Obesity: assessment, complications and treatment

A 10-year-old arrives because his BMI has crossed the 97th percentile. His father, who has type 2 diabetes, wants to know whether his son is "sick" and what to do. Three tasks sit in front of you at once. You must classify the weight accurately against age and sex, you must hunt for the comorbidities that make this a disease rather than a number, and you must build a staged plan the family can sustain without shame. This page teaches you to do all three, with the endocrinology lens the question demands. [1] [2]

Overview & Definition

Childhood obesity is a chronic, relapsing disease of excess adiposity in which biological, behavioural, psychosocial and environmental forces have pushed energy balance toward sustained fat storage. The 2023 American Academy of Pediatrics Clinical Practice Guideline reframes it this way deliberately, moving the conversation away from blame and toward long-term, treatable disease. [1]

Clinically you define the physical dimension with body mass index plotted against age and sex on a growth reference. From ages two through nineteen, obesity is a BMI at or above the 95th percentile, overweight spans the 85th to below the 95th percentile, and severe obesity carries stricter thresholds that change management. The Endocrine Society guideline sits alongside the AAP framework and gives the same percentile-based definition. [1] [2]

The reframe matters because it changes what you do next. Once obesity is a disease, your job is to assess it, stage it, screen for its complications and treat it longitudinally — exactly as you would asthma or diabetes — rather than waiting for the child to "grow out of it." Watchful waiting is no longer the recommended stance. [1]

These numbers orient you. The tracking figure explains why childhood is the strategic window, and the comorbidity figure explains why you screen at the first visit rather than waiting. [4] [1]

Classification

Classification answers two questions: how heavy is the body, and does the severity demand escalation beyond lifestyle? Both matter, because the tier you assign drives the treatment ladder. [1] [2]

These tiers come from the CDC and WHO growth references for ages two to nineteen and are reproduced in both the AAP and Endocrine Society guidance. [1] [2] [5]

The severe-obesity threshold is the gateway to escalation, so learn it precisely. Severe obesity is defined as a BMI at least 120 percent of the 95th percentile, or an absolute BMI of at least 35, whichever is lower. Once a child crosses into severe obesity, the AHA scientific statement and the AAP guideline agree that lifestyle alone is unlikely to suffice, and you should plan toward pharmacotherapy and, where eligible, surgery. [5] [1]

When the child turns eighteen you switch to adult cut-offs: overweight is BMI at least 25 and obesity is BMI at least 30. The crossover matters because a young person who looked "obese" on paediatric centiles at seventeen may appear only "overweight" on adult cut-offs at eighteen, yet carry the same comorbidities and the same need for care. [1]

Epidemiology & Risk Factors

Childhood obesity has risen steeply over two decades, and the severe obesity category is growing fastest of all. Prevalence varies widely by region, ethnicity and socioeconomic position, and Indigenous, Pacific Islander, South Asian and Hispanic children often carry a higher burden that reflects upstream environmental and historical drivers rather than individual behaviour. [1] [9]

The risk factors that cluster around a child are worth naming so you can act on them: family history of obesity or type 2 diabetes, socioeconomic disadvantage, food insecurity, high recreational screen time, short sleep duration, and exposure to weight-based teasing. Several are modifiable, and the lifestyle section returns to each of them. [1]

Perinatal and early-life factors programme later risk in ways that matter for the endocrinology lens. Maternal obesity, gestational diabetes, maternal smoking, and rapid infant weight gain all raise the probability of childhood obesity, which is why prevention starts before the child is born and continues through infancy feeding practice. [2]

Weight-based victimisation is strikingly common. Depending on the study, upward of half of children with higher weight report teasing or bullying about their body, and that experience independently predicts depression, disordered eating, lower physical activity and a worsened obesity trajectory. Treat it as a clinical problem in its own right, not background noise. [9]

The single most useful prognostic statistic is tracking. The systematic review by Simmonds and colleagues found that a child with obesity is roughly five times more likely to become an adult with obesity than a peer without, and that the probability rises with the severity and persistence of the childhood disease. This is why childhood is the window for management, not merely for observation. [4] [10]

Pathophysiology

The simplest truthful sentence about childhood obesity is that sustained positive energy balance expands adipose stores, and that the expanded adipose tissue then becomes metabolically active in ways that reinforce the disease. The real teaching lies in why the balance tilts and why it tilts more for some children than others. [1] [2]

On the biological side, obesity is substantially polygenic, and the hypothalamic systems that regulate appetite through leptin and ghrelin signalling do not simply obey a person's intentions. This is why "willpower" is a biologically inaccurate and clinically harmful frame — it blames a child for a regulated system that is set against them. [2] [1]

The behavioural drivers are the ones lifestyle intervention targets: an energy intake that exceeds expenditure, a diet shifted toward ultra-processed foods, sedentary behaviour and high recreational screen time, and short sleep. Each of these is independently associated with adiposity in youth. [1]

The psychosocial drivers fuse obesity with mood. Depression and obesity are bidirectional — the prospective meta-analysis by Mannan and colleagues shows that childhood and adolescent depression predicts later obesity, and obesity predicts later depression, in both sexes. Emotional eating and chronic stress reinforce the cycle. [11] [9]

The environmental drivers are upstream and powerful: food insecurity that paradoxically links to obesity through cheap energy-dense food, an obesogenic built environment, and socioeconomic disadvantage that constrains every "choice" a family appears to make. Naming these protects the child from blame and directs advocacy as well as clinical care. [1] [9]

Finally, adipose tissue dysfunction produces low-grade systemic inflammation and insulin resistance, which is the engine of the comorbidities — type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, dyslipidaemia and hypertension. Understanding this link is why the endocrinology assessment always screens downstream of the adipose tissue, not just the weight itself. [2] [5]

Clinical Presentation

Most children with obesity present at a routine health-supervision visit, or at a visit for an unrelated problem where the BMI is noted. The presentation you must not miss is the one where a comorbidity rather than the weight is the chief complaint — a limp from slipped capital femoral epiphysis, snoring from sleep apnoea, or abdominal discomfort from fatty liver. [1]

Symptoms that point toward a comorbidity deserve targeted questioning. Polyuria and polydipsia suggest hyperglycaemia or type 2 diabetes; snoring, witnessed apnoea and daytime sleepiness suggest obstructive sleep apnoea; headache and blurred vision suggest hypertension; right-upper-quadrant or diffuse abdominal discomfort can accompany fatty liver. Each changes the work-up and the urgency. [1] [7]

On examination, look for the markers of insulin resistance and comorbidity: acanthosis nigricans (velvety hyperpigmentation in neck folds and flexures), blood pressure taken with an appropriately sized cuff, central adiposity and waist circumference, striae, hepatomegaly, and in females any hirsutism or menstrual irregularity that overlaps with polycystic ovary syndrome. A limping overweight child needs an urgent hip assessment for slipped capital femoral epiphysis. [2] [1]

Disordered eating travels with higher weight more often than clinicians expect. Binge eating, loss-of-control eating and restrictive "dieting" can all coexist with a larger body, and restrictive eating in a higher-weight child can constitute atypical anorexia with the same medical danger as classic anorexia. Ask directly and without assumption. [9] [11]

Differential Diagnosis

Most childhood obesity is primary (exogenous, common, polygenic) and driven by the multifactorial balance described above. The differential diagnosis exists to catch the minority in whom the obesity is secondary to an endocrine, genetic or medication cause, because those children need the underlying driver treated, not lifestyle alone. [2]

These causes are uncommon, but each has a clinical fingerprint that should trigger targeted testing rather than a blanket endocrine panel. Short stature plus obesity, dysmorphism, developmental delay, hyperphagia, or a clear temporal link to a medication are the triggers to investigate. [2]

The clinical decision rule is simple and saves unnecessary testing. Order secondary-cause tests only when red-flag features are present — short stature relative to the family, developmental delay, Cushingoid features, hypotonia in infancy, hyperphagia, or a drug history that explains the trajectory. In a thriving child of normal height with a straightforward family history, the yield of a blanket endocrine screen is low. [2]

Clinical & Bedside Assessment

A good assessment measures the disease, screens for comorbidity, excludes secondary causes selectively, and captures the psychosocial context — all in language that does not shame the child. Plot height and weight accurately and derive BMI for age and sex on a recognised growth reference (CDC or WHO, or national charts such as the UK90 in Britain). [1] [2]

Beyond BMI, waist circumference and central adiposity add risk stratification, because abdominal fat tracks insulin resistance and cardiometabolic risk more tightly than total adiposity. Pubertal stage matters too: early puberty and PCOS cluster with obesity in girls, and body composition shifts across puberty in both sexes. [2]

Take a focused history that captures diet quality, physical activity, sedentary and screen time, sleep duration, family history of obesity and type 2 diabetes, and the social determinants that shape them. Ask directly about weight-based teasing, mood and eating behaviour. The family interview is where motivational interviewing earns its place: explore the family's own goals, their readiness, and what they have already tried. [1]

This table is your bedside filter: it tells you when to broaden the work-up beyond comorbidity screening into secondary-cause testing. [2]

Investigations

Investigations serve two purposes: screen every child with obesity for comorbidity, and test selectively for secondary causes. The baseline comorbidity panel is the same regardless of severity. [1]

These four — glucose metabolism, lipids, liver enzyme and blood pressure — catch most of the modifiable comorbidity early. Abnormal results direct referral and treatment, and normal results give you a baseline to track. [1] [2]

For metabolic dysfunction-associated steatotic liver disease, the NASPGHAN guideline recommends ALT as the first-line screen, with liver ultrasound and gastroenterology referral when ALT is persistently elevated or other risk factors accumulate. A normal ultrasound does not exclude early steatosis, because the scan is insensitive for it. [7]

Tests to exclude secondary causes are not universal — they are triggered by red-flag features. Check TSH when thyroid dysfunction is suspected (short stature, bradycardia, cold intolerance); consider a morning cortisol or low-dose dexamethasone suppression test for Cushingoid features; and measure IGF-1 and pursue genetic testing (Prader-Willi, MC4R pathway) when hyperphagia, developmental delay or dysmorphism are present. [2]

A sleep study (polysomnography) is indicated when an obese child snores, has witnessed apnoea, daytime sleepiness or unexplained pulmonary hypertension, to evaluate obstructive sleep apnoea. Untreated sleep apnoea worsens metabolic and cardiovascular outcomes and impairs learning and mood, so it deserves active detection rather than reassurance. [1] [5]

Mental-health screening is an investigation in its own right. Administer a validated depression and anxiety screen appropriate to age, and a screen for disordered eating such as the SCOFF or EAT-26, and ask directly about self-harm and weight-based victimisation. Repeat these at intervals, because the picture changes and the stakes are high. [9] [11]

Management — Resuscitation

There is no traditional resuscitation phase in childhood obesity, because the disease is chronic rather than acute. But several scenarios demand urgent action, and you must recognise them at the first visit rather than booking routine follow-up. [1]

First is symptomatic or markedly deranged type 2 diabetes discovered on screening — significant hyperglycaemia, ketosis, or features of hyperosmolarity. This needs same-day diabetes-team involvement, fluid and electrolyte assessment, and consideration of insulin, because paediatric type 2 diabetes can present in metabolic crisis. [1] [5]

Second is severe hypertension with target-organ features, and obstructive sleep apnoea with desaturation or cor pulmonale. Both are emergencies that redirect the entire visit toward stabilisation and specialist involvement, and both are easy to miss if attention stays fixed on the weight number. [5]

Third is a restrictive eating disorder in a higher-weight child — atypical anorexia with bradycardia, orthostatic vital-sign changes, hypothermia or electrolyte disturbance. These are emergencies that belong on an eating-disorder pathway, not a weight-loss pathway, and a disclosure of self-harm or suicidality always outranks a discussion of BMI. [9] [11]

Beyond these, escalation to paediatric endocrinology, gastroenterology, sleep medicine or a specialist weight-management service is appropriate when comorbidities are complex, when severe obesity needs intensification, or when primary-care management is not succeeding. [1]

Management — Definitive & Stepwise

Definitive management is staged, and the staging is the structure examiners reward. Each stage builds on the last, escalation is deliberate, and comorbidity treatment runs in parallel with the weight intervention rather than being bolted on at the end. [1]

Stage 1 — Lifestyle (all patients). Lifestyle modification is the foundation for every child with obesity, regardless of severity, and the Cochrane reviews confirm that diet, physical activity and behavioural interventions produce modest but real benefit. Frame it around health behaviours, not weight: at least 60 minutes of moderate-to-vigorous physical activity daily, a sustainable healthy eating pattern, sleep optimisation, and limiting recreational screen time. Deliver it with motivational interviewing. [3] [8] [1]

Stage 2 — Structured multidisciplinary paediatric weight management. When Stage 1 is insufficient, intensify to a structured programme with dietetics, psychology, exercise physiology and medical input. This is team-based care, still behaviour-anchored, with more structure and closer follow-up than primary care can offer. [1] [8]

Stage 3 — Anti-obesity pharmacotherapy. For moderate-to-severe obesity, escalate to medication alongside continued lifestyle. Orlistat inhibits pancreatic lipase (a typical adolescent dose is orlistat 120 mg three times daily with fat-containing meals, with fat-soluble-vitamin monitoring). Liraglutide, a GLP-1 receptor agonist, was shown by Kelly and colleagues to reduce BMI in adolescents with obesity in a randomised controlled trial, given subcutaneously and titrated up to a maximum of 3 mg daily where approved. Semaglutide, a once-weekly GLP-1 receptor agonist, extended this benefit in the Weghuber trial, with attention to gastrointestinal effects and nutritional adequacy. [12] [13] [1]

Stage 4 — Metabolic and bariatric surgery. Surgery is endorsed for carefully selected children and adolescents with severe obesity. Typical eligibility is a BMI at least 35 with a significant comorbidity such as type 2 diabetes, or at least 40 without comorbidity, performed at a specialist centre with lifelong follow-up. The Teen-LABS data show that surgery can achieve remission of type 2 diabetes and substantial comorbidity improvement, dramatically outperforming medical therapy in severely obese adolescents. [6] [5]

The trigger to escalate is failure to improve after three to six months at the current stage, combined with comorbidity burden and the family's readiness. Throughout, treat the comorbidities alongside the weight: metformin for insulin resistance or type 2 diabetes, positive airway pressure for obstructive sleep apnoea, dietary and statin management of dyslipidaemia per regional paediatric lipid guidance, and liver-directed care for steatotic liver disease. [1] [7]

Measure success with health behaviours, comorbidity resolution and psychosocial function — the scale is one datum among many, never the verdict. A child whose diabetes has remitted, whose sleep apnoea is treated and who is back in sport has succeeded, even if the BMI moves modestly. [1] [6]

Specific Subtypes & Scenarios

Severe obesity changes the conversation. Once the BMI reaches 120 percent of the 95th percentile or an absolute 35, lifestyle alone rarely suffices, and you should plan early toward pharmacotherapy and surgical referral rather than waiting through cycles of unsuccessful lifestyle attempts. The AHA statement is explicit about this. [5] [1]

Obesity in the pre-school child (two to five years) is managed predominantly with family-focused lifestyle change rather than medication, because pharmacotherapy and surgery are largely reserved for older children and adolescents. Focus on healthy family eating patterns, age-appropriate activity, sleep and screen-time habits, with referral when severe or accelerating. [1] [3]

Syndromic and monogenic obesity — Prader-Willi, Bardet-Biedl, Alström, and leptin or MC4R-pathway disorders — present with hyperphagia, developmental delay and dysmorphism, and require genetic diagnosis and multidisciplinary care. Targeted therapies exist for some (recombinant leptin for leptin deficiency; setmelanotide for certain MC4R-pathway defects), which is why accurate genetic sub-typing matters rather than lumping these children under "lifestyle failure." [2]

Obesity with type 2 diabetes is the highest-priority comorbidity scenario. Screen for it at baseline, and when it is present, involve the diabetes team early and treat the glucose disorder with metformin and lifestyle as first-line, escalating to insulin for symptomatic or ketotic presentation. Inge and colleagues showed that severely obese adolescents with type 2 diabetes had markedly better glycaemic outcomes after bariatric surgery than with medical therapy. [6] [1]

Obesity with binge eating or loss-of-control eating needs integrated care. Address the eating behaviour with psychology before or alongside weight-management pharmacotherapy, because some weight-loss medications interact with eating-disorder pathology. A higher-weight child with atypical anorexia belongs on an eating-disorder pathway first. [9] [11]

Complications & Pitfalls

The complications of childhood obesity span six systems, and screening for them is the core of the endocrinology assessment. The most damaging complication of care, however, is often the weight stigma the child encounters in clinical settings, including from clinicians. Stigmatising language reduces engagement, worsens mental health, and paradoxically worsens the obesity. [9]

Missing a comorbidity because attention stayed fixed on the BMI is a recurring failure. Type 2 diabetes, steatotic liver disease, obstructive sleep apnoea and hypertension are all treatable, and all are easy to overlook if the only metric discussed is weight. Screen systematically at baseline and repeat. [1] [7]

Under-treatment of severe obesity — leaving a child on lifestyle alone when the evidence supports pharmacotherapy and surgery — is the mirror image of over-treatment and is equally a failure. The guideline endorsement of intensification exists precisely because lifestyle is insufficient for severe disease. [5] [6]

Pharmacotherapy has its own pitfalls: orlistat causes fat-soluble-vitamin deficiency and gastrointestinal effects; GLP-1 receptor agonists cause nausea and require attention to nutritional adequacy and, in the context of pregnancy planning, cessation given teratogenicity concerns. Surgery carries perioperative risk and lifelong nutritional and adherence requirements. [12] [13] [6]

A close second pitfall is triggering or worsening a restrictive eating disorder through weight-centric lifestyle advice. Overemphasising weight loss in a vulnerable child can tip them into atypical anorexia with real medical danger. Frame every lifestyle conversation around behaviours and function, never around the weight number. [9]

Finally, deferring transition to adult care until the young person is lost to follow-up leaves comorbidities unmanaged. Plan transition deliberately, with a structured handover, from late adolescence. [1]

Prognosis & Disposition

The long-term cardiometabolic prognosis of a child with obesity is shaped by severity, comorbidity, engagement and the social determinants that surround them. The tracking evidence is stark: childhood obesity is a strong predictor of adult obesity and adult morbidity, and the risk scales with how severe and persistent the childhood disease is. [4] [10]

Comorbidity trajectories matter. Untreated type 2 diabetes in childhood carries a high lifetime burden of complications; steatotic liver disease can progress to steatohepatitis and fibrosis; hypertension and dyslipidaemia seed adult cardiovascular disease. Treating the comorbidities early and well is among the most consequential things a clinician can do for the adult this child will become. [1] [7]

Psychosocial prognosis is just as important. Untreated depression and weight-based distress worsen every other outcome — engagement, adherence, lifestyle success, quality of life. Conversely, sustained, family-centred, weight-neutral care that addresses stigma can substantially improve function and wellbeing even when the BMI moves modestly. [9] [11]

Follow-up frequency is higher during active management, often every few months, and relaxes to annual health-supervision once the plan is stable and comorbidities are controlled. Comorbidity resolution — diabetes remission after surgery, liver-enzyme normalisation with weight loss — measurably improves long-term outlook and should be tracked explicitly. [1] [6]

Transition to adult care is planned, not drifted into. For a young person with chronic obesity, comorbidities and an established multidisciplinary team, a structured handover to adult endocrinology, hepatology or a weight-management service preserves continuity and protects the gains made in childhood. [1]

Special Populations

Culturally safe obesity care for Indigenous children (Aboriginal, Torres Strait Islander, Maori, Pacific Islander) means engaging family and community, acknowledging the historical and structural determinants of the higher metabolic severity, and refusing individualistic framing of a population-level problem. [1] [9]

For migrant, refugee and asylum-seeking children, language barriers, food insecurity, trauma exposure and different cultural dietary patterns all shape the assessment and the plan. Use professional interpreters, screen for the psychological consequences of displacement, and adapt dietary advice to culturally familiar foods rather than imposing unfamiliar prescriptions. [9]

Children in out-of-home care often arrive with incomplete records, disrupted food security and care discontinuity. Prioritise coordination, continuity and practical support; a perfect lifestyle prescription is useless if the child has no stable kitchen or schedule. [1]

Socioeconomic disadvantage shapes every layer — access to healthy food, safe places for physical activity, specialist services, pharmacotherapy and surgery. Recognising these constraints is not making excuses; it is diagnosing a real part of the disease and directing advocacy alongside clinical care. [1] [9]

Children with intellectual disability or neurodevelopmental conditions, and those with medical complexity or technology dependence, need integrated care that accounts for communication, feeding, mobility and the baseline condition, and in which obesity is interpreted against that baseline rather than in isolation. Several syndromic obesity causes sit in this group and demand accurate genetic sub-typing. [2]

Evidence, Guidelines & Regional Differences

The 2023 AAP Clinical Practice Guideline (Hampl and colleagues) is the current landmark. It reframes obesity as a chronic disease, endorses immediate and intensive treatment rather than watchful waiting, and lays out a staged approach from lifestyle through pharmacotherapy to surgery, with concurrent behavioural and mental-health support. [1]

The 2017 Endocrine Society guideline (Styne and colleagues) sits alongside the AAP framework and offers complementary detail on assessment, comorbidity screening, secondary-cause exclusion and prevention, with broadly concordant percentile-based definitions and management principles. [2]

The Cochrane reviews (Mead on diet, physical activity and behavioural interventions; Ells on the overview of interventions) establish the evidence base for lifestyle: the benefit is real but modest, which is precisely why severe disease needs escalation beyond lifestyle alone. [3] [8]

Pharmacotherapy evidence has expanded rapidly. The liraglutide adolescent trial (Kelly and colleagues) demonstrated BMI reduction in a randomised controlled trial, and the once-weekly semaglutide trial (Weghuber and colleagues) extended the GLP-1 receptor agonist benefit to a once-weekly formulation. These trials underpin Stage 3 escalation. [12] [13]

Surgical evidence comes from the Teen-LABS cohort and related studies; Inge and colleagues showed that bariatric surgery achieved markedly better type 2 diabetes outcomes than medical therapy in severely obese adolescents, supporting surgery as a legitimate option for selected patients. The AHA scientific statement on severe obesity (Kelly) and the NASPGHAN steatotic-liver-disease guideline (Vos) round out the guideline landscape for comorbidity-specific management. [6] [5] [7]

Evidence controversies remain: the modest magnitude of lifestyle benefit, the long-term safety of newer pharmacotherapy in growing children, the optimal timing of surgery, and how best to measure success beyond BMI. [12] [6]

Exam Pearls

The high-yield points a fellowship candidate must hold: screen every child with obesity for comorbidity (fasting glucose or HbA1c, lipids, ALT, blood pressure) and for secondary causes selectively, guided by short stature, developmental delay, Cushingoid features or hyperphagia. [1] [2]

Lifestyle is the foundation for every patient — but lifestyle language targets health behaviours, never the weight number, to avoid triggering eating disorders. [3] [9]

Escalate to pharmacotherapy and surgery for severe obesity; do not leave severe disease on lifestyle alone. GLP-1 receptor agonists (liraglutide, semaglutide) are now evidence-based Stage 3 therapy, and bariatric eligibility commonly runs at BMI at least 35 with a comorbidity or at least 40 without, at a specialist centre. [12] [13] [5] [6]

Atypical anorexia occurs in higher-weight children and carries the same medical risk as anorexia at low weight — recognise it and escalate to eating-disorder care, not a weight-loss pathway. [9]

Weight stigma worsens every outcome; addressing it with weight-neutral, person-first language is core management, not an optional courtesy. Outcome measures are health behaviours, comorbidity resolution and psychosocial function — the scale is one datum among many, never the verdict on a child's worth or your care. [9] [1]

References

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2. [2]Styne DM, Arslanian SA, Connor EL Pediatric Obesity-Assessment, Treatment, and Prevention: An Endocrine Society Clinical Practice Guideline. Journal of clinical endocrinology and metabolism, 2017.PMID 28359099
3. [3]Mead E, Brown T, Rees K Diet, physical activity and behavioural interventions for the treatment of overweight or obese children from the age of 6 to 11 years. Cochrane Database of Systematic Reviews, 2017.PMID 28639319
4. [4]Simmonds M, Llewellyn A, Owen CG Predicting adult obesity from childhood obesity: a systematic review and meta-analysis. Obesity reviews, 2016.PMID 26696565
5. [5]Kelly AS, Barlow SE, Rao G Severe obesity in children and adolescents: identification, associated health risks, and treatment approaches: a scientific statement from the American Heart Association. Circulation, 2013.PMID 24016455
6. [6]Inge TH, Laffel LM, Jenkins TM Comparison of Surgical and Medical Therapy for Type 2 Diabetes in Severely Obese Adolescents. JAMA pediatrics, 2018.PMID 29532078
7. [7]Vos MB, Abrams SH, Barlow SE NASPGHAN Clinical Practice Guideline for the Diagnosis and Treatment of Nonalcoholic Fatty Liver Disease in Children. Journal of pediatric gastroenterology and nutrition, 2017.PMID 28107283
8. [8]Ells LJ, Rees K, Brown T Interventions for treating children and adolescents with overweight and obesity: an overview of Cochrane reviews. International journal of obesity, 2018.PMID 30301964
9. [9]Puhl RM, Lessard LM Weight Stigma in Youth: Prevalence, Consequences, and Considerations for Clinical Practice. Current obesity reports, 2020.PMID 33079337
10. [10]Llewellyn A, Simmonds M, Owen CG Childhood obesity as a predictor of morbidity in adulthood: a systematic review and meta-analysis. Obesity reviews, 2016.PMID 26440472
11. [11]Mannan M, Mamun A, Doi S Prospective Associations between Depression and Obesity for Adolescent Males and Females- A Systematic Review and Meta-Analysis of Longitudinal Studies. PLoS one, 2016.PMID 27285386
12. [12]Kelly AS, Auerbach P, Barrientos-Perez M A Randomized, Controlled Trial of Liraglutide for Adolescents with Obesity. New England Journal of Medicine, 2020.PMID 32233338
13. [13]Weghuber D, Chanoine JP, Hadjiyannakis S Once-Weekly Semaglutide in Adolescents with Obesity. New England Journal of Medicine, 2022.PMID 36322838