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Childhood obesity Dr Michal Ajzensztejn The Evelina London Children’s Hospital July 2014.

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Presentation on theme: "Childhood obesity Dr Michal Ajzensztejn The Evelina London Children’s Hospital July 2014."— Presentation transcript:

1 Childhood obesity Dr Michal Ajzensztejn The Evelina London Children’s Hospital July 2014

2 Overview  Definition  Size of the problem?  Aetiology  What is the cause for concern?  Management  prevention  Investigation  Treatment

3 Definition of obesity  Gold standard is body composition  MRI / Dexa / bioimpedence (proxy)  Waist circumference  BMI = Kg/M² A child's weight status is determined using an age- and sex-specific percentile for BMI rather than the BMI categories used for adults because children's body composition varies as they age and varies between boys and girls.

4 Definition Obesity expert committee- pediatrics 1998 Overweight: th Centile Obese: >95 th Centile International Obesity Task Force Overweight>91 st centile Obese>99 th centile

5 International obesity task force definition (IOTF) Cole et al BMJ 2000;320:1  Centiles for body mass index for British males and females. Centile curves are spaced two thirds of z score apart. Also shown are body mass index values of 25 and 30 kg/m2 at age 18, with extra centile curves drawn through them

6 Types of obesity in childhood

7 The scale of the problem  WHO- childhood obesity one of the most serious global public health challenges of 21 st century.  The National Child Measurement Program (CCMP) measures the height and weight of ~1M school children in England/yr. Latest figures show:  14.4% of children aged 10-11yrs – obese  18.9% of children aged 10-11yrs- overweight  9.3% of children aged 4-5yrs – obese  13% of children aged 4-5yrs - overweight. 1/3 rd of 10-11yrs old + >1/5 th of 4-5 yr olds were overweight or obese.  According to the National Audit Office- weight problems costs the Health Service £500million in consultations, drugs and other therapies.  Obesity causes 30,000 deaths a year.  Research from British Heart Foundation suggests children and young people could die from complications of obesity before their parents  By 2030 up to 48% of men and 43% of women in the UK could be obese if current trends in rise of obesity continue

8 Trends in adult prevalence of obesity (BMI > 30kg/m2)

9 Trend in childhood obesity US children

10 Causes of primary obesity  Interaction between genetic predisposition (50- 90%)& environment affecting food intake and energy expenditure  Twin studies offer some insight into the genetics of common obesity  Data from > 25,000 twin pairs and 50,000 biological and adoptive family members  Estimates for mean correlations for BMI are:  0.74 for monozygotic twins,  0.32 for dizygotic twins  0.25 for siblings  0.19 for parent–offspring pairs,  0.06 for adoptive relatives  0.12 for spouses

11 Environmental factors Increase risk  History of SGA- increased rates of obesity and metabolic syndrome  Poor infant feeding  Reduced energy expenditure  Social concerns- fear to let children play outside  Parental obesity/ eating disorders  Increased high fat / carb food intake  Increased sedentary lifestyle  Screen time (TV, computers, phones, ipad) Protective factors  Family meals  Self esteem  Breastfeeding

12 Foetal origin hypothesis “Barker Hypothesis”  ‘Foetal undernutrition in middle to late gestation leads to disproportionate foetal growth’ programmes later coronary heart disease’  ‘The most unfavourable outcome is thinness at birth followed by a rapid increase in body weight ’

13 Foetal programming  The way the mother prepares the foetus for the world in which it will be born  A communication through placental nutrition  Nutrition may alter the expression of maternal genes involved in foetal growth – ‘imprinting’ – gene methylation  The ‘Thrifty Phenotype’ - a mismatch between fetal programming and the environment

14 Genetics  Polygenic inheritance pattern with 2 subtypes (generalised and abdominal)  multiple polymorphic single genes likely involved  no genes for common obesity identified  very rare monogenic forms of obesity  Gene defects  ob/ob mouse – genes mutant – leptin deficient  db/db mouse- mutation in leptin receptor  POMC/ MC4R / neuronal insulin receptor mutations

15 Genetics Of Obesity Study (GOOS) Cambridge Sadaf Farooqi and Stephen O’Rahilly  BMI >4SDs for age /sex  Consanguineous or  FH of early onset < 10 yrs  Over 3000 samples analysed

16 Monogenic causes of obesity  Leptin deficiency  Leptin receptor deficiency  Hypogonadotrophin hypogonadism and other pituitary hormone abnormalities  Prohormone convertase1 (PC1) defect  Abnormal glucose tolerance  Hypocortisolism, hypog/hypog.  Melanocortin – 4-receptor defect  POMC deficiency  Red hair, adrenal insufficiency  PPARγ defect

17 Ghrelin  Hunger-stimulating peptide  produced by P/D1 cells in lining of the fundus of stomach  Ghrelin receptors are expressed in the pituitary, stomach, intestine + pancreas.  Gherlin levels increase before meals and decrease post meals  When a person loses weight-  ghrelin levels, which causes  food consumption and weight gain  When a person gains weight  ghrelin levels, causing a  in food consumption and weight loss

18 Leptin "satiety hormone"  Leptin is made by adipose tissue, it acts via receptors in the brain (LRb) to regulate energy balance and satiety.  Leptin stimulates the hypothalamus to give us the sensation of satiety resulting in decreased appetite and increases metabolism to aid wt loss.  The less fat you have, the less leptin you produce, resulting in increased appetite and decreased metabolism to enables wt gain.  However if you have increased fat stores there is increased leptin, which can lead to leptin resistance. So despite lots of leptin, appetite is not suppressed, metabolism is slowed down resulting in increased appetite and wt gain.

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20 Medical causes of obesity  Endocrine  Hypothyroid  Cushing syndrome  Pseudohypoparathyroidism  PCOS  Monogenic  Leptin deficiency  POMC deficiency  MC4R mutation 5% BMI>3 or 4SD  Hypothalamic  Eg tumours/craniopharyngioma  Syndromes  Prader-Willi  Bardel-Biedl  Cohen  Carpenter

21 Why is childhood obesity getting so much attention!  Tracking into adult life( 60%)  Metabolic syndrome (IRS)  Secondary effects

22 Implications of childhood obesity  Obese children become obese adults  Comorbidities:  Hypertension  Metabolic syndrome: hyperlipidaemia  PCOS  Non-alcoholic fatty liver  Insulin resistance/ impaired fasting and glucose tolerance  Type 2 DM  Slipped femoral capital epiphysis/ joint pain  Sleep apnea  Asthma  Benign raised intracranial pressure  Emotional + psychological effects of being overweight  Teasing/ bullying  Low self esteem  Anxiety  Depression

23 Insulin resistance Syndrome  Metabolic syndrome (syndrome X)  Central obesity (apple shape)  Hypertension  Raised triglycerides  Low HDL  Insulin resistance PCOS  Steatohepatitis  Glomerulonephritis  Atherosclerosis  Impaired glucose tolerance

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25 Insulin resistance syndrome  A velvety brown change to the skin  Mostly in neck, axilla, groin  Looks like dirt but doesn’t wash off!  Usually obese  Almost always have insulin resistance  Leads to Type 2 diabetes

26 Local problem  In 2000, the first cases of Type 2 diabetes in children were diagnosed in overweight girls aged 9 to 16 of Pakistani, Indian or Arabic origin in the UK.  Nationally incidence of type 2 diabetes amongst children is 1.5%  In Lambeth and Southwark the incidence of type 2 is closer to 5%.

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28 Obesogenic Environement Family Excess weight in parents Breast feeding practices Parent’s health Much Sedentary activity e.g TV, computers etc. Knowledge Budgeting, shopping and cooking skills Genetic predisposition Education & information School lessons Lifestyles Nutrition Cooking Media messages Fashions Body image Cultural beliefs Conflicting information Sports & Leisure Lack of school facilities Few local playing areas Widely available indoor- passive entertainment Unsafe streets Few cycle routes

29 Social + economic inequalities in diet and physical activity

30 Management  Primary Prevention  Community based weight management service  Tertiary obesity service  Severe obesity  Obesity with co-morbidities

31 Primary Prevention  Ante-natal care of the obese mother  Use of appropriate standards  WHO-UK Growth charts  Focus on early intervention (under 5s)  Education of midwives and HVs  Better infant feeding advice  Promotion of breast feeding  Better management of SGA/IUGR infants

32 Community based services  Not just an issue for health workers- community-wide approach  Input from education, LAs, sports bodies and voluntary groups  Specialised school nurse  An Information Resource  Educators  Give basic dietary advice  Risk assessment for referral  MEND- Mind, Exercise, Nutrition, Do it / Ready Steady Go  Planning permission- locality of sweet shops / fast food shops to schools  Media + Advertising companies- also have a duty

33 Tertiary level  Severe ‘morbid’ obesity  Pre-diabetic, insulin resistance, Type 2 diabetes  Adverse FH diabetes, ↑BP, ↑cholesterol, Ischaemic heart disease  Health co-morbidities  Cardiac  Renal  Neurological/muscular disorders  Steroids induced  Monogenic / syndrome

34 Tertiary service  Multi-disciplinary team  Psychologist / Family therapy  Dietician  Sports trainer  Paediatrician  ?Social worker  An initial team assessment  Motivational Interviewing skills  Understanding eating behaviours  Fuller family analysis

35 Classification for Investigation  Primary obesity with no family risk  Primary obesity with adverse family risk or signs/ suspicion of hyperinsulinism/ type II diabetes  Suspicion of secondary obesity/ genetic cause

36 Investigations  Simple obesity with no adverse family risk If well grown in height and normal on examination:  liver & renal function +/- liver USS  TFT  Fasting lipids  Fasting glucose/insulin  blood pressure (ambulatory if possible)  Simple obesity with family risk history or clinical suspicion of hyperinsulinism  As above plus  OGTT with insulins  Secondary / genetic cause  Investigate cause Eg UFC for cushings. Overnight Dex suppression test  Genetics for GOOS study

37 Who to treat?  Those with BMI > IOTF 30  Those with BMI >IOTF 25 with  strong family history diabetes/early CVD  impaired glucose tolerance  Age:  Rx should focus on >8 yrs  Those obese < 8yrs with obese parents IOTF- international obesity task force

38 Treatment  Treatment of obesity  Diet  Drugs  Exercise programs  Psychological approaches  Multi-disciplinary approaches  Surgery- Bariatric surgery / intragastric balloon  Treatment of obesity complications

39 Treatment targets  5% loss is standard adult weight loss target  10% is doing very well!  but losses are maintained better in children than adults  Weight maintenance in growing children  Imperative to start Rx before growth ceases

40 Treatment of Choice  comprehensive treatments including:  behavioral modification procedures  dietary intervention  an exercise program  reduction of sedentary behaviours  family centred  motivational enhancement

41 Drugs Drug trials for obesity in children & adolescents  Extremely few published  Drugs not licensed  We cannot assume risks and benefits same as in adult

42 What’s available  Orlistat – binds intestinal and pancreatic lipase and reduces dietary fat absorption by 30%  2.5 kg to 3.0 kg over 3-4 yrs. Compared with placebo  Reduces absorption of fat soluble vitamins  Metformin – useful in diabetes, impaired glucose intolerance and possibly insulin resistance  May improve cardiovascular outcome and reduce risk of PCOS/ metabolic syndrome

43 Surgery  UK: NICE guidelines recommend consideration of surgery for young people in exceptional circumstances  “Surgery...has the best chance of significant weight loss, reversal or improvement of current co-morbidities, and reduction of risk for future co- morbidities” Brown &Inge 2009

44 Criteria for Bariatric Surgery in children  BMI of 40 (kg/m 2 ) or more - OR  BMI >30 + other significant disease  All non-surgical measures have failed for at least 6 months  Receiving intensive management in a specialist service  Generally fit for anaesthesia and surgery  Commitment to long-term follow-up  Physiological and psychological maturity

45 Bariatric Surgery  Types  Gastric banding  Gastric bypass  Gastric sleeve surgery  No surgery without risk- High risk group  Post surgical complications  Long term follow up  Long term supplement therapy

46 Intragastric balloon Rx?  Less invasive  No long term complications  However are the results as sustainable?

47 The Evelina London Children’s Hospital obesity service  Still in the job planning phase  Will integrate community to tertiary level care  Bridge between medical and surgical intervention  Provide intragastric balloons  Multidisciplinary team:  Psychological/ family approach  Dietician  Sport/ activity  Nurse  Doctor  Speciality care: sleep study, orthopaedic, referral to King’s for liver and bariatric surgery

48 Thank you QUESTIONS?


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