Physiology of hunger

1. Subject: biological foundations of behaviour –II
Presenter- Ms Nisha Upadhyay
Topic: Hunger: theories, neural
signal, human obesity: Anorexia
nervosa

2. Outline
 Introduction
 Brain process in hunger
 Theories of hunger
 Obesity
 Anorexia nervosa
 Bulimia nervosa
 Conclusion
 References

3. Introduction
 Hunger is a feeling experienced by animal when glycogen
level of the liver falls below a certain point, usually
followed by a desire to eat
 Our bodies contain complex mechanism that maintain
proper levels of these essentials
 Our body has a tendency to maintain a steady state called
homeostasis
 when we are hungry, the walls of the stomach contract
producing ‘hunger pangs’.
 When we have eaten, the stomach is full and we satiated.

4.  Cannon and Washburn (1912) suggested that hunger
resulted from an empty stomach the walls of an empty
stomach rubbed again each other, producing what we
commonly identify as hunger pangs
 Inglefinger (1944) interviewed patients whose
stomach had been removed because of the cancer ;
their oesophagi had been attached directly to their
small intestines. Because they had no stomachs to
catch and hold the food, they had to eat small,
frequent meals. Despite their lack of a stomach, these
people reported the same feelings of hunger and
satiety that they had experienced before the operation.
 A more likely cause of hunger is depletion of the body
store of nutrients

5.  The primary fuels for the cells of our body are
glucose ( a simple sugar) and fatty acid (
chemicals produced when fat is broken down )
 Our digestive system contains food, these
nutrients are absorbed into the blood and
nourishes our cells.
 But the digestive tract is sometimes empty so
there has been reservoir that stores nutrients to
keep the cells of the body nourished when the
gut is empty.
 There are 2 reservoir
 SHORT TERM RESERVOIR

6. SHORT TERM RESERVOIR
 The short term reservoir is located in the cells of
the muscles and the liver and it is filled with a
carbohydrates
 When glucose is received from meal, some of it is
used for fuel and some is converted into glycogen
and stored in the liver

7. LONG TERM RESERVOIR
 Consist of adipose tissue (fat tissue), which is found
beneath the skin and in various locations in abdomen
 Adipose tissue consist of cells capable of absorbing
nutrients from the blood, converting them to triglycerides
( fats ) and storing them
 The long term reservoir is obviously what keeps us alive
during a prolonged fast.

8.  The brain lives primarily on glucose, and the
rest of the body lives on fatty acids, glycerol
is converted into glucose, so the brain
continues to be nourished even after the
short term reservoir is depleted

9. Brain process
 Most specifically the activity in 2 areas of the
hypothalamus conribute to our understanding
 The Lateral Hypothalamus- is involved in stimulation of
eating
 The ventro medial hypothalamus is involved in reducing
hunger
 Role of Leptin: it influence eating by inhibiting the
production of neurotransmitter in the lateral
hypothalamus that induces eating
 Neurotransmitter “ serotonin” is particularly responsible
for satiety and drugs that blocks serotonin have been
used to treat obesity in humans

10. Hunger theories
 Set-Point Assumption
 Glucostatic and Lipostatic Set-Point
Theories of Hunger and Eating
 Positive-Incentive Perspective

11. Set-Point Assumption
 Most people attribute hunger (the motivation to eat) to the
presence of an energy deficit, and they view eating as the
means by which the energy resources of the body are
returned to their optimal level that is, to the energy set
point.
 Set-point models assume that hunger and eating work in
much the same way as a thermostat regulated heating
system in a cool climate.
 The heater increases the house temperature until it
reaches its set point (the thermostat setting).
 The heater then shuts off, and the temperature of the
house gradually declines until it becomes low enough to
turn the heater back on.

12.  All set-point systems have three components: a
setpoint mechanism, a detector mechanism, and an
effector mechanism.
 The set-point mechanism defines the set point,the
detector mechanism detects deviations from the set
point ,and the effector mechanism acts to eliminate
the deviations.
 All set-point systems are negative feedback system

13. Glucostatic and Lipostatic Set-Point
Theories of Hunger and Eating
 Several researchers suggested that eating is
regulated by a system that is designed to maintain a
blood glucose set point
 the idea being that we become hungry when our
blood glucose levels drop significantly below their
set point and that we become satiated when eating
returns our blood glucose levels to their set point.
 The various versions of this theory are collectively
referred to as the Glucostatic theory.
 It seemed to make good sense that the main
purpose of eating is to defend a blood glucose set
point, because glucose is the brains primary fuel.

14.  Lipostatic theory: According to this theory, every
person has a set point for body fat, and deviations
from this set point produce compensatory
adjustments in the level of eating that return levels
of body fat to their set point.

15. Positive-Incentive Perspective
 The central assertion of this perspective,
commonly referred to as positive-incentive theory,
is that:
 humans and other animals are not normally
driven to eat by internal energy deficits but are
drawn to eat by the anticipated pleasure of eating
the anticipated pleasure of a behavior is called its
positive-incentive value

16.  According to the positive-incentive perspective, the
degree of hunger you feel at any particular time
depends on the interaction of all the factors that
influence the positive incentive value of eating These
include the following:
the flavor of the food you are likely to consume,
 what you have learned about the effects of this
food either from eating it previously or from other
people,
 the amount of time since you last ate,
 the type and quantity of food in your gut

17. Ventromedial hypothalamus
 Also called as Ventromedial nucleus of the
hypothalamus
 It is involve in terminating hunger, fear,
thermoregulation,and sexual activity
 The nuclear region is involved with the
recognition of the feeling of the fullness

18. Obesity
 It is an excessive accumulation of body fat
 In general fat should constitute about 20-27 percent of
body tissue in women and about 15-22% in men
 According to WHO
 600 million people worldwide are obese and 1.9 billion are
overweight, including 42 million children under 5 years
 RISK OF OBESITY : obesity is a risk factor for many
disorders.
 it contributes to death rates for all cancers
Obesity is chief cause of disability

19. Why Do Some People Become
Obese While Others Do Not?
 Differences in Consumption:
 There are many factors that lead some people to eat
more than others who have comparable access to food.
 For example, some people consume more energy
because they have strong preferences for the taste of
high-calorie foods
 Differences in Energy Expenditure :
The most obvious difference is that people differ
substantially in the amount of exercise they do

20.  Sedentary Lifestyle Is a Major Cause of Obesity:
Regular physical activity and physical training
are known to increase muscle mass and
decrease body fat mass and vice versa.
 Abnormal Feeding Behavior Is an Important
Cause of Obesity: environmental, social,
psychological factors contribute to abnormal
feeding.
 Genetic Factors as a Cause of Obesity:
evidence, however, suggests that 20 to 25 per
cent of cases of obesity may be caused by
genetic factors.

21. (1) mutations of MCR-4, the most common
monogenic form of obesity
(2) congenital leptin deficiency caused by
mutations of the leptin gene, which are very
rare; and
(3) mutations of the leptin receptor, also very
rare

22. BMI{ body mass index}
 It is defined as the body mass divided by the square
of the body height and universally expressed in units
of kg/m2
 In clinical terms BMI between 25 & 29.9 kg /m2 is called
obese
 Obesity is usually defined as 25% or greater total body
fat in men and 35% or greater in women
 Cut off value: 30.0 BMI and above is consider to be
obese.

23. Leptin and the Regulation of Body
Fat
 Fat release a peptide hormone called leptin
 Leptin as a Treatment for Human Obesity
 The early studies of leptin seemed to confirm the
hypothesis that it could function as an effective
treatment for obesity.
Receptors for leptin were found in the brain,and
injecting it into ob/ob mice reduced both their
eating and their body fat ( Seeley & Woods,
2003).

24. Treatment of Obesity
 Treatment of obesity depends on decreasing energy
input below energy expenditure
 Also creating a sustained negative energy balance until
the desired weight loss is achieved this means either
reducing energy intake or increasing energy expenditure.
 The current National Institutes of Health (NIH) guidelines
recommend a decrease in caloric intake of 500
kilocalories per day for overweight and moderately obese
persons (BMI greater than 25 but less than 35 kg/m2) to
achieve a weight loss of approximately 1 pound each
week

25.  To decrease energy intake, most reducing diets are
designed to contain large quantities of “bulk,” which is
generally made up of non-nutritive cellulose substances
 Various drugs for decreasing the degree of hunger have
been used in the treatment of obesity.
 The most widely used drugs are :
 amphetamines (or amphetamine derivatives), which directly
inhibit the feeding centers in the brain.
 sibutramine : it reduces food intake and increases energy
expenditure.

26. Anorexia nervosa
 In contrast to obesity, anorexia nervosa is a disorder of
under consumption.
 Anorexics eat so little that they experience health
threatening weight loss; and despite their emaciated
appearance, they often perceive themselves as fat
 Anorexia nervosa is a serious condition; In approximately
10% of diagnosed cases, complications from starvation
result in death, and there is a high rate of suicide among
anorexic
 Anorexia nervosa is an obssessive disorder amounting
to self starvation, in which an individual diets and
exercise to the point that body weight falls below the
optimum level, threatning health and potentiality leading

27. Anorexia and Positive Incentives
 The positive-incentive perspective on eating suggests that
the decline in eating that defines both anorexia (and
bulimia) is likely a consequence of a corresponding decline
in the positive-incentive value of food.
 However, the positive-incentive value of food for anorexia
patients has received little attention in part, because
anorexic patients often display substantial interest in food.
 The fact that many anorexic patients are obsessed with
food continually talking about it, thinking about it, and
preparing it for others (Crisp, 1983) seems to suggest that
food still holds a high positive-incentive value for them.

28. Bulimia nervosa
 The term “Bulimia nervosa” derives from the
“oxhunger” in Greek.
 Bulimia nervosa is a disorder characterized by
periods of not eating interrupted by bingeing (eating
huge amounts of food in short periods of time)
followed by efforts to immediately eliminate the
consumed calories from the body by voluntary
purging (vomiting); by excessive use of
laxatives,enemas,or diuretics; or by extreme
exercise.
 Bulimics may be obese or of normal weight.

29. Conclusion
When the glycogen level of the body decrease the
person feels desire to eat. It is affected by both
biological and environmental, factors. Research
believes that genetic differences among individuals
play a role in hunger. The brain, the digestive system
, etc are involved in hunger at the biological level.

30. Refrences
 Pinel, J.P.J. (2000). Biopsychology (4th
ed.).Boston: Allyn & Bacon.
 Taylor, S.E . Health psychology.McGraw Hill Education.
India
 Gross, R & Mcllveen, R.Biopsychology. Hodder education:
United Kingdom