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.

There is increasing evidence that obesity may be associated with chronic inflammation. Adiponectin, a peptide with anti-inflammatory properties, occurs in reduced levels in obese patients as 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 pro-inflammatory peptides such interleukin (IL)-6 and tumor necrosis factor-α (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 (Chapters 669, 670.4).

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 compared to 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.

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 comorbid conditions.

Examination of the growth chart reveals the severity, duration, and timing of obesity onset. Children who are overweight (BMI in the 85th-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 even 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 years), and adolescence. Severe obesity and obesity of long duration can require more intensive family intervention unless the family is highly motivated to make dietary and activity changes. 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 expand understanding of 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 44-1). 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 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 physical activity can lead to secondary obesity. Some medications can cause excessive appetite and hyperphagia, resulting in obesity. Atypical antipsychotic medications most commonly have this dramatic side effect. Rapid weight gain in a child or adolescent taking one of these medications might require a discontinuation of that medication. Poor linear growth and rapid changes in weight gain are indications for evaluation of possible medical causes.

Exploration of family eating and nutritional and activity patterns begins with a description of regular meal and snack times and family habits for walking, bicycle riding, active recreation, television, computer, and video-game time. It is useful to request a 24-hour 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 physical activity 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 44-2). Developmental delay and visual and hearing impairment can be associated with genetic disorders. Difficulty sleeping, snoring, or daytime sleepiness suggests the possibility of sleep apnea. Abdominal pain might suggest nonalcoholic fatty liver disease. 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. 44-3).

image

Figure 44-3 Acanthosis nigricans.

(From Gahagan S: Child and adolescent obesity, Curr Probl Pediatr Adolesc Health Care 34:6–43, 2004.)

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, cardiovascular disease, or metabolic syndrome indicates increased risk for developing these obesity-associated conditions. If one 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 physical activity.

Physical examination should be thorough, focusing on possible comorbid conditions (see Table 44-2). 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 (LDL) and high-density lipoprotein (HDL) cholesterol, and liver function tests are recommended as part of the initial evaluation for newly identified pediatric obesity (Table 44-3). Overweight children (BMI 85th-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.

Table 44-3 NORMAL LABORATORY VALUES FOR RECOMMENDED TESTS

LABORATORY TEST NORMAL VALUE
Glucose <110 mg/dL
Insulin <15 mU/L
Hemoglobin A1c <5.7%
AST 2-8 yr <58 U/L
AST 9-15 yr <46 U/L
AST 15-18 yr <35 U/L
ALT <35 U/L
Total cholesterol <170 mg/dL
LDL <110 mg/dL
HDL <35 mg/dL
Triglycerides 2-15 yr <100 mg/dL
Triglycerides 15-19 yr <125 mg/dL

AST, aspartate aminotransferase; ALT, alanine aminotransferase; LDL, low-density lipoprotein; HDL, high-density lipoprotein.

From Children’s Hospital of Wisconsin: The NEW (nutrition, exercise and weight management) kids program (PDF file). www.chw.org/display/displayFile.asp?docid=33670&filename=/Groups/NEWKids/08_Referral_Form.pdf. Accessed February 2, 2011.

Intervention

Successful intervention for obesity is challenging and is best accomplished using multimodal approaches to accomplish substantial lifestyle change. In adults, long-term weight loss is uncommon despite the availability of a wide variety of diet plans, commercial products, and medications. Cognitive-behavioral therapy approaches to improve motivation have been promising. A combination of nutritional advice, exercise, and cognitive behavioral approaches usually work best. Bariatric surgery can accomplish considerable weight loss in adolescents. It is not yet clear whether these patients will maintain a healthy weight permanently, and long-term safety has yet to be established.

It is important to begin with clear recommendations about appropriate caloric intake for the obese child (Table 44-4). Working with a dietitian is very helpful. Meals should be based on fruits, vegetables, whole grains, lean meat, fish, and poultry. Prepared foods should be chosen for their nutritional value, with attention to calories and fat. Foods that provide excessive calories and low nutritional value should be reserved for infrequent treats. Because many obese children are consuming calories greatly in excess of their needs, it is often impossible to achieve an immediate reduction to the recommended daily calorie level. Instead, a gradual approach is recommended. A 10 yr old child who requires 2000 kcal/day and consumes 3500 kcal/day could reduce his typical daily intake by 280 kcal by forgoing two cans of high-carbohydrate beverage and drinking water instead. Although this dietary change will not result in weight loss, it will probably result in slightly slower weight gain. Once this change has been successfully incorporated, the child could make another change such as cutting out a snack, thereby eliminating an additional 300 kcal.

Weight-reduction diets in adults generally do not lead to sustained weight loss. Therefore, the focus should be on changes that can be maintained for life. Attention to eating patterns is helpful. Families should be encouraged to plan family meals, including breakfast. It is almost impossible for a child to make changes in nutritional intake and eating patterns if other family members do not make the same changes. Dietary needs also change developmentally, as adolescents require greatly increased calories during their growth spurts, and adults who lead inactive lives need fewer calories than active and growing children.

Psychological strategies are helpful. The “traffic light” diet groups foods into those that can be consumed without any limitations (green), in moderation (yellow), or reserved for infrequent treats (red) (Table 44-5). The concrete categories are very helpful to children and families. This approach can be adapted to any ethnic group or regional cuisine. Motivational interviewing, a strategy with proven efficacy for decreasing tobacco and substance use, shows promise for assisting patients in changing their nutritional patterns. This approach begins with assessing how ready the patient is to make important behavioral changes. The professional then engages the patient in developing a strategy to take the next step toward the ultimate goal of healthy nutritional intake. This method allows the professional to take the role of a coach, helping the child and family reach their goals. Other behavioral approaches include family rules about where food may be consumed—for example, “not in the bedroom.” Evidence-based strategies can be used to tailor interventions, given individual and environmental differences.

It is very difficult to achieve weight loss by increasing physical activity alone. Nonetheless, increasing fitness improves cardiovascular health even without weight loss. Therefore, increasing physical activity can decrease risk for cardiovascular disease, improve well-being, and contribute to weight loss. Increased physical activity can be accomplished by walking to school, engaging in physical activity during leisure time with family and friends, or enrolling in organized sports. Children are more likely to be active if their parents are active. Just as family meals are recommended, family physical activity is recommended.

Active pursuits can replace more sedentary activities. The American Academy of Pediatrics recommends that screen time be restricted to no more than 2 hr/day for children >2 yr old and that children <2 yr old not watch television. Television watching is often associated with eating, and many highly caloric food products are marketed directly to children during child-oriented television programs.

Pediatric providers should assist families to develop goals to change nutritional intake and physical activity. They can also provide the child and family with needed information. The family should not expect immediate lowering of BMI percentile related to behavioral changes but can instead count on a gradual decrease in the rate of BMI percentile increase until it stabilizes, followed by a gradual decrease in BMI percentile. Referral to multidisciplinary, comprehensive pediatric weight-management programs is ideal for obese children whenever possible. As part of a comprehensive program, adolescents may receive adjunctive pharmacologic therapy. In adults, the addition of antiobesity drugs to comprehensive lifestyle modification can produce more weight loss than lifestyle modification alone, with a BMI-lowering effect of 4%. Sibutramine, a norepinephrine and serotonin reuptake inhibitor, and Orlistat, an intestinal lipase inhibitor, is as effective as adjunctive therapy to behavior modification for weight loss in overweight adolescents (Table 44-6). The effect on long-term weight maintenance is not yet known. The pediatric provider also makes referrals to specialists to treat comorbid conditions, including type 2 diabetes, hypertension, nonalcoholic fatty liver disease, and orthopedic disorders.

Table 44-6 MEDICATIONS USED FOR WEIGHT LOSS IN ADULTS

DRUG MECHANISM OF ACTION SIDE EFFECTS
Sibutramine* Appetite suppressant: combined norepinephrine and serotonin reuptake inhibitor Modest increases in heart rate and blood pressure, nervousness, insomnia
Phentermine* Appetite suppressant: sympathomimetic amine Cardiovascular, gastrointestinal
Diethylpropion* Appetite suppressant: sympathomimetic amine Palpitations, tachycardia, insomnia, gastrointestinal
Orlistat* Lipase inhibitor: decreased absorption of fat Diarrhea, flatulence, bloating, abdominal pain, dyspepsia
Bupropion Appetite suppressant: mechanism unknown Paresthesia, insomnia, central nervous system effects
Fluoxetine Appetite suppressant: selective serotonin reuptake inhibitor Agitation, nervousness, gastrointestinal
Sertraline Appetite suppressant: selective serotonin reuptake inhibitor Agitation, nervousness, gastrointestinal
Topiramate Mechanism unknown Paresthesia, changes in taste
Zonisamide Mechanism unknown Somnolence, dizziness, nausea

* Approved by the U.S. Food and Drug Administration for weight loss.

Drug Enforcement Administration schedule IV.

From Snow V, Barry P, Fitterman N, et al: Pharmacologic and surgical management of obesity in primary care: a clinical practice guideline from the American College of Physicians, Ann Intern Med 142:525–531, 2005.

In some cases, it is reasonable to refer adolescents for evaluation for bariatric surgery. The American Pediatric Surgical Association Guidelines recommends that surgery be considered only in children with complete or near-complete skeletal maturity, a BMI ≥40, and a medical complication resulting from obesity, after they have failed 6 mo of a multidisciplinary weight management program. Current surgical approaches include the Roux-en-Y and the adjustable gastric band.

Prevention

Prevention of child and adolescent obesity is essential for public health in the USA and most other countries (Tables 44-7 and 44-8). Efforts by pediatric providers can supplement national- and community-level public health programs. The National Institutes of Health (NIH) and Centers for Disease Control and Prevention (CDC) recommend a variety of initiatives to combat the current obesigenic environment, including promotion of breast-feeding, access to fruits and vegetables, walkable communities, and 60 min/day of activity for children. The USDA sponsors programs promoting 5.5 cups of fruits and vegetables per day. Incentives for the food industry to promote consumption of healthier foods should be considered. Marketing of unhealthy foods to children has begun to be regulated. We expect to see changes in federal food programs including commodity foods, the Women, Infant, and Children Supplemental Food Program (WIC), and school-lunch programs to meet the needs of today’s children.

Table 44-7 PROPOSED SUGGESTIONS FOR PREVENTING OBESITY

PREGNANCY

POSTPARTUM AND INFANCY

FAMILIES

SCHOOLS

COMMUNITIES

HEALTH CARE PROVIDERS

INDUSTRY

GOVERNMENT AND REGULATORY AGENCIES

From Speiser PW, Rudolf MCJ, Anhalt H, et al: Consensus statement: childhood obesity, J Clin Endocrinol Metabol 90:1871–1887, 2005.

The Ways to Enhance Children’s Activity and Nutrition (WE CAN) program is an example of a community-based child obesity prevention effort aimed at 8- to 12-year old children. This national program, designed for families and communities, focuses on three important behaviors: improved food choices, increased physical activity, and reduced screen time. Child health professionals can serve as leaders and topic experts for community programs. Speeches at schools, at community centers, and on local radio and television programs emphasize the importance of nutrition and physical activity for health.

Pediatric prevention efforts begin with careful monitoring of weight and BMI percentiles at health care maintenance visits. Attention to changes in BMI percentiles can alert the pediatric provider to increasing adiposity before the child becomes overweight or obese. All families should be counseled about healthy nutrition for their children because the current prevalence of overweight and obesity in adults is 65%. Therefore, approximately 2/3 of all children can be considered at risk for becoming overweight or obese at some time in their lives. Those who have an obese parent are at increased risk. Prevention efforts begin with promotion of exclusive breast-feeding for 6 mo and total breast-feeding for 12 mo. Introduction of infant foods at 6 months should focus on cereals, fruits, and vegetables. Lean meats, poultry, and fish may be introduced later in the 1st year of life. Parents should be specifically counseled to avoid introducing highly sugared beverages and foods in the 1st year of life. Instead, they should expose their infants and young children to a rich variety of fruits, vegetables, grains, lean meats, poultry, and fish to facilitate acceptance of a diverse and healthy diet. Parenting matters, and authoritative parents are more likely to have children with a healthy weight than those who are authoritarian or permissive. Families who eat regularly scheduled meals together are less likely to have overweight or obese children. Child health professionals are able to address a child’s nutritional status and to provide expertise in child growth and development.

Child health professionals can also promote physical activity during regular health care maintenance visits. Parents who spend some of their leisure time in physical activity promote healthy weight in their children. Beginning in infancy, parents should be cognizant of their child’s developmental capability and need for physical activity. Because television, computer, and video-game time can replace health-promoting physical activity, physicians should counsel parents to limit screen time for their children. Snacking during television watching should be discouraged. Parents can help their children to understand that television commercials intend to sell a product. Children can learn that their parents will help them by responsibly choosing healthy foods.

Bibliography

Ahima RS, Antwi DA. Brain regulation of appetite and satiety. Endocrinol Metab Clin. 2008;37:811-823.

American Heart Association. Dietary recommendations for children and adolescents: a guide for practitioners. Pediatrics. 2006;117:544-559.

Astrup A, Rössner S, Van Gaal L, et al. Effects of liraglutide in the treatment of obesity: a randomized, double-blind, placebo-controlled study. Lancet. 2009;374:1606-1616.

August GP, Caprios S, Fennoy I, et al. Prevention and treatment of pediatric obesity: an endocrine society clinical practice guideline based on expert opinion. J Clin Endocrinol Metab. 2008;93:4576-4599.

Bochukova EG, Huang N, Keogh J, et al. Large, rare chromosomal deletions associated with severe early-onset obesity. Nature. 2010;463:666-670.

Cecchini M, Sassi F, Lauer JA, et al. Tackling of unhealthy diets, physical inactivity, and obesity: health effects and cost-effectiveness. Lancet. 2010;376:1775-1784.

Cecil JE, Tavendale R, Watt P, et al. An obesity-associated FTO gene variant and increased energy intake in children. N Engl J Med. 2008;359:2558-2566.

Centers for Disease Control and Prevention. CDC grand rounds: childhood obesity in the United States. MMWR. 2011;60:42-46.

Centers for Disease Control and Prevention. Effect of switching from whole to low-fat/fat-free milk in public schools—New York City, 2004–2009. MMWR. 2010;59:70-73.

Centers for Disease Control and Prevention. Recommended community strategies and measurements to prevent obesity in the United States. MMWR. 2009;58:1-29.

Centers for Disease Control and Prevention. Obesity prevalence among low-income, preschool-aged children—United States, 1998–2008. MMWR. 2009;58:769-772.

Centers for Disease Control and Prevention. Differences in prevalence of obesity among black, white, and Hispanic adults—United States, 2006–2008. MMWR. 2009;58:740-744.

Centers for Disease Control and Prevention. Availability of less nutritious snack foods and beverages in secondary schools—selected states, 2002–2008. MMWR. 2009;58:1102-1104.

Chan G, Chen CT. Musculoskeletal effects of obesity. Curr Opin Pediatr. 2009;21:65-70.

Daniels SR, Jacobson MS, McCrindle BW, et al. American Heart Association childhood obesity research summit report. Circulation. 2009;119:e489-e517.

Dunn W, Schwimmer JB. The obesity epidemic and nonalcoholic fatty liver disease in children. Curr Gastroentero Reports. 2008;10:67-72.

Eckel RH, Alberti KGMM, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2010;375:181-183.

Ford AL, Bergh C, Södersten P, et al. Treatment of childhood obesity by retraining eating behaviour: randomized controlled trial. BMJ. 2010;340:b5388.

Franks PW, Hanson RL, Knowler WC, et al. Childhood obesity, other cardiovascular risk factors, and premature death. N Engl J Med. 2010;362:485-492.

Glaser Pediatric Research Network Obesity Study Group. Metformin extended release treatment of adolescent obesity. Arch Pediatr Adolesc Med. 2010;164:116-123.

Han JC, Lawlor DA, Kimm SYS. Childhood obesity. Lancet. 2010;375:1737-1746.

2010 Evidence for effective obesity treatment: Pediatricians on the right track!. Pediatrics. 2010;125:37-38.

Ibáñez L, Lopez-Bermejo A, Diaz M, et al. Pubertal metformin therapy to reduce total, visceral, and hepatic adiposity. J Pediatr. 2010;156:98-102.

Kavey REW. Treatment for obese children: a ray of hope? J Pediatr. 2010;157(3):357-359.

The Lancet. Childhood obesity: affecting choices. Lancet. 2010;375:611.

Lane MD, Cha SH, et al. Effect of glucose and fructose on food intake via malonyl-CoA signaling in the brain. Biochem Biophys Res Comm. 2009;382:1-5.

Larsen TM, Dalskov SM, van Baak M, et al. Diets with high or low protein content and glycemic index for weight-loss maintenance. N Engl J Med. 2010;363(22):2102-2113.

Lee IM, Djoussé L, Sesso HD, et al. Physical activity and weight gain prevention. JAMA. 2010;303:1173-1179.

Meyre D, Delphanque J, Chévre JC, et al. Genome-wide association study for early-onset and morbid adult obesity identifies three new risk loci in European populations. Nature Genetics. 2009;41:157-159.

Murry R, Bttista M. Managing the risk of childhood overweight and obesity in primary care practice. Curr Prob Pediatr Adoles. 2009;39:145-166.

Nadler EP, Brotman LM, Miyoshi T, et al. Morbidity in obese adolescents who meet the adult National Institutes of Health criteria for bariatric surgery. J Pediatr Surg. 2009;44:1869-1876.

Nguyen NT, Slone JA, Nguyen XM, et al. A prospective randomized trial of laparoscopic gastric bypass versus laparoscopic adjustable gastric banding for the treatment of morbid obesity. Ann Surg. 2009;250:631-641.

O’Brien PE, Sawyer SM, Laurie C, et al. Laparoscopic adjustable gastric banding in severely obese adolescents. JAMA. 2010;303:519-526.

Ogden CL, Carroll MD, Curtin LR, et al. Prevalence of high body mass index in US children and adolescents, 2007–2008. JAMA. 2010;303:242-249.

Paz-Priel I, Cooke DW, Chen AR. Cyclophosphamide for rapid-onset obesity, hypothalamic dysfunction, hypoventilation, and autonomic dysregulation syndrome. J Pediatr. 2011;158(2):337-339.

Plum L, Lin HV, Dutia R, et al. The obesity susceptibility gene Cpe links FoxO1 signaling in hypothalamic pro-opiomelanocortin neurons with regulation of food intake. Nature Med. 2009;15:1195-1201.

Reinehr T, Hinney A, Toschke AM, Hebebrand J. Aggravating effect of INSIG2 and FTO on overweight reduction in a one-year lifestyle intervention. Arch Dis Child. 2009;94:965-967.

Ruiz JR, Labayen I, Ortega FB, et al. Attenuation of the effect of the FTO rs9939609 polymorphism on total and central body fat by physical activity in adolescents. Arch Pediatr Adolesc Med. 2010;164:328-333.

Sacher PM, Kolotourou M, Chadwick PM, et al. Randomized controlled trial of the MEND program: a family-based community intervention for childhood obesity. Obesity. 2010;18:S62-S68.

Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med. 2009;360:859-872.

Savoye M, Nowicka P, Shaw M, et al. Long-term results of an obesity program in an ethnically diverse pediatric population. Pediatrics. 2011;127(3):402-410.

Spyropoulos C, Kehagias I, Panagiotopoulos S, et al. Revisional bariatric surgery. Arch Surg. 2010;145:173-177.

Swinburn B, Sacks G, Ravussin E. Increased food energy supply is more than sufficient to explain the US epidemic of obesity. Am J Clin Nutr. 2009;90:1453-1456.

Taveras EM, Rifas-Shiman SL, Belfort MB, et al. Weight status in the first 6 months of life and obesity at 3 years of age. Pediatrics. 2009;123:1177-1183.

U.S. Department of Agriculture. Dietary guidelines for Americans, 2005 (website). www.health.gov/DIETARYGUIDELINES/dga2005/document/html/chapter2.htm. Accessed May 23, 2010

Van Cauter E, Knutson K. Sleep and the epidemic of obesity in children and adults. Eur J Endocrinol. 2008;159:S59-S66.

Van Cleave J, Gortmaker SL, Perrin JM. Dynamics of obesity and chronic health conditions among children and youth. JAMA. 2010;303:623-630.

Vandanmagsar B, Youm YH, Ravussin A, et al. The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance. Nat Med. 2011;17(2):179-188.

Vanselow MS, Pereira MA, Neumark-Sztainer D, Raatz SK. Adolescent beverage habits and changes in weight over time: finding from Project EAT. Am J Clin Nutr. 2009;90:1489-1495.

Weiss R, Kaufman F. Metabolic complications of childhood obesity: identifying and mitigating the risk. Diabetes Care. 2008;31:S310-S316.

Wilfley DE, Stein RI, Saelens BE, et al. Efficacy of maintenance treatment approaches for childhood overweight: a randomized controlled trial. JAMA. 2007;298:1661-1673.

Williams G. Withdrawal of sibutramine in Europe. BMJ. 2010;340:377-378.