There is a key distinction between major depression (unipolar depression) and manic depression (bipolar depression). According to DSM-IV, major depressive episodes require 5 symptoms to occur nearly every day for a minimum of two weeks. These symptoms include emotional symptoms (sad, depressed mood), motivational symptoms (changes in activity levels, passivity), somatic symptoms (insomnia, hypersomnia), and cognitive symptoms (negative self concept, hopelessness). Patients with bipolar depression experience both depression and mania (a mood state involving elation, talkativeness, and unjustified high self esteem).
Around 10% of men and 20% of women become clinically depressed at some time in their lives and over 90% of these people will suffer from unipolar rather than bipolar depression. In addition to the distinction between the two types of depression, unipolar depression is split into a further two categories; reactive depression- a reaction to a stressful event, such as the death of a loved one and the event triggers and episode of depression and endogenous depression- depression from within a person, for instance it may be due to hormonal imbalances.
Endogenous depression is linked to biological factors, whereas with reactive depression an individual may have a genetic predisposition to depression but it is still psychological factors that are the primary cause. Family studies suggest the involvement of genetic factors. Gershon (1990) presented the findings from numerous family studies in which depression was assessed in the first degree relatives of patients of depression. It was found that compared with the general population, unipolar depression rates were 2-3 times higher where a first degree relative had depression.
One particular study which lends weight to genetic involvement in depression is that of Egeland et al. (1987). Egeland et al studied a small religious community living in Pennsylvania which had relatively low incidences of major depressive illness in comparison with the surrounding communities. One family that was studied had an extremely high level of bipolar disorder. 11/81 members had manic depression and on examination of their genes it was found that two marker genes on chromosome 11 appeared to be different.
Importantly, these genes were ‘neighbours’ of those that are involved in the production of monoamines, a biochemical implicated depression. The genetic element to depression is also supported by the study that found that the biological parents of adopted children who later developed depression were 8 times more likely to have had clinical depression when compared with adoptive parents (Wender et al. 1986). The clearest evidence about the role of genetic factors in the development of major depression and bipolar depression comes from studies on monozygotic (MZ) and dizygotic (DZ) twins.
Allen (1976) reviewed twin studies and reported that the concordance rates for bipolar depression were MZ= 72% and DZ= 14%. For unipolar depression he found concordance rates of MZ= 40% and DZ= 11%. This was replicated by Bertelsen et al (1977) who also found similar concordance rates of (for unipolar disorder) MZ= 59% and DZ=30% and for bipolar disorder found rates of MZ= 80% and DZ= 16%. These findings suggest that genetic factors are involved in both types of depression, and that their involvement is greater for bipolar than for major depression.