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CHILDHOOD OBESITY
APPROACH AND MANAGEMENT
MODERATOR: DR. ARPITA GOGOI
Assistant Professor
Dept. of Pediatrics.
PRESENTED BY: DR. ABHISHEK SAINI. PGT
Assam Medical College & Hospital, Dibrugarh
INTRODUCTION
• Childhood obesity complex multifactorial
challenging problem in western world and
also in developing nations like India, most
common, in the urban populations.
• Obesity in childhood is a well established risk
factor for obesity in adulthood and lead to
medical complicationss so initiate prevention
and treatment programes during childhood.
TOPIC TO DISCUSSED
•
•
•
•
•

Definition
Epidemiology
Etiology
Pathophysiology
Health consequences of
obesity
• Evaluation of obesity
• Management
• Prevention
Obesity
Definition based on BMI
• Pediatrics
– Obese - BMI> 95th percentile for gender and age
– At risk/overweight - BMI=85-95th percentile

• Adults
–
–
–
–

Obese – BMI> 30
Overweight – BMI=25-30
Morbid obesity>40
Super obesity>60
( nelson 19TH )
EPIDEMIOLOGY
Obesity is a global health problem.

•
• More than 1.6 billion persons > 15 year are over weight or
obese.(WHO,2008)
• In children, the prevalence of obesity increased 300% over
approximately 40 years.(nelson 19th)
• 31% of children older than 2 yr to be overweight or obese, in
USA. .(NHANESIV ,nelson 19th).
• INDIA,prevalence delhi 26%(7-16yr),in chennai 22%(7-16yr).(IAP
mishra at 2006)
• In India obesity more in preadolescent and adolescent children
rich families, from urban areas and those with an obese parent
or sibling.
Obesity
Trends in children and adolescents (WHO)
20%

15%

2 -5 yrs
6 - 11 yrs
12 - 19 yrs

10%

5%

0%

1963- 1965

1966- 1970

1971- 1974

1976- 1980

1988- 1994

1999- 2002
ETIOLOGY (NELSON 19

ENVIRONM
ENTAL

OBESI
TY
GENETIC &
SYDROME

CONSTITUT
IONAL&
FAMILIAL

TH)
Etiology of obesity in children NELSON 19TH
Causes:
A) NON ORGANIC(95-96%)
• FAMILIAL OR CONSTITUTINAL
Parental obesity(obese mother),inheritance of BMR
• ENVIRONMENTAL CAUSES:
– Life style and pattern of eating
– Sedentary life styles
– TV viewing
– Drugs (anticonvulsants, antipsychotics, glucocorticoids)
– Caloric excess

• PSYCHOSOCIAL
– Psychiatric disturbances
– Depression and attention seeking behaviour
ETIOLOGY CONTD
• B)ORGANIC CAUSES(4-5%)
CNS CAUSE
– Tumours Craniopharyngioma
– Infection
– Surgery
– Trauma involving hypothalamus
– Post irradiation
ENDOCRINE
– Hypothyroidism
– cushing syndrome
– hyperinsulinism
– GH deficiency
– pseudohypoparathyroidism
SYNDROMES AND MUTATIONS ASSOCIATED WITH OBESITY
There are numerous complex syndromes in which obesity is
associated finding with other features.
DISEASE

SYMPTOMS

Alstrom syndrome

Cognitive impairment, retinitis pigmentosa,
diabetes mellitus, hearing loss,
hypogonadism, retinal degeneration

Bardet-Biedl syndrome

Retinitis pigmentosa, renal abnormalities,
polydactyly, hypogonadism

Down syndrome

Short stature, dysmorphic facies, mental
retardation
DISEASE

SYMPTOMS

Albright hereditary osteodystrophy

Short stature, skeletal defects, and impaired olfaction

Turner syndrome

Ovarian dysgenesis, lymphedema, web neck, short
stature, cognitive impairment

Fragile X syndrome

Mental retardation, hyperkinetic behavior,
macroorchidism,
large ears, prominent jaw, high-pitched jocular
speech

Prader-Willi Syndrome

Neonatal hypotonia, slow infant growth, small hands
and feet, mental retardation, hypogonadism,
hyperphagia leading to severe obesity, paradoxically
elevated ghrelin

RARE SYNDROMES

Leptin or leptin receptor gene deficiency,Cohen
sydrome,MC4R deficiency,PC1 deficiency,Borjesonfrossman-lehman syndrome,Simpson-golabi-behmal
type2,Ulnar mammary syndrome,Wilson turner
syndrome,
DIFFRENCES

(MEHARBAN SINGH)

FEATURES

CONSTITUTIONAL OR
FAMILIAL OBESITY

PATHOLOGICAL OR
ENDOCRINAL OBESITY

FAMILY HISTORY

MAY BE PRESENT

USUALLY ABESENT

EATING BEHAVIOR

EXCESSIVE OR FAST AND
FAULTY,LAZY LIFE STYLE

EATING NORMAL OR
ACTIVITY IS EFFECTED
AFTER THE ONSET OF
OBESITY

DISTRIBUTION OF FAT

GENERALIZED

“BUFFLO HUMP”BECAUSE
OF GREATER DEPOSITION
OF FAT OVER FACE AND
CERVICO-DORSAL AREA.

HEIGHT

USUALLY INCREASED
WITH ADVANCED BONE
AGE

USUALLY DECREASED
WITH RETARDED BONE
AGE

BLOOD PRESSURE

NORMAL

MAY BE RAISED
FEATURES

ENDOCRINAL EFFECTS

HYPOGONADISM

CNS FEATURES

CONSTITUTIONAL OR
FAMILIAL OBESITY

NIL

NONE BUT PENIS MAY BE
EMBEDDED IN PUBIC PAD
OF FAT

NONE

PATHOLOGICAL OR
ENDOCRINAL OBESITY

ACNE,HIRSUTISM,AMENOR
RHEA OR MENSTRUAL
IRREGULARITY

MAY BE ASSOCIATED WITH
SOME
SYNDROMES(PRADERWILLI SYDROME,ALSTROM
SYDROME etc.)

EXCESSIVE
SLEEPINESS,HYDROCEPHAL
US WITH VISUAL
DEFECTS,RETINAL
DEGENERATION etc.
PATHOPHYSIO LOGY (OF FOOD INTAKE)
NELSON 19TH and BROOKS PEDIATRIC ENDOCRINOLOGY

• Role of hypothalamus
• Leptin
• Ghrelin and other gastrointestinal
peptides.
• Biochemical changes
a) Energy balance. b)Dyslipidemia
c)Vascular disease d)metabolic syndrome
Role of hypothalamus
NEUROPEPTIDES
&
PEPTIDES
LEPTIN
&MELANOCORTIN

NEURAL CONTROL

PATHWAY

HYPOTHALAMUS
Principal polypeptides and proteins that may be
involved in regulation of food intake:

Increases food intake

Decreases food intake

Neuropeptide Y
Orexin –A
Orexin – B
β-endorphin
GHRH
Ghrelin

Leptin
POMC (esp MSH)
GI peptides like : peptide yy ,CCK
somatostatin ,glucagon
Neuropeptides in
hypothalamous like CART
Control of appetite
Arcuate nucleus
ACTION OF LEPTIN
Increased food intake
Decreased energy expenditure
Fat depots (AD tissue)
Increased fat deposition
Increased leptin synthesis

Inhibit

Hypothalamus
increased activation
of leptin receptors

Increased plasma
leptin conc.
GHRELIN AND OTHER GI PEPTIDE
• Ghrelin increases food intake ,produced in stomach.
• GI peptides inhibits food intake
peptide YY
glucagon
somatostatin
CCK
enterostatin.
BIOCHEMICAL CHANGES IN OBESITY
Components of energy balance:
• Energy intake: fat provide 9kcal/gm carbohydrate and protein
4kcal/gm.
• Energy expenditure:
– Resting metabolic rate + meal induced thermogenesis + physical
activity energy expenditure.
• Energy storage:
– When energy intake exceeds energy expenditure a state of +ve
energy balance occurs. .
• Even though obesity is the end result of positive energy balance
due to over eating and lack of physical activity, it is caused by many
complex and inter related factors. Major factors are:
– Elevated levels of free fatty acid
– Insulin resistance.
contd
• High levels of FFA lead several adverse metabolic
effects.
• The high FFA level may be due to two factors
Increased release of FFA from adipose tissue
Decreased uptake of FFA by other tissues

• Insulin resistance two factors:
Excess cytokines & TNF- by adipocyte
Resistin hormone by adipocyte

• FFA and cytokines produce B-CELL lipotoxicity
DYSLIPIDEMIA IN
OBESITY

• High TG
• Low HDL
• HighLDL
particles
• Increased VLDL
• related to the
elevated
FFA
level in obesity.

METABOLIC
SYNDROME(SYNDROME X)

•Obesity, dyslipidemia,
raised BP, insulin
resistance (with or
without
gluc.intolerance)& a
prothrombotic
inflammatory vascular
states.
•Increases the risk of C.V.
diseases in children at an
younger age& early death.
Vascular disease
CO-MORBIDITIES&HEALTH
CONSEQUENCES OF OBESITY(nelson 19
• People with a BMI of
25 or above have an
increased risk of
developing
comorbidities which is
further
increased
with BMI of>30

th)
DISEASE

POSSIBLE SYMPTOMS

LABORATORY CRITERIA

CARDIOVASCULAR
Dyslipidemia

Hypertension

HDL <40, LDL >130, total
cholesterol >200

Fasting total cholesterol, HDL,
LDL, triglycerides

SBP >95% for sex, age, height

Serial testing, urinalysis,
electrolytes, blood urea
nitrogen, creatinine

ENDOCRINE(CONSULT PEDIATRIC ENDOCRINOLOGIST)

Type 2 diabetes mellitus

Acanthosis nigrans, polyuria,
polydipsia

Fasting blood glucose >110,
hemoglobin, A1c, insulin level, Cpeptide, oral glucose tolerance
test

Metabolic syndrome

Central adiposity, insulin
resistance, dyslipidemia,
hypertension, glucose
intolerance

Fasting glucose, LDL and HDL
cholesterol

Polycystic ovary syndrome

Irregular menses, hirsutism,
acne, insulin resistance,
hyperandrogenemia

Pelvic ultrasound, free
testosterone, LH, FSH
GASTROINTESTINAL
Gallbladder disease

possible symptoms
Abdominal pain,
vomiting, jaundice

labortory criteria
Ultrasound

Nonalcoholic fatty liver
disease (NAFLD)
Hepatomegaly,
abdominal pain,
dependent edema, ↑
transaminases
Can progress to
fibrosis, cirrhosis

AST, ALT, ultrasound,
CT, or MRI

NEUROLOGIC
Pseudotumor cerebri

Cerebrospinal fluid
Headaches, vision
opening pressure, CT,
changes, papilledema
MRI
ORTHOPEDIC

POSSIBLE SYMPTOMS

LABORATORY CRITERIA

Blount disease (tibia vara)

Severe bowing of tibia, knee
pain, limp

Musculoskeletal problems

Back pain, joint pain, frequent
strains or sprains, limp, hip
X-rays
pain, groin pain, leg bowing

Slipped capital femoral
epiphysis

Hip pain, knee pain, limp,
decreased mobility of hip

Knee x-rays

Hip x-rays

PSYCHOLOGICAL

Behavioral complications

Anxiety, depression, low selfesteem, disordered eating,
signs of depression, worsening
Consult pediatric psychologist
school performance, social
isolation, problems with
bullying or being bullied
PULMONARY

POSSIBLE SYMPTOMS

LABORATORY CRITERIA

Asthma

Shortness of breath,
wheezing, coughing,
exercise intolerance

Obstructive sleep apnea

Polysomnography, hypoxia,
Snoring, apnea, restless
electrolytes (respiratory
sleep, behavioral problems acidosis with metabolic
alkalosis)

Pulmonary function tests,
peak flow
EVALUATION
NELSON 19TH and BROOKS PEDIATRIC ENDOCRINOLOGY

HISTORY

EXAMIN
ATION

OBESITY

SPECIAL
TESTS

LAB

INVESTI
GATION
ASSESMENT OF CHILD
• HISTORY
• AGE OF ONSET
•
•
•
•
•
•
•
•

DURATION OF OBESITY
DEVELOPMENTAL HISTORY
PERINATAL HISTORY
FAMILY PROFILE
LIFE STYLE(DIET,ACTIVITY,HABBITS)
PSYCHOLOGICAL PROFILE
PUBERTAL DEVELOPMENTAL
SPECIFIC CAUSES
CNS CAUSE,ENDOCRINE,DRUGS
ASSESMENT OF CHILD(CONTD)
• EXAMINATION
• GENERAL & SYSTEMIC
 ANTHROPOMETRY
OBESITY MEASUEMENTS
PARENTAL HEIGHT
SHORT STATURE
 SKIN
 FUNDUS EXAMINATION
 PUBERTAL STAGING
 DYSMORPHIA OR SKELETAL ABNOMALITIES
Obesity
Measurement
• Weight
• Weight:Height
• BMI
– kg m2

• Skin Thickness
• Waist:Hip Ratio
BMI
• Weight in kg divided by height in m2
• BMI has got good correlation with BP, blood lipids,
lipoproteins and can predict obesity and its comorbidities in young adults.
Weight for height/length:
in <2years or if BMI charts is not available W/L chart can be used.

>95 centile is obese. If both the charts are not available
– Wt. up to 120% of ideal body weight: over weight
– Wt. >120% of ideal body weight: obese

Waist hip ratio:
– >0.95 in males and >0.8 in females associated with significant
health risk like insulin resistance etc.
Skin fold thickness:
Most common site used is triceps.
In healthy children normal values 10mm or more.
Value >120% of age or >85 percentile indicate obesity.
• Accurate measurement of body fat is possible through
DEXA (dual energy x-ray absorptiometry), CT, MRI,
Ultrasonography
to
estimate
subcutaneous
and
intraabdominal fats.
Diagnostic algorithm
• BROOKS PEDIATRIC ENDOCRINOLOGY
DIAGNOSTIC TESTS FOR EVALUATION OF OBESITY
• ROUTINE:
Fasting sugar, lipid profile & LFT;
• SPECIFIC:
Serum insulin ; in non syndromic cases.
Thyroid function test; when suspicion of hypothyroidsm
Urine free cortisol: features of cushing
Growth hormone: short sature, hypoglycemia ,micropenis.
Karyotype/FISH: dysmorphic features/Syndromes
Urine specific gravity or osmolality: Polydipsia
Androgens: hirsutism, oligomenorrhea, amenorrhea,
MRI or CT of brain: Hyperphagia, polydipsia, and polyuria,
headaches, visual complaints.
MANAGEMENT (nelson 19

th)

• Diet ,lifestyle changes,exercise and behaviour
modification are the corner stone of therapy.
• Anorectic drugs and surgery to be avoided in
childhood obesity.
• Pathological causes treated separtely.
GUIDELINES FOR MANAGEMENT
DO:
• Interview parents and child at length
• Examine child thoroughly
• Calculate BMI and ideal body weight
• Chart height for weight
• Record waist – hip ration and triceps skinfold thickness
• Obtain detailed diet diary
• Obtain detailed activity chart of child and family
• Baseline lab work
• Prescribe low fat, low caloric, high fibre, small frequent meals –
allowing enough calories for growth
• Prescribe activity that is aerobic, sustained and interesting.
GUIDELINES FOR MANAGEMENT (contd…)
DO NOT:
• Allow the parents to discuss the child in front of the
child and his or her sibling
• Encourage use of terms like fat, obese etc.
• Do extensive lab work to rule out rare conditions.
• Be harsh or insensitive if weight reduction progress is
not satisfactory.
DIETARY MANAGMENT
•
•
•
•
•

Education of parents and children
Avoid strict “negative dieting”
Avoid rapid weight loss.
Maintain food diary.
Avoid energy dense,high fat,fried food,fast
foods,non nutritive sweet drinks.
• Inclusion of food without processing,with
nutritive value and high fiber.
• Whole family follow diet modifications.
CATEGORIZATION OF FOOD- STUFFS
• traffic light diet plan groups food into categories.
– ‘RED’ FOODS; sweets, puddings, chocolates, ice-creams,
fried foods,red meat, nuts. As far as possible
consumption should be avoided.
– ‘YELLOW FOODS’ ; whole grain breads, lentils , beans,
sweet potatoes, vegetables cooked with minimum fat.
Should be consumed in limited amount
– ‘GREEN FOODS’ ; most fruits , vegetables, fat free
milk/cheese , fish. Can be consumed in unlimited
quantities.
( nelson 19th)
PHYSICAL ACTIVITY
•
•
•
•
•
•
•

Decrease sedantary activities,TV watching.
Increase daily routine activities.
Activities fit into life style prefered.
Sports and games prefered.
Consider weight bearing exercises.
Develop a daily exercise routine.
Gradually increase time and intensity exercise.
PHSICAL ACTIVITY
START SLOWLY WITH 30 MINS/DAY,MODERATE
INTENSITY EXERCISE

GRADUALLY INCREASE SESSIONS OF 45
MINS/DAY

INCREASE TIME AND INTENSITY EXERCISE
60 MINS/DAY 5 DAYS/WEEK(MULTIPLE
SEESIONS)
BEHAVIORAL MODIFICATIONS
•
•
•
•
•
•
•
•

Develop a daily exercise routine & diet chart.
Self monitoring; maintain diet & exercise diary.
Regular Counseling with positive reinforcement.
Encouragement & rewards for good performance
Education regarding foods calories & food options
Limiting TV viewing, video games, &net surfing
Build self confidence, positive attitude.
Support by families & friends.
FOLLOW UP GOALS
100 kcal deficit/day could lead to
5kg loss over one year.
BMI>95TH

CHILD

CHILD

2-7 YR

<2YR

NO
COMPLICATIONS

COMPLICATIONS
WT

MAINTAIN
BASELINE

WT
MAINTENANCE

LOSS

WT
CHILD>7 YEAR

BMI 85TH-95TH
NO

BMI>95TH
OR

COMPLICATIONS

COMPLICATIONS

WT MAINTENANCE

WT LOSS
DRUG THERAPY
• Drug therapy is not recommended for appetite suppression in
children & adolescents.
• 2 drugs approved for obesity in adults orlistat & sibutramine.
• Drug shouldnot be used as the sole element of treatment.

• Drug treatment is discontinued if wt. loss is < 5% after the first
12 weeks or if the pt. gains wt. at any time during the treatment.
• Insulin sensitizers, like metformin have been used in adult.
DRUGS

MECHANISM OF ACTION

SIDE EFFECTS

Bupropion

Appetite suppressant:
mechanism unknown

Paresthesia, insomnia, central
nervous system effects

Fluoxetine

Appetite suppressant:
Agitation, nervousness,
selective serotonin reuptake
gastrointestinal
inhibitor

Sertraline

Appetite suppressant:
Agitation, nervousness,
selective serotonin reuptake
gastrointestinal
inhibitor

Topiramate

Mechanism unknown

Paresthesia, changes in taste

Zonisamide

Mechanism unknown

Somnolence, dizziness,
nausea
DRUG

MECHANISM OF ACTION

SIDE EFFECTS

Sibutramine*[†]

Appetite suppressant:
combined norepinephrine
and serotonin reuptake
inhibitor

Modest increases in heart
rate and blood pressure,
nervousness, insomnia

Phentermine*[†]

Appetite suppressant:
sympathomimetic amine

Cardiovascular,
gastrointestinal

Diethylpropion*[†]

Appetite suppressant:
sympathomimetic amine

Palpitations, tachycardia,
insomnia, gastrointestinal

Orlistat*

Lipase inhibitor: decreased
absorption of fat

Diarrhea, flatulence,
bloating, abdominal pain,
dyspepsia
BARIATRIC SURGERY
• INDICATION
Children with BMI>40,more than 15 year of
age with medical complications
resulting from obesity,after they have failed
six months of a multidisciplinary weight
management program.
nelson 19th
BARIATRIC SURGERY
.

• Surgical options include
Gastric bypass or Roux- en-y
bypass(RYGB)

•

It include partial gastrectomy
creating small stomach pouch
Into which a distial segment of
jejunem is inserted.
CONTD
• Laproscopic Adjustable gastric banding(LAGB)
Gastric banding utilizes a prosthetic band to encircle the
proximal stomach. The ability to adjust band tension as
stomach volume changes provides an important
advantage .
PREVENTION (NELSON 19
• Children’s with risk
factor obesity(1 or both
obese parents, obese
siblings, maternal
age>35yr at birth, single
child ,single parent)
should be focused early.
• Consider obesity as a
disease & not , only as a
cosmetic problem

TH)
Nelson,19th

Proposed Suggestions for the Prevention of Obesity
PREGNANCY
• Normalize body mass index beforepregnancy.
Do not smoke.
• Maintain moderate exercisee as tolerated.
• In gestational diabetics, provide meticulous glucose
control
POSTPARTUM AND INFANCY
• Breast-feeding is preferred for a minimum of 3 mo.
• Postpone the introduction of solid foods and sweet
liquids.
.
CONTD
FAMILIES
• Eat meals as a family in a fixed place and time.
• No television during meals.
• Avoid unnecessary sweet or fatty foods and soft
drinks.
• Remove televisions from children's bedrooms;

SCHOOL
• Educate teachers & chidren in school.
• Mandate physical excercise 30–45 min/day,23/week.
• Encourage “the walking schoolbus”:
Contd.
COMMUNITIES
•
•

Avoid use of elevators and moving walkways.
Avoid culture-specific foods. (high fat)

HEALTH CARE PROVIDERS
• Biological and genetic counselling.
• Early recognition,proper care,provide treatment.

INDUSTRY and GOVERNMENT
•
•
•
•

Mandate nutrition labeling for products
Use celebrity advertising.
Start government- sponsored nutritional programs.
Ban advertising of fast foods.
CONCLUSION
• Obesity is a challenging & frustrating medical problem.
The results of treatment for obesity are generally poor
and disappointing. Prevention is the only hope to
decrease the incidence.

• Childhood is a critical period for the initiation of
obesity & therefore is the ideal time for the beginning
preventive programmes . A team approach with
involvement by families, school authorities, health care
providers, & governmental bodies are needed for
ensuring the health of the community.
THANK YOU

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Childhood Obesity Approach and Management

  • 1. CHILDHOOD OBESITY APPROACH AND MANAGEMENT MODERATOR: DR. ARPITA GOGOI Assistant Professor Dept. of Pediatrics. PRESENTED BY: DR. ABHISHEK SAINI. PGT Assam Medical College & Hospital, Dibrugarh
  • 2. INTRODUCTION • Childhood obesity complex multifactorial challenging problem in western world and also in developing nations like India, most common, in the urban populations. • Obesity in childhood is a well established risk factor for obesity in adulthood and lead to medical complicationss so initiate prevention and treatment programes during childhood.
  • 3. TOPIC TO DISCUSSED • • • • • Definition Epidemiology Etiology Pathophysiology Health consequences of obesity • Evaluation of obesity • Management • Prevention
  • 4. Obesity Definition based on BMI • Pediatrics – Obese - BMI> 95th percentile for gender and age – At risk/overweight - BMI=85-95th percentile • Adults – – – – Obese – BMI> 30 Overweight – BMI=25-30 Morbid obesity>40 Super obesity>60 ( nelson 19TH )
  • 5. EPIDEMIOLOGY Obesity is a global health problem. • • More than 1.6 billion persons > 15 year are over weight or obese.(WHO,2008) • In children, the prevalence of obesity increased 300% over approximately 40 years.(nelson 19th) • 31% of children older than 2 yr to be overweight or obese, in USA. .(NHANESIV ,nelson 19th). • INDIA,prevalence delhi 26%(7-16yr),in chennai 22%(7-16yr).(IAP mishra at 2006) • In India obesity more in preadolescent and adolescent children rich families, from urban areas and those with an obese parent or sibling.
  • 6. Obesity Trends in children and adolescents (WHO) 20% 15% 2 -5 yrs 6 - 11 yrs 12 - 19 yrs 10% 5% 0% 1963- 1965 1966- 1970 1971- 1974 1976- 1980 1988- 1994 1999- 2002
  • 7. ETIOLOGY (NELSON 19 ENVIRONM ENTAL OBESI TY GENETIC & SYDROME CONSTITUT IONAL& FAMILIAL TH)
  • 8. Etiology of obesity in children NELSON 19TH Causes: A) NON ORGANIC(95-96%) • FAMILIAL OR CONSTITUTINAL Parental obesity(obese mother),inheritance of BMR • ENVIRONMENTAL CAUSES: – Life style and pattern of eating – Sedentary life styles – TV viewing – Drugs (anticonvulsants, antipsychotics, glucocorticoids) – Caloric excess • PSYCHOSOCIAL – Psychiatric disturbances – Depression and attention seeking behaviour
  • 9. ETIOLOGY CONTD • B)ORGANIC CAUSES(4-5%) CNS CAUSE – Tumours Craniopharyngioma – Infection – Surgery – Trauma involving hypothalamus – Post irradiation ENDOCRINE – Hypothyroidism – cushing syndrome – hyperinsulinism – GH deficiency – pseudohypoparathyroidism SYNDROMES AND MUTATIONS ASSOCIATED WITH OBESITY There are numerous complex syndromes in which obesity is associated finding with other features.
  • 10. DISEASE SYMPTOMS Alstrom syndrome Cognitive impairment, retinitis pigmentosa, diabetes mellitus, hearing loss, hypogonadism, retinal degeneration Bardet-Biedl syndrome Retinitis pigmentosa, renal abnormalities, polydactyly, hypogonadism Down syndrome Short stature, dysmorphic facies, mental retardation
  • 11. DISEASE SYMPTOMS Albright hereditary osteodystrophy Short stature, skeletal defects, and impaired olfaction Turner syndrome Ovarian dysgenesis, lymphedema, web neck, short stature, cognitive impairment Fragile X syndrome Mental retardation, hyperkinetic behavior, macroorchidism, large ears, prominent jaw, high-pitched jocular speech Prader-Willi Syndrome Neonatal hypotonia, slow infant growth, small hands and feet, mental retardation, hypogonadism, hyperphagia leading to severe obesity, paradoxically elevated ghrelin RARE SYNDROMES Leptin or leptin receptor gene deficiency,Cohen sydrome,MC4R deficiency,PC1 deficiency,Borjesonfrossman-lehman syndrome,Simpson-golabi-behmal type2,Ulnar mammary syndrome,Wilson turner syndrome,
  • 12. DIFFRENCES (MEHARBAN SINGH) FEATURES CONSTITUTIONAL OR FAMILIAL OBESITY PATHOLOGICAL OR ENDOCRINAL OBESITY FAMILY HISTORY MAY BE PRESENT USUALLY ABESENT EATING BEHAVIOR EXCESSIVE OR FAST AND FAULTY,LAZY LIFE STYLE EATING NORMAL OR ACTIVITY IS EFFECTED AFTER THE ONSET OF OBESITY DISTRIBUTION OF FAT GENERALIZED “BUFFLO HUMP”BECAUSE OF GREATER DEPOSITION OF FAT OVER FACE AND CERVICO-DORSAL AREA. HEIGHT USUALLY INCREASED WITH ADVANCED BONE AGE USUALLY DECREASED WITH RETARDED BONE AGE BLOOD PRESSURE NORMAL MAY BE RAISED
  • 13. FEATURES ENDOCRINAL EFFECTS HYPOGONADISM CNS FEATURES CONSTITUTIONAL OR FAMILIAL OBESITY NIL NONE BUT PENIS MAY BE EMBEDDED IN PUBIC PAD OF FAT NONE PATHOLOGICAL OR ENDOCRINAL OBESITY ACNE,HIRSUTISM,AMENOR RHEA OR MENSTRUAL IRREGULARITY MAY BE ASSOCIATED WITH SOME SYNDROMES(PRADERWILLI SYDROME,ALSTROM SYDROME etc.) EXCESSIVE SLEEPINESS,HYDROCEPHAL US WITH VISUAL DEFECTS,RETINAL DEGENERATION etc.
  • 14. PATHOPHYSIO LOGY (OF FOOD INTAKE) NELSON 19TH and BROOKS PEDIATRIC ENDOCRINOLOGY • Role of hypothalamus • Leptin • Ghrelin and other gastrointestinal peptides. • Biochemical changes a) Energy balance. b)Dyslipidemia c)Vascular disease d)metabolic syndrome
  • 16. Principal polypeptides and proteins that may be involved in regulation of food intake: Increases food intake Decreases food intake Neuropeptide Y Orexin –A Orexin – B β-endorphin GHRH Ghrelin Leptin POMC (esp MSH) GI peptides like : peptide yy ,CCK somatostatin ,glucagon Neuropeptides in hypothalamous like CART
  • 19. ACTION OF LEPTIN Increased food intake Decreased energy expenditure Fat depots (AD tissue) Increased fat deposition Increased leptin synthesis Inhibit Hypothalamus increased activation of leptin receptors Increased plasma leptin conc.
  • 20. GHRELIN AND OTHER GI PEPTIDE • Ghrelin increases food intake ,produced in stomach. • GI peptides inhibits food intake peptide YY glucagon somatostatin CCK enterostatin.
  • 21. BIOCHEMICAL CHANGES IN OBESITY Components of energy balance: • Energy intake: fat provide 9kcal/gm carbohydrate and protein 4kcal/gm. • Energy expenditure: – Resting metabolic rate + meal induced thermogenesis + physical activity energy expenditure. • Energy storage: – When energy intake exceeds energy expenditure a state of +ve energy balance occurs. . • Even though obesity is the end result of positive energy balance due to over eating and lack of physical activity, it is caused by many complex and inter related factors. Major factors are: – Elevated levels of free fatty acid – Insulin resistance.
  • 22. contd • High levels of FFA lead several adverse metabolic effects. • The high FFA level may be due to two factors Increased release of FFA from adipose tissue Decreased uptake of FFA by other tissues • Insulin resistance two factors: Excess cytokines & TNF- by adipocyte Resistin hormone by adipocyte • FFA and cytokines produce B-CELL lipotoxicity
  • 23. DYSLIPIDEMIA IN OBESITY • High TG • Low HDL • HighLDL particles • Increased VLDL • related to the elevated FFA level in obesity. METABOLIC SYNDROME(SYNDROME X) •Obesity, dyslipidemia, raised BP, insulin resistance (with or without gluc.intolerance)& a prothrombotic inflammatory vascular states. •Increases the risk of C.V. diseases in children at an younger age& early death.
  • 25. CO-MORBIDITIES&HEALTH CONSEQUENCES OF OBESITY(nelson 19 • People with a BMI of 25 or above have an increased risk of developing comorbidities which is further increased with BMI of>30 th)
  • 26. DISEASE POSSIBLE SYMPTOMS LABORATORY CRITERIA CARDIOVASCULAR Dyslipidemia Hypertension HDL <40, LDL >130, total cholesterol >200 Fasting total cholesterol, HDL, LDL, triglycerides SBP >95% for sex, age, height Serial testing, urinalysis, electrolytes, blood urea nitrogen, creatinine ENDOCRINE(CONSULT PEDIATRIC ENDOCRINOLOGIST) Type 2 diabetes mellitus Acanthosis nigrans, polyuria, polydipsia Fasting blood glucose >110, hemoglobin, A1c, insulin level, Cpeptide, oral glucose tolerance test Metabolic syndrome Central adiposity, insulin resistance, dyslipidemia, hypertension, glucose intolerance Fasting glucose, LDL and HDL cholesterol Polycystic ovary syndrome Irregular menses, hirsutism, acne, insulin resistance, hyperandrogenemia Pelvic ultrasound, free testosterone, LH, FSH
  • 27. GASTROINTESTINAL Gallbladder disease possible symptoms Abdominal pain, vomiting, jaundice labortory criteria Ultrasound Nonalcoholic fatty liver disease (NAFLD) Hepatomegaly, abdominal pain, dependent edema, ↑ transaminases Can progress to fibrosis, cirrhosis AST, ALT, ultrasound, CT, or MRI NEUROLOGIC Pseudotumor cerebri Cerebrospinal fluid Headaches, vision opening pressure, CT, changes, papilledema MRI
  • 28. ORTHOPEDIC POSSIBLE SYMPTOMS LABORATORY CRITERIA Blount disease (tibia vara) Severe bowing of tibia, knee pain, limp Musculoskeletal problems Back pain, joint pain, frequent strains or sprains, limp, hip X-rays pain, groin pain, leg bowing Slipped capital femoral epiphysis Hip pain, knee pain, limp, decreased mobility of hip Knee x-rays Hip x-rays PSYCHOLOGICAL Behavioral complications Anxiety, depression, low selfesteem, disordered eating, signs of depression, worsening Consult pediatric psychologist school performance, social isolation, problems with bullying or being bullied
  • 29. PULMONARY POSSIBLE SYMPTOMS LABORATORY CRITERIA Asthma Shortness of breath, wheezing, coughing, exercise intolerance Obstructive sleep apnea Polysomnography, hypoxia, Snoring, apnea, restless electrolytes (respiratory sleep, behavioral problems acidosis with metabolic alkalosis) Pulmonary function tests, peak flow
  • 30. EVALUATION NELSON 19TH and BROOKS PEDIATRIC ENDOCRINOLOGY HISTORY EXAMIN ATION OBESITY SPECIAL TESTS LAB INVESTI GATION
  • 31. ASSESMENT OF CHILD • HISTORY • AGE OF ONSET • • • • • • • • DURATION OF OBESITY DEVELOPMENTAL HISTORY PERINATAL HISTORY FAMILY PROFILE LIFE STYLE(DIET,ACTIVITY,HABBITS) PSYCHOLOGICAL PROFILE PUBERTAL DEVELOPMENTAL SPECIFIC CAUSES CNS CAUSE,ENDOCRINE,DRUGS
  • 32. ASSESMENT OF CHILD(CONTD) • EXAMINATION • GENERAL & SYSTEMIC  ANTHROPOMETRY OBESITY MEASUEMENTS PARENTAL HEIGHT SHORT STATURE  SKIN  FUNDUS EXAMINATION  PUBERTAL STAGING  DYSMORPHIA OR SKELETAL ABNOMALITIES
  • 33. Obesity Measurement • Weight • Weight:Height • BMI – kg m2 • Skin Thickness • Waist:Hip Ratio
  • 34. BMI • Weight in kg divided by height in m2 • BMI has got good correlation with BP, blood lipids, lipoproteins and can predict obesity and its comorbidities in young adults.
  • 35. Weight for height/length: in <2years or if BMI charts is not available W/L chart can be used. >95 centile is obese. If both the charts are not available – Wt. up to 120% of ideal body weight: over weight – Wt. >120% of ideal body weight: obese Waist hip ratio: – >0.95 in males and >0.8 in females associated with significant health risk like insulin resistance etc.
  • 36. Skin fold thickness: Most common site used is triceps. In healthy children normal values 10mm or more. Value >120% of age or >85 percentile indicate obesity. • Accurate measurement of body fat is possible through DEXA (dual energy x-ray absorptiometry), CT, MRI, Ultrasonography to estimate subcutaneous and intraabdominal fats.
  • 37. Diagnostic algorithm • BROOKS PEDIATRIC ENDOCRINOLOGY
  • 38.
  • 39.
  • 40. DIAGNOSTIC TESTS FOR EVALUATION OF OBESITY • ROUTINE: Fasting sugar, lipid profile & LFT; • SPECIFIC: Serum insulin ; in non syndromic cases. Thyroid function test; when suspicion of hypothyroidsm Urine free cortisol: features of cushing Growth hormone: short sature, hypoglycemia ,micropenis. Karyotype/FISH: dysmorphic features/Syndromes Urine specific gravity or osmolality: Polydipsia Androgens: hirsutism, oligomenorrhea, amenorrhea, MRI or CT of brain: Hyperphagia, polydipsia, and polyuria, headaches, visual complaints.
  • 41. MANAGEMENT (nelson 19 th) • Diet ,lifestyle changes,exercise and behaviour modification are the corner stone of therapy. • Anorectic drugs and surgery to be avoided in childhood obesity. • Pathological causes treated separtely.
  • 42. GUIDELINES FOR MANAGEMENT DO: • Interview parents and child at length • Examine child thoroughly • Calculate BMI and ideal body weight • Chart height for weight • Record waist – hip ration and triceps skinfold thickness • Obtain detailed diet diary • Obtain detailed activity chart of child and family • Baseline lab work • Prescribe low fat, low caloric, high fibre, small frequent meals – allowing enough calories for growth • Prescribe activity that is aerobic, sustained and interesting.
  • 43. GUIDELINES FOR MANAGEMENT (contd…) DO NOT: • Allow the parents to discuss the child in front of the child and his or her sibling • Encourage use of terms like fat, obese etc. • Do extensive lab work to rule out rare conditions. • Be harsh or insensitive if weight reduction progress is not satisfactory.
  • 44. DIETARY MANAGMENT • • • • • Education of parents and children Avoid strict “negative dieting” Avoid rapid weight loss. Maintain food diary. Avoid energy dense,high fat,fried food,fast foods,non nutritive sweet drinks. • Inclusion of food without processing,with nutritive value and high fiber. • Whole family follow diet modifications.
  • 45. CATEGORIZATION OF FOOD- STUFFS • traffic light diet plan groups food into categories. – ‘RED’ FOODS; sweets, puddings, chocolates, ice-creams, fried foods,red meat, nuts. As far as possible consumption should be avoided. – ‘YELLOW FOODS’ ; whole grain breads, lentils , beans, sweet potatoes, vegetables cooked with minimum fat. Should be consumed in limited amount – ‘GREEN FOODS’ ; most fruits , vegetables, fat free milk/cheese , fish. Can be consumed in unlimited quantities. ( nelson 19th)
  • 46. PHYSICAL ACTIVITY • • • • • • • Decrease sedantary activities,TV watching. Increase daily routine activities. Activities fit into life style prefered. Sports and games prefered. Consider weight bearing exercises. Develop a daily exercise routine. Gradually increase time and intensity exercise.
  • 47. PHSICAL ACTIVITY START SLOWLY WITH 30 MINS/DAY,MODERATE INTENSITY EXERCISE GRADUALLY INCREASE SESSIONS OF 45 MINS/DAY INCREASE TIME AND INTENSITY EXERCISE 60 MINS/DAY 5 DAYS/WEEK(MULTIPLE SEESIONS)
  • 48. BEHAVIORAL MODIFICATIONS • • • • • • • • Develop a daily exercise routine & diet chart. Self monitoring; maintain diet & exercise diary. Regular Counseling with positive reinforcement. Encouragement & rewards for good performance Education regarding foods calories & food options Limiting TV viewing, video games, &net surfing Build self confidence, positive attitude. Support by families & friends.
  • 49. FOLLOW UP GOALS 100 kcal deficit/day could lead to 5kg loss over one year.
  • 52. DRUG THERAPY • Drug therapy is not recommended for appetite suppression in children & adolescents. • 2 drugs approved for obesity in adults orlistat & sibutramine. • Drug shouldnot be used as the sole element of treatment. • Drug treatment is discontinued if wt. loss is < 5% after the first 12 weeks or if the pt. gains wt. at any time during the treatment. • Insulin sensitizers, like metformin have been used in adult.
  • 53. DRUGS MECHANISM OF ACTION SIDE EFFECTS Bupropion Appetite suppressant: mechanism unknown Paresthesia, insomnia, central nervous system effects Fluoxetine Appetite suppressant: Agitation, nervousness, selective serotonin reuptake gastrointestinal inhibitor Sertraline Appetite suppressant: Agitation, nervousness, selective serotonin reuptake gastrointestinal inhibitor Topiramate Mechanism unknown Paresthesia, changes in taste Zonisamide Mechanism unknown Somnolence, dizziness, nausea
  • 54. DRUG MECHANISM OF ACTION SIDE EFFECTS Sibutramine*[†] Appetite suppressant: combined norepinephrine and serotonin reuptake inhibitor Modest increases in heart rate and blood pressure, nervousness, insomnia Phentermine*[†] Appetite suppressant: sympathomimetic amine Cardiovascular, gastrointestinal Diethylpropion*[†] Appetite suppressant: sympathomimetic amine Palpitations, tachycardia, insomnia, gastrointestinal Orlistat* Lipase inhibitor: decreased absorption of fat Diarrhea, flatulence, bloating, abdominal pain, dyspepsia
  • 55. BARIATRIC SURGERY • INDICATION Children with BMI>40,more than 15 year of age with medical complications resulting from obesity,after they have failed six months of a multidisciplinary weight management program. nelson 19th
  • 56. BARIATRIC SURGERY . • Surgical options include Gastric bypass or Roux- en-y bypass(RYGB) • It include partial gastrectomy creating small stomach pouch Into which a distial segment of jejunem is inserted.
  • 57. CONTD • Laproscopic Adjustable gastric banding(LAGB) Gastric banding utilizes a prosthetic band to encircle the proximal stomach. The ability to adjust band tension as stomach volume changes provides an important advantage .
  • 58. PREVENTION (NELSON 19 • Children’s with risk factor obesity(1 or both obese parents, obese siblings, maternal age>35yr at birth, single child ,single parent) should be focused early. • Consider obesity as a disease & not , only as a cosmetic problem TH)
  • 59. Nelson,19th Proposed Suggestions for the Prevention of Obesity PREGNANCY • Normalize body mass index beforepregnancy. Do not smoke. • Maintain moderate exercisee as tolerated. • In gestational diabetics, provide meticulous glucose control POSTPARTUM AND INFANCY • Breast-feeding is preferred for a minimum of 3 mo. • Postpone the introduction of solid foods and sweet liquids. .
  • 60. CONTD FAMILIES • Eat meals as a family in a fixed place and time. • No television during meals. • Avoid unnecessary sweet or fatty foods and soft drinks. • Remove televisions from children's bedrooms; SCHOOL • Educate teachers & chidren in school. • Mandate physical excercise 30–45 min/day,23/week. • Encourage “the walking schoolbus”:
  • 61. Contd. COMMUNITIES • • Avoid use of elevators and moving walkways. Avoid culture-specific foods. (high fat) HEALTH CARE PROVIDERS • Biological and genetic counselling. • Early recognition,proper care,provide treatment. INDUSTRY and GOVERNMENT • • • • Mandate nutrition labeling for products Use celebrity advertising. Start government- sponsored nutritional programs. Ban advertising of fast foods.
  • 62. CONCLUSION • Obesity is a challenging & frustrating medical problem. The results of treatment for obesity are generally poor and disappointing. Prevention is the only hope to decrease the incidence. • Childhood is a critical period for the initiation of obesity & therefore is the ideal time for the beginning preventive programmes . A team approach with involvement by families, school authorities, health care providers, & governmental bodies are needed for ensuring the health of the community.