Obesity is a state of excess adipose tissue mass. A massive psychosocial, pathophysiological problem that results in a high rate of mortality as well as morbidity. The basic mechanisms of the illness and its management as of 2017 are described in this presentation

1. Obesity

2. Origin of the problem
 Food supplies used to be intermittent
 Storing energy in excess of what is required for immediate use
was and is essential for survival.
 Adipose tissue - stores excess energy efficiently as triglycerides
 Releases stored energy as free fatty acids for use when needed
 This physiologic system, orchestrated through endocrine and
neural pathways, permits humans to survive starvation for as long
as several months.
 Now however… nutritional abundance & a sedentary lifestyle, and
influenced importantly by genetic  this system increases
adipose energy stores and produces adverse health
consequences.

3. Definition
Def: Obesity is a state of excess adipose tissue mass.
Although often viewed as equivalent to increased body
weight  need not be the case
Although not a direct measure of adiposity, the most
widely used method to gauge obesity is the body mass
index (BMI) i.e. kg/cm2

4. Definition

5. Dwayne (The Rock) Johnson
Height: 190 cm
Weight: 113 kg
BMI: 31.3
Is he obese??

6. Introduction
Other approaches to quantify obesity
Anthropometry (skinfold thickness)
Densitometry (underwater weighing)
Computed tomography (CT)
Magnetic resonance imaging (MRI)
Electrical impedance
Other indices
 Lean mass index
 Fat percentage

7. Introduction
The distribution of
adipose tissue in different
anatomic depots also has
substantial implications
for morbidity
This distinction is made
clinically by the waist-to-
hip ratio (WHR)
>0.9 in women
>1.0 in men
ABNORMAL

8. Prevalence
Estimated that over 12% of the world’s adult
population is obese
Estimations in India reveal that 5-12% are
obese
⅓ of the adult population of the US  Obese

9. Physiological regulation of energy balance
 Body weight is regulated by both endocrine and neural components
 Alterations in stable weight by forced overfeeding or food deprivation
induce physiologic changes that resist these perturbations

10. The Leptin Pathway

11. Effects of Leptin
Leptin resistance

12. Factors affecting appetite

13. Etiology of obesity
LIFESTYLE
PSYCHOLOGICAL MEDICAL
GENETIC
OBESITY

14. Environmental/Psychosocial
 Increased caloric
intake
▪ Availability, price
▪ Extra 50 cal/day (1 tsp
sugar) = 2.25 kg/year
= 25 kg over 10 years
 More sedentary
▪ Television/Computer
▪ Emphasis on
academics

15. Medical causes
 Cushing’s syndrome
 Hypothyroidism
 Insulinoma
 Craniopharyngioma and other disorders
involving the hypothalamus
 Drug induced

18. Complications of Obesity

19. Complications of Obesity

20. Complications associated with Obesity
Hypertriglyceridemia
Hypertension
Hyperuricemia
Venous insufficiency
DM
Cardiovascular disease
Cholelithiasis
Carcinomas
Pickwickian syndrome
Cardiac failure
Death
Duration of obesity

21. Management of
Obesity

22. Work up
Physical exam – Focus on possible complications
Investigations:
 Blood sugar, lipid profile, liver function tests
Other tests based on clinical features
 TSH, Sleep studies
 Dexamethasone suppression test for Cushing’s syndrome*

23. Treatment
Prevention
Diet
Increased physical activity
Behavior modification
Medicines

24. Guide to treatment options

25. Weight loss &
weight maintenance
Integrated weight management

26. Behaviour modification
Self monitoring of weight
Stress management
Social support

27. Diet
 The primary focus of diet therapy
is to reduce overall calorie
consumption
 Very low energy diets (e.g., 400 to 600
kcal/d)
 Low-calorie diets, >800 kcal/d
 very low fat diets
 very low carbohydrate “Atkins” style
diets
 Guidelines recommend initiating
treatment with a calorie deficit of 500–
1000 kcal/d compared with the
patient's habitual diet.

28. Diet
The revised Dietary Reference Intakes for
Macronutrients released by the Institute of Medicine
recommends
45–65% of calories from carbohydrates,
 20–35% from fat, and 10–35% from protein.
daily fiber intake of 38 g (men) and 25 g (women) for
persons over 50 years of age and
30 g (men) and 21 g (women)for those under age 50.

29. Diet
Low-carbohydrate, high-protein diets appear to be
more effective in lowering BMI;
improving coronary heart disease risk factors, including
an increase in HDL cholesterol and a decrease in
triglyceride levels;
controlling satiety in the short term compared with
low-fat diets

30. Diet
Occasionally, very low calorie diets (VLCDs) are
prescribed as a form of aggressive dietary therapy.
The primary purpose of a VLCD is to promote a rapid
and significant (13–23 kg) short-term weight loss over a
3- to 6-month period.
These propriety formulas typically supply 800 kcal, 50–
80 g protein, and 100% of the recommended daily
intake for vitamins and minerals.

31. Exercise
 Increased energy expenditure is the
most obvious mechanism for an
effect of exercise
 Exercise appears to be a valuable
means to sustain diet therapy
 Valuable in the obese individual for its
effects on cardiovascular tone and
blood pressure

32. Pharmacotherapy
Recommended if BMI >/= 27 with
comorbidities or BMI >/= 30
Facts:
Drugs alone cause modest weight loss
Diet with drugs improves efficacy
Effects maintained for duration of treatment
only
Long term safety data not available

33. Pharmacotherapy
Medications for obesity have traditionally
fallen into two major categories:
1. Appetite suppressants (anorexiants)
2. Gastrointestinal fat blockers

34. Pharmacotherapy
Centrally Acting Anorexiant Medication
Anorexiants increases satiety and decreases hunger,
these agents help patients reduce caloric intake without
a sense of deprivation.
Targets the ventromedial and lateral hypothalamus
Eg PHEN/TPM (Phenteramine and Topiramate)  9.3%
and 8.6% weight lost in 2 large trials

35. Pharmacotherapy
Centrally Acting Anorexiant Medication
Lorcaserin is a selective 5-HT2C receptor agonist
thought to decrease food intake through the pro-
opiomelanocortin system of neurons.

36. Pharmacotherapy
Peripherally Acting Medications
(Gastrointestinal fat blockers)
 Orlistat is a synthetic hydrogenated derivative of a
naturally occurring lipase inhibitor, lipostatin
 Potent, slowly reversible inhibitor of pancreatic, gastric,
and carboxylester lipases and phospholipase A2 
required for the hydrolysis of dietary fat into fatty acids.
 Acts in the lumen of the stomach and small intestine
 Blocks the digestion and absorption of ~30% of dietary
fat
 Weight loss of ~9–10%

37. Pharmacotherapy
In development
Bupropion and naltrexone
Liraglutide

38. Surgery
Indications
BMI > 35 with an associated comorbidity or a BMI > 40
(irrespective)
Repeated failures of other therapeutic approaches
Capability of tolerating surgery

39. Surgery
 Weight loss surgeries have traditionally been classified into 3
categories on the basis of anatomic changes:
 Restrictive
 Restrictive-malabsorptive
 Malabsorptive
 Clinical benefits of bariatric surgery in achieving weight loss and
alleviating metabolic comorbidities have been attributed largely to
changes in the physiologic responses of gut hormones and in
adipose tissue metabolism.

40. Surgery
 Restrictive surgeries limit the
amount of food the stomach can
hold and slow the rate of gastric
emptying.
 Malabsorptive surgeries reduce the
amount of absorption
A. Laparoscopic gastric band (LAGB)
B. The Roux-en-Y gastric bypass.
C. Biliopancreatic diversion with duodenal
switch.
D. Biliopancreatic diversion.vertical-banded
gastroplasty
E. Biliopancreatic diversion

41. Surgery
 These procedures generally produce a 30–35% average total body weight
loss that is maintained in nearly 60% of patients at 5 years.
 Significant improvement in multiple obesity-related comorbid conditions,
including type 2 diabetes, hypertension, dyslipidemia, obstructive sleep
apnea, quality of life and long-term cardiovascular events.
 The most common surgical complications include stomal stenosis or
marginal ulcers
 The restrictive-malabsorptive procedures carry an increased risk for
micronutrient deficiencies of vitamin B12, iron, folate, calcium, and
vitamin D.
 Patients with restrictive-malabsorptive procedures require lifelong
supplementation with these micronutrients.