Approximately 5 percent of bile acids in the small intestine are not reabsorbed in the ileum and reach the colon. Here, bacterial action results in deconjugation and dehydroxylation, producing the secondary bile acids, deoxycholate and lithocholate. These secondary bile acids play a key role in stimulating electrolyte and water secretion. These effects increase colonic motility and shorten the colonic transit time. Highly elevated levels of these secondary bile acids can result in watery diarrhea, as well as other gastrointestinal symptoms such as bloating, urgency and faecal incontinence. This is known as bile acid malabsorption (BAM), sometimes called bile acid diarrhea.
Although assessments of the prevalence of BAM vary, an estimate of 1 percent of the general population has been derived from data from a systematic review of 18 completed studies that estimated the prevalence of primary bile acid diarrhea using a test known as75Se-Homocholic Acid Taurine (SeHCAT) in patients with diarrhea-predominant irritable bowel syndrome (IBS-D).
There are no medicines currently approved to treat BAM. The current approach relies on binding excess bile acids to reduce their secretory actions, using a bile acid sequestrant such as cholestyramine or a variant such as colestipol. However, many patients cannot tolerate these medications because of the texture or taste or because they worsen the diarrhea or cause intolerable nausea, heartburn, wind or bloating. In addition, these medications can, over time, reduce fat-soluble vitamins, increase triglycerides or interfere with uptake of other medications.