Inflammatory and Cardiovascular Responses to Active and Passive Acute Psychological Stress

Q: What is the clinical evidence from this study?

Study design: RCT. Population: Healthy young adults (n=88). Intervention: Active psychological stress task (PASAT) vs. Passive psychological stress task (IAPS). Primary outcome: Circulating IL-6 at 45-minutes post-task (p=>0.05).

Q: What does this research mean for the field?

Both active and passive acute psychological stress elicit similar increases in circulating IL-6 and systemic inflammation response index (SIRI), despite active stress producing higher cardiovascular responses. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Victoria G. Linsley; Nicolette C. Bishop; Matthew J Roberts; Malik Hamrouni; Mayada Demashkieh; Nicola J. Paine

doi:10.1097/psy.0000000000001367

February 1, 2025Biopsychosocial Science and MedicineOpen Access

Inflammatory and Cardiovascular Responses to Active and Passive Acute Psychological Stress

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Key result

Active and passive psychological stress trigger similar inflammatory increases despite differing cardiovascular reactivity.

P>0.05
n=88

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Why the study?

Acute psychological stress promotes inflammation and cardiovascular risk, but whether immune responses to active stressors translate to passive stressors was unclear.

Does active psychological stress elicit a different inflammatory and cardiovascular response compared to passive psychological stress in healthy young adults?

Key Points

To investigate whether immune and cardiovascular responses differ between active and passive acute psychological stress modalities.
Completed by 88 participants (mean age = 21.5 years, 41% female) who underwent both an active stressor (Paced Auditory Serial Addition Test [PASAT]) and a passive stressor (International Affective Picture System [IAPS]) in randomized order.
Cardiovascular markers (systolic blood pressure, diastolic blood pressure, heart rate, cardiac output) were monitored continuously, followed by 45 minutes of rest post-task.
Serial blood samples were collected to quantify circulating and stimulated interleukin-6 (IL-6), systemic inflammation response index (SIRI), neutrophil/lymphocyte ratio (NLR), TNF-α, and P- and E-selectin.
Cardiovascular reactivity (HR, SBP, DBP, and cardiac output) was significantly higher during the active PASAT compared to the passive IAPS task (all p < .001).
Circulating IL-6 increased significantly from baseline to 45 minutes post-task for both PASAT and IAPS (p ≤ .001), with no significant difference between tasks at 45 minutes (p > .05).
SIRI increased from baseline to 45 minutes post-PASAT (p < .001) and post-IAPS (p = .004; no between-task difference at 45 minutes), NLR increased from baseline to 45-minute post-PASAT (p = .008), while TNF-α, P-selectin, and E-selectin showed no significant time effects (all p > .05).

Study Design

Type

RCT (n=88)

Randomization

randomized order (crossover)

Multicenter

No

Structured PICO

Does active psychological stress elicit a different inflammatory and cardiovascular response compared to passive psychological stress in healthy young adults?

P

Population

88 healthy young adults (mean age 21.5, 41% female) without chronic conditions or medication use underwent active and passive stress tasks to evaluate cardiovascular and inflammatory reactivity.

I

Intervention

Active psychological stress task (Paced Auditory Serial Addition Test [PASAT] for 8 minutes) including elements of social evaluation, competition, and aversive noise.

C

Comparator

Passive psychological stress task (International Affective Picture System [IAPS] negative valence images for 6 minutes).

O

Outcome

Inflammatory responses (including circulating and stimulated IL-6, SIRI, NLR, TNF-α, P-selectin, and E-selectin) and continuous cardiovascular measures (SBP, DBP, HR, cardiac output).surrogate

Main Result

Absolute Event Rate: 1.11% vs 1.01%

p-value: p=>0.05

Both active and passive psychological stress significantly elevate systemic inflammation markers (like IL-6 and SIRI), suggesting even passive stressors may contribute to long-term cardiovascular risk.

Limitations

Lack of a nonstress control condition to differentiate stress reactivity from diurnal variation
Young, healthy sample limits generalizability to clinical or older populations
Blood sampling timepoints (up to 45 minutes) may have missed peak responses for certain markers like TNF-α and selectins
Did not measure stress hormones like cortisol or catecholamines
Lack of nonstress control condition
Healthy young population restricts generalizability
Missing cortisol or catecholamine measurements
45-minute follow-up may have been too short for peak selectin or TNF-α expression

Implication

Passive stress elevates IL-6 and SIRI similarly to active stress; extends acute psychological stress research to passive modalities as a cardiovascular risk pathway.

Abstract

OBJECTIVE: Acute psychological stress is a risk factor for cardiovascular disease (CVD), possibly through promoting a heightened inflammatory profile. Active stressors are commonly used to investigate cardiovascular and immune reactivity; however, this response may not translate to other stress modalities. We aimed to decipher potential differences in immune responses to passive and active stressors. METHODS: Eighty-eight participants completed this study. After a baseline period, a passive (International Affective Picture System [IAPS]) and active stress task (Paced Auditory Serial Addition Test [PASAT]) were completed in a randomized order, with 45-minute rest post-tasks. Cardiovascular measures (including SBP, DBP, HR) were collected continuously. Blood samples were collected after each time point determining inflammatory responses, including circulating and stimulated interleukin-6 (IL-6), systemic inflammation response index (SIRI), neutrophil/lymphocyte ratio (NLR), TNF-α, and P- and E-selectin. RESULTS: Cardiovascular measures were higher during the PASAT than IAPS (p < .001). Circulating IL-6 levels increased from baseline to 45-minutes after both tasks (p ≤ .001), with no difference between 45-minute post-PASAT and 45-minute post-IAPS (p > .05). SIRI increased from baseline to post-IAPS (p = .013), 45-minute post-IAPS (p = .004), and 45-minute post-PASAT (p < .001). No difference in SIRI between 45-minute post-PASAT and 45-minute post-IAPS existed. NLR increased from baseline to 45-minute post-PASAT (p = .008). There were no significant time effects for TNF-α, P-selectin, or E-selectin (all p > .05). CONCLUSION: Both stressors increased circulating IL-6 levels and SIRI. Cardiovascular measures were higher during the active task, but the magnitude of inflammatory responses did not significantly differ between tasks. Regardless of stress modality, an immune response ensues, potentially increasing the risk of CVD over time.

Discussion

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Cite This Study

Linsley et al. (2025) conducted an RCT in Healthy young adults (n=88). Active psychological stress task (PASAT) vs. Passive psychological stress task (IAPS) was evaluated on Circulating IL-6 at 45-minutes post-task (p=>0.05). Both active and passive psychological stress tasks significantly increased circulating IL-6 and SIRI levels to a similar magnitude, despite higher cardiovascular reactivity during the active task.

synapsesocial.com/papers/6a242ce79ed8aa0626a0a956 https://doi.org/10.1097/psy.0000000000001367

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Inflammatory and Cardiovascular Responses to Active and Passive Acute Psychological Stress

Figures

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

Inflammatory and Cardiovascular Responses to Active and Passive Acute Psychological Stress

Figures

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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