Psychology: Unit 4 - Depression

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Depression Symptoms

  • Depression is an affective disorder in that it is characterised by disturbances of affect (or mood). It is accompanied by symptoms such as:
  • Emotional symptoms: The symptoms we most associate with depression, those feelings of sadness, loss of mood and loss of pleasure from what were previously enjoyable activities.  Mood may also alter during the course of the day, typically being lowest in the morning and gradually showing improvement as the day progresses. 
  • Physical symptoms: Disturbances of sleep: patients sometimes report insomnia, but sleeping longer than before is also common. Appetite can also decrease or it may increase in the form of comfort eating.
  • Cognitive symptoms: These can vary from negative self thoughts, loss of self esteem and self confidence, feelings of despair and hopelessness, inability to concentrate on tasks for any length of time to feelings of inadequacy and blaming themselves for their situation and on occasions and suicidal thoughts.
  • Motivational symptoms: Apathy and loss of drive are common.  Typically the depressed person will sit around waiting for things to happen, making no attempt to initiate activity or social contact. 
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Classification

  • For a formal diagnosis of depression to be made the patient needs to be suffering from low mood (most of the day, nearly every day for at least two weeks) and or loss of interest and pleasure together with at least four of the previous symptoms e.g lack of sleep.
  • Unipolar (major or clinical depression): This is what we normally consider to be depression and can comprise a combination of any of the symptoms mentioned above.  Minor depression occurs when the patient suffers the low mood but without any of the cognitive or other disturbances.
  • Dysthimic disorder (or chronic depression): DSM-IV-TR now recognises a milder form of depression with a lower level of diagnosis.  The patients only needs three of the symptoms rather than the usual five to be considered to be suffering from dysthimic disorder.  Note: dysthimic does not include suicidal thoughts.
  • Bipolar (manic depression): Involves bouts of clinically depressed symptoms that alternate with periods of near normal mood and/or elevated mood (mania). 
    • Bipolar 1: usually consists of mania and depression but can on rare occasions be mania on its own
    • Bipolar 2: major depression with hypomania (a less extreme form of mania).
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Diagnosis

  • Endogenous depression (as the name suggests) comes from within and is thought to be caused by chemical imbalance and is explained and treated best by the medical model.
  • Reactive depression on the other hand is caused by external factors such as loss of job, death of relative etc. and is usually explained using psychological approaches such as behaviourist or cognitive models.
  • Diagnosis: DSM (Diagnostic and Statistical Manual) devised by the American Psychiatric Association in 1952.  Its last major revision was 2013 when DSM-v was published. 
  • ICD (International Statistical Classification of Diseases and Related Health Problems) devised by the World Health Organisation and categorises all illnesses. Currenty we are on ICD-10 with ICD-11 due in 2015.
  • Advantages: Treatments are often specific to one disorder e.g. certain drugs wouldn't help certain disorders. An accurate diagnosis can provide valuable information about the likely cause of the disorder, which can be helpful in planning treatment. Often those suffering with mental disorders have numerous symptoms. It is much easier to sort these into one diagnosis which makes communication better.
  • Disadvantaged: Diagnosis leads to labeling which can be stigmatising and can lead to self fulfilling prophecy. Mis-diagnosis can lead to inappropriate therapy or even being wrongly institutionalised.
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Reliabilty

  • Reliability
     Considers the extent to which a diagnosis of depression is consistent: over time (test-retest) and between professionals (inter-rater).
  • Beck: Looked at the relability between two psychologists when examining 154 patients and found that they had a 54% reliability meaning that 71 cases weren't diagnosed the same.
  • Keller et al: Found that inter rater reliability using DSM was 'fair to good' whereas test-retest reliability (after a 6 month interval) was 'fair' at best.
  • Zanarini et al: Found an inter rater reliability correlation of 0.80 for major depressive disorder and a test retest correlation of 0.61 with one week between diagnosis sessions.
  • This could have happened because not all the psychiatrists may have used the same tests e.g. either used ICD or DSM. Demand characteristics could have come into play. Patients may give different symptoms e.g. may be more open to a person they are more comfortable with.
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Validity

  • The validity looks at to what extent the classification and diagnosis reflects the true nature of the problem the patient is suffering; the course that the disorder is expected to take (prognosis) and how great a positive effect the proposed treatments will actually have.
  • Wittchen et al: Asked 20,421 patients who attended their doctor's surgery to fill out a depression questionnaire. 4.2% of the patients fulfilled the criteria for a major depressive episode according to DSM-IV; considerably higher rates of 11.3% were obtained using ICD-10 criteria. This suggests that these classifications have low concurrent validity as they got very different results when used on the same people.
  • Co-morbidity: There is a growing trend in clinical psychology to diagnose patients as suffering from "co-morbid" disorders (disorders that often seem to occur together) e.g. anxiety. These co-morbid disorders could be symptoms of depression, so it could be the depression is causing it. Diagnosis may not be measuring what it is supposed to.
  • There is many different types of classifications for depression - this could effect the diagnosis as this could make it more likely for people to get the wrong diagnosis, which would make these diagnosis innacurate, thus having low validity.
  • Diagnosising someone with depression means labelling them and these labels are hard to remove e.g. doctors may always say that a patients problems are down to their depression.
  • Cultural bias can lead to depression being overlooked as a doctor may not understand the cultural differences and my not understand what is really wrong with the patient.
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Biochemistry: AO1

  • A growing number of researchers believe that genetic factors influence the amount of catecholamines (a group of neurotransmitters which include noradrenaline, dopamine and serotonin) in specific areas of the brain.According to the catecholamine hypothesis, depression is caused by a deficit in these neurotransmitters at brain synapses.
  • Packets of serotonin molecules are released from the presynaptic neurone into the space between the two nerve cells (the synaptic gap). These molecules may then be taken up by serotonin receptors on the postsynaptic nerve cell and thus pass along the chemical message. Excess molecules are taken back up by the presynaptic cell and reprocessed.
  • Neurotransmitters that are not re-taken by the releasing neuron are broken down by an enzyme called monoamine oxidase (MAO).
  • There are a number of ways that can cause a lack of neurotransmitters such as: There may be too much MAO activity, which clears the synaptic cleft of neurotransmitters too effectively; re-uptake of the neurotransmitters may be too efficient so the sending neuron doesn't recieve enough neurotransmitters; too little production of neurotransmitters so there are not enough chemicals in the synapse or a lack of sensitivity of the recieveing neuron (not enough receptor sites).
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Biochemistry: AO2

  • Wender and Klein: Administered drugs to rats which lower levels of noradrenaline; the behaviour of the rats became sluggish and innactive - characteristic of depression.
  • Mintun: Brain imaging in a PET scan to comapre brain activity of severly depressed people to a non-depressed control group. Serotonin receptors were shown by a chemical tracer. The depressed people had fewer serotonin receptors than the control group.
  • Both studies are low in internal/ecological validity because extraneous variables may be influencing the studies - could be a different reason as to why depressed people had less serotonin receptors or why the rats acted in that way.
  • Wender and Klein's study used rats which means it can't fully be generalised to humans as rats could have a very different reaction from humans. Also, its very unethical.
  • Both studies wouldn't have demand characteristics as animals don't know they are being researched and people can't change what their brain looks like.
  • Mintun's study has high external validity as it used people who are already depressed from real life settings which means the findings are more generalisable.
  • Wender and Klein's study had controlled conditions - easier to show cause and effect relationship.
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Gentics: AO1

  • The genetic explanation suggests that we inherit a predisposition towards the disorder from our parents. Depression seems to run in families and a number of studies have shown an increased risk for depression in first degree relatives of people with uni-polar depression.
  • There seems to be a link between the biological closeness of the relationship and the likelihood of developing depression.
  • More recent research has identified an abnormality in the 5-HTT gene in people that are depressed. This gene is responsible for the transmission of the neurochemical serotonin. Low levels of serotonin have been implicated in depression. This means that those who inherit the faulty gene may not produce significant levels of serotonin, thus leading to that individual becoming depressed.
  • In terms of genes, family research - especially twin and adoption studies - has shown there to be a genetic link to depression, and that this suggests some people may carry genes that predispose them to depression.
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Genetics: AO2

  • Weissman, Kidd and Prusoff: Found more than twice as many cases of depression in the first degree relatives of people suffering from depression, compared to first degree relatives who do not suffer from the disorder. Intrestingly, this figure is higher for female relatives.
  • The problem with using family studies is that they share the same environment so it is difficult to say whether the problem is genetic or through environment/socialisation. To solve this we could look at people who didn't live with their parents e.g. adoption studies.
  • McGuffin: Studied 212 pairs of twins, one or both of whom were being treated for uni-polar depression. There was a 46% concordance rate for MZ twins, and 20% rate for DZ twins.
  • Allen: Found similar findings with a 40% concordance rate for MZ twins, and 11% for DZ twins.
  • A problem with twin studies is that they will most likely grow up together, so it could be their environment that is causing depression, which is why they both have it. Also MZ twins are usually treated more similarly because of their appearance.
  • Wendler et al: Found that the biological relatives of adopted sufferers of uni-polar depression were about 7 times more likely than adoptive parents to have depression themselves. This suggests genes are the main factor, as if it were environment, we would expect adoptive parents to be more depressed. However, the adoption itself could be an extraneous varibale which caused the biological parents and twins to get depressed, and not the adoptive parents.
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Biological Evaluation

  • The consequences of proposing a biological explanation of depression is that it treats the symptoms rather than its causues; a positive consequence could be that they would know it wasn't there fault that they have depression and it could make them feel as if they are unlikely to get better, which is damaging.
  • The useful applications of this research is that drug therapies have been shown to lessen the symptoms of depression and it could stop people from blaming those who are depressed.
  • It is very difficult to isolate the biological cause as most of the methods of research are natural - you couldn't scientifically make people have depression as it is unethical.
  • Research suggests that drug therapy alone is not as successful at treating depression as drug therapy combined with cognitive therapies. This contradicts the view that biology is the only cause as if it were biology alone then we wouldn't expect cognitive therapy to help at all.
  • The stress diathesis model may be a more realistic explanation as it seems unlikely that biology alone causes depression, it is more likely that some people are predisposed to depression and when it is triggered by an event e.g. stress this causes depression.
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Psychodynamic: AO1

  • The seed of depression is sown in childhood during the oral stage of development.
  • The child seeks to satisfy their needs via oral gratification.
  • The child is overly gratified by the caregiver (e.g. it is over fed).
  • The child develops a fixation in the oral stage.
  • The child becomes excessively dependent on others to maintain their self esteem due to the over gratification.
  • The person the suffer is dependant on is taken away from them e.g. seperation or death.
  • The child attempts to get affection and attention back lost from the person they were dependent on.
  • The child 'introjects' (takes on the personality) of the person whose affection they have lost e.g. parent.
  • Freud believed that deep in our unconscious are feelings of negativity towards the people we love.
  • Sufferer begins to hate themselves as they continue trying to act like the person they have lost.
  • Thus they become depressed.
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Psychodynamic: AO2

  • Shah & Waller: Found that many people who have suffered depression describe their parents as "affectionless". This supports the theory as in their unconscious mind they secretly hate their parents which may have caused their depression. It is also a loss.
  • Barnes & Prosen: Found that men who had lost their fathers through death during their childhood scored higher on a depression scale than those who's fathers had not died.
  • Bifulco et al: Found that children whose mothers died in childhood were more likely than other children to experience depression later in life.
  • Both these studies support the theory as they were probably dependent on their parents who died, then they will become depressed later in life as they introject and start to hate themselves
  • However, Bifulco found that the depression could be explained through the lack of care that the children received following the death of their mother. This highlights the issue of nature as it shows there could be other reasons why these children become depressed, which would decrease the validityas the study may not be accurate and give us false conclusions.
  • We wouldn't be able to get higher validity as we can't manipulate a child's relationship with their parent or cause the child loss, as this could cause irraparable damage.
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Psychodynamic: AO3

  • It is estimated that only 10% of those who experience parental loss become depressed later which suggests there has to be other reasons for depression as we would expect a 100% rate.
  • Psychoanalysis, the therapy based on the psychodynamic theory, has been found not to be very effective in treating depression. This is a criticism of theory as if the therapy of the explanation does not work then it suggests that the explanation is wrong.
  • This research may also be socially sensitive as it is putting the blame of depression on parents, which is wrong as there are most likely other factors involved.
  • There could be obvious reasons to why children become depressed if a parent dies, such as losing a loved one, which could cause most people depression, whether or not they became orally fixated.
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Cognitive Model: AO1

  • According to Beck, depression is the result of faulty or maladaptive thinking. The emotional and physical symptoms are a consequence of the thinking patterns.
  • There are three main aspects shown in the cognitive triad: Negative thinking of the self e.g. I am a bad person; the world e.g. My life is terrible and the future e.g. Life will never get better.
  • Beck suggested that many secondary symptoms of depression can be understood in terms of negative beliefs e.g. lack of motivation could be the result of pessimism.
  • Silent Assumptions: Beck believed that the inner life of depressed people is dominated by a set of assumptions that shape cognition. These assumptions come from parents, friends, teachers etc (intentional or not). Examples are "I must get people's approval", "I must do things perfectly or not at all", "I must be valued by others or my life has no meaning". These beliefs aren't uncommon, its just that depressed people subscribe to them.
  • Information Processing: Concerns how depressed people are prone to distorting and misinterpreting information and turn it into negativity. E.g. Catastrophising: Exaggerating a minor setback into a disaster (failing a test --> never getting a job); Personalising: Taking responsibility and blame for all bad things that happen (blaming yourself if friend is hurt); Selective Thinking: Focusing on negative details/events whilst ignoring positive ones (cake gets ruined, but party was still fun) and Arbitary Inferences: Drawing negative conclusions based on a single incidence (being rejected and thinking that you always will be). 
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Cognitive Model: AO2

  • Lewinsohn, Joiner and Rohde: Measured negative or dsyfunctional attitudes in adolescents not having major depressive disorder at the onset of the study. One year later they assessed the negative life events experienced by the participants and whether they had developed the disorder. Only those who had dsyfunctional attitudes had a higher risk of depression.
  • The major advantage of this study is that it is over the period of a year which means it isb a longitudinal study which means that the findings will be more accurate and high in temporal validity. This will increase the support for the theory.
  • Evans et al: Assessed negative or dsyfunctional self beliefs in women in the 18th week of pregnancy. Women with the highest test scores were 60% more likely to become depressed than those with the lowest scores. They predicted the onset of depression 3 years later. It supports the theory as it shows those with negative thoughts are more prone to depression. An issue with this study is that women's thoughts could change when they are pregnant due to hormones and stress. This would decrease support for the theory as it is less valid.
  • Butler and Beck: Reviewed 14 meta-analyses investigating the effectiveness of Beck's cognitive therapy and concluded that about 80% benefited from it. It was more successful than drug therapy and had a lower relapse rate.
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Cognitive Model: AO3

  • This supports the theory as it shows that it has an effective therapy as most benefited from ioit and it had a lower relapse rate. Because it is a meta analysis, this means they will be using a wide range of data which is good. The research could lack validity as they were only looking at secondary data, so it is hard to tell how truthful it is, which could lead to false conclusions.
  • One strength of the theory is that it isn't determinist. It doesn't suggest that we have no free will and suggests we do have control over our actions. This is good as it means people can take some responsibility and make them feel as if they can change the way they are.
  • However, it only considers the role of the thought process, which is problematic because other studies have shown that different therapies do have a positive effect on people's depression e.g. drug therapies have been quite successful.
  • There is a lot of research supporting the theory which suggests that the research has reliability as when the research is repeated similar results are got and this therefore increases the validity as because so many studies support the theory it suggests that it is accurate.
  • The theory might be considered socially sensitive as it suggests that the blame for the disorder lies with the person, which could lead to people blaming sufferers for their depression, which is very wrong, especially when there is evidence of biological factors. It could also be positive as it shows people can take control, which could make them feel better.  
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Drug Therapy: AO1

  • Tricyclics (TCAs): They were found to help alleviate the symptoms of depression. The most commonly used drug in the tricyclic group is Tofranil which operates by blocking the re-uptake of noradrenaline and serotonin and so making more neurotransmitters avaliable.
  • Selective Serotonin Reuptake Inhibitors (SSRIs): They are very similar to TCAs as they also inhibit the re-uptake of serotonin and thus make more of this neurotransmitter avaliable. However, only SNRIs also inhibit noradrenaline which has been created more recently.
  • Serotonin and noradrenaline are relased into the synapse. On the pre-synaptic side there are re-uptake sites that reasorb the chemicals very quickly. Tricyclics act by blocking these sites or channels so again result in more of the chemical being avaliable in the synapse for a longer of period of time. Serotonin has been shown to have an inhibitory effect and helps to stop people from becoming depressed, so making more of this avaliable helps.
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Drug Therapy: AO2

  • Arroll et al: Found that both TCAs and SSRIs produce a more significant reduction in depressive symptoms compared to a placebo.
  • Kirsch et al: Concluded that only in cases of the most servere depression was there any significant advantage to using SSRIs over a placebo. However this may be because among moderately depressed individuals even the placebo seemed to offer them some hope which lessened symptoms. For severely depressed, the expectation of anything working was absent, thus removing any placebo effect.
  • Derublis et al: Compared depressed people who were given SSRIs to depressed people who were given cognitive treatments; in both groups 58% of people showed a reduction in symptom
  • Hollon: Continued to study these participants for 12 months and found those in the cognitive group had a 31% relapse rate; those who had drug therapy throughout the 12 months had a 47% relapse rate and those who had the drug but didn't continue had a 76% relapse rate.
  • This shows that SSRIs are not very effective as even if they stay on the drug for the full 12 months, 47% still relapsed which is almost half and those who didn;t come off 76% relapsed comapred to 31% for cognitive therapy, suggesting that it is more effective.
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Drug Therapy: AO3

  • Turner et al: Claimed that there is publication bias with regard to effectiveness of drugs. Publication bias is where studies give positive results are much more likely to be published than those with negative results. This matters because it could lead to false conclusions as it may seem like drug therapy is more effective than it really is.
  • Montgomery et al: Found SSRIs had an important advantage over TCAs with respect to tolerability. SSRIs are better tolerated than TCAs, therefore patients are more likely to continue with treatment and recover.
  • Geller et al: Double blind studies have consistently failed to demonstrate the superiority of antidepressant medications over placebos when given to children and adolescents.
  • Barbui et al: A review of studies found that although the use of SSRIs increased the risk of suicide among adolescents, the risk was decreased among adults, and particularly so for adults aged 65+ where it appeared to have a protection effect against the risk of suicide.
  • They would intially be appropriate because they are easier to administer and are a good place to start. They also work quicker than a lot of treatments e.g. CBT.
  • People can grow addicated and become dependent on drugs and drugs only help to relieve people of their symptoms, they don't actually deal with the cause of depression.
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ECT: AO1

  • It is where electric currents are passed through the brain to create seizures which are thought to help re-start brain chemistry and help alleviate patients depression.
  • Patients are given muscle relaxants and then an electric current between 70 and 130 volts is passed through the non-dominant hemisphere of the brain. The current is adminstrated for 1 and 3 seconds but the resulting seizure lasts for around a minute.
  • The electric currents stimulate patients to develop seizures which are thought to help re-set their brain chemistry and stop their depression.
  • It is usually given as a last resort as it can have dangerous side effects e.g. memory loss but the effect it gives is immediate, so it would be used when all other treatments had already been given.
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ECT: AO2

  • Gregory et al: Have shown that when ECT is compared to 'sham' ECT, there tends to be a significant difference in outcome in favour of real ECT.
  • Folkerts et al: ECT is effective in cases of treatment resistant depression.
  • Hussain: Found no significant improvement following the adminstration of ECT for treatment resistant depression.
  • Scott: A review of 18 studies with 1,144 patients comparing ECT with antidepressant medication showed that ECT is more effective in the short term treatment of depression.
  • None of these trials compared ECT with the newer types of antidepressants e.g. SSRIs.
  • Rose et al: Concluded that at least one third of patients complained of persistent memory loss after ECT.
  • A Department of Health report in 2007 found that among those recieving ECT in the previous 2 years; 30% reported that it had results in permanent fear and anxiety.
  • ECT would be good to use when other methods fail as ECT can immediately help someone with mental illness which can help suicidal people especially with depression when nothing else has helped them.
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CBT: AO1

  • It is a type of therapy that encourages people to consider the beliefs and expectations that are the root of their depression and to replace their irrational, negative thoughts with more positive, adaptive ones. It aims to change the way they think and therefore end their depression.
  • The therapist encourages the client to become aware of their beliefs that led to their depression. The client and therapist then test the beliefs using reality, either by role play in the session or outside the session in everyday life. The aim of this reality testing is to show the client the consequences of their irrational thinking.
  • Techniques are then used to encourage the client to develop more rational, positive beliefs. Once these are adopted, the client's depression should end.
  • The aim of this therapy is to replace this maladaptive thoughts using the ABC model with rational thoughts. Typically this therapy will last for 20 weeks.
  • The ABC Model: Activating Event - the actual event and the clients immediate interpretations of the event; Beliefs about the event - this evaluation can be rational or irrational and Consequences - how you feel and what you or other thoughts.
  • E.g. lost your job --> I'll never get another job/I'm worthless --> Depressed -----> Lost your job --> Rational Belief: I will get another job --> Neutral emotion.
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CBT: AO2

  • Doesn't just treat symptoms but the actual cause - It can make a real change in a person's outlook and behaviour and help them face every day problems and adapt to stressful situations in a way that ECT or drug therapy never could.
  • Holmes: Has identified some limitations of the evidence to support CBT such as the trials are of highly selected patients with only depression and no additional symptoms. There is far less evidence for real patient problems with more complex problems.
  • Blackburn and Moorhead: Suggested CBT is highly superior, especially over periods of more than a year.
  • Rush: Claimed that CBT is at least as effective as anti-depressants.
  • CBT is not as cost effective as other treatments such as drug therapy and isn't always avaliable on the NHS.
  • Bulter: Reviewed 16 meta-analysis of CBT and depression and based on this very large body of evidence concluded it was very effective for treating depression.
  • There are no side effects, withdrawl symptoms or dependance.
  • Not an overnight cure - A depressed person has to do a cost benefit analysis at the beginning of treatment as CBT takes time and motivation. Lack of motivation is a symptom of depression, so it may not be appropriate.
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Psychodynamic Treatment: AO1

  • The aim of this therapy is to enable the individual to cope better with the inner emotional conflicts that are causing depression. The first step of the therapy is to uncover the root cause of depression from childhood; to do this the unconscious must be investigated.
  • Psychoanalysis therapy: Is intense, can last for years, usually includes several sessions a week and traditionally involves the client lying on a couch.
  • Psychoanalytic therapy: Is less intense, has fewer sessions per week, may not last for years and involves the client and therapoist in a face to face scenario.
  • It explores the patients past and then links this to their current emotional state. Experiences of chilhood loss and rejection are particularly concentrated on as they are key to the beginning of depression; the therapy may involve making unconscious memories conscious.
  • Free Association: The client is asked to allow the free flow of feelings, thoughts and images and then to express them in words without cencorship. It would be hoped that this could show what the root of the persons depression is as they express their feelings freely.
  • Transference: This occurs when the client redirects feelings e.g. hostility towards the therapist that are unconsciously directed towards a significant person in their life. It would alwso be hoped that this could show who rather than what is the root cause of their depression.
  • The client is encouraged to relive childhood experiences in this safe environment.
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Psychodynamic Treatment: AO2

  • Whether it works is not clear - the evidence has been mixed in the past and there have been few empirical studies of the effectiveness compared to other treatments.
  • Burnand et al: Investigated 74 patients between 29 and 65 to compare treatment by anti-depressants alone and anti-depressants combined with psychotherapy. Whilst both groups improved, the group with combined treatment was associated with less treatment failure and global functioning. This shows the therapy is effective to a degree as people seem to relapse less, especially when combined with another treatment.
  • Driessen et al: Compared the efficacy of psychodynamic therapy with that of CBT. 341 adults who had major depression were randomly assigned to 16 sessions of CBT or short term psychodynamic therapy. Severely depressed patients also got anti-depressants. No statistically significant treatment differences were found after one year, although the average post treatment remission rate was 22.7%. Driessen stated that 16 weeks is not enough to treat many patients. This tells us that the psychodynamic therapies are just as effective as CBT. These findings can be seen as internally valid as there weren't as only the severely depressed got any other treatment.
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Psychodynamic Treatment: AO3

  • This treatment is good as it helps to find the cause of depression rather than lessen the symptoms like drug therapy does.
  • Someone with depression may not be able to engage with the treatment as they might not want to open up about their problems especially if they are painful memories.
  • Some critics argue that this therapy can cause emotional harm. This could cause emotional harm as they might not be able to deal with their memories, this the therapy could actually make their depression a lot worse.
  • People who are severely depressed and possibly suicidal would not gain from this treatment as they would need immediate help and with this treatment it could be a long time before they start to get better.
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