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Describe and evaluate two treatments of unipolar depression Essay

Describe and evaluate two treatments for unipolar depression (25 marks).

It has been believed that psychological disorders, like physical illnesses, have organic causes. Therefore, mental disorders are treated just like physical ones. Earlier treatments have included things like trepanning which was carried out in the stone again. Nowadays we have much safer and effective treatments such as therapies and drug treatment.

Low levels of both noradrenaline (nora) and serotonin (sero) have been found as being important in unipolar depression (UD) and so it seems logical to treat depression with drugs which increase the availability of these neurotransmitters.

Tricyclic, a type of anti-depressant, appears to work by blocking the reuptake of nora and sero. They block the transport route that would normally allow these neurotransmitters to be taken back into the pre-synaptic neurones. This means that nora and sero remain in the synapse longer which leads to an increase in the synaptic activity in the neurones. This helps the transmission of impulses to neurones which use up nora and sero.

Another type of drug treatment is the use of selective serotonin reuptake inhibitors (SSRIs). SSRIs work in a similar way to tricyclics but affect only the levels of serotonin in the synapses. In order to make efficient use of the body’s resources there is a system whereby serotonin isn’t wasted in the synapse but ‘taken back’ by the pre-synaptic neuron. If this mechanism is impaired by using inhibitor drugs then the sero which isn’t received by the post-synaptic neuron remains in the synapse. This extends the duration of the message being transmitted and/or increases the message intensity. Both SSRIs and tricyclics reduce the symptoms of depression and improves mood.

However, these drug treatments don’t always work. The success rate for them is around 60% but it varies from person to person, as do the side effects. There is, however, many different types of drug and each may have a different success rate. It must be remembered that the ‘success’ of drug treatments for one person may be seen as something completely different to another.

Kirsch et al collected data for the licensing of four new-generation anti-depressants. These were all SSRIs. A meta-analysis was carried out comparing the improvements seen in patients taking SSRIs with the improvements in control patients who had received placebos. They found that there was ‘no difference at moderate levels of initial depression’ between the improvements of those receiving SSRIs and those receiving placebos. This shows that the placebo appeared to benefit moderately depressed individuals. This could be due to the sufferers being presented with hope of reducing their symptoms. This contrasts with the results found of severely depressed groups who experienced lessened symptoms, which discredits the placebo effect. It could be argued that the drug itself may have a ‘placebo effect’ where a person feels that they are getting better because they are taking a pill, no matter what the pill is. It could be that the person is helping themselves and the drug is simply supplying the idea that they’re getting better when it does nothing to them.

Geller et al found that double blind studies showed anti-depressants to be more effective than placebos for children and adolescents. This could be because there are differences in development between children’s and adult’s brains concerning their neurochemistry. Therefore, children and teenagers may not need to use chemistry altering drugs and could just take a placebo instead as they seen to work better than anti-depressants.

Furthermore, Ferguson et al found that those treated with SSRIs were twice more likely to attempted suicide than those treated with a placebo. However, a later review found that a higher risk of suicide was amongst adolescents and decreased amongst adults. This supports Geller’s theory that SSRIs are more effective on adults than adolescents, reinforcing Geller’s view.

Drugs have been found to be appropriate and effective at preventing relapse and giving the sufferer a good quality of life meaning they can integrate back into society and return to everyday tasks. Alternatively, research such as Kirsch, Geller and Ferguson is based on correlational studies. This makes it difficult to say whether UD is caused by low levels of neurotransmitters or if it’s visa-versa.

Cognitive behavioural therapy (CBT) is a therapy which treats depression by combining both cognitive and behavioural techniques. The aim of this is to help people who have mental disorders to cope better with their lives and coincidentally feel better.

Ellis suggests that depression is due to irrational beliefs but is also maintained by reinforcement. Rational Emotive Behavioural therapy (REBT) aims to replace self-defeating beliefs with adaptive beliefs and uses the ABC model. An example of this is a student getting a good grade for their essay. This is the ‘activating’ of an event. How the person interprets an event or situation is where the ‘belief system’ comes in.

The emotional response is then observed which is the ‘consequence’ of the action is. The aim of REBT is to develop a ‘D’ aspect adding a ‘dispute system’ to replace B, adding an adaptive belief, so the person realises they do not have to be perfect. The therapist will ‘test’ patient’s beliefs with actions which challenge their faulty thinking. Often they can be blunt with clients and not show sympathy in order to avoid reinforcing the problem.

Cognitive therapy (CT) by Beck involves the use of ‘thought catching’ and ‘behavioural activation’. Thought catching involves the observation of client’s thinking and see how their thoughts influence their feelings. This brings around the realisation that even though their thoughts can seem factual, they are often not. Behavioural activation is where the client is encourage to find activities they might enjoy and put themselves in a position where they may have to deal with ‘cognitive obstacles’ so they can see that they are getting better whilst being active.

Butler et al looked at a meta-analyse of the effectiveness of CBT in the treatment of a variety of conditions and found it was ‘somewhat superior to anti-depressants in the treatment of adult depression’. This shows that CBT is highly effective for treating UD as supporting evidence was found across an entire range of data, making the results more reliable due to the large amount of information covered.

However, Holmes reported that in ‘the single largest study’ of treatments for depression, CBT appeared to be less effective than other psychotherapies and drug treatments. It was also pointed out that evidence for the effectiveness of CBT comes from studies of patients who have depression but no other symptoms. This suggests that CBT may be less effective for people who have multiple diagnoses or are considered to have comorbidity. It may be that CBT’s nature is to only focus on one mental illness due to how quick it is compared to other treatments for mental health disorders and therefore isn’t able to relieve all.

In conclusion, the diathesis-stress model would suggest that someone is born with a predisposition for UD but something from their environment must trigger it in order for them to suffer from it. Therefore it makes sense that a physiological treatment such as drug therapy should be used alongside a psychological therapy such as REBT in order to ensure that the treatment does in fact work as Holmes’, Geller’s and Ferguson’s research has shown it may not.

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