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This theoretical paper suggests a novel gut-centric cause for a subset of Post-Finasteride Syndrome (PFS) cases, which are not fully explained by androgen deprivation. It hypothesizes that a chronic overgrowth of hydrogen sulphide (H₂S)-producing bacteria in the small intestine acts as a systemic mitochondrial toxin. This condition may create a dysbiotic feedback loop that perpetuates the epigenetic silencing initially triggered by finasteride exposure. The paper proposes that this acquired metabolic dysfunction, driven by gut-derived toxins, could explain the persistence of PFS symptoms and highlights the small intestinal microbiome as a potential therapeutic target.

This theoretical paper suggests a novel gut-centric cause for a subset of Post-Finasteride Syndrome (PFS) cases, which are not fully explained by androgen deprivation. It hypothesizes that a chronic overgrowth of hydrogen sulphide (H₂S)-producing bacteria in the small intestine acts as a systemic mitochondrial toxin. This condition may create a dysbiotic feedback loop that perpetuates the epigenetic silencing initially triggered by finasteride exposure. The paper proposes that this acquired metabolic dysfunction, driven by gut-derived toxins, could explain the persistence of PFS symptoms and highlights the small intestinal microbiome as a potential therapeutic target.