| Popis: |
Doll and Peto1 suggested that 35% (range 10–70%) of all human cancers among the U.S. population were associated in some way with diet or nutrition. Despite this alarming statistic, there is very little firm understanding of the factors present in the diet that lead to cancer development. This arises for several reasons. First, the literature on diet and cancer is both vast and self-contradictory. Two committees sponsored by the U.S. National Academy of Sciences (U.S. National Research Council2; U.S. National Academy of Sciences3) reached different conclusions about the relative importance of the amount of diet consumed and the level and type of fat in the diet. Second, there has been, until recently, a prudent reluctance to base anti-cancer recommendations for the modification of human diets on well founded and repeated observations in experimental animals. Epidemiologic evidence on the nature of the human diet and the incidence of cancer is often unreliable because of difficulties patients and controls have in recalling what they ate years or decades ago. The value of animal experiments is now being recognized by the massive research program on the beneficial effects of dietary restriction being undertaken by Dr. Hart and his colleagues at the National Center for Toxicological Research.4–9 Third, there has been a reluctance to examine food components for their carcinogenic potential. This has arisen because the only remedial action following discovery of a naturally occurring carcinogen as a component of an important food crop has, until the past few years, been to cease using the food crop, an action that might substantially reduce the human food supply. Biogenetic engineering now provides the opportunity to reduce the levels of undesirable substances naturally occurring in food crops or, if it is used unwisely, to increase this level and thus increase human cancer risk. This problem is far from theoretical. It has recently been shown that background sister chromatid exchanges, a genotoxic event sometimes linked to carcinogenesis, are dependent in primary rat hepatocytes on the diet to which the rats were previously exposed.10 The background rate of sister chromatid exchanges in hepatocytes was lower when a purified diet was fed to the rats than when a commercial chow was used. |
