Hyodeoxycholic Acid Test

The trillions of bacteria living in your intestine quietly convert the digestive juices your liver makes into a small library of signaling molecules. One of those, HDCA (hyodeoxycholic acid), is showing up in research as a possible early window into how well your gut, liver, and metabolism are talking to each other.

Standard liver and lipid panels can look normal even when these gut-derived signals are off. Measuring HDCA in stool offers a different angle on what your microbiome is producing, and the early human research links higher levels to less liver fat and lower cardiovascular mortality in people with heart disease.

What HDCA Actually Is

Bile acids start in your liver, which makes them from cholesterol and releases them into the small intestine to help digest fat. Once they reach the gut, bacteria chemically rework them into dozens of different forms. HDCA is one of those bacterial reworkings, called a secondary bile acid, and most of it is found in stool, which is why this test uses a stool specimen rather than blood.

Beyond its role in digestion, HDCA acts as a chemical messenger. It can switch on receptors in your intestine and immune cells, including FXR (a sensor that regulates bile acid and fat metabolism) and TGR5 (a sensor involved in blood sugar control and inflammation). HDCA and its glycine-attached form can also activate LXR-alpha, a sensor that helps cells handle cholesterol. The same molecule can act as both an activator and a brake on FXR depending on the tissue, which is unusual for a bile acid and part of why researchers find it interesting.

Why It Matters

HDCA is not a routine clinical biomarker yet. It belongs to a research category of gut-derived metabolites that may add information your standard labs cannot provide. The most consistent human findings so far point to three areas: fatty liver disease, cardiovascular outcomes, and inflammatory bowel disease.

Fatty Liver Disease

In a study of adults evaluated for NAFLD (non-alcoholic fatty liver disease, the buildup of fat in the liver not caused by alcohol), people with more liver fat and more histologic injury had lower fecal HDCA levels. The relationship was an inverse correlation, meaning HDCA fell as the disease got worse. The finding fits a broader pattern in which a healthier secondary bile acid pool tracks with a healthier liver, but it comes from a small cross-sectional study and should be read as suggestive rather than definitive.

Heart Disease and Survival

A cohort of people with established coronary artery disease found that higher blood levels of unconjugated bile acids, including HDCA, were linked to lower cardiovascular mortality and lower all-cause mortality during follow-up. This evidence comes from serum measurements rather than stool, so it is biologically related but not a direct measurement of what this test reports. A separate study reported that serum HDCA was reduced in people with atherosclerosis, which lines up with the survival data: less HDCA, more disease.

Inflammatory Bowel Disease

The IBD (inflammatory bowel disease) research is mixed and reveals an important nuance about specimen type. In a serum bile acid profile of IBD patients and healthy controls, HDCA was elevated in both Crohn's disease and ulcerative colitis compared with healthy people, regardless of disease activity. In stool, the picture flips. A study of IBD patients found that the glycine-attached form of HDCA in stool helped distinguish ulcerative colitis from Crohn's disease, with about 67 out of 100 ulcerative colitis cases correctly identified and about 79 out of 100 Crohn's cases correctly cleared at a research cutoff. Stool HDCA also dropped in ulcerative colitis patients with the highest levels of intestinal inflammation.

Reconciling Conflicting Findings

HDCA is not a simple higher-is-better or lower-is-better marker. The same bile acid can rise in blood while falling in stool, or rise in one disease state and fall in another, because it travels through several tissues that handle it differently. In stool, more HDCA generally tracks with a healthier secondary bile acid pool and less liver fat. In blood, the picture depends on what the underlying disease is doing to bile acid recycling and detoxification. The practical takeaway: this is a phenotype indicator that adds context to other markers, not a single number that gives a verdict.

Reference Ranges

There are no clinical guideline cutpoints for HDCA. Reference values come from individual research cohorts and vary by laboratory, by specimen type (stool versus blood), and by the analytical method used (most often a lab technique called mass spectrometry, which separates and weighs molecules to count them precisely). The closest research-derived threshold is from a small ulcerative colitis study, which used a glycine-attached HDCA cutpoint based on a percentage of total bile acids to help distinguish ulcerative colitis from Crohn's disease. That cutoff was set in a small cohort to answer one specific clinical question and is not a general health threshold.

Because no consensus ranges exist, treat any single HDCA value as orientation, not a verdict. The most useful comparison is your own previous result from the same lab using the same assay.

When Results Can Be Misleading

HDCA reflects the activity of your gut microbiome, which is sensitive to short-term influences. The most common ways a single reading can be thrown off:

• Recent antibiotics: broad-spectrum antibiotics taken in the weeks before testing reshape the bacteria that produce HDCA, and can lower or distort the level temporarily.
• Acute diarrhea or constipation: stool transit time changes how much bacterial conversion happens before the sample is collected.
• Major diet shifts: a sudden change to a very low-fat or very high-fat diet, or a sudden surge in fiber, alters bile acid production and microbial conversion within days.
• Active flares of gut inflammation: active ulcerative colitis can lower stool HDCA independent of any treatment effect.

Tracking Your Trend

A single HDCA reading is most useful as a baseline. Bile acid output naturally varies day to day, and the underlying microbiome shifts in response to diet, sleep, illness, and medications. The signal that matters is direction over time, especially after a deliberate change such as a new diet pattern, a course of probiotics, or treatment of a gut condition.

A reasonable cadence is a baseline measurement, a follow-up at three to six months if you are making changes you expect to influence your gut microbiome, and an annual recheck thereafter to watch the trajectory.

What to Do With an Abnormal Result

An out-of-range HDCA value on its own does not diagnose anything. Use it as one input alongside the rest of the picture:

• If your liver markers are also off: look at ALT (alanine aminotransferase, a liver enzyme), AST (aspartate aminotransferase, another liver enzyme), and GGT (gamma-glutamyl transferase, a liver and bile duct enzyme), and consider an ultrasound or FibroTest to assess for fatty liver. A gastroenterologist or hepatologist can interpret the combined pattern.
• If you have gut symptoms: pair the result with calprotectin (an inflammation marker measured in stool) and a broader bile acid and microbiome profile. A gastroenterologist is the right next stop.
• If your cardiovascular markers are also concerning: focus on the established drivers of heart risk first, including ApoB (apolipoprotein B, the protein on cholesterol-carrying particles), Lp(a) (lipoprotein little a, an inherited heart risk particle), and hs-CRP (high-sensitivity C-reactive protein, a general inflammation marker). HDCA adds context but does not replace those tests.
• If everything else is normal: retest in three to six months before drawing any conclusions. A single off result in an otherwise healthy picture is rarely actionable on its own.