Alcohol intake and risk of rheumatoid arthritis: a Mendelian randomization study
- Alcohol intake and risk of rheumatoid arthritis: a Mendelian randomization study
- Alcohol intake; Rheumatoid arthritis; Mendelian randomization; Genetic predisposition to disease; Genome-wide association study
- Issue Date
- SPRINGER HEIDELBERG
- ZEITSCHRIFT FUR RHEUMATOLOGIE, v. 78, no. 8, Page. 791-796
- Objective. To examine whether alcohol intake is causally associated with rheumatoid arthritis (RA).
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 a GWAS meta-analysis of 5539 autoantibody-positive RA patients and 20,169 controls as the outcome.
Results. We selected 24 single nucleotide polymorphisms (SNPs) associated with alcohol intake frequency at genome-wide significance as instrumental variables (IVs) to improve inference, 16 of which were inversely associated with RA. The IVW method showed no evidence of a causal association between alcohol intake and RA (beta = 0.218, SE = 0.213, p = 0.306). The MR-Egger regression revealed that directional pleiotropy was unlikely to bias the result (intercept = 0.027, p = 0.292). The MR-Egger analysis and the weighted median approach showed no causal association between alcohol intake and RA (beta = -0.778, SE = 0.947, p = 0.420 and beta = -0.286, SE = 0.302, p = 0.344, respectively). Cochran's Q test did not indicate heterogeneity between IV estimates based on the individual variants, and results from a "leave-one-out" analysis demonstrated that no single SNP was driving the IVW point estimate.
Conclusion. The MR analysis does not support a causal inverse association between alcohol intake and RA occurrence.
- 0340-1855; 1435-1250
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