Kalman 2011.

Methods	Double‐blind parallel‐group placebo‐controlled randomised clinical trial Study period: June 2005 to April 2010
Participants	N = 143 Participants were in recovery from alcohol problems and were recruited from a residential substance abuse treatment programme and from the community. Inclusion criteria: smoked ≥ 10 cigarettes/d, history of alcohol abuse or dependence, and between 2 and 12 months of abstinence from alcohol Exclusion criteria: older than age 70; diagnosis of schizophrenia; current psychotic episode; cardiac problems in the past 3 months; uncontrolled hypertension; history of seizure; history of head injury with neurological sequelae or prolonged loss of consciousness; and use of medications that lower the seizure threshold
Interventions	Bupropion + nicotine patch (n = 73) Placebo + nicotine patch (n = 70) Participants were taking study medication for 8 weeks. They began study medication (bupropion 150 mg SR tablets or placebo) 1 week before their quit day. Participants were instructed to take 1 tabletd for 3 days, then one 150‐mg tablet twice per day for the remainder of the treatment phase of the study. All participants received a nicotine patch for 7 weeks, starting 1 week after starting study medication on their quit day. They received a 21‐mg patch for 4 weeks, a 14‐mg patch for 2 weeks, and a 7‐mg patch for 1 week.
Outcomes	Outcomes: 7‐day point prevalence smoking abstinence at week 7 (end of treatment), week 11, and week 24. At week 7, smoking abstinence was defined via self‐report (complete abstinence during the 7 days before the time of assessment) and biochemical verification (CO reading < 8 ppm). At week 11 and week 24, smoking abstinence was defined via self‐report and biochemical verification (salivary cotinine levels ≤ 15 ng/mL)
Funding source	Study was sponsored through personal funding by David Kalman: NIDA R01‐DA11713‐01; Peter Monti: NIAAA K05 Senior Scientist Award; and Marc Mooney: NIDA K01‐DA‐019446. NIDA and NIAAA had no further role in study design; in collection, analysis, and interpretation of data; in writing of the report; or in the decision to submit the paper for publication.
Declaration of interest	No conflicts were declared. None of the review authors have any connection with the tobacco, alcohol, pharmaceutical, or gaming industries or with any body substantially funded by 1 of these organizations.
Notes	Analysis of pharmacogenetics was reported in McGeary 2012.
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	Urn randomisation with 4 variables was used to allocate participants.
Allocation concealment (selection bias)	Low risk	Randomisation was based on 4 variables.
Blinding of participants and personnel (performance bias) All outcomes	Unclear risk	Active and placebo medications were identical in appearance. No further details are presented.
Blinding of outcome assessment (detection bias) All outcomes	Low risk	Outcome of the study was objective.
Incomplete outcome data (attrition bias) All outcomes	High risk	Excluded from analysis participants who did not receive the study medication; no ITT analysis was performed.
Selective reporting (reporting bias)	High risk	Weeks of abstinence assessment are different from those listed on clinicaltrials.gov (NCT00304707).
Other bias	Unclear risk	Additional analyses of pharmacogenetics were conducted in a subset of the original randomised trial population in McGeary 2012, but comparability of baseline characteristics between treatment groups is unclear.