Recurrent urinary tract infection (rUTI) affects a large proportion of women after an initial episode and consumes a substantial share of community antibiotic prescribing, yet prevention remains unsatisfactory and recurrence incompletely explained. Approximately half of recurrences are caused by the strain responsible for the index infection, implying a host reservoir that antimicrobial treatment does not eradicate. That reservoir is the intestine. This review applies to that reservoir an established mechanism that governs its size. Depletion of butyrate-producing Clostridia reduces peroxisome proliferator-activated receptor gamma signalling in colonocytes, shifts epithelial metabolism away from beta-oxidation, raises luminal oxygen and nitrate availability and permits an aerobic expansion of Enterobacteriaceae, including Escherichia coli. Butyrate sustains the physiological hypoxia that restrains this expansion by stabilising hypoxia-inducible factor, and the pathway is pharmacologically reversible in animal models. Women with rUTI show depletion of richness and of butyrate-producing bacteria without a corresponding difference in E. coli abundance, an apparent paradox that the proposed mechanism resolves, because what is lost is the epithelial capacity to restrain expansion rather than the organism itself. At population scale, butyrate-producer abundance is inversely associated with hospitalisation for infection. Antibiotics deplete these taxa profoundly and for prolonged periods, which closes a plausible self-perpetuating loop. Restoration of the intestinal community by faecal microbiota transplantation reduces recurrence. Butyrate nevertheless does not appear among interventions evaluated in current syntheses of non-antibiotic prophylaxis. We set out the evidence, state the falsifiable predictions of the model, and outline the trial required to test it. We locate butyrate-directed intervention within the wider class of postbiotic and microbial-metabolite strategi