Abstract

Background: Observational studies showed that educational attainment (EA) is associated with cardiometabolic diseases, but the long interval between exposure and outcome makes it difficult to infer causality. We herein used Mendelian randomization (MR) to examine the causal effects of EA on adiposity, type 2 diabetes (T2D), and coronary artery disease (CAD).Methods: A two-sample MR analysis was conducted using genome-wide association study (GWAS) summary statistics. Seventy-four instrumental variables (IVs) were used to determine the causal effect of EA on cardiometabolic diseases. Sensitivity analyses were also performed to detect the pleiotropy of the IVs.Results: Using the MR approach, we found that each additional year in EA is associated with a reduction in the body mass index (BMI) (β −0.17 [95% CI −0.23, −0.10], P = 8.85 × 10−7), a 39% reduction in the odds of having T2D (OR 0.61 [95% CI 0.50, 0.75], P = 1.16 × 10−6), and a 36% reduction in the odds of having CAD (OR 0.64 [95% CI 0.55, 0.75], P = 2.38 × 10−8) at the Bonferroni-adjusted level of significance.Conclusion: Our findings suggest a causal role of EA on the cardiometabolic diseases including adiposity, T2D, and CAD.

Highlights

  • Observational studies have consistently showed that socioeconomic status such as low education is associated with an increased risk of cardiovascular disease (CVD) and mortality [1,2,3,4], but disentangling causality is challenging due to the long interval between exposure and outcome

  • Standard inverse variance–weighted (IVW) Mendelian randomization (MR) analysis showed that 1 year longer education was associated with a reduction in the body mass index (BMI)

  • The intercept term estimated for the BMI from MR-Egger regression did not differ from 0, suggesting that individual single nucleotide polymorphisms (SNPs) heterogeneity was largely balanced (Table 1)

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Summary

Introduction

Observational studies have consistently showed that socioeconomic status such as low education is associated with an increased risk of cardiovascular disease (CVD) and mortality [1,2,3,4], but disentangling causality is challenging due to the long interval between exposure and outcome. A recent MR study indicated a causal association between low EA and increased risk of smoking, which might explain the observational associations between EA and adverse health outcomes such as coronary artery disease (CAD) [8]. Observational studies showed that educational attainment (EA) is associated with cardiometabolic diseases, but the long interval between exposure and outcome makes it difficult to infer causality. We used Mendelian randomization (MR) to examine the causal effects of EA on adiposity, type 2 diabetes (T2D), and coronary artery disease (CAD)

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