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At least 19 recordsLinked to original sources
PubMed2026

Role of nicotine metabolite ratio in pharmacological interventions on smoking cessation: A systematic review and meta-analyses of randomized controlled trials.

BACKGROUND AND OBJECTIVES: Emerging evidence suggests that the nicotine metabolite ratio (NMR) may influence the efficacy of smoking cessation, yet its role across pharmacotherapies remains unclear. This study aims to investigate how NMR affects cessation outcomes under different medications to guide personalized treatment. METHODS: We searched PubMed, Medline, EMBASE, and the Cochrane Central Register of Controlled Trials (inception to September 30, 2024) for randomized controlled trials on pharmacotherapy for smoking cessation with NMR data. Data were synthesized using random-effects models, with heterogeneity assessment. The primary outcome was verified smoking cessation rate at the end of treatment or the closest time-point. RESULTS: Eleven RCTs with accessible full text were included in the qualitative analyses and nine were included in the quantitative synthesis. For non-titratable nicotine replacement therapy (NRT), normal/fast metabolizers demonstrated lower odds of smoking cessation than slow metabolizers (Odds Ratio, OR=0.81, 95% confidence interval, CI=0.68-0.96; 5 studies, I²=62.5%). No significant associations were shown between normal/fast and slow metabolizers using titratable NRT (OR=1.04, 95% CI=0.95-1.14; 2 studies, I²=0%), bupropion (OR=0.67, 95% CI=0.38-1.16; 2 studies, I²=51.4%), or varenicline (OR=1.17, 95% CI=0.79-1.74; 4 studies, I²=59.8%). CONCLUSION: Current evidence demonstrates that NMR moderates' treatment efficacy among those who smoke using non-titratable NRT, with slow metabolizers achieving significantly better cessation outcomes than normal/fast metabolizers. Substantial further research is needed to determine optimal medication hierarchies across metabolic profiles.

Humans↗
PubMed2026

Optimizing smoking cessation pharmacotherapy and counseling for adult primary care patients: a factorial randomized controlled trial.

BACKGROUND: Even with the most effective smoking cessation pharmacotherapies (i.e., varenicline or combination nicotine replacement [C-NRT]), the majority of people ultimately return to smoking. This research explored how to optimize the use of varenicline and C-NRT to promote smoking cessation. METHODS: Primary care patients participated in a 2x2x2x2 factorial experiment that evaluated 4 factors: 1) Medication Type (Varenicline vs. C-NRT [patch + mini-lozenge]), 2) Preparation (pre-quit) Medication (4 Weeks vs. Standard); 3) Medication Duration (Extended [24 weeks] vs. Standard [12 weeks]); and 4) Counseling Type (Cessation Counseling [4 sessions] vs. Referral Support [2 sessions focused on use of referral resources]). This study was discontinued prior to reaching the proposed sample size (N = 608) due to pandemic-related budgetary constraints. RESULTS: Participants (N = 496) were 55% women and 45.6% Black individuals. There were no statistically significant main effects of the 4 factors on abstinence at 12, 26 or 52 weeks. There was a 3-way interaction between Medication Type, Preparation Medication, and Counseling Type (p = 0.04) predicting the primary outcome of biochemically confirmed abstinence at 52 weeks; cessation counseling vs. referral support improved varenicline quit rates when 4 weeks versus 1 week of pre-quit medication was offered. For C-NRT, counseling type did not significantly improve quit rates regardless of the use of preparation medication. CONCLUSIONS: There was no robust evidence that enhanced pre-quit or extended duration of varenicline or C-NRT increased abstinence rates. More intensive counseling may support cessation for different pharmacotherapy regimens. Given the lack of consistent findings, this research should be viewed as exploratory to guide future research.

Humans↗
PubMed2025

Genome-Wide Association Study of Varenicline-Aided Smoking Cessation.

INTRODUCTION: Varenicline is an &#x3b1;4&#x3b2;2 nicotinic acetylcholine receptor partial agonist with the highest therapeutic efficacy of any pharmacological smoking cessation aid and a 12-month cessation rate of 26%. Genetic variation may be associated with varenicline response, but to date, no genome-wide association studies of varenicline response have been published. METHODS: In this study, we investigated the genetic contribution to varenicline effectiveness using two electronic health record-derived phenotypes. We defined short-term varenicline effectiveness (SVE) and long-term varenicline effectiveness (LVE) by assessing smoking status at 3 and 12 months, respectively, after initiating varenicline treatment. In Stage 1, comprising five European cohort studies, we tested genome-wide associations with SVE (1405 cases, 2074 controls) and LVE (1576 cases, 2555 controls), defining sentinel variants (the most strongly associated variant within 1&#xa0;Mb) with p-value < 5&#x2005;&#xd7;&#x2005;10-6 to follow up in Stage 2. In Stage 2, we tested association between sentinel variants and comparable smoking cessation endpoints in varenicline randomized controlled trials. We subsequently meta-analyzed Stages 1 and 2. RESULTS: No variants reached genome-wide significance in the meta-analysis. In Stage 1, 10 sentinel variants were associated with SVE and five with LVE at a suggestive significance threshold (p-value&#x2005;<&#x2005;5&#x2005;&#xd7;&#x2005;10-6); none of these sentinels were previously implicated in varenicline-aided smoking cessation or in genetic studies of smoking behavior. CONCLUSIONS: We provide initial insights into the biological underpinnings of varenicline-aided smoking cessation, through implicating genes involved in various processes, including gene expression, cilium assembly, and early-stage development. IMPLICATIONS: Leveraging electronic health records, we undertook the largest genetic study of varenicline-aided smoking cessation to date, and the only such study to test genome-wide associations. We showed distinct genetic variants associated (p-value&#x2005;<&#x2005;5&#x2005;&#xd7;&#x2005;10-6) with varenicline-aided smoking cessation which implicate diverse cellular functions, including transcriptional regulation, RNA modification, and cilium assembly. These provide insights which, if independently corroborated, will improve understanding of varenicline response. The growing availability of biobank resources with genetic and varenicline response data will provide future opportunities for larger studies using the approach we developed.

Humans↗
PubMed1986

Clinical pharmacology of nicotine.

Nicotine is the primary reason why people consume tobacco products and it may contribute to causation of tobacco-related diseases. This chapter reviews the human pharmacology of nicotine, the evidence for a role of nicotine in human disease, and the use of nicotine (gum) as a therapeutic agent in smoking cessation therapy.

Animals↗
PubMed1992

Effects of differing nicotine-replacement doses on weight gain after smoking cessation.

OBJECTIVE: To prospectively assess effects of doses of a nicotine-replacement agent on weight gain in men and women after smoking cessation. DESIGN: Four-week, randomized, double-blind clinical trial. SETTING: Outpatient medical clinic. STUDY PARTICIPANTS: Healthy volunteers who smoked at least 10 cigarettes per day. INTERVENTION: Pharmacologic: Random assignment to 0, 2, or 4 mg of nicotine polacrilex on a fixed-dose schedule (one piece per hour while awake). Behavioral: Brief, medical/behavioral counseling regarding smoking cessation. MAIN OUTCOME MEASURE: Weight change as a function of dose and gender only in participants abstinent for all 4 week. (Self-reported abstinence verified by breath carbon monoxide levels). RESULTS: Weight change in women abstinent for 4 weeks (n = 16) was +1.69, +0.33, and -0.26 kg in the placebo, 2-mg, and 4-mg groups, respectively, compared with +1.60, +1.45, and +1.18 kg for the men who were abstinent for 4 weeks (n = 19). Medication use did not differ as a function of dose or gender. CONCLUSIONS: Nicotine polacrilex suppressed, in a dose-related fashion, weight gain after smoking cessation in successfully treated women. Weight gain was not shown to be suppressed in men, possibly because of small sample size.

Adult↗
PubMedDate not supplied

Affect regulation, nicotine addiction, and smoking cessation.

Numerous investigators have examined the role of negative affective states and affect regulation in the initiation and development of cigarette smoking behavior, smoking cessation, and relapse prevention. Affect regulation refers to any attempt to alleviate negative mood states by means of pharmacologic-, cognitive-, behavioral- or environmental-change methods. The psychological construct/process of affect regulation is examined in relation to (1) the initiation, development, and maintenance of the cigarette smoking habit; (2) the process of quitting smoking; and (3) the long-term maintenance of smoking abstinence versus relapse. Various psychosocial factors and physiological mechanisms are explored that have been hypothesized to be links between negative mood states, nicotine addiction, and smoking cessation. Implications for smoking cessation treatment are discussed in the areas of (1) the use of pharmacologic agents, such as clonidine, in the reduction of nicotine withdrawal symptoms; (2) nicotine replacement therapy; and (3) skills-training approaches to smoking cessation and relapse prevention.

Emotions↗
PubMedDate not supplied

Affect regulation, nicotine addiction, and smoking cessation.

Numerous investigators have examined the role of negative affective states and affect regulation in the initiation and development of cigarette smoking behavior, smoking cessation, and relapse prevention. Affect regulation refers to any attempt to alleviate negative mood states by means of pharmacologic-, cognitive-, behavioral- or environmental-change methods. The psychological construct/process of affect regulation is examined in relation to (1) the initiation, development, and maintenance of the cigarette smoking habit; (2) the process of quitting smoking; and (3) the long-term maintenance of smoking abstinence versus relapse. Various psychosocial factors and physiological mechanisms are explored that have been hypothesized to be links between negative mood states, nicotine addiction, and smoking cessation. Implications for smoking cessation treatment are discussed in the areas of (1) the use of pharmacologic agents, such as clonidine, in the reduction of nicotine withdrawal symptoms; (2) nicotine replacement therapy; and (3) skills-training approaches to smoking cessation and relapse prevention.

Affect↗
PubMed1992

Nicotine and the central nervous system: biobehavioral effects of cigarette smoking.

The effects of nicotine, like those of other drugs with potential for abuse and dependence, are centrally mediated. The impact of nicotine on the central nervous system is neuroregulatory in nature, affecting biochemical and physiological functions in a manner that reinforces drug-taking behavior. Dose-dependent neurotransmitter and neuroendocrine effects occur as plasma nicotine levels rise when a cigarette is smoked. Circulating levels of norepinephrine and epinephrine increase, and the bioavailability of dopamine is altered as well. Among the neuroendocrine effects are release of arginine vasopressin, beta-endorphin, adrenocorticotropic hormone, and cortisol. Notably, several of these neurochemicals are psychoactive and/or known to modulate behavior. Thus, affective states or cognitive demands may be favorably modified (at least temporarily) by nicotine intake. When nicotine is inhaled, the neuroregulatory effects just described are immediately available and the reinforcing effects of the drug are maximized. On the other hand, nicotine gum and most other nicotine replacement vehicles in current use have a slower onset of action, resulting in less reinforcement value. Recent data suggest that smoking cessation rates may be optimized by tailoring the dose of nicotine replacement (for example, 2 or 5 mg of nicotine gum) to the individual degree of nicotine dependence. In view of the dynamic interactions between the neuroregulatory effects of nicotine and a host of environmental conditions, nicotine replacement therapy is best carried out in combination with behavior modification techniques.

Behavior↗
PubMed2026

Effect of flavored on!&#xae; nicotine pouch products on smoking behaviors: A sequential, multiple assignment, randomized controlled trial.

PURPOSE: To evaluate whether flavored versus unflavored nicotine pouch (NP) access affects cigarette reduction and smoke exposure among adults who smoke daily, and whether delayed flavor introduction affects these outcomes. METHODS: Adults who smoked &#x2265;&#x2009;5 cigarettes/day (CPD) with interest in replacing cigarettes with NPs were enrolled in a remote, six-week, sequential multiple assignment randomized trial (n&#x2009;=&#x2009;402 randomized; n&#x2009;=&#x2009;400 analyzed). Participants were randomized to immediate access to seven NP flavors (Flavor), unflavored-only access for six weeks (Original), or unflavored-only for three weeks followed by flavor access (Delayed Flavor). Primary outcomes were &#x2265;&#x2009;50% reduction in weekly mean expired-air carbon monoxide (CO) from baseline and mean CO at Week 6. Secondary outcomes included &#x2265;&#x2009;50% CPD reduction, mean CPD, CO-verified 7-day abstinence, and incident smoke-free days. RESULTS: At Week 6, Flavor and Original did not differ in &#x2265;&#x2009;50% CO reduction (14.3% vs 14.2%; IRR=1.0, 95% CI=0.6-1.8) or mean CO (18.3 vs 16.5&#x2009;ppm; &#x3b2;=1.9, 95% CI=-1.3-5.0). CPD decreased across groups by Week 6, with no differences between Flavor and Original in &#x2265;&#x2009;50% CPD reduction (50.3% vs 51.6%; IRR=1.0, 95% CI=0.8-1.2) or CO-verified abstinence (9.3% vs 8.9%; IRR=1.0, 95% CI=0.5-2.2). Flavor increased smoke-free days early, with attenuation over time. Among Week 3 non-responders, delayed flavor access increased &#x2265;&#x2009;50% CPD reduction at Week 6 (33.3% vs 18.6%; IRR=1.8, 95% CI=1.0-3.2). CONCLUSIONS: NP access supported cigarette reduction regardless of flavor availability, but flavors may accelerate smoke-free days and improve response among individuals who do not reduce cigarette consumption with unflavored products alone.

Humans↗
PubMed1990

The mechanism of lung carcinogenesis and smoking cessation.

Mathematical modeling of risk of lung cancer upon smoking cessation suggests increasing risk, whereas the facts show decreasing mortality. This discordance is resolved by taking into account the mechanistically distinct steps in chemical carcinogenesis: (1) neoplastic conversion by genotoxic carcinogens and (2) neoplastic growth and development by agents with epigenetic and promoting effects. Tobacco smoke contains relatively small amounts of several types of genotoxic carcinogens, the effect of which is considerably and vitally enhanced by nongenotoxic promoting factors. Upon smoking cessation, the effect of the second type of agent is abruptly eliminated. Therefore, any preneoplastic lesions remain static or regress, whereas in the continuing smoker they progress. These sequences also apply, with different chemicals involved, in nutritional carcinogenesis.

Cell Transformation, Neoplastic↗
PubMed1991

Epidemiologic perspectives on life-style modification and health promotion in cancer research.

The clinical, patient-oriented focus of medicine and psychology is contrasted with the epidemiologic (public health) approach in assessing the role of life-style factors and health promotion in cancer research. The unifying host-agent-environment epidemiologic paradigm is applied to contemporary cancer prevention issues, principally smoking cessation and dietary modification, to demonstrate differences in inferences, prevention strategies, and research opportunities. An integration of population-based approaches with the dynamics of patient behavior and risks for cancer is especially salient when considering the role of psychosocial stress and personal and social resources. The social epidemiologic perspective, the study of the psychosocial determinants of physical health status, offers one approach for resolving the outlined differences in perspectives and is particularly relevant for understanding the etiology of life-style behaviors and how they might be altered.

Epidemiologic Methods↗
PubMed1988

The effect of clonidine on the cessation of cigarette smoking.

The effect of clonidine on smoking cessation was studied by randomly assigning 186 smokers in a double-blind fashion to either placebo or clonidine. Abstinence from smoking was reported more frequently by subjects receiving clonidine, but the difference was statistically significant only at the end of the first week (34.4% vs 21.5%; p less than 0.05). Bothersome side effects were common and resulted in the early discontinuation of the study medication by 23 of the subjects taking clonidine and eight taking placebo (p less than 0.05). Although this study did not demonstrate a significant effect of clonidine on smoking cessation, a beneficial trend was detected and therefore further trials with transcutaneous delivery of this agent in combination with behavior modification techniques are warranted.

Adult↗
PubMed1991

Cancer prevention: recent progress and future opportunities.

Knowledge gathered during the past few decades from the fields of cancer epidemiology, carcinogenesis, biochemistry, and molecular biology, much of which was communicated through the pages of the journal Cancer Research, provides powerful new strategies for cancer prevention. Indeed, I believe that it is possible to draft a blueprint for a comprehensive approach to cancer prevention, to be used as we approach the 21st century. This plan includes: (a) expanded epidemiological and laboratory studies to identify the specific causes of human cancers; (b) intervention studies, such as risk reduction by the cessation of cigarette smoking, dietary modifications, chemoprevention, and the development of vaccines for viral agents implicated in human cancer (i.e., hepatitis B, human papilloma virus, Epstein-Barr virus, and certain retroviruses), and (c) early detection and screening. Concepts and methods that have developed in the field of cellular and molecular biology will accelerate this progress. Indeed, we are currently in a very exciting phase of cancer research that brings together fields of cancer research which in the past were often disparate and disconnected, i.e., basic laboratory studies, epidemiology, prevention, and treatment. Thus, the astounding advances in our understanding of the molecular biology of cancer provide a unified concept of the nature of the cancer cell and also suggest new clinical approaches to cancer etiology, prevention, and treatment. Many of the biomarkers being developed for etiological studies, using the approach of molecular epidemiology, can also serve as biomarkers or intermediate end points to evaluate the efficacy of dietary intervention and chemoprevention studies. Some of these biomarkers will also be useful for evaluating the efficacy of cancer therapy. Furthermore, certain compounds being developed for cancer chemoprevention, e.g., the retinoids, may also be useful in the therapy of fully established neoplasms. It seems likely, therefore, that even before the year 2000 these powerful and unifying themes will accelerate advances in both cancer prevention and treatment, thus leading to major reductions in both the incidence and mortality of human cancer.

Humans↗
PubMed1989

Pharmacotherapy for smoking cessation.

Nicotine dependence and the role of various pharmacotherapeutic adjuncts in the medical management of nicotine withdrawal and smoking cessation are reviewed. Nicotine has been shown to be the drug in tobacco that causes addiction. The nicotine withdrawal syndrome is primarily characterized by craving, irritability, frustration, anger, anxiety, poor concentration, restlessness, weight gain, and decreased heart rate. Pharmacotherapeutic interventions can be classified into four groups: therapy that (1) replaces nicotine, (2) antagonizes nicotine, (3) provides symptomatic treatment for nicotine withdrawal, and (4) deters smoking. Nicotine replacement therapy with nicotine polacrilex gum has had minimal effect on increasing-smoking cessation among patients seen in a general medical practice setting. It is most effective in nicotine dependent smokers when it is used concomitantly with behavioral or psychological counseling. Nicotine antagonist therapy with mecamylamine may be useful in recalcitrant cases of nicotine dependence. Clonidine, in both oral and transdermal forms, has been shown to be effective for reduction of symptoms and craving associated with smoking cessation. Research on using the tricyclic antidepressants imipramine and doxepin to promote smoking cessation by reducing withdrawal symptoms is in its preliminary phases. Lobeline, an alkaloid with effects similar to those of nicotine, is an FDA Category III drug (i.e., safe, but of unknown efficacy) and is available without prescription. Silver acetate chewing gum deters smoking by producing an unpleasant metallic taste on concomitant ingestion of the agent and tobacco. It is an FDA Category III drug and is available without prescription. Drugs used in therapy of nicotine withdrawal include nicotine replacements, nicotine antagonists, agents to lessen the symptoms of withdrawal, and smoking deterrents. None of the drugs is completely effective. Successful drug use for smoking cessation involves consideration of the psychological, as well as physiological, aspects of nicotine addiction.

Humans↗