The Hidden Driver of SIBO and Chronic Gut Dysfunction: Bile Acid Malabsorption, Dysbiosis, and the Mitochondrial Cascade — Part II: Dysbiosis as the Origin of Bile Acid Malabsorption

The Dysbiosis-Driven Loss of BSH and Bai Operon Function SIBO and other forms of chronic dysbiosis are characterized by a profound phylogenetic and functional contraction: the loss of the specific bacterial lineages that produce bile salt hydrolase and bile acid 7&#945;-dehydroxylase. In SIBO, microbial communities are dominated by: Aerotolerant and facultative organisms ( Klebsiella , E. coli , Enterococcus , Staphylococcus ) Pathogenic anaerobes ( C. difficile , overgrown C. perfringens ) Reduced diversity of saccharolytic Clostridium species ( C. scindens , C. hiranonis ) Severely depleted Bacteroides , Faecalibacterium , Roseburia , and other butyrate-producing bacteria These dysbiotic communities lack the enzymatic capacity for bile acid metabolism. Research from the past decade confirms this repeatedly: Hang et al. (2014, Cell) demonstrated that germ-free mice reconstituted with dysbiotic microbiota show profound impairment of secondary bile acid synthesis and loss of FXR and TGR5 signaling, with downstream consequences for intestinal permeability, immune tolerance, and metabolic endotoxemia. Wahlstr&#246;m et al. (2016, Gut) showed that antibiotic-induced dysbiosis eliminates secondary bile acid synthesis and increases fecal primary bile acid concentration 10-fold, with persistent alterations lasting months after antibiotic cessation. Devlin et al. (2016, Cell Metabolism