Irritable bowel syndrome (IBS)
IBS is a diagnosis of exclusion, so subtyping it into SIBO, bile acid malabsorption or visceral hypersensitivity is what turns a label into something treatable.
IBS describes a symptom pattern once other disease has been excluded. That exclusion is necessary, and it is not the same as an explanation. A meaningful share of patients diagnosed with IBS have an identifiable mechanism: bacterial overgrowth, bile acid malabsorption, enzyme deficiency, or genuine visceral hypersensitivity. Each responds to something different.
SIBO, present in a substantial proportion of diarrhea-predominant IBS. Bile acid malabsorption, which is common, easily treated and almost never tested for. Post-infectious IBS following gastroenteritis. Disaccharidase deficiency. Visceral hypersensitivity mediated through the gut–brain axis. Dysbiosis. And in constipation-predominant IBS, slow transit or pelvic floor dysfunction.
By subtype, which is the point of establishing one. Low-FODMAP as a structured, time-limited diagnostic elimination with proper reintroduction — not a permanent diet, which harms the microbiome. Antimicrobials for confirmed SIBO. Bile acid sequestrants where malabsorption is demonstrated. Gut-directed hypnotherapy or CBT for visceral hypersensitivity, both of which have real evidence.
Breath testing for SIBO. Bile acid malabsorption testing where diarrhea predominates. Calprotectin, to separate IBS from inflammatory bowel disease. Celiac serology, which must be done before gluten is removed. Stool analysis. Red flags requiring gastroenterology first: rectal bleeding, unintentional weight loss, anemia, nocturnal symptoms, onset after fifty, or family history of colorectal cancer.
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