Johnson-Laird’s (1983, 1988) theory of mental models overcomes many of the limitations of current cognitive theories of depression. This approach lends itself readily to an account of depression that emphasises both the psychological and the social levels of vulnerability. It proposes that the depression-prone individual is likely to have a narrow range of valued goals and roles with few other sources of self worth. The threat to or loss of an overvalued goal or role should lead to depression, because no other sources, of self-worth are available to the individual.
However, in recent years research has been more focused on social factors, which attempts to examine the massive role of the socio-cultural environment into individual who is depressed. Research has generally support evidence that depression is expected to occur more commonly among working-class women. However, in recent reviews it has been suggested that ‘middle-aged, middle class, married, never divorced housewives, those women who assumed the traditional roles of wife and mother have a higher rate of depression than working women or women who have been divorced’ (Bart, 1974). To support this Becker (1964) states also that depression is more common among middle-class women. He describes this as middle-class women have an expected higher expectation and/or role which if not reached will inevitably cause feelings of guilt, low self esteem and depression. Working class women would explain her disappointment in terms of social deprivation whilst the middle class women would put it down to personal failure. Costello (1976) also agrees with the expectation developed for middle-class women to be responsible for it. However, with this research there is no systematic epidemiological research to support. The cognitive models focus on depressive cognitions the cause of clinical depression. Researches from others, particularly Brown & Harris (1978), illustrate the role of social factors. They looked at community surveys in urban and rural populations. 220 women who reported clinical levels of depressive symptoms were interviewed to find out about their life events and personal difficulties. They found four vulnerability factors:
- Women from lower social class were more vulnerable to depression than middle class women
- Absence of a confiding relationship
- Three or more children at home under 14 years of age
- Loss of own mother at age 11 or under
From these results they devised their socio-economic model of depression which entailed two aetiological elements:
- Provoking agents - severe life stress: events with severely threatening long term implications/long standing difficulties (e.g. redundancy).
- Vulnerability Factors - Social/personal characteristics which increase the likelihood of an individual developing an affective disorder in presence of sever life stress (a provoking agent).
Brown & Harris (1998) hypothesised that vulnerability factors reduced the individuals psychological resourced to cope. It reduces their self-esteem. However, they found it is not individual provoking agent or vulnerability factors that cause depression; it is their combined effect which causes depression.
Kendler et al (2000) found previous evidence had suggested that the etiologic role of stressful life events in major depression is reduced in recurrent versus first-onset cases.
Rutter et al (1975) carried out interviews on working class mothers and found evidence to support that lower social class groups were at a higher risk of depression. It has been suggested that psychosocial factors might play a role in creating vulnerability to depression as well as provoking it. Cassel & Kaplan (1972) showed that women without social support stood more chance of complications in life and therefore leading to depression. Provoking agents have contributed to depression and also illustrates a vulnerability factor. There is evidence to suggest that events can act as symptom formation factors and that the link is much what would be expected from everyday emotional responses to events. In general, feelings of depression will follow something that has happened and about which little or nothing can be done. If social factors are to be blamed, then attention to a person’s environment would be more effective than physical treatment. It has been commonly argued that quite trivial stimuli can at times produce illness.
Environmental factors that are known to affect mood include stresses such as financial or family difficulties, losses such as bereavements, relationship break-ups, and loss of employment. Losses and stresses appear to be particularly important prior to the first episode in that they tend to precipitate the illness, but subsequently mood-swings may occur without the same level of upsetting events occurring in the person's life. Alcohol, drugs, medication can all cause depression or elation in people who are predisposed to mood-swings. While most peoples' moods are minimally affected, at most, by these substances, people who have a biochemical tendency towards depression, in that they have a family history or past history of the disorder, can often find that they experience a major depression or elation with these chemicals.
Biological theorists have suggested that malfunctions in the brain caused by a chemical imbalance involving the neurotransmitters which prevent transmission by the nerve cells is one explanation for depression. There has been extensive research done in the past twenty years by genetic researchers in order to identify the genes that cause depression. As recent genes have not been identified and one reason may be that several genes contribute to the problem. This means that each gene makes a small contribution and is therefore, hard to spot. Much of the existing body of knowledge concerning the causes of depression points to genetics. Many scientists have isolated single genes to which they believe depression can be attributed; however, very few agree on which gene it is. Egeland (1987) announced that she had found a gene that provided a strong diathesis toward depression on chromosome 11. Two different groups of researchers (Detera-Wadleigh et al., 1987 and Hodgkinson et al., 1987) found no connection between the same gene and depression, which led to the theory that more than one gene, may be responsible for the disorder. At the same time, Baron et al (1987) announced they had found a genetic link between depression and a different gene. Both Baron and Egeland later stated that their findings may be inconclusive. Bredbecka et al (1993) announced that the gene for depression is on the X-chromosome; the next year Berrettini et al. (1994) reported to have found the gene that contributes to the disorder on chromosome 18 and Straub et al (1994) reported it to be on chromosome 21. McMahon et al (1995) found evidence to suggest that depression was more likely to be inherited from mothers than from fathers, proposing that the gene for the disorder would be different in women and men. At the same time, Stine (1995) published a paper supporting the theory that the gene for depression is on chromosome 18. Gershon’s research found that cases of depression in which there is a connection to chromosome 18 was not present in cases where the disorder seemed to be inherited from the mother. Nurnberger (1997) stated that he and his colleagues found evidence that points to as many as eight different chromosomes that may contain genes for depression, hypothesising that the various genes may work in different combinations; this might explain the different manifestations of depression. Recently, Stine reported that there are “three or four locations that look about equally promising for finding depression genes,” one of them chromosome 18. His research also seems to support Gershon’s; Stine believes that a predisposition from chromosome 18 is present only if inherited from the father.
Research on adults with depression generally points to both biological and psychosocial factors, but there has been considerably less research on children and adolescents (Kendler, 1995). Between 20 per cent and 50 per cent of depressed children and adolescents have a family history of depression. It is not clear whether the relationship between parent and childhood depression derives from genetic factors or if the depressed parents create an environment in which children are more likely to develop mental disorders (Kendler, 2000). Biochemical and physiological correlates of depression have been studied by medical researchers, with results that generally point to a chemical imbalance in the brain as a causal factor (Birmaher et, 1996). Most of these studies have been conducted with adults, so the findings may not apply to children and adolescents (Guetzloe, 1991). Brown & Harris (1998) found evidence that social support reduced risk of depression.
In addition to the number of competing biological theories, many people believe that psychological factors play an equally important role in the development of depression, focusing on environmental stressors; other schools of thought assert that it is entirely psychological, having its foundation in poor early parental relationships (Klein, 1935). The only thing that can be ascertained from the current theories of the origins of depression is that psychology is still very far from discovering the true cause of the disorder. Though treatment is becoming more available and socially acceptable, the origins of depression are still highly personal. Dobson (2001) explains that people get depressed as a result of a complex interaction of various factors.
There are individuals who may become depressed in almost any social circumstances and there are social circumstances in which almost any individual may become depressed (Champion et al, 1995).
Reference
American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders. Washington, D.C.
American Psychiatric Association (2000). Stressful Life Events and Previous Episodes in the Etiology of Major Depression in Women: An Evaluation of the "Kindling" Hypothesis. 157:1243-1251
Brown, G.W. & Harris, T (1979). Social Origins of Depression. London: Tavistock Publication.
Brown, G.W. & Moran, P (1994). Clinical and psychosocial origins of chronic depressive episodes. I: A community survey. The British Journal of Psychiatry 165: 447-456.
Brown, G.W., Harris T.O., Hepworth C., Robinson R (1998). Clinical and psychosocial origins of chronic depressive episodes. II. A patient enquiry. The British Journal of psychiatry, 135: 231-246.
Klein, M. (1935) A contribution to the psychogenesis of manic-depressive states. The Selected Melanie Klein, 116-145. Macmillan, New York.
Nicholi, A (1988). The New Harvard Guide to Psychiatry. The Belknap Press of Harvard University Press: Cambridge