In addition to this, medical questionnaires are prejudiced against those who suffer from affective disorders – questions appear to be aimed at those with fewer resources, less education and more stressors. Self Rating Scales such as The Beck Inventory (a four point rating scale) are just as problematic, as they suggest that there is a linear relationship between scores – this is clearly not the case – depression is a purely subjective illness, what may be four times as bad for one, may not be so, for another, so to score items as such may be misleading (Bennet, 2006). There are many different types of depression and reasons for it, yet only a few rudimentary (non biological) mechanisms by which to diagnose it; as a result diagnosis is not definitive as one would like to believe and this is almost certain to have an effect on who reports themselves as effectively treated and who does not. Nonetheless, once an individual is diagnosed as depressed, whether they receive pharmacological therapy or behavioural therapy is the next issue to deal with.
Pharmacological treatments work with the biological model of depression. The biological underpinnings comprise of the locus coeruleus (in the brain stem), which is responsible for the physiological response to panic and pain – it is the principal site in the brain for the synthesis of norepinephrine, and is linked with arousal of the stress response system and the release of cortisol (Toates, 2001). It also activates the nucleus accumbens, which has been linked with the brain reward system, ultimately resulting in the release of dopamine and/or endogenous opiates. The raphe nuclei, made up of serotonergic neurons in the brain stem, releases serotonin (neurotransmitter linked with mood) to the rest of the brain as and when activation occurs (Anderson,et al, 2004). It is at this point in the brain that Serotonin Selective Re-uptake Inhibitors work, inhibiting the reuptake of serotonin, thus freeing up more of the neurotransmitter for use in the synapses. Although this has been reported to lift the ‘black cloud’ that individuals feel is enshrouding them, it does not come without its costs. Firstly, it takes time to work – a matter of weeks, and secondly, side effects are often so unbearable that individuals stop treatment, as the depression was more bearable than the side effects. Sexual dysfunction, appetite disorders, anxiety and sleep problems name but a few. Although depressed patients often report lack of interest in sex to begin with, sexual dysfunction may add to their problems, not ease them. Intimacy within a romantic relationship can be a source of strength to many individuals (Hogg & Vaugn, 2005), and if the drug they are taking to treat their depression takes that away from them, one may question just how much of a benefit that drug is. The same may be said for the myriad of other side effects that have been listed by patients. Casacalenda (2002) did a meta analysis of six studies, and reported that 37% of the pharmacological patients dropped out due to side effects.
Although all individuals have the same biological components inside them, biochemical and biological theories have not yet been proven (Antonuccio, 1999). In addition to this, how each persons systems work with regards to the activation and inhibition of particular parts of the brain is unique to them and is reliant on their world view – their experiences and how they perceive and categorise things within their mind. This is where the difficulty arises in predicting benefits from a group of drugs that in short, only affects the reuptake or breakdown of serotonin. This is reflected in another meta-analysis where out of fifty two studies; only 47% of them were independently significant (Khan, 2002). Results like this do little to authenticate claims of origin. If anything, they lead one to question three things; firstly - the strength of the placebo effect – does this mean, in fact, that if people think they are taking something that will help them, that they self heal? As depression mainly affects one’s psychological state, perhaps this may be so. Secondly, as only the best results are ever published by drug companies (publisher bias), how poor are the results that are not published? Are individuals actually being prescribed drugs that at best only show significance less than half of the time? Thirdly, perhaps it may be viewed as irresponsible to treat a disorder that causes emotional pain with a pharmacological intervention, without talking to the individual and offering emotional support. As depression is a purely subjective experience, unique to the person in question, it seems fair to say that one class of drugs is unable to deal with the multiple and complex issues involved, and consequently the illness should not be labelled as biological. It is not that simple.
The phenomenology of depression may be viewed as further evidence to disprove the claim of biological origin. Depression is typified by omnipresent feelings of an-hedonia. However, what makes one individual depressed, does not necessarily do so to another. In other words, there is no definitive route to depression, unlike many of the other biological illnesses. An individual suffering from depression experiences little or no pleasure or satisfaction from anything, lacks motivation and interest in even the most mundane tasks (such as personal hygiene) and suffers from feelings of guilt and inadequacy (Hogg & Vaugn, 2005). Although depression is not tangible, one may discriminate sufferers from non-sufferers by their pervasive low affect and ‘no approach’ mannerisms. The sufferer may lack concentration, memory may be decreased and decision making appears to be really difficult, (possibly) due to their lack of self confidence. Often sufferers withdraw into themselves, isolating themselves further from sources of help and support. In addition, talk with regards to ones-self is normally of a derogatory manner - the deeper the individual sinks into depression, the more morbid their thoughts become, sometimes including thoughts surrounding their own death and suicide (Beckham & Leber, 1997). How one views the world around them, and how one interacts with those around them is based on a vast number of variables. Developmental and attachment factors, social class, gender issues, social justice and one’s personal schema’s of the world and one’s self will all impact upon how an individual responds to any given stressor at any given time. Talking therapies such as behavioural cognitive therapy have received much merit for their contribution to the treatment of depression as they assist individuals in challenging their world view and correcting schema’s that may be contributing to their psychological ill health (Champion & Power, 1995). A study by Ward et al and Bower et al (2000) did in fact reveal that patients treated psychologically were significantly better, four months later than their conventionally treated co-horts.
From the information and evidence provided, it is clear to see that depression is not merely an illness that can be treated with drugs. In many cases the drugs do not work, and in other cases the side effects are so pronounced that the patients would rather suffer the feelings of depression that take their medication. Although depression has been linked with certain bio-chemical make up and biological responses, these responses are triggered by an individuals perceived cognitions of the world around them. Hitherto, change the perceptions and the triggers change with them. Ward and Bower’s evidence supports this. If anything, one may consider that to label depression as biological is to pass the buck – it avoids change to social policy, which costs money, and places the problem in its entirety with the individual. For someone who is already at their wits end and psychologically suffering, this may be a cruel blow. Particularly if the medication does not work – it may leave them feeling like more of an outcast than they did in the first place. Where do they turn to then? Drug companies and government policy should be more careful how they label and treat affective disorders, as lives are affected by it, sometimes in a detrimental way.
References
Anderson, A. D., Oquendo, M. A., Parsey, R. V., Milak, M. S., Campbell, C., & Mann, J. J. (2004). Regional brain responses to serotonin in major depressive disorder. Journal of Affective Disorders, 82, 411-417.
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Bennet, P. (2006). Abnormal and Clinical Psychology. Berkshire: Open University Press
Casacalenda, J. (2002). Comaprison psycotherapy, pharmacology and control. Anerican Journa of Psychology, 159:1534.
Champion, L. A., & Power, M. J. (1995). Social and cognitive approaches to depression: Towards a new synthesis. British Journal of Clinical Psychology, 34, 485-503.
Hogg , M. A. & Vaugn, G. M. (2005) Social psychology. London: Pearson Prentice Hall.
Khan, I. (2002) Meta-analysis. International Journal of Neuropsychopharmacology, 5:193.
Toates, F. (2001). Biological Psychology. London Prentice Hall
Ward, E., King, M., Lloyd, M., Bower, P., Sibbald, B., Farrelly, S., et al. (2000). Randomised controlled trial of non-directive counselling, cognitive-behaviour therapy, and usual general practitioner care for patients with depression. I: Clinical effectiveness. British Medical Journal, 321, 1383-1388.
