Seligman experiments

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More than thirty-five years ago Seligman and his colleagues discovered and reported on two experiments which were to begin an ever-growing field of research, and to fuel continuing debates (Overmeir & Seligman, 1967; Seligman & Maier, 1967). The astonishing feature of these studies was that when dogs were exposed to inescapable shock they adopted behaviour patterns that were passive in nature, even when they were given continued shocks they remained inactive.

This phenomenon was labelled “learned helplessness” and instigated a theory around the findings. The theory postulated that only inescapable events produced giving up, because the identical pattern of shock, if it was under the animal’s control, did not produce giving up. The design used for these types of experiments was known as the “yoked triadic design” which involved three groups of subjects. A contingent group: These subjects are allowed to escape, or avoid a stimulus.

A non-contingent group: These subjects are exposed to a stimulus of the same duration by a yoking procedure. And, a no treatment group: These subjects are not exposed to any response outcome contingencies (Hejka, 1994). What this experimental design assumed was that animals in the non-contingent group have the cognitive ability to learn that their actions are futile and therefore will no longer try to escape, instead they will become passive.

Therefore, the original learned helplessness theory hypothesised that instead of learning occurring only when a response produces a reward or punishment, much to the behaviourists’ acknowledgement; it can occur independent of whether or not a reward or punishment has been given. Maier and Seligman (1976) and Seligman (1975) developed the original learned helplessness hypothesis, which proposed that exposing organisms to uncontrollable outcomes (outcomes that are independent of responding) would produce a motivational deficit, a cognitive deficit and an emotional deficit.

Seligman (1975) also postulated that human depression shares similar symptoms to that of learned helplessness and that the two conditions may be instigated by the same factors, that non-aversive outcomes can cause learned helplessness, and learned helplessness can be applied to all organisms not just dogs and humans. The early experiments investigating the phenomenon of learned helplessness were confined to animal subjects, but it was not long before it was tested in the human context (Hiroto & Seligman, 1975).

Indeed, a number of early studies set out to test that symptoms of depression paralleled the original theory of learned helplessness, which involved depressed subjects and their ability to solve anagram patterns and to turn off inescapable noise (Klein, Fencil-Morse & Seligman, 1976; Miller & Seligman, 1975; Klein & Seligman, 1976). It must be noted however, that not all early studies demonstrated the effect of learned helplessness in other animal species as Seligman had suggested it would (Seligman, 1975).

Indeed, a study conducted by Beatty (1979, cited in Hejka, 1994) failed to show any decrements in test task performance of rats following inescapable shock, while others found an improvement in test task performance (Anisman, & Waller 1971, cited in Hejka, 1994). The original theory sparked much debate and critiques to the original theory of learned helplessness were intensifying. The behaviourists’ headed the list believing that the animals’ had learned to remain passive, which would thus give a reward of the shock being turned off. Others believed that subjects differed in their sensitivity to shock.

While some would be able to sit there and take the shock, others were said to have a low tolerance and would therefore try to escape, and the sensitivity subjects had to the shock fluctuated over time. As evident as Seligman thought the early studies were in supporting the phenomenon of learned helplessness resulting in the same symptoms seen in naturally occurring depression, the theory still failed to account for ‘boundary conditions’, such as two out of three people becoming helpless but one resisting and no matter what happened to them to make them helpless, they would not give up (Peterson, Maier, & Seligman, 1993).

In the reformulated theory (Abramson, Seligman & Teasdale, 1978) cognition was refined in the form of attribution which postulated that human behaviour is controlled not just by the schedule of reinforcement in the environment but by an internal mental state, the explanations people make for why the environment has scheduled their reinforcements this way. More specifically the reformulated theory focussed on the following three dimensions of attributions for negative life events: internal-external, stable-unstable and global-specific (Abramson et al. 1978). Internal attributions explain causes of negative events in self-referent terms, whereas external attributions assign causes to factors outside the self. Internal and external attributions may also be unstable or stable. Stable attributions explain causes of negative events in terms of permanent factors, whereas unstable attributions explain events in terms of temporary factors. Moreover, internal and external attributions, stable or unstable, are divided into global and specific attributions.

Global attributions explain the causes of negative events in pervasive terms and span many situations, unlike specific attributions which explain events in limited, context-specific terms. Thus, when failure in tennis is explained due to lack of tennis ability, the cause is internal and stable; when failure is explained by lack of effort, the cause is internal and unstable (Harald, 2001). The theory hypothesises that individuals who attribute negative events to internal, stable and global causes are more predisposed toward depression than individuals who make external, unstable and specific attributions.

According to Abramson et al. (1978) the generality of the depressive deficits will depend on the globality of the attribution of helplessness. The persistence of the depression deficits will depend on the stability of the attribution for helplessness. Whether self-esteem is lowered or not, will depend on the internality of the attribution for the helplessness. Also, the amount of self-esteem lost is closely connected to the importance of the consequence to the individual.

Thus, the reformulation proposed that once people perceive that their helplessness is contingent on some other factor, the personal meaning of that factor determines their expectation of future helplessness. A key concept in the reformulated theory is explanatory style. Supposedly attributing a negative explanatory style to a wide number of events will predispose the individual to be more susceptible to depression than someone who has a positive explanatory style (Peterson et al. , 1993).

Nolen-Hoeksema, Girgus, and Seligman’s (1986) study of learned helplessness in third, fourth, and fifth-grade children tested the prediction that children with a maladaptive explanatory style who are not depressed are more likely to become depressed over time than are children who do not have a maladaptive explanatory style. These children were expected to show an increased incidence of helpless behaviours in the classroom. The results of the study supported the reformulated theory of helplessness.

The children who, according to psychological testing, were judged to be depressed and who showed more achievement-related problems tended to explain bad events by internal, stable, and global causes and good events by external, unstable, and specific causes. Children who experience a serious, uncontrollable event that affects much of their lives over time may show motivational, cognitive, and emotional deficits of depression that could lead to additional negative events.

They may then think that these events were their fault and begin to manifest a maladaptive explanatory style, which would make them susceptible to depression. A study concerning adults was carried out by Metalsky, Abramson, Seligman, Semmel, and Peterson (1982), which tested reactions to receiving low grades on a midterm exam. Those students that attributed their bad marks to internal, stable and global causes predicted increases in depressed mood state. But are the symptoms of learned helplessness produced in laboratory experiments the same as the symptoms depressed people have?

In order to determine an answer to that question a distinction of what the symptoms of depression are must be made. According to the DSM-IV-R to be diagnosed as suffering a “major depressive episode” you must have five of the following symptoms: depressed mood, loss of interest in usual activities, loss of appetite, insomnia, psychomotor retardation, loss of energy, feelings of worthlessness and guilt, diminished ability to think and poor concentration, and suicidal thought or action (Diagnostic and Statistical Manual of Mental Disorders, 1994).

If the list of symptoms from the DSM-IV-R are taken and applied to the people and animals that had taken part in the learned helplessness experiments, it was found that the groups allowed to control events had none of the nine critical symptoms, but the groups not permitted to control these very same events showed no less than eight of the nine symptoms (Peterson et al. , 1993). The only symptom that was not seen was suicidal thought and action, may be because the experimental failures were so minor e. g. ailure to turn off noise or solve anagrams. We all inevitably become sad and depressed at some time in our life. The future looks bleak and going forward seems like the last thing you want to do. Some people recover almost immediately; “all the symptoms of learned helplessness dissipate within hours” (Seligman, 1991, pg. 76). Others stay helpless for a couple of days, or weeks, and sometimes for months or longer. Seligman (1975) states, that this is the critical difference between brief demoralisation and an episode of depression.

It is acknowledged that you must have five of the nine symptoms of depression in the DSM-IV-R, however one more factor is needed: The symptoms cannot be momentary; they have to last at least two weeks. Based on the former experiments mentioned above concerning explanatory style, it is clear to see that people who have a pessimistic outlook on events seem to be more susceptible to depression than those that have an optimistic outlook. Indeed, the difference between people whose learned helplessness disappears swiftly and people who suffer their symptoms for two weeks or more is because of their explanatory style (Seligman, 1991).

People who have a pessimistic explanatory style and suffer bad events will be more predisposed to depression, whereas people who have an optimistic explanatory style and suffer bad events will tend to resist depression. According to the reformulated model of learned helplessness, by adding the premise of a depressive (pessimistic) explanatory style, the theory could account for the boundary conditions, or the variations in depression.

Seligman (1991) states that by removing this pessimistic explanatory style we must undergo therapy, more importantly cognitive therapy. Cognitive therapy specifically works by making patients more optimistic. Not only that, it prevents relapse because patients acquire a skill they can use again and again without relying on drugs. Drugs relieve depression, but only temporarily; unlike cognitive therapy, drugs fail to change the underlying pessimism which is at the root of the problem (Peterson et al. 1993). Other cures which relieve learned helplessness and are common to depression are electroconvulsive shock, time, anticholinergics and norepinephrine stimulants (Seligman, 1975). Controversies arise when trying to determine whether or not learned helplessness actually fits a model of depression. Are the laboratory experiments really testing the phenomenon or are they testing for other factors that the ardent supporters of the learned helplessness theory are too blind to see?

For instance, Barber and Winefield (1986) conducted a study which found that uncontrollable events do not invariably produce helplessness and that conditioned inattention may be a separate mechanism to that of learned helplessness and may be the true reason as to why some people have performance deficits. Winefield (1982) also stipulates that never has any experiment shown that humans do not learn like dogs. This maybe due to the experimental procedures not being the same for both animal and human subjects.

As has been stipulated earlier, explanatory style is said to play a large part in the reformulated theory of learned helplessness but a suggestion made by Abramson, Metalsky & Alloy (1989) assumes that expectations play just as big a role as does explanatory style in producing depression. Indeed, their revised theory of the reformulated theory, dubbed the “hopelessness theory of depression”, believes that depressed people generalise inappropriately from situations which are uncontrollable to situations which are controllable and that hopelessness is the proximal cause of depression.

In addition, if learned helplessness is going to fit a model of depression it must account for who actually distorts reality. It is assumed that depressed people distort reality but evidence contrary to the fact has been found by Alloy and Abramson (1979), who found that depressed subjects were actually more in touch with reality than were the non-depressed subjects. May be it is the individual who is more in touch with reality that might be more liable of suffering from depression than the individual who has an illusion of his or her control.

Another area of controversy for the learned helplessness theory fitting a model of depression is concerned with discontinuity and continuity (Peterson et al. , 1993). The discontinuity view believes that those with a mild form of depression are not susceptible to experiencing severe depression and vice versa. Another view is that mild depression has separate symptoms to that of severe depression and should not be judged along the same continuum. However, Peterson et al. 1993) believe that mild depression and severe depression are correlated and research into depressive symptoms must take this into account. The role that the learned helplessness theory has on depression is that we can understand that the major symptoms of learned helplessness all have parallels in the symptoms of depression and that cognitive therapy may be a more productive cure for unipolar depression than drugs. That the theory points out that depressed people make internal, stable, and global explanations of bad events and tend to make external, unstable, and specific explanations for good events.

That the explanatory style of the person, if pessimistic can predispose people to depression and help changing that negative explanatory style can help them overcome the depression. Therapy can work by helping the patient realise that some events in life are just not controllable no matter what you do. However, some events are controllable and reinforcing into the individual that responding produces reinforcement can be an effective way in breaking up learned helplessness. Further research into the phenomenon will give us an even better understanding of the theoretical concept that is learned helplessness.

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