Cited by 93Smoking Behavior and CessationNicotinic Acetylcholine Receptors StudySubstance Abuse Treatment and Outcomes

Developing human laboratory models of smoking lapse behavior for medication screening

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McKee, Sherry A.·2009·Addiction Biology

Abstract

Use of human laboratory analogues of smoking behavior can provide an efficient, cost-effective mechanistic evaluation of a medication signal on smoking behavior, with the result of facilitating translational work in medications development. Although a number of human laboratory models exist to investigate various aspects of smoking behavior and nicotine dependence phenomena, none have yet modeled smoking lapse behavior. The first instance of smoking during a quit attempt (i.e. smoking lapse) is highly predictive of relapse and represents an important target for medications development. Focusing on an abstinence outcome is critical for medication screening as the US Food and Drug Administration approval for cessation medications is contingent on demonstrating effects on smoking abstinence. This paper outlines a three-stage process for the development of a smoking lapse model for the purpose of medication screening. The smoking lapse paradigm models two critical features of lapse behavior: the ability to resist the first cigarette and subsequent ad libitum smoking. Within the context of the model, smokers are first exposed to known precipitants of smoking relapse (e.g. nicotine deprivation, alcohol, stress), and then presented their preferred brand of cigarettes. Their ability to resist smoking is then modeled and once smokers 'give in' and decide to smoke, they participate in a tobacco self-administration session. Ongoing and completed work developing and validating these models for the purpose of medication screening is discussed.

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Crossref · 10.1111/j.1369-1600.2008.00135.x

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  • Prior evidence indicates the interventions can activate mechanistic targets and that these targets relate to clinical outcomes at effect sizes larger than the powered values.

    “Preliminary evidence shows that our interventions have the ability to activate mechanistic targets, and for mechanistic targets to be related to clinical outcomes, at effect sizes beyond these powered values (Ashare et al., 2014; M. W. Otto et al., 2010; McKee, 2009; Patterson et al., 2010; Tang et al., 2013).”

    From A randomized controlled trial protocol for engaging distress tolerance and working memory to aid smoking cessation in low socioeconomic status (SES) adults (2020) · cites this paper as McKee, 2009

    The Introduction reports that nicotine gum and naltrexone altered craving responses to smoking cues, providing limited evidence that interventions can affect a potential mechanistic target. It also says the relationship of those craving effects to actual smoking behavior is unknown. The Summary and Conclusions calls for validation against clinical-response markers; the paper does not establish the claimed target–clinical outcome relationship or compare its effect size with the powered values. Page numbers are unavailable in our copy. (LLM, conf=0.79)

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  • The McKee protocol uses monetary rewards derived from empirical work so that smokers typically delay smoking during a 50-minute assessment, and it measures both resistance to the first cigarette and smoking after giving in.

    “This protocol uses empirically-derived monetary rewards so that smokers, on average, are able to delay smoking for effective assessment during a 50-minute assessment window, and provides measures of two critical features of lapse behavior: (a) the ability to resist the first cigarette and (b) subsequent smoking if a participant decides to “give in” and starts to smoke (McKee, 2009; McKee et al., 2”

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2 of the 88 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Brady KT Sinha R Co-occurring mental and substance use disorders. Am J Psychiatry 2005 162 1483 1493 16055769
  2. Brandon TH Tiffany ST Obremski KM Baker TB Post cessation cigarette use: theprocess of relapse. Addict Behav 1990 15 105 114 2343783

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Authors
McKee, S. A.
Affiliations
Yale University (US)
Corresponding author
McKee, Sherry A.
Venue
Addiction Biology
Publisher
Wiley
Published
2008-12-04
Volume
14
Issue
1
Pages
99-107
ISSN
  • 1355-6215 (ISSN-L)
  • 1369-1600
OpenAlex
W2122948329
Cited by
93
References
88
Citations by year
2026: 3 · 2025: 2 · 2023: 3 · 2022: 4 · 2021: 10 · 2020: 5 · 2019: 8 · 2018: 9 · 2017: 8 · 2016: 3 · 2015: 4 · 2014: 12 · 2013: 6 · 2012: 5
FWCI
0.40
Type
journal article
Language
en
Open access
Locations
  • Addiction Biology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Yale University
  • National Institutes of Health (1ul1rr024925-01)
  • National Institute on Alcohol Abuse and Alcoholism (P50AA015632)
  • National Institute on Drug Abuse (RL1DA024857, R21DA017234, PL1DA024859)
  • National Center for Research Resources (M01RR000125, UL1-RR024925, UL1RR024139)
Topics
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
Keywords
smoking lapse, smoking relapse, smoking cessation medication, drug screening, nicotine dependence, smoking abstinence, nicotine self-administration, nicotine deprivation, alcohol, stress, model validation
MeSH terms
Smoking Prevention, Alcohol Drinking, Arousal, Cues, Drug Evaluation, Preclinical, Humans, Models, Psychological, Motivation, Naltrexone, Nicotine, Psychotropic Drugs, Smoking, Social Environment, Social Facilitation, Tobacco Use Disorder, Smoking Cessation, Bupropion, Secondary Prevention

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