Conditions Misdiagnosed as IBS: 7 to Rule Out

IBS is a real diagnosis. It also happens to be the diagnosis that gets given when a workup is incomplete. This page walks through the seven conditions most commonly missed in that scenario, the specific red-flag features that should trigger further investigation, and the tests that distinguish each from true IBS. The goal is to give you the language to ask for what you need from your clinician, not to convince you that something rare is going on.

IBS is defined by the Rome IV criteria as recurrent abdominal pain at least one day per week on average for the prior three months, associated with two or more of the following: pain related to defecation, change in stool frequency, or change in stool form. The symptoms must have started at least six months before diagnosis. Crucially, Rome IV is a positive symptom-based definition, not a results-of-investigation definition. There is no blood test, scan, or biopsy that confirms IBS. There is only a clinical pattern that, after the relevant alternative diagnoses have been excluded, is consistent with IBS.

That structure creates a predictable failure mode. Many of the alternative diagnoses share substantial symptom overlap with IBS. Bloating, irregular bowel habits, abdominal pain, and post-meal distension are all features of IBS, of inflammatory bowel disease, of celiac disease, of small intestinal bacterial overgrowth, of endometriosis, of bile acid malabsorption, and so on. A clinician who matches the symptom pattern to IBS without running the exclusion panel can land on a diagnosis that fits the surface symptoms but misses the underlying condition.

There are several structural reasons this happens, and they are worth naming because understanding them changes how you advocate for yourself. First, primary care visits are short. A focused IBS workup involves a directed history, a small panel of bloodwork, a stool test, and sometimes a referral. Done well it takes more than one visit. Done quickly it gets compressed into a single appointment with the diagnosis given before the labs come back, or with the labs not ordered at all.

Second, the conditions that mimic IBS often have nonspecific early presentations. Crohn's disease can smoulder for years with mild symptoms before a flare. Celiac disease can present with bloating and bowel changes long before the classic textbook features (weight loss, malabsorption, anemia) become obvious. Endometriosis with bowel involvement can produce symptoms identical to IBS-M until you notice the cyclical pattern. None of these announce themselves clearly. They have to be looked for.

Third, jurisdictional defaults vary. In some places fecal calprotectin is part of the standard IBS exclusion panel. In others it is only ordered with red flags. Hydrogen and methane breath testing for SIBO is widely available in some regions and almost unavailable in others. Bile acid malabsorption testing is routine in the United Kingdom (the SeHCAT scan) but inconsistently available across Canada. The result: where you live changes which alternative diagnoses actually get ruled out.

Fourth, budget and resource pressures shorten investigations. A more thorough workup costs more (in tests, in scope time, in specialist visits) and produces a positive finding in a minority of patients. From a population-level view it can look efficient to default to IBS and reserve full workups for red flags. From an individual-level view it can mean a missed diagnosis for the person who does have IBD or celiac but presented without the textbook red flags.

The practical implication of all of this is straightforward. If you were given an IBS diagnosis after a brief visit with no labs, no stool tests, and no follow-up plan, your diagnosis was a working hypothesis at best. That is not a criticism of you or your clinician. It is a description of how the system produces incomplete workups under time pressure. The good news is the workup can be completed later. The seven conditions covered below are the ones worth making sure got ruled out.

Inflammatory bowel disease is the umbrella term for Crohn's disease and ulcerative colitis, two chronic autoimmune conditions in which the immune system attacks the lining of the gastrointestinal tract. Crohn's can affect any part of the GI tract from mouth to anus and tends to involve patchy full-thickness inflammation. Ulcerative colitis is limited to the colon and involves continuous inflammation of the inner lining. Both produce structural damage, both can lead to serious complications if untreated, and both can begin with symptoms that look identical to IBS in the early phase.

The reason IBD gets missed in IBS workups is that the early presentation is often mild. A patient may have intermittent loose stools, cramping, occasional bloating, and fatigue. None of those features differentiate from IBS on their own. The classic textbook IBD picture (significant rectal bleeding, dramatic weight loss, high fevers, severe abdominal pain) is the late presentation. The early presentation is much subtler and can persist for years before a flare forces the diagnosis.

The features that should make any clinician pause before settling on IBS rather than considering IBD are: visible blood in the stool (any amount, any frequency), unintentional weight loss, persistent diarrhea that wakes you at night, unexplained anemia or low ferritin, recurrent low-grade fevers, mouth ulcers, joint pain or skin lesions appearing alongside the bowel symptoms, family history of IBD, and onset after age 50. None of these features are diagnostic in isolation, but any one of them shifts the prior probability away from IBS enough to warrant active investigation.

The first-line test is fecal calprotectin. Calprotectin is a protein released by neutrophils into the bowel lumen during active intestinal inflammation. The test is a single stool sample, inexpensive, and widely available. A low calprotectin (typically below 50 micrograms per gram, though laboratory cutoffs vary) makes active IBD very unlikely and supports a functional diagnosis like IBS. An elevated calprotectin (often above 150 to 250) is the trigger for colonoscopy with biopsies, which is the gold standard for diagnosing IBD and determining its extent.

The structural advantage of calprotectin over older inflammation markers like C-reactive protein and erythrocyte sedimentation rate is that calprotectin reflects bowel-specific inflammation. CRP and ESR rise with systemic inflammation from any cause (infection, autoimmune disease elsewhere, etc.) and can also be normal in early IBD. Calprotectin specifically asks whether neutrophils are migrating into the gut wall, which is the relevant pathophysiology for IBD.

If your calprotectin comes back elevated, the next step is colonoscopy with biopsies, ideally with terminal ileum intubation so that Crohn's involving the small bowel is not missed. Biopsies are essential because the histological features (crypt distortion, granulomas, transmural inflammation) often clarify the diagnosis even when the visual appearance is borderline. If the colonoscopy is negative but calprotectin remains persistently elevated, small bowel imaging (MR enterography) may be warranted to look for Crohn's confined to the small bowel.

A note on overlap: some people genuinely have IBD plus an IBS-like overlay. After IBD is brought into remission with appropriate medical therapy, residual visceral hypersensitivity and altered gut motility can produce ongoing symptoms that meet Rome IV IBS criteria. This is not the same as the IBD being undertreated. It is a known phenomenon called IBS in IBD, and it is treated as IBS once active inflammation is excluded by repeat calprotectin and clinical review. We will revisit this overlap later when we discuss where gut-directed hypnotherapy fits.

The take-home: if you have any IBD red flags and your workup did not include calprotectin, ask for it specifically. The phrasing that works in primary care: “Given the bleeding I've been noticing, can we run a fecal calprotectin to make sure we're not missing inflammation?” A reasonable clinician will agree. For more on how IBD differs structurally from IBS and from SIBO, see our detailed differential breakdown of SIBO, IBS, and IBD.

Celiac disease is an autoimmune reaction to gluten that produces inflammation and progressive damage to the lining of the small intestine. The damage, villous atrophy, blunts the absorptive surface and impairs digestion of many nutrients. The classic textbook presentation involves diarrhea, weight loss, iron deficiency, and malabsorption. The more common modern presentation is much subtler: bloating, intermittent loose or soft stools, fatigue, mild iron or ferritin deficiency, and a symptom pattern that looks indistinguishable from IBS-D or IBS-M.

Estimates of celiac disease prevalence in the general population are around 1 percent, and a meaningful fraction of people meeting Rome IV IBS criteria turn out to have celiac when properly screened. This is precisely why celiac serology is part of the standard IBS exclusion panel in most modern guidelines. Skipping that test risks years of an IBS label sitting on top of undiagnosed celiac, with the ongoing villous damage producing slow-burning consequences (osteoporosis from impaired calcium absorption, infertility, neurological symptoms) that are completely preventable with treatment.

The first-line test is the tissue transglutaminase IgA antibody (tTG-IgA), with a total IgA level run alongside it. The total IgA matters because around 2 to 3 percent of celiac patients are also IgA-deficient, in which case tTG-IgA gives a false negative. If total IgA is low, the lab should reflex to an IgG-based test (deamidated gliadin peptide IgG or tTG-IgG) instead. Asking specifically for “tTG-IgA with total IgA” is the right phrasing.

There is one critical procedural point that catches more people than almost any other testing pitfall in this area: you must be eating gluten for the test to work. The antibodies measured by celiac serology are produced in response to ongoing immune activation by gluten. If you have been gluten-free for weeks to months, the antibody levels fall and the test can come back negative even when you have celiac disease. The same applies to the confirmatory small bowel biopsy, where the villous architecture begins to recover off gluten. The practical consequence is that self-experimenting with a gluten-free diet before getting tested can delay diagnosis for years.

If your tTG-IgA is positive, the diagnostic confirmation is upper endoscopy with duodenal biopsies (multiple biopsies, including from the duodenal bulb). The histology grades villous atrophy on the Marsh scale. A confirmed diagnosis opens up a structured management pathway: dietitian-supported gluten-free diet, dual-energy x-ray absorptiometry (DEXA) for bone density, and follow-up serology to monitor adherence and recovery.

A common scenario worth flagging: a person with IBS-pattern symptoms tries a gluten-free diet, feels better, and concludes they have celiac or non-celiac gluten sensitivity. The improvement is real but the cause is ambiguous. Removing gluten also removes a major source of fructans (a FODMAP), which often explains the symptom improvement in people who actually have FODMAP-sensitive IBS rather than celiac. The two conditions need very different long-term management. Test first, then interpret.

If you have already gone gluten-free without testing, your clinician may recommend a gluten challenge: a defined re-introduction period of normal gluten intake before testing. Six weeks is a common minimum. This is not pleasant if you actually have celiac, but it is the only way to get a reliable test result. If you cannot tolerate a challenge, HLA-DQ2 and HLA-DQ8 genetic testing can be useful: a negative result effectively rules out celiac (you cannot have celiac without these alleles), though a positive only tells you that you are genetically capable of developing it, not that you have it.

Small intestinal bacterial overgrowth is the presence of excessive bacteria in the small intestine, where bacterial counts are normally much lower than in the colon. When small bowel bacteria proliferate beyond normal levels, they ferment ingested carbohydrates locally, producing hydrogen and methane gas. That fermentation produces the symptom pattern most associated with SIBO: significant bloating that worsens within an hour or two of eating, abdominal distension, gas, and altered bowel habits. Symptoms can mirror IBS-D, IBS-M, or in methane-predominant SIBO, IBS-C.

The overlap between SIBO and IBS is substantial enough that estimates of how many people meeting Rome IV IBS criteria actually have SIBO range widely depending on the testing method and threshold used. The exact percentage is debated in the literature. What is not debated is that a meaningful subset of IBS-pattern presentations have an underlying SIBO component that, once treated, produces clear symptom improvement.

The standard non-invasive test is the hydrogen and methane breath test. After an overnight fast, you ingest a defined amount of a fermentable substrate (lactulose or glucose) and provide breath samples at intervals over two to three hours. The breath samples are analysed for hydrogen and methane gas. Bacteria produce these gases as byproducts of fermentation, and rising levels in the small bowel time window suggest excess bacterial activity in the small intestine. There are competing protocols and interpretation criteria (the North American Consensus on breath testing addresses this) and the test is not without controversy in the literature, but it remains the most accessible non-invasive screen.

The clinical features that should prompt a SIBO breath test in an IBS-labelled patient include: bloating-dominant symptom picture, post-meal distension within 60 to 90 minutes, gas as a major complaint, response to short courses of antibiotics in the past, and a history of conditions that predispose to SIBO (prior abdominal surgery, especially anything that altered the ileocecal valve; diabetes; scleroderma; chronic proton pump inhibitor use; any condition that slows small bowel motility).

If SIBO is confirmed, treatment is primarily medical: a course of rifaximin (an antibiotic with minimal systemic absorption that targets the gut), sometimes combined with neomycin or metronidazole if methane is dominant. Dietary approaches (low-FODMAP, elemental diets) are sometimes used as adjuncts. Recurrence is common and points to the importance of identifying and addressing the underlying motility or anatomical predisposition.

The reason this matters for an IBS-labelled patient is that rifaximin treatment of underlying SIBO can produce dramatic and sustained symptom improvement that no IBS treatment will reproduce. If your bloating is the dominant symptom, if it is worse within an hour of eating, and if you have never had a breath test, that is a reasonable conversation to have with your clinician.

A practical caveat: SIBO testing is not universally available, and access varies by region. In some Canadian provinces breath testing is straightforward through gastroenterology referral. In others it requires private-pay through specialty labs. If breath testing is not accessible, an empirical trial of rifaximin guided by a gastroenterologist is sometimes used, particularly when the symptom picture is highly suggestive.

Endometriosis is a condition in which tissue similar to the lining of the uterus grows outside the uterus, often on the ovaries, fallopian tubes, the pelvic peritoneum, the bladder, or the bowel. When endometriotic implants or adhesions involve the bowel, they produce symptoms that can be indistinguishable from IBS: cramping abdominal pain, bloating, altered bowel habits, painful bowel movements, and bouts of diarrhea or constipation.

The reason endometriosis is so commonly misdiagnosed as IBS is partly a consequence of the symptom overlap and partly a consequence of how diagnostic attention is allocated. A woman presenting to primary care with cyclical pelvic and abdominal pain is sometimes triaged into a gastroenterology pathway when the dominant symptoms are bowel-pattern, even though the underlying problem is gynecological. The cycle of symptoms is the clue, but it is easy to miss without explicitly looking for it.

Diagnostic delay for endometriosis averages around 7 to 10 years from symptom onset, depending on the population studied. Many women in that delay window receive an IBS diagnosis along the way, and the IBS label can actively interfere with the eventual workup by anchoring clinicians on a functional explanation when a structural one is present.

The features that should prompt consideration of endometriosis in any woman with an IBS diagnosis include: pain that worsens predictably around menstruation, painful periods (dysmenorrhea) more severe than typical, pain with deep penetration during intercourse (dyspareunia), pain with bowel movements that intensifies during menstruation, infertility or difficulty conceiving, and symptoms that do not respond to standard IBS interventions. Cyclical patterning is the most useful single feature: keep a symptom diary for two to three menstrual cycles and look for clustering around specific days of the cycle.

Diagnostic workup for suspected endometriosis starts with gynecological referral. Imaging plays a role: transvaginal ultrasound by an operator experienced in endometriosis can identify deep infiltrating endometriosis and ovarian endometriomas, and pelvic MRI provides additional detail. The definitive diagnosis remains laparoscopy with histological confirmation of endometriotic implants. Treatment options range from hormonal suppression to surgical excision, and management is best done at an endometriosis-experienced centre.

The take-home for women who have been told they have IBS but suspect their symptoms are cyclical: track your symptoms against your cycle for two to three months. If a clear pattern emerges, take that diary to a clinician and ask directly whether endometriosis has been considered. This is not a fringe question. Asking it changes management for a substantial share of women who have been mislabelled as having IBS.

The pancreas produces digestive enzymes (lipase, amylase, proteases) that the small intestine needs to break down fat, carbohydrate, and protein. Exocrine pancreatic insufficiency is the condition in which the pancreas fails to produce enough of these enzymes to digest food adequately. The result is malabsorption, especially of fat, with characteristic symptoms: greasy, pale, foul-smelling stools that are difficult to flush (steatorrhea), bloating and excessive gas after eating, weight loss despite adequate intake, and fatigue.

EPI is most commonly associated with chronic pancreatitis, cystic fibrosis, pancreatic cancer, and prior pancreatic surgery. It can also occur in long-standing diabetes and after some abdominal surgeries that alter normal digestion. The IBS-misdiagnosis pattern arises in milder cases where the steatorrhea is intermittent rather than dramatic, where weight loss is gradual, and where the bloating and altered bowel habits dominate the clinical picture. Those patients can spend years labelled as IBS-D before someone runs the right test.

The first-line screening test is fecal elastase. Elastase is a pancreatic enzyme that survives intestinal transit and can be measured in a single stool sample. Low fecal elastase (typically below 200 micrograms per gram, with values below 100 indicating severe insufficiency) suggests pancreatic insufficiency and warrants further workup, usually with cross-sectional imaging of the pancreas (MRI or CT) and gastroenterology referral.

The clinical features that should prompt fecal elastase testing in an IBS-labelled patient include: stools that are visibly greasy or pale, stools that are difficult to flush or float prominently, weight loss that does not fit a functional diagnosis, history of pancreatitis or significant alcohol use, long-standing diabetes, and bloating that is dominant after fatty meals specifically. Steatorrhea is the most specific feature. If you have been labelled IBS-D and have visibly greasy stools, that combination is worth a fecal elastase test.

If EPI is confirmed, treatment is pancreatic enzyme replacement therapy (PERT), which is straightforward and highly effective when dosed correctly. Many people see dramatic symptom improvement within days of starting appropriate replacement. The reason this matters: the IBS label keeps the wrong treatment going (low FODMAP, antispasmodics, none of which address the underlying enzyme deficiency) while a simple intervention is being missed.

Microscopic colitis is a chronic inflammatory condition of the colon that produces persistent watery diarrhea but cannot be seen on standard colonoscopy. The colon looks normal to the eye. The diagnosis is made on biopsy: the pathologist sees abnormal lymphocytes infiltrating the lining (lymphocytic colitis) or a thickened collagen band beneath the surface epithelium (collagenous colitis). Both subtypes are managed similarly.

Microscopic colitis is most common in middle-aged and older women, and the incidence has been rising. The classic presentation is chronic, often debilitating, watery diarrhea that can include several to many bowel movements per day, urgency, and occasional nocturnal diarrhea. Weight loss is variable. Crampy abdominal pain is common. The picture can look very similar to IBS-D, particularly in patients in whom standard colonoscopy was performed and reported as normal: the assumption becomes that nothing structural is going on and IBS becomes the working diagnosis.

The crucial procedural point is that colonoscopy alone does not rule out microscopic colitis. The colon needs to be biopsied even when it looks normal, with biopsies taken from multiple segments (right and left colon) because the disease can be patchy. If you have had a colonoscopy and were told it was normal, ask whether random biopsies were taken to rule out microscopic colitis specifically. If not, this is worth raising, particularly if your dominant symptom is chronic watery diarrhea.

Microscopic colitis is often triggered or worsened by certain medications. Non-steroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), selective serotonin reuptake inhibitors (SSRIs), and statins are the most commonly implicated. A careful medication review, including over-the-counter products, is part of the workup. In some cases stopping the offending medication produces resolution.

Treatment of established microscopic colitis is medical, most commonly with budesonide (a topical corticosteroid with limited systemic effect). Bile acid sequestrants are sometimes added when bile acid malabsorption coexists, which it often does. With appropriate treatment most people improve significantly, which makes the missed diagnosis all the more frustrating: years of being told you have IBS-D when a single round of budesonide would have changed your life.

Bile acids are produced by the liver, stored in the gallbladder, and released into the small intestine to help digest fats. Under normal conditions the bile acids are reabsorbed in the terminal ileum and recycled. Bile acid malabsorption is the condition in which this reabsorption fails, allowing excess bile acids to spill into the colon where they irritate the lining, accelerate motility, and produce watery diarrhea. The symptom pattern can be indistinguishable from IBS-D.

Estimates of how many people with an IBS-D label actually have underlying bile acid malabsorption have ranged as high as roughly 30 percent in some series. The condition is meaningfully under-recognised in part because the most accurate diagnostic test (the SeHCAT scan, a nuclear medicine study) is routinely available in the United Kingdom but inconsistently available across North America. Where SeHCAT is not accessible, the diagnosis is often made empirically by trial of bile acid sequestrants (cholestyramine, colesevelam, colestipol) and observed response.

The features that suggest bile acid malabsorption in an IBS-D-labelled patient include: chronic watery diarrhea with urgency, post-meal urgency (often worsening within an hour of eating, particularly fatty meals), nocturnal diarrhea, history of cholecystectomy (gallbladder removal), prior ileal surgery, Crohn's disease affecting the terminal ileum, or pelvic radiation history. Steatorrhea is variable and is not required to suspect bile acid malabsorption.

A reasonable conversation to have with a gastroenterologist if you have IBS-D and these features: ask whether bile acid malabsorption has been considered and whether SeHCAT testing is available locally. If not, ask whether an empirical trial of a bile acid sequestrant is reasonable as a diagnostic and therapeutic step. Many patients with bile acid malabsorption see response within days to weeks of starting an appropriate sequestrant, which is both useful clinically and diagnostic by inference.

The four scenarios that justify pushing for further workup are straightforward. First: standard IBS interventions are not working. If you have given a reasonable trial to dietary changes, antispasmodics, fibre adjustments, low-FODMAP under dietitian supervision, and (where indicated) gut-directed hypnotherapy, and your symptoms are not meaningfully better, the diagnosis deserves another look. The principle is simple: if treatment is not working, the first question is the diagnosis.

Second: any red-flag symptom that was not specifically worked up. Visible blood in stool, unintentional weight loss, persistent nocturnal diarrhea, fevers, anemia, family history of IBD or colorectal cancer, and onset after age 50 are all features that warrant active investigation regardless of whether the rest of the picture looks like IBS. If any of these are part of your story and your workup did not include the corresponding tests (calprotectin for bleeding and inflammation, colonoscopy with biopsies for any of the above, full bloodwork for anemia and inflammation), that gap is worth closing.

Third: a symptom pattern that does not actually fit Rome IV cleanly. The Rome IV criteria require recurrent abdominal pain related to defecation, change in stool frequency, or change in stool form. If your symptoms are dominantly bloating without abdominal pain, or your pain is not related to bowel movements, or your symptom pattern is clearly cyclical with menses, then the Rome IV positive criteria are not actually met and the IBS label is being applied loosely. A clinician should be able to walk you through which Rome IV criteria your symptoms specifically meet.

Fourth: a workup that was clearly incomplete. If your IBS diagnosis was given in a single visit with no labs ordered, no stool tests, and no follow-up plan, the workup is not done. That is not a failing on your part. It is a system outcome. The right next step is to advocate for completion: the baseline bloodwork, fecal calprotectin, celiac serology, and any further testing indicated by the specific symptom pattern.

A short word on what “rule out” actually means in my hypnotherapy practice. It does not mean ruling out every conceivable rare condition. That is impossible and would not be good medicine. It means actively excluding the conditions that share substantial symptom overlap with the working diagnosis, using the tests with the right sensitivity and specificity for those conditions. For an IBS workup, that is the baseline panel plus calprotectin plus celiac serology, with additional targeted tests added based on the specific symptom pattern. That is the bar.

On asking for a second opinion: in Canada you have the right to request a referral to a specialist or to seek a second opinion within the public system. The wording matters. Rather than “I want a second opinion because I don't trust the diagnosis,” try “I'd like to make sure we have not missed anything that needs different treatment. Could we either run additional tests or refer to gastroenterology so that the workup is complete?” That framing is collaborative and harder to refuse. If your primary care clinician still declines and cannot offer a clinical reason, walk-in clinics and provincial telehealth services are reasonable alternatives for initiating the bloodwork.

Everything above has been about getting the diagnosis right. The reason this page exists, written by a clinical hypnotherapist, is that the same dynamic shows up on the other side: people whose diagnosis is correct, who arrive looking for gut-directed hypnotherapy, and who deserve a clinician who will actually check that the diagnosis is solid before starting work. The point of this section is to be honest about where gut-directed hypnotherapy belongs in the pathway: at the end, after the diagnosis has been confirmed, not before.

Gut-directed hypnotherapy (GDH) is an evidence-based treatment for IBS, developed at the University of Manchester and structured around what is now called the Manchester Protocol. It works by using focused, absorbed attention to recalibrate the gut-brain axis: reducing visceral hypersensitivity, normalising motility patterns, and resetting the threat appraisal that the central nervous system applies to gut sensations. The clinical literature supporting it is substantial and spans decades.

The largest single-clinic case series, Miller 2015 (PMID 25736234), reported a 76 percent response rate in 1,000 consecutive refractory IBS patients treated on the Manchester Protocol, where response was defined as at least 50 percent improvement on validated symptom scoring. This is real-world clinic data, not a randomised trial, and it should be interpreted as an outcome benchmark from a specialist centre rather than as RCT-quality evidence. The point worth holding onto: in patients whose IBS diagnosis was correct, GDH produced meaningful response in roughly three-quarters of them.

Two qualifications matter here. First, GDH is for confirmed IBS. It is not for undifferentiated abdominal symptoms. If your workup is incomplete, the right next step is the workup, not GDH. Starting hypnotherapy on top of an unconfirmed diagnosis can produce symptom modification (reduced perception of pain, reduced anxiety around symptoms) that masks an underlying structural or inflammatory condition that is still progressing. That is not a path you want.

Second, GDH is appropriate as part of the management of overlap presentations, but only after the structural component has been addressed. A person with Crohn's in remission who continues to have IBS-pattern symptoms is a reasonable candidate for GDH, because the active inflammation has been brought under control and the residual visceral hypersensitivity is the right target. A person with active untreated IBD is not.

The same principle applies across the seven conditions covered above. Treat the celiac with a gluten-free diet and follow-up serology. Treat the SIBO with rifaximin. Treat the endometriosis with hormonal suppression or surgery. Treat the EPI with enzyme replacement. Treat the microscopic colitis with budesonide. Treat the bile acid malabsorption with a sequestrant. If, after the underlying condition is appropriately managed, residual IBS-pattern symptoms remain and meet Rome IV criteria, that is the moment GDH belongs in the conversation.

For more on what GDH actually involves, the protocol structure, and what the evidence supports, see our detailed page on gut-directed hypnotherapy for confirmed IBS. For the underlying mechanisms of IBS that GDH targets, see what actually causes IBS. For the formal diagnostic criteria, see our walkthrough of the Rome IV criteria for IBS.