Abstract
Over the years, numerous observational studies have substantiated that various dietary choices have opposing effects on cardiovascular disease. However, the causal effect has not yet been established. Thus, we conducted a Mendelian randomization (MR) analysis to reveal the causal impact of dietary habits on cardiovascular disease (CVD). Genetic variants strongly associated with 20 dietary habits were selected from publicly available genome-wide association studies conducted on the UK Biobank cohort (n = 449,210). Summary-level data on CVD were obtained from the FinnGen study, MEGASTROKE consortium, CARDIoGRAMplusC4D consortium, HERMES consortium, and other consortia (n=159 836 - 977 323). The inverse variance weighted method (IVW) was the primary outcome, while MR-Egger, weighted median, and MR Pleiotropy RESidual Sum and Outlier were used to assess heterogeneity and pleiotropy. We found compelling evidence of a protective causal effect of genetic predisposition towards cheese consumption on myocardial infarction (IVW OR = 0.67; 95% CI = 0.544-0.826; P = 1.784×10-4) and heart failure (IVW OR = 0.646; 95% CI = 0.513-0.814; P = 2.135×10-4). Poultry intake was found to be a detrimental factor for hypertension (IVW OR = 4.306; 95% CI = 2.158-8.589; P = 3.416×10-5), while dried fruit intake was protective against hypertension (IVW OR = 0.473; 95% CI = 0.348-0.642; P = 1.683×10-6). Importantly, no evidence of pleiotropy was detected. Mendelian randomization estimates provide robust evidence for a causal relationship between genetic predisposition to different dietary habits and CVD risk, suggesting that well-planned diets may help prevent and reduce the risk of CVD.
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