The prevalence of inflammatory bowel diseases (IBD), which include ulcerative colitis (UC) and Crohn’s disease (CD), has increased over recent decades in Western countries. While the lack of dietary fiber from these populations could therefore be one factor to blame, dietary fibers are often overlooked by IBD patients who fear that following a high-fiber diet will worsen their symptoms. Such exclusion diets can improve symptoms but may deprive patients of the benefits of fibers. However, recently, scientists are moving away from the concept that dietary fiber should be avoided in patients with IBD. Indeed, from fermentation, the gut microbiota releases short-chain fatty acids (SCFAs), that regulate metabolism, cell turnover, and the immune system.

In a new research article published in Gastroenterology, Armstrong et al. investigated the effects of different β-fructans  on barrier function and inflammation using colonic biopsies from pediatric patients with IBD and healthy controls. They based their hypothesis on the fact that some patients with IBD are sensitive to high-fiber diet and that they have a dysbiotic gut microbiota with fewer fiber-fermenting microorganisms, meaning that fibers are not fully fermented and remain in the gut where they could trigger inflammation.

The authors first tested the effect of β-fructans on inflammation response from monocytes, peripheral blood mononuclear cells (PBMCs) and ex-vivo colonic biopsy culture, as well as the fermentation capacity of gut microbiota. Unfermented β-fructans lead to an inflammatory response, gut barrier changes and pro-inflammatory cytokines, whereas when these fibers are fermented by gut microbes, they reduce inflammation by releasing SCFAs.

Unfermented dietary fructooligosaccharides (FOS) and inulin, but not barley, maltodextrin or dextrin, increased the release of the pro-inflammatory cytokine IL-1β by human monocytes, PBMCs, and in some patient biopsy tissues cultured ex vivo. More particularly, biopsy samples from UC and CD patients in flare-up phase showed an increased pro-inflammatory profile (IL-1β, IL-5, IL-23) compared with CD and UC in remission and non-IBD patient biopsies, in which a decrease in IL-1β secretion was observed with FOS supplementation. The authors also found higher levels of CD45+ cells in biopsies from patients with UC and CD. Altogether, these findings suggest that the fiber type, immune status and the fermentative capacity of their gut microbiota influence the proinflammatory role of dietary fibers.

To validate their hypothesis the authors cultured anaerobically fecal samples with FOS and applied the resulting supernatant of these fecal cultures onto monocytes and measured their inflammatory response. In order to down regulate inflammation, a decreased concentration of FOS and increased concentration of SCFAs by fermentation were required. The authors found that the fermentative capacity of the gut microbiota as reflected by decreased FOS levels and increased SCFAs, was lower in UC and CD patients in flare-up compared with IBD patients in remission and non-IBD patients.

To validate their findings, in a randomized controlled trial cohort, they supplemented UC patients in remission with β-fructans (15 g/d over 6 months) or placebo. In UC patients in remission, β-fructans significantly reduced the risk of flare as indicated by the lower level of fecal calprotectin (a marker of intestinal inflammation) compared with placebo. Nevertheless, 31% of UC patients in the β-fructans group experienced a flare-up at the study endpoint with increased pro-inflammatory cytokines in response to β-fructans supplementation. Armstrong et al found a low FODMAP diet among IBD patients correlated with a pro-inflammatory response to FOS. This finding raises the possibility that FOS consumption during remission may lessen the degree of inflammation thereafter.

The study of Armstrong et al highlights the intricacy of the variables influencing everyone’s response to fiber. Indeed, when fiber-fermenting microbes are present in an uninflamed gut, fermentation strengthens the intestinal barrier and reduces the inflammatory response. In contrast, when the capacity of the gut microbiota to ferment fiber is reduced and the gut environment is inflammatory, β-fructans stimulate inflammation. In the future, dietary fiber advice should be tailored to each patient’s pathological condition.



Wang R, Li Z, Liu S, et al. Global, regional and national burden of inflammatory bowel disease in 204 countries and territories from 1990 to 2019: a systematic analysis based on the Global Burden of Disease Study 2019. BMJ Open. 2023;13:e065186.

Haskey N, Gold SL, Faith JJ, et al. To Fiber or Not to Fiber: The Swinging Pendulum of Fiber Supplementation in Patients with Inflammatory Bowel Disease. Nutrients. 2023;15:1080.

Armstrong HK, Bording-Jorgensen M, Santer DM, et al. Unfermented β-fructan Fibers Fuel Inflammation in Select Inflammatory Bowel Disease Patients. Gastroenterology. 2023;164(2):228-240.

Shin A et Kashyap PC. Promote or Prevent? Gut Microbial Function and Immune Status May Determine the Effect of Fiber in Inflammatory Bowel Disease. Gastroenterology. 2023; 164(2):182-184.