Gut Microbiota Linked to Benign Prostatic Hyperplasia - EMJ

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Gut Microbiota Links to Benign Prostatic Hyperplasia

benign prostatic hyperplasia

A NEW systematic review suggests that alterations in gut microbiota composition may play a meaningful role in the pathogenesis of benign prostatic hyperplasia (BPH). The analysis evaluated clinical and preclinical research exploring the so-called gut–prostate axis, highlighting how microbial imbalance could influence inflammation, intestinal barrier function, and prostate enlargement. As interest grows in microbiome-driven disease mechanisms, the findings position gut dysbiosis as a potential diagnostic and therapeutic target in BPH management. 

Systematic Review Examines Clinical and Preclinical Evidence 

The authors conducted a comprehensive search of PubMed, MEDLINE, and Web of Science databases through October 2025, identifying 16 relevant studies, including 10 preclinical investigations and six clinical studies. Overall, the review encompassed 413 patients with BPH, 338 controls, and five distinct mouse models. Across studies, significant differences in gut microbial β-diversity were consistently observed between BPH populations and healthy controls, supporting the hypothesis that microbial shifts accompany disease progression. 

One of the most notable findings was an increased Firmicutes/Bacteroidetes (F/B) ratio in patients with BPH, which the researchers suggest may serve as a marker of pathological status. Specific genera, including PrevotellaRuminococcus, and Lactobacillus, were also implicated. Reduced abundance of Lactobacillus in particular was associated with inflammatory and metabolic disturbances relevant to prostate growth. 

Inflammation and Gut Barrier Dysfunction May Drive Disease Mechanisms 

Beyond microbial composition, the review highlights potential mechanistic pathways linking the gut to prostate pathology. Dysregulation of inflammatory cytokines such as interleukin-6 (IL-6) and interleukin-18 (IL-18) appeared repeatedly across studies. In addition, altered levels of intestinal tight junction proteins, including tight junction protein-1 and claudin-1, suggested compromised gut barrier integrity, which may promote systemic inflammation and contribute to BPH development. 

Clinical Implications and Future Research Directions 

Although the authors emphasise that current evidence remains limited by heterogeneity and relatively small clinical cohorts, the findings underscore the growing relevance of microbiome research in urology. Targeting gut microbial balance through diet, probiotics, or novel therapeutics could emerge as a complementary strategy for managing BPH in the future. Larger longitudinal studies and mechanistic trials will be necessary to determine whether modifying gut microbiota can translate into meaningful clinical outcomes for patients. 

Reference 

Xu Y et al. The gut-prostate axis in benign prostatic hyperplasia: systematic review of microbial dysbiosis and pathogenic mechanisms. BMC Urol. 2026;26:26. 

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