Why It's Impossible to Treat Chronic Gut Dysfunction at the Bacterial Level — Layer 6: Motility — How the Collapse Produces the Stasis That Creates the Overgrowth

This is the layer that most patients actually feel, every day, and that most practitioners have never properly explained. Here is the truth about motility dysfunction in chronic gut patients: it is not a separate problem from the host capacity collapse. It is one of its most direct consequences. What healthy motility requires Gut motility &#8212; the coordinated, rhythmic contractions that move food, bacteria, and waste through your digestive tract &#8212; is not a passive process. It is an energy-intensive, tightly coordinated, multi-system operation that depends on every single thing we&#8217;ve covered above. Specifically, it requires: Functional smooth muscle in the gut wall (which needs ATP). Functional pacemaker cells called interstitial cells of Cajal (ICCs) that generate the electrical rhythm that drives peristalsis. A functional enteric nervous system (ENS) &#8212; the &#8220;second brain&#8221; of around 500 million neurons embedded in your gut wall &#8212; that coordinates contractions. Proper vagal tone &#8212; the parasympathetic signaling from your brain stem that tells your gut to digest and move. Functional enteroendocrine cells that release signaling molecules like serotonin, GLP-1, motilin, and CCK at the right times. Proper bile acid signaling through receptors like TGR5, which regulate both motility and gut hormone release. The migrating motor complex (MMC)