Abstract 370: Corticosterone-mediated Associations Between Neighborhood Environment Perceptions and Lysosomal Acid Lipase Levels - Data From The Washington, D.C. Cardiovascular Health and Needs Assessment

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Experiences of adverse social determinants of health (SDoH), like less favorable neighborhood environment perceptions, are associated with cardiovascular disease (CVD). Lysosomal acid lipase (LAL) plays an important role in lipid metabolism, and genetic LAL deficiency has been linked to CVD risk. We aimed to determine the potential relationship between neighborhood perceptions and LAL and to evaluate stress-related biomarkers as mediators of this relationship in the D.C. Cardiovascular Health and Needs Assessment cohort (60 African American participants, mean age 61yr, 93% female), biomarkers were measured using ELISA, and perceptions of neighborhood violence, physical and social environment, social cohesion, and safety were determined using validated questionnaires with higher scores indicating more favorable perceptions. We explored neighborhood perceptions-LAL relationships with regression models adjusted for BMI and ASCVD risk score and stratified by hyperlipidemia due to the potential confounding role of LDL. Mediation analysis was used to evaluate cortisol and corticosterone as potential mediators of the neighborhood perceptions-LAL relationship. Of the neighborhood perceptions measured, more favorable perceptions of physical and social environment associated with greater LAL (β=0.23, p=0.09); this association persisted only among participants without hyperlipidemia (β=0.42, p=0.04). Only corticosterone associated with both perceived physical and social environment and LAL (Figure); corticosterone mediated 73.1% of this relationship in all participants and 89.9% of this relationship in participants without hyperlipidemia. Our data highlight the relationship between perceived physical and social environment and LAL mediated by corticosterone. Results also emphasize the importance of future interdisciplinary work to better understand mechanisms by which SDoH and associated biomarkers contribute to CVD disparities.

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