I.   Prevalence, trends, and definitions

               A.   Obesity is a maladaptive increase in body fat stores. The global epidemic of obesity is a serious public health concern that has affected both adults and children. Worldwide, approximately 42 million children under the age of five were overweight or obese in 2013 (1). While the prevalence of overweight and obesity in western and industrialized countries is almost double that in developing countries, the relative increase over the last two decades has been higher in developing countries (2). In the United States, obesity has more than doubled in children and quadrupled in adolescents over the past three decades. Currently, almost one third of children and adolescents in the United States are either overweight or obese and 17% of youth are obese (3). However, recent reports suggest that the prevalence of childhood obesity has begun to plateau (3). In the United States, childhood obesity is more commonly seen among African–American, Mexican–American, and American–Indian children, especially in low-income populations (3–5).

               B.   Body mass index (BMI) is an accepted screening tool for initial assessment of obesity in children and adolescents. Although BMI does not measure body fat directly, it correlates to direct measures of body fat, such as underwater weighing and dual-energy X-ray absorptiometry (6). BMI is calculated as weight (in kilograms) divided by the square of height (in meters). Adults with a BMI between 25 and 30 are considered overweight; those with a BMI more than 30 are considered obese. In children, the amount and distribution of body fat changes with age and it differs between girls and boys. To take these changes into account, the child’s BMI value is plotted on the Centers for Disease Control and Prevention (CDC) gender-specific growth charts developed in 2000 to determine the corresponding BMI-for-age percentile. Children with a BMI between the 85th and 95th percentile for age and sex are considered overweight while children with a BMI at or above the 95th percentile are considered obese. Severe obesity in children is defined as BMI ≥120% of the 95th percentile value or a BMI ≥35 kg per m² (whichever is lower), which corresponds to approximately the 99th percentile (Table 41.1). Approximately 6% of children and adolescents in the United States are severely obese (7).

               C.   Childhood obesity typically persists into adulthood depending on several factors including degree of obesity, older age of child, and parental obesity. While obesity at <3 years of age is not associated with an increased risk of adult obesity, the probability of obesity in adulthood exceeds 50% among obese 6-year-old children and 80% among obese 10- to 14-year-old children (8). Parental obesity more than doubles the risk of adult obesity among both obese and nonobese children (8). The severity of obesity during adolescence is an important predictor of persistent obesity in adulthood (9).

TABLE 41.1  Classification of obesity based on gender-specific BMI-for-age percentile

     II.   Etiology

               A.   Obesity is the result of a net imbalance of caloric intake over energy expenditure over time. However, the etiology of this imbalance is multifactorial. Adiposity in humans represents complex interactions between environmental factors, genetic predisposition, and developmental influences.

               B.   Several environmental and behavioral factors have been associated with the development of childhood obesity, including increased consumption of sugar-sweetened beverages, high glycemic index foods, large portion sizes, fast food restaurants, television viewing, decreased physical activity, and shortened sleep duration (10–12). The effect of lifestyle interventions to reduce childhood obesity has been limited, but school-based programs and parent-focused interventions targeting young children (ages 6 to 12 years) by promoting physical activity, healthy nutrition, and spending less time in screen-based activities have been found to be the most effective (13).

               C.   Genetic factors play a crucial role in the development of obesity with growing evidence that the amount of body fat is biologically regulated. Twin studies indicate that the heritability of body fatness and fat distribution in adulthood is 30% to 70% (14). Several single-gene mutations capable of producing profound increases in body fat have been identified (15). A mutation in melanocortin receptor (MCR) 4 is the most common single gene defect identified in the obese population (16). Obesity is also a component of several genetic syndromes including Prader–Willi syndrome, Alström syndrome, Bardet–Biedl syndrome, Borjeson–Forssman–Lehmann syndrome, Carpenter syndrome, and Cohen syndrome.

               D.   Endocrine causes of obesity are rare (<1% of cases) and include hypothyroidism, cortisol excess (Cushing syndrome), and pseudohypoparathyroidism. Hypothalamic lesions following surgery for craniopharyngioma, cranial irradiation, and traumatic brain injury can also result in obesity (16). Several medications can also cause weight gain including chronic glucocorticoid therapy, progestins, valproate, cyproheptadine, and psychoactive drugs like risperidone and olanzapine (16).

               E.   There is increasing evidence to support a role for “metabolic programming”, which refers to the effects of maternal nutrition and endocrine profile during pregnancy on the child’s predisposition to obesity (17). Intrauterine exposure to gestational diabetes among Pima Indians is associated with an increased risk of childhood and early adult obesity in offspring (18). Children born to mothers after undergoing bariatric surgery for severe obesity appear to have a lower prevalence of obesity than siblings born before the weight loss (19). High birth weight babies and small-for-gestational age babies who exhibit rapid catch up growth during infancy are at increased risk for childhood obesity (20).

   III.   Comorbidities. Obesity affects almost every organ system in the body, resulting in several immediate and long-term health consequences. Obesity markedly decreases life expectancy, especially among younger individuals (21).

               A.   Cardiovascular disease

                       1.   Childhood obesity is associated with an increased risk of cardiovascular disease in adulthood. Overweight or obese children who remained obese as adults have an increased risk of type 2 diabetes, hypertension, dyslipidemia, and carotid-artery atherosclerosis (22). Higher childhood BMI values increase the risk of coronary heart disease in adulthood (23). Overweight or obese children who are no longer obese as adults have a cardiovascular risk profile similar to individuals who are never obese (22).

                       2.   Previously considered rare, obese children are at a three-fold higher risk for hypertension (24). The risk increases linearly across the entire range of BMI values and systolic hypertension and associated left ventricular hypertrophy occurs early. The pathophysiology of obesity-related hypertension is multifactorial and includes hyperactivity of the sympathetic nervous system, insulin resistance, and altered vascular structure and function (24).

                       3.   Dyslipidemia is common among obese children with mildly elevated levels of serum low-density lipoprotein (LDL)-cholesterol, substantially increased triglyceride levels, and decreased levels of high-density lipoprotein (HDL)-cholesterol. Dyslipidemia during childhood and adolescence is associated with increased risk of atherosclerosis and cardiovascular disease in adulthood (25). The Bogalusa Heart study and other autopsy studies have demonstrated that the atherosclerotic process begins early in childhood with deposits of fatty streaks and fibrous plaques in the aorta and coronary arteries (26,27).

               B.   Endocrine disorders

                       1.   The epidemic of childhood obesity has led to a dramatic increase in the incidence of type 2 diabetes mellitus (T2DM) among children and adolescents (28,29). Currently, in the United States, T2DM is diagnosed in nearly one third of new cases of diabetes mellitus in youth between 10 and 19 years of age, especially in minority populations (30,31). Earlier onset of T2DM among children and adolescents leads to earlier onset of microvascular and macrovascular complications such as diabetic neuropathy, nephropathy, retinopathy, and atherosclerosis (28).

                       2.   Insulin resistance is strongly associated with childhood obesity and is a critical link between adiposity and increased risk for T2DM and other metabolic disorders (32). Insulin resistance refers to the inability of a given quantity of insulin to increase glucose utilization peripherally in muscle, liver, adipose tissue, etc. Risk factors for the development of insulin resistance include obesity, visceral adiposity, puberty, race/ethnicity, family history of T2DM, female sex, small for gestational age, and premature children (32). Obesity is the most important determinant of insulin resistance, with more than 50% of obese adolescents in the United States exhibiting insulin resistance (33).

                       3.   Metabolic syndrome is characterized by abdominal obesity, hypertension, glucose intolerance, atherogenic dyslipidemia, prothrombotic and proinflammatory state, increasing the risk of T2DM and cardiovascular disease in adults (34). Unfortunately, there is lack of consistency in the diagnostic criteria used in children and adolescents (35). Using the National Cholesterol Education Program (Adult Treatment Panel III) definition modified for age, nearly 30% of overweight adolescents in the United States meet criteria for metabolic syndrome (36). For each half-unit increase in BMI, there is a 50% increase in the risk for metabolic syndrome in overweight and obese children (37).

                       4.   Obese adolescent girls are at increased risk for hyperandrogenism and early onset polycystic ovary syndrome (PCOS), which is characterized by menstrual irregularities, hirsutism, acne, and obesity (38). PCOS is strongly associated with insulin resistance and is a major risk factor for the development of metabolic syndrome and T2DM in women.

               C.   Liver disorders

                       1.   Childhood obesity and insulin resistance are strongly associated with nonalcoholic fatty liver disease (NAFLD), which is the most common cause of chronic liver disease in children and adolescents (39). NAFLD is characterized by the accumulation of macrovesicular fat in hepatocytes in the absence of alcohol consumption. NAFLD is a spectrum of histopathologic features ranging from simple steatosis (fatty liver) to steatosis with inflammation and fibrosis (nonalcoholic steatohepatitis [NASH]) to cirrhosis (39). The true prevalence of NAFLD in children is unknown as most children with NAFLD are asymptomatic. In an autopsy study in children and adolescents, the prevalence of fatty liver was estimated to be 9.6% overall and 38% in obese children (40). Serum biomarkers (liver transaminases) and noninvasive imaging studies (ultrasound) are commonly used for the evaluation and monitoring of pediatric NAFLD, but are insensitive. Magnetic resonance imaging is more sensitive, but is not used clinically. Liver biopsy remains the gold-standard for diagnosis of NAFLD and NASH.

               D.   Respiratory disorders

                       1.   Childhood obesity quadruples the risk of obstructive sleep apnea syndrome (OSAS) (41); for each increase of 1 kg per m² of BMI above the mean in children, the risk of OSAS increases by 12% (41). The pathophysiology of OSAS in obese children is multifactorial (42). Adenotonsillar hypertrophy due to increased somatic growth is common in obese children. MRI studies have revealed that obese children with OSAS have a smaller oropharynx with larger adenoids, tonsils, and retropharyngeal nodes (43). In addition to anatomical factors, increased critical airway closing pressures, altered chest wall mechanics, and abnormalities of ventilatory control contribute to the pathophysiology of OSAS in obese children (42). Following adenotonsillectomy, obese children are at increased risk for residual OSAS (44). Both obesity and OSAS are strongly associated with metabolic syndrome; adolescents with OSAS are at an approximately seven-fold increased risk for metabolic syndrome (45).

                       2.   The prevalence of asthma is significantly increased in obese children (46). Increased BMI among children with asthma is associated with increased asthma symptoms, exacerbations, and emergency department visits (47). However, the nature of the relationship between childhood obesity and asthma remains unclear.

               E.   Orthopedic diseases

                       1.   Obesity is strongly associated with slipped capital femoral epiphysis (SCFE), which is the most common hip disorder in adolescents (48). SCFE usually occurs during the adolescent growth spurt and is characterized by nontraumatic displacement of the proximal femoral epiphysis from the metaphysis (49). A combination of mechanical and constitutional factors contributes to SCFE. Another orthopedic disorder commonly associated with childhood obesity is Blount’s disease, which is characterized by progressive varus deformity of the tibia and tibial torsion, resulting in bowed legs, abnormal gait, and pain (49).

                       2.   The prevalence of musculoskeletal pain is higher among obese children and unlike obese adults they have an increased risk of fractures (50). Obesity also affects gait, with increased loading on the medial compartment of the knee (49).

               F.   Psychosocial issues

                       1.   Psychosocial consequences of childhood obesity are widespread. The risk of psychosocial issues increases with age and girls are at greater risk than boys (51). Symptoms of depression and lower self-esteem are higher among obese adolescents (52,53). Overweight and obese adolescents are frequent targets of teasing and bullying and they are more likely to be socially marginalized (54,55).

                       2.   Obese children and adolescents report significantly lower health-related quality of life (QOL) scores than normal weight peers and similar QOL scores as those diagnosed with cancer (56). Obese children and adolescents with OSA report lower QOL scores than obese children and adolescents without OSA. Obese adolescents and young adults complete fewer years of advanced education and have decreased family income, lower rates of marriage, and higher rates of poverty compared to their nonobese peers (57).

   IV.   Adipose tissue as an endocrine organ

               A.   Adipose tissue is no longer considered just a passive reservoir for energy storage but rather a complex, highly active endocrine organ that plays a critical role in energy homeostasis (58,59). Adipose tissue secretes bioactive peptides called adipokines that control food intake, energy expenditure, carbohydrate, and lipid metabolism. In addition, receptors on adipose tissue respond to afferent signals from traditional hormone systems and the central nervous system. Metabolism of steroid hormones and glucocorticoids also occurs in adipose tissue (58).

               B.   Functionally, the two groups of adipose tissue are brown adipose tissue and white adipose tissue. In humans, brown adipose tissue (BAT) plays an important role in the regulation of body temperature in newborns, but its role in the post-newborn period is only now being studied. White adipose tissue (WAT) is the predominant adipose tissue in mammals and consists of adipocytes surrounded by loose connective tissue that is highly vascular and richly innervated, containing fibroblasts, macrophages, immune cells, and adipocyte precursors (58,59). WAT is primarily distributed in the subcutaneous region and around abdominal viscera (mesenteric, omental, and retroperitoneal fat) (58,59). Women generally have a higher percentage of body fat than men and store excess fat in the gluteo-femoral region, whereas men store excess fat in the abdominal (visceral) region (60). Increased visceral adiposity has been associated with insulin resistance, T2DM, and cardiovascular disease (61).

               C.   Nonesterified (free) fatty acids as well as several adipokines including leptin, adiponectin, resistin, retinol binding protein 4, are secreted by adipose tissue. Obesity is characterized by dysregulation of adipokine secretion and response (62). Under normal circumstances, leptin plays a major role in energy homeostasis by signaling satiety to the brain through hypothalamic receptors. Leptin levels increase with weight gain and decrease with weight loss or starvation and subcutaneous adipose tissue secretes more leptin than visceral adipose tissue. However, despite increased leptin levels, obese patients become insensitive to the actions of leptin secondary to hypothalamic leptin resistance (62). On the other hand, adiponectin levels are negatively correlated with obesity, insulin resistance, T2DM, and cardiovascular disease. Adiponectin increases insulin sensitivity and has anti-atherogenic and anti-inflammatory properties (62). Resistin increases insulin resistance and has pro-inflammatory properties (62). In addition to the dysregulated secretion of adipokines, obesity has been linked to a low-grade, chronic inflammatory state with increased release of inflammatory cytokines including tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and C-reactive protein from macrophages in adipose tissue and elsewhere (62).

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