Cancer: Diets and Nutrition

Since the turn of the century, new methods of processing and storage have resulted in a proliferation of the kinds and numbers of food items available to the U.S. population. Unfortunately, little is known about the ways in which such innovations have altered the specific composition of the diet. The only components of food that have been monitored regu larly are the nutrients. The dietary levels of most nutrients have changed relatively little over the past 80 years.

Attempting to determine which constituents of food might be associ ated with cancer, epidemiologists have studied population subgroups, including migrants to the United States, to examine the relationship between specific dietary patterns or the consumption of certain foods and the risk of developing particular cancers. In general, the evidence suggests that some types of diets and some dietary components (e.g., high fat diets or the frequent consumption of salt-cured, salt-pickled, and smoked foods) tend to increase the risk of cancer, whereas others (e.g., low fat diets or the frequent consumption of certain fruits and vegetables) tend to decrease it. The mechanisms responsible for these effects are not fully understood, partly because nutritive and non nutritive components of foods may interact to exert effects on cancer incidence.

In the laboratory, investigators have attempted to shed light on the mechanisms by which diet may influence carcinogenesis. They have ex amined the ability of Individual nutrients, food extracts, or non nutritive components of food to enhance or inhibit carcinogenesis and mutagenesis, thereby providing epidemiologists with testable hypotheses regarding specific components of the diet. Because the data from both types of studies are generally grouped according to dietary constitu ents, the committee found it advantageous to organize its report in a similar fashion.

Total Caloric Intake

The committee reviewed many studies in which the variable examined was the total amount of food consumed by humans or animals, rather than the precise composition of the diet. This review is contained in Chapter 4, which is entitled "Total Caloric Intake," even though the studies did not indicate whether the observed effects resulted from the changes in the proportion of specific nutrients in the diet or from the modification of total caloric intake.

Since very few epidemiologists have been able to examine the effect of caloiric intake per se on the risk of cancer, their reports have pro vided largely indlrect^evidence for such a relationship, and much of it is based on associations between body weight or obesity and cancer.

In laboratory experiments, the incidence of tumors is lower and the lifespan much longer for animals on restricted food intake than for ani mals fed ad libitum. However, because the intake of all nutrients was simultaneously depressed in these studies, the observed reduction in tumor incidence might have been due to the reduction of some specific nutrient, such as fat. It is also difficult to Interpret experiments In which caloric Intake has been modified by varying dietary fat or fiber, both of which may by themselves exert effects on tumorlgenesis.

Thus, the committee concluded that neither the epidemiological stud ies nor the experiments in animals permit a clear interpretation of the specific effect of total caloric intake on the risk of cancer. Nonethe less, the studies conducted in animals show that a reduction in total food Intake decreases the age-specific Incidence of cancer. The evi dence Is less clear for human beings.

Lipids (Fats and Cholesterol)

Many epidemiological and laboratory studies have been conducted to examine the association between cancer and intake of lipids, i.e., total dietary fat, saturated fat, polyunsaturated fat, and cholesterol.
Fats. Epidemiological studies have repeatedly shown an association between dietary fat and the occurrence of cancer at several sites, espe cially the breast, prostate, and large bowel. In various populations, both the high incidence of and mortality from breast cancer have been shown to correlate strongly with higher per capita fat consumption; the few case-control studies conducted have also shown this association with dietary fat. Like breast cancer, increased risk of large bowel cancer has been associated with higher fat Intake in both correlation and case control studies. The data on prostate cancer are more limited, but they too suggest that an increased risk Is related to high levels of dietary fat. In general, it Is not possible to identify specific components of fat as being clearly responsible for the observed effects, although total fat and saturated fat have been associated most frequently.
The epidemiological data are not entirely consistent. For example, the magnitude of the association of fat with breast cancer appears greater in the correlation data than in the case-control data, and several reports on large bowel cancer fail to show an association with fat. Possible reasons for these discrepancies are apparent . These are discussed in Chapter 5 (see pages 5-5 and 5-18).
Like epidemiological studies, numerous experiments in animals have shown that dietary lipids Influence tuti*origenesls, especially IB the breast and the colon. An increase In fat intake from 5% to 20% of the weight of the diet (i.e., approximately 10% to 40% of total calories) Increases tumor incidence in various tissues; conversely, animals con suming low fat diets have a lower tumor incidence. When the intake of total fat Is low, polyunsaturated fats appear to be more effective than saturated fats In enhancing tumorigenesis. However, this distinction becomes less prominent as total fat Intake Is increased.

Dietary fat appears to have a promoting effect on tumorigenesis. For example, some studies suggest that the development of colon cancer is enhanced by the increased secretion of certain bile steroids and bile acids that accompanies high levels of fat intake. Nonetheless, there is little or no knowledge concerning the specific mechanisms involved In tumor promotion. This lack of understanding contributes to our overall uncertainty about the mechanisms that underlie the effect of diet on carcinogenesis. Although most of the data suggest that dietary fat has promoting activity, there is not enough evidence to warrant the complete exclusion of an effect on initiation.

The committee concluded that of all the dietary components It studied, the combined epidemiological and experimental evidence Is most suggestive for a causal relationship between fat intake and the occur rence of cancer. Both epidemiological studies and experiments in ani mals provide convincing evidence that increasing the intake of total fat increases the incidence of cancer at certain sites, particularly the breast and colon, and, conversely, that the risk Is lower with lower Intakes of fat. Data from studies in animals suggest that when fat Intake Is low, polyunsaturated fats $re more effective than saturated fats In enhancing tumorigenesis, whereas the data on humans do not permit a clear distinction to be made between the effects of different components of fat. In general, however, the evidence from epidemlolog Ic4l and laboratory studies is consistent.

Cholesterol

The relationship between dietary cholesterol and cancer Is not clear. Many studies of serum cholesterol levels and cancer mortality In human populations have demonstrated an Inverse correlation with colon cancer among men, but the evidence is not con clusive. Data on cholesterol and cancer risk from studies in animals are too limited to permit any inferences to be drawn.

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