Considering that vascular endothelial cell dysfunction is the pathological basis of erectile dysfunction (ED), and recognizing the beneficial effects of 25-hydroxyvitamin D (25(OH)D) on vascular endothelial cell protection, the researchers diligently investigated the causal relationship between serum 25(OH)D levels and ED. However, inconsistent clinical evidence has left the association between serum 25(OH)D levels and ED unclear. The objective of this work was to employ Mendelian randomization (MR) analysis to ascertain the potential causal relationship between serum 25(OH)D levels and ED. We conducted a two-sample MR analysis utilizing data from publicly available genome-wide association studies (GWASs). The primary analysis method for the MR analysis was the inverse-variance weighted (IVW) method, supplemented by the MR-Egger and weighted median methods. In addition, we evaluated heterogeneity with Cochran’s Q test, assessed pleiotropy using the MR-Egger intercept test, and performed a leave-one-out analysis to identify single-nucleotide polymorphisms (SNPs) with potential effects. Outliers were detected using MR-pleiotropy residual sum and outlier (MR-PRESSO). Genetically predicted serum 25(OH)D levels were not found to be causally associated with ED in IVW method (OR = 1.028, 95% CI = 0.845–1.250, P = 0.785), MR-Egger method (OR = 1.057, 95% CI = 0.782–1.430, P = 0.720), and weighted median method (OR = 1.225, 95% CI = 0.920–1.633, P = 0.165). The results of sensitivity analyses reinforced our conclusion, indicating no evidence of heterogeneity or directional pleiotropy. In summary, our findings do not substantiate a genetic-level causal link between serum 25(OH)D levels and the prevalence of ED. Nonetheless, future research, including larger MR studies, clinical trials, and additional observational studies, is essential to validate and reinforce the outcomes of our present study.

考虑到血管内皮细胞功能障碍是勃起功能障碍（ED）的病理基础，并认识到25-羟基维生素D（25（OH）D）对血管内皮细胞保护的有益作用，研究人员深入研究了血清25与(OH)D 水平和 ED。然而，不一致的临床证据使得血清 25(OH)D 水平与 ED 之间的关联尚不清楚。这项工作的目的是采用孟德尔随机化 (MR) 分析来确定血清 25(OH)D 水平与 ED 之间的潜在因果关系。我们利用公开的全基因组关联研究 (GWAS) 的数据进行了两个样本的 MR 分析。MR分析的主要分析方法是逆方差加权(IVW)法，辅以MR-Egger法和加权中值法。此外，我们使用 Cochran's Q 检验评估异质性，使用 MR-Egger 截距检验评估多效性，并进行留一分析以识别具有潜在影响的单核苷酸多态性 (SNP)。使用 MR 多效性残差和和离群值 (MR-PRESSO) 检测离群值。IVW 方法（OR = 1.028，95% CI = 0.845–1.250， P  = 0.785）、MR-Egger 方法（OR = 1.057，95%）中未发现基因预测的血清 25(OH)D 水平与 ED 存在因果关系。CI = 0.782–1.430，P  = 0.720）和加权中位数法（OR = 1.225，95% CI = 0.920–1.633，P  = 0.165）。敏感性分析的结果强化了我们的结论，表明没有异质性或方向性多效性的证据。总之，我们的研究结果并未证实血清 25(OH)D 水平与 ED 患病率之间存在基因水平因果关系。尽管如此，未来的研究，包括更大规模的 MR 研究、临床试验和其他观察性研究，对于验证和强化我们当前研究的结果至关重要。