Dietary Restrictions and Cancer
Ronald Wilson Hart and Angelo Turturro
Division of Biometry and Risk Assessment, National Center for Toxicological Research, Jefferson, Arkansas
Abstract
Dietary restriction (DR) alters a significant environmental factor in carcinogenesis, dietary intake, thus inhibiting both spontaneous and induced tumorigenesis. Potential mechanisms for the inhibition of spontaneous cancer may include the effects of DR to do the following: decrease body weight, which decreases cellular proliferation and increases apoptosis in a number of organs that increase and decrease with body size; decrease body temperature, thereby lowering the amount of endogenous DNA damage temperature generates; decrease oxidative damage, by increasing antioxidant damage defense systems; decrease, generally, cellular proliferation; and protect the fidelity of the genome by decreasing DNA damage, increasing DNA repair, and preventing aberrant gene expression. Potential mechanisms for reducing induced tumor incidence include lowering agent activation, changing agent disposition, decreasing the adducts most associated with agent toxicity, and inhibiting tumor progression through mechanisms similar to those that can effect spontaneous tumorigenesis. As a method to control a major source of environmental cancer, and as the major modulator of the agent induction of this disease, understanding how DR works may significantly contribute to the efforts to explain how diet impacts on development of cancer in the United States, and may suggest methods to reduce the adverse impacts of other environmental agents on the disease. -- Environ Health Perspect 105(Suppl 4):989-992 (1997)
Key words: dietary restriction, cancer, diet, spontaneous carcinogenesis, induced carcinogenesis, body weight and cancer, oxidative damage, cellular proliferation
This paper is based on a presentation at the symposium on Mechanisms and Prevention of Environmentally Caused Cancers held 21-25 October 1995 in Santa Fe, New Mexico. Manuscript received at EHP 16 April 1996; accepted 4 September 1996.
The authors acknowledge the support of the National Institute of Aging/National Center for Toxicological Research Interagency Agreement for the Project on Caloric Restriction for its ongoing support.
Address correspondence to Dr. R.W. Hart, Division of Biometry and Risk Assessment, HFT-020, National Center for Toxicological Research, 3900 NCTR Drive, Jefferson, AR 72079. Telephone: (501) 543-7232. Fax: (501) 543-7332. E-mail: rhart@nctr.fda.gov
Abbreviations used: AL, ad libitum; BW, body weight; DEN, diethylnitrosamine; DR, dietary restriction; PR, protein restriction.
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Last Update: July 1, 1997