Why Dysbiosis, SIBO, Hydrogen Sulfide Intolerance, MCAS, and Long COVID May All Be Downstream of a Single Event — Glutathione is not a supply problem. It's a capacity problem.

The same logic — and it is the signature logic of this entire model — applies to glutathione, your master cellular antioxidant. Low glutathione is almost universally read as a building-block problem: the body lacks the raw materials (cysteine, glycine, glutamate) to make it, so we supply precursors and call it solved. Sometimes that's right. In chronic inflammatory gut dysfunction, it is frequently wrong, and the wrongness matters. Glutathione can run low for reasons that have nothing to do with how much you're making: it is being consumed too fast — persistent oxidative stress and lipid peroxides relentlessly burn through reduced glutathione; recycling is broken — used (oxidized) glutathione has to be regenerated by an enzyme called glutathione reductase, which requires both NADPH (a cellular reducing-power molecule) and FAD (derived from vitamin B2, riboflavin), and if NADPH or riboflavin run short, the recycling stalls and glutathione "looks low" even when synthesis is fine; NADPH itself is depleted — drained by immune activation, by NADPH-oxidase activity producing superoxide, and by the constant demand to recharge antioxidants; selenium is limiting, so the selenium-dependent glutathione peroxidases that neutralize lipid hydroperoxides can't keep up. So when glutathione is low, the right question is never just "are we deficient in sulfur amino acids?" It is a capacity quest