Definition, epidemiology, and etiology of obesity in children and adolescents

INTRODUCTION — Obesity has become one of the most important public health problems in the United States and many other resource-abundant settings and transitional economies [1-3]. As the prevalence of obesity has increased, so has the prevalence of the comorbidities associated with obesity [2]. For this reason, it is imperative that health care providers identify overweight and obese children so that counseling and treatment can be provided.

The definition, epidemiology, and etiology of obesity in children and adolescents will be presented here. Related content on childhood obesity can be found in the following topic reviews:

●(See "Prevention and management of childhood obesity in the primary care setting".)

●(See "Clinical evaluation of the child or adolescent with obesity".)

●(See "Overview of the health consequences of obesity in children and adolescents".)

●(See "Surgical management of severe obesity in adolescents".)

DEFINITIONS — The term "obesity" refers to an excess of fat. However, the methods used to directly measure body fat are not available in daily practice. For this reason, obesity usually is assessed by the relationship between weight and height (ie, anthropometrics), which provides an estimate of body fat that is sufficiently accurate for clinical purposes.

Body mass index (BMI) is the widely accepted standard measure of overweight and obesity for children two years of age and older [4-6]. BMI provides a guideline for weight in relation to height and is equal to the body weight (in kilograms) divided by the height (in meters) squared (table 1). Other indices of childhood obesity, including weight-for-height (which is particularly useful for the child younger than two years), measures of regional fat distribution (eg, waist circumference and waist-to-hip ratio), and the growth standards developed by the World Health Organization (WHO), are discussed separately. (See "Measurement of body composition in children" and "Measurement of growth in children", section on 'Growth references and standards'.)

Because children grow in height as well as weight, the norms for BMI in children vary with age and sex. In 2000, the National Center for Health Statistics (NCHS) and the Centers for Disease Control and Prevention (CDC) published BMI reference standards for children between the ages of 2 and 20 years (figure 1A-B). BMI percentiles also can be determined using a calculator for females (calculator 1) and for males (calculator 2). As children approach adulthood, the thresholds for defining overweight and obesity (85^th and 95^th percentiles for BMI) are approximately 25 and 30 kg/m², respectively, which represent the same thresholds for defining overweight and obesity in adults.

The following definitions are used to categorize weight status for children between 2 and 20 years of age (table 2) [4]:

●Underweight – BMI <5^th percentile for age and sex.

●Normal weight – BMI between the 5^th and <85^th percentile for age and sex.

●Overweight – BMI between >85^th and 95^th percentile for age and sex.

●Obesity – Classified by severity, using the following thresholds ( (figure 2A-B) or CDC extended BMI growth charts) [4,7,8]:

•Class I – BMI ≥95^th percentile for age and sex or BMI ≥30 (whichever is lower).

•Class II – BMI ≥120 percent of the 95^th percentile values or a BMI ≥35 kg/m² (whichever is lower). This threshold approximates the 98^th percentile after age seven years but is above the 98^th percentile in younger children [9].

•Class III obesity – BMI ≥140 percent of the 95^th percentile values or a BMI ≥40 kg/m². This threshold is between the 99^th and 99.9^th percentiles after age seven years [9].

The above definition of severe obesity in children and adolescents is recommended because it is clinically practical and because the CDC growth standards are not sufficiently precise to use percentile curves or Z-scores at the extremes [10,11]. In males, the curve for 120 percent of the 95^th percentile reaches a BMI of 35 kg/m² at age 18 years, corresponding to class II obesity in adults. In females, the corresponding curve reaches a BMI of 35 kg/m² around age 16.5 years. (See "Obesity in adults: Prevalence, screening, and evaluation".)

Children with severe obesity represent approximately 5 percent of children and adolescents in the United States, with the highest prevalence in Black and Mexican-American youth [7,12,13]. Among adolescents between 12 and 19 years of age, the prevalence of severe obesity is approximately 7 percent in females and 9.7 percent in males [7]. This group has significantly more cardiovascular risk factors and a greater risk for having obesity in adulthood [13]. Therefore, this threshold appears to define a group with medically significant obesity in children and adolescents. (See "Surgical management of severe obesity in adolescents", section on 'Consequences of severe obesity'.)

The term "morbid obesity" is sometimes used to identify individuals with obesity-related comorbidities. However, this term is often inappropriately used as a synonym for severe obesity, and it also may have pejorative connotations to patients, so its use is discouraged. (See "Overview of the health consequences of obesity in children and adolescents".)

In the discussion that follows, the term "obesity" refers to children with BMI ≥95^th percentile for age and sex and "overweight" refers to children with BMI between the 85^th and 95^th percentile for age and sex, unless otherwise noted.

EPIDEMIOLOGY

Prevalence

●United States – Approximately one-third of children and adolescents in the United States are either overweight or obese [7]. The population is distributed into higher weight categories with advancing age, as shown below (in which each weight category is inclusive of the higher weight categories) (figure 3):

•Overweight (body mass index [BMI] ≥85^th to 95^th percentile)

-12.3 percent of preschool-aged children (2 to 5 years)

-15.4 percent of school-aged children (6 to 11 years)

-19.4 percent of adolescents (12 to 19 years)

•Class I obesity (BMI ≥95^th percentile to <120 percent of the 95^th percentile and <35 kg/m²)

-11.7 percent of preschool-aged children

-12.3 percent of school-aged children

-8.9 percent of adolescents

•Class II or III obesity (BMI that is either ≥120 percent of the 95^th percentile or ≥35 kg/m²)

-2 percent of preschool-aged children

-6.4 percent of school-aged children

-10.1 percent of adolescent females and 13.2 percent of adolescent males

The BMI percentiles are defined by the growth charts developed by the Centers for Disease Control and Prevention (CDC) to reflect a generally healthy population, in which the prevalence of overweight and obesity are 15 and 5 percent, respectively, by definition. The actual prevalence of overweight and obesity listed above indicates that the weight status of the population is considerably less healthy than the reference population. The prevalences of overweight and obesity are somewhat lower if the percentiles are adjusted for pubertal status, but this adjustment is not routinely performed in clinical care or research [14].

Childhood obesity is more common among Native American, Black, and Mexican American children than in non-Hispanic White children [3,7,15]. A child’s risk of having obesity is two- to three-fold higher if they have one birth parent with obesity, and up to 15-fold if they have two birth parents with obesity [16]. Obesity is also more prevalent among populations with lower income, education levels or those living in rural environments [15,17]. As an example, 14.9 percent of low-income preschool-aged children had obesity in 2010, compared with 12.1 percent in this age group in the general population [18].

●Other countries – The prevalence of childhood overweight and obesity is high in most resource-abundant settings worldwide [2,19]. It is difficult to directly compare prevalence rates between countries because of differences in definitions and dates of measurements. Use of the International Obesity Task Force (IOTF) standards typically results in lower prevalence estimates than other standards [20,21]. However, studies using comparable statistics show that rates are particularly high (greater than 30 percent) in most countries in North and South America, as well as in Great Britain, Greece, Italy, Malta, Portugal, and Spain (figure 6B) [22]. There are somewhat lower rates in Nordic countries, France, and Central Europe [2]. In Russia and most of the countries of Eastern Europe, the prevalence of overweight is lower (approximately 15 percent) but increasing. In China, the prevalence of overweight among children is approximately one-half of that in the United States, but rates are substantially higher in young children than in adolescents [23].

Trends

●United States – In the United States, the prevalence of obesity rose dramatically in the last few decades of the 20^th century and beginning of the 21^st century. After the early 2000s, there was a plateau in the overall prevalence of obesity, but the prevalence of severe obesity has continued to climb. The pattern varied slightly by age group: Among school-aged children (6 to 11 years), the prevalence of obesity increased dramatically from 6.5 percent in 1976-1980 to 19.3 percent in 2015-2018 (figure 4) [3,24]. In this age group, the trend was increasing until 2007-2008 and then remained more or less stable through 2018 [3]. Among adolescents (12 to 19 years), the prevalence of obesity increased from 5 percent in 1976-1980 to 20.9 percent in 2015-2018, with no significant plateau [3,24].

For preschool-aged children (aged two to five years) in the United States, data from the National Health and Nutrition Examination Survey (NHANES) are mixed but show an overall plateau since the early 2000s (figure 4) [3,25,26]. Modestly decreasing trends in this young age group were reported in various studies and subgroups between 2004-2012 [26-32], but this was followed by resumption of an upward trend through 2018 [3,7].

Despite the plateau in overall prevalence of childhood obesity in the United States, the prevalence of severe obesity continues to increase. Severe obesity among children 2 to 19 years old increased across the NHANES survey from 2.6 percent (1988-1994), to 5.1 percent (2003-2004), to 6.0 percent (2015-2016) [25]. In 2016, 6 percent of children had class II obesity (BMI ≥120 percent of the 95^th percentile or ≥35 kg/m²) and 1.9 percent had class III obesity (BMI ≥140 percent of the 95^th percentile or ≥40 kg/m²) [7].

●Other countries – Worldwide, overweight and obesity in children have generally increased across a wide range of resource-abundant and resource-limited countries during the past 50 years (figure 5 and figure 6A-B), with several higher-income countries reporting more recent plateauing or decreases [19]. The rate at which childhood obesity is increasing in middle- and low-income countries is 30 percent higher than the rate of increase in high-income countries [33,34]. Plateaus in the prevalence of childhood obesity are reported in population studies from Australia [35] and France [36], and decreasing rates were reported in Germany [37], Switzerland [38], Spain [39], and Canada [40]. For preschool-aged children, stable or decreasing trends were reported in New Zealand, Victoria (Australia), England and Germany [41,42].

●Coronavirus disease 2019 (COVID-19)-related changes – The COVID-19 pandemic was associated with increases in childhood obesity in several countries [43-46]. As an example, in a large health care system in California, the prevalence of obesity rose among all age groups during the first year of the pandemic; the greatest change was among children 5 to 11 years old, among whom the prevalence of obesity rose from 19 to 26 percent [43]. Similar trends were seen in a nationwide sample [47]. Other studies report that the pandemic exacerbated risk factors for obesity, disproportionately impacting urban and low-income populations [46,48,49]. (See "COVID-19: Management in children", section on 'Physical health effects'.)

Persistence into adulthood — Many but not all obese children will become obese adults. The likelihood of persistence of childhood obesity into adulthood (sometimes called "tracking") is related to age [50-54], parental obesity [16,55,56], severity of obesity [53,57-59], and BMI trajectory during childhood [60]. These observations provide support for the concept of interventions early in life to prevent and treat obesity. (See "Prevention and management of childhood obesity in the primary care setting", section on 'Evidence for efficacy'.)

Longitudinal studies reveal that a substantial component of adolescent obesity is established before five years of age. In a large study from the United States, children who were overweight at entry into kindergarten were four times as likely to become obese by 8^th grade as compared with those who were not overweight [58]. Moreover, the severity of obesity was an important predictor of persistence. Among children who had mild obesity at entry into kindergarten (mean age 5.6 years), 47 percent remained obese in 8^th grade (mean age 14.1 years). Among those who had severe obesity (BMI 99^th percentile) in kindergarten, more than 70 percent remained obese in 8^th grade (figure 7). Similar findings were reported in a large population study from Germany, in which almost 90 percent of children who were obese at three years of age remained overweight or obese during adolescence [61]. For this group, the greatest acceleration in BMI standard deviation (SD) score occurred between two and six years of age. The analysis did not adjust for other known risk factors for obesity, such as parental weight or poverty. In a separate analysis from the same report, children who were large for gestational age at birth or whose mothers had obesity had particularly high risk for obesity, as has been shown in other studies. A separate long-term study found that obesity at age five years (compared with normal weight) was associated with higher BMI in mid-adulthood (mean BMI difference 6.5 kg/m² at age 50) [54]. The tracking of obesity from age 5 to 50 years was modest (positive predictive value 67 percent). These studies demonstrate that excessive weight gain during the preschool years is a strong predictor of persistent obesity but do not determine whether the association is causal versus a marker of underlying inherent or environmental risk.

Studies with longer-term follow-up reveal that childhood obesity typically persists into adulthood, particularly for children with an obese parent. Among obese six-year-old children with an obese parent, 50 percent remained obese as adults, and among obese 10- to 14-year-old children with an obese parent, 80 percent remained obese as adults [16]. Similar findings were reported in a large international cohort in which 82 percent of individuals who were obese as children (age 11.4±4.0 years) remained obese as adults at follow-up approximately 23 years later [62]. A separate study used data from several large national datasets in the United States to simulate growth trajectories into adulthood and predicted that almost 60 percent of all United States children who are alive today will be obese by the time they reach 35 years of age [53]. The risk for adult obesity increases with age and childhood BMI. For children with severe obesity, tracking is strong and occurs early in life: A two year-old child with severe obesity has an 80 percent chance of being obese at age 35, while a five-year-old child with severe obesity has a 90 percent chance of remaining obese. These long-term studies must be interpreted with caution since the dietary habits and activity levels of today's children may differ from those of the children in the studies, thereby altering the risk of obesity in adulthood [63].

Most adolescents with obesity will continue to have obesity in adulthood. In a study of adolescents from a single city in the United States, obesity persisted into young adulthood in approximately two-thirds of adolescents, while one-third "exited" obesity [64]. The severity of obesity during adolescence is an important predictor of whether the obesity is likely to persist into adulthood [12,53]. In a large population study in the United States, approximately 75 percent of adolescents with severe obesity (BMI >120 percent of the 95^th percentile) continued to have severe obesity as adults (BMI >40 kg/m²) [65]. Meanwhile, 8 percent of adolescents with more moderate obesity developed severe obesity as adults. In adolescents, the tracking of severe obesity is even stronger than in younger age groups [13].

Whether sex affects the risk that obesity will persist into adulthood varies markedly among studies in different populations. In one study from 1980, obesity during adolescence persisted into adulthood for approximately 80 percent of females but only 30 percent of males [66]. This was presumably related to changes in body composition that occur at puberty, when body fat decreases in males and increases in females [67]. However, in later cohorts, obesity in adolescent males is more likely to be persistent and the risk of persistent obesity is similar to that of females [68-70]. In one study from Australia, both males and females who had obesity during adolescence had a 50 to 60 percent chance of having obesity as young adults [70]. However, among adolescents who had overweight but not obesity during adolescence, males were more likely than females to have ongoing obesity during young adulthood (15 versus 12 percent).

Other risk factors for obesity in adulthood are discussed in greater detail separately. (See "Obesity in adults: Etiologies and risk factors".)

ETIOLOGY — The sections below summarize important factors that contribute to obesity in childhood and adolescence. The etiology and pathogenesis of obesity are discussed in greater detail separately. (See "Obesity in adults: Etiologies and risk factors" and "Obesity: Genetic contribution and pathophysiology".)

Environmental factors — Almost all obesity in children is strongly influenced by environmental factors, either a sedentary lifestyle or a caloric intake that is greater than needs. The contributions of specific environmental influences are the subject of considerable discussion and research. Environmental factors explain only part of obesity risk but are important targets for treatment because they are potentially modifiable [71,72].

Increasing trends in glycemic index of foods, sugar-containing beverages, portion sizes for prepared foods, and fast food service; diminishing family presence at meals; decreasing structured physical activity; increasing use of computer-, electronic-, and/or digital-oriented play activity; school meal nutrition content; and elements of the built environment (eg, availability of sidewalks and playgrounds) have all been considered as causal influences on the rise in obesity [72,73]. In particular, a number of well-designed studies have shown associations between intake of sugar-containing beverages or low physical activity and obesity or metabolic abnormalities [74-81]. Causal associations seem likely but are difficult to establish with certainty. Evidence supporting each of these factors is summarized in the sections below.

Sugar-sweetened beverages — Accumulating evidence suggests that consumption of sugar-sweetened beverages (including fruit juice) is an important contributor to the development of obesity in some individuals [82-84]. according to nationally representative surveys of children in the United States, sugar-sweetened beverages supplied an average of 270 kcal/day, representing 10 to 15 percent of total caloric intake [85]. Moreover, a randomized trial demonstrated that reducing consumption of sugar-sweetened beverages among adolescents with overweight and obesity was associated with a modest decrease in body mass index (BMI) [86]. In a separate randomized trial in 5- to 12-year-old children (primarily normal-weight), consumption of one serving of an artificially sweetened beverage daily was associated with less weight gain and fat accumulation as compared with consumption of a sugar-sweetened beverage [87].

In each of these studies, the observed effect sizes were small. Nonetheless, these findings support the concept that population-focused approaches to reduce intake of sugar-sweetened beverages, such as changes in school or public policy, including taxation, could be beneficial [88-92].

Recreational screen media use — Devices and format for screen media use continue to evolve, and all recreational (ie, not school-related) screen use should probably be considered together when setting goals for clinical purposes. One randomized study suggests that if a substantial reduction in screen media use can be achieved, it effectively increases physical activity [93].

Other studies associating screen time with obesity focused on specific types of media:

●Television – Television viewing is perhaps the best-established environmental influence on the development of obesity during childhood. The amount of time spent watching television or the presence of a television in a child's bedroom are directly related to the prevalence of obesity in children and adolescents [94-100], although some other studies found only a weak correlation [101-103]. The effects may persist into adulthood: In two longitudinal cohort studies, television viewing at ≥5 years was independently associated with increased BMI at age 26 to 30 years [104,105].

Several mechanisms have been proposed to explain this association [106-109]:

•Displacement of physical activity

•Depression of metabolic rate

•Adverse effects on diet quality (purported mechanism is that food consumption may not be appetite-driven in this setting, eg, prompted by food commercials)

•Effects of television on sleep

One study provides evidence that the effects of television on obesity are mediated primarily by changes in energy intake. In a randomized trial, reducing television viewing and computer use among overweight four- to seven-year-old children was effective in reducing both BMI and energy intake during the two-year intervention, without apparent changes in physical activity [107]. Similar associations between television viewing and energy intake have been shown in studies of older or non-overweight youth [110].

●Video games – The use of electronic games also has been associated with obesity during childhood [111,112]. The effect is small and may be mediated in part through increased consumption of sugar-sweetened beverages and irregular bedtimes [112]. In the few studies that analyze the influences separately, the association with obesity is somewhat weaker for electronic games than for television [98,111,113,114], perhaps because the games do not include food advertising.

●Exergames – A few video games are designed to require interactive physical activity by the player; these are sometimes called "exergames" [115].

The efficacy of exergames to increase physical activity or treat obesity has not been systematically studied. A few studies suggest that they generally induce a small or moderate increase in energy expenditure during playing time [116-120]. As examples, two studies found that energy expenditure of playing some common sport-simulating exergames was higher than that of sedentary games but not as high as playing the sport itself [118,121]. The energy expenditure depends on the game: In one study, energy expenditure during six different activity-enhancing games ranged from 4.2 metabolic equivalents (mets) for Wii boxing to 7.1 mets for Sportwall, compared with 4.9 mets for walking at 3 miles/hour [122].

The long-term effect of activity-enhancing games probably depends on the intensity and participant enjoyment of the game, activities replaced by the gaming, and motivating support systems. One report described good patient retention and clinically significant reductions in BMI among adolescent patients participating in a multifaceted obesity management program, which featured one-hour group exergaming sessions or provision of exergame equipment for home use [123]. A systematic review of controlled trials of exergaming interventions reported mixed outcomes; 4 of 10 trials reported statistically significant beneficial effects on weight outcomes over 12 to 24 weeks [115].

Sleep — Mounting evidence suggests an association between shortened sleep duration or irregular sleep schedules and obesity. This association has been shown in multiple cross-sectional studies, after adjustment for a number of potential environmental confounders [73,124-128]. The effects are more marked in children at the upper end of the weight range [129]. Similar findings have been seen in adult populations [130]. Moreover, several longitudinal studies also showed associations after adjustment for confounders, suggesting that the association may be causal [131-140]. As an example, in a large longitudinal study among preschool-aged children with early bedtimes (8:00 PM or earlier), 10 percent developed obesity by adolescence, compared with 23 percent of those with late bedtimes (9:00 PM or later) [137]. Children with early bedtimes had a relative risk of adolescent obesity of 0.48 compared with late bedtimes, after adjustment for several confounding variables, including maternal obesity, maternal education, and income level. Additional support for a causal association comes from a short-term experimental study in which sleep deprivation for one week was associated with increased food intake, weight gain, and higher leptin levels as compared with the child's usual sleep [141]. Behavioral strategies for improving sleep in children are discussed in a separate topic review. (See "Behavioral sleep problems in children".)

Sleep may have an association with insulin resistance and cardiometabolic risk factors, independent of its association with obesity. In several studies of adolescents with obesity and sleep-disordered breathing, sleep fragmentation and intermittent hypoxemia were associated with decreased insulin sensitivity, independent of adiposity [128,142-145]. Similarly, shorter sleep duration was associated with markers of cardiometabolic risk factors, including abdominal obesity, increased blood pressure, and abnormal lipid profile [146].

The mechanism for an association between sleep duration and obesity has not been established but may include alterations in serum leptin and ghrelin levels, both of which have been implicated in the regulation of appetite. Sleep deprivation is also associated with increased neural reward processing, which may lead to increased food intake in susceptible individuals [147]. Alternatively, short sleep duration may be associated with reduced physical activity levels and/or provide a longer opportunity to ingest food. (See "Obesity in adults: Etiologies and risk factors", section on 'Sleep patterns'.)

Medications — A number of drugs can cause weight gain, including certain psychoactive drugs (particularly olanzapine and risperidone), antiseizure medication, and glucocorticoids (table 3). Weight gain and hyperlipidemia induced by olanzapine may be particularly severe in adolescents as compared with adults [148]. Brief courses of oral or inhaled glucocorticoids (eg, several days for an exacerbation of asthma) are unlikely to have long-term effects on body weight unless they are prescribed frequently. Medication-induced weight gain is discussed separately. (See "Obesity in adults: Etiologies and risk factors", section on 'Medications associated with weight gain' and "Schizophrenia in adults: Maintenance therapy and side effect management", section on 'Endocrinologic and metabolic side effects' and "Schizophrenia in adults: Maintenance therapy and side effect management", section on 'Metabolic dysregulation'.)

Other — Other environmental factors that have been proposed as possible contributors to obesity include the influences of gut microbiota, environmental toxins, and viruses. The role of each of these factors remains speculative but is supported by preliminary evidence and is the subject of ongoing investigation.

●Gut microbiome – Several lines of investigation have suggested that there is a relationship between the gut microbiome and the potential for weight gain [149-151]. Several observational studies have suggested an association between obesity and exposure to antibiotics (or maternal infection) during gestation [152-155] or infancy [152,156-161]. Contrasting results were seen in another large study, which found no such association including in a secondary analysis of twin pairs [162]. If there is an association, the effect size appears to be small and may not be clinically important.

Studies in animal models generally support the possibility of an association between the gut microbiome and weight gain or loss. These include studies on antibiotic exposure [163,164] and models of gastric bypass surgery [165-167].

●Toxins – Epidemiologic studies raise the possibility that obesity could be triggered or exacerbated by exposure to environmental endocrine-disrupting chemicals, such as the pesticide dichlorodiphenyltrichloroethane (DDT) [168] or bisphenol A (BPA). BPA is a compound used to manufacture polycarbonate resin and is a common contaminant of foods sold in cans and plastic packaging [169]. Most individuals in the United States have detectable levels of BPA in urine, and most of the exposure is from food [170]. Experimental studies in cell culture and animals suggest that BPA is a selective modulator of estrogen receptors and accelerates adipogenesis and postnatal somatic growth [171-173]. Epidemiologic studies in adults and children demonstrate an association between urinary BPA concentrations and obesity or obesity-related diseases, including diabetes and cardiovascular disease [174-177]. It is possible that the observed association is due to dietary or environmental variables that were not included in the analysis, or by increased storage of BPA in adipose tissue among obese individuals, rather than a direct causal effect. (See "Endocrine-disrupting chemicals".)

Exposure to such endocrine-disrupting chemicals could also be a mechanism for the "metabolic programming" phenomenon described below. (See 'Metabolic programming' below.)

●Viruses – A few studies suggest the possibility that obesity can be triggered or exacerbated by exposure to a virus. Adenovirus 36 increases body fat in several animal models, and human studies have found conflicting results about an association between the presence of this serotype and obesity. These data are discussed in a separate topic review. (See "Pathogenesis, epidemiology, and clinical manifestations of adenovirus infection", section on 'Possible association with obesity'.)

Genetic factors

●Polygenic factors – There is strong evidence that genetic factors play a permissive role and interact with environmental factors to produce obesity. Studies suggest that heritable factors are responsible for 40 to 85 percent of the variation in adiposity [178], but most of the genetic polymorphisms responsible have not yet been isolated. Thus, genetic contributions to common obesity likely exist, but most of the molecular mechanisms for these factors have yet to be determined. Moreover, genetic and environmental factors interact, such that a healthy home environment can attenuate the effect of genetic factors. In a large study of twin pairs, the heritability of BMI was greater among children living in obesogenic home environments compared with those living in healthier environments during early childhood [179]. (See "Obesity: Genetic contribution and pathophysiology", section on 'Common (multifactorial) obesity'.)

●Syndromic obesity – A variety of specific syndromes in which obesity is a primary manifestation have been identified (table 4). These are rare causes of obesity, accounting for less than one percent of childhood obesity in tertiary care centers [24,180,181]. Obesity is also a component of several relatively common genetic syndromes, including Down syndrome.

In addition to being overweight, children with genetic syndromes associated with obesity typically have early-onset obesity and characteristic findings on physical examination. These include dysmorphic features, short stature, developmental delay, intellectual disability, retinal changes, or deafness. Prader-Willi is the most common of these syndromes and is characterized by hypotonia and feeding difficulties during infancy (often with failure to thrive), with hyperphagia and obesity developing during early childhood, with developmental delay. For most of the syndromes, including Prader-Willi and Bardet-Biedl syndromes, the genetic cause has been sufficiently isolated to permit specific testing, but the exact mechanism through which they cause obesity is not understood or is attributable to multiple genes (table 4). (See "Prader-Willi syndrome: Management".)

●Monogenic obesity – Single-gene defects in which obesity is the primary manifestation are even more rare (table 5). Several of these affect the melanocortin pathway in the central nervous system. Melanocortin 4 receptor defects (MIM *155541) are the most common but are still rare, contributing to obesity in approximately 2 to 6 percent of individuals with early-onset obesity [182-185]. Mutations causing deficiencies in leptin (MIM #614692) or its receptor (MIM #614963) are rare and usually are associated with consanguinity [186-188]. (See "Obesity: Genetic contribution and pathophysiology", section on 'Monogenic forms of obesity'.)

Endocrine disorders — Endocrine causes of weight gain are identified in less than 1 percent of children and adolescents with obesity [181,189]. These disorders usually are associated with overweight or mild obesity rather than severe obesity (table 6). Most children with these problems have short stature and/or hypogonadism [181]. The primary considerations are:

●Cortisol excess (eg, the use of corticosteroid medication, Cushing syndrome) (see "Epidemiology and clinical manifestations of Cushing syndrome")

●Hypothyroidism (see "Acquired hypothyroidism in childhood and adolescence")

●Growth hormone deficiency (see "Diagnosis of growth hormone deficiency in children")

●Pseudohypoparathyroidism type 1a (Albright hereditary osteodystrophy) (see "Etiology of hypocalcemia in infants and children", section on 'End-organ resistance to PTH (pseudohypoparathyroidism)')

Hypothalamic obesity — Hypothalamic lesions may cause rapidly progressive severe obesity, which is particularly difficult to treat (table 6). In the pediatric age group, hypothalamic obesity most often arises after surgical treatment for craniopharyngioma and usually is associated with panhypopituitarism. Similar patterns may be caused by trauma, tumor, or an inflammatory disease affecting the hypothalamus. (See "Craniopharyngioma" and "Obesity in adults: Etiologies and risk factors", section on 'Hypothalamic obesity'.)

A rare cause of hypothalamic obesity is a syndrome consisting of rapid-onset obesity, hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD), which may be associated with neuroendocrine tumors, leading to the expanded acronym, ROHHADNET. Patients may present in infancy or early childhood with central hypoventilation (resembling congenital central hypoventilation syndrome) and a variety of abnormalities in the hypothalamic-pituitary axis, with autonomic dysregulation, including episodes of hyperthermia or hypothermia (table 7) [190,191]. (See "Congenital central hypoventilation syndrome and other causes of sleep-related hypoventilation in children", section on 'Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD)'.)

Metabolic programming — There is increasing evidence that environmental and nutritional influences during critical periods in development can have permanent effects on an individual's predisposition to obesity and metabolic disease. The precise mediators and mechanisms for these effects have not been established but are the subject of ongoing investigations [192,193]. This phenomenon has been called "metabolic programming" and may account for a component of intergenerational transmission of obesity via epigenetic mechanisms (see "Principles of epigenetics"), in addition to genetic and environmental factors. The best evidence for metabolic programming focuses on gestation. There is modest information about effects during infancy and early childhood and minimal information about any effects during later life stages. Examples of the evidence supporting metabolic programming of body weight are provided in the following sections.

Gestation — Maternal body weight and nutritional factors during gestation are probably an important determinant of metabolic programming. Several key areas demonstrate the link between the intrauterine environment and child health and weight:

●Effect of maternal nutrition during pregnancy – During the Dutch famine of 1944 to 1945, exposure to famine during early gestation (first trimester) was associated with obesity, metabolic disease, and cardiovascular mortality and overall mortality [194-198], while exposure to famine at any stage of gestation was associated with higher rates of insulin resistance [199,200].

●Effect of maternal prepregnancy weight – Some studies suggest that a mother's prepregnancy weight and weight gain during pregnancy are predictors of the child's birth weight and/or weight during childhood [201], and the association persists after adjusting for genetic and other prenatal environmental factors [202-207]. However, another large study found a minimal effect of incremental increases in maternal BMI during pregnancy on offspring BMI during childhood, after rigorous adjustment for genetic factors [208]. (See "Gestational weight gain".)

The possibility of a causal relationship between the intrauterine environment and obesity in the offspring is supported by studies in women who have had gastric bypass surgery: Children born to women who have had gastric bypass surgery appear to have a lower prevalence of obesity than those born before the gastric bypass, suggesting that reversal of maternal obesity had beneficial long-term effects on the metabolic profile of the offspring [209]. In contrast, a separate study was unable to detect an effect of maternal BMI on metabolic programming in the offspring: Mother-offspring associations for BMI were equally as strong as the father-offspring association, suggesting that the effect was not mediated through the intrauterine environment [210]. Thus, the mechanism involved in the intergenerational transmission of obesity is complex and/or difficult to detect in clinical studies in humans.

●Association of birth weight with long-term metabolic outcomes – Individuals born small for gestational age, large for gestational age, or prematurely have higher rates of insulin resistance during childhood and young adulthood, even after controlling for obesity status [202,211-213], as well as associations between birth weight (reflecting fetal nutrition) and later diabetes, heart disease, insulin resistance, and obesity [214-218].

●Association with other maternal endocrine factors – Other markers of the maternal endocrine milieu are also associated with childhood obesity, although the mechanisms for the association are not established, as illustrated by the following studies:

•Maternal diabetes mellitus during gestation is associated with an increased BMI in adult male offspring, independent of maternal BMI in early pregnancy [219].

•Maternal preeclampsia, with or without prematurity, is associated with higher BMI in the offspring by adolescence [220,221]. Studies conflict in their results as to whether this association is limited to male [221,222] or female offspring [223].

Infancy and early childhood — Infancy and early childhood may also be critical periods for metabolic programming. Studies in a variety of populations have shown consistent associations between rates of weight gain during infancy or early childhood and subsequent obesity or metabolic syndrome during early childhood [224-226], adolescence, or adulthood [227] (for systematic reviews, see references [228-231]), or with intermediate outcomes such as adiposity, blood pressure, and other cardiovascular risk factors in early childhood [232-235].

In particular, some (but not all) studies suggest that breastfeeding has a protective effect against childhood obesity, as detailed in a separate topic review (see "Infant benefits of breastfeeding", section on 'Limited evidence for benefit'). Other studies suggest that this effect may be mediated by protein intake since high protein intakes during the first two years of life appear to promote weight gain (although not necessarily adiposity) [236-238]. In a randomized trial, formulas with standard concentrations of protein (11.7 percent of energy for infant formula and 17.6 percent of energy for follow-on formula) were associated with higher BMI at school age compared with formulas with lower concentrations of protein that are similar to breast milk (7.1 percent of energy for infant formula) [236,237]. It should be noted that these studies did not determine whether the difference in weight was attributable to adipose versus lean mass.

Clinical implications — The above evidence describing metabolic programming during gestation and early life suggest that early intervention might be an important tool in preventing obesity.

Controlled trials of early nutritional interventions with long-term outcomes are still lacking. Nonetheless, there is ample circumstantial evidence to support clinical efforts to optimize nutrition during gestation, infancy, and early childhood. Appropriate goals are to optimize glycemic control in pregnant women and target moderate rates of weight gain in infants and young children. Breastfeeding may have a protective effect on the later development of obesity, in addition to its many other benefits to the infant. The effect appears to be small, and the mechanism of the association is unclear. (See "Infant benefits of breastfeeding", section on 'Chronic disease' and "Prevention and management of childhood obesity in the primary care setting", section on 'Prevention'.)

Nutritional goals are less clear for low birth weight infants, for whom catch-up growth is associated with improved neurodevelopmental outcomes but also with increased risks for metabolic disease [239-242]. Increasing the protein component of feeding (eg, a maximum protein content of 3.6 g/100 kcals) appears to improve growth and metabolic health, including normalizing serum insulin-like growth factor 1 (IGF-1) concentrations [239]. This strategy has been proposed to achieve improved neurodevelopmental and metabolic outcomes for these infants, but it is not yet tested. (See "Nutritional composition of human milk and preterm formula for the premature infant", section on 'Protein'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Obesity in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Weight and health in children (The Basics)")

SUMMARY

●Body mass index (BMI) – BMI is the accepted standard measure of overweight and obesity for children two years of age and older. BMI provides a guideline for weight in relation to height and is equal to the body weight (in kilograms) divided by the height (in meters) squared (table 1). Reference standards vary by age and sex (figure 1A-B). (See 'Definitions' above.)

●Weight categories – For children between 2 and 20 years of age, the following weight categories are used (table 2) (see 'Definitions' above):

•Overweight – BMI between the 85^th and 95^th percentile for age and sex.

•Obesity – Classified by severity, using the following thresholds ( (figure 2A-B) or CDC extended BMI growth charts):

-Class I: BMI ≥95^th percentile for age and sex or BMI ≥30 (whichever is lower)

-Class II: BMI ≥120 percent of the 95^th percentile values or BMI ≥35 (whichever is lower)

-Class III: BMI ≥140 percent of the 95^th percentile values or BMI ≥40 kg/m² (whichever is lower)

●Epidemiology

•Prevalence – Approximately one-third of children and adolescents in the United States are either overweight or obese (figure 3). The prevalence of obesity among children and adolescents tripled from the late 1970s to 2000 and subsequently plateaued for most age and weight categories, although the prevalence of severe obesity continues to increase (figure 4). Several regions or subpopulations have shown slight decreases in childhood obesity since 2008. The prevalence of childhood overweight and obesity also increased in many other resource-abundant countries worldwide (figure 5). (See 'Prevalence' above.)

•Tracking – The likelihood of persistence of childhood obesity into adulthood is related to age, parental obesity, and severity of obesity. A substantial component of adolescent obesity is established before five years of age. (See 'Persistence into adulthood' above.)

●Etiology of obesity

•Environmental factors – Factors that contribute to obesity include increasing trends in glycemic index of foods, sugar-containing beverages, larger portion sizes for prepared foods, fast food service, diminishing family presence at meals, decreasing structured physical activity, increased sedentary activities (eg, screen time), shortened sleep duration, and changes in elements of the built environment (eg, availability of sidewalks and playgrounds). For a few children, medications (eg, certain psychoactive drugs) have an important causal role. (See 'Environmental factors' above and 'Medications' above.)

•Genetic factors – Genetic factors play a permissive role and interact with environmental factors to produce obesity. Studies suggest that heritable factors are responsible for 40 to 85 percent of the variation in adiposity, but most of the genetic polymorphisms responsible have not yet been isolated. A few specific syndromes and single-gene defects which are linked to obesity in childhood have been identified (table 4 and table 5). (See 'Genetic factors' above.)

•Endocrine causes – Endocrine disorders are identified in less than 1 percent of children and adolescents with obesity. The disorders include hypothyroidism, cortisol excess (eg, the use of corticosteroid medication, Cushing syndrome), growth hormone deficiency, and pseudohypoparathyroidism. Most children with these problems have short stature and/or hypogonadism (table 6). (See 'Endocrine disorders' above.)

•Hypothalamic obesity – Hypothalamic lesions tend to cause rapidly progressive severe obesity, which is particularly difficult to treat. In the pediatric age group, hypothalamic obesity most often arises after surgical treatment for craniopharyngioma and usually is associated with panhypopituitarism. Similar patterns may be caused by trauma, tumor, or an inflammatory disease affecting the hypothalamus. (See 'Hypothalamic obesity' above.)

•Metabolic programming – Metabolic programming refers to the concept that environmental and nutritional influences during critical periods in development, particularly during gestation, can have permanent effects on an individual's predisposition to obesity and metabolic disease. (See 'Metabolic programming' above.)