The Iron-Sulfur Cluster Crisis: Why Your Mitochondria Can't Recover (And Why Practitioners Don't Talk About It) — Why This Matters in SIBO and Chronic Dysbiosis

SIBO isn&#8217;t primarily a bacterial overgrowth problem&#8212;it&#8217;s a host compartmentalization failure . The small intestine should be hostile to fermentation. Rapid transit, alkaline pH, low substrate availability, and robust intestinal motility should prevent bacterial dominance. But SIBO persists because the host has failed. And a major part of that failure is mitochondrial. When colonocyte (and small intestinal epithelial cell) mitochondria lose Fe-S cluster integrity: ATP production collapses, so tight junctions weaken Motility drivers&#8212;the migrating motor complex&#8212;require ATP-dependent coordination. Dysfunction spreads upward The local immune response becomes incoherent; dysbiosis-driving microbes aren&#8217;t cleared effectively Butyrate, normally a fuel, becomes a toxin that accumulates due to impaired oxidative metabolism The redox gradient that selects against facultative anaerobes collapses, further favoring dysbiosis The microbes aren&#8217;t the primary driver. They&#8217;re the consequence of host failure. And the failure isn&#8217;t just about butyrate sensitivity or epithelial permeability&#8212;it&#8217;s about the inability to manufacture and maintain the substratum of all aerobic life: functional Fe-S clusters.