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ARTICLE
Unraveling the bidirectional association between mental disorders and prostatitis: insights from a genetic perspective
Guancan Liang#, Jian Pan#, Ruixiang Dai, Ziyi Lin, Xunbao Wang, Teng Hou, Zhicheng Luo, Xiaoming Wang*
Department of Urology, South China Hospital of Shenzhen University, Shenzhen, China
* Corresponding Author: Xiaoming Wang. Email: 
# Equal contribution
(This article belongs to the Special Issue: From Mechanisms to Models: Data-Driven Innovation in Urological Disease Research)
Canadian Journal of Urology https://doi.org/10.32604/cju.2026.074252
Received 06 October 2025; Accepted 06 January 2026; Published online 06 February 2026
Abstract
Background: The causal link between mental illness and prostatitis remains inconclusive, largely due to heterogeneity and potential confounders. This study explored the causal link between mental illness and prostatitis in men using Mendelian randomization (MR), and offered recommendations for enhancing future research. Methods: Publicly accessible genome-wide association study (GWAS) data were accessed via the IEU OpenGWAS platform and FinnGen database for this research. The inverse variance weighted (IVW) approach served as the primary Mendelian randomization analysis, while MR-Egger, weighted median, weighted mode, and simple mode methods were additionally applied to evaluate potential relationships between prostatitis and four psychiatric disorders (schizophrenia, depression, bipolar disorder, and anxiety). Results: The analysis indicated a significant causal association between depression and prostatitis (OR = 1766.294, p = 0.01), whereas no evidence of a causal relationship was observed for schizophrenia, bipolar disorder, or anxiety with prostatitis (p > 0.05). In the reverse-direction MR analysis, prostatitis showed no evidence of a causal effect on psychiatric disorders. Further sensitivity analyses did not reveal pleiotropy or heterogeneity, and leave-one-out analyses indicated that the overall results were not significantly affected by any single instrumental variable. Sensitivity analyses provided no indication of pleiotropy or heterogeneity, and leave-one-out testing suggested that the overall results remained stable regardless of the exclusion of any single instrumental variable. Conclusion: The present study provides genetic evidence that depression may increase the risk of prostatitis, highlighting the need for early preventive strategies. Additional studies are needed to clarify the mechanisms connecting depression and prostatitis in men.
Keywords
Prostatitis; mental disorders; mendelian randomization; genetics; causal effect
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