Genetically predicted insomnia causally increases the risk of erectile dysfunction

Abstract

Sleep has attracted extensive attention due to its significance in health. However, its association with erectile dysfunction (ED) is insufficiently investigated. To investigate the potential causal links between sleep traits (insomnia, sleep duration, and chronotype) and ED, this study was performed. The single-nucleotide polymorphisms (SNPs) associated with insomnia, sleep duration, and chronotype were retrieved from previous genome-wide association studies (GWAS). A conventional two-sample Mendelian randomization (MR) was used to estimate the causal links between sleep traits and ED. The summary statistics of ED were from individuals of European ancestry (6175 cases vs 217 630 controls). As shown by the random effect inverse-variance-weighting (IVW) estimator, genetically predicted insomnia was causally associated with a 1.15-fold risk of ED (95% confidence interval: 1.07–1.23, P < 0.001). Sleep duration and morningness were not causally associated with ED, as indicated by the IVW (all P > 0.05). These findings were consistent with the results of sensitivity analyses. Based on genetic data, this study provides causal evidence that genetically predicted insomnia increases the risk of ED, whereas sleep duration and chronotype do not.

Insights into modifiable risk factors of erectile dysfunction, a wide-angled Mendelian Randomization study

“…Therefore, to prevent ED, we recommend giving up cigarette and alcohol consumption. In line with previous observational studies and MR analyses, we also report a significant association between insomnia, snoring, and ED [43] , [44] , [45] . Clinicians should recognize and treat sleep disorders in the general population, especially in patients with ED.…”

Causal association of cardiovascular disease with erectile dysfunction: a two‐sample bidirectional Mendelian randomization analysis

“…32,33 Snoring and insomnia were also shown, in previous MR studies, to contribute to the development of ED, but in view of the high data overlap, they were excluded in the confounders. 34,35 With adjustment for confounders, our MVMR further revealed that the casual effects of genetic susceptibility to IS on ED were not mediated by relevant screening confounders, as compared with CHD and HF. Thus, physicians should pay more attention to ED progression in patients with IS.…”

“…Thus, it is necessary to include confounders in MVMR analysis (both the recognized risk factors and diseases recently proven by MR studies, such as T2D, dyslipidaemia, obesity, smoking, and COVID‐19) 32,33 . Snoring and insomnia were also shown, in previous MR studies, to contribute to the development of ED, but in view of the high data overlap, they were excluded in the confounders 34,35 . With adjustment for confounders, our MVMR further revealed that the casual effects of genetic susceptibility to IS on ED were not mediated by relevant screening confounders, as compared with CHD and HF.…”

Causal relationship between air pollution, lung function, gastroesophageal reflux disease, and non-alcoholic fatty liver disease: univariate and multivariate Mendelian randomization study

“…Furthermore, we excluded palindromic SNPs with ambiguous minor allele frequencies falling outside the range of >0.45– < 0.55, as well as incompatible allele combinations from different individuals at two or more loci, to ensure the integrity of the dataset ( 25 ). We also calculated the F statistic, F = beta^2/SE^2, to assess the strength of the IVs, excluding those with corresponding F-statistic values below 10 as weak IVs ( 26 ). Additionally, we performed leave-one-out sensitivity analysis, excluding one SNP at a time and conducting IVW analysis on the remaining SNPs to exclude specific SNPs driving significant effects ( 27 ).…”