Addiction Rehab: A Systematic Review of the Relationships Between Craving and Smoking Cessation.

A Systematic Review of the Relationships Between Craving and Smoking Cessation.

Filed under: Addiction Rehab

Nicotine Tob Res. 2013 Jan 4;
Wray JM, Gass JC, Tiffany ST

INTRODUCTION: Craving is often portrayed as a defining feature of addiction, but the role of craving in the addictive process is controversial. Particularly contentious is the extent to which drug craving predicts subsequent relapse. METHODS: This review synthesizes findings from 62 smoking cessation studies published through December 2011. Eligible studies measured craving for cigarettes in treatment-seeking smokers and related this to subsequent smoking status. The relationships of general craving and cue-specific craving with treatment outcome were examined separately. Further, analyses that related general craving to smoking status were divided into those that used craving data collected before the quit attempt, after the quit attempt, and those that used change in craving over time as a predictor. RESULTS: Results across studies revealed a total of 198 indices of association with 94 (47%) of these being significant. In general, the findings indicated (a) there were only a few cases of significant associations between craving collected as part of cue-reactivity studies and treatment outcome, (b) postquit craving was a stronger predictor of treatment outcome than prequit craving, and (c) several moderators likely influence the relationship between craving and cessation outcome. CONCLUSIONS: The overall results suggest that craving is not a necessary condition of relapse. In addition, inconsistent relationships between craving and treatment outcome call into question the value of craving as a target of treatment and underscore limitations in the prognostic utility of craving.
HubMed – addiction

 

Socioeconomic, demographic and smoking-related correlates of the use of potentially reduced exposure to tobacco products in a national sample.

Filed under: Addiction Rehab

Tob Control. 2013 Jan 4;
Shaikh RA, Siahpush M, Singh GK

BACKGROUND AND AIM: In recent years, new non-traditional, potentially reduced exposure products (PREPs), claiming to contain fewer harmful chemicals than the traditional products, have been introduced in the market. Little is known about socioeconomic, demographic and smoking-related determinants of the likelihood of using these products among smokers. The aim of this study was to examine these determinants. METHODS: Data from the 2006-2007 Tobacco Use Supplement to the Current Population Survey was used. We limited the analysis to current smokers (n=40 724). Multivariate logistic regression analyses were conducted to estimate the association between covariates and the probability of the use of PREPs. RESULTS: We found that younger age, lower education, higher nicotine addiction and having an intention to quit are associated with higher likelihood of the use of PREPs. The likelihood of using these products was found to be higher among respondents who are unemployed or have a service, production, sales or farming occupation than those with a professional occupation. Smokers living in the midwest, south or west, were found to have a greater likelihood of the use of PREPs than those living in the northeast. CONCLUSIONS: Because there is little evidence to suggest that PREPs are less harmful that other tobacco products, their marketing as harm-minimising products should be regulated. Smokers, in particular those who are younger, have a lower socioeconomic status, and are more nicotine-dependent, should be the target of educational programmes that reveal the actual harm of PREPs.
HubMed – addiction

 

Susceptibility to ethanol sensitization is differentially associated with changes in pCREB, trkB and BDNF mRNA expression in the mouse brain.

Filed under: Addiction Rehab

Behav Brain Res. 2013 Jan 2;
Nona CN, Guirguis S, Nobrega JN

Repeated exposure to ethanol in mice induces behavioural sensitization, a progressive increase in locomotor activity that is common to drugs of abuse. Not all mice however show sensitization to ethanol. The goal of the present study was to examine whether variability in the sensitization response to ethanol (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely BDNF and its receptor trkB, and levels of phosphorylated cyclic AMP-regulated element-binding protein (pCREB), 14 days after withdrawal from chronic, intermittent EtOH exposure. Male DBA/2NCrl mice received 7 biweekly EtOH (2.2g/kg, i.p.) or saline (SAL) injections and were classified as Sensitized or Non-sensitized on the basis of final locomotor activity (LMA) scores. Brains were removed two weeks later for immunohistochemical and in situ hybridization analyses. Compared to SAL-treated and Non-sensitized mice, Sensitized animals showed a higher number of pCREB-immunoreactive cells in the nucleus accumbens shell (+68% and +50%, respectively) and in the bed nucleus of the stria terminalis (+ 61% and 46%, respectively), whereas SAL and Non-sensitized groups did not differ from each other. A different pattern was seen when BDNF and trkB mRNA levels were analyzed in the same groups. Non-sensitized mice displayed lower BDNF mRNA in several brain areas and significantly lower trkB levels throughout the brain when compared to either the Sensitized or to SAL groups, which did not differ from each other. These results indicate that sensitization to EtOH is differentially associated with increased pCREB levels in specific brain areas. The observed decrease in BDNF and trkB mRNA in the Non-sensitized group suggests the possibility that EtOH may have neurotoxic effects in a subpopulation of mice, which might in turn prevent the development of behavioural sensitization. The lack of a difference in BDNF and trkB mRNA expression between Sensitized and SAL mice suggests that EtOH sensitization may be mediated by mechanisms different from those mediating sensitization to other psychostimulants.
HubMed – addiction

 

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