The knowledge regarding the biological causes of depression is somewhat rudimentary compared to other illness due to the lack of thorough knowledge regarding the complexities of the human brain. However, the monoamine theory, hypothesizes that a predisposition to depression can occur in individuals whose serotonin, norepinephrine, and dopamine have been depleted (Bunney & Davis 1965; Delgado 2000; Hirschfield 2000) Serotonin, norepinephrine, and dopamine are neurotransmitters responsible for regulating mood, focus and motivation by carrying chemical signals from one part of the brain to another, however, in depressed patients, these signals are low or interpreted and hence fail to function effectively. The two pieces of evidence which support the monoamine theory is the effect of reserpine on brain activity and the
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Additionally, the theory does not explain why all drugs which aim to enhance monoamines are not necessarily effective in treating depression. (Hirschfield 2000). Moreover, researchers are unable to determine yet a clear explanation for the reasons as to why antidepressant drugs take up to 12 weeks to effectively combat the depressive-like symptoms (Uher et. Al 2011). However, there is undeniable evidence of the success of treatment, as it is widely accepted that one of most effective way to alleviate depression is to increase monoamines in the brain (Delgado & Moreno 1999). ‘Selective serotonin reuptake inhibitors’ and ‘serotonin-norepinephrine reuptake inhibitors’ are examples of antidepressant medication aimed at increasing the concentration of monoamines in the brain to subsequently counteract the depleted sources that exist in depressed patients. Thus through an analysis of the presented evidence, the monoamine theory of depression is a hypothesis with much repute due to its success in the treatment of patients and reducing depressive-like systems. However, the lack of knowledge surrounding the complexities of the brain cannot be
Additionally, the theory does not explain why all drugs which aim to enhance monoamines are not necessarily effective in treating depression. (Hirschfield 2000). Moreover, researchers are unable to determine yet a clear explanation for the reasons as to why antidepressant drugs take up to 12 weeks to effectively combat the depressive-like symptoms (Uher et. Al 2011). However, there is undeniable evidence of the success of treatment, as it is widely accepted that one of most effective way to alleviate depression is to increase monoamines in the brain (Delgado & Moreno 1999). ‘Selective serotonin reuptake inhibitors’ and ‘serotonin-norepinephrine reuptake inhibitors’ are examples of antidepressant medication aimed at increasing the concentration of monoamines in the brain to subsequently counteract the depleted sources that exist in depressed patients. Thus through an analysis of the presented evidence, the monoamine theory of depression is a hypothesis with much repute due to its success in the treatment of patients and reducing depressive-like systems. However, the lack of knowledge surrounding the complexities of the brain cannot be