ppt on obesity

1. OBESITY AND OVERWEIGHT

2. 1. Definition
2. Epidemiology
3. Pathophysiology
4. Etiology
5. Obesity Associated Co morbidities
6. Intervention and Management
7. Prevention
8. References
CONTENTS

3.  Obesity is defined using Body Mass Index.
 BMI = Weight in Kg/ (Height in meters)2
 Obesity and overweight are defined using
BMI percentiles for children ≥ 2years and
weight/length percentiles for <2 year old.
 The criterion for obesity is BMI ≥95TH
percentile, and overweight between 85th
to
95th
percentile
Definition1

4. Available methods of body fat/body
composition assessment

6. During childhood, levels
of body fat change
begin with high adiposity
during infancy,
decreases for
approximately 5.5 years
until adiposity rebound,
adiposity then increases
until early adulthood
Fig. Source: Developed by the National Centre for Health Statistics in
collaboration with the National centre for chronic disease prevention and
Health Promotion (2000) http://www.cdc.gov/growthcharts

7.  According to NFHS-5 report, the prevalence
of overweight children under 5 years of age
has increased from 2.1% (2015-2016) to
3.4% (2019-2021)2
 According to the WHO, approximately 39
million under 5 year old children are
overweight or obese2
 The Global Burden of Disease report shows
that in India, 11.5% children were overweight
in 2017 and is projected to increase to 17.5%
by 20302

8.  Appetite and satiety control is a complex interplay
between leptin and ghrelin with support from other
cytokine and hormones.
 During fasting, low leptin levels increase appetite and
decrease energy expenditure by stimulating
neuropeptide-Y synthesis, inhibiting sympathetic and
other catabolic pathways.
 During feeding, increased leptin levels decrease appetite
and increase energy expenditure through release of
melanocortin and corticotropin-releasing hormone (CRH).
 Both leptin and insulin enter the brain and act as
inhibitors of food intake, activate thermogenesis and
inhibit the production of propiomelanocortin (POMC)
which has catabolic properties.
PATHOPHYSIOLOGY

10. ETIOLOGY
CONSTITUTI
ONAL 95%
ENDOCRINE
DRUGS
GENETIC
HYPOTHA
LAMIC
MONOGENIC
DISORDERS

11. FEATURE CONSTITUTIONAL PATHOLOGICAL
PATTERN GENERALISED CENTRAL
GROWTH RATE ACCELERATED RETARDED
SKELETAL MATURITY ADVANCED RETARDED
DYSMORPHIC FEATURES ABSENT MAY BE PRESENT
ENDOCRINE FEATURES ABSENT MAY BE PRESENT
CONSTITUTIONAL VS PATHOLOGICAL
OBESITY

12.  Constitutional obesity: 95% etiology, tall for age,
proportionate obesity and normal development.
 Endocrine:
1. Cushing syndrome- Central obesity, hirsutism,
moon face, hypertension.

13. 1. GH deficiency- short stature and slow
linear growth
2. Hypothyroidism- short stature, weight
gain, fatigue, constipation, cold
intolerance

14.  Genetic causes: Some examples include
1. Prader Willi Syndrome- Partial deletion of
chromosome 15 or partial loss
Neonatal hypotonia, slow infant growth, small
hands and feet, mental retardation,
hypogonadism, hyperphagia

17.  Monogenic obesity is associated with a
single gene mutation (e.g., a mutation in the
leptin/melanocortin pathway, resulting in
severe obesity). Eg, Melanocortin-4 receptor
(MC4R) and others such as ADCY5, ETV5,
KCTD15, GNPDA2 and TMEM18 loci.
 Polygenic obesity results from a complex
interaction of multiple genetic, social,
environmental, and behavioral influences,
e.g., single nucleotide polymorphisms of the
PSMA6 and PSMA3 proteosomal genes
affecting gene expression.

18. HYPOTHALAMIC CAUSES

19. MEDICATIONS ASSOCIATED WITH OBESITY
1. PREDNISOLONE AND OTHER GLUCOCORTICOIDS
2. THIORIDAZINE
3. OLANZAPINE
4. CLOZAPINE
5. QUETAPINE
6. RISPERIDONE
7. LITHIUM
8. AMITRIPTYLINE AND OTHER TCA
9. VALPROATE
10.CARBAMAZEPINE
11.GABAPENTIN
12.PROPANOLOL AND OTHER BETA BLOCKERS
DRUGS

20. APPROACH TO A CASE OF OBESITY
BMI> 95TH
PERCENTILE
HISTORY AND PHYSICAL EXAMINATION
ABNORMAL
ANTIPSYCHOTIC DRUG
USE
NORMAL
REEVALUATE DRUG
THERAPY/ CHOICE EVALUATE FOR
OBESITY CO
MORBIDITIES
IF YES, INITIATE LIFE
STYLE CHANGES AND
TREAT CO MORBIDITY
IF NO, INITIATE
LIFESTYLE CHANGES
CONTINUE WEIGHT
GAIN> 6 MONTHS,
CONSIDER
PHARMACOTHERAPY
AND SURGERY

21. ABNORMAL
GENETIC
EVALUATION
ENDOCRINE
EVALUATION
CNS INJURY
NEURODEVELOPMENTAL
ABNORMALITIES
ATTENUATED
GROWTH VELOCITY
YES, KARYOTYPE: DNA
METHYLATION STUDY
IS THERE DEVELOPMENTAL DELAY?
HYPOTHALAMIC
OBESITY
YES, PRADER
WILLI SYNDROME
NO, MEASURE LEPTIN,
INSULIN, PROINSULIN
LEPTIN RECEPTOR
DEFICIENCY, MC4R
DEFICIENCY
MOLECULAR
GENETIC STUDY
YES, CONGENITAL
LEPTIN
DEFICIENCY,
PCSK1 DEFN
RETINAL
DYSTROPHY,
PHOTOPHOBIA,
NYSTAGMUS?
NO, ALBRIGHTS
HERIDITARY
OSTEODYSTROPH,
BDNF
YES, BARDET BIEDL
SYNDROME, TUB
DEFICIENCY

22. INVESTIGATIONS

23. Non pharmacological management

24.  The AAP recommends no television viewing for less
than 2-yearsold and the advised screen time
(inclusive of television, computer and internet)
should not exceed more than 1–2 hours per day for
older children.
 Younger children and toddlers should have daily half
to one hour of outdoor play. Older children should
have moderate to vigorous exercise for 60 minutes
daily of which 30 minutes should be during school
time.
 Sleep should be sufficient and timings should be
regular. Sleep debt is associated with decrease leptin
and increase ghrelin levels leading to obesity
 Exclusive breastfeeding for 6 months and breastfeed
for 12 months in infants

25.  The Expert Committee on Prevention and Pediatric
Obesity (Endocrine Society Clinical Practice Guidelines)
recommends the use of drugs on individualized
assessment after conservative trial (generally for 6
months) has failed.
 Pharmacotherapy has been prescribed in children above
16 years of age who suffer from obesity-related
complications.
 The only drug which has been approved by US Food
and Drug Administration (FDA) is orlistat, and for use in
12–16 years old adolescents with obesity.
 ORLISTAT 120MG PO TID BEFORE MEALS
(Pancreatic Lipase Inhibitor)
PHARMACOLOGICAL

26.  The two commonly used procedures are
 1. Laparoscopic adjustable gastric banding (LAGB)
 2. Roux-en-Y gastric bypass (RYGB).
They may be offered to adolescents
 who have completed puberty (at least Tanner stage 4 or
5) with failed attempts to reduce weight by conservative
methods with or without a trial of pharmacotherapy for at
least 6 months
 BMI more than 50 kg/m2 in the absence of any
comorbidity
 BMImore than 40 kg/m2 and comorbidities like type 2
diabetes, obstructive sleep apnea or pseudotumor cerebri.
Surgical

27. The Global Strategy on Diet, Physical Activity and Health
(DPAS) was developed by the WHO in 2004. The four main
objectives were:
1. To encourage the implementation of public health action
and preventative intervention to reduce the risk factors
resulting from unhealthy diet and physical inactivity.
2. To increase recognition of the implications of unhealthy diet
and inadequate physical activity levels and knowledge of
preventative measures.
3. To promote policies and action plans at all levels to address
diet and physical activity behaviors.
4. To encourage monitoring, evaluation and further research.
The preventive strategies at individual level include changes
in diet, lifestyle and physical activity as well as behavior

28. 1. TEXTBOOK OF NELSON
2. Saha J, Chouhan P, Ahmed F, Ghosh T, Mondal
S, Shahid M, Fatima S, Tang K.
Overweight/Obesity Prevalence among Under-
Five Children and Risk Factors in India: A Cross-
Sectional Study Using the National Family
Health Survey (2015-2016). Nutrients. 2022 Sep
1;14(17):3621
3. PIYUSH GUPTA TEXTBOOK OF PAEDIATRICS
REFERENCES

29. THANK YOU