O-58 - Each +300 mg-day dietary cholesterol associated with higher CVD (HR 1.17) and mortality (1.18) across 6 US cohorts
The dietary-cholesterol exposure result. Associations were monotonic with no significant nonlinear terms (P for nonlinear 0.19-0.83), i.e. no apparent threshold.
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Individual-participant-data pooling of 6 US prospective cohorts (ARIC, CARDIA, CHS, Framingham Offspring, Jackson Heart Study, MESA — the NHLBI Lifetime Risk Pooling Project; D-1), 29,615 participants (mean age 51.6; 44.9% men; 31.1% Black), data 1985-2016, median follow-up 17.5 years (max 31.3); 5,400 incident CVD events, 6,132 deaths. Self-reported diet (mostly a single baseline FFQ/diet-history per cohort) was harmonized across instruments via a standardized protocol. Exposures: dietary cholesterol (mg/day) and egg consumption (number/day). Outcomes: incident CVD (composite of fatal/nonfatal CHD, stroke, heart failure, other CVD death) and all-cause mortality, reported as HR and absolute risk difference over follow-up, adjusted for demographic, socioeconomic, and behavioral factors; a further model adds dietary cholesterol to the egg model. Observational design with mostly single-baseline diet (regression-dilution and residual-confounding vulnerability).
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Why this is evidence
H-27 is framed as harm operating through dietary cholesterol (of which eggs are a major source), so a monotonic, threshold-free dietary-cholesterol dose-response on hard CVD and mortality endpoints is close to its core prediction. H-21 (no causal egg/mortality effect) and H-6 (protection) predict no such positive cholesterol gradient. The observation is on dietary cholesterol rather than eggs directly, hence it discriminates the harm anchor only to the extent egg cholesterol carries the exposure — the egg-specific version is O-59.