The Hidden Driver of SIBO and Chronic Gut Dysfunction: Bile Acid Malabsorption, Dysbiosis, and the Mitochondrial Cascade — Part I: The Physiology—Enterohepatic Circulation and Bacterial Conversion

The Two Forms of Bile Acid and Their Metabolic Fates The human liver synthesizes approximately 400&#8211;800 mg of bile acids daily from cholesterol. These are released into the duodenum conjugated&#8212;bound to glycine or taurine&#8212;which increases their solubility and prevents premature absorption in the proximal small intestine. This conjugation is deliberate: it ensures that primary bile acids (cholic and chenodeoxycholic acid) remain in solution and perform their lipid emulsification function across the entire small intestine. However, the human liver itself cannot convert primary bile acids into secondary bile acids . This conversion&#8212;the deconjugation and 7&#945;-dehydroxylation of cholic acid to deoxycholic acid and chenodeoxycholic acid to lithocholic acid&#8212;is entirely dependent on a specific and vulnerable subset of anaerobic bacteria. Without these bacteria, the entire enterohepatic circulation becomes dysfunctional. The Bacterial Enzymes That Control Bile Acid Fate Two distinct bacterial enzyme systems are required: 1. Bile Salt Hydrolase (BSH) Bile salt hydrolase is responsible for deconjugating glycine- and taurine-conjugated bile acids. This is a gate-keeping step : without functional BSH activity, conjugated primary bile acids accumulate in the small intestinal lumen and cannot proceed to secondary bile acid synthesis. BSH is produced by a narrow p