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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.
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.
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.
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.
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
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.
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.
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.
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.