Confirmatory factor analyses and reliability of the modified cigarette evaluation questionnaire

Cappelleri, Joseph C.; Bushmakin, Andrew G.; Baker, Christine L.; Merikle, Elizabeth; Olufade, Abayomi O.; Gilbert, David G.

doi:10.1016/j.addbeh.2006.06.028

Cited by 213 publications

(167 citation statements)

References 6 publications

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“…Participants were prompted once daily to complete a short assessment at random times between 8 AM and 10 PM. Assessment items included daily Subjective State Scale 24,25 for measurement of positive and negative affect, weekly Edinburgh Postnatal Depression Scale 26,27 for assessment of depressive symptoms, and in the event of a smoking "slip," the modified Cigarette Evaluation Questionnaire 28 measuring the degree to which subjects experienced the reinforcing effects of smoking (results of the Subjective State Scale and modified Cigarette Evaluation Questionnaire analyses are forthcoming). Weekly phone calls were made to troubleshoot issues, further collect data regarding smoking status and offer brief relapse prevention counseling.…”

Section: Methodsmentioning

confidence: 99%

Progesterone and Postpartum Smoking Relapse: A Pilot Double-Blind Placebo-Controlled Randomized Trial

Allen

Lunos

et al. 2016

NICTOB

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Introduction: Pregnancy is a strong motivator to quit smoking, yet postpartum relapse rates are high. Growing evidence suggests a role of sex hormones in drug abuse behavior and given the precipitous drop in sex hormones at delivery, they may play a role in postpartum relapse. This pilot study evaluates the feasibility and potential role of exogenous progesterone in postpartum smoking relapse. Methods: This 12-week double-blind placebo-controlled randomized pilot trial randomized 46 abstinent postpartum women to active progesterone (PRO; 200 mg twice a day) versus placebo (PBO) for 4 weeks. Participants were followed for relapse for 12 weeks. Main study outcomes include abstinence (point prevalence), feasibility (compliance per number of clinic visits attended, pill counts and Electronic Data Capture [EDC] completed) and self-reported acceptability. Safety was also measured by depressive symptom scores, adverse events, and breastfeeding. Results: Overall retention rate was 87% at week 12. At week 4, abstinence rates were 75% in the PRO group and 68.2% in the PBO group (p = .75). Medication adherence was 68% and clinic visit attendance was 80%, with no differences by randomization. Depressive symptom scores, adverse events, and breastfeeding did not vary by randomization. Conclusions: Although the study was not powered to evaluate abstinence rates, we did observe a higher prevalence of abstinence at week 4 in the PRO group. Further, exogenous progesterone was well tolerated and did not adversely affect depressive symptoms or breastfeeding. Thus, the results of this pilot study indicate further investigation into progesterone as a postpartum relapse prevention strategy is warranted. Implications: This innovative pilot trial determined the feasibility of delivering exogenous progesterone as a potential prevention of postpartum smoking relapse. We observed high retention and moderate adherence rates, as well as high acceptability among participants. Further, though not statistically significant, more women in the treatment group remained abstinent from smoking during follow-up. This project adds to the growing body of literature on the role of sex hormones in smoking relapse and also provides support for a fully powered clinical trial.

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Section: Methodsmentioning

confidence: 99%

Progesterone and Postpartum Smoking Relapse: A Pilot Double-Blind Placebo-Controlled Randomized Trial

Allen

Lunos

et al. 2016

NICTOB

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“…The breath expired CO level change from pre-to postcigarette was 4.95 (SD = 1.73) after the nicotine cigarette and 3.27 (SD = 1.42) after the denicotinized cigarette (T = −4.71, P = 1 × 10 −4 ). After smoking, participants completed a questionnaire to evaluate the smoking reward they experienced from the cigarette (44). Female participants were scanned during their early follicular phase (2-9 d after menses) to minimize the effects of rising levels of es-trogen on the endogenous opioid system (45).…”

Section: Methodsmentioning

confidence: 99%

Human Mu Opioid Receptor ( OPRM1 A118G) polymorphism is associated with brain mu-opioid receptor binding potential in smokers

Ray

Ruparel²,

Newberg³

et al. 2011

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

133

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Evidence points to the endogenous opioid system, and the muopioid receptor (MOR) in particular, in mediating the rewarding effects of drugs of abuse, including nicotine. A single nucleotide polymorphism (SNP) in the human MOR gene (OPRM1 A118G) has been shown to alter receptor protein level in preclinical models and smoking behavior in humans. To clarify the underlying mechanisms for these associations, we conducted an in vivo investigation of the effects of OPRM1 A118G genotype on MOR binding potential (BP ND or receptor availability). Twenty-two smokers prescreened for genotype (12 A/A, 10 */G) completed two [ 11 C]carfentanil positron emission tomography (PET) imaging sessions following overnight abstinence and exposure to a nicotine-containing cigarette and a denicotinized cigarette. Independent of session, smokers homozygous for the wild-type OPRM1 A allele exhibited significantly higher levels of MOR BP ND than smokers carrying the G allele in bilateral amygdala, left thalamus, and left anterior cingulate cortex. Among G allele carriers, the extent of subjective reward difference (denicotinized versus nicotine cigarette) was associated significantly with MOR BP ND difference in right amygdala, caudate, anterior cingulate cortex, and thalamus. Future translational investigations can elucidate the role of MORs in nicotine addiction, which may lead to development of novel therapeutics.genetics | neuroimaging | tobacco W ith 1 billion tobacco users worldwide, nicotine dependence has a major impact on global health. Advances in medication development for nicotine dependence require an improved understanding of the neurobiology of this complex, relapsing brain disorder (1). Although multiple neurobiological mechanisms have been implicated, a growing body of evidence points to the endogenous opioid system, and the mu-opioid receptor (MOR) in particular, in mediating the reinforcing effects of drugs of abuse, including nicotine (2-5). Nicotine upregulates MOR mRNA and protein expression in brain regions important in drug reward in rodents (4, 6) and stimulates endogenous opioid release (7,8), resulting in MOR activation and dopamine release (9).Genetic variation in MORs can modulate the endogenous opioid system, thereby altering behavior. A common single nucleotide polymorphism (SNP) in the mu-opioid receptor gene (OPRM1 A118G) results in an amino acid exchange at a putative glycosylation site in the extracellular terminus of the MOR (10). This OPRM1 SNP has been associated with a variety of drug dependence phenotypes in rodent and human studies (11), including nicotine reward, nicotine withdrawal severity, and smoking relapse (12)(13)(14).Despite substantial attention to the OPRM1 A118G in drug addiction research, the precise function of this SNP has yet to be clarified. Although the minor (G) allele was originally thought to be a "gain-of-function" variant, on the basis of increased affinity of MOR agonists (15), other data suggest that the G allele is associated with reduced mRNA and protein expression (16,17)....

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“…[4][5][6] Because of its dual agonistantagonist properties, varenicline offers the potential therapeutic benefit of simultaneously relieving symptoms of nicotine withdrawal and cigarette craving during abstinence, while attenuating the reinforcing effects of nicotine and psychological reward associated with smoking. 4,7 Clinical evidence from self-report data have indeed indicated that, unlike other cessation medications, abstinence increased over the first weeks of varenicline use; this suggests that smoking whilst on varenicline is gradually less rewarding, thereby helping to initiate abstinence and perhaps setting the stage for a more stable quit. [8][9][10] Similar findings have been reported from laboratory investigations with varenicline when self-reporting smoking reward was assessed immediately after smoking.…”

Section: Introductionmentioning

confidence: 99%

Pharmacokinetic-Pharmacodynamic Modeling of the Effect of Varenicline on Nicotine Craving in Adult Smokers

Ravva

Gastonguay

Faessel

et al. 2014

Nicotine &Amp; Tobacco Research

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Introduction: Varenicline has been shown to significantly reduce craving and several aspects of smoking reinforcement in clinical trials, compared with placebo. This is the first report describing the concentration-effect relationship of varenicline on relief of craving. Methods: The pharmacokinetics (PK) and pharmacodynamics (PD) of a single 2 mg dose of varenicline were investigated in 40 smokers in a randomized, crossover study comparing the effect of varenicline with placebo on ameliorating abstinence-and cue-induced craving and withdrawal symptoms. Subjects were asked to complete self-reported questionnaires (Smoking Urges Scale and Minnesota Nicotine Withdrawal Scale [MNWS]) and blood samples were simultaneously collected for measurement of varenicline concentrations. Only the data from the 4-hr postdose abstinence period (just prior to the cue session) were analyzed. Data were described by a 2-compartment PK model and a linear PD model with first-order onset/offset rate constants describing the placebo response "kinetics. " Response was described as the net effect of the baseline, placebo, and drug responses. Results: Varenicline significantly decreased mean craving score when compared with placebo and the magnitude of this response was related to varenicline concentration. The time-course and magnitude of both placebo and varenicline craving response were characterized by a large degree of unexplained variability. Simulations were used to illustrate the expected craving response over time and its associated random variability after chronic dosing. Conclusions: Craving reduction is associated with increased varenicline concentrations. The relatively rapid onset of this effect within 4 hr postdose suggests that, smokers may experience some craving relief after acute administration of varenicline.

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Confirmatory factor analyses and reliability of the modified cigarette evaluation questionnaire

Cited by 213 publications

References 6 publications

Progesterone and Postpartum Smoking Relapse: A Pilot Double-Blind Placebo-Controlled Randomized Trial

Progesterone and Postpartum Smoking Relapse: A Pilot Double-Blind Placebo-Controlled Randomized Trial

Human Mu Opioid Receptor ( OPRM1 A118G) polymorphism is associated with brain mu-opioid receptor binding potential in smokers

Pharmacokinetic-Pharmacodynamic Modeling of the Effect of Varenicline on Nicotine Craving in Adult Smokers

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