SynthesisInternational journal of impotence research2025
The impact of cannabis use on erectile dysfunction and sex hormones: a Mendelian randomization analysis.
Synthesis in International journal of impotence research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Multi-Ancestry Mendelian Randomization Reveals Lipid-Associated Genetic Risk Factors for COPD.International journal of chronic obstructive pulmonary disease · 2025Pooled it
- Synthetic Cannabinoid AB-FUBINACA Negatively Impacted the Male Fertility and Induced Testicular Toxicity.Forensic toxicology · 2026Article
- Disentangling Nicotine vs Non-Nicotine Components of Tobacco Exposure in Psoriasis and Psoriatic Arthritis: A Multivariable and Trans-Ethnic Mendelian Randomization Study.Clinical, cosmetic and investigational dermatology · 2026Article
- Drugs Used in "Chemsex"/Sexualized Drug Behaviour-Overview of the Related Clinical Psychopharmacological Issues.Brain sciences · 2025Review
- Mapping the Four Adiposity Axes-Inflammatory Cytokine-Venous Thromboembolism Risk Landscape: A Two-Step Mediation Mendelian Randomization Analysis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.