BETHESDA, MD (Oct. 2, 2026) — A new study, to be published in Gastroenterology, finds that gut inflammation can change the way gut bacteria break down food — possibly triggering immune reactions to foods that were previously fine to eat. The findings may help explain why so many people with inflammatory bowel disease (IBD) react badly to foods like dairy or gluten, even in remission.
IBD, which includes Crohn's disease and ulcerative colitis , is marked by flare-ups of severe inflammation, and many patients change their diets to manage symptoms, despite limited evidence that this helps. About two-thirds of IBD patients report food-related symptoms. Dairy, wheat, and fiber are the most frequently blamed triggers, but why they cause problems has remained unclear.
The gut microbiota, the trillions of bacteria living in the intestines, may hold the answer. These bacteria help digest foods that human enzymes can't process alone, and prior research has shown IBD patients often have altered gut bacteria. This study identifies a novel mechanism by which that alteration drives food reactions.
"The microbiome acts as a metabolic organ, helping us digest food components, including those that can trigger gut reactions," said study author Alberto Caminero, PhD. "Our study shows that inflammation impairs this microbial digestive capacity, potentially contributing to adverse food reactions and opening new possibilities for microbiome-based therapies to restore this function in IBD patients."
Other key authors involved in this research from The McMaster University Medical Centre included Bruna Barbosa, PhD, and senior clinical collaborators Neeraj Narula, MD, and Premysl Bercik, MD.
Using two mouse models of colitis, researchers found that inflammation made animals more prone to developing food sensitivities. After inflammation, exposure to dairy or gluten triggered an allergic-type immune response in the colon; reintroducing those foods later caused heightened gut sensitivity and worse colitis symptoms.
The cause traced back to the microbiota: inflammation depleted the specific bacteria that normally break down these food triggers. That shift alone was enough to increase sensitization risk — transferring gut bacteria from inflamed mice into germ-free mice made those mice more prone to sensitization to the same foods, while restoring the missing bacteria reduced these effects.
The pattern held in people, too. Among IBD patients, those who self-reported food intolerances were more likely to have both a reduced ability to break down common trigger foods and lower levels of the bacteria responsible for that job.
The researchers note that microbiota disruption is likely just one piece of a larger picture that also includes genetics, infections, and stress — all of which need further research.
Together, the findings point to a possible mechanism behind food sensitivities in IBD: Inflammation disrupts the gut bacteria that normally process certain foods, and this disruption — not the foods themselves — helps trigger the immune reactions patients experience.
Learn more about IBD in the AGA GI Patient Center .
