IBS: Dysbiosis or Malabsorption?

Recurring abdominal pain, bloating, alternating bowel habits, diarrhea or constipation are among the most common symptoms seen in clinical practice. The risk, especially in the context of integrative medicine, is interpreting them too quickly as dysbiosis or irritable bowel syndrome, without distinguishing between functional syndromes, malabsorption, organic inflammation, and iatrogenic conditions.

Irritable bowel syndrome (IBS, irritable bowel syndrome) is a disorder of gut-brain interaction, not an endless exclusionary diagnosis or a residual category for patients “with nothing wrong.” According to the Rome IV framework (the international classification and diagnostic criteria system developed by the Rome Foundation), functional gastrointestinal disorders are today defined and diagnosed as disorders of gut-brain interaction (DGBI, disorders of gut-brain interaction), characterized by integrated alterations in motility, visceral sensitivity, mucosal/immune function, microbiota, and central pain processing (1).

The clinical point is therefore twofold: recognize IBS as a real condition with meaningful impact on quality of life, but at the same time avoid diagnosing malabsorption, celiac disease, inflammatory bowel diseases, bile acid diarrhea, or exocrine pancreatic insufficiency as simply “irritable colon.” An integrated approach makes sense only if it starts from an essential work-up, identifies red flags, and uses diet, fiber, probiotics, and lifestyle in a targeted way, with measurable outcomes.

Irritable bowel syndrome: a positive diagnosis, not one of exclusion

The Rome IV criteria define IBS as recurring abdominal pain, at least 1 day per week in the last 3 months, associated with at least two among: relation to defecation, change in stool frequency, or change in stool form. The subtypes are classified based on the Bristol Stool Form Scale (BSFS, Bristol stool form scale):

• IBS with constipation predominance (IBS-C, constipation-predominant IBS);
• IBS with diarrhea predominance (IBS-D, diarrhea-predominant IBS);
• IBS mixed (IBS-M, mixed IBS), or unclassified (IBS-U, unclassified IBS) (2). 

This classification guides treatment. A patient with IBS-D and postprandial urgency requires different priorities than a patient with IBS-C, bloating, and a sense of incomplete evacuation. Likewise, the presence of anticipatory anxiety, visceral hypervigilance, insomnia, or chronic pain suggests a gut-brain–dominant phenotype where diet and drugs alone may be insufficient.

Guidelines from the British Society of Gastroenterology (BSG) and the American College of Gastroenterology (ACG)support a positive diagnostic approach when clinical criteria are met and there are no alarm features. This reduces repeated diagnostic workups, medicalization, and costs, but it does not justify laxity: thorough history-taking, physical examination, medication review, first-line tests, and attention to symptoms not compatible with a functional form are required (3,4).

Dysbiosis: a useful concept, a weak diagnosis

The term “dysbiosis” denotes a qualitative or functional alteration of the microbiota relative to a presumed eubiotic ecosystem. However, in clinical practice, “dysbiosis” is not a stand-alone diagnosis with universally validated cutoffs.

This point is crucial. Commercial microbiota tests can yield impressive reports, but rarely change patient management in an evidence-based way. The risk is shifting focus to bacterial abundances that are difficult to interpret, while overlooking more solid information: the duration and features of symptoms, unintentional weight loss, anemia, nocturnal diarrhea, family history, medications, diet, prior infections, travel, abdominal surgery, alcohol use, and eating disorders.

The microbiota should be treated as a “functional interface,” not as an isolated target. The physician should not chase the normalization of a chart, but instead improve symptoms, quality of life, dietary tolerance, bowel function, and clinical markers. The practical question becomes: «Which interventions increase the resilience of the intestinal ecosystem without creating unnecessary restrictions or diagnostic delays?»

When to think about malabsorption

Malabsorption implies a defect in the digestion or absorption of nutrients. It can involve fats, carbohydrates, proteins, micronutrients, or bile salts. Unlike IBS, it tends to produce more systemic signs: unintended weight loss, steatorrhea, iron deficiency, vitamin B12 or folate deficiency, hypoalbuminemia, edema, osteopenia, cramps, neuropathy, and disproportionate fatigue.

The main causes to consider include celiac disease, exocrine pancreatic insufficiency, bile acid diarrhea, inflammatory bowel disease, intestinal resections, enteropathies, chronic infections, lactose intolerance, small intestinal bacterial overgrowth (SIBO), and medications. The BSG guidelines on chronic diarrhea specifically call for excluding inflammation, neoplasia, celiac disease, and commonly underdiagnosed conditions like bile acid diarrhea and microscopic colitis (5).

A note on celiac disease: it can mimic IBS-D or IBS-M, but requires proper serologic and histologic diagnosis. Updated ACG guidelines recommend performing serologic tests while the patient is consuming gluten; starting a gluten-free diet before work-up can make diagnosis more difficult (6). The same applies to DIY restrictive diets: they can temporarily reduce symptoms but mask organic pathology.

Essential work-up: a few tests, but well chosen

In a patient with symptoms compatible with IBS, and no red flags, the work-up must be proportionate. In cases with chronic diarrhea or IBS-D, the American Gastroenterological Association (AGA) suggests targeted testing to exclude treatable conditions such as Giardia infection, celiac disease, inflammatory bowel disease, and bile acid diarrhea, avoiding indiscriminate panels (7).

A reasonable first-line panel may include: complete blood count (CBC), ferritin, vitamin B12, folates; C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), thyroid-stimulating hormone (TSH), liver function tests, albumin, electrolytes, serology for celiac disease with anti-tissue transglutaminase IgA (tTG-IgA) and total IgA. In patients with persistent diarrhea or suspected inflammatory patterns, fecal calprotectin helps distinguish a functional phenotype from possible inflammatory bowel disease (IBD), though it does not replace specialist assessment (3,5,7).

If the picture suggests fat malabsorption, weight loss, or steatorrhea, exocrine pancreatic insufficiency (EPI) should be considered, especially in patients with chronic pancreatitis, pancreatic surgery, long-standing diabetes, alcoholism, cystic fibrosis, or pancreatic neoplasms. The AGA Clinical Practice Update 2023 identifies fecal elastase as the noninvasive reference test in practice, to be interpreted with care in the setting of watery stools (8).

SIBO: a diagnosable condition, but frequently overdiagnosed

SIBO can occur in predisposed contexts: anatomical changes, surgery, motility disorders, scleroderma, chronic opioid use, hypochlorhydria, diabetes with autonomic neuropathy (9). However, bloating and gas alone are not sufficient to diagnose SIBO. Glucose- or lactulose-based breath tests can be helpful in select patients, but there are diagnostic limitations and a risk of overdiagnosis, necessitating targeted use. The growing risk is labeling every IBS patient with bloating as SIBO. In practice, evaluate for SIBO when there is a clear clinical rationale: predisposing factors, diarrhea/malabsorption, nutritional deficiencies, atypical responses to fermentable carbohydrates, prior surgery or dysmotility.

Diet: low-FODMAP yes, but not a definitive diet

The low-FODMAP diet (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) is the dietary intervention with the strongest evidence in IBS. A meta-analysis by Black, Staudacher, and Ford showed that the low-FODMAP diet sits among the most effective dietary strategies for global IBS symptoms (10). The AGA Clinical Practice Update 2023 on the role of diet in IBS also regards it as the most evidence-supported dietary approach (11).

The critical point is how to apply it. The low-FODMAP diet should not be prescribed as a permanent exclusion, but as a three-phase protocol: short-term restriction (usually 4–6 weeks), structured reintroduction of FODMAP groups, and long-term personalization. The reintroduction phase is the most important: it helps distinguish true triggers from unnecessary restrictions and helps recover dietary diversity, fiber, and overall diet quality.

In patients with a history of eating disorders, fear of foods, underweight, or many restrictions, the low-FODMAP approach can be counterproductive. In these cases, starting with adapted “healthy eating” guidance is preferable: regular meals, limiting very fatty meals, alcohol, caffeine, and polyols, staying well hydrated, choosing soluble fiber, and managing stress.

Fiber, prebiotics, and probiotics: precision before trendiness

In IBS, soluble and viscous fibers, such as Psyllium (Ispaghula), have a more favorable profile than insoluble, highly fermentable fibers that can worsen bloating and pain in some patients. The AGA recognizes the effectiveness of soluble fiber on global symptoms (11).

Prebiotics, such as inulin, fructo-oligosaccharides or galacto-oligosaccharides, can modulate the microbiota, but in IBS patients they should be titrated with caution: start with low doses, increase gradually, monitor bloating, pain, and sleep quality. “Feeding the microbiota” does not mean forcing fermentable fibers into a hypersensitive gut.

Regarding probiotics, the stance should be measured. AGA guidelines on probiotics recommend using them in IBS only within clinical trials, reflecting heterogeneity of strains, endpoints, and quality of evidence. (12) This does not mean no patient will respond, but that the notion “probiotic for IBS” is too generic. If a trial is chosen, define the strain, formulation, dose, duration (4–8 weeks), outcome, and stopping criteria. A probiotic without a measurable response should not be continued for months “to rebalance the flora.”

Gut-brain interaction: real symptoms, multimodal treatment

IBS is heavily modulated by the central nervous system, stress, and visceral hypervigilance. Pain, urgency, and bloating can amplify anticipatory anxiety; anxiety increases visceral sensitivity and hyperarousal, and fragmented sleep lowers the pain threshold. This circuit explains why some patients do not respond to a single diet, even when technically well implemented. Guidelines from the ACG and BSG include therapies targeting the gut-brain axis, such as gut-directed psychotherapy, cognitive-behavioral therapy, and gut-directed hypnosis, for patients with persistent symptoms (3,4). This means offering interventions on sleep, activity, breathing, stress, and the relationship with food not as “alternatives,” but as part of the pathophysiology-driven treatment.

Medications, supplements, and iatrogenesis

Many intestinal symptoms are amplified or sustained by medications: metformin, magnesium, antacids, proton pump inhibitors, antibiotics, nonsteroidal anti-inflammatory drugs, opioids, iron, antidepressants, laxatives, sweeteners, and supplements. A comprehensive medication review is often more useful than a new microbiota test. In IBS, pharmacologic treatment should be tailored to the subtype (IBS-D or IBS-C) and aligned with specialist guidelines.

Malabsorption, dysbiosis, and IBS share symptoms but are not interchangeable. An integrated approach is useful if it maintains clinical discipline: a positive IBS diagnosis where appropriate, targeted exclusion of organic pathologies, prudent use of the dysbiosis concept, and interventions with measurable outcomes. The true goal is not to “clear out” or “reset” the gut, but to restore function: less pain, more predictable bowel movements, better tolerance to foods, reduced anticipatory anxiety, and improved quality of life.

Red flags and diagnoses not to miss

Alarm signs

• Unintentional weight loss.
• Blood in stools, iron-deficiency anemia, fever.
• Nocturnal or progressive diarrhea.
• Onset of symptoms after age 50.
• Family history of colorectal cancer, celiac disease, or IBD.
• Persistent vomiting, dysphagia, progressive pain.
• Abdominal mass, ascites, or significant abnormal laboratory results.

Diagnoses to consider before concluding IBS

• Celiac disease.
• IBD: Crohn’s disease and ulcerative colitis.
• Microscopic colitis.
• Diarrea da acidi biliari (bile acid diarrhea).
• Exocrine pancreatic insufficiency.
• Lactose intolerance or other malabsorption disorders.
• SIBO in predisposed patients.
• Gastrointestinal neoplasms in compatible presentations.
• Endocrine/metabolic causes: hyperthyroidism, diabetes, adrenal insufficiency in specific contexts.
• Iatrogenic causes: medications, supplements, alcohol, sweeteners.

First-line tests

• CBC, ferritin, B12, folates.
• CRP, ESR, albumin, liver function.
• TSH.
• tTG-IgA + total IgA for celiac disease.
• Fecal calprotectin, if persistent diarrhea or suspected inflammatory process.
• Giardia testing if risk or exposure.
• Fecal elastase if suspected EPI (Exocrine Pancreatic Insufficiency).
• Assessment for bile acid diarrhea when available and clinically indicated.

Stepwise protocol

Step 1 – Phenotype. Define IBS subtype, duration, triggers, relation to meals/defecation, Bristol score, pain, urgency, bloating, red flags, medications, and dietary history. Add simple scores: IBS-SSS (Irritable Bowel Syndrome Severity Scoring System), Bristol, dietary-symptom diary, and quality-of-life scale.

Step 2 – Exclude what changes management. Request only essential tests: celiac testing before gluten elimination; calprotectin in persistent diarrhea; ferritin, B12, folates if malabsorption is suspected; fecal elastase if signs of EPI are present.

Step 3 – Stabilize the baseline. Regular meals, limit ultra-processed foods, alcohol, caffeine, and polyols; slow chewing; proper hydration; titrated soluble fiber; physical activity; and sleep. This phase can already improve many patients.

Step 4 – Targeted diet. If symptoms persist and the phenotype is compatible, guided low-FODMAP for 4–6 weeks, then reintroduction. Avoid indefinite restrictions. In vulnerable or highly restricted patients, favor less drastic interventions.

Step 5 – Selective interventions. Probiotics only as a time-limited trial; prebiotics at low doses; evidence-based drugs tailored to the subtype; gut-brain therapy if pain, anxiety, avoidance, or hypervigilance dominate the picture.

Step 6 – Reassess. After 8–12 weeks, reassess symptoms, Bristol score, quality of life, and safety; if there is no response, reconsider the diagnosis and refer to a gastroenterologist.

Minimal outcomes at 8–12 weeks

Intestinal symptoms

• IBS-SSS reduction of at least 50 points.
• Reduction in days with abdominal pain.
• Improvement in urgency/incomplete evacuation.
• Normalization or improvement of Bristol score.

Function and quality of life

• Less dietary and social avoidance.
• Better tolerance of full meals.
• Reduced work absence or daily life limitations.
• Greater confidence in managing triggers.

Nutrition

• Progressive reintroduction of previously excluded foods.
• Adequate intake of tolerated fiber.
• Avoid unintentional weight loss.
• Monitor for risk of overly restrictive dieting.

Safety

• No anemia, no unintended weight loss, or adverse biochemical changes.
• Review of medications and supplements.
• Referral to a gastroenterologist if red flags, abnormal markers, or lack of response.

Article excerpt from the October 2026 issue of Karla Miller

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