Psychological explanations of depression

However, it is not known whether the MZ and DZ twin pairs experienced equally similar environments. As a result, it is possible that some of the higher concordance rate for MZ than for DZ twins reflects environmental rather than genetic influences. This is supported by studies such as Kendler & Prescott (1999) who tested 3.790 twin pairs and found the hereditability factor of 39% but also an environmental factor of 61%. Thus, there is some degree of evidence for a genetic component in depression, i.


genetics may be a predisposing factor and environment a precipitating cause. Numerous theories have also been put forward based on the notion that low levels of the neurotransmitters noradrenaline and serotonin may play a role in the development of depression. It has also been suggested that there may be increased levels of these neurotransmitters when bipolar disorder patients are in their manic phase. Kety (1975) put forward a permissive amine theory of mood disorder. According to this the level of noradrenaline is generally controlled by the level of serotonin.

When the level of serotonin is low, however, noradrenaline levels are less controlled and so they may fluctuate wildly. Dopamine also plays a role. In depression, the theory maintains that when serotonin is low (inherited factor) and this causes noradrenaline and dopamine levels to be inadequately controlled. Hence, depression is produced. It is hard to know whether the high or low levels of serotonin and noradrenaline helped to cause the depression, or whether the depression altered the levels of those neurotransmitters.

Support for this theory lies with the anti-depressant drugs (tricyclic drugs) which are effective in treating depression and are thought to increase noradrenergic levels. This suggests the potential importance of altered levels of serotonin and noradrenaline. However, the drugs rapidly affect neurotransmitter levels, but take much longer to reduce the symptoms of depression or mania. A further weakness of the drug evidence is that the drugs effects do not provide direct evidence of what caused the depression in the first place.

MacLeod (1998) called this treatment aetiology fallacy- the mistaken notion that success of a given form of treatment reveals the cause of the disorder. ` There are also psychological accounts of depression. Freud (1917/1950) proposed the psychodynamic approach which argues that depression is created in early childhood. If a child’s needs are over or under gratified during the oral stage, fixation occurs and the person may develop a tendency to be excessively dependent on others for self-esteem. Freud conceived depression to be like grief, in that it occurs as a reaction to the loss of an early relationship (Brown & Harris, 1978).

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