The impact of cannabis use on erectile dysfunction and sex hormones: a Mendelian randomization analysis.

Abstract

Previous study has highlighted an association between cannabis use (CU) and an increased risk of erectile dysfunction (ED), potentially due to indirect effects on sex hormonal balance. However, the evidence remains controversial, and the causal relationship is unclear. This study utilized genome-wide association study (GWAS) data to investigate the causal relationships between cannabis use disorder (CUD), lifetime cannabis use (LCU), and ED, as well as levels of sex hormones including estradiol (E2), bioavailable testosterone (BT), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) through Mendelian randomization (MR) analysis. The primary method of analysis was the inverse variance weighted (IVW) method. Data from the FinnGen and UK Biobank were used for replication and meta-analysis. The results indicated no causal relationship between genetically predicted CUD (OR = 0.97, 95% CI 0.87-1.10, P = 0.66) and LCU (OR = 1.13, 95% CI 0.84-1.50, P = 0.42) with the risk of ED. The meta-analysis provided consistent evidence (P > 0.05). No causal relationships were found between CUD and LCU with E2(CUD: β = 0.00, 95% CI 0.00-0.01, P = 0.37; LCU: β = 0.00, 95% CI -0.02-0.01, P = 0.62), BT (CUD: β = 0.00, 95% CI -0.03-0.02, P = 0.90; LCU: β = 0.02, 95% CI -0.04-0.09, P = 0.46), FSH (CUD: β = 0.01, 95% CI -0.18-0.20, P = 0.92; LCU: β = 0.01, 95% CI -0.44-0.47, P = 0.95), and LH (CUD: β = 0.01, 95% CI -0.18-0.21, P = 0.90; LCU: β = 0.13, 95% CI -0.22-0.49, P = 0.46). Sensitivity analyses detected no evidence of horizontal pleiotropy or heterogeneity, ensuring the robustness of the results. In conclusion, this MR analysis did not provide evidence supporting a causal relationship between CU and ED or sex hormone levels.