PREVENTIVE
MEDICINE
4, 322-327
(1975)
Overview:
Nutrition
and Cancer
ERNST L. WYNDER’ Division
of Epidemiology, American Health New York, New York 10019
Foundation,
You Are What You Eat is the title of a popular book on nutrition. Whatever else one might think about the contents of the book, the title hits the mark. It is well recognized that the food intake of infants affects their mental development and that the lack of certain nutrients relates to a wide variety of deficiency diseases. What is less well accepted is that “overnutrition” (so aptly called by Rene Dubos “malnutrition of the affluent”) similarly induces a variety of “excess” diseases. These are the types of diseases particularly common in the U.S. and most of the developed world today. Investigators experienced with atherosclerosis and cardiovascular diseases have been convinced for some time now that excess-particularly in the intake of saturated fats and cholesterol - significantly contributes to the development of these diseases, and scientists have already recommended dietary modifications as the best hope of reducing their incidence. These investigations have shown that the types of nutrients consumed, rather than obesity caused by increased food consumption, are the main culprits in the development of heart disease. The public at large, however, usually considers overnutrition in relation to obesity. How often does one hear an expression of surprise by lay people that an individual who was as thin as a rail has just died of a heart attack? It is well recognized that one can have a nutrition-induced hyperlipidemia primarily resulting from an excessive intake of saturated fats and cholesterol and not be overweight. These types of nutrients are the main culprits, not only because we are a sedentary population, but also because we consume these nutrients in excess. One reason the relationship between nutrition and cancer is ignored is that, in spite of some early experimental observations such as those by Tannenbaum and Silverstone (1 l), few oncologists have given much thought to this problem. Obviously, if we as scientists or physicians do not think about a given issue, its significance will elude us even if it confronts us directly. Evidence is now at hand that nutrition-not so much in terms of food additives or food contaminants, but rather, specific deficiencies and excesses-significantly contributes to the development of a whole variety of human cancers. Within the confines of this brief communication, we shall not deal with food additives such as cyclamates, saccharin, or antioxidants, since these subjects have been discussed extensively in the scientific and lay literature. We do recognize the importance of looking at each of these factors on the basis of their overall risk or 1 This work has been supported by National can Cancer Society Grant CI-I 15.
Cancer Institute 322
Copyright @I 1975 by Academic Press, Inc. All rights of reproduction in any form reserved.
Contract
# NOI-CP-43378,
Ameri-
OVERVIEW:
NUTRITION
AND
CANCER
323
benefit and of judging experimental data realistically as to their possible application to human cancer. NUTRITIONAL
DEFICIENCY
The main “deficiency cancers” are those of the upper alimentary tract where these cancers have been observed to develop with a relatively high frequency in smokers who are heavy consumers of alcohol (15). Current evidence suggests that the effect of alcohol in increasing the risk for these cancers does not so much relate to the likelihood that alcohol per se is carcinogenic but rather to the fact that alcoholism is often associated with nutritional deficiencies, particularly deficiencies in the B vitamin group. We at the American Health Foundation speculate that the mechanism whereby alcohol increases the risk of cancer in these areas is by impeding mitochondrial function in the epithelial cells of the upper alimentary tract. This mechanism would then be similar to that of Plummer-Vinson disease, a disease induced by a long-standing iron deficiency, which is also associated with a high risk of cancer in this anatomic area (14). Other examples of deficiency include iodine deficiency, which is known to increase the risk of thyroid cancer, and protein deficiency, which is believed to increase the risk of liver cancer in certain parts of Africa. We believe that gastric cancer may be related to a diet high in carbohydrate intake and relatively low in the intake of fat and fat-soluble vitamins, although this concept is still speculative. It is’ also possible that cervix cancer, so common in developing countries and known to be related to early intercourse and poor genital hygiene, may also be affected by vitamin A deficiency, a vitamin that plays a role in preserving the integrity of squamous mucous-producing epithelium of the type that covers the cervix. NUTRITIONAL
EXCESSES
Of particular importance is current evidence indicating that dietary excesses contribute to cancers of the lower gastrointestinal tract and cancer of the endocrine system. Epidemiologically, a correlation between fat consumption and colon cancer has been demonstrated. We recognize, of course, that association does not equate with causation; association makes up a part of the total epidemiological evidence. One pertinent epidemiological clue is that each of these cancers is quite uncommon in Japan, but their incidence tends to increase as the Japanese immigrate to Hawaii or California concomitant w.ith their adoption of American dietary habits (4). Colon cancer, which affects about 100,000 Americans each year, has an average annual age-adjusted incidence rate of 30.9/100,000 for both sexes and all races combined. When contrasted to an incidence rate of only 41100,000 in Japan, these figures suggest that cancer of the colon, like most other cancers, is related to environmental causes. Indeed, it should be comforting for man to know that most cancers are not an inevitable consequence of being human. Studies on stool specimens have shown that high-risk populations for colon cancer differ from low-risk populations in that they have a relatively high content of anaerobic bacteria as well as bile acid and cholesterol metabolites in their feces-fecal constituents distinctly in-
324
ERNST
L.
WYNDER
fluenced by dietary intake, especially in terms of fat and cholesterol. Our studies do not suggest that fiber content of food per se or that constipation, and thus transit time, are of etiological significance in the development of colon cancer. The specific carcinogen for the large bowel mucosa remains to be identified experimentally. Tumor-promoting activity in the colon of rats has been shown for lithocholic and taurodesoxycholic bile acids. Recently, it has been shown by Hill et al. (5) in England and by Reddy (9) that patients with colon cancer have a higher output of anaerobic bacteria and of bile acid and cholesterol metabolites in their feces than the general population. Epidemiologically, we have also shown a correlation between a high fat or cholesterol diet and cancer of the pancreas and kidney. The migration clue-namely, that migrant populations to the U.S. tend to approximate the cancer rate prevalent in the U.S. as shown in particular in studies by Staszewski and Haenszel (IO)-applies also to endocrine-related cancers such as breast, ovary, endometrium, and prostate. The mechanism whereby diet may affect these hormonal-related cancers, either by affecting their production, interaction, and/or storage or by their effect on cell-and-hormone interaction, is most complex. We believe there might be a phase where a cell is “initiated” by a carcinogen resulting from a hormonal milieu, which, in turn, is influenced by diet. Such influence may lead to the modification of a few susceptible cells. MacMahon and Cole have shown a change in the estriol to estradioh estrone ratio in Japanese, Japanese immigrants, and U.S. populations that is likely due to dietary differences (7). The initiating phase is followed by a promotion phase later in life that is probably affected by another kind of hormonal setting, which, in turn, is controlled by dietary factors. The initiation phase also appears to be related to the age of menarche, which is shown to be linked to diet and specifically to weight. In Western populations, the critical average weight when menarche begins seems to be about 46 kg. The age of menarche has continuously declined in the last 100 years and correlated with an increase in breast cancer. The present increase of breast cancer in U.S. women in the 30-50 age group may be a result of this earlier onset of menarche as a consequence of dietary modification. The fact that the American-Japanese differences for these female cancers, as well as for prostate cancer, increases with advancing age indicates that the dietary effect may be greatest for the promoting phase. Laboratory studies (2) in rats have shown that this promotor phase may be due to an increase in the ratio of prolactin to estrogen, a ratio that is influenced by the amount of fat in the diet. In humans the role of prolactin remains unclear. We have said relatively little about the role of obesity in increasing one’s risk for cancer. A clear association has been shown for obesity only to endometrium and to female kidney cancer (16). The relationship shown by de Waard and Baanders-von Halewyn (3) that obesity relates to breast cancer in postmenopausal women might relate to socioeconomic factors peculiar to the Netherlands, although suggestive evidence in this field has been also shown by Lin et al. (6) for data from Taiwan and Valaoras et al. (12). Our own data, when matched for socioeconomic factors, show no significant increased role for obesity. Nor for height that obesity per se is not the bona fide factor is suggested by
OVERVIEW:
NUTRITION
AND
CANCER
325
the fact that even though black U.S. women are significantly more obese postmenopausally than white women at the same stage of life, their risk for developing breast cancer is, in fact less (8). Obesity must be judged in terms of the nutritional factors that have induced it. While experimental and epidemiological studies are continuing in this area to identify the specific hormonal factors and interrelationship of factors that relate to these diseases, one may well ask what we as physicians should recommend to our patients at the present time. PREVENTIVE
ACTION
Most of us recognize that our nutritional education was relatively poor while in medical school. We may have had a few lectures on specific vitamins, but few of us have been instructed in how to look at nutrition as a whole, particularly as it relates to man’s continued and optimal well-being. Many of us have little knowledge about what a normal serum cholesterol level should be, and in instructing our patients, we frequently confuse average with normality. The fact is that the average American is hyperlipidemic. We would like to see no American adult exceed a serum cholesterol level of 180 mg%. I am reminded of my favorite definition of average, which I initially heard quoted by the economist Walter Heller: A man stands with one foot on hot coals and the other foot on dry ice-and on the average he is comfortable! Average does not necessarily mean normal. Even if we were going to place our patients on a low-cholesterol diet, perhaps with the aid of some booklets from the American Heart Association, we have very little personal knowledge of what an adequate diet should be for a largely sedentary population. Furthermore, even if we took the time to instruct our patients as to how to modify their behavior, we have had negligible training in the behavioral sciences. We have learned from the history of medicine that man prevented illnesses long before he understood their specific mechanism of causation. The same concept applies to nutrition and cancer. Where diseases are caused by deficiencies, it is easier to convince people that nutrition supplements ought to be introduced than it is to alter their dietary habits. Where diseases are due to excesses, recommendations for reducing various intakes would appear more difficult, for commercial as well as for behavioral reasons. We should join our colleagues involved in cardiovascular disease prevention in advocating “the prudent diet,” a fat-controlled, low-cholesterol eating style (1). Such a diet suggests that we reduce our total calories by about 20%, that we reduce the total intake of saturated fats to no more than 10% of the total caloric intake in an effort to increase significantly the present P/S ratio of 0.3 : 1.0, that we decrease our dietary cholesterol from the present average of 600 mg to around 300 mg daily, and that we adjust our carbohydrate intake so that complex types predominate. In terms of fat and cholesterol intake, The Prudent Diet (1) suggests limiting the consumption of red meat to four portions per week, eating no more than two eggs a week, limiting the intake of organ foods, and avoiding fat-rich dairy products and saturated fats. We should encourage our patients to eat more fish and poultry, egg substitutes, and highly polyunsaturated margarine and oils and to replace whole milk with skimmed milk.
326
ERNST
L. WYNDER
At the same time, we should advocate supplements to certain foods in areas where deficiency prevails. Supplements added to flour in Sweden, such as iron and vitamins, have reduced Plummer-Vinson disease in that country. The addition of iodine to salt has led to reduction of goiter. Supplementing vitamin B to alcohol in the diet might well be considered. We should encourage the egg industry and the U.S. Department of Agriculture to undertake studies to lower the cholesterol content of eggs. We should reduce the fat content of milk and other dairy products and of beef, which can be accomplished through greater use of range feeding. In these days of high grain prices, this would obviously be economically as well as nutritionally advantageous. We should also encourage our baking industry to use more polyunsaturated and less saturated fats in their food processing. Additionally, physicians should be encouraged to investigate the new nutritional labeling practices of various manufacturers in order to be able to discuss and interpret the meanings of such labels with their patients. Naturally, in conjunction with this increased attention to labels, physicians should urge their patients to use the more nutritionally acceptable products, which, in turn, should influence the availability of such products. These recommendations for dietary modification should also be applied to children. Their early years of development are of particular importance, both in terms of following in their parents’ footsteps and of establishing metabolic pathways. Preventive medicine should have its start in infancy if it is to be fully successful. At the American Health Foundation, we are engaged in clinical and experimental research toward the discovery and elucidation of environmental factors that appear to relate to cancer in humans. In terms of education, the American Health Foundation hopes to promote a diet that, on the one hand, is suitable for proper growth but, on the other, will not lead to an accumulation of lipids and other nutrients that the increasingly sedentary human body cannot properly utilize and metabolize. Philosophically, if not scientifically, human beings are not biochemically adapted to metabolize many dietary excesses. We are strong advocates of the prudent diet as well as a generally prudent life-style with regard to other high-risk factors. Each physician should serve as an exemplar in his or her own life-style. Not only will we prolong our life expectancy in this way, but we will be in a better position to advise our patients, especially with regard to the behavioral problems involved in changing life-styles in the areas of diet, smoking, alcohol, and physical activity. Personal knowledge and experience will enable all of us to live better. It is important to remember that the major advances in the history of medicine have been made by immunization programs and modification of environmental factors rather than by therapeutic measures. It is hoped that modification of diet will play a significant role, as has already been shown by cigarette modification, in the conquest of cancer. REFERENCES 1. Bennett, I., and Simon, M. “The Prudent Diet.” David White, Inc., New York, 1973. 2. Chan, P. C., and Cohen, L. A. Effect of dietary fat, antiestrogen and antiprolactin on the development of mammary tumors in rats. J. Nat. Cancer Inst. 52, 25-30 (1974).
OVERVIEW:
NUTRITION
AND CANCER
327
3. De Waard, F., and Baanders-von Halewyn, E. A. A prospective study in general practice on breast-cancer risk in post-menopausal women. Int. J. Cancer 14, 153- 160 (1974). 4. Haenszel. W. M., and Kurihara, M. Studies of Japanese migrants: (I) mortality from cancer and other diseases among Japanese in the U.S. J. Nat. Cancer Ins?. 40, 43-51 (1968). 5. Hill, M. J., Crowther, J. S., Drasar, B. S., Hawksworth, G., Aries, V. and Williams, R. E. 0. Bacteria and aetiology of cancer of the large bowel. Lancer i, 95-100 (1971). 6. Lin, T. M., Chen, K. P., and MacMahon, B. Epidemiological characteristics of cancer of the breast in Taiwan. Cancer 27, 1497-1504 (1971). 7. MacMahon, B., and Cole, P. Ovarian etiology activity of breast cancer, in “Epidemiology of Cancer Leukemias and Lymphomas.” Springer Verlag, Zurich, 1970. 8. National Cancer Institute. “The Third National Cancer Survey Advanced Three Year Report 1969-197 1 Incidence (excluding carcinoma in situ).” National Institutes of Health HEW Publication No. (NIH) 74-637, Bethesda, MD, 1974. 9. Reddy, B. S., and Wynder, E. L. Large bowel carcinogenesis: fecal constituents of populations with disease incidence rates of colon cancer. J. Nat. Cancer Inst. 50, 1437-1442 (1973). 10. Staszewski, J., and Haenszel, W. Cancer mortality among the Polish-born in the United States. J. Nat. Cancer Inst. 35, 291-297 (1965). 11. Tannenbaum, A., and Silverstone, H. Nutrition in relation to cancer. Advan. Cancer Res. 1, 451-501 (1953). 12. Valaoras, V. G., et al. Lactation and reproductive histories of breast cancer patients in Greater Athens, 1965-67. Int. J. Cnncer 4, 350-363 (1969). 13. Wynder, R. L., Escher, G. C., and Mantel, N. An epidemiological investigation of cancer of the endometrium. Cancer 19, 489-520 (1966). 14. Wynder, E. L., Hultberg, J., Jacobsson, F., and Bross, I. D. J. Environmental factors in cancer of the upper alimentary tract: a Swedish study with special reference to Plummer-Vinson (PattersonKelly) syndrome. Cancer 19, 470-487 (1957). 15. Wynder, E. L., and Mabuchi, K. Etiological and preventive aspects of human cancer. Prev. Med. 1, 300.-334 (1972). 16. Wynder, E. L., Mabuchi, K., and Whitmore, W. F. Epidemiology of adenocarcinoma of the kidney. J. Nat. Cancer Inst. 53, 1619-1634 (1974).
MEDICINE
4, 322-327
(1975)
Overview:
Nutrition
and Cancer
ERNST L. WYNDER’ Division
of Epidemiology, American Health New York, New York 10019
Foundation,
You Are What You Eat is the title of a popular book on nutrition. Whatever else one might think about the contents of the book, the title hits the mark. It is well recognized that the food intake of infants affects their mental development and that the lack of certain nutrients relates to a wide variety of deficiency diseases. What is less well accepted is that “overnutrition” (so aptly called by Rene Dubos “malnutrition of the affluent”) similarly induces a variety of “excess” diseases. These are the types of diseases particularly common in the U.S. and most of the developed world today. Investigators experienced with atherosclerosis and cardiovascular diseases have been convinced for some time now that excess-particularly in the intake of saturated fats and cholesterol - significantly contributes to the development of these diseases, and scientists have already recommended dietary modifications as the best hope of reducing their incidence. These investigations have shown that the types of nutrients consumed, rather than obesity caused by increased food consumption, are the main culprits in the development of heart disease. The public at large, however, usually considers overnutrition in relation to obesity. How often does one hear an expression of surprise by lay people that an individual who was as thin as a rail has just died of a heart attack? It is well recognized that one can have a nutrition-induced hyperlipidemia primarily resulting from an excessive intake of saturated fats and cholesterol and not be overweight. These types of nutrients are the main culprits, not only because we are a sedentary population, but also because we consume these nutrients in excess. One reason the relationship between nutrition and cancer is ignored is that, in spite of some early experimental observations such as those by Tannenbaum and Silverstone (1 l), few oncologists have given much thought to this problem. Obviously, if we as scientists or physicians do not think about a given issue, its significance will elude us even if it confronts us directly. Evidence is now at hand that nutrition-not so much in terms of food additives or food contaminants, but rather, specific deficiencies and excesses-significantly contributes to the development of a whole variety of human cancers. Within the confines of this brief communication, we shall not deal with food additives such as cyclamates, saccharin, or antioxidants, since these subjects have been discussed extensively in the scientific and lay literature. We do recognize the importance of looking at each of these factors on the basis of their overall risk or 1 This work has been supported by National can Cancer Society Grant CI-I 15.
Cancer Institute 322
Copyright @I 1975 by Academic Press, Inc. All rights of reproduction in any form reserved.
Contract
# NOI-CP-43378,
Ameri-
OVERVIEW:
NUTRITION
AND
CANCER
323
benefit and of judging experimental data realistically as to their possible application to human cancer. NUTRITIONAL
DEFICIENCY
The main “deficiency cancers” are those of the upper alimentary tract where these cancers have been observed to develop with a relatively high frequency in smokers who are heavy consumers of alcohol (15). Current evidence suggests that the effect of alcohol in increasing the risk for these cancers does not so much relate to the likelihood that alcohol per se is carcinogenic but rather to the fact that alcoholism is often associated with nutritional deficiencies, particularly deficiencies in the B vitamin group. We at the American Health Foundation speculate that the mechanism whereby alcohol increases the risk of cancer in these areas is by impeding mitochondrial function in the epithelial cells of the upper alimentary tract. This mechanism would then be similar to that of Plummer-Vinson disease, a disease induced by a long-standing iron deficiency, which is also associated with a high risk of cancer in this anatomic area (14). Other examples of deficiency include iodine deficiency, which is known to increase the risk of thyroid cancer, and protein deficiency, which is believed to increase the risk of liver cancer in certain parts of Africa. We believe that gastric cancer may be related to a diet high in carbohydrate intake and relatively low in the intake of fat and fat-soluble vitamins, although this concept is still speculative. It is’ also possible that cervix cancer, so common in developing countries and known to be related to early intercourse and poor genital hygiene, may also be affected by vitamin A deficiency, a vitamin that plays a role in preserving the integrity of squamous mucous-producing epithelium of the type that covers the cervix. NUTRITIONAL
EXCESSES
Of particular importance is current evidence indicating that dietary excesses contribute to cancers of the lower gastrointestinal tract and cancer of the endocrine system. Epidemiologically, a correlation between fat consumption and colon cancer has been demonstrated. We recognize, of course, that association does not equate with causation; association makes up a part of the total epidemiological evidence. One pertinent epidemiological clue is that each of these cancers is quite uncommon in Japan, but their incidence tends to increase as the Japanese immigrate to Hawaii or California concomitant w.ith their adoption of American dietary habits (4). Colon cancer, which affects about 100,000 Americans each year, has an average annual age-adjusted incidence rate of 30.9/100,000 for both sexes and all races combined. When contrasted to an incidence rate of only 41100,000 in Japan, these figures suggest that cancer of the colon, like most other cancers, is related to environmental causes. Indeed, it should be comforting for man to know that most cancers are not an inevitable consequence of being human. Studies on stool specimens have shown that high-risk populations for colon cancer differ from low-risk populations in that they have a relatively high content of anaerobic bacteria as well as bile acid and cholesterol metabolites in their feces-fecal constituents distinctly in-
324
ERNST
L.
WYNDER
fluenced by dietary intake, especially in terms of fat and cholesterol. Our studies do not suggest that fiber content of food per se or that constipation, and thus transit time, are of etiological significance in the development of colon cancer. The specific carcinogen for the large bowel mucosa remains to be identified experimentally. Tumor-promoting activity in the colon of rats has been shown for lithocholic and taurodesoxycholic bile acids. Recently, it has been shown by Hill et al. (5) in England and by Reddy (9) that patients with colon cancer have a higher output of anaerobic bacteria and of bile acid and cholesterol metabolites in their feces than the general population. Epidemiologically, we have also shown a correlation between a high fat or cholesterol diet and cancer of the pancreas and kidney. The migration clue-namely, that migrant populations to the U.S. tend to approximate the cancer rate prevalent in the U.S. as shown in particular in studies by Staszewski and Haenszel (IO)-applies also to endocrine-related cancers such as breast, ovary, endometrium, and prostate. The mechanism whereby diet may affect these hormonal-related cancers, either by affecting their production, interaction, and/or storage or by their effect on cell-and-hormone interaction, is most complex. We believe there might be a phase where a cell is “initiated” by a carcinogen resulting from a hormonal milieu, which, in turn, is influenced by diet. Such influence may lead to the modification of a few susceptible cells. MacMahon and Cole have shown a change in the estriol to estradioh estrone ratio in Japanese, Japanese immigrants, and U.S. populations that is likely due to dietary differences (7). The initiating phase is followed by a promotion phase later in life that is probably affected by another kind of hormonal setting, which, in turn, is controlled by dietary factors. The initiation phase also appears to be related to the age of menarche, which is shown to be linked to diet and specifically to weight. In Western populations, the critical average weight when menarche begins seems to be about 46 kg. The age of menarche has continuously declined in the last 100 years and correlated with an increase in breast cancer. The present increase of breast cancer in U.S. women in the 30-50 age group may be a result of this earlier onset of menarche as a consequence of dietary modification. The fact that the American-Japanese differences for these female cancers, as well as for prostate cancer, increases with advancing age indicates that the dietary effect may be greatest for the promoting phase. Laboratory studies (2) in rats have shown that this promotor phase may be due to an increase in the ratio of prolactin to estrogen, a ratio that is influenced by the amount of fat in the diet. In humans the role of prolactin remains unclear. We have said relatively little about the role of obesity in increasing one’s risk for cancer. A clear association has been shown for obesity only to endometrium and to female kidney cancer (16). The relationship shown by de Waard and Baanders-von Halewyn (3) that obesity relates to breast cancer in postmenopausal women might relate to socioeconomic factors peculiar to the Netherlands, although suggestive evidence in this field has been also shown by Lin et al. (6) for data from Taiwan and Valaoras et al. (12). Our own data, when matched for socioeconomic factors, show no significant increased role for obesity. Nor for height that obesity per se is not the bona fide factor is suggested by
OVERVIEW:
NUTRITION
AND
CANCER
325
the fact that even though black U.S. women are significantly more obese postmenopausally than white women at the same stage of life, their risk for developing breast cancer is, in fact less (8). Obesity must be judged in terms of the nutritional factors that have induced it. While experimental and epidemiological studies are continuing in this area to identify the specific hormonal factors and interrelationship of factors that relate to these diseases, one may well ask what we as physicians should recommend to our patients at the present time. PREVENTIVE
ACTION
Most of us recognize that our nutritional education was relatively poor while in medical school. We may have had a few lectures on specific vitamins, but few of us have been instructed in how to look at nutrition as a whole, particularly as it relates to man’s continued and optimal well-being. Many of us have little knowledge about what a normal serum cholesterol level should be, and in instructing our patients, we frequently confuse average with normality. The fact is that the average American is hyperlipidemic. We would like to see no American adult exceed a serum cholesterol level of 180 mg%. I am reminded of my favorite definition of average, which I initially heard quoted by the economist Walter Heller: A man stands with one foot on hot coals and the other foot on dry ice-and on the average he is comfortable! Average does not necessarily mean normal. Even if we were going to place our patients on a low-cholesterol diet, perhaps with the aid of some booklets from the American Heart Association, we have very little personal knowledge of what an adequate diet should be for a largely sedentary population. Furthermore, even if we took the time to instruct our patients as to how to modify their behavior, we have had negligible training in the behavioral sciences. We have learned from the history of medicine that man prevented illnesses long before he understood their specific mechanism of causation. The same concept applies to nutrition and cancer. Where diseases are caused by deficiencies, it is easier to convince people that nutrition supplements ought to be introduced than it is to alter their dietary habits. Where diseases are due to excesses, recommendations for reducing various intakes would appear more difficult, for commercial as well as for behavioral reasons. We should join our colleagues involved in cardiovascular disease prevention in advocating “the prudent diet,” a fat-controlled, low-cholesterol eating style (1). Such a diet suggests that we reduce our total calories by about 20%, that we reduce the total intake of saturated fats to no more than 10% of the total caloric intake in an effort to increase significantly the present P/S ratio of 0.3 : 1.0, that we decrease our dietary cholesterol from the present average of 600 mg to around 300 mg daily, and that we adjust our carbohydrate intake so that complex types predominate. In terms of fat and cholesterol intake, The Prudent Diet (1) suggests limiting the consumption of red meat to four portions per week, eating no more than two eggs a week, limiting the intake of organ foods, and avoiding fat-rich dairy products and saturated fats. We should encourage our patients to eat more fish and poultry, egg substitutes, and highly polyunsaturated margarine and oils and to replace whole milk with skimmed milk.
326
ERNST
L. WYNDER
At the same time, we should advocate supplements to certain foods in areas where deficiency prevails. Supplements added to flour in Sweden, such as iron and vitamins, have reduced Plummer-Vinson disease in that country. The addition of iodine to salt has led to reduction of goiter. Supplementing vitamin B to alcohol in the diet might well be considered. We should encourage the egg industry and the U.S. Department of Agriculture to undertake studies to lower the cholesterol content of eggs. We should reduce the fat content of milk and other dairy products and of beef, which can be accomplished through greater use of range feeding. In these days of high grain prices, this would obviously be economically as well as nutritionally advantageous. We should also encourage our baking industry to use more polyunsaturated and less saturated fats in their food processing. Additionally, physicians should be encouraged to investigate the new nutritional labeling practices of various manufacturers in order to be able to discuss and interpret the meanings of such labels with their patients. Naturally, in conjunction with this increased attention to labels, physicians should urge their patients to use the more nutritionally acceptable products, which, in turn, should influence the availability of such products. These recommendations for dietary modification should also be applied to children. Their early years of development are of particular importance, both in terms of following in their parents’ footsteps and of establishing metabolic pathways. Preventive medicine should have its start in infancy if it is to be fully successful. At the American Health Foundation, we are engaged in clinical and experimental research toward the discovery and elucidation of environmental factors that appear to relate to cancer in humans. In terms of education, the American Health Foundation hopes to promote a diet that, on the one hand, is suitable for proper growth but, on the other, will not lead to an accumulation of lipids and other nutrients that the increasingly sedentary human body cannot properly utilize and metabolize. Philosophically, if not scientifically, human beings are not biochemically adapted to metabolize many dietary excesses. We are strong advocates of the prudent diet as well as a generally prudent life-style with regard to other high-risk factors. Each physician should serve as an exemplar in his or her own life-style. Not only will we prolong our life expectancy in this way, but we will be in a better position to advise our patients, especially with regard to the behavioral problems involved in changing life-styles in the areas of diet, smoking, alcohol, and physical activity. Personal knowledge and experience will enable all of us to live better. It is important to remember that the major advances in the history of medicine have been made by immunization programs and modification of environmental factors rather than by therapeutic measures. It is hoped that modification of diet will play a significant role, as has already been shown by cigarette modification, in the conquest of cancer. REFERENCES 1. Bennett, I., and Simon, M. “The Prudent Diet.” David White, Inc., New York, 1973. 2. Chan, P. C., and Cohen, L. A. Effect of dietary fat, antiestrogen and antiprolactin on the development of mammary tumors in rats. J. Nat. Cancer Inst. 52, 25-30 (1974).
OVERVIEW:
NUTRITION
AND CANCER
327
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