Twin studies suggest that as like schizophrenia, depression has a higher concurrence rate when it comes to monozygotic (MZ) twins compared to dizygotic (DZ) twins. Research by Bertelsen et al (1977) estimated that in a Danish sample the concordance rate for MZ twins was 43% in comparison to the 20% in DZ twins.
However the same pattern is not proved true for all forms of clinical depression. A study by Kendler, where twins suffering from mild clinical depression were studied, showed that there was little difference between MZ twins and DZ twin, the MZ concordance rate was 49%, which was similar to the 42% concordance rate of the DZ twins. This suggests that some forms of depression, especially the mild ones may be less affected by genes then the more severe ones. Bipolar disorder is said to be more influenced by genetic factors than unipolar disorders (Weissman et al, 1984)
As like schizophrenia, neither family nor twin studies show decisive evidence that depression is genetically transmitted as family members encounter similar life events. If family attitude is full of misery then these attitudes are likely to be transferred on to children. It has often been observed that MZ twins are treated more similarly then DZ twins especially when the DZ twins consist of one boy and one girl.
Adoption studies provide us with most concrete evidence of differentiating between environment and genes. Research by Wendler et al (1986) traced the biological relatives of adoptee’s who had been hospitalised due to severe depression; they found an excessively high occurrence of unipolar depression in these relatives.
In conclusion evidence points towards genetics playing a part in depression, in some parts more than others. However it is suggested that instead of being the direct cause of it, it makes a person more prone to getting depression then others. This pattern represents the diathesis-stress model of abnormality, that genetic factors may make a person more constitutionally vulnerable when they are experiencing general forms of stress, which may involve biological stress such as viral infection or illness.
Another biological explanation into depression is the biochemistry explanation. At the cellular level depression has clear biochemical roots, affecting the way nerve cells in the brain. Severely depressed people have unusual levels of the hormone cortisol, and several brain chemicals, i.e.: the neurotransmitters serotonin and noradrenalin.
According to the catecholamine theory, unipolar depression is caused by the lack of noradrenalin in ones body. According to Ayd 1956 the drug resprine, a treatment for high blood pressure, causes depression in some people. This drug is meant to lower the levels of noradrenalin.
The drug monoamine oxidase (MAO) inhibitors act as an anti depressant, these drugs work by increasing the level of noradrenalin in ones body. Trycylics another group of antidepressants also work in the same way as MAO by increasing the supply of noradrenalin to the brain.
The indoleamine theory suggests that the lack of serotonin could equally be responsible for depression (Golden and Gilmore, 1990). Research has indicated that serotonin plays a similar part to noradrenalin in the cause of depression. Resprine works in the same way as it does with noradrenalin by decreasing the levels of serotonin. MAO inhibitors and trycyclics also increase the levels of serotonin (Amsterdam et al, 1980). The neurons in the brain which use serotonin are in the same location as those that use noradrenalin.
