44 resultados para Alcohol-dependence

em University of Queensland eSpace - Australia


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There is no specific self-efficacy measure that has been developed primarily for problem drinkers seeking a moderation drinking goal. In this article, we report the factor structure of a 20-item Controlled Drinking Self-Efficacy Scale (CDSES Sitharthan et al., 1996; Sitharthan et al., 1997). The results indicate that the CDSES is highly reliable, and the factor analysis using the full sample identified four factors: negative affect, positive mood/social context, frequency of drinking, and consumption quantity. A similar factor structure was obtained for the subsample of men. In contrast, only three factors emerged in the analysis of data on female participants. Compared to women, men had low self-efficacy to control their drinking in situations relating to positive mood/social context, and subjects with high alcohol dependence had low self-efficacy for situations relating to negative affect, social situations, and drinking less frequently. The CDSES can be a useful measure in treatment programs providing a moderation drinking goal. (C) 2003 Wiley Periodicals, Inc.

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Background: Because alcohol has multiple dose-dependent consequences, it is important to understand the causes of individual variation in the amount of alcohol used. The aims of this study were to assess the long-term repeatability and genetic or environmental causes of variation in alcohol intake and to estimate the degree of overlap with causes of susceptibility to alcohol dependence. Methods: Data were used from three studies conducted between 1980 and 1995 on volunteer adult male and female Australian twin subjects. In each study, alcohol intake was reported both as quantity X frequency and as past-week data. Repeatability was calculated as correlations between occasions and between measures, and the effects of genes and environment were estimated by multivariate model fitting to the twin pair repeated measures of alcohol use. Relationships between mean alcohol use and the lifetime history of DSM-III-R alcohol dependence were tested by bivariate model fitting. Results: Repeatability of the alcohol intake measures was between 0.54 and 0.85, with the highest repeatability between measures within study and the lowest repeatability between the first and last studies. Reported alcohol consumption was mainly affected by genetic factors affecting all times of study and by nonshared environmental factors (including measurement error) unique to each time of study. Genes that affect alcohol intake do affect alcohol dependence, but genetic effects unique to dependence are also significant; environmental effects are largely unique to either intake and dependence. Conclusions: Nearly all the repeatable component of variation in alcohol intake is due to genetic effects. Genes affecting intake also affect dependence risk, but there are other genes that affect dependence alone. Studies aiming to identify genes that affect alcohol use disorders need to test loci and candidate genes against both phenotypes.

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Background. Genetic influences have been shown to play a major role in determining the risk of alcohol dependence (AD) in both women and men; however, little attention has been directed to identifying the major sources of genetic variation in AD risk. Method. Diagnostic telephone interview data from young adult Australian twin pairs born between 1964 and 1971 were analyzed. Cox regression models were fitted to interview data from a total of 2708 complete twin pairs (690 MZ female, 485 MZ male, 500 DZ female, 384 DZ male, and 649 DZ female/male pairs). Structural equation models were fitted to determine the extent of residual genetic and environmental influences on AD risk while controlling for effects of sociodemographic and psychiatric predictors on risk. Results. Risk of AD was increased in males, in Roman Catholics, in those reporting a history of major depression, social anxiety problems, and conduct disorder, or (in females only) a history of suicide attempt and childhood sexual abuse; but was decreased in those reporting Baptist, Methodist, or Orthodox religion, in those who reported weekly church attendance, and in university-educated males. After allowing for the effects of sociodemographic and psychiatric predictors, 47 % (95 % CI 28-55) of the residual variance in alcoholism risk was attributable to additive genetic effects, 0 % (95 % CI 0-14) to shared environmental factors, and 53 % (95 % CI 45-63) to non-shared environmental influences. Conclusions. Controlling for other risk factors, substantial residual heritability of AD was observed, suggesting that psychiatric and other risk factors play a minor role in the inheritance of AD.

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Objectives: To examine the health-related quality of life of alcohol-dependent patients across a 12-week cognitive behaviour treatment (CBT) program and identify whether the patient selection of the anticraving medication naltrexone further enhanced these outcomes. Method: One hundred and thirty-six consecutive alcohol-dependent subjects voluntarily participated and were offered naltrexone, of which 73 (54%) participants declined medication. A matched design was used. Of the 136 subjects, 86 (43 naltrexone and CBT; 43 CBT only) could be individually matched (blind to outcome measures) for gender, age, prior alcohol detoxification and dependence severity. Measures of health status and mental health wellbeing included the Rand Corporation Medical Outcomes Short Form 36 Health Survey (SF-36) and the General Health Questionnaire (GHQ-28). Results: Pre-treatment, all had SF-36 and GHQ-28 scores markedly below national norms. Post-treatment, significant improvement in seven of the eight SF-36 subscales and all of the GHQ-28 subscales occurred, approximating national normative levels. Patients in the CBT + naltrexone group were significantly more likely to have increased days abstinent (p = 0.002) and to complete the program abstinent (p = 0.051). The adjunctive use of naltrexone did not provide additional benefit as reflected in SF-36 and GHQ-28 scores, beyond CBT alone. Conclusions: Patients who completed the CBT-based treatment program reported significant improvements in self-reported health status (SF-36) and wellbeing (GHQ-28). The adjunctive use of naltrexone demonstrated no additional improvement in these measures.

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Objective: The Temptation and Restraint Inventory (TRI) is commonly used to measure drinking restraint in relation to problem drinking behavior. However, as yet the TRI has not been validated in a clinical group with alcohol dependence. Method: Male (n = 111) and female (n = 57) inpatients with DSM-IV diagnosed alcohol dependence completed the TRI and measures of problem drinking severity, including the Alcohol Dependence Scale and the quantity, frequency and week total of alcohol consumed. Results: The factor structure of the TRI was replicated in the alcohol dependent sample. Cognitive Emotional Preoccupation (CEP), one of the two higher order factors of the TRI, demonstrated sound predictive power toward all dependence severity indices. The other higher order factor, Cognitive Behavioral Control (CBC), was related to frequency of drinking. There was limited support for the CEP/CBC interactional model of drinking restraint. Conclusions: Although the construct validity of the TRI was sound, the measure appears more useful in understanding the development, maintenance and severity of alcohol-related problems in nondependent drinkers. The TRI may show promise in detecting either continuous drinking or heavy episodic type dependent drinkers.

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The present study evaluated the effectiveness of attendance at a clinically based, short-term, in-patient group CBT program largely based on Monti, Abrams, Kadden, and Cooney(1) to treat problem drinking. Participants were 37 males and 34 females diagnosed with alcohol dependence. Patients attended 42 CBT sessions over three weeks, with each session being one hour in duration. Measures included the Khavari Alcohol Test (KAT), the Short Alcohol Dependence Data Questionnaire (SADD), the Beck Anxiety Index (BAI), the Symptom Checklist-90-Revised (SCL-90), a General Self-Efficacy scale (GSE), and the Drinking Expectancy Profile (DEP). Group attendance rates were monitored daily. Two structured phone calls were conducted at one month and three months post-discharge. Results showed that attendance rates at CBT group sessions were not associated with improvements found at the end of therapy or in drinking behaviors at three-month follow-up. Full support could not be found for the effectiveness of group CBT and cognitive models of problem drinking.

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Background: The low-activity variant of the aldehyde dehydrogenase 2 (ALDH2) gene found in East Asian populations leads to the alcohol flush reaction and reduces alcohol consumption and risk of alcohol dependence (AD). We have tested whether other polymorphisms in the ALDH2 gene have similar effects in people of European ancestry. Methods: Serial measurements of blood and breath alcohol, subjective intoxication, body sway, skin temperature, blood pressure, and pulse were obtained in 412 twins who took part in an alcohol challenge study. Participants provided data on alcohol reactions, alcohol consumption, and symptoms related to AD at the time of the study and subsequently. Haplotypes based on 5 single-nucleotide polymorphisms (SNPs) were used in tests of the effects of variation in the ALDH2 gene on alcohol metabolism and alcohol's effects. Results: The typed SNPs were in strong linkage disequilibrium and 2 complementary haplotypes comprised 83% of those observed. Significant effects of ALDH2 haplotype were observed for breath alcohol concentration, with similar but smaller and nonsignificant effects on blood alcohol. Haplotype-related variation in responses to alcohol, and reported alcohol consumption, was small and not consistently in the direction predicted by the effects on alcohol concentrations. Conclusions: Genetic variation in ALDH2 affects alcohol metabolism in Europeans. However, the data do not support the hypothesis that this leads to effects on alcohol sensitivity, consumption, or risk of dependence.

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Background: Previous research has reported both a moderate degree of comorbidity between cannabis dependence and major depressive disorder (MDD) and that early-onset cannabis use is associated with increased risks for MDD. Objective: To examine whether associations between both lifetime cannabis dependence and early cannabis use and measures of MDD, suicidal ideation, and suicide attempt persist after controlling for genetic and/or shared environmental influences. Design: Cross-sectional survey of twin pairs discordant for lifetime cannabis dependence and those discordant for early cannabis use. Setting: General population sample of twins (median age, 30 years). Participants: Two hundred seventy-seven same-sex twin pairs discordant for cannabis dependence and 311 pairs discordant for early-onset cannabis use (before age 17 years). Main Outcome Measures: Self-report measures of DSM-IV-defined lifetime MDD, suicidal ideation, and suicide attempt. Results: Individuals who were cannabis dependent had odds of suicidal ideation and suicide attempt that were 2.5 to 2.9 times higher than those of their non-cannabis-dependent co-twin. Additionally, cannabis dependence was associated with elevated risks of MDD in dizygotic but not in monozygotic twins. Those who initiated cannabis use before age 17 years had elevated rates of subsequent suicide attempt (odds ratio, 3.5 [95% confidence interval, 1.4-8.6]) but not of MDD or suicidal ideation. Early MDD and suicidal ideation were significantly associated with subsequent risks of cannabis dependence in discordant dizygotic pairs but not in discordant monozygotic pairs. Conclusions: Comorbidity between cannabis dependence and MDD likely arises through shared genetic and environmental vulnerabilities predisposing to both outcomes. In contrast, associations between cannabis dependence and suicidal behaviors cannot be entirely explained by common predisposing genetic and/or shared environmental predispositions. Previously reported associations between early-onset cannabis use and subsequent MDD likely reflect shared genetic and environmental vulnerabilities, although it remains possible that early-onset cannabis use may predispose to suicide attempt.

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Consistent relationships have been demonstrated between problem drinking and certain personality characteristics. A contemporary cognitive model of alcohol misuse, drinking restraint, has recently shown promise in furthering our understanding of problematic drinking. This study examined the potential association between drinking restraint and personality characteristics in 168 alcohol dependent inpatients. Subjects completed the short-scale Revised Eysenck Personality Scales (EPS-R; Eysenck, Eysenck, & Barrett, 1985), Temptation and Restraint Inventory (TRI; Collins & Lapp, 1992), Alcohol Dependence Scale (ADS; Skinner & Allen, 1982) and drinking measures including quantity, frequency and weekly drinking total. Results indicated that although there was some conceptual overlap between drinking restraint and personality factors, the TRI had a unique relationship with indices of problem drinking once personality factors were taken into account. This indicates that restrained drinking and personality, although related, are discrete constructs. While restrained drinking may aid in the understanding of current drinking behavior, personality characteristics appear to contribute to the etiology and maintenance of drinking problems. (c) 2005 Elsevier Ltd. All rights reserved.

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After ingestion of a standardized dose of ethanol, alcohol concentrations were assessed, over 3.5 hours from blood (six readings) and breath (10 readings) in a sample of 412 MZ and DZ twins who took part in an Alcohol Challenge Twin Study (ACTS). Nearly all participants were subsequently genotyped on two polymorphic SNPs in the ADH1B and ADH1C loci known to affect in vitro ADH activity. In the DZ pairs, 14 microsatellite markers covering a 20.5 cM region on chromosome 4 that includes the ADH gene family were assessed, Variation in the timed series of autocorrelated blood and breath alcohol readings was studied using a bivariate simplex design. The contribution of a quantitative trait locus (QTL) or QTL's linked to the ADH region was estimated via a mixture of likelihoods weighted by identity-by-descent probabilities. The effects of allelic substitution at the ADH1B and ADH1C loci were estimated in the means part of the model simultaneously with the effects sex and age. There was a major contribution to variance in alcohol metabolism due to a QTL which accounted for about 64% of the additive genetic covariation common to both blood and breath alcohol readings at the first time point. No effects of the ADH1B*47His or ADH1C*349Ile alleles on in vivo metabolism were observed, although these have been shown to have major effects in vitro. This implies that there is a major determinant of variation for in vivo alcohol metabolism in the ADH region that is not accounted for by these polymorphisms. Earlier analyses of these data suggested that alcohol metabolism is related to drinking behavior and imply that this QTL may be protective against alcohol dependence.

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This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October, 2004. Chronic alcoholism follows a fluctuating course, which provides a naturalistic experiment in vulnerability, resilience, and recovery of human neural systems in response to presence, absence, and history of the neurotoxic effects of alcoholism. Alcohol dependence is a progressive chronic disease that is associated with changes in neuroanatomy, neurophysiology, neural gene expression, psychology, and behavior. Specifically, alcohol dependence is characterized by a neuropsychological profile of mild to moderate impairment in executive functions, visuospatial abilities, and postural stability, together with relative sparing of declarative memory, language skills, and primary motor and perceptual abilities. Recovery from alcoholism is associated with a partial reversal of CNS deficits that occur in alcoholism. The reversal of deficits during recovery from alcoholism indicates that brain structure is capable of repair and restructuring in response to insult in adulthood. Indirect support of this repair model derives from studies of selective neuropsychological processes, structural and functional neuroimaging studies, and preclinical studies on degeneration and regeneration during the development of alcohol dependence and recovery from dependence. Genetics and brain regional specificity contribute to unique changes in neuropsychology and neuroanatomy in alcoholism and recovery. This symposium includes state-of-the-art presentations on changes that occur during active alcoholism as well as those that may occur during recovery-abstinence from alcohol dependence. Included are human neuroimaging and neuropsychological assessments, changes in human brain gene expression, allelic combinations of genes associated with alcohol dependence and preclinical studies investigating mechanisms of alcohol induced neurotoxicity, and neuroprogenetor cell expansion during recovery from alcohol dependence.