Alcoholism, clinical and experimental research
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Alcohol. Clin. Exp. Res. · Jul 2010
Comparative StudyPolymorphisms of alcohol dehydrogenase-1B and aldehyde dehydrogenase-2 and the blood and salivary ethanol and acetaldehyde concentrations of Japanese alcoholic men.
The effects of genetic polymorphism of aldehyde dehydrogenase-2 (ALDH2) on alcohol metabolism are striking in nonalcoholics, and the effects of genetic polymorphism of alcohol dehydrogenase-1B (ADH1B) are modest at most, whereas genetic polymorphisms of both strongly affect the susceptibility to alcoholism and upper aerodigestive tract (UADT) cancer of drinkers. ⋯ The ADH1B/ALDH2 genotype affected the blood and salivary ethanol and acetaldehyde levels of nonabstinent alcoholics in a different manner from nonalcoholics, and clear effects of ADH1B genotype and less clear effects of ALDH2 were observed in the alcoholics. Alterations in alcohol metabolism as a result of alcoholism may modify the gene effects, and these findings provide some clues in regard to associations between the genotypes and the risks of alcoholism and UADT cancer.
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Alcohol. Clin. Exp. Res. · Jul 2010
Randomized Controlled Trial Comparative StudyPhysical health and drinking among medical inpatients with unhealthy alcohol use: a prospective study.
Unhealthy alcohol use is common in medical inpatients, and hospitalization has been hypothesized to serve as a "teachable moment" that could motivate patients to decrease drinking, but studies of hospital-based brief interventions have often not found decreases. Evaluating associations between physical health and subsequent drinking among medical inpatients with unhealthy alcohol use could inform refinement of hospital-based brief interventions by identifying an important foundation on which to build them. We tested associations between poor physical health and drinking after hospitalization and whether associations varied by alcohol dependence status and readiness to change. ⋯ Among medical inpatients with nondependent unhealthy alcohol use and those who do not view their drinking as problematic, alcohol-attributable illness may catalyze decreased drinking. Brief interventions that highlight alcohol-related illness might be more successful.
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Alcohol. Clin. Exp. Res. · Jul 2010
Comparative StudyChronic ethanol disrupts circadian photic entrainment and daily locomotor activity in the mouse.
Chronic ethanol abuse is associated with disrupted circadian rhythms and sleep. Ethanol administration impairs circadian clock phase-resetting, suggesting a mode for the disruptive effect of alcohol abuse on circadian timing. Here, we extend previous studies to explore the effects of chronic forced ethanol on photic phase-resetting, photic entrainment, and daily locomotor activity patterns in C57BL/6J mice. ⋯ These results confirm that chronic ethanol consumption and withdrawal markedly impair circadian clock photic phase-resetting. Ethanol also disturbs the temporal structure of nighttime locomotor activity and photic entrainment. Collectively, these results suggest a direct action of ethanol on the SCN clock.