LCA/DCA Ratio

Two bile acids can both fall during a bowel illness without their ratio changing much. If they fall by the same proportion, the ratio stays exactly the same. That's the main limitation to understand when looking at your LCA/DCA result: the relationship between these molecules doesn't reveal how much of either one is present.

This is an exploratory biomarker. There are no standardized clinical cutpoints or validated optimal targets, and trials haven't established that using this ratio to guide care improves health. Research on its individual components helps explain the biology, but it doesn't establish the ratio as a diagnostic or treatment-monitoring tool.

What This Ratio Compares

Your liver makes cholic acid and chenodeoxycholic acid from cholesterol. These primary bile acids help your intestine absorb fat. Most are reabsorbed, while some reach bacteria in the colon. Certain bacteria convert cholic acid into deoxycholic acid, or DCA, and chenodeoxycholic acid into lithocholic acid, or LCA. These bacterial products are called secondary bile acids.

This test compares stool LCA with stool DCA using LC-MS. The laboratory method separates and identifies individual molecules before measuring their amounts. The reported ratio divides LCA by DCA. A rise can therefore reflect more LCA, less DCA, or changes in both.

Several processes shape those amounts. They include the supply of primary bile acids, bacterial conversion, movement through the bowel, and absorption. DCA is partly absorbed and returned to the liver. Much of the LCA formed in the intestine leaves in stool; the absorbed portion can undergo further chemical changes that help its elimination. A stool ratio doesn't isolate bacterial activity from these other processes.

Evidence About the Ratio Itself

One study directly examining the lithocholate-to-deoxycholate ratio included 171 people and found that heavier stool output was associated with a lower ratio. It used gas chromatography and grouped some related bile acid derivatives with the reported components. That measurement isn't directly interchangeable with this LC-MS result. The association also doesn't show that changing stool bulk improves health by changing the ratio.

A more recent analytical study examined bile acid profiles and this ratio using LC-MS/MS in stool extracts and dried fecal spots prepared from those extracts. It included five people in each of three groups: healthy participants, people with diarrhea, and people with Clostridioides difficile infection. This was a small study of measurement methods and group differences. It didn't establish diagnostic accuracy or a treatment target.

Direct measurement of this ratio isn't limited to these two studies. An older colorectal cancer case-control study also reported the ratio directly; that finding is discussed in the colorectal cancer section below.

Inflammatory Bowel Disease

A study of 62 people with inflammatory bowel disease and 17 healthy controls measured individual stool bile acids using LC-MS/MS. Among those with ulcerative colitis, looser stools were associated with lower DCA and LCA concentrations. The same relationship wasn't found in Crohn's disease. The study also found a lower secondary-to-primary bile acid ratio in ulcerative colitis, which is a different calculation from LCA/DCA.

That absence of a stool-consistency link in Crohn's disease describes this particular study, not bile acid chemistry in Crohn's disease generally. A separate 2026 study found reduced stool LCA and a reduced secondary-to-primary bile acid ratio in both Crohn's disease and ulcerative colitis, though that finding doesn't validate LCA/DCA either.

These findings connect bowel inflammation and stool consistency with bile acid composition. They don't establish that a low LCA/DCA result identifies a flare, or that a change between flare and remission measures recovery.

Diarrhea-Predominant Irritable Bowel Syndrome

In a study comparing 55 people with diarrhea-predominant irritable bowel syndrome with 28 healthy controls, stool LCA was lower and primary bile acids were higher. DCA was numerically lower, but that difference wasn't statistically significant. Both LCA and DCA concentrations were associated with bowel movement frequency.

Faster passage through the bowel could reduce the time available for bacterial conversion, and differences in bacterial populations could also contribute. The study couldn't establish which process caused the observed pattern. It didn't validate LCA/DCA for diagnosing irritable bowel syndrome or bile acid diarrhea.

Liver Disease

In a study comparing 47 people with cirrhosis, 24 of whom had advanced disease, with 14 healthy controls, more advanced disease was associated with lower stool secondary bile acids and lower secondary-to-primary bile acid ratios. Those findings concern the amount of bacterial products relative to their precursors, rather than the balance between LCA and DCA.

A separate study included 199 people with biopsy-confirmed fatty liver disease and 88 healthy controls. Stool DCA and LCA concentrations were roughly twice as high in the advanced-fibrosis group as in healthy controls. That comparison wasn't a doubling from mild to advanced fibrosis: LCA didn't differ significantly between those two disease groups. Differences in DCA and LCA also weren't statistically significant after adjustment for body mass index and insulin resistance.

These observations don't establish opposite diagnostic rules for fatty liver and cirrhosis. The populations, disease stages, and other influences differ. Neither study showed that this ratio can detect liver scarring or track its progression.

Colorectal Cancer

Studies comparing people with and without colorectal tumors have reported differences in some stool bile acids, but the findings vary by molecule and comparison group. A meta-analysis of observational studies reported higher concentrations of several bile acids in some higher-risk groups. It didn't establish that the LCA/DCA ratio predicts future cancer or provides a useful screening result.

An older case-control study measured the LCA/DCA ratio directly and found it was higher in people with colorectal cancer than in cancer-free controls. That single historical association doesn't establish that the ratio predicts future cancer, performs as a screening test, or responds to treatment.

A study involving 215 people with inflammatory bowel disease and 51 controls found no significant direct association between individual fecal bile acids and colorectal cancer or precancerous changes. Only six participants with inflammatory bowel disease had cancer, which limits what a negative finding can establish.

Another study found no significant difference in DCA or LCA between 14 people with advanced colorectal adenomas and 32 controls. It measured fluid from the small intestine during colonoscopy, a different specimen from stool. Neither study validates this stool ratio as a cancer screen.

Aging and the Gut Barrier

A study comparing 100 older adults with 100 younger adults found differences in stool bile acid composition, including higher LCA in the older group. Bile acid patterns were associated with blood markers related to inflammation and intestinal barrier function. Because participants were compared at one point in time, the study couldn't determine whether the bile acid changes caused those findings. It didn't establish this ratio as a measure of biological age or intestinal barrier damage.

When Results Can Be Misleading

• Missing component values: a ratio can look similar when both acids are abundant or when both are scarce. Without the individual LCA and DCA results, you can't distinguish those situations.
• Very little DCA: DCA is the denominator. If its measured amount is close to the laboratory's quantification limit, small measurement errors can produce a large change in the ratio.
• Stool consistency and transit: diarrhea, constipation, and inflammation can change bile acid composition. Dilution by stool water alone would cancel out if both components were affected equally, but changes in absorption and bacterial conversion need not affect them equally.
• LC-MS measurement differences: stool contains compounds that can interfere with the instrument's signal. Extraction, separation of closely related molecules, calibration, and correction for interference affect accuracy. Results from different laboratories aren't automatically interchangeable.
• Sample handling: collection, storage, and preparation can affect the measured bile acid profile. A result from a dried fecal spot or a pooled collection shouldn't automatically be compared with an ordinary stool sample.
• Medication and diet: antibiotics, bile acid medications, and changes in diet or bowel transit can alter individual bile acids. The direction of change in LCA/DCA often hasn't been established, and a medication-related change doesn't by itself indicate new disease.

Serial Trending

Laboratory precision and biological stability are different questions. In a population study of 136 adults with measurements taken at baseline and again six months later, individual fecal bile acids showed meaningful change over that interval. In a separate check, baseline samples from 50 randomly selected participants were each measured twice to test the laboratory method's technical reproducibility, which was generally good. Good reproducibility of a single measurement doesn't mean the underlying biology stays stable. The study didn't establish the variability of LCA/DCA itself.

Repeated measurements may describe changes in stool chemistry, but no validated size or direction of change indicates improved gut health. An apparent trend also needs comparable collection conditions, component measurements, and laboratory methods.