- Pediatric obesity remains an ongoing serious international health concern affecting ~17% of US children and adolescents, threatening their adult health and longevity.
- Pediatric obesity has its basis in genetic susceptibilities influenced by a permissive environment starting in utero and extending through childhood and adolescence.
- Genetic screening for rare syndromes is indicated only in the presence of specific historical or physical features.
- Endocrine etiologies for obesity are rare and usually are accompanied by attenuated growth patterns.
- Pediatric comorbidities are common, and long-term health complications often result. Screening for comorbidities of obesity should be applied in a hierarchal, logical manner for early identification before more serious complications result.
- The psychological toll of pediatric obesity on the individual and family necessitates screening for mental health issues and counseling as indicated.
- The prevention of pediatric obesity by promoting healthful diet, activity, and environment should be a primary goal, since achieving effective, long-lasting results with lifestyle modification once obesity occurs is difficult.
Diagnosing Overweight and Obesity
- ES recommends using body mass index (BMI) and the Centers for Disease Control and Prevention (CDC) normative BMI percentiles to diagnose overweight or obesity in children and adolescents ≥2 years of age. (1|⊕⊕⊕◯)
- ES recommends diagnosing a child or adolescent >2 years of age as overweight if the BMI is ≥85th percentile but <95th percentile for age and sex, as obese if the BMI is ≥95th percentile, and as extremely obese if the BMI is ≥120% of the 95th percentile or ≥35 kg/m2 (1|⊕⊕◯◯). ES suggests that clinicians take into account that variations in BMI correlate differently to comorbidities according to race/ethnicity and that increased muscle mass increases BMI. (2|⊕◯◯◯)
- ES suggests calculating, plotting, and reviewing a child's or adolescent's BMI percentile at least annually during well-child and/or sick-child visits. (U)
- ES suggests that a child <2 years of age be diagnosed as obese if the sex-specific weight for recumbent length is ≥97.7th percentile on the World Health Organization (WHO) charts, since US and international pediatric groups accept this method as valid. (2|⊕◯◯◯)
- ES recommends against routine laboratory evaluations for endocrine etiologies of pediatric obesity unless the patient's stature and/or height velocity are attenuated (assessed in relationship to genetic/familial potential and pubertal stage). (1|⊕⊕⊕◯)
- ES recommends that children or adolescents with a BMI of ≥85th percentile be evaluated for potential comorbidities (see Table 2 and Fig. 1). (1|⊕⊕⊕◯)
- ES recommends against measuring insulin concentrations when evaluating children or adolescents for obesity. (1|⊕⊕⊕◯)
Genetic Obesity Syndromes
- ES suggests genetic testing in patients with extreme early onset obesity (before 5 years of age) and that have clinical features of genetic obesity syndromes (in particular extreme hyperphagia) and/or a family history of extreme obesity (2|⊕⊕◯◯)
Table 1. Prevalence of Pediatric Overweight and Obesity in the United States
|Obesity||Combined Overweight and Obesity|
|12–19 y by race||Hispanic||21.9%||43.3%||34.3%||38.1%|
Table 2. Screening for Comorbidities of Pediatric Overweight or Obesity
|Comorbidity||Tests and Interpretation|
(To convert mg/dL to mmol/L, multiply by 0.0555 for glucose, 0.0259 for cholesterol, and 0.0113 for triglycerides.)
IFG (verify fasting status)
IGT (if OGTT is used)
|Prehypertension and hypertension||3–11 y: (standardized according to sex, age, and height percentile)|
|Obstructive sleep apnea|
b In the absence of unequivocal hyperglycemia, should be confirmed by repeat testing.
c Given variability in testosterone levels and the poor standardization of assays, it is difficult to define an absolute level that is diagnostic of PCOS or other causes of hyperandrogenism (familiarity with local assays recommended). The preferred assay is HPLC tandem mass spectroscopy.
Derived from (a) American Diabetes Association. Diabetes Care 2014;37(Suppl 1):S14–S80; (b) Expert Panel. Pediatrics 2011;128(Suppl 5): S213–S256; (c) Schwimmer JB et al. Gastroenterology 2010;138:1357–1364. e1–2; (d) Legro RS et al. J Clin Endocrinol Metab. 2013;98:4565–4592; (e) Wise MS et al. Sleep 2011;34:389–398; (f )Zametkin AJ. J Am Acad Child Adolesc Psychiatry 2004;43:134–150.
- ES suggests that clinicians promote and participate in the ongoing healthy dietary and activity education of children and adolescents, parents, and communities, and encourage schools to provide adequate education about healthy eating. (2|⊕◯◯◯)
- ES recommends that clinicians prescribe and support healthy eating habits such as:
- avoiding the consumption of calorie-dense, nutrient-poor foods (e.g., sugar-sweetened beverages, sports drinks, fruit drinks, most "fast foods" or those with added table sugar, high-fructose corn syrup, high-fat or high-sodium processed foods, and calorie-dense snacks)
- encouraging the consumption of whole fruits rather than fruit juices. (1|⊕⊕◯◯)
- ES recommends that children and adolescents engage in at least 20 minutes, optimally 60 minutes, of vigorous physical activity ≥5 days per week to improve metabolic health and reduce the likelihood of developing obesity. (1|⊕⊕◯◯)
- ES suggests fostering healthy sleep patterns in children and adolescents to decrease the likelihood of developing obesity due to changes in caloric intake and metabolism related to disordered sleep. (2|⊕⊕◯◯)
- ES recommends balancing unavoidable technology-related screen time in children and adolescents with increased opportunities for physical activity. (1|⊕⊕◯◯)
- ES suggests that a clinician’s obesity prevention efforts enlist the entire family rather than only the individual patient. (2|⊕◯◯◯)
- ES suggests that clinicians assess family function and make appropriate referrals to address family stressors to decrease the development of obesity. (2|⊕⊕◯◯)
- ES suggests using school-based programs and community engagement in pediatric obesity prevention. (2|⊕⊕◯◯)
- ES recommends using comprehensive behavior-changing interventions to prevent obesity. Such programs would be integrated with school- or community-based programs to reach the widest audience. (1|⊕⊕◯◯)
- ES recommends breast-feeding in infants based on numerous health benefits. However, we can only suggest breast-feeding for the prevention of obesity, as evidence supporting the association between breast-feeding and subsequent obesity is inconsistent. (2|⊕◯◯◯)
Figure 1. Diagnosis and Management Flowchart —footnotesa Measure insulin and proinsulin in patients with clinical features of PCSK1 deficiency.
Adapted from: August GP et al. J Clin Endocrinol Metab. 2008;93:4576–4599. with permission, ©Endocrine Society. Republished with permission of Springer Science and Bus Media BV from Farooqi S and O'Rahilly S In: Grant S, ed. The Genetics of Obesity. New York, NY: Springer; 2104:23–32.; permission conveyed through Copyright Clearance Center, Inc.
Table 3. Genetic Obesity Syndromes With and Without Developmental Delay
|Genetic Obesity Syndrome||Clinical Features|
|Obesity WITH Developmental Delay|
|Prader-Willi syndrome||Hypotonia, failure to thrive in infancy followed by weight gain, short stature (due to GH deficiency), hyperphagia, hypogonadotropic hypogonadism, sleep disturbance, obsessive behaviors|
|Albright's hereditary osteodystrophy||Short stature in some but not all patients, skeletal defects, impaired olfaction, and hormone resistance (e.g., parathyroid hormone) if a mutation is maternally inherited|
|SIM1 deficiency||Hyperphagia with autonomic dysfunction (characterized by low systolic blood pressure), speech and language delay, neurobehavioral abnormalities, including autistic type behaviors|
|BDNF/TrkB deficiency||Hyperactivity, impaired concentration, limited attention span, impaired short-term memory and pain sensation|
|Bardet-Biedl syndrome||Dysmorphic extremities (syndactyly/brachydactyly/polydactyly), retinal dystrophy or pigmentary retinopathy, hypogonadism, renal abnormalities/impairment|
|TUB deficiency||Retinal dystrophy, deafness|
|Obesity WITHOUT Developmental Delay|
|Alström syndrome||Retinal dystrophy; extreme insulin resistance; deafness; dilated cardiomyopathy; progressive pulmonary, hepatic, and renal dysfunction|
|MC4R deficiency||Hyperphagia, accelerated linear growth, disproportionate hyperinsulinemia, low/normal blood pressure|
|SH2B1 deficiency||Hyperphagia, disproportionate hyperinsulinemia, early speech and language delay that often resolves, behavioral problems including aggression|
|KSR2 deficiency||Mild hyperphagia and reduced basal metabolic rate, insulin resistance often with acanthosis nigricans, irregular menses, early development of T2DM|
|Leptin deficiency||Extreme hyperphagia, frequent infections, hypogonadotropic hypogonadism, mild hypothyroidism|
|Leptin receptor deficiency||Extreme hyperphagia, frequent infections, hypogonadotropic hypogonadism, mild hypothyroidism|
|POMC deficiency||Hyperphagia, cholestatic jaundice or adrenal crisis due to ACTH deficiency, pale skin, and red hair in whites|
|PCSK1 deficiency||Small bowel enteropathy, hypoglycemia, hypothyroidism, ACTH deficiency, diabetes insipidus|