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The food environment as a cardiometabolic exposure: mechanisms, inequities, and interacting environmental risk
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This review paper summarizes existing research on how neighborhood food environments, such as access to and cost of food, relate to heart and metabolic disease risk. It discusses how ultra-processed food exposure may contribute to obesity, diabetes, and heart disease, and notes these effects often overlap with other neighborhood risks, including air pollution and microplastics.
Background The exposome framework has expanded understanding of how cumulative environmental exposures influence cardiometabolic health. Although air pollution, green space, and socioeconomic factors are increasingly recognized within this framework, the food environment remains less consistently conceptualized as a structural cardiometabolic exposure. Methods This narrative review synthesizes current literature on food environment determinants, including availability, accessibility, affordability, and food insecurity, alongside common approaches used to operationalize food environments in research. We also review mechanistic and epidemiologic evidence linking unhealthy food environments, particularly those characterized by high exposure to ultra-processed foods, with cardiometabolic outcomes. Finally, we discuss interactions with walkability, air pollution, climate stressors, socioeconomic vulnerability, and emerging exposures such as microplastics. Results Food environments shape dietary behaviors through structural constraints that influence food choice, purchasing, and consumption. Unhealthy food environments may promote higher intake of ultra-processed foods and lower intake of minimally processed foods, contributing to obesity, insulin resistance, type 2 diabetes, cardiovascular disease, and chronic kidney disease through interconnected metabolic, inflammatory, and vascular pathways. These effects frequently cluster with other adverse neighborhood conditions, amplifying persistent and cumulative cardiometabolic risk contributing to health inequities. Current research is limited by heterogeneous exposure definitions, cross-sectional designs, residual confounding, and underrepresentation of low- and middle-income settings. Conclusions The food environment should be considered a major structural component of the cardiometabolic exposome. Improving its measurement and prioritizing longitudinal, equity-focused, and policy-relevant research will be essential to inform interventions that reduce cardiometabolic disease burden and disparities.
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