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Executive Summary

The twentieth century has witnessed noticeable shifts in the direction of nutrition programs, policy, and research in industrialized nations—from identification and prevention of nutrient deficiency diseases in the first three decades of the century to refinement and application of knowledge of nutrient requirements in the subsequent two decades. In the second half of the century, emphasis on nutrient deficiency diseases decreased as the major causes of mortality shifted from infectious to chronic diseases. Attention then turned to investigating the role of diet in the maintenance of health and the reduction of the risk of such chronic diseases as heart disease and cancer. Subsequently, epidemiologic, clinical, and laboratory research demonstrated that diet is one of the many important factors involved in the etiology of these diseases. During the past few decades, scientists have been faced with the challenge of identifying dietary factors that influence specific diseases and defining their pathophysiological mechanisms. Simultaneously, public health policymakers, the food industry, consumer groups, and others have been debating how much and what kind of evidence justifies giving dietary advice to the public and how best to mitigate risk factors on which there is general agreement among scientists.

Purpose, Approach, and Scope of the Study

This study on diet, chronic diseases, and health was launched in an effort to address the scientific issues that are fundamental to nutrition policy on reducing the risk of these diseases. The Committee on Diet and Health was appointed to conduct the study within the Food and Nutrition Board of the National Research Council's Commission on Life Sciences. The committee began with the understanding that lack of consensus on the role of diet in the etiology of chronic diseases derived partly from incomplete knowledge and partly from the absence of generally accepted criteria for interpreting the evidence. It also noted that the totality of the evidence relating dietary components to the entire spectrum of major chronic diseases had yet to be examined systematically. Several reports issued to date have addressed many issues of public health importance. However, most have not been sufficiently comprehensive and have not crossed the boundary separating the simple assessment of dietary risk factors for single chronic diseases from the complex task of determining how  these risk factors influence the entire spectrum of chronic diseases—atherosclerotic cardiovascular diseases, cancer, diabetes, obesity, osteoporosis, dental caries, and chronic liver and kidney diseases.



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Page 3 1— Executive Summary The twentieth century has witnessed noticeable shifts in the direction of nutrition programs, policy, and research in industrialized nations—from identification and prevention of nutrient deficiency diseases in the first three decades of the century to refinement and application of knowledge of nutrient requirements in the subsequent two decades. In the second half of the century, emphasis on nutrient deficiency diseases decreased as the major causes of mortality shifted from infectious to chronic diseases. Attention then turned to investigating the role of diet in the maintenance of health and the reduction of the risk of such chronic diseases as heart disease and cancer. Subsequently, epidemiologic, clinical, and laboratory research demonstrated that diet is one of the many important factors involved in the etiology of these diseases. During the past few decades, scientists have been faced with the challenge of identifying dietary factors that influence specific diseases and defining their pathophysiological mechanisms. Simultaneously, public health policymakers, the food industry, consumer groups, and others have been debating how much and what kind of evidence justifies giving dietary advice to the public and how best to mitigate risk factors on which there is general agreement among scientists. Purpose, Approach, and Scope of the Study This study on diet, chronic diseases, and health was launched in an effort to address the scientific issues that are fundamental to nutrition policy on reducing the risk of these diseases. The Committee on Diet and Health was appointed to conduct the study within the Food and Nutrition Board of the National Research Council's Commission on Life Sciences. The committee began with the understanding that lack of consensus on the role of diet in the etiology of chronic diseases derived partly from incomplete knowledge and partly from the absence of generally accepted criteria for interpreting the evidence. It also noted that the totality of the evidence relating dietary components to the entire spectrum of major chronic diseases had yet to be examined systematically. Several reports issued to date have addressed many issues of public health importance. However, most have not been sufficiently comprehensive and have not crossed the boundary separating the simple assessment of dietary risk factors for single chronic diseases from the complex task of determining how  these risk factors influence the entire spectrum of chronic diseases—atherosclerotic cardiovascular diseases, cancer, diabetes, obesity, osteoporosis, dental caries, and chronic liver and kidney diseases.

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Page 4 This report attempts to cross that boundary. It complements the recent Surgeon General's Report on Nutrition and Health and other efforts of government agencies and voluntary health and scientific organizations by providing an in-depth analysis of the overall relationship between diet and the full spectrum of major chronic diseases. In this report, the committee reviews the evidence regarding all major chronic public health conditions that diet is believed to influence. It draws conclusions about the effects of nutrients, foods, and dietary patterns on health, proposes dietary recommendations that have the potential for diminishing risk, and estimates their public health impact. The committee focuses on risk reduction rather than on management of clinically manifest disease. It recognizes, however, that the distinction between prevention or risk reduction and treatment may be blurred in conditions where dietary modification might delay the onset of clinical diseases (e.g., the cardiovascular complications in diabetes mellitus) or might slow the progression of impaired function; therefore, conditions such as these are addressed, but only briefly. The committee defined risk reduction broadly to include decreased morbidity as well as mortality from chronic diseases and believes that consideration should be given to dietary modification to reduce the risk for both. The difficulty of quantifying the role of diet in the etiology of chronic diseases and the potential public health impact of dietary modification are discussed in Chapters 2 and 28. In Chapter 2, the committee presents criteria for assessing the data from single studies and explains its procedure for evaluating the overall evidence. Special attention is given to the role of nutrient interactions and to the assessment of benefits and risks in arriving at conclusions and formulating dietary recommendations. Throughout the report, the committee recognizes that genetically dependent variability among individuals, and variability due to age, sex, and physiological status, may all affect physiological requirements for nutrients, responses to dietary exposures, the risk of chronic diseases, and consequently the effectiveness of dietary recommendations in reducing the risk of chronic diseases. The report addresses in detail the risks that apply to the general population and comments on the feasibility of defining risks for subpopulations and individuals with different susceptibilities. Finally, the committee discusses the limitations of data on diet-disease relationships, emphasizes the necessarily interim nature of its conclusions and recommendations, and proposes directions for research. Criteria for Assessment The strengths and weaknesses of different kinds of clinical, epidemiologic, and laboratory studies and the methodologies for dietary assessment are reviewed in Chapter 2. To the extent possible, the committee evaluated data from studies in humans as well as in animals. It noted that ecological correlations of dietary factors and chronic diseases among human populations provide valuable data but cannot be used alone to estimate the strength of the association between diet and diseases. The effect of diet on chronic diseases has been most consistently demonstrated in comparisons of populations with substantially different dietary practices, possibly because it is more difficult to identify such associations within a population whose diet is fairly homogeneous. Thus in general, associations within populations based on case-control and prospective cohort studies underestimate the association. In intervention studies, long exposure is usually required for the effect of diet on chronic disease risk to be manifested. Furthermore, the strict criteria for selecting participants in such studies may result in more homogeneous study samples, which limit the applicability of results to the general population. Despite the limitations of various types of studies in humans, the committee concluded that repeated and consistent findings of an association between certain dietary factors and diseases are likely to be real and indicative of a cause-and-effect relationship. Experiments on dietary exposure of different animal strains can take genetic variability into account and permit more intensive observation. However, extrapolation of data from animal studies to humans is limited by the ability of animal models to simulate human diseases and the comparability of absorption and metabolic phenomena among species. The committee placed more confidence in data derived from studies on more than one animal species or test system, on results that have been reproduced in different laboratories, and on data that indicate a dose-response relationship. The committee concluded that assessments of the strength of associations between diet and chronic diseases cannot simply be governed by criteria commonly used for inferring causality in other areas of human health. Faced with the special characteristics of studies on nutrients, dietary patterns, and chronic diseases, the commit-

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Page 5 tee first assessed the strengths and weaknesses of each kind of study and then evaluated the total evidence against six criteria: strength of association, dose-response relationship, temporally correct association, consistency of association, specificity of association, and biologic plausibility. Finally, it assessed the overall strength of the evidence on a continuum from highly likely to very inconclusive. Overall, the strength, consistency, and preponderance of data and the degree of concordance in epidemiologic, clinical, and laboratory evidence determined the strength of the conclusions in this report. Integration of the Overall Evidence In Section II of this report, Evidence on Dietary Components and Chronic Diseases (Chapters 6 through 18), the committee uses the approach described briefly above and more fully in Chapter 2. Throughout this section, the committee considers the epidemiologic, clinical, and experimental data pertaining to each nutrient or dietary factor and specific chronic diseases, including cardiovascular diseases, specific cancers, diabetes, hypertension, obesity, osteoporosis, hepatobiliary disease, and dental caries. Nutrient interactions and mechanisms of action are discussed where applicable. In Section III, Impact of Dietary Patterns on Chronic Diseases, the evidence relating nutrients to specific chronic diseases and diet-related conditions is briefly reassembled and leads to the committee's conclusions on the role of dietary patterns in the etiology of the diseases and assessment of the potential for reducing their frequency and severity. These conclusions are drawn directly from the research data, where the evidence pertains to dietary patterns or foods and food groups, or from  extrapolations from  the evidence on individual nutrients. In its overall review and integration of the evidence, the committee moved from a consideration of individual nutrients to foods, to food groups, and then to dietary patterns as they relate to the spectrum of chronic diseases. Criteria and Process for Formulating Dietary Recommendations Absolute proof is difficult to obtain in any branch of science. As evidence accumulates, however, it often reaches the point of proof in an operational sense, even though proof in an absolute sense may be lacking. In law, proof beyond a reasonable doubt is generally accepted as a standard for making decisions and taking action. The degree of evidence as well as the severity of the crime are the bases for the relative intrusiveness of legal actions taken, e.g., issuing a warning for a misdemeanor compared to the imposition of severe penalties for a felony. A similar paradigm can be applied to evidence on dietary patterns and associated health risks. For example, public education might be sufficient to warn against the potential hazard of excess caffeine intake, whereas evidence on the toxicity and carcinogenicity of aflatoxin warrants government regulation to curtail aflatoxin contamination of grains and milk. The strength of the evidence might not be the only relevant criterion for determining the course of action; other factors include the likelihood and severity of an adverse effect, potential benefits of avoiding the hazard, and the feasibility of reducing exposure. Much remains to be learned about the impact of diet on chronic disease risk. Nonetheless, in accordance with this paradigm, the committee concluded that the overall evidence regarding a relationship between certain dietary patterns (e.g., a diet high in total fat and saturated fat) and chronic diseases (e.g., cardiovascular diseases and certain cancers) supports (1) a comprehensive effort to inform the public about the likelihood of certain risks and the possible benefits of dietary modification and (2) the use of technological and other means (e.g., production of leaner animal products) to facilitate dietary change. Assessing Risks and Benefits The committee hopes to contribute to knowledge about the process of arriving at dietary recommendations by documenting the considerations and the logic that underlie its dietary recommendations. An essential step in developing dietary recommendations for overall health maintenance is the synthesis of recommendations pertaining to single diseases into a single coherent set of recommendations to reduce the overall risk of diet-related chronic diseases. For example, recommendations to enhance calcium intake for possible protection against osteoporosis might, in isolation, be viewed as conflicting with recommendations for coronary  heart disease, because dairy products—which contribute the most calcium to the U.S. diet—are also rich sources of saturated fats, which increase coronary heart disease risk. Thus,

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Page 6 recommendations for maintaining adequate bone mass as well as for preventing coronary disease would logically stress consumption of low-fat dairy products. The committee also considered the synergistic and antagonistic effects of dietary interactions. For example, the potential benefits of encouraging adequate trace element intake for reducing the risk of certain cancers could in principle be offset by a recommendation to increase vegetable intake for the possible prevention of colon cancer, because high plant food diets are also high in fiber, which could initially inhibit absorption of certain trace elements. To a large extent, the task of assessing such potential competing risks and benefits and nutrient interactions was simplified by an inherent consistency in dietary recommendations to maintain good health. For example, the advisability of consuming a diet low in saturated fatty acids, total fat, and cholesterol is supported by strong evidence of potential benefit in reducing the risk of cardiovascular diseases as well as comparatively weaker evidence that low-fat diets decrease the risk of certain kinds of cancers. Other Considerations The committee also considered whether to base recommendations on individual nutrients, on single foods or food groups, or on overall pattern of dietary intake. Although recommendations based on nutrients or food groups are of value, in the committee's experience guidelines directed toward overall dietary patterns are the most useful because they address the total diet and are more easily interpreted by the general public. Moreover, because many studies on diet and chronic diseases in humans have focused on foods rather than on single nutrients, food-based recommendations may more accurately reflect current understanding about the relationship between chronic diseases and diet. Nonetheless, many of the diet-disease relationships examined required consideration of single foods, food groups, and specific nutrients. This is reflected in the committee's recommendations. The committee agreed that quantitative guidelines should be proposed when warranted by the strength of the evidence and the potential importance of recommendations to public health. Such guidelines can take into account nutrient interactions, they are less susceptible to misinterpretation when translated into food choices, and they provide specific targets that can serve as a basis for nutrition programs and policy. The committee has attempted to explain the degree of certainty warranted by the evidence and to make quantitative recommendations to the extent justified. Recommendations for Individuals as Opposed to Populations There are two complementary approaches to reducing risk factors in the target population. The first, the public health or population-based approach, is aimed at the general population, and the second, the high-risk or individual-based approach, is aimed at individuals with defined risk profiles. Most chronic diseases etiologically associated with nutritional factors (e.g., atherosclerotic cardiovascular diseases, hypertension, obesity, many cancers, osteoporosis, and diabetes mellitus) also have genetic determinants, and genetic-environmental interactions play an important role in determining disease outcome. For most diseases, however, it is not yet possible to identify susceptible genotypes and thus risks to specific individuals. Furthermore, the variability in nutrient requirements among individuals is not well defined. Therefore, it is usually not possible to make recommendations for individuals. On the other hand, because the major chronic disease burden falls on the general population (approximately 70% of all deaths in the U.S. population are due to cardiovascular diseases and cancer), the most benefit is likely to be achieved by a public-health prevention strategy to shift the distribution of dietary risk factors by means of dietary recommendations to reduce chronic disease risk in the general population. The public health approach to prevention recognizes that even though reduction of risk for individuals with average risk profiles (e.g., an average serum cholesterol level) might be small or negligible, because these people represent the great majority of the population, the benefit for the total population is likely to be paradoxically large (e.g., because most coronary deaths occur among those who have only moderate elevations in serum cholesterol levels). However, when it is possible to identify high-risk persons, such as those with certain hyperlipidemias, special attention can be directed to their management. Therefore, in the committee's judgment, an effective prevention strategy should be aimed at the general public and, where knowledge permits, it should be complemented with recommendations for those at high risk.

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Page 7 Major Conclusions and their Bases The committee analyzed trends in the major chronic diseases as well as in eating patterns (Chapters 3 and 5). It reviewed the epidemiologic, clinical, and laboratory evidence pertaining to dietary factors and chronic diseases (Chapters 6 through 26) and attempted to put into perspective the role of diet as it relates to other environmental and genetic factors in the etiology of these diseases (Chapters 4 and 5). Following are the general conclusions drawn from the committee's in-depth review, as well as the specific conclusions pertaining to the major dietary components and specific chronic diseases. General Conclusions · A comprehensive review of the epidemiologic, clinical, and laboratory evidence indicates that diet influences the risk of several major chronic diseases. The evidence is very strong for atherosclerotic cardiovascular diseases and hypertension and is highly suggestive for certain forms of cancer (especially cancers of the esophagus, stomach, large bowel, breast, lung, and prostate). Furthermore, certain dietary patterns predispose to dental caries and chronic liver disease, and a positive energy balance produces obesity and increases the risk of noninsulin-dependent diabetes mellitus. However, the evidence is not sufficient for drawing conclusions about the influence of dietary patterns on osteoporosis and chronic renal disease. · Most chronic diseases in which nutritional factors play a role also have genetic and other environmental determinants, but not all the environmental risk factors have been clearly characterized and susceptible genotypes usually have not been identified. Furthermore, the mechanisms of genetic and environmental interactions involved in disease are not fully understood. It is evident that dietary patterns are important factors in the etiology of several major chronic diseases and that dietary modifications can reduce such risks. Nevertheless, for most diseases, it is not yet possible to provide quantitative estimates of the overall risks and benefits. Fats, Other Lipids, and High-Fat Diets The following conclusions derive from the committee's extensive review of the data described in Chapters 6 (Calories), 7 (Fats and Other Lipids), 19 (Atherosclerotic Cardiovascular Diseases), 21 (Obesity and Eating Disorders), 22 (Cancer), and 25 (Hepatobiliary Disease). General Conclusion · There is clear evidence that the total amounts and types of fats and other lipids in the diet influence the risk of atherosclerotic cardiovascular diseases and, to a less well-established extent, certain forms of cancer and possibly obesity. The evidence that the intake of saturated fatty acids and cholesterol are causally related to atherosclerotic cardiovascular diseases is especially strong and convincing. Total Fats · In several types of epidemiologic studies, a high-fat intake is associated with increased risk of certain cancers, especially cancers of the colon, prostate, and breast. The epidemiologic evidence is not totally consistent, but it is supported by experiments in animals. The combined epidemiologic and laboratory evidence suggests that a reduction of total fat intake is likely to decrease the risk of these cancers. · High-fat intake is associated with the development of obesity in animals and possibly in humans. In short-term clinical studies, a marked reduction in the percentage of calories derived from dietary fat has been associated with weight loss. · Although gallbladder disease is associated with obesity, there is no conclusive evidence that it is associated with fat intake. · Intake of total fat per se, independent of the relative content of the different types of fatty acids, is not associated with high blood cholesterol levels and coronary heart disease. A reduction in total fat consumption, however, facilitates reduction of saturated fatty acid intake; hence, in addition to reducing the risk of certain cancers, and possibly obesity, it is a rational part of a program aimed at reducing the risk of coronary heart disease. Saturated Fatty Acids · Clinical, animal, and epidemiologic studies demonstrate that increased intakes of saturated fatty acids (12 to 16 carbon atoms in length) increase the levels of serum total and low-density-lipoprotein (LDL) cholesterol and  that these higher levels in turn lead to atherosclerosis and increase the risk of coronary heart disease. Satu-

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Page 8 rated fatty acid intake is the major dietary determinant of the serum  total cholesterol and LDL cholesterol levels in populations and thereby of coronary heart disease risk in populations. Lowering saturated fatty acid intake is likely to reduce serum total and LDL cholesterol levels and, consequently, coronary heart disease risk. · The few epidemiologic studies on dietary fat and cancer that have distinguished between the effects of specific types of fat indicate that higher intakes of saturated fat as well as total fats are associated with a higher incidence of and mortality from cancers of the colon, prostate, and breast. In general, these findings are supported by data from animal experiments. Polyunsaturated Fatty Acids · Clinical and animal studies provide firm evidence that omega-6 polyunsaturated fatty acids when substituted for saturated fatty acids result in a lowering of serum total cholesterol and LDL cholesterol and usually also some lowering of high-density-lipoprotein (HDL) cholesterol levels. · Laboratory studies in rodents suggest that diets with high levels of vegetable oils containing omega-6 polyunsaturated fatty acids promote certain cancers more effectively than diets with high levels of saturated fats, whereas there is some evidence that diets with a high content of omega-3 polyunsaturated fatty acids may inhibit these same cancers. However, these findings are not supported by the limited number of epidemiologic studies that have distinguished between the effects of different types of fat. There are no human diets that naturally have very high levels of total polyunsaturated fatty acids, and there is no information about the long-term consequences of high polyunsaturated fatty acid intakes. · Fish oils containing large amounts of omega-3 polyunsaturated fatty acids reduce plasma triglyceride levels and increase blood clotting time. Their effects on LDL cholesterol vary, and data on the long-term health effects of large doses of omega-3 polyunsaturated fatty acids are limited. Limited epidemiologic data suggest that consumption of one or two servings of fish per week is associated with a lower coronary heart disease risk, but the evidence is not sufficient to ascertain whether the association is causal or related to the omega-3 polyunsaturated fatty acid content of fish. Monounsaturated Fatty Acids · Clinical studies indicate that substitution of monounsaturated for saturated fatty acids results in a reduction of serum total cholesterol and LDL cholesterol without a reduction in HDL cholesterol. Dietary Cholesterol · Clinical, animal, and epidemiologic studies indicate that dietary cholesterol raises serum total cholesterol and LDL cholesterol levels and increases the risk of atherosclerosis and coronary heart disease. There is substantial inter- and intra-individual variability in this response. High dietary cholesterol clearly seems to contribute to the development of atherosclerosis and increased coronary heart disease risk in the population. Trans Fatty Acids · Clinical studies indicate that trans fatty acids and their cis isomers have similar effects on plasma lipids. Animal studies do not indicate that trans fatty acids have a greater tumor-promoting effect than their cis isomers. Carbohydrates, Vegetables, Fruits, Grains, Legumes, and Cereals and Their Constituents The committee's conclusions on carbohydrates and foods containing complex carbohydrates—i.e., vegetables, fruits, grains, legumes, and cereal products—derive from a review of direct and indirect evidence throughout the report, especially in Chapters 9 (Carbohydrates), 10 (Dietary Fiber), 11 (Fat-Soluble Vitamins), 12 (Water-Soluble Vitamins), and 22 (Cancer). · Diets high in plant foods—i.e., fruits, vegetables, legumes, and whole-grain cereals—are associated with a lower occurrence of coronary heart disease and cancers of the lung, colon, esophagus, and stomach. Although the mechanisms underlying these effects are not fully understood, the inverse association with coronary heart disease may be largely explained by the usually low saturated fatty acid and cholesterol content of such diets. Such diets are also low in total fat, which is directly associated with the risk of certain cancers, but rich in complex carbohydrates (starches and fiber) and certain vitamins, minerals, trace elements, and nonnutritive constituents, and these factors probably also confer protection against certain cancers and coronary heart disease. · Compared to nonvegetarians, complete vegetarians and lacto-ovovegetarians have lower serum levels of total and LDL cholesterol and triglycerides. These lower levels may be the combined

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Page 9 result of lower intakes of saturated fatty acids and total fat and higher intakes of water-soluble fiber (e.g., pectin and oat bran). In clinical and animal studies, such fiber has been found to produce small reductions in serum  total cholesterol independently of the effect due to fat reduction. · Populations consuming high-carbohydrate diets, which are high in plant foods, have a comparatively lower prevalence of noninsulin-dependent diabetes mellitus, possibly because of the higher proportion of complex carbohydrate intake and lower prevalence of obesity—a risk factor for noninsulin-dependent diabetes mellitus. In clinical studies, such diets have been shown to improve glucose tolerance and insulin sensitivity. · Epidemiologic studies indicate that consumption of carotenoid-rich foods, and possibly serum carotene concentration, are inversely associated with the risk of lung cancer. · Laboratory studies in animals strongly and consistently indicate that certain retinoids prevent, suppress, or retard the growth of chemically induced cancers at a number of sites, including the esophagus, pancreas, and colon, but especially the skin, breast, and bladder. However, most epidemiologic studies do not show an association between preformed vitamin A and cancer risk or a relationship between plasma retinol level and cancer risk. · Epidemiologic studies suggest that vitamin C-containing foods such as citrus fruits and vegetables may offer protection against stomach cancer, and animal experiments indicate that vitamin C itself can protect against nitrosamine-induced stomach cancer. The evidence linking vitamin C or foods containing that vitamin to other cancer sites is more limited and less consistent. · Some investigators have postulated that several other vitamins (notably vitamin E, folic acid, riboflavin, and vitamin B12) may block the initiation or promotion of cancer, but the committee judged the evidence too limited to draw any conclusions. · Epidemiologic and clinical studies indicate that a diet characterized by high-fiber foods may be associated with a lower risk of coronary heart disease, colon cancer, diabetes mellitus, diverticulosis, hypertension, or gallstone formation, but there is no conclusive evidence that it is dietary fiber, rather than the other components of vegetables, fruits, and cereal products, that reduces the risk of those diseases. Although soluble fibers can decrease serum cholesterol and glucose levels, and certain insoluble fibers inhibit chemically induced tumorigenesis, it is difficult to compare the effects of specific dietary fibers tested in the laboratory with the effects of fiber-containing foods or of other potentially protective substances present in these foods. · Although human and animal studies indicate that all fermentable carbohydrates can cause dental caries, sucrose appears to be the most cariogenic. The cariogenicity of foods containing fermentable carbohydrates is influenced by the consistency and texture (e.g., stickiness) of the food as well as by the frequency and sequence of consumption. Sugar consumption (by those with an adequate diet) has not been established as a risk factor for any chronic disease other than dental caries in humans. Protein and High-Protein Diets Studies of the association of protein and high-protein diets with chronic diseases are reviewed in Chapters 8 (Protein), 13 (Minerals), 19 (Atherosclerotic Cardiovascular Diseases), 22 (Cancer), and 23 (Osteoporosis) and form the basis of the following major conclusions. · In intercountry correlation studies, diets high in meat—a major source of animal protein—have a strong positive association with increased atherosclerotic coronary artery disease and certain cancers, notably breast and colon cancer. Such diets are often characterized by a high content of saturated fatty acids and cholesterol, which probably accounts for a large part of the association with coronary heart disease, and by a high content of total fat, which is directly associated with the risk of these cancers. However, these diets also tend to have low levels of plant foods, the consumption of which is inversely associated in epidemiologic and animal studies with the risk of heart disease and certain cancers. Total serum cholesterol can be reduced in people with high blood cholesterol by replacing animal foods in their diet with plant foods. · High protein intake can lead to increased urinary calcium excretion. The impact of this finding on the development of osteoporosis in the general population is unclear. · The data linking elevated intakes of animal protein to increased risk of hypertension and stroke are weak, and no plausible mechanisms have been posited for either effect. Energy The following conclusions are based on assessment of the roles of energy intake and expenditure

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Page 10 in chronic disease risk as described in Chapters 6 (Calories) and Chapter 21 (Obesity and Eating Disorders). · Positive energy balance can result from increased energy intake, reduced energy expenditure, or both, and over the long term, can lead to obesity and its associated complications. · Although data from clinical and animal studies demonstrate that overfeeding leads to obesity, increased body weight in cross-sectional and longitudinal population surveys of adults cannot be accounted for by increased energy intake. Thus, it is likely that obesity develops in adult life either because of reduced physical activity, or overfeeding, or both. Obesity is enhanced not only by this energy imbalance but also by a genetic predisposition to obesity and altered metabolic efficiency. · Epidemiologic studies indicate that increased energy expenditure is inversely associated with the risk of coronary heart disease. · Epidemiologic and clinical studies and some experiments in animals demonstrate that obesity is associated with an increased risk of noninsulin-dependent diabetes mellitus, hypertension, gallbladder disease, endometrial cancer, and osteoarthritis. It may also be associated with a higher risk of coronary heart disease and postmenopausal breast cancer. · Studies in humans suggest that fat deposits in the abdominal region pose a higher risk of noninsulin-dependent diabetes mellitus, coronary heart disease, stroke, hypertension, and increased mortality than do fat deposits in the gluteal or femoral regions. · Experience in long-term management of obesity indicates that neither frequent fluctuations in body weight nor extreme restrictions of food intake are desirable. · Long-term follow-up studies indicate that extreme leanness is associated with increased mortality and that the causes of mortality are different from those associated with excess weight. · The specific causes of obesity are not well known, although some obese people clearly consume more energy compared to people of normal weight, whereas others are very sedentary or may have increased metabolic efficiency. Compared to maintenance of stable weight, weight gain in adult life is associated with a greater risk of cardiovascular disease, noninsulin-dependent diabetes mellitus, hypertension, gallbladder disease, and endometrial cancer. Certain risk factors—e.g., high serum cholesterol, elevated serum glucose, and high blood pressure—can be curtailed by weight reduction in overweight adults. Alcoholic Beverages The extensive data on the health effects of alcohol consumption are examined in Chapters 16 (Alcohol), 19  (Atherosclerotic Cardiovascular Diseases), 20 (Hypertension), 22 (Cancer), and 25 (Hepatobiliary Disease). Following are the committee's major conclusions related to alcohol. · When consumed in excess amounts, alcohol replaces essential nutrients including protein and micronutrients and can lead to multiple nutrient deficiencies. · Sustained, heavy intake of alcoholic beverages leads to fatty liver, alcoholic hepatitis, and cirrhosis. It also increases the risk of cancers of the oral cavity, pharynx, esophagus, and larynx, especially in combination with cigarette smoking, whereupon the effects on cancer risk become synergistic. There is some epidemiologic evidence that alcohol consumption is also associated with primary liver cancer and that moderate beer drinking is associated with rectal cancer. The association of alcohol consumption with increased risk of pancreatic or breast cancer is less clear. · Excessive alcohol consumption is associated with an increased incidence of coronary heart disease, hypertension, stroke, and osteoporosis. · Alcohol consumption during pregnancy can damage the fetus, cause low infant birth weight, and lead to fetal alcohol syndrome. No safe level of alcohol intake during pregnancy has been determined. Salt and Related Compounds The following conclusions derive from the evidence on salt and related compounds and their relation to chronic diseases. This evidence is reviewed in Chapters 15 (Electrolytes), 20 (Hypertension), and 22 (Cancer). · Blood pressure levels are strongly and positively correlated with the habitual intake of salt. In populations with a sustained salt intake of 6 g or more per day, blood pressure rises with age and hypertension is frequent, whereas in populations consuming less than 4.5 g of salt per day, the age-related rise in blood pressure is slight or absent and the frequency of hypertension is uniformly low. Clinical studies demonstrate that once hypertension is established, it cannot always be fully

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Page 11 corrected by resumption of a moderately low (<4.5 g/day) salt intake. · Although clinical and epidemiologic studies indicate that some people are more susceptible to salt-induced hypertension than others, there are no reliable markers to predict individual responses. Epidemiologic evidence suggests that blacks, people with a family history of hypertension, and all those over age 55 are at a higher risk of hypertension. · Epidemiologic and animal studies indicate that the risk of stroke-related deaths is inversely related to potassium intake over the entire range of blood pressures, and the relationship appears to be dose dependent. The combination of a low-sodium, high-potassium intake is associated with the lowest blood pressure levels and the lowest frequency of stroke in individuals and populations. Although the effects of reducing sodium intake and increasing potassium intake would vary and may be small in some individuals, the estimated reduction in stroke-related mortality for the population is large. · A high salt intake is associated with atrophic gastritis in epidemiologic and animal studies, and there is also epidemiologic evidence that a high salt intake and frequent consumption of salt-cured and salt-pickled foods are associated with an elevated incidence of gastric cancer. The specific causative agents in these foods have not been fully identified. Minerals and Trace Elements The conclusions listed below are based on a review of the evidence on calcium, magnesium, trace elements, and chronic diseases discussed in Chapters 13 (Minerals), 14 (Trace Elements), 20 (Hypertension), 22 (Cancer), and 23 (Osteoporosis). · Epidemiologic, clinical, and animal studies suggest that sustained low calcium intake is associated with a high frequency of fractures in adults, but the role of dietary calcium in the development of osteoporosis and the potential benefits of calcium supplements—in amounts that exceed the Recommended Dietary Allowances (RDAs)—in decreasing the risk of osteoporosis are unclear. · Some epidemiologic studies have shown an association between calcium  intake and blood pressure, but a causal association between low calcium intake and high blood pressure has not been established. · A few data from epidemiologic and animal studies suggest that a high calcium intake may protect against colon cancer, but the evidence is preliminary and inconclusive. · Unequivocal evidence from epidemiologic and clinical studies indicates that fluoridation of drinking water supplies at a level of 1 ppm protects against dental caries. Such concentrations are not associated with any known adverse health effects, including cancer. · Low selenium intake in epidemiologic and animal studies and low selenium levels in human sera have been associated with an increased risk of several cancers. Moreover, some studies in animals suggest that diets supplemented with large doses of selenium offer protection against certain cancers. These data should be extrapolated to humans with caution, however, because high doses of selenium can be toxic. · The data on most trace elements examined in this report (e.g., copper and cadmium) are too limited or weak to permit any conclusions about their effects on chronic disease risk. Dietary Supplements Claims for the health benefits of dietary supplements have drawn substantial attention in recent decades. The committee has reached the following conclusion on the basis of the evidence reviewed in Chapter 18 (Dietary Supplements). · A large percentage of people in the United States take dietary supplements, but not necessarily because of nutrient needs. The adverse effects of large doses of certain nutrients (e.g., vitamin A) are well documented. There are no documented reports that daily multiple vitamin-mineral supplements, equaling no more than the RDA for a particular nutrient, are either beneficial or harmful for the general population. The potential risks or benefits of the long-term use of small doses of supplements have not been systematically examined. Coffee, Tea, and Other Nonnutritive Dietary Components The following major conclusions pertaining to coffee, tea, and other nonnutritive dietary components are based on a review of the evidence in Chapter 17 (Coffee, Tea, and Other Nonnutritive Dietary Components). · Coffee consumption has been associated with slight elevations in serum cholesterol in some epidemiologic studies. Epidemiologic evidence linking coffee consumption to the risk of coronary

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Page 12 heart disease and cancer in humans is weak and inconsistent. · Tea drinking has not been associated with an increased risk of any chronic disease in humans. · The use of such food additives as saccharin, butylated hydroxyanisole, and butylated hydroxytoluene does not appear to have contributed to the overall risk of cancer in humans. However, this lack of evidence may be due to the relatively recent use of many of these substances or to the inability of epidemiologic techniques to detect the effects of additives against the background of common cancers from other causes. The association between food additives and cancer is also complicated by the long latency period between initial exposure to a carcinogen and the subsequent development of cancer. · A number of environmental contaminants (e.g., some organochlorine pesticides, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons) cause cancer in laboratory animals. The committee found no evidence to suggest that any of these compounds individually makes a major contribution to the risk of cancer in humans; however, the risks from simultaneous exposure to several compounds and the potential for adverse effects in occupationally exposed people have not been adequately investigated. · Certain naturally occurring contaminants in food (e.g., aflatoxins and N-nitroso compounds) and nonnutritive constituents (e.g., hydrazines in mushrooms) are carcinogenic in animals and thus pose a potential risk of cancer in humans. Naturally occurring compounds shown to be carcinogenic in animals have been found in small amounts in the average U.S. diet. There is no evidence thus far that any of these substances individually makes a major contribution to cancer risk in the United States. · Most mutagens detected in foods have not been adequately tested for carcinogenic activity. Although mutagenic substances are generally suspected of having carcinogenic potential, it is not yet possible to assess their contribution to the incidence of cancer in the United States. · Overall, there is a shortage of data on the complete range of nonnutritive substances in the diet. Thus, no reliable estimates can be made of the most significant exposures. Exposure to nonnutritive chemicals individually, in the minute quantities normally present in the average diet, is unlikely to make a major contribution to the overall cancer risk to humans in the United States. The risk from simultaneous exposure to many such compounds cannot be quantified on the basis of current evidence. The Committee's Dietary Recommendations The dietary recommendations of the Committee on Diet and Health, given below, are directed to healthy, North American adults and children. Wherever evidence permits, the committee attempts to identify the special dietary needs of population subgroups at high risk for specific diseases or with different dietary requirements because of age, sex, or physiological status. The special dietary needs of the elderly are largely unknown. As discussed in Chapter 28, the quantities proposed in the committee's recommendations are goals for intake by individuals. To achieve these goals, the mean intake by the population (the public health goal) would have to be higher or lower than the recommended intake for individuals, depending on the direction of the proposed dietary modification. For example, a recommendation that all individuals should reduce their fat intake to 30% or less of calories can be expected to lead to a population mean intake substantially below 30% of calories from fat. Similarly, a recommendation that individuals increase their carbohydrate intake to more than 55% of total calories can be expected to lead to a population mean intake clearly above 55% of calories from carbohydrates. Thus, the guidelines for individuals differ somewhat from the public health (population) goals, which need to be more stringent in order to achieve the goals for individuals. The extent to which the public health goal for a nutrient differs from the goal for individuals in the population will depend on the distribution of intake for that nutrient in the population. In most cases, however, the variation in nutrient intakes in the population is not well known. The recommendations in this report are the product of a systematic and extensive analysis of the literature by a multidisciplinary committee that considered the criteria and the process for arriving at recommendations and documented the extensive literature on which they are based. They are generally in agreement with the advice provided by other expert panels in the United States and abroad, although in most cases they include more  specific  quantitative  recommendations. These recommendations are appropriate for current patterns of dietary intake and disease morbidity and mortality in the United States and are

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Page 13 based on conclusions regarding the association of dietary factors with the entire spectrum of chronic diseases. They take into account competing risks for different diseases as well as nutrient interactions. These recommendations should be reexamined as new knowledge is acquired and as the patterns of morbidity and mortality change over the next decades. The committee's recommendations are presented in a logical sequence that also reflects a general order of importance. For example, all dietary macrocomponents are addressed  first. Among these, highest priority is given to reducing fat intake, because the scientific evidence concerning dietary fats and other lipids and human health is strongest and the likely impact on public health the greatest. Lower priority is given to recommendations on other dietary components, because they are derived from weaker evidence or because the public health impact is likely to be comparatively less. Where the evidence is strongest, the committee presents quantitative recommendations. It recognizes that setting specific quantitative goals is somewhat arbitrary and is based on informed judgment rather than on scientifically derivable formulas; however, quantification facilitates translation of goals into dietary patterns and food choices. Goals are needed to develop and evaluate programs aimed at achieving dietary changes and serve as the basis for regulatory actions such as those relating to food labeling and the validity of health claims for foods and nutrients. The committee's recommendations derive from an assessment of the evidence on chronic diseases, but should be used in combination with the RDAs to achieve an optimal and highly desirable dietary pattern for the maintenance of good health. In the committee's judgment, these recommendations have the potential for a substantial reduction in the risk of diet-related chronic diseases in the general population. · Reduce total fat intake to 30% or less of calories. Reduce saturated fatty acid intake to less than 10% of calories, and the intake of cholesterol to less than 300 mg daily. The intake of fat and cholesterol can be reduced by substituting fish, poultry without skin, lean meats, and low- or nonfat dairy products for fatty meats and whole-milk dairy products; by choosing more vegetables, fruits, cereals, and legumes; and by limiting oils, fats, egg yolks, and fried and other fatty foods. A large and convincing body of evidence from studies in humans and laboratory animals shows that diets low in saturated fatty acids and cholesterol are associated with low risks and rates of atherosclerotic cardiovascular diseases. High-fat diets are also linked to a high incidence of some types of cancer and, probably, obesity. Thus, reducing total fat and saturated fatty acid intake is likely to lower the rates of these chronic diseases. Fat intake should be reduced by curtailing the major sources of dietary fats rather than by eliminating whole categories of foods. For example, by substituting fish, poultry without skin, lean meats, and low- or nonfat dairy products for high-fat foods, one can lower total fat and saturated fatty acid intake while ensuring an adequate intake of iron and calcium—two nutrients of special importance to women. Dietary fat can also be reduced by limiting intake of fried foods, baked goods containing high levels of fat, and spreads and dressings containing fats and oils. Different types of fatty acids have different effects on health. Saturated fatty acids and dietary cholesterol tend to increase total and LDL serum cholesterol and, consequently, the risk of cardiovascular disease. The extent of this activity differs among saturated fatty acids; palmitic, myristic, and lauric acids have the greatest cholesterol-raising effect. The main dietary sources of these cholesterol-raising saturated fatty acids are dairy and meat products and some vegetable oils, such as coconut, palm, and palm-kernel oils. Dietary cholesterol is found mainly in egg yolks, certain shellfish, organ meats, and, to a lesser extent, in other meats and dairy products. Thus, the intake of these foods should be curtailed. Monounsaturated fatty acids are found in a variety of foods but are especially abundant in olive oil and canola oil. Polyunsaturated fatty acids are of two types—omega-6 and omega-3; both are essential nutrients and cannot be synthesized endogenously. Omega-6 polyunsaturated fatty acids are common in several plant oils, including corn, safflower, soybean, and sunflower oils. Omega-3 polyunsaturated fatty acids are found in cold-water marine fish (such as salmon and mackerel) and in some plant oils (e.g., soybean and canola oils). Omega-6 polyunsaturated fatty acids and monounsaturated fatty acids (and carbohydrates) lower LDL cholesterol when substituted for saturated fatty acids. Omega-3 polyunsaturated fatty acids also lower LDL-cholesterol when substituted for saturated fatty acids, but they are more effective in lowering elevated serum triglyceride levels. Although consumption of fish one or more times a week has been associated with a reduced risk of coronary heart disease, the committee does not

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Page 14 recommend the use of concentrated fish oil supplements, because there is insufficient evidence that they are beneficial and the absence of long-term adverse effects has not been established. The evidence linking high-fat diets to increased cancer risk is less persuasive than that associating saturated fatty acids and dietary cholesterol to coronary heart disease, but the weight of evidence indicates that high-fat diets are associated with a higher risk of several cancers, especially of the colon, prostate, and breast. Most evidence from studies in humans suggests that total fat or saturated fatty acids adversely affect cancer risk. No studies in humans have yet examined the benefits of changing to low-fat diets; however, such evidence exists from experiments in animals. The combined evidence from epidemiologic and laboratory studies suggests that reduction of total fat is likely to reduce the risk of these cancers. Epidemiologic data on the possible association of low serum cholesterol levels with an increased incidence of and mortality from cancer in general or colon cancer in men in particular are inconsistent and do not suggest a causal association. Rather, they indicate that the lower serum cholesterol levels in some of these studies were in part the consequence of undetected cancers. The overall evidence indicates that dietary modification to lower serum total cholesterol and coronary heart disease risk is likely to reduce the risk of colon cancer without increasing the risk of other cancers. Animal studies also suggest that high-fat diets may lead to obesity, possibly because dietary fat is converted to body fat more efficiently than are other sources of calories. Short-term clinical studies in humans indicate that a substantial reduction in fat intake may be accompanied by weight loss; however, reduced caloric intake was observed in some of these reports and although not specifically noted is likely to have occurred in others. This indicates that a substantial reduction in fat intake may result in overall caloric reduction, perhaps because of the caloric density of dietary fat. From a public health perspective, this phenomenon may be important, regardless of whether fat reduction per se results in weight loss or whether weight loss results from an overall reduction in caloric intake. In the committee's judgment, concerns that reduced fat intake may curtail intake of meats and dairy products and thus limit intakes of iron and calcium  by women and children or that young children on reduced-fat diets might not obtain adequate calories to support optimal growth and development are not justified. Fat intake can be reduced to approximately 30% of calories without risk of nutrient deficiency, and this level of fat intake after infancy has not been associated with any detrimental effects. Furthermore, adequate caloric intake can readily be maintained in children on diets containing 30% of calories from fat. Although the committee recommends that the total fat intake of individuals be 30% or less of calories, there is evidence that further reduction in fat intake may confer even greater health benefits. However, the recommended levels are more .likely to be adopted by the public because they can be achieved without drastic changes in usual dietary patterns and without undue risk of nutrient deficiency. Furthermore, they permit gradual adaptation to lower-fat diets as more lower-fat foods become available on the market. The committee recommends that people who should not lose weight should compensate for the caloric loss resulting from decreased fat intake by consuming greater amounts of foods containing complex carbohydrates (e.g., vegetables, certain fruits, legumes, and whole-grain cereal products). Although the committee recommends that saturated fatty acid intake be maintained at less than 10% of total calories by individuals, it is highly likely that further reduction, to 8 or 7% of calories or lower, would confer greater health benefits. Such further reductions can best be achieved by substituting additional complex carbohydrates and monounsaturated for saturated fatty acids in the diet. Larger reductions in cholesterol intakes—e.g., to 250 or 200 mg or even less per day—may also confer health benefits. The committee recommends that the polyunsaturated fatty acid intake of individuals not exceed 10% of total calories and that polyunsaturated fatty acid intake in the population be maintained at current levels in the U.S. diet, i.e., an average of approximately 7% of total calories. (The requirement for omega-6 polyunsaturated fatty acids can be met by 1 to 2% of calories as linoleic acid.) Concern that an increase in polyunsaturated fatty acid intake may increase risk of certain cancers derives primarily from studies of animals on very-high-polyunsaturated fatty acid diets. Given the absence of human diets naturally very high in total polyunsaturated fatty acids and the lack of information about the long-term consequences of high polyunsaturated fatty acid intake (see Chapter 7), it seems prudent to recommend that polyunsaturated fatty acid intake not be increased above the current average in the U.S. population. However, since most of the polyunsaturated fatty acids in the

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Page 15 current U.S. diet are of the omega-6 rather than the omega-3 type, and since the committee's recommendation is directed mainly at omega-6 polyunsaturated fatty acids, any increase in total polyunsaturated fatty acid resulting from an increase in foods containing omega-3 polyunsaturated fatty acids (e.g., by eating more fish containing such fatty acids) is reasonable. · Every day eat five or more servings* of a combination of vegetables and fruits, especially green and yellow vegetables and citrus fruits. Also, increase intake of starches and other complex carbohydrates by eating six or more daily servings of a combination of breads, cereals, and legumes. The committee recommends that the intake of carbohydrates be increased to more than 55% of total calories by increasing primarily complex carbohydrates. Fats and carbohydrates are the two major sources of calories in the diet. National food consumption surveys indicate that the content of the average U.S. diet is high in fat and low in complex carbohydrates (e.g., starches, vegetables, legumes, breads, cereals, and certain fruits). Green and yellow vegetables; fruits, especially citrus fruits; legumes; and whole-grain  cereals and breads, which constitute a small portion of the present U.S. diet, generally contain low levels of fat; thus, they are good substitutes for fatty foods and good sources of several vitamins, minerals, complex carbohydrates, and dietary fiber. The recommended number of servings is derived from experience in planning nutritionally balanced diets that would meet the committee's dietary recommendations. The amounts recommended would facilitate an increase in the total carbohydrate and complex carbohydrate content of the diet, make up for the caloric deficit due to fat reduction, and supply sufficient quantities of essential vitamins and minerals. The committee does not recommend increasing the intake of added sugars, because their consumption is strongly associated with dental caries, and, although they are a source of calories for those who may need additional calories, they provide no nutrients. Furthermore, foods high in added sugars (e.g., desserts and baked goods) are generally also high in fat. Studies in various parts of the world indicate that people who habitually consume a diet high in plant foods have low risks of atherosclerotic cardiovascular diseases, probably largely because such diets are usually low in animal fat and cholesterol, both of which are established risk factors for atherosclerotic cardiovascular diseases. Some constituents of plant foods, e.g., soluble fiber and vegetable protein, may also contribute—to a lesser extent—to the lower risk of atherosclerotic cardiovascular diseases. The mechanism  for the link between frequent consumption of vegetables and fruits, especially green and yellow vegetables and citrus fruits, and decreased susceptibility to cancers of the lung, stomach, and large intestine is not well understood because the responsible agents in these foods and the mechanisms for their protective effect have not been fully determined. However, there is strong evidence that a low intake of carotenoids, which are present in green and yellow vegetables, contributes to an increased risk of lung cancer. Fruits and vegetables also contain high levels of fiber, but there is no conclusive evidence that the dietary fiber itself, rather than other nutritive and nonnutritive components of these foods, exerts a protective effect against these cancers. The committee does not recommend the use of fiber supplements. Vegetables and fruits are also good sources of potassium. A diet containing approximately 75 mEq of potassium (i.e., approximately 3.5 g of elemental potassium) daily may contribute to reduced risk of stroke, which is especially common among blacks and older people of all races. Potassium supplements are neither necessary nor recommended for the general population. · Maintain protein intake at moderate levels. Protein is an essential nutrient, and protein-containing foods are important sources of essential amino acids in the diet. However, because there are no known benefits and possibly some risks in consuming diets with a high animal protein content, the committee recommends that protein intake not be increased to compensate for the caloric loss that would result from the recommended reduction in fat intake. In general, average protein intake by adults in the United States considerably exceeds the RDA, which is 0.8 g/kg of desirable body weight for adults. The committee recommends maintaining total protein intake at levels lower than twice the RDA for all age groups (e.g., less than 1.6 g/kg body weight for adults). Increased risks of certain cancers and coronary heart disease have been associated in some epidemiologic studies with diets high in meat and, as a *An average serving is equal to a half cup for most fresh or cooked vegetables, fruits, dry or cooked cereals and legumes, one medium piece of fresh fruit, one slice of bread, or one roll or muffin.

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Page 16 consequence, in animal protein, and with high protein intake alone in laboratory studies. It is not known whether these adverse effects are due solely to the usually high total-fat, saturated fatty acid, and cholesterol content of diets that are rich in meat or animal protein, or to what extent protein per se or other factors also contribute. High protein intake may also lead to increased urinary calcium loss. The committee is aware of concerns among some scientists that animal protein restriction might curtail the ability of some population subgroups with habitually lower protein intakes (e.g., women and the elderly) to meet the RDA for certain other essential nutrients such as iron. However, the recommendation to maintain intake below twice the RDA for all age groups would require no reduction of current average intakes in the United States. The committee does not recommend against eating meat; rather, it recommends consuming lean meat in smaller and fewer portions than is customary in the United States. · Balance food intake and physical activity to maintain appropriate body weight. Excess weight is associated with an increased risk of several chronic disorders, including noninsulin-dependent diabetes mellitus, hypertension, coronary heart disease, gallbladder disease, osteoarthritis, and endometrial cancer. The risks appear to decline following a sustained reduction in weight. Increased abdominal fat carries a higher risk for these disorders than do comparable fat deposits in the hips and thighs. New standards for healthy body composition take into account such differences in regional body fat distribution as well as weight-to-height ratios. Neither large fluctuations in body weight nor extreme restrictions in food intake are desirable. In the U.S. population and other westernized societies, body weight and body mass index are increasing while the overall caloric intake of the population is decreasing. These trends as well as the association of moderate, regular physical activity with reduced risks of heart disease lead to the committee's recommendation that the U.S. population increase its physical activity level and that all healthy people maintain physical activity at a moderately active level, improve physical fitness, and moderate their food intake to maintain appropriate body weight. For adult men and women of normal weight, this will also allow the ingestion of adequate calories to meet all known nutrient needs. Overweight people should increase their physical activity and reduce their caloric intake, and people with a family history of obesity should avoid calorically dense foods and select low-fat foods. · The committee does not recommend alcohol consumption. For those who drink alcoholic beverages, the committee recommends limiting consumption to the equivalent of less than 1 ounce of pure alcohol in a single day. This is the equivalent of two cans of beer, two small glasses of wine, or two average cocktails. Pregnant women should avoid alcoholic beverages. Excessive alcohol drinking increases the risk of heart disease, high blood pressure, chronic liver disease, some forms of cancer, neurological diseases, nutritional deficiencies, and many other disorders. Even moderate drinking carries some risk in circumstances that require neuromotor coordination and judgment, e.g., driving vehicles, working around machinery, and piloting airplanes or boats. Consumption of even small amounts of alcohol can lead to dependence. Approximately 10% of those who consume alcoholic beverages in the United States are alcoholics. Pregnant women and women who are attempting to conceive should avoid alcoholic beverages because there is a risk of damage to the fetus and no safe level of alcohol intake during pregnancy has been established. Although several studies show that moderate alcohol drinking is associated with a lower coronary heart disease risk, it would be unwise to recommend moderate drinking for those who do not drink because, in the committee's judgment, a causal association has not been established and because even moderate drinking poses certain other risks, including the risk of alcohol addiction. · Limit total daily intake of salt (sodium  chloride) to 6 g or less. Limit the use of salt in cooking and avoid adding it to food at the table. Salty, highly processed salty, salt-preserved, and salt-pickled foods should be consumed sparingly. Studies in human populations in different parts of the world show that a diet containing more than 6 g of salt per day is associated with elevated blood pressure, and many Americans habitually exceed this level. It is probable that susceptibility to salt-induced hypertension (salt sensitivity) is genetically determined, but no reliable genetic marker has yet been identified. Thus, those who are most susceptible to developing salt-induced hypertension, and therefore likely to benefit most from this recommendation, cannot yet be identified. In salt-sensitive people, the recommended level of salt intake is unlikely to contribute to

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Page 17 blood pressure elevation and may even lead to blood pressure reduction. In the general population, the recommended level will have no detrimental effect. The committee is aware that a greater reduction in salt intake (i.e., to 4.5 g or less) would probably confer greater health benefits than its present recommendation, but chose 6 g as an initial goal that can be achieved more readily. This does not preclude a subsequent recommendation for further reduction. The evidence linking salt intake per se to stomach cancer is less persuasive than that for salt and hypertension. There is consistent evidence, however, that frequent consumption of salt-preserved or salt-pickled foods increases the risk of stomach cancer. The specific causative agents in those foods have not been identified. · Maintain adequate calcium intake. Calcium is an essential nutrient; it is necessary for adequate growth and skeletal development. Certain segments of the population, especially women, because of their low caloric intake, and adolescents, because of their higher nutrient requirements, need to make careful food choices to obtain adequate calcium from the food supply. The committee recommends consumption of low- or nonfat dairy products and dark-green vegetables, which are rich sources of calcium and can assist in maintaining calcium intake at approximately RDA levels. Although low calcium intake is associated with a higher frequency of fractures and possibly with high blood pressure, the potential benefits of calcium intakes above the RDAs to prevent osteoporosis or hypertension are not well documented and do not justify the use of calcium supplements. · Avoid taking dietary supplements in excess of the RDA in any one day. A large percentage of the U.S. population consumes some vitamin or mineral supplement daily. The supplements are often self-prescribed and not based on known nutrient deficiencies. It is not known what, if any, benefits or risks accrue to individuals or the general population from taking small doses of supplements. Some population subgroups (e.g., those suffering from malabsorption syndromes) may require supplements, but they should take them only under professional supervision. A single daily dose of a multiple vitamin-mineral supplement containing 100% of the RDA is not known to be harmful or beneficial; however, vitamin-mineral supplements that exceed the RDA  and other supplements (such as protein powders, single amino acids, fiber, and lecithin) not only have no known health benefits for the population but their use may be detrimental to health. The desirable way for the general public to obtain recommended levels of nutrients is by eating a variety of foods. Thus, the committee supports the general scientific opinion and the opinions of several other expert panels that have recently commented specifically on supplement use. It emphasizes, however, that the long-term health effects (risks and benefits) of supplements have not been adequately studied. · Maintain an optimal intake of fluoride, particularly during the years of primary and secondary tooth formation and growth. There is convincing evidence that consumption of optimally fluoridated water (i.e., 0.7 to 1.2 ppm fluoride, depending on ambient temperature) significantly reduces the risk of dental caries in people of all ages, especially in children during the years of primary and secondary tooth formation and growth. There is no evidence that such fluoride concentrations have any adverse effects on health, including cancer risk. In the absence of optimally fluoridated water, the committee supports the use of dietary fluoride supplements in the amounts generally recommended by the American Dental Association, the American Academy of Pediatrics, and the American Academy of Pediatric Dentistry. Implications of Recommendations for Food Choices What do the committee's recommendations imply with regard to selection of foods and food groups? To some extent, this issue is addressed under each recommendation. Therefore, only a synthesis is provided here. Principles of food selection will also be explained in more detail in the committee's forthcoming report to the general public. In summary, the diet recommended by the committee should contain moderately low levels of fat, with special emphasis on restriction of saturated fatty acids and cholesterol; high levels of complex carbohydrates; only moderate levels of protein, especially animal protein; and only low levels of added sugars. Caloric intake and physical activity should be balanced to maintain appropriate body weight. The recommendation to maintain total fat intake at or below 30% of total caloric

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Page 18 intake and saturated fatty acid intake at less than 10%, combined with the recommendation to maintain protein intake only at moderate levels, means that for most North Americans it will be necessary to select leaner cuts of meat, trim off excess fat, remove skin from poultry, and consume fewer and smaller portions of meat and poultry. Fish and many shellfish are excellent sources of low-fat protein. By using plant products (e.g., cereals and legumes) instead of animal products as sources of protein, one can also reduce the amount of saturated fatty acids and cholesterol in the diet. Dairy products are an important source of calcium and protein, but whole milk, whole-milk cheeses, yogurt, ice cream, and other milk products are also high in saturated fatty acids. Therefore, low-fat or skim milk products should be substituted. Furthermore, it is desirable to change from butter to margarine with a low saturated fatty acid content, to use less oils and fats in cooking and in salad dressings, and to avoid fried foods. For most people, the recommended restriction of fat intake, coupled with the recommendation for moderation in protein intake, implies an increase in calories from carbohydrates. These calories should come from  an increased intake of whole-grain cereals and breads rather than from foods or drinks containing added sugars. For example, bakery goods, such as pies, pastries, and cookies, although they provide complex carbohydrates also tend to contain high levels of total fat, saturated fatty acids, and added sugars, all of which need to be curtailed to meet the committee's recommendations. In general, vegetables and fruits are unlikely to contribute substantially to caloric intake but are major sources of vitamins, minerals, and dietary fiber. The committee places special emphasis on increasing consumption of green and yellow vegetables as well as citrus fruits, particularly since their consumption in North America is relatively low. The committee's recommendations would lead to a substantial increase in consumption frequency and portion sizes, especially of vegetables, for the average person. Thorough washing of fresh vegetables (especially leafy ones) and fruits will minimize the consumption of pesticide residues in the diet. The need for restriction of certain dietary components—such as egg yolks; salt; salty, smoked, and preserved foods; and alcoholic beverages—is clearly explained in the recommendations. Further considerations include methods of preparation, cooking, and processing, which can have important effects on the composition of foods. The committee emphasizes the need to read the labels on prepared, formulated, and other processed foods to identify their contribution of nutrients in general and of salt, fats and cholesterol, and sugars in particular. With regard to the risk of chronic diseases, maximum benefit can be attained and any unknown, potentially harmful effects of dietary constituents minimized by selecting a variety of foods from each food group, avoiding excessive caloric intake (especially excessive intake of any one item or food group), and engaging regularly in moderate physical exercise. Impact on Public Health: Benefits and Risks of Dietary Modification The committee used several approaches and lines of evidence to assess potential adverse consequences of its dietary recommendations for the general population (see Chapter 28). For example, it examined the degree of concordance in death rates and mortality trends between the two leading diet-related causes of death—i.e., coronary heart disease and cancer—to assess the degree to which common dietary risk and protective factors may be operating. It also analyzed the possible adverse consequences of reducing the intake of total fat, saturated fatty acids, and cholesterol, which would lead to a reduction in serum cholesterol levels and in the risk of atherosclerotic cardiovascular disease. In some studies, low serum cholesterol is associated with increased colon cancer mortality. However, this finding is inconsistent and the data do not suggest that lowering serum cholesterol by dietary modification would increase the risk of any cancer. Furthermore, the committee considered the effect of reducing total serum cholesterol on increasing risk of hemorrhagic stroke in hypertensives; the possible adverse effects of increased intakes of polyunsaturated fatty acids, carbohydrates, vegetables, and carotene and of moderate intakes of alcohol (as opposed to total avoidance); the effect of potential increases in exposure to pesticides; and the potential for nutrient deficiencies or toxicity among population subgroups (see Chapter 28). It concluded that despite using the worst-case hypothetical scenarios, the benefits of dietary modification far outweigh the potential for adverse effects, which is minimal if any, as summarized below. The lines of evidence examined in Chapter 28 indicate that risk factors and protective character-

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Page 19 istics for the major diet-related chronic diseases and causes of death are concordant. In general, dietary intervention to reduce the risk of one disease (e.g., coronary heart disease) is also likely to reduce the risk of other diseases (e.g., several cancers). Central to the committee's deliberations was the extent to which the overall risk of chronic diseases in the general U.S. population might be reduced by dietary modification. Because the role of dietary factors in the etiology of chronic diseases differs by factor and disease (see Major Conclusions), the impact of dietary modification on the risk of different diseases is likely to vary considerably. As discussed in Chapter 28, the committee used several approaches in developing quantitative estimates of the potential public health impact if its dietary recommendations were to be fully adopted by the public. It recognized at the outset that the accuracy of such estimates is determined by the strength, consistency, and congruence of the evidence from a variety of sources, especially from extensive, long-term observations and dietary interventions in human populations, which provide the most reliable estimates of association. The best of these data pertain to serum cholesterol levels and the risk of coronary heart disease; those on dietary factors as they relate to coronary heart disease, cancer, and other major causes of mortality are not as extensive. Estimates of the reduction of coronary heart disease risk in human populations can be derived by extrapolating the effects of a downward shift in average serum cholesterol levels, by comparing coronary heart disease risk in populations with greatly different saturated fatty acid or total fat intakes or wide ranges in mean serum cholesterol levels, or by examining the results of serum-cholesterol-lowering trials on cardiovascular disease incidence. The many drawbacks to these approaches are explained in Chapter 28. In general, however, by using these approaches, the committee estimates that its recommendations for reducing intake of saturated fatty acids, dietary cholesterol, and total fat could lead to at least a 10% reduction in serum cholesterol levels and a 20% reduction in coronary heart disease risk in the United States beyond the 1987 levels. More stringent dietary modification provides the potential for even greater reduction in coronary disease risk in the future. This underestimates the potential benefits of dietary modification because it only focuses on certain lipids and does not take into account the potential benefits of reductions in body weight and blood pressure in the population. The picture is less clear for the risk of cancer and other chronic diseases. Some epidemiologists estimate that as much as 90% of all cancer in humans can be attributed to various environmental factors, including diet. Others attribute 30 to 40%  of cancers in men and 60% of cancers in women to diet. Still others have estimated that 10 to 70% of the deaths from  cancer could be prevented by dietary modifications, especially for cancers of the stomach, the large bowel, and to a lesser extent, the breast, the endometrium, and the lung. The conclusions of the Committee on Diet and Health are in general agreement with those of the National Research Council's Committee on Diet, Nutrition, and Cancer, which in 1982 concluded that cancers of most major sites are influenced by dietary patterns. The data are not sufficient, however, to quantify the contribution of diet to the overall cancer risk or to determine the quantitative reduction in risk that might be achieved by dietary modifications. The committee notes that several countries with dietary patterns similar to those recommended in this report have about half the U.S. rates for diet-associated cancers. This suggests that the committee's dietary recommendations could have a substantial impact on reducing the risk of cancer in the United States. For the other chronic diseases and conditions considered in this report (i.e., hypertension, obesity, osteoporosis, diabetes mellitus, hepatobiliary disease, and to a lesser extent, dental caries), the magnitude of risk reduction expected through full implementation of the committee's guidelines on diet and health cannot be reliably estimated at this time due to limitations in the data. Nevertheless, on the basis of its overall assessment of the data, the committee concludes that implementation of its dietary recommendations through readily available natural diets is likely to greatly reduce the overall risk of these chronic diseases without discernibly increasing the risk of any cause of death or disability. In Chapter 28, the committee categorizes dietary factors according to the strength of the evidence and relates each to the risk of chronic diseases and the potential public health benefit of dietary modification. In the committee's judgment, modification of the total diet along the lines recommended in this report is necessary to achieve the maximum public health benefit; and among dietary factors, reduced intakes of total fat, satu-

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Page 20 rated fatty acids, and cholesterol are likely to have the greatest impact. Implementation of Dietary Recommendations What strategies are needed to implement the committee's dietary recommendations, and what are their implications for different sectors of society? These issues are the subject of a separate study by the Food and Nutrition Board. Therefore, they only receive brief consideration below and in Chapter 28 of this report. It is apparent to the committee and the Food and Nutrition Board that if one of our national goals is to reduce the risk of chronic diseases and if dietary modification is likely to assist in achieving that goal, then various sectors of society need to collaborate in implementing dietary recommendations of the type proposed by the committee. The committee is aware that many nutrition programs and regulatory actions that are already in place or under way under the auspices of government agencies and in the private sector are consistent with implementing the proposed recommendations. Nevertheless, it wishes to draw special attention to the following general issues. A concerted effort will be needed to make the changes in the food supply and in nutrition policy and programs that will be required to increase the availability of low-fat and low-salt foods in supermarkets and in public eating facilities such as school cafeterias and restaurants. Consideration needs to be given to the most effective means of achieving such modification: through technological changes, massive public education efforts, legislative measures such as food labeling, or a combination of such strategies. Although the committee's report to the public, which will be issued in the near future, will explain its major conclusions and recommendations in lay terms, leaders in government agencies, the health professions, the food industry, and the mass media face the challenge of interpreting the committee's nine recommendations for the general public as well as for high-risk groups. They will need to convey in practical terms the concept of certainty or uncertainty of benefit, competing risks, dietary interactions, and target populations. There is a need to develop adequate educational tools and to identify the best means of educating and motivating the public. Health professionals, government agencies, and the industry must also undertake additional research to identify ways of effecting dietary change. In the committee's judgment, it is feasible to implement the proposed recommendations within the framework of the average lifestyle in the United States, and the committee is encouraged by the knowledge that dietary habits in this country have already changed markedly in many ways that are consistent with these recommendations. To convey a full understanding of these recommendations to the public and to implement them will require close collaboration among government agencies, the food industry, health professionals (physicians, nutritionists, dietitians, and public health personnel), educational institutions, leaders in mass media, and the general public. Research Directions Fundamental scientific discoveries generally occur in completely unexpected ways. Thus it is impossible to predict where the major discoveries will be made or which research directions will prove to be the most fruitful. Therefore, the committee does not wish to stifle creativity by specifying experimental protocols or directing research. Nevertheless, it is possible and desirable to propose a scheme for organizing research to seek more definitive data on the associations between diet and chronic diseases. The committee's conclusions and dietary recommendations reflect its assessment of current knowledge and actions justified now; they can be made more definitive only through additional research of the kind recommended in this section. The seven categories of research proposed below are not presented in order of priority. Rather, taken together, they reflect a conceptual framework for interdisciplinary collaborative research that encompasses different kinds of investigations: short- and long-term experiments in vitro and in vivo, food consumption surveys, food composition analyses, descriptive and analytical epidemiologic studies, metabolic studies and clinical trials in humans, and social and behavioral research. More detailed and specific research recommendations are summarized in Chapter 28 and presented in Chapters 4 and 6 through 26. · Identification of foods and dietary components that alter the risk of chronic diseases and elucidation of their mechanisms of action. Much needed research falls in this category. Many dietary constituents are already known to play a role in the etiology of chronic diseases, but additional and more specific knowledge, especially

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Page 21 concerning mechanisms of action, will lead to more definitive conclusions and provide more precise guidance about ways to reduce the risk of different chronic diseases. · Improvement of the methodology for collecting and assessing data on the exposure of humans to foods and dietary constituents that may alter the risk of chronic diseases. Methodological shortcomings inhibit the interpretation and analysis of data and often prevent the derivation of precise conclusions about the association of diet and chronic diseases. Thus, the committee recommends that high priority be given to development of better methods for data collection, quantification of dietary exposures and effects, and data analysis. · Identification of markers of exposure and early indicators of the risk of various chronic diseases. This category of research is designated for two purposes: first, to circumvent the shortcomings of using the disease itself as the sole end point—i.e., because of the long latency period of many chronic diseases evidenced by the delay between dietary exposure and disease expression; and second, to circumvent problems due to exposure misclassification when dietary recall methods are used. In the committee's judgment, there is a pressing need to identify biochemical/biological markers of dietary exposure, early biological markers that can forecast the emergence of clinical disease, and genetic markers that can identify high-risk subgroups in the population. In addition, the committee proposes greater use of the techniques of molecular biology to study gene-nutrient interactions that can help characterize individual variability in nutrient requirements and response to various chronic diseases. · Quantification of the adverse and beneficial effects of diet and determination of the optimal ranges of intake of dietary macro- and micro-constituents that affect the risk of chronic diseases. Although most dietary constituents are known to have some effect on the risk of certain chronic diseases, much less is known about the magnitude of this effect. The committee believes that there is a strong need to quantify these effects in order to estimate the contribution of diet to the risk of chronic diseases. These efforts should include a study of nutrient interactions, competing risks, and dose-response relationships. The ultimate aim of such research should be to determine the optimal ranges of intake of various dietary components for health maintenance, keeping in mind the desirability of identifying their effects and the shape of the dose-response curve. ·Through intervention studies, assessment of the potential for chronic disease risk reduction. Carefully designed intervention studies should be conducted to assess the public health impact of dietary modification. Although many such studies have been conducted for heart disease, hypertension, dental caries, and obesity, and a few have focused on osteoporosis, no such long-term studies have yet been completed for cancer. The committee has considered whether priority should be given to additional large-scale trials or whether current knowledge is sufficient to undertake dietary interventions in the population and subsequently to assess their effectiveness by carefully monitoring trends in disease incidence and mortality. Intervention trials should be undertaken only when a substantial body of data indicates a high likelihood of benefit without discernible risk. Such trials might be warranted to obtain more definitive data, especially because the kinds of diets tested in such trials might yield data about potential benefits of dietary intervention to simultaneously reduce the risk of multiple chronic diseases, but they should not be used as a basis for delaying prudent dietary modifications warranted by current knowledge. Any intervention studies should be accompanied by effective monitoring to assess disease incidence, prevalence, and mortality rates. · Application of knowledge about diet and chronic diseases to public health programs. Social and behavioral research should be undertaken to achieve a better understanding of factors that motivate people to modify their food habits. This knowledge is indispensable for designing effective public health programs to reduce the risk of chronic diseases. Furthermore, improved technologies are needed to increase the availability of foods that conform  to the committee's dietary recommendations. · Expansion of basic research in molecular and cellular nutrition. The six categories described above focus on research to enhance knowledge of the interrelationship among dietary factors, chronic diseases, and health, and this research includes an understanding of the underlying mechanisms. The committee wishes to emphasize the need for such

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Page 22 fundamental research to advance our knowledge of basic cellular and molecular mechanisms. Research in disciplines ranging from the physical sciences, to biochemistry, physiology, applied biology, nutrition, medicine, epidemiology, biophysics, cellular and molecular biology, and genetics is needed to fill the gaps in our understanding of how dietary, environmental, and genetic factors interact to influence the risk of chronic diseases. The committee hopes that the findings contained in this report will be as widely disseminated as possible and urges that all those with an interest in and responsibility for public health participate in this effort. Recognizing the limitations of current knowledge, it strongly believes that periodic updates of its findings will be necessary as new data emerge to shed more light on associations between diet and chronic diseases.