Experimental and Clinical Psychopharmacology1996, Vol. 4, No. 1,55-60

Copyright 1996 by the American Psychological Association, Inc.1064-1297/96/S3.00

Models of Relapse and Relapse Prevention: A Commentary

G. Alan MarlattUniversity of Washington

The author provides a commentary on a series of articles published on relapse to substance abuse.The following points summarize this commentary: animal and human studies of drug primingeffects are limited as an analogue for relapse because they fail to address drug self-administration;relapse is exacerbated following events (contextual initiating conditions) that indicate reducedaccess to alternative reinforcers; relapse has multiple determinants including internal cognitiveprocesses that may differentiate between urges and substance use; relapse prevention (RP) can bematched with stages of change in treatment; and RP may be associated with emergent effects overtime in substance abuse treatment outcome studies.

As the discussant for the 1993 Symposium on Relapse toSubstance Abuse conducted at the 101st Annual Conventionof the American Psychological Association (August, 1993,Toronto, Ontario, Canada), I was asked to provide a briefcommentary on the published articles in this series. The set ofarticles as a whole covers a good deal of territory in that itprovides linkages between basic and clinical research in thetreatment of substance abuse and is based on research withboth human and animal subjects. Both experimental research-ers and scientist-practitioners will find relevant material andprovocative issues in reading through this material. Also, avariety of theoretical perspectives is represented among theauthors, ranging from basic conditioning and operant modelsto cognitive-behavioral approaches rooted in social learningtheory. Treatment issues are addressed in terms of motivationand treatment matching and relapse prevention. In summary,there is something here for everyone even though not everyonewill find the coverage comprehensive in scope and definitive interms of conclusions.

Each article raises a number of questions, many of which canbe addressed in future research efforts. I share some of my ownreactions and questions as they occurred to me listening to(and later reading) the symposium articles. In my role asdiscussant, I would like to make a few brief comments on eachof the articles. Before doing so, let me clarify my ownbackground and orientation in the substance abuse field sothat my biases will be more transparent in the followingdiscussion. Although I have done basic research studies ondeterminants of alcohol consumption in humans, most of mycurrent interests are in the areas of prevention and treatmentof addictive behaviors. As a clinical psychologist serving as aprofessor in an academic setting, I define myself as a scientist-practitioner working as principal investigator on NationalInstitutes of Health-funded research and training grants. Inaddition to conducting research studies on the effectiveness ofprevention and treatment programs for alcohol and substanceabuse, I have seen clients with these problems in my limitedprivate practice. My theoretical orientation is based on cogni-

Correspondence concerning this article should be addressed to G.Alan Marlatt, Department of Psychology, NI-25, Box 35125, Universityof Washington, Seattle, Washington 98195-1525. Electronic mail maybe sent via Internet to marlatt@u.washington.edu.

live and social learning theory and includes basic conditioningand behavioral models. In the treatment arena, my work hasmost closely been identified with relapse prevention, a cogni-tive-behavioral approach that is designed to prevent andmanage relapse problems in substance-abuse treatment (e.g.,Marlatt & Barrett, 1994). More recently, I have been applyingthe harm reduction model, a public-health approach to reduc-ing the harm and risks associated with alcohol and substanceuse among active users (Marlatt & Tapert, 1993).

The first two articles in the symposium series addressed thetopic of priming effects and animal models of relapse (M. E.Carroll & Comer, 1996; de Wit, 1996). Animal models havecontributed significantly to researchers' understanding of ad-dictive behaviors and how they develop. The range of suchcontributions is impressive: strengthening researchers' under-standing of the basic mechanisms of drug action and reinforce-ment, genetic models of drug preference, teratogenic effects ofalcohol and other drugs (e.g., animal studies of the fetalalcohol syndrome), self-administration of drugs and schedulesof reinforcement, animal studies of opiate antagonists andother pharmacotherapeutic agents that are used in the treat-ment of addiction problems in humans—the list goes on andon. In both articles the authors presented an animal model ofrelapse. Can an animal model provide a useful analogue of theprocess of relapse in humans who are motivated to abstaineither under their own efforts or in conjunction with atreatment program? Here I have a mixed response.

In the priming effect model of relapse, animals are firsttrained to self-administer a reinforcing drug and are then puton an extinction schedule. Stimuli are then presented (such aspriming dose of the drug) and the animal is observed todetermine if behavior previously rewarded by the drug isreinstated. Research with rats showed that priming injectionsof the previously self-administered drug reinstate extinguishedresponding whereas other drugs do not.

M. E. Carroll and Comer (1996) noted that both externaland internal (interoceptive) cues can trigger reinstatement ofdrug-seeking behavior: "Often, external stimuli lead to druguse and then the internal stimuli associated with drug usesustain relapse" (p. 11). It is interesting that one high-risksituation for drug relapse in animals is food deprivation:"Under even slightly restricted feeding conditions drug

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intake dramatically increases, and it is markedly suppressedwhen unlimited access to food is offered" (M. E. Carroll &Comer, 1996, p. 15). It is clear that hunger potentiates drugrelapse in animals, but is it hunger (craving) for drugs or forfood that drives the behavior? Although the underlying mech-anism for drug reinstatement behavior has yet to be confirmed,the authors emphasize one plausible explanation—appetitive-incentive motivational theory—which states that drugs thatproduce a priming effect have strong motivational-appetitiveeffects, acting much like appetizers that stimulate increasedhunger and augment subsequent eating behavior.

This research has a number of important implications forsubstance abuse treatment. One is that cue exposure isrecommended as part of an abstinence-based treatment pro-gram. According to M. E. Carroll and Comer (1996), "Extin-guishing responding to external or internal stimuli (cue expo-sure) along with the extinction of the primary reinforcingeffects of the drug (abstinence) has been suggested as aneffective strategy for reducing relapse in humans" (p. 12).However, according to a comprehensive review of the cueexposure treatment literature (Drummond, Tiffany, Glautier,& Remington, 1995), the passive extinction paradigm has notbeen shown effective in reducing relapse rates in humans indrug treatment. Teaching skills to actively cope with urges andcraving triggered by exposure to drug-associated stimuli maybe a more effective strategy (Marlatt, 1990).

Although I agree that these animal studies provide a goodmodel of drug reinstatement behavior (after a period ofextinction), I find one major problem in accepting this as amodel of drug relapse in humans. In the animal studies, thepriming dose of the drug is administered by the experimenter.In humans, the priming dose is self-administered. Humanshave a choice and they select a drug. Animals, if given a choice,seem to prefer food. What do the animal studies tell us aboutthe choice behavior of previously drug-administered animalswhen they are presented with food and drug alternatives?Some would say that only people who decide to change theirdrug use (either to abstain or to moderate use) and arecommitted to their goal are candidates for relapse. If one doesnot make an effort to change, how can one relapse? Confirmedsmokers and alcoholics do not relapse, they just continue touse. In this narrower sense, clinical studies of relapse arerestricted to individuals who are committed and motivated toabstain (on their own or via treatment) and yet experiencelapses or setbacks. To what extent is the first lapse (after aperiod of abstinence) to be considered a voluntary or involun-tary behavior? Must every lapse serve as a primer for aninevitable relapse? In the animal model, there is little choiceinvolved.

The discussion of priming effects is expanded to includehuman studies in the article by de Wit (1996). Again, it isquestionable as to whether these studies represent an ecologi-cally valid model of human relapse to drug use after a period ofvoluntary abstinence. In each of the human priming effectstudies reviewed in the article, participants were first adminis-tered a preload of the drug (alcohol, heroin, or nicotine,depending on the study) before measures of craving or drugconsumption were obtained. In no study were participantsgiven the choice between initial self-administration of the drug

and alternative behavioral responses. Nor is it clear thatparticipants were motivated to abstain from drug use whenthey participated in the research (in one study, regularsmokers were paid to abstain for 4 days before receiving thenicotine preload).

De Wit (1996) then reviewed literature showing that prim-ing effects have also been found with a variety of nondrugreinforcers, including rewarding stimuli such as food andaversive stimuli (e.g., shock). Most of the data presentedseemed to fit within the framework of incentive motivationaltheory, one of several theories that could explain observedpriming effects. According to this theory, "Incentive motiva-tional theory... holds that all incentive, or motivationallysignificant, stimuli (unconditioned as well as conditioned) havethe ability to induce motivation for that stimulus. This increasein motivation is manifested by an increase in the likelihood ofactivities related to that stimulus" (de Wit, 1996, p. 9). Thismodel appears to fit well when applied to cases in which anexternally administered reward (food or drug preload) is foundto enhance craving or subsequent consumption. The model islimited, however, as an analogue of the human relapse processin which an individual who has made a prior commitment toabstinence later self-administers the forbidden substance. Thislimitation arises because cognitive processes such as outcomeexpectancies (e.g., positive expectancies for drug effects),self-efficacy (subjective confidence that one will be able toexecute an alternative coping response to drug-taking in atemptation situation), and attributions people make for whythey resumed drug use may all have significant impact onwhether a lapse occurs and whether the lapse will be followedby further relapse (Marlatt & Gordon, 1985). Attributing alapse to internal states beyond the individual's control (e.g., "Iwent back to smoking because I lacked the willpower to controlmy nicotine addiction") is more likely to lead to further relapsethan an external attribution that focuses on behavior that canbe changed (e.g., "I smoked a cigarette when I went out for adrink with an old smoking buddy—next time I will have to bemore careful"). In both cases, the first cigarette acts as aprimer in terms of pharmacological effects and should equallyenhance subsequent smoking behavior. Research on the absti-nence violation effect (AVE) shows that cognitive attributionsalso play a significant role in determining whether the firstdrug use (lapse) after a period of voluntary abstinence triggersfurther relapse (Curry, Marlatt, & Gordon, 1987). Becausemost (but not all) lapses are likely to trigger subsequentrelapse, the combined impact of both drug priming effects anda pessimistic attributional style may exacerbate the relapseoutcome.

The third article (Vuchinich & Tucker, 1996) provided afurther elaboration of factors that may differentiate a discretelapse from a chronic relapse. In a prospective treatmentoutcome study, alcoholic men were followed for a 6-monthperiod following inpatient treatment. Before discharge, allpatients were asked about the extent to which their drinkinghad disrupted their functioning in six life-health areas (inti-mate relations, family relations, social relations, vocationalfunctioning, financial status, and physical health). Drawingfrom behavioral choice theory, the authors defined the poten-tial for relapse as a choice between a smaller earlier reinforce-

SPECIAL SECTION: RELAPSE AND PREVENTION 57

ment (e.g., taking a drink) and a larger later reinforcer (e.g.,reward from significant others for maintaining abstinence).The authors hypothesized that, following treatment, "Suchevents would lower the value of life-health rewards so thatalcohol would be preferred, even if alcohol was not immedi-ately available at the time of the event. This event-drinkingassociation should be strongest when the events are relevant tolife-health areas that previously had been disrupted by drink-ing" (Vuchinich & Tucker, 1996, p. 21). Results supported thehypotheses. The more the patients' pretreatment drinking hadimpaired their intimate relations, family relations, or voca-tional functioning, the more likely negative events occurring inthese life-health areas following treatment were found to beassociated with relapse. It was also found that relapse episodeswere more severe when preceded by a negative event in one ofthese life-health areas compared with drinking that was notpreceded by such events.

I recently worked with a client in therapy whose relapseepisodes matched the pattern described above. The client wasa married woman who experienced problems with both alcoholand depression. In her attempt to stop drinking, she experi-enced several setbacks. On one occasion, she accepted a drink(one glass of wine) that was offered to her at a women's literarydiscussion group; this episode was only a lapse as she refrainedfrom any additional drinking. On another occasion, she drankto intoxication after speaking on the phone to her husbandwho was out of town on a business trip. During the conversa-tion, her husband criticized her because he mistakenly thoughtshe had been drinking during his absence. After the call, shereacted by drinking almost a whole bottle of sherry and wasstill intoxicated when her husband returned from his trip.These clinical findings are in line with behavioral choicetheory. In the first example, the lapse did not escalate furtherrelapse because the event (taking a drink at a social gathering)did not signal decreased access to subsequent rewards. In thesecond case, the drinking was more severe, presumably be-cause the precipitating event (being accused by her husband ofdrinking even when she had not) signaled to her that she wasunlikely to gain any future rewards from her husband on hisreturn. Both environmental antecedents to drinking and cogni-tive processes that occur subsequent to drinking (e.g., theabstinence violation effect) may be involved as determinants oflapse and relapse episodes. I agree with the conclusion drawnby Vuchinich and Tucker: "Most likely the lapse-relapsedistinction depends both on the contextual initiating condi-tions and on internal processes activated after drinking be-gins" (p. 25).

The article by Brandon, Wetter, and Baker (1996) providedadditional information on cognitive and internal processes thatare hypothesized to influence smoking relapse. In this con-trolled laboratory study, college student smokers were as-signed to either a withdrawal condition (24 hr of abstinence) ora continued smoking group (no prior abstinence). All partici-pants also received a mood manipulation by varying perfor-mance feedback (positive vs. negative) on the block design taskof the Wechsler Adult Intelligence Scale. Measures wereobtained to assess outcome expectancies for smoking, urges orcraving to smoke, and smoking topography (latency to first puffand total number of puffs in an ad lib smoking task). Results

showed a significant correlation between positive outcomeexpectancies and urge to smoke for all participants. Urges tosmoke were increased significantly by the negative affectmanipulation, but only for participants in the continuedsmoking group. Among continuing smokers, smoking consump-tion was influenced by negative affect only for those smokerswho held low expectancies for negative reinforcement fromsmoking. Overall, Brandon et al. found almost no covariancebetween urges and smoking motivation or smoking consump-tion: Urge was best predicted by negative affect, whereasactual smoking was best predicted by outcome expectancies.As Brandon et al. concluded, "Urge and state affect self-reports may tend to covary, and expectancy measures and drugconsumption-intake may tend to covary, but there may be littlerelation between the two pairs of measures" (p. 35).

Whether this study represents a valid analogue of smokingcessation and relapse remains open to question. As acknowl-edged by Brandon et al. (1996) "participants in the withdraw-ing condition were not actually attempting to quit, nor didmost express even a desire to quit" (p. 35). Despite thisimportant limitation, the results provided support for the roleof internal factors such as the experience of negative affect andoutcome expectancies as determinants to smoke in a givensituation. The findings also provided support for models ofrelapse that focus on proximal mood and cognitive expectan-cies as determinants of substance use.

Part of the difficulty in studies such as this is developingdefinitions and measures of internal states that can be repli-cated by other investigators. In the Brandon et al. (1996) study,positive outcome expectancies were found to significantlycorrelate with self-reports of smoking urges and craving. Thisfinding is consistent with social-learning models of the relapseprocess. In my cognitive-behavioral model of relapse, I definedcraving as a "subjective state that is mediated by the incentiveproperties of positive outcome expectancies. In other words,craving is a motivational state associated with a strong desirefor an expected positive outcome" (Marlatt, 1985, p. 138).Outcome expectancies, in a high-risk situation for relapse, areinfluenced both by proximal mood or affect (prior negativeaffect increases expectancies for "relief following substanceuse) and by the individual's self-efficacy for coping to remainabstinent. Further research is needed to untangle and under-stand the relation between these proximal motivational con-structs and more distal environmental events that are thoughtto be involved in the relapse process.

The final two articles addressed the topic of relapse preven-tion (RP) in the treatment of alcohol and substance abuseproblems. In the article by Annis, Schober, and Kelly (1996) ofthe Addiction Research Foundation, Toronto, Ontario,Canada, the role of structured RP counseling in an outpatienttreatment setting is described in an intriguing five-componentcounseling program matched to the five stages of changeoutlined by Prochaska and DiClemente (1984). Followingcompletion of the first three components of the program(assessment, motivational interviewing to provide assessmentfeedback, and development of an individualized treatmentplan), clients who decide to proceed sign a formal treatmentcontract to enter the structured RP program. The RP programconsists of two components: initiation and stabilization of

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change followed by the long-term maintenance stage. Annis etal. described a new procedure to assess the client's stage ofchange, the commitment to change algorithm.

Annis et al. (1996) described the program but gave nooutcome data to gauge its effectiveness. Although the programcomponents appear well-grounded in terms of motivationaland stage theory matched with treatment interventions, onewonders whether clients would actually follow the varioussteps and stages in the linear, lock-stepped manner suggestedby the model. As with any developmental stage model, there isan implicit assumption that clients will graduate from onestage to the next, as they proceed from "precontemplation" to"maintenance." In my own clinical experience, my clientsoften failed to follow this linear progression of stages—somemoved back and forth between stages (e.g., from maintenanceback to contemplation), whereas others skipped over stagesaltogether (e.g., a client who received a citation for drivingwhile intoxicated and jumps from precontemplation to actionin a single day).

Another concern is the potential barrier set up for clientsbefore they can enter the formal RP program: Only those whomake an explicit decision, formalized by the signing of atreatment contract, are allowed to proceed. This policy isdictated by the rationale that "it can be detrimental to useaction-oriented counseling procedures with clients who havenot yet reached a decision to change" (Annis et al., 1996, p.41). What happens to those clients to fail to sign the contract?How many drop out when faced with this formal admissionrequirement? For clients who are unwilling to continue intreatment, perhaps a harm-reduction program could be madeavailable as an alternative to dropping out. Harm-reductionprocedures can be used to stabilize and reduce drug-takingrisks until the client is ready to move on to the next level oftreatment (Marlatt & Tapert, 1993).

One of the most useful clinical tools developed by Annis(Annis & Davis, 1988) is the Inventory of Drinking Situations(and the parallel Inventory of Drug-Taking Situations). Theseinventories assess situational antecedents or triggers for druguse and are based on the taxonomy of high-risk situations forrelapse that Marlatt & Gordon (1980) originally developed.Clients fill out the inventory and a profile of high-risk situa-tions (see Figure 2 of Annis et al., 1996) is generated that canbe used to develop targets for coping skill training in the RPprogram. Despite the apparent limitations of our originalrelapse taxonomy (e.g., possible attributional bias based onretrospective self-reports given by individuals who had recentlyexperienced a relapse episode), recent research that uses aprospective design has replicated the initial findings of Marlattand Gordon (Hodgins, el-Guebaly, & Armstrong, 1995). Thisstudy confirmed what Marlatt and Gordon have found to bethe most frequent trigger for relapse—the experience ofnegative emotional states. In another recent article by Cunning-ham, Sobell, Sobell, Gavin, and Annis (1995), it was reportedthat negative emotional states are a primary determinant ofdrinking for both individuals in treatment for alcohol problemsand for heavy drinkers in the general population.

Annis et al. (1996) also proposed a unique approach totraining clients to cope with high-risk situations for relapse.Clients in the initial "action stage" of RP are encouraged to

use avoidance coping (e.g., avoidance of drug use settings),whereas those further along in the "maintenance stage" are"requested additionally to take steps that will proactivelyexpose them to high-risk situations . . . in a way that will fadereliance on external supports (e.g., a particular person, activ-ity, or medication) in order to promote self-attribution ofcontrol" (p. 43). Although this is an interesting hypothesis, itmay be difficult to test because most clients, as Annis et al.admitted "use a combination of action and maintenancestrategies over the course of counseling" (p. 42). It may be thetype of situation that dictates the appropriate coping responserather than the client's position in the temporal stage ofchange model.

In the final article in this series, K. M. Carroll (1996)provided a review of controlled clinical trials that have evalu-ated RP in the treatment of smokers, alcoholics, and drugusers. Across substances, RP is found to be generally effectivecompared with no-treatment controls, whereas evidence regard-ing RP's superiority relative to other active treatments is lessconsistent. K. M. Carroll concluded that RP holds particularpromise in three areas: reducing severity of relapses when theyoccur, enhancing durability of effects following cessation ofacute treatment, and matching patient to treatment particu-larly for patients at higher levels of impairment.

Although RP can be used as an intervention to initiateabstinence (and to prevent relapse), it also has been applied asa maintenance strategy designed to minimize relapse episodeswhen and if they occur during and following formal treatment.K. M. Carroll (1996) concluded the following in her review of24 studies: "Although no single study has directly contrastedthe effectiveness of relapse prevention as a maintenance versusabstinence initiation treatment, taken together the studiesreviewed here suggest the effectiveness of relapse preventionin both formats appears roughly comparable" (p. 52). In termsof abstinence initiation, the goal of RP is to identify potentialhigh-risk situations and to provide the client with effectivecoping skills to prevent relapse. The primary focus here ispreparation for coping with ongoing and future events thatmay cause problems. For those who do relapse, RP proceduresare designed to minimize the degree of setback and get theclient back on track. In this case, the primary goal is relapsemanagement that would prevent lapses from escalating intofull-blown relapse episodes or to help the client recover fromsuch episodes should they occur, or both. In this case, the goalof relapse management is consistent with a harm-reductionapproach—to reduce the harmful consequences of ongoingdrug use.

Many RP programs fail to make this distinction between thegoals of abstinence initiation and relapse management. As anexample, AVE refers to the self-defeating attributions clientsoften make after a lapse occurs (e.g., the lapse is attributed tointernal causes beyond the client's control). When should thisinformation about the AVE be presented to clients? Ifpresented only during the abstinence initiation phase, it ispossible that this information could be perceived by someclients as "permission-giving" in that it may undermine theclient's commitment to total abstinence. Conversly, if a client isin the midst of a relapse episode and is on the verge ofdropping out or giving up, helping the person cope with the

SPECIAL SECTION: RELAPSE AND PREVENTION 59

AVE and its demoralizing consequences is often the bestcourse of action. The problem with presenting RP as a fixedpackage (based on manuals administered to groups of clientsin randomized clinical trials) is that it fails to take into accountindividual differences in each client's progress. Applied on anindividual basis, however, RP techniques can be applied on atreatment-matching basis to fit the client's unique circum-stances and conditions.

K. M. Carroll (1996) noted that some RP treatment outcomestudies showed delayed emergence of effects, suggesting that"even though minimal treatments may be sufficient over shortperiods of time, sustained or continuing improvement may beassociated with the implementation of generalizable copingskills conferred through relapse prevention treatment" (p. 52).In her study comparing RP and pharmacotherapy in thetreatment of cocaine abuse, K. M. Carroll noted that onlythose clients who received RP showed significant continuingimprovement at the 1-year follow-up. These results are consis-tent with data previously reported in a study assessing theeffectiveness of RP in the treatment of alcohol dependence(Chancy, O'Leary, & Marlatt, 1978). In that study, thosepatients who received RP during inpatient treatment and whorelapsed during a 1-year follow-up showed significantly lessdrinking and shorter relapse episodes compared with patientsin the control conditions. Subsequent analyses (Marlatt, 1983)revealed that relapsed patients continued to show greaterimprovement over the course of the posttreatment year, afinding similar to the delayed emergent effect described byK. M. Carroll.

This delayed emergent effect of RP is consistent with theskills acquisition basis of this approach. As clients becomemore experienced in acquiring and performing new copingskills, their overall performance should improve over time.Acquiring self-management skills takes time, and mistakes orerrors (lapses and relapses) are common, particularly in theearly stages of recovery. Such setbacks can be viewed asopportunities for new learning rather than as indications ofpersonal failure or lack of motivation. A delayed emergenteffect is congruent with the notion that RP is based more onthe principles of prevention than on treatment itself. In RP, aswith most prevention programs, an attempt is made to teachclients basic self-management skills that can be applied tofuture risks and problems. From a public health perspective,RP can be considered a form of tertiary prevention, the goal ofwhich is to prevent relapse (and promote progress) in individu-als who have already developed an addiction problem and havemade a commitment to abstinence. Delayed emergent effectshave also been obtained in secondary prevention programs foralcohol abuse; recent work in teaching moderate drinkingskills to college student binge drinkers showed that those whoreceived the cognitive-behavioral prevention program contin-ued to improve over a 3-year follow-up period compared withno-treatment controls (Marlatt, Baer, & Larimer, 1995).

The delayed emergent effect associated with RP makes it agood candidate for clinical trials in which it is combined withactive treatment methods such as pharmacotherapy in thetreatment of addictive behaviors. With pharmacotherapeutictreatment (e.g., desipramine for cocaine dependence or naltrex-one for alcohol dependence), one would expect an initial

period of maximum benefit in terms of symptom reduction,followed by a period of gradual decay as the initial treatmenteffect wears out over time. One would expect a bettermaintenance outcome if the effects of RP continue to emergeat the same time as the treatment effects subside. One can thusavoid the mixed message that clients sometime experiencewhen they are told that their treatment involves both takingmedications (treatment relying on an external agent) andlearning new coping skills (prevention based on internalmastery of self-management skills).

Taken as a set, the articles in this symposium provide anintegrative and tantalizing overview of relapse theory andresearch in the addictions field. The study of relapse is itself anemergent area, one that is open to many perspectives andexperimental approaches spanning both animal and humanstudies. Much (perhaps most) of this work has yet to develop,both in terms of understanding the multiple (biopsychosocial)determinants of the relapse process and in developing moreeffective interventions to prevent and manage relapse in theclinical setting. In my view, the authors whose work is pre-sented in this series have made outstanding contributions byproviding fresh insights and by suggesting new directions toguide future research efforts.

References

Annis, H. M., & Davis, C. S. (1988). Cognitive Assessment ofexpectancies. In D. M. Donovan & G. A. Marlatt (Eds.), Assessmentof Addictive Behaviors (pp. 84-111). New York: Guilford Press.

Annis, H. M., Schober, R., & Kelly, E. (1996). Matching addictionoutpatient counseling to client readiness for change: The role ofstructured relapse prevention counseling. Experimental and ClinicalPsychopharmacology, 4, 37—45.

Brandon, T. H., Wetter, D. W., & Baker, T. B. (1996). Affect,expectancies, urges, and smoking: Do they conform to models ofdrug motivation and relapse? Experimental and Clinical Psychophar-macology, 4, 29-36.

Carroll, K. M. (1996). Relapse prevention as a psychological treat-ment: A review of controlled clinical trials. Experimental and ClinicalPsychopharmacology, 4, 46-54.

Carroll, M. E., & Comer, S. D. (1996). Animal models of relapse.Experimental and Clinical Psychopharmacology, 4, 11-18.

Chaney, E. F., O'Leary, M. R., & Marlatt, G. A. (1978). Skill trainingwith alcoholics. Journal of Consulting and Clinical Psychology, 46,1092-1104.

Cunningham, J. A., Sobell, M. B., Sobell, L. C., Gavin, D. R., & Annis,H. M. (1995). Heavy drinking and negative affect situations in ageneral population and a treatment sample: Alternative explana-tions. Psychology of Addictive Behaviors, 9, 123-127.

Curry, S., Marlatt, G. A., & Gordon, J. R. (1987). Abstinence violationeffect: Validation of an attributional construct with smoking cessa-tion. Journal of Consulting and Clinical Psychology, 55, 145-149.

de Wit, H. (1996). Priming effects with drugs and other reinforcers.Experimental and Clinical Psychopharmacology, 4, 5-10.

Drummond, D. C., Tiffany, S. T., Glautier, S., & Remington, R. (Eds.).(1995). Addictive behavior: Cue exposure theory and practice. NewYork: Wiley.

Hodgins, D. C., el-Guebaly, N., & Armstrong, S. (1995). Prospectiveand retrospective reports of mood stages before relapse to substanceuse. Journal of Consulting and Clinical Psychology, 63, 400-407.

Marlatt, G. A. (1983). The controlled drinking controversy: A commen-tary. American Psychologist, 38, 1097-1110.

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Marlatt, G. A. (1985). Cognitive factors in the relapse process. In G. A.Marlatt & J. R. Gordon (Eds.), Relapse prevention: Maintenancestrategies in the treatment of addictive behaviors (pp. 128-200). NewYork: Guilford Press.

Marlatt, G. A. (1990). Cue exposure and relapse prevention in thetreatment of addictive behaviors. Addictive Behaviors, 15, 395-399.

Marlatt, G. A., Baer, J. S., & Larimer, M. E. (1995). Preventing alcoholabuse in college students: A harm-reduction approach. In G. M.Boyd, J. Howard, & R. A. Zucker (Eds.), Alcohol problems amongadolescents: Current directions in prevention research (pp. 147-172).Northvale, NJ: Erlbaum.

Marlatt, G. A., & Barrett, K. (1994). Relapse prevention. In M.Galanter & H. D. Kleber (Eds.), The textbook of substance abusetreatment. New York: American Psychiatric Press.

Marlatt, G. A., & Gordon, J. R. (1980). Determinants of relapse:Implications for the maintenance of behavior change. In P. O.Davidson & S. M. Davidson (Eds.), Behavioral medicine: Changinghealth lifestyles (pp. 410^152). New York: Brunner/Mazel.

Marlatt, G. A., & Gordon, J. R. (1985). Relapse prevention: Mainte-nance strategies in the treatment of addictive behaviors. New York:Guilford Press.

Marlatt, G. A., & Tapert, S. F. (1993). Harm reduction: Reducing therisks of addictive behaviors. In J. S. Baer, G. A. Marlatt, & R. J.McMahon (Eds.), Addictive behaviors across the lifespan (pp. 243-273). Newbury Park, CA: Sage.

Prochaska, J. O., & DiClemente, C. C. (1984). The transtheoreticalapproach: Crossing traditional boundaries of therapy. Homewood, IL:Dow Jones/Irwin.

Vuchinich, R. E., & Tucker, J. A. (1996). Alcoholic relapse, life events,and behavioral theories of choice: A prospective analysis. Experimen-tal and Clinical Psychopharmacology, 4, \ 9-28.

Received June 30,1995Accepted June 30,1995

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