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Seligman (1973) referred to depression as the ‘common cold’ of psychiatry because of its frequency of diagnosis.  According to BPS figures a staggering 9 million people in Britain reported feelings of depression to their GP in 1998!  However to continue Seligman’s analogy, although this ‘cold’ may have reached epidemic proportions in the West it is certainly not pandemic since many cultures and areas of the World report little or no depression


Characteristics of depression

Depression is an affective disorder in that it is characterised by disturbances of affect (or mood).  During the course of any period of time it is not unusual for a person’s mood to alter.  However with affective disorders this variation is more marked and is accompanied by other symptoms.

These symptoms of depression do vary; the DSM-IV recognise three main types of depression, only two of which will be mentioned here, and only one of which will be covered in detail.  A possible 6 mark question on the paper could ask you to describe the symptoms or characteristics of depression.  Clearly ‘feeling sad’ is not going to earn you very much credit!

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.  This may be associated with circadian rhythms

Physical symptoms

Disturbances of sleep: patients sometimes report insomnia, but sleeping longer than before is also common, perhaps as patients attempt to escape their problems. 

Appetite can also decrease or it may increase in the form of comfort eating.  Part of this may be due to boredom since typically depressed people tend to have lower activity levels.

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.  This could be because they don’t want people to see them in a depressed state.

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.


Famously Sir Winston Churchill suffered from manic depression and referred to his low moods as his ‘Black dog.’

Bit of trivia for those of that persuasion: this particular photograph, perhaps the most famous of Churchill was taken by the great *Karsh of Ottawa.  Legend has it that having problems getting the picture he wanted he leaned forward and pulled the cigar from Churchill’s mouth.  This was the result!


*Yousuf Karsh, although always referred to as ‘Karsh of Ottawa’ was actually born in Armenia!



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 four of the following:




Like some of the other symptoms this can swing either way.  Sometimes patients report insomnia, other times a desire to sleep all the time


As above, sometimes patients lose their appetite resulting in weight loss, others engage in comfort eating and show noticeable weight gain.


This usually decreases (except during a manic phase of bipolar) and patients can be lethargic.  To be diagnosed this needs to be observable rather than just the patient feeling there’s been a change. 


Usually energy levels take a sharp decline with general lack of interest


A major symptom is the negative feelings experienced by most patients.  These can be about self, World, future (see Beck)


Usually manifested by difficulties holding concentration


In the more severe cases of depression, recurrent thoughts of death and/or suicide.


All of these in the absence of bereavement. 

Also as with schizophrenia, symptoms and severity vary between patients.  Some unipolar patients experience delusions and hallucinations (more common in bipolar).  Many patients don’t respond to SSRI or MAOI drug treatments whereas others do.  Sometimes patients diagnosed with depression will respond better to a combination of antidepressants and anti-psychotics such as chlorpromazine.  This all tends to suggest that like schizophrenia, major depression should not be seen as a unitary disorder but rather a collection of related disorders with some overlapping symptoms, but with different causes and prognoses. 



Age of onset of depression appears to have fallen in the second half of the twentieth century.  Increasingly adolescents are beginning to display symptoms of depression.  If depression goes untreated then each bout typically lasts about six months, although this can be reduced to a more typical three months following treatment. 

Women are up to four times more likely than men to be diagnosed with depression and we’ll consider possible reasons for this later.  Up to 9% of women are diagnosed with depression compared to only 2 0r 3% of men. 

About 10% of patients diagnosed with unipolar depression will commit suicide.


Categories of depression

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)..


Differences between unipolar and bipolar disorders



Persistent low mood

Swings between high and low mood

Up to 3 times more common in women

Similar incidence in men and women

Around 5% incidence in the general population

Around 1% incidence in the general population


Far more common in creative people (writers, actors, comedians etc).

In twin studies about a 46% concordance rate between MZ twins

In twin studies about a 72% concordance rate between MZ twins.


Mania is rare on its own, usually being accompanied by bouts of depression. 

Symptoms include:

  • Rushing around but achieving very little.
  • Sense of euphoria
  • ‘Flight of ideas’ in which sentences seem to skip all over the place
  • Puns and word-play
  • Occasional grandiose delusions
  • Increased sexual appetite
  • Sending sprees

A common feature is starting a huge task, or many tasks simultaneously but not finishing them off… presumably because the mania wanes and the depression kicks back in.




These are the two most widely used and quoted methods of categorising mental illness. 

DSM (Diagnostic and Statistical Manual) devised by the American Psychiatric Association in 1952.  Its last major revision was 1994 when DSM-IV was published.  DSM-V is currently under construction and is expected in 2013.

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.



Famous manic depressives

Stephen Fry

Ben Stiller

Robin Williams

Robbie Williams


Endogenous or reactive depression

This is a second way of distinguishing between depressions that relates more to causes rather than symptoms.

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.


Depression is also a major factor in a number of other related disorders such as Seasonal Affective Disorder (SAD), Premenstrual syndrome (PMS) and Postpartum depression (PPD).  The latter was formerly known as post natal depression.


Depression and Anxiety

Generally speaking the general population are accepting of depression but tend to be more concerned about psychotic disorders such as schizophrenia.  Mood disorders, like anxiety disorders are not seen as threatening and are usually not too far removed from ‘normal’ or everyday behaviour.  They are also far more common than psychoses. 

There tends to be lots of overlap between depression and anxiety, both in terms of symptoms and in terms of diagnosis.  It’s thought that as many as 90% of patients suffering from depression also exhibit symptoms of anxiety, such as interruptions of sleep, ability to concentrate and panic.  Some have even suggested a new category of ‘mixed anxiety depression’ with the unfortunate abbreviation ‘MAD.’  It’s also worth mentioning that stress can be a symptom of both, as well as a potential cause! 

Famous manic depressives (continued)

John Cleese

Van Gogh (probably)

Jim Carey




Reliability and Validity of a Diagnosis of Depression


Considers the extent to which a diagnosis of depression is consistent:

  1. over time (test-retest)
  2. between professionals (inter-rater)

Keller et al (1995) found the following concordance rates:

  • Test-retest (0.61) which was classed as ‘fair’
  • Inter-rater reliability (0.8) which was classed as ‘fair to good.’

The reason given for what seems like the low figure for test-retest reliability was the strict diagnosis criteria for major depression.  Criteria such as ‘lethargy’ and ‘change in activity’ are very subjective and prone to change over time.  If one of these items is seen as present on first test but absent on the second then such a fickle diagnosis can be altered.



Considers the extent to which the different types of depression are really that distinct from one another.  For example is it valid to distinguish between MDD and dysthimic disorder. 

When these are compared there does appear to be plenty of overlap leading some to question whether they are distinct disorders. 

A major issue with diagnosis of depression, particularly in the UK is the GP making the decision.  As there title suggests, these are general practitioners and not specifically trained for diagnosing psychological disorders.  Often their diagnosis of depression is based more on their prior knowledge of the patient rather than by adhering to the DSM criteria. 


Factors reducing reliability and validity

1. Categorical

Think back to your AS and the issue of defining abnormality.  One of the main issues with the definitions is the idea of a cut-off point.  Psychopathology still tends to be very black and white.  A person either has depression or they don’t (and similarly for schizophrenia, PTSD etc).  Is a person who has six of the above symptoms for 10 days or four of the symptoms for two months really not suffering from depression?  Many psychologists prefer to see depression as a continuum ranging from relatively mild and short-lived symptoms through to a more extreme higher end.    Kendler and Gardner (1998) believe that the DSM diagnosis is pitched towards the higher end of this spectrum. 

2. Arbitrary classification and measurement of symptoms

Many of the diagnostic criteria are very loosely defined.  How much energy does a person need to lose?  How much does the ability to concentrate need to be reduced…and so on.  It seems to be assumed by the diagnosis, that people with just a few of the symptoms are healthy and pucker.  However, over half of these patients go on to develop other symptoms and become officially depressed. 

3. Co-morbidity

It isn’t unusual for a patient to be suffering from two or more psychological conditions simultaneously.  As we’ve already seen, depression and anxiety seem to be closely related and it is common for a patient to be suffering from both in some form.  For example, 39% of agoraphobics also suffer from MDD.

This suggests that different disorders as classified by the DSM and ICD may not be quite so distinct as they suggest.  It also raises a more practical issue; which disorder should be treated first?


Reliability and Validity of Beck’s Depression Inventory (BDI)

The BDI is one of the most widely used tests for assessing the severity of depression.  When it was first published in 1961 it signalled a major shift in the view of depression which until that time had been viewed in psychodynamic terms.  Aaron Beck considered the cognitive symptoms of depression rather than seeing it as a self destructive and inwardly displaced anger. 

The BDI consists of 21 item self-report questionnaire.  Each item is designed to test the severity of a specific symptom.

Items 1 to 14 consider psychological symptoms.  For example:

1. Sadness

0.  I do not feel sad

1.  I feel sad much of the time

2.  I am sad all of the time

3.  I am so sad or unhappy that I can’t stand it


Items 15 to 21 consider the more physical symptoms.  For exampl

14. Loss of Energy

0.  I have as much energy as ever

1.  I have less energy than I used to have

2.  I don’t have enough energy to do very much

3.  I don’t have enough energy to do anything


As you can see, each item is rated 0 to 3 and a cumulative total gives an indication of severity of depression.

0–9 indicates that a person is not depressed,

10–18 indicates mild-moderate depression,

19–29 indicates moderate-severe depression and

30–63 indicates severe depression.


Reliability of BDI

Beck et al (1996) gave the test to 26 outpatients during two therapy sessions one week apart.  The test-retest concordance was a very high 0.93.

The test is also high on split-test reliability (0.85)

Most studies carried out on reliability find that the BDI is a reliable test of depressive severity.


Validity of BDI

The BDI has concurrent validity in that it tends to agree with other measures of depression.

It is also high on construct validity.  An obvious way to judge validity of a test is to observe the person in real life situations.  If the person scores as suffering severe depression then this should be observable in their behaviour. 

BDI-II was introduced specifically to bring it into line with the DSM-IV diagnosis.  BDI-II is seen as having higher content validity than its predecessor BDI-1A.

Note: the BDI is not intended to diagnose depression.  It was designed by Beck to measure the severity of depression in patients aged 13 and over, who had already been psychiatrically diagnosed with depression.  The danger of using it as a diagnostic tool is that the characteristics it is measuring may well be the symptoms of other unknown disorders. 


Medical model

A combination of genetic evidence and discussion of the permissive amine theory is needed here.  Remember too that these are not mutually exclusive.  A decreased sensitivity to a particular neurotransmitter is likely to be caused by a genetic abnormality!

Genetic explanation

All the usual points need to be borne in mind and spelt out to the examiner.  Clearly you will want to mention trends within families, twin studies (MZ and DZ), adoption studies and gene research.  These then need to be evaluated in terms of environmental influences and the extent to which they can explain patterns such as sex differences.

Family patterns and studies

Depression does tend to ‘run in families.’  Gershon (1990) found that the incidence of depression is up to three times higher in families with a history of the disorder than it is within the general population as a whole.  Others have put this figure even higher.  Weissman (1987) looked at the prevalence of affective disorders in general and found that family members with first degree relatives (parent, sibling) with a mood disorder were up to ten times more likely to suffer from one too.

Twin studies

We’ll distinguish here between unipolar and bipolar disorders:

Unipolar or major depression

Allen (1976) reported the following concordance rates:

MZ twins 40%

DZ twins 11%

Suggesting a genetic component to explain the difference between the two.

Bipolar (or manic) depression

MZ twins 72%    (This is the highest concordance rate for any psychological disorder).

DZ twins 14% 

It is worth mentioning that different studies have produced varying percentage figures but the overall trend is usually the same.

You must point out however the shortcomings of twin research:

  1. Environmental factors cannot be ruled out.  Clearly MZ twins share a more similar environment than DZ twins so influences of events, family, friends, education etc. are more likely to be similar on both.
  2. In earlier research it wasn’t always possible to distinguish between MZ and DZ twins so figures may be inaccurate. 
  3. Even in MZ twins reared apart environments may not be that different.
  4. Depression is not entirely genetic since no studies have shown a 100% concordance rate between MZ twins!


Adoption studies

Wender et al (1986) found that the biological parents of adopted children who had developed depression, were eight times more likely to have the disorder than the adoptive parents.  As usual, adoption studies like this provide some of the most powerful evidence for a genetic component.

Genes as diathesis

Clearly there are environmental factors involved in depression.  A negative environment acting on a person genetically predisposed to depression has more of an impact than a similar environment acting on a person without that predisposition.  Kendler et al (1995) found the highest levels of depression in those scoring high on negative life events and having the genetic predisposition. 


Identifying specific genes for depression

The first attempt was by Egeland et al (1987) who researched 81 members of the Old Order Amish Community of Pennsylvania.  Four families within the community showed a much higher than expected incidence of bipolar (manic) depression.  Of the 81 studied 14 were diagnosed with bipolar disorder and all had abnormalities on the tip of chromosome 11.  This caused particular interest at the time since this location is adjacent to genes known to be involved in the production of serotonin (see biochemical section below). 

However, other studies have failed to replicate the findings suggesting that either this gene is not responsible or more likely; more than one gene is involved.  Nemeroff (1998) has implicated a gene on the X chromosome.  Recent research has also suggested a possible lo=ink with genes on chromosomes 4,6,11,12,13,15,18,and 22.  Clearly genetically complex!

A possible link between genetic and biochemical influences…

Ogilvie et al (1996) found that people with depression were far more likely to have abnormalities on a gene known as SERT that is used to make serotonin-transporter protein.  New drugs used to treat depression are believed to act on serotonin-transporter protein.


Biochemical explanations

Noradrenalin and serotonin are the likely candidates.  Both are classed as monoamines (as is dopamine).

Background evidence

Schildkraut (1965) found that too high a level of noradrenalin led to mania and too little to depression.  The first finding should not come as a surprise if you consider the chemical similarity between noradrenalin and adrenalin!  Schildkraut believed that serotonin behaved in the same way.  We now know that this is not the case.

Lemonick (1997) found that drugs used to treat depression increased levels of both noradrenalin and serotonin.

Lithium carbonate used to level out some of the mood swings of manic depressives (such as Valerie in the video) decrease levels of noradrenalin and serotonin.

How do these two neurotransmitters work to create depression?


The permissive amine theory:

Kety (1975) believed that fluctuations in noradrenalin levels affect our mood: high levels of noradrenalin leading to heightened mood and eventually mania, low levels to a lowering of mood and eventually to depression.  But what about the role of serotonin which is clearly playing an important role too?

Kety concluded that it is serotonin that controls the levels of noradrenalin by restraining the fluctuations.


Evidence for the permissive amine theory.

Teuting et al (1981) examined the urine of depressed patients and found chemicals that suggest lowered levels of both serotonin and noradrenalin.

Imagine Mr Teuting speaking to the careers adviser at school.  ‘And what would you like to do when you grow up master Teuting?’   ‘I’d like to collect urine samples’ comes the reply.  ‘You’re taking the **ss!!!’ exclaims the careers officer!

Kety (1975) found higher than expected levels of noradrenalin in manic patients.  Bunney et al (1972) reported fluctuating levels of noradrenalin in bipolar disorder patients.

The amino acid tryptophan is an essential pre-cursor of serotonin.  A mutant gene that reduces levels of tryptophan, and results in an 80% reduction in serotonin levels, is ten times more likely to be found in depressed patients. 

Bit more complicated…but bear with me:  Patients in remission that are given an amino acid that lowers levels of tryptophan suffer a brief relapse.  However, patients that have never had depression, given the same amino acid, suffer no symptoms of depression.  This suggests that a previous period of depression alters the serotonin system and makes a future bout more likely. 


Evidence against the permissive amine theory

Deakin & Graeff (1991) report that even following recovery from depression the deficits in serotonin and noradrenalin levels still remain which questions the cause and effect relationship assumed by the model.

Research evidence for the other models of depression can be used to question the theory.


Evaluation of the permissive amine theory

Firstly there are problems of cause and effect (as always).  We cannot be certain that fluctuating levels of noradrenalin are causing altered mood states.  It could be altered mood states causing the fluctuation or a third variable that is causing both.

Secondly, anti-depressives such as MAOIs (monoamine oxidase inhibitors) and SSRIs (selective serotonin reuptake inhibitors) increase the levels of noradrenalin and serotonin within minutes.  However, they have no effect on mood for many weeks suggesting that they are not working simply by increasing the levels of chemical in the brain.  In fact by the time the drugs start to work, it seems likely that levels of serotonin and noradrenaline have probably returned to normal.  There are a few theories as to why drugs such as Prozac (SSRI) might be taking so long to work:

  1. Kennett (1999) believes drugs like Prozac are causing structural changes within the brain such as making neurons more sensitive to amines. 
  2. The post-synaptic neurons need time to adapt to the increased levels of serotonin in the synapse
  3. A more recent theory: The SSRI is increasing levels of neural growth in the hippocampus.  People with a more negative affective style (and more prone to depression) often have increased levels of stress hormones such as cortisol.  These are known to ‘kill off or prune’ (Haidt 2006) certain key cells in the hippocampus.  Prozac and other SSRIs are known to release neural growth hormone which takes about four or five weeks to repair this damage to the hippocampus (Nestler et al 2001).

Thirdly, not all depressives show reduced levels of these chemicals and similarly not all patients benefit from anti-depressives that work by increasing chemical activity.

Finally there is the issue of ‘treatment aetiology fallacy.’  Just because increasing the level of a chemical solves a problem it doesn’t necessarily follow that it was lack of that chemical that caused the problem in the first place.  MacLeod (1998) cites the example of aspirin curing headache as a more obvious example.  Although taking aspirin cures our headache we would not assume that it was lack of aspirin that caused it in the first place!

Treatment aetiology fallacy

Prozac reduces the symptoms of depression probably by increasing levels of serotonin.

But can we be certain that it was lack of serotonin that led to the depression in the first place?



For a fuller account of this theory see the back two pages borrowed and adapted from the ‘find the light’ mental health support group website.


Hormones and depression

Hormones are another family of biochemicals that we need to consider.  These seem to be implicated in disorders such as PMS, PMD and possibly SAD.  They may also help us explain why women are far more prone to depression.  More on gender differences later when we briefly consider other, more feminist, perspectives.


Pre-menstrual syndrome (PMS)

Halbreich et al (1983) found that 43% of women report depressive symptoms at some point in their menstrual cycle.  These are most likely in the week before menstruation and include irritability, bloating, breast tenderness, mood swings and decreased ability to concentrate. 

Abramowitz et al (1982) reported that 41% of women admitted to a psychiatric hospital were admitted either on the first day of their monthly cycle or the day before.


Post-partem depression (PPD)

20% of women report feelings of depression after the birth of a child.  Normally this occurs within a few days but typically only lasts for about a week or so.

It is still unclear whether this is due to levels of oestrogen or progesterone or to increased levels of cortisol which make it difficult to cope with stress.  It is known that in normal people the level of cortisol in the bloodstream peaks in the morning, then decreases as the day progresses.

In depressed people, however, cortisol peaks earlier in the morning and does not level off or decrease in the afternoon or evening. Although the exact mechanism that causes depression is uncertain, clinical studies suggest that chronically elevated cortisol may induce clinical depression by somehow affecting the serotonin system in the brain. 

The chemical dexamethasone lowers levels of cortisol in non-depressed people.  However, when given to patients suffering from depression there appears to be little or no drop in levels of cortisol.  The Conclusion is that their levels are so high the drop appears negligible.  Any drop is also short-lived.  It is thought that the HPA (hypothalamic-pituitary-adrenal) axis acts very quickly to restore cortisol levels in patients suffering depression. 

PPD appears to be more common in women from families with a history of clinical depression suggesting that there may be a family predisposition to mood disorders of this kind.


Seasonal affective disorder

You are already familiar with this from the work we did on biological rhythms.  When I say that it may be linked to melatonin production does that ring any bells?  If you recall we also mentioned that there is a close link between melatonin and serotonin…you see it all starts to fall into place by the time it’s almost too late!

The most common form of SAD is experienced in the winter and is associated with falling light levels.  In the summer light levels suppress melatonin production and darkness stimulates its production which is a factor in the onset of sleep.

It is thought that lack of natural light in the winter months desynchronises our daily fluctuations of melatonin which in turn will affect serotonin production.

Summer SAD is not so easy to explain.  Kay (1994) suggests that changes within the Earth’s magnetic field may cause the alternation between winter and summer SAD.  At first glance this does sound unlikely but there is surprisingly increasing evidence to support it.  I’m not sure where you could tie this in but I’ll include it for general interest and in the hope (rather than the expectation) that a question on external factors of depression may come up.

Following geomagnetic storms admissions to psychiatric wards for summer SAD increase significantly.  Westhead (1996) found that pregnant women and new mothers are 60% more likely to suffer from depression if they live near power cables that also disrupt local magnetic fields.

Bush (aaaaaaaaaaaaaaarghhhhh) just the mention of that name… reported significantly higher suicide rates (six times higher than expected) in 15 to 24 year olds living in the Alaskan hinterland.  He put this down to the aurora borealis (or northern lights) that create changes within the Earth’s magnetic field.  I will leave you to hypothesise about other possible causes of depression in young people living in a freezing cold climate in the back end of nowhere!


Psychological explanations of depression

No surprises here!  The usual collection of explanations based on some all too familiar approaches to the subject.  As always I think it’s a useful exercise to spend a few minutes attempting to predict how each approach will seek to explain a given topic… useful since not only will it boost your confidence but also be good practice for the approaches section of the synoptic paper. 

As always with the approaches there is a mixture of the good, the bad and the downright ugly!  Work out which is which for yourselves but as always keep opinions on the paper as objective as possible and always be sure to back up arguments with research!


Psychodynamic approach

As always Freud (in this case 1917) was the first to offer possible explanations of depression and was also the first to notice the similarity in feelings reported by patients suffering from depression (he called it melancholia) and those who had recently suffered bereavement (mourning).

Freud’s theory has a number of interconnecting strands.  What follows is only a brief overview of what he saw as a complex process:

Loss could be ‘actual,’ as in the case of death of a close friend or relative, or it could be ‘symbolic’, as in the case of a lost job etc.  Either way loss in adulthood causes us to relive childhood experiences of loss explaining the clingy behaviour of some types of bereavement.  In extreme cases regression to childhood may occur, particularly if the child had suffered bereavement during their own childhood.

Hostility and aggression are also involved.  Death causes feelings of anger at our loss and this has to be displaced inwards towards ourselves since outward expression of anger at such a sensitive time would not be acceptable to the superego.  Anger directed towards ourselves causes the feelings of guilt and despair associated with many forms of depression. 

Freud also assumed that in most cases we would have had fallings out with the deceased which would also cause guilt on their death.


Evidence and evaluation

Research for Freud’s ideas that early loss can make us more susceptible to depression in later life is mixed.  At AS we looked at Bowlby’s work on maternal deprivation and separation.  Bowlby suggested that early separation or loss can cause problems in forming later attachments (his so called ‘internal working model’).  This inability to form loving relationships later in life may result in depression.  Others, such as Parker (1992) have failed to find any link between early loss and later depression 

Loss is a factor in relatively few cases of depression (probably as little as 10%).  So what causes depression on the other 90%?

Generally speaking, psychoanalysis has not been successful at treating depression, suggesting the theory behind the treatment lacks validity.

Freud also offered an explanation of bipolar disorder.  The depressed phase is due to the Superego gaining overall control of personality and creating an overwhelming feeling of guilt and unworthiness.  Eventually the Ego strikes back and is able to regain control of personality, but in so doing swings the balance too far the other way producing the manic backlash.  This then leads to a further counter attack by the Superego producing alternating mood swings.


Behaviourist-Cognitive approach

Cognitive explanations of depression can broadly be split into two:

  • Cognitive-behavioural explanations that combine cognitive and behavioural approaches
  • Cognitive explanations that adopt a purely cognitive approach

We’ll look at the first category for starters:

Cognitive-behavioural explanation

It should come as no surprise that these are combined; i. We have seen them used in this way before and ii. They do complement each other nicely, one concentrating on events outside the person and the other considering only events within the mind.

Learned helplessness

Seligman & Maier (1967) carried out their classic study in which dogs were given electric shocks to the feet.  In the control condition the dogs could jump a small barrier and escape the shocks, but in the experimental condition the barrier was higher and the foot shocks were therefore inescapable

In the follow up trial dogs that could not escape in the first part of the study made no attempt to escape the shocks even when they were given the opportunity.  Past experience had taught them that they had no control over outcomes, in effect they had learned to be helpless!

Seligman noticed the similarity between learned helplessness and some of the symptoms of human depression in which patients become passive and accepting of their situation and make little or no attempt to resolve their problems.  This similarity was reinforced by findings that showed a reduction in serotonin and noradrenalin levels in rats that had become helpless in this way.

Would humans placed in a similar situation behave in a similar way?  Hiroto (1974) got participants to endure inescapable loud noise.  In a follow up trial when they were provided with a handle that would turn the sound off they sat back and endured it.


For Seligman, therefore, learned helplessness results in a feeling that the person is unable to exercise control in their lives. 

Seligman’s theory however, did not provide a full picture.  Not everyone becomes helpless in these situations and Seligman was unable to explain the culture of self-blame or blaming others for their predicament.  For example, many depressed patients blame themselves for their failings which does not tie in with Seligman’s idea that they see themselves as helpless. 

The experience of feeling out of control in one particular situation is an experience common to most people at some time but very rarely does it lead to clinical depression.

Later Seligman came to realise the importance of cognitions and particularly the way a depressed person tends to view negative events in an overly pessimistic way.  This brings us nicely to the next theory:


Cognitive explanations

Seligman is seen as a link between behaviourist and cognitive explanations. 

Abramson et al’s theory (1978) can be seen as a logical extension of learned helplessness theory.  It draws attribution theory which is a very well established concept from social psychology and combines it with Seligman’s work on learned helplessness.  Basically any kind of experience we have in life we try and account for using attributions.  However, according to this theory the depressed patient faced with an experience of failure, attributes the failure in a particular way according to three variables.  We shall consider each using the unfamiliar experience of examination failure as an example:

Internal or external?

  • Internal

The person blames themselves.  In the case of exams, I failed to put in the necessary work or I wasn’t up to the task.

  • External

The person blames others or look for external excuse.  We had a crap teacher or there was too much noise in the exam hall.


Stable or unstable?

  • Stable

The idea that things will always be this bad and won’t get better in future.  I just can’t do exams!

  • Unstable

Things will improve.  Next time I’ll be prepared and will succeed.


Global or specific?

  • Global

The failure will apply in all other situations.  There’s no point in sitting other exams because I’m no good at them.

  • Specific

The failure applies only to this examination.  Maths and psychology will be fine.

Learned helplessness would equate to an internal, stable and global outlook.  It’s all my fault, it will always be like this and regardless of the situation!

In 1989 Abramson termed his idea ‘Hopelessness Theory’ believing that the patients pessimistic view of the future creates the expectation that the future will only bring bad things.

Metalsky et al (1987) questioned students who had just failed a psychology exam.  Those found to have an internal, stable, global outlook were still suffering mild depression two days later. 



As always we have the problem of chicken or egg (cause and effect).  Does this particular attribution lead to depression (as the theory implies) or does negative attribution arise from a depressed state of mind?  Peterson & Seligman (1978) believe that it is causal and suggested that this internal, stable, global outlook is present in people prone to depression and acts to trigger depression in those suffering negative life events.

The cause of this depressed attributional style is thought to arise in childhood.  Rose et al (1994) attributed it (that word again) to abuse, parents being overly protective, harsh discipline within the family and to very high expectations from parents.  In fact very similar to some of the possible triggers for anorexia.  Generally however, the theory doesn’t provide a very thorough account of how the negative attributional style develops.

Much of the research is questionnaire based (Peterson & Seligman’s Attributional style questionnaire), with all the problems that arise because of this… demand characteristics, fibs etc…


Beck’s cognitive triad

A cognitive perspective would not be complete without schemas!  Memory, Piaget etc?

The triad involves unrealistically negative views about self, the world and the future.  According to Beck this negative outlook would have originated in childhood, perhaps due to bereavement, overly critical parents or teachers etc.

Essentially Beck believes that a depressed person has developed a negative set of schemas (schemata) upon which their expectations about life are based.  For example they may have developed a self-blame schema which makes them feel responsible for all the things in their life that go wrong or an ineptness schema that causes them to expect failure every time.

These negative schemas are caused by cognitive biases (faulty perceptions if you like):  Some examples of cognitive biases suggested by Neck:

Over-generalisation: an overall negative conclusion about all situations based on one, perhaps trivial event.   For example a bad test result in a maths lesson convinces the person that they are stupid and should not be going to University!

Arbitrary interference: an assumption arising from no evidence at all.  For example you arrange a barbecue and it rains.  Person assumes they are useless!

According to Beck these three types of cognition: views, schemas and biases interact and in doing so reinforce each other eventually leading to clinical depression.



The very kindly looking Mr. Aaron Beck.



There is plenty of evidence to suggest that Beck’s views on negative thinking do apply to depressed people.  However, we still have the issue of what causes what.  Davison & Neale (1998) and later Beck himself believe that the process is two way.  Depression leads to negative thinking which in turn worsens the effects of the depressed mood.  This is called bi-directional. 

A number of successful therapies have built up based on the cognitive approach such as Ellis’ Rational Emotive Therapy (RET) which encourages patients to recognise their negative thoughts and replace them with more realistic outlooks.  Cognitive Behaviour Therapies in general have proved to be most effective in treating a variety of disorders including depression, eating disorders and anxiety disorders.  This also provides indirect evidence for the validity of the theory on which the therapies are based.  More on these in the next section. 


Culture, society, gender and depression

Perhaps not a likely topic for an entire essay, this could certainly be questioned as a six-marker warm up question!

Culture and depression

Depression is far more widely reported in Western society.  Is this due to its higher prevalence, its wider diagnosis or differences in diagnosis in other cultures?


In the West we associate depression mostly with lowered mood, although as we saw at the outset there are distinct physical symptoms too.  In Asian culture depression is very rarely reported or diagnosed.  However, the physical symptoms that we associate with depression do appear to be common, namely apathy, tiredness, lack of volition (no attempt to initiate actions or interactions), loss of appetite etc.  This unwillingness to report psychological symptoms may be due to the stigma some societies associate with illnesses of the mind and the discrimination that families may face as a result.

The Hopi of North America have no word for ‘depression.’  Does this mean it doesn’t exist in their culture?  Perhaps the social support in their culture alleviates the worst effects of stress and depression.

Or could it be that they only report the physical symptoms so suffer from increased incidence of lethargy, tiredness etc.?


Family could provide another explanation of the apparent rarity in Asian culture.  Extended families provide social support that we know can alleviate problems that are stress related (recall your AS).  Stress and depression are known to be closely correlated. 


How some other cultures refer to ‘depression.’   Just as a matter of general interest/knowledge


‘Exhaustion of the nerves’ and ‘Hearts being weighed down.’


‘Ants crawling in parts of my brain.’  (Anatomically closer than the Chinese)


Gender and depression

More likely to be examined since it does shed some light on the possible causes of depression.

Williams & Hargreaves (1995) reported that women are up to three times more likely to suffer depression than men.  One theory for this discrepancy is that in fact men do suffer just as much depression as women but they fail to report it.  Some of it may be hidden behind other behaviours such as alcohol or drug abuse or behind aggression.  Research, however, suggests that men who do suffer depression were just as likely to report it as women.

Some possible explanations for sex differences:


Biological factors:

Menstrual cycle that results in cyclical changes in the body’s hormones.  We have already seen that PMS and PPD are associated with such fluctuations.

Diet appears increasingly likely as a cause of the sex difference.  Diksic et al (1997) found that men make 52% more serotonin than women, which according to the medical model would make men far less prone to depression than women.  Smith, in the same year attributed some of this difference to dieting, particularly in the teenage years.  Low calorie diets reduce the amount of the essential amino acid tryptophan.  Tryptophan is a vital ingredient in the production of serotonin.  (Meat, milk and eggs are the most common sources of tryptophan).

Biological factors alone seem unlikely as an explanation of the huge sex difference that exists.  Other, non-biological factors have been implicated:


Social and cultural factors:

Physical and sexual abuse in early years is known to be a contributory factor to later depression.  Girls are far more prone to these kinds of abuse.

Housewife role.  Jessie Bernard (1976) said that ‘being a housewife makes women sick.’  Unlike men who seem to fair better in a relationship, women (particularly in the housewife role) are far more likely to suffer from depression than unmarried women.   The housewife has little control in her life which can lead to stress, (stress and depression closely linked remember!).  The feeling of lack of control may also contribute to learned helplessness.  Staying at home, looking after children can also be isolating, cutting the woman off from her network of social support, which would normally act as a buffer against stress.  Cochrane (1983) goes further, suggesting that depression may actually be a coping strategy for what they see as an intolerable situation.

Socio economic status: women generally are lower paid than men and far more likely to claim state benefits (particularly single parents who are predominantly women).  Again poverty and lack of control is a major factor in stress and again we have the link between stress and depression.

Generally the links between culture and gender and depression are complex, but in both cases stress and social support appear important.


Behaviourist explanations of depression

Nothing to do with culture or sex differences but instead a very weak explanation of depression in general 

Lewinsohn (1974) believed that death of a person close to you reduces the amount of positive reinforcement you receive (because they can no longer say or do nice things).  As a response to a loss the person may become withdrawn and avoid social contact.  This causes concern from those around, in the form of increased attention, which seeks to reinforce the withdrawn behaviour making it more likely.

Eventually, as the depression continues, the interest by others begins to decline reducing positive reinforcement and furthering the depressed mood.


Peterson (1993) did report fewer pleasurable experiences however, yet again we have issues of cause and effect.  Unfortunately, as always, the behaviourist explanation offers little insight into individual differences, is very reductionist in that it seeks to explain complex issues in overly simplistic ways and is unable to explain the subjective feelings of low mood.



Brain Chemistry Basics

This provides useful extension to what has preceded on the medical model.  However, the first part is also useful background information for what is to follow on medical treatments since it provides a basic explanation of what happens at the synapse. 

Neurotransmitters are chemical messengers within the brain that facilitate communication between nerve cells. 

Let's illustrate with serotonin.  Packets of serotonin molecules are released from the end of the presynaptic cell (the axon) into the space between the two nerve cells (the synapse).  These molecules may then be taken up by serotonin receptors of the postsynaptic nerve cell (the dendrite) and thus pass along their chemical message.  Excess molecules are taken back up by the presynaptic cell and reprocessed.

Several things might potentially go wrong with this process and lead to a serotonin deficit.  Just to enumerate a few possibilities:

1.       Not enough serotonin is produced,

2.       There are not enough receptor sites to receive  serotonin,

3.       Serotonin is being reabsorbed too quickly before it can reach receptor sites, 

4.       Chemical precursors to serotonin (molecules from which serotonin is manufactured) may be in short supply, or

5.       Molecules that facilitate the production of serotonin may be in too short supply.

As you can see, if there is a breakdown anywhere along the path, neurotransmitter supplies may not be adequate for your brain's needs.  Inadequate supplies lead to the symptoms that we know as depression.

The Primary Players (extension)


In the 1960s Schildkraut cast his vote with noadrenaline as the causative factor for depression in the now classic "catecholamine" hypothesis of mood disorders. He proposed that depression stems from a deficiency of noradrenaline in certain brain circuits and that mania arises from too much of this substance.  There is indeed a large body of evidence that supports this hypothesis, however, changes in noradrenaline levels do not affect mood in everyone. 



Obviously there must be some other factor that interacts with noradrenaline to cause depression.  Serotonin has been found to be this other factor. Serious investigations into serotonin's role in mood disorders, however, have been going on for almost 30 years, ever since Prange et al put forward the so-called "permissive amine hypothesis". This view held that synaptic depletion of serotonin was another cause of depression, one that worked by promoting, or "permitting," a fall in noradrenaline levels. 

So, although, noradrenaline still played a major role in depression, serotonin levels could be altered to indirectly raise noradrenaline levels.  Newer antidepressants like Effexor are actually targeted at both serotonin and noradrenaline. Tricyclics (TCAs) also affect both noradreanline and serotonin, however, they have the added effect of influencing histamine and acetylcholine, which produces the side-effects that TCAs are known for, such as dry mouth or eyes, peculiar taste in mouth, sensitivity to light of the eyes, blurry vision, constipation, urinary hesitancy, and others.  SSRIs (selective serotonin reuptake inhibitors)  do not affect histamine and acetylcholine and thus do not have the same side-effects as the older medications.


Treatments for Depression


We shall now consider how the models of depression outlined above, have attempted to produce effective methods of treatment for depression. 

As always these can be split into medical treatments that assume physical intervention such as drugs are needed to put right altered brain chemistry and psychological methods that assume talking cures are required to put right irrational thinking or solve unconscious conflicts. 

As we shall see, depression is unusual in that both medical and psychological interventions seem to be crucial and work particularly well in conjunction with oneanother.  This is not always the case, for example, schizophrenia seems better suited to medical approaches and phobias and anxiety disorders are mostly best resolved using psychological.  Although this is an over-simplification and others would undoubtedly disagree.


Medical treatments

Drugs appear to be the treatment of choice.  Go to your GP suffering from depression and by far the most likely treatment will taking two tablets a day.  However, over the past thirty years the drugs have changed and the choice has increased and improved.  We shall look at three major categories, two of which have a similar mechanism at the synapse.

1. MAOIs (monoamine oxidase inhibitors)

Do exactly what they say on the tin… albeit a rather complex tin!  

For example: Nardil (phenelzine) and Iproniazid


Remember our American cousins refer to adrenaline as epinephrine (hence the epi-pen) that releases adrenaline.

Therefore there should be no surprise to find that noradrenaline becomes norepinephrine. 


Note: adrenaline is Latin for ‘on the kidney.’ 

Epinephrine is Greek for ‘on the kidney.’


Having been released into the synapse, serotonin and noradrenaline are quickly broken down by the enzyme monoamine oxidase.  This will obviously reduce the amount of these two chemicals available.  MAOIs inhibit (or prevent) the action of monoamine oxidase so results in higher levels of serotonin and noradrenaline in the synapse. 


Evaluation of MAOIs

These are seen as being the least effective of the anti-depressants.  According to Bennett (2006) they have a 50% success rate.

Side effects include increased blood pressure and increased risk of cerebral haemorrhage, especially if taken with yeast products, bananas or fish!


2. Tricyclics


For example: Dosulepin (dothiepin), imipramine and amitriptyline



Serotonin and noradrenaline are released into the synapse.  On the pre-synaptic side there are re-uptake sites that reabsorb the chemicals very quickly.  Tricyclics act by blocking these sites (or channels) so again result in more of the chemical being available in the synapse for a longer period of time.  Tricyclics (0ften referred to as TCA for tricyclic antidepressant) are so called because of their three carbon ring structure. 


Evaluation of tricyclics

They are diagnosed for both mild and severe depression and claim to have a 60-65% success rate.

However, they are probably the most troublesome of all the antidepressants usually prescribed.  Since they work on serotonin and noradrenaline pathways they have a number of side-effects, particularly effecting the heart and arteries.  Others include:

Dry mouth  

Constipation -bran cereals, prunes, fruit, and vegetables should be in the diet

Bladder problems -emptying the bladder completely may be difficult

Sexual problems

Blurred vision, dizziness and drowsiness. 

However, these pale into insignificance compared to their major side effect.  They are potentially lethal in large doses!  Not good to be prescribed to any patient and certainly not to people suffering from depression, one of whose symptoms may be thoughts of death and suicide.

Newer tricyclics generally have fewer side effects. 


3.  SSRIs (Selective Serotonin Re-uptake Inhibitors)

These again do exactly what they say on the tin.  They work in a similar way to tricyclics by inhibiting re-uptake, but unlike tricyclics they are selective for serotonin… that is, they have no effect on noradrenaline. 

Examples include: citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline.  By far the most famous of these is fluoxetine or Prozac.  ‘Vitamin P’ as it is often called! 


This should look familiar since it is the right hand side of the diagram on the previous page.  SSRIs work in the same way as tricyclics but only impact on serotonin pathways, rather than serotonin and noradrenaline. 


Evaluation of SSRIs

Because they only alter one pathway (serotonin) they generally have fewer side effects than the tricyclics.  Most importantly it is almost impossible to overdose on SSRIs. 

The most widely experienced side effects are dry mouth and constipation, as with tricyclics.

However, there have been some reported cases of extreme violence and even murder that have been attributed to SSRIs.  Apparently Eli Lilly who make Prozac are currently contesting over 200 cases brought by patients, victims and/or the relatives of victims.

There have also been 250,000 reported attempted suicides (25,000) of which have been successful, by patients on SSRIs.  However, according to Fergusson et al (2005) there is no greater likelihood of suicide than with tricyclics and both are probably fewer than with non-use of drugs.

The risk of suicide seems most acute in under-18s and in the UK prescribing of SSRIs (with the exception of Prozac) to this age group has been stopped. 


General evaluation of antidepressants

It is worth pointing out that all of these drugs take weeks to work which suggests their mechanism of action is far more complex than the above explanations would seem to suggest.  In fact we don’t know exactly how antidepressants bring about the alteration in mood.  As mentioned earlier when looking at the medical model, SSRIs may work by altering the serotonin system in the brain.  Some even believe that the change is to neural growth in the hippocampus (which would explain the four or five week delay). 

There are concerns that antidepressants are being over-prescribed (compare to anxiolytics such as valium in the 1970s).  In 2004 a survey of GPs in the UK found that 80% admitted prescribing Prozac or Seroxat when patients probably just needed someone to talk to!  


Research into the effectiveness of SSRIs

To achieve highest grades you really must provide evidence for the effectiveness or otherwise of antidepressants.  Although the above points are all valid, you don’t need to be an A2 psychology student to point out that drugs often have side effects.  What will separate la crème de la crème from your run of the mill student is the ability to cite and evaluate relevant research and explain why the research is important. 

When discussing drugs it is useful to consider the extent to which they’re curative or palliative.  When we take drugs I suppose we like to think they’re the former.  Curative drugs will eliminate the cause of the problem in this case depression.  If this were the case of course, then when the course of medication ended we wouldn’t return to our former state of illness.  Generally however, as we saw with anxiolytics at AS, antidepressants seem to be palliative.  They ease the symptoms, improve our mood and generally make us feel all better… temporarily. 


Key Study:  Hollon et al (2005)

We don’t really have key studies anymore, but this is a good one to cite.   The initial study was actually carried out by DeRubeis et al (2005)

Depressed patients were treated for 16 weeks.  They received either:

  • An SSRI (paroxetine) or
  • Cognitive therapy

Similar numbers of each group (about 60%) showed considerable improvement. 

Hollon et al (2005) then picked up the reigns and followed these successes for a further 12 months.  They were broken down as follows:


Initial 16 weeks

Continuation period

Relapse rate

Cognitive therapy

No treatment


Drug therapy (SSRI)

No treatment


Drug therapy

Drug therapy



What this tells us

When cognitive therapy was stopped and no further treatment was received, relatively few suffered relapse into depression.  This suggests that cognitive therapy has dealt with the cause of the depression. 

When drug therapy is given and maintained relapse rate is relatively low (though not as low as therapy) which suggests the drugs are working provided they are maintained. 

The most telling figure however, is the 76% that relapse when the drugs are withdrawn.  This confirms that drugs are fine until medication stops.  During the prescribed period the drugs are reducing the symptoms but not dealing with the causes.  If they were then the patient would be fine when medication stopped.  In fact three quarters of patients become depressed again.  Drugs appear to be palliative


Do drugs permanently alter the brain’s serotonin system?

De Rubeis and Hollon join forces along with others in this well thought out study.  They found that patients being treated for a second or third time with antidepressants are far less likely to derive benefits from the medication.  Effectiveness dropped from 60% (first timers) to below 20% in those who had previously been prescribed similar drugs. 

This is easiest explained by assuming that these must be difficult cases, having clearly relapsed in the past.  However, when these repeat patients are treated with cognitive therapy the success rate is just as high (40%) as first timers.  The researchers conclude that taking drugs such as SSRIs alters brain chemistry and makes future treatments less effective.  

Electro convulsive therapy (ECT)

ECT is the most controversial of treatments for depression, if not for any psychological disorder. 



Convulsions have been deliberately induced in psychiatric patients for hundreds of years but it wasn’t until the 1930s that Hungarian psychiatrist Meduna used camphor to deliberately induce seizures in schizophrenics, believing that this would act as an antagonist to the disorder.  Two Italian psychiatrists Cerletti and Bini began using electricity to produce the seizures in 1938, having earlier experimented on animals.  Initially the whole procedure was very experimental as they varied the voltage.  It soon became clear that it produced better results in patients suffering from severe depression and during the 1940s it became a popular in the UK and USA.  Although the number of treatments have dropped significantly in recent years, there are still over 12,000 uses in the UK annually.

Spooky or what?  It’s 8.10 am Sunday 11th April and I’m watching Sky Sunrise as I write.  Paper review headline in News of the World: ‘Frankenstein op save me from suicide.’  Apparently some woman from a soap opera called Coronation Street has had ECT.  Sounds like it’s been effective too.

The above story does highlight the negative way in which the treatment is usually viewed. 




 The procedure

ECT is very much a last-resort treatment, generally only used when all other treatments, chemical and talking, have failed, and when the patient is seen as being at imminent risk if suicide. 




The patient is given a general anaesthetic followed a few minutes later by a muscle relaxant

Oxygen is provided throughout.  A current of about 0.6 amps (voltage between 70 and 150V) is passed through the temple of the non-dominant side of the brain (usually the right). 

The current is administered for between 1 and 3 seconds but the resulting seizure lasts around one minute.  In fact it seems as though the seizure is the crucial factor.  Usually there are about three treatments a week for up to five weeks. 


How does it work?

As with drugs, the exact mechanism of ECT is unknown.  Certainly it seems to be the seizure (as opposed to the current per se) that seems to be crucial but exactly what this is doing is unclear.  Theories include improving blood flow in the brain or increasing the transportation of neurochemicals. 


Does it work?

There is plenty of evidence to suggest that ECT can be effective.  Petrides et al (2001) found that between 65% and 85% of patients had a ‘favourable response’ to ECT.  A meta-analysis of studies found ECT to be more effective than drug treatment or placebo ECT.

Placebo ECT

Patients are told they are to receive ECT, are anaesthetised, given muscle relaxants etc. but never receive the shock treatment.  There is a placebo effect with ECT (as you would expect with any form of treatment for depression) however, placebo ECT falls well short of genuine ECT in its effectiveness.  This provides evidence for the validity of ECT as a form of treatment.

De Vreed et al (2005) found that the following groups respond best to ECT:

  • Patients over 65 years of age (41% of ECT patients are over 65)
  • Patients with depression lacking psychotic symptoms such as delusions
  • Patients without personality disorders
  • Patients that respond well to antidepressants (which raises the question; why ECT?)


Side effects and other evaluation points

The most widely reported is memory loss.  This has been reduced since ECT was administered to only one hemisphere of the brain.  In fact the treatment is most effective when given bilaterally (across both sides) but the memory loss that followed was considered too great a risk.  Memory loss is reported by a bout a third of patients. 

Nearly a third of patients report long lasting fear and anxiety following the procedure. 

Cognitive processes also slow for a number of weeks or even months, following the procedure.  Although most psychiatrists seem to think these risks are worth taking, others, most notably Peter Breggin, believe that the treatment is not as effective as widely stated and that the side effects are more severe than most practitioners admit.  Breggin (1997) has found little evidence to show that the beneficial effects last longer than four weeks. 



The WHO guidelines (2005) clearly state ‘"ECT should be administered only after obtaining informed consent."  In the USA doctors should make the patient aware of the risks and the number of treatments that are likely to be needed.  Patients are also told of their right to withdraw from the treatment at any point during the course of shocks.  In the UK the situation seems to be ‘less formal.’  The British Journal of Psychology (2005) found that only half of patients felt they had received sufficient information in advance.

“Approximately a third did not feel they had freely consented to ECT even when they had signed a consent form.”

Amendments to the Mental Health Act in 2009 made it unlawful to administer ECT to any patient who has the ability to refuse consent.  However, it can still be administered against a patient’s will in an emergency and about 2,000 patients annually are still given ECT without consent in the UK. 

ECT is very rarely administered in European countries outside of the UK. 



Psychological Treatments for Depression


Cognitive Behaviour Therapy (CBT)

CBT is currently seen as being the most effective psychological method of treating depression.  Originally devised by Aaron T. Beck it combines primarily the cognitive model with aspects of psychoanalysis and behaviour therapy. 

The basic aim of CBT is ‘cognitive restructuring’ designed to bring about ‘lasting changes in target emotions and behaviour’ (Wessler 1986).  To this end the therapist and the patient (from here on in referred to as ‘the client’) form a relationship in which the irrational and overly negative beliefs of the client are recognised and challenged by the therapist.

CBT has been widely used by many therapists for many years.  During that time it has undergone many revisions with each therapist tailoring the procedure to their own needs.  As a result there are many forms of CBT in use.  However, they all have various characteristics in common and Beck and Weishaar (1989) suggest the following five common elements:

Patients are taught to:

  1. Monitor their negative and automatic cognitions
  2. Recognise the link between cognitions, affect (mood) and behaviour
  3. Consider evidence for and against these automatic thoughts
  4. Replace biased thoughts with more realistic ones
  5. Learn to identify and then change the beliefs that predispose the client to distorted thinking.

Making the client aware of the way cognitive and behavioural aspects feed into mood is referred to as the educational phase. 


Thought catching (cognitive element)

Considers the link between irrational thinking and low mood.  Typically the therapist will set homework in which the client is set clear and achievable goals such as talking to a member of the opposite sex or a stranger or perhaps recognising their automatic thoughts and challenging these.  Homework extends the therapy into everyday life.  However, the therapist needs to be certain that the homework set is realistic.  Setting a task that cannot be achieved is likely to reinforce the client’s negative thinking still further.

Behavioural activation (behaviourist element)

The client is encouraged to take part in enjoyable activities.  It is common for patients with depression to cut themselves off and stop socialising.  Here the therapist encourages the client to get out and engage in activities that they enjoyed before the depression.  For example, play sports, go to the cinema, socialise with friends..

Exercise is seen as being particularly beneficial:

Babyak et al (2006) randomly allocated 156 depressed patients into one of three groups:

  1. Four months of aerobic exercise
  2. Drug treatment
  3. Combination of exercise and drug treatment

After the four months all showed significant improvement.  Six months later when the patients were revisited the groups taking exercise had a significantly lower level of relapse.

With CBT there are usually about 20 sessions followed by ‘boosters’ in the first year to help prevent relapse. 


Does CBT work?

An early study by Rush et al (1977) showed CBT to be more effective in reducing low mood than the drug imimprimine (a tricyclic).  However, in this particular study the most striking feature was the lack of success of the drug!

Elkin (1994) made a similar comparison and found that both CBT and imiprimine resulted in ‘almost complete removal’ of depressed symptoms in 55% of patients.  Both were significantly better than placebo, but the drug did work faster.


Hollon et al (2005)

This will sound familiar because we’ve looked at it as evidence for the effectiveness of drugs, but here it is again.  Depressed patients were treated for 16 weeks.  They received either:

An SSRI (paroxetine) or Cognitive therapy

Similar numbers of each group (about 60%) showed considerable improvement.  These successes were then followed up for a further 12 months.  They were broken down as follows:

Initial 16 weeks

Continuation period

Relapse rate

Cognitive therapy

No treatment


Drug therapy (SSRI)

No treatment


Drug therapy

Drug therapy



What this tells us

When CBT was stopped and no further treatment was received, relatively few suffered relapse into depression.  This suggests that cognitive therapy has dealt with the cause of the depression. 

When drug therapy is given and maintained relapse rate is relatively low (though not as low as therapy) which suggests the drugs are working provided they are maintained. 

The most telling figure however, is the 76% that relapse when the drugs are withdrawn.  This confirms that drugs are fine until medication stops.  During the prescribed period the drugs are reducing the symptoms but not dealing with the causes.  If they were then the patient would be fine when medication stopped.  In fact three quarters of patients become depressed again.  Drugs appear to be palliative.  This suggests that CBT is to be preferred to drugs.

Further evidence for the curative nature of CBT was produced by Segal et al (2005).  Groups of patients were treated with either CBT or drugs.  As with the Hollon study, both were similarly successful. 

Later the recovered patients were ‘made to feel sad.’* Those who had been treated with drugs returned to their negative and dysfunctional thinking (evidence for palliative) whereas those who had received CBT remained more positive and rational (evidence for curative). 

*Was intrigued as to how they did this… here’s the answer: ”Patients listened through headphones to a piece of music presented on a CD player while following instructions to recall a time in their lives when they felt sad. The piece of music was “Russia under the Mongolian Yoke,” composed by Sergei Prokofiev. This piece was re-mastered at half speed and runs for approximately 8 min. This piece, played at half speed, has been shown to be very effective in inducing a negative or depressed mood.”


Note: a lot is made in the literature about the competence of the therapist in ensuring a positive outcome.  However, there have been recent and successful attempts to produce more automated forms of CBT that can be delivered online.  This would seem to negate the need for a therapist at all!


Psychodynamic Interpersonal Theory (PIT)

Devised by Hobson (1985) and originally called ‘conversation model’ since it is based on the therapist and patient having a ‘therapeutic conversation.’ 

The basic assumption of the treatment is that depression arises from disruption of personal relationships.  These are explored during therapy as part of another relationship, the one between therapist and patient. 

The treatment is designed as a short term measure that explores past relationships, particularly those during childhood and adolescence, many of which might have failed.  Its primary aim is to reduce the symptoms of depression ad improve social adjustment.  PIT claims to produce more satisfying current relationships by exploring what has gone wrong with previous ones. 

In order to keep the therapy as brief as possible, the patient and therapist agree during the first few sessions which relationships will be explored.  Future sessions then concentrate on these.  In this way, PIT is unlike the more typical open-ended therapies preferred by the psychodynamic approach.


Three components of depression

  1. Development of symptoms due to biological, genetic and/or psychodynamic factors.
  2. Social interactions that are learned and change over the course of a lifetime
  3. Personality; the enduring dispositional characteristics which may predispose a person to depression

IPT tackles the first two.  It doesn’t consider or attempt to influence personality.

Although PIT has been used to treat a host of psychological issues such as eating disorders, panic disorder and issues relating to HIV, its main focus has always been on depression.  In particular PIT is designed to manage four basic problem areas:


1. Unresolved grief

Grief is normal following bereavement.  However, this considers delayed grief or grief that has become distorted.  For example grief that lacks sadness but manifests itself in non-emotional ways such as odd behaviours. 

Aim of PIT: to facilitate mourning


2. Role disputes

When there are differing expectations about the nature or outcome of a relationship between the people involved.  Perhaps one wanting it to become more serious when the other doesn’t.

Aim of PIT; to recognise the nature of the dispute and decide a plan of action that will resolve the misunderstanding.


3. Role transitions

Depression caused by an inability to cope with life changes and events.  Typical examples would include divorce, retirement, leaving home.  The depressed person is far more likely to see these as a loss rather than an opportunity.

Aim of PIT: Get the patient to give up the old role and accompanying sadness, guilt or anger.


4. Interpersonal deficits

The patient has too few or total lack of supportive relationships, for example no intimate relationships resulting in feelings of inadequacy and low self-esteem.

Aim of PIT: to reduce social isolation.  In this case PIT is more likely to focus on past relationships. 


Does PIT work?

Paley et al (2008) concluded that PIT is as effective as CBT.

They followed 62 patients over a 52 month period.  The effectiveness of the PIT was measured using the BDI (Beck Depression Inventory). 34% of patients showed significant reduction in depressed symptoms. 

However, this study was poorly controlled (by the authors’ own admission) so it is difficult to be certain that it was just the PIT bringing about the improvements. 

Brief interventions can also be useful.  54 NHS patients were either given 12 weeks of PIT or placed on a waiting list for treatment (control group).

In the 33 patients that completed the study there were significant improvements.  However, there was a very high drop out rate, mostly from the ones on the waiting list.


Overall evaluation


Many psychologists consider CBT to be too limited in its approach, considering mostly the cognitive processes underlying the negative cognitions.  PIT recognises the importance of relationships in the development and treatment of depression so adds a new dimension to therapy. 

PIT is especially useful in depression known to be at least partly due to relationship issues, such as divorce and bereavement.