Clinical Evidence Concise
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Obesity In Children
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Am Fam Physician. 2007 Dec 1;76(11):1701-1702.
What are the effects of lifestyle interventions for the treatment of childhood obesity?
LIKELY TO BE BENEFICIAL
Multifactorial Interventions. Multifactorial interventions (particularly those that included problem solving) delivered to the family were more effective at reducing body mass index (BMI), decreasing the number of overweight children, or both, than the interventions delivered to children alone.
Behavioral Interventions Alone. We found insufficient evidence that behavioral interventions alone can effectively promote weight loss in children and adolescents.
Diet Alone. One randomized controlled trial found no significant difference in reduction in overweight between two dietary interventions of higher and lower protein levels.
Physical Activity Alone. We found insufficient evidence that physical activity interventions alone can effectively promote weight loss in children and adolescents.
Obesity is a chronic condition characterized by an excess of body fat. It is most often defined by the BMI, which is highly correlated with body fat.1 BMI is weight in kilograms divided by height in meters squared (kg per m2). In children and adolescents, BMI varies with age and sex. It typically rises during the first months after birth, falls after the first year, and rises again around the sixth year of life.2 A given BMI value is usually compared against reference charts to obtain a ranking of BMI percentile for age and sex. The BMI percentile indicates the relative position of the child's BMI compared with a historical reference population of children of the same age and sex. Worldwide, there is little agreement on the definition of overweight and obesity among children; however, a BMI above the 85th percentile is generally considered to be at least “at risk for overweight” in the United States and United Kingdom. A BMI above the 95th percentile is variably defined as overweight or obese, but generally indicates a need for intervention.
The prevalence of obesity (generally BMI above the 95th percentile) is steadily increasing among children and adolescents. In the United Kingdom in 2004, it was estimated that 14 percent of boys and 17 percent of girls two to 15 years of age were obese.3 The prevalence of overweight among children and adolescents in the United States increased from 14 percent in 1999 to 2000, to 16 percent in 2003 to 2004, among females and from 14 to 18 percent among males.4
Obesity is the result of long-term energy imbalances in which daily energy intake exceeds daily energy expenditure.5 Energy balance is modulated by a myriad of factors, including metabolic rate, appetite, diet, and physical activity.6 Although these factors are influenced by genetic traits in a moderate number of children, the increase in obesity prevalence in the past few decades cannot be explained by changes in the human gene pool, and is more often attributed to environmental changes that promote excessive food intake and discourage physical activity.6,7 The risk of childhood obesity is related to childhood diet and sedentary time. Other risk factors are parental obesity, low parental education, social deprivation, infant feeding patterns, early or more rapid puberty (both a risk factor and an effect of obesity), extreme (both high and low) birth weights, and gestational diabetes.2 Specifically, physical activity levels have decreased over the years and now only 36 percent of children and adolescents in the United States are meeting recommended levels of physical activity.8 Less commonly, obesity may also be induced by medications (e.g., high-dose glucocorticoids), neuroendocrine disorders (e.g., Cushing's syndrome), or inherited disorders (e.g., Down syndrome, Prader-Willi syndrome).2 In this review, we have considered treatment of children for overweight and obesity in a clinical setting (not broader public health settings, such as interventions given to a whole school). We have included interventions given to the children, their parents, or both.
Most obese adolescents will become obese adults. For example, a five-year longitudinal study of obese adolescents, 13 to 19 years of age, found that 86 percent remained obese as young adults.9 Obesity is associated with a higher prevalence of insulin resistance, elevated blood lipid levels, increased blood pressure, and impaired glucose tolerance, which in turn may increase the risk of several chronic diseases in adulthood, including hypertension, dyslipidemia, diabetes, cardiovascular disease, sleep apnea, osteoarthritis, and some cancers.2,10 Perhaps the most significant short-term morbidities for overweight and obese children are psychosocial, and include social marginalization, low self-esteem, and an impaired quality of life.2 Physicians should emphasize improvements in diet, physical activity, and health independent of changes in body weight.
Author disclosure: Nothing to disclose.
search date: August 2006
Adapted with permission from Arterburn DE. Obesity in children. Clin Evid Handbook Dec 2007:110–1.
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2. Lobstein T, Baur L, Uauy R, IASO International Obesity Task Force. Obesity in children and young people: a crisis in public health. Obes Rev. 2004;(5 suppl 1):4–104.
3. Association for the Study of Obesity. The prevalence of obesity in the UK. Association for the Study of Obesity, 2004. Accessed April 21, 2007 at: http://www.aso.org.uk/portal.aspx?mlmenuid=1990&TargetPortal=36&ApplicationID=116.
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5. Schwartz MW, Woods SC, Porte D Jr, et al. Central nervous system control of food intake. Nature. 2000;404:661–71.
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8. Eaton DK, Kann L, Kinchen S, et al. Youth risk behavior surveillance—United States, 2005. MMWR Surveill Summ. 2006;55:1–108.
9. Gordon-Larsen P, Adair LS, Nelson MC, et al. Five-year obesity incidence in the transition period between adolescence and adulthood: the National Longitudinal Study of Adolescent Health. Am J Clin Nutr. 2004;80:569–75.
10. Must A, Spadano J, Coakley EH, et al. The disease burden associated with overweight and obesity. JAMA. 1999;282:1523–9.
This is one in a series of chapters excerpted from the Clinical Evidence Handbook, published by the BMJ Publishing Group, London, U.K. The medical information contained herein is the most accurate available at the date of publication. More updated and comprehensive information on this topic may be available in future print editions of the Clinical Evidence Handbook, as well as online at http://www.clinicalevidence.com (subscription required). Those who receive a complimentary print copy of the Clinical Evidence Handbook from United Health Foundation can gain complimentary online access by registering on the Web site using the ISBN number of their book.
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