Even a modest loss of 5 to 10 per cent of starting weight can result in significant health benefits.. The current evidence base indicates that low-fat ad libitum eating plans, resulting
Trang 1ENDORSED 18 SEPTEMBER 2003
of Overweight and Obesity in Adults
Trang 2© Commonwealth of Australia 2003
Paper-based publications
This work is copyright Apart from any use as permitted under the Copyright Act 1968, no part may be
reproduced by any process without prior written permission from the Commonwealth available from the Department of Communications, Information Technology and the Arts Requests and inquiries concerning reproduction and rights should be addressed to the Commonwealth Copyright Administration, Intellectual Property Branch, Department of Communications, Information Technology and the Arts,
GPO Box 2154, Canberra ACT 2601 or posted at http://www.dcita.gov.au/cca.
© Commonwealth of Australia 2003
Electronic documents
This work is copyright You may download, display, print and reproduce this material in unaltered form only (retaining this notice) for your personal, non-commercial use or use within your organisation
Apart from any use as permitted under the Copyright Act 1968, all other rights are reserved Requests
for further authorisation should be directed to the Commonwealth Copyright Administration, Intellectual Property Branch, Department of Communications, Information Technology and the Arts, GPO Box 2154, CanberraACT 2601, or posted at http://www.dcita.gov.au/cca.
ISBN Print: 1 864961 90 2 ISBN Online: 1 864961 96 1
For copies of this document contact:
Phone: 1800 020 103 extension 8654 (toll free number)
Email: phd.publications@health.gov.au
Website: www.obesityguidelines.gov.au
Trang 3C O N T E N T S
Preface vii
Summary ix
Evidence-based statements and recommendations xv
1 Setting the scene 1
1.1 The obesity epidemic 1
1.2 The health burden 2
1.3 The financial burden 7
1.4 The benefits of weight loss 7
1.5 Possible detrimental effects of weight loss 8
1.6 Normal regulation of body weight 8
1.7 Abnormal regulation of body weight and the 10
aetiology of obesity 1.8 At-risk groups 11
1.9 Obesity and eating disorders 12
2 Assessment 21
2.1 How is energy balance disturbed? 21
2.2 Why is energy balance disturbed? 22
2.3 Other considerations 31
3 Measuring overweight and obesity 43
3.1 'Gold standard' measures 43
3.2 Anthropometric measures 44
4 Treatment: general 53
4.1 A global approach to treatment and prevention 53
4.2 A treatment model 54
4.3 Treatment expectations 55
4.4 Treatment goals 56
4.5 Treatment duration 58
4.6 Treatment providers 58
4.7 Treatment emphasis 59
4.8 Selection of patients for treatment 60
4.9 The quality of obesity treatment studies 60
Trang 4C ONTENTS C ONTENTS
5 Treatment: energy intake 65
5.1 Existing evidence of the effectiveness of diet therapy 66
5.2 Recent evidence on dietary therapy 67
5.3 Types of dietary approaches 67
5.4 Summary 80
5.5 Gaps in knowledge 80
6 Treatment: physical activity 91
6.1 Secular changes in obesity and physical activity 92
6.2 Recent findings on physical activity 94
6.3 Summary 109
6.4 Gaps in knowledge 109
7 Treatment: behavioural therapy 119
7.1 Approaches to behavioural therapy 119
7.2 Behavioural treatment outcomes 121
7.3 Behavioural-drug combination therapy 129
7.4 Other psychological factors 129
7.5 Gaps in knowledge 131
8 Treatment: pharmacotherapy 137
8.1 Who should be treated with pharmacotherapy? 139
8.2 Pharmacotherapy treatment options 139
8.3 Drugs that inhibit nutrient absorption 145
8.4 Combined drug therapy 148
8.5 Potential new compounds 148
8.6 The ability of drugs to sustain weight loss 149
8.7 Cost-effectiveness of weight-loss drugs 150
8.8 Summary 150
8.9 Gaps in knowledge 151
9 Treatment: surgery 157
9.1 Who should be treated with surgery? 157
9.2 The effectiveness of bariatric surgery 158
9.3 Types of procedures 158
9.4 Benefits of surgical intervention 168
9.5 Risks of surgical intervention 169
9.6 Summary 170
9.7 Gaps in knowledge 170
10 Weight-loss supplements and alternative treatments 177
10.1 Weight-loss supplements 177
10.2 Commercial weight-loss programs 188
10.3 Gaps in knowledge 188
Trang 5Appendix A The guideline-development methodology 197
Appendix B Diet therapy evidence (1997-2001) 206
Appendix C Physical activity evidence (1996-2001) 220
Appendix D Behavioural therapy evidence 228
Appendix E Sibutramine therapy evidence 234
Appendix F Orlistat therapy evidence 238
Appendix G Surgical treatment evidence 246
Appendix H Sources for appendixes 258
Trang 6P REFACE
P R E FA C E
In recent decades the number of Australians who are overweight or obese has continued to increase: in 1999-2000 an estimated 67 per cent of adult males and
52 per cent of adult females were classified as overweight or obese In 1992-93,
it was estimated that obesity was costing Australia $840 million a year, of which about 63 per cent was being directly borne by the health care system
In 1997 the National Health and Medical Research Council’s Expert Panel on
Prevention of Obesity and Overweight prepared Acting on Australia’s Weight: a strategic plan for the prevention of overweight and obesity The primary outcomes
of that plan were the goals to ‘prevent further weight gain in adults and eventually reduce the proportion of the adult population that is overweight or obese; and to ensure healthy growth of children’
Undoubtedly, most of the work required to tackle overweight and obesity in
Australia will take the form of population-wide strategies seeking to modify the
‘obesogenic’ modern social environment However, during the development of Acting
on Australia’s Weight and the subsequent strategy, the need for clinical practice
guidelines for the management of overweight and obesity in Australian adults and children became apparent So, in 2000, in collaboration with the Population Health Division of the Commonwealth Department of Health and Ageing, the NHMRC initiated the development of the guidelines
In working on the project, and having determined that separate guidelines were required for adults and for children and adolescents, the NHMRC researched
practices for managing overweight and obesity and ensured that the practices
identified were multi-faceted—for example, strategies that span physical activity, diet and self-esteem
These guidelines for adults are the result of a comprehensive assessment of the current scientific evidence They provide detailed evidence-based guidance for assessing and managing overweight and obesity in Australia They also highlight important health concerns associated with overweight and obesity and, through the provision of clinical practice information for at-risk groups, aim to improve health outcomes for people with conditions such as diabetes, cardiovascular disease and some cancers The evidence has been reviewed in detail up to January 2002 After review of the document by stakeholders, only key additional references to March
2003 have been added, in order to expedite the process of publication
The guidelines focus primarily on the majority population in Australia It should be recognised that the problem among specific groups, and Aboriginal and Torres Strait Islander peoples in particular, has distinct characteristics that are currently less well understood and need urgent, detailed examination
Trang 7The guidelines are designed for use by general practitioners and allied health
professionals when providing advice to patients in the clinical setting Information for consumers is also being developed It is stressed that the guidelines are for clinical practice They do not represent a comprehensive population-based approach to
overweight and obesity in adults: that was the task of Acting on Australia’s Weight,
and it will be addressed again in future NHMRC publications
It is recommended that these guidelines be updated and revised by 2006
Trang 8S U M M A RY
B AC K G RO U N D
Overweight and obesity are in epidemic proportions throughout Australia: it is estimated that 67 per cent of adult males and 52 per cent of adult females were overweight or obese in 1999-2000 The figures are even higher for some ethnic and age groups
This epidemic of overweight and obesity is part of a worldwide trend, and it is contributing to increasing levels of non-communicable metabolic and mechanically induced disorders such as diabetes, cardiovascular disease, joint problems,
obstructive sleep apnoea, and some cancers
While the causes of the problem are diverse, it is the interaction between humans’ varying levels of genetic, cultural and socio-economic predisposition to weight gain, and an increasingly ‘obesogenic’ modern environment, that is propelling the epidemic and explains the inter-individual differences in response
A S S E S S M E N T
As well as the assessment of weight related co-morbidities (such as dislipidaemia, hypertension and hyperglycaemia), clinical assessment of overweight and obesity requires two other important aspects: examining energy intake and physical activity levels to assess how energy imbalance has occurred; and considering the nature
of the environment, personal reasons and other factors to understand why it has occurred
Clinicians should take into account a person’s weight history, background, family, work and social environments, the presence of medical co-morbidities, motivation and readiness to change, and the costs and benefits of weight loss before prescribing any treatment
Trang 9T R E AT M E N T: G E N E R A L
Obesity is a chronic problem There is no single, effective treatment for all
overweight and obese people, and the problem tends to recur after weight loss
Some treatments (such as surgery) may be more effective than others in terms
of total weight loss in certain circumstances
People’s expectations of weight loss often exceed the capabilities of available
programs, making successful treatment more difficult However, weight loss has a
strongly beneficial effect on the co-morbidities of obesity, with the degree of benefit
usually related to the amount of weight loss Even a modest loss of 5 to 10 per cent
of starting weight can result in significant health benefits
All successful treatments involve some form of lifestyle change affecting energy
intake (food) or energy expenditure (physical activity), or both Among the aids to
treatment are behaviour modification, some medications, low-energy or very low
energy diets, and surgery
Treatment can be considered in a step-wise fashion, as shown in the following figure
The bottom steps suggest that that the clinical role must be supported by public
health measures for an integrated approach to the problem
A stepped model for clinical management of overweight and obesity
Source: Reproduced with permission—reference 10, Chapter 4.
Individual education and skills training
Behaviour modification Medical surgical Rx
Population education and awareness raising General population
Overweight/obese
Overweight/obese
(with disordered eating patterns or cognitions)
Obese or overweight with risk factors
(BMI >30 or BMI >27 with risk factors)
Intervention Target population
Trang 10S UMMARY S UMMARY
T R E AT M E N T: E N E R G Y I N TA K E
The effectiveness of any diet depends on the energy imbalance produced by a reduction in energy intake in relation to energy expenditure This can be done in many ways, but some methods are more effective and have less deleterious effects than others
A variety of diets involving a reduction in energy intake lead to short-term weight loss The current evidence base indicates that low-fat ad libitum eating plans, resulting in a daily energy reduction of 2 to 4 megajoules a day, in combination with increased physical activity, appear to be the most effective for long-term weight loss
It is possible that the primary mechanism through which low-fat diets exert their influence is reduction of energy density Other forms of low-energy density diets are being researched and may prove equally effective However, the evidence
is not currently available
Low-energy (that is, 4 to 5 megajoules a day) and very low energy (1.7 to 3.3 megajoules
a day) formula diets can lead to significant weight loss in the short term in motivated people under strict supervision In the long term (say, five years), however, they result in no greater weight losses than an ad libitum low-fat eating plan
Regular, weight-bearing exercise (for example, walking) that the person enjoys
is most effective for weight loss A non-weight bearing form of activity (such as swimming, walking in water or cycling) may, however, be best for very immobile, obese patients until their level of fitness increases and weight-bearing activities can be more easily carried out
Trang 11T R E AT M E N T: P H A R M AC OT H E R A P Y
There are currently four prescription medications that have been approved by the
Therapeutic Goods Administration for use in Australia—phentermine, diethylpropion,
orlistat and sibutramine—and may offer benefits as adjunct therapy for weight loss in
people with a BMI greater than 30 or greater than 27 with co-morbidities Of these,
phentermine and diethylpropion are indicated only for short-term use
Some antidepressant medications help some people lose weight
T R E AT M E N T: S U R G E RY
Surgery—mainly of the types that restrict the intake or absorption of food—is the
most effective weight-loss treatment in severely obese patients In general, surgery
is indicated for patients with a BMI greater than 40 or with a BMI greater than
35 and serious medical co-morbidities, although it is increasingly being used
in patients with BMIs lower than this
Surgically induced weight loss results in a marked reduction in some of the
co-morbidities associated with obesity (particularly diabetes) and an improvement
in quality of life
Although it may appear expensive relative to other treatments, obesity surgery
is one of the most cost-effective treatments available
A LT E R N AT I V E T R E AT M E N T S
At present no herbal or other over-the-counter supplements demonstrate sufficient
evidence of long-term weight loss and lack of significant side effects
D E A L I N G W I T H C O - M O R B I D I T I E S
The severity of a co-morbidity will determine the type of treatment, but weight loss
should nevertheless be a primary consideration when dealing with all co-morbidities
related to obesity
In cases of moderately elevated risk factors (such as raised blood sugars or
cholesterol), attempts should be made to manage weight through lifestyle change
before resorting to more intensive treatments
S U M M A RY O F T R E AT M E N T S
The following table summarises the effect of weight-loss treatments in overweight or
obese adults
Trang 12S UMMARY S UMMARY
The effects of weight-loss treatments in overweight or obese adults: a summary
Treatment Weight loss/gain (kg) Weight loss/gain (kg) Ability to prevent regain?
over 1-2 years a over >2 years a
Sibutramine plus -10.8 (-16.6 to -5.2) Not known Yes, while drug is taken
lifestyle modification 10.7%
Orlistat plus a mildly -8.4 (-13.1 to -6.2) g -6.9 h Yes, while drug is taken
Surgery Gastric bypass -46 (-53 to -35) -42 (-62 to -29) over 3-14 years Yes
a Results expressed as mean weight loss, with range of weight loss in parentheses and % weight loss in italics.
b Based on the placebo arms of 31 treatment studies lasting 1-2 years and 8 studies lasting more than 2 years.
c After 4-20 weeks.
d After 1-2 years without diet or behavioural therapy.
e After 1-2 years with diet or behavioural therapy.
f With 3-5 hours of moderate or vigorous activity per week.
g Weight loss due to orlistat alone is 2.8 kilograms.
h Not yet published in peer-reviewed literature (abstract only) Note: Most treatment studies have been carried out on people of European descent, predominantly female Many obesity treatment studies report high attrition rates (see Appendixes B to G) These high attrition rates are not associated with any particular intervention They diminish the effectiveness of weight-reduction programs and suggest caution in the interpretation of data based on the weight losses of people who remain in the programs.
Source: Randomised controlled trials reported in the literature cited throughout this publication
Trang 13E V I D E N C E - B A S E D S TAT E M E N T S A N D
R E C O M M E N DAT I O N S
The information in this publication is summarised in two formats, as shown in Appendix A The evidence-based statements are founded on the levels of evidence for clinical interventions set by the National Health and Medical Research Council The grades of recommendation are less formally determined, being based on
previous guidelines
B AC K G RO U N D
Overweight and obesity are becoming an increasingly serious problem in Australia, causing more and more, and graver, ill-health This is part of a worldwide trend towards obesity, and it is associated with modernisation and changing lifestyles
Overweight and obesity are present in epidemic proportions throughout III-2Australia: it is estimated that over 67 per cent of adult males and
52 per cent of adult females were overweight or obese in 1999–2000
Overweight poses a health burden at all ages, being associated with a III-2number of diseases caused by metabolic complications or the excess
weight itself, or both
A modest weight loss of 5 to 10 per cent of starting body weight III-2
is sufficient to achieve clinically relevant health benefits
A S S E S S M E N T
Clinical assessment involves two aspects: examining energy intake and expenditure
to determine how energy imbalance has occurred; and considering the nature of the environment and personal and other factors to understand why it has occurred Factors such as a person’s motivation, co-morbidities, and the costs and benefits of weight loss also need to be considered
Food intake and levels of physical activity can be estimated only III-2approximately in a clinical setting
Recommendation: level B
• Although it may be necessary to evaluate food intake and energy expenditure in the clinical situation, the currently available measures should be interpreted with caution
Trang 14E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS
Evidence level
The modern environment is a potent stimulus for obesity III-2
Some rare cases of single-gene mutations cause severe obesity III-2
disorders, which are usually manifest early in life
Recommendations: level B
• Before initiating treatment, known single-gene mutations should be considered
in early-onset cases of severe obesity
• When single-gene mutation obesity is confirmed, the patient should be referred
to a specialist who deals with these problems
Statement
In general, cases of severe obesity are more likely to have Expert opinion
basis than cases of overweight, which may result from
environmental influences alone
Recommendations: level D
• A different, more intensive care strategy may be needed when dealing with cases
of severe obesity compared with cases of overweight
• Information about the age of onset and the presence of parental obesity may help
clinicians identify people with a genetic predisposition to excessive weight gain
Psychological stress can have variable effects on a person’s III-3
body weight
Recommendation: level C
• Stress may need to be considered as a factor in obesity
Several prescription medications can cause weight gain II
Recommendation: level B
• A person’s current medication use should be assessed as a potential
cause of weight gain or failure to lose weight
Trang 15Evidence-based statements Evidence level
Obesity in childhood and adolescence is a risk factor for III-2obesity later in life
The tracking of childhood obesity into adult obesity is stronger III-2for older children than for younger ones
Recommendation: level B
• When treating adults for overweight or obesity, the past history shouldinclude height and weight in childhood
Pregnancy and menopause are critical periods for weight gain III-2
when compared with a placebo
Certain life events—for example, marriage, holidays, and giving IV
up sport—can have an influence on body fatness
Quitting smoking can cause significant weight gain—on Iaverage 5 to 6 kilograms in the first year
Recommendation: level B
• Instituting a weight-loss program at the time of quitting smoking may help attenuate the weight gain that usually occurs after quitting
Lack of motivation and a history of failed attempts to lose III-3 weight may make it more difficult to maintain a low body weight
Psychological factors—including early life experiences—can IVplay an important part in the development of overweight or obesity
Recommendation: level C
• Case histories for weight management should include an assessment of life events, past history of weight-loss attempts, and psychological factors
Trang 16E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS
M E A S U R E M E N T
There are no perfect clinical measures of overweight and obesity, and in some
cases there may be counter-productive effects of measurement on people who
are clearly overweight For adults, a combination of waist circumference and BMI
is recommended for the clinical measurement of overweight and obesity A BMI
above 25 or a waist circumference above 80 centimetres in women or 94 centimetres
in men is regarded as overweight A BMI above 30 or a waist circumference above
88 centimetres in women or 102 centimetres in men is regarded as obesity It
should be noted, however, that these cut-offs for overweight and obesity have
been derived in predominantly Caucasian populations and are likely to vary in
other population groups
At present there are no data on the best measures to use for Aboriginal and
Torres Strait Islander peoples
BMI is an acceptable approximation of total body fat at III-2
the population level and can be used to estimate the relative
risk of disease in most people However, it is not always an
accurate predictor of body fat or fat distribution, particularly
in muscular individuals, because of differences in body-fat
proportions and distribution
Recommendation: level B
• Interpret BMI with caution when this is the only measure of body fatness
in a person, particularly when measuring older people and muscular,
mesomorphic individuals such as athletes
Waist circumference is a valid measure of abdominal fat III-2
mass and disease risk in individuals with a BMI less than 35
If BMI is 35 or more, waist circumference adds little to the
absolute measure of risk provided by BMI
Recommendations: level B
• To reduce the risk of disease, Caucasian men should aim for a waist circumference
of less than 102 centimetres and women less than 88 centimetres In Asians and
Indians the target could be 10 centimetres lower, and in Pacific Islanders it could
be significantly higher
• If patients wish to be measured, a combination of BMI and waist circumference,
or weight and waist circumference, should be used
Trang 17Recommendations: level D
• Both weight and waist circumference should be used to assess relative changes
in body fatness over time
• For some obese patients measurement may be counter-productive; these patients should be allowed to choose whether to have their fat mass measured Other patients may prefer not to know the results of measurement
T R E AT M E N T: G E N E R A L
Obesity is a chronic problem There is no single, effective treatment, and the problem tends to recur after weight loss People’s expectations of weight loss are often
unrealistic, but even a modest loss of 5 to 10 per cent of starting weight can result
in significant health benefits At present, most research focuses on weight loss rather than end-point diseases
People’s expectations of weight-loss programs IVare often unrealistic
Recommendation: level D
• Efforts should be made to moderate people’s unrealistic expectations
of weight-loss programs
Obesity is a chronic disorder that tends to recur IVafter weight loss
Recommendation: level C
• People suffering from obesity should have long-term contact with, and support from, health professionals
Trang 18E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS
Statement
As a complex disorder with multiple causes, obesity often Expert opinion
calls for multi-disciplinary attention
Recommendations: level D
• If needed, clinicians should seek assistance from health professionals in other
disciplines with specialist knowledge in obesity management
• The health benefits and personal costs involved in weight loss vary considerably
between individuals, so consideration of treatment should take into account the
number of quality life-years to be gained, co-morbidities, the potential for successful
change, and the patient’s motivation
Statement
There is no single effective treatment for long-term Expert opinion
weight loss Lifestyle changes underlie all currently
effective treatments and should be emphasised
T R E AT M E N T: E N E R G Y I N TA K E
The effectiveness of any changes to eating behaviour depends on the
energy imbalance produced by a reduction in energy intake relative
to energy expenditure There are many ways of achieving this, although
some of them are potentially dangerous
The main requirement of a dietary approach to weight I
loss is a reduction in total energy intake
Recommendation: level A
• A reduction in total energy intake remains the basic mechanism whereby all dietary
weight loss occurs Evidence to date shows that low-fat ad libitum diets can result
in long-term weight loss Other strategies have shown short-term effectiveness but
have not yet been assessed for long-term effect
Low-fat ad libitum diets that reduce daily energy intake by I
2 to 4 megajoules can lead to a weight loss of 2 to 6 kilograms
and a waist-circumference loss of 2 to 5 centimetres after
one year of treatment
There is some evidence that these diets, if intensively monitored, may II
be more effective in maintaining weight loss than more restrictive
Trang 19Recommendation: level B
• Patients can benefit from being taught how to recognise and reduce fat in their diet
in such a way as to maintain the micronutrient integrity of the diet
Nutritionally balanced low-energy diets of 4 to 5 megajoules a Iday can result in weight losses of 7 to 13 kilograms and significant
decreases in abdominal fat after six months’ treatment But this weight loss is not sustained: half of the weight lost is regained after one to two years of treatment
Recommendation: level B
• Low-energy diets should not be considered for continuous long-term treatment
of overweight and obesity When they are used, close supervision is essential
Very low energy diets produce greater initial weight loss Ithan other forms of energy restriction (9 to 26 kilograms
over four to 20 weeks) Long-term maintenance of this weight loss over one to two years is variable (–14 to 0 kilograms), and success is more likely if behavioural or drug therapy is used as a follow-up
Use of meal replacements for one to five years can IIproduce weight losses of 3.0 to 9.5 kilograms and significant
improvements in several co-morbid factors in overweight and obese people
Recommendation: level B
• Clinically significant weight loss can be achieved using meal-replacement programs
Trang 20E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS
There is curently no long-term evidence supporting the use Long-term
of 'popular'diets (for example, low-carbohydrate diets and evidence
single-food diets) Some diets—such as those involving modified not available
fats, increased protein and a low glycaemic index—show
promise in short-term studies No long-term data are available
Although epidemiological studies show little relationship between III-I
alcohol intake and BMI in men, and even an inverse relationship
in women, experimental studies suggest that alcohol energy
is additive to the normal diet, and that it contributes
to excess energy intake and fat storage
T R E AT M E N T: E N E R G Y E X P E N D I T U R E
In the short term it is more difficult to cause an energy imbalance that leads
to weight loss through physical activity than it is through dietary restriction
A regular pattern of daily activity is, however, one of the keys to long-term
maintenance of weight loss
In modern societies there is an association between III-3
low levels of physical activity and obesity
In the absence of dietary change, moderate to vigorous I
exercise at the level usually prescribed—three to five hours
a week—produces a modest weight loss (about 2 kilograms)
over one year
Physical activity appears to be associated with a reduction III-2
in abdominal fat
Physical activity as part of a weight-loss program can help II
decrease total body fat while generally preserving fat-free mass
Weight loss can be expected to occur in a dose-response III-2
fashion, increasing with an increasing volume of physical activity
Recommendation: level B
• Recommendations for physical activity for weight loss should be based on activity
volume, where volume is defined by frequency, duration and intensity
Recommendations: level D
• When overweight or obesity is associated with low cardiovascular fitness, the volume
of physical activity should be based on frequency and duration but not intensity
• When a person’s cardiovascular fitness is high but overweight or obesity
persists, more intense levels of activity may be considered
Trang 21Evidence-based statement Evidence level
Lifestyle-based increases in physical activity—as opposed II
to a structured exercise program—are likely to be more successful for weight loss in the long term
There is no single ‘best’ exercise for weight loss Resistance III-1training may provide benefits in terms of retention of lean body
mass, but it offers no apparent extra advantages, for either weight loss or fat loss, over accumulated aerobic activity
Recommendations: level D
• Depending on initial fitness, health status, personal preferences, and lifestyle, any
of several types of physical activity may be the right one for a particular individual
• It is important to prescribe physical activity that a patient prefers and is therefore likely to maintain in the long term
• For very immobile obese patients, a reduced weight-bearing form of activity (such as swimming, walking in water, or cycling) may be best in the early stages
of a weight-loss program, until their fitness increases and weight-bearing activities (such as walking) can be more easily carried out
There can be significant individual differences in the weight-loss IIresponse to a set amount of physical activity
Even in the absence of weight loss, increases in physical activity III-2can improve metabolic health and may protect against certain
diseases (diabetes and cardiovascular disease, for example) and early mortality
Long-term (more than two years) studies have demonstrated IIthat physical activity can limit fat mass and weight regain more
effectively than diet
Trang 22E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS
There is an inverse relationship between the volume of physical III-1
activity carried out and weight regain
Weight regain after one year is likely to be up to 40 per cent with II
30 minutes of moderate activity daily but less than 15 per cent with
80 minutes or more of daily activity Therefore, an activity level equivalent
to about 45 kilojoules per kilogram per day (about 80 minutes a day)
is probably the minimum required for effective weight maintenance
Physical activity is likely to be more effective when combined with II
energy restriction, leading to a further 3 to 6 kilograms of weight
loss and greater loss of abdominal fat than ad lib low-fat diets or
physical activity alone over one year
A mean weight loss of 7.5 kilograms observed one year after II
diet-plus-physical activity therapy falls to 3.1 kilograms with longer
treatment, although this remains a significantly better outcome than
that associated with no treatment at all
Recommendation: level B
• Physical activity should be a component of any weight-loss program, particularly for
improving the effectiveness of weight maintenance
T R E AT M E N T: B E H AV I O U R A L T H E R A P Y
Behavioural therapy can increase the effectiveness of other weight-loss treatments;
the duration of the therapy is related to the extent of weight-loss maintenance
Evidence level
Overall, behavioural therapy used in combination with II
other weight-loss approaches can induce a mean weight
loss of about 5 kilograms, although this is variable
(0 to 13 kilograms) Three to five years after intervention
ceases, weight loss falls to about 3 kilograms (0 to 10 kilograms)
Recommendation: level B
• For optimal results, aspects of behavioural therapy should be combined
with nutrition and physical activity
Trang 23Evidence-based statements Evidence level
Long-term (more than a year) behavioural therapy used in IIcombination with other weight-loss interventions can be
associated with reductions in abdominal fat, even in the absence
of weight loss
Behavioural therapy can
• improve compliance with dietary and physical activity requirements II
No single behavioural therapy strategy appears to be superior II
to any other in the population as a whole
Increased duration of behavioural treatment increases the IIlikelihood of maintaining weight loss; in the absence of continued
behavioural intervention, a return to baseline weight occurs in the great majority of subjects
Behavioural therapy adds to the benefits associated with all other IIforms of weight-loss treatment
Recommendation: level B
• Consideration should be given to making aspects of behavioural therapy—
for example, self-monitoring, social support and stimulus control—a part
of all weight-loss interventions
T R E AT M E N T: P H A R M AC OT H E R A P Y
Research into new anti-obesity drugs is moving quickly, and recommendations may need to be updated The four medications currently available in Australia—orlistat, sibutramine, phentermine, and diethylpropion—appear to be effective for continued weight loss, although phentermine and diethylpropion are indicated only for short-term use Because there is no long-term (over two years) information published in the peer-reviewed literature on the potential harmful effects of these medications,
it is incumbent on the practitioner to prescribe with caution
Trang 24E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS
The dopaminergic agents phentermine and diethylpropion can II
produce effective weight losses of 6 to 7 kilograms (3 to 3.6
kilogram more than placebo), but are currently indicated only
for short-term use
Some SSRI (selective serotonin re-uptake inhibitor) II
antidepressant medications can result in weight loss in some
people under well-controlled conditions, although the effect
may be transient despite continued use of drugs
Sibutramine can lead to a weight loss of 5.6 kilograms or about I
6 per cent (4.3 kilogram more placebo), and improve some co-morbid
factors after one to two years of treatment If it is preceded by, or
combined with, lifestyle and dietary modifications, weight loss in some
individuals can almost double, to 10.8 kilograms, ranging from 5 to
17 kilograms (4 to 5 kilogram above placebo), or about 10.7 per cent
The safety of prolonged (more than two years) therapeutic
use of sibutramine has, however, not been demonstrated
The medication should be used with caution in patients
with a history of hypertension, and its use is not recommended
in patients with coronary artery disease, arrhythmias,
congestive heart failure, or stroke
Orlistat combined with a low-energy, low-fat diet can I
lead to a weight loss of 8.4 kilograms ranging from 6 to
13kilograms (1.1 to 4.5 kilogram above placebo), or about
8.6 per cent, and improve some co-morbid factors after one
to two years of treatment Two-thirds of this weight loss is
the result of diet modification
A recently completed study published in abstract format Level of evidence
has shown efficacy and safety in patients over a four-year yet to be assigned
treatment period
Both sibutramine and orlistat can increase the likelihood I
of long-term maintenance of weight loss while the drug
is being taken
Recommendation: level A
• Pharmacotherapy can be a useful adjunct to lifestyle change to induce weight loss in
some patients with a BMI greater than 30 and in patients with a BMI greater than 27
with co-morbidities It is, however, clear that—like therapy for other chronic disorders
such as hypertension, diabetes and dyslipidaemia—the medication is effective only
while it is being taken In the absence of long-term (more than two years)
peer-reviewed data, the long-term risk-benefit ratio of new drugs cannot be predicted
Drugs should be used only under careful medical supervision and in the context
of a long-term treatment strategy
Trang 25T R E AT M E N T: S U R G E RY
Surgery is the most effective treatment for severe obesity: for most procedures good weight maintenance has been observed three to eight years after surgery
in most patients
Surgical procedures in motivated, morbidly obese patients III-2can result in weight losses of from 16 to 43 per cent
(varying between 22 and 63 kilograms) that are reasonably well maintained over three to eight years
Recommendation: level B
• Surgery is the most effective treatment for morbid obesity: for most procedures and most patients, good weight maintenance has been observed three to eight years after surgery
Surgically induced weight loss results in a marked reduction III-2
in the incidence and severity of some of the co-morbidities associated with obesity (particularly diabetes) and improved quality of life
Obesity surgery may prove cost-effective in morbidly obese IV patients after two years
In patients with acceptable operative risks, mortality as a III-2consequence of bariatric surgery is low Bariatric surgery is,
however, often associated with impaired absorption of micronutrients, which requires lifelong monitoring and often folate or vitamin B supplementation
Recommendation: level B
• Assessing both peri-operative risk and possible long-term complications
is important; the risk-benefit ratio should be assessed in each case
Trang 26E VIDENCE - BASED STATEMENTS AND RECOMMENDATIONS 1—S ETTING THE SCENE
A LT E R N AT I V E T R E AT M E N T S
A wide range of alternative treatments, including non-prescription supplements,
are available for weight loss, but none of them has produced supporting evidence
at the level required for these guidelines
Statement
At present no non-prescription supplements have Good-quality
demonstrated sufficient evidence of long-term weight evidence not
loss and lack of significant side effects available
Recommendation: level D
• It is important to advise patients about the lack of evidence for the use of alternative,
over-the-counter weight-loss medications and, in some cases, the possible dangers of
their use
Trang 27is double the prevalence recorded in 1986.5 In numerical terms, this translates to almost 8 million adults and 600 000 children and adolescents in Australia who were overweight or obese around the turn of the century
Notes: Body mass index = weight (kg) divided by height (m)2 Overweight is defined as a BMI of
25 to 30; obese is defined as a BMI greater than 30.
Obesity is regarded as a disease in its own right1, but it is also a risk factor for a large number of other diseases (see Table 1.2) Using the prevalence figures shown in Table 1.1, more than 50 per cent of patients visiting a general practitioner are likely
to have overweight or obesity as a co-morbidity, if not a primary cause of disease There is no sign of the problem abating, so this situation will probably persist
At the superficial level, the answers seem simple: eat less and move more But in reality this is one of the most complex and difficult physiological problems to deal with in modern disease management, and there is much misleading and sometimes confusing information to be found in both the lay and the scientific literature It is for these reasons that we need guidelines providing an evidence-based assessment of the most effective ways of managing the problem in a clinical setting
Trang 281—S ETTING THE SCENE 1—S ETTING THE SCENE
Evidence-based statement
Overweight and obesity are present in epidemic III-2
proportions throughout Australia: it is estimated that
over 67 per cent of adult males and 52 per cent of
adult females were overweight or obese in 1999-2000
1 2 T H E H E A LT H B U R D E N
The relationship between excess weight, disease and early death has been known
since the time of Hippocrates, although only recently have scientifically controlled
studies been carried out to verify it These studies are not comprehensively reviewed
here since several recent reviews exist.1,6-12 Their main findings are, however,
discussed in the following paragraphs to provide a rationale for the guidelines
1 2 1 M O RTA L I T Y
A number of studies carried out in the last three decades have shown a clear
relationship between excess body weight, as measured by body mass index, and
increased mortality and morbidity Summaries of these studies can be found in
several meta-analyses and reviews.10,12-16 Many of the earlier studies were marred
by methodological difficulties,16,17 making their conclusions of dubious value, but
more recent studies have tended to overcome these problems18,19 and have arrived
at similar conclusions After accounting for increased mortality at a low BMI as a
consequence of smoking and physical disorders causing weight loss, the relationship
between mortality ratios (deaths per 100 000 people) and BMI appears to be either
linear or curvilinear, beginning at a BMI of around 20 to 22.18-21 This relationship
BMI (kg/m 2 )
Trang 29The relationship holds good for both males and females19, although it may be modified by age19, race22 and fitness level.23 Cardiovascular disease and cancer appear to be the main sources of the increased mortality.18,24 In a recent update of data from the Framingham study in the United States, being overweight (BMI 24.0
to 29.9) reduced life expectancy by 3.1 and 3.3 years in overweight 40-year-old male and female non-smokers and by 5.8 and 7.1 years in obese (BMI >30) non-smokers Obese male and female smokers lost 13.7 and 13.3 years respectively.25 Figures 1.2 and 1.3 show the impact of BMI on the risk of all-cause mortality, stroke, coronary heart disease, and type 2 diabetes in overweight and mildly obese subjects The Y-axis represents relative risk, which is a measure of the risk of disease compared with a baseline measure (in this case a BMI of 20)
The figures show clear relationships for both women (Figure 1.2) and men (Figure 1.3) Type 2 diabetes is one of the most immediate outcomes of excess body fat, with by far the highest level of risk with increased weight in both sexes, even in subjects who are mildly overweight In the longer term, heart disease, stroke and all-cause mortality tend to become more significant, as both figures show Mortality (and morbidity) are also associated with the amount of weight gained in adult life
A weight gain of 10 kilograms or more since young adulthood is associated with increased mortality18, coronary heart disease26, hypertension27, stroke28 and diabetes.29
For example, the US Nurses Health Study showed an increased relative risk of mortality ranging from 1.25 for a weight gain of 5 to 8 kilograms from the age of
18 years to 2.65 for a weight gain of 20 kilograms or more.26 This is supported
by other studies in the United States30, the United Kingdom31 and Japan.32
Figure 1.2 Age-adjusted relative risk, by BMI, for different end points among
US women (from the Nurses Health Study)
Source: Reproduced with permission—reference 8.
3.5 3 2.5 2 1.5 1 0.5
0
All cause mortality Stroke
Coronary heart disease Type 2 diabetes mellitus
BMI (kg/m 2 )
Trang 301—S ETTING THE SCENE 1—S ETTING THE SCENE
Figure 1.3 Age-adjusted relative risk, by BMI, for different end points among
US men (from the Health Professionals Follow-up Study)
Source: Reproduced with permission—reference 8.
There are some discrepancies in the literature relating to risk but these could be
a result of the historical use of BMI as an indicator of fatness The risks associated
with obesity are known to stem from increased adiposity, particularly around
the waist.10 BMI offers only a crude measure of this at the individual level and in
fact may discriminate against some muscular individuals with low body fat (male
athletes, for example) Recent epidemiological studies have found that fat-distribution
measures, such as waist circumference or waist-to-hip ratio, are better predictors
of mortality 8,14,33,34 (see also Section 1.2.5)
There are two main causal links between obesity and morbidity: indirect links, as a
result of metabolic consequences; and direct links, as a result of excess body weight
Table 1.2 shows diseases and conditions linked through these mechanisms; they
are classified into three categories of relative risk for obese individuals (BMI >30)
compared with non-obese individuals (BMI <30), and the major references that have
established the causal link are included
All cause mortality
Stroke
Coronary heart disease Type 2 diabetes mellitus
BMI (kg/m 2 )
Trang 311—S ETTING THE SCENE 1—S ETTING THE SCENE
Relative risk Associated with metabolic Associated with excess
Greatly increased (RR >3) Type 2 diabetes 35,36 Sleep apnoea 44,45
Gall bladder disease 37 Breathlessness 46,47
Dyslipidaemia 40 Social isolation and
depression 49 Insulin resistance 41,42 Daytime sleepiness and
fatigue 50 Non-alcoholic fatty liver disease 43
Moderately increased Coronary heart disease 31,51 Osteoarthritis 54
Gout/hyperuricaemia 53 Hernia 56
Psychological problems 49 Slightly increased (RR 1-2) Cancer (breast, endometrial, colon Varicose veins
and others) 57,58 Musculoskeletal problems 63 Reproductive abnormalities/ Bad back 64
impaired fertility 59 Stress incontinence Polycystic ovaries 60 Oedema/cellulitis Skin complications 61
of end-point diseases such as coronary artery disease, stroke and diabetes.13
Obesity is often not considered to be the cause of some of the conditions listed in Table 1.2, such as bad back, breathlessness, sleep apnoea, and daytime sleepiness Increases in body weight can, however, cause mechanical pressures on the lower back, increased diaphragmatic pressure, or increased occlusion of the pharynx
by excess body fat which can lead to these conditions Psychological problems, such
as social isolation, depression and difficulty with interpersonal relationships, can also be a consequence of being too fat Finally, there is evidence that obesity results
in self-reported decreases in health, even in the absence of chronic disease.66
Obesity-related disease generally becomes manifest in the long term, so adverse health outcomes are not usually seen in childhood and adolescence The most pernicious exception to this is type 2 diabetes, which is now becoming increasingly common in obese children.67 Dyslipidaemia, hypertension and insulin resistance are also often present in obese children,68,69 as are certain orthopaedic complications.70
More immediate for the child, however, may be psychosocial problems associated with being overweight.71
Trang 321—S ETTING THE SCENE 1—S ETTING THE SCENE
Several epidemiological studies have suggested an age-related weakening of the link
between obesity and mortality, especially over the age of 75 years.19,72 This may be
due to the greater likelihood of diseases increasing mortality and causing weight loss
in the aged73 or the fact that those most sensitive to obesity-related disorders have
died before reaching an older age It could also be a consequence of using BMI as
the measure of obesity BMI has particular disadvantages in older groups because of
the natural decrease in height with age74 and the differential loss of lean mass with
age, which could increase the relative risk of excess weight with age In support of
this, recent work suggests that obesity, as measured by the distribution of abdominal
fat, indicates a health risk associated with ageing more similar to that in younger
age groups.14
Body fat is distributed primarily around the abdomen in males (‘android’ obesity)
and around the hips and buttocks in females (‘gynoid’ obesity) In the last 5 to 10
years, life insurers have been aware of the importance of android fat in mortality
risk This was brought to scientific attention in the 1950s by French endocrinologist
Jean Vague,75 although little attention was paid to it at that time Interest was
re-awakened in the 1980s, when Swedish research showed a high ratio of waist-to-hip
circumference was more important as a risk factor for heart disease than BMI in
both men76 and women.77 The finding stimulated an interest in the waist-to-hip ratio
as a clinical measure of health risk.78 More recently, however, it has emerged that
waist circumference alone,33,79 or in combination with other metabolic measures80, is
a better indicator of risk and reduces the errors in waist-to-hip ratio measurements
It is also closely associated with visceral, or internal, trunkal fat,81 which is an even
better predictor of risk than subcutaneous abdominal fat.82 The fact that BMI does not
distinguish fat mass from lean mass may explain why fat distribution measures such
as waist circumference and the waist-to-hip ratio have recently been found to be
better predictors of mortality in epidemiological studies than BMI.8,14,33,34 In general,
waist circumference is also associated with a higher risk of the disorders listed in
Table 1.2 than BMI, suggesting that body composition has a major impact on health
Overweight poses a health burden at all ages, being III-2
associated with a number of diseases caused by metabolic
complications and/or the excess weight itself
Trang 331 3 T H E F I N A N C I A L B U R D E N
Several studies attempting to estimate the costs of obesity to the community have recently been reviewed by Caterson.83 The direct costs have been estimated to be around 9 per cent of total health care costs in the United States84 and 1 to 5 per cent
in Europe.85 The direct costs in Australia were estimated at A$464 million in 1989-90,
or 2 per cent of total health care costs; the indirect costs—such as loss of income and productivity losses—were estimated at a further A$272 million.86 It should be noted, however, that, because of its closer relationship with morbidity and disability than with mortality, obesity will significantly increase the number of years during which
an individual suffers from ill-health and so may add much more to indirect, as well
as direct, costs.8 It has been estimated that about 10 per cent of the total cost of lost productivity in Sweden, for example, is ascribable to sick leave and work disability related to obesity.87 Importantly, the costs of health care associated with an obesity-related disorder such as diabetes have been calculated as almost doubling over time with the normal progression of the disease.88 This suggests that the economic burden
is not only significant but is likely to get worse, even if there is no further growth in obesity prevalence
1 4 T H E B E N E F I T S O F W E I G H T L O S S
There appears to be little question that weight gain is associated with an increased risk of a number of health disorders A related, but not necessarily contingent, question is whether weight loss leads to improvement in these conditions A second question concerns the cost of the interventions required to achieve these benefits,
if there are any The benefits may be not only financial but also in the psychosocial costs incurred by an individual
Modest weight losses of 5 to 10 per cent have been shown to confer health benefits,89-91 among them decreases in hypertension-in both hypertensive92 and non-hypertensive individuals93 and improvements in blood lipids.94 A more substantial
15 to 20 per cent weight loss in the first year after diagnosis can reverse the elevated mortality risk of type 2 diabetes91,95 and reduce sleep apnoea50 and other risk factors.96
In evaluating the two-year effects of obesity surgery, Sjostrom et al.97 showed that
a 30-kilogram weight loss can reduce the risk of diabetes 14-fold and hypertension, dyslipidaemia and hypertriglyceridaemia four-fold, as well as reduce plasma triglyceride levels by 60 per cent and hypertension by 10 per cent In quantitative terms, it has been shown that each 1 per cent decrease in body weight can lead
to a fall of about 1mmHg in systolic blood pressure and 2mmHg in diastolic.98 LDL cholesterol has been estimated to reduce by 1 per cent for every kilogram lost.94
In situations where the cause of weight loss is unknown, some studies have actually shown an increase in mortality with weight loss99 or weight cycling.100,101 However, when weight loss is intentional, modest losses have been shown to increase survival102 and reduce total mortality by 25 to 50 per cent.103,104 This reduction in mortality is most apparent (28 per cent) in overweight individuals with diabetes.105
The large weight loss in the Swedish Obese Subjects Study106 also points to a reduced 10-year mortality in the surgical intervention group
Trang 341—S ETTING THE SCENE 1—S ETTING THE SCENE
Preliminary results from the Swedish Obese Subjects Study show significant economic
benefits from weight loss Narbro et al.107 compared diabetes medication costs for
patients who had lost more than 15 kilograms with those for patients who had lost
less than 5 kilograms and found more than a 50 per cent reduction in costs As
noted, diabetes costs have also been shown to almost double with progression of
the disease88, but the progression can be considerably retarded by weight loss.95
Among the non-economic benefits of weight loss are improved quality of life108 and
improvements in psychological factors such as self-esteem.109
In summary, an increasing number of well-conducted studies show that modest
weight loss does appear to offer significant benefits in terms of medical, economic
and personal outcomes The benefit-cost ratio is dependent on the type and extent
of the weight-loss intervention However, surgery, which is one of the most costly
approaches to dealing with the problem, has been shown to have one of the most
positive benefit-cost ratios.110,111
A modest weight loss of 5 to 10 per cent of starting body III-2
weight is sufficient to achieve clinically relevant health benefits
1 5 P O S S I B L E D E T R I M E N TA L E F F E C T S O F
W E I G H T L O S S
Although voluntary weight loss generally has overwhelmingly positive health
benefits, it needs to be noted that there are some possible adverse effects with
voluntary weight losses, in some cases, even including premature death.112 Although
this has been inadequately researched,113 there are several possible reasons:
increased stress levels from the pressure to lose weight; increased arterial plaque
formation from excessive fatty acids liberated from fat stores; a rise in homocysteine
levels resulting from reduced food intake (particularly vitamin B intake);114 and/or
intensification of environmental toxins in reduced fat stores.115
1 6 N O R M A L R E G U L AT I O N O F B O DY W E I G H T
Normal regulation of body weight is generally considered to occur when energy
intake equals energy expenditure However, the traditional ‘physics’ approach
defined in the formula ‘weight = energy in – energy out’ is a static one and fails to
reflect the complexity of homeostatic mechanisms in a biological organism.116 It also
fails to highlight the external influences on energy balance, which can have a major
effect on the amount of control an individual has over his or her body weight
A more encompassing approach is that shown in Figure 1.4.117
Trang 35Figure 1.4 An ‘ecological’ approach to obesity
Source: Modified from reference 117.
Figure 1.4 suggests that there are three main influences on equilibrium levels
of body fat: environmental, biological and behavioural These are mediated through energy intake (foods and fluids) and/or energy expenditure (metabolic rate, thermogenesis and physical activity) Levels of body fat are also moderated by physiological adjustments to changes in the energy balance—for example, changes
in metabolism, hunger, or the energy costs of physical activity.118,119 Changes in the body’s fat stores may not necessarily be reflected in changes in body weight, although in the long term this will probably be the case Equilibrium stores are the result of a dynamic balance between a variety of opposing forces and could be considered as ‘settling points’
Regulation of body weight is highly complex and tightly controlled The search for food and water is so important that multiple overlapping mechanisms control and integrate this behaviour The central role in weight regulation is given to the hypothalamic region of the brain,120 and recent work has identified many neurotransmitters involved in weight regulation in this area.121 There is also evidence that body weight is defended, as shown by the moderating effects of physiological adjustment illustrated in Figure 1.4 Subjects who gain or lose 10 to 20 per cent of their body weight by overeating or restricting their intake produce compensatory changes in energy expenditure that oppose the change in body weight.122,123 The central integrating unit in the brain can function only if it is aware of the size of nutrient stores, so there must be signals from the fat stores to the hypothalamus One recently discovered signal of this kind is the hormone leptin, which is synthesised in fat cells in proportion to the amount of fat in the cell and transported to the brain, where it interacts with several neuropeptides to reduce food intake and increase energy expenditure.124 Most obese people have high levels of circulating leptin but
do not respond to this; that is, they appear to be leptin insensitive The defence of body weight by central regulatory mechanisms set at a high level may be one reason why it is so difficult for obese individuals to maintain weight loss in the long term
Behaviour
= – Energy outEnergy in x
Equilibriumfat stores
Physiologicaladjustments
Influences
Trang 361—S ETTING THE SCENE 1—S ETTING THE SCENE
1 7 A B N O R M A L R E G U L AT I O N O F B O DY W E I G H T
A N D T H E A E T I O L O G Y O F O B E S I T Y
If the second law of thermodynamics can be taken as immutable, it follows that
weight gain can occur only if total energy intake exceeds total energy expenditure
But this has often led to the belief that abnormal regulation—as in the case of weight
gain—can come only from voluntary manipulation of energy from the environment
The implication of this is that ‘sloth’ or ‘gluttony’, or both, fully explain obesity.125 As
the model outlined in Figure 1.4 shows, however, energy balance can be modified
by a number of factors beyond the voluntary control of the individual Energy
intake, for example, is modified by individual differences in nutrient partitioning
and oxidation,126 while energy expenditure is influenced by metabolic rate and
levels of spontaneous physical activity.127
The obese statuette known as the Venus of Wilendorf and other ancient artefacts
suggest that obesity has existed in human societies throughout history.128 Indeed, it
is clear that most mammals have the genetic propensity to store excess energy as
an energy reserve.129 Genuine cases of obesity throughout history seem, however,
to have been limited, suggesting that in most individuals excess body weight will
not develop in the absence of an obesogenic environment or significant changes in
behaviour, or both Thus, both the degree of obesogenicity of the environment and
the degree of genetic predisposition will influence body weight
The relative contributions of environmental and biological (genetic) factors to
energy intake and expenditure may vary according to the degree of obesity121 (see
Figure 1.5) For example, at modest increases in BMI (that is, at a BMI of 25 to
30), environment appears to play the dominant role, with genetic predisposition
contributing only a little.130 At the other extreme, in morbidly obese individuals, the
disorder is likely to be largely due to a genetic defect, with environment playing a
permissive role Because people in developed societies are rarely, if ever, subjected
to food deprivation and much of the food offered for sale is high in fat or sugar,
or both, the modern, affluent society is obesogenic The combination of a genetic
predisposition and an obesogenic environment is therefore a potent one, and for
many individuals weight gain is almost impossible to escape
Trang 37Figure 1.5 The relative contributions of genes and the environment to the
aetiology of obesity
Source: Reproduced with permission—reference 121.
The environmental changes wrought by the industrial and technological revolutions have increased the chances of energy imbalance in a larger proportion of the population and made obesity a normal response to an ‘abnormal’ (in evolutionary terms) environment.131 Given the range of genetic, behavioural and biological responses to excess energy, it is easy to conclude that abnormalities in regulation
of body weight have fuelled the modern obesity epidemic
1 8 AT- R I S K G RO U P S
While everyone is at risk of at least becoming overweight in the modern obesogenic environment, there are some people who are biologically prone to morbid and prolonged obesity People with an endocrine or medical abnormality are the first and most obvious candidates; examples are monogenetic disorders such as Cushing’s syndrome, Prader-Willi syndrome and hypothyroidism, which generally show
up early in life There are also other rare, but instructive, cases of monogenetic abnormalities (such as leptin deficiencies) that can result in obesity early in life (see Section 2.2.2) It is likely, however, that most obesity is polygenic—that is, a result of the interaction of several genes This genetic mix is now considered an abnormality, but it would once have increased an individual’s chance of surviving food shortages People from lower socio-economic groups, people with low education levels, and people from rural areas have also been shown to be more prone to weight gain in the current environment
In addition to these physio-demographic indicators of risk, there are particular life stages when the risk of weight gain is increased for all individuals, in the right
Environment
Genes
BMI
Trang 381—S ETTING THE SCENE 1—S ETTING THE SCENE
environmental conditions; these are childhood,132 early adolescence,133 pregnancy11
and menopause134 in women, and middle age in men and women Other factors,
such as quitting smoking,135 changes in lifestyle (marriage, divorce, and so on)
and medication, can also increase the risk of weight gain All of these need to be
considered in the management of obesity; they are discussed further in Chapter 2
1 9 O B E S I T Y A N D E AT I N G D I S O R D E R S
The current public emphasis on obesity—which has arisen because of the increased
prevalence of the problem in modern societies—has generated concern about the
health impact of over-reaction It is often proposed that undereating disorders such
as anorexia nervosa and bulimia nervosa are the result of public and media emphasis
on reduced body weight, which can be taken to unhealthy extremes by some On
the other hand, overeating can also be regarded as an eating disorder, and it is
much more widespread in modern societies Although guidelines for dealing with
obesity must consider overeating as a significant influence on energy imbalance, it
is incumbent on a regulatory or other authoritative body to take into account the
possible impact of any approaches aimed at reducing obesity in terms of stimulating
an increase in undereating disorders These disorders are generally considered to
constitute a special group of problems, so they are not considered in this document
R E F E R E N C E S
1 World Health Organization Obesity: preventing and managing the global
epidemic Report of a WHO consultation WHO Tech Rep Ser 2000;894(3):
i–xii, 1–253
2 International Diabetes Institute Diabesity and associated disorders in
Australia, 2000: the Australian Diabetes, Obesity and Lifestyle Study (AusDiab)
Melbourne: International Diabetes Institute, 2001
3 Bennett SA, Magnus P Trends in cardiovascular risk factors in Australia: results
from the National Heart Foundation’s Risk Factor Prevalence Study, 1980–1989
Med J Aust 1994;161(9):519–27.
4 Ball K, Crawford D, Ireland P, Hodge A Patterns and demongraphic predictors
of five-year weight change in a multi-ethnic cohort of men and women in
Australia Pub Hlth Nutr, 2003 (in press).
5 Booth ML, Wake M, Armstrong T, Chey T, Hesketh K, Mathur S The
epidemiology of overweight and obesity among Australian children and
adolescents, 1995–97 Aust NZ J Pub Hlth 2001;25(2):162–9.
6 Seidell JC, Kahn HS, Williamson DF, Lissner L, Valdez R Report from a Centers
for Disease Control and Prevention workshop on use of adult anthropometry
for public health and primary health care Am J Clin Nutr 2001;73(1):123–6.
7 Pi-Sunyer FX Medical hazards of obesity Ann Intern Med 1993;119
(7 Pt 2):655–60
8 Visscher TL, Seidell JC The public health impact of obesity
Trang 399 Bray G Overweight, mortality and morbidity In: Bouchard C, ed Physical activity and obesity Champaign, IL: Human Kinetics, 2000:31–54.
10 National Institutes of Health Identification, evaluation and treatment of overweight and obesity in adults Washington, DC: NHLBI, 1998.
11 British Nutrition Foundation Obesity London: Blackwell Science, 1999.
12 National Task Force on the Prevention and Treatment of Obesity
Overweight, obesity and health risk Arch Int Med 2000;160(7):898–904.
13 Sjostrom L The metabolic syndrome of human obesity In: Bouchard C, Bray
G, eds Regulation of body weight: biological and behavioral mechanisms
New York: John Wiley & Sons, 1996
14 Seidell JC, Visscher TL Body weight and weight change and their health
implications for the elderly Eur J Clin Nutr 2000;54(suppl 3):S33–S39.
15 Falsom A, Kushi L, Hong C Physical activity and incident diabetes mellitus
in postmenopausal women Am J Pub Hlth 2000;90(1):134–8.
16 Troiano RP, Frongillo EA, Sobal J, Levitsky DA The relationship between body weight and mortality: a quantitative analysis of combined information from
existing studies Int J Obes Relat Metab Disord 1996;20(1):63–75.
17 Willett WC, Dietz WH, Colditz GA Guidelines for healthy weight
N Engl J Med 1999;341(6):427–34.
18 Manson JE, Willett WC, Stampfer MJ, Colditz GA, Hunter DJ, Hankinson
SE et al Body weight and mortality among women
N Engl J Med 1995;333(11):677–85.
19 Stevens J, Cai J, Pamuk ER, Williamson DF, Thun MJ, Wood JL The effect
of age on the association between body-mass index and mortality
N Engl J Med 1998;338(1):1–7.
20 Garrison RJ, Castelli WP Weight and thirty-year mortality of men in the
Framingham Study Ann Intern Med 1985;103(6 Pt 2):1006–9.
21 Bray G Overweight is risking fate Definition, classification, prevalence
and risks Ann NY Acad Sci 1987;499:14–28.
22 Jones CO, White NG Adiposity in Aboriginal people from Arnhem Land, Australia: variation in degree and distribution associated with age, sex and
lifestyle Ann Hum Biol 1994;21(3):207–27.
23 Lee CD, Blair SN, Jackson AS Cardiorespiratory fitness, body composition,
and all-cause and cardiovascular disease mortality in men Am J Clin Nutr
1999;69(3):373–80
24 Manson JE, Stampfer MJ, Hennekens CH, Willett WC Body weight and
longevity: a reassessment JAMA 1987;257(3):353–8.
25 Peeters A, Barendregt JJ, Willekens F, Mackenbach JP, Al Mamun A, Bonneux L Obesity in adulthood and its consequences for life expectancy:
a life-table analysis Ann Intern Med, 2003;138:24–32.
26 Willett WC, Manson JE, Stampfer MJ, Colditz GA, Rosner B, Speizer FE et al Weight, weight change, and coronary heart disease in women: risk within
the ‘normal’ weight range JAMA 1995;273(6):461–5.
Trang 401—S ETTING THE SCENE 1—S ETTING THE SCENE
27 Huang Z, Willett WC, Manson JE, Rosner B, Stampfer MJ, Speizer FE et al
Body weight, weight change, and risk for hypertension in women
Ann Intern Med 1998;128(2):81–8.
28 Rexrode KM, Hennekens CH, Willett WC, Colditz GA, Stampfer MJ,
Rich-Edwards JW et al A prospective study of body mass index, weight
change, and risk of stroke in women JAMA 1997;277(19):1539–45.
29 Colditz GA, Willett WC, Rotnitzky A, Manson JE Weight gain as a risk factor
for clinical diabetes mellitus in women Ann Intern Med 1995;122(7):481–6.
30 Kannel WB, D’Agostine RB, Cobb JL Effect of weight on cardiovascular
disease Am J Clin Nutr 1996;63(suppl.):419S–422S.
31 Shaper A, Wannamethee S, Walker M Body weight: implication for the
prevention of coronary heart disease, stroke and diabetes mellitus in
a cohort study of middle aged men BMJ 1997;314:1311–17.
32 Tokunaga K, Matsuzawa Y, Kotani K, Keno Y, Kobatake T, Fujioka S et al
Ideal body weight estimated from the body mass index with the lowest
mortality Int J Obes 1991;15:1–5.
33 Baik I, Ascherio A, Rimm EB, Giovannucci E, Spiegelman D, Stampfer MJ
et al Adiposity and mortality in men Am J Epidem 2000;152(3):264–71.
34 Folsom AR, Kushi LH, Anderson KE, Mink PJ, Olson JE, Hong CP et al
Associations of general and abdominal obesity with multiple health
outcomes in older women: the Iowa Women’s Health Study Arch Intern
Med 2000;160(14):2117–28.
35 Carey VJ, Walters EE, Colditz GA, Solomon CG, Willett WC, Rosner BA et al
Body fat distribution and risk of non-insulin-dependent diabetes mellitus
in women: the Nurses Health Study Am J Epidem 1997;145(7):614–19.
36 Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC Obesity, fat
distribution, and weight gain as risk factors for clinical diabetes in men
Diab Care 1994;17(9):961–9.
37 Pacchioni M, Nicoletti C, Caminiti M, Calori G, Curci V, Camisasca R et
al Association of obesity and type II diabetes mellitus as a risk factor for
gallstones Dig Dis Sci 2000;45(10):2002–6.
38 Brown CD, Higgins M, Donato KA, Rohde FC, Garrison R, Obarzanek E et al
Body mass index and the prevalence of hypertension and dyslipidemia
Obes Res 2000;8(9):605–19.
39 Wilsgaard T, Schirmer H, Arnesen E Impact of body weight on blood pressure
with a focus on sex differences: the Tromso Study, 1986–1995 Arch Intern
Med 2000;160(18):2847–53.
40 Pan D, Hulbert A, Storlien L Dietary fats, membrane phospholipids
and obesity J Nutr 1994;124:1555–65.
41 Boden G Free fatty acids—the link between obesity and insulin resistance
Endocr Pract 2001;7(1):44–51.