Amanda R. Mathew

Co-morbidity between major depressive disorder and anxiety disorders: shared etiology or direct causation?

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.

Clinical strategies to enhance the efficacy of nicotine replacement therapy for smoking cessation: a review of the literature.

A number of smoking cessation pharmacotherapies have led to increases in quitting and thus to significant benefits to public health. Among existing medications, nicotine replacement therapy (NRT) has been available the longest, has the largest literature base in support, and is the only option for over-the-counter access. While the short-term efficacy of NRT is well documented in clinical trials, long-term abstinence rates associated with using NRT are modest, as most smokers will relapse. This literature review examines emerging clinical strategies to improve NRT efficacy. After an initial overview of NRT and its FDA-approved indications for use, we review randomized trials in which clinical delivery of NRT was manipulated and tested, in an attempt to enhance efficacy, through (1) duration of use (pre-quit and extended use), (2) amount of use (high-dose and combination NRT), (3) tailoring to specific smoker groups (genotype and phenotype), or (4) use of NRT for novel purposes (relapse prevention, temporary abstinence, cessation induction). Outcomes vary within and across topic area, and we highlight areas that offer stronger promise. Combination NRT likely represents the most promising strategy moving forward; other clinical strategies offer conflicting evidence but deserve further testing (pre-quit NRT or tailored treatment) or offer potential utility but are in need of further, direct tests. Some areas, though based on a limited set of studies, do not offer great promise (high-dose and extended treatment NRT). We conclude with a brief discussion of emergent NRT products (e.g., oral nicotine spray, among others), which may ultimately offer greater efficacy than current formulations. In order to further lower the prevalence of smoking, novel strategies designed to optimize NRT efficacy are needed.

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

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 upon 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 to December 2014, which yielded 852 papers. 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 determined independently whether papers met review criteria. We included 297 papers 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 upon correcting adverse internal states and beliefs about the high value of smoking in those states to improve cessation outcomes for depressed smokers.

Restructuring Reward Mechanisms in Nicotine Addiction: A Pilot fMRI Study of Mindfulness-Oriented Recovery Enhancement for Cigarette Smokers

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 (rs = .68 to .91) and increased positive affect (rs = .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.

Post‐traumatic stress disorder symptoms, underlying affective vulnerabilities, and smoking for affect regulation

BACKGROUND AND OBJECTIVES Post-traumatic stress disorder (PTSD) is overrepresented among cigarette smokers. It has been hypothesized that those with PTSD smoke to alleviate negative affect and counteract deficient positive affect commonly associated with the disorder; however, limited research has examined associations between PTSD symptoms, smoking motives, and affective vulnerability factors. In the current study, we examined (1) whether PTSD symptoms were associated with positive reinforcement and negative reinforcement smoking motives; and (2) whether two affective vulnerability factors implicated in PTSD-anxiety sensitivity and anhedonia-mediated relationships between PTSD symptoms and smoking motives. METHODS Data were drawn from a community sample of non-treatment-seeking smokers recruited without regard for trauma history (N = 342; 10+ cig/day). We used the Posttraumatic Stress Disorder Checklist-Civilian Version (PCL-C) to assess overall PTSD symptom severity as well as individual PTSD subfactors. RESULTS Overall, PTSD symptom severity was significantly associated with negative reinforcement, but not positive reinforcement, smoking motives. Variation in anxiety sensitivity significantly mediated the relation between PTSD symptom severity and negative reinforcement smoking motives, whereas anhedonia did not. Regarding PTSD subfactors, emotional numbing was the only PTSD subfactor associated with smoking rate, while re-experiencing symptoms were uniquely associated with both positive reinforcement and negative reinforcement smoking motives. CONCLUSIONS AND SCIENTIFIC SIGNIFICANCE Findings suggest that anxiety sensitivity may be an important feature associated with PTSD that enhances motivation to smoke for negative reinforcement purposes. Smoking cessation interventions that alleviate anxiety sensitivity and enhance coping with negative affect may be useful for smokers with elevated PTSD symptoms.

Smoking Behavior and Alcohol Consumption in Individuals With Panic Attacks

Individuals with anxiety often report greater smoking and drinking behaviors relative to those without a history of anxiety. In particular, smoking and alcohol use have been directly implicated among individuals experiencing panic attacks, diagnosed with panic disorder, or high on panic-relevant risk factors such as anxiety sensitivity. Less is known, however, about specific features of panic that may differentiate among those who do or do not use cigarettes or alcohol. The purpose of the current study was to replicate previous research findings of an association between panic symptomatology, cigarette smoking, and alcohol consumption, as well as extend findings by examining whether specific symptoms of panic attacks differentiated among those who do or do not use cigarettes or alcohol. Participants (n = 489) completed the Panic Attack Questionnaire-IV, a highly detailed assessment of panic attacks and symptoms, as well as self-report measures of smoking history and alcohol use. Consistent with previous research, participants who reported a history of panic attacks (n = 107) were significantly more likely to report current daily or lifetime daily cigarette smoking, and significantly greater hazardous or harmful alcohol use than participants with no panic history (n = 382). Although smoking and hazardous alcohol use were highly associated regardless of panic status, participants with panic attacks showed elevated hazardous alcohol use after controlling for daily or lifetime smoking. Surprisingly, although participants who reported having had at least one panic attack were more likely to smoke, panic attack symptoms, intensity, or frequency did not differentiate panickers who did or did not smoke. Furthermore, panic-related variables were not shown to differentially relate to problematic drinking among panickers. Implications for understanding the complex relationship between panic attacks and smoking and drinking behaviors are discussed.

Negative mood reverses devaluation of goal-directed drug-seeking favouring an incentive learning account of drug dependence.

BackgroundTwo theories explain how negative mood primes smoking behaviour. The stimulus–response (S-R) account argues that in the negative mood state, smoking is experienced as more reinforcing, establishing a direct (automatic) association between the negative mood state and smoking behaviour. By contrast, the incentive learning account argues that in the negative mood state smoking is expected to be more reinforcing, which integrates with instrumental knowledge of the response required to produce that outcome.ObjectivesOne differential prediction is that whereas the incentive learning account anticipates that negative mood induction could augment a novel tobacco-seeking response in an extinction test, the S-R account could not explain this effect because the extinction test prevents S-R learning by omitting experience of the reinforcer.MethodsTo test this, overnight-deprived daily smokers (n = 44) acquired two instrumental responses for tobacco and chocolate points, respectively, before smoking to satiety. Half then received negative mood induction to raise the expected value of tobacco, opposing satiety, whilst the remainder received positive mood induction. Finally, a choice between tobacco and chocolate was measured in extinction to test whether negative mood could augment tobacco choice, opposing satiety, in the absence of direct experience of tobacco reinforcement.ResultsNegative mood induction not only abolished the devaluation of tobacco choice, but participants with a significant increase in negative mood increased their tobacco choice in extinction, despite satiety.ConclusionsThese findings suggest that negative mood augments drug-seeking by raising the expected value of the drug through incentive learning, rather than through automatic S-R control.

Relationship of Childhood Trauma to Depression and Smoking Outcomes in Pregnant Smokers

OBJECTIVE We evaluated whether childhood trauma moderated the treatment effect on depression and smoking outcomes in pregnant smokers. METHOD The sample included pregnant smokers participating in a randomized trial evaluating the efficacy of a 10-session interpersonally focused therapy-cognitive behavioral analysis system of psychotherapy (CBASP)-versus a time-matched health and wellness control (HW) for smoking cessation and depression reduction. Women (N = 248) who completed the Childhood Trauma Questionnaire (CTQ) were included. On average, women were 25 years old (SD = 5.91) and smoked 10 (SD = 6.9) cigarettes per day. Depressive symptoms were assessed with the Center for Epidemiological Studies Depression Scale (CES-D), and women had an average score of 21 (SD = 11.03). Seventy-six percent of women had experienced some form of moderate to severe childhood trauma as assessed by the CTQ. RESULTS In women with a history of moderate to severe childhood trauma, there was a dose-response association of treatment on depression outcome through 6 months postpartum; those with increasing amounts of childhood trauma benefitted more from CBASP, whereas those in the HW condition did not. Childhood trauma did not moderate the treatment effect on abstinence, although increasing amounts of trauma were associated with reduced likelihood of abstinence at 6 months posttreatment. CONCLUSIONS An interpersonally focused therapy may be beneficial for the treatment of depression during the prenatal period in pregnant smokers with childhood trauma histories, and such treatment becomes increasingly more important with cumulative trauma experience. Childhood trauma increases risk for cessation failure in pregnant smokers. (PsycINFO Database Record (c) 2013 APA, all rights reserved).

Current major depression is associated with greater sensitivity to the motivational effect of both negative mood induction and abstinence on tobacco-seeking behavior

BACKGROUND Although depression and smoking commonly co-occur, the mechanisms underpinning this association are poorly understood. One hypothesis is that depression promotes tobacco dependence, persistence and relapse by increasing sensitivity to acute negative mood and abstinence induced tobacco-seeking behavior. METHODS Twenty nine daily smokers of >10 cigarettes per day, nine with major depression and 20 without, completed two laboratory sessions one week apart, smoking as normal prior to session 1 (sated session), and 6h abstinent prior to session 2 (abstinent session). In both sessions, tobacco-seeking was measured at baseline by preference to view smoking versus food images. Negative mood was then induced by negative ruminative statements and sad music, before tobacco-seeking was measured again at test. RESULTS In the sated session, negative mood induction produced a greater increase in tobacco choice from baseline to test in depressed (p<0.001, ηp2=0.782) compared to non-depressed smokers (p=0.045, ηp2=0.216, interaction: p=0.046, ηp2=0.150). Abstinence also produced a greater increase in baseline tobacco choice between the sated and abstinent sessions in depressed (p=0.002, ηp2=0.771) compared to non-depressed smokers (p=0.22, ηp2=0.089, interaction: p=0.023, ηp2=0.189). These mood and abstinence induced increases in tobacco choice were positively associated with depression symptoms across the sample as a whole (ps≤0.04, ηp2≥0.159), and correlated with each other (r=0.67, p<0.001). CONCLUSIONS Current major depression or depression symptoms may promote tobacco dependence, persistence and relapse by increasing sensitivity to both acute negative mood and abstinence induced tobacco-seeking behavior. Treatments should seek to break the association between adverse states and smoking to cope.

A mechanistic test of nicotine replacement therapy sampling for smoking cessation induction.

Studies that explore the mechanisms of treatment effect are needed in the area of smoking cessation induction, the primary goal of which is to promote the occurrence of a quit attempt among individuals who report little interest in smoking cessation. This study tested the mediational effect of 5 psychological variables (motivation to quit, abstinence self-efficacy, knowledge of nicotine replacement therapy (NRT), and both positive and negative attitudes toward NRT) on the relationship between NRT sampling and smoking outcomes. Adults who reported low levels of intention to quit in the next month (n = 593) were recruited for a nationwide randomized clinical trial of NRT sampling. Participants provided self-report data via telephone interview on multiple occasions, with the final follow-up at 6 months. Motivation to quit, and to a lesser degree, abstinence self-efficacy at the end of the 6-week intervention best accounted for the effect of NRT sampling as a promoter of quit attempts, smoking reduction, and 7-day point prevalence abstinence. Providing smokers with free NRT samples, in addition to encouraging them to engage in temporary abstinence, results in meaningful change in motivation and self-efficacy, which in turn influence smoking outcomes. Cessation induction interventions should aim to increase motivation to quit and abstinence self-efficacy, above and beyond any efforts to increase knowledge or prompt attitudinal shifts. (PsycINFO Database Record