Unipolar depression is both viewed as a disorder resulting from dysfunctional thinking processes, and as a disorder resulting from irregularities in neurotransmitters such as serotonin. Compare these two theories and the implications that result from these two contrasting approaches.
Unipolar depression also known as major depression or clinical depression is a mood disorder that consists of long-term depressive episodes including extreme feelings of sadness and worthlessness, low-self esteem, lack of motivation and sometimes trouble sleeping and a loss of appetite. The cognitive models of depression say that mood disorders originate and are sustained by maladaptive thoughts and beliefs. Whereas the biochemical models of depression state that depression originates from irregularities in neurotransmitters and hormones such as serotonin and norepinephrine/ noradrenalin.
Beck's model, the cognitive triad of depression is one of the first theory's that explains depression in this way. The model consists of negative views of self, the environment and the future. Beck says that people are more likely to develop depression after negative thoughts in stressful life events. Negative thinking or 'cognitive desertions' is thought to develop in childhood though learning and dictates how the persons will interpret events in their life. It has been suggested that different types of disorder are characterised by different types of automatic thoughts. Specific depressive thoughts would be ones like 'I will never be able to do this' or 'I'm hopeless'. (Beck, 1967). This is supported by a study by Icoviello, Alloy, Abramson, Whitehouse & Hogan 2006. It examines whether the cognitive risk of onset of depression can also predict the course of the depression and the recurrence in a prospective design. The results show that cognitive high-risk participants had more episodes of depression which were more severe and chronic than low-risk participants when observed over 2.5 years. There were not differences observed in the risk groups during the episodes. This shows that negative cognitive styles predict a worse course of depression as well as rendering an individual prone to depression onset. Therefore the cognitive models state that depressed people have more dysfunctional thoughts than non depressed people do and this dysfunctional attitude increases peoples vulnerability to depression after stressful like events. These negative attributions mean a higher chance of lifetime depression. Relapses are more likely for people who maintain the cognitive distortions, the thought processes that maintain the depressive symptoms. However the sample was chosen to include people with high and low cognitive vulnerability to depression, so it may not be able to be generalized to everyone. Also it may mean there is a biochemical bases that makes them vulnerable to depression.
Evidence suggests that treatments that increase the levels of certain neurotransmitters in the brain relieves the symptoms of depression. However it is not the case that a lack of these neurotransmitters causes the depression as the treatment increases the level of these neurotransmitters within a very short time, but their therapeutic effects take longer to establish. More complex interactions within the neurotransmitters such as receptor irregularities or receptor sensitivity may help to explain this delay in treatment efficacy. Evidence for the role of these systems in the development of depression comes from monoamine depletion study by Booij, Van der Does & Riedel (2003) where healthy participants are subjected to procedures which mimic deficiency in certain neurotransmitter systems (including serotonin, dopamine and noradrenaline) that play a role in regulating mood and cognitive functions, which has an effect in depression. The evidence suggests that the interventions are specific, to their short-term effects on one or two neurotransmitter systems. The AMPT (alpha-methyl-para-tyrosine) procedure is less specific, affecting both the dopamine and norepinephrine systems. Neither procedure has an immediate effect on the symptoms of depressed patients; however, both induce transient depressive symptoms in some remitted depressed patients. The evidence also suggests that ATD (acute tryptophan depletion) and APTD (acute phenylalanine/tyrosine depletion) affect different cognitive functions, in particular different memory systems. (Booij, Van der Does & Riedel, 2003) These suggest that lowering serotonin for example induce mild symptoms of depression in some healthy participants particularly those with a family history of depressive disorder. Therefore those people who do experience a mood response to such procedure may suggest a genetic vulnerability to depression.
A study has shown that genetics' may be a potential risk factor in the development of depression. Although the neurobiological equivalent of the predisposition remains unclear, it seems as though the brain serotonin system plays an important mediating role. Therefore, individuals with a family history of depression may be more likely to develop depression due to an innate altered serotonergic neurotransmission in the brain. A problem, however, is that the role of brain serotonin in depression is complex and this serotonin-related innate vulnerability is not sufficient enough to cause a depression. Stressful life events have been investigated for an additional factor influencing the onset of depression. Furthermore, depression is associated with stress hormone dysregulation and bidirectional interactions are thought to occur between stress-related changes in the neuroendocrine stress system and the serotonergic system. The study shows that healthy individuals with a positive family history of depression are more likely to develop depression due to a genetic serotonergic susceptibility, which deteriorates stress coping mechanisms and increases stress vulnerability. (Firk & Markus, 2007) Although the biochemical model does not take into account individual differences in peoples thought patterns.
It has been proposed that differences between individuals in the kind of negative thinking they show once depressed may be associated with differences in the future course of their depression. In a prospective investigation, a group of depressed women were initially assessed on measures of depression and of negative depressive thinking. They were reassessed 5 months later. Their final levels of depression were significantly and independently predicted, by initial level of depression and by the number of global negative trait adjectives women used to describe themselves at initial assessment. For a given level of depression, women with much globally self-devaluative thinking recovered more slowly than equally depressed women showing less of such thinking (Dent & Teasdale, 1988).
If the cognitive model is believed than the implications is the treatment of patients. They will be treated with cognitive therapies, the cause of the problem will be tackled and the aim will be to reverse the negative thought processes. With practice relapses can be treated quickly as well, this is a long term solution and is specific to each person, although it takes along time and the patient would have to carry on with life during this time. If the biochemical model is to be believed then depressed patients will be treated with drugs or electroconvulsive therapy. The symptoms of depression will be addressed but the cause of the depression may not be tackled. It is a quick solution and allows the patient to carry on with normal life, although the treatment is not specific to each person. (Mitchell, Higgs & Lee, 2008)
In conclusion both explanations can explain some parts of depression. The biochemical model explains how abnormalities in neurotransmitters in the brain can make people vulnerable to depression. The cognitive model can explain how depression is sustained as thought processes certainly maintain depressive symptoms. Both can explain how depression can relapse. No one model can fully explain the onset or continuation of depression. A way to treat depression effectively would be to use a combination of both drugs to cope while doing Cognitive Behavioural Therapy.
- Beck, A.T., (1967). Depression: Clinical, Experimental, and Theoretical Aspects. Harper and Row, New York.
- Booij, L., Van der Does, A.J.W., Riedel, W.J. (2003). Monoamine depletion in psychiatric and healthy populations: review. Molecular Psychiatry, 8, 12, p951-973
- Dent, J., Teasdale, J.D., (1988). Negative cognition and the persistence of depression. Abnormal Psychology. 97, 29-34.
- Firk, C., Markus, C.R. (2007). Serotonin by stress interaction: a susceptibility factor for the development of depression? Journal of Psychopharmacology, 21, p538-544
- Icoviello, B.M., Alloy, L.B., Abramson, L.Y., Wayne G., Whitehouse, Hogan M.E. (2006). The course of depression in individuals at high and low cognitive risk for depression: A perspective study. Journal of Affective Disorders, 93, p61-69
- Mitchell, I., Higgs, S., Lee, J. (2008). Biological Bases of Behaviour. Second Edition. Pearson Education Limited.