Rudolph's Pediatrics, 22nd Ed.

CHAPTER 32. The Overweight or Obese Child

Michelle Smith-Beckley and Brian M. Fidlin

The percentage of overweight children in the United States has more than tripled since 1980 with the greatest impact occurring among minority and economically disadvantaged children.1 Globally, it is currently estimated that 1 in 10 school-aged children is overweight (roughly 155 million children) and 30 to 45 million of those children are considered obese.2 For children under the age of 5 years, a further 22 million children are considered overweight.3These findings suggest a very troubling future given that the likelihood of obesity persisting into adulthood increases from 20% at 4 years of age to 80% by adolescence and that obesity increases the risk for a myriad of weight-related health complications.4

To better understand the pathobiology of obesity, it is useful to review the process by which adipose tissue is created. From an evolutionary prospective, it is beneficial to store energy during periods of energy availability in preparation for very likely periods of food scarcity. The body stores the available excess energy in the form of triglycerides within fat cells that reside within the adipose tissue. This tissue is widely distributed throughout the body and can store a tremendous amount of excess energy. When food scarcity limits energy intake, the body then releases the stored energy in the form of free fatty acids, providing a survival advantage. A delicate balance exists, and even small, subtle changes in lifestyle can begin leading a person toward obesity. A small but regular increase in calories or cessation of a regular physical activity can tip the balance toward overweight and obesity. In our current Western environment, food scarcity is uncommon with readily available high-density caloric foods being relatively inexpensive.

The factors that influence an individual’s intake-to-expenditure ratio are nearly limitless. Children are confronted on a daily basis with a tremendous amount of marketing encouraging the consumption of high-calorie, high-fat, and high-sugar foods and drinks. They become progressively more sedentary as they are encouraged to engage in activities like video games, the Internet, and television. More subtle influences may include neighborhoods that are too dangerous for children to play outside, inadequate sleep, parents who do not model appropriate health behaviors, and governmental policies. These influences alter the child’s intake-to-expenditure energy ratio.

An individual’s genetics also plays a significant role in the development of weight and weight-related problems. Children who are adopted possess body mass indices that are more closely related to their biological than to their adoptive parents.5 Apart from genetic risk, an individual’s obesity risk is also shaped by the environment and biological factors, such as leptin, ghrelin, adiponectin, and other hormones that affect specific metabolic functioning, such as appetite, satiety, and fat distribution.6


The most practical and widely used means for determining weight status is to calculate body mass index (BMI).

Results are plotted on age and gender–appropriate charts. Routine plotting of a child’s BMI allows the physician to not only determine weight status but also examine weight trajectory over time by evaluation of changes in BMI percentile channels. While BMI does not directly measure excess adipose tissue, it is a reliable indicator of body fat for most children.7 A BMI over the 85th percentile is considered overweight, and over the 95th percentile is classified as obese. BMI charts for boys and girls are available at the Centers for Disease Control and Prevention Web site:

Table 32-1. Genetic Syndromes and Gene Defects Associated with Obesity

HHMO (hypogonadism, hypomentia, hypotonia, and obesity)

Lawrence-Moon-Bardet-Biedl syndrome (includes retinitis pigmentosa)

Prader-Willi syndrome (loss of imprinted genes on 15q11-13)

Alstrom syndrome

Cohen syndrome

Albright hereditary osteodystrophy (pseudohypo-parathyroidism)

Carpenter syndrome

MOMO (macrosomia, obesity, macrocephaly, and ocular abnormalities) syndrome

Rubinstein-Taybi syndrome

Deletions of 6q16, 1p36, 2q37, and 9q34

Maternal uniparental disomy of chromosome 14

Fragile X syndrome

Börjeson-Forssman-Lehman syndrome

POMC (proopiomelanocortin) deficiency syndromes (severe early-onset obesity, adrenal insufficiency, red hair due to a complete loss of function mutation of the human POMC gene)

Table 32-2. Complications of Overweight and Obesity Cardiovascular Hypertension

Table 32-3. History, Symptoms, and Signs of Conditions Caused by or Associated with Overweight and Obesity History and Symptoms Polyuria, polydipsia, weight loss anxiety, school avoidance, social isolation

A dual-energy x-ray absorptiometry scan can determine the amount of an individual’s body fat and bone mineral content. Computer tomography (CT) and magnetic resonance imaging (MRI) scans allow examination of the placement of specific fat distributions. Bioelectrical impedance examines body fat as well as the amount of body water an individual possesses.


Obesity is almost always due to an imbalance of caloric intake and expenditures, as described previously. Obesity is rarely secondary to genetic or endocrine conditions. Very early–onset obesity is more likely to be associated with an underlying genetic syndrome, although in some cases, such as Prader-Willi syndrome, weight gain may be slow during infancy because of feeding difficulties. Decreased linear growth in the face of obesity is a major red flag for a primary genetic or endocrine condition. The most common genetic syndromes are the hypogonadism, hypomentia, hypotonia, and obesity (HHHO) syndromes. Two forms are well known: Prader-Willi Syndrome (the most common obesity syndrome due to loss of imprinted genes on 15q11-13) and Lawrence-Moon-Bardet-Biedl syndrome. Others are listed in Table 32-1.8-10

Iatrogenic agents that contribute to obesity include glucocorticoids, appetite stimulants such as megestrol acetate, certain antidepressants, antipsychotics and oral hypoglycemic agents. Injury or malformation of the satiety center in the hypothalamus can also lead to hyperphagia and obesity. This condition is rare and is diagnosed anatomically or by association with other hypothalamic defects. Endocrine disorders associated with obesity include Cushing disease and hypothyroidism, but these are rare, and other symptoms and signs are observed such that routine measurement of hormone levels in overweight and obese children is not recommended.11

Comorbidities of overweight and obesity are summarized by organ system in Table 32-2, and a list of symptoms and signs for conditions either associated with obesity or caused by obesity are shown in Table 32-3.


Evaluation of the overweight or obese child or adolescent begins with a careful assessment of the degree of obesity, lifestyle issues (diet, sleep, and physical activity) and screening for complications. The American Medical Association, Health Resources and Services Administration, and Centers for Disease Control and Prevention released their expert recommendations on the assessment, prevention, and treatment of child and adolescent overweight and obesity in 2007.12 The document is available at

The most effective treatment of overweight and obesity is prevention. Community efforts to prevent obesity encourage healthier lifestyles with better food choices and availability of healthy food, increased activity, and reduced television viewing, video-game playing, and computer use (or “screen time”). Unfortunately, positive lifestyle messages are diluted by a substantial amount of marketing of unhealthy products and lifestyles. Well-child care visits represent an opportunity for screening and counseling. Most interventions consist of lifestyle modifications. Pharmacologic therapies and surgical therapy are reserved for those with severe obesity and/or comorbidities.

Table 32-4. Prevention and Treatment of Overweight and Obesity

Assess all children for obesity at well-child care visits from age 2 to 18 years

Accurately measure height and weight, calculate BMI

Categorize weight: underweight (< 5%), healthy weight (5–84%), overweight (85–94%), obese (≥ 95%)

Measure blood pressure (use appropriately sized cuff)

Perform a focused family history for:

Obesity (especially in parents)

Type 2 diabetes



Early deaths from heart disease or stroke

Assess behaviors and attitudes that increase risk for overweight

Sweetened beverage consumption

Unhealthy diet habits

Frequency of eating out

Portion sizes

Physical activity levels

Screen time

Physical examination (see Table 32-3)

Order laboratory tests to screen for comorbidities if appropriate

BMI 85–94%: fasting lipid profile

BMI 85–94%, age ≥ 10 yrs, with risk factors or BMI > 95% and age ≥ 10 yrs: fasting lipid profile, aspartate aminotransferase, alanine aminotransferase, fasting glucose and other tests as indicated (consider fasting insulin and HgbA1c)

Provide counseling using motivational interviewing techniques that engage patient and family. Common useful interventions include:

Limit sugar-sweetened beverages

Eat at least 5 servings of fruits and vegetables

Moderate to vigorous physical activity for at least 60 min a day

Limit screen time to no more than 2 hr/day

Remove television and video games from children’s bedrooms

Eat breakfast every day

Limit eating out, especially at fast food restaurants

Have regular family meals

Limit portion sizes

Utilize appropriate tools

Health education materials

Behavioral risk assessment and self-monitoring tools

Action planning and goal setting tools

Referral to other health professionals, including dietitians, psychologists, and health educator

Individual or group visits with frequency individualized to family needs and risk factors; consider monthly

BMI, body mass index.


All children benefit from weight screening at all health care visits. Table 32-4 outlines some of the important aspects of such screening. In those with a high BMI, counseling to achieve lifestyle modifications is recommended. Informing the family of the child’s weight-associated risks is generally helpful. Using more neutral terms to describe weight, such as excess weight, body mass index, or risk for diabetes and heart disease can reduce the risk of stigmatization or harm to self-esteem in the child and may allow the family to engage in therapeutic changes. A focused family history is important to identify additional risk factors. A child with 1 obese parent has a 3-fold increased risk, and with 2 obese parents, a 13-fold increased risk of becoming obese. A family history of type 2 diabetes, hypertension, hypercholesterolemia, and early deaths from heart disease or stroke increases risk in the child. Assessment of risk behaviors and attitudes allows intervention. The family’s perception or concern about weight, readiness to change, successes, and barriers to change should be evaluated. Primary care providers can access a useful toolkit at that includes a health habit screening form, educational handouts for families, tips on how to implement the program in the pediatric office, and tips on using motivational interviewing with patient families. Increased activity, decreased sedentary time (especially screen time), improved sleep habits, and reduced intake of sweetened beverages and fatty foods are initial steps to promote weight loss. In children with a BMI higher than the 95th percentile, formal programs that focus on lifestyle change should be considered if the family can be motivated to participate. Interdisciplinary teams, including dietitians, physical therapists, psychologists, social workers, and physicians, can provide effective care for select patients, but community efforts are required to address the needs of most children. Weight loss targets appropriate for specific age and BMI are shown in eTable 32.1.


Adjunct pharmacotherapy should be considered only in obese children with severe comorbidities if a formal program of intensive lifestyle modification has been ineffective. Treatment effects are often modest and not well sustained. Most therapies are associated with potential complications. Drug treatments may include sibutramine, which is not approved for use in those younger than 16 years; orlistat, which is approved only for those older than 12 years; and metformin, which is not approved for treatment of obesity but is approved for those who are at least 10 years old with type 2 diabetes mellitus. Medications sometimes discussed for treatment but with even less pediatric experience include octreotide, leptin, topiramate, and growth hormone, none of which have been approved for the treatment of obesity.11


Bariatric surgery should be considered for adolescents with a BMI of more than 40 kg/m2 in whom lifestyle modifications have been unsuccessful and for those who have severe comorbidities.13 It should be performed only in those who have attained a majority of skeletal maturity (generally age 13 years for girls and age 15 years for boys). The patient and family need to be committed to lifelong change and adherence to prescribed nutritional, behavioral, and medical follow-up. These procedures should be performed only by experienced surgeons in the context of a multidisciplinary team that can evaluate the benefits and risks for surgery in each individual patient. Bariatric surgery is not recommended for preadoles-cent children; for pregnant or breast-feeding adolescents; for those planning to become pregnant within 2 years of surgery; or for any patient with an unresolved eating disorder, untreated psychiatric disorder, or Prader-Willi syndrome.

Bariatric surgical procedures include restrictive procedures that decrease the reservoir capacity of the stomach, malabsorptive procedures that decrease absorption of nutrients, and combinations of these. The gastric banding (“lapband”) procedure consists of placement of a fluid-filled balloon band around the upper end of the stomach. This creates a small pouch and narrow passage into the rest of the stomach. The vertical banded gastroplasty creates the pouch with both a band and staples. Gastric bypass procedures create a small stomach pouch that restricts food ingestion and constructs a bypass of the duodenum and other parts of the small intestine to cause malabsorption. This is most commonly achieved with a Roux-en-Y segment of small intestine being connected to the gastric pouch.

There is limited experience with the Roux-en-Y gastric bypass in adolescent patients, with good results being reported in more than half of the patients, but complications can be substantial and include pulmonary embolism, shock, intestinal obstruction, postoperative bleeding, staple line leak, beriberi, and severe malnutrition.14,15 Fewer adolescent patients have received lapband therapy with good efficacy. Reported complications of lapband include band slippage, micronutrient deficiency, band erosion, port/tube dysfunction, hiatal hernia, wound infection, and pouch dilation.15,16 Thus, careful follow-up is essential after any type of bariatric surgery.