BACKGROUND: Cognitive models explaining medically unexplained complaints propose that activating illness-related memory causes increased complaints such as pain. However, our previous studies showed conflicting support for this theory. PURPOSE: Illness-related memory is more likely to influence reporting of complaints when its activation is enmeshed with that of self-related memory. We, therefore, investigated whether inducing this association would cause a stronger decrease in pain tolerance. In addition, we examined whether SFA acted as a moderator of this effect. METHODS: We used subliminal evaluative conditioning (SEC) to induce an association between activated self-related and illness-related memory. Seventy-six participants were randomly assigned to four combinations of two priming factors: (1) the self-referent word "I" versus the nonself-referent "X" to manipulate activated self-related memory and (2) health complaint (HC) words versus neutral words to manipulate activated illness-related memory. Pain tolerance was assessed using a cold pressor task (CPT). RESULTS: Participants primed with the self-referent "I" and HC words did not demonstrate the expected lower pain tolerance. However, SFA acted as a moderator of the main effect of the self-prime: priming with "I" resulted in increased pain tolerance in participants with low SFA. CONCLUSIONS: The current study did not support the hypothesis that associations between activated self-related memory and illness-related memory cause increased reporting of complaints. Instead, activating self-related memory increased pain tolerance in participants with low SFA. This seems to indicate that the self-prime might cause an increase in SFA and suggests possible new ways to promote adaptive coping with pain.
RCT Entities:
BACKGROUND: Cognitive models explaining medically unexplained complaints propose that activating illness-related memory causes increased complaints such as pain. However, our previous studies showed conflicting support for this theory. PURPOSE: Illness-related memory is more likely to influence reporting of complaints when its activation is enmeshed with that of self-related memory. We, therefore, investigated whether inducing this association would cause a stronger decrease in pain tolerance. In addition, we examined whether SFA acted as a moderator of this effect. METHODS: We used subliminal evaluative conditioning (SEC) to induce an association between activated self-related and illness-related memory. Seventy-six participants were randomly assigned to four combinations of two priming factors: (1) the self-referent word "I" versus the nonself-referent "X" to manipulate activated self-related memory and (2) health complaint (HC) words versus neutral words to manipulate activated illness-related memory. Pain tolerance was assessed using a cold pressor task (CPT). RESULTS:Participants primed with the self-referent "I" and HC words did not demonstrate the expected lower pain tolerance. However, SFA acted as a moderator of the main effect of the self-prime: priming with "I" resulted in increased pain tolerance in participants with low SFA. CONCLUSIONS: The current study did not support the hypothesis that associations between activated self-related memory and illness-related memory cause increased reporting of complaints. Instead, activating self-related memory increased pain tolerance in participants with low SFA. This seems to indicate that the self-prime might cause an increase in SFA and suggests possible new ways to promote adaptive coping with pain.