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Inflammatory Hypothesis

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The inflammatory hypothesis of depression looks at an immunological causes of depression. One model is called the sickness behaviour which refers to the non-specific reaction to infection. Sickness behaviour is characterised by weakness, lethargy, malaise, inability to concentrate and reduced apatite. This symptomology is due to proinflammatory cytokines which have a very similar pathway to neurotransmitters ie serotonin indicating that more research is needed to fully explain causes of depression3.
Other research has shown however that ADT did not dramatically effect mood indicating that levels of serotonin may not actually have a direct influence on depression more a predisposing or contributory factor4. The evidence from ADT research
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These are generally considered a symptom of depression even though some studies have looked into them being responsible for depressive behaviour. So rather than serotonin levels being treated as the single cause of depression they should be considered another symptom.
Especially in the United States there has been an increase in prescriptions and sales of serotonin reuptake inhibitors antidepressants. This upturns in sales were only possible because of the claim of serotonin being the main chemical responsible for depression. Therefore antidepressants like (SSRI’s) which correct a possible chemical imbalance regarding serotonin levels are often considered first when patients’ are diagnosed with mental health disorders like depression, anxiety, bipolar disorder, etc.6
Attempts were also made to induce depression by depleting serotonin levels, but these experiments reaped no consistent results. Likewise, researchers found that huge increases in brain serotonin, arrived at by administering high-dose L-tryptophan, were ineffective at relieving depression” (Lacasse & Leo, 2005) This statement perfectly highlights that even though a lack of serotonin is considered the main cause of depression, studies trying to prove this have been continuing to fail showing consistent
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In randomized controlled trials, buproprion and reboxetine were just as effective as the SSRI’s in the treating of depression9.It is still to be proven that a singular neurochemical abnormality could be the cause of so many differing behavioral manifestations.
However, serotonin is not affected to a significant degree.
Exercise is just as effective as the SSRI’s.
SSRI’s are considered ‘antidepressants’, however they are also used for a wide range of psychiatric disorders (e.g. anxiety, obsessive compulsive disorder, …)
Genes encoding for the 5-HT-Transporter and 5HT2A receptor are proposed candidates for involvements in mood disorder10.
His452Tyr polymorphism of the 5HT2A receptor gene has had functional consequences with the Tyr-allele à associated mobilization and a different time response of calcium10.
The 5HT induced calcium response was found to be enhanced in depressed patients10.
Study showed that the 5HT2A polymorphism is not significantly associated with major
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