Alcoholism, clinical and experimental research
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Alcohol. Clin. Exp. Res. · Feb 2010
Randomized Controlled TrialBrief motivational interviewing for DWI recidivists who abuse alcohol and are not participating in DWI intervention: a randomized controlled trial.
Driving while impaired (DWI) recidivists with unresolved alcohol use problems pose an ongoing risk for traffic safety. Following conviction, many do not participate in mandated alcohol evaluation and intervention programs, or continue to drink problematically after being relicensed. This study investigated if, in DWI recidivists with alcohol problems and not currently involved in DWI intervention, Brief Motivational Interviewing (BMI) produced greater reductions in risky drinking at 6- and 12-month follow-up compared to an information-advice control condition. Additional analyses explored whether BMI was associated with greater readiness to change, subsequent substance abuse treatment service utilization, and satisfaction compared to the control condition. ⋯ Brief MI approaches warrant further implementation and effectiveness research as an opportunistic DWI intervention strategy to reduce risks associated with alcohol use outside of clinical and DWI relicensing settings.
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Alcohol. Clin. Exp. Res. · Feb 2010
Opioids in the hypothalamic paraventricular nucleus stimulate ethanol intake.
Specialized hypothalamic systems that increase food intake might also increase ethanol intake. To test this possibility, morphine and receptor-specific opioid agonists were microinjected in the paraventricular nucleus (PVN) of rats that had learned to drink ethanol. To cross-validate the results, naloxone methiodide (m-naloxone), an opioid antagonist, was microinjected with the expectation that it would have the opposite effect of morphine and the specific opioid agonists. ⋯ The delta-opioid receptor agonist in the PVN increased ethanol intake in strong preference over food and water, while the kappa-opioid agonist suppressed ethanol intake. Prior studies show that learning to drink ethanol stimulates PVN expression and production of the peptides enkephalin and dynorphin, which are endogenous agonists for the delta- and kappa-receptors, respectively. These results suggest that enkephalin via the delta-opioid system can function locally within a positive feedback circuit to cause ethanol intake to escalate and ultimately contribute to the abuse of ethanol. This is in contrast to dynorphin via the kappa-opioid system, which may act to counter this escalation. Naltrexone therapy for alcoholism may act, in part, by blocking the enkephalin-triggered positive feedback cycle.