Why Does SIBO Keep Coming Back After Treatment? — The H2S Complex IV recurrence loop

In hydrogen-sulfide-dominant SIBO, an additional mechanism deepens the recurrence pattern. When the displaced community is dominated by sulfate-reducing taxa, particularly Desulfovibrio piger and Bilophila wadsworthia , the metabolic byproduct is hydrogen sulfide. At low concentrations, H2S is a signaling molecule with vasodilatory and anti-inflammatory effects. At sustained high concentrations, it is a respiratory toxin. H2S binds the heme iron in the active site of cytochrome c oxidase, Complex IV of the electron transport chain. It competitively inhibits oxygen reduction at the terminal step of electron transport. When Complex IV is inhibited, the upstream complexes back up, electron flow stalls, ATP synthesis falls further, and the cell shifts further toward glycolysis. The colonocyte that was already struggling to oxidize butyrate now cannot perform oxidative phosphorylation either. This produces the most distinctive recurrence pattern of H2S SIBO. The bioenergetic lesion that allowed sulfate-reducers to expand has been deepened by the metabolic byproduct of their expansion. Antimicrobial treatment reduces the population. H2S falls. Complex IV inhibition lifts. Colonocyte metabolism partially recovers. But the underlying substrate failure was never addressed. As antimicrobial pressure ends, the niche reopens, the sulfate-reducers expand back, H2S production returns, Comple