Childhood obesity

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

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Childhood obesity. Dr Michal Ajzensztejn The Evelina London Children’s Hospital July 2014. Overview. Definition Size of the problem? Aetiology What is the cause for concern? Management prevention Investigation Treatment. Definition of obesity. Gold standard is body composition - PowerPoint PPT Presentation

Transcript of Childhood obesity

Page 1: Childhood obesity

Childhood obesityDr Michal AjzensztejnThe Evelina London Children’s Hospital July 2014

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OverviewDefinition

Size of the problem?

Aetiology

What is the cause for concern?

ManagementpreventionInvestigationTreatment

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Definition of obesityGold standard is body composition MRI / Dexa / bioimpedence (proxy)Waist circumference BMI = Kg/M²A 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.

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DefinitionObesity expert

committee- pediatrics 1998

Overweight: 85-95th Centile

Obese: >95th Centile

International Obesity Task Force

Overweight>91st centileObese>99th centile

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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

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Types of obesity in childhood

Primary

SecondaryEndocrine Hypothyroidism Cushings syndrome pseudohypoparathyroidismHypothalamic MonogenicSyndromes

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The scale of the problem WHO- childhood obesity one of the most serious global public health

challenges of 21st 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.1/3rd of 10-11yrs old + >1/5th 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

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

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Trend in childhood obesity US children 1971-2006

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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

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Environmental factors Increase riskHistory of SGA- increased rates of obesity and metabolic syndromePoor infant feedingReduced energy expenditureSocial concerns- fear to let children play outsideParental obesity/ eating disordersIncreased high fat / carb food intakeIncreased sedentary lifestyle

Screen time (TV, computers, phones, ipad)Protective factorsFamily mealsSelf esteemBreastfeeding

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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’

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Foetal programming

The way the mother prepares the foetus for the world in which it will be born

A communication through placental nutritionNutrition 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

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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

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Genetics Of Obesity Study (GOOS) Cambridge

Sadaf Farooqi and Stephen O’Rahilly

BMI >4SDs for age /sexConsanguineous or

FH of early onset < 10 yrsOver 3000 samples analysed

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Monogenic causes of obesityLeptin deficiencyLeptin receptor deficiency

Hypogonadotrophin hypogonadism and other pituitary hormone abnormalities

Prohormone convertase1 (PC1) defect Abnormal glucose tolerance Hypocortisolism, hypog/hypog.

Melanocortin – 4-receptor defectPOMC deficiency

Red hair, adrenal insufficiencyPPARγ defect

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GhrelinHunger-stimulating peptide produced by P/D1 cells in lining of the fundus

of stomachGhrelin receptors are expressed in the

pituitary, stomach, intestine + pancreas.Gherlin levels increase before meals and

decrease post mealsWhen 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

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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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Medical causes of obesityEndocrine

HypothyroidCushing syndromePseudohypoparathyroidismPCOS

MonogenicLeptin deficiencyPOMC deficiencyMC4R mutation 5% BMI>3 or 4SD

Hypothalamic Eg tumours/craniopharyngioma

SyndromesPrader-WilliBardel-BiedlCohenCarpenter

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Why is childhood obesity getting so much attention!

Tracking into adult life( 60%)Metabolic syndrome (IRS)Secondary effects

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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

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Insulin resistance SyndromeMetabolic syndrome (syndrome X)Central obesity (apple shape)HypertensionRaised triglyceridesLow HDL Insulin resistance PCOSSteatohepatitisGlomerulonephritisAtherosclerosis Impaired glucose tolerance

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Insulin resistance syndrome

A velvety brown change to the skinMostly in neck, axilla, groinLooks like dirt but doesn’t wash off!Usually obeseAlmost always have insulin resistanceLeads to Type 2 diabetes

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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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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

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Social + economic inequalities in diet and physical activity

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ManagementPrimary Prevention

Community based weight management service

Tertiary obesity serviceSevere obesityObesity with co-morbidities

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Primary PreventionAnte-natal care of the obese motherUse of appropriate standards

WHO-UK Growth chartsFocus on early intervention (under 5s)

Education of midwives and HVsBetter infant feeding advicePromotion of breast feedingBetter management of SGA/IUGR

infants

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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

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Tertiary levelSevere ‘morbid’ obesityPre-diabetic, insulin resistance, Type 2

diabetesAdverse FH diabetes, ↑BP, ↑cholesterol,

Ischaemic heart diseaseHealth co-morbidities

CardiacRenalNeurological/muscular disordersSteroids induced

Monogenic / syndrome

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Tertiary serviceMulti-disciplinary team

Psychologist / Family therapyDieticianSports trainerPaediatrician?Social worker

An initial team assessmentMotivational Interviewing skillsUnderstanding eating behavioursFuller family analysis

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Classification for InvestigationPrimary 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

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InvestigationsSimple obesity with no adverse family

riskIf well grown in height and normal on

examination: liver & renal function +/- liver USSTFTFasting lipidsFasting glucose/insulin blood pressure (ambulatory if possible)

Simple obesity with family risk history or clinical suspicion of hyperinsulinismAs above plusOGTT with insulins

Secondary / genetic cause Investigate cause Eg UFC for cushings. Overnight

Dex suppression test Genetics for GOOS study

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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 yrsThose obese < 8yrs with obese parents

IOTF- international obesity task force

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TreatmentTreatment of obesity

DietDrugsExercise programsPsychological approachesMulti-disciplinary approachesSurgery- Bariatric surgery /

intragastric balloonTreatment of obesity complications

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Treatment targets5% loss is standard adult weight loss

target10% 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

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Treatment of Choicecomprehensive treatments

including:behavioral modification proceduresdietary interventionan exercise programreduction of sedentary behavioursfamily centred

motivational enhancement

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Drugs

Drug trials for obesity in children & adolescents

Extremely few publishedDrugs not licensedWe cannot assume risks and

benefits same as in adult

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What’s availableOrlistat – 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 vitaminsMetformin – useful in diabetes, impaired

glucose intolerance and possibly insulin resistance

May improve cardiovascular outcome and reduce risk of PCOS/ metabolic syndrome

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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

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Criteria for Bariatric Surgery in children BMI of 40 (kg/m2) 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

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Bariatric Surgery

Types Gastric banding Gastric bypass Gastric sleeve surgery

No surgery without risk- High risk groupPost surgical complicationsLong term follow upLong term supplement therapy

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Intragastric balloon Rx?

Less invasiveNo long term complicationsHowever are the results as

sustainable?

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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

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Thank youQUESTIONS?