Major depression also known as unipolar depression is a mood disorder describing an individual's emotional state that affects the mind and body physically, psychologically and socially. The American Psychiatric Association (1994) describes Major Depressive Disorder (MDD) as more severe than other mood disorders with respect to severity such as mild, moderate and severe with or without psychotic features and can often be chronic or recurrent. Out of all psychiatric disorders MDD is the most common and related to high morbidity and mortality (Neugebauer 1989, 1999) nevertheless according to the DSM-IV-TR criteria (APA 2000) at least five to nine symptoms of depression within the course of two weeks are required to be present for a diagnosis of MDD even though other symptoms have also been found correlated to the disorder. MDD can be treated in many different ways particularly pharmacologically through the use of antidepressants medication or cognitive behavioural therapy.
Cognitive theories of depression assume that an individual's negative ways of thinking can increase their chances of them developing depression when they experience a stressful event in their life. Those prone to depression consider themselves as being worthless, unlovable, deficient, inadequate and portray their environment as being overwhelming, consisting of obstacles and failure as well as their future to be bleak and hopeless (Beck 1979, 1983). The hopelessness theory of depression (Abraham, Metalsky and Alloy 1989) puts forward the idea that when an individual is confronted by a negative event in their life, if they display a depressogenic inferential style they are more likely to be at risk of developing depression due to their thinking style that they are worthless because of a negative event they have experienced and the thought that another negative event will occur as a result (Beck 1991).
The revised cognitive theories of depression led to the introduction of cognitive behavioural treatment (CBT) which was primarily developed as a treatment for depression (Beck 1979, 1983) and requires the adoption of certain experiential strategies that concentrate on depressogenic information processing and behaviour (Lewinsohn 1975, Lewinsohn et al 1986). To diagnose the depressive affect of a patient, treatment is focussed mainly on the individual's cognition, behaviour and physiology (Klosko and Sanderson 1999). This is because in the cognitive domain underlies the patient's ability to apply cognitive restructuring techniques in order to correct their negative thoughts which form the basis for depression by adopting a more logical and rational way of thinking. Similarly in the behavioural domain underlies the patient's behavioural deficits which maintain and contribute to the onset of depression such as their loss of social reinforcement and social withdrawal and in order to remediate these deficits techniques such as activity scheduling, social skills and assertiveness training are employed. Finally the physiological domain accountable for the patient's anxiety and agitation symptoms such as weight loss, aches, pains, tiredness and constipation is remediated by teaching the patient procedures such as relaxation, mediation and imagery to calm their bodies.
CBT helps patients to recognize their abnormal beliefs and processing tendencies and to analytically test the accuracy of those beliefs and tendencies by making regular use of behavioural strategies in order to shape and restructure the patient's lives and to test their beliefs (Beck, Rush, Shaw and Emery 1979). Patients are encouraged to participate in experiments in which they predict what the outcome of the experiment will be and then conduct the experiment and gather data to see if the prediction they made was correct. Patients usually find that they are overly pessimistic in predicting their likelihood of success and in their own abilities. CBT aims to help the patient make more accurate self assessments and perceptions of the world and in particular their future by teaching patients how to assess the accuracy of their own beliefs; a skill that they can use even after therapy is over.
Research has shown that CBT has performed well in many controlled trials in clinical settings (Hollon and Shelton 2001) and early trials of the treatment suggested that it might be more effective than antidepressants (Blackburn, Bishop, Glen, Whalley, & Christie, 1981; Rush, Beck, Kovacs, & Hollon, 1977) particularly in the reduction of acute distress (Dobson 1989; Robson et al 1990). However, the use of pharmalogical treatments was applied less in these trials (Meterissian and Bradwejn 1989) and studies applying an adequate amount of pharamacological treatment have suggested that both pharmacological and cognitive behavioural treatments are comparably efficient in outpatients samples (Hollon et al., 1992; Murphy, Simons, Wetzel, & Lustman, 1984).
CBT relies mainly upon the quality of how it is applied and it is evident that a lot of the time therapists do not implement it adequately (DeRubies et al 2001, Elkin et al 1999). An earlier study of Jarrett et al (1998) highlighted that patients continuing with their therapy after remission were less likely to relapse than those patients who were withdrawn from their treatment which suggested that CBT past the point of remission can reduce risk of patient relapse and recurrence. Research has shown that continuation of the therapy has reduced the risk of symptoms returning over a 36 month follow-up which suggests that patients will benefit more from the maintenance and continuation of the therapy (Blackburn and Moore 1997). The continuation treatment phase shown that cognitive therapy has a long-term effect that lasts after the end of treatment because patients are treated to the point of remission and therefore are less likely to relapse after the termination of the treatment than those who enter remission after the treatment of medications (Blackburn, Eunson and Bishop 1992, Evan et al 1992, Kovacs, Rush, Beck, Hollon 1981, Simons, Murphy, Levine and Wetzel 1986). The Vanderbilt-Pennsylvania study comparing CBT and pharmacotherapy showed that 25% of patients treated by CBT relapsed within the same year the treatment ended compared to 81% of patients treated with medication relapsed within the same year that the treatment ended.
The pharmacological theories of depression suggest that neurotransmitters; norepinephrine, dopamine and serotonin are involved in the regulation of mood and therefore involved in the process of depression. This led to the belief that use of antidepressants could block out the neurotransmitters into the presynaptic neuron (Duman, Heninger and Nestler 1997). Noradrenal levels also seem to be abnormal in depression and are affected by antidepressants (Wong and Licinio 2001). The National Institute of Mental Health Consensus development conference highlighted that 50% to 85% of patients who have an episode of depression are likely to have a recurring episode therefore treatment of depression has 3 phase; acute treatment where use of antidepressants relieves symptoms (Rockville 1993), continuation treatment where use of antidepressants suppresses symptoms to prevent relapse (Sturm and Wells 1995, Mintz, Mintz, Arruda and Hwang 1992, APA 1993) and finally the maintenance treatment which involves long term use of antidepressants in order to prevent recurrence or emergence of symptoms (Ramana, Paykel, Cooper, Hayhurst, Saxty, and Surtees 1995).
The malaise theory of depression suggests that the state or emotion of malaise should be considered as the main factor of depression rather than sadness of mood consequently MDD is recognised to be the result of inappropriate sickness behaviour caused by the immune activation including malfunction in cytokines. A high amount of research supports the belief that MDD is mediated by abnormalities in cytokines (Smith et al 1998, Maes et al, 1991; Joyce et al, 1992; Maes et al, 1993; Hickie & Lloyd, 1995; Yirmaya, 1997; Connor & Leonard, 1998). Therefore MDD is known as a normal brain response to an abnormal body state suggesting that low mood is the product of malaise concluding that the feeling of malaise should be considered as the main factor of depression (Healy, 1990). Pharmacological treatments such as antidepressants are suggested to apply their effects through an analgesic on the main dysphoric symptoms of malaise. It is seen easier to be happy without malaise just like the way it is seen to happier to be without chronic pains for example a headache and the role of antidepressants therefore is to remove obstacle to happiness through their analgesic effect (Charlton 2000). Moreover the malaise theory would predict that the antidepressant would have an effect on the symptoms of malaise only within hours however mood could take a number of weeks to change (Healy 1990). These notions are in line with those of various other published literature which leads to a large series of predictions being made and tested (Charlton 2000).
It has been well noted that antidepressants have comparable efficacy and similar onsets and action to other forms of treatment to depression (APA 2000). The Depression Guideline Panel (1993) showed that response rates for four categories of medication were higher than they were for pill placebo. The first antidepressant to be identified was Monoamine Oxidase (MAO) which operates by inhibiting the monoamine oxidase making more neurotransmitters available to transmit impulses across the synapse therefore are very efficacious in treating depressions characterized by abnormal symptoms (Thase, Trivedi and Rush 1995). Although efficient they can be fatal causing heart attack or strokes when combined with food such as cheese, red wine, beer and high blood pressure drugs (Thase et al 1995). Tricyclic antidepressants (TCAs) are the most widely used antidepressants and work by inhibiting norepinephrine reuptake or inhibit both norepinephrine and serotonin reuptake which has effect on both neurotransmitter systems (Thase and Kupfer 1996). A major drawback of TCAs is the side effects and up to 30% of patients stop taking TCAs due to the side effects (Depression Guideline Panel 2003). The side effects include dry mouth, blurred vision, drowsiness as well as receptors in the brain being blocked (Preskon and Burke 1992) which blocks the reuptake of norepinephrine and may cause fainting (Roose 1992).It also reduced the number of receptors that participate in serotonin uptake.
Selective Serotonin Reuptake Inhibitors (SSRIs) are favoured by the majority (Olfson et al 2002) and have replaced TCAs because of their ease to use, lower side effects and safety in overdose (Thase and Kupfer 1996). They block the reuptake of serotonin back in to the presynaptic neurons. The main drawbacks are their expense and side effects which are nausea, diarrhoea, headache, tremor, daytime sleepiness, nervousness and insomnia. Several new antidepressants such as bupropion have advantages over the old ones (Croft et al 1999) and can particularly be useful for treatment of depression characterised by weight gain, loss of energy and overly sleeping. Venlafaxine inhibits reuptake of serotonin but also inhibits reuptake of norepinephrine and of dopamine at higher (Haney, Rudolph and Preskon 2000).
About 50% of patients who begin pharmacotherapy respond to all antidepressant medication (Depression Guideline Panel 1993, Murlow et al 1999) although almost 30% respond to pill placebo alone. Research also shows that about 29-46% respond fully, 15% respond partially and 40% do not respond at all (Depression Guideline Panel 2003). According to Charlton (1995) the psychological nature of depression is unclear therefore the way antidepressants act upon depression is unclear which makes the rationale for drug treatment for MDD also unclear.
A study carried out by Rush et al (1979) found that cognitive therapy was more effective than tricyclic antidepressant therapy in patients who were suffering from clinical depression which was refuting the findings of previous research that stated cognitive therapy was not any more effective than placebo therapy and furthermore less effective than pharmacological treatments for depression (Hollon, Shelton and Loosen 1991). One study that suggesting that CBT was less effective than pharmacotherapy was that of Elkin et al (1989) which showed that CBT was less effective than medication and not any more effective than placebo therapy. However, other studies have reported CBT to be just as effective as medication (DeRubeis, Gelfand, Tang, & Simons, 1999). A point to be noted is that neither of the studies included a placebo control which makes it hard to see if the medication treatment was adequately implemented or if any portion of the sample displayed a true drug effect (Klein 1996). A recent study addresses this issue where findings suggested that CBT was as effective as antidepressants and more effective than pill-placebo control (Jarrett et al 1999).
In conclusion it can be said that although antidepressants are the most commonly used pharmacological treatments; they can be problematic and have side effects even though there are studies attesting to their efficacy some patients still do not respond to the medication and there is a chance of patient relapse. CBT on the other hand is a therapeutic alternative with a large amount of empirical evidence attesting to its efficacy whether applied alone or in combination with pharmacological interventions or other treatments. In regard to MDD several studies have suggested that a combination of MDD and pharmacological interventions would be more efficient (Hollon, Shelton and Loosen 1991, Friedman, Wright, Jarrett and Thase 2006). Alternatively there are some studies suggesting that CBT and pharmacotherapy both perform equally well for example a study comparing CBT to Pharmacology which also included a placebo group found that CBT and medication performed equally well for the acute treatment phase of depression (DeRubeis and Hollon 2005). Moreover the use of CBT is more effective in helping patients with depression and apathy, adjust socially and to recover both their interpersonal and professional performance (Oleveria 1998).