Defining Childhood Overweight and Obesity

Body mass index (BMI) is a practical measure used to determine overweight and obesity. BMI is a measure of weight in relation to height that is used to determine weight status. BMI can be calculated using either English or metric units. BMI is the most widely accepted method used to screen for overweight and obesity in children and adolescents because it is relatively easy to obtain the height and weight measurements needed to calculate BMI, measurements are non-invasive and BMI correlates with body fatness.6 While BMI is an accepted screening tool for the initial assessment of body fatness in children and adolescents, it is not a diagnostic measure because BMI is not a direct measure of body fatness.

Use of BMI to Screen for Overweight and Obesity in Children

Child and Teen
BMI Calculator

For children and adolescents (aged 2-19 years), the BMI value is plotted on the CDC growth charts to determine the corresponding BMI-for-age percentile.

• Overweight is defined as a BMI at or above the 85th percentile and lower than the 95th percentile.

• Obesity is defined as a BMI at or above the 95th percentile for children of the same age and sex.

These definitions are based on the 2000 CDC Growth Charts for the United States and expert committee. A child's weight status is determined based on an age- and sex-specific percentile for BMI rather than by the BMI categories used for adults. Classifications of overweight and obesity for children and adolescents are age- and sex-specific because children's body composition varies as they age and varies between boys and girls.

Prevalence

Obesity is a serious health concern for children and adolescents. Data from NHANES surveys (1976-1980 and 2003-2006) show that the prevalence of obesity has increased: for children aged 2-5 years, prevalence increased from 5.0% to 12.4%; for those aged 6-11 years, prevalence increased from 6.5% to 17.0%; and for those aged 12-19 years, prevalence increased from 5.0% to 17.6%.^{1, 46}

Healthy People 2010 identified overweight and obesity as 1 of 10 leading health indicators and called for a reduction in the proportion of children and adolescents who are overweight or obese,⁹ but the United States has made little progress toward the target goal.

Progress toward reducing the national prevalence of overweight and obesity is monitored using data from the National Health and Nutrition Examination Survey (NHANES). The most recent NHANES data (2003-2006) showed that for children aged 6 -11 years and 12-19 years, the prevalence of overweight was 17.0% and 17.6% respectively.¹ These prevalence figures are more than three times the target prevalence of 5% set in Healthy People 2010.

Trends in Childhood Obesity

The following graphs show trends in childhood overweight based on NHANES data for various age groups, beginning with NHANES I (1971-1974) and ending with NHANES 2003-2006 (the most recently available published data).

Data from NHANES I (1971-1974) to NHANES 2003-2006 show increases in overweight among all age groups:

• Among preschool-aged children, aged 2-5 years, the prevalence of overweight increased from 5.0% to 12.4%.8, 46

• Among school-aged children, aged 6-11 years, the prevalence of overweight increased from 4.0% to 17.0%.8, 46

• Among school-aged adolescents, aged 12-19 years, the prevalence of overweight increased from 6.1% to 17.6%.8, 46

Obesity Among Racial/Ethnic Groups

Although obesity has increased for all children and adolescents over time, NHANES data indicate disparities among racial/ethnic groups. The following graphs compare the prevalence for racial/ethnic groups of adolescent boys and girls aged 12 through 19 years.

Racial/Ethnic Comparison: Boys Aged 12-19 Years
The most recent NHANES data (2003-2006) showed that for boys, aged 12-19 years:

• The prevalence rate of obesity was higher among adolescent Mexican-American boys (22.1%) and than among non-Hispanic white boys (17.3%) and black boys (18.5%).⁴⁶

Data from NHANES III (1988-1994) through NHANES 2003-2006 showed that the largest increases in the prevalence of obesity occurred among adolescent non-Hispanic black boys (7.8%) and Mexican American boys (8.0%) compared to non-Hispanic white boys (5.7%).

• Among non-Hispanic white boys, the prevalence of obesity increased from 11.6% to 17.3%.

• Among non-Hispanic black boys, the prevalence of obesity increased from 10.7% to 18.5%.

• Among Mexican American boys, the prevalence of obesity increased from 14.1% to 22.1%.

Racial/Ethnic Comparison: Girls Aged 12-19 Years
The most recent NHANES data (2003-2006) showed that for girls, aged 12-19 years:

• Non-Hispanic black girls had the highest prevalence of obesity (27.7%) compared to that of non-Hispanic white (14.5%) and Mexican American 19.9%) girls.⁴⁶

Data from NHANES III (1988-1994) through NHANES 2003-2006 showed that non-Hispanic black adolescent girls experienced the largest increase in the prevalence of obesity (14.5%) compared to non-Hispanic white adolescent (7.1%) and Mexican American adolescent (10.7%) girls.

• Among non-Hispanic white girls, the prevalence of obesity increased from 7.4% to 14.5%.

• Among non-Hispanic black girls, the prevalence of obesity increased from 13.2% to 27.7%.

• Among Mexican American girls, the prevalence of obesity increased from 9.2% to 19.9%.

Contributing Factors

On this Page

• Genetic Factors

• Behavioral Factors

• Environmental Factors

At the individual level, childhood obesity is the result of an imbalance between the calories a child consumes as food and beverages and the calories a child uses to support normal growth and development, metabolism, and physical activity. In other words, obesity results when a child consumes more calories than the child uses. The imbalance between calories consumed and calories used can result from the influences and interactions of a number of factors, including genetic, behavioral, and environmental factors.¹⁰ It is the interactions among these factors - rather than any single factor - that is thought to cause obesity.¹¹

Genetic Factors

Studies indicate that certain genetic characteristics may increase an individual's susceptibility to excess body weight.^{12, 13} However, this genetic susceptibility may need to exist in conjunction with contributing environmental and behavioral factors (such as a high-calorie food supply and minimal physical activity) to have a significant effect on weight. Genetic factors alone can play a role in specific cases of obesity . For example, obesity is a clinical feature for rare genetic disorders such as Prader-Willi syndrome.¹⁴ However, the rapid rise in the rates of overweight and obesity in the general population in recent years cannot be attributed solely to genetic factors. The genetic characteristics of the human population have not changed in the last three decades, but the prevalence of obesity has tripled among school-aged children during that time.^{8, 46}

Behavioral Factors

Because the factors that contribute to childhood obesity interact with each other, it is not possible to specify one behavior as the "cause" of obesity . However, certain behaviors can be identified as potentially contributing to an energy imbalance and, consequently, to obesity .

• Energy intake: Evidence is limited on specific foods or dietary patterns that contribute to excessive energy intake in children and teens. However, large portion sizes for food and beverages, eating meals away from home, frequent snacking on energy-dense foods and consuming beverages with added sugar are often hypothesized as contributing to excess energy intake of children and teens.¹⁵ In the area of consuming sugar-sweetened drinks, evidence is growing to suggest an association with weight gain in children and adolescents.^{16, 17, 18} Consuming sugar-sweetened drinks may be associated with obesity because these drinks are high in calories.¹⁹ Children may not compensate at meals for the calories they have consumed in sugar-sweetened drinks, although this may vary by age.^{20, 21} Also, liquid forms of energy may be less satiating than solid forms and lead to higher caloric intake.^{22, 23}

• Physical activity: Participating in physical activity is important for children and teens as it may have beneficial effects not only on body weight, but also on blood pressure and bone strength.²⁴ Physically active children are also more likely to remain physically active throughout adolescence and possibly into adulthood.²⁵
  
  Children may be spending less time engaged in physical activity during school. Daily participation in school physical education among adolescents dropped 14 percentage points over the last 13 years - from 42% in 1991 to 28% in 2003.26 In addition, less than one-third (28%) of high school students meet currently recommended levels of physical activity.²⁷

• Sedentary behavior: Children spend a considerable amount of time with media. One study found that time spent watching TV, videos, DVDs, and movies averaged slightly over 3 hours per day among children aged 8-18 years.28 Several studies have found a positive association between the time spent viewing television and increased prevalence of obesity in children.^{29, 30, 31} Media use, and specifically television viewing, may

  • displace time children spend in physical activities,^{32, 33}

  • contribute to increased energy consumption through excessive snacking and eating meals in front of the TV,^{34, 35}

  • influence children to make unhealthy food choices through exposure to food advertisements,¹⁵ and

  • lower children's metabolic rate.³⁶

Environmental Factors

Home, child care, school, and community environments can influence children's behaviors related to food intake and physical activity.¹⁵

• Within the home: Parent-child interactions and the home environment can affect the behaviors of children and youth related to calorie intake and physical activity. Parents are role models for their children who are likely to develop habits similar to their parents.¹⁵

• Within child care: Almost 80% of children aged 5 years and younger with working mothers are in child care for 40 hours a week on average.³⁷ Child care providers are sharing responsibility with parents for children during important developmental years. Child care can be a setting in which healthy eating and physical activity habits are developed.

• Within schools: Because the majority of young people aged 5-17 years are enrolled in schools and because of the amount of time that children spend at school each day, schools provide an ideal setting for teaching children and teens to adopt healthy eating and physical activity behaviors. According to the Institute of Medicine (IOM), schools and school districts are, increasingly, implementing innovative programs that focus on improving the nutrition and increasing physical activity of students.¹⁵

• Within the community: The built environment within communities influences access to physical activity opportunities and access to affordable and healthy foods. For example, a lack of sidewalks, safe bike paths, and parks in neighborhoods can discourage children from walking or biking to school as well as from participating in physical activity.¹⁵ Additionally, lack of access to affordable, healthy food choices in neighborhood food markets can be a barrier to purchasing healthy foods.³⁸

Consequences

Childhood obesity is associated with various health-related consequences. Obese children and adolescents may experience immediate health consequences and may be at risk for weight-related health problems in adulthood.

Psychosocial Risks

Some consequences of childhood and adolescent obesity are psychosocial. Obese children and adolescents are targets of early and systematic social discrimination.³⁹ The psychological stress of social stigmatization can cause low self-esteem which, in turn, can hinder academic and social functioning, and persist into adulthood.⁴⁰

Cardiovascular Disease Risks

Obese children and teens have been found to have risk factors for cardiovascular disease (CVD), including high cholesterol levels, high blood pressure, and abnormal glucose tolerance.³⁹ In a population-based sample of 5- to 17-year-olds, 70% of obese children had at least one CVD risk factor while 39% of obese children had two or more CVD risk factors.²

Additional Health Risks

Less common health conditions associated with increased weight include asthma, hepatic steatosis, sleep apnea and Type 2 diabetes.

• Asthma is a disease of the lungs in which the airways become blocked or narrowed causing breathing difficulty. Studies have identified an association between childhood obesity and asthma.^{41, 42}

• Hepatic steatosis is the fatty degeneration of the liver caused by a high concentration of liver enzymes. Weight reduction causes liver enzymes to normalize.³⁹

• Sleep apnea is a less common complication of obesity for children and adolescents. Sleep apnea is a sleep-associated breathing disorder defined as the cessation of breathing during sleep that lasts for at least 10 seconds. Sleep apnea is characterized by loud snoring and labored breathing. During sleep apnea, oxygen levels in the blood can fall dramatically. One study estimated that sleep apnea occurs in about 7% of obese children.⁴³

• Type 2 diabetes is increasingly being reported among children and adolescents who are obese.44 While diabetes and glucose intolerance, a precursor of diabetes, are common health effects of adult obesity, only in recent years has Type 2 diabetes begun to emerge as a health-related problem among children and adolescents.⁴⁵ Onset of diabetes in children and adolescents can result in advanced complications such as CVD and kidney failure.⁴⁵

References

1. NHANES data on the Prevalence of Overweight Among Children and Adolescents: United States, 2003-2006. CDC National Center for Health Statistics, Health E-Stat. (http://www.cdc.gov/nchs/products/pubs/pubd/hestats/overweight/overwght_child_03.htm)

2. Freedman DS, Mei Z, Srinivasan SR, Berenson GS, Dietz WH. Cardiovascular risk factors and excess adiposity among overweight children and adolescents: the Bogalusa Heart Study. J Pediatr. 2007 Jan;150(1):12-17.e2.

3. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997; 37(13):869-873.

4. Serdula MK, Ivery D, Coates RJ, Freedman DS. Williamson DF. Byers T. Do obese children become obese adults? A review of the literature. Prev Med 1993;22:167-177.

5. Freedman DS, Khan LK, Dietz WH, Srinivasan SR, Berenson GS. Relationship of childhood overweight to coronary heart disease risk factors in adulthood: The Bogalusa Heart Study. Pediatrics 2001;108:712-718.

6. Mei Z, Grummer-Strawn LM, Pietrobelli A, Goulding A, Goran MI, Dietz WH. Validity of body mass index compared with other body-composition screening indexes for the assessment of body fatness in children and adolescents. Am J Clin Nutr 2002;978-985.

7. Barlow SE and the Expert Committee. Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: summary report. Pediatrics 2007;120 Supplement December 2007: S164-S192.

8. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999-2000. JAMA 2002;288(14):1728-1732.

9. U.S. Department of Health and Human Services. Healthy People 2010. 2nd edition. 2 volumes. Washington, DC: U.S. Department of Health and Human Services, 2000.

10. U.S. Department of Health and Human Services. The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity. Rockville, MD: Public Health Service, Office of the Surgeon General, 2001.

11. World Health Organization. WHO Technical Report Series 894: Obesity: Preventing and Managing the Global Epidemic. A Report of a WHO Consultation. Geneva, 2000.

12. Farooqi IS, O'Rahilly S. Recent advances in the genetics of severe obesity. Arch Dis Child 2000;83:31-34.

13. LeStunff C, Fallin D, Bougneres P. Paternal transmission of the very common class I INS VNTR alleles predisposes to childhood obesity. Nat Genet 2001;29:96-99.

14. Bouchard C, Perusse L, Rice T, Rao DC. The genetics of human obesity. In Bray GA, Bouchard C, James WPT, eds. Handbook of obesity. New York: Marcel Dekker, Inc., 1998: 157-190.

15. Institute of Medicine. Preventing Childhood Obesity-Health in the Balance. The National Academies Press, Washington, DC; 2005.

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17. Welsh JA, Cogswell ME, Rogers S, Rockett H, Mei Z, Grummer-Strawn LM. Overweight among low-income preschool children associated with the consumption of sweet drinks: Missouri 1999-2002. Pediatrics 2005;155:e223-e229.

18. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr 2006;84:274-288.

19. Sherry B. Food behaviors and other strategies to prevent and treat pediatric overweight. Intl J Obesity 2005;29:S116-S126.

20. Birch LL, McPhee L, Sullivan S. Children's food intake following drinks sweetened with sucrose or aspartame: time course effects. Physiol Behav 1989;45:387-395.

21. Louis-Sylvestre J, Tournier A, Verger P, Chabert M, Delorme B, Hossenlop J. Learned caloric adjustment of human intake. Appetite 1989;12:95-103.

22. DiMeglio DP, Mattes RD. Liquid versus solid carbohydrate; effects on food intake and body weight. Intl J Obes Relat Metab Disord 2000;24:794-800.

23. Crombie C, Anderson GH, Leiter LA, et al. Effects of sucrose pre-load on subjective measures of appetite and food intake in children. In Black RM, Anderson GH. Sweeteners, food intake and selection. In Fernstrom JD, Miller GD, eds. Cited in Appetite and Body Weight Regulation: Sugar, Fat and Macronutrient Substitutes. Boca Raton, FL: CRC Press 1994;125-136.

24. Strong WB, Malina RM, Blimkie CJ, et al. Evidence based physical activity for school-age youth. J. Pediatr 2005;146:732-737.

25. Malina RM. Tracking of physical activity and physical fitness across the lifespan. Res Q Exerc Sport 1996;67:S48-S57.

26. Lowry R, Brener N, Lee S, Epping J, Fulton J, Eaton D. Participation in high school physical education - United States, 1991-2003. MMWR 2004; 53(36): 844-847, 2004.

27. Eaton DK, Kann L, Kinchen S, Ross J, Hawkins J, Harris WA, et al., Youth Risk Behavior Surveillance - United States, 2005. MMWR Surveillance Summary 2006; SS-5 (55).

28. Roberts D, Foehr U, Rideout V. Generation M: media in the lives of 8 to 18 year-olds. The Henry J. Kaiser Family Foundation; Menlo Park, 2005.

29. Dietz WH, Gortmaker SL. Do we fatten our children at the television set? Obesity and television viewing in children and adolescents. Pediatrics 1985;75:807-812.

30. Gortmaker SL, Must A, Sobol AM, Peterson K, Colditz GA, Dietz WH. "Television viewing as a cause of increasing obesity among children in the United States, 1986-1990." Arch Pediatr Adolesc Med 1996;150(4):356-62. (http://archpedi.ama-assn.org/cgi/content/abstract/150/4/356)

31. Crespo CJ, Smit E, Troiano RP, Bartlett SJ, Macera CA, Andersen RE. Television watching, energy intake, and obesity in US children: results from the third National Health and Nutrition Examination Survey, 1988-1994. Arch Pediatr Adolesc Med 2001;155 (3):360-365.

32. Lowry R, Wechsler H, Galuska DA, Fulton JE, Kann L. Television viewing and its associations with overweight, sedentary lifestyle, and insufficient consumption of fruits and vegetables among U.S. high school students: differences by race, ethnicity, and gender. J Sch Health 2002;72:413-421.

33. Robinson TN, Hammer LD, Killen JD, et al. Does television viewing increase obesity and reduce physical activity? Cross-sectional and longitudinal analyses among adolescent girls. Pediatrics 1993;91:273-280.

34. Coon KA, Tucker KL. Television and children's consumption patterns. A review of the literature. Minerva Pediatr 2002;54:423-436.

35. Francis LA, Birch LL. Does eating during television viewing affect preschool children's intake? J Am Diet Assoc 2006;106:598-600.

36. Treuth MS, Butte NF, Wong WW. Effects of familial predisposition to obesity on energy expenditure in multiethnic prepubertal girls. Am J Clin Nutr 2000;71:893-900.

37. National Research Council and the Institute of Medicine. Working Families and Growing Kids: Caring for Children and Adolescents, 2003. Washington, DC: The National Academies Press.

38. Morland K, Wing S, Diez Roux A, Poole C. Neighborhood characteristics associated with the location of food stores and food service places. Am J Prev Med 2002;1:23-29.

39. Dietz W. Health consequences of obesity in youth: Childhood predictors of adult disease. Pediatrics 1998;101:518-525.

40. Swartz MB and Puhl R. Childhood obesity: a societal problem to solve. Obesity Reviews 2003; 4(1):57-71.

41. Rodriguez MA, Winkleby MA, Ahn D, Sundquist J, Kraemer HC. Identification of populations subgroups of children and adolescents with high asthma prevalence: findings from the Third National Health and Nutrition Examination Survey. Arch Pediatr Adolesc Med 2002;156:269-275.

42. Luder E, Melnik TA, Dimaio M. Association of being overweight with greater asthma symptoms in inner city black and Hispanic children. J Pediatr 1998;132:699-703.

43. Mallory GB, Fiser DH, Jackson R. Sleep-associated breathing disorders in morbidly obese children and adolescents. J Pediatr 1989;115:892-897.

44. Fagot-Campagna A, Narayan KMV, Imperatore G. Type 2 diabetes in children: exemplifies the growing problem of chronic diseases [Editorial]. BMJ 2001;322:377-378.

45. Must A, Anderson SE. Effects of obesity on morbidity in children and adolescents. Nutr Clin Care 2003;6:1;4-11.

46. Ogden CL, Carroll MD, Flegal KM. High Body Mass Index for Age Among US Children and Adolescents, 2003-2006. JAMA 2008;299:2401-2405.

47. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997; 37(13):869-873.

48. Serdula MK, Ivery D, Coates RJ, Freedman DS. Williamson DF. Byers T. Do obese children become obese adults? A review of the literature. Prev Med 1993;22:167-177.

49. http://www.aap.org/family/tv1.htm, accessed 12/18/06.

50. This physical activity recommendation is from the Dietary Guidelines for Americans 2005: http://www.health.gov/dietaryguidelines/dga2005/document/html/chapter4.htm