Biological Explanations Of Depression
Depression
Diagnosis and classification of depression
Depression is classified under the DSM as a mood disorder. Most depressed individuals will suffer from only one type of depression (unipolar), whereas others may experience states of mania that alternate with depression (bipolar).
Comer (2001) claimed depression is ‘a low, sad state marked by significant levels of sadness, lack of energy, low self-worth, guilt or related symptoms’.
Diagnosis requires the presence of 5 of the following symptoms (which must include either depressed mood or loss of interest and pleasure). These symptoms must cause significant distress or impairment in general functioning, and must not be accounted for by bereavement.
* Sad, depressed mood (e.g. …show more content…
feeling sad or appearing tearful). * Loss of interest and pleasure in usual activities. * Difficulties in sleeping (insomnia or hypersomnia). * Shift in activity levels (lethargic or agitated). * Poor appetite or increased appetite. * Negative self-concept, feelings of worthlessness and guilt. * Difficulty in concentrating. * Recurrent thoughts of death and/or suicide.
Reliability of diagnosis
The consistency of a measuring instrument such as a questionnaire or scale to assess whether two independent assessors give similar diagnoses (inter-rater reliability) or whether tests used to deliver diagnoses are consistent over time (test re-test reliability).
Inter-rater reliability:
Low levels of inter-rater reliability related to any classification procedure suggest it might lead to faulty diagnosis and inappropriate treatment.
Lobbestael et al (2011) assessed inter-rater reliability of the structured clinical interview for assessments of major clinical depressive disorder in a mix of patient/ non-patient controls. Results found moderate agreement with inter-rater coefficient of 0.66.
Test-retest reliability:
This is a major goal in the new version of DSM. Current measurement scales = BDI (Beck Depression Inventory).
Evaluation of diagnosis criteria of the DSM:
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The DSM is constantly changing with the developments of technology and science. This makes the research and content more valid and reliable, as up-to-date information is constantly being used.
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Keller et al (1995) carried out a study to explore the reliability of the classification of depression using 524 outpatients. They were interviewed using the DSM criteria then re-interviewed 6 months later. The inter-rater reliability were fair to good and the test re-test reliability was poor to fair.
According to Keller (1995) the reason for low reliability was due to the high requirements of the diagnosis. One item difference can make the difference between a diagnosis of MDD and a less serious diagnosis.
It can sometimes be hard to determine each type of depression and their symptoms. GP’s may also give invalid diagnosis accounts based on previous knowledge of the patient. Tiller (2001) found only a ¼ of doctors could remember all 9 symptoms= unreliable.
Synoptic; observer-bias
Subjectivity of diagnosis- judging whether patients have any given symptom is subjective because they cannot be measured. For example, loss of pleasure in usual activities is a symptom of MDD, but how much loss of pleasure is needed to qualify?
Beck Depression Inventory (BDI)
What is the BDI?
A self-report questionnaire designed to measure the severity of symptoms in individuals with depression. Each question assesses a specific symptom (items 1-14 measure psychological symptoms, while items 15-21 measure physical symptoms). Every item is accompanied by four alternative responses, graded for severity from 0-3.
How do you test severity?
The sum of the BDI items indicated the severity of depression. For the general population anything over 21 indicated depression, for those who have been diagnosed a score of 0-9 represents minimal depressive symptoms compared to a score of 30 representing severe depression. This therefore allows us to distinguish between different types of depression.
Evaluation of the BDI:
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Beck et al (1996) used the responses of 26 outpatients tested at 2 therapy sessions (1 week apart). There was a correlation of 0.93 indicating high test- retest reliability.
Visser et al (2006) assessed 92 outpatients for depression using the DSM criteria and the BDI. 60 patients completed a BDI postal-survey, producing a test-retest correlation of 0.88.
Content validity- this refers to whether the items in the test are representative of what’s being measured. The BDI has a high content validity because it was constructed by mental health clinicians.
Concurrent validity- this measures the extent to which the test concurs with already existing assessing methods. Again, the BDI has a high concurrent validity as it can be measured with other scales.
Construct validity- this assesses the degree to which the test measures an internal variable. The BDI scores have a positive correlation of related symptoms, showing high construct validity.
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The BDI does not take into account personal circumstances, which could lead to the wrong diagnosis being given (for example, bereavement may be occurring).
Synoptic; social desirability bias (individuals could easily lie or not write certain answers due to external pressures).
Validity of diagnosis
Validity = the extent that a diagnosis reports something that is real and distinct from other disorders and the extent that a classification such as DSM measures what it claims to measure. Reliability and validity are linked- it cannot be valid if it is not reliable.
Comorbidity:
Refers to the extent that two or more conditions co-occurs
Research has shown the presence of an anxiety disorder is the single biggest risk for the development of depression as it serves as a compounding stressor that leads to major depression (especially patients with a genetic vulnerability).
Content validity:
Refers to whether items in a test are representative of that which is being measured. The BDI is high in content validity because it is a result of a consensus of mental health clinicians.
Concurrent validity:
It is a measure of the extent to which a test concurs with already existing standards.
Beck et al (1998) has consistently demonstrated concurrent validity between BDI and other measures of depression.
Factors that reduce reliability/validity
Types of depression:
McCollough et al (2003) compared 861 outpatients with various types of depression and found few differences on a range of clinical, psychological and treatment responsible variables suggesting that distinction between subtypes of depression may not be valid.
Are GP diagnoses valid?
Van Weel-Baumgarten et al (2006) suggests that diagnoses given by GP’s (rather than secondary specialist are made against the background of a patient so could be biased).
Consequences of Comorbidity:
The presence of this has repeatedly shown to have a negative impact on social and occupational functioning and a poorer response to treatment for patients with depression.
Goodwin et al (2001) found having suicidal thoughts occurred 5X higher in MDD compared to no disorder. But major depression comorbids with panic disorder.
Cultural difference in the diagnosis of depression
Members of ethnic minority groups are less likely to seek professional help for depression. This could be due to the stigma or that they tend to view depression as a disease treated by professionals.
Karasz (2005) gave symptoms to 36 South Asian Immigrants and 37 European Americans.
SA said that symptoms were a problem in social and moral terms and suggested self-management and non-professional help. EA emphasized biological explanations for symptoms including hormonal imbalance and neurological problems.
Biological explanations of depression
Genetics:
Family studies- having a first-degree relative with depression appears to be a risk factor for depression. Family studies select people that already have depression and examine whether their family members have or may have depression.
Gershon (1990) carried out a meta-analysis of 10 family studies and found clinical depression in first-degree relatives ranged from 7% to 30% (which is higher than the general population.
Twin studies- By comparing genes in both MZ (identical) and DZ (non-identical) twins, we are able to see the effects of genetics within disorders.
McGuffin et al (1996) studies 177 people with depression and their same sex twin. The concordance rate (similarity rate) was 46% in MZ twins and 20% in DZ twins, suggesting that depression has a hereditary component.
Adoption …show more content…
studies-
Wender et al (1986) studied biological relatives of adopted individuals with depression. It was found that there was a higher incidence (8X higher) in depression in these relatives, than with those of a non-depressed control group.
Gene diatheses- some individuals are thought to be born with a genetic predisposition to developing depression, and when this interacts with environmental stressors it can create depressive episodes.
Kendler et al (1995) found that women who were a co-twin of a depressed individual were more likely to be depressed later in life than those without the genetic vulnerability. Most significantly, the highest levels of depression were found in the group who were exposed to significant negative life events and were more genetically at risk for depression.
Evaluation of the genetic explanations
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Synoptic; psychology is a science and it supports the biological and social learning approaches.
Research support; a mutant gene that starves the brain of serotonin is found 10X more in depressed individuals than in control groups.
Zhang et al (2005); it can result in 80% reduction of normal serotonin levels in the brain.
Caron et al; found gene was carried by 9/87 depressed patients and only 2/219 control patients.
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It is clear that depression is not caused solemnly by genetic factors, as if this was true, findings would consistently show 100% results.
Kendler et al 1992) found a higher incidence of mental disorders (lower genetic concordance) when looking at both depression and generalised anxiety disorder (comorbidity disorders) - indicating that genetic links may be a result of another disorder/vulnerability.
Synoptic: * Nature vs. Nurture- it may not be the twin’s genetics but their upbringing which causes depression. * Cause or consequence- it is unclear whether the results are a cause or consequence of depression. * Non-ethical- by using already depressed patients and adopted individuals.
Biochemical factors:
Serotonin- research has found that there is a link between low serotonin levels and depression. Prozac and other antidepressant drugs (which block serotonin) have confirmed this link.
Delagdo et al (1990) gave depressed patients a diet which lowered tryptophan and found the majority of patients experienced a return of normal depressive symptoms, which disappeared when their diet returned to normal.
Cortisol Hypersecretion- cortisol is one of the hormones released by the adrenal gland during periods of stress, and stressful events have been shown to trigger depression- this works as elevated cortisol levels reduce serotonin levels, which in turn leads to depression.
Noradrenaline- it has been proposed that a deficiency of the neurotransmitter, noradrenaline causes depression. Findings show that levels of indirect markers of noradrenaline were low in depressed individuals. Post-mortem studies reveal increased noradrenaline receptor in the brains of depressed suicide victims.
Evaluation of the biochemical factors
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Kraft et al (2005) studied 96 depressed patients who were treated using dual SNRIs; these patients showed a more positive response than those treated using a placebo.
Research support (Leonard) - shows that drugs that lower levels of noradrenaline bring depressive states and those that increase it bring anti-depressive effects.
Synoptic; psychology is a science and is supports the biological approach- reliable statistical results.
When testing the serotonin theory on individuals with no past of depression, no changed were seen to their behaviour after being given a tryptophan diet- this suggests that serotonin levels dont always cause depression.
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Strickland et al (2002) - conflicting evidence; found no evidence of increased cortisol levels in a large group of depressed women. They did however find individuals going through stressful periods did have increased levels. This shows that stressful life events can result in elevated cortisol levels but this doesn’t always lead to depression.
Synoptic; correlation not causation, cause or consequence, deterministic, un-ethical studies (e.g. getting patients to re-live depression), not reliable.
Psychological explanations of depression
Psychodynamic theories:
Mourning and melancholia- according to Freud (1917) when a loved one is lost (through bereavement or, for children, separation or withdrawal) there is a period of mourning, and then life returns to normal. For some however this period of mourning does not end and is called a permanent stage of melancholia. Freud claimed this then become melancholia depression. Mourning and melancholia are similar- a reaction to loss etc. but whereas mourning is a natural process, melancholia is a pathological illness.
The pathology of depression- Freud also suggested that we unconsciously harbour negative feelings towards the ones we love, and that when we lose these loved ones we direct the negative feelings towards ourselves. We then normally begin a period of mourning were we separate ourselves from the loved one, however for some this goes astray, the individual resents being deserted by them and end up in a state of self-abuse and self-blame because the anger against the lost person is turned inwards.
Evaluation of the psychodynamic approach
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Bifulco et al (1992) found that children whose mothers died in childhood, were more likely (than other children) to develop depression later in life. However this could be a result of the lack of nurture rather than loss.
Research support- many studies have found that many people who have suffered depression had unaffectionate parents. This supports Freud’s theory of loss through withdrawal of affection.
Research support- it was also found that men who lost their fathers through death in early childhood scored higher on the depression scale than those who hadn’t died.
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Research has found only 10% of those who had experienced an early loss, later developed depression.
Freud’s psychoanalytic approach and therapy (psychoanalysis) has not proved very effective with depression cases. However this may be due to the fact depressives find it difficult to communicate in the way this therapy requires.
The DSM criterion clearly states that mourning should not be included within a diagnosis.
Synoptic; Nature vs. Nurture (unclear which is more dominant), deterministic, unfalsifiable (doesn’t support psychology is a science).
Cognitive theories:
Becks theory of depression
According to Aaron Beck (1967) depressed people have acquired a negative schema (a tendency to adopt a negative view of the world) during childhood due to parental or peer rejection/criticisms.
These negative schemas are activated whenever the individual encounters a new situation that resembles the original conditions in which this schema was learnt. Negative schemas are also subject to cognitive-biases in thinking (e.g. over-generalisations/ sweeping conclusions of self-worth on the basis of one negative piece of feedback) - which lead Back to develop the Negative Triad, a pessimistic view of the self, the world and the
future.
Learned Helplessness (Seligman 1975)
Depression may be learned when a person tried but fails to control unpleasant experiences. As a result they acquire a sense of being unable to control many aspects of their life, and so they become depressed (impairing their performance in situations that can be controlled- a characteristic of depression).
Hopelessness
Abramson et al (1989) modified the helplessness theory, and explained depression as a pessimistic expectation of the future. It suggests depression is internal (it’s my fault), stable (people hate me) and global (everything i do goes wrong). A person prone to depression is therefore thought to show a depressive attributional style where they attribute bad outcomes to personal, stable and global characteristics. However, some people with negative attributional styles dont become depressed (by avoiding negative thinking and traumatic experiences), however, the hopeless person believes the worst (pessimistic) and doesn’t believe they have the resources to change that situation.
Evaluation of the cognitive approach
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Beck’s theory of depression- Bates et al (1999) found that depressed participants who were given negative automatic-thought statements became more and more depressed. Just because there is a link this does not mean that negative thoughts cause depression.
Hiroto et al- supports learned helplessness showed that college students who were exposed to uncontrollable adverse events were more likely to fail on cognitive tasks. These findings show that having some degree of control and not feeling completely helpless greatly improves performance, especially for those who are depressed.
Maier and Seligman (1967) created hopeless dogs by continuously shocking them in a cage, when moved to a box in which they could escape they simply didn’t attempt to run.
Kwon et al (2002) - supports the hopelessness model. Participants were assessed on a weekly basis and found those with increased negative attributional style also showed more of symptoms when associated with depression when stressed. It is possible that a NAS is more common in women because throughout social development they are taught to think in a negative way about themselves. This might explain why more women suffer depression than men.
Research support- has found that cognitive-based therapies are 80% effective in treating depressed adults.
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Synoptic; Nurture vs. Nature (developed from childhood), non-ethical, ignored the psychodynamic theories.
Maier and Seligman (1967) - learned helplessness; results from animal studies cannot be generalised to humans, due to different brain cognitions and structures.
Barnett and Gottlib (1988) - learned helplessness; showed that people who were formally depressed are actually no different from people who have never been depressed in terms of their tendencies to view negative events with an attitude to helplessness.
Beck’s theory of depression - there is a shadow over the issue of whether or not negative thinking comes before depression or is a result of depression. So research in this area is lacking.
Segal and Ingram (1994) - compared depressed people against recovered depressed people. Found negative thinking to be a consequence of depression rather than causing depression.
Sociocultural factors
Life events and diathesis- Life events act as a trigger for those with a genetic vulnerability for depression. Cognitive models believe that the presence of a negative attributional style acts as a ‘diathesis’ that predisposes the person to interpret events and its consequences in a way that facilitates depression. In this war even minor events can trigger depressive episodes if they are subject to the biased interpretation that arises from this cognitive vulnerability. Kendler- the highest levels of depression were found in women who were most genetically at risk for depression.
Social networks and support- Billings et al (1983) found that depressed individuals reported having sparse social networks providing little social support, making them less able to handle negative life events and more vulnerable to continuing depression. Research has shown that the behaviour of depressed people reflects a deficit in social skills (i.e. interpersonal problem solving, lack of eye contact and frequently elicit rejection from others). Evaluation of the cognitive approach
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These theories can be supported by early bereavement (and psychodynamic theories) because bereavement is a major life event. Evidence that suggests that women rely on social support and are adversely affected by its absence
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Research suggests that males are more likely to internalise feelings, and females are more likely to share their feelings in social networks. Women have a 20% likelihood of depression compared to 10% of men. This leads to research being gender bias. Synoptic; Gender-bias, cause or consequence (lack of social support) Diathesis-stress model
Diathesis-stress model = underlying predispositions such as genetic vulnerability, childhood loss or patterns of negative thinking can give rise to depression if activated by stressors in the environment e.g. bereavement, unemployment, divorce etc. There is considerable evidence to support this.
Brown and Harris (1978) - the social origins of depression. A major study of housewives in London and identified 2 factors- severe life events and long-term difficulties- come into play with vulnerability factors. Depression among working class mothers incorporates early life experiences. 8 year follow up – early life experiences were a strong predictor of adult depression. Most significant childhood adversities were parental indifference/physical or sexual =abuse. Bifulco confirmed these findings.
Mazure et al (2000): 43 patients and 43 controls.
Standard scales to assess the number, the severity and the type of stressful events that occurred in 6 months.
Found; adverse life events, socio-trophy and need for control were significantly related to depression and the type of stressful event had impact on the effectiveness of treatment.
Evaluation:
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Controlled study that looked at 7 variables
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Ignored some factors, social networks/coping strategies, early trauma Found gender differences in response to treatment needs investigating.
Biological therapies for depression
Anti-depressants
How do they work? A lack of neurotransmitters (serotonin and noradrenaline) being produced in the nerve endings leads to depression. In normal brains, neurotransmitters are constantly released from the nerve endings, stimulating the neighbouring cells. To terminate their action, neurotransmitters are re-absorbed into the nerve endings or are broken down by an enzyme. Relive symptoms of depression.
Typically taken for 4-6 months (can be longer). Antidepressants work either by reducing the rate of re-absorption or by blocking the enzyme which breaks down the neurotransmitters. Both of these increase the amount of neurotransmitter available.
Tricyclics- these block the transported mechanism that re-absorbs both serotonin and noradrenaline, after it has fired. As a result more of the neurotransmitters are left in the synapse, prolonging their activity and making the next impulse easier. Slow-acting and mild. SSRIs (Selective Serotonin Re-uptake Inhibitors) - work by blocking the re-uptake of serotonin, this then increases the quantity available within the synapse. Moderate side effects (example is Prozac- “the wonder drug”). MAOIs (Monoamine Oxidise Inhibitors) - work by blocking enzymes that break down neurotransmitters available (noradrenaline and serotonin) so increases their activity.
There are 3 stages to the treatment: 1) Acute phase- the treatment of current symptoms 2) Continuation phase- this occurs for 4-6 months, after which the drugs are gradually withdrawn to prevent relapse. And symptoms have diminished. 3) Maintenance phase- this is used by those with recurrent depressive episodes. Evaluation of antidepressants
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This explanation supports the biological approach to depression.
The use of drugs as a treatment is beneficial for general use because they are cheap to make in large quantities, meaning if effective they could help dramatically.
Synoptic; psychology is a science, falsifiable.
65-70% effective in reducing symptoms compared to placebos.
Combining drugs and psychological treatments- for therapies can be effective, clients must have some insight (they must recognise that they have a problem) often they have no insight.
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Kirsch et al (2008) reviewed trials of anti-depressants and found that they only help people with severe depression. However, it was also found that even a placebo helped these individuals.
Research indicated that those treated with SSRIs were twice as likely to attempt suicide (compared to those treated by other measures).
Double-blind studies (the experimenter and participant’s dont know what they are searching for) have failed to demonstrate the superiority of antidepressants over placebos, when used on children.
Synoptic; unethical (the use of placebo instead of effectively treating a patient), deterministic and reductionist
Brown and Harris (1978) - showed that episodes of depression were almost always preceded by a significant life event.
Only treats symptoms not the underlying cause- does not necessarily offer a long-term cure because in many cases symptoms recur when drugs have stopped being taken
Turner et al (2008) and Goldacre- claim that there is evidence of publication bias towards studies that show positive effects of antidepressants
Effects are not immediate.
ECT (Electro-convulsive therapy)
Should only be used as a last resort where all other treatments have failed or when the condition is considered to be potentially life-threatening. This is because of its risky procedures and fast acting effect.
How does it work? Electrodes are placed on either the temple of the non-dominant side of the brain and the forehead, or placed on both temples. A short-acting general anaesthetic is then injected into the patient to place then in an unconscious state, while oxygen is also given to keep their breathing regular. To prevent damaging muscles, a nerve-blocking agent is also administered. After preparation, a small amount of electric current is passed through the patient’s brain producing a seizure lasting about one minute. This is repeated three times a week, with patients requiring between 3-15 treatments. The mechanisms of ECT- we are unsure why ECT works, however it is clear that it is the seizure which benefits the patient and not the electrical stimulus. It appears the seizure restores the brains ability to regulate mood- thus altering the depressive moods and episodes. Evaluation of ECT
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Gregory et al (1985) that have compared real ECT with ‘sham ECT’ (i.e. where the patient is anaesthetised but does not receive ECT), have found significant differences between the outcomes (in favour of real ECT).
Scott (2004) carried out a meta-analysis of patients, comparing ECT to drug therapy. He found ECT was more effective than drug therapy in the short-term of depression.
Synoptic; psychology is a science.
Richards and Lyn (2006) - studies indicated that 60-70% of patients improve with ECT.
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Research highlights a range of possible side effects of ECT including: * Impaired memory * Cardiovascular changes * Headaches * Fear and anxiety
Other research identifies that of 700 patients who received ECT, 59% has not consented to the treatment despite its risks. It was claimed they were given the treatment due to their un-clear mental state.
Despite its clear effectiveness, the cost of ECT is too high to provide to all patients, and it is therefore extremely hard to determine who can and can’t receive this treatment.
Synoptic; un-ethical (non consent, not sure how it works, side-effects) Psychological therapies for depression CBT (Cognitive Behavioural Therapy)
The aim of CBT is to identify and alter an individual’s maladaptive cognitions, as well as any dysfunctional behaviours that might be contributing towards the depression. CBT is relatively brief (with between 16-20 sessions) and is focused on current problems and current dysfunctional thinking.
There are many factors to CBT, two of which are explained below:
Thought catching- individuals are taught how to see the link between their thoughts and the way they feel. They are taught to challenge negative associations (e.g. an individual has heard something and assumes it’s about them) by replacing them with more constructive ones (e.g. is here any evidence to support this?).
Behavioural activation- a characteristic of depression is that the individuals no longer participate in activities that they have previously enjoyed. In CBT the therapist and client identify potentially pleasurable activities and anticipate/deal with any cognitive obstacles.
Evaluation of CBT
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March et al (2007) enrolled 327 adolescents who were diagnosed with depression, and randomly assigned a treatment of SSRIs, CBT or a combination of both. After 12 weeks, 62% has responded positively to the drug treatment, 48% to CBT and 73% to a combination of the two. They also found that CBT significantly reduced suicidal thoughts and behaviour (in comparison to the drug treatments).
Synoptic; free-will not determinism, more ethical than drug treatments and ECT
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Research evidence; indicates that when compared to a placebo treatment, CBT was no significantly more effective. Research also indicates that a 15% variance can be seen between treatments as a result of varied therapist competence.
CBT is very expensive- therefore becoming a hard treatment to offer- due to the lack of expertise capable administering the treatment.
CBT requires the individual involved to be committed through ‘homework’ tasks, this involvement predicts their outcomes.
CBT is not effective for those who are highly stressed- which given that is a characteristic of depression, is a large proportion of individuals.
Synoptic; age-bias, gender-bias (socialisation means males are less likely to talk about their problems, compared to women who are more likely to discuss their problems).
PIT (Psychodynamic Interpersonal Therapy)
In an attempt to move away from the traditional psychoanalytic approach of a one-sided relationship between therapist and client, this treatment placed emphasis on conversation between them. Problems are discussed not only as past events, but also relived in the present and resolved within the therapeutic relationship (it was believed that problems arouse due to disturbances within interpersonal relationships, and could therefore only be resolved through positive relationships with the therapist).
Components of PIT:
* Exploratory rationale- interpersonal difficulties are identified, and the therapist attempts to find an explanation for the individual by linking their current symptoms with these difficulties. * Share understanding- the therapist tries to understand what the individual is experiencing or feeling. * Staying with feelings- an attempt is made to recreate feelings in a therapeutic environment. * Focus on difficult feelings- the individual may express an emotion of which they are not aware (e.g. anger) or may not display appropriate emotions (e.g. being calm while discussing a distressing event). * Gaining insight- patterns or consistencies of behaviours are identified through different types of relationships. * Sequencing of interventions- different aspects of the model must be used in a coherent manner. * Change- therapists acknowledge and encourage change throughout the therapy.
Evaluation of PIT
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Paley et al (2008) investigated 62 patients receiving PIT in a hospital environment and assessed them using the BDI. They found significant results, although they were just as good as CBT.
Guthrie (1999) indicated that most cognitive therapies fail to recognise the importance of interpersonal relationship and their contribution to depression. This makes PIT important for treatment of depression that may have arisen due to childhood or dysfunctional relationship.
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Research evidence; identified the importance of the quality of the relationship established between the therapist and client. Due to this, this treatment takes a lot of time, effort and finance.
Diagnosis and classification of depression
Depression is classified under the DSM as a mood disorder. Most depressed individuals will suffer from only one type of depression (unipolar), whereas others may experience states of mania that alternate with depression (bipolar).
Comer (2001) claimed depression is ‘a low, sad state marked by significant levels of sadness, lack of energy, low self-worth, guilt or related symptoms’.
Diagnosis requires the presence of 5 of the following symptoms (which must include either depressed mood or loss of interest and pleasure). These symptoms must cause significant distress or impairment in general functioning, and must not be accounted for by bereavement.
* Sad, depressed mood (e.g. …show more content…
feeling sad or appearing tearful). * Loss of interest and pleasure in usual activities. * Difficulties in sleeping (insomnia or hypersomnia). * Shift in activity levels (lethargic or agitated). * Poor appetite or increased appetite. * Negative self-concept, feelings of worthlessness and guilt. * Difficulty in concentrating. * Recurrent thoughts of death and/or suicide.
Reliability of diagnosis
The consistency of a measuring instrument such as a questionnaire or scale to assess whether two independent assessors give similar diagnoses (inter-rater reliability) or whether tests used to deliver diagnoses are consistent over time (test re-test reliability).
Inter-rater reliability:
Low levels of inter-rater reliability related to any classification procedure suggest it might lead to faulty diagnosis and inappropriate treatment.
Lobbestael et al (2011) assessed inter-rater reliability of the structured clinical interview for assessments of major clinical depressive disorder in a mix of patient/ non-patient controls. Results found moderate agreement with inter-rater coefficient of 0.66.
Test-retest reliability:
This is a major goal in the new version of DSM. Current measurement scales = BDI (Beck Depression Inventory).
Evaluation of diagnosis criteria of the DSM:
+
The DSM is constantly changing with the developments of technology and science. This makes the research and content more valid and reliable, as up-to-date information is constantly being used.
-
Keller et al (1995) carried out a study to explore the reliability of the classification of depression using 524 outpatients. They were interviewed using the DSM criteria then re-interviewed 6 months later. The inter-rater reliability were fair to good and the test re-test reliability was poor to fair.
According to Keller (1995) the reason for low reliability was due to the high requirements of the diagnosis. One item difference can make the difference between a diagnosis of MDD and a less serious diagnosis.
It can sometimes be hard to determine each type of depression and their symptoms. GP’s may also give invalid diagnosis accounts based on previous knowledge of the patient. Tiller (2001) found only a ¼ of doctors could remember all 9 symptoms= unreliable.
Synoptic; observer-bias
Subjectivity of diagnosis- judging whether patients have any given symptom is subjective because they cannot be measured. For example, loss of pleasure in usual activities is a symptom of MDD, but how much loss of pleasure is needed to qualify?
Beck Depression Inventory (BDI)
What is the BDI?
A self-report questionnaire designed to measure the severity of symptoms in individuals with depression. Each question assesses a specific symptom (items 1-14 measure psychological symptoms, while items 15-21 measure physical symptoms). Every item is accompanied by four alternative responses, graded for severity from 0-3.
How do you test severity?
The sum of the BDI items indicated the severity of depression. For the general population anything over 21 indicated depression, for those who have been diagnosed a score of 0-9 represents minimal depressive symptoms compared to a score of 30 representing severe depression. This therefore allows us to distinguish between different types of depression.
Evaluation of the BDI:
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Beck et al (1996) used the responses of 26 outpatients tested at 2 therapy sessions (1 week apart). There was a correlation of 0.93 indicating high test- retest reliability.
Visser et al (2006) assessed 92 outpatients for depression using the DSM criteria and the BDI. 60 patients completed a BDI postal-survey, producing a test-retest correlation of 0.88.
Content validity- this refers to whether the items in the test are representative of what’s being measured. The BDI has a high content validity because it was constructed by mental health clinicians.
Concurrent validity- this measures the extent to which the test concurs with already existing assessing methods. Again, the BDI has a high concurrent validity as it can be measured with other scales.
Construct validity- this assesses the degree to which the test measures an internal variable. The BDI scores have a positive correlation of related symptoms, showing high construct validity.
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The BDI does not take into account personal circumstances, which could lead to the wrong diagnosis being given (for example, bereavement may be occurring).
Synoptic; social desirability bias (individuals could easily lie or not write certain answers due to external pressures).
Validity of diagnosis
Validity = the extent that a diagnosis reports something that is real and distinct from other disorders and the extent that a classification such as DSM measures what it claims to measure. Reliability and validity are linked- it cannot be valid if it is not reliable.
Comorbidity:
Refers to the extent that two or more conditions co-occurs
Research has shown the presence of an anxiety disorder is the single biggest risk for the development of depression as it serves as a compounding stressor that leads to major depression (especially patients with a genetic vulnerability).
Content validity:
Refers to whether items in a test are representative of that which is being measured. The BDI is high in content validity because it is a result of a consensus of mental health clinicians.
Concurrent validity:
It is a measure of the extent to which a test concurs with already existing standards.
Beck et al (1998) has consistently demonstrated concurrent validity between BDI and other measures of depression.
Factors that reduce reliability/validity
Types of depression:
McCollough et al (2003) compared 861 outpatients with various types of depression and found few differences on a range of clinical, psychological and treatment responsible variables suggesting that distinction between subtypes of depression may not be valid.
Are GP diagnoses valid?
Van Weel-Baumgarten et al (2006) suggests that diagnoses given by GP’s (rather than secondary specialist are made against the background of a patient so could be biased).
Consequences of Comorbidity:
The presence of this has repeatedly shown to have a negative impact on social and occupational functioning and a poorer response to treatment for patients with depression.
Goodwin et al (2001) found having suicidal thoughts occurred 5X higher in MDD compared to no disorder. But major depression comorbids with panic disorder.
Cultural difference in the diagnosis of depression
Members of ethnic minority groups are less likely to seek professional help for depression. This could be due to the stigma or that they tend to view depression as a disease treated by professionals.
Karasz (2005) gave symptoms to 36 South Asian Immigrants and 37 European Americans.
SA said that symptoms were a problem in social and moral terms and suggested self-management and non-professional help. EA emphasized biological explanations for symptoms including hormonal imbalance and neurological problems.
Biological explanations of depression
Genetics:
Family studies- having a first-degree relative with depression appears to be a risk factor for depression. Family studies select people that already have depression and examine whether their family members have or may have depression.
Gershon (1990) carried out a meta-analysis of 10 family studies and found clinical depression in first-degree relatives ranged from 7% to 30% (which is higher than the general population.
Twin studies- By comparing genes in both MZ (identical) and DZ (non-identical) twins, we are able to see the effects of genetics within disorders.
McGuffin et al (1996) studies 177 people with depression and their same sex twin. The concordance rate (similarity rate) was 46% in MZ twins and 20% in DZ twins, suggesting that depression has a hereditary component.
Adoption …show more content…
studies-
Wender et al (1986) studied biological relatives of adopted individuals with depression. It was found that there was a higher incidence (8X higher) in depression in these relatives, than with those of a non-depressed control group.
Gene diatheses- some individuals are thought to be born with a genetic predisposition to developing depression, and when this interacts with environmental stressors it can create depressive episodes.
Kendler et al (1995) found that women who were a co-twin of a depressed individual were more likely to be depressed later in life than those without the genetic vulnerability. Most significantly, the highest levels of depression were found in the group who were exposed to significant negative life events and were more genetically at risk for depression.
Evaluation of the genetic explanations
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Synoptic; psychology is a science and it supports the biological and social learning approaches.
Research support; a mutant gene that starves the brain of serotonin is found 10X more in depressed individuals than in control groups.
Zhang et al (2005); it can result in 80% reduction of normal serotonin levels in the brain.
Caron et al; found gene was carried by 9/87 depressed patients and only 2/219 control patients.
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It is clear that depression is not caused solemnly by genetic factors, as if this was true, findings would consistently show 100% results.
Kendler et al 1992) found a higher incidence of mental disorders (lower genetic concordance) when looking at both depression and generalised anxiety disorder (comorbidity disorders) - indicating that genetic links may be a result of another disorder/vulnerability.
Synoptic: * Nature vs. Nurture- it may not be the twin’s genetics but their upbringing which causes depression. * Cause or consequence- it is unclear whether the results are a cause or consequence of depression. * Non-ethical- by using already depressed patients and adopted individuals.
Biochemical factors:
Serotonin- research has found that there is a link between low serotonin levels and depression. Prozac and other antidepressant drugs (which block serotonin) have confirmed this link.
Delagdo et al (1990) gave depressed patients a diet which lowered tryptophan and found the majority of patients experienced a return of normal depressive symptoms, which disappeared when their diet returned to normal.
Cortisol Hypersecretion- cortisol is one of the hormones released by the adrenal gland during periods of stress, and stressful events have been shown to trigger depression- this works as elevated cortisol levels reduce serotonin levels, which in turn leads to depression.
Noradrenaline- it has been proposed that a deficiency of the neurotransmitter, noradrenaline causes depression. Findings show that levels of indirect markers of noradrenaline were low in depressed individuals. Post-mortem studies reveal increased noradrenaline receptor in the brains of depressed suicide victims.
Evaluation of the biochemical factors
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Kraft et al (2005) studied 96 depressed patients who were treated using dual SNRIs; these patients showed a more positive response than those treated using a placebo.
Research support (Leonard) - shows that drugs that lower levels of noradrenaline bring depressive states and those that increase it bring anti-depressive effects.
Synoptic; psychology is a science and is supports the biological approach- reliable statistical results.
When testing the serotonin theory on individuals with no past of depression, no changed were seen to their behaviour after being given a tryptophan diet- this suggests that serotonin levels dont always cause depression.
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Strickland et al (2002) - conflicting evidence; found no evidence of increased cortisol levels in a large group of depressed women. They did however find individuals going through stressful periods did have increased levels. This shows that stressful life events can result in elevated cortisol levels but this doesn’t always lead to depression.
Synoptic; correlation not causation, cause or consequence, deterministic, un-ethical studies (e.g. getting patients to re-live depression), not reliable.
Psychological explanations of depression
Psychodynamic theories:
Mourning and melancholia- according to Freud (1917) when a loved one is lost (through bereavement or, for children, separation or withdrawal) there is a period of mourning, and then life returns to normal. For some however this period of mourning does not end and is called a permanent stage of melancholia. Freud claimed this then become melancholia depression. Mourning and melancholia are similar- a reaction to loss etc. but whereas mourning is a natural process, melancholia is a pathological illness.
The pathology of depression- Freud also suggested that we unconsciously harbour negative feelings towards the ones we love, and that when we lose these loved ones we direct the negative feelings towards ourselves. We then normally begin a period of mourning were we separate ourselves from the loved one, however for some this goes astray, the individual resents being deserted by them and end up in a state of self-abuse and self-blame because the anger against the lost person is turned inwards.
Evaluation of the psychodynamic approach
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Bifulco et al (1992) found that children whose mothers died in childhood, were more likely (than other children) to develop depression later in life. However this could be a result of the lack of nurture rather than loss.
Research support- many studies have found that many people who have suffered depression had unaffectionate parents. This supports Freud’s theory of loss through withdrawal of affection.
Research support- it was also found that men who lost their fathers through death in early childhood scored higher on the depression scale than those who hadn’t died.
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Research has found only 10% of those who had experienced an early loss, later developed depression.
Freud’s psychoanalytic approach and therapy (psychoanalysis) has not proved very effective with depression cases. However this may be due to the fact depressives find it difficult to communicate in the way this therapy requires.
The DSM criterion clearly states that mourning should not be included within a diagnosis.
Synoptic; Nature vs. Nurture (unclear which is more dominant), deterministic, unfalsifiable (doesn’t support psychology is a science).
Cognitive theories:
Becks theory of depression
According to Aaron Beck (1967) depressed people have acquired a negative schema (a tendency to adopt a negative view of the world) during childhood due to parental or peer rejection/criticisms.
These negative schemas are activated whenever the individual encounters a new situation that resembles the original conditions in which this schema was learnt. Negative schemas are also subject to cognitive-biases in thinking (e.g. over-generalisations/ sweeping conclusions of self-worth on the basis of one negative piece of feedback) - which lead Back to develop the Negative Triad, a pessimistic view of the self, the world and the
future.
Learned Helplessness (Seligman 1975)
Depression may be learned when a person tried but fails to control unpleasant experiences. As a result they acquire a sense of being unable to control many aspects of their life, and so they become depressed (impairing their performance in situations that can be controlled- a characteristic of depression).
Hopelessness
Abramson et al (1989) modified the helplessness theory, and explained depression as a pessimistic expectation of the future. It suggests depression is internal (it’s my fault), stable (people hate me) and global (everything i do goes wrong). A person prone to depression is therefore thought to show a depressive attributional style where they attribute bad outcomes to personal, stable and global characteristics. However, some people with negative attributional styles dont become depressed (by avoiding negative thinking and traumatic experiences), however, the hopeless person believes the worst (pessimistic) and doesn’t believe they have the resources to change that situation.
Evaluation of the cognitive approach
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Beck’s theory of depression- Bates et al (1999) found that depressed participants who were given negative automatic-thought statements became more and more depressed. Just because there is a link this does not mean that negative thoughts cause depression.
Hiroto et al- supports learned helplessness showed that college students who were exposed to uncontrollable adverse events were more likely to fail on cognitive tasks. These findings show that having some degree of control and not feeling completely helpless greatly improves performance, especially for those who are depressed.
Maier and Seligman (1967) created hopeless dogs by continuously shocking them in a cage, when moved to a box in which they could escape they simply didn’t attempt to run.
Kwon et al (2002) - supports the hopelessness model. Participants were assessed on a weekly basis and found those with increased negative attributional style also showed more of symptoms when associated with depression when stressed. It is possible that a NAS is more common in women because throughout social development they are taught to think in a negative way about themselves. This might explain why more women suffer depression than men.
Research support- has found that cognitive-based therapies are 80% effective in treating depressed adults.
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Synoptic; Nurture vs. Nature (developed from childhood), non-ethical, ignored the psychodynamic theories.
Maier and Seligman (1967) - learned helplessness; results from animal studies cannot be generalised to humans, due to different brain cognitions and structures.
Barnett and Gottlib (1988) - learned helplessness; showed that people who were formally depressed are actually no different from people who have never been depressed in terms of their tendencies to view negative events with an attitude to helplessness.
Beck’s theory of depression - there is a shadow over the issue of whether or not negative thinking comes before depression or is a result of depression. So research in this area is lacking.
Segal and Ingram (1994) - compared depressed people against recovered depressed people. Found negative thinking to be a consequence of depression rather than causing depression.
Sociocultural factors
Life events and diathesis- Life events act as a trigger for those with a genetic vulnerability for depression. Cognitive models believe that the presence of a negative attributional style acts as a ‘diathesis’ that predisposes the person to interpret events and its consequences in a way that facilitates depression. In this war even minor events can trigger depressive episodes if they are subject to the biased interpretation that arises from this cognitive vulnerability. Kendler- the highest levels of depression were found in women who were most genetically at risk for depression.
Social networks and support- Billings et al (1983) found that depressed individuals reported having sparse social networks providing little social support, making them less able to handle negative life events and more vulnerable to continuing depression. Research has shown that the behaviour of depressed people reflects a deficit in social skills (i.e. interpersonal problem solving, lack of eye contact and frequently elicit rejection from others). Evaluation of the cognitive approach
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These theories can be supported by early bereavement (and psychodynamic theories) because bereavement is a major life event. Evidence that suggests that women rely on social support and are adversely affected by its absence
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Research suggests that males are more likely to internalise feelings, and females are more likely to share their feelings in social networks. Women have a 20% likelihood of depression compared to 10% of men. This leads to research being gender bias. Synoptic; Gender-bias, cause or consequence (lack of social support) Diathesis-stress model
Diathesis-stress model = underlying predispositions such as genetic vulnerability, childhood loss or patterns of negative thinking can give rise to depression if activated by stressors in the environment e.g. bereavement, unemployment, divorce etc. There is considerable evidence to support this.
Brown and Harris (1978) - the social origins of depression. A major study of housewives in London and identified 2 factors- severe life events and long-term difficulties- come into play with vulnerability factors. Depression among working class mothers incorporates early life experiences. 8 year follow up – early life experiences were a strong predictor of adult depression. Most significant childhood adversities were parental indifference/physical or sexual =abuse. Bifulco confirmed these findings.
Mazure et al (2000): 43 patients and 43 controls.
Standard scales to assess the number, the severity and the type of stressful events that occurred in 6 months.
Found; adverse life events, socio-trophy and need for control were significantly related to depression and the type of stressful event had impact on the effectiveness of treatment.
Evaluation:
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Controlled study that looked at 7 variables
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Ignored some factors, social networks/coping strategies, early trauma Found gender differences in response to treatment needs investigating.
Biological therapies for depression
Anti-depressants
How do they work? A lack of neurotransmitters (serotonin and noradrenaline) being produced in the nerve endings leads to depression. In normal brains, neurotransmitters are constantly released from the nerve endings, stimulating the neighbouring cells. To terminate their action, neurotransmitters are re-absorbed into the nerve endings or are broken down by an enzyme. Relive symptoms of depression.
Typically taken for 4-6 months (can be longer). Antidepressants work either by reducing the rate of re-absorption or by blocking the enzyme which breaks down the neurotransmitters. Both of these increase the amount of neurotransmitter available.
Tricyclics- these block the transported mechanism that re-absorbs both serotonin and noradrenaline, after it has fired. As a result more of the neurotransmitters are left in the synapse, prolonging their activity and making the next impulse easier. Slow-acting and mild. SSRIs (Selective Serotonin Re-uptake Inhibitors) - work by blocking the re-uptake of serotonin, this then increases the quantity available within the synapse. Moderate side effects (example is Prozac- “the wonder drug”). MAOIs (Monoamine Oxidise Inhibitors) - work by blocking enzymes that break down neurotransmitters available (noradrenaline and serotonin) so increases their activity.
There are 3 stages to the treatment: 1) Acute phase- the treatment of current symptoms 2) Continuation phase- this occurs for 4-6 months, after which the drugs are gradually withdrawn to prevent relapse. And symptoms have diminished. 3) Maintenance phase- this is used by those with recurrent depressive episodes. Evaluation of antidepressants
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This explanation supports the biological approach to depression.
The use of drugs as a treatment is beneficial for general use because they are cheap to make in large quantities, meaning if effective they could help dramatically.
Synoptic; psychology is a science, falsifiable.
65-70% effective in reducing symptoms compared to placebos.
Combining drugs and psychological treatments- for therapies can be effective, clients must have some insight (they must recognise that they have a problem) often they have no insight.
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Kirsch et al (2008) reviewed trials of anti-depressants and found that they only help people with severe depression. However, it was also found that even a placebo helped these individuals.
Research indicated that those treated with SSRIs were twice as likely to attempt suicide (compared to those treated by other measures).
Double-blind studies (the experimenter and participant’s dont know what they are searching for) have failed to demonstrate the superiority of antidepressants over placebos, when used on children.
Synoptic; unethical (the use of placebo instead of effectively treating a patient), deterministic and reductionist
Brown and Harris (1978) - showed that episodes of depression were almost always preceded by a significant life event.
Only treats symptoms not the underlying cause- does not necessarily offer a long-term cure because in many cases symptoms recur when drugs have stopped being taken
Turner et al (2008) and Goldacre- claim that there is evidence of publication bias towards studies that show positive effects of antidepressants
Effects are not immediate.
ECT (Electro-convulsive therapy)
Should only be used as a last resort where all other treatments have failed or when the condition is considered to be potentially life-threatening. This is because of its risky procedures and fast acting effect.
How does it work? Electrodes are placed on either the temple of the non-dominant side of the brain and the forehead, or placed on both temples. A short-acting general anaesthetic is then injected into the patient to place then in an unconscious state, while oxygen is also given to keep their breathing regular. To prevent damaging muscles, a nerve-blocking agent is also administered. After preparation, a small amount of electric current is passed through the patient’s brain producing a seizure lasting about one minute. This is repeated three times a week, with patients requiring between 3-15 treatments. The mechanisms of ECT- we are unsure why ECT works, however it is clear that it is the seizure which benefits the patient and not the electrical stimulus. It appears the seizure restores the brains ability to regulate mood- thus altering the depressive moods and episodes. Evaluation of ECT
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Gregory et al (1985) that have compared real ECT with ‘sham ECT’ (i.e. where the patient is anaesthetised but does not receive ECT), have found significant differences between the outcomes (in favour of real ECT).
Scott (2004) carried out a meta-analysis of patients, comparing ECT to drug therapy. He found ECT was more effective than drug therapy in the short-term of depression.
Synoptic; psychology is a science.
Richards and Lyn (2006) - studies indicated that 60-70% of patients improve with ECT.
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Research highlights a range of possible side effects of ECT including: * Impaired memory * Cardiovascular changes * Headaches * Fear and anxiety
Other research identifies that of 700 patients who received ECT, 59% has not consented to the treatment despite its risks. It was claimed they were given the treatment due to their un-clear mental state.
Despite its clear effectiveness, the cost of ECT is too high to provide to all patients, and it is therefore extremely hard to determine who can and can’t receive this treatment.
Synoptic; un-ethical (non consent, not sure how it works, side-effects) Psychological therapies for depression CBT (Cognitive Behavioural Therapy)
The aim of CBT is to identify and alter an individual’s maladaptive cognitions, as well as any dysfunctional behaviours that might be contributing towards the depression. CBT is relatively brief (with between 16-20 sessions) and is focused on current problems and current dysfunctional thinking.
There are many factors to CBT, two of which are explained below:
Thought catching- individuals are taught how to see the link between their thoughts and the way they feel. They are taught to challenge negative associations (e.g. an individual has heard something and assumes it’s about them) by replacing them with more constructive ones (e.g. is here any evidence to support this?).
Behavioural activation- a characteristic of depression is that the individuals no longer participate in activities that they have previously enjoyed. In CBT the therapist and client identify potentially pleasurable activities and anticipate/deal with any cognitive obstacles.
Evaluation of CBT
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March et al (2007) enrolled 327 adolescents who were diagnosed with depression, and randomly assigned a treatment of SSRIs, CBT or a combination of both. After 12 weeks, 62% has responded positively to the drug treatment, 48% to CBT and 73% to a combination of the two. They also found that CBT significantly reduced suicidal thoughts and behaviour (in comparison to the drug treatments).
Synoptic; free-will not determinism, more ethical than drug treatments and ECT
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Research evidence; indicates that when compared to a placebo treatment, CBT was no significantly more effective. Research also indicates that a 15% variance can be seen between treatments as a result of varied therapist competence.
CBT is very expensive- therefore becoming a hard treatment to offer- due to the lack of expertise capable administering the treatment.
CBT requires the individual involved to be committed through ‘homework’ tasks, this involvement predicts their outcomes.
CBT is not effective for those who are highly stressed- which given that is a characteristic of depression, is a large proportion of individuals.
Synoptic; age-bias, gender-bias (socialisation means males are less likely to talk about their problems, compared to women who are more likely to discuss their problems).
PIT (Psychodynamic Interpersonal Therapy)
In an attempt to move away from the traditional psychoanalytic approach of a one-sided relationship between therapist and client, this treatment placed emphasis on conversation between them. Problems are discussed not only as past events, but also relived in the present and resolved within the therapeutic relationship (it was believed that problems arouse due to disturbances within interpersonal relationships, and could therefore only be resolved through positive relationships with the therapist).
Components of PIT:
* Exploratory rationale- interpersonal difficulties are identified, and the therapist attempts to find an explanation for the individual by linking their current symptoms with these difficulties. * Share understanding- the therapist tries to understand what the individual is experiencing or feeling. * Staying with feelings- an attempt is made to recreate feelings in a therapeutic environment. * Focus on difficult feelings- the individual may express an emotion of which they are not aware (e.g. anger) or may not display appropriate emotions (e.g. being calm while discussing a distressing event). * Gaining insight- patterns or consistencies of behaviours are identified through different types of relationships. * Sequencing of interventions- different aspects of the model must be used in a coherent manner. * Change- therapists acknowledge and encourage change throughout the therapy.
Evaluation of PIT
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Paley et al (2008) investigated 62 patients receiving PIT in a hospital environment and assessed them using the BDI. They found significant results, although they were just as good as CBT.
Guthrie (1999) indicated that most cognitive therapies fail to recognise the importance of interpersonal relationship and their contribution to depression. This makes PIT important for treatment of depression that may have arisen due to childhood or dysfunctional relationship.
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Research evidence; identified the importance of the quality of the relationship established between the therapist and client. Due to this, this treatment takes a lot of time, effort and finance.