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Challenges to tacking the obesity epidemic:
Why public health approaches do not work
Joe ProiettoUniversity of Melbourne
Department of Medicine
Repatriation Hospital
Austin Health
Heidelberg Victoria
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THE EPIDEMIC
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Prevalence
Overweight Obese Overweight plusObese
Men 48.2% 19.3% 67.5%
Women 29.9% 22.3% 52.1%
Cameron AJ et al MJA 178: 427-432 2003
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The Scourge
2. NHMRC 2003
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How Should we tackle the Obesity
Epidemic?
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“Common sense” tells us that obesity is caused by eating too much and not exercising enough.
If so, the solution is clear and easy.
To stem the obesity epidemic, we must simply educate the public about their eating and lifestyle behaviours.
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From the “NorthEast & Region”
Wednesday March 10 2004
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The Minnesota Heart Health Program
•A 13 year research and demonstration program•Included 3 demonstration communities and 3 matched control communities•Primary end-point was reduction in cardiovascular risk achieved mainly by lifestyle modification leading to weight loss.
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The Minnesota Heart Health Program
•Mass media campaigns were conducted for the duration of the program•These media campaigns educated the people on: * the link between obesity and cardiovascular risk
* behaviours that could contribute to the development of obesity* Services available to assist them with weight loss
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Impact of education on body weight
Cohort Study
Jeffery RW et al.Int J Obes Relat Metab Disord 19:30-39 1995
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Why did the public health measures in the Minnesota Heart Health Program fail to
influence the weight gain?
The Authors concluded that there were too many “negative” messages and that these overwhelmed the healthy messages.
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What negative messages do we have?
Australian children watch an average of 2.5 hours of television per day.
Advertisements can occur at the rate of 30 per hour
Food ads, as a percentage of total ads on television, range from 25%-48% (average 34%). (Hill and Radimer, 1997). Young Media Australia
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A junk food advertising audit conducted by the Australian Divisions of General Practice National Divisions Youth Alliance in January 2003 analysed 50 hours of child targeted TV on commercial stations.
Dr Andrew Binns Medicine Australia
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Children watching two and a half hours of TV a day during the holiday period would have been exposed to 406 advertising messages encouraging them to eat junk food.
Dr Andrew Binns Medicine Australia
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What do you think the chances are of reducing this
exposure to negative messages ?
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The Age 28 July 2006
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Controlling food intake
Can we reduce the exposure to negative messages?
Probably over time
Can we reduce the exposure of the population to energy dense food available in abundance all year round?
Probably not
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Physical activity
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The World Today - Tuesday, 29 June, 2004 12:30:00PM promises to spend on childhood obesity solutionsReporter: Alexandra KirkThe Prime Minister has promised to spend $116 million to tackle the problem of childhood obesity.
Mr Howard said the plan was built on "common sense", as he called for support from the whole community to get children moving and eating well.
Mr Howard has already rejected Labor's plan to ban fast food advertising during children's television programs, saying that would take responsibility away from parents.
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The Age 9 May 2007
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Contribution of timetabled physical education to total physical activity in primary school children: cross sectional study Katie M Mallam,et al. BMJ 327:592-593 2003
Monitored physical activity during waking hours for 7 days using accelerometers in 3 schools.
Studied 120 boys and 95 girls aged 7.5-10.5 years.
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School 1 was wealthy with extensive facilities and 9.0 a week timetabled physical activity.
School 2 was and award winning village school with 2.2 hours per week of timetabled physical education sessions.
School 3 was an inner city school with limited or no sporting facilities and 1.8 hours timetabled physical education per week.
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Katie M Mallam,et al BMJ 327:592-593 2003
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Katie M Mallam,et al BMJ 327:592-593 2003
Conclusion
“The total amount of physical activity done by primary school children does not depend on how much physical education is timetabled at school because children compensate out of school.”
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Moodie ML, Carter RC, Swinburn BA, Haby MM. The cost-effectiveness of Australia's Active After-School Communities program. Obesity (Silver Spring). 2010 Aug;18(8):1585-92. Epub 2009 Nov 5.
“For 1 year, the intervention cost is Australian dollars (AUD) 40.3 million (95% uncertainty interval AUD 28.6 million; AUD 56.2 million), and resulted in an incremental saving of 450 (250; 770) DALYs. The resultant cost-offsets were AUD 3.7 million, producing a net cost per DALY saved of AUD 82,000 (95% uncertainty interval AUD 40,000; AUD 165,000).
Although the program has intuitive appeal, it was not cost-effective under base-case modeling assumptions.”
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Reduced Physical Activity:
3 types of activity Past Now(5,000,000 BC -1800) (1800-2010)
a) Obligatory + + + + -
b) Voluntary + +
c) Spontaneous + +
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CHOICE
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Can we engineer society to force increased physical
activity?
Probably not
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Summary
There are significant political, social, economic and cultural impediments to stemming the obesity epidemic.
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Biological impediments to
limiting the obesity epidemic
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NH&MRC 2003
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Long term effects of weight loss – diet therapy
Diet Weight loss
1-2 years
Weight loss
> 2 years
Ad lib low fat -3.9 kg -2.7 kg
Low energy -6.7 kg -1.1 kg
Very low energy
-11.8 kg -4.1 kg
Meal replacement
-5.5 kg -6.5 kg
‘Popular’ diets Not known Not known
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Long term effects of weight loss – Physical activity
Weight loss
1-2 years
Weight loss
> 2 years
Physical activity
- 1.8 kg - 1.3 kg
Diet plus activity
-7.5 kg - 3.1 kg
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Long term effects of weight loss – Behaviour therapy
Weight loss
1-2 years
Weight loss
> 2 years
Behaviour therapy
- 4.7 kg -2.8 kg
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Long term effects of weight loss –Surgery
Weight loss
1-2 years
Weight loss
> 2 yearsGastric bypass - 46 kg - 42 kg
Biliopancreatic bypass
- 53 kg - 54 kg
Non-adjustable gastroplasty
- 41 kg - 25 kg
Adjustable gastroplasty
- 31 kg - 34 kg
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WHY THESE RESULTS?
Why is it that for most, the only therapy that works long term is the one that removes choice?
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Weight is Homeostatically
Regulated
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Arcuate NucleusNPY CARTAGRP MSH Lateral
HypothalamusOrexin MCH
Paraventricular Hypothalamic NucleusOxytocin CRH
Brain Stem
FOOD INTAKE
ENERGY EXPENDITURE
Cerebral Cortex conscious will
Ghrelin
Leptin
CCKPYY3-36
GLP-1Oxyntomodulin
InsulinAmylin
PP
OpioidsDopamine Endocannabinoids
-
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The consequence of the homeostatic regulation of body weight is that after weight loss, the body puts in place mechanisms to drive weight regain.
What are these mechanisms?
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Geldszus et al. Eur J Endocrinol 1996; 135: 659-62
Changes in Leptin levels with dieting
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0
1.0
2.0
3.0
4.0
5.0
6.0
7.0
0 60 120 180 240
Time (min)
Pla
sm
a C
CK
(p
mol/
L)
0
10
20
30
CC
K A
UC
(p
mol/L/4
h)
p=0.016
Week 0Week 9
Post- breakfast CCK release pre and post weight loss
Chearskul S. et al. American Journal of Clinical Nutrition, 87: 1238-1246, May 2008
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Ghrelin levels after weight loss
8. Cummings 2002
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What determines the weight that the homeostatic
mechanisms try to defend?
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Weight is Genetically Determined
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Genes and Obesity
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BMI- Intrapair Correlations
Type CorrelationMen
Correlation Women
MonozygoticReared apartReared Together
0.700.74
0.660.66
DizygoticReared ApartReared Together
0.150.33
0.250.27
Stunkard AJ et al New Engl J Med 322:1483-7 1990
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Twin A
Twin BAbd
omin
al F
at g
ain
Abdominal Fat gain
Effect of 100 days of overfeeding in 12 pairs of identical twins
Bouchard C et al New Engl J Med 322:1477-82 1990
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So Obesity is genetic……
BUT……
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Prevalence (cont)
1980 2000
ObeseBMI > 30
kg/m2
7.1% 18.4%
Cameron AJ et al. MJA 178: 427-432 2003
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Obesity is more prevalent among lower socioeconomic groups
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How can these contradictory results be
explained?
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Obesity is more prevalent among lower
socioeconomic groups
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The current explanations are that:
1. There are more junk food outlets in underprivileged areas.
2. There is an inverse relation between energy density and energy cost.
3. The high energy density and palatability of sweets and fats are associated with higher energy intakes.
However all of this ignores the intrinsic regulation of body weight
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Published 2009 Penguin Books London
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How could social inequality cause
obesity?
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Psychoneuroendocrinology 32: 824-33 2007
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Prevalence (cont)
1980 2000
ObeseBMI > 30
kg/m2
7.1% 18.4%
Cameron AJ et al. MJA 178: 427-432 2003
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Levin BE et al Am J Physiol 278:R231-R237 2000
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CONCLUSION 1 The Pessimistic view
To overcome the powerful biological mechanisms causing and maintaining obesity we would need to recreate an environment where food is limited and physical activity is obligatory.
Such a society is unthinkable in a free democratic country.
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CONCLUSION 2 The optimistic view
We will limit the obesity epidemic by identifying and avoiding the environmental (dietary) triggers to genetic obesity
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UniMelb ObesityAustin Health –Weight Control Clinic PhysiotherapyAustin Health – Department of Respiratory Medicine RMH– Metabolic Disorders ClinicAustralian Centre for Science, Innovation and Society Royal Women’s HospitalBariatric Surgery (AH/ WH) School of Population Health - Key
Centre Women's Health/Public Health
Centre for Adolescent Health School of Behavioural ScienceCentre for Meolecular, environmental, genetic andanalytical epidemiologyCentre for Community Child Health School of NursingCentre for Health, Exercise and Sports Medicine SVH HospitalCSIRO Molecular & Health Technologies St Vincents InstituteDepartment of Economics Victorian Centre of Excellence for
Eating DisordersEating Disorders Foundation Walter and Eliza Hall InstituteFaculty of Land and Food Resources Western Hospital Obesity ClinicMercy Hospital For Women Lymphoedema ClinicMetabolic Disorders Centre (A/H)Northern Hospital Healthy Eating ClinicPaediatric Obesity (RCH)Physiology