The causal association between seven drugs and erectile dysfunction: a Mendelian randomization study

Many studies have shown that patients develop erectile dysfunction (ED) after taking or aggravating certain drugs. However, other studies have considered such conclusions to be inaccurate. To explore the genetically predicted associations between drug treatment and ED, we used publicly available genome-wide association study (GWAS) data to evaluate the relationship between seven drug treatment regimens and ED using two-sample Mendelian randomization (MR) analysis.

In this study, a two-sample Mendelian randomized design was used to evaluate the causal relationship between 40 drugs and the risk of ED using publicly available pooled data from the GWAS.

We employed five methods for MR analysis: MR-Egger, weighted median, inverse variance weighted (IVW), simple mode, weighted mode, MR-Egger intercept test, MR pleiotropy residual sum, and outlier global test to identify horizontal pleiotropy. Cochran's Q statistics were used for instrument heterogeneity tests, and the leave-one-out method was used for sensitivity analysis.

The results showed that simvastatin (p = 0.023), ramipril (p = 0.041), metformin (p = 0.00061), gliclazide (p = 0.015), atorvastatin (p = 0.037), atenolol (p = 0.0052), aspirin (p = 0.051), and simvastatin, and five other drugs were potentially associated with ED. After excluding confounding single-nucleotide polymorphisms (SNPs), the p-value of aspirin was slightly above 0.05, suggesting that aspirin may not have a potential causal relationship with ED, warranting further investigation to confirm this finding. No potential causal relationships were found between the remaining 33 exposures and ED.

Genetically predicted associations suggest that there may be potential causal relationships between simvastatin, ramipril, metformin, gliclazide, atorvastatin, atenolol, and ED, which require further research.