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DRUG THERAPY, CBT AND DEPRESSION

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DRUG THERAPY, CBT AND DEPRESSION

 

introduction

Depression is highly prevalent in the current world which makes it a considerable disease burden that results in high economic costs and loss of the quality of life for victims and their family members. Severe depression is believed to be one of the four leading causes of disability in the world and the next 20 years; it may become the 2nd major disability cause after cardiovascular diseases (Racagni & Popoli 2008).

Various effective interventions for depression have been established over the years including drug therapy and cognitive behavioral therapy (CBT). Although drugs are known to produce useful results in treating depression, they are associated with adverse side effects and the issues of placebo effects. Some physicians argue that CBT is more effective in treating depression because it does not include the errors of drug therapy. This essay aims to compare the efficiency of drug therapy and cognitive behavioral therapy (CBT) in treating depression.

Literature Review

According to clinical evidence and meta-analyses, drug therapy in depression therapy is effective because patients indicate positive results when given medication. Additionally, patients who have issued placebo drugs for depression showed significant clinical improvement. However, because physicians do not prescribe placebo drugs to their patients, there are no substantial means of comparing the effectiveness of drug therapy to placebos.

According to Imel, Malterer, McKay & Wampold (2008, p. 197), a meta-analysis was conducted to evaluate the efficiency of psychological interventions such as CBT and pharmacotherapy that involved ten studies as well as one research that compared psychological treatment with the different categories of antidepressant drugs. An analysis of the studies indicated that psychotherapy produced more effects than pharmacotherapy. Moreover, supportive counseling for depression such as CBT is significantly less effective than pharmacotherapy. However, the side effect differences between drug therapy and psychotherapy are small to non-significant for great depression (Fourneir et al. 2010).

In the past 20 years, the efficacy of various antidepressant drugs has been assessed concerning depression. However, there has been no significant evidence on the treatment side-effects of antidepressants. The overall side-effects caused by the new generation antidepressant drugs makes them under-recommended for clinical importance, and little evidence exists on the prescription of antidepressants for majorly depressed victims when alternative interventions such as CBT fail to offer positive results (Parker 2009).

Most experiments on antidepressant drugs, however, include out-patients but significantly exclude in-patients with severe depression and those with suicidal symptoms, alcohol addictions, personality disorders and anxiety complications as a result of a recession. When the degree of depression severity decreases, drug therapy may be more ineffective than useful. From the results obtained in Randomized Controlled Trials (RCTs), any clinical model should prioritize severe depression with psychosis as critical conditions for evaluating discrete and discriminatory response to antidepressant medication. Kirsch et al. (2008, p. 220) state that research conducted in the 1960s to differentiate placebos from antidepressants indicated 60-70% feedback rates to various antidepressant medication and only 10% feedback rates for placebos.

Parker (2009, p. 2) argues that drug therapy is highly effective for patients with brain damages and diseases as a result of melancholic and psychotic depression while psychotherapies such as cognitive behavioral therapy are more useful for slight depression caused by causal personality factors and extreme life incidences. Hence, the main argument is that no intervention should be considered as having a general application across diverse disorders caused by depression- less than half of the patients under drug therapy show full recovery. There is a however great need for more effective pharmacotherapies, but recent efforts to establish better antidepressants have yielded little results.

The principal reason to unsuccessful efforts in the development of novel antidepressant drugs is inadequate knowledge of the pathological system of depression and the mechanism of antidepressant medications. Moreover, there lacks a model that significantly displays the etiological conditions attributing to human depression as well as the symptoms (Vos, Corry, Haby, Carter & Andrews 2005). Antidepressant drugs are more beneficial to patients with extreme depression symptoms compared to placebo and less advantageous to patients with minimal to common depression symptoms.

In the 1960s, the first generation of antidepressant drugs (FGAs) was developed which included tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs) are considered highly effective for drug therapy however their utilization is limited because of their potential lethal side effects such as hypertension (Imel et al. 2008). The TCAs which were developed shortly after the MAOIs are highly efficient and have been used for drug therapy for many years although they are associated with a variety of side effects. According to Racagni & Popoli (2008, p. 288), in the 1980s and 1990s the second generation antidepressant medication (SGAs) were developed which consisted of noradrenergic and specific serotogenic antidepressants (NaSSAs), selection serotonin reuptake inhibitors (SSRIs), noradrenaline reuptake inhibitors (NARIs), reuptake inhibitors (SARIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs). NaSSAs composed of mirtazapine and NARIs comprised of reboxetine are the critical choices for depression treatments. Although many SGAs display less adverse effects to TCAs, they do not indicate significant signs of higher efficacy levels or substantial improvement to drug therapy than the latter drugs.

Discussion

Patients who are given placebos may indicate improvements in depression symptoms even when they are aware the medication is not real (Kirsch et al. 2008). Several researchers from the National Institute of Mental Health (NIMH) conducted a study to analyse the neurochemical system of the placebo effect during drug therapy. The scientists sampled 35 participants with severe depression patients who were not on medication. In the first stage of the research, the participants were simultaneously given placebo drugs which were described as effective antidepressants and others with no antidepressant results, otherwise inactive. The two different groups took their placebo medication for seven days and then switched after a few days. In the 2nd stage of the research, all participants received a ten-week treatment with antidepressant drugs comprising of selective serotonin reuptake inhibitors (SSRIs) and their depression symptoms evaluated.

Participants reported a reduction in depression symptoms when they received the active placebo in comparison to when they received inactive placebo. The significant decrease in depression symptoms was associated with increased µ-opioid receptor activities in some regions of the brain. Furthermore, the expanded µ-opioid mechanism activated by the active placebo was linked with overall better results to subsequent drug therapy. Vos et al. (2005, p. 687) state that the study’s findings indicate that some depression victims are more responsive to drug therapy and may report better results if cognitive behavioral therapies (CBT) that establish physician-patient relationship are integrated into their intervention as well as antidepressants.

There is an increasing prevalence of depression despite the significant increase in the use of antidepressants. However, it has been reported that depression is underdiagnosed and poor compliance is the main reason. It is predicted that only 30% of patients take antidepressant medication according to prescription probably due to their adverse side effects, for example, sexual disorders associated with SSRIs as well as the disappearance of obvious therapeutic influences for several weeks (Fournier et al. 2010). Hence, the fear of adverse effects discourages patients from drug therapy which makes them remain in an untreated or undertreated state; therefore, antidepressant drugs are not necessarily inefficacious.

Antidepressants are considered ineffective because of the concept that they are less beneficial for depression that displays minimal to moderate symptoms, which is the category whereby many victims of depression are found. A majority of depressed patients in the primary healthcare setting are offered pharmacological treatment because it is the only available depression intervention.

Evidence indicates that sertraline offers better outcome to placebo and is equivalent to CBT for patients with chronic depression (Vos et al. 2005). Despite significant enhancements in drug therapy over the years, various types of depression are resistant to treatment thus accounting for failure to respond to antidepressants positively.

Research also indicates that some antidepressants increase the harmful effects of patients, for instance, depressed patients prescribed with fluoxetine display signs of suicidal thoughts. Additionally, a meta-analysis reported the risk of suicidality in 18-24-year-old depression patients partaking SSRIs. The study also revealed that non-psychiatric patients had a higher chance of suicidal symptoms when given antidepressant drugs however the risk was lower for depressed patients (Imel et al. 2008). The drugs fluoxetine and venlafaxine do not indicate a significant increase in suicide risk for adolescents and the youth however are useful for treating depression. Parker (2009, p. 2) argues that although antidepressant drugs offer short and long-term benefits, their efficacy is limited because of the persistence of problems such as regression issues, limited potency, intolerance, and deferred therapeutic inception.

The main reason why drug therapy has limited potency is the mechanism of antidepressants in increasing the levels of monoamine, however; depression victims do not suffer lower neurotransmitter levels (Imel et al. 2008). When antidepressant drugs are consumed, they cause an immediate increase in the levels of monoamine despite a delay in therapeutic symptoms. However, other factors apart from monoamine attribute to depression which indicates the reason for the regulated sufficiency of the drug therapy.

Different meta-analyses and systematic surveys conclude that cognitive behavioral therapy (CBT) is an effective depression intervention; therefore, it is the most recommended as the principal treatment option (Vos et al. 2005).

Conclusion

The drug therapy offers significant aid in the short and long-term to millions of depression victims. However, pharmacotherapy is limited due to crucial issues such as physical side effects, limited efficiency perseverance, intolerance, placebo effects and delayed therapeutic inception. The cognitive behavioral therapy (CBT) is an effective intervention for mild to moderate depression, and it excludes the physical side effects and placebo incidences associated with drug therapy. CBT also enhances the physician-patient relationship thus improving the patient’s outcome. However, the efficacy of CBT in the treatment of depression needs more research.

References

Fournier, J.C. et al. (2010) Antidepressant drug effects and depression severity: a patient-level

meta-analysis, JAMA, 303(1), 47-53.

Imel, Z.E., Malterer, M.B., McKay, K.M. & Wampold, B.E. (2008). A meta-analysis of

psychotherapy and medication in unipolar depression and dysthymia. Journal of Affective Disorders, 110(3), 197-206.

Kirsch, I. et al. (2008). Challenging received wisdom: antidepressants and the placebo effect.

McGill Journal of Medicine, 11(2), 219-222.

Parker, G. (2009) Antidepressants on trial: how valid is the evidence? British Journal of

Psychiatry, 194, 1-3.

Racagni, G. & Popoli, M. (2008). Cellular and molecular mechanisms in the long-term action of

antidepressants. Dialogues in Clinical Neuroscience, 10, 385-400.

Vos, T., Corry, J., Haby, M. M., Carter, R., & Andrews, G. (2005). Cost-effectiveness of

cognitive–behavioural therapy and drug interventions for major depression. Australian and New Zealand Journal of Psychiatry, 39(8), 683-692.

 

 

 

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