Obesity - MD Connect · Doctor of Medicine Objectives • Discuss the aetiology of obesity for...

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Transcript of Obesity - MD Connect · Doctor of Medicine Objectives • Discuss the aetiology of obesity for...

Obesity a Clinical problem and a National problem

Joe Proietto Matt Sabin

Rob Moodie

Doctor of Medicine

Objectives

• Define obesity • Revise normal energy balance and its

regulation • Revise energy in food and basal metabolic rate

Doctor of Medicine

Objectives

• Discuss the aetiology of obesity for individuals (nature vs nuture) including the social determinants of health

• Discuss the aetiology and evolution of the obesity epidemic in Australia over the last three decades

• Discuss the future projections of obesity and outline the health service demands and cost implications

Doctor of Medicine

Objectives

• List the common complications of obesity • Describe the social implications of obesity • Describe treatment options available for

patients with obesity (including individual and family approaches)

• Discuss the ways of managing the obesity epidemic at community, national and international levels

Doctor of Medicine

History

• Mrs Grosso comes to your surgery with her 8 year old son who has a sore throat and feels hot.

• You examine the child and diagnose a viral URTI. • You notice however that both mum and child are

obese. • Knowing the consequences of obesity and the

fact that weight loss has many benefits, you explore the issue further.

Doctor of Medicine

First let’s revise the regulation of energy balance.

Consider the energy in food and the

influence of basal metabolic rate

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What is obesity?

Why does it occur and how common is this condition?

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What questions would you like to ask Mrs Grosso?

What important complications should you consider with this condition?

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History (Cont)

• You learn that all of the family are obese. Mr Grosso in particular is a very heavy man. In addition, the eldest child (aged 15) is obese. Finally there is a 9 month old baby who is still being breast fed.

• After discussing the issue with Mrs Grosso, with her agreement, you refer the family to a newly established Family Obesity Clinic at the Austin hospital staffed by both adult and paediatric obesity experts.

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In the clinic the following histories are obtained for each of the Grosso Family

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Mr Grosso • Age 42 years • Overweight all of his life but gained even more

weight recently • Has never attempted weight loss • Gives a past history of

– Hypertension diagnosed 3 years ago – Obstructive sleep apnoea diagnosed 1 year ago

now treated with CPAP – No diabetes but has been found to have an

elevated fasting blood glucose

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Mr Grosso

On Examination: Wt: 144 kg Ht: 175 cm BMI: 47.0 kg/m2 Waist: 135 cm BP: 154/86 Lipids: T Chol 4.5 mmol/L, Tg 3.6 mmol/L, HDL-C 0.7 mmol/L Rest of examination normal

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Does Mr Grosso have the Metabolic Syndrome?

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Definitions of the MetSyn….

• All agree on the core components of the metabolic syndrome: – Obesity – Insulin resistance/glucose intolerance – Hypertension – Dyslipidaemia

• However key criteria differ between groups

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WHO Definition • Mandatory component:

– High insulin levels, an elevated fasting blood glucose or an elevated post meal glucose

• With at least 2 of the following criteria:

– Abdominal obesity as defined by: • a waist to hip ratio of greater than 0.9 • BMI of at least 30 kg/m2 • waist measurement over 94 cm

– Triglyceride level of at least 1.7 mmol/L – HDL cholesterol lower than 0.9 mmol/L – Blood pressure of 140/90 or above (or on treatment for

high blood pressure).

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NCEP - ATP III criteria

National cholesterol education program

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IDF Criteria

• Mandatory component: – Central obesity - waist circ. ethnicity specific

• Europid >=94cm men, >=80cm women • Asian (not Japanese) >=90cm men,>=80cm women • Japanese >=85cm men, >=90cm women

• Plus two or more of other criteria: – Triglycerides >1.7mmol/L or on specific treatment – HDL cholesterol <1.03mmol/L in men, <1.29 in women or on

specific treatment – Blood Pressure >/= 130/85 or on treatment – FBG >/=5.6mmol/L or previously diagnosed T2DM

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Mrs Grosso Mrs Grosso is a 38 year woman who has always struggled with her weight. She has had many attempts at weight loss always with some initial success but she has ineviatably regained. General Health is good

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Mrs Grosso On Examination: Weight 130 kg Height 168 cm BMI 46.1 kg/m2 Waist 105 cm BP 120/84 Normal lipids All other examination normal

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Why does the equally obese Mrs Grosso not have the same co-morbidities as her husband?

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Miss Angela Grosso Miss Grosso has just turned 15. She is in year 10 at her local high school. She has been overweight from early childhood. Lately she has not enjoyed going to school as she has become self-conscious about her body shape and has been the target of teasing from other girls.

Doctor of Medicine

Miss Angela Grosso On Examination: Weight 95kg Height 170 cm BMI 32.9kg/m2 Waist 105 cm BP 135/85 Lipids: Chol 4.5 mmol/l; Tg 1.2 mmol/l; HDL 1.6 mmol/l LFT’s: Abnormal, ALT 60 Rest of examination normal

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What is the most pressing problem for Miss Grosso?

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Rebecca Puhl and Kelly D. Brownell Bias, Discrimination, and Obesity Obesity Research (2001) 9, 788–805 This article reviews information on discriminatory attitudes and behaviors against obese individuals, integrates this to show whether systematic discrimination occurs and why, and discusses needed work in the field. Clear and consistent stigmatization, and in some cases discrimination, can be documented in three important areas of living: employment, education, and health care. Among the findings are that: 1.28% of teachers in one study said that becoming obese is the worst thing that can happen to a person; 2.24% of nurses said that they are "repulsed" by obese persons; and, 3.controlling for income and grades, parents provide less college support for their overweight than for their thin children. 4.There are also suggestions but not yet documentation of discrimination occurring in adoption proceedings, jury selection, housing, and other areas. Given the vast numbers of people potentially affected, it is important to consider the research-related, educational, and social policy implications of these findings.

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What treatment options do we have for Mr and Mrs Grosso and possibly Miss Grosso?

What are the pros and cons of each

approach?

Could we precipitate an eating disorder in Miss Grosso?

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Is there an optimal way to lose weight?

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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

NH&MRC Evidence-based guidelines 18 September 2003

Doctor of Medicine

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

NH&MRC Evidence-based guidelines 18 September 2003

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Long term effects of weight loss – Behavior therapy

Weight loss 1-2 years

Weight loss > 2 years

Behaviour therapy

- 4.7 kg -2.8 kg

NH&MRC Evidence-based guidelines 18 September 2003

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Weight Loss Agents : • SSRI’s – Fluoxetine

• Phentermine (Duromine) • [Topiramate (Topamax)] • (Duromine + Topamax (Qsymia)) • (Lorcaserin (Belviq)) • (Bupropion + Naltraxone (Contrave)) • (Leptin + Amylin) • Orlistat

[ ] = Off Label use ( ) = under investigation () = available USA

Doctor of Medicine

Weight Loss Agents (Cont)

• [Exenatide (Byetta)] • [Liraglutide (Victoza)] • Amylin (long acting) • Leptin (long acting)

[ ] = Off Label use ( ) = under investigation () = available USA

Bariatric Surgery

• Adjustable gastric Banding • Sleeve Gastrectomy • Roux-en-Y bypass

Gastric banding Sleeve gastrectomy Roux-en-Y bypass

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Master Anthony Grosso Anthony will be 8 in a few weeks. He loves his food and is “solid” On Examination: Weight: 45kg Height: 140 cm BMI: 23kg/m2 Otherwise healthy

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Do we need to do anything to treat Anthony?

With a BMI of 23 kg/m2 is Anthony obese?

Should we do blood tests on Anthony to exclude metabolic illness?

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In a child: Overweight is being 85-94 percentile for weight with a BMI of 18 kg/m2

Obesity is being > 95 percentile for weight with a BMI of 20 kg/m2

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Master Joseph Grosso Joseph is 9 months old and has been largely breast fed although lately mum has been supplementing with formula and started to introduce solids. On Examination he is a healthy baby

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What should we advise Mrs and Mr Grosso to do to prevent Joseph becoming obese?

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Why is it that Mrs and Mr Grosso and their children are not rare cases?

What are the changes?

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QUESTIONS

Is it better to treat the adults in an adult clinic or should we treat the whole family at once?

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Why have the obesity rates in Australian adults risen from 10% in 1980, to 28% in 2011 in just 30 years? Why has the prevalence of overweight and obesity in Australian children 7-15yrs gone from 11% in 1995 to 25% in 2007? (see Swinburn et al The Global Obesity epidemic: shaped by Global drivers and local environments Lancet 2100;378:804-14; Gortmaker et al Changing the future of obesity: science, policy and action Lancet 2011;378:838-47; Swinburne, Sacks Commonwealth Ministers Reference Book 2012)

What are the predictions for overweight and obesity in Australia?

Doctor of Medicine

Between 2000 and 2025, the adult prevalence of obesity is estimated to increase from 20.5 to 33.9%, while the prevalence of normal [sic] weight is estimated to decrease from 40.6 to 28.1%. [See Walls et al Projected progression of the prevalence of Obesity in Australia Obesity Volume 20, Issue 4, 11 SEP 2012, http://onlinelibrary.wiley.com/doi/10.1038/oby.2010.338/pdf]

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Why has this occurred? What are the drivers?

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It has started in most high income countries in 1970s/1980s. Although the behavioural patterns and their environmental determinant are complex and vary from country to country the following important causes include:

• Major change in global food systems – processing (energy densification) of food

• Ensuring food is more appealing – market and laboratory research by food and drink companies to “addict” consumers through added fats, sugar and flavour enhancers

Doctor of Medicine

• Food becoming much cheaper with quicker, more convenient supply – the rise of the fast food industry

• Movement from individual to mass preparation of food

• Greater availability and ubiquity of food (e.g. vending machines)

• Massive ongoing advertising, promotion to children and adults; sponsorship of sport – normalising of their products in the culture of Australia

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This occurred at the same time as: • Decreased incidental (the exercise we get in

carrying out in our daily activities) physical exercise – rise in car ownership and use, (more so in Australia and USA compared to European countries and Japan)

• Children not walking but being driven to school, decreased emphasis on physical education in schools

• Rapid rise in sedentary entertainments e.g. TV, videos, video games, internet, social media

• Mechanisation of the workplace and in the home – decreased manual labour

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• These are all modified in different countries and sub populations by: • National wealth • Government policy • Cultural norms • The built environment • Genetic and epigenetic mechanisms • Biological bases for food preferences and

regulate motivation for physical activity

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What impact will this have on your clinical practice? What impact will this have on health services demands and costs?

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QUESTIONS

How are we to stop the obesity epidemic?

What can be done by governments, by industry and in local communities?

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Norm and the “Life- be in it” campaign (run on television in the 1980”s)

From The Science Show ABC Radio (www.abc.net.au)

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“Insanity is doing more of the same thing and

expecting a different outcome.”

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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

© Copyright The University of Melbourne 2016 Last updated: January 2013