AJCN Cancer Health Disparities Conference
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wargovich, M. J.
Right arrow Articles by Levin, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wargovich, M. J.
Right arrow Articles by Levin, B.
Agricola
Right arrow Articles by Wargovich, M. J.
Right arrow Articles by Levin, B.

American Journal of Clinical Nutrition, Vol 54, 202S-205S, Copyright © 1991 by The American Society for Clinical Nutrition, Inc

REVIEW ARTICLES

Modulating effects of calcium in animal models of colon carcinogenesis and short-term studies in subjects at increased risk for colon cancer

MJ Wargovich, PM Lynch and B Levin
Department of Medical Oncology, University of Texas MD Anderson Cancer Center, Houston 77030.

A substantive amount of evidence from animal models supports the hypothesis that dietary fat is an etiological factor in colon cancer. Although various theories account for possible mechanisms, it is clear that under the influence of a basic colonic pH, fatty acids and bile acids may become highly surfactant in the colon, causing cell loss and compensatory hyperproliferation. Calcium likely reduces lipid damage in the colon by complexing with fat to form mineral-fat complexes or soaps. It has been shown in an increasing number of animal experiments that calcium has the ability to inhibit colon cancer. In limited studies in man, the colonic hyperproliferation associated with increased risk for colon cancer has been reversed for short periods by administration of supplemental dietary calcium. Taken together the available evidence suggests that increases in the daily intake of calcium in the diet may provide a means of colorectal-cancer control.


This article has been cited by other articles:


Home page
 JNCI J Natl Cancer InstHome page
A. Schatzkin and U. Peters
Advancing the Calcium-Colorectal Cancer Hypothesis
J Natl Cancer Inst, June 16, 2004; 96(12): 893 - 894.
[Full Text] [PDF]

Home page
 J. Am. Coll. Nutr.Home page
R. M. Ortega, A. M. Requejo, A. M. Lopez-Sobaler, P. Andres, M. E. Quintas, B. Navia, M. Izquierdo, and T. Rivas
The Importance of Breakfast in Meeting Daily Recommended Calcium Intake in a Group of Schoolchildren
J. Am. Coll. Nutr., February 1, 1998; 17(1): 19 - 24.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1991 by The American Society for Nutrition