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Unit 4 – Section B – Psychology in Action PACK 2 Biological Explanations and Treatments for Depression Specification: Clinical characteristics of depression Issues surrounding the classification and diagnosis of depression, including reliability and validity Biological explanations of depression, for example, genetics, biochemistry Psychological explanations of depression, for example, cognitive and psychodynamic Biological therapies for depression, including their evaluation in terms of appropriateness and effectiveness Psychological therapies for depression, for example, psychodynamic and cognitive-behavioural, including their evaluation in terms of appropriateness and effectiveness This pack will cover the following part of the specification: Biological explanations of depression, for example, genetics, biochemistry Note: Research evidence can be used as part of AO1 (particularly for biological explanations) or as part of AO2. If you use evidence as AO1 (outline), you only need to describe the findings/conclusions. If you use evidence as AO2 (evaluation), you need to explain how the research supports/contradicts the explanation. Biological therapies for depression, including their evaluation in terms of appropriateness and effectiveness 1 Biological explanations of depression: Note from the mark scheme: Genetics – genetic explanations are difficult to describe in detail, so AO1 credit can be awarded for straight descriptions of family, adoption or twin studies (eg McGuffin 1996, Wender 1986) which are used to demonstrate the genetic explanation. Genetics The genetic explanation of depression suggests that we inherit a predisposition towards the disorder from our parents. Depression seems to run in families and a number of studies have shown an increased risk for depression in first degree relatives of people with uni-polar depression. There seems to be a link between the biological closeness of the relationship and the likelihood of developing depression. More recent research has identified an abnormality in the 5-HTT gene in people who are depressed. This gene is responsible for the transmission of the neurochemical serotonin. Low levels of serotonin have been implicated in depression. This means that those who inherit the faulty gene may not produce sufficient levels of serotonin, thus leading to that individual becoming depressed. Research evidence Family studies Gershon et al. (1982) reported the risk for depression to be higher (over 16%) in first degree relatives compared to non-relatives (almost 6%). Weissman et al. (1984) found first degree relatives had a higher risk of suffering depression before the age of 20 (24%) compared to non-relatives (5%). The evidence points to a genetic component that runs in families, particularly for early onset of depression. Twin studies Why study twins and why might twin studies be preferable to family studies? 2 Here is a table showing some of the research on twins in relation to depression. In each case, briefly comment on what the study suggests about genes as a cause for major (unipolar) depression (weak, moderate or strong evidence). Allen et al. 1976 (review of studies) Mean concordance rate MZs 40% DZs 11% McGuffin et al. 1996 MZs 46% DZs 20% Kendler et al. 2006 Largest study, Swedish 42,161 twins including 15,493 complete pairs MZs 38% Females 42% Males 29% Adoption studies Wendler et al (1986) found that the biological relatives of adopted sufferers from uni-polar depression were about 7 times more likely to than adoptive parents to have had the depression themselves. General evaluation points Comment on the concordance rates. To what extent do twin studies support the suggestion that major depression is heritable? 3 Explain why concordance rates are not 100% for MZs or 50% for DZs (as would be expected if the cause of major depression was entirely genetic). It is possible that females are genetically predisposed to suffer depression more than men. However, there could be other explanations. What might they be? Biochemical: Neurotransmitters A growing number of researchers believe that genetic factors influence the amount of catecholamines, a group of neurotransmitters which include noradrenaline [norepinephrine in the US], dopamine and serotonin) in specific sites in the brain. According to the catecholamine hypothesis, depression is caused by an imbalance of brain chemicals. Low levels of serotonin have an effect on noradrenaline and dopamine, all of which are involved in arousal. Serotonin is thought to be involved in depression because drugs that increase serotonin levels reduce symptoms of depression. Serotonin is broken down by an enzyme (mono-amine oxidase). There are a number of possibilities for insufficient serotonin. Delete as appropriate. a) There may be too much/ too little MAO activity, which clears the synaptic cleft of neurotransmitters too efficiently b) Re-uptake of the neurotransmitters may be too efficient /not efficient c) There may be under production / over production of the neurotransmitters d) The receiving neuron may be under sensitive / over sensitive (e.g. not enough receptor sites) 4 Hormones An association has been found between the menstrual cycle and depression. 43% of women in one study suffered depressive symptoms in the pre-menstrual phase. Cortisol might be involved in depression. In one study, 70% of depressed, hospitalised patients had increased levels of cortisol, which is a stress hormone. Further research evidence for biochemical/hormone for depression Wender and Klein (1981) administered dugs to rats which lower levels of noradrenaline; the behaviour of the rats became sluggish and inactive. Mintun et al (2004) used the brain imaging technique of Positron Emission Tomography (PET scan) to compare the brain activity of severely depressed people to a non-depressed control group. Serotonin receptors are shown up in the scan by marking them with the chemical tracer of altanserin. The depressed people had fewer serotonin receptors throughout their brains than the control group. Anti-depressants such as reboxetine decrease depression in humans; they increase levels of noradrenaline by inhibiting reuptake. There have been cases were taking reboxetine has led to mania. While the drug has an immediate effect on the level of noradrenaline in the synapse, they take three to four weeks to work to alleviate the symptoms of depression. Also Prozac (an anti-depressant) has been found to be effective in reducing depression by increasing the availability of serotonin but has no effect on noradrenaline. 5 EVALUATION OF BIOLOGICAL EXPLANATIONS 1. Any of the research above can be used as supporting evidence for the biological explanations, just remember to ground it back to the explanation! 2. Why is it difficult to draw firm conclusions about the role of genes and biochemistry in depression? (Think about the methods of research – AO3) 3. What are the possible consequences of proposing a biological explanation of depression? Try to make both a positive and a negative point: 4. Research suggests that drug therapy alone is not as successful at treating depression as drug therapy combined with cognitive (psychological) therapies. Why does this contradict the view that biology alone is the cause of depression? 5. Explain why the biological explanations of depression fall on the nature side of the nature/nurture debate and why this matters. 6. Are there any useful applications of the research? 6 Biological treatments for Depression Drug treatments & ECT AO1: Drug treatment Drug treatments aim to restore the balance of neurotransmitters, particularly by increasing serotonin levels. Outline how each of these therapies work: Tricyclics (TCAs) SSRIs (e.g. Prozac) Side effects: SSRIs may cause digestive problems but they usually wear off quite quickly. They can cause drowsiness. They can also cause withdrawal symptoms if a person stops taking them suddenly. TCAs: include a dry mouth, constipation, sweating, slight hesitancy in passing urine, and slight blurring of vision. Quite severe, so SSRIs now preferred. ECT (you have studied this at AS) Answer the following questions: What is it? How is it administered? 7 What is it supposed to do for the patient? Who is most likely to receive it? Evaluation: effectiveness and appropriateness of biological treatments Effectiveness of drug therapies: Some psychologists claim that antidepressants do not work and they simply act as a placebo, others claim that they are highly effective; the picture is not clear. Read the article The depressing news about anti-depressants from the VLE for more information on a view of them not working. Effectiveness of TCAs versus SSRIs… Both TCAs and SSRIs have been shown to produce a more significant reduction in depressive symptoms compared to a placebo (Arroll et al.) SSRIs may only be effective in cases of severe depression… Kirsch et al. concluded that only in cases of the most severe depression was there any significant advantage to using SSRIs over a placebo. However… This may be because, among moderately depressed individuals, even the placebo appeared to offer them some hope, which contributed to a lessening of symptoms. For the severely depressed, the expectation of anything working was absent, thus removing any placebo effect. DeRubeis et al. (2005) compared cognitive therapy with drug therapy (an SSRI). After 16 weeks 58% showed improvement in each group. However, Hollon et al. (2005) followed up on the same patients. They studied three groups and were interested in relapse. Cognitive therapy then no further treatment 31% relapse Drug therapy then no further treatment 76% relapse Drug therapy – continuing treatment 47% relapse What does this say about the effectiveness of SSRIs in the long term? 8 Turner et al. claim that there is publication bias with regard to the effectiveness of drugs. What would the publication bias be and why does it matter? Appropriateness of drug therapies: Appropriateness of TCAs and SSRIs… SSRIs have an important advantage over TCAs with respect to tolerability. SSRIs are better tolerated than TCAs, therefore patients are more likely to continue with treatment and recover (Montgomery et al.). Antidepressants are not suitable for children and adolescents… Double blind studies (e.g. Geller et al.) have consistently failed to demonstrate the superiority of antidepressant medications over placebos when given to children and adolescents. There may be an increased risk of suicide… A review of studies (Barbui et al.) found that, although the use of SSRIs increased the risk of suicide among adolescents, the risk was decreased among adults, and particularly so for adults aged 65+ where it appeared to have a protection effect against the risk of suicide. Why drugs may initially be more appropriate than other treatment Why may drugs not be a suitable long term treatment for depression? Effectiveness of ECT Research (e.g. Gregory et al.) have shown that when ECT is compared to ‘sham’ ECT, there tends to be a significant difference in outcome in favour of real ECT. This suggests that there is no placebo effect from receiving ECT. ECT is effective in cases of treatment resistant depression (Folkerts et al.) although other studies have found no improvement following the administration of ECT for treatment-resistant depression (Hussain). There are mixed findings regarding its effectiveness. Given the ethical difficulties associated with ECT, it is questionable whether ECT should be used. Patients may be encouraged to have ECT because it is effective, when that may not be the case. 9 ECT versus antidepressants… A review of 18 studies with 1,144 patients comparing ECT with antidepressant medication showed that ECT is more effective in the short-term treatment of depression (Scott). This suggests that ECT is effective compared with anti-depressants although it may depend on the type of drug offered. Appropriateness of ECT It is considered appropriate for treating depression but not for those suffering from schizophrenia or severe anxiety disorders. However, remember that there can be co-morbidity of disorders (see Diagnosis and Classification), so it may not always be appropriate for treating depression, particularly if it combines with anxiety disorders. Rose et al. concluded that at least one-third of patients complained of persistent memory loss after ECT. A Department of Health report in 2007 found that, among those receiving ECT in the previous 2 years, 30% reported that it had results in permanent fear and anxiety. It may be considered appropriate as a last resort. Why? In cases of severe depression, a person may be sectioned under the mental health act, particularly if they are suicidal, in which case a relative would have to give consent to the treatment. It may be ethical to use ECT if the benefits outweigh the costs. Do you think they do? How do they compare, ethically, with drug treatments? 10