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1 Executive Sunday Scientific pronouncements are usually viewed by the public as carry- ing a rather high level of certainty. Therefore, scientists must be especially careful in their choice of words whenever they are not total- ly confident about their conclusions. For example, it has become abso- lutely clear that cigarettes are the cause of approximately one-quarter of all the fatal cancers in the United States. If the population had been persuaded to stop smoking when the association with lung cancer was first reported, these cancer deaths would now not be occurring. Twenty years ago the stop-smoking message required some rather cautious word- ing. Today, the facts are clear, and the choice of words is not so important. The public often demands certain kinds of information before such information can be provided with complete certainty. For example, weather forecasting is often not exact; nevertheless, the public asks that the effort be made, but has learned to accept the fact that the results are not always reliable. The public is now asking about the causes of cancers that are not associated with smoking. What are these causes, and how can these cancers be avoided? Unfortunately, it is not yet possible to make firm scientific pronouncements about the association between diet and cancer. We are in an interim stage of knowledge similar to that for cigarettes 20 years ago. Therefore, in the judgment of the committee, it is now the time to offer some interim guidelines on diet and cancer. Approximately 20% of all deaths in the United States are caused by cancer. Although the number of cancer cases is steadily increasing as the population grows, the age-adjusted total cancer incidence and mor- tality rates for sites other than the respiratory tract (cancers of which are primarily due to cigarette smoking) have as a whole remained stable during the last 30 to 40 years. The search for the causes of cancer has been an important branch of cancer research. Considerable effort has been devoted to studying the influence of both environmental and genetic factors on the incidence of cancer. In the course of this research, it has become clear that most cancers have external causes and, in principle, should therefore be pre- ventable. For example, blacks and Japanese residing in the United States develop the spectrum of cancers that is typical for the United States but different from that in Africa and Japan. But what might these external causes be? Many factors in our en- vironment are potential causes of cancer. They include substances in the air we breathe, the water we drink, the regions in which we work and 1 1 - 1

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2 DIET, NUTRITION, AND CANCER live, and the foods we eat. Our exposure to some of these factors var- ies in ways that can be precisely measured. For most factors, however, the measurement of the exposures and the assessment of their effects are neither precise nor straightforward. Among the factors whose precise effects are difficult to assess are the diets consumed by different groups of people. The measurements are difficult not only because it is hard to learn what people eat but also because the foods comprising their diets are so complex. Studies of the association between diet and cancer have focused on cancers of the gastrointestinal tract, the breast and other tissues susceptible to hormonal influence, and, to a lesser extent, the respi- ratory tract and the urinary bladder. After assessing the resultant literature, the committee concluded that the differences in the rates at which various cancers occur in different human populations are often correlated with differences in diet. The likelihood that some of these correlations reflect causality is strengthened by laboratory evidence that similar dietary patterns and components of food also affect the incidence of certain cancers in animals. Chapters 16 and 17 provide information about the trends in cancer incidence and the relationship between diet and the incidence of cancer at specific sites. Epidemiologists have found it relatively easy to demonstrate a cor- relation between diets consumed in modern affluent societies and the incidence of cancers in such organs as the breast, colon, and uterus. But it has proved to be much more difficult to establish causal rela- tionships and to determine which, if any, of the dietary components is responsible. Similarly, difficulties are encountered in laboratory experiments. Like humans, most animals have a significant incidence of cancer in old age, and the rates of these cancers often tend to be affected by changes in diet. However, the influence of diet on spontaneous and experimen- tally induced cancers is not easily investigated because the underlying mechanisms and molecular biology of the cancers are still not fully understood. Indeed, the effects of diet were often regarded as a nuisance--i.e., yet another variable standing between the investigators and their measurement of carcinogenicity. As a consequence, researchers have only recently returned to the study of diet as a factor in carcino- genesis. It is possible that research in progress will generate more defini- tive information that will be useful in formulating dietary recommenda- tions to minimize the risk of cancer. In the meantime, the committee believes that the evidence at hand justifies certain interim guidelines. These guidelines appear at the end of this chapter following a summary of the committee's findings and the conclusions it believes can be drawn from the scientific evidence. 1 - 2

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Executive Summary 3 SUMMARY AND CONCLUSIONS - Dietary Patterns and Components of Food 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 caloric intake per se on the risk of cancer, their reports have pro- vided largely indirect evidence for such a relationship, and much of it is based on associations between body weight or obesity and cancer. 1 - 3

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4 DIET, NUTRITION, 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 tumorigenesis. 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 tumorigenesis, especially in 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 1 - 4

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Execahve Summary 5 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 are 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 epidemiolog- ical 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. Chapter 5 contains a more detailed discussion of these studies. Protein At, The relationship between protein intake and carcinogenesis has been studied in human populations as well as in the laboratory. These stud- ies are discussed in Chapter 6. Results of epidemiological studies have suggested possible associa- tions between high intake of dietary protein and increased risk for can- cers at a number of different sites, although the literature on protein is much more limited than the literature concerning fats and cancer. In addition, because of the very high correlation between fat and protein 1-5

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6 DIET, NUTRITION, AND CANCER in the diets of most Western countries, and the more consistent and often stronger association of these cancers with fat intake, it seems likely that dietary fat is the more active component. Nevertheless, the evidence does not completely preclude the existence of an inde- pendent effect of protein. In most laboratory experiments, carcinogenesis is suppressed by diets containing levels of protein at or below the minimum required for optimal growth. Chemically induced carcinogenesis appears to be enhanced as protein intake is increased up to 2 or 3 times the normal requirement; however, higher levels of protein begin to inhibit car- cinogenesis. There is some evidence to suggest that protein may affect the initiation phase of carcinogenesis and the subsequent growth and development of the tumor. Thus, in the judgment of the committee, evidence from both epidemio- logical and laboratory studies suggests that high protein intake may be associated with an increased risk of cancers at certain sites. Because of the relative paucity of data on protein compared to fat, and the strong correlation between the intakes of fat and protein in the U.S. diet, the committee is unable to arrive at a firm conclusion about an independent effect of protein. Carbohydrates As discussed in Chapter 7, information concerning the role of carbo- hydrates in the development of cancer in humans is extremely limited. Although some studies suggest that a high intake of refined sugar or starch increases the risk of cancer at certain sites, the results are insufficient to permit any firm conclusions to be drawn. The data obtained from studies in animals are equally limited, providing too little evidence to suggest that carbohydrates (possibly excluding fiber) play a direct role in experimentally induced carcino- genesis. However, excessive carbohydrate consumption contributes to caloric excess, and this in turn has been implicated as a modifier of carcinogenesis. Dietary Fiber Considerable effort has been devoted to studying the effects of dietary fiber and fiber-containing foods (such as certain vegetables, fruits, and whole grain cereals) on the occurrence of cancer (see Chapter 8~. Most epidemiological studies on fiber have examined the hypothesis that high fiber diets protect against colorectal cancer. Results of correlation and case-control studies of dietary fiber have sometimes supported and sometimes contradicted this hypothesis. In both types of 1 - 6

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Executive Summary 7 studies, correlations have been based primarily on estimates of fiber intake obtained by grouping foods according to their fiber content. In the only case-control study and the only correlation study in which total fiber consumption was quantified rather than estimated from the consumption of high fiber foods, no association was found between high fiber intake and a lower risk of colon cancer. However, the correla- tion study indicated that the incidence of colon cancer was inversely related to the intake of one fiber component--the pentosan fraction, which is found in whole wheat products and other food items. Laboratory experiments also have indicated that the consumption of some high fiber ingredients (e.g., cellulose and bran) inhibits the in- duction of colon cancer by certain chemical carcinogens. However, the results are inconsistent. Moreover, they are difficult to equate with the results of epidemiological studies because most laboratory investi- gations have focused on specific fibers or their individual components, whereas most epidemiological studies have been concerned with fiber- containing foods whose exact composition has not been determined. Thus, the committee found no conclusive evidence to indicate that dietary fiber (such as that present in certain fruits, vegetables, grains, and cereals) exerts a protective effect against colorectal cancer in humans. Both epidemiological and laboratory reports suggest that if there is such an effect, specific components of fiber, rather than total fiber, are more likely to be responsible. Vitamins . In recent years, there has been considerable interest in the role of vitamins A, C, and E in the genesis and prevention of cancer. In con- trast, less attention has been paid to the B vitamins and others such as vitamin K. Chapter 9 contains more detailed information on the evidence summarized below. Vitamin A. A growing accumulation of epidemiological evidence indi- cates that there is an inverse relationship between the risk of cancer and the consumption of foods that contain vitamin A (e.g., liver) or its precursors (e.g., the carotenoids in green and yellow vegetables). Most of the data do not show whether the effects are due to carotenoids, to vitamin A itself, or to some other constituent of these foods. In these studies, investigators found an inverse association between estimates of vitamin A intake and carcinoma at several sites, e.g., the lung, the urinary bladder, and the larynx. Studies in laboratory animals indicate that vitamin A deficiency generally increases susceptibility to chemically induced neoplasia and that an increased intake of the vitamin appears to protect against car- cinogenesis in most, but not all cases. Because high doses of vitamin A are toxic, many of these studies have been conducted with its synthetic 1 - 7

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8 DIET, NUTRITION, AND CANCER analogues (retinoids), which lack some of the toxic effects of the vitamin. Retinoids have been shown to inhibit chemically induced neoplasia of the breast, urinary bladder, skin, and lung in animals. The committee concluded that the laboratory evidence shows that vitamin A itself and many of the retinoids are able to suppress chemi- cally induced tumors. The epidemiological evidence is sufficient to suggest that foods rich in carotenes or vitamin A are associated with a reduced risk of cancer. The toxicity of vitamin A in doses exceed- ing those required for optimum nutrition, and the difficulty of epi- demiological studies to distinguish the effects of carotenes from those of vitamin A, argue against increasing vitamin A intake by the use of supplements. Vitamin C (Ascorbic Acid). The epidemiological data pertaining to the effect of vitamin C on the occurrence of cancer are not exten- sive. Furthermore, they provide mostly indirect evidence since they are based on the consumption of foods, especially fresh fruits and vegetables, known to contain high concentrations of the vitamin, rather than on actual measurements of vitamin C intake. The results of several case-control studies and a few correlation studies suggest that the con- sumption of vitamin-C-containing foods is associated with a lower risk of certain cancers, particularly gastric and esophageal cancer. In the laboratory, ascorbic acid can inhibit the formation of car- cinogenic N-nitroso compounds, both in vitro and in viva. On the other hand, studies of its inhibitory effect on preformed carcinogens have not provided conclusive results. In recent studies, the addition of ascor- bic acid to cells grown in culture prevented the chemically induced transformation of these cells and, in some cases, caused reversion of transformed cells. Thus, the limited evidence suggests that vitamin C can inhibit the formation of some carcinogens and that the consumption of vitamin-C- containing foods is associated with a lower risk of cancers of the stomach and esophagus. Vitamin E (~-Tocopherol). Because vitamin E is present in a variety - of commonly consumed foods (particularly vegetable oils, whole grain cereal products, and eggs), it is difficult to identify population groups with substantially different levels of intake. Consequently, it is not surprising that there are no epidemiological reports concerning vitamin E intake and the risk of cancer. Vitamin E, like ascorbic acid, inhibits the formation of nitrosa- mines in viva and in vitro. However, there are no reports about the effect of this vitamin on nitrosamine-induced neoplasia. Limited evi- dence from studies in animals suggests that vitamin E may also inhibit the induction of tumorigenesis by other chemicals. 1 - 8

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Execahve Summary 9 The data are not sufficient to permit any firm conclusion to be drawn about the effect of vitamin E on cancer in humans. The B Vitamins. No specific information has been produced by epi- demiological studies, and there have been only a few inadequate labora- tory investigations to determine whether there is a relationship between various B vitamins and the occurrence of cancer. Therefore, no conclu- sion can be drawn. Minerals Of the many minerals present in the diet of humans, the committee reviewed the evidence for nine that have been suspected of playing a role in carcinogenesis. The assessment was severely limited by a pau- city of relevant studies on all but two minerals--selenium and iron. Where data on dietary exposure and carcinogenesis were insufficient, the committee used information from studies of occupational exposure or laboratory experiments in which the animals were exposed through routes other than diet. Chapter 10 contains more detailed information on the evidence summarized below. Selenium. Selenium has been studied to determine its role in both the causation and the prevention of cancer. The epidemiological evi- dence is derived from a few geographical correlation studies, which have shown that the risk of cancer is inversely related to estimates of per capita selenium intake, selenium levels in blood specimens, or selenium concentrations in water supplies. It is not clear whether this relation- ship applies to all types of cancer or only to cancer at specific sites such as the gastrointestinal tract. There have been no case-control or cohort studies. Experiments in animals have also demonstrated an antitumorigenic effect of selenium. But the relevance of these results to cancer in humans is not apparent since the selenium levels used in most of the studies far exceeded dietary requirements and often bordered on levels that are toxic. Earlier reports suggesting that selenium was carcino- genic in laboratory animals have not been confirmed. Therefore, both the epidemiological and laboratory studies suggest that selenium may offer some protection against the risk of cancer. However, firm conclusions cannot be drawn from the limited evidence. Increasing the selenium intake to more than 200 ~g/day1 by the use of supplements has not been shown to confer health benefits exceeding The upper limit of the Range of Safe and Adequate Daily Dietary Intakes published in the Recommended Dietary Allowances (see Chapter 10~. 1 - 9

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10 DIET, NUTRITION,AND CANCER those derived from the consumption of a balanced diet. Such supple- mentation should be considered an experimental procedure requiring strict medical supervision and is not recommended for use by the public. Iron. Iron deficiency has been related to an increase in the risk of Plummer-Vinson syndrome, which is associated with cancer of the upper alimentary tract. Some evidence suggests that iron deficiency may be related to gastric cancer, also through an indirect mechanism. Although epidemiological reports have suggested that inhalation exposures to high concentrations of iron increase the risk of cancer, there is no evidence pertaining to the effect of high levels of dietary iron on the risk of cancer in humans. The limited evidence from animal experiments suggests that a deficiency of dietary iron may increase susceptibility to some chemically induced tumors. The data are not sufficient for a firm conclusion to be drawn about the role of iron in carcinogenesis. Copper, Zinc, Molybdenum, and Iodine. Some epidemiological studies suggest that dietary zinc is associated with an increase in the inci- dence of cancer at certain sites; others suggest that blood and tissue levels of zinc in cancer patients are lower, and those of copper are higher, than in the controls. Results of experiments in animals are also inconclusive. Different levels of dietary zinc either enhance or retard tumor growth, depending on the specific test design. High levels of copper have been observed to protect against chemical induction of tumors. There is some epidemiological evidence that a deficiency of molyb- denum and other trace elements is associated with an increased risk of esophageal cancer. Limited experiments in animals suggest that dietary molybdenum supplementation may reduce the incidence of nitrosamine- induced tumors of the esophagus and forestomach. Studies conducted in Colombia, Iceland, and Scotland indicated that iodine deficiency, and also excessive iodine intake, may increase the risk of thyroid carcinoma. These observations have not been confirmed in other countries or in other studies. In general, the results of studies in animals support the association between iodine deficiency and thyroid cancer. The committee concluded that the data concerning dietary exposure to zinc, copper, molybdenum, and iodine are insufficient and provide no basis for conclusions about the association of these elements with cancer risk. Arsenic, Cadmium, and Lead. Occupational exposure to these elements is associated with an increased risk of cancer at several sites. Expo- sure to high concentrations of arsenic in drinking water has been linked with skin cancer. However, the evidence for cancer risk resulting from exposure to the normally low levels of these elements in the diet is not 1-10

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Executive Summary 11 conclusive. No carcinogenic effects of dietary cadmium and arsenic have been observed in laboratory experiments, whereas high intakes of certain lead compounds appear to increase the incidence of cancer in mice and rats. On this basis, the committee believes that no firm conclusions can be drawn about the risk of cancer due to normal dietary exposure to arsenic, cadmium, and lead. Inhibitors of Carcinogenesis Foods and numerous nutritive and nonnutritive components of the diet have been examined for their potential to protect against carcino- genesis. In epidemiological studies, investigators have attempted to correlate the intake of specific foods (and by inference, certain vita- mins and trace elements) and the incidence of cancer. In laboratory experiments, vitamins, trace elements, nonnutritive food additives, and other organic constituents of foods (e.g., indoles, phenols, flavones, and isothiocyanates) have been tested for their ability to inhibit neoplasia (see Chapter 15~. The committee believes that there is sufficient epidemiological evidence to suggest that consumption of certain vegetables, especially carotene-rich (i.e., dark green and deep yellow) vegetables and cru- ciferous vegetables (e.g., cabbage, broccoli, cauliflower, and Brussels sprouts), is associated with a reduction in the incidence of cancer at several sites in humans. A number of nonnutritive and nutritive com- pounds that are present in these vegetables also inhibit carcinogenesis in laboratory animals. Investigators have not yet established which, if any, of these compounds may be responsible for the protective effect observed in epidemiological studies. Alcohol The effects of alcohol consumption on cancer incidence have been studied in human populations. In some countries, including the United States, excessive beer drinking has been associated with an increased risk of colorectal cancer, especially rectal cancer. This observation has not been confirmed in other studies. There is limited evidence that excessive alcohol consumption causes hepatic injury and cirrhosis, which in turn may lead to the formation of hepatomas (liver cancer). When consumed in large quantities, alcoholic beverages appear to act syner- gistically with inhaled cigarette smoke to increase the risk for cancers of the mouth, larynx, esophagus, and the respiratory tract. The studies of alcohol consumption and cancer are discussed in Chapter ll. 1-11

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12 DIET, NUTRITION, AND CANCER Naturally Occurring Carcinogens In addition to nutrients, a variety of nonnutritive substances (e.g., hydrazines) are natural constituents of foods. Furthermore, metabolites of molds (e.g., mycotoxins such as the potent carcinogen aflatoxin) and of bacteria E.g., carcinogenic nitrosamines) may con- taminate foods. Many of these are occasional contaminants, whereas others are normal components of relatively common foods. In Chapter 12, the committee examines evidence linking consumption of some of these substances to carcinogenesis. The committee concluded that certain naturally occurring contami- nants in food are carcinogenic in animals and pose a potential risk of cancer to humans. Noteworthy among these are mycotoxins (especially aflatoxin) and N-nitroso compounds, for which there is some epidemio- logical evidence. Studies in animals indicate that a few nonnutritive constituents of some foods, such as hydrazines in mushrooms, are also carcinogenic. The compounds thus far shown to be carcinogenic in animals have been reported to occur in the average U.S. diet in small amounts; how- ever, there is no evidence that any of these substances individually makes a major contribution to the total risk of cancer in the United States. This lack of sufficient data should not be interpreted as an indication that these or other compounds subsequently found to be car- cinogenic do not present a hazard. Mutagens in Foods Mutagens are substances that cause heritable changes in the genet- ic material of cells. If a chemical is mutagenic to bacteria or other organisms, it is generally regarded as a suspect carcinogen, although carcinogenicity must be confirmed in long-term tests in whole animals. As is evident from the discussion in Chapter 13, considerable attention has recently been directed toward mutagenic activity in foods. Many vegetables contain mutagenic flavonoids such as quercetin, kaempferol, and their glycosides. Furthermore, some substances found in foods can enhance or inhibit the mutagenic activity of other com- pounds. Mutagens in charred meat and fish are produced during the pyrolysis of proteins that occurs when foods are cooked at very high temperatures. Mutagens can also be produced during normal cooking of meat at lower temperatures. Smoking of foods as well as charcoal broiling results in the deposition of mutagenic and carcinogenic poly- nuclear organic compounds such as benzo~a~pyrene on the surface of the food. Most mutagens detected in foods have not been adequately tested for their carcinogenic activity. Thus, the committee believes that it is not yet possible to assess whether such mutagens are likely to contrib- ute significantly to the incidence of cancer in the United States. 1-12

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Executive Summary 13 Food Additives In the United States, nearly 3,000 substances are intentionally added to foods during processing. Another estimated 12,000 chemi- cals (e.g., vinyl chloride and acrylonitrile, which are used in food- packaging materials) are classified as indirect (or unintentional) additives, and are occasionally detected in some foods. Large amounts of some additives, such as sugar, are consumed by the general popula- tion, but the annual per capita exposure to most indirect additives represents only a minute portion of the diet. Although the Food Safety Provisions and, in many cases, the "Delaney Clause" of the Federal Food, Drug, and Cosmetic Act prohibit the addition of known carcinogens to foods, only a small proportion of the substances added to foods have been tested for carcinogenicity according to protocols that are considered acceptable by current standards. Moreover, except for the studies on nonnutritive sweeteners, only a few epidemiological studies have been conducted to assess the effect of food additives on cancer incidence. Chapter 14 contains detailed information on certain additives, i.e., selected nonnutritive sweeteners, antioxidants, and additives used in packaging or for promoting the growth of animals used for food. Particular attention is given to substances to which humans are widely exposed. Of the few direct food additives that have been tested and found to be carcinogenic in animals, all except saccharin have been banned trom use in the food supply. Only minute residues of a few indirect additives that are known either to produce cancer in animals (e.g., acrylonitrile) or to be carcinogenic in humans (e.g., vinyl chloride and diethylstilbestrol) are occasionally detected in foods. The evidence reviewed by the committee does not suggest that the increasing use of food additives has contributed significantly to the overall risk of cancer for humans. However, this lack of detectable effect may be due to their lack of carcinogenicity, to the relatively recent use of many of these substances, or to the inability of epide- miological techniques to detect the effects of additives against the background of common cancers from other causes. Environmental Contaminants Very low levels of a large and chemically diverse group of environ- mental contaminants may be present in a variety of foods. The dietary levels of some of these substances are monitored by the Market Basket Surveys conducted by the Food and Drug Administration. Many of them have been extensively tested for carcinogenicity. 2Sec. 402(a)~2~(C) and Sec. 409(c)~1~(A), respectively. 1-13

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14 DIET, NUTRITION, AND CANCER In Chapter 14, the committee has summarized the evidence concern- ing exposure of humans to, and the carcinogenicity of, selected pesti- cides, some industrial chemicals, and other environmental contaminants. As with food additives, consideration was given primarily to compounds to which humans are widely exposed. The results of standard chronic toxicity tests indicate that a num- ber of environmental contaminants (e.g., some organochlorine pesticides, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons) cause cancer in laboratory animals. The committee found no epidemiological evidence to suggest that these compounds individually make a major con- tribution to the risk of cancer in humans. However, the possibility that they may act synergistically and may thereby create a greater car- cinogenic risk cannot be excluded. Contribution of Diet to Overall Risk of Cancer - By some estimates, as much as 90% of all cancer in humans has been attributed to various environmental factors, including diet (see Chapter 18~. Other investigators have estimated that diet is respon- sible for 30% to 40% of cancers in men and 60% of cancers in women. Recently, two epidemiologists suggested that a significant proportion of the deaths from cancer could be prevented by dietary means and that dietary modifications would have the greatest effect on the incidence of cancers of the stomach and large bowel and, to a lesser extent, on cancers of the breast, the endometrium, and the lung. The evidence reviewed by the committee suggests that cancers of most major sites are influenced by dietary patterns. However, the committee concluded that the data are not sufficient to quantitate the contribution of diet to the overall cancer risk or to determine the percent reduction in risk that might be achieved by dietary modifica- tions. INTERIM DIETARY GUIDELINES It is not now possible, and may never be possible, to specify a diet that would protect everyone against all forms of cancer. Nevertheless, the committee believes that it is possible on the basis of current evi- dence to formulate interim dietary guidelines that are both consistent with good nutritional practices and likely to reduce the risk of cancer. These guidelines are meant to be applied in their entirety to obtain maximal benefit. 1. There is sufficient evidence that high fat consumption is linked to increased incidence of certain common cancers (notably breast and colon cancer) and that low fat intake is associated with a lower inci- dence of these cancers. The committee recommends that the consumption 1-14

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Execahve Summary 15 of both saturated and unsaturated fats be reduced in the average U.S. diet. An appropriate and practical target is to reduce the intake of fat from its present level (approximately 40%) to 30% of total calo- ries in the diet. The scientific data do not provide a strong basis for establishing fat intake at precisely 30% of total calories. Indeed, the data could be used to justify an even greater reduction. However, in the judgment of the committee, the suggested reduction (i.e., one- quarter of the fat intake) is a moderate and practical target, and is likely to be beneficial. 2. The committee emphasizes the importance of including fruits, vegetables, and whole grain cereal products in the daily diet. In epidemiological studies, frequent consumption of these foods has been inversely correlated with the incidence of various cancers. Results of laboratory experiments have supported these findings in tests of individual nutritive and nonnutritive constituents of fruits (especially citrus fruits) and vegetables (especially carotene-rich and cruciferous vegetables). These recommendations apply only to foods as sources of nutrients-- not to dietary supplements of individual nutrients. The vast litera- ture examined in this report focuses on the relationship between the consumption of foods and the incidence of cancer in human populations. In contrast, there is very little information on the effects of various levels of individual nutrients on the risk of cancer in humans. There- fore, the committee is unable to predict the health effects of high and potentially toxic doses of isolated nutrients consumed in the form of supplements. 3. In some parts of the world, especially China, Japan, and Ice- land, populations that frequently consume salt-cured (including salt- pickled) or smoked foods have a greater incidence of cancers at some sites, especially the esophagus and the stomach. In addition, some methods of smoking and pickling foods seem to produce higher levels of polycyclic aromatic hydrocarbons and N-nitroso compounds. These com- pounds cause mutations in bacteria and cancer in animals, and are sus- pected of being carcinogenic in humans. Therefore, the committee recom- mends that the consumption of food preserved by salt-curing (including salt-pickling) or smoking be minimized. 4. Certain nonnutritive constituents of foods, whether naturally occurring or introduced inadvertently (as contaminants) during pro- duction, processing, and storage, pose a potential risk of cancer to humans. The committee recommends that efforts continue to be made to minimize contamination of foods with carcinogens from any source. Where such contaminants are unavoidable, permissible levels should continue to be established and the food supply monitored to assure that such levels are not exceeded. Furthermore, intentional additives (direct and indi- rect) should continue to be evaluated for carcinogenic activity before they are approved for use in the food supply. 1-15

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16 DIET, NUTRITION, AND CANCER 5. The committee suggests that further efforts be made to identify mutagens in food and to expedite testing for their carcinogenicity. Where feasible and prudent, mutagens should be removed or their con- centration minimized when this can be accomplished without jeopardizing the nutritive value of foods or introducing other potentially hazard- ous substances into the diet. 6. Excessive consumption of alcoholic beverages, particularly com- bined with cigarette smoking, has been associated with an increased risk of cancer of the upper gastrointestinal and respiratory tracts. Consump- tion of alcohol is also associated with other adverse health effects. Thus, the committee recommends that if alcoholic beverages are consumed, it be done in moderation. * * * The committee suggests that agencies involved in education and pub- lic information should be encouraged to disseminate information on the relationship between dietary and nutritional factors and the incidence of cancer, and to publicize the conclusions and interim dietary guide- lines in this report. It should be made clear that the weight of evi- dence suggests that what we eat during our lifetime strongly influences the probability of developing certain kinds of cancer but that it is not now possible, and may never be possible, to specify a diet that protects all people against all forms of cancer. The cooperation of the food industry should be sought to help implement the dietary guidelines de- scribed above. Since the current data base is incomplete, future epidemiological and experimental research is likely to provide new insights into the relationship between diet and cancer. Therefore, the committee suggests that the National Cancer Institute establish mechanisms to review these dietary guidelines at least every 5 years. 1-16