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The Wistar Institute, Philadelphia, PA 19104
3 To whom correspondence should be addressed. E-mail: kritchevsky{at}mail.wistar.upenn.edu.
Our advances in knowledge of the epidemiology of cancer and of the nutritional and genetic effects on this disease have not yet been translated into successful treatment. This is due in part to our tendency toward reductionist thinking, dating to the days when one drug killed one bug. We could learn something by trying to reconcile the differences. Cancer is a degenerative disease that develops over a long time and goes through many stages. Perhaps different nutritional approaches are needed at each stage. The same dietary treatment may not exert the same effects during all stages of tumor development. Obesity is one risk factor that is generally agreed upon. Energy (caloric) restriction has been shown to inhibit experimental carcinogenesis, and energy expenditure affects human carcinogenesis. It would be interesting to combine energy restriction with nutritional treatment. One neglected area of inquiry is that of interactions among nutrients. Substitution of nutrient A for nutrient B can precipitate a series of interactions between nutrient B and the rest of the diet. If more experimental work were done with spontaneous tumors, it would eliminate possible effects of carcinogen metabolism in carcinogenesis and might provide a more accurate reflection of human carcinogenesis. Focusing on one specific dietary component or class of components belies the complexity of the problem.
KEY WORDS: energy (caloric) restriction nutritional epidemiology
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