Impulsivity is an Independent Predictor of 15-Year Mortality Risk among Individuals Seeking Help for Alcohol-Related Problems

In yesterday’s blog we looked at how AA membership and the 12 step program of recovery helped reduce impulsivity in recovering alcoholics.

We mentioned also that impulsivity was present as a pathomechanism of alcoholism from vulnerability in “at risk” children from families, were there was a history of alcoholism, right the way through to recovering alcoholics in long term recovery (i.e. many years of recovery).

We cited and used excerpts from a study written by the same authors as the study we cite now (1).

This study shows and highlights how, if untreated, by recovery programs such as AA’s 12 steps, that “trait” impulsivity can lead to increased mortality in alcoholics.

This study interestingly shows there is a difference from “state-like” impulsivity in early recovery when recovering people are still distressed and “trait-like” which is after Year 1 of recovery when some of the severity of withdrawal from alcohol has long since abated and some recovery tools have been learnt.

The fact that this impulsivity continues to contribute to relapse and mortality may suggest it is a trait state in alcoholics and possibly a vulnerability to later alcoholism also.

In effect, it illustrates the role impulsivity plays as a pathomechanism in alcoholism, i.e. it is a psychological mechanism that drives addiction and alcoholism forward to it’s chronic endpoint.

Again research shows us how we can learn about a pathology from the recovery from it!

 

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“Abstract

Background

Although past research has found impulsivity to be a significant predictor of mortality, no studies have tested this association in samples of individuals with alcohol-related problems or examined moderation of this effect via socio-contextual processes. The current study addressed these issues in a mixed-gender sample of individuals seeking help for alcohol-related problems.

Results

…higher impulsivity at baseline was associated with an increased risk of mortality from Years 1 to 16; higher impulsivity at Year 1 was associated with an increased risk of mortality from Years 1 to 16, and remained significant when accounting for the severity of alcohol use, as well as physical health problems, emotional discharge coping, and interpersonal stress and support at Year 1. In addition, the association between Year 1 impulsivity and 15-year mortality risk was moderated by interpersonal support at Year 1, such that individuals high on impulsivity had a lower mortality risk when peer/friend support was high than when it was low.

Conclusions

The findings highlight impulsivity as a robust and independent predictor of mortality.

Introduction

…personality traits related to impulsivity (e.g., low conscientiousness) have been identified as significant predictors of poor health-related outcomes including mortality (Bogg and Roberts, 2004; Roberts et al., 2007). Although there is a well-established association between disinhibitory traits and alcohol use disorders (AUDs) (Labouvie and McGee, 1986; McGue et al., 1999;Sher et al., 2000), to our knowledge, no studies have tested these traits as predictors of mortality among individuals with alcohol-related problems or examined moderation of this effect via socio-contextual processes.

Predictors of Mortality Risk among Individuals with Alcohol Use Disorders

Relative to the general population, individuals with AUDs are more likely to die prematurely (Finney et al., 1999; Johnson et al., 2005; Valliant, 1996). Accordingly, several longitudinal studies have aimed to identify the most salient risk factors for mortality in this population (for a review, see Liskow et al., 2000)

…more reliance on avoidance coping, less social support, and more stress from interpersonal relationships increase the risk of mortality among individuals with AUDs (Finney and Moos, 1992; Holahan et al., 2010; Mertens et al., 1996; Moos et al., 1990).

Impulsivity and Risk for Mortality: Relevance for Individuals with Alcohol Use Disorders

Despite the litany of variables that have been examined as predictors of mortality among individuals with AUDs, tests of the significance of individual differences in personality are noticeably absent from this literature. In the clinical and health psychology literatures, however, personality traits have long been identified as possible risk factors for mortality (Friedman and Rosenman, 1959), with low conscientiousness emerging as one of the most consistent, trait-based predictors of poor health and reduced longevity (Kern and Friedman, 2008; Roberts et al., 2007). Conscientiousness is a broad domain of personality reflecting individual differences in the propensity to control one’s impulses, be planful, and adhere to socially-prescribed norms (John et al., 2008).

(previously) no studies in this literature have tested impulsivity as an independent predictor of mortality in a sample of individuals with alcohol-related problems. This is a surprising omission, given that impulsivity is a well-established risk factor for alcohol misuse (Elkins et al., 2006; McGue et al., 1999; Sher et al., 2000) and therefore may be an especially potent predictor of mortality among individuals with AUDs. Furthermore, the role of impulsivity as an independent predictor of mortality risk among individuals with AUDs is relevant from the standpoint of the stage of the alcohol recovery process.

Thus, we sought to examine the impulsivity-mortality link at baseline and one year after participants had initiated help-seeking for their alcohol use problems. At baseline, participants were in a state of distress due to their problematic alcohol use, whereas at Year 1 most participants had obtained help for their alcohol-related problems and reduced their drinking (Finney and Moos, 1995).

Given prior research on acute clinical states and self-report assessments of personality (e.g., Brown et al., 1991; Peselow et al., 1994;Reich et al., 1987), we hypothesized that individuals’ self-reports of impulsivity at Year 1 would be less a reflection of their alcohol problems – and therefore more likely to be independently linked to mortality risk – than their reports at baseline, which may be more closely associated with concurrent alcohol use and problems (i.e., state effects).

Discussion

…impulsivity at baseline was a significant predictor of mortality risk from Years 1 to 16; however, this effect was accounted for by the severity of alcohol use at baseline. In contrast, impulsivity at Year 1 was associated with an increased risk of mortality over the subsequent 15 years…

In addition, a significant interaction was observed between impulsivity and peer/friend support at Year 1, which suggested that, among individuals high on impulsivity, the mortality risk may be reduced for those high on support from peers/friends. Collectively, these findings highlight impulsivity as an independent risk factor for mortality in AUD samples…

…It is also conceivable that, given participants were in a state of crisis at baseline, their reports of their impulsive tendencies at that time partly captured “state” effects (e.g., psychiatric distress from concurrent substance use; withdrawal symptoms) and therefore were less an indication of their typical or “characterological” pattern of impulsivity, independent of alcohol use. However, at Year 1, most participants had reduced their drinking and were not in a state of crisis; thus, their reports at that time may have been a better reflection of their “trait-like” pattern of impulsivity, which in turn may be a more robust independent predictor of long-term outcomes such as mortality. Accordingly, future studies that seek to test impulsivity as an independent predictor of mortality among individuals with AUDs should consider the stage of the alcohol recovery process.

Moderation of the Impulsivity-Mortality Link via the Social Context

The results of the moderator analyses suggest that the effects of impulsivity on mortality may become manifest through interactions between traits and socio-contextual process (Friedman, 2000). That is, the dire effects of impulsivity on risk for mortality may not reach fruition for individuals who are able to maintain a strong peer support network. Conceivably, by virtue of their strong bond with a high-risk individual, such peers may have sufficient leverage to discourage expression of the individual’s impulsive tendencies and encourage consideration of the long-term consequences of his/her actions.

Such a perspective is consistent with evidence from the AUD treatment-outcome literature that social support networks are a key mechanism by which Alcoholics Anonymous (AA) and other psychosocial treatments can improve long-term drinking-related outcomes (Humphreys and Noke, 1997; Kaskutas et al., 2002).

Furthermore, from the standpoint of treatment, the present findings suggest that interventions for AUDs may benefit from an ecological perspective that considers the contexts in which dispositional tendencies, such as impulsivity, become expressed in individuals’ everyday lives. Notably, based on prior work with this sample, longer duration in AA and alcohol treatment was associated with a decline in impulsivity (Blonigen et al., 2009). In combination with the present findings, it appears that formal and informal help for AUDs may include “active ingredients” that can help curtail expression of impulsive tendencies (e.g., social integration, peer bonding; Moos, 2007,2008) and buffer the otherwise deleterious impact of such tendencies on health and longevity.

References

1. Blonigen, D. M., Timko, C., Moos, B. S., & Moos, R. H. (2011). Impulsivity is an Independent Predictor of 15-Year Mortality Risk among Individuals Seeking Help for Alcohol-Related Problems. Alcoholism, Clinical and Experimental Research, 35(11), 2082–2092. doi:10.1111/j.1530-0277.2011.01560.x

Alcoholics Anonymous and Reduced Impulsivity: A Novel Mechanism of Change

Impulsivity or lack of behaviour inhibition, especially when distressed, is one psychological mechanisms which is implicated in all addictive behaviour from substance addiction to behaviour addiction.

It is, in my view, linked to the impaired emotion processing as I have elucidated upon in various blogs on this site.

This impulsivity is present for example in those vulnerable to later alcoholism, i.e. sons and daughters of alcoholic parents or children  from a family that has a relatively high or concentrated density of alcoholics in the family history, right through to old timers, people who have decades of recovery from alcoholism.

It is an ever present and as a result part of a pathomechanism of alcoholism, that is it is fundamental to driving alcoholism to it’s chronic endpoint.

It partly drives addiction via it’s impact on decision making – research shows people of varying addictive behaviours choose now over later, even if it is a smaller short term gain over a greater long term gain. We seem to react to relieve a distress signal in the brain rather than in response to considering and evaluating the long term consequences of a decision or act.

No doubt this improves in recovery as it has with me. Nonetheless, this tendency for rash action with limited consideration of long term consequence is clearly a part of the addictive profile. Not only do we choose now over then, we appear to have an intolerance of uncertainty, which means we have difficulties coping with uncertain outcomes. In other words we struggle with things in the future particularly if they are worrying or concerning things, like a day in court etc. The future can continually intrude into the present. A thought becomes a near certain action, again similar to the though-action fusion of obsessive compulsive disorder. It is as if the thought and possible future action are almost fused, as if they are happening in unison.

Although simple, less worrying events can also make me struggle with leaving the future to the future instead of endless and fruitlessly ruminating about it in the now. In early recovery  especially I found that I had real difficulty dealing with the uncertainty of future events and always thought they would turn out bad. It is akin to catastrophic thinking.

If a thought of a drink entered into my head it was so distressing, almost as if I was being dragged by some invisible magnet to the nearest bar. It was horrendous. Fortunately I created my own thought action fusion to oppose this.

Any time I felt this distressing lure of the bar like some unavoidable siren call of alcohol I would turn that thought into the action of ringing my sponsor. This is why sponsees should ring sponsors about whatever, whenever in order to habitualize these responses to counteract the automatic responses of the addicted brain.

I think it is again based on an inherent emotion dysregulation. Obsessive thoughts are linked to emotion dysregulation.

My emotions can still sometimes control me and not the other way around.

Apparently we need to recruit the frontal part of the brain to regulate these emotions and this is the area most damaged by chronic alcohol consumption.

As a result we find it difficult to recruit this brain area which not only helps regulate emotion but is instrumental in making reflective, evaluative decisions about future, more long term consequence. As a result addicts of all types appear to use a “bottom up” sub-cortical part of the brain centred on the amgydala region to make responses to decisions instead of a “top down” more cortical part of the brain to make evaluative decisions.

We thus react, and rashly act to relieve the distress of undifferentiated emotions, the result of unprocessed emotion rather than using processed emotions to recruit the more cortical parts of the brain.

Who would have though emotions were so instrumental in us making decisions? Two parts of the brain that hold emotions in check so that they can be used to serve goal directed behaviour are the orbitofrontal cortex and the ventromedial prefrontal cortex.

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These areas also keep amgydaloid responding in check. Unfortunately these two areas are impaired in alcoholics and other addictive behaviours so their influence on and regulation of the amgydala is also impaired.

This means the sub cortical areas of the amgydala and related regions are over active and prompt not a goal directed response to decision making but a “fight or flight” response to alleviate distress and not facilitate goal directed behaviour.

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Sorry for so much detail. I have read so much about medication recently which does this or that to reduce craving or to control  drinking but what about the underlying conditions of alcoholism and addictive behaviour? These are rarely mentioned or considered at all.

 

We always in recovery have to deal with alcoholism not just it’s symptomatic manifestation of that which is chronic alcohol consumption. This is a relatively simple point and observation that somehow alludes academics, researchers and so-called commentators on this fascinating subject.

Anyway that is some background to this study which demonstrates that long term AA membership can reduce this impulsivity and perhaps adds validity to the above arguments that improved behaviour inhibition and reducing impulsivity is a very possible mechanism of change brought about by AA membership and the 12 step recovery program.

It shows how we can learn about a pathology from the recovery from it!

Indeed when one looks back at one’s step 4 and 5 how many times was this distress based impulsivity the real reason for “stepping on the toes of others” and for their retaliation?

Were we not partly dominated by the world because we could not keep ourselves in check? Didn’t all our decisions get us to AA because they were inherently based on a decision making weakness? Isn’t this why it is always useful to have a sponsor, someone to discuss possible decisions with?

Weren’t we out of control, regardless of alcohol or substance or behaviour addiction? Isn’t this at the heart of our unmanageability?

I think we can all see how we still are effected by a tendency not to think things through and to act rashly.

The trouble it has caused is quite staggeringly really?

Again we cite a study (1) which has Rudolf H. Moos as a co-author. Moos has authored and co-authored a numbered of fine papers on the effectiveness of AA and is a rationale beacon in a sea of sometimes quite controversial and ignorant studies on AA, and alcoholism in general.

“Abstract

Reduced impulsivity is a novel, yet plausible, mechanism of change associated with the salutary effects of Alcoholics Anonymous (AA). Here, we review our work on links between AA attendance and reduced impulsivity using a 16-year prospective study of men and women with alcohol use disorders (AUD) who were initially untreated for their drinking problems. Across the study period, there were significant mean-level decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity…

Among individuals with alcohol use disorders (AUD), Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [1, 2]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [3]. To our knowledge, however, there have been no efforts to examine links between AA and reductions in impulsivity-a dimension of personality marked by deficits in self-control and self-regulation, and tendencies to take risks and respond to stimuli with minimal forethought.

In this article, we discuss the conceptual rationale for reduced impulsivity as a mechanism of change associated with AA, review our research on links between AA and reduced impulsivity, and discuss potential implications of the findings for future research on AA and, more broadly, interventions for individuals with AUD.

Impulsivity and related traits of disinhibition are core risk factors for AUD [5, 6]. In cross-sectional research, impulsivity is typically higher among individuals in AUD treatment than among those in the general population [7] and, in prospective studies, impulse control deficits tend to predate the onset of drinking problems [811]

Although traditionally viewed as static variables, contemporary research has revealed that traits such as impulsivity can change over time [17]. For example, traits related to impulsivity exhibit significant mean- and individual-level decreases over the lifespan [18], as do symptoms of personality disorders that include impulsivity as an essential feature [21, 22]. Moreover, entry into social roles that press for increased responsibility and self-control predict decreases in impulsivity [16, 23, 24]. Hence, individual levels of impulsivity can be modified by systematic changes in one’s life circumstances [25].

Substance use-focused mutual-help groups may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [26]. Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations.

…the idea of reduced impulsivity as a mechanism of change…it is consistent with contemporary definitions of recovery from substance use disorders that emphasize improved citizenship and global health [31], AA’s vision of recovery as a broad transformation of character [32], and efforts to explore individual differences in emotional and behavioral functioning as potential mechanisms of change (e.g., negative affect [33,34]).

Several findings are notable from our research on associations between AA attendance and reduced impulsivity. First, consistent with the idea of impulsivity as a dynamic construct [18, 19], mean-levels of impulsivity decreased significantly in our AUD sample. Second, consistent with the notion that impulsivity can be modified by contextual factors [25], individuals who participated in AA longer tended to show larger decreases in impulsivity across all assessment intervals.

References

Blonigen, D. M., Timko, C., & Moos, R. H. (2013). Alcoholics anonymous and reduced impulsivity: a novel mechanism of change. Substance abuse, 34(1), 4-12.

Alcoholics Anonymous Effectiveness: Faith Meets Science

There has much, if not too much, talk of the effectiveness of AA in recent weeks,months and year. Whether there is a concerted controlled drinking agenda is for you to decide.

Controlled drinking for an alcoholic, for me and particularly a chronic alcoholic, is a mirage. Period.

Once you have been pickled to a gherkin you never return to being a cucumber again!

Check the methodology of studies that state it is possible as I have yet to come across a single study that has not been refuted years later by  follow up study.

In order to address this complicated area of studying the effectiveness of a group which does not lend itself easily to being studied we will refer to cite and choose excerpts from an excellent study on AA from a number of years ago (1).

This is the most definitive study of how and why AA works. If you are a newcomer read well.

Given the amount of dubious journalism and studies cited recently it is hugely important to put a study out there which gives those seeking recovery a true picture of how and why AA works.

Another point – if you are reading about recovery in glossy magazines, even if they purport to be aiding those in recovery, think twice about these journalistic pieces.  If it is controversial it sells. Common sense and diligent, unbiased experimental studies which give a fair appraisal of all points don’t sell in the same way.

I even wonder if this glossy recovery mags do more harm than good? Put it this way, an alcoholic could leave these sites thinking of a drink just as much as thinking about recovery.

 

 

Research on the effectiveness of Alcoholics Anonymous (AA) is controversial and is subject to widely divergent interpretations. The goal of this paper is to provide a focused review of the literature on AA effectiveness that will allow readers to judge the evidence for AA effectiveness 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, 2, 3, 4 and 6 is very 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).

The Cochrane Group  [1] review recommended that people considering attending AA or a twelve step facilation (TSF) should be made aware that there is a lack of experimental evidence on 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 [4], and that those who attend AA before attending treatment tend to attend AA longer than those who attend treatment first [5].

Prior efforts to summarize the findings on AA effectiveness have included literature reviews [6, 7] and meta analyses [810]. The most recent meta analysis [10] 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, no corroboration of self-report, etc.) somewhat inflated the case for AA effectiveness [9].

A review summarizing the state of the literature 7 years later [7] argued that there was a consistent, rigorous body of evidence supporting AA effectiveness. Again, there seems to be something for everybody, and the literature really does seem 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. 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 six 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 evaluate the totality of the evidence of a causal effect for smoking on lung cancer in the absence of experimental data [13, 14].

The criterion offer a framework for judging the “totality” of the evidence [12 p.191], implicitly acknowledging that the evidence may not be strong for all criteria, and leaving the final decision to the individual evaluator. These are the criterion:

  • The relationship between an exposure (here, exposure to AA) and the outcome (abstinence, as 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
  • There should be a dose-response relationship, such that more involvement in AA relates to higher levels of abstinence.
  • The consistency of the association matters. If some studies find a strong relationship between number of AA meetings attended and rate of abstinence, but many do not, this would call into question whether the dose-response relationship should be trusted, as evidence goes.
  • 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.
  • 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 select sample who would be sober anyway, 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; 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.
  • Coherence with existing knowledge is needed to establish causation. 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.

Figure 1

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Criterion:-

Criterion 1 – strength of association

.  As shown in Figure 1, which draws on a longitudinal study of male inpatients in Veterans Administration programs, rates of abstinence are about twice as high for those who attended a 12-step group such as AA following treatment… The rates of abstinence were about twice as high among those who had attended AA or another 12-step group (but no other form of aftercare).

Criterion 2 – dose response relationship

.  Do higher levels of AA attendance or involvement relate to higher levels of abstinence? There is evidence of a dose response relationship for number of 12-step meetings (Figure 2a), frequency of 12-step meetings (Figure 2b), and duration of AA meeting attendance (Figure 2c).

Figure 2a

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Again studying male residential patients in the VA system, and considering AA meeting attendance for the 90 days prior to the 1-year follow-up, the dose response curve looks almost linear (Figure 2a), with more 12-step meetings associated with higher rates of alcohol and drug abstinence [4]

In a smaller outpatient sample, over 70% of those attending 12-step groups weekly for the 6 months prior to the 2-year follow-up were alcohol abstainers, while alcohol abstinence rates among those attending less than weekly were the same as those who never attended during that period [18]; this suggests a threshold dose-response effect for weekly attendance at 12-step groups (Figure 2b).

Figure 2b

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In a longitudinal study of previously untreated problem drinkers, 70% of those with 27 weeks or more of sustained AA meeting attendance any given year (whether at year 1, at years 2–3, or at years 4–8) were abstinent from alcohol at the 16-year follow-up [4]; those with shorter duration of attendance had lower rates of abstinence, with the dose response most evident for AA attendance years 1 and years 4–8 (figure 2c). This study is the reason for Moos’ recommendation to send people to AA first, because those who went to AA first were more likely to be involved in AA for longer duration [5].

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Criterion 3 – consistency of association

The similarities in abstinence rates between the weekly or near-weekly AA attenders (70%) in these two latter studies with different populations and follow-up periods is relevant to this criteria, consistency of association.

Another example is shown in Figure 3, which presents rates of abstinence for those who attended AA but no other treatment (third bar, labeled ‘AA only’), in two different samples (VA inpatients, and previously untreated problem drinkers in the general population), with different follow-up periods (1, 3, and 8 years).

The 1-year study considered alcohol and drug abstinence as a function of 12-step group attendance, while the 3- and 8-year data focused specifically on AA attendance and alcohol abstinence. About 50% of those who had attended AA/12-step meetings only were abstinent at 1 year [15] and at 3 and 8 years [19]; and about one-fifth of those who did not attend AA/12-step meetings or treatment were abstinent at the parallel follow-up interviews.

Another study of the general population [20] found that individuals with lifetime alcohol dependence who went to 12-step meetings but no formal treatment were more likely to be abstinent than those who did nothing (not shown).

Figure 3

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Criterion 4-  temporally correct association

Moos’ work that studied 16-year alcohol abstinence in a previously untreated problem drinking sample as a function of AA during years 2–3 and years 4–8 [4] (Figure 2c) and met the 4th criterion for evidence of causality.

Criterion 5 – specificity

We will return to this issue in the conclusion as it concerns the mixed results among experimental evidence that has considered evidence of specificity. It is here that methodological differences play a role in clouding the results.

Criterion 6, coherence with existing knowledge

To evaluate the literature on AA effectiveness according to this criterion, theoretical plausibility will be discussed; that is, does AA work in a way that is consistent with major theoretical perspectives on health behavior and behavior change?

For example, a recent interpretation of contemporary psychodynamic theory has characterized alcoholism as an interaction between one’s abilities to express feelings and self-regulate one’s behavior [27]. The theory argues that despite low self esteem, many alcoholics have a narcissistic personality [28] and a sense of omnipotence. They drink to self-medicate, as a way of addressing unmet needs and uncomfortable psychological states.

AA solutions consistent with this characterization of the problem are evident at meetings, in the AA steps, and through people in the AA fellowship.

Meetings provide an opportunity to share one’s own struggles (and learn how to talk about one’s feelings), to increase one’s motivation to abstain, and to get outside of one’s self (and change one’s mood) by hearing others talk about their problems and how AA helped them.

The steps help with self-governance, narcissism and omnipotence: accepting powerlessness over alcohol (step 1); recognizing that one cannot do it alone (but that a higher power, which can be operationalized as the AA group, is there to help; steps 2–3); realizing how one’s behavior affected and affects others (step 4–9); treating other people better (step 10); finding meaning in life (step 11); and relinquishing one’s negative self-focus by helping others (step 12). Through the people in AA, one learns how to live a sober life, and how to regulate one’s behavior one day at a time.

Bandura’s social learning theory [29] adds to the psychodynamic perspective (noting the problem) of  social influences and from self-efficacy: if everyone around you drinks, and if you don’t think it is within your ability to not drink, you will be unable to abstain. The antidote includes changing environmental cues (such as staying away from bars), role modeling (seeing others succeed at not drinking), and self-efficacy (believing you can abstain).

AA meetings, and spending time with people in AA, represent changes in environmental cues; that is, you’re not at a bar, seeing alcohol and seeing people drink alcohol, when you’re at a meeting or out with AA friends.

At an AA meeting, you are exposed to successful role models, instead of current drinkers, who suggest a new approach to abstinence: not drinking 1 day at a time (instead of saying you are “quitting forever”). Seeing yourself able to abstain for one day begins to build self-efficacy, which accumulates with the passage of every sober day.

Spending time at AA meetings and with people in AA also leads to relapse prevention mechanisms put forward by standard behavioral modification techniques. These include learning how to say no to a drink when offered, having a plan of action when confronted with likely drinking conditions, and choosing alternative behaviors to take the place of drinking.

Several studies offer empirical support for these mechanisms. The positive relationship between AA involvement and abstinence has been shown to be partially mediated (explained) by (a) psychological and spiritual mechanisms including finding meaning in life [30], greater motivation for abstinence [31], and changes in religious beliefs and spiritual experiences [32]; (b) social influences such as fewer pro-drinking influences [33], more friends in general [34], having AA friends supportive of abstinence [35], and enhanced friendship networks [36]; and (c) social learning and behavioral mechanisms including improved self-efficacy [31, 37] and effective coping and relapse prevention skills [34, 36] to abstain. These mechanisms (and theories) are inter-related. For example, AA friends represent a particularly effective source of social support, because they provide expertise in preventing relapse.

Conclusions

The goal was not to provide an exhaustive review of the evidence, but rather to present representative studies that address AA effectiveness according to six accepted criterion for establishing scientific causation. This framework may be especially appropriate for considering AA effectiveness, because it acknowledges the value and limitations of experimental evidence in the context of other criterion for determining treatment effectiveness.

As stated at the outset, the experimental evidence for AA effectiveness (addressing specificity) is the weakest among the six criteria considered crucial for establishing causation. Only two studies provided strong proof of a specific AA or TSF effect: the outpatient arm of Project MATCH (with effects at 1 and 3 years) [2, 3], and the intensive referral condition in Timko’s trial (with effects for abstinence at 6 months and 1 year) [24]. The effect sizes were similar, with the TSF/Intensive referral conditions having a 5-10% advantage in abstinence rates. It is noteworthy that neither of these studies attempted to randomize patients to AA per se; instead, they focused on interventions intended to facilitate AA involvement.

One reason that several of the other trials may not have found positive effects for AA/ TSF is because many individuals randomized to the non-AA/non-TSF conditions also attended AA; thus, the AA or TSF condition ended up being compared to a condition consisting of an alternative treatment plus AA.

This was the case in Walsh’s hospital inpatient treatment vs. AA study [23] and in the aftercare arm of Project MATCH [22], and arose because the patients in the non-AA/non-TSF conditions also had attended 12-step-based inpatient treatment, which in turn engendered strong participation in AA. Thus, AA attendance levels were high in the inpatient hospital condition in the former study, and in the CBT and MET conditions among the Project MATCH aftercare subjects. In fact, CBT and MET aftercare patients attended more meetings than the TSF outpatients, and the aftercare patients overall attended twice the number of meetings at every follow-up compared to the outpatients [22, see pp.191–192].

As for the scorecard for the other criteria, the evidence for AA effectiveness is quite 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 evident at AA meetings and through the AA steps and fellowship (criteria 6, plausibility).”

Reference

Kaskutas, L. A. (2009). Alcoholics Anonymous effectiveness: Faith meets science. Journal of addictive diseases, 28(2), 145-157.