Individual Dynamics in Stress-Related Pain Responses

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Abstract

Background Stress and pain are adaptive, bidirectionally related systems, modulated by shared factors. However, how stress reactivity relates to individual differences in pain-related distress and pain sensitivity remains unclear. This preregistered study therefore investigates how physiological reactivity to acute stress relates to trait pain-related distress and stress-induced changes in pain sensitivity, and whether pain-related distress acts as moderator. Methods Trait pain-related distress was assessed in 148 healthy males using questionnaires. Baseline blood pressure, pulse rate, alpha-amylase, and cortisol were obtained as well as initial heat pain thresholds and tolerances. One group underwent the Maastricht Acute Stress Task, while another group performed the placebo version. Consecutively all stress- and experimental pain indicators were examined again. Results Trait pain-related distress was not associated with stress reactivity (MAST-induced changes in physiological stress indicators), while stress-induced changes in pain sensitivity showed high individual variability, but were not associated with stress reactivity. Finally, we found preliminary evidence that in individuals with a higher tendency to catastrophize and to fear pain, stronger alpha-amylase increases were associated with larger stress-induced increases in pain threshold ( p-FDR = .07). Conclusion Our study illustrates the idiosyncrasy of the complex interplay between trait pain-related distress, physiological stress reactivity, and stress-induced changes in pain sensitivity. While our preliminary results require replication, they suggest that stable individual differences influence the link between stress and pain beyond physiology. This underscores the importance of considering trait differences in future research on stress-pain interactions to, ultimately, better tailoring preventions and treatments for patients with chronic pain.
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Abstract

Background Stress and pain are adaptive, bidirectionally related systems, modulated by shared factors. However, how stress reactivity relates to individual differences in pain-related distress and pain sensitivity remains unclear. This preregistered study therefore investigates how physiological reactivity to acute stress relates to trait pain-related distress and stress-induced changes in pain sensitivity, and whether pain-related distress acts as moderator.

Methods

Trait pain-related distress was assessed in 148 healthy males using questionnaires. Baseline blood pressure, pulse rate, alpha-amylase, and cortisol were obtained as well as initial heat pain thresholds and tolerances. One group underwent the Maastricht Acute Stress Task, while another group performed the placebo version. Consecutively all stress- and experimental pain indicators were examined again.

Results

Trait pain-related distress was not associated with stress reactivity (MAST-induced changes in physiological stress indicators), while stress-induced changes in pain sensitivity showed high individual variability, but were not associated with stress reactivity. Finally, we found preliminary evidence that in individuals with a higher tendency to catastrophize and to fear pain, stronger alpha-amylase increases were associated with larger stress-induced increases in pain threshold (p-FDR = .07).

Conclusion

Our study illustrates the idiosyncrasy of the complex interplay between trait pain-related distress, physiological stress reactivity, and stress-induced changes in pain sensitivity. While our preliminary results require replication, they suggest that stable individual differences influence the link between stress and pain beyond physiology. This underscores the importance of considering trait differences in future research on stress-pain interactions to, ultimately, better tailoring preventions and treatments for patients with chronic pain. Competing Interest Statement The authors have declared no competing interest. Footnotes Our main changes in the revised manuscript include: - Greater emphasis on the non-significant findings following correction for multiple testing, with more cautious wording adopted throughout to better reflect the strength of the evidence. - Subjective responses to the MAST and AUCi cortisol measures were removed from the primary analyses, - Terminology was standardized throughout the manuscript to improve consistency (e.g., using stress response versus stress reactivity). - Additional clarification and background information, including clearer identification of the involved stress systems, stronger theoretical grounding for the hypotheses based on existing literature, greater depth in the discussion section (e.g., regarding the absence of significant findings), and increased transparency concerning the studys limitations.

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last seen: 2026-05-20T01:45:00.602351+00:00