Over the past two decades, convincing evidence has emerged linking defined risk factors with atherosclerosis, the pathologic basis for cardiovascular disease. Postmortem studies have clearly shown that elevated total and low-density lipoprotein (LDL) cholesterol levels are associated with strong evidence of accelerated atherosclerosis beginning in childhood.1,2
In this issue of American Family Physician
, Shamir and Fisher3
review the guidelines for lipid testing in children and provide a complete and practical guide to the initial approach to dietary treatment.
The guidelines for lipid measurement were developed by the Pediatric Panel of the National Cholesterol Education Program (NCEP) in 1991.4
It is important to emphasize that universal screening of children was not recommended. Cholesterol levels measured in childhood correlate statistically with levels measured in young adults, but the correlation is not strong. Less than one half of children with total cholesterol levels above the 90th percentile in childhood will remain at that level as young adults. For an individual, only 25 percent of an adult cholesterol level can be predicted from the pediatric value.5
In response to this information, the NCEP Pediatric Panel recommended a policy of selective screening with lipid determination only in children with a positive family history of premature cardiovascular disease in an expanded first-degree pedigree (i.e., to include not only parents and siblings, but also aunts, uncles and grandparents), or a history of parental hypercholesterolemia. This algorithm aims to identify the majority of children at greatest risk of having high cholesterol as adults, without inappropriately labeling normal young people as “diseased.” Overall, this conservative approach appears reasonable, but it has some limitations. As in the original screening protocol for adults, the focus is exclusively on identification and modification of elevated total and LDL cholesterol levels. An important missing element is the role of high-density lipoprotein (HDL) cholesterol.
HDL cholesterol levels vary inversely with risk for cardiovascular disease: an isolated low HDL cholesterol is a powerful independent predictor of premature coronary artery disease.6
Among men younger than 45 years of age hospitalized with a myocardial infarction, a low HDL cholesterol level is identified as the major lipid abnormality more often than an elevated LDL cholesterol level. HDL levels are largely unaffected by diet composition, but they decrease significantly with obesity and exposure to cigarette smoke, and increase with habitual exercise and alcohol intake. Identification of low HDL cholesterol levels in a child from a family with a positive history of premature coronary disease is as critical as identification of elevated total and LDL cholesterol levels. It is a significant limitation of the NCEP Pediatric Panel guidelines that the issues surrounding HDL cholesterol are not addressed.
With a dramatic increase in prevalence over the past 20 years, obesity is now one of the most serious health problems facing young persons in this country. Depending on definition, as many as 25 percent of U.S. children and adolescents are overweight.7
The increased prevalence of childhood obesity parallels the large increase in adult obesity that has occurred over the past two decades: from NHANES III, with data collected between 1960 and 1994, the prevalence of obesity in adults increased from nearly 13 percent to 22.5 percent of the U.S. population, with most of that increase occurring in the past decade.8
Almost all coronary risk factors are increased with obesity, including elevated total and LDL cholesterol levels, reduced HDL cholesterol levels, hypertension and insulin resistance.9
In an autopsy study of children dying traumatically, elevated body mass index was the risk factor that correlated most highly with increased histologic extent of atherosclerosis.10
Importantly, even small amounts of weight loss have been shown to result in normalization of the lipid profile in obese adolescents.11
In comparison, in children with genetically based lipid abnormalities, diet interventions are often only minimally effective.
As Shamir and Fisher state in their article,3
obesity in and of itself should be considered an indication for lipid measurement in children. Appreciating the difference in response to diet therapy means that practitioners can confidently recommend diet change in obese children. Pediatric care professionals are in a unique position to attempt to prevent obesity by identifying a positive family history for obesity in infancy. Early identification of weight for height disproportion as it develops, especially in the setting of family obesity, can lead to diet and exercise recommendations that may help prevent the development of progressive obesity.12
Finally, nutrition counseling requires knowledge, training, experience and time, all of which physicians frequently lack.13
Shamir and Fisher3
provide some excellent aids for evaluation of current diet and handouts to assist families in making recommended diet changes. Referral to a registered dietitian is an option in helping families learn to translate prescribed levels of fat and saturated fat intake into practical recommendations for shopping and eating.14
In particular, referral to a registered dietitian is useful for institution of the step II diet, where fat intake is less than 20 percent of total calories and saturated fat is less than 7 percent. In managing hypercholesterolemia in childhood, recommended diet changes represent a potential lifetime commitment so all available resources including referral to a registered dietitian need to be considered.
Beginning in childhood, elevated cholesterol levels represent a major risk factor for premature cardiovascular disease. Cholesterol-lowering diets have been shown to be a safe and effective method of reducing total and LDL cholesterol levels without impairment of growth and development in children. Shamir and Fisher3
provide a very useful guide to the identification and management of hypercholesterolemia in childhood.