Factors That Influence How Much We Eat

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PowerPoint Presentation for
Biopsychology, 8th Edition
by John P.J. Pinel
Prepared by Jeffrey W. Grimm
Western Washington University
Copyright © 2011 Pearson Education,
Inc. All rights reserved.
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Chapter 12
Hunger, Eating, and Health
Why Do Many People Eat Too
Much?
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Control of Eating
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Is there a “set point” for the body’s energy
reserves that determines when we eat?
The prevalence of eating disorders suggests that
this may not be the case
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Over half of 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

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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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FIGURE 12.1 The gastrointestinal
tract and the process of digestion.
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Energy Storage in the Body

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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

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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
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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 Continued

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Energy availability controlled by two pancreatic
hormones
Insulin: high during cephalic and absorptive phases
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Triggers glucose use as fuel by body cells
Triggers conversion of blood-borne energy to fat, glycogen,
and protein
Triggers energy storage in adipose cells, liver, and muscles
Glucagon: high during fasting phase

Triggers change of stored energy to usable fuel: fat to free
fatty acids and then ketones; protein to glucose
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FIGURE 12.3 The major events
associated with the three phases of
energy metabolism: the cephalic,
absorptive, and fasting phases.
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Theories of Hunger and
Eating: Set Points vs. Positive
Incentives

The Set-Point Assumption:
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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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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
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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
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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
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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
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Adaptive species-typical preferences
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Adaptive species-typical aversions
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Sweet and fatty foods = high energy
Salty = sodium-rich
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 What
We Eat
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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
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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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FIGURE 12.5 The sham-eating
preparation.
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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 Continued
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Appetizer effect: small amounts of food may
increase hunger
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Due to cephalic-phase responses?
Serving size: the larger the serving, generally
the more consumed
Social influences
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Even rats eat more when in a group
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Sensory-Specific Satiety
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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 (outline)
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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
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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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Experiments suggested two hypothalamic
centers
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Ventromedial (VMH): a satiety center
Lateral (LH): a hunger center
Lesions of VMH produce hyperphagia
Lesions of LH produce aphagia and adipsia
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FIGURE 12.8 The locations in the rat
brain of the ventromedial
hypothalamus and the lateral
hypothalamus.
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FIGURE 12.9 Postoperative
hyperphagia and obesity in a rat with
bilateral VMH lesions. (Based on
Teitelbaum, 1961.)
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Myth of Hypothalamic Hunger
and Satiety Centers Continued
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The VMH likely is not a satiety center
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The LH likely is not a feeding center
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VMH lesion rats maintain a new higher weight
VMH lesions may non-specifically destroy other brain
regions (noradrenergic bundle; paraventricular nucleus)
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 the Gastrointestinal
Tract in Satiety
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Cannon and Washburn (1912)
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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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FIGURE 12.12 Transplantation of an
extra stomach and length of intestine
in a rat. Koopmans (1981) implanted
an extra stomach and length of
intestine in each of his experimental
subjects.
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Hunger and Satiety
Peptides
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Gut peptides that decrease meal size:
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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
Continued
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Hunger peptides usually synthesized in the
hypothalamus:
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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
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Microinjections of some peptides have major
effects on eating
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Serotonin and Satiety
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Serotonin agonists consistently reduce
rats’ food intake
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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
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Food-related: insatiable appetite, extremely slow
metabolism; eventual death in adulthood from obesityrelated 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
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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
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Variability of body weight
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Set points and health
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According to the set-point assumption, it should be
very difficult to gain weight
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
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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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FIGURE 12.13 The
diminishing effects on
body weight of a lowcalorie diet and a highcalorie diet.
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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?
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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
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Why is there an Epidemic of Obesity?
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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?
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Energy input differences
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Energy output differences
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Craving for high-calorie foods
Cultural norms
Large cephalic-phase response to sight and smell of
food
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?
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Considering the leaky-barrel model, longterm 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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FIGURE 12.16 An ob/ob mouse and a
control mouse.
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Leptin, Insulin, and the
Arcuate Melanocortin System
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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
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Serotonin appears to increase short-term satiety
signals associated with the consumption of a
meal and decrease…
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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
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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
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Anorexia
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Voluntary self-starvation
Fatal in 10% of patients
Bulimia: bingeing and purging
Similar symptoms, difficult to distinguish
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Distorted body image
Most often affects educated, affluent young
females
Associated with obsessive-compulsive disorder
and depression
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Anorexia and Positive
Incentives
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It is not clear whether anorexics find food
less appealing
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Some evidence suggests the opposite
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Anorexia Nervosa: A
Hypothesis
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A person out of homeostatic balance might
find a full meal to be aversive
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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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