Why It's Impossible to Treat Chronic Gut Dysfunction at the Bacterial Level — The Bigger Point

Across genetics, mitochondrial metabolomics, immune markers, bile acid chemistry, motility assessment, and stool sequencing &#8212; six different testing layers, twenty-five-plus data points &#8212; every finding that keeps appearing in my patient population converges on the same place: the colonocyte, and the immune interface adjacent to it, and the mitochondrial network that powers both, and the entire operational architecture that depends on them. The microbiome is a downstream readout. The calprotectin is the wrong marker. The serum B6 is misleading. The butyrate production is intact. The motility problem is not a separate problem. The colonocyte has lost the capacity to use any of it. This is the Host Capacity Model. It is not a theory I am defending. It is a pattern that the data is forcing me to accept. Every client I have worked with has confirmed it. Every piece of research I have reviewed has been consistent with it. Every treatment protocol that has been aimed above the host layer has worked, and every protocol that has been aimed below it has failed. If any of this recognized you &#8212; the decade of relapsing SIBO, the calprotectin that came back &#8220;normal&#8221; while your gut fell apart, the methylation protocol that didn&#8217;t help, the supplement stack that keeps growing, the antimicrobials that worked for six weeks and failed for six years, the prokinet