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(Circulation. 1996;94:1795-1800.)
© 1996 American Heart Association, Inc.

Articles

Dietary Guidelines for Healthy American Adults

A Statement for Health Professionals From the Nutrition Committee, American Heart Association

Ronald M. Krauss, MD, Chair; Richard J. Deckelbaum, MD; Nancy Ernst, RD; Edward Fisher, MD; Barbara V. Howard, PhD; Robert H. Knopp, MD; Theodore Kotchen, MD; Alice H. Lichtenstein, DSc; Henry C. McGill, MD; Thomas A. Pearson, MD, PhD; T. Elaine Prewitt, DPH; Neil J. Stone, MD; Linda Van Horn, PhD, RD; Richard Weinberg, MD, Members

Key Words: AHA Medical/Scientific Statements • diet • atherosclerosis • cholesterol

	Introduction

Top Introduction Dietary Guidelines for Americans Dietary Guidelines for Children Dietary Issues Requiring Further... References

 
In 1957 the American Heart Association proposed that modification of dietary fat intake would reduce the incidence of coronary heart disease (CHD), which had become the leading cause of disability and death in the United States and other industrialized countries.¹ Since then the AHA has issued seven policy statements on diet and CHD as reliable new information has become available.^{2 3 4 5 6 7 8} In each of these statements emphasis was placed on consumption of total fat, saturated and certain unsaturated fatty acids, dietary cholesterol, and sodium because of their significant contribution to risk of CHD. Later, excessive alcohol intake was considered because of its association with hypertension, stroke, and other diseases. Such knowledge has encouraged other health organizations and the federal government to make similar recommendations.

In May 1989 representatives of nine health organizations and governmental bodies met under the aegis of the AHA, reviewed the scientific evidence, and concluded that most Americans can improve their overall health and maintain it with a few specific but fundamental dietary changes.⁹ The following guidelines are consistent with those promoted by each organization:

Eat a nutritionally adequate diet consisting of a variety of foods.

Reduce consumption of fat, especially saturated fat, and cholesterol.

Achieve and maintain an appropriate body weight.

Increase consumption of complex carbohydrates and dietary fiber.

Reduce intake of sodium.

Consume alcohol in moderation, if at all. Children, adolescents, and pregnant women should abstain.

Current AHA recommendations regarding diet and related lifestyle practices for the general population are based on evidence indicating that modification of specific risk factors will decrease incidence of CHD.⁸ These risk factors include cigarette smoking; elevated levels of plasma cholesterol, particularly low-density lipoprotein (LDL) cholesterol; low levels of high-density lipoprotein (HDL) cholesterol; increased blood pressure; diabetes mellitus; obesity, especially visceral adiposity; and physical inactivity.

To reduce the impact of these risk factors on the occurrence of CHD in the general population, in 1996 the AHA recommends the following population-wide dietary and lifestyle goals:

Elimination of cigarette smoking

Appropriate levels of caloric intake and physical activity to prevent obesity and reduce weight in those who are overweight

Consumption of 30% or less of the day's total calories from fat

Consumption of 8% to 10% of total calories from saturated fatty acids

Consumption of up to 10% of total calories from polyunsaturated fatty acids

Consumption of up to 15% of total calories from monounsaturated fatty acids

Consumption of less than 300 mg/d of cholesterol

Consumption of no more than 2.4 g/d of sodium

Consumption of 55% to 60% of calories as complex carbohydrates

For those who drink and those for whom alcohol (ethanol) is not contraindicated, consumption should not exceed 2 drinks (1 to 2 oz of ethanol) per day

	Dietary Guidelines for Americans

Top Introduction Dietary Guidelines for Americans Dietary Guidelines for Children Dietary Issues Requiring Further... References

 
In formulating the following dietary recommendations, the AHA Nutrition Committee endeavored to make them consistent with those issued by the US Dietary Guideline Committee.¹⁰ Although the AHA guidelines were developed specifically for prevention of heart and blood vessel disease, they can contribute to prevention of other diseases, including some forms of cancer, renal disease, and osteoporosis. The AHA guidelines are also consistent with current recommendations for prevention and management of diabetes.¹¹ These chronic diseases account for the majority of the morbidity and mortality in the population, highlighting the importance of providing the public with scientifically based dietary and lifestyle guidelines.

1. Eat a variety of foods.
The AHA strongly endorses consumption of a variety of foods and believes that all dietary recommendations should enable individuals to adopt eating patterns consistent with their own lifestyles and that will supply the calories, protein, essential fatty acids, carbohydrates, vitamins, minerals, and fiber needed for good health. This pattern can be achieved by eating foods from all the food groups, including fruits and vegetables; nonfat and low-fat dairy products; whole-grain breads, cereals, pasta, starchy vegetables, and beans; and lean meat, skinless poultry, and fish. The AHA recommends that healthy individuals obtain an adequate nutrient intake from foods eaten in variety, balance, and moderation. Vitamin and mineral supplements are not a substitute for a balanced and nutritious diet designed to emphasize intake of fruits, vegetables, and whole-grain foods. Excessive intake of calories, sugar, and salt should be avoided.

2. Balance food intake with physical activity and maintain or reduce weight.
Loss of excess weight and long-term maintenance of a healthy weight can improve blood lipid levels and blood pressure and reduce risk for heart disease, the most common form of diabetes, stroke, and certain cancers.¹² In many individuals with increased abdominal or visceral fat, even modest weight reduction may result in improvement in many metabolic CHD risk factors, particularly those associated with insulin resistance, including low HDL level, elevated triglyceride level, and small dense LDL.^{13 14} Successful long-term maintenance of a healthy body weight can be promoted by regular physical activity in conjunction with a diet that is limited in calories, particularly those derived from fat, and relatively rich in complex carbohydrates and fiber.^{15 16}

3. Choose a diet low in fat, saturated fatty acids, and cholesterol.
The AHA's population-wide recommendation to consume no more than 30% of total calories as fat is aimed at reducing saturated fatty acid intake and maintaining a healthy body weight. This guideline applies to the average of total calories consumed over a period of 1 week. A common misinterpretation is that the total calories must be consumed in one day, which can limit the variety of food choices in the diet.

Diets with very low total fat intake have been tested with favorable results in studies of persons at high risk, but such diets have not been demonstrated to be of value for the general population and may have adverse consequences, including potential nutrient deficiencies in certain subgroups such as children, pregnant women, and the elderly.^{17 18 19} For this reason, the AHA endorses the recommendation of the World Health Organization for a lower limit of 15% of calories as total fat.²⁰ Moreover, the AHA recommends that for the general population, the level of fat intake in the diet should be guided by emphasis on adequate consumption of fruits, vegetables, and grains; a healthy weight goal; and, as described below, dietary intake of saturated fatty acids and cholesterol appropriate to individual risk for CHD.

The AHA emphasizes restriction of saturated fatty acid intake because this is the strongest dietary determinant of plasma LDL cholesterol levels.^{21 22} Different saturated fatty acids have varying abilities to raise blood cholesterol. Total plasma and LDL cholesterol levels are mainly affected by lauric (12 carbon atoms), myristic (14 carbon atoms), and palmitic (16 carbon atoms) acids. Reduced intake of these cholesterol-raising saturated fatty acids has resulted in a reduction in plasma LDL cholesterol levels in well-controlled dietary studies. Short-chain (less than 10 carbon atoms) fatty acids and stearic acid (18 carbon atoms) have little effect on cholesterol levels.²³

Currently the AHA recommendation for the general population is that less than 10% of total calories come from saturated fatty acids. Equations developed from carefully controlled clinical studies indicate that reducing saturated fat intake from the current average intake of 12% to 14%^{21 22 23 24} of calories can lead to an average reduction of 3% to 5% in CHD risk in the population as a whole. There is, however, interindividual variation in plasma LDL cholesterol response to reduced intake of saturated fatty acids, partially influenced by genetic factors.^{25 26 27} For this reason and also because of varying CHD risk status, population-wide guidelines do not address the specific needs of all individuals. In particular, persons with elevated LDL cholesterol levels that are responsive to diet can benefit from even greater limitation of dietary saturated fatty acids, such as 7% or less of total calories. Specific dietary guidelines for persons at higher risk have been developed by the AHA and the Expert Panel of the National Cholesterol Education Program.²⁸

Because foods contain fatty acids in varying types and amounts, it is not practical to design an eating pattern that selectively eliminates or replaces one fatty acid with another. For example, food labels list total fat by category. For the purpose of designing an eating pattern, all saturated fatty acids are considered equivalent.

Reduction in caloric intake resulting from limitation of total saturated fatty acids may be beneficial for achieving and maintaining a healthy body weight. When it is appropriate to reduce plasma lipid and lipoprotein levels while maintaining caloric intake, saturated fatty acids in the diet can be replaced by either polyunsaturated or monounsaturated fatty acids,^{29 30 31 32 33 34} carbohydrates,^{35 36} or protein,³⁷ all of which have differing effects on plasma serum lipids and lipoproteins. High intakes of -6 polyunsaturated fatty acids, however, have been reported to increase risk of formation of gallstones. In addition, results of animal studies suggest that high intake of polyunsaturated fatty acids (more than 10% of calories) may promote cancer.³⁸ The AHA currently recommends that intake of -6 fatty acids be no more than 10% of total calories. -3 polyunsaturated fatty acids, derived primarily from fish, can also be substituted for dietary saturated fatty acids and as discussed below may have beneficial effects beyond those associated with lowering LDL cholesterol levels.³⁹

In recent years there has been an interest in monounsaturated fatty acids as a suitable replacement for saturated fatty acids. Although their net effect on serum lipids and lipoproteins is not much different from that of polyunsaturated fatty acids,^{30 31 32 33 34} they may have some advantages. Unlike polyunsaturates, monounsaturates are not as susceptible to oxidation, which may play a role in atherogenesis. The AHA therefore recommends a monounsaturated fatty acid intake in the range of 10% to 15% of total calories.²⁸

Another factor deserving attention is the use of trans fatty acids. Trans fatty acids found primarily in hydrogenated vegetable oils tend to raise cholesterol levels relative to their nonhydrogenated counterparts.^{40 41} This increase appears to be less than occurs with similar amounts of saturated animal fat or highly saturated vegetable oils, eg, coconut and palm kernel oils. Among the few data available, analyses using plasma or tissue levels of trans fatty acids as a measure of intake suggest that CHD risk is associated with trans fatty acids derived from animal products⁴² but not with those from hydrogenation of oils. In addition, there is no clear dose-response effect for trans fatty acid intake and CHD risk. Based on this limited information, the AHA recommends limiting trans fatty acid intake, for example, by substituting soft margarine for hard. The AHA also encourages the food industry to develop more products with reduced trans fatty acid content.

Dietary cholesterol⁴³ can increase plasma and LDL cholesterol levels and in epidemiological studies^{44 45 46 47} has been shown to be related to CHD risk independent of its effects on blood cholesterol levels. When compared with the effects of saturated fatty acids, the effects of dietary cholesterol on LDL cholesterol levels are weaker but can be substantial in some individuals. As with intake of saturated fatty acids, there is considerable interindividual variation in response to dietary cholesterol, which should be considered when making individual dietary recommendations. Currently the AHA recommends that dietary cholesterol intake be less than 300 mg/d.

4. Choose a diet with plenty of vegetables, fruits, and whole-grain products.
These foods should contribute the majority of daily energy intake—between 55% and 60% of total calories. Fruits, vegetables, whole grains, and legumes provide important vitamins, minerals, fiber, and complex carbohydrates as part of a diet moderate in total fat and low in saturated fat content.

Diets high in unrefined carbohydrates also tend to be high in both soluble and insoluble fiber. Foods rich in soluble fiber, including oats, barley, beans, soy products, guar gum, and pectin found in apples, cranberries, currants, and gooseberries can help maximize a reduction in plasma total and LDL cholesterol levels as part of a fat-modified diet.^{48 49 50} Total dietary fiber intake of 25 to 30 g/d from foods, not supplements, will help ensure an eating pattern high in complex carbohydrates and low in fat.

5. Choose a diet moderate in sugar.
The AHA encourages consumption of complex carbohydrates in the form of grains, vegetables, and legumes. Sugar intake has not been directly related to risk for cardiovascular disease, but diets high in refined carbohydrates are often high in calories and low in complex carbohydrates, fiber, and essential vitamins and minerals.

6. Use salt and sodium in moderation.
The AHA recommends that the general public consume no more than 6 grams of sodium chloride per day. This recommendation is based on the evidence for an association between dietary sodium chloride intake and blood pressure derived from a substantial number of epidemiological observations^{51 52 53 54} and clinical trials of salt restriction.^{55 56 57}

Results of therapeutic trials of sodium chloride restriction in hypertensive individuals also document modest but significant reductions in blood pressure.^{55 56 57} However, there is considerable variation among blood pressure responses to sodium chloride restriction, and there is no simple, reliable test to accurately predict salt sensitivity.

Although there is general agreement in the scientific community that salt restriction can improve blood pressure in hypertensive individuals, there are no clear data that allow definition of a desirable upper limit for salt intake. In the United States most current estimates of average sodium chloride intake range from 7.5 to 10.0 g/d. The AHA has elected to support the recommendation of the US Dietary Guideline Committee to limit sodium chloride intake to 6 g/d. However, slightly higher intakes (6.0 to 7.5 g/d) have not been demonstrated to increase cardiovascular risk or raise blood pressure in normotensive persons without other cardiovascular risk factors. The recommended guideline is an admittedly arbitrary recommendation for avoiding excessive salt intake rather than an attempt to impose low salt intake.

Based on the totality of the evidence, the AHA has concluded that the recommendation that the general public limit daily sodium chloride intake to 6 g/d is prudent and safe, will not restrict intake of other nutrients, and may have a significant impact on prevention of cardiovascular disease.

Reduced sodium intake should be only one component of a comprehensive nutritional approach to blood pressure lowering, which should also include prevention and treatment of obesity, limitation of alcohol intake, and strategies that ensure adequate intake of potassium, magnesium, and calcium.

7. If you drink, do so in moderation.
Incidence of heart disease in those who consume moderate amounts of alcohol (an average of 1 to 2 drinks per day for men and l drink per day for women) is lower than that in nondrinkers.^{58 59} However, with increased consumption of alcohol, there are increased public health dangers, such as alcoholism, hypertension, obesity, stroke, cardiomyopathy, a number of cancers, liver disease, accidents, suicides, and fetal alcohol syndrome. In addition, some persons with an inherited predisposition to a variety of metabolic conditions, such as hypertriglyceridemia, pancreatitis, and porphyria should not consume alcohol at all. For the person beginning to drink alcohol, alcohol addiction and alcoholism is a real threat, heightened by a familial predisposition to alcoholism. In consideration of these risks, the AHA concludes that it is not advisable to issue guidelines to the general population that may lead some persons to increase their intake of alcohol or start drinking if they do not already do so. The advisability of consuming alcohol in moderation (no more than 2 drinks per day) is best determined in consultation with the individual's primary care physician.

	Dietary Guidelines for Children

Top Introduction Dietary Guidelines for Americans Dietary Guidelines for Children Dietary Issues Requiring Further... References

 
The AHA emphasizes that these dietary guidelines are appropriate for children older than 2 years. Children between the ages of 2 and 5 can gradually adopt the diet habits of the family.⁶⁰ The Recommended Dietary Allowances for iron, zinc, calcium, and other nutrients essential for growth and development can easily be met using these guidelines. Children should eat foods from all food groups, including lean meats, low-fat dairy products, whole-grain enriched cereal products, fruits, vegetables, and legumes. The primary emphasis of diets for children is on providing adequate calories and nutrients for normal physical activity, growth, and development. This recommendation can easily be achieved while following these dietary guidelines.

	Dietary Issues Requiring Further Research

Top Introduction Dietary Guidelines for Americans Dietary Guidelines for Children Dietary Issues Requiring Further... References

 
In formulating these guidelines for dietary and lifestyle practices for reduction of cardiovascular disease risk in the general population, the AHA Nutrition Committee has attempted to limit its recommendations to those for which the body of scientific evidence provides adequate support. However, there are a number of additional dietary and nutritional factors potentially related to cardiovascular risk for which the available data are thought to be insufficient for the committee to recommend specific guidelines. These issues are briefly summarized below. The committee will prepare more detailed statements on these issues and will update its dietary guidelines to include recommendations on these issues when additional research findings allow a consensus to be reached.

Antioxidant Vitamin Supplements
There is considerable current interest in the use of supplemental antioxidant vitamins E, C, and A as a result of epidemiological observations suggesting a link between increased intake and decreased cardiovascular disease risk.⁶¹ These observational studies do not prove a cause-and-effect relationship. Moreover, supplementation with such vitamins poses both potential hazards at worst and undocumented efficacy at best. The AHA recommends that antioxidant vitamins and other nutrients be derived from foods in the context of a diet low in saturated fat.

Vitamins Affecting Homocysteine Levels
Interest in folic acid and vitamins B6 and B12 has been awakened because of their effects on the metabolism of homocyst(e)ine.⁶² Elevated homocyst(e)ine in plasma has a strong epidemiological association with CHD, peripheral vascular, and cerebrovascular disease. As with other vitamin supplements, no clinical trials have tested whether there is a clinical benefit to reduced homocysteine levels through increased intake of folic acid, B6, or B12.

Very Low-Fat Diets and Fat Substitutes
Diets in which less than 15% of calories are derived from fat have been advocated by some. There is little information about the potential value of such diets for the US population, and their consumption requires major lifestyle changes. This poses concern, particularly for healthy children and older persons, for whom other nutrient needs may be compromised by excessive restriction of fat. Moreover, in some persons reduced-fat, high-carbohydrate diets result in potentially adverse metabolic changes, including reduced HDL cholesterol and increased triglyceride levels.¹⁹ Therefore, the AHA believes that there is no justification to recommend widespread consumption of very low-fat diets.

The AHA recognizes that there may be a place for fat substitutes in the diet, but in the absence of evidence for overall health benefits, it discourages the use of these products. This is particularly true for children, who are encouraged to develop a taste for fruits, vegetables, and whole-grain foods rather than relying on foods containing fat or sugar substitutes and that are often of little nutritional value. There is also concern that in persons of all ages, emphasis on reduced-fat foods may override attention to total caloric intake, thereby contributing further to the rising incidence of obesity in this country.

-3 Fatty Acids Supplementation
High intake of -3 fatty acids at levels that can be achieved only by the use of supplements can reduce plasma levels of triglyceride-rich lipoproteins, with generally only a minor and variable effect on LDL cholesterol level. These fatty acids may influence atherogenesis by mechanisms other than their effects on lipoproteins,⁶³ such as altering thrombosis or reducing immune response. The AHA does not recommend the use of -3 fatty acid supplements because their long-term benefits have not been demonstrated, and such a practice may replace overall adherence to the recommended diet. The AHA recommends including fish in the diet because fish is a natural source of -3 fatty acids and is relatively low in saturated fatty acids.

Soy Protein
Data are accumulating that indicate that when soy protein is substituted for animal protein, total LDL cholesterol can be reduced.⁶⁴ This is not a consistent finding across all subgroups. Other recent studies have suggested that the phytoestrogen content of soybeans may contribute to lipid lowering and other cardiovascular effects. Further studies of those effects are under way. The use of soy protein, soy oil, and other soy products within the context of low total and saturated fatty acid intake is consistent with the AHA dietary guidelines, but further research is needed to test potential risks of high intake before a specific guideline can be developed.

Genetic Factors Affecting Dietary Response
There is emerging evidence that interindividual variation of certain responses to diet, such as reduction in LDL cholesterol with diets low in fat and cholesterol or the effects of weight-loss diets, may be related in part to underlying genetic influences.⁶⁵ Differences in responses to diet in different populations may also be important in designing specific guidelines in certain populations. As these influences become more specifically and clearly defined by ongoing research and as testing becomes available, individualized dietary and lifestyle recommendations may provide more effective approaches to prevention of CHD.

	Footnotes

 
Requests for reprints should be sent to the Office of Scientific Affairs, American Heart Association, 7272 Greenville Ave, Dallas, TX 75231-4596.

"Dietary Guidelines for Healthy Americans" was approved by the American Heart Association Science Advisory and Coordinating Committee on June 20, 1996.

	References

Top Introduction Dietary Guidelines for Americans Dietary Guidelines for Children Dietary Issues Requiring Further... References

 

1. Page IH, Stare FJ, Corcoran AC, Pollack H, Wilkinson CF Jr. Atherosclerosis and the fat content of the diet. JAMA. 1957;164:2048-2051.
   
2. Dietary fat and its relation to heart attacks and strokes: report by the Central Committee for Medical and Community Program of the American Heart Association. Circulation.. 1961;23:133-136.[Free Full Text]
   
3. American Heart Association. Diet and Heart Disease. New York, NY: American Heart Association; 1965.
   
4. American Heart Association. Diet and Heart Disease. New York, NY: American Heart Association; 1968.
   
5. American Heart Association. Diet and Coronary Heart Disease. New York, NY: American Heart Association; 1973.
   
6. American Heart Association. Diet and coronary heart disease: a statement for physicians and other health professionals. Circulation.. 1978;54:762A-766A.
   
7. American Heart Association. Dietary guidelines for healthy American adults: a statement for physicians and health professionals by the Nutrition Committee. Circulation.. 1986;74:1465A-1468A.
   
8. American Heart Association. Dietary guidelines for healthy American adults: a statement for physicians and health professionals by the Nutrition Committee. Circulation.. 1988;7:721A-724A.
   
9. American Heart Association. The healthy American diet. Circulation. 1991;82:1079.[Medline] [Order article via Infotrieve]
   
10. US Dietary Guideline Committee, US Department of Agriculture, US Department of Health and Human Services. Nutrition and Your Health: Dietary Guidelines for Americans. 4th ed. 1995. Home & Garden Bulletin 232.
    
11. Franz MJ, Horton ES Sr, Bantle JP, Beebe CA, Brunzell JD, Coulston AM, Henry RR, Hoogwerf BJ, Stacpoole PW. Nutrition principles for the management of diabetes and related complications. Diabetes Care. 1994;17:490-518.[Medline] [Order article via Infotrieve]
    
12. Stunkard AJ. Current views on obesity. Am J Med. 1996;100:230-236.[Medline] [Order article via Infotrieve]
    
13. Blackburn G. Effect of degree of weight loss on health benefits. Obes Res. 1995;3(suppl 2):211s-216s.
    
14. Goldstein DJ. Beneficial health effects of modest weight loss. Int J Obes Relat Metab Disord. 1992;16:397-415.[Medline] [Order article via Infotrieve]
    
15. Blair SN. Evidence for success of exercise in weight loss and control. Ann Intern Med. 1993;119:702-706.[Abstract/Free Full Text]
    
16. Grilo CM. Physical activity and obesity. Biomed Pharmacother. 1994;48:127-136.
    
17. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA, McLanahan SM, Kirkeeide RL, Brand RJ, Gould KL. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet. 1990;336:129-133.[Medline] [Order article via Infotrieve]
    
18. Gould KL, Ornish D, Scherwitz L, Brown S, Edens RP, Hess MJ, Mullani N, Bolomey L, Dobbs F, Armstrong WT, et al. Changes in myocardial perfusion abnormalities by positron emission tomography after long-term, intense risk factor modification. JAMA. 1995;274:894-901.[Abstract]
    
19. Schaefer EJ, Lichtenstein AH, Lamon-Fava S, McNamara JR, Schaefer MM, Rasmussen H, Ordovas JM. Body weight and low-density lipoprotein cholesterol changes after consumption of a low-fat ad libitum diet. JAMA. 1995;274:1450-1455.[Abstract]
    
20. Food and Agriculture Organization. Fats and Oils in Human Nutrition: Report of a Joint Expert Consultation (WHO.FAO). 1994. FAO Paper 57.
    
21. Keys A, Anderson JT, Grande F. Serum cholesterol response to changes in the diet, IV: particular saturated fatty acids in the diet. Metabolism. 1965;14:776-787.
    
22. Hegsted DM, McGandy RB, Myers ML, Stare FJ. Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr. 1965;17:281-295.[Medline] [Order article via Infotrieve]
    
23. Hegsted DM, Ausman LM, Johnson JA, Dallal GE. Dietary fat and serum lipids: an evaluation of the experimental data. Am J Clin Nutr. 1993;57:875-883. Correction in Am J Clin Nutr 1993;58:245.[Abstract/Free Full Text]
    
24. Keys A, Anderson JT, Grande F. Prediction of serum cholesterol responses of man to change in fats in the diet. Lancet. 1957;2:959-966.
    
25. Brown MS, Goldstein JL. A receptor-mediated pathway for cholesterol homeostasis. Science. 1986;232:34-47.[Free Full Text]
    
26. Mahley RW, Weisgraber KH, Innerarity TL, Rall SC Jr. Genetic defects in lipoprotein metabolism: elevation of atherogenic lipoproteins caused by impaired catabolism. JAMA. 1991;265:78-83.[Abstract]
    
27. Heller DA, de Faire U, Pedersen NL, Dahlen G, McClearn GE. Genetic and environmental influences on serum lipid levels in twins. N Engl J Med. 1993;328:1150-1156.[Abstract/Free Full Text]
    
28. National Cholesterol Education Program. Second report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). Circulation. 1994;89:1333-1445.[Medline] [Order article via Infotrieve]
    
29. Howard BV, Hannah JS, Heiser CC, Jablonski KA, Paidi MC, Alarif L, Robbins DC, Howard WJ. Polyunsaturated fatty acids result in greater cholesterol lowering and less triacylglycerol elevation than do monounsaturated fatty acids in dose-response comparison in a multiracial study group. Am J Clin Nutr.. 1995;62:392-402.[Abstract/Free Full Text]
    
30. Mensink RP, Katan MB. Effect of a diet enriched with monounsaturated or polyunsaturated fatty acids on levels of low-density and high-density lipoprotein in healthy women and men. N Engl J Med. 1989;321:436-441.[Abstract]
    
31. Dreon DM, Uranizan KM, Krauss RM, Austin MA, Wood PD. The effects of polyunsaturated fat vs monounsaturated fat on plasma lipoproteins. JAMA. 1990;263:2462-2466.[Abstract]
    
32. Grundy SM, Denke MA. Dietary influences on serum lipids and lipoproteins. J Lipid Res. 1990;31:1149-1172.[Abstract]
    
33. Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins: a meta-analysis of 27 trials. Arterioscler Thromb. 1992;12:911-919.[Abstract/Free Full Text]
    
34. Ginsberg HN, Barr SL, Gilbert A, Karmally W, Deckelbaum R, Kaplan K, Ramakrishnan R, Holleran S, Dell RB. Reduction of plasma cholesterol levels in normal men on an American Heart Association Step I diet or a Step II diet with added monounsaturated fat. N Engl J Med. 1990;322:574-579.[Abstract]
    
35. Ullmann D, Connor WE, Hatcher LF, Connor SL, Flavell DP. Will a high-carbohydrate, low-fat diet lower plasma lipids and lipoproteins without producing hypertriglyceridemia? Arterioscler Thromb. 1991;11:1059-1067.[Abstract/Free Full Text]
    
36. Frayn KN, Kingman SM. Dietary sugars and lipid metabolism in humans. Am J Clin Nutr. 1995;62(suppl):250S-263S.
    
37. Carroll KK. Review of clinical studies on cholesterol-lowering response to soy protein. J Am Diet Assoc. 1991;91:820-827.[Medline] [Order article via Infotrieve]
    
38. Welsch CW. Relationship between dietary fat and experimental mammary tumorigenesis: a review and critique. Cancer Res. 1992;52(suppl):2040S-2048S.
    
39. Connor WE, DeFrancesco CA, Connor SL. N-3 fatty acids from fish oil: effects on plasma lipoproteins and hypertriglyceridemic patients. Ann N Y Acad Sci. 1993;638:16-34.
    
40. Feldman EB, Kris-Etherton PM, Kritchevsky D, Lichtenstein A, for the ASCN/AIN Task Force on Trans Fatty Acids of the American Society for Clinical Nutrition and American Institute of Nutrition. Position paper on trans fatty acids. Am J Clin Nutr. 1996;63:663-670.[Abstract/Free Full Text]
    
41. Report of the Expert Panel on Trans Fatty Acids and Coronary Heart Disease. Trans fatty acids and coronary heart disease risk. Am J Clin Nutr. 1995;62(suppl):655S-708S.
    
42. Wahle KWJ, James WPT. Isomeric fatty acids and human health. Eur J Clin Nutr. 1993;47:828-839.[Medline] [Order article via Infotrieve]
    
43. Stamler J, Shekelle R. Dietary cholesterol and human coronary heart disease: the epidemiologic evidence. Arch Pathol Lab Med. 1988;112:1032-1040.[Medline] [Order article via Infotrieve]
    
44. Shekelle RB, Shryock AM, Paul O, Lepper M, Stamler J, Liu S, Raynor WJ Jr. Diet, serum cholesterol, and death from coronary heart disease: the Western Electric study. N Engl J Med. 1981;304:65-70.[Abstract]
    
45. Kushi LH, Lew RA, Stare FJ, Ellison CR, el Lozy M, Bourke G, Daly L, Graham I, Hickey N, Mulcahy R, et al. Diet and 20-year mortality from coronary heart disease: the Ireland-Boston diet-heart study. N Engl J Med. 1985;312:811-818.[Abstract]
    
46. Kromhout D, Coulander CD. Diet, prevalence and 10-year mortality from coronary heart disease in 871 middle-aged men: the Zutphen study. Am J Epidemiol. 1984;119:733-741.[Abstract/Free Full Text]
    
47. McGee DL, Reed DM, Yano K, Kagan A, Tillotson J. Ten-year incidence of coronary heart disease in the Honolulu Heart Program: relationship to nutrient intake. Am J Epidemiol. 1984;119:667-676.[Abstract/Free Full Text]
    
48. Bell LP, Hectorn KJ, Reynolds H, Hunninghake DB. Cholesterol-effects of soluble-fiber cereals as part of a prudent diet for patients with mild to moderate hypercholesterolemia. Am J Clin Nutr. 1990;52:1020-1026.[Abstract/Free Full Text]
    
49. Whyte JL, McArthur R, Topping D, Nestel P. Oat bran lowers plasma cholesterol levels in mildly hypercholesterolemic men. J Am Diet Assoc. 1992;92:446-449.[Medline] [Order article via Infotrieve]
    
50. Ripsin CM, Keenan JM, Jacobs DR Jr, Elmer PJ, Welch RR, Van Horn L, Liu K, Turnbull WH, Thye FW, Kestin M, et al. Oat products and lipid lowering: a meta-analysis. JAMA. 1992;267:3317-3325. Correction in JAMA. 1992;268:3074.[Abstract]
    
51. He J, Tell GS, Tang Y-C, Mo P-S, He G-Q. Relation of electrolytes to blood pressure in men: the Yi people study. Hypertension. 1991;17:378-385.[Abstract/Free Full Text]
    
52. Stamler J, Rose G, Elliott P, Dyer P, Marmot M, Kesteloot H, Stamler R. Findings of the International Cooperative INTERSALT Study. Hypertension. 1991;17(suppl I):I-9-I-15.
    
53. Elliott P, Stamler J, Nichols R, Dyer AR, Stamler R, Kesteloot H, Marmot M, for the Intersalt Cooperative Research Group. Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. BMJ. 1996;312:1249-1253.[Abstract/Free Full Text]
    
54. Law MR, Frost CD, Wald NJ. By how much does dietary salt reduction lower blood pressure? I: analysis of observational data among populations. BMJ. 1991;302:811-815.
    
55. Australian National Health and Medical Research Council Dietary Salt Study Management Committee. Fall in blood pressure with modest reduction in dietary salt intake in mild hypertension. Lancet. 1989;1:399-402.[Medline] [Order article via Infotrieve]
    
56. Cutler JA, Follmann D, Elliott P, Suh I. An overview of randomized trials of sodium reduction and blood pressure. Hypertension. 1991;17(suppl I):I-27-I-33.
    
57. Midgley JP, Matthew AG, Greenwood CM, Logan AG. Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. JAMA. 1996;275:1590-1597.[Abstract]
    
58. Klatsky AL, Armstrong MA, Friedman GD. Alcohol and mortality. Ann Intern Med. 1992;117:646-654.
    
59. Steinberg D, Pearson TA, Kuller LH. Alcohol and atherosclerosis. Ann Intern Med. 1991;114:967-976.
    
60. American Academy of Pediatrics. National Cholesterol Education Program: report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents. Pediatrics. 1992;89(3, pt 2):525-584.
    
61. Jha P, Flather M, Lonn E, Forkouh M, Yusuf S. The antioxidant vitamins and cardiovascular disease: a critical review of epidemiologic and clinical trial data. Ann Intern Med. 1995;123:860-872.[Abstract/Free Full Text]
    
62. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease: probable benefits of increasing folic acid intakes. JAMA. 1995;274:1049-1057.[Abstract]
    
63. Harris WS. Fish oils and plasma lipid and lipoprotein metabolism in humans: a critical review. J Lipid Res. 1989;30:785-807.[Abstract]
    
64. Messena M, Erdman JW Jr, eds. First international symposium on the role of soy in preventing and treating chronic disease. J Nutr. 1995;125(suppl):567s-808s.
    
65. Dreon DM, Krauss RM. Gene-diet interactions in lipoprotein metabolism. In: Lusis AJ, Potter JI, Sparks RS, eds. Molecular Genetics of Coronary Heart Disease and Stroke. Basel, Switzerland: Karger; 1992;14:325-349.
    

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