CHILDREN’S HEALTH: INCREASED RISK OF CHRONIC HEALTH CONDITIONS IN ADULTHOOD

Most overweight children/adolescents already have cardiovascular disease (CVD) risk factors. Approximately 60% of overweight 5- to 10-year-old children and overweight 11- to 17-year-old adolescents already have one associated biochemical or clinical cardiovascular risk factor (such as hyperlipidemia, hypertension, or increased insulin levels), and 25% have two or more. Overweight schoolchildren (defined by Freedman et al as having a BMI > 95th percentile) had anywhere from two to twelve times the chance of having CVD risk factors as compared to schoolchildren with < 85th percentile BMI. For example, an overweight child is two times as likely to have total serum cholesterol of 200 mg/dL than is a lean child.

Coronary artery disease was found among post-adolescent U.S. soldiers (18-21 years old) killed in action in Korea (JAMA 152:1090-1093, 1953). The American Heart Association (AHA) recently stated that the pathological data proves that atherosclerosis begins in childhood, and that the extent of atherosclerotic plaque development in children and young adults correlates with the same risk factors identified in adults. The AHA asserted that it is eminently reasonable to initiate healthful lifestyle training in childhood to promote improved cardiovascular health in adult life.

Risk factors for the metabolic syndrome are defined in the study by Freedman et al as triglycerides > 130 mg/dL, low-density lipoproteins > 130 mg/dL, high-density lipoproteins < 35 mg/dL, insulin > 95th percentile, and either systolic or diastolic blood pressure > 95th percentile. Twenty-two percent of all children with one risk factor for the metabolic syndrome are overweight; 100% of all children with all four risk factors for the metabolic syndrome are overweight.

Obese children/adolescents already have risk factors for type 2 diabetes, and some have clinically overt type 2 diabetes. Children (4- to 10-year-olds) with BMI > 30 kg/m2 have increased fasting blood insulin. Hyperinsulinemia is the harbinger of insulin resistance, which is believed to be one of the major initiators of the metabolic syndrome cascade.

Some adolescents with BMI > 35 kg/m2 already have insulin resistance and elevated fasting C-peptide levels, both of which are manifestations of overt type 2 diabetes.

Given these alarming trends, it is reasonable to expect many adolescents with type 2 diabetes to present with microvascular and macrovascular complications of diabetes as early as young adulthood. This has indeed been the case, as shown by Young et al.

Overweight/obese children and adolescents with the highest BMIs are more likely to have clustering of factors in metabolic syndrome when they are adults. In one study, 15% of children with the highest BMIs had clustering of metabolic syndrome factors (i.e., high fasting insulin, systolic or mean blood pressures, and total cholesterol/triglycerides to HDL-cholesterol ratio) 11 years later.

Moreover, being overweight/obese as children/adolescents was associated with a disproportionately high prevalence of adverse health effects that were independent of adult body weight 55 years later in men and women. The follow-up to the Harvard Growth Study by Must et al also found that overweight male and female adolescents had greater difficulty with activities of daily living (ADL) later in life. Also, being an overweight adolescent male significantly predicted an increased relative risk of death, 55 years later.

Overweight adolescent females had no such increased mortality risk! An obese child has a high probability of becoming an obese adult.

An odds ratio of 2 or 20 means that the obese child has twice or 24 times the chance of being an obese adult, compared to a non-obese child. In fact, the incidence of childhood obesity doubled in a 13-year period. What changed from 1976-1980 to 1988-1994 to cause this dramatic doubling of obesity in U.S. children? The answer is found in lifestyle. Our children are much more physically inactive than previous generations. The increase in obesity is due to environmental changes - such as a marked decline in physical activity and a concomitant increase in sedentary behavior and ingestion of high-calorie foods and drinks - affecting existing susceptibility genes.

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