AMERICAN JOURNAL OF
Public Editorials Health November 1990 Volume 80, Number 11
EDITOR Michel A. Ibrahim, MD, PhD EDITOR (RETIRED) Alfred Yankauer, MD, MPH ASSISTANT EDITOR Ernest Schoenfeld, DrPH Jane E. Sisk, PhD EDITORIAL BOARD Irene H. Butter, PhD (1990) Chair Doris Bloch, RN, DrPH (1992) Suzanne E. Dandoy, MD, MPH (190) Joy G. Dryfoos, MA (1992) Herschel S. Horowitz, DDS (992) Sherman A. James, PhD 991) Dieter Koch-Weser, PhD, MDl (1991) Robert L. Kane, MD (1991) Philip J. Landrigan, MI) (1990) Jean Pakter, MD, MPH (1992) Lee N. Robins, PhD (1991) Jeannette J. Simmons, DSc, MPH (1990) Fernando M. Trevino, PhD, MPH (1990) Julian A. Waller, MD (1992) Rita Zemach, PhD (1991) STAFF William H. McBeath, MD, MPH Executive DirectorlManaging Editor Jaclyn Alexander Publications Director Doyne Bailey Assistant Managing Editor Cheryl N. Jackson Production Manager Mary Beth Kammann Advertising Manager Marilyn Butler Publication Assistant CONTRIBUTING EDITORS George J. Annas, JD, MPH Public Health and the Law Carol Jenkins, MLS Book Corner Mary Grace Kovar, DrPH, MS New from NCHS Elizabeth Fee, PhD Robert R. Korstad, PhD Public Health Then and Now Hugh H. Tilson, MD, DrPH Notes from the Field
AJPH November 1990, Vol. 80, No. 11
Established 1911
Challenges for Public Health Nutrition in the 1990s A scientific approach to public health nutrition includes: collection of evidence regarding the relation of nutritional factors to health and disease; assessment of current dietary practices; development of strategies to modify diets in a manner deemed to be beneficial; and the evaluation of intervention strategies. This approach has been successful in eliminating several nutritional deficiencies that were once widespread. Despite these successes, nutritional factors remain as probable major determinants of the dominant health problems, particularly cardiovascular diseases and cancer, in the United States and other affluent countries. As we enter a new decade, a consideration of challenges facing those working to improve our nation's health through nutrition may be appropriate. The Scientific Evidence
Establishing the relation between nutrition and chronic diseases such as cancer and cardiovascular diseases has been more elusive than for deficiency-related diseases such as pellagra and rickets. Unlike specific vitamin deficiencies, the common chronic diseases almost always have multiple causes, including interactions with genetic factors. Also, chronic diseases often have long latent periods, perhaps resulting from many years of continuous exposure, and occur with relatively low frequency even though the cumulative lifetime risk is high. Thus, it is a formidable challenge to obtain a high level of proof that a particular nutritional factor is a cause of disease. Several large, official reviews during the last 10 yearsl-3 have examined the relationship of diet and nutrition to health and disease. This information cannot be considered in detail in an editorial; however, several general comments can be made regarding coronary heart disease and cancer. Coronary Heart Disease
Despite the prominence given to the relation between diet and coronary heart disease (CHD) during the last 40 years, direct evidence is disappointingly meager. Very few human studies, either case-control or cohort observational studies or intervention trials, have directly examined the relationships between dietary factors and cardiovascular disease. Almost all were seriously limited in size or by their method of dietary assessments.4 Only two consistent findings have emerged: * an inverse relation between energy intake and the risk of coronary heart disease (almost surely reflecting the protective effects of physical activity), and * a strong protective effect of moderate alcohol intake. Although the focus of dietary recommendations is usually a reduction in saturated fat intake, no relation between saturated fat intake and risk of CHD was observed in the most informative prospective study to date.5 Even if such a relationship exists, the widely quoted ecological association found by Keys6 was probably fortuitously confounded, because the magnitude of the relationship between saturated fat intake and CHD rates was considerably stronger than expected on the basis of metabolic studies of diet and blood lipids and, in turn, epidemiologic studies of serum lipids and CHD risk.5 The classical diet/heart hypothesis-that risk of CHD is increased by dietary cholesterol and saturated fat and reduced by polyunsaturated fat-probably contains some element of truth. However, the hypothesis is over-simplified in many respects 1 295
EDITORIALS
and needs continued refinement. For example, it has been known for decades, but largely ignored, that only some saturated fats increase serum cholesterol.78 Stearic acid (18:0) is the predominant saturated fatty acid formed in the hydrogenation of vegetable fat and appears to have no adverse effect on serum lipids; it will increasingly contribute to total saturated fat intake as processed vegetable fats replace animal fats in our diet. Thus, as pointed out by Grundy9 the use of the generic term "saturated fat" to describe diets may be outmoded, both in research, and in policy and consumer education. Furthermore, a variety of hypotheses have arisen that relate other factors to risk of CHD; these include low intakes of antioxidants, fiber, vitamins B-6 and folic acid, and omega-3 fatty acids.5 These all remain to be fully evaluated, but the possibility exists that they will be more important than dietary lipids. A large volume of literature has developed using blood lipids as a surrogate endpoint to predict the influence of diet on risk of CHD. Although much has been learned, this approach is not entirely satisfactory for two fundamental reasons. First, because of the heterogeneity of blood lipids it is difficult to interpret predictions based on either total serum cholesterol (the only lipid measured in many studies) or a specific subfraction. For example, a general lowering of fat intake without alternation of the fatty acid composition may lower total cholesterol intake slightly, but this reduction is largely due to a decrease in HDL-cholesterol. '0 As HDL-C is strongly protective for CHD, the effect of a general fat reduction on risk of CHD is unclear and could conceivably be deleterious, depending on the original composition of fat in the diet. Second, it is likely that diet influences CHD risk through other causal pathways in addition to blood lipids, such as by influencing the propensity for thrombus formation. For example, based on his observation of increasing platelet aggregability with P/S ratios greater than about 0.7, Renaud has hypothesized that a goal of 1.0 for P/S ratio may not be desirable. "I Lacking adequate information about the relationship of diet and disease, policy makers have used inductive reasoning to translate metabolic information to recommendations about food intake. For example, the consistent observation that polyunsaturated fat reduces total serum cholesterol has promoted the dramatic shift from butter and lard to margarine and vegetable shortening in this country. However, persons who consume margarine instead of butter have not been shown to have a lower risk of CHD. Trans isomers of fatty acids formed in the processing of liquid vegetable oils, comprising up to 35 percent of some margarines, have recently been found to affect blood lipids adversely.'2 Thus, it is unclear whether those who switched from butter to margarine have increased, decreased, or not influenced their risk of CHD. Because foods are highly complex products that may affect the occurrence of CHD through multiple mechanisms, better empirical data relating foods and nutrients directly to risk of CHD and other major diseases are needed to develop scientifically based nutritional recommendations for the public. Diet and Cancer For the last decade, public policy reports have focused on fat as the most important dietary cause of cancer in the US; benefits from fat reduction have been anticipated for cancers of the breast, colon, and prostrate.'12 Particular
concerns have been raised regarding the possibility that polyunsaturated fat intake may increase risk of breast cancer. However, as described by Byers,'3 recently accrued data 1 296
have rendered these relations less rather than more clear, especially for breast cancer. In contrast, data have continued to accumulate that increased intake of fruits and vegetables is associated with lower risk of several cancers, most notably colon, lung, and stomach.3'4,'5 More information is needed, however, about the specific foods responsible for these benefits and whether they result from intake of fiber, betacarotene, or some other factors. Largely based on the reported inverse associations between intake of fruits and vegetables, the consumption of whole-grain breakfast cereals has been heavily promoted, even though there is at present limited evidence that cereal fiber influences the risk of colon cancer. Health Effects of Energy Balance
Although attention has focused on dietary composition, energy balance is clearly important in relation to cardiovascular disease, diabetes, several types of cancer, and total mortality. Even persons of average weight for their height in the US appear to be at increased risk for several important conditions compared with those weighing less than average.'6-'9 The health effects of weight loss are less clear and deserve further attention. Growing evidence suggests that fat distribution is an independent determinant of hypertension, diabetes, and cardiovascular disease; thus the findings by Laws, et al, in this issue,20 that behavioral factors are correlated with the waist-to-hip circumference ratio, are of interest. Additional data on body fat distribution and its determinants are likely to improve both the prediction of individual risk of disease and our understanding of the pathogenesis of several diseases. However, this knowledge may be of limited importance in disease prevention because body fat distribution appears to be more strongly determined by genetic factors than is overall obesity;2' the accumulation of abdominal fat (represented by a high waist-to-hip circumference ratio) is probably best avoided by preventing overall
obesity.
Prevention of obesity is a soundly supported nutritional objective; however, accumulating data regarding energy balance before adulthood raise complex issues. In both international studies22 and studies within countries,23-25 greater height (which reflects in part pre-adult energy balance) appears to be a risk factor for several cancers, particularly of the breast. These findings are consistent with the powerful cancer-inhibiting effect of energy restriction seen in animal studies. Translating this information into practice is clearly premature. However, those involved in childhood nutrition will need to weigh more seriously the hazards and benefits of promoting maximal growth rates and attained height, and consider whether any possibility exists for raising smaller rather than larger children, because the prospect of preventing a large proportion of breast cancer by other behavioral means appears bleak. Data Development
The need for better empirical data on the relation of nutritional factors and the incidence of cancer and heart disease has fueled controversy over the most fruitful methods of study. International correlations, case-control, cohort, randomized trials, and animal experiments all have strengths and limitations.26-29 It is likely that no specific combination of study design will be uniformly optimal for addressing all hypotheses; therefore, all approaches merit continued evaluation and refinement. A new generation of large prospective dietary studies started in the 1980s have enrolled over half a million persons collectively and will substantially increase knowledge during AJPH November 1990, Vol. 80, No. 11
EDITORIALS
the l990s.5 The increased use ofintermediate endpoints, such as adenomatous colon polyps and non-invasive measurements of atherosclerosis, may increase the efficiency of investigations, although the relation of these surrogates to clinical disease may be complex. Assessment of Dietary Practices and Development of Intervention Strategies Despite many uncertainties and the need for improved data on diet and disease, public health action is appropriate in several areas. Reasonable priorities include the prevention of obesity, a reduction of dietary cholesterol and animal fat (although the best choice of replacement energy sources is uncertain), and an increase in consumption of fruits and vegetables (although the specific types and amounts to be encouraged are less clear). Work such as that reported in this issue by Basch, et al,30 indicating encouraging progress on the assessment of diet in childhood, and by Patterson, et al,31 demonstrating that intakes of fruits and vegetables are considerably lower than recommended, are important elements in the development of a rational nutrition intervention. Further work identifying population subgroups with high intakes of animal fat and low consumption of fruits and vegetables should provide targets for education and nutritional assistance programs. Dietary intervention strategies may involve both public and private institutions as well as individuals. A combination of these should be most effective, however, because individuals can exert pressure on institutions and institutions can expand the options of individuals. For example, the feasibility study by Ellison, et al,32 in this issue provides encouraging evidence that major changes in the diets of boarding students can be made in a nonintrusive manner. Other notable insti-
tutional changes that immediately alter the diets of millions have been recent decisions by some of the fast food providers to fry their fish, chicken, and (soon) their potatoes in vegetable rather than animal fat. The fast food industry still has far to go in providing an attractive array of healthy alternatives, such as vegetarian middle-eastern, Indian, and Oriental foods, to their predominant products. A challenge to the nutrition community is to help make this a viable direction. As the scientific basis for a reduction in total fat is weak, and the concept of generic "saturated fat" is increasingly outmoded, nutrition educators and those involved in food labeling are challenged to provide clear and scientifically sound messages for the public. Just as messages based on the four food groups were effective in eliminating specific nutritional deficiencies in this country, approaches based on foods and dietary patterns rather than RDAs (recommended daily allowance), percentage of calories from fat, or grams of fiber per day may be the most effective method of communication to the public. Messages will need to include suggested limits for some foods as well as positive recommendations for others. Moreover, messages need to take into consideration the social and cultural aspect of food and health, because knowledge by itself may not necessarily translate into action. Whatever the strategies, they should be rigorously evaluated for effectiveness in producing changes in diet. Although the objective of preventing obesity is clear, the means of achieving it are not. The refractory nature of this problem can be appreciated by noting that the high prevalence of obesity has not decreased in this country despite obesity being a conspicuous and highly stigmatized risk AJPH November 1990, Vol. 80, No. 11
factor. Large sums are spent on treatments, but their longterm effectiveness is disappointing. Although obesity is a heterogeneous syndrome caused by multiple factors, sedentary life-style is probably the most important reason for its high prevalence in our society.33 A major impact on this problem will probably require a fundamental restructuring of society, necessitating a broad interdisciplinary approach. For example, our cities and towns will need to be modified so that it is once again safe, convenient, and pleasant to walk or ride a bicycle to work or school, and to go shopping. This task may be beyond our perceived responsibilities; but, by default, leadership in this effort must be assumed by those interested in public health. State and local public health workers may be particularly effective in this effort as they are close to relevant decision-making processes. In summary, new data gathered from the large studies started in the previous decade should provide substantial refinements in our knowledge about diet and health. Translating these findings into effective intervention strategies will require creativity and rigorous evaluation. The US public is clearly willing to make substantial changes in diet, as demonstrated by the large decreases in egg and red meat consumption and the substitutions of vegetable fat for animal fat that have already been accomplished. For these reasons, we should be optimistic that continued enhancement of dietary practices can substantially improve health in the US. REFERENCES 1. Committee on Diet, Nutrition, and Cancer, National Research Council: Diet, Nutrition, and Cancer. Washington, DC: National Academy Press, 1982. 2. The Surgeon General: The Surgeon General's Report on Nutrition and Health. DHHS (PHS) Pub No. 88-50210, Washington, DC: Govt Printing Office, 1988. 3. NAS/NRC Committee on Diet and Health: Diet and Health: Implications for reducing chronic disease risk. Washington, DC: National Academy Press, 1989. 4. Willett W: Nutritional Epidemiology. New York: Oxford University Press, 1990. 5. Shekelle RB, Shryock AM, Paul O: Diet, serum cholesterol and death from coronary heart disease. The Western Electric Study. N Engl J Med 1981; 304:65-70. 6. Keys A: Seven Countries: A multivariate analysis of death and coronary heart disease. Cambridge: Harvard University Press. 1980; 252. 7. Hegsted DM, McGandy RB, Myers ML, Stare FJ: Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr 1%5; 17:281-295. 8. Bonanome A, Grundy SM: Effect of dietary stearic acid on plasma cholesterol and lipoprotein levels. N Engi J Med 1986; 318:1244-1248. 9. Grundy SM: Trans monounsaturated fatty acids and serum cholesterol levels (editorial). N Engl J Med 1990; 323:480-481. 10. Lee-Han H, Cousins M, Beaton M, McGuire V, Krukov V, Chipman M, Boyd N: Compliance in a randomized clinical trial of dietary fat reduction in patients with breast dysplasia. Am J Clin Nutr 1988; 48:575-586. 11. Renaud S, Godsey F, Dumont E, Thevenon C, Ortchanian E, Martin JL: Influence of long-term diet modification on platelet function and composition in Moselle farmers. Am J Clin Nutr 1986; 43:136-150. 12. Meusink RP, Katan MB: Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects. N Engl J Med 1990; 323:439-444. 13. Byers T: Diet and Cancer: Any progress in the interim? Cancer 1988; 62:1713-1724. 14. Willett W: The search for the causes of breast and colon cancer. Nature
1989; 338:389-393. 15. Trock B, Lanza E, Greenwald P: Dietary fiber, vegetables, and colon cancer: critical review and meta-analysis of the epidemiologic evidence. JNCI 1990; 82:650-661. 16. Manson JE, Stampfer JM, Hennekens CH, Willett WC: Body weight and longevity. JAMA 1987; 257:353-358. 17. Manson JE, Colditz GA, Stampfer MJ, Willett WC, Rosner B, Monson RR, Speizer FE, Hennekens CH: A prospective study of obesity and risk of coronary heart disease in women. N Engl J Med 1990; 322:882-889. 18. Maclure KM, Hayes KC, Colditz GA, Stampfer MJ, Speizer FE, Willett WC: Weight, diet and risk of symptomatic gallstones in middle-aged women. N Engl J Med 1989; 321:563-569.
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EDITORIALS 19. Colditz GA, Willett WC, Stampfer MJ, Manson JE, Hennekens CH, Arky RA, Speizer FE: Weight as a risk factor for clinical diabetes in women. Am J Epidemiol 1990; 132:501-513. 20. Law A, Terry RB, Barrett-Conner E: Behavioral covariates of waist-to-hip ratio in Rancho Bernardo. Am J Public Health 1990; 80:1358-1362. 21. Bouchard C, Tremblay A, Despres JP, et al: The response to long-term overfeeding in identical twins. N Engl J Med 1990; 322:1477-1482. 22. Micozzi MS: Nutrition, body size, and breast cancer. Yearbook Phys Anthropol 1985: 28:175-206. 23. Valaoras VG, MacMahon B, Trichopoulos D: Lactation and reproductive histories of breast cancer patients in greater Athens 1965-67. Int J Cancer 1969; 4:350-363. 24. Swanson CA, Jones DY, Schatzkin A, Brinton LA, Ziegler RG: Breast cancer risk assessed by anthropometry in the NHANES I Epidemiological Follow-up Study. Cancer Res 1988; 48:5363-5367. 25. Vatten U, Kvinnsland S: Body height and risk of breast cancer. A prospective study of 23,831 Norwegian women. Int J Cancer 1990; 45:440. 26. Prentice RL, Kakar F, Hursting S, Sheppard L, Klein R, Kushi LH: Aspects of the rationale for the Women's Health Trial. JNCI 1988; 80:802-819. 27. Editorial. Should we case-control? Lancet 1990; 1:1127-1128. 28. Willett WC, Stampfer MJ: Dietary fat and cancer: another view. Cancer Causes and Control 1990; 1:103.
29. Goodwin PJ, Boyd NF: Critical appraisal of the evidence that dietary fat is related to risk of breast cancer in humans. JNCI 1987; 79:473-485. 30. Basch CE, Shea S, Arliss R, Contento IR, Rips J, Gufin B, Iricoyen M, Zybert P: Validation of mothers' report of dietary intake by four-to-seven year old children. Am J Public Health 1990; 80:1314-1317. 31. Patterson BH, Block G, Rosenberger WF, Pee D, Kahle LL: Fruits and vegetables in the American diet: data from the NHANES II Survey. Am J Public Health 1990; 80:(December), in press. 32. Ellison RC, Goldberg RJ, Witschi JC, Caper AL, Puleo EM, Stars FJ: Use of fat-modified food products to change dietary fat intake of young people. Am J Public Health 1990; 80:1374-1376. 33. Gortmaker SL, Dietz WH, Cheung LWY: Inactivity, diet, and the fattening of America. J Am Dietet Assoc 1990; 90:1247-1255.
WALTER WILLETT, MD From the Departments of Epidemiology and Nutrition, Harvard School of Public Health, and the Channing Laboratory, the Department of Medicine, Harvard Medical School and Brigham & Women's Hospital. Address reprint requests to Walter Willett, MD, Channing Laboratory, 180 Longwood Avenue, Boston, MA 02115.
Future APHA Meeting Dates/Site 1991 NOVEMBER 10-14 ATLANTA, GEORGIA 1992 NOVEMBER 8-12 WASHINGTON, DC 1993 OCTOBER 24-28 SAN FRANCISCO, CALIFORNIA 1994 OCTOBER 30-NOVEMBER 3 WASHINGTON, DC
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AJPH November 1990, Vol. 80, No. 11
Public Editorials Health November 1990 Volume 80, Number 11
EDITOR Michel A. Ibrahim, MD, PhD EDITOR (RETIRED) Alfred Yankauer, MD, MPH ASSISTANT EDITOR Ernest Schoenfeld, DrPH Jane E. Sisk, PhD EDITORIAL BOARD Irene H. Butter, PhD (1990) Chair Doris Bloch, RN, DrPH (1992) Suzanne E. Dandoy, MD, MPH (190) Joy G. Dryfoos, MA (1992) Herschel S. Horowitz, DDS (992) Sherman A. James, PhD 991) Dieter Koch-Weser, PhD, MDl (1991) Robert L. Kane, MD (1991) Philip J. Landrigan, MI) (1990) Jean Pakter, MD, MPH (1992) Lee N. Robins, PhD (1991) Jeannette J. Simmons, DSc, MPH (1990) Fernando M. Trevino, PhD, MPH (1990) Julian A. Waller, MD (1992) Rita Zemach, PhD (1991) STAFF William H. McBeath, MD, MPH Executive DirectorlManaging Editor Jaclyn Alexander Publications Director Doyne Bailey Assistant Managing Editor Cheryl N. Jackson Production Manager Mary Beth Kammann Advertising Manager Marilyn Butler Publication Assistant CONTRIBUTING EDITORS George J. Annas, JD, MPH Public Health and the Law Carol Jenkins, MLS Book Corner Mary Grace Kovar, DrPH, MS New from NCHS Elizabeth Fee, PhD Robert R. Korstad, PhD Public Health Then and Now Hugh H. Tilson, MD, DrPH Notes from the Field
AJPH November 1990, Vol. 80, No. 11
Established 1911
Challenges for Public Health Nutrition in the 1990s A scientific approach to public health nutrition includes: collection of evidence regarding the relation of nutritional factors to health and disease; assessment of current dietary practices; development of strategies to modify diets in a manner deemed to be beneficial; and the evaluation of intervention strategies. This approach has been successful in eliminating several nutritional deficiencies that were once widespread. Despite these successes, nutritional factors remain as probable major determinants of the dominant health problems, particularly cardiovascular diseases and cancer, in the United States and other affluent countries. As we enter a new decade, a consideration of challenges facing those working to improve our nation's health through nutrition may be appropriate. The Scientific Evidence
Establishing the relation between nutrition and chronic diseases such as cancer and cardiovascular diseases has been more elusive than for deficiency-related diseases such as pellagra and rickets. Unlike specific vitamin deficiencies, the common chronic diseases almost always have multiple causes, including interactions with genetic factors. Also, chronic diseases often have long latent periods, perhaps resulting from many years of continuous exposure, and occur with relatively low frequency even though the cumulative lifetime risk is high. Thus, it is a formidable challenge to obtain a high level of proof that a particular nutritional factor is a cause of disease. Several large, official reviews during the last 10 yearsl-3 have examined the relationship of diet and nutrition to health and disease. This information cannot be considered in detail in an editorial; however, several general comments can be made regarding coronary heart disease and cancer. Coronary Heart Disease
Despite the prominence given to the relation between diet and coronary heart disease (CHD) during the last 40 years, direct evidence is disappointingly meager. Very few human studies, either case-control or cohort observational studies or intervention trials, have directly examined the relationships between dietary factors and cardiovascular disease. Almost all were seriously limited in size or by their method of dietary assessments.4 Only two consistent findings have emerged: * an inverse relation between energy intake and the risk of coronary heart disease (almost surely reflecting the protective effects of physical activity), and * a strong protective effect of moderate alcohol intake. Although the focus of dietary recommendations is usually a reduction in saturated fat intake, no relation between saturated fat intake and risk of CHD was observed in the most informative prospective study to date.5 Even if such a relationship exists, the widely quoted ecological association found by Keys6 was probably fortuitously confounded, because the magnitude of the relationship between saturated fat intake and CHD rates was considerably stronger than expected on the basis of metabolic studies of diet and blood lipids and, in turn, epidemiologic studies of serum lipids and CHD risk.5 The classical diet/heart hypothesis-that risk of CHD is increased by dietary cholesterol and saturated fat and reduced by polyunsaturated fat-probably contains some element of truth. However, the hypothesis is over-simplified in many respects 1 295
EDITORIALS
and needs continued refinement. For example, it has been known for decades, but largely ignored, that only some saturated fats increase serum cholesterol.78 Stearic acid (18:0) is the predominant saturated fatty acid formed in the hydrogenation of vegetable fat and appears to have no adverse effect on serum lipids; it will increasingly contribute to total saturated fat intake as processed vegetable fats replace animal fats in our diet. Thus, as pointed out by Grundy9 the use of the generic term "saturated fat" to describe diets may be outmoded, both in research, and in policy and consumer education. Furthermore, a variety of hypotheses have arisen that relate other factors to risk of CHD; these include low intakes of antioxidants, fiber, vitamins B-6 and folic acid, and omega-3 fatty acids.5 These all remain to be fully evaluated, but the possibility exists that they will be more important than dietary lipids. A large volume of literature has developed using blood lipids as a surrogate endpoint to predict the influence of diet on risk of CHD. Although much has been learned, this approach is not entirely satisfactory for two fundamental reasons. First, because of the heterogeneity of blood lipids it is difficult to interpret predictions based on either total serum cholesterol (the only lipid measured in many studies) or a specific subfraction. For example, a general lowering of fat intake without alternation of the fatty acid composition may lower total cholesterol intake slightly, but this reduction is largely due to a decrease in HDL-cholesterol. '0 As HDL-C is strongly protective for CHD, the effect of a general fat reduction on risk of CHD is unclear and could conceivably be deleterious, depending on the original composition of fat in the diet. Second, it is likely that diet influences CHD risk through other causal pathways in addition to blood lipids, such as by influencing the propensity for thrombus formation. For example, based on his observation of increasing platelet aggregability with P/S ratios greater than about 0.7, Renaud has hypothesized that a goal of 1.0 for P/S ratio may not be desirable. "I Lacking adequate information about the relationship of diet and disease, policy makers have used inductive reasoning to translate metabolic information to recommendations about food intake. For example, the consistent observation that polyunsaturated fat reduces total serum cholesterol has promoted the dramatic shift from butter and lard to margarine and vegetable shortening in this country. However, persons who consume margarine instead of butter have not been shown to have a lower risk of CHD. Trans isomers of fatty acids formed in the processing of liquid vegetable oils, comprising up to 35 percent of some margarines, have recently been found to affect blood lipids adversely.'2 Thus, it is unclear whether those who switched from butter to margarine have increased, decreased, or not influenced their risk of CHD. Because foods are highly complex products that may affect the occurrence of CHD through multiple mechanisms, better empirical data relating foods and nutrients directly to risk of CHD and other major diseases are needed to develop scientifically based nutritional recommendations for the public. Diet and Cancer For the last decade, public policy reports have focused on fat as the most important dietary cause of cancer in the US; benefits from fat reduction have been anticipated for cancers of the breast, colon, and prostrate.'12 Particular
concerns have been raised regarding the possibility that polyunsaturated fat intake may increase risk of breast cancer. However, as described by Byers,'3 recently accrued data 1 296
have rendered these relations less rather than more clear, especially for breast cancer. In contrast, data have continued to accumulate that increased intake of fruits and vegetables is associated with lower risk of several cancers, most notably colon, lung, and stomach.3'4,'5 More information is needed, however, about the specific foods responsible for these benefits and whether they result from intake of fiber, betacarotene, or some other factors. Largely based on the reported inverse associations between intake of fruits and vegetables, the consumption of whole-grain breakfast cereals has been heavily promoted, even though there is at present limited evidence that cereal fiber influences the risk of colon cancer. Health Effects of Energy Balance
Although attention has focused on dietary composition, energy balance is clearly important in relation to cardiovascular disease, diabetes, several types of cancer, and total mortality. Even persons of average weight for their height in the US appear to be at increased risk for several important conditions compared with those weighing less than average.'6-'9 The health effects of weight loss are less clear and deserve further attention. Growing evidence suggests that fat distribution is an independent determinant of hypertension, diabetes, and cardiovascular disease; thus the findings by Laws, et al, in this issue,20 that behavioral factors are correlated with the waist-to-hip circumference ratio, are of interest. Additional data on body fat distribution and its determinants are likely to improve both the prediction of individual risk of disease and our understanding of the pathogenesis of several diseases. However, this knowledge may be of limited importance in disease prevention because body fat distribution appears to be more strongly determined by genetic factors than is overall obesity;2' the accumulation of abdominal fat (represented by a high waist-to-hip circumference ratio) is probably best avoided by preventing overall
obesity.
Prevention of obesity is a soundly supported nutritional objective; however, accumulating data regarding energy balance before adulthood raise complex issues. In both international studies22 and studies within countries,23-25 greater height (which reflects in part pre-adult energy balance) appears to be a risk factor for several cancers, particularly of the breast. These findings are consistent with the powerful cancer-inhibiting effect of energy restriction seen in animal studies. Translating this information into practice is clearly premature. However, those involved in childhood nutrition will need to weigh more seriously the hazards and benefits of promoting maximal growth rates and attained height, and consider whether any possibility exists for raising smaller rather than larger children, because the prospect of preventing a large proportion of breast cancer by other behavioral means appears bleak. Data Development
The need for better empirical data on the relation of nutritional factors and the incidence of cancer and heart disease has fueled controversy over the most fruitful methods of study. International correlations, case-control, cohort, randomized trials, and animal experiments all have strengths and limitations.26-29 It is likely that no specific combination of study design will be uniformly optimal for addressing all hypotheses; therefore, all approaches merit continued evaluation and refinement. A new generation of large prospective dietary studies started in the 1980s have enrolled over half a million persons collectively and will substantially increase knowledge during AJPH November 1990, Vol. 80, No. 11
EDITORIALS
the l990s.5 The increased use ofintermediate endpoints, such as adenomatous colon polyps and non-invasive measurements of atherosclerosis, may increase the efficiency of investigations, although the relation of these surrogates to clinical disease may be complex. Assessment of Dietary Practices and Development of Intervention Strategies Despite many uncertainties and the need for improved data on diet and disease, public health action is appropriate in several areas. Reasonable priorities include the prevention of obesity, a reduction of dietary cholesterol and animal fat (although the best choice of replacement energy sources is uncertain), and an increase in consumption of fruits and vegetables (although the specific types and amounts to be encouraged are less clear). Work such as that reported in this issue by Basch, et al,30 indicating encouraging progress on the assessment of diet in childhood, and by Patterson, et al,31 demonstrating that intakes of fruits and vegetables are considerably lower than recommended, are important elements in the development of a rational nutrition intervention. Further work identifying population subgroups with high intakes of animal fat and low consumption of fruits and vegetables should provide targets for education and nutritional assistance programs. Dietary intervention strategies may involve both public and private institutions as well as individuals. A combination of these should be most effective, however, because individuals can exert pressure on institutions and institutions can expand the options of individuals. For example, the feasibility study by Ellison, et al,32 in this issue provides encouraging evidence that major changes in the diets of boarding students can be made in a nonintrusive manner. Other notable insti-
tutional changes that immediately alter the diets of millions have been recent decisions by some of the fast food providers to fry their fish, chicken, and (soon) their potatoes in vegetable rather than animal fat. The fast food industry still has far to go in providing an attractive array of healthy alternatives, such as vegetarian middle-eastern, Indian, and Oriental foods, to their predominant products. A challenge to the nutrition community is to help make this a viable direction. As the scientific basis for a reduction in total fat is weak, and the concept of generic "saturated fat" is increasingly outmoded, nutrition educators and those involved in food labeling are challenged to provide clear and scientifically sound messages for the public. Just as messages based on the four food groups were effective in eliminating specific nutritional deficiencies in this country, approaches based on foods and dietary patterns rather than RDAs (recommended daily allowance), percentage of calories from fat, or grams of fiber per day may be the most effective method of communication to the public. Messages will need to include suggested limits for some foods as well as positive recommendations for others. Moreover, messages need to take into consideration the social and cultural aspect of food and health, because knowledge by itself may not necessarily translate into action. Whatever the strategies, they should be rigorously evaluated for effectiveness in producing changes in diet. Although the objective of preventing obesity is clear, the means of achieving it are not. The refractory nature of this problem can be appreciated by noting that the high prevalence of obesity has not decreased in this country despite obesity being a conspicuous and highly stigmatized risk AJPH November 1990, Vol. 80, No. 11
factor. Large sums are spent on treatments, but their longterm effectiveness is disappointing. Although obesity is a heterogeneous syndrome caused by multiple factors, sedentary life-style is probably the most important reason for its high prevalence in our society.33 A major impact on this problem will probably require a fundamental restructuring of society, necessitating a broad interdisciplinary approach. For example, our cities and towns will need to be modified so that it is once again safe, convenient, and pleasant to walk or ride a bicycle to work or school, and to go shopping. This task may be beyond our perceived responsibilities; but, by default, leadership in this effort must be assumed by those interested in public health. State and local public health workers may be particularly effective in this effort as they are close to relevant decision-making processes. In summary, new data gathered from the large studies started in the previous decade should provide substantial refinements in our knowledge about diet and health. Translating these findings into effective intervention strategies will require creativity and rigorous evaluation. The US public is clearly willing to make substantial changes in diet, as demonstrated by the large decreases in egg and red meat consumption and the substitutions of vegetable fat for animal fat that have already been accomplished. For these reasons, we should be optimistic that continued enhancement of dietary practices can substantially improve health in the US. REFERENCES 1. Committee on Diet, Nutrition, and Cancer, National Research Council: Diet, Nutrition, and Cancer. Washington, DC: National Academy Press, 1982. 2. The Surgeon General: The Surgeon General's Report on Nutrition and Health. DHHS (PHS) Pub No. 88-50210, Washington, DC: Govt Printing Office, 1988. 3. NAS/NRC Committee on Diet and Health: Diet and Health: Implications for reducing chronic disease risk. Washington, DC: National Academy Press, 1989. 4. Willett W: Nutritional Epidemiology. New York: Oxford University Press, 1990. 5. Shekelle RB, Shryock AM, Paul O: Diet, serum cholesterol and death from coronary heart disease. The Western Electric Study. N Engl J Med 1981; 304:65-70. 6. Keys A: Seven Countries: A multivariate analysis of death and coronary heart disease. Cambridge: Harvard University Press. 1980; 252. 7. Hegsted DM, McGandy RB, Myers ML, Stare FJ: Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr 1%5; 17:281-295. 8. Bonanome A, Grundy SM: Effect of dietary stearic acid on plasma cholesterol and lipoprotein levels. N Engi J Med 1986; 318:1244-1248. 9. Grundy SM: Trans monounsaturated fatty acids and serum cholesterol levels (editorial). N Engl J Med 1990; 323:480-481. 10. Lee-Han H, Cousins M, Beaton M, McGuire V, Krukov V, Chipman M, Boyd N: Compliance in a randomized clinical trial of dietary fat reduction in patients with breast dysplasia. Am J Clin Nutr 1988; 48:575-586. 11. Renaud S, Godsey F, Dumont E, Thevenon C, Ortchanian E, Martin JL: Influence of long-term diet modification on platelet function and composition in Moselle farmers. Am J Clin Nutr 1986; 43:136-150. 12. Meusink RP, Katan MB: Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects. N Engl J Med 1990; 323:439-444. 13. Byers T: Diet and Cancer: Any progress in the interim? Cancer 1988; 62:1713-1724. 14. Willett W: The search for the causes of breast and colon cancer. Nature
1989; 338:389-393. 15. Trock B, Lanza E, Greenwald P: Dietary fiber, vegetables, and colon cancer: critical review and meta-analysis of the epidemiologic evidence. JNCI 1990; 82:650-661. 16. Manson JE, Stampfer JM, Hennekens CH, Willett WC: Body weight and longevity. JAMA 1987; 257:353-358. 17. Manson JE, Colditz GA, Stampfer MJ, Willett WC, Rosner B, Monson RR, Speizer FE, Hennekens CH: A prospective study of obesity and risk of coronary heart disease in women. N Engl J Med 1990; 322:882-889. 18. Maclure KM, Hayes KC, Colditz GA, Stampfer MJ, Speizer FE, Willett WC: Weight, diet and risk of symptomatic gallstones in middle-aged women. N Engl J Med 1989; 321:563-569.
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EDITORIALS 19. Colditz GA, Willett WC, Stampfer MJ, Manson JE, Hennekens CH, Arky RA, Speizer FE: Weight as a risk factor for clinical diabetes in women. Am J Epidemiol 1990; 132:501-513. 20. Law A, Terry RB, Barrett-Conner E: Behavioral covariates of waist-to-hip ratio in Rancho Bernardo. Am J Public Health 1990; 80:1358-1362. 21. Bouchard C, Tremblay A, Despres JP, et al: The response to long-term overfeeding in identical twins. N Engl J Med 1990; 322:1477-1482. 22. Micozzi MS: Nutrition, body size, and breast cancer. Yearbook Phys Anthropol 1985: 28:175-206. 23. Valaoras VG, MacMahon B, Trichopoulos D: Lactation and reproductive histories of breast cancer patients in greater Athens 1965-67. Int J Cancer 1969; 4:350-363. 24. Swanson CA, Jones DY, Schatzkin A, Brinton LA, Ziegler RG: Breast cancer risk assessed by anthropometry in the NHANES I Epidemiological Follow-up Study. Cancer Res 1988; 48:5363-5367. 25. Vatten U, Kvinnsland S: Body height and risk of breast cancer. A prospective study of 23,831 Norwegian women. Int J Cancer 1990; 45:440. 26. Prentice RL, Kakar F, Hursting S, Sheppard L, Klein R, Kushi LH: Aspects of the rationale for the Women's Health Trial. JNCI 1988; 80:802-819. 27. Editorial. Should we case-control? Lancet 1990; 1:1127-1128. 28. Willett WC, Stampfer MJ: Dietary fat and cancer: another view. Cancer Causes and Control 1990; 1:103.
29. Goodwin PJ, Boyd NF: Critical appraisal of the evidence that dietary fat is related to risk of breast cancer in humans. JNCI 1987; 79:473-485. 30. Basch CE, Shea S, Arliss R, Contento IR, Rips J, Gufin B, Iricoyen M, Zybert P: Validation of mothers' report of dietary intake by four-to-seven year old children. Am J Public Health 1990; 80:1314-1317. 31. Patterson BH, Block G, Rosenberger WF, Pee D, Kahle LL: Fruits and vegetables in the American diet: data from the NHANES II Survey. Am J Public Health 1990; 80:(December), in press. 32. Ellison RC, Goldberg RJ, Witschi JC, Caper AL, Puleo EM, Stars FJ: Use of fat-modified food products to change dietary fat intake of young people. Am J Public Health 1990; 80:1374-1376. 33. Gortmaker SL, Dietz WH, Cheung LWY: Inactivity, diet, and the fattening of America. J Am Dietet Assoc 1990; 90:1247-1255.
WALTER WILLETT, MD From the Departments of Epidemiology and Nutrition, Harvard School of Public Health, and the Channing Laboratory, the Department of Medicine, Harvard Medical School and Brigham & Women's Hospital. Address reprint requests to Walter Willett, MD, Channing Laboratory, 180 Longwood Avenue, Boston, MA 02115.
Future APHA Meeting Dates/Site 1991 NOVEMBER 10-14 ATLANTA, GEORGIA 1992 NOVEMBER 8-12 WASHINGTON, DC 1993 OCTOBER 24-28 SAN FRANCISCO, CALIFORNIA 1994 OCTOBER 30-NOVEMBER 3 WASHINGTON, DC
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