Khera · The New England journal of medicine 2016 · prospective and cross-sectional cohort study · n=55685

Genetic Risk, Adherence to a Healthy Lifestyle, and Coronary Disease.

Cited 1507 times in the scientific literature.

Level 3 - non-randomized controlled study

Prospective cohort studies combined with a cross-sectional cohort analysis

PubMed 27959714 · doi:10.1056/NEJMoa1605086 · record verified 2026-08-28

What was done

Researchers assessed the relationship between genetic risk, lifestyle adherence, and coronary artery disease across four cohorts totaling 55,685 participants: three prospective cohorts (ARIC [n = 7,814], WGHS [n = 21,222], and MDCS [n = 22,389]) and one cross-sectional cohort (BioImage [n = 4,260]). Genetic risk was quantified using a polygenic risk score. Lifestyle was categorized based on four factors: no current smoking, no obesity, regular physical activity, and a healthy diet (favorable: ≥3 factors; unfavorable: 0-1 factor). Outcomes evaluated included incident coronary events and coronary-artery calcification.

What was found

Participants at high genetic risk (top quintile) had a 91% higher relative risk of incident coronary events compared to those at low genetic risk (bottom quintile) (hazard ratio [HR], 1.91; 95% CI, 1.75 to 2.09). Across all genetic risk tiers, a favorable lifestyle was associated with lower risk. Among participants at high genetic risk, a favorable lifestyle was associated with a 46% lower relative risk of coronary events compared to an unfavorable lifestyle (HR, 0.54; 95% CI, 0.47 to 0.63). Standardized 10-year incidence of coronary events decreased from 10.7% to 5.1% in ARIC, 4.6% to 2.0% in WGHS, and 8.2% to 5.3% in MDCS. In the BioImage study, a favorable lifestyle was associated with significantly less coronary-artery calcification across all genetic risk groups.

Why it matters

High genetic risk for coronary artery disease can be substantially offset; adhering to a healthy lifestyle is associated with nearly halving coronary event risk even among individuals in the highest genetic risk tier.

Limits

The observational design cannot establish causality. Ancestry, detailed demographic characteristics, and residual confounding factors are not described in the abstract. One cohort (BioImage) was cross-sectional and measured coronary-artery calcification rather than clinical outcomes.

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