Lithocholic acid (LCA)
Optimal Result:
24.16 - 75.75 %.
Lithocholic acid (LCA) is a bile acid formed from chenodeoxycholate by bacterial action, usually conjugated with glycine or taurine. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as cholagogue and choleretic.
Bile Acids are natural products of cholesterol synthesis that aid in the emulsification and absorption of dietary fats in the small intestine. Elevated total fecal bile acid is indicative of a diagnosis of bile acid malabsorption. Quantification of fecal bile acids aids in diagnosis for IBS and identification of patients with chronic diarrhea who may benefit from bile acid sequestrant therapy. There is a connection between the liver health, fecal bile acid concentrations, and gut microbiota composition. Bile acids have both direct antimicrobial effects on gut microbes and indirect effects through FXR-induced antimicrobial peptides. Cholic acid (CA), Chenodeoxycholic acid (CDCA), Deoxycholic acid (DCA), Lithocholic acid (LCA) are the major bile acids related to gut microbiome.
Chronically high levels of lithocholic acid are associated with several forms of cancer including colon cancer, pancreatic cancer, esophageal cancer, and many other GI cancers. High bile acid levels lead to the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and the development of reduced apoptosis capability upon chronic exposure.
Lab Results Explained and Tracked
What does it mean if your Lithocholic acid (LCA) result is too high?
Chronically high levels of lithocholic acid are associated with several forms of cancer including:
- colon cancer,
- pancreatic cancer,
- esophageal cancer,
- and many other GI cancers.
High bile acid levels lead to the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and the development of reduced apoptosis capability upon chronic exposure.
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