How best to manage cholesterol in pediatric practice? Solutions remain controversial, but a pediatric cardiologist clarifies how to proceed.
How best to manage cholesterol in pediatric practice remains controversial. By answering the questions that surround this issue, a pediatric cardiologist clarifies how to proceed.
Although mortality from cardiovascular disease steadily decreased from the 1960s to the early 1990s, these gains have reached a plateau.1 As a result, the spotlight is once again on how to prevent coronary artery disease (CAD) and lower cholesterol.
The role of the pediatrician in blood pressure assessment, smoking prevention, the encouragement of physical activity, and the prevention of obesity arouses little controversy. Yet the importance of measuring and controlling the cholesterol level in children continues to produce heated commentary.2-4 This is so, even though recent public health programs to reduce cholesterol through diet and drug treatment have been successful, whereas efforts to prevent tobacco use, increase physical activity, and control obesity in children and adolescents have not been effective.1,5-7
In 1992, the National Cholesterol Education Program (NCEP) issued a consensus report on the importance of reducing blood cholesterol in childhood.2,8 According to the report, the daily diet of a child older than 2 years should comprise less than 30% fatof which no more than one third (10% of total energy intake) should be saturated fatand less than 300 mg of cholesterol. The NCEP recommends cholesterol screening for children with a positive family history of early myocardial infarction or elevated cholesterol. More aggressive treatment is reserved for those with the highest levels of low-density lipoprotein (LDL) cholesterol. These recommendations have not been well implemented in pediatric practice, though the American Academy of Pediatrics recently re-endorsed them.2,9
To guide cholesterol management in pediatric practice, pediatricians need answers to several important questions:
We have known since the 1950s that coronary atherosclerosis begins in youth. In the past decade, the unambiguous relationship between risk factors for cardiovascular disease and premature atherosclerosis has become apparent. In the Bogalusa Heart Study, which assessed cardiovascular risk factors in children attending school in Bogalusa, La., between 1972 and 1992,10 autopsy studies were performed on 204 individuals who died prematurely of all causes. Investigators found a positive relationship between an elevated premortem cholesterol level and the extent of atherosclerotic lesions. In fact, the study showed relationships between all conventional risk factors for coronary artery disease and atherosclerosis and demonstrated that the presence of several such risk factors magnified the risk of disease.
The Pathobiological Determinants of Atherosclerosis in Youth Study (PDAY) performed autopsy studies of young adults who died between 15 and 35 years of age, measuring risk factors for cardiovascular disease.11,12 This study, too, showed strong relationships between atherosclerosis and the presence of risk factors for cardiovascular disease, particularly a high LDL cholesterol level, thick renal artery walls (a surrogate for blood pressure), high thiocyanate levels (a surrogate for tobacco use), and the presence of diabetes mellitus and obesity. Most important, fibrous plaque, the irreversible lesion of atherosclerosis, had a prevalence of 15% to 20% in the study group by the end of the second decade of life.
A comparison of the relationship among risk status, age, and atherosclerosis in young people with the relationship among risk status, age, and coronary mortality in adults offers insight into how the presence of risk factors for CAD affects the aging process of the coronary vasculature (Figure 1).11,13 The 15-year-old at high risk of a cardiovascular event because of high LDL levels, low high-density lipoprotein (HDL) cholesterol levels, and smoking has about the same amount of atherosclerosis as the 35-year-old nonsmoker with low LDL levels, and high HDL levels. In the Framingham Study, a long-range follow-up study of adults and their cardiovascular risk factors begun 50 years ago, the 35-year-old at high risk of cardiovascular disease has the same CAD mortality rate as the 60-year-old with no risk factors. Thus, the presence of risk factors, including elevated LDL cholesterol, appears to accelerate the aging process in the coronary vasculature, a process that begins in earnest in the second decade of life.
A low-risk state prevents subsequent CAD.14 Longitudinal studies of several hundred thousand adults followed for decades show that persons without cardiovascular risk factors are remarkably well-protected from cardiovascular disease, with rates of coronary disease from one third to one fifth that of persons with risk factors. It is useful to remember that, whereas only a few adults have no risk factors for cardiovascular disease, most 10-year-olds have a cholesterol level less than 180 mg/dL and a systolic blood pressure less than 120 mm Hg, do not smoke, and are not diabetic. Maintenance of this healthful state, called primordial prevention, should be a goal of pediatric care.
At least 30% of Americans either die of cardiovascular disease or experience substantial cardiovascular morbidity. Risk begins to rise at cholesterol levels below the 50th percentile for adults. Indeed, most heart attacks occur in persons with only a mild elevation of LDL cholesterol.15 Americans consume about 3% to 4% more fat than recommended and 2% to 4% more saturated fat. Daily cholesterol intake is now appropriate.16 Since the goal for children and adolescents is to prevent the rise of the cholesterol level with age, the entire family will benefit from implementing a diet low in cholesterol and saturated fat. Such a diet should be recommended before measuring the cholesterol level in children. Cholesterol levels have been shown to fall among children in the United States when changes are made to the diet.7
Following the recommended diet may not be sufficient for children with familial hypercholesterolemia (FH), which affects one in 500 people. Homozygotes (1:1,000,000 frequency) experience cardiovascular morbidity beginning in the second decade of life; more than half of male heterozygotes experience cardiovascular morbidity by age 50 and half of females by age 60.17 Coronary calcium, normally not recognized until the fourth decade of life, has been demonstrated in roughly 25% of adolescents with FH (Figure 2).18 Endothelial dysfunction, as assessed by brachial artery reactivity and increased carotid artery thickness as measured by ultrasound, is characteristic in adolescents with FH.19,20 Measuring cholesterol levels is a meaningful way to screen for this genetic disorder, particularly because more aggressive treatment may alter the natural history of the disease.
The literature discusses three cholesterol screening strategies for children: no screening, selective screening, and universal screening.21 Since young adults rarely go to the doctor, a person with FH who is not screened during childhood may not be identified until late in the third or fourth decade of life when he (or she) first undergoes cholesterol testing. NCEP guidelines recommend selective screening based on family history of either early myocardial infarction or elevated cholesterol. This strategy tests about 25% of the population and identifies only 50% of those with elevated cholesterol. Universal screening has the advantage of identifying everyone with FH (Table 1); the disadvantage is cost. Some observers argue that, in addition, the cost of beginning treatment in adolescenceincluding dietary counseling and medicationdoes not justify the benefit in health outcomes.3
Recent research on screening has uncovered other problems. The cholesterol level varies considerably from year to year, particularly at young ages and during puberty.22,23 This variability makes it difficult to classify accurately children in the 60th to 95th percentiles of risk distribution, which include those with a cholesterol level considered borderline high or high (Figure 3).
According to NCEP cut points, cholesterol of 170 mg/dL (110 mg/dL for LDL) is borderline high and 200 mg/dL (130 mg/dL for LDL) is high. A child's cholesterol level can be accurately predicted if the cholesterol level of both parents is known, but this information is rarely available. In addition, children are reluctant to have blood drawn, making it problematic to repeat the measurement to ensure accuracy, as recommended by NCEP.
Total cholesterol and HDL cholesterol can be measured without fasting. To calculate LDL cholesterol, use this formula: LDL cholesterol = total cholesterol - HDL cholesterol - (triglycerides/5). To use this equation and measure triglycerides (TG), the patient must fast for 12 to 14 hours.24 The formula cannot be used for TG greater than 400 mg/dL because chylomicrons are present in the blood.
Defining elevated cholesterol in children is not easy. The initial NCEP guideline was based on the distribution of cholesterol among American children in the Lipid Research Clinics Prevalence study.8 The borderline high level was established at the 75th percentile, the high level at about the 95th percentile.
Choosing a cut point based on statistical considerations can be problematic. Different population-based data sets provide different values for specific percentile cut points, as do different laboratory methodologies for measuring blood lipids. Pubertal-related changes in lipid levels confound interpretation.22 Last, decade-to-decade changes in the cholesterol level in the population make problematic an understanding of what is "normal." Is "normal" based on levels in the children of a country without significant coronary artery disease or on 50th percentile levels for US children?
Another way to identify abnormal values would be to select a level of cholesterol reliably associated with disease or a consensus point at which drug therapy would be initiated. Consider that an LDL cholesterol level of 160 mg/dL reliably segregates children of parents with FH into those with and without the genetic disorder.17 In long-term follow-up studies of adults, cardiovascular risk begins to increase at an LDL cholesterol level of about 110 mg/dL and increases at least twofold above baseline at about 160 mg/dL.14 In PDAY, an increase of 50 mg/dL of non-HDL cholesterol was associated with an approximate doubling of risk for the presence of atherosclerotic plaque, which is consistent with observations of myocardial infarction rates in adult populations.11
From a clinical treatment standpoint, an LDL cholesterol value of 190 to 220 mg/dL has generally been considered a reasonable starting point for drug treatment of younger patients.8,24 Thus, a disease-based rationale for cholesterol screening cut points should reliably identify all children with LDL cholesterol above 190 mg/dL and most of those above 160 mg/dL. Cut points recommended for adults meet this requirement: a total cholesterol (TC) of 200 mg/dL for borderline high and 240 mg/dL for high.23,25
No studies in the literature demonstrate that lowering cholesterol in youngsters prevents myocardial infarction or stroke as an adult. Because the time between youth and a myocardial event can be measured in decades, the case for a treatment benefit must be made by inference rather than from clinical trial data. Making the decision to treat a youngster rests on an understanding of the effectiveness of diet, the efficacy of various medications, and, because therapy will continue for many years, safety. Substantial progress has been made in all these areas since NCEP guidelines were published, with regard to treating the population at large and treating individuals.
Treating high cholesterol in the population at large. Two long-term randomized trials in youth provide data on the safety and efficacy of a low-saturated-fat, low-cholesterol diet. The Dietary Intervention Study in Childhood (DISC) compared dietary measures with conventional medical treatment and current diet during a three-year period in more than 600 children, from 8 to 11 years of age, with elevated LDL cholesterol.26 Dietary treatment was associated with a small but statistically significant reduction in LDL cholesterol, and the diet was found to be safe across a range of anthropometric, hormonal, psychologic, and nutritional endpoints.
The Turku Infant Study of a low-saturated-fat and low-cholesterol diet was begun in Finland with infants from 6 months to 1 year of age27; follow up has passed the five-year mark. Again, mild cholesterol lowering and the safety of such a diet across a broad range of endpoints and efficacy was demonstrated. Preliminary data also suggest that persons on the lower fat diet may be less obese than controls.
The diets in both these studies were slightly more restrictive than the low-fat, low-cholesterol population diet discussed above and were well accepted by participants. These studies therefore establish the safety of the population diet. In fact, this diet has been endorsed in the prevention of a wide range of chronic diseases of adulthood.28
Questions about the safety of a low-fat and low-cholesterol diet raised a decade ago have been put to rest, but questions about efficacy remain. This discussion has been clouded by confusion about the goals of treatment using diet. A critical goal of recommending a low- saturated-fat and low-cholesterol diet to an entire population is to lower that population's cholesterol level and coronary mortality. Think of this public health role as trying to lower the average cholesterol level where you live by 5 mg/dL.
In DISC, the control group had a diet similar to that of the typical American child; the treatment group had the recommended diet. Results of DISC suggest that a change from the typical diet to the recommended diet in the population at large would decrease the mean cholesterol level in children. Tracking of trends in diet, cholesterol level, and cardiovascular mortality in several countries around the world indicates that this lowering of cholesterol would be beneficial.5 Pediatricians can do their part by advising schools to change their lunch program, providing nutrition advice to supermarkets, and persuading restaurants to serve heart-healthy menu selections.
Treating high cholesterol in individuals. In contrast, studies suggest that following the standard dietary recommendation will not lower cholesterol enough to treat FH adequately or to prevent or delay significantly the onset of CAD in those who have this condition. In patients with high LDL cholesterol, it is important to restrict saturated fat to less than 7% of total calories and dietary cholesterol to less than 200 mg/day (Table 2).8,24
Although a high cholesterol level can sometimes be reduced substantially by dietary intervention, particularly if the patient's diet is poor at presentation, the patient typically comes from a family in which dietary management is already in place because a family member is affected by FH. Drug therapy usually is needed. Maintaining a good diet is important nonetheless because the cholesterol level will rise if the patient resumes a poor diet.
In middle-aged adults with a mild or severe elevation of LDL cholesterol, drug treatment prevents future CAD. HMG-CoA reductase inhibitors or statins provide the best results and offer the best long-term safety.29,30 Aggressive cholesterol lowering in those with manifest CAD has produced dramatic improvement in outcome, but the cost-benefit ratio of treatment in asymptomatic adults is not established.
At what age should treatment start? What level of LDL cholesterol should trigger treatment? These questions would be easier to answer if noninvasive testing for the presence of atherosclerosis were available. For adolescents with FH, abnormalities in carotid artery wall thickness, endothelial dysfunction, and coronary calcium are indicative.18,20 These tests are not sufficiently discriminating to be used clinically, however, and we have no longitudinal studies of the impact of treatment on these secondary endpoints.
Two principles drawn from the recent literature can be applied to improve treatment decisions in youngsters. First, irreversible plaque does not develop until well into the second decade of life, making it unlikely that treatment will be beneficial before adolescence unless extreme hyperlipidemia or other severe risk factors for artherosclerosis are present. Second, the presence of more than one risk factor intensifies the rate at which atherosclerosis progresses. Risk intensifiers include regular tobacco use, diabetes mellitus (or impaired glucose tolerance), an HDL cholesterol level of less than 35 mg/dL, hypertension, and a strong family history for early myocardial events.
Two factors can be protective against CAD: female gender and an HDL cholesterol level of 60 mg/dL or higher.24 Data are insufficient to assess how other risk factors (independent of those already mentioned), such as an elevated level of homocysteine and lipoprotein (a) and mild obesity, should affect pediatric treatment decisions.
I usually initiate drug treatment at the conclusion of the adolescent growth spurt in teens with an LDL cholesterol level above 190 mg/dL (Table 3); the cholesterol level will only rise after this stage of development. I delay treatment if protective factors are present and begin treatment at a younger age if multiple risk factors are present or LDL cholesterol is extremely highmore than 250 mg/dL. Most families are not eager for their child to begin medication, so the decision to treat often is made after a period of follow up and diet treatment. If the youngster has an atrocious diet, drug therapy always should be delayed until diet modification has been tried. Conversely, treatment should not be delayed if the youngster has multiple risk factors and is trying hard to adhere to the recommended diet.
Choice of medication depends on the severity of cholesterol elevation, age of the patient, and the family's experience. Three general classes of drugs are used in children. The resins prevent bile acid reabsorption in the gut. Commercially available products include different preparations of cholestyramine; some special margarines are available in supermarkets. Niacin blocks very low density lipoprotein (VLDL) release from the liver. Finally, the HMG-CoA reductase inhibitors or "statins" are the first choice for adults. Table 4 lists available drugs and pertinent information about them.
I prescribe cholestyramine for younger children and those closest to the 190 mg/dL cut point because a low dose of this medication is generally effective. I prescribe statins in older adolescents and when LDL cholesterol is very high; lovastatin has recently been shown safe and effective in adolescents.6 Niacin is reserved for the rare patient who is willing to comply with the drug initiation protocol and frequent safety monitoring. For patients with a very low HDL cholesterol or high triglycerides, I use atorvastatin or niacin for initial therapy. A good rule of thumb is to use a drug that an affected parent has taken successfully.
"Promoting a healthy cholesterol level" below summarizes how to make cholesterol management part of office practice.
NCEP guidelines have stood the test of time, or at least one decade. They could benefit from an update, not only to reflect evolving science but to ease implementation because their associated algorithms are cumbersome to execute.2-4,8,24
Institute a population-based intervention to improve the cardiovascular health of American children. Many studies have established the usefulness and safety of the population-based diet. The population-based approach cannot be limited to diet, however. CAD prevention guidelines should address a range of behaviors that lower risk for not only CAD but other diseases as well. Avoidance of tobacco products, participation in regular exercise, balanced nutrition, and appropriate caloric intake for body size should be incorporated into the primordial prevention or health promotion message. Physicians should advocate this approach more actively.
Provide universal cholesterol screening for FH. NCEP guidelines for adults should be extended into the pediatric age range, explicitly to identify potential candidates for medical therapy in adolescence (Table 5). As a corollary, the cut points for borderline high total, high total, and LDL cholesterol should be the same as for adults.24
High cholesterol would be defined as TC of 240 mg/dL or higher and LDL cholesterol of 160 mg/dL or higher; borderline high would be TC of 200 mg/dL or higher and an LDL cholesterol of 130 mg/dL or higher. Initial screening would be for TC and HDL cholesterol, for which fasting is not required, and screening would be conducted through physicians' offices so that counseling would be provided. Age at screening should be above 5 years so that the child can participate more fully in diet education.
These changes would simplify the current treatment algorithm. They would also more cleanly separate those who need dietary education from those who might require medicine, and focus attention in the physician's office on medical aspects of treatment.
Don't begin medical therapy until middle to late adolescence. Unless a youngster is at extremely high risk, treatment need not begin earlier. In deciding to initiate therapy, use the same cut points for borderline high TC, high TC, and LDL cholesterol as are used for adults.
The prevention of chronic diseases of adulthood that have their origin in youth is of increasing importance in pediatric practice. CAD is the leading cause of death in the United States; research performed in the last decade demonstrates the pediatric origins of atherosclerosis and supports a public health approach to CAD risk intervention in childhood. The outcome? A population that is maintained in the relatively low-risk state of childhoodnot only by keeping the cholesterol level low but by preventing obesity and tobacco usehas less CAD as it enters adulthood.1
Adolescents in the categories of highest risk are most likely to have premature atherosclerosis and may therefore have the most to gain from intervention. Pediatricians can lower the risk of CAD by participating in public health programs that prevent development of cardiovascular risk factors and by identifying and treating children who are at substantially increased risk from genetic diseases such as FH.
1. Pearson TA: Population benefits of cholesterol reduction: Epidemiology, economics, and ethics. Am J Cardiol 2000;85:20E
2. American Academy of Pediatrics, Committee on Nutrition: Cholesterol in childhood. Pediatrics 1998; 101:141
3. Newman TB, Garber AM: Cholesterol screening in children and adolescents (Commentary). Pediatrics 2000;105:637
4. Bricker JT: CVD Prevention. Cardiovascular Risk 2000 (in press)
5. Verschuren WM, Jacobs DR, Bloemberg BP, et al: Serum total cholesterol and long-term CAD mortality in different cultures: Twenty-five-year follow-up of the Seven Countries Study. JAMA 1995;274:131
6. Stein EA, Illingworth DR, Kwiterovich PO Jr, et al: Efficacy and safety of Lovastatin in adolescent males with heterozygous familial hypercholesterolemia. A randomized controlled trial. JAMA 1999;281:137
7. Hickman TB, Briefel RR, Carroll MD, et al: Distributions and trends of serum lipid levels among United States children and adolescents ages 4-19 years: Data from the Third National Health and Nutrition Examination Survey. Prev Med 1998;27:879
8. National Cholesterol Education Program: Report of the expert panel on blood cholesterol levels in children and adolescents. Pediatrics 1992;89:515
9. Kimm SY, Payne GH, Stylianou MP, et al: National trends in the management of cardiovascular disease risk factors in children: Second NHLBI survey of primary care physicians. Pediatrics 1998;102(5):e50
10. Berenson GS, Srinivasan SR, Bao W, et al: Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. N Engl J Med 1998;338:1650
11. PDAY Research Group: Relationship of atherosclerosis in young men to serum lipoprotein cholesterol concentrations and smoking: A preliminary report from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. JAMA 1990;264:3018
12. McGill HC, McMahan CA, Zieske AW, et al: For the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group: Association of coronary heart disease risk factors with microscopic qualities of coronary atherosclerosis in youth. Circulation 2000;102:374
13. Kannel WB, McGee D, Gordon T: A general cardiovascular risk profile: The Framingham Study. Am J Cardiol 1976;38:46
14. Daviglus ML, Liu K, Greenland P, et al: Benefit of a favorable cardiovascular risk-factor profile in middle age with respect to Medicare costs. N Engl J Med 1998;339:1122
15. Akosah KO, Gower E, Groon L, et al: Mild hypercholesterolemia and premature heart disease: Do the national criteria underestimate disease risk? Am Coll Cardiol 2000;35:1178
16. Daily dietary fat and total food-energy intakes: Third National Health and Nutrition Examination Survey, Phase 1, 1988-91 MMWR 1994;43:116
17. Kwiterovich PO Jr, Fredrickson DS, Levy RI: Familial hypercholesterolemia (one form of familial type II hyperlipoproteinemia): A study of its biochemical, genetic, and clinical presentation in childhood. J Clin Invest 1974; 53:1237
18. Gidding SS, Brookstein LC, Chomka EV: Usefulness of electron beam tomography in adolescents and young adults with heterozygous familial hypercholesterolemia. Circulation 1998;98:2580
19. Mietus-Snyder M, Malloy MJ: Endothelial dysfunction occurs in children with two genetic hyperlipidemias: improvement with antioxidant vitamin therapy. J Pediatr 1998;133:35
20. Tonstad S, Joakimsen O, Stensland-Bugge E, et al: Risk factors related to carotid intima-media thickness and plaque in children with familial hypercholesterolemia and control subjects. Arterioscler Thromb Vasc Biol 1996; 16:984
21. Gidding SS: The rational for lowering serum cholesterol levels in American children. Am J Dis Child 1993; 147:386
22. Labarthe DR, Nichaman MZ, Harrist RB, et al: Development of cardiovascular risk factors from ages 8 to 18 in Project HeartBeat! Study design and patterns of change in plasma total cholesterol concentration. Circulation 1997;95:2636
23. Benuck I, Gidding SS, Donovan M: Year-to-year variability of cholesterol levels in a pediatric practice. Arch Pediatr Adolesc Med 1995;149:292
24. National Cholesterol Education Program: Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II) JAMA 1993;269:3015
25. Gidding SS, Liu K, Bild DE, Flack J, et al: Prevalence and identification of abnormal lipoprotein levels in a biracial population of young adults: The CARDIA Study. Am J Cardiol 1996;78:304
26. DISC Collaborative Research Group: Efficacy and safety of lowering dietary intake of fat and cholesterol in children with elevated low-density lipoprotein cholesterol. The Dietary Intervention Study in Children (DISC). JAMA 1995;273:1429
27. Rask-Nissila L, Jokinen E, Terho P, et al: Neurological development of 5-year-old children receiving a low-saturated fat, low-cholesterol diet since infancy: A randomized controlled trial. JAMA 2000;284:993
28. Deckelbaum RJ, Fisher EA, Winston M, et al: Summary of a Scientific Conference on Preventive Nutrition: Pediatrics to Geriatrics. Circulation 1999;100:450
29. Shepherd J, Cobbe SM, Ford I, et al: Prevention of CAD with pravastatin in men with hypercholesterolemia: West of Scotland Coronary Prevention Study Group. N Engl J Med 1995;33:1301
30. Downs JR, Clearfield M, Weis S, et al: Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPA/TexCAPS (Air Force/Texas Coronary Atherosclerosis Prevention Study). JAMA 1998;279:1615
A good diet and appropriate cholesterol screening are cornerstones of maintaining healthy cholesterol levels.
Diet. Offer the following diet information to parents and patients during routine office counseling or when measuring cholesterol. This advice also can be used as preliminary counseling for children with hypercholesterolemia before referring to a dietitian.
For sophisticated diet assessment and counseling, which may be appropriate if a child's diet initially is poor, refer to a skilled dietitian. Frequent follow-up improves outcome. Patients who might benefit the most from counseling are those with FH who are too young for medicine and those with an LDL cholesterol level that is consistently between 110 mg/dL and 190 mg/dL.
Cholesterol screening. Perform cholesterol screening at an office visit, when you also can take the time to do some counseling. Between 5 and 7 years of age is optimal because children can learn to read food labels. They may also be more receptive to a health message at that age than when they are older. Measurement of total cholesterol or HDL cholesterol does not require fasting, which clears chylomicrons from the bloodstream; calculation of LDL cholesterol does require fasting.
The cholesterol level increases immediately before puberty and declines during the rapid growth spurt. It is lowest at 12 to 14 years of age in girls and 15 to 17 years of age in boys. Cholesterol assessment also can uncover several dyslipidemias. Reassure families of children with a mild elevation of cholesterol that diet may well be sufficient to reach a healthy level. A child with FH, on the other hand, probably needs cholesterol-lowering medical therapy at some point in life.
Last, in making cholesterol management part of office practice, forget about stereotypes. Many patients with genetic hyperlipidemia are lean and on a good diet. Overweight patients may have a normal lipid level. And don't forget that hypothyroidism can cause dyslipidemia.
Samuel Gidding. Controlling cholesterol in children. Contemporary Pediatrics 2001;0:77.