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
 MRI / Dexa / bioimpedence (proxy)
 Waist circumference
 BMI = Kg/M²
A child's weight status is determined using an ageand 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.
Definition
Obesity expert committeepediatrics 1998
Overweight: 85-95th Centile
Obese: >95th Centile
International Obesity Task
Force
Overweight>91st centile
Obese>99th centile
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
Types of obesity in childhood
Primary
Secondary
Endocrine
Hypothyroidism
Cushings syndrome
pseudohypoparathyroidism
Hypothalamic
Monogenic
Syndromes
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:
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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
Trends in adult prevalence
of obesity (BMI > 30kg/m2)
Trend in childhood obesity
US children 1971-2006
Causes of primary obesity
 Interaction between genetic predisposition (5090%)& 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
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
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’
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
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
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
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
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
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.
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
Why is childhood obesity
getting so much attention!
Tracking into adult life( 60%)
Metabolic syndrome (IRS)
Secondary effects
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
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
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
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%.
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
Obesogenic
Environement
Sports & Leisure
•Lack of school facilities
•Few local playing areas
•Widely available indoorpassive entertainment
•Unsafe streets
•Few cycle routes
Education & information
•School lessons
•Lifestyles
•Nutrition
•Cooking
•Media messages
•Fashions
•Body image
•Cultural beliefs
•Conflicting information
Social + economic inequalities
in diet and physical activity
Management
 Primary Prevention
 Community based weight management
service
 Tertiary obesity service
 Severe obesity
 Obesity with co-morbidities
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
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
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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
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
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
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
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
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
Treatment
 Treatment of obesity
 Diet
 Drugs
 Exercise programs
 Psychological approaches
 Multi-disciplinary approaches
 Surgery- Bariatric surgery / intragastric
balloon
 Treatment of obesity complications
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
Treatment of Choice
 comprehensive treatments including:
 behavioral modification procedures
 dietary intervention
 an exercise program
 reduction of sedentary behaviours
 family centred
 motivational enhancement
Drugs
Drug trials for obesity in children &
adolescents
Extremely few published
Drugs not licensed
We cannot assume risks and
benefits same as in adult
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
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 comorbidities” Brown &Inge 2009
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
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
Intragastric balloon Rx?
 Less invasive
 No long term complications
 However are the results as sustainable?
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
Thank you
QUESTIONS?