Cited by 169Tryptophan and brain disordersCardiac Health and Mental HealthAntioxidant Activity and Oxidative Stress

Multiple aberrations in shared inflammatory and oxidative & nitrosative stress (IO&NS) pathways explain the co-association of depression and cardiovascular disorder (CVD), and the increased risk for CVD and due mortality in depressed patients

Maes, Michael, Ruckoanich, Piyanuj, Chang, Young Seun, Mahanonda, Nithi, Berk, Michael·2011·Progress in Neuro-Psychopharmacology and Biological Psychiatry

Abstract

There is evidence that there is a bidirectional relationship between major depression and cardiovascular disorder (CVD): depressed patients are a population at risk for increased cardiac morbidity and mortality, and depression is more frequent in patients who suffer from CVD. There is also evidence that inflammatory and oxidative and nitrosative stress (IO&NS) pathways underpin the common pathophysiology of both CVD and major depression. Activation of these pathways may increase risk for both disorders and contribute to shared risk. The shared IO&NS pathways that may contribute to CVD and depression comprise the following: increased levels of pro-inflammatory cytokines, like interleukin-1β (IL-1β), IL-2, IL-6, IL-8, IL-12, tumor necrosis factor-α, and interferon-γ; T cell activation; increased acute phase proteins, like C-reactive protein, haptoglobin, fibrinogen and α1-antitrypsin; complement factors; increased LPS load through bacterial translocation and subsequent gut-derived inflammation; induction of indoleamine 2,3-dioxygenase with increased levels of tryptophan catabolites; decreased levels of antioxidants, like coenzyme Q10, zinc, vitamin E, glutathione and glutathione peroxidase; increased O&NS characterized by oxidative damage to low density lipoprotein (LDL) and phospholipid inositol, increased malondialdehyde, and damage to DNA and mitochondria; increased nitrosative stress; and decreased ω3 polyunsaturated fatty acids (PUFAs). The complex interplay between the abovementioned IO&NS pathways in depression results in pro-atherogenic effects and should be regarded as a risk factor to future clinical CVD and due mortality. We suggest that major depression should be added as a risk factor to the Charlson "comorbidity" index. It is advised that patients with (sub)chronic or recurrent major depression should routinely be assessed by serology tests to predict if they have an increased risk to cardiovascular disorders.

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Crossref · 10.1016/j.pnpbp.2010.06.008

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Authors
Maes, M., Ruckoanich, P., Chang, Y. S., Mahanonda, N., & Berk, M.
Affiliations
  • Piyavate Hospital (TH)
  • Mental Health Research Institute (AU)
Corresponding author
Maes, Michael
Venue
Progress in Neuro-Psychopharmacology and Biological Psychiatry
Publisher
Elsevier BV
Published
2011-04
Volume
35
Issue
3
Pages
769-783
ISSN
0278-5846 (ISSN-L)
OpenAlex
W2011854518
Cited by
169
References
288
Citations by year
2026: 4 · 2025: 17 · 2024: 10 · 2023: 9 · 2022: 8 · 2021: 7 · 2020: 13 · 2019: 10 · 2018: 9 · 2017: 10 · 2016: 13 · 2015: 15 · 2014: 12 · 2013: 12 · 2012: 12
FWCI
0.70
Type
journal article
Language
en
Open access
closed
Locations
  • Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Health and Mental Health
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
major depressive disorder, cardiovascular disease, inflammatory signaling, oxidative stress, nitrosative stress, inflammatory cytokines, acute phase proteins, complement system, lipopolysaccharide, tryptophan catabolites, indoleamine 2,3-dioxygenase, antioxidants, atherosclerosis, omega-3 polyunsaturated fatty acids, cardiovascular mortality, Charlson Comorbidity Index
MeSH terms
Animals, Antioxidants, Cardiovascular Diseases, Depression, Female, Humans, Inflammation, Male, Risk, Fatty Acids, Omega-3, Nitrosation, Comorbidity, Oxidative Stress

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