Overweigh-Assesment 1

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Clinical evaluation of the child or adolescent with obesity

Authors: Joseph A Skelton, MD, MS, William J Klish, MD
Section Editors: Kathleen J Motil, MD, PhD, Mitchell E Geffner, MD
Deputy Editor: Alison G Hoppin, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2022. | This topic last updated: Jun 06, 2022.
INTRODUCTION
Obesity is among the most prevalent and consequential public health problems in the United
States and many other countries [1]. As the prevalence of obesity increases, so does the
prevalence of the associated comorbidities [2].
The goal of a comprehensive evaluation of the child with overweight or obesity is to identify
treatable causes and comorbidities. The evaluation should include a focused history and
physical examination, with laboratory and radiologic studies for selected patients.
The clinical evaluation of the child or adolescent with overweight or obesity will be presented
here. Other aspects of clinical management of obesity in children are discussed in separate
topic reviews:
● (See "Definition, epidemiology, and etiology of obesity in children and adolescents".)

● (See "Overview of the health consequences of obesity in children and adolescents".)
● (See "Prevention and management of childhood obesity in the primary care setting".)
● (See "Surgical management of severe obesity in adolescents".)
BODY MASS INDEX
Body mass index (BMI) is equal to the body weight (in kilograms) divided by the height (in
meters) squared ( table 1). BMI should be calculated at least annually for all children older
than two years [3-6]. The results should be used to determine:
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● BMI percentile – The BMI percentile can be determined by plotting points on a BMI
growth curve ( figure 1A-B). For children with severe obesity, an extended growth chart
may be needed and facilitates tracking ( figure 2A-B). BMI percentiles also can be
determined using a calculator for boys (calculator 1) and for girls (calculator 2).
● Weight category – The BMI percentile is used to categorize the weight class ( table 2):
• Underweight – BMI <5th percentile for age and sex.
• Normal weight – BMI between the 5th and <85th percentile for age and sex.
• Overweight – BMI ≥85th to <95th percentile for age and sex.
• Obesity – BMI ≥95th percentile for age and sex.
• Severe obesity – BMI ≥120 percent of the 95th percentile values or a BMI ≥35 kg/m2
(whichever is lower) ( figure 2A-B) [7,8]. This corresponds to approximately the 99th
percentile. Some authors distinguish an additional subgroup with more severe obesity
with BMI ≥140 percent of the 95th percentile values or a BMI ≥40 kg/m2, which
corresponds to class III obesity in adults [7].
BMI is a clinically practical tool for the assessment of overweight and obesity in children. It
correlates with adiposity [9-11] and complications of excess childhood weight [12-15]. However,
because BMI does not directly measure body fat, it may overestimate adiposity in a child with
increased muscle mass (eg, an athlete) and underestimate adiposity in a child with reduced
muscle mass (eg, a sedentary child). (See "Measurement of body composition in children",
section on 'Estimates of adiposity'.)
HISTORY
Weight history — The child's historical pattern of weight gain should be evaluated based on
serial growth measurements (if available) or history.
The rapidity and age of onset is sometimes helpful in determining the cause or contributors to
the child's obesity:
● Gradual onset – Gradual onset of obesity is typical for the most common forms of obesity
(genetic predisposition combined with excess caloric intake or other environmental
contributors).
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● Abrupt onset of weight gain – Abrupt onset of obesity with rapid weight gain should
prompt investigation of a major psychosocial trigger such as a loss or change in the family
or new symptoms of anxiety or depression. (See 'Psychosocial history' below.)
Other possible causes include medication-induced weight gain and neuroendocrine

causes of obesity (eg, Cushing disease, hypothalamic tumor, or, rarely, ROHHADNET
syndrome [rapid-onset obesity with hypothalamic dysfunction, hypoventilation, autonomic
dysregulation, with or without neuroendocrine tumor]) ( table 10B) [16]. (See
"Definition, epidemiology, and etiology of obesity in children and adolescents", section on
'Endocrine disorders' and "Definition, epidemiology, and etiology of obesity in children
and adolescents", section on 'Hypothalamic obesity'.)
● Severe early-onset – Severe early-onset obesity is more likely to have a strong genetic
component. Some forms of syndromic or monogenic obesity have onset before two years
of age, while others (especially Prader-Willi syndrome) tend to have growth failure during
infancy followed by rapid weight gain and development of obesity after two years of age (
table 3A-B).
Diet — The dietary history should elicit the following information, as summarized in the table (
table 4) [2,17]:
● Caregiver(s) involved in feeding – Including meal planning, shopping, and preparing and
being present at meals.
● Eating patterns – Including timing, content, and location of meals and snacks. The
possibility of disordered eating is raised by (see "Eating disorders: Overview of
epidemiology, clinical features, and diagnosis"):
• Recurrent episodes of consuming large amounts of food with a sense of loss of control
(suspect binge eating disorder) [18]
• Inappropriate compensatory behavior to prevent weight gain (self-induced vomiting or

other purging, fasting, and/or excessive exercise) associated with binge eating (suspect
bulimia nervosa)
Children who eat less frequent meals (eg, those who skip meals) are more likely to have
obesity than those who eat more frequently [19], but this association may not be causal
and may be due to confounders (eg, increased snacking).
● Food frequency – Preliminary identification of foods high in calories and low in nutritional
value that can be reduced, eliminated, or replaced. Common sources of excess calories
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include:
• Sugar-containing beverages, including soda, juice, sugar-containing "sports" drinks,

and flavored milks
• Snack foods (chips, sweets)
• Other eating outside of meals (leftovers, quick-service foods)
● Food preferences and dislikes – While picky eating is not necessarily associated with the
development of obesity, several reports indicate higher prevalence of picky eating in
children with overweight and obesity [20-22], and addressing picky eating as part of
weight management can improve outcomes [20,23]. A picky eating pattern may also be a
relevant focus for nutritional and behavioral counseling.
● Restaurants and prepared foods – Fast food service and restaurant meals are often
higher in calories and lower in nutritional value compared with foods prepared at home.
Identifying the frequency and type of such meals facilitates counseling to reduce
frequency and/or optimize food selections. (See "Fast food for children and adolescents".)
Activity — The activity history should include the following factors, as summarized in the table (
table 5) [2,24]:
● Physical activity
• Time spent in play (especially outdoors)

• School recess and physical education (frequency, duration, and intensity)
• Sports participation
• Afterschool and weekend activities
• Lifestyle activity, such as walking or riding a bike to school; if none, document any
barriers to these activities
● Sedentary activity – In most cases, most sedentary behavior involves screen time.
Document both recreational activities (television, smart phone/device, recreational
internet use, and video games) and educational activities (homework, reading, and
computer-based learning).
Sleep — The sleep history should include:
● Sleep habits – Assess typical sleep duration, sleep quality, and sleep schedule, and
compare with recommended sleep times for children ( table 6). Short sleep duration or
irregular sleep schedules have been associated with obesity in children and adults; a
causal association has been proposed but not established (see "Definition, epidemiology,
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and etiology of obesity in children and adolescents", section on 'Sleep'). Strategies for
improving sleep are discussed separately. (See "Behavioral sleep problems in children".)
● Symptoms of sleep disorders – Obesity is associated with an increased risk for

obstructive sleep apnea. Any child who snores habitually (eg, ≥3 nights per week), has
loud snoring, or has pauses in breathing during sleep should be further evaluated.
Obstructive sleep apnea also may cause nocturnal enuresis or daytime symptoms
including inattention, learning problems, and hyperactivity, with or without sleepiness.
(See "Evaluation of suspected obstructive sleep apnea in children", section on 'Screening'.)
Medical history — The medical history should include review of all medications, particularly
those that are known to be weight-promoting (eg, certain psychoactive drugs such as
risperidone, antiseizure medication, and glucocorticoids) ( table 7). (See "Definition,
epidemiology, and etiology of obesity in children and adolescents", section on 'Medications'.)
In addition, document any known comorbidities of obesity, as outlined in the table ( table 8).
(See "Overview of the health consequences of obesity in children and adolescents".)
Review of systems — The review of systems should probe for further evidence of comorbidities
or underlying causes of obesity ( table 9) [2,4].
Developmental delay or dysmorphic features raise the possibility of a syndromic form of obesity
( table 3A). In particular, a history of hypotonia and feeding problems during infancy followed
by rapid weight gain during early childhood and developmental delay suggests the possibility of
Prader-Willi syndrome. (See "Clinical features, diagnosis, and treatment of Prader-Willi
syndrome".)
Family history — Key elements are:
● Obesity – Inquire about obesity in first-degree relatives (parents and siblings) [2]. Use
terms such as "overweight" or "unhealthy weight" because these terms are generally more
acceptable to patients than "obesity" (see "Prevention and management of childhood
obesity in the primary care setting", section on 'Strategies for discussing weight'). In
particular, obesity in one or both parents is an important predictor for whether a child's
obesity will persist into adulthood [25-28]. This association has both genetic and
environmental components. (See "Definition, epidemiology, and etiology of obesity in
children and adolescents", section on 'Persistence into adulthood'.)
● Comorbidities – Inquire about common comorbidities of obesity, such as cardiovascular

disease, hypertension, diabetes, liver or gallbladder disease, and respiratory problems
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(severe asthma or sleep apnea) in first- and second-degree relatives (grandparents, uncles,
aunts, half-siblings, nephews, and nieces). The presence of such comorbidities predicts the
child's future risk, regardless of whether the affected family member has obesity. Maternal
gestational diabetes is associated with adverse cardiometabolic outcomes in the offspring
[29].
Family dynamics — There is some evidence that family dynamics and family functioning are
associated with childhood obesity. A systematic review from 2014 found that 12 out of 17
included studies demonstrated significant associations between impaired family function and
increased risk of child obesity [30]. More recent studies have had similar findings [31-33]. More
research is needed to delineate mechanisms of this association, as well as prospectively
studying the impact of family functioning on child weight and behavior. Family dynamics and
approaches to discussing body weight with affected children and families are discussed
separately. (See "Prevention and management of childhood obesity in the primary care setting",
section on 'General approach to counseling about weight management'.)
Psychosocial history — Key elements are:
● Anxiety and depression – Anxiety and depression can disrupt eating patterns, promote
obesity, and interfere with weight management interventions. (See "Anxiety disorders in
children and adolescents: Assessment and diagnosis" and "Pediatric unipolar depression:
Epidemiology, clinical features, assessment, and diagnosis".)
● Events – Possible triggering events such as a loss of a loved one (death or relocation),
divorce, or changes in primary caregiver(s).
● School function and social issues – Academic performance and trends; social function
(eg, does the child have friends, and are they a target for teasing?).
● Smoking or vaping – Cigarette smoking increases long-term cardiovascular risk [4,34-37].

The risks of vaping nicotine (via e-cigarettes or other electronic devices) have not been
established but include nicotine dependence, which may, in turn, promote combustible
tobacco use. (See "Overview of the health consequences of obesity in children and
adolescents" and "Prevention of smoking and vaping initiation in children and
adolescents", section on 'Vaping and e-cigarettes'.)
In addition, fear of weight gain may be a barrier to smoking cessation in adolescents and
this concern should be addressed specifically in counseling. (See "Management of
smoking and vaping cessation in adolescents", section on 'Address barriers to quitting'.)
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● Social determinants of health – Key factors include poverty, food insecurity, access to
sources of healthy food and recreation, and transportation [38-40].
PHYSICAL EXAMINATION
The physical examination should evaluate for comorbidities and possible causes of the obesity
[4]. Key findings to note are shown in the table ( table 10A). Details about rare syndromic or
endocrine forms of obesity are summarized in these tables ( table 3A and table 10B) and
described separately. (See "Definition, epidemiology, and etiology of obesity in children and
adolescents", section on 'Etiology'.)
● General examination – Assess the general appearance/mood; look for dysmorphic

features, which may suggest a genetic syndrome ( table 3A-B) [2,4]. In addition, assess
the fat distribution:
• A markedly Cushingoid fat distribution (concentrated in the interscapular area, face,

neck, and trunk) suggests the possibility of Cushing syndrome, although this
distribution of fat may also be seen in exogenous obesity (caused by a combination of
genetic predisposition and excessive caloric intake). (See "Definition, epidemiology, and
etiology of obesity in children and adolescents", section on 'Endocrine disorders' and
"Epidemiology and clinical manifestations of Cushing's syndrome".)
• Abdominal obesity (also called central, visceral, android, or male-type obesity) is

associated with certain comorbidities, including metabolic syndrome, polycystic ovary
syndrome, and insulin resistance. Waist circumference or other indices of abdominal
obesity are associated with these comorbidities on a population level. However, these
measures are weak predictors of cardiovascular risk, so they have limited utility for
clinical care of individual patients. Abdominal obesity and measurement of the waist
circumference are discussed separately. (See "Measurement of body composition in
children", section on 'Fat distribution' and "Overview of the health consequences of
obesity in children and adolescents", section on 'Metabolic syndrome' and "Definition,
clinical features, and differential diagnosis of polycystic ovary syndrome in
adolescents".)
● Blood pressure – Blood pressure should be carefully measured using a properly sized
cuff. The bladder of the cuff should cover at least 80 percent of the arm circumference (the
width of the bladder will be approximately 40 percent of the arm circumference) (
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figure 3) [41]. In many children and adolescents with obesity, this will require use of
adult-sized or large adult-sized cuffs.
Hypertension is defined as systolic or diastolic blood pressure ≥95th percentile for children
1 to 13 years and ≥130/80 for adolescents 13 years and older on at least three occasions (
table 11) [41]. (See "Definition and diagnosis of hypertension in children and
adolescents".)
Hypertension increases the long-term cardiovascular risk in children with excess body
weight [4]. Occasionally, hypertension is a sign of Cushing syndrome [2]. (See
"Nonemergent treatment of hypertension in children and adolescents".)
● Stature – Assessment of stature and height velocity provides some clues to help
distinguish common exogenous obesity (caused by a combination of genetic
predisposition and excessive caloric intake) from obesity that is secondary to genetic or
endocrine abnormalities [42,43].
• Children with exogenous obesity are often tall for their age; the mechanism may
involve trophic factors such as hyperinsulinemia, which accelerates skeletal
maturation. However, they may also have earlier epiphyseal fusion, so the effects on
adult height are variable.
• By contrast, children with endocrine and genetic causes of obesity often have short
stature. As an example, decreased height velocity is an early sign in Cushing disease (
figure 4). Children with Prader-Willi syndrome are often short for their genetic
potential and/or fail to have a pubertal growth spurt. A useful (but imprecise and
unvalidated) screen for a possible endocrine cause of obesity is the combination of a
weight above the 95th percentile for age and sex but a height below the 50th percentile,
taking into account parental height. (See "Clinical features, diagnosis, and treatment of
Prader-Willi syndrome".)
● Examination of the head, eyes, ears, nose, and throat (HEENT)
• Enlarged tonsils suggest increased risk for obstructive sleep apnea. (See "Evaluation of
suspected obstructive sleep apnea in children".)
• Erosion of the tooth enamel may indicate self-induced vomiting in patients with an
eating disorder. (See "Eating disorders: Overview of epidemiology, clinical features, and
diagnosis".)
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• Blurred optic disc margins ( picture 1) may indicate pseudotumor cerebri, an

unexplained but not uncommon association with obesity [44]. (See "Idiopathic
intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis".)
• Nystagmus or visual complaints raise the possibility of a hypothalamic-pituitary lesion

[42]. Other findings that support this possibility are rapid onset of obesity or
hyperphagia, decrease in height velocity, precocious puberty, and neurologic
symptoms [42]. (See "Clinical manifestations and diagnosis of central nervous system
tumors in children".)
• Microcephaly is a feature of Cohen syndrome (in addition to other dysmorphic

features).
• Clumps of pigment in the peripheral retina may indicate retinitis pigmentosa, which
occurs in Bardet-Biedl syndrome.
● Skin and hair
• Acanthosis nigricans ( picture 2A-D) may signify insulin resistance with or without
type 2 diabetes [45-47].
• Hirsutism and acne are common features of polycystic ovary syndrome and Cushing
syndrome.
• Striae distensae (stretch marks) are linear atrophic plaques in susceptible sites (eg,
abdomen, breasts, thighs). They are initially pink or purple, then evolve to
hypopigmented scar-like depressions with fine wrinkling. They are usually the result of
rapid weight gain but also may be manifestations of Cushing syndrome. (See "Striae
distensae (stretch marks)".)
• Dry, coarse, or brittle hair may be present in hypothyroidism. (See "Clinical

manifestations of hypothyroidism".)
• Red hair (in White individuals), hyperphagia, and early onset of obesity are features of
proopiomelanocortin deficiency. In addition, people with this condition have low levels
of adrenocorticotropic hormone with associated adrenal insufficiency. (See "Obesity:
Genetic contribution and pathophysiology", section on 'Proopiomelanocortin'.)
● Abdomen
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• Abdominal tenderness, particularly in the right upper quadrant, may be a sign of

gallbladder disease or nonalcoholic fatty liver disease (NAFLD) [4].
• Hepatomegaly may be a clue to NAFLD [4]. (See "Nonalcoholic fatty liver disease in
children and adolescents".)
● Musculoskeletal
• Limited range of motion at the hip or a gait abnormality may be caused by slipped
capital femoral epiphysis. (See "Evaluation and management of slipped capital femoral
epiphysis (SCFE)".)
• Genu varum (bow legs) or valgus (knock-knees). (See "Overview of the health
consequences of obesity in children and adolescents", section on 'Genu varus or
valgus'.)
• Nonpitting edema may indicate hypothyroidism. (See "Clinical manifestations of

hypothyroidism".)
• Dorsal finger callousness may be a clue to self-induced vomiting in patients with an

eating disorder [2]. (See "Eating disorders: Overview of epidemiology, clinical features,
and diagnosis".)
• Postaxial polydactyly (an extra digit next to the fifth digit) may be present in Bardet-
Biedl syndrome [48], and small hands and feet may be present in Prader-Willi
syndrome ( table 3A-B) [2]. (See "Clinical features, diagnosis, and treatment of
• Pes planus (flat feet) and pronation of the feet are common in children with obesity and
frequently give rise to pain during exercise [49-51].
● Genitourinary – Endocrine or genetic causes of obesity are often associated with

hypogonadism [2]. Evaluation of pubertal stage is discussed separately. (See "Normal
puberty", section on 'Sexual maturity rating (Tanner stages)' and "Clinical features,
diagnosis, and treatment of Prader-Willi syndrome", section on 'Hypogonadism'.)
• Undescended testicles, small penis, and scrotal hypoplasia may indicate Prader-Willi
syndrome.
• Small testes may suggest Prader-Willi or Bardet-Biedl syndrome [48].
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• Delayed or absent puberty may occur in the presence of hypothalamic-pituitary

tumors, Prader-Willi syndrome, Bardet-Biedl syndrome, leptin deficiency, or leptin
receptor deficiency.
• Precocious puberty occasionally is a presenting symptom of a hypothalamic-pituitary

lesion or dysfunction, including in ROHHAD(NET) syndrome [42]. Children with Prader-
Willi syndrome often have premature adrenarche. (See "Clinical manifestations and
diagnosis of central nervous system tumors in children" and "Definition, etiology, and
evaluation of precocious puberty" and "Clinical features, diagnosis, and treatment of
● Development – Most of the syndromic causes of overweight in children are associated

with cognitive or developmental delay ( table 3A-B). Prader-Willi syndrome is also
associated with marked hypotonia during infancy and delayed development of gross
motor skills. (See "Clinical features, diagnosis, and treatment of Prader-Willi syndrome",
section on 'Behavior characteristics'.)
FURTHER EVALUATION
Routine blood tests — The laboratory evaluation for children with obesity is not fully
standardized. Most experts suggest routine screening for the following comorbidities (
table 12A) [4,43,52]:
● Dyslipidemia – Screening consists of a fasting lipid profile (total cholesterol, triglycerides,

and high- and low-density lipoprotein cholesterols). The approach to lipid screening and
follow-up is summarized in the algorithms ( algorithm 1A-B) and detailed in a separate
topic. (See "Dyslipidemia in children and adolescents: Definition, screening, and
diagnosis", section on 'Approach to screening'.)
● Type 2 diabetes mellitus – Laboratory testing for diabetes is suggested for children with
overweight or obesity and additional risk factors ( table 12B). Screening consists of
either fasting plasma glucose or hemoglobin A1c. Measurement of a fasting insulin level is
not recommended for screening or clinical decision-making [53]. (See "Epidemiology,
presentation, and diagnosis of type 2 diabetes mellitus in children and adolescents",
section on 'Screening'.)
● Fatty liver disease – Screening is performed with a serum alanine aminotransferase (ALT)
level. Measure starting between 9 and 11 years of age. If normal, repeat at least every two
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to three years [54]. Sustained elevations of ALT (eg, >2 times the upper limit of normal
[ULN] for six months) warrant further evaluation.
For ALT interpretation, use the ULN of 22 units/L for girls and 26 units/L for boys [55]. Note
that these values are substantially lower than the ULNs reported in most pediatric hospital
laboratories. However, it is important to note that liver transaminases have only moderate
sensitivity and specificity for detecting clinically significant nonalcoholic fatty liver disease
(NAFLD). (See "Overview of the health consequences of obesity in children and
adolescents", section on 'Nonalcoholic fatty liver disease' and "Nonalcoholic fatty liver
disease in children and adolescents".)
Tests for selected patients — Additional testing may be warranted for selected patients, as
outlined in the table ( table 12A) [52,56,57].
● Tests for causes of obesity
• Hypothyroidism or Cushing syndrome – Routine laboratory screening for

hypothyroidism or Cushing syndrome is not recommended [43,53,58]. However,
testing is appropriate if there are suggestive signs or symptoms, particularly evidence
of growth attenuation (decreased height velocity). Mildly elevated levels of thyroid-
stimulating hormone are more often found in children with obesity compared with
normal-weight peers, but this is a consequence rather than a cause of the obesity [59].
(See "Establishing the diagnosis of Cushing's syndrome" and "Acquired hypothyroidism
in childhood and adolescence".)
• Syndromic obesity – Children with developmental delay or dysmorphic features

should be evaluated for syndromic obesity ( table 3A).
● Tests for comorbidities
• Vitamin D deficiency – The American Academy of Pediatrics and others recommend

against routine screening for vitamin D deficiency in healthy children, including those
with overweight or obesity [53,60,61]. However, targeted screening may be appropriate
for children with very low dairy/vitamin D intake or those with genu varum/valgus
malformations. Although children and adolescents are somewhat more likely to have
low serum vitamin D concentrations compared with the general population [62], this
may be related to the sequestration of vitamin D in adipose tissue and a clinical
consequence has not been established. (See "Vitamin D insufficiency and deficiency in
children and adolescents", section on 'Obesity'.)
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• Hypertension – For children with hypertension, additional laboratory testing may be

warranted (eg, serum electrolytes, blood urea nitrogen, creatinine, and urinalysis). (See
"Evaluation of hypertension in children and adolescents".)
• Polycystic ovary syndrome – Laboratory testing is warranted in females with

symptoms suggesting polycystic ovary syndrome, ie, an irregular menstrual pattern,
hirsutism or treatment-resistant acne, or acanthosis nigricans with central obesity. (See
"Diagnostic evaluation of polycystic ovary syndrome in adolescents".)
Imaging — The radiographic evaluation of children with obesity is directed by findings on the

history and physical examination.
● Plain radiographs of the lower extremities should be obtained if there are clinical findings
consistent with slipped capital femoral epiphysis (hip or knee pain, limited range of
motion, abnormal gait) or Blount disease (bowed tibia). (See "Evaluation and management
of slipped capital femoral epiphysis (SCFE)", section on 'Radiologic evaluation'.)
● Abdominal ultrasonography may be indicated in children with findings consistent with

gallstones (eg, abdominal pain, abnormal transaminases) [4].
● Abdominal ultrasonography is not recommended as a routine screening test for NAFLD in

children with obesity, because it is not a useful predictor of clinically significant NAFLD.
However, for children with persistently elevated serum aminotransferases, ultrasound or
other radiographic evaluation may be indicated as part of a full evaluation for suspected
NAFLD. (See "Overview of the health consequences of obesity in children and adolescents",
section on 'Nonalcoholic fatty liver disease' and "Nonalcoholic fatty liver disease in
children and adolescents", section on 'Screening'.)
INITIAL MANAGEMENT
Management in primary care — Management strategies vary according to the child's age,

weight status and trend, and history of interventions. A clinical approach to management in the
primary care setting is summarized in the algorithm ( algorithm 2) and described in a
separate topic review. (See "Prevention and management of childhood obesity in the primary
care setting".)
Referrals
● Comprehensive weight management program – Referral is suggested for [4,63]:
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• Severe obesity (body mass index [BMI] ≥120 percent of the 95th percentile or BMI ≥35
kg/m2, whichever is lower), especially if any comorbidities are present or if BMI ≥40
kg/m2.
• Refractory obesity (progressive increase in BMI percentiles despite structured

interventions in the primary care setting).
• Severe obesity in a child younger than two years. These children warrant special
evaluation for the underlying cause of the obesity, as well as intensive support to
optimize diet.
A comprehensive weight management program usually includes coordinated and

intensive dietary and behavioral therapy and may offer pharmacologic and/or surgical
therapy. If such a program is not available, key services may be provided by separate
referrals to a clinician with special expertise in obesity, with support from a dietitian
and/or mental health specialist as needed.
● Weight loss surgery – For adolescents with severe obesity, and especially those with
major comorbidities (type 2 diabetes, severe sleep apnea, and/or steatohepatitis), referral
to an experienced weight loss surgery program may be appropriate. Some comprehensive
weight management programs include evaluation or referral for weight loss surgery,
whereas others require a separate referral. Patient selection is discussed in a separate
topic review. (See "Surgical management of severe obesity in adolescents".)
● Specialty referral for comorbidities – Children with suspected or established

comorbidities may require referral to an appropriate subspecialist. Further information
about comorbidities is outlined in a separate overview (see "Overview of the health
consequences of obesity in children and adolescents"), which includes links to disease-
specific topic reviews.
● Mental health specialists – Indications for referral include:
• Clinically significant depression or anxiety. Weight loss therapy may be ineffective

without concurrent psychological care [3].
• Suspected eating disorder (eg, inability to control consumption of large amounts of

food, self-induced vomiting or laxative use to avoid weight gain, dorsal finger lesions).
These patients should be evaluated by a therapist with experience in eating disorders;
such children require psychological treatment and should not participate in weight
management programs without the concurrence of a therapist [3].
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SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Obesity in children".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topic (see "Patient education: My child is overweight (The Basics)")
SUMMARY AND RECOMMENDATIONS
● Body mass index (BMI) – BMI is the accepted standard measure of obesity and
overweight in children. "Obesity" is defined by a BMI ≥95th percentile for age and sex, and
"overweight" is defined by a BMI ≥85th and <95th percentile for age and sex ( table 2).
(See 'Body mass index' above.)
Height and weight should be measured and BMI calculated at least yearly in children older
than two years. The results should be used to determine the child's weight category (
table 2) and plotted on an appropriate growth curve to determine the BMI percentile
and trend ( figure 1A-B). For children with severe obesity, use of an extended growth
chart facilitates tracking ( figure 2A-B). (See 'Body mass index' above.)
● History – The history should include information about (see 'History' above):
• Onset of obesity and historical patterns of weight gain

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• Child's diet and food preferences ( table 4)
• Physical activity patterns and sedentary activities (screen time) ( table 5)
• Sleep duration compared with recommended sleep time ( table 6) and sleep-related
symptoms such as snoring
• Review of systems for signs of comorbidities or syndromic obesity ( table 9)
• Family history of obesity and comorbidities
• Psychosocial history including possible triggering events, school/social functioning,

and social determinants of health (food insecurity and other challenges)
● Physical examination – The physical examination should evaluate for signs and
symptoms of comorbidities and genetic and endocrinologic causes of overweight (
table 10A-B). (See 'Physical examination' above.)
● Further evaluation – The laboratory evaluation for children with obesity is not
standardized. Most experts suggest routine screening for dyslipidemia, hypertension, and
fatty liver disease, as well as selective screening for type 2 diabetes in adolescents with
risk factors ( table 12A-B). Additional testing may be warranted for patients with signs or
symptoms suggesting polycystic ovary syndrome, obstructive sleep apnea,
hypothyroidism, Cushing syndrome, or orthopedic problems. (See 'Further evaluation'
above.)
● Initial management – Management strategies vary according to the child's age, weight
status and trend, and history of interventions. A clinical approach to management in the
primary care setting is summarized in the algorithm ( algorithm 2) and detailed in a
separate topic review. (See "Prevention and management of childhood obesity in the
primary care setting".)
● Referrals – Suggested referrals for children and adolescents with obesity include (see
'Referrals' above):
• For patients with severe or refractory obesity, and especially those with comorbidities,
refer to a comprehensive weight management program or pediatric obesity specialist.
• For adolescents with severe obesity, and especially those with major comorbidities,
consider referral to an experienced weight loss surgery program.
6/19/22, 5:58 PM 5861
• For patients with symptoms and signs of depression, anxiety, or an eating disorder,
refer for psychological evaluation and treatment.
Use of UpToDate is subject to the Terms of Use.
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17. Hoppin, AG. Obesity. In: Pediatric Gastrointestinal Disease: Pathopsychology, Diagnosis, Ma
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Management of High Blood Pressure in Children and Adolescents. Pediatrics 2017; 140.
42. Taylor M, Couto-Silva AC, Adan L, et al. Hypothalamic-pituitary lesions in pediatric patients:
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nigricans in an adult obese population. Arch Dermatol 1992; 128:941.
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high risk for metabolic abnormalities. J Pediatr 2010; 156:87.
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syndrome, a form of Laurence-Moon-Biedl syndrome. N Engl J Med 1989; 321:1002.
49. Riddiford-Harland DL, Steele JR, Baur LA. Are the feet of obese children fat or flat?
Revisiting the debate. Int J Obes (Lond) 2011; 35:115.
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Diagnosis and Treatment of Nonalcoholic Fatty Liver Disease in Children:
Recommendations from the Expert Committee on NAFLD (ECON) and the North American
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55. Schwimmer JB, Dunn W, Norman GJ, et al. SAFETY study: alanine aminotransferase cutoff
values are set too high for reliable detection of pediatric chronic liver disease.
Gastroenterology 2010; 138:1357.
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syndrome. Endocrinol Metab Clin North Am 1994; 23:487.
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58. Choosing Wisely. Avoid routinely measuring thyroid function and/or insulin levels in childre
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9, 2022).
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weight loss and is not related to lipids. J Clin Endocrinol Metab 2006; 91:3088.
60. Choosing Wisely. Avoid ordering Vitamin D concentrations routinely in otherwise healthy c
hildren, including children who are overweight or obese. 2017. Available at: https://www.ch
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Management of Nutritional Rickets. J Clin Endocrinol Metab 2016; 101:394.
62. Turer CB, Lin H, Flores G. Prevalence of vitamin D deficiency among overweight and obese
US children. Pediatrics 2013; 131:e152.
63. Young KL, Demeule M, Stuhlsatz K, et al. Identification and treatment of obesity as a
standard of care for all patients in children's hospitals. Pediatrics 2011; 128 Suppl 2:S47.
Topic 5861 Version 56.0
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GRAPHICS
Calculation of body mass index
English formula for BMI:

703 × weight in pounds ÷ (height in inches)2
Metric formula for BMI:

Weight in kilograms ÷ (height in meters)2
BMI: body mass index.
Graphic 71431 Version 5.0
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Body mass index-for-age percentiles, males 2 to 20 years, CDC

growth charts: United States
BMI: body mass index; CDC: Centers for Disease Control and Prevention.
Developed by the National Center for Health Statistics in collaboration with the National Center for
Chronic Disease Prevention and Health Promotion (2000).
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Body mass index-for-age percentiles, females 2 to 20 years,

CDC growth charts: United States
BMI: body mass index; CDC: Centers for Disease Control.
Developed by the National Center for Health Statistics in collaboration with the National Center for
Chronic Disease Prevention and Health Promotion (2000).
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BMI curves for females 2 to 20 years with severe obesity
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Severe obesity in pediatric patients is defined as a body mass index (BMI) that is either ≥120% of the 95th
percentile curve, or BMI ≥35 kg/m2 (whichever is lower). The area defining severe obesity is shaded in red in
the figure above. A BMI of 40 kg/m2 is typically used as a threshold for weight loss surgery in adults and
adolescents without major comorbidities. Note that this threshold is well above the curve representing 120%
of the 95th percentile at all ages.
The black curves (50 through 97) represent the standard BMI growth reference from the CDC, published in
2000. The blue curves (110% through 190%) are derived by multiplying the 95th percentile values by 1.1
through 1.9, respectively.
CDC: Centers for Disease Control and Prevention.
Adapted from: Kelly AS, Barlow SE, Rao G, et al. Severe obesity in children and adolescents: Identification, associated health risks, and
treatment approaches. A scientific statement from the American Heart Association. Circulation 2013; 128:1689.
6/19/22, 5:58 PM 5861
BMI curves for males 2 to 20 years with severe obesity
6/19/22, 5:58 PM 5861
Severe obesity in pediatric patients is defined as a body mass index (BMI) that is either ≥120% of the 95th
percentile curve, or BMI ≥35 kg/m2 (whichever is lower). The area defining severe obesity is shaded in red in
the figure above. A BMI of 40 kg/m2 is typically used as a threshold for weight loss surgery in adults and
adolescents without major comorbidities. Note that this threshold is well above the curve representing 120%
of the 95th percentile at all ages.
The black curves (50 through 97) represent the standard BMI growth reference from the CDC, published in
2000. The blue curves (110% through 190%) are derived by multiplying the 95th percentile values by 1.1
through 1.9, respectively.
CDC: Centers for Disease Control and Prevention.
Adapted from: Kelly AS, Barlow SE, Inge TH, et al. Severe obesity in children and adolescents: Identification, associated health risks, an
treatment approaches. A scientific statement from the American Heart Association. Circulation 2013; 128:1689.
6/19/22, 5:58 PM 5861
Weight categories for adults and youth
Adults
Youth 2 to 18 years
Category 18 years and older[1]

(CDC, AAP, IOM, ES,
(kg/m2 ) IOTF[2,3] )
Underweight BMI <18.5 BMI <5th percentile for age
Normal weight BMI 18.5 to 24.9 BMI ≥5th to <85th percentile
Overweight BMI 25 to 29.9 BMI ≥85th to <95th percentile
Obesity BMI ≥30 BMI ≥95th percentile
Severe obesity BMI ≥35 (class II obesity) BMI ≥120% of the 95th
percentile or a BMI ≥35
(whichever is lower)*[4,5]
BMI ≥40 (class III obesity) BMI ≥140% of the 95th

percentile or a BMI ≥40
(whichever is lower)[5]
CDC: Centers for Disease Control and Prevention; AAP: American Academy of Pediatrics; IOM:
Institute of Medicine; ES: Endocrine Society; IOTF: International Obesity Task Force; BMI: body mass
index.
* In children, several definitions of severe obesity have been used. The most widely accepted is BMI
≥120% of the 95th percentile or a BMI ≥35 kg/m2 (whichever is lower)[3] . This corresponds to
approximately the 99th percentile or BMI Z-score ≥2.33 (ie, 2.33 standard deviations above the
mean).
References:
1. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence
Report. National Institutes of Health. Obes Res 1998; 6 Suppl 2:51S.
2. Barlow SE, Expert Committee. Expert committee recommendations regarding the prevention, assessment, and
treatment of child and adolescent overweight and obesity: summary report. Pediatrics 2007; 120 Suppl 4:S164.
3. Wang Y. Cross-national comparison of childhood obesity: the epidemic and the relationship between obesity and
socioeconomic status. Int J Epidemiol 2001; 30:1129.
4. Kelly AS, Barlow SE, Rao G, et al. Severe Obesity in Children and Adolescents: Identification, Associated Health Risks,
and Treatment Approaches: A Scientific Statement From the American Heart Association. Circulation 2013.
5. Skinner AC, Skelton JA. Prevalence and Trends in Obesity and Severe Obesity Among Children in the United States,
1999-2012. JAMA Pediatr 2014.
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Selected neuroendocrine disorders associated with childhood obesity
Disorder Key features
Hypothyroidism Decreased linear growth, mildly accelerated weight gain, mostly due
to fluid retention.
Altered school performance, sluggishness, constipation, pubertal

delay.
Cortisol excess Decreased linear growth, mildly or moderately accelerated weight

(corticosteroid medication, gain, with central fat distribution.
Cushing syndrome)
Suprascapular fat pad, violaceous striae, acne, hirsutism, signs of
insulin resistance, neuropsychological changes.
Growth hormone deficiency Decreased linear growth, mildly accelerated weight gain, delayed
bone age.
Cherubic face with underdeveloped nasal bridge.
Pseudohypoparathyroidism Obesity with round facies, short stature, short fourth metacarpal
type 1a (Albright hereditary bones, developmental delay, hypocalcemia, subcutaneous
osteodystrophy) calcifications, and hyperparathyroid bone disease.
Hypothalamic lesions
After brain surgery (eg, Abrupt very rapid weight gain, hyperphagia. Often associated with
for craniopharyngioma) panhypopituitarism.
Diencephalic tumor Variable onset; may include headache, vomiting, vision defects, and
other symptoms of increased intracranial pressure.
ROHHAD/ROHHADNET Rapid onset of obesity, central hypoventilation, and autonomic

syndrome dysregulation (may include hyperthermia or hypothermia), with or
without neural crest tumors. Onset typically during early childhood.
Possible immune-mediated mechanism. In the past, some cases of
apparent "idiopathic" hypothalamic obesity may have been ROHHAD
without the hypoventilation.
Congenital central Prominent central hypoventilation and autonomic dysfunction;

hypoventilation associated with PHOX2B gene mutations. Obesity is not a prominent
syndrome (early- or late- symptom, and the reported association may be due to historical
onset) misclassification of ROHHAD.
ROHHAD/ROHHADNET: rapid-onset obesity, hypothalamic dysfunction, hypoventilation, autonomic

dysregulation, with or without neural crest tumors.
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Selected genetic syndromes associated with obesity
Obesity
MIM Clinical
Syndrome Locus Gene onset
phenotype features
(type)
Albright hereditary 103580 20q13.2 GNAS1 Early Short stature,

osteodystrophy (generalized) short metacar
(pseudohypoparathyroidism and metatarsa
type 1a) round facies,
delayed dentit
± hypocalcemi
and/or
subcutaneous
calcium or bon
deposition
(osteoma cutis
precocious
puberty, mild
cognitive defic
Alström 203800 2p13 ALMS1 Age 2 to 5 Blindness,

years deafness,
(central) acanthosis
nigricans, chro
nephropathy,
type 2 diabete
cirrhosis, prim
hypogonadism
males only,
normal cogniti
Bardet-Biedl syndrome 209900 11q13 BBS1 Age 1 to 2 Intellectual

years disability,
615981 16q21 BBS2
(central) hypotonia,
600151 3p12-q13 BBS3 retinitis
(ARL6) pigmentosa,
615982 15q22.3-q23 BBS4 polydactyly,
hypogonadism
615983 2q31 BBS5 glucose
605231 20p12 BBS6 intolerance,
(MKKS) deafness, rena
disease
615984 4q27 BBS7
615985 14q32 BBS8

(TTC8)
6/19/22, 5:58 PM 5861
615986 7p14 BBS9
615987 12q BBS10
615988 9q33.1 BBS11

(TRIM32)
615989 4q27 BBS12
615990 17q23 BBS13

(MKS1)
615991 12q21.3 BBS14

(CEP290)
615992 2p15 BBS15

(C2ORF86)
Beckwith-Wiedemann 130650 11p15.5 in Multiple – Hyperinsulinem

most cases; hypoglycemia,
deregulation hemihypertrop
of imprinted intolerance of
genes fasting
including
IGF2
Carpenter 201000 6p11 RAB23 (Central) Intellectual

disability, shor
stature,
brachycephaly
polydactyly,
syndactyly of f
cryptorchidism
umbilical hern
high-arched
palate,
hypogonadism
males only
Cohen 216550 8q22 COH1 Mid- Intellectual

(VPS13B) childhood disability,
(central) microcephaly,
small hands an
feet,
cryptorchidism
hypotonia and
failure to thriv
infancy,
prominent cen
incisors; long,
6/19/22, 5:58 PM 5861
thin fingers an
toes
Prader-Willi 176270 15q NDN Age 1 to 3 Early growth

years faltering follow
SNRPN
(generalized) by hyperphagi
and increased
weight gain by
to 3 years. Mild
moderate
cognitive defic
microcephaly,
short stature,
hypotonia,
almond-shape
eyes, high-arch
palate, narrow
hands and fee
delayed puber
(but premature
adrenarche).
MIM: Mendelian Inheritance in Man database.
Adapted from:
1. Pediatric Obesity. In: Pediatric Nutrition Handbook, 6th ed, Kleinman R (Ed), American Academy of Pediatrics, Elk
Grove Village, IL, 2009. p.751.
2. Hoppin AG. Obesity. In: Pediatric Gastrointestinal Disease: Pathopsychology, Diagnosis, Management, 4th ed, Walker
WA, Goulet O, Kleinman RE, et al (Eds), BC Decker, Ontario, 2004. p.311.
3. Leibel RL, Chua SC, Rosenbaum M. Obesity. In: The Metabolic and Molecular Bases of Inherited Disease, 8th ed,
Scriver CR, Beaudet AL, Sly WS, Valle D (Eds), McGraw-Hill, New York, 2001. p.3965.
6/19/22, 5:58 PM 5861
Genetic disorders in which obesity is an isolated or predominant feature
Disorder
Gene Clinical features
(gene)
Leptin deficiency
LEP Severe early-onset obesity, hypometabolic rate,
(various hyperphagia, pubertal delay, impaired glucose tolerance,
mutations hypothalamic hypogonadism, frequent infections. Leptin
interfering with levels are very low or undetectable. Obesity and
synthesis or hyperphagia respond to replacement with exogenous
secretion of recombinant leptin[1] .
leptin)
Leptin receptor LEPR Severe early-onset obesity, hypometabolic rate,

deficiency hyperphagia, pubertal delay, hypothalamic hypogonadism.
Leptin levels are high but are proportional to the degree of
obesity, so they are not a useful marker for this defect.
Responds to treatment with setmelanotide, a melanocortin
4 receptor agonist*, but not to exogenous leptin[2,3] .
Leptin LEP (LEP p.D100Y) Severe early-onset obesity, hyperphagia. Leptin level are
dysfunction
high (consistent with degree of obesity) but biologically
(biologically inactive. Obesity and hyperphagia respond to treatment
inactive leptin) with exogenous recombinant leptin[4] .
Pro- POMC Adrenal insufficiency (typically presenting in the neonatal

opiomelanocortin period), severe early-onset obesity, hyperphagia, with pale
deficiency skin and red hair in White individuals[5,6] . Responds to
treatment with setmelanotide*.
Proprotein PCSK1, also Early-onset obesity, diarrhea, abnormal glucose

convertase 1/3 known as homeostasis, hypogonadotropic hypogonadism,
deficiency prohormone hypocortisolism, elevated plasma proinsulin and POMC[7] .
convertase 1 Responds to treatment with setmelanotide*.
Melanocortin MC4R Early-onset moderate to severe obesity, early-onset

receptor 4 hyperphagia, increased bone density, accelerated linear
haploinsufficiency growth, severe hyperinsulinemia, mild central
hypothyroidism[8] .
Melanocortin 2 MRAP2 Severe nonsyndromic early-onset obesity (probably very

receptor rare)[9] .
accessory protein
2
GNAS mutations GNAS complex Severe early-onset obesity with or without developmental
locus delay, short stature, brachydactyly, subcutaneous
ossifications, pseudohypoparathyroidism (hypocalcemia,
PTH resistance) and thyrotropin resistance (elevated TSH
6/19/22, 5:58 PM 5861
with normal or low fT4)[10] (eg, Albright's hereditary

osteodystrophy). Obesity is likely mediated by disrupted
MC4R signaling.
POMC: pro-opiomelanocortin; PCSK1: proprotein convertase subtilisin/kexin type 1; PTH: parathyroid

hormone; GNAS: encodes the G-alphas (stimulatory G-protein alpha subunit) protein; TSH: thyroid-
stimulating hormone; fT4: free thyroxine.
* Setmelanotide, a melanocortin 4 receptor agonist, is available for the treatment of obesity due to
mutations in the POMC, PCSK1, or LEPR (leptin receptor) genes confirmed by genetic testing[11] .
Refer to UpToDate content on genetic contributions to obesity.
References:
1. Farooqi IS, Matarese G, Lord GM et al. Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and
neuroendocrine/metabolic function of human congenital leptin deficiency. J Clin Invest 2002; 110:1093.
2. Clement K, Vaisse C, Lahlou N et al. A mutation in the human leptin receptor gene causes obesity and pituitary
dysfunction. Nature 1998; 392:398.
3. Farooqi IS, Wangensteen T, Collins S et al. Clinical and molecular spectrum of congenital deficiency of the leptin
receptor. New Engl J Med 2007; 356:237.
4. Wabitsch M, Funcke JB, Lennerz B et al. Biologically inactive leptin and early-onset extreme obesity. New Engl J Med
2015; 372:48.
5. Krude H, Biebermann H, Luck W et al. Severe early-onset obesity, adrenal insufficiency and red hair pigmentation
caused by POMC mutations in humans. Nat Genet 1998; 19:155.
6. Anisimova AS, Rubtsov PM, Akulich KA, et al. Late diagnosis of POMC deficiency and in vitro evidence of residual
translation from allele with c.-11C>A mutation. J Clin Endocrinol Metab 2017; 102:359.
7. Jackson RS, Creemers JW, Ohaqi S et al. Obesity and impaired prohormone processing associated with mutations in
the human prohormone convertase 1 gene. Nat Genet 1997; 16:303.
8. Farooqi IS, Keogh JM, Yeo GS et al. Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene.
New Engl J Med 2003; 348:1085.
9. Asai M, Ramachandrappa S, Joachim M, et al. Loss of function of the melanocortin 2 receptor accessory protein 2 is
associated with mammalian obesity. Science 2013; 341:275.
10. Mendes de Oliveira E, Keogh JM, Talbot F, et al. Obesity-Associated GNAS Mutations and the Melanocortin Pathway. N
Engl J Med 2021; 385:1581.
11. Rhythm Pharmaceuticals. Imcivree: Highlights of Prescribing information. 2020. Available at:
https://www.rhythmtx.com/IMCIVREE/prescribing-information.pdf (Accessed on December 08, 2020).
Farooqi IS. The severely obese patient – a genetic workup. Nat Clin Pract Endocrinol Metab 2006; 2:172.
6/19/22, 5:58 PM 5861
Goals and counseling on nutritional factors related to childhood obesity
Nutritional Contribution to
Examples of goals* Counseling tips
factor weight gain
Parent/caregiver Parent/caregiver is an Family members Be a good role model

role important role model have diet and activity for healthy eating
for healthy eating. goals that are similar and exercise
to those expected of (regardless of your
the child. weight).
Try to get all family
members to do the
same.
Tell your child about
your diet and activity
goals; be honest if
you don't meet them
and say that you will
keep trying.
Parent/caregiver is Family plans and Control the grocery

often responsible for eats meals together. list – It's easier to
meal planning and Aim to have a single make healthy choices
influences the home meal prepared for if almost all of the
nutritional the entire family, foods in the house
environment[1] . rather than making are healthy.
separate items for Prepare the same
different members of meal for all family
the family. members.
Include at least 1
food that the child
likes and don't
pressure the child to
try every food.
Parent/caregiver Support a healthy Find positive things

shapes the child's self- body image for the to say about the child
image and eating child. that do not focus on
patterns. Model a healthy their weight.
relationship with Parents should use
food. the same positive talk
to themselves.
Be positive about
trying new foods.
6/19/22, 5:58 PM 5861
Model a healthy
relationship with
food – Focus on the
importance of food
for our bodies and
avoid negative
comments about
calories and eating.
Restaurants and Meals eaten away 1 or fewer take-out Practice more family
fast food from home increase or fast food meals meals; start with
portion size and total weekly. takeout that is
energy intake and are Plan meals for the brought home and
of poorer nutrient week, including put on plates to be
quality[2-4] . which meals will be eaten as a family.
Increased frequency at restaurants. Make a family meal
of eating meals away plan, including the
from home is children in planning.
associated with Schedule a day to
increased BMI[5,6] . grocery shop and
build the grocery list
from the meal plan.
Utilize meal planning
websites for the
family.
Explore cooking and
food preparation
classes and websites;
encourage the parent
and child to
participate together.
Sweetened High intake of sugar- Avoid all sugar- Main beverages

beverages sweetened beverages sweetened should be water or
is linked to increased beverages and juice. low-fat milk
prevalence of obesity This can be (unsweetened).
in children[7-8] , but facilitated by "Diet" (artificially
causality has not been eliminating these sweetened)
established[9,10] . beverages from the beverages are OK but
Fruit juice also should home environment. in moderation.
be considered a
sweetened beverage.
Artificially sweetened
beverages are safe
and may help with
weight control[11,12] .
6/19/22, 5:58 PM 5861
Portion sizes Larger portions lead Goals depend on Caution parents in

to increased energy child's age, degree of focusing too much
intake[13-14] . obesity, and level of on portion sizes to
physical activity. avoid disagreements
Use a balanced plate over food.
approach to subtly Encourage a
decrease portion balanced plate¶ .
size.
Energy-dense An association Avoid serving fried Have snacks at home

foods between energy- foods at meals. made from 2 food
dense foods and Eliminate high- groups.
obesity has been calorie snack foods Make homemade
established in adults from the house (eg, "snack packs" using
but not yet in cookies, chips, ice small bags or
children[15] . cream). containers.
Offer only low-fat or Schedule snack times
skim milk; limit instead of snacking
quantities of cheese; when hungry and
choose cereals with close to mealtimes.
relatively low sugar
content.
Fruits and Eating fruits and Encourage at least 5 Plan a "field trip" to
vegetables vegetables may servings of the grocery store or
displace more energy- vegetables and fruits produce stand,
dense foods and daily (fresh, cooked, allowing child to pick
increase satiety. There frozen, or canned). out fruits and
is some evidence that These should not be vegetables that the
low consumption of in the form of juice child wants to try.
these foods is or candy-like "fruit Involve the child in
associated with snacks." meal planning,
obesity[16-18] . allowing the child to
choose fruits and
vegetables for meals.
Serve fruits and
vegetables with
meals, but don't
pressure the child to
eat or try them
(which can cause
negative reactions).
Continue to offer
new foods, even if
child does not eat
them initially. Offer
6/19/22, 5:58 PM 5861
them gently but do

not force the child to
try them. Pair new
foods with familiar
ones.
Breakfast Skipping breakfast is Eat a moderate Allow the child to

associated with breakfast daily. Avoid have non-breakfast
obesity in children breakfast foods with food items in the
despite perceived high sugar or energy morning if desired
decrease in daily density (eg, high- ("breakfast doesn't
caloric intake[19-23] sugar cereals or have to be breakfast
and has adverse pastries). foods").
effects on school Prepare items ahead
performance[24-26] . of time or wake up
earlier in order to eat
breakfast.
If the child is
reluctant to eat
breakfast, allow them
to have smaller
breakfast meals to
establish the habit of
eating in the
morning.
Meal frequency Snacking tends to Offer 3 meals daily Schedule a snack

and snacking result in increased on a regular time.
energy intake and schedule. Establish "kitchen
poorer diet quality; a 1 or 2 additional hours" to encourage
direct association healthy snacks may children to eat at
between snacking and be appropriate for mealtimes.
obesity in children has some children. Teach about hunger
not been established. and fullness; if meals
are offered at regular
times, the children
will get the needed
nutrition.
* These are examples of optimal goals. Actual goals for counseling depend upon the child's age,
degree of obesity, current habits, and other considerations including family finances and local
resources. In most cases, more stringent goals should be set as counseling progresses. Goals need
not be absolute: For example, high-calorie snack foods should ideally be eliminated from the house
but might be permitted occasionally as a "treat." Refer also to UpToDate content and tables on tips
for maintaining a healthy weight.
6/19/22, 5:58 PM 5861
¶ The "balanced plate" approach gives approximately 1/4 of the meal plate to each of 4 food groups:
vegetables, grains, fruits, and protein. This is a way to teach and encourage ample intake of
vegetables, fruits, and fiber and may help to subtly limit portion size. Guidance is available at the
MyPlate website.
References:
1. Valdés J, Rodríguez-Artalejo F, Aguilar L, et al. Frequency of family meals and childhood overweight: a systematic
review. Pediatr Obes 2013; 8:e1.
2. Whitlock EP, O'Connor EA, Williams SB, et al. Effectiveness of weight management interventions in children: a targeted
systematic review for the USPSTF. Pediatrics 2010; 125:e396.
3. Hamano T, Li X, Sundquist J, Sundquist K. Association between Childhood Obesity and Neighbourhood Accessibility to
Fast-Food Outlets: A Nationwide 6-Year Follow-Up Study of 944,487 Children. Obes Facts 2017; 10:559.
4. Bowman SA, Gortmaker SL, Ebbeling CB, et al. Effects of fast-food consumption on energy intake and diet quality
among children in a national household survey. Pediatrics 2004; 113:112.
5. Ma Y, Gong W, Ding C, et al. The association between frequency of eating out with overweight and obesity among
children aged 6-17 in China: a National Cross-sectional Study. BMC Public Health 2021; 21:1005.
6. Lachat C, Nago E, Verstraeten R, et al. Eating out of home and its association with dietary intake: a systematic review
of the evidence. Obes Rev 2012; 13:329.
7. Pereira MA, Kartashov AI, Ebbeling CB, et al. Fast-food habits, weight gain, and insulin resistance (the CARDIA study):
15-year prospective analysis. Lancet 2005; 365:36.
8. Brownell KD, Farley T, Willett WC, et al. The public health and economic benefit of taxing sugar-sweetened beverages.
New Engl J Med 2009; 361:1599.
9. Malik VS, Pan A, Willett WC, Hu FB. Sugar-sweetened beverages and weight gain in children and adults: a systematic
review and meta-analysis. Am J Clin Nutr 2013; 98:1084.
10. Trumbo PR, Rivers CR. Systematic review of the evidence for an association between sugar-sweetened beverage
consumption and risk of obesity. Nutr Rev 2014; 72:566.
11. Baker-Smith CM, de Ferranti SD, Cochran WJ, Committee on Nutrition, Section on Gastroenterology, Hepatology and
Nutrition. The Use of Nonnutritive Sweeteners in Children. Pediatrics 2019; 144:e20192765.
12. de Ruyter JC, Olthof MR, Seidell JC, Katan MB. A trial of sugar-free or sugar-sweetened beverages and body weight in
children. N Engl J Med 2012; 367:1397.
13. Lewis CJ, Park YK, Dexter PB, Yetley EA. Nutrient intakes and body weights of persons consuming high and moderate
levels of added sugars. J Am Diet Assoc 1992; 92:708.
14. Rolls BJ, Engell D, Birch LL. Serving portion size influences 5-year-old but not 3-year-old children's food intakes. J Am
Diet Assoc 2000; 100:232.
15. Krebs NF, Himes JH, Jacobson D, et al. Assessment of child and adolescent overweight and obesity. Pediatrics 2007;
120 Suppl 4:S193.
16. Naude CE, Visser ME, Nguyen KA, et al. Effects of total fat intake on bodyweight in children. Cochrane Database Syst
Rev 2018; CD012960.
17. McCrory MA, Fuss PJ, Hays NP, et al. Overeating in America: association between restaurant food consumption and
body fatness in healthy adult men and women ages 19 to 80. Obes Res 1999; 7:564.
18. Bazzano LA, He J, Ogden LG, et al. Fruit and vegetable intake and risk of cardiovascular disease in US adults: the first
National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Am J Clin Nutr 2002; 76:93.
19. Maskarinec G, Novotny R, Tasaki K. Dietary patterns are associated with body mass index in multiethnic women. J
Nutr 2000; 130:3068-72.
20. Monzani A, Ricotti R, Caputo M, et al. A Systematic Review of the Association of Skipping Breakfast with Weight and
Cardiometabolic Risk Factors in Children and Adolescents. What Should We Better Investigate in the Future? Nutrients
2019; 11:387.
21. Okada C, Tabuchi T, Iso H. Association between skipping breakfast in parents and children and childhood
overweight/obesity among children: a nationwide 10.5-year prospective study in Japan. Int J Obes (Lond) 2018;
42:1724.
22. Wicherski J, Schlesinger S, Fischer F. Association between Breakfast Skipping and Body Weight-A Systematic Review
and Meta-Analysis of Observational Longitudinal Studies. Nutrients 2021; 13:272.
6/19/22, 5:58 PM 5861
23. Ardeshirlarijani E, Namazi N, Jabbari M, et al. The link between breakfast skipping and overweigh/obesity in children
and adolescents: a meta-analysis of observational studies. J Diabetes Metab Disord 2019; 18:657.
24. Adolphus K, Lawton CL, Champ CL, Dye L. The Effects of Breakfast and Breakfast Composition on Cognition in
Children and Adolescents: A Systematic Review. Adv Nutr 2016; 7:590S.
25. Kawabata M, Lee K, Choo HC, Burns SF. Breakfast and Exercise Improve Academic and Cognitive Performance in
Adolescents. Nutrients 2021; 13:1278.
26. Verduci E, Bronsky J, Embleton N, et al. Role of Dietary Factors, Food Habits, and Lifestyle in Childhood Obesity
Development: A Position Paper From the European Society for Paediatric Gastroenterology, Hepatology and Nutrition
Committee on Nutrition. J Pediatr Gastroenterol Nutr 2021; 72:769.

Information from:
120:S193.
2. Ross MM, Kolbash S, Cohen GM, Skelton JA. Multidisciplinary treatment of pediatric obesity: nutrition evaluation and
management. Nutr Clin Pract 2010; 25:327.
6/19/22, 5:58 PM 5861
Assessment and counseling to promote physical activity in children
Assessment of sedentary Examples of goals* Counseling tips

behaviors
Recreational screen time, Goals vary by age:[1] Household rules that may help
including: <2 years – Little or no to limit screen time:
Television, videos, or screen time Set a specific screen time
movies ≥2 years – Maximum 1 limit, which applies to all
Video games hour daily family members
Other internet, such as No television viewing
tablets during meals
Social media and smart No television in child's
phones bedroom
No smartphone in
bedroom at night
Develop a "Family Media
Agreement" that outlines
family rules and
objectives for online and
media use
Include
children/adolescents in
the goal-setting process;
this is important because
caregivers cannot
continuously monitor
and enforce these rules.
Educational screen time: Educational screen time is not

Homework restricted. However, advise the
Reading family to:
Computer-based learning Track these activities for

the purposes of
awareness
Do not mix with
recreational screen time
Balance with physical
activity
Assessment of physical Examples of goals* Counseling tips

activity
Record type, frequency, and Goals vary by age: Strategies to promote physical
duration of: activity:[5,6]
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Unstructured Preschool-aged – ≥2 Include family-based

activity/active play hours of unstructured physical activity for
Time outdoors activity daily[2] modeling and
Routine activity, such School-aged and older – encouragement ("game-
as walking to school ≥1 hour moderate or night," walks, hikes,
vigorous structured family sports)
Structured physical
activity physical activity daily[3,4] Start with appealing
recreational activities and
Sports
progress to more
Physical conditioning
structured activity as
tolerated
Offer options: team-
based or individual
sports; coached or self-
directed; competitive or
noncompetitive
Encourage children to
participate in choice of
activity
A step counter
(pedometer) may interest
and motivate some
children
Consider physical activity
levels when choosing
daycare or after-school
programming

To elicit practical options, ask

the family about:
Barriers to physical
activity, including cost
and access
What opportunities are
available (eg, school- or
community-based
programs or facilities)
Examples of questions to ask for a brief semiquantitative assessment of physical activity in children,
as well as tips for helping families achieve recommended goals. Evaluating activity in each of these
areas provides an estimate of the child's overall activity level and helps identify areas for potential
improvement.
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* These are examples of optimal goals. Actual goals for counseling depend upon the child's age,
degree of obesity, current habits, and other considerations including family finances and local
resources. In general, more stringent goals should be set as counseling progresses.
References:
1. Daniels SR, Hassink SG, Committee on Nutrition. The role of the pediatrician in primary prevention of obesity.
Pediatrics 2015; 136:e275.
2. World Health Organization. Guidelines on physical activity, sedentary behaviour and sleep for children under 5 years
of age. World Health Organization. Available at: http://www.who.int/iris/handle/10665/311664 (Accessed on June 9,
2021).
3. Spear BA, Barlow SE, Ervin C, et al. Recommendations for treatment of child and adolescent overweight and obesity.
Pediatrics 2007; 120 Suppl 4:S254.
4. United States Department of Health and Human Services: Physical activity guidelines for Americans, 2nd Edition
(2018). Available at: https://health.gov/our-work/physical-activity/current-guidelines (Accessed on August 06, 2021).
5. Foster C, Moore JB, Singletary CR, Skelton JA. Physical activity and family-based obesity treatment: a review of expert
recommendations on physical activity in youth. Clin Obes 2018; 8:68.
6. Brown HE, Atkin AJ, Panter J, et al. Family-based interventions to increase physical activity in children: a systematic
review, meta-analysis and realist synthesis. Obes Rev 2016; 17:345.
Information from: Krebs NF, Himes JH, Jacobson D, Nicklas TA, Guilday P, Styne D. Assessment of child and adolescent
overweight and obesity. Pediatrics 2007; 120 Suppl 4:S193-228.
6/19/22, 5:58 PM 5861
Recommended sleep times for children
Age group Recommended sleep time
Infants 4 to 12 months 12 to 16 hours (including naps)
Toddlers 1 to 2 years 11 to 14 hours (including naps)
Children 3 to 5 years 10 to 13 hours (including naps)
Children 6 to 12 years 9 to 12 hours
Teens 13 to 18 years 8 to 10 hours
For optimal health, daytime functioning, and development, the above sleep times are recommended
on a regular basis. These consensus recommendations were made by the American Academy of
Sleep Medicine[1] and endorsed by the American Academy of Pediatrics[2] .
References:
1. Paruthi S, Brooks LJ, D'Ambrosio C, et al. Recommended Amount of Sleep for Pediatric Populations: A Consensus
Statement of the American Academy of Sleep Medicine. J Clin Sleep Med 2016; 12:785.
2. Recommended Amount of Sleep for Pediatric Populations. Pediatrics 2016; 138.
6/19/22, 5:58 PM 5861
Categorization of certain medications by their effects on body weight[1]
Produce weight loss

Antiseizure medications: topiramate, zonisamide, lamotrigine
Antidepressants: bupropion, venlafaxine, desvenlafaxine
Antipsychotics: ziprasidone
Attention deficit hyperactivity disorder medications: eg, methylphenidate, amphetamine,

dextroamphetamine[2,3]
Are weight neutral
Antipsychotics: haloperidol, aripiprazole
Produce weight gain

Antidepressants: monoamine oxidase inhibitors, tricyclic antidepressants (nortriptyline,
amitriptyline, doxepin), paroxetine, citalopram, escitalopram, imipramine, mirtazapine
Antipsychotics: thioridazine, olanzapine, risperidone, clozapine, quetiapine
Diabetes medications: eg, insulin, sulfonylureas, thiazolidinediones, meglitinides
Glucocorticoids: eg, prednisone
Hormonal agents: especially progestins, eg, medroxyprogesterone
Antiseizure medications: eg, divalproex
Neurologic and mood-stabilizing agents: eg, lithium, carbamazepine, gabapentin, valproate
Antihistamines: cyproheptadine
Alpha blockers: especially terazosin
Beta blockers: especially propranolol
Reference:
1. Tsai AG, Wadden TA. In the Clinic: Obesity. Ann Intern Med 2013; 159:ITC3-1.
2. Catalá-López F, Hutton B, Núñez-Beltrán A, et al. The pharmacological and non-pharmacological treatment of
attention deficit hyperactivity disorder in children and adolescents: A systematic review with network meta-analyses
of randomised trials. PLoS One 2017; 12:e0180355.
3. Goldfield GS, Lorello C, Doucet E. Methylphenidate reduces energy intake and dietary fat intake in adults: a
mechanism of reduced reinforcing value of food? Am J Clin Nutr 2007; 86:308.
Adapted from: Bray GA, Ryan DH. Medical therapy for the patient with obesity. Circulation 2012; 125:1695.
6/19/22, 5:58 PM 5861
Comorbidities of obesity in children and adolescents
Cardiovascular
Hypertension
Dyslipidemia
Abnormal cardiac structure and function
Premature atherosclerotic cardiovascular disease
Adult cardiovascular disease
Dermatologic
Acanthosis nigricans
Striae
Intertrigo
Furunculosis
Hidradenitis suppurativa
Endocrine
Prediabetes
Diabetes mellitus
Metabolic syndrome
Hyperandrogenism and polycystic ovary syndrome
Growth and puberty
Gastrointestinal
Nonalcoholic fatty liver disease
Cholelithiasis
Neurologic
Idiopathic intracranial hypertension
Orthopedic
Genu varus (Blount disease) or valgus
Pes planus (flat feet)
Slipped capital femoral epiphysis
Fractures
Psychosocial
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Social isolation
Anxiety
Depression
Difficult peer relationships (teasing, bullying)
Disordered eating patterns
Pulmonary
Asthma
Obstructive sleep apnea
Obesity hypoventilation syndrome
Renal
Albuminuria, impaired kidney function
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Important aspects of the review of systems in overweight or obese children
Additional studies or referral
Symptom Potential significance

(consider)
Delayed Genetic syndrome Referral to pediatric geneticist and/or

development neurologist
Short stature or Genetic syndrome Referral to pediatric geneticist

reduced height
Endocrinologic etiology (eg, Cushing 24-hour urine collection for free
velocity
syndrome, hypothyroidism, cortisol, thyroid function tests; referral
ROHHADNET syndrome [rapid-onset to pediatric endocrinologist
obesity with hypothalamic dysfunction,
hypoventilation, autonomic
dysregulation, and neural crest
tumor])
Headaches Pseudotumor cerebri Referral to pediatric neurologist

(especially
morning)
Nausea/vomiting
Blurred or
decreased vision
Snoring Sleep apnea, obesity hypoventilation Polysomnogram (sleep study) and/or

syndrome referral to a pediatric sleep medicine,
Daytime
pulmonologist, or ENT specialist
sleepiness and/or Inattentive behaviors may be
inattentive symptoms of insufficient or disrupted
behaviors sleep
Nocturnal
enuresis
Abdominal pain Gallbladder disease, cholelithiasis AST, ALT, abdominal ultrasonography;

(generalized or referral to surgeon
right upper
Nonalcoholic fatty liver disease AST, ALT; referral to pediatric
quadrant)
gastroenterologist (refer to UpToDate
content on nonalcoholic fatty liver
disease)
Hip pain, knee Slipped capital femoral epiphysis or Radiographs; referral to pediatric
pain, limp Blount disease (tibia vara) orthopedist
Oligomenorrhea Polycystic ovary syndrome Referral to pediatric endocrinologist or

or amenorrhea adolescent specialist
Prader-Willi syndrome Referral to pediatric geneticist
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Urinary Type 2 diabetes Urinalysis, fasting blood glucose,

frequency, hemoglobin A1c, glucose tolerance
nocturia, test; referral to pediatric
polydipsia, endocrinologist
polyuria
Binge eating or Eating disorder Referral to specialist in eating

purging disorders
Insomnia Depression Referral to pediatric psychologist or

psychiatrist
Anhedonia
ENT: ear/nose/throat; AST: aspartate aminotransferase; ALT: alanine aminotransferase.
Adapted from:
1. Barlow SE, Dietz WH. Obesity evaluation and treatment: Expert Committee recommendations. The Maternal and Child
Health Bureau, Health Resources and Services Administration and the Department of Health and Human Services.
Pediatrics 1998; 102:E29.
2. Dietz WH, Robinson TN. Clinical practice. Overweight children and adolescents. N Engl J Med 2005; 352:2100.
6/19/22, 5:58 PM 5861
Findings of note on physical examination in children with obesity
Examination
Definition Clinical concern raised
finding
Anthropometrics
Short stature Height <50th percentile with weight Endocrine or genetic condition (eg,
>95th percentile* (if not explained Cushing syndrome)
or unexplained
by familial short stature)
decrease in height
velocity Growth velocity <5 cm/year in a
prepubertal child, or declining
across over 2 or more height
percentile curves on a standard
chart (eg, decreasing from the 90th
to the 50th percentile)
Vital signs
Hypertension Hypertension if systolic or diastolic Primary hypertension, renal

blood pressure >95th percentile for disease, or Cushing syndrome
age, gender, and height on ≥3
occasions
Skin
Acanthosis nigricans Hyperpigmented, thickened, Suggests insulin resistance and

velvety skin in body folds and increased risk for type 2 diabetes
creases, particularly neck
Excessive acne, Hirsutism is an abnormal amount Polycystic ovary syndrome

hirsutism, oligo- or of sexual hair that appears in a
amenorrhea male pattern (eg, face and neck)
Violaceous striae Linear lesions that are red, pink, or Cushing syndrome
purple in color, particularly on the
abdomen
HEENT
Papilledema, cranial Optic disc swelling on funduscopic Pseudotumor cerebri (idiopathic

nerve VI paralysis examination, caused by increased intracranial hypertension)
intracranial pressure
Tonsillar hypertrophy Tonsils occupy more than 50% of Obstructive sleep apnea
the lateral dimension of
oropharynx
Goiter Enlarged or swollen thyroid gland Hypothyroidism
Chest
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Wheezing High-pitched whistling on Asthma

auscultation
Abdomen
Hepatomegaly, right Increased liver span Nonalcoholic fatty liver disease or

upper quadrant gallstones
tenderness
Genitourinary
Micropenis Unusually small penis In most cases, the small-appearing

penis is actually normal size; the
length is buried under suprapubic
fat
Some endocrinologic or monogenic

forms of obesity are associated
with hypogonadism and
undervirilization in males
Undescended testes Testicle not palpable in scrotum Prader-Willi syndrome
Precocious puberty Secondary sex characteristic Hypothalamic-pituitary lesion,

development that is inappropriate including for
for chronological age ROHHAD/ROHHADNET syndrome
Children with Prader-Willi

syndrome often have premature
pubarche (due to adrenarche) but
not precocious puberty
Musculoskeletal
Abnormal gait, limp, Slipped capital femoral epiphysis

pain in hip or groin,
limited range of
motion in hip
Genu varum (bow Abnormal tibio-femoral angle Mild deformities may be

legs) or genu valgus physiologic in children <6 years; in
(knock-knees) older children, these are associated
with excessive weight
Clinically significant genu varum is

known as Blount disease
Small hands and Genetic condition (eg, Prader-Willi

feet, or polydactyly syndrome or Bardet-Biedl
syndrome)
HEENT: examination of the head, eyes, ears, nose, and throat; ROHHAD/ROHHADNET: rapid onset of
obesity, hypothalamic dysfunction, hypoventilation, autonomic dysregulation, with or without neural
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crest tumor.
* Most children with obesity who have not completed linear growth are relatively tall for their age.
Therefore, height <50th percentile is unusual.
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Determining appropriate blood pressure cuff size in children
The width of the bladder of the blood pressure cuff should be approximately 40%
of the circumference of the upper arm midway between the olecranon and the
acromion. The length of the bladder of the cuff should encircle 80 to 100% of the
circumference of the upper arm at the same position.
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2017 American Academy of Pediatrics updated definitions for pediatric

blood pressure categories
For children aged 1 to <13 years For children aged ≥13 years
Normal BP Systolic and diastolic BP <90th Systolic BP <120 and diastolic BP <80
percentile mmHg
Elevated BP Systolic and diastolic BP ≥90th Systolic BP 120 to 129 and diastolic BP
percentile to <95th percentile, or <80 mmHg
120/80 mmHg to <95th percentile
(whichever is lower)
Stage 1 HTN Systolic and diastolic BP ≥95th 130/80 to 139/89 mmHg

percentile to <95th percentile+12
mmHg, or 130/80 to 139/89 mmHg
(whichever is lower)
Stage 2 HTN Systolic and diastolic BP ≥95th ≥140/90 mmHg

percentile+12 mmHg, or ≥140/90
mmHg (whichever is lower)
BP: blood pressure; HTN: hypertension.
Reproduced with permission from: Pediatrics, Vol. 140, doi: 10.1542/peds.2017-1904. Copyright © 2017 by the AAP.
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Abnormal growth in a child with Cushing's disease
Growth chart of a girl diagnosed with Cushing's disease at age 11.25 years. The patient had
poor height velocity since age 9.6 years, in conjunction with a 2.25-year delayed bone age
(leftward arrow from height point at actual age 11.25 years), and excessive weight gain over
the same time period. An ACTH-producing pituitary adenoma was discovered and removed
by transsphenoidal surgery at age 11.5 years. The patient subsequently had full biochemical
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recovery, initially followed by a significant improvement in height velocity and a significant

reduction in weight (loss of 16 pounds over 6 months). With progressive puberty, the
patient's bone age delay decreased (1.25 years at actual age 12.25 years, and 0.5 years at
actual age 14 years) in association with physiological height plateauing. The progressive
acceleration in bone age was likely due to the effects of pubertal estrogen. The bracket at
the far right of the height curve represents the mid-parental target height range (±1 SDS). As
is typical in patients with childhood Cushing's disease, the mid-parental target height was
not achieved[1] .
BMI: body mass index; SDS: standard deviation score; ACTH: adrenocorticotropic hormone.
Reference:
1. Chan LF, Storr HL, Grossman AB, Savage MO. Pediatric Cushing's syndrome: Clinical features, diagnosis, and
treatment. Arq Bras Endocrinol Metabol 2007; 51:1261-1271.
Courtesy of Mitchell Geffner, MD.
6/19/22, 5:58 PM 5861
Papilledema
Papilledema, characterized by blurring of the optic disc margins,

loss of physiologic cupping, hyperemia, and fullness of the veins, in
a 5-year-old girl with intracranial hypertension due to vitamin A
intoxication.
Courtesy of Gerald Striph, MD.
6/19/22, 5:58 PM 5861
Close view of acanthosis nigricans on the posterior neck.

Hyperpigmented velvety plaques are present.
Reproduced with permission from: www.visualdx.com. Copyright VisualDx. All rights

reserved.
6/19/22, 5:58 PM 5861
A velvety, slightly verrucous plaque is present on the neck.
6/19/22, 5:58 PM 5861
Classic hyperpigmented axillary lesion in acanthosis nigricans.
Courtesy of Jeffrey Flier, MD.
6/19/22, 5:58 PM 5861
A velvety, hyperpigmented plaque with associated acrochordons is

present in the axilla.
6/19/22, 5:58 PM 5861
Additional assessment for weight-related comorbidities to be considered

for selected children with obesity[1-5]
Condition Tests Reason Note
Early atherosclerotic Fasting lipid profile Hyperlipidemia, Children with

cardiovascular disease hypertriglyceridemia, obesity or other risk
cardiovascular disease factors for early
risk cardiovascular
disease – Screen
after 2 years of age.
Children without
obesity or other
cardiovascular risk
factors – Universal
screening once
between ages 9 and
11 years and once
between ages 17
and 21 years.
Refer to UpToDate
content on
dyslipidemia in
children for
interpretation and
follow-up.
Hypertension BP measurement Multiple Use appropriately

measurements are sized cuffs and age-
required to diagnose appropriate norms.
or exclude Measure BP at all
hypertension health care visits (and
at least annually).
24-hour ambulatory BP Evaluate for "masked" Suggested if the

monitoring hypertension; rule out diagnosis is unclear
"white coat" from random office
hypertension measurements.
CBC, metabolic panel, Exclude other causes Suggested if

renin assay, urinalysis, of hypertension hypertension is
renal ultrasound confirmed.
Fatty liver disease Serum ALT Initial screening with

serum ALT for all
children with obesity
starting between 9 and
6/19/22, 5:58 PM 5861
11 years of age. If
normal, repeat at least
every 2 to 3 years*.
Evaluation for liver Determine cause of Perform this

disease: elevated evaluation if ALT is >80
Abdominal transaminases units/L, persistently
ultrasound to elevated >2 times the
evaluate for ULN* for 6 months, or
anatomical if other
abnormalities signs/symptoms of
Screening advanced liver disease
laboratory are present.
tests¶ ;
evaluation for
viral hepatitis,
autoimmune
hepatitis, and
endocrine
disorders
Exclude genetic
disorders in
selected patients
Liver biopsy Determine cause of Perform liver biopsy if

elevated ALT >2 times the ULN
transaminases, assess for >6 months.
degree of hepatitis Imaging cannot
accurately determine
inflammation and
fibrosis.
Type 2 diabetes Fasting glucose, Assess for insulin Perform in children

mellitus or impaired HbA1c, or oral glucose resistance and ≥10 years old with
glucose tolerance tolerance test hyperglycemia overweight or obesity
and 1 or more risk
factors for type 2
diabetesΔ .
Diabetes is
diagnosed if
fasting glucose
≥126 mg/dL or
hemoglobin A1c
≥6.5% on 2
occasions.
Prediabetes is
diagnosed if
6/19/22, 5:58 PM 5861
fasting glucose
100 to 125
mg/dL or
hemoglobin A1c
5.7 to 6.4% on 2
occasions.
Sleep apnea Polysomnogram (sleep Evaluate sleep-related Perform in patients

study) breathing disorders who have obesity and
symptoms suggesting
obstructive sleep
apnea◊ .
Orthopedic disease Hip radiographs Evaluate for SCFE Perform in patients

with unexplained
aching pain in hip,
groin, thigh, or knee.
Use frog-leg
positioning for
radiograph.
Knee radiographs Evaluate for genu Perform in patients

varus (Blount disease) with genu varum (bow
or valgus deformity legs) or genu valgum
(knock-knees).
Polycystic ovary Total testosterone (or To confirm whether Perform in females

syndrome free testosterone) hyperandrogenemia is with irregular menses
present and exclude or hirsutism. If
To evaluate for other
other causes of laboratory testing is
causes of menstrual
hyperandrogenemia abnormal, additional
abnormalities: TSH,
and/or abnormal workup is indicated.
prolactin, DHEAS, 17-
menses
hydroxyprogesterone
(early morning)
Impaired kidney BUN, creatinine Evaluate for impaired Perform in adolescents

function kidney function and with severe obesity,
Urine for UACR
albuminuria hypertension, or type 2
diabetes§ . UACR >30
mg/g is abnormal.
Precocious puberty LH, FSH, testosterone Early onset of obesity Physical examination
or estradiol, DHEAS often is sufficient to
evaluate.
Pseudotumor cerebri Funduscopic Increased intracranial Perform funduscopic

examination, lumbar pressure suggested by examination in
puncture papilledema and patients with frequent
confirmed by lumbar headaches.
puncture
6/19/22, 5:58 PM 5861
BP: blood pressure; CBC: complete blood count; ALT: alanine aminotransferase; ULN: upper limit of
normal; SCFE: slipped capital femoral epiphysis; TSH: thyroid-stimulating hormone; DHEAS:
dehydroepiandrosterone sulfate; BUN: blood urea nitrogen; UACR: urine albumin-to-creatinine ratio;
LH: luteinizing hormone; FSH: follicle-stimulating hormone; GGTP: gamma-glutamyl transpeptidase.
* For interpretation of serum ALT, use the ULN of 22 units/L for females and 26 units/L for males, as
determined from healthy lean children in the National Health and Nutrition Examination Survey
(NHANES)[3] . Note that these values are substantially lower than the ULNs reported in most
pediatric hospital laboratories.
¶ Screening laboratory tests for suspected fatty liver disease include a CBC with hemoglobin HbA1c.
Δ Risk factors for type 2 diabetes include: family history of type 2 diabetes, high-risk race/ethnicity
(Native American, African American, Latino, Asian American, Pacific Islander), signs of insulin
resistance (eg, acanthosis nigricans), or conditions associated with diabetes (hypertension,
dyslipidemia, polycystic ovary syndrome).
◊ Symptoms suggesting obstructive sleep apnea include persistent snoring (most nights, most
sleeping positions), observed gasping or apneas, nocturnal enuresis, and morning headaches.
§ Screening for impaired kidney function is recommended for patients with type 2 diabetes[5] .
UpToDate authors also suggest this screening for patients with other risk factors for developing
chronic kidney disease, including severe obesity and hypertension.
References:
1. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents,
National Heart, Lung, and Blood Institute. Expert panel on integrated guidelines for cardiovascular health and risk
reduction in children and adolescents: Summary report. Pediatrics 2011; 128:S213.
2. de Ferranti SD, Steinberger J, Ameduri R, et al. Cardiovascular Risk Reduction in High-Risk Pediatric Patients: A
Scientific Statement From the American Heart Association. Circulation 2019; 139:e603.
3. Barlow SE. Expert committee recommendations regarding the prevention, assessment, and treatment of child and
adolescent overweight and obesity: summary report. Pediatrics 2007; 120:S164.
120:S193.
5. Vos MB, Abrams SH, Barlow SE, et al. NASPGHAN Clinical Practice Guideline for the Diagnosis and Treatment of
Nonalcoholic Fatty Liver Disease in Children: Recommendations from the Expert Committee on NAFLD (ECON) and the
North American Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN). J Pediatr Gastroenterol
Nutr 2017; 64:319.
6. American Diabetes Association. 13. Children and Adolescents: Standards of Medical Care in Diabetes-2020. Diabetes
Care 2020; 43:S163.
6/19/22, 5:58 PM 5861
Our approach to lipid screening in children and adolescents
CVD: cardiovascular disease; CoA: coarctation of the aorta; AS: aortic stenosis; TGA: transposition of the grea
cardiomyopathy; SLE: systemic lupus erythematosus; JIA: juvenile idiopathic arthritis; HDL-C: high-density lip
cholesterol; LDL-C: low-density lipoprotein cholesterol.
* Initial screening can be performed with a fasting or nonfasting lipid profile (with the latter, non-HDL-C is c
measured TC and HDL-C levels). Confirmatory testing with a fasting lipid profile should be performed if adve
screen (ie, TC ≥200 mg/dL, HDL-C <40 mg/dL, LDL-C ≥130 mg/dL, or non-HDL ≥145 mg/dL). For additional d
topic on screening and diagnosis of dyslipidemia in children.
¶ These are general suggestions for the timing and interval of screening; they should be tailored to the child
example, for a child with a single risk factor that does not place him/her into the high-risk category (eg, non
exposure without any additional risk factors), it is reasonable to begin screening later and repeat it less freq
with risk factors that place him/her in the high-risk category (eg, Kawasaki disease with known coronary arte
perform lipid screening earlier and more frequently.
Δ Family history of premature CVD is generally defined as heart attack, treated angina, interventions for cor
cardiac death, or ischemic stroke in a male parent or sibling before 55 years of age or a female parent or sib
Adapted from:
1. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents, National Hea
panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: Summary report. Pedi
2. de Ferranti SD, Steinberger J, Ameduri R, et al. Cardiovascular risk reduction in high-risk pediatric patients: A scientific statemen
Circulation 2019; 139:e603.
6/19/22, 5:58 PM 5861
Overview of follow-up of children undergoing lipid screening
LDL-C and non-HDL-C units are mg/dL; divide by 38.67 to convert to mmol/L.
HDL-C: high-density lipoprotein cholesterol; LDL-C: low-density lipoprotein cholesterol; CVD: cardiovascular d
hypercholesterolemia; SLE: systemic lupus erythematosus; JIA: juvenile idiopathic arthritis; CoA: coarctation
transposition of the great arteries; HCM: hypertrophic cardiomyopathy.
* For children with underlying risk factors for premature CVD (listed below)Δ , lipid screening begins at the ti
(generally not earlier than age 2 years) with subsequent testing every 1 to 3 years depending on the nature
without underlying risk factors for premature CVD, routine lipid screening is performed twice during childho
years) and once after puberty (age 17 to 21 years). Refer to UpToDate topic on dyslipidemia screening in chi
¶ Lifestyle modifications may include low saturated fat diet; increased intake of dietary fiber through fruits,
supplementation with plant stanols and sterols; increasing physical activity; and, in obese children, weight lo
management of dyslipidemia in children for further details of nonpharmacologic management of hypercho
Δ Risk factors for premature CVD in children are similar to those in adults and include hypertension, diabete
and family history of premature atherosclerotic CVD. In addition, other medical conditions that can present
associated with increased risk of early CVD include: chronic kidney disease, Kawasaki disease (with current o
6/19/22, 5:58 PM 5861
childhood cancer, transplant vasculopathy, chronic inflammatory diseases (eg, SLE and systemic JIA), HIV, ce
(CoA, AS, TGA, congenital coronary artery anomalies), cardiomyopathy (eg, HCM), pulmonary hypertension,
bipolar disorder.
◊ Confirmatory testing consists of 2 fasting lipid profiles obtained 2 weeks to 3 months apart (ie, if the patie
performed as the initial screen, a second fasting lipid profile is obtained 2 weeks to 3 months later; if the pa
using nonfasting non-HDL-C, 2 separate fasting lipid profiles should be performed). Average the 2 results.
§ For further details on the management of hypercholesterolemia and FH, refer to separate UpToDate topic
¥ Secondary causes of hypercholesterolemia include diabetes mellitus, nephrotic syndrome, hypothyroidism

certain medications (eg, glucocorticoids, antiretrovirals). Refer to the UpToDate topic on screening and diag
further details.
6/19/22, 5:58 PM 5861
Testing for type 2 diabetes mellitus in asymptomatic children and

adolescents
Overweight or obese:
BMI ≥85th percentile for age and gender
Plus 1 or more of the following additional risk factors*:

Maternal history of diabetes or gestational diabetes mellitus during the child's gestation
Family history of type 2 diabetes mellitus in a first- or second-degree relative
High-risk race/ethnicity (Native American, African American, Latino, Asian American, Pacific
Islander)
Signs of insulin resistance on physical examination or conditions associated with insulin resistance
(acanthosis nigricans, hypertension, dyslipidemia, polycystic ovary syndrome, or small for
gestational age birth weight)
Screening frequency
Begin screening at age 10 years, or at onset of puberty if this occurs when the child is <10 years
old
Repeat screening every 3 years, or more frequently if BMI is increasing
* This criterion was updated as of the 2018 version of the Standards of Medical Care in Diabetes and
subsequent updates.
From: American Diabetes Association. Standards of medical care in diabetes--2014. Diabetes Care 2014; 37 Suppl 1:S14.
American Diabetes Association, 2014. Copyright and all rights reserved. Material from this publication has been used with
the permission of American Diabetes Association. The content within this table is still current as of the 2022 version of the
Standards of Medical Care in Diabetes.
6/19/22, 5:58 PM 5861
Staged approach to obesity management in children[1]
This algorithm is intended to guide the management of otherwise healthy children with obesity in a primary
care setting. Children with syndromic features, mental health concerns, or established obesity comorbidities
may require earlier referral and/or additional support.
* A sharp rise in BMI refers to an upward deflection on the BMI curve that is substantially steeper than the
nearby centile curves over 6 to 12 months.
¶ For weight management counseling, the timing of follow-up depends on the clinician's level of concern an
the patient and family's engagement. A typical interval between visits is 1 to 3 months.
6/19/22, 5:58 PM 5861
Δ Severe obesity is ideally defined as BMI ≥120% of the 95th percentile or ≥35 kg/m2 (whichever is lower).
This corresponds to approximately the 99th percentile or BMI Z-score ≥2.33 (ie, 2.33 standard deviations
above the mean).
◊ Pharmacotherapy is typically managed by clinicians with special expertise in weight management (eg, a
multidisciplinary weight management program) but may be appropriate for management of obesity in a
primary care setting if the clinician learns the limitations and potential adverse effects of the available optio
and follows the patient closely. Refer to UpToDate content on obesity management in the primary care setti
and on pharmacotherapy for obesity.
§ Weight loss surgery is an appropriate consideration for adolescents with severe obesity and with medical
comorbidities who have failed to lose weight through conventional dietary interventions and behavioral
modification. It should only be performed in the context of a multidisciplinary program with expertise in
adolescent medicine and extensive expertise in bariatric surgery. Early surgical intervention may improve
outcomes compared with intervention at an older age or higher BMI. Refer to UpToDate content on surgica
management of severe obesity in adolescents.
Reference:
1. Spear BA, Barlow SE, Ervin C, et al. Recommendations for treatment of child and adolescent overweight and obesity. Pediatrics
2007; 120:S254.
6/19/22, 5:58 PM 5861
Contributor Disclosures
Joseph A Skelton, MD, MS Other Financial Interest: Childhood Obesity journal EIC [Childhood obesity].
All
of the relevant financial relationships listed have been mitigated. William J Klish, MD No relevant financial
relationship(s) with ineligible companies to disclose. Kathleen J Motil, MD, PhD Consultant/Advisory
Boards: Acadia.
All of the relevant financial relationships listed have been mitigated. Mitchell E Geffner,
MD Grant/Research/Clinical Trial Support: Neurocrine Biosciences[Congenital adrenal hyperplasia];Novo
Nordisk [Growth].
Consultant/Advisory Boards: Adrenas[Congenital adrenal
hyperplasia];Ascendis[Growth];Calcilytix[Calcium];Eton[Congenital adrenal hyperplasia];Neurocrine
Biosciences[Congenital adrenal hyperplasia];Novo Nordisk[Growth];Nutritional Growth
Solutions[Growth];Pfizer[Growth].
Other Financial Interest: McGraw-Hill textbook royalties[Pediatric
endocrinology].
All of the relevant financial relationships listed have been mitigated. Alison G Hoppin,
MD No relevant financial relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

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Clinical evaluation of the child or adolescent with obesity

● (See "Definition, epidemiology, and etiology of obesity in children and adolescents".)

BODY MASS INDEX

• Underweight – BMI <5th percentile for age and sex.

• Overweight – BMI ≥85th to <95th percentile for age and sex.

• Obesity – BMI ≥95th percentile for age and sex.

Other possible causes include medication-induced weight gain and neuroendocrine

• Inappropriate compensatory behavior to prevent weight gain (self-induced vomiting or

• Sugar-containing beverages, including soda, juice, sugar-containing "sports" drinks,

• Time spent in play (especially outdoors)

Sleep — The sleep history should include:

● Symptoms of sleep disorders – Obesity is associated with an increased risk for

Family history — Key elements are:

● Comorbidities – Inquire about common comorbidities of obesity, such as cardiovascular

Psychosocial history — Key elements are:

● Smoking or vaping – Cigarette smoking increases long-term cardiovascular risk [4,34-37].

● General examination – Assess the general appearance/mood; look for dysmorphic

• A markedly Cushingoid fat distribution (concentrated in the interscapular area, face,

• Abdominal obesity (also called central, visceral, android, or male-type obesity) is

● Examination of the head, eyes, ears, nose, and throat (HEENT)

• Blurred optic disc margins ( picture 1) may indicate pseudotumor cerebri, an

• Nystagmus or visual complaints raise the possibility of a hypothalamic-pituitary lesion

• Microcephaly is a feature of Cohen syndrome (in addition to other dysmorphic

● Skin and hair

• Dry, coarse, or brittle hair may be present in hypothyroidism. (See "Clinical

• Abdominal tenderness, particularly in the right upper quadrant, may be a sign of

• Nonpitting edema may indicate hypothyroidism. (See "Clinical manifestations of

• Dorsal finger callousness may be a clue to self-induced vomiting in patients with an

● Genitourinary – Endocrine or genetic causes of obesity are often associated with

• Small testes may suggest Prader-Willi or Bardet-Biedl syndrome [48].

• Delayed or absent puberty may occur in the presence of hypothalamic-pituitary

• Precocious puberty occasionally is a presenting symptom of a hypothalamic-pituitary

● Development – Most of the syndromic causes of overweight in children are associated

● Dyslipidemia – Screening consists of a fasting lipid profile (total cholesterol, triglycerides,

● Tests for causes of obesity

• Hypothyroidism or Cushing syndrome – Routine laboratory screening for

• Syndromic obesity – Children with developmental delay or dysmorphic features

● Tests for comorbidities

• Vitamin D deficiency – The American Academy of Pediatrics and others recommend

• Hypertension – For children with hypertension, additional laboratory testing may be

• Polycystic ovary syndrome – Laboratory testing is warranted in females with

Imaging — The radiographic evaluation of children with obesity is directed by findings on the

● Abdominal ultrasonography may be indicated in children with findings consistent with

● Abdominal ultrasonography is not recommended as a routine screening test for NAFLD in

Management in primary care — Management strategies vary according to the child's age,

● Comprehensive weight management program – Referral is suggested for [4,63]:

• Refractory obesity (progressive increase in BMI percentiles despite structured

A comprehensive weight management program usually includes coordinated and

● Specialty referral for comorbidities – Children with suspected or established

● Mental health specialists – Indications for referral include:

• Clinically significant depression or anxiety. Weight loss therapy may be ineffective

• Suspected eating disorder (eg, inability to control consumption of large amounts of

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

● Basics topic (see "Patient education: My child is overweight (The Basics)")

SUMMARY AND RECOMMENDATIONS

• Onset of obesity and historical patterns of weight gain

• Child's diet and food preferences ( table 4)

• Physical activity patterns and sedentary activities (screen time) ( table 5)

• Review of systems for signs of comorbidities or syndromic obesity ( table 9)

• Family history of obesity and comorbidities