One-third of North American children are overweight or obese. Pathologic obesity accounts for only a small percentage of these cases. The vast majority are the result of a complex interaction of genetic and hormonal, nutritional, physical activity, and physical and social environmental factors. Obesity increases the risk for various cardiometabolic, pulmonary, and psychosocial complications for children, which often continues into adulthood. Multidisciplinary care, focusing on family-centered behavior change, is an evidence-based, essential part of the treatment, along with pharmacologic and surgical options for more complex cases. Prevention and early intervention strategies are key to reversing the obesity epidemic.
Key points
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Routine body mass index (BMI) screening of children on age-appropriate growth charts is necessary to identify those requiring further assessment.
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Central adiposity is associated with increased risk for type 2 diabetes (T2DM), dyslipidemia, hypertension, sleep-disordered breathing, nonalcoholic fatty liver disease, and polycystic ovarian syndrome (PCOS).
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Family-centered behavior therapy should focus on small goals to improve nutritional intake and physical activity and reduce sedentary behaviors.
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Studies demonstrate modest weight loss of 5% to 10% with improvement in cardiometabolic parameters.
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Psychosocial stressors and comorbidities may make behavior change difficult; empathetic counseling using techniques such as motivational interviewing may be useful adjuncts to therapy.
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Prevention strategies must be implemented across various domains, as children are influenced in the context of their families, cultures, communities, and on a broader population level.
Background
Obesity prevalence has increased during the past decades in children and adolescents, leading to a significant current and future health burden. In North America, approximately one-third of children are either overweight or obese. Although the overall proportion of children with obesity may be plateauing, the rates of severe obesity in children continue to rise, particularly in very young children. Furthermore, the incidence of overweight/obesity for children younger than 5 years in low- and middle-income countries is higher than the rates of wasting. As obesity tends to track into adulthood, especially for those with the most severe degrees of obesity and in older age groups, prevention and intervention strategies should begin at the earliest age possible.
Overweight and obesity in children are assessed clinically by calculation of BMI, obtained by dividing weight (in kilograms) by height squared (square meters). BMI values can be plotted on age- and sex-specific growth charts. Several definitions of pediatric obesity exist, as defined by growth charts compiled by the Centers for Disease Control (CDC), the World Health Organization (WHO), and the International Obesity Task Force. Most commonly, overweight is defined as BMI 85th to 95th percentile (CDC) or 85th to 97th percentile (WHO) and obesity as greater than or equal to 95th percentile (CDC) or greater than or equal to 97th percentile (WHO).
Background
Obesity prevalence has increased during the past decades in children and adolescents, leading to a significant current and future health burden. In North America, approximately one-third of children are either overweight or obese. Although the overall proportion of children with obesity may be plateauing, the rates of severe obesity in children continue to rise, particularly in very young children. Furthermore, the incidence of overweight/obesity for children younger than 5 years in low- and middle-income countries is higher than the rates of wasting. As obesity tends to track into adulthood, especially for those with the most severe degrees of obesity and in older age groups, prevention and intervention strategies should begin at the earliest age possible.
Overweight and obesity in children are assessed clinically by calculation of BMI, obtained by dividing weight (in kilograms) by height squared (square meters). BMI values can be plotted on age- and sex-specific growth charts. Several definitions of pediatric obesity exist, as defined by growth charts compiled by the Centers for Disease Control (CDC), the World Health Organization (WHO), and the International Obesity Task Force. Most commonly, overweight is defined as BMI 85th to 95th percentile (CDC) or 85th to 97th percentile (WHO) and obesity as greater than or equal to 95th percentile (CDC) or greater than or equal to 97th percentile (WHO).
Etiology/Risk factors
Childhood obesity is a complex condition, influenced by genetics, nutritional intake, level of physical activity, and social and physical environment factors. Rare pathologic causes may also lead to rapid weight gain; however, in most children, there is no single underlying cause. Red flags for pathologic obesity that may warrant further investigation include rapid onset of weight gain, very early age of onset, obesity discordant with parent weights, hypogonadism, short stature/poor linear growth, and association of dysmorphic features or developmental delay.
Environmental Factors
Intrauterine and postnatal factors
Substantial evidence from epidemiologic and experimental animal studies suggest that fetal and early postnatal environmental exposures impact significantly on the development of obesity, diabetes, and heart disease. The “developmental origins of health and disease (DOHaD)” hypothesis posits a stimulus or insult to an organism during a critical period of development can alter gene expression via epigenetic modifications. For example, being either small or large for gestational age is associated with an increased risk of developing childhood obesity. Prenatal exposure to gestational diabetes mellitus (hyperglycemia, hyperinsulinemia), maternal smoking, and high maternal adiposity are correlated with increased incidence of childhood obesity, independent of birth size. A systematic review found a strong increased risk of overweight and obesity in individuals delivered by cesarean section. Outcomes related to mode of delivery and obesity may be due to accumulation of differing bacteria in the gut (the microbiome), which influences inflammation, nutrient ingestion, and immune system development in the infant.
Exclusive breast-feeding in the first 6 months correlates with a lower incidence of childhood obesity in cohort studies, although a large randomized clinical trial promoting breast-feeding failed to show a protective effect at age 6.5 years. Rapid weight gain in the first few months of life, in addition to an earlier age of BMI rebound (the physiologic increase in slope of the BMI curve normally occurring at age 5–7 years), is also associated with higher rates of childhood obesity and adult cardiometabolic risk.
Nutrition/Feeding behaviors
Several dietary factors including higher caloric food intake during infancy, introduction of solid foods before 6 months of age, higher consumption of sweetened drinks (juice, soda), increased fast food consumption, eating while watching television (TV), skipping breakfast, reduced family meal times eating together, and lower daily milk, fruit, and vegetable intake have all been associated with increased rates of childhood obesity.
Most guidelines recommend 60 minutes of moderate to vigorous daily physical activity for children and adolescents. In Canada, approximately 93% and 96% of Canadian children aged 5 to 11 and 12 to 17 years, respectively, fail to meet these guidelines. Low habitual levels of physical activity are associated with higher obesity incidence in multiple studies. Sedentary behavior, in particular time spent at the TV or computer screen, is associated with higher BMIs, although systematic reviews examining reduced screen time showed no effect on BMI in children.
Obesity and sociodemographic influences
Cross-sectional studies have shown that members of certain ethnic groups (eg, Aboriginal, Hispanic, and South Asian) are more prone to obesity during childhood. Children from low-income countries with greater food security are more prone to becoming obese, as are those in urban areas as compared with children in rural areas. In high-income countries, children in the lowest socioeconomic classes have higher obesity rates in comparison to children from a more affluent socioeconomic position.
Pathologic Causes of Obesity
Endocrine causes
Endocrine disorders, such as hypothyroidism, Cushing syndrome, growth hormone deficiency, and pseudohypoparathyroidism, can present with weight gain and slowed growth. Of these, only Cushing syndrome typically presents with severe obesity; however, all disorders may lead to a more central pattern of weight deposition. Endocrine causes of obesity are rare and are found in less than 1% of children and adolescents with obesity, with hypothyroidism being the most common cause of endocrine-related weight gain. The level of leptin, a hormone produced by adipocytes that acts at the level of the hypothalamus to regulate weight and induce satiety, is elevated in obesity. However, similar to the insulin resistance that develops with increased adiposity, leptin resistance also occurs, and both of these may contribute to reduced satiety and subsequent weight gain.
Genetic causes
Rare single gene defects, which specifically result in obesity, are those that affect the leptin-melanocortin regulating pathway. The genes identified thus far include leptin, the leptin receptor, proopiomelanocortin, prohormone convertase 1, melanocortin receptors (MCR) 3 and 4, and the transcription factor single-minded 1. Of these, only MCR4 mutations are common, accounting for approximately 4% of early-onset and childhood cases of severe obesity. There are also several genetic syndromes associated with obesity, including Prader-Willi, Bardet-Biedl, Alström, and WAGR ( W ilms tumor, a niridia, g enitourinary anomaly, mental r etardation) syndromes, which generally exhibit some degree of neurocognitive delay and characteristic dysmorphic features.
Common genetic variants associated with high adiposity and weight gain, but having weak individual effects, have been identified through genome-wide association studies, although no single variant contributes in a large way to predict obesity.
Other causes
Central nervous system tumors such as craniopharyngioma located in the hypothalamic region and the subsequent surgery to debulk these tumors can result in reduced satiety, resistance to insulin and leptin, and enhanced insulin secretion due to autonomic dysregulation. The net result of these physiologic changes leads to rapid and unrelenting weight gain. Lastly, medication-induced obesity can occur from the use of atypical antipsychotics and high-dose glucocorticoids.
Comorbidities/Consequences of childhood obesity
There are multiple potential comorbidities associated with obesity, many of which track into adulthood. However, not all overweight or obese children exhibit medical or psychological sequelae; a subset of individuals may exhibit no clinical complications or health risks related to their weight.
In adults, the metabolic syndrome is defined as a clustering of features including insulin resistance/elevated glucose, hypertension, abdominal obesity and dyslipidemia that portends risk for T2DM, and cardiovascular disease. The metabolic syndrome is also prevalent in other conditions linked to insulin resistance, such as PCOS and nonalcoholic fatty liver disease (NAFLD). In children and adolescents, features of the metabolic syndrome cluster in a similar fashion, although there is no single accepted definition. A systematic review of studies performed in the pediatric age range indicates a prevalence of metabolic syndrome in population-based studies of 3.3%, 11.9%, and 29.2% of normal-weight, overweight, and obese children, respectively.
There is compelling evidence that the obesity-associated dyslipidemia tracks from early life into adulthood. In a report from the Bogalusa Heart Study, pathology studies of children and young adults aged 2 to 39 years who died primarily from traumatic injuries, fatty streaks in the aorta and coronary arteries were documented early in life, and these atherosclerotic changes were associated with elevated cholesterol and higher BMI. In the large population-based US study, the National Health and Nutrition Examination Survey (NHANES) reported that the overall prevalence of dyslipidemia in children and adolescents is 20.3% and increases to 42.9% in obese youth. Recommendations supporting the use of non–high-density lipoprotein (HDL) cholesterol (calculated as total cholesterol − HDL cholesterol) have been published, with further evaluation with fasting lipid profile if non-HDL cholesterol is abnormal.
Hypertension is defined as elevated systolic or diastolic blood pressure (BP) greater than or equal to 95th percentile for age, sex, and height-based tables. Studies in American children indicate a prevalence estimate of 10% with prehypertension (95th percentile > BP ≥90th percentile) and 3.7% with hypertension, increasing with increasing BMI and waist circumference. Recognition of elevated BP in the office setting is unrecognized in approximately 25% of cases.
Rates of T2DM in children have increased in parallel with increases in obesity. In 2009, the total prevalence of T2DM in a representative sample of youth younger than 20 years in the United States was 0.24 cases per 1000 individuals, with increasing prevalence with age, whereas the incidence of T2DM in Canada was 11.3 cases per 100,000 children (<18 years) per year, similar to American incidence statistics. Impaired glucose tolerance is particularly common in severely obese adolescents, with up to 25% exhibiting this finding. Of great concern are an increasing number of reports indicating that youth diagnosed with T2DM go on to develop significant microvascular and macrovascular complications of diabetes early in adulthood.
Fat deposition in the liver visualized by ultrasonography or elevated levels of hepatic alanine aminotransferase are distinctive for NAFLD, which can progress to more serious liver dysfunction and is a common consequence of obesity in all ages. In addition, gallstones are found to be more prevalent in obese adolescents (2%) as compared with nonobese teens (0.6%), although the mechanisms leading to this have not been completely elucidated.
PCOS is one of the most common endocrine disorders affecting 4% to 6% of young women and is the leading cause of infertility. PCOS is characterized by chronic oligo-ovulation or anovulation, hyperandrogenism, and the appearance of polycystic ovaries on ultrasound imaging. Challenges in diagnosing youth with PCOS include physiologic anovulation in the first year postmenarche, presence of acne during puberty, and multifollicular (but not polycystic) appearance of the ovaries during adolescence. Insulin resistance is a core feature of PCOS and leads to stimulation of increased androgen, as well as increased risk for the metabolic syndrome. These features, along with the presence of PCOS symptoms 1 to 2 years after menarche, should prompt further assessment.
Obstructive sleep apnea is 4 to 6 times higher in obese children and adolescents than in nonobese peers. Sleep-disordered breathing has been associated with insulin resistance and cardiometabolic risk, as has poor sleep quality in children and adolescents. The causal association between obesity and asthma is debatable. However, the apparent association may be due to the difficulty in subjectively distinguishing between shortness of breath related to obesity and increased work effort and wheezing-related symptoms due to asthma.
Excessive weight can lead to injury of the developing epiphyseal growth plates, resulting in pain and limited mobility. Blount disease (tibia vara), flatfoot, scoliosis, osteoarthritis, slipped capital femoral epiphysis, and spondylolisthesis leading to low back pain have all been associated with overweight/obesity.
Obese children and adolescents are susceptible to dermatologic conditions such as acanthosis nigricans (hyperpigmented, hyperkeratotic plaques) and intertriginous irritation or infection. Neurologic conditions include an increased risk for intracranial hypertension. Renal pathologies such as hyperfiltration and microalbuminuria may also be seen. Lastly, both vitamin D and iron deficiencies are shown to be increased in overweight and obese children.
Psychosocial Comorbidities
Anxiety, depression, stress, low self-esteem and body image, bullying, social withdrawal, and lower quality of life have all been reported to be more common in obese adolescents. Poor school performance, including difficulty with concentration, homework completion, and missed school days, are 4 times more likely in an adolescent obese population when compared with a healthy control sample. Clinical populations of overweight/obese adolescents also show higher lifetime rates of eating disorders, especially bulimia nervosa, than population-based samples. Binge eating disorder (BED), defined as repetitive loss of control of eating of large quantities of food over discrete time frames, without compensatory weight-reduction activity, is common. About 20% to 40% of adolescents seeking treatment of overweight/obesity report symptoms of BED.
Assessment/Screening
Calculation of BMI and plotting on age- and sex-appropriate growth charts for children older than 6 years are recommended by the US Obesity Task Force as routine screening approach for use in clinical practice. There is insufficient evidence to provide a similar recommendation for children younger than 6 years, although this recommendation will likely change over time given increasing obesity incidence in this age group. Although BMI is correlated with percent body fat, it is also correlated with lean tissue mass and height and represents an indirect measure of adiposity. Measurement of skinfold thickness, waist to height ratio, waist circumference, and bioelectrical impedance analysis, which have been shown to predict cardiometabolic risk, have been used as physical measures of adiposity in pediatric research populations, as BMI may not always be accurate in judging adiposity. However, as no reference standards for these measures have been developed for children, from a practical clinical standpoint, they are not recommended for clinical screening.
Tables 1 and 2 outline specific points to consider when gathering history and conducting a physical examination and list suggested investigations to screen for common obesity-related comorbidities. Additional laboratory tests that could be performed if history indicates risk factors include thyroid function, abdominal ultrasonography to assess fatty liver, renal function, albumin to creatinine ratio, and clinical screening for PCOS.
| Checklist | Rationale |
|---|---|
| History | |
| Past attempts at weight loss; recent weight gain/loss | Methods used in weight loss attempts; rate of weight changes |
| Developmental delay, stunted linear growth, pattern of weight gain (age of onset) | Genetic syndromes, endocrine disorders |
| Headaches, blurred vision | Hypertension, intracranial hypertension |
| Breathing difficulty while sleeping, snoring, daytime drowsiness | Obstructive sleep apnea |
| Joint pain | Slipped femoral capital epiphysis, Blount disease, spondylolisthesis |
| Menstrual history, hirsutism | Hyperandrogenism, PCOS |
| Polyuria, nocturia | T2DM |
| Increased fatigue, cold intolerance, constipation, dry skin | Hypothyroidism |
| Medications | Drug-induced obesity |
| Fetal/infant history | |
| Maternal BMI, maternal gestational diabetes, maternal nutrition Birth weight Breast-feeding, introduction of complementary food | To identify prenatal/postnatal exposure that may have contributed to the development of overweight/obesity |
| Nutrition, physical activity, and sedentary behaviors | |
| Food choices, daily caloric intake, eating behaviors—snacking, family meals, eating disorders Time spent in physical activity, intensity Screen time and other sedentary behaviors | To elucidate modifiable unhealthy sedentary and dietary behaviors |
| Environmental factors | |
| Access to fresh produce, grocery stores, food security Access to parks and recreational community centers Access to primary health care providers | To gather information about potential environmental barriers |
| Psychosocial factors | |
| Negative affect (depression, anxiety, stress) Body image, self-esteem Peer influence (bullying, support, teasing) Readiness to change, motivation, confidence School functioning | To identify psychosocial issues and need for intervention |
| Family history | |
| Obesity, T2DM, hypertension, dyslipidemia, coronary artery disease, sleep apnea | Genetic inheritance of risk factors and risk for comorbidities |
| Test | Age Group/Criteria | Outcomes/Thresholds |
|---|---|---|
| Dyslipidemia | ||
| FLP If nonfasting, calculate non-HDL (total cholesterol−HDL), and repeat with FLP if non-HDL cholesterol is high or HDL-cholesterol is low Repeat every 2 y | Children >2 y of age if BMI ≥85th percentile a | Total cholesterol >5.2 mmol/L (200 mg/dL), high Triglycerides >1.7 mmol/L (150 mg/dL), high HDL cholesterol <0.9 mmol/L (35 mg/dL), low Non-HDL >3.8 mmol/L (145 mg/dL), high Low-density lipoprotein >3.4 mmol/L (130 mg/dL), high a |
| IGT & T2DM | ||
| FPG 2-h OGTT, 1.75 mg/kg up to max 75 g. HbA1c Repeat every 3 y |
|
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| NAFLD | ||
| ALT/AST Repeat every 2 y | Children >10 y, with BMI 85th–94th percentile and metabolic risk factors, or BMI ≥95th percentile c | ALT/AST 2 × normal levels Upper limit of normal: ALT = 22–25 U/L |
| Sleep-disordered breathing | ||
| Sleep study (polysomnography or nocturnal pulse oximetry) Repeat if symptoms arise. | All, if symptoms to suggest OSA are documented | Detection of hypopneas, apneas, sleep disruption and fragmentation, or cyclic desaturations |
a Lipid threshold cutoffs may vary depending on number of individual risk factors.
b Guidelines for diabetes screening are those recommended by the American Diabetes Association, which differ slightly from those suggested by the Canadian Diabetes Association.
c Recommendations from the American Academy of Pediatrics expert committee on child obesity. The American Association for the Study of Liver Diseases does not support screening because of a lack of evidence and specific management guidelines of NAFLD in children.
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