Pain and substance use are highly prevalent and co-occurring conditions that continue to garner increasing clinical and empirical interest. Although nicotine and tobacco, alcohol, and cannabis each confer acute analgesic effects, frequent or heavy use may contribute to the development and progression of chronic pain, and pain may be heightened during abstinence. Additionally, pain can be a potent motivator of substance self-administration, and it may contribute to escalating use and poorer substance-related treatment outcomes. We integrated converging lines of evidence to propose a reciprocal model in which pain and substance use are hypothesized to interact in the manner of a positive feedback loop, resulting in the exacerbation and maintenance of both conditions over time. Theoretical mechanisms in bidirectional pain–substance use relations are reviewed, including negative reinforcement, social cognitive processes, and allostatic load in overlapping neural circuitry. Finally, candidate transdiagnostic factors are identified, and we conclude with a discussion of clinical implications and future research directions.
Although emerging research suggests that pain-related anxiety may play a role in the maintenance of tobacco dependence, no previous work has examined pain-related anxiety as a predictor of smoking cessation outcomes. The goal of the current study was to test the hypothesis that pain-related anxiety would predict early lapse and relapse to cigarette smoking. These data were collected in the context of a primary study examining the role of emotional vulnerabilities in smoking cessation. The current analyses were conducted among a sample of 55 daily cigarette smokers who attempted to quit smoking without using any psychosocial or pharmacological cessation aids. Pain-related anxiety was assessed at baseline using the PASS-20. Early lapse and relapse were assessed using timeline follow-back procedures. Cox regression analyses indicated that pain-related anxiety was a significant predictor of both early smoking lapse and relapse, such that for every one-point increase on the PASS-20, the risk of early lapse increased by 3.7% and the risk of early relapse increased by 3.6%. These effects were evident above and beyond the variance accounted for by tobacco dependence, past four-week pain severity, anxiety sensitivity, and the presence of current Axis I psychopathology. Kaplan-Meier survival analyses further revealed that among early lapsers, greater pain-related anxiety predicted a more rapid trajectory to lapse. Pain-related anxiety was also shown to be a significant predictor of early lapse when the sample was limited to smokers who endorsed past four-week pain. These findings lend empirical support to the notion that pain-related anxiety may contribute to the maintenance of tobacco dependence among smokers who experience varying levels of pain intensity.
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