RESEARCH ARTICLE
Obesity and Colorectal Cancer Risk: Impact of the Gut Microbiota and Weight-Loss Diets
Harry J. Flint*, R. John Wallace
Article Information
Identifiers and Pagination:
Year: 2010Volume: 2
First Page: 50
Last Page: 62
Publisher Id: TOOBESJ-2-50
DOI: 10.2174/1876823701002010050
Article History:
Received Date: 07/09/2009Revision Received Date: 23/09/2009
Acceptance Date: 23/09/2009
Electronic publication date: 14/7/2010
Collection year: 2010
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The link between obesity and colorectal cancer risk in man is well established. This review investigates the role that the intestinal microbial population plays in this link and the impact of weight-loss diets on colorectal cancer risk. Changes in the composition of the intestinal bacterial community have been implicated in contributing to obesity. The robustness of these claims is analysed here, along with the role of bacterial metabolism in colon cancer risk. Weight-loss diets, low in carbohydrate and high in protein and fat, present an additional hazard to individuals struggling with obesity. Intestinal bacteria ferment carbohydrates to products that are generally regarded as being beneficial to health and protective against cancer. Some commensal species also appear to suppress inflammation. On the other hand, when carbohydrate limits the growth of intestinal bacteria, protein is broken down and the amino acids released are fermented to products that are inflammatory and possibly carcinogenic. We advocate the inclusion of non-digestible but fermentable carbohydrate in weight-loss diets to avoid these problems. High-fat diets enhance the escape of fats to reach the intestine, the implications of which are not fully understood. Even more fat reaches the intestine when dietary lipase inhibitors or fat-absorbing non-digestible dietary additives are used. Consequences for gut health of the increased fat concentration in the intestine seem to vary between individuals, the possible reasons for which are discussed here.