Overweight and Obesity

Epidemiology

Obesity is an important pediatric public health problem associated with risk of complications in childhood and increased morbidity and mortality throughout adult life. Obesity is now linked to more deaths than underweight. In 2014, according to the World Health Organization (WHO), more than 1.9 billion persons ≥20 yr old were overweight or obese.

In the United States, 37% of adults are obese, and 35% are overweight. In children the prevalence of obesity increased 300% over approximately 40 yr. According to the National Health and Nutrition Examination Survey (NHANES), 2013–2014, 34% of children 2-19 yr old were overweight or obese, with 17% in the obese range. Risk for obesity in children 2-19 yr old varies significantly by race/ethnicity, with >20% for minority children compared with 15% for white children. Across all racial groups, higher maternal education confers protection against childhood obesity.

The first 1000 days, the period from conception to age 2 yr, are increasingly recognized as a modifiable period related to risk for childhood obesity. Parental obesity correlates with a higher risk for obesity in the children. Prenatal factors, including high preconceptual weight, gestational weight gain, high birthweight, and maternal smoking, are associated with increased risk for later obesity. Paradoxically, intrauterine growth restriction with early infant catch-up growth is associated with the development of central adiposity and adult-onset cardiovascular (CV) risk. Breastfeeding is modestly protective for obesity based on dose and duration. Infants with high levels of negative reactivity (temperament) are more at risk for obesity than those with better self-regulation.

Body Mass Index

Obesity or increased adiposity is defined using the body mass index (BMI) , an excellent proxy for more direct measurement of body fat. BMI = weight in kg/(height in meters) ² . Adults with a BMI ≥30 meet the criterion for obesity, and those with a BMI 25-30 fall in the overweight range. During childhood, levels of body fat change beginning with high adiposity during infancy. Body fat levels decrease for approximately 5.5 yr until the period called adiposity rebound, when body fat is typically at the lowest level. Adiposity then increases until early adulthood ( Fig. 60.1 ). Consequently, obesity and overweight are defined using BMI percentiles for children ≥2 yr old and weight/length percentiles for infants <2 yr old. The criterion for obesity is BMI ≥95th percentile and for overweight is BMI between 85th and 95th percentiles.

Etiology

Humans have the capacity to store energy in adipose tissue, allowing improved survival in times of famine. Simplistically, obesity results from an imbalance of caloric intake and energy expenditure. Even incremental but sustained caloric excess results in excess adiposity. Individual adiposity is the result of a complex interplay among genetically determined body habitus, appetite, nutritional intake, physical activity (PA) , and energy expenditure. Environmental factors determine levels of available food, preferences for types of foods, levels of PA, and preferences for types of activities. Food preferences play a role in consumption of energy-dense foods. Humans innately prefer sweet and salty foods and tend initially to reject bitter flavors, common to many vegetables. Repeated exposure to healthy foods promotes their acceptance and liking, especially in early life. This human characteristic to adapt to novel foods can be used to promote healthy food selection.

Endocrine and Neural Physiology

Monitoring of “stored fuels” and short-term control of food intake (appetite and satiety) occurs through neuroendocrine feedback loops linking adipose tissue, the gastrointestinal (GI) tract, and the central nervous system (CNS) ( Figs. 60.2 and 60.3 ). GI hormones, including cholecystokinin, glucagon-like peptide 1, peptide YY, and vagal neuronal feedback promote satiety. Ghrelin stimulates appetite. Adipose tissue provides feedback regarding energy storage levels to the brain through hormonal release of adiponectin and leptin. These hormones act on the arcuate nucleus in the hypothalamus and on the solitary tract nucleus in the brainstem and in turn activate distinct neuronal networks. Adipocytes secrete adiponectin into the blood, with reduced levels in response to obesity and increased levels in response to fasting. Reduced adiponectin levels are associated with lower insulin sensitivity and adverse CV outcomes. Leptin is directly involved in satiety; low leptin levels stimulate food intake, and high leptin levels inhibit hunger in animal models and in healthy human volunteers. However, the negative feedback loop from leptin to appetite may be more adapted to preventing starvation than excess intake.

Numerous neuropeptides in the brain, including peptide YY (PYY), agouti-related peptide, and orexin, appear to affect appetite stimulation, whereas melanocortins and α-melanocortin–stimulating hormone are involved in satiety ( Fig. 60.3 ). The neuroendocrine control of appetite and weight involves a negative-feedback system, balanced between short-term control of appetite and long-term control of adiposity (including leptin). PYY reduces food intake via the vagal-brainstem-hypothalamic pathway. Developmental changes in PYY are evident as infants have higher PYY levels than school-age children and adults. Obese children have lower fasting levels of PYY than adults. Weight loss may restore PYY levels in children, even though this does not happen in adults. In addition, patients homozygous for the FTO obesity-risk allele demonstrate poor regulation of the orexigenic hormone acyl-ghrelin and have poor postprandial appetite suppression.

Comorbidities

Complications of pediatric obesity occur during childhood and adolescence and persist into adulthood. An important reason to prevent and treat pediatric obesity is the increased risk for morbidity and mortality later in life. The Harvard Growth Study found that boys who were overweight during adolescence were twice as likely to die from CV disease as those who had normal weight. More immediate comorbidities include type 2 diabetes, hypertension, hyperlipidemia, and nonalcoholic fatty liver disease (NAFLD) ( Table 60.2 ). Insulin resistance increases with increasing adiposity and independently affects lipid metabolism and CV health. The metabolic syndrome (central obesity, hypertension, glucose intolerance, and hyperlipidemia) increases risk for CV morbidity and mortality. NAFLD has been reported in 34% of patients treated in pediatric obesity clinic. NAFLD is now the most common chronic liver disease in U.S. children and adolescents. It can present with advanced fibrosis or nonalcoholic steatohepatitis and may result in cirrhosis and hepatocellular carcinoma. Insulin resistance is often associated. Furthermore, NAFLD is independently associated with increased risk of CV disease.

Obesity may also be associated with chronic inflammation. Adiponectin, a peptide with antiinflammatory properties, occurs in reduced levels in obese patients compared to insulin-sensitive, lean persons. Low adiponectin levels correlate with elevated levels of free fatty acids and plasma triglycerides as well as a high BMI, and high adiponectin levels correlate with peripheral insulin sensitivity. Adipocytes secrete peptides and cytokines into the circulation, and proinflammatory peptides such interleukin (IL)-6 and tumor necrosis factor (TNF)-α occur in higher levels in obese patients. Specifically, IL-6 stimulates production of C-reactive protein (CRP) in the liver. CRP is a marker of inflammation and might link obesity, coronary disease, and subclinical inflammation.

Some complications of obesity are mechanical, including obstructive sleep apnea and orthopedic complications. Orthopedic complications include Blount disease and slipped femoral capital epiphysis (see Chapters 697 and 698.4 ).

Mental health problems can coexist with obesity, with the possibility of bidirectional effects. These associations are modified by gender, ethnicity, and socioeconomic status. Self-esteem may be lower in obese adolescent girls than in nonobese peers. Some studies have found an association between obesity and adolescent depression. There is considerable interest in the co-occurrence of eating disorders and obesity. Obese youth are also at risk for bullying based on their appearance.

Identification

Overweight and obese children are often identified as part of routine medical care. The child and family may be unaware that the child has increased adiposity. They may be unhappy with the medical provider for raising this issue and may respond with denial or apparent lack of concern. It is often necessary to begin by helping the family understand the importance of healthy weight for current and future health. Forging a good therapeutic relationship is important because obesity intervention requires a chronic disease management approach. Intervention and successful resolution of this problem require considerable effort by the family and the child over an extended period in order to change eating and activity behaviors.

Evaluation

The evaluation of the overweight or obese child begins with examination of the growth chart for weight, height, and BMI trajectories; consideration of possible medical causes of obesity; and detailed exploration of family eating, nutritional, and activity patterns. A complete pediatric history is used to uncover comorbid disorders. The family history focuses on the adiposity of other family members and the family history of obesity-associated disorders. The physical examination adds data that can lead to important diagnoses. Laboratory testing is guided by the need to identify comorbidities.

Examination of the growth chart reveals the severity, duration, and timing of obesity onset. Children who are overweight (BMI in 85–95th percentile) are less likely to have developed comorbid conditions than those who are obese (BMI ≥95th percentile). Those with a BMI ≥99th percentile are more likely to have coexisting medical problems. Once obesity severity is determined, the BMI trajectory is examined to elucidate when the child became obese. Several periods during childhood are considered sensitive periods, or times of increased risk for developing obesity, including infancy, adiposity rebound (when body fat is lowest at approximately age 5.5 yr), and adolescence. An abrupt change in BMI might signal the onset of a medical problem or a period of family or personal stress for the child. Examination of the weight trajectory can further reveal how the problem developed. A young child might exhibit high weight and high height because linear growth can increase early in childhood if a child consumes excess energy. At some point the weight percentile exceeds the height percentile, and the child's BMI climbs into the obese range. Another example is a child whose weight rapidly increases when she reduces her activity level and consumes more meals away from home. Examination of the height trajectory can reveal endocrine problems, which often occur with slowing of linear growth.

Consideration of possible medical causes of obesity is essential, even though endocrine and genetic causes are rare (see Table 60.1 ). Growth hormone deficiency, hypothyroidism, and Cushing syndrome are examples of endocrine disorders that can lead to obesity. In general, these disorders manifest with slow linear growth. Because children who consume excessive amounts of calories tend to experience accelerated linear growth, short stature warrants further evaluation. Genetic disorders associated with obesity may manifest extreme hyperphagia, or they can have coexisting dysmorphic features, cognitive impairment, vision and hearing abnormalities, or short stature. In some children with congenital disorders such as myelodysplasia or muscular dystrophy, lower levels of PA can lead to secondary obesity. Some medications, such as atypical antipsychotics, can cause excessive appetite and hyperphagia, resulting in obesity ( Table 60.3 ). Rapid weight gain in a child or adolescent taking one of these medications might require its discontinuation. Poor linear growth and rapid changes in weight gain are indications for evaluation of possible medical causes.

Exploration of family eating, nutritional, and activity patterns begins with a description of regular meal and snack times and family habits for walking, bicycle riding, active recreation, and screen time (TV, computer, video games). It is useful to request a 24-hr dietary recall with special attention to intake of fruits, vegetables, and water, as well as high-calorie foods and high-carbohydrate beverages. When possible, evaluation by a nutritionist is extremely helpful. This information will form the basis for incremental changes in eating behavior, caloric intake, and PA during the intervention.

Initial assessment of the overweight or obese child includes a complete review of bodily systems focusing on the possibility of comorbid conditions (see Table 60.2 ). Developmental delay and visual and hearing impairment can be associated with genetic disorders. Difficulty sleeping, snoring, or daytime sleepiness suggests sleep apnea. Abdominal pain might suggest NAFLD. Symptoms of polyuria, nocturia, or polydipsia may be the result of type 2 diabetes. Hip or knee pain can be caused by secondary orthopedic problems, including Blount disease and slipped capital femoral epiphysis. Irregular menses may be associated with polycystic ovary syndrome. Acanthosis nigricans can suggest insulin resistance and type 2 diabetes ( Fig. 60.4 ).

The family history begins with identifying other obese family members. Parental obesity is an important risk for child obesity. If all family members are obese, focusing the intervention on the entire family is reasonable. The child may be at increased risk for developing type 2 diabetes if a family history exists. Patients of African American, Hispanic, or Native American heritage are also at increased risk for developing type 2 diabetes. Identification of a family history of hypertension, CV disease, or metabolic syndrome indicates increased risk for developing these obesity-associated conditions. If the clinician helps the family to understand that childhood obesity increases risk for developing these chronic diseases, this educational intervention might serve as motivation to improve their nutrition and PA.

Physical examination should be thorough, focusing on possible comorbidities (see Table 60.2 ). Careful screening for hypertension using an appropriately sized blood pressure cuff is important. Systematic examination of the skin can reveal acanthosis nigricans, suggesting insulin resistance, or hirsutism, suggesting polycystic ovary syndrome. Tanner staging can reveal premature adrenarche secondary to advanced sexual maturation in overweight and obese girls.

Laboratory testing for fasting plasma glucose, triglycerides, low-density lipoprotein and high-density lipoprotein cholesterol, and liver function tests are recommended as part of the initial evaluation for newly identified pediatric obesity ( Table 60.4 ). Overweight children (BMI 85–95th percentile) who have a family history of diabetes mellitus or signs of insulin resistance should also be evaluated with a fasting plasma glucose test. Other laboratory testing should be guided by history or physical examination findings. Fig. 60.5 provides a recommended approach to categorization, evaluation, and treatment.