Indian J Pediatr (June 2018) 85(6):463–471
https://doi.org/10.1007/s12098-017-2531-x
REVIEW ARTICLE
Obesity in Children: Definition, Etiology and Approach
Bhawana Aggarwal 1 & Vandana Jain 2
Received: 31 May 2017 / Accepted: 11 October 2017 / Published online: 25 November 2017
# Dr. K C Chaudhuri Foundation 2017
Abstract Childhood obesity is an important public health
issue worldwide. Urbanization, sedentary lifestyle and
change in food habits are the chief reasons behind this
pandemic. In a small proportion of children, obesity is
the result of endocrine, syndromic or monogenic causes.
The present paper summarizes the methods, definitions and
cut-offs for identification of obesity in children. We have
briefly reviewed the various techniques used for estimation
of body fat in children and the cut-offs for defining obesity
based on body fat percentage, and the reference curves
based on body mass index and waist circumference. The
etiology of obesity in children, including individual behav-
iors, macro- and micro-environmental influences, and en-
docrine causes have been discussed, and an approach to
etiological assessment of obese children has been present-
ed. Special emphasis has been laid on clinical pointers that
suggest the presence of syndromic, endocrine or monogen-
ic forms of obesity, such as, short stature, dysmorphism,
neurocognitive impairment and early age at onset.
Keywords Body mass index . Body fat . Childhood obesity .
Endocrine obesity . Exogenous obesity . Overweight
* Vandana Jain
drvandanajain@gmail.com
1
Department of Pediatrics, All India Institute of Medical Sciences,
New Delhi, India
2
Division of Pediatric Endocrinology, Department of Pediatrics, All
India Institute of Medical Sciences, New Delhi 110029, India
Introduction
The prevalence of obesity in children has reached an
alarming level that mandates urgent action. In 2010, over
43 million children under the age of 5 y were reported to
be overweight worldwide [1]. A multicentric study con-
ducted in eleven affluent urban Indian schools found the
prevalence of overweight and obesity as 18.2% by the
International Obesity Task Force (IOTF) classification
and 23.9% by World Health Organization (WHO) stan-
dards in children aged 2–17 y [2]. It is important to halt
and reverse this epidemic as obese children are at risk of
developing several complications, both somatic and psy-
chosocial that adversely affect the quality of life as well
as longevity.
Having a focus on early recognition of childhood obe-
sity is all the more important for developing countries like
India that have been struggling to reduce the prevalence of
undernutrition and stunting in children for the past several
decades. The public mindset and governmental policies are
geared towards identification and nutritional rehabilitation
of the undernourished child, but the same concern is not
seen for identifying children who are overweight or show
upward crossing of centiles on growth curves. There is a
need for nutritional policies that promote not only ade-
quate, but qualitatively and quantitatively appropriate nu-
trition in children.
In the present paper, we have discussed the various
methods, reference curves and cut-offs used to define over-
weight and obesity from infancy to adolescence. We have also
reviewed the etiology of obesity in children and the approach
to etiological work-up in obese children, with a focus on clin-
ical pointers that help in delineating children with an underly-
ing genetic or endocrine cause from the much more common
exogenous obesity.
464 Indian J Pediatr (June 2018) 85(6):463–471

Definitions and Diagnosis of Overweight and Obesity
in Children
World Health Organisation (WHO) defines obesity as an ex-
cess in fat mass great enough to increase the risk of morbidity,
altered physical, psychological, or social well- being and/ or
mortality [3].
at 5 y and it shows a gradual increase to 24.6% at 18 y [7].
Similar reference curves for Indian children aged 7–17 y using
dual energy X-ray absorptiometry (DXA) have been pub-
lished by Khadgawat et al. [8].
Anthropometry Based Diagnosis of Overweight
and Obesity

Body Fat Measurement
Body fat can be estimated by several methods, such as dual
energy X-ray absorptiometry (DXA), bioelectrical impedance
assay (BIA), computed tomography (CT) and magnetic reso-
nance imaging (MRI) of abdomen, measurement of skinfold
thicknesses at multiple sites, air displacement plethysmogra-
phy and stable isotope dilution techniques [4]. A summary of
the principles of these methods is provided in Table 1. Air
displacement plethysmography and stable isotope dilution
technique are considered as the most robust methods for esti-
mation of body composition in infants and children [5]. In
adult men and women, body fat percentage above 25 and
35%, respectively is generally considered as obesity [6]. For
children, reference curves for body fat percentage for
Caucasian children aged 5–18 y were published by
McCarthy et al. in 2006 using bioelectrical impedance. The
2nd, 85th and 95th centiles for age and gender are considered
as cut-offs for underfat, overfat and obese [7]. The 50th centile
for boys is 15.6% at 5 y, increases to 20.8% at 11 y and again
decreases to 15.4% by 18 y. For girls, the 50th centile is 18%
For making a clinical diagnosis of overweight and obesity,
estimation of body fat percentage is not required. Body mass
index (BMI), calculated as weight in Kg/(height in meters)2,
shows a good correlation with body fat percentage, and is
widely used as an index of relative weight [9]. The most im-
portant consideration in choosing a BMI cut-off for defining
overweight/ obesity is the increased risk for complications.
The adult cut-off points of BMI of 25 and 30 kg/m2 for over-
weight and obesity, respectively, are used due to the observed
increased health risks at these levels. BMI of 30 kg/m2 corre-
sponds roughly to 25 and 30% of fat mass, respectively in
Caucasian men and women [9].
BMI however has some disadvantages. It does not dis-
tinguish reliably between lean and fat mass, and does not
predict percentage body fat consistently across ethnicities
[10]. Asian Indians have higher body fat compared with
Caucasians for similar BMI. For example, in a study by
Banerji et al., it was noted that a mean BMI of 24.5
corresponded to mean body fat of 33% in Asian Indian
men residing in the US [11]. Additionally, fat distribution
in Asian Indians is more in the central abdominal region

Table 1 Methods of body fat

estimation S.N. Technique Principle

1. Dual energy X-ray Fat mass (FM) and fat free mass (FFM) are calculated based
Absorptiometry (DXA) on differential absorption of X-rays of two different energies.
Uses low levels of ionizing radiation.
2. Stable isotope dilution Water labelled with a small dose of stable isotope of oxygen
or hydrogen is given orally. After equilibration, the concentration
of the stable isotope in urine or saliva allows estimation of total
body water (TBW). FFM is derived from it using an assumed
value for hydration factor of FFM.
3. Air displacement This technique is based on whole body densitometry.
plethysmography The equipment PEAPOD is used in infants below 6 mo
and BODPOD in older children and adults.
4. Bioelectrical Impedance Measures the impedance offered by the body to a small electric
Analysis (BIA) current. This is used to calculate total body water, from which FFM
is derived.
5. Magnetic resonance Measures the volume of abdominal fat by analysing the absorption
imaging (MRI) and emission of energy in the electromagnetic spectrum. Unlike
other methods, it does not measure total body FM.
6. Skinfold thickness Several equations have been derived using skinfold thickness at
based equations three to five sites (biceps, triceps, subscapular, suprailiac,
thigh etc.) to estimate FM. The accuracy and reliability of this
method is limited.
Indian J Pediatr (June 2018) 85(6):463–471 465

compared to peripheral subcutaneous region [12]. Hence
the risk of cardiovascular disease and type 2 diabetes
starts increasing at lower BMI in Asian Indians [12].
Therefore, the Indian Consensus Group has recommended
the BMI cut-offs of ≥23 and ≥25 kg/m2 for classifying
Asian Indian adults as overweight and obese, respectively
[12]. The American Diabetes Association (ADA) has also
recommended screening for type 2 diabetes at the BMI
cut-off of 23 kg/m2 for Asian Indians [13].
For children, several curves that give BMI distribution
as a function of age and sex have been elaborated, and
several definitions of overweight and obesity are in use
(Table 2) [14–18]. For Indian children, it is recommended
to use WHO multicentric growth reference standards
(WHO MGRS) and cut-offs for defining overweight and
obesity in children below 5 y of age [14, 18]. In the age
group of 5–18 y, the revised Indian Academy of Pediatrics
(IAP 2015) BMI curves that use cut-off percentiles equiv-
alent to adult BMI of 23 and 27 kg/m2 to define overweight
and obesity, respectively should be used [18].
Measurement of waist circumference is another easy tool
that is useful in identification of obesity. Waist circumfer-
ence being a measure of central obesity has been seen to
correlate more strongly than BMI with several complica-
tions such as insulin resistance, dyslipidemia and non-
alcoholic fatty liver disease [19]. Recently, Khadilkar et al.
have published waist circumference centiles for Indian chil-
dren aged 2–18 y and have suggested use of 70th centile as
the cut-off for screening for metabolic syndrome [20].
Alternatively, for adolescents, waist circumference more
than the adult cut-offs of 90 and 80 cm, respectively, for
Asian males and females can be considered as indicative
of abdominal obesity [19]. Higher waist to hip circumfer-
ence ratio (WHR) also denotes abdominal obesity, and
WHR is considered to be high if >0.95 and 0.85 for adoles-
cent boys and girls, respectively [19]. Waist circumference
to height ratio of >0.5 is also a convenient and age indepen-
dent method to identify adults [21] as well as children and
adolescents [22] at increased health risk.
Etiology of Childhood Obesity
On the basis of etiology, childhood obesity is broadly
subdivided into exogenous and endogenous. Exogenous
obesity is brought about by a chronic imbalance between
energy intake and expenditure; whereas endogenous obe-
sity is caused by various genetic, syndromic and endo-
crine causes. Metabolic programming, as observed in chil-
dren born small or large for gestational age, infants of
diabetic mothers and those with rapid or excessive
catch-up growth in first few years of life, compounds
the problem of obesity brought about by lifestyle and
dietary factors [23, 24]. Table 3 summarizes the etiology
of obesity in children.

Table 2 BMI reference curves

for children and adolescents Reference Methodology and cut-off points
curve

CDC • Based on representative data of US children aged 2–20 y

• Cut-off points of 85th and 95th centile are used for overweight and obesity, respectively [14]
IOTF • Based on data of nearly 2 lakh children aged 2–18 y from 6 countries (Brazil, USA,
Netherlands, Singapore, Hong Kong and UK)
• Centile curves drawn to correspond to BMI cut-offs of 25 and 30 kg/m2 at 18 y are used
to define overweight and obesity [15]
WHO • For children aged 0–5 y, data of healthy, breast fed children from high socioeconomic status
from 6 countries (Brazil, Ghana, India, Norway, Oman and the USA) was collected as part
of WHO Multicentric Growth Reference study
-Overweight: BMI or Weight for length/ height > +2SD
-Obese: BMI or Weight for length/ height > +3SD [16]
• For children aged 5–19 y, WHO reference 2007 charts are based on data collected
for the 1977 National Center for Health Statistics (NCHS) growth charts
-Overweight: BMI > +1SD
-Obesity: BMI > +2 SD [17]
IAP 2015 • These charts are based on pooled data from 9 previous Indian studies published in the last
decade. Data of more than 33,000 children from 14 Indian cities belonging to upper
or middle socioeconomic class was used to construct these charts.
• Centiles equivalent to adult BMI of 23 and 27 kg/m2 are used to define overweight
and obesity, respectively [18].

CDC Centers for Disease Control and Prevention; IOTF International Obesity Task Force; BMI Body Mass Index;
WHO World Health Organization; IAP Indian Academy of Pediatrics
466
Table 3 Etiology of obesity in children and adolescents
Exogenous
• Chronic imbalance between energy intake and expenditure.
Increased intake of processed and refined diet, sugar-sweetened
beverages, increased time spent on TV viewing, internet browsing or
playing electronic games, reduced physical activity, reduced sleep.
• Medications
Glucocorticoids, tricyclic antidepressants, risperidone
• Adverse metabolic programming (acts in conjunction with diet and
lifestyle factors)
Infants born small for gestational age (SGA), large for gestational age
(LGA), those born to mothers with obesity or diabetes, and those with
accelerated weight gain in infancy are predisposed to obesity in
childhood.
Endogenous
• Monogenic causes
Defects in genes encoding melanocortin 4 receptor (MC4R), leptin
(LEP), leptin receptor (LEPR) pro-opiomelanocortin (POMC) etc.
• Genetic syndromes
Alstrom, Bardet- Biedl, Prader Willi, Beckwith- Wiedemann,
Carpenter, Cohen, Albright Hereditary Osteodystrophy etc.
• Endocrine causes
Hypothyroidism, Cushing syndrome, hypothalamic obesity, growth
hormone deficiency, persistent hyperinsulinism etc.
Exogenous Obesity
Children of the present generation are living in an increasingly
obesogenic environment, where gaining excessive weight is
very easy, but remaining fit requires conscious and sustained
efforts [25]. Unhealthy or obesogenic individual behaviors are
linked to the surrounding microenvironments, including fami-
lies, schools, and neighbourhoods; which in turn are influenced
by macrosystems like food industry and government [26].
Individual Behaviors
& Unhealthy dietary habits: Consumption of energy
dense foods, packaged refined foods, sugar-sweetened
beverages, excessive snacking, skipping meals, large
portion size and poor intake of fruits and vegetables
are associated with obesity [27].
& Lack of physical activity
& Increased screen time and reduced sleep time [28]
& Increased television (TV) viewing time: TV viewing is
not just a sedentary behavior but also leads to over-
weight due to its association with unmindful munching,
and through influencing children’s food preferences by
exposure to TV advertisements [29].
Micro-environmental Influences
& Family: Parenting styles and behaviors as well as parents’
own diet and physical activity patterns have a very strong
Indian J Pediatr (June 2018) 85(6):463–471
influence on the food and exercise choice of the child.
There is increased risk of childhood obesity with maternal
diabetes, smoking and obesity, underlining the role of fetal
environment. Infant feeding style, sleep duration, rate of
postnatal weight gain and age of adiposity rebound are
also associated with obesity later [30–32].
& School: School environment can become obesogenic if
there is no emphasis on nutrition and physical education.
Lack of playgrounds and sports facilities, potentially un-
healthy school lunches, and availability of unwholesome
snacks and beverages in the school or its vicinity increase
the risk of obesity in children [33, 34].
& Neighbourhood: Factors such as availability of healthy
food and grocery, park spaces, stray dogs that hinder
walking or cycling can mediate the risk of obesogenic
behavior [35–37].
Macro-environmental Influences
& Food industry: Production of high fat, sugar and/ or salt
containing foods, use of complex marketing and advertis-
ing practices, aggressive sales tactics, and confusing food
labelling restrict the consumers’ ability to make rational
and healthy choices.
& Government: Government is responsible for providing
safe environment conducive to physical activity such as
play grounds, open gyms, cycle and pedestrian friendly
roads. Strong nutritional policies are also needed to restrict
availability of unhealthy snacks, taxation, clear food label-
ling, and price control of fruits and vegetables [26, 27].
According to a systematic review, the three environmental
exposures that have the most significant impact on childhood
obesity are the availability of sugar- sweetened beverages,
portion size, and food marketing [38].
Endogenous Obesity
Endocrinopathies, monogenic syndromes and other genetic
syndromes account for a small proportion of childhood obe-
sity. Monogenic and syndromic causes have been discussed in
detail in a separate paper in this volume. Role of metabolic
programming has also been discussed in another review paper
in this volume. We shall be briefly reviewing the endocrine
causes here.
Endocrine Causes
Children with identifiable endocrinopathies comprise a small
minority (about 2–3%) of children referred for evaluation of
overweight [39]. However it is important for physicians to be
able to suspect and diagnose these conditions, so that specific
Indian J Pediatr (June 2018) 85(6):463–471
treatment can ensue. An important clue to underlying endo-
crine etiology is deceleration or cessation of linear growth, so
that height is below the centile expected for the child’s genetic
potential. The clinical features of various endocrinopathies
associated with obesity are briefly discussed below [40, 41].
& Hypothyroidism– Clinical hypothyroidism with elevated
TSH and low T4 levels is typically associated with
mild weight gain (increase in BMI by 1–2 kg/m2 only).
Decreased resting energy expenditure, fluid retention
and diminished linear growth are the mechanisms im-
plicated in BMI gain. Subclinical hypothyroidism is
observed in roughly 10% of overweight/ obese chil-
dren, but is considered as a consequence rather than
cause of obesity and does not require treatment with
thyroxine [42].
& Cush ing s yn drome– C u s h i n g s y n d r o m e or
hypercortisolism in children can be exogenous or endog-
enous. Endogenous Cushing syndrome is rare in children.
It is mostly caused by adrenal tumor or hyperplasia in
children below 6 y of age, and pituitary micro adenoma
in older children. Exogenous iatrogenic hypercortisolism
due to long term treatment with glucocorticoids (as in
several autoimmune, dermatological, pulmonary or neo-
plastic conditions) or even off-label over the counter use
of steroids by quacks as medicine for minor respiratory
illness or ‘tonic’ is not uncommon [43]. Hypercortisolism
is associated with growth failure, central obesity, hirsut-
ism, increased appetite and hypertension.
& Growth hormone deficiency (GHD)– GHD is character-
ized by short stature (height generally below −3 standard
deviations), low growth velocity and mild truncal obesity.
& Hypothalamic obesity– The ventromedial, arcuate,
paraventricular and dorsomedial nuclei of the hypothal-
amus produce neuropeptides involved in appetite regu-
lation and energy expenditure. Hypothalamic obesity is
a consequence of congenital malformation or injury to
the hypothalamus, resulting in disruption of these nu-
clei. Craniopharyngioma treated surgically is the most
common cause of hypothalamic obesity in pediatric age
group. The other causes include pituitary tumors and
aneurysms, inflammatory and infiltrative diseases,
trauma, cranial irradiation or surgery. Affected patients
are generally lethargic with reduced energy expendi-
ture. They may also have other endocrinopathies, in-
cluding GHD, hypothyroidism, precocious or delayed
puberty, and diabetes insipidus [40, 41].
& Albright Hereditary Osteodystrophy (AHO)– AHO is a
genetic disorder due to heterogenous inactivating mu-
tation in GNAS, the gene that encodes the alpha chain
of Gs. AHO phenotype (short stature, round facies,
obesity, brachydactyly, ectopic ossification, develop-
mental delay and mental retardation) is associated with
467
pseudohypoparathyroidism types 1 a and c [40, 41].
This is further discussed in the paper by Koves et al.
in this issue.
& ROHHADNET (Rapid Onset obesity, Hypothalamic dys-
function, Hypoventilation, Autonomic Dysregulation and
Neuroendocrine tumors) syndrome: This syndromic cause
of childhood obesity typically manifests with accelerated
weight gain and decelerated linear growth between 2 and
4 y of age, along with evidence of autonomic dysfunction
and hypoventilation. It is associated with varying degree
of involvement of the hypothalamic-pituitary axis, includ-
ing GH deficiency with low IGF-I in some, glucocorticoid
deficiency or excess, hypogonadotropic hypogonadism,
hyperprolactinemia, hypothyroidism abnormalities of wa-
ter and sodium homeostasis, adrenal tumors etc. [44]. This
is further discussed in the paper by Koves et al. in this
issue.
& Persistent hyperinsulinemia– Mutations in several genes
resulting in excessive production of insulin by pancreatic
beta cells, or insulinomas can lead to obesity as the affect-
ed children increase their food intake to prevent
hypoglycemia.
Approach
Assessment of overweight/ obese children should begin with a
thorough history and examination directed to find the etiology
and the associated complications including metabolic, cardio-
vascular (e.g., hypertension), respiratory, gastrointestinal, or-
thopedic and psychological issues. Investigations and further
evaluation should be guided by the history and examination
[41, 45]. Since a majority of children and adolescents have
exogenous obesity, they should not be unnecessarily investi-
gated for endocrine or genetic causes. Some of the red flags
that should alert the physician to the possibility of endogenous
etiology of obesity are listed in Table 4.
History
History is important for identification of pointers towards un-
derlying etiology, modifiable lifestyle factors, current and fu-
ture risk of obesity related complications and assessment of
patient’s / family’s readiness to make behavioral changes [45].
Key points in history include the following:
& Birth weight, intrauterine exposure to maternal diabetes or
obesity
& Age of onset of obesity, rapidity of weight gain
& History of medication use– Steroids, antipsychotics,
antidepressants
& Socioeconomic status
468
Table 4 Clues to underlying endogenous obesity
S.N. Red flags in history or examination
1 Stature shorter than that expected for midparental height
2 Onset in infancy or early childhood (< 5 y)
3 Lack of satiety, food foaraging behavior, hyperphagia,
willingness to eat even food that is perceived as
lacking in taste
4 Dysmorphism
5 Intellectual impairment or significant behavioral problems
6 Sudden onset
7 Low birth weight, hypotonia and feeding difficulties in infancy
8 Features suggestive of neurological deficits e.g., squint, vision
or visual field impairment, evidence of pituitary hormone deficits
9 Hypogonadism
10 Stage 2 hypertension
11 Violaceous striae, fat deposition over nape of neck, interscapular area
12 History of cranial irradiation, chemotherapy, CNS pathology
ROHHADNET Rapid Onset obesity, Hypothalamic dysfunction, Hypoventilation, Autonomic Dysregulation and Neuroendocrine tumors; AHO
Albright Hereditary Osteodystrophy; MC4R Melanocortin-4 receptor
& Family history of obesity, cardiovascular disease, dyslip-
idemia, diabetes and hypertension
& Dietary pattern– Frequency of eating outside the home,
excessive consumption of sweetened beverages, energy
dense food, large food portion size, low consumption
of fruits and vegetables, meal frequency and quality,
snacking patterns.
& Physical activity assessment– Environmental and social
factors that support or pose barriers to physical activity,
time spent in mild, moderate and vigorous physical activ-
ity, in sedentary pursuits, especially screen (TV, mobile,
computer, etc.) time.
& Number of hours of sleep per day
& Psychological history– History suggestive of eating disor-
der, substance abuse, bullying or teasing, low self-esteem
should be noted.
& Developmental history should be taken, as intellectual dis-
ability may point towards endogenous etiology.
& Pubertal status, age at menarche and menstrual history in
girls
& History of cold intolerance, constipation, dry skin,
excessive hair growth, reduced linear growth for
endocrinopathies.
& History of central nervous system damage due to infec-
tion, trauma radiation or mass suggest hypothalamic
Indian J Pediatr (June 2018) 85(6):463–471
Possible etiology
Endocrine or syndromic (Prader Willi, ROHHADNET, AHO etc)
Monogenic or syndromic, rarely endocrine (e.g., adrenal tumor
or exogenous Cushing syndrome)
Monogenic syndromes (e.g., MC4R, leptin or leptin receptor gene
mutations), Prader Willi syndrome
Syndromic
Syndromic
Endocrine, e.g., exogenous Cushing syndrome or adrenal tumors;
Syndromic e.g., Prader Willi, ROHHADNET have relatively
sudden onset between 2 and 4 y of age
Prader Willi syndrome
Hypothalamic obesity or ROHHADNET
Syndromic, some monogenic and endocrine causes. However,
apparent small penis due to its being buried in pubic fat
is common in exogenous obesity as well.
Cushing syndrome
Children with exogenous obesity usually have milder degree
of hypertension but may occasionally have stage 2
hypertension as well.
Cushing syndrome
Endocrine obesity
obesity. History of morning headaches, vomiting, visual
disturbances, excessive urination/ drinking should be
noted.
& History of symptoms of complications/ comorbidities-
headache (pseudotumor cerebri), snoring and day time
somnolence (obstructive sleep apnea), abdominal pain
(cholelithiasis, non-alcoholic fatty liver disease), hip pain
(slipped capital femoral epiphyses), polyuria/ polydipsia
(type 2 diabetes), irregular menses/ increased hair growth
(polycystic ovarian disease) etc.
Physical Examination
The physical examination should evaluate presence of comor-
bidities and underlying etiologies.
& General appearance– Dysmorphic features for genetic
syndromes; assessment of fat distribution as centripetal
involvement with fat deposition in interscapular area, face,
neck and trunk may suggest Cushing syndrome.
& Anthropometry– Weight, height and waist circumfer-
ence should be measured and BMI calculated, and
compared with age and gender specific norms.
Children with exogenous obesity are generally tall for
Indian J Pediatr (June 2018) 85(6):463–471
their age and midparental height, whereas underlying
genetic/ endocrine causes in most cases are associated
with short stature (obesity due to MC4R mutation is not
associated with short stature).
& Vitals– Heart rate and blood pressure should be measured.
Care should be taken to use appropriate sized cuff to mea-
sure blood pressure. Hypertension may be present as a
complication of obesity or may suggest underlying
Cushing syndrome.
& Skin and hair– Dry and brittle hair are seen in hypothy-
roidism, red hair in POMC mutation, hirsutism in poly-
cystic ovarian disease and Cushing syndrome; dry and
coarse skin in hypothyroidism, violaceous striae in
Cushing syndrome, xanthelasma in dyslipidemia, skin
tags, keratosis pilaris and acanthosis nigricans are markers
of insulin resistance.
& Head, eyes, throat– Head circumference for microcephaly;
fundus for papilledema in pseudotumor cerebri and retini-
tis pigmentosa in syndromic obesity like Bardet-Biedl
syndrome (BBS); enlarged tonsils for obstructive sleep
Fig. 1 Diagnostic algorithm for
approach towards childhood
obesity
469
apnea, tooth enamel erosions in eating disorders and due
to increased sugar consumption.
& Abdomen– Tenderness in cholilithiasis, hepatomegaly in
non-alcoholic fatty liver disease
& Musculoskeletal system– Polydactyly in BBS; small
hands and feet with tapering fingers/ toes in Prader Willi
syndrome (PWS); abnormal gait and limited range of hip
motion in slipped capital femoral epiphysis; lower leg
bowing in Blount’s disease.
& Genitourinary system and pubertal stage assessment–
Undescended testis, small penis and scrotal hypoplasia
in PWS; delayed puberty in hypothalamic-pituitary le-
sions, PWS, BBS, and leptin deficiency; apparent
micropenis buried in fat in all forms of obesity; precocious
puberty occasionally in hypothalamic- pituitary lesions.
& Developmental assessment– Developmental delay/ intel-
lectual disability in some cases of syndromic obesity
Figure 1 depicts the diagnostic algorithm for etiological
assessment of childhood obesity.
470
Investigations
Only those children in whom genetic or endocrine causes are
suspected based on history and examination need to be spe-
cifically tested for these by appropriate tests. Investigations
such as thyroid function test, serum cortisol and overnight
dexamethasone test should not be a part of routine work-up
in obese children. The role of investigative work-up in
overweight/ obese children is to screen for cardiovascular,
metabolic and other complications of obesity including dys-
lipidemia, type 2 diabetes, non-alcoholic fatty liver disease,
obstructive sleep apnea and polycystic ovarian syndrome [45].
The guidelines for screening for these complications are in-
cluded in a separate paper by Vikram et al. in this issue.
Conclusions
Overweight and obesity are becoming increasingly common
in children. Measurement of BMI should be a part of all
health-related visits of children, as well as of school health
programs, and all efforts should be made to increase aware-
ness regarding the health complications of childhood obesity.
Although most cases of obesity in children are secondary to
positive energy balance, it is imperative to look for clinical
features common to monogenic mutations, endocrine causes
or genetic syndromes. Regardless of the etiology, all patients
should be assessed for modifiable lifestyle risk factors and
screened for the complications of obesity. However, preven-
tion remains the best approach to halt and reverse the current
epidemic of childhood obesity.
Contributions BA and VJ conceptualized the paper, searched the lit-
erature and drafted the paper. Both authors have seen and approved the
final version. VJ will act as guarantor for this paper.
Compliance with Ethical Standards
Conflict of Interest None.
Source of Funding None.
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