Transcript 03. Obesity lecture I.ppt

Obesity
Dr. Sumbul Fatma
Overview
 Definition
 Prevalence
 Consequences of Obesity
 Assessment of Obesity
 Causes of obesity
Definition
 Obesity is a disorder of body weight regulatory
systems characterized by an accumulation of excess
body fat usually 20 percent or more over an
individual's ideal body weight.
 A combination of abundance of food with reduced
activity levels found in industrialized societies, has
resulted in a tendency for the sustained deposition of
fat
Prevalence
 The prevalence of obesity increases with age.
Particularly alarming is the explosion of
childhood obesity, which has shown a three
fold increase in prevalence over the last two
decades.
 As adiposity has increased so has the risk of
developing associated diseases, such as
diabetes, hypertension, and cardiovascular
disease.
Prevalence of Obesity
 Childhood and adolescent obesity increased from 5% to
16% in the last 20 years
 Adulthood obesity increased from 12% to 21% in 10
years.
 16 million US adults with BMI over 35
 60 million US obese adults (BMI > 30)
Assessment
 Body mass index (BMI)— is an indirect
measure of obesity and correlates with the
amount of body fat in most individuals.
(exceptions are athletes who have large
amounts of lean muscle mass)
 The BMI gives a measure of relative weight,
adjusted for height. This allows comparisons
both within and between populations.
Calculating BMI
 Calculate Body Mass Index (BMI) =
weight (kg)
height squared (meters)
Or…
weight (pounds) x 703
height squared (inches)
Definition of Overweight & Obesity
 Using BMI
BMI
GRADE
UNDER WEIGHT
≤ 18.5
NORMAL
18.5 – 24.9
OVER WEIGHT
25.0 – 29.9
OBESITY
30.0 – 34.9
I
OBESITY
35.0 – 39.9
II
EXTREME OBESITY
≥ 40
III
Anatomic differences in fat deposition
It has a major influence on associated health
risks.
Android, “apple-shaped,” or upper body
obesity is the excess fat located in the central
abdominal area of the body
is associated with a greater risk for
hypertension, insulin resistance, diabetes,
dyslipidemia, and coronary heart disease
waist to hip ratio of more than 0.8 for
women and more than 1.0 for men.
Anatomic differences in fat deposition
Gynoid, “pear-shaped,” or lower body
obesity - Fat distributed in the lower
extremities around the hips or gluteal
region.
 waist to hip ratio of less than 0.8 for
women and less than 1.0 for men.
The pear shape is relatively benign
healthwise, and is commonly found in
females
Waist-to-hip ratio is a better predictor of
myocardial infarction than BMI
Biochemical differences in regional fat
depots
Abdominal fat cells are much larger and have a higher rate
of fat turnover than lower body fat cells
Hormonally more responsive than adipocytes in the legs
and buttocks
As men tend to accumulate the readily mobilizable
abdominal fat, they generally lose weight more readily
than women do
Substances released from abdominal fat are absorbed via
the portal vein and, thus, have direct access to the liver
Gluteal fat- free fatty acids from gluteal fat enter the general
circulation, and have no preferential action on hepatic
metabolism
Number of fat cells
 When triacylglycerols are deposited in adipocytes,




the cells increase in size and when the ability of a fat
cell to expand is limited, and when its maximal size is
reached, it divides
Obesity involves an increase in both the number and
size of adipocytes
Fat cells, once gained, are never lost
An obese individual, with increased numbers of
adipocytes, will have to reduce the size of those fat
cells in order to normalize fat stores. These
individuals will be in the doubly abnormal state of
having too many, too small fat cells.
Formerly obese patients have a particularly difficult
time maintaining their reduced body weight
Body weight regulation
 The body weight of most individuals tends to
range within ten percent of a set value
 This observation prompted the theory that
each individual has a biologically
predetermined “set point” for body weight
‘Set Point’ Theory
 The body attempts to add adipose tissue
when the body weight falls below the set
point, and to lose weight when the body
weight is higher than the set point
Weight loss
weight gain
Appetite increases
Appetite falls
Energy Exp. Falls
Increases
 Strict set point model does not explain why
some individuals fail to revert to their starting
weight after a period of overeating, or
 the current epidemic of obesity
 Body weight, rather than being irrevocably set,
seems to drift around a natural “settling point,”
which reflects a balance between factors that
influence food intake and energy expenditure
 Body weight is stable as long as the behavioral and
environmental factors that influence energy
balance are constant.
Factors predispose to obesity
 Genetic – familial tendency
 Environmental and behavioral
 Sex – women more susceptible
 Activity – lack of physical activity
 Psychogenic – emotional deprivation,
depression
 Social class – poorer classes
 Alcohol – problem drinking
 Smoking – cessation smoking
 Prescribed drugs – tricyclic derivatives
Genetic contributions to obesity
 Despite the widely held belief that obesity is a
result of uncontrolled, gluttonous eating
behavior, it is now evident that genetic
mechanisms play a major role in determining
body weight
 Obesity is often observed clustered in
families. If both parents are obese, there is a
70–80% chance of the children being obese.
In contrast, only 9% of children were fat when
both parents were lean
• The inheritance of obesity is not simple Mendelian
genetics as would be expected if the condition were a
result of a defect in a single gene. Rather, obesity
behaves as a complex polygenic disease involving
interactions between multiple genes and the
environment
• The importance of genetics as a determinant of obesity
is also indicated by the observation that children who
are adopted usually show a body weight that correlates
with their biologic rather than adoptive parents
• Furthermore, identical twins have very similar BMI,
whether reared together or apart, and their BMI are
more similar than those of nonidentical, dizygotic twins.
•
•
•
•
•
The epidemic of obesity occurring over the last decade cannot be
explained by changes in genetic factors, which are stable on this
short time scale
Environmental factors, such as the ready availability of palatable,
energy-dense foods, play a role in the increased prevalence of
obesity
Furthermore, sedentary lifestyles enhance the tendency to gain
weight
When Japanese or Chinese populations migrate to the United
States, their BMI increases. For example, men in Japan (aged 46–
49 years) are lean, with an average BMI of 20, whereas Japanese
men of the same age living in California are heavier, with an
average BMI of 2
Eating behaviors, such as snacking, portion size, variety of foods
consumed, an individual's unique food preferences, and the
number of people with whom one eats also influence food
consumption and the tendency toward obesity
Weight Gain: How Does It Happen?
 Energy imbalance

calories consumed not equal to calories used
 Over a long period of time
 Due to a combination of several factors
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Individual behaviors
Social interactions
Environmental factors
Genetics
Weight Gain: Energy In
3500 calories = 1 pound
 100 calories extra per day


= 36,500 extra per year
= 10.4 lbs weight gain
 Question: How much is 100 calories?
 Answer: Not very much!
 1 glass skim milk, or
 1 banana, or
 1 slice cheese, or
 1 tablespoon butter
Evolving Pathology
 More in and less out = weight gain
 More out and less in = weight loss
 Hypothalamus

control center for hunger and satiety
 Endocrine disorder

where are the hormones?
Reference
 Lippincott’s Illustrated Reviews of
Biochemistry 4th Edition
Thank You!