Depression (Unipolar Disorder)
· Describe the clinical characteristics of unipolar depression;
· Outline genetic and biochemical explanations of depression;
· Discuss psychological explanations of depression.
The shit from having a bad day to clinical depression can be very gradual and go unnoticed to the sufferer until quite late.
The term clinical depression refers to a state of depression where the persons ability to cope with everyday life is seriously impaired.
Everyone (Especially if they have had any family history of suffering from depression) is vulnerable to developing it.
Up to 5% of the population can be diagnosed as having some form of depression and there is a 20% chance of having an episode of clinical depression at some point in one’s life
List of symptoms, loosely divided into those that have psychological and those who have physical consequences – overlaps occur considerably.
· Loss of concentration
· Inability to experience pleasure
· Loss of appetite or food loosing its taste;
· Increase in harsh, negative, self-critical thoughts;
· Feeling that others are being over-critical;
· Guilt feelings;
· Feeling helpless and / or without hope that things can improve;
· Seeking to be alone more often;
· Changes in habitual behavior;
· Thoughts of suicide;
· Loss of interest in sexual matters or increased sexual promiscuity;
· Feeling exhausted after 12 hours sleep;
· Sleep disturbance;
· Headaches, chest pains;
· Appetite or weight change;
· Increased alcohol / drug use.
If someone experiences most of these for >2 weeks there is a good chance that they are suffering from depression.
The above is for unipolar depression.
For bipolar depression they’re:
· Reactive depression – resulting from a reaction to external events;
· Endogenous depression – resulting from conditions within oneself
(Aetiology refers to the causes of an illness.)
Who is most at risk?
· Typically appears at 18-22
· Possibly linked to stressors during these years
What causes depression?
Single personal trauma / stressful life event è stress è symptoms of depression.
More often it is evoked by combinations of bad experiences. Physical causes include:
· Side effects of surgical operation or medication;
· Alcohol / drug abuse;
· Withdrawal from drugs;
· Thyroid disease.
Biological explanations of depression:
Genetic Explanation of depression:
· Research concentrates on the individual sufferer, the families of sufferers, and the twin studies in which one twin suffers from unipolar depression.
· If an individual persistently has episodes of depression a genetic factor may be suspected. Several family and twin studies are reported that show concordance rates (when 1 member other than the twin suffering from the condition) between 30 – 40% which is higher than would occur by chance.
Evidence from family studies:
· Gershon (1990) reviewed ten family studies and found that rates of unipolar depression in 1st degree relatives ranged between 7 and 30%. However, this may arguably be genetically or environmentally produced.
· DSM-IV states that there is a high incidence of unipolar depression with those offspring of those with bipolar (manic) depression. However, that could be a reaction to exactly that situation.
Evidence from twin studies:
· Twin studies comparing MZ to DZ but cannot separate out the environmental and genetic effects.
· McGuffin et al. (1996) found 46% concordance in MZ twins compared with 20% DZ in total of 109 twin pairs with no evidence of the effect of shared environment.
· Bierut et al. (1999) carried out a study of 2662 pairs of twins in Australia and although they reported a hereditability factor of between 36 and 44 % they claimed that environmental factors played a larger role.
Evidence from adoption studies:
· Most show an increased risk in the biological relatives of people with depression rather than adopted relatives.
· Wender et al. (1986) found that biological relatives were 8 times more likely to have depression than adoptive relatives.
· It seems unlikely that a single unipolar gene will ever be identified.
Evaluation: Genetic explanations.
· Some genetic evidence, but, shared genes normally share the same environment; therefore it could equally be learned behavior.
· Risk seems to be increased for MZ twins however, the risks are never thought to be 100%. Genetics seems to be a risk factor but not a whole explanation.
· Predisposing factor: There may be a genetic component operating as a predisposing factor, with additional precipitating causes.
· Genetic uncertainty: Even if genetic factors do play a part in the origins of unipolar depression, it is not clear what the precise mechanism is that is transmitted. Without knowing the specific genes involved, it is impossible to understand how they code biological structures and functions that produce the symptoms of depression.
Biochemical explanations of depression:
The biochemical explanation claims that depression is the cognitive state resulting from imbalances in brain chemistry that can he controlled in many cases by antidepressant drugs known as tricyclic drugs. However, it does not claim that these imbalances are genetic in origin — and, indeed, they may be the consequence rather than the cause of some aspects of the depression. Three brain chemicals are principally involved. These are noradrenaline, serotonin, and dopamine.
Post-mortems of depressed people do not show abnormally low levels of noradrenaline. Serotonin levels are also associated with depressive symptoms, but we do not know whether a low serotonin level is the cause or the consequence of the depression. According to Iversen, low dopamine levels are associated with unipolar depression.
Cases of depression in old age were thought to be associated with the fact that dopamine production naturally diminishes after the age of 45. However, giving elderly sufferers a dopamine replacement doesn’t seem to help.
Although these three neurotransmitters may be involved in depression we do not know how. Researchers investigating the endocrine (hormonal) system have found that the adrenal cortex produces cortisol and cortisone — two hormones involved in metabolism of fats, carbohydrates and proteins. Cortisol production is increased as the individual experiences stress, and this may then trigger other physiological responses leading to the experience of depression. Hormonal (oestrogen and progesterone) imbalances are known to be involved in some menstruation-related depression, although the precise involvement isn’t known.
Some people appear to become more depressed and lethargic and have trouble sleeping during the winter months. This pattern can indicate a mood disorder called seasonal affective disorder (SAD). One suggestion is that this is caused by a lack of daylight.
Some evidence exists for links with the brain chemicals, particularly, serotonin and noradrenalin.
It’s been found that treatment with anti-depressive drugs, which contain serotonin are effective, whereas those drugs containing noradrenaline have no effect (Lam et al. 1996) Speculation concludes that SAD may be linked to serotonergic related mechanisms. Cannot be causal because treatment does not cure the problem, which returns when the drug treatment has ceased. Perhaps a genetic component?
Madden et al. (1996) reports a significant genetic influence in winter patterns SAD. Data was collected from 4,639 adult twins in Australia via a mailed questionnaire – however people lie.
Evaluation: Biochemical explanations.
1. Role of neurotransmitters:
· Significant body of evidence for this argument.
· Theories based on deficit of these chemicals are too simplistic – they do not have an immediate effect on neurotransmitter availability and take several weeks to affect mood.
2. Delayed effects:
· Much evidence implying noradrenaline comes from observations of resperine etc. these do not simply affect levels of noradrenaline – other properties of these drugs may relate to their reaction with noradrenaline.
3. Isolating cause and effect
4. Impairment of stress response system:
· Abnormal levels of regulation of cortisol suggest depression may be related to impairment of the stress response system.
· Such irregularities are not found in all people with depression and are sometimes found in people with other kinds of mental disorder.
5. Role of female hormones:
· Females more likely to suffer from depression, however, only few suffer from post natal depression – so not the inevitable response to hormonal changes.
6. Biological factors as predisposing factor:
· There is no definite evidence of biological features as the cause of depression, although there is a lot of support for the idea that they are a contributory factor. It is likely they predispose people to depression, but that environmental triggers are required before the disorder emerges.
Psychological explanations of depression:
1. Psychodynamic explanations for depression.
Freud’s view is that where early relationships with parents are unsatisfactory because parents are neglectful, unloving, or abusive the child represses its feelings of anger towards the parents and these manifest themselves later as self-criticism, and lack of self esteem and self confidence. Depression develops from these negative feelings.
Bowlby’s (1973) attachment theory supports the idea that inadequate attachments also contribute to depression. Bowlby was supported by Robert Hinde (1977) at London zoo involving the removal of half a dozen or so infant monkeys from their parents and other monkeys and rearing them at various periods. Hinde investigated the nature of early social relationships and one way of testing this was to see what happened when they were disrupted. This research, which Hinde admits that he would not want to carry out now, caused great disruption in the animals behavior from which most never recovered. However, to generalize these findings with baby monkeys to humans is potentially simplistic and misleading.
Evaluation: Psychodynamic explanations
· Difficult to test:
Impossible to tell if Freud’s theory is true as impossible to demonstrate unconscious motivations.
· Presence of anger:
Some evidence people with depression show increased anger but findings are inconsistent. Studies unable to show this anger is directed inwards.
· Effect of loss of parent:
Some evidence that loss of parent in childhood is associated with later depression. However, such loss effects the environment in which the child lives as well as the child’s psychological functioning. It might be that the social and financial hardships that such a loss might entail create a vulnerability to depression.
2. Behavioral explanations of depression:
Lewinsohn (1974) suggests that when someone is deprived of social reinforcement such as feeling appreciated and encouraged and enjoying social interaction, they may become depressed. The individual displays the symptoms of depression, which are then reinforced by others paying them attention, and giving the sympathy that was lacking in the first place.
Martin Seligman’s theory of learned helplessness is influential.
Basically Seligman found that dogs that couldn’t escape from an electric shock learned that escape and avoidance were impossible, and didn’t even attempt to escape subsequently when it was possible. They had learned a ‘helpless’ reaction. Something similar may explain human depression. If you simply cannot achieve something, no matter how hard you try, you may give up and become depressed, knowing that you will never be able to achieve your goals. However, there are many other variables here. Some people are even more motivated to try harder when they fail. There may be a gender difference here, too. One study found that females tend to become depressed, whilst males tend to get angry, when frustrated by failure.
Seligman incorporated an element of cognition in order to refine his ‘learned helplessness’ model, It was developed from Aaron Beck’s faulty self-perception theory (1963). This proposed that people who suffer the symptoms of depression are likely to have negative views about themselves, the situation they are in, and their future prospects. Such feelings become an obsession and interfere with the individual’s ability to deal with the world. This leads to the symptoms of depression.
Beck claims that we inherit strategies for dealing positively with the world. However, environmental factors such as divorce and unemployment can undermine them.
3. Cognitive—behavioral explanations and Beck’s cognitive theory of depression
Most of the evidence for the cognitive—behavioural model comes from Aaron Beck’s work. He believed that depression is largely the result of negative thinking (which he called ‘cognitive errors’).
Beck’s view (1991) states there are three components to depression:
· regarding oneself as worthless
· believing that the world is filled with obstacles
· believing that nothing much is ever likely to change.
This seriously gloomy view distorts the ability to think logically about the world and relationships with it.
Evaluation: cognitive – behavioral explanations
· Research subjects:
Most of Seligman’s studies were conducted on college students, rather than on clinically depressed patients.
· Perception of control:
One of the key elements of hopelessness theory is that the depressed people have little control over their lives. Ford & Neale (1985) however, found that depression students did not underestimate their degree of control.
· Hopelessness as cause or effect?
It is not clear whether hopelessness is a cause of depression or a side effect of becoming depressed. If it is the cause, then it would have to precede the onset of depression.
A 5 year longitudinal study of children by Nolen-Hoeksema et al. (1992) found no connection between attributional style and depression in young children. However, they did find a connection as the children grew older, suggesting that attributional styles may develop over a number of years.
· Hopelessness expectancy:
Abramson et al. (1989) further reinforced the theory of hopelessness to inc. the role of expectancy. Outlining the sequence of events that they thought would lead to hopelessness. This begins with the negative event which interacts with the persons already held negative schemas and a stable and global attribution is made of why the event occurred. These beliefs lead to hopelessness expectation in the future that then may result in depression. They even suggest that hopelessness expectation is a sub type of depression.
DeVellis and Blalock (1992) is a longitudinal study of 57 adults tested the claim that hopelessness expectancy is a sufficient cause for depression. They found support for the link between expectancy and depression, but as moderating, rather than mediating factor, i.e. it does not by itself cause the depression merely by the degree.
4. Diathesis stress model:
No single explanation can account for depression.
Stressful life events
There is no doubt that the traumatic effects of stressful life events can build up overwhelming the ability to cope.
Some people are more vulnerable, genetically, endocrinologically and socially.
Brown & Harris’s longitudinal studies (1993) identify severe life events and long term difficulties as the two factors that trigger depression, especially when the person is feeling vulnerable because of lack of support or an inability to do anything about the situation.
Lock & Key hypothesis:
Parker et al. (1998) proposed a ‘lock and key’ hypothesis of depression which posits that the early adverse experiences establish locks that can be activated by keys mirroring the earlier adverse experience. Theses in turn induce depression. Interviewing 270 severely clinically depressed patients this worked in 1/3rd of their sample (Approx.)
The remaining 2/3rds were diagnosed as reactive depression – therefore not chronic depression.
Unipolar depression is a medical condition, typically first appearing in adolescents and young adults, which is recognised by an enduring group of symptoms including feelings of isolation, guilt, helplessness and even thoughts of suicide. It can be precipitated by environmental and/or biological triggers. Up to 5 per cent of the population may be diagnosed with a depressive illness at any one time.
Some types of depression may run in families and there is growing evidence that vulnerability to depression may be genetically transmitted. However, many behavioural scientists believe that some types of depression may have roots in learning arising from childhood experiences. Where the consequences of one’s actions lead, even unintentionally, to a desired consequence, the behavior may become learned. Showing symptoms of sadness may attract attention and support, which may thus reinforce the sad behaviour, leading ultimately to the experience of depression.
Beck’s cognitive—behavioural model suggests that people’s thinking becomes negative when one’s endeavors’ fail. One becomes self-critical and convinced that one cannot succeed, slowly leading to increasingly severe symptoms of depression.
On balance, it is probable that depression is caused by a combination of several factors — notably genetic predisposition, biochemical imbalances, early psychological deprivation, inadequate parenting, and an excessive exposure to adolescent and adult stressors.
Gershon (1990) - Reviewed ten family studies and found that
rates of unipolar depression in 1st degree relatives ranged between 7 and 30%. However, this may arguably be genetically or environmentally produced.
McGuffin et al. (1996) - Found 46% concordance in MZ twins
compared with 20% DZ in total of 109 twin pairs with no evidence of the effect of shared environment.
Bierut et al. (1999) - Carried out a study of 2662 pairs of twins in
Australia and although they reported a hereditability factor of between 36 and 44 % they claimed that environmental factors played a larger role.
Wender et al. (1986) - Found that biological relatives were 8 times
more likely to have depression than adoptive relatives.
Robert Hinde (1977) - Supported Bowlby at London zoo involving
the removal of half a dozen or so infant monkeys from their parents and other monkeys and rearing them at various periods.
Lewinsohn (1974) - Suggests that when someone is deprived of
social reinforcement such as feeling appreciated and encouraged and enjoying social interaction, they may become depressed. The individual displays the symptoms of depression, which are then reinforced by others paying them attention, and giving the sympathy that was lacking in the first place.
Nolen-Hoeksema et al. (1992) - A 5 year longitudinal study of children
found no connection between attributional style and depression in young children. However, they did find a connection as the children grew older, suggesting that attributional styles may develop over a number of years.
Abramson et al. (1989) - Further reinforced the theory of
hopelessness to inc. the role of expectancy. Outlining the sequence of events that they thought would lead to hopelessness. This begins with the negative event which interacts with the persons already held negative schemas and a stable and global attribution is made of why the event occurred. These beliefs lead to hopelessness expectation in the future that then may result in depression. They even suggest that hopelessness expectation is a sub type of depression.
DeVellis and Blalock (1992) - Is a longitudinal study of 57 adults tested the
claim that hopelessness expectancy is a sufficient cause for depression. They found support for the link between expectancy and depression, but as moderating, rather than mediating factor, i.e. it does not by itself cause the depression merely by the degree.
Brown & Harris’s longitudinal
Studies (1993) - Identify severe life events and long term
difficulties as the two factors that trigger depression, especially when the person is feeling vulnerable because of lack of support or an inability to do anything about the situation.
Parker et al. (1998) - Proposed a ‘lock and key’ hypothesis of
depression which posits that the early adverse experiences establish locks that can be activated by keys mirroring the earlier adverse experience. These in turn induce depression. Interviewing 270 severely clinically depressed patients this worked in 1/3rd of their sample (Approx.) the remaining 2/3rds were diagnosed as reactive depression – therefore not chronic depression.
Concepts to note:
Define these terms:
· Bipolar (manic) depression
· Endogenous depression
· Reactive depression
· Seasonal affective disorder (SAD)
· Tricyclic drugs
· Unipolar depression
What did they do or say?
· Brown and Harris
· Ford and Neale
· Kendler and Prescott