{"version":"v1","chain":{"id":"motility-first-cascade","title":"(Competing) Motility failure → stagnation → microbial overgrowth → barrier stress","question":"Could primary motility disorder explain recurrent SIBO without invoking host bioenergetics?","summary":"Conventional view: MMC dysfunction (post-infectious autoimmunity, neuropathy, structural) is the primary lesion; ecological and bioenergetic changes are secondary.","steps":[{"nodeId":"concept:sibo-host-capacity-model","rationale":"Antibodies (e.g. anti-vinculin) or neuropathy impair MMC sweep.","evidence":"emerging"},{"nodeId":"concept:dysbiosis-ecology","rationale":"Stagnation favours microbial overgrowth in the small bowel.","evidence":"established"},{"nodeId":"concept:gut-barrier-dysfunction","rationale":"Persistent overgrowth and bile-acid deconjugation injure the mucosa.","evidence":"mechanistic-inference"}],"competingChains":["oxygen-leak-cascade"],"relatedConcepts":["sibo-host-capacity-model"],"relatedArticles":[],"evidenceFloor":"emerging","lastReviewed":"2026-05-11"}}