1. Welcome to Session on Obesity Meera Kaur, PhD, RD Assistant Professor Department of Family Medicine Faculty of Medicine

2. Outline Learning objectives Introduction Classification and diagnosis2
Learning objectives
Introduction
Classification and diagnosis
Obesity trend
Adipose tissue, adiposity, hypertrophy and hyperplasia
Energy balance
Regulation of body weight
Regulation of food intake and body weight
Regulatory factors in feeding and adiposity
Sound weight loss program
Conclusions
Questions and answers

3. Learning Objectives To understand3
Learning Objectives
To understand
the physiological and metabolic perspectives of obesity/overweight, and
the regulation of body weight with special reference to:
Regulatory factors involved in feeding and adiposity

4. 4
Introduction
Obesity is the disorder of body composition defined by a relative or absolute excess of body fat.
The WHO and NHLBI have classified obesity as an epidemic
In 2002, ~64% Americans overweight; 32% obese
16% or 9 million kids were overweight
Thus, a trend towards an ever-fatter America
By 2009, 70% of American expected to be overweight or obese
Obesity contributes to +300,000 deaths a year
From a global perspective, the increase in the prevalence of obesity is alarming

5. Classification and Diagnosis5
Classification and Diagnosis
Classification
BMI (kg/m2)
Risk of Co-morbidities
Underweight
<18.5
increased risk in other areas
Desirable
Average
Overweight
Mildly Increased
Obese
>30.0
Class I Obesity
Moderate
Class II Obesity
Class III Obesity
>40.0
Severe
Very severe

6. Classification for Children (<2 Years)6
Classification for Children (<2 Years)
BMI Status
Normal weight for height 10th-90th percentile
At risk for overweight 85th-95th percentile
Overweight >95 percentile
(Centre for Disease Control and Prevention, 2005)

7. Assessing Obesity Waist circumference at level of iliac crest7
Assessing Obesity
Waist circumference at level of iliac crest
Above 40 inches for men and 35 inches for women are indicative of health risk.
Waist-to-hip ratio: Circumference of the waist at the level of L3 divided by the circumference of the hip at the largest area of the gluteal region. (Helps identify central or android obesity.)
For men waist-to-hip ratio > 1
For women waist-to-hip ratio > 0.85

8. Obesity Trends in US Adults8
1991
1993
1995
1998
< 10%
10% to 15%
> 15%
AH, et al. JAMA. 1999

9. Obesity Trends in US Adults…9

10. Obesity Trends in US Adults, 200410
No Data <10% %–14% 15%–19% %–24% ≥25%

11. Adipose Tissue, Adipocytes, Hypertrophy and Hyperplasia11
Adipose Tissue, Adipocytes, Hypertrophy and Hyperplasia
Adipose tissue
White: energy, cushion, insulation
Brown: Key regulator of energy expenditure
Adipocytes
store 80-90% fat as tryglyceride
Hypertrophy
 adipose tissue due to enlarged adipocytes
Hyperplasia
 adipose tissue due to  number of adipocytes

12. Juvenile-Onset Obesity12
Juvenile-Onset Obesity
Develops in infancy or childhood
Increase in the number of adipose cells
Adipose cells have long life span and need to store fat
Makes it difficult to lose the fat (weight loss)
Causes
poor dietary patterns
lack of physical activity
43% of adolescents watch 2 hours or more of TV/day

13. Adult-Onset Obesity Develops in adulthood13
Adult-Onset Obesity
Develops in adulthood
Fewer (number of) adipose cells
These adipose cells are larger (stores excess amount of fat)
If weight gain continues, the number of adipose cells can increase

14. Regulation of Body Weight14
Regulation of Body Weight
Short-term regulation is governed by:
Hunger (postabsorptive), appetite and satiety (postprandial)
physical trigger for hunger > satiety
Long-term regulation is governed by:
feedback mechanism– adipocytokines (signaling protein is released from the adipose mass when normal body composition is disturbed. This mechanism plays a greater role in younger persons than older adults.

15. 15
Set-Point Theory
Fat storage in nonobase adult is regulated to preserve the specific weight.
deliberate effort to starve or overfeed are followed by a rapid return to original body weight (set-point).
if set-point theory is true, some form of obesity could be due to the abnormally established set-point.
Can we establish a new settling-point vs. Set-point to treat obesity?
However, data are not conclusive in this area. We need to do more research.

16. 16
Energy Production

17. 17
Energy Balance…
State in which energy intake, in the form of food and /or alcohol, matches the energy expended, primarily through basal metabolism and physical activity
Positive energy balance
Energy intake > energy expended
Results in weight gain
Negative energy balance
Energy intake < energy
Results in weight loss

18. Energy Balance 18

19. Regulation of Energy Intake and Body Weight19
Regulation of Energy Intake and Body Weight
Factors that regulate energy intake and body weights are:
Dietary thermogenesis and the Thermic Effect of Foods (TEF)/Specific Dynamic Action (SDA) of foods
Resting/Basal Metabolic Rate (RMR)/(BMR)
Energy expended in voluntary activity
Regulatory neurotransmitters and hormones

20. Thermic Effect of Foods20
Thermic Effect of Foods
Energy used to digest, absorb, and metabolize food nutrients
“Sales tax” of total energy consumed
~5-10% above the total energy consumed
TEF is higher for CHO and protein than fat
Less energy is used to transfer dietary fat into adipose stores
Meal size, meal composition, previous meal, insulin resistance, physical activity and aging influence the TEF.
Aerobic exercise the TEF

21. Resting Metabolic Rate (RMR)21
Resting Metabolic Rate (RMR)
RMR explains 60-70% of Total Energy expenditure (TEE). When body is deprived of energy
RMR adapts to conserve energy by dropping rapidly (up to 15% in two weeks).
RMR declines with age
During undernutrition, abnormalities in lipolysis may cause insulin resistance affecting RMR
The regulation of free fatty acid availability is an important area of research related to the RMR.

22. Activity Thermogenesis (AT)22
Activity Thermogenesis (AT)
Energy expended in voluntary activity – activity thermogenesis (AT) is the most important component of TEE (15-30% normally). Therefore, AT should be  when energy is not restricted.
RMR and Fat free mass (FFM) decrease with age. Hence adjustment between energy intake and AT should be adjusted for preserving normal weight.
All activity counts including nonexcercise activity thermogenesis (NEAT).
To reverse obesity standing and ambulatory time should be promoted at least 2.5 hours/day.

23. Energy Balance 23

24. Ultimate Energy Balance24
Ultimate Energy Balance
TEF
REE
NEAT
Physical activity
Dietary
Intake

25. Macronutrients and Fat Storage25
Macronutrients and Fat Storage
Body prefers to use CHO as energy source
Only excess intake of CHO and protein will be turned into fat
Fat will remain as fat for storage
Physical activity encourages the burning of dietary fat (Beta-oxidation)
High CHO diet decreases Beta-oxidation
Most endurance athletes burn fatty acids for energy

26. Fat Storage Fat Carbohydrates26
Fat Storage
Fat
Most fat is stored directly into adipose tissue
Body has ability to store fat (as fat)
Carbohydrates
Limited CHO can be stored as glycogen Most CHO is used as a energy source
Excessive CHO will be synthesized into fat (for storage)

27. Protein and Fat Storage27
Protein and Fat Storage
Protein is primarily used for tissue synthesis
Adults generally consume more protein than needed for tissue synthesis
Excess protein is used as a energy source
Some protein will be synthesized into fat (for storage)

28. Regulatory Factors in Feeding and Adiposity28
Regulatory Factors in Feeding and Adiposity
Brain Neurotransmitters
Gut hormones
Other hormones

29. Brain Neurotransmitters29
Brain Neurotransmitters
Norepinephrine and Dopamine
Released by symphathetic nervous system (SNS)
Fasting & starvation  SNS activity, epinephrine that govern feeding behaviour and subatrate mobilization
Dopaminnergic pathway in the brain play a role in reinforcement properties of foodds.
Serotonin
 In serotonin leads to carbohydrate appetite.
Corticotrophin-releasing Factor (CRF)
CRF is a potent anorexic agent and weakens the feeding response produced by norepinephrine and neuropeptide Y.
CRF is released during exercise.

30. Gut Hormones… Incretins is a G-I peptide Cholecystokinin (CCK)30
Gut Hormones…
Incretins is a G-I peptide
 insulin release after eating , even before blood glucose level is elevated. Serotonin is a G-I peptide
Cholecystokinin (CCK)
At brain level inhibits food intake. Stimulates pancreatic enzymes
Bombesin
 Food intake and enhances the release of CCK.
Enterostatin
Part of pancreatic lipase;  satiety following fat consumption

31. Gut Hormones Adiponectin - Adipocytokine secreted by adipose tissue31
Adiponectin - Adipocytokine secreted by adipose tissue
Level of this hormone is inversely related to BMI. Plays role in metabolic disorders.
Glucagon causes hypoglycemia
Glucagon-like-peptide-1 (GLP-1)
Released in presence of glucose rich food, delays gastric emptying time and promote satiety.
Leptin is an adipocytokine and regulates appetite.
In obesity it loses the ability to inhibit energy intake.
Resistin - An adipocytokine that antagonizes insulin action
Ghrelin – Produced in stomach and stimulate hunger.
Peotide YY-3-36 (PYY ) is secreted in small bowel in response to foods.

32. Other Hormones 32
Thyroid hormone – Modulates the tissue responsiveness to the catecholamines secreted by SNS. A  in thyroid hormone lpwers the SNS activity and adaptive thermogenesis.
Vispatin - An adipocytokine protein that has an insulin-like-effect. Plasma level  with  adiposity and insulin resistance.
Adrenomedullin - A new peptide secreted by adipocytesas a result of inflammatory process

33. Satiety Regulator The hypothalamus Sympathetic nervous system33
Satiety Regulator
The hypothalamus
When feeding cells are stimulated, they signal us to eat
When satiety cells are stimulated, they signal us to stop eating
Sympathetic nervous system
When activity increases, it signals us to stop eating
When activity decreases, it signals us to eat

34. Influences of Satiety…34
Influences of Satiety…

35. 35
Influences of Satiety

36. What it Takes to Lose a Pound36
What it Takes to Lose a Pound
Body fat contains 3500 kcal per pound
Fat storage (body fat plus supporting lean tissues) contains 2700 kcal per pound
Must have an energy deficit of kcal to lose a pound per week

37. 37
Do the Math
To lose one pound, you must create a deficit of kcal
So to lose a pound in 1 week (7 days), try cutting back on your kcal intake and increase physical activity so that you create a deficit of kcal per day
- 500 kcal x 7 days = kcal = 1 pound of weight loss
day week in 1 week

38. Sound Weight Loss Program38
Sound Weight Loss Program
Meets nutritional needs, except for kcal
Slow & steady weight loss
Adapted to individuals’ habits and tastes
Contains enough kcal to minimize hunger and fatigue
Contains common foods
Fit into any social situation
Change eating problems/habits
Improves overall health
See a physician before starting

39. Summary and Conclusion39
Summary and Conclusion
To treat obesity and/or develop an effective weight loss program, understanding of
the physiological and metabolic perspectives of obesity/overweight is important
the regulation of body weight with special reference to:
Regulatory factors involved in feeding and adiposity is crucial
Energy balance is the key point
Team approach is important in developing a sustainable weight loss program

40. Thank you for gracing the session!
Any question?