Why Butyrate Supplementation Makes Chronic Gut Dysfunction Worse: The Data They Don't Show You — The Inflammatory Bowel Disease Connection: Why Conventional Medicine Gets It Wrong

IBD (Crohn&#8217;s disease, ulcerative colitis) is conventionally treated with increasing attention to butyrate, based on studies showing butyrate&#8217;s anti-inflammatory potential. Butyrate enemas. High-dose SCFA supplementation. Dietary protocols designed to maximize butyrate production. But here&#8217;s what&#8217;s actually happening in IBD: IBD is fundamentally a disease of colonocyte bioenergetic failure compounded by dysbiosis-driven mucosal inflammation. The inflammatory cascade is secondary to epithelial dysfunction, not primary. When you add high-dose butyrate to an IBD patient whose colonocytes are already struggling to oxidize it, you&#8217;re not targeting the upstream problem. You&#8217;re flooding the system with a molecule that, in that context, drives HDAC inhibition, mast cell activation, and further epithelial chaos. Yes, some IBD studies show butyrate benefit. But look closely: They typically show modest, short-term improvements, often confounded by changes in diet or concurrent interventions. The long-term outcomes? Mixed at best. The patients who respond to butyrate supplementation? Likely those with milder disease, better-preserved colonocyte function, and capacity to actually oxidize it. The patients who don&#8217;t respond, or deteriorate? Their colonocytes can&#8217;t. And the mechanism I&#8217;ve described explains why.