What is addiction relapse?

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Since the 1980s, relapse has been conceptualized as a dynamic process through which an abstinent person gives in to the urge to resume substance use (such as drinking, smoking, or self-administering drugs). Relapse is distinguished from slips or lapses that are one-time (slip) or brief occurrences (lapses) during the recovery process. Relapse is not generally considered a failure of treatment but rather a common consequence of an attempt to change any chronic behavior, not just addictive behaviors.
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What Is Relapse?

There has been a major shift in how relapse is conceptualized by addiction researchers. Before the 1980s, the term relapse was used to signify any return to substance use following a period of abstinence, much as a disease state recurs following a period of remission. However, largely as a result of work by G. Alan Marlatt and colleagues, relapse is now viewed as a dynamic process through which a person gives in to the urge to resume drinking, smoking, or taking drugs following a period of sobriety or abstinence. An important feature of the dynamic process approach is that relapse is distinguished from slips or lapses that are one-time (slip) or brief occurrences (lapses) of substance use during the recovery process.

Despite wide variations in relapse criteria (from a single drink, cigarette, or drug use episode to a return to pretreatment substance use levels), studies have shown that recovery from substance abuse is typically characterized by repeated episodes of relapse, with the first episode most often occurring within one year of treatment. For alcohol-dependent persons who have undergone treatment, relapse is the most common outcome, with less than 25 percent remaining abstinent after one year. Approximately one-half of recovering cocaine addicts are reported to relapse within one year of detoxification. However, relapse rates for addictive behaviors are not significantly different from those of other chronic conditions such as asthma, diabetes, and hypertension.

Risk Factors

The use of electronic devices, such as ecological momentary assessment (EMA), for real-time monitoring has provided valuable information about external events, thoughts, and mood states that precede a slip, lapse, or relapse. Among the most common triggers reported for abstinence cessation are exposure to substance-related cues, negative mood states or stress, social interactions, and substance use even in small quantities.

In a 1996 analysis, negative mood states and interpersonal conflict were identified as triggers for more than 50 percent of all relapse episodes involving alcohol and smoking and for more than 40 percent for those involving heroin. However, these triggers do not inevitably precipitate a relapse. Researchers are paying more attention to individual differences in relapse risk and in the potential for predisposing factors, such as severity of dependence, genetics, and beliefs about drug effects and coping skills to moderate or interact with precipitating factors that increase the risk for relapse.

In studies of alcohol dependency, Marlatt and his colleagues described an emotional reaction to a lapse that can influence progression to a relapse. Persons who blame themselves for lapsing subsequently experience guilt and negative emotions and are then more likely to continue drinking than persons who perceive the lapse as an occasion to improve their coping skills. Studies using retrospective reports of the lapse suggest that the magnitude of this reaction is related to relapse; however, EMA studies have not observed this relationship.

Brain imaging studies have shown that specific regions of the corticostriatal limbic circuitry involved in stress-induced and drug-cue-induced craving states are associated with drug relapse outcomes. Moreover, some persons have less effective orbitofrontal cortex circuitry, making it more challenging to manage their urge to seek drugs and more difficult to make good decisions. These studies are important for developing new medications for use in relapse prevention.

Genetic differences have been shown to influence susceptibility to relapse through their interaction with medications. In a 2003 study using naltrexone to reduce craving in alcohol-dependent patients, the relapse rate was significantly higher (47.9 percent) in patients with the Asn40 variant in an opioid receptor gene compared with patients with the Asp40 variant (26.1 percent).

Theories of Relapse

A number of models have been constructed to explain the phenomenon of relapse. One of the most influential models is Marlatt’s cognitive-behavioral approach to relapse prevention. This model bases relapse risk on self-efficacy, outcome expectancies, attributions of causality, and decision-making processes. An abstinent person who encounters a high-risk situation (trigger) and engages in a successful coping response will heighten self-efficacy (confidence in ability to remain abstinent).

In contrast, an abstinent person with poor coping skills will be unable to manage the craving elicited by the trigger, leading to a reduction in self-efficacy, an increase in the expectation of a positive outcome, and an increased risk of lapsing. Lapses that are attributed to personal failure generate guilt and negative emotions and a further reduction in self-efficacy, thereby heightening the risk of relapse.

Conditioning models also have contributed prominently to the understanding of relapse. Cues associated with substance use are thought to be Pavlovian conditioned stimuli that come to elicit various conditioned responses, including drug craving. Human cue-reactivity studies have confirmed this account of craving. Several studies also have tested the prediction that exposure to such cues in the absence of substance use (cue exposure therapy, or CET) should be an effective extinction procedure for eliminating craving and guarding against relapse. Results have been mixed.

Researchers Peter Monti, Damaris Rohsenow, and colleagues showed that cue exposure combined with coping-skills training may result in increased use of skills, increases in days abstinent, and decreases in drinking. Other studies of alcohol dependency, however, have found little impact of CET in eliminating craving and reducing relapse.

Laboratory studies of extinction in animals may provide some insight in clinical studies about the apparent fragility of CET for relapse prevention. The phenomena of reinstatement, renewal, retraining, and spontaneous recovery collectively illustrate that extinction does not remove original learning. In a 2002 review paper, researcher Mark Bouton discussed how each of these phenomena may underlie relapse. For example, his research on renewal has shown that extinction is context specific, such that when an extinguished CS is presented in its original conditioning context, responses to the CS are renewed.

Future Directions

Addiction researchers are in general agreement that a multivariate, biopsychosocial approach to relapse is essential. In a 2006 commentary on relapse in the addictive behaviors, researchers Stephen Maisto and Gerard Connors recommended that more attention be paid to the operational definition of relapse, theory development and its systematic testing, modeling of the relapse process, and the role of moderating variables on relapse outcome.


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Conklin, C. A., and S. T. Tiffany. “Applying Extinction Research and Theory to Cue-Exposure Addiction Treatments.” Addiction 97 (2002): 155–67. Print.

Daley, Dennis C., and Antoine Douaihy. Relapse Prevention Counseling: Clinical Strategies to Guide Addiction Recovery and Reduce Relapse. Eau Claire: PESI, 2015. Print.

Granfield, Robert, and Craig Reinarman. Expanding Addiction: Critical Essays. New York: Routledge, 2015. Print.

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Pool, Eva, Tobias Brosch, Sylvain Delplanque, and David Sander. "Stress Increases Cue-Triggered 'Wanting' for Sweet Reward in Humans." Journal of Experimental Psychology 41.2 (2015): 128–36. Print.

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Sinha, Rajita, and Chiang-Shan R. Li. “Imaging Stress- and Cue-Induced Drug and Alcohol Craving: Association with Relapse and Clinical Implications.” Drug and Alcohol Review 26 (2007): 25–31. Print.

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