Introduction: Cardiometabolic disease (CMD) may influence lung cancer risk through shared biological pathways and treatment effects. We examined clinical and genetic factors underlying comorbidity between CMD and lung cancer. Method: We analyzed 214,096 adults with CMD or lung cancer using electronic health record data. Variables included age, sex, body mass index, smoking status, CMD subtype, statin use, and cancer history. We used logistic regression to estimate the association of CMD phenotypes with lung cancer incidence, adjusting for demographics and smoking. We conducted age-stratified analyses and performed Mendelian randomization using genome-wide association summary statistics to assess genetic correlations between CMD traits and lung cancer. Results: Atrial fibrillation (OR 1.24, 95% CI 1.19–1.29), myocardial infarction (OR 1.20, 95% CI 1.16–1.25), heart failure (OR 1.35, 95% CI 1.30–1.39), and coronary atherosclerosis (OR 1.36, 95% CI 1.31–1.41) were associated with higher lung cancer risk. Dyslipidemia (OR 0.75, 95% CI 0.66–0.86), hypertension (OR 0.69, 95% CI 0.65–0.73), and type 2 diabetes (OR 0.95, 95% CI 0.92–0.99) were inversely associated. Statin use modestly increased risk (OR 1.05, 95% CI 1.01–1.08), with fluvastatin and atorvastatin showing the strongest effects. Mendelian randomization indicated a genetic association between type 2 diabetes liability and lung cancer (OR 1.14, 95% CI 1.08–1.21). Conclusion: We found that cardiometabolic conditions and their treatments are associated with lung cancer risk through both clinical and genetic pathways. Understanding these shared determinants may improve risk stratification and support integrated prevention strategies targeting cardiovascular and pulmonary health.
Adebamowo et al. (2026) studied this question.