Obesity in Children

Updated: Jan 23, 2023
Author: Steven M Schwarz, MD, FAAP, FACN, AGAF; Chief Editor: Jatinder Bhatia, MBBS, FAAP 



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.


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]

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.


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. Excess androgens lead to menstrual irregularities, including amenorrhea and oligomenorrhea. 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]


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]


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.

A study by Perry et al that included BMI data from 597,017 children reported that children 5-6 years of age with severe obesity had almost 6 times the risk for slipped capital femoral epiphysis and children 11-12 years of age with severe obesity had 17 times the risk compared to children with normal BMI.[21]

Liver and gallbladder dysfunction

Evidence of liver dysfunction (non-alcoholic liver disease, NAFLD), with elevated plasma concentrations of transaminases, is observed in 20% of children with obesity; the liver dysfunction most commonly reflects hepatic steatosis. Increasingly, hepatic steatosis may progress to steatohepatitis, hepatic fibrosis and cirrhosis. The prevalence of NAFLD is particularly high in individuals of Hispanic descent, because of a single nucleotide polymorphism in the PNPLA3 gene[22] . Vitamin E supplements may be effective in reversing steatohepatitis in some patients, suggesting that the disorder reflects, at least in part, a relative state of vitamin E deficiency.[23] 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.[24]

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.[25]  

A study by Lang et al that included the data from 507,496 children reported that approximately 23% to 27% of new pediatric asthma cases are directly caused by obesity.[26, 27]


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.[28]

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.[29]

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.[30, 31]

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.



History and Physical Examination

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 central nervous system (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.

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. However, excessive facial hair, acne, and irregular periods in a teenage girl suggest that the weight gain may be caused by cortisol excess or polycystic ovary syndrome (PCOS). Obesity itself may be accompanied by facial hair, irregular menses, and hypertension.

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 central nervous system (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



Diagnostic Considerations

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 polycystic ovary syndrome (PCOS).

Differential Diagnoses



Approach Considerations

Identify any genetic or hormonal disorder that may be a cause of obesity in a child.

In the evaluation of type II diabetes mellitus, a serum hemoglobin A1c level as well as fasting and 2-hour post glucola glucose and insulin levels (for evaluation of glucose tolerance and insulin resistance) are recommended. To identify high-risk patients, Maffeis et al reported that obese children and adolescents with a fasting plasma glucose value greater than or equal to 86 mg/dL are most likely to manifest impaired glucose tolerance.[32]

The following laboratory studies may also be indicated in patients with obesity:

  • 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 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

  • Liver function studies (transaminases), to screen for non-alcoholic fatty liver disease (non-alcoholic steatohepatitis)

When clinically indicated, obtain magnetic resonance imaging (MRI) of the brain with focus on the hypothalamus and pituitary.



Approach Considerations

Theoretically, any therapeutic interventions in the child with obesity must achieve control of weight gain and reduction in body mass index (BMI) safely and effectively and should prevent the long-term complications of obesity in childhood and adulthood.

Manage any acute or chronic complications of obesity (see Prognosis) 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. Consultations with a pulmonary (sleep) medicine specialist, orthopedist, and/or gastroenterologist may be appropriate in some cases. Avoid a punitive approach and reward positive behaviors.

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.

Behavioral Treatment

Kalarchian et al found that family-based behavioral weight control is effective for severely obese children.[33] In a randomized, controlled trial in 192 children aged 8-12 years whose average body mass index (BMI) percentile for age and sex was 99.18, intervention was associated with significant decreases in percentage of child overweight at 6 months compared with usual care. Small significant improvements in medical outcomes were observed at 6 and 12 months.[33] Children who attended 75% or more of intervention sessions maintained decreases in percentage overweight through 18 months.

Wildes et al found that in severely obese children, binge eating affects initial response to family-based behavioral treatment.[34] In a randomized controlled trial in 192 children aged 8-12 years, children who self-reported binge eating showed a 2.6% increase in percentage overweight in response to acute treatment, whereas those without binge eating showed an 8.5% decrease; this difference was not maintained during longer-term follow-up. Children who reported binge eating comprised 11.5% of study subjects, and they were younger; had more depressive, anxiety, and eating disorder symptoms; and had lower self-esteem than those without binge eating.[34]

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.

In contrast to the above findings, DeBar et al recently reported that an intensive, group therapy approach was superior to standard, family-based therapy in achieving lifestyle changes (eg, less consumption of fast foods) and in reducing the BMI of overweight adolescents.[35]

Lifestyle Modifications, Exercise, and Physical Activity

Oude et al concluded that, although no one treatment program can be conclusively recommended, combined behavioral lifestyle interventions produce a significant reduction in weight. Although orlistat and sibutramine (withdrawn from US market) may be used as adjuncts to lifestyle interventions, they must be carefully considered.[36]

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.

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 high-density lipoprotein (HDL) levels, and improves psychologic well-being. Controlled trials have demonstrated that lifestyle exercise programs, in association with dietary restrictions, provide long-term weight control in children and adolescents.

The results from a systematic review and meta-analysis study noted that exercise referral schemes have not been proven as an effective means of increasing physical activity or reducing depression in sedentary individuals when compared with usual care. Further studies are needed to assess the effect on health-related outcomes.[37] However, the results from a 2012 study suggest that low levels of cardiorespiratory fitness have also been associated with elevated depressive symptoms in obese adolescents.[5]

The World Health Organization released guidelines on sugar intake.[38]

The guidelines include the following:

  • WHO recommends a reduced intake of free sugars throughout the life course.
  • In both adults and children, WHO recommends reducing the intake of free sugars to less than 10% of total energy intake.
  • WHO suggests a further reduction of the intake of free sugars to below 5% of total energy intake. Free sugars include monosaccharides and disaccharides added to foods and beverages by the manufacturer, cook or consumer, and sugars naturally present in honey, syrups, fruit juices, and fruit juice concentrates.
  • For countries with a low intake of free sugars, levels should not be increased. Higher intakes of free sugars threaten the nutrient quality of diets by providing significant energy without specific nutrients.
  • These recommendations were based on the totality of evidence reviewed regarding the relationship between free sugars intake and body weight and dental caries.
  • Increasing or decreasing free sugars is associated with parallel changes in body weight, and the relationship is present regardless of the level of intake of free sugars. The excess body weight associated with free sugars intake results from excess energy intake.
  • Although exposure to fluoride reduces dental caries at a given age and delays the onset of the cavitation process, it does not completely prevent dental caries, and dental caries still progresses in populations exposed to fluoride.
  • Intake of free sugars is not considered an appropriate strategy for increasing caloric intake in individuals with inadequate energy intake if other options are available.
  • These recommendations do not apply to individuals in need of therapeutic diets, including for the management of severe and moderate acute malnutrition. Specific guidelines for management of severe and moderate acute malnutrition are being developed separately.

Reduced Fat and Very Controlled–Energy Diets

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. One study noted that patients who attended 12-week commercial weight-management programs realized greater weight loss than those who received primary care programs, which were more costly to provide.[39]

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. Studies in adult subjects demonstrate that lower fat intake is associated with relatively lower body weight, BMI and waist circumference. While similar findings have not been confirmed in children, a meta-analysis of available pediatric studies suggests a direct relationship between fat intake and weight gain.[40]

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, epidemiologic 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.

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 year-long study of 73 pediatric patients aged 7-17 years showed significant reductions in the percentage overweight, total body fat (TBF), body mass index (BMI), total and low-density lipoprotein (LDL) 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.

Duckworth et al found that a high-protein diet does not reduce obese children's desire to eat.[41] Overweight and obese children who were assigned to 1 of 2 isoenergetic diets, a standard 15% protein diet or a 25% protein diet, achieved similar effects on weight loss, body composition, and changes in appetite or mood. Overall, children lost 5.2 ± 3 kg in body weight and reduced their BMI standard deviation score by 0.25. However, with both diets, ratings of desire to eat significantly increased over the duration of the intervention.[41]

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.

Psychopathology – 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 tricyclic antidepressants (TCAs), stimulate appetite and weight gain. Offer psychologic support to patients who have obesity, and refer these patients for psychiatric evaluation and care if evidence of psychopathology or dysfunction is present.

As noted earlier, 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. (See Family-Based Behavioral Treatment)

Surgical Intervention

Various bariatric surgical procedures have been used in adults and some adolescents (in most centers, patients ≥ 15 y) with a body mass index (BMI) of more than 40 kg/m2 or weight exceeding 100% of ideal body weight (IBW).

Vertical-banded gastroplasty

The most common procedures involve gastric restriction. In the vertical-banded gastroplasty (VBG), a pouch of 15-30–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.

Laparoscopic adjustable gastric banding

Laparoscopic placement of an adjustable gastric band (LAGB) has supplanted the VBG, both because of its relative safety and because of its reversibility. Use of 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.

Data suggest that the LAGB is associated with superior outcomes relative 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.

O'Brien et al found that in adolescents, laparoscopic adjustable gastric banding resulted in a greater percentage of patients achieving a loss of 50% of excess weight, compared with lifestyle intervention.[42] In a prospective, randomized controlled trial in 50 patients aged 14-18 years with a BMI higher than 35 kg/m2, 21 patients (84%) in the gastric banding and 3 (12%) in the group assigned to supervised lifestyle intervention lost more than 50% of excess weight, corrected for age. Overall, the mean changes in the gastric banding group were a weight loss of 34.6 kg, representing an excess weight loss of 78.8%, 12.7 BMI units, and a BMI z-score change from 2.39 to 1.32.[42] The mean losses in the lifestyle group were 3 kg, representing an excess weight loss of 13.2%, 1.3 BMI units , and a BMI z-score change from 2.41 to 2.26.

In 2015, the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition released the following guidelines on bariatric surgery in children and adolescents:[43, 44]

  • Consider bariatric surgery in “carefully selected” patients with a body mass index (BMI) >40 kg/m2 who have severe comorbidities such as nonalcoholic fatty liver disease (NAFLD), or in those with a BMI > 50kg/m2 who have milder comorbidities.

  • Additional factors to consider in deciding whether a child or adolescent should undergo bariatric surgery include physical and psychological maturity, personal desire to undergo the procedure, previous attempts at weight loss, and ability to adhere to follow-up care.

  • The Roux-en-Y gastric bypass, laparoscopic adjustable gastric band, and sleeve gastrectomy are the most widely used procedures in pediatric obesity, but their use is associated with subsequent nutritional deficiencies. Temporary intragastric devices could represent a better option for initial treatment in pediatric populations.

  • Current evidence suggests that bariatric surgery can decrease the grade of steatosis, hepatic inflammation, and fibrosis in NAFLD.

  • Uncomplicated NAFLD is not an indication for bariatric surgery.

  • Roux-en-Y gastric bypass is considered a safe and effective option for extremely obese adolescents, as long as appropriate long-term follow-up is provided.

  • Laparoscopic adjustable gastric banding has not been approved by the FDA for use in adolescents and therefore should be considered investigational.

  • Sleeve gastrectomy and other types of weight loss surgery that have grown increasingly common in adults still need to be considered investigational.

Guidelines released in 2023 from the American Academy of Pediatrics recommend that physicians offer bariatric surgery as an option to adolescents with obesity who are aged 13 years or older and have a BMI at the 95th percentile or higher (see Guidelines).[45]


In the absence of a clear, organic etiopathogenesis (eg, leptin deficiency, other hormonal abnormalities), 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 (see Long-term complications of childhood obesity under Prognosis).

Further studies are needed to achieve the following:

  • Identify young children who are predisposed to adolescent and adult obesity

  • Identify interventions that prevent the development of obesity in children at risk

  • Assess the long-term risks of obesity in prepubertal children

  • Identify measures that prevent further weight gain in children and adolescents with obesity

In 2008, The Endocrine Society released guidelines for the prevention and treatment of childhood obesity.[46]

In 2010, the American Heart Association/American Stroke Association (AHA/ASA) issued guidelines for the primary prevention of stroke. A few of the recommendations were as follows[47] :

  • Diet and nutrition: A diet that is low in sodium and high in potassium is recommended to reduce blood pressure; diets that promote the consumption of fruits, vegetables, and low-fat dairy products such as the Dietary Approaches to Stop Hypertension (DASH)–style diet help lower blood pressure and may lower risk of stroke

  • Physical inactivity: Increasing physical activity is associated with a reduction in the risk of stroke; the goal is to engage in at least 30 minutes of moderate intensity activity on a daily basis

  • Obesity and body fat distribution: Weight reduction among overweight and obese persons is recommended to reduce blood pressure and risk of stroke

Learning life-long habits that incorporate exercise and healthy eating is essential and research is emerging regarding various methods of educating youth.

In a systematic review and meta-analysis to determine the effect of school-based physical activity interventions on body mass index (BMI) in children, Harris et al concluded that current population-based policies that mandate increased physical activity in schools are unlikely to have a significant effect on the increasing prevalence of childhood obesity.[48] Meta-analysis showed that BMI did not improve with physical activity interventions.

In contrast, a Swedish study by Marcus et al determined that school-based intervention can reduce obesity in children aged 6-10 years and may affect home-based eating habits.[49] The study of 3135 boys and girls found a 3.2% decrease in prevalence of obesity and overweight at schools where intervention was attempted. A German study also concluded that school-based intervention was effective, after noting that intervention resulted in 31% reduction in the risk of overweight,[50] and a Dutch study reported beneficial effects of a Dutch Obesity Intervention program.[51]

The results of another study suggest that school wellness policies, mandated by the 2004 Child Nutrition and WIC Reauthorization, can significantly reduce the risk of adolescent obesity. Specifically, wellness policies related to diet were significantly associated with lower BMI, while those related to physical activity were significantly associated with lower odds of severe obesity only.[52]

A Cochrane Database of Systemic Reviews study notes that child obesity prevention programs implemented in the health, education and care systems and targeted to children aged 6-12 years may have a positive effect on BMI.[53]

A European Youth Heart Study confirms that improving fitness habits in children correlates with a lower incidence of obesity in adolescence.[15]

Long-Term Monitoring

Regular follow-up is indicated in patients with obesity 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



Guidelines Summary

Endocrine Society, European Society of Endocrinology, and Pediatric Endocrine Society

Clinical practice guidelines from the Endocrine Society, European Society of Endocrinology, and Pediatric Endocrine Society[54, 55]

Children or teens with a body mass index (BMI) ≥85th percentile should be evaluated for related conditions such as metabolic syndrome, diabetes, prediabetes, or hypertension.

Youth being evaluated for obesity do not need to have their fasting insulin values measured, because it has no diagnostic value.

Children or teens affected by obesity do not need routine laboratory evaluations for endocrine disorders that can cause obesity unless their height or growth rate is less than expected based on age and pubertal stage.

About 7% of children with extreme obesity may have rare chromosomal abnormalities or genetic mutations. Specific genetic testing is suggested when there is early-onset obesity (before 5 yr of age), an increased drive to consume food known as extreme hyperphagia, other clinical findings of genetic obesity syndromes, or a family history of extreme obesity.

American Academy of Pediatrics

Clinical practice guidelines from the American Academy of Pediatrics for the evaluation and treatment of children and adolescents with obesity[45, 56]

Children and adolescents aged 12 years and older with obesity (defined as a BMI at the 95th percentile or higher) should be offered the option of receiving weight-loss medication in addition to continuing support for lifestyle modifications, such as increased exercise and a healthier diet.

Adolescents aged 13 years and older with severe obesity (defined as a BMI at 120% or greater of the 95th percentile for age and sex) should be offered the option of bariatric surgery in addition to continuing support for lifestyle changes.

BMI should be calculated starting at age 2 years, with particular attention to patients at the 85th percentile or higher for their age and sex (defined as overweight), at the 95th percentile or higher (obesity), or at the 120th percentile and higher (severe obesity).

Blood pressure should be measured at every visit beginning at age 3 years in patients with overweight (BMI at the 85 percentile or higher) and obesity (BMI at the 95th percentile or higher).

Fasting lipid tests should be performed in children aged 10 years and older with overweight (BMI at the 85th percentile or higher) and obesity (BMI at the 95th percentile or higher). Lipid testing may be performed in children aged 2-9 years with obesity.



Medication Summary

The glucagonlike peptide-1 (GLP-1) agonists liraglutide (Saxenda) and semaglutide (Wegovy) have gained FDA approval for adjunctive therapy to a reduced calorie diet and increased physical activity for chronic weight management in adolescents meeting criteria for obesity. Studies of liraglutide or semaglutide plus lifestyle intervention results in greater reduction in BMI than lifestyle intervention alone.[57, 58]  

Orlistat (Alli, Xenical), a pancreatic lipase inhibitor, is approved for long-term obesity management in patients aged 12 years and older in the United States. Remaining available weight loss products in the US for short-term use in adults include phentermine (Adipex-P) and diethylpropion.

Setmelanotide (Imcivree) is a melanocortin-4 agonist. It was approved by the US Food and Drug Administration (FDA) in November 2020 for patients aged 6 years and older for weight control caused by rare genetic conditions (eg, proopiomelanocortin [POMC], proprotein convertase subtilisin/kexin type 1 [PCSK1], leptin receptor [LEPR] deficiencies). Phase 3 clinical trials observed 80% of patients with obesity owing to POMC or PCSK1 deficiency achieved greater than 10% weight loss and 45.5% of patients with obesity due to LEPR deficiency achieved greater than 10% weight loss after 1 year of treatment. Additionally, hunger scores improved from baseline to 1 year.[59, 60]

FDA weight loss drug withdrawals


Sibutramine (Meridia),[61, 62] a selective serotonin norepinephrine reuptake inhibitor (SNRI), was withdrawn from the US market on October 8, 2010 because of an increased risk of myocardial infarction (MI) and stroke.[63] Europe suspended sibutramine from the market earlier in 2010. 

The FDA requested the market withdrawal after reviewing data from the Sibutramine Cardiovascular Outcomes Trial (SCOUT),[63] which was initiated as part of a postmarket requirement to look at the cardiovascular safety of sibutramine after the European approval of this drug. The trial demonstrated a 16% increase in the risk of serious heart events, including nonfatal MI, nonfatal stroke, the need to be resuscitated once the heart stopped, and death, in a group of patients given sibutramine and another given placebo. A very small difference (2.5%) in weight loss was noted between the placebo group and the group that received sibutramine.[63]


Rimonabant (Acomplia), an anorectic agent with specific cannabinoid receptor inhibition, was approved in several European countries in 2006; however, it was unanimously denied approval 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 neurologic and psychiatric side effects that have been associated with the drug, including seizures, depression, anxiety, insomnia, aggressiveness, and suicidal thoughts. Nonetheless, rimonabant is approved for sale in 42 countries and is marketed for obesity with associated cardiovascular risk in 20 countries.

Fenfluramine and dexfenfluramine

Two previously and widely used agents, the serotoninergic drugs fenfluramine and dexfenfluramine, were 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.

Long-term weight loss and/or life-style modifications

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 US include benzphetamine (Didrex), diethylpropion, phendimetrazine (Bontril), and phentermine (Ionamin).

Adverse effects

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 US (eg, phenylpropanolamine, mazindol) or are banned by the FDA (eg, ephedrine alkaloids ephedra, ma huang) as the consequence of potentially fatal cardiovascular effects.

Pediatric experience

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.[64] However, a second study failed to demonstrate any significant benefit from orlistat treatment.[65] 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 body mass index (BMI) (sibutramine, -8.2% vs placebo, 0.8%,without any observed cardiodynamic effects.[61]

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.

Pastor- Villaescusa et al conducted a randomized, prospective, double-blind, placebo-controlled, multicenter trial to determine the effects of oral metformin on 140 obese children. The study reported that in prepubertal children, metformin decreased the BMI z score vs the placebo (−0.8 vs −0.6) and also improved inflammatory and cardiovascular-related obesity parameters. However, the effects were not seen in pubertal children. Further study is needed to investigate if the difference is related to a dosing issue.[66, 67]


Class Summary

Anorexiants are administered to manage obesity. Indications include weight loss and maintenance of weight loss, in conjunction with a reduced calorie diet, specifically in patients who are obese with an initial body mass index (BMI) of 30 or 27 mg/m2 and other risk factors (eg, diabetes mellitus, dyslipidemia, hypertension).

Orlistat (Alli, Xenical)

Orlistat is a gastrointestinal lipase inhibitor that induces weight loss by inhibiting nutrient absorption. The effectiveness of this agent in producing weight loss does not depend on systemic absorption, and it may reduce the absorption of some fat-soluble vitamins (A, D, E, K) and beta-carotene. Administer a daily oral multivitamin supplement containing fat-soluble vitamins 2 hours before meals or 1 hour after meals.

Glucagon-like Peptide-1 Agonists

Liraglutide (Saxenda)

Indicated as adjunctive therapy to a reduced-calorie diet and increased physical activity for chronic weight management in adolescents aged 12 years and older with weight > 60 kg and an initial body mass index (BMI) corresponding to greater than 30 kg/m2 for adults (obese) by international cutoffs.

Semaglutide (Wegovy)

Indicated as an adjunct to a reduced calorie diet and increased physical activity for chronic weight management for pediatric patients aged 12 years and older with an initial BMI at ≥95th percentile standardized for age and sex (obesity). 

Adrenergic Agonists

Class Summary

Adrenergic agonists are stimulants that release tissue stores of epinephrine, causing subsequent alpha- and/or beta-adrenergic stimulation. These drugs have provided benefits to patients with obesity and are approved in adults for short-term use (8-12 wk).


Caffeine is a natural xanthine derivative that directly stimulates all levels of the central nervous system (CNS), cardiovascular system, and voluntary muscles. This agent increases gastric acid secretion and renal blood flow and also has mild diuretic activity.

Phentermine (Adipex-P)

Phentermine is a sympathomimetic amine that increases the release and reuptake of norepinephrine and dopamine. The anorexiant effect of this agent occurs as result of satiety-center stimulation in the hypothalamic and limbic areas of brain. Phentermine is the pharmacologic component of a comprehensive weight-reduction program (including behavioral modification, caloric restriction, exercise) intended for patients with an initial body mass index (BMI) of 30 or 27 kg/m2 and other risk factors (eg, diabetes, hyperlipidemia, hypertension).


Diethylpropion is a sympathomimetic amine that is effective as an adjunct for anoretic therapy of exogenous obesity. The anorexiant effect of this drug occurs as a result of satiety-center stimulation in the hypothalamic and limbic areas of brain. Note that diethylpropion is a controlled substance with high potential for abuse and addiction.

Melanocortin Agonists

Class Summary

Melanocortin-4 (MC4) receptors in the brain are involved in regulation of hunger, satiety, and energy expenditure. Setmelanotide may reestablished MCR receptor pathway activity in patients with obesity due to rare genetic conditions associated with insufficient activation of the MC4 receptor.

Setmelanotide (Imcivree)

MC4 agonist designed to restore impaired MC4 pathway function caused by genetic variants that occur upstream of the receptor. It is indicated for chronic weight management in patients with obesity owing to proopiomelanocortin (POMC), proprotein convertase subtilisin/kexin type 1 (PCSK1), or leptin receptor (LEPR) deficiency in adults and children aged 6 years and older. 


Questions & Answers


What is the prevalence of obesity in children and adolescents in the US?

Which health conditions are associated with childhood obesity?

What are the trends in the prevalence of obesity in children, and what factors are believed to have a role in its development?

How is obesity in children defined?

What is body mass index (BMI)?

What BMI values are considered overweight or obese in children and adolescents?

What is the role of insufficient cardiorespiratory fitness in weight gain and the risk of being overweight in children aged 6-15 years?

What is the role of sleep in the body mass index (BMI) of children?

What is the relationship between the birth of a sibling and body mass index (BMI) in young children?

Which genetic syndromes are associated with childhood obesity?

Which hormonal disorders are associated with childhood obesity?

Which medications may cause weight gain in children and adolescents?

What is energy imbalance, and what is its role in childhood obesity?

What is the role of hormone dysfunction in weight gain and childhood obesity?

What are the roles of familial and environmental factors in childhood obesity?

Are twins affected similarly in the development of childhood obesity?

How does excess abdominal fat contribute to insulin resistance, dyslipidemia, and hypertension in childhood obesity, and what are the long-term effects of these conditions?

What is the role of fatty liver in insulin sensitivity and beta cell function in obese adolescents?

What is the prevalence of obesity in children and adolescents in the US?

What are the international prevalence rates of obesity in children?

What are the race-related demographics of obesity in children, and which ethic groups have the highest incidence of childhood obesity?

Is obesity more common in adolescent males or females?

What is the relationship between obesity in adolescence and obesity in adulthood?

What long-term complications of obesity are seen in adults who were obese in childhood or adolescence?

What is the effect of dieting and unhealthy weight-control behaviors in young adults?

What is the risk of hypertension in childhood and adolescent obesity?

What are the acute complications of childhood obesity?

Which orthopedic disorders occur more frequently in children with obesity?

How do liver and gallbladder dysfunction manifest in children with obesity?

What emotional and psychosocial complications are common in children and adolescents with obesity?

What are the cardiovascular and endocrine complications associated with childhood and adolescent obesity?

How does body fat distribution correlate to cardiovascular and endocrine complications in childhood and adolescent obesity?

Does childhood obesity increase the risk of atherosclerosis?

What is the correlation between childhood or adolescent obesity and obesity in adulthood?

What is the correlation between BMI and long-term complications of childhood obesity?

What is the relationship between adolescent obesity and diabetes in adulthood?

What is the relationship between adolescent obesity and coronary artery disease (CAD) in adulthood?

How is childhood obesity associated with significant changes in myocardial geometry and function?

What is the role of childhood and adolescent obesity in the risk of gout and colorectal cancer in adulthood?

What are the effects of childhood obesity on psychosocial dysfunction in adulthood?


Which characteristics of the physical exam may indicate a hormone or genetic condition in childhood obesity?

Which symptoms suggest hypothyroidism in children with obesity?

Which condition may be indicated when a child with obesity presents with polyuria and polydipsia?

What are the signs and symptoms of hypothalamic obesity and pituitary hypothyroidism in children with obesity?

What are the signs of excessive cortisol in children with obesity?

Which conditions related to childhood obesity may be indicated by signs of sexual development at an early age?

What are the clinical clues that suggest a hormonal etiology for childhood obesity?


How do the rate of linear growth and the timing of puberty contribute to the diagnostic picture in obesity in children?

What are the differential diagnoses for Obesity in Children?


What is the role of genetic or hormone tests in the workup of obesity in children?

Which lab tests are used in the evaluation of type II diabetes mellitus in children with obesity?

Which lab studies may be indicated in patients with obesity?

When should MRI of the brain be obtained in the workup of obesity in children?


What are the goals of therapeutic interventions for childhood obesity?

What is the most effective approach to managing obesity in children?

What are the effects of weight loss and reductions in BMI in childhood obesity?

Is behavioral therapy effective for the treatment of obesity in children?

What is the role of binge eating in childhood obesity?

What is the role of family support in the treatment of childhood obesity?

What is the role of group therapy in the treatment of childhood obesity?

What are the WHO guidelines on sugar intake?

What is the most effective approach to treatment of childhood obesity?

Is smoking tobacco a reasonable approach to weight management in adolescents and adults with obesity?

What is the role of physical activity in the treatment of childhood obesity?

What is the role of exercise in the treatment of childhood obesity?

Are exercise referral schemes an effective approach to the treatment of childhood obesity?

How can weight gain be limited in mild or moderate childhood obesity?

Which weight-management programs are most effective in the treatment of obesity in children?

Are reduced-fat diets effective in the treatment of childhood obesity?

What is the WHO recommended dietary fat intake in the management of childhood obesity?

How can children and adolescents with obesity achieve rapid weight loss?

Does a high-protein diet reduce the desire to eat in children with obesity?

Are very controlled-energy diets effective in the treatment of obesity in children, and what are the risks?

Which psychiatric disorders are associated with severe obesity in children?

What are the potential adverse effects of psychiatric treatment in children with obesity?

What is the role of family participation in the treatment of obesity in children and adolescents?

Is laparoscopic adjustable gastric band (LAGB) more effective than lifestyle intervention in the treatment of adolescent obesity?

When is surgical intervention considered in the treatment of adolescent obesity?

What is the role of vertical-banded gastroplasty (VBG) in the treatment of adolescent obesity?

What is the role of laparoscopic adjustable gastric band (LAGB) in the treatment of adolescent obesity?

How effective is laparoscopic adjustable gastric band (LAGB) in comparison to vertical-banded gastroplasty (VBG) in the treatment of adolescent obesity, and when is it considered?

What are the ESPGHN guidelines on bariatric surgery in children and adolescents with obesity?

What are the long-term advantages of preventing the development of obesity in childhood and adolescence?

What are the AHA/ASA guidelines for primary prevention of stroke related to obesity in childhood?

Are school-based interventions effective in reducing the prevalence of obesity in children?

Are child obesity prevention programs effective?

Why is regular follow-up important for patients with obesity?


Which medications are available for long-term obesity management in adults?

Can sibutramine (Meridia) be used to treat obesity?

Can rimonabant (Acomplia) be used to treat obesity?

Can fenfluramine and dexfenfluramine (“fen-phen”) be used to treat obesity?

Are sibutramine and orlistat effective medications for the treatment and long-term management of obesity?

What are the adverse effects associated with weight loss drugs for the treatment of obesity?

When are noradrenergic agents contraindicated in the treatment of obesity?

Are weight loss drugs effective for the treatment of adolescent obesity?

When are anorectic drugs indicated for the treatment of obesity in children?

What are the effects of oral metformin in children with obesity?

Which medications in the drug class Anorexiants are used in the treatment of Obesity in Children?

Which medications in the drug class Glucagon-like Peptide-1 Agonists are used in the treatment of Obesity in Children?

Which medications in the drug class Adrenergic Agonists are used in the treatment of Obesity in Children?

Which medications in the drug class Melanocortin Agonists are used in the treatment of Obesity in Children?