κ-Opioid Signaling in the Lateral Hypothalamic Area Modulates Nicotine-Induced Negative Energy Balance

Several studies have reported that nicotine, the main bioactive component of tobacco, exerts a marked negative energy balance. Apart from its anorectic action, nicotine also modulates energy expenditure, by regulating brown adipose tissue (BAT) thermogenesis and white adipose tissue (WAT) browning. These effects are mainly controlled at the central level by modulation of hypothalamic neuropeptide systems and energy sensors, such as AMP-activated protein kinase (AMPK). In this study, we aimed to investigate the kappa opioid receptor (κOR)/dynorphin signaling in the modulation of nicotine’s effects on energy balance. We found that body weight loss after nicotine treatment is associated with a down-regulation of the κOR endogenous ligand dynorphin precursor and with a marked reduction in κOR signaling and the p70 S6 kinase/ribosomal protein S6 (S6K/rpS6) pathway in the lateral hypothalamic area (LHA). The inhibition of these pathways by nicotine was completely blunted in κOR deficient mice, after central pharmacological blockade of κOR, and in rodents where κOR was genetically knocked down specifically in the LHA. Moreover, κOR-mediated nicotine effects on body weight do not depend on orexin. These data unravel a new central regulatory pathway modulating nicotine’s effects on energy balance.     

Measurement of chemical emission rates from cigarette butts into air

This study examined airborne emissions from cigarette butts for styrene, 2-methyl-2-cyclopenten-1-one, naphthalene, triacetin, and nicotine. Ten experiments were conducted by placing butts in a stainless steel chamber and measuring the chemical concentrations in chamber air. Emission rates were determined from the concentrations. Triacetin and nicotine concentrations were roughly 50% of initial concentrations after 100 hours, while concentrations of other chemicals decayed to less than 10% of initial concentrations within 24 hours. Initial emission rates per cigarette butt ranged from 200 to 3500 ng h⁻¹. Triacetin and nicotine emission rates at 25°C were 1.6 to 2.2 times higher than the rates at 20°C, while the emission rates of other chemicals at 25°C were 1.1 to 1.3 times higher than the rates at 20°C only during the first sampling period. The chemical concentrations and emission rates at 30°C were comparable or lower than the values at 25°C, possibly due to different batches of cigarettes used. The 24-hours emitted mass of nicotine from a cigarette butt at 25°C could be up to 14% of the literature reported nicotine masses emitted from a burning cigarette.     

Environmental and individual exposure to secondhand aerosol of electronic cigarettes in confined spaces: Results from the TackSHS Project†

Secondhand electronic cigarette (e-cigarette) aerosol (SHA) might impair indoor air quality and expose bystanders. This study aims to investigate exposure to SHA in controlled conditions of enclosed settings simulating real-world scenario. An experiment was performed in a car and in a room, in which SHA was generated during a 30-minute ad libitum use of an e-cigarette. The experiment was replicated on five consecutive days in each setting. We measured PM_2.5, airborne nicotine concentrations, and biomarkers of exposure to SHA, such as nicotine metabolites, tobacco-specific nitrosamines, propylene glycol, and glycerol in bystanders’ saliva samples before, during, and after the exposure period. Self-reported health symptoms related to exposure to SHA were also recorded. The results showed that the highest median PM_2.5 concentration was recorded during the exposure period, being 21 µg/m³ in the room setting and 16 µg/m³ in the car setting—about twofold increase compared to the baseline. Most concentrations of the airborne nicotine and all biomarkers were below the limit of quantification in both settings. Bystanders in both settings experienced some short-term irritation symptoms, expressed as dry throat, nose, eyes, and phlegm. In conclusion, short-term use of an e-cigarette in confined spaces increased indoor PM_2.5 level and caused some irritation symptoms in bystanders.     

Nicotine dependence subtypes among adolescent smokers: Examining the occurrence, development and validity of distinct symptom profiles.

To increase understanding of the etiology and epidemiology of nicotine dependence among adolescent smokers, the present study examined the occurrence and development of distinct nicotine dependence symptom profiles in a sample of adolescent smokers. A total of 25 secondary schools throughout the Netherlands participated in a 1-year longitudinal study. Multiple dimensions of nicotine dependence were assessed, at two time points, among 641 adolescents (aged 14–17 years) who were classified as smokers. Results showed 4 distinct, yet stable, nicotine dependence subtypes that could be characterized by quantitative as well as qualitative differences. The symptom profiles were similar for males and females but differentially associated with previously identified correlates of nicotine dependence, namely parental smoking, peer smoking, and depressive mood. Finally, differential links of the 4 subtypes were found with regard to smoking uptake and cessation. The finding of qualitative different subgroups of adolescent smokers may have important implications for intervention efforts regarding nicotine dependence and smoking cessation. Such efforts may need to be tailored to the specific subgroups’ needs. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of night smoking, sleep disturbance, and their co-occurrence on smoking outcomes.

Recent evidence suggests that smoking during the night is an indicator of nicotine dependence and predicts smoking cessation failure. Night smokers are likely to experience disturbance to their sleep cycle when they wake to smoke, but we are not aware of the prevalence of night smokers' self-reported sleep disturbance. Because sleep disturbance also predicts smoking cessation failure, we examined how the pre-cessation risk factors of night smoking and sleep disturbance, and their co-occurrence, predict smoking cessation failure in a 6-week double-blind randomized controlled trial examining whether naltrexone augments the efficacy of the nicotine patch (O'Malley et al., 2006). Smokers (N = 385) completed the Pittsburgh Sleep Quality Index (Buysse, Reynolds, Monk, Berman, & Kupfer, 1989) and a single item of waking at night to smoke pre-cessation. Smoking status was determined at weeks 1, 6, 24, and 48 weeks after quitting. The two main findings were: (a) night smokers reported significantly greater sleep disturbance than nonnight smokers; and (b) smokers with co-occurring night smoking and sleep disturbance experienced significantly greater risk for smoking than smokers with neither risk factor. Results suggest that individuals who both wake during the night to smoke and report clinically-significant sleep disturbance represent a high-risk group of smokers. Future smoking cessation treatment might incorporate strategies related to managing these smokers' sleep habits and physiological dependence on nicotine in order to bolster their cessation outcomes. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

The relationship between in-treatment abstinence and post-treatment abstinence in a smoking cessation treatment.

Previous research has indicated that abstinence early in a smoking cessation program is predictive of successful posttreatment abstinence. However, it has not been established whether or not this effect is independent of other in-treatment abstinence patterns. In this paper the relationship between three potentially important aspects of in-treatment smoking abstinence and posttreatment smoking abstinence are examined: early abstinence, extended abstinence, and end-of-treatment abstinence. We examined the relationship between smoking behavior measured each weekday over 70 visits (approximately 14 weeks) of a contingency management smoking cessation program and at a follow-up visit 6 months after study entry (3 months after the scheduled end of treatment). Ninety-five of 102 participants were successfully followed-up. Seven of these 95 participants were confirmed abstinent. Early abstinence, defined as abstinence during the first 10 treatment visits, was significantly and independently related to follow-up abstinence (OR = 56.67 [7.29–440.63]). Extended abstinence and end-of-treatment abstinence were related to follow-up abstinence, but not independent of early abstinence based on multiple regression models. Inclusion of a variety of demographic and environmental characteristics did not significantly alter this relationship. Thus, consistent with the previous literature, the establishment of early abstinence appears to be crucial to establishing longer-term abstinence, independent of other in-treatment abstinence patterns. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Subjective responses to intravenous nicotine: Greater sensitivity in women than in men.

Although approximately 45% of smokers in the United States are women, the influence of sex on nicotine dependence remains incompletely understood. Evidence from preclinical and clinical studies has indicated that there are significant sex differences in nicotine's effects. The authors' goal in this report was to determine whether men and women differ in their acute response to intravenous nicotine, which has not been examined in previous studies. Twelve male and 12 female smokers received saline followed by 0.5 mg/70 kg and 1.0 mg /70 kg nicotine intravenously. In response to nicotine, women, as compared with men, had enhanced ratings for drug strength, head rush, and bad effects. Women and men experienced similar suppression of smoking urges by nicotine as assessed by the Brief Questionnaire on Smoking Urges. Nicotine-induced heart rate and systolic and diastolic blood pressure increases were also similar in magnitude in men and women. The findings, consistent with those of several previous studies, support greater sensitivity of female smokers to some but not all of the subjective effects of nicotine. Further studies are warranted to examine the role of this differential nicotine sensitivity to development of nicotine dependence and response to nicotine replacement treatments in men and women. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Brain fMRI reactivity to smoking-related images before and during extended smoking abstinence.

[Correction Notice: An erratum for this article was reported in Vol 18(3) of Experimental and Clinical Psychopharmacology (see record 2010-11933-011). In the article the authors find it necessary to redefine the thresholding procedure used for data analyses, due to problems in the Brain Voyager software. This does not affect the main findings of the paper.] Reactivity to smoking-related cues may play a role in the maintenance of smoking behavior and may change depending on smoking status. Whether smoking cue-related functional MRI (fMRI) reactivity differs between active smoking and extended smoking abstinence states currently is unknown. We used fMRI to measure brain reactivity in response to smoking-related versus neutral images in 13 tobacco-dependent subjects before a smoking cessation attempt and again during extended smoking abstinence (52 ± 11 days) aided by nicotine replacement therapy. Prequit smoking cue induced fMRI activity patterns paralleled those reported in prior smoking cue reactivity fMRI studies. Greater fMRI activity was detected during extended smoking abstinence than during the prequit assessment subcortically in the caudate nucleus and cortically in prefrontal (BA 6, 9, 44, 46), primary somatosensory (BA 1, 2, 3), temporal (BA 22, 41, 42), parietal (BA 7, 40) anterior cingulate (BA 24, 32), and posterior cingulate (BA 31) cortex. These data suggest that during extended smoking abstinence, fMRI reactivity to smoking versus neutral stimuli persists in brain areas involved in attention, somatosensory processing, motor planning, and conditioned cue responding. In some brain regions, fMRI smoking cue reactivity is increased during extended smoking abstinence in comparison to the prequit state, which may contribute to persisting relapse vulnerability. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Pain, nicotine, and smoking: Research findings and mechanistic considerations.

Tobacco addiction and chronic pain represent 2 highly prevalent and comorbid conditions that engender substantial burdens upon individuals and systems. Interrelations between pain and smoking have been of clinical and empirical interest for decades, and research in this area has increased dramatically over the past 5 years. We conceptualize the interaction of pain and smoking as a prototypical example of the biopsychosocial model. Accordingly, we extrapolated from behavioral, cognitive, affective, biomedical, and social perspectives to propose causal mechanisms that may contribute to the observed comorbidity between these 2 conditions. The extant literature was 1st dichotomized into investigations of either effects of smoking on pain or effects of pain on smoking. We then integrated these findings to present a reciprocal model of pain and smoking that is hypothesized to interact in the manner of a positive feedback loop, resulting in greater pain and increased smoking. Finally, we proposed directions for future research and discussed clinical implications for smokers with comorbid pain disorders. We observed modest evidence that smoking may be a risk factor in the multifactorial etiology of some chronically painful conditions and that pain may come to serve as a potent motivator of smoking. We also found that whereas animal studies yielded consistent support for direct pain-inhibitory effects of nicotine and tobacco, results from human studies were much less consistent. Future research in the emerging area of pain and smoking has the potential to inform theoretical and clinical applications with respect to tobacco smoking, chronic pain, and their comorbid presentation. (PsycINFO Database Record (c) 2011 APA, all rights reserved)