All You Need to Know About Depression

ALL YOU NEED TO KNOW ABOUT DEPRESSION

CLINICAL CHARACTERISTICS OF DEPRESSION BE SELECTIVE FROM THE FOLLOWING – THERE WILL PROBABLY ONLY BE A MAXIMUM OF 4 MARKS ON OFFER FOR THIS. Five (or more) of the following symptoms have been present for the same two-week period and represent a change from previous functioning; at least one of the first two symptoms (depressed mood or loss of interest or pleasure) is included in these:  Depressed mood most of the day, nearly every day (as indicated by either subjective report or observation by others). In children and adolescents, this can be irritable mood.

 Markedly diminished interest or pleasure in all (or almost all) activities most of the day, nearly every day (as indicated by either subjective report of observation by others).

 Significant weight loss when not dieting, or weight gain (e.g. a change of more than 5 per cent of body weight in a month), or decrease or increase in appetite nearly every day. In children, consider failure to make expected weight gains.

 Insomnia (not being able to sleep) or hypersomnia (sleeping too much) nearly every day.

 Psychomotor agitation or retardation nearly every day (observable by others not merely subjective feelings of restlessness or being slowed down).

 Fatigue or loss of energy every day

 Feelings of worthlessness or excessiveness or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).

 Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others)

 Recurrent thoughts of death (not just fear of dying) recurrent suicidal ideation without a specific plan or a suicide attempt or a specific plan committing suicide.

 In addition, the symptoms:

- Cause clinically significant distress or impairment in social, occupational, or other important areas of functioning

ISSUES WITH CLASSIFICATION AND DIAGNOSIS OF DEPRESSION BE SELECTIVE – YOU WILL NOT BE ABLE TO WRITE ABOUT ALL OF THESE EFFECTIVELY EVEN IF THE QUESTION IS FOR 24 MARKS. CHOOSE THE ONES YOU CAN COMPETENTLY DISCUSS.  Not everyone agrees that depression should be medicalised. All humans have moods so some people think it is wrong to call it pathology. However, supporters of the medical model say that mood can show extreme manifestations, like other natural biological phenomena such as blood pressure or blood sugar, and can cause illness in some people. We all experience sadness at times but in some cases a depressed mood causes serious impairment of functioning.

 The symptoms of depression as outlined in the DSM criteria could be experienced by a range of people in unhappy situations or with abnormal personalities. A minimum of five symptoms form the DSM are required for diagnosis. One problem is that two individuals could score their five symptoms from a completely different set of alternatives. This means that their depression could look quite different. ALL YOU NEED TO KNOW ABOUT DEPRESSION

 It can sometimes be difficult for clinicians to make the distinction between one type of depression and another. One clear distinction would seem to be between unipolar and bipolar disorder, but even this is not straightforward. About 10 per cent of people diagnosed with major depressive disorder go on to develop bipolar episodes (Coryell et al., 1995). Similarly, someone with dysthymic disorder can have a major depressive episode as well. This is called ‘double depression’ and was observed in about 25 per cent of depressed patients in a large study conducted by the National Institute of Mental health (NIMH) (Keller et al., 1983)

 The diagnostic manuals do not distinguish between endogenous depression and reactive depression. There is little conclusive evidence to support this distinction in terms of the causes of depression (Hammen, 1995) but there do seem to be two fairly reliable different symptom clusters with the so-called melancholic (endogenous) depression characterised by more severe symptoms and a greater likelihood of suicide. Endogenous means that it arises from internal, biological factors rather than as a reaction to something in the person’s life circumstances as in reactive depression). It might simply be that the two types exist along a continuum and that melancholic depression is simply at the most severe end. However, it does seem to have implications for therapy, with melancholic depression responding more positively to ECT and to certain antidepressant medication.

 It can be difficult to determine whether mood disorder symptoms in a patient who has another medical condition (e.g. dementia, cancer, thyroid disorders) are:

 secondary to the effects on the brain of the medical condition (classified as a mood disorder caused by general medical condition)

 secondary to the effects on the brain of drugs used to treat the medical condition (classified as substance- induced mood disorder

 reflective of a primary mood disorder unrelated to the medical condition (e.g. MDD)

 Co-morbidity is often a problem. Depression frequently occurs alongside other disorders such as substance abuse, alcoholism, eating disorders and schizophrenia, and it can be difficult for clinicians to decide which is the primary disorder. Anxiety so frequently coexists with depression that a new category has appeared in the DSM of ‘anxiety not otherwise specified’ that is a mixture of anxiety/depression symptoms.

 While psychiatrists are doctors who specialise in mental disorders, the GP is usually the first point of reference for someone suffering the symptoms of depression. It is estimated that about 3 per cent of the general population in the UK are treated by their GP for depression. However, it has also been suggested that approximately half of the people who go to their GP with depressive symptoms are not recognised as having depression (Goldberg and Huxley, 1992)

 Cultural background should also be taken into account when making a diagnosis. While depression is a universal disorder and symptoms are similar around the world, there are some cultural differences, the most pronounced being between Western and non-Western cultures. As American and western cultural ideals have shaped the construction of both the diagnostic manuals, they are emic constructs. To impose these on other cultures is to assume that here is no difference between cultures. This is referred to as imposing an etic. This assumption that there is no difference or that Western ideals are the correct ones is culturally biased (ethnocentrism). Therefore, when the DSM and ICD are used to classify and diagnose depression in non-western cultures they are an imposed etic and may not be measuring what they claim to be measuring which means they may not be a valid classification tool. If they lack consistency across cultures, they also lack reliability. ALL YOU NEED TO KNOW ABOUT DEPRESSION

BIOLOGICAL EXPLANATIONS FOR DEPRESSION GENETIC FACTORS AO1 Description and outline Research on the heredity of depression within families, shows that some individuals are more likely to develop the disorder than others. Individuals with a parent or sibling with clinical depression are 1.5 to 3 times more likely to develop the condition than those who do not have a close relative with the condition. This suggests there may be some kind of genetic factor in the cause for depression. A genetic factor can be investigated by: Twin studies - Concordance rates can be compared between MZ twins (monozygotic – identical sharing 100% genes) and DZ twins (dizygotic – fraternal twins sharing 50% genes like any other siblings). Research has been less consistent for unipolar disorder but they are still of interest: McGuffin et al., 1996 used the Maudsley Hospital Twin Register and found concordance rates of 46% in MZ twins and 20% in DZ twins. AO2 Evaluative commentary Both of these rates are considerably higher than the normal lifetime risk of developing depression that applies to the general population. However, the concordance rates are never 100 per cent so genetics cannot offer a complete explanation. Twins usually share a very similar life experience (even more so for identical twins who will always be the same sex, maybe dressed in the same outfits and can even pose as each other). There appears to be strong evidence that a predisposition to mood disorders is genetically transmitted (Andrew et al., 1998) but this is likely to be a general predisposition rather than for a specific mental disorder. The diathesis-stress model suggests that certain individuals have a strong genetic predisposition which makes them more susceptible to developing depression when they are exposed to environmental stressors. Kendler et al., 1995 provided support for this model in their Virginia twin study. They found that women who were genetically predisposed to depression (i.e. they had a twin already diagnosed with the disorder) were far more likely to develop depressive symptoms when faced with negative life events than women who were at less risk of depression (i.e. they had a twin who did not have the disorder. BIOCHEMICAL FACTORS AO1 Description and outline Amine Hypothesis - This suggests that depression is caused by low activity of certain monoamine neurotransmitter – noradrenaline. The link between noradrenaline and depression was established way back in the 1950s by accident. A number of drug trials were being done to explore the effectiveness of certain drugs to lower blood pressure. One of these drugs, reserpine also lowered noradrenaline as a side effect. It was observed that participants whose noradrenaline levels were lowered seemed to develop periods of acute depression. This suggested that low levels of noradrenaline may be implicated in depression. AO2 Evaluation of the catecholamine hypothesis. There is a great deal of research that supports the catecholamine hypothesis. However, much research also contradicts Schildkraut’s hypothesis. While there does seem to be a relationship between low levels of noradrenaline and MDD, levels of noradrenaline do not affect the moods of everyone in the same way, if they affect them at all. This variability can be further seen in sufferers of depression who are prescribed drugs which increase the levels of noradrenaline in the body, but have little effect on the depressive disorder. AO2 Support for this idea has come from the effectiveness of drug therapy  Antidepressant drugs such as tricyclics and MAOIs, which work by increasing the available amount of noradrenaline and 5HT (serotonin receptors) in the brain were found to be effective in alleviating the symptoms of depression.  Selective Serotonin Reuptake Inhibitors (SSRIs e.g. Prozac) work by increasing the availability of serotonin and work well for some people in reducing the symptoms of depression. They have a negligible effect on noradrenaline.

 Conversely, depression is an unwanted side-effect of reserpine, a drug used to treat high blood pressure, which acts by depleting levels of noradrenaline.

Such findings led to the idea that depression is simply caused by a depletion of the amines, primarily noradrenaline and serotonin, while mania is caused by too much of these amines. However, it now seems that the mechanism is more complex than that. One problem for the original theory is that antidepressant drugs do not simply target these particular ALL YOU NEED TO KNOW ABOUT DEPRESSION neurotransmitter levels – they have other effects in the brain as well. This means that we can’t be sure that it is the change in the neurotransmitter levels that accounts for the effectiveness of the drug. It follows that we cannot conclude that these neurotransmitters cause the depression in the first place. Another problem to consider is that they exert an immediate effect on neurotransmitter levels but take several weeks to have an effect on the mood symptoms of depression. It is also the case that newer, equally effective antidepressant medications do not work by increasing neurotransmitter availability in the same way as the first generation of drugs. These problems with the simple, basic theory have led researchers to suggest that depression arises from a much more complex interaction of neurochemical factors. Research into the amine hypothesis continues, but the precise link to depression is not yet clear. It could even be the case that the dysregulation of the amine system is the result of depression rather than the cause. BIOLOGICAL TREATMENTS FOR DEPRESSION INTRODUCTION The most widely used treatment for depression is chemotherapy, i.e. the use of antidepressant drugs. Effective drug treatments for depression developed rapidly in the 1960s with the introduction of two groups of drugs.  AO1 Monoamine-oxidase inhibitors (MAOIs)

These work by inhibiting the work of an enzyme (Mono-amine oxidase) which flushes neurotransmitters such as serotonin and norepinephrine (noradrenaline) out of the synapse like a waste product. MAOIs reduce this action which means that there is more availability of these neurotransmitters in the synapse.

AO2 Effectiveness and appropriateness

They are effective, and are still used for severe cases of depression, but they have severe side-effects if taken with certain food and drink, e.g. marmite, red wine. This is due to the fact that blood pressure is raised which can result in death. For this reason they are not used so much now and patients taking them have to be carefully monitored. Adolescents are not usually prescribed MAOs as they may not monitor their diet so carefully. Sometimes they are used when other drug treatments have failed and/or the patient is hospitalised and their diet can be controlled.

 AO1 Tricyclic antidepressants

These drugs work in a different way by blocking the reuptake of neurotransmitters like norepinephrine (noradrenaline) and serotonin so that more remains in the synapse. The end result is the same – there is more neurotransmitter available to pass to the next neurone. AO1 Later, a new class of drug was discovered - Selective serotonin reuptake inhibitors (SSRIs) These work in the same way as tricyclics but they target serotonin specifically and have fewer side effects.

AO2 Appropriateness of drug therapy in the treatment of depression The development of anti-depressant drugs was welcomed when they first appeared. They were thought of as a quick, easy and cheap alternative to lengthy psycho therapies. However these features are also their downfall as they are becoming over prescribed. While they might offer hope to some, they only treat the symptoms; the root causes of the depression may remain so that when the patient comes off the medication, the low mood may return. Depressed individuals usually have to continue to take drugs for some time after they have shown improvement. This ‘maintenance therapy’ (Kessler et al, 2002) significantly reduces the rates of relapse. However, anti-depressant drugs are not thought to be addictive (unlike tranquilizers). If addiction does occur, it is only in a minority of people. Nevertheless, it is advisable to come off them slowly and under medical supervision. A number of studies have reported a much higher rate of reduction of symptoms for drugs compared to placebos – more than twice as high (Thase and Kupfer, 1996). However, depression covers a wide range of symptoms which may respond differentially to different treatments and so the same drug doesn’t work for everyone. One of the main problems of using drugs as a treatment for depression is that scientists don’t really know why they work. One curiosity is that serotonin levels are altered immediately by the use of SSRIs and yet symptoms may are not usually ALL YOU NEED TO KNOW ABOUT DEPRESSION relieved for a couple of weeks or even longer. This suggests that there is something else involved apart from the serotonin levels. All of the drugs have potential unwanted side-effects e.g. drowsiness, nausea, decreased sex drive etc. These are far less severe with the more recent SSRI drugs and disappear fairly soon. It seems clear that very few, if any, depressions arise solely from biological factors. Antidepressants seem to be quite effective in reducing some of the symptoms of depression, but they can have no effect on the life circumstances of the individual. For this reason, drug therapy is often combined with various psychological interventions.

ELECTRIC CONVULSIVE THERAPY (ECT) AO1 ECT was first introduced as a therapeutic technique in the 1930s. It was frequently misused and caused physical and emotional damage to many patients. However, its use today is highly controlled and it is administered under considerably safer conditions. Patients are given sedatives and muscle relaxants. Electrodes are attached to the scalp and a small electric current is passed through the brain for a fraction of a second inducing a convulsion that lasts for approximately one minute. When the patient comes round from the anaesthetic, they will normally have no recollection of the treatment. Clinicians differ in the precise way that they administer the procedure. For example it is not clear exactly how much current should be passed through the brain or whether the treatment is effective when electrodes are only placed on one side of the head instead of both. Similarly there is variability in the number and regularity of treatments offered within a course. A double-blind study (Lerer et al, 1995) comparing the efficacy of the treatment when given twice or three times weekly found little difference in clinical outcomes but there were fewer cognitive side-effects in the twice- weekly programme. It is thought that ECT increases the availability of monoamines e.g. serotonin and norepinephrine (noradrenaline) and that it reduces blood flow in the frontal temporal regions, but the precise mechanisms are unclear. It is extremely effective in cases of severe depression particularly where there are psychotic features or suicidal intent (Sackheim and Rush, 1995). AO2 Effectiveness There are contradictory findings regarding the effectiveness of ECT. Rey and Walter (1997) claim that up to 70% of patients with severe depression get relief with ECT. On the other hand, Schwartz (1995) says that 85% of those who are initially helped by ECT relapse, so any benefits can be short-lived. This is supported by Breggin (1997) who found that ECT may have some benefits to certain patients, but that these benefits do not generally last for more than four weeks. Overall, research indicates that ECT is successful for some individuals with depression, although it is often a last resort. For severe cases where the sufferer is suicidal it is thought that ECT has saved many lives as it is fast acting compared to drugs. When compared with sham ECT the real treatment is more effective (according to Buchan et al, 1992) but only when the patient suffers delusions as well as depression (which is rare). Buchan concluded that ECT has few benefits.

AO2 Appropriateness ECT remains a controversial treatment because it is an invasive assault on the brain and no one is entirely clear how it works. Although modern techniques have eliminated some of the more serious side-effects associated with ECT, there is some evidence that it causes short-term memory loss. There is some disagreement about this. Rogers et al (1993) state that about one third of patients receiving ECT report the experience as distressing and say that they have experienced significant memory loss as a result of their treatment. However in a review of research in this area, Devanand et al (1994) found no convincing evidence that ECT causes long-term memory deficits or that it causes any structural brain damage. There are also ethical considerations with the use of ECT. Although informed consent should be given before this treatment is carried out, it is questionable whether severely depressed people really understand the procedures or the implications of the treatment.

PSYCHOLOGICAL EXPLANATIONS OF DEPRESSION

1. PSYCHOANALYTIC THEORIES

Freud’s original view was set out in his essay ‘Mourning and Melancholia’ in 1917. Freud related the origins of depression back to the first stage of development, the oral stage. This stage is characterised by dependency on the caregiver. Individuals whose needs are not met by parents during this stage become fixated and are inclined to be excessively dependent on other people this dependent personality style makes them particularly ALL YOU NEED TO KNOW ABOUT DEPRESSION vulnerable to depression. They spend much of their time and energy on seeking the love and approval of others, often at considerable personal cost. They also become angry when their needs are not met, but this anger is turned inwards. This is an unconscious process and the individual does not recognise the emotion as anger and certainly does not connect it with anger towards the parents. If an actual loss occurs in later life e.g. the death of a loved one, or a symbolic loss such as being made redundant from a job, the individual feels the loss more acutely than other people and may regress to the oral stage. The individual feels anger at being deserted, but turns the anger inwards because the outer expression of anger is unacceptable to the superego.

AO2 Freud’s theory was important for stressing the role of early experience in creating a vulnerability to depression and this idea is central to other psychodynamic and cognitive theories.

There have also been studies which have shown that depressed people show more anger than controls who are not experiencing depression, but this is overt anger rather than anger turned inward as predicted by psychoanalytic theory.

Bifulco et al, 1987) found some support for the idea that the loss of a parent to death or divorce can be linked to later depression.

There is also some evidence for the idea that a set of dependent personality traits characterise people with depression. However, these traits appear to fluctuate with the level of depression so they might be an effect of the disorder rather than a cause

There are links here with Bowlby’s attachment theory. He believed that insecure parent-child attachments or separations could lead to later depression and this supports Freud’s theory about the importance of early child/parent relationships especially with the mother. Studies of depressed adolescents (e.g. Hammen et al, 1995) provide evidence for this.

A key problem with Freud’s ideas is that many of the concepts are not defined well enough for clear cut hypothesis to be formulated and tested. It does not necessarily mean that his ideas are wrong, only that they cannot be rigorously tested.

2. BECK’S COGNTIVE THEORY

Aaron Beck (1967, 1976) claims that depression is a disorder of thought, rather than of mood – the depressed individual thinks about themselves, the environment and the future in pessimistic terms. Beck originally trained as a psychoanalyst and believes that the foundations for depression are often laid in childhood. As a result of early traumas and unhappy experiences, the individual develops negative schemas or core beliefs that lead to negative automatic thoughts (NATs). These are habitual ways of thinking which arise spontaneously without deliberate choice and are constantly critical and derogatory.

When faced with stressors such individuals tend to apply faulty logic to their interpretation of events. Beck calls these errors of logic cognitive distortions or biases for example minimising successes and maximising failures or picking out the negative aspects of an event and focusing on that.

Certain stressful situations tend to trigger memories in the individual of the circumstances which fist led them to acquire negative schemas. For example, a child who was frequently criticised and corrected for making mistakes might develop a schema about being incompetent. If in later life the individual’s performance at ALL YOU NEED TO KNOW ABOUT DEPRESSION work is criticised, this schema is reactivated – he/she is reminded of past failures and now expects only failure in the future too.

AO2 Cognitive theories of depression have been extremely influential and have stimulated huge amounts of research that have contributed to our understanding of the disorder and how to treat it. They have given rise to a range of therapies and, on the whole, these seem to have been very helpful for people with depression. Beck’s later idea that individual personality differences can predict the type of event that triggers depression could be used to explain some of the different symptom sub-types.

However, it is difficult to determine the extent to which distorted cognitive patterns cause depression. Numerous studies (Gotlib and Hammen, 1992 review) have sown that depressed people do show more negative thinking than the controls. However, as yet there is no convincing evidence that such thinking precedes a depressive episode. It seems likely that negative thinking is a consequence of depression and that it might well serve to maintain the disorder rather than explain its origins. It is therefore impossible to be sure that negative thinking is the cause of depression as it might be the effect of it instead.

PSYCHOLOGICAL TREATMENTS FOR DEPRESSION 1. PSYCHOANALYTIC THERAPY Psychoanalytic therapy was developed by Freud in the late 1800s. The aim of the therapy is to bring to consciousness repressed wishes and painful memories from childhood, in the process making the client aware of the unconscious causes for their symptoms. The goal of classical psychoanalysis is to allow the client to work through their intensive depressive and angry feelings and to find more realistic standards for self- evaluation. It also allows them to develop more appropriate internal working models for relationships.

Several techniques are used such as free association, dream analysis, projective tests etc. And underpinning the whole process is transference in which self-directed hostility and criticism and ideas of abandonment and loss of autonomy are projected onto the therapist. The therapist helps the client to interpret this transference by pointing out the similarities between the patient-parent relationship and the patient analyst relationship.

Ao2 Effectiveness and appropriateness There is some evidence from controlled trials that brief psychodynamic psychotherapy is an effective treatment for people with depression (Holmes, 1999), but it is not appropriate for everyone.

Psychodynamic therapy is expensive and takes place over a long period of time. Some key clinical characteristics of depression such as a sense of helplessness, low motivation, self-esteem and apathy make it very unlikely that a depressed person would ‘last the course’. Since psychoanalysis depends on the client wanting to know where their illness has come from, a depressed person who has little or no interest in the causes of their problem is unlikely to benefit from analysis. Concerns have been expressed about the appropriateness of using psychodynamic therapy with depressed individual. Because depressed people tend towards dependency on others, the nature of the client/therapist relationship may be unsuitable and may foster more dependency which may be inappropriate. It has been claimed the likelihood of recovering from a mental disorder is less with psychoanalytic treatment than without. In a classic critique of psychoanalyst therapy, Eysenck (1952) gathered evidence from outcome studies which showed that people on a waiting list for therapy were more likely to recover spontaneously from their symptoms than those actually receiving treatment. He compared the results of 24 studies, to see if psychoanalysis was more likely than other forms of therapy to result in positive mental health changes. He ALL YOU NEED TO KNOW ABOUT DEPRESSION found that whilst patients did recover with psychoanalysis, the rate was comparable to that experienced without treatment, and that psychoanalysis was less effective than behavioural therapies. For Eysenck, the conclusion was quiet clear – psychoanalysis does not work. It has since been suggested however that Eysenck was rather selective in the choice and analysis of his data. Bergin (1971) re-examined Eysenck’s data and reached the opposite conclusion- whilst some people do indeed spontaneously recover without treatment psychoanalysis was over twice as effective as no treatment at all.

According to Grunbaum (1993) any apparent benefits of psychoanalysis are the result of unintended placebo effects. Basically, it is the action of being treated itself that results in improvement, not actually what the psychoanalyst does, that leads to improvement. The reason why psychoanalysis might lead to a cure is that the client is in a powerful relationship with the therapist. Part of the power of a therapist is that they can never be wrong: for example, should the patient challenge the therapist then their challenging behaviour could be interpreted as just another symptom of their disorder. This means that the client is under strong pressure to conform to the therapists’ expectations. Grunbaum also points out that the very earliest evidence for the effectiveness of psychoanalysis is flawed. Freud himself only ever presented 12 cases of psychoanalysis for public scrutiny, and none of these was fully evaluated in terms of outcomes and benefits to the client. Traditional forms of psychoanalysis have not generally been considered effective treatments for depression. However, research into the success of more modern forms of the therapy has been more positive in this regard. Elkin et al (1989) for example found that a more modern form of psychoanalysis called interpersonal psychodynamic therapy compared favourably to cognitive behavioural therapy.

1. COGNITIVE-BEHAVIOURAL THERAPY (CBT) This therapy was developed by Beck and is based on his theory of depression. It aims to identify and alter negative beliefs and expectations (the cognitive element) and to alter dysfunctional behaviours that are contributing to or maintaining the depression (behavioural element). The therapy is intended to be relatively brief consisting of about 20 sessions over 16 weeks. It is an active, directive therapy which focuses on the here and now although, in the initial session, the therapist often asks for background information about the past to throw some light on current circumstances there are several aspects to the therapy including behavioural activation, graded homework assignments, thought-catching, cognitive restructuring and problem solving. Behavioural activation is a technique for encouraging the client to identify pleasurable activities and to overcome obstacles in carrying them out. Graded homework assignments are given to allow the client to experiment with the activity and to engage in progressively more rewarding activities. Thought catching is a technique that encourages the client to record their own thoughts and feelings and, with the help of the therapist, to challenge these thoughts when they are unhelpful. The client keeps a written record usually divided in to three columns and the therapist teaches techniques for challenging the negative thoughts, e.g. ‘What is the evidence?’; ‘Is there another way to interpret the situation?’; ‘What is the worst thing that could happen?’ Once the therapist has addressed the ‘surface’ negative thought, he or she will start to challenge and dispute deeper core beliefs, e.g. ‘If people ignore me or do not like me, it means that I am worthless’. For example if a client has had a bad day because someone they saw while out shopping ignored them the therapist might help them to understand that the automatic negative thought behind this is that the person doesn’t like them which makes them feel rejected. The challenge might be that maybe the person was preoccupied and didn’t actually see the client at all. Where appropriate the therapist will also teach practical techniques such as improved conversational skills.

Ao2 Effectiveness of CBT There have been numerous studies that have shown that CBT is effective in reducing symptoms of depression and in preventing relapse: (Kuyken et al 2007).

A number of studies have also compared the effectiveness of CBT with antidepressants and other types of psychotherapy. Findings are not conclusive and studies have been beset by methodological and sampling problems. However, CBT appears to be as effective as medication in reducing symptoms of depression in the acute phase and some research (e.g. Fava et al 1994) has shown that CBT is superior to drug therapy in treating the residual symptoms, i.e. the symptoms that remain after a medication programme.

CBT is often used effectively in conjunction with antidepressant medication. For example in a large comparison study (Keller et al 2000) found that recovery rates were: ALL YOU NEED TO KNOW ABOUT DEPRESSION

56 %r cent using the drugs alone, 52 % using CBT alone, 85 % when the two therapies were used in combination.

It is difficult to predict which clients will respond well to CBT. Research is inconclusive, but it appears to be suitable for both severe and milder forms of depression. However, Simons et al, 1995 found that CBT is not effective for people who have high stress levels in response to genuinely difficult life circumstances that brief therapy cannot resolve.

AO2 Appropriateness of CBT The client undergoing CBT is a more active participant than is possible with biological treatments and needs to commit themselves to the therapy. This can be a positive aspect as the commitment and cooperation required can result in effort on the part of the client which may motivate them and help to lift the depression. On the other hand, the kind of effort involved may not suit a severely depressed person who is apathetic.

CBT therapy is not physically invasive and therefore does not have the difficulty of side-effects or addiction. However, clients do sometimes become dependent on their therapist and the effectiveness of the therapy depends on client cooperation. CBT is not always available on the NHS and if it is, there is often a waiting list. This is not helpful if someone needs immediate help. Furthermore, even if CBT is readily available it may be several weeks before the effects of it are evident. It is quicker than psychoanalysis, but medication may be a quicker solution. The client is provided with techniques to help themselves which may be used in the future if depression threatens to re- occur. This can mean that the client does not relapse in the same way as they might if they were to just take medication. CBT provides long-term coping mechanisms.

Previous exam questions

Note that from 2012 questions will be out of 24 marks rather than 25 (Split 8 AO1 and 16 AO2 marks)

Jan 2010

a) Outline clinical characteristics of depression. (5 marks)

b) Explain issues associated with the classification and/or diagnosis of depression.

(10 marks) ALL YOU NEED TO KNOW ABOUT DEPRESSION

c) Outline and evaluate one biological therapy used in the treatment of depression. (4 + 6 marks)

Jun 2010 a) Outline at least one biological explanation of depression and at least one psychological explanation of depression (9 marks) b) Evaluate biological and psychological explanation s of depression. (16 marks)

Jan 2011

Outline and evaluate two or more psychological therapies for depression. (9 + 16 marks)

Jun 2011

Discuss biological therapies for depression. (9 + 16 marks)