IBS: Beyond the Diagnosis of Exclusion
IBS — Irritable Bowel Syndrome — is not a diagnosis. It is a description.
IBS: Beyond the Diagnosis of Exclusion
The Laziest Diagnosis in Medicine
IBS — Irritable Bowel Syndrome — is not a diagnosis. It is a description. Telling someone they have IBS is like telling someone their car is broken because it makes a noise. You have described the symptom. You have explained nothing.
Rome IV criteria define IBS as recurrent abdominal pain at least one day per week for three months, associated with defecation, change in stool frequency, or change in stool form. Notice what is missing: any mention of why. This is a pattern-recognition label, not a root cause identification. Conventional gastroenterology hands you this label after a colonoscopy comes back normal, maybe a celiac panel, and then offers antispasmodics, fiber, and the suggestion to “manage stress.”
Functional medicine refuses to stop there. Behind every case of “IBS” lies one or more identifiable, treatable mechanisms. The question is never do you have IBS — the question is what is causing your IBS symptoms?
The Hidden Causes Behind “IBS”
SIBO: The Elephant in the Room
Small Intestinal Bacterial Overgrowth is present in 60-80% of IBS patients according to the landmark work of Dr. Mark Pimentel at Cedars-Sinai. Bacteria that belong in the colon have migrated upstream into the small intestine, where they ferment food prematurely, producing hydrogen, methane, or hydrogen sulfide gas. The result: bloating within 30-90 minutes of eating, distension, pain, altered motility.
Hydrogen-dominant SIBO tends toward diarrhea (IBS-D). Methane-dominant overgrowth — now called Intestinal Methanogen Overgrowth (IMO) — slows transit and causes constipation (IBS-C). Hydrogen sulfide SIBO causes diarrhea with a rotten-egg odor. Diagnosis: lactulose or glucose breath test. Treatment: see the dedicated SIBO protocol.
Post-Infectious IBS: The Autoimmune Gut
Here is a story that conventional medicine rarely tells. You get food poisoning — Campylobacter, Salmonella, E. coli, Shigella. You recover. But weeks later, IBS symptoms begin and never leave. This is post-infectious IBS, and it accounts for roughly 10-15% of all IBS cases.
The mechanism: bacterial toxins called Cytolethal Distending Toxin B (CdtB) trigger an immune response. Your body produces anti-CdtB antibodies that cross-react with vinculin, a structural protein in the interstitial cells of Cajal — the pacemaker cells of your gut. This autoimmune attack damages the Migrating Motor Complex (MMC), the sweeping wave that clears bacteria from the small intestine between meals. Damaged MMC means stagnant small intestine means SIBO.
The IBS Smart test (Gemelli Biotech) measures anti-vinculin and anti-CdtB antibodies. Elevated levels confirm post-infectious IBS with autoimmune motility damage. This changes the entire treatment approach: you must support the MMC aggressively with prokinetics (low-dose erythromycin 50mg at bedtime, prucalopride 1-2mg, or herbal options like ginger 1000mg + 5-HTP 50-100mg at bedtime) and treat recurrent SIBO as a chronic management issue rather than a one-time fix.
Bile Acid Malabsorption (BAM)
Up to 30% of patients diagnosed with IBS-D actually have bile acid malabsorption. Bile acids produced by the liver are supposed to be reabsorbed in the terminal ileum. When they are not, they spill into the colon where they act as a potent laxative — watery, urgent diarrhea, often bright yellow or green.
Testing: SeHCAT scan is the gold standard (available in the UK, limited elsewhere), serum C4 level is a surrogate marker (elevated = bile acid overproduction), or a therapeutic trial of cholestyramine. Treatment: cholestyramine 4g before meals (start low — it causes bloating), ox bile 125-250mg with fatty meals if bile production is low rather than high, TUDCA (tauroursodeoxycholic acid) 250-500mg for bile quality optimization.
Visceral Hypersensitivity
Some guts are simply wired to feel more. Visceral hypersensitivity means the pain threshold of gut neurons is lowered — normal distension that a healthy person would not notice registers as pain. This is often post-infectious or trauma-related. The gut-brain axis has been recalibrated toward threat.
This is not “in your head.” This is measurable central sensitization — the same process seen in fibromyalgia and chronic pain syndromes.
Treatment approaches:
- Peppermint oil (IBgard 90mg enteric-coated, 3x/day): Khanna 2014 meta-analysis showed an NNT of 2.5 — meaning for every 2.5 patients treated, one achieves significant relief. Peppermint is a calcium channel blocker in smooth muscle and a TRPM8 agonist that produces an analgesic cooling sensation.
- Gut-directed hypnotherapy: The Monash University protocol achieves 70-80% response rates with effects lasting years after treatment ends. This is not stage hypnosis. This is targeted neuroplasticity work that resets visceral pain processing in the brain.
- Low-dose amitriptyline 10-25mg at bedtime: Acts as a visceral analgesic at sub-antidepressant doses by modulating descending pain inhibition pathways.
- Vagal toning: Breathing exercises, cold water face immersion, humming — all activate the vagus nerve and shift the autonomic nervous system toward parasympathetic calm.
Dysbiosis Without SIBO
Not all microbial imbalance is in the small intestine. Large intestinal dysbiosis — low Bifidobacterium, low Akkermansia muciniphila, low Faecalibacterium prausnitzii, high pathobionts like Klebsiella, Citrobacter, or Proteus — creates inflammation, altered motility, impaired short-chain fatty acid production, and barrier dysfunction. GI-MAP testing with PCR quantification guides targeted treatment: specific probiotics, prebiotics, antimicrobials, and dietary shifts.
Food Sensitivities and FODMAP Intolerance
IgG-mediated food sensitivities, histamine intolerance, and FODMAP intolerance all produce IBS-like symptoms. The low-FODMAP diet (developed at Monash University, best tracked with their app) achieves a 75% response rate. But here is the critical point most practitioners miss: the low-FODMAP diet is a SHORT-TERM diagnostic tool, not a permanent lifestyle. It should last 4-6 weeks, followed by systematic reintroduction of each FODMAP group to identify specific triggers.
Long-term FODMAP restriction starves beneficial bacteria — particularly Bifidobacterium — and impoverishes the microbiome. You solve one problem by creating another.
Histamine intolerance deserves its own screening: DAO enzyme level in serum, OAT test for histamine metabolites, and a careful dietary history. Treatment includes DAO enzyme supplementation, low-histamine diet, and addressing the underlying cause (often SIBO, dysbiosis, or mast cell activation).
Parasites
Blastocystis hominis, Dientamoeba fragilis, and Giardia lamblia all cause IBS-like symptoms and are routinely missed by conventional stool O&P testing. GI-MAP uses PCR — far more sensitive. Post-travel IBS should always prompt parasite screening.
Candida Overgrowth
Especially suspect in IBS-D with bloating, brain fog, sugar cravings, and a history of antibiotic use or oral contraceptives. OAT test shows elevated arabinose and tartaric acid. GI-MAP shows yeast overgrowth. Treatment: antifungals (fluconazole or herbal — oregano oil, caprylic acid, Pau d’Arco), biofilm disruptors, low-sugar diet, Saccharomyces boulardii.
Pancreatic Exocrine Insufficiency
More common than recognized, especially in older patients and those with IBS-D. Symptoms: greasy stools, undigested food, bloating after fatty meals, weight loss. GI-MAP measures pancreatic elastase-1: below 200 mcg/g indicates insufficiency. Treatment: pancreatic enzyme replacement — prescription Creon or OTC pancreatin 500mg with meals. Response is often dramatic and rapid.
Motility Disorders
Gastroparesis, colonic inertia, pelvic floor dysfunction — these are specific motility diagnoses hiding under the IBS umbrella. Testing: SmartPill wireless motility capsule, sitz marker study (for colonic transit), anorectal manometry (for pelvic floor function).
Dyssynergic defecation deserves special attention: paradoxical contraction of the pelvic floor muscles during straining. The patient pushes, and the exit door closes instead of opens. Biofeedback pelvic floor physical therapy has greater than 70% cure rate for this condition — yet most patients are never tested and cycle through laxatives for years.
Stress and the Gut-Brain Axis
Rome IV now officially classifies IBS as a “disorder of gut-brain interaction.” This is not dismissive — it is mechanistic. Autonomic nervous system dysregulation drives altered motility, mast cell activation in the intestinal mucosa, increased intestinal permeability, and visceral hypersensitivity. The CRH (corticotropin-releasing hormone) pathway links psychological stress directly to gut inflammation.
Psycho-neuro-gastroenterology is the emerging field addressing this axis with gut-directed hypnotherapy, CBT for IBS (NICE-recommended), vagal toning, and comprehensive stress management.
Endometriosis: The Hidden Mimic
In women with IBS-like symptoms that worsen cyclically with the menstrual period, always consider endometriosis. Forty to fifty percent of women with endometriosis receive an IBS diagnosis first. Dyschezia (painful bowel movements) during menses is a red flag. See the dedicated endometriosis protocol.
The Testing Approach
Do not guess. Test systematically:
- GI-MAP: Comprehensive stool PCR — pathogens, parasites, yeast, bacterial balance, elastase-1, calprotectin, zonulin, beta-glucuronidase, secretory IgA, anti-gliadin IgA
- SIBO breath test: Lactulose preferred (tests entire small intestine), 3-gas if available (hydrogen, methane, hydrogen sulfide)
- IBS Smart test: Anti-vinculin and anti-CdtB antibodies (post-infectious IBS)
- Calprotectin: Elevated = inflammatory bowel disease (IBD) until proven otherwise — refer for colonoscopy
- Celiac panel: tTG IgA + total IgA (2-3% of “IBS” is undiagnosed celiac, and IgA deficiency causes false negatives)
- Thyroid panel: Hypothyroidism → constipation, hyperthyroidism → diarrhea
- Food sensitivity panel: IgG-mediated (controversial but clinically useful as guide)
- OAT (Organic Acids Test): Yeast markers, bacterial metabolites, neurotransmitter metabolites
- DAO level: Serum diamine oxidase for histamine intolerance
- Bile acid testing: Serum C4 or cholestyramine trial if IBS-D
IBS-C Specific Protocol
Rule out: hypothyroidism, low magnesium, pelvic floor dysfunction (anorectal manometry), methane SIBO/IMO.
- Magnesium citrate: 400-800mg at bedtime (osmotic laxative + muscle relaxant)
- PHGG (Partially Hydrolyzed Guar Gum): 5g/day (Sunfiber) — prebiotic fiber that does NOT worsen bloating like psyllium or inulin
- Vitamin C: Titrate to bowel tolerance (2000-5000mg) — osmotic effect
- Motility support: Ginger root extract 1000mg, prokinetics for MMC (see SIBO protocol)
- Hydration: Minimum 2-3 liters daily — dehydration is the most overlooked cause of constipation
- Caution: Do NOT add more fiber if SIBO is suspected. Feeding bacteria in the wrong place makes everything worse.
IBS-D Specific Protocol
Rule out: bile acid malabsorption, celiac disease, microscopic colitis (requires biopsy — colonoscopy looks normal but biopsies show collagenous or lymphocytic inflammation), carcinoid syndrome (24-hour urine 5-HIAA), pancreatic insufficiency.
- Berberine: 500mg 2-3x/day — antimicrobial, anti-inflammatory, AND slows intestinal transit. A multi-target molecule.
- SBI (Serum Bovine Immunoglobulins): EnteraGam (prescription) or MegaIgG2000 (OTC) — binds microbial toxins, supports mucosal immunity. Particularly effective in post-infectious IBS.
- Bile acid binders: Cholestyramine 4g if BAM confirmed
- Probiotics: Saccharomyces boulardii 250-500mg 2x/day (anti-diarrheal, anti-Clostridium, restores brush border enzymes), Lactobacillus plantarum 299v (Ducrotté 2012 — significant improvement in IBS symptoms, abdominal pain, bloating)
- L-glutamine: 5g 2-3x/day for intestinal barrier repair (Zhou 2019 — reduced IBS-D symptoms and intestinal permeability)
- Bismuth subsalicylate: Short-term for acute flares
The Functional Medicine Message
IBS is a starting point, not an endpoint. It is the smoke, not the fire. Every patient labeled with IBS deserves a thorough investigation into what is actually happening — whether that is SIBO, post-infectious autoimmunity, bile acid malabsorption, pelvic floor dysfunction, parasites, food sensitivities, or the downstream consequences of a nervous system stuck in survival mode.
The gut does not malfunction randomly. It malfunctions for reasons. Find the reasons, and the irritable bowel becomes a bowel at peace.