What Actually Causes IBD? A Mechanistic Reading of Crohn's Disease and Ulcerative Colitis — What the microbiome looks like in IBD

The microbial signature of IBD is one of the most consistent findings in the literature. Specific taxa are reliably depleted. Specific taxa are reliably expanded. Depleted in IBD: Faecalibacterium prausnitzii, the dominant butyrate producer in the healthy gut, falls dramatically. The depletion correlates with disease severity and predicts flare risk. Roseburia intestinalis and other butyrate producers in the Lachnospiraceae family are similarly depleted. Akkermansia muciniphila, the dominant mucus-resident commensal, is reduced or absent. Overall microbial diversity is reduced — alpha diversity metrics consistently show lower values in active IBD compared to healthy controls. Expanded in IBD: Enterobacteriaceae (E. coli, Klebsiella) expand, often substantially. Specific adherent-invasive E. coli strains have been identified in Crohn's disease and may contribute to pathogenesis. Sulfate-reducing taxa (Desulfovibrio, Bilophila) often expand in ulcerative colitis. Fusobacterium has been associated with both IBD and colorectal cancer. Several Candida species, particularly Candida albicans, expand in some patients. This microbial pattern is not a primary cause of IBD. It is the predictable consequence of the colonocyte bioenergetic failure. The taxa that depend on physiological hypoxia (the obligate anaerobic core) are displaced when the hypoxia is lost. The taxa that thrive in the