- Created by: poppet1107
- Created on: 15-04-15 10:44
Unipolar Depression, also known as clinical depression, or major depressive disorder, unipolar depression is a mood disorder, characterised by varying degrees of sadness, lack of energy, lack of self-worth, hopelessness and guilt.
Depressive disorders are the most common mental health disorders, with an estimated 3.5 million sufferers in the UK and every 1 in six having a diagnosable depressive condition at some point in their lives.
Unipolar disorder should be distinguished from bipolar disorder. Whereas unipolar depression is a mood disorder which is seen as a constant negative disturbance to mood, bipolar disorder involves fluctuations between moods of manic depression and mania, unlike in the case of unipolar depression.
Depression has long been argued to be either a physiological or psychological condition, and there is strong evidence that both biological and mental factors contribute to depression, for example some factors may cause the development of depression in the first place, whereas others maintain it.
There has been research into the physiological explanations of depression which include genetic factors and neurotransmitter dysfunction.
For example research using twins indicates a genetic basis for depression. The basis of twin studies is that identical or monozygotic (MZ) twins are naturally occurring clones of each other, sharing all of their genes.
On the other hand, non-identical or dizygotic (DZ) twins share on average half of their genes. Therefore if we assume that the environment shared by twins is roughly the same for both types of twin, then any greater similarities in MZ twins rather than DZ twins shows the action of genes over environment.
It has been found that the closer related you are to someone with depression, the more likely you are to develop it.
McGuffin et al (1996)
Studied 117 pairs of twins, with at least one having unipolar depression and was being treated. They found that 46% of the other MZ twin and 20% of the DZ twin had also suffered depression.
This suggests a link between genetic makeup and unipolar as the MZ twins who have identical genetics had a higher chance of suffering from depression, this in turn supports the hypothesis that being more closely related increases the chance of developing unipolar.
(-) However this study can be criticised due to there not being a 100% concordance rate; if unipolar was 100% genetic then there should be a 100% concordance rate among MZ twins, however McGuffin et al showed that it was not ensured that both twins would experience depression.
(+) This suggests that although there is a link between genetic makeups and unipolar, there must be other factors, environmental for example, that contribute to its development. The aetiology reduces the cause of a major illness to simply being genetics and ignored the idea of environmental factors influencing someone having unipolar.
Another more holistic Physiological explanation of depression is that genes act as a diatheses, within which genetic factors play the role of a diathesis in a diathesis-stress relationship. T
his explanation suggests that there is a genetic predisposition for depression interacting with environmental stressors to produce the end depressive reaction. We therefore may expect such environmental stressors to affect those with this genetic predisposition differently to those without it.
Kendler et al (1995)
Provided support for this explanation, as they found that women who were genetically predisposed to depression were far more likely to develop depressive symptoms when faced with negative life events.
Wilhelm et al (2006)
Conducted a study where 150 Australian teachers were interviewed every five years. At each interview they were then asked about positive and negative life events (such as bereavement, unemployment and marital break-up) and assessed for clinical depression.
The researchers found that negative life events were linked to depression but, most importantly, those individuals who had the short-short allele of the serotonin transporter gene, which has been linked with depression, were particularly vulnerable to depression.
Evaluation of Wilhelm et al.
However variation within this gene alone were not directly correlated with depression, but the vulnerability the gene created only become apparent when an individual also experienced negative life events.
This model demonstrates that genes do not determine who will develop depression but if there has been depression within a family, this may leave a genetic vulnerability to depression, which could be triggered by other environmental factors.
Consequently this also supports the genetic aetiology as acknowledges genetics being a factor of unipolar but acting as a vulnerability which is exposed when an environmental factor (such as the death of a family member) occurs.
An alternative physiological explanation of depression is the belief that a certain group of neurotransmitters called monoamines, which include noradrenaline and serotonin, exists in lower levels in the brains of depressed individuals.
In the 1960’s, it was first proposed that depression stems from a deficiency of noradrenaline in certain brain circuits.
Bunney and Davis (1965)
Found evidence of this through the discovery that indirect markers of noradrenaline levels, such as bi-products found in urine, were often low in depressed individuals.
The role of noradrenaline in depression is supported by the fact that drugs which cause noradrenaline depletion induces depressive states, while those that increase these levels show antidepressant effects (Leonard, 2000).
Ketty's Serotonin Theory
Suggests that serotonin controls the levels of other transmitters and that if low levels of serotonin occur, other transmitters (noradrenaline + dopamine) can fluctuate wildly, producing depression.
NcNeil and Cimbolic’s (1986)
Found the major serotonin-by product is not found in the cerebrospinal fluid of suicidal depressed patients, suggesting it is deficient in depressive's brains.
(-)However, this research study does not establish a cause-effect relationship and such it is difficult to know whether the levels of serotonin caused the depression or whether depression alters the level of neurotransmitters.
The introduction of Prozac and other antidepressant drugs that selectively block serotonin reuptake confirm the association between serotonin and depression.
Delgado et al (1990)
Gave depressed patients who were relieving antidepressant medication a special diet which lowered their levels of one of the precursors of serotonin - tryptophan.
The majority of patients experienced a return of their depressive symptoms, which disappeared again when their diet was returned to normal.
(-) Despite these findings it has been found that individuals without a personal or family history of depression tend not to show any mood changes following tryptophan depletion, despite the fact that tryptophan depletion alters the activity of the same mood-regulating regions of the brain, such as the amygdala, in these individuals as it does in patients with depression in all people. Therefore, lowering serotonin levels does not induce depression in all people
Therefore, lowering serotonin levels does not induce depression in all people. One suggestion by Ann het Rot et al. (2009) is that it is possible that a depressive episode alters the serotonin system such that a person becomes more vulnerable to the effects of future changes in serotonin levels.
Becks Theory of Depression
Which was developed by Beck in 1967 as he believed that depressed individuals feel as the do because their thinking is biased towards negative schema - which is a tendency to adopt a negative view of the world – during childhood.
This could have been caused by a variety of factors, including parental and/or peer rejection, being criticized or by depressive attitudes of parents.
These negative schemas, for example expecting to fail, are then activated whenever the individual encounters a new situation, such as an exam, that resembled the original conditions, such as teacher’s criticism, in which the schema was originally learned.
Negative schema maintain what Beck calls the negative triad which is a pessimistic view of the self, the world (by not being able to cope with the demands of their environment) and the future.
Hammen and Krantz (1976)
This theory is supported by research such as Hammen and Krantz (1976) who found that depressed women made more errors in logic when asked to interpret written material than non-depressed women.
Bates et al. (1999)
As well as Bates et al. (1999) who found that depressed participants who were given negative automatic-thought-like statements became more and more depressed.
(-) However, as with many of these explanations, the link between negative thoughts and depression does not mean that the former caused the latter. Additionally, the process of thinking in depressed individuals has been explained, but the disorder has not.
(-) Some psychologists argue that this theory is simplistic and deterministic in the sense that it has over simplified the theory of depression; Beck’s theory is also seen to be reductionist as it fails to acknowledge that other factors, apart from cognitive ones, may be responsible.
Seligmans 'Learned Helplessness'
Alternatively, Seligman proposed that depression may be learned when a persona tries but fails to control negative experiences.
As a result of this they then acquire a sense of being unable to exercise control over their life, and therefore become depressed.
For example only so many times someone will try to 'get back on their feet' after a tragic event; if a number of tragic events occur one after the other, it is argued the person will learn that 'getting back on your feet' is pointless and not try; when they can overcome a situation, they don't because they've learnt from past experiences that any actions result in failure.
This ‘Learned Helplessness’ then impairs their performance in situations than can be controlled which is a characteristic of many depressives who fail to initiate coping strategies in the face of stress.
Maier and Seligman (1976)
The theory of learned helplessness was tested and supported by Maier and Seligman in 1976, as they subjected participants to inescapable noise shock and insoluble problems, after which the participants failed to escape from similar situations later even where escape was possible.
(-) However, causation cannot be inferred from this study as associations haven't been identified as a lack of reinforcement in social interactions or helplessness may be a consequence of being depressed rather than a cause.
(-) This theory can also be criticised as being reductionist as the behavioural explanation oversimplifies the condition by focusing only on environmental factors, and reduces depression to your past experiences, thus ignoring the influence of biology.