A review of the efficacy of smoking-cessation pharmacotherapies in nonwhite populations

Robles, Gisela I.; Singh-Franco, Devada; Ghin, Hoytin Lee

doi:10.1016/j.clinthera.2008.05.010

Cited by 66 publications

(51 citation statements)

References 32 publications

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“…Smoking leads to the development of a strong dependency, and the efficacy of smoking cessation treatments is very low (1,2). One vital issue in developing improved strategies to assist with smoking cessation is to understand the mechanisms that underlie nicotine dependence in cigarette smokers.…”

mentioning

confidence: 99%

Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing ¹¹ C-nicotine

Rose

Mukhin

Lokitz

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

117

103

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Tobacco smoking is a chronic, relapsing disorder that constitutes one of the primary preventable causes of death in developed countries. Two of the popular hypotheses to explain the development and maintenance of strong nicotine dependence in cigarette smokers posit (i) a rapid brain nicotine accumulation during cigarette smoking and/or (ii) puff-associated spikes in brain nicotine concentration. To address these hypotheses, we investigated the dynamics of nicotine accumulation in the smoker's brain during actual cigarette smoking using PET with 3-s temporal resolution and 11 C-nicotine loaded into cigarettes. The results of the study, performed in 13 dependent smokers (DS) and 10 nondependent smokers (NDS), suggest that puff-associated spikes in the brain nicotine concentration do not occur during habitual cigarette smoking. Despite the presence of a puff-associated oscillation in the rate of nicotine accumulation, brain nicotine concentration gradually increases during cigarette smoking. The results further suggest that DS have a slower process of brain nicotine accumulation than NDS because they have slower nicotine washout from the lungs and that DS have a tendency to compensate for their slower rate of brain nicotine accumulation compared with NDS by inhaling a larger volume of smoke. For these reasons, smokers' dependence on cigarette smoking, or the resistance of NDS to becoming dependent, cannot be explained solely by a faster brain nicotine accumulation.cigarette smoking | nicotine dependence | tobacco | addiction | lung T obacco smoking is a chronic, relapsing disorder that constitutes one of the leading preventable causes of death in developed countries. Smoking leads to the development of a strong dependency, and the efficacy of smoking cessation treatments is very low (1, 2). One vital issue in developing improved strategies to assist with smoking cessation is to understand the mechanisms that underlie nicotine dependence in cigarette smokers.Nicotine is the one of the ingredients of cigarette smoke that is most closely linked to tobacco dependence (3). This alkaloid interacts with both central and peripheral neuronal nicotinic acetylcholine receptors (nAChRs). The nAChRs belong to the superfamily of ligand-gated ion channels and are composed of five protein subunits. To date, nine α-subunits (α2-α10) and three β-subunits (β2-β4) have been identified in the nervous system (reviewed in ref. 4). Most of these subunits may form a heteromeric complex, but others (α7-α9) appear to function predominantly as a homomeric group. High diversity in neuronal nAChR subunits can potentially lead to an enormous variety of these receptors in the nervous system.After acute administration of nicotinic agonists, the nAChR channel complex is activated and becomes permeable for sodium, potassium, and calcium ions. Nonetheless, prolonged exposure of nAChRs to nicotinic agonists leads to desensitization of the receptors. The desensitization diminishes channel permeability and the capability of the receptors to be activate...

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mentioning

confidence: 99%

Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing ¹¹ C-nicotine

Rose

Mukhin

Lokitz

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

117

103

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“…[1][2][3][4]. A meta-analysis indicates that there are measurable benefits in studies of 12 to 18 months of continued NRT use for relapse prevention (5), and other studies also indicate that this use is cost effective (6).…”

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confidence: 99%

Long-term Nicotine Replacement Therapy: Cancer Risk in Context

Shields

2011

Cancer Prevention Research

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Nicotine replacement therapy (NRT) for up to 12 weeks is well established, safe and efficacious for fostering smoking cessation. Some smokers at a high risk of relapse may benefit from long-term use, and so long-term NRT safety and efficacy have become a paramount question for the FDA and others. Laboratory studies have indicated a carcinogenic potential of nicotine. Animal model studies reported in this issue of the journal by Maier and colleagues (beginning on page 1743) and Murphy and colleagues (beginning on page 1752), however, provide additional reassurance that NRT does not promote lung cancer. Very long-term studies of NRT effects do not yet exist and would be needed to definitively answer the question about NRT efficacy and cancer risk and some decision making will need to be made based on limited human data and experimental studies. The overall NRT safety question is complex and requires consideration of three contexts and comparator groups (long-term NRT/abstinence vs. smoking, long-term intermittent NRT/ reduced smoking vs. smoking, and long-term NRT/abstinence vs. abstinence without long-term NRT). Although the data on these issues are insufficient, the first comparison seems intuitive and may be compelling enough to allow the FDA to approve a long-term indication for NRT. An important public health goal is to help smokers and their health care providers understand the implications of potential long-term NRT risks in the context of its potential benefits and the far greater risks of continued smoking. Cancer Prev Res; 4(11); 1719-23. Ó2011 AACR.The efficacy and safety of short-term nicotine replacement therapy (NRT) for fostering long-term smoking cessation is well established, and up to 12 weeks of therapy is approved by the U.S. Food and Drug Administration (FDA; refs. 1-4). A meta-analysis indicates that there are measurable benefits in studies of 12 to 18 months of continued NRT use for relapse prevention (5), and other studies also indicate that this use is cost effective (6). An important question of considerable interest that remains today, however, is whether NRT can be recommended for long-term use, even years, to continue to promote smoking abstinence. The answer to this question requires both an efficacy and safety assessment. In this context, NRT conceptually has substantial benefits compared with long-term smoking but also, as explained later and addressed in this issue of the journal, laboratory studies suggest a potential for nicotine to foster the development of cancer.The premise of long-term NRT use is that it would prevent smoking relapse, and the risks would be limited to maintaining nicotine addiction, but without the adverse consequences of continued smoking, such as increased lung cancer risk. Like the consideration of other long-term medications, on face value it is a simple risk-benefits equation. In actuality, however, this question is not simple to answer because the risk can be considered in 3 different contexts and comparator groups namely: (i) what is the risk o...

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“…The present study showed that the patients who used varenicline for smoking cessation therapy had a significantly higher quitting rate than those who used NRT and bupropion at the end of therapy (at weeks [4][5][6][7][8][9][10][11][12]. Several studies that assessed the success rate of pharmacological therapies reported different rates.…”

Section: Discussionmentioning

confidence: 82%

“…Smoking cessation interventions generally include counseling and/or pharmacological therapies like varenicline, bupropion, and NRT alone or in combination. Research findings suggest that smoking-cessation self-help strategies alone are usually ineffective while counseling and pharmacotherapy either alone or in combination can improve abstinence rates (7). The comparison between bupropion and NRT suggests no advantage for either treatment.…”

Section: Introductionmentioning

confidence: 97%

Success Rates of Pharmacological Therapies Used for Smoking Cessation and Factors that Affect Smoking Cessation Rates

et al. 2015

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A review of the efficacy of smoking-cessation pharmacotherapies in nonwhite populations

Cited by 66 publications

References 32 publications

Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing ¹¹ C-nicotine

Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing ¹¹ C-nicotine

Long-term Nicotine Replacement Therapy: Cancer Risk in Context

Success Rates of Pharmacological Therapies Used for Smoking Cessation and Factors that Affect Smoking Cessation Rates

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A review of the efficacy of smoking-cessation pharmacotherapies in nonwhite populations

Cited by 66 publications

References 32 publications

Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing 11 C-nicotine

Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing 11 C-nicotine

Long-term Nicotine Replacement Therapy: Cancer Risk in Context

Success Rates of Pharmacological Therapies Used for Smoking Cessation and Factors that Affect Smoking Cessation Rates

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Product

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Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing ¹¹ C-nicotine

Kinetics of brain nicotine accumulation in dependent and nondependent smokers assessed with PET and cigarettes containing ¹¹ C-nicotine