Abstract
BACKGROUND: The causal relationship between the level of serum 25-hydroxyvitamin D [25(OH)D] and the risk of erectile dysfunction (ED) is still unclear. AIM: We tried to determine the causal relationship between the level of serum 25(OH)D and ED risk. METHODS: In this study, we used genome-wide association study data from the UK Biobank to analyse the relationship between serum 25(OH)D (as the exposure) and ED (as the outcome). Linkage disequilibrium score regression (LDSC) was used to assess the genetic correlation between 2 traits. The CAUSE (Causal Analysis using Summary Effect estimates) method and Mendelian randomization (MR) were employed to evaluate the bidirectional causal relationship. The MRlap method was utilized to assess the impact of sample overlap on the results. To assess potential heterogeneity and horizontal pleiotropy, we utilized methods such as MR-Egger, MR-PRESSO (Mendelian Randomization Pleiotropy Residual Sum and Outlier), weighted median, and others. OUTCOMES: The primary outcome was defined as self or physician-reported ED, or using oral ED medication, or a history of surgery related to ED. RESULTS: The LDSC analysis did not reveal a significant genetic correlation between serum 25(OH)D and ED (r(g) = 0.2787, P = .3536). Additionally, the CAUSE (P value testing that the causal model is a better fit >.05) and MR analyses (odds ratio, 0.8951; 95% confidence interval, 0.7480-1.0710; P = .2260) did not support a causal relationship between 25(OH)D and ED, and our study did not detect any heterogeneity and pleiotropy. CLINICAL IMPLICATIONS: This study provides evidence on whether vitamin D needs to be ingested to prevent or treat ED. STRENGTHS AND LIMITATIONS: We used LDSC and MR to avoid bias. However, the population in this study was limited to European ancestry. CONCLUSION: No causal relationship was found between 25(OH)D and ED.