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BIOPSYCHOLOGY 8e

John P.J. Pinel

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Topics
12.1 Digestion, Energy Storage, and
Energy Utilization
12.2 Theories of Hunger and Eating: Set
Points versus Positive Incentives
12.3 Factors that Determine What, When,
and How Much We Eat
12.4 Physiological Research on Hunger
and Satiety
12.5 Body Weight Regulation: Set Points
versus Settling Points
12.6 Human Obesity: Causes,
Mechanisms, and Treatments
12.7 Anorexia and Bulimia Nervosa
Control of Eating

Is there a “set point” for the body’s energy


reserves that determines when we eat?
•The prevalence of eating disorders suggests
this may not be the case
• Over ½ the adult population in the U.S.
meets clinical criteria for obesity
• The average American consumes 3,800
calories per day—about twice the average
requirement
• 3% of U.S. adolescents suffer from
anorexia or bulimia

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Digestion, Energy Storage, and Energy Utilization

• Purpose of eating is to
provide the body with
molecular building blocks
and energy
• Digestion: breaking down
food and absorbing its
constituents

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Digestion, Energy Storage, and Energy Utilization

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Energy Storage in the Body

• Energy delivered to the body as lipids,


amino acids, and glucose
• Energy storage in the body as fats,
glycogen, and proteins
• Fats are most efficient for energy storage
• One gram of fat stores twice as much
energy as one gram of glycogen
• Fat does not attract and hold as much
water as glycogen, and so provides
denser energy storage

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Three Phases of Energy Metabolism

• Energy metabolism: Chemical


changes that make energy available
for use
• Cephalic phase: preparation for
eating
• Absorptive phase: energy absorbed
• Fasting phase
• Withdrawing energy from reserves
• Ends with next cephalic phase

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Three Phases of Energy Metabolism

• Energy availability
controlled by two
pancreatic hormones
• Insulin: high during
cephalic and
absorptive phases
• Glucagon: high
during fasting phase

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Theories of Hunger and Eating: Set Points vs. Positive
Incentives
• The Set-Point Assumption
• Hunger is a response to an
energy need; we eat to
maintain an energy set
point
• Typical assumption: Eating
works like a thermostat, a
negative feedback system:
turns on when energy is
needed, off when set point
is reached

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Theories of Hunger and Eating

FIGURE 12.4:
The energy set-point
view that is the basis of
many people’s thinking
about hunger and eating.

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Glucostatic and Lipostatic Set-Point Theories of Hunger

• If we eat to maintain an
energy level (homeostasis),
what is monitored? (c. 1940s
and 1950s)
• Glucostatic theories –
glucose levels determine
when we eat
• Lipostatic theories – fat
stores determine how much
we eat over long term
(explaining why weight tends
to be constant)

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Problems with Set-Point Theories of Hunger and Eating

• Contrary to evolutionary pressures


that favored energy storage for
survival
• Reductions in blood glucose or
body fat do not reliably induce
eating
• Do not account for the influence of
external factors on eating and
hunger

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Positive-Incentive Perspective

• We are drawn to eat by the


anticipated pleasure of eating
• We have evolved to “crave” food
• Multiple factors interact to
determine the positive-incentive
value of eating
• Accounts for the impact of
external factors on eating behavior

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Factors that Determine What, When, and How Much
We Eat

• Adaptive species-typical
preferences
– Sweet and fatty foods = high
energy
– Salty = sodium-rich
• Adaptive species-typical aversions
– Bitter = often associated with
toxins
• Learned preferences and
aversions
– Rats prefer diet with vitamins,
foods they smell in mother’s
milk or other rats’ breaths

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Factors That Influence When We Eat

• We tend to get hungry at mealtime


• As mealtime approaches, the
body enters the cephalic phase
leading to a decrease in blood
glucose
• Pavlovian conditioning of hunger
demonstrated experimentally

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Factors that Influence How Much We Eat

• Satiety: may stop a meal,


“being full”
• Satiety signals: food in gut
and glucose in the blood
can induce satiety signals
• Sham eating studies
demonstrate that satiety
signals are not necessary
for meal termination
• Rats initially sham eating
eat normal-sized meal if
food is familiar

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Factors that Influence How Much We Eat

FIGURE 12.5:
The sham-eating
preparation.

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Factors that Influence How Much We Eat

FIGURE 12.6:
Change in the magnitude of
sham eating over repeated
sham-eating trials. The rats
in one group sham ate the
same diet they had eaten
before the sham eating
phase; the rats in another
group sham ate a diet
different from the one they
had previously eaten.
(Based on Weingarten,
1990.)

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Factors that Influence How Much We Eat

• Appetizer effect: small


amounts of food may
increase hunger
• Serving size: the larger the
serving, generally the more
consumed
• Social influences
• Even rats eat more when in
a group

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Sensory-Specific Satiety

• Tasting a food immediately


decreases the positive-
incentive value of similar
tastes and decreases the
palatability of all foods about
30 minutes later
• Adaptive – encourages a
varied diet
• Some foods are resistant to
sensory-specific satiety: rice,
bread, potatoes, sweets, and
green salads

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Physiological Research on Hunger and Satiety

• Role of blood glucose levels


• Myth of hypothalamic centers
• Role of the GI tract
• Hunger and satiety peptides
• Serotonin and satiety

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Role of Blood Glucose Levels in Hunger and
Satiety

• Blood glucose drops prior to a


meal as preparation to eat – not a
cue to eat
• Must decrease blood glucose by
50% to trigger feeding
• Premeal glucose infusions often
do not suppress eating
• Reduced blood glucose may
contribute to hunger, but changes
in blood glucose do not prevent
hunger or satiety

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Myth of Hypothalamic Hunger and Satiety Centers

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Myth of Hypothalamic Hunger and Satiety
Centers

The VMH likely is not a satiety center


• VMH lesion rats maintain a new higher weight
• VMH lesions may non-specifically destroy
other brain regions (noradrenergic bundle;
paraventricular nucleus)
The LH likely is not a feeding center
• LH lesioned rats will recover if kept alive by
tube feeding
• LH lesions may produce sensory and motor
disturbances that affect food seeking
Most supported role of the hypothalamus:
regulation of energy metabolism

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Role of Gastrointestinal Tract in Satiety

• Cannon and Washburn (1912)


 Studies suggested stomach
contractions led to hunger, distension
to satiety
• However, hunger is still experienced with
no stomach (but rest of GI tract
remaining)
• In a rat study, rats with a transplanted
stomach and intestine expressed sated
behavior when food was injected
• Led to hypothesis of blood borne satiety
signal(s)

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Role of Gastrointestinal Tract in Satiety

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Hunger and Satiety Peptides

• Gut peptides that decrease meal size:


cholecystokinin (CCK), bombesin, glucacon, alpha-
melanocyte-stimulating hormone, somatostatin
• Must first establish that peptide does not merely create
illness
• CCK causes nausea at high doses, but suppresses food
intake at doses insufficient to induce taste aversions

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Hunger and Satiety Peptides

• Hunger peptides usually synthesized in the hypothalamus:


neuropeptide Y, galanin, orexin-A, ghrelin
• Overall, many different neural signals control eating (not
just glucose and fat)
• Hypothalamus plays a central role in eating behaviors
• Microinjections of some peptides have major effects on
eating

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Serotonin and Satiety

• Serotonin agonists consistently


reduce rats’ food intake
– Even intake of palatable food
is affected
– Reduces amount eaten per
meal
– Preferences shift away from
fatty foods
• Similar effects seen in humans

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Prader-Willi Syndrome: Patients with Insatiable Hunger

Symptoms:
• Food-related: insatiable appetite, extremely slow
metabolism; eventual death in adulthood from
obesity related diseases
• Other symptoms: weak muscles, small hands
and feet, triangular mouth, stubbornness,
feeding difficulties in infancy, tantrums,
compulsivity, skin picking
Damage or absence of a section of
chromosome 15
• Study of the syndrome may lead to advances in
understanding eating behaviors in humans

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Body Weight Regulation: Set Points vs. Settling Points

Variability of body weight


• According to the set-point
assumption, it should be very
difficult to gain weight
Set points and health
• Free-feeding does not lead to
optimum health
• Positive effects seen with caloric
restriction
Diet-induced thermogenesis –
body temperature drops with fat
loss, making weight-loss diets
gradually less effective

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Set Points and Settling Points in Weight Control

• Body weight drifts around a


natural settling point – “the level
at which the various factors that
influence body weight achieve
an equilibrium”
• A new body weight will be
established if conditions remain
constant
• A loose kind of homeostatic
regulation
• Modeled by “The leaky-barrel”

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Set Points and Settling Points in Weight Control

FIGURE 12.13:
The diminishing effects
on body weight of a low-
calorie diet and a high-
calorie diet.

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Set Points and Settling Points in Weight Control

FIGURE 12.14:
The leaky-barrel model: a
settling-point model of
eating and body weight
homeostasis.

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Who Needs to Be Concerned about Obesity?

•Everyone, as rates of obesity are


increasing in most parts of the
world
•Obesity is related to many other
health problems

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Human Obesity: Causes, Mechanisms, and Treatments

Why Is There an Epidemic of


Obesity?
•Evolution favored preferring high-
calorie food, eating to capacity,
storing fat, and using energy
efficiently
•Cultural practices and beliefs
promote consumption

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Why Do Some People Become Obese While Others Do Not?

Energy input differences


• Craving for high-calorie foods
• Cultural norms
• Large cephalic-phase response to sight and smell of food
Energy output differences
• Exercise
• Diet-induced thermogenesis
• NEAT (nonexercise activity thermogenesis)
Genetics interacts with both energy input and output

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Why Are Weight-Loss Programs Typically Ineffective?

• Considering the leaky-barrel


model, long-term weight loss will
require a permanent lifestyle
change
• Exercise also can make you
hungry
– Often people eat more
calories after the workout
than they burned during the
workout

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Leptin and the Regulation of Body Fat

• Leptin – a negative feedback fat signal


• Hormone released by fat cells
• Leptin receptors found in the brain
• ob/ob mice are three times normal weight
• Homozygous for a mutant gene ob
• Lack leptin
• Eat more, and store fat more efficiently
than controls
• Human leptin research
• However, most obese humans have
high leptin levels. Leptin injections help
the few ob/ob humans

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Leptin, Insulin, and the Melanocortin System

• Insulin brain levels reflect


visceral fat; leptin levels
reflect subcutaneous fat
• Both insulin and leptin
receptors found in the
arcuate nucleus of the
hypo-thalamus
• Leptin and insulin in the
brain have some effects
on eating behavior, but
are (again) not the only
eating/sating signals

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Treatment of
Obesity:
Serotonergic
Agonists • Serotonin appears to increase short-
term satiety signals associated with the
consumption of a meal and decrease…
• Urge to eat high-calorie foods
• Consumption of fat
• Intensity of hunger
• Size of meals
• Number of snacks and bingeing
• Early serotonin agonists produced
heart disease in some patients and were
withdrawn from the market

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Treatment
of Obesity:
Gastric
Surgery • Gastric bypass and the adjustable
gastric band create a smaller
stomach
• Treatments are for extreme obesity
• These treatments are effective in
some patients

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Anorexia Bulimia Nervosa
• Anorexia
• Voluntary self-starvation
• Fatal in 10% of patients
• Bulimia: bingeing and purging
• Similar symptoms, difficult to
distinguish
• Distorted body image
• Most often affects educated,
affluent young females
• Associated with obsessive-
compulsive disorder and
depression

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Anorexia Nervosa: A Hypothesis

• A person out of homeostatic


balance might find a full meal
to be aversive
• Eating a meal would then
lead to development of food
aversions
• For example, feeding meals
to famine victims sometimes
leads to anorexia
• Implication is for anorexics to
eat small amounts of food
throughout the day as part of
therapy

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Watch: Thinking About Hunger
Watch: Eating and the Brain
Watch: Anorexia
Animation: Leptin and Obesity

Note: To view the MyPsychLab assets, please make sure you are connected to the
internet and have a browser opened and logged into www.mypsychlab.com.

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Acknowledgments
Slide Image Description Image Source

template lightning ©istockphoto.com/Soubrette

template background texture ©istockphoto.com/Hedda Gjerpen

Ch12 image eating ©istockphoto.com/aldomurillo

3, 13 head ©istockphoto.com/Suzanne Tucker

3, 13, 30 food - burger & fries ©istockphoto.com/Adolfo Lazo

4 blue sky & clouds, open arms ©istockphoto.com/kertlis

5 Figure 12.1 Pinel 8e, p. 300

6 messy files ©istockphoto.com/Jelena Popic

7 laughing ©istockphoto.com/Stratesigns, Inc.

8 Figure 12.3 Pinel 8e, p. 302

9, 19 hungry ©istockphoto.com/Neil Wysocki

9, 19 bowl ©istockphoto.com/Jill Chen

9, 19 dish of noodles ©istockphoto.com/Jamesmcq24

10 Figure 12.4 Pinel 8e, p. 303

11 woman observing & taking notes ©istockphoto.com/Claudio Arnese

12 Man's head ©istockphoto.com/Nicolas Hansen

14 box of chocolates ©istockphoto.com/The Desktop Studio

15 pressure gauge ©istockphoto.com/Mark Evans

16 bucket of popcorn ©iStockphoto.com/PMSI Web Hosting and Design

17 Figure 12.5 Pinel 8e, p. 307

18 Figure 12.6 Pinel 8e, p. 308

20 person thinking ©istockphoto.com/akurtz

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Acknowledgments
Slide Image Description Image Source

21 book ©istockphoto.com/Carmen Martínez Banús

22, 24, 40 brain ©istockphoto.com/Stephen Kirklys

23 Figure 12.8 Pinel 8e, p. 310


23 Figure 12.9 Pinel 8e, p. 311

25, 39 white rat ©iStockphoto.com/Elena Butinova

25, 26, 39 blue sky & clouds ©istockphoto.com/kertlis

26 Figure 12.12 Pinel 8e, p. 313

27, 28 head - woman ©istockphoto.com/Angel Herrero de Frutos

29 hand holding rat ©iStockphoto.com/sidsnapper

31, 32, 33, 34 DNA ©istockphoto.com/HooRoo Graphics

31, 32, 43 scale ©istockphoto.com/Luca di Filippo

33 Figure 12.13 Pinel 8e, p. 316

34 Figure 12.14 Pinel 8e, p. 317

35, 36 globe w/ flags ©istockphoto.com/Stay Media Productions

37 friends sitting on a bench ©istockphoto.com/Aldo Murillo

38 people on treadmills ©istockphoto.com/ShaneKato

41, 42 medical clipboard ©istockphoto.com/Anastasia Pelikh

44 notebook ©istockphoto.com/stockcam

44 yellow pad ©istockphoto.com/DNY59

45 laptop ©istockphoto.com/CostinT

45 table and wall ©istockphoto.com/David Clark

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