Is depression an inflammatory disorder?

Raison, Charles L.; Miller, Andrew H.

doi:10.1007/s11920-011-0232-0

Cited by 524Tryptophan and brain disordersStress Responses and CortisolTreatment of Major Depression

Is depression an inflammatory disorder?

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Raison, Charles L., Miller, Andrew H.·2011·Current Psychiatry Reports

DOI 10.1007/s11920-011-0232-0PMC PMC3285451

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Abstract

Studies consistently report that groups of individuals with major depressive disorder (MDD) demonstrate increased levels of a variety of peripheral inflammatory biomarkers when compared with groups of nondepressed individuals. These findings are often interpreted as meaning that MDD, even in medically healthy individuals, may be an inflammatory condition. In this article, we examine evidence for and against this idea by looking more closely into what the actual patterns of inflammatory findings indicate in terms of the relationship between MDD and the immune system. Data are presented in support of the idea that inflammation only contributes to depression in a subset of patients versus the possibility that the depressogenic effect of inflammatory activation is more widespread and varies depending on the degree of vulnerability any given individual evinces in interconnected physiologic systems known to be implicated in the etiology of MDD. Finally, the treatment implications of these various possibilities are discussed.

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Individuals with distress, including informal caregivers, may experience increased systemic inflammatory biomarkers such as C-reactive protein.
“Individuals with distress, including ICs, may experience increased systemic inflammatory biomarkers (eg, C-reactive protein [CRP]) (24–26)”
From A Randomized Controlled Trial of Emotion Regulation Therapy for Psychologically Distressed Caregivers of Cancer Patients (2020) · cites this paper as [25]
The mild increases from typhoid vaccination are comparable to elevations in inflammation seen in some depressed individuals.
“A strength of these studies is that the mild increases elicited by typhoid vaccination are comparable to the elevations in inflammation seen in some individuals with depression (Dowlati et al., 2010; Raison and Miller, 2011).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison and Miller, 2011
Only 33-47% of depressed individuals show elevated peripheral inflammation markers.
“For example, only 33–47% of depressed individuals demonstrate elevated peripheral markers of inflammation (Raison and Miller, 2011; Rethorst et al., 2014).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison and Miller, 2011
It is biologically plausible that inflammatory cytokines serve as mediators of both environmental and genetic factors that may trigger depressive disorders.
“Nonetheless, it is biologically plausible that inflammatory cytokines serve as mediators of both environmental and genetic factors that may trigger the development of depressive disorders (Raison and Miller, 2011).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Raison and Miller, 2011
In humans, chronic stress is one of the main precursors of depressive symptoms.
“In humans, chronic stress is one of the main precursors of depressive symptoms [78, 79].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [79]

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[65]Raison CL Demetrashvili M Capuron L Miller AH Neuropsychiatric adverse effects of interferon-alpha: recognition and management. CNS Drugs 2005 19 105 23 15697325 PMC1255968
[68]Capuron L Raison CL Musselman DL Association of exaggerated HPA axis response to the initial injection of interferon-alpha with development of depression during interferon-alpha therapy. Am J Psychiatry 2003 160 1342 5 12832253

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Background
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Authors: Raison, C. L., & Miller, A. H.
Affiliations: Emory University (US)
Corresponding author: Raison, Charles L.
ORCID: Raison, Charles L.
Miller, Andrew H.
Venue: Current Psychiatry Reports
Publisher: Springer Science and Business Media LLC
Published: 2011-09-17
Volume: 13
Issue: 6
Pages: 467-475
ISSN: 1523-3812 (ISSN-L)
1535-1645
DOI: 10.1007/s11920-011-0232-0
PMC: PMC3285451
OpenAlex: W2034040607
Cited by: 524
References: 92
Citations by year: 2026: 13 · 2025: 22 · 2024: 26 · 2023: 23 · 2022: 28 · 2021: 45 · 2020: 36 · 2019: 39 · 2018: 57 · 2017: 37 · 2016: 41 · 2015: 47 · 2014: 38 · 2013: 41 · 2012: 29
FWCI: 1.82
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Current Psychiatry Reports (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: H. Lundbeck A/S
National Institutes of Health (UL1TR000454)
National Institute of Mental Health (R01MH083746, R01MH087604, R01MH075102)
National Center for Advancing Translational Sciences
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords: major depressive disorder, depression, inflammation, inflammatory markers, immune system, neuroinflammation, depression vulnerability, depression treatment
MeSH terms: Anti-Inflammatory Agents, Autonomic Nervous System, Major Depressive Disorder, Humans, Inflammation, Stress, Psychological, Biomarkers, Cytokines

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