The factors that regulate methanogenesis in humans have not been established. The presence of bile acid, which is lost into the colon from the small intestine, may be an important regulatory factor of methanogenesis. To examine this possibility, the effect of human bile on methane production by faecal cultures, and the in vivo effect of biliary diversion on breath methane excretion in a methanogenic choledochostomy patient, were investigated. Faecal suspensions (0.1%) from five methanogenic humans were incubated anaerobically with bile (0.3-30%) from three choledochostomy patients, and headspace methane measured by gas chromatography. All biles inhibited headspace methane. Inhibition of methanogenesis was dose dependent, plateaued at 10-30% bile concentration, and was abolished by 0.6% cholestyramine. The maximum inhibition by bile, median (range), was 38 (0.9-56)% of control methane values. Reversal of the bile fistula in the fourth choledochostomy patient converted that subject from methanogenic to 'non-methanogenic' status, It is concluded that inhibition of methanogens in the caecum by bile acid could significantly reduce the number of methanogens in the colon. This and the effect of transit time could explain much of the known epidemiology of 'non-methanogenesis', which has been related to obesity, (comparatively) fast colonic transit in healthy persons, and to small intestinal Crohn's disease.
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