Understanding Bile Acid Malabsorption: A Complete Guide to Causes, Diagnosis, and Treatment of Bile Acid–Related Chronic Diarrhea

Table of Contents

• Key Points
• Background: Why Bile Acid Malabsorption Matters
• How Bile Acids Normally Work
• The Four Types of Bile Acid Malabsorption
• How the Researchers Reviewed the Evidence
• How Common Is BAM, and Who Is at Risk?
• Diagnosing BAM: What Tests Are Available
• Treatment Options for BAM
• What This Means for Patients
• Limitations of the Evidence
• Practical Recommendations for Patients
• Frequently Asked Questions
• Source Information

Key Points

• BAM is a common, treatable cause of chronic diarrhea, found in roughly 25% to 35% of patients with unexplained chronic diarrhea in a US clinic population.
• Up to half of patients with BAM report symptoms lasting more than five years before receiving the correct diagnosis.
• The 75SeHCAT scan is the most accurate test for BAM, but it is not widely available and requires a nuclear medicine department.
• About two-thirds of patients with unexplained diarrhea and confirmed BAM improved on bile acid sequestrant therapy, compared with one-third without BAM.
• Emerging treatments include FXR agonists, FGF19 analogues, GLP-1 receptor agonists, and approaches that modify the gut microbiome.

Background: Why Bile Acid Malabsorption Matters

Bile acid malabsorption (BAM) means the gut does not reabsorb bile acids the way it should. Bile acids are detergent-like molecules the liver makes to digest fat. When too many of them reach the lower intestine, they trigger chronic diarrhea — a condition doctors sometimes call cholorrhea (bile-acid diarrhea).

This is not a minor nuisance condition. The symptoms can include an urgent need to pass stool, fecal incontinence (loss of bowel control), fatigue, dizziness, and a feeling of faintness. Together, these problems can lead to depression and a significantly reduced quality of life.

The review's authors make a blunt point: BAM is treatable, but it is missed far too often. A diagnostic delay is common, and up to one-half of patients with BAM report symptoms lasting more than five years before they receive the correct diagnosis. Timely and accurate identification of BAM is therefore "a major unmet need" in digestive medicine.

How Bile Acids Normally Work

To understand what goes wrong in BAM, it helps to understand the normal bile acid cycle, known as the enterohepatic circulation (the loop between the liver and the intestine).

Making and releasing bile acids

• The liver builds bile acids from cholesterol. The "classical pathway" uses the enzymes cholesterol 7α-hydroxylase (CYP7A1) and CYP8B1; the "alternative pathway" uses CYP27A1.
• The two primary bile acids are cholic acid (CA) and chenodeoxycholic acid (CDCA).
• The liver attaches (conjugates) these acids to taurine or glycine using two enzymes: bile acid CoA synthase (BACS) and BA-CoA-amino acid N-acetyltransferase (BAAT).
• The finished bile acids are pumped into bile by the bile salt export pump (BSEP). A separate transporter, MRP2, handles other substances such as bilirubin and glutathione.

The gallbladder stores and concentrates bile between meals. During fasting, roughly 20% of gallbladder contents empty at the end of phase II of the migrating myoelectric complex. The migrating myoelectric complex is a periodic wave of gut muscle activity. This emptying is under the control of the vagus nerve and the hormone motilin. After a meal, more than 50% empties because fat triggers release of the hormone cholecystokinin (CCK).

In healthy people, fasting blood levels of bile acids run about 0.2 to 0.7 µM (micromoles per liter). After each meal they rise to about 4 to 5 µM. This rhythm is tightly controlled.

The feedback loop between gut and liver

When bile acids reach the terminal ileum (the last part of the small intestine), they switch on a receptor called the farnesoid X receptor (FXR). Working with a partner receptor called RXR, FXR increases production of a hormone-like protein called fibroblast growth factor 19 (FGF19). In mice the equivalent protein is FGF15.

FGF19 then travels through the bloodstream to the liver and gallbladder. In the gallbladder it binds to the FGFR4/β-Klotho receptor and inhibits gallbladder contraction. In the liver, the same receptor activates JNK/ERK signalling, which shuts down CYP7A1 and CYP8B1 and therefore reduces bile acid production. A second braking pathway, FXR–SHP, works alongside it.

Bile acids also act through a different receptor, GPBAR-1 (G-protein bile acid receptor 1). In the intestine this triggers release of peptide YY (PYY), glucagon-like peptide 1 (GLP-1) and glucagon-like peptide 2 (GLP-2). These hormones influence glucose and insulin metabolism and appetite, and they act on GPBAR-1 receptors in brown fat (heat-generating fat tissue) and muscle. In gallbladder muscle, GPBAR-1 signalling raises cAMP and PKA, opens ATP-regulated potassium channels, and relaxes the muscle so the gallbladder can refill.

Recycling — and what happens when recycling fails

The terminal ileum reabsorbs more than 95% of bile acids — roughly 19 out of every 20 molecules. Only about 5% are lost in stool each day (about 1 in 20). Reabsorbed bile acids travel back to the liver through the portal vein, completing a circuit that runs 4 to 12 times daily. About 10 to 50% of the reabsorbed bile acids spill over into the general circulation rather than staying in the loop.

Whatever reaches the colon meets gut bacteria, which convert primary bile acids into secondary bile acids. Some of these are reabsorbed by passive diffusion. The kidney also contributes: it takes up bile acids through the apical sodium-dependent bile acid transporter (ASBT) in the proximal tubule, and filtration is regulated by MRP2, 3 and 4 transporters.

When this system breaks down, too many bile acids collect in the lower gastrointestinal tract. The consequences are a chain reaction:

• Abnormal transport of water and sodium in the bowel
• Damage to the mucosal lining (the surface layer of the gut)
• Increased mucus secretion
• Faster intestinal motility (quicker transit of stool)
• Gut dysbiosis (an imbalanced gut bacterial community)

The Four Types of Bile Acid Malabsorption

Doctors divide BAM into four types based on what is causing it. Knowing the type guides treatment.

• Type 1 — ileal disease. Defective bile acid reabsorption because the terminal ileum is damaged or removed. This is frequently seen in Crohn's disease, both with and without surgical removal of the ileum, where reported rates range from 11% to 76%, and higher still in some reports. It also occurs after ileal resection for any reason and after radiation enteropathy (bowel injury from radiation therapy). It can show up as osmotic diarrhea (caused by substances pulling water into the bowel) or as true steatorrhea (fatty stool from fat malabsorption).
• Type 2 — idiopathic (primary) BAM. Here no structural defect in absorption can be documented. It may appear as primary bile acid diarrhea or as the diarrhea-predominant form of irritable bowel syndrome (IBS-D). It is associated with reduced bacterial conversion of primary bile acids into secondary bile acids.
• Type 3 — non-ileal conditions causing BAM. Other diseases or surgeries disrupt bile acid handling without direct ileal damage. Examples include post-cholecystectomy diarrhea, which occurs after gallbladder removal. Examples include post-vagotomy diarrhea, which occurs after vagus nerve surgery. Examples include chronic pancreatitis with impaired bicarbonate secretion. Examples include celiac disease with villous atrophy, which is flattening of the intestinal absorptive surface. Examples include impaired gallbladder and small bowel motility. In some cases, prevalence is comparable to healthy people.
• Type 4 — excessive bile acid synthesis without primary malabsorption. The liver simply makes too many bile acids. This occurs mainly in hypertriglyceridemia (high blood triglycerides) and during diabetes treatment with metformin. It is also seen in metabolic dysfunction-associated steatotic liver disease (MASLD, formerly called fatty liver disease) and in people with obesity.

Genetic contributors to Type 2 BAM

Genetics matter, but only rarely cause the problem on their own. Identified genetic variants explain roughly 1% of primary BAM cases. Key findings include:

• The rs3808607 T>G polymorphism in the promoter region of CYP7A1 is associated with a higher ratio of 7α-hydroxy-4-cholesten-3-one (C4) to cholesterol in patients who develop bile acid diarrhea after ileal resection surgery. People carrying the TT (AA) genotype appear to have about a twofold increase in bile acid synthesis.
• Heterozygotes for the rs8192877 A>G variant (people carrying one copy) show about double the fecal primary bile acids compared with AA homozygotes, and GG homozygotes show even higher levels. This variant also relates to colorectal adenoma (polyp) risk.
• Other variants may alter the ASBT transporter, reduce FGF19 production, or blunt the liver's ability to shut down bile acid synthesis.
• Mutations affecting the FGF19/FGFR4-β-Klotho/ERK1/2/CYP7A1 axis can disrupt the feedback brake. Notably, impaired release of ileal FGF19 occurs in IBS-D patients who respond to cholestyramine, suggesting that excess liver bile acid production can indeed result from broken FGF19 signalling.
• The GPBAR-1 SNP rs11554825 has a minor allele frequency of 41%. This SNP was correlated with symptoms in a study. The study compared scintigraphically assessed small bowel and colonic transit in 230 healthy controls and 414 patients with functional gastrointestinal disorders. Of those patients, 84 had alternating IBS, 157 had constipation-predominant IBS, and 173 had diarrhea-predominant IBS.

The authors note that the role of gut microbiota in type 2 BAM still requires further study.

Type 3 in focus: after gallbladder removal

Cholecystectomy (gallbladder removal) is a common trigger. Without a gallbladder, bile drips more continuously and is less concentrated. People who have had their gallbladder removed show about double the recycling of the bile acid pool through the intestine. This accelerated recycling is tied to a twofold increase in liver bile acid synthesis and higher bile acid and cholesterol secretion into bile.

Even so, the bile acid pool stays constant and fat is digested and absorbed normally. The problem is exposure: gut bacteria now meet more primary bile acids, converting them into secondary bile acids — mainly deoxycholic acid (DCA). The pool becomes enriched in more hydrophobic (water-repelling), less hydrophilic bile acids, which can disrupt cell membranes and cause cell lysis (cell breakdown). After surgery, cholic acid synthesis dips slightly, but the pathway CA → 7α-dehydroxylation → DCA increases, delivering more DCA back to the liver and suppressing cholic acid production. This profile does not change in the long term.

The reported incidence of diarrhea after cholecystectomy varies widely — from 2% to 50% — depending on the population studied, the study design, and how diarrhea was defined. It usually resolves or improves over weeks to months — about 1 in 50 to 1 in 2 patients depending on the group studied. Some authors report BAM in 68% to 86% of cholecystectomy patients. But a larger analysis of 25 studies found that only 9.1% of patients with diarrhea after cholecystectomy had BAM. Two-thirds of those patients were diagnosed with BAM.

Type 3 in focus: microscopic colitis and other causes

In microscopic colitis, BAM results from villous atrophy, inflammation, and collagen deposition in the ileum. A 75SeHCAT retention below 10% was found in about 44% of patients with collagenous colitis and chronic diarrhea — nearly 1 in 2. Almost 80% of those patients responded to bile acid sequestrant therapy, which suggests treating all patients with microscopic colitis even if their 75SeHCAT test is negative.

Type 4 causes deserve attention too. About 20% of patients taking metformin (1 in 5) had accelerated bowel transit times. Patients with obesity and hypertriglyceridemia can also show increased bile acid synthesis and idiopathic BAM.

How the Researchers Reviewed the Evidence

The authors ran a systematic literature search in PubMed for studies on BAM published from 1965 to May 19, 2024. The search combined keywords and medical subject headings (MeSH) related to BAM:

• "bile acid malabsorption," "bile acid diarrhoea," "bile salt malabsorption," "bile salt diarrhoea," or "BAM"
• Combined with "diarrhoea," "chronic diarrhoea," or "malabsorptive diarrhoea"

Studies were included if they (1) focused on BAM and its association with bile-acid-induced diarrhea, and (2) provided original data. Reviews, editorials, and letters were excluded unless they contained relevant data. The researchers also checked the reference lists of selected articles to find cited studies that might have been missed in the initial search.

How Common Is BAM, and Who Is at Risk?

BAM is common in people with unexplained chronic diarrhea — and the numbers vary widely depending on who is tested and how.

In a US population study of patients referred to a gastroenterology outpatient clinic, the prevalence of chronic diarrhea was about 1%. Among those with unexplained chronic diarrhea, BAM was found in roughly 25% to 35% — between 1 in 4 and 1 in 3 patients. About 30% of patients treated for diarrhea-predominant irritable bowel syndrome (IBS-D) — nearly 1 in 3 — have idiopathic BAM.

Risk is higher in specific groups. These groups include people who have had ileal resection. They include people with terminal ileal disease, such as Crohn's disease or radiation-induced injury. They include people with diseases affecting gut motility or absorption, such as celiac disease. They include people whose bile acid delivery to the small intestine is disturbed, most notably after cholecystectomy. BAM may also contribute to post-vagotomy diarrhea, since these patients show higher fecal bile acid excretion.

A Danish study conducted between 2003 and 2021 identified 5,264 people with BAM based on the 75SeHCAT test. The BAM group was compared with age- and sex-matched controls from the general population. Those in the BAM group had more other medical conditions. They used more healthcare services. They had lower levels of education and income.

Prevalence by type

• Type 1: In patients with chronic watery diarrhea, 75SeHCAT testing found BAM in 34% (about 1 in 3).
• Type 2: Prevalence is estimated in only a few studies and appears as low as 1% of new cases of chronic diarrhea and 3% of all chronic diarrhea cases — suggesting widespread underdiagnosis. Yet 51% of patients with unexplained diarrhea who underwent 48-hour fecal bile acid testing had BAM. About two-thirds of them improved with bile acid sequestrant therapy, compared with only one-third when BAM was absent. In patients with chronic diarrhea tested by 75SeHCAT, BAM was detected in 38% of cases, with type 2 accounting for 28%. Other reports found BAM by 75SeHCAT in 50% of patients, with one-third having IBS-D.
• Type 3: In patients with chronic watery diarrhea, 75SeHCAT found BAM in 28%.

A systematic review estimated the population prevalence of BAM at more than 1% and reported that about 30% of patients with chronic diarrhea had been tested by 75SeHCAT. In 15 prospective studies of patients with IBS-D-like symptoms, the prevalence of BAM by 75SeHCAT was 10% overall — moderate BAM in 32% and mild BAM in 26% of those tested. Response rates to cholestyramine (a bile acid sequestrant) were 96% in severe BAM and 70% in mild BAM.

About one-fourth of IBS-D or functional diarrhea patients test positive for bile acid diarrhea. BAM is also linked to post-infectious diarrhea. Of patients with a history of acute gastroenteritis, 55% had a positive 75SeHCAT test. Of patients with post-infectious diarrhea, 18% had BAM that responded to cholestyramine.

Bile acid levels differ across IBS subtypes. Patients with IBS-D who secrete more bile acids showed high fecal levels of primary unconjugated bile acids. These patients also showed high serum C4, especially at higher body size. Levels were lower in IBS with constipation (IBS-C) and in healthy volunteers. This supports a role for bile acids in IBS itself and points to serum C4 and fecal primary and secondary unconjugated bile acids as potential biomarkers.

Diagnosing BAM: What Tests Are Available

BAM is frequently underdiagnosed, and early diagnosis matters because it prevents unnecessary tests and improves quality of life. Every available test has limitations, but each can identify patients who will benefit most from treatment. Because of limited availability and cost, these tests are rarely used in combination.

1. Empiric trial of bile acid sequestrants

This is the practical first step. Empiric diagnosis of BAM is based mainly on the clinical response to bile acid sequestrants. This approach is recommended in patients with unexplained chronic diarrhea when specific tests are not available. No studies have compared the accuracy of empiric treatment against specific testing.

The most important limitation is poor patient compliance — patients may not tolerate the medication. False-negative results can occur partly because bile acid sequestrants taste unpleasant.

2. The 75SeHCAT test

This is the most accurate test for identifying both the presence and the severity of BAM. It works by measuring how much bile acid remains in the abdomen seven days after the patient swallows it. The test uses a synthetic conjugated bile acid (homotaurocholic acid) labelled with the isotope selenium-75.

How it is done:

1. Patients must avoid bile acid sequestrant medication for a few days before the test.
2. They fast for four hours before swallowing the 75SeHCAT capsule.
3. A gamma camera takes the first scan within three hours of ingestion.
4. A second scan is taken after seven days, which makes the result less dependent on day-to-day diet.

Low retention of 75SeHCAT signals fecal bile acid loss. Results are graded by how much radioactive selenium is retained:

• Severe BAM: less than 5% retained
• Moderate BAM: 5% to 10% retained
• Mild BAM: 10% to 15% retained

In a systematic review of 43 studies enrolling 1,223 IBS patients, 10% had retention below 5%, 27% had retention below 10%, and 13% had retention below 15%.

Radiation exposure is limited. The 75SeHCAT activity is small (370 KBq), the radiation dose is 0.26 mSv, and the total absorbed radiation is 0.3 Gy/kBq. Despite its high accuracy, 75SeHCAT is not widely available and is inaccessible to most clinicians. It requires a nuclear medicine department with trained personnel and is time-consuming for the patient. These limits can lead to missed diagnoses, diagnostic delay, or unnecessary radiological and endoscopic examinations.

3. Fecal bile acid test

Directly measuring the bile acids that reach the colon and leave in stool is an alternative when 75SeHCAT is unavailable. The protocol requires a four-day diet containing 100 g of fat, followed by a 48-hour stool collection to measure total and individual fecal bile acids.

Diagnostic cut-offs:

• Total fecal bile acids above 2,337 µmol per 48 hours, or a fraction of primary bile acids (CDCA and CA) exceeding 10% of the total
• An alternative recommended cut-off: total fecal bile acids above 1,000 µmol per 48 hours plus a fraction of primary bile acids exceeding 4%

Stool frequency and consistency correlate with concentrations of primary fecal bile acids. The test is simple and safe, but both patients and healthcare workers may find it time-consuming and inconvenient. Measuring individual bile acid species is mainly reserved for research; for clinical purposes, simply measuring total fecal bile acids is considered satisfactory.

Reported accuracy: fecal bile acid content has 45% sensitivity and 63% specificity for detecting a 75SeHCAT result below 15% when measuring primary bile acids above 10%. It is advisable to combine the measurement of total fecal bile acid content with the percentage of primary bile acids.

4. Fasting serum C4

C4 (7α-hydroxy-4-cholesten-3-one) is the precursor of liver bile acid synthesis, so fasting serum C4 directly measures how active that pathway is. Levels above 48.9 ng/mL can indicate BAM. The C4 and FGF19 measurements have been validated against 75SeHCAT.

Because C4 naturally fluctuates during the day, blood must be sampled before 9 a.m. False-positive or false-negative results are possible in patients with cholestatic chronic liver disease, which is liver disease with blocked bile flow. False-positive or false-negative results are also possible in patients with hypertriglyceridemia. They are also possible in people taking statins. All of these can interfere with bile acid synthesis. C4 levels can also shift with factors affecting circadian rhythm. Because of these confounders, combination testing is suggested, such as fecal bile acids plus C4 levels.

5. Fasting serum FGF19

FGF19 works in the opposite direction from C4. Low FGF19 levels mean less inhibition of the conversion of cholesterol to bile acids, while BAM diagnosis relies on decreased FGF19 and elevated C4 together. Serum FGF19 can serve as an index of ileal bile acid reabsorption. When measured in patients with chronic diarrhea, the cut-off for diagnosing BAM is a fasting FGF19 below 60 pg/mL. Like C4, the sample should be taken in the morning while fasting.

6. Emerging diagnostic tests

Newer approaches need more validation, including machine learning techniques. Several experimental tests are in development:

• Molecular imaging techniques to analyze how different bile acids bind to the GPBAR-1 and FXR receptors
• Serum lipidome profiles (the pattern of fats in the blood) to distinguish people with BAM
• Detection of microbial metabolites called volatile organic compounds (VOCs), which may mark gut dysbiosis in BAM compared with healthy people

VOC testing is appealing and promising, but it requires complex experimental procedures, standardization, and data analysis. The current scarcity of reliable, widely available tests is an unmet need. This is especially true when a bile acid sequestrant trial is not enough to confirm the diagnosis. It is also true when a bile acid sequestrant trial is not enough to justify using newer therapeutic agents.

Treatment Options for BAM

Treatment must address the underlying condition when the cause is known. When the cause is unknown, current approaches start with dietary modification and bile acid sequestrants, with newer drug classes emerging.

Bile acid sequestrant therapy (BAST)

Bile acid sequestrants bind bile acids in the gut so they cannot irritate the colon. This was an Italian retrospective study of chronic diarrhea in 136 patients with ileal disease, cholecystectomy, or post-prandial diarrhea. BAM was confirmed in 28.1% of cases. Patients improved after six months of treatment with cholestyramine.

Treatment does more than reduce stool frequency. BAST also improves scores on the "Role limitation due to physical health" dimension. BAST also improves scores on the overall mental component summary of the 36-Item Short Form Survey (SF-36), a standard quality-of-life questionnaire. And notably, the review reports that about two-thirds of patients with unexplained diarrhea and confirmed BAM improved on sequestrant therapy, compared with only one-third of those without BAM.

Emerging drug treatments

Beyond bile acid sequestrants, the review highlights several therapeutic approaches now being explored. These target the specific molecular pathways that control bile acid production and recycling:

• FXR agonists — drugs that activate the farnesoid X receptor, mimicking the body's natural signal to reduce bile acid production
• FGF19 analogues — laboratory-made versions of the hormone that tells the liver to slow bile acid synthesis
• GLP-1 receptor agonists — drugs that mimic the gut hormone glucagon-like peptide 1
• Microbiota modulation — treatments aimed at changing the gut bacterial community

The authors argue that these novel agents can only make their way into routine care if BAM stops being treated as a "diagnosis of exclusion". A "diagnosis of exclusion" is a label given only after everything else has been ruled out. Ignoring BAM as a specific condition will continue to drive up healthcare costs and reduce patients' quality of life.

What This Means for Patients

If you have chronic diarrhea that has never been explained, BAM should be on your doctor's list. Between 1 in 4 and 1 in 3 people with unexplained chronic diarrhea have it, and roughly 1 in 3 people treated for IBS-D have the idiopathic form.

The condition is treatable. Bile acid sequestrants helped about two-thirds of patients with confirmed BAM in the studies reviewed, and they improve quality-of-life scores as well as stool symptoms. When BAM is absent, only about one-third of patients improve on the same therapy — which is why an accurate diagnosis matters.

Certain situations raise the odds. Ask about BAM testing if you have had ileal surgery or radiation to the abdomen. Ask about BAM testing if you have Crohn's disease or celiac disease. Ask about BAM testing if you have had your gallbladder removed and developed diarrhea afterward. Ask about BAM testing if you take metformin and have developed loose stools. About 1 in 5 people on metformin show accelerated bowel transit.

Watch for the red flags the review highlights as quality-of-life threats: urgency, fecal incontinence, fatigue, dizziness, and fainting feelings. These are not "just diarrhea" — they are the symptoms that drive depression and lost work and social time in this condition.

Limitations of the Evidence

The reviewers are candid about gaps in the evidence. Several key limitations stand out.

• No diagnostic standardization exists for BAM, which the authors say "may account for poor recognition and delayed management."
• No studies have compared the accuracy of empiric treatment with bile acid sequestrants against specific diagnostic testing.
• The most accurate test, 75SeHCAT, is unavailable to most clinicians. It requires a nuclear medicine department and trained staff, and it is time-consuming for patients.
• Fecal bile acid testing is valid but inconvenient for patients and staff, limiting real-world use.
• C4 and FGF19 measurements can be distorted by cholestatic liver disease, hypertriglyceridemia, statin use, and circadian rhythm factors.
• Genetic variants explain only about 1% of primary BAM cases, and the role of gut microbiota in type 2 BAM needs more research.
• Emerging tests such as molecular imaging, serum lipidomics, and volatile organic compound detection still require validation, standardization, and better data analysis.
• The incidence of diarrhea after cholecystectomy ranges so widely (2% to 50%) that comparisons across studies are difficult.

Finally, poor compliance with bile acid sequestrants is a real barrier. The medications are unpleasant to take, and that can produce false-negative results when the diagnosis rests on a treatment trial.

Practical Recommendations for Patients

1. Keep a symptom record. Note stool frequency, urgency, incontinence episodes, fatigue, and dizziness. Correlating these with diet and stress helps your doctor judge whether BAM is likely.
2. Ask specifically about BAM testing. If you have chronic diarrhea that has not been explained, ask whether bile acid malabsorption is on the differential diagnosis. Name it — underdiagnosis is the core problem this review describes.
3. Ask whether testing is available locally. If 75SeHCAT is not accessible, alternatives include a 48-hour fecal bile acid test and fasting blood tests for C4 and FGF19.
4. Prepare correctly for testing. Stop bile acid sequestrants a few days before a 75SeHCAT test, fast for four hours beforehand, and have C4 or FGF19 blood drawn in the morning before 9 a.m. while fasting. For a fecal bile acid test, follow the four-day, 100 g fat diet and complete the full 48-hour stool collection.
5. Take a sequestrant trial seriously. If your doctor prescribes a bile acid sequestrant as a diagnostic trial, stick with it long enough to judge the response. Report side effects or difficulty taking it. Poor palatability can cause a false-negative result.
6. Do not accept a five-year delay. Up to half of patients wait more than five years for a BAM diagnosis. If testing is negative but symptoms persist, discuss combination testing or referral to a gastroenterologist with an interest in bile acid disorders.
7. Ask about newer options. If sequestrants do not work or are poorly tolerated, ask about FXR agonists, FGF19 analogues, GLP-1 receptor agonists, and microbiome-directed approaches.
8. Treat the whole picture. Because BAM affects mood and daily functioning, ask about quality-of-life assessment alongside stool symptoms.

Frequently Asked Questions

What is bile acid malabsorption (BAM)?

BAM means the gut does not reabsorb bile acids properly. Bile acids are detergent-like molecules the liver makes to digest fat. When too many reach the lower intestine, they trigger chronic diarrhea, sometimes called cholorrhea. Symptoms can include urgency, fecal incontinence, fatigue, dizziness, and faintness, and together these can lead to depression and reduced quality of life.

How common is BAM in people with unexplained chronic diarrhea?

In a US population study of patients referred to a gastroenterology outpatient clinic, BAM was found in roughly 25% to 35% of those with unexplained chronic diarrhea — between 1 in 4 and 1 in 3. About 30% of patients treated for diarrhea-predominant irritable bowel syndrome (IBS-D) have idiopathic BAM.

Who is at higher risk of BAM?

Risk is higher in people who have had ileal resection. Risk is higher in people with terminal ileal disease such as Crohn's disease or radiation-induced injury. Risk is higher in people with diseases affecting gut motility or absorption such as celiac disease. Risk is higher in people whose bile acid delivery to the small intestine is disturbed, most notably after gallbladder removal. About 1 in 5 people on metformin show accelerated bowel transit.

What tests are available for diagnosing BAM?

Tests include an empiric trial of bile acid sequestrants, the 75SeHCAT scan, a 48-hour fecal bile acid test, and fasting blood tests for C4 and FGF19. The 75SeHCAT scan is the most accurate for identifying presence and severity, but it is not widely available. C4 and FGF19 can be distorted by liver disease, hypertriglyceridemia, statins, and circadian rhythm.

What does a 75SeHCAT result mean?

The 75SeHCAT test measures how much bile acid remains in the abdomen seven days after swallowing a capsule. Results are graded by retention: severe BAM is less than 5% retained, moderate BAM is 5% to 10%, and mild BAM is 10% to 15%. Low retention signals fecal bile acid loss. The test requires avoiding bile acid sequestrants for a few days beforehand.

What treatments are available for BAM?

Treatment starts with dietary modification and bile acid sequestrants, which bind bile acids in the gut. In the studies reviewed, about two-thirds of patients with unexplained diarrhea and confirmed BAM improved on sequestrant therapy, compared with only one-third of those without BAM. Emerging options include FXR agonists, FGF19 analogues, GLP-1 receptor agonists, and microbiota modulation.

How should I prepare for BAM testing?

For a 75SeHCAT test, stop bile acid sequestrants a few days before. Fast for four hours beforehand. Expect a first scan within three hours and a second after seven days. For C4 or FGF19 blood tests, have blood drawn in the morning before 9 a.m. while fasting. For a fecal bile acid test, follow a four-day, 100 g fat diet and complete the full 48-hour stool collection.

I have had unexplained chronic diarrhea for years and my doctor says it is IBS. When should I seek a second opinion about bile acid malabsorption?

Seek a second opinion if chronic diarrhea has never been explained. Between 1 in 4 and 1 in 3 people with unexplained chronic diarrhea have bile acid malabsorption. Up to half of patients wait more than five years for the correct diagnosis. Ask specifically whether BAM is on the differential. Ask whether testing such as the 75SeHCAT scan, a 48-hour fecal bile acid test, or fasting C4 and FGF19 blood tests is available. A second opinion can confirm the diagnosis and clarify treatment options. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article title: Advances in the pathophysiology, diagnosis and management of chronic diarrhoea from bile acid malabsorption

Authors: Agostino Di Ciaula, Mohamad Khalil, Gyorgy Baffy, and Piero Portincasa

Author affiliations: Clinica Medica "A. Murri," Department of Precision and Regenerative Medicine and Ionian Area (DiMePre-J), University of Bari "Aldo Moro," Medical School, Bari, Italy; Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; and Section of Gastroenterology, Department of Medicine, VA Boston Healthcare System, Boston, MA, USA.

Publication details: European Journal of Internal Medicine, volume 128 (2024), pages 10–19. Invited Review Article. Received 25 April 2024; revised 4 July 2024; accepted 5 July 2024; available online 27 July 2024. DOI: 10.1016/j.ejim.2024.07.008. Published as an open-access article under a CC BY license on behalf of the European Federation of Internal Medicine.

Note: This patient-friendly article is based on peer-reviewed research. It summarizes a systematic review of published studies and is intended for educational purposes. It is not a substitute for personalized medical advice. Discuss any changes to your care with your own physician.