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Obesity in Children

  • Author: Steven M Schwarz, MD, FAAP, FACN, AGAF; Chief Editor: Jatinder Bhatia, MBBS, FAAP  more...
 
Updated: Mar 29, 2016
 

Background

Obesity is the most prevalent nutritional disorder among children and adolescents in the United States. Approximately 21-24% of American children and adolescents are overweight, and another 16-18% is obese; the prevalence of obesity is highest among specific ethnic groups.

Childhood obesity predisposes to insulin resistance and type 2 diabetes, hypertension, hyperlipidemia, liver and renal disease, and reproductive dysfunction. This condition also increases the risk of adult-onset obesity and cardiovascular disease.[1]

Obesity in children is a complex disorder. Its prevalence has increased so significantly in recent years that many consider it a major health concern of the developed world. The National Health and Nutrition Examination Survey (NHANES) indicates that the prevalence of obesity is increasing in all pediatric age groups, in both sexes, and in various ethnic and racial groups. Many factors, including genetics, environment, metabolism, lifestyle, and eating habits, are believed to play a role in the development of obesity. However, more than 90% of cases are idiopathic; less than 10% are associated with hormonal or genetic causes.

Definitions

Operational definitions of obesity in adults are derived from statistical data that analyze the association between body mass and the risk of acute and long-term morbidity and mortality. Because acute medical complications of obesity are less common in children and adolescents than in adults, and because longitudinal data on the relation between childhood weight and adult morbidity and mortality are more difficult to interpret, no single definition of obesity in childhood and adolescence has gained universal approval.

Some investigators have used the terms overweight, obese, and morbidly obese to refer to children and adolescents whose weights exceed those expected for heights by 20%, 50%, and 80-100%, respectively. The body mass index (BMI) has not been consistently used or validated in children younger than 2 years. Because weight varies in a continuous rather than a stepwise fashion, the use of these arbitrary criteria is problematic and may be misleading. Nevertheless, children and adolescents defined as overweight or obese according to published criteria are highly likely to maintain this ponderal status as adults.

Body mass index

The BMI is a continuous, although imperfect, measure of body fatness. Calculated as weight (kg) divided by height (m2), BMI corrects for body size and can be readily and reliably quantified in clinical settings. The BMI correlates closely with total body fat (TBF), which is estimated using dual-energy x-ray absorptiometry (DEXA) scanning in children who are overweight and obese.

Normal values for BMI vary with age, sex, and pubertal status, and standard curves representing the 5th through the 95th percentiles for BMI in childhood and adolescence were generated using data from the 1988-1994 NHANES.[2] Consensus committees have recommended that children and adolescents be considered overweight or obese if the BMI exceeds the 85th or 95th percentiles, on curves generated from the 1963-1965 and 1966-1970 NHANES, or exceeds 30 kg/m2 at any age.[3]

McGavock et al demonstrated that low cardiorespiratory fitness and reductions in fitness over time are significantly associated with weight gain and the risk of being overweight in children aged 6-15 years.[4] Analysis on a cohort of 902 schoolchildren showed higher waist circumference and disproportionate weight gain over a 12-month follow-up period in those children with low cardiorespiratory fitness. The 12-month risk of overweight classification was 3.5-fold higher in youth with low cardiorespiratory fitness, relative to fit peers.[4] Reductions in cardiorespiratory fitness were significantly and independently associated with increasing BMI. Low levels of cardiorespiratory fitness have also been associated with elevated depressive symptoms in obese adolescents.[5]

One study suggests that a lack of adequate sleep time in young children is associated with increased BMI; this observation is independent of other confounding variables (eg, physical activity).[6]

Furthermore, data indicate that over a 5-year period an increase in BMI among overweight children 6 to 11 years of age is associated with increases in both systolic and diastolic blood pressure, as well as with a decrease in sleep time.[7]

A study by Mosli et al found that a birth of a sibling when the child is 24 to 54 months old is associated with a healthier body mass index z-score trajectory.[8, 9]

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Etiology and Pathophysiology

Genetic syndromes associated with childhood obesity include the following:

  • Prader-Willi syndrome
  • Pseudohypoparathyroidism
  • Laurence-Moon-Biedl (Bardet-Biedl) syndrome
  • Cohen syndrome
  • Down syndrome
  • Turner syndrome

Hormonal disorders associated with childhood obesity include the following:

  • Growth hormone deficiency
  • Growth hormone resistance
  • Hypothyroidism
  • Leptin deficiency or resistance to leptin action
  • Glucocorticoid excess (Cushing syndrome)
  • Precocious puberty
  • Polycystic ovary syndrome (PCOS)
  • Prolactin-secreting tumors

Medications that may cause weight gain in children and adolescents include the following:

  • Cortisol and other glucocorticoids
  • Megace
  • Sulfonylureas
  • Tricyclic antidepressants (TCAs)
  • Monoamine oxidase inhibitors (MAOIs), such as phenelzine
  • Oral contraceptives
  • Insulin (in excessive doses)
  • Thiazolidinediones
  • Risperidone
  • Clozapine

Energy imbalance

During childhood and adolescence, excess fat accumulates when total energy intake exceeds total energy expenditure. This energy imbalance can result from excessive energy intake and/or reduced energy expenditure, the latter is usually a consequence of a sedentary lifestyle. This is particularly associated with excessive television viewing, excessive computer use, and insufficient physical activity. In infancy, excess fat deposition occurs when excess energy is provided, especially when the protein-to-energy ratio is altered. This is often seen when feedings are supplemented with additives such as carbohydrates or fat and protein content remains the same. In addition, one study reported an increased incidence of obesity at age 3 years in infants weaned to solid foods by 4 months.[10]

Ghrelin/leptin hormonal pathway dysfunction

In individuals who are obese, dysfunction in the gut-brain-hypothalamic axis via the ghrelin/leptin hormonal pathway has been suggested to have a role in abnormal appetite control and excess energy intake. See the image below.

Central nervous system (CNS) neurocircuitry for sa Central nervous system (CNS) neurocircuitry for satiety and feeding cycles. AGRP = Agouti-related protein; CB = cannabinoid; CCK = cholecystokinin; CRH = corticotropin-releasing hormone; GLIP = glucagonlike peptide; Mc-3 and 4 = melanocortin-3 and 4; MCH = melanin concentrating hormone; α-MSH = alpha–melanocyte-stimulating hormone; POMC = pro-opiomelanocortin; TNF = tumor necrosis factor.

Studies indicate that dysfunction in this hormonal axis may be the causative factor in as many as 10% of obese subjects, with emphasis particularly on those individuals who appear to manifest familial morbid obesity. In these families, several reports have shown a dramatic, weight loss response to hormone replacement therapy in patients with leptin deficiency. Reductions in energy expenditure characterize other hormonal deficiency states, including hypothyroidism and growth hormone deficiency. Increases in energy intake are observed in genetic syndromes, such as Prader-Willi syndrome, Cushing syndrome, and drug-induced obesity.

Weight gain factors

Despite observations of an etiologic role for genetic and hormonal disorders, these factors alone do not explain the excess weight gain observed in most patients who have obesity and are referred to physicians for evaluation and treatment. Although most overweight children have a familial form of obesity, with 1 or 2 obese parents, excess weight gain in obese children clearly depends on both genetic and environmental factors. Correlations between parent and child habitus likely reflect, at least in part, the familial patterns of food intake, exercise, and selection of leisure activity (including amount of television watching), as well as familial and cultural patterns of food selection. Nevertheless, evidence from twin, adoption, and family studies suggests that genetic factors also play a considerable role in the development of childhood obesity.

Genetics

Concordance rates for obesity and type 2 diabetes mellitus are higher in monozygotic twins than in dizygotic twins, and measures of total body fat (TBF) correlate nearly as strongly in monozygotic twins reared apart as in monozygotic twins reared together. Still, genetic factors cannot explain the increased prevalence of obesity observed among American adolescents over the past generation.

Insulin resistance, dyslipidemia, and hypertension

The accumulation of body fat, particularly in a visceral distribution, reduces the sensitivity to insulin in skeletal muscle, liver tissue, and adipose tissue; this "insulin resistance" predisposes to glucose intolerance and hypertriglyceridemia. Low levels of high-density lipoprotein (HDL), observed both genetically and in association with a sedentary lifestyle, likely contribute to the increase of premature coronary artery disease observed in adults with obesity. Increases in circulating levels of insulin and insulin-like growth factor I may increase blood pressure (BP) and may stimulate the production of androgens from ovarian and adrenocortical cells, with consequent dysmenorrhea and virilization in females. Aromatization of adrenal androgens to estrone leads to gynecomastia in males. The insulin resistance, dyslipidemia, and hypertension predispose to type 2 diabetes and cardiovascular disease, reducing life expectancy.

In a study by D’Adamo et al that evaluated the role of fatty liver in the alteration of insulin sensitivity and β-cell function in obese patients, the investigators concluded that fatty liver, independent of visceral fat and intramyocellular lipid content (ICML), has a central role in insulin resistance in obese adolescents.[11] Patients were divided into 2 groups: 23 obese adolescents with and 20 obese adolescents with low HFF were matched for age, Tanner stage, BMI score, and percentage of body fat, visceral fat, and IMCL. The group with a high hepatic fat fraction (HFF) had lower whole-body insulin sensitivity index and lower estimates of insulin secretion, as well as a significantly lower glucose disposal rate, than the group with low HFF.

While insulin resistance represents an important associated finding in adolescents with steatosis, a recent study reported that in younger children with fatty liver, markers for oxidative stress (eg, oxidized glutathione) were the most significant, independent risk factors.[12]

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Epidemiology

United States statistics

Using body mass index (BMI) criteria, the most recent national surveys demonstrate that 21-24% of American children and adolescents are overweight and that another 16-18% are obese. A 2012 study noted a 16.9% prevalence of obesity in children and adolescents in 2009-2010, which is comparable to the prevalence rates reported in 2007-2008.[13] These findings indicate that the prevalence of overweight (BMI ≥ 85th percentile) children and adolescents in the US has increased by 50-60% in a single generation, and the prevalence of obesity has doubled. The prevalence of obesity in American Indians, Hawaiians, Hispanics, and blacks is 10-40% higher than in whites.

International statistics

International data reporting regarding childhood obesity varies, and accuracy may be less than optimal; however, Eneli and Dele Davies reported that in 77% of the countries analyzed, the prevalence rate for children who were overweight was at least 10%.[14] Notably, the highest rates for children at risk for obesity were found in Malta (25.4%) and the United States (25.1%). Lithuania (5.1%) and Latvia (5.9%) had the lowest rates. A recent European Youth Heart Study suggests Swedish children have a lower risk of becoming overweight or obese in adolescence compared with Estonian children.[15]

Racial, sexual, and age differences in incidence

Race and ethnicity are associated with increased rates of obesity in children and adolescents. Puerto Rican, Cuban American, and Native American preschoolers have an increased incidence of obesity; black, Native American, Puerto Rican, Mexican, and native Hawaiian school-aged children have the highest rates of obesity in this age group. Approximately 25% of black adolescents are obese. Rosen reported that obstructive sleep apnea hypoventilation (OSA/H) is more commonly seen in black children than in Hispanic or white children.[16] Tonsils and adenoids are at their peak size, relative to the size of the oropharynx, when children are aged 2-7 years.

During the second decade of life, females are more likely to be obese than males, except for black teenagers, among whom males are more likely to be obese than females. Although the male sex is associated with an increased incidence of OSA in adults, no differences have been identified in children before puberty.

Adolescent obesity is predictive of adult obesity, with 80% of teenagers who are obese continuing on to be obese as adults. Obesity is more likely to occur during specific periods of life, such as when children are aged 5-7 years and during adolescence. A recent European Youth Heart Study suggests male sex confers a higher risk of obesity in adolescence.[15]

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Prognosis

For many years, complications arising from obesity were considered unusual in childhood. However, a plethora of minor and major problems may arise in children and adolescents with obesity; most of these problems have considerable impact on quality of life, and some may reduce life expectancy.

Childhood and, especially, adolescent obesity is predictive of adult obesity, which is associated with an increased incidence of diabetes, hypertension, gallstones, and hypercholesterolemia.[1] Pulmonary consequences observed in children and adolescents include an increased frequency of reactive airways, poor exercise tolerance, increased work of breathing, and increased oxygen consumption. The few people who develop obesity-hypoventilation syndrome experience right-sided heart failure with right ventricular hypertrophy.

From an analysis of 4 prospective cohort studies, data suggest that overweight or obese adults who were also obese as children are at increased risk of type 2 diabetes, hypertension, dyslipidemia, and carotid-artery atherosclerosis. However, obese children who achieved a normal BMI by adulthood realized similar risks of these outcomes to individuals who were never obese.[17]

The results from one study suggest that dieting and unhealthy weight-control behaviors in adolescence are associated with greater weight and BMI increases into young adulthood.[18]

A study by Parker et al observed that compared with those who maintained a healthy weight, children and adolescents who became obese or maintained obesity had a more than threefold increased risk of incident hypertension.[19, 20]

Acute complications of childhood obesity

Acute complications of childhood obesity include type 2 diabetes, hypertension, hyperlipidemia, accelerated growth and bone maturation, ovarian hyperandrogenism and gynecomastia, cholecystitis, pancreatitis, and pseudotumor cerebri. Fatty liver is common; rarely, patients develop cirrhosis and renal disease (focal glomerulosclerosis). Sleep apnea and sleep-disordered breathing are common in children and adolescents with obesity; in some cases, the apnea is accompanied by neurocognitive dysfunction. Tonsillectomy and adenoidectomy and/or bilevel positive airway pressure/continuous positive airway pressure (BIPAP/CPAP) may be beneficial in patients with reduced oxygenation or carbon dioxide retention.

Orthopedic disorders

Numerous orthopedic disorders, including genu valgum, slipped capital femoral epiphysis, and tibia vara, are observed more commonly in children with obesity. Excess weight in young children can cause bowing of the tibia and femurs; the resulting overgrowth of the proximal tibial metaphysis is called Blount disease.

Liver and gallbladder dysfunction

Evidence of liver dysfunction, with elevated plasma concentrations of transaminases, is observed in 20% of children with obesity; the liver dysfunction most commonly reflects hepatic steatosis, but cirrhosis may develop in rare instances. Vitamin E supplements may be effective in reversing this so-called steatohepatitis, suggesting that the disorder reflects a relative state of vitamin E deficiency.[21] Cholelithiasis is more common in adults with obesity than in adults with normal weight. Although gallstones are unusual in childhood, nearly one half of all cases of cholecystitis in adolescents are associated with obesity. Cholecystitis may be even more common during rapid weight loss, particularly with very controlled–energy diets.

Psychologic complications

Emotional and psychosocial sequelae are widespread. Anecdotal evidence suggests that depression and eating disorders are common in children and adolescents referred to obesity clinics. Prejudice and discrimination against individuals with obesity are ubiquitous within US culture; even young children have been found to regard their peers who have obesity in negative ways. Social isolation, peer problems, and lower self-esteem are frequently observed.

Cardiovascular and endocrine complications

Obesity during childhood and adolescence is associated with numerous cardiovascular risk factors, including hyperinsulinism and insulin resistance, hypercholesterolemia, hypertriglyceridemia, reduced levels of high-density lipoprotein (HDL), and hypertension. A hallmark of insulin resistance is acanthosis nigricans, the presence of which indicates an increased risk of type 2 diabetes. Adolescent girls with obesity also demonstrate a hyperandrogenic profile, consisting of elevated serum concentrations of androstenedione, dehydroepiandrosterone-sulfate (DHEA-S), and testosterone, as well as reduced levels of sex hormone–binding globulin. The clinical picture resembles that of polycystic ovary syndrome (PCOS). The excess androgens are of adrenal and ovarian origin and may be related, at least in part, to increased serum concentrations of insulin and insulin growth factor 1 (IGF-I).

Among sexually mature adolescents, changes in serum lipids and androgens seem to correlate more strongly with body fat distribution than with absolute weight. Thus, adolescents with central obesity (ie, android or abdominal fat pattern) are more likely to manifest these cardiovascular risk factors than individuals with peripheral obesity (ie, gynoid or gluteal pattern). In prepubertal children, however, the cardiovascular risk factors correlate better with body weight than with body fat distribution. The increasing prevalence of obesity in childhood and adolescence, accompanied by insulin resistance, appears to explain the increasing incidence of type 2 diabetes in adolescents, particularly in minority populations.

Studies indicate that obese children with nonalcoholic fatty liver disease may be at increased risk for atherosclerosis.[22]

Long-term complications of childhood obesity

Obesity during childhood and adolescence is associated with an increased risk of obesity during adulthood, with its attendant long-term health risks. This increased risk appears most pronounced for adolescent males with moderate to severe obesity. The long-term implications of obesity during infancy and early childhood on subsequent health are less clear. In general, the proportion of children with obesity who have obesity as adults increases with increased age at onset of obesity, such that 26-41% of preschoolers with obesity have obesity as adults, compared with 42-63% of school-aged children. Additionally, the higher the degree of obesity during childhood, the higher the risk of adult obesity.

Individuals aged 18 years with a body mass index (BMI) at or above the 95th percentile have a 66-78% risk of being overweight at age 35 years. A recently published study reported that at age 18 years, a BMI of 35 or greater was independently associated with an increased risk of lower extremity edema, walking limitation, polycystic ovary syndrome, abnormal kidney function, asthma, obstructive sleep apnea, and type 2 diabetes.[23]

Diabetes

Epidemiologic data, although limited, indicate that adolescent obesity is associated with increased morbidity and mortality in later life. Accordingly, the dramatic increase in the prevalence of type 2 diabetes among adolescents with obesity is likely to be accompanied by a host of diabetic-related complications in adulthood and a reduction in life span. Although obesity, per se, is associated with a heightened risk of morbidity related to abnormalities in glucose homeostasis, recent data indicate that the rate of increase in BMI during adolescence may also represent a significant risk factor for diabetes.[24]

Cardiovascular disease

An increased risk of death from all causes and from coronary artery disease (CAD) has been consistently observed in males, but not in females, who had obesity during adolescence. In a follow-up of the Harvard Growth Study, the risk of morbidity from CAD and atherosclerosis was increased among men and women who had been overweight (BMI > 75th percentile) as teenagers. The trend towards higher BMI values among adolescents in the US has also been associated with increases in left ventricular mass, when compared to similar cohorts in earlier generations, further suggesting that early obesity increases the long-term risk for development of cardiac disease.[25]

Mangner et al conducted a study to assess geometric and functional changes of the heart in obese compared with nonobese children and adolescents. The authors found thicker left ventricular (LV) walls and an increased LV mass, as well as impaired measures of systolic function, among the obese children when compared with nonobese children. The authors also reported no difference in ejection fractions between the obese and nonobese children, but the average LV strain, strain rate, and displacement, which are markers of LV longitudinal function assessed by 2D speckle-tracking echocardiography (2D-STE), were significantly impaired among the obese children. The results of this study demonstrate that childhood obesity is associated with significant changes in myocardial geometry and function, indicating an early onset of potentially unfavorable alterations in the myocardium.[26, 27]

Gout and colorectal cancer

Gout and colorectal cancer increased among men who had obesity as adolescents, and arthritis increased among women who had obesity as adolescents. Many of these adverse health outcomes appear to be independent of adult weight, suggesting a direct effect of adolescent obesity on adult health and mortality.

Psychosocial dysfunction

Psychosocial dysfunction in individuals who have obesity in childhood and adolescence is a serious concern. Among teens and young adults who were tracked after 7 years, overweight females were found to have completed less schooling, were less likely to have married, and had higher rates of household poverty compared with their non-overweight peers. For overweight males, the only adverse outcome was a decreased likelihood of being married.

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Contributor Information and Disclosures
Author

Steven M Schwarz, MD, FAAP, FACN, AGAF Professor of Pediatrics, Children's Hospital at Downstate, State University of New York Downstate Medical Center

Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American Association for Physician Leadership, New York Academy of Medicine, Gastroenterology Research Group, American Gastroenterological Association, American Pediatric Society, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Jatinder Bhatia, MBBS, FAAP Professor of Pediatrics, Medical College of Georgia, Georgia Regents University; Chief, Division of Neonatology, Director, Fellowship Program in Neonatal-Perinatal Medicine, Director, Transport/ECMO/Nutrition, Vice Chair, Clinical Research, Department of Pediatrics, Children's Hospital of Georgia

Jatinder Bhatia, MBBS, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, American Society for Nutrition, American Society for Parenteral and Enteral Nutrition, Academy of Nutrition and Dietetics, Society for Pediatric Research, Southern Society for Pediatric Research

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Gerber.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Michael Freemark, MD, to the development and writing of the source article.

References
  1. Ogden CL, Yanovski SZ, Carroll MD, Flegal KM. The epidemiology of obesity. Gastroenterology. May 2007. 132:2087-2102. [Medline]. [Full Text].

  2. Fiore H, Travis S, Whalen A, Auinger P, Ryan S. Potentially protective factors associated with healthful body mass index in adolescents with obese and nonobese parents: a secondary data analysis of the third national health and nutrition examination survey, 1988-1994. J Am Diet Assoc. 2006 Jan. 106(1):55-64; quiz 76-9. [Medline].

  3. Flegal KM, Ogden CL, Wei R, et al. Prevalence of overweight in US children: comparison of US growth charts from the Centers for Disease Control and Prevention with other reference values for body mass index. Am J Clin Nutr. 2001 Jun. 73(6):1086-93. [Medline].

  4. McGavock JM, Torrance BD, McGuire KA, Wozny PD, Lewanczuk RZ. Cardiorespiratory fitness and the risk of overweight in youth: the Healthy Hearts Longitudinal Study of Cardiometabolic Health. Obesity (Silver Spring). 2009 Sep. 17(9):1802-7. [Medline].

  5. Shomaker LB, Tanofsky-Kraff M, Zocca JM, Field SE, Drinkard B, Yanovski JA. Depressive symptoms and cardiorespiratory fitness in obese adolescents. J Adolesc Health. 2012 Jan. 50(1):87-92. [Medline]. [Full Text].

  6. Carter PJ, Taylor BJ, Williams SM, Taylor RW. Longitudinal analysis of sleep in relation to BMI and body fat in children: the FLAME study. BMJ. 2011 May 26. 342:d2712. [Medline]. [Full Text].

  7. Archbold KH, Vasquez MM, Goodwin JL, Quan SF. Effects of Sleep Patterns and Obesity on Increases in Blood Pressure in a 5-Year Period: Report from the Tucson Children's Assessment of Sleep Apnea Study. J Pediatr. 2012 Jan 25. [Medline]. [Full Text].

  8. Mosli RH, Kaciroti N, Corwyn RF, Bradley RH, Lumeng JC. Effect of Sibling Birth on BMI Trajectory in the First 6 Years of Life. Pediatrics. 2016 Mar 11. [Medline].

  9. Garcia J. Birth of a Sibling May Decrease Obesity Ris. Medscape Medical News. Available at http://www.medscape.com/viewarticle/860298. March 14, 2016; Accessed: March 30, 2016.

  10. Huh S, Rifas-Shiman S, Taveras E, Oken E, Gillman M. Timing of solid food introduction and risk of obesity in preschool-aged children. Pediatrics. 2011 Mar. 127(3):e544-51. [Medline]. [Full Text].

  11. D'Adamo E, Cali AM, Weiss R, Santoro N, Pierpont B, Northrup V. Central role of fatty liver in the pathogenesis of insulin resistance in obese adolescents. Diabetes Care. 2010 Aug. 33(8):1817-22. [Medline].

  12. Ruiz-Extremera A, Carazo A, Salmerón A, et al. Factors associated with hepatic steatosis in obese children and adolescents. J Pediatr Gastroenterol Nutr. 2011 Aug. 53(2):196-201. [Medline].

  13. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity and trends in body mass index among US children and adolescents, 1999-2010. JAMA. 2012 Feb 1. 307(5):483-90. [Medline].

  14. Eneli I, Dele Davis H. Epidemiology of childhood obesity. Dele Davis H, ed. Obesity in Childhood & Adolescence. Westport, Conn: Praeger Perspectives; 2008. Vol 1.: 3-19.

  15. Ortega FB, Labayen I, Ruiz JR, et al. Improvements in fitness reduce the risk of becoming overweight across puberty. Med Sci Sports Exerc. 2011 Oct. 43(10):1891-7. [Medline].

  16. Rosen CL. Clinical features of obstructive sleep apnea hypoventilation syndrome in otherwise healthy children. Pediatr Pulmonol. 1999 Jun. 27(6):403-9. [Medline].

  17. Juonala M, Magnussen CG, Berenson GS, et al. Childhood adiposity, adult adiposity, and cardiovascular risk factors. N Engl J Med. 2011 Nov 17. 365(20):1876-85. [Medline].

  18. Neumark-Sztainer D, Wall M, Story M, Standish AR. Dieting and unhealthy weight control behaviors during adolescence: associations with 10-year changes in body mass index. J Adolesc Health. 2012 Jan. 50(1):80-6. [Medline]. [Full Text].

  19. Parker ED, Sinaiko AR, Kharbanda EO, Margolis KL, Daley MF, Trower NK, et al. Change in Weight Status and Development of Hypertension. Pediatrics. 2016 Mar. 137 (3):1-9. [Medline].

  20. Brown T. Obesity, High BMI Raise Hypertension Risk in Kids, Teenagers. Medscape Medical News. Available at http://www.medscape.com/viewarticle/859416. February 25, 2016; Accessed: March 30, 2016.

  21. Di Sario A, Candelaresi C, Omenetti A, Benedetti A. Vitamin E in chronic liver diseases and liver fibrosis. Vitam Horm. 2007. 76:551-73. [Medline].

  22. Akin L, Kurtoglu S, Yikilmaz A, Kendirci M, Elmali F, Mazicioglu M. Fatty liver is a good indicator of subclinical atherosclerosis risk in obese children and adolescents regardless of liver enzyme elevation. Acta Paediatr. 2012 Nov 28. [Medline].

  23. Inge TH, King WC, Jenkins TM, et al. The effect of obesity in adolescence on adult health status. Pediatrics. 2013 Dec. 132(6):1098-104. [Medline].

  24. Tirosh A, Shai I, Afek A, Dubnov-Raz G, et al. Adolescent BMI trajectory and risk of diabetes versus coronary disease. N Engl J Med. 2011 Apr 7. 364(14):1315-25. [Medline].

  25. Crowley D, Khoury P, Urbina E, Ippisch H, Kimball T. Cardiovascular Impact of the Pediatric Obesity Epidemic: Higher Left Ventricular Mass is Related to Higher Body Mass Index. J Pediatr. 2011 May. 158(5):709-714.e1. [Medline].

  26. Mangner N, Scheuermann K, Winzer E, Wagner I, Hoellriegel R, Sandri M, et al. Childhood obesity: impact on cardiac geometry and function. JACC Cardiovasc Imaging. 2014 Dec. 7(12):1198-205. [Medline].

  27. O'Riordan M. Obesity in Kids Affects Heart Shape, Functional Impairments. Medscape Medical News. Available at http://www.medscape.com/viewarticle/832982. Accessed: December 17, 2014.

  28. Maffeis C, Pinelli L, Brambilla P, Banzato C, Valzolgher L, Ulmi D, et al. Fasting plasma glucose (FPG) and the risk of impaired glucose tolerance in obese children and adolescents. Obesity (Silver Spring). 2010 Jul. 18(7):1437-42. [Medline].

  29. Kalarchian MA, Levine MD, Arslanian SA, et al. Family-based treatment of severe pediatric obesity: randomized, controlled trial. Pediatrics. 2009 Oct. 124(4):1060-8. [Medline].

  30. Wildes JE, Marcus MD, Kalarchian MA, et al. Self-reported binge eating in severe pediatric obesity: impact on weight change in a randomized controlled trial of family-based treatment. Int J Obes (Lond). 2010 Jul. 34(7):1143-8. [Medline]. [Full Text].

  31. DeBar LL, Stevens VJ, Perrin N, Wu P, Pearson J, Yarborough BJ, et al. A primary care-based, multicomponent lifestyle intervention for overweight adolescent females. Pediatrics. 2012 Mar. 129(3):e611-20. [Medline]. [Full Text].

  32. Oude Luttikhuis H, Baur L, Jansen H, et al. Interventions for treating obesity in children. Cochrane Database Syst Rev. 2009 Jan 21. CD001872. [Medline].

  33. Pavey TG, Taylor AH, Fox KR, et al. Effect of exercise referral schemes in primary care on physical activity and improving health outcomes: systematic review and meta-analysis. BMJ. 2011 Nov 4. 343:d6462. [Medline]. [Full Text].

  34. Guideline: Sugars Intake for Adults and Children. Geneva: World Health Oganization, 2015. Available at http://www.ncbi.nlm.nih.gov/books/NBK285537/.

  35. Jolly K, Lewis A, Beach J, Denley J, Adab P, Deeks JJ, et al. Comparison of range of commercial or primary care led weight reduction programmes with minimal intervention control for weight loss in obesity: Lighten Up randomised controlled trial. BMJ. 2011 Nov 3. 343:d6500. [Medline]. [Full Text].

  36. Hooper L, Abdelhamid A, Moore HJ, Douthwaite W, Skeaff CM, Summerbell CD. Effect of reducing total fat intake on body weight: systematic review and meta-analysis of randomised controlled trials and cohort studies. BMJ. 2012 Dec 6. 345:e7666. [Medline].

  37. Duckworth LC, Gately PJ, Radley D, Cooke CB, King RF, Hill AJ. RCT of a high-protein diet on hunger motivation and weight-loss in obese children: an extension and replication. Obesity (Silver Spring). 2009 Sep. 17(9):1808-10. [Medline].

  38. O'Brien PE, Sawyer SM, Laurie C, et al. Laparoscopic adjustable gastric banding in severely obese adolescents: a randomized trial. JAMA. 2010 Feb 10. 303(6):519-26. [Medline].

  39. Tucker ME. New Guidelines Address Bariatric Surgery in Children. Medscape Medical News. Available at http://www.medscape.com/viewarticle/838351. Accessed: February 27, 2015.

  40. Nobili V, Vajro P, Dezsofi A, Fischler B, Hadzic N, Jahnel J, et al. Indications and Limitations of Bariatric Intervention in Severely Obese Children and Adolescents With and Without Non-alcoholic Steatohepatitis: the ESPGHAN Hepatology Committee Position Statement. J Pediatr Gastroenterol Nutr. 2015 Feb 2. [Medline].

  41. [Guideline] August GP, Caprio S, Fennoy I, et al. Prevention and treatment of pediatric obesity: an endocrine society clinical practice guideline based on expert opinion. J Clin Endocrinol Metab. 2008 Dec. 93(12):4576-99. [Medline].

  42. [Guideline] Goldstein LB, Bushnell CD, Adams RJ, Appel LJ, Braun LT, Chaturvedi S, et al. Guidelines for the Primary Prevention of Stroke. A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2010 Dec 6. [Medline].

  43. Harris KC, Kuramoto LK, Schulzer M, Retallack JE. Effect of school-based physical activity interventions on body mass index in children: a meta-analysis. CMAJ. 2009 Mar 31. 180(7):719-26. [Medline].

  44. Marcus C, Nyberg G, Nordenfelt A, Karpmyr M, Kowalski J, Ekelund U. A 4-year, cluster-randomized, controlled childhood obesity prevention study: STOPP. Int J Obes (Lond). 2009 Apr. 33(4):408-17. [Medline].

  45. Muckelbauer R, Libuda L, Clausen K, Toschke AM, Reinehr T, Kersting M. Promotion and provision of drinking water in schools for overweight prevention: randomized, controlled cluster trial. Pediatrics. 2009 Apr. 123(4):e661-7. [Medline].

  46. Singh AS, Chin A Paw MJ, Brug J, van Mechelen W. Dutch obesity intervention in teenagers: effectiveness of a school-based program on body composition and behavior. Arch Pediatr Adolesc Med. 2009 Apr. 163(4):309-17. [Medline].

  47. Coffield JE, Metos JM, Utz RL, Waitzman NJ. A multivariate analysis of federally mandated school wellness policies on adolescent obesity. J Adolesc Health. 2011 Oct. 49(4):363-70. [Medline].

  48. Waters E, de Silva-Sanigorski A, Hall BJ, et al. Interventions for preventing obesity in children. Cochrane Database Syst Rev. 2011 Dec 7. 12:CD001871. [Medline].

  49. Daniels SR, Long B, Crow S, et al. Cardiovascular effects of sibutramine in the treatment of obese adolescents: results of a randomized, double-blind, placebo-controlled study. Pediatrics. 2007 Jul. 120(1):e147-57. [Medline].

  50. Berkowitz R, Fujioka K, Daniels S, et al. Effects of sibutramine treatment in obese adolescents. A randomized trial. Ann Intern Med. July 2006. 145:81-90. [Medline].

  51. Abbott Laboratories agrees to withdraw its obesity drug Meridia. FDA, U.S. Food and Drug Administration. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm228812.htm. Accessed: October 8, 2010.

  52. Dunican KC, Desilets AR, Montalbano JK. Pharmacotherapeutic options for overweight adolescents. Ann Pharmacother. 2007 Sep. 41(9):1445-55. [Medline].

  53. Bray GA, Ryan DH. Drug treatment of the overweight patient. Gastroenterology. May 2007. 132:2239-2252. [Medline].

  54. Badman MK, Flier JS. The adipocyte as an active participant in ebergy balance and metabolism. Gastroenterology. May 2007. 132:2103-2115. [Medline].

  55. Elder KA, Wolfe BM. Bariatric surgery: A review of procedures and outcomes. Gastroenterology. May 2007. 132:2253-2271. [Medline].

 
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Central nervous system (CNS) neurocircuitry for satiety and feeding cycles. AGRP = Agouti-related protein; CB = cannabinoid; CCK = cholecystokinin; CRH = corticotropin-releasing hormone; GLIP = glucagonlike peptide; Mc-3 and 4 = melanocortin-3 and 4; MCH = melanin concentrating hormone; α-MSH = alpha–melanocyte-stimulating hormone; POMC = pro-opiomelanocortin; TNF = tumor necrosis factor.
 
 
 
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