@article{10.37349/edd.2026.1005112,
abstract = {This review goes over the impact of caffeine consumption in inflammatory bowel disease (IBD), examining epidemiology, clinical outcomes, mechanistic studies, and translational research. Caffeine, a widely consumed methylxanthine, exerts diverse physiological effects on the gastrointestinal tract. Mechanistic and preclinical data offer plausible biological pathways by which caffeine could influence the IBD course. Caffeine’s antagonism of adenosine receptors may modulate immune cell activation and cytokine release; its effects on gut motility and secretion can alter symptom perception, and caffeine-mediated changes in intestinal epithelial barrier function, oxidative stress, and the gut microbiome have been demonstrated. These effects make it a lucrative investigational option, and various studies have demonstrated that caffeine intake may reduce the incidence of IBD and may even have disease-modifying effects in regular consumers. However, differences in caffeine source (coffee, tea, soda), dose, concurrent dietary patterns, and disease subtype (Crohn’s disease versus ulcerative colitis) limit definitive causal inference. Clinical implications remain cautious: while moderate caffeine intake may be tolerable and even helpful for many patients, individualized assessment is advisable, particularly for those with symptom-triggering sensitivity or overlapping functional bowel disorders. Future research should target mechanistic links and clinically meaningful outcomes to inform evidence-based dietary guidance for people with IBD.},
author = {Mohamed, Mohamed Ahmed and Chokr, Dima and Sundaram, Harini and Hafeez, Shameelah and Areebah, Zainab and Santhalingam, Subishwar and Bishop, Faith},
doi = {10.37349/edd.2026.1005112},
journal = {Exploration of Digestive Diseases},
elocation-id = {1005112},
title = {The impact of caffeine in inflammatory bowel disease: a review of the literature},
url = {https://www.explorationpub.com/Journals/edd/Article/1005112},
volume = {5},
year = {2026}
}