Journal of addiction & prevention最新文献

Background: The military has stringent anti-tobacco regulations for new recruits. While most tobacco products have declined in recent years, e-cigarette use has tripled among this population. However, little is known about the factors facilitating this inverse relationship.

Objectives: Examine the facilitators of e-cigarette use during a high risk period following initial enlistment among young adults.

Methods: Focus groups were conducted with Airmen, Military Training Leaders (MTLs) and Technical Training Instructors (TTIs) to qualitatively explore unique characteristics of e-cigarettes leading to use in Technical Training.

Results: The most commonly used tobacco product across participants was cigarettes (42.7%), followed by e-cigarettes (28.0%) and smokeless tobacco (22.6%). Almost a third (28.7%) of participants reported using more than one tobacco product. E-cigarette use was much more common among Airmen (76.1%), compared to MTLs (10.9%) and TTIs (13.0%).Four main facilitators around e-cigarette use were identified including: 1) There is no reason not to use e-cigarettes; 2) Using e-cigarettes helps with emotion management; 3) Vaping is a way of fitting in; and 4) Existing tobacco control policies don't work for vaping. E-cigarettes were not perceived as harmful to self and others, which could explain why Airmen were much less likely to adhere to existing tobacco control regulations. Subversion was viewed as the healthy option compared to utilizing designated tobacco use areas due to the potential exposure to traditional tobacco smoke. This coupled with a lack of understanding about e-cigarette regulations and difficulties with enforcement, promoted use among this young adult population.

Conclusion: Findings suggest that e-cigarettes are used for similar reasons as traditional tobacco products, but their unique ability to be concealed promotes their widespread use and circumvents existing tobacco control policies. In order to see reductions in use, environmental policies may need to be paired with behavioral interventions at the personal and interpersonal level.

Cocaine use disorder is characterized not only by the high rate of relapse, but also by deficits in cognition and prefrontal cortical function. Still, the relationship between cognitive impairment and cocaine-seeking remains poorly understood. The current study used a rodent model to determine the effects of extended access cocaine self-administration on cognitive performance in a prefrontal cortex-dependent delayed match-to-sample/non-match-to-sample (DMS/DNMS) task. Further, this study sought to investigate how post-cocaine changes in cognitive performance correlate with cue/context-induced cocaine-seeking following a prolonged period of abstinence. Animals were trained to self-administer cocaine during 6 daily 1 hour-long sessions followed by 12 days of extended, 6 hour-long access. The extended access cocaine rats exhibited robust self-administration behavior and escalation of cocaine intake. Next, DMS/DNMS task was used to evaluate working memory capacity and reversal learning performance over a range of 0 - 30 s delays. Although this study failed to detect a major cognitive impairment, extended access to cocaine resulted in the persistent working memory/DMS deficit at a moderate cognitive load (10 s delay). There were no changes in the reversal learning/DNMS performance. It is likely that the parameters of the DMS/DNMS task, as used in the current study, exceeded acquisition capacity of rats thus obscuring cocaine effects at longer delays. Finally, rats showed a robust relapse of context/cue-elicited cocaine-seeking following the 45 - day abstinence. However, the intensity of cocaine-seeking did not correlate with the deficit in the DMS task. In conclusion, future studies must re-evaluate whether a more robust relationship between post-cocaine cognitive performance and cocaine-seeking can be detected under adjusted DMS/DNMS conditions.

Latinos are exposed to adverse psychosocial factors that impact their health outcomes. Given the heterogeneity and rapid growth of this population, there is an urgent need to understand the mechanisms through which psychosocial factors impact substance abuse and anxiety between immigrant and U.S. born Latino adults. The present study employs a multi-group path analysis using Mplus 7.2 to examine generational differences in the paths between affiliation culture, years of formal education, contact with important people, and length of full-time employment to substance abuse and anxiety in immigrant and U.S. born Latino adults who completed substance abuse treatment. A total of 131 participants (Mage= 36.3, SD ± 10.5, 86.3% males, 48.1% non-U.S. born with a mean length of stay of 19 years in the U.S. (SD ± 13.71) in recovery from substance abuse completed self-report measures. Results from the multi-group path analysis suggest that being more affiliated to the U.S. culture is associated with substance abuse, whereas years of formal education and longer full-time employment is associated with reduced anxiety in the immigrant group. Conversely, frequent contact with important people and affiliation to the U.S. culture are associated with fewer years of substance abuse, whereas longer full-time employment is associated with substance abuse in the U.S. born group. Anxiety and substance abuse was correlated only in the U.S. born group. The implications of these findings are discussed.

Objective: The Post - Traumatic Stress Disorder (PTSD) factor structure is not a generally agreed upon concept. It has remained controversial and its' efficacy regarding different trauma presentations is still in question. Therefore, it is imperative that we evaluate different conceptualizations of the PTSD factor structure. This study aims to understand how PTSD is structured when comorbid with Substance Use Disorder (SUD).

Method: We evaluated presentations of PTSD - SUD from a Latino community based sample. This was done using several accepted models of the PTSD factor structure. We then performed an exploratory factor analysis of the factor structure of PTSD when comorbid with SUD.

Results: We found that the factor structure of PTSD - SUD was different from the structure presented in the DSM - IV and other empirically validated structural models.

Conclusion: The factor structure of PTSD may need to include a separate structure when PTSD is comorbid with SUD. Cultural differences when structuring the PTSD diagnosis should also be considered.

Objective: Alcohol-impaired driving persists as a major cause of traffic fatalities and injuries among young drivers. This meta-analysis examined whether brief alcohol interventions were effective in reducing driving after drinking among adolescents and young adults.

Method: Our systematic search identified 12 experimental/quasi-experimental evaluations (16 intervention groups) that measured driving while intoxicated and related consequences and provided data for effect size calculation (N = 5,664; M age =17 years; 57% male). The studies were published between 1991 and 2011. Three-level random-effects meta-analyses using a structural equation modeling approach were used to summarize the effects of the interventions.

Results: Compared with controls, participants in brief alcohol interventions reported reduced drinking and driving and related consequences (ḡ = 0.15, 95% CI [0.08, 0.21]). Supplemental analyses indicated that reductions in driving while intoxicated were positively associated with the reduced post-intervention heavy use of alcohol. These findings were not attenuated by study design or implementation factors.

Conclusions: Brief alcohol interventions under 5 hours of contact may constitute a promising preventive approach targeting drinking and driving among adolescents and young adults. Reducing heavy episodic alcohol consumption appeared to be a major factor in reducing drunk-driving instances. Interpretation of the findings must be made with caution, however, given the possibility of publication bias and the small observed effect size. Future research should focus on the exact mechanisms of behavior change leading to beneficial outcomes of brief alcohol interventions and the potential effectiveness of combined brief interventions and other preventive approaches.

Amphetamine (AMPH) is a psychostimulant and the most prescribed drug to treat attention deficit hyperactive disorder (ADHD). Although therapeutically used doses are generally well tolerated, numerous side effects are still known to occur, such as jitteriness, loss of appetite and psychosis. Moreover, AMPH is liable to be abused by users looking for increased alertness, weight loss or athletic performance. A growing body of evidence indicates that drugs of abuse, including AMPH, control gene expression through chromatin modifications. However, while numerous studies have investigated the molecular mechanisms of AMPH action, only a small number of studies have explored changes in gene expression caused by AMPH. This review examines the epigenetic changes induced by chronic and acute treatments with AMPH and includes, where relevant, data obtained with other psychostimulants such as methamphetamine and cocaine.

Methamphetamine is the second most widely used illicit drug worldwide. More than 290 tons of methamphetamine was synthesized in the year 2005 alone, corresponding to approximately ~3 billion 100 mg doses of methamphetamine. Drug addicts abuse high concentrations of methamphetamine for months and even years. Current reports in the literature are consistent with the interpretation that methamphetamine-induced neuronal injury may render methamphetamine users more susceptible to neurodegenerative pathologies. Specifically, chronic exposure to psychostimulants is associated with increases in striatal alpha-synuclein expression, a synaptic protein implicated in the pathogenesis of neurodegenerative diseases. This raises the question whether methamphetamine exposure affects alpha-synuclein levels in the brain. In this short report, we examined alpha-synuclein protein and mRNA levels in the striatum, hippocampus and cortex of adolescent male mice following a neurotoxic regimen of methamphetamine (24mg/kg/daily/14days). We found that methamphetamine exposure resulted in a decrease in the monomeric form of alpha-synuclein (molecular species <19 kDa), while increasing higher molecular weight alpha-synuclein species (>19 kDa) in the striatum and hippocampus, but not in the cortex. Despite the elevation of high molecular weight alpha-synuclein species (>19 kDa), there was no change in the alpha-synuclein mRNA levels in the striatum, hippocampus and cortex of mice exposed to methamphetamine. The methamphetamine-induced increase in high molecular weight alpha-synuclein protein levels might be one of the causal mechanisms or one of the compensatory consequences of methamphetamine-mediated neurotoxicity.