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Canadian Journal of Gastroenterology
Volume 12, Issue 2, Pages 133-146
Nutritional Review

Altered Colonic Environment, a Possible Predisposition to Colorectal Cancer and Colonic Inflammatory Bowel Disease: Rationale of Dietary Manipulation with Emphasis on Disaccharides

A Szilagyi

Division of Gastroenterology, Department of Medicine, The Sir Mortimer B Davis Jewish General Hospital, Faculty of Medicine, McGill University, Montreal, Quebec, Canada

Received 12 August 1997; Accepted 8 December 1998

Copyright © 1998 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.


A recurrent theme in the schema of pathogenetic mechanisms attributed to colorectal cancer (CRC) and inflammatory bowel disease (IBD) is the interaction between genes and environment. Dietary and other environmental factors, and lower intestinal flora and their chemical interactions occur in the pathogenesis of both. Events at the mucosal surface may be influenced by factors in the luminal environment and by contributions of the host. In addition, both forms of IBD - Crohn's disease (CD) and ulcerative colitis (UC) - have distinctive associated host events. Even within CD and UC, different clinical patterns and prognoses may have different specific host mechanisms. Some of the current putative pathogenetic processes in CRC and IBD are reviewed. Particular attention is given to hypotheses relating to the role of dietetic substances, mainly fibre and dairy products, and how they may affect disease formation. It is argued that within the context of hypotheses proposed for possible beneficial effects of these two dietetic factors, CRC and IBD may be considered together. Further support is lent to arguments that similar and additional hypothetical features ascribed to beneficial effects of fibre may be attributed to disaccharides, lactose and its derivatives, lactulose and lactitol.