~NEW FILE BEGINS - Dec #9 i t t ‘ \ i _ oF , THe PRIMARY -PREVENTION OF THE ATHEROSCLEROTIC DISVASES ere gare " Position Paper for the ~~ ° é + . . . . fj a, INTER-SOQCIETY COMMISSION FoR HEART DISEASE RESCURCES , j oo : so Prepared by the n _ , ~. Atherosclerosis Study Group __. 4 , \- -Chairman: Jeremiah Stamler, M.D. Members: Rodney Re ‘Beard, M.D. ‘. William E. Connor, M.D. - + Victor G. deWolfe, M.D, . s+. .Jeseph Stokes: III, M.D. Park W. Willis III, M.D. i Epidemiology Study Group 4 oo Chairman: Abraham M, Lilienfeld, M.D, “Members: Thomas R. Dawber, M.D. , Joseph T. Doyle, M.D. Frederick H, Epstein, M.D. Lewis oH. Kuller, M.D.” . Warren Winkelstein, Jr., M.D, Lo POO HEMSIREEE Ag | Li Biwi a eed, ! : i FOR i 74 at hoP TD SEN ! PATER SAL { ia T, x e cis, Gi 4 id) , | - = “ Peg SS ‘ USE OLY | - vt . . "In view of the fact that atherosclerotic complica- “tions cause a majority of the deaths in this country and a substantial proportion of the disability, it is recommended that immediate efforts be made to prevent premature athero- sclerotic complications." ~ - Second National Conference on . ' Cardiovascular Diseases, Summary Papers, i964. "Coronary Heart Disease has reached enormous propor- tions, striking more and more at younger subjects. It will result.in coming years in the greatest epidemic mankind has faced unless we are able to reverse the trend by concentrated research into its cause and prevention. "The Board expressed a wish that countries most affected by cardiovascular diseases increase their efforts both to set up efficient services for control and to carry out more exten- sive research programmes." ae / Executive Board, World Health ' Organization, 1969. ~ Contents wre The Need, for a National Commitment to Primary Prevention as the fe Principal Means of Controlling a Major Public Health Problem -- Coronary Heart Disease and Other Atherosclerotic Dis@ases........ ce aeeeee De ‘. II, The Possibility of Achieving Primary Prevention of Atherosclerotic DESCASCS. eee ee cere eens ee ceeeser eer eenessessseeeeeteececceacsveteeeeecces “A. Association of risk factors with atherosclerotic.diseases “- - \major risk FACEOUS +o veeceeseeeeceeseeerereeenee ener eneeeee ewes Diet and serum Lipids. ce cecscceccccccccaceccccccceccccceccce Hypertension. ..cecessececcesecsecsseccteccseccceseeeccceccce, Cigarette SMOKING. sss cececcecccccccesccccvscccvccccccecccuece Lee} Combinations of major risk EACtOLS. cc ececccccccccccccceccucee B. | Association of risk factors with atherosclerotic diseases -- other risk EACCOLS + oe caceecerecccccccccccesescccccccsccccccveces Diabetes mellitus and asymptomatic hyperglycemia. ...cccccccae ODESLEY. coc cececcccccccccccccccccccce Sedentary Living. .ceccccccccceccececes Psycho-social tensions...iceccaccocece Family RLSTOLY. ccccecccccccvcccccccece C. Modification of risk Lactors.ccccsccececee Changes in diet composition.......eee. Control of cigarette’ smoking.....seeee Drug treatment of hypertension......e. eeoeeeeeeenerceveseneeannene eP@eoevesereoerevrseevneecenmesaee cece cece nceseccesccrece i eeeeveereeseeeseenenenene eeeesavraneeterseeseencania eoeereorcesececoreeeececeye eeeeeteoeonesseeoasneseseosnane Control of multiple risk EACCOYSs ceesececceccecccscececceeccs SUMMATY. ccc cceeccccccccccccccccuccecseccccces III. Recommendations for Primary Prevention. ..cccescece eeeveceeerereoreoscenevneeeucne oeeeeeeeeseeersesesnenteese A. A National Policy Commitment to a Strategy of Primary PLEVENCLON. coveccescccccccscccccceccccece “ * @eeeenveveseereereternanees 10 10 Ll. 13 14 16 17 17 . ‘B, Definitive Field Trials of Primary PLOVCNELON. .. ee eee e cece es ee De 17 a C. ‘Diet and Food Modifications. .....cceecececccevcccecccecccccces 17 1. CAlOTICS. ..o esas cece cece cc ec eee ceccecescccecvcvaccce 18 / 2. Cholesterol. .eeeececccccccccccccncccccscuveceeccccsccce 18 3. Saturated LACS Looe ee cesenceeceecsncecsecsecieeces. 18 . 4. MEALS see seeeeeee eee eecerereeeeeenseteeectaeeeeeceeeees 20 3. Dairy PLOGUCE Ss cee ees eeeecercccccsccncscncccacvsceccnce 21 v . 6. Baked GOONS vee esererecseeeccccccssccceecscseessecceees 22 , ” . \ . 7. Fats and OLLSecceccecenccccerccccccnccccccceccsccecucce 22 8. Ege YOLKS. oe eeececccccccncccccccccccccccccccccccccccece 22 9. Definition and labeling of LOOdS. cc cccecccccccccccesece 23 -10. Government food and nutrition programs weet e cececenece 24 ll. Public and professional nutrition education... ..e.eeeee 24 D. . Elimination of cigarette SMOKING. cc ccccescecscccccccccccccecce 26 1. Advertising and sale of cigarettes. ..ccccecceceeecceces 26 2. Mass media education Programs. cececccscecccccccvencces , 26 ,3. Education program in the SCHOOLS. ssececensesececceceese 26 4, Cigarette vending machines.:cs.eseseceececescocececcee, 27 3. Smoking in public factlities...ccccececcccecceceeeccece 27 6. Use of tobacco tax LUNGS. cece ceeccccccnccnccccesscccccs 27 7. - Government subsidies for tobacco cultivation and CXPOLE sees esecececeaceceeeceeeccuseececcccececececcc, 27 8. Socioeconomic planning for the phase-out of the _ tobacco UNGUSELY. es esc ececceccceccecsceccecececceceeece 27 E. Detection and control of hypertension. sseeseseessseceeeenneees 27 F. Community programs for individuals highly susceptible to _ premature atherosclerotic discases..ceccsceccececceccccccccece 28 G. Drugs for the treatment of hyperlipidemia; exercise programs... 29 “IV, Primary Prevention of Premature Atherosclerotic Dischses -- Perspective. 30 I. THE NEED FOR A NATIONAL COMMITMENT TO PRIMARY PREVENTION AS THE PRINCIPAL MEANS OF CONTROLLING A MAJOR PUBLIC HEALTH PROBLEM -- ~ ~ . y CORONARY HEART DISEASE AND OTHER ATHEROSCLEROTIC DISEASES, Atherosclerosis is the major specific type of arteriosclerosis afflicting mankind. Its halimark is an accumulation of fatty materials 7 (lipids), cholesterol most prominently, in 1 the walls of medium and large arteries, The clinical manifestations of this disease reflect \ the ischemic complications of severe atherosclerosis. _The central problen, therefore, is the prevention of the severe form of this disease, particularly its premature occurrence, e.g., before age 65. Morbidity, disability and mortality rates from atherosclerotic diseases -- coronary heart disease (CHD), cerebrovascular, aortic, renal vascular and peripheral vascular disease -- remain extremely high in the United States and constitute one of the principal challenges to medical science and public health. This report is based principally on the extensive research data available concerning the critical problem of coronary heart disease. However, its conclusions are probably applicable to atherosclerosis wherever it occurs. | The National Health Examination Survey of 1960-62 estimated that 3.1 million American adults age 18 to 79 had definite coronary heart disease and 2.4 million had suspect CHD, together xvepresenting about 5 per cent of this population (Table 1 ) ¢ 1 ). It was further estimated that of Americans under age 65, almost 1.9 million had definite CHD and 1.6 million had suspect CHD. Every year about a million persons in the United States experience either a myocardial infarction or sudden CHD death. There are over 600,000 deaths each year due to CHD. (Table 2) (2), over 200,000 . | | | more succumb to atherothrombotic disease of Major. arterial vessels ._ 2 in other Parts of the body, Approximately 165, 000 of ‘the coronary £ deaths occur in persons under 65 years of age, with a “greater toll (3 to 1) among men than women, For middle-aged men, the United States has one of the highest CHD death rates in ‘the world (Table: 3) ¢ 4,5), Analysis of mortality trends give 1 no sign’ that these high death rates are decreasing (Fig. 1) ¢ 3 >). A North American man has about one chance in five of developing clinical CHD before age 60, mostly in the form of myocardial infarction (Fig. 2) ¢ 6, 6a-k ). About 25 per cent of those experiencing ‘a first premature heart attack die within three hours of onset of . symptons, often prior to hospitalization and before medical care can be obtained (Table 4) 6, ark, 7). Another 10 pet cent die within the first Weeks after their attack. For those middle-aged persons fortunate enough to recover, Prognosis for Tongevity is markedly impaired.” They are approximately five times as likely to die within the next. five years as | . those without a history of previous coronary disease (6, 6a-k, 7-9), In most cases death is due to recurrent acute eoronary episodes, Clinical atherosclerotic disease in the arteries. of other organs is similarly associated with a reduced life expectancy. These facts strongly indicate that major progress in controlling atherosclerotic diseases is possible only by primary prevention -+ reducing first clinical episodes by preventing severe atherosclerosis — and its complications. This must be the main strategic thrust of a national effort to control coronary heart disease during the years ahead. o- MA es II. THE POSSIBILITY OF ACHIEVING PRIMARY PREVENTION OF ATHERO- SCLEROTIC DISEASES. A. ‘Association of tisk factors with atherosclerotic diseases «+ major risk factors: Many studies conducted over the past 25 years have &. demonstrated associations between certain biochemical, physiological and environmental factors and the development of premature coronary heart 7 disease. Numerous risk factors for CHD. have been identified-such as high in saturated fat-cholesterol-calories, } habitual diet, elevated blood lipids", hypertension, cigarette smoking, hyperglycemia (diabetes mellitus), obesity, sedentary living, psycho- a positive .social tensions, and,jfamily history of premature atherosclerotic disease, Of central importance ‘in evaluating the association between risk factors and CHD is the finding that arterial lesions cannot generally be produced experimentally in animals without a substantial modification oo. of the diet involving increased intake of cholesterol and fat, leading to elevation of serum lipid levels.* Similarly, with very few exceptions, human populations consuming diets high in saturated fat ! and cholesterol have high mean serum cholesterol levels and high te eee Fee ee we ee ws ne -~ . +"Hyperlipidemia" is the generic term for elevation of one or more of the blood (serum) lipids, i.e., cholesterol, triglycerides, phospholipids. The most extensive research on the relationship between the blood lipids and the atherosclerotic diseases has involved serum cholesterol. Recent evidence suggests that elevated serum triglycerides may also be related to increased tisk of CHD. - The water-insoluble serum lipids are dissolved in the blood stream ‘by combination with proteins to form several types of serum lipoproteins. The association between lipoprotein patterns and CHD is currently under further study to assess whether any of the types have predictive or diagnostic value over and above that of serum cholesterol and triglyceride levels alone or in combination (38). *Comprehensive reviews of research (animal, experimental, clinicopathologic and epidemiologic) on the atherosclerotic diseases are available in the recent scientific literature (10-37), This section summarizes evidence considered most pertinent to the matter of achieving primary prevention. ~ - . . . % wee . 3 | | ’ incidence and mortality rates from premature CED. Human populations consuming diets low in cholesterol and saturated fat have low mean serum cholesterol levels and low incidence and mortality rates from " premature CHD. Within any population group, again with few exceptions, the risk of developing premature CHD increases as the serum enoteeter rol | Lo “, level Yises, This fact has been extensively documented fou the American male population in several prospective epidemiologic studies (Fig. 3, , : “” cf, also Fig. 11 below ) ( 6, 6a-k ), The relationship -— --", between level of serum cholesterol and disease is continuous. With increasing cholesterol concentration risk is ; ,inereased. There is no evidence of a critical level of serum cholesterol which separates high from low risk individuals. ‘ Detailed data on relationships among. diet, serum lipids and premature CHD are available from many studies. For example, the International Atherosclerosis Project quantitated the degree of athero- sclerosis of the aorta and coronary arteries at autopsy in over 31,000 persons age 10 to 69 who died during 1960-65 in 15 cities throughout the world. Marked geographic differences in the extent and severity of atherosclerosis were observed (Fig. 4 5) ( 227 )}. Populations in those countries with a high intake of saturated fat and high serum cholesterol levels had more severe atherosclerotic lesions than did populations in countries with low saturated fat intake and low serum cholesterol levels, Decedents from the Waited States showed the greatest degree of. involvement. Repeated analyses of international mortality statistics have “ yielded comparable findings. The most recent data deal with mortality’ rates for 22 developed countries including the British Commonwealth, Europe and North America (Table 3 ) ( 4, 5 ). The sizeable * ‘ e differences in CHD mortality rates for middle-aged males correlate positively with differences in nutritional factors, eee, total calories, saturated fat, and cholesterol. The United States is near « _the top of. the list with high per capita levels for ae of these indices and for mortality. * Data collected in research on living populations are consistent with those obtained from autopsy studies ‘and mortality statistics. An extensive report from a prospective international study of 18 population samples in seven countries -- Finland, Greece, Tealy, Japan, Netherlands, United States and Yugoslavia -~- deals with observations on approximately 12,000 men originally age 40-59 who have been studied ‘for about a decade ( 39, 40 ). On initial examination, marked differences in prevalence of CHD were recorded among the population samples from the seven countries (Fig. 5 d) ¢ _ 40 . ). For samples with high prevalence of CHD, including middle-aged American men, the rate was over four times greater than for those from countries with low prevalence. . Data on five year CHD incidence. and mortality rates are consistent with the prevalence data (Fig. 5 ‘and Table 5) (40). The highest five year — incidence rates were recorded for men "from Eastern Finland and the United States -- over 120 and 80 per 1,000 respectively. In contrast, five year incidence rates were about 20 per 1,000 or less for men in Corfu, Crete, Dalmatia and Japan. Differences in CHD mortality rates were frequer "dy paralleled by differences in total mortality rates (Table 2) “( 40 ». This finding supports the conclusion that the differences . in CHD rates were not due to diagnostic variability. Differences in CHD prevalence, incidence and mortality rates among the populations of these countries were significantly related to saturated fat intake and . 8erum cholesterol level (Figs. 6-8 ) ( 40. , ).* « ‘ | | ' | Recent. clinical studies using angiography to assess narrowing of coronary arteries have further strengthened the evidence on the association between serum lipid levels and CHD. Middle-aged patients with substantial narrowing of the coronary arteries had levels of serum cholesterol, triglycerides or ' bath significantly higher than those, of patients with- out such narrowing ( al ). ‘Hypertension also aggravates the atherosclerotic process, particularly in the presence of hyperlipidemia. This conclusion is supported by “Tipressive clinical ‘and experimental data as well as by prospective epidemiologic findings demonstrating significant correlations between blood pressure and the subsequent development of CHD . (Fig, 9, 11 ).6, ba-k), This relationship between blood pressure and CHD risk is continuous, At each higher step of the blood pressure scale risk is increased, Hypertension has also been established as a major risk factor for cerebrovascular disease, including atherothrombotic cerebral infarction and cerebral hemorrhage (Fig. 9 ). (6, 6a+k), The 1964 Surgeon General's report on cigarette smoking established that on the average Cigarette smokers in, the United States have a 70 per cent greater chance of developing CHD than non-smokers (. 420 >). Recent data from several prospective studies in this country have con- firmed this finding and strengthened the association between smoking and atherosclerotic diseases (6, Ga-k, 43-45). “The largest of these has involved one million men and women ( 46 ). ‘This showed . that for each sex and age group CHD mortality increased with increased intensity of cigarette smoking (Table 6) ¢ 46° ).« Men age 45-54 smoking two Or more packs of cigarettes a day were at highest risk, , The younger the age group, the higher the relative risk t we associated with cigarette smoking (Table 7) (6, Ga-k, 47, 48). It has also been demonstrated that the association between cigarette smoking and CHD risk is inde- pendent of such’ other risk factors as serum cholesterol level and blood | pressure me, (Fig.10) (6, 6ak, 49, 50). In addition, three studies have recently shown '.that atherosclerosis of aorta and/or coronaty arteries is more severe at autopsy . > ‘ in persons who had been habitual cigarette smokers prior to eeerh compared to those ‘who had never smoked (Fig.1l ) © 51, 54). Finally, as the annual supplements to the Surgeon General? S report have noted, research Progress has been recorded in elucidating possible mechanisms whereby smoking may exert its deleterious effect on the atherogenic process (43-45), | Morbidity and mortality rates # were high in polyunsaturated fat. In the New York Anti-Coronary Club, polyunsaturates were used for partial replacement of saturates. This study also placed obese volunteers on weight reducing diets during their initial months in the project. | The Los Angeles study was a double blind random trial among veterans living in domiciliary facilities. The Helsinki study is a comparison of two mental hospital populations. The New York study compared volunteers placed on a fat modified diet with a somewhat similar group of volunteers on their usual diet. Several hundred men have participated in each study for several years. _ These three studies reported a sizeable decrease in the incidence of new coronary events in the experimental compared with their respective comparison groups " (Pigs. 18-20) (85-87)... | «*%In the Los Angeles study, the effect appeared Ry : to be substantially greater in men under age 65 at entry. Two studies (Los Angeles and Helsinki) also reported mortality findings. Their data indicate that -diet change was associated with reductions in CHD mortality rates, although statistical significance was not reached. The Helsinki study also recorded a sizeable reduction in total mortality rate, paralleling the decrease in CHD death rate but again, statistical significance was not reached, The Los Angeles study did not note any decrease in total mortality. ‘The lower death rate from ~ 12 atherosclerotic disease was offset in the experimental group by a — - ~* nigher death rate from non-cardiovascular causes, including a statistically \significant excess of deaths from malignant neoplasms. 3 ‘ ‘VW This last finding has posed a question concerning possible ‘ “carcinogenic effects of diats very high in polyunsaturated fats. The results of these three studies are encouraging with regard to . a ee j “. the possibility of - preventing CHD and other atherosclerotic . . . Nee . : . diseases by dietary fat modification. However, they are not conclusive as to the preventive value of dietary change. Each dealt with a relatively small group and had one or another additional flaws, e.¢., high drop-out rates, absence of a suitable control group, lack of double blind design (88,89), Nonetheless, all are consistent in showing a reduction in CHD incidence and indicate the potential for CHD prevention through _ “ modification of dietary fat composition. — ° Control of cigarette smoking: The Surgeon General's reports on “The Health Consequences of Smoking'' have concluded that cessation of cigarette smoking is followed by a reduction in CHD risk ( 42 = 45). . This determination was based on evidence obtained from several studies. Two were large prospective studies designed to assess differential mortality among adults classified according to their smoking history. Both reported that CHD ‘mortality rates of former cigarette smokers were well below rates of current smokers, especially among younger 7 “groups ( Fig. 21). ¢ 46 - 48, 54), The differential CHD mortality between former and current smokers was greater when the group of former smokers was restricted to those who stopped smoking. for reasons other than doctor's orders. Similar findings were ob- - served in a longitudinal study of mortality among British physicians and in the Western Collaborative Group Study (Table'12) ¢ 44, 90, 91). In the latter it was found that the CHD incidence rate for middle- ~aged male ex-smokers was intermediate between rates for men who never smoked and men who were heavy cigarette smokers at entry. This finding was recorded after see adjusting for several concomitant risk factors (e.g., serum cholesterol, blood pressure, physical activity). | Further, the combined experience of adult males followed prospectively by the . . studies cooperating in the Pooling Project showed that the age-adjusiy ineidence rate of severe forms of CHD among male ex-smokers was about as low" a as that observed for males who had never smoked, and was “much “Lower the \a package or more of cigarettes per day ) the rate for men smoking. at entry ( Fig. 11) (6, 6a-k). ‘Again, the findings were independent of serum cholesterol and blood pressure, The consistent findings of all these studies provide highly suggestive evidence in support of the concept that cessation of cigarette smoking is of value in the effort to prevent CHD, Drug treatment for hypertension: Drug treatment for patients with diastoli blood pressures averaging from 115 to 129 m,, Hg has produced marked reductions in morbidity from hypertensive complications (Table 13) (77). Recently an important report was published on the Veterans Administration Cooperative Study of drug therapy for male hypertensive patients wita alastolic blood pressures averaging between 90 and 114 mm, Hg (so-called "mild" hyper- tension) (78 ). Three hundred eighty such hypertensive men were randomly assigned to either active antihypertensive agents or placebos and followed for periods of one to 5.5 years (average 3,3 years), Fifty-six of the placebo . treated patients developed morbid events, as contrasted with 22 of the actively treated patients, Life-table analysis indicated that the estimated risk of developing a mordid event over a five year period was reduced from 55 to 18 per cent by treatment (Fig, 22) (78), Major nonfatal and fatal cardiovascular events (terminating morbid events) occurred in 35 patients of ,the control group as compared to 9 patients in the lala group. Nineteen deaths related to hyper- ° 14 , tension or atherosclerosis occurred in the control Broup anc 8 in the act ivoly trec ‘In addition to the morbid events, 20 patients — all in the control group—déeveloped - persistent elevation of diastolic blood pressure to 125 mn, Hg or greater. The bene ficial effect of treatment was more evident in the patients with higher initial blood pressures than in those with lower levels at entry.’ * Treatment apparently was most effective in the prevention of congestive heart failure and stroke, and least effective in preventing clinical manifestations of severe. coronary atherosclerosis. The limited size of the study. precluded a definitti- “assessment of ability to prevent premature CHD by drug treatment of hypertension, However, the data currently available support the judgment | that effective long-term therapy for hypertension may help to prevent CHD and other atherosclerotic diseases, Control of multiple risk factors: Only one investigation has attempted to explore the possibility of prevention by control of multiple risk factors — hyperlipidemia, obesity, hypertension, cigarette smoking and sedentary living, . This Chicago Coronary Prevention Evaluation Program has used diets low in saturated fat and cholesterol, and moderate in calories, total fat, polyunsaturated fat, carbohydrate and salt (29), It has avoided recommending diets high in polyun- saturated fat. It has encouraged cigarette smokers to abandon this habit and urged sedentary men to take up regular, frequent, moderate exercise to enhance cardiopulmonary fitness. Its percicipants are 519 coronary- prone men originally age 40-59. They are being compared with over 3,200 marched men from the U.S, national cooperative Pooling Project (6, 6a-k). This study, still in progress, has reported encouraging effects on.CHD and ‘total mortality (Fig, 23) (88), Like the other "first generation" field trials described above, the investigation is limited by relatively small sample size, | @s well as lack of a randomly assigned control group, Therefore, its findings on the possibility of preventing premature death in high risk middle-aged males can be viewed only as suggestive (88, 89). e 15 . SUMMARY Converging lines of epidemiological, clinical and experimental evidence, both animal and human, supvort the judement that the relation- : 5 : — ; ship between the risk factors, particularly the major risk factors -- i.e,, -! hypercholesterolenia,’ cigarette smoking, hypertension -- and the develop- ment of coronary heart disease is probably causal. This should not “Be interpreted as implying that the evidence on this matter is con-~ clusive.. Nevertheless, the data strongly indicate that to a considerable degree coronary heart disease in the United States, particularly in the under 60 age group, results principally from the impact of these three widely prevalent risk factors. This critically important con- clusion rests on the following foundations: Confirmatory data are available from many sources on the epidemiologic associations; these associations persist when confounding variables are taken into account; the associations are strong and consistent; they are in accord with findings from other research disciplines and are biologically plausible in terms of reasonable pathogenetic mechanisms and concepts of multi- factorial etiology relating apparent cause and disease. Alternative hypotheses to account for the associations do not fit the majority of observations to date. : The research findings on risk factors stronely indicate the possibility of effective primary prevention c£ atherosclerotic disease, Particularly premature coronary heart disease (Tables 14-16) (76 92), TIq. RECOMMENDATIONS FOR PRIMARY PREVENTION, A. The Commission recommends that a strateoy of primary prevention of premature atherosclerotic diseases be adopted as lone-term national policy for the United States and ko implement this stratesy that adecuate resources of money and manpower be committed to accomplish: t£sources or be LO : oeeeChanges in diet to prevent or control hyperlipidemia, obesity, aw hypertension and diabetes .+ssElimination of ciparette smoking e+e+Pharmacologic control of elevated blood pressure, B. The Commission recommends that a Special Committee be established at al high level of the Federal Government to develop coordinated plans for large-scale, long-term trials fo determine the effect of various inter- ‘wentions, particularly diet modification, on the rates of premature atherosclerotic diseases in the United States, The Commission recognizes that differences of opinion exist with regard to the likely beneficial effect of various types of change, particularly fat modification of the diet, on premature CED in the United States. The public health importance of CHD makes it mandatory to conduct such trials ( 76, 94, 95). The Commission further recognizes that even if planning were to start immediately, the American public would probably have to wait at least 10 years for results of these ; studies. At times urgent public health decisions must be made on the basis of incomplete evidence. Therefore, the Commission recommends that actions with regard to the reasonable and safe changes described below be piompely implemented. C. The Commission recommends the following modifications Of diet for the general public, and particularly for individuals with marked increase 17 in risk of premature atherosclerotic disease, 1. Caloric intake be adjusted to achieve and maintain optimal Weight. Correction of obesity is known to be frequently 4 , toe associated “with significant control of certain CHD: ; “risk factors, | «@e8., fall in blood pressure of some hyper- tensive patients, decregse in blood glucose levels in some patients with maturity-onset diabetes, decline in elevated serum triglyceride levels. It is generally agreed that this meagure is a reasonable and: gage “aspect of any prophylactic regimen. . 2. A reduction of dietary cholesterol to less than 300 mg. ' per day. The average daily diet in the United States contains approximately 600 mg. of cholesterol. Substantial reduction in amount of cholesterol in the diet has been found to lower con-~ centration of cholesterol in the serum of most people. Since cholesterol is present in many protein sources of high biological quality, careful planning is necessary to lower intake of cholesterol without impairing intake of protein. 3. A substantial reduction of dietary saturated fats. This change will lower concentration of cholesterol in the serum of most people. The ideal quantity of fat needed in the diet is not known but moderation in intake is considered desirable, e.g., Kh less than 35 per cent of total calories from all fats. Intake of [9 rh jess than 10 per cent of total calories from saturated fats is fritical importance for attainment of optimal serum cholesterol - levels for most people. Unsaturated fats may be used in moderation to replace a portion of the saturated fats, i,e,, 10 percent of calories from mono-+ and up to 10 percent from polyunsaturated fats, With ‘proper ’ control of saturated fat, cholesterol and calorie intake, as recommended 18 , , * above, ingestion of large amounts of polyunsaturated fats -- i.e., 10 per cent or more of total calories -- is generally not necessary for control of serum lipid levels. International data indicate that populations with low serum lipid levels and low CHD mortality rates habitually consume diets low in saturated ‘fat and cholesterol, and low or moderate ; in total fat and poly- unsaturated fat -- not high in the latter (5, 40 ). “ With these dietary principles, requirements for optimal nutrition can be met for all sectors of the population, including infants, children, adolescents, pregnant and lactating women, and older persons. Changes in the environment to aid the American people to improve their diet should be a major aspect of this effort at prevention. Recent research has shown that it is entirely possible to prepare foods commercially in ways that will contribute sub- stantially to the control of hyperlipidemia. In the National Diet-Heart Study, many foods were prepared with sizeable reductions in content of total fat, saturated fat, cholesterol and calories (°° 76 © ). This was done with dairy and meat products, baked goods, frozen desserts and other foodstuffs. It was demonstrated that modified” foods can be made in forms that are highly acceptable to the consumer, The Commission therefore ‘recormends that the food industry be encouraged by the medical profession and the government “and supported by the general public to make available leaner meats and processed meats, dairy products, frozen desserts and baked goods reduced in saturated fats, cholesterol and calories, and a 0 . be Reduction ain saturated fat and cholesterol content of _ = Lo ~~ dairy procucts, beee Industry and government should review and establish _ policies (including prici ing policies) that will encourace development of iow: fat, low incholesterol milk .and milk 4 . - products, and use ‘of cows produci _ large amounts of high ‘protein, low fat milk, Wholesale pricing of dairy products wis still based on butter fat content, a practice persisting ; , "from the days when measurement of butter fat was used to detect skimming or watering of milk, i. ‘ ts eevee The dairy industry enourd be helped and encourazed : to. develop techniques for reducing saturated fat and cholesterol in cheeses of all varieties. Total fluid milk consumption in the United States is decreasing while consumption of cheese is steadily increasing. At current levels of consumption _ significant control of hyperlipidemia seems unlikely unless , . . . composition of cheeses can be altered. The National Diet-Heart Study demonstrated that limited progress has been made in this. area, and further progress certainly is possible, : , eee. Industry should be stimulated to develop creamers iow in total fats, saturated fats and cholesterol, Chances ( in labeling and advertising of cream substitutes are needed, SO that their actual fat composition is clear. The so-called non-dairy-fat creamers currently on the market present a special problem. These products are characterized by a high content “ of coconut oil and/or hydrogenated vegetable oil and therefore of saturated fat’ (96). -Coconut oil is one of the most potent > agents for elevating serum cholesterol level. Labels that 21 ~ read “made with vegetable oil" give an erroneous implication that the product is to be preferred Over one containing dairy fat. ce . Reduction of-saturated fat, cholesterol and calorie content of baked goods. As the National Diet-Heart Study demonstrated, nutritionally excellent baked goods , of all _ types can be prepared commercially in completely acceptable forms with reduced saturated fat, cholesterol and calorie content. Wide- spread. marketing of these fat modified products should be encoureged, d. Promotion of fats and oils Low in saturated fats and cholesterol for table spreads, shortenings, cooking and salad dressings, ete. In some areas of the country, state and/or local laws prohibit the use of butter substitutes in restaurants and institutions. These laws should be repealed, e. Reduction of egg yolk consumption. The yolk of the egg is.the single highest source of cholesterol in the average American diet, as well as a source of considerable saturated fat. Ingestion of two eggs a day -- in visible and/or invisible form (i.e, in prepared foods) ~- will seriously hamper dietary programs aimed at reducing serum cholesterol, Consequently the public should be encouraged to avoid ese yolk consumption, and the food industry should be persuaded to minimize’ ege yolk content of commercially prepared foods. Food manufacturers have recently developed low’ cholesterol and low saturated fat ege Substitutes which may be used successfully in quantity cookery and for scrambled eggs, omelettes, etc. Such developments should be encouraged, £, Modernization of resulations on lebeling and definition "of foods. In December 1959 the Focd and Drug Administration introduced into the Federal Register the statement: "The role of cholesterol in heart and artery diseases has not been established " (97. ), Consequently, it ruled that advertising claiming that the consumption of a food product might protect against diseases of the heart and arteries was false and misleading. The Federal Register in May, 1965 published a proposal favorable to the labeling of edible fats. This was supported by the American Heart ‘Association and the American Diabetes Association. In February 1966. however, the FDA rejected the recommendation to label edible fats and Oils, but endorsed a study of this problem to be conducted by the Council on Foods and Nutrition of the American _ Medical Association. The Council completed its report and transmitted it to the FDA, The report favored such labeling but the FDA took no action. | - t The FDA's resulation with respect fo labeling of foods . should be reviewed and updated. A new approach fo labeling is needed -- to allow the consumer easily to identify nutrient content (particularly the amount and type of fat and cholesterol) in all foods, including commercially prepared mixed dishes, and 0 Qu to. encourage the manufacture of nutritious Products low in saturat fats and cholesterol, = : Correspondingly rules and reeulations of the USDA, state and local agencies on foodstuff definition, adulteration, etc., should be modernized to pernit and encourage production, advertising and — the sale o of products ow in saturated fats and cholesterol (e.2., —— ame 23 processed meats), made with moderate amounts of unsaturated oils instead of large amounts of saturated fats, &. Improvement in school lunch, food stamp, other supplementary food programs and government administer ed nutrition practices fe.c., Armed Forces, Veterans Administration facilities). Policies, regulations, practices and educational aspects of these programs ” should be revised to encourage improved eating habits including consumption of low saturated fat, low cholesterol diets among children, teenagers, young adults and ~ low income groups ( 98 >. . . Ww: . he. Development of a comprehensive and sustained public and professional nutrition education program. To effect the- required changes in dictary habits, ‘it is cy essential that the entire community be actively involved through a comprehensive and sustained public and professional education program. This will deepen understanding and appreciation of the need for primary prevention and inform the public and health professions on ways Of selecting and preparing foods consistent with sound nutritional practices, Special emphasis must be directed toward developing effective instructional programs on nutrition in the educational curricula at all levels. For this purpose, particular attention should be given to the institutions training health professionals with expertise in nutrition -- e.g., college and university home " economics departments, hospital dietitian instruction programs, schools of medicine, dentistry and nursing, and teachers! colleges, These sources should. develop educational programs | based on modern concepts of sound ‘nutrition, Succeeding generations should have the advantage of this’ — knowledge beginning in “elementary school, VN 24 Food manufacturers have an excellent opportunity to provide — 7 public education through advertising. They should be encouraged to call attention in their advertising to the type and amount of fat and the cholesterol content of their products. for Ls foi a There “is a great need for extensive and continuous ~ . _ - . nal . . , , . . . . , ao , j * zs . s . . * ° * 4 co dissemination by the news media of information on diet, as well as other risk factors. Public service communications in this area should be substantially strengthened and broadened, 5 , With proper education, information and the availability of fat modified foods, it will be possible for most Americans to make desirable changes in their diets without major dislocation of . personal eating habits. Americans should be encouraged to modify habits with recard to all five major sources of fat in the U.S. diet -- meats, Specifically a superior pattern of nutrient intake can be achieved : by altering habits along the following lines: cess .Use lean cuts of beef, lamb, pork and veal, cooked _to dispose of saturated fat and eaten in moderate portion sizes;’ sess *° Use lean meat of poultry and fish; eens Use fat-modified™ processed meat products (frank- furters, sausage, salami, etec.)$ Levee Use organ meats (e.g., liver) and shellfish in 7 : moderation since they are higher in cholesterol than muscle “of red meat, chicken and fish; . . seve Avoid fat cuts of meat, addition of saturated fat in cooking meat, large meat portions and processed meats high in saturated fat; *Throughout this set of guidelines fat modified refers to products made with reduced caturated far na pbaleseamal ppweawe ; ee. Use low fat and fat modified dairy products; cece Avoid high saturated fat dairy products; ee. Use fat modified baked goods (pies, cookies, cakes, - sweet rolls, doughnuts, crullers); bees - Avoid baked goods high in saturated fat and . cholesterol; . —_ \ | eee Use salad and cooking oils, new soft margarines and ° ‘shortenings low in saturated fat; _. 1 ‘ epee ; Avoid butter, margarine and shortenings high in saturated tat: oe 4 Avoid candies high in saturated fat: wee! Avoid egg yolk, bacon, lard, suet; | I cece ‘Use. grains, fruits, vegetables, legumes , elimination of cigarette smokins as a national habit. 1. Efforts should be made to reduce smoking among young . people by strict restraints on advertising and the sale of civarettes, All ‘advertising of tobacco in the mass media (including television, | radio, newspapers and magazines) should de discontinued, Short of this all advertising should carry an honest, frank, highly visible warning for potential consumers. 2. he mass media education vroeran emphasizing the health ae hazards of smoking should be continued indefinitely to redress: x oa the imbalance created by decades of cigarette advertising. 3. Education programs on the risks of smoking should be . 0 the early primary grades,. Parents, teachers, health professionals 26 and other adults in positions of responsibility (e.g., television , entertainers and sports personalities) should be made avere of a : the serious adverse influence of their own smoking habit as a poor example for children who may become lifelong cigarette smokers. It is noteworthy that physicians have been particularly successful \ in giving up cigarette smoking and are in a unique position to 7 exezt great influence in helping their patients stop smoking. 4, Cigarette vending machines should be removed from all medical facilities and public buildings or, preferably, banned altocether,. 3+ The prohibition against smoking in laree meetings and mass poe transit facilities should be vigorously enforced. 6. Revenues from progressive increases in taxes on tobacco . should be earmarked for smoking control programs and the care of patients with diseases associated with smoking, exporting tobacco should be critically reviewed with the objective £ making economic supports for agriculture consonant with national - g Pp ag health goals, 8. Planning by appropriate social science experts should ZO forward for the orderly phase out of the tobacco industry without major economic dislocation of those whose livelihood is involved. +. E. The Commission recommends 2 major national effort to detect and. control hypertension. Recent studies have shown that the prevalence of elevated blood pressure is gencrally high inthe United States, 27 tions of the major risk factors, especially in the Negro population (Table 17 ) ( 99 ). Many hyper- “tensives have not been identified; many others known to have the disease are not receiving adequate therapy. . Programs are urgently . needed to. identify hypertensives in the community and assure their subsequent treatment. The recently published positive results from the Veterans Administration field trial of drug therapy for so-called "mild" hypertension underscore the potential significance of such woot programs ( 78 . ooee F. The Commission recommends that community programs be developed and expanded for the detection and treatment of ve rsons of all ‘ages’ “who am ‘are very susceptible to premature atherosclerotic diseases due to combins- ” This recommendation is premised on extensive experience demonstrating i that effective community programs for prevention of diséase generally combine measures addressed to the entire population with concerted efforts for the detection and care of high risk individuals. All available evidence indicates that this well-established principle applies to the | prevention of the atherosclerotic diseases, - On the basis of recent experience detection prosrams are likely to identify a very large proportion of the population “- @.2., about 20 or 30 per cent of middle-aged adults -- as being at unusually high risk. For such individuals, community seryices should be provided to , ; * assist their physicians in long-term management, Such programs will a “ .require the training and use of large numbers of allied health pro- fessionals, as well as physicians. foe mH HF ee me ee *Detailed proposals concerning these conmunity services will be presented in subsequent reports of the Commission, 28 G, The Commission presents the followine observations on drut treatment of hyperlipidemia and on exercise programs, and their possible role in the — preventive effort: _ Drugs for the treatment of hyperlipidemia have been developed in recent "years, For example, several years. of experience with cholestyramine, -clofi- & brate, dextrothyroxine and nicotine acid have demonstrated that they will ‘reduce cholesterol and triglyceride levels in the blood of many patients especially if they are abnormally high. What is yet to be determined is whether the biochemical action of these or similar drugs will exert any favor-— able effect on the course of the atherosclerotic diseases and whether ‘long term continued use of these substances produces significant deleterious effects. Clinical indications for the prescription of these drugs are now being defined, For example, they are possibly indicated for specific types of patients with marked hyperlipidemia, incapable of being normalized by diet alone. In this situation the risk of progression of atherosclerotic disease may outweigh any as yet unrecognized ‘hazards of long-term medication, There is a need for fur-' ther development and evaluation of relatively nontoxic drugs for the lowering of elevated blood lipids, Regular exercise, particularly those forms of endurance exercise which enhance cardiovascular fitness, may have a role. to play in the prevention of atheroscletoric diseases, It is important to emphasize, however, that exer- cise is not free of danger both to the musculoskeletal and the cardiovas- cular systems, This is particularly true for middle-aged individuals— especially coronary~prone persons—who suddenly take up vigorous exercise after years of minimal physical activity. 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Coronary Heart Disease Mortality Ratios among Current Cigarette Smokers Only by Amount Smoxed Daily ‘== American Cancer Society Study of One’ Million ‘Men’ and@ Women (49) Non- Cigarettes Sioked Daily ‘Age and Sex Smokers " * Under 10 10-19 20-39 G0+_ Men: ‘ 45 to .54-------~~~ 1.0 : 2.45 ft 3.2 3,1 3.4 [55° to 6dnnnnnnnnn 1.0 . 1.5 1.9 2.0 | ° 2.1 65 to Dare rmmmmmie} 1,0 1.3 . 1,6 1.6 * 75 to 84rr--nen 1.0 , 1.2 . 4 1.10 j---~--- Women: ' 45 to 54--------—~ 1.0 ‘10.9 2.0 2.7 [------ 55 to Sdorersgane 1.0 1,3 . 1.6 2,0 Jerenne 65 i) 1,0 1,1 1.4 1,9 |-----~ 75 to Baarqrrenee 1,0 TT med eee Aan ene x ; Expected deaths were less than 10, : & OS . . “syuqeep 6 03 ¢ ATuUC~UOdN peseq Sajey. *oRer- peqoedxe euq Aq DepPTATP e7eA poearosgo oy ST of jer AQTTeqxow oun. . a 8z°T] lS" €3° 00°t ~--- Let 86° 92° 00'T ~STedA 6L~OL seem €8'T ST*2 9c co't |Veo*z }| s80°Z 6L°T vO'T OO°T = FeSzeeA 69~09 SE L9°Z 04°? 9Z°T OO'T EL°E 89°C LEZ ST*T 00°T ~-szeak 65295 pL*S| O62; o9°% | ost] oo'Tt | glete co‘e | 80°% Te*t OO'T = fPSsxe04 Gy~OF % . rsaTeuaz Bo" ZZ°T ze’ | s6t 00°T Let 6P'T Trt Pit oo'tT fp esxve& S7>0L ZL°T} -ZO°T] HTT | OE* T= OOTT S| 6L'T T6'T ee't SFT oo'T = peszead 69-09 ov'z{ e0°C) Br't} S6e't] oo't | 6L'z on'z et'z 6s*T Oo'T fsszeok eshos | po'T Tete} Pit 6L°Z| = 00°T Ts's 9L°E 6S" 09°T OO"T.. 4--SzeeA GP-OP ‘ 7 SOTRH _ SOMME ALITWIAOW ! . . , . i ~- 229 VOLe 70? 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United States, Current Ponuitiion Survey, Ture 2068, Auausr L967 enc Augues Mook - Turmer { : : ot | » Cigarette Smoxing Status -- Rate Per 1,000 Sex and Age — Date Persons - in | Total Present Former Never l Unknown ie ‘ Thous ands pesulation ! smoker smoker smoked ever smok. j : . BOTH SEXES Fo. Total, 17 years and over ~----/ June 1966. 124,500 1,000 396 115 464 ° 25 f t . . Aug., 1957 126,579 1,000 391 ) “123 462 . 2 | so , Aug. 1968 128,556 ; 1,000 377 132 469 23 a . : . . ; . . : 17~24 yeatge~-eoe- Some orem of June 1966 22,711 1,000 376 44 557. 23 “ : Aug. 1967 23,377 : 1,000 370. 49 558 24 Aug. 1968 23,962 1,000 348 58 573 21 - : ae ~” ‘ + 25-44 yeargen-nn wenn n ne coee--4 June 1966 45,132 1,000 496 117 367 | - 20 Aug. 1957 45,488 1,000 465 126 369 20 ; ~ Aug. 1968 45,985 1,000 47. 136__ 375 17 4 45-64 YOALE Mmmm enna eee nn June 1966 38,960 1,000 402 145 424 30 : NCU Rug. 1967 39 ,649 1,000 400 152 420 28 Aug. 1968 40,227 1,000 385 161 427 27 65 years, and overeren-e~~= awee-| June 1986 |° 17,697 1,000 153 138 680 29 . : Aug. 1967 18,064 21,000 160 144 665 32 ' Aug. 1968 18,381 1,000 159 152 659 29 MALE . . : Total, 17 years and over-~--~-~ June 1966 58,469 1,000 466 172 314 28 . Aug. 1967 59 ,248 2,000 478 | 182 314 26 Aug. 1968 60,073 1,000 459 7 192 326 23 17-24 YEarSrnmmmmen mse enn memes June 1966 10,529 \ 1,000 444 46 483 27 Aug. 1967 10,739 3} 1,000 438 52 483 27 Aug. 1968 10 ,987 1,000 413 65 500 22 25-44 yeargnemacnmemeremaceneseny June 1966 21,536 2,000 579 1909 239 22 Aug. 1957 21,733 1,000 563 169 249 20 Aug. 1968 21,987 1,000 547 178 258 2170 : 45-64 FOALS Wm ween nme nem enn nn June 1966 18,688 1,000 501 213 248 33 , Aug. 1967 18,956 1,000 496° 231 24% 29 . Aug. 1968 19,169 1,000 473 240 260 27 65. years ‘and. over=-------e-----4 June 1935 7,717 | 1,000 246 267 454 32 . . Rug. 1967 7,821, 2,000 255 278 434 33 Aug, 1968 7,910 1,000 245 288 434 33 FEMALE : : , Total, 17 years and over--~--- June 1966 66,031 1,000 316 ' 65 597 22 . Aug. 1967 67,330 1,000 314 t 70 593 23 Aug. 1968 68,483 - 1,000 305 79 594 22 17-24 years~emeen anne nee nen ene June 1956 12,182, 1,060 316 42 622 20 . Aug. 1967 | 12 ,638 1,000 312 47 621 20 Aug. 1968 12,975 1,000 294 53 634 19 . . . . ¢ ” o 25-44 years~~---~ Hoe wen wmmmmanmn! June 1966 23,596 1,000 421 79 483 17 . Aug. 1967 23,755 1,000 413 88 480 19) a . ‘Aug. 1968 23,998 1,000 402 98 482 17 45-64 yeargnmnnnnnnnnnn--2-----] June 1966 20,272 1,000 311 76 587 ” 26 Aug. 1967 20 ,694 1,000 313 79 581 : 27 Aug. 1968 21,039 1,000 305 88 579 27 65 years and over-~---~-~----~--4 June 1966 9,950 1,000 81 38 855 26 * Aug. 1967 10,243 1,600 87 42 B42 29 Aug. 1968 10,471 1,000 95 49 829 27 NOTE: For official population estimates for more seneral use, see U.S, Bureau of the Census reports on the civilian population of the United States in Current Population FRenorts, Series P20, P-25 and P-60. % Te . - TABLE 10 - Cigarette Smoking Status, by Age and Sex, Whites me Chicago Heart Association Detection Project 1967 - 1969” Age-Adjusted Rate Per 1,000* Cigarette 3,262 Men 958 Women| .2,137 Men 1,249 Women Smoking Status — Age 25-44 Age 25-44 Age 45-64 Age 45-64 . \ \ . ‘ . / . ‘ Never Smoked 261.5 : 369.6 245.0 511.3 : : . : : é Ex-Smokers - 261.2 171.9 340.7 147.2, i|<10 Pex Day 71.8 109.6 63.8.] 119.6 210 Per Day | 405.5 348.9 350.5 221.9 Ex-Smokers 353.7 272.7 451.3 301.2 Ever Smoked * 1,000 ‘ , *All rates age-adjusted by five year age groups to U.S, white population 1960. ° __ be 7 . . - ‘Table Ll Regression of Coronary Atherosclerosis with Cessation of Atherogenic Diet, Male ‘Rhesus Monkeys (83) Group Nutritional © Luminal Narrowing Regimen . . . Main Coronary Left Anterior | Left ---- Distal ‘ ’ Left Right Descending | | Circumflex Continuation, : , Right Main 1 ‘High Egg Yolk Fat, , ‘ High Cholesterol ~- 17 Months “} 60 £ 8] 56 4.7 53 £8 57 +9 65 + 10 2. | High Egg Yolk Fat, High Cholesterol ~- 17 Weeks; Low Fat, Low Cholesterol ~~ 40 Months 17+ 4/142 3 2144 22 + 6 is +5 3-0 High Egg Yolk Fat, ‘ High Cholesterol ~~ 17 Weeks; High Corn Oil Fat, Low Cholesterol -- ; : +5; 26 + 3 20 + 5 23 4 6 18 +5 40 Months 25 Values are means + standard errors. u , mo, a i oe oo, . ; Table 12 Hy, . . : ~ . . 1 “Incidence of New Coronary Heart Disease by Smoking Category:. Western Collaborative Group Study, Males 30-49 Years of Age at Entry — ~~. 4 1/2 Years Average Observation Data (44,96) « vee Rate per 10,000 Population Smoking Category . Number © Adjusted for Not a of Men Concomitant Adjusted . , Variables . Never smoked . 540 - _ 36 7 | 29 Former cigarette smokers | 241 67 92 Pipe and cigar only 406 - 27 16 1-15 cigarettes ° | 212 51 52 16-25 cigarettes 436 89 | ge os 26 cigarettes and over 425 98 104 , Table 13 Effects of Treatment on Norbidity and Mortality in Hypertension -~ Male Patients with Diastolic Blood Pressures Averaging 115 - 129 mm. Ug at Entry -- Veterans Administration Cooperative Study on Antihypertensive Agents (77) baad . df k. a ™ Dype of * Number of Events Event | Placebo Hydrochlorothiazide + | , ‘ . o se Reserpine + hydralazine |- ™ 70 Nen 73..Men \> - mo, Deaths 4 0 Class A events _- 10 0. ‘ Subtotal 14 | 0 Other treatment failures 7 1 , Total terminating events 21 | i Class B events (nonterminating) 6 L | Total 27 2 Average period ox observation: 15.7 months for the placebo group, 20.7 months . ‘for the active- dup group. . ‘Of the four deaths, two were attributed to dissecting aneurysm, one to ruptured ‘abdominal aortic aneurysm and one was a sudden death. Class A (terminating) morbid events: hypertensive complications as defined in .the protocol which required treatment with known active agents and permanent removal from protocol assigned therapy, including: fundoscopic evidence of “grade 3 or 4 hypertensive retinopathy; doubling of “blood urea nitrogen to levels above 60 mg./dl.; dissecting aortic aneurysm} cerebrovascular hemorrhage (as opposed to thrombosis); subarachnoid hemorrhage; congestive heart failure persisting despite digitalis and mercurial diuretics; elevation of diastolic blood pressure to 140 ma. Hg or higher on three repeated visits and average rehospitalization diastolic pressure to 130 ma. Hg or higher. " - Class B (nonterminating) morbid events: as opposed to class A events, were those which did not require permanent discontinuation of protocol treatments. Patients with developing B events could be treated with known antihypertensive agents for _ ‘as long as six months, after which protocol treatment: had to be reinstituted. Class B events included organic complications associated with atherosclerosis, such as cerebrovascular thrombosis (as contrasted -to hemorrhage which was considered a class A event) or myocardial infarction. Congestive heart failure which responded . to routine therapy with digitalis or mercurials and did not require antihypertensive a agents also was classified as a B event. ” “ POTENTIAL IMPACT OF _ PRIMARY PREVENTION . OF CORONARY HEART DISRASE (TABLES 14,15,16) Because of the high incidence and mortality from clinical corénary heart disease, the impact of a program of primary prevention may be substantial. Most coronary heart disease deaths occur within the first - few hours after the onset of the clinical event, before adequate medical care is available.* In theory, therefore, the majority of these deaths can be prevented only by preventing the occurrence of the initial event. The impact of a program of primary prevention depends upon three variables: 1. The magnitude of the disease in the community as measured by incidence, prevalence, or mortality, 2. The potential effectiveness of the program in reducing the number of events, , 3. The percentage of the population at risk that will - accept the program. The estimated incidence of clinical coronary heart disease per year ‘is 4/1,000 at age 35-44, 10/1,000 at age 45-54, and 20/1,000 age 55-64 for white men. Approximately 20 per cent of the new events will result in deaths and about two-thirds of the deaths will be sudden, i.e., occurring within the first few hours after the event. Incidence data for the black population are not available at present but are probably similar to thase for whites, *Studies indicate that from 60-70% of coronary heart disease deaths occur outside the hospital. The median time of survival from onset of attack to death for these patients is about 25 minutes, . Based on current United States population estimates, the incidence and number of deaths from an initial coronary event for white males age 35-64 is shown in Table ll. The estimated impact ‘of a primary prevention program is shown in Table 12. These projections are based on varying percentages of potential efficacy and the percentage of the population that igs included, ee Note that even if the effectiveness of primary prevention is small — ' --(10%) but is available to a large seement of the population, the impact in terms of reduction of mortality and morbidity will be substantial. Thus, the potential for primary prevention of coronary heart disease when based on a community effort as recommended in this report is’ very great, aT, Table 14 *. t . . : * . . . . . . . . ». Estimated Number of New Cases and Deaths from an Initial Coronary 2 Event for White Males (92) Population ‘Number of Cases Number of Deaths” 35+-44 10, 000, 000 40,000 8,000 | 5-54 10, 000, 000 100, 000 20, 000 55-64 8, 000, 000 160, 000: 32,000 TOTAL 28, 000, 000 300, 000 60, 000 " Deaths following initial event only. 000‘09 000‘00€.} 000 ‘0¢ 000 ‘ost 000 “zt. — 00009 | - 000%9 | gootog |.” ; quested QQ: 000 ‘0 000 ‘0ST 000 *St - 000 ‘Sz 000 £9 000 ‘OE o00‘E |. op0%st fF qUdOTEg OS - 000 ‘ZT 000 £a9 000 9° -000°0E | ~—s gov *z 000 ‘2T 002 ‘T 000 ‘9 qUDD1ag OZ 000 ‘9 0000 | ooofe . 000‘st | goer 000°9 009 ooofe |. quested 7 | poqyusaorg poquaAdrg pojUoAdIg | pajzuaaorg . paquoaerg paquencrg pejquoserg | pojRuoaarg syqeog Sose) sy ee Ssoseg sy2eoq sosey syqeoqg soseg I ; . | 84T299FI9 FU9OL9gG OOT Joatqoo7 zy 2UZ9I1Eg OS VATIOVJFA QUID OZ DATIOOFIA JUBIIDT OT —UOTIeOTTTpoy SutTjdeoo. ° poQuoADIgT squaaq yo JOqUNN pue -- SSOUBATIIOJJY TeTQuojog . : uotqe{ndog zo aSequooza; (26) ¥9-SE e8y setey SFTUM. ipaepnyTouy uotqe{ndog ‘842 Jo eSequeozeg pue einpsosozrg 42 Fs0 SSOUBATIOVTJY uo paseg poqueaoxzg 2q PINON 3ey2 Ssyyeeg puke squeaq zo TeqUnN JO uoTRIeUTAS| . 1 “CT OTs \ . Table 16 Estimuted Relative Reduction in Coronury Heurt Disease © Incidence (v ). Associated with Relative Reduction in Serum Cholesterol’ (u) (76) Relative — Relative decrease Relative , Relative decreas decrease in coronary heart decrease “ain coronary heart | in serun disease incidence in serwn disease incidence cholesterol . ; cholesterol: ; , (u) (v) (a) fv) _ «OL too +026 — 26. 551 .02 . .052 , eT 567 +03 +078 © 28 583 04 * 103 29 6598 205 128: - 230°: -613 «06 . -152 , 231 627 OT "176 ne 232 642° 08 - . -199 Jd... | 33 «655 «09 2222 , "34 -669 .10 2h . £35 682 ell 267) ; 236 ; -695 12 -288 ~37 -707 Po +310 -.38 «720 wh 2330 5, 1239 “731 015 , 2351 «40 - «Th3 «16 371 Al 2754 “17 2392 , 42 «765 18 «410 ” 43 -776 219 «a9 bh, +786 220 . AL8 ws 19 221 466 ‘ 6 805 122 - 48h : 47 .815 ' 623 501 . «48 82h 2h ; +518 hg .833 025 0535 . - 250 842 ‘ Note: Values of v were obtained from the reiationship, v = 1 ~ (1-266 - described in reference (93), These data illustrate the potential for prevention, and the possibility of achieving declines in CHD morbidity and mortality as projected in the preceding table (Table 15). For example, a ten per cent reduction in serum cholesterol level of the U. S. population ( u = +10) is estimated to yield a 24.4 per cent decrease in CHD incidence (v= .244). - Similar estimates can readily be made of the potential for prevention inherent in continuing further decreases in the prevalence of cigarette smoking in the . . 7 Toose 17 White and Negro Adults with Blood Pressures of at Least 160 Systolic or 95 Diastolic, by Sex and Age: United States, 1960-62 -- U.S. National Health Examination Survey (99) , \ a \ _ os - Systolic at least | Diastolic at least| Systolic at least ™ 160 mm. Hg 95 mm. Hg . 160 ma. Ig or © } “Sex and Age ft Diastolic 95 mn. is ’ ft \ _ . j White Negro: ' White Negro White - Negro Prevalance Rate per 1,000 Both sexes-18-79 Yar Saran neem w ne men- 105 188 87 220 147 | 276 _ Men Total-18-79 years-------- go | 6168 226 136 276 18-24 yeats-------n-nennnen ee 2 - 7 “19° 17. 19 25-34 years---~-------- meeeen 7 46 . "34 11S 37 125 35-44 years--------~---- a 39 162 109 259 “f° 118 265 45-54 yearsernnen nnn cnc enn sen 87 108 . 138 » 295 173 _ 308 55-64 years-m-nen nn nen cnn n ne 159 294 119 ' 316 214 446 65-74 yearsrernnenennee erenee 261 632 123 405 273 660 75°79 yearSenncncn nnn e wen en en 391 598 133 212 402 598 - Women _ Total-18-79 years-------~- 123 "204 . | = 83 215 156 276 18-24 yearse-----nnenn wenn en- - 7. 8 34 8 34 - 25-34 yeargennneannnenrennnn- . 7 |. 34 21 85 23 85 35-44 yearsennncnnn neem nnn nn 23 143 , 53. 241 62 256 45-54 years-nnnneneewnennenne 107 308 109 343 155 419 55-64 yearsqn-nnn wenn mewn ennnn 253 338 164 367 310 410 65-74 yearsenrq-nn nn we wenn nnn 454 685 | 179 321 486 710 75-79 yearsqnnnnmennncwennewne 427 694 120 263 449 "694 U.S. population (cf. Tables 6, 7, 9, 12 and Figs. 11, 16, 21). 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L SONG BAILOY , eg Le a Sonya WY . 4 we ~ . a, ° * 2 a . - JO . 1 2 8 ' F ——- | 7 8 | Td Ea 2 Ee ES "4 . | ~ / > Pm a3 Aff cn = ’ . . 43 7 Im - oF wil “-i02 - , - . 3SY3UOHT : ~~ -35¥auD3d 3SYRVONI | | SVEIO ° . “105 c ; ; ’ - “ . ‘ ' ° + ~ -{07 ° “f - - 0939%1d 0 Ro ie - i 1 . 3 ; - 2 eT Th Se ; | TOVEUIS ANO UO OF 03 ore Ady tsatssop®@ z svy cy aanSty 7SURINING OF BION a Oo ff © & ¢ 9 a - NOILASIULSIG IN3OY2g | - 10 _ = bn MALE FEMAL sere ee — . [] Unknown’ 2 see * ~ Tot ee ns a ee Oe pee ane» 7 pais e Ae ¢ i tee t ; ‘ . . G2 | . ARMSTRONG, WARNER, CONNOR . e - ’ - " a ' we N . . a 3°: | ’ 41 a . , & foe . ilo, te. > waa - - . ee : ‘0 t nf * -- . . . ce . : nf . . ” : . . . : e . ‘ , ; . vue ve, ' ye ls t : . «4 Biwi et ok L 5 - . s ay + 7 . ra : . FIGURE 7 (aj) fe ' Top left: Baseline atherosclerosis. Markeel luminal occlusion by encroachment of intinia - - showing several of the features found: cellular accunudation including lipid-leden macrophases, . : >. fibrous proliferation, and cellular breakdown, Yematoxylin and eosin, & 109. Top right if . Baseline atherasclerosis. A downstream section from the artery shown in top left figure Gfter ye staining for fat. A relatively fet-free collar of fivrous tissue encircles the lumen. Through- 7 out the rest of the intima mixtures of fat-free and fat-Leaiing celly are found among varying amounts of intimal scarring, Oil-Red-O, x GO. Micdle left: Baseline atherosclerosis. Lard ‘ . of [ masses af acellular material are seen at the outer third of the intima. Hematoxylin and eosin, ° ve X 70. Middie right: Baseline «therosclerosis, In the larger artery a redial arrangement of , mn the outer fibrous structure Of the intima orients a mixed population of cells, the mitdie partion — “ee : of the intimal lesion is aceupied Ly a circumferential fibrous collar, and the innermost portion of : 1 shows cellular hyperplasia This form of intense arteritis may be seen frequeutly as a response ms ‘ to the hyperlipidemia, The portion of branch erery shown at the lefé has a &readier acellular : L portion in the intimal mass. Hematoxylin and cosin, x% 110, Bottom left: Regression athero- . : “E sclerosis. Visible intimal lipid (black) is small within an unusually large residual masy of fibrous . ue . T , - + Gireubition Research, Vol. XXVIL, July 1976 ' , a . we - . ' ” + ; . Teg OT terme mee ee ee ee, ad *. ~ ae I . . 3 c ft ‘ get i | onda : : 4 . ° | fot. | wey ; oe | e[- : yg | “yt i . : : ‘ ‘ ’ ‘fe < ty Ls ‘ ole . ri a t 1 . eet : ba te -*. ", Sat : ee. . t af 5 ont Pt oof ok , ft mn ; : 1 i . ; i wa + oe . ola x “ | . ’ r | Po ; . re ! . 4 > : . ok : th pf 1 ' ee, % aoc. tr ea . a nah ssf “ : “y eo bt Ua fu. a" 3} ~ § ‘ : « af Jf t : : “sf : a t 3 4, ok . toe Po atl . . ae 7 mo 4 { “af a . e o3 oe ~ : wae Pn of PA Ie = ee toe les ram - t _ Figure z 17 Top lefts Regression atherosclerosis. Numerous small gaps accur in an otherwise intact internal elastic membrane, Residual medial damage is present at top left. Vernuefs, % 109, Top right: Regression atherosclerasis. The intima stains dark (collesen} and the media pale (smooth muscle) with nearly intact architecture. Van Gieson, X G0. Bottom left: Regression atherosclerosis. “The intima consists largely of connective tissue. Hematoxylin aud eosin, X 99. Botton right: Regression atherosclerosis. Grusually small areas of intimal thickening occur, the largest of tehich is ut the bottom of the section, Hematoxylin anc ecosia, X 120, . ‘ 7 total transverse area among the groups: Pinkaon or distension cannot be ruled out in baselhe atherosclerosis, however, avcrag regression study. One was the-erdss observa- tion of dictinetly fewer lesiéns throughout accessible arterial tree, including the aorta, in y tae since the average Crosssaquonal area of the regression animals than were seen in animals arteries of this group was arger than in the With baseline atherosclerosis. This finding will * . : , rae os regression animals, although tra regression be-rénorted separately. A second observation monkeys: were more than 3 ycars™s! autopsy, The decreased narrowing of the lumens o the coronary arteries in animals-fed regression regimens was accompanjed’by several features that would be looked for at the end of . al der at pertains to the gross appearance of the “unopened, intact core nary arteries themsclves, Group 1 had beaded, ivory-colored arteries, puithe regression groups had smoother, paler arteries~suggesting thinner walls. The third, and to us, mdstNagtabie evidence in favor of £ i a ottom right: Regression atherosclerosis, The residual intimal lesio en (dark), and collagen scary are seen also in the media, Van Gieson, X 90 tissue. Sudan IV, «% 90. ¥% is rich in collaz Circulation Research, Vol. XXVU, July 1970 * . Meet nt oe rene cere toe en rey Uteirene mee mom are corr mmvars@e sie meee ee ay gt th see ete eee ep me ee me ee eee ee . € ' ‘ 5 : . : ‘. E h ws 4 . ‘ t oi 4 boy i mete vee ae i . . ' ‘ 1 . mt nein nee et A ae, Feet NM Ree le eee armen oe fete Cte mee eae A seer ee teeta EES ee See. 40 CUMULATIVE INCIDENCE , Fy u 7 4 ' 50 . ° STRATED BY AGE 20 . . i en ne) , 20 e ‘Ze t : or? 1, EXPE . » « 337 - ' a 7 he fr a * / : “ i ve? : ta + ade * f 10 of a on - . . faci 2 eet at tet” . sey ween A ® O et edne : : - . : . . - ‘ . \ , a’ . + T # 160 STRATIFIED BY leon. .. INITIAL SERUM CHOLESTEROL ts sol-- 1 S = So ue vo teen OY uy = a. a O° STRATED BY PRE-EXISTING COMPLICATIONS N pe Prwwany 40 eT 1 + . “i ce ‘ a Wn Oo “ oO ©. x - : ' es ‘ foe a Tee 9 0” oO! ~ o e a ¢ —_— - 0 caren ) WITH J p=0.0) 40, .¥ ° . ~ 7 Exp, p=0.03 - 307 — tr Wh en Se Oem os we EXP. f , a eal eon? 9 O icoeceegreege ea : 7 / 50. , ° “2 Teon7 cane - { ! ALL CASES * * Y p=0.02 : of - . | T EXPT eee In A 20d. 304 . | . ? 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NY 6 i ed A VY I GS es 4 edeo3 PF Gi AIGGCUG NON dido CEI £2¢ ALY VLUOW UVIAG OG ee eee OTE ry ce oscar ee ; . | : ve . | . roa + . i . . : ” , * a cae - - — .~ ~ : oo . =_ . Le 6 60 6. 6. 6. = | References Coronary Heart Disease in Adults, United States, 1960-1962, Data from the National Health Survey, Vital and Health Statistics. Scrics 11, No. 10, UeS. Department of Health, Education and.Welfare. Public Health Service, Wabhington, DeCo, 1965, Vital Statistics of the United States, 1967, Vol. 2, Parts A and B, Mortality, U.S» Department of Health, Education and Welfare Public Health Service, Washington, D.C., 1969. Moriyama, I.M., Stamler, J. and Krueger, DeEo The Major Cardiovascular Diseases’-- An Epidemiolocic: Analysis, Amer, Public Health Assoc., New York, NeYo, in press. Mortality Statistics, Cardiovascular Diseases, Annual Statistics 1955-1964 by Sex and Age. . . ‘ Epidemiological and Vital Statistics Report, World Health Organization, 20, 539, 1967, Stamler, Jo, Stamler, R. and Shekelle, R. Regional Differences in Mortality, Prevalence and Incidence of Ischaemic Heart Disease. Snellen, H.A., Edo, Boerhaave Course on Ischaemic Heart Disease, 1969, Leiden, the Netherlands, in press. Data from the Pooling Project, Council on Epidemiology, American Heart ‘Association -- a national cooperative project for pooling data from the Albany civil servant, Chicago Peoples Gas Company, Chicago Western Electric Company, Framingham community, Los: Angeles civil servant, Minneapolis-St, Paul business men, and other prospective epidemiologic studies of adult cardiovascular disease in the United States, The following are representa- tive references on the individual studies and on the results of the Pooling Project presented to date: , oe Doyle, JoTe Risk Factors in Coronary Heart Disease, New York State Je Med., 63, 1317,- 1963, b. Stamler, J. - Cardiovascular Diseases in the United States, a Amer. Jo Cardiol., 10, 319, 1962. . Ce. Paul, 0., Lepper, MoH«, Phelan, WeH., Dupertuis, G.We, MacMillan, A., McKean, He and Park, Ho A Longitudinal Study of Coronary Heart Disease, Circulation, 28, 20, 1963, de Dawber, T.Re, Kannel, W.B. and McNamara, PoM. The Prediction of Coronary Heart Disease, Trans. Assoc. Life Insur. Med. Dir. Amer., 47, 70, 1964, Bo Moore, FoEo Ge Ce Chapman, JoM. and Massay, FoJe The Interrelationship of Serum Cholesterol, Hypertension, Body Weight, and Risk of Coronary Diseases Results of the First Ten Years Follow-up in the Los Angeles Ilcart Study. Je Chrone Dise, 17, 933, 1964. _£e Keys, Ao, "taylor, Hole, Blackburn, He, Brozek, Jo, Anderson, JeT. and Simonson, Ee ~~ Coronary Heart Disease among Minnesota Business and Profes Sional Men Followed Fifteen Years. «Circulation, 28, 381, 15963, Some Preliminary Findings from the Pooling Project of the Council on . Epidemiology, American Heart Association, Paper Presented at the Conference: on Cardiovascular Disease Epidemiology, Council on Epidemiology, American Heart Association, March 3-4, 1969, New Orleans, La. b he Doyle, JoT. and Kinch, S.-H. Coronary Heart Disease in the United States: Some Preliminary Findings £rom the Pooling Project o£ the Council on Epidemiology of the American - Heart Association. Presented at the 42nd Scientific Sessions, American Heart Association, Nov. 14, 1969. - ie Epstein, F.He and Moore, F.Ee Progress Report to the National Heart Institute on the National Cooperative Pooling Project, 1968, , je Paul, 0. The Risks of Mild Hypertension: A Ten Year Report. Pooling Project, Council on Epideaiology, American Heart Association. Paper presented to the VI World Congress of Cardiology, London, England, September, 1970. of Brit. Heart J., in press. ; L ke Doyle, J.T. and Kannel, W.Be Coronary Risk Factors: 10 Year Pindings in 7,446 Americans. Pooling Project, Council on Epidemiology, American Heart Association. ‘Paper presented to the VI World Congress of Cardiology, London, England, September, 1970, Brite Heart Je, in press. Kuller, Le Sudden Death in Arteriosclerotic Heart Diséase--The Case for Preventive Medicine. . Amer. Jo Cardiole, 24, 617, 1969. ” Gubner, Re Mortality Ratios in Coronary Heart Disease, in Councils for Arteriosclerosis, Clinical Cardiology and Rehabilitation, American Heart Association, New York, Sept. 15, 1967, Conference on Coronarv Artery Discase. Trans, Assoc, Life Insur. Meds Dir. Amere,. 51, 231, 1967. Coronary Drug Project Research Group. Control of Hyperlipidemia: 4. Progress in Drug Trials of Secondary Prevention, with Particular Reference to the Coronary Drug Project, in JoncsS, Rode, Edey Atherosclerosis, Second International Symposiun, Springer-Verlag, New York, NeYeo, in presse : . 12. ‘Lio 19. 10. li. 13. 15. L660 18. 20, 21, 22), 24 . oe ‘ Blological Aspects of Occlusive Vascular Disease, Adams, CoWoMe Vascular Histochemistry. 9. Lloyd-Luke, Loudoh, England, 1967. Allen, E., Barker, N. and Mines, EoAc, Jre Peripheral Vascular Disease, 3rd Edition, W.B. Saunders, Philadelphia, Pao, 1962, Blumenthal, HoT., Editor, Cowdry's Arberioscteruss, 2nd Edition, C Chaxles Co Thomas , Springfield, Ill., 196: a Brest, AeNo and Moyer, Je He, Editors. ; ; Atherosclerotic Vascular Disease, 7 a ey Appleton-Century-Crofts, New York, NeYo, 1967. Chalmers, DeGe and Gresham, G.A., Editors. Cambridge University Press, Cumbridge, England, 1964. Constantinides, Pe Experimental Atherosclerosis, Elsevier, Amsterdam, Netherlands, 1965. Friedman, Me Pathogenesis of Coronary Artery Disease, McGraw-Hill Book Co., New York, No Yos 1969, Jones, AoMo, Editor. Modern Trends in Cardiolosy ~ 2, Butterworths, London, 1969, Jones, ReJc, Editor. Evolution of the Atherosclerotic Plaque, University of Chicago Press, Chicago, Ill., 1963, ; Jones, RoJe, Editor, Atherosclerosis, Second International Symposium, Springer-Verlag, New York, 23). NeYe, in presse Likoff, W. and Moyer, JoH., Editors. Coronary Heart: Disease, Grune and Stratton, New York, N.Ye, 1963, Mann, GoeVe, Editor, 7 Symposium on Atherosclerosis. Amero Je Med., 46, 655, 1969, McGill, 1.C., Jre, Editor. : oo Geographic Pathology of Atherosclerosis, Williams and Wilkins, Baltimore, Mde, 1968. Millikan,. C. He, Sickert, ReGe and Whisnant, J.P., Editors. Cerebral Vascular Diseases, Fifth Confer ence, Grune and Stratton, New York, Ne Yo> 1966.6 : Miras, C. Jey Howard, AeNe and Becletel, Rey Editors. S. Karger, Basel/new York, i965. Raab, We Prevention of Ischemic llcart Disease, Charles C. Thomas, Springficld, T1l,, 1966. 30. 31, 32) 336 34. - 35.1 36. 37.6 38. 39. 40. +e Ok create OR Roberts, J.Co, Ir. and Straus, Re, Editors, Comparative Atherosclerosis, Hocber-ilarper, New York, NoYo, 1965, Sandler, M. and Bourne, GLE., Editors. _ Atherosclerosis and its Oricin, Academic Press, New York, NoYe, 1963, _ Schettler, F.G. and Boyd, GoS., Editors, -- Atherosclerosis, Elsevier, Amsterdam, 1969, + STE BCR CPOSAS Stamler, J. , . . Lectures on Preventive Cardiology, Grune and Stratton, New York, NoYo, 1967, Strandness, D.Eo, Jre Peripheral Arterial Disease -- A Physiologic Approach, voee ‘ Little, Brown and Company, Boston, Masso, 1969, Toole, J.F.e and Patel, A.Ne, Editors, . . Cerebrovascular Disorders, McGraw-Hill Book Co., New York, NeYo, 1967, Toole, J.Fe, Siekert, RC. and Whisnant, J.P., Editors, Cerebral Vascular Diseases, Sixth Conference. Grune and Stratton, New York, NeYe, 1968, Atherosclerosis: Recent Advances, . Ann. New York Acad, Scie, 149, Art. 2, Pp. 585-1068, Nov, 21, 1968, New York Heart Association Conference on Coronary Heart Disease: Preventive and Therapeutic Aspects, Bull, NoYe Acad. Mede, 44, Noo 8, Aug., 1968, The President's Commission on Heart Disoase Cancer ard Stroke, 3 1 Report to the President, A National Program to Conguer Heart Disease. Cancer and Stroke, Vols. 1 and 2, Washington, D.C., Dec. 1964 and Feb. 1965, Andrus, EeC. and Maxwell, C.H., Editors, : The Heart _and Circulation -- Second National Conference on Cardiovascular Diseases, Vols, 1 and ii, Federation of American Societies ror Experimental Biology, Washington, D.C., 1965, Symposium on Coronary Heart Disease, 2nd Edition (Revised), American Heart Association Monograph No, 2, American Heart Association, New York, NoYo, 1968, Fredrickson, D.Se, Levy, RoI. and Lees, RS, | Fat Transport in Lipoproteins--An Integrated Approach to Mechanisms and Disorders. New Engl. Jo Mede, 276, 34, 94, 148, 215 and 273, 1967, Keys, A.,. Aravanis, Ce, Blackburn, H.W., vanBuchem, FoSePe, Buzina, Ro, Djordjevic, B.S., Dontas, A.S., Fidanza, F., Karvonen, Mode, Kimura, Ne, | Lekos, Do, Monti, Me, Puddu, V. and Taylor, H.Le Epidemiological Studias Related to Coronary Heart Disease: Characteristics of Men Aged 40-59 in Seven Countrias, }Acta Ned. Scand., Suppl. 460, 1966, Keys, Ao , Editor, ee boo Coronary Heart Disease in Seven Countries, | Circulation, 41, Suppl, 1, 1970, 41, 42, 432 bag: 454 47, 48.6 49.) 50.) "51. | D2 ~ Documented Coronary Artery Dis A « and Gorlin, Re in Patients with Angiographically se Amere Jo Cardiol., 24, 178, 1969. Smoking and Health: Report of the Advisory Committee to the Surgeon General of the Public liealth Service, U.S. Department of Health, Education and Welfare Public Health Service Publication No, 1103, Suporintendont of Documents, UoSo Government Printing Office, Washington, DoCo, 196%. k The Health Consecuences of Smokine--A Public Health Service Review: 1967. 7 _ US. Department of Health, Education and Welfare Public liealth Service Publication No. 1696, Washington, DeCo, 1967, The Tiealth Consenuences of Smoking--1968 Susplement to the 1967 Public Health Service Reviews UseS. Department of Health, Education and Welfare, 1968 a te Supplement to Public Health Service Publication 1696, Washington, D.C., 1968. The jiealth Consequences of Smoking~-1969 Supplement to the 1967 Public Health Service Review. U.S. Department of Health, Education and Welfare Public Health Service Publication No. 1969-2, Washington, DoC., 1969. Hammond, EoCo Smoking in Relation to the Death Rates of-One Million Men and Women, in Naenszel, We, Ede, Epidemiological Approaches to the Study of Cancer and Other Diseases, National Cancer Institute monograph No, 19, ppe 127-204, UeSe Public Health Service, Bethesda, Md., Jan. 1966, Hammond, EC. and Garfinkel, Lo - . . Coronary Heart Disease, Stxoke, and Aortic Aneurysm--Factors in the Etiology. Arch. Environ. Health, 19, 167, 1969, Kahn, HoAe . . The Dorn Study of Smoking and % rtality among UeS. Veterans: Report on 8 1/2 Years of Observation, in Haenszel, We, Ede, Epidemiological Approaches to the Study of Cancer and Other iseases, National Cancer Instituce Monograph No. 19, pp. 1-125, U.S. Public Health Service, Bethesda, Md., Jan. 1966, Borhani, NoOe, Hechter, HoH. and Breslow, R. Report of a 10-year Follow-up Study of the San Francisco Longshoremen, Mortality from Coronary Heart Disease and from All Causes, Jo Chron, Dis., 16, 1251, 1963. : . ° Doyle, J.T., Dawber, ToRe, Kannel, WoBe, Kinch, S.ll, and Kahn, HA. The Relationship of Cigarette Smoking to Coronary Heart Disease, The “Second Report of the Combined Experience of the Albany, NeY. and Framingham, Mass. Studies, .- . , - JeActioAe, 190, 856, 1964, Auerbach, 0., Hammond, E.C. and Garfinkel, L. Smoking in Relation to Atherosclerosis of the Coronary Arteries. (New Engl. Jo Med., 273, 775, 1965, Sackett, DyLe, Gibson, RoW., Bross, I.DeJe and Pickron, JeWe Relation between Aortic Atherosclerosis and the Use of Cigarettes and Alcohol, An Autopsy Study. New Engl. J. Meds, 279, 1413, 1968, . oe Veene, 55k 564 57) 286 596 606} 61. 62. | 63. 64, 65, " JoAoMeAsy 202, 10, 1967. Strong, JoPeoy Richards, M.L., MeGill, WeCe, Tro, Eggen, DoA. and Meturry, MT. On the Association of Cigarette Sioking with Coronary and Aortic Atherosclerosis, Jo Atherosclex, Rese, 106, 503, 1969, , Stanler, Jo * Cigarette Smoking and Atherosclerotic Coronary Heart Disease, Bull, NoY. Acad. Mede, 44, 1476, 1968, Epstein, Follo ; : - 2 - Hyperglycemia: A Risk Factor in Coronary Heart Disease, Circulation, 36, 609, 1967, oe Pell, S. and D'Alonzo, C.A. Some Aspects of Hypertension in Diabetes Mellitus. eee Epstein, Foe, Ostrander, LoDo, Jre, Johnson, BeC., Payne, MoWe, Hayner, NoS., Keller, J.B. and Francis, T., Jr. Epidemiological Studies of Cardiovascular Disease in a Total Conmunity-Tecumseh, Michigan, Anne Intern, Med. 62, 1170, 1965, Ostrander, LeDo, Jro, Francis, Te, Jre, Hayner, NeSe, Kjelsberg, M.O. and Epstein, F.H. oO The Relationship of Cardiovascular Disease to Hyperglycemia, Anne Intern. 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