Alcohol RSS feed: Articles in Press. 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//inpress?rss=yesElsevier Inc.en © 2010 Elsevier Inc. All rights reserved. Alcohol0741-83292010-01-11 © 2010 Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.alcoholjournal.org/article/PIIS0741832909001967/abstract?rss=yesAbstract: Directional asymmetry, the systematic differences between the left and right body sides, is widespread in human populations. Changes in directional asymmetry are associated with various disorders that affect craniofacial development. Because facial dysmorphology is a key criterion for diagnosing fetal alcohol syndrome (FAS), the question arises whether in utero alcohol exposure alters directional asymmetry in the face. Data on the relative position of 17 morphologic landmarks were obtained from facial scans of children who were classified as either FAS or control. Shape data obtained from the landmarks were analyzed with the methods of geometric morphometrics. Our analyses showed significant directional asymmetry of facial shape, consisting primarily of a shift of midline landmarks to the right and a displacement of the landmarks around the eyes to the left. The asymmetry of FAS and control groups differed significantly and average directional asymmetry was increased in those individuals exposed to alcohol in utero. These results suggest that the developmental consequences of fetal alcohol exposure affect a wide range of craniofacial features in addition to those generally recognized and used for diagnosis of FAS.Prenatal alcohol exposure alters the patterns of facial asymmetry - Corrected ProofC.P. Klingenberg, L. Wetherill, J. Rogers, E. Moore, R. Ward, I. Autti-Rämö, Å. Fagerlund, S.W. Jacobson, L.K. Robinson, H.E. Hoyme, S.N. Mattson, T.K. Li, E.P. Riley, T. Foroud, the CIFASD Consortium10.1016/j.alcohol.2009.10.016Alcohol (2010)2010-01-11Alcohol2010-01-11http://www.alcoholjournal.org/article/PIIS0741832909001827/abstract?rss=yesAbstract: Fetal alcohol spectrum disorders (FASD) are the leading preventable causes of developmental disabilities with serious permanent consequences. Regardless of the increased awareness of fetal alcohol syndrome (FAS), 13% of women in the United States drink alcohol during pregnancy. Health care professionals do not routinely assess the frequency and quantity of alcohol use by their patients. This study examined the knowledge, skills, and practices of family medicine residency and clerkship directors and assessed the time devoted and format of FAS curricula in the programs. A self-administered anonymous survey was sent to the residency and clerkship directors (N=571). Response rate of clerkship directors was 52% and residency directors 46%. Both groups showed high level of knowledge of FASD and of alcohol counseling practices for pregnant women. Although almost two thirds of the residency programs had FASD integrated in the curriculum, an equivalent fraction of predoctoral programs did not. More than half of the clerkship directors without FASD in their curriculum agreed that a need exists for its inclusion. These findings raise important medical education and policy issues and provide insight into the disparity in FASD content of curricula between predoctoral and family medicine residency programs in the United States. The role of physician counseling in primary prevention of FAS should continue to be stressed in predoctoral and residency education.Fetal alcohol syndrome: knowledge and attitudes of family medicine clerkship and residency directors - Corrected ProofRoger Zoorob, Muktar H. Aliyu, Carmela Hayes10.1016/j.alcohol.2009.10.012Alcohol (2010)2010-01-07Alcohol2010-01-07http://www.alcoholjournal.org/article/PIIS074183290900158X/abstract?rss=yesAbstract: Preventing fetal alcohol spectrum disorders (FASDs) requires detection of in-pregnancy maternal risk drinking. The widely used T-ACE screen has been applied in various ways, although the impact of those different uses on effectiveness is uncertain. We examined relations among different T-ACE scoring criteria, maternal drinking, and child outcome. Self-reported across-pregnancy maternal drinking was assessed in 75 African-American women. The different T-ACE criteria used varied the level of drinking that defined tolerance (two or three drinks) and the total T-ACE score cut-points (two or three). Receiver operator curves and regression analysis assessed the significance of relations. Increasing the total T-ACE score cut-point to 3 almost doubled specificity in detecting risk drinking whereas maintaining adequate sensitivity, equivalent to that in the original report, and identified substantially more neurobehavioral deficits in children. Redefining tolerance at three drinks did not improve T-ACE effectiveness in predicting outcomes. This study is among the first to show the ability of an in-pregnancy T-ACE assessment to predict child neurodevelopmental outcome. In addition, increasing the total T-ACE score criterion (from 2 to 3) improved identification of non-drinking mothers and unaffected children with little loss in detection of drinkers and affected children. Efficient in-pregnancy screens for risk drinking afford greater opportunities for intervention that could prevent/limit FASDs.Validity of the T-ACE in pregnancy in predicting child outcome and risk drinking - Corrected ProofLisa M. Chiodo, Robert J. Sokol, Virginia Delaney-Black, James Janisse, John H. Hannigan10.1016/j.alcohol.2009.08.009Alcohol (2010)2010-01-06Alcohol2010-01-06http://www.alcoholjournal.org/article/PIIS0741832909001608/abstract?rss=yesAbstract: Fetal alcohol spectrum disorders (FASD) are a common cause of developmental disability, birth defects, and mortality. The performance characteristics of current diagnostic tools for FASD are not adequately reported. This study examines the performance characteristics of the Fetal Alcohol Syndrome Diagnostic Checklist (FASDC). In a population of 658 subjects from North Dakota, we used the FASDC score to examine the agreement between FASDC score, clinical diagnosis, and the Institute of Medicine criteria for FASD. All subjects were seen for evaluation in the genetic/dysmorphology clinics, which are funded by the state to provide genetic diagnostic services for residents of North Dakota. We compared the clinical diagnosis and the FASDC scores to determine the performance characteristics of the FASDC in the categorical diagnosis of fetal alcohol spectrum (FAS), other-FASD, and a group with No-FASD. Comparisons were made using univariate and logistic models of outcomes using both the presence and the absence of alcohol exposure or FASDC phenotype data. The FASDC performance characteristics for differentiation of the FAS group from non-FASD were excellent (accuracy 99%, sensitivity 99%, and specificity 99%). Logistic models for subjects with scores in the FASD range were differentiated with an accuracy of 82%, sensitivity 85%, and specificity 80% using the data on phenotype and exposure. We were able to delineate subjects with scores in the No-FASD range with an accuracy of 78%, sensitivity 64%, and specificity 81% without including the exposure and phenotype data by use of the other descriptive data (maternal characteristics, birth records, and demographic data) from the FASDC. All diagnostic tools should have performance characteristics assessed and available before adoption for use in clinical settings. The FASDC scores produce diagnostic groupings that approximate expert clinical judgment. The tool may be useful in other clinical settings for the diagnosis of FASD or as an FASD registry or research database.Diagnosis of fetal alcohol spectrum disorders: a validity study of the fetal alcohol syndrome checklist - Corrected ProofLarry Burd, Marilyn G. Klug, Qing Li, Jacob Kerbeshian, John T. Martsolf10.1016/j.alcohol.2009.08.010Alcohol (2010)2010-01-06Alcohol2010-01-06http://www.alcoholjournal.org/article/PIIS0741832909001694/abstract?rss=yesAbstract: Many children adversely affected by maternal drinking during pregnancy cannot be identified early in life using current diagnostic criteria for fetal alcohol spectrum disorder (FASD). We conducted a preliminary investigation to determine whether ethanol-induced alterations in placental gene expression may have some utility as a diagnostic indicator of maternal drinking during pregnancy and as a prognostic indicator of risk for adverse neurobehavioral outcomes in affected offspring. Pregnant Long-Evans rats voluntarily consumed either a 0 or 5% ethanol solution 4 h each day throughout gestation. Ethanol consumption produced a mean maternal daily intermittent peak serum ethanol concentration of 84 mg/dL. Placentas were harvested on gestational day 20 for gene expression studies. Microarray analysis of more than 28,000 genes revealed that the expression of 304 known genes was altered twofold or greater in placenta from ethanol-consuming dams compared with controls. About 76% of these genes were repressed in ethanol-exposed placentas. Gene expression changes involved proteins associated with central nervous system development; organ morphogenesis; immunological responses; endocrine function; ion homeostasis; and skeletal, cardiovascular, and cartilage development. To date, quantitative real-time polymerase chain reaction analysis has confirmed significant alterations in gene expression for 22 genes, including genes encoding for three calcium binding proteins, two matrix metalloproteinases, the cannabinoid 1, galanin 2 and toll-like receptor 4, iodothyronine deiodinase 2, 11-β hydroxysteroid dehydrogenase 2, placental growth factor, transforming growth factor alpha, gremlin 1, and epithelial growth factor (EGF)-containing extracellular matrix protein. These results suggest that the expression of a sufficiently large number of placental mRNAs is altered after moderate drinking during pregnancy to warrant more detailed investigation of the placenta as a biomarker system for maternal drinking during pregnancy and as an early indicator of FASD. Furthermore, these results provide new insights into novel mechanisms on how ethanol may directly or indirectly mediate its teratogenic effects through alterations in placental function during pregnancy.Effects of moderate drinking during pregnancy on placental gene expression - Corrected ProofMartina J. Rosenberg, Christina R. Wolff, Ahmed El-Emawy, Miranda C. Staples, Nora I. Perrone-Bizzozero, Daniel D. Savage10.1016/j.alcohol.2009.10.002Alcohol (2010)2010-01-06Alcohol2010-01-06http://www.alcoholjournal.org/article/PIIS0741832909001803/abstract?rss=yesAbstract: Currently, no single marker is sensitive and specific enough to be considered a reliable biomarker for prenatal alcohol exposure. To identify a proteomic signature profile for maternal alcohol consumption, we carried out high-throughput proteomics on maternal endothelial caveolae exposed to moderate binge-like alcohol conditions. In these specialized lipid-ordered microdomains that contain a rich assembly of proteins, we demonstrate that moderate binge-like alcohol resulted in a distinctive maternal caveolar proteomic signature with important proteins being dramatically decreased/knocked out in the alcoholic profile. These proteins span from histones and basic structural proteins like α tubulin to proteins involved in trafficking, deubiquitination, cell signaling, and cell–cell adhesion. The profile also suggests an important role for the mother and the uteroplacental compartment in the pathogenesis of fetal alcohol spectrum disorders (FASD). These data demonstrate that the caveolar proteomic signature created by alcohol shows a promising direction for early detection of FASD.High-throughput caveolar proteomic signature profile for maternal binge alcohol consumption - Corrected ProofJayanth Ramadoss, Wu-xiang Liao, Dong-bao Chen, Ronald R. Magness10.1016/j.alcohol.2009.10.010Alcohol (2010)2010-01-06Alcohol2010-01-06http://www.alcoholjournal.org/article/PIIS0741832909001475/abstract?rss=yesAbstract: The Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD) was created in 2003 to further understanding of fetal alcohol spectrum disorders. Clinical and basic science projects collect data across multiple sites using standardized methodology. This article describes the methodology being used by the clinical projects that pertain to assessment of children and adolescents. Domains being addressed are dysmorphology, neurobehavior, 3-D facial imaging, and brain imaging.Collaborative initiative on fetal alcohol spectrum disorders: methodology of clinical projects - Corrected ProofSarah N. Mattson, Tatiana Foroud, Elizabeth R. Sowell, Kenneth Lyons Jones, Claire D. Coles, Åse Fagerlund, Ilona Autti-Rämö, Philip A. May, Colleen M. Adnams, Valentina Konovalova, Leah Wetherill, Andrew D. Arenson, William K. Barnett, Edward P. Riley, CIFASD10.1016/j.alcohol.2009.08.005Alcohol (2009)2009-12-28Alcohol2009-12-28http://www.alcoholjournal.org/article/PIIS0741832909001487/abstract?rss=yesAbstract: Detecting patterns of maternal drinking that place fetuses at risk for fetal alcohol spectrum disorders (FASDs) is critical to diagnosis, treatment, and prevention but is challenging because information on antenatal drinking collected during pregnancy is often insufficient or lacking. Although retrospective assessments have been considered less favored by many researchers due to presumed poor reliability, this perception may be inaccurate because of reduced maternal denial and/or distortion. The present study hypothesized that fetal alcohol exposure, as assessed retrospectively during child adolescence, would be related significantly to prior measures of maternal drinking and would predict alcohol-related behavioral problems in teens better than antenatal measures of maternal alcohol consumption. Drinking was assessed during pregnancy, and retrospectively about the same pregnancy, at a 14-year follow-up in 288 African-American women using well-validated semistructured interviews. Regression analysis examined the predictive validity of both drinking assessments on pregnancy outcomes and on teacher-reported teen behavior outcomes. Retrospective maternal self-reported drinking assessed 14 years postpartum was significantly higher than antenatal reports of consumption. Retrospective report identified 10.8 times more women as risk drinkers (≥ one drink per day) than the antenatal report. Antenatal and retrospective reports were moderately correlated and both were correlated with the Michigan Alcoholism Screening Test. Self-reported alcohol consumption during pregnancy based on retrospective report identified significantly more teens exposed prenatally to at-risk alcohol levels than antenatal, in-pregnancy reports. Retrospective report predicted more teen behavior problems (e.g., attention problems and externalizing behaviors) than the antenatal report. Antenatal report predicted younger gestational age at birth and retrospective report predicted smaller birth size; neither predicted teen IQ. These results suggest that if only antenatal, in-pregnancy maternal report is used, then a substantial proportion of children exposed prenatally to risk levels of alcohol might be misclassified. The validity of retrospective assessment of prior drinking during pregnancy as a more effective indicator of prenatal exposure was established by predicting more behavioral problems in teens than antenatal report. Retrospective report can provide valid information about drinking during a prior pregnancy and may facilitate diagnosis and subsequent interventions by educators, social service personnel, and health-care providers, thereby reducing the life-long impact of FASDs.A 14-year retrospective maternal report of alcohol consumption in pregnancy predicts pregnancy and teen outcomes - Corrected ProofJohn H. Hannigan, Lisa M. Chiodo, Robert J. Sokol, James Janisse, Joel W. Ager, Mark K. Greenwald, Virginia Delaney-Black10.1016/j.alcohol.2009.03.003Alcohol (2009)2009-12-28Alcohol2009-12-28http://www.alcoholjournal.org/article/PIIS0741832909001499/abstract?rss=yesAbstract: This study was designed to develop a zebrafish experimental model to examine defects in retinoic acid (RA) signaling caused by embryonic ethanol exposure. RA deficiency may be a causative factor leading to a spectrum of birth defects classified as fetal alcohol spectrum disorder (FASD). Experimental support for this hypothesis using Xenopus showed that effects of treatment with ethanol could be partially rescued by adding retinoids during ethanol treatment. Previous studies show that treating zebrafish embryos during gastrulation and somitogenesis stages with a pathophysiological concentration of ethanol (100mM) produces effects that are characteristic features of FASD. We found that treating zebrafish embryos with RA at a low concentration (10−9M) and 100mM ethanol during gastrulation and somitogenesis stages significantly rescued a spectrum of defects produced by treating embryos with 100mM ethanol alone. The rescued phenotype that we observed was quantitatively more similar to embryos treated with 10−9M RA alone (RA toxicity) than to untreated or 100mM ethanol-treated embryos. RA rescued defects caused by 100mM ethanol treatment during gastrulation and somitogenesis stages that include early gastrulation cell movements (anterior–posterior axis), craniofacial cartilage formation, and ear development. Morphological evidence also suggests that other characteristic features of FASD (e.g., neural axis patterning) are rescued by RA supplement.Zebrafish fetal alcohol syndrome model: effects of ethanol are rescued by retinoic acid supplement - Corrected ProofJames A. Marrs, Sherry G. Clendenon, Don R. Ratcliffe, Stephen M. Fielding, Qin Liu, William F. Bosron10.1016/j.alcohol.2009.03.004Alcohol (2009)2009-12-28Alcohol2009-12-28http://www.alcoholjournal.org/article/PIIS0741832909001530/abstract?rss=yesAbstract: Many previous attempts by fetal alcohol spectrum disorders researchers to compare data across multiple prospective and retrospective human studies have failed because of both structural differences in the collected data and difficulty in coming to agreement on the precise meaning of the terminology used to describe the collected data. Although some groups of researchers have an established track record of successfully integrating data, attempts to integrate data more broadly among different groups of researchers have generally faltered. Lack of tools to help researchers share and integrate data has also hampered data analysis. This situation has delayed improving diagnosis, intervention, and treatment before and after birth. We worked with various researchers and research programs in the Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CI-FASD) to develop a set of common data dictionaries to describe the data to be collected, including definitions of terms and specification of allowable values. The resulting data dictionaries were the basis for creating a central data repository (CI-FASD Central Repository) and software tools to input and query data. Data entry restrictions ensure that only data that conform to the data dictionaries reach the CI-FASD Central Repository. The result is an effective system for centralized and unified management of the data collected and analyzed by the initiative, including a secure, long-term data repository. CI-FASD researchers are able to integrate and analyze data of different types, using multiple methods, and collected from multiple populations, and data are retained for future reuse in a secure, robust repository.Implementation of a shared data repository and common data dictionary for fetal alcohol spectrum disorders research - Corrected ProofAndrew D. Arenson, Ludmila N. Bakhireva, Christina D. Chambers, Christina A. Deximo, Tatiana Foroud, Joseph L. Jacobson, Sandra W. Jacobson, Kenneth Lyons Jones, Sarah N. Mattson, Philip A. May, Elizabeth S. Moore, Kimberly Ogle, Edward P. Riley, Luther K. Robinson, Jeffrey Rogers, Ann P. Streissguth, Michel C. Tavares, Joseph Urbanski, Yelena Yezerets, Radha Surya, Craig A. Stewart, William K. Barnett10.1016/j.alcohol.2009.08.007Alcohol (2009)2009-12-28Alcohol2009-12-28http://www.alcoholjournal.org/article/PIIS0741832909001797/abstract?rss=yesAbstract: Despite considerable data published on cognitive and behavioral disabilities in children with fetal alcohol spectrum disorders (FASD), relatively little information is available on behavioral or pharmacological interventions for alcohol-affected children. The main goals of this article, therefore, are to summarize published intervention studies of FASD and to present a neurodevelopmental framework, based on recent findings from a number of disciplines, for designing new therapies for alcohol-affected children. This framework assumes a neuroconstructionist view, which posits that reciprocal interactions between neural activity and the brain's hardware lead to the progressive formation of intra- and interregional neural connections. In this view, behavioral interventions can be conceptualized as a series of guided experiences that are designed to produce neural activation. Based on evidence from cognitive neuroscience, it is hypothesized that specific interventions targeting executive attention and self-regulation may produce greater generalizable results than those aimed at domain-specific skills in children with FASD. In view of reciprocal interactions between environmental effects and neural structures, the proposed framework suggests that the maximum effects of interventions can eventually be achieved by optimally combining behavioral methods and cognition-enhancing drugs.A neurodevelopmental framework for the development of interventions for children with fetal alcohol spectrum disorders - Corrected ProofPiyadasa W. Kodituwakku10.1016/j.alcohol.2009.10.009Alcohol (2009)2009-12-28Alcohol2009-12-28http://www.alcoholjournal.org/article/PIIS0741832909001542/abstract?rss=yesAbstract: Many ethanol dependent women also use other drugs of abuse that may affect pregnancy outcome and long-term child neurodevelopment. This study investigated the association between drugs of abuse and concurrent use of ethanol in pregnancy. A study cohort of neonates with FAEE levels above 2nmol per gram meconium, indicative of heavy in utero ethanol exposure, was identified (n=114). Meconium and hair analyses for the presence of other drugs of abuse were obtained for some of these neonates and the rates of drug exposure were compared with the rates in a cohort of neonates who were tested negative (FAEE below 2nmol per gram meconium) for ethanol exposure (n=622). Odds ratios (ORs) for various drugs were calculated with ethanol exposure. A 15.5% positive rate for intrauterine ethanol exposure was detected. A high rate of in utero drug exposure was detected in neonates with and without in utero ethanol exposure, 60.5% versus 62.7% respectively. Neonates with heavy in utero ethanol exposure were almost twice as likely to be exposed to narcotic opiates (OR=1.90; 95% confidence interval [CI]: 1.13–3.20) and 3.3 times as likely to be exposed to amphetamine (OR=3.30; 95% CI 1.06–10.27) when compared to neonates with no ethanol exposure. Exposure to cannabinoids predicted less likely exposure to ethanol (OR=0.61; 95% CI: 0.38–0.98) and no significant difference was noted in the exposure to cocaine (OR=1.24, 95% CI: 0.81–1.91). Neonates suspected of heavy in utero ethanol exposure should be tested for other drugs of abuse and vice versa. Early detection of drug exposures can facilitate early intervention to both the neonate and the mother, thus decreasing the risk of long-term neurodevelopmental outcomes for the child, including secondary disabilities associated with fetal alcohol spectrum disorder.Heavy in utero ethanol exposure is associated with the use of other drugs of abuse in a high-risk population - Corrected ProofSarit Shor, Irena Nulman, Vivian Kulaga, Gideon Koren10.1016/j.alcohol.2009.08.008Alcohol (2009)2009-12-23Alcohol2009-12-23