Key result
Ultraprocessed food intake links to incident CVD, mediated partially by central adiposity and IL-6.
Why the study?
Higher consumption of ultraprocessed foods has been consistently associated with increased cardiovascular disease risk, but the biological pathways underlying this relationship remain incompletely understood.
Do central adiposity and systemic inflammation mediate the association between ultraprocessed food intake and incident cardiovascular disease in adults free of baseline CVD?
Cohort (n=6,531)
Do central adiposity and systemic inflammation mediate the association between ultraprocessed food intake and incident cardiovascular disease in adults free of baseline CVD?
Effect estimate: β 0.012 (95% CI 0.007-0.017)
The increased risk of cardiovascular disease associated with ultraprocessed food consumption is partially mediated by central adiposity and systemic inflammation, supporting dietary strategies that limit UPFs.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“While much dietary guidance focuses on nutrient composition, our results underscore the relevance of food processing as a determinant of cardiometabolic health. Reducing [ultraprocessed food] consumption may confer cardiovascular benefits by limiting excess adiposity and attenuating chronic inflammation: two key drivers of atherosclerotic cardiovascular disease.”
Central adiposity and IL-6 may mediate UPF-CVD links; extends observational data but leaves causal inference and practice change open.
BACKGROUND: Higher consumption of ultraprocessed foods (UPFs) has been consistently associated with increased cardiovascular disease (CVD) risk, but the biological pathways underlying this relationship remain incompletely understood. OBJECTIVES: The study aims to examine whether body composition, systemic inflammation, and metabolic biomarkers mediate the association between UPF consumption and incident CVD. METHODS: MESA (Multi-Ethnic Study of Atherosclerosis) is a population-based, prospective cohort study of men and women aged 45 to 84 years who were free of clinically apparent CVD at baseline. UPFs were classified according to the Nova classification system. To evaluate potential pathways linking UPF intake with incident CVD, mediation analyses were conducted using generalized structural equation modeling and counterfactual-based causal mediation analysis. RESULTS: Among 6,531 participants, higher UPF intake was associated with adverse cardiometabolic profiles. In single-mediator generalized structural equation models, both waist-to-height ratio (β: 0.012; CI: 0.007-0.017) and interleukin (IL)-6 (β: 0.003; CI: 0.001-0.006) significantly mediated the association between UPF intake and incident CVD, with waist-to-height ratio mediating 44% and IL-6 mediating 13% of the total association. In parallel mediation models including waist-to-height ratio and IL-6 simultaneously, both mediators retained independent indirect effects, with adiposity contributing 38% and IL-6 contributing 9% of the proportion mediated. Results were consistent in magnitude and direction across counterfactual mediation analyses. CONCLUSIONS: The association between UPF consumption and CVD risk appears to be partially mediated through central adiposity and systemic inflammation. These findings provide mechanistic insight into how UPFs may contribute to CVD risk and support dietary strategies that limit UPFs to reduce cardiometabolic risk.
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Haidar et al. (2026) conducted a cohort in Cardiovascular disease risk (n=6,531). Ultraprocessed food intake was evaluated on Incident CVD (β 0.012, 95% CI 0.007-0.017). Ultraprocessed food intake association with incident cardiovascular disease was partially mediated by waist-to-height ratio (β 0.012; CI 0.007-0.017) and interleukin-6 (β 0.003; CI 0.001-0.006).
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