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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 notavailable 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].
Definition; epidemiology; and etiology of obesity in
children and adolescents
Last literature review for version 17.3: September 30, 2009 | This topic last updated:
September 29, 2009
AuthorWilliam J Klish, MD
Section EditorsKathleen J Motil, MD, PhDJohn L Kirkland, MDCraig Jensen, MD
Deputy EditorAlison G Hoppin, MD
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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 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 5years) 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 children12.6 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 developedcountries 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]. Activity-
enhancing 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 energyexpenditure 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) (table3) [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 notestablished. 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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58. Flint, J, Kothare, SV, Zihlif, M, et al. Association between inadequate sleep and insulinresistance in obese children. J Pediatr 2007; 150:364.
59. Sekine, M, Yamagami, T, Handa, K, et al. A dose-response relationship between shortsleeping hours and childhood obesity: results of the Toyama Birth Cohort Study. Child CareHealth Dev 2002; 28:163.
60. Jiang, F, Zhu, S, Yan, C, et al. Sleep and obesity in preschool children. J Pediatr 2009;154:814.
61. Bayer, O, Rosario, AS, Wabitsch, M, von Kries, R. Sleep duration and obesity in children: isthe association dependent on age and choice of the outcome parameter?. Sleep 2009;32:1183.
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62. Lumeng, JC, Somashekar, D, Appugliese, D, et al. Shorter sleep duration is associated withincreased 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 forobesity: a 32-year prospective birth cohort study. Pediatrics 2008; 122:955.
64. Touchette, E, Petit, D, Tremblay, RE, et al. Associations between sleep duration patternsand overweight/obesity at age 6. Sleep 2008; 31:1507.
65. Cappuccio, FP, Taggart, FM, Kandala, NB, et al. Meta-analysis of short sleep duration andobesity in children and adults. Sleep 2008; 31:619.
66. Bouchard, C. Genetic determinants of regional fat distribution. Hum Reprod 1997; 12 Suppl1:1.
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 childrenand adolescents. J Pediatr 2007; 150:618.
69. Vaisse C, Clement K, Durand E, et al. Melanocortin-4 receptor mutations are a frequent andheterogeneous 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-4receptor and severe early-onset obesity. J Pediatr 2007; 150:613.
71. Leibel, RL, Chua, SC, Rosenbaum, M. Obesity. In: The Metabolic and Molecular Bases ofInherited 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), AmericanAcademy of Pediatrics, Elk Grove Village, IL, 2009. p. 733.
73. Mantzoros, CS, Rifas-Shiman, SL, Williams, CJ, et al. Cord blood leptin and adiponectin aspredictors of adiposity in children at 3 years of age: a prospective cohort study. Pediatrics2009; 123:682.
74. Chiavaroli, V, Giannini, C, D'Adamo, E, et al. Insulin resistance and oxidative stress inchildren 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 heartdisease 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 heartdisease. Lancet 1989; 2:577.
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78. Plagemann, A. Perinatal nutrition and hormone-dependent programming of food intake.Horm Res 2006; 65 Suppl 3:83.
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82. Monteiro, PO, Victora, CG. Rapid growth in infancy and childhood and obesity in later life--asystematic review. Obes Rev 2005; 6:143.
83. Ong, KK, Loos, RJ. Rapid infancy weight gain and subsequent obesity: systematic reviewsand hopeful suggestions. Acta Paediatr 2006; 95:904.
84. Owen, CG, Martin, RM, Whincup, PH, et al. Effect of infant feeding on the risk of obesityacross the life course: a quantitative review of published evidence. Pediatrics 2005;
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88. Gardner, DS, Hosking, J, Metcalf, BS, et al. Contribution of early weight gain to childhoodoverweight 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.
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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 sex-
specific 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 growthcharts: 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
Adults
(21+yrs)
Youth (2-20 yrs) AAP,
IOM, ES, IOTF
Youth (2-20yrs)
CDC
Underweight BMI
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AAP: American Academy of Pediatrics; IOM: Institute of Medicine; ES: Endocrine society; CDC: Centers for Disease Control;
IOTF: International obesity task force
Obesity BMI 30 BMI 95th percentile Not used
Class III obesity (super
obesity)
BMI 40 Not used Not used
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Rising prevalence of overweight children (5-11)
For this figure, the prevalence of overweight children is defined as the percentof 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. InternationalObesity Task Force EU Platform Briefing Paper. Brussels 2005. Copyright 2005
European Association for the Study of Obesity.
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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 Basesof Inherited Disease, 8th ed, Scriver, CR, Beaudet, AL, Sly, WS, Valle, D (Eds), McGraw-Hill, New York, 2001. p.
3965.
failure to thrive with hyperphagia and
increased weight gain by 2-3 years, mild tomoderate cognitive deficit;
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Single gene defects associated with obesity
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 andLeibel, 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.
Single gene disorder Chromosome Clinical features
Leptin deficiency 7q31.3 Severe, early onset obesity, hypometabolic rate,
hyperphagia, pubertal delay, impaired glucosetolerance, hypothalamic hypogonadism
POMC deficiency 2p23.3 Severe, early onset obesity, red hair, hyperphagia,
adrenal insufficiency, hyperpigmentation
Prohormone convertase
impairment
5q15-q21 Early onset obesity, abnormal glucose homeostasis,
hypogonadotropic hypogonadism, hypocortisolism,elevated plasma proinsulin and POMC
Melanocortin receptor 4
haploinsufficiency
18q21.3-q22 Early onset, moderate-severe obesity, early onset
hyperphagia, increased bone density
Leptin receptor
deficiency
1p31-p22 Severe, early onset obesity, hypometabolic rate,
hyperphagia, pubertal delay, hypothalamichypogonadism
Decreased growth in Cushing's disease
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2009 UpToDate, Inc. All rights reserved. | Subscription and License Agreement | Support Tag:[ecapp0503p.utd.com-76.6.71.5-EAD8E8D1EB-6]
Licensed to: UpToDate Individual Web - Blanca Peruzzi
Chronological height and weight chart of a boy who developed overtCushing's disease at about age seven years. He stopped growing andminimized his weight gain for about five years with a strict diet and vigorousexercise program. He was treated with conventional megavoltage pituitaryirradiation at age 13 years (arrows). He resumed growth at the same velocityas 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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