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(Circulation. 1997;95:1646-1650.)
© 1997 American Heart Association, Inc.

Articles

National Cholesterol Education Program Recommendations for Cholesterol Testing in Young Adults

A Science-Based Approach

James I. Cleeman, MD; Scott M. Grundy, MD, PhD

From the National Cholesterol Education Program (J.I.C.), National Heart, Lung, and Blood Institute, Bethesda, Md, and the Center for Human Nutrition (S.M.G.), University of Texas Southwestern Medical Center at Dallas.

Correspondence to James I. Cleeman, MD, Coordinator, National Cholesterol Education Program, National Heart, Lung, and Blood Institute, 31 Center Dr, Bldg 31, Room 4A16, Bethesda, MD 20892-2480.

Key Words: cholesterol screening • coronary disease • cholesterol • lipoproteins • adults, young

	Introduction

Top Introduction References

 
The National Cholesterol Education Program (NCEP) recommends that all adults 20 years old have their serum cholesterol concentrations measured.^{1 2} The NCEP guidelines have been endorsed by representatives of more than 40 medical and health organizations, including the American College of Cardiology, American Academy of Family Physicians, American Medical Association, American College of Preventive Medicine, and American Heart Association. A dissent from this recommendation has been registered in a recent report of the American College of Physicians (ACP),³ which maintains that it is not necessary to measure serum cholesterol levels in young adult men (ages 20 to 35 years) and premenopausal women (ages 20 to 45 years) and in older individuals (>65 years old). The arguments against cholesterol measurement in young adults and older patients are restated by Garber and Browner, the authors of the ACP guidelines, in the present issue of Circulation.⁴ The NCEP is planning to publish a detailed position paper on cholesterol lowering in the elderly population later in 1997. In this article, we outline the NCEP recommendations regarding cholesterol testing in young adults and the scientific rationale for the recommendations.

The second report of the NCEP Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II [ATP II]) recommends that total cholesterol levels be measured at least once every 5 years in all adults 20 years old and that HDL cholesterol levels be measured at the same time if accurate results are available.^{1 2} These recommendations are based on a large and diverse body of evidence derived from animal, pathological, genetic, biochemical, metabolic, and epidemiological studies and clinical trials, as extensively referenced in the ATP II report.² The 25 members of ATP II were selected, not as mischaracterized by Garber and Browner⁴ "from several professional organizations," but rather because of their independent expertise in a range of disciplines, including epidemiology, health statistics, primary care, lipidology, cardiology, nutrition, pharmacology, and health economics, that were required to develop appropriate science-based guidelines. The several drafts of the ATP II report were reviewed and commented on by the members of the NCEP Coordinating Committee. Over 18 months, careful examination of the evidence and thorough scrutiny of the proposed guidelines by both the panel and the Coordinating Committee generated a widely agreed-on set of recommendations that are grounded in solid science.

In ATP II, the preferred approach to cholesterol measurement is case finding. Case finding means using the opportunity presented by a visit to the physician to perform a total and HDL cholesterol blood test in the setting of a medical examination in which inquiries are made regarding other coronary heart disease (CHD) risk factors, ie, prior CHD and other atherosclerotic disease, age, gender, family history, cigarette smoking, high blood pressure, diabetes, obesity, and physical inactivity. Underlying this recommendation is the idea that the primary care physician has a vital role to play in assessing the CHD risk of an individual and in prescribing ways to reduce an elevated risk and that cholesterol measurement to detect a high total cholesterol and/or low HDL cholesterol level is a crucial element in developing an accurate assessment of a person's overall CHD risk.

This general recommendation is meant to include young adult men (ages 20 to 35 years) and premenopausal women (ages 20 to 45 years). One fundamental rationale for this recommendation is to detect persons who have an increased risk for CHD on the basis of the finding of an elevated serum cholesterol level. The detection of such individuals serves two purposes. First, for some patients, it enables the physician to start a program of early intervention for high serum cholesterol in the medical setting to reduce the long-term risk for CHD, primarily through changes in diet, physical activity, and weight control. For many others, detection of an elevated cholesterol level allow the physician to provide counsel on an individualized basis so patients can make informed choices about modification of life habits on their own. A second important rationale is that cholesterol measurement in young adulthood is one component of a broad public health effort to reduce risk for CHD through population-wide education and modification of risk factors.^{5 6} In our view, both reasons justify early detection of high serum cholesterol levels.

There is now strong evidence that coronary atherosclerosis begins in late adolescence and young adulthood. For example, in the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study,⁷ pathological examination of 15- to 34-year-old men and women who died suddenly revealed that atherosclerosis is present in the abdominal aorta and right coronary arteries in this age range and increases across the range. Moreover, the percentage of the intimal surface affected by raised atherosclerotic lesions is positively correlated with measured levels of LDL and VLDL cholesterol and negatively correlated with HDL cholesterol levels. This study convincingly demonstrates that young men and women with higher LDL plus VLDL cholesterol levels and lower HDL cholesterol levels are developing atherosclerosis at an accelerated rate. This basic fact militates in favor of taking the results of cholesterol measurement into account when evaluating the risk-factor status of young adults.

Furthermore, elevated cholesterol levels in young adulthood increase the risk for developing CHD later in life. Klag et al⁸ reported that a cholesterol level determined at age 22 predicts the rate of development of CHD over the following 30 to 40 years. Young adult men whose serum cholesterol is in the top quartile have five times the risk of a CHD event and nine times the risk of a myocardial infarction compared with those with levels in the bottom quartile over the ensuing 30 to 40 years. This is a dramatic demonstration of the high risk associated with elevated serum cholesterol in young adulthood; this high risk is borne by fully 25% of such individuals. Framingham Heart Study⁹ results likewise document that cholesterol levels measured in young adulthood predict cardiovascular mortality and total mortality rates 30 years later. Knowledge of an individual's cholesterol level is thus indispensable in the assessment of long-term CHD risk in young adults. The ACP guidelines³ give the long-term outlook short shrift and instead focus exclusively on the short-term risk for CHD, which is obviously quite low in young adults. But, for persons with many decades of life still to come, it is clearly relevant to know whether their present cholesterol level forecasts a high or low risk for CHD in the long run.

The long-term power of serum cholesterol to predict CHD has recently been reevaluated by Law et al.¹⁰ These researchers indicate that observational studies systematically underestimate the association between serum cholesterol concentrations and the development of ischemic heart disease. This underestimation occurs as a result of two factors: (1) regression dilution bias, which results from random fluctuation of cholesterol levels in individuals over time and which affects studies in which only a single cholesterol measurement is made, and (2) a surrogate dilution effect, which results from the fact that differences in total cholesterol levels reflect smaller differences in LDL cholesterol levels, with the latter being the major atherogenic lipoprotein. In addition, most observational studies have not included HDL cholesterol levels, which represent another powerful indicator of CHD risk. Law et al¹¹ further demonstrated that the earlier a change is made in cholesterol levels, the greater will be its long-term effects on CHD risk. For example, based on epidemiological and clinical trial data, they estimate that a 10% reduction in total cholesterol levels will reduce lifetime risk for CHD by 50% if the reduction occurs before age 40 but by only 39% if it occurs at age 50 and only 27% if it occurs at age 60. This impressive estimate of a 50% reduction differs from the 20% reduction in risk observed for the same cholesterol lowering in many short-term studies (5 years).² Even the large cholesterol reductions achieved in the recent statin trials^{12 13 14} and sustained for 5 years produced reductions in CHD rates that were significantly smaller than would be expected on the basis of epidemiological data. The long-term effects on CHD risk of differences in baseline cholesterol levels noted by Klag et al⁸ and Framingham Heart Study researchers⁹ are consistent with the thesis of Law et al^{10 11} ; however, even these long-term data ^{8 9} may have underestimated the impact of cholesterol levels because they included only single cholesterol measurements at baseline and did not correct for regression dilution bias.

One common misconception that is explicitly subscribed to by the authors of the ACP guideline is that cholesterol-lowering therapy can be instituted later in life and the risk associated with years of atherosclerosis buildup can be nullified. It is true that recent clinical trials^{12 13 14} show that cholesterol-lowering therapy in patients with advanced atherosclerotic disease reduces the risk for acute coronary syndromes (acute myocardial infarction and unstable angina). This beneficial effect probably is the result of stabilization of vulnerable plaques, which prevents plaque rupture and ensuing thrombotic events. This favorable response is observed in high-risk patients whether in primary¹⁴ or secondary^{12 13} prevention trials. However, in these trials, there is an unacceptably high rate of CHD even in the treated groups. This holds true not only for secondary prevention trials but also for primary prevention studies in which a statin drug was used to treat high-risk individuals, such as the West of Scotland Coronary Prevention Study.¹⁴ Letting atherosclerosis go unchecked for an additional 20 years before measuring cholesterol levels in midlife means that many people will be carrying a greater burden of coronary plaque and some of these people will have a CHD event before cholesterol-lowering therapy is started. Approximately 25% of first CHD events manifest as sudden death,^{15 16} and efforts at secondary prevention are too late for these persons. Mass treatment of the general population with powerful cholesterol-lowering drugs to reduce CHD risk seems a poor alternative to long-term, nondrug prevention of CHD. Once a middle-aged and older population has accumulated a large amount of coronary atherosclerosis, rates of acute myocardial infarction will be unacceptably high no matter how effective are plaque-stabilizing regimens.

Moreover, there is little evidence that cholesterol-lowering therapy initiated late in the course of atherosclerotic disease will have much of an impact on stable angina pectoris. At present, a substantial portion of cardiology is concerned with management of angina pectoris. Even in the absence of acute thrombotic events in the coronary arteries, angina pectoris causes significant morbidity in middle-aged and older Americans. Most of coronary angioplasty and much of coronary surgery are performed to relieve the symptoms of angina. These symptoms arise from atherosclerotic narrowing of the coronary arteries. Angiographic studies¹⁷ show that cholesterol-lowering therapy produces modest changes in existing coronary lesions of the type responsible for angina pectoris. The most promising way to modify the incidence and morbidity of angina is to prevent the development of atherosclerosis in the first place. This can be achieved only through reduction in risk factors on a long-term basis. Lowering cholesterol levels in young adulthood is thus a necessary element of the long-term prevention of atherosclerosis and reduction in the burden of CHD on our society.

One of the distinctions that Garber and Browner⁴ make between the NCEP and ACP guidelines is that, in their view, the latter are based on quantitative inferences, whereas the former are not. This is an erroneous assertion. The NCEP developed numerous quantitative estimates of the downstream consequences of the ATP II recommendations, including estimates of the percentage of adults who would be candidates for various steps of the ATP II diagnostic and treatment algorithm. When the NCEP ATP II guidelines were released on June 15, 1993, it was stated that implementation of the guidelines would mean that 40% of adults would have a full lipoprotein profile, 29% would require dietary therapy under medical supervision, and 7% would be candidates for drug treatment.¹⁸ In contrast, the ACP guidelines³ did not quantify the number of young adults with high cholesterol levels who will be missed if their cholesterol levels are not measured and who will thereby be denied the knowledge that they have a proven personal stake in lowering their cholesterol level.

One category of young adults who will be missed by the ACP approach is those with familial hypercholesterolemia (FH) and other genetic dyslipidemias. Most investigators agree that early detection of FH is useful for the purpose of initiating early therapy. The ACP guidelines suggest that screening of young adults for FH is inefficient. However, at least half of young adults with FH will go undetected if family history is relied on to decide whether cholesterol should be measured.¹⁹ The number who will remain undetected on the basis of family history is 79 000 individuals. This estimate is based on the assumption that the prevalence of FH in the population is 1 per 500 persons. In fact, severe polygenic hypercholesterolemia and other genetic dyslipidemias have a higher prevalence in young adults, ie, 1 per 100 to 200 persons. Few of these affected patients will be detected on the basis of family history alone. Thus, the total number of people with severe hypercholesterolemia or other genetic dyslipidemias who would be detected by cholesterol measurement in young adults will considerably exceed those with definite FH. Many of these more severely affected persons will need intensive cholesterol-lowering efforts. Most will be missed by the ACP guidelines.

Another category of individuals who will be missed by the ACP guidelines are young adults with LDL cholesterol levels of 190 to 219 mg/dL. The NCEP^{1 2} has recommended that the use of cholesterol-lowering drugs be delayed in young adult men (<35 years old) and premenopausal women whose LDL cholesterol levels are <220 mg/dL. Nevertheless, special attention must be given to those in whom LDL cholesterol levels range from 190 to 219 mg/dL. At the least, maximal dietary therapy should be instituted and patients should be monitored for response. If the LDL cholesterol level persists in the range of 190 to 220 mg/dL after maximal dietary therapy, consideration can be given to the use of drugs whose long-term safety is known, such as bile acid sequestrants. In young adults who have other risk factors (eg, cigarette smoking or diabetes mellitus), LDL cholesterol levels in the range of 190 to 220 mg/dL deserve more aggressive management. The NCEP guidelines for management of very high LDL levels in young adults are influenced by the fact that such patients are not at high risk for CHD in the short term (eg, the next 10 years). On the other hand, such patients are developing coronary atherosclerosis at an increased rate. Consequently, efforts to reduce LDL cholesterol levels and, in turn, retard coronary atherogenesis appear to be fully warranted. Of course, a safe approach should be adopted. This generally means the use of maximal dietary therapy and, in some cases in which relative risk is particularly high, the use of cholesterol-lowering drugs with a known long-term safety profile.

Perhaps even more important from the viewpoint of public health is the detection of young adults with borderline high-risk (130 to 159 mg/dL) and high-risk (>160 mg/dL) LDL cholesterol levels who will be missed by use of the ACP guidelines. According to data from NHANES III,² 12% of men ages 20 to 34 have LDL cholesterol levels in the high-risk range. Approximately 8% of premenopausal women have high-risk LDL cholesterol levels. These young adults with high-risk levels of LDL cholesterol deserve individualized attention for risk-factor modification. Although most persons with such LDL levels do not require cholesterol-lowering drugs, they should receive special attention to modify any other risk factors, and dietary therapy should be implemented in the effort to reduce LDL cholesterol levels to <160 mg/dL. An additional 23% of young adult men and 20% of premenopausal women have borderline high-risk LDL cholesterol levels.² At the very least, these persons should be informed that they carry a long-term risk for CHD that is greater than that of most young adults, ie, greater than the risk for 65% of young adult men and 72% of premenopausal women. The physician can play several roles in working with young adults with borderline high-risk LDL cholesterol: first, the physician has the responsibility of informing a patient of a relatively increased long-term risk for CHD; second, the physician should provide advice on modification of life habits and monitor for long-term results; and third, the physician should pay increased attention to other cardiovascular risk factors and modify them appropriately. As shown in long-term prospective studies,^{8 9} patients with borderline high-risk and high-risk LDL cholesterol levels are those most likely to develop premature CHD. Therefore, low-cost and safe forms of intervention to lower cholesterol levels are justified.

The NCEP has recommended that HDL cholesterol levels be measured at the time of cholesterol testing. An HDL cholesterol level of <35 mg/dL is listed as a major and independent risk factor for CHD.^{1 2} Approximately 15% of young adult men and 5% of premenopausal women have categorically low HDL cholesterol levels (<35 mg/dL).² Failure to detect a low serum HDL cholesterol level leaves another risk factor out of the assessment of CHD risk. A low HDL cholesterol level is increasingly being recognized as a marker for high CHD risk. It is a frequent component of the insulin-resistance syndrome.²⁰ Therefore, detection of a low HDL cholesterol level can alert the physician to another set of risk parameters. Special attention should be given to mitigating the insulin-resistance state through changes in life habits, ie, weight control and exercise.

A prominent assumption of the ACP recommendations is that "diet does not work." In other words, it is futile to advise dietary change because patients will refuse to heed advice. Very few investigators hold that dietary change cannot lower serum LDL cholesterol levels if truly adopted. A large number of dietary studies document that a change from the current American diet to the NCEP recommended diet will produce, on average, an approximate 10% reduction in serum LDL cholesterol levels.²¹ More intensive dietary therapy will produce even greater lowering. The pessimistic attitude adopted by ACP does not seem justified by the facts. For the entire US population, diet has worked. Over the past two decades, intakes of saturated fat, total fat, and dietary cholesterol have declined.²² LDL cholesterol levels in the entire population have declined in parallel.²³ If such a change can occur, it is probable that a greater change in eating habits can be brought about in the medical care setting when required because of a high cholesterol level, since studies²¹ demonstrate that the degree of cholesterol lowering achieved through dietary therapy of an individual is greater than that achieved in the population approach. At the very least, young adults with borderline high-risk or high-risk levels of LDL cholesterol deserve to be identified, informed of their elevated risk, and offered the opportunity for dietary change. The choice should be theirs.

The decline in population-wide cholesterol levels has come at the same time as a sharp increase in the percentage of adults who have had their cholesterol checked and have been told their level.²⁴ Informing people of their cholesterol level has an impact on their dietary behaviors and on the magnitude of cholesterol lowering they achieve.²⁵ It is quite likely that the documented increase in cholesterol measurement has contributed significantly to the observed population effects of increased cholesterol awareness and reduced cholesterol levels.

The nondrug approach to the treatment of patients with elevated LDL cholesterol goes beyond reduction in saturated fats and dietary cholesterol. Many young adults with elevated LDL cholesterol are in the process of gaining weight. Much of the weight gain with aging, which contributes significantly to the rise of LDL cholesterol levels with aging, occurs in the years between 20 and 35. Data from NHANES have shown that increasing obesity has a particularly strong effect on cholesterol levels in this age range.^{26 27} Therefore, special attention should be given to weight control in young adults with elevated LDL cholesterol. The NCEP has placed increased emphasis on exercise as a component of risk reduction in patients with high serum cholesterol levels.^{1 2} Exercise also is helpful in weight control. The finding of elevated serum cholesterol in a young adult thus should cause a physician to redouble the advice for weight control and increased exercise. This advice is particularly important for young adults who have low serum HDL cholesterol levels, which as stated above often is an indicator of insulin resistance.

Another major concern that contributed to the ACP recommendations was the assumption that cholesterol screening will necessarily lead to inappropriate use of drugs to control elevated serum cholesterol levels in young adults. The data say otherwise.²⁴ Only 0.2% of adults 25 to 34 years old are taking cholesterol-lowering drugs, whereas 61% have had their cholesterol measured and only 1% of adults 35 to 44 years old are taking cholesterol-lowering medication, whereas 76% have been tested. These statistics support the view of the NCEP, which holds that internists and other primary care physicians can be trusted to continue measuring cholesterol levels and exercising sound clinical judgment to avoid inappropriate drug treatment in young adults. The NCEP guidelines are quite explicit on who among young adults are candidates for drug therapy.^{1 2} It is inappropriate that millions of young adults should be denied the advice of their physician regarding cholesterol levels simply because the authors of the ACP guidelines hold that neither physician nor patient can be trusted to use this information wisely and must therefore be kept in the dark. In our view, a more reasoned approach is to encourage physicians to routinely make the appropriate measurements and to act on them with sound judgment.

	References

Top Introduction References

 

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This Article Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cleeman, J. I. Articles by Grundy, S. M. Search for Related Content PubMed PubMed Citation Articles by Cleeman, J. I. Articles by Grundy, S. M.