Behavioral Activation for Smoking Cessation in Veterans With PTSD
Phase: NA
Conditions: Tobacco Dependence, PTSD
Sponsor: VA Office of Research and Development

Version 5; 3/5/2015 
1
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Behavioral Activation for Smoking Cessation in Veterans with PTSD 
 
 
Study PI:  
Jessica W. Cook, PhD.,  
William S. Middleton Memorial Veterans Affairs Hospital 
Center for Tobacco Research and Intervention 
 
 
NCT01995123 
 

Version 5; 3/5/2015 
2
 
Project Summary 
 
Aims and Rationale: The primary objective of this research is to produce an empirically 
validated treatment that increases smoking cessation in veterans with posttraumatic stress disorder 
(PTSD), one that can be easily integrated into smoking cessation clinics and/or mental health clinics 
within Veterans Administration (VA) facilities. PTSD is highly prevalent in the VA patient 
population and is associated with a rate of smoking (53% - 66%) that far exceeds that of VA 
enrollees in general (22%). PTSD is also associated with unusually high rates of smoking 
cessation treatment failure. The disparity in smoking cessation outcomes amongst veterans with 
PTSD may occur because standard smoking cessation treatment does not address PTSD-
specific vulnerabilities. Veterans with smoking-PTSD comorbidity may respond optimally to 
treatment that addresses PTSD and associated affective symptoms, because such symptoms 
can both reinforce smoking and undermine quit attempts. Recent evidence shows that 
behavioral activation therapy (BA), a behavioral treatment that increases engagement in 
reinforcing activities, significantly reduces PTSD symptoms.  BA may improve smoking 
cessation outcomes amongst veterans with PTSD because it reduces overall PTSD symptom 
severity and affective distress (low positive affect, high negative affect), which can cause 
smoking relapse. The proposed research will determine whether BA as an adjunct to standard 
smoking cessation treatment (ST+BA) is superior to a comparably intense combination of 
standard smoking cessation treatment + health and smoking education (ST+HSE) in improving 
smoking cessation outcomes among veterans with PTSD.  The HSE intervention is intended to 
constitute a credible intervention that controls for contact time.  Secondary objectives are to 
determine if BA improves PTSD symptomatology and associated affective distress, and to 
identify potential mediators of BA on smoking outcomes. 
Methods: A total of 120 veterans with PTSD who are motivated to quit smoking will 
attend an initial diagnostic and baseline assessment session.  Those who are interested, 
eligible, and who provide consent will be randomly assigned to receive ST+BA or ST+HSE and 
will be contacted by their individual study therapist to schedule the first treatment session. 
Participants will be stratified into treatment groups based on: 1) major depressive disorder 
(MDD; present versus absent), and 2) PTSD symptom severity. All participants will receive 
eight, individual sessions of ST+BA or ST+HSE. All participants will receive 20 minutes of 
identical standard smoking cessation treatment in each of the eight sessions. Those in the 
ST+BA condition will receive an additional 30 minutes of behavioral activation therapy; those in 
the ST+HSE condition will receive an additional 30 minutes of health education and information 
about smoking.  All participants will receive 12 weeks of the nicotine patch and either nicotine 
gum or lozenge. Smoking cessation outcomes will be assessed 1, 2, 3, 4, 12, 20, and 26 weeks 
after the quit date. 
 
Significance: This research has important clinical and public health significance because 
smoking is especially common among veterans with PTSD and it is the leading preventable cause 
of disease and disability. Reducing smoking rates among veterans with PTSD would result in 
substantially lower smoking-related illness and death in this vulnerable group of smokers. It 
would also reduce tobacco related healthcare costs charged to the VA. Study methods and 
findings may potentially be extended to smoking cessation treatment for patients with mental 
health disorders other than PTSD.   
 
 
Background and Significance 
 
PTSD is associated with an unusually high smoking prevalence and low cessation rates 
The health, economic, and human costs of tobacco use are profound. Cigarette smoking 
remains the single largest preventable contributor to premature morbidity and mortality in the 
United States20,21. Approximately 443,000 Americans die prematurely each year from tobacco-

Version 5; 3/5/2015 
3
related cancer, cardiovascular, cerebrovascular, and respiratory diseases22. The economic 
costs of tobacco use are also substantial. In the US, the annual costs of medical expenses and 
lost productivity resulting from tobacco-related disease, disability, and death are estimated at 
more than $193 billion22.  
US veterans suffer disproportionately from smoking and smoking-related illness. 
Accordingly, a large portion of smoking-related healthcare costs are passed on to the nation’s 
largest healthcare provider: the VA. PTSD, a highly prevalent mental health disorder among 
veterans (18%)23, is associated with an especially high prevalence of cigarette smoking and low 
cessation rates15,24,25. Between 53-66% of veterans with PTSD smoke14-16, nearly three times 
the rate of VA enrollees in general (22%)17. A greater proportion of veterans with PTSD smoke 
heavily (> 25 cigarettes per day), compared with VA patients who smoke but do not have PTSD 
(48% versus 28%)15. Moreover, there is evidence that smoking contributes to the significantly 
poorer physical health and higher use of medical care services for veterans with PTSD 
compared with those without the disorder26-28. Individuals with PTSD also have close to the 
worst quit rates in comparison with patients with 13 other mental health disorders25. Little is 
known about helping smokers with PTSD quit smoking, in part, because this group is typically 
excluded from smoking cessation clinical trials. We propose to examine whether behavioral 
activation (BA), a behavioral treatment that increases engagement in reinforcing activities, 
improves the efficacy of standard smoking cessation treatment (relative to a health and smoking 
educational adjuvant to standard cessation treatment: ST+HSE).  
Standard smoking cessation treatment is ineffective for veterans with PTSD  
Standard smoking cessation treatment is relatively ineffective for smokers with PTSD. A 
recent trial of 943 smokers with military-related PTSD compared the effectiveness of referral to 
a specialized VA smoking cessation clinic versus smoking cessation treatment that was 
integrated into mental health care (Integrated Care)29. McFall (co-investigator for proposed 
work) and colleagues found a 12-month prolonged abstinence rate of only 4.5% among 
veterans who received treatment from a VA smoking cessation clinic vs. a rate of 8.9% among 
veterans who received Integrated Care. Despite the boost in cessation achieved through 
Integrated Care, over 90% failed to maintain abstinence for a one-year period. In addition, only 
about a third of VA enrollees with PTSD engage in PTSD treatment30; thus, veterans with PTSD 
are insufficiently exposed to smoking treatment via Integrated Care. Clearly, there is a need to 
develop more effective smoking treatments for people with PTSD – especially treatments that 
can be delivered across diverse settings to increase treatment access. We aim to improve quit 
rates by augmenting standard smoking cessation treatment with BA, a novel and easily 
administered smoking cessation treatment for veterans with PTSD. Because BA selectively 
treats the components of PTSD that motivate smoking and may hinder quit attempts, it should 
be an especially efficacious smoking cessation treatment for veterans with PTSD.  
Smokers with PTSD may smoke to regulate PTSD symptoms and affective distress  
PTSD Symptoms. Regardless of the causal relation between smoking and PTSD (i.e., 
PTSD leads to smoking31 or vice versa32), there is evidence that smoking may help regulate 
PTSD symptoms and associated mood states. PTSD is an anxiety disorder involving an 
extreme and often sustained psychological and biochemical stress response to trauma 
exposure. Pervasive efforts to avoid distress are central to PTSD symptomatology. Regular self-
administration of nicotine may serve as one strategy for tolerating PTSD-related symptoms (re-
experiencing, avoidance, emotional numbing, hyperarousal). VA PTSD patients, in particular, 
report being motivated to smoke in response to distressing military memories14. They have also 
been shown to experience nicotine withdrawal symptoms in response to encounters with 
trauma-related stressors33, and they report that smoking reduces PTSD symptoms elicited by 
exposure to laboratory-based trauma cues34. In addition, research35 including ours36, shows that 
higher emotional numbing symptoms of PTSD (loss of interest, detachment from others) are 
associated with heavier smoking. These results suggest that smoking may be used to 
counteract the automatic blunting of positive emotion following trauma exposure.  
Negative Affect. In addition to relatively specific PTSD symptoms, individuals with PTSD 

Version 5; 3/5/2015 
4
also experience severe negative affective disturbances, and may smoke to regulate these 
events37. In fact, compared with other smokers, those with PTSD have extraordinarily high 
levels of negative affect37,38, react more strongly to stressors39,40, and have a greater perceived 
need to blunt or suppress negative affect38. Also, data show that smoking reduces negative 
affect among veterans with PTSD after they have been exposed to laboratory-based trauma 
cues41. If smoking helps regulate negative mood, quitting smoking may unmask heightened 
negative affect among smokers with PTSD. Negative affect is associated with failure to quit 
smoking (e.g., 5), and those with PTSD may experience withdrawal-related negative affect as 
particularly intolerable42, prompting a return to smoking.  
Positive Affect. Smokers with PTSD may also self-administer nicotine to counter 
deficient positive affect, a deficit that is central to the emotional numbing component of PTSD. 
Evidence shows that individuals with PTSD report lower global positive affect than do those 
without PTSD37, potentially because their pervasive pattern of avoidance disrupts contact with 
positively reinforcing activities that engender positive emotions. Nicotine administration 
stimulates brain reward systems43 and produces positive mood improvement among smokers44. 
Thus, those with PTSD may rely on cigarettes as an accessible and reliable source of positive 
reinforcement. When veterans with PTSD attempt to quit smoking, they may be particularly 
likely to relapse because they miss the positive mood enhancing effects of cigarettes. Indeed, 
post-quit declines in positive affect have been implicated with difficulties quitting smoking45,46. 
We posit that veterans with PTSD may increase their likelihood of quitting smoking by learning 
to engage in new, non-smoking, sources of positive reinforcement that enhance positive 
emotions. BA was chosen as a smoking cessation adjuvant because it increases engagement in 
valued life activities in order to increase contact with positive reinforcement.     
In summary, smoking may regulate PTSD symptoms as well as two affective 
vulnerabilities associated with PTSD: elevated negative affect and low positive affect. Quitting 
smoking may interfere with such regulation and further exacerbate these vulnerabilities, 
prompting a return to smoking. Thus, an optimal smoking cessation treatment for PTSD may be 
one that augments standard smoking cessation treatment with strategies that address PTSD 
symptoms as well as withdrawal-related affective distress. We propose to examine whether 
behavioral activation (BA), a treatment that targets these PTSD-associated vulnerabilities, 
improves the efficacy of standard smoking cessation treatment among veterans with PTSD.   
Behavioral activation was first developed as a treatment for depression   
The primary goal of Behavioral activation (BA) is to increase engagement in valued life 
activities in order to increase contact with positive reinforcement. BA was originally validated as 
a stand-alone treatment for depression. It has received very strong empirical support, with 
results equal to or better than cognitive therapy and antidepressant medications47-51. From the 
functional analytic framework of BA, depression is viewed as resulting from antecedent risk 
factors (e.g., environmental stressors) that initiate depression by disrupting contact with 
positively reinforcing activities. For example, a stressor like losing a job may lead to negative 
mood states. A common reaction to negative emotions is avoidance behaviors, because 
avoidance can reduce exposure to further stress. However, continued avoidance narrows the 
depressed person’s behavioral repertoire and ultimately denies him/her access to sources of 
positive reinforcement. Entrenched patterns of avoidance result in depression. BA attempts to 
re-engage depressed individuals in their lives through focused activation strategies that 
encourage patients to approach sources of positive reinforcement that are consistent with their 
long-term goals.  
Behavioral activation reduces symptoms of PTSD 
BA may be an effective treatment for PTSD because of evidence that PTSD, similar to 
depression, results in a pervasive pattern of avoidance38 that leads to disruption in contact with 
positively reinforcing activities. Behavioral theories of PTSD hold that PTSD develops by 
conditioning: a traumatic event becomes associated with the context in which the trauma 
occurred and generalizes broadly to other contexts. Individuals with PTSD then avoid situations 
and experiences (including those that would typically be experienced as enjoyable, such as 

Version 5; 3/5/2015 
5
eating at a restaurant), to forestall negative affect. However, because of continued avoidance, 
the original conditioning remains intact (i.e., does not extinguish). Further, through the process 
of secondary conditioning (by which conditioned stimuli can create further conditioned 
associations), avoidance can become more pervasive and entrenched over time.  
The application of BA for the treatment of PTSD is supported by both theory and 
research. As with depression, BA treats PTSD by re-engaging individuals in activities and 
experiences that are positively reinforcing by overcoming patterns of avoidance. Evidence 
suggests that BA should help regulate deficient positive affect and excessive negative affect 
associated with PTSD (including during tobacco abstinence). BA increases positive emotions 
resulting from engagement in appetitive events52, and increased frequency of positively 
reinforcing activities is associated with increased positive affect and decreased negative 
affect53. Several open label, non-randomized trials support the efficacy of BA for treatment of 
PTSD. Civilians with PTSD (n=14) who received BA reported a significant pre- to post-treatment 
reduction in PTSD symptoms (assessed via Clinician Administered PTSD Scale; CAPS). The 
pre- versus post-treatment effect was large (d=1.29 6). Veterans with PTSD also reported a 
significant reduction in CAPS-assessed PTSD symptoms following BA treatment in two open-
label trials (n=8, pre- versus post-treatment d = 1.44, 8; n=11, pre-versus post-treatment d=.62 
11). In addition, in a pilot randomized trial of BA versus treatment as usual (TAU) (n=8), BA 
produced greater PTSD symptom reduction than TAU19. The pre- versus post-treatment effect 
of BA was large (d=1.0), as was the BA versus TAU effect (d=1.19). The large average pre- 
versus post-treatment BA effect from these studies (d=1.10) is comparable to the large average 
pre- versus post-treatment effect for all evidence-based PTSD treatments (d=1.43; from a 
recent meta-analysis of evidence-based PTSD treatments54).  
Finally,  a recent open label trial of 117 veterans with PTSD7 shows that BA produces 
reductions in PTSD symptoms (via PCL self-report) that are comparable to those produced by 
manualized Prolonged Exposure (PE) (i.e., β10= -1.21: see 55). Further, trauma imaginal 
exposure (the central element of PE) did not accelerate BA effects on PTSD7. These data add 
to the mounting evidence that BA can serve as an independent treatment for PTSD, producing 
effects that are similar to those produced by other evidence based treatments.    
Behavioral activation is ideal for integration with smoking cessation treatment  
Because BA treats PTSD and affective reactions that are implicated in cessation failure, 
we propose that it will improve the efficacy of standard smoking cessation treatment in veterans 
with PTSD. Several features of BA make it an ideal smoking cessation adjuvant. First, BA is 
inherently targeted at the challenges posed by quitting smoking; e.g., increased contact with 
nonsmoking reinforcers should mitigate the impact of nicotine abstinence on affect. That is, BA 
may facilitate cessation by reducing withdrawal symptoms such as negative affect (in addition to 
influencing cessation through reduction of PTSD symptoms). Second, the idiographic nature of 
BA allows it to be flexibly tailored to the unique needs of smokers with PTSD. Third, its 
uncomplicated nature allows it to be used with smokers varying in insight and intellectual 
capacity. Fourth, BA is straightforward to administer and extremely time-efficient, which 
facilitates its integration into smoking cessation treatment in diverse settings (e.g., BA has been 
effectively administered by nurses in primary care56). These latter features are especially 
promising regarding the potential flexibility and generalizability of BA for smoking cessation in 
different VA treatment settings. Therefore, BA is both feasible and functionally appropriate for 
smoking cessation without altering its central tenets or application.    
Importantly, veterans who are interested in quitting smoking may accept BA more than 
they do other PTSD therapies such as prolonged exposure (PE). The primary goal of PE is to 
elicit fear and anxiety through exposing the individual to memories of the trauma. BA differs 
from PE in that the goal is to increase exposure to reinforcing activities vs. those that elicit fear 
or anxiety. In this respect, BA is a more suitable smoking cessation adjuvant treatment because 
it does not involve a trauma-focus component, and might therefore be less distressing and more 
acceptable to smokers with PTSD. This should also permit widespread use of BA in diverse 
treatment settings.   

Version 5; 3/5/2015 
6
Behavioral activation improves smoking cessation outcomes  
Dr. Lejuez (consultant for proposed research) and colleagues9 found that BA plus 
standard smoking cessation treatment versus expanded standard smoking cessation treatment 
alone increased 6-month point prevalence abstinence among community smokers. Although the 
study was underpowered to detect treatment mediators (n = 42), importantly, smokers 
randomized to BA experienced a significant reduction in depressed mood at 6-months postquit 
relative to those who received a control therapy. This suggests that BA may have boosted 
cessation rates via its amelioration of post-quit affective distress. Because such affective 
distress hinders quit attempts in veterans with PTSD, we posit that BA will similarly improve 
cessation rates in this population.  
The proposed treatment (ST+BA) is based on the BA treatment manual developed by 
Dr. Lejuez “Life Enhancement Treatment for Smoking”. This treatment manual includes all the 
standard components of BA, but is made relevant for smoking cessation. For example, 
treatment goals are made relevant to developing a healthy non-smoking lifestyle; i.e., engaging 
in positively reinforcing activities in the absence of smoking. We have made minor adaptations 
to Dr. Lejuez’s manual so that the BA exercises are also made relevant to  
PTSD. For example, the therapeutic exercises and examples have been tailored to address 
PTSD-specific barriers to engaging in reinforcing activities (e.g., tolerating anxiety while 
engaging in an activity in a public setting). Importantly, any adaptations to BA are 
psychoeducational and related to building a rationale for how BA addresses PTSD and 
smoking. The central tenets of BA remain unchanged: veterans increase engagement in 
positively reinforcing activities (see Appendix 3a; Session 1 of ST+BA treatment manual and 
Section D.8.e for detailed description of treatment protocol).    
BA treats PTSD-specific smoking relapse risk factors 
In addition to examining whether BA affects smoking outcomes (the “Intervention 
Hypothesis”: see Figure 1), a secondary objective of the proposed research is to examine the 
treatment effects of BA on PTSD symptoms and affective distress. Examining these treatment 
effects will also identify potential mediators of BA on smoking outcomes. Although this initial 
research is not powered for mediation analyses, such analyses may nevertheless suggest how 
BA works for smokers with PTSD and provide critical pilot data for future treatment process 
research. A secondary benefit is that the proposed work will produce additional data on BA as a 
treatment for PTSD. The following are hypothesized treatment effects of BA that may promote 
smoking cessation:   
PTSD Treatment Effect. Consistent with prior research6,7,8,11,19, we posit that BA will 
reduce overall PTSD symptom severity. Exploratory analyses will also examine the BA effects 
on each PTSD symptom cluster (re-experiencing, avoidance, emotional numbing, hyperarousal) 
to refine analyses of potential mediators. Self-report PTSD symptom severity will be measured 
at treatment visits and at each follow-up visit.  In addition, a structured clinical assessment of 
PTSD (via the Clinical Administered PTSD Scale; CAPS) will occur at baseline and end-of-
treatment.  
Negative Affect Treatment Effect. BA has been shown to reduce depressed mood during 
smoking cessation9, and increased engagement in reinforcing activities is associated with 
decreased negative affect51. Thus, we posit that BA will decrease negative affect following 
quitting smoking. We will also explore the effects of BA on other tobacco withdrawal symptoms 
(e.g., craving) since negative affect may be causally linked with such symptoms. In addition, 
exploratory analyses will examine the influence of BA on depressed mood because depression 
often co-occurs with PTSD59. Negative affect, depressed mood, and withdrawal symptoms will 
be assessed at every study visit and follow-up visit. A structured clinical assessment of current 
depression, in addition to PTSD, will occur at baseline and end-of-treatment.  
Positive Affect Treatment Effect. Evidence suggests that increasing the frequency of 
engagement in reinforcing activities elevates positive affect51. Therefore, we posit that BA will 
lead to increased global positive affect. In general, there is evidence that BA modulates reward 
functioning (i.e., approach toward rewarding events). Administration of BA results in functional 

Version 5; 3/5/2015 
7
changes in brain structures that mediate both reward anticipation (incentive value) and reward 
feedback60. It is unclear how BA’s enhancement of the brain reward system maps onto actual 
behavior. It is possible that BA will also increase the sensitivity of the Behavioral Activation 
System (BAS), one of the major motivational systems associated with goal attainment and 
reward seeking. Thus, exploratory analyses will examine whether BA increases the sensitivity of 
the Behavioral Activation System. Positive affect and sensitivity of the Behavioral Activation 
System will be measured at every study visit (albeit, with only questionnaire measures).   
Exploratory Mediation Analyses. Separate treatment effect hypotheses address whether 
BA, on top of a common smoking cessation base, affects PTSD symptoms, negative affect, and 
positive affect. Separate analyses will determine the relations of these latter variables with 
likelihood of smoking abstinence (the outcome hypotheses). We will conduct exploratory 
mediation analyses for variables that are influenced by BA and that also predict smoking 
outcomes. Although the proposed research is not powered for mediation, detecting treatment or 
outcome effects will provide relevant information about how BA works (or does not work), and 
how it can be improved. Finally, while not a meditational analysis, exploratory analyses will 
analyze the extent to which improvement in PTSD symptoms and affect in the ST+BA condition 
depends upon execution of behavioral assignments (e.g., engaging in reinforcing activities). 
This is an important test of the model by which BA is thought to work.  
Significance 
Smoking in persons with PTSD is common, hard-to-treat, and refractory, and exacts 
incredibly high human and health costs. This work is significant because it will contribute to the 
development of a smoking cessation treatment tailored for people with PTSD that could boost 
quit rates in this hard-to-treat comorbid population. Stopping smoking would reduce the elevated 
risk of tobacco-related cancer, cardiovascular, cerebrovascular, respiratory diseases and 
premature death in smokers with PTSD, and associated healthcare costs. The rapidly 
expanding number of veterans returning from deployment to Iraq and Afghanistan with comorbid 
nicotine dependence and PTSD62 presages an increasing demand for smoking cessation 
services and medical care from these veterans for years to come. Failure to develop more 
effective smoking cessation treatments for this large and expanding group of smokers will result 
in unnecessary tobacco-related disease, disability, and death in a vulnerable, comorbid 
population.    
 BA holds a great deal of promise for smoking cessation in veterans with PTSD. First, 
BA is extremely time-efficient and easily integrated with standard smoking treatment. Second, 
BA affects factors that are central to both PTSD and smoking cessation. Third, BA has already 
been shown to successfully increase cessation rates among smokers with symptoms of 
depression. Fourth, BA is feasible for delivery in VA settings and is acceptable to veterans. 
Adding to the significance of this work is evidence that suggests BA will not only boost smoking 
cessation rates in this population, but will also ameliorate symptoms of PTSD. Finally, this work 
will provide additional insight into how BA works, which will guide future treatment development 
and evaluation research.  
In sum, we posit that BA — used as an adjuvant to standard smoking cessation 
treatment — will overcome major shortcomings of tobacco use treatment provided for veterans 
with PTSD by the VA (i.e., poor outcomes). It will do so by treating PTSD symptomatology that 
motivates smoking and undermines quit attempts using a treatment that is highly acceptable to 
veterans with PTSD. 
Innovation 
 It is imperative to develop innovative, more effective smoking cessation interventions 
that accommodate the unique treatment needs of smokers with PTSD. No clinical trials have 
tested a smoking treatment tailored for this vulnerable comorbid population. The present 
research will, therefore, build on limited previous research and constitute the only trial that 
compares a novel treatment (BA) versus a contact control condition on long-term smoking 
abstinence. This research is highly innovative because BA is designed to treat both the 
symptoms of PTSD as well as enhance smoking outcomes. Thus, BA is a rare or unique 

Version 5; 3/5/2015 
8
smoking cessation adjuvant because it could promote cessation by simultaneously treating both 
PTSD and tobacco withdrawal symptoms (e.g., negative affect).   
In addition, BA’s simplicity and lack of aversive elements should enhance its clinical 
delivery in health care contexts and enhance patient acceptance and participation. Finally, the 
measures of mechanism of action (e.g., affect, PTSD symptoms) should produce unique 
information on why smoking is so highly comorbid with PTSD, and why veterans with PTSD are 
unable to quit.   
Relevance to Veteran Health 
 
Smoking claims 443,000 lives each year, making it the leading cause of death in the 
US22. In fact, smoking kills more people each year than AIDS, drugs and alcohol, 
homicide, suicide and motor vehicle accidents combined63. US veterans suffer 
disproportionately from smoking and smoking-related illness. Accordingly, a large portion of 
smoking-related healthcare costs are passed on to the VA. In 2008, the VA spent over $5 billion 
to treat chronic obstructive pulmonary disease (COPD) alone, a condition that is highly linked 
with tobacco use17. Stopping smoking before the age of 50 reduces risk of death by 50% over 
the ensuing 15 years64, and health benefits extend to older smokers who stop as well64.   
Veterans with PTSD represent a large group of patients who would reap the known 
health benefits of stopping smoking64 if the effectiveness of cessation treatment is improved. 
The VA has placed high priority on providing specialized care to approximately 560,217 
veterans with PTSD65. Stopping smoking would reduce the risk of tobacco-related cancer, 
cardiovascular, cerebrovascular, and respiratory diseases in those with PTSD22. In addition, the 
rapidly expanding number of veterans returning from deployment to Iraq and Afghanistan with 
comorbid nicotine dependence and PTSD62 suggests there will be an increasing demand for 
smoking cessation services and medical and psychiatric care from these veterans for years to 
come. A decline in smoking in veterans with PTSD would result in substantially lower smoking-
related illness and death in this vulnerable clinical population. It would also dramatically reduce 
tobacco-related healthcare costs charged to the VA. The relevance of this research is further 
enhanced because the tested intervention targets both PTSD symptoms as well as smoking 
cessation. Finally, the relevance of the proposed work is underscored by the fact that BA is a 
brief and easily administered treatment that is readily accepted by veterans with PTSD8,11. Thus, 
ST+BA could easily and readily be translated into VA clinical practice.   
 
 
Research Design and Methods 
 
Study Objective 
The primary goal of the proposed research is to examine whether behavioral activation as an 
adjuvant to standard smoking cessation treatment (ST+BA) improves smoking cessation 
outcomes among veterans with PTSD relative to a comparably intense combination of standard 
smoking cessation treatment + health and smoking education (ST+HSE).  
 
Specific Aims/Study Objectives 
Primary Aim: 
Aim 1: Compare the effects of behavioral activation (BA) and health and smoking education 
(HSE) on abstinence rates, when each is used as an adjuvant to standard smoking 
cessation treatment (ST+BA vs. ST+HSE). 
 
Secondary Aims: 
Aim 2: Compare the effects of behavioral activation (BA) and health and smoking education 
(HSE) on PTSD symptoms and affective distress when each is used as an adjuvant to 
standard smoking cessation treatment. 
Aim 3: Identify potential mediators of the effects of BA on smoking cessation outcomes.   
 

Version 5; 3/5/2015 
9
Design Overview 
A total of 120 veterans with PTSD who are motivated to quit smoking will attend an initial 
diagnostic and baseline assessment session. Those who are interested and eligible and who 
provide consent will be randomly assigned to receive ST+BA or ST+HSE and will be contacted 
by the study therapist to schedule the first treatment session. Randomization of participants into 
treatment will be stratified on: 1) major depressive disorder (MDD; present vs. absent), and 2) 
bupropion use. All participants will receive eight, individual sessions of ST+BA or ST+HSE. All 
will receive 20 minutes of identical standard smoking cessation treatment in each of the eight 
sessions. Those in the ST+BA condition will receive an additional 30 minutes of behavioral 
activation therapy; those in the ST+HSE condition will receive an additional 30 minutes of health 
education and information about smoking. All participants will receive 12 weeks of the nicotine 
patch and either nicotine gum or lozenge. Smoking cessation outcomes will be assessed 1, 2, 3, 
4, 12, 20, and 26 weeks after the quit date.  
Recruitment 
The proposed research will be conducted at the Madison VAMC in collaboration with the 
UW-CTRI. Due to challenges associated with recruiting a specialized population, we have 
devised a recruitment plan using two major recruitment pipelines.  
Pipeline 1: We will recruit veterans from the Madison VAMC and other local VAMCs 
(e.g., Tomah, Milwaukee, and community-based outpatient clinics). During regular mental health 
treatment, primary care visits, and other medical appointments at VAMCs, veterans will be 
queried by providers not affiliated with the study about their interest in the study. Clinicians who 
identify potential subjects will co-sign study staff to a note.  Study staff will then call the 
interested study candidate for an initial telephone screening. Additionally, approved recruitment 
fliers will be posted within the Madison and other local VAMCs. . Potential subjects may call 
study staff directly. An automated list of VA patients who have both PTSD and tobacco 
dependence in their medical record will be generated. Informational letters may be mailed to 
veterans who meet these two basic eligibility criteria for the study. Data will be reviewed from 
the Mental Health Research Cooperative (MHRC) registry and informational letters may be 
mailed to veterans who have previously joined the registry and meet basic criteria.  Veterans 
who receive the informational letter may call study staff directly if interested, and study staff may 
place a follow-up phone call to letter recipients if they do not reply.  
 Pipeline 2: We will also recruit veterans from the greater Madison area and Southern 
Wisconsin. who may not be receiving VA care. We will use our ongoing collaboration with the 
Wisconsin State Department of Veterans Affairs (DVA) to recruit non-VA enrolled veterans. As 
in the past, the DVA has agreed to provide information about the proposed research program 
within Mission Welcome Home packets. Research program information will include a flier and 
interested veterans can contact study staff. As part of our collaboration with the Wisconsin DVA, 
we will also continue collaborating with County Veteran Service Officers (CVSOs) in southern 
Wisconsin, who work directly with veterans and who will refer veterans to the research program.  
Approved recruitment fliers will be posted in the community and potential subjects may call 
study staff directly. 
In addition to screening for smoking status and interest in quitting, the phone screen will 
include a validated four-item PTSD screening questionnaire used by the Department of Defense 
Post-Deployment Health Assessment Program, which identifies veterans with possible PTSD88.   
Inclusion and Exclusion Criteria 
One hundred and twenty participants will be enrolled. For inclusion in the study, 
participants must: 1) report smoking an average of 6 or more cigarettes daily for at least six 
months; 2) report a desire to quit smoking; 3) meet criteria for current PTSD; 4) speak and read 
English; 5) agree to participate in the study; and 6) be ≥ 18 years old.   
Participants will be excluded from the study based on the following: 1) meeting criteria 
for psychotic or bipolar disorder; 2) psychoactive substance abuse or dependence (excluding 
nicotine dependence) within the past 6 months; 3) inability to give informed, voluntary, written 
consent to participate; 4) current use of any pharmacotherapy for smoking cessation not 

Version 5; 3/5/2015 
10
provided by the researchers during the quit attempt; 5) use of non-cigarette tobacco or nicotine 
products as a primary form of tobacco/nicotine use; 6) being currently suicidal or homicidal, as 
assessed by VA suicide/homicide template questions administered to all veterans; 7) being 
medically unable to use the nicotine patch or nicotine gum/lozenge; 8) psychotropic medication 
changes within 2 months of study initiation and during active treatment; 9) current engagement 
in evidence-based therapies for PTSD or depression; 10) pregnant or trying to become 
pregnant; or 11) incarceration.  
In addition, we will inform participants that, for research purposes, we prefer that they 
remain on the same psychotropic medication regimen throughout the trial. However, if it is 
necessary for a participant to alter treatment for his/her welfare, we will ask the participant to 
notify us immediately. Such participants will remain in the trial, but primary study analyses will 
be conducted with such participants excluded.  
Any concerns regarding nicotine patch, gum, or lozenge use will be reviewed by the 
study clinician, who may interview patients should further information be required. All women of 
childbearing potential will be required to agree to use an approved method of birth control to 
prevent pregnancy during the period of nicotine replacement therapy (NRT) use. Participants 
with suicidal or homicidal ideation at screening will be referred for VA psychiatric care, and they 
will be excluded from the study. Study candidates who express imminent intent for harm to self 
or others at any point in the study will be referred for VA emergency care.  
Assessments 
The following assessments will be conducted during the study: 1) Screening/diagnostic 
assessments used to determine inclusion into the study, 2) baseline descriptive assessments, 
3) smoking status assessments, 4) treatment effect assessments, and 5) treatment adherence 
assessments. See Table 1 for the schedule of assessments. 
Table 1. Therapy and Assessment Schedule for the Study    
 
Baseline 
Therapy Sessions 
 
Follow-ups 
V1 
 
 
V2 
Wk -4 
V3 
Wk -3 
V4 
Wk -2 
V5 
Wk -1 
V6 
Target 
Quit 
Day 
V7 
Wk 1 
Post-
quit 
V8 
Wk 2 
Post-
quit 
V9 
Wk 3 
Post-
quit 
V10 
Wk 4 
Post- 
quit 
PA1, 2 
Wk 
12,20 
Post-quit 
V11 
Wk 26 
Post-
quit 
In-person Counseling  
    (ST+BA or ST+HSE)  
 
TS1 
TS2  TS3 
TS4 
TS5 
TS6 
TS7 
TS8 
 
 
 
Screening/Diagnostic Assessments 
 
 
 
 
 
 
 
 
 
 
 
 
        PTSD phone screen (PC-PTSD) 
 X* 
 
 
 
 
 
 
 
 
 
 
 
        Axis I Disorders (SCID-I) 
X 
 
 
 
 
 
 
 
 
 
 
 
        PTSD (CAPS) 
X 
 
 
 
 
 
 
 
 
X 
 
 
        Depression (SCID-I) 
X 
 
 
 
 
 
 
 
 
X 
 
 
        Suicidal/Homicidal Ideation    
              Assessment  
X 
 
 
 
 
 
 
 
 
 
 
 
        Medical History 
        X 
 
 
 
 
 
 
 
 
 
 
 
Baseline Descriptive Measures 
 
 
 
 
 
 
 
 
 
 
 
 
        Demographics 
X 
 
 
 
 
 
 
 
 
 
 
 
        Smoking history 
X 
 
 
 
 
 
 
 
 
 
 
 
        FTND 
X 
 
 
 
 
 
 
 
 
 
 
 
        WSWS 
X 
 
 
 
 
 
 
 
 
 
 
 
Smoking Status Assessments 
 
 
 
 
 
 
 
 
 
 
 
 
        Smoking/Alcohol use Status 
 
X 
X 
    X  
X 
X 
X 
X 
X 
 
X 
X 
        Calendar data  
 
X 
X 
X 
X 
X 
X 
X 
X 
 
X 
X 
        CO assessment  
X 
 
 
  
 
X 
X 
X 
X 
 
 
X 
        Cotinine Assessment  
 
 
 
 
 
 
 
 
 
 
 
X 
Treatment Effects Assessments 
 
 
 
 
 
 
 
 
 
 
 
 
 PANAS 
X 
X 
 
X 
    
X 
X 
X 
X 
X 
X 
X 
 PTSD symptoms (PCL) 
X 
 
 
X 
 
 
X 
X 
 
X 
X 
X 
        Depressed mood (PHQ-9) 
X 
 
 
 
 
 
 
 
X 
 
 
 
        Behavioral Activation (BAS)  
X 
 
 
 
X 
 
X 
 
X 
 
X 
X 
        WSWS-11 
X 
 
 
 
 
X 
 
X 
 
X 
X 
X 

Version 5; 3/5/2015 
11
 
*Occurs at the phone screen, prior to the in-person screening visit; **Follow-ups at Weeks 5 and 
26 are in-person, to permit PTSD and depression assessments and abstinence bioverification, 
respectively. Other follow-ups, at Weeks 12 & 20, are phone assessments (PA). 
Screening/Diagnostic Assessments  
Primary Care PTSD Screen (PC-PTSD). The PC-PTSD88 is a validated, four-item 
measure of PTSD with yes-no response options used by the Department of Defense Post-
Deployment Health Assessment Program to identify veterans with possible PTSD. Two yes 
answers have been shown to yield sensitivity of .96 and specificity of .7889. Study candidates 
who yield one or more yes answers on the PC-PTSD at the phone screen will be further 
assessed by an in-person diagnostic interview.   
Clinician Administered PTSD Scale (CAPS). The CAPS90 will be used to determine 
PTSD diagnostic status and severity. It will be administered at baseline and at the end of 
treatment (V10; see Table 1). The CAPS is a widely used and validated clinician interview for 
the assessment of PTSD. PTSD diagnosis on the CAPS is based on meeting the symptom 
criteria as defined in the most recent version of the Diagnostic and Statistical Manual of Mental 
Disorders (DSM).  The CAPS shows strong internal validity90. In addition, time since trauma, 
number of traumatic exposures, type of trauma, and time since original PTSD diagnosis will be 
assessed to aid in identifying factors that may be associated with treatment outcomes. 
Structured Clinical Interview for DSM Axis I Disorders (SCID-I). The SCID91 is a widely 
used structured interview that assesses psychiatric disorders. The SCID-I has been shown to 
have very good reliability and validity92. The SCID-I will be administered at baseline, and only 
the depression module of the SCID-I will administered at the end of treatment (V10). If 
depression is noted in the SCID and participants are not already receiving clinical care, they will 
be referred to a clinical care provider.  Questions pertaining to illicit drug use will be asked, but 
not recorded to protect participant privacy. 
Suicidal Ideation/Homicidal Ideation (SI/HI) Screening Form. Participants will be asked 
standard VA clinical questions regarding suicidality and homicidality (e.g., “In the last month, 
have you thought about harming or killing anyone?” “Are you feeling hopeless about your 
future?”). Participants who endorse homicidal ideation or suicidal ideation with intent or plan will 
be excluded from the study, thoroughly evaluated for safety, and referred for VA mental health 
care. Dr. Cook, a VA psychologist, will be available via pager at all times so that study staff can 
consult with her about assessing risk for harm and making appropriate referrals. In addition, all 
study staff will receive standard VA suicide prevention training.  
Medical History. Participants will complete a brief medical history questionnaire used in 
our prior research that focuses primarily on contraindications for using the nicotine patch, gum, 
and lozenge. Positive responses will be followed up by the study clinician, Maria Wopat. All 
women will receive additional questions regarding current pregnancy/nursing, plans to become 
pregnant during the period of medication use, and use of birth control. 
Baseline Descriptive Measures 
Demographic Information Questionnaire. Standard demographic information will be 
gathered via self-report at baseline to describe the study sample and to allow examination of 
any systematic differences between the two treatment groups. 
Smoking History Questionnaire and Nicotine Dependence Assessment. Standard 
smoking history information such as number of previous quit attempts and years smoked will be 
        Tripartite Pleasure Scale  
X 
 
 
 
X 
 
X 
 
 
X 
 
X 
        Snaith-Hamilton Pleasure 
X 
 
 
X 
 
X 
 
X 
 
X 
X 
X 
Stress and Pleasure  
X 
 
 
 
 
 
 
 
X 
 
X 
X 
Treatment Adherence Measures  
 
 
 
 
 
 
 
 
 
 
 
 
Therapist adherence to treatment  
 
 
 
 
 
 
 
 
 
 
 
 
        Adherence to nicotine patch and  
               side effects  
 
 
 
 
 
X 
X 
X 
X 
 
X (Wk 12 
only) 
 
        Participant adherence to BA 
 
X 
X 
X 
X 
X 
X 
X 
X 
 
 
 

Version 5; 3/5/2015 
12
collected. The Fagerstrom Test for Nicotine Dependence (FTND)93 will be used as a continuous 
measure of nicotine dependence.  
Smoking Status Assessments  
Measures of Smoking Status. Number of cigarettes smoked each day will be assessed 
at baseline and every visit. Abstinence (both point-prevalence and continuous) will be assessed 
on the quit day and at 1, 2, 3, 4, 12, 20, and 26-weeks post-quit day. We will assess long-term 
outcomes in a manner consistent with the recommendations of the Society for Research on 
Nicotine and Tobacco (SRNT) Workgroup on Biochemical Confirmation1. The main outcome 
analyses are based on 7-day point prevalence abstinence (i.e., reported abstinence for at least 
the 7 days prior to the assessment). Time-line follow-back (TLFB)95 procedures will be used, as 
in our previous work, to assess continuous abstinence and to establish dates of initial lapse 
(smoking the first postquit cigarette), relapse (smoking for 7 consecutive days), and total days 
smoking.  
Biochemical Verification. Self-reported abstinence will be biochemically verified at every 
in-person visit (from the Quit Day through 4 Weeks postquit and at 26-Weeks postquit) by 
carbon monoxide (CO) analysis of breath samples (8 ppm cutoff96). We chose the 26-week 
postquit follow up to biochemically verify abstinence as this is the smoking cessation outcome 
time point used in major meta-analytic studies (e.g., 86), and it serves as a good index of later 
smoking outcomes86. 
 In addition to CO verification, urinary cotinine (cutoff value of 20 ng/ml) for stated 
abstinence of 2 weeks or more (cotinine may be incompletely metabolized before this time) will 
be assessed at 26-Weeks postquit. All participants will be queried as to NRT use as this could 
affect cotinine levels. Expired air CO levels will be assessed with a carbon monoxide monitor96. 
Detected values above the stated cutoff scores will be considered indicative of smoking.  
Treatment Effect Measures  
Positive and Negative  Affect. The Positive Affect-Negative Affect Schedule (PANAS)97 
will be used to assess positive and negative affect. The PANAS is a self-report state mood 
questionnaire consisting of 10 adjectives describing positive mood states and 10 adjectives 
describing negative mood states that are rated on 5-point scales ranging from 1 (very slightly or 
not at all) to 5 (extremely). The PANAS possesses good reliability and validity97. Positive and 
negative affect will be measured at all treatment and follow-up sessions.  Anhedonia, the ability 
to experience pleasure will also be assessed by the Pleasure Activity Scale and Hedonic Tone 
questionnaires. 
PTSD Symptoms. Posttraumatic Stress Disorder Checklist-Military Version (PCL)98 is a 
17-item self-report scale that assesses PTSD symptom severity. Items are rated on a 5-point 
Likert scale according to how much the symptom bothered the respondent over the past month. 
The psychometric properties of this measure are excellent98. In addition, a structured clinical 
assessment of PTSD via the CAPS will occur at baseline and end-of-treatment (V10). 
Depressed Mood. We will use the Personal Health Questionnaire Depression Scale 
(PHQ) to assess depression. The PHQ is a well-validated tool for the assessment of depressive 
symptoms. The PHQ will be administered during active treatment and follow-up assessments. 
The depression module of the SCID-I will also be administered at baseline and end of treatment 
(V10).  
Behavioral Activation. The Behavioral Activation Scale100 assesses the sensitivity of the 
Behavioral Activation System, an index of the strength of motivation to engage in reinforcing 
activities (including goal-directed activity). Although those in the ST+BA group will record the 
actual frequency of engagement in reinforcing activities, self-monitoring is an important 
component of the ST+BA and could introduce poor treatment fidelity if utilized in the ST+HSE 
group. Thus, we have chosen to measure sensitivity of the Behavioral Activation System, which 
theoretically is the primary factor affected by BA. Sensitivity of the Behavioral Activation System 
will be assessed during active treatment and follow-up sessions. The psychometric properties of 
the Behavioral Activation Scale are strong100.  
Withdrawal. We will monitor withdrawal severity at baseline, throughout treatment, and 

Version 5; 3/5/2015 
13
follow-up using the Wisconsin Smoking Withdrawal Scale, a 28-item scale that assesses 
nicotine withdrawal. It will allow for the assessment of the frequency, duration, severity, and 
temporal variability in withdrawal symptoms.   
Ecological Momentary Assessment (EMA).  For 2 weeks (1 week prior to the quit date 
and 1 week after the quit date), participants will receive automated assessment calls every 
evening (14 calls) at a pre-arranged time. Two calls will also be made prior to initiating therapy 
and two calls after completion of therapy.  The Interactive Voice Response (IVR) assessments 
will evaluate: 1) PTSD symptoms, 2) positive and negative affect, 3) withdrawal, 4) use of NRT 
(after the quit date), 5) number of cigarettes smoked that day, and 6) activity engagement (e.g., 
Did you engage in a recreational activity today?). Four activity engagement EMA items will 
provide an additional measure of adherence to the behavioral exercises, as well as a measure 
of the primary mechanism through which BA is thought to work; i.e., whether BA leads to 
reduction in PTSD as a result of increased activity level. Moreover, EMA will provide information 
about whether symptom improvement is related to the overall level of activity and/or type of 
activity (e.g., social versus non-social reinforcers). EMA data will also allow us to examine 
whether increased activity is directly associated with smoking abstinence (in addition to PTSD 
reduction).  Finally, we will be able to examine whether BA’s effects on PTSD symptoms 
(assessed via EMA) influence smoking abstinence.  
The brief assessment items—Ecological  Momentary Assessment (EMA)—have been 
shown in our prior work to sensitively reflect treatment effects, predict relapse, and reveal 
treatment mediation47,64. The calls will last approximately 4 minutes; this assessment burden is 
much less than has been used successfully in many other studies, including our own, using 
EMA assessments46,98. Importantly, research shows that veterans with PTSD have similar EMA 
compliance rates as individuals without PTSD34,65. Participants will use either their own cell 
phone or one provided by the study. They will earn $2.00 for completing each EMA assessment.  
We believe the EMA assessment schedule will produce the data needed for the study 
although it is less intensive (only one assessment per day) than other EMA protocols. In 
contrast to most research involving EMA , we are not attempting to characterize the relationships 
among measures at particular points in time (e.g., examining affect before and after individual 
cigarettes), which would require a much more frequent assessment schedule. Instead, we are 
interested in whether BA exerts effects on behavior and ratings on a more tonic basis, 
consistent with BA’s putative mechanisms of action, and are using EMA in order to obtain time-
stamped measures. 
Treatment Adherence Measures 
Therapist Competence and Adherence to Treatment. All treatment sessions in both 
conditions will be audiotaped, and a random selection of 25% (about 2 tapes per participant) of 
the audiotapes will be rated shortly thereafter by Drs. Cook and Messina to assess therapist 
adherence to and competence with the treatment protocol. Audio tapes will be maintained in a 
locked area accessible only the study staff and will be stored at the VA indefinitely, per VA 
policy.  Separate rating checklists developed for the ST+BA and ST+HSE protocols will be 
used. Kappa will be reported for rated variables.  
Adherence to Nicotine Replacement Therapy and side effects. Adherence to the nicotine 
patch, gum, and lozenge will be queried at each visit following initiation of NRT (Visits 6–9) and 
during the 12-week post-quit follow up call. Participants will be asked to return unused patches 
and gum/lozenge, which will be counted at each visit before dispensing new medication. NRT 
side effects will also be assessed at each visit. Potential differences in NRT use between 
treatment groups will be examined and incorporated into statistical models if a meaningful 
relation with outcomes is detected.   
Adherence to BA. Patient treatment adherence to the ST+BA condition will be assessed 
by study personnel during weekly counseling sessions.  
 
Study Procedures  
Timing of Events   

Version 5; 3/5/2015 
14
The study involves three basic phases:1) Study Consent and Baseline; 2) Therapy 
Sessions; and 3) Follow-up. Figure 4 illustrates the timing of study events, and the procedures 
associated with these phases are included in the text that follows.  
 
 
   
 
 
Study Consent and Baseline   
Screening Telephone Call. Prior to entry into the study, participants will complete a 
screening phone call that will provide a brief overview of the study and ask preliminary 
screening questions. Study staff will obtain verbal consent to review the potential participant’s 
VA medical chart to confirm that they meet basic criteria.  The medical chart will be reviewed to 
confirm PTSD and depression diagnosis and treatment, other mental health disorders, current 
medications, and medication contraindications.  Only information that is directly discussed with 
the potential participant will be recorded and no information regarding illicit drug use will be 
recorded.  For those who are interested in learning more and who meet the criteria for entry into 
the study, an in-person screening session appointment (V1) will be scheduled.  
In-Person Screening Assessment (V1). At the first visit, study staff will explain the study 
in detail and obtain written informed consent. Study staff will also obtain consent to audiotape 
treatment sessions on VA form 10-3203.  For study candidates who provide informed consent, 
study staff will then proceed with screening and baseline assessments. All participants will 
complete an interview assessment including: 1) the Clinician Administered PTSD Scale (CAPS) 
for PTSD diagnostic status; 2) the Structured Clinical Interview for DSM (SCID) to assess for 
Axis I disorders (including depression); 3) assessment of suicidality or homicidality, and 4) 
medical history assessment. Any person who reports thoughts of suicide/self-harm or harm to 
others will be seen by VA Mental Health triage. Those judged to be at risk will be excluded and 
referred to appropriate VA treatment resources. Those who do not meet criteria for inclusion in 
the study will be referred to the VA smoking cessation clinic. Participants who meet 
inclusion/exclusion criteria will then be asked to complete a series of baseline self-report 
questionnaires including: 1) a demographic information questionnaire; 2) measures of PTSD 
symptom severity; 3) measures of proposed treatment effects; and 4) smoking history and 
dependence measures. 
Randomization Process. After the in-person screening assessment is complete, the 
participant  will be assigned into ST+BA or ST+HSE. The following variables will be blocked in 
this order: 1) severity of PTSD, 2) depression status (MDD versus no MDD), and 3) bupropion 
use. Separate randomization tables will also be developed for those presenting via the two 
different pipelines (VA vs. community [via DVA]). This will ensure that any characteristics that 
are related to such entities are counterbalanced across groups. Following randomization, study 
staff will contact the participant to schedule the first treatment session.  
Treatment 
All participants will attend eight study visits in which they will receive ST+BA or ST+HSE 

Version 5; 3/5/2015 
15
(V2-V9). The quit day will occur on the same day as the fifth treatment visit (V6: see Figure 4). 
At the beginning of each visit (prior to the administration of therapy), participants will complete a 
series of self-report measures that may include assessments of: 1) positive and negative affect 
(PANAS), 2) PTSD symptom severity (PCL), 3) depressed mood (PHQ), 4) level of behavior 
activation (BAS), and 5) withdrawal symptoms. Some assessments will not be administered at 
every visit to reduce assessment burden (see Table 1 for specific assessment schedule). 
Smoking status (continuous and point prevalence) will be assessed at every in-person visit 
following the quit date. Sessions may be completed via telemental health (TMH) at a community 
based outpatient clinic (CBOC) that is closer to a Veteran’s home or via phone in rare cases in 
which a Veteran is unable to travel a session in person. 
Follow-up 
All participants will receive follow-up phone calls at Weeks 12 and 20 (PA1 and PA2). 
They will also attend an in-person post-treatment follow-up visit to receive structured clinical 
assessments of PTSD and depression (V10). Participants will also attend an in-person follow-up 
visit at 26-weeks post-quit for nicotine abstinence bioverification (V11). Follow-up assessments 
will include measures of smoking status, positive and negative mood, PTSD symptom severity, 
depressed mood, sensitivity of the Behavioral Activation System, and withdrawal (see Table 1 
for schedule).   
Treatment Conditions 
Treatment Conditions Overview 
The experimental treatment group will receive ST+BA, and the contact control group will 
receive ST+HSE. BA is being examined as an adjunct to ST, with the latter an evidence-based 
treatment for smoking cessation. Both treatments will be delivered in eight, individual therapy 
sessions. Treatment sessions 1–4 (V2–V5) will occur prior to the quit day, therapy session 5 
(V6) will occur on the quit day, and therapy sessions 6–8 (V7–V9) will occur each week until 4 
weeks post-quit (see Figure 4). Participants in the ST+BA and ST+HSE conditions will 
participate in 20 minutes of identical, standard smoking cessation treatment during each 
session. The ST+BA condition will include an additional 30 minutes of behavioral activation 
therapy, and the ST+HSE condition will include an additional 30 minutes of health and smoking 
education. In addition to receiving ST+BA or ST+HSE, all participants will receive 12 weeks of 
the nicotine patch and either nicotine gum or lozenge. 
Standard Smoking Cessation Therapy (ST) 
Participants in both treatment groups will receive a standard, individual smoking 
cessation treatment based on the 2008 US PHS Clinical Practice Guideline, Treating Tobacco 
Use and Dependence86. The investigative team has considerable expertise in delivering 
behavioral and pharmacological treatments for smoking cessation. Treatment will be delivered 
in eight, 20-minute individual sessions over an 8-week period, with existing treatment manuals 
modified for this delivery format (see Table 2). The use of manuals will help ensure that the ST 
intervention does not differ between treatment arms (which will be checked with treatment 
fidelity assays). The same smoking cessation treatment has been used successfully in previous 
CTRI research (e.g., 4,46). This cessation treatment is similar in content to that used at VA 
facilities18, increasing the generalizability of the current research.   
Table 2. Standard Smoking Cessation Treatment Overview 
Therapy Session 
Standard Smoking Cessation Therapy Content  
Therapy Session 
1 
(V2) 
• 
Provide reinforcement and support for quitting.   
• 
Discuss past quit experiences. 
• 
Address pros and cons of quitting.  
• 
Initiate self-monitoring.  
• 
Provide self-help materials (Clearing the Air USDHHS) 105  
Therapy 
Sessions 2 (V3) 
• 
Identify high-risk situations.  
• 
Discuss abstinence violation effect.   
• 
Develop coping strategies.  

Version 5; 3/5/2015 
16
• 
Discuss link between alcohol use and smoking.  
Therapy Session 
3 
(V4) 
 
• 
Discuss how to enlist social support.  
• 
Demonstrate how to use nicotine patch and nicotine gum or 
lozenge.  
• 
Prepare for quitting.  
Therapy 
Sessions 4 
through 8 
(V5–V9) 
• 
Discuss past quitting experiences.  
• 
Provide intratreatment support and reinforcement.  
• 
Anticipate high-risk situations and generate coping plan.   
• 
Develop social support for nonsmoking.   
Nicotine Replacement 
Participants in both groups will begin using the nicotine patch and gum or lozenge 
starting on the morning of their assigned quit day. Nicotine patch and gum or lozenge will be 
provided to participants, at no cost, by the Madison VAMC. Consistent with the 2008 PHS 
Guideline86, participants smoking ten or more cigarettes/day will receive 12 weeks of the 
following patch dosing: 6 weeks of 21 mg, 4 weeks of 14 mg, and 2 weeks of 7 mg nicotine 
patches. Participants smoking less than ten cigarettes/day will receive 12 weeks of the following 
patch dosing: 8 weeks of 14 mg and 4 weeks of 7 mg nicotine patches. Participants may taper 
down on patch dosage more slowly if needed as suggested by the 2010 VHA Tobacco Use 
Cessation Treatment Guidance. They will be instructed to apply one patch daily.  As per the 
PHS Guideline, VHA Guideline, and package insert, gum/lozenge dose will be based on 
cigarettes smoked per day.  Participants who smoke less than 25 cigarettes/day will only 
receive 2-mg gum/lozenge; participants smoking 25 or more cigarettes/day will receive 4-mg 
gum/lozenge.  Participants will be told to try to use one piece of gum every 1-2 hours.  However, 
participants will also be told that they may not be able to take a full, recommended dose of oral 
NRT given their conjoint use of the patch.  Participants will be urged to use at least 5 
pieces/day, unless this amount of use produces negative (toxic) effects.   All participants will be 
given complete instructions on proper NRT use86 and on signs of nicotine overdose/toxicity. 
Medication usage and side effects will be assessed at all visits. Maria Wopat, the VA smoking 
cessation coordinator, clinical pharmacist, and study clinician, will recommend dosage/use 
alterations as per good clinical practice if the participant experiences symptoms of nicotine 
toxicity or side-effects. Changes in recommended medication use will be considered in analyses 
of adherence outcomes. Participants will be asked to continue taking the medication for the full 
12 weeks unless they are smoking regularly and heavily (≥ 10 cigarettes per day every day).  
Standard Smoking Cessation Treatment Plus Health and Smoking Education (ST+HSE) 
The ST+HSE treatment protocol will include all elements of standard smoking cessation 
treatment and nicotine replacement therapy (described above) along with health and smoking 
education. We will use a health and smoking education control treatment similar to that used by 
Hall and colleagues84 — one that is currently being used successfully at UW-CTRI for a 
federally-funded grant (NIDA 5 P50 DA019706). The intervention includes information adapted 
from the Freedom from Smoking - American Lung Association, with additional information from 
the Mayo Clinic Nicotine Dependence Center Treatment Program Manual. This intervention is 
intended to produce the effects of a generic, extended cessation intervention and to control for 
clinical contact. We will present additional information beyond that presented in the ST 
intervention, so that the HSE intervention is not repetitive or boring. Participants will be 
encouraged to discuss presented information to reinforce what they are learning, and to discuss 
how the presented information is related to their situation and history (see 84). Thus, while the 
HSE treatment will present more information than the ST intervention by itself, therapists will 
relate the information delivered in the HSE intervention to the patient’s life situation, health 
status, desired quitting benefits, or self-reports (family history, withdrawal, level of nicotine 
dependence). This will be done because it is consistent with good clinical practice (also see84), 
and because the patient should not see the HSE intervention as being distinctly different/not 
integrated with the ST intervention. Therefore, in the ST+HSE condition, the first 20 minutes of 

Version 5; 3/5/2015 
17
each session will have the same agenda as in the other conditions, but the rest of the agenda 
will present new information, encourage discussion of that information, and relate the 
information to the patient’s situation and health. Thus, the ST+HSE intervention is designed to 
produce the effects of a generic smoking cessation intervention that has the same duration and 
clinical contact as does ST+BA (see Table 3; also cf. 83,84). This intervention is not designed to 
be inert. But, because standard cessation interventions have had poor success in the PTSD 
population, we do not expect this intervention to produce significant benefit.   
Table 3. Health and Smoking Education Overview   
Therapy Session 
Health and Smoking Education Content  
Therapy Session 
1 (V2) 
• 
Smoking is a true addiction: the meaning and implications. 
• 
Symptoms of physical and psychological addiction and withdrawal 
and why it is so difficult to quit.   
• 
Smoking involves habitual behaviors: implications for heaviness of 
smoking and quitting.   
• 
Relate and discuss topics relative to participant’s smoking history 
and experiences. 
Therapy Session 
2 (V3) 
• 
Surgeon General Report: Health Consequences of Smoking (e.g., 
present data on health risks). 
• 
Immediate health benefits of quitting. 
• 
Delayed health benefits of quitting. 
• 
Relate to the patient’s own health, smoking history, and concerns. 
Therapy Session 
3 (V4) 
• 
Negative health effects of second-hand smoke and implications for 
family members. 
• 
Components of a cigarette (e.g., thousands of chemicals, 400 of 
which are toxic).  
• 
Nature and consequences of nicotine withdrawal symptoms, 
including urges (e.g., relapse), and the highly variable time course 
of symptoms. 
• 
Physical and psychological readiness for quitting smoking and the 
relation to cessation success.  
• 
Relate to patient’s family/living context, withdrawal experiences, 
and readiness. 
Therapy Session 
4 (V5) 
• 
The personal, social, and economic costs of smoking (time spent, 
money spent).    
• 
Relation of smoking to weight, and relation of quitting to weight 
gain. 
• 
Relative health effects of excess weight vs. smoking.  
• 
Relation of smoking to lifestyle, health behaviors (e.g., diet, 
exercise).  
• 
Relate to patient’s reasons for quitting, concerns about costs of 
quitting, and lifestyle. 
Therapy Session 
5 (V6) 
• 
Effect of quitting smoking on other behaviors (e.g., sleep).  
• 
Effects of quitting smoking on your physical appearance. 
• 
Importance of adherent use of nicotine replacement. 
• 
Information on safety of nicotine replacement products vs. smoking.  
• 
Relate to patient’s concerns about appearance, use of NRT, and 
commitment to abstinence. 

Version 5; 3/5/2015 
18
Therapy Session 
Health and Smoking Education Content  
Therapy Session 
6 (V7) 
• 
Effect of nicotine on the brain (e.g., time to reach brain, systems 
affected, risks for stroke, etc.). 
• 
Effect of quitting smoking on the brain (e.g., reduced risk of stroke).  
• 
Smoking and other health effects (e.g., infertility). 
• 
Threats to cessation that occur late vs. early in the cessation 
attempt. 
Therapy Session 
7 (V8) 
• 
Relapse triggers and the course of a relapse.  
• 
Relate to patient’s likely future encounters with triggers. 
• 
What a slip will do to health and smoking motivation (relation of slip 
to full relapse). 
• 
How smoking is related to psychological symptoms (e.g., may be 
triggered by anxiety). 
• 
Occurrence of unanticipated benefits of cessation. 
Therapy Session 
8 (V9) 
• 
Years of potential life gained by quitting smoking.   
• 
Answer questions about cessation. 
• 
Reinforce success.   
 
Standard Smoking Cessation Treatment Plus Behavioral Activation (ST+BA) 
The ST+BA treatment will include all elements of standard smoking cessation treatment 
and nicotine replacement therapy (described above) along with the key elements of behavioral 
activation.  Treatment will be delivered in eight, 50-minute (20 minutes of standard smoking 
treatment followed by 30 minutes of BA) individual sessions over an 8-week period. BA will be 
made relevant to smoking cessation, but this will occur within the BA portion of the treatment, 
ensuring that both conditions comprise the same smoking cessation base. As with the HSE 
treatment, therapists will make the BA relevant to the patient’s life and will ensure appropriate 
integration with the ST. The following components of behavioral activation will be provided in 
ST+BA sessions:  
Therapy Session 1 (V2)  
Rationale for ST+BA and Monitoring. At the start of the BA component of Session 1, 
patients will receive a thorough rationale for the ST+BA treatment. Following this presentation, 
patients will discuss current activities (i.e., smoking lifestyle) and consider the reinforcing value 
of these activities. As homework, they will begin engaging in a self-monitoring exercise to 
examine already-occurring daily activities. The primary goals of this assignment are to: (a) 
provide a baseline measure to index progress following behavioral activation; (b) make the 
patient more cognizant of the quality and quantity of his/her activities; and (c) provide ideas for 
potential activities to increase during treatment. Psychoeducation information about how PTSD 
can undermine engagement in reinforcing activities will be presented.  
Therapy Session 2 (V3) 
Identification of Overall Values and Goals within a Nonsmoking Lifestyle. Following self-
monitoring homework, the emphasis shifts to identifying a person’s values and goals within a 
variety of life areas. This exercise will generate a target activity hierarchy (i.e., reinforcing 
activities). Next, the patient will be introduced to the Master Activity Log. Using the Master 
Activity Log, the therapist and patient will collaboratively determine the final goals regarding the 
frequency and duration of activities per week. The three easiest reinforcing activities from the 
hierarchy will be selected, and the patient will be given the Behavioral Checkout for use in 
monitoring engagement in these activities over the upcoming week.  Study staff will not limit the 
type of activity in which the patient chooses to participate, and will encourage whatever activities 
the patient finds enjoyable, meaningful, and rewarding.  Most likely, activities will be things that 
the patient has done in the past and study staff will encourage them to reinitiate activities or to 
increase the frequency.  Common activities include gardening, going on walks, or doing 
volunteer work. 

Version 5; 3/5/2015 
19
Therapy Session 3 (V4) 
Monitoring Progress and Continuing to Reevaluate Nonsmoking Lifestyle. The session 
will begin with a discussion of the patient’s weekly Behavioral Checkout. As a function of 
success in engaging in the previously selected activities, new activities will be added for 
monitoring in the upcoming week so that the patient moves through the hierarchy from the 
easier to the more difficult reinforcing activities. The session also focuses on the upcoming quit 
day and the importance of continuing with selected appropriate reinforcing activities in the 
absence of smoking. 
Therapy Sessions 4–8: Quit Week and Beyond (V5–V9) 
Maintenance. Participants will continue to monitor engagement in reinforcing activities in 
the absence of smoking. Based on their success, participants will continue to move through 
their activity hierarchy. As difficulties arise, participants will be encouraged to revisit their overall 
goals within a nonsmoking lifestyle and to work with their therapist to modify their activity 
hierarchy.  
Reasons for stopping assigned treatment  
 
BA has been shown to improve mood and anxiety disorders. BA has not been 
associated with significant adverse events. However, we will monitor biweekly for patient reports 
of affective distress and PTSD symptoms to inform decisions to stop treatment early in 
consultation with the study Data Safety Monitoring Board (DSMB). In addition, as indicated in 
the informed consent, participants can choose to stop treatment at any time, and we will 
terminate individual treatment in the event of associated and concerning adverse events.  
 
Retention of Participants 
The integrity of the data is highly dependent on retention of a large proportion of 
participants. Our extensive experience with smoking cessation and PTSD intervention studies 
has shown that retention of participants is fostered by the following strategies that we will follow 
in the proposed research; 
• 
Providing state-of-the-art smoking cessation interventions at no cost to participants; 
• 
Willingness to negotiate scheduling of contacts to fit with the participant’s schedule; 
• 
Dispensing medications at in-person visits (i.e., not requiring additional trips to a 
pharmacy); 
• 
Compensation of, and recognition for, completion of study milestones; 
• 
Providing participant who would like to discontinue treatment the option of continuing to 
receive study assessments only.   
We will also enhance retention via providing incentives for all phone assessment and in-
person visits. Subjects will receive $30 for each in-person treatment visit (V2–V9) to help defray 
the costs of travel or potential child care, $25 for completing each follow-up phone assessment 
(at Weeks 12 and 20 post-quit (PA1–PA2)), and $50 for attending each in-person follow-up visit 
(at Weeks 5 and 26 post-quit (V10-V11)). Participants will also receive $2 for each automated 
call answered and an extra $24 if they answer 80% or more of the automated calls.  Total 
subject payment is thus $450/subject if all visits, phone calls, and follow-ups are completed.    
 
 
Data and Safety Monitoring Plan 
 
To identify unanticipated problems or complications, study participants will be provided 
at enrollment with contact information for the study coordinator, principal investigator, and the 
VA hospital patient relations representative.   Any unanticipated problems or complications will 
be reported to the MR IRB per UW-Madison campus policy.  Corrective actions, such as 
changes to the research protocol or informed consent process, will be taken in order to protect 
the safety, welfare or rights of study subjects or others.  Researchers will monitor biweekly for 
patient reports of affective distress and PTSD symptoms to inform decisions to stop treatment 

Version 5; 3/5/2015 
20
early in consultation with the data monitoring committee.  Additionally, the Clinical Science 
Research and Development (CSRD) Data Monitoring Committee will review safety data. 
 
 
Safety and Protection of Human Subjects 
 
Subject privacy will be protected during the course of this study and HIPAA regulation 
will be followed. Only relevant, applicable study data will be collected, and will be entered in a 
secure web-based system with restricted access.   Any required paper data will be kept in a 
confidential locked area, with no personal identifying information in our data set.  This will be 
available only to primary study staff directly responsible for this data, and to representatives of 
the VA Research and Development Committee or University of Wisconsin IRB.  Access to data 
will be removed if study staff are no longer part of the study team.  Informed consent will be 
obtained by study staff. A data and safety monitoring committee will review all adverse events.  
Medical emergency and safety plans will be established, and adverse events will be reported in 
a timely manner to appropriate committees.  
In accordance with VA policy, in the case of reporting incidents, i.e. theft or loss of data 
or storage media, unauthorized access of sensitive data or storage devices or non-compliance 
with security controls, the Information Security Officer and Privacy Officer will be notified within 
one hour to determine an appropriate course of action.   
 
 
Statistical Considerations 
 
Power considerations   
Estimated effect sizes for the primary treatment comparison and the power available to 
detect these effects with two-tailed tests are provided below for the total N = 120 participants 
with 25% attrition, using intent-to-treat approach. We computed power for the GLMM 
longitudinal analysis using a SAS macro developed by Dang and colleagues108.  
Specific Aim 1: Dr. Lejuez’s recent trial of BA for smoking cessation in smokers with 
symptoms of depression showed that 19% of smokers who received ST+BA were abstinent at 
6-months post-quit, relative to those who received a contact-control smoking cessation 
treatment (0% abstinence rate at 6-months post-quit). For a treatment of this intensity (ST+BA), 
we believe that an improvement of at least 15% at 26-weeks post-quit would be sufficiently large 
to support additional research. For the current study, we predict that 6-month point prevalence 
abstinence rates will be 20% for ST+BA and approximately 5% for ST+HSE. We computed 
power for the GLMM longitudinal analysis using a SAS macro developed by Dang and 
colleagues109 with the following parameters: N=45 per group; 5 time-points; drop-out rate of 
0.25; 5% vs. 20% treatment effect over time; random effects variance=1; and within-subject 
correlation=0.6. Power for this scenario is 0.85. Even though power estimates have accounted 
for an estimated 25% attrition for a sample of N=90, we increased the sample size by 30 
participants (N=120) to ensure that we have sufficient statistical power (which accounts for 25% 
attrition). Thus, the current study will have strong statistical power in the GLMM analyses.  
 
 
Data and Record Keeping 
 
Data elements will be collected and stored during the screening assessment and all 
visits and phone assessments. During the screening session, data resulting from structured 
clinical interviews assessing Axis I Disorders will be collected and stored. In addition, 
questionnaires measuring mood, medical history, smoking characteristics, craving, withdrawal 
symptoms, CO levels, behavioral activation, and demographic information will be collected and 

Version 5; 3/5/2015 
21
stored. During later visits, questionnaires measuring mood, craving, withdrawal symptoms, CO 
levels, cotinine levels, and behavioral activation will be collected and stored.    
Screening assessment data will be collected and stored in paper format.  A summary of 
the screening assessment and all study questionnaires at study visits will be administered to 
participants via a web-based computer program called Qualtrics that presents questions on the 
screen that are answered by entering keystrokes on the computer keyboard.  Qualtrics is 
available and funded through UW DoIT and provides a HIPAA-compliant, encrypted data 
collection system that allows completion of questionnaires without paper data.  Data are stored 
on a secure password-protected UW server but not on the computer on which the participant 
completes the Qualtrics questionnaires.   
The study will utilize a unique study ID for storing all data related to individual 
participants.  Information linking that study ID to participant identifying information will be 
maintained by the PI. Subject identifying information will only be available to those study staff 
with whom subjects have direct contact. Data being used for analysis will be identified with the 
study ID only. Aside from the screening assessment, the study will not routinely utilize any 
paper or non-electronic records; if paper records are used as a back-up during a period when a 
functioning computer is not available, they will be maintained in a locked area after their entry 
has been properly verified.  Paper data will likely be kept in room G22 (VHAMADCookJ) or G13 
(VHAMADWebstK) of the VA hospital.  Electronic records may be obtained on a mobile device 
that is protected with VA approved encryption technology that is FIPS 140-2 validated. 
The name, contact information, and study schedule for interested and enrolled 
participants will be kept in a separate database.  The automated list of potential participants to 
whom informational letters will be sent will be maintained in a separate database as well.  This 
identifiable information is maintained in order to contact and follow-up with interested potential 
participants or enrolled participants.  No study data will be stored in these databases.  All 
identifiable data will be stored on secure, password-protected servers located at the Madison 
VA and only study personnel will be granted access.  All data that is not identifiable (forms 
collected after enrollment that are identified only by study number) is stored on a UW DoIT 
server with a copy of this data retained on a VA server. 
Data will be maintained by the Madison, WI VAMC following the completion of the study. 
 
Safety and Protection of Data Collected in Qualtrics 
 
The research team will manage study data through Qualtrics.  Qualtrics is an electronic 
data management system that will be used to capture, edit, manage, and export study data for 
analysis.  Qualtrics is a HIPAA-secure survey tool obtained through licensing agreement with 
the University of Wisconsin System and promoted for research by DoIt.  Subject identifiable 
information is restricted at multiple levels; 
1. Access to the Qualtrics system is restricted to those that have been granted access by 
the software administrators. User access requires supervisor approval, completion of 
HIPAA and Human Subjects Protection training, and completion of role-based training in 
the Qualtrics system.  
2. In addition, users’ access is limited to protocols for which they have some responsibility 
of protocol, subject, or data management.  
3. Within those protocols, the ability to view and modify data is restricted based on their 
role in the conduct of the research project (e.g. regulatory staff do not have the privilege 
to view subject identifiable information). 
 
In addition, the technical components of this software are managed by the UW-
Madison’s Bioinformatics Computing Group (for server maintenance, software upgrades, etc.), 
and security and software support is provided by CTRI staff. CTRI staff are able to access 
subject information in order to help end users of the software program when questions arise.  

Version 5; 3/5/2015 
22
All communication between the clients and the Qualtrics application takes place via 
Hypertext Transfer Protocol over Secure Socket Layer or HTTPS. HTTPS provide the ability for 
normal web based communication over an encrypted Secure Socket Layer (SSL) connection. 
This ensures that data passing between the client and Qualtrics is protected from unauthorized 
attempts to access the data. 
The Qualtrics system is web-based software, with data stored on secure servers. Data 
exported from the Qualtrics System, is exported with indirect identifiers (i.e. with study ID 
number per subject) for statistical and data monitoring purposes in an MS Excel or SAS format. 
Upon exportation, the clinical research management system has no control over how it is 
manipulated or managed.  Qualtrics data is backed up regularly.  In addition, a copy of all 
Qualtrics data for the study is stored at the VA. 
 
 

Version 5; 3/5/2015 
23
References 
  
1. 
Bray RM, Hourani LL, Olmsted KLR, et al. 2005 Department of Defense survey of health 
related behaviors among active duty military personnel. Available at: 
http://www.ha.osd.mil/special_reports/2005_Health_Behaviors_Survey_1-07.pdf. 
Accessed Nov, 2009. 
2. 
Cook J, Jakupcak M, Rosenheck R, Fontana A, McFall M. Influence of PTSD symptom 
clusters on smoking status among help-seeking Iraq and Afghanistan veterans. Nicotine 
Tob Res. Jul 31 2009;11(10):1089-1095. 
3. 
Seal K, Maguen S, Cohen B, et al. VA mental health services utilization in Iraq and 
Afghanistan veterans in the first year of receiving new diagnoses. J Trauma Stress. in 
press. 
4. 
Beckham JC, Kirby AC, Feldman ME, et al. Prevalence and correlates of heavy smoking 
in Vietnam veterans with chronic posttraumatic stress disorder. Addict Behav. Sep-Oct 
1997;22(5):637-647. 
5. 
Feldner MT, Babson KA, Zvolensky MJ. Smoking, traumatic event exposure, and post-
traumatic stress: a critical review of the empirical literature. Clin Psychol Rev. Jan 
2007;27(1):14-45. 
6. 
Lasser K, Boyd JW, Woolhandler S, Himmelstein DU, McCormick D, Bor DH. Smoking 
and mental illness: A population-based prevalence study. JAMA. Nov 22-29 
2000;284(20):2606-2610. 
7. 
McFall M, Saxon AJ, Thompson CE, et al. Improving the rates of quitting smoking for 
veterans with posttraumatic stress disorder. Am J Psychiatry. Jul 2005;162(7):1311-
1319. 
8. 
Piper ME, Federmen EB, McCarthy DE, et al. Using mediational models to explore the 
nature of tobacco motivation and tobacco treatment effects. J Abnorm Psychol. Feb 
2008;117(1):94-105. 
9. 
McCarthy DE, Piasecki TM, Lawrence DL, Jorenby DE, Shiffman S, Baker TB. 
Psychological mediators of bupropion sustained-release treatment for smoking 
cessation. Addiction. Sep 2008;103(9):1521-1533. 
10. 
Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United 
States, 2000. JAMA. 2004;291(10):1238-1245. 
11. 
U.S. Department of Health and Human Services. The health consequences of smoking: 
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; 2004. 
12. 
Centers for Disease Control and Prevention. Cigarette smoking among adults - United 
States, 2007. MMWR. 2008;57(45):1221-1226. 
13. 
Brown DW. Smoking prevalence among U.S. veterans. J Gen Intern Med. Nov 6 
2009;Epub ahead of print]. 
14. 
Lynch JP, Hanson K, Kao TC. Health-related behaviors in young military smokers. Mil 
Med. Mar 2004;169(3):230-235. 
15. 
Beckham JC, Roodman AA, Shipley RH, et al. Smoking in Vietnam combat veterans 
with post-traumatic stress disorder. J Trauma Stress. Jul 1995;8(3):461-472. 
16. 
Shalev A, Bleich A, Ursano RJ. Posttraumatic stress disorder: somatic comorbidity and 
effort tolerance. Psychosomatics. Spring 1990;31(2):197-203. 
17. 
Beckham JC, Moore SD, Feldman ME, Hertzberg MA, Kirby AC, Fairbank JA. Health 
status, somatization, and severity of posttraumatic stress disorder in Vietnam combat 
veterans with posttraumatic stress disorder. Am J Psychiatry. Nov 1998;155(11):1565-
1569. 
18. 
Schnurr PP, Jankowski MK. Physical health and post-traumatic stress disorder: review 
and synthesis. Semin Clin Neuropsychiatry. Oct 1999;4(4):295-304. 

Version 5; 3/5/2015 
24
19. 
Friedman MJ, Schnurr PP. The relationship between trauma, post-traumatic stress 
disorder, and physical health. In: Friedman MJ, Charney DS, Deutch AY, eds. 
Neurobiological and clinical consequences of stress: From normal adaptation to PTSD. 
Philadelphia: Lippincott-Raven; 1995:507-524. 
20. 
Institute of Medicine. Combating tobacco use in military and veteran populations. 
Available at: 
http://www.iom.edu/~/media/Files/Report%20Files/2009/MilitarySmokingCessation/Com
bating%20Tobacco%20Military%20for%20web.ashx. Accessed Dec 9, 2009. 
21. 
Breslau N, Kessler RC, Chilcoat HD, Schultz LR, Davis GC, Andreski P. Trauma and 
posttraumatic stress disorder in the community: the 1996 Detroit Area Survey of Trauma. 
Arch Gen Psychiatry. Jul 1998;55(7):626-632. 
22. 
Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of DSM-
III-R psychiatric disorders in the United States. Results from the National Comorbidity 
Survey. Arch Gen Psychiatry. Jan 1994;51(1):8-19. 
23. 
Hankin CS, Spiro A, 3rd, Miller DR, Kazis L. Mental disorders and mental health 
treatment among U.S. Department of Veterans Affairs outpatients: the Veterans Health 
Study. Am J Psychiatry. Dec 1999;156(12):1924-1930. 
24. 
Seal KH, Metzler TJ, Gima KS, Bertenthal D, Maguen S, Marmar CR. Trends and risk 
factors for mental health diagnoses among Iraq and Afghanistan veterans using 
Department of Veterans Affairs health care, 2002-2008. Am J Public Health. Sep 
2009;99(9):1651-1658. 
25. 
Jakupcak M, Cook J, Imel Z, Fontana A, Rosenheck R, McFall M. Posttraumatic stress 
disorder as a risk factor for suicidal ideation in Iraq and Afghanistan War veterans. J 
Trauma Stress. Aug 2009;22(4):303-306. 
26. 
Jakupcak M, Luterek J, Hunt S, Conybeare D, McFall M. Posttraumatic stress and its 
relationship to physical health functioning in a sample of Iraq and Afghanistan War 
veterans seeking postdeployment VA health care. J Nerv Ment Dis. May 
2008;196(5):425-428. 
27. 
Jakupcak M, Conybeare D, Phelps L, et al. Anger, hostility, and aggression among Iraq 
and Afghanistan War veterans reporting PTSD and subthreshold PTSD. J Trauma 
Stress. Dec 2007;20(6):945-954. 
28. 
Centers for Disease Control and Prevention. Cigarette smoking among adults and trends 
in smoking cessation - United States, 2008. MMWR. 2009;58(44):1227-1232. 
29. 
Breslau N, Davis GC, Schultz LR. Posttraumatic stress disorder and the incidence of 
nicotine, alcohol, and other drug disorders in persons who have experienced trauma. 
Arch Gen Psychiatry. Mar 2003;60(3):289-294. 
30. 
Miller DR, Kalman D, Ren XS, Lee AF, Niu Z, Kazis L. Health behaviors of veterans in 
the VHA: Tobacco use: 1999 large health survey of VHA enrollees. Washington, D.C: 
Office of Quality and Performance, Veterans Health Administration, Department of 
Veterans Affairs; 2001. 
31. 
Zvolensky MJ, Stewart SH, Vujanovic AA, Gavric D, Steeves D. Anxiety sensitivity and 
anxiety and depressive symptoms in the prediction of early smoking lapse and relapse 
during smoking cessation treatment. Nicotine Tob Res. Mar 2009;11(3):323-331. 
32. 
Comings DE, Ferry L, Bradshaw-Robinson S, Burchette R, Chiu C, Muhleman D. The 
dopamine D2 receptor (DRD2) gene: a genetic risk factor in smoking. 
Pharmacogenetics. Feb 1996;6(1):73-79. 
33. 
Comings DE, Muhleman D, Gysin R. Dopamine D2 receptor (DRD2) gene and 
susceptibility to posttraumatic stress disorder: a study and replication. Biol Psychiatry. 
Sep 1 1996;40(5):368-372. 
34. 
Koenen KC, Hitsman B, Lyons MJ, et al. A twin registry study of the relationship 
between posttraumatic stress disorder and nicotine dependence in men. Arch Gen 
Psychiatry. 2005;62(11):1258-1265. 

Version 5; 3/5/2015 
25
35. 
van der Velden PG, Kleber RJ, Koenen KC. Smoking predicts posttraumatic stress 
symptoms among rescue workers: a prospective study of ambulance personnel involved 
in the Enschede Fireworks Disaster. Drug Alcohol Depend. Apr 1 2008;94(1-3):267-271. 
36. 
Cook JW, McFall MM, Calhoun PS, Beckham JC. Posttraumatic stress disorder and 
smoking relapse: A theoretical model. J Trauma Stress. Dec 2007;20(6):989-998. 
37. 
Beckham J. Smoking and anxiety in combat veterans with chronic posttraumatic stress 
disorder:  A review. J Psychoactive Drugs. 4/1999 1999;31(2):103-110. 
38. 
Brown PJ, Wolfe J. Substance abuse and post-traumatic stress disorder comorbidity. 
Drug Alcohol Depend. Mar 1994;35(1):51-59. 
39. 
Beckham JC, Feldman ME, Barefoot JC, et al. Ambulatory cardiovascular activity in 
Vietnam combat veterans with and without posttraumatic stress disorder. J Consult Clin 
Psychol. Apr 2000;68(2):269-276. 
40. 
Coyne JC. Self-reported distress: analog or Ersatz depression? Psychol Bull. Jul 
1994;116(1):29-45. 
41. 
Watson D, Clark LA, Tellegen A. Development and validation of brief measures of 
positive and negative affect: The PANAS scales. J Pers Soc Psychol. Jun 
1988;54(6):1063-1070. 
42. 
Cook JW, Spring B, McChargue D, Hedeker D. Hedonic capacity, cigarette craving, and 
diminished positive mood. Nicotine Tob Res. Feb 2004;6(1):39-47. 
43. 
Davidson RJ. Anterior cerebral asymmetry and the nature of emotion. Brain Cogn. Sep 
1992;20(1):125-151. 
44. 
Roemer L, Litz BT, Orsillo SM, Wagner AW. A preliminary investigation of the role of 
strategic withholding of emotions in PTSD. J Trauma Stress. 2001/01// 2001;14(1):149-
156. 
45. 
Litz BT, Gray MJ. Emotional numbing in posttraumatic stress disorder: current and future 
research directions. Aust N Z J Psychiatry. Apr 2002;36(2):198-204. 
46. 
Rauch SL, van der Kolk BA, Fisler RE, et al. A symptom provocation study of 
posttraumatic stress disorder using positron emission tomography and script-driven 
imagery. Arch Gen Psychiatry. May 1996;53(5):380-387. 
47. 
Baker TB, Piper ME, McCarthy DE, Majeskie MR, Fiore MC. Addiction motivation 
reformulated: An affective processing model of negative reinforcement. Psychol Rev. 
2004;111(1):33-51. 
48. 
Beckham JC, Wiley MT, Miller SC, et al. Ad lib smoking in post-traumatic stress 
disorder: an electronic diary study. Nicotine Tob Res. Jul 2008;10(7):1149-1157. 
49. 
Beckham JC, Dennis MF, McClernon FJ, Mozley SL, Collie CF, Vrana SR. The effects of 
cigarette smoking on script-driven imagery in smokers with and without posttraumatic 
stress disorder. Addict Behav. Dec 2007;32(12):2900-2915. 
50. 
Kenford SL, Fiore MC, Jorenby DE, Smith SS, Wetter D, Baker TB. Predicting smoking 
cessation. Who will quit with and without the nicotine patch. JAMA. Feb 23 
1994;271(8):589-594. 
51. 
Cook JW, Spring B, McChargue D. Influence of nicotine on positive affect in anhedonic 
smokers. Psychopharmacology (Berl). May 2007;192(1):87-95. 
52. 
Corrigall WA. Understanding brain mechanisms in nicotine reinforcement. Br J Addict. 
May 1991;86(5):507-510. 
53. 
Ferster CB. A functional anlysis of depression. Am Psychol. Oct 1973;28(10):857-870. 
54. 
Lewinsohn PM. A behavioral approach to depression. In: Friedman RM, Katz MM, eds. 
The psychology of depression: Contemporary theory and research. New York: Wiley; 
1974. 
55. 
Beck AT, Steer RA, Brown GK. Manual for Beck Depression Inventory II (BDI-II). San 
Antonio, TX: Psychology Corporation; 1996. 
56. 
Jacobson NS, Martell CR, Dimidjian S. Behavioral activation treatment for depression: 
Returning to contextual roots. Clin Psychol: Science and Practice. 2001;8:255-270. 

Version 5; 3/5/2015 
26
57. 
Gortner ET, Gollan JK, Dobson KS, Jacobson NS. Cognitive-behavioral treatment for 
depression: relapse prevention. J Consult Clin Psychol. Apr 1998;66(2):377-384. 
58. 
Dimidjian S, Hollon SD, Dobson KS, et al. Randomized trial of behavioral activation, 
cognitive therapy, and antidepressant medication in the acute treatment of adults with 
major depression. J Consult Clin Psychol. Aug 2006;74(4):658-670. 
59. 
Lejuez CW, Hopko DR, LePage JP, Hopko SD, McNeil DW. A brief behavioral activation 
treatment for depression. Cognit Behav Practice. 2001///Spr 2001;8(2):164-175. 
60. 
Hopko DR, Lejuez CW, LePage JP, Hopko SD, McNeil DW. A brief behavioral activation 
treatment for depression. A randomized pilot trial within an inpatient psychiatric hospital. 
Behav Modif. Sep 2003;27(4):458-469. 
61. 
Daughters SB, Braun AR, Sargeant MN, et al. Effectiveness of a brief behavioral 
treatment for inner-city illicit drug users with elevated depressive symptoms: the life 
enhancement treatment for substance use (LETS Act!). J Clin Psychiatry. Jan 
2008;69(1):122-129. 
62. 
Hopko DR, Armento ME, Cantu MS, Chambers LL, Lejuez CW. The use of daily diaries 
to assess the relations among mood state, overt behavior, and reward value of activities. 
Behav Res Ther. Oct 2003;41(10):1137-1148. 
63. 
Wagner AW, Zatzick DF, Ghesquiere A, Jurkovich GJ. Behavioral activation as an early 
intervention for posttraumatic stress disorder and depression among physically injured 
trauma survivors. Cognit Behav Practice. 2007/11// 2007;14(4):341-349. 
64. 
Mulick PS, Naugle AE. Behavioral activation for comorbid PTSD and major depression: 
A case study. Cognit Behav Practice. 2004///Fal 2004;11(4):378-387. 
65. 
Jakupcak M, Roberts LJ, Martell C, et al. A pilot study of behavioral activation for 
veterans with posttraumatic stress disorder. J Trauma Stress. Jun 2006;19(3):387-391. 
66. 
Foa EB, Rothbaum BO. Treating the trauma of rape: Cognitive behavioral therapy for 
PTSD. New York: Guilford Press; 1998. 
67. 
Johnson DR, Lubin H. Treatment preferences of Vietnam veterans with posttraumatic 
stress disorder. J Trauma Stress. Jul 1997;10(3):391-405. 
68. 
MacPherson L, Tull MT, Matusiewicz A, al. e. Randomized controlled trial of behavioral 
activation smoking cessation treatment for smokers with elevated depressive symptoms. 
J Consult Clin Psychol. in press. 
69. 
Frueh BC, Gold PB, Dammeyer M, et al. Differentiation of depression and PTSD 
symptoms in combat veterans. Depress Anxiety. 2000;11(4):175-179. 
70. 
Leventhal AM, Ramsey SE, Brown RA, LaChance HR, Kahler CW. Dimensions of 
depressive symptoms and smoking cessation. Nicotine Tob Res. Mar 2008;10(3):507-
517. 
71. 
Kinnunen T, Leeman RF, Korhonen T, et al. Exercise as an adjunct to nicotine gum in 
treating tobacco dependence among women. Nicotine Tob Res. Apr 2008;10(4):689-
703. 
72. 
McCarthy DE, Piasecki TM, Fiore MC, Baker TB. Life before and after quitting smoking: 
an electronic diary study. J Abnorm Psychol. Aug 2006;115(3):454-466. 
73. 
Brady KT, Killeen TK, Brewerton T, Lucerini S. Comorbidity of psychiatric disorders and 
posttraumatic stress disorder. J Clin Psychiatry. 2000;61 Suppl 7:22-32. 
74. 
Dichter GS, Felder JN, Petty C, Bizzell J, Ernst M, Smoski MJ. The effects of 
psychotherapy on neural responses to rewards in major depression. Biol Psychiatry. Nov 
1 2009;66(9):886-897. 
75. 
Johnson JG, Cohen P, Pine DS, Klein DF, Kasen S, Brook JS. Association between 
cigarette smoking and anxiety disorders during adolescence and early adulthood. JAMA. 
Nov 8 2000;284(18):2348-2351. 
76. 
Gray J. A critique of Eysenck's theory of personality. In: Eysenck HJ, ed. A model for 
personality. Berlin: Springer-Verlag; 1981:246-276. 

Version 5; 3/5/2015 
27
77. 
Fiore MC, Kenford SL, Jorenby DE, Wetter DW, Smith SS, Baker TB. Two studies of the 
clinical effectiveness of the nicotine patch with different counseling treatments. Chest. 
Feb 1994;105(2):524-533. 
78. 
Jorenby DE, Leischow SJ, Nides MA, et al. A controlled trial of sustained-release 
bupropion, a nicotine patch, or both for smoking cessation. N Engl J Med. Mar 4 
1999;340(9):685-691. 
79. 
Piper ME, Federman EB, McCarthy DE, et al. Efficacy of bupropion alone and in 
combination with nicotine gum. Nicotine Tob Res. Sep 2007;9(9):947-954. 
80. 
Smith SS, Jorenby DE, Leischow SJ, et al. Targeting smokers at increased risk for 
relapse: Treating women and those with a history of depression. Nicotine Tob Res. Feb 
2003;5(1):99-109. 
81. 
Jorenby D. Clinical efficacy of bupropion in the management of smoking cessation. 
Drugs. 2002;62 Suppl 2:25-35. 
82. 
Jorenby DE, Hays JT, Rigotti NA, et al. Efficacy of varenicline, an alpha4beta2 nicotinic 
acetylcholine receptor partial agonist, vs placebo or sustained-release bupropion for 
smoking cessation: a randomized controlled trial. JAMA. 2006;296(1):56-63. 
83. 
Smith SS, Jorenby DE, Fiore MC, et al. Strike while the iron is hot: can stepped-care 
treatments resurrect relapsing smokers? J Consult Clin Psychol. Jun 2001;69(3):429-
439. 
84. 
McCarthy DE, Bolt DM, Baker TB. The importance of how: A call for mechanistic 
research in tobacco dependence treatment studies. In: Treat T, Bootzin RI, Baker TB, 
eds. Psychological clinical science: recent advances in theory and practicer. Integrative 
perspectives in honor of Richard M. McFall. New York: Lawrence Erlbaum Associates; 
2007:133-163. 
85. 
Hopko DR, Sanchez L, Hopko SD, Dvir S, Lejuez CW. Behavioral activation and the 
prevention of suicidal behaviors in patients with borderline personality disorder. J Pers 
Disord. Oct 2003;17(5):460-478. 
86. 
Hopko DR, Lejuez CW, Hopko SD. Behavioral activation as an intervention for co-
existent depressive and anxiety symptoms. Clinical Case Studies. 2004:37-48. 
87. 
Hopko DR, Lejuez CW, LePage J, Hopko SD, McNeil DW. A brief behavioral activation 
treatment for depression: A randomized trial within an inpatient psychiatric hospital. 
Behav Modif. 2002:255-286. 
88. 
Cohen J. Statistical power analysis for the behavioral sciences. Hillsdale, NJ: Lawrence 
Erlbaum Associates; 1988. 
89. 
McNair DM, Lorr M, Droppleman LF. Profile of mood states manual. San Diego, CA: 
Educational and Industrial Testing Service; 1971. 
90. 
Spring B, Doran N, Pagoto S, et al. Fluoxetine, smoking, and history of major 
depression: A randomized controlled trial. J Consult Clin Psychol. Feb 2007;75(1):85-94. 
91. 
Piper ME, Federman EB, Smith SS, Fiore MC, Baker TB. Efficacy of bupropion SR alone 
and combined with 4-mg nicotine gum. Talk to be presented at the 10th Annual Meeting 
of the Society for Research on Nicotine and Tobacco, Scottsdale, AZ,. 2004. 
92. 
Jorenby DE, Fiore MC. Smoking cessation. In: Crapo JD, Glassroth J, Karlinsky J, King 
TE, eds. Baum's Textbook of Pulmonary Diseases. 7 ed. Philadelphia: Lippincott, 
Williams & Wilkins; 2003:279-288. 
93. 
Piper ME, Smith SS, Schlam TR, et al. A randomized placebo-controlled clinical trial of 5 
smoking cessation pharmacotherapies. Arch Gen Psychiatry. Nov 2009;66(11):1253-
1262. 
94. 
Shiffman S, Paty J. Smoking patterns and dependence: contrasting chippers and heavy 
smokers. J Abnorm Psychol. Aug 2006;115(3):509-523. 
95. 
Weathers FW, Keane TM, Davidson JR. Clinician-administered PTSD scale: a review of 
the first ten years of research. Depress Anxiety. 2001;13(3):132-156. 

Version 5; 3/5/2015 
28
96. 
Brigham GS, Feaster DJ, Wakim PG, Dempsey CL. Choosing a control group in 
effectiveness trials of behavioral drug abuse treatments. J Subst Abuse Treat. Dec 
2009;37(4):388-397. 
97. 
Fiore MC, Jaen CR, Baker TB, et al. Treating tobacco use and dependence: 2008 
update. Rockville, MD: U.S. Department of Health and Human Services, U.S. Public 
Health Service.; 2008. 
98. 
Hall SM, Humfleet GL, Reus VI, Munoz RF, Cullen J. Extended nortriptyline and 
psychological treatment for cigarette smoking. Am J Psychiatry. Nov 2004;161(11):2100-
2107. 
99. 
Hall SM, Munoz RF, Reus VI. Cognitive-behavioral intervention increases abstinence 
rates for depressive-history smokers. J Consult Clin Psychol. Feb 1994;62(1):141-146. 
100. 
Ussher M, West R, McEwen A, Taylor A, Steptoe A. Efficacy of exercise counselling as 
an aid for smoking cessation: A randomized controlled trial. Addiction. Apr 
2003;98(4):523-532. 
101. 
Ussher M, West R, McEwen A, Taylor A, Steptoe A. Randomized controlled trial of 
physical activity counseling as an aid to smoking cessation: 12 month follow-up. Addict 
Behav. Dec 2007;32(12):3060-3064. 
102. 
Galvin K, Webb C, Hillier V. Assessing the impact of a nurse-led health education 
intervention for people with peripheral vascular disease who smoke: the use of 
physiological markers, nicotine dependence and withdrawal. Int J Nurs Stud. Feb 
2001;38(1):91-105. 
103. 
Klesges RC, DeBon M, Vander Weg MW, et al. Efficacy of a tailored tobacco control 
program on long-term use in a population of U.S. military troops. J Consult Clin Psychol. 
Apr 2006;74(2):295-306. 
104. 
Williamson GM. The central role of restricted normal activities in adjustment to illness 
and disability: A model of depressed affect. Rehab Psychol. 1998///Win 1998;43(4):327-
347. 
105. 
Barlow DH, Allen LB, Choate ML. Toward a Unified Treatment for Emotional Disorders. 
Behav Ther. 2004///Spr 2004;35(2):205-230. 
106. 
Bliese PD, Wright KM, Adler AB, Cabrera O, Castro CA, Hoge CW. Validating the 
primary care posttraumatic stress disorder screen and the posttraumatic stress disorder 
checklist with soldiers returning from combat. J Consult Clin Psychol. Apr 
2008;76(2):272-281. 
107. 
Prins A, Ouimette P, Kimerling R, et al. The primary care PTSD screen (PC-PTSD): 
Development and operating characteristics. Primary Care, Psychiatry. 2004;9:9-14. 
108. 
Blake DD, Weathers RW, Nagy LM, et al. A clinician rating scale for assessing current 
and lifetime PTSD: The CAPS-1. Behaviour Therapist. 1990;13:187-188. 
109. 
Spitzer RL, Williams JB, Gibbon M, First MB. The Structured Clinical Interview for DSM-
III-R (SCID). History, rationale, and description. Arch Gen Psychiatry. 1992;49:624-629. 
110. 
Williams JB, Gibbon M, First MB, et al. The Structured Clinical Interview for DSM-III-R 
(SCID). II. Multisite test-retest reliability. Arch Gen Psychiatry. Aug 1992;49(8):630-636. 
111. 
Heatherton TF, Kozlowski LT, Frecker RC, Fagerstrom KO. The Fagerstrom Test for 
Nicotine Dependence: a revision of the Fagerstrom Tolerance Questionnaire. Br J 
Addict. Sep 1991;86(9):1119-1127. 
112. 
Baker TB, Piper ME, McCarthy DE, et al. Time to first cigarette in the morning as an 
index of ability to quit smoking: implications for nicotine dependence. Nicotine Tob Res. 
Nov 2007;9 Suppl 4:S555-570. 
113. 
SRNT Subcommittee on Biochemical Verification. Biochemical verification of tobacco 
use and cessation. Nicotine Tob Res. 2002;4:149-159. 
114. 
Sobell LC, Sobell MB, Leo GI, Cancilla A. Reliability of a timeline method: Assessing 
normal drinkers' reports of recent drinking and a comparative evaluation across several 
populations. Br J Addict. Apr 1988;83(4):393-402. 

Version 5; 3/5/2015 
29
115. 
Jarvis MJ, Tunstall-Pedoe H, Feyerabend C, Vesey C, Saloojee Y. Comparison of tests 
used to distinguish smokers from nonsmokers. Am J Public Health. Nov 
1987;77(11):1435-1438. 
116. 
Blanchard EB, Jones-Alexander J, Buckley TC, Forneris CA. Psychometric properties of 
the PTSD Checklist (PCL). Behav Res Ther. Aug 1996;34(8):669-673. 
117. 
Armento ME, Hopko DR. The Environmental Reward Observation Scale (EROS): 
development, validity, and reliability. Behav Ther. Jun 2007;38(2):107-119. 
118. 
Carver S, White T. Behavioral inhibition, behavioral activation and affective responses to 
impending reward and punishment: The BIS/BAS scales. J Pers Soc Psychol. 
1994;67:319-333. 
119. 
Meyer B, Johnson SL, Winters R. Responsiveness to threat and incentive in bipolar 
disorder: Relations of the BIS/BAS scales with symptoms. J Psychopathol Behav 
Assess. 2001/09// 2001;23(3):133-143. 
120. 
Hughes JR, Hatsukami D. Signs and symptoms of tobacco withdrawal. Arch Gen 
Psychiatry. Mar 1986;43(3):289-294. 
121. 
Piasecki TM, Niaura R, Shadel WG, et al. Smoking withdrawal dynamics in unaided 
quitters. J Abnorm Psychol. 2000;109(1):74-86. 
122. 
Gwaltney CJ, Shiffman S, Balabanis MH, Paty JA. Dynamic self-efficacy and outcome 
expectancies: prediction of smoking lapse and relapse. J Abnorm Psychol. Nov 
2005;114(4):661-675. 
123. 
Hufford MR, Shields AL, Shiffman S, Paty J, Balabanis M. Reactivity to ecological 
momentary assessment: an example using undergraduate problem drinkers. Psychol 
Addict Behav. Sep 2002;16(3):205-211. 
124. 
U.S. Department of Health and Human Services. Clearing the air: How to quit 
smoking...and quit for keeps. NIH publication no. 95-1647: Public Health Service, 
National Institutes of Health, National Cancer Institute; 1995. 
125. 
Waltz J, Addis ME, Koerner K, Jacobson NS. Testing the integrity of a psychotherapy 
protocol: assessment of adherence and competence. J Consult Clin Psychol. Aug 
1993;61(4):620-630. 
126. 
Schafer JL, Graham JW. Missing data: our view of the state of the art. Psychol Methods. 
Jun 2002;7(2):147-177. 
127. 
Graham JW. Missing data analysis: making it work in the real world. Annu Rev Psychol. 
2009;60:549-576. 
128. 
Collins LM, Schafer JL, Kam CM. A comparison of inclusive and restrictive strategies in 
modern missing data procedures. Psychol Methods. Dec 2001;6(4):330-351. 
129. 
Piasecki TM, Jorenby DE, Smith SS, Fiore MC, Baker TB. Smoking withdrawal 
dynamics: I. Abstinence distress in lapsers and abstainers. J Abnorm Psychol. Feb 
2003;112(1):3-13. 
130. 
Piasecki TM, Jorenby DE, Smith SS, Fiore MC, Baker TB. Smoking withdrawal 
dynamics: II. Improved tests of withdrawal-relapse relations. J Abnorm Psychol. Feb 
2003;112(1):14-27. 
131. 
Cole DA, Maxwell SE. Testing mediational models with longitudinal data: Questions and 
tips in the use of structural equations modeling. J Abnorm Psychol. in press. 
132. 
MacKinnon DP, Lockwood CM. Distribution of products tests for the mediated effect. 
2001:Unpublished manuscript. 
133. 
Sobel ME. Asymptomatic confidence intervals for indirect effects for structural equation 
models. In: Leinhardt S, ed. Sociological methodology. Washington, DC: American 
Sociological Association; 1982:290-312. 
134. 
MacKinnon DP, Fritz MS, Williams J, Lockwood CM. Distribution of the produce 
confidence limits for the indirect effect: Program PRODCLIN. Behav Res Methods. 
2007;39:384-389. 
135. 
Fritz MS, Mackinnon DP. Required sample size to detect the mediated effect. Psychol 
Sci. Mar 2007;18(3):233-239. 

Version 5; 3/5/2015 
30
136. 
Yehuda, R., Giller, E. L., Southwick, S. M., Lowy, M. T., & Mason, J. W. (1991). 
Hypothalamic-pituitary-adrenal dysfunction in posttraumatic stress disorder. Biological 
Psychiatry, 30, 1031-1048.