This study aimed to examine whether smoking behavior is causally related to gout. Summary statistics of publicly available data from genome-wide association studies (GWAS) of smoking behavior (n = 85,997) served as the exposure dataset, while meta-analysis results of 14 studies including 2115 cases and 67,259 controls of European descent served as the outcome dataset. The data were subjected to two-sample Mendelian randomization (MR) analysis using the inverse-variance weighted (IVW), weighted median, and MR-Egger regression methods. Five single-nucleotide polymorphisms (SNPs) from GWAS of smoking behavior were selected as instrumental variables (IVs) to improve inference: CHRNA3 (rs1051730), PDE1C (rs215614), CYP2A6 (rs4105144), CHRNB3 (rs6474412), and CYP2B6 (rs7260329). The IVW data did not support a causal association between smoking behavior and gout (beta = − 0.035, SE = 0.036, p = 0.333). MR-Egger regression indicated that directional pleiotropy did not bias the result (intercept = 0.021; p = 0.560). MR-Egger analysis revealed no causal association between smoking behavior and gout (beta = − 0.074, SE = 0.070, p = 0.366). The weighted median approach did not support a causal association between smoking behavior and gout (beta = − 0.043, SE = 0.040, p = 0.279). Cochran’s Q test indicated no evidence of heterogeneity between IV estimates based on individual variants. The results of “leave one out” analysis demonstrated that no single SNP drove the IVW point estimate. MR estimates using IVW, weighted median, and MR-Egger analysis were consistent and did not support a causal inverse association between smoking behavior and gout.
- Mendelian randomization
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