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Definition; epidemiology; and etiology of obesity in children and adolescents

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Definition; epidemiology; and etiology of obesity in children and adolescents


Author William J Klish, MD Section Editors Kathleen J Motil, MD, PhD John L Kirkland, MD Craig Jensen, MD Deputy Editor Alison G Hoppin, MD

Last literature review for version 17.3: September 30, 2009 | This topic last updated: September 29, 2009 INTRODUCTION Obesity has become one of the most important public health problems in the United States (graph 1) [1-3]. As the prevalence of obesity increases so does the prevalence of the comorbidities associated with obesity [4]. For this reason it is imperative that health care providers identify overweight and obese children so that counseling and treatment can be provided. The definition, epidemiology, and etiology of obesity in children and adolescents will be presented here. Comorbidities of obesity in children and adolescents and the clinical evaluation of the obese child or adolescent are discussed separately. (See "Comorbidities and complications of obesity in children and adolescents" and "Clinical evaluation of the obese child and adolescent".) DEFINITIONS "Overweight" technically refers to an excess of body weight, whereas "obesity" refers to an excess of fat. However, the methods used to directly measure body fat are not available in daily practice. For this reason, obesity is often assessed by means of indirect estimates of body fat (ie, anthropometrics) [5]. The body mass index (BMI) is the accepted standard measure of overweight and obesity for children two years of age and older [6]. Body mass index provides a guideline for weight in relation to height and is equal to the body weight divided by the height squared (table 1). Other measures of childhood obesity, including weight-for-height (which is particularly useful for the child younger than two years) and measures of regional fat distribution (eg, waist circumference and waist-to-hip ratio) are discussed separately. (See "Measurement of growth in children", section on 'Obesity'.) Adults with a BMI between 25 and 30 are considered overweight; those with a BMI 30 are considered to be obese. Unlike adults, children grow in height as well as weight. Thus, the norms for BMI in children vary with age and sex. In 2000, the National Center for Health Care Statistics and the Centers for Disease Control (CDC) published BMI reference standards for children between the ages of 2 and 20 years (graph 2A-B). BMI percentiles also can be determined using a calculator for boys (calculator 1) and for girls (calculator 2). As children approach adulthood, the 85th and 95th percentile BMI for age and sex are approximately 25 and 30, the thresholds for overweight and obesity in adults, respectively [7].

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There remains some variability in the terminology used to distinguish between categories of adiposity (table 2), but a growing consensus supports the following definitions for children between 2 and 20 years of age: Underweight BMI <5th percentile for age and sex. Normal weight BMI between the 5th and 85th percentile for age and sex. Overweight BMI between the 85th and 95th percentile for age and sex. The CDC uses the term "at risk for overweight" for this category. Obese BMI 95th percentile for age and sex. The CDC uses the term "overweight" for this category. In adults, a BMI threshold of 40 kg/m(2) distinguishes individuals with severe obesity and the highest risks for comorbidities. This category is sometimes termed "class III obesity" or "super obesity". (See "Screening for and clinical evaluation of obesity in adults".) A similar category of severe obesity has not been defined in childhood. However, a large population study used a BMI >99th percentile to define a population of children with the most severe obesity [8]. This group represents approximately 4 percent of children and adolescents (ages 5 to 17) in the United States, and has significantly more cardiovascular risk factors and a greater risk for having obesity in adulthood. Therefore, the 99th percentile for BMI (z-score >2.33) appears to be a useful cutoff to define a group with medically significant obesity in children and adolescents [9]. Adolescents with this severe degree of obesity should be treated with tertiary care intervention with a multidisciplinary pediatric weight management team, which may include consideration for weight loss surgery [9]. (See "Surgical management of severe obesity in adolescents".) The term "morbid obesity" is sometimes used to identify individuals with obesity-related comorbidities. However, this term is often inappropriately used as a synonym for severe obesity, and it also may have pejorative connotations to patients, so its use is discouraged. (See "Comorbidities and complications of obesity in children and adolescents".) In the discussion that follows, the term "obesity" refers to children with BMI >95 percentile for age and sex and "overweight" refers to children with BMI between the 85th and 95th percentile for age and sex, unless otherwise noted. EPIDEMIOLOGY The prevalence of obesity among school-aged children (6 to 11 years) and adolescents (12 to 19 years) in the United States dramatically increased between 1976 to 1980 and 2003 to 2006 (from 6.5 to 17.0 percent in children, and from 5.0 to 17.6 percent in adolescents) [1,10]. The prevalence of obesity also tripled for preschool-aged children (2 to 5 years) from 5 percent in 1976 to 1980 to 12.4 percent in 2003 to 2006. Of note, the increase in obesity prevalence reached a plateau around 2000; the percentage of children and adolescents in each weight category remained stable between 2000 and 2006 [10]. Currently, almost one third of children and adolescents in the United States are either overweight or obese [10]. The population is distributed into higher weight categories with advancing age, as shown below:

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Overweight or obese (BMI85 percentile) 24 percent of preschool children (2 to 5 years) 33 percent of school-aged children (6 to 11 years) 34 percent of adolescents (12 to 19 years) Obese (BMI95 percentile) 12.4 percent of preschool children 17.0 percent of school-aged children 17.6 percent of adolescents Severe obesity (BMI97 percentile) 8.5 percent of preschool children 11.4 percent of school-aged children 12.6 percent of adolescents Childhood obesity is more common among American Indian, non-Hispanic blacks, and Mexican Americans than in non-Hispanic whites [4,10-12]. Having an obese parent increases the risk of obesity by two-to three fold. Obesity is also more prevalent among low-income populations. As an example, 14.6 percent of low-income preschool aged children were obese in 2008, as compared with 12.4 percent in this age group in the general population [12]. In the same study, the prevalence of obesity among the low-income preschool-aged population increased from 1998 to 2003, but plateaued between 2003 to 2008. The prevalence of childhood overweight and obesity is also increasing in most other developed countries worldwide (graph 3). It is difficult to directly compare prevalence rates between countries because of differences in definitions and dates of measurements. Use of the International Obesity Task Force (IOTF) standards typically results in lower prevalence estimates than other standards [13,14]. However, studies using comparable statistics show that rates are particularly high (greater than 30 percent) in most countries in North and South America, as well as in Great Britain, Greece, Italy, Malta, Portugal, and Spain [15]. There are somewhat lower rates in the Nordic countries, and the central portion of western Europe. In Russia and most of the countries of Eastern Europe the prevalence of overweight is lower (less than 10 percent), but increasing. In China, the prevalence of overweight among children is approximately 1/3 of that in the US, but a greater proportion of pre-school-aged children are affected [14]. Thus, across a wide range of developed and developing countries, and using a variety of measures, studies show increasing prevalence of obesity in children. Only one small study, examining children in Scotland, showed a reversal of the trend between 2001 and 2004 [16]. The reasons for the apparent improvement were not addressed in the study. The increased prevalence of childhood obesity has resulted in an increased prevalence of the comorbidities associated with obesity [4]. As an example, the prevalence of conditions such as sleep apnea and gall bladder disease in US children and adolescents tripled between 1979 to 1981

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and 1997 to 1999 [17]. Comorbidities of childhood obesity are discussed separately. (See "Comorbidities and complications of obesity in children and adolescents".) Persistence into adulthood It is difficult to predict which overweight children will become obese adults. The likelihood of persistence of childhood obesity into adulthood is related to age [18-20], parental obesity [21,22], and severity of obesity [23,24]. In longitudinal studies, approximately 25 percent of obese preschool children remain obese as adults [25], compared to approximately 50 percent of obese 6-year olds, and 80 percent of obese 10- to 14-year olds who had one obese parent [21]. These statistics must be interpreted with caution since the dietary habits and activity levels of today's children may differ from those of the children in the studies, thereby altering the risk of obesity in adulthood [7]. As a general rule, a sedentary obese child who does not alter his or her caloric intake and lifestyle is unlikely to be of normal weight as an adult. Girls are more prone than boys to develop persistent obesity during adolescence [7,26]. This is related to changes in body composition that occur at puberty, when body fat decreases in boys and increases in girls [27]. Approximately 80 percent of obese adolescent girls remain obese, whereas approximately 30 percent of obese adolescent males do so [26]. The natural history of obesity and risk factors for persistence into adulthood is discussed in greater detail separately. (See "Etiology and natural history of obesity", section on 'Age at which overweight develops'.) ETIOLOGY The etiology and pathogenesis of obesity are discussed in greater detail separately. (See "Etiology and natural history of obesity" and "Pathogenesis of obesity".) Environmental factors Almost all obesity in children is strongly influenced by environmental factors, caused by either a sedentary lifestyle or a caloric intake that is greater than needs. The contributions of specific environmental influences are the subject of considerable discussion and research. Increasing trends in glycemic index of foods, sugar-containing beverages, portion sizes for prepared foods, fast food service, and decreasing structured physical activity have all been considered as causal influences on the rise in obesity. In particular, a number of well-designed studies have shown associations between intake of sugar-containing beverages or low physical activity and obesity or metabolic abnormalities [28-34]. Causal associations seem likely but are difficult to establish with certainty. Television Television viewing is perhaps the best established environmental influence on the development of obesity during childhood. The amount of time spent in watching television is directly related to the prevalence of obesity in children and adolescents [35-39]. The effects may persist into adulthood. In two longitudinal cohort studies, television viewing at 5 years was independently associated with increased BMI at age 26 to 30 years [40,41]. Other studies suggest that the association between television viewing and obesity is considerably weaker [42,43]. There are several proposed mechanisms for this association [44,45]: Displacement of physical activity Depression of metabolic rate

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Adverse effects on diet quality One study provides evidence that the effects of television on obesity are mediated primarily by changes in energy intake. In a randomized trial, reducing television viewing and computer use among overweight four to seven year-old children was effective in reducing both BMI and energy intake during the two year intervention, without apparent changes in physical activity [45]. Similar associations between television viewing and energy intake have been shown in studies of older or non-overweight youth [46]. Video games The use of electronic games also has been associated with obesity during childhood [47]. In the few studies that analyze the influences separately, the association with obesity is somewhat weaker for electronic games than for television [47,48], perhaps because the games do not include food advertising. A few video games have been specifically designed to provide nutritional education and encourage healthy habits [49,50]. Others require interactive physical activity by the player [51]. Activityenhancing games generally cause a modest increase in energy expenditure during playing time [52-54]. Two studies examined some of the most commonly used games and found that energy expenditure of playing active games was higher than that of sedentary games, but not as high as playing the simulated sport itself [54,55]. In general, the activity levels of the games were comparable to moderate-intensity walking, and not of sufficiently high intensity to contribute to the recommended daily amount of exercise for children. A small study reported that use of one of these games had no long-term effect on obesity status, and that use of the game declined sharply over time [56]. Otherwise, the efficacy of these games to increase physical activity or treat obesity has not been systematically studied. Sleep Cross-sectional studies suggest an association between shortened sleep duration and obesity or insulin resistance, after adjustment for a number of potential environmental confounders [57-60]; the effects are more marked in children at the upper end of the weight range [61]. Three longitudinal studies also showed associations after adjustment for confounders, suggesting that the association may be causal [62-64]. Similar findings have been seen in adult populations [65]. The mechanism for the association has not been established, but may include alterations in serum leptin and ghrelin levels, both of which have been implicated in the regulation of appetite, or perhaps a longer opportunity to ingest food. (See "Etiology and natural history of obesity", section on 'Sleep deprivation'.) Genetic factors Genetic factors play a permissive role and interact with environmental factors to produce obesity. Studies suggest that heritable factors are responsible for 30 to 50 percent of the variation in adiposity [66], but most of the genetic polymorphisms responsible have not yet been isolated. Thus, genetic contributions to common obesity likely exist, but the molecular mechanisms for these factors have yet to be determined. (See "Pathogenesis of obesity", section on 'Common obesity'.) A variety of specific syndromes and single-gene defects which are linked to obesity in childhood have been identified (table 3). These are rare causes of obesity, accounting for less than one percent of childhood obesity in tertiary care centers [1,67,68]. In addition to being overweight, children with genetic syndromes associated with obesity typically have characteristic findings on

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physical examination. These include dysmorphic features, short stature, developmental delay or intellectual disability (mental retardation), retinal changes, or deafness. (See "Clinical features, diagnosis, and treatment of Prader-Willi syndrome".) For most of the syndromes, including Prader-Willi syndrome, the genetic cause has been sufficiently isolated to permit specific testing, but the exact mechanism through which they cause obesity is not understood or is attributable to multiple genes (table 4). Other disorders are attributable to a mutation in a single gene involved in regulation of body weight, although the mutations also may have effects on pigmentation (POMC) and the reproductive system (table 5). Several of these affect the melanocortin pathway in the central nervous system. The most common single gene defect currently identified in populations with severe obesity are mutations in the melanocortin 4 receptor, but this is still rare, accounting for only about four to six percent of severe obesity [69,70]. Endocrine disease Endocrine causes of obesity are identified in fewer than 1 percent of children and adolescents with obesity [68]. The disorders include hypothyroidism, cortisol excess (eg, the use of corticosteroid medication, Cushing syndrome), growth hormone deficiency, and acquired hypothalamic lesions (eg, infection, vascular malformation, neoplasm, trauma) (table 3) [67,71,72]. Most children with these problems have short stature and/or hypogonadism (graph 4) [68]. These disorders are discussed in detail separately. (See "Acquired hypothyroidism in childhood and adolescence" and "Clinical manifestations of Cushing's syndrome" and "Diagnosis of growth hormone deficiency in children".) Metabolic programming There is increasing evidence that environmental and nutritional influences during critical periods in development can have permanent effects on an individual's predisposition to obesity and metabolic disease. The precise mediators and mechanisms for these effects have not been established, but are the subject of ongoing investigations [73]. Nutrition during gestation and early life Maternal nutrition during gestation is probably an important determinant of metabolic programming, as illustrated by the following studies: Individuals born small for gestational age (SGA) or large for gestational age (LGA) have higher rates of insulin resistance during childhood, even after controlling for obesity status [74]. Similarly, many population-based studies confirm an association between birthweight (reflecting fetal nutrition) and later diabetes, heart disease, insulin resistance, and obesity [75,76]. Studies of a cohort of individuals exposed to the Dutch famine in 1944 to 1945, and controlled studies of over- and under-feeding in animals, support the notion that there are causal associations between nutritional exposures during gestation and later obesity and metabolic disease [77,78]. Children born to women who have had gastric bypass surgery appear to have a lower prevalence of obesity than those born before gastric bypass, suggesting that reversal of maternal obesity had beneficial permanent effects on the metabolic profile of the offspring [79]. Infancy and early childhood are probably also critical periods for metabolic programming. Studies in a variety of populations have shown consistent associations between rates of weight gain during infancy or early childhood and subsequent obesity or metabolic syndrome during early childhood

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[80], adolescence or adulthood [81] (for systematic reviews, see references [82-85]), or with intermediate outcomes such as adiposity and blood pressure in early childhood [86-88]. In conjunction with the evidence supporting metabolic programming, these observations suggest that early intervention might be an important tool in preventing obesity. Controlled trials of early nutritional interventions with long-term outcomes are still lacking. Nonetheless, there is ample circumstantial evidence to support clinical efforts to optimize nutrition during gestation, infancy and early childhood. Appropriate goals are to optimize glycemic control in pregnant women and target moderate rates of weight gain in infants and young children. Nutritional goals are less clear for low-birthweight infants, for whom catch-up growth is associated with improved neurodevelopmental outcomes, but also with increased risks for metabolic disease [89-91]. Increasing the protein component of feeding (eg, a maximum protein content of 3.6 g/100 kcals) appears to normalize serum IGF-1 concentrations [89]. This strategy has been proposed to achieve improved neurodevelopmental and metabolic outcomes for these infants, but it is not yet tested. Other maternal endocrine factors Other markers of the maternal endocrine milieu are also associated with childhood obesity, although the mechanisms for the association are not established. In a study of 6009 children and their mothers, younger age of the mother at menarche was an independent predictor of the child's obesity status, after adjustment for the maternal obesity status as well as socioeconomic factors [92]. The children whose mothers had earlier menarche also had more rapid growth during the first two years of life, whereas birthweight and growth after two years were similar. The results of this study do not distinguish between mechanisms of metabolic programming versus genetic mechanisms for the transgenerational obesity transmission observed in this study. Environmental mechanisms are less likely because of the adjustment for maternal BMI and socioeconomic factors, but these cannot be excluded. A large longitudinal study failed to demonstrate intergenerational acceleration mechanisms (maternal-child transmission) from maternal weight status during pregnancy [93]. Among 4654 parent-child pairs, the father-offspring and mother-offspring associations for BMI were equally strong. Parental height and weight were self-reported during the pregnancy, and the child's BMI was measured at approximately 7.5 years of age. This study did not detect any effects of maternal obesity transmitted to the child through the intrauterine environment. Thus, if metabolic programming is a mechanism for intergenerational transmission of obesity, the effect is either subtle, or the mediators are more complex than maternal BMI. It is also possible that the study systematically under-estimated parental BMIs because measurements were self-reported.

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62. Lumeng, JC, Somashekar, D, Appugliese, D, et al. Shorter sleep duration is associated with increased risk for being overweight at ages 9 to 12 years. Pediatrics 2007; 120:1020. 63. Landhuis, CE, Poulton, R, Welch, D, Hancox, RJ. Childhood sleep time and long-term risk for obesity: a 32-year prospective birth cohort study. Pediatrics 2008; 122:955. 64. Touchette, E, Petit, D, Tremblay, RE, et al. Associations between sleep duration patterns and overweight/obesity at age 6. Sleep 2008; 31:1507. 65. Cappuccio, FP, Taggart, FM, Kandala, NB, et al. Meta-analysis of short sleep duration and obesity in children and adults. Sleep 2008; 31:619. 66. Bouchard, C. Genetic determinants of regional fat distribution. Hum Reprod 1997; 12 Suppl 1:1. 67. Speiser, PW, Rudolf, MC, Anhalt, H, et al. Childhood obesity. J Clin Endocrinol Metab 2005; 90:1871. 68. Reinehr, T, Hinney, A, de Sousa, G, et al. Definable somatic disorders in overweight children and adolescents. J Pediatr 2007; 150:618. 69. Vaisse C, Clement K, Durand E, et al. Melanocortin-4 receptor mutations are a frequent and heterogeneous cause of morbid obesity. J Clin Invest 2000; 106:253. 70. Dubern, B, Bisbis, S, Talbaoui, H, et al. Homozygous null mutation of the melanocortin-4 receptor and severe early-onset obesity. J Pediatr 2007; 150:613. 71. Leibel, RL, Chua, SC, Rosenbaum, M. Obesity. In: The Metabolic and Molecular Bases of Inherited Disease, 8th ed, Scriver, CR, Beaudet, AL, Sly, WS, Valle, D (Eds), McGraw-Hill, New York, 2001. p. 3965. 72. Pediatric Obesity. In: Pediatric Nutrition Handbook, 6th ed, Kleinman, R (Ed), American Academy of Pediatrics, Elk Grove Village, IL, 2009. p. 733. 73. Mantzoros, CS, Rifas-Shiman, SL, Williams, CJ, et al. Cord blood leptin and adiponectin as predictors of adiposity in children at 3 years of age: a prospective cohort study. Pediatrics 2009; 123:682. 74. Chiavaroli, V, Giannini, C, D'Adamo, E, et al. Insulin resistance and oxidative stress in children born small and large for gestational age. Pediatrics 2009; 124:695. 75. Huxley, R, Owen, CG, Whincup, PH, et al. Is birth weight a risk factor for ischemic heart disease in later life?. Am J Clin Nutr 2007; 85:1244. 76. Barker, DJ, Winter, PD, Osmond, C, et al. Weight in infancy and death from ischaemic heart disease. Lancet 1989; 2:577. 77. Fernandez-Twinn, DS, Ozanne, SE. Mechanisms by which poor early growth programs type2 diabetes, obesity and the metabolic syndrome. Physiol Behav 2006; 88:234. 78. Plagemann, A. Perinatal nutrition and hormone-dependent programming of food intake. Horm Res 2006; 65 Suppl 3:83. 79. Kral, JG, Biron, S, Simard, S, et al. Large maternal weight loss from obesity surgery prevents transmission of obesity to children who were followed for 2 to 18 years. Pediatrics 2006; 118:e1644. 80. Taveras, EM, Rifas-Shiman, SL, Belfort, MB, et al. Weight status in the first 6 months of life and obesity at 3 years of age. Pediatrics 2009; 123:1177. 81. Leunissen, RW, Kerkhof, GF, Stijnen, T, Hokken-Koelega, A. Timing and tempo of first-year rapid growth in relation to cardiovascular and metabolic risk profile in early adulthood. JAMA 2009; 301:2234.

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82. Monteiro, PO, Victora, CG. Rapid growth in infancy and childhood and obesity in later life--a systematic review. Obes Rev 2005; 6:143. 83. Ong, KK, Loos, RJ. Rapid infancy weight gain and subsequent obesity: systematic reviews and hopeful suggestions. Acta Paediatr 2006; 95:904. 84. Owen, CG, Martin, RM, Whincup, PH, et al. Effect of infant feeding on the risk of obesity across the life course: a quantitative review of published evidence. Pediatrics 2005; 115:1367. 85. Baird, J, Fisher, D, Lucas, P, et al. Being big or growing fast: systematic review of size and growth in infancy and later obesity. BMJ 2005; 331:929. 86. Belfort, MB, Rifas-Shiman, SL, Rich-Edwards, J, et al. Size at birth, infant growth, and blood pressure at three years of age. J Pediatr 2007; 151:670. 87. Shehadeh, N, Weitzer-Kish, H, Shamir, R, et al. Impact of early postnatal weight gain and feeding patterns on body mass index in adolescence. J Pediatr Endocrinol Metab 2008; 21:9. 88. Gardner, DS, Hosking, J, Metcalf, BS, et al. Contribution of early weight gain to childhood overweight and metabolic health: a longitudinal study (EarlyBird 36). Pediatrics 2009; 123:e67. 89. Yeung, MY. Postnatal growth, neurodevelopment and altered adiposity after preterm birth-from a clinical nutrition perspective. Acta Paediatr 2006; 95:909. 90. Lucas, A, Morley, R, Cole, TJ. Randomised trial of early diet in preterm babies and later intelligence quotient. BMJ 1998; 317:1481. 91. Thureen, PJ. The neonatologist's dilemma: catch-up growth or beneficial undernutrition in very low birth weight infants-what are optimal growth rates?. J Pediatr Gastroenterol Nutr 2007; 45 Suppl 3:S152. 92. Ong, KK, Northstone, K, Wells, JC, et al. Earlier Mother's Age at Menarche Predicts Rapid Infancy Growth and Childhood Obesity. PLoS Med 2007; 4:e132. 93. Davey Smith, G, Steer, C, Leary, S, Ness, A. Is there an intrauterine influence on obesity? Evidence from parent child associations in the Avon Longitudinal Study of Parents and Children (ALSPAC). Arch Dis Child 2007; 92:876.

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GRAPHICS

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Prevalence of obesity* among children and teenagers, by age group and selected period--United States, 1963-2004

* Children with body mass index (BMI) values at or above the 95th percentile of CDC sexspecific BMI growth charts for 2000.

National Health and Nutrition Examination Surveys. Additional information is available at http://www.cdc.gov/nchs/products/pubs/hestats/overwght99.htm.

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Calculation of BMI
English formula for BMI: [Weight in pounds Height in inches Height in inches] x 703 Metric formula for BMI: Weight in Kilograms Height in meters Height in meters

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Body mass index-for-age percentiles, boys, 2 to 20 years, CDC growth charts: United States

Developed by the National Center for Health Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion (2000).

Body mass index-for-age percentiles, girls, 2 to 20 years, CDC growth charts: United States

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Developed by the National Center for Health Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion (2000).

Weight categories for adults and youth

Category
Underweight Normal weight At risk of overweight Overweight

Adults (21+yrs)
BMI <18.5 BMI 18.5-24.9 Not used BMI 25-29.9

Youth (2-20 yrs) AAP, IOM, ES, IOTF


BMI <5th percentile for age BMI 5th to 85th percentile Not used BMI 85th to 95th percentile

Youth (2-20yrs) CDC


BMI <5th percentile for age BMI 5th to 85th percentile BMI 85th to 95th percentile BMI 95th percentile

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Definition; epidemiology; and etiology of obesity in children and adolescents

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Obesity Class III obesity (super obesity)

BMI BMI

30 40

BMI 95th percentile Not used

Not used Not used

AAP: American Academy of Pediatrics; IOM: Institute of Medicine; ES: Endocrine society; CDC: Centers for Disease Control; IOTF: International obesity task force

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Definition; epidemiology; and etiology of obesity in children and adolescents

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Rising prevalence of overweight children (5-11)

For this figure, the prevalence of overweight children is defined as the percent of children aged 5 to 11 with BMI >85 percentile, using IOTF standards.
IOTF: International Obesity Task Force.

Reproduced with permission from: Lobstein, T, Rigby, N, Leach, R. International Obesity Task Force. EU platform diet, physical activity, and health. International Obesity Task Force EU Platform Briefing Paper. Brussels 2005. Copyright 2005 European Association for the Study of Obesity.

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Specific syndromes linked to childhood obesity


Genetic syndromes Albright hereditary osteodystrophy Alstrom-Hallgren syndrome Bardet-Biedl syndrome

Carpenter syndrome Cohen syndrome Prader-Willi syndrome Selected single gene disorders:
Leptin deficiency Leptin receptor deficiency Propiomelanocortin (POMC) deficiency Prohormone convertase 1 impairment Melanocortin receptors 3 and 4 deficiency

Endocrine disorders Cushing's disease Hypothyroidism Growth hormone deficiency Acquired hyopthalamic lesions

Genetic syndromes associated with obesity

Syndrome
Albright hereditary osteodystrophy

Obesity Chromosome onset (type)


20q13.11 Early (generalized)

Clinical features
Short stature, short metacarpals and metatarsals, round facies, delayed dentition, +/- hypocalcemia and/or vicarious mineralization, precocious puberty, mild cognitive deficit Blindness, deafness, acanthosis nigricans, chronic nephropathy, type 2 diabetes, cirrhosis, primary hypogonadims in males only, normal cognition Mental retardation, hypotonia, retinitis pigmentosa, polydactyly, hypogonadism +/glucose intolerance, deafness, renal disease

Alstrom-Hallgren 2p14-p13

Age 2 - 5 yrs (central)

Bardet-Biedl

BeckwithWiedeman Carpenter

16q21 15q22-q23 3p13-p12 11q13 20p12 11p15.5 Unknown

Age 1 - 2 yrs (central)

Cohen

8q22

Prader- Willi

15q

Hyperinsulinemia, hypoglycemia, hemihypertrophy, intolerance of fasting (central) Mental retardation, short stature, brachycephaly, polydactyly, syndactyly of feet, cryptorchidism, umbilical hernia, high-arched palate, hypogonadism in males only Mid-childhood Mental retardation, microcephaly, small hands (central) and feet, cryptorchidism, hypotonia and failure to thrive in infancy, prominent central incisors, long, thin fingers and toes Age 1 - 3 yrs Microcephaly, short stature, hypotonia, (generalized) almond- shaped eyes, high-arched palate, narrow hands and feet, delayed puberty, early

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failure to thrive with hyperphagia and increased weight gain by 2-3 years, mild to moderate cognitive deficit;
Adapted from: Pediatric Obesity. In: Pediatric Nutrition Handbook, 5th ed, Kleinman, R (Ed), American Academy of Pediatrics, Elk Grove Village, IL, 2004. p. 551 and Hoppin, AG. Obesity. In: Pediatric Gastrointestinal Disease: Pathopsychology, Diagnosis, Management, 4th ed, Walker, WA, Goulet, O, Kleinman, RE, et al (Eds), BC Decker, Ontario, 2004. p. 311 and Leibel, RL, Chua, SC, Rosenbaum, M. Obesity. In: The Metabolic and Molecular Bases of Inherited Disease, 8th ed, Scriver, CR, Beaudet, AL, Sly, WS, Valle, D (Eds), McGraw-Hill, New York, 2001. p. 3965.

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Single gene defects associated with obesity

Single gene disorder Chromosome


Leptin deficiency 7q31.3

Clinical features
Severe, early onset obesity, hypometabolic rate, hyperphagia, pubertal delay, impaired glucose tolerance, hypothalamic hypogonadism Severe, early onset obesity, red hair, hyperphagia, adrenal insufficiency, hyperpigmentation Early onset obesity, abnormal glucose homeostasis, hypogonadotropic hypogonadism, hypocortisolism, elevated plasma proinsulin and POMC Early onset, moderate-severe obesity, early onset hyperphagia, increased bone density Severe, early onset obesity, hypometabolic rate, hyperphagia, pubertal delay, hypothalamic hypogonadism

POMC deficiency

2p23.3

Prohormone convertase 5q15-q21 impairment Melanocortin receptor 4 18q21.3-q22 haploinsufficiency Leptin receptor 1p31-p22 deficiency
POMC: propiomelanocortin.

Adapted from: Hoppin, AG. Obesity. In: Pediatric Gastrointestinal Disease: Pathopsychology, Diagnosis, Management, 4th ed, Walker, WA, Goulet, O, Kleinman, RE, et al (Eds), BC Decker, Ontario, 2004. p. 311 and Leibel, RL, Chua, SC, Rosenbaum, M. Obesity. In: The Metabolic and Molecular Bases of Inherited Disease, 8th ed, Scriver, CR, Beaudet, AL, Sly, WS, Valle, D (Eds), McGraw-Hill, New York, 2001. p. 3965.

Decreased growth in Cushing's disease

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Chronological height and weight chart of a boy who developed overt Cushing's disease at about age seven years. He stopped growing and minimized his weight gain for about five years with a strict diet and vigorous exercise program. He was treated with conventional megavoltage pituitary irradiation at age 13 years (arrows). He resumed growth at the same velocity as boys of his age, but there was no catch-up growth.
Reprinted with permission from Williams Textbook of Endocrinology, 8th ed, Foster, DW, Wilson, JD (Eds), WB Saunders, Philadelphia, 1996.

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