Why Dysbiosis, SIBO, Hydrogen Sulfide Intolerance, MCAS, and Long COVID May All Be Downstream of a Single Event — Hydrogen sulfide: a host clearance problem wearing a microbial costume

Hydrogen sulfide (H₂S) deserves its own section, because it is so badly misunderstood. H₂S is not a villain. At physiological levels it is a gasotransmitter — a signaling gas your body makes on purpose, involved in blood-vessel tone, mitochondrial signaling, neuromodulation, and mucosal defense. The problem is never the existence of hydrogen sulfide. The problem is always concentration, location, rate of production, and rate of clearance. On the production side, certain microbes generate H₂S from sulfur substrates — sulfate-reducing bacteria like Desulfovibrio, and bile-tolerant sulfur metabolizers like Bilophila wadsworthia. When these expand, sulfide production rises. This is the part most testing focuses on. But here is what almost everyone misses: clearing hydrogen sulfide is a mitochondrial job. Your body disposes of H₂S through a dedicated enzymatic unit. SQOR (sulfide quinone oxidoreductase) initiates clearance by oxidizing sulfide and passing its electrons into the CoQ pool — the same coenzyme-Q hub the electron transport chain uses. ETHE1, TST/rhodanese, and SUOX carry the downstream steps that finish converting sulfide into harmless, excretable forms. Read that again, because it's the whole point: sulfide clearance dumps electrons into the same electron transport chain that's already failing in our model. If the CoQ pool and the ETC are congested — because iron-sulfur