Alcoholism, clinical and experimental research
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Alcohol. Clin. Exp. Res. · Jun 2007
College attendance and its effect on drinking behaviors in a longitudinal study of adolescents.
While college attendance has been shown to be associated with increased drinking behaviors, there are no studies to our knowledge that have examined whether college attendance moderates genetic influences for drinking. We first tested for changes in alcohol consumption in adolescents who did and did not subsequently attend college, and then tested for variation of the genetic and environmental determinants of drinking in these 2 groups. ⋯ Exposure to a college environment acts as an environmental moderator, supporting the hypothesis that the magnitude of genetic influence on certain aspects of alcohol consumption is greater in environments where drinking behaviors are more likely to be promoted.
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Alcohol. Clin. Exp. Res. · May 2007
Randomized Controlled TrialA pilot double-blind treatment trial of memantine for alcohol dependence.
There is growing evidence that N-methyl-d-aspartate (NMDA) receptor antagonists may have potential for the treatment of alcohol disorders. Memantine is a selective noncompetitive NMDA receptor antagonist that has been shown to decrease alcohol craving in moderate drinkers. This 16-week double-blind outpatient pilot clinical trial determined if memantine was more effective than placebo at reducing alcohol use in actively drinking alcohol-dependent patients. ⋯ The results of this double-blind placebo-controlled pilot trial do not support the use of memantine for the treatment of actively drinking alcohol-dependent patients. However, voucher incentives did facilitate retention.
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Alcohol. Clin. Exp. Res. · Apr 2007
Randomized Controlled TrialOpioid receptor gene (OPRM1, OPRK1, and OPRD1) variants and response to naltrexone treatment for alcohol dependence: results from the VA Cooperative Study.
Pharmacotherapy of alcohol dependence (AD) is at an early stage of development; currently available medications have limited efficacy. It would be clinically valuable to identify, before initiation of a course of treatment, those patients who, based on genetic markers, are most likely to respond to a specific pharmacotherapy. A previous report suggested that a functional variant at the genetic locus encoding the mu opioid receptor (Asn40Asp) is such a marker, in short-term (3-month) treatment with the opioid-blocking drug naltrexone (NTX). ⋯ These results do not support association of the OPRM1 Asn40Asp polymorphism with NTX treatment response for AD.
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Alcohol. Clin. Exp. Res. · Apr 2007
Randomized Controlled TrialMultidimensionality of the Alcohol Withdrawal Symptom Checklist: a factor analysis of the Alcohol Withdrawal Symptom Checklist and CIWA-Ar.
This study evaluated the factor structure of 2 scales for measuring the severity of the alcohol withdrawal syndrome (AWS): a self-rated scale, the Alcohol Withdrawal Symptoms Checklist (AWSC), and an observer-rated scale, the Clinical Institute Withdrawal Assessment-Alcohol, Revised (CIWA-Ar). ⋯ Self-rated measures of AWS could play an important role in complementing observer-rated measures in clinical and research settings. In this sample, the AWSC appeared to identify multiple dimensions of AWS with face validity for clinical relevance.
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Alcohol. Clin. Exp. Res. · Apr 2007
Alcohol binge before trauma/hemorrhage impairs integrity of host defense mechanisms during recovery.
Alcohol abuse, both chronic and acute, is a known modulator of immune function and is associated with increased incidence of traumatic injury. Previously, we demonstrated that acute alcohol intoxication before hemorrhagic shock impairs hemodynamic and neuroendocrine counterregulation, suppresses early lung proinflammatory cytokine expression, and increases mortality from infection during recovery. In the present study, we examined the impact of a 3-day alcohol binge on host responses during trauma/hemorrhage (T x Hem) and following overnight recovery. ⋯ These results indicate that a 3-day alcohol binge results in hemodynamic instability associated with attenuated neuroendocrine activation and increased mortality during T x Hem as well as sustained suppression of the proinflammatory cytokine response of blood and pleural-derived cells to a "second-hit" inflammatory challenge. As a result, we speculate that the net shift toward an anti-inflammatory state may contribute to enhanced susceptibility to infection during the recovery period.