Obesity in Pediatric Patients

Etiology

Obesity is multifactorial, originating from a complex interplay between genetic, biological, environmental, socioeconomic, and cultural factors. Genetics and biology are predetermined, while other factors can be modified. Modifiable factors include family behaviors related to eating, sleeping, and exercise, access to healthy food in schools and communities, availability of safe places for physical activity, and adverse childhood experiences.

Weight gain occurs when energy intake, measured in calories, chronically exceeds energy expenditure, eventually leading to obesity.[5] Genetic determinants play a lesser role. Shifting food preferences in recent decades have been influenced by marketing and the availability of high-calorie processed foods like fast food and sugar-sweetened beverages. The consumption of hyperpalatable, energy-dense foods, along with eating supersized portions and snacking, correlates with a drastic increase in obesity in industrialized nations.[6]

Decreased physical activity and increased screen time—via smartphones, computers, televisions, and video games—contribute to the problem.[7] Studies show obesity rates rose during the COVID-19 pandemic when school closures led to more screen and sedentary time, replacing active play and physical activities.[8]

Feeding patterns are culturally driven, with children modeling after their parents and families from a young age. Research demonstrates that higher parental education and structured family meals positively influence healthy food choices in children. Families eating together, exposing children to a variety of nutritious foods, and avoiding television during meals foster a positive food environment that reduces the likelihood of obesity.[9] The amount of time a child spends watching television and playing video games correlates with increased distracted eating and obesity.[10]

Other critical risk factors may predispose individuals to obesity. Perinatal and postnatal conditions that increase risk include elevated maternal BMI during pregnancy, large-for-gestational-age birth weight, rapid weight gain in infancy and early childhood, and the contrast between breastfeeding, which is a protective factor, and formula feeding. Environmental chemicals, microbiota, early antibiotic use, and adverse life experiences are also considered potential risk factors.[11][12][13]

Polygenic and monogenic obesity, though uncommon, merit consideration. Polygenic obesity results from the interaction of several polygenic variants with environmental factors, increasing the likelihood of obesity. Further genetic and molecular studies are needed to determine the clinical significance of these genetic variations. Monogenic obesity is severe and has an early onset, typically caused by an autosomal recessive mutation in the leptin-melanocortin pathway. Deficiencies in melanocortin 4 receptor (MC4R) and proopiomelanocortin increase food-seeking behaviors in children, while leptin and leptin receptor deficiencies result in early-onset extreme obesity.[14]

Genetic syndromes, including Prader-Willi, Bardet-Biedl, and Beckwith-Wiedemann syndromes and Albright hereditary osteodystrophy, are also associated with obesity.[15] Secondary etiologies of obesity, such as endocrine, neurologic, psychological, and drug-induced causes, should be considered when obesity onset is sudden or unexpected. The resulting hormonal imbalances affecting satiety and food-seeking behaviors are the likely mechanisms promoting the condition in these cases.

Epidemiology

The prevalence of obesity in children aged 6 to 11 years rose from 4.2% between 1963 and 1965 to 15.3% between 1999 and 2000.[16] Data from the National Health and Nutrition Examination Survey for 2015 to 2016 show that the trend has continued. According to this survey, the prevalence of obesity in the U.S. among children and teens is 18.5%. The rate is even higher for adolescents, at 20.6% for 12- to 19-year-olds.

Approximately 13.5 million American adolescents struggle with obesity. Disparities exist across racial and ethnic groups, with non-Hispanic Black and Mexican American children exhibiting higher rates of obesity than non-Hispanic White children. Factors such as parental educational level and income, access to healthy food options, and availability of safe physical activity opportunities contribute to disparities in obesity prevalence. Additionally, children with disabilities, including autism and intellectual disabilities, are at higher risk for developing obesity.[17]

Pathophysiology

Appetite and satiety are controlled through neuroendocrine feedback mechanisms. Gastrointestinal hormones, such as ghrelin, stimulate appetite, while glucagon-like peptide-1 (GLP-1), Peptide YY, cholecystokinin (CCK), and vagal neural feedback inhibit appetite and promote satiety.[18]

Adipose tissue contributes to energy balance through adiponectin and leptin, which signal satiety. These hormones provide feedback to the arcuate nucleus in the hypothalamus, which, in turn, sends behavioral and autonomic outputs to the solitary tract nucleus in the brainstem, stimulating gastrointestinal hormone secretion.

Neuropeptides in the brain, including peptide YY (PYY), agouti-related peptide (AgRP), and orexin, stimulate appetite, whereas melanocortin and α-melanocyte-stimulating hormones promote satiety.[19][20] A genetic deficiency of MC4R has been associated with increased food-seeking behavior.[21]

Lack of sleep has been shown to decrease levels of leptin, which signals fullness, and increase levels of ghrelin, which stimulates hunger. Ghrelin, the "hunger hormone," activates PYY and AgRP, which stimulate appetite.

The neuroendocrine interaction between the gut, adipose tissue, and brain maintains the balance between appetite stimulation and adiposity. Mutations in genes involved in the secretion of these hormones are of interest in epigenetic modifications and may represent potential therapeutic targets.

History and Physical

Evaluation of patients with obesity begins with a comprehensive medical history and a careful physical examination to identify the etiology and any comorbid conditions. This process typically occurs during a well-child visit at the medical home but may also take place during problem-focused appointments. The clinician should first inquire whether the family or patient has concerns about the child’s growth or weight. History-taking should begin with reviewing prenatal factors, such as maternal weight gain during pregnancy or gestational diabetes, which may increase the likelihood of obesity. Perinatal history should include questions about intrauterine growth retardation followed by rapid catch-up growth or whether the child was large for gestational age at birth.

A nonjudgmental approach is essential when probing the details of a child’s nutritional intake and energy expenditure. Reviewing family feeding patterns, meal composition, snacking habits, and screen time can help uncover the cause of excessive weight gain. A 24-hour diet recall, which lists the servings of fruits, vegetables, and high-carbohydrate and high-calorie foods in meals, snacks, and beverages, provides valuable information. Additionally, noting the duration and type of physical activity can help assess energy expenditure.

Reviewing height and weight growth charts for abrupt changes in weight, height, and BMI trajectories may suggest an underlying etiology. Extreme appetite and food-seeking behaviors are observed in some genetic conditions.

A family history of obesity and obesity-related comorbid conditions can provide further insights. Genetic susceptibility may be present, particularly if family members have experienced severe obesity requiring bariatric surgery or if obesity affects multiple generations. The presence of diabetes, hypertension, or cardiovascular disease in a family member increases the risk of a child developing similar conditions. Parental obesity is another risk factor, likely influenced by the interplay of genetics, shared environment, and social determinants of health. Clinicians should help families understand that childhood obesity increases the likelihood of developing several chronic diseases.

History may provide vital clues to less common, secondary causes of obesity. Significant head trauma preceding the onset of sudden weight gain may suggest a hypothalamic cause. Symptoms such as easy bruising, muscle weakness, fatigue, and central obesity could indicate Cushing syndrome. Cold intolerance, dry skin, and swelling of the anterior neck may point to hypothyroidism. However, fewer than 1% of children with obesity are diagnosed with an endocrine cause despite many families believing weight gain is due to a hormone imbalance. Reviewing medications associated with obesity, such as steroids, antipsychotics (eg, risperidone), and antiepileptics (eg, valproate), is important in evaluating drug-induced obesity.[22] 

Signs and symptoms elicited on history that suggest the presence of comorbidities include the following:

• Diabetes mellitus: Polyuria and polydipsia
• Pseudotumor cerebri: Headache and vision changes
• Blount disease and slipped capital femoral epiphysis (SCFE): Painful limp and hip or knee pain
• Gallbladder disease and nonalcoholic fatty liver disease (NAFLD): Abdominal pain, vomiting, and jaundice
• Behavioral or psychological problems: Anxiety and depression, worsening school performance, and experiences of bullying
• Asthma and obstructive sleep apnea: Shortness of breath, snoring, and daytime sleepiness or fatigue
• Polycystic ovary syndrome (PCOS): Irregular menses, hirsutism, and acne

Assessing behavioral and emotional concerns with validated screening tools, such as the Patient Health Questionnaire-9 (PHQ-9), can help diagnose psychological comorbidities.

Physical examination begins with measuring height, weight, and blood pressure and calculating the BMI, which has the following formula:

BMI = Weight in kg ÷ (Height in m)²

Blood pressure should be measured with an appropriately sized cuff to ensure accuracy. A head-to-toe examination should follow to identify potential causes and complications of obesity.

Facial and body dysmorphism may indicate genetic disorders. For example, almond-shaped eyes, hypogonadism, and small hands and feet may suggest Prader-Willi syndrome. Other features, such as hypotonia, upward-slanting eyes, a short neck, and transverse palmar creases, are associated with Down syndrome. A round face, central obesity, and excess fatty tissue on the upper back between the shoulders may be signs of Cushing syndrome. Cognitive impairment may also suggest a genetic syndrome. Short stature is often linked to hormone deficiencies and Albright hereditary osteodystrophy.

Eye findings, such as papilledema (possibly from pseudotumor cerebri), retinal degeneration, and nystagmus (associated with Bardet-Biedl syndrome), should be followed up by a specialist. Skin changes, such as acanthosis nigricans, characterized by thickened and darkened skin on the nape of the neck, along with acne and hirsutism, may point to insulin resistance or PCOS. Sexual maturity ratings may reveal premature adrenarche in obese girls.

The clinician should also look for any dyspnea or wheezing, which may suggest asthma, as well as abdominal tenderness or hepatomegaly, which may indicate NAFLD. Restriction in hip and knee mobility may be signs of SCFE and Blount disease, respectively.

Evaluation

Obesity is typically diagnosed by the primary care clinician during health maintenance visits. The growth chart not only reveals the onset and severity of this condition but also provides clues about its potential causes. The BMI trajectory helps differentiate between a gradual increase during sensitive growth periods, such as infancy, childhood, and adolescence, and an abrupt acceleration. Sudden BMI changes may signal personal or family stress or medical issues such as tumors, trauma, hypothyroidism, and medication use.

Comparing weight and height trajectories can be particularly informative. In a young child consuming excess calories, both weight and height typically increase in a linear pattern. However, if weight increases disproportionately, it may suggest a sedentary lifestyle with low physical activity. A deceleration in linear growth over time may point to endocrine issues, such as hypothyroidism.

Laboratory investigation should focus on the early detection of comorbidities, as the risk increases with a child’s age and the severity of obesity. The prevalence of comorbidities also varies by race and ethnicity. Black and Hispanic youth have higher rates of prediabetes and type 2 diabetes mellitus (T2DM), while Hispanic children experience higher rates of metabolism-associated fatty liver disease (MAFLD). These differences are likely influenced by socioeconomic and environmental factors rather than genetic ones.

For children with obesity, evaluation for lipid abnormalities, prediabetes, diabetes, and hepatic dysfunction should begin at age 10. Assessments should include a fasting lipid panel, fasting glucose, alanine transaminase, and aspartate transaminase every 2 years. If fasting glucose is elevated, further testing with hemoglobin A1C (HbA1C) or a 2-hour plasma glucose level after an oral glucose tolerance test may be considered.

For children aged 2 to 9 years, routine evaluation for lipid abnormalities is unnecessary but may be conducted if indicated based on a positive family history. The risk of prediabetes, T2DM, and NAFLD is lower in this age group, so testing is not universally recommended. However, screening for glucose abnormalities or liver dysfunction is appropriate if physical examination findings, such as acanthosis nigricans, are suggestive or if diabetes has been elicited in the family history.

When PCOS is suspected, testing for levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone should be performed. A thyroid hormone assessment is indicated for concerns about thyroid function and serum cortisol levels to diagnose Cushing syndrome.

Other studies may also be considered when clinically indicated. Imaging modalities include radiographs of the hip and knee joints to look for signs of SCFE and Blount disease, as well as ultrasound of the abdomen and pelvis to search for features consistent with PCOS. Brain computed tomography or magnetic resonance imaging may be used to assess for hypothalamic tumors. Polysomnography tests are used to search for signs of obstructive sleep apnea, while pulmonary function tests help determine the presence of asthma. Additionally, a lumbar puncture and cerebrospinal fluid (CSF) opening pressure measurement can assist in detecting pseudotumor cerebri.

The 2025 Global Commission outlined the following 13 diagnostic criteria that signal obesity-related organ dysfunction:

• Symptoms of increased intracranial pressure, including vision loss and recurrent headaches
• Sleep apnea
• Breathlessness or wheezing due to weight
• Hypertension
• Presence of hyperglycemia, hypertriglyceridemia, and low high-density lipoprotein cholesterol (HDL-C)
• Elevated liver function tests due to MAFLD
• Microalbuminemia
• Recurrent urinary incontinence
• PCOS
• Recurrent pain, tripping, or falling due to pes planus or leg malalignment
• Recurrent pain or limited mobility due to tibia vara
• SCFE
• Limitations of day-to-day activities or mobility

Treatment / Management

Lifestyle and Behavioral Interventions

Evidence supports treating obesity and its comorbidities to achieve weight loss, prevent further weight gain, and improve related complications. Guidelines do not recommend a "watchful waiting" approach. Clinicians must document the presence of obesity and clearly explain to caregivers the importance of addressing this problem while avoiding stigmatizing the child. Asking for permission to discuss the child's BMI and weight can help facilitate this conversation. Labels like "obese child" must be avoided, and neutral terms, such as "unhealthy weight" or "gaining too much weight for age or height," must be used instead. The primary focus should remain on the child's health.

Behavioral change is the cornerstone of managing pediatric obesity. Family-based interventions should focus on reducing BMI by limiting the intake of sweetened beverages and fast food, increasing fruit and vegetable consumption, and promoting physical activity. Clinicians should provide clear recommendations on healthy food choices and portion sizes while also encouraging daily exercise. Simply advising "eat less and exercise more" is too simplistic. Families should be encouraged to plan meals that take children's preferences into account while ensuring a balanced, nutrient-rich diet.[23](A1)

Evidence does not support any single specific diet for weight loss. Approaches like the "traffic light diet plan" can help families make healthy changes that align with their cultural beliefs and ethnicity.[24] Another recommendation is the "5-2-1-0" guideline: 5 daily servings of fruits and vegetables, no more than 2 hours of screen time, at least 1 hour of physical activity, and no sugar-sweetened beverages. Primary care clinicians can encourage behaviors such as removing unhealthy foods from the home, keeping a food diary, rewarding positive changes, and setting specific eating and exercise goals. Clinicians must also be mindful of any family experiencing food insecurity or challenges in obtaining enough food or living in neighborhoods without safe spaces for play and exercise.

Creating a healthy food environment at home involves incorporating nutritious food choices for meals and snacks while avoiding TV watching during meals. Children often model after the behaviors of adults in the home, and positive family changes can play a key role in preventing and treating obesity.[25][26] Motivational interviewing helps assess the family's understanding of the health problems linked to obesity and guides them in adopting strategies aligned with their values and beliefs.[27] Involving both patients and their parents in goal-setting fosters sustainable and beneficial behavioral changes.(B3)

The Physical Activity Guidelines for Americans recommend that children aged 6 to 17 engage in at least 60 minutes of moderate-to-vigorous exercise daily, while children aged 3 to 5 years should be physically active throughout the day.[28] Both aerobic and resistance exercises have been shown to improve the metabolic profile of children and reduce the risk of cardiovascular events.[29] Increasing physical activity can involve activities such as walking to school, participating in sports, unstructured outdoor play, and exercising with family members during leisure time. Encouraging family-wide physical activity is more effective in promoting a healthy, active lifestyle than focusing on the child alone.[30](A1)

The American Academy of Pediatrics recommends limiting screen time to less than 1 hour daily for children aged 2 to 5 years and 2 hours daily for older children. For children younger than 2 years, no screen time is advised, except for video chats with friends and family. Increased screen time is linked to lower levels of physical activity.

Primary care clinicians, often working with limited resources and time, may find it difficult to provide the intensive behavior and lifestyle interventions recommended for obesity. A structured weight management plan typically involves motivational interviewing and referrals to a registered dietitian or nutrition specialist. The next step often involves a comprehensive, multifaceted approach, which includes increased intensity and frequency of behavior change sessions, often led by an interprofessional team, with up to 22 sessions over 3 to 12 months. In some cases, patients may benefit from tertiary care interventions that include expert advice on nutrition and exercise, behavior counseling, pharmacologic therapy, and consideration of bariatric surgery.

Pharmacologic Treatment

No evidence supports weight loss medication use as a standalone therapy. However, this approach may be recommended as an adjunct when intensive behavioral interventions have not been successful. Many drugs used for weight loss in adults are not approved by the Food and Drug Administration (FDA) for children, and additional studies are ongoing to assess their efficacy and safety.

Orlistat, approved by the FDA for children aged 12 years and older with obesity, is a pancreatic lipase inhibitor that promotes mild-to-moderate weight loss by blocking fat absorption. Despite its effectiveness, adverse effects, including flatulence, fecal urgency, and steatorrhea, can limit its use. The recommended dose is 120 mg orally 3 times daily.[31](B3)

Metformin is FDA-approved for children aged 10 years and older for treating T2DM. This drug has not been approved for weight loss, but studies show a mild-to-modest weight reduction in patients who take it for T2DM. Metformin is also used to treat PCOS by decreasing hepatic glucose production, reducing gut glucose absorption, and increasing insulin sensitivity. The starting dose is 500 mg orally, either daily or twice daily, and it can be increased up to a maximum of 2,500 mg per day.

GLP-1 receptor agonists help reduce hunger by slowing gastric emptying and influencing central nervous system targets. Liraglutide, injected daily, is FDA-approved for children aged 12 years and older with obesity. Exenatide, administered weekly, is approved for treating children aged 10 to 17 with T2DM. Common adverse effects of GLP-1 medications include nausea and vomiting.

MC4R agonists, such as setmelanotide, are FDA-approved for children aged 6 years and older with rare genetic conditions, including proopiomelanocortin and leptin deficiency. Setmelanotide, which is injected daily, decreases appetite. Adverse effects may include nausea and injection site reactions.[32](B3)

Phentermine and topiramate extended-release capsules are approved for weight loss in adults. Recent data show significant weight loss and improved lipid profiles in teens. However, this medication is not currently FDA-approved for children. Topiramate suppresses appetite but is known to cause cognitive slowing and teratogenic effects. Consequently, this medication must be prescribed with caution, especially for older teens.

Lisdexamfetamine is a stimulant sometimes used off-label in adults with obesity. This agent is approved for treating binge eating disorder in adults and attention-deficit/hyperactivity disorder (ADHD) in pediatric patients. Lisdexamfetamine may be beneficial when a teen requires treatment for both combined ADHD and obesity.

Surgery

Weight loss surgery can be a safe and effective option for pediatric patients with severe obesity. Candidates typically have a BMI greater than or equal to 35 kg/m² or 120% of the 95th percentile for age and sex, whichever is lower. The American Pediatric Surgical Association recommends surgical management for adolescents who have near-complete skeletal maturity and are at risk for medical complications related to obesity after failing intensive behavioral interventions in an interprofessional weight management program lasting at least 6 months.[33]

Bariatric and metabolic surgeries, such as laparoscopic vertical sleeve gastrectomy and Roux-en-Y gastric bypass, are options for pediatric patients with severe obesity. Laparoscopic adjustable gastric band procedures are only approved for patients aged 18 and older and tend to have worse long-term success and higher complication rates. Patients must be referred to comprehensive surgical centers experienced in working with the youth and their families.

Similar to adults, pediatric bariatric patients can experience significant reductions in BMI and improvement or resolution of many obesity-related comorbid conditions, including hypertension, T2DM, dyslipidemia, and weight-related quality of life. Postoperative complications are typically minor, such as nausea and dehydration, but up to a quarter of patients may require additional procedures within the next 5 years. Close follow-up and long-term monitoring for micronutrient deficiencies and malabsorption are necessary, and vitamin and mineral supplements may be required.

Before receiving bariatric and metabolic surgery, patients and their families must undergo a thorough evaluation and education regarding the surgical risks and benefits, ensuring they can make informed decisions. The family must understand that lifestyle modifications are essential after bariatric procedures and that surgery is not a "quick fix." The interprofessional surgical team should conduct a comprehensive physiological and psychosocial assessment to determine whether the patient is a suitable candidate for surgery.

Differential Diagnosis

Uncommon secondary causes of obesity and medical conditions associated with obesity should be considered. Attenuated height growth velocity suggests endocrine causes like hypothyroidism, hypothalamic tumor, growth hormone deficiency, and Cushing syndrome. A history of significant head trauma requires ruling out central nervous system injury as the cause of hypothalamic obesity. In such cases, an abrupt change in the weight gain trajectory is usually observed following the inciting event.

Hyperphagia, atypical facial features, and neurodevelopmental delays may indicate genetic disorders accompanied by obesity. DNA methylation studies can confirm Prader-Willi syndrome. Ocular abnormalities like retinal dystrophy and nystagmus are associated with Bardet-Beidl and Alstrom syndrome and warrant further investigation. Developmental delays in the presence of severe obesity should raise suspicion for rare conditions, such as congenital leptin or proprotein convertase subtilisin/kexin type 1 (PCSK1) deficiencies, which may be identified by measuring serum leptin, proinsulin, and insulin levels.[34] MC4R deficiency is a cause of early-onset pediatric obesity and is diagnosed through molecular genetic studies.

Idiopathic intracranial hypertension, also known as pseudotumor cerebri, is a rare but serious neurological condition most commonly affecting young women with obesity or overweight. Obesity does not cause idiopathic intracranial hypertension but is a typical association. Initial symptoms include vision changes and headaches. Papilledema may be present on physical examination. Computed tomography and brain magnetic resonance imaging may be performed, but the definitive diagnostic test is the measurement of the CSF opening pressure upon lumbar puncture.[35]

Prognosis

Meta-analysis of studies evaluating the efficacy of behavioral and family-based interventions in reducing childhood obesity have shown encouraging outcomes in preschool children. The reduction of screen time has emerged as a critical strategy.[36]

Early diagnosis and prompt intervention lead to a decline in comorbidities and an improved overall prognosis. As the burden of complications increases with age and severity, early diagnosis and treatment offer the best chance for good health. When lifestyle changes and behavioral interventions fail, clinicians must refer patients for pharmacological and surgical interventions promptly. Without appropriate treatment, children with obesity likely become adults with obesity, at risk for long-term adverse health outcomes.

Complications

Treating pediatric obesity and its comorbid conditions is challenging, time-consuming, and often frustrating for both clinicians and families. Obesity impacts multiple organ systems, most notably the cardiovascular and endocrine systems.[37] Dyslipidemia, characterized by low high-density lipoprotein and high low-density lipoprotein and total cholesterol, as well as hypertension, increases the risk of future adverse cardiovascular events. Central adiposity, in particular, causes metabolic imbalances that lead to insulin resistance and metabolic syndrome, and it is commonly associated with PCOS. Excess adipose tissue can also interfere with the liver's metabolic and synthetic functions, contributing to the development of NAFLD. Obesity is also associated with an increased risk of gallstones.

Orthopedic problems are more common when increased pressure from excess body weight affects growing bones. While Blount disease and SCFE are likely multifactorial, obesity is often a contributing factor. Patients with Blount disease typically present with knee pain, a limp, and severe bowing of the tibias. SCFE should be suspected when a child presents with hip pain and decreased internal limb rotation on examination.[38]

Pulmonary comorbidities include asthma and obstructive sleep apnea. Children with asthma may report shortness of breath, cough, and exercise intolerance, while those with obstructive sleep apnea may exhibit snoring, restlessness, daytime sleepiness, and behavioral problems. Pulmonary function tests and polysomnography may be warranted for further evaluation.

The psychological complications of obesity can significantly impact a child's daily life and should be addressed early. Interviewing children nonjudgmentally with open-ended questions can encourage them to share any concerns they may have. Additionally, clinicians should inquire about symptoms of anxiety or depression, worsening grades, or experiences of bullying at school. Professional counseling may be necessary to prevent the progression of psychological symptoms.