History of Alcoholism and the Justice System

ORIGINAL ARTICLE

Changes in depression mediate the effects of AA attendance on alcohol use outcomes Claire E. Wilcox, MDa and J. Scott Tonigan, PhD b

aDepartment of Psychiatry, University of New Mexico, Albuquerque, NM, USA; bCenter on Alcoholism, Substance Abuse, and Addiction, University of New Mexico, Albuquerque, NM, USA

ABSTRACT Background: Depression may contribute to increased drinking in individuals with alcohol use disorder. Although Alcoholics Anonymous (AA) attendance predicts drinking reductions, there is conflicting information regarding the intermediary role played by reductions in depression. Objectives: We explored whether AA attendance reduces depressive symptoms, the degree to which improvement in depression results in reductions in drinking, and in which subgroups these effects occur. Methods: 253 early AA affiliates (63%male) were recruited and assessed at baseline 3, 6, 9, 12, 18, and 24months. Depression was measured using the Beck Depression Inventory (BDI) and was administered at baseline 3, 6, 12, 18, and 24months. AA attendance and alcohol use outcomes were obtained with the Form 90. Mediation analyses were performed at early (3, 6, and 9 months) and late (12, 18, and 24 months) follow-up to investigate the degree to which reductions in depression mediated the effect of AA attendance on drinking, controlling for concurrent drinking. In addition, a series of moderated media- tion analyses were performed using baseline depression severity as a moderator. Results: At early follow-up, reductions in depression (6 months) mediated the effects of AA attendance (3 months) on later drinking (drinks per drinking day) (9 months) (b = −0.02, boot CI [−0.055, −0.0004]), controlling for drinking at 6months. Baseline depression severity did notmoderate the degree towhich BDImediated the effects of AA attendance on alcohol use (ps > .05). Conclusion: These findings provide further evidence that depression reduction is a mechanism by which AA attendance leads to reductions in alcohol use. Improving depression may help reduce alcohol use in individuals with AUD, and AA attendance may be an effective way to achieve that goal.

ARTICLE HISTORY Received 18 July 2016 Revised 7 October 2016 Accepted 13 October 2016

KEYWORDS 12-step; alcoholics anonymous; depression; alcohol use disorders; negative affect

Background

Relatively consistent evidence has accumulated, indicating that community-basedAlcoholics Anonymous (AA) atten- dance is predictive of decreased alcohol use for many, but not all, problem drinkers (1–5). Importantly, self-selection bias does not appear to account for AA-related benefit (6–8), and the salutary effects of AA have been observed in diverse populations including urban Native Americans (9), dually diagnosed adults (10,11), and ethnic minorities (12,13). Factors that do appear to account for AA-related benefit during early AA affiliation include acquiring an AA sponsor (14–16) social support for abstinence (17,18), gains in spiritual practices (19,20), and increased abstinence self- efficacy (21–24).

Central in the core AA literature (25) is the proposi- tion that negative affect is a leading precipitant to relapse and much of the prescribed step work in 12-step programs is therefore directed at reducing the unbridled expression of anger, depression, and selfish- ness. The degree to which AA attendance influences

AA member depression and, in turn, how changes in depression among AA members actually explains the beneficial effect of AA on drinking, remains unclear, however. Specifically, three rigorous longitudinal stu- dies have investigated changes in depression among AA members (26–28) (hereafter referred to as Wilcox et al. (26), Worley et al. (27) and Kelly et al. (28), respec- tively). Found in each of these studies, AA exposed adults reported significant reductions in depressive symptoms over time, with such pre-post reductions observed at 6-month follow-up among veterans with substance use and major depressive disorder [Worley et al. (27); Hedges g (g, Cohen’s d adjusted for small sample bias) = 0.55], at 9 months in both outpatient and aftercare treatment seeking Project MATCH sam- ples (Kelly et al. (28); g = 0.29), and over the course of 2 years in a community-recruited sample (Wilcox et al. (26); g = 0.18). Lagged analyses in each aforementioned study showed that frequency of AA attendance was associated with later reductions in depression.

CONTACT Claire E. Wilcox, MD [email protected] Department of Psychiatry, University of New Mexico, MSC 09-5030, 1 University of New Mexico, Albuquerque, NM 87131, USA.

THE AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE, 2018 VOL. 44, NO. 1, 103–112 http://dx.doi.org/10.1080/00952990.2016.1249283

© 2018 Taylor & Francis

Findings diverge, however, when changes in depres- sive symptoms were examined after statistically con- trolling for concurrent drinking. In the Kelly et al. (28) study, for example, the inclusion of current drink- ing in the lagged models eliminated the direct and independent effect of AA attendance on levels of depression symptoms, so reductions in depressive symptoms were attributed to the direct effect of AA attendance on reducing drinking. Furthermore, Kelly et al. (28) determined that changes in depressive symp- toms did not mediate that association between fre- quency of AA attendance and later drinking in either the aftercare or outpatient MATCH samples. A differ- ent relationship between AA attendance and changes in depression was presented in Worley et al. (27) and Wilcox et al. (26). Specifically, these studies found that the independent effect of AA on later levels of depression symptoms remained even after controlling for concurrent alcohol and substance use, suggesting that reductions in levels of depression symptoms may be attributable to the influence of AA beyond that explained by reductions in alcohol or substance use. Also noteworthily, Worley et al. (27) reported that reductions in depression significantly mediated 15% of the direct effect of AA on drinking. Wilcox et al. (26) did not examine whether reductions in depression mediated the effect of AA on drinking.

There are some possible explanations for the con- flicting results between these three studies. Foremost, at baseline, the absolute severity of depressive symptoms was significantly different across the three studies, with the MATCH aftercare and outpatient samples for Kelly et al. (28) reporting significantly lower levels of depres- sion. Combining the MATCH aftercare and outpatient samples, for example, yielded a mean Beck Depression Inventory-II (BDI) (29) score at intake of 10.16 (SD 8.25). The mean score for the community-based AA sample for Wilcox et al. (26) was 19.79 (SD 11.35), almost twice as depressed as the Kelly et al. (28) sample, and approached the BDI cutoff score of 20 for moder- ate depression. The most depressed sample studied was that of Worley et al. (27) which had a mean Hamilton Depression Scale score of 28.55 (SD 10.82), well above the cutoff of 17 for moderate depression (30), and all subjects had a diagnosis of major depressive disorder. We therefore suspected that adults with major depres- sive disorders were disproportionately represented in Worley et al. (27) and Wilcox et al. (26), and that, to some extent, the significantly lower levels of depression symptoms found in the MATCH sample from Kelly et al. (28) could have resulted in lower effects of AA

on depression. Other related work, using multiple med- iator analyses, has also found a stronger relationship between AA, depression, and later drinking (media- tion) in individuals with more severe depression (19).

Objectives

The objective of this study was to shed light on the reasons for conflicting findings in studies of the rela- tionship between AA exposure, changes in depression, and drinking outcomes by performing additional ana- lyses on the dataset used in the Wilcox et al. (26) study, with a particular focus on whether or not changes in depression mediated the reductions in drinking observed AA attendance. To do so, we investigated whether changes in levels of depression could explain the effects of AA exposure on later drinking in our sample, using similar approaches to those utilized by Kelly et al. (28) and Worley et al. (27). Furthermore, we investigated whether or not the presence or absence of a clinically relevant depression score at study entry moderated the strength of these associations. We hypothesized that since our sample was more depressed than that of Kelly et al. (28), and therefore more similar to that of Worley et al. (27), changes in depression would mediate the effects of AA on drinking (Aim 1), similar to the results in Worley et al. (27), but unlike those in Kelly et al. (28). Furthermore, if differences in baseline depression levels between the Worley et al. (27) and Kelly et al. (28) studies were driving the differences in findings, we hypothesized that baseline depression would moderate the meditational effect, and that mediation would be more pronounced (larger indirect effect) in those with greater baseline depression (Aim 2).

Methods

Participants and procedure

This is a follow-up report to a previously published paper (26), and details about the community-based AA sample can be obtained from the original paper. In brief, participants were early AA affiliates with little previous exposure to 12-step programs (participants were excluded for more than 16 weeks of lifetime AA exposure and if they reported ever having had a period of alcohol abstinence of at least 12 months at any time in their life after their alcohol use had become a pro- blem). Two hundred and fifty-three adults with alcohol use problems were recruited from AA groups; from

104 C. E. WILCOX AND J. S. TONIGAN

outpatient substance abuse treatment facilities; and from community sources including homeless shelters, advertisement in local newspapers, and flyers (68 were recruited from community-based AA, 87 were recruited from outpatient treatment abuse treatment centers, and 98 at shelters or through advertisements and flyers). Participants were also required to have attended one or more AA meetings in the prior 3 months, to have consumed alcohol in the prior 90 days, and to meet Diagnostic and Statistical Manual of Mental Disorders (31) criteria for alcohol dependence or abuse (32). All procedures were approved by the institutional review board at the University of New Mexico (UNM Protocol No. 24028).

Breathalyzers were used to ensure that participants’ blood alcohol concentration did not exceed 0.05 prior to the consent process, or at any subsequent interview. Once consented, participants were administered a base- line interview that included 15 self-report question- naires, 3 semi-structured interviews, and a urine toxicology screen. Follow-up interviews were con- ducted in 3-month increments for one year and then at 18 and 24 months. More than 85% of the original sample provided follow-up data at 24 months. No intervention was offered in this assessment-only study, although clinical referrals were made upon participant request, or when deemed warranted by clinical staff.

Measures

Alcohol use Alcohol use data were obtained using the Form 90 (33), which is a calendar-based semi-structured interview. Two alcohol use measures from the Form 90 were computed. Proportion of days abstinent from alcohol (PDA) was defined as the number of alcohol-abstinent days in an assessment period divided by the total num- ber of days in the period. Drinks per drinking day (DPDD) was defined as number of drinks consumed per drinking (i.e., non-abstinent) days in the assess- ment period.

12-step meeting attendance A single item from the Form 90 interview documented frequency of 12-step meeting attendance during an interview period. The proportion days of 12-step atten- dance for each participant was calculated as a ratio of days 12-step meeting attendance divided by the number of days in an interview period.

Depression The Beck Depression Inventory (BDI) (29), commonly used in both clinical and research settings to screen for

and establish severity of depression, was used as a measure of depressive symptomatology. The BDI is composed of 21 questions each scored on a scale of 0 to 3 asking about symptoms over the past 2 weeks such as hopelessness, irritability, guilt, feelings of being pun- ished, fatigue, weight loss, and lack of interest in sex. Total scores on the BDI of 0–13 indicate minimal depression, 14–19 mild depression, 20–28 moderate depression, and 29–63 severe depression. For mediation analyses, we used the BDI as a continuous variable to mark the degree of depressive symptomatology. When used as a moderator, we used a dichotomous modera- tor variable by grouping individuals with minimal or mild depression into one group, and those with mod- erate or severe depression into the other group as a marker of the presence or absence of clinically relevant depression.

Statistical analyses

To examine whether the effect of AA attendance on drink- ing (DPDD, PDA) could be partially or fully accounted for by changes in BDI scores, we conducted mediation tests using the bias-corrected bootstrap (34) as implemented in the PROCESS macro for SPSS (35), which uses ordinary least squares regression. In all models, we bootstrapped 1000 samples and significant effects were determined by 95%bias-corrected confidence intervals that do not contain zero. We conducted two single-mediation models (Aim 1: Analysis 1 for PDA, Analysis 2 for DPDD) in which we examined the total, direct, and indirect effects of AA atten- dance on alcohol use via BDI scores at early follow-up (3-month AA; 6-month BDI; 9-month alcohol use; n = 194). For these two models, drinking and BDI at study entry (baseline) were entered as covariates, and con- current drinking (6 months) was entered as a mediator operating in parallel [Figure 1; Model 4 in PROCESS Macro (36)]. We then conducted two tests of moderated mediation (Aim 2: Analysis 3 for PDA, Analysis 4 for DPDD) by entering baseline categorical depression as a moderator into the two single-mediation models defined above [Figure 2; Model 58 in PROCESS Macro (36)]. Although we did not formally test for heteroskedasticity, we used the heteroskedasticity-consistent standard errors option in the process macro (37). For our post hoc late follow-up analyses, we used exactly the same methods described above, except that we used 12 month AA, 18 month BDI and 24 month alcohol use (n = 183) instead of the 3-, 6-, and 9-month time points described above (Figures 1 and 2; Analyses 5, 6, 7, 8). The outcome variables were transformed prior to the analyses using a transforma- tion that eliminated extreme outliers (DPDD was square root transformed; PDA was arc sin of square root

THE AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE 105

transformed), although this may not have been necessary, as bootstrapping (as opposed to the Sobel test for indirect effects) significantly minimizes the need for normally dis- tributed outcome variables (38). We note for the reader that p values are appropriate for all of the reported para- meters except the indirect effects. In this case, we are interested in whether the CI contains 0 or not.

Results

Participant information

Of the 253 participants, 194 participants had complete data for the planned analyses at early follow-up. Of these 194 participants, 63% of the sample was male (n=123) and the mean age of participants was 39.14 years (SD 9.84). A

majority of the reduced sample had a high school degree (22.2%nodegree, 12.4%GED, 38.1%high school diploma), were unemployed (63.9%), and were single or divorced (48.1%, 34.5%); 16.0% of the participants reported being homeless. Of the 194 participants, 42.9% were Hispanic, 32.1% were non-Hispanic White, 18.7% were Native American, and the remaining participants were of African, Asian, or unspecified ancestry. Finally, at study entry, participants reported that they were attending AA meetings 16.0%of the days (SD18.5%) andhad ameanBDI score of 20.1 (SD11.3), amean proportion of days abstinent of alcohol of 52.7 (SD 30.5) and amean drinks per drinking day of 17.60 (12.81).

Simple correlations between primary measures [alcohol use (baseline), BDI (baseline), AA (3 month), BDI (6 month), alcohol use (9 month)] were in the expected

Figure 1. Pictorial representation of statistical mediation model used for Aim 1/Analysis 1 and 2 (early follow-up for PDA and DPDD) and Analysis 5 and 6 (late follow-up for PDA and DPDD). Definitions: AA = AA attendance; PDA = percent days abstinent; DPDD = drinks per drinking day; BDI = Beck Depression Inventory; Early = early follow-up; Late = late follow-up; A = path A, B = path B, C = path C representing total effect beforemediator is entered intomodel, C’ = path C’ representing direct effect after mediator is entered intomodel. Coefficients and significance values for Analysis 1 and 2 are in Table 2, and for Analysis 5 and 6 are in Table 3.

Figure 2. Pictorial representation of statistical moderated mediation model used for Aim 2/Analysis 3 and 4 (early follow-up for PDA and DPDD) andAnalysis 7 and 8 (late follow-up for PDA andDPDD). Definitions: AA=AA attendance; PDA=percent days abstinent; DPDD=drinks per drinking day; BDI = Beck Depression Inventory; Early = early follow-up; Late = late follow-up; A = path A, B = path B, C = path C representing total effect before mediator is entered into model, C’ = path C’ representing direct effect after mediator is entered into model. Coefficients and significance values for Analysis 7 and 8 are in Table 4.

106 C. E. WILCOX AND J. S. TONIGAN

directions such that greater AA attendance was associated with lower BDI scores and lower alcohol consumption, and lower BDI scores were associated with lower alcohol con- sumption (Table 1). Of note, the full sample (n = 253) and the complete data sample for the early follow-up analyses (n = 194) had very similar mean values for the key variables in our analyses (Supplementary Table 1).

Mediation analyses—Aim 1/early follow-up (Analysis 1, 2)

There was a significant direct effect of AA (3 months) on drinking (6 months) for both PDA (p = 0.000, b = 0.441, t= 5.88) andDPDD (p= 0.009, b= −1.482, t=−3.388). The direct effect of AA (3 months) on drinking (9 months) was not significant, although the total effect was highly signifi- cant for both PDA (p=0.006, b = 0.102, t = 2.757) and DPDD (p = 0.008, b = −1.177, t = −2.694). Furthermore, in support of previous findings (26), there were significant effects of AA (3 months) on BDI (6 months) for PDA (p = 0.040, b = −5.043, t = −2.073) and DPDD (p = 0.050, b = −4.723, t = −1.973) (path A; Figure 1). For DPDD, but not PDA, BDI (6 month) was associated with DPDD (9 months) (p = 0.041, b = 0.023, t = 2.060) (path B; Figure 1), and the indirect effect of AA (3 months) on alcohol use at 9 months via BDI (6 months) was also significant. Not surprisingly, alcohol use at 6 months (PDA and DPDD) was a significant mediator of the effects of AA (3 months) on alcohol use (9 months) (Table 2).

Moderated mediation—Aim 2/early follow-up (Analysis 3, 4)

We then entered a BDI categorical moderator variable (as a marker of the likely presence or absence of a depressive disorder diagnosis) into the mediation mod- els (Figure 2). When we did so, none of the indirect effects via BDI for either category of depression and neither of the indices of moderated mediation were statistically significant for the two models tested, indi- cating that baseline depression severity did not moder- ate the degree to which BDI (6 months) mediated the

relationship between AA attendance (3 months) and alcohol use (9 months). The interaction terms were not significant for either model for either path A or path B, indicating that the baseline BDI categorical variable did not moderate either the relationship between AA (3 months) and alcohol use 6 months) or

Table 1. Correlations between AA attendance, depression, and alcohol use (early). PDA BL DPDD BL BDI BL AA 3 months PDA 6 months DPDD 6 months BDI 6 months PDA 9 months

DPDD BL −0.046, 253 BDI BL −0.247**, 227 −0.014, 227 AA 3 months 0.196**, 239 0.238**, 239 −0.201**, 215 PDA 6 months 0.269**, 239 0.077, 239 −0.227**, 214 0.438**, 236 DPDD 6 months −0.113, 239 0.020, 239 0.202*, 214 −0.282**, 236 −0.817**, 239 BDI 6 months −0.097, 215 −0.133, 215 0.455**, 199 −0.235**, 215 −0.381**, 214 0.327**, 214 PDA 9 months 0.278**, 237 0.072, 237 −0.212**, 213 0.370**, 233 0.705**, 234 −0.532**, 234 −0.362**, 211 DPDD 9 months −0.142*, 237 0.076, 237 0.172*, 213 −0.258**, 233 −0.573**, 234 0.575**, 234 0.305**, 211 −0.837**, 237

*p < 0.05, ** p< 0.01. All values are reported in the format: Spearman’s rho, number of participants; BL = baseline, BDI = Beck Depression Inventory, PDA = percent days abstinent, DPDD = drinks per drinking day (transformed variables for PDA and DPDD).

Table 2. Results from mediation analyses to examine whether changes in depression mediate the effect of AA attendance on alcohol use outcomes at early follow-up (3, 6, 9 months; Fig.1; Aim 1; Analysis 1, 2). PDA early (n = 194) Coeff SE t p

Path A (to BDI 6 months) AA 3 months −5.043 2.432 −2.073 0.040 PDA baseline −0.009 2.336 −0.004 0.997

Path A (to PDA 6 months) AA 3 months 0.441 0.075 5.875 0.000 BDI baseline −0.004 0.002 −1.751 0.082

Path B (to PDA 9 months) BDI 6 months −0.004 0.003 −1.415 0.159 AA 3 months −0.059 0.088 −0.669 0.505 BDI baseline 0.001 0.003 0.526 0.599

Total Effect (to PDA 9 months) AA 3 months 0.282 0.102 2.757 0.006 BDI baseline −0.003 0.003 −1.195 0.234

Coeff Boot SE

Boot LLCI

Boot ULCI

Indirect effect (BDI 6 months is mediator)

0.013 0.012 −0.002 0.051

Indirect Effect (PDA 6 months is mediator)

0.221 0.043 0.141 0.310

DPDD early (n=194) Coeff SE t p

Path A (to BDI 6 months) AA 3 months −4.723 2.394 −1.973 0.050 DPDD baseline −0.293 0.507 −0.579 0.563

Path A (to DPDD 6 months) AA 3 months −1.482 0.437 −3.388 0.001 BDI baseline 0.023 0.010 2.204 0.029

Path B (to DPDD 9 months) BDI 6 months 0.023 0.011 2.060 0.041 AA 3 months −0.293 0.347 −0.845 0.399 BDI baseline −0.0001 0.010 0.008 0.994

Total Effect (to DPDD 9 months) AA 3 months −1.177 0.437 −2.694 0.008 BDI baseline 0.022 0.011 2.023 0.044

Coeff Boot SE

Boot LLCI

Boot ULCI

Indirect effect (BDI 6 months is mediator)

−0.019 0.013 −0.055 −0.0004

Indirect effect (DPDD 6 months is mediator)

−0.138 0.043 −0.234 −0.065

PDA = percent days abstinent, DPDD = drinks per drinking day, BDI = beck depression inventory, AA = AA attendance, Coeff = coefficient, SE = standard error, LLCI = lower level of confidence interval, ULCI = upper level of con- fidence interval. All indirect effect values are completely standardized.

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BDI (6 months) or the relationship between BDI (6 months) and alcohol use (9 months), respectively (Table 4).

Post hoc mediation Analysis—late follow-up (Analysis 5, 6)

In the aforementioned analyses looking at the 3-, 6-, and 9-month follow-up time points, we supported our findings from previous work in Wilcox et al. (26), showing that AA attendance was associated with reduc- tions in later depression, controlling for concurrent drinking (26). Since our previous analysis included all time points (baseline to 24 months) and did not look at early and late time points separately, we wanted to

explore whether or not changes in depression mediated the effect of AA on alcohol use.

As seen at early follow-up, at late follow-up, AA (12 month) was significantly associated with alcohol use (18months) for PDA (p= 0.009, b= 0.397, t= 2.627) and at a trend level for DPDD (p = 0.064, b = −1.478, t = −1.864). In addition, AA (12 months) was significantly associated with BDI (18 months) for PDA (p = 0.047, b = −7.947, t = −2.004) and at a trend level for DPDD (p = 0.053, b = 7.801, t = −1.945) (path A; Figure 1), supporting pre- vious findings from Wilcox et al. (26). However, BDI (18 months) was not significantly associated with alcohol use (24 months) (path B; Figure 1) for either DPDD or PDA, and the indirect effects via BDI were not significant, indicating that at late follow-up, BDI (18 months) did not mediate the effects of AA (12 month) on alcohol use (24 months) (Table 3).

Post hoc moderated mediation analysis—late follow-up (Analysis 7, 8)

When the baseline BDI categorical variable was entered into the model, none of the indirect effects via BDI for either category of depression and neither of the indices of moderated mediation were statistically significant for the two models tested, indicating that baseline depres- sion severity as a categorical variable did not moderate the degree to which BDI (18 months) mediated the relationship between AA (12 months) and alcohol use (24 months). For path A for the PDA analysis, both the BDI moderator variables and the interaction terms in the moderated mediation analysis were significant for AA (12 months) to both BDI (18 months) and PDA (18 months) (Table 4, Figure 2). For path A for the DPDD analysis, the BDI moderator variable and the interac- tion term for AA (12 months) to BDI (18 months) were significant (Table 4, Figure 2). Plotting slopes by group indicated that those with greater depression levels at baseline were more likely to show a decrease in BDI scores (18 months) with higher levels of AA attendance (12 months).

Discussion

This study investigated the relationship between AA attendance, depression, and alcohol consumption in individuals new to AA. In particular, our primary aim was to see whether the beneficial effects of AA atten- dance on drinking were mediated by effects on depres- sion. Previous work has shown conflicting results using similar approaches at similar time points (26–28), and our findings help clarify things, somewhat. First, and most interestingly, we found that changes in depression

Table 3. Results from analyses to examine whether changes in depression mediate the effect of AA attendance on alcohol use outcomes at late follow-up (12, 18, 24 months; Fig. 1; Analysis 5, 6). PDA late (n = 183) Coeff SE t p

Path A (to BDI 18 months) AA 12 months −7.947 3.966 −2.004 0.047 PDA baseline 0.134 2.114 0.064 0.949

Path A (to PDA 18 months) AA 12 months 0.397 0.151 2.627 0.009 BDI baseline −0.004 0.003 −1.779 0.077

Path B (to PDA 24 months) BDI 18 months 0.000 0.003 0.080 0.937 AA 12 months 0.067 0.097 0.691 0.490 BDI baseline 0.001 0.003 0.169 0.866

Total effect (to PDA 24 months) AA 12 months 0.351 0.131 2.680 0.008 BDI baseline −0.003 0.003 −0.839 0.403

Coeff Boot SE

Boot LLCI

Boot ULCI

Indirect Effect (BDI 18 months is mediator)

−0.006 0.103 −0.293 0.159

Indirect effect (PDA 18 months is mediator)

0.137 0.050 0.033 0.234

DPDD late (n=183) Coeff SE t p

Path A (to BDI 18 months) AA 12 months 7.801 4.010 −1.945 0.053 DPDD baseline −0.109 0.486 −0.225 0.823

Path A (to DPDD 18 months) AA 12 months −1.478 0.793 −1.864 0.064 BDI baseline 0.029 0.012 2.417 0.017

Path B (to DPDD 24 months) BDI 18 months −0.004 0.012 −0.362 0.718 AA 12 months −0.356 0.807 −0.441 0.660 BDI baseline 0.006 0.011 0.570 0.570

Total effect (to DPDD 24 months) AA 12 months −1.358 0.730 −1.860 0.065 BDI baseline 0.024 0.012 2.021 0.045

Coeff Boot SE

Boot LLCI

Boot ULCI

Indirect effect (BDI 18 months is mediator)

−0.004 0.012 −0.015 0.034

Indirect effect (DPDD 18 months is mediator

−0.122 0.066 −0.257 0.001

PDA = percent days abstinent, DPDD = drinks per drinking day, BDI = beck depression inventory, AA = AA attendance, Coeff = coefficient, SE = standard error, LLCI = lower level of confidence interval, ULCI = upper level of confidence interval. All indirect effect values are completely standardized.

108 C. E. WILCOX AND J. S. TONIGAN

mediated the beneficial effects of AA attendance at 3 months on drinking (DPDD) at 9 months controlling for concurrent drinking, consistent with Worley et al. (27), but in contrast to Kelly et al. (28). Our results were in support of our hypothesis, given that our sample was more similar to that of Worley et al. (27) than that of Kelly et al. (28) in terms of baseline depression levels. By contrast, in our sample, for PDA, the indirect effects were not significant, although they were still in the expected directions; changes in depression appeared to have a greater effect on the quantity consumed, rather than the decision to drink or not drink on a particular day. Other related work has also found that drinking mediated the relationship between AA and later drink- ing (19), and that the effect was stronger for DPDD.

We also hypothesized that baseline depression severity would moderate the indirect effect, but this hypothesis was not supported. Had it been supported, this would

have indicated that differences in depression levels were driving the differences in results between the three stu- dies. The absence of an observed effect could have resulted from the fact that BDI scores are fluid in this population and that a single time point measurement of BDI (our dichotomous moderator variable) is not a reli- able marker of the presence or absence of a depressive syndrome. An alternative explanation for the differences lies in the variability in rates of AA attendance. Namely, our sample and that of Worley et al. (27) had higher AA attendance frequency than that of Kelly et al. (28); in our sample, rates were 29%, 19%, and 15% of days attending AA meetings during the preceding assessment periods at 3, 6, and 9 months, respectively (26), whereas in Kelly et al. (28) participants had minimal AA attendance. Moreover, a clear majority of the participants in Wilcox et al. (26) attended AA throughout the 24 months and, in the Worley et al. (27) study, participants reported, on

Table 4. Results from moderated mediation analyses to examine whether baseline depression severity moderates the degree to which changes in depression mediate the effect of AA attendance on alcohol use outcomes at late follow-up (12, 18, 24 months; Fig. 2; Analysis 7, 8). PDA late with baseline depression severity moderator variable (n=194) Coeff SE t p

Path A (to BDI 18 months) BDI mod 6.227 3.108 2.004 0.047 BDI mod × AA 12 months −15.811 7.644 −2.068 0.040

Path A (to PDA 18 months) BDI mod −0.403 0.124 −3.242 0.001 BDI mod × AA 12 months 0.712 0.284 2.507 0.013

Path B (to PDA 24 months) BDI mod 0.080 0.227 0.351 0.726 BDI mod ×BDI 18 months 0.001 0.006 0.209 0.835 BDI mod × PDA 18 months −0.055 0.139 −0.396 0.692

Coeff Boot SE Boot LLCI Boot ULCI

Indirect effect (BDI 18 months is mediator); minimal/mild sepression 0.001 0.042 −0.036 0.065 Indirect effect (BDI 18 months is mediator); moderate/severe depression −0.009 0.067 −0.139 0.135 Indirect effect (PDA 18 months is mediator); minimal/mild depression 0.073 0.157 −0.254 0.346 Indirect effect (PDA 18 months is mediator); moderate/severe depression 0.570 0.129 0.326 0.844 Index of moderated mediation (BDI 18 months is mediator) −0.009 0.072 −0.155 0.132 Index of moderated mediation (PDA 18 months is mediator) 0.497 0.204 0.137 0.922

DPDD late with baseline depression severity moderator variable (n=183) Coeff SE t p

Path A (to BDI 18 months) BDI mod 6.157 3.115 1.977 0.050 BDI mod ×AA 12 months −15.868 7.628 2.080 0.039

Path A (to DPDD 18 months) BDI mod 0.447 0.475 0.942 0.602 BDI mod × AA 12 months −0.169 1.680 −0.101 0.920

Path B (to DPDD 24 months) BDI mod 0.667 0.606 1.100 0.273 BDI mod × BDI 18 months 0.014 0.029 0.476 0.635 BDI mod × DPDD 18 months 0.117 0.192 0.610 0.542

Coeff Boot SE Boot LLCI Boot ULCI

Indirect effect (BDI 18 months is mediator); minimal/mild depression −0.0042 0.119 −0.412 0.172 Indirect effect (BDI 18 months is mediator); moderate/severe depression 0.129 0.238 −0.266 0.687 Indirect effect (DPDD 18 months is mediator); minimal/mild depression −1.094 0.758 −2.806 0.156 Indirect effect (DPDD 18 months is mediator); moderate/severe depression −1.028 0.945 −2.954 0.487 Index of moderated mediation (BDI 18 months is mediator) 0.133 0.262 −0.301 0.733 Index of moderated mediation (DPDD 18 months is mediator) 0.066 1.180 −2.282 2.389

BDI mod = Categorical BDI moderator variable, DPDD = drinks per drinking day, BDI = beck depression inventory, AA = AA attendance, Coeff = coefficient, SE = standard error, LLCI = lower level of confidence interval, ULCI = upper level of confidence interval; none of the paths for the analysis using percent days abstinent as the outcome were significant so these results are not reported in a table.

There were no significant interaction terms nor were the indices of moderated mediation significant for PDA or DPDD at early follow-up (Analyses 3,4) and so no table was created.

THE AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE 109

average, attending more than 10 AAmeetings prior to the 3-month follow-up. By contrast, in Kelly et al. (28) study, a majority of the outpatient participants did not attend AA during any follow-up and, by the 9-month follow-up, the percent of outpatient MATCH participants reporting any AA attendance had declined to 29%. The absence of mediation in the Kelly et al. (28) study may have occurred because participants had significantly less overall expo- sure to AA.

Although we used different methods than we had used in our previous paper (26), we still observed that AA attendance was associated with reductions in later depressive symptoms, controlling for concurrent drink- ing (path A; Figures 1 and 2). Moreover, we obtained further detail about the time points at which these effects were stronger (early follow-up) and in which populations (greater baseline depression levels for late follow-up). One possible reason that baseline depres- sion severity did not moderate the relationship between AA attendance and later depression at early follow-up is that there was more room for improvement in all individuals, and due to the powerful effect of novelty, otherwise known as the “pink cloud” by AA attendees early in their AA exposure. At late follow-up, there may have been a stronger effect for those with greater depression at baseline, perhaps because they were the individuals for whom depression was not tightly linked with alcohol consumption, and who took longer to improve in their depressive symptom levels. Finally, that those with moderate or severe depression scores at baseline benefited even more at late follow-up than those with minimal or mild depression also supports findings in the literature that individuals with co-occur- ring psychiatric issues are just as likely to benefit from AA (11,39), and that drinking reduction improves chances of recovery from psychiatric illness.

Negative affect has long been considered a trigger for drinking and is considered a reasonable target for AUD treatment both within the AA literature (25) and treat- ment literature at large (40). This is supported by studies showing that compulsive alcohol use is driven by negative reinforcement (41), that people with AUD report drinking to relieve negative affect (42–44), that depression precedes relapse and is associated with greater drinking in individuals with AUD seeking treat- ment (45–49), and that treatments targeting negative affect and emotion regulation result in improvements in drinking (42,50). On the other hand, previous work has also shown that antidepressants in individuals with AUD but without depression are not effective at redu- cing drinking (51), and has shown a minimal role of depression in predicting later drinking (52). Our results supported the possibility that changes in negative affect

(depression) do indeed mediate the effects of AA on later drinking, that this effect occurs above and beyond the effect of AA on drinking (for DPDD at early follow- up), and that improving negative affect is a reasonable treatment target.

One limitation of our study has to do with the fact that we only had a single measurement tool, the BDI, for negative affect. Although anger has been explored as a mediator of AA’s effect on drinking (53), to our knowledge, neither anxiety nor irritability has been. Furthermore, we had some limitations to our analysis methods. For one, we only analyzed subjects with com- plete data, which could have limited our power to detect effects and may have caused us to have null effects at late follow-up, for example. Second, although lagging the time points in our analyses for the indepen- dent, mediator, and dependent variables was a strength in our study in terms of being able to make inferences about causality, latent growth curve modeling would have allowed us to include all time points and may have had more sensitivity to detect effects (54). Finally, this is an observational cohort study rather than, say, a randomized trial targeting depression or assigning individuals to degrees of AA attendance fre- quency, and therefore, causality cannot be definitively attributed to the independent variable or mediator in such a design; associations could have been driven by unmeasured variables.

Conclusions

In conclusion, we observed that changes in depression mediated the effects of AA attendance on later drinking (DPDD) at early follow-up consistent with some but not all studies. However, baseline depression severity did not moderate the indirect effect and therefore did not provide support to the hypothesis that baseline depression differ- ences were driving the differences between studies. Importantly, however, these findings have clinical signifi- cance by increasing support for models that ameliorating negative affect may help to reduce alcohol use in indivi- duals with AUD and that encouraging AA attendance may be one way to achieve drinking reduction via this mechanism.

Disclosure statement

The authors report no relevant financial conflicts.

Funding

This research was supported by National Institute on Alcohol Abuse and Alcoholism (NIAAA) Grants K02-AA00326

110 C. E. WILCOX AND J. S. TONIGAN

and R01-AA014197. CEW is supported by NIA-AA Grant K23-AA021156. JST is supported by NIAAA Grant K24-AA021157. The views expressed are those of the authors and do not necessarily represent the views of the NIAAA.

ORCID

J. Scott Tonigan http://orcid.org/0000-0002-6668-2038

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