Summary/Abstract

Research on the effectiveness of Alcoholics Anonymous (AA) is controversial and subject to widely divergent interpretations. The goal of this article is to provide a focused review of the literature on AA effectiveness that will allow readers to judge the evidence effectiveness of AA for themselves.

Content

ABSTRACT. Research on the effectiveness of Alcoholics Anonymous (AA) is controversial and subject to widely divergent interpretations. The goal of this article is to provide a focused review of the literature on AA effectiveness that will allow readers to judge the evidence effectiveness of AA for themselves. The review organizes the research on AA effectiveness according to six criterion required for establishing causation: (1) magnitude of effect; (2) dose response effect; (3) consistent effect; (4) temporally accurate effects; (5) specific effects; (6) plausibility. The evidence for criteria 1- 4 and 6 is strong: rates of abstinence are about twice as high among those who attend AA (criteria 1, magnitude); higher levels of attendance are related to higher rates of abstinence (criteria 2, dose-response); these relationships are found for different samples and follow-up periods (criteria 3, consistency); prior AA attendance is predictive of subsequent abstinence (criteria 4, temporal); and mechanisms of action predicted by theories of behavior change are present in AA (criteria 6, plausibility). However, rigorous experimental evidence establishing the specificity of an effect for AA or Twelve Step Facilitation/TSF (criteria 5) is mixed, with 2 trials finding a positive effect for AA, 1 trial finding a negative effect for AA, and 1 trial finding a null effect. Studies addressing specificity using statistical approaches have had two contradictory findings, and two that reported significant effects for AA after adjusting for potential confounders such as motivation to change.

INTRODUCTION

Research on the effectiveness of Alcoholics Anonymous (AA) is controversial and subject to widely divergent interpretations. For example, the Cochrane Group published a review of the AA literature that considered outcome studies of AA and of 12-step facilitation (TSF), a form of specialty treatment that introduces clients to the 12-step philosophy and support system. Their review recommended that people considering at­tending AA or a TSF treatment program should be made aware that there is a lack of experi­mental evidence about the effectiveness of such programs.¹ This is despite optimal outcomes for TSF at 1 and 3 years for outpatients in the Project MATCH trial.^2,3 At the other end of the spec­trum, 12-step scholar Rudy Moos has recom­mended that referral agencies should consider referring people to AA first rather than to treat­ment first. This is based on his own observational studies, which have found that longer duration of AA attendance is associated with less drinking at 8 and 16 years,⁴and that those who attend AA before attending treatment tend to attend AA longer than those who attend treatment first.⁵ The goal of this article is to provide a focused review of the literature on AA effectiveness that will allow readers to judge the evidence for AA effectiveness themselves.

Prior efforts to summarize the findings on AA effectiveness have included literature reviews^6,7 and meta analyses.⁸⁻¹⁰ The most recent meta-analysis¹⁰ concluded that attending AA led to worse outcomes than no treatment at all. An ear­lier meta-analysis focusing on moderating ef­fects found that the evidence for AA effective­ness was stronger in outpatient samples, and that poorer quality studies (based on volunteers, self-selection rather than random assignment, and no corroboration of self-report) somewhat inflated the case for AA effectiveness.⁹ A review sum­marizing the state of the literature 7 years later⁷ argued that there was a consistent, rigorous body of evidence supporting AA effectiveness. Again, there seems to be something for everybody and the literature seems to be widely subject to in­terpretation. This may stem from the criterion being used to judge effectiveness.

At the heart of the debate is the quality of the evidence. AA critics have argued that AA is a cult that relies on God as the mechanism of action,¹¹ and that rigorous experimental stud­ies are necessary to convince them of AA’s ef­fectiveness. Their concern is well-founded. As will be evident from this review, experimental studies represent the weakest of the available evidence. However, the review also will high­light other categories of evidence that are over­whelmingly convincing with respect to AA ef­fectiveness, including the consistency with es­tablished mechanisms of behavior change. This review will organize the research on AA effec­tiveness according to 6 formal criterion for estab­lishing causation,¹² which should help readers to integrate the sometimes conflicting conclu­sions discussed above. These criterion were first introduced to assist policymakers in evaluating the totality of the evidence of a causal effect for smoking on lung cancer in the absence of ex­perimental data (as randomizing individuals to smoker and non-smoker conditions was not an option).^13,14 The criterion offer a framework for judging the “totality” of the evidence,¹²implicitly acknowledging that the evidence may not be strong for all criteria, and leaving the final de­cision to the individual evaluator. These are the criterion:

1. The relationship between an exposure (here, exposure to AA) and the outcome (here, ab­stinence because AA does not recommend any drinking for alcoholics) must be strong. According to this criteria, weak relationships between AA and abstinence would not be as convincing of causality as strong ones nor would they be as clinically relevant.
2. There should be a dose–response relation­ship, such that more involvement in AA re­lates to higher levels of abstinence. Building on the first criterion, the size of the dose– response effect also is important.
3. The consistency of the association matters. If some studies find a strong relationship be­tween the number of AA meetings attended and the rate of abstinence but many do not, this would call into question whether the dose–response relationship should be trusted, as evidence goes.
4. The timing of the purported influence must be correct. This means that the measurement of AA exposure must be prior to the period of abstinence that is being studied; otherwise, it could mean that abstinent people tend to go to AA rather than AA causing people to be abstinent. Concurrent relationships do not count here; thus, according to this criterion, AA attendance for the past month cannot be considered as causal evidence for being ab­stinent during the past month.
5. The specificity of the association must be demonstrated. One must be able to rule out other explanations than AA exposure for hav­ing led to abstinence. This addresses the con­cern that those who attend AA are a part of a select sample who would be sober without ever going to AA. For example, if those who attend AA are highly motivated to do some­thing about their drinking, it could be that this motivation is the cause of their abstinence and it would be unfair to credit AA for their suc­cessful outcome. Evidence of specificity ide­ally requires experimental manipulation of exposure to AA. For example, individuals in a study might be randomized to attend AA or to attend psychotherapy; they do not select their treatment. Because of randomization, motivated people would end up being ran­domized both to psychotherapy and to AA, so it would not be the case that the “deck was stacked” in favor of AA. If those randomized to attend AA were more likely than those ran­domized to psychotherapy to be abstinent 2 years later, this would demonstrate an effect specific to AA that could not be due to a se­lection bias in which only motivated people attend AA. Randomization would also equal­ize other pre-existing conditions (known and unknown) that might confound AA’s effect.
6. Coherence with existing knowledge is needed to establish causation. In drug trials, this is addressed by considering biological plausi­bility. For example, the drug neurontin stops seizures because it reduces the electrical ac­tivity in the brain. Here, in studying AA ef­fectiveness, biological plausibility is of no help. The notion of theoretical plausibility is suggested as a way of addressing coher­ence with existing knowledge; that is, are the mechanisms of action that explain be­havior change present in AA? Several the­ories and different aspects of AA exposure will be considered in addressing this final criterion.

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