Can We Prevent Atherosclerotic Disease? Yes.
Disclosure:Dr. Kuller has no conflicts.
Pub Date: Monday, March 2, 2009
Author: Lewis Kuller, MD, DrPH
Implementing nutrition guidelines for the pediatric and adult populations provides a structure for new efforts to reduce cardiovascular disease (CVD) by modifying the diet of both the pediatric and adult populations. We have a long legacy of documents and proposals for modifying diet and other risk factors to reduce coronary heart disease (CHD) and stroke. In a 1971 report, Stamler noted that the prevalence of CVD was very high and required action. "Wisdom and responsibility call for widespread professional implementation now of reasonable, safe nutritional-hygienic approaches to primary prevention." The 1966 paper by Brown and Farrand, two eminent nutritionists, noted that the key to an adequate diet for serum cholesterol reduction was the proper selection of fat-containing products resulting in a diet that was low in saturated fat and high in polyunsaturated fat. The 1968 report from the National Diet Heart Study was a major advance for approaches to reducing blood cholesterol levels.
In 1978, Henry Blackburn documented that mass hyperlipidemia in the population is the primary requisite for mass atherosclerosis, manifested as premature CVD, disability, and death. A diet high in saturated fat and cholesterol was the cause of the mass hyperlipidemia. The great potential for preventing atherosclerosis would not be realized unless programs involved the entire population, including children. He recommended changes in national dietary goals that affected cultural and personal eating patterns, as well as public and professional health education on a national basis. Specifically, he recognized that atherosclerosis was caused by a common source epidemic due to the adverse diet that required not only mass health education but also changes in food production.
The implementation of current nutrition guidelines, as noted in the report, "Implementing American Heart Association Pediatric and Adult Nutrition Guidelines," requires: (a) a healthy food environment, (b) marketing of nutrition to counterbalance unhealthy food messages, (c) empowering consumers, and (d) trained professionals to create a food-, nutrition-literate society.
The choices of foods in a population are driven to a considerable degree by social changes over time, such as the impact of two-parent employed families, migration to suburbia with long commutes and limited leisure time, the decrease in job-related energy expenditure, and much greater availability of high calorically dense snack foods that can be mass produced at low cost. These factors have clearly contributed to changes in the American diet and, especially, the increase in obesity. Dietary interventions cannot succeed without a broader understanding of the impact of these important social changes over time and, especially, how they impact less educated and low socioeconomic populations that are at higher risk of CVD. Eating is now our number one social outlet. Each meal cannot be treated as a "therapeutic challenge." The report stresses approaches to change eating behavior.
Animal experimental studies of diet and atherosclerosis, cross cultural and longitudinal epidemiologic studies, and clinical trials of both diet and several types of lipid lowering drugs have substantiated the relationship between dietary saturated fat and cholesterol and poly- and monounsaturated fats, and have substantiated the development and extent of atherosclerosis and risk of CHD.[6-8] There is a strong linear relationship, for example, between the amount of low-density lipoprotein (LDL) cholesterol lowering and the reduction of risk of CHD.
Over the past 40 years there have been substantial changes in the American diet, with a reduction in saturated fat, probably from about 18% to 10% or 11% in dietary cholesterol. This led to reduction in blood total and LDL cholesterol in the population. This has contributed to the remarkable decline in CHD morbidity and mortality. Higher caloric intake has led to the epidemic of obesity, the leveling off in the reduction in blood cholesterol levels, increased prevalence of hypertension [10,11] and a flattening of the decline in CHD mortality, especially in younger age groups. The continued very high salt intake of the American diet due primarily to the amount of salt added to processed food is a major contributor to the very high prevalence of hypertension. Numerous studies have shown that the reduction of sodium in diet decreased blood pressure (BP) levels, prevented hypertension, and decreased mortality.[13-15]
Unfortunately, emphasis on the diet to reduce CHD and stroke has lost its focus both in public health and clinical medicine communities. The diet-heart hypothesis and the importance of blood LDL cholesterol or apolipoprotein-B (ApoB) has been questioned wrongly both in the lay press and by clinical investigators.
CHD is not primarily an inflammatory disease. Inflammation is important but only in the context of the diet-atherosclerosis and elevated LDL cholesterol, ApoB, and other risk factors. Modest attempts to change the diet, especially in adults, such as in the Women’s Health Initiative (WHI), have had little effect on LDL cholesterol and therefore, on the risk of CHD, further raising a red flag about the importance of diet without recognizing that the basic problem is the failure to substantially modify the diet, not the lack of the effects of diet on lipid levels or atherosclerosis. The failure of some recent lipid lowering drug trials to reduce CHD or the extent of atherosclerosis has unfortunately provided misguided ammunition for putting dietary approaches for the prevention of atherosclerosis and CHD on the back burner and led investigators to suggest that the diet-heart relationship remains an unproven hypothesis.
It is extremely difficult to further lower the amount of saturated fat within the American diet or the amount of salt without major changes in food production and shifts in their availability to the population. New genetic approaches have led to the misinterpretation that we will soon be able to identify a substantial segment of the population that is susceptible, as well as nonsusceptible individuals, to the risk of CHD and subsequently limit our dietary recommendations to the susceptibles only. Grocery stores for those susceptible to high saturated fat diets or too high salt intake (i.e., salt sensitivity and nonsensitivity) are extremely unlikely. Genetic host susceptibility in relationship to the diet is clearly of considerable importance in determining the results in both the LDL or ApoB cholesterol levels and the relationship between diet, lipoprotein levels, extent of atherosclerosis, and subsequent risk of CHD. Clinical guidelines for the treatment of high-risk factors such as using the Framingham risk score have arbitrarily defined an at-risk LDL cholesterol level(s) without recognizing that the relationship between lipoproteins and atherosclerosis or CHD risk is continuous from relatively low cholesterol levels. These guidelines have unfortunately focused on individuals at high risk and with extensive atherosclerosis and lost the emphasis on a population approach for reducing risk factors and CV morbidity and mortality.[19,21]
Steinberg noted that "the long-standing controversy over the validity of the lipid hypothesis of atherosclerosis has been settled." The basic problem, however, is that aggressive interventions using drugs such as statins to lower LDL cholesterol, especially among older individuals or those at very high risk, are very effective but still do not reduce the CV incidence to the same levels of those found in very low risk populations such as in Japan. The basic problem, they note, is the need for more aggressive efforts to lower lipid levels, especially at an earlier age to prevent the development of the atherosclerotic lesions.[22,23]
The following proposal for implementing the AHA Pediatric Adult Nutrition Guidelines should provide a template for a much more aggressive effort to prevent CHD:
- LDL cholesterol or ApoB levels, high BP, cigarette smoking, obesity, and type II diabetes are the primary determinants of the risk of CHD.
- Elevated blood LDL cholesterol and higher BP and diabetes are examples of common source diet epidemics. The common sources are the availability and amount of specific foods in the American diet, high salt intake, high intake of saturated fat and trans fatty acids, lower intake of polyunsaturated fats ,and higher caloric intake. This results in elevated LDL cholesterol and especially ApoB or LDL particles, elevated BP due to high salt consumption from processed foods and the excess caloric intake resulting in obesity and diabetes.
- Clinical CHD is a preventable disease. Populations and individuals with low blood cholesterol, low BP, no diabetes, and noncigarette smoking have very low risk of CHD and stroke and low total mortality. It is not our lack of knowledge of the determinants of CVD but primarily a lack of implementation of what we know.
- Future substantial reductions of CVD morbidity and mortality in the United States and reduction in health care costs due to these diseases is feasible now with implementation of the recommendations as proposed in these guidelines. The continued higher incidence of CVD in the United States is due in large part to our continued failure to implement an effective prevention program based on current knowledge.
- The primary disease of interest is atherosclerosis. This disease begins in childhood, is directly related to the level of LDL cholesterol, ApoB, or LDL particles, and BP levels.[25,26] Individuals will vary in response to their diet LDL cholesterol, ApoB, or LDL particle levels and to the extent of atherosclerosis. This is due to both genetic and host susceptibility and other lifestyle factors. Further research to identify protective factors in the diet, such as in the Mediterranean diet in southern Europe , high omega-3 polyunsaturated as found in the Japanese population , or plant-based diets  should have high priority so as to maximize the prevention of atherosclerosis in the population.
- Common source epidemics require that the environment, (i.e., the food sources) must be modified. Collaboration and a close working relationship with the food industry are absolutely imperative, as noted in this report and also, many years ago, by the first nutrition committee of the AHA, chaired by the late Dr. Ed Bierman. Collaboration with governmental agencies with impact on the food industry, such as the U.S. Department of Agriculture, the Food and Drug Administration, the Department of Education, and the Department of Health and Human Services, is also very important.
- Individual-based interventions to reduce LDL cholesterol levels, BP levels, or obesity have difficulty in demonstrating major long-term reductions in risk factors. The short-term changes are often lost when the behavioral, nutritional efforts are reduced or even stopped. Thus, short-term studies (i.e., 6 months, 1 year, 2 years, etc.) are probably of very limited value. The implementation, therefore, of individualized or even group interventions should probably be limited to higher risk individuals, especially younger and middle-aged individuals with elevated risk factors and/or genetic risk [30,31] who are interested in making lifelong commitments to substantial dietary changes. Further research to improve the delivery and implementation of these guidelines, as noted, especially at lower cost using modern technologies such as the Internet, which can be shown to have substantial effectiveness in reducing the risk factors, should have a high priority.
- Prevention of atherosclerosis through implementation of nutritional guidelines as recommended in this report in both children and adults will have no impact unless voluntary agencies such as the AHA, public health agencies, and the National Institutes of Health, for example, recognize that CHD is a preventable disease. The primary prevention of atherosclerosis in the population must have a high priority. Common source epidemics generally involve the entire population. The high risk and treatment approaches alone, although successful, have less impact on substantially reducing CHD morbidity and mortality.
A much greater commitment to nutritional research is needed, especially the evaluation of other foods that may modify both the lipoprotein levels and the extent of atherosclerosis. The role of specific nutrients on the conversion of atherosclerotic disease to clinical CAD (i.e., thrombogenesis, plaque characteristics, etc.) beyond saturated and trans fatty acids, polyunsaturated fat, and total cholesterol should also be a high priority.
The message must be that atherosclerosis is preventable, that elevated LDL, ApoB, or LDL particles, smoking, hypertension, diabetes, obesity, and lack of physical activity are the primary determinants of the evolving atherosclerotic disease. The focus on prevention of atherosclerosis now and the elimination of severe atherosclerosis in future generations should be the highest priority, and these new recommended guidelines can be a template for national public health and clinical preventive medicine programs in the United States and in other countries. We have succeeded in the past in substantially reducing the saturated fat and cholesterol in the American diet and blood cholesterol levels. A new population level of blood cholesterol should be the goal (i.e. 160 to 180 mg/dL), obtainable based on the recommendations in the report to reduce the prevalence of the obesity, bring about a decline in BP levels, and prevent hypertension in children and adults.
- Gidding SS, Lichtenstein AH, Faith MS, et al. Implementing American Heart Association pediatric and adult nutrition guidelines: a scientific statement from the American Heart Association Nutrition Committee of the Council on Nutrition, Physical Activity and Metabolism, Council on Cardiovascular Disease in the Young, Council on Arteriosclerosis, Thrombosis and Vascular Biology, Council on Cardiovascular Nursing, Council on Epidemiology and Prevention, and Council for High Blood Pressure Research. Circulation. 2009;119:1161-1175.
- Stamler J. Acute myocardial infarction--progress in primary prevention. Br Heart J 1971;33:163.
- Brown HB, Farrand ME. Pitfalls in constructing a fat-controlled diet. J Am Diet Assoc 1966;49:303-308.
- National Diet-Heart Study Research Group with the Approval of the Executive Committee on Diet and Heart Disease. The National Diet-Heart Study Final Report. Circulation 1968;37:I1-428.
- Blackburn H. How nutrition influences mass hyperlipidemia and atherosclerosis. Geriatrics 1978;33:42-46.
- McGill HC, McMahan A, Gidding SS. Preventing heart disease in the 21st century. Implications of the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study. Circulation. 2008;117:1216-1227.
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- O’Keefe JH, Jr., Cordain L, Harris WH, et al. Optimal low-density lipoprotein is 50 to 70 mg/dl. Lower is better and physiologically normal. J Am Coll Cardiol 2004;43:2142-2146.
- Schober SWE, Carroll MD, Lacher DA, Hirsch R. High serum total cholesterol-an indicator for monitoring cholesterol lowering efforts: U.S. adults, 2005-2006. NCHS Data Brief December 2007, No. 2.
- Cutler JA, Sorlie PD, Wolz M, et al. Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988 and 1999-2004. Hypertension 2008;52:818-827.
- Ford ES, Capewell S. Coronary heart disease mortality among young adults in the U.S. from 1980 through 2002. J Am Coll Cardiol 2007;50:2128-2132.
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- Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease. The Women’s Health Initiative randomized controlled dietary modification trial. JAMA 2006;295:655-666.
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- Arnett DK, Baird AE, Barkley RA, et al. Relevance of genetics and genomics for prevention and treatment of cardiovascular disease. A scientific statement from the American Heart Association Council on Epidemiology and Prevention, the Stroke Council, and the Functional Genomics and Translational Biology Interdisciplinary Working Group. Circulation 2007;115:2878-2901.
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-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association