Obesity 125657

WHY THIS TOPIC??
Data from the National Health and Nutrition

Examination Surveys (NHANES)
obesity (BMI >30) has increased from 14.5%
(between 1976 and1980) to 35.7% (between 2009 and
2010).
Extreme obesity (BMI ≥40) has also increased and
affects 5.7% of the population.
•As many as 68% of U.S. adults aged ≥20 years
were overweight (defined as BMI >25) between
the years of 2007 and 2008.
•The prevalence in children and adolescents has

been rising at a worrisome rate, reaching 15.9% in
2009/2010, but may be levelling off.
•Incurs an expenditure on heath accounting to nearly

5.7% of total health budget.
•Obesity and overweight together are the second

leading cause of preventable death in the U.S.,
accounting for 300,000 deaths per year.
INDIAN DATA
NFHS 2007 National family Health Survey
DEFINITION
Obesity is a state of excess adipose
tissue mass.
Although often viewed as equivalent to
increased body weight, this need not be the
case—Eg:lean but very muscular individuals
SOME FACTS!!
The distinction between lean and obese is
somewhat arbitrary and obesity is therefore
better defined by assessing its linkage to
morbidity or mortality.
Although not a direct measure of adiposity,
the most widely used method to gauge obesity
is the body mass index (BMI).At a similar BMI,
women have more body fat than men.
Other methods – Skinfold thickness,
Densitometry(underwater weighing), CT
/MRI, Electrical Impedence
•Based on data of substantial morbidity, a BMI of
30 is obesity in both men and women.
•Most studies suggest that all-cause, metabolic,

cancer, and cardiovascular morbidity begin to rise
(albeit at a slow rate) when BMIs are ≥25.
•A BMI between 25 and 30 should be viewed as

medically significant and worthy of therapeutic
intervention in the presence of risk factors that are
influenced by adiposity, such as hypertension and
glucose intolerance.
•Anatomic distribution of fat depots also has
substantial implications for morbidity.
•Specifically, intraabdominal and abdominal

subcutaneous fat have more significance than
subcutaneous fat present in the buttocks and lower
extremities.
•This distinction is most easily made clinically by

determining the waist-to-hip ratio, with a ratio >0.9
in women and >1.0 in men being abnormal.
ANATOMY
Adipocytes+ Stromal /Vascular component
(Preadipocystes/ macrophages)
Store excess energy as Triglycerides
Release stored energy as free fatty acids for
utilization at other sites when in need.
Controlled by neuroendocrie pathways
Adipocyte is an Endocrine cell !!!!
PHYSIOLOGIC
REGULATION OF ENERGY
BALANCE
Balance between Energy Intake and Expenditure
0.3% positive imbalance X 30 yrs =9Kg Weight gain!!!!
Neural Signaling Endocrine
Components pathways components
Hypothalamus •Serotonergic •Leptin,
Vagal Inputs •Catecholaminergic •Insulin
•Endocanabinoid •Cortisol
•Opiod signalling •Gut Peptides:
pathway Ghrelin, CCK, Peptide
YY
•Glucose
•Hypothalamic
Peptides:
Neuropeptide Y,
Agouti related
Leptin and its effects
ETIOLOGY
Obesity is a heterogeneous group of
disorders.
Role of genes:
Heritability of body weight is similar to that
for height. (POLYGENIC)
Inheritance is usually not Mendelian.
Adoptees more closely resemble their
biologic than adoptive parents with respect to
obesity
• Identical twins have very similar BMIs whether
reared together or apart, and their BMIs are much
more strongly correlated than those of dizygotic
twins.
• Affect both limbs of energy balance intake and
expenditure.
• Currently, identified genetic variants, both
common and rare, account for less than 5% of the
variance of body weight
Role of Environment:
•The environment plays a key role in obesity as
evidenced by the fact that famine prevents obesity
in even the most obesity-prone individual
•Cultural factors are also important—these relate

to both availability and composition of the diet
and to changes in the level of physical activity.
•In children, obesity correlates to some degree with

time spent watching television.
•
Both epidemiologic correlations and experimental
data suggest that sleep deprivation leads to
increased obesity.
OTHER GENETIC SYNDROMES
Prader-Willi Syndrome
Laurence-Moon-Biedl Syndrome
Ahlstrom’s Syndrome
Cohen’s Syndrome
Carpenter’s Syndrome
CONSEQUENCES OF
OBESITY
Reproductive
Menstrual Disorders
Infertility
Complications during pregnancy
, during labour
Biirth defect
IUFD
EVALUATION
i. The Obesity-Focused History
• What factors contribute to the patient’s obesity?
• How is the obesity affecting the patient’s health?
• What is the patient’s level of risk from obesity?
• What does the patient find difficult about managing
weight?
• What are the patient’s goals and expectations?
• Is the patient motivated to begin a weight management
program?
• What kind of help does the patient need?
ii. Body Mass Index (BMI) and Waist
Circumference:
BMI, calculated as weight (kg)/height (m)2 or as
weight (lbs)/height (inches)2 × 703, is used to
classify weight status and risk of disease.
Excess abdominal fat, assessed by measurement of
waist circumference or waist-to-hip ratio, is
independently associated with a higher risk for
diabetes mellitus and cardiovascular disease.
Waist circumference is a surrogate for visceral
adipose tissue.
iii. Assessment of comorbid conditions

iv. Determination of fitness level
Reported by questionnaire or measured by a
maximal treadmill exercise test, is an important
predictor of all-cause mortality rate independent of
BMI and body composition.
v. Assessment of the patient’s readiness to
adopt lifestyle changes:
An attempt to initiate lifestyle changes when the
patient is not ready usually leads to frustration
and may hamper future weight-loss efforts.
This exercise helps establish readiness to change
and also serves as a basis for further dialogue.
TREATMENT
Consists of 3 modalities:
1.Diet, exercise, behavioral therapy
2.Pharmacotherapy
3.Bariatric Surgery
WHEN TO CHOOSE
WHICH MODALITY??
DIET
Reduce overall calories
NHLBI guidelines: calorie deficit of 500-
1000kcal/d compared to habitual diet (
1-2lb/week)
Smaller proportions, more fruits vegetables, more
whole grains, leaner cuts of meat, decrease fried
food, beverages
Calorie intake 45-65% from carbohydrates, 20-
35% from fats, 10-35% from proteins
Low carbohydrate – High protein diet –ATKINS
diet
PHYSICAL ACTIVITY
150min/week of moderate intensity
75min /week of vigorous intensity aerobic
exercise in intervals of atleast 10min
BEHAVIOURAL THERAPY
Reinforce new dietary and physical activity
behaviours
 Self monitoring
 Stress management
 Stimulus control
 Social support
 Cognitive restructuring
PHARMACOTHERAPY
BMI>30
Or BMI>27 with obesity related complications
Failure of diet/activity/ behavioural change
MEDICATIONS
Two major categories:
i. Appetite suppressants (anorexiants):
Primarily targets three monoamine receptor systems in the
hypothalamus: noradrenergic, dopaminergic, and
serotonergic receptors.
Sibutramine : SSNRI
Two new appetite suppressants were approved by the
U.S.FDA in 2012: lorcaserin 10 mg bid and
phentermine/topiramate (PHEN/TPM) extended release 15-
mg/92-mg dose
ii. GI fat blockers. Reduce the absorption of selective
macronutrients, such as fat, from the GI tract. Orlistat
120 mg tid
Rimonabant ( CB1 receptor antagonist)
SURGERIES
Weight loss surgeries have traditionally been classified
into three categories on the basis of anatomic changes:
BMI>40kg/m2 or >35kg/m2 with serious comorbidities
i. Restrictive
ii. Restrictive and Malabsorptive
THANK YOU!!

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WHY THIS TOPIC??

Data from the National Health and Nutrition

•The prevalence in children and adolescents has

•Incurs an expenditure on heath accounting to nearly

•Obesity and overweight together are the second

•Most studies suggest that all-cause, metabolic,

•A BMI between 25 and 30 should be viewed as

•Specifically, intraabdominal and abdominal

•This distinction is most easily made clinically by

•Cultural factors are also important—these relate

•In children, obesity correlates to some degree with

iii. Assessment of comorbid conditions

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