Why It's Impossible to Treat Chronic Gut Dysfunction at the Bacterial Level — Why It Is Mechanistically Impossible to Fix This at the Bacterial Level

Once you see these six layers stacked, the conclusion becomes unavoidable. Let me walk through why every bacteria-focused intervention has to fail in this patient population: Antibiotics (rifaximin, Xifaxan, herbals). These reduce the microbial load temporarily. They do nothing to restore IAP. They do nothing to restore SLC5A8 expression. They do not reverse DNMT3A methyl-donor deficits. They do not rebuild secondary bile acid-producing guilds &#8212; in fact, they often destroy the remaining 7&#945;-dehydroxylators as collateral damage. They do not restore motility. They do not reduce LPS translocation after the course ends. When the patient stops the antibiotic, the same host environment that selected for dysbiosis the first time selects for it again. Hence the 44% relapse rate on rifaximin in the published data, and the much higher relapse rate in post-antibiotic chronic cases. Probiotics. These add organisms to a lumen that can no longer support them. Lactic acid bacteria can&#8217;t colonize a colon where the oxygen gradient has collapsed. Faecalibacterium and Akkermansia are obligate anaerobes &#8212; they die in the lumen that dysbiotic patients present with. The probiotic passes through. Some patients feel worse during the transient exposure because adding live organisms to a permeable, inflamed gut is not benign. Few feel meaningfully better six months later. Prebiotic