Neurohormonal and inflammatory hyper-responsiveness to acute mental stress in depression.
Open accessAbstract
Depression is associated with dysregulated hypothalamic-pituitary-adrenal (HPA) axis function, overactivity of the sympathoadrenal system, and increased levels of inflammation markers. It is not known whether these biological processes are disproportionately elevated in response to acute negative emotional arousal by mental stress (MS). The present study investigates responses of neurohormones and inflammatory markers to MS in 14 clinically depressed (age: 42+/-10 years; 50% female) and 14 non-depressed control (age: 39+/-6 years; 50% female) participants. Heightened acute MS reactivity was documented in depressed participants (adrenocorticotropic hormone, rho=0.001; norepinephrine, rho=0.042; epinephrine, rho=0.039), and a delayed increase in cortisol was observed (rho=0.002). Inflammation markers increased more strongly in depressed versus non-depressed participants (IL-6, rho=0.027; tumor necrosis factor-alpha, rho=0.050; and recovery C-reactive protein, rho=0.003). It is concluded that depressed individuals display hyper-reactivity of neuroimmunological markers in response to acute negative emotions. This hyper-reactivity may serve a pathologic role in the elevated morbidity and mortality risk associated with depression.
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Depressed participants exhibited greater TSST-induced increases in several markers of SNS and HPA axis activity, including epinephrine, norepinephrine, adrenocorticotropic hormone, and cortisol, compared to nondepressed participants.
“Compared to nondepressed participants, depressed participants exhibited greater TSST-induced increases in several markers of SNS and HPA axis activity, including epinephrine, norepinephrine, adrenocorticotropic hormone, and cortisol.”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Weinstein et al., 2010
The Results (Neurohormonal Response to Acute Mental Stress) report greater ACTH, cortisol, norepinephrine, and epinephrine responses in depressed participants than in controls. But the Methods (Procedures) identify the stressors as anger recall and mental arithmetic tasks, not the TSST, so the claim misidentifies what induced those responses. (LLM, conf=0.91)
Experimental — accuracy not yet measuredDepressed participants also exhibited greater increases in plasma levels of the proinflammatory cytokines TNFα and IL-6 and the inflammatory marker CRP.
“Depressed participants also exhibited greater increases in plasma levels of the proinflammatory cytokines TNFα and IL-6 and the inflammatory marker CRP”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Weinstein et al., 2010
Individuals with diagnosed depression have demonstrated stronger increases in proinflammatory cytokines in response to laboratory stress than non-depressed individuals.
“Individuals with diagnosed depression have demonstrated stronger increases in proinflammatory cytokines in response to laboratory stress than non-depressed individuals (Weinstein et al., 2010; Fagundes et al., 2013)”
From The interplay between stress, inflammation, and emotional attention: relevance for depression (2019) · cites this paper as Weinstein et al., 2010
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- Authors
- Weinstein, A. A., Deuster, P. A., Francis, J. L., Bonsall, R. W., Tracy, R. P., & Kop, W. J.
- Affiliations
- George Mason University (US)
- Uniformed Services University of the Health Sciences (US)
- Emory University (US)
- University of Vermont (US)
- University of Maryland Medical Center (US)
- Corresponding author
- Weinstein, Ali A.
- Venue
- Biological Psychology
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 84
- Issue
- 2
- Pages
- 228-234
- ISSN
- 0301-0511 (ISSN-L)
- PMC
- PMC2875322
- OpenAlex
- W2163435166
- Cited by
- 113
- References
- 71
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 8 · 2023: 12 · 2022: 6 · 2021: 5 · 2020: 5 · 2019: 12 · 2018: 6 · 2017: 4 · 2016: 7 · 2015: 8 · 2014: 6 · 2013: 7 · 2012: 4
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychology (publishedVersion)
- Research portal (Tilburg University) (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL079376)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- depression, acute psychological stress, neurohormones, inflammatory markers, hypothalamic-pituitary-adrenal axis, sympathoadrenal system, ACTH, cortisol, norepinephrine, epinephrine, interleukin-6, TNF-α, C-reactive protein, neuroinflammation, stress reactivity
- MeSH terms
- Adrenocorticotropic Hormone, Adult, Analysis of Variance, C-Reactive Protein, Catecholamines, Depression, Female, Humans, Hydrocortisone, Male, Middle Aged, Stress, Psychological, Tumor Necrosis Factor-alpha, Interleukin-6, Cytokines
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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