|Grant Number:||5R01CA127491-04 Interpret this number|
|Primary Investigator:||Shadel, William|
|Project Title:||Evaluating the Casual Pathways From Lapse to Relapse in Smokers|
DESCRIPTION (provided by applicant): The overwhelming majority of smoking lapses lead to full blown relapse. Because lapses almost always occur and cannot always be avoided, cognitive-behavioral relapse prevention techniques have focused on helping smokers to manage their reactions to lapses so that they can avoid relapses. Unfortunately, cognitive- behavioral relapse prevention training has not been especially promising for smokers in this regard. This may be due to the fact that the field has no good information available about the psychological processes and mechanisms that cause a lapse to become a relapse. One way to begin to refine or to develop new cognitive- behavioral relapse prevention interventions is to focus on testing and evaluating newer theories of relapse in order to understand more about the psychological processes that cause lapses to become relapses. Driven by the recent revision of relapse prevention theory and the results of field research, this application proposes to conduct two studies designed to provide a clinically-relevant experimental analogue model of how lapses causally contribute to relapse. In relapse prevention theory, lapses are followed by phasic changes in self- efficacy and in combination (either additively or interactively) with tonic levels of smoking outcome expectancies, contribute to relapse. In other words, self-efficacy and outcome expectancies mediate the relationship between lapse and relapse. Mediational analyses, by definition, model the direct causal force that an initial variable (in our case, a lapse) exerts on an outcome variable (relapse) through an intervening variable(s) the mediator(s) (self-efficacy and outcome expectancies). The mediator both is caused by the initial variable (lapses cause changes in self-efficacy and outcome expectancies) and causes the outcome variable (lapse induced changes in self-efficacy and outcome expectancies cause changes relapse likelihood). Thus, our analogue model of relapse will: 1) experimentally create a lapse after a period of programmed abstinence and then measure time to relapse over a brief 14-day follow-up period to determine whether lapse is causally related to relapse and what the mediating roles of self-efficacy and smoking outcome expectancies are in this relationship (Study 1); and 2) experimentally manipulate self-efficacy and outcome expectancies after a period of programmed abstinence and a programmed lapse, and then measure time to relapse over a brief follow-up period to determine whether experimentally controlled changes to self-efficacy and smoking outcome expectancies causally contribute to relapse (Study 2). Smokers who are motivated to quit will participate in these studies to enhance the clinical applicability and external validity of the findings. As such, all participants will be offered clinical treatment for smoking cessation after completing the experimental portion of each study. The long range goals of this research are threefold: 1) to promote an improved understanding of the proposed mechanisms of action of relapse prevention treatment; 2) to build on these results to build a more complex model of relapse; and 3) to improve clinical efficacy of relapse prevention training with smokers. Cigarette smoking contributes to over half a million deaths annually in the United States and quitting smoking substantially reduces the death and disease associated with smoking. Unfortunately, however, most smokers who attempt to quit smoking will not be successful; in other words, most smokers who attempt to quit relapse. One reason is that very little good information is available about the psychological variables that cause relapses. PUBLIC HEALTH RELEVANCE: This research seeks to uncover the psychological variables that cause relapses and the results will be used to inform a new generation of more successful smoking cessation treatments.