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. Author manuscript; available in PMC: 2025 Jun 1.
Published in final edited form as: Addiction. 2024 Mar 14;119(6):1059–1070. doi: 10.1111/add.16472

Co-action and changes in alcohol use during a smoking cessation attempt

Christine Vinci 1, Cho Y Lam 2, Paul E Etcheverry 3, Virmarie Correa-Fernandez 4, Miguel Ángel Cano 5, Paul M Cinciripini 6, David W Wetter 2
PMCID: PMC11831237  NIHMSID: NIHMS2053555  PMID: 38482972

Abstract

Aims:

Three smoking cessation studies (CARE, Break Free, Por Nuestra Salud [PNS]) were used to measure changes in average alcohol consumption, binge drinking and alcohol-related problems during a smoking cessation attempt and to explore co-action with smoking abstinence.

Design:

CARE and PNS were longitudinal cohort cessation studies; Break Free was a two-arm randomized clinical trial.

Setting:

Texas, USA.

Participants:

Participants were current smokers who were recruited from the community and received smoking cessation interventions. All participants received nicotine replacement therapy and smoking cessation counseling. CARE included 424 smokers (1/3 White, 1/3 African American and 1/3 Latino); Break Free included 399 African American smokers; PNS included 199 Spanish-speaking Mexican-American smokers.

Measurements:

Weekly alcohol consumption was collected multiple times pre and post-quit, and binge drinking and alcohol-related problems were collected at baseline and 26 weeks post-quit. Analyses included only those who indicated current alcohol use.

Findings:

Average alcohol consumption decreased from baseline to 26 weeks post-quit in CARE (F = 17.09, P < 0.001), Break Free (F = 12.08, P < 0.001) and PNS (F = 10.21, P < 0.001). Binge drinking decreased from baseline to 26 weeks post-quit in CARE (F = 3.94, P = 0.04) and Break Free (F = 10.41, P < 0.001) but not PNS. Alcohol-related problems decreased from baseline to 26 weeks post-quit in CARE (Chi-sq = 6.41, P = 0.010) and Break Free (Chi sq = 14.44, P = 0.001), but not PNS.

Conclusions:

Among current drinkers, alcohol use/problems appear to decrease during a smoking cessation attempt and remain low through 26 weeks after the quit attempt. Little evidence was found for co-action, with smoking abstainers and relapsers showing similar change in alcohol use/problems.

Keywords: alcohol use, binge drinking, co-action, problematic drinking, race/ethnicity, smoking cessation

INTRODUCTION

Tobacco remains the leading cause [1] and alcohol the third leading cause of preventable death and disability in the United States [2]. Moreover, co-use of tobacco and alcohol has a synergistic adverse effect on health, with co-use increasing the risk for morbidity and mortality over and above the use of either substance alone [35]. Co-use clusters together within both individuals (e.g. smokers are more likely to drink, binge drink and misuse alcohol than non-smokers) [68] and situations (e.g. co-use often happens within the same day and the same use episode) [912]. However, the consequences of cigarette smoking, alcohol use and their co-use can be ameliorated by quitting smoking and consuming less alcohol [1315].

Theory and research on multiple health-risk behaviors highlight the importance of understanding the degree to which a change in one risky health behavior (e.g. attempt to quit smoking) induces changes in another [16, 17]. Here, we investigate (1) changes in alcohol use during a smoking quit attempt; and (2) co-action, defined as the degree to which a successful versus an unsuccessful change in smoking (e.g. smoking abstinence versus relapse) is associated with a change in alcohol use. Understanding co-action and changes in alcohol use during a smoking cessation attempt has the potential to contribute to the development of targeted interventions [17, 18].

There are several reasons to expect a change in alcohol use among smokers trying to quit. One hypothesis is that alcohol use increases during a quit attempt to combat nicotine withdrawal [19]. Quitting smoking is associated with increases in negative affect and stress, which may increase alcohol use [2023]. In addition, quitting smoking is associated with a decrease in dopamine levels, which contributes to withdrawal symptoms [24], whereas alcohol use can increase dopamine levels [2527].

Attempting to quit smoking may reduce alcohol use, and strategies used while quitting smoking may extend to alcohol use. For instance, avoiding locations associated with smoking may also decrease exposure to alcohol (e.g. bars, parties) [28]. Smoking acts as a behavioral cue for drinking such that quitting smoking may reduce cues for drinking [29], leading to a decrease in alcohol use. Smokers who know that drinking increases smoking urges might reduce alcohol use to decrease craving for cigarettes [3033]. Finally, smokers trying to quit may be motivated to live healthier and drink less [17].

Unfortunately, most smoking cessation attempts fail [34], and relapse may impact alcohol use during a cessation attempt. Returning to smoking may decrease stress and/or increase dopamine levels, which decreases the desire to drink [20, 24] or smoking resumption may expose one to drinking cues and increase their alcohol use [29, 32, 33].

Prior research on co-action of smoking and alcohol use during a smoking cessation attempt

Two smoking cessation studies have examined smoking abstinence as a moderator of change in alcohol use during a smoking cessation attempt with mixed findings. One study found that abstainers showed a larger decrease in alcohol consumption and heavy drinking than did relapsers [35]. Another study found that compared to women who relapsed, men who remained quit for a year decreased alcohol consumption. Women showed a decrease in alcohol use at a year follow-up regardless of abstinence status [36].

Other studies found no evidence of co-action. A study with HIV+ smokers found no association of smoking status with alcohol use, but abstinence was defined as quitting smoking for even 1 day, which is a non-standard definition of quitting [10]. Among light smokers, alcohol consumption and binge drinking decreased after quitting smoking, but no difference was found between smoking abstainers and relapsers 6 months post-quit day [37]. Another cessation study found alcohol consumption decreased for the 2 weeks post-quit day, but no difference was found between abstainers and relapsers [19]. Additional studies measuring alcohol use during a smoking cessation attempt have also found decreases in alcohol use, but these studies did not examine whether decreases differed by smoking abstinence status [3841].

Several conclusions can be drawn from prior research. First, evidence supports a potential decrease in alcohol consumption and binge drinking during a smoking cessation attempt with no identified studies indicating an increase in alcohol use. Second, studies examining co-action of smoking cessation with alcohol use found inconsistent results, with abstainers showing greater drops in alcohol use than relapsers in some studies, but not others. Therefore, it is unclear if decreases in alcohol use during a smoking cessation attempt occur regardless of smoking abstinence status or whether there is co-action, with decreases in alcohol use being higher among smoking abstainers than relapsers.

Although valuable, prior research examining co-action of smoking cessation and alcohol use is limited. Several studies exploring co-action examined very specific populations including the homeless [35], light smokers [37] and HIV+ smokers [10], whose results may not generalize to broader populations. Two other studies that examined co-action either examined alcohol use for only 2 weeks following quit day [19] or examined populations that were largely White (83%, 96%) [19, 36].

The goal of the current research was to examine co-action of abstinence status and alcohol use during a smoking cessation attempt among relatively large, diverse samples of adult smokers. Data from three smoking cessation studies were used to examine changes in alcohol use during a smoking quit attempt and to test for moderation by smoking abstinence. Gender and race/ethnicity were also tested as potential moderators. This research expands on past work by (1) examining three different measures of alcohol use (average weekly alcohol consumption, binge drinking, and alcohol-related problems); (2) examining moderation by smoking abstinence at both early and long-term post-quit follow-ups (the first several weeks and 26 weeks post-quit); and (3) including multiple studies with racially/ethnically diverse samples.

METHOD

Procedures

Participants

Data were collected as part of three separate smoking cessation studies: CARE, Break Free and Por Nuestra Salud (PNS). All participants were recruited in the Houston, Texas area. Approval was received from the Institutional Review Board of the University of Texas MD Anderson Cancer Center. Informed consent was obtained from all participants. The analysis was not pre-registered and the results should be considered exploratory.

CARE was a longitudinal cohort study examining the social determinants of smoking cessation. Participant recruitment and the study procedures have been reported elsewhere [42, 43]. Eligibility criteria included age 21 or older, ≥5 cigarettes/day and motivated to quit smoking within 30 days.

Break Free was a two-arm randomized clinical trial evaluating the efficacy of a palmtop computer-delivered smoking cessation intervention among African American smokers (both conditions were included in the present analysis). Participant recruitment and the study procedures have been reported elsewhere [44]. Eligibility criteria included age 21 to 65, ≥5 cigarettes/day and motivated to quit smoking within 2 weeks.

PNS was a longitudinal cohort study examining the social determinants of smoking cessation among Spanish-speaking individuals of Mexican heritage. Participant recruitment and the study procedures have been reported elsewhere [45]. Eligibility criteria included age 18 to 65, self-reported Mexican heritage, prefer to speak in Spanish, ≥5 cigarettes/day and motivated to quit smoking within 30 days.

All three studies shared similar exclusionary criteria: contraindication for nicotine patch use, active substance use dependence (including alcohol dependence and excluding nicotine), regular use of tobacco products other than cigarettes, use of other smoking cessation medications, pregnancy, participated in a smoking cessation program or study during the past 90 days or another household member enrolled.

Smoking cessation treatment

Participants from all three studies received 4 to 6 weeks of nicotine patches. Counseling is described in more detail below for each study. Note that none of the studies explicitly addressed alcohol use (i.e. it was not a module or pre-specified aspect of the intervention) unless it was relevant to that participant. For instance, if someone indicated that alcohol use was a trigger for smoking, it was then discussed.

In CARE, participants also received six counseling sessions based on the Treating Tobacco Use and Dependence Clinical Practice Guideline [34] and self-help materials [43]. Counseling sessions lasted 10 to 20 min. In-person sessions occurred 1 week before quit day, on quit day and at weeks 1, 2 and 4 post-quit. A telephone counseling session occurred 3 weeks post-quit.

Break Free participants were randomly assigned to standard cessation treatment or the standard treatment supplemented with treatment delivered via palmtop computer (computer-delivered treatment [CDT] condition) [44]. Standard treatment included culturally sensitive self-help materials (Pathways to Freedom) [46], and five in-person counseling sessions based on the Treating Tobacco Use and Dependence Clinical Practice Guideline [34]. In-person sessions were provided 12 and 5 days pre-quit day and at 3, 10 and 31 days post-quit day, and each session lasted 15 to 30 min. The CDT condition included everything the standard condition provided, in addition to 6 weeks of CDT, which began 12 days pre-quit day and continued to 31 days post-quit day.

In PNS, participants received cessation treatment that included Spanish-language self-help materials (Guia Para Dejar de Fumar) [47], and three brief in-person and three telephone counseling sessions based on an empirically validated intervention for Spanish-speaking smokers [48]. In-person counseling sessions occurred 1 week before quit day, on quit day and 3 weeks after. Telephone counseling sessions, which were conducted in Spanish and lasted about 15 min, occurred 3 days, 1 week and 2 weeks post-quit.

Measures

Analyses included individuals who endorsed drinking alcohol (i.e. those reporting no alcohol use were excluded). Alcohol users were identified by the following questions: CARE and Break Free—‘What is the maximum number of drinks you have consumed on any one occasion in the past 3 months?’ (must select 1 or more drinks); PNS—‘Do you ever drink alcohol?’ (must have indicated yes).

Alcohol use measures

Weekly alcohol consumption

Participants completed the Alcohol Quantity and Frequency Questionnaire, self-reporting how many standard alcoholic drinks they consumed on average each day of the week (e.g. ‘How many drinks do you consume on an average Monday’). These daily averages were summed to create an average number of drinks consumed per week [49]. Weekly alcohol consumption was collected as follows: CARE—baseline, quit day and 4 and 26 weeks post-quit; Break Free—baseline and 4.5 and 26 weeks post-quit; and PNS—baseline, quit day and 3 and 26 weeks post-quit.

Binge drinking

In CARE, participants responded to: ‘How often in the past three months have you consumed 5 or more drinks’. In Break Free, participants responded to: ‘How often (or how many occasions) in the past three months have you consumed 5 or more drinks?’ In PNS, participants responded to: ‘How often in the past 30 days have you consumed (4 if female; 5 if male) or more drinks?’ In all three studies, binge drinking was measured at baseline and 26 weeks post-quit [50].

Hazardous and harmful alcohol use (alcohol-related problems used here)

Participants in all three studies completed the alcohol module of the Patient Health Questionnaire (PHQ) [51]. Participants indicated if they ever drank alcohol followed by five questions asking if they had experienced a negative event associated with drinking (e.g. drunk or hungover at work, drove drunk) in the last 3 months. A positive response to one or more questions indicates hazardous and harmful alcohol use (note that the original PHQ uses the term ‘probable alcohol abuse’, but we have modified this to ‘hazardous and harmful alcohol use’ to be current with recent terminology; for ease of reading, this will be termed ‘alcohol-related problems’ throughout the article). In all three studies, alcohol-related problems were measured at baseline and 26 weeks post-quit.

Smoking status

Abstinence was defined in all studies as no smoking beginning on the quit date, verified by expired carbon monoxide level ≤10 ppm [52] or salivary cotinine value <20 ng/mL [53, 54]. Both an intention-to-treat (ITT) approach (participants lost to follow-up coded as relapsed), and a completers-only approach (participants lost to follow-up coded as missing), were used in the analyses. Relapse was not modeled as time-varying. Once a participant was classified as relapsed at one time point that status carried over to all subsequent time points. Smoking abstinence was analyzed at both early (4 weeks post-quit in CARE, 4.5 weeks in Break Free and 3 weeks in PNS) and long-term (26 weeks post-quit) follow-ups.

Time

Time was examined as a categorical variable. For the alcohol consumption analyses, four time points were examined in CARE and PNS (CARE: baseline [1-week pre-quit date], quit day, week 4 and week 26; PNS: baseline [1-week pre-quit date], quit day, week 3 and week 26) and three in Break Free (baseline [19 days pre-quit date], week 4.5 and week 26). For the binge drinking and alcohol-related problems analyses, baseline and week 26 were used in analyses for all three datasets.

Analysis plan

Three sets of longitudinal analyses were conducted for each dataset. Age, gender, race/ethnicity (in CARE), partner status, education level, cigarettes per day, time to first cigarette on waking and experimental condition (in Break Free) were included as covariates. Although we report results including current alcohol drinkers only here, we ran another set of analyses with the entire sample (i.e. drinkers and non-drinkers). Results were remarkably similar between the two sets of analyses.

The first set of analyses examined weekly alcohol consumption using mixed linear modeling with Proc Mixed in SAS (Enterprise Guide, Vers 6.1). These analyses used a categorical time variable to predict weekly alcohol consumption. Weekly alcohol consumption was skewed and kurtotic in all three datasets. Therefore, the weekly alcohol consumption measure was log transformed in CARE, Break Free and PNS, which helped normalize the variable.

The second set of analyses examined change in binge drinking from baseline to 26 weeks with generalized estimating equations using Proc Mixed in SAS (Enterprise Guide, Vers 6.1). Binge drinking was kurtotic and was log transformed in all datasets, which helped normalize the variable. Proc Mixed in SAS can analyze longitudinal data with multiple time points without dropping participants who have missing data at some time points [55]. Therefore, as binge drinking was collected at two time points, participants were retained in the analyses even if they had missing binge drinking data.

The third set of analyses examined change in the percentage meeting alcohol-related problems criteria from baseline to week 26. Generalized estimating equation analyses were conducted using Proc Genmod in SAS (Enterprise Guide, Vers 6.1) using a binomial distribution. Only participants who provided alcohol-related problems data at both baseline and week 26 were included in these analyses.

Covariates

Covariates were collected at baseline. Baseline smoking (i.e. average cigarettes smoked per day, time to first cigarette on waking [<5 min vs >5 min] [56]) and demographic (i.e. age, gender, relationship status, education level and race/ethnicity) measures were included as covariates in the statistical models examining alcohol consumption, binge drinking and alcohol-related problems in all three datasets. Treatment condition was also included as a covariate in all statistical models for Break Free.

Co-action analyses

For each of the above sets of analyses, smoking abstinence status (abstinent or relapsed) was tested as a moderator of differences in the alcohol use variables over time. Moderation was tested by both abstinence as measured at the early follow-up (week 4 in CARE, week 4.5 in Break Free and week 3 in PNS) and the long-term follow-up (week 26 in all data sets).

For alcohol consumption, if a significant interaction was found between time and abstinence status (early or long-term), a targeted contrast was completed comparing the pre-quit measures (baseline and quit day; baseline only in Break Free) versus the appropriate alcohol consumption measure post-quit day (week 4 in CARE, week 4.5 in Break Free and week 3 in PNS for early follow-up and week 26 for long-term follow-ups). For binge drinking and alcohol-related problems, abstinence status at both the early and long-term follow-up were tested as moderators of change from baseline to week 26. Results for analyses examining abstinence using the ITT and completers-only principles led to similar conclusions. Therefore, only the moderation by ITT abstinence results are presented.

Moderation by race and gender

For each data set, gender was tested as a moderator. In CARE, race/ethnicity was also examined as a moderator. All moderation analyses controlled for the other covariates. Note that these moderation analyses may be underpowered to detect significant effects.

RESULTS

Participant characteristics

In CARE, 424 participants were enrolled, but after excluding non-drinkers, 284 were included in the weekly alcohol consumption analyses. Of these 284, 29% (83) were non-Latino White, 31% (89) were African American and 40% (112) were Latino. Participants were included in binge drinking and alcohol-related problems analyses if they provided data at both baseline and week 26. In CARE, 281 participants provided binge drinking data and 284 provided alcohol-related problems data at both time points.

In Break Free, 399 African Americans were enrolled, but after excluding non-drinkers, 273 were included in the weekly alcohol consumption and probable alcohol abuse analyses. Binge drinking outcomes were available from 270 participants.

In PNS, 199 participants were enrolled, but after excluding non-drinkers, 170 were included in the weekly alcohol consumption and alcohol-related problems analyses. Binge drinking outcomes were available from 158 participants.

Regarding tobacco abstinence data, in CARE, there were 46 participants with missing data at week 4 and 44 participants with missing data at week 26. In Break Free, there were 49 participants missing abstinence data at week 4.5 and 42 participants with missing data at week 26. In PNS, 25 participants were missing abstinence data at week 3 and 32 participants were missing data at week 26. Table 1 presents descriptive statistics and abstinence percentages for all three studies.

TABLE 1.

Participant characteristics for CARE, Break Free and PNS.

CARE Break Free PNS
Age 39.6 (11.5) 40.6 (10.0) 37.1 (10.1)
Gender (% female) 52% 54% 34%
Education (% > high school) 60% 48% 24%
Partner status (% married/living with partner) 37% 42% 68%
% smoking within 5 min of waking 60% 57% 17%
Baseline cigarettes per day 20.3 (10.6) 20.6 (12.8) 16.0 (8.4)
Early abstinence (ITT) 15% 8% 21%
Early abstinence (completers) 18% 10% 25%
Late abstinence (ITT) 4% 3% 5%
Late abstinence (completers) 4% 4% 9%
Weekly alcohol consumption
 Baseline
  Mean 11.63 (14.86) 13.62 (22.75) 10.82 (19.72)
  Median 6 7 4
  Range 0–94 0–250 0–150
 Quit day
  Mean 10.38 (14.25) 9 (16.81)
  Median 6 2
  Range 0–102 0–86
 Week 4 (abstainers)
  Mean 8.20 (12.45) 16.86 (24.73) 7.69 (15.39)
  Median 3 11 0.5
  Range 0–60 0–71 0–66
 Week 4 (relapsers)
  Mean 8.05 (11.76) 9.18 (11.76) 5.64 (9.80)
  Median 5 5 1
  Range 0–86 0–62 0–61
 Week 26 (abstainers)
  Mean 4.90 (4.72) 4.5 (6.59) 14.88 (21.38)
  Median 2.5 1.5 4
  Range 0–15 0–16 0–64
 Week 26 (relapsers)
  Mean 9.02 (12.68) 10.10 (10.85) 6.11 (13.05)
  Median 4 6.5 1
  Range 0–66 0–47 0–92

Note: Early abstinence refers to abstinence collected in the immediate weeks post-quit day (CARE: 4 weeks; Break Free: 4.5 weeks; PNS: 3 weeks). Late abstinence refers to abstinence collected at Week 26 post-quit. Completers refer to only participants who completed the assessment.

Abbreviations: ITT, intention to treat; PNS, Por Nuestra Salud.

Alcohol consumption analyses

In CARE, significant differences were found between alcohol consumption at different time points, with alcohol consumption at baseline significantly higher than alcohol consumption at quit day, week 4 and week 26 (see Table 2, Model 1A). Additional comparisons indicated that weekly alcohol consumption on quit day was significantly higher than at week 4 (t(275) = 3.82, P < 0.001) and week 26 (t(275) = 3.75, P < 0.001) post-quit. The week 4 and week 26 post-quit measures were not significantly different from each other (t(275) = −1.08, P = 0.28). Figure 1 presents results of the adjusted means.

TABLE 2.

Mixed linear analyses to predict weekly alcohol consumption.

Predictors β (SE) 95% CI P df F P
CARE Model 1A
 Time variable 3, 275 17.09 <0.001
  Intercept 2.00 (3.29) (1.39, 2.61) <0.001
  Quit day −0.13 (0.53) (−0.21, −0.04) 0.003
  Week 4 post-quit −0.31 (0.58) (−0.41, −0.21) <0.001
  Week 26 post-quit −0.38 (0.71) (−0.51, −0.25) <0.001
Break Free Model 1B
 Time variable 2, 265 12.08 <0.001
  Intercept 2.68 (0.41) (1.87, 3.50) <0.001
  Week 4.5 post-quit −0.31 (0.07) (−0.44, −0.18) <0.001
  Week 26 post-quit −0.28 (0.09) (−0.45, −0.11) 0.002
PNS Model 1C
 Time variable 3, 162 10.21 <0.001
  Intercept 1.28 (0.42) (0.44, 2.12) <0.001
  Quit day −0.19 (0.07) (−0.32, −0.06) 0.004
  Week 3 post-quit −0.43 (0.08) (−0.58, −0.27) <0.001
  Week 26 post-quit −0.34 (0.10) (−0.54, −0.14) 0.001

Note: In all three data sets, the baseline time point is the comparison group for the time variable results. F and the corresponding P provide results for the type III tests of the significance for the time categorical variable fixed effect.

Abbreviation: PNS, Por Nuestra Salud.

FIGURE 1.

FIGURE 1

Adjusted log transformed means for alcohol consumption over time. The vertical axis indicates the average number of drinks (log transformed) per week that participants reported.

In Break Free’s preliminary analyses, the experimental treatment variable (CDT vs. no CDT) did not predict weekly alcohol consumption nor did it interact with time, therefore, the condition was only included as a covariate. The time variable was significant, and week 4.5 and week 26 alcohol consumption were both significantly lower than at baseline (Table 2, Model 1B). Follow-up analyses indicated that week 4.5 and week 26 weekly alcohol consumption were not significantly different from each other (t(265) = −0.33, P = 0.74) (see Figure 1 for graph of adjusted means).

In PNS, the time effect was a significant predictor (Table 2, Model 1C) with alcohol consumption at quit day, week 3 and week 26 significantly lower than at baseline. Follow-up analyses indicated that weekly alcohol consumption at week 3 was significantly lower than quit day (t(162) = 3.60, P < 0.001). Weekly alcohol consumption at week 26 was not significantly lower than quit day consumption (t(162) = 1.60, P = 0.11). Week 3 and 26 alcohol consumption were also not significantly different from each other (t(162) = −0.92, P = 0.36) (see Figure 1 for graph of adjusted means).

Binge drinking analyses

The next set of analyses used the categorical time variable (baseline and week 26) and covariates to predict binge drinking. In CARE, the time variable was a significant predictor (see Table 3, Model 2A) of binge drinking. In Break Free, the experimental condition variable did not predict binge drinking or interact with time, therefore, condition was only included as a covariate. The time variable was a significant predictor (see Table 3, Model 2B). The significant time effect found in CARE and Break Free indicated a decrease in binge drinking from baseline to 26 weeks post-quit. For PNS, the time variable was not a significant predictor (F(1, 161) = 0.14, P = 0.71). See Figure 2 for graphs of adjusted means.

TABLE 3.

Mixed linear analyses to predict binge drinking.

Predictors β (SE) 95% CI P df F P
CARE Model 2A
 Time variable 1, 274 3.94 0.04
  Intercept 1.28 (0.26) (0.77, 1.80) <0.001
  Week 26 post-quit −0.14 (0.07) (−0.28, −0.01) 0.04
Break Free Model 2B
 Time variable 1, 263 10.41 0.001
  Intercept 1.64 (0.32) (1.00, 2.27) <0.001
  Week 26 post-quit −0.22 (0.07) (0.08, 0.34) 0.001
PNS Model 2C
 Time variable 1, 161 1.14 0.29
  Intercept 0.29 (0.30) (−0.30, 0.90) 0.33
  Week 26 post-quit 0.08 (007) (−0.70, 0.22) 0.29

Note: F and the corresponding P provide results for the type III tests of the significance for the time categorical variable fixed effect.

Abbreviation: PNS, Por Nuestra Salud.

FIGURE 2.

FIGURE 2

Adjusted log transformed binge drinking episodes over time. The vertical axis indicates the number of times (log transformed) participants reported binge drinking in the last 3 months for CARE and Break Free or in the last month for Por Nuestra Salud (PNS).

Alcohol-related problems analyses

The next set of analyses used the time variable and covariates to predict alcohol-related problems. In CARE, the time variable was a significant predictor (estimate = 0.43 (0.17), 95% CI = −0.09, 0.77, P = 0.01), indicating that the percentage of participants with alcohol-related problems decreased from baseline to week 26. In Break Free, the experimental condition did not predict alcohol-related problems nor did it interact with time, therefore, condition was only included as a covariate. The time variable was significant (estimate = 0.77 (0.21), 95% CI = 0.36, 1.18, P < 0.001), indicating a decrease in the percentage of participants with alcohol-related problems from baseline to week 26. In PNS, the time variable was non-significant (estimate = 0.11 (0.25), 95% CI = −0.37, 59, P = 0.65). See Figure 3 and Table 4 for alcohol-related problems results.

FIGURE 3.

FIGURE 3

Adjusted percentages for alcohol-related problems over time. The vertical axis indicates the percentage of participants who met criteria for alcohol-related problems at each time point.

TABLE 4.

Generalized estimating equation to predict alcohol-related problems.

Predictors β (SE) 95% CI P df χ2 P
CARE Model 3A
 Time variable 1 6.41 0.01
  Intercept 0.11 (0.63) (−1.10, 1.32) 0.86
  Week 26 post-quit 0.43 (0.17) (0.09, −0.77) 0.01
Break Free Model 3B
 Time variable 1 14.44 0.001
  Intercept 0.58 (0.78) (−0.97, 2.12) 0.46
  Week 26 post-quit 0.77 (0.21) (0.36, 1.18) 0.001
PNS Model 3C
 Time variable 1 0.20 0.65
  Intercept −1.15 (0.87) (−2.84, 0.55) 0.18
  Week 26 post-quit 0.11 (0.24) (−0.37, 0.59) 0.65

Note: F and the corresponding P provide results for the type III tests of the significance for the time categorical variable fixed effect.

Abbreviation: PNS, Por Nuestra Salud.

Co-action analyses

Co-action analyses were performed using both early abstinence status and late abstinence status as moderators of the time variable predicting alcohol consumption, binge drinking and alcohol-related problems in CARE, Break Free and PNS. In total, 18 co-action moderation analyses were performed; two (early and late abstinence status) each for alcohol consumption, binge drinking and probable alcohol use for each of the three data sets. Of the 18 co-action analyses, all of the interactions of time and abstinence status (i.e. the effect of time was not moderated by abstinence status) were non-significant (all P >0.25), except for late abstinence status moderating the time variable predicting alcohol consumption in Break Free. For this analysis, ITT abstinence from week 26 post-quit was added as a predictor along with time and the covariates. Week 26 ITT abstinence was a non-significant (F(1, 264) = 0.55, P = 0.50) predictor of weekly alcohol consumption. Next, the interaction between abstinence status and time was added to the model and it was significant (F(2, 264) = 5.29, P = 0.005). Pair-wise comparisons indicated that weekly alcohol consumption was not significantly different between smokers who remained abstinent at week 26 and smokers who lapsed by week 26 at either baseline or week 3. However, abstainers reported significantly fewer drinks per week than abstainers at 26 weeks post-quit (t = −2.11, P = 0.03). For relapsers, their weekly alcohol consumption increased significantly from baseline to week 26 post-quit (t = 2.85, P = 0.004), Abstainers’ weekly alcohol consumption did not change significantly from baseline to week 26 post-quit (t = −1.62, P = 0.11) (see Figure 4).

FIGURE 4.

FIGURE 4

Adjusted log transformed means for weekly alcohol consumption for relapsers versus abstainers in Break Free. The vertical axis indicates the average log transformed number of drinks per week reported by participants.

Moderation by race and gender

For all three measures of alcohol use in all three datasets, gender was not a significant moderator of time. In CARE, race/ethnicity was not a significant moderator for any of the three measures of alcohol use. Results available from authors on request.

DISCUSSION

The current study examined changes in alcohol use during a smoking quit attempt, including testing for co-action (i.e. that success or failure at quitting smoking will be associated with differential changes in alcohol use). Results are generally consistent with previous research indicating that alcohol consumption decreases during a smoking cessation attempt. In all three studies, decreases in weekly alcohol consumption were present at 3 to 5 weeks post-quit day, and this decrease was maintained through 6 months in two of the three data sets. We found mixed results for binge drinking with decreases in CARE and Break Free, but not PNS. This research also provides some of the first evidence that alcohol-related problems decrease during a smoking cessation attempt as both CARE and Break Free demonstrated this effect. Finally, there was very little evidence for co-action as changes in alcohol use were not limited to those who were abstinent. Abstainers showed a larger decrease than relapsers only for the long-term follow-up of alcohol consumption in Break Free.

Decreases in alcohol consumption occurred for both abstainers and relapsers. In the one analysis that found moderation by smoking abstinence status (Break Free), decreases were larger for abstainers, but were also found for relapsers. These findings could potentially be accounted for by behavioral changes that occur and are maintained during a smoking quit attempt. That is, if smokers make and maintain behavioral changes (e.g. avoiding bars or friends who smoke and drink), those changes may lead to decreases in alcohol consumption, regardless of their success at influencing smoking cessation. Similarly, motivation to make healthy lifestyle changes might reduce alcohol consumption and continue even after a lapse to smoking. It is unclear whether explanations emphasizing the role of smoking abstinence in decreasing alcohol consumption, including smoking acting as a cue to drink or avoiding drinking to reduce cravings for a cigarette [29, 32, 33] can be answered by these findings. Assessing smoking and alcohol use more frequently (e.g. daily, weekly) would provide a more thorough assessment. Nonetheless, when decreases in binge drinking (Break Free) and alcohol-related problems (CARE, Break Free) were found, they occurred equally for both relapsers and abstainers. As with alcohol consumption, behavioral change and motivational explanations may be a better fit for these results than explanations focused on the role of smoking abstinence, although future research is needed to fully investigate this hypothesis.

Results have important clinical implications. The current findings fit with a growing literature suggesting that fear of increased alcohol use during a quit attempt is unwarranted and that smokers who attempt to quit smoking, regardless of success, will at worst experience no change in alcohol use and at best decrease alcohol use [2024, 26, 27]. These benefits occur with average alcohol consumption, binge drinking and alcohol-related problems. The smoking cessation treatments in the current studies did not explicitly focus on alcohol use, although drinking was discussed if it was an area of concern for the participant. This suggests that decreases in alcohol during a smoking quit attempt can occur with standard smoking cessation treatment (the combination of nicotine replacement therapy and brief smoking cessation counseling) [57]. Additionally, alcohol use may be reduced even further with treatments specifically designed to address both smoking cessation and alcohol risk reduction, at least among smokers who are able to successfully quit [18]. An important caveat is that in all three studies, participants used nicotine patches and received counseling. It is unclear whether these results would generalize to smoking quit attempts that do not involve these treatment components or that entail different treatments.

PNS results were different than the other data sets. The lack of significant results in PNS could be because of a smaller sample size or because the sample consisted of Spanish speaking, predominantly Mexican immigrants to the United States, and change in alcohol use during a cessation attempt could be culturally dependent or influenced by acculturation status. Further research is warranted.

Co-action was defined as a change in alcohol use that differed by abstinence status (abstinent vs smoking). However, measures of smoking abstinence and alcohol use were only measured together at several time points and in a relatively gross fashion. Therefore, these findings could mask co-action that occurs at a more ‘micro’ or ‘episodic’ level. For example, choosing to refrain from smoking at a party might contribute to reduced alcohol consumption, versus choosing to smoke contributing to increase drinking. A more detailed measurement procedure such as ecological momentary assessment could better pinpoint when smoking occurs during a quit attempt and how that influences alcohol use.

Limitations and strengths

Despite using multiple studies with diverse samples, there are several limitations to note. Alcohol use was self-reported, relying on participants to accurately recall their use. The measures of binge drinking in CARE and Break Free did not adjust the definition of binge drinking by participant gender. In addition, participants were not recruited based on their alcohol use, which might lead to underpowered analyses. Missing data were present across all three studies and should be considered on interpretation of the results. It is possible that for some analyses (e.g. co-action) we were underpowered to detect significant effects. It is unclear how well these results would generalize to smokers trying to quit without nicotine replacement and counseling. Future research should explore explanations for decreases in alcohol use during a cessation attempt, which the current studies were not designed to test. Finally, the sample excluded those with alcohol dependence, and recruitment for all studies was conducted in a single city, which could limit generalizability. Strengths include the consideration of several types of alcohol use outcomes, inclusion of measures of alcohol use and smoking abstinence in both the short and long-term, and examination of racially and ethnically diverse samples.

CONCLUSION

Across three unique data sets using diverse samples, little support was found for co-action of smoking abstinence and change in alcohol use during a smoking cessation attempt. Results indicate that decreases in alcohol use during a smoking cessation attempt are not dependent on successfully achieving and maintaining smoking abstinence. These findings have important clinical implications as there was no evidence of a negative impact (and some evidence of a positive impact) of smoking cessation treatment on alcohol use.

Funding information

National Institute on Drug Abuse, Grant/Award Number: R01DA014818; National Cancer Institute, Grant/Award Numbers: R01CA094826, R25TCA57730, U54CA153505, P30CA016672, P30CA042014; National Center on Minority Health and Health Disparities, Grant/Award Numbers: P60MD000503, R00MD010468; American Cancer Society, Grant/Award Number: MRSG-15-018-01-CPPB. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Footnotes

DECLARATION OF INTERESTS

P.M.C. has served on the scientific advisory board of Pfızer Pharmaceuticals and has conducted educational talks sponsored by Pfızer on smoking cessation for physicians in 2008. No other financial disclosures were reported by the authors of this paper.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the corresponding author upon reasonable request.

REFERENCES

  • 1.U.S. Department of Health and Human Services. The health consequences of smoking—50 years of progress: a report of the surgeon general Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2014. [Google Scholar]
  • 2.Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United States, 2000. JAMA. 2004;291(10):1238–45. 10.1001/jama.291.10.1238 [DOI] [PubMed] [Google Scholar]
  • 3.Hart CL, Smith GD, Gruer L, Watt GC. The combined effect of smoking tobacco and drinking alcohol on cause-specific mortality: a 30 year cohort study. BMC Public Health. 2010;10(1):1. 10.1186/1471-2458-10-789 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Pelucchi C, Gallus S, Garavello W, Bosetti C, La Vecchia C. Cancer risk associated with alcohol and tobacco use: focus on upper aero-digestive tract and liver. Alcohol Res. 2006;29(3):193. [PMC free article] [PubMed] [Google Scholar]
  • 5.Taylor B, Rehm J. When risk factors combine: the interaction between alcohol and smoking for aerodigestive cancer, coronary heart disease, and traffic and fire injury. Addict Behav. 2006;31(9):1522–35. 10.1016/j.addbeh.2005.11.008 [DOI] [PubMed] [Google Scholar]
  • 6.Bobo JK, Husten C. Sociocultural influences on smoking and drinking. Alcohol Res Health. 2000;24(4):225–32. [PMC free article] [PubMed] [Google Scholar]
  • 7.Dani JA, Harris RA. Nicotine addiction and comorbidity with alcohol abuse and mental illness. Nat Neurosci. 2005;8(11):1465–70. 10.1038/nn1580 [DOI] [PubMed] [Google Scholar]
  • 8.Substance Abuse and Mental Health Services Administration. Results from the 2013 National Survey on Drug Use and Health: summary of National Findings, NSDUH Series H-48, HHS Publication No. (SMA) 14-4863 Rockville, MD: Substance Abuse and Mental Health Services Administration; 2014. [Google Scholar]
  • 9.Dierker L, Lloyd-Richardson E, Stolar M, Flay B, Tiffany S, Collins L, et al. The proximal association between smoking and alcohol use among first year college students. Drug Alcohol Depend. 2006;81(1):1–9. 10.1016/j.drugalcdep.2005.05.012 [DOI] [PubMed] [Google Scholar]
  • 10.Lisha NE, Carmody TP, Humfleet GL, Delucchi KL. Reciprocal effects of alcohol and nicotine in smoking cessation treatment studies. Addict Behav. 2014;39(3):637–43. 10.1016/j.addbeh.2013.11.018 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Piasecki TM, McCarthy DE, Fiore MC, Baker TB. Alcohol consumption, smoking urge, and the reinforcing effects of cigarettes: an ecological study. Psychol Addict Behav. 2008;22(2):230–9. 10.1037/0893-164X.22.2.230 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Shapiro D, Jamner LD, Davydov DM, James P. Situations and moods associated with smoking in everyday life. Psychol Addict Behav. 2002;16(4):342–5. 10.1037/0893-164X.16.4.342 [DOI] [PubMed] [Google Scholar]
  • 13.Bjartveit K, Tverdal A. Health consequences of sustained smoking cessation. Tob Control. 2009. [DOI] [PubMed] [Google Scholar]
  • 14.Bosetti C, Garavello W, Gallus S, La Vecchia C. Effects of smoking cessation on the risk of laryngeal cancer: an overview of published studies. Oral Oncol. 2006;42(9):866–72. 10.1016/j.oraloncology.2006.02.008 [DOI] [PubMed] [Google Scholar]
  • 15.Hayes RB, Bravo-Otero E, Kleinman DV, Brown LM, Fraumeni JF, Harty LC, et al. Tobacco and alcohol use and oral cancer in Puerto Rico. Cancer Causes Control. 1999;10(1):27–33. 10.1023/A:1008876115797 [DOI] [PubMed] [Google Scholar]
  • 16.Cairney J, Leatherdale ST, Faulkner GE. A longitudinal examination of the interrelationship of multiple health behaviors. Am J Prev Med. 2014;47(3):283–9. 10.1016/j.amepre.2014.04.019 [DOI] [PubMed] [Google Scholar]
  • 17.Prochaska JJ, Spring B, Nigg CR. Multiple health behavior change research: an introduction and overview. Prev Med. 2008;46(3):181–8. 10.1016/j.ypmed.2008.02.001 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Correa-Fernández V, Díaz-Toro EC, Reitzel LR, Guo L, Chen M, Li Y, et al. Combined treatment for at-risk drinking and smoking cessation among Puerto Ricans: a randomized clinical trial. Addict Behav. 2017;65:185–92. 10.1016/j.addbeh.2016.10.009 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19.Berg KM, Piper ME, Smith SS, Fiore MC, Jorenby DE. Defining and predicting short-term alcohol use changes during a smoking cessation attempt. Addict Behav. 2015;48:52–7. 10.1016/j.addbeh.2015.04.004 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Brady KT, Sonne SC. The role of stress in alcohol use, alcoholism treatment, and relapse. Alcohol Res. 1999;23(4):263. [PMC free article] [PubMed] [Google Scholar]
  • 21.Piasecki TM, Jorenby DE, Smith SS, Fiore MC, Baker TB. Smoking withdrawal dynamics: I. Abstinence distress in lapsers and abstainers. J Abnorm Psychol. 2003;112(1):3–13. 10.1037/0021-843X.112.1.3 [DOI] [PubMed] [Google Scholar]
  • 22.Piasecki TM, Jorenby DE, Smith SS, Fiore MC, Baker TB. Smoking withdrawal dynamics: II. Improved tests of withdrawal-relapse relations. J Abnorm Psychol. 2003;112(1):14–27. 10.1037/0021-843X.112.1.14 [DOI] [PubMed] [Google Scholar]
  • 23.Sayette MA. Does drinking reduce stress? Alcohol Res Health. 1999;23(4):250–5. [PMC free article] [PubMed] [Google Scholar]
  • 24.D’souza MS, Markou A. Neuronal mechanisms underlying development of nicotine dependence: implications for novel smoking-cessation treatments. Addict Sci Clin Pract. 2011;6(1):4–16. [PMC free article] [PubMed] [Google Scholar]
  • 25.Boileau I, Assaad JM, Pihl RO, Benkelfat C, Leyton M, Diksic M, et al. Alcohol promotes dopamine release in the human nucleus accumbens. Synapse. 2003;49(4):226–31. 10.1002/syn.10226 [DOI] [PubMed] [Google Scholar]
  • 26.Söderpalm B, Ericson M. Neurocircuitry involved in the development of alcohol addiction: the dopamine system and its access points. In: Behavioral neurobiology of alcohol addiction Berlin: Springer; 2011. p. 127–61. [DOI] [PubMed] [Google Scholar]
  • 27.Söderpalm B, Löf E, Ericson M. Mechanistic studies of ethanol’s interaction with the mesolimbic dopamine reward system. Pharmacopsychiatry. 2009;42(S 01):S87–94. [DOI] [PubMed] [Google Scholar]
  • 28.Kahler CW, Spillane NS, Metrik J. Alcohol use and initial smoking lapses among heavy drinkers in smoking cessation treatment. Nicotine Tob Res. 2010;12(7):781–5. 10.1093/ntr/ntq083 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Drobes DJ. Cue reactivity in alcohol and tobacco dependence. Alcohol Clin Exp Res. 2002;26(12):1928–9. 10.1111/j.1530-0277.2002.tb02506.x [DOI] [PubMed] [Google Scholar]
  • 30.Burton SM, Tiffany ST. The effect of alcohol consumption on craving to smoke. Addiction. 1997;92(1):15–26. 10.1111/j.1360-0443.1997.tb03634.x [DOI] [PubMed] [Google Scholar]
  • 31.Sayette MA, Martin CS, Wertz JM, Perrott MA, Peters AR. The effects of alcohol on cigarette craving in heavy smokers and tobacco chippers. Psychol Addictive Behav. 2005;19(3):263–70. 10.1037/0893-164X.19.3.263 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32.Businelle MS, Lam CY, Kendzor DE, Cofta-Woerpel L, McClure JB, Cinciripini PM, et al. Alcohol consumption and urges to smoke among women during a smoking cessation attempt. Exp Clin Psychopharmacol. 2013;21(1):29–37. 10.1037/a0031009 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33.Lam CY, Businelle MS, Cofta-Woerpel L, McClure JB, Cinciripini PM, Wetter DW. Positive smoking outcome expectancies mediate the relation between alcohol consumption and smoking urge among women during a quit attempt. Psychol Addict Behav. 2014;28(1):163–72. 10.1037/a0034816 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Clinical Practice Guideline Treating Tobacco Use and Dependence 2008 Update Panel, Liaisons, and Staff. A clinical practice guideline for treating tobacco use and dependence: 2008 update: a US public health service report. Am J Prev Med. 2008;35(2):158–76. 10.1016/j.amepre.2008.04.009 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.Reitzel LR, Nguyen N, Eischen S, Thomas J, Okuyemi KS. Is smoking cessation associated with worse comorbid substance use outcomes among homeless adults? Addiction. 2014;109(12):2098–104. 10.1111/add.12688 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36.Murray RP, Istvan JA, Voelker HT. Does cessation of smoking cause a change in alcohol consumption? Evidence from the Lung Health Study. Subst Use Misuse. 1996;31(2):141–56. 10.3109/10826089609045804 [DOI] [PubMed] [Google Scholar]
  • 37.Stahre MA, Toomey TL, Erickson DJ, Forster JL, Okuyemi KS, Ahluwalia JS. The effects of a tobacco intervention on binge drinking among African American light smokers. J Addict Dis. 2013;32(4):377–86. 10.1080/10550887.2013.849972 [DOI] [PubMed] [Google Scholar]
  • 38.Hughes JR, Hatsukami D. Signs and symptoms of tobacco withdrawal. Arch Gen Psychiatry. 1986;43(3):289–94. 10.1001/archpsyc.1986.01800030107013 [DOI] [PubMed] [Google Scholar]
  • 39.Metrik J, Spillane NS, Leventhal AM, Kahler CW. Marijuana use and tobacco smoking cessation among heavy alcohol drinkers. Drug Alcohol Depend. 2011;119(3):194–200. 10.1016/j.drugalcdep.2011.06.004 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Mitchell JM, Teague CH, Kayser AS, Bartlett SE, Fields HL. Varenicline decreases alcohol consumption in heavy-drinking smokers. Psychopharmacology (Berl). 2012;223(3):299–306. 10.1007/s00213-012-2717-x [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Stamford BA, Matter S, Fell RD, Papanek P. Effects of smoking cessation on weight gain, metabolic rate, caloric consumption, and blood lipids. Am J Clin Nutr. 1986;43(4):486–94. 10.1093/ajcn/43.4.486 [DOI] [PubMed] [Google Scholar]
  • 42.Businelle MS, Kendzor DE, Reitzel LR, Costello TJ, Cofta-Woerpel L, Li Y, et al. Mechanisms linking socioeconomic status to smoking cessation: a structural equation modeling approach. Health Psychol. 2010;29(3):262–73. 10.1037/a0019285 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43.Kendzor DE, Costello TJ, Li Y, Vidrine JI, Mazas CA, Reitzel LR, et al. Race/ethnicity and multiple cancer risk factors among individuals seeking smoking cessation treatment. Cancer Epidemiol Prevention Biomarkers. 2008;17(11):2937–45. 10.1158/1055-9965.EPI-07-2795 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Kendzor DE, Cofta-Woerpel LM, Mazas CA, Li Y, Vidrine JI, Reitzel LR, et al. Socioeconomic status, negative affect, and modifiable cancer risk factors in African-American smokers. Cancer Epidemiol Biomarkers Prev. 2008;17(10):2546–54. 10.1158/1055-9965.EPI-08-0291 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 45.Kendzor DE, Businelle MS, Reitzel LR, Castro Y, Vidrine JI, Mazas CA, et al. The influence of discrimination on smoking cessation among Latinos. Drug Alcohol Depend. 2014;136:143–8. 10.1016/j.drugalcdep.2014.01.003 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46.Robinson RG. Pathways to freedom: winning the fight against tobacco US Department of Health and Human Services, Centers for Disease Control and Prevention; 2006. [Google Scholar]
  • 47.Pérez-Stable EJ, Sabogal F, Marín G, Marín BV, Otero-Sabogal R. Evaluation of “Guia para Dejar de Fumar,” a self-help guide in Spanish to quit smoking. Public Health Rep. 1991;106(5):564–70. [PMC free article] [PubMed] [Google Scholar]
  • 48.Wetter DW, Mazas C, Daza P, Nguyen L, Fouladi RT, Li Y, et al. Reaching and treating Spanish-speaking smokers through the National Cancer Institute’s cancer information service: a randomized controlled trial. Cancer. 2007;109(S2):406–13. 10.1002/cncr.22360 [DOI] [PubMed] [Google Scholar]
  • 49.Sobell LC, Agrawal S, Sobell MB, Leo GI, Young LJ, Cunningham JA, et al. Comparison of a quick drinking screen with the timeline follow-back for individuals with alcohol problems. J Stud Alcohol. 2003;64(6):858–61. 10.15288/jsa.2003.64.858 [DOI] [PubMed] [Google Scholar]
  • 50.National Institute on Alcohol Abuse and Alcoholism. The physicians’ guide to helping patients with alcohol problems U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism; 1995. [Google Scholar]
  • 51.Spitzer RL, Kroenke K, Williams JB, Group PHQPCS. Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. JAMA. 1999;282(18):1737–44. 10.1001/jama.282.18.1737 [DOI] [PubMed] [Google Scholar]
  • 52.Hajek P, West R, Lee A, Foulds J, Owen L, Eiser JR, et al. Randomized controlled trial of a midwife-delivered brief smoking cessation intervention in pregnancy. Addiction. 2001;96(3):485–94. 10.1046/j.1360-0443.2001.96348511.x [DOI] [PubMed] [Google Scholar]
  • 53.McBride CM, Curry SJ, Lando HA, Pirie PL, Grothaus LC, Nelson JC. Prevention of relapse in women who quit smoking during pregnancy. Am J Public Health. 1999;89(5):706–11. 10.2105/AJPH.89.5.706 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54.Reitzel LR, Vidrine JI, Businelle MS, Kendzor DE, Costello TJ, Li Y, et al. Preventing postpartum smoking relapse among diverse low-income women: a randomized clinical trial. Nicotine Tob Res. 2010;12(4):326–35. 10.1093/ntr/ntq001 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55.Singer JD, Willett JB. Applied longitudinal data analysis: modeling change and event occurrence. Oxford; New York: Oxford University Press; 2003. xx, 644 p. 10.1093/acprof:oso/9780195152968.001.0001 [DOI] [Google Scholar]
  • 56.Heatherton TF, Kozlowski LT, Frecker RC, Rickert W, Robinson J. Measuring the heaviness of smoking: using self-reported time to the first cigarette of the day and number of cigarettes smoked per day. Br J Addict. 1989;84(7):791–800. 10.1111/j.1360-0443.1989.tb03059.x [DOI] [PubMed] [Google Scholar]
  • 57.Fiore MC, Jaén CR, Baker TB, Bailey WC, Benowitz N, Curry S, et al. Clinical practice guideline US Department of Health and Human Services. Public Health Service; 2008. p. 1196–9. [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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