AUTHOR INFORMATION

Section 1 of 10

Authored by Michael Freemark, MD, Professor of Pediatrics, Duke University; Chief, Division of Pediatric Endocrinology, Department of Pediatrics, Duke University Medical Center

Michael Freemark, MD, is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Federation for Medical Research, Endocrine Society, Juvenile Diabetes Foundation International, Lawson-Wilkins Pediatric Endocrine Society, North Carolina Medical Society, and Society for Pediatric Research

Edited by Steven M Schwarz, MD, FAAP, FACN, Chair, Department of Pediatrics, Long Island College Hospital; Professor of Pediatrics, State University of New York, Downstate Medical Center College of Medicine; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Jatinder Bhatia, MD, Professor of Pediatrics, Chief, Section of Neonatology, Vice Chairman for Clinical Research, Department of Pediatrics, Medical College of Georgia; Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences; and Jatinder Bhatia, MD, Professor of Pediatrics, Chief, Section of Neonatology, Vice Chairman for Clinical Research, Department of Pediatrics, Medical College of Georgia

Author's Email:	Michael Freemark, MD
Editor's Email:	Steven M Schwarz, MD, FAAP, FACN

eMedicine Journal, April 25 2006, VOLUME 7, Number 4

INTRODUCTION

Section 2 of 10

Background: Obesity is the most prevalent nutritional disorder among children and adolescents in the United States. Childhood obesity predisposes to insulin resistance and type 2 diabetes, hypertension, hyperlipidemia, liver and renal disease, and reproductive dysfunction and increases the risks of adult obesity and cardiovascular disease.

Operational definitions of obesity in adults are derived from statistical data analyzing the association between body mass and risks 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. Given that weight varies in a continuous rather than a stepwise fashion, the use of these arbitrary criteria is problematic and may be misleading.

The body mass index (BMI) is a continuous, though imperfect, measure of body fatness. Calculated as weight (kg) divided by height (m²), BMI corrects for body size and can be quantified readily and reliably in clinical settings. The BMI correlates closely with total body fat (TBF, estimated by dual-energy x-ray absorptiometry (DEXA) scan 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 have been generated using data from the National Health and Nutrition Examination Surveys of 1988-1994. Recently, 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 surveys or is more than 30 kg/m² at any age.

Pathophysiology: 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 for body metabolism, thermoregulation, and physical activity. Increases in energy intake are observed in genetic syndromes, such as Prader-Willi syndrome, Cushing syndrome, drug-induced obesity, and certain mutations in genes that control appetite. Reductions in energy expenditure characterize hormonal deficiency states, including hypothyroidism and growth hormone deficiency.

Genetic and hormonal disorders, however, do not explain the excess weight gain observed in most patients who have obesity and are referred to physicians for evaluation and treatment. Most overweight children have a familial form of obesity that results from environmental as well as genetic factors. Correlations between parent and child habitus likely reflect, at least in part, the family patterns of food intake, exercise, selection of leisure activity (including amounts of TV watching), and family 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.

Concordance rates for obesity and type 2 diabetes mellitus are higher in monozygotic twins than in dizygotic twins, and measures of TBF correlate nearly as strongly in monozygotic twins reared apart (r = 0.61) as in monozygotic twins reared together (r = 0.75). Still, genetic factors cannot explain the increased prevalence of obesity observed among American adolescents during the past generation.

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) likely contribute to the increase of premature coronary artery disease observed in adults with obesity. Increases in circulating levels of insulin and insulinlike growth factor I may increase BP and 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.

Frequency:

• In the US: Using BMI criteria, the most recent national surveys demonstrate that 21-24% of American children and adolescents are overweight and that nearly 15% are obese. These findings indicate that the prevalence of overweight (BMI = ³85th percentile) children and adolescents in the United States has increased by 50-60% in a single generation, while the prevalence of obesity has doubled. The prevalence of obesity in American Indians, Hawaiians, Hispanics, and blacks is 10-40% higher than that in whites.

Mortality/Morbidity: 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.

• Acute complications
  
  
  • 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; rare 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.
    
    
  • A number of 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.
    
    
  • 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. One recent study indicates that vitamin E supplements may be effective in reversing this so-called steatohepatitis, suggesting that the disorder reflects a relative state of vitamin E deficiency. 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.
    
    
  • 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 frequently are observed.
    
    
  • Obesity during childhood and adolescence is associated with a number of cardiovascular risk factors, including hyperinsulinism and insulin resistance, hypercholesterolemia, hypertriglyceridemia, reduced levels of 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.

Race: See Frequency.

Sex: See Mortality/Morbidity.

CLINICAL

Section 3 of 10

History:

• Short stature or a reduced rate of linear growth in a child with obesity suggests the possibility of growth hormone deficiency, hypothyroidism, cortisol excess, pseudohypoparathyroidism, or a genetic syndrome such as Prader-Willi syndrome.



• A history of dry skin, constipation, intolerance to cold, or fatigability suggests hypothyroidism.



• Polyuria and polydipsia may be noted if the adolescent with obesity develops overt diabetes.



• A history of damage to the CNS (eg, infection, trauma, hemorrhage, radiation therapy, seizures) suggests hypothalamic obesity with or without pituitary growth hormone deficiency or pituitary hypothyroidism. A history of morning headaches, vomiting, visual disturbances, and excessive urination or drinking also suggests that the obesity may be caused by a tumor or mass in the hypothalamus.

Physical:

• Two particularly useful clinical measures are the rate of linear growth and the timing of puberty. Most patients who have familial or diet-induced obesity grow at a normal or excessive rate and enter puberty at the appropriate age; many mature more quickly than children with normal weight, and bone age commonly is advanced. In contrast, growth rate and pubertal development are diminished or delayed in growth hormone deficiency, hypothyroidism, cortisol excess, and a variety of genetic syndromes. Conversely, growth rate and pubertal development are accelerated in precocious puberty and in some girls with PCOS.



• Clinical clues that suggest a hormonal etiology for childhood obesity include the following:


• • Weight gain out of character for the family
  
  
  
  • Obesity in a short child
  
  
  
  • Progressive weight gain without a comparable increase in linear growth
  
  
  
  • Dry skin, constipation, intolerance to cold, and fatigability
  
  
  
  • History of CNS damage (eg, trauma, hemorrhage, infection, radiation, seizures)
  
  
  
  • Accumulation of fat in the neck and trunk but not in the arms or legs
  
  
  
  • Purple striae (stretch marks)
  
  
  
  • Hypertension
  
  
  
  • Inappropriate sexual development at an early age
  
  
  
  • Excess facial hair, acne, and/or irregular menses in a teenage girl
  
  
  
  • Headaches, vomiting, visual disturbances, or excessive urination and drinking
  
  
  
  • Treatment with certain drugs or medications
  
  
  
• Selective accumulation of fat in the neck, trunk, and purple striae suggest an excess of cortisol, particularly if the rate of linear growth has declined.



• The appearance of signs of sexual development at an early age suggests that the weight gain is caused by precocious puberty. On the other hand, excessive facial hair, acne, and irregular periods in a teenage girl suggest that the weight gain may be caused by cortisol excess or PCOS. Obesity itself may be accompanied by facial hair, irregular menses, and hypertension.

Causes:

• 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
  
  
  
  • 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

  • Monoamine oxidase inhibitors (MAOIs), such as phenelzine

  • Oral contraceptives

  • Insulin (in excessive doses)

  • Thiazolidinediones

  • Risperidone

  • Clozapine
  
  
  

WORKUP

Section 4 of 10

Lab Studies:

• Fasting and 2-hour postglucola glucose and insulin levels and hemoglobin A1c (for evaluation of insulin resistance and glucose tolerance)



• Fasting lipid panel for detection of dyslipidemia



• Thyroid function tests



• Serum leptin



• Adrenal function tests, when indicated, to assess the possibility of Cushing syndrome



• Karyotype (with fluorescence in situ hybridization [FISH] for Prader-Willi [15q-]), when indicated by clinical history and physical examination



• Growth hormone (GH) secretion and function tests, when indicated



• Assessment of reproductive hormones (including prolactin), when indicated



• Serum calcium, phosphorus, and parathyroid hormone levels to evaluate for suspected pseudohypoparathyroidism

Imaging Studies:

• MRI scan of the brain with focus on the hypothalamus and pituitary, when clinically indicated

Procedures:

• Sleep studies to detect sleep apnea

TREATMENT

Section 5 of 10

Medical Care: Theoretically, any therapeutic interventions in the child with obesity must achieve control of weight gain and reduction in BMI safely and effectively and should prevent the long-term complications of obesity in childhood and adulthood. First, manage any acute or chronic complications of obesity and request psychiatric assistance for unusual eating disorders or severe depression. Devise a care plan that emphasizes long-term diet and exercise, family support, and the avoidance of dramatic swings in body weight. A team approach to therapy, involving the efforts of nurse educators, nutritionists, exercise physiologists, and counselors, is likely to prove most effective. Avoid a punitive approach and reward positive behaviors.

Any intervention is likely to fail if it does not involve the active participation and support of family members. The child at hand may be only one of many family members who have obesity, and successful treatment often requires a change in the entire family's approach to eating. In selected cases, family therapy may be highly beneficial.

Recognize that a loss of 5-20% of total body weight can reduce many of the health risks associated with obesity in adults; however, whether modest weight loss or moderate reductions in BMI can improve outcomes in pediatric patients or reduce the long-term risks of obesity in adulthood is not known. Because dramatic reductions in BMI are difficult to achieve and sustain in children and adolescents as well as adults, initiating counseling and therapy may be prudent with realistic goals that emphasize gradual reductions in body fat and BMI and maintenance of weight loss rather than a rapid return to ideal body weight. Reductions in body weight are accompanied by equivalent reductions in energy expenditure. Consequently, maintenance of a given weight in a patient with obesity necessitates a lower energy intake than maintenance of an equivalent weight in a patient who has never been obese.

Smoking prevention. Smoking of tobacco reduces appetite and is used by many adults and some teenagers to prevent or limit weight gain. The deleterious consequences of smoking clearly outweigh the benefits achieved by weight control, and all children and adolescents should be urged never to smoke. Measures to prevent excessive weight gain should be undertaken in obese adolescents who discontinue smoking.

• General measures


• • Exercise and physical activity: Physicians and parents should encourage children to participate in vigorous physical activity throughout adolescence and young adulthood and to limit time spent watching television and videos and playing computer games. Even regular walking for 20-30 minutes per day can facilitate weight control. Exercise reduces weight accretion through increases in energy expenditure and has favorable effects on cardiovascular status, decreases body fat and total cholesterol levels, increases lean body mass and HDL levels, and improves psychological well-being. Controlled trials have demonstrated that lifestyle exercise programs, in association with dietary restrictions, provide long-term weight control in children and adolescents.
  
  
  
  • Nutritional counseling and reduced fat diet
    • An energy-restricted balanced diet, in association with patient and parent education, behavioral modification, and exercise can limit weight gain in many pediatric patients who have mild or moderate obesity. Programs that modify family patterns of eating are most likely to be successful. Reductions in total and saturated fat may be particularly useful in adolescents who consume large quantities of high fat, snack, and packaged fast foods, including French fries, pizza, chips, and crackers.

    • The average diet for children and adolescents in the United States contains approximately 35% fat. Reducing fat intake to 30% of total energy, as recommended by the World Health Organization (WHO); however, little evidence exists, epidemiological or experimental, that supports the idea that a reduced fat but otherwise unlimited diet suffices for substantial weight reduction in obese individuals. A reduced fat diet may be more useful for primary or secondary prevention of weight gain in individuals with previous obesity individuals, particularly in those with a familial susceptibility.
  
  
  
• Intensive intervention


• • Mental health counseling and support: Anecdotal evidence suggests that children with severe obesity may develop major psychiatric disorders (eg, suicide attempts, manic depression, other depressive disorders) that require hospitalization or long-term medication. Whether most of these psychiatric disorders predate, cause, or result from the obesity or its treatment is unclear. Like adults, children who enter obesity treatment programs may be at particularly high risk for the development of psychopathology.

  • Treatment of the psychiatric conditions may complicate or exacerbate problems associated with weight control because a number of antidepressant medications, particularly tricyclics, stimulate appetite and weight gain. Offer patients who have obesity psychological support and refer these patients for psychiatric evaluation and care if evidence of psychopathology or dysfunction is present. As noted previously, any therapeutic intervention in the child or adolescent with obesity is unlikely to succeed without the understanding, approval, and active participation of family members. Family therapy is effective in patients resistant to other therapeutic interventions, particularly those with parents who have obesity.
  
  
  
• Very controlled–energy diets
  • A protein-sparing modified fast can achieve rapid weight loss in an inpatient or outpatient setting and has been used successfully by a number of investigators in children and adolescents with obesity. For example, a yearlong study of 73 pediatric patients aged 7-17 years showed significant reductions in the percent overweight, TBF, BMI, total and low-density lipoprotein cholesterol, triglycerides, and fasting serum insulin with no change in fat-free mass. Unfortunately, this study and many others combined the diet with behavior modification and a vigorous exercise program, making it impossible to assess the effects of the diet itself.

  • In general, very controlled–energy diets are hampered by high dropout rates and, in adults, have been associated with losses in lean weight, gallstone formation, cardiac arrhythmias, and sudden death. Moreover, some studies suggest that regain of weight after severe dieting may lead to overshoot, with excess weight deposited as a higher percentage of body fat. Concerns have been raised regarding the long-term cardiovascular risks of such weight cycling in adults, but the potential hazards of dramatic or cyclical weight changes in children and adolescents are unknown.

  • More important, the long-term effects of very controlled–energy diets on adolescent growth and development and subsequent reproductive function, musculoskeletal development, and intermediary metabolism remain poorly understood. Given these uncertainties and the difficulties inherent in maintaining severe caloric restriction, the very controlled–energy diets cannot be recommended for the great majority of children and adolescents with obesity.

Surgical Care: A variety of bariatric surgical procedures have been used in adults and some adolescents with BMI exceeding 40 or weight exceeding 100% of ideal body weight (IBW). The most common procedures involve gastric restriction. In the vertical-banded gastroplasty, a pouch of 15- to 30-mL capacity is constructed, greatly reducing the amount of food that can be eaten at any time. In the gastric bypass, a larger pouch that empties into the jejunum is created. As a result, nutrients bypass the duodenum and most of the stomach, which often creates a dumping syndrome. Overall effectiveness is good with significant weight loss, reduction in obesity complications, and increased life expectancy; however, mortality rate of the procedure is 1% in adults, and complications include encephalopathy, nephrolithiasis, cholelithiasis, protein-losing enteropathy, and other nutritional deficiencies. Consider these procedures only in the most severe cases of late-adolescent obesity that are resistant to all other forms of therapy.

Consultations:

• Nutrition



• Exercise physiology



• Psychiatry



• Pulmonary (sleep) medicine



• Orthopedics



• Gastroenterology

Diet: See Treatment.

Activity: See Treatment.

MEDICATION

Section 6 of 10

The use of anorectic drugs for the treatment of obesity has a checkered history. In general, anorectic agents have little or no effect on weight gain in the absence of a controlled diet and exercise program. The drugs have modest effects on total body weight, with long-term weight losses amounting to 2-10 kg in adults with obesity, and the responses of individuals to drug therapy vary considerably. Most of the weight loss resulting from drug therapy is achieved within the first 6 months of treatment, with subsequent maintenance of the reduced weight or slight regain of weight. Unfortunately, discontinuation of the drug therapy is accompanied by rebound weight gain and loss of the selective advantage over placebo.

Of more concern, the drugs may have potentially serious adverse effects, particularly in patients with psychiatric disorders. For example, adrenergic agents (eg, phentermine, sibutramine) may cause dry mouth, insomnia, nervousness, diaphoresis, hypertension, nausea, and constipation. Tolerance to most adverse effects is achieved within 2 weeks of continuous treatment. Contraindications to the use of noradrenergic agents include angina and other forms of atherosclerotic disease, cardiac arrhythmias, hyperthyroidism, and/or the concomitant use of MAOIs. Several adrenergic drugs have either been withdrawn from the market in the United States (eg, phenylpropanolamine, mazindol) or are banned by the FDA (eg, ephedrine alkaloids [ephedra, Ma Huang]) due to adverse events including hypertension, myocardial infarction, stroke, and death.

The serotoninergic preparations, fenfluramine and dexfenfluramine, recently were withdrawn from the commercial market because of their association with valvular heart disease and primary pulmonary hypertension. These drugs also were associated with drowsiness, insomnia, tremor, and short-term memory loss. High doses of fenfluramine and dexfenfluramine are neurotoxic in rats and monkeys, raising concerns about the long-term use of other serotoninergic preparations, such as fluoxetine, in children.

Essentially, no information exists regarding the use of anorectic agents in children. In general, do not use anorectic drugs routinely for the prevention or treatment of obesity in childhood or adolescence. Indeed, do not administer anorectic drugs to prepubertal children until carefully controlled clinical studies are performed to assess their safety and efficacy. Administer anorectic drugs only after the patient has failed to respond to vigorous attempts to modify behavior, diet, and family interactions. Unless prohibited by a specific investigational protocol, all adolescents who are administered anorectic agents should receive concurrent nutritional and family counseling and should implement a plan of regular exercise and physical activity.

FOLLOW-UP

Section 7 of 10

Further Outpatient Care:

• Regular follow-up is indicated for the following reasons:


• • Reinforcement of nutritional goals and exercise objectives
  
  
  
  • Identification of social and emotional barriers to therapy
  
  
  
  • Family support and counseling (if indicated)
  
  
  
  • Assessment of growth, pubertal development, and reproductive function
  
  
  
  • Assessment of glucose tolerance and fasting lipid levels
  
  
  
  • Identification and management of obesity-related acute and chronic complications
  
  
  

In/Out Patient Meds:

• See Treatment.

Deterrence/Prevention:

• Clearly, the long-term management of moderate or morbid obesity in adulthood is highly problematic and rarely successful. Preventing the development of obesity in childhood and adolescence is more likely to reduce long-term complications than treatment of obesity in adults. Thus, further studies are needed to (1) identify young children who are predisposed to adolescent and adult obesity, (2) identify interventions that prevent the development of obesity in children at risk, (3) assess the long-term risks of obesity in prepubertal children, and (4) identify measures that prevent further weight gain in children and adolescents with obesity.

Complications:

• Complications are variable, depending on the severity of the disorder and the effectiveness of therapy. See Mortality/Morbidity.

Prognosis:

• See Mortality/Morbidity

Patient Education:

• See Treatment.



• For excellent patient education resources, visit eMedicine's Diabetes Center, Cholesterol Center, and Eating Disorders Center. Also, see eMedicine's patient education articles, Diabetes, Cholesterol and Children, Obesity, Obesity in Children, Weight Loss and Control, and Gallstones.

MISCELLANEOUS

Section 8 of 10

Medical/Legal Pitfalls:

• Failure to identify a genetic or hormonal disorder in a child with obesity



• Overaggressive or inappropriate use of anorectic medications

TEST QUESTIONS

Section 9 of 10

CME Question 1: What is the single best way to differentiate childhood Cushing syndrome from diet-induced obesity?

A: Bone age
B: Buffalo hump
C: Striae
D: Growth velocity
E: Blood pressure

The correct answer is D: Glucocorticoid excess causes growth failure in nearly all cases of childhood Cushing syndrome, whereas most children with diet-induced obesity grow at a normal or accelerated rate.

CME Question 2: Which of the following is the best predictor of childhood obesity?

A: The weights of the parents
B: Size of the child at birth
C: The child's food intake
D: Frequency of exercise
E: Type of food eaten

The correct answer is A: The best predictor of childhood obesity is parental obesity. Correlations between parent and child habitus likely reflect, at least in part, the family patterns of food intake, exercise, selection of leisure activity (including amounts of TV watching), and family 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.

Pearl Question 1 (T/F): Rapid weight gain at age 5 years is of little consequence; children outgrow the problem when they enter puberty.

The correct answer is False: Rapid weight gain during the period of adiposity rebound is a marker for obesity in adolescence and adulthood. Dietary intervention is prudent, even at this age.

Pearl Question 2 (T/F): The most reliable sign of insulin resistance in a child with obesity is acanthosis nigricans.

The correct answer is True: A hallmark of insulin resistance is acanthosis nigricans, the presence of which indicates an increased risk of type 2 diabetes.

Pearl Question 3 (T/F): Premature adrenarche in the prepubertal child may predispose to polycystic ovary syndrome (PCOS) in adolescence and adult life.

The correct answer is True: Recent studies reveal that premature adrenarche in girls may predispose them to PCOS and glucose intolerance later in life.

Pearl Question 4 (T/F): Breast enlargement in the overweight adolescent boy represents the natural accumulation of fatty tissue.

The correct answer is False: In males with obesity, true gynecomastia occurs as the consequence of increased serum estrone levels. Estrone is derived from the aromatization of adrenal androgens by adipose tissue.

BIBLIOGRAPHY

Section 10 of 10

• Artz E, Haqq A, Freemark M: Hormonal and metabolic consequences of childhood obesity. Endocrinology and Metabolism Clinics of North America 2005; 34: 643-658[Medline].
• Barsh GS, Farooqi IS, O'Rahilly S: Genetics of body-weight regulation. Nature 2000 Apr 6; 404(6778): 644-51[Medline].
• Dietz WH: Health consequences of obesity in youth: childhood predictors of adult disease. Pediatrics 1998 Mar; 101(3 Pt 2): 518-25[Medline].
• Epstein LH, Myers MD, Raynor HA: Treatment of pediatric obesity. Pediatrics 1998 Mar; 101(3 Pt 2): 554-70[Medline].
• Goran MI: Measurement issues related to studies of childhood obesity: assessment of body composition, body fat distribution, physical activity, and food intake. Pediatrics 1998 Mar; 101(3 Pt 2): 505-18[Medline].
• Montague CT, O'Rahilly S: The perils of portliness: causes and consequences of visceral adiposity. Diabetes 2000 Jun; 49(6): 883-8[Medline].
• Pi-Sunyer FX, Laferrere B, Aronne LJ: Therapeutic controversy: Obesity--a modern-day epidemic. J Clin Endocrinol Metab 1999 Jan; 84(1): 3-12[Medline].
• Rosenbaum M, Leibel RL: The physiology of body weight regulation: relevance to the etiology of obesityin children. Pediatrics 1998 Mar; 101(3 Pt 2): 525-39[Medline].
• Speiser PW, Rudolf MC, Anhalt H, et al: Childhood obesity. J Clin Endocrinol Metab 2005 Mar; 90(3): 1871-87[Medline].
• Theriot JA, Sayat J, Franco S, Buchino JJ: Childhood obesity: a risk factor for omental torsion. Pediatrics 2003 Dec; 112(6 Pt 1): e460[Medline].
• Troiano RP, Flegal KM: Overweight children and adolescents: description, epidemiology, and demographics. Pediatrics 1998 Mar; 101(3 Pt 2): 497-504[Medline].
• Weiss R, Dziura J, Burgert TS, et al: Obesity and the metabolic syndrome in children and adolescents. N Engl J Med 2004 Jun 3; 350(23): 2362-74[Medline].

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