Lapse-induced surges in craving influence relapse in adult smokers: an experimental investigation.

The overwhelming majority of smokers who attempt to quit using any method or delivery channel are unsuccessful (Shiffman, Brockwell, Pillitteri, & Gitchell, 2008). One of the central challenges for smokers who achieve initial abstinence is that they are at high risk for lapsing. A lapse is a circumscribed period of smoking after a smoker has achieved abstinence (see Hughes, Keely, Niaura, et al., 2003); after a lapse, individuals return to a period of abstinence. However, periods of abstinence following a lapse are typically short-lived: nearly every smoker who lapses eventually relapses (Brandon, Tiffany, Obremski, & Baker, 1990; Garvey et al., 1992; Chornock, Stitzer, Gross, & Leischow, 1992). Unfortunately, the mediating mechanisms that cause lapses to become relapses are poorly understood and interventions designed to stop the progression from lapse to relapse have not been especially effective. Advancing the field’s understanding of the mechanisms that turn lapses into relapses has been recommended as a way to improve smoking cessation treatments (Abrams, Emmons, Niaura, Goldsten, & Sherman, 1991; Niaura & Abrams, 2002; Piasecki, Fiore, McCarthy, & Baker, 2002; Shiffman, 2006). Once these mechanisms are identified treatments could be developed or existing treatments could be modified to target those mechanisms and improve cessation outcomes. This study experimentally investigates the role that craving plays in turning smoking lapses into relapses. Craving plays a central role many theories of relapse (for reviews, see Brandon, Vidrine, & Litvin, 2007; Marlatt & Donovan, 2005; Skinner & Aubin, 2010; Tiffany,Warthen, & Goedeker, 2009). Two types of craving have been identified (see Shiffman, 2000). Background craving occurs on a more or less steady basis throughout the day, diminishing in intensity over time. Increasing levels of deprivation from smoking typically lead to stronger levels of background cravings (Payne, Smith, Sturges, & Holleran, 1996) and smokers with more intense levels of background craving have increased risk of relapse (Killen & Fortman, 1997; Shiffman et al., 1997). However, periodic episodes of intense surges in craving (episodic craving) can persist even as the intensity of background craving declines (Shiffman, Paty, Gnys, Kassel, & Hickcox, 1996b; Shiffman et al, 1997). Episodic craving can be triggered by contextual cues (Shiffman et al., 1996b) and can predict both lapses and relapses (e.g., Shiffman et al, 1996b). Owing to its importance in predicting smoking cessation outcomes and relapse, cognitive-behavioral treatments offer strategies to help smokers manage cravings (Brown, 2003). Pharmacological treatments for smoking cessation are thought to operate, in part, by blunting levels of background craving (Tiffany, Cox, & Elash, 2000). Some nicotine replacement medications (e.g., nicotine gum) can be used as “rescue” medications to help smokers manage episodic craving in response to provocative cues (Shiffman et al., 2003). Less well studied is what happens to craving after a smoking lapse and whether it prompts relapsing. Studies have suggested that craving can both decrease (Juliano, Donny, Houtsmuller, & Stitzer, 2006) and increase (Shiffman et al., 1996b; see also Shiffman & Paty, 2006) after a lapse. Post-lapse decreases in craving can be explained by negative reinforcement models (Baker, Piper, McCarthy, Majeskie, & Fiore, 2004). In this view, increased craving during an abstinent period (i.e., pre-lapse craving) represents an aversive state from which the smoker seeks relief by smoking (i.e., smoking reduces craving). A resumption of smoking (i.e., relapse) results from the drive to alleviate episodic increases in craving. Post lapse increases in craving can be explained by reinstatement models of drug use (Chiamulera, Borgo, Falchetto, Valerio, & Tessari, 1996; Shaham, Adamson, Grocki, & Corrigall, 1997; see Epstein, Preston, Stewart, & Shaham, 2006). In this view, the small priming dose of nicotine provided by a smoking lapse (perhaps combined with the context or cues associated with the lapse; see Niaura et al., 1988) creates an appetitive motivational state, indexed by increased craving, which then stimulates further smoking (Baker, Morse, & Sherman, 1986; Robinson & Berridge, 1993; Wise & Bozarth, 1987). Regardless of the direction of post-lapse changes in craving, no studies have examined whether these changes contribute to relapse. The purpose of this study is to experimentally evaluate the effects of a programmed smoking lapse on smoking relapse and the effects of post-lapse changes in craving on relapse. We enrolled smokers who were motivated to quit smoking as participants. After 48 hours of biochemically confirmed abstinence (achieved with a minimal brief cognitive-behavioral intervention; see Shadel & Niaura, 2003), we experimentally manipulated lapse by randomly assigning participants to either a lapse or no-lapse condition, after which we tracked daily levels of craving and smoking behavior through a brief follow-up (14-days). Relapse was defined as the first instance of smoking at least one cigarette a day for seven consecutive days following the manipulation day (Hughes et al., 2003). We hypothesized that participants assigned to the lapse condition would relapse more quickly compared to participants in the no-lapse condition and that the effect of lapse on relapse would be explained (mediated) by post-lapse changes in craving. Experimental studies of relapse such as the one reported in this paper permit stronger causal inferences compared to field studies and quasi experimental designs and allow for controlled evaluation of theoretical mechanisms that are thought to underlie an observed phenomenon (see Chow, 1995; see also McKee, 2009; Perkins, Stitzer, & Lerman, 2006). The current design was inspired by the only two smoking studies that have used experimental designs to model relapse in the laboratory (Chornick et al., 1992; Juliano et al., 2006). These studies manipulated lapses by having individuals smoke five cigarettes after an abstinent period (vs not smoking and/or smoking de-nicotinzed cigarettes) and measured time to first cigarette puff (after the manipulation) as the outcome. Findings from these studies suggested that lapse is causally related to subsequent smoking in recently quit individuals. However important these findings, these studies were limited by their use of individuals who were not motivated to quit, short follow-up periods (< one week), non-standard definitions of relapse, and lack of an attention to mechanisms that link lapse to relapse. The current study was designed to address these concerns with this previous work and to enhance the clinical utility of laboratory models of relapse.