THE COURSE OF DEPRESSION:
THEORIES AND THERAPIES OF UNIPOLAR DEPRESSION
THEORIES AND THERAPIES OF UNIPOLAR DEPRESSION
THE COURSE OF DEPRESSION
When a vulnerable individual becomes depressed, what is likely to happen if
the individual fails to seek out treatment? If anything good about depression
can be said, it is that it usually dissipates in time. After the initial attack,
which comes on suddenly about three-quarters of the time, depression
seems to last an average of about three months in outpatients. Among inpatients,
who are usually more severely depressed, it lasts about six months on
the average. At first, the depression gets progressively worse, eventually
reaching the bottom, but then the depressed individual begins to recover
gradually to the state that existed before the onset (Beck, 1967; Robins and
Guze, 1972). What our grandmothers told us about our own personal tragedies-
time heals all wounds-is certainly true for depression. The mind,
or the body, seems incapable of sustaining a dark mood forever, and unknown
homeostatic mechanisms take over and, in time, correct the disorder.
The time that a depressive episode lasts, however, is painfully long, and to
an individual suffering from it, it seems like forever. For this reason, a therapist
will always emphasize that the depressive episode will go away in time.
Without minimizing the suffering the patient is feeling now, the therapist
should tell the patient that complete recovery from the episode occurs in 70
to 95 percent of the cases. For some, this ray of hope may speed the time
when the depression will lift.
Once a depressive episode has occurred, one of three patterns may develop.
The first is recovery without recurrence. About half the patients who
have had a depressive episode will not have another one, at least during the
following ten years. Generally, the more stable a person is before the episode,
the less likely depression will recur. On the other hand, half of depressed
individuals will show the second pattern: recovery with recurrence. The second depressive
episode, if it occurs, will tend to be of about the same
duration as the first attack. On the average, however, most individuals who
have recurrent episodes of depression can expect an average symptom-free
interval of more than three years before the next episode, and the interval
between episodes in recurrent depression tends to become shorter over the
years. For some individuals, the third pattern will develop: chronic depression.
Roughly 10 percent of those individuals who have a major depressive
episode will not recover and will remain chronically depressed (Perris, 1968;
Kerr, Roth, Schapira, and Gurney, 1972; Schuyler, 1974). Therapy for depression usually
attempts to make the current episode shorter or to postpone
the time at which another episode might strike. The therapies for
depression derive from four different theories, and it is to these theories and
therapies we now turn.
THEORIES AND THERAPIES OF UNIPOLAR DEPRESSION
What causes depression, and how is depression most effectively treated? In
the last fifteen years, we have moved out of the dark ages in our understanding
of depression. Substantial strides have been made in the understanding
and treatment of the disorder. Between 80 and 90 percent of severe
depressions can now be markedly alleviated with a brief course of therapy.
Although several theories, with substantial research support, have emerged
to explain the origins of depression, we still cannot say with certainty what
the cause of depression is or how it can best be treated. We can, however,
make highly educated guesses. There are four main theories and therapies
for depression: the biological model, the psychodynamic model, the behavioral
model, and the cognitive model. These theories overlap, and there is
also a good deal of overlap in the therapies each recommends, but each
tends to focus on one aspect of depression. At the end of this section, we will
attempt a synthesis of these models.
THE BIOLOGICAL MODEL OF DEPRESSION
According to the biological model, depression is a disorder of the body.
While in principle, depression could be caused by a problem in any bodily
organ-the liver, the blood, the stomach-speculation has centered almost
entirely on the brain, and in particular on depletion of those substances
(biogenic amines) that help transmit nerve implulses across the gaps (synapses)
between nerve cells (neurons). There are four clues that the body is
intimately involved in depression (Schuyler, 1974). First of all, depression
occurs with some frequency following periods of natural physiological
change in women: after giving birth to a child, at menopause, and just before
menstruation. Second, there is considerable similarity of symptoms across
cultures, sexes, ages, and races, indicating an underlying biological process.
Third, somatic therapies, in particular drugs like tricyclic antidepressants
and MAO inhibitors, and electroconvulsive shock, are effective treatments
of depression. Fourth, depression is occasionally induced in normal individuals
as a side effect of medications; in particular depression may be induced
by reserpine, a high-blood-pressure reducing drug (Schuyler, 1974). These
clues have fueled the search for a biological basis of depression.
The Neurochemical Basis of Depression
The biological model holds that depression is a disorder of motivation
caused by insufficiencies of the biogenic amines. The biogenic amines are
neurochemicals that facilitate neural transmission. They divide into two
groups with different chemical structures: the catecholamines, which include
norepinephrine, epinephrine, and dopamine; and the indaleamines,
which include serotonin and histamine.
The biogenic amines play significant roles in neural transmission in the
medial forebrain bundle (MFB) and the periventricular system (PVS). The
MFB and PVS are two major pathways that run through lower centers of the
brain. Research with animals indicates that the MFB and PVS may be the
neuroanatomical basis of reward and punishment respectively (Stein,
1968). Electrical stimulation of the MFB is highly reinforcing to rats, and
electrical stimulation of the periventricular system is very punishing. The
MFB may function as a "go" system that facilitates active behavior, whereas
the PVS may act as a "stop" system. When the biogenic amines are depleted,
the functioning of these systems is reduced and depression, with its
loss of motivation, may ensue. Speculation about the neurochemical basis
of depression has centered primarily around decreased availability of one of
the catecholamines, norepinephrine (NE) (Schildkraut, 1965).
The hypothesized mode of action of norepinephrine in
transmission of a nerve impulse from one neuron
across the synapse to a second neuron in the brain.
When a nerve impulse occurs in neuron l,
norepinephrines discharged into the synapse (the gap between neuron land
neuron 2). This stimulates neuron 2 to fire when the NE makes contact with
the receptors on the membrane of neuron 2. Norepinephrine is now sitting
in the synapse and on the membrane of neuron 2. Neuron 2 will continue to
fire until the NE is inactivated. There are two relevant ways that norepinephrine
can now be inactivated. The first way is by reuptake, in which
neuron 1 reabsorbs norepinephrine, thereby decreasing the amount of norepinephrine at the
receptors. The second is by breakdown. This is facilitated
by the enzyme, monoamine oxidase (MAO), among others. This enzyme
breaks down the norepinephrine chemically and renders it inactive. As we
said above, norepinephrine is a catecholamine, which is one of two classes of
biogenic amines. The biogenic amines affect our motivation. And when we
decrease the amount of biogenic amines (in this case, norepinephrine), we
will have less motivation. The catecholamine hypothesis claims that when
reuptake and/or breakdown are doing their job too well, our norepinephrine
level drops too low, and we become highly unmotivated, in short, depressed.
Two groups of drugs are used to treat depression: tricyclic antidepressants
and MAO inhibitors. Each affects the availability of NE in the brain. It was a
serendipitous finding that led to their use as antidepressants. Individuals
with tuberculosis, who are frequently depressed, were tested with a new
drug, iproniazid. It turned out that the drug didn't help cure their tuberculosis,
but it did produce a much brighter mood in the patients, and they became
less depressed. Why did this happen? The drug, iproniazid, is an MAO
inhibitor. As we have seen, the enzyme MAO facilitates breakdown, thereby
making less norepinephrine available for neural transmission. So this drug,
iproniazid, inhibited the enzyme MAO in the patients with tuberculosis,
and in part prevented breakdown of NE. The catecholamine hypothesis
claims that, as a result, more norepinephrine was available, and with more
NE available, the tuberculosis patients became less depressed. Since then,
MAO inhibitors have been successfully used in treating depression, thereby
rendering support for the biological model, specifically the catecholamine
hypothesis.
Also discovered by accident, the tricyclic antidepressants affect the availability
of NE. These drugs block the process of reuptake. As we saw above,
reuptake occurs when the neuron that released NE absorbs it back. If reuptake
is blocked, then less NE is absorbed, and more will be available. As a
result of more NE, the patient will become less depressed. This provides further
evidence for the catecholamine hypothesis.
Further evidence for this hypothesis has come from reserpine-induced
depression. Reserpine is a powerful sedative given to high blood pressure patients.
Physicians discovered that it produces an unwanted side effect, depression
with suicidal tendencies, in about 15 percent of the people who
take it. It turns out that reserpine, among other actions, depletes norepinephrine.
With less NE, these high blood pressure patients became depressed.
Despite the favorable evidence supporting the catecholamine hypothesis
based on the action of these drugs, advocates of the hypothesis are appropriately cautious. The reason is that reserpine, the tricyclics, and the MAO inhibitors all have a large number of effects other than their effect on norepinephrine. Because of this, it is very possible that their effects might be due to some other properties of the drugs and not necessarily to their effect on norepinephrine.
Depression and Suicide
Post-Traumatic Stress Disorder (PTSD)
Social Anxiety
Generalized Anxiety
Panic Disorder
Major Depression Disorder
Agoraphobia
For the Therapy I recommend click here:
The Liberator Method
When a vulnerable individual becomes depressed, what is likely to happen if
the individual fails to seek out treatment? If anything good about depression
can be said, it is that it usually dissipates in time. After the initial attack,
which comes on suddenly about three-quarters of the time, depression
seems to last an average of about three months in outpatients. Among inpatients,
who are usually more severely depressed, it lasts about six months on
the average. At first, the depression gets progressively worse, eventually
reaching the bottom, but then the depressed individual begins to recover
gradually to the state that existed before the onset (Beck, 1967; Robins and
Guze, 1972). What our grandmothers told us about our own personal tragedies-
time heals all wounds-is certainly true for depression. The mind,
or the body, seems incapable of sustaining a dark mood forever, and unknown
homeostatic mechanisms take over and, in time, correct the disorder.
The time that a depressive episode lasts, however, is painfully long, and to
an individual suffering from it, it seems like forever. For this reason, a therapist
will always emphasize that the depressive episode will go away in time.
Without minimizing the suffering the patient is feeling now, the therapist
should tell the patient that complete recovery from the episode occurs in 70
to 95 percent of the cases. For some, this ray of hope may speed the time
when the depression will lift.
Once a depressive episode has occurred, one of three patterns may develop.
The first is recovery without recurrence. About half the patients who
have had a depressive episode will not have another one, at least during the
following ten years. Generally, the more stable a person is before the episode,
the less likely depression will recur. On the other hand, half of depressed
individuals will show the second pattern: recovery with recurrence. The second depressive
episode, if it occurs, will tend to be of about the same
duration as the first attack. On the average, however, most individuals who
have recurrent episodes of depression can expect an average symptom-free
interval of more than three years before the next episode, and the interval
between episodes in recurrent depression tends to become shorter over the
years. For some individuals, the third pattern will develop: chronic depression.
Roughly 10 percent of those individuals who have a major depressive
episode will not recover and will remain chronically depressed (Perris, 1968;
Kerr, Roth, Schapira, and Gurney, 1972; Schuyler, 1974). Therapy for depression usually
attempts to make the current episode shorter or to postpone
the time at which another episode might strike. The therapies for
depression derive from four different theories, and it is to these theories and
therapies we now turn.
THEORIES AND THERAPIES OF UNIPOLAR DEPRESSION
What causes depression, and how is depression most effectively treated? In
the last fifteen years, we have moved out of the dark ages in our understanding
of depression. Substantial strides have been made in the understanding
and treatment of the disorder. Between 80 and 90 percent of severe
depressions can now be markedly alleviated with a brief course of therapy.
Although several theories, with substantial research support, have emerged
to explain the origins of depression, we still cannot say with certainty what
the cause of depression is or how it can best be treated. We can, however,
make highly educated guesses. There are four main theories and therapies
for depression: the biological model, the psychodynamic model, the behavioral
model, and the cognitive model. These theories overlap, and there is
also a good deal of overlap in the therapies each recommends, but each
tends to focus on one aspect of depression. At the end of this section, we will
attempt a synthesis of these models.
THE BIOLOGICAL MODEL OF DEPRESSION
According to the biological model, depression is a disorder of the body.
While in principle, depression could be caused by a problem in any bodily
organ-the liver, the blood, the stomach-speculation has centered almost
entirely on the brain, and in particular on depletion of those substances
(biogenic amines) that help transmit nerve implulses across the gaps (synapses)
between nerve cells (neurons). There are four clues that the body is
intimately involved in depression (Schuyler, 1974). First of all, depression
occurs with some frequency following periods of natural physiological
change in women: after giving birth to a child, at menopause, and just before
menstruation. Second, there is considerable similarity of symptoms across
cultures, sexes, ages, and races, indicating an underlying biological process.
Third, somatic therapies, in particular drugs like tricyclic antidepressants
and MAO inhibitors, and electroconvulsive shock, are effective treatments
of depression. Fourth, depression is occasionally induced in normal individuals
as a side effect of medications; in particular depression may be induced
by reserpine, a high-blood-pressure reducing drug (Schuyler, 1974). These
clues have fueled the search for a biological basis of depression.
The Neurochemical Basis of Depression
The biological model holds that depression is a disorder of motivation
caused by insufficiencies of the biogenic amines. The biogenic amines are
neurochemicals that facilitate neural transmission. They divide into two
groups with different chemical structures: the catecholamines, which include
norepinephrine, epinephrine, and dopamine; and the indaleamines,
which include serotonin and histamine.
The biogenic amines play significant roles in neural transmission in the
medial forebrain bundle (MFB) and the periventricular system (PVS). The
MFB and PVS are two major pathways that run through lower centers of the
brain. Research with animals indicates that the MFB and PVS may be the
neuroanatomical basis of reward and punishment respectively (Stein,
1968). Electrical stimulation of the MFB is highly reinforcing to rats, and
electrical stimulation of the periventricular system is very punishing. The
MFB may function as a "go" system that facilitates active behavior, whereas
the PVS may act as a "stop" system. When the biogenic amines are depleted,
the functioning of these systems is reduced and depression, with its
loss of motivation, may ensue. Speculation about the neurochemical basis
of depression has centered primarily around decreased availability of one of
the catecholamines, norepinephrine (NE) (Schildkraut, 1965).
The hypothesized mode of action of norepinephrine in
transmission of a nerve impulse from one neuron
across the synapse to a second neuron in the brain.
When a nerve impulse occurs in neuron l,
norepinephrines discharged into the synapse (the gap between neuron land
neuron 2). This stimulates neuron 2 to fire when the NE makes contact with
the receptors on the membrane of neuron 2. Norepinephrine is now sitting
in the synapse and on the membrane of neuron 2. Neuron 2 will continue to
fire until the NE is inactivated. There are two relevant ways that norepinephrine
can now be inactivated. The first way is by reuptake, in which
neuron 1 reabsorbs norepinephrine, thereby decreasing the amount of norepinephrine at the
receptors. The second is by breakdown. This is facilitated
by the enzyme, monoamine oxidase (MAO), among others. This enzyme
breaks down the norepinephrine chemically and renders it inactive. As we
said above, norepinephrine is a catecholamine, which is one of two classes of
biogenic amines. The biogenic amines affect our motivation. And when we
decrease the amount of biogenic amines (in this case, norepinephrine), we
will have less motivation. The catecholamine hypothesis claims that when
reuptake and/or breakdown are doing their job too well, our norepinephrine
level drops too low, and we become highly unmotivated, in short, depressed.
Two groups of drugs are used to treat depression: tricyclic antidepressants
and MAO inhibitors. Each affects the availability of NE in the brain. It was a
serendipitous finding that led to their use as antidepressants. Individuals
with tuberculosis, who are frequently depressed, were tested with a new
drug, iproniazid. It turned out that the drug didn't help cure their tuberculosis,
but it did produce a much brighter mood in the patients, and they became
less depressed. Why did this happen? The drug, iproniazid, is an MAO
inhibitor. As we have seen, the enzyme MAO facilitates breakdown, thereby
making less norepinephrine available for neural transmission. So this drug,
iproniazid, inhibited the enzyme MAO in the patients with tuberculosis,
and in part prevented breakdown of NE. The catecholamine hypothesis
claims that, as a result, more norepinephrine was available, and with more
NE available, the tuberculosis patients became less depressed. Since then,
MAO inhibitors have been successfully used in treating depression, thereby
rendering support for the biological model, specifically the catecholamine
hypothesis.
Also discovered by accident, the tricyclic antidepressants affect the availability
of NE. These drugs block the process of reuptake. As we saw above,
reuptake occurs when the neuron that released NE absorbs it back. If reuptake
is blocked, then less NE is absorbed, and more will be available. As a
result of more NE, the patient will become less depressed. This provides further
evidence for the catecholamine hypothesis.
Further evidence for this hypothesis has come from reserpine-induced
depression. Reserpine is a powerful sedative given to high blood pressure patients.
Physicians discovered that it produces an unwanted side effect, depression
with suicidal tendencies, in about 15 percent of the people who
take it. It turns out that reserpine, among other actions, depletes norepinephrine.
With less NE, these high blood pressure patients became depressed.
Despite the favorable evidence supporting the catecholamine hypothesis
based on the action of these drugs, advocates of the hypothesis are appropriately cautious. The reason is that reserpine, the tricyclics, and the MAO inhibitors all have a large number of effects other than their effect on norepinephrine. Because of this, it is very possible that their effects might be due to some other properties of the drugs and not necessarily to their effect on norepinephrine.
Depression and Suicide
Post-Traumatic Stress Disorder (PTSD)
Social Anxiety
Generalized Anxiety
Panic Disorder
Major Depression Disorder
Agoraphobia
For the Therapy I recommend click here:
The Liberator Method