Systematic Evaluation of the Impact of a Wide Range of Dietary Habits on Myocardial Infarction: A Two-Sample Mendelian Randomization Analysis

Abstract

Background: Myocardial infarction is a cardiovascular disease that significantly contributes to global morbidity and disability. Given the significant role of diet in the pathogenesis and prevention of cardiovascular diseases, this study rigorously investigates the causal relationship between dietary habits and myocardial infarction.

Methods and results: This study used large-scale genome-wide association studies with pooled UK Biobank data to explore associations between 9 dietary categories (83 types) and myocardial infarction. A 2-sample Mendelian randomization approach was applied to assess these associations, while multivariate Mendelian randomization and mediation analyses investigated the role of lipids in mediating the effects of diet on myocardial infarction. Univariate Mendelian analyses revealed genetic associations among 9 categories of dietary habits (83 types) and myocardial infarction. Notably, robust evidence indicates the "tablespoons of cooked vegetables per day" as the most significant risk factor for myocardial infarction development. "Coffee consumption(cups per day)" and "frequency of adding salt to food" were also identified as supplementary risk factors. In contrast, "overall alcohol intake" showed a protective effect, potentially by increasing high-density lipoprotein cholesterol (4.48% mediation) and reducing triglycerides (6.24% mediation). Cereal category, particularly "cereal consumption (bowls per week)" was associated with reduced myocardial infarction risk, contributing by raising high-density lipoprotein cholesterol (3.69% mediation) and lowering total cholesterol (8.33% mediation). Additionally, "overall cheese consumption" was also protective against myocardial infarction.

Conclusions: Our findings elucidate the influence of dietary habits on myocardial infarction, showing underlying genetic mechanisms and emphasizing the regulatory role of lipids as an intermediate.

Keywords: Mendelian randomization; dietary habits; lipids; myocardial infarction.

Figure 1. Outline of the study design.

CARDIoGRAMplusC4D indicates Coronary Artery Disease Genome‐Wide Replication and Meta‐Analysis Plus the Coronary Artery Disease Genetics; GLGC, Global Lipids Genetics Consortium; HDL‐C, high‐density lipoprotein cholesterol; LDL‐C, low‐density lipoprotein cholesterol; MR, Mendelian randomization; MRC‐IEU, Medical Research Council Integrative Epidemiology Unit at the University of Bristol; TC, cholesterol; and TG, triacylglycerol.

Figure 2. Effect of dietary habits on myocardial infarction.

The type of dietary habits in the gray picture represents no causal relationship with the risk of myocardial infarction; the type of dietary habits in the color picture represents causal relationship with the risk of myocardial infarction. IVW indicates inverse variance weighted; MR, Mendelian randomization; MR‐PRESSO, Mendelian randomization Pleiotropy Residual Sum and Outlier; and MR‐RAPS, Mendelian randomization Robust Adjusted Profile Score.

Figure 3. Mediation analysis of the effect of dietary habits on myocardial infarction via potential mediators.

The blue arrow indicates the initial variable that decreases the risk associated with the tail variable. The red arrows represent the initial variables that elevate the risk associated with the subsequent variables. HDL‐C indicates high‐density lipoprotein cholesterol; TC, cholesterol; and TG, triacylglycerol.