Chapter 14 Abnormal Psychology1

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Chapter 14 Abnormal Psychology- The Serotonin Theory Of Depression A fundamental reason for the use of antidepressants is the long-held belief that depression is caused by imbalances in brain chemicals, particularly serotonin. First proposed in the 1960s, a connection between decreased serotonin and depression became generally known in the 1990s with the introduction of selective serotonin reuptake inhibitor (SSRI) antidepressants. The serotonin theory of depression is still typical, despite more recent doubts. According to surveys, most people today think it is proven that depression is brought on by a "chemical imbalance" in the brain. It has been hypothesized that there may be a connection involving depression and the repeat length polymorphism in the SERT gene's promoter location, notably the presence of the short repeats variant, which results in decreased SERT expression. It's interesting to note that higher levels of synaptic serotonin would result from lower levels of SERT. With the assumption that the short form of the polymorphism may only cause depression in the presence of stressful life events, this hypothesis has since been overtaken by a concentration on the interaction impact between this polymorphism, depression, and stress. In contrast to other areas of serotonin research, a great deal of systematic reviews and meta-analyses of genetic research have been carried out. A very sizable study based on a sample from two genetic data banks was completed most recently.
There isn't strong evidence that reduced serotonin concentrations or activity is related to or responsible for depression, according to their analysis of the main lines of serotonin research. The majority of studies revealed no indication of diminished serotonin activity in depressed individuals compared to those without depression, and techniques to lower serotonin availability by depleting tryptophan do not reliably worsen mood in volunteers. Effectively eliminating any connection between serotonin system-related polymorphisms and depression, including a potential interaction with stress, are high quality, well-powered genetic research. However, earlier antidepressant treatment and their impacts on the serotonin system are likely to have an influence on these findings. Antidepressants might also enhance the impact of tryptophan deprivation in some overlapping studies involving individuals with depression, yet these results are not always observed. The meta-analysis's authors additionally emphasized data showing that long-term antidepressant use lowers 5-HIAA levels. These results imply that antidepressants may cause compensatory changes over time that are the opposite of their acute effects. Animal studies showing decreased serotonin availability after extended antidepressant therapy have also been conducted. The effects of various medicines on neurochemical systems, such as the serotonin system, particularly during and after long-term usage, in addition to the physical and psychological repercussions of such impacts, need to be further studied. According to this analysis, the extensive research on the serotonin theory has not led to strong proof that depression has a physiological basis. This is in line with the findings of numerous previous biological marker studies. We argue that it is past time to admit that the serotonin theory of depression lacks supporting evidence.
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