Although a large body of literature reported that high intake of vitamin E played a possible role in reducing risk of cardiometabolic diseases, conflicting results were also found in some observational studies due to confounding factors. Hence, we used a Mendelian randomization study as an alternative way to examine the causality between circulating vitamin E and cardiometabolic diseases. Summary-level data were extracted from consortia and three single nucleotide polymorphisms were used as instrumental variables. Our study showed that a one-SD increase in circulating vitamin E levels was causally associated with an increased risk of coronary artery disease [odds ratio (OR) 3.16 (95%CI 1.74, 5.73); p = 1.91 × 10−3] at the Bonferroni-adjusted level of significance (p<0.005). Moreover, a one-SD increase in circulating vitamin E levels was associated with a 0.572-SD increase in low density lipoprotein cholesterol (mg/dl), a 0.693-SD increase in total cholesterol (mg/dl), and a 1.45-SD increase in triglyceride (mg/dl), but a 0.502-SD decrease in high density lipoprotein cholesterol (mg/dl) at the Bonferroni-adjusted level of significance (p<0.0028). Our findings indicated that genetically elevated vitamin E was associated with increased risk of coronary artery disease, suggesting an adverse causality between circulating vitamin E and coronary artery disease.
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