Childhood Obesity — A Looming Disaster
Abstract & Commentary
By Jonathan Abrams, MD
Professor of Medicine, Division of Cardiology, University of New Mexico, Albuquerque.
Dr. Abrams serves on the speaker's bureau for Merck, Pfizer, and Parke-Davis.
Sources: Baker, et al. Childhood body-mass index and the risk of coronary heart disease in adulthood. N Engl J Med. 2007;357:2329-2337. Ludwig, DS. Childhood obesity — The shape of things to come. N Engl J Med. 2007;357:2325-2327.
This remarkable study is a population analysis of a huge cohort of children in Denmark who were followed, since 1930 or later, for the presence of coronary heart disease (CHD), and had all mandatory annual examinations at schools in Copenhagen. The study analyzed data from 277,000 children, aged 7-13. During a 46-year period, over 10,000 CHD events occurred among men and 4,300 among women; there were 5 million person-years of follow-up! Body Mass Index (BMI) was identified for each child from years 1955-1960; the BMI score was calculated by subtracting the child's BMI from the mean BMI in this fixed-reference population and dividing the result by the standard deviation of the reference population. The investigators employed the National Death Registry in Denmark, as well as the ICD-8 and ICD-10 curves (International Classification of Diseases). Late follow-up of subjects began at age of 28, or in 1977 (when the Hospital Discharge Registry was established). Almost 281,000 subjects were eligible for analysis. Cox proportional-hazards regression data were used to assist in the analysis of data to determine the probability of adult CHD events. Probabilities for children were calculated separately at ages 7 and 13.
Results: During the 46 years of surveillance, more than 14,000 CHD events were recorded. When the data were assessed for the effect of childhood BMI on the effect of any CHD event, it was found that the risk for events in adulthood increased significantly for each one unit increase for BMI score. The risk of adult CHD was highest for boys who had the highest BMI values and lowest for boys with the lowest BMI levels. The risk of an adult event increased as the children's age increased for both boys and girls; risk for girls was lower for all events. The risk of non-fatal events was associated with childhood BMI, and these increased with the age of the child; the association between childhood BMI and adult non-fatal events was linear. Fatal events occurred in 32,000 women with risk, and were associated with increasing age in those with a high childhood BMI. Probabilities of CHD events during adulthood was not high in either group of children, but were elevated when compared to non-obese subjects. For instance, an average-sized boy of 13 had a 33% higher risk of a CHD event in adulthood if he was obese in childhood.
The authors conclude that "higher childhood BMI values elevated the risk of having a CHD event in adult-hood, with risk increasing linearly in boys and girls."
Birth weight was not shown to have an interaction with subsequent obesity or with an increase in events.
"Childhood BMI, even after the effects of birth weight have been taken into account, is associated with CHD in adulthood."
Many studies and publications emphasize risk factors for CHD, which are essentially the same in childhood as in adults. These include hypertension, abnormal glucose, and dyslipidemia. Body weight in childhood is associated with the presence of these risk factors in children, linking high childhood BMI with an increased risk of adult CHD. Identifying at-risk boys and girls is important, in that subsequent CHD events can be ameliorated. The authors note that the BMI relationship to coronary events began before the "emergence of the obesity epidemic," and all birth cohorts showed the same relationships to adult CHD. The investigators believe that "the associations. . .observed are based on the biologic effects of the children's BMI," as childhood obesity is already associated with distinct biologic risk factors. They note that contemporary children are heavier than their counterparts from the past, with no evidence of a slowdown in childhood overweight and obesity; this situation occurs in Denmark and presumably many other countries. The authors calculated the probability of a child having a future CHD event, with the example of a 13-year-old boy who weighs 11 kilos more than average and who has a 33% increase in probability of a CHD event before age 60. Between 7 and 13 years old, there is a substantial increase in risk, which suggests "the possibility of intervention during this period of childhood can reduce the risk of future CHD.
An accompanying editorial stresses the history of weight gain over the past 40 years, "with average weight increasing progressively among children from all social and economic levels, racial and ethnic groups, and regions of the country." The author, David Ludwig, suggests that one in three children in adolescence are overweight (BMI in to the 85th-95th percentile for age and sex) or obese (BMI above the 95th percentile), with risk ratio close to one in two in minority groups. Phase one of the obesity revolution was the last 40-50 years, and phase two is now characterized by serious weight-related problems in children, including diabetes, fatty liver, orthopedic problems, sleep apnea, psychological problems, including social isolation, eating disorders, and often an adverse socio-economic background. Other data confirm these statements. Ludwig states that "pediatric obesity may shorten life expectancy in the United States by 2-5 years by mid century, an effect equal to that of all cancers combined." A true epidemic will become possible through acceleration of the obesity rates through multiple mechanisms over many years. "Obese children tend to be heavy in adulthood, in part because obesity-promoting habits persist." In addition to metabolic problems, many abnormalities are related to childhood obesity and subsequent adverse events. He calls for a comprehensive national strategy, involving junk food meals and advertising, adequate funding for healthy lunches, regular physical activity, and the restructuring of the foreign subsidy program to favor nutrient-dense rather than calorie-dense foods that are of high quality.
The data from this very large study speaks for itself. This elegant analysis of many decades, with remarkably complete follow-up, and confirmation that CHD risks have been accelerating over decades, calls for immediate and major public action. The overall prevalence of obesity in adults has been steadily increasing. Enormous effort and literally billions of dollars have been spent on adult obesity in the past decade or more, and there has been some suggestion of a slowing of the atherogenic conditions in our adult population. How much better it would be to link childhood, early adulthood, and full adulthood together in educational programs, emphasizing changing our dietary patterns, emphasizing healthy nutrients, including vegetables and fruits, demanding healthy lunches in our schools, and providing our children and adults with regular exercise programs. The Danish study should be a clarion call for national policy makers, industry, and health care workers of all types, resulting in an increase expenditure of funds for fighting obesity in children.