Maintenance of a positive outlook during acute stress protects against pro-inflammatory reactivity and future depressive symptoms
Open accessAbstract
Unlabelled Cognitive and affective responses to acute stress influence pro-inflammatory cytokine reactivity, and peripheral cytokines (particularly interleukin-1 beta (IL-1β)), can act on the brain to promote depressive symptoms. It is unknown whether acute stress-induced changes in positive affect and cognitions (POS) and pro-inflammatory reactivity predict future depressive symptoms. We examined acute stress responses among women, to determine prospective predictors of depressive symptoms.Hypotheses (1) Stress-induced decreases in POS will be associated with stress-related increases in circulating IL-1β. (2) Acute stress-induced decreases in POS and increases in IL-1β reactivity will predict increases in depressive symptoms 1 year later. Thirty-five post-menopausal women were exposed to acute stress with the Trier Social Stress Task (TSST) and provided blood samples under resting conditions and 30 min after the conclusion of the TSST, which were assayed for IL-1β. IL-1β reactivity was quantified as post minus pre-TSST. Failure to maintain POS was quantified as the decrease in POS during the TSST. Change in depressive symptoms from the study baseline to the following year was determined. Greater acute stress-induced declines in POS were significantly associated with increased IL-1β reactivity (p≤.02), which significantly predicted increases in depressive symptoms over the following year (p<.01), controlling for age, body mass index, chronic stress, antidepressant use and baseline depressive symptoms. IL-1β reactivity was a significant mediator of the relationship between POS decline and future increases in depressive symptoms (p=.04). Difficulty maintaining positivity under stress and heightened pro-inflammatory reactivity may be markers and/or mechanisms of risk for future increases in depressive symptoms.
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The greater the inflammatory response to a psychosocial stressor, the more probable the subject is to develop depression over the ensuing months.
“the greater the inflammatory response to a psychosocial stressor, the more probable the subject is to develop depression over the ensuing months5.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [5]
The Results (Hypothesis 2; page not provided) report that greater IL-1β reactivity to acute stress was associated with greater increases in depressive symptoms one year later. The Methods (Inventory of Depressive Symptoms; page not provided) show that the outcome was a change in symptom score, not the probability of developing depression; the prospective sample was also limited to post-menopausal women. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIncreases in circulating IL-1β predicted increases in depressive symptoms over the following year.
“increases in circulating IL-1 β in turn predicted increases in depressive symptoms over the following year”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Aschbacher et al., 2012
Greater difficulty in maintaining a positive cognitive-affective state during the TSST was associated with greater increases in circulating IL-1β.
“greater difficulty in maintaining a positive cognitive-affective state during the TSST was associated with greater increases in circulating IL-1 β”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Aschbacher et al., 2012
IL-1β reactivity to the TSST significantly mediated the relation between cognitive-affective responses to the TSST and future increases in depressive symptoms over the 1-year follow-up period.
“IL-1 β reactivity to the TSST significantly mediated the relation between cognitive-affective responses to the TSST and future increases in depressive symptoms over the 1-year follow-up period”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Aschbacher et al., 2012
Increases in IL-1β in response to TSST predicted the increase of depressive symptoms 1 year later.
“increases in IL-1β in response to TSST predicted the increase of depressive symptoms 1 year later (Aschbacher et al., 2012).”
From The interplay between stress, inflammation, and emotional attention: relevance for depression (2019) · cites this paper as Aschbacher et al., 2012
Inappropriate inflammation increases the risk and severity of mood disorders.
“This elevated inflammatory state has also been associated with increased risk and severity of mood disorders including depression (Aschbacher et al, 2012;Danese et al, 2008;Pace et al, 2012).”
From Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders (2017) · cites this paper as Aschbacher et al, 2012
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- Authors
- Aschbacher, K., Epel, E., Wolkowitz, O. M., Prather, A. A., Puterman, E., & Dhabhar, F. S.
- Affiliations
- University of California, San Francisco (US)
- Stanford Medicine (US)
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 26
- Issue
- 2
- Pages
- 346-352
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC4030538
- OpenAlex
- W2015010043
- Cited by
- 112
- References
- 48
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 6 · 2023: 9 · 2022: 8 · 2021: 11 · 2020: 6 · 2019: 16 · 2018: 12 · 2017: 6 · 2016: 11 · 2015: 3 · 2014: 7 · 2013: 5 · 2012: 2
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- University of California, San Francisco
- National Institute on Aging (R01AG030424)
- National Heart, Lung, and Blood Institute (K23HL112955)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
- Keywords
- acute stress, positive affect, IL-1β, inflammatory cytokines, depressive symptoms, Trier Social Stress Test, postmenopausal women, mediation
- MeSH terms
- Affect, Aged, Depression, Female, Humans, Inflammation, Middle Aged, Psychiatric Status Rating Scales, Stress, Psychological, Time Factors, Interleukin-6, Interleukin-1beta
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