1. CHILDHOOD OBESITY

2. CRITERIA FOR OBESITY Body mass index (BMI)
BMI= Weight (Kg) / Height (m)2
BMI more than 85th percentile - Overweight
BMI more than 95th percentile – Obese
BMI is a good indicator of body fat
BMI is unreliable in short muscular individuals

3. Weight for height
Weight for height compares the child’s weight to the expected weight for his/her height
Weight for height more than 120% - Obese

4. Skin fold thickness
Skin fold thickness (SFT)– indicator of subcutaneous fat.
Measured over subscapular, triceps or biceps region.
Age specific cut-offs should be used.
SFTmore than 85th percentile is considered as abnormal.

5. Waist circumference Marker of abdominal adiposity.
Key risk factor for metabolic and cardiovascular effects of obesity.

6. INCIDENCE &PREVALENCE

7. ETIOLOGY CONSTITUTIONAL OBESITY ENVIRONMENTAL FACTORS ENDOCRINE CAUSES
HYPOTHALAMIC OBESITY
DRUGS
GENETIC SYNDROMES
MONOGENIC DISORDERS

8. CONSTITUTIONAL OBESITY
Over 95% of all cases
Imbalance in energy intake and expenditure
Proportional obesity
Tall for age
Normal development
Avoid unnecessary investigations
Family history

9. ENVIRONMENTAL FACTORS
Excessive calorie intake
Sedentary lifestyle
Television viewing
Computer games
Decreased physical
activity

10. ENDOCRINE CAUSES Cushing syndrome Hypothyroidism GH Deficiency
Pseudohypoparathyroidism
Growth failure in obese child is an important indicator

11. Cushing syndrome Central obesity Hypertension Striae
Retarded skeletal maturation
Hirsutism
Myopathy

12. Hypothyroidism Rare cause of isolated obesity Developmental delay
Coarse skin
Retarded skeletal maturation
Constipation
Cold intolerance etc

13. GH Deficiency Short stature Body proportions are normal
Immature facies “doll like”
Delayed teeth development
Bone age is delayed

14. Pseudohypoparathyroidism
Growth retardation
Hypocalcemia
Round facies
Brachydactyly
Brachymetacarpia
Subcutaneous calcifications
Bony deformities

15. DRUGS Antiepileptic drugs Steroids Estrogen Glucocorticoids,
sulfonylureas,
MAOIs
oral contraceptives,
risperidone,
clozapine

16. HYPOTHALAMIC OBESITY Head injury Infection Brain tumors Radiation
Post-neurosurgery

17. HYPOTHALAMIC OBESITY Excessive appetite
Signs & symptoms of CNS involvement
Hypothalamic pituitary defects

18. GENETIC SYNDROMES Prader willi syndrome
Laurence Moon Biedle Bardet syndrome
Beckwith weidmann syndrome
Carpenter syndrome

19. Prader willi syndrome Infantile hypotonia Hyperphagia Almond like eyes
Behavioural abnormality
Hypogonadism

20. Laurence Moon Biedle Bardet syndrome
Hypogonadism
Retinitis pigmentosa
Polydactyly mental retardation
Type 2 diabetes mellitus
Renal abnormalities

21. Beckwith weidmann syndrome
Organomegaly
Earlobe creases
hemihypertrophy

22. MONOGENIC DISORDERS Leptin deficiency Leptin resistance
Abnormalities of MC4R & proconvertase

24. EVALUATION
History
Age of onset – use of growth charts and family photographs. Early onset (_5 years of age) suggests a genetic cause
Duration of obesity – short history suggests endocrine or central cause

25. History(cont….)
A history of damage to the CNS (e.g. infection, trauma, hemorrhage, radiation therapy, seizures) suggests hypothalamic obesity with or without pituitary GH deficiency or pituitary hypothyroidism.

26. History(cont….)
A history of morning headaches, vomiting, visual disturbances and excessive urination or drinking also suggests that the obesity may be caused by a tumor or mass in the hypothalamus

27. History(cont….)
A history of dry skin, constipation, intolerance to cold or fatigue suggests hypothyroidism.
Mood disturbance and central obesity suggest Cushing syndrome.
Frequent infections and fatigue may suggest ACTH deficiency due to POMC mutations

28. History(cont….)
Hyperphagia – often denied but sympathetic approach needed and specific questions, such as waking at night to eat and/or demanding food very soon after a meal, suggest hyperphagia. If severe, especially in children, suggests a genetic cause for obesity

29. History(cont….)
Developmental delay – milestones, educational history, behavioral disorders.
Consider craniopharyngioma or structural causes(often relatively short history) and genetic causes

30. History(cont….)
Visual impairment and deafness can suggest genetic causes
Onset and tempo of pubertal development – onset can be early or delayed in children and adolescents.
Primary hypogonadotropic hypogonadism or hypogenitalism associated with some genetic disorders

31. History(cont….)
Family history – consanguineous relationships, other children affected, family photographs useful.
Severity may differ due to environmental effects
Treatment with certain drugs or medications. Glucocorticoids, sulfonylureas, MAOIs oral contraceptives, risperidone, clozapine

32. Examination Document weight and height compared with normal centiles.
Calculate BMI and WHR (in adults). In children, obtain parentalheights and weights where possible
Head circumference if clinically suggestive

33. Examination(cont…)
Short stature or a reduced rate of linear growth in a child with obesity suggests the possibility of GH deficiency, hypothyroidism, cortisol excess, pseudohypoparathyroidism or a genetic syndrome such as Prader–Willi syndrome

34. Examination(cont…)
Obese children and adolescents are often tall (on the upper centiles), however, accelerated linear growth (height SDS >2) is a feature of MC4R deficiency
Body fat distribution – central distribution with purple striae suggests Cushing syndrome.
Selective fat deposition (60%) is a feature of leptin and leptin receptor deficiency
Dysmorphic features or skeletal dysplasia

35. Examination(cont…)
Pubertal development/secondary sexual characteristics.
Most obese adolescents grow at a normal or excessive rate and enter puberty at the appropriate age; many mature more quickly than children with normal weight, and bone age is commonly
advanced.
In contrast, growth rate and pubertal development are diminished or delayed in GH deficiency, hypothyroidism, cortisol excess and a variety of genetic syndrome.
Conversely, growth rate and pubertal development are accelerated in precocious puberty and in some girls with PCOS

36. Examination(cont…) Acanthosis nigricans
Valgus deformities - in severe childhood obesity
Hair color – red hair (if not familial) may suggest mutations in POMC (pro-opiomelanocortin) in white Caucasians

37. Investigations
Fasting and 2-h post glucose and insulin levels. Proinsulin if PC1( prohormone convertase 1) deficiency considered
Fasting lipid panel for detection of dyslipidemia
Thyroid function tests
Serum leptin if indicated

38. Investigations(cont…)
Karyotype
DNA for molecular diagnosis
Bone age
GH secretion and function tests, when indicated
Assessment of reproductive hormones, when indicated

39. Investigations(cont…)
Serum calcium, phosphorus and parathyroid hormone levels to evaluate for suspected pseudohypoparathyroidism
MRI scan of the brain with focus on the hypothalamus and pituitary, when clinically indicated

42. Screening for glucose intolerance and the metabolic syndrome in children and adolescents.
High-risk populations
Obese (BMI z-score >95th percentile) children or adolescent, plus
High-risk ethnic group and/or
Family history of type 2 diabetes or GDM and/or
Acanthosis nigricans and/or
Prominent abdominal fat deposition
Ovarian hyperandrogenism

43. Fasting glucose and insulin levels
Screening for glucose intolerance and the metabolic syndrome in children and adolescents
Screening procedures
Blood pressure
Fasting glucose and insulin levels
Fasting lipid panel (_FFA if possible)
2-h glucose level (_insulin if possible)
HbA1c (less useful)

44. COMPLICATIONS CNS – Benign intracranial hypertension
Respiratory – Obstructive sleep apnea
Cardiovascular – Atherosclerosis, Hypertension
Hepatobiliary – Nonalcoholic steatohepatitis,
gall stones
Endocrine – PCOD, Type 2 DM, Dislipidemia
Orthopedic – Osteoarthritis, slipped capital femoral epiphyses

45. Management Treatment of obesity aims to:
Reduce BMI and visceral fat mass;
Decrease circulating insulin concentrations;
Increase insulin sensitivity
Decrease hepatic glucose production and fasting and post-prandial glucose concentrations;

46. Management( cont…) Reduce circulating FFA and TG concentrations;
Decrease blood pressure;
Reduce the expression of inflammatory cytokines;
Normalize vascular and endothelial function

47. Management( cont…) Dietary measures 30-40% caloric restriction
Improve nutritive value of diet
Reduction in consumption of junk food, carbonated drink , saturated fat
Increase in fiber, fruits, vegetables.

48. Management( cont…) Lifestyle modification
Increase in physical activities min/day
Swimming
Running
Playing outdoors

49. Management( cont…) Drugs Orlistat – gastric lipase inhibitor
Sibutramine – neurotransmitter modulator
Metformin – in children with insulin resistance
Leptin – for leptin deficiency
Octreotide – for hypothalamic obesity

50. Surgery Indicated for morbid obesity BMI>40 kg/m2
Last resort in treatment
Laparoscopic gastric banding-
procedure of choice
directed at reducing gastric capacity

51. Learning Points There is a global epidemic of obesity
A very few obese children have a monogenic cause of their condition
Consequences of obesity include insulin resistance and type 2 diabetes, dyslipidemia, hepatic steatosis/steatohepatitis (fatty liver), hypertension, focal glomerulosclerosis, accelerated growth and bone maturation, ovarian hyperandrogenism, gynecomastia,
cholecystitis, pancreatitis and pseudotumorcerebri

52. Learning Points Non-metabolic complications include sleep apnea,
orthopedic disorders and stress incontinence
Long-standing obesity and insulin resistance
increase the risk of cardiovascular disease, stroke,
orthopedic complications, sleep apnea, some
malignancies and psychosocial disorders in adults
Treatment is by lifestyle intervention (including
behavior therapy), pharmacotherapy and
surgery but success is very limited
Prevention is better than cure

53. Thank you