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Published in final edited form as: Drug Alcohol Depend. 2013 Sep 27;134:391–395. doi: 10.1016/j.drugalcdep.2013.09.019

Achieving smoking abstinence is associated with decreased cocaine use in cocaine-dependent patients receiving smoking-cessation treatment

Theresa M Winhusen a, Frankie Kropp a, Jeff Theobald a, Daniel F Lewis a
PMCID: PMC3889710  NIHMSID: NIHMS528012  PMID: 24128381

Abstract

Background

Past research suggests that a significant relationship exists between cigarette smoking and illicit-stimulant abuse. The present study evaluated the association between achieving smoking abstinence in response to smoking-cessation treatment (SCT) and illicit-stimulant abstinence in cocaine- and/or methamphetamine-dependent participants.

Methods

Secondary analysis of a randomized, 10-week trial conducted at 12 substance use disorder (SUD) treatment programs. Two hundred and sixty seven adults, meeting DSM-IV-TR criteria for cocaine and/or methamphetamine-dependence and interested in quitting smoking were randomized to SUD treatment as usual plus SCT consisting of weekly individual smoking cessation counseling, extended-release (XL) bupropion (300 mg/day), nicotine inhaler, and contingency management for smoking abstinence. Illicit-stimulant-abstinence was measured by self-report and urine drug screens. Smoking abstinence was assessed via self-report and carbon monoxide levels.

Results

A significant effect was found for the cocaine-dependent subsample (N=147) in which participants who stopped smoking were abstinent for illicit stimulants an average of 78.2% of the post-smoking-quit weeks (weeks 4-10) relative to 63.6% in participants who continued smoking (X2(1)=8.55, p<.01, d=0.36). No significant effects were found for the sample as a whole (N=249) or for the methamphetamine-dependent subsample (N=102).

Conclusions

The present results suggest that cocaine-dependent patients achieving smoking abstinence in response to SCT might evidence not only improved smoking outcomes but improved cocaine-use outcomes as well. Future research to replicate this finding appears warranted.

Keywords: cocaine, smoking cessation, methamphetamine

1. INTRODUCTION

A link between cigarette smoking and cocaine abuse has been established in pre-clinical, human laboratory, and clinical studies. In mice, exposure to nicotine prior to cocaine increases behaviors associated with cocaine and results in synaptic changes in the striatum and amygdala that are not associated with nicotine or cocaine alone (Huang et al., 2013; Levine et al., 2011). Pre-treatment of rhesus monkeys with nicotine prior to cocaine enhances the preference for cocaine (Mello and Newman, 2011) while the combination of nicotine and cocaine results in greater drug administration than either substance alone (Mello et al., 2013; Mello and Newman, 2011). Human laboratory studies have found that cocaine administration increases the rate of cigarette smoking (Nemeth-Coslett et al., 1986; Roll et al., 1997) and that mecamylamine, a nicotine antagonist, reduces cue-induced cocaine craving (Reid et al., 1999) while nicotine increases it (Reid et al., 1998).

Clinically, the rates of cocaine dependence are significantly higher in cocaine users who initiated cocaine after having started smoking compared to both non-smokers and those who initiated cocaine before smoking (Levine et al., 2011). The rate of smoking in cocaine abusers is 75-80% (Budney et al., 1993; Gorelick et al., 1997; Sees and Clark, 1993) and smoking cigarettes is associated with more severe cocaine addiction, including more frequent cocaine use, a greater likelihood of injecting or smoking cocaine, and more severe employment and legal difficulties (Budney et al., 1993; Roll et al., 1997). In addition, smoking status is a significant predictor of cocaine use (Frosch et al., 2000; Patkar et al., 2003; Roll et al., 1996) and cocaine users who smoke concurrently smoke more cigarettes (Brewer et al., 2013; Roll et al., 1996) and experience greater cravings for both nicotine and cocaine (Brewer et al., 2013).

A smaller body of research also suggests that there is a connection between methamphetamine use and cigarette smoking. In rats, co-administration of nicotine and methamphetamine results in expression of different genes in the brain than those expressed when either drug is administered alone (Saint-Preux et al., 2013). It has been suggested that nicotine and methamphetamine may substitute for each other, to some extent (Gatch et al., 2008; Hiranita, et al., 2006). In nicotine-naïve rats, nicotine priming alone reinstates methamphetamine-seeking, though to a lesser degree than methamphetamine-priming and cue-induction (Hiranita et al., 2006). In contrast, Neugebauer and colleagues (2010) found that nicotine priming reinstated methamphetamine-seeking only in rats that had been previously treated with nicotine rather than saline. In humans, a laboratory study found that d-amphetamine dose-dependently increases cigarette smoking (Tidey et al., 2000). A secondary analysis of a clinical trial of bupropion for methamphetamine dependence revealed a positive association between number of cigarettes smoked and methamphetamine use, but only in the placebo group (Brensilver et al., 2013). The high prevalence of smoking in methamphetamine abusers, estimated to be over 87% (Grant et al., 2007; Weinberger and Sofuoglu, 2009), also suggests a link between cigarette smoking and methamphetamine use.

Given the link between illicit stimulant use and cigarette smoking, we have hypothesized that better illicit stimulant-use outcomes would be obtained for stimulant-dependent patients who achieved smoking cessation abstinence in response to smoking-cessation treatment (Winhusen et al., 2012a). The data to test this hypothesis came from a recent multi-site trial conducted by the National Institute on Drug Abuse (NIDA) National Drug Abuse Treatment Clinical Trials Network (CTN) which evaluated the impact of concurrent substance use disorder (SUD) and nicotine dependence treatment for cocaine and/or methamphetamine-dependent patients who were also nicotine dependent. The primary analyses from the trial revealed that there were no significant treatment effects on stimulant-use outcomes (Winhusen et al., in press). The present analyses evaluated the association between achieving smoking abstinence and illicit-stimulant abstinence in the post-smoking-quit phase of the study for participants randomized to the smoking-cessation condition. Because there are important differences between cocaine and methamphetamine (Newton et al., 2005; Winhusen et al., 2013), we evaluated the association for the entire sample as well as separately for the cocaine-dependent and methamphetamine-dependent participants.

2. METHODS

2.1 Study Design

Details of the trial are provided elsewhere (Winhusen et al., 2012a). Briefly, the study was a 10-week, intent-to-treat, 2-group randomized controlled trial with follow-up visits at 3 and 6 months post-smoking quit date conducted at 12 SUD outpatient treatment programs. Treatment programs which did not provide smoking-cessation treatment were eligible to participate. Eligible participants were randomized to treatment as usual (TAU) or TAU with smoking-cessation treatment (TAU+SCT). During the 10-week treatment phase, participants were scheduled to attend two research visits per week for efficacy and safety assessments. There were single follow-up visits at 3-months and 6-months post-quit date. Participants randomized to the TAU+SCT arm participated in the SUD treatment as typically provided by the study site and also received SCT consisting of extended-release (XL) bupropion 300 mg/day, nicotine inhaler, individual 10 minute smoking-cessation counseling weekly for 10 weeks, and prize-based contingency management for smoking abstinence (Carbon Monoxide (CO)< 4ppm) during the post-quit phase.

2.2 Participants

Recruitment was primarily from clinic patients entering substance use disorder (SUD) treatment at a participating site. Eligible participants were adults enrolled in outpatient SUD treatment, and interested in quitting smoking. The main inclusion criteria were: meeting DSM-IV-TR criteria for cocaine- and/or methamphetamine-dependence, smoking at least 7 cigarettes daily and a CO level ≥ 8 ppm, and being in good physical health as determined by medical history, vital signs, and electrocardiogram. The decision to require 7 CPD was based on a prior trial completed by our group in which the more standard ≥10 CPD criterion was a primary reason for excluding African-American, but not Caucasian, smokers. Exclusion criteria included a medical or psychiatric condition potentially making study participation unsafe, current treatment for nicotine dependence; for women, pregnancy, breastfeeding, or unwillingness to use adequate birth control. The present study evaluated the association between smoking abstinence and illicit-stimulant abstinence in the cocaine-dependent (n=147), methamphetamine-dependent (n=102), and pooled (n=249) samples.

2.3 Measures

Abstinence from cocaine/methamphetamine was defined by stimulant-negative urine drug screens (UDS) and self-report of no stimulant use at each research visit. A rapid UDS system that screened for drugs of abuse including cocaine, methamphetamine, amphetamine, opioids, benzodiazepines, and marijuana was used to analyze the urine samples (Branan Medical Corporation). To avoid falsification, urine samples were collected using temperature monitoring and the validity of urine samples was checked with the use of a commercially available adulterant test. Self-report of substance use was assessed using the Timeline Follow-back (TLFB) method (Sobell and Sobell, 1992; Fals-Stewart et al., 2000), which is widely employed and well-validated. Achievement of smoking cessation was defined as achieving smoking-point prevalence abstinence (PPA) during the final treatment week (week 10). PPA is a standard measure and is defined as self-report of not smoking in the previous seven days, confirmed by a CO level <8 ppm (Hurt et al., 2003). In accordance with National Institutes of Health policy, participants self-reported their race and ethnicity based on the race/ethnicity classifications used in the 2000 United States Census.

2.4. Data analysis

All analyses were completed using SAS, Version 9. 3 (SAS Institute, 2010). Illicit-stimulant abstinence weeks during the post-smoking-quit phase (e.g., study weeks 4-10) were regressed using a mixed model regression including smoking-cessation status (e.g., continued smoking vs. smoking abstinent), and study week randomizing on participant. To determine whether any differences in stimulant abstinence were specific to smoking-cessation status, participant demographic and baseline characteristics on which the groups significantly differed were evaluated, via the corrected Akaike Information Criteria (AICC), for inclusion as covariates in the regressions. This approach allowed an evaluation of the association of illicit-stimulant abstinence with smoking-cessation status when other variables related to smoking-cessation status were controlled. It has been recommended that effect sizes be reported along with p-values to provide information about the clinical significance of an effect in addition to its statistical significance (Nakagawa, 2004). Consistent with this recommendation, we calculated the Cohen's d (Cohen, 1988), using mean and standard deviation estimates generated from the raw data, for statistically significant effects.

3. RESULTS

Demographic and baseline characteristics for the participants are provided in Table 1. The association between smoking abstinence and illicit stimulant abstinence was evaluated for the pooled sample and for the subsets of cocaine-dependent and methamphetamine-dependent participants. As can be seen in Table 2, the results revealed a significant difference only for the cocaine-dependent subsample in which participants who stopped smoking were abstinent for illicit stimulants an average of 78.2% of the post-smoking-quit weeks (weeks 4-10) relative to 63.6% in participants who continued smoking; the effect size for this difference is d=0.36.

Table 1.

Participant demographic and baseline characteristics as a function of dependence diagnosis and smoking-cessation abstinence

Pooled Sample TAU+SCT (N=249) Cocaine-Dependent TAU+SCT (N=147) Methamphetamine-Dependent TAU+SCT (N=102)
Continued Smoking N=174 Smoking Abstinent N=75 Smoking Analysisa Continued Smoking N=107 Smoking Abstinent N=40 Smoking Analysisa Continued Smoking N=67 Smoking Abstinent N=35 Smoking Analysisa
Age, mean (SD), y 37.7 (9.9) 36.2 (10.1) W=1.1 41.4 (9.1) 40.4 (9.9) W=0.3 31.8 (8.0) 31.5 (8.2) W=0.4
Sex, male, n (%) 89 (51.1) 47 (62.7) X2(1)=2.8 57 (53.3) 29 (72.5) X2(1)=4.4* 32 (47.8) 18 (51.4) X2(1)=0.1
Race, n (%) X2(2)=0.9 F=0.017 X2(1)=0.1
    African-American 56 (32.4) 27 (36.0) 56 (52.8) 27 (67.5) 0 (0) 0 (0)
    Caucasian 105 (60.7) 41 (54.7) 48 (45.3) 12 (30.0) 57 (85.1) 29 (82.9)
    Other/mixed 12 (6.9) 7 (9.3) 2 (1.9) 1 (2.5) 10 (14.9) 6 (17.1)
Ethnicity, Hispanic, n (%) 20 (11.6) 11 (14.7) X2(1) =0.5 10 (9.4) 1 (2.5) F=0.117 10 (14.9) 10 (28.6) X2(1)=2.7
Baseline use (prior 28 days)
    Days/stimulant use 2.3 (5.2) 1.3 (4.1) T(174.0)=1.5 2.7 (5.7) 2.2 (5.5) W=1.4 1.5 (4.1) 0.3 (0.9) T(76.6)=2.3*
    Stimulant-free, n (%) 118 (67.8) 61 (81.3) X2(1)=4.7* 68 (63.6) 31 (77.5) X2(1)=2.6 50 (74.6) 30 (85.7) X2(1)=1.7
    Days/drug use 5.1 (8.7) 2.1 (5.4) T(218.4)=3.3** 5.7 (9.3) 3.5 (6.9) T(93.1)=1.6 4.1 (7.8) 0.5 (1.6) T(76.3)= 3.6***
    Drug-free, n (%) 90 (51.7) 55 (73.3) X2(1)=10.1** 51 (47.7) 26 (65.0) X2 (1)=3.5 39 (58.2) 29 (82.9) X2(1)=6.3*
Smoking history
    No. of Smoking years 21.1 (9.5) 19.4 (9.7) W=1.4 24.2 (9.0) 22.4 (9.8) W=1.0 16.1 (8.1) 16.0 (8.4) W=0.2
    No. of cigarettes/day 17.1 (8.6) 14.8 (7.6) W=2.1* 18.1 (8.9) 16.1 (7.5) W=1.4 15.5 (7.7) 13.3 (7.5) W=1.3
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Note.

a

W= Wilcoxon rank-sum test; X2(df)= Pearson chi-square test; T(df)= Student's t-test; F= Fisher's exact test.

*

p<.05

**

p<.01

***

p<.001. Where not specifically indicated, numbers represent means (standard deviations).

Table 2.

Stimulant-abstinence during the post-smoking-quit phase as a function of dependence diagnosis and smoking-cessation abstinence

n % Weeks abstinent Smoking Analysis (X2)
Pooled sample (N=249)
Continued smoking 174 71.0 (39.4) 2.97
Smoking abstinent 75 83.3 (31.4)
Cocaine-dependent (N=147)
Continued smoking 107 63.6 (41.8) 8.55**
Smoking abstinent 40 78.2 (35.7)
Methamphetamine-dependent (N=102)
Continued smoking 67 83.3 (31.7) 0.04
Smoking abstinent 35 89.2 (24.7)
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Note. X2(1)= Type III Wald chi-square.

**

p<.01.

4. DISCUSSION

The present study evaluated the association between smoking abstinence and illicit-stimulant abstinence in cocaine- and/or methamphetamine-dependent participants receiving smoking-cessation treatment. The results revealed a significant association for the cocaine-dependent participants with no significant differences for the sample as a whole or for the methamphetamine-dependent participants.

The present results are consistent with a fairly substantial literature finding a significant relationship between cigarette smoking and cocaine abuse. They are also consistent with the finding that methadone-maintained participants receiving smoking-cessation treatment provided significantly more cocaine-free urines during weeks in which they were smoking abstinent (Shoptaw et al., 2002). In the present study, a significant association between smoking cessation and illicit-stimulant abstinence was not found for the methamphetamine-dependent patients and, thus, the effect in the cocaine-dependent patients appears to be more than a matter of patients who are able to stop one substance (cigarettes) being better able to stop using substances in general (e.g., illicit stimulants). The effect observed in the cocaine-dependent patients had a Cohen's d (Cohen, 1988) of .36, which is in the range of a clinically-meaningful effect.

A potential explanation for the observed significant association between smoking cessation and illicit-stimulant use in cocaine- but not methamphetamine-dependent participants comes from a secondary analysis exploring the relationship between menthol cigarettes and illicit stimulant abuse in these participants (Winhusen et al., 2013). Specifically, the results revealed that 67% of the cocaine-dependent participants smoked menthol cigarettes and that menthol cigarettes were associated with self-reported prolongation of the cocaine high and with greater illicit stimulant use, associations not seen in the methamphetamine-dependent participants. Thus, for a majority of cocaine-dependent participants, achieving smoking abstinence could directly impact the reinforcing effects of cocaine by removing a substance that prolongs the illicit-stimulant high whereas methamphetamine-dependent participants achieving smoking abstinence would not obtain a similar benefit.

The present finding is of interest for several reasons. First, because the prevalence of smoking in cocaine-dependent patients is 75-80% (Budney et al., 1993; Gorelick et al., 1997; Sees and Clark, 1993), the proposed treatment approach would be applicable for the majority of cocaine-dependent patients. Second, cigarette smoking is deadly, accounting for 443,000 deaths annually in the United States (Centers for Disease Control and Prevention, 2008). Thus, using smoking-cessation treatment to intervene with both cocaine use and cigarette smoking would impact two important public health issues.

The present study has several strengths and a few limitations. First, this trial was conducted at 12 sites, which enhances the generalizability of the results, and included a large sample of stimulant-dependent participants. Another study strength is that it was conducted with individuals seeking treatment at SUD treatment programs and, thus, the results are likely generalizable to individuals in treatment for stimulant-dependence disorders (Winhusen et al., 2012b). A limitation is that the findings are correlational in nature and, thus, cause and effect determinations cannot be made. Second, this study included a treatment-seeking population of outpatients who were interested in quitting smoking, so the findings may not be generalizable to individuals not seeking treatment. Finally, bupropion may decrease cocaine use in some cocaine-dependent patients (Margolin et al., 1995; Poling et al., 2006; Stoops et al., 2012) and, thus, the observed connection between smoking cessation and illicit stimulant use may reflect a bupropion-induced global decline in addiction in some participants.

In conclusion, the present results suggest that cocaine-dependent patients achieving smoking cessation in response to smoking-cessation treatment might evidence not only improved smoking outcomes but improved cocaine-use outcomes as well. Future research to replicate this finding appears warranted.

Acknowledgments

Role of Funding Source

Funding for this study was provided by the National Institute on Drug Abuse (NIDA) Clinical Trials Network: U10-DA013732 to University of Cincinnati (Dr. Winhusen); U10-DA020036 to University of Pittsburgh (Dr. Daley), U10-DA013720 to University of Miami School of Medicine (Drs. Szapocznik and Metsch); U10-DA013045 to University of California Los Angeles (Dr. Ling); U10-DA013727 to Medical University of South Carolina (Dr. Brady); U10-DA020024 to University of Texas Southwestern Medical Center (Dr. Trivedi); U10-DA015815 to University of California San Francisco (Drs. Sorensen and McCarty). The publications committee of the Clinical Trials Network (CTN) gave final approval of the analysis and interpretation of the data and approved the manuscript.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Contributors

Dr. Winhusen conceptualized the research hypotheses, contributed to the analysis and interpretation of the data, and led the drafting of the manuscript. Mr. Lewis conducted analyses and critically reviewed the manuscript. Ms. Kropp and Mr. Theobald contributed to the interpretation of the findings and critically revised the manuscript for important intellectual content. All authors have approved the final manuscript.

Conflict of Interest

The authors have no potential conflicts of interest to report.

Author Disclosure for: Achieving smoking abstinence is associated with decreased cocaine use in cocaine-dependent patients receiving smoking-cessation treatment

REFERENCES

  1. Brensilver M, Heinzerling KG, Swanson A-N, Telesca D, Furst BA, Shoptaw SJ. Cigarette smoking as a target for potentiating outcomes for methamphetamine abuse treatment. Drug Alcohol Rev. 2013;32:96–99. doi: 10.1111/j.1465-3362.2012.00423.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Brewer AJ, 3rd, Mahoney JJ, 3rd, Nerumalla CS, Newton TF, De la Garza R., 2nd The influence of smoking cigarettes on the high and desire for cocaine among active cocaine users. Pharmacol. Biochem. Behav. 2013;106:132–136. doi: 10.1016/j.pbb.2013.03.008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Budney AJ, Higgins ST, Hughes JR, Bickel WK. Nicotine and caffeine use in cocaine-dependent individuals. J. Subst. Abuse. 1993;5:117–130. doi: 10.1016/0899-3289(93)90056-h. [DOI] [PubMed] [Google Scholar]
  4. Centers for Disease Control and Prevention Smoking-attributable mortality, years of potential life lost, and productivity losses--United States, 2000-2004. MMWR. 2008;57:1226–1228. [PubMed] [Google Scholar]
  5. Cohen J. Statistical Power Analysis for the Behavioral Sciences. L. Erlbaum Associates; Hillsdale, N.J: 1988. [Google Scholar]
  6. Frosch DL, Shoptaw S, Nahom D, Jarvik ME. Associations between tobacco smoking and illicit drug use among methadone-maintained opiate-dependent individuals. Exp. Clin. Psychopharmacol. 2000;8:97–103. doi: 10.1037//1064-1297.8.1.97. [DOI] [PubMed] [Google Scholar]
  7. Gatch MB, Flores E, Forster MJ. Nicotine and methamphetamine share discriminative stimulus effects. Drug Alcohol Depend. 2008;93:63–71. doi: 10.1016/j.drugalcdep.2007.08.020. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Gorelick DA, Simmons MS, Carriero N, Tashkin DP. Characteristics of smoked drug use among cocaine smokers. Am. J. Addict. 1997;6:237–245. [PubMed] [Google Scholar]
  9. Grant KM, Kelley SS, Agrawal S, Meza JL, Meyer JR, Romberger DJ. Methamphetamine use in rural Midwesterners. Am. J. Addict. 2007;16:79–84. doi: 10.1080/10550490601184159. [DOI] [PubMed] [Google Scholar]
  10. Hiranita T, Nawata Y, Sakimura K, Anggadiredja K, Yamamoto T. Suppression of methamphetamine-seeking behavior by nicotinic agonists. Proc. Natl. Acad. Sci. U. S. A. 2006;103:8523–8527. doi: 10.1073/pnas.0600347103. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Huang YY, Kandel DB, Kandel ER, Levine A. Nicotine primes the effect of cocaine on the induction of LTP in the amygdala. Neuropharmacology. 2013;74:126–134. doi: 10.1016/j.neuropharm.2013.03.031. [DOI] [PubMed] [Google Scholar]
  12. Hurt RD, Krook JE, Croghan IT, Loprinzi CL, Sloan JA, Novotny PJ, Kardinal CG, Knost JA, Tirona MT, Addo F, Morton RF, Michalak JC, Schaefer PL, Porter PA, Stella PJ. Nicotine patch therapy based on smoking rate followed by bupropion for prevention of relapse to smoking. J. Clin. Oncol. 2003;21:914–920. doi: 10.1200/JCO.2003.08.160. [DOI] [PubMed] [Google Scholar]
  13. Levine A, Huang Y, Drisaldi B, Griffin EA, Jr., Pollak DD, Xu S, Yin D, Schaffran C, Kandel DB, Kandel ER. Molecular mechanism for a gateway drug: epigenetic changes initiated by nicotine prime gene expression by cocaine. Sci. Transl. Med. 2011;3:107ra109. doi: 10.1126/scitranslmed.3003062. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Margolin A, Kosten TR, Avants SK, Wilkins J, Ling W, Beckson M, Arndt IO, Cornish J, Ascher JA, Li SH, Bridge P. A multicenter trial of bupropion for cocaine dependence in methadone-maintained patients. Drug Alcohol Depend. 1995;40:125–131. doi: 10.1016/0376-8716(95)01198-6. [DOI] [PubMed] [Google Scholar]
  15. Mello NK, Fivel PA, Kohut SJ. Effects of chronic buspirone treatment on nicotine and concurrent nicotine+cocaine self-administration. Neuropsychopharmacology. 2013;38:1264–1275. doi: 10.1038/npp.2013.25. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Mello NK, Newman JL. Discriminative and reinforcing stimulus effects of nicotine, cocaine, and cocaine + nicotine combinations in rhesus monkeys. Exp. Clin. Psychopharmacol. 2011;19:203–214. doi: 10.1037/a0023373. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Nemeth-Coslett R, Henningfield J, Katz J, Goldberg S. Pharmacol. Biochem. Behav. 1986;25:303. doi: 10.1016/0091-3057(86)90156-5. [DOI] [PubMed] [Google Scholar]
  18. Neugebauer NM, Harrod SB, Bardo MT. Nicotine elicits methamphetamine-seeking in rats previously administered nicotine. Drug Alcohol Depend. 2010;106:72–78. doi: 10.1016/j.drugalcdep.2009.07.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Newton TF, De La Garza R, 2nd, Kalechstein AD, Nestor L. Cocaine and methamphetamine produce different patterns of subjective and cardiovascular effects. Pharmacol. Biochem. Behav. 2005;82:90–97. doi: 10.1016/j.pbb.2005.07.012. [DOI] [PubMed] [Google Scholar]
  20. Patkar AA, Vergare MJ, Thornton CC, Weinstein SP, Murray HW, Leone FT. Nicotine dependence and treatment outcome among African American cocaine-dependent patients. Nicotine Tob. Res. 2003;5:411–418. doi: 10.1080/1462220031000094178. [DOI] [PubMed] [Google Scholar]
  21. Poling J, Oliveto A, Petry N, Sofuoglu M, Gonsai K, Gonzalez G, Martell B, Kosten TR. Six-month trial of bupropion with contingency management for cocaine dependence in a methadone-maintained population. Arch. Gen. Psychiatry. 2006;63:219–228. doi: 10.1001/archpsyc.63.2.219. [DOI] [PubMed] [Google Scholar]
  22. Reid MS, Mickalian JD, Delucchi KL, Berger SP. A nicotine antagonist, mecamylamine, reduces cue-induced cocaine craving in cocaine-dependent subjects. Neuropsychopharmacology. 1999;20:297–307. doi: 10.1016/S0893-133X(98)00076-1. [DOI] [PubMed] [Google Scholar]
  23. Reid MS, Mickalian JD, Delucchi KL, Hall SM, Berger SP. An acute dose of nicotine enhances cue-induced cocaine craving. Drug Alcohol Depend. 1998;49:95–104. doi: 10.1016/s0376-8716(97)00144-0. [DOI] [PubMed] [Google Scholar]
  24. Roll JM, Higgins ST, Budney AJ, Bickel WK, Badger GJ. A comparison of cocaine-dependent cigarette smokers and non-smokers on demographic, drug use and other characteristics. Drug Alcohol Depend. 1996;40:195–201. doi: 10.1016/0376-8716(96)01219-7. [DOI] [PubMed] [Google Scholar]
  25. Roll JM, Higgins ST, Tidey J. Cocaine use can increase cigarette smoking: evidence from laboratory and naturalistic settings. Exp. Clin. Psychopharmacol. 1997;5:263–268. doi: 10.1037//1064-1297.5.3.263. [DOI] [PubMed] [Google Scholar]
  26. Saint-Preux F, Bores LR, Tulloch I, Ladenheim B, Kim R, Thanos PK, Volkow ND, Cadet JL. Chronic co-administration of nicotine and methamphetamine causes differential expression of immediate early genes in the dorsal striatum and nucleus accumbens of rats. Neuroscience. 2013;243:89–96. doi: 10.1016/j.neuroscience.2013.03.052. [DOI] [PMC free article] [PubMed] [Google Scholar]
  27. Sees KL, Clark HW. When to begin smoking cessation in substance-abusers. J. Subst. Abuse Treat. 1993;10:189–195. doi: 10.1016/0740-5472(93)90044-3. [DOI] [PubMed] [Google Scholar]
  28. Shoptaw S, Rotheram-Fuller E, Yang X, Frosch D, Nahom D, Jarvik ME, Rawson RA, Ling W. Smoking cessation in methadone maintenance. Addiction. 2002;97:1317–1328. doi: 10.1046/j.1360-0443.2002.00221.x. [DOI] [PubMed] [Google Scholar]
  29. Stoops WW, Lile JA, Glaser PE, Hays LR, Rush CR. Influence of acute bupropion pre-treatment on the effects of intranasal cocaine. Addiction. 2012;107:1140–1147. doi: 10.1111/j.1360-0443.2011.03766.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. Tidey JW, O'Neill SC, Higgins ST. d-amphetamine increases choice of cigarette smoking over monetary reinforcement. Psychopharmacology (Berl.) 2000;153:85–92. doi: 10.1007/s002130000600. [DOI] [PubMed] [Google Scholar]
  31. Weinberger AH, Sofuoglu M. The impact of cigarette smoking on stimulant addiction. Am. J. Drug Alcohol Abuse. 2009;35:12–17. doi: 10.1080/00952990802326280. [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Winhusen TM, Adinoff B, Lewis DF, Brigham GS, Gardin JG, II, Sonne SC, Theobald J, Ghitza U. A tale of two stimulants: Mentholated cigarettes may play a role in cocaine, but not methamphetamine, dependence. Drug Alcohol Depend. doi: 10.1016/j.drugalcdep.2013.09.002. Available online 2013, http://dx.doi.org/10.1016/j.drugalcdep.2013.09.002. [DOI] [PMC free article] [PubMed]
  33. Winhusen T, Brigham GS, Kropp F, Lindblad R, Gardin JG, 2nd, Penn P, Hodgkins C, Kelly TM, Douaihy A, McCann M, Love LD, DeGravelles E, Bachrach K, Sonne SC, Hiott B, Haynes L, Sharma G, Lewis DF, VanVeldhuisen P, Theobald J, Ghitza U. A randomized trial of concurrent smoking-cessation and substance use disorder treatment in stimulant-dependent smokers. J. Clin. Psychiatry. doi: 10.4088/JCP.13m08449. In press. [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Winhusen T, Lewis D, Adinoff B, Brigham G, Kropp F, Donovan DM, Seamans CL, Hodgkins CC, Dicenzo JC, Botero CL, Jones DR, Somoza E. Impulsivity is associated with treatment non-completion in cocaine- and methamphetamine-dependent patients but differs in nature as a function of stimulant-dependence diagnosis. J. Subst. Abuse Treat. 2013;44:541–547. doi: 10.1016/j.jsat.2012.12.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
  35. Winhusen T, Stitzer M, Woody G, Brigham G, Kropp F, Ghitza U, Lindblad R, Adinoff B, Green C, Sharma G, Somoza E. Design considerations for a study to evaluate the impact of smoking cessation treatment on stimulant use outcomes in stimulant-dependent individuals. Contemp. Clin. Trials. 2012a;33:197–205. doi: 10.1016/j.cct.2011.09.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  36. Winhusen T, Winstanley EL, Somoza E, Brigham G. The potential impact of recruitment method on sample characteristics and treatment outcomes in a psychosocial trial for women with co-occurring substance use disorder and PTSD. Drug Alcohol Depend. 2012b;120:225–228. doi: 10.1016/j.drugalcdep.2011.06.014. [DOI] [PMC free article] [PubMed] [Google Scholar]

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