END2.21 - Obesity Dr Gul Bano © S Nussey. What is obesity?

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END2.21 - Obesity Dr Gul Bano © S Nussey

Transcript of END2.21 - Obesity Dr Gul Bano © S Nussey. What is obesity?

Page 1: END2.21 - Obesity Dr Gul Bano © S Nussey. What is obesity?

END2.21 - Obesity

Dr Gul Bano

© S Nussey

Page 2: END2.21 - Obesity Dr Gul Bano © S Nussey. What is obesity?

What is obesity?

Page 3: END2.21 - Obesity Dr Gul Bano © S Nussey. What is obesity?
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Page 5: END2.21 - Obesity Dr Gul Bano © S Nussey. What is obesity?

How is obesity defined?

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How to measure obesity?

BMI = Weight/height2 - using metric not Imperial measures

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How to measure obesity?

cm

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Who is obese?

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Age and sex effects

Who is obese?

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Effect of ethnic group

Who is obese?

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Effect of educational level

Who is obese?

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Who is obese?

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Why treat obesity?

Effect of obesity on all-cause deaths

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Why treat obesity?Effect of obesity on coronary disease deaths

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Why treat obesity?

Effect of obesity onType 2 DM

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Quantification of weight gain as a risk factor for diabetes

• US female nurses study - 114,281 - age 30-55 y with no DM, stroke, CAD or cancer at entry.

• Prospective cohort study 1976-90 (98% White).

• Outcome measure - NIDDM

• 2204 cases during 1.49 million woman-years.

• After age adjustment, BMI was the dominant predictor of NIDDM

Ann Intern Med 1995, 122: 481.

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US Nurses study

1

10

100

<22 22.0-22.9

23.0-23.9

24.0-24.9

25.0-26.9

27.0-28.9

29.0-30.9

31.0-32.9

33.0-34.9

>35.0

Rel

ativ

e ri

sk a

djus

ted

for

age

Attained BMI

2.94.3

replotted

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US Nurses study

0.1

1

10

100

>20.0 11.0-19.9

5.0-10.9

4.9-4.9

5.0-7.9

8.0-10.9

11.0-19.9

>20.0Rel

ativ

e ri

sk a

djus

ted

for

a

ge a

nd B

MI

at 1

8y

Loss (kg) Gain (kg)

Weight change from age 18 to 1976

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Effect of weight gain from 18y to 1982 on relative risk stratified for

FHFamilyhistory

Relative Risk adjusted for Age and BMI at 18y

Loss of11-19 kg

Loss of5-10 kg

Loss/Gain5 kg

Gainof 5-9

kg

Gain of10-19 kg

Gain of>20 kg

No FH 0.47 0.9 1.0 2.3 6.1 20.1

One parent 2.1 1.9 3.6 6.8 12.6 27.9

Siblingalone

4.3 1.0 5.8 11.9 32.8

Both parentsand sibling

3.7 1.6 11.7 21.3 48.7

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Quantification of weight gain as a risk factor for diabetes

• NHANES I - 14,407 US adults >25y 1971-5, followed to 1992.

• Weight change from recruitment to first follow up in 1982-4.

• Outcome measure - NIDDM

• 27% increased risk for gains of 5kg or more

• Every kg increase produces 4.5% increase in risk

Am J Epidemiol 1997, 146: 214

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NHANES I Study

Weight change Relative risk corrected*

BMI <25 BMI 25-<29 BMI >29

at recruitment

Loss > 5kg 2.3 0.7 1.25

Loss <5 kg to gain <5kg 1.0 1.0 1.0

Gain 5-<8 kg 1.84 2.38 2.11

Gain 8-<11kg 1.02 1.34 1.1

Gain 11-<20 kg 3.33 2.3 2.64

Gain > 20 kg 2.83 6.1 2.3

*corrected for age, sex, race,education, smoking, cholesterol, bp, alcohol

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Effects of weight loss on diabetes associated mortality

• US Cancer Prevention Study I• 1959-60 - 1,078,894 men & women age > 30y with

91% follow up to 1972.• 52,207 white women age >40 and <64y who had

never smoked and had BMI > 27 at recruitment, 15,069 with ‘obesity related health condition’ (heart disease, stroke, diabetes, hypertension).

• Outcome measure - Death certificate ICD-7 code 260

Am J Epidemiol 1995, 141:1128

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Cancer Prevention Study I

Weight change Diabetes related deaths*Corrected Mortality Rate Ratios

mean 95% CI

None 1.0

Not known 1.41 1.06-1.87

Unintentional loss 0.98 0.67-1.56

Unintentional gain 1.02 0.67-1.56

Intentional loss of 0.5-9 kg 0.56 0.38-0.82

Intentional loss of >9.1 kg 0.69 0.53-0.9

*corrected for initial age and BMI, education, alcohol, physical activity, other illnesses

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How to treat obesity?

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Representative outcomes of therapy

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Treating obesity

Overlapping activities in an integrated approach

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Current potential integration

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Effectiveness of lifestyle changes in general practice

• Meta-analysis - smoking, alcohol, diet and exercise.

• Randomised trials including ‘usual care’ arm, published in English.

• 6 electronic databases and 37 trials. Only smoking intervention could be analysed.

• None showed substantial changeFamily Practice 1997, 14:160

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Shared Care Approach - 1

• Australian study of shared care vs hospital based

• 37 shared care vs 101 gender-, age- and BMI- matched hospital care patients.

• Food habits by questionnaire, weight, BMI with comparisons at 10 and weeks.

• Jointly designed protocol. NB fewer GPs signed up for obesity shared-care protocol than for other protocols.

Int J Obesity 1996, 20:413

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Shared Care Approach - 2

Shared care Hospital based

Week 10-week 1

Weight loss (kg) 4.8 + 0.6 2.6 + 0.4

BMI 1.8 + 0.2 0.9 + 0.2

Retention 76% 59%

Week 26-week 1

Weight loss (kg) 5.0 + 1.2 5.0 + 0.9

BMI 1.9 + 0.5 1.9 + 0.4

Retention 45% 30%

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Changes in BMI in the Minnesota Heart Health Program

• 6 communities in 3 states - 500,000 people

• Mass media, physician education, risk factor screening, adult education, environmental programs, youth education for 7 years in 3.

• Obesity not primary outcome but included.

• Cross-sectional and cohort studies• BMI increased with time and was

unaffected by intervention. Int J Obesity 1995, 19:30.

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Changes in BMI in the Stanford 5-city project

• 2 treatment cities n=122,800 received 6 yr mass media and community cardiovascular risk reduction program.

• BMI a primary outcome• Cross-sectional and cohort

studies• BMI increased with time and

was unaffected by intervention. Am J Epidemiol 1991, 134:235

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Physician

Surgeon

Psychologist

Dietitian

Community

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Mechanism - 1

‘Medicalise’ the problem

Provide means

Motivate

Reinforce

Establish individual responsibility

Set individual long-term targets

Focus

Use individualised objective measures

Measure

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Mechanism - 2

‘Medicalise’ the problem

Entry into main-stream medicine

Avoids suggestionof moral turpetude

Establishes patho-physiologicalmechanism

Provides mechanism by whichsocio-political issues can be addressed

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Mechanism - 3

Individual Responsibility

Clear definition of risk, comparablewith smoking, bp, lipids

Motivation

Clarity of purposeand targets for therapy

Reinforces medical model

Avoids comparisons

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Conclusion

• Obesity should be managed as a disease entity by a physician-centred multidisciplinary team.

• Evidence for long-term success of commercial community-based treatment is sparse.

• Evidence for the success of non-commercial community-based management (however desirable) is negligible.

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Means

• Eating pattern modification– + Behaviour therapy eg eating situation – + Appetite suppression eg sibutramine– + Fat malabsorption eg orlistat– + Group therapy eg ‘Weight Watchers’– + Gastric balloon or waist cord– + Surgery eg banded gastroplasty

• Exercise

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Medical treatment of obesity

• Dexfenfluramine - withdrawn

• Orlistat - fat malabsorption

• Sibutramine - centrally acting

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Sibutramine

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Orlistat

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Conclusion

• Moderate weight loss (~10% or 10kg) is associated with - – A significant reduction in diabetes incidence and

associated mortality

– Improved metabolic control in established diabetes

• This can be achieved with medical therapies

• More significant weight loss in morbid obesity can currently only be achieved by surgical techniques