The results of the current study, in combination with the results of other experimental studies (Chornock et al., 1992
; Juliano et al., 2006
), firmly establish that lapse has a causal relationship to relapse in smokers. The current study goes beyond these previous studies in that it provides new information about mediating mechanisms that link smoking lapses to relapses. Compared with participants in the no lapse condition, participants who were assigned to lapse experienced an initial acute decrease in craving followed by a significant surge in craving. The surges in craving experienced by those in the lapse condition, which were observed after controlling for their baseline craving levels, explained their faster rate of relapse relative to participants in the control condition.
The field of tobacco control has long struggled to understand why smoking lapses nearly always lead to relapses. As a result, cognitive-behavioral and pharmacological interventions have had little success in helping smokers to avoid relapse. Research that clearly identifies the mechanisms that govern the relationship between lapse and relapse would have a substantial impact on smoking cessation and relapse prevention treatments, pointing the way toward the development of new treatments and modification of existing ones to target those mechanisms for change (Shiffman, 2006
). Our results therefore have implications for relapse prevention treatments in addition to having implications for theories that explain why lapses almost inevitably lead to relapses.
Cognitive-behavioral treatments (Brown, 2003
) and medications for smoking cessation (Shiffman et al., 2003
; Tiffany et al., 2000
) target craving to help smokers maximize their successes with quitting, but neither is currently employed specifically to prevent lapses from turning into relapses. Currently, cognitive-behavioral treatments emphasize management of the abstinence violation effect that is thought to result from lapses (Brown, 2003
), even though data supporting the existence of the abstinence violation effect are not particularly strong (Shiffman, Kassel, Gwaltney, & McChargue, 2005
). The results of this study suggest that cognitive-behavioral treatment efforts could, instead, focus on helping smokers prepare for and manage episodic increases in craving that follow lapses. For example, cognitive-behavioral craving management strategies such as relaxation or guided imagery, or cognitive restructuring to manage cue provoked cravings after smokers quit (see Brown, 2003
) could be included in advice to smokers on how to manage increases in craving that follow a lapse. Medications like the nicotine patch are ineffective at blunting episodic surges of craving that result from exposure to smoking cues (Tiffany et al., 2000
), but faster acting nicotine replacement therapies such as the nicotine gum (Shiffman et al., 2003
) are effective at reducing episodic cravings. As such, nicotine gum could potentially be used immediately after a lapse to manage the episodic surge in craving that follows a lapse, that is, to “rescue” the smoker from the negative consequences of a lapse. Of course, these suggestions would need to be evaluated in controlled clinical trials to ensure safety and efficacy.
The study results are neither fully consistent with negative reinforcement models (Baker et al., 2004
) nor are they fully consistent with nicotine reinstatement models (Epstein et al., 2006
). The initial craving relief experienced by participants in the lapse condition is predicted by negative reinforcement models (see Juliano et al., 2006
). However, the subsequent increases in craving participants experienced between the programmed lapse and relapse, and the finding that this increase was related to subsequent relapse, are more consistent with reinstatement models than with negative reinforcement models (see Shiffman et al., 1996b
). Though not consistent with either theory individually, the findings are broadly consistent with the nicotine regulation model of smoking (reviewed in Benowitz et al., 2008
; see also Chandra, Scharf & Shiffman, in press
; Koob & Le Moal, 1997
) which incorporates elements of both negative reinforcement models (Baker et al., 2004
) and nicotine reinstatement models (Epstein et al., 2006
). According to the nicotine regulation model, smoking will alleviate craving related to nicotine deprivation (i.e., lapse), but only for a short time. Once nicotine has been metabolized and blood levels begin to drop, craving will re-emerge motivating the person to smoke again (i.e., relapse). These rises and falls in levels of nicotine and corresponding changes in craving are hypothesized to maintain long-term patterns of smoking. Additional research is needed to further refine the conceptual explanations that best account for the role that craving plays in explaining the link between smoking lapse and relapse.
There are limitations to this study. First, the generalizability of the study is limited given that the sample was composed of reactively recruited, healthy, and heavier smokers. The results may not apply to lighter smokers and/or to those with more significant health problems. The extent to which these results generalize to smokers quitting on their own in the field and/or with medications or more intensive cognitive-behavioral treatments is also not known. Second, there are several processes likely involved in lapsing and relapsing (see Marlatt & Donovan, 2005
) and this paper only examined craving. Third, we inferred the motivational effect of increased craving but did not assess the affective qualities of craving. Thus, we cannot draw conclusions about the relative positive or negative valence of participants’ experience of craving following the lapse (see Baker et al., 1986; Ferguson et al., 2006). Fourth, the lapse was experimentally-induced; although this represents a strength from a causal inference standpoint, whether the results generalize to an actual (non-programmed) lapse is not known. Finally, although we observed significant levels of relapse, we only followed participants for 14 days after the experimentally manipulated lapse. In general, a majority of relapses occur within a two week window of quitting (Shiffman et al., 1996a
). Nonetheless, a longer follow-up period would have provided a richer source of data.
These limitations notwithstanding, this study fills an important gap in the smoking literature by illuminating the relationship between lapse and relapse and specifying a new, mediating role for craving in the relapse process. The study is distinguished by its use of an experimental design to examine these questions in a way that enhanced the clinical utility and applicability of the model and findings. As such, these results have implications for modifying the treatment protocols for existing cognitive-behavioral and pharmacological treatments designed to help smokers prevent lapses from becoming relapses.