PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY

LESSON 14. Ingestive Behavior

PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
Ingestive behaviors encompass all eating and drinking behaviors. These actions are
influenced by physiological regulatory mechanisms; these mechanisms exist to
control and establish homeostasis within the human body. Disruptions in these
ingestive regulatory mechanisms can result in eating disorders such as obesity,
anorexia, and bulimia.

Homeostasis and Allostasis

Physiologist Walter B. Cannon (1929) introduced the term homeostasis to refer to

temperature regulation and other biological processes that keep body variables
within a fixed range. Homeostatic processes in animals trigger physiological and
behavioral activities that keep certain variables within a set range. In many cases,
the range is so narrow that we refer to it as a set point, a single value that the
body works to maintain. Processes that reduce discrepancies from the set point are
known as negative feedback. Much of motivated behavior can be described as
negative feedback: Something causes a disturbance, and behavior proceeds until it
relieves the disturbance.

However, the concept of homeostasis is not fully satisfactory, because the body
does not maintain complete constancy. For example, your body temperature is
about half a Celsius degree higher in mid-afternoon than in the middle of the
night.
We can describe these alterations as changes in the set point, but even changes in
the set point don’t fully account for many observations. Much of our behavior
anticipates a need before it occurs.

To describe these dynamic changes, researchers use the term allostasis (from the
Greek roots meaning “variable” and “standing”), which means the adaptive way in
which the body anticipates needs depending on the situation, avoiding errors
rather than just correcting them (McEwen, 2000; Sterling, 2012).

Drinking
Mechanisms of Water Regulation

Humans vary their strategy depending on circumstances. If an individual cannot

find enough to drink or if the water tastes bad, he/she conserve water by
excreting more concentrated urine and decreasing your sweat, somewhat like a
gerbil, although not to the same extreme. Your posterior pituitary releases the
hormone vasopressin that raises blood pressure by constricting blood vessels.
Vasopressin is also known as antidiuretic hormone (ADH) because it enables the
kidneys to reabsorb water from urine and therefore make the urine more
concentrated. (Diuresis means “urination.”)

Two Types of Thirst

 Osmotic Thirst
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
Eating salty foods causes osmotic thirst, and losing fluid by bleeding or sweating
induces hypovolemic thirst.

Osmotic pressure is the tendency of water to flow across a semipermeable

membrane from the area of low solute concentration to the area of higher
concentration. The membrane surrounding a cell is almost a semipermeable
membrane because water flows across it freely and various solutes flow either
slowly or not at all between the intracellular fluid inside the cell and the
extracellular fluid outside it. Osmotic pressure occurs when solutes are more
concentrated on one side of the membrane than on the other.

If you eat something salty, sodium ions spread through the blood and the
extracellular fluid but do not cross the membranes into cells. The result is a higher
concentration of solutes (including sodium) outside the cells than inside. The
resulting osmotic pressure draws water from the cells into the extracellular fluid.
Certain neurons detect their own loss of water and then trigger osmotic thirst, a
drive for water that helps restore the normal state.

a.) Greater concentration of b.) Water ows out of the

solutes (green dots) outside cell, equalizing the solute
the cell than inside. concentration and shrinking
the cell.

How does the brain detect osmotic pressure? It has receptors around the third
ventricle, including the OVLT (organum vasculosum laminae terminalis) and the
subfornical organ (SFO) (Hiyama, Watanabe,Okado, & Noda,2004)

Those receptors detect osmotic pressure and

the sodium content of the blood (Tiruneh,
Huang, & Leenen, 2013). The OVLT also
receives input from receptors in the digestive
tract, enabling it to anticipate an osmotic
need before the rest of the body experiences
it (Bourque, 2008).

The subfornical organ has one population of

neurons that increases thirst and another
population that suppresses it (Abbott,
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
Machado, Geerling, & Saper, 2016; Oka, Ye, & Zuker, 2015). Those axons combine
with input from the OVLT, the stomach, and elsewhere to provide input to the
hypothalamus. The lateral preoptic area and surrounding parts of the
hypothalamus control drinking (Saad, Luiz, Camargo, Renzi, & Manani, 1996). The
supraoptic nucleus and the paraventricular nucleus (PVN) control the rate at
which the posterior pituitary releases vasopressin.

 Hypovolemic Thirst and Sodium Specific Hunger

Receptors in your kidneys and on your blood vessels react to the decreased blood
pressure by sending messages to the brain to release vasopressin, which constricts
blood vessels and conserves the fluid you still have. Also, the kidneys release the
enzyme renin, which splits a portion off angiotensinogen, a large protein in the
blood, to form angiotensin I, which other enzymes convert to angiotensin II. Like
vasopressin, angiotensin II constricts the blood vessels, compensating for the drop
in blood pressure

Angiotensin II also helps trigger thirst, in conjunction with receptors that detect
blood pressure in the large veins. However, this thirst is different from osmotic
thirst, because you need to restore lost salts and not just water. This kind of thirst
is known as hypovolemic (HI-po-vo-LEE-mik) thirst, meaning thirst based on low
volume. When angiotensin II reaches the brain, it stimulates neurons in areas
adjoining the third ventricle (Fitts, Starbuck, & Ruhf, 2000; Mangiapane &
Simpson, 1980; Tanaka et al., 2001). Those neurons send axons to the
hypothalamus, where they release angiotensin II as their neurotransmitter
(Tanaka, Hori, & Nomura, 2001). The connection between a neurotransmitter and
its function is not arbitrary. The brain uses a chemical that was already performing
a related function elsewhere in the body.

An animal that becomes deficient in sodium shows an immediate strong preference

for salty tastes, known as sodium-specific hunger (Richter, 1936), even for
extremely concentrated salt solutions that it would ordinarily reject (Robinson &
Berridge, 2013). Neurons in several brain areas suddenly react much more strongly
than usual to salty tastes (Tandon, Simon, & Nicolelis, 2012).

Sodium-specific hunger depends partly on hormones (Schulkin, 1991). When the

body’s sodium reserves are low, the
adrenal glands produce aldosterone, a
hormone that causes the kidneys, salivary
glands, and sweat glands to retain salt
(Verrey & Beron, 1996). Aldosterone and
angiotensin II together change the
properties of taste receptors on the
tongue, neurons in the nucleus of the
tractus solitarius (part of the taste
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
system), and neurons elsewhere in the brain to increase salt intake (Krause &
Sakal, 2007).
Hunger/Eating
Digestion and Food Selection

Consumption of Dairy Products

Most mammals at about the age of weaning
lose the intestinal enzyme lactase, which is
necessary for metabolizing lactose, the sugar
in milk. Adult mammals can drink a little
milk, but consuming too much causes
stomach. The declining level of lactase may
be an evolved mechanism to encourage
weaning at the appropriate time.

Humans are a partial exception to this rule.

Many adults have enough lactase levels to
consume milk and other dairy products
throughout life. However, the prevalence of
the necessary genes varies. Nearly all the
adults in China and surrounding countries are
unable to metabolize lactose, as do varying
numbers of people in other parts of the world
(Curry, 2013; Flatz, 1987; Rozin & Pelchat,
1988). People who are lactose intolerant can
consume a little milk, and larger amounts of
cheese and yogurt, which are easier to digest, but they generally learn to limit
their intake.

Food Selection and Consumption

The belief that sugar causes hyperactivity is apparently an illusion based on

people’s tendency to see what they expect to see.

Another common misconception is that eating turkey causes sleepiness, supposedly

because eating turkey increases the supply of tryptophan, which enables the brain
to make serotonin and melatonin. However, turkey has only an average amount of
tryptophan.

Nevertheless, it is true that tryptophan helps the brain produce melatonin, which
aids sleepiness. Other than taking tryptophan pills, the most reliable way to
increase tryptophan in the brain is to eat a diet high in carbohydrates. Tryptophan
enters the brain by an active-transport protein that it shares with phenylalanine
and other large amino acids. When you eat carbohydrates, your body reacts by
increasing secretion of insulin, which moves sugars into storage, and also moves
phenylalanine into storage (in liver cells and elsewhere). By reducing the
competition from phenylalanine, this process makes it easier for tryptophan to
reach the brain, inducing sleepiness (Silber & Schmitt, 2010).
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY

Eating: What is Metabolism?

The Short-term Reservoir

The short-term reservoir sustains our fuel needs for several hours between meals.
It is located in the cells of the liver and the muscles, and it is filled with a
complex, insoluble carbohydrate called glycogen. Cells in the liver convert glucose
(a simple, soluble carbohydrate) into glycogen and store it. They are prompted to
do so by the presence of insulin, a peptide hormone generated by the pancreas.
When glucose and insulin are present in the blood, some of the glucose is used as
fuel and some is stored as glycogen. When all of the food has been absorbed from
the digestive tract, the level of glucose in the blood begins to fall.

The fall in glucose is detected by cells in the pancreas and in the brain. The
pancreas responds by stopping its secretion of insulin and starting to secrete a
different peptide hormone: glucagon. The liver soaks up excess glucose and stores
it as glycogen when plenty of glucose is available, and it releases glucose from its
reservoir when the digestive tract becomes empty and the level of glucose in the
blood begins to fall.
The carbohydrate reservoir in the
liver is reserved primarily for the
central nervous system (CNS).

The Long-term Reservoir

Our long-term reservoir consists of adipose tissue (fat tissue). This reservoir is
filled with fats or, more precisely, with triglycerides.Triglycerides are complex
molecules that contain glycerol (a soluble carbohydrate, also called glycerine)
combined with three fatty acids (stearic acid, oleic acid, and palmitic acid).

The long-term fat reservoir is what keeps us alive when we are fasting. As we
begin to use the contents of our short-term carbohydrate reservoir, fat cells start
converting triglycerides into fuels that the cells can use and releasing these fuels
into the bloodstream.

When the digestive system is empty, there is an increase in the activity of the
sympathetic axons that innervate adipose tissue, the pancreas, and the adrenal
medulla. All three effects (direct neural stimulation, secretion of glucagon, and
secretion of catecholamines) cause triglycerides in the long-term fat reservoir to
be broken down into glycerol and fatty acids. The fatty acids can be directly
metabolized by cells in all of the body except the brain, which needs glucose. That
leaves glycerol. The liver takes up glycerol and converts it to glucose. That
glucose, too, is available to the brain.
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
Insulin has several other functions besides causing glucose to be converted to
glycogen. One of these functions is controlling the entry of glucose into cells.
Glucose easily dissolves in water, but it will not dissolve in fats.
To be taken into a cell, glucose must be transported there by glucose transporters
—protein molecules that are situated in the membrane and are similar to those
responsible for the reuptake of transmitter substances. Glucose transporters
contain insulin receptors, which control their activity; only when insulin binds with
these receptors can glucose be transported into the cell.

Fasting Phase

Physiologists refer to the metabolism that takes place while the digestive tract is
empty as fasting phase of metabolism.

A fall in blood glucose level causes the pancreas to stop secreting insulin and to
start secreting glucagon. The absence of insulin means that most of the cells of the
body can no longer use glucose. The presence of glucagon and the absence of
insulin instruct the liver to start drawing on the short-term carbohydrate reservoir
—to start converting its glycogen into glucose. The presence of glucagon and the
absence of insulin, along with increased activity of the sympathetic nervous
system, also instruct fat cells to start drawing on the long-term fat reservoir—to
start breaking down triglycerides into fatty acids and glycerol.

Absorptive Phase

The phase of metabolism that occurs when food is present in the digestive tract is
called the absorptive phase.

Suppose that we eat a balanced meal of carbohydrates, proteins, and fats. The
carbohydrates are broken down into glucose, and the proteins are broken down
into amino acids. The fats basically remain as fats. Let us consider each of these
three nutrients:
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
(1) Glucose: As we start absorbing the nutrients, the level of glucose in the blood
rises. This rise is detected by cells in the brain, which causes the activity of the
sympathetic nervous system to decrease and the activity of the parasympathetic
nervous system to increase. This change tells the pancreas to stop secreting
glucagon and to begin secreting insulin. The insulin permits all the cells of the
body to use glucose as a fuel. Extra glucose is converted into glycogen, which fills
the short-term carbohydrate reservoir. If some glucose is left over, it is converted
into fat and absorbed by fat cells.
(2) Amino acids: A small proportion of the amino acids received from the digestive
tract are used as building blocks to construct proteins and peptides; the rest are
converted to fats and stored in adipose tissue.
(3) Fat: Fat is not used as a fuel at this time; it is simply stored in adipose tissue.

Eating: Signals to Start a Meal

Signals from the Digestive System

An empty stomach and upper

intestine provide an important
endocrine signal to the brain that it is
time to start thinking about finding
something to eat. A peptide hormone
called ghrelin is released from the
gastrointestinal system when
individuals are in the fasting phase
and the digestive system is empty
(Kojima et al., 1999). Ghrelin then binds to receptors in the hypothalamus
to help stimulate eating behavior.

Blood levels of ghrelin increase

with fasting and are reduced after
a meal. Blocking the ghrelin signal
inhibits eating and increasing
ghrelin can cause weight gain by
increasing food intake and
decreasing the metabolism of fats.
Blood levels of ghrelin increase
shortly before each meal, which
suggests that this peptide is
involved in the initiation of a meal
(Cummings, 2006).

Ghrelin is a potent stimulator of

food intake, and it even stimulates
thoughts about food. Schmid et al.,
(2005) found that a single
intravenous injection of ghrelin not
only enhanced appetite in typical
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
participants; it also elicited vivid images of foods that the participants liked to
eat.

Metabolic Signals

GLUCOSE AND LIPIDS

A fall in blood glucose level (a condition known as hypoglycemia) is a potent
stimulus for hunger. When (nonradioactive) 2-DG is given in large doses, it
interferes with glucose metabolism by competing with glucose for access to the
mechanism that transports glucose through the cell membrane and for access to
the enzymes that metabolize glucose. Both hypoglycemia and 2-DG cause
glucoprivation;that is, they deprive cells of glucose. And glucoprivation, whatever
its cause, stimulates eating.

Hunger can also be produced by causing lipoprivation—depriving cells of lipids.

More precisely, they are deprived of the ability to metabolize fatty acids through
injection of a drug such as mercaptoacetate.

DETECTORS
Two sets of detectors:
(1) The detectors in the brain monitor the nutrients that are available on their
side of the blood–brain barrier, and
(2) the detectors in the liver monitor the nutrients that are available to the
rest of the body.

Liver Detectors
A study by Novin et al.,
(1973) suggested that
receptors in the liver can
stimulate glucoprivic hunger.
The investigators infused 2-
DG into a vein to the liver.
The infusions of 2-DG caused
immediate eating.

Lipoprivic hunger
appears to be
stimulated by receptors
in the liver as well.
Ritter and Taylor (1990)
induced lipoprivic
hunger and found that
cutting the vagus nerve
abolished this hunger.
Thus, the liver appears
to contain receptors
that detect low
availability of glucose
or fatty acids
(glucoprivation or lipoprivation) and send this information to the brain
through the vagus nerve (Friedman et al., 2005).

Brain Detectors
PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY
Because the brain can use only glucose, it would make sense that these detectors
respond to glucoprivation—and,
indeed, they do. Ritter et al., (2000) found that injections of a drug that produces
glucoprivation into two regions of the hindbrain—the dorsomedial and
ventrolateral medulla— induced eating.

The brain contains detectors that monitor the availability of glucose (its only fuel)
inside the blood– brain barrier, and the liver contains detectors the monitor the
availability of nutrients (glucose and fatty acids) outside the blood–brain barrier.

End of Lesson 14 Handout Part 1

PSYC103 BIOLOGICAL/PHYSIOLOGICAL PSYCHOLOGY