This document discusses obesity in children. It defines obesity and related terms like overweight, defines it using BMI percentiles. It discusses the pathogenesis involving hormones like leptin and ghrelin. Risk factors include genetic predisposition and lifestyle factors. Obesity can cause medical conditions like diabetes, hypertension, fatty liver disease. Evaluation involves history, exam and investigations. Management focuses on diet modification, physical activity and lifestyle changes.

1. OBESITY
P R E S E N T E R : D R . S M I T H A M
D R . VA N I

2. INTRODUCTION
• Obesity refers to presence of excess of fat in body.
• Important paediatric public health problem across the
world, associated with the risk of complications in
childhood & increased morbidity & mortality throughout
adult life.

3. DEFINITION
OVERWEIGHT OBESE EXTREMELY
OBESE
Weight for length as
per WHO sex
specific charts
(<2years)
>/= 97th percentile
BMI percentiles as
per revised CDC
charts
(2-20years)
>/=85th to <95th >/=95th >/=120% of 95th
or >/= 35kg/m2
BMI as per IAP BMI
charts
(5-18years)
>/=23 adult equivalent
percentile:
Boys-71st
Girls-75th
>/=27 adult equivalent
percentile:
Boys-90th
Girls-95th

4. BMI
• BMI= weight in kg/(height in meters)2
• During childhood body fat levels change, beginning with
high adipocity in infancy, then decrease approximately
5.5yrs until a period called ADIPOCITY REBOUND.
• BMI varies with age & puberty, hence Z scores are
accurate
• OVERWEIGHT is defined as BMI >1 SD
• OBESITY is defined as BMI >2 SD above the WHO growth
reference medium

5. BMI
• Does not take into account lean mass of an individual
• Muscular children can also have higher BMI
• Racial & ethnic differences in fat content of individuals
with same BMI
• 25% children with normal BMI have excess body fat
• Higher fat content & its distribution(central adipocity)
correlate better with risk of obesity complications
• Hence waist circumference is better paramater for
predicting complications

6. • WAIST CIRCUMFERENCE
-more than 70th percentile
• WAIST-TO-HIP ration (WHR)
-WHR index for adolescent boys >0.95 & for girls >0.85 is
considered abdominal obesity
• WAIST –TO-HEIGHT ratio
-values <0.5 exclude central obesity
-values >0.5 indicate central obesity even in children with
normal weight & height
(Review article IJP- obesity in children 25.11.2017

7. PREDICTIVE FACTORS
• If one or both parents are obese
• Over-nutrition & bottle feeding during infancy
• Childhood obesity leads to adult obesity
• Factors increasing risk of adult obesity are younger age of
onset, greater severity of obesity & having an obese
parent, adipocity rebound at lower age
• Managing obesity at younger age reduces risk of adult
obesity & morbidities associated with it.

8. EPIDEMIOLOGY
• Obesity has become number one public health
problem worldwide
• Prevalence is increasing in developing countries
• In 5-19yrs age group number of obese children
increased from 11million in 1975 to 124 million in
2016 globally & 213million were obese in 2016
( IAP textbook on pediatric endocrinology)

9. EPIDEMIOLOGY
• In 0-5yrs group overweight & obese children no
increased from 32million in 1990 to 41million in 2016
• According to 52 studies conducted in India across 16
states prevalence increased from 16.3% in 2001-2005
to 19.3% after 2010
( IAP textbook on pediatric endocrinology)

10. PATHOGENESIS
• Obesity occurs when energy intake exceeds energy
expenditure
• Neuro endocrine feedback loops linking to adipose
tissue, GIT & CNS
• 3 components
1)AFFERENT SYSTEM
2)CENTRAL PROCESSING UNIT
3)EFFERENT SYSTEM

11. 1) AFFERENT SYSTEM: generates signals from adipose
tissue ( LEPTIN & ADIPONECTIN) , pancreas(insulin)
& stomach( ghrelin), ileum & colon( peptide YY)
2) CENTRAL PROCESSING UNIT: located in
hypothalamus
-ARCUATE NUCLEUS: processes & integrates peripheral
signals & generates efferent signal
-contains 2 subsets of neurons
: POMC (propiomelanocortin)/ CART ( cocaine &
amphetamine regulated transcripts)
:NPY (neuropeptide y) & AgRP ( agouti related
peptide)
1) EFFERENT SYSTEM: carry out orders from
hypothalamus in form of feeding behaviour &
energy expenditure

12. GIT harmones,
cholecystokinin,
glucagon like peptide-1,
peptide YY,
vagal neuronal feedback
promote satiety
HYPOTHALAMU
S
POMC/CART: enhance
energy expenditure by
production of
ANOREXIGENIC alpha
MSH & activation of
melanocortin
receptors 3 & 4
NPY/AgRP: promote
food intake
(OREXIGENIC EFFECT) &
weight gain through
activation of Y1/5
receptors
Hunger
Vagal neurons
Ghrelin stimulate
appetite

13. • Ghrelin stimulates appetite
• Adipose tissue provide feedback through release of
adiponectin & leptin regarding energy stores
• Adiponectin- also called fat burning molecule &
guardian angel against obesity
• Low leptin levels stimulate food intake & hight leptin
inhibit hunger

14. ETIOLOGY
• LIFESTYLE & DIET
*lack of physical activity
-pressure for academic performance have led to less time for
physical education in schools
-perception of poor neighbourhood safety
-advent of computers, video games leading to sedentary
lifestyle
*differences in food choices
-increased consumption of high carbohydrate beverages,
including sodas, fruit punch & juice
-increase in consumption of sugar sweetened beverages

15. ETIOLOGY
• Strong correlation with TV watching
(according to National Health
& Nutrition Examination Survey,
childhood obesity prevalence
is lowest among children
watching TV <1hr/day
& highest among those
watching TV for >4hrs/day)
• Having TV in bedroom is a risk
factor

16. • SOCIAL FACTORS
 Abuse, neglect & nonsupportive family environment
 Neglected children are at 9 times higher risk to
become obese than normal children
• ENDOCRINE
 Hypothyroidism
 Steroid excess
 Growth hormone deficiency
 Pseudohypoparathyroidism
 Hyperinsulinism/Insulin resistance

17. ETIOLOGY
• CNS
 Hypothalamic tumors
 Malformations
 Trauma/surgery
 ROHHAD ( Rapid-onset Obesity with Hypothalamic
dysregulation, Hypoventilation & Autonomic
dysregulation )

18. ETIOLOGY
• SYNDROMES
 Prader-Willi syndrome
 Alstrom syndrome
 Bardet-Biedl syndrome
 Beckwith-Weidemann syndrome
 Carpenter syndrome
 Cohen syndrome
 Down’s syndrome
 Turner syndrome
 Biemond syndrome

19. ETIOLOGY
• MONOGENIC DISORDERS
 Leptin deficiency
 Leptin receptor deficiency
 Pro-opimelanocortin deficiency
 Melanocortin receptor deficiency (commonly known
genetic defect)
• PSYCHIATRIC
 Anxiety
 Depression

20. ETIOLOGY
• DRUGS
 Atypical antipsychotics: olanzapine, clozapine,
risperidone
 Antiepileptics: carbamazepine, valproate, vigabatrin,
gabapentin
 Lithium
 Tricyclic antidepressants

21. • HERITABILITY or METABOLIC PROGRAMMING
 Tendency to gain weight is often inherited &
determines the risk of developing obesity. Ex: studies
showed identical twins & adopted children brought up
in different environment have BMI similar to biological
parents
• Other factors contributing to metabolic
programming are
 In utero environment or maternal malnutrition
 Birth weight ( small or large for gestation)
 Gestation ( term or preterm)

22. • GENETICS
 Important in severe forms of obesity
 Genetic disorders result in severe obesity with onset
at young age
 Major genetic factors contributing to obesity are
MONOGENIC GENE DISODERS & GENETIC
SYNDROMES

23. • MONOGENIC OBESITY
 Include abnormalities in genes involved in energy
expenditure & intake.
 More than 430 genes, chromosomal regions &
markers are associated with human obesity phenotypes.
 Fat mass & obesity associated (FTO) genes variants are
implicated in common form of obesity
 Other important genes are leptin, POMC & MCR4

24. CLASSIFICATION
• PRIMARY/CONSTITUTIONAL
 Most common type
 Cause is primarily nutritional & results from
imbalance betwwen energy intake & expenditure
• SECONDARY/ PATHOLOGIC
 Monogenic, endocrine, syndromic causes

25. HEALTH CONSEQUENCES OF
OBESITY

26. HEALTH CONSEQUENCES OF
OBESITY
• TYPE 2 DIABETES MELLITUS
 Most patients are obese
 Insulin resistance is strongest risk factor
 ADA (American Diabetes Association) suggests screening
of at risk children i.e. those with BMI >/= 85th percentile
plus >/= to 2 of the risk factors:
 High risk ethnic group
 Affected 1st/2nd degree relative
 Signs of insulin resistance
 Screening performed at puberty or 10yrs( whichever
occurs 1st) & thereafter every 3yrs.
If any symptom noticed screening can be done earlier.

27. • DYSLIPIDEMIA
• HYPERTENSION
 75% of HTN patients are obese hence obesity is most
common cause of pediatric hypertension.
• NON ALCOHOLIC FATTY LIVER DISEASE
 Prevalence in obese children & adolescents is 34.2%
 Aggravates hepatic insulin resistance, hence
increasing risk of developing T2DM

28. • METABOLIC SYNDROME
• Syndrome X, clustering of cardiovascular risks
• Characterized by
 Abdominal obesity ( WC>90th centile for age, gender, &
ethnicity) plus 2 or more of following
 Triglycerides more than 150mg/dl
 HDL <40mg/dl
 BP >/= 95th percentile adjusted for height, age & gender
 Fasting glucose >/=100mg/dl
• International Federation of Diabetes has proposed MS
should not be defined in children<10yrs

29. • POLYCYSTIC OVARY SYNDROME
 Excess adipocity, especially abdominal is associated
with hyperandrogenemia
• PSYCHIATRIC
 High rates of depression
 Low self esteem & anxiety
• MISCELLANEOUS
 More prone for orthopedic problems: Blount’s
disease & slipped capital epiphyses
 Prone for gallstones, pseudotumor cerebri &
obstructive sleep apnea.

32. EVALUATION OF OBESE
CHILDREN
• HISTORY: Onset (infancy or childhood)
 Infantile onset-> monogenic obesity
• Duration
• Rapidity of weight gain
• Recent increase in appetite with rapid weight gain
associated with headache/ visual disturbances ->
intracranial mass
• Antenatal history- GDM status
• Birth weight, SGA, LGA

33. • H/O developmental milestones : delayed motor
milestones, feeding difficulty during infancy F/B
voracious appetite suggests Prader-Willi syndrome
• Family history: obesity, DM, HTN & dyslipidemia
• Social/psychologic history: tobacco use, depression

34. • Environment
 Details of activity patterns
 Availability of safe play areas
 Duration of TV viewing
• Dietary history
 Diet details, total fat intake
 Total caloric intake
 Attitudes towards food

35. EVALUATION OF OBESE
CHILDREN
• HISTORY
HISTORY
Mental retardation Genetic etiology
Short stature, decreased height velocity Endocrine etiology
Medication Drugs
Snoring, morning headaches Obstructive sleep apnea
Knee or hip pain Orthopedic morbidity
Polyuria, polydipsia Type 2 DM
Hirsutism, irregular menses PCOS

36. EXAMINATION
• ANTHROPOMETRY
 BMI
 Waist to hip ratio
• Vital signs- blood pressure
• Head to toe
 Dysmorphic features-> genetic syndrome
 Cushingoid facies
 Papilledema
 Cranial nerve VI paralysis
 Hump on back
 Stretch striae

37.  Dry skin, enlarged thyroid gland
 Acanthosis nigricans
 Hirsutism & acne
 Shortening of 4th & 5th metacarpal->
pseudohypoparathyroidism
 Gynaecomastia
 Tanner staging- premature puberty
 Undescended testes & micropenis

39. DIFFERENCE BETWEEN CONSTITUTIONAL &
PATHOLOGIC OBESITY
CONSTITUTIONAL PATHOLOGICAL
AGE OF
ONSET
Usually 5-6yrs or peripubertal No age predilection
FAMILY
HISTORY
Present due similar socio-
demographic factors
Definite inheritance pattern
seen in genetic causes
EXAMINATIO
N
Proportional increase in weight
,height,
Fat distribution is proportionate
Dysmorphic features absent
No neurodevelopmental delay
Discordant growth due to
rapid weight gain &
faltering height
Fat distribution
disproportionate
Dysmorphic features may
be present
Neurodevelopmental delay
may be present
BONE AGE Normal Delayed
TREATMENT Responds to lifestyle measures Poor response to lifestyle
measures

40. METHODS FOR BODY FAT
ASSESSMENT
• BMI
• WAIST CIRCUMFERENCE
• WHR
• SKIN FOLD THICKNESS
• HYDRODENSITOMETRY( Underwater Weighing)
• ULTRASOUND
• BIOELECTRICAL IMPEDENCE
• DUAL ENERGY X RAY ABSORPTIOMETRY( DEXA)
 Gold standard

41. INVESTIGATIONS
• Routinely required
CBC, LFT, RFT, SE
Oral glucose tolerance test
In all children above 3yrs of age
• Fasting lipid levels
• Fasting glucose
• HBA1C
• SGPT
• Insulin levels

42. TO KNOW CAUSE OF
OBESITY
DISEASE SUSPECTED INVESTIGATION
Hypothyroidism FT4,TSH
Cushing syndrome Urine free cortisol, serum cortisol,
GH deficiency GH stimulation test, IGF-1
Genetic syndrome Genetic testiing
CNS disorder MRI brain
Monogenic obesity MC4R gene testing, leptin levels

43. IF COMORBIDITIES PRESENT
• Dyslipidemia - Fasting total cholesterol, HDL, LDL,
triglycerides
• Hypertension -Serial testing, urinalysis, electrolytes,
blood urea nitrogen, creatinine
• Type 2 diabetes mellitus -Fasting blood glucose,
hemoglobin A1c, insulin level, C-peptide
• Metabolic syndrome-Fasting glucose, LDL and HDL
cholesterol
• Polycystic ovary syndrome - Pelvic ultrasound, free
testosterone, LH, FSH

44. • Gallbladder disease - Ultrasound
• Nonalcoholic fatty liver disease (NAFLD) -AST, ALT,
ultrasound, CT, or MRI
• Pseudotumor cerebri -Cerebrospinal fluid opening
pressure, CT, MRI
• Blount disease - Knee x-rays
• Musculoskeletal problems -X-rays
• Slipped capital femoral epiphysis -Hip x-rays
• Obstructive sleep apnea- Polysomnography, hypoxia,
electrolytes

45. MANAGEMENT
• Diet modification
• Behavioural therapy
• Physical activity
• Pharmacotherapy
• Bariatric surgery

46. MANAGEMENT
1)DIET THERAPY
• Normal balanced pattern—fat intake less than 25% of
total calories, protein 15–20%, rest 55% as complex
carbohydrates
• Fibre and micronutrients, plenty of liquids.
• Weight loss of 0.5 kg/week
• Protein (0.8–1 g/kg/day)
• Avoid large meals with long gaps, and missed meals

47. • DIET STRATERGIES
 5 servings of fruits and vegetables everyday
 Minimize sugar-sweetened beverages, such as soda
and punches
 Prepare more meals at home rather than purchasing
restaurant food

48. DIET STRATEGIES
Eat the table as a family at least 5 or 6 times per week
Allow the child to self-regulate his or her meals
Avoid overly restrictive feeding behaviors

49. TRAFFIC LIGHT DIET PLAN
FEATURE GREEN LIGHT
FOODS
YELLOW LIGHT
FOODS
RED LIGHT
FOODS
QUALITY Low calorie, high
fibre, low fat,
nutrient dense
Nutrient dense
but higher in
calories & food
High in calories,
sugar & fat
TYPES OF FOOD Fruits &
vegetables
Lean meats, dairy
products,
starches, grains
Fatty meals
,sugar, sugar
sweetened
beverages, fried
foods
QUANTITY unlimited limited Infrequent or
avoided

50. 2)EXERCISE
• Active games-walking with friends, swimming,
dancing, and sports are encouraged
• Initially low impact, moderate-intensity exercise (30
minutes × 5 days/week)
• The time and intensity of exercise should be
increased to about an hour daily.
• Screen time should be less than 2 hours/day

51. 3)BEHAVIORAL MODIFICATION AND SOCIAL SUPPORT
This includes various techniques
❑ Monitoring
❑ Goal setting
❑ Stimulus control
❑ Social reinforcement

52. ❑Reward and punishment
❑Aversion therapy
❑ Managing high-risk situations
❑ Relapse prevention
• Initially a monthly review with reinforcement may be
necessary for a period of 3-6 months

53. MANAGEMENT
• Stepwise approach recommended by AMERICAN
ACADEMY OF PEDIATRICS
STAGE 1-PREVENTION PLUS
 Diet strategies
 Physical activity 1 hour daily
 Reinforce gaols
 Avoid extremely strict eating regimens
 Limit screen time <2hrs/day (no TV viwing for <2yrs
children)

54. • STAGE 2- If no improvement after 3months of stage 1
STRUCTURED WEIGHT MANAGEMENT
 Planned daily meals, 1 or 2 snacks with balanced
macronutrients
 Consumption of low energy density foods
 Reduce quantity & frequency of high energy density
foods
 Limit portion size
 Monthly patient-provider contact
 Positive reinforcement techniques
 Strong parental involvement for school going children

55. WEIGHT GOALS
• 2-5YRS - 85-94th: maintain weight until BMI is <85th
perentile/ slowing of weight gain
 >95th: maintain until BMI is <85th percentile ( weight
loss 0.5kg/month acceptable)
• 6-11yrs- 85-94th: until BMI <85th percentile/ slowing
of weight gain
 95-99th: gradual weight loss( 0.5kg/month)
 >99th : weight loss maximum 1kg/week

56. WEIGHT GOALS
• 12-18yrs – 85-94th with no health risks: weight
management
 85-94th with health risks: weight maintenance or
gradual weight loss
 95-99th : weight loss (max 1kg/week)
 >99th : weight loss (max 1kg/week)

57. • COMPREHENSIVE MULTIDISCIPLINARY INTERVENTION
 Same as stage 2, with diet & physical activity
structured to achieve negative energy balance
Weekly patient provider contact for at least 8-12weeks
Parent training in behavioral techniques to improve
home eating & activity environment

58. MANAGEMENT
• If fail to achieve weight goals after 3-6months of
stage 2
TERTIARY CARE INTERVENTION
 Pharmacotherapy
 Bariatric surgery
 Children falling in stage 2 intervention
 Should be willing to maintain healthy diet &
adequate physical activity

59. 4) PHARMACOTHERAPY
It should be considered only after
Significant efforts at diet, exercise and behavior control
have failed
As an add-on to these efforts
Medications have been used:
1)Orlistat- inhibits gastric & pancreatic lipases resulting in
reduced fat absorption
 Approved for more than12 years of age.
Side effects: fatty/oily stool, abdominal cramps, fecal
incontinence, reduced absorption of fat soluble vitamins

60. 1) Sibutramine is a serotonin reuptake inhibitor- FDA
approved for more than 16years age
3)Metformin (not approved by FDA)
• Indicated for T2DM children >10yrs
• Can also be used for obese girls with PCOS
• Reduces hepatic glucose production, increases
peripheral insulin sensitivity & decreases intestinal
absorption of glucose
• SE- nausea, vomiting, vitamin B12 deficiency

61. • Other drugs only in certain situations
 Growth hormone : Prader willi syndrome
 Octreotide: hypothalamic obesity
 Leptin: leptin deficiency
• Medications should be discontinued if there is no
0.4% reduction in BMI or BMI Z scores after taking
medications for 12weeks

62. BARIATRIC SURGERY
• Prerequisites ( Endocrine society recommendations)
 Adolescent with final or near final adult height &
Tanner stage 4-5
 BMI 40kg/m2 or BMI >35kg/m2 with significant
comorbidities
 Extreme obesity & persistance of comorbidities
despite lifestyle modification, with or without
pharmacotherapy trial

63. Patient has ability to maintain healthy dietary &
activity habits
Competent & stable family confirmed by
psychological evaluation
Access to experienced surgeon in medical centre
• CONTRAINDICATIONS
Preadolescents
Untreated psychiatric disorder
Unresolved eating disorder
Prader willi syndrome

64. PREVENTION
Overweight and obesity are becoming increasingly
common in children
• Measurement of BMI should be part of all health-
related visits of children, as well as of school health
programmes.
• Efforts should be made to increase awareness
regarding the health complications of childhood
obesity
• Children with obesity-related comorbidities should
have early intervention.

65. PREVENTIVE MEASURES
INFANCY
Breast feeding: exclusive BF up to 6months
• Continue BF for 12 months with other foods
FAMILIES
• Eat meals as a family in a fixed place & time
• Do not skip meals, especially breakfast
• Avoid junk food, aerated drinks and fried foods
• Encourage fruits, salads and whole dals and water as
drink
• Encourage physical activity
• Do not use food as a reward
• Controlled screen time: TV, computers, video games

66. • SCHOOLS
No sugary or sports drinks, juices, fried snacks
available in or near school
Install water fountains & hydration stations
Educate teachers regarding physical education,
nutrition
Educate children about appropriate diet & lifestyle
Mandate minimum standards for physical education
Encourage WALKING SCHOOL BUS : groups of
children walking to school with adult supervision
Identify, counsel those at risk/ already obese
Early referral if there is rapid weight gain

67. • COMMUNITIES
Increase family friendly exercise & safe play facilities
Discourage use of elevators & moving walkways
• HEALTHCARE PROVIDERS
Explain biologic & genetic contributions to obesity
Give age appropriate expectations for BMI
Work toward classifying obesity as disease &
providing treatment

68. • INDUSTRY
Mandate age appropriate nutrition labeling for
products aimed at children
Reduce portion size
Use celebrity advertizing directed at children for
healthful foods

69. • GOVERNMENT & REGULATORY AGENCIES
Fund healthy lifestyle programs
Provide financial incentives to industry to develop
healthful products
Ban toys as gift to children for purchasing fast foods
Ban advertising fast foods, junk foods

70. THANK YOU