COMORBIDITIES OF OBESITY
From Sizing Up the Childhood Overweight Epidemic for the Primary Care Provider, presented by Nemours
| METABOLIC SYNDROME —Samuel S. Gidding, MD, Professor of Pediatrics, Thomas Jefferson University, Jefferson
Medical College, Philadelphia, PA, and Director, Outreach Services, Nemours Cardiac Center, Wilmington, DE
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| Atherosclerosis: autopsy study of individuals 15 to 34 yr of age (accidental deaths) showed atherosclerosis increased with
increasing abdominal obesity, body mass index (BMI; >30 increases risk 3-fold), and glycohemoglobin (4- to 5-fold increase)
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| Metabolic syndrome: cluster includes elevated blood pressure (BP), elevated triglycerides, low levels of high-density
lipoprotein cholesterol (HDL-C), increased heart size, diminished physical fitness, increased levels of C-reactive protein
(CRP) and other inflammatory markers, and prothrombotic state
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| Evaluation of insulin resistance: methods—fasting blood glucose (preferred), 2-hr glucose tolerance test; random
measurement of blood glucose; insulin resistance —fasting insulin and hemoglobin A1c (HbA1c ) levels provide markers
of insulin resistance before blood glucose increases; fasting insulin <17 µU/mL generally eliminates diagnosis; upper
limit of normal HbA1c , 6.0%; note—measures highly variable, so check several times before diagnosing patient
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| Blood pressure: mean BP in overweight children elevated by 1 SD (6-8 mm Hg); weight loss decreases BMI and BP;
hypertension and obesity—≈10% of overweight children have high BP (3-fold risk compared to general population);
overweight leads to high cardiac output, abnormal resistance in peripheral vasculature, and elevated levels of aldosterone
and insulin
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 | Diagnosing hypertension in children: regular routine facilitates accurate measurement; eg, speaker always measures BP
in right arm with child sitting (right arm BP 5-10 mm Hg higher than left arm); initial measurements often high (child
nervous), so take several until BP levels off; using aneroid or mercury devices best; technical pointers—use appropriate-sized
cuff (bladder should reach ≥50% around arm; cuff should cover ≥50% of upper arm length); undercuffing
increases margin of error; BP tables—provide standards based on sex, age, and height
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| Left ventricular hypertrophy (LVH): study in adults classified participants as “optimal” or “nonoptimal”; <25% of men
and women met criteria for optimal group; mean LV mass ≈5 g less (ie, 10%-12% smaller) in optimal group; greater
LV mass significantly impacts risk for cardiac disease
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| Indications for medical treatment in children: symptomatic hypertension; secondary hypertension (eg, secondary to kidney
disease); hypertensive damage to target organs (eg, LVH); coexisting diabetes; persistent hypertension despite
nonpharmacologic measures
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| Dyslipidemia: diagnostic guidelines for children different from guidelines for adults; low-density lipoprotein cholesterol
(LDL-C)—medication appropriate for children \>10 yr of age with LDL-C ≥190 mg/dL; diet and behavioral intervention
preferred for children with levels between 100 mg/dL and 129 mg/dL; HDL-C—levels <40 mg/dL low; 40
to 59 mg/dL borderline; triglycerides—100 mg/dL upper limit of normal; ≥500 mg/dL requires medical therapy;
non–HDL-C—measurement less variable than LDL-C (which is affected by day-to-day variation in very low-density
lipoproteins [VLDL]); triglycerides—primarily carried by VLDL and chylomicrons; elevated in patients with type 2
diabetes, insulin resistance, or overweight; VLDL—remnants atherogenic; factors that increase VLDL decrease HDL-
C; predictive value—non–HDL-C may predict risk better than LDL-C, especially in overweight patients
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| Lipoproteins: atherogenicity varies with type of particle; elevated triglycerides associated with small dense LDL-C and increased
catabolism of HDL-C; small dense LDL particles easily enter atheroma and easily oxidized (increase inflammation)
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| Genetic predisposition: familial hypercholesterolemia (heterozygous condition affects 1 in 500; homozygous condition
affects 1 in 1 million); lipoprotein lipase (LPL) deficiency associated with triglyceride levels \>750 mg/dL (increased
risk for pancreatitis)
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| Diet: managing hypercholesterolemia—<30% of calories from fat, and <7% of calories from saturated fat; limit cholesterol
to <200 mg/day; diet must supply appropriate energy for normal growth and sufficient micronutrients; managing
triglycerides and HDL-C—manage weight; restrict or eliminate sugar; limit fruit juice to ≤12 oz/day; incorporate
mono- and polyunsaturated fats into diet
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| Treating comorbidities: decision to treat medically based on multiple factors, including age (speaker rarely treats children
<10 yr of age), sex (girls have slower progression; wait until after puberty), and family history; safety, compliance,
and goal of therapy affect choice of medication
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| Weight loss: primary treatment; 10% decrease in BMI decreases BP (≥10 mm Hg), triglycerides (1 risk class), and sometimes
LDL-C (up to 30%) and increases HDL-C (3-5 mg/dL)
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| Medical management: BP—use once-daily medications; first-line therapy includes angiotensin-converting enzyme
(ACE) inhibitors or thiazide diuretics; angiotensin-receptor blockers (ARBs) also used, but generic formulations not
available; 65% of patients need combination therapy for effective management; dyslipidemia—begin with fish oil for
patients with triglycerides \>500 mg/dL; consider statins (pravastatin or atorvastatin [Lipitor])
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| Definitions of clinical success: nonpharmacologic management eliminates need for drug therapy; weight decreases by
1 lb every 2 wk (in patients with BMI \>30 or with comorbidities); weight maintenance (for most children); BMI maintenance
(especially in younger children)
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| ASSESSING AND IMPROVING OBESITY-RELATED COMORBIDITIES —Sandra G. Hassink, MD, Assistant Professor
of Pediatrics, Thomas Jefferson University, Jefferson Medical College, Philadelphia, PA, and Director, Weight Management
Program, A.I. DuPont Hospital for Children, Wilmington, DE
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| Prevention: although weight loss can improve obesity-related comorbidities, residual effects generally occur; weight
management should emphasize importance of prevention
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| Pulmonary effects: structural—accumulation of adipose tissue in upper airway contributes to obstruction; abdominal
obesity may compromise respiratory excursion; functional—infiltration of adipocytes into diaphragm and lung parenchyma
affects pulmonary function; metabolic—inflammatory cytokines produced by adipocytes may exacerbate asthma
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| Sleep-disordered breathing: continuum beginning with primary snoring through Pickwickian syndrome; even primary
snoring in early school-age children may affect academic achievement later in life
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| Obstructive sleep apnea syndrome (OSAS): prevalence—affects up to 3.5% of children; obesity significantly increases
risk (abnormal sleep patterns reported in almost all obese children studied); OSAS noted in obese infants as young as 5
mo of age; consequences—pulmonary hypertension leads to right ventricular hypertrophy (RVH); LVH; systemic hypertension;
impaired academic performance; lower scores on standardized testing; problems with learning and memory;
deficits in attention, motor efficiency, and graphomotor ability (may appear similar to attention deficit disorder [ADD]);
cardiac effects; history—nighttime symptoms include snoring, restless sleeping, heavy or noisy breathing, orthopnea,
frequent awakening, enuresis, apnea, diaphoresis, cyanosis; daytime symptoms include morning headache, daytime
tiredness, napping, poor academic functioning, inattentiveness, memory deficit, irritability, elevated BP; physical
examination—check for adenotonsillar hypertrophy (symptoms include mouth breathing, nasal obstruction during
wakefulness, adenoidal facies, and hypernasal speech); diagnosis—symptom checklists used in research settings; definitive
diagnosis requires nighttime sleep study (polysomnography); severity—neither degree of obesity nor severity
of sleep symptoms correlates with severity of obstruction; components of sleep study—assessment of respiratory effort,
airflow at nose and mouth, and arterial O2 ; electrocardiography; electroencephalography; treatment—weight loss
(definitive treatment); tonsillectomy or adenoidectomy may temporize symptoms, but not curative; positive airway pressure
(continuous or bilevel) effective, but compliance difficult; corrective surgery (eg, uvulopalatopharyngoplasty, craniofacial
surgery, or tracheostomy)
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| Pearls: ask about sleep disturbances, snoring, and sleep position; suspect OSAS in obese children with poor school performance
or concentration; remember that sleep-disordered breathing may progress over time
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| Asthma: rise in asthma parallels rise in obesity; weight reduction reduces asthma symptoms; obesity associated with increased
bronchial hyperresponsiveness, gastroesophageal reflux, leptin production (may increase inflammation), decreased
lung volume and thoracic distensibility, and altered breathing pattern (higher frequency, lower tidal volume);
evaluation—because inactive children may not report symptoms, specifically ask about activity patterns (eg, if and
when out of breath, chest tightness, cough, dropping out of sports, slowing down, losing interest); treatment—as exercise
increases (as part of weight-loss program), symptoms may emerge; symptom management especially important in
obese children, because corticosteroids may cause weight gain; asthma severity—among asthmatics, obese children miss
more school days, receive more medication, and have lower peak expiratory flow rates than nonobese children; they also
have increased incidence of coughing, wheezing, and dyspnea; vicious cycle—obesity exacerbates asthma, and asthma
may reduce activity (leading to weight gain)
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| Ankle and foot pain: magnetic resonance imaging (MRI) may show edema of bone marrow; abnormal gait in obese
child warrants investigation
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| Slipped capital femoral epiphysis (SCFE): high index of suspicion in obese patient with limp; obese patients represent
50% to 66% of SCFE cases; presentation may include pain in groin, thigh, or knee (referred); diagnosis—limited
motion of hip with abduction and internal rotation; bilateral x-ray of hips diagnostic; bilateral disease occurs in up to 20%
of patients; medial and posterior displacement of femoral epiphysis relative to femoral neck, occurring through growth
plate; pathology—occurs most commonly in zone of hypertrophic cartilage cells; causes include excessive weight gain,
renal failure, radiation therapy, hypothyroidism, treatment with gonadotropin-releasing hormone (GnRH) agonists or
growth hormone; pearls—routinely examine knees and hips of obese children; pay attention to symptoms in lower extremities
and to gait abnormalities
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| Blount disease: unilateral or bilateral bowing of tibia and femur caused by overgrowth of medial aspect of tibial metaphysis;
66% of patients obese; patients may present with pain, limp, or peripheral neuropathies; treatment—weight loss;
corrective surgery; bracing in very young children
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| Nonalcoholic steatohepatitis (NASH): nonalcoholic fatty liver disease (NAFLD) progresses from simple steatosis
through NASH and may continue to cirrhosis and end-stage liver disease; 15% of obese children have inflammation and fibrosis
of liver; diagnosis—elevated liver enzymes; echogenicity seen on ultrasonography; biopsy definitive; etiology—
obesity associated with fatty liver; second insult (genetic predisposition or environmental “hit”) results in inflammation and
fibrosis; risk—obesity and type 2 diabetes strong predictors for progression; young age increases risk by increasing duration
of risk for second hit; fatty liver more easily damaged by variety of insults (eg, infection, alcohol, industrial toxins); predictors
of elevated liver enzymes include male sex, Hispanic ethnicity, and elevated BMI; predictors of fibrosis include BMI,
insulin resistance, and, possibly, leptin levels; treatment—modest weight loss normalizes liver enzymes and decreases evidence
of fatty infiltration (but effect on fibrosis unknown); metformin appears to normalize liver enzymes in ≈50% of children,
reduce hepatic steatosis in ≈33%, and improve insulin sensitivity (clinical trial in progress); cautions—rapid weight
loss not recommended for children (may increase free fatty acids and oxidation); pearls—even mild obesity may result in
elevated liver enzymes and hepatic steatosis; metabolic evaluation of obese children should always include liver function;
diagnosis of NAFLD requires exclusion of other causes of liver disease
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| Cholelithiasis: diagnosis based on abdominal pain, tenderness, ultrasonography, and laboratory studies; rapid weight
loss increases risk in adults; obese adolescent girls have 4-fold increased risk; 50% of cholecystitis in adolescents associated
with obesity
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| Psychologic comorbidities: obesity associated with depression, anxiety, low self-esteem, victimization (eg, teasing,
bullying), and binge eating disorder; psychologic conditions that may affect treatment of obesity include attention-deficit/
hyperactivity disorder (ADHD) or ADD, bipolar disorder, adjustment disorder, and oppositional defiant disorder
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| Depression: study showed depressed mood in adolescents (grades 7-12) predicted obesity, but obesity did not predict depression;
chronically obese children had significantly higher rates of oppositional defiant disorder and depression (in
boys); obese children and their parents reported lower scores for health-related quality of life (especially in children with
OSAS); BMI inversely correlated with physical functioning
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Educational Objectives
| The goal of this activity is to provide the clinician with information to aid in the identification and management of obesity-
related comorbidities in children. After hearing and assimilating this program, the clinician will be better able to:
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| 1. Discuss obesity-related comorbidities and their associated risks with overweight patients and their families.
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| 2. Diagnose hypertension, dyslipidemia, and glucose intolerance in children.
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| 3. Incorporate screening for obesity-related comorbidities into routine examinations of overweight children.
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| 4. Discuss the effect of weight loss on various comorbidities associated with obesity.
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| 5. Discuss risk for psychologic disorders and their effects on management of obesity in children.
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Suggested Reading
Barros R et al: Obesity and airway inflammation in asthma. J Allergy Clin Immunol 117:1501, 2006; Chia DJ, Boston
BA: Childhood obesity and the metabolic syndrome. Adv Pediatr 53:23, 2006; Emmet GA et al: Primary ambulatory
care of overweight children. Pediatr Ann 35:838, 2006; Glazebrook C et al: Asthma as a barrier to children’s
physical activity: implications for body mass index and mental health. Pediatrics 118:2443, 2006; Kirk S et al: Pediatric
obesity epidemic: treatment options. J Am Diet Assoc 105(5 Suppl 1):S44, 2005; Landrigan PJ et al: The National
Children’s Study: a 21-year prospective study of 100,000 American children. Pediatrics 118:2173, 2006; Libman IM,
Arslanian SA: Prevention and treatment of type 2 diabetes in youth. Horm Res 67:22, 2006; Manoff EM et al: Relationship
between body mass index and slipped capital femoral epiphysis. J Pediatr Orthop 25:744, 2005; Meyer AA et
al: Improvement of early vascular changes and cardiovascular risk factors in obese children after a six-month exercise program.
J Am Coll Cardiol 48:1865, 2006; Patton HM et al: Pediatric nonalcoholic fatty liver disease: a critical appraisal
of current data and implications for future research. J Pediatr Gastroenterol Nutr 43:413, 2006; Rand CM et al: Preventive
counseling at adolescent ambulatory visits. J Adolesc Health 37:87, 2005; Schwimmer JB et al: Prevalence of
fatty liver in children and adolescents. Pediatrics 118:1388, 2006; Shine NP et al: Adenotonsillectomy for obstructive
sleep apnea in obese children: effects on respiratory parameters and clinical outcome. Arch Otolaryngol Head Neck Surg
132:1123, 2006; Tauman R et al: Persistence of obstructive sleep apnea syndrome in children after adenotonsillectomy.
J Pediatr 149:803; Zappalla FR: Evaluation of dyslipidemia in children. Pediatr Ann 35:808, 2006.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported
nothing to disclose.
Drs. Gidding and Hassink were recorded in Newark, DE, at Sizing Up the Childhood Overweight Epidemic for the Primary
Care Provider, sponsored by Nemours Health and Prevention Services, and held October 18, 2006. The Audio-Digest
Foundation thanks the speakers and Nemours Health and Prevention Services for their cooperation in the production of
this program.
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