Precessation treatment with nicotine skin patch facilitates smoking cessation

ArticleinNicotine & Tobacco Research 8(1):89-101 · March 2006with26 Reads
DOI: 10.1080/14622200500431866 · Source: PubMed
Abstract
Nicotine replacement therapy (NRT) is a well-established treatment to aid smoking cessation, and current products recommend using NRT only after quitting smoking. However, theoretical arguments and previous data support the hypothesis that precessation use of NRT might be useful in reducing dependence on inhaled nicotine and serve as a helpful prelude to smoking cessation. The present study explored the use of NRT for 2 weeks before a target quit-smoking date, during which subjects continued to smoke ad libitum. Three experimental conditions varied the nicotine delivery of the cigarettes smoked during these 2 weeks so that we could examine the effects of concurrent nicotine administration on compensatory smoking of low tar and nicotine cigarettes. Subjects smoked (a) their usual brands of cigarettes, (b) conventional low tar and nicotine cigarettes, or (c) denicotinized cigarettes. After the quit date, subjects received pharmacotherapy consisting of various doses of NRT (0, 21, or 42 mg/24-hr) in combination with the nicotinic antagonist mecamylamine (10 mg/day). Results showed that precessation nicotine patch treatment was associated with a significantly higher rate of continuous smoking abstinence at 4 weeks, regardless of cigarette condition. Ad libitum smoking before the target quit date was modulated by nicotine patch treatment, and compensatory increases in smoking low tar and nicotine cigarettes were prevented by concurrent use of nicotine patches. These results suggest that use of NRT before a target quit-smoking date deserves further evaluation as a possible smoking cessation treatment. Moreover, while nicotine patches were well tolerated when subjects smoked nicotine-containing cigarettes, the use of nicotine skin patches with reduced-nicotine cigarettes potentially offers the advantage of increased efficacy without introducing concern about toxic effects of excessive nicotine intake.
    • "The underlying rationale behind pharmacological therapies of substance abuse has been, by large, the " substitution strategy " which, by replacing the abused compound with a different molecule with similar pharmacological activity (but different pharmacokinetics) aims, in general, at harm reduction. Methadone (Dole and Nyswander, 1965; Senay, 1973a, 1973b) represents probably the best example of this philosophy, but similar cases are the various pharmaceutical formulations (patches, spray, gums etc.) of nicotine for smokers (Malaiyandi et al., 2006; Rose et al., 2006 ) and gammahydroxybutyric acid (GHB) for alcoholics (Gallimberti et al., 1989). While this approach has been of great value in the past, it has the disadvantage of very long therapeutic times (many years) thereby post-poning the drug-free status sine-die. "
    [Show abstract] [Hide abstract] ABSTRACT: Drug addiction is a compulsive behavioral abnormality. In spite of pharmacological treatments and psychosocial support to reduce or eliminate drug intake, addiction tends to persist over time. Preclinical and human observations have converged on the hypothesis that addiction represents the pathological deterioration of neural processes that normally serve affective and cognitive functioning. The major elements of persistent compulsive drug use are hypothesized to be structural, cellular and molecular that underlie enduring changes in several forebrain circuits that receive input from midbrain dopamine neurons and are involved in affective (e.g. ventral striatum) and cognitive (e.g. prefrontal cortex) mechanisms. Here we review recent progress in identifying crucial elements useful to understand the pathophysiology of the disease and its treatments. Manipulation of neuropeptides brain systems and pharmacological targeting of κ-opioid receptors and/or drug metabolism may hold beneficial effects at affective and cognitive level. Non-pharmacological, highly innovative approaches such as Transcranial Magnetic Stimulation may reveal unsuspected potential and promise to be the first neurobiology-based therapeutics in addiction.
    Full-text · Article · Apr 2016
    • "In this planned replication study there was little evidence overall that smoking reduction while using nicotine replacement therapy and smoking predicted subsequent abstinence. We hypothesized that the association between reduction and quitting reported previously [1][2][3]5] could have arisen, because people felt that they ought to reduce smoking intentionally while using cessation medication. We did not find strong evidence that the strength of association between reduction and cessation varied by trial arm. "
    [Show abstract] [Hide abstract] ABSTRACT: AND AIMS: Previous studies have reported that people who use a smoking cessation medication while smoking and reduce cigarette consumption spontaneously are three times more likely to stop smoking after a quit date. The aim was to replicate this and assess whether it arises because of willed effortful reduction rather than unwilled reduced drive to smoke caused by medication. DESIGN: Secondary analysis of a trial where participants were randomised to smoke as normal or reduce by 75% over 2 weeks prior to quit date, using nicotine replacement therapy (NRT) in both arms. SETTING: Thirty-one UK primary care practices. PARTICIPANTS: A total of 517 adult smokers seeking quitting support in the carbon monoxide (CO) analyses and 421 in the cigarettes/day analyses. MEASUREMENTS: Russell Standard abstinence was recorded 4 weeks after quit date. The randomized groups were combined and the association between reduction and abstinence examined. The second analysis assessed whether this association differed by whether smokers were, or were not, instructed to reduce. FINDINGS: In all participants, there was no evidence that reducing cigarettes/day or CO by at least half compared with not reducing predicted abstinence at 4 weeks [risk ratio (RR) = 0.88; 95% confidence interval (CI) = 0.68-1.14 and RR = 1.20; 95% CI = 1.00-1.44, respectively]. However, in smokers instructed to reduce, CO reduction was associated with 4-week abstinence (RR = 1.52; 95% CI = 1.16-2.00), but not among people advised not to reduce (RR = 0.91; 95% CI = 0.67-1.24). CONCLUSIONS: Smoking reduction prior to a target quit date while on a smoking cessation medication may only predict subsequent abstinence when smokers are consciously attempting to reduce.
    Full-text · Article · Mar 2016
    • "Most of the studies described earlier demonstrate an acute reduction in craving and cigarette use during denicotinized cigarette use; however, it is less clear whether denicotinized cigarette smoking promotes abstinence. One study indicates that the use of nicotine patches is a strong predictor of abstinence, but not the use of denicotinized cigarettes , suggesting drug replacement therapy may be more effective than extinction procedures in promoting abstinence (Rose et al. 2006). As it stands, instrumental extinction using denicotinized cigarettes or similar methods appear promising, but further research is required to clarify whether the acute effects on craving and use extend into abstinence. "
    [Show abstract] [Hide abstract] ABSTRACT: One of the principal barriers to overcoming addiction is the propensity to relapse, even after months or years of abstinence. Relapse can be precipitated by cues and contexts associated with drug use; thus, decreasing the conditioned properties of these cues and contexts may assist in preventing relapse. The predictive power of drug cues and contexts can be reduced by repeatedly presenting them in the absence of the drug reinforcer, a process known as extinction. The potential of extinction to limit relapse has generated considerable interest and research over the past few decades. While pre-clinical animal models suggest extinction learning assists relapse prevention, treatment efficacy is often lacking when extinction learning principles are translated into clinical trials. Conklin and Tiffany (Addiction, 2002) suggest the lack of efficacy in clinical practice may be due to limited translation of procedures demonstrated through animal research and propose several methodological improvements to enhance extinction learning for drug addiction. This review will examine recent advances in the behavioural and pharmacological manipulation of extinction learning, based on research from pre-clinical models. In addition, the translation of pre-clinical findings-both those suggested by Conklin and Tiffany () and novel demonstrations from the past 13 years-into clinical trials and the efficacy of these methods in reducing craving and relapse, where available, will be discussed. Finally, we highlight areas where promising pre-clinical models have not yet been integrated into current clinical practice but, if applied, could improve upon existing behavioural and pharmacological methods.
    Full-text · Article · Dec 2015
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