A Mendelian randomization study between metabolic syndrome and its components with prostate cancer

Abstract Previous research has produced inconsistent findings concerning the connection between metabolic syndrome and prostate cancer. It is challenging for observational studies to establish a conclusive causal relationship between the two. However, Mendelian randomization can provide stronger evidence of causality in this context. To examine the causal link between a metabolic composite and its components with prostate cancer, we performed a two-sample Mendelian randomization (MR) study utilizing aggregated data from genome-wide association studies, followed by meta-analyses. In our study, we employed inverse variance weighting as the primary method for MR analysis. Additionally, we assessed potential sources of heterogeneity and horizontal pleiotropy through the Cochran’s Q test and MR-Egger regression. Moreover, we used multivariate MR to determine whether smoking versus alcohol consumption had an effect on the outcomes. We found no causal relationship between metabolic syndrome and its components and prostate cancer(MetS, odds ratio [OR] = 0.95, 95% confidence interval [CI] = 0.738–1.223, p = 0.691; TG, [OR] = 1.02, 95%[CI] = 0.96–1.08, p = 0.59); HDL, [OR] = 1.02, 95% [CI] = 0.97–1.07, p = 0.47; DBP, [OR] = 1.00, 95%[CI] = 0.99–1.01, p = 0.87; SBP, [OR] = 1.00, 95%[CI] = 0.99–1.00, p = 0.26; FBG [OR] = 0.92, 95%[CI] = 0.81–1.05, p = 0.23; WC, [OR] = 0.93, 95%[CI] = 0.84–1.03, p = 0.16). Finally, the MVMR confirms that the metabolic syndrome and its components are independent of smoking and alcohol consumption in prostate cancer. We didn’t find significant evidence to determine a causal relationship between the metabolic syndrome and its components and prostate cancer through MR analysis. Further research is necessary to explore the potential pathogenesis between the two diseases.