Affective Disorders (Depression)
Disorders of affect (emotion) are probably the most common form of psychological disturbance. Whereas it can be hard for us to understand and imagine the symptoms of schizophrenia, we are all familiar with the symptoms of depression, and we all have had some experience of 'low mood' at many points in our lives. However, it is perhaps precisely because it seems more familiar, that people with major depression still feel misunderstood, as we often feel that people should be able to 'snap out of it' like we might do with a bad mood. For the 15% of people who it is estimated will have a major depressive episode at some point in their lives, this is not a condition that can be easily shaken off...
Symptoms and prevalence of major depression
Types of abnormal affect conditionsDepression is the main symptom of a number of mood disorders, which include the following.
Major depression (Unipolar) Manic depression (bi-polar) Seasonal affective disorder (SAD) Far less studied and seemingly much rarer is the opposite of depression... unipolar mania! For this unit, however, we will focus entirely on major depression. |
Prevalence - sex differences in depressionIn adults, major depressive disorder affects twice as many women as men. For both genders it is most common in those who are 25-65 years of age, and least common for those over the age of 65. In children, clinical depression affects girls and boys at about the same rate.
What is not clear is whether this sex difference is due to nature or nurture factors. For example, a nurture explanation could be that females typically have more stressful lives in many countries (due to inequalities between genders, a lack of social status and so on) and this may contribute to higher levels of depression. A nurture explanation would suggest that some biological difference between men and women (perhaps due to genetic or hormonal factors) affects the likelihood of acquiring the condition. Gender differences in depression are also explored in this useful InThinking worksheet.
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Unipolar depression (major depression)
Unipolar depression is the term used when a person’s mood changes from normal to depressed. People suffering from this type of depression are usually aware their mood has changed and will seek help or make a spontaneous recovery. Unipolar depression can be divided into two different types:
1) Reactive – caused by factors external to the person such as stressful life events, bereavement, divorce etc. This is the type that people are most likely to experience.
2) Endogenous – caused by factors within the person such as genes or brain chemistry
1) Reactive – caused by factors external to the person such as stressful life events, bereavement, divorce etc. This is the type that people are most likely to experience.
2) Endogenous – caused by factors within the person such as genes or brain chemistry
Diagnosis of Unipolar depressionMay appear gradually or suddenly and it occurs in all social classes and all ages. Severe forms mostly occur in middle and old age. In the UK more women than men are diagnosed. But the male suicide rate is much higher than the female rate.
Depression can be diagnosed through clinical interview and use of DSM-IV and ICD-10, which are manuals used in the clinical diagnosis of psychological/psychiatric disorders. There are several factors that the clinician must take into consideration: · Five of the physical, emotional, cognitive, behavioural and social symptoms to occur along with persistent low mood for a minimum of two weeks
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Difficulties in diagnosing depression· Many of the symptoms reported by those suffering mental illness are very subjective (e.g. I feel depressed) – reliant on self-report by the client.
· The reliability of diagnosis may be questionable as DSM-IV and ICD-10 are based on the assumption that we can assign individuals neatly into categories. However, many of the symptoms of depression for example, are found in much of the population. · There may be cultural, social and gender biases in diagnosing people according to classification systems which are devised by western practitioners. Notions of abnormality vary across groups and time (see the 'Concepts and Diagnosis page'. Two great examples of cultural variation in diagnosis of depression are given on that page - 'brain fag' and 'neurasthenia'. You can use them to discuss cultural variations in the prevalence of depression. |
Implications/Consequences of being diagnosed with depression
· Once a person has been classified as having a mood disorder a suitable treatment can be decided upon. Patients therefore get access to specialist help.
· A diagnosis of mood disorder can lead to labelling. The stigma of a psychiatric diagnosis may create expectations in the person and others. · There are also issued to be considered concerning the person’s safety. Doctor’s need to assess whether the person is at risk of suicide and if they feel they are, they would need to section them under the mental health act. In turn, this leads to ethical issues pertaining to consent and enforcing treatment. |
NOW STOP and think like a psychologist! These issues reoccur!!The difficulties and implications with diagnosing depression are often the same as with diagnosing any psychological condition! You can reuse the same ideas to answer different questions, as long as you adjust the point you're making to the specific question being asked.
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Assignment 1 - Test your memory(a) Explain what is meant by the term ‘abnormal affect’.
(b) Describe two types of abnormal affect. Assignment 2 - ERQAlthough there are no SAQs in the Paper 2 exam, you can still be asked them as a part of a longer ERQ. For example:
Describe the symptoms and prevalence of one psychological disorder. Discuss cultural and/or gender variations in the prevalence of one psychological disorder. (22) This may seem like a difficult question at first... but you can also reuse loads of the material from the 'Concepts and Diagnosis' page here! There IS enough to say if you think carefully.
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Etiologies of major depression
Etiology (or aetiology if you're British) means the set of causes for a particular condition. Here we will look at three main explanations suggested for the causes of depression; biological, cognitive and diathesis-stress/sociocultural.
Biological explanations of depression - genetic
Assignment 3 - interpreting research evidenceAbove is the abstract of a research article into the genetics of depression. Summarise what you think these findings show (in your own words) and bring them to the next lesson.
Traingulating evidence... what about Caspi et al (2003)? |
McGuffin et al (1996)AIM – To examine the impact of genes on unipolar depression.
METHOD – 177 people with unipolar depression and twins of the same sex were recruited. RESULTS – Concordance rate of 46% for 68 pairs of MZ twins. For 109 pairs of DZ twins it was 20%. Assignment 5 - You draw the conclusionWhat conclusions can you draw from the above study. Make the inferences you draw as detailed as possible and try to consider both what the data shows and what it doesn't show! Write your conclusions down and send them to me.
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Twin, family and adoption studies in genetic research
The direction of causality - a major issue in mental illness researchAs you can see from the evaluation issues to the right, it is sometimes hard to tell what causes what in psychological illness. We are left with a 'chicken and egg' scenario, where we know that things have changed, but do not know exactly what has caused the change.
This is a major problem for lots of research. For example, if we find that a person with a condition has unusual neurotransmitter levels (see below), we don't know if the condition caused the neurotransmitter levels or if the neurotransmitter levels caused the condition! It is therefore an evaluation issue that you can use repeatedly in your essays, providing you understand it and link it clearly to the topic you have been asked about! |
Evaluating the genetic explanation
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Biochemical explanations for major depression
You should remember from studying neurotransmission in BLoA that the brain produces chemicals to pass messages between different parts of the brain and nervous systems. The biochemical explanation for depression argues that depression involves the neurotransmitters serotonin and norepinephrine, both of which play a role in appetite and emotion. Lower levels of these chemicals may lead to depression.
Study - Teuting (1981)AIM: to investigate any abnormalities in the urine samples of depressed persons
METHOD: when norepinephrine and serotonin are broken down by enzymes, a chemical compound is present in the person’s urine. Teuting compared the urine samples from depressed and non-depressed people. RESULTS: There were lower levels of the chemical compound in the depressed samples urine in comparison to the non-depressed group. CONCLUSION: this suggests that depressed people have lower than normal activity of NTs in the brain which causes the depressed mood. EVALUATION: difficult to establish cause and effect (AGAIN!) - SEE ABOVE. Criticism of biochemical explanations for depression· Anti-depressants do not work for all patients. Also, the drugs increase the levels of the biochemicals immediately but can take weeks for the depression to be alleviated. Why is this? This seems to challenge a direct link between NTs and depression.
· Cause, effect or correlation? It is difficult to establish whether the low levels of NTs cause depression, are an effect of having the disorder or are merely associated with it. Causation cannot be inferred as only associations have been identified. · The (partial) success of treatments which block serotonin receptors doesn't necessarily mean that serotonin caused the condition in the first place. This is the treatment aetiology fallacy (sometimes also called 'backwards reasoning')! Taking paracetomol relieves a headache but does not mean the headache was cause by a lack paracetomol. This is an issue for ALL DRUG TREATMENTS! |
Other evidence supporting a biochemical explanation for depression· The 2 neurotransmitters that are thought to be involved in depression, norepinephrine and seratonin, are part of the ‘monoamine group’ that play a role in normal arousal and emotion. That these NTs would be involved in depression therefore seems to have face validity.
· Anti-depressant drugs (MAOIs) which increase levels of norepinephrineand serotonin are often successful at reducing the symptoms of depression as do SRRIs which inhibit the re-uptake of serotonin. |
Assignment 6 - Memory test
a) Explain, in your own words, what is meant by a biological explanation of depression
(b) Describe a study investigating the biological explanation of abnormal affect
(b) Describe a study investigating the biological explanation of abnormal affect
Beck's cognitive theory of depression
Beck (1987) proposed that people with depression develop negative schemas; they tend to view the world and the future in pessimistic ways. These can become self fulfilling prophesies. Beck (1991) maintains that there are three components to depression:
He called these the cognitive triad. Thus the person sees him/herself as: 1. Worthless 2. Living in a world full of obstacles 3. Contemplating a future continuing in much the same way. The cognitive triad can lead to errors in judgement known as ‘cognitive errors’ such as magnification, minimisation and personalisation, underemphasising strengths and exaggerating weaknesses. |
Evaluating cognitive theories of depression
REVISION - Quizlet on cognitive explanations for depressionHave a go at this quizlet on cognitive explanations for depression.
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Assignment 7 - Memory testa) Explain, in your own words, what is meant by a cognitive explanation of depression.
(b) Describe a study investigating the cognitive explanation of major depression |
Socio-cultural factors in depression: the Diathesis-stress Model
The diathesis-stress model is a way of explaining how people end up suffering from mental disorders by assuming that mental disorders come from the interaction of two things, genetics and life experience (nature and nurture). It highlights the importance of SOCIAL factors, as well as biological and personality ones, in the development of any abnormality condition
Using the example of depression, two people are born with a genetic predisposition for depression. One of them has a normal upbringing and life, so despite this genetic predisposition, never actually develops it. The other however may suffer some event that combined with the depression genetic trait pushes them 'over the edge' and they end up with depression.
Using the example of depression, two people are born with a genetic predisposition for depression. One of them has a normal upbringing and life, so despite this genetic predisposition, never actually develops it. The other however may suffer some event that combined with the depression genetic trait pushes them 'over the edge' and they end up with depression.
Major life events, such as bereavement, unemployment, divorce and serious illness may be significant precipitating factors in reactive depression (though less so in endogenous depression).
Zubin and Spring (1977) suggested that we inherit a vulnerability to a disorder, which could be revealed by certain events (precipitating factors). Brown & Harris (1978) identified two types of these precipitating factors for depression – severe life events and vulnerability factors (lack of paid employment outside the home, two or more children under the age of 5, early loss of mother, lack of close relationship etc). The diathesis-stress model has received a great deal of support - such as from Caspi et al (2003). Life events may be precipitating factors which interact with other vulnerability factors such as genetics and early experiences. This model supports an interactionist view – the idea that mental illness is the result of a combination of biological and environmental factors. |
STOP AND THINK... WHERE CAN YOU USE THIS EVIDENCE?The Brown and Harris (1978) study is very influential in a number of ways. It helps us to explain depression from a sociocultural perspective, avoiding the reductionism of just using one explanation... BUT IT CAN BE USED FOR MORE.
Another of your learning objectives is 'discuss cultural gender variations in prevalence of disorders'. Look at the stressful 'precipitating factors' that they list... are some of them gender specific? Can this be used to possibly explain why Kessler et al (2005) and other have found that depression rates were higher in women than men (see 'prevalence' section above)? Can we also use this to explain why Marsella (1995) found higher levels of depression in urban settings? |
USE STUDIES CAREFULLY, AND BE AWARE THAT THEY CAN BE APPLIED TO MORE THAN ONE ARGUMENT! If you want more information, then this free page on the InThinking site has lots of useful detail and more studies to compare.
Assignment 8 - SAQ1 page from memory (about major depression):
(This would be a good starting point for an ERQ asking you to evaluate etiologies) |
Assignment 9 - SAQ with alternative command term
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Implementing Treatments for Depression
Biomedical, individual and group approaches to treatment
Examining the assumptions of treatment options for depression
Each approach has its own assumptions about the aetiology of the condition that it is trying to treat. Your ideas about where the condition comes from will naturally influence the treatment that you try to design for it. If you think that depression is purely a neurochemical imbalance, you will be more likely to prescribe a drug therapy than cognitive therapies, for example. One major assumption that comes out of this, which you could mention in an 'examine' essay, is that each therapy assumes that it is targeting the underlying cause of the condition.
Biomedical treatments for depression - drug therapy
Exam Hint!!! Think like a psychologist and know the links!Although the actual drugs given to treat different psychological conditions vary; how they actually work and the evaluation issues around them have a lot of features in common. If you know them well, you can use the same issues in essays on ANY biological/drug treatments! Before you read this section, look back at the way that neurotransmission works.
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You should remember from the above section on biological explanations, that the biochemical explanation for depression suggests that the condition is the result of low levels of serotonin and norepinephrine. If so, it follows that an effective drug therapy for depression
might involved using drugs that increase the supply of these
neurotransmitters. See the video to the right for an introduction to how this might happen.
Both serotonin and norepinephrine belong to a group of neurotransmitters called monoamines. Drug therapy is the most commonly used treatment for depression. Two of the most common drugs used are SSRIs and MAOIs. |
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SSRIs (selective serotonin reuptake inhibitors)SSRIs are specific to serotonin. For example, fluoxetine (trade name Prozac) prevents the re-uptake of serotonin by the presynaptic neuron, so leaving it to have an enhanced effect on the postsynaptic neuron.
SSRIs are currently the most widely used anti-depressant drugs (often used in cases of bipolar disorder as well as major depression) |
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MAOIs (monoamine oxidase inhibitors)Monoamine Oxidase (MAO) is an enzyme which normally breaks down monoamines at the synapse. MAOIs block MAO, thus the monoamines remain longer in the synapse and continue to act on the postsynaptic neuron.
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The InThinking site has a free page on biomedical approaches to treatment which also covers the information given here, and the evaluations below. Read it and then answer the questions at the bottom of the page FROM MEMORY.
Evaluating drug treatments for depression
Assignment 9 - Video analysisThe video to the right is a very nice, not too detailed look at some of the controversies surrounding the use of anti-depressant medication (and, by extension, many of the issues surrounding drug therapy as a whole).
Many of the key evaluation ideas that we have looked at already in the course are referred to (if not in name), such as:
Make a list of the major points raised in the discussion, and try to relate them to the theories and evaluations that we have talked about for major depression. |
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Assignment 10 - SAQ
Complete the following question from memory, about depression - writing a page
Describe a biomedical approach to treatment in one disorder (8)
A 22 mark ERQ could ask you to 'examine', or maybe 'evaluate' the things that you describe in this question. Plan how you would do this.
Describe a biomedical approach to treatment in one disorder (8)
A 22 mark ERQ could ask you to 'examine', or maybe 'evaluate' the things that you describe in this question. Plan how you would do this.
An individual therapy for depression - Beck's Cognitive Restructuring/CBT
Individual therapy involves a therapist working one on one with a client. They are common, popular and often effective forms of psychological treatment.
Remember Beck's cognitive triad for depression? Re-read the section above on this page if you don't.
Cognitive therapy believes that:
In recent years, there have been increasing efforts to add some of the more successful features of behavioural therapy to cognitive therapy. This combination is referred to as cognitive-behavioural therapy. CBTs will attempt to change or restructure BOTH the client’s cognitions AND their behaviours in combination. |
Beck (1976) argued that therapy for depression should involve uncovering and challenging and replacing the negative and unrealistic beliefs of depressed clients.
Beck’s therapy consists of challenging the negative cognitive triad (see earlier). There are four phases: 1. Increasing confidence and elevating mood 2. Challenging automatic negative thoughts 3. Identifying negative thoughts 4. Changing key attitudes and beliefs |
Clients examine the evidence on which their thougts are based, thus making them recognise they are faulty. The behavioural part then comes into play. Beck instructs his patients to monitor and log their thought processes between therapy sessions and gives them tasks that require patients to adopt new behaviours.
It is hoped that the client will come to accept that many of his or her negative thoughts are irrational and unrealistic. For example, a depressed client who argues that people are always avoiding him or her can be asked to keep a diary of specific occasions when it happens. It is very likely that it happens much less often than they imagine. |
Evaluating CBT...
Research evidence - Hollon et al (2006)Aim – to compare the effectiveness of cognitive and drug therapy.
Method – People with moderate to severe depression were given either drug therapy or CBT for 16 weeks. Both groups were followed for a year. Results – CBT relapse rates were around 40%. Drug therapy rates were around 45%. A control group (on placebo) showed relapse rates of 80%. Conclusion – CBT appears to be as effective as drug therapy for treating depression. BUT… still a relapse rate of 40% or so, showing that using therapies on their own may not be the most effective form of treatment. Using an interaction of a number of different treatments may be the most effective form of treatment. Paykel et al (1999) supports this view. They conducted a controlled trial of 158 patients who had experienced one episode of major depression. The patients received antidepressant medication but some of them also received cognitive therapy. The CBT group had a relapse rate of 29% compared to those who only had medication. Therefore CBT in combination with medication may be most effective at preventing relapse. |
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Assignment 11 - SAQComplete the following question from memory, about depression - writing a page
Analyse how one individual therapy can be used to treat a disorder (8) The cartoon on the right satirises the common consequence of thinking of depression as a cognitive disorder - that if it's all to do with thinking then the person should just be able to 'think' themselves better. Most of us probably still have a feeling that people with low mood should sometimes just 'pull themselves together' or 'cheer up'. Hopefully you now understand that this is not always as easy as it can seem.
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Group treatment for depression
Group therapies (as the name suggests) involve a number of people with a similar condition meeting with a therapist at the same time. There are many different types of group therapy, but one type of treatment which is becoming increasingly popular is therapy based on the ideas of 'mindfulness'
Mindfulness-based cognitive therapy (MBCT)
Mindfulness is an interesting mixture of the old and the new. Meditation as a form or relaxation or religious ritual has been around for thousands of years, practised most famously by Buddhists, amongst others. Interest in the potential value of this ancient practice was rekindled in the 1970s by the American researcher Jon Kabat-Zinn (seen here giving a talk to the very trendy employees of Google), originally for stress, but this practice soon spread into a treatment for depression as well.
How is it supposed to work?Think for a moment about all of the things that you have to do today. What about this week, or this month? With deadlines piling up on us and increasingly busy and interconnected lives, it can sometimes become overwhelming, even for the most efficient of us.
The basic idea of mindfulness therapy is to encourage us to become more 'present-centred'. We focus all of our attention on the present, on our immediate sensations thoughts and feelings. The breeze on your face, the ticking of the clock, the slight rumbling of your stomach (I'm writing this just before lunch!) This present-centred approach helps us to place our worries in context (in effect, we learn to be able to selectively ignore them - thoughts are seen as 'clouds' drifting past us, rather than being intimately associated with us). See this useful NHS information page for more information. |
How does MCBT work?The original MBCT program designed by Segal, Williams and Teasdale (2001) consisted of an eight-week course of group therapy and meditation sessions, with the following elements built in (taken from http://mbct.co.uk/):
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Evaluating MBCT
Research evidence - Piet and Hougard (2011)Background: Mindfulness-based cognitive therapy (MBCT) is a group-based clinical intervention program designed to reduce relapse or recurrence of major depressive disorder (MDD) by means of systematic training in mindfulness meditation combined with cognitive-behavioural methods.
Objective: By means of a meta-analysis to evaluate the effect of MBCT for prevention of relapse or recurrence among patients with recurrent MDD in remission. Method: Electronic databases were searched and researchers were contacted for further relevant studies. Studies were coded for quality. Meta-analyses were performed by means of the Cochrane Collaboration Review Manager 5.1. Results: Six randomized controlled trials with a total of 593 participants were included in the meta-analysis. MBCT significantly reduced the risk of relapse/recurrence with a risk ratio of 0.66 for MBCT compared to treatment as usual or placebo controls, corresponding to a relative risk reduction of 34%. In a pre-planned subgroup analysis the relative risk reduction was 43% for participants with three or more previous episodes, while no risk reduction was found for participants with only two episodes. In two studies, MBCT was at least as effective as maintenance antidepressant medication. Conclusion: Results of this meta-analysis indicate that MBCT is an effective intervention for relapse prevention in patients with recurrent MDD in remission, at least in case of three or more previous MDD episodes. Assignment 13 - SAQComplete the following question from memory, about depression - writing a page
Explain how one group therapy can be effective in treating a disorder (8) |
Assignment 12 - Summarise the research studyThe Piet and Hougard (2011) study summary to the left illustrates results from a meta-analysis of MBCT.
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22 mark Extended Response Questions
The 4 possible essay questions for this section (though remember that the command terms could change) are:
• Examine biomedical, individual and group approaches to treatment. • Evaluate the use of biomedical, individual and group approaches to the treatment of one disorder. • Discuss the use of eclectic approaches to treatment. • Discuss the relationship between etiology and therapeutic approach in relation to one disorder. NOTE HOW MUCH ALL OF THESE ESSAYS WILL OVERLAP! THE SAME INFORMATION CAN BE USED, REGARDLESS OF THE TITLE OF THE ESSAY (AS LONG AS YOU REMEMBER TO ANSWER THE QUESTION) You should plan an essay which will be about 2-3 sides of A4 long, including a detailed focus on the command term. The marking criteria are below. ALWAYS refer to these before you begin to plan your essay. It is crucial that you know what the examiners are looking for so that you can write exactly what is needed for top marks! |
Planning a great 22 mark questionKNOW THE COMMAND TERM! This is absolutely crucial! A different command term requires a different style of essay, so you need to tailor what you write to the question. You will still be able to use the same pieces of information, but how you use them may vary.
PLAN PLAN PLAN! Every year the examiners' comments mention that essays which are clearly planned score the best marks. FOLLOW THEIR ADVICE! Don't be afraid to spend up to 10 minutes in an exam planning your essay (and longer earlier in the year when are learning and practising). USE EVIDENCE! You have 2 detailed studies here to use, but you should also look to find triangulating evidence using other experimental methods or from other areas of the syllabus EVALUATE! You must evaluate the studies you present. Evaluating means talking about the strengths and weaknesses of the study as well as the strengths and weaknesses of the level of analysis as a whole with reference to the question (e.g. reductionist explanation of genetics in some behaviour) |
Revision |
ExtensionBelow is an interesting research article on the use of RET - a form of cognitive therapy similar to CBT in treating women who have undergone genital mutilation.
The serotonin hypothesis for depression is not 50 years old. This very recent review gives an excellent (if complex) overview of its strengths and weaknesses, and the evidence which shows why it cannot be considered a full explanation of the condition.
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