The phenotype of recovery XII: A reinforcer pathology perspective on associations between delay discounting and pain catastrophizing in substance use disorder recovery.

Autor: Dwyer CL; Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke, VA, United States of America; Department of Psychology, Virginia Tech, Blacksburg, VA, United States of America., Craft WH; Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke, VA, United States of America., Yeh YH; Psychology Department, Illinois College, Jacksonville, IL, United States of America., Cabral DAR; Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke, VA, United States of America., Athamneh LN; Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke, VA, United States of America., Tegge AN; Department of Statistics, Virginia Tech, Blacksburg, VA, United States of America. Electronic address: ategge@vt.edu., Stein JS; Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke, VA, United States of America., Bickel WK; Fralin Biomedical Research Institute at Virginia Tech Carilion, Roanoke, VA, United States of America. Electronic address: wkbickel@vtc.vt.edu.
Jazyk: angličtina
Zdroj: Journal of substance use and addiction treatment [J Subst Use Addict Treat] 2024 Nov 09; Vol. 169, pp. 209573. Date of Electronic Publication: 2024 Nov 09.
DOI: 10.1016/j.josat.2024.209573
Abstrakt: Background: Substance use disorder (SUD) and pain are highly comorbid conditions and several pain indices (e.g., pain intensity) are associated with an increased risk of relapse. However, the cognitive-emotional experience of pain (i.e., pain catastrophizing) is understudied in SUD recovery. Further, how the association between pain catastrophizing and delay discounting - a posited biomarker of addiction, impacts multidimensional aspects of SUD recovery, including remission and quality of life (QOL), has yet to be examined.
Methods: Individuals (n = 170) in SUD recovery reporting pain were asked about their chronic pain status, completed the Brief Pain Inventory, the Pain Catastrophizing Scale, an Adjusting Amount Delay Discounting Task, and the World Health Organization QOL-BREF scale. Univariate logistic and linear regressions examined associations between delay discounting and several pain indices with remission and QOL. Mediation analyses were investigated whether pain catastrophizing mediates the relationship between delay discounting and 1) sustained remission and 2) QOL.
Results: Significant negative associations were found between delay discounting (p < .001) and pain catastrophizing (p = .001) with sustained remission. Pain catastrophizing significantly mediated the relationship between delay discounting and physical QOL (p = .044), psychological QOL (p = .009), social (p = .018), and environmental QOL (p = .014). Pain catastrophizing did not mediate the relationship between DD and sustained remission.
Conclusion: Individuals with greater DD exhibited greater pain catastrophizing, contributing to poorer QOL in SUD recovery. Our findings support that a Reinforcer Pathology framework is useful to understanding the cognitive-emotional experience of pain within the context of SUD recovery. Interventions that target both delay discounting and maladaptive cognitive and emotional responses to pain may lessen the negative impact of pain on SUD recovery and improve SUD outcomes.
Competing Interests: Declaration of competing interest Although the following activities/relationships do not create a conflict of interest pertaining to this manuscript, in the interest of full disclosure, Dr. Bickel would like to report the following: W. K. Bickel is a principal of HealthSim, LLC; BEAM Diagnostics, Inc.; and Red 5 Group, LLC. In addition, he serves on the scientific advisory board for Ria Health; and serves as a consultant for Lumanity. Dr. Tegge would like to report the following works on a project supported by Indivior, Inc. None of the other authors has any conflicts of interest to report.
(Copyright © 2024. Published by Elsevier Inc.)
Databáze: MEDLINE
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