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Most bile acid stories stop at the liver. This one starts in your gut. Lithocholic acid (LCA) is made when specific gut bacteria chemically rework one of your liver's bile acids in the lower intestine, and the amount you produce mirrors the health of that microbial community.
Levels can swing in either direction depending on what is happening inside you. Low fecal LCA shows up in inflammatory bowel conditions and certain liver diseases. High LCA shows up in advanced liver fibrosis, certain metabolic patterns, and impaired antitumor immunity. The number alone is not a verdict, but it is a window into a pathway that standard liver and gut tests cannot see.
Your liver makes a set of starting bile acids from cholesterol. When those reach the lower intestine, certain bacteria (notably Clostridium scindens, members of Ruminococcaceae, and related groups) strip off a chemical group in a process called 7α-dehydroxylation. The result is LCA. The amount of LCA in your stool is therefore a readout of two things at once: how much primary bile acid your liver is sending down, and how active these specific microbes are at converting it.
LCA is not just a waste product. It binds to several cellular receptors that influence bile acid synthesis, fat and sugar handling, immune balance in the gut wall, and inflammatory tone. That is why disturbances in LCA show up across a wide range of conditions, from gut inflammation to liver scarring to metabolic disease.
Fatty liver, now often called metabolic dysfunction-associated steatotic liver disease (MASLD), shows a consistent fingerprint in bile acids. In adults with biopsy-proven nonalcoholic fatty liver disease, both fecal and serum bile acid levels rise as fibrosis worsens, and LCA in particular tracks with more advanced scarring. A meta-analysis pooling circulating bile acid data in MASLD found that several LCA-related species rise alongside disease progression.
In adult NAFLD with advancing fibrosis, fecal and serum LCA tend to climb. In children with NAFLD, the pattern is the opposite: fecal LCA is reduced because the bacteria that make it are depleted. The takeaway is that LCA is a stage-specific signal, and pairing it with a fibrosis test like FIB-4 or an elastography scan gives a sharper picture than either alone.
In ulcerative colitis (UC) and in pouchitis after surgical pouch creation, fecal LCA is markedly reduced. The reason is mechanical: the bacteria that produce LCA are depleted in active inflammation, and their absence leaves the gut bathed in primary bile acids that drive further inflammation. Restoring secondary bile acids, including LCA, calms colitis in animal models, which suggests the deficit is not just a marker but part of the disease.
If you have UC and your fecal LCA is low, that pattern is consistent with active dysbiosis. It does not by itself prove disease activity, but combined with calprotectin (a stool inflammation marker) it can give you a more nuanced sense of whether you are in remission at the microbial level, not just symptom-free.
Diarrhea-predominant irritable bowel syndrome (IBS-D) generally shows reduced fecal LCA, with more primary bile acids spilling into the colon and triggering more frequent, looser stools. Lower LCA correlates with higher defecation frequency and visceral hypersensitivity in this group. There is a subtype of IBS-D where LCA is actually higher with more severe symptoms, which is why interpretation always benefits from clinical context.
LCA is not a simple high-bad, low-good marker. It is a phenotype indicator. Low fecal LCA usually signals loss of the bacteria that produce it, which is harmful in colitis and IBS-D contexts. High fecal or serum LCA usually signals dysregulated bile acid handling, which is harmful in advancing liver fibrosis. But in chronic liver disease, higher serum LCA has been linked to better preserved muscle mass and survival, and one human study found that lower LCA predicted higher coronary atheroma risk. The framework that resolves these findings is that LCA reflects the state of a complex gut-liver-microbe axis, and the same number can mean different things in different bodies. This is why a single reading is rarely actionable on its own and why pairing the test with disease-specific context (liver enzymes, calprotectin, gut symptoms, imaging) is essential.
Fecal LCA correlates positively with body mass index and triglyceride levels in community-based studies, and patterns of secondary bile acids including LCA shift after bariatric surgery in line with weight loss. In a randomized Mediterranean diet trial in 284 adults, the way gut bacteria handle bile acids modified how much cardiometabolic benefit people got from the diet, suggesting the LCA pathway is part of why some people respond to diet better than others.
In newly diagnosed type 2 diabetes, a 1,234-person cohort linked higher unconjugated secondary bile acids (a category that includes LCA) to greater cardiovascular disease risk. Animal-fat-rich diets push fecal LCA higher and are associated with fewer normal stools, while higher insoluble fiber intake associates with lower LCA.
There are no standardized clinical reference ranges or risk-stratification cutpoints for fecal lithocholic acid. Major guideline bodies do not recommend specific thresholds, and population-derived reference intervals vary by assay (most labs use liquid chromatography with mass spectrometry, a method that separates and identifies molecules), specimen handling, and study cohort. What follows is research-derived orientation, not a clinical target.
Treat any single result as a baseline data point. The most useful comparison is your own number over time within the same lab, not against a universal cutpoint. If your lab provides a reference range, ask whether it was derived from healthy controls in their assay system or borrowed from research literature.
LCA varies meaningfully day to day with diet, transit time, and microbial fluctuations. A single reading carries less information than a trend across two or three time points. If you are testing because of a specific concern (fatty liver, ulcerative colitis, gut symptoms, or a major dietary or microbial intervention), get a baseline, retest in 3 to 6 months if you are making changes, and continue at least annually thereafter. Watching the trajectory matters far more than any single absolute number, especially for a research-grade marker without consensus thresholds.
Pair retesting with companion tests where appropriate. Tracking fecal LCA alongside calprotectin (gut inflammation) is more informative for colitis than either alone. Tracking fecal LCA alongside ALT and a non-invasive fibrosis score is more informative for fatty liver than either alone.
An unexpected LCA result is a starting point for a workup, not an endpoint. The pattern of results around it determines what to do next.
If your LCA is high alongside elevated ALT, GGT, or a high non-invasive fibrosis score, the priority is investigating liver disease. A FibroScan or an Enhanced Liver Fibrosis (ELF) score helps stage fibrosis, and a hepatology referral is reasonable if scores cross intermediate or high-risk thresholds. If your LCA is low alongside elevated calprotectin or ongoing diarrhea, the priority is gastrointestinal: a stool microbiome panel and a gastroenterology consult are reasonable next steps. If your LCA is abnormal but your liver, inflammation, and gut markers are all reassuring, the most defensible move is to retest in 3 to 6 months, ideally after a sustained dietary or microbial intervention, before chasing it further.
Evidence-backed interventions that affect your Lithocholic Acid level
Lithocholic Acid is best interpreted alongside these tests.