UPDATE ON OBESITY
From the Cape Cod Conference on Pediatrics for the Primary Care Physician, presented by Nemours
Sandra G Hassink, MD, Director, Weight Management Program, AI DuPont Hospital for Children, Wilmington,
DE, and Clinical Instructor in Pediatrics, Jefferson Medical College, Philadelphia, PA
| Obesity epidemic: rapid progression since 1980; 60% of adults in United States obese or overweight, ie, body mass
index (BMI) >85th percentile; reference standards growth charts and weight distributions from 1980; reference population
from 1980s; 33% of children and 25% of those <5 yr of age obese and overweight; prevalence—crosses time and
ethnic groups (minorities more severely)
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| Pathophysiology: excess adipose tissue; in research, measured by underwater weighing, dual-energy x-ray absorptiometry
(DEXA), or computed tomography (CT) or magnetic resonance imaging (MRI); measured clinically by BMI,
which correlates with fat (correlation greater as degree of overweight increases); anthropometry and bioelectric impedance
other clinical tools
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| White adipose tissue: not just fuel storage for energy needed in time of deprivation; contains—adipocytes; multipotent
stem cells (differentiate into muscle, cartilage, adipose tissue, and bone); macrophages (inflammatory); vascular
tissue; metabolically active organ system—adipocytes store fuel, produce cytokines, and involved in hormonal regulation
and energy regulation in central nervous system (CNS) and periphery; cytokines—tumor necrosis factor (TNF)-
α alters insulin signaling, increasing insulin resistance; interleukin (IL)-6 increases acute-phase proteins;
adiponectin—modulates endothelial adhesion and inhibits inflammatory responses; decreases in obesity; resistin—
thought to affect insulin resistance
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| Inflammatory component: macrophages migrate into adipose tissue; secreted TNF-α stimulates preadipocytes and
endothelial cells to produce monocyte chemoattractant protein-1; increased leptin and decreased adiponectin stimulates
macrophage migration; inflammatory component provides insight into link between obesity and cardiovascular disease
(CVD)
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| Energy regulation in obesity: leptin—discovery in 1996 provided first insight into obesity as dysfunction of energy
regulatory state; 4 hypothalamic nuclei—input on energy storage, feeding behavior, hunger, vagal regulation and leptin;
all affect development of, and dysregulated in, obesity
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| Intrauterine environment: unborn child responsive and vulnerable to changes in intrauterine environment; intrauterine
programming may affect short- and long-term energy balance; infants of diabetic mothers—have increased adiposity
in childhood; increased risk for obesity, impaired glucose tolerance, type 2 diabetes; diabetes in pregnancy
alters genetic response to environment; exposure to excess glucose results in hyperinsulinemia, alters insulin-receptor
expression and sensitivity to extrauterine environment; children of obese mothers—predisposed to obesity and diabetes,
more sensitive to toxic environment; mothers have impaired glucose tolerance, gestational diabetes, diabetes; infants
who are small for gestational age (SGA)—at risk for obesity, diabetes, and CVD; now thought that restricted
intrauterine nutritional environment may lead to exposure to increased amounts of fatty acids that stimulate adipose tissue
hyperplasia and insulin resistance; children on either side of appropriate-for-gestational age spectrum prone to insulin
resistance and predisposition to diabetes and obesity; intrauterine environment affects adulthood
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| Growth: child kept on normal growth curve by balance between genetics, environment, and healthy physiology; adipose
tissue has its own growth trajectory; adiposity—in newborns, 15% in girls, 12% in boys; nadir at preschool age;
at puberty, decreases in boys, increases in girls
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| Obesity in childhood: heterogeneous disease with unique weight-gain trajectories, environmental triggers, and physiologic
responses; each family and child has unique genetic, behavioral, relational, and physiologic characteristics that contribute
to development and maintenance of excess adiposity
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| Patient case: boy 3.5 yr of age; height >97th percentile; weight peaked over 97th percentile then flattened after starting
clinic; physiologic changes—clavicle fractured at playground; asthma treated with steroids; toxic synovitis of hip (immobilized;
possible inflammatory component)
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| Stress: activates hypothalamic-pituitary-adrenal axis; high glucocorticoid, high glucose and lipid levels; increased cardiovascular
tone; immunosuppression if severe; stress-obesity connection—stress of social subordination in female
monkeys associated with increased central fat deposition; chronic uncontrollable stress in rats resulted in increased adipocyte
size and heavier fat pads (independent of eating and activity); physiologic components of stress look like metabolic
syndrome (eg, increased blood pressure [BP], waist-hip ratio, cholesterol, glycosylated hemoglobin)
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| Patient case, continued: dysregulation—history of colic (disturbed autoregulation?); mother pregnant when boy
brought to clinic; describes child as strong-willed; perhaps dyadic change between mother and boy and possible loss of
external regulation for him; boy described as big eater who eats rapidly (satiety cues lost?)
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| Cardiac vagal tone: marker for functional status of parasympathetic nervous system; measure of heart period variability,
respiratory sinus arrhythmia, general reactivity, and regulation of arousal; low tone associated with emotional
dysregulation, social wariness, and behavioral inhibition; high tone associated with ability to self-soothe after display
of negative affect
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 | Link to parenting style: study found bidirectional and longitudinal relationship between child’s vagal tone and parenting
behavior; given stable vagal tone over 2 to 4 yr, low vagal tone at 2 yr predicted maternal restricted overcontrolling
parenting at 2 and 4 yr; high vagal tone predicted more supportive parenting; new recommendations on obesity
from American Medical Association (AMA) and Centers for Disease Control and Prevention (CDC)—
authoritative parenting style associated with low overweight while rigid authoritarian style associated with high
overweight
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| Patient case, continued: child dependent; afraid of dark; likes junk food; fights with mother over food; sneaks food;
upset when told “no”; difficult to get to bed; child in dysregulatory relationship with environment; father present, but
busy professional; patient did well; weight flat for 4 yr
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| Questions: how is individual vulnerability determined? how is multidimensional risk and effect assessed? how does
parent/environmental interaction modify physiology? which factors allow for resilience?
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| Patient A: parent of patient morbidly obese; rapid early weight gain in child; satiety and food sneaking and seeking issues;
obstructive sleep apnea (OSA); ankle pathology (pain with walking); look at—genetic etiology; ineffective
parenting from mother and grandmother (permissive); decision making; absence of metabolic sequelae; poor school
function and poor self-esteem; sleep apnea—children with sleep-disordered breathing more likely to suffer from tiredness,
poor school function, attention and memory deficits, and, in older children, poor decision-making; deficits compromise
participation in activities that may prevent weight gain; child appears tired and inattentive and often labeled
“lazy and unmotivated”; physiologic process results in behavior ramifications, labeling, and how others relate to child;
parenting style affected, eg, parent may adopt authoritarian style and become angry with child
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| Depression and obesity: study—chronically obese children have higher rates of oppositional defiance disorder, and,
in boys, depression; chronic and childhood obesity associated with undereducated parents and low family income; further
interactions—food used to soothe and self-medicate distress; food mimics drug effects in prefrontal cortex (affects
mood); decision-making deficits greater in women with higher BMIs than in normal-weight women; in another
study, obese children of normal intelligence have deficits in cognitive function and decision-making; cortical functions
that inhibit short-term rewards in face of long-term negative consequences may be impaired in obesity (increases difficulty
of making lifestyle and behavior changes); risk factors for obesity—depression, divorce, and family stress
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| Quality of life: obese children and adolescents rate themselves as having lower quality of life in all domains; parents
rate children lower than children rate themselves; patients with OSA rate themselves even lower
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| Summary: 1% to 3% of adolescents have BMI >40; more common than cystic fibrosis, juvenile diabetes, and childhood
cancer combined; obesity chronic disease that moves into adulthood with its comorbidities (sleep apnea, hypertension,
liver disease, PCOS); pathologic implications—earlier onset of type 2 diabetes; end-stage liver disease if
fibrosis and inflammation develop (≈15% of children with fatty livers); new explanation for old disease, eg, sleep apnea;
obesity-related emergencies—hyperglycemia; hyperosmolarity; diabetic ketoacidosis; cardiomyopathy
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| OBESITY: “HOW TO” IN THE OFFICE
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| Body mass index: one point in time on growth trajectory (must look at child’s entire trajectory); meaning found in
context of gene-environment interactions and individual child; classify, calculate, and chart; classifications—
overweight 85th to 94th percentiles; obese 95th to 99th percentiles; severe morbid obesity >99th percentile (risk factor
for cardiovascular abnormalities); validity—associated with subcutaneous and total body fat; correlates with physiologic
changes associated with excess adiposity (elevated insulin, BP, lipids, and cardiovascular risk factors); higher
BMI more specific for excess adiposity
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| Key concepts: genetic predisposition determines susceptibility to energy imbalance; the worse the environment, the less
predisposition needed; expression triggered by biologic, psychologic, and social factors; obesity result of common final
pathway, in which energy intake exceeds expenditure; interaction with environment may change way energy managed;
chronic disease, ie, predisposition lifelong and often multigenerational; no quick fix; treatment aimed at long-term
change of underlying causes (difficult concept for adolescents)
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| Treatment: based on chronic-care model; flexible; goals— make realistic and base on individual circumstances; main
goal weight loss, ie, BMI reduction (may not be first goal chosen by patient; might need to start with weight stabilization);
metabolic fitness, eg, normalize cholesterol, normalize insulin; targeted behavioral change, eg, not sneaking
food; functional improvement, eg, ability to bend down and tie shoes; improvement in psychosocial factors, eg, more
peer activity; improvement in comorbidities; start with relatively short-term goal
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| Comprehensive approach: more successful than dieting alone; multidisciplinary; want behavior change in diet and
activity level; family and patient skill-building; treat as family problem; support groups helpful if targeted to adolescents’
needs; treating parents alone also works; address underlying comorbidities; social disapproval—due to culture
of thinness; cycle of blame and guilt—parent may blame child; readjust it as family issue; expectations—may be for
medical diagnosis or easy solution; frame problem; prioritize needed change; offer skill-building and realistic goal-setting;
help patients understand chronicity of condition; engage patients in conversation; familial obesity—may lead to
pessimism about treatment; best long-term outcome data seen in pediatric age group; behavioral change can ameliorate
genetic influences; 10% weight loss can modify genetic risk factors; barriers to treatment—lack of health insurance;
fear of triggering eating disorder, eg, anorexia
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| Strategy: BMI 5th to 84th percentile—primary prevention; track growth and BMI; educate on nutrition, activity,
screen time; develop practice-based prevention strategies; school and community involvement; children at specific
risk—parental obesity; family history of syndrome X; intrauterine risk; crossing BMI percentiles, eg, normal trajectory,
then inflection point (weight gain; determine trigger factor, eg, family problem or death); high-risk nutrition and
activity environments, eg, family grazes, eats in front of television (TV), snack foods; high-risk behavior, eg, child rewarded
with food; 85th to 94th percentile—secondary prevention; identify BMI and overweight; do fasting lipid
panel, glucose, and liver function tests; screen for high-risk environment and behaviors; assess families for resilience
and barriers to change; keep child on growth chart; identify comorbidities; 95th to 99th percentile—focus on decreasing
high-risk behavior and weight reduction to reduce impact of comorbidities and prevent progression; 2-yr trajectory
from impaired glucose tolerance to diabetes; obesity-related comorbidities that may require attention include pseudotumor
cerebri, slipped capital femoral epiphysis, Blount’s disease, sleep apnea, liver and gallbladder disease, >99th
percentile—weight management multidisciplinary clinic; targeted weight reduction with hypocaloric diet; consider
surgery
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| Prevention, intervention, and treatment: visits—address obesity, ask if weight of concern to parent or child;
components of successful outcome—return visits (depends on bond established with child and family on first visit);
one change made between visits; family involvement; monitoring, eg, self-monitoring, family monitoring, keeping diet
records; learn what parents have said to child and child’s concerns; assess environment—access to food; enablers;
high-calorie beverages; portions; fast food; snacking; poor nutrition; meal skipping; activity—safety; cost; incorporation
into lifestyle; family patterns; motor and social skills; inactivity—number and locations of TVs and amount of
screen time per day (as high as 12-15 hr during summer); family patterns that may be influenced by parental illness,
obesity, and media savvy
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| Assessment: be sensitive to body image; interview child while clothed, provide gown for physical; complete
examination—looking for acanthosis, striae, hirsutism, skin infection, skin picking, adipose tissue distribution, gynecomastia
in boys, funduscopic examination, hips and knees, Tanner stage; histories—family; diet; activity and inactivity;
identify caregivers and environments; eating patterns; discretion with snacks
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| Nutrition and problems: encourage self-monitoring; diet records predictors of success; promote breast-feeding; teach
cued feeding and satiety skills; preschool problems—inappropriate access to food; inconsistent responses to hunger demands;
multiple caregivers; after school—child often alone with TV and food; adolescence—meal skipping; dysregulation
with night eating; eating becomes social; more discretion
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| Activity:promote sports; does not have to be physical activity, just away from TV; partner child with parents to do
something together; infants—should not be watching TV; preschool children—free play; schedule time; school
age—after-school inactivity and safety; inactive family equals inactive children; if caregivers older, their lifestyle affects
child; most activities involve transportation, and parents often do not have time; morbidly obese adolescent—
may have social isolation, poor self-esteem, lack of social skills; longer obesity lasts, the harder to mainstream child
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| Emotions: be aware of own feelings about obesity; defuse blame and guilt; be ready to deal with sadness and discouragement;
establish trust; first job to get patient to come back
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| Intervention: externalize problem, eg, genetics, environment, comorbidities; make it objective problem family can
work on, rather than personal problem; define success in terms of problems identified to solve; even coming back to report
failure is positive; keep trying
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Suggested Reading
Calkins SD: Cardiac vagal tone indices of temperamental reactivity and behavioral regulation in young children. Dev
Psych 31:125, 1997; Caprio S et al: Prevalence of impaired glucose tolerance among children and adolescents with
marked obesity. N Engl J Med 346:802, 2002; Dabelea D et al: Intrauterine diabetic environment confers risk for type
II diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. J Pediatr Endocrinol Metab 14:1085,
2001; Davis C et al: Decision-making deficits and overeating: a risk model for obesity. Obes Res 12:929, 2004; Freedman
DS: Cardiovascular risk factors and excess adiposity among overweight children and adolescents: The Bogalusa
Heart Study. J Pediatr 150:12, 2007; Fox NA: Heart Rate Variability and Behavioral Activity: Indirect Differences in
Autonomic Patterning and Their Relation to Infant and Child Temperaments. In: Perspectives on Behavioral Inhibition.
Chicago, IL: Univ Chicago Press; 1989:117-195. Freinkel N: Of pregnancy and progeny (Banting Lecture). Diabetes
29:1023, 1980; Hassink SG: A Clinical Guide to Pediatric Weight Management and Obesity. Lippincott, Williams,
and Wilkins: 2006; Mustillo S et al: Obesity and psychiatric disorder: developmental trajectories. Pediatrics 111:851,
2003; Narayan KM et al: Lifetime risk of diabetes mellitus in the United States. JAMA 290:1884, 2003; Ogden CL et
al: Prevalence of overweight and obesity in the US 1999-2004. JAMA 295:1549, 2006; Pelchat ML: Of human bondage:
food craving, obsession, compulsion, and addiction. Physiol Behav 76:347, 2002; Rhodes SK et al: Neurocognitive
deficits in morbidly obese children with obstructive sleep apnea. J Pediat 127:741, 1995; Schwimmer JB et al: Health-
related quality of life of severely obese children and adolescents. JAMA 289:1813, 2003
Educational Objectives
| The goal of this activity is to improve understanding of the pathophysiology of obesity and develop intervention strategies
for children at risk. After hearing and assimilating this program, the clinician will be better able to:
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| 1. List physiologic, social, and psychologic factors associated with obesity.
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| 2. Apply the knowledge of obesity pathophysiology to prevention, intervention, and treatment.
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| 3. Recommend lifestyle changes for prevention and treatment of obesity.
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| 4. Recognize the impact of obesity on physiologic function and its association with other disease states.
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| 5. Explain how obesity management and treatment may differ from typical office practice.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose relevant
financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified
conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business
or commercial interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
Dr. Hassink spoke at the Cape Cod Conference on Pediatrics for the Primary Care Physician, presented August 3-5,
2007, in Hyannis, MA, by Nemours Children’s Clinic. The Audio-Digest Foundation thanks the speaker and the sponsor for
their cooperation in the production of this program.
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