Cognitive Theory Of Depression

The following academic paper highlights the up-to-date issues and questions of Cognitive Theory Of Depression. This sample provides just some ideas on how this topic can be analyzed and discussed.

In this essay, the symptoms of depression will be described and aetiology discussed from a cognitive viewpoint. In particular, Seligman’s learned helplessness (1975); Abramson’s (1978) revision of learned helplessness; Beck’s ‘cognitive distortion’ model (1976), and Teasdale’s differential activation hypothesis (1988) shall be evaluated. Cognitive theorists generally regard thought processes as causative factors in depression.

The treatment of depression proposed by cognitive theorists will also be assessed in detail, and empirical evidence shall be considered.

Finally, a conclusion of the efficacy of cognitive theory regarding depression shall be presented and suggestions offered regarding the direction in which research should go in the future. Many psychologists and psychiatrists alike have described the symptoms of depression; however, one description is particularly apt. “Mood is sometimes dominated by a profound inward dejection and gloomy hopelessness, sometimes more by indefinite anxiety and restlessness.

The patient’s heart is heavy, nothing can permanently rouse his interest, nothing gives him pleasure . . . ” Kraeplin (1921, p. 6).

Depression is termed an affective mood disorder due to the foremost feature of abnormally low mood. Depression occurs when feelings of sadness or grief are prolonged and exaggerated beyond what seems reasonable. Depression therefore ceases to be a symptom and becomes an illness, involving widespread depression of mental and physical functions. The patient appears slow and indecisive, increasingly unable to cope with everyday problems. Physical symptoms are often prominent because bodily functions are upset and because depression lowers the tolerance for discomfort and pain.

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Cognitive Triad Theory

Seligman (1975) describes depression as the common cold of psychiatry because it is also so widespread. Following the cognitive revolution in the 1960’s, theorists began to use cognitive theories to explain affective disorders. Cognitive theories are mainly based on unipolar rather than bipolar depression, which is believed to have an entirely different aetiology. Therefore unipolar depression shall be only investigated in this paper. Stated simply, cognitive therapy is based on the assumption that negative cognition distortion of experience underlies depression.

This approach shall be analysed in consideration of Aaron Beck (1974) and additions by others, including Teasdale (1988) and Seligman (1975). Seligman’s original learned helplessness theory (1975) was based on the experimental examination of two groups of dogs. The experimental group were given unavoidable electric shocks repeatedly, while the control group were given the same shocks but with the option of escaping them. The experimental group demonstrated what Seligman described as ‘learned helplessness’. This was characterised by lethargy, sluggishness, and loss of appetite.

Seligman theorised that this phenomenon was a result of a perceived lack of control, and he generalised it into a theory of human clinical depression. He proposed that if you expose a person to a stressor and they perceive no control over it, they will respond with learned helplessness. Criticisms of Seligman’s theory include: is it really possible to generalise from a sample of one species of animal to humans? And why do some people deal with stressors well and others poorly? Clearly Seligman’s theory is inadequate because it fails to explain individual differences.

Abramson (1978) revised the learned helplessness theory in an attempt to deal with the individual differences criticism. In order to do this, he introduced attributional styles into the theory. The four basic premises are displayed in Table 1. Expected aversiveness (Expecting that highly aversive outcomes are probable) Expected uncontrollability (Expecting that you will be unable to control situations) Attributional style > Internal – bad events caused by self rather than external sources > Stable – the source of a bad event is stable and will therefore happen again Global – the repercussions of a bad event are far reaching (Maladaptive, so negative events are attributed to having internal, stable or global characteristics) Severity of symptoms (The more certain an aversive state of affairs is, the greater the resultant cognitive and motivational deficits) Table 1 basic premises of Abramson’s (1978) revision of learned helplessness Criticisms of Seligman (1975) and Abramson (1978) tend to centre on the idea that the theory is simply too basic. It needs a richer framework and it needs to explain how structures and processes are organised.

Seligman fails to even attempt this, however sis repertoire was within the animal field and not human beings, and the latter are more complex in certain faculties. The previous theories also ignore the consequences of people’s actions and the moral aspects of their thoughts. Seligman sees attributional style as a stable ‘trait’. Whilst, clinical observation of depressives shows that attributional style fluctuates with mood state. Studies of non-depressives and recovered depressives show no differences in their attributional style.

Additionally, learned helplessness has been shown to be non-predictive. In a longitudinal study, Lewinsohn (1981/1988) found that dysfunctional attitudes/belief sets do not predict depressive symptoms in a 4 month follow up of college students. Therefore stable, maladaptive cognitions were not found to be vulnerability factors, thus contradicting the theory. In other words, learned helplessness is a descriptive account of depression as opposed to an aetiological explanation (Lewinsohn, 1981). Clearly, the aforementioned theories have been insufficient as causal theories of depression.

Research has focused uttermost on Beck’s (1976) cognitive theory of depression. He devised a schema-based model of depression, aiming to provide a coherent account of the beliefs a depressed person expresses about themselves, the future and the world. To outline his model: Previous negative events are encoded in the form of schemas. Beck defined schemas as ‘relatively stable cognitive patterns which form the basis for the regularity of interpretations of a particular set of situations’. Beck’s schemas are latent, i. e. nly activated or influenced by similar events to the ones that defined them. These schemas contain prepositional information (e. g. ‘I am worthless’). When focused on three interlocking beliefs in a negative way (the cognitive triad), this causes and maintains depression. The cognitive triad causes negative, automatic thoughts (i. e. depressive thoughts occurring beyond the conscious control of the sufferer) and to systematic or logical errors. Systematic errors are a variety of errors of reasoning a depressive shows, which serve to perpetuate their depression.

Examples include: over-generalisation, which is arbitrarily drawing a conclusion about a wide variety of things on the basis of single events (e. g. ‘I failed my exam so I will fail in everything I do’). Arbitrary inference is the drawing of a negative conclusion in the absence of supporting information (e. g. ‘my friend did not want to meet me therefore she hates me). Dichotomous thinking describes thinking in polar opposites. So something is either all good or a total disaster, (e. g. if I fail this year at university I might as well be dead’).

Effectively, Beck defines the maintenance of depression as an interaction between all these factors causing a vicious cycle. See Figure 1. However, Beck’s theory has many criticisms. Beck argues that the cognitive triad is a stable ‘trait’ that depressives develop; yet research shows that attributions fluctuate with mood. Beck sidesteps this problem by saying that the schemas are latent, but this is not an adequate solution. Additionally, Beck’s schemas are vaguely defined and therefore inadequate and he doesn’t state how they are activated.

Beck states that Depressogenic schemas are caused by a ‘critical incident’, so how do you account for depression that isn’t caused by a ‘critical incident’? Most importantly, the evidence supporting Beck’s theory is correlational. So we know there is a strong association between negative thoughts and depression, but there is no evidence that it is causal. Therefore Beck’s theory is a good description of the cognitive symptoms of depression, but there is no evidence that it is anything more. This leads us to wonder ‘how do cognitive theorists actually explain the aetiology of depression? Teasdale’s differential activation hypothesis (1988) was an extension of Beck’s work. He revised Bower’s 1981 network theory for prepositional memory and made it into a cognitive theory of depression. The network is made up of links and nodes, each node either being a prepositional item or a ‘depression emotion node’ termed ‘DEMON’. The more related two nodes are, the stronger the link. Past experience is the basis of these links and activation spreads passively through the network according to the strength of each link.

A depressive tends to focus on the Demon’s, strengthening the links to them; thereby creating a viscous cycle that keeps on strengthening the links to the DEMON’s. The Teasdale model is certainly a major theory that has stimulated a lot of research. A major strength of Teasdale’s theory is that it doesn’t rely on identifying a critical incident whilst Beck’s does. This is due to the nature of the nodes and links in the network; therefore less related incidents can still trigger the demon. However, this theory again doesn’t attempt to explain the aetiology by definition.

Teasdale saw the maintenance of depression as cognitive, but not the cause. On a personal note, this theory seems rather abstract and scientific as a theory of an only too human mood disorder. It makes you wonder exactly how is depression caused according to cognitive theorists? However, cognitive therapy of depression is a rather different story from cognitive aetiology of the mood disorder. It has been widely accepted by the clinical community since it was introduced and cognitive therapy has generally being supported in controlled trials (Dobson, 1989).

Cognitive therapy is based on the assertion that individuals can learn to recognise and modify their negative beliefs and maladaptive information processing capabilities, resulting in preventing or alleviating depression. Cognitive therapy has typically proven superior to no treatment or wait-list controls in college students (Shaw, 1977). Cognitive behaviour therapy is ‘an active, directive, time-limited, structured approach . . . based on an underlying theoretical rationale that an individual’s affect and behaviour are largely determined by the way in which he structures the world’ (Beck et al, 1979, p. ) Beck’s theory is described in a manual (Beck et al. , 1979). It is an individual approach with many individual decisions and therapist choices of techniques. The manual suggests a typical structure for the sequence of sessions. Specific cognitive techniques are used to provide entry points into the patient’s cognitive organization. The techniques of questioning, of identifying illogical thinking are employed to help the patient and therapist to understand and modify the patient’s construction of reality.

Findings do appear to provide impressive support for the efficacy of cognitive therapy in the treatment of depression. In 1977 Rush et al found cognitive therapy superior to imipramine pharmacotherapy in an outpatient sample. However, levels of depression actually increased for the pharmacologically treated patients during the 2 weeks before the end of treatment, when the medication was withdrawn. This increase could account for the pharmacotherapy’s poorer performance at post treatment.

Moreover, Hollon et al (1991) suggests that cognitive therapy may prevent symptom return following successful treatment. Patients previously treated with cognitive therapy, either alone or in combination with medication, evidenced a lower rate of symptom return than patients treated with pharmacotherapy only. Rush, Khatami, and Beck (1975) reported the treatment of three patients with chronic depression using a combination of cognitive and behavioural techniques. The cognitive approach was directed at exposing and correcting the patient’s negative distortions of the activities undertaken.

These patients showed rapid and persistent improvement with therapy as reflected by their scores on clinical and self-report measures. The three major cognitive theories in depression have been considered: Seligman’s (& Abramson’s revised) Learned Helplessness; Beck’s Cognitive distortion model and Teasdale’s Differential activation hypothesis. However, there are certain criticisms that apply to these models in general: the experimental samples used were mainly college students; the models are so general that they can apply equally well to anorexics, alcoholics etc and are therefore not very specific to depression.

Most of the terms used are vaguely defined, leaving many processes and organisations unexplained. However, cognitive theories of depression generally suggest that mistaken beliefs and maladaptive information processing play a role in the onset and maintenance of depression (Beck, 1976). On the other hand, cognitive therapies based on Beck’s (1976) model are usually the therapy of choice by practitioners, especially in cases of mild to moderate depression.

Therefore although cognitive theory may not be adequate to explain the aetiology of depression it is sufficient as a treatment for depression. Looking to the future, new theories need to take a broader view and begin to model the interaction between biological, environmental, and physiological factors. Although the cognitive idea of aetiology of depression is hazy, the treatment they suggest for the disorder clearly works yet more work needs to be done before cognitive therapy can be regarded as a preventative of depression and supported empirically.