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Healthcare professional Resource for Gluten Related Disorders.

Dr. Schär Institute

Etiology and pathogenesis: What causes IBS?

It is unlikely that there is one unifying factor that will explain the pathogenesis of IBS, and more likely that it is the outcome of the complex interplay between a number of factors involving the gut and the central nervous system [1].

Post infectious IBS

Between 3.7-36% of patients who have suffered bacterial or viral gastroenteritis will go on to develop IBS [2,3], a recent meta-analysis of published trials reported a sevenfold increased risk of developing IBS after an infectious gastroenteritis [4].

Gut bacteria

There are over 1000 species of human gut bacteria and each individual is populated by at least 160 different species, including a core of 18 species present in all humans. The role of these gut bacteria in the pathogenesis of IBS is being increasingly recognized. Research has shown that there are alterations in the bacteria levels in patients with IBS and that gut bacteria can be adversely affected by gut infections and gastroenteritis [6]. IBS patients had lower levels of Lactobacilli and Bifidobacteria [5].

Gut permeability

The lining of the intestine and the mucus that it secretes protect the body from absorbing unwanted molecules as they pass along the gut. However, studies into IBS show that the gut lining in some patients is damaged resulting in unwanted molecules crossing the gut wall into the body and potentially activating the body’s immune system [7,8]. This defect is principally seen in diarrhea dominant IBS patients and interestingly is most notable in non-post infectious IBS [7].

Immune activation

Increased activity of the innate immune system is seen in subgroups of IBS patients [6]. There is some suggestion of immune mast cell involvement, particularly in those with diarrhea dominant IBS, where allergic type responses may result in the release of inflammatory chemicals in the gut [9,10]. Increased mast cell infiltration has been observed in close proximity to nerve fibers in the colon in IBS patients, which could explain increased levels of pain in these subjects [11]. Some studies speculate as to whether there are subgroups of IBS patients for whom food allergy is responsible for this immune activation [12]. The adaptive immune system has also been implicated in IBS with raised numbers of T cells being noted in the gut of some IBS patients [13]. However, research is conflicting and more work is needed to look into immune involvement in IBS symptoms.

Stress Factors

Corticotrophin-releasing hormone (CRH) mediates the stress response and has been shown to increase gut motility. It has also been shown to promote inflammation by increasing intestinal permeability in IBS patients. CRH can also alter gut bacteria, gut secretions, sensitivity of the gut wall and the blood flow to the intestine [1]. These effects may go part of the way to explaining why some people find that their symptoms are exacerbated during periods of stress. What we don’t yet fully understand however is how significant stress and the body chemicals associated with stress are in the development of IBS as a condition.

Food ingestion

Half of IBS patients report increases in gut symptoms after eating [1]. Research has suggested that food allergy may be relevant in a subset of patients [12,14]. However, adult allergy, which predominantly affects the gut, is often non-IgE in nature and therefore will not show up on allergy tests making it difficult to confirm [15].

Role of FODMAPs in IBS symptoms

There is increasing evidence that many IBS patients exhibit an intolerance to poorly absorbed carbohydrates such as fructose, lactose, polyols, fructans and galacto-oligosaccharides, known commonly as ‘FODMAPs’ [16-18]. These foods can cause fermentation in the gut resulting in gas, flatulence and bloating in sensitive individuals. These foods also increase water delivery into the bowel resulting in loose stools. The low FODMAP diet removes these foods for an 8 week period and then reintroduces the foods. The foods are added one at a time and the patient is monitored for tolerance. The diet is now widely used and is recommended by both the NICE Guidelines [19] and the British Dietetic Association IBS Guidelines [20].

Both celiac disease and the more recently recognized condition - non coeliac gluten sensitivity, can exhibit IBS-type symptoms. Benefits of gluten restriction on IBS-type symptoms have been reported [21], however wheat contains high levels of the fermentable ‘fructans’ so it is plausible that the improvement in symptoms, at least for some individuals, may simply be related to the reduction/exclusion of FODMAPs.
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  8. Marshall JK, Thabane M, Garg AX, Clark W, Meddings J, Collins SM, et al. Intestinal permeability in patients with irritable bowel syndrome after a waterborne outbreak of acute gastroenteritis in Walkerton, Ontario. Alimentary pharmacology & therapeutics. 2004;20(11-12):1317-22.
  9. Guilarte M, Santos J, de Torres I, Alonso C, Vicario M, Ramos L, et al. Diarrhoea-predominant IBS patients show mast cell activation and hyperplasia in the jejunum. Gut. 2007;56(2):203-9.
  10. Walker MM, Talley NJ, Prabhakar M, Pennaneac'h CJ, Aro P, Ronkainen J, et al. Duodenal mastocytosis, eosinophilia and intraepithelial lymphocytosis as possible disease markers in the irritable bowel syndrome and functional dyspepsia. Alimentary pharmacology & therapeutics. 2009;29(7):765-73.
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  13. Ohman L, et al. A controlled study of colonic immune activity and B7 blood T lymphocytes in patients with irritable bowel syndrome. Clinical Gastroenterology & Hepatology. 2005;3:980-6.
  14. Carroccio A, Brusca I, Mansueto P, D'Alcamo A, Barrale M, Soresi M, et al. A comparison between two different in vitro basophil activation tests for gluten- and cow's milk protein sensitivity in irritable bowel syndrome (IBS)-like patients. Clinical chemistry and laboratory medicine : CCLM / FESCC. 2013;51(6):1257-63.
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  16. Staudacher HM, Irving PM, Lomer MC, Whelan K. Mechanisms and efficacy of dietary FODMAP restriction in IBS. Nat Rev Gastroenterol Hepatol. 2014.
  17. Staudacher HM, Lomer MC, Anderson JL, Barrett JS, Muir JG, Irving PM, et al. Fermentable carbohydrate restriction reduces luminal bifidobacteria and gastrointestinal symptoms in patients with irritable bowel syndrome. The Journal of nutrition. 2012;142(8):1510-8.
  18. Shepherd SJ, Lomer MC, Gibson PR. Short-chain carbohydrates and functional gastrointestinal disorders. Am J Gastroenterol. 2013;108(5):707-17.
  19. National Institute for Health and Care Excellence. Irritable bowel syndrome in adults: diagnosis and management of irritable bowel syndrome in primary care. London: NICE; 2015.
  20. McKenzie YA, Alder A, Anderson W, Wills A, Goddard L, Gulia P, et al. British Dietetic Association evidence-based guidelines for the dietary management of irritable bowel syndrome in adults. J Hum Nutr Diet. 2012;25(3):260-74.
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