The biological model of diagnosis would fundamentally disagree with the view that depression can primarily be explained through psychological factors. This is because the biological model holds that all psychological illnesses, such as depression, are caused by biological factors such as genetics, illnesses in the womb, or being caused as a side-effect of other illnesses. There are other, more in depth explanations.
For example, one view holds that the endocrine system is responsible for depression due to high levels of hormones such as cortisol resulting in depression. However, it may be that cortisol is actually a by-product of stressful psychological events that act as a precursor to depression, suggesting that can primarily be explained through psychological factors. One other explanation suggests that dopamine is controlled by serotonin, associating low levels with depression and higher levels with mania. However, it is not clear how hormones affect depression yet.
Allen supported the view that depression has a genetic cause by carrying out a twins study aimed at proving that depression can primarily be explained through biological, not psychological, factors. Allen studied monozygotic, or identical, twins, and he found that the concordance rating for major depression in monozygotic twins was 40%, while it was only 11% for dizygotic twins. For bipolar depression, the figure for dizygotic twins was modified to 72%. This study suggests that one can inherit major depression, a finding corroborated by a study from Egeland.
Egeland studied an Amish community, finding that the community had a low rate of major depression, but one family in particular had 11 out of 81 members with bipolar depression. Egeland found that these members shared a gene that was neighbours with the genes involved with monoamine production. This is concordant with the suggestion that psychological diseases have a biological cause, also suggested by the prevalence of depression in families such as that of Lord Tennyson. There are, however, problems with the above studies, as well as their findings.
First, the nature/nurture argument could well be used against Allen’s study to explain that depression in monozygotic twins may have such a high concordance because of shared upbringing. A pair of seemingly ‘identical’ twins may be treated as though they are very similar in the home (even dressed similarly), and thus those on the ‘nurture’ side of the psychological debate may argue that because the two are treated similarly, the concordance rate for depression when it occurs will indeed be high.
Seligman, however, suggested that depression was down to a mix of cognitive defects and classical conditioning that he called ‘learned helplessness’, suggesting that depression can primarily be explained through psychological factors. Seligman proposed that humans attribute failure to a cause, and if they subconsciously learn to generalise these causes, then ‘learned helplessness’, and thus depression, can result. These causes refer to the balance between: internal and external factors; stable or instable factors (that is, factors that modify over time or not); and global or specific factors (i.
e. factors that cause all problems, or those that have a specific cause, such as failing an exam due to a lack of revision). A maladaptive attribution style, hailed by Seligman as the main cause of major depression, would involve labelling failure as internal, stable, and global (‘everything is my fault, and there is nothing I can do about it’). To measure this Seligman devised the ‘Attributional Style Questionnaire’, which aimed to measure how people attributed things to external or internal factors.
To experiment and test the theory of learned helplessness, Seligman gave the Attributional Style Questionnaire to college students who had recently failed some of their exams. Seligman found that most pupils who attained poor exam results, unsurprisingly, were depressed after the exams. Two days later, however, those who had made specific attributions to their failure were less depressed due to the fact that they had identified that they could work towards achieving better grades. There are, however, problems with Seligman’s study.
First, it suffers from what can only be described as a rather inferior sample size, which is also unrepresentative due to its composition. This leads to experimental invalidity, although the ecological validity of the experiment is credible due to its real life setting. Finkelstein and Ramey (1977) supported Seligman’s theory by carrying out a further experiment, consisting of two groups of human babies. One group was placed into a crib with a sensory pillow, designed so that the movement of the baby’s head could control the rotation of a mobile.
The other group had no control over the movement of the mobile and could only enjoy looking at it. Later, both groups of babies were tested in cribs that allowed the babies to control the mobile. Although all the babies now had the power to control the mobile, only the group that had already learned about the sensory pillow bothered to use it. This suggests that the role of classical conditioning, or learning by association, can indeed be implicated in the causes of depression. Both this, and Seligman’s study, suggest that depression can primarily be explained through psychological factors.