Antidepressants for smoking cessation.
Ontology highlight
ABSTRACT:
SUBMITTER: Howes S
PROVIDER: S-EPMC7175455 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Genetic Architecture of Smoking and Smoking Cessation
| PRJNA75689 | ENA
Project description:Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. Methods: SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 10 healthy never-smokers and 10 healthy smokers, before and after they quit for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. Results: There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy never-smokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway the top enriched pathway of the target genes of the persistent deregulated miRNAs. Conclusions: In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammation diseases or lung cancer, it is likely that persistent smoking-related changes in small airway epithelium miRNAs play a role in the subsequent development of these disorders.
2015-11-23 | GSE53519 | GEO
Project description:Despite being highly motivated to quit, many of my patients struggle with smoking cessation during pregnancy. Can you comment on the current treatment options and discuss their safety and efficacy during pregnancy?Given the considerable and well-documented adverse effects of antenatal smoking on mother and fetus, pharmacotherapy for smoking cessation should be considered. Available medications include nicotine replacement therapy, sustained-release bupropion, and varenicline. Nicotine replacement therapy and bupropion do not appear to increase the risk of major malformations; however, there is currently limited evidence on the use of varenicline during pregnancy. Given that these agents are only marginally successful in smoking cessation, their use should always be accompanied by behavioural counseling and education to maximize quit rates.
| S-EPMC3352787 | biostudies-other
Project description:One way to enhance therapeutic development is through the identification and development of evaluative tools such as biomarkers. This review focuses on putative diagnostic, pharmacodynamic, and predictive biomarkers for smoking cessation. These types of biomarkers may be used to more accurately diagnose a disease, personalize treatment, identify novel targets for drug discovery, and enhance the efficiency of drug development. Promising biomarkers are presented across a range of approaches including metabolism, genetics, and neuroimaging. A preclinical viewpoint is also offered, as are analytical considerations and a regulatory perspective summarizing a pathway toward biomarker qualification.
| S-EPMC3772534 | biostudies-literature
Project description: Not available
| S-EPMC9009295 | biostudies-literature
Project description:A significant proportion of COPD patients (∼40%) continue smoking despite knowing that they have the disease. Smokers with COPD exhibit higher levels of nicotine dependence, and have lower self-efficacy and self-esteem, which affects their ability to quit smoking. Treatment should be adapted to the needs of individual patients with different levels of tobacco dependence. The combination of counselling plus pharmacotherapy is the most effective cessation treatment for COPD. In patients with severe COPD, varenicline and bupropion have been shown to have the highest abstinence rates compared with nicotine replacement therapy. There is a lack of evidence to support that smoking cessation reduction or harm reduction strategies have benefits in COPD patients. The long-term efficacy and safety of electronic cigarettes for smoking cessation need to be evaluated in high-risk populations; therefore, it is not possible to recommend their use for smoking cessation in COPD. Future studies with the new generation of nicotine vaccines are necessary to determine their effectiveness in smokers in general and in COPD patients.
| S-EPMC10032588 | biostudies-literature
Project description:IntroductionWe conducted a preliminary proof-of-concept study evaluating gabapentin for the treatment of tobacco dependence.MethodsSubjects (N = 80) were randomized to gabapentin (600 mg three times per day or 900 mg three times per day) or placebo. After a 2-week dose titration, the target dose was maintained for 9 weeks and then tapered over 1 week. Follow-up was for 12 weeks after the medication phase.ResultsThe study had high dropout rates with more than one half of participants in each arm discontinuing study. Gabapentin-treated participants exhibited lower abstinence rates than placebo-treated participants; however, this difference was not significant. Smoking reduction was observed across all treatment arms compared with baseline (p < .01) but did not differ across treatment groups.DiscussionAlthough not definitive, our findings suggest that gabapentin administered at these doses with this dosing regimen holds little promise for the treatment of tobacco dependence in a population of smokers seeking treatment.
| S-EPMC2825098 | biostudies-literature
Project description: Not available
| S-EPMC6635501 | biostudies-literature
Project description: Not available
| S-EPMC6568235 | biostudies-literature
Project description:ImportanceMillions of Americans are forced to quit smoking as they enter tobacco-free prisons and jails, but most return to smoking within days of release. Interventions are needed to sustain tobacco abstinence after release from incarceration.ObjectiveTo evaluate the extent to which the WISE intervention (Working Inside for Smoking Elimination), based on motivational interviewing (MI) and cognitive behavioral therapy (CBT), decreases relapse to smoking after release from a smoke-free prison.DesignParticipants were recruited approximately 8 weeks prior to their release from a smoke-free prison and randomized to 6 weekly sessions of either education videos (control) or the WISE intervention.SettingA tobacco-free prison in the United States.ParticipantsA total of 262 inmates (35% female).Main outcome measureContinued smoking abstinence was defined as 7-day point-prevalence abstinence validated by urine cotinine measurement.ResultsAt the 3-week follow-up, 25% of participants in the WISE intervention (31 of 122) and 7% of the control participants (9 of 125) continued to be tobacco abstinent (odds ratio [OR], 4.4; 95% CI, 2.0-9.7). In addition to the intervention, Hispanic ethnicity, a plan to remain abstinent, and being incarcerated for more than 6 months were all associated with increased likelihood of remaining abstinent. In the logistic regression analysis, participants randomized to the WISE intervention were 6.6 times more likely to remain tobacco abstinent at the 3-week follow up than those randomized to the control condition (95% CI, 2.5-17.0). Nonsmokers at the 3-week follow-up had an additional follow-up 3 months after release, and overall 12% of the participants in the WISE intervention (14 of 122) and 2% of the control participants (3 of 125) were tobacco free at 3 months, as confirmed by urine cotinine measurement (OR, 5.3; 95% CI, 1.4-23.8).Conclusions and relevanceForced tobacco abstinence alone during incarceration has little impact on postrelease smoking status. A behavioral intervention provided prior to release greatly improves cotinine-confirmed smoking cessation in the community.Trial registrationclinicaltrials.gov Identifier: NCT01122589.
| S-EPMC4438989 | biostudies-literature