Psychoneuroendocrinology · 2026
Individual dynamics in stress-related pain responses.
СтатьяНазвание и аннотация: Перевод в очереди
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Vyverman Joren, Timmers Inge, Meeuwis Stefanie H, Smeets Tom, Hilger Kirsten
Аннотация
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 observed non-significant trend-level effects suggesting that in individuals with a higher tendency to catastrophize and to fear pain, stronger alpha-amylase increases might be associated with larger stress-induced increases in pain thresholds (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 trend-level results require replication, they suggest that stable individual differences could potentially 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 tailor prevention and treatment for individuals with chronic pain.
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 observed non-significant trend-level effects suggesting that in individuals with a higher tendency to catastrophize and to fear pain, stronger alpha-amylase increases might be associated with larger stress-induced increases in pain thresholds (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 trend-level results require replication, they suggest that stable individual differences could potentially 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 tailor prevention and treatment for individuals with chronic pain.