Gut microbes and benign prostatic hyperplasia: the role of dysbiosis.

Abstract

Benign prostatic hyperplasia (BPH) is a common age-related condition characterized by stromal and epithelial proliferation within the prostate and is influenced by androgen signaling, ageing, obesity, metabolic dysfunction, and inflammation. Increasing interest has focused on whether the gut microbiota may contribute to these processes through a putative gut-prostate axis. The human gut contains a complex microbial ecosystem comprising thousands of bacterial species whose metabolites and immune-modulatory activities influence host physiology. Alterations in microbial composition and function have been associated with numerous chronic inflammatory and metabolic disorders. Emerging clinical and preclinical evidence suggests that gut dysbiosis may also be associated with prostate enlargement and lower urinary tract symptoms. Proposed mechanisms include altered production of short-chain fatty acids, impaired intestinal barrier integrity with increased lipopolysaccharide translocation, Toll-like receptor signaling, changes in tryptophan and serotonin metabolism, vagal pathways, and systemic cytokine-mediated inflammation. However, current evidence remains largely associative and mechanistic, with relatively few human studies directly linking alterations in the gut microbiota to BPH pathogenesis. This narrative review examines current evidence supporting the gut-prostate axis in BPH, evaluates potential biological mechanisms such as the vagus nerve and tryptophan, discusses dietary influences on microbiota composition, and highlights limitations in the existing literature together with priorities for future research and therapeutic development.