Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 665
Page 665 28 Recommendations on Diet, Chronic Diseases, and Health The committee's overall recommendations on diet, chronic diseases, and health are presented in this chapter along with a discussion of the criteria, the process, and the factors considered in formulating them. There is also a discussion of the nature of the recommendations and the target populations and comparisons with recommendations of other expert groups in the United States and abroad. In addition, this chapter includes an assessment and some quantitative estimates of the potential benefits and adverse consequences of dietary modifications as they relate to chronic disease risk and recommendations for research to increase knowledge in this area. 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. The Committee on Diet and Health adopted this approach of gearing dietary recommendationsthe proposed level of actionto such critical features as the level of certainty, the potential for public health benefit, and the likelihood of minimal risk. Thus, although much remains to be learned before firm conclusions and recommendations can be made regarding the total impact of diet on chronic disease risk, in the committee's judgment it would be derelict to ignore the large body of evidence while waiting for absolute proof of benefit from dietary change. The committee concluded that the overall evidence regarding a relationship between certain dietary patterns (e.g., a diet high in saturated fat and total fat) and chronic diseases (e.g., cardiovascular diseases or certain cancers) supports (1) a comprehensive
OCR for page 666
Page 666 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 meat) to facilitate dietary change. The process of arriving at dietary recommendations, rather than the recommendations themselves, previously has received little attention. One relevant attempt is the development of the Public Health Objectives for the Nation by the Office of Disease Prevention and Health Promotion of the U.S. Department of Health and Human Services (DHHS, 1983). That office proposed 17 priority objectives for improving nutrition during the 1990s as well as an implementation plan for meeting these objectives. A midcourse review of the status of these objectives documented the process of developing the objectives and suggested that substantial progress has been made in achieving certain nutrition-related objectives (DHHS, 1986). The logic, criteria, and philosophy for formulating dietary recommendations are also discussed in reports by the Health Education Council in the United Kingdom (NACNE, 1983), the American Heart Association in its Dietary Guidelines for Healthy American Adults (AHA, 1986), the National Research Council's Committee on Diet, Nutrition, and Cancer (NRC, 1982), and a Food and Nutrition Board report entitled Toward Healthful Diets (NRC, 1980b). Several individual attempts to define or analyze the process of developing dietary recommendations also provide insights into the philosophy underlying recommendations issued in different countries (e.g., Grobstein, 1983; Langsford, 1979; Molitor, 1979; Palmer, 1983). The committee hopes to contribute to this nascent field through the discussions that follow. A special feature of the present study is its attempt to develop recommendations and strategies for risk reduction across the entire spectrum of major diet-related chronic diseases. Several factors were considered in this process: risks and benefits; the advantages of making recommendations by nutrient, by food, or by dietary pattern; the basis for proposing quantitative as opposed to qualitative recommendations; recommendations for individuals as opposed to populations; and the feasibility of implementation. These are discussed in the following sections. Assessment of Risks and Benefits To develop dietary recommendations for reducing the overall risk of diet-related chronic diseases, it is essential to analyze and compare recommendations pertaining to individual diseases. For example, recommendations to increase calcium intake to provide possible protection against osteoporosis might in isolation be viewed as conflicting with recommendations for coronary heart disease (CHD) prevention, because dairy productswhich contribute the most calcium to the U.S. dietare also major sources of saturated fatty acids (SFAs), which are known to increase plasma cholesterol levels and CHD risk. Thus, recommendations for maintaining adequate bone mass and for preventing CHD would both have to stress consumption of low-fat dairy products. Other important considerations are dietary interactions and their synergistic or antagonistic effects. For example, the potential benefits of enhanced trace element intake for certain cancers might be offset by increasing the intake of vegetables and cereals in an attempt to reduce risk for colon cancer, because such foods are also high in fiber, which could in principle initially inhibit intestinal absorption of certain trace elements. As exemplified systematically at the end of this chapter, the committee considered such potential risks as well as dietary interactions and dose-response relationships in assessing the probable impact of dietary modification on risk factors across the range of chronic diseases. To some extent, this task was simplified by the inherent concordance in dietary risk and protective factors. For example, a recommendation to lower fat intake would be consistent with evidence that low-fat intake may reduce the risk of certain cancers and with stronger evidence that decreased SFA and cholesterol intakes reduce cardiovascular disease risk. Recommendations by Nutrients, Foods, or Dietary Patterns The committee discussed whether to base its recommendations on individual nutrients, single foods or food groups, or the overall pattern of dietary intake. Nutrient-based recommendations (e.g., fluoridation of water for the general population or iron fortification to reduce the risk of iron deficiency) might be easy for public health personnel to interpret and implement (e.g., through supplementation or food fortification); however, they may fail to take into account needs that arise from interactions among nutrients (e.g., increased selenium requirements for those on a high-vitamin C diet or enhanced iron absorption in the presence of vitamin C). Furthermore, such recommenda-
OCR for page 667
Page 667 tions may be difficult for the public to interpret or translate into diets, e.g., understanding how to plan diets to obtain at least 800 mg of calciumthe Recommended Dietary Allowance (RDA) per day. Thus, recommendations pertaining to nutrient intake would usually need to be translated by professionals into guidance about food choices for the public. Recommendations based on single foods or food groups are easier to implement when only a few foods serve as the major sources of an essential dietary component (e.g., dairy products, which are the primary source of calcium in the U.S. diet). However, such guidance can be misleading. Rich sources of nutrients are not necessarily good dietary sources unless the food is eaten frequently or in large amounts and the nutrient is bioavailable. For example, although the calcium content of spinach is higher than that of dairy products, dairy products are better sources of calcium because of greater bioavailability and more frequent consumption. Furthermore, such recommendations may ignore food group commonalities (i.e., foods with similar nutrient profiles can be exchanged for each other). As summarized later in this chapter, guidelines issued by other expert groups, including the American Diabetes Association (1987), the American Heart Association (AHA, 1988), the National Research Council's Committee on Diet, Nutrition, and Cancer (NRC, 1982), the U.S. Department of Agriculture and the Department of Health and Human Services (USDA/DHHS, 1985), and the U.S. Surgeon General (DHHS, 1988), are in general based on overall dietary patterns. Furthermore, epidemiologic evidence on chronic diseases pertains more often to foods or diets and less often to single nutrients or other nonnutritive substances (e.g., coffee and tea). Therefore, nutrient-based recommendations must be derived often from the epidemiologic data on dietary patterns. For example, the statement that diets with a high plantfood and low fat content are associated with reduced rates of certain cancers more accurately reflects present knowledge than do conclusions that diets high in selenium or isothiocyanates are likely to reduce cancer risk. The latter requires an inference about cause and effect that is not yet justified by the data. Recommendations about overall dietary patterns may be difficult to implement, however, if they are too general, devoid of quantification, or provide quantitative information that the average person cannot interpret. For example, the basic five food groups recommended by the USDA are represented in the average fast-food cheeseburger, but not in the desirable proportions (i.e., only a small proportion from the fruit and vegetable group, but high proportions of salt and fat). Alternatively, few people would be able to translate a recommendation to consume a ''lower-fat" diet or only "30% of calories from fat" into appropriate food choices. In light of these considerations, the committee concluded that dietary guidelines to prevent chronic diseases and improve the health of the general U.S. population should emphasize overall dietary patterns but should also incorporate relevant information about food groups, foods, and nutrients. Quantitative Versus Qualitative Recommendations The committee considered the extent to which its recommendations could be quantified. In general, its decisions were based on the strength of the evidence. The need for quantification also depended on whether dietary effects have a threshold and whether the effects seem to be linear or curvilinear in nature. Quantitative guidelines can take into account nutrient interactions, they are less susceptible to misinterpretation when translated into food choices, and they can be presented as single numbers or as ranges. Furthermore, they are more likely to result in dietary modification because they provide specific targets. The committee weighed these advantages against the possibility that specifying quantities might in some cases give the appearance of greater certainty than is justified by the evidence. Overall, the committee found the arguments for quantification compelling. Recommendations for Individuals as Opposed to Populations There are two approaches to reducing dietary risk factors for chronic diseases: the first is the individual-based approach aimed at identifying and treating individuals at high risk and the second a more global population-based or public health approach aimed at the general population (Blackburn and Jacobs, 1984; Goldbourt, 1987; Olson, 1986). These two approaches are complementary to each other (Rose, 1985; WHO, 1982). Recommendations tailored to special needs of individuals based on age, sex, physiological status (e.g., pregnancy and lactation), genetic background, and body build, as well as to special conditions such as occupational exposures and
OCR for page 668
Page 668 metabolic defects, would be ideal. Recommendations to individuals or special population subgroups could also take into consideration thresholds for nutrient requirements (e.g., upper limits or ranges of nutrient intake set to avoid deficiency or toxicity) or specify an optimal average nutrient intake over time. Recommendations suited to individual needs are desirable because every person is genetically unique, and genetic determinants influence the etiology and pathogenesis of practically all chronic diseases associated with nutritional factors. For example, high blood pressure, obesity, hyperlipidemia and atherosclerosis, and certain cancers appear to aggregate in families because of interaction of genetics and a shared environment. Public health recommendations to modify undesirable dietary patterns are unlikely to apply equally to everyone because genetic-environmental interactions as well as dietary exposures contribute to the outcome in specific individuals. For conditions such as the hyperlipidemias, we can identify some persons at high risk and concentrate specific preventive efforts in this subpopulation. For other conditions, where specific tests are lacking, a strong family history of the disease may suggest that special preventive approaches are needed. It is usually not feasible, however, to identify people at high risk or to screen the entire population. Moreover, people at only moderate or slightly increased riske.g., those with borderline-high blood cholesterol levelswill also benefit greatly from the dietary recommendations given to high-risk individuals (National Cholesterol Education Program, 1988). For most diseases, we are prevented from making individually based recommendations because of a lack of knowledge about susceptible genotypes or risks to particular individuals and about the distribution of dietary requirements in the population. Nevertheless, dietary recommendations aimed at reducing the risk in the general population can have a major benefit for the nation's health. This is because even a relatively small reduction in risk for a disease that occurs in a large number of people who are at moderate risk could lead to a larger reduction in risk for the total population than a large reduction in risk for a smaller number of people at higher risk. For example, the majority of CHD deaths occurs not among those at high risk because of high serum cholesterol levels, but in people who have only moderate elevations in serum cholesterol (i.e., <240 mg/dl; National Cholesterol Education Program, 1988). Thus, any reduction in the intake of saturated fatty acids, total fat, and cholesterol in this segment of the population could result in a large absolute decrease in CHD deaths. Similarly, for the general population, decreased salt intake may substantially reduce the risk of hypertension and a reduced fat intake may curtail the risk of certain cancers, although the effects on many individuals may be small or absent. Furthermore, although genetic factors can affect individual susceptibility, they appear to account for only a small part of the observed variation in disease incidence among populations, as exemplified by the tendency of migrants to acquire the disease rates of their adoptive countries (see Chapter 5). Thus, a major focus of any preventive strategy should be to shift the distribution of risk factors (including adverse dietary exposures) in the entire population, thereby decreasing overall disease risk. This is best accomplished through recommendations for the general population. This public health approach requires special strategies, including support of the media, the food industry, nutritionists, public health personnel, the medical profession, educators, and government. Such a policy has many merits if it is feasible to implement without harm to individuals, since it may benefit many people, is simpler to implement, and the overall costs to society are usually low. Examples of such policies in other arenas are mass vaccinations against poliomyelitis despite a wide range of genetic susceptibility to paralysis, fluoridation of the entire water supply to prevent caries despite differences in caries susceptibility (see Chapters 14 and 26), or iron fortification of cereals, even though only children and adult women are at risk of iron deficiency and such fortification may adversely affect those few with hemochromatosis (see Chapters 4 and 14). With advances in knowledge of genetic variability and its interaction with the environment, in the future we will be increasingly able to supplement general recommendations for the population with more sophisticated, individually based dietary intervention. The committee also considered the relationship between public health goals and dietary recommendations aimed at individuals. Dietary recommendations for individuals are derived almost entirely from data on benefit or risk in certain populations and thus require considerable discretion and clinical judgment in their application. Goals or guidelines for the general population attempt to consider the wide variation in the distribution of dietary or nutrient requirements in the population, but they fail to consider individual
OCR for page 669
Page 669 FIGURE 28-1 Hypothetical distribution of serum total cholesterol levels (mean ± 2 SD) in a population associated with a public health goal of 200 mg/dl. needs and are therefore not identical to guidelines for the individual. For example, the recommendation that individuals limit SFA intake to less than 10% of total calories derives mainly from evidence that populations with mean intakes of less than 10% of calories as SFA have low mean serum total cholesterol levels and are relatively free of atherosclerotic diseases. However, this recommended goal for individuals is different from the goal for a population. Figures 28-1 and 28-2 illustrate the different bases of recommendations for individuals and for the population as a whole. In the hypothetical example in Figure 28-1, serum cholesterol levels in a population range from 140 to 260 mg/dl with a mean of 200 mg/dl. This distributioni.e., the mean ± 2 standard deviations (SD)is compatible with a goal of 200 mg/dl for the general population (National Cholesterol Education Program, 1988). In contrast, Figure 28-2 shows the population serum cholesterol distribution that might be associated with a recommendation that all individuals lower their serum total cholesterol to 200 mg/dl or less. To achieve this goal (i.e., where very few individuals would have levels above 200 mg/dl) would require a much lower population average of serum total cholesterol levels (i.e., approximately 150 mg/dl). The dietary recommendations in the following section are directed to individuals, but they incorporate public health goals for the general population as well. Feasibility of Implementation Should the feasibility of implementation affect dietary recommendations? For example, if an expert committee concludes that the population would be healthier if fat consumption were reduced from an average of 40% to no more than 10% of total calories, should it consider not only the feasibility of designing nutritionally balanced diets with only 10% of calories from fat but also the FIGURE 28-2 Hypothetical distribution of serum total cholesterol levels (mean ± 2 SD) in a population associated with a public health goal that all individuals lower their serum total cholesterol to 200 mg/dl or less. The range of cholesterol levels is assumed to be narrower than that shown in Figure 28-1. feasibility of achieving such dietary change? If such a recommendation would fit within a balanced diet, it could be made in principle, despite the recognition that fat consumption would decline gradually at best and that a more readily attainable goal may encourage more change. The committee carefully considered the feasibility of designing nutritionally balanced diets based on its recommendations and, to a limited extent, the factors involved in the implementation of its recommendations. In general, however, its recommendations are based on the scientific principles described above. 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 above, 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
OCR for page 670
Page 670 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 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 calciumtwo 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. SFAs 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 SFAs; palmitic, myristic, and lauric acids have the greatest cholesterol-raising effect. The main dietary sources of these cholesterol-raising SFAs 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
OCR for page 671
Page 671 shellfish, organ meats, and, to a lesser extent, in other meats and dairy products. Thus, the intake of these foods should be curtailed. MUFAs are found in a variety of foods but are especially abundant in olive oil and canola oil. PUFAs are of two typesomega-6 and omega-3; both are essential nutrients and cannot be synthesized endogenously. Omega-6 PUFAs are common in several plant oils, including corn, safflower, soybean, and sunflower oils. Omega-3 PUFAs are found in coldwater marine fish (such as salmon and mackerel) and in some plant oils (e.g., soybean and canola oils). Omega-6 PUFAs and MUFAs (and carbohydrates) lower LDL cholesterol when substituted for saturated fatty acids. Omega-3 PUFAs also lower LDL cholesterol when substituted for SFAs, 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 CHD, the committee does not 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 CHD, 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 CHD 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 adequate iron and calcium in 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 SFA 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 MUFAs for SFAs in the diet. Larger reductions in cholesterol intakese.g., to 250 to 200 mg or even less per daymay also confer health benefits. The committee recommends that the PUFA
OCR for page 672
Page 672 intake of individuals not exceed 10% of total calories and that PUFA 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 PUFAs can be met by 1 to 2% of calories as linoleic acid.) Concern that an increase in PUFA intake may increase risk of certain cancers derives primarily from studies of animals on very-high-PUFA diets. Given the absence of human diets naturally very high in total PUFAs and the lack of information about the long-term consequences of high PUFA intake (see Chapter 7), it seems prudent to recommend that PUFA intake not be increased above the current average in the U.S. population. However, since most of the PUFAs in the 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 PUFAs, any increase in total PUFA resulting from an increase in foods containing omega-3 PUFAs (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 calorie 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 contributeto a lesser extentto 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 *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.
OCR for page 673
Page 673 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 CHD have been associated in some epidemiologic studies with diets high in meat and, as a 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 NIDDM, hypertension, CHD, 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 CHD 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
OCR for page 674
Page 674 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 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.
OCR for page 675
Page 675 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 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 SFA 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 componentssuch as egg yolks; salt; salty, smoked, and preserved foods; and alcoholic beveragesis 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. Comparison of the Committee's Recommendations with those by Other Expert Groups Recommendations to the General Population In the recent history of dietary recommendations for overall health, an expert group from Sweden, Norway, and Finland was among the first to propose in 1968 that the general population should avoid excessive caloric intake, reduce fat intake from 40 to 25-30% of calories, reduce saturated fatty acid intake while increasing dietary polyunsaturated fatty acids, reduce consumption of sugar and sugar-containing foods, and increase the consumption of vegetables, potatoes, skim milk, fish, lean meat, and cereal products (Anonymous, 1968). The next two decades were characterized by a proliferation of dietary recommendations by authoritative groups in the United States, Canada, many western European countries, Japan, Australia, and New Zealand. In the past decade alone, more than a dozen expert committees, voluntary health organizations, and government agencies in the United States have issued dietary guidelines to promote good health in general or to lower the risk of specific chronic diseases (see Table 28-1). The recommendations for general health mainte-
OCR for page 700
Page 700 TABLE 28-7 Health Impact of Major Cancers Associated with Dietary and Other Interventions in the United States in 1980a Cancer Sites Risk Factor (AR %)b Total Number of Cancer Deaths in 1980 Number of Cancer Deaths in 1980 Attributed to the Risk Factorc Lung Smoking (75.9) 67,140 50,959 Occupation (12) 10,615 1,274 Colon and Rectum Diet (20) 11,444 2,289 Breast Diet (20) 7,504 1,501 Pancreas Smoking (25.8) 5,931 1,530 Bladder Smoking (39.0 M) (16.4 F) 4,347 d Occupation (23) 2,530 582 Larynx Smoking (74) 2,552 1,888 Alcohol (16.9) 583 99 Cervix Smoking (24.1) 1,320 318 Total 113,966 % of all cancers 28 a Adapted from Amler and Dull (1987). b AR = attributable risk. c Number of attributable deaths in 1980 = attributable risk (as a percentage) x total number of cancer deaths in 1980. d Cannot calculate using combined male and female deaths. Table 28-7 provides estimates (column 2), by cancer site, of the percentage of total risk attributable to major risk factors. Multiplying these attributable risks by the total number of 1980 cancer deaths (column 3) gives the number of cancer deaths for each site (column 4) attributable to each risk factor. Although attributable risk estimates are only approximate, Table 28-7 suggests that dietary recommendations similar to those of the Committee on Diet and Health could prevent more than 2,000 deaths from colorectal cancer and approximately 1,500 from breast cancer annually. These calculations also probably underestimate the real potential of dietary change, because these apparently diet-related tumors are very rare in some populations. All these estimates about the extent of cancer attributable to diet should be interpreted cautiously, since they are based on data that are subject to considerable error and require making a number of assumptions about which opinions might reasonably differ. Overview and Summary of Risks and Benefits of Dietary Modification In summary, the committee used several approaches and various lines of evidence to assess possible adverse consequences of its dietary recommendations for the general population. For example, it examined the degree of concordance in death rates and mortality trends among the major diet-related causes of death (i.e., coronary heart disease and cancers) to determine the commonality in dietary risk factors and protective characteristics. It also analyzed the possible consequences of reducing the intake of total fat, SFAs, and cholesterolactions that would reduce serum cholesterol and CHD risk but that in some studies are also associated with increased risk of colon cancer mortality. Furthermore, it considered the effect of reducing serum total cholesterol in the population on the risk of hemorrhagic stroke in hypertensives, the possible adverse effects of increased PUFA or MUFA intake, increased carbohydrate intake, increased intake of vegetables and carotene, possible increased exposure to pesticides, moderate alcohol intake versus avoidance, and the potential for nutrient deficiency or toxicity among population subgroups. Using worst-case scenarios, the committee concluded that the potential for adverse effects (e.g., increased colon cancer risk due to a reduction in the population mean for serum total cholesterol) is minimal at best and is far outweighed by the many potential benefits. Various lines of evidence indicate that risk factors and protective factors for the major diet-related chronic diseases and causes of death run in parallel and that,
OCR for page 701
Page 701 in general, dietary intervention to reduce the risk of one disease (e.g., CHD) is likely also 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 U.S. population might be reduced by dietary modification. Because the extent to which dietary factors are involved in the etiology of different chronic diseases varies considerably (see Chapter 27), the impact of dietary modification on the risk of different diseases will also vary. The committee used several approaches for developing quantitative estimates of the expected public health impact if its dietary recommendations were to be fully adopted by the public. The accuracy of such an estimate is determined by the availability of strong, consistent, and congruent evidence from a variety of sources, especially from extensive, long-term observations of dietary interventions in human populations. Such data are most extensive for serum cholesterol levels and the risk of CHD and much less extensive for dietary factors and CHD, cancer, and other major causes of death. Estimates for the reduction in CHD risk were derived by extrapolating the effects of a downward shift in average serum cholesterol levels, by comparing CHD risk in populations with substantially different diets and mean serum cholesterol levels, and by examining the results of cholesterol-lowering trials on cardiovascular disease incidence. There are many drawbacks to using any of these approaches, as explained above. Taken together, however, these approaches strongly suggest that following the committee's recommendations for reducing intake of SFAs, cholesterol, and total fats and a consequent modest (at least 10%) reduction in serum cholesterol levels should lead to at least a 20% reduction in CHD risk in the United States beyond the 1987 levels. More stringent dietary modification provides the potential for even greater reduction in coronary disease in the future. This underestimates the 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. The committee's conclusions are generally in 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 (NRC, 1982). The data are not sufficient, however, to quantitate the contribution of diet to overall cancer risk or to determine the quantitative reduction in risk that might be achieved by dietary modifications. The committee notes that several countries (e.g., Mediterranean countries) with dietary patterns similar to those recommended here have about half the U.S. rates for diet-associated cancers (see Chapter 22). This suggests that the committee's dietary recommendations could also have a substantial impact on reducing the risk of cancers 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 dental caries), the magnitude of risk reduction expected through full implementation of the committee's guidelines on diet and health cannot be reliably estimated due to limitations in the data. Nevertheless, the committee concluded that implementation of its dietary recommendations through readily available natural diets is likely to result in considerable reductions in the overall risk of these chronic diseases without a discernible increase in the risk of any cause of death or disability. The committee also categorized dietary factors according to the strength of the evidence relating each to the risk of chronic diseases and the potential public health impact of dietary modification. In the committee's judgment, modification of the total diet along the lines of its recommendations is necessary to achieve the maximum public health benefit, and among dietary factors, modifications in the intake of total fat, SFAs, and dietary 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 society? These questions are the subject of a separate study by the Food and Nutrition Board. Therefore, these issues are considered only briefly in this report. As summarized in Tables 28-1 through 28-4, a comparison of dietary guidelines from diverse, authoritative sources in the United States and abroad suggests that scientists and public health agencies now widely agree on general nutrition principles to promote good health, but the best way to implement these principles has not been determined. It is apparent to the committee and the Food and Nutrition Board that if one of our
OCR for page 702
Page 702 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. The committee is aware that a number of efforts to implement dietary recommendations are already under way both within and outside the U.S. government. The U.S. Department of Health and Human Services, for example, has developed implementation plans to coincide with 17 priority objectives for improving nutrition during the decade 1980 to 1990. These plans include measures to improve health, reduce risk factors, increase public and professional changes in the macronutrient composition of the awareness, and improve services and surveillance(DHHS, 1983), and many of them are consistent with implementing dietary changes. Voluntary health organizations, health professionals, and the food industry are also taking actions that pertain to implementation of nutrition policies. Nevertheless, the committee wishes to draw special attention to the following general issues pertaining to implementation. A concerted effort will be needed to make changes in the food supply and in nutrition policy average U.S. diet. and programs to increase the availability of low- fat, low-saturated fat, and low-salt foods in super- markets and in public eating facilities such as school cafeterias and restaurants. Consideration may need 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 follow this report, 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 dietary recommendations for the general public and their implications 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 food and agriculture industries must also undertake additional research to identify ways of effecting dietary change. Health professionals specifically need to under- take more definitive research to determine the suitability of traditional nutrition education tools such as the Basic Four Food Guide (Page and Phipard, 1957) for use with the current recommendations and to consider new food guidance systems, such as the ones discussed by Cronin et al. (1987), that take into account the proposed The food industry has traditionally exerted a major influence on eating patterns. Although producers of meat, poultry, fats, and oils have in the past taken issue with certain dietary recommendations, they have been increasingly responsive to dietary guidance. For example, there is an increasingly wide variety of diet menus in restaurants (Burros, 1985), and the food industry has undertaken research that attempts to implement current recommendations (e.g., the production of leaner animals) and has voluntarily adopted measures to control additives and contaminants of concern. The challenge to the private sector now is to undertake more scientifically based advertising, to develop suitable educational materials, and to make more nutritionally desirable and affordable foods more widely available in grocery stores, restaurants, hospitals, and other public eating facilities. Food marketing research suggests that the public is now better informed and more intensely interested in matters pertaining to diet, chronic diseases, and health and that it actively seeks nutrition guidance (Jones and Weimer, 1981; Louis Harris & Associates, Inc., 1978, 1979; Mark Clements Research, Inc., 1980). However, food marketing surveys also demonstrate that the general public does not necessarily apply the advice it seeks. The multiple forces that compete for the public's attention in the marketplace and the absence of criteria for separating fact from fallacy underscore the need for a coordinated approach to implementing dietary recommendationsa strategy that involves cooperation among government agencies, professionals, and the private sector. It is apparent to the Food and Nutrition Board and its Committee on Diet and Health that many actions within and outside the federal government directly or indirectly influence the development and implementation of dietary recommendations. However, these actions appear fragmented, often pertain to a single disease or a single dietary recommendation, and are not necessarily consistent. Furthermore, their effectiveness is unclear. In view of these concerns, another Food and Nutrition Board committee is developing a strategy for implementing the dietary recommendations proposed in this report.
OCR for page 703
Page 703 The committee is confident that it is feasible to implement its recommendations within the framework of the current U.S. lifestyle, and it is encouraged by knowledge that dietary habits in the United States already have changed markedlyin many ways that are consistent with current recommendations. Thus, it seeks the collaboration of government agencies, the food industry, health professionals (physicians, nutritionists, dietitians, and public health personnel), educational institutions, leaders in mass media, and the general public in interpreting and implementing the proposed dietary modifications. 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 below. 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 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 concerning mechanisms of action, will lead to more definitive conclusions and provide more precise guidance about the ways to reduce the risk of different chronic diseases. With regard to macroconstituents, the committee recommends that additional research focus on the following issues. · Separating the effects of energy intake per se from those of specific sources of calories, e.g., fats, on disease risk, especially the risk of certain cancers, obesity, and noninsulin-dependent diabetes mellitus (NIDDM). · The effects of increasing the proportion of carbohydrates in the diet on CHD morbidity and mortality among individuals with diabetes. · The mechanism for regional fat accumulation, the feedback signals for regulation of fat stores, the means to modify body fat distribution, and the relative risks associated with regional fat deposits. · The role of postprandial lipoproteins and their remnants in atherogenesis and in the risk of coronary heart disease and their relationship to dietary fat intakes. · The nature and the regulation (including regulation by dietary intake) of heterogeneity within each major class of lipoproteins and the role of different lipoprotein subclasses in atherosclerosis and CHD. · The major dietary determinants of plasma HDL and the role of HDL in preventing coronary heart disease. · The mechanism whereby the type and amount of dietary fat influence different stages of carcinogenesis, e.g., PUFA (omega-3 and omega-6) and cancer risk, or MUFA intake and breast cancer risk. · The relative importance of different types of proteins (animal and vegetable) compared to different types and amounts of fats in chronic disease etiology and their mechanisms of action (e.g., in coronary heart disease, different cancers, hypertension, and stroke). · The relative effects of different types and amounts of fibers in chronic disease etiology and the mechanisms whereby they may affect serum lipid levels, CHD, different cancers, NIDDM, and gallstones. · The influence of dietary factors other than fats on serum lipids, the atherosclerotic process, and cardiovascular diseases. · The nutritional, environmental, behavioral, and genetic factors in the etiology of obesity associated with NIDDM.
OCR for page 704
Page 704 · The potential link between the intake of total carbohydrates, different types of carbohydrates, and stomach cancer. · Further identification of eating patterns that are protective against dental caries and the contributory role of sugars in the pathogenesis of caries versus the effect of fluoride in caries prevention. · The mechanisms whereby chronic alcohol ingestion increases the risk of hypertension and possibly that of breast cancer. With regard to research directions for foods and their microconstituents, the committee wishes to draw attention to the following topics. · Further identification of the constituents in plant foods (vegetables, whole-grain products, and citrus fruits) that may modify the risk of different chronic diseases and elucidation of their mechanisms of action. · The specific dietary and other environmental factors associated with vegetarian lifestyles and their relative contribution to the overall maintenance of health and reduction of the risk of specific chronic diseases. · The mechanisms whereby various ions (e.g., sodium, potassium, chloride, and possibly calcium) affect blood pressure. · The potential role of specific B vitamins in carcinogenesis and of carotenoids as potential chemopreventive agents for specific neoplasms. · The mechanism whereby vitamin E deficiency combined with a high PUFA intake may enhance carcinogenesis. · The mechanisms, other than nitrosamine-inhibition, whereby vitamin C may influence carcinogenesis and the specific effects of vitamin C versus those of other substances in plant foods that are associated with a lower cancer risk. · The potential role of calcium and vitamin D in the etiology and prevention of osteoporosis. · The relative role of different types of coffee and constituents of coffee and tea in altering cancer risk and in affecting serum cholesterol levels and heart disease risk. · Further identification of nutritive and nonnutritive dietary constituents that may cause, or protect against, various chronic diseases. · Evaluation of the carcinogenic potential of suspect carcinogens in common foods, e.g., certain mycotoxins, polycyclic aromatic hydrocarbons, and naturally occurring constituents such as flavonoids. · The effect of diet on the endogenous formation of mutagens, such as nitrosamines and fecal and urinary mutagens, and the carcinogenicity of such mutagens. 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 limit the interpretation 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 the following types of research. · Development of better methods to monitor and quantify dietary exposures in human populations. This includes improvement in food composition data for both nutritive and nonnutritive substances (especially fiber and microconstituents), methods for more frequent and long-term monitoring of dietary intake, and better methods to quantify dietary intake, especially for energy and alcohol. In particular, the methodology of USDA's Nationwide Food Consumption Surveys and the National Center for Health Statistics' Health and Nutrition Examination Surveys should be improved to permit assessment of the long-term health effects of dietary factors, both nutritive and nonnutritive. · Development of better methods for data analysis from epidemiologic studies, for example, statistical methods that take into account collinearity and multiple interactions among dietary variables and that permit simultaneous analysis of the association between specific foods, food classes and food constituents, and disease end points. · Additional techniques for assessing the mutagenic effects of chemicals on human cells in vivo and application of such techniques to assess mutagenicity of diets that are believed to present a high or a low risk for cancer. 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 of exposure misclassification
OCR for page 705
Page 705 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 further use of molecular biology techniques to study gene-nutrient interactions that can help characterize individual variability in nutrient requirements and susceptibility to various chronic diseases. The following are examples of specific topics that deserve attention. · Additional and better biochemical markers of exposure to dietary fats and early biological markers of neoplasia. · Genetic control of response to dietary fats, the interaction of genetic factors and dietary fats, and their impact on specific chronic diseases, especially cardiovascular diseases, cancer, and gallbladder disease. · The role of gene-nutrient interactions in the etiology of NIDDM, alcohol dependence, hypertension, osteoporosis, certain cancers, food intake and obesity, and dental caries. · Simpler methods for identifying high-risk groups. Quantification of the Adverse and Beneficial Effects of Diet and Determination of the Optimal Ranges of Intake of Dietary Macro- and Microconstituents 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. The following are examples of specific areas that deserve attention. · More discriminating data on the effect of the type and amount of fat on the risk of cardiovascular diseases and cancers of the breast, colon, and prostate and on the levels of fat intake associated with the maximum risk reduction. Special attention is needed to determine the effects on cancer and cardiovascular disease risk of very high intakes of polyunsaturated fats (e.g., of the kind found in fish oils) and to determine the optimal proportion of polyunsaturated, monounsaturated, and saturated fatty acids in the diet. · The optimal range of protein intake by identifying the effects of the amounts and types of protein on chronic diseases including atherosclerosis, certain cancers, hypertension and stroke, and osteoporosis. · The long-term effects of excessive protein intake on renal function in humans and its relationship to the risk of end-stage renal disease. · The role of specific amino acids or combinations of amino acids in augmenting chronic disease risk. · The nature of interaction between protein and different carcinogens in experimentally induced carcinogenesis. · The long-term effects of increasing the proportion of complex carbohydrates (starches and fibers) in the diet on the risk of, and biochemical markers for, several diseases, especially stomach and pancreatic cancers, NIDDM, and atherosclerotic cardiovascular diseases, and the specific roles of individual fibers in disease onset. · The potential beneficial or adverse effects of mild to moderate alcohol consumption on coronary heart disease risk. · The optimal range of intake of water-soluble vitamins for prevention of chronic diseases, especially cancer and liver disease at all stages of the life cycle. · Dose-response curves for trace elements with the potential for reducing chronic disease risk (e.g., selenium and copper). · Interactions among nutrients or among nutrients and other environmental risk factors at ranges of exposure that have the potential for modifying chronic disease risk. These would include interactions of physical activity, fat intake, and obesity; alcohol and vitamin A or alcohol and the B vitamins and cancer; fiber and micronutrients such as calcium, zinc, or vitamin C and various diseases; vitamin E, polyunsaturated fatty acids, and CHD; vitamin E, selenium, and cancer; sodium, potassium, and their anions, alcohol, lipids, proteins, and hypertension, or dietary electrolytes and calcium and hypertension; fluoride, the spectrum of carbohydrate intake, and dental caries; diet, phys-
OCR for page 706
Page 706 ical fitness, and blood pressure; and synergistic and antagonistic interactions among food additives, contaminants, nutrients, and cancer risk. 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 large-scale trials or whether current knowledge is sufficient to undertake interventions in the population and subsequently to assess their effectiveness by careful monitoring of 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. A few such trials (e.g., fat-reduction for breast cancer risk; a trial to examine multiple risk factors to test multiple disease end points; a trial with sodium restriction, potassium supplementation, and weight control for hypertension; b-carotene supplements for the risk of cancers of the lung, gastrointestinal tract, and cervix; increased dietary fiber for the risk of colon cancer; and especially trials that can simultaneously measure the impact of dietary modification on multiple disease end points) might be justified to obtain more definitive data, 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 enhance the availability of foods that conform to the committee's dietary recommendations. Examples of the type of research are listed below. · Comparisons of the behavior and motivations of people who have changed their food habits with those who have not. · Natural history of dietary change in humans to identify periods of vulnerability to change in eating habits. · Methods for reducing obesity and maintaining weight loss. · Methods for controlling alcohol abuse and alcohol dependence. · Methods for monitoring and evaluating the impact of dietary recommendations on chronic disease risk. · Ethnic and cultural differences in response to dietary modification and means of incorporating these differences in strategies for risk reduction. · Animal husbandry and food technology research to produce leaner animals, plant foods with less pesticide or toxic chemical residues, and a greater variety of processed foods with less fat, modified fatty acid composition, less salt, more complex carbohydrates, and less refined sugars. 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 emphasizes the need for such fundamental research to further 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. References AAP (American Academy of Pediatrics). 1983. Toward a prudent diet for children. Pediatrics 71:78-80. ACS (American Cancer Society). 1984. Nutrition and Cancer: Cause and Prevention. American Cancer Society Special Report. American Cancer Society, New York. 10 pp. ADA (American Dietetic Association). 1986. The American Dietetic Association's nutrition recommendations for women. J. Am. Diet. Assoc. 86:1663-1664.
OCR for page 707
Page 707 ADA (American Dietetic Association). 1987. Recommendations concerning supplement usage: ADA statement. J. Am. Diet. Assoc. 87:1342-1343. Ad Hoc Working Group on Coronary Prevention. 1982. Prevention of coronary heart disease in the United Kingdom. Lancet 1:846-847. AHA (American Heart Association). 1982. Rationale of the diet-heart statement of the American Heart Association: Report of Nutrition Committee. Circulation 65: 839A-854A. AHA (American Heart Association). 1983. Diet in the healthy child: task force committee of the Nutrition Committee and the cardiovascular disease in the young council of the American Heart Association. Circulation 67: 1411A-1414A. AHA (American Heart Association). 1986. Dietary guidelines for healthy American adults: a statement for physicians and health professionals by the Nutrition Committee, American Heart Association. Circulation 74:1465A-1468A. AHA (American Heart Association). 1988. Dietary guidelines for healthy American adults: a statement for physicians and health professionals by the Nutrition Committee, American Heart Association. Circulation 77:721A-724A. American Diabetes Association. 1987. Nutritional recommendations and principles for individuals with diabetes mellitus: 1986. Diabetes Care 10:126-132. American Health Foundation. 1972. Position statement on diet and coronary heart disease. Prev. Med. 1:255-286. American Health Foundation. 1979. Conference on the health effects of blood lipids: optimal distributions for populations. Prev. Med. 8:580-759. American Health Foundation. 1983. Summary and recommendations of the conference on blood lipids in children: optimal levels for early prevention of coronary artery disease. Prev. Med. 12:728-740. Amler, R.W., and H.B. Dull, eds. 1987. Closing the Gap: The Burden of Unnecessary Illness. Oxford University Press, New York. 210 pp. Beaglehole, R., M.A. Foulkes, I.A.M. Prior, and E.F. Eyles. 1980. Cholesterol and mortality in New Zealand Maoris. Br. Med. J. 280:285-287. Blackburn, H., and D. Jacobs. 1984. Sources of the diet-heart controversy: confusion over population versus individual correlations. Circulation 70:775-780. Breslow, L., and J.E. Enstrom. 1980. Persistence of health habits and their relationship to mortality. Prev. Med. 9: 469-483. Burros, M. 1985. Dining choices for healthier food. New York Times, May 11, p. 52. Byington, R., A.R. Dyer, D. Garside, K. Liu, D. Moss, J. Stamler, and Y. Tsong. 1979. Recent trends of major coronary risk factors and CHD mortality in the United States and other industrialized countries. Pp. 340-380 in R.J. Havlik, M. Feinleib, T. Thom, B. Krames, A.R. Sharrett, and R. Garrison, eds. Proceedings of the Conference on the Decline in Coronary Heart Disease Mortality. DHEW Publ. No. (NIH) 79-1610. National Heart, Lung, and Blood Institute, National Institutes of Health, Public Health Service, Department of Health, Education, and Welfare, Bethesda, Md. Callaway, C.W., K.W. McNutt, R.S. Rivlin, A.C. Ross, H.H. Sandstead, and A.P. Simopoulos. 1987. Statement on vitamin and mineral supplements. The Joint Public Information Committee of the American Institute of Nutrition and the American Society for Clinical Nutrition. J. Nutr. 117:1649. Cambien, F., P. Ducimetiere, and J. Richard. 1980. Total serum cholesterol and cancer mortality in a middle-aged male population. Am. J. Epidemiol. 112:388-394. Canadian Cancer Society. 1985. Facts on Cancer & Diet: Your Food Choices May Help You Reduce Your Cancer Risk. Canadian Cancer Society, Toronto. 23 pp. Canadian Consensus Conference on Cholesterol. 1988. Preliminary Report. A Conference on the Prevention of Heart and Vascular Disease Through Altering Serum Lipids and Lipoprotein Risk Factors, March 9-11, 1988. Government Conference Centre, Ottawa, Ontario, Canada. 16 pp. Castelli, W.P. 1979. How many drinks a day? J. Am. Med. Assoc. 242:2000. Commonwealth Department of Health/National Health and Medical Research Council. 1983. Nutrition Policy Statements. C.J. Thompson, Commonwealth Government Printer, Canberra, Australia. 39 pp. Council on Scientific Affairs. 1979. American Medical Association concepts of nutrition and health. J. Am. Med. Assoc. 242:2335-2338. Council on Scientific Affairs. 1987. Vitamin preparations as dietary supplements and as therapeutic agents. J. Am. Med. Assoc. 257:1929-1936. Cronin, F.J., A.M. Shaw, S.M. Krebs-Smith, P.M. Marsland, and L. Light. 1987. Developing a food guidance system to implement the dietary guidelines. J. Nutr. Educ. 19:281-302. Department of Health, Ireland. 1984. Guidelines for Preparing Information and Advice to the General Public on Healthy Eating. Food Advisory Committee, Department of Health, Dublin, Ireland. 26 pp. Department of National Health and Welfare, Canada. 1977. Recommendations for Prevention Programs in Relation to Nutrition and Cardiovascular Disease. Report of the Committee on Diet and Cardiovascular Diseases, Bureau of Nutritional Sciences, Health Protection Branch, Ottawa, Ontario, Canada. 46 pp. Department of National Health and Welfare, Canada. 1982. Canada's Food Guide Handbook (revised). Report of the Committee on Diet and Cardiovascular Diseases. Ottawa Supply and Services, Ottawa, Ontario, Canada. 52 pp. DHEW (U.S. Department of Health, Education, and Welfare). 1979. Healthy People: the Surgeon General's Report on Health Promotion and Disease Prevention. DHEW (PHS) Publ. No. 79-55071. Office of the Assistant Secretary for Health and Surgeon General, Public Health Service, U.S. Department of Health, Education, and Welfare. U.S. Government Printing Office, Washington, D.C. 177 pp. DHHS (U.S. Department of Health and Human Services). 1983. Public health service implementation plans for attaining the objectives for the nation: improved nutrition, summary of the problem. Public Health Reports 98:132-155. DHHS (U.S. Department of Health and Human Services). 1986. The 1990 Health Objectives for the Nation: A Midcourse Review. Office of Disease Prevention and Health Promotion, Public Health Service. U.S. Government Printing Office, Washington, D.C. 253 pp. DHHS (U.S. Department of Health and Human Services). 1987. Monthly Vital Statistics Report, Vol. 36: The Advance Report of Final Mortality Statistics, 1985. DHHS Publ. No. (PHS) 87-1120. National Center for Health
OCR for page 708
Page 708 Statistics, Public Health Service, U.S. Department of Health and Human Services, Hyattsville, Md. 48 pp. DHHS (U.S. Department of Health and Human Services). 1988. The Surgeon General's Report on Nutrition and Health. DHHS (PHS) Publ. No. 88-50210. Public Health Service, U.S. Department of Health and Human Services. U.S. Government Printing Office, Washington, D.C. 712 pp. DHSS (Department of Health and Social Security). 1984. Diet and Cardiovascular Disease. Report on Health and Social Subjects No. 28. Report of the Panel on Diet in Relation to Cardiovascular Disease, Committee on Medical Aspects of Food Policy. Her Majesty's Stationery Office, London. 32 pp. Doll, R., and R. Peto. 1981. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J. Natl. Cancer Inst. 66:1191-1308. Dupin, H., et al. 1981. Apports Nutritionnels Conseillés pour la population française. Technique et Documentation, Lavoisier, France. 101 pp. Dyer, A.R., J. Stamler, O. Paul, R.B. Shekelle, J.A. Schoenberger, D.M. Berkson. M. Lepper, P. Collette, S. Shekelle, and H.A. Lindberg. 1981. Serum cholesterol and risk of death from cancer and other causes in three Chicago epidemiological studies. J. Chronic Dis. 34:249-260. ECP/IUNS (European Organization for Cooperation on Cancer Prevention Studies/International Union for Nutritional Sciences). 1986. Proceedings of a joint ECP-IUNS workshop on diet and human carcinogenesis (Arhus, Denmark; June 1985). Nutr. Cancer 8:1-40. Farchi, G., A. Menotti, and S. Conti. 1987. Coronary risk factors and survival probability from coronary and other causes of death. Am. J. Epidemiol. 126:400-408. Finnish Heart Association. 1987. Prevention of Coronary Heart Disease in Finland. National Board of Health, National Public Health Institute, Finnish Cardiac Society. Finnish Heart Association, Helsinki, Finland. 96 pp. Food and Nutrition Council, Netherlands. 1983-1984. Food Policy Note (Nota Voedingsbeleid). Ministry of Health, Welfare, and Culture, Ministry of Agriculture, and the Ministry of Economics. The Hague. 94 pp. Garcia-Palmieri, M.R., P.D. Sorlie, R. Costas, Jr., and R.J. Havlik. 1981. An apparent inverse relationship between serum cholesterol and cancer mortality in Puerto Rico. Am. J. Epidemiol. 114:29-40. Garn, S.M., and M. LaVelle. 1985. Two-decade follow-up of fatness in early childhood. Am. J. Dis. Child. 139:181-185. German Society of Nutrition. 1985. Ten Guidelines for Sensible Nutrition. Deutsche Gesellschaft für Ernährung e.V. Frankfurt, Federal Republic of Germany. 6 pp. Goldbourt, U. 1987. High risk versus public health strategies in primary prevention of coronary heart disease. Am. J. Clin. Nutr. 45 suppl. 5:1185-1192. Goldman, L., and E.F. Cook. 1984. The decline in ischemic heart disease mortality rates. An analysis of the comparative effects of medical interventions and changes in lifestyle. Ann. Intern. Med. 101:825-836. Greenwald, P., and E.W. Sondik, eds. 1986. Cancer control objectives for the nation: 1985-2000. J. Natl. Cancer Inst. Monogr. 2:1-105. Grobstein, C. 1983. Should imperfect data be used to guide public policy? Science 83 4:18. Hakama, M., and E.A. Saxén. 1967. Cereal consumption and gastric cancer. Int. J. Cancer 2:265-268. Hardell, L., M. Eriksson, P. Lenner, and E. Lundgren. 1981. Malignant lymphoma and exposure to chemicals, especially organic solvents, chlorophenols and phenoxy acids: a case-control study. Br. J. Cancer 43:169-176. Hegsted, D.M. 1986. Serum-cholesterol response to dietary cholesterol: a re-evaluation. Am. J. Clin. Nutr. 44:299-305. Hennekens, C.H., W. Willett, B. Rosner, D.S. Cole, and S.L. Mayreut. 1979. Effects of beer, wine, and liquor in coronary deaths. J. Am. Med. Assoc. 242:1973-1974. Higginson, J., and C.S. Muir. 1979. Environmental carcinogenesis: misconceptions and limitations to cancer control. J. Natl. Cancer Inst. 63:1291-1298. Hoar, S.K., A. Blair, F.F. Holmes, C.D. Boysen, R.J. Robel, R. Hoover, and J.F. Fraumeni, Jr. 1986. Agricultural herbicide use and risk of lymphoma and soft-tissue sarcoma. J. Am. Med. Assoc. 256:1141-1147. Inter-Society Commission for Heart Disease Resources. 1970. Primary prevention of the atherosclerotic diseases. Circulation Suppl. 42:A55-A95. Inter-Society Commission for Heart Disease Resources. 1984. Optimal resources for primary prevention of atherosclerotic diseases. Circulation 70:153A-205A. Iso, H., D.R. Jacobs, Jr., D. Wentworth, J.D. Neaton, and J. Cohen. 1988. Relationship of serum cholesterol to risk of different types of stroke: 28th conference on cardiovascular disease epidemiology. CVD Epidemiol. Newsletter (AHA) 43:40. Jain, M., G.M. Cook, F.G. Davis, M.G. Grace, G.R. Howe, and A.B. Miller. 1980. A case-control study of diet and colo-rectal cancer. Int. J. Cancer 26:757-768. Japanese Ministry of Health and Welfare. 1985. Dietary Guidelines for Health Promotion, Vol. 29. Health Promotion and Nutrition Division, Health Services Bureau. Ministry of Health and Welfare, Tokyo. 6 pp. Jenkins, D.J.A. 1988. Carbohydrates (B) dietary fiber. Pp. 52-71 in M.E. Shils and V.R. Young, eds. Modern Nutrition in Health and Disease, 7th ed. Lea & Febiger, Philadelphia. Jones, J.L., and J. Weimer. 1981. Health-related food choices. Fam. Econ. Rev. Summer:16-19. Kagan, A., D.L. McGee, K. Yano, G.G. Rhoads, and A. Nomura. 1981. Serum cholesterol and mortality in a Japanese-American population: the Honolulu Heart Program. Am. J. Epidemiol. 114:11-20. Kannel, W.B., and P.A. Wolf. 1983. Epidemiology of cerebrovascular disease. Pp. 1-24 in R.W.R. Russell, ed. Vascular Disease of the Central Nervous System, 2nd ed. Churchill Livingstone, Edinburgh. Kark, J.D., A.H. Smith, and C.G. Hames. 1980. The relationship of serum cholesterol to the incidence of cancer in Evans County, Georgia. J. Chronic Dis. 33:311-322. Kelsay, J.L. 1986. Update on fiber and mineral availability. Pp. 361-372 in G.V. Vahouny and D. Kritchevsky, eds. Dietary Fiber: Basic and Clinical Aspects. Plenum Press, New York. Keys, A. 1968. Official Collective Recommendation on Diet in the Scandinavian Countries. Nutr. Rev. 26:259-263. Keys, A. 1980. Pp. 345-359 in Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Harvard University Press, Cambridge, Mass. Keys, A. 1984. Serum cholesterol response to dietary cholesterol. Am. J. Clin. Nutr. 40:351-359. Kozarevic, D., D. McGee, N. Vojvodic, T. Gordon, Z. Racic, W. Zukel, and T. Dawber. 1981. Serum cholesterol and
OCR for page 709
Page 709 mortality: the Yugoslavia Cardiovascular Disease Study. Am. J. Epidemiol. 114:21-28. Langsford, W.A. 1979. A food and nutrition policy. Food Nutr. Notes Rev. 36:100-103. Louis Harris & Associates, Inc. 1978. Health Maintenance. Pacific Mutual Life Insurance Co., Newport Beach, Calif. 88 pp. Louis Harris & Associates, Inc. 1979. The Perrier Study: Fitness in America. Great Waters of France, Inc., New York. 59 pp. LSRO (Life Sciences Research Office). 1987. Physiological Effects and Health Consequences of Dietary Fiber. Federation of American Societies for Experimental Biology, Bethesda, Md. 236 pp. MacGregor, G.A. 1985. Sodium is more important than calcium in essential hypertension. Hypertension 7:628-640. Macquart-Moulin, G., E. Riboli, J. Cornée, B. Charnay, P. Berthezène, and N. Day. 1986. Case-control study on colorectal cancer and diet in Marseilles. Int. J. Cancer 38: 183-191. Mark Clements Research, Inc. 1980. Trends in Nutrition, I. The Benchmark Survey, February, 1980. Self Magazine, New York. (various pagings) Marmot, M.G., A.M. Adelstein, N. Robinson, and G.A. Rose. 1978. Changing social-class distribution of heart disease. Br. Med. J. 2:1109-1112. Marshall, J.R., R. Priore, S. Graham, and J. Brasure. 1981. On the distortion of risk estimates in multiple exposure level case-control studies. Am. J. Epidemiol. 113:464-473. McMichael, A.J., and J.D. Potter. 1984. Parity and death from colon cancer in women: a case-control study. Comm. Health Study 8:19-25. Miller, A.B. 1978. An overview of hormone-associated cancers. Cancer Res. 38:3985-3990. Miller, A.B. 1982. Risk factors from geographic epidemiology for gastrointestinal cancer. Cancer 50 suppl. 11:2533-2540. Miller, J.Z., M.H. Weinberger, and J.C. Christian. 1987. Blood pressure response to potassium supplementation in normotensive adults and children. Hypertension 10:437-442. Miller, J.Z., M.H. Weinberger, S.A. Daugherty, N.S. Fineberg, J.C. Christian, and C.E. Grim. 1988. Blood pressure response to dietary sodium restriction in healthy normotensive children. Am. J. Clin. Nutr. 47:113-119. Molitor, G.T. 1979. National nutrition goals: how far have we come? Pp. 135-141 in M. Chou and D.P. Harmon, Jr., eds. Critical Food Issues of the Eighties. Pergamon Press, New York. NACNE (National Advisory Committee for Nutrition Education). 1983. A Discussion Paper on Proposals for Nutritional Guidelines for Health Education in Britain. Health Education Council, London. 40 pp. National Advisory Committee, New Zealand. 1982. Nutrition goals for New Zealanders. Health 34:11-12. National Cholesterol Education Program. 1988. Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Arch. Intern. Med. 148:36-69. National Heart Foundation of Australia, Committee on Diet and Heart Disease. 1979. Diet and coronary heart disease: a review. Med. J. Aust. 2:294-307. National Heart Foundation of New Zealand. 1976. Coronary Heart Disease: A Progress Report, 1976. Report by a Committee Convened by the Scientific Committee of the National Heart Foundation of New Zealand. National Heart Foundation of New Zealand, Dunedin, New Zealand. 132 pp. NCI (National Cancer Institute). 1984a. Cancer Prevention: Good News, Better News, Best News. NIH Publ. No. 842671. National Institutes of Health, Public Health Service, U.S. Department of Health and Human Services. U.S. Government Printing Office, Washington, D.C. 20 pp. NCI (National Cancer Institute). 1984b. Diet, Nutrition, and Cancer Prevention: A Guide to Food Choices. NIH Publ. No. 85-2711. National Institutes of Health, Public Health Service, U.S. Department of Health and Human Services. U.S. Government Printing Office, Washington, D.C. 52 pp. NCI (National Cancer Institute). 1987. Diet, Nutrition, and Cancer Prevention: A Guide to Food Choices. NIH Publ. No. 87-2878. National Institutes of Health, Public Health Service, U.S. Department of Health and Human Services. U.S. Government Printing Office, Washington, D.C. 39 pp. NHLBI (National Heart, Lung, and Blood Institute). 1980. Summary Report of the NHLBI Cholesterol Workshop, February 26-27, 1980. Division of Heart and Vascular Disease, National Institutes of Health. U.S. Government Printing Office, Washington, D.C. NIAAA (National Institute on Alcohol Abuse and Alcoholism). 1986. Toward a National Plan to Combat Alcohol Abuse and Alcoholism: A Report to the United States Congress. National Institutes of Health, Public Health Service, U.S. Department of Health and Human Services, Rockville, Md. 81 pp. NIH (National Institutes of Health). 1984a. Health Implications of Obesity: National Institutes of Health Consensus Development Conference Statement. Ann. Intern. Med. 103:1073-1077. NIH (National Institutes of Health). 1984b. Osteoporosis: Consensus Development Conference Statement, Vol. 5. Publ. No. 421-132:4652. National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases and the Office of Medical Applications of Research. U.S. Government Printing Office, Washington, D.C. 6 pp. NIH (National Institutes of Health). 1985. Lowering blood cholesterol to prevent heart disease: consensus conference. J. Am. Med. Assoc. 253:2080-2086. NRC (National Research Council). 1980a. Recommended Dietary Allowances. 9th ed. A Report of the Committee on Dietary Allowances, Food and Nutrition Board, Assembly of Life Sciences, National Academy of Sciences. National Academy Press, Washington, D.C. 185 pp. NRC (National Research Council). 1980b. Toward Healthful Diets. Report of the Food and Nutrition Board, Division of Biological Sciences, Assembly of Life Sciences. National Academy of Sciences, Washington, D.C. 24 pp. NRC (National Research Council). 1982. Diet, Nutrition, and Cancer. Report of the Committee on Diet, Nutrition, and Cancer, Assembly of Life Sciences, National Academy Press, Washington, D.C. 496 pp. Oliver, M.F., J.A. Heady, J.N. Morris, and J. Cooper. 1978. A co-operative trial in the primary prevention of ischaemic heart disease using clofibrate: report from the Committee of Principal Investigators. Br. Heart J. 40:1069-1118. Oliver, M.F., J.A. Heady, J.N. Morris, and J. Cooper. 1980. W.H.O. cooperative trial on primary prevention of ischaemic heart disease using clofibrate to lower serum cho-
OCR for page 710
Page 710 lesterol: mortality follow-up. Report of the Committee of Principal Investigators. Lancet 2:379-385. Olson, R.E. 1986. Mass intervention vs screening and selective intervention for the prevention of coronary heart disease. J. Am. Med. Assoc. 255:2204-2207. Page, I.H., E.V. Allen, F.L. Chamberlain, A. Keys, J. Stamler, and F.J. Stare. 1961. Dietary fat and its relation to heart attacks and strokes. Circulation 23:133-136. Page, L., and E.F. Phipard. 1957. Essentials of an Adequate Diet. Home Economics Research Report No. 3. Agricultural Research Service, U.S. Department of Agriculture. U.S. Government Printing Office, Washington, D.C. 21 pp. Pahlke, G. 1975. Dietary fat and degenerative vascular diseases. Nutr. Metab. 18:113-115. Palmer, S. 1983. Diet, nutrition, and cancer: the future of dietary policy. Cancer Res. 43 suppl. 5:2509s-2514s. Panel on Nutrition and Prevention of Diseases. 1983. Dietary guidelines and nutrition policies in Japan. Ministry of Health and Welfare, Public Health Bureau. Japan Dietetic Association, Tokyo. 168 pp. Phillips, R.L. 1975. Role of life-style and dietary habits in risk of cancer among Seventh-Day Adventists. Cancer Res. 35: 3513-3522. Reed, D., K. Yano, and A. Kagan. 1986. Lipids and lipoproteins as predictors of coronary heart disease, stroke, and cancer in the Honolulu Heart Program. Am. J. Med. 80: 871-878. Risch, H.A., M. Jain, N.W. Choi, J.G. Fodor, C.J. Pfeiffer, G.R. Howe, L.W. Harrison, K.J. Craib, and A.B. Miller. 1985. Dietary factors and the incidence of cancer of the stomach. Am. J. Epidemiol. 122:947-959. Rose, G. 1985. Sick individuals and sick populations. Int. J. Epidemiol. 14:32-38. Rose, G., and M.J. Shipley. 1980. Plasma lipids and mortality: a source of error. Lancet 1:523-526. Rose, G., H. Blackburn, A. Keys, H.L. Taylor, W.B. Kannel, O. Paul, D.D. Reid, and J. Stamler. 1974. Colon cancer and blood-cholesterol. Lancet 1:181-183. Royal Ministry of Health and Social Affairs. 1981-1982. On the Follow-up of Norwegian Nutrition Policy. Report No. 11 to the Storting (1981-1982). Oslo. 79 pp. Shapiro, L.R., P.B. Crawford, M.J. Clark, D.L. Pearson, J. Raz, and R.L. Huenemann. 1984. Obesity prognosis: a longitudinal study of children from the age of 6 months to 9 years. Am. J. Public Health 74:968-972. Sidney, S., and J.W. Farquhar. 1983. Cholesterol, cancer, and public health policy. Am. J. Med. 75:494-508. Silverberg E., and J.A. Lubera. 1988. Cancer statistics, 1988. CA Mag. 38:5-22. Swedish National Food Administration. 1981. Swedish Nutrition Recommendations. National Food Administration, Uppsala. 11 pp. Tuomilehto, J., J. Geboers, J.T. Salonen, A. Nissinen, K. Kuulasmaa, and P. Puska. 1986. Decline in cardiovascular mortality in North Karelia and other parts of Finland. Br. Med. J. 293:1068-1071. Upton, A.C. 1979. Statement on Diet, Nutrition, and Cancer. Hearings of the Subcommittee on Nutrition of the Senate Committee on Agriculture, Nutrition, and Forestry, October 2, Washington, D.C. U.S. Senate. 1977. Dietary Goals for the United States, 2nd ed. Report of the Select Committee on Nutrition and Human Needs. Stock No. 052-070-04376-8. U.S. Government Printing Office, Washington, D.C. 83 pp. USDA (U.S. Department of Agriculture). 1984. Nationwide Food Consumption Survey. Nutrient Intakes: Individuals in 48 States, Year 1977-78. Report No. 1-2. Consumer Nutrition Division, Human Nutrition Information Service, Hyattsville, Md. 439 pp. USDA (U.S. Department of Agriculture). 1987. Nationwide Food Consumption Survey. Continuing Survey of Food Intakes by Individuals. Women 19-50 Years and Their Children 1-5 Years, 4 Days, 1985. Report No. 85-4. Nutrition Monitoring Division, Human Nutrition Information Service, U.S. Department of Agriculture, Hyattsville, Md. 182 pp. USDA/DHHS (U.S. Department of Agriculture/Department of Health and Human Services). 1980. Nutrition and Your Health: Dietary Guidelines for Americans. Home & Garden Bulletin No. 228. U.S. Department of Agriculture and Department of Health and Human Services, Washington, D.C. 20 pp. USDA/DHHS (U.S. Department of Agriculture/Department of Health and Human Services). 1985. Nutrition and Your Health: Dietary Guidelines for Americans, 2nd ed. Home & Garden Bulletin No. 228. U.S. Government Printing Office, Washington, D.C. 24 pp. Waterhouse, J., C. Muir, K. Shanmugaratnam, and . Powell, eds. 1982. Cancer Incidence in Five Continents, Vol. IV. International Agency for Research on Cancer, Lyon, France. 812 pp. Westlund, K., and R. Nicolaysen. 1972. Ten-year mortality and morbidity related to serum cholesterol. Scand. J. Clin. Lab. Invest. 30 suppl. 127:1-24. WHO (World Health Organization). 1982. Prevention of Coronary Heart Disease. Report of a WHO Expert Committee. Technical Report Series No. 678. World Health Organization, Geneva. 53 pp. WHO (World Health Organization). 1987. World Health Statistics Annual 1987. World Health Organization, Geneva. 455 pp. Wilhelmsen, L., G. Berglund, D. Elmfeldt, G. Tibblin, H. Wedel, K. Pennert, A. Vedin, C. Wilhelmsson, and L. Werkö. 1986. The multifactor primary prevention trial in Göteborg, Sweden. Eur. Heart J. 7:279-288. Williams R.R., P.D. Sorlie, M. Feinleib, P.M. McNamara, W.B. Kannel, and T.R. Dawber. 1981. Cancer incidence by levels of cholesterol. J. Am. Med. Assoc. 245:247-252. Wynder, E.L., and G.B. Gori. 1977. Contribution of the environment to cancer incidence: an epidemiologic exercise. J. Natl. Cancer Inst. 58:825-832. Yaari, S., U. Goldbourt, S. Even-Zohar, and H.N. Neufeld. 1981. Associations of serum high density lipoprotein and total cholesterol with total, cardiovascular, and cancer mortality in a 7-year prospective study of 10,000 men. Lancet 1:1011-1015.
Representative terms from entire chapter: