All treatments for mental health conditions are based on hypotheses that seek to explain their aetiology. These tend to be reductionist models approaching the problem from one dimension of the biopsychosocial paradigm. Unsurprisingly this approach is far from effective.
Four models and therapies will be described and evidence that offers support or otherwise will be discussed. It will then be concluded that to improve therapy success rates a multidimensional approach faithful to the biopsychosocial paradigm is required.
The monoamine hypothesis of mood disorders is a biological model which states that low levels of monoamine neurotransmitters cause depression. Evidence for this comes from the observation in drug studies that decreasing levels of monoamines caused depression and increasing levels lift it. The low levels of serotonin metabolites in the cerebrospinal fluid of depressed people, and up-regulation of serotonin receptors in the brains of suicide victims is also suggestive (Datta, 2010, pp. 58-61).
If the hypothesis is accurate then anti-depressant medications (ADM) which increase monoamine levels should offer relief. These are first-line treatments for depression but only 50% of depressed people are 'cured' when taking a single ADM. Different formulations or mixes of drugs are more successful (DeRubeis et al. (2008) in McLannahan, (2010, p. 99)). Also their mechanism of action is not clear because although neurotransmitter levels rise very quickly the therapeutic effect isn't felt for many weeks. Increased neurogenesis may be a factor (McLannahan, 2010, pp. 98-99).
Therefore the monoamine hypothesis does not provide a complete picture of depression. The non-universality of the up-regulation of monoamine receptors in suicides, and the wide spectrum of results in serotonin manipulation studies suggest other biological factors play a role (Datta, 2010, pp.60-62). It is also noted that although ADMs are better than placebo they are not better than cognitive therapy, a psychological approach (McLannahan, 2010, pp. 98-99).
Classical conditioning postulates that a behaviour can be triggered by a neutral stimulus if it has previously been associated with an unconditional stimulus. In Pavlov's famous experiment dogs were conditioned to salivate on hearing a bell because it was previously associated with food (Toates, 2010, P. 23-24).
Classical conditioning could explain phobia acquisition if we assume that phobias are learned behaviour and classical conditioning is a type of learning. Support for this comes from the 'Little Albert' experiment where an infant was 'conditioned' to be scared of a rat by pairing its exposure with a loud noise (McLannahan, 2010, pp. 107-108).
Treatment using the classical conditioning model would be to 'extinguish' the conditioned response. Graded exposure therapy is used to achieve this whereby the feared stimulus is gradually presented to the patient without the unconditional stimulus until the fearful...