Alcohol RSS feed: Current Issue. Alcohol is an international, peer-reviewed journal that is devoted to publishing multi-disciplinary biomedical research on all aspects of the actions or effects of alcohol on the nervous system or on other organ systems. Emphasis is given to studies into the causes and consequences of alcohol abuse and alcoholism, and biomedical aspects of diagnosis, etiology, treatment or prevention of alcohol-related health effects. Intended for both research scientists and practicing clinicians, the journal publishes original research on the neurobiological, neurobehavioral, and pathophysiological processes associated with alcohol drinking, alcohol abuse, alcohol-seeking behavior, tolerance, dependence, withdrawal, protracted abstinence, and relapse. In addition, the journal reports studies on the effects alcohol on brain mechanisms of neuroplasticity over the life span, biological factors associated with adolescent alcohol abuse, pharmacotherapeutic strategies in the treatment of alcoholism, biological and biochemical markers of alcohol abuse and alcoholism, pathological effects of uncontrolled drinking, biomedical and molecular factors in the effects on liver, immune system, and other organ systems, and biomedical aspects of fetal alcohol spectrum disorder including mechanisms of damage, diagnosis and early detection, treatment, and prevention. Articles are published from all levels of biomedical inquiry, including the following: molecular and cellular studies of alcohol's actions in vitro and in vivo ; animal model studies of genetic, pharmacological, behavioral, developmental or pathophysiological aspects of alcohol; human studies of genetic, behavioral, cognitive, neuroimaging, or pathological aspects of alcohol drinking; clinical studies of diagnosis (including dual diagnosis), treatment, prevention, and epidemiology. The journal will publish 9 issues per year; the accepted abbreviation for Alcohol for bibliographic citation is Alcohol . Alcohol subscribes to the tenets of The Farmington Consensus (see http://www.elsevier.com/framework_products/promis_misc/525453fc.pdf or http://www1.elsevier.com/homepage/sab/alcohol/fconsensus.htm ). Submission of a paper to the journal will be taken as evidence that the authors have complied with the tenets set forth in the Consensus. All submitted material will be subject to peer review. Alcohol considers three types of manuscripts for publication: - Original research articles are full-length reports of the authors' original research addressing topics consistent with the Aims and Scope of the journal. Submissions outside the scope of the journal, or incomplete or fragmentary submissions, will not be considered. - Rapid communications are original, high-quality manuscripts that describe new data of high impact and major importance to the field. These contributions are typically short (e.g., 4 journal pages), and will be peer-reviewed by at least one expert in the field of the research and an Editor, and will be either accepted with minimal or no revisions or rejected. Publication of accepted rapid communications will be expedited. - Invited review articles will be considered for publication, upon invitation from the Editor-in-Chief, as full-length papers or mini-reviews. These contributions will be peer-reviewed. Contact the Editor-in-Chief concerning the suitability of a topic for an invited review. There are no page charges for articles published in Alcohol , and the current practice is to provide the corresponding author with 50 free reprints of his/her article. Effective May 2006, authors from all countries are invited to submit manuscripts, complete in all respects and following the Instructions to Authors (revised May 2006), to Charles R. Goodlett, Editor-in-Chief, via Elsevier electronic submission at http://ees.elsevier.com/alcohol Contact for questions: Charles R. Goodlett Editor-in-Chief, Alcohol Department of Psychology IUPUI 402 North Blackford Street Indianapolis, IN 46202-3275 Tel: +1-317 274-6772 Fax: +1-317 278-7181 E-mail: alcojrnl@iupui.edu http://www.alcoholjournal.org/?rss=yesElsevier Inc.en © 2010 Elsevier Inc. All rights reserved. Alcohol0741-8329445August 2010 © 2010 Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.alcoholjournal.org/article/PIIS0741832910000479/abstract?rss=yesAbstract: In this study, alcohol was administered intravenously to study whether its effects on mood should preferably be studied as a bi- or unipolar phenomenon. This was studied in a double-blind, placebo-balanced, design on six healthy male volunteers. Of the three bipolar aspects of mood (calmness, activity, and pleasantness), only calmness was significantly affected by intravenous alcohol. In contrast, there were significant differences between alcohol and placebo for five of the six unipolar indexes. This support the hypothesis that subjective effects of alcohol on mood are preferably studied with self-ratings that allows positive and negative aspects to be analyzed separately. Further, our data suggest that the effects of alcohol are primarily on negative aspects of mood rather than on positive.Should mood during intravenous alcohol administration be studied as a bi- or unipolar phenomenon? a pilot studyLars Saxon, Stefan Skagerberg, Stefan Borg, Arto J. Hiltunen10.1016/j.alcohol.2010.05.007Alcohol 44, 5 (2010)2010-06-21Alcohol2010-06-21445S0741-8329(10)X0005-2393400http://www.alcoholjournal.org/article/PIIS0741832910000480/abstract?rss=yesAbstract: A serotonin deficiency state has been implicated in alcohol-dependent individuals' experience of obsessive–compulsive alcohol craving. Because the serotonin transporter (5-HTT) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high-expressing LA alleles present in the 5-HTT gene-linked polymorphic region [5-HTTLPR] of the SLC6A4 gene) is associated with an increase in obsessive–compulsive alcohol craving. The current pilot investigation sought to explore this hypothesis by examining the extent to which obsessive–compulsive alcohol craving varies by 5-HTTLPR genotype among participants enrolled in an ongoing pharmacogenetics trial. All participants were screened with a semi-structured diagnostic interview, completed self-report measures of alcohol-related behavior, and underwent peripheral venous blood draw for DNA genotyping. Cross-sectional data obtained at baseline from 176 currently drinking alcohol-dependent individuals were analyzed using multiple regression. Preliminary findings suggest that 5-HTTLPR is not predictive of Obsessive Compulsive Drinking Scale total and factor scores. Although the 5-HTTLPR polymorphism was not related to obsessive–compulsive alcohol craving in this pilot study, additional research is needed to clarify the possible role of serotonergic mechanisms in alcohol craving.Relationship between the serotonin transporter polymorphism and obsessive–compulsive alcohol craving in alcohol-dependent adults: a pilot studyRachel D. Thompson, Jaimee L. Heffner, Judith A. Strong, Thomas J. Blom, Robert M. Anthenelli10.1016/j.alcohol.2010.05.008Alcohol 44, 5 (2010)2010-07-05Alcohol2010-07-05445S0741-8329(10)X0005-2401406http://www.alcoholjournal.org/article/PIIS0741832910000625/abstract?rss=yesAbstract: Knowledge of alcohol use disorder and of substance-related problems has recently found some initial support in genetic studies. With a view to further understanding of this particular aspect, in the light of the “self-medication hypothesis,” we focused our attention on the gamma aminobutyric acid system and, in particular, on single nucleotide polymorphisms (SNPs) in the glutamate decarboxylase 67 or glutamic acid decarboxylase 67 (GAD67) gene region in association with alcohol dependence. The research was structured as a case–control study. The patient cohort included 283 Caucasian males from the Veneto region, North-east Italy; 107 were alcohol dependent according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV TR) criteria, and 176 were controls recruited from blood donors. We analyzed 26 SNPs located in the coding and untranslated regions of the GAD67 gene with the GenomeLab SNPStream Genotyping System (Beckman Coulter, Fullerton, CA). Fisher's Chi-square test for allele and genotype distributions and Hardy–Weinberg equilibrium analysis for cases and controls were performed. Ten SNPs at the GAD67 gene were valid for further statistics. Preliminary results show a difference in genotype distribution (P=.003; χ2=11.6081) between alcoholic subjects and controls of SNP rs 11542313 located in exon 3 of the GAD67 gene, responsible for a silent mutation (His37His). This is the first genetic study regarding the GAD67 gene in relation to the condition of alcohol dependence in an Italian population of subjects all coming from the same region (Veneto). The results highlight a statistical association between one SNP of GAD67 and the condition of alcohol dependence. To clarify the possible meaning of this association, further genetic analyses are being undertaken. In particular, we are investigating other genetic polymorphisms, both upstream and downstream from rs 11542313, which may interfere with splicing and/or GAD67 mRNA stability.Alcohol dependence and glutamate decarboxylase gene polymorphisms in an Italian male populationClaudio Terranova, Marianna Tucci, Giovanni Forza, Luisa Barzon, Giorgio Palù, Santo Davide Ferrara10.1016/j.alcohol.2010.05.011Alcohol 44, 5 (2010)2010-07-02Alcohol2010-07-02445S0741-8329(10)X0005-2407413http://www.alcoholjournal.org/article/PIIS0741832910000662/abstract?rss=yesAbstract: The most well-known metabolic pathways from ethanol to acetaldehyde include alcohol dehydrogenase (ADH) and the microsomal ethanol oxidizing system that involves cytochrome P450 2E1 (CYP2E1). Acetaldehyde is further oxidized to acetate by aldehyde dehydrogenase (ALDH). The genetic variation of ADH1B, ALDH2, and CYP2E1 is different among racial populations and cause difference in elimination rates of alcohol. The aim of this study was to determine the polymorphisms of ADH1B (rs1229984; Arg47His), ALDH2 (rs671; Glu487Lys), CYP2E1*6 (rs6413432; T7632A), and CYP2E1*7B (rs6413420; G-71T) in unrelated healthy Turkish population and compare it with other populations. ADH1B and ALDH2 polymorphisms were analyzed with an allele-specific polymerase chain reaction (PCR) assay, and CYP2E1*6 and CYP2E1*7B polymorphisms were genotyped by PCR-restriction fragment length polymorphism method. ADH1B polymorphism analysis yielded the genotype distribution as 83.9% ADH1B*1/1 and 16.1% ADH1B*1/2, and no individuals with ALDH2*1/2 and ALDH2*2/2 genotypes were found in Turkish population. The genotype frequencies for CYP2E1*6 polymorphism were found as 85.3% for homozygote common, 14.1% for heterozygote, and 0.6% for homozygote uncommon. For CYP2E1*7B polymorphism, the genotype frequencies were determined to be 86.5% G/G, 13.5% for G/T; however, no individuals with homozygote uncommon genotype were detected. According to our study results, the genotype distributions of ADH1B, ALDH2, CYP2E1*6, and CYP2E1*7B in Turkish population were similar compared with Caucasian and some European populations, whereas differed significantly from East Asian populations. This study may be useful in epidemiological studies of the influence of ADH1B, ALDH2, CYP2E1*6, and CYP2E1*7B polymorphisms on diseases, including several types of cancer related to alcohol consumption and alcohol dependence.Distribution of ADH1B, ALDH2, CYP2E1∗6, and CYP2E1∗7B genotypes in Turkish populationZeliha Kayaaltı, Tülin Söylemezoğlu10.1016/j.alcohol.2010.06.002Alcohol 44, 5 (2010)2010-07-02Alcohol2010-07-02445S0741-8329(10)X0005-2415423http://www.alcoholjournal.org/article/PIIS0741832910000492/abstract?rss=yesAbstract: Nonsynonymous single nucleotide polymorphisms (nsSNPs) are thought as potential disease modifiers because they alter the encoded amino acid sequence and are likely to affect the function of the proteins accounting for susceptibility to disease. Distinguishing the functionally significant nsSNPs from tolerant nsSNPs is helpful to characterize the genetic basis of human diseases and assess individual susceptibility to diseases. Many nsSNPs have been found in alcohol metabolism-related genes but there is poor knowledge on the relationship between the genotype and phenotype of nsSNPs in these genes. In this study, we have identified a total of 203 nsSNPs in 29 human alcohol metabolism-related genes from the National Center for Biotechnology Information (NCBI) dbSNP and SWISS-Prot databases. Using the PolyPhen and SIFT algorithms, 43% of nsSNPs in alcohol metabolism-related genes were predicted to have functional impacts on protein function with a significant concordance of the prediction results between the two algorithms. The prediction accuracy is about 77–81% of all the nsSNPs based on the results of in vivo and in vitro studies. These amino acid substitutions are supposed to be the pathogenetic basis for the alteration of metabolism enzyme activity and the association with disease susceptivity. The phenotype of nsSNPs predicted as deleterious needs to be clarified in further studies and the prediction of nsSNPs in human alcohol metabolism-related genes would be useful hints for further genotype–phenotype studies on the individual difference in susceptivity to alcohol-related diseases.Phenotype prediction of deleterious nonsynonymous single nucleotide polymorphisms in human alcohol metabolism-related genes: a bioinformatics studyLin-Lin Wang, An-Kui Yang, Yong Li, Jun-Ping Liu, Shu-Feng Zhou10.1016/j.alcohol.2010.05.009Alcohol 44, 5 (2010)2010-06-21Alcohol2010-06-21445S0741-8329(10)X0005-2425438http://www.alcoholjournal.org/article/PIIS0741832910000431/abstract?rss=yesAbstract: This study investigated regional cerebral flood flow (CBF) in chronic alcoholic patients, focusing primarily on the limbic system, including the hippocampus and the callosomarginal region, because of their susceptibility to damage in such patients. The degree of hippocampal atrophy in such patients was also examined. Regional CBF and the degree of parahippocampal gyrus atrophy were studied in 22 chronic alcoholic male patients with no neurological or psychological symptom (mean age, 59.3±4.1 years). Their findings were compared with those of 22 age-matched, male, normal controls (mean age, 59.7±3.9 years). Single-photon emission computed tomography was performed using the 99mTc-ethylcysteinate dimer ( 99mTc-ECD) Patlak Plot method, and the three-dimensional stereotaxic region of interest (ROI) template (3DSRT) and the fine stereotaxic ROI template (fine SRT) developed by Takeuchi et al were used to evaluate regional CBF, focusing primarily on the limbic system. These methods make it possible to precisely and objectively measure the details of regional CBF. The voxel-based specific regional analysis system for Alzheimer's disease (VSRAD) was used to determine the degree of parahippocampal gyrus atrophy in chronic alcoholic patients. VSRAD is a method developed by Hirata et al for evaluating the degree of atrophy of the parahippocampal gyrus. The results were analyzed using Z scores (>2 indicating significant atrophy). Blood flows in the callosomarginal region, pericallosal region, thalamus, hippocampus, parahippocampal gyrus, amygdaloid body, anterior cingulate gyrus, and middle cingulate gyrus were lower in the chronic alcoholic group than in the control group. Parahippocampal gyrus atrophy was not observed in the control group (average Z score, 0.62±0.29). In contrast, an atrophic tendency was observed in the chronic alcoholic group (average Z score, 1.88±0.44). Clinically intact, chronic alcoholic patients with no neurological or psychological symptom had decreased CBF in the limbic system and a tendency to parahippocampal gyrus atrophy.Atrophy of the parahippocampal gyrus and regional cerebral blood flow in the limbic system in chronic alcoholic patientsYutaka Suzuki, Minoru Oishi, Katsuhiko Ogawa, Tomohiko Mizutani10.1016/j.alcohol.2010.05.003Alcohol 44, 5 (2010)2010-06-21Alcohol2010-06-21445S0741-8329(10)X0005-2439445http://www.alcoholjournal.org/article/PIIS0741832910000443/abstract?rss=yesAbstract: Alcohol and nonsteroidal anti-inflammatory drugs are noxious agents that can disrupt the integrity of the gastroduodenal mucosal and damage the epithelial barrier and lead to increased gastroduodenal permeability. Moreover, it is not uncommon that patients are exposed to these two barrier stressors at the same time. It is thus important to know how simultaneous exposure affects the gastroduodenal barrier, and acquiring that knowledge was the goal of this study. We used a method that has been widely used for the assessment of injury to the gastroduodenal barrier induced by these noxious agents—measurement of gastroduodenal permeability as indicated by urinary excretion of ingested sucrose. We used gas chromatography to measure the amount of sucrose excreted in the urine over the 5–12h after ingestion of a bolus of sucrose. The 148 participants in the study included 92 alcoholics and 56 healthy controls. All study subjects had a baseline permeability test. To determine whether addition of a second noxious agent, in addition to chronic alcohol, further decreases gastroduodenal barrier integrity, a subset of 118 study subjects participated in another permeability test in which they were exposed to aspirin. For this test, participants ingested 1,300mg aspirin twice, 12 and 1h before the final permeability test. The baseline permeability test showed that alcoholics have significantly higher gastroduodenal permeability than controls. Aspirin caused a significant within-group absolute increase in gastroduodenal permeability in both alcoholics and controls (+7.72%, P=.003 and +2.25%, P=.011, respectively), but the magnitude of these increases was not significantly different from each other. Baseline permeability did vary by gender, self-reported illegal drug use, and employment type. The extent of the permeability increase after aspirin ingestion varied with illegal drug use and recruitment site (a surrogate marker of socioeconomic status). Our data show that alcoholics have greater gastroduodenal permeability than healthy controls. This difference was independent of the duration of any preceding period of sobriety, gender, smoking history, or illicit drug abuse. The injurious effects of alcohol on the gastroduodenal epithelial barrier are long lasting, persisting even after 7 days of sobriety. Although, acute aspirin and chronic alcohol each increase intestinal permeability in alcoholics, their effects appear to be additive rather than synergistic.Effects of aspirin on gastroduodenal permeability in alcoholics and controlsAshkan Farhadi, Ali Keshavarzian, Mary J. Kwasny, Maliha Shaikh, Louis Fogg, Cynthia Lau, Jeremy Z. Fields, Christopher B. Forsyth10.1016/j.alcohol.2010.05.004Alcohol 44, 5 (2010)2010-07-05Alcohol2010-07-05445S0741-8329(10)X0005-2447456http://www.alcoholjournal.org/article/PIIS0741832910000807/abstract?rss=yesAbstract: Serum total sialic acid (TSA) concentration is a sensitive marker of excessive alcohol consumption and is the sum of protein-bound sialic acid, lipid-bound sialic acid (LSA), and free sialic acid. The LSA is the fraction of SA attached to gangliosides that are transported in the blood by the lipoproteins. In this article, the effect of chronic alcohol consumption on the serum levels of LSA was evaluated. The objective of the study was to understand the mechanism of elevated serum TSA concentration during alcohol abuse. Additionally, the association of LSA with serum lipid profile was tested. For this purpose, the levels of LSA, TSA, lipids, lipoproteins, and apolipoproteins (apos) in the sera of 106 alcoholics were measured. The serum level of LSA in alcohol abusers was significantly elevated. This increase was because of the elevated level of LSA in patients drinking alcohol up to 2 days before sampling. The elevated level of LSA positively correlated with TSA, and also with biochemical indices of hepatocellular injury such as aspartate aminotransferase and γ-glutamyltransferase, but did not correlate with any lipids, apos, and lipoproteins. The increase in LSA level is not related with the status of serum lipid profile but is related to the liver status estimated by the biochemical markers of liver cell damage. On the basis of our results, we conclude that the elevated level of LSA in alcohol abusers contributes to an increase in the serum concentration of TSA, and contrary to TSA, is affected by the status of liver cells.Lipid-bound sialic acid in alcoholics participates in increased level of total sialic acidBogdan Cylwik, Lech Chrostek, Agnieszka Krawiec, Zbigniew Supronowicz, Alicja Koput, Maciej Szmitkowski10.1016/j.alcohol.2010.06.005Alcohol 44, 5 (2010)2010-08-13Alcohol2010-08-13445S0741-8329(10)X0005-2457462http://www.alcoholjournal.org/article/PIIS0741832910001059/abstract?rss=yesAbstract: The aims of this study were to study suicide rates in youths aged 15–29 years in the European Union (EU), to identify differences between early members and new members to the EU since 2004, and to evaluate the association between alcohol-related variables and suicide rates, while controlling for indicators of social stress. We explored temporal trends in age-adjusted suicide rates for youths aged 15–29 years resident in EU nations since 1980. Social changes in EU nations were associated with increased inequalities between the countries in suicide, especially in male youths (new/early EU members: relative risk=1.55; 95% confidence interval: 1.48/1.61). Pure alcohol consumption predicts suicide rates in female youths, whereas social stress related to violence against youths predicts suicide rates in male youths. EU political and heath agencies should devise policies to prevent youth suicide with a focus on alcohol misuse and societal stress associated with violence against youths.Alcohol consumption predicts the EU suicide rates in young women aged 15–29 years but not in men: analysis of trends and differences among early and new EU countries since 2004Marco Innamorati, David Lester, Mario Amore, Paolo Girardi, Roberto Tatarelli, Maurizio Pompili10.1016/j.alcohol.2010.07.007Alcohol 44, 5 (2010)2010-08-01Alcohol2010-08-01445S0741-8329(10)X0005-2463469