Parallels between Depression and Learned Helplessness
We have now examined the basic learned helplessness phenomena in animals
and humans and the theory behind it. Learned helplessness has been
suggested as a model for depression. The similarity in symptoms, cause, cure,
prevention, and predisposition between learned helplessness in the
laboratory and unipolar depression as it occurs in real life.
SYMPTOMS
The failure to escape noise and to solve problems after experience
with uncontrollable events is the basic passivity deficit of learned
helplessness. This passivity seems similar to the motivational deficits of depression.
Failure to initiate responses by depressed individuals has been systematically
demonstrated in the laboratory: depressed students and patients
fail to escape noise and fail to solve anagrams. The more depressed they are,
the more severe is this deficit (Miller and Seligman, 1975, 1976; Price,
Tryon, and Raps, 1978).
Non-depressed individuals given inescapable noise or unsolvable problems
show the cognitive deficit of learned helplessness: they have difficulty
learning that responding is successful, even when it is. Depressed individuals
show exactly the same deficit. Non-depressed human beings made helpless
fail to see patterns in anagrams and fail to change expectancy for future success
when they succeed and fail in skill tasks. Depressed students and patients
show these same deficits in the laboratory (Miller and Seligman, 1975,
1976; Abramson, Garber, Edwards, and Seligman, 1978). These results suggest
that the cognitive deficit both in learned helplessness and depression
may be produced by the expectation that future responding will be ineffective,
and this expectation seems central to the negative beliefs about self,
ongoing experience, and about the future, which cognitive therapists like
Beck postulate as the central cause of depression.
When individuals are made helpless by inescapable noise and attribute
their failure to their own shortcomings as opposed to external causes, not
only are the motivational and cognitive deficits of helplessness and depression
observed, but self-esteem drops as well. In contrast, when helpless subjects
are led to make external attributions and blame the task difficulty for
their failure, the motivational and cognitive deficits are observed but self esteem
deficits are not. This parallels the low self-esteem that occurs in depressives,
particularly among individuals who blame themselves for their
troubles (Abramson, 1978).
Parallel mood changes occur both in learned helplessness and depression.
When non-depressed subjects are made helpless by inescapable noise or
unsolvable problems, they become sadder, more hostile, and more anxious.
These reports parallel the emotional changes in depression: more sadness,
anxiety, and perhaps more hostility.
In the laboratory, rats who receive inescapable shock eat less food, lose
more weight, aggress less against other rats, and lose out in competition for
food with rats who had received either escapable shock or no shock. This
loss of appetite and loss of aggression produced by helplessness in the laboratory
parallels the somatic symptoms of depressives: they lose weight, eat less,
their social desires and status drop, and they become less aggressive Finally,
learned helplessness in the rat is accompanied by norepinephrine
depletion. In an exciting series of studies over the last decade, Jay Weiss at
Rockefeller University has demonstrated that the brains of rats who have
received inescapable shock have less available norepinephrine than the
brains of animals who receive no shock or escapable shock. Weiss argues
that it is the norepinephrine depletion and not the expectation of
response out come independence that causes learned helplessness. While the evidence
is not yet in on whether it is the norepinephrine depletion, the expectancies
of response-outcome independence, or both that are fundamental in
learned helplessness, it is important that norepinephrine depletion is probably
a correlate of depression in humans (Weiss, Glazer, and Pohoresky, 1976).
In summary:
There are several parallel symptoms in laboratory-created
learned helplessness and depression as found in nature. In both conditions,
the four basic symptoms of depression are displayed: motivational deficits,
thought deficits, mood changes, and physical deficits. Since these four deficits
were created in the laboratory by a known factor-by imposing the expectation
that future responses and important outcomes will be
independent-could it be that when we observe the same four symptoms in
nature and call the condition depression, that the same cause-a belief in
the futility of responding-is at work?
CAUSE
The learned helplessness hypothesis says that depressive deficits,
which parallel the learned helplessness deficits, are produced when an
individual expects that bad events may occur and that they will be independent
of his responding. When this is attributed to internal factors, self-esteem
will drop; to stable factors, the depression will be long-lived; and to
global factors, the depression will be general. Recent evidence confirms this.
This attributional style has been found in depressed students, children, and
patients. Depressed patients, moreover, believe that the important goals in
their life are less under their control than do other psychiatric patients (Seligman,
et al., 1979; Eidelson, 1977; Raps and Seligman, 1980). Most important,
individuals who have this attributional style but are not depressed,
become depressed when they later encounter bad events (Peterson and Seligman, 1999).
THERAPY
(See below for my recommendation)
Since the cause of learned helplessness and depression is hypothesized
to be the expectation that responding will be ineffective in controlling
future events, the basic therapeutic theme should be to change this
belief to one in which the individual believes that responding will be effective
and anticipated bad events will be avoided. The attributional theory of
learned helplessness suggests some basic strategies for doing this.
So, for example, learned helplessness theory suggests that therapies such as teaching
social skills and assertiveness training should be anti-depressive because they
teach the individual that he can control affection and the esteem of other
people by his own actions. Further tactics such as criticizing automatic
thoughts (it's not that I'm an unfit mother, rather I'm grouchy at 7 A.M.)
help alleviate depression because they change attributions for failure from
internal, stable, and global (unfit mother) to external, unstable, and specific
(7 A.M.). Notice how similar these stategies are to the techniques of cognitive
and behavioral therapies that we have just reviewed. In addition to cognitive
and behavior therapy parallels, there are somatic therapy parallels as well.
Four kinds of somatic therapy appear to break up learned helplessness in animals:
electroconvulsive shock, MAO inhibitors, tricyclics, and dream deprivation.
(Dorworth, 1971; Porsolt, et al., 1978; Brett, Burling, and Pavlik, 1981)
These are the four somatic therapies that also can break up unipolar depression.
In summary, there is reason to believe that the somatic, the cognitive, and
the behavioral therapies that reverse learned helplessness also reverse depression.
PREVENTION AND PREDISPOSITION
Learned helplessness in animals is prevented by prior experience with mastery and immunization.
If an animal first controls important events, such as shock and food, then later
helplessness never occurs. In effect, it is prevented. Such immunization seems to
be lifelong: rats who learn to escape shock as weanlings do not become helpless
when as adults they are given inescapable shock. Conversely, lifelong
vulnerability to helplessness is produced by early experience with inescapable
shock: rats who receive inescapable shock as weanlings become helpless
adults (Hannum, Rosellini, and Seligman, 1976). This parallels the data on
the prevention of and vulnerability to depression. Individuals whose mother
dies before the child is eleven years old are more vulnerable to depression
than those whose mother does not. There are, however, invulnerability factors
that prevent depression from occurring in such individuals: a job, an
intimate relationship with a spouse or lover, not having life burdened with
child care, and religious belief (Brown and Harris, 1978). These invulnerability
factors may all increase the expectation of future control, and vitiate
the expectations of future helplessness.
The final parallel in the predisposition to helplessness and depression is
that depressed individuals have an insidious attributional style: when they
fail, they tend to attribute their failure to internal, global, and stable factors;
but when they succeed, they attribute their success to external, unstable, and
specific factors (Seligman, Abramson, Semmel, and von Baeyer, 1979). This
is a style that maximizes the expectation that responding will be ineffective
in the future. The helplessness model suggests that it is this attributional
style that predisposes an individual to depression, and recent evidence confirms this.
Two groups of equally non-depressed students with the opposite attributional
styles for failure-one internal, stable, and global, the other external,
unstable, and specific-were followed for one semester. Those students with
the insidious attributional style became more depressed when confronted
with later failure (i.e., disappointing mid-term grades) than those students
with the opposite attributional style. This suggests that it is a catastrophizing
attributional style that is common in depression-it's me, it's going to last
forever, and it's going to affect everything I do- that predisposes an individual
to depression and that the opposite attributional style may prevent
depression when bad events occur (Peterson and Seligman, 1984).
~~~~~~~~~~~~
Treating:
Depression
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
and humans and the theory behind it. Learned helplessness has been
suggested as a model for depression. The similarity in symptoms, cause, cure,
prevention, and predisposition between learned helplessness in the
laboratory and unipolar depression as it occurs in real life.
SYMPTOMS
The failure to escape noise and to solve problems after experience
with uncontrollable events is the basic passivity deficit of learned
helplessness. This passivity seems similar to the motivational deficits of depression.
Failure to initiate responses by depressed individuals has been systematically
demonstrated in the laboratory: depressed students and patients
fail to escape noise and fail to solve anagrams. The more depressed they are,
the more severe is this deficit (Miller and Seligman, 1975, 1976; Price,
Tryon, and Raps, 1978).
Non-depressed individuals given inescapable noise or unsolvable problems
show the cognitive deficit of learned helplessness: they have difficulty
learning that responding is successful, even when it is. Depressed individuals
show exactly the same deficit. Non-depressed human beings made helpless
fail to see patterns in anagrams and fail to change expectancy for future success
when they succeed and fail in skill tasks. Depressed students and patients
show these same deficits in the laboratory (Miller and Seligman, 1975,
1976; Abramson, Garber, Edwards, and Seligman, 1978). These results suggest
that the cognitive deficit both in learned helplessness and depression
may be produced by the expectation that future responding will be ineffective,
and this expectation seems central to the negative beliefs about self,
ongoing experience, and about the future, which cognitive therapists like
Beck postulate as the central cause of depression.
When individuals are made helpless by inescapable noise and attribute
their failure to their own shortcomings as opposed to external causes, not
only are the motivational and cognitive deficits of helplessness and depression
observed, but self-esteem drops as well. In contrast, when helpless subjects
are led to make external attributions and blame the task difficulty for
their failure, the motivational and cognitive deficits are observed but self esteem
deficits are not. This parallels the low self-esteem that occurs in depressives,
particularly among individuals who blame themselves for their
troubles (Abramson, 1978).
Parallel mood changes occur both in learned helplessness and depression.
When non-depressed subjects are made helpless by inescapable noise or
unsolvable problems, they become sadder, more hostile, and more anxious.
These reports parallel the emotional changes in depression: more sadness,
anxiety, and perhaps more hostility.
In the laboratory, rats who receive inescapable shock eat less food, lose
more weight, aggress less against other rats, and lose out in competition for
food with rats who had received either escapable shock or no shock. This
loss of appetite and loss of aggression produced by helplessness in the laboratory
parallels the somatic symptoms of depressives: they lose weight, eat less,
their social desires and status drop, and they become less aggressive Finally,
learned helplessness in the rat is accompanied by norepinephrine
depletion. In an exciting series of studies over the last decade, Jay Weiss at
Rockefeller University has demonstrated that the brains of rats who have
received inescapable shock have less available norepinephrine than the
brains of animals who receive no shock or escapable shock. Weiss argues
that it is the norepinephrine depletion and not the expectation of
response out come independence that causes learned helplessness. While the evidence
is not yet in on whether it is the norepinephrine depletion, the expectancies
of response-outcome independence, or both that are fundamental in
learned helplessness, it is important that norepinephrine depletion is probably
a correlate of depression in humans (Weiss, Glazer, and Pohoresky, 1976).
In summary:
There are several parallel symptoms in laboratory-created
learned helplessness and depression as found in nature. In both conditions,
the four basic symptoms of depression are displayed: motivational deficits,
thought deficits, mood changes, and physical deficits. Since these four deficits
were created in the laboratory by a known factor-by imposing the expectation
that future responses and important outcomes will be
independent-could it be that when we observe the same four symptoms in
nature and call the condition depression, that the same cause-a belief in
the futility of responding-is at work?
CAUSE
The learned helplessness hypothesis says that depressive deficits,
which parallel the learned helplessness deficits, are produced when an
individual expects that bad events may occur and that they will be independent
of his responding. When this is attributed to internal factors, self-esteem
will drop; to stable factors, the depression will be long-lived; and to
global factors, the depression will be general. Recent evidence confirms this.
This attributional style has been found in depressed students, children, and
patients. Depressed patients, moreover, believe that the important goals in
their life are less under their control than do other psychiatric patients (Seligman,
et al., 1979; Eidelson, 1977; Raps and Seligman, 1980). Most important,
individuals who have this attributional style but are not depressed,
become depressed when they later encounter bad events (Peterson and Seligman, 1999).
THERAPY
(See below for my recommendation)
Since the cause of learned helplessness and depression is hypothesized
to be the expectation that responding will be ineffective in controlling
future events, the basic therapeutic theme should be to change this
belief to one in which the individual believes that responding will be effective
and anticipated bad events will be avoided. The attributional theory of
learned helplessness suggests some basic strategies for doing this.
So, for example, learned helplessness theory suggests that therapies such as teaching
social skills and assertiveness training should be anti-depressive because they
teach the individual that he can control affection and the esteem of other
people by his own actions. Further tactics such as criticizing automatic
thoughts (it's not that I'm an unfit mother, rather I'm grouchy at 7 A.M.)
help alleviate depression because they change attributions for failure from
internal, stable, and global (unfit mother) to external, unstable, and specific
(7 A.M.). Notice how similar these stategies are to the techniques of cognitive
and behavioral therapies that we have just reviewed. In addition to cognitive
and behavior therapy parallels, there are somatic therapy parallels as well.
Four kinds of somatic therapy appear to break up learned helplessness in animals:
electroconvulsive shock, MAO inhibitors, tricyclics, and dream deprivation.
(Dorworth, 1971; Porsolt, et al., 1978; Brett, Burling, and Pavlik, 1981)
These are the four somatic therapies that also can break up unipolar depression.
In summary, there is reason to believe that the somatic, the cognitive, and
the behavioral therapies that reverse learned helplessness also reverse depression.
PREVENTION AND PREDISPOSITION
Learned helplessness in animals is prevented by prior experience with mastery and immunization.
If an animal first controls important events, such as shock and food, then later
helplessness never occurs. In effect, it is prevented. Such immunization seems to
be lifelong: rats who learn to escape shock as weanlings do not become helpless
when as adults they are given inescapable shock. Conversely, lifelong
vulnerability to helplessness is produced by early experience with inescapable
shock: rats who receive inescapable shock as weanlings become helpless
adults (Hannum, Rosellini, and Seligman, 1976). This parallels the data on
the prevention of and vulnerability to depression. Individuals whose mother
dies before the child is eleven years old are more vulnerable to depression
than those whose mother does not. There are, however, invulnerability factors
that prevent depression from occurring in such individuals: a job, an
intimate relationship with a spouse or lover, not having life burdened with
child care, and religious belief (Brown and Harris, 1978). These invulnerability
factors may all increase the expectation of future control, and vitiate
the expectations of future helplessness.
The final parallel in the predisposition to helplessness and depression is
that depressed individuals have an insidious attributional style: when they
fail, they tend to attribute their failure to internal, global, and stable factors;
but when they succeed, they attribute their success to external, unstable, and
specific factors (Seligman, Abramson, Semmel, and von Baeyer, 1979). This
is a style that maximizes the expectation that responding will be ineffective
in the future. The helplessness model suggests that it is this attributional
style that predisposes an individual to depression, and recent evidence confirms this.
Two groups of equally non-depressed students with the opposite attributional
styles for failure-one internal, stable, and global, the other external,
unstable, and specific-were followed for one semester. Those students with
the insidious attributional style became more depressed when confronted
with later failure (i.e., disappointing mid-term grades) than those students
with the opposite attributional style. This suggests that it is a catastrophizing
attributional style that is common in depression-it's me, it's going to last
forever, and it's going to affect everything I do- that predisposes an individual
to depression and that the opposite attributional style may prevent
depression when bad events occur (Peterson and Seligman, 1984).
~~~~~~~~~~~~
Treating:
Depression
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