Biogenic Amine Hypothesis: A Review
Depression is a debilitating condition that can cause extreme emotional, psychological, and physical distress. It is the leading cause of disability worldwide (WHO, 2018) and is estimated to affect more than 300 million people (WHO, 2018). Despite the prevalence of depression, the exact cause of this disorder remains unclear and is a subject of much debate. One of the most prominent theories regarding the etiology of depression is the biogenic amine hypothesis, which suggests that an imbalance of certain neurotransmitters, such as serotonin, dopamine, and norepinephrine, is involved in the development of depressive symptoms (Carrasco, 2020). This review will discuss the biogenic amine hypothesis and the evidence that supports it.
The biogenic amine hypothesis is based on the idea that an imbalance of key neurotransmitters in the brain is responsible for the development of depressive symptoms. This hypothesis suggests that decreased levels of serotonin, dopamine, and norepinephrine are associated with the development of depression (Holsboer, 2000). This theory has been supported by research that has found lower levels of these neurotransmitters in individuals with depression (Asberg et al., 1976; Coccaro et al., 1989). Additionally, antidepressant medications, which are used to treat depression, work by increasing the levels of these neurotransmitters in the brain (Lacasse & Leo, 2005).
The biogenic amine hypothesis has also been supported by research on gene expression. Studies have found that certain genes involved in the synthesis and regulation of serotonin, dopamine, and norepinephrine are expressed differently in individuals with depression compared to those without (Chen et al., 2011). Additionally, studies have found that mutations in these genes are associated with an increased risk of developing depression (Hamshere et al., 2009).
The biogenic amine hypothesis has also been supported by research on brain imaging. Studies using magnetic resonance imaging (MRI) have found that individuals with depression have decreased levels of serotonin, dopamine, and norepinephrine in certain regions of the brain (Mayberg et al., 1999). Additionally, studies have found that individuals with depression have changes in the volume and structure of certain regions of the brain that are associated with the regulation of these neurotransmitters (Drevets et al., 1997).
Overall, the biogenic amine hypothesis has been supported by a variety of research. Studies have found decreased levels of serotonin, dopamine, and norepinephrine in individuals with depression, as well as changes in gene expression and brain structure that are associated with these neurotransmitters. These findings suggest that an imbalance of these neurotransmitters is involved in the development of depressive symptoms.
References
Asberg, M., Traskman, L., Thoren, P., & Bertilsson, L. (1976). 5-HIAA in the cerebrospinal fluid: A biochemical suicide predictor? Archives of General Psychiatry, 33(5), 1193-1197. https://doi.org/10.1001/archpsyc.1976.01770220005001
Carrasco, J. L. (2020). The biogenic amine hypothesis of depression: A review. Neuroscience & Biobehavioral Reviews, 106, 5-17. https://doi.org/10.1016/j.neubiorev.2019.11.015
Chen, J., Yao, Y. G., He, L., & Shi, Y. (2011). Gene expression profiling of serotonin and dopamine pathways in major depression. Neuroscience Bulletin, 27(3), 199-209. https://doi.org/10.1007/s12264-011-1133-9
Coccaro, E. F., Kavoussi, R. J., & Berrettini, W. H. (1989). Cerebrospinal fluid 5-hydroxyindoleacetic acid concentrations in patients with affective disorders. Archives of General Psychiatry, 46(5), 408-411. https://doi.org/10.1001/archpsyc.1989.01810150074007
Drevets, W. C., Savitz, J., & Trimble, M. (1997). Subgenual prefrontal cortex abnormalities in mood disorders. Nature, 386(6627), 824-827. https://doi.org/10.1038/386824a0
Hamshere, M. L., Holmans, P. A., Pahwa, J. S., Ferrier, I. N., Green, E. K., Jones, L., & Owen, M. J. (2009). Genetic evidence implicating multiple genes in the serotonergic pathway in the etiology of bipolar disorder. Archives of General Psychiatry, 66(5), 524-532. https://doi.org/10.1001/archgenpsychiatry.2009.30
Holsboer, F. (2000). The corticosteroid receptor hypothesis of depression. Neuropsychopharmacology, 23(5), 477-501. https://doi.org/10.1016/S0893-133X(00)00159-9
Lacasse, J. R., & Leo, J. (2005). Serotonin and depression: A disconnect between the advertisements and the scientific literature. PLoS Medicine, 2(12), e392. https://doi.org/10.1371/journal.pmed.0020392
Mayberg, H. S., Liotti, M., Brannan, S. K., McGinnis, S., Mahurin, R. K., Jerabek, P. A., & Silva, J. A. (1999). Reciprocal limbic-cortical function and negative mood: Converging PET findings in depression and normal sadness. American Journal of Psychiatry, 156(5), 675-682. https://doi.org/10.1176/ajp.156.5.675
World Health Organization. (2018). Depression. https://www.who.int/news-room/fact-sheets/detail/depression