To what extent can cognitive theories of depression explain the onset as well as maintenance of the disorder?
To what extent can cognitive theories of depression explain the onset as well as maintenance of the disorder?
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 showed what Seligman described as 'learned helplessness' (characterized by lethargy, sluggishness, loss of appetite)
Seligman theorized that this phenomenon was a result of a perceived lack of control, and he generalized it into a theory of human clinical depression. In other words, he theorised that if you expose a person to a stressor and they perceive no control over it, they will respond with learned helplessness.
However, Seligman's theory has received major criticisms, namely:
you cant generalise from a sample of one species of animal to humans: Blankley, 1978
Seligman's theory doesn't explain individual differences: why do some people deal with stressors well and others poorly?
In an attempt to deal with the individual differences criticism, Abramson introduced attributional styles into the theory of learned helplessness
4 basic premises:
Expected aversiveness (expecting that highly aversive outcomes are probable)
Expected uncontrollability (expecting that you will be unable to control situations)
Attributional style (maladaptive, so negative events are attributed to having internal, stable or global characteristics)
internal (cf external) bad events caused by self rather than external sources
stable (cf unstable) the source of a bad event is stable & will therefore happen again, rather than being a one off
global (cf specific): the repercussions of a bad event are far reaching
Severity of symptoms (the more certain an aversive state of affairs is, the greater the resultant cognitive and motivational deficits)
it is a basic theory - it needs a richer framework and it needs to explain how structures and processes are organized. Seligman doesn't even attempt this.
it ignores the consequences of people's actions and moral aspects of their thoughts
Seligman sees attributional style as a stable 'trait'. Clinical observation of depressive shows that attributional style fluctuates with mood state. Studies of non-depressives and recovered depressives show no differences in their attributional style. (Dobson & Shaw 1986)
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 symptomatology in a 4 month follow up of college students. Therefore stable, maladaptive cognitions were not found to be ...
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it ignores the consequences of people's actions and moral aspects of their thoughts
Seligman sees attributional style as a stable 'trait'. Clinical observation of depressive shows that attributional style fluctuates with mood state. Studies of non-depressives and recovered depressives show no differences in their attributional style. (Dobson & Shaw 1986)
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 symptomatology 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)
Beck (1976) 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 memory 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. only activated or influenced by similar events to those that defined them.
these schemas contain propositional information (eg 'I am worthless')
When focused on three interlocking beliefs in a negative way (the cognitive triad), this causes and maintains depression:
SELF : deflective
WORLD : insuperable difficulties
FUTURE : hopeless
The cognitive triad causes negative, automatic thoughts (ie depressive thoughts occurring beyond the conscious control of the sufferer) and to systematic or logical errors.
Systematic/logical errors are a variety of errors of reasoning a depressive shows, which serve to perpetuate their depression, for example:
over-generalization: arbitrarily drawing a conclusion about a wide variety of things on the basis of single events (eg 'I failed my driving test so I will fail everything')
arbitrary inference: the drawing of a negative conclusion in the absence of supporting information (eg My girlfriend did not telephone me therefore she hates me)
dichotomous thinking: thinking in polar opposites (also called 'black and white' thinking) so something is either all good or a total disaster, (eg if my wife leaves me then I may as well be dead)
Effectively, Beck defines the maintenance of depression as an interaction between all these factors causing a vicious cycle:
However, Beck's theory has many criticisms:
Beck says the cognitive triad is a stable 'trait' that depressives develop, but 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. Beck's schemas are vaguely defined & therefore inadequate He doesn't state how they are activated He states that depressogenic schemas are caused by a 'critical incident': this doesn't account for when depression is not caused by a 'critical incident.
Modern research (eg Power & Champion, 1986) suggests that depressives are not as unrealistic as Beck thought: instead it is postulated that non-depressives are 'over-optimistic' and depressives, while pessimistic, are relatively more realistic. 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 Beck doesn't attempt to explain how schemas work at an unconscious level: Shevrin & Dickman (1980) suggest that the conscious aspect may occur late in processing.
Teasdale's differential activation hypothesis (1988)
Looks specifically at mood states
An extension of Beck's work
Bower's 1981 took a network theory devised for propositional memory (Collins & Quallin (date?)), and incorporated mood states into the propositional network.
Teasdale revised Bower's theory, making it into a cognitive theory of depression.
How does the network work?
the network is made up of links and nodes, each node either being a propositional 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
Activation spreads passively through the network- according to the strength of each link
A depressive focuses on the DEMONs, strengthening the links to them, thereby creating a vicious cycle that keeps on strengthening the links to the DEMONs
Strengths of Teasdale's model
A major theory that has stimulated a lot of research
Doesn't rely on identifying a critical incident (Beck's does) this is due to the nature of the nodes & links in the network: less related incidents can still trigger the DEMON
Critique of Teasdale's differential activation hypothesis:
Doesn't attempt to explain aetiology by definition: Teasdale saw the maintenance as cognitive, but not the cause.
the propositional network model on which it is based was not originally developed for mood disorders, it was originally developed as a model of semantic memory (Collins & Quallin)
Semantic memory (word meanings) is a small knowledge domain: Teasdale added events, actions and situations to the network: is molar organization more useful?
Teasdale treats the links between the nodes in an ad hoc and atheoretical manner- the nodes have:
different statuses
are uni-directional / bi-directional
labeled differently
different types of concepts are represented
therefore, what processes could be involved in a so called 'passive' spread of activation?
"A theory that gives depression the same status as 'has four legs' is the cognitive equivalent of putting a bull in a china shop."
Conclusions:
Thus the 3 major cognitive theories in depression have been considered: Seligman's (& Abramson's revised) Learned Helplessness (an explanatory style model); Beck's Cognitive distortion model (a schema model) and Teasdale's Differential activation hypothesis (a network model). However there are certain criticisms that apply to these models in general:
The experimental samples used were mainly college students
Zajonic (1984) and others suggest that emotion and cognition are separately operating systems
The models are to general in that they can apply equally well to anorexics, alcoholics (etc), ie they aren't very specific to depression
Most of the terms used are vaguely defined, leaving many processes and organisations unexplained
Most importantly, they miss out on the social (Brown & Harris, 1978) and humanistic domain of human life (Rogers..).
there is some genetic basis for developing mood disorders: Wender et al (1986); Egeland et al (1987)
Biochemical models of depression are becoming increasingly detailed (eg Kety's permissive amine theory (1975)). Seratonin and Norepinephrine have been isolated as playing a key role, which modern drugs like Prozac target and successfully alleviate symptoms of depression, although biochemical therapies given on their own have a high rate of relapse when the course finishes
However, while this essay has stressed the criticisms of cognitive models of depression, praise must be given where it is due. Cognitive therapies based on Beck's (1976) model (often in conjunction with modern drug therapies) are usually the therapy of choice by practitioners, especially in cases of mild to moderate depression
Looking to the future, new theories need to take a broader view and begin to model the interaction between biological, environmental, and psychological factors.
