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

Michael J Wargovich, Patrick M. Lynch, Bernard Levin

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

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 colorectalcancer control.

Original languageEnglish (US)
JournalAmerican Journal of Clinical Nutrition
Volume54
Issue numberSUPPL. 1
StatePublished - 1991
Externally publishedYes

Fingerprint

colorectal neoplasms
Colonic Neoplasms
carcinogenesis
colon
Colon
Carcinogenesis
Animal Models
animal models
Calcium
calcium
Fats
Dietary Calcium
Soaps
lipids
Dietary Fats
Bile Acids and Salts
Surface-Active Agents
Minerals
soaps
animal experimentation

Keywords

  • Calcium
  • Colon cancer
  • High-risk subjects
  • Proliferation

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

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AB - 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 colorectalcancer control.

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