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

Dec 13, 2018Lupus

Alcohol consumption and the risk of developing lupus: a genetic analysis study

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Abstract

No causal association was found between alcohol intake and systemic lupus erythematosus (SLE) in a study of 336,965 participants.

Analysis utilized 20 genetic variants linked to alcohol intake to assess potential causal relationships.
The inverse-variance weighted method showed no significant association (beta = -0.413, p = 0.421).
MR-Egger regression and weighted median methods also indicated no causal link (beta = -1.494, p = 0.464; beta = -0.538, p = 0.349, respectively).
Directional pleiotropy was unlikely to influence the results, as indicated by MR-Egger regression (intercept = 0.031, p = 0.582).
Findings suggest that alcohol consumption does not causally influence the occurrence of SLE.

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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.

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

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