Bhave S, Bavdekar A, Otiv M. IAP National Task Force for Childhood Prevention of Adult Diseases: Childhood Obesity. Indian Pediatr 41, 559-575

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INDIAN PEDIATRICS 559 VOLUME 41
__
JUNE 17, 2004
IAP National Task Force for
Childhood Prevention of Adult
Diseases: Childhood Obesity
6.1 Primary prevention of childhood
obesity: Public Health Approach
6.2 Do interventions work ?
6.3 Strategies and Aims
6.4 Special strategies for target groups
6.5 Channels of intervention
7. Management of established obesity
7.1 Approach to assessment
7.2 Approach to therapy
7.3 Principles of therapy
7.4 Intensive therapy
8. Key Messages
9. References
10. Annexures
1. Preamble
India is in the midst of a rapidly escalating
‘epidemic’ of Type II Diabetes and Coronary
Heart Disease (CHD). Today, India has more
diabetic patients than any other country in the
world, and it is predicted that CHD will soon
become the leading cause of death in our
country. Indians, as an ethnic group are
particularly at high risk for insulin resistance
(syndrome X) and central obesity, both
forerunners of diabetes, CHD and other
‘life style’ disorders. It is now emerging
convincingly that these disorders begin in
childhood (or even earlier, in fetal life), and
manifest due to interactions and accumulation
of various risk factors, throughout the life
course. Pediatricians, therefore, have an
important role in the prevention and control of
the ‘epidemic’. It is indeed ironic that a problem
of “plenty” viz., childhood obesity, has emerged
while we are still fighting undernutrition and
infectious disease. As such, conflict in public
health messages, is a distinct possibility and
must be avoided at all costs.
Writing Committee:
Sheila Bhave*
Ashish Bavdekar**
Madhumati Otiv***
Contents
1. Preamble
2. Introduction
2.1 Obesity is a global epidemic
2.2 Indian is fattening too
3. What is obesity and how do we measure
it?
3.1 Measurement of Obesity
3.2 Reference Charts for children
3.3 Other markers of obesity
4. Epidemiology
4.1 Determinants of obesity and its
persistence
4.2 Indians at high risk; our special
concerns
5. Causes of the epidemic in India
5.1 Changes in life style (urbanisation)
5.2 Genetic/constitutional predisposition
5.3 Other factors
6. How can we control this epidemic ?
Department of Pediatrics, KEM Hospital, Pune
411 011, India.
Correspondence: *Dr. Sheila Bhave, Consultant in
Pediatric Research, Department of Pediatrics,
KEM Hospital, Pune 411 011, India.
Email : kemhrc@vsnl.com
**Associate Consultant , Pediatric Gastroenterology.
*** Research Associate.

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The Indian Academy of Pediatrics has
established a National Task Force on ‘Child-
hood Prevention of Adult Chronic Disease’,
and earlier issues of Indian Pediatrics have
carried reviews and recommendations on
(i) Childhood Physical Activity and
Prevention of Adult Disease, and
(ii) Insulin Resistance and Type II Diabetes
Mellitus in Childhood.
Presented here is the third in the series, on
“Childhood Obesity”.
The members of the task force are listed in
Annexure 1.
2. Introduction
Traditionally, a fat child is considered as an
‘attractive’ child, and is often referred to as a
‘healthy’ child. However, the adverse and
serious consequences of childhood obesity are
now proven beyond doubt(1,2) (Table I).
Psychosocial stigmatization may not be a big
problem in our country, and severe
complications of obesity (such as obstructive
sleep apnea, and pseudotumor cerebrii) are
rare. However, obese children have substantial
risks for morbidity such as hypertension and
dyslipedemia even before they reach
adulthood(3,4). Type 2 diabetes is beginning
to emerge in children(5). Importantly, 50 to
80% of obese children become obese adults
and all complications of adult obesity are made
worse if the obesity begins in childhood(1) .
Several elegant reviews and recom-
mendations by expert committees have been
published for prevention and treatment of
childhood obesity in the developed
countries(6,7). The aim of this paper is to
highlight some of the unique features of
obesity in India, and to suggest interventions
TABLE I– Consequences of Childhood Obesity(1-7).
Immediate Effects and Complications (usually in severe obesity)
Psychosocial stress Blount’s disease
Respiratory embarrassment Slipped femoral epiphysis
Obstructive airway disease Flat feet
Restrictive airway disease Hepatic steatosis
(most severe, Pickwickian syndrome) Endocrine effects*
Pseudotumor cerebrii increased skeletal growth
Cholelithiasis (and cholecystitis) early puberty (reduced final growth)
* (Endocrine causes of obesity such as Cushing's not considered here)
Co-morbidities
Dyslipidemias (especially with visceral fat / central obesity)
Hypertension
Insulin Resistance Syndrome (Syndrome X)
Childhood Type 2 diabetes mellitus
Ovarian hyperandrogenism (hirsutism, oligomenorrhea and infertility ± ovarian cysts)
Reduced bone density
Raised C reactive protein / systemic inflammation
Future Risks
Adult obesity (Increased mortality and morbidity from all obesity related disorders)
Coronary Heart Disease and cerebrovascular disease
Type 2 Diabetes Mellitus
Osteoporosis

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based on the prevailing health and social
infrastructure systems in our country.
2.1 Obesity is a global epidemic(8)
According to WHO (2000) atleast 50% of
adults and 20% of children in U.K. and U.S.A.
are currently overweight. Prevalence of
overweight amongst Australian children has
increased from 11% in 1985 to 20% in
1995(8). Childhood obesity has tripled in
Canada in last 20 years. It has been estimated
that, in 1995, the direct costs of treatment of
obesity in USA accounted for $70 billion with
far greater indirect costs(9).
Obesity does not seem to have spared
developing countries either. Thailand, Iran,
Nigeria and Brazil have all reported
unprecedented levels of obesity with trends
that are substantially rising every year(2). The
calculated global prevalence of overweight
(including obesity) in children aged 5-17 years
is estimated by the International Obesity Task
Force (IOTF) to be approximately 10%, but
this is ‘unequally distributed’ with prevalence
ranging from over 30% in Americas to <2% in
sub Saharan Africa(2).
2.2 India is fattening too
In a recent study by Reddy, et al., more
than 28% of adult males and 47% of adult
females in urban Delhi were overweight by
WHO standards(9). In the same study the
corresponding figures for overweight in a
neighbouring Haryana rural area were 7% in
males and 9% in females. Conversely, as many
as 38% of males and 36% of females in the
rural area were actually ‘underweight’ by BMI
standards. Such an ‘urban, rural divide’ has
been documented in other Indian studies
too(10).
In children, the difference between the rich
and the poor is fairly evident in recently
conducted urban studies. Ramachandran, et al.
studied children from six schools in Chennai,
two each from high, middle and lower income
groups(11). The prevalence of overweight
(including obese) adolescents ranged from
22% in better off schools to 4.5% in lower
income group schools. In a Delhi school with
tution fees more than Rs. 2,500 per month, the
prevalence of overweight was 31%, of which
7.5% were frankly obese(12). In Pune the
figures for overweight children are 24% in a
well off school and 6% in a ‘corporation’
school (unpublished data).
3. What is obesity and how do we
measure it?
Obesity is defined as a condition of
abnormal or excessive fat accumulation in
adipose tissue, to the extent that health may be
impaired (WHO consultation on obesity,
2000)(8). It has to be pointed out that the terms
overweight and obese are often used some-
what loosely and interchangeably. However,
standardization is necessary for international
and secular comparisons.
3.1 Measurement of obesity
Body weight is reasonably correlated with
body fat, but is also highly correlated with
height. Therefore, weight adjusted for height
squared [body mass index (BMI in kg/m
2
)] is a
useful index to assess overweight and is a
fairly reliable surrogate for adiposity. It is
calculated easily from weight and height and it
correlates with other measures of body fatness
in children and adolescents. BMI also cor-
relates with markers of secondary complica-
tions of obesity, including current blood
pressures, blood lipids and with long-term
mortality(13). A limitation of BMI however is
that it cannot differentiate an obese individual
from a muscular one. It also cannot locate the
site of fat e.g., people with ‘central obesity’
may have normal BMIs. Inspite of several
limitations, BMI as of now appears to be the

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most practical way of measuring and
comparing obesity for clinical and epidemio-
logical purposes.
As per WHO classification (for adults)
BMI >25 = overweight and BMI >30 =
obesity
However, as these WHO criteria may
underestimate obesity in Asians, the Inter-
national Obesity Task Force (IOTF) has
proposed the standards for adult obesity in
Asia and India as follows(14).
BMI >23 = overweight and BMI >25 =
obesity.
3.2 Reference charts for children
BMI values for adults, are age independent
and same for both sexes. However in children,
BMI changes physiologically (substantially)
with age and sex. At birth the median BMI is as
low as 13 kg/m
2
, increasing to 17 kg/m
2
at age
1, decreasing to 15.5 kg/m
2
at age 6, then
increasing to 21 kg/m
2
at age 20. Many
countries have published BMI-for-age charts
for their populations, and some have also
defined cut-off points on these charts to define
overweight and obesity. A recent Indian study
by Agarwal, et al. has described indices
including BMI and skinfolds for affluent
Indian school children(15). However, the
sample size of the study is probably not large
enough to generate internationally accepted
standards.
The two BMI charts that can be used as a
reference, for Indian children, as of now,
therefore are:
(1) The NCHS/CDC charts from USA(16).
The American Obesity Association uses
the 85th percentile of BMI for age and
sex as a reference point for overweight
and the 95th percentile for obesity in
children. These charts can be readily
downloaded from the internet sites,
but are however, based on well off
populations from USA.
(2) Recently, new BMI standards in children
using a large internationally represen-
tative sample from six different countries
(not India), with widely differing
prevalence rates for obesity have been
published(17). Age- and sex-specific
BMI cut-off points for defining
overweight and obesity in children have
been derived by identifying percentiles in
children analogous to adult BMIs of 25
kg/m
2
and 30 kg/m
2
, respectively. These
are referred to as IOTF cutoff points and
are now recommended as standards for
international comparison of data(2).
3.3 Other markers of obesity
Other markers and measures of obesity are
summarised in Table II.
All these markers have their individual
advantages (e.g., waist circumference for
central obesity, DEXA for actual fat
percentage) but none are really standardized as
yet for children.
4. Epidemiology
4.1 Determinants of obesity and its
persistence
Atleast 30% of obesity begins in
childhood. Conversely 50 to 80% of obese,
children become obese adults(1). Many
longitudinal studies have demonstrated
convincingly, the substantially higher risks of
child onset obesity(18,19). In the Harvard
study, morbidity from cardiovascular disease,
diabetes, obesity related cancers and arthritis
was 50 -100% higher in obese individuals who
were also obese as children and generally the
cardiovascular mortality in such individuals
was doubled(20).

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TABLE II–Other Markers of Obesity and Comments.
Skinfold thickness (SFT)(53) Skinfold thickness by itself has not been validated as a marker of obesity in
population studies. Body fat % can be calculated from prediction equations
using multiple skinfold measurements.
Cut-off values for obesity - 30% body fat (girls) and 20-25% body fat (boys).
Disadvantages – Significant inter and intra-observer variation, affected by
gender and ethnicity, no Indian reference data, no significant advantage over
BMI.
Waist circumference(54) Highly sensitive and specific measure of central obesity.
Cut off values for risk - 102 cm (adult males), 88 cm (adult females), 71 cm
(pre-pubertal children).
No Indian data.
Waist hip ratio(53) Waist circumference / Hip circumference > 0.9 = Central Obesity. No added
advantage of WHR over waist circumference in assessing central obesity.
Bioelectrical impedence analyses Non-invasive, safe, cheap, reliable estimation of body composition using a
small portable instrument.
Requires standardised conditions, experienced personnel, adequate hydration
status, overpredicts body fat in lean and muscular individuals and underpredicts
in obese.
Dual energy X-ray Accurately estimates whole-body as well as regional bone mineral density, lean
absorptiometry (DEXA) mass, and fat mass over a wide range of ages and body sizes.
Cut off values for body fat % : adults males >25% and females >35%.
Non-invasive, minimal radiation, but very expensive.
Air displacement plethy- A sophisticated new technique. Accurate, non-invasive, comfortable but very
smography(BOD-POD) expensive. May be unsuitable for younger children as it needs considerable co-
operation.
rebound remains obscure(23). However, the
most important predictor of adult obesity
appears to be adolescent weight and changes
of BMI during this time(24). The older a child
is, when he or she remains overweight, the
greater the likelihood that overweight will
remain in adulthood.
4.2 Indians at high risk; our special
concerns
The prevalence of diabetes, CHD and other
life style disorders is increasing alarmingly in
India, and is affecting much younger
populations than in the West. A large pool
of young Indians demonstrate ‘prediabetics’
The crucial periods for persistence of
obesity appear to be (i) gestational period
(ii) adiposity rebound age (5-7yrs) and
(iii) adolescence. A number of studies have
shown that high birthweight is positively
related to subsequent fatness(21) but higher
prevalence of obesity is also seen in
lower birthweights–the U or J shaped
relationship(22). The tendency for indicators
of adiposity such as BMI to fall around the age
of one year, and then increase again by around
5th year is referred to as ‘adiposity rebound’.
It is now evident, that earlier the rebound the
greater the risk of subsequent obesity,
although what drives the timing of adiposity

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(i.e., insulin resistance and or glucose
intolerance)(25). Gestational diabetes is
common in mothers. The association of these
problems with high BMIs and importantly
central obesity is now well accepted(26). In
transitional economies such as in India obesity
and malnutrition often coexist (‘double burden
of disease’) causing confusion in health
messages(8).
Infact, frank obesity may not be as high in
India as in the west, but the body composition
and metabolism of Indians (and Asians in
general) make them especially prone to
adiposity and its consequences(27). South
Asians have atleast 3 to 5% higher body fat for
the same BMI as compared to Caucasians(28).
The fat is typically located centrally, and
around visceral organs where it is meta-
bolically more dangerous than peripheral fat.
Recent Pune studies have demonstrated the
‘thin fat Indian Phenotype’ with evidence of
hyperinsulinemia even at birth(29). Moreover,
recent longitudinal studies in India have
highlighted the deleterious effect of acce-
lerated weight gain in childhood ‘crossing of
centiles’ especially in LBW babies(30,31).
Indices of insulin resistance and cardio-
vascular risk factors were found to be highest
in those that were born ‘small’ but were big by
8 years in the Pune study, even though they
were not obese in absolute terms. The recent
Delhi study in young adults showed that an
increase of BMI of 1 SD from 2 to 12 years of
age, increased the odds ratio for disease by
1.36(31). Further, continuing cohort studies in
Pune suggest that accelerated growth in
childhood is associated with early maturation
and greater risk of obesity (unpublished
results).
It is now evident that our traditional
understanding of concepts of ‘catch up
growth’, weight gain in pregnancy and birth
weight may need redefining.
5. Causes of the epidemic (in India)
In India there is a tremendous ‘Urban/
Rural’ and ‘Rich / Poor’ divide, prevalence in
the urban rich being much higher than in rural
areas and poor communities. The causes
include:
5.1 Changes in life style (‘urbanisation’)
With improving standards of living, and
availability of food in plenty, the upper class
societies of India in recent years have
urbanized to western levels. The components
of life style changes are:
• Unhealthy eating patterns, wrong choices
of food: Traditional micronutrient rich
foods are being replaced by energy dense
highly processed, micronutrient poor foods
with greatly increased portions ‘Dil Mange
More’. High calorie snacks, junk food
revolution, cool cola (‘thanda matlab’)
colonisation, and food as rewards or
demonstration of love are all part of new
life styles. All celebrations and festivals
seem to be centered around rich foods.
• Sedentary pursuits: TV and movie
watching, video games, internet gazing
and telephone gossip sessions are now
important activities of children. TV also
affects by heavy marketing of colas and
other fatty foods. The number of TV sets
and telephone connections are touted as
indices of development!
• ‘Obesogenic schools’ and Tution classes:
An important factor for obesity in India is
the intense competition for admissions to
schools and colleges with flourishing
tuition classes right from nursery levels !
Children are forced to use their play time
for additional studies. Games or physical
training sessions are restricted or non
existent in many schools. Some schools do
not have any playgrounds at all.

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• Inadequate play areas: Due to unsafe
roads (traffic, crime) children are dis-
couraged form walking or cycling to
school. Motorized vehicles are popular and
they are perceived to be quicker and safer
for transport. Erosion of open spaces for
exercise and lack of parental time to
supervise play are all part of new
obesogenic lifestyles. As against food as
rewards, ironically exercise is meted out as
a punishment - ‘100 sit ups,’ ‘run round
the field.’
5.2 Genetic ‘Constitutional’ pre-
disposition
The factors responsible could be:
• Modern environment may have unmasked
previously silent obesogenic genes ‘thrifty
genotypes’(32).
• Programming of previously malnourished
populations to accumulate fat more
intensely in an attempt to store for future
starvation (‘early life origins’)(33,34).
• Stunting in childhood (short height for age)
may increase the risk of central obesity
especially in transitional economies(35).
• High rate of gestational diabetes in
pregnant women causing higher birth
weights in babies leading to inter-
generational effects of obesity in childhood
and its attendants problem(36).
• Familial pattern of eating, exercise and
behavior.
5.3 Other factors
• Prolonged and exclusive breast feeding
is associated with a significantly lower rate
of obesity and hypertension in later
life(37). It is not clear if early introduction
of energy dense supplements in infancy
has contributed to childhood obesity in
India.
• The high glycemic index of our
predominantly carbohydrate diet may be
responsible for hyperinsulinism, weight
gain and eventual type 2 diabetes(38).
• Yet other factors controlling body weight
regulation such as `low body metabolic
rate (BMR)' and probably governed by
hypothalamus - these factors as of now are
all speculative(1,2).
6. How can we control this epidemic?
6.1 Primary prevention of childhood
Obesity: Public health approach
Atleast 1 in 10 urban middle class children
in India is overweight. If we allow this
epidemic to continue we will top the world in
Diabetes and CHD earlier than estimated. The
cost of treating diabetes mellitus and
associated disorders alone will consume a
major chunk of our resources which we can ill
afford. Only community based approaches
can address such large numbers of affected
children. Further, results of treating estab-
lished obesity at clinics are dis-appointing,
though on a positive note children do better
than adults(6). Obesogenic lifestyle behaviors
are less well developed in children and
therefore more amenable to change. An
overwhelming body of evidence now indicates
that prevention must begin in childhood to
reduce the burden and cost of obesity in
society(2,8).
In India, Public health efforts so far, have
been directed towards improving nutrition
(and thereby implied weights of newborns,
infants, children and mothers). Obesity
prevention campaigns will have to be carefully
worded to avoid conflicting messages and
deleterious results! However the only way to
cut short the escalating epidemic appears to be
prevention of obesity and other lifestyle
problems in childhood itself.

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The control of this epidemic is a challenge
and requires strong social and political will in
addition to medical management. A concerted
public health approach will be required for
effective prevention. The whole family,
indeed the whole society must be targeted for
the health of the future generation.
6.2 Do interventions/preventive methods
work?
In India, we have just about started
reporting high prevalence of obesity in
children. Obviously then, no intervention
studies have been carried out as yet. But a
number of studies have been carried out and
reported from the western countries(2,39,40).
Some reports from developing countries have
started to emerge(41). By and large recent
studies in children (as against adult studies)
have shown some positive short term and long
term results with programs that target the
whole life style of children.
The CATCH study (Child and adolescent
trial for cardiovascular health) in multi racial
American school children and the ‘Go Girls’
community based study in African American
girls showed that children can be taught to eat
less fat and exercise more!(40,42). Larger
numbers and longer time inputs could have
shown positive influence on prevalence of
obesity too. An important UK school based
study (APPLES) which targeted whole
community reported successful imple-
mentation of the program but unsuccessful
result (in fact the study group had reduced
activity and no weight loss!)(43). Obviously
more time or different approaches will have to
be tried to improve outcome. Perhaps the most
optimistic results have come from Singapore;
an 8 year school based campaign with
government support (Health Promotion
Board) was successful in implementation as
well as reduction in prevalence of obesity
(from a high of 16.6% in early 90s to less than
14.6% in 1998)(44). This study however was
targeted at obese children only, and the
possibility of causing psychosocial stigmas by
such an approach must be considered. In
Brazil, an ambitious programme to promote
physical activity in children was launched in
1997, in Sau Paulo, and because of its impact
has now been adopted throughout the country -
‘Agita Brasil’(41). The Brazil programme has
highlighted psychosocial and educational
benefits as well as physical benefits but, is yet
to be assessed in terms of obesity prevalence.
Obviously many lessons can be learnt from
the successful and the not so successful
programs in other countries.
The following strategies suggested
specifically for our country, are based not only
on the above evidence, but on observational
data and also on logic.
6.3 Strategies and Aims: Public Health
Approch(2,7,8,45)
As a Public Health Approach, essentially
all children, adolescents and families should
benefit from counseling to prevent excess
weight gain and obesity.
• Life style approach
(i) Healthy eating patterns: Emphasis should
be on nutrition rather than ‘dieting’. It is
important to maintain healthy components of
traditional diets (i.e., micronutrient rich food
such as fruits, vegetables and whole grain
cereals) and guard against heavily marketed
energy dense fatty and salty foods (e.g., pre-
packaged snacks, ice-creams and chocolates)
and the sugary cold drinks. The strategy
should be to recognise and eliminate risk
features of high calorie intake such as frequent
snacking (samosas, potato chips, chiwdas),
eating out frequently (burgers, dosas),
celebrating with food (cake, chocolates) and

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drinks (colas, beers). Healthier alternatives can
be suggested. Habits attained early have more
chance of remaining throughout life.
A simple Indianised message based on
recommendations of AHA(7) could be–“think
of a day’s food composition as a ‘Thali’
wherein 50% (half) is full of vegetables, salads
and fruits. A quarter (25%) should be made up
of cereals such as rice and/or chapattis and the
remaining quarter should be protein based
(dal/milk/egg/animal protein)”. Fried, snacks
and ‘sweet dishes’ are only for a very few
special occasions ! (Fig. 1).
(ii) Increase physical activity levels: Children
should be encouraged to be active not only for
weight control but for general well being.
Many adolescents/pre adolescents find
defined physical exercises (aerobics, tread-
mills) boring and punitive and are more likely
to continue activity if it is incorporated into
their daily routines, e.g., walking or cycling to
school and playing with friends in the grounds.
The WHO recommends atleast 30 minutes of
cumulative moderate exercise (equivalent to
walking briskly) for all ages; plus for children,
an additional 20 minutes of vigorous exercise
(equivalent to running), three times a
week(46). These recommendations are basi-
cally for prevention of CHD; prevention of
obesity may require more physical exertion. In
general, moderate to vigorous activities for a
period of atleast one hour a day may be a more
practical recommendation for all school going
children.
(iii) Decrease sedentary behavior: Perhaps
even more important is decreasing sedentary
behavior. In our country, chief sedentary
behaviors are television (should be restricted
to no more than 2 hours a day), computers,
telephone conversations and importantly
tution classes (restriction may not be
possible!).
• Avoid Overfeeding Stunted Populations.
Assess stature, and prevent feeding excess
calories to children with low weight for age
but normal weight for height i.e., ‘stunted
children’. Most PEM prevention programs
(school mid day meals) use food
supplements that provide ample energy
and protein but may be deficient in
micronutrients. Such programs may induce
weight gain in underweight children while
length deficit may not be reversed, thereby
creating a risk for obesity(47). Quality of
Fig. 1. Showing recommended constituents of day’s food intake in a ‘Thali’ based visual.
Salads
Vegetables
Fruits
Protein b
ased:
eg.
Milk, egg,
`dal’, meat
Carbohydrate
based: eg.
R
ice, `chappati’
Increase NSP fibre
Decrease oily foods
`No’ to soft drinks
Based on AHA (AHOY)(7)
Recommended constituent of day’s
food intake

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foods provided in ‘feeding programs’ is
crucial–fruits and vegetables should be
included and energy excess should be
avoided(47).
• ‘Target’ populations most in need of
interventions; in India this would probably
mean urban children from higher and mid
socio economic status. Targeting avoids
confusing messaging directed towards
opposite segments of society.
• ‘Tailor the interventions’ to suit the
specific needs of the community. Use
culture appropriate messages e.g., urban
Indians need to know that ‘chubby’ or fat
infants are not equal to ‘healthy’ babies !
• Address ‘Behavior’ Change. Behavior is
culture based. Consider socio-cultural and
ethnic issues–these would be important in
suggesting diets and activity. For example,
adolescent girls from conservative families
are often discouraged from playing
outdoor games but can be encouraged to
perform physical household chores.
• Focus on involvement of entire family
(parents, grandparents) indeed the entire
community for better results. Average
Indian families have poor knowledge of
‘healthy eating’.
• Confront vested interests e.g., advertising
of colas.
• Build supportive infrastructure e.g., safe
play grounds, transport and town
planning.
6.4 Special strategies to target specific age
groups(8)
Infants and Young Children
• Mothers should prevent excess weight gain
in pregnancy; control diabetes or impaired
glucose tolerance in pregnancy.
• Promote exclusive breast feeding for six
months.
• Avoid adding sugars, starches or oils to
feeding formulas.
• Assure appropriate micronutrient intake
especially of iron, calcium and vitamins.
• Monitor growth with weight for height and
BMI. Discourage ‘accelerated crossing of
centiles’.
• Make clear differentiation of ‘catch up
growth’ from accelerated weight gain.
Catch up growth should be associated
with gain in height proportional to weight
gain.
• Instruct mothers to accept the child's
appetite and not to force feed.
• Instruct families that ‘fat infants make fat
adults’.
Children and adolescents
The fat rebound age (5-8years) and
adolescence are particularly high risk periods
for accumulating fat. Strategies for prevention
include
• Promote active lifestyles including at least
one hour of vigorous ‘play’ per day. Limit
TV and other sedentary activities to
<2 hr/day. Physical activity is as important,
if not more than didactic lessons.
• Promote sensible eating–increase fruit and
vegetables and restrict energy dense
sweets and soft drinks. Impart health
education skills to make healthy food
choices e.g., early home cooked dinners to
avoid TV snacking. Substitute soups/
salads/baked foods for wafers, chocolates /
fried foods.
• Modify environments to promote physical
activity e.g., safe roads for cycling,
jogging.
• Celebration should be in the form of
outdoor play/picnics rather than fast food
joint parties.

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• Educate about the evils of alcohol/tobacco
to adolescents.
6.5 Channels of interventions / health
education
School Based Programs
Schools are probably the ideal medium of
intervention as they are central to children’s
lives and information can be relatively quickly
dissipated through this channel.
Aspects to be considered are:
• Training of teachers in lifestyles, nutrition
and activity.
• Introduction of ideal school meals or
provision of canteens offering only
healthy options based on Indian foods.
• Introduction of ‘nutrition and physical
education’ in school curriculum. These
activities should become compulsory and /
or a ‘scoring subject’ with marks to be
added to total grades. Only then will
parents/students give the required attention
and time to this in this competitive world of
academics!
• After school games (supervised/
unsupervised) to be encouraged. Opening
up of school playgrounds on weekends and
holidays.
• Obese children should not be teased,
targeted or bullied or isolated.
• Involve parent associations.
• School health check ups should monitor
BMI along with height and weight
annually.
Media involvement
Another powerful channel especially for
upper and middle class societies is media
coverage. Regular columns and supplements
have already started making a mark.
Health centers/Doctors/Other Professionals
• It is important for doctors and other health
professionals to think ‘prevention of
obesity’ at all visits and incorporate
relevant health education. The success of
this channel in recent years with ORS,
immunizations, breast feeding and
prevention of malnutrition makes this an
optimistic channel for such a campaign.
• Incorporate BMI charts / IOTF cut offs and
waist circumference (in addition to height,
weight and head circumference) in routine
health records. Monitor BMI every year,
particularly for children from high risk
families.
• Identify children with BMI >75th centile
(and with accelerated crossing of centiles)
for frequent monitoring and ‘life style’
interventions.
• Discourage parent's obsession with food
intake and pleas for tonics.
Governmental authorities
Both health and infrastructural authorities
should be responsible for
• Devising national strategies
• Encouraging food outlets/restaurants to
serve healthy choices
• Providing safe exercise opportunities.
• Regulate advertisements aimed at children
and insist on food labelling.
• Consider taxation on ‘fatty food’ or
alternatively reduce taxation/promote
production of fresh food and vegetables.
As said earlier this sort of a Public Health
Approach requires strong social and political
will with concurrent medical motivation and
management.
7. Management of established obesity
Whereas the public health campaign is to

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7.3 Principles of therapy (Table III)
Theoretically, obesity management is
energy balance (eat less and exercise more).
However, in practice the treatment can be
challenging and frustrating because of
frequent relapses.
The principles of therapy are generally
same as in prevention viz.:
(a) Reduced calorie intake;
(b) Increased activity levels;
(c) Decreased sedentary behavior;
(d) Family involvement;
(e) Behavioral changes.
Limiting energy intake of growing
children can result in decreased linear growth
velocity in obese children and is therefore
risky(45). Dieting could also increase
prevalence of inadequate nutrients, such as
iron, calcium, zinc and vitamins A, C and E.
High degrees of parental dietary control may
infact have adverse psychobehavioral effects
on young children with treatment failures(49).
Hence the aim should be provision of well
balanced healthy meals with a healthy
approach to eating. Several different dietary
studies have shown successful reduction
of calorie intake and improved eating
behaviors(45). The advise usually centres
around reducing calories from fat, saturated
fats, cholesterol and sugars (high density
foods) while increasing fruits, vegetables and
whole grain cereals (lower density foods).
Counting of calories can be tedious and
inaccurate and it is more advantageous to
supply indigenous versions of Food Guide
Pyramids or Epstein’s traffic light diets(50).
Trials of hypocaloric diets, protein modified
fasts, fibre supplementation and anorectic
drugs have been shown to be by and
large, ineffective in children in the long
range(48).
be targeted to the society as a whole,
individual or clinic based approach is
necessary for the treatment of the obviously
obese child. A guideline for assessment by
pediatricians in their clinic based practice is
provided in the accompanying Table III.
Principles of therapy are outlined in the
following section.
7.1 Management of obesity–clinic /
individual approach
Management of established obesity in
children needs a concerted and a sustained
effort from a team of experienced health
professionals. Treatment is more likely to be
successful in children than adults. Western
guidelines by and large apply to our clinics and
are outlined below(2,6,48).
Goals of therapy: Approach to therapy
Medical Goal: Medical goal should be
resolution of complications and co-morbidites
such as hypertension and hyperlipidemias.
Behavioral Goal: Achievement of healthy
eating and activity patterns rather than
achievement of ideal body weight .
Weight Goal: Weight maintenance rather than
weight loss (unless moribund obesity) in
young children–‘Let the child grow into his
weight’. Prolonged weight maintenance will
allow a gradual decline in the BMI as the child
grows in height.
7.2 General Approach to Therapy(1,6,38)
• Institute small, gradual and permanent
changes, not short-term diets or exercise
programs aimed at rapid weight loss.
• Involve the family and all care givers in the
treatment program.
• Intervention should begin early (later than
age 3 yrs but earlier than adolescence).
• Clinicians should encourage and empa-
thize and not criticise.

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
TABLE III–Clinic Based Approach to Childhood Obesity.
BMI Clinical evaluation Assessments Comments
>95th centile NCHS Rule out underlying causes* Developmental Delay, All are relatively rare conditions
e.g., Hypothyroidism (1-2/1000 children), Short Stature, and have distinctive clinical
Prader Willi (1/25000 population), Dysmorphism, features.
Cushings syndrome Abnormal genitalia *May require referral to
Endocrinologist
>95th centile NCHS
Look out for severe complications* Blurred optic disks, Breathing Rare, but some severe
(See Table 1) difficulties , Painful walking, complications are potentially
Abdominal pain fatal.
*Appropriate reference to
experts
>75th centile, NCHS &
Screen for co morbidities
Family history of obesity Such as Hypertension (25% obese children) Blood pressure Comorbidities are very
/ related morbidities Dyslipidemias (20% obese children) Lipid Profile common (upto 30%)
Polycystic ovaries (20% obese children) Blood sugar levels
Childhood Type II Diabetes Mellitus Fasting insulin Further investigation and
Insulin Resistance Syndrome USG referral according to findings
All overweight and obese
Assess for Psychological disorders Counsellors Could be cause or effect of
children e.g., Depression, Binge eating, Bulimea obesity

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Addition of physical activity and reduction
in sedentary behavior, both (supervised
and unsupervised) improves long term
outcome(48). The important components of
behavioral therapy include treatment of
families as a whole, identification of problem
behaviors and their modifications, and `tailor'
made advise and support component.
Parenting skills recommended in treatment
plans are praising the child's behavior, never
using food as reward, establishing firm daily
family meal and snack times, providing only
healthy options, removing temptations and
being a good role model(51).
7.4 Intensive therapy
Yanovski (2001) reviewed the limited data
on intensive therapies that have been proposed
and tried in children(52). These include
(a) severe energy restriction below 1000 kcal /
day (b) drugs-fenfluramine, metformin, sibu-
tramine, leptin, octreotide and (c) bariatric
surgery such as gastric bypass and gastric
stapling. Although initial weight loss can be
dramatic, most of these approaches are fraught
with significant adverse consequences and
need constant long term monitoring. These are
therefore, to be considered only in the rare
gross cases with potential life threatening
complications. None of the treatment
modalities can be successful without positive
behavioral changes.
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Annexure 1
Members of the Task Force
Ashish Bavdekar, Swarnarekha Bhat, Vijayalakshmi
Bhatia, Sheila Bhave, Panna Choudhury, Umesh
Kapil, Anita Khalil, Anura V.Kurpad, M.K.C. Nair,
Madhumati Otiv, P.Raghupathy, H.P.S. Sachdev
(Chairperson), R.N.Salhan, Nitin Shah, Sumathi
Swaminathan and Anju Virmani.