Symptoms and features, two explanations and two treatments of unipolar depression Symptoms and features of unipolar depression

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1 D 3.6 Unipolar depression Symptoms and features, two explanations and two treatments of unipolar depression Symptoms and features of unipolar depression Also known as clinical depression, or major depressive disorder, unipolar depression is a mood disorder, characterised by varying degrees of sadness, disappointment, loneliness, hopelessness and guilt. It is a relatively common mental health disorder, with an estimated 3.5 million sufferers in the UK. Unipolar disorder should be distinguished from bipolar disorder. Whereas unipolar depression is a mood disorder which is seen as a constant disturbance to mood, bipolar disorder involves fluctuations between moods of manic depression and mania, which is not the case with unipolar depression. Other than the depressive emotions listed above, common symptoms of unipolar depression are lethargy (lack of will or energy), permanent anxiety issues and problems with sleep (including waking early or continually through the night and difficulty getting to sleep). Some of the features of unipolar depression are listed below: Depression is twice as common in women as in men, although men are more likely to commit suicide Different people have different courses of the disorder, some are only affected once, for others it is chronic The peak time for depression is between the ages of 50 and 60, although it typically occurs between 30 and 40 People who suffer any form of depression usually live shorter lives, possibly due to a link between depression and heart disease and other stress-related illnesses There are as many as 3.5 million UK sufferers and 20 million American sufferers of unipolar depression One specific subtype of unipolar depression is postpartum depression, for which there is usually no obvious reason. This is a temporary form of unipolar depression which occurs, almost exclusively in women, but also sometimes in men, where distressed mothers suffer severe mood disorders. This is especially distressing for the mother when they have looked forward to having the baby for months. Feelings include guilt, and feeling unable to cope and as though you are a bad parent. Some women can go weeks or months without seeking treatment, and in some cases, even years! It is a very common disorder affecting as many as 1 in 10 new mothers. The monoamine hypothesis: a biological explanation One biological explanation for unipolar depression is the monoamine hypothesis. The monoamines are a group of neurotransmitters which include serotonin, noradrenaline and dopamine. You will recognise the latter, dopamine, from the biological offering of an explanation for schizophrenia. The monoamines are believed to regulate mood. One of the functions of serotonin is to regulate the other neurotransmitters. Without the regulation provided by serotonin, erratic brain functioning and thinking patterns occur. Low levels of serotonin produces low levels of noradrenaline (a neurotransmitter needed for alertness, energy, anxiety and attention to life). Evidence suggests that low levels of noradrenaline cause depression, and high levels cause mania, which suggests it is involved both in unipolar and bipolar depression. Dopamine is also related to feelings of alertness, motivation and attention, and so it is suggested low levels of dopamine similarly are linked to depression. Essentially the monoamine hypothesis suggests that low levels of dopamine and low levels of noradrenaline result in depressive moods, and low levels of serotonin mean low levels of noradrenaline. It can therefore be low levels of dopamine or noradrenaline that result in depression, or a mixture of both. The hypothesis is used to work with drug treatment, so that the correct drugs (antidepressants) can be prescribed based on the particular monoamine in question. In other words, when a clinician is presented with a patient, they will choose the correct drug that alleviates the presented symptoms of depression. Most antidepressants work by increasing levels of serotonin. It cannot be concluded that the explanation for depression is strictly biological. The diathesis-stress model explains how some mental disorders can have a biological underlying cause but require an environmental trigger to become active.

2 Studies have indicated that there may be a genetic link for depression. Although the role of genes in depression is an alternative biological explanation, they share some similarities, and the genetic explanation also offers a diathesis-stress model. McGuffin (1996) studied 214 pairs of twins, where at least one of each twin pair was being treated for unipolar depression. It was found that 46% of the identical twins shared the disorder, and only 20% of fraternal non-identical twins shared the disorder. This indicates a genetic link. Whilst genetic makeup may predispose somebody to develop depression, a stressful life event might be needed to act as a trigger for that depression (diathesis-stress). An evaluation for the monoamine hypothesis for depression is shown below: There is much sound evidence to support the theory, particularly in treatment if the hypothesis suggests the symptoms are due to monoamine deficiencies and drugs which replace those monoamines alleviate the symptoms, there is evidence for the hypothesis Further evidence is seen from studies involving monoamine oxidase inhibitor enzymes, which prevent the inhibition of monoamines, so they can function properly which alleviates depression However, it could be argued that some drugs such as opipramol help relieve depression yet do not adjust monoamine imbalances, reducing the validity of the explanation Furthermore, in some studies, levels of monoamines have been deliberately depleted, which does not seem to reproduce the symptoms of depression Much of the research comes from animal studies, and we must take care when generalising from such data Beck s model of depression: a cognitive explanation A different explanation for unipolar depression comes from the cognitive approach, from Aaron Beck, who is considered the father of cognitive therapy. There are three aspects to Beck s cognitive model of depression: the cognitive triad three areas Beck considered suffered negative automatic thoughts the individual s cognitive errors faulty thought patterns and negative or unrealistic tasks the schemata patterns of maladaptive thoughts and beliefs of the world of the self of the future The cognitive triad The first part of Beck s cognitive model of depression is the cognitive triad. This suggests three areas where there are negative automatic thoughts. The thoughts consist of negative views of the self (feeling inadequate and unworthy), negative views of the world (feeling defeated or deprived) and negative views of the future (believing that your suffering will continue). A sufferer of depression tends to think life will always be that way for them, and that nothing can improve: this comes from the future aspect. The cognitive errors Cognitive errors mean that an individual gives selective attention to the negative side of a situation, and always ignore the positive aspects. Beck described this as the faulty thought patterns. The downside is overestimated so that the most negative conclusion possible is reached when in a situation. Schemata Schemata are built up through experiences of the world, and involve developing positive and negative beliefs and attitudes to interpret the world. A generalised negative belief pattern makes someone vulnerable to depression. A new situation is interpreted through the use of a person s relevant existing schemata, including a self-schemata (for example, if someone is regularly criticised by their parents, they are going to develop a negative set of beliefs about themselves). The way to overcome depression according to the cognitive model by Beck is to change the maladaptive thought interpretations by considering alternative thoughts and interpretations of events. If evidence is presented that there are other interpretations, an individual can change their cognitions. The likely schemata of a depressed person include: cognitive schemata lead a person to seeing actual or threatened loss affective schemata lead a person to feelings of sadness, loneliness and guilt physiological schemata (biological schemata) lead to feelings of tiredness, lack of energy and activity motivational schemata lead to helplessness and a lack of direction behavioural schemata lead to social withdrawal and inactivity

3 The cognitive model is shown in the flow diagram to the right. There is some evidence which supports the cognitive model of depression. Koster et al. (2005) examined the role of attention to negative stimuli in depression. There were 15 depressed students and 15 non-depressed students in the participant sample, and they were each given a selective attention test on a computer screen, where they were presented with positive (e.g. powerful, successful), negative (e.g. loser, failure) and neutral (e.g. paper) words for one and a half seconds each. Half a second after the word disappeared, a square would appear onscreen on either the lefthand or right-hand side, and participants had to press q when it appeared on the left, and p when on the right. Early experiences and interactions with the real world Core beliefs Rules and assumptions (if then ) Trigger Thoughts The time for them to react and press the right key was measured, and it was found that depressed people took an average of 12ms to disengage from negative words, compared to non-depressed students who only took 2ms. This supports Beck s cognitive model as it shows depressed people respond to negative stimuli. Consequences Behaviour Feelings Strengths of Beck s cognitive explanation of depression: Research has shown that depressed people have negative thoughts and that the cognitive model is backed up both by self-report data and other test measures. The model is evidence-based, with many studies supporting Beck s ideas, including Ingram (2001) who found that those with adverse childhood experiences had depression later in life, as the model suggests The theory takes into account other aspects, such as genes, development and early experiences and acknowledges that such developmental issues can lead to certain thinking patterns and core beliefs which lead to depression After treatment for depression, patients biased negative thought patterns seem to disappear, which seems to be evidence for the cognitive model for depression Weaknesses of Beck s cognitive explanation of depression: Strict evidence that shows negative thinking precisely causes depression is hard to find whilst you could argue that since faulty thinking stops when depression disappears this must be in favour of the model, it might also be seen that perhaps faulty thinking and negative beliefs come with depression, rather than are the cause of depression It is difficult from a methodological point of view to distinguish between thinking which causes depression and thinking that is caused by depression, so objective measure is difficult Some studies, such as Dykman et al. (1991) have not shown the cognitive biases Beck suggests, observing that depressed people do not seem to have a distorted perception of their own abilities, and whilst perhaps still focusing on the negative parts of events, they do in fact understand the events accurately, against what the model suggests Drug therapy: a biological treatment Just as with schizophrenia, depression is treatable with the use of drug treatment, from the biological approach. Drug treatment for depression tends to happen in the community: rarely are depressed people hospitalised, unless they are at risk of endangering themselves or others. Antidepressants are used to treat depression, and these drugs usually work by increasing the levels of serotonin in the brain, since some of the symptoms of depression come about due to low levels of serotonin (leading to low levels of noradrenaline). This is how the well-known drug Prozac works, although this is not to say this is strict proof that the monoamine hypothesis is correct, it does provide some sound evidence. Such drugs used to treat depression are called SSRIs (selective serotonin reuptake inhibitors). The SSRIs include drugs like Prozac, and others such as Fluvoxamine and Citalopram, as well as some more modern and less-in-use atypical antidepressants (drugs which target individual monoamines, such as specifically noradrenaline).

4 Another group of drug used to treat depression is the MAOIs (monoamine oxidase inhibitors), which work to prevent the breakdown of the monoamines (serotonin, noradrenaline and dopamine), so in effect achieving the same results: increased levels of the monoamines in the brain. As you would expect, no drug treatment comes without its potential side effects. Side effects of the SSRIs include nausea, insomnia, anxiety, dizziness, weight fluctuations, headaches, fatigue and blurred vision, and the MAOIs have more severe side effects and so are only used as a last resort if other drugs don t work; similarly, another group of drugs, the tricyclic antidepressants, are a subtype of SSRIs which are nowadays outdated, and also have more severe side effects. Treatment of depression with antidepressants has to be withdrawn gradually in order to avoid suffering withdrawal symptoms, which develop with what is known as antidepressant discontinuation syndrome and involve crying spells, insomnia, aches and pains and muscle spasms. Kuyken et al. (2008) In this study, Kuyken et al. compared drug treatment and a form of cognitive-behavioural therapy, finding that a group version of CBT was at least as successful as drug therapy. They divided 123 people with depression into two groups: one continued with their medication, and the other had the psychotherapy (with the option to remain on or come off of their drug treatment). Over 8 weeks, the therapy group met and carried out group exercises, such as how to focus on the present and not the past. About 47% of the CBT participants had a relapse rate over the 15 months after the course had ended, whilst those who had drug therapy alone had a relapse rate of 60% and so it was thought that the person-centred therapy gave the patients skills for life that drug therapy could not. This study showed that whilst drug treatment for depression can be effective, it is not as effective as it could be without having another type of therapy used as well. Antidepressants can be used to boost mood so that other therapies, such as CBT, can take place: without drug therapy these other treatments cannot happen Research is constantly undergoing to find more effective drugs with bigger success rates and fewer side effects (atypical antidepressants, for example, have far fewer side effects than the old tricyclic drugs) Drugs are easy, quick and cheap to prescribe and are the favoured treatment for the NHS The use of antidepressants is based on a scientific hypothesis, generally accepted by psychiatrists Although drugs are cheap and quick to prescribe and are readily available, it may be the case sometimes that doctors prescribe them over other treatments for their own convenience, rather than the good of the patient Drugs are often criticised for only masking the problem, they do not cure the disorder A common effect of discontinuation of drugs, especially with antidepressants, is withdrawal symptoms, which can prove troublesome and may need more drugs to treat the withdrawal symptoms, which is not ideal Patients may forget to take their drugs or purposefully choose not to take them to avoid the side effects Cognitive-behavioural therapy: a cognitive treatment A therapy from the cognitive approach, actually based around the work of Beck, cognitive-behavioural therapy (CBT) which you may have met from schizophrenia also is a person-centred form of psychotherapy used to work with the patient to try and overcome the symptoms of depression, rather than (or as well as) using chemotherapy. Usually it takes place once a week and consists of at least five-to-twenty sessions, progress is reviewed at around 20 sessions. The therapy works to try and help the patient identify negative and unhelpful thoughts and to try and change them. This may involve drawing diagrams for the patients to try and show them the links between their thinking, behaviour and emotions. The rationale of CBT is that our thoughts affect our feelings and behaviour, and so by changing our thoughts, we can make ourselves feel better. Some forms of CBT also focus directly on changing behaviour. The therapy is collaborative, the therapist and the patient will agree on what the patient wants to change. The therapist may then ask the patient to express their negative belief, for example, in relation to their social life. A depressed patient might believe that there is no point in going out as they won t enjoy it: the therapist will try and respond by convincing them that they should try it and will in fact enjoy going out.

5 Stiles et al. (2006) This study looked at cognitive-behavioural therapy and other therapies (one person-centred therapy and psychodynamic therapy) over a three-year period, in 58 NHS settings around the UK. They found that no therapy stood out as being more successful than any of the others, but they were all very effective: there were reductions in relapse rates and improvements according to self-report data. Whilst this study did not show CBT to be any more effective than other psychotherapies, it did prove the therapy to be effective at treating depression. Below is an evaluation for the use of cognitive-behavioural therapy for treating unipolar depression: The individual is helped to recognise any problems and taught how to overcome difficulties, so solutions will be more lasting than therapies outside the patient s control, such as token economy programmes Cognitive restructuring has been used successfully, for example in stress management by having a sense of control and coping mechanisms, a person is better able to deal with stressful situations in real life Studies such as Seligman et al. (1998) and Kuyken et al. (2008) have shown CBT to be particularly effective, especially when used alongside drug treatment The therapy relies on the assumption that the individual can change their own thought patterns and control their beliefs, so this isn t a treatment which everyone will get results from Whilst most studies support CBT as a treatment for depression, many studies have suggested a mix of therapies is more effective A weakness of Beck s cognitive model is that it may be depression which causes negative thoughts, not the other way around and if this is the case, the therapy (based on the rationale changing thoughts changes behaviour) is not going to be effective