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Obesity
Clinical Assessment and Management of Adult Obesity
Robert F. Kushner, MD
O
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verweight and obesity are the most common medical
problems seen in primary care practice, affecting ⬎68%
of adults and 33.0% of children and adolescents in the United
States.1,2 Obesity is a risk factor for several of the leading
causes of preventable death, including cardiovascular disease,
diabetes mellitus, and many types of cancer. Thus, successful
treatment and control of obesity should be major imperatives.
However, multiple studies have shown that detection and
counseling rates among physicians remain low.3– 6 Thus, a
gap exists between the need to provide obesity care and the
actual provision of care. In this article, current recommendations for the medical evaluation of the obese adult patient are
reviewed, followed by management approaches to using
lifestyle therapy, pharmacotherapy, and surgery.
Preventive Services Task Force has concluded that behaviorbased treatments are safe and effective for weight loss and
maintenance.16 As a result, the Centers for Medicare and
Medicaid Services recently approved coverage for intensive
behavioral therapy for obesity for Medicare beneficiaries in
the primary care setting.17 Whether these initiatives will
reduce the clinical inertia that surrounds obesity care is less
certain.
Identification and Evaluation of the Patient
With Obesity
Broaching the Subject of Obesity
National studies have shown that obesity counseling rates
remain low among healthcare professionals.4 The reasons
vary and include time restraints during a busy practice, lack
of effective treatment options and practical tools, low confidence or insufficient training in weight management skills
and counseling, or concern that raising the topic will be
interpreted by the patient as being insensitive.5,18 There is
reason to be concerned. There are few other conditions in
medical practice and in our society that are as stigmatized and
shunned as obesity.19 In reality, obesity is a complex disease
caused by genetic, biological, economic, environmental, psychosocial, and behavioral determinants. Rather than blaming
patients for their weight, recognizing obesity as a medical
condition will pave the way a frank, open, and respectful
dialog.
There is no clearly established method for telling patients
that they are overweight or obese.20 However, initiating talk
about weight is an interactive process with information
sharing between patient and physician. When the topic of
body weight is first raised, words matter. The approach that
physicians use to broach this potentially sensitive topic may
influence how patients react emotionally and cognitively to
the discussion and advice provided. Language used by the
physician sets the stage for the interaction.21 The reason for
the concern is that the word obesity is a highly charged
emotive term.22 It has a significant pejorative meaning with
many patients, leaving them feeling judged and blamed when
labeled as obese. The bottom line is that the physician and
patient must use shared terminology that is agreeable, inoffensive, and understandable to both individuals.23 Recently,
the American Medical Association issued a pamphlet titled
Weigh What Matters, a family prevention program designed
A Case for Physician Involvement
Few other chronic public health conditions parallel the
prevalence of overweight and obesity. They affect two thirds
of adults and one third of children and adolescents in the
United States.1,2 Minority racial and ethnic groups are especially affected; nearly 76.6% of blacks and 80% of Mexican
Americans are overweight or obese.1 Per capita medical
expenditures and the cost of both absenteeism and presenteeism (workers being on the job but, because of medical
conditions, not fully functioning) attributable to obesity range
from $1143 (obese I men) to $6684 (obese III women).7
Clinically, determination of height and weight functions as
a simple and inexpensive surrogate measure for percent body
fat when the values are entered into the Quetlet index (weight
[kg]/height [m2]), commonly referred to as body mass index
(BMI).8,9 Categorization of patients by BMI also serves as a
useful risk estimate for morbidity and mortality that is
supported by multiple population studies.10,11 The relationship is particularly striking for the development of type 2
diabetes mellitus.12,13 BMI tables are conveniently used to
facilitate patient evaluation. The importance of detection was
reinforced in 2009 when the Healthcare Effectiveness Data
and Information Set measure included assessment of adult
BMI for the first time14 and the Centers for Medicare and
Medicaid Services mandated that the electronic medical
record be capable of calculating BMI as part of the Core
Measures on Vitals.15 However, treatment is more difficult to
implement and to sustain given the limited resources and time
available in the primary care setting.5 Nonetheless, the US
From the Northwestern University Feinberg School of Medicine, Chicago, IL.
Correspondence to Robert F. Kushner, MD, Professor of Medicine and Clinical Director, Northwestern Comprehensive Center on Obesity,
Northwestern University Feinberg School of Medicine, 750 N Lake Shore Dr, Rubloff 9 –976, Chicago, IL 60611. E-mail rkushner@northwestern.edu
(Circulation. 2012;126:2870-2877.)
© 2012 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org
DOI: 10.1161/CIRCULATIONAHA.111.075424
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Kushner
Clinical Assessment and Management of Obesity
2871
Figure. Lifestyle events– body weight graph.
Patients are asked to mark life events and diet
attempts that have contributed to their current
weight. This patient has experienced a progressive
weight gain that has recently been accelerated by
smoking cessation and increased commute to
work. Adapted from Kushner et al26 with permission from the publisher. © 2009 American Dietetic
Association.
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to provide resources needed to address weight with patients
and their families.24 The pamphlet contains several additional
conversation starters to broach this sensitive topic.
Taking an Obesity-Focused History
The first step in initiating obesity care is to take a comprehensive history that addresses issues and concerns specific to
obesity treatment. This obesity-focused history allows the
physician to develop tailored treatment recommendations that
are more consistent with the needs and goals of the individual
patient. A useful, practical, and reflective technique to
quickly identify the behavioral and biopsychosocial determinants of weight gain is to ask patients to complete a lifestyle
events– body weight graph (the Figure).26 For many patients,
weight gain initially occurs with or is accelerated coincident
to smoking cessation, initiation of a medication, or change in
life events such as a change in marital status, change in
occupation, or illness.26 At-risk times for women include
pregnancy and menopause. Stressful life events often result in
a change in eating and physical activity habits. Using the
lifestyle events– body weight graph as a conversation map is
an efficient and productive means to facilitate discussion
from the patient’s perspective. Insight into predisposing
genetic factors is obtained by taking a family history.27
Similarly, it is important to ascertain whether the patient was
overweight as a child or adolescent because early onset of
obesity is a predictor of severe obesity in adulthood.28
A dietary and physical activity history should be assessed
in all patients before counseling is initiated. In today’s
society, walking to or from the car, train, or bus or keeping
the home clean often represents the extent of daily physical
activity for many individuals. Assessment of psychological
health and psychiatric history should be done routinely during
the history. Particular attention should be paid to the presence
of mood and anxiety disorders, which are the most common
disorders in the general population and occur with high rates
among persons with obesity.29 Probing for conditions of
disordered eating such binge eating disorder, bulimia, or
night-eating syndrome or other psychological conditions that
may impair treatment such as attention deficit disorder or
posttraumatic stress disorder should be part of a comprehensive obesity history. The occurrence of a major depressive
episode, eating disorder, or serious psychological condition
should trigger a referral to a mental health provider.
Determining a patient’s readiness for weight loss is an
essential part of the initial evaluation. The National Heart,
Lung, and Blood Institute’s Practical Guide on the Identification, Evaluation, and Treatment of Overweight and Obesity
in Adults30 recommends that physicians assess patient motivation and support, stressful life events, psychiatric status,
time availability and constraints, and appropriateness of goals
and expectations to help establish the likelihood of lifestyle
change. It is important to remember that most patients are
ambivalent about changing longstanding lifestyle behaviors,
fearing that it will be difficult, uncomfortable, or depriving.
Motivational interviewing is a particularly useful technique to
explore ambivalence31 and has been shown to modestly
enhance weight loss in obese patients.32 Once a healthcare
provider is trained and skilled in motivational interviewing,
the technique can be delivered in a time-efficient manner.33
Physical Examination of the Obese Patient
According to the National Heart, Lung, and Blood Institute
“Clinical Guidelines on the Identification, Evaluation, and
Treatment of Overweight and Obesity in Adults,”34 the
Practical Guide on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults,30 and the World
Health Organization,35 assessment of risk status resulting
from overweight or obesity is based on the patient’s BMI,
waist circumference, and existence of comorbid conditions. A
desirable or healthy BMI is 18.5 to 24.9 kg/m2; overweight is
25 to 29.9 kg/m2; and obesity is ⱖ30 kg/m2. Obesity is
further subdefined into class I (30.0 –34.9 kg/m2), class II
(35.0 –39.9 kg/m2), and class III (ⱖ40 kg/m2; Table 1),
although lower cut points have been suggested for the Asian
population.36 Although BMI does not directly measure body
fat, its utility as a risk estimate has been demonstrated in
multiple population studies.10,11 Nonetheless, in some instances, the use of height and weight alone for calculation of
BMI as a surrogate measure of body fat may lead to an
incorrect estimation of risk.37 Patients with an unusual body
habitus, body builders with increased muscularity, or the
elderly with reduced lean body mass may be misclassified.
Although accurate methods to assess body fat such as
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December 11, 2012
Table 1. Classification of Overweight in Adults According to BMI
2
Classification
BMI, kg/m
Underweight
⬍18.5
Normal range
18.5–24.9
Risk of Comorbidities
Identifying the High-Risk Obese Patient
ⱖ25.0–29.9
Overweight
Increased
Class I obesity
30.0–34.9
High
Class II obesity
35.0–39.9
Very high
Class III obesity
ⱖ40.0
Extremely high
BMI indicates body mass index. Adapted from National Institutes of Health
and North American Association for the Study of Obesity30 with permission of
the publisher. © 2000 National Institutes of Health.
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dual-energy x-ray absorptiometry or air displacement plethysmography exist, they are impractical and too expensive for
routine clinical application. The inherent problems with using
BMI alone to estimate risk is exemplified by the obesity
paradox, the observed inverse correlation between BMI and
mortality in patients with existing chronic heart failure,
coronary heart disease, and chronic kidney disease.38,39 Although reasons for the obesity paradox remain uncertain,
proposed confounding factors include the poor sensitivity of
BMI to detect excess adiposity versus lean muscle mass, body
fat distribution, and the independent contribution of
fitness.40 – 42
In addition to BMI, the risk of overweight and obesity is
independently associated with excess abdominal fat and
fitness level. Population studies have shown that people with
large waist circumferences have elevated obesity-related
health risk compared with those with normal waist circumferences and within similar BMI categories.43– 45 The threshold for excessive abdominal fat appears to vary between
racial and ethnic groups. Proposed cut points have been
suggested by the International Diabetes Federation (Table
2).46 Determination of fitness level is another modifier of
assessing risk associated with BMI. Longitudinal studies have
shown that cardiorespiratory fitness (as measured by a maximal treadmill exercise test) is an important predictor of
all-cause mortality independently of BMI and body composition. More specifically, fit obese men had a lower risk of
all-cause and CVD mortality that did unfit lean men.47
Similarly, among women, cardiorespiratory fitness was a
Table 2.
more important predictor of all-cause mortality than was
baseline BMI.48
Ethnic Specific Values for Waist Circumference
Waist Circumference, cm
Country/Ethnic Group
Male
Female
North American
ⱖ102
ⱖ88
European
ⱖ94
ⱖ80
South Asian/Chinese
ⱖ90
ⱖ80
Japanese
ⱖ85
ⱖ90
Ethnic South and Central
Americans
Use South Asian
recommendations
Use South Asian
recommendations
Sub-Saharan Africans
Use European data
Use European data
Eastern Mediterranean and
Middle East (Arab) populations
Use European data
Use European data
Adapted from Alberti et al46 with permission from the publisher. © 2006
John Wiley and Sons Inc.
With the high prevalence of obesity and the imprecision of
BMI and waist circumference alone to estimate individual
risk, identifying which patient to treat is an important clinical
decision. Among US adults, 51.3% of overweight adults and
31.7% of obese adults are metabolically healthy, defined as
having 0 or 1 cardiometabolic abnormality.49 Obesity increases the risk for CVD predominantly through its effects on
other risk factors.50 According to a meta-analysis of 21 cohort
studies including ⬎300 000 persons, the adverse effects of
overweight on blood pressure and cholesterol levels account
for ⬇45% of the increased risk of coronary heart disease.51
Conflicting data exist on whether BMI or waist circumference independently contributes to cardiovascular outcomes in
addition to the predicted Framingham Risk Score.46,52 It is
suggested that overweight patients with clinical markers of
insulin resistance would benefit most by losing weight.
Specific markers include elevated triglyceride concentration,
a low high-density lipoprotein cholesterol concentration, a
high ratio of triglycerides to high-density lipoprotein cholesterol, or a combination of an enlarged waist and elevated
triglyceride concentration.53–57
According to the practical guide,30 patients at very high
absolute risk who trigger the need for intense risk factor
modification and management include those with established
atherosclerotic diseases, type 2 diabetes mellitus, and sleep
apnea. Presence of the metabolic syndrome should also
prompt urgent treatment.58 Obesity is associated with ⬎60
medical conditions, the incidence and prevalence of which
vary by BMI class, sex, and age.59,60 A direct relationship
with increasing BMI categories is particularly observed for
diabetes mellitus, hypertension, and dyslipidemia.61 Unique
aspects of the physical examination for patients with obesity
have recently been reviewed.62 No single laboratory test or
diagnostic evaluation is indicated for all patients with obesity,
although a fasting glucose and lipid profile is consistent with
current guidelines.63,64 The specific evaluation performed
should be based on the presentation of symptoms, risk
factors, index of suspicion, and screening guidelines appropriate for the patient.
Although BMI and waist circumference are useful anthropometric markers to identify potential risk, they do not
accurately reflect the presence or severity of the health risk.
Analogous to other staging systems commonly used for
congestive heart failure and chronic kidney disease, Sharma
and Kushner65 recently proposed the use of a new functional
staging system for obesity that would complement the current
anthropometric classification (Table 3). This riskstratification construct, called the Edmonton Obesity Staging
System, classifies individuals with obesity into 5 graded
categories based on their morbidity and health-risk profile.
The staging system was recently shown to predict increased
mortality among 2 large population cohorts.66,67 Future studies will need to determine whether the Edmonton Obesity
Staging System improves risk stratification over other tools
such as the Framingham Risk Score.
Kushner
Table 3.
Clinical Assessment and Management of Obesity
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Edmonton Obesity Staging System
Obesity-Related Risk Factors
Physical Symptoms, Psychopathology, Functional
Limitations, and Impairment of Well-being
0
None (blood pressure, serum lipids, fasting glucose, etc)
None
1
Subclinical (borderline hypertension, impaired fasting glucose, elevated liver enzymes, etc)
Mild
2
Established (hypertension, type 2 diabetes mellitus, sleep apnea, osteoarthritis, reflux disease,
polycystic ovary syndrome, anxiety disorder, etc)
Moderate
3
Established end-organ damage (myocardial infarction, heart failure, diabetic complications,
incapacitating osteoarthritis, etc)
Significant
Severe disabilities (potentially end-stage disabilities, etc)
Severe
Stage
4
Adapted from Sharma and Kushner65 with permission from the publisher. © 2009 Nature Publishing Group.
Approaching Obesity as a Chronic Disease
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The cause of obesity is multifaceted, brought about by an
interaction between predisposing genetic and metabolic factors and a rapidly changing modern environment. There is a
strong selection bias in favor of regulatory systems that
vigorously defend against deficits in body weight.68 The
regulatory changes with weight loss include significant reductions in levels of leptin and the gastrointestinal hormones
peptide YY, cholecystokinin, and amylin and increases in the
levels of ghrelin, hormonal changes that are associated with
increased hunger and urges to eat.69 Energy expenditure with
weight loss is disproportionately reduced, attributable largely
to increased skeletal muscle work efficiency and reduced
physical activity.70,71 As a result of these underlying adaptive
physiological factors and the behavioral challenges of balancing caloric intake and expenditure, weight loss maintenance is difficult. According to self-report data from ⬎14 000
participants in the 1999 to 2006 National Health and Nutrition Examination Survey (NHANES), only 17.3% of adults
reported losing 10% of maximum body weight and keeping it
off for at least 1 year.72 For these reasons, obesity should be
considered a chronic relapsing disease in which we use
multiple modalities of treatment, including lifestyle counseling, pharmacotherapy, and surgery.
Lifestyle Treatment
The foundation of obesity care is assisting the patient in
making healthier dietary and physical activity choices that
will lead to a net negative energy balance. The initial goal is
to achieve a 5% to 10% weight loss over the initial 6 months
of treatment.34 For some patients, weight maintenance may be
a reasonable goal. A comprehensive review of lifestyle
modification for obesity was previously provided by Wadden
et al.73 It is important to remember that personal choices are
heavily influenced by exposure to environmental factors, ie,
home and work life, access, affordability, media, and advertising, so all recommendations must have a contextual perspective.74 Caloric reduction is the most important component in achieving weight loss, whereas increased and
sustained physical activity is particularly important in maintaining the lost weight.75–79 Weight loss is dependent primarily on reducing total caloric intake, not the proportions of
carbohydrate, fat, and protein in the diet.78 The macronutrient
composition (ie, proportion of calories from carbohydrate,
fat, and protein) will ultimately be determined by the patient’s
taste preferences, cooking style, and culture. However, the
patient’s underlying medical problems are also important in
guiding the recommended dietary composition. As Table 4
shows, the dietary prescription may vary according to the
patient’s metabolic profile and risk factors. A consultation
with a registered dietitian for medical nutrition therapy is
particularly useful,84 along with the importance of emphasizing collaborative care and self-management of chronic disease.85 Incorporating meal replacements into the diet is
another useful strategy. Meal replacements are foods designed to take the place of a meal or snack while providing
nutrients and good taste within a fixed caloric limit.86,87 An
alternative dietary strategy is to refer the patient to one of
several commercial weight loss programs that have demonstrated weight loss outcomes.88,89
In addition to reducing caloric intake, patients are encouraged to burn more calories. There is a distinction between
physical activity and exercise. Whereas physical activity
consists of any bodily movement that increases energy
expenditure, eg, activities of daily living like walking, climbing stairs, and gardening, exercise is defined as planned,
structured, and repetitive bodily movement done to improve
or maintain 1 or more components of physical fitness.90
Weight loss counseling should encourage both entities as part
of treatment. Studies have demonstrated that lifestyle activities are as effective as structured exercise programs in
Table 4. Dietary Recommendations for Overweight or Obese
Patients With Components of the Metabolic Syndrome58
Metabolic Syndrome Component
Increased waist circumference (population
and country specific)
Elevated blood pressure
Dietary Recommendation
Caloric reduction
DASH diet79–81
Systolic ⱖ130 mm Hg and/or diastolic
ⱖ85 mm Hg
Elevated fasting glucose
Carbohydrate controlled diet82
ⱖ5.5 mmol/L (100 mg/dL)
Elevated triglycerides
Mediterranean diet or TLC83
ⱖ1.7 mmol/L (ⱖ150 mg/dL)
Lower high-density lipoprotein cholesterol
Mediterranean diet or TLC83
⬍1.0 mmol/L (40 mg/dL) in men
⬍1.3 mmol/L (50 mg/dL) in women
DASH indicates Dietary Approaches to Stop Hypertension; TLC, Therapeutic
Lifestyle Change. All diets are energy reduced by 500 to 1000 kcal/d and
should be accompanied by exercise to maximize metabolic benefit .
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Table 5.
December 11, 2012
A Guide to Selecting Treatment
BMI Category
Treatment
Diet, exercise,
behavior therapy
25–26.9 kg/m
27–29.9 kg/m
30 –34.9 kg/m2
35–39.9 kg/m2
ⱖ40 kg/m2
With comorbidities
With comorbidities
⫹
⫹
⫹
With comorbidities
⫹
⫹
⫹
With comorbidities
⫹
2
Pharmacotherapy
2
Surgery
Prevention of weight gain with lifestyle therapy is indicated in any patient with a body mass index (BMI) ⬎25 kg/m2,
even without comorbidities, whereas weight loss is not necessarily recommended for those with a BMI of 25 to 29.9
kg/m2 or a high waist circumference unless they have 2 or more comorbidities. Combined intervention made up of
a low-calorie diet, increased physical activity, and behavior therapy provides the most successful therapy for weight
loss and weight maintenance. Adapted from National Institutes of Health and North American Association for the Study
of Obesity30 with permission from the publisher. © 2000 National Institutes of Health.
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improving cardiorespiratory fitness and weight loss.91 The
most useful strategy in achieving lifestyle goals is to include
self-monitoring. Patients are asked to track their food intake,
physical activity, and weight throughout treatment.92 The
benefits of tracking include having real-time data on dietary
intake as it relates to caloric and other nutritional goals,
allowing reflection and planning of diet, introducing restraint,
and providing information to share with the provider. Similar
benefits are achieved by tracking physical activity by recording time or steps. Finally, it is important to remember that
lifestyle management is 1 component of a comprehensive
approach to the patient with obesity and cardiovascular
disease. Control of glucose, blood pressure, and lipid levels,
along with secondary prevention of recurrent events, is
optimized with the use of concurrent medication
management.93
Pharmacotherapy
According to current Food and Drug Administration guidance, pharmacotherapy is approved for patients with a BMI
ⱖ30 kg/m2 or ⱖ27 kg/m2 when complicated by an obesity
comorbidity (Table 5). Although sound in principle, few
agents are currently approved for treatment of obesity. They
fall into 2 major categories: appetite suppressants or anorexiants and gastrointestinal fat blockers. The 2 most commonly
used sympathomimetic amines are phentermine and diethylpropion, both labeled schedule IV drugs by the Drug Enforcement Agency. A full discussion of pharmacological treatment
for obesity was previously provided by Bray and Ryan.94
Three medications were submitted to the Food and Drug
Administration for a new drug application.95–97 However, at
the time of this writing, none of the medications has been
approved. A concern about two of these medications, phentermine/topiramate extended release (Qnexa; Vivus, Inc,
Mountain View, CA) and naltrexone/buproprion (Contrave;
Orexigen, La Jolla, CA), is the potential cardiovascular risk
from the slight increase in pulse rate.98 Regardless of whether
new antiobesity agents are available, it is important to avoid
or minimize weight-gaining medications when possible.99
Bariatric Surgery
According to the 1991 NIH Consensus Development Conference Panel on bariatric surgery,100 patients with a BMI ⱖ40
kg/m2 or those with a BMI ⱖ35 kg/m2 who have associated
high-risk comorbid conditions such as cardiopulmonary disease or type 2 diabetes mellitus could be considered surgical
candidates (Table 5). Consequently, Medicare and other
third-party insurance payers have followed these criteria for
reimbursement qualifications. The bariatric laparoscopic adjustable gastric banding surgical procedures were previously
reviewed by Dixon et al.101 Compared with standard care,
differences in BMI levels from baseline to year 1 are ⫺2.4
kg.m2 for laparoscopic adjustable gastric band, ⫺10.1 kg/m2
for laparoscopic gastric sleeve, ⫺9.0 kg.m2 for Roux-en-Y
gastric bypass, and ⫺11.3 kg.m2 for biliopancreatic diversion.102 Significant improvement in multiple obesity-related
comorbid conditions, including type 2 diabetes mellitus,
hypertension, dyslipidemia, obstructive sleep apnea, and
quality of life, has been reported.103 A recent meta-analysis of
controlled clinical trials comparing bariatric surgery and no
surgery showed that surgery was associated with a reduced
odds ratio risk of global mortality (odds ratio, 0.55), cardiovascular mortality (odds ratio, 0.58), and all-cause mortality
(odds ratio, 0.70).104
The decision to recommend bariatric surgery is dependent
primarily on the patient’s BMI and the presence of comorbid
conditions that are likely to be responsive to weight loss.
Other patient-related factors such as psychosocial health,
adherence, expectations, and past weight loss attempts are
taken into consideration. There is not enough predictive
information available to differentially select 1 procedure over
another for an individual patient. However, restrictivemalabsorptive procedures appear to result in greater weight
loss and improvement in comorbid conditions than restrictive
procedures. Furthermore, the surgeon’s experience and riskto-benefit ratio are considered. Contraindications include an
extremely high operative risk, active substance abuse, or a
major unstable or uncontrolled psychopathological condition
such as major depressive disorder, schizophrenia, or bulimia.
All patients who are considering weight loss surgery
should undergo a comprehensive assessment by a multidisciplinary team of healthcare providers that includes a physician, registered dietitian, and mental health professional.59
During the preoperative process, patients are typically instructed on healthy eating and physical activity patterns,
behavioral strategies to implement the lifestyle changes, and
the importance of stress reduction and social support for
Kushner
long-term success. Evidence-based recommendations for best
practice patient care have recently been published.59,105
Conclusions
Obesity is a serious and highly prevalent disease associated
with increased morbidity and mortality. Healthcare providers
must take an active role in the identification, evaluation, and
treatment of high-risk individuals. Broaching the topic of
weight and conducting an obesity-focused history need to be
incorporated by all physicians. All patients should be provided lifestyle therapy with consideration for pharmacotherapy and bariatric surgery when indicated. Primary treatment
should be directed at preventing further weight gain for
overweight patients and achieving a modest 10% weight loss
for obese patients.
Disclosures
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Dr Kushner has served on the medical advisory boards for Vivus,
Amylin, Orexigen, GI Dynamics, Novo Nordisk, Zafgen, and Retrofit. He serves on the Board of Directors for the Obesity Action
Coalition.
References
1. Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and
trends in the distribution of body mass index among US adults,
1999 –2010. JAMA. 2012;307:491– 497.
2. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity and
trends in body mass index among US children and adolescents,
1999 –2010. JAMA. 2012;307:483– 490.
3. Jackson JE, Doescher MP, Saver BG, Hart LG. Trends in professional
advice to lose weight among obese adults, 1994 –2000. J Gen Intern
Med. 2005;20:814 – 818.
4. McAlpine DD, Wilson AR. Trends in obesity-related counseling in
primary care: 1995–2004. Med Care. 2007;45:322–329.
5. Kushner RF. Tackling obesity: is primary care up to the challenge? Arch
Intern Med. 2010;170:121–123.
6. Haire-Joshu D, Klein S. Is primary care practice equipped to deal with
obesity? Arch Intern Med. 2011;171:313–315.
7. Finkelstein EA, DiBonaventura MD, Burgess SM, Hale BC. The costs
of obesity in the workplace. J Occup Environ Med. 2010;52:971–976.
8. Garrow JS, Webster J. Quetlet’s index (W/H2) as a measure of fatness.
Int J Obes (Lond). 1985;9:147–153.
9. Gallagher D, Heymsfield SB, Heo M, Jebb SA, Murgatroyd SA,
Sakamoto Y. Healthy percentage body fat ranges: an approach for
developing guidelines based on body mass index. Am J Clin Nutr.
2000;72:694 –701.
10. Prospective Studies Collaboration. Body-mass index and cause-specific
mortality in 900,000 adults: collaborative analysis of 57 prospective
studies. Lancet. 2009;373:1083–1096.
11. Berrington de Gonzalez A, Hartge P, Cerhan JR, Flint AJ, Hannan L,
MacInnis RJ, Moore SC, Tobias GS, Anton-Culver H, Freeman LB,
Beeson WL, Clipp SL, English DR, Folsom AR, Freedman M, Giles G,
Hakansson N, Henderson KD, Hoffman-Bolton J, Hoppin JA, Koenig
KL, Lee IM, Linet MS, Park Y, Pocobelli G, Schatzkin A, Sesso HD,
Weiderpass E, Willcox BJ, Wolk A, Zeleniuch-Jacquotte A, Willett WC,
Thun MJ. Body-mass index and mortality among 1.46 million white
adults. N Engl J Med. 2010;363:2211–2219.
12. Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk
factor for clinical diabetes mellitus in women. Ann Intern Med. 1995;
122:481– 486.
13. Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC. Obesity,
fat distribution, and weight gain as risk factors for clinical diabetes in
men. Diabetes Care. 1994;17:961–969.
14. National Committee for Quality Assurance. 2009 Healthcare effectiveness data and information set (HEDIS). http://www.ncqa.org/Portals/
0/HEDISQM/HEDIS2010/2010_Measures.pdf. Accessed April 8, 2012.
15. Eligible professional meaningful use table of contents core and menu set
objectives. Centers for Medicare and Medicaid Services. https://
www.cms.gov/EHRIncentivePrograms/Downloads/EP-MU-TOC.pdf.
Accessed April 8, 2012.
Clinical Assessment and Management of Obesity
2875
16. LeBlanc ES, O’Connor E, Whitlock EP, Patnode CD, Kapka T. Effectiveness of primary care-relevant treatments for obesity in adults: a
systematic evidence review for the U.S. Preventive Services Task Force.
Ann Intern Med. 2011;155:434 – 447.
17. Decision memo for intensive behavioral therapy for obesity (CAG00423N). Centers for Medicare and Medicaid Services. http://www.cms.
gov/medicare-coverage-database/details/nca-decision-memo.aspx?&
NcaName⫽Intensive%20Behavioral%20Therapy%20for%20Obesity&
bc⫽ACAAAAAAIAAA&NCAId⫽253&. Accessed April 8, 2012.
18. Rao, Burke LE, Spring BJ, Ewing LJ, Turk M, Lichtenstein AH, Cornier
MA, Spence JD, Coons M. New and emerging weight management
strategies for busy ambulatory settings: a scientific statement from the
American Heart Association. Circulation. 2011;124:1182–1203.
19. Puhl RM. Heuer CA. The stigma of obesity: a review and update.
Obesity. 2009;17:941–964.
20. Baron RB. Telling patients they are overweight or obese: an insult or an
effective intervention? Arch Intern Med. 2011;171:312–322.
21. Tailor A, Ogden J. Avoiding the term “obesity”: an experimental study
of the impact of doctors’ language on patients’ beliefs. Patient Educ
Couns. 2009;76:260 –264.
22. Wadden TA, Didie E. What’s in a name? Patients’ preferred terms for
describing obesity. Obes Res. 2003;11:1140 –1146.
23. Dutton GR, Tan F, Perri MG, Stine CC, Dancer-Brown M, Goble M,
Van Vessem N. What words should we use when discussing excess
weight? J Am Board Fam Med. 2010;23:606 – 613.
24. Weigh What Matters. American Medical Association. http://www.amaassn.org/resources/weighwhatmatters/physicians.html. Accessed April
8, 2012.
25. Kushner RF, Kushner N, Jackson Blatner D, eds. Counseling Overweight Adults: The Lifestyle Patterns Approach and Toolkit. Chicago,
IL: American Dietetic Association; 2009.
26. Ogden J, Stavinaki M, Stubbs J. Understanding the role of life events in
weight loss and weight gain. Psychol Health Med. 2009;14:239 –249.
27. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting
obesity in young adulthood from childhood and parental obesity. N Engl
J Med. 1997;337:869 – 873.
28. The NS, Suchindran C, North KE, Popkin BM, Gordon-Larsen P.
Association of adolescent obesity with risk of severe obesity in
adulthood. JAMA. 2010;304:2042–2047.
29. Luppino FS, De Wit LM, Bouvy PF, Stijnen T, Cuijpers P, Penninx
BWJH, Zitman FG. Overweight, obesity, and depression: a systematic
review and meta-analysis of longitudinal studies. Arch Gen Psychiatry.
2010;67:220 –229.
30. National Heart, Lung, and Blood Institute and North American Association for the Study of Obesity. Practical Guide on the Identification,
Evaluation, and Treatment of Overweight and Obesity in Adults.
Bethesda, MD: National Institutes of Health; October 2000. NIH publication No. 00-4084.
31. Rollnick S, Butler CC, Kinnersley P, Gregory J, Mash B. Motivational
interviewing. BMJ. 2010;340:1242–1245.
32. Armstrong MJ, Mottershead TA, Ronksley PE, Campbell TS, Hammelgarn BR. Motivational interviewing to improve weight loss in overweight and/or obese patients: a systematic review and meta-analysis of
randomized controlled trials. Obes Rev. 2011;12:709 –723.
33. Pollak KI, Alexander SC, Coffman CJ, Tulsky JA, Lyna P, Dolor RJ,
James IE, Brouwer RJN, Manusov JRE, Ostbye T. Physician communication techniques and weight loss in adults: project CHAT. Am J Prev
Med. 2010;394:321–328.
34. National Heart, Lung, and Blood Institute. Clinical guidelines on the
identification, evaluation, and treatment of overweight and obesity in
adults: the evidence report. Obes Res. 1998;6(suppl):51S–210S.
35. Obesity: Preventing and Managing the Global Epidemic. Geneva, Switzerland: World Health Organization; 1998.
36. WHO Expert Consultation. Appropriate body-mass index for Asian
populations and its implications for policy and intervention strategies.
Lancet. 2004;363:157–163.
37. Romero-Corral A, Somers VK, Sierra-Johnson J, Thomas RJ, CollazoClavell ML, Korinek J, Allison TG, Batsis JA, Sert-Kuniyoshi FH,
Lopez-Jimenez F. Accuracy of body mass index in diagnosing obesity in
the adult general population. Int J Obes (Lond). 2008;32:959 –966.
38. Ades PA, Savage P. The obesity paradox: perception vs knowledge.
Mayo Clin Proc. 2010;85:112–114.
39. Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ,
Allison TG, Mookadam F, Lopez-Jimenez F. Association of bodyweight
with total mortality and with cardiovascular events in coronary artery
2876
40.
41.
42.
43.
44.
45.
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
Circulation
December 11, 2012
disease: a systematic review of cohort studies. Lancet. 2006;368:
666 – 678.
Lavie CJ, Milani RV, Ventura HO, Romero-Corral A. Body composition and heart failure prevalence and prognosis: getting to the fat of the
matter in the “obesity paradox.” Mayo Clin Proc. 2010;85:605– 608.
Oreopoulos A, Ezekowitz JA, McAlister FA, Kalantar-Zakeh K,
Fonarow GC, Norris CM, Johnson JA, Padawal RJ. Association between
direct measures of body composition and prognostic factors in chronic
heart failure. Mayo Clin Proc. 2010;85:609 – 617.
McAuley PA, Kokkinos PF, Oliveira RB, Emerson BT, Myers JN.
Obesity paradox and cardiorespiratory fitness in 12,417 male veterans
aged 40 to 70 years. Mayo Clin Proc. 2010;85:115–121.
Balkau B, Deanfield JE, Despres JP, Bassand JP, Fox KAA, Smith SC,
Barter P, Tan CE, Gaal LV, Wittchen HU, Massien C, Haffner SM.
International Day for the Evaluation of Abdominal Obesity (IDEA): a
study of waist circumference, cardiovascular disease, and diabetes
mellitus in 168,000 primary care patients in 63 countries. Circulation.
2007;116:1942–1951.
Ghandehari H, Le V, Kamal-Bahl S, Bassin SL, Wong ND. Abdominal
obesity and the spectrum of global cardiometabolic risk in US adults. Int
J Obes (Lond). 2009;33:239 –248.
Dhaliwal SS, Welborn TA. Central obesity and multivariable cardiovascular risk as assessed by the Framingham Prediction Scores. Am J
Cardiol. 2009;103:1403–1407.
Alberti KG, Zimmet P, Shaw J. Metabolic syndrome: a new world-wide
definition: a consensus statement from the International Diabetes Federation. Diabet Med. 2006;23:469 – 480.
Lee CD, Blair SN, Jackson AS. Cardiorespiratory fitness, body composition, and all-cause and cardiovascular disease mortality in men. Am J
Clin Nutr. 1999;69:373–380.
Farrell SW, Braun L, Barlow CE, Cheng YJ, Blair SN. The relation of
body mass index, cardiorespiratory fitness, and all-cause mortality in
women. Obes Res. 2002;10:417– 423.
Wildman RP, Muntner P, Reynolds K, McGinn AP, Rajpathak S, WylieRosett J, Sowers M. The obese without cardiometabolic risk factors
clustering and the normal weight with cardiometabolic risk factor clustering: prevalence and correlates of 2 phenotypes among the US population (NHANES 1999 –2004). Arch Intern Med. 2008;168:1617–1624.
Wilson PWF, D’Agostino RB, Sullivan L, Parise H, Kannel WB. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med. 2002;162:1867–1872.
Bogers RP, Bemelmans WJE, Hoogenveen RT, Boshuizen HC,
Woodward M, Knekt P, van Dam RM, Hu FB, Visscher TLS, Menotti
A, Thorpe RJ, Jamrozik K, Calling S, Strand BH, Shipley MJ. Association of overweight with increased risk for coronary heart disease
partly independent of blood pressure and cholesterol levels: a meta-analysis of 21 cohort studies including more than 300,000 persons. Arch
Intern Med. 2007;167:1720 –1728.
Mora S, Yanek LR, Moy TF, Fallin D, Becker LC, Becker DM. Interaction of body mass index and Framingham Risk Score in predicting
incident coronary disease in families. Circulation. 2005;111:1871–1876.
Reaven GM. Importance of identifying the overweight patient who will
benefit the most by losing weight. Ann Intern Med. 2003;138:420 – 423.
McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven G. Use
of metabolic markers to identify overweight individuals who are insulin
resistant. Ann Intern Med. 2003;139:802– 809.
Kahn HS, Valdez R. Metabolic risks identified by the combination of
enlarged waist and elevated triacylglycerol concentration. Am J Clin
Nutr. 2003;78:928 –934.
Lemieux I, Pascot A, Couillard C, Lamarche B, Tchernof A, Almeras N,
Bergeron J, Gaudet D, Tremblay G, Prud’homme D, Nadeau A, Despres
JP. Hypertriglyceridemic waist: a marker of the atherogenic metabolic
triad (hyperinsulinemia; hyperapolipoprotein B; small, dense LDL) in
men? Circulation. 2000;102:179 –184.
Despres JP, Lemieux I, Prud’homme D. Treatment of obesity: need to
focus on high risk abdominally obese patients. BMJ. 2001;322:716 –720.
Alberti FKMM, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI,
Donato KA, Fruchart JC, James WPT, Loria CM, Smith SC. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart
Association; World Heart Federation; International Atherosclerosis
Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640 –1645.
59. Mechanick JI, Kushner RF, Sugerman HJ; Writing Group. AACE/
TOS/ASMBS guidelines: the American Association of Clinical Endocrinologists, the Obesity Society, and American Society for Metabolic &
Bariatric Surgery medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric
surgery patient. Obesity. 2009;17(suppl):S1–S70.
60. Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The
disease burden associated with overweight and obesity. JAMA. 1999;
282:1523–1529.
61. Bays HE, Chapman RH, Grandy S. The relationship of body mass index
to diabetes mellitus, hypertension and dyslipidemia: comparison of data
from two national surveys. Int J Clin Pract. 2007;61:737–747.
62. Silk AW, McTigue KM. Reexamining the physical examination for
obese patients. JAMA. 2011;305:193–194.
63. Standards of medical care in diabetes: 2012. Diabetes Care. 2012;35:
S11–S63.
64. Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. Executive summary of the third reports of the
National Cholesterol Education Program (NCEP) Expert Panel on
Detection, Evaluation, and Treatment of High Blood Cholesterol in
Adults (Adult Treatment Panel III). JAMA. 2001;285:2486 –97. http://
www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf.
65. Sharma AM, Kushner RF. A proposed clinical staging system for
obesity. Int J Obes (Lond). 2009;33:289 –295.
66. Padwal RS, Pajewski NM, Allison DB. Using the Edmonton obesity
staging system to predict mortality in a population-representative cohort
of people with overweight and obesity. CMAJ. 2011;183:E1059 –E1066.
67. Kuk JL, Ardern CI, Church TS, Sharma AM, Padwal R, Sui Z, Blair SN.
Edmonton Obesity Staging System: association with weight history and
mortality risk. Appl Physiol Nutr Metab. 2011;36:570 –576.
68. Schwartz MW, Woods SC, Seeley RJ, Barash GS, Baskin DG, Leibel
RL. Is the energy homeostasis system inherently biased toward weight
gain? Diabetes. 2003;52:232–238.
69. Sumithran P, Predergast LA, Delbridge E, Purcell K, Shulkes A,
Kriketos A, Proietto J. Long-term persistence of hormonal adaptations to
weight loss. N Engl J Med. 2011;365:1597–1604.
70. Rosenbaum M, Kissileff HR, Mayer LES, Hirsch J, Leibel RL. Energy
intake in weight-reduced humans. Brain Res. 2010;1350:95–102.
71. Redman LM, Heilbronn LK, Martin CK, de Jonge L, Williamson DA,
Delany JP, Ravussin E. Metabolic and behavioral compensation in
response to caloric restriction: implications for the maintenance of
weight loss. PloS One. 2009;4:e4377.
72. Kraschnewski JL, Boan J, Espisito J, Sherwood NE, Lehman EB,
Kephart DK, Sciamanna CN. Long-term weight loss maintenance in the
United Sates. Int J Obes (Lond). 2010;34:1644 –1654.
73. Wadden TA, Webb VL, Moran CH, Bailer BA. Lifestyle modification
for obesity: new developments in diet, physical activity, and behavior
therapy. Circulation. 2012;125:1157–1170.
74. Lowe MR. Self-regulation of energy intake in the prevention and
treatment of obesity: is it feasible? Obes Res. 2003;11(suppl):44S–59S.
75. US Department of Agriculture and US Department of Health and
Human Services. Dietary Guidelines for Americans 2010. 7th ed. Washington, DC: US Government Printing Office; December 2010.
76. Jakicic JM. The effect of physical activity on body weight. Obesity.
2009;17(suppl 3):S34 –S38.
77. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK;
American College of Sports Medicine. American College of Sports
medicine position stand: appropriate physical activity intervention
strategies for weight loss and prevention of weight regain for adults.
Med Sci Sports Exerc. 2009;41:459 – 471.
78. Saks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD,
McManus K, Champagne CM, Bishop LM, Laranjo N, Leboff MS,
Rood JC, de Jonge L, Greenway FL, Loria CM, Obarzanek E, Williamson DA. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med. 2009;360:
859 – 873.
79. Sacks FM, Svetkey LP, Vollmr WM, Appel LJ, Bray GA, Harsha D,
Obarzanek E, Conlin PR, Miller ER, Simons-Morton DG, Karanja N,
Lin PH, Aickin M, Most-Windhauser MM, Moore TJ, Proschan MA,
Cutler JA; DASH–Sodium Collaborative Research Group. Effects on
blood pressure of reduced dietary sodium and the Dietary Approaches to
Stop Hypertension (DASH) diet. N Engl J Med. 2001;344:3–10.
80. Elmer PJ, Obarzanek E, Vollmer WM, Simons-Morton D, Stevens VJ,
Young DR, Lin PH, Champagne C, Harsha DW, Svetkey LP, Ard J,
Brantley PJ, Proschan MA, Erlinger TP, Appel LJ. Effects of compre-
Kushner
81.
82.
83.
84.
85.
86.
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
87.
88.
89.
90.
91.
92.
93.
hensive lifestyle modification on diet, weight, physical fitness, and
blood pressure control: 18-month results of a randomized trial. Ann
Intern Med. 2006;144:485– 495.
Blumenthal JA, Babyak MA, Hinderliter A, Watkins LL, Craighead L,
Lin PH, Caccia C, Johnson J, Waugh R, Sherwood A. Effects of the
DASH diet alone and in combination with exercise and weight loss on
blood pressure and cardiovascular biomarkers in men and women with
high blood pressure: the ENCORE study. Arch Intern Med. 2010;170:
126 –135.
A position statement of the American Diabetes Association: nutrition
recommendations and interventions for diabetes. Diabetes Care. 2008;
31(suppl):S61–S78.
Nordmann AJ, Suter-Zimmerman K, Bucher HC, Shai I, Tuttle KR,
Ramon, Estruch R, Briel M. Meta-analysis comparing Mediterranean to
low-fat diets for modification of cardiovascular risk factors. Am J Med.
2011;124:841– 851.
Position of the American Dietetic Association: weight management.
J Am Diet Assoc. 2009;109:330 –346.
Bodenheimer T, Lorig K, Holman H, Grumbach K. Patient selfmanagement of chronic disease in primary care. JAMA. 2002;288:
2469 –2475.
Keogh JB, Clifton PM. The role of meal replacements in obesity
treatment. Obes Rev. 2005;6:229 –234.
Wadden TA, West DS, Neiberg RH, Wing RR, Ryan, Johnson KC,
Foreyt JP, Hill JO, Trence DL, Vitolins MZ; Look AHEAD Research
Group. One-year weight losses in the Look AHEAD Study: factors
associated with success. Obesity. 2009;17:713–722.
Rock CL, Flatt SW, Sherwood NE, Karanja N, Pakiz B, Thompson CA.
Effect of a free prepared meal and incentivized weight loss program on
weight loss and weight loss maintenance in obese and overweight
women: a randomized trial. JAMA. 2010;304:1803–1811.
Jebb SA, Ahern AL, Olson AD, Aston LM, Holzopfel C, Stoll J,
Amann-Gassner U, Simpson AE, Fuller NR, Pearson S, Lau NS, Mander
AP, Hauner H, Caterson ID. Primary care referral to a commercial
provider for weight loss treatment versus standard care: a randomized
controlled trial. Lancet. 2011;378:1485–1492.
American College of Sports Medicine. ACSM’s Guidelines for Exercise
Testing and Prescription. 7th ed. Philadelphia, PA: Lippincott Williams
& Wilkins; 2006.
2008 Physical activity guidelines for Americans. US Department of
Health and Human Services. 2008. www.health.gov/paguidelines.
Accessed April 8, 2012.
Burke LE, Wang J, Sevick MA. Self-monitoring in weight loss: a
systematic review of the literature. J Am Diet Assoc. 2011;111:92–102.
Smith SC, Benjamin EJ, Bonow RO, Braun LT, Creager MA, Franklin
BA, Gibbons RJ, Grundy SM, Hiratzka LF, Jones DW, Lloyd-Jones
DM, Minissian M, Mosca L, Peterson ED, Sacco RL, Spertus J, Stein
JH, Taubert KA. AHA/ACCF secondary prevention and risk reduction
therapy for patients with coronary and other atherosclerotic vascular
disease: 2011 update: a guideline from the American Heart Association
and American College of Cardiology Foundation. Circulation. 2011;
124:2458 –2473.
Clinical Assessment and Management of Obesity
2877
94. Bray GA, Ryan DH. Medical therapy for the patient with obesity.
Circulation. 20102;125:1695–1703.
95. Smith SR, Weissman NJ, Anderson CM, Sanchez M, Chuang E, Stubbe
S, Bays H, Shanahan WR; Behavioral Modification and Lorcaserin for
Overweight and Obesity Management (BLOOM) Study Group. Multicenter, placebo-controlled trial of lorcaserin for weight management.
N Engl J Med. 2010;363:245–256.
96. Greenway FL, Fujioka K, Plodkowski RA, Mudaliar S, Guttadauria M,
Erickson J, Kim DD, Dunayevich E; COR-I Study Group. Effect of
naltrexone plus bupropion on weight loss in overweight and obese adults
(COR-1): a multicenter, randomized, double-blind, placebo-controlled,
phase 3 trial. Lancet. 2010;376:595– 605.
97. Gadde KM, Allison DB, Ryan DH, Peterson CA, Troupin B, Schwiers
ML, Day WW. Effects of low-dose, controlled-release, phentermine
plus topiramate combination on weight and associated comorbidities in
overweight and obese adults (CONQUER): a randomized, placebocontrolled, phase 3 trial. Lancet. 2011;377:1341–1352.
98. Hiatt WR, Thomas A, Goldfine AB. What cost weight loss? Circulation.
2012;125:1171–1177.
99. Leslie WS, Hankey CR, Lean MEJ. Weight gain as an adverse effect of
some commonly prescribed drugs: a systematic review. Q J Med. 2007;
100:395– 404.
100. Gastrointestinal surgery for severe obesity: National Institutes of Health
Consensus Development Conference statement. Am J Clin Nutr. 1992;
55:615S– 619S.
101. Dixon J, Straznicky NE, Lambert EA, Schlaich MP, Lambert GW.
Laparoscopic adjustable gastric banding and other devices for the management of obesity. Circulation. 2012;126:774 –785.
102. Padwal R, Klarenbach S, Wiebe N, Birch D, Karmali S, Manns B, Hazel
M, Sharma AM, Tonelli M. Bariatric surgery: a systematic review and
network meta-analysis of randomized trials. Obes Rev. 2011;12:
602– 621.
103. Buchwald H, Avidor Y, Braunwald E, Jenson MD, Pories W, Fahrbach
K, Schoelles K. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292:1724 –1737.
104. Pontiroli AE, Morabito A. Long-term prevention of mortality in morbid
obesity through bariatric surgery: a systematic review and meta-analysis
of trials performed with gastric banding and gastric bypass. Ann Surg.
2011;253:484 – 487.
105. Blackburn GL, Hutter MM, Harvey AM, Apovian CM, Boulton HR,
Cummings S, Fallon JA, Greenberg I, Jiser ME, Jones DB, Jones SB,
Kaplan LM, Kelly JJ, Rayford SRS, Lautz DB, Lenders CM, LoNigro
R, Luce H, McNamara A, Mulligan AT, Paasche-Orlow MK, Perna
FM, Pratt JSA, Stancel SM, Robinson MK, Romanelli JR, Saltzman
E, Schumann R, Shikora SA, Snow RL, Sogg S, Sullivan MA,
Tarnoff M, Thompson CC, Wee CC, Ridley N, Auerbach J, Hu FB,
Kirle L, Buckley RB, Annas CL. Expert Panel on Weight Loss surgery:
executive report update. Obesity. 2009;17:842– 862.
KEY WORDS: diet
䡲
life style
䡲
obesity
䡲
primary health care
䡲
therapy
Clinical Assessment and Management of Adult Obesity
Robert F. Kushner
Circulation. 2012;126:2870-2877
doi: 10.1161/CIRCULATIONAHA.111.075424
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