BIOPSYCHOLOGY

BOOK / DOC EDGE / 1st YR - 2nd SEM

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[TRANS] UNIT 12: HUNGER, EATING, AND HEALTH

● Many people—and we assume this includes organisms that live inside our gastrointestinal
you—believe that hunger and eating are normally tract)
triggered when the body’s energy resources fall ▪ Gut microbiome aka probiotic bacteria-
below a prescribed optimal level, or set point. helps us digestion food, then we help
them get the nutrients
○ The leftovers of what we ingest are
The Case of the Man Who Forgot Not to Eat jettisoned from the other end
● strictly speaking, food has not been consumed
○ development of severe amnesia for long-term until it has been digested
explicit memory
○ On one occasion, he was offered a second
meal about 15 minutes after he had eaten the
first, and he ate it. When offered a third meal
15 minutes later, he ate that, too. When
offered a fourth meal he rejected it, claiming
that his “stomach was a little tight.”
○ R.H.’s hunger (i.e., motivation to eat) did not
result from an energy deficit

DIGESTION, ENERGY STORAGE, AND

ENERGY UTILIZATION
● The primary purpose of hunger is to increase the
probability of eating
● The primary purpose of eating is to supply the
body with the molecular building blocks and
energy it needs to survive and function

HUNGER -> EATING -> SUPPLY

● In short,
DIGESTION AND ENERGY STORAGE 1. chewing (mastication )
IN THE BODY ○ with the help of the tongue and teeth
then mixing it with the saliva which
contains salivary enzymes thus,
DIGESTION
initiating chemical digestion. There are
● Digestion is the gastrointestinal process of two types of digestion- mechanical and
breaking down food and absorbing its chemical.
constituents into the body 2. esophagus
3. stomach (breaks down food)
● In order to appreciate the basics of digestion, it is ○ Another process of digestion occurs
useful to consider the body without its wherein the muscles of the stomach
protuberances, as a simple living tube with a hole contracts and turns the food around and
at each end. at the same time mixes it with chemicals
○ To supply itself with energy and other released by the stomach (pepsin and
nutrients, the tube puts food into one of its hydrochloric acid
two holes—the one with teeth—and passes 4. small intestine(absorption)
the food along its internal canal so that the ○ Duodenum (connected to the liver and
food can be broken down and partially pancreas)
absorbed from the canal into the body ▪ Bile helps in the emulsification of fat
○ Much of the work of breaking down the food ○ Jejunum- propelled forward with
we ingest is done by the constituents of our peristalsis
gut microbiome (the bacteria and other

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 ▪ As the food goes through the small ○ Consequently, if all your fat calories were
intestine, the nutrients are absorbed stored as glycogen, you would likely weigh
by the microvilli well over 275 kilograms (600 pounds)
○ Ileum-by the time it reaches this place,
almost all of the nutrients have been
absorbed
5. Large intestine- contains the undigested
portion. Absorbs water and fluid as the food
passes through the colon.
○ Ascending colon
○ Transverse colon
○ Descending colon
○ Sigmoid colon (muscular part)

ENERGY STORAGE IN THE BODY

● As a consequence of digestion, energy is
delivered to the body in three forms:
○ Lipids (fats) -for fats
○ Amino acids (breakdown products of
proteins) -for proteins
○ Glucose (a simple sugar that is the
breakdown product of complex
carbohydrates, that is starches and sugars)
- for glucose
○ When the body reacts to them, it
immediately creates energy
● The body uses energy continuously, but its
consumption is intermittent
○ therefore, it must store energy for use in the
intervals between meals.
THREE PHASES OF ENERGY METABOLISM
● There are three phases of energy metabolism
● If theyre not used, theyre being stored
(the chemical changes by which energy is made
somewhere
available for an organism’s use):
● Energy is stored in three forms:
○ the cephalic phase
○ Fats (for lipids, stored in the adipose tissue)
▪ The condition of the body before we
○ Glycogen (for glucose, stored usually in the
start eating
liver but sometimes in the muscle)
▪ The body prepares itself as the food
○ Proteins (for amino acids, stored as protein
comes in
in the muscles)
▪ the preparatory phase
● Most of the body’s energy reserves are stored as
▪ often begins with the sight, smell, or
fats, relatively little as glycogen and proteins
even just the thought of food, and it
○ changes in the body weights of adult
ends when the food starts to be
humans are largely a consequence of
absorbed into the bloodstream
changes in the amount of their stored body
▪ the pancreas releases a great deal of
fat
insulin into the bloodstream (para
● Why is fat the body’s preferred way of storing
bumaba ang blood glucose level) and
energy?
very little glucagon
○ Glycogen, which is largely stored in the liver
▪ Lowering of the blood glucose level
and muscles, might be expected to be the
triggers a sensation called hunger
body’s preferred mode of energy storage
pangs (nagugutom ka)
because it is so readily converted to
○ the absorptive phase
glucose—the body’s main directly utilizable
▪ period during which the energy
source of energy
absorbed into the bloodstream from the
○ But there are two reasons why fat, rather
meal is meeting the body’s immediate
than glycogen, is the primary mode of
energy needs
energy storage:
▪ the pancreas releases a great deal of
▪ a gram of fat can store almost twice as
insulin into the bloodstream and very
much energy as a gram of glycogen
little glucagon
▪ glycogen, unlike fat, attracts and holds
▪ The insulin will now then be utilized in
substantial quantities of water
this phase by converting the

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 carbohydrates into glucose for use as ● On the other hand, the high levels of
energy fasting-phase glucagon promote the release of
▪ Pagsumobra then glucose can now be free fatty acids from adipose tissue and their use
stored as glycogen as the body’s primary fuel
▪ In this phase,all the free glucose are ● The high glucagon levels also stimulate the
already utilized the glucagon can conversion of free fatty acids to ketones, which
convert glycogen in the liver into energy are used by muscles as a source of energy
for the body during the fasting phase
▪ Pag na absorb na lahat ng nutrients ● After a prolonged period without food, however,
required for that time, you enter the next the brain also starts to use ketones, thus further
stage conserving the body’s resources of glucose
○ the fasting phase
▪ period during which all of the unstored
energy from the previous meal has been
used and the body is withdrawing
energy from its reserves to meet its
immediate energy requirements
▪ ends with the beginning of the next
cephalic phase
▪ characterized by high blood levels of
glucagon and low levels of insulin
▪ Pag naubos ang glycogen, it’s followed
by the fats. Icoconvert into 3 fatty acids
para magamit as source of energy. Then
pagnaubos na yung fats, sunod yung
proteins sa muscles
● The flow of energy during the three phases of
energy metabolism is controlled by two
pancreatic hormones:
○ insulin
○ Glucagon
● insulin does three things: THEORIES OF HUNGER AND EATING: SET
○ it promotes the use of glucose as the primary POINTS VERSUS POSITIVE INCENTIVES
source of energy by the body
○ it promotes the conversion of bloodborne SET-POINT ASSUMPTION
fuels to forms that can be stored: glucose to ● Most people attribute hunger (the motivation to
glycogen and fat and amino acids to proteins eat) to the presence of an energy deficit, and
○ it promotes the storage of glycogen in liver they view eating as the means by which the
and muscle, fat in adipose tissue, and energy resources of the body are returned to
proteins in muscle their optimal level—that is, to the energy set point
● In short, the function of insulin during the cephalic
phase is to lower the levels of bloodborne fuels,
primarily glucose, in anticipation of the impending
influx; and its function during the absorptive
phase is to minimize the increasing levels of
bloodborne fuels by utilizing and storing them
● In contrast to the cephalic and absorptive
phases, the fasting phase is characterized by
high blood levels of glucagon and low levels of
insulin
○ Without high levels of insulin, glucose has
difficulty entering most body cells; thus,
glucose stops being the body’s primary fuel
○ In effect, this saves the body’s glucose for
the brain, because insulin is not required for
glucose to enter most brain cells
● The low levels of insulin also promote the ● After a meal (a bout of eating), a person’s energy
conversion of glycogen and protein to glucose. resources are assumed to be near their set point
○ The conversion of protein to glucose is and to decline thereafter as the body uses energy
called gluconeogenesis to fuel its physiological processes

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 ○ When the level of the body’s energy we become satiated when eating returns our
resources falls far enough below the set blood glucose levels to their set point
point, a person becomes motivated by ● The various versions of this theory are
hunger to initiate another meal. The meal collectively referred to as the glucostatic theory
continues, according to the set-point ● It seemed to make good sense that the main
assumption, until the energy level returns to purpose of eating is to defend a blood glucose
its set point and the person feels satiated set point because glucose is the brain’s primary
(not hungry). fuel
● All set-point systems have three components: a
set-point mechanism, a detector mechanism, and LIPOSTATIC THEORY
an effector mechanism ● Also 1940s, 1950s
○ set-point mechanism defines the set point ● According to this theory, every person has a set
○ detector mechanism detects deviations point for body fat, and deviations from this set
from the set point point produce compensatory adjustments in the
○ effector mechanism acts to eliminate the level of eating that return levels of body fat to
deviations their set point
▪ For example, the set-point, detector, and ● The glucostatic and lipostatic theories were
effector mechanisms of a heating viewed as complementary, not mutually exclusive
system are the thermostat, the ○ The glucostatic theory was thought to
thermometer, and the heater, account for meal initiation and termination,
respectively whereas the lipostatic theory was thought to
● All set-point systems are negative feedback account for long-term regulation
systems ○ Thus, the dominant view in the 1950s was
○ negative feedback systems- systems in that eating is regulated by the interaction
which feedback from changes in one between two set-point systems: a short-term
direction elicit compensatory effects in the glucostatic system and a long-term lipostatic
opposite direction system
▪ Negative feedback systems are
common in mammals because they act PROBLEMS WITH SET-POINT THEORIES OF
to maintain homeostasis—a stable
internal environment—which is critical
HUNGER AND EATING
for mammals’ survival ● three more major weaknesses of set-point
● Set-point systems combine negative feedback theories of hunger and eating
with a set point to keep an internal environment ○ set-point theories of hunger and eating are
fixed at the prescribed point inconsistent with basic eating-related
evolutionary pressures as we understand
● By science, the body always tries to maintain a them
homeostatic ambition- balance condition ○ major predictions of the set-point theories of
● For this may certain levels that need to be met hunger and eating have not been confirmed
para masabing balance ○ set-point theories of hunger and eating are
● If the glucose level increases or decreases, it deficient because they fail to recognize the
triggers the set-point, na there’s a change in the major influences on hunger and eating of
set-point such important factors as taste, learning, and
● The body then reacts thru a negative feedback social influences
system. Yung level na yun, that’s what you call ● Wild animals laging may high metabolic rate kasi
the set point they are always on the move
○ Glucostatic set-point ● Before, in humans, there is no obesity pero
○ Lipostatic set-point ngayon marami because of the changes in our
● Problem is it does not apply to satiety and hunger lifestyle which is not similar to the natural lifestyle
of animals
GLUCOSTATIC THEORY
● (1940s, 1950s) researchers working under the
POSITIVE-INCENTIVE PERSPECTIVE
● Eating is pleasurable even for animals
assumption that eating is regulated by some type
● Pleasure increases because of
of set-point system speculated about the nature
○ Preferred flavors
of the regulation
○ Past experiences
● Several researchers suggested that eating is
○ Time since last meal
regulated by a system designed to maintain a
○ Others eating
blood glucose set point—the idea being that we
● The inability of set-point theories to account for
become hungry when our blood glucose levels
the basic phenomena of eating and hunger led to
drop significantly below their set point and that

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 the development of an alternative theoretical and salty tastes are characteristic of sodium-rich
perspective foods.
● central assertion of this perspective ○ In contrast, bitter tastes, for which most
○ Aka positive-incentive theory humans have an aversion, are often
○ that humans and other animals are not associated with toxins
normally driven to eat by internal energy ○ Superimposed on our species-typical taste
deficits but are drawn to eat by the preferences and aversions, each of us has
anticipated pleasure of eating the ability to learn specific taste preferences
▪ the anticipated pleasure of a behavior is and aversions
called its positive-incentive value
○ There are several different positive-incentive LEARNED TASTE PREFERENCES AND
theories, and we refer generally to all of AVERSIONS
them as the positive-incentive perspective
● Animals learn to prefer tastes that are followed by
● The major tenet of the positive-incentive
an infusion of calories, and they learn to avoid
perspective on eating is that eating is controlled
tastes that are followed by illness
in much the same way as sexual behavior: We
● humans and other animals learn what to eat from
engage in sexual behavior not because we have
their conspecifics
an internal deficit but because we have evolved
○ rats learn to prefer flavors they experience in
to crave it
mother’s milk and those that they smell on
● According to the positive-incentive perspective, it
the breath of other rats
is the presence of good food, or the anticipation
○ in humans, many food preferences are
of it, that normally makes us hungry, not an
culturally specific—for example, in some
energy deficit
cultures, various nontoxic insects are
● According to the positive-incentive perspective,
considered to be a delicacy
the degree of hunger you feel at any particular
time depends on the interaction of all the factors
that influence the positiveincentive value of
LEARNING TO EAT VITAMINS AND
eating MINERALS
○ These include the following: the flavor of the ● researchers have studied how dietary
food you are likely to consume, what you deficiencies influence diet selection
have learned about the effects of this food ● How do animals select a diet that provides all of
either from eating it previously or from other the vitamins and minerals they need?
people, the amount of time since you last ○ Two patterns of results have emerged: one
ate, the type and quantity of food in your gut, for sodium and one for the other essential
whether or not other people are present and vitamins and minerals.
eating, whether or not your blood glucose ○ When an animal is deficient in sodium, it
levels are within the normal range develops an immediate and compelling
● positive-incentive theories do not single out one preference for the taste of sodium salt
factor as the major determinant of hunger and ○ an animal deficient in some vitamin or
ignore the others mineral other than sodium must learn to
consume foods that are rich in the missing
FACTORS THAT DETERMINE WHAT, WHEN, nutrient by experiencing their positive effects;
AND HOW MUCH WE EAT this is because vitamins and minerals other
● Animals than sodium normally have no detectable
○ Prefer sweet and salty foods kasi ito yung taste in food
edible ○ For example, rats maintained on a diet
○ Aversion to bitter deficient in thiamine (vitamin B1) develop an
○ Conditioned taste aversions aversion to the taste of that diet, and if they
○ Conditioned taste preferences are offered two new diets, one deficient in
○ Cravings for deficiencies thiamine and one rich in thiamine, they often
develop a preference for the taste of the
FACTORS THAT INFLUENCE WHAT WE EAT thiamine-rich diet over the ensuing days, as
it becomes associated with improved health
● Certain tastes have a high positive-incentive
● If we, like rats, are capable of learning to select
value for virtually all members of a species
diets rich in the vitamins and minerals we need,
○ Humans- special fondness for sweet, fatty,
why are dietary deficiencies so prevalent in our
and salty taste
society?
● This species-typical pattern of human taste
○ One reason is that, in order to maximize
preferences is adaptive because in nature sweet
profits, manufacturers produce foods that
and fatty tastes are typically characteristic of
high-energy foods rich in vitamins and minerals,

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 have the tastes we prefer but lack many of mealtimes are not cries from your body for food;
the nutrients we need to maintain our health they are the sensations of your body’s
○ The second reason is illustrated by the preparations for the expected
classic study of Harris and associates homeostasis-disturbing meal.
(1933). ● Mealtime hunger is caused by the expectation of
▪ When thiamine-deficient rats were food, not by an energy deficit
offered two new diets, one with thiamine
and one without, almost all of them PAVLOVIAN CONDITIONING OF HUNGER
learned to eat the complete diet and ● Weingarten provided strong support for the view
avoid the deficient one. that hunger is often caused by the expectation of
▪ However, when they were offered 10 food, not by an energy deficit
new diets, only one of which contained ● During the conditioning phase of one of his
the badly needed thiamine, few experiments, Weingarten presented rats with six
developed a preference for the complete meals per day at irregular intervals, and he
diet signaled the impending delivery of each meal
● The number of different substances, both with a buzzer-and-light conditional stimulus
nutritious and not, consumed each day by most ○ This conditioning procedure was continued
people in industrialized societies is immense, and for 11 days.
this makes it difficult, if not impossible, for their ○ Throughout the ensuing test phase of the
bodies to learn which foods are beneficial and experiment, the food was continuously
which are not available.
○ Despite the fact that the subjects were never
FACTORS THAT INFLUENCE WHEN WE EAT deprived during the test phase, the rats
● Collier and his colleagues found that most started to eat each time the buzzer and light
mammals choose to eat many small meals were presented—even if they had recently
(snacks) each day if they have ready access to a completed a meal
continuous supply of food
○ most people, particularly those living in FACTORS THAT INFLUENCE HOW
family groups, tend to eat a few large meals MUCH WE EAT
each day at regular times
● The motivational state that causes us to stop
○ We eat at a time basis- Weingarten research
eating a meal when there is food remaining is
○ Interestingly, each person’s regular
satiety
mealtimes are the very same times at which
● Satiety mechanisms play a major role in
that person is likely to feel most hungry; in
determining how much we eat.
fact, many people experience attacks of
malaise (headache, nausea, and an inability
to concentrate) when they miss a regularly
SATIETY SIGNALS
scheduled meal ● Satiety signals- the time when we feel satisfied
○ Volume- the amount of food determines our
PREMEAL HUNGER satisfaction
○ Nutritive density
● According to Woods, the key to understanding
● food in the gut and glucose entering the blood
hunger is to appreciate that eating meals
can induce satiety signals, which inhibit
stresses the body
subsequent consumption
○ Before a meal, the body’s energy reserves
● These signals depend on both the volume and
are in reasonable homeostatic balance; then,
the nutritive density (calories per unit volume)
as a meal is consumed, there is a major
of the food
homeostasis-disturbing influx of fuels into the
● The effects of nutritive density have been
bloodstream
demonstrated in studies in which laboratory rats
○ The body does what it can to defend its
have been maintained on a single diet.
homeostasis
○ Once a stable baseline of consumption has
○ At the first indication that a person will soon
been established, the nutritive density of the
be eating—for example, when the usual
diet is changed.
mealtime approaches—the body enters the
● Some rats eventually learn to adjust the volume
cephalic phase and takes steps to soften the
of food they consume to keep their caloric intake
impact of the impending
and body weights relatively stable.
homeostasis-disturbing influx by releasing
○ However, there are major limits to this
insulin into the blood and thus reducing
adjustment: Rats rarely increase their intake
blood glucose
sufficiently to maintain their body weights if
● Woods’s message is that the strong, unpleasant
the nutritive density of their conventional
feelings of hunger you may experience at

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 laboratory feed is reduced by more than 50 particularly effective in eliciting
percent or if there are major changes in the cephalic-phase responses
diet’s palatability SERVING SIZE AND SATIETY
● amount of consumption is influenced by serving
SHAM EATING size
● The study of sham eating indicates that satiety ● The larger the servings, the more we tend to eat
signals from the gut or blood are not necessary to
terminate a meal SOCIAL INFLUENCE AND SATIETY
● In sham-eating experiments, food is chewed and ● Feelings of satiety also depend on whether we
swallowed by the subject; but rather than passing are eating alone or with others.
down the subject’s esophagus into the stomach, ● People consume more when eating with others.
it passes out of the body through an implanted ● Laboratory rats do the same
tube
● Because sham eating adds no energy to the SENSORY-SPECIFIC SATIETY
body, setpoint theories predict that all
sham-eaten meals should be huge. ● The number of different tastes available at each
○ But this is not the case meal has a major effect on meal size
○ The first sham meal of rats sham eating their ● the effect of offering a laboratory rat a varied diet
usual diet is typically the same size as of highly palatable foods—a cafeteria diet—is
previous normal meals, thus indicating that dramatic
satiety is a function of previous experience, ○ The spectacular effects of cafeteria diets on
not the current increases in the body’s consumption and body weight clearly run
energy resources. However, after the first counter to the idea that eating is rigidly
few sham meals, rats begin to sham eat controlled by internal energy set points
larger meals ○ The effect on meal size of cafeteria diets
results from the fact that satiety is to a large
degree sensory-specific.
● As you eat one food, the positive-incentive value
of all foods declines slightly, but the
positive-incentive value of that particular food
plummets.
○ As a result, you soon become satiated on
that food and stop eating it
○ However, if another food is offered to you,
you will often begin eating again
● Rolls (1990) suggested that sensory-specific
satiety has two kinds of effects:
○ relatively brief effects that influence the
selection of foods within a single meal
○ relatively enduring effects that influence the
selection of foods from meal to meal
▪ Some foods seem to be relatively
immune to long-lasting sensory-specific
satiety; foods such as rice, bread,
potatoes, sweets, and green salads can
be eaten almost every day with only a
slight decline in their palatability
● The phenomenon of sensory-specific satiety has
two adaptive consequences
○ it encourages the consumption of a varied
diet
▪ If there were no sensory-specific satiety,
APPETIZER EFFECT AND SATIETY a person would tend to eat their
preferred food and nothing else, and the
● appetizer effect- If appetizers are served, you result would be malnutrition
will notice that small amounts of food consumed ○ sensory-specific satiety encourages animals
before a meal actually increase hunger rather that have access to a variety of foods to eat
than reduce it a lot
○ Presumably, it occurs because the
consumption of small amounts of food is

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 ▪ an animal that has eaten its fill of one
food will often begin eating again if it
encounters a different one
▪ This encourages animals to take full
advantage of times of abundance, which
are all too rare in nature
PHYSIOLOGICAL RESEARCH ON HUNGER
AND SATIETY

ROLE OF BLOOD GLUCOSE LEVELS IN

HUNGER AND SATIETY
● efforts to link blood glucose levels to eating have
been largely unsuccessful
● In the classic experiment of Campfield and Smith
(1990), rats were housed with free access to food
and water, and their blood glucose levels were
continually monitored
○ In this situation, baseline blood glucose
levels rarely fluctuated more than 2 percent
○ However, about 10 minutes before a meal
was initiated, the levels quickly dropped
about 8 percent
VMH SATIETY CENTER
● Evidence does not support the glucostatic
interpretation of this observation: that the ● In 1940, it was discovered that large bilateral
premeal decline in blood glucose produces electrolytic lesions to the ventromedial
hunger and eating hypothalamus produce hyperphagia (excessive
○ Indeed, evidence suggests that the eating) and extreme obesity in rats
causation goes in the opposite direction: that ● This VMH syndrome has two different phases:
the intention to start eating triggers the ○ dynamic phase
decline in blood glucose ▪ begins as soon as the subject regains
● Four relevant observation consciousness after the operation
○ The time course of the glucose decline is not ▪ characterized by several weeks of
consistent with the idea that it reflects a grossly excessive eating and rapid
gradual decline in the body’s energy—it weight gain
occurs suddenly just before eating begins ▪ However, after that, consumption
○ Eliminating the premeal drop in blood gradually declines to a level just
glucose does not eliminate the meal sufficient to maintain a stable level of
○ If an expected meal is not served, blood obesity; this marks the beginning of the
glucose soon returns to its previous level static phase
○ The glucose levels in the extracellular fluids ○ static phase
that surround CNS neurons stay relatively ▪ important feature- the animal maintains
constant, even when blood glucose levels its new body weight
drop ▪ If a rat in the static phase is deprived of
food until it has lost a substantial
MYTH OF HYPOTHALAMIC HUNGER AND amount of weight, it will regain the lost
weight once the deprivation ends;
SATIETY CENTERS
conversely, if it is made to gain weight
● experiments on rats seemed to suggest that
by forced feeding, it will lose the excess
eating behavior is controlled by two different
weight once the forced feeding is
regions of the hypothalamus:
curtailed
○ satiety by the ventromedial hypothalamus
● Ventromedial hypothalamus is not the hunger
(vmh)
center
○ feeding by the lateral hypothalamus (lh)
○ After they destroyed the ventromedial
hypothalamus at may hyperphagia, ang
reason pla for the hyperphagia is because
there is an increase in metabolic requirement
○ Nung nasira yung ventromedial
hypothalamus, there’s a need in the increase
of metabolism

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 ○ Kapag kumain ng marami and na meet yung ➢ they are like misers who run to the
demand ng metabolism, nawala yung bank each time they make a bit of
hyperphagia money and deposit it in a savings
account from which withdrawals
LH FEEDING CENTER cannot be made
● In 1951, Anand and Brobeck reported that ○ The second line of evidence that undermined
bilateral electrolytic lesions to the lateral the theory of a VMH satiety center has
hypothalamus produce aphagia—a complete shown that many of the effects of VMH
cessation of eating lesions are not attributable to VMH damage
○ concluded that the lateral region of the ▪ A large fiber bundle, the ventral
hypothalamus is a feeding center noradrenergic bundle, courses past
● Teitelbaum and Epstein (1962) subsequently the VMH and is thus inevitably damaged
discovered two important features of the LH by large electrolytic VMH lesions; in
syndrome: particular, fibers that project from the
○ they found that the aphagia was nearby paraventricular nuclei of the
accompanied by adipsia—a complete hypothalamus are damaged
cessation of drinking ▪ Bilateral lesions of the noradrenergic
○ they found that LH-lesioned rats partially bundle or the paraventricular nuclei
recover if they are kept alive by tube feeding produce hyperphagia and obesity, just
▪ First, they begin to eat wet, palatable as VMH lesions do
foods, such as chocolate chip cookies
soaked in milk, and eventually they will MODERN RESEARCH ON THE ROLE OF
eat dry food pellets if water is HYPOTHALAMIC NUCLEI IN HUNGER AND
concurrently available SATIETY
● Aphagia and Adipsia is the effect of the overall ● recent evidence suggests that certain distinct cell
damage of the lateral hypothalamus, specifically populations within the hypothalamus can
in the arcuate nucleus, which also triggers the influence hunger and satiety
feeling of satisfaction ○ For example, certain neurons within the
paraventricular nucleus of the hypothalamus
REINTERPRETATION OF THE EFFECTS OF have been shown to act as nutrient sensors
VMH AND LH LESIONS that can influence feeding and satiety
● The theory that the VMH is a satiety center ● several distinct neuronal populations within the
crumbled in the face of two lines of evidence arcuate nucleus of the hypothalamus have been
○ One of these lines showed that the primary shown to either:
role of the hypothalamus is the regulation of ○ control the metabolism of adipose tissue
energy metabolism, not the regulation of ○ reduce feeding
eating ○ increase feeding
▪ The initial interpretation was that
VMH-lesioned animals become obese ROLE OF THE GASTROINTESTINAL
because they overeat; however, the TRACT IN SATIETY
evidence suggests the converse—that ● One of the most influential early studies of
they overeat because they become hunger was published by Cannon and Washburn
obese in 1912
▪ Bilateral VMH lesions increase blood ● It was a perfect collaboration: Cannon had the
insulin levels, which increases ideas, and Washburn had the ability to swallow a
lipogenesis (the production of body fat) balloon
and decreases lipolysis (the ○ First, Washburn swallowed an empty balloon
breakdown of body fat to utilizable forms tied to the end of a thin tube.
of energy) ○ Then, Cannon pumped some air into the
▪ Both are likely to be the result of the balloon and connected the end of the tube to
increases in insulin levels that occur a water-filled glass U-tube so that
following the lesion Washburn’s stomach contractions produced
▪ Because the calories ingested by a momentary increase in the level of the
VMH-lesioned rats are converted to fat water at the other end of the U-tube
at a high rate, the rats must keep eating ○ Washburn reported a “pang” of hunger each
to ensure they have enough calories in time a large stomach contraction was
their blood to meet their immediate recorded
energy requirements

SIY, CHANTELLE 1P4 9

● Cannon and Washburn’s finding led to the theory
that hunger is the feeling of contractions caused
▪ Koopmans found that food injected into
by an empty stomach, whereas satiety is the
the transplanted stomach and kept there
feeling of stomach distention
by a noose around the pyloric sphincter
○ However, support for this theory and interest
decreased eating in proportion to both
in the role of the gastrointestinal tract in
its caloric content and volume
hunger and satiety quickly waned with the
▪ Because the transplanted stomach had
discovery that human patients whose
no functional nerves, the gastrointestinal
stomach had been surgically removed and
satiety signal had to be reaching the
whose esophagus had been hooked up
brain through the blood.
directly to their duodenum (the first segment
▪ And because nutrients are not absorbed
of the small intestine, which normally carries
from the stomach, the bloodborne
food away from the stomach) continued to
satiety signal could not have been a
report feelings of hunger and satiety and
nutrient.
continued to maintain their normal body
▪ It had to be some chemical or chemicals
weight by eating more meals of smaller size
that were released from the stomach in
● In the 1980s, there was a resurgence of interest
response to the caloric value and
in the role of the gastrointestinal tract in eating
volume of the food—which leads us
○ Koopmans (1981) transplanted an extra
nicely into the next section
stomach and length of intestine into rats and
● The illustration above shows na gumawa sila ng
then joined the major arteries and veins of
another stomach na nagssupply ng nutrition tot
the implants to the recipients’ circulatory
the intestine pero no nervous connection to the
systems
brain
● Despite the fact that there was no nervous
connection, it did trigger so they figured out that it
might be in the blood

HUNGER AND SATIETY PEPTIDES

SIY, CHANTELLE 1P4 10

● Soon after the discovery that the stomach and ● Still it is clear that hypothalamic circuits are only
other parts of the gastrointestinal tract release one part of a two-way communication system
chemical signals to the brain, evidence began to between the brain and gut that influences hunger,
accumulate that these chemicals were peptides, eating, digestion, and the regulation of energy
short chains of amino acids that can function as resources
hormones and neurotransmitters ● Peptide
● Ingested food interacts with receptors in the ○ Satiety
gastrointestinal tract and in so doing causes the ▪ CCK
tract to release peptides into the bloodstream ▪ Bombesin
● In 1973, Gibbs, Young, and Smith injected one of ▪ Glucagon
these gut peptides, cholecystokinin (ccK), into ▪ Alpha-melanocyte-stimulating hormones
hungry rats and found that they ate smaller meals ▪ Somatostatin
○ This led to the hypothesis that circulating gut ○ Hunger
peptides provide the brain with information ▪ Neuropeptide Y
about the quantity and nature of food in the ▪ Galanin
gastrointestinal tract and that this information ▪ Orexin A
plays a role in satiety ▪ Ghrelin
○ There has been considerable support for the
hypothesis that peptides can function as SEROTONIN AND SATIETY
satiety signals ● Serotonin- a neurotransmitter that has
○ Several gut peptides have been shown to hormone-like capability
bind to receptors in the brain, particularly in ○ Agonists reduce food intake
areas of the hypothalamus involved in ○ Desire to create serotonin agonist without
energy metabolism, and a dozen or so side effects
alpha-melanocyte-stimulating hormone, and ● Serotonin- mood disorder
somatostatin) have been reported to reduce ○ If depressed ka, binibigyan ka ng serotonin
food intake to go back to your contented state
○ These have become known as satiety ○ Psychological effect- feeling of contentment
peptides (peptides that decrease appetite) ● The monoaminergic neurotransmitter serotonin is
● evidence suggests that one peptide in particular, another chemical that plays a role in satiety
CCK, induces illness: ○ The initial evidence for this role came from a
○ CCK administered to rats after they have line of research in rats
eaten an unfamiliar substance induces a ○ In these studies, serotonin-produced satiety
conditioned taste aversion for that was found to have three major properties
substance, and CCK induces nausea in ▪ It caused the rats to resist the powerful
humans attraction of highly palatable cafeteria
○ However, CCK reduces appetite and eating diets
at doses substantially below those required ▪ It reduced the amount of food consumed
to induce taste aversion in rats, and thus it during each meal rather than reducing
qualifies as a legitimate satiety peptide the number of meals
● Several hunger peptides (peptides that increase ▪ It was associated with a shift in food
appetite) have also been discovered preferences away from fatty foods
○ These peptides tend to be synthesized in the ● This profile of effects suggested that serotonin
brain, particularly in the hypothalamus might be useful in combating obesity in humans
○ The most widely studied of these are ● Indeed, serotonin agonists (e.g., fenfluramine,
neuropeptide Y, galanin, orexin-A, and dexfenfluramine, fluoxetine) have been shown to
ghrelin reduce hunger, eating, and body weight in obese
● The discovery of the hunger and satiety peptides humans under some conditions
has had two major effects on the search for the
neural mechanisms of hunger and satiety PRADER-WILLI SYNDROME: PATIENTS WITH
○ the sheer number of these hunger and INSATIABLE HUNGER
satiety peptides indicates that the neural ● Problem with this is the genetic abnormality
system that controls eating likely reacts to ● Accidental of chromosomal replication Gene #15,
many different signals, not just to one or two usually inherited from the father
○ the discovery that many of the hunger and ● Prader-Willi syndrome could prove critical in the
satiety peptides have receptors in the discovery of the neural mechanisms of hunger
hypothalamus has renewed interest in the and satiety
role of the hypothalamus in hunger and ● Individuals with prader-willi syndrome, which
eating results from an accident of chromosomal

SIY, CHANTELLE 1P4 11

 replication, experience insatiable hunger, little or SET POINTS AND HEALTH
no satiety, and an exceptionally slow metabolism ● one implication of setpoint theories of
○ In short, the Prader-Willi patient acts as body-weight regulation is that each person’s set
though he or she is starving point is optimal for that person’s health—or at
● If untreated, most patients become extremely least not incompatible with good health.
obese, and they often die in early adulthood from ● Experimental results indicate that this common
diabetes, heart disease, or other obesity-related prescription for good health could not be further
disorders from the truth
● Two kinds of evidence suggest that typical ad
Prader-Willi Syndrome: The Case of Miss A libitum (free-feeding) levels of consumption are
unhealthy
○ was born with little muscle tone ○ First are the results of nonexperimental
○ Was tube fed because her sucking reflex studies of humans who consume fewer
was so weak calories than others
○ By the time she was 2 years old, her ▪ low-calorie diets seem to slow down the
hypotonia (below-normal muscle tone) aging process
had resolved itself, but a number of ○ Evidence suggests that dietary restriction
characteristic deformities and can have beneficial effects even if it is not
developmental delays began to appear initiated until later in life
○ At 3½ years of age, Miss A. suddenly ● evidence that dietary restriction can be used to
began to display a voracious appetite and treat some neurological conditions
quickly gained weight. Fortunately, her ○ reduce seizure susceptibility in human
family maintained her on a low-calorie diet epileptics
and kept all food locked away ○ improve memory in the elderly
○ Miss A. is moderately intellectually
disabled, and she suffers from psychiatric REGULATION OF BODY WEIGHT BY
problems. Her major problem is her CHANGES IN THE EFFICIENCY OF ENERGY
tendency to have tantrums any time UTILIZATION
something changes in her environment ● Of course, how much someone eats plays a role
(e.g., a substitute teacher at school). in his or her body weight, but it is now clear that
the body controls its fat levels, to a large degree,
● This increase has been stimulated by the recent by changing the efficiency with which it uses
identification of the genetic cause of the energy
condition: an accident of reproduction that ● As a person’s level of body fat declines, that
deletes or disrupts a section of chromosome 15 person starts to use energy resources more
coming from the father efficiently, which limits further weight loss
○ conversely, weight gain is limited by a
progressive decrease in the efficiency of
BODY-WEIGHT REGULATION: SET POINTS
energy utilization
VERSUS SETTLING POINTS ● Rothwell and Stock (1982) created a group of
○ One strength of set-point theories of eating is that obese rats by maintaining them on a cafeteria
they also explain body-weight regulation diet, and they found that the resting level of
energy expenditure in these obese rats was 45
SET-POINT ASSUMPTIONS ABOUT BODY percent greater than in control rats
WEIGHT AND EATING ● Initially, low- calorie diets produce substantial
● Calory-restricted weight loss. But the rate of weight loss
○ Hindi kumakain diminishes with each successive week on the
VARIABILITY OF BODY WEIGHT diet, until an equilibrium is achieved and little or
● Set-point theories of body-weight regulation no further weight loss occurs
suggest that the best method of maintaining a ● diet-induced thermogenesis- The mechanism
constant body weight is to eat each time there is by which the body adjusts the efficiency of its
a motivation to eat because, according to the energy utilization in response to its levels of body
theory, the main function of hunger is to defend fat
the set point ○ Increases in the levels of body fat produce
○ However, many people avoid obesity only by increases in body temperature, which require
resisting their urges to eat additional energy to maintain them—and
decreases in the level of body fat have the
opposite effects

SIY, CHANTELLE 1P4 12

● There are major differences among humans both ○ t in those cases in which both models make
in basal metabolic rate (the rate at which energy the same prediction, the settling-point model
is utilized to maintain bodily processes when does so more parsimoniously—that is, with a
resting) and in the ability to adjust the metabolic simpler mechanism that requires fewer
rate in response to changes in the levels of body assumptions
fat ● leaky-barrel analogy to see how the two models
● research on calorie-restricted diets suggests that account for four key facts of weight regulation
these people (people who remain slim even
though they eat a lot) may not eat with impunity:
There seems to be a health cost to pay for
overeating even in the absence of obesity

SET POINTS AND SETTLING POINTS IN

WEIGHT CONTROL
● According to the settling-point model, body
weight tends to drift around a natural settling
point—the level at which the various factors that
influence body weight achieve an equilibrium
○ The idea is that as body-fat levels increase,
changes occur that tend to limit further
increases until a balance is achieved
between all factors that encourage weight
gain and all those that discourage it
● The settling-point model provides a loose kind of
homeostatic regulation, without a set-point
mechanism or mechanisms to return body weight
to a set point
● According to the settling-point model, body
weight remains stable as long as there are no
long-term changes in the factors that influence it;
and if there are such changes, their impact is
limited by negative feedback
● In the settling-point model, the negative feedback
merely limits further changes in the same
direction, whereas in the set-point model,
negative feedback triggers a return to the set
point
● An analogy to think about the settling-point
mechanism
○ the amount of water entering the hose is
analogous to the amount of food available to
the subject
○ the water pressure at the nozzle is
analogous to the positive-incentive value of
the available food
○ the amount of water entering the barrel is
analogous to the amount of energy
consumed
○ the water level in the barrel is analogous to
the level of body fat
○ the amount of water leaking from the barrel
is analogous to the amount of energy being
expended
○ the weight of the barrel on the hose is
analogous to the strength of the satiety
signal
● The main advantage of the settling-point model of
body-weight regulation over the body-fat set-point
model
○ it is more consistent with the data

SIY, CHANTELLE 1P4 13

 ○ (For the next generation) how are they going
to handle the growing obesity-related health
problem

OBESITY: WHY IS THERE AN EPIDEMIC?

● Evolution
○ Inconsistent food supplies were one of the
main threats to survival
○ As a result, the fittest individuals were those
who preferred high-calorie foods, ate to
capacity when food was available, stored as
many excess calories as possible in the form
of body fat, and used their stores of calories
as efficiently as possible
○ Individuals who did not have these
characteristics were unlikely to survive a
food shortage or a harsh winter, and so
these characteristics were passed on to
future generations
● Cultural practices that promote consumption has
augmented the effects of evolution
○ it is commonly believed that one should eat
three meals per day at regular times,
● the leaky-barrel model suggests that it is possible whether one is hungry or not
to permanently change your body weight by ○ that food should be the focus of most social
permanently changing any of the factors that gatherings
influence energy intake or output ○ that meals should be served in courses of
progressively increasing palatability
○ and that salt, sweets (e.g., sugar), and fats
(e.g., butter or cream) should be added to
foods to improve their flavor and thus
increase their consumption
● Parents
○ tendency to make unhealthy food choices by
parents tends to be passed on to their
offspring

WHY DO SOME PEOPLE BECOME OBESE

WHILE OTHERS DO NOT?
● Why do some people become obese while others
living under the same obesity-promoting
conditions do not?
○ Those who are obese are those whose
energy intake has exceeded their energy
HUMAN OBESITY: CAUSES, MECHANISMS, output; those who are slim are those whose
AND TREATMENTS energy intake has not exceeded their energy
output
OBESITY: WHO NEEDS TO BE ● two kinds of individual differences play a role in
obesity:
CONCERNED?
○ those that lead to differences in energy input
● Concerns
○ those that lead to differences in energy
○ obese individuals who are metabolically
output
healthy run a greater risk of developing
● Food preferences
health problems
● Social factors
○ Obese women are at increased risk of
● Basal metabolism
having infants with health problems
● Differences in consumption and energy
○ many people who are slim as youths develop
● Genetics
serious weight problems as they age
● Differences in nonexercise activity thermogenesis

SIY, CHANTELLE 1P4 14

DIFFERENCES IN CONSUMPTION
● Many factors lead some people to eat more than
others who have comparable access to food
○ have strong preferences for the taste of
high-calorie foods
○ were raised in families and/or cultures that
promote excessive eating
○ have particularly large cephalic-phase
responses to the sight or smell of food

DIFFERENCES IN ENERGY EXPENDITURE

● With respect to energy output, people differ ● Most weight-loss programs are unsuccessful in
markedly from one another in the degree to the sense that, as predicted by the settling-point
which they can dissipate excess consumed model, most of the lost weight is regained once
energy. the dieter stops following the program and the
● The most obvious difference is that people differ original conditions are reestablished
substantially in the amount of exercise they get; ● .The key to permanent weight loss is a
however, there are others permanent lifestyle change
○ differences in basal metabolic rate ● Exercise has many health-promoting effects;
○ in the ability to react to fat increases by however, despite the general belief that exercise
diet-induced thermogenesis is the most effective method of losing weight,
○ NEAT, or nonexercise activity several studies have shown that it often
thermogenesis, which is generated by contributes little to weight loss
activities such as fidgeting and the ● One reason is that physical exercise normally
maintenance of posture and muscle tone accounts for only a small proportion of total
▪ plays a small role in dissipating excess energy expenditure: Most of the energy you
energy expend is used to maintain the resting
physiological processes of your body (e.g., body
DIFFERENCES IN GUT MICROBIOME temperature) and to digest your food
COMPOSITION ● Another reason is that our bodies are efficient
● Our gastrointestinal tract is replete with microbes, machines, burning only a small number of
such as bacteria, that help us digest the food we calories during a typical workout
eat—collectively known as our gut microbiome ● Moreover, after exercise, many people feel free
● these microbes are so numerous that they to consume extra drinks and foods that contain
outnumber our own bodily cells by 10 to 1 more calories than the relatively small number
● Influence of microbes to the brain that were expended during the exercise
○ they can influence neurodevelopment
○ the blood–brain barrier, LEPTIN AND THE REGULATION
○ myelination of certain CNS axons OF BODY FAT
● Fat is more than a passive storehouse of energy
GENETIC AND EPIGENETIC FACTORS ○ it actively releases a peptide hormone called
● many genes can influence body weight leptin
● about 100 human chromosome loci (regions) ● Leptin
have already been linked to obesity ○ Hormone produced by fat cells
● some of these genes seem to influence the ○ In animals decreases eating
likelihood of obesity by affecting one’s gut ○ In animals decreases body fat
microbiome ○ Correlated with subcutaneous fat
○ Receptors in arcuate nucleus
WHY ARE WEIGHT-LOSS PROGRAMS ○ In humans who have low levels,
OFTEN INEFFECTIVE? administration can maintain reasonable
weight
○ Pagtumataba ka sobra, nawawala ang leptin
○ Pagnawala, di ka na papayat
● Insulin
○ Positively correlated with body fat
○ Receptors found in the brain, arcuate
nucleus

SIY, CHANTELLE 1P4 15

 ○ Low doses reduce eating and body weight ● At first, the suggestion that insulin serves as a
● The following three subsections describe negative feedback signal for body fat regulation
○ the discovery of leptin was viewed with skepticism
○ how its discovery has fueled the ○ After all, how could the level of insulin in the
development of a new approach to the body, which goes up and then comes back
treatment of human obesity down to normal following each meal, provide
○ how the understanding that leptin and insulin the brain with information about gradually
are feedback signals led to the discovery of changing levels of body fat?
a hypothalamic nucleus that plays an ○ It turns out that insulin does not readily
important role in the regulation of body fat penetrate the blood–brain barrier, and its
levels in the brain were found to stay
OBESE MICE AND THE DISCOVERY OF relatively stable
LEPTIN ● following findings supported the hypothesis that
insulin serves as a negative feedback signal in
● In 1950, a spontaneous genetic mutation
the regulation of body fat:
occurred in the mouse colony being maintained
○ brain levels of insulin were found to be
in the Jackson Laboratory at Bar Harbor, Maine.
positively correlated with levels of body fat
○ The mutant mice were homozygous for the
○ Receptors for insulin were found in the brain
gene (ob), and they were grossly obese,
○ Infusions of insulin into the brains of
weighing up to three times as much as
laboratory animals were found to reduce
typical mice.
eating and body weight
○ These mutant mice are commonly referred to
● Why are there two fat feedback signals?
as ob/ ob mice
○ One reason may be that leptin levels are
▪ 1950s genetically obese mouse (can’t
more closely correlated with subcutaneous
produce leptin) ob/ob mouse
fat (fat stored under the skin), whereas
▪ Ob/ob mice eat more than control mice
insulin levels are more closely correlated
▪ they convert calories to fat more
with visceral fat (fat stored around the
efficiently
internal organs of the body cavity)
▪ they use their calories more efficiently
▪ Thus, each fat signal could provide
● Coleman (1979) hypothesized that ob/ob mice
different information. Visceral fat is more
lack a critical hormone that normally inhibits fat
common in males than females and
production and maintenance
poses the greater threat to health
● In 1994, Friedman and his colleagues
● The discovery that leptin and insulin are signals
characterized and cloned the gene that is
that provide information to the brain about fat
mutated in ob/ob mice
levels in the body provided a means for
○ They found that this gene is expressed only
discovering the neural circuits that participate in
in fat cells, and they characterized the
fat regulation.
protein it normally encodes, a peptide
● Receptors for both peptide hormones are located
hormone they named leptin
in many parts of the nervous system, but most
○ Because of their mutation, ob/ob mice lack
are in the hypothalamus, particularly in the
leptin.
arcuate nucleus.
○ This finding led to an exciting hypothesis:
● A closer look at the distribution of leptin and
Perhaps leptin is a negative feedback
insulin receptors in the arcuate nucleus indicated
signal normally released from fat stores to
that these receptors are not randomly distributed
decrease appetite and increase fat
throughout the nucleus.
metabolism
○ They are located in two classes of neurons:
▪ neurons that release neuropeptide y
LEPTIN, INSULIN, AND THE ARCUATE (the gut hunger peptide that you read
MELANOCORTIN SYSTEM about earlier in the chapter)
● There was great fanfare when leptin was ▪ neurons that release melanocortins, a
discovered class of peptides that includes the gut
● it was not the first peptide hormone to be satiety peptide α-melanocyte-stimulating
discovered that seems to function as a negative hormone (alpha-melanocyte-stimulating
feedback signal in the regulation of body fat hormone).
○ More than 30 years ago, Woods and ● Attention has been mostly focused on the
colleagues (1979) suggested that the melanocortin-releasing neurons in the arcuate
pancreatic peptide hormone insulin serves nucleus (often referred to as the melanocortin
such a function system) because injections of
α-melanocytestimulating hormone have been

SIY, CHANTELLE 1P4 16

 shown to suppress eating and promote weight ○ However, they were subsequently withdrawn
loss from the market because chronic use was
● It seems, however, that the melanocortin system found to be associated with heart disease in
is only a minor component of a much larger a small but significant number of users.
system: Elimination of leptin receptors in the ○ Currently, there is only one approved
melanocortin system produces only a slight serotonin agonist for the treatment of obesity
weight gain that has a more favorable side-effect profile:
lorcaserin
LEPTIN AS A TREATMENT FOR HUMAN ○ However, the efficacy of lorcaserin for the
OBESITY treatment of obesity is only modest
● The early studies of leptin seemed to confirm the
hypothesis that it could function as an effective GASTRIC SURGERY
treatment for obesity ● gastric bypass is a surgical treatment for
● Receptors for leptin were found in the brain, and extreme obesity that involves short-circuiting the
injecting it into ob/ob mice reduced both their normal path of food through the digestive tract so
eating and their body fat that its absorption is reduced
● All that remained was to prove leptin’s ○ The first gastric bypass was done in 1967,
effectiveness in human patients and it is currently the most commonly
● However, when research on leptin turned from prescribed surgical treatment for extreme
ob/ ob mice to obese humans, the program ran obesity
into two major snags
○ First, obese humans—unlike ob/ob
mice—were found to have high, rather than
low, levels of leptin
○ Second, injections of leptin did not reduce
either the eating or the body fat of obese
humans
○ In short, the actions of leptin are different in
humans and ob/ ob mice

TREATMENT OF OBESITY
● The following two subsections discuss two
treatments that are at different stages of
development: serotonergic agonists and gastric
surgery

SEROTONERGIC AGNOSIS ● An alternative is the adjustable gastric band

● serotonin agonists have been shown to reduce procedure, which involves surgically positioning
food consumption in both human and nonhuman a hollow silicone band around the stomach to
subjects reduce the flow of food through it; the
○ they have considerable potential in the circumference of the band can be adjusted by
treatment of obesity injecting saline into the band through a port that
● Serotonin agonists seem to act by a mechanism is implanted in the skin
different from that for leptin and insulin, which ○ One advantage of the gastric band over the
produce long-term satiety signals based on fat gastric bypass is that the band can readily
stores be removed
● Serotonin agonists seem to increase short-term ● A meta-analysis of studies comparing the two
satiety signals associated with the consumption procedures found both to be highly effective
of a meal ● In general, gastric bypass was found to be more
● Serotonin agonists have been found in various effective than the adjustable gastric band
studies of obese patients to reduce the following: procedure but was associated with more
the urge to eat high-calorie foods, the surgery-related complications
consumption of fat, the subjective intensity of ○ However, neither procedure is effective
hunger, the size of meals, the number of unless patients change their eating habits.
between-meal snacks, and bingeing
● Because of this extremely positive profile of ANOREXIA AND BULIMIA NERVOSA
effects and the severity of the obesity problem, ● two eating disorders of underconsumption:
serotonin agonists (fenfluramine and anorexia nervosa and bulimia nervosa.
dexfenfluramine) were rushed into clinical use.

SIY, CHANTELLE 1P4 17

 ANOREXIA AND BULIMIA NERVOSA controlling their appetites and thus enter into
a cycle of starvation, bingeing, and purging
ANOREXIA NERVOSA ● other similarities that support the view that
anorexia and bulimia are variants of the same
● anorexia nervosa is a disorder of
disorder
underconsumption
○ Individuals with anorexia or bulimia both tend
● Individuals with anorexia eat so little that they
to have distorted body images, seeing
experience health threatening weight loss, and
themselves as much fatter and less
despite their emaciated appearance, they often
attractive than they are in reality
perceive themselves as fat
○ In practice, many patients seem to straddle
● Anorexia nervosa is a serious condition: In
the two diagnoses and cannot readily be
approximately 4 percent of diagnosed cases,
assigned to one or the other categories, and
complications from starvation result in death, and
many patients flip-flop between the two
there is a high rate of suicide among persons
diagnoses as their circumstances change
with anorexia
○ Both anorexia and bulimia are highly
correlated with obsessive-compulsive
BULIMIA NERVOSA disorder and depression
● Bulimia nervosa is a disorder characterized by ● Anorexic’s complication
periods of not eating interrupted by bingeing ○ Reduced metabolism
(eating huge amounts of food in short periods of ○ Bradycardia
time) followed by efforts to immediately eliminate ○ Hypotension
the consumed calories from the body by ○ Hypothermia
voluntary purging (via vomiting or excessive use ○ anemia
of laxatives, enemas, or diuretics) or by extreme ● Bulimic’s compilation
exercise ○ Irritation and inflammation of the esophagus
● Related to guilt ○ Vitamin and mineral deficiencies
○ You let yourself eat the when you reach the ○ Electrolyte imbalance
lvl of satiety, you feel guilty which leads to ○ Dehydration
purging ○ Acid reflux
● Persons with bulimia may be obese or of normal ● Relationship between the two
weight ○ May be variants of same disorder
● binge-eating/ purging anorexia- underweight ○ Both have distorted body images
● Bulimia nervosa is a serious condition: The ○ Both are comorbid with
mortality rate for individuals with bulimia is about obsessive-compulsive disorder
4 percent. ○ Both are comorbid with depression
○ Patients can straddle the two diagnoses or
RELATION BETWEEN ANOREXIA AND flip flop between the two
BULIMIA ○ From bulimia to anorexia, bihira ang
● Different treatment for each disorder anorexia to bulimia, pwede rin ang nagstart
○ Anorexia- treatment for reduced metabolism, sa bulimia to anorexia to bulimia again
bradycardia (slow heart rate), hypotension
(low blood pressure), hypothermia (low body ANOREXIA AND POSITIVE INCENTIVES
temperature), and anemia (deficiency of red ● No pleasure or motivation to eat - anorexia
blood cells) ● The positive-incentive perspective on eating
○ Bulimia- treatment for irritation and suggests that the decline in eating that defines
inflammation of the esophagus, vitamin and both anorexia and bulimia is likely a
mineral deficiencies, electrolyte imbalance, consequence of a corresponding decline in the
dehydration, and acid reflux positive-incentive value of food
● Although anorexia and bulimia nervosa may ○ However, the positive-incentive value of food
seem like very different disorders from a for anorexia patients has received little
physician’s perspective, scientists often find it attention—in part, because anorexia patients
more appropriate to view them as variations of often display substantial interest in food. The
the same disorder fact that many anorexia patients are
○ According to this view, both anorexia and obsessed with food— continually talking
bulimia begin with an obsession about body about it, thinking about it, and preparing it for
image and slimness and extreme efforts to others—seems to suggest that food still
lose weight holds a high positive-incentive value for them
○ Persons with anorexia or bulimia both ○ However, to avoid confusion, it is necessary
attempt to lose weight by strict dieting, but to keep in mind that the positive- incentive
those with bulimia are less capable of value of interacting with food is not

SIY, CHANTELLE 1P4 18

 necessarily the same as the ● So why do individuals with severe anorexia not
positive-incentive value of eating food—and experience a massive increase in the
it is the positive-incentive value of eating positive-incentive value of eating, similar to the
food that is critical when considering increase experienced by other starving
anorexia nervosa individuals?
● studies have found that the positive-incentive ○ The answer may be meals. Meals consumed
value of various tastes is lower in anorexia by a person with anorexia may produce a
patients than in controls variety of conditioned taste aversions that
○ However, these studies grossly reduce the motivation to eat.
underestimate the importance of reductions ○ This hypothesis needs to be addressed
in the positive-incentive value of food in the because of its implication for treatment:
etiology of anorexia nervosa, because the Patients with anorexia—or anybody else who
participants with anorexia have been is severely undernourished—should not be
compared to normal-weight control encouraged, or even permitted, to eat meals
participants ○ They should be fed—or infused with—small
● We can get some insight into the effects of amounts of food intermittently throughout the
anorexia nervosa on the positive-incentive value day
of food only by comparing individuals with ● Hypothesis:
anorexia to starving people of the same weight. ○ Anorexia is related to conditioned taste
Consider the behavior of volunteers undergoing aversion
semistarvation and compare it to people with ○ At the beginning of meals, homeostatic
anorexia. When asked how it felt to starve, one balance is disrupted by an infusion of
starving volunteer replied: calories
○ In people who eat little, the aversive effects
are greater
○ Supported by starving concentration camp
victims finding eating noxious
○ Meals consumed by anorexics produce taste
aversion
ANOREXIA NERVOSA: A HYPOTHESIS ○ Potentially treatment is small amounts of
● Why does the adaptive massive increase in the food intermittently
positive-incentive value of eating that occurs in
victims of starvation not occur in persons starving
due to anorexia?
○ Under conditions of starvation, the
positive-incentive value of eating normally
increases to such high levels that it is difficult
to imagine how anybody who was
starving—no matter how controlled, rigid,
obsessive, and motivated that person
was—could refrain from eating in the
presence of palatable food
○ Why this protective mechanism is not
activated in severe anorexia is a pressing
question about the etiology of anorexia
nervosa.
● research of Woods and his colleagues on the
aversive physiological effects of meals
○ At the beginning of meals, people are
normally in reasonably homeostatic balance,
and this homeostasis is disrupted by the
sudden infusion of calories.
● The other part of the answer lies in the finding
that the aversive effects of meals are much
greater in people who have been eating little
● Meals, which produce adverse, but tolerable,
effects in healthy individuals, may be extremely
aversive for individuals who have undergone food
deprivation

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The Case of the Student with Anorexia

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