Dataset Information

Sleep as a Target for Optimized Response to Smoking Cessation Treatment.

ABSTRACT: Declining national rates of current tobacco use to an all-time low of 15.1% represents a public health victory. Undermining this progress, however, are smoking rates of up to 50% among high-risk, low-income populations. Current FDA-approved treatments for nicotine dependence are ineffective with between 70-95% of treatment-seekers relapsing within the first year of attempted abstinence. Thus, identification of novel intervention targets to optimize response to currently available treatments for nicotine dependence is a critical next step. One such target may be sleep insomnia. Insomnia is a clinically verified nicotine withdrawal symptom but, to date, addressing insomnia or other sleep disturbance symptoms as an adjunctive smoking cessation therapy has yet to be fully considered. To this end, this manuscript presents a narrative review of: (1) sleep continuity and architecture in smokers versus nonsmokers; (2) effects of nicotine abstinence on sleep; (3) possible mechanisms linking sleep with smoking cessation outcomes; (4) plausible adjunctive sleep therapies to promote smoking cessation; (5) possible treatments for unhealthy sleep in smokers; and (6) directions for future research. Taken together, this will provide conceptual support for sleep therapy as an adjunctive treatment for smoking cessation.

Implications

This narrative literature review presents a comprehensive discussion of the relationship between habitual sleep and cigarette smoking. The extent to which unhealthy sleep in smokers may be a viable intervention target for promoting response to smoking cessation treatment is considered. Ultimately, this review provides conceptual support for sleep therapy as an adjunctive treatment for smoking cessation.

SUBMITTER: Patterson F

PROVIDER: S-EPMC6329404 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Sleep as a Target for Optimized Response to Smoking Cessation Treatment.

Patterson Freda F Grandner Michael A MA Malone Susan K SK Rizzo Albert A Davey Adam A Edwards David G DG

Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco 20190101 2

Declining national rates of current tobacco use to an all-time low of 15.1% represents a public health victory. Undermining this progress, however, are smoking rates of up to 50% among high-risk, low-income populations. Current FDA-approved treatments for nicotine dependence are ineffective with between 70-95% of treatment-seekers relapsing within the first year of attempted abstinence. Thus, identification of novel intervention targets to optimize response to currently available treatments for ...[more]

PMID: 29069464

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Project description:ImportanceCigarette smoking leads to upregulation of nicotinic acetylcholine receptors (nAChRs) in the human brain, including the common α4β2* nAChR subtype. While subjective aspects of tobacco dependence have been extensively examined as predictors of quitting smoking with treatment, no studies to our knowledge have yet reported the relationship between the extent of pretreatment upregulation of nAChRs and smoking cessation.ObjectiveTo determine whether the degree of nAChR upregulation in smokers predicts quitting with a standard course of treatment.Design, setting, and participantsEighty-one tobacco-dependent cigarette smokers (volunteer sample) underwent positron emission tomographic (PET) scanning of the brain with the radiotracer 2-FA followed by 10 weeks of double-blind, placebo-controlled treatment with nicotine patch (random assignment). Pretreatment specific binding volume of distribution (VS/fP) on PET images (a value that is proportional to α4β2* nAChR availability) was determined for 8 brain regions of interest, and participant-reported ratings of nicotine dependence, craving, and self-efficacy were collected. Relationships between these pretreatment measures, treatment type, and outcome were then determined. The study took place at academic PET and clinical research centers.Main outcomes and measuresPosttreatment quit status after treatment, defined as a participant report of 7 or more days of continuous abstinence and an exhaled carbon monoxide level of 3 ppm or less.ResultsSmokers with lower pretreatment VS/fP values (a potential marker of less severe nAChR upregulation) across all brain regions studied were more likely to quit smoking (multivariate analysis of covariance, F8,69 = 4.5; P < .001), regardless of treatment group assignment. Furthermore, pretreatment average VS/fP values provided additional predictive power for likelihood of quitting beyond the self-report measures (stepwise binary logistic regression, likelihood ratio χ21 = 19.8; P < .001).Conclusions and relevanceSmokers with less upregulation of available α4β2* nAChRs have a greater likelihood of quitting with treatment than smokers with more upregulation. In addition, the biological marker studied here provided additional predictive power beyond subjectively rated measures known to be associated with smoking cessation outcome. While the costly, time-consuming PET procedure used here is not likely to be used clinically, simpler methods for examining α4β2* nAChR upregulation could be tested and applied in the future to help determine which smokers need more intensive and/or lengthier treatment.Trial registrationclinicaltrials.gov Identifier: NCT01526005.

Dataset Information

Sleep as a Target for Optimized Response to Smoking Cessation Treatment.

Implications

Publications

Sleep as a Target for Optimized Response to Smoking Cessation Treatment.

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