cigarette smoking and depression comorbidity: systematic ... · cigarette smoking and depression...

Cigarette smoking and depression comorbidity:systematic review and proposed theoretical model

Amanda R. Mathew1, Lee Hogarth2, Adam M. Leventhal3, Jessica W. Cook4,5 & Brian Hitsman1

Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA,1 School of Psychology, University of Exeter, Exeter, UK,2

Departments of Preventive Medicine and Psychology, University of Southern California Keck School of Medicine, Los Angeles, CA, USA,3 University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA4 and William S. Middleton Memorial Veterans Hospital, Madison, WI, USA5

ABSTRACT

Background and Aims Despite decades of research on co-occurring smoking and depression, cessation rates remainconsistently lower for depressed smokers than for smokers in the general population, highlighting the need for theory-drivenmodels of smoking and depression. This paper provides a systematic reviewwith a particular focus upon psycholog-ical states that disproportionately motivate smoking in depression, and frame an incentive learning theory account ofsmoking-depression co-occurrence. Methods We searched PubMed, Scopus, PsychINFO and CINAHL to December2014, which yielded 852 papers. Using pre-established eligibility criteria, we identified papers focused on clinical issuesand motivational mechanisms underlying smoking in established, adult smokers (i.e. maintenance, quit attempts andcessation/relapse) with elevated symptoms of depression. Two reviewers determined independently whether papers metreview criteria. We included 297 papers in qualitative synthesis. Results Our review identified three primary mecha-nisms that underlie persistent smoking among depressed smokers: low positive affect, high negative affect and cognitiveimpairment. We propose a novel application of incentive learning theory which posits that depressed smokers experiencegreater increases in the expected value of smoking in the face of these three motivational states, which promotesgoal-directed choice of smoking behavior over alternative actions. Conclusions The incentive learning theory accountsfor current evidence on how depression primes smoking behavior and provides a unique framework for conceptualizingpsychological mechanisms of smoking maintenance among depressed smokers. Treatment should focus upon correctingadverse internal states and beliefs about the high value of smoking in those states to improve cessation outcomes fordepressed smokers.

Keywords Depression, nicotine dependence, review, smoking, smoking cessation, treatment.

Correspondence to: Amanda R. Mathew, Northwestern University Feinberg School of Medicine, Department of Preventive Medicine, 680 North Lake ShoreDrive, Suite 1400, Chicago, IL 60611, USA. E-mail: [email protected] 22 January 2016; 29 April 2016; final version accepted 5 September 2016

INTRODUCTION

Individuals with depression are more likely to smoke,smoke more cigarettes per day and are less likely to quitsmoking successfully than individuals without depression,and this health disparity is an important clinical and publichealth concern. Recent epidemiological data show that thesmoking rate for clinically depressed individuals is approx-imately twice the rate in the general population [1–6]. Fur-ther, smokers with depression report greater nicotinewithdrawal symptoms [7,8], due in part probably togreater nicotine dependence among depressed versusnon-depressed smokers [9–12]. Although depressedsmokers endorse levels of motivation to quit that are

similar to, or even higher than, smokers in the generalpopulation [13–15] and attempt to quit at similar rates[16], odds of successful abstinence at 1 month are30–50% lower for those with current depression andelevated depressive symptoms [16].

As smoking prevalence continues to decline in thegeneral population, those with mental illness are over-represented increasingly among smokers and constitutean important tobacco use disparity group [17]. Those withmental illness die up to 25 years earlier than those inthe general population, due largely to chronicillnesses associated with smoking (e.g. cardiovascular dis-ease [18–20]). Given that smoking cessation improvesboth mental [21–26] and physical health outcomes [27],

© 2016 Society for the Study of Addiction Addiction

REVIEW doi:10.1111/add.13604

even among smokers with chronic health conditions, de-velopment of smoking cessation interventions targeted tothose with various forms of mental illness (i.e. mood andanxiety disorders, substance use disorders, serious mentalillness) are greatly needed. Herein, we focus our reviewon continuous depressive symptomatology [28–30], rang-ing from subsyndromal levels of depression to clinical disor-ders (i.e. current or past diagnosis of major depression).

Although promising cessation treatments exist (e.g.[31]), no treatment has been shown to attenuate fullythe elevated relapse risk associated with depression, andfurther innovations in treatment development are needed.One major limitation to advances in treatment of comorbidsmoking–depression has been a lack of comprehensivetheories of the psychology of nicotine dependence and de-pression. Identifying the psychological mechanisms thatunderlie smoking persistence among those with elevateddepressive symptoms is critical for (1) a comprehensivecharacterization of the causal connection betweendepression and smoking and (2) developing innovative,theory-based and effective treatment strategies whichtarget these psychological mechanisms specifically indepressed smokers.

This systematic review provides an update of the cur-rent state of evidence on the topic of co-occurring smokingand depression and proposes a novel application of incen-tive learning theory to conceptualize smoking persistenceamong depressed smokers. As detailed below, the incentivelearning account has gained considerable empirical sup-port in the study of drug dependence [32–40], and offersa unique lens through which to view the clinical problemof smoking and depression. In particular, incentivelearning theory proposes that specific states drive goal-directed selection of smoking behavior over alternatechoices for depressed smokers. We believe that the incen-tive learning theory accounts for current evidence onhow depression primes smoking and identifies novelpsychological targets to optimize smoking cessationtreatment for depressed smokers.

MATERIALS AND METHODS

Data sources and searches

We searched the PubMed, Scopus, PsycINFO and CINAHLdatabases to December 2014, using Medical SubjectHeadings or Major Concept search terms when available.We combined smoking-related (i.e. smoking, tobacco,nicotine, smoking cessation, tobacco use, tobacco usedisorder, tobacco use cessation) and depression-relatedterms (i.e. depression, depressive, major depression).Search delimiters were ‘adult’, ‘human’ and ‘Englishlanguage’. We also performed manual searches ofreference lists of pertinent papers.

Study eligibility

Two authors reviewed abstracts and full-text publicationsindependently. Inclusion criteria stipulated that studiesexamine clinical issues relevant to established, adultsmokers (age ≥ 18 years), such as causes and correlatesof smoking maintenance, willingness to quit andcessation/relapse among established smokers, rather thansmoking initiation or progression to regular smoking. Thereview included both current/past major depression andelevated depressive symptoms. Studies not assessingdepression through clinical diagnostic instrument or vali-dated, continuous scale (i.e. by self-reported diagnosis orsingle-item only) were excluded. Studies of specialpopulations of smokers (e.g. psychiatric, medical) withoutmajor depression were excluded. We includedqualitative/quantitative reviews and clinical trial, humanlaboratory-based, observational and epidemiological studydesigns. Non-peer-reviewed publications and case studieswere excluded.

We excluded publications that both reviewers agreeddid not meet eligibility criteria. Authors resolved disagree-ments by consensus.

RESULTS

Results of literature searches

Our searches of databases identified 852 unique citations(Fig. 1). We screened 852 records by abstract and 453full-text papers. Of these, 297 papers were included in thequalitative synthesis. Publications incorporated in thenarrative review were those which contributed mostdirectly to our theoretical framework.

PSYCHOLOGICAL MECHANISMSPROMOTING SMOKING MAINTENANCEAND RELAPSE IN DEPRESSED SMOKERS

Affective processes

While depression is characterized by a wide range of affec-tive, cognitive, behavioral and somatic features [41],evidence is mounting that the affective disturbances indepression may play a qualitatively unique role indepression–smoking comorbidity over and above mostnon-affective depressive symptoms [15,42,43]. Indeed,symptom-level analyses have shown that high negativeaffect (NA; experience of subjective distress) and low posi-tive affect (PA; low engagement with the environment[44,45]) are associated uniquely with nicotine dependenceseverity [46,47], smoking heaviness [48] and smokingrelapse risk [42,49–53]. Moreover, low PA accounts forindependent variance in relapse risk, above and beyondhigh NA [42,49], suggesting that these two processesreflect unique etiological influences on smoking.

2 Amanda R. Mathew et al.


The notion that two distinct affective processes promotesmoking is consistent with multi-dimensional models ofpsychopathology and personality which purport that lowPA and high NA are empirically distinct overarchingpsychological dimensions that have unique psychosocialand biological etiologies [54–56]. The low PA dimensionincludes constructs related to appetitive emotion, includingdiminished pleasure, interest, expectancy, motivation andreinforcement learning [54,57]), whereas the NA dimen-sion includes constructs related to aversive emotion includ-ing sadness, irritability, anxiety, low distress tolerance andneuroticism [54]. In the proposed theoretical model, lowPA and high NA represent distinct states that each worsenmore rapidly following abstinence for depressed versusnon-depressed smokers [58,59] and serve to augmentsmoking motivation.

First, as nicotine dependence increases, low PA signalsthe greater reinforcement value of smoking. In the overallpopulation of smokers and non-smokers, nicotine moder-ately improves PA and reward responsivity [60]. Crucially,smokers with prominent symptoms of anhedonia (i.e. thedecreased capacity to experience pleasure) experiencefrequent bouts of low PA and endorse greater nicotine-induced increases in PA and reward responsivity followingsmoking [61]. While smoking itself is more reinforcing inthe anhedonic state, a greater experience of reward mayalso be derived from other non-nicotine reinforcers, suchas music, and contribute to the greater net value ofsmoking in the anhedonic state [62]. Following acute

withdrawal, regular smokers show moderate-sized reduc-tions in PA and reward responsivity [51,59,63], whileanhedonic smokers exhibit greater reductions in PA,reward responsivity and urge to smoke to enhance PA[64–67]. Potentially, pre-existing deficits in hedonic experi-ence among depressed smokers may be unmasked andexacerbated by nicotine withdrawal, producing strongmotivation to resume smoking to end a temporary ‘timeout’ in reward experience and obtain smoking’s positivereinforcing effects [57]. Thus, low PA is established as asignal for the increased reinforcement value of smoking,particularly among depressed smokers with prominentsymptoms of anhedonia.

Secondly, elevated NA also serves as a motivationalstate driving smoking maintenance among depressedsmokers. Although escape or avoidance of NA is thoughtto be the pre-potent motive for addictive drug use [68],the relationship between smoking and NA is complex.Nicotine is thought to have antidepressant proper-ties [69–72] and experience of NA is shown, reliably, todecrease latency to smoke and increase number of puffsconsumed [73]. However, while smoking reverseswithdrawal-induced NA [74–77], there is little evidencethat it alleviates experimentally induced NA [77–82].

Depressed smokers probably fail to distinguish NAprovoked by withdrawal versus other sources (i.e. environ-mental stressors), and thus seek out smoking in response toboth states. Nicotine withdrawal is characterized by amarked increase in NA among smokers in the

Figure 1 Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) diagram: summary of search and selection

Smoking and depression 3


generalpopulation [83,84]. Depression-prone smokersexperience even greater deprivation-induced increases inNA [85–87], which could reflect an unmasking of a pro-pensity towards negative affective states [57]. Accordingly,depressed smokers [88] and individuals prone to depression[89] are especially likely to smoke for affect regulationmotives. NA thus provides a reliable signal for the greaterreinforcement value of smoking and becomes establishedas a motivational state which primes smoking behavior,particularly in depressed smokers.

Cognitive impairment

In addition to affective disturbances, depression is charac-terized by non-specific cognitive deficits that span domainsof attention, memory, processing speed and all aspects ofexecutive functioning [90–96]. Although the aggregatedeffect size estimates of cognitive deficits in major depressionare small to medium [93,97], these deficits are clinicallysignificant [93,97], functionally impairing [98–100] andmay persist even after an acute depressive episode hasabated [90]. Crucially, cognitive impairment associatedwith depression is similar to that observed during nicotinewithdrawal, particularly in domains of executive function-ing and attention [101–103]. In a general population ofsmokers, smoking abstinence is associated with impairedsustained attention, working memory and response inhibi-tion [104], and biases cognition towards the perceived sa-lience of smoking-related stimuli ([105,106], but also see[107]). Depressed smokers are shown to experience evengreater withdrawal-induced deficits in cognitive perfor-mance [108], which may reflect the overlap (or perhapsadditive effect) of cognitive deficits in depression withcognitive deficits induced by smoking abstinence. Accord-ingly, depressed smokers may maintain smoking behaviorin order to attenuate cognitive deficits, especially whenengaged in effortful or cognitively demanding tasks[109,110]. Importantly, cognitive deficits are associatedprospectively with smoking relapse for both smokers inthe general population [111,112] and depression-pronesmokers [113]. Thus, background cognitive deficits indepression may summate with acute withdrawal-relatedcognitive deficits to prime smoking [108].

Our theoretical model posits that cognitive impairmentcomes to signal the additional reinforcement of smokingproduced by the resulting improvement in cognitive func-tioning. However, far fewer studies have examined cogni-tive versus affective processes underlying smokingmaintenance in depressed smokers, limiting the definitiveconclusions that can be drawn. Preliminary evidencesuggests that depressed smokers endorse smoking in partto manage negative intrusive thoughts and facilitateconcentration and problem-solving [114]. Additionally,depressed versus non-depressed smokers showed improved

reaction-time performance after smoking, suggesting thatthey experienced greater cognitive enhancementcompared to baseline [115]. Further studies are neededto test whether depressed versus non-depressed smokersexperience greater reinforcement value of smoking in theface of cognitive impairment, as suggested by an incentivelearning theory account.

Proposed incentive learning model of smoking anddepression and distinction from negativereinforcement-based models

Negative reinforcement models may be divided into threecategories based upon the proposed mechanisms by whichadverse states promote drug use. All three categories makethe common prediction that depressed smokers experiencefrequent bouts of high NA, low PA and cognitive impair-ment, which intensify rapidly during acute abstinenceand function to promote smoking maintenance andrelapse [80–83]. The distinction between the three catego-ries of negative reinforcement accounts lies in their depic-tion of the learning processes by which these adversestates acquire control over smoking behavior. The earlynegative reinforcement accounts referred to the adversestates as internal instrumental discriminative stimuli(or SDs for short) because they ‘set the occasion’ or providethe context [116] in which smoking is more reinforcing;but exactly how these internal SDs prime smoking behaviorwas not specified fully [117,118].

The later wave of negative reinforcement theories[119], allostasis theories [120,121] andmore recent incen-tive habit theories [122] have sought to specify howadverseinternal states prime smoking behavior. These theories fol-low Hull’s [123] stimulus–response/reinforcement view ofinstrumental discrimination learning, according to whichadverse internal stimuli (S) form a direct association withsmoking response sequences (R) as a result of reinforce-ment from smoking. The S–R association between adversestates and smoking responses is especially strong becausesmoking is more reinforcing in the adverse states, whichstrengthens the S–R association. This learning enables ad-verse states to elicit smoking behavior directly, without re-trieving knowledge of the consequences of the behavior.Accordingly, S–R-based control of smoking has been calledautomatic, unconscious, pre-conscious, habitual and com-pulsive. Such S–R accounts are attractive because they canexplain howadverse internal states could promote smokingbehavior bypassing the individual’s intentions to remainabstinent, which could account for depressed smokers’elevated rates of smoking cessation failure, despite highmotivation to quit. These accounts ascribe to internalstimuli the same form of direct control over response selec-tion that ‘standard’ habit theories of addiction haveascribed to external drug-related cues [124–126].



However, S–R accounts of action control by internalstates have been challenged on logical grounds by re-searchers from the behavior-analyst tradition [127–130].The grounds for this challenge are that the behavioralsequences needed to yield nicotine reinforcement differvastly depending on the context (e.g. purchasing cigarettesfrom a store versus from a machine; smoking during abreak versus in a bar). Internal states on their own arenot sufficiently discriminating to elicit the responsesequence that is required to produce nicotine reinforce-ment in these various external contexts via simpleS–R/reinforcement learning [127–130]. Instead, from thebehavior-analyst perspective, adverse internal states func-tion as motivating operations (or MOs) because they pre-dict that smoking has greater reinforcement valueindependently of the external context and the responsecurrently required to produce that reinforcer. MOs arethought to motivate behavior by interacting with theexternal SDs. Specifically, by virtue of signaling that asmoking reinforcement has a greater value, MOs lowerthe threshold of activation required for external SDs to elicitthe specific response sequences required to producesmoking reinforcement in the external context. On thisaccount, adverse states do not elicit smoking directly(as predicted by S–R theories) but, rather, modulate theability of external discriminative stimuli to evoke smokingbehavior through S–R learning. The main weakness of thisaccount is that it does not explain fully the nature of theinteraction which allows adverse states (MOs) to modulatecontrol by external stimuli over response selection.

Incentive learning theory addresses this limitation bysuggesting that adverse states promote smoking behaviorthrough a conjunction of explicit desire and goal-directedinstrumental knowledge [32–34]; see also [35]. On thisview, adverse states function as motivational states (likeMOs) which, by virtue of predicting the greater reinforce-ment value of smoking, come to elicit an expectation ofthe greater reinforcement value of smoking (i.e. greatersubjective desire to smoke). Smokers also acquire explicitgoal-directed instrumental knowledge of the specificresponse sequences that yield nicotine reinforcement indifferent external contexts. These two forms of knowledgeare then synthesized in a cognitive inference. The experi-ence of an adverse state generates an expectation of thegreater reinforcement value of smoking which is combinedwith goal-directed instrumental knowledge of the responsesequence required to produce the desired smokingoutcome given the specific external context [36–39]. Theincentive learning account is unique among the categoriesof negative reinforcement theory in predicting that adverseinternal states prime smoking behavior via a conjunctionof subjective desire to smoke and instrumental knowledgeof the responses required to produce that outcome in thecurrent context.

Proposed theory

As shown in Fig. 2, we propose a novel application of theincentive learning account to co-occurring smoking anddepression. Figure 2a illustrates the acute smoking phasein which depressed smokers develop an expectation ofgreater reinforcement value of smoking in three specificmotivational states: NA, low PA and cognitive impairment.As smoking persists, Fig. 2b displays the role of chronicsmoking in worsening NA, low PA and cognitive impair-ment over time due to frequent bouts of nicotinewithdrawal. Belief about the high reward value of smokingin these motivational states, particularly during absti-nence, is conceptualized as the primary trigger for smokingmaintenance and relapse following a quit attempt indepressed smokers.

Although this theoretical framework is relevant tosmokers in the general population, we believe that themotivational states are especially effective in depressedsmokers. First, those with depression experience moreintense adverse states and greater reinforcement value ofsmoking in these states, so these states become morepowerful motivators of smoking. Secondly, depression isassociated with a more severe withdrawal syndrome,adding further intensity to the adverse states as motivatorsof smoking behavior. Lastly, depression is thought to coun-ter acute satiety, so depressed smokers sustain a greater ex-pected value of smoking even immediately after smoking.

The unique prediction of the incentive learningaccount(compared to the S–R account) is that subjective desire tosmoke prompted by adverse states and goal-directed instru-mental knowledge of the effective smoking response ineach context are integrated to drive smoking behavior.One source of support for this claim is the finding thatexperimental induction of stress or NA provoke increasesin both smoking desire and smoking behavior[79,82,131–139]. Although the mood-induced increasein smoking desire may cause the smoking behavior, asanticipated by incentive learning theory, S–R-basednegative reinforcement accounts would argue that theincrease in smoking desire is actually epiphenomenal inrelation to smoking behavior. The causal status of subjec-tive desire in controlling behavior remains an unresolvedscientific question [34,140].

We recently reported direct empirical evidencesupporting the incentive learning account over the S–Raccount of how negative mood provokes smoking [40]. Aunique prediction of the incentive learning account is thatinduced negative mood should be able to augment a noveltobacco-seeking response in an extinction test throughintegration of (1) expected high value of tobacco and(2) knowledge of the instrumental response required toproduce that outcome in the context. By contrast, theS–R account predicts that an induced negative moodshould not be able to augment a novel tobacco-seeking



response in an extinction test. This is because the S–Raccount requires direct experience of the greater value oftobacco in the induced mood state to strengthen the asso-ciation between that state and the novel tobacco-seekingresponse. Such S–R learning is not possible because the to-bacco reinforcer is omitted from the extinction test. The re-sults of our study [40] showed that inducing a negativemood state in smokers augmented tobacco-seeking in anextinction test, confirming that NA primes tobacco-seekingthrough an inference of knowledge about the greater valueof tobacco in the mood state and knowledge of whichresponse produces tobacco in the current context.

We generalize this finding to suggest that whendepressed individuals experience an adverse state (NA,low PA or cognitive impairment), which is heightened dur-ing abstinence, this state provokes an expectation of thecurrent high value of smoking, which is integrated withknowledge of the response sequence required to smoke in

the context, to drive selection of that behavior over alterna-tives [38]. Below, we review implications of our proposedtheory for pharmacological and behavioral interventionsfor smoking cessation in depressed smokers.

DISCUSSION

Treatment implications of the incentive learning-basedtheoretical model: guiding principles

The foremost prediction made by the incentive learning ac-count is that adverse internal states are the primary driversof smoking behavior in depressed individuals. Accordingly,experimental treatment approaches which seek to modifyreactivity to external smoking cues (e.g. via cognitive biasmodification [141]) are unlikely to be effective in depressedsmokers. Rather, treatments should identify the adversemotivational states that are the primary drivers of smokingin each individual and personalize treatment to target

Figure 2 (a) Acute effect of smoking in depressed smokers. (b) Chronic effect of smoking in depressed smokers. (a) Incentive learning processes bywhich specific states (i.e. negative affect, low positive affect, and cognitive impairment) are alleviated acutely by smoking, and thus signal the enhancedincentive value of smoking. (b) Enhanced incentive reward value fosters persistence of smoking though goal-directed selection of this behavioralchoice. Chronically, smoking engages allostatic processes such that the aversive states are augmented. These aversive states in turn signal the higherincentive value of acute smoking, thus completing the vicious cycle



those states. Further, effective intervention strategiesshould address smokers’ beliefs about the high rewardvalue of smoking in these motivational states. In sum,our theory suggests that treatments which (1) attenuateadverse internal states and (2) reverse positive expectan-cies associated with smoking are most likely to achievecessation among depressed smokers.

Targeted pharmacological interventions

Consistent with our theory, pharmacological interventionsmay be particularly effective in depressed smokers by ame-liorating the motivational states which raise the expectedvalue of smoking: high NA, low PA and cognitive impair-ment. In particular, varenicline has cognitive-enhancingeffects in both treatment-motivated smokers [142] andnon-smokers [143], and reduces the cognitive impairmentthat accompanies withdrawal [144]. Bupropion is alsoshown to be an effective pharmacological interventionamong depressed smokers [145,146], possibly through itseffects on affective functioning [88,147]. Further, giventhat multiple withdrawal-related motivational states mayinteract or summate to motivate smoking among de-pressed smokers, combination pharmacotherapy (i.e. com-bined varenicline and bupropion or combination nicotinereplacement therapy [148–150] may be particularly war-ranted for this population to address each state optimally.As studies of pharmacological agents have focused largelyupon cessation outcomes rather than mediating variables,future research testing the effects of medications on themotivational states identified in this review could help toguide pharmacological treatment for depressed smokers.

Targeted behavioral interventions

To date, NA has been the primary component of depressiontargeted characteristically by behavioral interventions insmokers with comorbid depression [151–154]. Expandingbehavioral interventions to also target low PA explicitlycould improve smoking outcomes for smokers with depres-sion. Behavioral activation—an efficacious treatment formajor depressive disorder that increases engagement in re-inforcing activities congruent with a person’s goals [155]—may counteract withdrawal-related anhedonia andincrease quit rates by increasing exposure to alternativesources of non-smoking reinforcement [156].

Our model states further that relations between moti-vational states and goal-directed smoking behavior are me-diated by expectancies that smoking will improve thesestates. Behavioral interventionswhich address these expec-tancies (i.e. by challenging maladaptive beliefs about thelong-term mood regulating effects of nicotine) could helpto break the link between cognitive/affective deficits andsmoking maintenance among depressed smokers.

Although smokers with depression believe commonly thatsmoking helps to regulate their negative mood states[157,158], evidence suggests that smoking actually leadsto worsening of mental health symptoms over time and,conversely, quitting leads to improved mental health status[159]. Thus, behavioral interventions should emphasizethe distinction between withdrawal reversal and truemood improvement to allow smokers to learn that the ben-efits of smoking are short- but not long-term, and restrictedto the withdrawal syndrome and not environmentalstressors. Novel strategies incorporating self-monitoringand personalized feedback could help to improve thesalience and credibility of this message, particularly amongdepressed smokers.

Conclusions

Our proposed theory posits that smoking is maintainedamong depressed smokers through the expectation thatsmoking will alleviate specific states, in integration withthe goal-directed choice of smoking over alternate behav-iors. Drawing from a systematic review of the smoking-depression literature, we propose high NA, low PA andcognitive impairment as the three motivational states thatdrive this process. While we have chosen a narrativereview format in order to frame our conceptual model, thisapproach limited our ability to systematically assess for riskof bias and strength of evidence across studies. As the treat-ment literature on smoking and depression expands, it willbe increasingly important for future reviews of this topic toinclude both qualitative and quantitative methods ofanalysis.

Our review identifies several directions for futureresearch. First, it remains unclear how awareness of cogni-tive deficits interacts with awareness of affective states (i.e.low PA and high NA) to provide the motivational signalpromoting goal-directed smoking behavior. Studies thatcharacterize each of these withdrawal-related statesamong depressed smokers, as well as their unique andshared contribution to tobacco-seeking behavior, areneeded. Secondly, although our theory holds that expec-tancies play a causal role in smoking maintenance, it hasnot been specified fully how knowledge of reward valuesand context-dependent response requirements translateinto actual action selection. Thirdly, cognitive processesamong depressed smokers have received relatively little re-search attention, but we believe cognitive impairment rep-resents a key motivational state maintaining smokingbehavior in this population [160]. Future research shouldelucidate further the extent to which depressed smokerssmoke for cognitive enhancement motives, benefit differen-tially from smoking in terms of functional cognitive out-comes and respond to pro-cognitive agents as part of asmoking cessation intervention. Lastly, as depression and



smoking co-occur commonly with other mental healthconcerns (i.e. substance use disorders, anxiety disorders)[161–163], identifying the unique versus shared incentivestates underlying each of these conditions in order to guideintegrated treatment is an important priority.

Declaration of interests

Dr. Histman has served on a scientific advisory board forPfizer and receives study medication and placebo free ofcharge from Pfizer for use in ongoing National Institutesof Health funded clinical trials.

Acknowledgments

This work is supported by the National Cancer Instituteand National Institute on Drug Abuse of the UnitedStates National Institutes of Health (Grant NumbersF32DA036947 and R01CA184211). J.W.C. is supportedby Merit Review Award 101CX00056 from the US Depart-ment of Veterans Affairs. We thank Dr Robert West forfeedback on an earlier draft of this manuscript.

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