Management of Obesity

1. Kyaw Soe win, Asso Prof / Senior Consultant Cardiologist
Vintage Luxury Yachet Hotel, 30 May 2015

2. Treating Patients with Obesity:
Who, Why, How and to What Ends

3. Guide for Selecting Obesity Treatment
The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. October 2000, NIH Pub. No.00-4084
Treatment 23-26.9 27-29.9 30-34.9 35-39.9 >40
Diet, Exercise,
Behavior Tx + + + + +
Pharmaco-
therapy
With co-
morbidities
+ + +
Surgery
With co-
morbidities
+
BMI Category (kg/m2)
Take Home Massage

4.  Definition : Obesity is a state of excess adipose tissue mass.
(Harrison’s :17th )
 Obesity is a disease of caloric imbalance that results from an
excess intake of calories above their consumption by the body.
(Robbins : 8th)
 Obesity can be defined as an excess of body fat accumulation or
adiposity, with multiple organ-specific adaptive or maladaptive
consequences, and has been considered more prone to develop
cardiovascular diseases.

5. • Calling it a disease would define one-third of Americans as being ill and
could lead to more reliance on costly drugs and surgery rather than
lifestyle changes
• Some people might be overtreated because their BMI was above a line
designating them as having a disease, even though they were healthy
Why Obesity is NOT a Disease
• It is a lifestyle choice
• No specific symptoms associated with it
• It is a risk factor for disease, not a disease itself*
* What about high cholesterol or hypertension?

6. Why Obesity IS a Disease
• It is associated with impaired body function
• Like other diseases, it results from physiological
dysfunction (precipitated by numerous forces in modern
society)
• It causes, exacerbates or accelerates more than 65
significant comorbid diseases
• It is associated with a substantial burden of morbidity
and premature death

7. 7
Consequences of Obesity
Hippocrates
recognized that :
“sudden death is more
common in those who
are naturally fat than
in lean.”
(in BC 400)

8. Complications of Obesity
Several of these complications exacerbate the
underlying obesity, creating a vicious cycle:
Diabetes Many diabetes drugs
cause weight gain
PCOS Insulin resistance
promotes lipogenesis
Sleep apnea Disrupted sleep
can cause weight gain
Arthritis Limit exercise capacity
Back pain
Inflammatory Steroids often cause
disorders weight gain
Depression Eating disorders and
Psychological many psychotropic agents
cause weight gain
Psychological
Neoplastic
Inflammatory
Structural
Metabolic
Degenerative

9. Medical Complications of Obesity
Phlebitis
venous stasis
Coronary heart disease
Pulmonary disease
abnormal function
obstructive sleep apnea
hypoventilation syndrome
Gallstones
Gout
Diabetes
Osteoarthritis
Fatty liver
disease
steatosis
steatohepatitis
cirrhosis
Hypertension
Dyslipidemia
Cataracts
Skin disorders
Pancreatitis
Intracranial hypertension
Cognitive dysfunction
Cancer
breast, uterus, cervix, ovary,
prostate, kidney, colon, esophagus
pancreas, gallbladder, liver
Gynecologic abnormalities
abnormal menses
infertility
polycystic ovarian syndrome
Stroke

10.  Affects men and women of all ages
 Predominates in developed countries.
obesity?

11. PREVALENCE OF RISK FACTORS FOR NON-COMMUNICABLE
DISEASES IN MYANMAR
Risk Factors
Yangon*
(2003-2004) (%)
National**
(2009) (%)
Male Female Both Sexes Male Female Both Sexes
Current smoking 36.00 11.11 23.20 33.61 6.13 16.68
Current drinking 25.96 1.09 11.96 31.17 1.47 12.87
Physical inactivity 7.32 7.86 7.62 10.44 14.1 12.69
Fruits and vegetable consumption (% Who
eat 5servings of fruits and vegetables/day)
98.64 98.73 98.69 89.8 90.6 90.29
Hypertension 27.94 24.11 25.87 30.99 29.34 29.97
Overweight (BMI 25) 20.60 29.96 23.80 17.74 30.27 25.38
Obesity (BMI 30) 4.77 10.35 7.85 4.27 8.37 6.8
Raised Blood cholesterol level
(5.2mmol/L)
21.16 35.12 27.42 - - -
Diabetes (diagnosed by OGTT) 11.51 12.64 12.14 - - -
*STEP Survey in Yangon Division (2003-2004)
** National STEP Survey (2009) ((Prof. TSLatt et al, JAFES vol 26 no 2, November 2011)

15. Assessment of Overweight and
Obesity
 Body Mass Index (BMI)
 Weight (kg)/height (m2)
 Weight (lb)/height (in2) x 703
 Waist Circumference (WC)
 High risk:
 Men >102 cm (40 in.)
 Women >88 cm (35 in.)
 Waist Hip Ratio (WHR)
 Skin-fold thickness
 Measurement of Abdominal Fat by CT

16. Classification BMI (kg/m2) Risk of co-morbidities
Underweight <18.5 Low (but risk of other clinical problems
increased)
Normal range 18.5-24.9 Average
Overweight* ≥25
Pre-obese 25.0-29.9 Mildly increased
Obese >30.0
Class I 30.0-34.9 Moderate
Class II 35.0-39.9 Severe
Class III 40.0 Very severe
WHO Classification of adult categories of BMI
Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report. NIH
Publication # 98-4083, September 1998, National Institutes of Health.

17. Classification BMI
(kg/m2)
Risk of co-morbidities
Waist circumference
< 90 cm (men)
< 80 cm (women)
≥ 90 cm (men)
≥ 80 cm (women)
Underweight <18.5 Low (but risk of other
clinical problems
increased)
Average
Normal range 18.5-22.9 Average Increased
Overweight ≥23
At risk 23.0-24.9 Increased Moderate
Obese I 25-29.9 Moderate Severe
Obese II ≥ 30.0 Severe Very severe
World Health Organization, 1998
WHO classification of BMIs for adults
of Asian origin

18.  Values are age independent & same for both sexes.
 At similar BMI, fat content in women > men BMI 30 is
threshold for obesity.
 BMI 25 - 30 medically significant & requires intervention
• At a given BMI, women, on average, have more body fat.
• Morbidity and mortality increase with BMI similarly for
men and women

19. Limits of using BMI
 BMI is not an index of regional fat distribution
 BMI may overestimate body fat in athletes and individuals with
a muscular build
 BMI DOES NOT
 show the difference between excess fat and muscle.
 identify whether the fat is laid down in particular sites. eg,
abdominal fat has more serious health consequences than fat
located elsewhere
 BMI may underestimate body fat in older persons and
individuals who have lost muscle mass

20. Measuring Waist Circumference
Waist circumference is calculated by comfortably measuring the waist
halfway between the bottom of the rib cage and the top of the pelvis.

21. Measuring Waist Circumference
 WC is a good surrogate index of visceral adiposity.
 WC is an independent and powerful risk factor for CAD
and MI.
 WC is related to increased risk of DM, hypertension,
stroke, sleep apnoea and dyslipidaemia.
Increased risk Substantially increased risk
Men 94 cm 102 cm
Women 80 cm 88 cm

22. Country/Ethnic group Waist circumference
Europids
Male
Female
≥ 94 cm
≥ 80 cm
South Asians
Male
Female
≥ 90 cm
≥ 80 cm
Chinese
Male
Female
≥ 90 cm
≥ 80 cm
Japanese
Male
Female
≥ 90 cm
≥ 80 cm
Ethnic South and Central Americans
Use South Asian recommendations until
more specific data are available
Sub-Saharan Africans Use European data until more specific
data are available
Eastern Mediterranean and Middle
East (Arab) populations
Country/ethnic specific values for waist circumference

23. Measuring obesity
Measuring Waist Circumference
 Large waist circumference (WC) can identify some at increased
risk over BMI alone
 If BMI and other cardiometabolic risk factors are assessed,
currently there is insufficient evidence to:
 Substitute WC for BMI
 Measure WC in addition to BMI
Klein, et al. Waist Circumference and Cardiometabolic Risk. Diabetes Care. 2007 0: dc07-9921v1-0.

24. Other methods
 Waist hip ratio - >0.9 for women
- > 1 for men
 Anthropometry ( skin fold thickness )
 Harpenden skin calliper
 < 40 mm in males, < 50 mm in females
 Densitometry ( under water weighing )
 CT Scan, MRI, Electric impedance

25. Waist-to-hip ratio
Ratio =
WAIST
HIPS
TO FIND RATIO
Waist: Measure at
narrowest point with
stomach relaxed
Hips: Measure at
fullest point
Desired Ratio
Women : <0.8
Men : < 1.0
Risk increases if
waist circumference
is >94 cm in men and
>80 cm in women

26. Skin Fold Thickness
 Harpenders callipers / MRNL callipers
 It is measured at biceps/triceps/illiac
and interscapular.
 Total of all four sites is considered
15-45 mm – 8-22 % of total body fat
46-75 mm – 23-30 % of total body fat
76-150 mm – 31-40 % of total body fat
151-170 mm – 41-45 % of total body fat
Upto 22% it is normal (males)
Upto 30% it is normal (females)

27. Measuring Abdominal Fat by CT

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29. Obesity Phenotypes
 Peripheral adiposity
 Collection of fat on hips and buttocks
 Women are more likely to have a peripheral distribution
 Associated with mechanical problems
 Abdominal adiposity or central obesity
 More likely to have a waist distribution
 Associated with insulin resistance and heart disease
 Mixed central – peripheral adiposity
 Severely obese women and men ( BMI >40 kg/m2)

30. Peripheral adiposity central obesity

31. Measuring Waist Hip Ratio

32. •Mixed central – peripheral adiposity

33. “Super obese" male
A "super obese" male with a BMI of 47 kg/m2: weight 146 kg (322 lb), height 177 cm (5 ft 10 in)

34. WHY is it HARD to maintain the weight loss for those
who lose after dietary restriction?
- Constant number of adipocytes
- -Higher no. in obese

35. Fat Cells
 Adipose cells store majority of the body’s fat. Vary in size and number.
 Increase in body fatness is due to:
 Fat cell hypertrophy
 Fat cell hyperplasia
Fat Cell Number
 Number of fat cells appears to be biggest factor in determining risk for obesity.
 Determined mostly in adolescent years
 Average non-obese person: 25-30 bill.
 Moderately obese: 60-100 bill.
 Massively obese: 300 bill. +
 Fat cells development (significant ):
 Last trimester of pregnancy
 First year of life
 During adolescent “growth spurt”

36. ..

37. Fat Cells and Weight Gain
 Typically only see an increase in size of existing cells in adults. (Hypertrophy)
 If cells begin to reach their maximum size of 1.0 micrograms of lipid per cell then
new cells may develop. (Hyperplasia)
Fat Cells and Weight Loss
 Cells decrease in size, not number:
 Studies have proven, fat cells ONLY decrease in size not number.
 Individuals with higher number of cells, regained weight more readily.
 Person’s with smaller, more numerous cells reported more “cravings” for food
 Leptin?
Development of Adipose tissues
As expected, studies have shown that nutritional and exercise
interventions in the growing years, results in a LOWER FAT CELL
NUMBER, and a subsequent decrease in relative RISK of obesity!!!

38. All Fat Cells Are Not Created Equal
• Large Insulin-
Resistant
Adipocytes
• Adrenergic
Receptors 
• Insulin-Mediated
Antilypolysis
• Catecholamine-
Mediated
Lipolysis 
• Small Insulin-Sensitive
Adipocytes
• Adrenergic Receptors

Fatty Acids 

39. Adipose Tissue is
an Endocrine Organ!!!

40. LEPTIN
ADIPONECTIN
INTERLEUKIN-6
Cortisol
(11betaHSD)
Angiotensinogen
Angpt4/PGAR/FIAF
SAA2
Retinol Binding Protein
Adipokines (adipose hormones) and other key secretory
products produced by fat cells.

41. LEPTIN
ADIPONECTIN
INTERLEUKIN-6
Cortisol
(11betaHSD)
Angiotensinogen
Angpt4/PGAR/FIAF
Serum Amyloid A
Omentin
Visfatin
Adipokines are also produced by non-adipose cells within adipose tissue.
TNF-ALPHA
Interleukin-8
PAI-1

42. Resistance
Hyperinsulinemia
+
Hyperglycemia
Activation of the
sympathetic nervous
system
Increase of arterial tone
Na+ reabsorption
Hypertension
Overstimulation of
pancreatic -cell
function
Reduction of insulin
secretion
Type 2 Diabetes

43. Risk Factor Defining Level
Abdominal obesity
Men
Women
Waist circumference
>102 cm (>40 in)
>88 cm (>35 in)
Triglycerides ≥150 mg/dL (1.7 mmol/L)
HDL cholesterol
Men
Women
<40 mg/dL (1.04 mmol/L)
<50 mg/dL (1.29 mmol/L)
Blood pressure ≥130/ ≥85 mmHg
Fasting glucose ≥100 mg/dL (5.6 mmol/L)
In order to make a diagnosis of the metabolic syndrome a patient must present
with three or more of the following five risk factors:
Metabolic syndrome:
The NCEP ATP III definition*
*2001, updated 2005

44. Metabolically Healthy Obesity
Features of MHO subjects
 Predominant subcutaneous peripheral adiposity
 Younger age when compared with complicated obese subjects
 Normal fasting glucose and glucose tolerance
 Normal systolic and diastolic BP (≤120/80 mmHg)
 Normal lipid profile, including normal levels of TG (≤150 mg/dl)
and HDL cholesterol (≥40 and ≥50 mg/dl in men and women,
respectively)
The existence of MHO subjects is a well-defined clinical entity.

45.  when compared with complicated obese subjects
 Lower prevalence of small LDL particles
 Better insulin sensitivity
 Lower inflammatory status
 Normal liver enzymes
 Normal resting electrocardiogram
 Appropriate echocardiographic left ventricular mass or no LV
hypertrophy
 Low c-IMT
 No clinical evidence of coronary artery disease or heart
failure
Metabolically Healthy Obesity
Features of MHO subjects

46.  MHO subjects show a more prevalent subcutaneous,
peripheral obesity phenotype rather than the central,
visceral obesity phenotype.
 MHO subjects also need clinical management and weight loss
strategies similar to morbidly obese subjects.
 Their better insulin sensitivity and lower visceral adiposity
may contribute to a better response to weight-loss
interventions.
Metabolically Healthy Obesity
Management of MHO subjects

47. Managing the Obesity

48. 48
What causes Obesity?
 Genetics
 Nutrient and Energy model of
obesity:
 Energy output (physical activity)
 Energy input (dietary intake)
 Behavioral and cultural factors
 Medications

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52. Genetic Links
 Study in Cambridge University has isolated at least two genes that
when manipulated…control weight gain / loss (Leptin)
 Genetics account for ~40% of weight differences
 Genes affect metabolic rate, fuel use, brain chemistry
 A child with no obese parents has a 10% chance of becoming obese
 A child with 1 obese parent has a 40% chance
 A child with 2 obese parents has a 80% chance

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69. Obesity results from a failure of normal weight and
energy regulatory mechanisms

71. Berthoud HR. Curr Opin Neurobiology 2011;21:888-896

72. Satiety Regulator
The hypothalamus
When feeding cells are stimulated, they signal you to
eat
When satiety cells are stimulated, they signal you to
stop eating
Sympathetic nervous system
When activity increases, it signals you to stop eating
When activity decreases, it signals you to eat

73.  Produced by adipocytes
 Product of ‘ob’ gene
 Provides signal for “energy
sufficiency”.
 Abundant fat  Leptin
secretion
 Regulated by insulin
stimulated glucose
metabolism
 Stimulates thermogenesis,
activity, energy expenditure
Leptin
+ POMC/CART
neurons
Anorexic
neuropeptides-
(MSH)
Leptin
-
NPY/AgRP
neurons
Produce
orexinergic
neuropeptides

74.  Produced mainly by adipocytes
 Low levels in obesity
 Stimulates fatty acid oxidation
 “Fat-burning molecule”
 “Guardian angel against
obesity”
 ↓ fatty acid influx in liver, liver
glucose production
 ↓ Protects against Metabolic
syndrome
Adiponectin
AdipoR1, AdipoR2 in
skeletal muscle,
liver, brain
+ cAMP activated
protein kinase
Inactivates acetyl
coenzyme A
carboxylase (Key
enzyme in Fatty
acid synthesis)

75. GI Hormonal influence
Peptide Where
synthesized
Effect on feeding
Ghrelin Stomach Orexigenic
CCK Duodenum Anorexigenic
PYY Distal small
intestine
Anorexigenic
GLP-1 Small intestine Anorexigenic
Amylin Pancreas Anorexigenic
CCK = cholecystokinin; PYY = polypeptide YY;
GLP-1 = glucagon-like peptide 1; [exenatide, liraglutide]; Amylin [pramlintide]

76. “Age and Obesity”
 Greatest fat gain is from 25 – 44 years of age in most people.
 Average man will gain 0.2 to 0.8 kg per year. This equates to
an average of over a pound a year.
 14% of all women will gain over 30 lbs from age 25 to 34.

77. Medication-induced Weight Gain
Medications account for 5-10% of obesity in the U.S.
In each relevant category, remove or substitute
weight gain-promoting medications with weight
neutral or weight loss-promoting alternatives

78. Selected Medications That Can Cause Weight
Gain
 Psychotropic medications
 Tricyclic antidepressants
 Monoamine oxidase inhibitors
 Specific SSRIs
 Atypical antipsychotics
 Lithium
 Specific anticonvulsants
 -adrenergic receptor blockers
SSRI=selective serotonin reuptake inhibitor
 Diabetes medications
– Insulin
– Sulfonylureas
– Thiazolidinediones
 Highly active antiretroviral
therapy
 Tamoxifen
 Steroid hormones
– Glucocorticoids
– Progestational
steroids

79. Macroenvironmental Influences*
• 24-hour lifestyle
• Economic structure
• Time pressures
• Workload
• Loss of downtime
• Speed of life
• Global stressors
*Amenable only to societal intervention

80. Microenvironmental Influences*
• Types of nutrients
• Eating schedules
• Physical activity
• Sleep health
• Drugs and medications
• Local stressors
*Amenable to individual action

81. The goal of lifestyle-based therapies is to
normalize the patient’s microenvironment

82. Management of Obesity and Goals
Goal is to reduce or prevent co-morbidities.
 Short term Goal: Decrease body weight by 10 percent from
baseline.
 If goal is achieved, further weight loss can be attempted if
indicated.
 Reasonable timeline: 6 months of therapy.
• Interim goal: Maintenance
– May need to be continued indefinitely.
• Long-term goal: If unable to lose weight, prevent
further weight gain.

83. How much weight loss is significant?
A 5-10% reduction in weight (within 6 months)
and
weight maintenance should be stressed in any
weight loss program and contributes
significantly to decreased morbidity

84. Benefits of Modest Intentional Weight
Loss
 Improvement in comorbid
diseases
 Type 2 diabetes
 Hypertension
 Dyslipidemia
 Fatty liver disease
 Obstructive sleep apnea
 Asthma
 Osteoarthritis
 Cancer risk
• Improved quality of life
• Decreased health care costs
• Decreased surgical
complication rates
• Orthopedic surgery
• Heart surgery
• General and thoracic
surgery
• The effect on cardiovascular risk is less clear

85. Obesity Treatment Pyramid
Surgery
Pharmacotherapy
Lifestyle Modification
Diet Physical Activity

86. Requires two steps:
 Assessment
 Degree of obesity
 Determine absolute risk status
 Management
 Weight management
 Weight loss
 Weight maintenance
 Control of associated risk factors
Management of Overweight/Obese Patients

87. Assessment of Overweight and
Obesity
 Body Mass Index (BMI)
 Weight (kg)/height (m2)
 Weight (lb)/height (in2) x 703
 Waist Circumference (WC)
 High risk:
 Men >102 cm (40 in.)
 Women >88 cm (35 in.)
 Waist Hip Ratio (WHR)
 Skin-fold thickness
 Measurement of Abdominal Fat by CT

88. Determine Absolute Risk Status
Evaluate:
 Disease conditions (e.g., CHD, type 2 diabetes, sleep apnea)
(+ = very high risk)
 Cardiovascular risk factors: smoking, hypertension,
high LDL, low HDL, IGT, family h/o (>3 = high risk
 Other obesity-associated diseases (e.g., gynecological
abnormalities, osteoarthritis)
 Other risk factors:
 Physical inactivity
 High serum TG (>200 mg/dL)

89. Classification Of Obesity (Clinical staging)
 Stage 0: no apparent obesity-related risk factors
 Stage 1: presence of obesity-related sub-clinical risk factors, mild
physical symptoms.
 Stage 2: presence of established obesity-related chronic disorders
 Stage 3: established end-organ damage
 Stage 4: severe (end-stage?) disabilities

90. Treatment Algorithm
Patient Encounter
Hx of 25 BMI?
• Measure weight,
height, and waist
circumference
• Calculate BMI
Examination
Brief reinforcement/
educate on weight
management
Periodic weight
check
Advise to maintain
weight/address
other risk factors
Clinician and patient
devise goals and
treatment strategy
for weight loss and
risk factor control
Assess reasons for
failure to lose
weight
Maintenance counseling:
Dietary therapy
Behavior therapy
Physical activity:
Treatment
Assess risk
factors
No
Yes
1
2
14
15 13
12
11 1016
3
4 6
5 7
8
9
Yes
No
Yes
No
Hx BMI 25?
No
Yes
Yes
No
Does
patient want to
lose weight?
Yes
No
Progress
being made/goal
achieved?
BMI 25 OR
waist circumference
> 88 cm (F)
> 102 cm (M)
BMI
 30 OR
{[BMI 25 to 29.9
OR waist circumference
>88 cm (F) >102 cm (M)]
AND 2 risk
factors}
BMI
measured in
past
2 years?

91. No
BMI
³ 30 OR
{[BMI 25 to 29.9
OR waist >88 cm (F)
>102 cm (M)]
AND ³ 2 risk
factors}
Treatment Algorithm
(Part 1 of 3)Patient Encounter
Hx of 25
BMI?
• Measure
weight, height,
and waist
circumference
• Calculate BMI
Assess risk
factors
No
Yes
1
2
3
4
6
5
7
Yes
No
BMI
measured in
past
2 years?
BMI  25 OR
waist > 88 cm (F)
> 102 cm (M)
Yes
Examination
Treatment

92. Devise goals and
treatment strategy for
weight loss and risk
factor control
Assess reasons for
failure to lose weight
Maintenance
counseling
12
11 10
8
9
No
Yes
Yes
No Desire to
lose weight?
Yes
No
Progress
made?
BMI
30 OR
{[BMI 25 to 29.9
OR waist >88 cm (F)
>102 cm (M)]
AND  2 risk
factors}
Examination
Treatment
7
Periodic weight
check
• Advise to maintain weight
• Address other risk factors
13
16
Treatment Algorithm
(Part 2 of 3)

93. • Brief reinforcement
• Educate on weight
management
Periodic weight
check
• Advise to maintain
weight
• Address other risk
factors
14
15
13
16
5
Yes
No
Yes
No
Hx BMI  25?
BMI 25 OR
waist > 88 cm (F)
> 102 cm (M)
Examination
Treatment
Treatment Algorithm
(Part 3 of 3)
* This algorithm applies only to
the assessment for overweight
and obesity and subsequent
decisions based on that
assessment. It does not
include any initial overall
assessment for cardiovascular
risk factors or diseases that are
indicated.

94. Dietary Therapy (Total Fasting)
 Not recommended
 There is diuresis, natriuresis
 All deficiencies
 Re Feeding Syndrome-severe an potentially fatal
electrolyte, fluid and metabolic abnormalities when
feeding is resumed.

95. Why Diets Don’t Work
 Obesity is a chronic disease
 Treatment requires long-term lifestyle changes
 Dieters are misdirected
 More concerned about weight loss than healthy lifestyle
 Unrealistic weight expectations
 Body defends itself against weight loss
 Thyroid hormone concentrations (BMR) drop during weight loss and make it more
difficult to lose weight
 Activity of lipoprotein lipase increases making it
more efficient at taking up fat for storage
 Weight cycling (yo-yo dieting)
 Typically weight loss is not maintained
 Weight lost consists of fat and lean tissue
 Weight gained after weight loss is primarily adipose tissue
 Weight gained is usually more than weight lost
 Associated with upper body fat deposition

96. Clinical Application
 “Doctor, I know I need to reduce my calories and
exercise more in order to lose weight. I have done
it more times that I would like to admit. But I get
hungry and its hard to stay on a calorie reduced
diet. What is it about my metabolism that causes
me to be so hungry?”

97. Nutrients Influence
Presence of energy yielding nutrient registers satiety in
the brain
Apolipoprotein A-IV on the chylomicrons signals satiety
in the brain
Absence of these nutrients will signal hunger

98. Behavior Therapy:
Important Concepts
Techniques to conquer eating triggers
 eating regular meals
 eating at the same time and place
 use smaller plates
 keeping accessible food out of sight
 eating only when hungry
 avoiding activities that encourage
eating
• slowing pace of eating
• reducing portion sizes
• measuring food intake
• leaving food on plate
• improving food choices
• eliminating second
servings
•

99. Physical Activity, Exercise, and Physical Fitness
 Physical activity: Any bodily movement produced by skeletal
muscles that results in energy expenditure.
 Exercise: A subset of physical activity That is planed,
structured, and repetitive and is done to improve or
maintain physical fitness.
 Physical fitness: A set of attributes that are either health or
skill related Health- endurance, strength, flexibility, Skill-
balance, agility, power, reaction time, speed and
coordination

100. Regular Physical Activity
 Fat use is enhanced with regular physical
activity
 Increases energy expenditure
 Duration and regularity are important
 Make it a part of a daily routine

101. Physical Activity
 Activity blunts the weight gain seen with aging.
 Studies in active adults
 No statistical relationship between caloric
consumption and body fat percentage
 Linear relationship between activity level and body
fat%.
 Reduced physical activity is the MAIN cause of adult obesity!

102. Increasing energy expenditure:
exercise is very effective in preventing long term
weight regain.
At least, doing aerobic exercise 3-5 times /week
for 45 minute
Include 5-10 minute warm up and cool down

103. Pharmacological Therapies

104. Drug Treatment of Obesity: Indicated when
 BMI is greater than 30
 BMI is higher than 27 and there are other
cardiovascular complications
 After several attempts diet alone is not enough

105. Anti-Obesity Medication – General Principles
 Should not be first-line in treatment of obesity
 Should only be used in conjunction with a healthy
eating and good exercise programme.
 Should not be prescribed to children in General
Practice – if all other advice on behavioural changes,
exercise and diet is failing – refer to secondary care.

106. Pharmacotherapy: sibutramine
 Sibutramine is a centrally acting inhibitor of serotonin
and noradrenaline reuptake. A starting dose of 10 mg
once daily is recommended; after 4 weeks this can be
titrated to 15 mg once daily.
 Sibutramine induces ≥10% loss of initial body weight
in almost 50% of overweight/obese patients.

109. Treatment Options 2012
Phentermine
 Short term medication
Orlistat
 Fat blocker with limited efficacy and well known
side effects
Metformin

110. Pharmacotherapy: Orlistat
 Orlistat is a reversible lipase inhibitor for obesity
management that acts by inhibiting the absorption of
dietary fats.
 Orlistat may induce ≥10% loss of initial body weight in
almost 30% of obese patients.
 Orlistat produces beneficial effects on
cardiometabolic profile in overweight/obese
individuals.

111. Orlistat - Mechanism of Action
FA
MG
GI lipase +
orlistat
TG
Intestinal lumen Mucosal cell Lymphatics
MicelleBile acids
MG
30% not absorbed
FFA

112. Orlistat inhibits absorption of approximately 30%
of dietary fat
30
25
20
15
10
5
0
Mean faecal fat (g/day)
-5 -4 -3 -2 -1 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Study days
Guerciolini, Int J Obesity 1997; 21 (Suppl. 3): S12-23
Orlistat 120 mg tid

113. Orlistat (Xenical)
 License – BMI 30+ or BMI 27+ with associated risk
factors.
 Continue after 3mths only if patient has lost at least
5% of body wt since starting.
 Continue for longer than 12mths only after discussing
benefits / limitations with pt.
 Vitamin supplementation (esp D) may be considered if
concern about absorption of fat soluble vitamins.

114.  Contra-indications – chronic malabsorption syndrome,
cholestasis, breast-feeding
 Cautions – pregnancy
 Side Effects – GI – flatulence, faecal urgency and
incontinence, oily stools, abdo pain and distension.
Tooth and gingival disorders, fatigue, headache,
anxiety.
 Dose – 120mg during or up to an 1hr after a meal up
to TDS. If a meal is missed or contains no fat – omit
the dose of orlistat.
Orlistat (Xenical)

115. Meta-analysis of RCTs Evaluating Effect of
Orlistat Therapy on Weight Loss at 1-Year
Study
or Sub-category
WMD (random)
95% CI
Hollander 1998*
Sjostrom 1998
Davidson 1999
Finer 2000
Heuptman 2000
Lindgarde 2000
Rossner 2000
Bakris 2002
Broom 2002
Kelley 2002*
Miles 2002*
Total (95% CI)
Padwal et al. Int J Obes 2003;27:1437
*All subjects had type 2 diabetes
WMD=weighted mean difference Favours
Treatment
Favours
Control
-10 -5 0 105

116. -12
-9
-6
-3
0
Effect of Long-term Orlistat Therapy on Body Weight
0
Weeks
52
Torgenson et al. Diabetes Care 2004;27:155
ChangeinWeight(kg)
104 156 208
P<0.001 vs placebo
-4.1 kg
-6.9 kg
Placebo
Orlistat

117. Gastrointestinal Side Effects of Orlistat
Therapy
Year 1 Year 2
Placebo Orlistat Placebo Orlistat
Fatty/oily stool 5 31 1 8
Increased defecation 7 20 2 2
Liquid stools 10 13 5 8
Fecal urgency 3 10 2 3
Flatulence 3 7 2 3
Flatus with discharge 0 7 0 1
Fecal incontinence 0 7 0 2
Oily evacuation 1 6 0 5
Low plasma vitamin conc:
Vitamin A 0.6 0.3 0.8 0
Vitamin D 0.6 5.1 0.8 3.1
Vitamin E 0.9 4.6 0 1.6
Sjostrom et al. Lancet 1998;352:167.
Values are percentage of subjects.

118. Pharmacotherapy: Metformin
 Metformin is an oral anti-diabetic drug that improves glucose
tolerance and insulin sensitivity.
 Metformin can be used alone or in combination with
sibutramine, orlistat or rimonabant for weight-loss management
in overweight and obese patients with and without diabetes.
 Metformin significantly improves the cardiometabolic profile in
overweight and obese subjects with and without diabetes.

119.  Medications approved in 2013
● Lorcaserin
● Phentermine/Topiramate ER
 Medications going to the FDA for possible approval
● Liraglutide
● Bupropion SR/ Naltrexone SR
Treatment Options 2014

120. Indications
and Dose
• Approved by FDA,
July 2012, schedule IV
• Indication
Weight loss in pts
with BMI ≥30 kg/m2
or BMI ≥27 kg/m2
with weight-related
co-morbid condition(s)
• Treatment Dose Daily
phentermine 7.5 mg
topiramate ER 46 mg
• Max Dose Daily
phentermine 15 mg
topiramate ER 92 mg
Phentermine/Topiramate ER
Phentermine and topiramate extended-release [package insert]. Mountain View, CA : Vivus; 2012.
Mechanism of
Action
Phentermine
• Sympathomimetic
amine, NE release
• Blunts appetite
Topiramate
• Increases GABA
activity, antagonize
AMPA/ kainate
glutamate receptor,
carbonic anhydrase
inhibitor
• Prolongs satiety
Contraindications
and Warnings
Contraindications
Pregnancy, glaucoma,
hyperthyroidism, MAOIs
Warnings
• Fetal toxicity
• Increased heart rate
• Suicide and mood and
sleep disorders
• Acute myopia and
glaucoma
• Cognitive impairment
• Metabolic acidosis
• Creatinine elevations
• Hypoglycemia with diabetes
meds
2012

121. Lancet. 2011 Apr 16;377(9774):1341-52
Topiramate/Phentermine (Qsymia) Effects on Weight

122. Phentermine/Topiramate ER Improves Risk Factors and Manifestations of
Cardiometabolic Disease CONQUER Study
Variable
Phentermine
7.5mg/
Topiramate
46 mg ER Placebo P value
Waist circumference
(cm)
 -7.6 -2.4 <0.0001
Systolic BP (mm Hg)  -4.7 -2.4 0.0008
Diastolic BP (mm Hg) -3.4 -2.7 0.1281
Triglycerides (%)  -8.6 4.7 <0.0001
LDL–C (%) -3.7 -4.1 0.7391
HDL–C (%)  5.2 1.2 <0.0001
CRP (mg/L)  -2.49 -0.79 <0.0001
Adiponectin (µg/mL)  1.40 0.33 <0.0001
Changes from baseline to week 56 in secondary endpoints
Gadde KM, et al. Lancet. 2011;377(9774):1341-1352.

123. Phentermine/Topiramate ER: EQUIP and CONQUER
Most Commonly Reported Treatment Emergent Adverse Events
Adverse Event (%)
(N=3749)
Placebo
PHEN/TPM ER
3.75/23
PHEN/TPM ER
7.5/46
PHEN/TPM ER
15/92
Paresthesia 1.9 4.2 13.7 19.9
Dry mouth 2.8 6.7 13.5 19.1
Constipation 6.1 7.9 15.1 16.1
Upper respiratory
tract infection
12.8 15.8 12.2 13.5
Headache 9.3 10.4 7.0 10.6
Dysgeusia 1.1 1.3 7.4 9.4
Nasopharyngitis 8.0 12.5 10.6 9.4
Insomnia 4.7 5.0 5.8 9.4
Dizziness 3.4 2.9 7.2 8.6
Sinusitis 6.3 7.5 6.8 7.8
Nausea 4.4 5.8 3.6 7.2
Back pain 5.1 5.4 5.6 6.6
Fatigue 4.3 5.0 4.4 5.9
Blurred vision 3.5 6.3 4.0 5.4
Diarrhea 4.9 5.0 6.4 5.6
Phentermine and topiramate extended-release [package insert]. Mountain View, CA: Vivus; 2012.

124. Phentermine and Topiramate Neuropsychiatric
Safety
 No serious AEs related to depression, anxiety or
cognition
 No increase in the risk of suicidality
(C-SSRS*, PHQ-9**, and AE reporting) in a population
where 20% had a prior history
of depression
 Can be prescribed in patients with stable depression and
patients on SSRIs
*Columbia Suicide Severity Rating Scale
** Patient Health Questionnaire 9-item depression scale
Phentermine and topiramate extended-release [package insert]. Mountain View, CA : Vivus; 2012.

125. Phentermine/Topiramate
 Combination gives greater effectiveness with fewer
side effects
 Cost: $150.00/month
 Side effects: dry mouth, numbness, tingling,
insomnia, dizziness, anxiety, irritability and
disturbance in attention

126. Lorcaserin
Lorcaserin hydrochloride [package insert]. Woodcliff Lake, NJ: Eisai Inc.; 2012.
Mechanism of
Action
• Selective 5-HT2C
receptor agonist
• Stimulates α-MSH
production from
POMC neurons
resulting in
activation of MC4R
• Increases satiety
Indications and
Dose
• Approved by FDA
June 2012
• Indication: Weight
loss in patients with
BMI ≥30 kg/m2 or
BMI ≥27 kg/m2 with
weight-related co-
morbid condition(s)
• 10 mg po bid
• Schedule IV
• Discontinue if 5%
weight loss is not
achieved in 12 wks
Contraindications and
Warnings
Contraindications
• Pregnancy
Warnings
• Co-administration with
other serotonergic or anti-
dopaminergic agents
• Valvular heart disease
• Cognitive impairment
• Psychiatric disorders
(euphoria, suicidal
thoughts, depression)
• Priapism
• Risk of hypoglycemia with
diabetes meds
2012

127. Increase in serotonin bioavailability (due to food intake or pharmacological
compounds such as sibutramine and fenfluramine) or direct agonism of
5HT2CRs and 5HT1BRs modulates firing of POMC/CART and AgRP NPY
neurones within the arcuate nucleus of the ARC
Anorectic POMC neurones expressing 5HT2CR depolarize on receptor
activation and release α-melanocyte-stimulating hormone (α-MSH), which in
turn activates second-order melanocortin 4 receptor (MC4R) expressing
neurones, principally within the paraventricular nucleus of the hypothalamus
(PVH; Balthasar et al. 2005)
Concomitant activation of 5HT1BRs expressed on orexigenic AgRP/NPY
neurones within the ARC causes membrane hyperpolarization and subsequent
inhibition of neuropeptide release
Inhibitory 5HT1BR activation also attenuates inhibitory postsynaptic currents
onto POMC/CART neurones further potentiating anorexigenesis
Subsequent downstream neuroendocrine signalling promotes satiety and the
cessation of food intake
Garfield A S , and Heisler L K. J Physiol. 2009;587:49-60.
Proposed Model of a Serotonergic
Pathway Modulating Food Intake

128. Lorcaserin Phase 3 Trials
• n=3,182
• 2 years tx
• Dosage 10 mg QD1
1. Smith SR, et al. N Engl J Med 2010;363:245-56.
2. Fidler MC, et al. J Clin Endocrinol Metab, October 2011, 96(10):3067–3077.
3. O’Neil PM, et al. Obesity (16 March 2012) | doi:10.1038/oby.2012.66
Arena Pharmaceuticals
• n=4,008
• 1 year tx
• Dosage 10 mg QD2
• n=604 obese/ overweight
with type 2 DM
• 1 year+ tx
• Dosage 10 mg BID
or 10 mg QD3
128

129. Endpoint Lorcaserin Placebo P value
Waist
circumference
(cm)
 −6.8 −3.9 <0.001
SBP/DBP (mm Hg)  −1.4 / −1.1 −0.8 / −0.6 0.04/0.01
Cholesterol (% Δ)
Total
LDL
HDL


−0.90
2.87
0.05
0.57
4.03
−0.21
0.001
0.049
0.72
Triglycerides (%)  −6.15 −0.14 <0.001
Safety
HR (beats/min)
Beck depression II
 −2.0
−1.1
−1.6
−0.9
0.049
0.26
Lorcaserin ─ BLOOM Study:
Key Secondary Endpoints
Intention-to-Treat Analysis with LOCF Imputation
Smith SR, et al. NEJM. 2010;363:245-256.

130. Lorcaserin: Adverse Events Reported by >5% in Any
Group
N (%) Lorcaserin
(N = 3195)
Placebo
(N = 3185)
Headache 537 (16.8) 321 (10.1)
Dizziness 270 (8.5) 122 (3.8)
Nausea 264 (8.3) 170 (5.3)
Constipation 186 (5.8) 125 (3.9)
Fatigue 229 (7.2) 114 (3.6)
Dry mouth 169 (5.3) 74 (2.3)
Smith SR, et al. NEJM. 2010;363:245-256.
Intention-to-Treat Analysis with LOCF Imputation

131. Naltrexone SR/Bupropion
2011

132. Naltrexone/Bupropion
• Mechanism of Action
– Naltrexone ─ Opioid receptor antagonist
– Bupropion ─ Dopamine/noradrenaline reuptake inhibitor
• Approved by FDA committee but FDA did not approve until a CVD outcome
study is performed due to concerns about blood pressure and pulse in
some patients
• The Light Study (CVD outcomes) is under way; estimated completion: July
2017
Apovian C, et al. Obesity. 2013.
Clinicaltrials.gov. Cardiovascular Outcomes Study of Naltrexone SR/Bupropion SR in Overweight and Obese
Subjects With Cardiovascular Risk Factors (The Light Study). 2012. http://clinicaltrials.gov/show/NCT01601704

133. Mean Weight Loss
Greenway FL, et al. Lancet 2010 Aug 21; 376:595. DOI:10.1016/S0140-6736(10)60888-4.
Naltrexone/ Bupropion
56 Weeks – Completer PopulationCOR-I Phase 3

134. Side Effects
Most frequent events:
– Nausea
• N=171 (29.8%) naltrexone 32 mg plus bupropion
• N=155 (27.2%) naltrexone 16 mg plus bupropion
• N=30 (5.3%) placebo
– Headache, constipation, dizziness, vomiting, and dry mouth were
also more frequent in the naltrexone plus bupropion groups vs.
placebo
– Transient increase of ~1·5 mm Hg in mean systolic and diastolic
blood pressure was followed by a reduction of around 1 mm Hg
below baseline in the naltrexone plus bupropion groups
– Combination treatment was not associated with increased
depression or suicides vs. placebo
Naltrexone/Bupropion
Greenway FL, et al. Lancet. 2010 Aug 21;376(9741):595-605.PMID: 20673995.

135. Liraglutide
2010

136. Liraglutide
 Glucagon-Like Peptide 1 (GLP-1) receptor agonist approved in 2010
for treatment of type 2 diabetes (1.8 mg/day)
 Appetite effect mediated by both the activation of GLP-1
receptors expressed on vagal afferents and hypothalamus
 Affects visceral fat adiposity, appetite, food preference, and
cardiovascular biomarkers in patients with type 2 diabetes
 Suppresses appetite, and delays gastric emptying
 Phase III trials assessing effects of doses as high as 3.0 mg/day
submitted to FDA

137. Effects of Liraglutide and Orlistat on Body
Weight in Nondiabetic Obese Adults
Data are mean (95% CI) for the ITT population
Astrup A, et al. Lancet. 2009 Nov 7;374(9701):1606-16.

138. • Generally well tolerated and improved quality of life
• Adverse events mostly mild or moderate
• Gastrointestinal events (particularly nausea and vomiting), consistent
with the known physiological effects of GLP-1, were more frequent
than with placebo
• At year 1, nausea and/or vomiting was associated with greater weight
loss with liraglutide 3.0 mg, but even those who did not experience
these events lost more weight than those on placebo or orlistat
• Injection regimen did not impair adherence or cause significant
withdrawal during treatment or run-in
Liraglutide: Adverse Events
Astrup A, et al. Int J Obes (Lond). Jun 2012; 36(6): 843–854.

139. Obesity Drugs in the Pipeline
Beloranib
Phase 2 Trial

140. Anti-obesity
Medications
in
Development
Kim GW, et al. Clin Pharmacol Ther. 2013 Oct 8. doi: 10.1038/clpt.2013.204. [Epub ahead of print]

141. Medications Approved for Obesity
Medication
Average Weight
Loss*
Mechanism of Action Potential Side Effects
Phentermine (short-term
treatment)
~ 5% Adrenergic Tachycardia, hypertension
Phentermine /
Topiramate
10% Adrenergic, CNS
Tachycardia, hypertension,
cognitive dysfunction, neuropathy,
teratogenicity
Lorcaserin 3.5% Serotonergic (5HT2C) Headache
Orlistat 3% Lipase inhibitor Steatorrhea, incontinence
* Beyond placebo

142. Weight Loss from Other Medications
Medication Indicated Uses Comments
Bupropion Depression Avoid in bipolar disease
Topiramate
Seizures
Migraines
Mood disorders
May produce neurological side effects
Zonisamide
Seizures
Mood disorders
Few studies
Metformin
Type 2 diabetes
PCOS
Rare liver toxicity
Liraglutide. Exenatide Type 2 diabetes Injectable
Pramlintide Type 2 diabetes Injectable
Pramlintide Type 2 diabetes Injectable
Strategy: Aim for Double Benefits when Possible

143. Pharmacological Treatment of Obesity
 Current medications 5-12% wt loss
 Benefits only last as long as patient takes the medication.
Chronic treatment likely needed.
 Drugs probably not paid for by insurance so cost is a big
issue for patients.
 Issues of FDA approval, long term safety, and efficacy.
 Are medications an appropriate treatment modality for
obesity?

144. Practical Use of Weight Loss Medications
 Understand risks, cautions and monitoring essentials
 Start when weight is stable (within 3% over 3 months)
 Aim for weight stability with lifestyle management
 Assess effects at 1 and 3 months
 Continue medication beyond 3 months if ≥ 5% total weight loss
 Some use “4x3” rule - ≥ 4 lbs. weight loss/month x 3 months
 Weight plateau with increased hunger is expected
 Medication still working if substantial weight regain absent

145. Proper Use of Obesity Medications
 Recognizing non-responders
An obese patient is started on a weight loss medication and is
not losing adequate amounts of weight
● STOP the medication
 Lorcaserin patient should lose 5% or more of their weight by 3
months, otherwise stop
 Phentermine/topiramate patient should lose 3% by 3 months or 5%
by 6 months

146. The super-obese (BMI 40 + )
 Incidence in U.S. population: 2.1% (4.4 million).
 Increased risk of OA, cardiopulmonary failure, OSA, all
consequences of metabolic syndrome (DM, NASH,
HTN, hyperlipidaemia).
 Medical treatment essentially hopeless, though met
syndrome improves with 5-10% weight loss.
 >2x mortality with BMI>40 kg/m2 due to
cardiopulmonary failure, sleep apnea, diabetes

147. Gastric BypassLap Band
Effectiveness
Risk
Low High

148. C. Biliopancreatic diversion with
duodenal switch.
D. Biliopancreatic diversion.

149. Comparison of Operations
 Lap band: 20% weight loss, very low mortality,
1% serious or 2.4% any complication
 Sleeve gastrectomy: 25% weight loss, 0.1%
mortality, 2.4% serious or 6.3% any complication
 Gastric bypass: 30% weight loss, 0.2% mortality,
2.5% serious or 10% any complication
Ann Surg 2013;257: 791–797; Flum DR, N Engl J Med. 2009 Jul 30;361(5):445-54

150. Who is a Good Candidate?
 BMI>35 with co-morbidities or >40 without
 Age 20-60
 Co-morbidities: Diabetes, sleep apnea, reflux > Hypertension, DJD
 Failed other forms of therapy
 No serious, active cardiac, pulmonary, or psychiatric disease
 Must be psychologically stable and wiling to follow postoperative
diet instruction
 No endocrine cause for obesity
 Surgical intervention work by decreasing energy intake

151. Surgical Treatment
Morbidity and mortality
 Mortality ranges from 0.1% for gastric banding and 0.5% for
Roux-en-Y gastric bypass to 1% for biliopancreatic bypass and
duodenal switch.
 Laparoscopic gastric banding provides a better post-operative
safety profile and therefore represents the least invasive of
the frequently performed bariatric procedures.
 Laparoscopic adjustable gastric banding and roux-en-Y gastric
bypass are the most common bariatric surgical procedures.

152. Effect of bariatric surgery on body fatness
parameters
Changes After 2 years After 10 years
Body weight 22% decrease 16% decrease
Waist circumference 16% decrease 12% decrease
BMI 22% decrease 16% decrease

153. Bariatric Surgery is Associated with a
Reduced Mortality: the SOS Study
Sjostrom L NEJM 2007: 357-741-752
30% lower risk
Of dying
MI: 25 in control
Group 13 in the
Surgery group
Cancer: 47 in
The control group
29 in the surgery
group

154. Stampede Trial: Benefits of Surgery for Type 2
DM
Parameter Medical Therapy
(n=41)
Bypass
(n=50)
Sleeve
(n=49)
P Value
HbA1c<6 12% 42% 37% 0.008
HbA1C<6 without DM
med
0% 42% 27% 0.003
% change in Tg -14% -44% -42% 0.08
% change in HDL 11% 28% 28% 0.001
N Engl J Med 2012;366:1567-76

155. Guide for Selecting Obesity Treatment
The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. October 2000, NIH Pub. No.00-4084
Treatment 23-26.9 27-29.9 30-34.9 35-39.9 >40
Diet, Exercise,
Behavior Tx + + + + +
Pharmaco-
therapy
With co-
morbidities
+ + +
Surgery
With co-
morbidities
+
BMI Category (kg/m2)

156. A Call to Action
 Obesity IS a disease, regardless of its designation
 Counsel patients with obesity on the risks of excess weight and
the benefits of weight loss
 Identify the medical comorbidities of obesity in each patient
 Pursue a step-wise strategy for weight loss – lifestyle, medications
and surgery as needed
 Help patients maintain weight loss by optimizing the patients
lifestyle – healthy diet, regular exercise, adequate sleep, stress
reduction
15

157. Take-home Messages
Obesity Treatment
• Lifestyle adjustment is the mainstay of therapy
• Medications can be effective
• In selected patients
• Medications work differently in different patients – requires
‘trial and error’ approach
• Combination therapies look particularly promising
• Go Slow and Try Different Approaches

158. Currently Available Options
 Accept weight where it is
 Diet/Exercise: 3-10% weight loss
 Drugs: 5-12% weight loss
 Medically Supervised/Combination
of Diet + Drug: 10-15% weight loss
 Surgery: 15-30% weight loss
Low
High
Effectiveness

159. Currently Available Options
 Accept weight where it is
 Diet/Exercise: 3-10% weight loss
 Drugs: 5-12% weight loss
 Medically Supervised/Combination
of Diet + Drug: 10-15% weight loss
 Surgery: 15-30% weight loss
Low
High
Risks/Time/Money

160.  In 2008, 1.5 billion adults, 20 and older, were
overweight
 65% of the world's population live in countries
where overweight and obesity kills more
people than underweight.
 Nearly 43 million children under the age of five
were overweight in 2010.
 Obesity is preventable.

161. Prevention of Obesity
Eat less
Eat less
Eat less ……
……………….
Use legs

165. Health benefits
Whether or not liposuction provides the health benefits commonly associated
with achieving weight loss through other means is a matter of debate in
scientific circles. Mainstream doctors agree that liposuction does not help to
combat obesity related metabolic disorders like insulin resistance.
"Liposuction does not achieve metabolic benefits of weight loss". BMJ 328 (7454): 1457–1450. doi:10.1136/bmj.328.7454.1457-a.
PMC 428545.
liposuction