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Childhood Obesity and Cardiovascular Disease: A Societal Call for Action

Disclosure: None
Pub Date: Tuesday, January 15, 2008
Authors: Stephen R. Daniels, MD, PhD, FAHA

Article Text

It is well-known that adults with obesity are at risk for cardiovascular disease outcomes including myocardial infarction, left ventricular hypertrophy, heart failure, and stroke. In large part, this relationship operates through the relationship that obesity has with known cardiovascular disease risk factors, such as dyslipidemia, hypertension, and type 2 diabetes mellitus. It has been more controversial to determine whether obesity in adults has a more direct effect on cardiovascular risk. The growing body of evidence in support of these relationships led Eckel and Krauss to publish a call to action from the American Heart Association regarding obesity as an increasingly important factor in the development of cardiovascular disease.[1]

The relationship of obesity in childhood to subsequent risk of cardiovascular disease in adulthood has been less clear. In part, this is due to the fact that the relationship, if it exists, must play out over decades. However, with a clear epidemic of childhood obesity, it is becoming increasingly important to understand the health ramifications of childhood obesity both in the short and long term. The Centers for Disease Control and Prevention have reported analyses indicating that obesity has become as important as cigarette smoking as a cause of death.[2] In addition, Olshansky and colleagues have reported the results of mathematical modeling, which suggests that because of obesity in children, this current generation of children is likely to have a shorter average lifespan than their parents.[3] Caution has been urged in the interpretation of both these results; nevertheless, even the suggestion of such trends is disconcerting. For these reasons, it is important to evaluate the evidence regarding the impact of childhood obesity on cardiovascular disease.

The prevalence and severity of childhood obesity are both increasing. The current best estimates show that approximately 17% of children and adolescents have body mass index (BMI) greater than the 95th percentile, a level that is considered obese.[4] This has increased from a prevalence of about 5% in 1971-1974 when the percentile cutpoints were established. In addition, the severity of childhood obesity appears to be increasing. Current estimates are that 4% of children and adolescents have a BMI above the 99th percentile for BMI, a level that is associated with an even more dramatic increase in cardiovascular risk factors in young individuals.[5]

An important question is whether childhood obesity results in obesity during adulthood. If this is the case, then even if obesity in childhood is not associated with short-term problems, young obese individuals will acquire the increased risks of obesity in adulthood when they reach that age range. The data on this issue are quite clear. BMI is quite likely to track over time. Whitaker et al. have shown that the childhood factors that make adult obesity more likely are a higher level of BMI during childhood, the presence of obesity at an older age during childhood and adolescence, and the presence of obesity in the parents.[6]

It is also important to examine the concept that childhood obesity may create an even greater risk of future cardiovascular events by having a negative impact on risk factors for cardiovascular disease earlier in life. Having those risk factors operative on a vulnerable cardiovascular system may result in an adverse outcome at an even younger age in adulthood than would the presence of obesity in adulthood alone.

Much evidence has accumulated that obesity in young individuals has a similar short-term effect to that observed in adults. Type 2 diabetes mellitus was once considered a disease that exclusively affected adults. This is no longer true. Over the past 15 years, it has become clear that obesity can also lead to type 2 diabetes in adolescents.[7] Diabetes has been established as a very potent risk factor for cardiovascular disease. In fact, the most recent report from the NHLBI National Cholesterol Education Program has established diabetes as a cardiovascular disease risk equivalent, meaning that patients with diabetes should be treated as aggressively to lower cardiovascular risk as a patient who already has established cardiovascular disease.[8] While it remains to be seen if the time course of cardiovascular disease in adolescents with type 2 diabetes is similar to that in adults, and it remains unclear how aggressively to treat adolescents with diabetes to lower cardiovascular risk, these relationships seen in adults are an important cause for concern.

Childhood obesity is also associated with dyslipidemia.[9] The elevation of triglycerides and decrease in HDL-cholesterol found in obese individuals have been called atherogenic dyslipidemia. Obesity may also adversely affect LDL-cholesterol, which can increase risk of cardiovascular disease. Childhood obesity and increase in BMI from childhood to adulthood are also important determinants of adult dyslipidemia.

Obesity in children and adolescents may also result in elevation of blood pressure. The risk of elevated blood pressure is increased for children with BMI greater than the 90th percentile when compared to children with BMI below the 10th percentile.[10] Muntner et al. have demonstrated trends for increasing levels of blood pressure in children across national surveys over time.[11] This increase in average systolic and diastolic blood pressure has been shown to be due, at least in part, to secular trends for increased obesity in childhood. Furthermore, Din-Dzietham et al. have shown increasing prevalence of high blood pressure in children and adolescents by following national surveys from 1967 to 2002.[12] Again, an important factor in these trends is the role of the increasing prevalence and severity of obesity among children and adolescents.

Left ventricular hypertrophy has also been shown to be associated with increased BMI in children and adolescents. This relationship may be due in part to the impact of obesity on blood pressure elevation, which in turn results in increased left ventricular mass. However, obesity appears to also have an independent effect on increasing left ventricular mass.[13] The mechanism involved is not completely known but may be due to increased circulating growth factors, including insulin resulting from obesity.

Obesity has also been shown to have a more direct effect on vascular disease. The two major pathology studies, the Pathobiologic Determinants of Atherosclerosis in Youth (PDAY) and the Bogalusa Study, both showed BMI to be associated with early and more advanced atherosclerotic lesions in the aorta and coronary arteries in adolescents and young adults who died of accidental causes.[14,15] In the Muscatine Study, Mahoney et al. found that weight in childhood was the strongest childhood predictor of the presence of coronary artery calcium in young adulthood.[16] Childhood obesity has also been found to be associated with endothelial dysfunction and increased carotid intima-media thickness, both of which are recognized to be associated with atherosclerotic cardiovascular disease and increased risk of adverse cardiovascular disease outcomes in adults.[17,18]

Recently, Bibbins-Domingo et al. reported the results of a computer simulation to estimate the impact of adolescent obesity on adult coronary heart disease.[19] In this analysis, they estimated the prevalence of obesity in 35-year-olds in 2020 based on the prevalence of overweight in adolescents in 2000. They then used the CHD Policy Model, a computer simulation of U.S. residents who are over 35 years of age, to predict the annual excess incidence and prevalence of coronary heart disease (CHD). They also evaluated the effect of treating obesity-related increases in hypertension and dyslipidemia on subsequent outcome.

They found that the incidence of CHD and the total number of CHD events and deaths would be expected to increase in young adulthood as a result of ongoing obesity.[19] This increase is then projected to continue as the population reaches middle age. Aggressive treatment of hypertension and dyslipidemia would reduce the predicted number of CHD deaths due to obesity in childhood but would not eliminate the projected increase. These results provide a somewhat better estimate of the potential effects of childhood obesity but largely rely on known relationships between obesity and cardiovascular disease in adulthood. It is possible that the results, in reality, could be somewhat worse than projected due to earlier and longer term effects of obesity on cardiovascular disease risk factors and the cardiovascular system.

While all of these results present a very strong circumstantial case against childhood obesity, direct evidence for the relationships of obesity in childhood and adverse cardiovascular events in adulthood has been harder to find. Baker et al. provide more direct evidence of a relationship between childhood obesity and cardiovascular disease in adulthood based on the results of a cohort study.[20] They studied the relationship of BMI from age 7-13 years and CHD in adulthood after 25 years of age. The subjects in this study were a cohort of over 275,000 Danish school children. These individuals had height and weight measurements available from school and then had CHD outcomes tracked during adulthood via linkage to national health registers. The investigators found that the risk of a CHD event, including both nonfatal and fatal events, during adulthood was positively associated with BMI at age 7-13 years for boys and at age 10-13 years for girls. The risk increased across the entire BMI distribution.

Unfortunately, they did not have data on BMI or other anthropometric measures in adulthood. This leaves open the question concerning whether the effect of childhood BMI is largely on adult BMI, which then, in turn, results in cardiovascular disease, or whether increased BMI in childhood has a more direct effect on the cardiovascular system and adult outcomes. In one study that had data on both childhood and adult anthropometric measures, the observed association between increased BMI in childhood and total cholesterol, LDL-cholesterol, HDL-cholesterol, fasting insulin, and systolic and diastolic blood pressure in adulthood was eliminated after controlling for BMI in adulthood.[9]

These results take what has been a theoretical risk of childhood obesity and show that it is now quite real. Whether increased BMI in childhood operates independently or largely via resulting in increased BMI in adulthood, the adverse outcomes are important. While better treatments for obesity-related comorbid conditions are being developed, it is unlikely that such treatments can keep pace with the widespread impact of obesity. Unfortunately, treatment for obesity itself is often quite difficult, especially in our current obesogenic environment. These results make the AHA call to action of Eckel and Krauss [1] even more important. It can no longer be a call to action with a focus on adults. It must now be a trans-societal call for action. There is a major concern that all of the hard-won gains regarding cardiovascular disease outcomes over the last 70 years are now in jeopardy because of the growing epidemic of childhood obesity. Intervention now, across all aspects of society, to prevent and treat childhood obesity is imperative.


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-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association. --