Biogenic Amines Hypothesis: A Review
Abstract
The biogenic amine hypothesis has been proposed as a mechanism for the development of major depression. The hypothesis suggests that the reduced levels of biogenic amines such as serotonin, norepinephrine and dopamine in the synaptic cleft are contributory factors to the development of depression. This paper reviews the evidence for the biogenic amine hypothesis, highlighting the strengths and weaknesses of the current evidence. It also discusses the potential implications of the hypothesis for the diagnosis and treatment of depressive disorders.
Introduction
Major depression is a common mental disorder that affects an estimated 350 million people worldwide (WHO, 2016). The etiology of depression is complex and likely involves a combination of biological, psychological and social factors (Kupfer & Frank, 2016). One of the most widely accepted theories of the etiology of depression is the biogenic amine hypothesis. This hypothesis postulates that depressive disorders are caused by a deficiency of biogenic amines, such as serotonin, norepinephrine and dopamine, in the synaptic cleft (Kupfer & Frank, 2016). The purpose of this paper is to review the evidence for the biogenic amine hypothesis and to discuss its implications for the diagnosis and treatment of depressive disorders.
Evidence for the Biogenic Amine Hypothesis
The biogenic amine hypothesis has been supported by a range of evidence from animal and human studies. Animal studies have demonstrated that the depletion of serotonin, norepinephrine and dopamine can lead to depressive-like behavior (Drevets et al., 1997; Willner, 1997). In humans, there is evidence that reduced levels of biogenic amines are associated with depression (Asberg et al., 1976; Ordway et al., 1987). Furthermore, antidepressant medications, such as tricyclic antidepressants and selective serotonin reuptake inhibitors, are known to increase levels of biogenic amines in the synaptic cleft (Kupfer & Frank, 2016). This suggests that restoring biogenic amine levels may be an effective treatment for depression.
Limitations of the Biogenic Amine Hypothesis
Despite the evidence in support of the biogenic amine hypothesis, there are a number of limitations that should be noted. First, there is evidence that biogenic amine levels are not always reduced in depressed individuals. For example, research has found that biogenic amine levels can be normal or even elevated in some depressed individuals (Kupfer & Frank, 2016). This suggests that the biogenic amine hypothesis may not be applicable to all cases of depression. Second, the evidence from animal studies is limited by the fact that animal models of depression cannot fully replicate the complex nature of depression in humans. Finally, the effects of antidepressant medication on biogenic amine levels are still not fully understood.
Conclusion
The biogenic amine hypothesis is a widely accepted theory of the etiology of depression. The hypothesis suggests that reduced levels of biogenic amines, such as serotonin, norepinephrine and dopamine, in the synaptic cleft may be a contributory factor to the development of depression. This hypothesis has been supported by a range of evidence from animal and human studies. However, there are a number of limitations that should be noted, including the fact that biogenic amine levels are not always reduced in depressed individuals and that the effects of antidepressant medication on biogenic amine levels are still not fully understood.
References
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