta KH, Balasubramanian R, Huang T, Jha SC, Zeleznik OA, Kroenke CH, Tinker LF, Smoller JW, Casanova R, Tworoger SS, Manson JE, Clish CB, Rexrode KM, Hankinson SE, Kubzansky LD. Plasma metabolomic profiles associated with chronic distress in women. Psychoneuroendocrinology, 2021; 133:105420. PMCID: PMC8547060.