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Depression is a widespread phenomenon across the world, affecting many groups and individuals within society. According to the American Psychiatry Association (APA) depression is defined as “a medical illness that causes feelings of sadness and/or a loss of interest in activities once enjoyed and can lead to a variety of emotional and physical problems that can decrease a person’s ability to function at work and at home” (American Psychiatric Association, 2013).It is therefore important to research and conduct studies about depression in order to gain a wider insight into its causes and effecting factors as well as a means of treating the disorder. Each of these factors will be discussed in this paper through the use of critical analyses and the evaluation of empirical evidence from numerous sources as a means of determining the level of efficacy of the treatment of depression and whether the chosen model of depression can be related to other human behaviours.
Depression is a phenomenon amongst many that have been rigorously studied in psychology; in the hopes of finding new ways of treating the disorder, as well as aiming to gain a deeper insight and understanding into the variables and factors that may lead to the diagnosis of, or have an effect on depression. This constant research by numerous psychologists and practitioners has led to the discovery and development of many treatments, including antidepressant drugs. Most notably – selective serotonin reuptake inhibitors (SSRIs).
SSRIs are a form of antidepressant drugs that are used for the treatment of depression as well as other disorders such as anxiety disorders. Although there are some explanations and theories pertaining to how SSRIs function in the treatment of depression; the exact biological mechanism of action of SSRIs still remains undiscovered. The most popular and widely accepted theory is usually explained using the serotonin hypothesis – a long-standing model of depression – especially within the biological approach to psychology. According to this approach, neurotransmitters are believed to play a key role in human behaviour, character and emotion. Therefore, with the support of research, levels of the transmission of different types of neurotransmitters such as serotonin in the brain are believed to be a fundamental determinant of mood: high serotonin activity has been associated with the result of happiness, whereas low serotonin activity has been associated with sadness or depressive moods (Jenkins, Nguyen, Polglaze & Bertrand, 2016). Depression is considered to be caused by low levels of serotonin being transmitted between neurons. SSRIs were, therefore, developed to interfere with the activity of the serotonin transporter – a reuptake molecule that removes serotonin from the synapse and stops it from being reabsorbed by the postsynaptic neuron; causing, the presumed low levels of synaptic serotonin in a depressed individual to become elevated, alleviating the individual of depression.
Different versions and variations of the general serotonin model of explaining depression, are a representation of the most widely accepted explanation for SSRI action and are also consistent with most empirical data findings (Leonard, 1995a; Potter, 1996). However, there are some findings that contradict or at least lead us to question the validity of the serotonin model of depression. For example, if levels of serotonin are in direct correlation with mood – this would lead us to believe that clinically healthy individuals that are then treated with SSRIs would be expected to experience; euphoria and a reduction in serotonin would, therefore, induce depression, however, that is not the case. In fact, this type of manipulation of serotonin levels has a very limited effect on mood except for in individuals who have already been diagnosed with or have recently recovered from depression (McAllister-Williams & Young 1998; Smith, K. A., Fairburn, C. G., & Cowen, P. J., 1997). These findings can be used to support the argument that serotonin plays a small role in depression rather than the major role it is believed to play and is more likely to affect vulnerable individuals who already have a susceptibility towards depression. This consequently makes it difficult for the explanation of how levels of serotonin cause depression, to remain tenable. Overall, these findings indicate not only that the relationship between serotonin and depression is; much more complex than previous research has assumed but that the empirical evidence shown by McAllister-Williams and Young (1998) may also lead us to believe that there must be at least one more variable playing either a catalytic or an intermediary role between serotonin and depression.
Furthermore, although many successful drugs used to treat mood disorders block the reabsorption of serotonin, a number of antidepressants that have been found to be effective in treating depression do not. This includes selective norepinephrine reuptake inhibitors (SNRIs). This type of drug enhances rather than inhibits serotonin reuptake thus illustrating that although serotonin does seem to play some sort of role in depression, there must be other factors playing a significant role. Moreover, we can infer that the relationship between neurotransmitters and mood must be more complicated than the current serotonin model of explaining depression would imply.
Alternatively, rather than looking at an SSRI’s ability to increase levels of serotonergic transmission, most current versions of the serotonin model postulate that SSRIs are successful against depression due to changes in monoamine neurotransmission that occur as a result of continuous repression of serotonin reuptake (Leonard, 1995b). This hypothesis suggests that long-term activation of the serotonin transporter (5-HTT) by SSRIs lead to a typical set of adaptive responses including – changes in the responsiveness of multiple monoamine and GABA receptors in the brain which may be an alternative explanation of why SSRIs are effective in treating depression rather than their ability to decrease serotonin levels.
In order to truly evaluate both the importance and effectiveness of SSRIs, it may be necessary to look, not only at the general relationship between neurotransmitters and emotions/mood; but also at the relationships between serotonin and other human behaviours. By studying how levels of serotonergic transmission interact with other human behaviours, emotions or moods we may be able to distinguish key features or components of how serotonin behaves and affects human behaviour that may be successfully applied to depression and how we treat it. For example, some research has found support for serotonin being associated with aggression, neuroticism and impulsiveness (Nielsen, D. A., Goldman, D., Virkkunen, M., Tokola, R., Rawlings, R., & Linnoila, M., 1994; Retz, W., Retz‐Junginger, P., Supprian, T., Thome, J., & Rösler, M., 2004; Skuse, D., 2006). Furthermore, research has also found a positive correlation between serotonin and “harm – avoidant” personality traits (Gerra et al. 2000; Hansenne, M., & Ansseau, M., 1999), if this is the case, it could help us to explain why decreased levels of serotonin may lead to depression since behavioural traits or side-effects of having depression often tend to lead to both direct and indirect harmful behaviours or characteristics in individuals whether to themselves or others. Croquette et al (2010) conducted a study to test the hypothesis that elevated levels of serotonin would result in individuals being more likely to behave in more morally acceptable behaviours. This was carried out through a within-subjects study in which one group of participants were given SSRIs and the control group were given placebo’s then asked to answer some moral dilemmas that included both personal and impersonal variations. They found that those who had taken SSRIs were less likely to approve of or support the theoretical harming of an individual even if it would save a group of people. From this research, it can be concluded that serotonin clearly plays a role in how humans make morally just or “harm-avoidant” decisions and behaviours. However most of the research that has been carried out in regards to the relationship between serotonin and morality/”harm-avoidant” personality traits have been correlational, so we are therefore unable to determine the direction of the relationship between the co-variables thus making it difficult for us to apply this evidence to the serotonin model of explaining depression. Additionally, as these are correlational studies, we are unable to tell whether there may be an unaccounted third variable that may be causing a correlational relationship to be found between serotonin and “harm-avoidant” personality traits. In Kédia et al’s (2008) study of how neural activity is connected to emotions experienced by individuals when given moral dilemmas – or in this case – asked to think about situations in which themselves or someone else was being hurt or inflicting pain; it was found that four main areas in the brain became active – ventromedial prefrontal cortex, anterior cingulate cortex, striatum and amygdala. All of which, are areas of the brain that are understood to have compact serotonergic projections, consequently leading us to infer that serotonin may, in fact, play a role in “harm avoidant” behaviours and personality traits.
In conclusion, basic biological approaches to theorising how serotonin is associated with depression may no longer be considered to be tenable. However, more current experimental adaptations of these theories using new empirical evidence, create an interesting premise on the neuropsychology of depression and the application to pharmaceutical aspects of treatment. Furthermore, the application of serotonin to theories of other human behaviours such as individuals with “harm-avoidant” personality traits and behaviours has allowed researchers to gain a deeper insight into the functions of serotonin whilst allowing us to develop theories as to how this can be applied to the understanding of depression and hopefully it’s treatment. Further research must be carried out in order to find more supporting empirical evidence to solidify these theories as well as to develop them enough to create a possibility of predicting as well as improving clinical response to SSRIs as well as other treatments of depression.
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