The Real Cause of SIBO — Why Everything You’ve Been Told Is Incomplete — The Host Capacity Model: What I Have Been Building

Over years of research into SIBO, chronic gut dysfunction, mast cell activation, the epigenetics of gut barrier function, and the intersection of metabolic biology and microbial ecology, I have developed a framework I call the Host Capacity Model. The central argument is that SIBO &#8212; and most chronic gut dysfunction &#8212; is not primarily a microbial problem. It is a host capacity problem. Host capacity refers to the metabolic, immune, structural, and neurological capacity of the gut lining and its supporting systems to maintain conditions that make the small intestine inhospitable to the wrong organisms. When host capacity is high, bacteria cannot establish regardless of exposure. When host capacity falls &#8212; through any combination of the mechanisms described in this article &#8212; establishment becomes possible, and eventually inevitable. The model is organized around the colonocyte as the central unit of analysis. Not the microbiome, not the bacteria, not the breath test result &#8212; the cell that lines the intestine and whose metabolic state determines whether the lumen is hospitable or hostile. The CD38-NAD&#8314; depletion cascade, SLC5A8 epigenetic silencing of the butyrate transporter, colonocyte mitochondrial dysfunction, PPAR-&#947; downregulation, and the resulting oxygen-nitrate-lactate leak &#8212; these are the mechanistic nodes where host capacity