Background and Aims Despite decades of research on co-occurring smoking and depression, cessation rates remain consistently lower for depressed smokers than for smokers in the general population, highlighting the need for theory-driven models of smoking and depression. This paper provides a systematic review with a particular focus on psychological states that disproportionately motivate smoking in depression, and frame an incentive learning theory account of smoking-depression co-occurrence. Methods We searched PubMed, Scopus, PsychINFO, and CINAHL through December 2014, which yielded 852 articles. Using pre-established eligibility criteria, we identified papers focused on clinical issues and motivational mechanisms underlying smoking in established, adult smokers (i.e., maintenance, quit attempts, and cessation/relapse) with elevated symptoms of depression. Two reviewers independently determined whether articles met review criteria. We included 297 articles in qualitative synthesis. Results Our review identified three primary mechanisms that underlie persistent smoking among depressed smokers: low positive affect, high negative affect, and cognitive impairment. We propose a novel application of incentive learning theory which posits that depressed smokers experience greater increases in the expected value of smoking in the face of these three motivational states, which promotes goal-directed choice of smoking behavior over alternative actions. Conclusions The incentive learning theory accounts for current evidence on how depression primes smoking behavior and provides a unique framework for conceptualizing psychological mechanisms of smoking maintenance among depressed smokers. Treatment should focus on correcting adverse internal states, and beliefs about the high value of smoking in those states, to improve cessation outcomes for depressed smokers.

Background Major depressive disorder (MDD) and anxiety disorders (ANX) are debilitating and prevalent conditions that often co-occur in adolescence and young adulthood. The leading theoretical models of their co-morbidity include the direct causation model and the shared etiology model. The present study compared these etiological models of MDD–ANX co-morbidity in a large, prospective, non-clinical sample of adolescents tracked through age 30. Method Logistic regression was used to examine cross-sectional associations between ANX and MDD at Time 1 (T1). In prospective analyses, Cox proportional hazards models were used to examine T1 predictors of subsequent disorder onset, including risk factors specific to each disorder or common to both disorders. Prospective predictive effect of a lifetime history of one disorder (e.g. MDD) on the subsequent onset of the second disorder (e.g. ANX) was then examined. This step was repeated while controlling for common risk factors. Results The findings supported relatively distinct profiles of risk between MDD and ANX depending on order of development. Whereas the shared etiology model best explained co-morbid cases in which MDD preceded ANX, direct causation was supported for co-morbid cases in which ANX preceded MDD. Conclusions Consistent with previous research, significant cross-sectional and prospective associations were found between MDD and ANX. The results of the present study suggest that different etiological models may characterize the co-morbidity between MDD and ANX based upon the temporal order of onset. Implications for classification and prevention efforts are discussed.

Effective management of chronic diseases involves sustained changes in health behavior, which often requires substantial effort and patient burden. As treatment burden is associated with reduced adherence across several chronic conditions, its assessment and treatment are important clinical priorities. The balance between patient demands and capacity (e.g., coping resources) may be indexed by patients’ subjective experience of treatment fatigue. We present a modified workload-capacity model that incorporates evidence that treatment fatigue may 1) be caused by increased workload due to treatment burden (e.g., intensity, complications) and 2) undermine adherence. Emerging technology-based interventions may be well-suited to reduce treatment burden, prevent treatment fatigue, and increase treatment adherence.

Background: Former smokers now outnumber current smokers in many developed countries, and current smokers are smoking fewer cigarettes per day. Limited data suggest that lung function decline normalizes with smoking cessation; however, mechanistic studies suggest ongoing risk. We hypothesized that former smokers and low-intensity current smokers have accelerated lung function decline compared with never-smokers, including among those without prevalent lung disease.Methods: Longitudinal spirometry measures and self-reported smoking behaviors were harmonized across six US population-based cohorts. FEV1 decline of sustained former smokers and current smokers was compared to that of never-smokers using mixed models adjusted for socio-demographic and anthropometric factors. Differential FEV1 decline was also evaluated according to duration of smoking cessation and cumulative (pack-years) and current (cigarettesper-day) cigarette consumption.Findings: 25,352 participants (ages 17-93 years) completed 70,228 valid spirometry exams. Over median 7-year follow-up (interquartile range, 3-20), FEV1 decline at the median age (57 years) was 31•01, 34•97, and 39•92 mL/year in sustained never-smokers, former smokers, and current smokers, respectively. With adjustment, former smokers demonstrated 1•82 mL/year accelerated FEV1 decline (95% CI, 1•24-2•40) compared to never-smokers, which was 20% of the effect estimate for current smokers. Compared to never-smokers, accelerated FEV1 decline was observed for decades after smoking cessation and in smokers with low cumulative cigarette consumption (<10 pack-years). With respect to current cigarette consumption, the effect estimate for FEV1 decline in current smokers of <5 cigarettes-per-day was 68% of those in current smokers of ≥30 cigarettes-per-day, and 5 times greater than in former smokers. Among participants without prevalent lung disease, associations were attenuated but were consistent with the main results.

The primary goal of this pilot feasibility study was to examine the effects of Mindfulness-Oriented Recovery Enhancement (MORE), a behavioral treatment grounded in dual-process models derived from cognitive science, on frontostriatal reward processes among cigarette smokers. Healthy adult (N = 13; mean (SD) age 49 ± 12.2) smokers provided informed consent to participate in a 10-week study testing MORE versus a comparison group (CG). All participants underwent two fMRI scans: pre-tx and after 8-weeks of MORE. Emotion regulation (ER), smoking cue reactivity (CR), and resting-state functional connectivity (rsFC) were assessed at each fMRI visit; smoking and mood were assessed throughout. As compared to the CG, MORE significantly reduced smoking (d = 2.06) and increased positive affect (d = 2.02). MORE participants evidenced decreased CR-BOLD response in ventral striatum (VS; d = 1.57) and ventral prefrontal cortex (vPFC; d = 1.7) and increased positive ER-BOLD in VS (dVS = 2.13) and vPFC (dvmPFC = 2.66). Importantly, ER was correlated with smoking reduction (r's = .68 to .91) and increased positive affect (r's = .52 to .61). These findings provide preliminary evidence that MORE may facilitate the restructuring of reward processes and play a role in treating the pathophysiology of nicotine addiction.