A recent Scientific Reports study used Mendelian randomization (MR) trials to explore the causal link between erectile dysfunction (ED) and inflammatory bowel disease (IBD).
The study found a causal association between IBD and ED. However, further research was needed to explore the potential mechanism of the causative relationship between IBD and ED.
Study: A Mendelian randomization study on causal effects of inflammatory bowel disease on the risk of erectile dysfunction. Image Credit: ciobanetre/Shutterstock.com
Background
IBD is a non-specific and chronic disease of the gastrointestinal tract. Ulcerative colitis (UC) and Crohn’s disease (CD) are its two main subtypes.
The former causes chronic inflammation of the mucosa of the colon and rectum, while the latter is associated with the inflammation of the tissues of the entire gastrointestinal tract.
Abdominal pain, diarrhea, various extraintestinal manifestations, and weight loss are frequently experienced by IBD patients, which significantly hampers their quality of life.
Research has shown that IBD could also influence sexual function. Patients of ED are unable to sustain or attain an erection for successful sexual intercourse. Although previous studies have demonstrated a correlation, the causal link between ED and IBD remains unclear.
About the study
The present study used MR trials to explore the causal link between ED and IBD. MR uses an instrumental variables (IV) approach and can eliminate the influence of reverse causality and confounding factors.
For successful MR trials, certain conditions must be met, namely, the existence of a correlation between the exposure and the IV, the absence of a correlation between the IV and confounding variables, and the ability of the IV to affect the outcome through exposure solely.
Concerning IVs, single nucleotide polymorphisms (SNPs) are frequently used. These genetic elements are, therefore, free from time, lifestyle, and the environment.
Genome-wide association studies (GWAS) were used to obtain data for this study, where ED was deemed an outcome factor and IBD was the exposure factor.
Key findings
The MR analyses conducted here suggested that IBD indeed has a causal effect on ED. The subtype analysis found that UC may not lead to heightened ED risk, but CD could. Various sensitivity analyses established the robustness of these results.
With respect to heterogeneity, no significant heterogeneity was noted between IBD and ED. However, heterogeneity was noted in the UC subgroup.
The fact that UC may not cause ED was demonstrated through an inverse variance-weighted random-effects model. Furthermore, no significant horizontal pleiotropy was observed.
Several studies have highlighted that IBD patients report a higher prevalence of ED. In fact, one cross-sectional study of 208 IBD patients and 190 normal individuals showed that the IBD patients reported a prevalence of ED, which was three times that of normal subjects. This study additionally highlighted depression as an independent risk factor for ED.
Another related study documented that the prevalence of ED in IBD patients was as high as 30.3%. Contrary to these results, there exists at least one other study that did not report an increased prevalence of ED among IBD patients compared to healthy controls.
Despite the presence of many studies suggesting a potential correlation between IBD and ED risk, there have been no causal studies establishing the link between IBD and ED.
Moreover, in many of the cross-sectional studies, confounding factors and reverse causality have made causal inference difficult. This study is the first to establish a causal link between IBD and ED, and it could facilitate a better understanding of the sexual activity in IBD patients.
Here, it was hypothesized that depression may be a mediator for ED in IBD patients because, like most other chronic diseases, IBD adversely affects psychological health.
An additional concern to keep in mind is that IBD medications may cause ED, as evidenced by the cases of sulfasalazine-induced ED.
Stoma and rectal surgery are common surgical procedures for IBD, but there exists the risk of damage to pelvic nerves. This study avoided confounding factors related to age, treatment, and mental state due to the use of MR trials.
Conclusions
This study also has some limitations. The key limitation is that the data was sourced from GWAS, which comprises mainly European nationals. This raises questions about the generalizability of the findings and the extension to non-European populations.
Secondly, no mediation analyses were conducted despite the possibility of mediating factors.
Thirdly, an ED subtype analysis could not be performed due to the lack of data. Finally, the results could have been affected by the fact that the ratio of the overlapping subgroup was not sufficiently clear in the sample.
In sum, this is the first study that documented a causal link between IBD and ED. Furthermore, it was also shown that IBD and its subtype CD could lead to an increased risk of ED, but this causal link could not be established in the case of UC. Future research should focus on the underlying mechanisms through which IBD leads to ED.
IBD increases type 1 diabetes risk, revealing a bidirectional link between the two conditions