Cited by 113Stress Responses and CortisolTryptophan and brain disordersNeuropeptides and Animal Physiology

Neurohormonal and inflammatory hyper-responsiveness to acute mental stress in depression.

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Weinstein, Ali A., Deuster, Patricia A., Francis, Jennifer L., Bonsall, Robert W., Tracy, Russell P., Kop, Willem J.·2010·Biological Psychology

Abstract

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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Crossref · 10.1016/j.biopsycho.2010.01.016

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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 measured
  • Depressed 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”
  • 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)”

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Research works printed but not linked: 1

  1. Hedlund JL Virmani R 1979 The Hamilton rating scale for depression: A comprehensive review Journal of Operational Psychiatry 11 48 65

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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)
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
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

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