Roles of micronutrients in cancer prevention: recent evidence from the laboratory.
In addition to differences in needs for dietary quality and quantity, humans, as individuals and as subsets of the population, are exposed to variations in climate, stress, environmental contaminants and other confounding factors which likely impinge on susceptibility to cancer. Despite the complexity of lifestyles and dietary habits, it is impressive to review available data on the relation of nutrients to cancer. There is sufficient parallelism between controlled animal studies and human behavior that we are compelled to believe that a variety of essential nutrients can modify carcinogenesis in humans and in lower animals. The micronutrients which appear to meet criteria for classifying them as protective agents in animal models include vitamin A and some of the synthetic retinoids; beta carotene; folic acid; vitamin C; choline/methionine; zinc, and selenium. Some of the others have suggestive effects but in the view of this author, the data are often equivocal, inadequate, or conflicting. These observations clearly support the proposal that animal studies have made enormous contributions in the past 15-20 years to our understanding of carcinogenesis and that this will continue into the future. From the data now available we can state with confidence that animal studies have shown that nutrients can modify the carcinogenesis process at specific sites and through a variety of mechanisms. These include effects on the formation of carcinogens from precursors; effects on metabolism of the carcinogen; effects on one or more stages of initiation, promotion, and progression; host defense mechanisms; cellular differentiation and on growth and metastasis of the tumor. The tools of the molecular biology, just now emerging in the field of nutrition, should have an immense impact on determining more accurately where nutrients exert their effects, how this is accomplished, and to suggest appropriate prevention and intervention techniques. Using molecular biology, combined with traditional and newer methods of toxicology and pathology, we should be able within a few years to better understand carcinogenesis and with such knowledge in hand to make sound recommendations about dietary habits to the public.
Newberne
P M
PM
Boston University School of Medicine, Mallory Institute of Pathology, MA 02118.
Locniskar
M
M
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology; D002794:Choline / Q000494:pharmacology; D005260:Female; D005492:Folic Acid / Q000494:pharmacology; D008715:Methionine / Q000494:pharmacology; D051379:Mice; D008903:Minerals / Q000494:pharmacology*; D009374:Neoplasms, Experimental / Q000517:prevention & control*; D051381:Rats; D012643:Selenium / Q000494:pharmacology; D014801:Vitamin A / Q000494:pharmacology; D014815:Vitamins / Q000494:pharmacology*; D015032:Zinc / Q000494:pharmacology
D008903:Minerals; D014815:Vitamins; D014801:Vitamin A; D005492:Folic Acid; D008715:Methionine; D012643:Selenium; D015032:Zinc; D002794:Choline; D001205:Ascorbic Acid