Post-Finasteride Syndrome (PFS) is conventionally framed as a persistent endocrine or neurosteroid disorder. However, a significant subset of patients presents with metabolic and somatic symptoms that androgen deprivation alone cannot fully explain. This theoretical paper proposes a gut-centric aetiology for this subset: a chronic, hydrogen sulphide (H₂S)-dominant overgrowth of bacteria in the small intestine. This paper puts forth the hypothesis that H₂S produced by enteric sulphate-reducing bacteria acts as a systemic mitochondrial toxin, creating a dysbiotic feedback loop that effectively 'locks' indefinitely the epigenetic silencing initially triggered by finasteride exposure. By reframing this subset of PFS as an acquired metabolic dysfunction driven by gut-derived toxins, this framework provides a novel mechanism for the persistence of the condition and underlines the small intestinal microbiome as a potential therapeutic target.