An alternative psychological approach of depression is the behavioral theory of ‘learned helplessness’ developed by Seligman (1974) which suggests that if people attempt to deal with negative experiences but fail to this successfully, as a consequence feelings of depression will arise as a result of the self-belief of their incapability of succeeding in anything, they therefore stop trying. He tested this by conducting a highly controlled experiment placing dogs in a confided area where electric shocks pulsed through. Once the dogs learned there was no escape, they no longer reacted to the shocks and accepted their fate. Even when opportunities to prevent these shocks arose, there was no attempt. Immediately the issue of psychological harm is raised due depressive symptoms the dogs incurred after shocks. As the experiment was administered in a laboratory it allows the study to be replicated however when conducted on humans the results were not duplicated. These dissimilarities suggests there is low ecological validity and as the experiment uses dogs, it cannot be generalised onto humans. Despite this, Hiroto and Seligman (1974) conducted an alternative experiment results indicate that individuals who had repeatedly encountered challenging events and failed had an increased chance of being unsuccessful in subsequent tasks. Although the behavioural theory helps us to understand depression farther, it is deterministic because it assumes that once behaviour is learnt the individual has no control over stressors when in reality there is. Furthermore, not all bad situations leads to depression as ‘learnt helplessness’ theory suggests.
The second approach to depression is biological, in which the first explanation looks at neurochemical activity in brain. This theory involves the balance of chemicals in the brain, it looks at the deficiency of neurotransmitters; noradrenanaline (NA) which is concerned with emotions and serotonin (5-HT) which regulates NA activity. The permissive amine hypothesis put forward by Kety (1975) suggests depression is caused by the fluctuation of NA causing mood swings due to insufficient levels of 5-HT. Teuting et al (1981) compared substances found in urine of depressed and normal patients. The results showed lower levels of NA and 5-HT in depressed patients, supporting the permissive amine hypothesis. However, it is difficult to know whether its the levels of NA and 5-HT that cause depression, or whether depression itself changes the levels of neurotransmitters. It is known that those anti-depressants that raise NA and 5-HT such as Effexor are an effective treatment in reducing the symptoms of depression. This helps to validates the hypothesis however it is only true for 60% of cases therefore doesn’t account for non-responsive cases indicating there are other biological factors involved. Furthermore, Deakin and Graeff (1991) found that even subsequent to recovery some patients still lacked NA and 5-HT, again suggesting the involvement of other factors. The neurochemical theory focuses on physiological features allowing for accurate measurement and manipulation of variables however the model is based on a correlation between depression and neurotransmitters consequently there is no direct link and therefore doesn’t constitute the cause of the disorder.
The second biological explanation for depression suggests that genetics factors cause the disorder. Gerschon (1990) evaluated family studies and found that the rate of depression in patients who also have depressive first-degree relatives is two to three times compared to the rate of the overall population. His work was supported by Harrington et al (1993) who also assessed family studies and found 20% more likely to have depression if a first-degree relative is also depressive in comparison to a 10% of non-relatives. The results of these studies clearly show a link between the disorder and genetics. McGuffin et al (1996) goes further in verifying this link by looking at the concordance rates of the closest of matched pairs, twins. Monozygotic twins (MZ) are expected to have a higher concordance rate as they have identical genes whereas dizygotic twins (DZ) only share 50% of genes. The results showed a 46% concordance rate for MZ twins and 20% for DZ twins. Supporting results were found by Allen (1976) where the concordance rate for MZ twins was 40 per cent and only 11 per cent for DZ twins. However, it is difficult to tell whether its purely genetic links influencing depression or if similar environment and upbringing have an effect on the occurrence of the disorder. In 1986, Wender et al carried out adoption studies, separating genes and the environment by looking at the biological relatives of adopted depressive patients and found that a higher incidence rate compared to those in the control group indicating that the role of genes play a large part in depression. This can helps sufferers as it removes the ‘blame’ culture from them onto others, namely relatives.
Although higher rates of depression within genetically tied groups are expected to assure justification of the theory, the genetic explantation of depression far exceeds the psychodynamic, behavioural and neurochemical theories as its evidence clearly demonstrate a direct connection between genes and the disorder, basing it on well-established scientific disciplines which can be reliably measured. It also takes into account how environmental factors may induce the depression and separate these whereas all other theories are oversimplistic by reducing the cause of depression down to either the unconcious, learnt behaviour or neurotransmitters and ignoring all other influences.
References
A-level Psychology Psychopathology Revision - Explanations for Depression | S-cool, the revision website. 2011. A-level Psychology Psychopathology Revision - Explanations for Depression | S-cool, the revision website. [ONLINE] Available at: . [Accessed 26 February 2011].
Revision:Psychopathology - The Student Room. 2011. Revision:Psychopathology - The Student Room. [ONLINE] Available at: . [Accessed 26 February 2011].
-Kety (1975)
-Teuting et al (1981)
Cardwell,M (2003) Complete A-Z Psychology Handbook. 3rd Edition. Kent: Hodder and Stoughton.
Cardwell, M. Flanagan,C. (2005) Psychology AS, The Complete Companion. Cheltenham:
-Allen (1976)
-Deakin and Graeff (1991)
-Freud
-Gerschon (1990)
-Harrington et al (1993)
-Hiroto and Seligman (1974)
-McGuffin et al (1996)
-Paykel and Cooper (1992)
-Seligman (1974)
-Wender et al (1986)
Jean-marc Lawton, 2009. Aqa (A) As Psychology (Exams Revision Notes). Edition. Philip Allan Updates.
Roz Brody, 2002. Revise Psychology for AS Level. Edition. Psychology Press.
