Dietary FODMAP Restriction in IBS

Irritable bowel syndrome (IBS) is a condition affecting up to 21% of the general population. Previously a diagnosis of exclusion, diagnosis now relies on the presence of chronic gastrointestinal symptoms with the absence of alarm features suggestive of organic disease (e.g., rectal bleeding, anaemia, weight loss, severe pain, family history of inflammatory bowel disease, coeliac disease, or colorectal malignancy).

Since 2005, a diet low in fermentable short-chain carbohydrates—termed the low FODMAP (fermentable oligo-, di-, mono-saccharides, and polyols) diet—has been the focus of many robust clinical trials and is now used internationally as the first-line dietary approach for managing functional gastrointestinal symptoms seen in IBS. To date, the concept of FODMAPs inducing symptoms was thought to originate from the large intestine, where luminal distension would result from both colonic gas and the osmotic load caused by bacterial fermentation of unabsorbed FODMAPs. However, a study using magnetic resonance imaging recently showed that osmotic load from FODMAPs also distends the small intestine, contributing further to our understanding of FODMAP-mediated symptoms in IBS patients.

Multiple high-quality studies have now shown that restricting problematic FODMAPs improves overall gastrointestinal symptoms in up to 86% of IBS sufferers. Moreover, symptom improvement has been shown to be effective and durable in all IBS subtypes (diarrhoea predominant, constipation predominant, and mixed type-IBS).

The low FODMAP diet requires guidance from specialist dietitians to implement an elimination phase and assess tolerance levels. Testing tools like hydrogen/methane breath tests are essential for personalising the diet and reducing unnecessary dietary restrictions, as the diet’s success depends on excluding only the FODMAPs that trigger symptoms while maintaining as varied a diet as possible.

Case Study

A 25-year-old otherwise well male presented with a 12-month history of peri-umbilical pain and some altered bowel habits. He consulted his general practitioner, who performed a stool sample, which was positive for Blastocystis Hominis. He was prescribed a one-week course of metronidazole, but despite a follow-up negative stool culture, his symptoms persisted.

He was referred for gastroscopy and colonoscopy, both of which were normal. Biopsies taken from the duodenum ruled out coeliac disease, and random colonic biopsies were also normal. A CT scan of the abdomen revealed a small mass in his right kidney. The urologist reassured him that this was an anatomical variant of the kidney and unlikely to be the cause of his symptoms.

Further questioning revealed the patient’s diet was high in fructose. A hydrogen/methane breath test confirmed fructose malabsorption. Following dietary intervention under specialist dietetic supervision, the patient restricted fructose from his diet, resulting in complete symptom resolution. He continues to work with a dietitian to maintain a minimally restrictive, symptom-free diet.

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