Clinical depression and inflammatory risk markers for coronary heart disease
Abstract
Despite mounting evidence that psychiatric depression heightens risk for cardiac morbidity and mortality, little is known about the mechanisms responsible for this association. The present study examined the relation between depression and the expression of inflammatory risk markers implicated in the pathogenesis of coronary heart disease (CHD). One hundred adults were enrolled (68% women, 48% Caucasian, 48% African-American, mean age 30 +/- 2 years). Fifty subjects met the diagnostic criteria for clinical depression; the remaining 50 were demographically matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or regular medication regimen aside from oral contraceptives. The depressed subjects exhibited significantly higher levels of the inflammatory markers C-reactive protein (3.5 +/- 0.5 vs 2.5 +/- 5 mg/L, p = 0.04) and interleukin-6 (3.0 +/- 0.3 vs 1.9 +/- 0.2 pg/ml, p = 0.007) compared with control subjects. Mediational analyses aimed at identifying the pathways contributing to this association revealed that neither cigarette smoking nor subclinical infection with cytomegalovirus or Chlamydia pneumoniae had been responsible. However, depressed subjects exhibited greater body mass than control subjects, and analyses were consistent with adiposity accounting for a portion of the relation between clinical depression and increased expression of inflammatory markers.…
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Resistance to glucocorticoids and mild systemic inflammation have been implicated in the pathogenesis of depression, suggesting that the dynamics observed may help explain affective difficulties among caregivers.
“Notably, resistance to glucocorticoids and mild, systemic inflammation have also been implicated in the pathogenesis of depression (15,40–42), suggesting that the dynamics observed herein may help explain the affective difficulties often found among caregivers (43).”
From A Functional Genomic Fingerprint of Chronic Stress in Humans: Blunted Glucocorticoid and Increased NF-κB Signaling (2008) · cites this paper as [41]
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- Authors
- Miller, G. E., Stetler, C. A., Carney, R. M., Freedland, K. E., & Banks, W. A.
- Affiliations
- Washington University in St. Louis (US)
- Saint Louis University (US)
- Corresponding author
- Miller, Gregory E
- Venue
- The American Journal of Cardiology
- Publisher
- Elsevier BV
- Published
- 2002-12
- Volume
- 90
- Issue
- 12
- Pages
- 1279-1283
- ISSN
- 0002-9149 (ISSN-L)
- OpenAlex
- W1981466881
- Cited by
- 424
- References
- 3
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 7 · 2023: 10 · 2022: 9 · 2021: 5 · 2020: 11 · 2019: 15 · 2018: 16 · 2017: 8 · 2016: 24 · 2015: 18 · 2014: 12 · 2013: 13 · 2012: 24
- FWCI
- 12.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The American Journal of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Health and Mental Health
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- major depressive disorder, coronary artery disease, inflammatory markers, C-reactive protein, interleukin-6, adiposity, body mass, cigarette smoking, cytomegalovirus, Chlamydia pneumoniae, asymptomatic infection, mediation analysis, heart disease risk
- MeSH terms
- Adult, C-Reactive Protein, Coronary Disease, Cross-Sectional Studies, Depressive Disorder, Female, Humans, Inflammation, Male, Obesity, Risk Factors, Smoking, Tumor Necrosis Factor-alpha, Biomarkers, Interleukin-6, Body Mass Index, Odds Ratio, Case-Control Studies, Chemokine CCL2
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