AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Obesity is the most prevalent nutritional disorder among children and adolescents in the United States. Currently available data report that approximately 40% of children in the United States are either overweight or 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. It also increases the risk of adult obesity and cardiovascular disease.

Operational definitions of obesity in adults are derived from statistical data analyzing 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 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.

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 have been generated using data from the National Health and Nutrition Examination Surveys of 1988-1994.¹ 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 exceeds 30 kg/m² at any age.²

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, 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 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. 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. 

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.

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), 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 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.

Frequency

United States

Using BMI criteria, the most recent national surveys demonstrate that 21-24% of American children and adolescents are overweight and that nearly 16-18% 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, 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.

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; 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.
  • 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. Vitamin E supplements may be effective in reversing this so-called steatohepatitis, suggesting that the disorder reflects a relative state of vitamin E deficiency.³ 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 are frequently 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.
• Long-term complications
• • 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 individuals with a BMI at or above the 95th percentile have a 66-78% risk of being overweight at age 35 years.
  • 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. The epidemiological data, although limited, indicate that adolescent obesity is associated with increased morbidity and mortality in later life.
  • 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. 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 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 to their nonoverweight peers. For overweight males, the only adverse outcome was a decreased likelihood of being married.

Race

See Frequency.

Sex

See Mortality/Morbidity.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 is commonly advanced. In contrast, growth rate and pubertal development are diminished or delayed in growth hormone deficiency, hypothyroidism, cortisol excess, and various 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 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Procedures

• Sleep studies to detect sleep apnea

TREATMENT

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 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 is recommended by the World Health Organization (WHO); however, little evidence, epidemiological or experimental, 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
• • 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 numerous 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 above, 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 successfully used by numerous 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; thus, assessing the effects of the diet itself is impossible.
  • 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. Because of these uncertainties and the difficulties inherent in maintaining severe caloric restriction, the very controlled–energy diets cannot be recommended for the vast majority of children and adolescents with obesity.

Surgical Care

Various bariatric surgical procedures have been used in adults and some adolescents (in most centers, patients >15 y) with a BMI of more than 40 or weight exceeding 100% of ideal body weight (IBW).

The most common procedures involve gastric restriction. In the vertical-banded gastroplasty (VBG), 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. 

Accordingly, laparoscopic placement of an adjustable gastric band (LAGB) has recently supplanted the VBG, both because of its relative safety and because of its reversibility. The LAGB involves placing a collar with an internal, saline-filled balloon around the upper stomach, 1-2 cm below the esophagogastric junction. This creates a 30-mL upper gastric pouch that can be modified by injecting a small amount of saline into a subcutaneous port linked to the balloon. Recent data suggest that the LAGB is associated with superior outcomes to those observed following VBG, and its low complication rate and reversibility make LAGB a viable alternative treatment for the adolescent patient. Nevertheless, the LAGB, or any surgical approach, should be considered only in the most severe cases of 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 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medications approved for long-term obesity management in adult patients in the United States include sibutramine (Meridia), a selective serotonin norepinephrine reuptake inhibitor, and orlistat (Alli, Xenical), a pancreatic lipase inhibitor. Sibutramine may be classified as an anorectic drug, whereas orlistat's mechanism of action involves induction of lipid maldigestion. Although each of these medications significantly increases weight loss when compared with placebo, in long-term studies, the anorectic agents have also been shown to maintain effectiveness only in conjunction with an appropriate diet and exercise program.
 
Indeed, these drugs mediate only modest effects on total body weight, with long-term weight losses amounting to 2-10 kg in adults with obesity. Furthermore, responses of individuals to drug therapy widely vary. Most weight loss is achieved within the first 6 months of treatment, followed either by weight stabilization or by a slight regain of lost weight. Discontinuation of drug therapy is usually accompanied by rebound weight gain and loss of the selective advantage over placebo, unless significant lifestyle modifications have been achieved. Other older anorectic agents approved in the United States include benzphetamine (Didrex), diethylpropion, phendimetrazine (Bontril), and phentermine (Ionamin).

Rimonabant (Acomplia), an anorectic agent with specific cannabinoid receptor inhibition, was recently denied approval by the US Food and Drug Administration (FDA). The approval was unanimously rejected by the FDA's Endocrinologic and Metabolic Drugs Advisory Committee in June 2007. The FDA committee said that more detailed long-term safety information with larger patient numbers was needed with regard to neurological and psychiatric side effects that have been associated with the drug, including seizures, depression, anxiety, insomnia, aggressiveness, and suicidal thoughts. Rimonabant was approved in several European countries in 2006. Rimonabant is approved for sale in 42 countries and is marketed for obesity with associated cardiovascular risk in 20 countries.

All of these weight loss drugs are associated with significant side effects that often limit their use. With orlistat, resulting nausea, bloating, and discomfort from steatorrhea are common, although these symptoms tend to decrease with long-term use. 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 monoamine oxidase inhibitors (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) as the consequence of potentially fatal cardiovascular effects.

Two previously and widely used agents, the serotoninergic drugs fenfluramine and dexfenfluramine, were recently withdrawn from the commercial market because of their association with valvular heart disease and primary pulmonary hypertension. These drugs were also 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 (eg, fluoxetine) in children.

Pediatric experience with the use of weight loss drugs is beginning to emerge. One multicenter, randomized trial of orlistat in obese adolescents demonstrated weight stabilization and reduced body fat in the orlistat group, whereas significant weight gain was observed in patients receiving placebo.⁴ However, a second study failed to demonstrate any significant benefit from orlistat treatment.⁵ Regarding the use of anorectic agents, a 12-month, randomized placebo-controlled trial of sibutramine in 498 adolescents demonstrated a significant, drug-associated reduction in BMI (sibutramine vs placebo = -8.2% vs -0.8%, P<0.001), without any observed cardiodynamic effects.⁶

Despite some of these promising findings, anorectic drugs should never be routinely used for the prevention or treatment of obesity in childhood or adolescence. Clearly, these agents must be absolutely proscribed for prepubertal children until carefully controlled clinical studies are performed to assess their safety and efficacy. Administration of anorectic drugs may be considered in the postpubertal adolescent, but 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 prescribed 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 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 vary depending on the severity of the disorder and the efficacy 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 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to identify a genetic or hormonal disorder in a child with obesity
• Overaggressive or inappropriate use of anorectic medications

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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2. 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. Jun 2001;73(6):1086-93. [Medline].
3. 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].
4. Dunican KC, Desilets AR, Montalbano JK. Pharmacotherapeutic options for overweight adolescents. Ann Pharmacother. Sep 2007;41(9):1445-55. [Medline].
5. Bray GA, Ryan DH. Drug treatment of the overweight patient. Gastroenterology. May 2007;132:2239-2252. [Medline].
6. 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. Jul 2007;120(1):e147-57. [Medline].
7. American Academy of Pediatrics, Committee on Nutrition. Prevention of pediatric overweight and obesity. Pediatrics. Aug 2003;112:424-430. [Medline]. [Full Text].
8. 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].
9. Badman MK, Flier JS. The adipocyte as an active participant in ebergy balance and metabolism. Gastroenterology. May 2007;132:2103-2115. [Medline].
10. Barsh GS, Farooqi IS, O'Rahilly S. Genetics of body-weight regulation. Nature. Apr 6 2000;404(6778):644-51. [Medline].
11. Berkowitz R, Fujioka K, Daniels S, Hoppin A, Owen S, Perry A, et al. Effects of sibutramine treatment in obese adolescents. A randomized trial. Ann Intern Med. July 2006;145:81-90. [Medline].
12. Dietz WH. Health consequences of obesity in youth: childhood predictors of adult disease. Pediatrics. Mar 1998;101(3 Pt 2):518-25. [Medline].
13. Elder KA, Wolfe BM. Bariatric surgery: A review of procedures and outcomes. Gastroenterology. May 2007;132:2253-2271. [Medline].
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Article Last Updated: Nov 1, 2007