Understanding the basic and clinical pharmacology of nicotine provides a basis for improved prevention and treatment of tobacco addiction. Nicotine acts on nicotinic cholinergic receptors in the ...brain to release dopamine and other neurotransmitters that sustain addiction. Neuroadaptation and tolerance involve changes in both nicotinic receptors and neural plasticity. Nicotine addiction can occur in the context of physical dependence characterized by self‐medication to modulate negative affect and/or to relieve withdrawal symptoms, as well as, in light or occasional smokers, primarily for positive reinforcement in specific situations. Nicotine is metabolized primarily by CYP2A6. Its clearance exhibits considerable individual variability that is determined by genetic, racial, and hormonal (sex) factors. Genetically slow metabolism of nicotine appears to be associated with a lower level of dependence. Nicotine dependence is highly heritable and appears to be influenced by genes coding for some nicotine receptor subtypes, some neurotransmitter genes, and genes involved in neural connectivity. Novel pharmacotherapies for nicotine dependence include partial agonists for nicotinic receptors and nicotine vaccines. Pharmacogenetic studies suggest various candidate genes and a nicotine metabolism phenotype that influence outcome. Human pharmacology studies of nicotine and smoking behavior also provide a basis for assessing the benefits and risks of long‐term nicotine use for harm reduction and for a potential cigarette regulatory strategy that includes reducing nicotine content of cigarettes to nonaddictive levels.
Clinical Pharmacology & Therapeutics (2008); 83, 4, 531–541. doi:10.1038/clpt.2008.3
Socioeconomic status and smoking: a review Hiscock, Rosemary; Bauld, Linda; Amos, Amanda ...
Annals of the New York Academy of Sciences,
February 2012, Letnik:
1248, Številka:
1
Journal Article
Recenzirano
Smoking prevalence is higher among disadvantaged groups, and disadvantaged smokers may face higher exposure to tobacco's harms. Uptake may also be higher among those with low socioeconomic status ...(SES), and quit attempts are less likely to be successful. Studies have suggested that this may be the result of reduced social support for quitting, low motivation to quit, stronger addiction to tobacco, increased likelihood of not completing courses of pharmacotherapy or behavioral support sessions, psychological differences such as lack of self‐efficacy, and tobacco industry marketing. Evidence of interventions that work among lower socioeconomic groups is sparse. Raising the price of tobacco products appears to be the tobacco control intervention with the most potential to reduce health inequalities from tobacco. Targeted cessation programs and mass media interventions can also contribute to reducing inequalities. To tackle the high prevalence of smoking among disadvantaged groups, a combination of tobacco control measures is required, and these should be delivered in conjunction with wider attempts to address inequalities in health.
Significant progress has been made in reducing the prevalence of tobacco use in the United States. However, tobacco cessation efforts have focused on the general population rather than individuals ...with mental illness, who demonstrate greater rates of tobacco use and nicotine dependence.
To assess whether declines in tobacco use have been realized among individuals with mental illness and examine the association between mental health treatment and smoking cessation.
Use of nationally representative surveys of noninstitutionalized US residents to compare trends in smoking rates between adults with and without mental illness and across multiple disorders (2004-2011 Medical Expenditure Panel Survey MEPS) and to compare rates of smoking cessation among adults with mental illness who did and did not receive mental health treatment (2009-2011 National Survey of Drug Use and Health NSDUH).The MEPS sample included 32,156 respondents with mental illness (operationalized as reporting severe psychological distress, probable depression, or receiving treatment for mental illness) and 133,113 without mental illness. The NSDUH sample included 14,057 lifetime smokers with mental illness.
Current smoking status (primary analysis; MEPS sample) and smoking cessation, operationalized as a lifetime smoker who did not smoke in the last 30 days (secondary analysis; NSDUH sample).
Adjusted smoking rates declined significantly among individuals without mental illness (19.2% 95% CI, 18.7-19.7% to 16.5% 95% CI, 16.0%-17.0%; P < .001) but changed only slightly among those with mental illness (25.3% 95% CI, 24.2%-26.3% to 24.9% 95% CI, 23.8%- 26.0%; P = .50), a significant difference in difference of 2.3% (95% CI, 0.7%-3.9%) (P = .005). Individuals with mental illness who received mental health treatment within the previous year were more likely to have quit smoking (37.2% 95% CI, 35.1%-39.4%) than those not receiving treatment (33.1% 95% CI, 31.5%-34.7%) (P = .005).
Between 2004 and 2011, the decline in smoking among individuals with mental illness was significantly less than among those without mental illness, although quit rates were greater among those receiving mental health treatment. This suggests that tobacco control policies and cessation interventions targeting the general population have not worked as effectively for persons with mental illness.
Chronic obstructive pulmonary disease (COPD), lung cancer, asthma and pulmonary tuberculosis are common pulmonary diseases that are caused or worsened by tobacco smoking. Growing observational ...evidence suggests that symptoms and prognosis of these conditions improve upon smoking cessation. Despite increasing numbers of (small) randomised controlled trials suggesting intensive smoking cessation treatments work in people with pulmonary diseases many patients are not given specific advice on the benefits or referred for intensive cessation treatments and, therefore, continue smoking.This is a qualitative review regarding smoking cessation in patients with COPD and other pulmonary disorders, written by a group of European Respiratory Society experts. We describe the epidemiological links between smoking and pulmonary disorders, the evidence for benefits of stopping smoking, how best to assess tobacco dependence and what interventions currently work best to help pulmonary patients quit. Finally, we describe characteristics and management of any "hardcore" smoker who finds it difficult to quit with standard approaches.
•Addictive smoking is common among people with severe mental illness (SMI).•Tobacco use disorder(TUD)/nicotine dependence(ND) reflect an evolving nomenclature.•Females with a primary diagnosis of any ...SMI have lower prevalence rates of TUD.•Bupropion and varenicline represent common strategies for SMI with TUD/ND.•Forthcoming rigorous randomized controlled studies should focus on varying SMIs.
The prevalence, correlates, and management of tobacco use disorder (TUD) or nicotine dependence (ND) among people with severe mental illness (SMI), namely schizophrenia, bipolar disorder (BD), and major depressive disorder (MDD), remain unclear. Therefore, a systematic review and meta-analysis was conducted. Electronic databases were systematically searched from inception to July 12, 2020, for observational studies documenting the prevalence, odds, and correlates of TUD/ND among people with SMI; randomized controlled trials (RCTs) informing the management of TUD/ND in people with SMI were also included. Random-effects meta-analyses were conducted. Sources of heterogeneity were explored. Nineteen observational studies, including 7527 participants with SMI met inclusion criteria. TUD/ND co-occurred in 33.4–65% of people with SMI. Rates were higher among males. While bupropion and varenicline represent promising treatment opportunities for schizophrenia with TUD/ND, non-pharmacological interventions require further research, mainly for people with primary mood disorders. TUD/ND represent prevalent co-occurring conditions among people with SMI. Further well-designed RCTs are warranted to inform their management.
Context Rapid developments in e-cigarettes, or electronic nicotine delivery systems (ENDS), and the evolution of the overall tobacco product marketplace warrant frequent evaluation of the published ...literature. The purpose of this article is to report updated findings from a comprehensive review of the published scientific literature on ENDS. Evidence acquisition The authors conducted a systematic review of published empirical research literature on ENDS through May 31, 2016, using a detailed search strategy in the PubMed electronic database, expert review, and additional targeted searches. Included studies presented empirical findings and were coded to at least one of nine topics: (1) Product Features; (2) Health Effects; (3) Consumer Perceptions; (4) Patterns of Use; (5) Potential to Induce Dependence; (6) Smoking Cessation; (7) Marketing and Communication; (8) Sales; and (9) Policies; reviews and commentaries were excluded. Data from included studies were extracted by multiple coders (October 2015 to August 2016) into a standardized form and synthesized qualitatively by topic. Evidence synthesis There were 687 articles included in this systematic review. The majority of studies assessed patterns of ENDS use and consumer perceptions of ENDS, followed by studies examining health effects of vaping and product features. Conclusions Studies indicate that ENDS are increasing in use, particularly among current smokers, pose substantially less harm to smokers than cigarettes, are being used to reduce/quit smoking, and are widely available. More longitudinal studies and controlled trials are needed to evaluate the impact of ENDS on population-level tobacco use and determine the health effects of longer-term vaping.
Background: Cigarette smoking is the main cause of preventable death in developed
countries. While the direct positive behavioral reinforcing effect of nicotine has historically been
considered the ...primary mechanism driving the development of TUD, accumulating contemporary
research suggests that the cognitive-enhancing effects of nicotine may also significantly contribute
to the initiation and maintenance of TUD, especially in individuals with pre-existing cognitive
deficits.
Methods: We provide a selective overview of recent advances in understanding nicotine’s effects on
cognitive function, a discussion of the role of cognitive function in vulnerability to TUD, followed
by an overview of the neurobiological mechanisms underlying the cognitive effects of nicotine.
Results: Preclinical models and human studies have demonstrated that nicotine has cognitiveenhancing
effects. Attention, working memory, fine motor skills and episodic memory functions are
particularly sensitive to nicotine's effects. Recent studies have demonstrated that the α4, β2, and α7
subunits of the nicotinic acetylcholine receptor (nAChR) participate in the cognitive-enhancing
effects of nicotine. Imaging studies have been instrumental in identifying brain regions where nicotine
is active, and research on the dynamics of large-scale networks after activation by, or withdrawal
from, nicotine hold promise for improved understanding of the complex actions of nicotine
on human cognition.
Conclusion: Because poor cognitive performance at baseline predicts relapse among smokers who
are attempting to quit smoking, studies examining the potential efficacy of cognitive-enhancement
as strategy for the treatment of TUD may lead to the development of more efficacious interventions.
Acute rupture or erosion of a coronary atheromatous plaque and subsequent coronary artery thrombosis cause the majority of sudden cardiac deaths and myocardial infarctions. Cigarette smoking is a ...major risk factor for acute coronary thrombosis. Indeed, a majority of sudden cardiac deaths attributable to acute thrombosis are in cigarette smokers. Both active and passive cigarette smoke exposure seem to increase the risk of coronary thrombosis and myocardial infarctions. Cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors. This creates an imbalance of antithrombotic/prothrombotic factors and profibrinolytic/antifibrinolytic factors that support the initiation and propagation of thrombosis.
The ratio of 3'hydroxycotinine to cotinine, or nicotine metabolite ratio (NMR), is strongly associated with CYP2A6 genotype, CYP2A6-mediated nicotine and cotinine metabolism, and nicotine clearance. ...Higher NMR (faster nicotine clearance) is associated retrospectively with heavier smoking and lower cessation rates.
NMR as a predictive biomarker of cessation outcomes is being investigated (NCT01314001). In addition to strong CYP2A6 genetic influences on NMR, demographic and hormonal factors alter NMR. Here, we analyzed, for the first time together, these sources of variation on NMR in smokers screened for this clinical trial (N = 1,672).
Participants (mean age = 45.9) were 65.1% Caucasian, 34.9% African American, and 54.8% male. Mean NMR (SD) was higher in Caucasians versus African Americans 0.41 (0.20) vs. 0.33 (0.21); P < 0.001, and in females versus males 0.41 (0.22) vs. 0.37 (0.20); P < 0.001. Among females, birth control pill use (N = 17) and hormone replacement therapy (N = 14) were associated with 19.5% (P = 0.09) and 29.3% (P = 0.06) higher mean NMR, respectively, albeit nonsignificantly. BMI was negatively associated with NMR (Rho = -0.14; P < 0.001), whereas alcohol use (Rho = 0.11; P < 0.001) and cigarette consumption (Rho = 0.12; P < 0.001) were positively associated with NMR. NMR was 16% lower in mentholated cigarette users (P < 0.001). When analyzed together in a linear regression model, these predictors (each ≤2%) accounted for <8% of total NMR variation.
Although these factors significantly affected NMR, they contributed little (together <8%; each ≤2%) to total NMR variation.
Thus, when using NMR, for example, to prospectively guide smoking cessation therapy, these sources of variation are unlikely to cause NMR misclassification.
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