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Relapse and Craving
There is evidence that approximately 90 percent of alcoholics are likely to experience at least one relapse over the 4-year
period following treatment. Despite some promising leads, no controlled studies definitively have shown any single or combined
intervention that prevents relapse in a fairly predictable manner. Thus, relapse as a central issue of alcoholism treatment
warrants further study. Similar relapse rates for alcohol, nicotine, and heroin addiction suggest that the relapse mechanism
for many addictive disorders may share common biochemical, behavioral, or cognitive components. Thus, integrating relapse
data for different addictive disorders may provide new perspectives for relapse prevention.
Impaired control has been suggested as a determinant for relapse, yet is defined differently among investigators. Keller
suggested that impaired control has two meanings: the unpredictability of an alcoholic's choice to refrain from the first
drink and the inability to stop drinking once started. Other investigators limit the use of "impaired control" to
the inability to stop drinking once started. They suggest that one drink does not lead inevitably to uncontrolled drinking.
Research has shown that severity of dependence affects the ability to stop drinking after the first drink.
Several relapse theories utilize the concept of craving. Use of the term "craving" in a variety of contexts,
however, has led to confusion about its definition. Some behavioral researchers argue that the idea of craving is circular,
hence meaningless, since in their view, craving can only be recognized retrospectively by the fact that the subject drank.
They de-emphasize physiological urges and stress the relationship between the behavior of drinking and environmental stimuli
that prompt the behavior. On the other hand, Ludwig and Stark find no problem with the term "craving": craving is
recognized simply by asking whether a subject who has not yet drunk alcohol feels a need for it, much as one can inquire about
another person's hunger before he or she eats. Ludwig and associates suggested that alcoholics experience classical conditioning
(Pavlovian), by pairing external (e.g., familiar bar) and internal (e.g., negative mood states) stimuli to the reinforcing
effects of alcohol. This theory suggests that craving for alcohol is an appetitive urge, similar to hunger, that varies in
intensity and is characterized by withdrawal-like symptoms. The symptoms are elicited by internal and external cues that evoke
memory of the euphoric effects of alcohol and of the discomfort of withdrawal.
Physiological responses to alcohol cues have been described. For example, research has shown that exposure to alcohol,
without consumption, can stimulate an increased salivary response in alcoholics. Similarly, skin conductance levels and self-reported
desire for alcohol were correlated for alcoholic subjects in response to alcohol cues; the relationship was strongest for
those most severely dependent. Alcoholics demonstrated significantly greater and more rapid insulin and glucose responses
than nonalcoholics following the consumption of a placebo beer.
Several relapse prevention models incorporate the concept of self-efficacy, which states that an individual's expectations
about his or her ability to cope in a situation will affect the outcome. According to Marlatt and colleagues, the transition
from the initial drink following abstinence (lapse) to excessive drinking (relapse) is influenced by an individual's perception
of and reaction to the first drink. These investigators formulated a cognitive-behavioral analysis of relapse, positing that
relapse is influenced by the interaction of conditioned high-risk environmental situations, skills to cope with the high-risk
situations, level of perceived personal control (self-efficacy), and the anticipated positive effects of alcohol. An analysis
of 48 episodes revealed that most relapses were associated with three high-risk situations:
frustration and anger
social pressure
interpersonal temptation
Cooney and associates supported this model by demonstrating that, among alcoholics, exposure to alcohol cues was followed
by diminished confidence in the ability to resist drinking.
Marlatt and Gordon argue that an alcoholic must assume an active role in changing drinking behavior. Marlatt advises the
individual to achieve three basic goals: modify lifestyle to enhance the ability to cope with stress and high-risk situations
(increase self-efficacy); identify and respond appropriately to internal and external cues that serve as relapse warning signals;
and implement self-control strategies to reduce the risk of relapse in any situation.
Rankin and colleagues tested the effectiveness of cue exposure in extinguishing craving in alcoholics. The investigators
gave severely dependent alcoholic volunteers a priming dose of alcohol, which had been shown to evoke craving. Volunteers
were urged to refuse further alcohol; their craving for more alcohol diminished with each session. After six sessions, the
priming effect almost completely disappeared. Volunteers who participated in imaginal cue exposure did not have the same outcome.
This treatment was performed in a controlled, inpatient setting; the long-term effectiveness of cue exposure for diminishing
craving after discharge remains to be demonstrated.
Chaney and associates investigated the effectiveness of skills-training intervention to help alcoholics cope with relapse
risk. The alcoholics learned problem-solving skills and rehearsed alternative behaviors for specific high-risk situations.
The investigators suggested that skills training may be a useful component of a multi-modal behavioral approach to prevent
relapse.
A relapse prevention model for alcoholics emphasizes a strategy that helps each individual develop a profile of past drinking
behavior and current expectations about high-risk situations. The therapy promotes use of coping strategies and behavioral
change by engaging the patient in performance-based homework assignments related to high-risk situations. Preliminary outcome
data revealed a decrease in the number of drinks consumed per day as well as in drinking days per week. Forty-seven percent
of the clients reported total abstinence over the 3-month follow-up period, and 29 percent reported total abstinence over
the entire 6-month follow-up period.
Disulfiram (Antabuse) is used as an adjunct to enhance the probability of long-term sobriety. Although patient compliance
is problematic, disulfiram therapy has successfully decreased frequency of drinking in alcoholics who could not remain abstinent.
A study of supervised disulfiram administration reported significant periods of sobriety of up to 12 months in 60 percent
of patients treated.
Preliminary neurochemical studies have revealed that decreased levels of brain serotonin may influence appetite for alcohol.
Alcohol-preferring rats have lower levels of serotonin in various regions of the brain. In addition, drugs that increase brain
serotonin activity reduce alcohol consumption in rodents.
Four studies have evaluated the effect of serotonin blockers - zimelidine, citalopram, and fluoxetine on alcohol consumption
in humans, each using a double-blind, placebo-controlled design. These agents produced a decrease in alcohol intake and, in
some cases, a significant increase in the number of abstinent days. These effects, however, were found among small samples
and were short lived. Controlled trials in larger dependent populations are needed before serotonin blockers can provide hope
as a possible adjunct for relapse prevention.
In both pharmacological and behavioral prevention strategies, it is important to consider severity of alcohol dependence
as a critical factor.
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