Alcohol intake and risk of systemic lupus erythematosus: a Mendelian randomization study

Abstract

Objectives: This study aimed to examine whether alcohol intake is causally associated with systemic lupus erythematosus (SLE).

Methods: We performed a two-sample Mendelian randomization (MR) analysis using the inverse-variance weighted (IVW), weighted median, and MR-Egger regression methods. We used the publicly available summary statistics of alcohol intake frequency from the UK Biobank genome-wide association studies (GWASs; n = 336,965) as the exposure and an SLE GWAS consisting of 1311 SLE and 1783 control subjects of European descent as the outcome.

Results: We selected 20 single nucleotide polymorphisms (SNPs) associated with alcohol intake frequency at genome-wide significance as instrumental variables to improve inference. The IVW method found no evidence to support a causal association between alcohol intake and SLE (beta = -0.413, SE = 0.513, p = 0.421). The MR-Egger regression revealed that directional pleiotropy was unlikely to bias the result (intercept = 0.031, p = 0.582). The MR-Egger analysis found no causal association between alcohol intake and SLE (beta = -1.494, SE = 1.996, p = 0.464). Likewise, the weighted median approach also did not provide evidence of a causal association between alcohol intake and SLE (beta = -0.538, SE = 0.574, p = 0.349). The MR estimates determined using the IVW, weighted median, and MR-Egger regression methods were consistent and results from a "leave-one-out" analysis demonstrated that no single SNP was driving the IVW point estimate.

Conclusions: The results of MR analysis do not support a causal inverse association between alcohol intake and SLE occurrence.

Keywords: Alcohol intake; Mendelian randomization; systemic lupus erythematosus.