This test is most useful if any of these apply to you.
If your bowels run fast, slow, or unpredictably, it can help to know how much of your liver's own digestive acid makes it all the way out in your stool. That amount shifts with diarrhea, constipation, gut bacteria, and liver health, and none of it appears on a routine blood panel.
This is a research-grade marker. There are no standardized clinical cutpoints, and most of the evidence comes from studies comparing groups of people. A single result is best used to start a line of questions about your gut and to set a baseline you can track.
CDCA (chenodeoxycholic acid) is one of the two main bile acids your liver makes from cholesterol. Bile acids are soap-like molecules that let you absorb fat and fat-soluble vitamins. Your liver attaches most of its CDCA to glycine or taurine before releasing it into bile, and most of it is reabsorbed at the end of the small intestine and sent back to the liver for reuse.
The fraction that escapes reabsorption reaches the colon. There, certain bacteria strip off the attached glycine or taurine and then reshape the molecule into lithocholic acid. CDCA counts as a primary bile acid because your liver makes it, and lithocholic acid counts as a secondary bile acid because bacteria make it.
So the amount in your stool, reported in nanograms per gram of stool, reflects three things at once: how much your liver made, how much your gut failed to reclaim, and how much your colon bacteria converted before it left. A high level usually means bile is moving through quickly or the converting bacteria are scarce. A low level can mean less bile reaching the colon, or slower transit that gives bacteria more time to work.
The clearest human data on stool CDCA concern bowel habits. In the colon, primary bile acids like CDCA draw water into the bowel and speed things along, so a large pool of unconverted CDCA tends to travel with faster, looser stools. Three groups of studies fit that picture.
| Who Was Studied | What Was Compared | What They Found |
|---|---|---|
| Adults with diarrhea-predominant irritable bowel syndrome and healthy comparison groups | Stool CDCA and bowel symptoms | CDCA was markedly higher with diarrhea, and higher levels went with more frequent bowel movements and a more sensitive rectum |
| Adults with functional constipation | Stool CDCA and stool quality | CDCA was higher than in controls, and higher levels went with more complete bowel movements and softer stools |
| Adults with constipation-predominant irritable bowel syndrome | Stool bile acids and how fast the colon moved | About 15 in 100 had low stool bile acids, with a smaller share of primary bile acids such as CDCA, and that group had slower colon transit |
Sources: Wei et al. 2020; Li et al. 2023; Vijayvargiya et al. 2017.
The constipation finding looks like it contradicts the diarrhea finding, but both point the same way. CDCA in the colon pushes toward more water and faster movement. In someone with diarrhea, a high level goes with too much of that push, and in someone with constipation, a higher level went with stools closer to normal. The number hints at which way bile acids are pulling your bowel, and whether that's a problem depends on where your bowel habits already sit.
What this means for you: if you have chronic loose stools and a high result, bile acids are a reasonable suspect and worth a proper workup. If you're constipated and your result is low, that fits a known subgroup whose colon gets too little bile.
Because bacteria turn CDCA into lithocholic acid, stool CDCA partly reports on whether those converting bacteria are present in numbers. Across studies of irritable bowel syndrome with diarrhea, cirrhosis, fatty liver disease, ulcerative colitis, and alcohol-associated hepatitis, fewer converting bacteria went with more unconverted primary bile acid in stool and less secondary bile acid.
In these groups, primary bile acids, CDCA included, often rose alongside potentially harmful bacteria and inflammation markers and fell as beneficial bacteria became more common. In healthy young adults, though, people whose stool was rich in primary bile acids had a distinct mix of gut bacteria and more normal stools, which fits the idea that context decides what the number means.
This is why stool CDCA pairs well with a microbiome test. A high result alongside a thin population of bile-converting species points toward a bacterial explanation, and a high result with a normal microbiome points back toward gut speed or bile supply.
The liver makes CDCA and gut bacteria finish it, so liver disease shows up in stool bile acids from both ends. In nonalcoholic fatty liver disease, which is fat buildup in the liver unrelated to heavy drinking, stool total bile acids including CDCA were higher, alongside signs of disrupted gut bacteria.
In a study of 287 people with biopsy-confirmed fatty liver, higher bile acid levels in both stool and blood went with more advanced liver scarring. The primary bile acid share and the ratio of primary to secondary bile acids rose as scarring advanced, though bacteria-made secondary bile acids still made up most of the stool bile acid pool at every stage. In cirrhosis, especially advanced disease, and in alcohol-associated hepatitis, the gut's conversion of primary bile acids into secondary ones was impaired.
A high stool result doesn't diagnose a liver problem. If yours is high and you carry risk factors for fatty liver, such as extra weight around the middle, high triglycerides, or prediabetes, it's a good reason to check liver enzymes and, if those are off, to get imaging that measures liver stiffness.
Ulcerative colitis is a form of inflammatory bowel disease that inflames the lining of the colon. In people with it, stool carried more conjugated primary bile acids, including CDCA's conjugated forms, and fewer secondary bile acids. Those shifts tracked with changes in gut bacteria and with inflammatory signaling molecules in the blood.
A separate study found that the disrupted stool bile acid pattern followed disease severity and symptoms in active ulcerative colitis, but not in Crohn's disease. If your stool CDCA is high alongside bloody or persistent diarrhea, the next test to add is fecal calprotectin. Calprotectin measures inflammation in the gut lining, and a high value is the usual trigger for a colonoscopy.
Bile acids have long been studied as a possible contributor to colon cancer. A 2025 meta-analysis pooling 23 studies found stool CDCA modestly higher on average in people with colorectal cancer or at higher risk than in lower-risk comparison groups, with a somewhat larger gap in people who already had cancer. The size of the difference varied a lot from study to study.
These were case-control and cross-sectional studies, which compare people with and without a disease at one point in time. They show that stool CDCA differs in people who have colorectal cancer, which is a weaker claim than showing it predicts who will develop it. Older studies often found the stronger signal in the secondary bile acids deoxycholic and lithocholic acid rather than CDCA, and at least one blood study found CDCA lower, not higher, in people with colorectal cancer.
Stool CDCA doesn't replace colorectal cancer screening. If you're at screening age or colon cancer runs in your family, you still need a stool blood test, a stool DNA test, or a colonoscopy on schedule, and a high CDCA result is one more reason to stay current.
Studies of blood CDCA tell a different story, and the two shouldn't be mixed. In a large Chinese cohort of adults with normal blood sugar, higher blood levels of CDCA in its free form, without glycine or taurine attached, went with a somewhat lower chance of developing type 2 diabetes, while the attached forms of primary bile acids went with a higher chance. Other settings, such as obesity with type 2 diabetes, have shown a higher CDCA share in blood, so the blood link to diabetes depends on context. In people with coronary artery disease followed for years, higher blood CDCA went with a lower risk of dying from heart disease or any cause.
Blood CDCA mostly reflects bile acids your gut reabsorbed and sent back toward the liver, while stool CDCA reflects what got away. That's why a high blood level and a high stool level can mean opposite things about the same system, and why the blood findings can't be borrowed to interpret your stool result.
Stool bile acids swing with whatever your gut did in the days before you collected, so a single sample is noisy. These are the factors most likely to throw a reading off.
One stool sample captures one stretch of bowel activity. Because this marker answers to gut speed, bacteria, and bile supply all at once, the useful information is in how it moves across samples collected under similar conditions.
Get a baseline when your bowels are behaving the way they usually do, and when you're off laxatives, antidiarrheals, and antibiotics. If you're treating chronic diarrhea, a falling number alongside firmer stools is the pattern that fits improvement.
This is a newer measurement without standardized cutpoints, which is exactly why your own earlier results become the most useful comparison you have. No study has yet shown that tracking it changes health outcomes. Use the same lab each time so the numbers stay comparable.
Read the number alongside your symptoms and the rest of the stool bile acid panel. CDCA alone can't separate bile supply, gut speed, and missing bacteria, and the full panel narrows it down: total bile acids, the share of primary versus secondary bile acids, and the secondary bile acids deoxycholic and lithocholic acid.
Blood in your stool, unexplained weight loss, or a change in bowel habits that lasts for weeks needs prompt evaluation, usually including a colonoscopy, whatever this number says.
Evidence-backed interventions that affect your CDCA level
Chenodeoxycholic Acid is best interpreted alongside these tests.
Chenodeoxycholic Acid is included in these pre-built panels.