Overview of the health consequences of obesity in children and adolescents

Authors:: Joseph A Skelton, MD, MS; William J Klish, MD
Section Editor:: Mitchell E Geffner, MD
Deputy Editor:: Alison G Hoppin, MD

Literature review current through: Jan 2024.

This topic last updated: Oct 27, 2023.

INTRODUCTION — Obesity has become one of the most important public health problems in the United States (figure 1) [1] and many other countries [2]. As the prevalence of obesity increases, so does the prevalence of associated comorbidities, resulting in an enormous burden of obesity-related disease worldwide [2]. For this reason, it is imperative that clinicians identify children with overweight and obesity so that counseling and treatment can be provided. Certain comorbidities such as type 2 diabetes mellitus (T2DM) and steatohepatitis that were once considered "adult diseases" are now regularly seen in children with obesity. Moreover, obesity during adolescence increases the risk for cardiovascular disease and premature death during adulthood, independent of obesity during adulthood [3-10].

This topic presents an overview of the comorbidities of obesity in children and adolescents, which include abnormalities in cardiovascular, dermatologic, endocrine, gastrointestinal, neurologic, orthopedic, psychosocial, and pulmonary health, as well as functional limitations (table 1) [11]. Evaluation and monitoring for these comorbidities are important components of health care for individuals with obesity. (See "Clinical evaluation of the child or adolescent with obesity".)

The clinical evaluation for these comorbidities is summarized in the table (table 2) and described in more detail in a separate topic review. (See "Clinical evaluation of the child or adolescent with obesity".)

UpToDate topics with related material include:

●(See "Definition, epidemiology, and etiology of obesity in children and adolescents".)

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

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

●(See "Overweight and obesity in adults: Health consequences".)

DEFINITIONS — In the discussion that follows, the term "obesity" refers to children with body mass index (BMI) ≥95^th percentile for age and sex and the term "overweight" refers to children with BMI between the 85^th and 95^th percentile for age and sex, unless otherwise noted. Calculation of BMI and definitions of obesity and severe obesity (often categorized as class 1, 2, or 3 obesity) are discussed in detail separately. (See "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Definitions'.)

CARDIOVASCULAR — Obesity in children and adolescents is associated with a number of cardiovascular changes that are linked to increased cardiovascular risk in adulthood. Two cardiovascular risk factors, hypertension and dyslipidemia, are components of the metabolic syndrome. A minority of children and adolescents with obesity have no evidence of cardiovascular risk factors (termed "metabolically healthy obesity"). These individuals also show no signs of preclinical atherosclerotic disease (as measured by carotid intima-media thickness) and tend to remain metabolically healthy in adulthood [12]. Cardiovascular risk in children is stratified based on multiple risk factors including obesity, lipids, blood pressure, and the presence of other comorbidities. Understanding this risk stratification can guide assessment and management of these cardiovascular risk factors. (See "Overview of the management of the child or adolescent at risk for atherosclerosis".)

Hypertension — The risk of hypertension (table 3) is increased in children and adolescents with overweight and obesity and increases with the severity of obesity [13-15]. In a cross-sectional study, the prevalence of hypertension was approximately 4 percent in children with moderate obesity and 9 percent in those with severe obesity [16]. Similarly, the risk of hypertension is approximately twofold higher in children with mild obesity and fourfold higher in those with severe obesity compared with children with normal weight status [17]. When hypertension is assessed using ambulatory blood pressure monitoring, approximately 50 percent of children with obesity have hypertension [18,19]. When casual office blood pressure measurements are used, substantially fewer cases of hypertension are detected [20]. This discrepancy, termed "masked" hypertension, is particularly common in children with obesity and has clinically important consequences. (See "Ambulatory blood pressure monitoring in children", section on 'Masked hypertension'.)

The presence of hypertension during childhood predicts hypertension and metabolic syndrome during adulthood, even after adjustment for body mass index (BMI) during childhood [21]. The presence of obesity during childhood also predicts hypertension during adulthood, but that risk resolves if the individual loses weight by adulthood [22,23]. The evaluation and management of hypertension in children and adolescents is discussed separately. (See "Definition and diagnosis of hypertension in children and adolescents" and "Nonemergent treatment of hypertension in children and adolescents".)

Dyslipidemia — Dyslipidemia occurs among children and adolescents with overweight and obesity, particularly those with a central fat distribution [15,24] and increased adiposity (as measured by triceps skinfold thickness ≥85^th percentile) [25]. The typical pattern is one of elevated concentrations of serum low-density lipoprotein (LDL)-cholesterol and triglycerides and a decreased concentration of high-density lipoprotein (HDL)-cholesterol [13,15]. The risk for these abnormalities increases with the severity of obesity [14]. (See "Dyslipidemia in children and adolescents: Definition, screening, and diagnosis".)

The evaluation of dyslipidemia in children and adolescents with obesity includes measurement of a fasting lipid panel (total cholesterol, triglycerides, and HDL-cholesterol) (algorithm 1A-B). Treatment for dyslipidemia is discussed separately. (See "Clinical evaluation of the child or adolescent with obesity", section on 'Routine blood tests' and "Dyslipidemia in children and adolescents: Management" and 'Society guideline links' below.)

Cardiac structure and function — Obesity in children is associated with alterations in cardiac structure and function that are similar to those seen in middle-aged adults. Findings include increased left ventricular mass, which is seen in both hypertensive and nonhypertensive children with obesity [13,26-31]; increased left ventricular and left atrial diameter; greater epicardial fat; and systolic and diastolic dysfunction [31,32].

Premature atherosclerotic cardiovascular disease — Childhood obesity is also associated with several markers for subclinical atherosclerosis. These include endothelial dysfunction, carotid intima-media thickening, premature development of aortic and coronary arterial fatty streaks and fibrous plaques, and increased arterial stiffness [19,33-35]. For individuals with obesity during childhood and adolescence, the intima-media thickening persists even if they lose weight by adulthood [23]. These observations lend support to the idea that atherosclerotic processes begin at an early age and are associated with obesity, inflammation, hypertension, and abnormal lipid profiles [36,37]. Even modest degrees of excess adiposity contribute to cardiovascular risk. One study demonstrated that cardiovascular risk factors are elevated in youth who are overweight (BMI 85^th to 95^th percentile), with further abnormalities in those with obesity (BMI ≥95^th percentile) [38] and increasing with severe obesity [14]. Insulin resistance is an independent risk factor for premature carotid atherosclerosis, after adjustment for a variety of other cardiovascular risk factors, including hypertension and dyslipidemia [39,40]. (See "Overview of risk factors for development of atherosclerosis and early cardiovascular disease in childhood".)

Adult cardiovascular disease — The studies outlined above describe intermediate cardiovascular outcome; increasing evidence demonstrates an association between obesity during childhood and cardiovascular disease during adulthood.

The origins of adult cardiovascular disease begin in childhood and adolescence, with evidence that the presence of high BMI in adolescence is associated with cardiovascular disease and acute cardiovascular events in adulthood [41-44], even when controlling for adult BMI [41]. Other studies have also shown an increased prevalence of cardiovascular risk factors for adults who first developed obesity during childhood, although resolution of that obesity decreased those risks [22]. A predictive model estimated that the prevalence of coronary heart disease in the United States will increase 5 to 16 percent by 2035, with more than 100,000 excess cases attributable to the increase in childhood obesity [45].

DERMATOLOGIC

Acanthosis nigricans — Acanthosis nigricans (picture 1A-B) is a common skin abnormality in individuals with obesity and is associated with insulin resistance. The pathophysiology, diagnosis, and management of acanthosis nigricans are discussed separately. (See "Acanthosis nigricans".)

Other — Other dermatologic comorbidities of obesity include striae distensae (stretch marks), intertrigo, furunculosis, and hidradenitis suppurativa. Striae are common and are caused by mechanical factors (skin distension), possibly acting in concert with hormonal factors such as relatively high levels of adrenocorticosteroids [46]. Hidradenitis suppurativa is characterized by inflammatory nodules or deep fluctuant cysts in the intertriginous skin of the axillae and groin (picture 2). (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis" and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Intertrigo".)

ENDOCRINE — Endocrine comorbidities of obesity in children and adolescents include impaired glucose tolerance, diabetes mellitus, hyperandrogenism in females, and abnormalities in growth and puberty.

Type 2 diabetes mellitus — Subclinical insulin resistance (as occurs with prediabetes) is common among adolescents with obesity and is an important predictor of developing type 2 diabetes mellitus (T2DM) during adulthood. T2DM is diagnosed in only a small minority of adolescents but has important clinical implications, including more rapid progression of diabetes-related complications compared with adult-onset T2DM. Definitions of prediabetes and diabetes are shown in the tables (table 4A-B). (See "Epidemiology, presentation, and diagnosis of type 2 diabetes mellitus in children and adolescents".)

Prevalence and association with obesity — The reported prevalence of prediabetes and T2DM in children with obesity varies considerably, presumably because of different degrees of obesity, racial and ethnic variation, and age range of the sampled population [47-50]. Prevalence rates also vary somewhat depending on the method used to detect dysglycemia.

In the United States, the prevalence of T2DM in youth 10 to 19 years old rose from 0.34 cases per 1000 in 2001 to 0.46 cases per 1000 in 2017 [51]. This trend follows but lags behind the rise of severe obesity in this population. (See "Epidemiology, presentation, and diagnosis of type 2 diabetes mellitus in children and adolescents".)

Estimated prevalence of prediabetes in the United States is difficult to determine, but one study found that nearly 18 percent of adolescents had prediabetes (not differentiating between type 1 diabetes and T2DM) [52]. The association of prediabetes with obesity severity was illustrated by a population-based study of adolescents 12 to 19 years in the United States [14]. Prediabetes (defined as hemoglobin A1c >5.7 percent) was reported in 3 percent of subjects with class I obesity (body mass index [BMI] ≥95^th percentile), 6 percent of those with class II obesity (BMI ≥120 to <140 percent of the 95^th percentile), and 13 percent of those with class III obesity (BMI ≥140 percent of the 95^th percentile). Moreover, there is evidence that youth with obesity have impaired insulin sensitivity even below the thresholds that are used to define prediabetes [53-55].

A longitudinal study of young men in Israel indicates an association between BMI during adolescence and later development of T2DM [41]. This association was seen even within the range of BMI that is considered normal. Interestingly, the association disappeared after adjusting for BMI during adulthood, suggesting that T2DM is primarily associated with obesity at or near the time of diagnosis, rather than the effects of chronic obesity since childhood.

Clinical implications of prediabetes — Children and adolescents who meet criteria for prediabetes (table 4A) should be monitored closely. The first and most appropriate approach to prevent development of T2DM in individuals with obesity is lifestyle modification (predominantly exercise and weight loss), which was shown to have modest efficacy based on large studies in adults. Pharmacologic intervention with metformin is less effective but may be appropriate for select patients. The efficacy of these interventions for preventing T2DM has been studied only in adults. (See "Prevention of type 2 diabetes mellitus".)

The likelihood that prediabetes in an adolescent with obesity will progress to T2DM is not well established. In one small study, 25 percent of youth with prediabetes and obesity progressed to diabetes over two years, while almost 50 percent reverted to normal glucose tolerance [55]. In adults with obesity and prediabetes, almost 30 percent progress to T2DM over three years [56].

Clinical implications of type 2 diabetes — Early diagnosis of T2DM (table 4B) is imperative because aggressive treatment can slow the development of complications including progressive neuropathy, retinopathy, nephropathy, and atherosclerotic cardiovascular disease [57]. Moreover, individuals who present with T2DM during adolescence appear to have more rapid progression of diabetes-related complications as compared with those who present later in life. As an example, among adolescent patients with newly diagnosed T2DM, a large percentage had comorbidities (13.0 percent had microalbuminuria, 80.5 percent had dyslipidemia, and 13.6 percent had hypertension) [58]. (See "Management of type 2 diabetes mellitus in children and adolescents".)

Metabolic syndrome — The "metabolic syndrome" is a term used to describe the clustering of metabolic risk factors for T2DM and atherosclerotic cardiovascular disease in adults: abdominal obesity, hyperglycemia, dyslipidemia, and hypertension. Clustering of cardiovascular risks also occurs in children and adolescents, particularly those with obesity [59,60]. The presence of obesity in early childhood predicts increased risk for metabolic syndrome and other biomarkers of cardiometabolic risk in early adolescence [61]. Several studies estimate that approximately 10 percent of United States adolescents have metabolic syndrome, as defined by modifications of adult criteria [62-64]. However, because puberty is associated with changes in several of the traits that characterize metabolic syndrome, there is considerable instability to the diagnosis. In one study, approximately one-half of the adolescents initially classified as having metabolic syndrome lost the diagnosis during a three-year observation period, while others acquired the diagnosis [65].

The long-term implications of the metabolic syndrome in children and adolescents are unknown. As a result, screening and treatment should be focused on the individual cardiometabolic risk factors (obesity, dysglycemia, dyslipidemia, and hypertension), while recognizing that these are often clustered together [60]. The metabolic syndrome-associated cardiometabolic risks can be addressed by following recommendations for addressing obesity itself and for each of these risk factors, with special attention to children with multiple risk factors. (See 'Cardiovascular' above.)

Several different sets of criteria have been used to define the metabolic syndrome in adolescents (table 5) [66,67]. These and other aspects of the metabolic syndrome are discussed in detail separately. (See "Metabolic syndrome (insulin resistance syndrome or syndrome X)", section on 'Children and adolescents'.)

Hyperandrogenism — Adolescent females with obesity are at increased risk of hyperandrogenism and early-onset polycystic ovary syndrome (PCOS). Upwards of 7 percent of reproductive-age women are affected by PCOS, and the risk increases with increasing obesity. In a large cohort study of adolescents in California, PCOS was diagnosed in approximately 1 to 2.5 percent of females with moderate obesity and 3 to 5.7 percent of those with extreme obesity [68]. PCOS can include a variety of clinical abnormalities, including menstrual irregularities, acne, hirsutism, acanthosis nigricans, and seborrhea. In some patients, the diagnosis may be difficult to establish during adolescence. The clinical manifestations, diagnosis, and management of PCOS in adolescents are discussed separately. (See "Definition, clinical features, and differential diagnosis of polycystic ovary syndrome in adolescents" and "Diagnostic evaluation of polycystic ovary syndrome in adolescents" and "Treatment of polycystic ovary syndrome in adolescents".)

The association of obesity with PCOS is partially responsible for the association between obesity and reduced fertility in adult women.

Growth and puberty — Obesity in children and adolescents may be accompanied by accelerated linear growth and bone age [69]. It is uncertain whether this accelerated growth results in stature different than that which is genetically programmed. (See "The child with tall stature and/or abnormally rapid growth", section on 'Obesity'.)

Overweight has been associated with early onset of sexual maturation in females [70,71]. However, this relationship is inconsistent [72]. The relationship between obesity and pubertal onset in males is also inconsistent [70,73]. (See "Normal puberty", section on 'Trends in pubertal timing'.)

GASTROINTESTINAL

Metabolic dysfunction-associated steatotic liver disease (nonalcoholic fatty liver disease) — Obesity is associated with a clinical spectrum of liver abnormalities collectively known as metabolic dysfunction-associated liver disease (MASLD), which was previously known as nonalcoholic fatty liver disease [74]. MASLD is the most common cause of liver disease in children [75-77]. It is subdivided into three categories, defined by histologic findings: steatotic liver disease alone, metabolic dysfunction-associated steatohepatitis (MASH), and MASH with fibrosis or cirrhosis (table 6). The prevalence of MASLD is approximately 7 percent among children and adolescents in the general population and up to 34 percent among children with obesity [78]. The screening, evaluation, and management of MASLD in children and adolescents are discussed in a separate topic review. (See "Metabolic dysfunction-associated steatotic liver disease in children and adolescents".)

Cholelithiasis — Obesity is the most common cause of gallstones in children without predisposing conditions (eg, hemolytic anemia, history of parenteral nutrition) [79-81]. The risk for gallstones increases with body mass index (BMI) and is greater for females than for males. As an example, one study reported a sevenfold greater risk for gallstones among females with severe obesity as compared with those with healthy weight (adjusted odds ratio 7.71) [82]. The risk was further increased for those who used oral contraceptives. Hispanic ethnicity is an independent risk factor for nonhemolytic gallstone disease [83]. One study examined the prevalence of gallstones in 493 asymptomatic children and adolescents between 8 and 18 years of age, with obesity defined as a BMI ≥2 standard deviation scores (approximately 97^th percentile). Ultrasound screening detected gallstones in 10 of the children (2 percent; eight females and two males), all of whom were postpubertal [84].

Signs and symptoms of gallstones in children and adolescents are nonspecific [81,85]. They include epigastric pain, jaundice, right upper quadrant pain, nausea, vomiting, and fatty food intolerance [79,80,85]. Because early recognition is necessary for successful management, gallbladder disease should be considered in the differential diagnosis of persistent abdominal pain in adolescents with obesity [86]. Ultrasonography is the test of choice for diagnosis. (See "Choledocholithiasis: Clinical manifestations, diagnosis, and management".)

NEUROLOGIC

Idiopathic intracranial hypertension — Idiopathic intracranial hypertension (pseudotumor cerebri) is uncommon in children and adolescents, but its prevalence is increased in those with obesity [87,88]. The prevalence is approximately 4 cases per 100,000 in normal-weight children, and the risk increases with the severity of obesity (odds ratio 6.45 for obesity and 16.14 for severe obesity) [88]. Although as many as one-half of children who present with idiopathic intracranial hypertension have obesity, the onset of symptoms does not appear to correlate with weight gain [89].

Children and adolescents with idiopathic intracranial hypertension typically present with headache. Associated complaints may include nausea, vomiting, retroocular eye pain, transient visual obscurations, visual loss, and diplopia. Papilledema is the characteristic examination finding (picture 3A-C). (See "Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis".)

Idiopathic intracranial hypertension can cause severe visual impairment or blindness. Thus, weight loss is an important component of treatment for patients with obesity and idiopathic intracranial hypertension [90]. (See "Idiopathic intracranial hypertension (pseudotumor cerebri): Prognosis and treatment".)

NUTRITIONAL

●Vitamin D deficiency appears to be common among children and adolescents with obesity, although the prevalence varies among populations and regions [91-94]. However, the clinical implications of this finding in children with obesity remain unclear, and the utility of routine screening is controversial [95]. (See "Vitamin D insufficiency and deficiency in children and adolescents", section on 'Obesity'.)

●Iron deficiency and obesity are also seemingly associated, with a 1.3 higher odds of deficiency compared with normal-weight individuals [96]. This meta-analysis found an even stronger correlation in children and adolescents, possibly due to higher iron demand during normal growth. An older study found upwards of 40 percent of children with overweight or obesity were iron deficient compared with 4 percent of children of normal weight [97]. (See "Iron deficiency in infants and children <12 years: Screening, prevention, clinical manifestations, and diagnosis" and "Iron requirements and iron deficiency in adolescents", section on 'Epidemiology'.)

ORTHOPEDIC — Orthopedic comorbidities of obesity include slipped capital femoral epiphysis (SCFE) and tibia vara (Blount disease). In addition, children with obesity have an increased prevalence of fractures, other sport injuries, genu valgum, musculoskeletal pain (eg, back, leg, knee, ankle, and foot), impaired mobility, and lower extremity malalignment compared with children without obesity [98-100]. (See "Approach to the child with knock-knees" and "Approach to the child with bow-legs", section on 'Blount disease'.)

Slipped capital femoral epiphysis — SCFE is characterized by a displacement of the capital femoral epiphysis from the femoral neck through the physeal plate (image 1). It typically occurs in early adolescence. Obesity is a significant risk factor [101]. The classic presentation is that of an adolescent with obesity who presents with nonradiating, dull, aching pain in the hip, groin, thigh, or knee and no history of preceding trauma. Diagnosis is confirmed by radiographs. Patients with SCFE should be referred to an orthopedic surgeon for management and an obesity specialist for an appropriate weight-loss program to prevent occurrence of contralateral SCFE [8,102]. The epidemiology, presentation, evaluation, and management of SCFE are discussed in detail separately. (See "Evaluation and management of slipped capital femoral epiphysis (SCFE)", section on 'Clinical manifestations'.)

Genu varus or valgus — Genu varus (also known as tibia varus or Blount disease) is characterized by progressive bowed legs and tibial torsion [103]. It results from inhibited growth of the medial proximal tibial growth plate due to excessive abnormal weight-bearing [104,105]. Genu varus is associated with obesity [103,105-109] and is particularly common among individuals with darkly pigmented skin [104,106,108,110]. In one report, the prevalence of genu varus among 80 Black males (aged 13 to 19 years) who weighed ≥210 pounds was 2.5 percent [110].

Clinical features of genu varus include complaints of knee pain or instability and bowlegs that gradually increase in severity [111,112]. Severe adiposity may obscure the physical findings and delay the diagnosis. Radiographs are necessary for diagnosis (image 2). (See "Approach to the child with bow-legs", section on 'Blount disease'.)

Genu valgus is a deformity in which the tibiofemoral angle points towards the midline (knock-knees). Physiologic genu valgus is more common in children with obesity [113]. The association with obesity is less strong than for genu varus, and the deformity rarely warrants surgical correction. (See "Approach to the child with knock-knees".)

Fractures — Children with obesity are more susceptible to fractures than those with healthy body weight [114,115]. Unlike adults, children with obesity generally have reduced bone mass when adjusted for body size [116-118]. The relative contributions of stress from body weight during falls, vitamin D deficiency, reduced bone mass from lack of exercise, and other biomechanical effects of obesity on bone have not been established [119,120].

PSYCHOSOCIAL — Psychosocial consequences of childhood obesity are widespread [90,121]. These include social isolation [122,123], distorted peer relationships, poor self-esteem [124,125], distorted body image [126], anxiety [127], and depression [128-133]. The risk of psychosocial morbidity increases with increasing age and is greater among females than males [121,124,134-136]. Representative studies include:

●Quality of life – In community-based and referral populations, children and adolescents with obesity and their parents or caregivers report decreased health-related quality of life (physical, emotional, social, and school functioning) compared with healthy, nonoverweight children and adolescents [132,137-140]. In the referral population, health-related quality of life among children and adolescents with severe obesity was similar to that reported by children and adolescents with cancer [137].

●Weight bias and stigma – In the early school years (age 6 to 10 years), overweight and obese children may become targets of discrimination by their peers [141]. In one study from the 1960s of male schoolchildren from Indiana, obesity was associated with a peer stereotyping of negative characteristics (eg, laziness, lying, cheating, ugliness, dirtiness, and stupidity) [142]. In another study, schoolchildren preferred children with a variety of handicaps to children with obesity as their friends [90,143]. In a 2006 study from southwest England, males and females who were obese at 7.5 years of age were more likely to be victims of bullying at 8.5 years of age than average-weight children [144]. In addition, males who were obese at 7.5 years were more likely to be overt bullies at 8.5 years than average-weight males. Despite these issues, many young children with overweight and obesity appear to maintain a positive self-image and have normal self-esteem [125,145,146].

Adolescents with obesity also experience bias and bullying from their peers; many, particularly females, develop a negative self-image that persists into adulthood [76,126]. Data from the National Longitudinal Survey of Youth indicate that women, but not men, who were obese in late adolescence and early adulthood completed fewer years of advanced education and had lower household income, lower rates of marriage, and higher rates of poverty compared with their nonobese peers [147]. Similar data were reported from a British cohort [148].

●Body image and eating patterns – Several studies report an association between obesity and eating disorders [149]. As an example, in one study, approximately one-third of adolescents being treated for eating disorders were previously overweight or obese [150]. The obesity or excessive weight gain usually precedes the disordered eating, suggesting that overweight children and adolescents may engage in unhealthy eating behaviors in an attempt to lose weight [150-153]. However, reverse causality is also possible, given the overlap between restrictive messages used for obesity management (portion control, reducing calories) and the inevitable focus on weight and thus physical appearance. Thus, efforts to promote weight loss could prompt or worsen an eating disorder, and care should be taken to minimize this risk through counseling that supports a positive body image and healthy eating patterns, and vigilance for signs of disordered eating patterns [149].

PULMONARY — Pulmonary comorbidities of obesity in children and adolescents include obstructive sleep apnea (OSA) and the obesity hypoventilation syndrome (OHS).

Asthma — Results are conflicting regarding the relationship between obesity and asthma severity. Obesity and adiposity are associated with an increased incidence of asthma, and higher body mass index (BMI) is associated with greater asthma severity. However, biologic causality has not been proven, and the relationship could be explained by reverse causation (ie, asthma limiting physical activity, leading to obesity). Obesity and asthma share common physiologic pathways, which are complex and not fully elucidated; their commonalities may be demonstrated in the improved asthma outcomes after successful weight management [154]. (See "Asthma in children younger than 12 years: Initial evaluation and diagnosis", section on 'Obesity'.)

Obstructive sleep apnea — OSA describes complete obstruction of the upper airway during sleep and cessation of air movement despite ongoing respiratory effort; partial airway obstruction is termed obstructive hypoventilation. OSA is typically but not always associated with persistent snoring. Obesity is an important predisposing factor; the prevalence of OSA is markedly increased in children and adolescents with obesity as compared with those with healthy weight. As an example, in a study of adolescents with moderate to severe obesity (BMI >97^th percentile), 45 percent had OSA on polysomnogram (defined as an apnea-hypopnea index [AHI] >1.5 in this study) [155]. The pathogenesis and evaluation of OSA in children are discussed separately. (See "Mechanisms and predisposing factors for sleep-related breathing disorders in children" and "Evaluation of suspected obstructive sleep apnea in children".)

The relationship between sleep and obesity is complex. There is some evidence that shortened sleep duration or sleep fragmentation (ie, poor sleep quality) promotes obesity and also that OSA is associated with decreased insulin sensitivity in adolescents, independent of adiposity. These associations are discussed separately. (See "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Sleep'.)

Children and adolescents with obesity and sleep-disordered breathing should be referred for specialty care [8]. They require an aggressive weight loss program since weight loss can improve ventilation and general health. In addition, they may require continuous positive airway pressure (CPAP) until weight loss is sufficient to restore adequate ventilation. (See "Management of obstructive sleep apnea in children".)

Obesity hypoventilation syndrome — OHS is defined by extreme obesity and alveolar hypoventilation during wakefulness. This disorder is rare but life-threatening and requires prompt diagnosis and therapy.

More commonly, patients with obesity also may have hypoventilation during sleep in the absence of airway obstruction, perhaps due to the restrictive ventilatory defect caused by obesity. In a study of 64 children, 17 percent had episodes of hypoventilation, often with severe oxygen desaturation [156], which was associated with abdominal distribution of fat mass. (See "Clinical manifestations and diagnosis of obesity hypoventilation syndrome".)

RENAL — We suggest screening for impaired kidney function in selected patients with obesity and risk factors for chronic kidney disease by measuring urine albumin-to-creatinine ratio (UACR); UACR >30 mg/g is abnormal. The glomerular filtration rate should also be estimated at baseline and repeated as indicated based on the UACR and the patient's clinical status. Performing this screening annually is recommended by consensus for patients with type 2 diabetes [10]. We suggest similar screening for patients with primary hypertension and/or severe obesity, although there is no expert consensus on this approach. (See "Chronic complications and screening in children and adolescents with type 2 diabetes mellitus", section on 'Nephropathy (albuminuria)'.)

The above suggestion for screening is supported by observations that obesity is associated with impaired renal function. Obesity is a known risk factor for chronic kidney disease in adults, as indicated by a rise in the prevalence of end-stage renal disease in parallel with the rise in obesity rates (see "Overweight and obesity in adults: Health consequences", section on 'Chronic kidney disease'). Studies in children with obesity report impaired glomerular filtration rates that may predict later chronic kidney disease [157]. Furthermore, impaired kidney function in youth with obesity may be reversible, as suggested by observations that adolescents undergoing bariatric surgery experience improvement in estimated glomerular filtration rate after surgically-induced weight loss. (See "Surgical management of severe obesity in adolescents", section on 'Comorbidity improvement'.)

CANCER — Excess weight in adulthood is a known risk factor for several types of cancer, especially mouth, gastrointestinal, biliary, pancreatic, breast, ovarian, endometrial, kidney, and blood cancers. (See "Overweight and obesity in adults: Health consequences", section on 'Cancer'.)

In addition, several studies specifically link excess weight during childhood to cancer risk during adulthood, especially leukemia, Hodgkin disease, and colorectal and breast cancer [158,159]. As an example, a registry study of Swedish men found robust associations between childhood overweight/obesity and adult cancers (hazard ratio [HR] 1.51, 95% CI 1.26-1.8), even for those who were overweight during childhood but had a healthy weight by young adulthood (HR 1.38, 95% CI 1.09-1.75) [160]. By contrast, individuals who first became overweight during adolescence did not have a significantly increased risk for cancers during adulthood (HR 1.04, 95% CI 0.81-1.31). These findings are limited by the lack of data about weight status later in adulthood.

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: Lipid disorders and atherosclerosis in children" and "Society guideline links: Obesity in children" and "Society guideline links: Nonalcoholic fatty liver disease".)

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SUMMARY

●Overview – The comorbidities of obesity in childhood and adolescence include abnormalities in cardiovascular, dermatologic, endocrine, gastrointestinal, neurologic, orthopedic, psychosocial, and pulmonary health, as well as functional limitations (table 1). Evaluation and monitoring for these comorbidities is summarized in the table (table 2).

●Cardiovascular

•Hypertension is probably the most common comorbidity associated with obesity. Children with obesity are three times more likely to have hypertension than those without obesity. (See 'Hypertension' above.)

•More than 50 percent of children with obesity have lipid abnormalities as measured by a fasting profile, typically elevated low-density lipoprotein (LDL)-cholesterol and triglycerides and a decreased high-density lipoprotein (HDL)-cholesterol. (See 'Dyslipidemia' above.)

•Childhood obesity is associated with several markers of subclinical atherosclerosis and changes in cardiac function, including carotid intima-media thickening and preclinical aortic and coronary arterial fatty streaks and fibrous plaques. (See 'Premature atherosclerotic cardiovascular disease' above and 'Cardiac structure and function' above.)

•Obesity during childhood is associated with an increased risk for major cardiovascular events during adulthood, independent of adult obesity status (figure 2). (See 'Adult cardiovascular disease' above.)

●Dermatologic – Acanthosis nigricans (picture 1A-B) is a common skin abnormality in individuals with obesity and is associated with insulin resistance. Less common abnormalities include intertrigo and hidradenitis suppurativa (picture 2). (See 'Dermatologic' above.)

●Endocrine

•Among adolescents with obesity, 7 to 25 percent have increased risk for developing type 2 diabetes mellitus (T2DM), sometimes called "prediabetes," and 0.5 to 4 percent have overt T2DM. Diagnostic criteria for prediabetes and T2DM are shown in the tables (table 4A-B). Indications and methods for screening are discussed separately. (See 'Type 2 diabetes mellitus' above and "Epidemiology, presentation, and diagnosis of type 2 diabetes mellitus in children and adolescents", section on 'Screening'.)

•The metabolic syndrome describes the clustering of abdominal obesity, hyperglycemia, dyslipidemia, and hypertension, which are risk factors for T2DM and atherosclerotic cardiovascular disease. Several different sets of criteria have been used to define the metabolic syndrome in adolescents (table 5). (See 'Metabolic syndrome' above.)

•Adolescent females with obesity are at increased risk of hyperandrogenism and early-onset polycystic ovary syndrome (PCOS). PCOS can include a variety of clinical abnormalities, including menstrual irregularities, acne, hirsutism, acanthosis nigricans, and seborrhea. In some cases, the diagnosis may be difficult to establish during adolescence. Obesity during adulthood is also associated with reduced fertility. (See 'Hyperandrogenism' above.)

●Gastrointestinal

•Obesity is associated with a clinical spectrum of liver abnormalities collectively known as metabolic dysfunction-associated steatotic liver disease (MASLD; previously known as nonalcoholic fatty liver disease), the most common cause of liver disease in children. MASLD is subdivided into three categories, defined by histologic findings: steatotic liver disease alone, metabolic dysfunction-associated steatohepatitis (MASH), and MASH with fibrosis or cirrhosis (table 6). (See "Metabolic dysfunction-associated steatotic liver disease in children and adolescents".)

•Asymptomatic gallstones can be detected in approximately 2 percent of adolescents with obesity, most of whom are females. If symptoms develop, they tend to include epigastric pain, jaundice, right upper quadrant pain, nausea, vomiting, and fatty food intolerance. (See 'Cholelithiasis' above.)

●Orthopedic

•Orthopedic comorbidities of obesity include slipped capital femoral epiphysis (SCFE) and tibia vara (Blount disease). In addition, obese children have an increased prevalence of fractures, genu valgum, musculoskeletal pain (eg, back, leg, knee, ankle, and foot), impaired mobility, and lower extremity malalignment than children without obesity. (See 'Orthopedic' above.)

●Psychosocial

•Psychosocial consequences of childhood obesity are common and include alienation, distorted peer relationships, poor self-esteem, distorted body image, anxiety, depression, and disordered eating patterns. The risk of psychosocial morbidity increases with increasing age and is greater among females than males. (See 'Psychosocial' above.)

●Pulmonary

•Approximately 10 percent of children and adolescents with obesity have clinically significant sleep apnea, and the risk is higher among children with severe obesity and/or consistent snoring. The diagnosis is made with polysomnography. (See 'Obstructive sleep apnea' above and "Evaluation of suspected obstructive sleep apnea in children".)

●Renal

•Children with obesity have increased risk for impaired kidney function, which develops gradually. Risk factors include the presence of type 2 diabetes, hypertension, and severe obesity. (See 'Renal' above.)

●Cancer

•Excess weight in childhood is associated with an increased risk of cancer in adulthood, especially leukemia, Hodgkin disease, and colorectal or breast cancer. (See 'Cancer' above.)

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Topic 5869 Version 71.0

خرید پکیج

Overview of the health consequences of obesity in children and adolescents

References