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.
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OBESITY IN CHILDREN: CAUSES, COMPLICATIONS & MANAGEMENT
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
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
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.
30.
31.
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
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
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
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