Diet and carcinogenesis.

In summary there is a wealth of information on dietary and nutritional effects on carcinogenesis in laboratory rodents. Experimental studies based on epidemiological evidence, earlier experimental studies and known or predicted cellular, biochemical and molecular effects of nutrients have produced clear evidence that carcinogenesis in laboratory rodents is influenced by dietary intake of calories, fat, lipotropes (choline, methionine), vitamin A and related retinoids, Se, calcium, zinc, fiber, ethanol and a large number of non-nutrient components of foods. For these substances or groups of substances mechanistic hypotheses supported by experimental data and are leading to further research. The information provided will contribute to understanding of basic processes in carcinogenesis as well as of the specific interactions studied, and should contribute to significant advances in preventive medicine. Restriction of caloric intake of rodents by amounts > 10% over a significant portion of their lifetime reduces tumorigenesis. That level of restriction reduces the rate of growth and maturation, and most experiments in this area employ greater restrictions that virtually abolish growth from a young age. Therefore, the observations are of interest in mechanistic studies, but their applicability to preventive medicine requires better definition of the degree and duration of restriction required for a significant effect and the age at which it must be imposed. Restriction of total fat intake and modifications to increase the intake of omega-3 fats have a reasonably consistent effect on tumorigenesis in rodents but a much less consistently demonstrable effect in humans. Again, the observations in rodents are providing a major stimulus to mechanistic studies. The lipotropes are extremely valuable as tools for investigating mechanisms of carcinogenesis in rodents. Their importance in the epidemiology of human cancer has yet to be demonstrated clearly and is a subject of research at present. The naturally occurring vitamins and minerals, as well as fiber, derive their importance in this context from investigations to explain the consistent epidemiological demonstrations of reduction of tumor risk with increased consumption of fruits and vegetables. The activity of the isolated nutrients as anticarcinogens in rodents has generally not matched the activity expected from epidemiological studies. The anticarcinogenic activity of many of the non-nutrient components of fruits and vegetables is remarkable in particular models, however, as is the activity of natural and synthetic retinoids. At present the results must be interpreted to indicate an important effect of combinations of the whole foods with identification of particular nutrients or non-nutrients in specific cases.(ABSTRACT TRUNCATED AT 400 WORDS)