Stress and pain: modality-specific opioid mediation of stress-induced analgesia.
Level 2 - randomized trial
Individual double-blind randomized crossover trial in humans
PubMed 34405305 · doi:10.1007/s00702-021-02401-4
What was done
Eighty-four participants (34 women) completed a within-subject, double-blind, counterbalanced crossover trial to evaluate whether the endogenous opioid system mediates stress-induced analgesia. Across two sessions, participants received either oral placebo or the opioid antagonist naltrexone (50 mg). In each session, participants underwent two evoked pain tests (cold pressor test and heat pain) after an extended rest period and after an acute combined stressor (public speaking and mental arithmetic challenge). Hormonal, cardiovascular, and pain responses were measured.
What was found
The abstract reports statistical significance and directions of effect without numerical values, effect sizes, or test statistics. Both acute stress and naltrexone produced significant changes in cardiovascular and hormonal measures. Stress significantly increased cold pressor test tolerance (indicating stress-induced analgesia), an effect that was most pronounced in participants experiencing the stress condition first. Naltrexone abolished the stress-induced increase in cold pressor tolerance. No significant stress-induced analgesia was observed for heat pain responses.
Why it matters
This trial demonstrates in humans that endogenous opioids mediate stress-induced analgesia for cold pain, while showing that this analgesic response is modality-specific rather than uniform across all pain types.
Limits
The abstract provides no raw numbers, means, standard deviations, or effect sizes. The sample was limited to 84 healthy volunteers undergoing acute laboratory stressors and experimental pain, which may not generalize to clinical pain. Analgesia was observed only for cold pressor tolerance and did not generalize to heat pain.
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