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Canadian Journal of Gastroenterology
Volume 9 (1995), Issue 5, Pages 273-276

Gut-Brain Interactions in Inflammatory Bowel Disease: A Clinician’s Perspective

Theodore M Bayless

Meyerhoff DD-IBD Center, Johns Hopkins Hospital, Baltimore, Maryland, USA

Copyright © 1995 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


While most physicians and some patients consider psychosocial factors important in aggravating already existing inflammatory bowel disease (IBD), most of the information is based on a few recent scientific studies, varied anecdotal observations and a tendency for patients and some physicians to view psychosocial and stress-related issues with speculation, bias and some stigmatization. Patients with proctitis who have experienced recrudescence of mucosal friability and rectal bleeding within a day of a severe life stress provide a dramatic example of such anecdotes. Time-lag studies have indicated that stress, especially major life events, precedes illness aggravation in patients with IBD but that stress is not disease-specific. The symptoms studied, pain and diarrhea, were more likely to be physiological responses to acute stress rather than reflections of increased disease activity. Current scientific research supposes the prospect that environmental factors influence disease susceptibility through the central nervous system. Stress is associated with alterations in both humoral and cellular immune mechanisms in humans and in experimental animals. While psychosocial factors may not initiate inflammation in IBD, it is possible that they lead to alterations in the immune response and thereby alter disease activity. Mind-gut interactions affect salivation, gastric secretion, gastric motility and colonic motility, as well as numerous other gastrointestinal functions. These ‘physiological’ responses are expected in the IBD patient and perhaps will be accentuated by inflammation and its multiple effects on gut function. Because 10 to 13% of the general population have a tendency to suffer from irritable bowel syndrome (IBS), it is expected that the same percentage of IBD patients will have both IBD and IBS. An example of clinically relevant alterations in pathophysiology is the association of acute proctosigmoiditis with an increase in IBS symptoms in the left colon. Pain and diarrhea based on distension of an irritable left colon after ileocolonic resection result from excessive distension of the left colon by the larger stool volume following loss of absorptive surface of the ileum and right colon. Patients with IBS are also more symptomatic with small amounts of unabsorbed carbohydrates, such as fructose, sorbitol and lactose. Patients with severe IBS have an irritable small bowel, especially when it is formed into a closed reservoir, such as an ileoanal pouch; these patients have at least eight to 10 bowel movements per day because of the spasticity and small capacity of the ileoanal pouch. The stomach to pouch transit time may also be quite rapid. Explaining the coexistence of IBD and IBS to the patient is often quite helpful to the patient and to the doctor. One hopes that the scientific explanations of these mind-gut interactions are forthcoming.