The National Institute of Mental Health (NIMH) convened a meeting in September 2005 to review tobacco use and dependence and smoking cessation among those with mental disorders, especially individuals with anxiety disorders, depression, or schizophrenia. Smoking rates are exceptionally high among these individuals and contribute to the high rates of medical morbidity and mortality in these individuals. Numerous biological, psychological, and social factors may explain these high smoking rates, including the lack of smoking cessation treatment in mental health settings. Historically, "self-medication" and "individual rights" have been concerns used to rationalize allowing ongoing tobacco use and limited smoking cessation efforts in many mental health treatment settings. Although research has shown that tobacco use can reduce or ameliorate certain psychiatric symptoms, overreliance on the self-medication hypothesis to explain the high rates of tobacco use in psychiatric populations may result in inadequate attention to other potential explanations for this addictive behavior among those with mental disorders. A more complete understanding of nicotine and tobacco use in psychiatric patients also can lead to new psychiatric treatments and a better understanding of mental illness. Greater collaboration between mental health researchers and nicotine and tobacco researchers is needed to better understand and develop new treatments for cooccurring nicotine dependence and mental illness. Despite an accumulating literature for some specific psychiatric disorders and tobacco use and cessation, many unstudied research questions remain and are a focus and an emphasis of this review.

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Objective-Adolescence is an important period of risk for the development of lifelong smoking behaviors. Compelling, although inconsistent, evidence suggests a relation between parental smoking and the risk of smoking initiation during adolescence. This study investigates unresolved issues concerning the strength and nature of the association between parent smoking and offspring smoking initiation.Methods-We enrolled 564 adolescents aged 12-17, along with one of their parents, into the New England Family Study between [2001][2002][2003][2004]. Lifetime smoking histories were obtained from parents and their adolescent offspring. Discrete-time survival analysis was used to investigate the influence of parental smoking histories on the risk of adolescent smoking initiation.Results-Parental smoking was associated with a significantly higher risk of smoking initiation in adolescent offspring (odds ratio=2.81, 95% CI=1.78, 4.41). In addition, the likelihood of offspring smoking initiation increased with the number of smoking parents and the duration of exposure to parental smoking, suggesting a dose-response relation between parental smoking and offspring smoking. Offspring of parents who had quit smoking were no more likely to smoke than offspring of parents who had never smoked. The effects of parental smoking on offspring initiation differed by sex (with a stronger effect of father's smoking on boys than girls), developmental period (with a stronger effect of parental smoking before the adolescent was age 13 than afterwards), and residence of parents (with effects of father's smoking being dependent on living in the same household as the adolescent). Parental smoking was also associated with stronger negative reactions to adolescents' first cigarette, a potential marker of the risk of progression to higher levels of use.Conclusions-Parental smoking is an important source of vulnerability to smoking initiation among adolescents, and parental smoking cessation might attenuate this vulnerability. KeywordsSmoking; adolescents; parent-offspring transmissionMost adult smokers began smoking during adolescence; 1-3 preventing adolescent smoking initiation is therefore important for reducing the public health burden of smoking-related illnesses over the life course. There is accumulating evidence that parental smoking increases the risk for adolescent smoking initiation; 4-19 however, unresolved issues persist concerning the strength and nature of the association between parent smoking and initiation of smoking in offspring. 20 For example, while parental smoking and parental nicotine dependence have each been linked with an increased risk of offspring smoking, 21,22 few studies of intergenerational transmission have addressed their comparative effects. Evidence from one such study suggests that the effect of maternal smoking on offspring smoking is largely irrespective of maternal nicotine dependence. 18Prior evidence of a dose-response relationship between parental smoking and offspring initiation is also mixed. In...

The authors conducted a meta-analysis of published studies to (a) evaluate the premise that a history of major depression is associated with failure to quit smoking and (b) identify factors that moderate the relationship between history of depression and cessation outcome. Fifteen studies met the selection requirements and were coded for various study methodology and treatment characteristics. DSTAT was used to calculate individual study effect sizes, determine the mean effect size across studies, and test for moderator effects. No differences in either short-term (Յ 3 months) or long-term abstinence rates (Ն 6 months) were observed between smokers positive versus negative for history of depression. Lifetime history of major depression does not appear to be an independent risk factor for cessation failure in smoking cessation treatment.

Most of the PTSD-ND association is explained by shared genetic effects. However, there is a substantial, robust PTSD-ND association not explained by shared risk factors. Multiple explanations for the association were supported; however, the strongest association was consistent with preexisting ND increasing the risk of PTSD onset. These data suggest that male veterans with a history of ND may be at increased risk for PTSD. Further research on the biological mechanisms underlying PTSD-ND comorbidity is needed.

A meta-analysis of published studies with adult human participants was conducted to evaluate whether physical fitness attenuates cardiovascular reactivity and improves recovery from acute psychological stressors. Thirty-three studies met selection criteria; 18 were included in recovery analyses. Effect sizes and moderator influences were calculated by using meta-analysis software. A fixed effects model was fit initially; however, between-studies heterogeneity could not be explained even after inclusion of moderators. Therefore, to account for residual heterogeneity, a random effects model was estimated. Under this model, fit individuals showed significantly attenuated heart rate and systolic blood pressure reactivity and a trend toward attenuated diastolic blood pressure reactivity. Fit individuals also showed faster heart rate recovery, but there were no significant differences in systolic blood pressure or diastolic blood pressure recovery. No significant moderators emerged. Results have important implications for elucidating mechanisms underlying effects of fitness on cardiovascular disease and suggest that fitness may be an important confound in studies of stress reactivity.

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.

People with mental health and addictive (MHA) disorders smoke at high rates and require tobacco treatment as a part of their comprehensive psychiatric care. Psychiatric care providers often do not address tobacco use among people with mental illness, possibly owing to the belief that their patients will not be able to quit successfully or that even short-term abstinence will adversely influence psychiatric status. Progress in the development of treatments has been slow in part because smokers with current MHA disorders have been excluded from most smoking cessation trials. There are several smoking cessation treatment options, including psychological and pharmacological interventions, that should be offered to people with an MHA disorder who smoke. Building motivation and readiness to quit smoking is a major challenge, and therefore motivational interventions are essential. We review the treatment options for people with tobacco dependence and MHA disorders, offer recommendations on tobacco assessment and tailored treatment strategies, and provide suggestions for future research. Treatment efficacy could be enhanced through promoting smoking reduction as an initial treatment goal, extending duration of treatment, and delivering it within an integrated care model that also aims to reduce the availability of tobacco in MHA treatment settings and in the community.