A link between stress and depression: Shifts in the balance between the kynurenine and serotonin pathways of tryptophan metabolism and the etiology and pathophysiology of depression
Open accessAbstract
Alteration of tryptophan (TRP) metabolism elicited by proinflammatory cytokines has gained attention as a new concept to explain the etiological and pathophysiological mechanisms of major depression. The kynurenine (KYN) pathway, which is initiated by indoleamine 2,3-dioxygenase (IDO), is the main TRP metabolic pathway. It shares TRP with the serotonin (5-HT) pathway. Proinflammatory cytokines induce IDO under stress, promote the KYN pathway, deprive the 5-HT pathway of TRP, and reduce 5-HT synthesis. The resultant decrease in 5-HT production may relate to the monoamine hypothesis of major depression. Furthermore, metabolites of the KYN pathway have neurotoxic/neuroprotective activities; 3-hydroxykynurenine and quinolinic acid are neurotoxic, whereas kynurenic acid is neuroprotective. The hippocampal atrophy that appears in chronic depression may be associated with imbalances in neurotoxic/neuroprotective activities. Because proinflammatory cytokines also activate the hypothalamo-pituitary-adrenal (HPA) axis, these imbalances may inhibit the hippocampal negative feedback system. Thus, changes in the TRP metabolism may also relate to the HPA axis-hyperactivity hypothesis of major depression. In this article, we review the changes in TRP metabolism by proinflammatory cytokines under stress, which is assumed to be a risk factor for major depression, and the relationship between physiological risk factors for major depression and proinflammatory cytokines.
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The neurodegeneration hypothesis (cytokine-5-HT interaction) can explain individual differences in depression among the elderly and chronically ill.
“One hypothesis that can explain these differences is the neurodegeneration hypothesis: Cytokine-5-HT interaction[47,48].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [47]
Eating tryptophan-deficient foods worsens mood, while the administration of tryptophan improves depressive symptoms.
“Eating tryptophan-deficient foods worsens mood, while the administration of tryptophan improves depressive symptoms[47].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [47]
According to the neurodegeneration hypothesis, acute psychological stress triggers tryptophan defects and mood swings; chronic stress increases proinflammatory cytokines; excessive proinflammatory cytokines activate IDO, accelerate tryptophan metabolism to kynurenine, decrease brain 5-HT, and aggravate depression in vulnerable individuals.
“According to this hypothesis, acute psychological stress triggers tryptophan defects and mood swings. To correct the 5-HT imbalance, 5-HT synthesis and receptor expression are modified. This is the first stage of coping with psychological stress. If the psychological stress is chronic, the levels of proinflammatory cytokines increase.”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [47]
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Palhano-Fontes, F., Alchieri, J. C., Oliveira, J. P. M., Soares, B. L., Hallak, J. E. C., Galvao-Coelho, N., & de Araujo, D. B. (2014) · The Therapeutic Use of Ayahuasca · doi:10.1007/978-3-642-40426-9_2 · Cited by 36 · see citing works
Xie, S., Wang, C., Song, J., Zhang, Y., Wang, H., Chen, X., & Suo, H. (2024) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.4c03870 · Cited by 27 · see citing works
- Authors
- Miura, H., Ozaki, N., Sawada, M., Isobe, K., Ohta, T., & Nagatsu, T.
- Affiliations
- Nagoya University (JP)
- Fujita Health University (JP)
- Corresponding author
- Miura, Hideki
- Venue
- Stress
- Publisher
- Informa UK Limited
- Published
- 2008-01
- Volume
- 11
- Issue
- 3
- Pages
- 198-209
- ISSN
- 1025-3890 (ISSN-L)
- 1607-8888
- OpenAlex
- W2003808704
- Cited by
- 282
- References
- 94
- Citations by year
- 2026: 23 · 2025: 23 · 2024: 29 · 2023: 26 · 2022: 28 · 2021: 9 · 2020: 19 · 2019: 14 · 2018: 8 · 2017: 7 · 2016: 14 · 2015: 9 · 2014: 10 · 2013: 10 · 2012: 11
- FWCI
- 4.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Stress (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- major depressive disorder, tryptophan metabolism, kynurenine pathway, serotonin pathway, indoleamine 2,3-dioxygenase, inflammatory cytokines, 3-hydroxykynurenine, quinolinic acid, kynurenic acid, hippocampal atrophy, hypothalamic-pituitary-adrenal axis, monoamine hypothesis, neuroinflammation
- MeSH terms
- Animals, Antidepressive Agents, Brain, Depression, Major Depressive Disorder, Humans, Hypothalamo-Hypophyseal System, Kynurenine, Models, Biological, Pituitary-Adrenal System, Serotonin, Stress, Psychological, Tryptophan, Biogenic Monoamines, Cytokines, Metabolic Networks and Pathways
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