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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

Page 1 of 23Definition; epidemiology; and etiology of obesity in children and adolescents

11/24/2009http://www.uptodateonline.com/online/content/topic.do?topicKey=pedigast/15483&view ...


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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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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.

77. Fernandez-Twinn, DS, Ozanne, SE. Mechanisms by which poor early growth programs type-2 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 surgeryprevents transmission of obesity to children who were followed for 2 to 18 years. Pediatrics2006; 118:e1644.

80. Taveras, EM, Rifas-Shiman, SL, Belfort, MB, et al. Weight status in the first 6 months of lifeand 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-yearrapid growth in relation to cardiovascular and metabolic risk profile in early adulthood. JAMA2009; 301:2234.




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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;

115:1367.

85. Baird, J, Fisher, D, Lucas, P, et al. Being big or growing fast: systematic review of size andgrowth 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 bloodpressure 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 andfeeding 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 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.

90. Lucas, A, Morley, R, Cole, TJ. Randomised trial of early diet in preterm babies and laterintelligence quotient. BMJ 1998; 317:1481.

91. Thureen, PJ. The neonatologist's dilemma: catch-up growth or beneficial undernutrition invery low birth weight infants-what are optimal growth rates?. J Pediatr Gastroenterol Nutr2007; 45 Suppl 3:S152.

92. Ong, KK, Northstone, K, Wells, JC, et al. Earlier Mother's Age at Menarche Predicts RapidInfancy 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 andChildren (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 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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21/23

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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