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 Introduction

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

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

Body Fat Measurement For making a clinical diagnosis of overweight and obesity,
estimation of body fat percentage is not required. Body mass
Body fat can be estimated by several methods, such as dual index (BMI), calculated as weight in Kg/(height in meters)2,
energy X-ray absorptiometry (DXA), bioelectrical impedance shows a good correlation with body fat percentage, and is
assay (BIA), computed tomography (CT) and magnetic reso- widely used as an index of relative weight [9]. The most im-
nance imaging (MRI) of abdomen, measurement of skinfold portant consideration in choosing a BMI cut-off for defining
thicknesses at multiple sites, air displacement plethysmogra- overweight/ obesity is the increased risk for complications.
phy and stable isotope dilution techniques [4]. A summary of The adult cut-off points of BMI of 25 and 30 kg/m2 for over-
the principles of these methods is provided in Table 1. Air weight and obesity, respectively, are used due to the observed
displacement plethysmography and stable isotope dilution increased health risks at these levels. BMI of 30 kg/m2 corre-
technique are considered as the most robust methods for esti- sponds roughly to 25 and 30% of fat mass, respectively in
mation of body composition in infants and children [5]. In Caucasian men and women [9].
adult men and women, body fat percentage above 25 and BMI however has some disadvantages. It does not dis-
35%, respectively is generally considered as obesity [6]. For tinguish reliably between lean and fat mass, and does not
children, reference curves for body fat percentage for predict percentage body fat consistently across ethnicities
Caucasian children aged 5–18 y were published by [10]. Asian Indians have higher body fat compared with
McCarthy et al. in 2006 using bioelectrical impedance. The Caucasians for similar BMI. For example, in a study by
2nd, 85th and 95th centiles for age and gender are considered Banerji et al., it was noted that a mean BMI of 24.5
as cut-offs for underfat, overfat and obese [7]. The 50th centile corresponded to mean body fat of 33% in Asian Indian
for boys is 15.6% at 5 y, increases to 20.8% at 11 y and again men residing in the US [11]. Additionally, fat distribution
decreases to 15.4% by 18 y. For girls, the 50th centile is 18% 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 cut-off for screening for metabolic syndrome [20].
the risk of cardiovascular disease and type 2 diabetes Alternatively, for adolescents, waist circumference more
starts increasing at lower BMI in Asian Indians [12]. than the adult cut-offs of 90 and 80 cm, respectively, for
Therefore, the Indian Consensus Group has recommended Asian males and females can be considered as indicative
the BMI cut-offs of ≥23 and ≥25 kg/m2 for classifying of abdominal obesity [19]. Higher waist to hip circumfer-
Asian Indian adults as overweight and obese, respectively ence ratio (WHR) also denotes abdominal obesity, and
[12]. The American Diabetes Association (ADA) has also WHR is considered to be high if >0.95 and 0.85 for adoles-
recommended screening for type 2 diabetes at the BMI cent boys and girls, respectively [19]. Waist circumference
cut-off of 23 kg/m2 for Asian Indians [13]. to height ratio of >0.5 is also a convenient and age indepen-
For children, several curves that give BMI distribution dent method to identify adults [21] as well as children and
as a function of age and sex have been elaborated, and adolescents [22] at increased health risk.
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 Etiology of Childhood Obesity
obesity in children below 5 y of age [14, 18]. In the age
group of 5–18 y, the revised Indian Academy of Pediatrics On the basis of etiology, childhood obesity is broadly
(IAP 2015) BMI curves that use cut-off percentiles equiv- subdivided into exogenous and endogenous. Exogenous
alent to adult BMI of 23 and 27 kg/m2 to define overweight obesity is brought about by a chronic imbalance between
and obesity, respectively should be used [18]. energy intake and expenditure; whereas endogenous obe-
Measurement of waist circumference is another easy tool sity is caused by various genetic, syndromic and endo-
that is useful in identification of obesity. Waist circumfer- crine causes. Metabolic programming, as observed in chil-
ence being a measure of central obesity has been seen to dren born small or large for gestational age, infants of
correlate more strongly than BMI with several complica- diabetic mothers and those with rapid or excessive
tions such as insulin resistance, dyslipidemia and non- catch-up growth in first few years of life, compounds
alcoholic fatty liver disease [19]. Recently, Khadilkar et al. the problem of obesity brought about by lifestyle and
have published waist circumference centiles for Indian chil- dietary factors [23, 24]. Table 3 summarizes the etiology
dren aged 2–18 y and have suggested use of 70th centile as 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 Indian J Pediatr (June 2018) 85(6):463–471

Table 3 Etiology of obesity in children and adolescents influence on the food and exercise choice of the child.
Exogenous There is increased risk of childhood obesity with maternal
• Chronic imbalance between energy intake and expenditure. diabetes, smoking and obesity, underlining the role of fetal
Increased intake of processed and refined diet, sugar-sweetened environment. Infant feeding style, sleep duration, rate of
beverages, increased time spent on TV viewing, internet browsing or postnatal weight gain and age of adiposity rebound are
playing electronic games, reduced physical activity, reduced sleep.
• Medications also associated with obesity later [30–32].
Glucocorticoids, tricyclic antidepressants, risperidone & School: School environment can become obesogenic if
• Adverse metabolic programming (acts in conjunction with diet and there is no emphasis on nutrition and physical education.
lifestyle factors) Lack of playgrounds and sports facilities, potentially un-
Infants born small for gestational age (SGA), large for gestational age
(LGA), those born to mothers with obesity or diabetes, and those with healthy school lunches, and availability of unwholesome
accelerated weight gain in infancy are predisposed to obesity in snacks and beverages in the school or its vicinity increase
childhood. the risk of obesity in children [33, 34].
Endogenous & Neighbourhood: Factors such as availability of healthy
• Monogenic causes food and grocery, park spaces, stray dogs that hinder
Defects in genes encoding melanocortin 4 receptor (MC4R), leptin
(LEP), leptin receptor (LEPR) pro-opiomelanocortin (POMC) etc. walking or cycling can mediate the risk of obesogenic
• Genetic syndromes behavior [35–37].
Alstrom, Bardet- Biedl, Prader Willi, Beckwith- Wiedemann,
Carpenter, Cohen, Albright Hereditary Osteodystrophy etc.
• Endocrine causes
Hypothyroidism, Cushing syndrome, hypothalamic obesity, growth Macro-environmental Influences
hormone deficiency, persistent hyperinsulinism etc.
& Food industry: Production of high fat, sugar and/ or salt
containing foods, use of complex marketing and advertis-
Exogenous Obesity ing practices, aggressive sales tactics, and confusing food
labelling restrict the consumers’ ability to make rational
Children of the present generation are living in an increasingly and healthy choices.
obesogenic environment, where gaining excessive weight is & Government: Government is responsible for providing
very easy, but remaining fit requires conscious and sustained safe environment conducive to physical activity such as
efforts [25]. Unhealthy or obesogenic individual behaviors are play grounds, open gyms, cycle and pedestrian friendly
linked to the surrounding microenvironments, including fami- roads. Strong nutritional policies are also needed to restrict
lies, schools, and neighbourhoods; which in turn are influenced availability of unhealthy snacks, taxation, clear food label-
by macrosystems like food industry and government [26]. ling, and price control of fruits and vegetables [26, 27].

According to a systematic review, the three environmental

Individual Behaviors
exposures that have the most significant impact on childhood
obesity are the availability of sugar- sweetened beverages,
& Unhealthy dietary habits: Consumption of energy
portion size, and food marketing [38].
dense foods, packaged refined foods, sugar-sweetened
beverages, excessive snacking, skipping meals, large
Endogenous Obesity
portion size and poor intake of fruits and vegetables
are associated with obesity [27].
Endocrinopathies, monogenic syndromes and other genetic
& Lack of physical activity
syndromes account for a small proportion of childhood obe-
& Increased screen time and reduced sleep time [28]
sity. Monogenic and syndromic causes have been discussed in
& Increased television (TV) viewing time: TV viewing is
detail in a separate paper in this volume. Role of metabolic
not just a sedentary behavior but also leads to over-
programming has also been discussed in another review paper
weight due to its association with unmindful munching,
in this volume. We shall be briefly reviewing the endocrine
and through influencing children’s food preferences by
causes here.
exposure to TV advertisements [29].
Endocrine Causes

Micro-environmental Influences Children with identifiable endocrinopathies comprise a small

minority (about 2–3%) of children referred for evaluation of
& Family: Parenting styles and behaviors as well as parents’ overweight [39]. However it is important for physicians to be
own diet and physical activity patterns have a very strong able to suspect and diagnose these conditions, so that specific
Indian J Pediatr (June 2018) 85(6):463–471 467

treatment can ensue. An important clue to underlying endo- pseudohypoparathyroidism types 1 a and c [40, 41].
crine etiology is deceleration or cessation of linear growth, so This is further discussed in the paper by Koves et al.
that height is below the centile expected for the child’s genetic in this issue.
potential. The clinical features of various endocrinopathies & ROHHADNET (Rapid Onset obesity, Hypothalamic dys-
associated with obesity are briefly discussed below [40, 41]. function, Hypoventilation, Autonomic Dysregulation and
Neuroendocrine tumors) syndrome: This syndromic cause
& Hypothyroidism– Clinical hypothyroidism with elevated of childhood obesity typically manifests with accelerated
TSH and low T4 levels is typically associated with weight gain and decelerated linear growth between 2 and
mild weight gain (increase in BMI by 1–2 kg/m2 only). 4 y of age, along with evidence of autonomic dysfunction
Decreased resting energy expenditure, fluid retention and hypoventilation. It is associated with varying degree
and diminished linear growth are the mechanisms im- of involvement of the hypothalamic-pituitary axis, includ-
plicated in BMI gain. Subclinical hypothyroidism is ing GH deficiency with low IGF-I in some, glucocorticoid
observed in roughly 10% of overweight/ obese chil- deficiency or excess, hypogonadotropic hypogonadism,
dren, but is considered as a consequence rather than hyperprolactinemia, hypothyroidism abnormalities of wa-
cause of obesity and does not require treatment with ter and sodium homeostasis, adrenal tumors etc. [44]. This
thyroxine [42]. is further discussed in the paper by Koves et al. in this
& Cush ing s yn drome– C u s h i n g s y n d r o m e or issue.
hypercortisolism in children can be exogenous or endog- & Persistent hyperinsulinemia– Mutations in several genes
enous. Endogenous Cushing syndrome is rare in children. resulting in excessive production of insulin by pancreatic
It is mostly caused by adrenal tumor or hyperplasia in beta cells, or insulinomas can lead to obesity as the affect-
children below 6 y of age, and pituitary micro adenoma ed children increase their food intake to prevent
in older children. Exogenous iatrogenic hypercortisolism hypoglycemia.
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 Approach
illness or ‘tonic’ is not uncommon [43]. Hypercortisolism
is associated with growth failure, central obesity, hirsut- Assessment of overweight/ obese children should begin with a
ism, increased appetite and hypertension. thorough history and examination directed to find the etiology
& Growth hormone deficiency (GHD)– GHD is character- and the associated complications including metabolic, cardio-
ized by short stature (height generally below −3 standard vascular (e.g., hypertension), respiratory, gastrointestinal, or-
deviations), low growth velocity and mild truncal obesity. thopedic and psychological issues. Investigations and further
& Hypothalamic obesity– The ventromedial, arcuate, evaluation should be guided by the history and examination
paraventricular and dorsomedial nuclei of the hypothal- [41, 45]. Since a majority of children and adolescents have
amus produce neuropeptides involved in appetite regu- exogenous obesity, they should not be unnecessarily investi-
lation and energy expenditure. Hypothalamic obesity is gated for endocrine or genetic causes. Some of the red flags
a consequence of congenital malformation or injury to that should alert the physician to the possibility of endogenous
the hypothalamus, resulting in disruption of these nu- etiology of obesity are listed in Table 4.
clei. Craniopharyngioma treated surgically is the most
common cause of hypothalamic obesity in pediatric age History
group. The other causes include pituitary tumors and
aneurysms, inflammatory and infiltrative diseases, History is important for identification of pointers towards un-
trauma, cranial irradiation or surgery. Affected patients derlying etiology, modifiable lifestyle factors, current and fu-
are generally lethargic with reduced energy expendi- ture risk of obesity related complications and assessment of
ture. They may also have other endocrinopathies, in- patient’s / family’s readiness to make behavioral changes [45].
cluding GHD, hypothyroidism, precocious or delayed Key points in history include the following:
puberty, and diabetes insipidus [40, 41].
& Albright Hereditary Osteodystrophy (AHO)– AHO is a & Birth weight, intrauterine exposure to maternal diabetes or
genetic disorder due to heterogenous inactivating mu- obesity
tation in GNAS, the gene that encodes the alpha chain & Age of onset of obesity, rapidity of weight gain
of Gs. AHO phenotype (short stature, round facies, & History of medication use– Steroids, antipsychotics,
obesity, brachydactyly, ectopic ossification, develop- antidepressants
mental delay and mental retardation) is associated with & Socioeconomic status
468 Indian J Pediatr (June 2018) 85(6):463–471

Table 4 Clues to underlying endogenous obesity

S.N. Red flags in history or examination Possible etiology

1 Stature shorter than that expected for midparental height Endocrine or syndromic (Prader Willi, ROHHADNET, AHO etc)
2 Onset in infancy or early childhood (< 5 y) Monogenic or syndromic, rarely endocrine (e.g., adrenal tumor
or exogenous Cushing syndrome)
3 Lack of satiety, food foaraging behavior, hyperphagia, Monogenic syndromes (e.g., MC4R, leptin or leptin receptor gene
willingness to eat even food that is perceived as mutations), Prader Willi syndrome
lacking in taste
4 Dysmorphism Syndromic
5 Intellectual impairment or significant behavioral problems Syndromic
6 Sudden onset 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
7 Low birth weight, hypotonia and feeding difficulties in infancy Prader Willi syndrome
8 Features suggestive of neurological deficits e.g., squint, vision Hypothalamic obesity or ROHHADNET
or visual field impairment, evidence of pituitary hormone deficits
9 Hypogonadism 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.
10 Stage 2 hypertension Cushing syndrome
Children with exogenous obesity usually have milder degree
of hypertension but may occasionally have stage 2
hypertension as well.
11 Violaceous striae, fat deposition over nape of neck, interscapular area Cushing syndrome
12 History of cranial irradiation, chemotherapy, CNS pathology Endocrine obesity

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- obesity. History of morning headaches, vomiting, visual
idemia, diabetes and hypertension disturbances, excessive urination/ drinking should be
& Dietary pattern– Frequency of eating outside the home, noted.
excessive consumption of sweetened beverages, energy & History of symptoms of complications/ comorbidities-
dense food, large food portion size, low consumption headache (pseudotumor cerebri), snoring and day time
of fruits and vegetables, meal frequency and quality, somnolence (obstructive sleep apnea), abdominal pain
snacking patterns. (cholelithiasis, non-alcoholic fatty liver disease), hip pain
& Physical activity assessment– Environmental and social (slipped capital femoral epiphyses), polyuria/ polydipsia
factors that support or pose barriers to physical activity, (type 2 diabetes), irregular menses/ increased hair growth
time spent in mild, moderate and vigorous physical activ- (polycystic ovarian disease) etc.
ity, in sedentary pursuits, especially screen (TV, mobile,
computer, etc.) time.
& Number of hours of sleep per day Physical Examination
& Psychological history– History suggestive of eating disor-
der, substance abuse, bullying or teasing, low self-esteem The physical examination should evaluate presence of comor-
should be noted. bidities and underlying etiologies.
& Developmental history should be taken, as intellectual dis-
ability may point towards endogenous etiology. & General appearance– Dysmorphic features for genetic
& Pubertal status, age at menarche and menstrual history in syndromes; assessment of fat distribution as centripetal
girls involvement with fat deposition in interscapular area, face,
& History of cold intolerance, constipation, dry skin, neck and trunk may suggest Cushing syndrome.
excessive hair growth, reduced linear growth for & Anthropometry– Weight, height and waist circumfer-
endocrinopathies. ence should be measured and BMI calculated, and
& History of central nervous system damage due to infec- compared with age and gender specific norms.
tion, trauma radiation or mass suggest hypothalamic Children with exogenous obesity are generally tall for
Indian J Pediatr (June 2018) 85(6):463–471 469

their age and midparental height, whereas underlying apnea, tooth enamel erosions in eating disorders and due
genetic/ endocrine causes in most cases are associated to increased sugar consumption.
with short stature (obesity due to MC4R mutation is not & Abdomen– Tenderness in cholilithiasis, hepatomegaly in
associated with short stature). non-alcoholic fatty liver disease
& Vitals– Heart rate and blood pressure should be measured. & Musculoskeletal system– Polydactyly in BBS; small
Care should be taken to use appropriate sized cuff to mea- hands and feet with tapering fingers/ toes in Prader Willi
sure blood pressure. Hypertension may be present as a syndrome (PWS); abnormal gait and limited range of hip
complication of obesity or may suggest underlying motion in slipped capital femoral epiphysis; lower leg
Cushing syndrome. bowing in Blount’s disease.
& Skin and hair– Dry and brittle hair are seen in hypothy- & Genitourinary system and pubertal stage assessment–
roidism, red hair in POMC mutation, hirsutism in poly- Undescended testis, small penis and scrotal hypoplasia
cystic ovarian disease and Cushing syndrome; dry and in PWS; delayed puberty in hypothalamic-pituitary le-
coarse skin in hypothyroidism, violaceous striae in sions, PWS, BBS, and leptin deficiency; apparent
Cushing syndrome, xanthelasma in dyslipidemia, skin micropenis buried in fat in all forms of obesity; precocious
tags, keratosis pilaris and acanthosis nigricans are markers puberty occasionally in hypothalamic- pituitary lesions.
of insulin resistance. & Developmental assessment– Developmental delay/ intel-
& Head, eyes, throat– Head circumference for microcephaly; lectual disability in some cases of syndromic obesity
fundus for papilledema in pseudotumor cerebri and retini-
tis pigmentosa in syndromic obesity like Bardet-Biedl Figure 1 depicts the diagnostic algorithm for etiological
syndrome (BBS); enlarged tonsils for obstructive sleep assessment of childhood obesity.

Fig. 1 Diagnostic algorithm for

approach towards childhood
obesity
470 Indian J Pediatr (June 2018) 85(6):463–471

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