SUMMARY The relationship between the degree of obesity and the incidence of cardiovascular disease (CVD) THE IMPORTANCE of body weight, body mass and other measures of adiposity in the prediction of cardiovascular disease (CVD) has been the subject of longstanding debate. Many studies have shown that the incidence of certain types of CVD, particularly coronary heart disease and stroke, is greater in heavier persons,'`but only a few suggest that any obesity index makes an additional contribution to risk once the levels of coexisting risk factors are taken into account. '.2'4 Obesity is associated with elevated blood pressure, blood lipids and blood glucose,7 1 and changes in body weight are coincident with changes in these risk factors for disease.", 113 Thus, the consensus has been that the increased risk among heavier persons is due primarily to the influence of the associated risk factor profile and not to the degree of obesity per se. The existing data have also been interpreted to suggest that obesity is benign when it exists without other major risk factors for CVD.In this report, we reexamine the obesity question and describe the influence of relative weight on the 26-year incidence of CVD in Framingham men and women. Earlier results from this study suggested that the degree of obesity is not a potent independent risk factor for CVD in general, particularly among women. 14, 15 However, these conclusions were based on analyses of the influence of relative weight over shorter periods of follow-up and may not have conveyed the true impact of disease risk.Such a reevaluation appears timely in view of the current revisions to the original Metropolitan Life In-
The relation between high density lipoprotein cholesterol (HDL-C) and the development of myocardlal Infarction was examined In 2425 subjects, aged 50 to 79 years, who were enrolled In the Framingham Study from 1969 to 1971. After 12 years of follow-up, men in the bottom three quartiles of HDL-C (<52 mg/dl) experienced a 60% to 70% excess of myocardlal Infarction as compared to men whose HDL-C levels were higher (p<0.05). The effect of HDL-C was especially strong In women. In separate comparisons to the 4th quartlle of HDL-C (> 67 mg/dl), the risk of myocardial Infarction Increased from a fourfold excess In the adjacent 3rd quartlle (56 to 66 mg/dl, p<0.01) to a nearly sixfold excess In the 1st quartile (<46 mg/dl, p < 0.001). These results persisted after adjusting for age and other risk factors. In addition, a significant effect of HDL-C remained In subjects who had the lowest concentrations of total cholesterol (=s 192 mg/dl In men and 211 mg/dl In women) In which 29% had levels of HDL-C (s 36 mg/dl In men and 46 mg/dl In women) that were associated with a marked elevation In the Incidence of myocardlal Infarction. We conclude that screening for total cholesterol alone In men and women aged 50 and older may not adequately Identify the coronary candidate. In addition, selective screening of HDL-C only for Individuals with high concentrations of total cholesterol can leave the false Impression that low total cholesterol Is uniformly associated with a healthy risk profile. S everal epidemiologic studies have demonstrated that high density lipoprotein cholesterol (HDL-C) is inversely related to the incidence of coronary heart disease morbidity and mortality.1 " 7 Fewer studies have established a relation between HDL-C and specific coronary manifestations, including angina pectoris, coronary insufficiency, and myocardial infarction. while most fail to provide data for women. 3 " 10 In this report, a closer examination of the effect of HDL-C as a determinant of the specific manifestation of myocardial infarction is presented for men and women aged 50 and older. We describe the incidence of myocardial infarction as it occurred for various ranges of HDL-C, after adjusting for age and other cardiovascular risk factors. We further examine the effect of HDL-C within groups of subjects with low and high concentrations of total cholesterol and the resulting implications for screening for total cholesterol alone. Findings for this report are based on 12 years of follow-up of a sample of subjects originally enrolled in the Framingham Study. MethodsSince 1948, the Framingham Study has biennially followed 5209 men and women for the development of cardiovascular disease. Sampling methods, response rates, follow-up, and examination procedures have been described elsewhere.11 - 12From 1969 to 1971, fasting levels of HDL-C were first determined among study participants after heparin-manganese chloride precipitation of fresh plasma, following a modified protocol adopted by the Lipid Research Clinics. 13For this report, subjects we...
SUMMARY The relationships of total cholesterol and the proportion of cholesterol in individual lipoprotein classes to coronary heart disease are complex. To help simplify these relationships, cholesterol values are often combined into one summary estimate to form a single risk factor with a relationship to disease that is more easily described. Although summary estimates result in convenient expressions relating cholesterols to coronary heart disease, there is the potential for sacrificing information by ignoring the joint configuration of cholesterols that make up these estimates. We investigated the extent of this possibility for the ratio of total cholesterol to high-density lipoprotein cholesterol and the ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol. The findings suggest that the summary estimates are useful expressions for combining cholesterol information and are strong predictors of coronary heart disease. Clinicians who choose to use a summary estimate for screening purposes should recognize that a single ratio estimate is not always as informative as the joint configuration of the cholesterols that make up the estimate. This possibility is most clearly exhibited for the ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol, and it may become more apparent in future studies as the capabilities of exploring lipoprotein cholesterol relationships improve.TOTAL CHOLESTEROL (T-C) and the amount of cholesterol in individual lipoprotein density classes have been shown to be related to the development of coronary heart disease (CHD). 11 With the discovery of these relationships, attempts have often been made to reduce the complex explanations of causality among the lipoprotein density classes. These attempts have resulted in the derivation of summary estimates, which combine information contained in more than one cholesterol value.5 -0 The summary estimates are not intended to replace the need to jointly consider individual pieces of information concerning lipid profiles. Rather, they are convenient measures of disease risk because they provide a single value that quantifies the
Margarine is a major source of trans fatty acids, the intake of which has risen since the early 20th century. Some data indicate that consumption of trans fatty acids increases the risk of coronary heart disease (CHD). In 1966-1969, 832 men from the Framingham Study, age 45-64 years and free of CHD, were administered a single 24-hour dietary recall, from which we estimated total daily margarine intake. We calculated CHD cumulative incidence rates and, using proportional hazards regression, CHD incidence rate ratios over 21 years of follow-up. Mean energy intake was 2,619 kcal; mean margarine intake was 1.8 (range 0-12) tsp per day. There were 267 incident cases of CHD. Age-adjusted CHD cumulative incidence rose over categories of margarine intake, but the increased risk was apparent only in the second half of the follow-up period. Adjusted for age and energy intake, the risk ratio for CHD for each increment of 1 teaspoon per day of margarine was 0.98 [95% confidence interval (CI) = 0.91-1.05] for the first 10 years of follow-up and 1.10 (95% CI = 1.04-1.17) for follow-up years 11-21. Adjustment for total fat intake and for cigarette smoking, glucose intolerance, left ventricular hypertrophy, body mass index, blood pressure, physical activity, and alcohol intake did not materially change the results. Butter intake did not predict CHD incidence. These data offer modest support to the hypothesis that margarine intake increases the risk of coronary heart disease.
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