Overweight and Obesity

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Chapter 44 Overweight and Obesity

Obesity is an important pediatric public health problem associated with risk of complications in childhood and increased morbidity and mortality throughout adult life. The prevalence of childhood obesity has increased, and the prevention and treatment of obesity has emerged as an important focus of pediatric research and clinical care.

Body Mass Index

Health care professionals define obesity or increased adiposity using the body mass index (BMI), which is 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. 44-1). Consequently, obesity and overweight are defined using BMI percentiles; children >2 yr old with a BMI ≥95th percentile meet the criterion for obesity, and those with a BMI between the 85th and 95th percentiles fall in the overweight range. The terminology used for pediatric obesity previously was “overweight” and “risk for overweight.” This terminology has changed to improve consistency with the adult criteria and international definitions of pediatric obesity.

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, and energy expenditure. Environmental factors determine levels of available food, preferences for types of foods, levels of physical activity, and preferences for types of activities.

Environmental Changes

Over the last 4 decades, the food environment has changed dramatically. Changes in the food industry relate in part to social changes, as extended families have become more dispersed. Few families have someone at home to prepare meals. Foods are increasingly prepared by a “food industry,” with high levels of calories, simple carbohydrates, and fat. The price of many foods has declined relative to the family budget. These changes, in combination with marketing pressure, have resulted in larger portion sizes and increased snacking between meals. The increased consumption of high-carbohydrate beverages, including sodas, sport drinks, fruit punch, and juice, adds to these factors.

One third of U.S. children consume “fast food” daily. A typical fast food meal can contain 2000 kcal and 84 g of fat. Many children consume 4 servings of high-carbohydrate beverages per day, resulting in an additional 560 kcal of low nutritional value. Sweetened beverages have been linked to increased risk for obesity because children who drink high amounts of sugar do not consume less food. The dramatic increase in the use of high-fructose corn syrup to sweeten beverages and prepared foods is another important environmental change. Fructose-laden products mighty increase obesity risk through a mechanism related to appetite control. Unlike glucose, which decreases food intake through the malonyl-CoA signaling pathway, consumption of fructose does not result in a similar decrease.

Since World War II, levels of physical activity in children and adults have declined. Changes in the built environment have resulted in more reliance on cars and decreased walking. Work is increasingly sedentary, and many sectors of society do not engage in physical activity during leisure time. For children, budgetary constraints and pressure for academic performance have led to less time devoted to physical education in schools. Perception of poor neighborhood safety is another factor that can lead to lower levels of physical activity when children are required to stay indoors. The advent of television, computers, and video games has resulted in opportunities for sedentary activities that do not burn calories or exercise muscles.

Changes in another health behavior, sleep, might also contribute. Over the last 4 decades, children and adults have decreased the amount of time spent sleeping. Reasons for these changes may relate to increased time at work, increased time watching television, and a generally faster pace of life. Chronic partial sleep loss can increase risk for weight gain and obesity, with the impact possibly greater in children than in adults. In studies of young, healthy, lean men, short sleep duration was associated with decreased leptin levels and increased ghrelin levels, along with increased hunger and appetite. Sleep debt also results in decreased glucose tolerance and insulin sensitivity related to alterations in glucocorticoids and sympathetic activity. Some effects of sleep debt might relate to orexins, peptides synthesized in the lateral hypothalamus that can increase feeding, arousal, sympathetic activity, and/or neuropeptide Y activity.

Genetics

The rapid rise in obesity prevalence relates to dramatic environmental changes, but genetic determinants may be important for individual susceptibility. Rare single-gene disorders resulting in human obesity are known, including FTO (fat mass and obesity) and INSIG2 (insulin-induced gene 2) mutations as well as leptin deficiency and pro-opiomelanocortin deficiency. In addition, other genetic disorders associated with obesity such as Prader-Willi syndrome have long been recognized (Table 44-1). It is likely that genes are involved in behavioral phenotypes related to appetite regulation and preference for physical activity. More than 600 genes, markers, and chromosomal regions have been associated with human obesity.

Table 44-1 ENDOCRINE AND GENETIC CAUSES OF OBESITY

DISEASE SYMPTOMS LABORATORY
ENDOCRINE
Cushing syndrome Central obesity, hirsutism, moon face, hypertension Dexamethasone suppression test
Growth hormone deficiency Short stature, slow linear growth Evoked GH response, IGF-1
Hyperinsulinism Nesidioblastosis, pancreatic adenoma, hypoglycemia, Mauriac syndrome Insulin level
Hypothyroidism Short stature, weight gain, fatigue, constipation, cold intolerance, myxedema TSH, FT4
Pseudohypoparathyroidism Short metacarpals, subcutaneous calcifications, dysmorphic facies, mental retardation, short stature, hypocalcemia, hyperphosphatemia Urine cAMP after synthetic PTH infusion
GENETIC
Alstrom syndrome Cognitive impairment, retinitis pigmentosa, diabetes mellitus, hearing loss, hypogonadism, retinal degeneration ALMS1 gene
Bardet-Biedl syndrome Retinitis pigmentosa, renal abnormalities, polydactyly, hypogonadism BBS1 gene
Biemond syndrome Cognitive impairment, iris coloboma, hypogonadism, polydactyly  
Carpenter syndrome Polydactyly, syndactyly, cranial synostosis, mental retardation Mutations in the RAB23 gene, located on chromosome 6 in humans
Cohen syndrome Mid-childhood-onset obesity, short stature, prominent maxillary incisors, hypotonia, mental retardation, microcephaly, decreased visual activity Mutations in the VPS13B gene (often called the COH1 gene) at locus 8q22
Deletion 9q34 Early-onset obesity, mental retardation, brachycephaly, synophrys, prognathism, behavior and sleep disturbances Deletion 9q34
Down syndrome Short stature, dysmorphic facies, mental retardation Trisomy 21
ENPP1 gene mutations Insulin resistance, childhood obesity Gene mutation on chromosome 6q
Frohlich syndrome Hypothalamic tumor  
Leptin or leptin receptor gene deficiency Early-onset severe obesity, infertility (hypogonadotropic hypogonadism) Leptin
Melanocortin 4 receptor gene mutation

MC4R mutation Prader-Willi Syndrome Neonatal hypotonia, slow infant growth, small hands and feet, mental retardation, hypogonadism, hyperphagia leading to severe obesity, paradoxically elevated ghrelin Partial deletion of chromosome 15 or loss of paternally expressed genes Pro-opiomelanocortin deficiency Obesity, red hair, adrenal insufficiency, hyperproinsulinemia Loss-of-function mutations of the POMC gene Turner syndrome Ovarian dysgenesis, lymphedema, web neck, short stature, cognitive impairment XO chromosome

cAMP, cyclic adenosine monophosphate; FT4, free throxine; GH, growth hormone; IGF, insulin-like growth factor; PTH, parathyroid hormone; TSH, thyroid-stimulating hormone.

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 (Fig. 44-2). 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 cardiovascular outcomes. Leptin is directly involved in satiety, as low leptin levels stimulate food intake and high leptin levels inhibit hunger in animal models and in healthy human volunteers. Adiposity correlates to serum leptin levels among children and adults, with the direction of effect remaining unclear.

Numerous neuropeptides in the brain, including neuropeptide Y, agouti-related peptide, and orexin, appear to affect appetite stimulation, whereas melanocortins and α-melanocortin-stimulating hormone are involved in satiety. The neuroendocrine control of appetite and weight involves a negative-feedback system, balanced between short-term control of appetite (including ghrelin, PPY) and long-term control of adiposity (including leptin).

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 cardiovascular disease as those who had normal weight. More immediate comorbidities include type 2 diabetes, hypertension, hyperlipidemia, and nonalcoholic fatty liver disease (Table 44-2). Insulin resistance increases with increasing adiposity and independently affects lipid metabolism and cardiovascular health. Nonalcoholic fatty liver disease occurs in 10-25% of obese adolescents and can progress to cirrhosis.

Table 44-2 OBESITY-ASSOCIATED COMORBIDITIES

DISEASE POSSIBLE SYMPTOMS LABORATORY CRITERIA
CARDIOVASCULAR
Dyslipidemia HDL <40, LDL >130, total cholesterol >200 Fasting total cholesterol, HDL, LDL, triglycerides
Hypertension SBP >95% for sex, age, height Serial testing, urinalysis, electrolytes, blood urea nitrogen, creatinine
ENDOCRINE
Type 2 diabetes mellitus Acanthosis nigrans, polyuria, polydipsia Fasting blood glucose >110, hemoglobin, A1c, insulin level, C-peptide, oral glucose tolerance test
Metabolic syndrome Central adiposity, insulin resistance, dyslipidemia, hypertension, glucose intolerance Fasting glucose, LDL and HDL cholesterol
Polycystic ovary syndrome Irregular menses, hirsutism, acne, insulin resistance, hyperandrogenemia Pelvic ultrasound, free testosterone, LH, FSH
GASTROINTESTINAL
Gallbladder disease Abdominal pain, vomiting, jaundice Ultrasound
Nonalcoholic fatty liver disease (NAFLD)

AST, ALT, ultrasound, CT, or MRI NEUROLOGIC Pseudotumor cerebri Headaches, vision changes, papilledema Cerebrospinal fluid opening pressure, CT, MRI ORTHOPEDIC Blount disease (tibia vara) Severe bowing of tibia, knee pain, limp Knee x-rays Musculoskeletal problems Back pain, joint pain, frequent strains or sprains, limp, hip pain, groin pain, leg bowing X-rays Slipped capital femoral epiphysis Hip pain, knee pain, limp, decreased mobility of hip Hip x-rays PSYCHOLOGICAL Behavioral complications Anxiety, depression, low self-esteem, disordered eating, signs of depression, worsening school performance, social isolation, problems with bullying or being bullied Child Behavior Checklist, Children’s Depression Inventory, Peds QL, Eating Disorder Inventory 2, subjective ratings of stress and depression, Behavior Assessment System for Children, Pediatric Symptom Checklist PULMONARY Asthma Shortness of breath, wheezing, coughing, exercise intolerance Pulmonary function tests, peak flow Obstructive sleep apnea Snoring, apnea, restless sleep, behavioral problems Polysomnography, hypoxia, electrolytes (respiratory acidosis with metabolic alkalosis)

ALT, alanine aminotransferase; AST, aspartate aminotransferase; CT, computed tomography; FSH, follicle-stimulating hormone; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LH, luteinizing hormone; MRI, magnetic resonance imaging; Peds QL, Pediatric Quality of Life Inventory.

In adults, the combination of central obesity, hypertension, glucose intolerance, and hyperlipidemia is the metabolic syndrome. Persons with the metabolic syndrome are at increased risk for cardiovascular morbidity and mortality. Experts do not uniformly agree that this symptom cluster in the pediatric age group has prognostic significance.

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