Position Paper \'Argue your position on the biomedical model of depression\' PDF

Preview

Summary

Position Paper...

Description

Argue Your Position on The Biomedical Causal Model for Depression PSYC232 Dr Susan Giles 201349906 Word Count: 1868

The biomedical model (BMM) of depression assumes that mental disorders like depression are biologically based brain diseases. The BMM was described by psychiatrist George Engel (1977) as a dominant model of disease which is biomedical and assumes diseases to be fully accounted for by deviations from the norm of measurable biological variables, which leaves no room for the social, psychological and behavioural dimensions of illness. The main assumptions of the BMM of asserts that depression is caused by neurotransmitter/hormone dysregulation, genetics and brain structure or function. This paper will propose the argument against the biomedical model of depression, arguing that depressive disorder is not solely biologically based, by providing disputing arguments for the serotonin hypothesis, neurotransmitter imbalances, genetic heritability and the serotonin uptake gene.

The biomedical model of depression asserts that depression is caused by a deficiency of monoamine neurotransmitters (serotonin). The monoamine hypothesis of depression was proposed by Schildkraut [26] and this theory was later further developed by Coppen [7] to emphasise the possible role of serotonin. The ‘serotonin hypothesis’ of depression is almost 50 years old and, at its simplest, proposes that lessened activity of serotonin pathways plays a causal role in the pathophysiology of depression. Evidence that serotonin plays a role in depression comes from studies involving ‘tryptophan depletion’, in which serotonin levels are lowered via acute dietary manipulation through administration of large neutral amino acids (LNAA) which limits the transport of endogenous tryptophan (TRP) across the blood brain barrier by competition of other LNAAs and subsequently deceases serotonergic neurotransmission [4]. One study found that in healthy participants with no risk

factors for depression, tryptophan depletion does not produce clinically significant changes in mood; however, recovered depressed patients free of medication can show brief, clinically relevant, depression symptomatology [22].

However, serotonin levels in the brain itself cannot actually be measured, the only way serotonin can be measured is in the blood, but is serotonin in the blood the same as brain chemistry? The serotonin within blood does not correlate with the serotonin in the brain, therefore research can never fully provide evidence for the lack of serotonin within the brain. Additionally, the research conducted within the industry is likely to be funded by the pharmaceutical industry therefore facing a conflict of interest between producing good science and results that will enhance the sales of their products as there is an apparent bias in the favour of industry [19]. Research found describes the influence of this sponsoring and concludes that companies exploit a wide variety of possibilities of manipulating study results. Apart from financing the study, financial links to the authors may tend to make the results of the study more favorable for the company and in some publications, evidence was detected that sponsors from the pharmaceutical industry had influenced study protocols. For example, research found that placebos were more frequently used in drug studies than was the case with independently financed studies [3]. Additionally, marketing campaigns by companies frequently emphasize biological causation simply because by doing so makes drug treatment seen like the obvious remedy, although it is a lot more complex than this.

An assumption of the BMM, in its original form known as the serotonin hypothesis states that the deficit in serotonin is a primary case, and would be reversed by anti-

depressants, resultingly restoring normal function in depressed patients. A further assumption of the biomedical model is that neurotransmitter imbalances can be corrected by psychotropic medications, therefore supporting a biomedical cause [11]. Research to support the efficacy of antidepressants has shown that by carrying out double-blind, randomized controlled trials (RCTs) in order to compare antidepressants with a placebo, antidepressants were resultingly found to be more effective than placebo [6].

However, this research does have some faults which leads us to question whether we can support the assumption made by the BMM. The research conducted by Cipriani on the efficacy of antidepressants had a median duration of 8 weeks. Therefore, we cannot be sure that antidepressants are a long-term solution for depression, as it is much more complex than this. Research has been carried out looking into such long-term effects of antidepressants as told by participants themselves, and found that out of 180 participants, 30.7% reported moderate-tosevere depression while on antidepressants. Additionally, ten adverse effects were reported by more than half of the participants, including withdrawal effects (73.5%), sexual difficulties (71.8%) and feeling emotionally numb (64.5%). Problems with antidepressants, also highlighted the long process of finding an antidepressant that ‘worked’, problems with discontinuation, the negative impact of antidepressants on views of self and other adverse effects [5]. We can therefore argue that antidepressants may work for short-term effects in reducing feelings of depression, however they may also lead to other adverse, negative effects on the individual. Moreover, there is limited and unclear research to show that antidepressants prevent actual recurrence of depression in the longer term therefore disputing the efficacy of

antidepressants on depression [24]. This further argues the biomedical assumption that the deficit in serotonin could be reversed by antidepressants as if antidepressants could restore the normal neurotransmitter function in depressed patients, there would be high success rates and no chance of relapse.

As there is limited research to provide support for antidepressants preventing relapse, it is therefore appropriate to look at alternative explanations for the treatment of depression. For example, research has been conducted into the effectiveness of cognitive therapy in depressed patients, finding that cognitive therapy (CT) appeared significantly better than antidepressants [15]. Hollon et al (2006) further asserts that CT has lower relapse rates than drug therapy, so it is more effective in the long-term and disproves the assumption of the BMM as CT targets the cognitive underlying factors of depression.

A further assumption of the biomedical model of depression involves the theory of genetics. The most compelling theories come from twin studies, most of which compare the diagnosis of depression in identical (monozygotic/MZ) twins with the prevalence in same sex, non-identical (dizygotic/DZ) twins, providing evidence for high genetic contribution to major depressive disorder. Research suggests a heritability rate of 37% in twin studies supporting this genetic assumption.

However, twin studies as an explanation for the genetic theory of genetics can be faulted by its methodology. Twin studies rest on two fundamental assumptions; that MZ twins are genetically identical, and the world treats MZ and DZ twins equivalently, this is known as the so-called ‘equal environments assumption’. Neither

assumptions are true nor have been proven and displays a reductive approach to the complexity of our genetic structure. Additionally, no twin studies have been proven to find concordance rates of 100%, therefore this evidence cannot be fully supported as it is clear there is room for other variance and other factors effecting these concordance rates, for example environment, further supporting the idea that depression cannot be purely biological and arguing the assumptions of the BMM.

Furthermore, adoption studies of biologically related and biologically unrelated adopted siblings have found no evidence for genetic evidence [13], therefore conflicting with the results of most twin studies, disputing the biological influence of genetics. Results from adoption studies have resultingly suggested that the contribution of genetic factors to depression is negligible.

The biomedical model of depression further asserts the relationship of genetic variants of the serotonin transporter gene (SLC6A4), being a key regulator of the serotonergic neurotransmission with depressive symptoms. Research has found genetic vulnerability involving the SLC6A4 gene is significantly associated with increased depressive symptoms. As serotonin influences mood, this gene variant may lead to less serotine uptake and resultingly lower mood in individuals [27].

However, this evidence comes with some problems making us question the assumptions of the biomedical model of depression. The assumption of the serotonin transporter gene has failed to produce further research that replicates the results. One study found no evidence that the serotonin transporter genotype is associated with an elevated risk of depression in men alone, women alone, or in both sexes

combined [25]. Additionally, research into genetic theories of depression have proposed alternative explanations to rely solely on the biomedical model and to involve other situational and environmental factors such as stressful live events in being a cause of depression. In a meta-analysis, it was found that the number of stressful life events was significantly associated with depression and the addition of the serotonin trans porter genotype did not improve this prediction of risk of depression. [25]. This therefore disputes the assumptions of the BMM and proving that is it more complex than a biological explanation and other factors need to be taken into account.

As detailed above, this paper argues against the assumptions of the biomedical model as the cause and effect of depression cannot be simplified into a solely biological disorder. There are other factors that come into play in the development of depression such as environmental stressors. If the development of depression was simply due to biological factors like genetics, everyone could have a predisposition to developing the disorder, so therefore something must have to occur in order to become clinically depressed. The cause of depression involves a complex network of variables, some of which include; stressful life events, trauma, lack of social supportive networks, childhood experiences, poverty, occupational status, all of which do not have biological influence. A further point which suggests the complexity of depression and argues the biological argument is that some patients are able to be treated and cured for depression without the use of drugs and just through a therapy treatment, further suggesting the influence of other factors such as the environment, and a potential cognitive basis of depression, and how such factors have a influence and play a larger role in the cause of depression.

Nowadays, the dominant way of thinking about depression is the role that biology plays, and that the primary causes of depression are considered to be biological influences such as genetic vulnerabilities and the influence and relative availability of neurotransmitters. However, as described, there are other factors that majorly dispute and disprove the assumptions of the BMM. The main argument of this paper disputes the assumptions made by the biomedical model of depression, including that depression is caused by a deficiency of monoamine neurotransmitters (serotonin). This hypothesis proposes that idea that lessened activity in serotonin pathways plays a causal role in the pathophysiology of depression and is contradicted by lack of evidence of not only a causal relationship, but a lack of ability to collect data about serotonin in the brain in general. The genetic argument of the BMM is disputed not only by adoption studies providing evidence for a further underlying environmental cause and lack of 100% concordance rates in twin studies, but also the lack of research able to support and replicate the serotonin transporter gene assumption. In order to provide an explanation for depressive disorder, it is necessary to consider the complexity of depression and reflect on the number of other factors that come into play when thinking about the cause of depression; environmental, social, relational. The biomedical model of depression is therefore argued as described by the evidence above, and it is concluded that there is not one sole explanation for depression and biological factors are only a fraction of the complexity.

References

1.

Belmaker, R. H., & Agam, G. (2008). Major depressive disorder. New England Journal of Medicine, 358(1), 55-68.

2.

Biskup, C. S., Sánchez, C. L., Arrant, A., Van Swearingen, A. E., Kuhn, C., & Zepf, F. D. (2012). Effects of acute tryptophan depletion on brain serotonin function and concentrations of dopamine and norepinephrine in C57BL/6J and BALB/cJ mice. PLoS One, 7(5), e35916.

3.

Breidert, M., & Hofbauer, K. (2009). Placebo: misunderstandings and prejudices. Deutsches Ärzteblatt International, 106(46), 751.

4.

Cadoret, R. J., O'Gorman, T. W., Heywood, E., & Troughton, E. (1985). Genetic and environmental factors in major depression. Journal of Affective Disorders, 9(2), 155-164

5.

Cartwright, C., Gibson, K., Read, J., Cowan, O., & Dehar, T. (2016). Long-term antidepressant use: patient perspectives of benefits and adverse effects. Patient preference and adherence, 10, 1401.

6.

Cipriani, A., Furukawa, T. A., Salanti, G., Geddes, J. R., Higgins, J. P., Churchill, R., ... & Tansella, M. (2009). Comparative efficacy and acceptability of 12 newgeneration antidepressants: a multiple-treatments meta-analysis. The lancet, 373(9665), 746-758.

7.

Coppen, A. (1973). Role of serotonin in affective disorders. In Serotonin and behavior (pp. 523-527). Academic Press.

8.

Coppen, A. J., & Doogan, D. P. (1988). Serotonin and its place in the pathogenesis of depression. The Journal of clinical psychiatry.

9.

Cowen, P. J. (2008). Serotonin and depression: pathophysiological mechanism or marketing myth?. Trends in Pharmacological Sciences, 29(9), 433-436

10.

Cowen, P. J., & Browning, M. (2015). What has serotonin to do with depression?. World Psychiatry, 14(2), 158.

11.

Deacon, B. J. (2013). The biomedical model of mental disorder: A critical analysis of its validity, utility, and effects on psychotherapy research. Clinical psychology review, 33(7), 846-861.

12.

Drevets, W. C., Frank, E., Price, J. C., Kupfer, D. J., Holt, D., Greer, P. J., ... & Mathis, C. (1999). PET imaging of serotonin 1A receptorbinding in depression. Biological psychiatry, 46(10), 1375-1387.

13.

Eley, T. C., Deater-Deckard, K., Fombonne, E., Fulker, D. W., & Plomin, R. (1998). An adoption study of depressive symptoms in middle childhood. The Journal of Child Psychology and Psychiatry and Allied Disciplines, 39(3), 337345.

14.

Engel, G. L. (1977). The need for a new medical model: a challenge for biomedicine. Science, 196(4286), 129-136.

15.

Gloaguen, V., Cottraux, J., Cucherat, M., & Blackburn, I. M. (1998). A metaanalysis of the effects of cognitive therapy in depressed patients. Journal of affective disorders, 49(1), 59-72.

16.

Hollon, S. D., Stewart, M. O., & Strunk, D. (2006). Enduring effects for cognitive behavior therapy in the treatment of depression and anxiety. Annu. Rev. Psychol., 57, 285-315.

17.

Ji, Y., Biernacka, J. M., Hebbring, S., Chai, Y., Jenkins, G. D., Batzler, A., ... & Mushiroda, T. (2013). Pharmacogenomics of selective serotonin reuptake inhibitor treatment for major depressive disorder: genome-wide associations and functional genomics. The pharmacogenomics journal, 13(5), 456.

18.

Leo, J., & Lacasse, J. R. (2008). The media and the chemical imbalance theory of depression. Society, 45(1), 35-45.

19.

Lexchin, J. (2012). Sponsorship bias in clinical research. International Journal of Risk & Safety in Medicine, 24(4), 233-242.

20.

Malison, R. T., Price, L. H., Berman, R., Van Dyck, C. H., Pelton, G. H., Carpenter, L., ... & Baldwin, R. M. (1998). Reduced brain serotonin transporter availability in major depression as measured by [123I]-2β-carbomethoxy-3β-(4iodophenyl) tropane and single photon emission computed tomography. Biological psychiatry, 44(11), 1090-1098

21.

Meltzer, H. Y. (1990). Role of Serotonin in Depression a. Annals of the New York Academy of Sciences, 600(1), 486-499

22.

Murphy, F., Smith, K., Cowen, P., Robbins, T., & Sahakian, B. (2002). The effects of tryptophan depletion on cognitive and affective processing in healthy volunteers. Psychopharmacology, 163(1), 42-53.

23.

Oberbeck, R., Schmitz, D., Wilsenack, K., Schüler, M., Biskup, C., Schedlowski, M., ... & Exton, M. S. (2003). Prolactin modulates survival and cellular immune functions in septic mice. Journal of Surgical Research, 113(2), 248-256.

24.

Pies, R. (2012). Are antidepressants effective in the acute and long-term treatment of depression? Sic et Non. Innovations in clinical neuroscience, 9(5-6), 31.

25.

Risch, N., Herrell, R., Lehner, T., Liang, K. Y., Eaves, L., Hoh, J., ... & Merikangas, K. R. (2009). Interaction between the serotonin transporter gene (5HTTLPR), stressful life events, and risk of depression: a metaanalysis. Jama, 301(23), 2462-2471.

26.

Schildkraut JJ (1965) The catecholamine hypothesis of affective disorders: A review of supporting evidence. J Neuropsychiatry Clin Neurosci 7: 524–533.

27.

Su, S., Zhao, J., Bremner, J. D., Miller, A. H., Tang, W., Bouzyk, M., ... & Vaccarino, V. (2009). Serotonin transporter gene, depressive symptoms, and interleukin-6. Circulation: Cardiovascular Genetics, 2(6), 614-620....