Key result
Ultra-processed food intake is linked to ~5% higher heart failure risk per daily serving.
Why the study?
Ultra-processed foods are linked to adverse cardiometabolic outcomes and increased atherosclerotic CVD risk, but the relationship between UPF intake and incident HF, along with its potential biological mediators, remained incompletely understood.
Does higher ultra-processed food consumption increase the risk of incident heart failure in adults free of baseline cardiovascular disease?
Cohort (n=6,531)
Does higher ultra-processed food consumption increase the risk of incident heart failure in adults free of baseline cardiovascular disease?
Answers are grounded in this paper and cite their sources.
Higher consumption of ultra-processed foods is significantly associated with an increased risk of incident heart failure—specifically HFpEF—with central adiposity statistically accounting for roughly half of this relationship.
Background Ultra-processed foods (UPFs) are associated with adverse cardiometabolic outcomes and increased atherosclerotic cardiovascular disease (CVD) risk. However, the relationship between UPF intake and incident heart failure (HF) remains incompletely understood. Objective To examine the relationship between UPF consumption and incident HF, and to evaluate potential biological mediators. Methods A sample of 6,531 U.S. adults aged 45–84 years without CVD at baseline from the Multi-Ethnic Study of Atherosclerosis was analyzed. UPF intake was classified according to the Nova system. Multivariable Cox proportional hazards models evaluated associations between UPF intake and incident HF. Phenotypes were classified as HF with reduced ejection fraction (HFrEF; EF <50%) or HF with preserved ejection fraction (HFpEF; EF ≥50%). Mediation analyses were conducted to evaluate the potential mediating role of waist-to-height ratio as a surrogate measure for central adiposity. Results Higher UPF intake was significantly associated with increased risk of incident HF across sequentially adjusted models. In the primary model (Model 2), each additional daily serving of UPF was associated with a 5% higher risk of incident HF (HR 1.052; 95% CI 1.002–1.103). When stratified by phenotype, UPF intake remained significantly associated with HFpEF (HR 1.096; 95% CI 1.016–1.183), but not HFrEF. Participants in the upper 80% of UPF intake had a more than two-fold higher risk of HFpEF compared with the lowest 20% (HR 2.234; 95% CI 1.289–3.874). In mediation analyses, waist-to-height ratio statistically accounted for approximately 51% of the association between UPF intake and total HF and 49% of the association between UPF intake and HFpEF. Conclusion Higher UPF consumption was significantly associated with an increased risk for incident HF, with associations primarily driven by the HFpEF phenotype. Central adiposity, measured by waist-to-height ratio, demonstrated a potential mediating role, suggesting that obesity-related cardiometabolic pathways may represent an important pathway linking UPF consumption to HF risk.
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Haidar et al. (2026) conducted a cohort in Free of cardiovascular disease at baseline (evaluated for incident heart failure) (n=6,531). Ultra-processed food (UPF) consumption (Nova system) vs. Lower UPF intake (including lowest 20% of UPF intake) was evaluated on Incident heart failure (HF) (HR 1.052, 95% CI 1.002-1.103). Each additional daily serving of ultra-processed food was associated with a 5% higher risk of incident heart failure (HR 1.052; 95% CI 1.002-1.103), driven by HFpEF (HR 1.096).
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