Declining Cholesterol Levels in US Youths
Authors: Sarah D. de Ferranti
Journal: JAMA (2012)

ATHEROSCLEROTIC DISEASE APPEARS TO BE LESS DEADLY than it was in the past; from 1998 to 2008, fatalities fromcardiovasculardisease (CVD)declinedby31%. However, that CVD is still listed as the cause for 1 of every 3 US deaths indicates a persistent burden of disease related to the obesity epidemic, inactive lifestyles, and poor eating habits, which contribute both to obesity and to CVD risk directly. Some epidemiologists project that by the year 2030, the rate of myocardial infarction may increase again by as much as 16.6% more than current levels. Despite this bleak picture, the improvement in lipid values in US children and adolescents reported by Kit and colleagues in this issue of JAMA, is a reason for optimism. In this study based on cross-sectional National Health and Nutrition Examination Survey (NHANES) data involving more than 16 000 participants from 1988-1994 to 2007-2010, the authors report that total cholesterol (TC) declined a mean 5 mg/dL in children aged 6 to 19 years over the past 2 decades. Atherogenic lipoproteins, represented by non–highdensity lipoprotein (non-HDL), decreased a mean of 8 mg/dL across all ages. Among adolescents aged 12-19 years with available fasting serum specimens, low-density lipoprotein (LDL) and triglyceride levels both declined (5 mg/dL and 9 mg/dL, respectively). Furthermore, high-density lipoprotein (HDL) increased by 2 mg/dL. There were important decreases in rates of high TC (11.3%-8.1%) and high nonHDL (17.3%-14.8%), as rates of low HDL also declined, although the change did not reach statistical significance (P=.05). In adolescents, the prevalence of high LDL and high triglycerides also declined. When considered on a population basis, the changes Kit et al report are clinically meaningful, and since they likely reflect population trends, are cause for optimism. The strong relationship between TC, LDL and non-HDL, and CVD events, and the effect in adults of lowering lipid levels on CVD mortality whether by pharmacotherapy or diet, suggest these types of changes could modify future mortality. For example, a 10% decline in TC is associated with a 15% lower rate of coronary heart disease (CHD) mortality; similar relationships are seen with LDL and non-HDL. But why would childhood cholesterol improve? The concurrent increase in pediatric obesity, decrease in physical activity, increase in screen time, and the overall poor diet of the US population would suggest lipid levels should worsen, not improve. Several possible explanations are worth considering. Although unlikely, it is conceivable that the data are inaccurate. NHANES has set standards for state-of-the art health surveillance. However, temporal changes in laboratory techniques may have caused or contributed to the findings. The authors chose not to include data sets from 2003-2004 and 2005-2006, in part, because the HDL-C values were “positive[ly] biased”. They noted that a change in laboratory methods did occur over the course of the survey; early on, HDL was measured by heparin manganese precipitation and later a direct immunoassay was used. An increase in HDL levels related to changes in laboratory methods could explain an improvement in LDL if TC and triglyceride levels remained constant; based on the Friedewald calculation, LDL would by necessity be calculated at a lower value. However, Kit et al found not only an increase in HDL levels, but also a decline in both TC and triglyceride levels, indicating that the change in HDL methods is unlikely to be the sole explanation for the improvement in US childhood cholesterol profiles. Another possible explanation is that the changes in pediatric lipid values reported by Kit et al merely represent a temporary decline that will worsen in the coming years and be reflected in the next survey. However, cholesterol levels also declined in US adults between 1960 to 2006, according to NHANES data, suggesting a population-wide trend may also be at play during childhood. A plausible explanation for improved childhood lipid values could be individual interventions to improve CVD risk— either lifestyle modification or pharmacotherapy. For a number of years lipid-lowering interventions have been recommended by the American Academy of Pediatrics and the American Heart Association, including statins for select high-risk children. Controversy in the popular and scientific press around lipid screening and treatment is long