Nature and Causes of Depression A Level Psychology Resources
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People who are more unhappy than usual often say that they are “Depressed”. In most cases, however, they are describing a normal mood change in response to sad events or fatigue. In psychopathology, however, depression does not refer to a normal mood, but to a dysfunctional clinical syndrome. An ordinary, short-lived depressed mood can often be beneficial, in that it allows a person to explore themselves, their values and the situation.
People may emerge from a normal depressed mood with a sense of greater strength, clarity and resolve (Comer, 1995). Clinical depression, on the other hand is so severe and long lasting that it can seriously debilitate a person and may even intensify over a period of time. Depressed patients may find the simplest of tasks so difficult that they cannot complete them. Some people with depression even try to end their lives.
This article examines what depression is and several theories regarding the causes of the disorder. Depressing Statistics 20% – 26% of women and 8% – 12% of men develop depression at some point in their lives 78% will experience more than one episode over the next 10 years; only 22% remain continuously well. Many will show a tendency over time for episodes to become more frequent and closer together The average duration of Major Depression is 8 – 12 months. Half of people therefore go on being depressed for longer than this time.10% – 15% develop persistent, chronic, depression At any given time about 5% to 9% of women and 2% to 3% of men are suffering from depression 10% of those attending GPs have depression; 5% have Major Depression There are 300,000 GPs in the UK each of whom will see 250 patients with depression each year.13% of mothers develop postnatal depression Depression is consistently associated with increased morbidity and mortality from a range of physical illnesses (particularly cardiovascular)8%-15% of people with depressive disorders in contact with psychiatric services eventually commit suicide. The rate amongst community depressives is 3%. Between 3000 and 7000 people each year take their lives whilst suffering from depression.(Blacker, 2000)To be diagnosed with Major Depressive Disorder a person must have had at least one depressive episode, but have no symptoms of mania or hypomania Genetic Factors.
A large number of theorists believe that some people inherit a predisposition for unipolar depression and this view has been supported by family pedigree studies, twin studies and adoption studies. Family Pedigree Studies.
Researchers select “probands” with depression and examine whether their close relatives have a higher incidence of depression than the general population (or the relatives of non-depressed probands). This type of research has confirmed that as many as 20% of the relatives of depressed probands are depressed, compared with 5-10% of the general population (Harrington et al, 1993; Nurnberger & Gershon, 1992). Twin Studies
Studies of monozygotic and dizygotic twins have also supported the genetic theory. One Danish study, for example, found that when a monozygotic twin has unipolar depression there is a 43% chance that the other twin will develop the disorder. If a dizygotic twin has the disorder the probability is only 20% (Bertelsen et al, 1977). Moreover, there is research evidence that suggests that being around a person that is depressed can lower a persons mood. Coyne (1976), for example, found that participants reported feeling worse than usual after a short telephone conversation with a depressed person. Interacting with a depressed person, may, therefore, contribute to the development of depression in that person’s relatives. Additionally, the twin studies demonstrate that factors other than genetics contribute to the disorder: in Bertelsen el al’s study 57% of the MZs of depressives did not develop depression, despite having identical genes.Adoption Studies
A study of the families of adoptees who were hospitalised with severe depression found that their biological parents were more likely to have severe depression than the biological parents of a non depressed control group (Wender et al, 1986), but this was not the case with mild depression.
How could genes cause depression?
The mechanism of how genes lead to depression was investigated in a fascinating piece of research was by Kendler & Karkowski-Shuman (1997). They examined female MZ and DZ twins who were sufferers of major depression using the degree of genetic similarity as an index of genetic predisposition to depression. The number of stressful life events experienced by the participants was measured, these included: assault, serious marital problems, divorce/breakup, job loss, serious illness and major financial problems.
They found that exposure to these stressful events was predicted by the closeness of the genetic relationships. Stressful life events that occurred during depressive episodes were not included in the analysis.
In women, genetic risk factors for Major Depression increase the probability of experiencing Stressful Life Events in the interpersonal and occupational/financial domains. Genes can probably impact on the risk for psychiatric illness by causing individuals to select themselves into high risk environments.While this may appear to be compelling evidence for a genetic basis of depression there are a number of issues to be considered:
The research is based on the premise that genetic factors predispose a person to develop depression. I.e., twins of those who are depressed are more likely to develop depression because of genetic factors.
The increased risk of developing the disorder in MZ twins of sufferers may be due to shared environmental factors.
These shared environmental factors may be what leads them to “select themselves into high risk environments”.
Alternatively, the shared environment itself may be high risk and, thus, account for the findings of the above study. Biochemical factors
During the 1950s it was discovered that the blood pressure medication “reserpine” causes depression in some people (Ayd, 1956). Reserpine was found to lower levels of the neurotransmitter norepinephrine in the brain, which suggests that depression may be related to a lowered supply of norepinephrine. Evidence for the role of norepinephrine in depression:
Reserpine lowers norepinephrine levels
Monoamine Oxidase (MAO) inhibitors increase the supply of norepinephrine in many neurons and at the same time alleviate symptoms of depression
Another type medication used to treat depression, the tricyclics, also increase norepinephrine supplies (Snyder, 1984; 1976).
Because norepinephrine belongs to the class of chemicals called catecholamines this is known as the catecholamine theory. Problems with the catecholamine theory Reserpine also lowers the levels of serotonin in the brain.
This led many researchers to believe that low levels of serotonin may also cause unipolar depression (Golden & Gilmore, 1990). This is known as the indolamine theory, as serotonin belongs to the class of chemicals known as indolamines.
There are a number of possibilities regarding the biochemical contributions to unipolar depression:
Low norepinephrine + Low serotonin = depression
Low serotonin or low norepinephrine = depression
Neither low serotonin, nor low norepinephrine lead to depression.
Low norepinephrine + low serotonin = depression
However, some people become depressed when they take the blood pressure medicine “Aldomet” which lowers norepinephrine levels, but not serotonin levels (Comer, 1995)
Low levels of serotonin or norepinephrine
There is a considerable amount of research that supports the theory that for some people depression is caused by low norepinephrine and that for others, low serotonin. For example, MHPG, a metabolite of norepinephrine is excreted in low levels in some, but not all depressed people (Yazici et al, 1993; Maas, 1975). Similar results have been found with 5-HIAA a major metabolite of serotonin (Yazici et al, 1993; Maas, 1975).
Another line of research involves administering precursors of serotonin or norepinephrine to depressed participants. If they alleviate the symptoms it would support the theory. Van Praag (1984) found that tryptophan, a precursor of serotonin, does indeed reduce symptoms of depression in some, but not all cases. Similarly, Gelenberg et al (1980) found that tyrosine, a precursor of norepinephrine, alleviates depressive symptoms in some cases.
There is also evidence that norepinephrine depression is different to serotonin depression. Indeed, serotonin and norepinephrine are very different chemically and the structures that contain the structures that use these neurotransmitters are also different. Asberg et al (1976) found that depressed participants whose serotonin was depleted were more apathetic and suicidal than those whose norepinephrine was depleted. Suicide attempts by those with low serotonin were more frequent and more violent than those whose serotonin was not depleted.
Some researchers, however, believe that it is not the supply of these neurotransmitters that is responsible for unipolar depression; they believe that ineffective norepinephrine and serotonin receptors are responsible for depression and this creates the illusion of a low supply (Newman et al, 1993).
Other researchers believe that other neurotransmitters, such as acetylcholine may be involved in depression: exposure to insecticides that increase acetylcholine levels causes some adults to become depressed (Gershon & Shaw, 1961). Also, Intravenous administration of physostigmine, which increases acetylcholine supplies, can cause depression in previously nondepressed participants (Risch et al, 1983). It is, of course possible that an overall imbalance between norepinephrine, serotonin and acetylcholine causes symptoms of unipolar depression (Ballenger, 1988).
Evaluation of neurotransmitter theories
Much of the research that has led to the development of these theories has involved chemically generating depression like symptoms in laboratory animals; it may be incorrect to infer that these symptoms are akin to human depression (Overstreet, 1993). Nevertheless, the studies quoted above did involve human participants.
Another difficulty is that many of the studies measured neurotransmitter activity indirectly. It was assumed, for example, that precursors such as tryptophan were converted into neurotransmitters such as serotonin after administration, which in turn increased the activity of that chemical in the brain. Moreover, measurement of neurotransmitter metabolites in urine was believed to reflect neurotransmitter activity in the brain; however, this is not necessarily the case.
Also, it is not certain whether neurotransmitter activity is a cause or an effect of depression. Cognitive theorists, for example, suggest that faulty cognitions precede low neurotransmitter activity and depression, while the biological position claims the opposite. Research has so far failed to confirm either position; negative cognitions can lower the activity of serotonin and norepinephrine, and low levels of these neurotransmitters can cause negative cognitions (Comer, 1995).