Alcohol intake and risk of systemic lupus erythematosus: a Mendelian randomization study. (February 2019)

• Record Type: Journal Article
• Authors: Bae, S C; Lee, Y H
• Is Part Of: Lupus. Volume 28:Number 2(2019)
• Page Start: 174
• Page End: 180
• Publication Date: 2019-02
• Subjects: Alcohol intake -- systemic lupus erythematosus -- Mendelian randomization; Systemic lupus erythematosus -- Periodicals; 616.772005
• DOI: 10.1177/0961203318817832
• Languages: English
• ISSNs: 0961-2033

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.