Evaluating Treatment Mechanisms of Varenicline: Mediation by Affect and Craving.

Evaluating Treatment Mechanisms of Varenicline: Mediation by Affect and Craving.
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评估伐尼克兰的治疗机制:通过情感和渴望进行调节。

DOI:
10.1093/ntr/ntac138
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发表时间:
2022
期刊:
Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco
影响因子:
--
通讯作者:
Hawk,LarryW
Hawk,LarryW
中科院分区:
--
文献类型:
--
作者:
Tonkin,SarahS;Colder,Craig;Mahoney,MartinC;Swan,GaryE;Cinciripini,Paul;Schnoll,Robert;George,TonyP;Tyndale,RachelF;Hawk,LarryW

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负强化模型认为,在戒烟过程中,情感和渴望的变化部分地驱动了吸烟的复发。伐仑克林可以通过减轻这些变化来帮助戒烟;然而,这一中介途径尚未在安慰剂对照试验中得到正式评估。因此,我们测试了消极情绪(NA)、积极情绪(PA)和渴望的轨迹作为伐尼克兰对戒烟效果的中介。目的和方法在一项戒烟随机对照试验(NCT01314001)中,对828名被分配到伐尼克兰或安慰剂组的成年人进行了二级数据分析。在戒烟前1周、目标戒烟日(TQD)和戒烟后1周和4周评估自我报告的NA、PA和渴望。结果在戒烟后1周内,NA达到峰值,PA没有变化,渴望度下降。NA的上升幅度较小(间接效应95% CI:。01到。30),戒烟后1周的平均渴望度降低(CI:。06到。50)是伐尼克兰与治疗结束时较高戒烟率之间关系的中介因子。PA与戒烟有关,但不是显著的中介。结论这些结果部分支持了伐尼克兰通过减轻特定心理过程的变化而提高戒烟率的假设,并支持了NA和渴望可能是伐尼克兰的治疗机制。本研究提供了来自安慰剂对照随机临床试验的第一个证据,证明伐尼克兰的疗效部分是由于戒烟后NA和渴望的减弱。在尝试戒烟的过程中减少NA和在尝试戒烟的早期渴望可能是有效干预的重要治疗机制。此外,戒烟后的NA、PA和渴望都与复发有关,代表了未来干预发展的治疗目标。
IntroductionNegative reinforcement models posit that relapse to cigarette smoking is driven in part by changes in affect and craving during the quit attempt. Varenicline may aid cessation by attenuating these changes; however, this mediational pathway has not been formally evaluated in placebo-controlled trials. Thus, trajectories of negative affect (NA), positive affect (PA), and craving were tested as mediators of the effect of varenicline on smoking cessation.Aims and MethodsSecondary data analysis was conducted on 828 adults assigned to either varenicline or placebo in a randomized controlled trial for smoking cessation (NCT01314001). Self-reported NA, PA, and craving were assessed 1-week pre-quit, on the target quit day (TQD), and 1 and 4 weeks post-TQD.ResultsAcross time, NA peaked 1-week post-quit, PA did not change, and craving declined. Less steep rises in NA (indirect effect 95% CI: .01 to .30) and lower mean craving at 1-week post-quit (CI: .06 to .50) were mediators of the relationship between varenicline and higher cessation rates at the end of treatment. PA was associated with cessation but was not a significant mediator.ConclusionsThese results partially support the hypothesis that varenicline improves smoking cessation rates by attenuating changes in specific psychological processes and supported NA and craving as plausible treatment mechanisms of varenicline.ImplicationsThe present research provides the first evidence from a placebo-controlled randomized clinical trial that varenicline’s efficacy is due, in part, to post-quit attenuation of NA and craving. Reducing NA across the quit attempt and craving early into the attempt may be important treatment mechanisms for effective interventions. Furthermore, post-quit NA, PA, and craving were all associated with relapse and represent treatment targets for future intervention development.
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