Abstract
BACKGROUND: The relationship between Metabolic Syndrome and cancer remains controversial. The authors aimed to assess the association between Metabolic Syndrome and cancer risk at different locations using a Mendelian randomization approach. METHODS: The authors extracted single nucleotide polymorphisms (SNPs) of MetS and its components from public databases for populations of European ancestry. Causal effects were estimated using inverse variance weighting, MR-Egger, weighted median, and MR-PRESSO. Sensitivity analyses were performed using Cochran's Q test, MR-Egger intercept test, MR-PRESSO, leave-one-out analysis, and funnel plots. In addition, the authors calculated the Statistical power. Finally, the authors applied the False Discovery Rate (FDR) to correct our results. RESULTS: IVW methods showed that Genetically predicted Metabolic Syndrome may be a potential risk factor for hepatocellular carcinoma ( P =0.031, P-FDR=0.093). Metabolic Syndrome was not causally associated with cancers at other sites (lung, thyroid, breast, prostate, kidney, bladder, colorectal, esophagus, and stomach). In further analyses, WC may increase the risk of lung ( P =0.003, P-FDR=0.018), and esophageal ( P =0.011, P-FDR=0.066) cancers and decrease the risk of prostate cancer ( P =0.006, P-FDR=0.001). Furthermore, hypertension may reduce the risk of Hepatic cancer ( P =0.014, P-FDR=0.084). CONCLUSION: Our study suggests that genetically predicted Metabolic Syndrome may increase the risk of some cancers. Prevention and treatment of Metabolic Syndrome may help to prevent the development of related cancers.