recent Scientific report The study used Mendelian randomization (MR) trials to explore the causal link between erectile dysfunction (ED) and inflammatory bowel disease (IBD).
Studies have found a causal relationship between IBD and ED. However, further studies were needed to explore the potential mechanism of the causal relationship between IBD and ED.
Study: A Mendelian Randomization Study on the Causal Effect of Inflammatory Bowel Disease on the Risk of Erectile Dysfunction. Image credit: ciobanetre/Shutterstock.com
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 inflammation of tissues throughout the gastrointestinal tract.
Abdominal pain, diarrhea, various external manifestations and weight loss are often experienced by IBD patients, which significantly disrupts their quality of life.
Studies have shown that IBD can also affect sexual function. Patients with ED are unable to sustain or have an erection for successful intercourse. Although previous studies have demonstrated a correlation, the causal link between ED and IBD remains unclear.
About the study
The current study used MR trials to explore the causal link between ED and IBD. MR uses an instrumental variables (IV) approach and can eliminate the effects of reverse efficacy and confounding factors.
For a successful MR trial, certain conditions must be met, namely, the existence of correlation between exposure and IV, the absence of correlation between IV and confounding variables, and the ability of IV to influence the outcome through exposure alone. .
For IV, single nucleotide polymorphisms (SNPs) are often used. These genetic factors are therefore independent of time, lifestyle and environment.
Genome-wide association studies (GWAS) were used to obtain data for this study, in which ED was believed to be an outcome factor and IBD was an exposure factor.
The MR analyzes conducted here suggested that IBD indeed has a causal effect on ED. Subtype analysis showed that UC may not increase ED risk, but CD may. Various sensitivity analyzes established the robustness of these results.
In terms of diversity, no significant differences were noted between IBD and ED. However, heterogeneity was observed in UC subgroups.
The fact that UC does 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. Indeed, a cross-sectional study of 208 IBD patients and 190 normal individuals showed that 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 was as high as 30.3% in IBD patients. In contrast to these findings, there is at least one other study that did not report an increased prevalence of ED in IBD patients compared with healthy controls.
Despite the presence of many studies indicating a possible correlation between IBD and ED risk, there have been no causal studies establishing a link between IBD and ED.
Furthermore, in many cross-sectional studies, established causality and reverse causality make causal inference difficult. This study is the first to establish a causal link between IBD and ED and may facilitate a better understanding of sexual activity in IBD patients.
Here, it was hypothesized that depression may be a mediator for ED in IBD patients because, like other chronic diseases, IBD adversely affects mental health.
An additional concern to keep in mind is that IBD medications can cause ED, as evidenced in cases of sulfasalazine-induced ED.
Stoma and rectal surgery are common surgical procedures for IBD, but there is a risk of pelvic nerve damage. This study avoided confounding factors related to age, treatment, and psychiatric status due to the use of MR trials.
This study also has some limitations. The main limitation is that the data were derived from GWAS, which mainly consisted of European citizens. This raises questions about the generalizability of the findings and the extension to non-European populations.
Second, no mediation analysis was performed despite the possibility of mediating factors.
Third, an ED subtype analysis could not be performed due to lack of data. Finally, the results may have been influenced by the fact that the proportion of overlapping subgroups was not sufficiently clear in the sample.
In summary, this is the first study to document a causal link between IBD and ED. Furthermore, it was also shown that IBD and its subtype CD may increase the risk of ED, but this causal link could not be established for UC. Future research should focus on the underlying mechanisms by which IBD leads to ED.