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Alcohol Effects (alcohol + effects)
Kinds of Alcohol Effects Selected AbstractsAcute Alcohol Effects on Inhibitory Control and Implicit Cognition: Implications for Loss of Control Over DrinkingALCOHOLISM, Issue 8 2010Matt Field Alcohol impairs inhibitory control, and it alters implicit alcohol cognitions including attentional bias and implicit associations. These effects are seen after doses of alcohol which do not lead to global impairments in cognitive performance. We review studies which demonstrate that the effects of alcohol on inhibitory control are associated with the ability of alcohol to prime alcohol-seeking behavior. We also hypothesize that alcohol-induced changes in implicit alcohol cognitions may partially mediate alcohol-induced priming of the motivation to drink. Based on contemporary theoretical models and conceptualizations of executive function, impulsivity, and the motivational salience of alcohol-related cues, we speculate on other aspects of cognition that may underlie alcohol's effects on alcohol seeking. Inconsistencies in existing research and priorities for future research are highlighted, including dose effects and the potential interactions between chronic heavy drinking and the acute effects of alcohol on these cognitive processes. [source] Alcohol Effects on Central Nervous System Gene Expression in Genetic Animal ModelsALCOHOLISM, Issue 2 2005William J. McBride This article summarizes the proceedings of a symposium presented at the 2004 annual meeting of the Research Society on Alcoholism in Vancouver, British Columbia, Canada. The organizers and chairs were William J. McBride and Michael F. Miles. The presentations were (1) Molecular Triangulation on Gene Expression Patterns in Behavioral Responses to Acute Ethanol, by Robnet T. Kerns; (2) Gene Expression in Limbic Regions After Ethanol Self-Infusion Into the Posterior Ventral Tegmental Area, by Zachary A. Rodd; (3) Microarray Analysis of CNS Limbic Regions of Inbred Alcohol-Preferring and -Nonpreferring rats and Effects of Alcohol Drinking, by Wendy N. Strother and Howard J. Edenberg; and (4) Microarray Analysis of Mouse Lines Selected for Chronic Ethanol Withdrawal Severity: The Convergence of Basal, Ethanol Regulated, and Proximity to Ethanol Quantitative Trait Loci to Identify Candidate Genes, by Joel G. Hashimoto and Kristine M. Wiren. [source] Fetal Alcohol Spectrum,The Hidden Epidemic in Our CourtsJUVENILE AND FAMILY COURT JOURNAL, Issue 4 2001KATHRYN PAGE PH.D. ABSTRACT This article discusses the basics of Fetal Alcohol Syndrome and Fetal Alcohol Effects (FAS/E): the history, nature, prevalence, causes, and effects of prenatal exposure to alcohol. Some of the unique features of FAS/E are explored, particularly those that make it so hard to spot and those that predispose people to nonproductive or criminal activity. The presentation of FAS/E in Juvenile Court is discussed and put in the context of the multiplicity of factors pertaining to delinquency; finally, innovative interventions, approaches and resources are laid out. Issues surrounding FAS/E as they appear in Family Court are then explored, with emphasis on the intergenerational transmission of this array of conditions and how we might interrupt such transmission. [source] Intoxication With Bourbon Versus Vodka: Effects on Hangover, Sleep, and Next-Day Neurocognitive Performance in Young AdultsALCOHOLISM, Issue 3 2010Damaris J. Rohsenow Background:, This study assessed the effects of heavy drinking with high or low congener beverages on next-day neurocognitive performance, and the extent to which these effects were mediated by alcohol-related sleep disturbance or alcoholic beverage congeners, and correlated with the intensity of hangover. Methods:, Healthy heavy drinkers age 21 to 33 (n = 95) participated in 2 drinking nights after an acclimatization night. They drank to a mean of 0.11 g% breath alcohol concentration on vodka or bourbon one night with matched placebo the other night, randomized for type and order. Polysomnography recordings were made overnight; self-report and neurocognitive measures were assessed the next morning. Results:, After alcohol, people had more hangover and more decrements in tests requiring both sustained attention and speed. Hangover correlated with poorer performance on these measures. Alcohol decreased sleep efficiency and rapid eye movement sleep, and increased wake time and next-day sleepiness. Alcohol effects on sleep correlated with hangover but did not mediate the effects on performance. No effect of beverage congeners was found except on hangover severity, with people feeling worse after bourbon. Virtually no sex differences appeared. Conclusions:, As drinking to this level affects complex cognitive abilities, safety could be affected, with implications for driving and for safety-sensitive occupations. Congener content affects only how people feel the next day so does not increase risk. The sleep disrupting effects of alcohol did not account for the impaired performance so other mechanisms of effect need to be sought. As hangover symptoms correlate with impaired performance, these might be contributing to the impairment. [source] Alcohol expectancies in convicted rapists and child molestersCRIMINAL BEHAVIOUR AND MENTAL HEALTH, Issue 2 2001Anu S. Aromäki PhD Background Previous findings suggest that cognitive factors and expectancies related to drinking can mediate subjective sexual arousal as well as aggression in men. Our aim was to investigate the drinking habits and alcohol-related expectancies that might predispose men to sexually aggress in two groups of sexual offenders. Method Men convicted of rape (n = 10) were compared with men convicted of child molesting (n = 10) and with control subjects (n = 31). Current drinking habits (while not in prison) were assessed by self-report, and the extent of alcohol abuse was mapped by the Michigan Alcoholism Screening Test (MAST; Selzer, 1971). Cognitive expectancies related to alcohol use were explored by the standard Alcohol Expectancy Questionnaire (AEQ; Brown et al., 1980). Results The majority of the men who committed rape (70%) but only a third of the men convicted of child molesting were diagnosed with antisocial personality disorder. Alcohol abuse was common in men convicted of both rape and child molesting and the men convicted of rape expected significantly more positive effects from drinking than the control group. Both sex offender groups were the only groups to express significant alcohol-related cognitive expectancies linked to arousal and aggression. Expectancy patterns were directly linked to the antisocial personality characteristics. Conclusion Alcohol abuse is common in men who commit both rape and child molesting. Heavy drinking and the anticipation of alcohol effects such as sexual enhancement, arousal and aggression may facilitate sexual aggression in offenders with antisocial personality disorder. Copyright © 2001 Whurr Publishers Ltd. [source] Alcohol and mortality: methodological and analytical issues in aggregate analysesADDICTION, Issue 1s1 2001Thor Norström This supplement includes a collection of papers that aim at estimating the relationship between per capita alcohol consumption and various forms of mortality, including mortality from liver cirrhosis, accidents, suicide, homicide, ischaemic heart disease, and total mortality. The papers apply a uniform methodological protocol, and they are all based on time series data covering the post-war period in the present EU countries and Norway. In this paper we discuss various methodological and analytical issues that are common to these papers. We argue that analysis of time series data is the most feasible approach for assessing the aggregate health consequences of changes in population drinking. We further discuss how aggregate data may also be useful for judging the plausibility of individual-level relationships, particularly those prone to be confounded by selection effects. The aggregation of linear and curvilinear risk curves is treated as well as various methods for dealing with the time-lag problem. With regard to estimation techniques we find country specific analyses preferable to pooled cross-sectional/time series models since the latter incorporate the dubious element of geographical co-variation, and conceal potentially interesting variations in alcohol effects. The approach taken in the papers at hand is instead to pool the country specific results into three groups of countries that represent different drinking cultures; traditional wine countries of southern Europe, beer countries of central Europe and the British Isles and spirits countries of northern Europe. The findings of the papers reinforce the central tenet of the public health perspective that overall consumption is an important determinant of alcohol-related harm rates. However, there is a variation across country groups in alcohol effects, particularly those on violent deaths, that indicates the potential importance of drinking patterns. There is no support for the notion that increases in per capita consumption have any cardioprotective effects at the population level. [source] Evaluating theories of alcohol-related aggression using observations of young adults in barsADDICTION, Issue 6 2000Kathryn Graham Aims. The objective of the present study is to evaluate 36 explanations of alcohol-related aggression that have been proposed in the research literature in terms of their relevance to naturally-occurring incidents of aggression involving alcohol. Design. The study involved content analysis of descriptions of 105 incidents of aggression. Setting and participants. Bars frequented by young adults. Measurements. Step-by-step descriptions of incidents of aggression reported by researcher-observers based on 93 nights of observation in bars between midnight and 3 a.m. Findings. Some explanations relating to the effects of alcohol (e.g. focused on the present, reduced anxiety about sanctions or danger, heightened emotionality) and the environment (e.g. generally permissive environment, expectation by patrons that aggression will be tolerated) were found to be relevant to most incidents, while other explanations (e.g. crowding, release of pent-up anger) were directly relevant to only a few or no incidents. Incidents involving male-to-male aggression were more likely than incidents involving both males and females to be attributable to expectations, acceptance of aggression, power concerns, male honor and "macho" values. Principal components analysis identified five groupings of explanations: risk-taking effects of alcohol, cognitive impairment from alcohol, hyperemotional effects of alcohol, "macho" subculture, and permissive environment. Conclusions. The findings are consistent with a model of alcohol-related aggression that involves multiple contributing factors including alcohol effects and situational contexts. The greater relevance of certain explanations and the natural groupings of explanations point to directions for future research. [source] Alcohol inhibition of neurogenesis: A mechanism of hippocampal neurodegeneration in an adolescent alcohol abuse modelHIPPOCAMPUS, Issue 5 2010Stephanie A. Morris Abstract Adolescents diagnosed with an alcohol use disorder show neurodegeneration in the hippocampus, a region important for learning, memory, and mood regulation. This study examines a potential mechanism by which excessive alcohol intake, characteristic of an alcohol use disorder, produces neurodegeneration. As hippocampal neural stem cells underlie ongoing neurogenesis, a phenomenon that contributes to hippocampal structure and function, we investigated aspects of cell death and cell birth in an adolescent rat model of an alcohol use disorder. Immunohistochemistry of various markers along with Bromo-deoxy-Uridine (BrdU) injections were used to examine different aspects of neurogenesis. After 4 days of binge alcohol exposure, neurogenesis was decreased by 33 and 28% at 0 and 2 days after the last dose according to doublecortin expression. To determine whether this decrease in neurogenesis was due to effects on neural stem cell proliferation, quantification of BrdU-labeled cells revealed a 21% decrease in the dentate gyrus of alcohol-exposed brains. Cell survival and phenotype of BrdU-labeled cells were assessed 28 days after alcohol exposure and revealed a significant, 50% decrease in the number of surviving cells in the alcohol-exposed group. Reduced survival was supported by significant increases in the number of pyknotic-, FluoroJade B positive-, and TUNEL-positive cells. However, so few cells were TUNEL-positive that cell death is likely necrotic in this model. Although alcohol decreased the number of newborn cells, it did not affect the percentage of cells that matured into neurons (differentiation). Thus, our data support that in a model of an adolescent alcohol use disorder, neurogenesis is impaired by two mechanisms: alcohol-inhibition of neural stem cell proliferation and alcohol effects on new cell survival. Remarkably, alcohol inhibition of neurogenesis may outweigh the few dying cells per section, which implies that alcohol inhibition of neurogenesis contributes to hippocampal neurodegeneration in alcohol use disorders. © 2009 Wiley-Liss, Inc. [source] Transcallosal White Matter Degradation Detected With Quantitative Fiber Tracking in Alcoholic Men and Women: Selective Relations to Dissociable FunctionsALCOHOLISM, Issue 7 2010Adolf Pfefferbaum Introduction:, Excessive alcohol consumption can adversely affect white matter fibers and disrupt transmission of neuronal signals. Here, we examined six anatomically defined transcallosal white matter fiber bundles and asked whether any bundle was specifically vulnerable to alcohol, what aspect of white matter integrity was most affected, whether women were more vulnerable than men, and whether evidence of compromise in specific bundles was associated with deficits in balance, sustained attention, associative learning, and psychomotor function, commonly affected in alcoholics. Methods:, Diffusion tensor imaging quantitative fiber tracking assessed integrity of six transcallosal white matter bundles in 87 alcoholics (59 men, 28 women) and 88 healthy controls (42 men, 46 women). Measures included orientational diffusion coherence (fractional anisotropy, FA) and magnitude of diffusion, quantified separately for axial (longitudinal; ,L) and radial (transverse; ,T) diffusivity. The Digit Symbol Test and a test of ataxia were also administered. Results:, Alcoholism negatively affected callosal FA and ,T of all but the sensory-motor bundle. Women showed no evidence for greater vulnerability to alcohol than men. Multiple regression analyses confirmed a double dissociation: higher diffusivity in sensory-motor and parietal bundles was associated with poorer balance but not psychomotor speed, whereas higher diffusivity in prefrontal and temporal bundles was associated with slower psychomotor speed but not balance. Conclusions:, This study revealed stronger alcohol effects for FA and radial diffusivity than axial diffusivity, suggesting myelin degradation, but no evidence for greater vulnerability to alcohol in women than men. The presence of brain-behavior relationships provides support for the role of alcoholism-related commissural white matter degradation as a substrate of cognitive and motor impairment. Identification of a double dissociation provides further support for the role of selective white matter integrity in specific domains of performance. [source] Increased Activation of the ACC During a Spatial Working Memory Task in Alcohol-Dependence Versus Heavy Social DrinkingALCOHOLISM, Issue 5 2010Sabine Vollstädt-Klein Background:, Activation of the anterior cingulate cortex (ACC) in a spatial working memory task has been associated with risk factors for alcohol use disorders such as low alcohol effects and positive alcohol expectations in adolescents. To transfer these results into adults, we used the same task in adults. Methods:, During functional magnetic resonance imaging, 12 light social, 7 heavy social, and 11 non-abstinent-dependent alcohol drinkers performed a spatial working memory task and completed measures of automatic alcohol-related thoughts and behavior (Obsessive,Compulsive Drinking Scale,OCDS), alcohol use of the last 90 days, and general intelligence. Results:, Behavioral performance in the spatial working memory task was not significantly different in all 3 groups. Controlling for differences in general intelligence alcohol-dependent participants showed a higher task-related activation of the dorsal ACC (dACC) in comparison with light and heavy social drinkers. Measures of the OCDS were positively correlated with the activation in the left hippocampus and right thalamus in all participants. Conclusions:, Our results support the findings of increased dACC activation during a spatial working memory task as a risk factor for alcohol dependence. Increased task-related activation in the dACC was only observed in alcohol-dependent participants and not in heavy social drinkers with comparable alcohol consumption. Furthermore, the absence of behavioral performance differences between groups as well as an association between dACC activation and working memory performance indicates subtle working memory deficits. Low capacity of working memory has been linked to more automatic and less self-regulated behavior in studies on natural reward processing. Therefore, additional neural activation during performance of the non-alcohol-related working memory task in participants with higher OCDS values in the left hippocampus and the right thalamus may be a consequence of decreased neural capacity because of distracting alcohol-related thoughts. [source] Effects of Straight Chain Alcohols on Specific Isoforms of Adenylyl CyclaseALCOHOLISM, Issue 4 2010Mohammad Hasanuzzaman Background:, Our previous studies showed that the activity of adenylyl cyclase (AC) was enhanced by pharmacologically relevant concentrations of ethanol, that this enhancing effect of ethanol on AC activity was AC isoform specific, and that the alcohol cutoff effect for n -alkanol potentiation of AC activity was also AC isoform specific. Therefore, we hypothesized that within the cyclic AMP-generating system, AC is the target of ethanol's action and that alcohols interact directly with the AC molecules. To characterize the interaction between alcohols and AC proteins, the effects of a series of straight chain alcohols would be very valuable in understanding alcohol action at the molecular level. To our knowledge, straight chain alcohols other than n- alkanols and 1,,-diols have not been used extensively to study alcohol effects on the activity of AC or other proteins important in the alcohol research field. Methods:, The effects of a series of straight chain alcohols on D1A dopamine receptor-stimulated activity of AC isoforms type 6, 7, and 9 (AC6, AC7, and AC9) were examined in transfected Hela cells by a cAMP accumulation assay. Results:, In general, all 3 AC isoforms responded to a series of straight chain alcohols in a similar manner. The order of responsiveness is as follows: monoalcohol > diol > triol and tetraol. Within monoalcohols, 1-alcohols had larger effects than 2-alcohols. Two of 3 stereoisomers of 2,3-butanediol, [D-(-)-2,3-butanediol and meso -2,3-butanediol] showed similar enhancing effects on all 3 AC isoforms. However, the third stereoisomer, L-(+)-2,3-butanediol, inhibited AC7 activity, while it stimulated AC6 and AC9. Conclusion:, The number and the position of hydroxyl groups in straight chain alcohols play an important role in the magnitude of the enhancement on AC activity. Regardless of AC isoforms, the most effective of the straight chain alcohols seems to be the 1-alcohol (n -alkanol) for a given chain length. We found that one of the stereoisomers of 2,3-butanediol had opposite effects on AC activity depending on the AC isoform. Overall, the results are consistent with the hypotheses and demonstrate that a series of straight chain alcohols can be a valuable tool to study AC-alcohol interactions. [source] Subjective Response to Alcohol: A Critical Review of the LiteratureALCOHOLISM, Issue 3 2010Meghan E. Morean Background:, Subjective response to alcohol (SR), which reflects individual differences in sensitivity to the pharmacological effects of alcohol, may be an important endophenotype in understanding genetic influences on drinking behavior and alcohol use disorders (AUDs). SR predicts alcohol use and problems and has been found to differ by a range of established risk factors for the development of AUDs (e.g., family history of alcoholism). The exact pattern of SR associated with increased risk for alcohol problems, however, remains unclear. The Low Level of Response Model (LLR) suggests that high-risk individuals experience decreased sensitivity to the full range of alcohol effects, while the Differentiator Model (DM) asserts that high risks status is associated with increased sensitivity to alcohol's positive effects but decreased sensitivity to negative effects. Aims:, The current paper (1) reviews two prominent models of subjective response, (2) reviews extant laboratory-based research on subjective response, (3) highlights remaining gaps in our understanding and assessment of subjective response, and (4) encourages collaborative efforts to address these methodological and conceptual concerns. Methods:, This paper reviews studies which employed placebo-controlled and non-placebo-controlled alcohol challenge paradigms to assess a range of alcohol effects including impairment, stimulation, and sedation. Results:, The research literature provides at least partial support for both the LLR and DM models. High-risk individuals have been shown to have a reduced response to alcohol with respect to sedative or impairing effects, particularly on the descending limb of the blood alcohol curve (BAC). There is also evidence that ascending limb stimulant effects are more pronounced or operate differently for high-risk individuals. Discussion:, Despite commendable advances in SR research, important questions remain unanswered. Inconsistent results across studies may be attributable to a combination of an inadequate understanding of the underlying construct and methodological differences across studies (e.g., number and timing of assessments across the BAC, inclusion of a placebo condition). With respect to the underlying construct, existing measures fail to adequately distinguish between cognitive/behavioral impairment and sedation, aspects of which may be perceived positively (e.g., anxiolysis) due to their ability to act as negative reinforcers. Conclusions:, Addressing the concerns raised by the current review will be integral to making meaningful scientific progress in the field of subjective response. [source] Alcohol, Psychological Dysregulation, and Adolescent Brain DevelopmentALCOHOLISM, Issue 3 2008Duncan B. Clark While adolescent alcohol consumption has been asserted to adversely alter brain development, research in human adolescents has not yet provided us with sufficient evidence to support or refute this position. Brain constituents actively developing during adolescence include the prefrontal cortex, limbic system areas, and white matter myelin. These areas serving cognitive, behavioral, and emotional regulation may be particularly vulnerable to adverse alcohol effects. Alternatively, deficits or developmental delays in these structures and their functions may underlie liability to accelerated alcohol use trajectories in adolescence. This review will describe a conceptual framework for considering these relationships and summarize the available studies on the relationships among risk characteristics, alcohol involvement and brain development during this period. The cross-sectional designs and small samples characterizing available studies hamper definitive conclusions. This article will describe some of the opportunities contemporary neuroimaging techniques offer for advancing understanding of adolescent neurodevelopment and alcohol involvement. [source] Only Male Mice Show Sensitization of Handling-Induced Convulsions Across Repeated Ethanol Withdrawal CyclesALCOHOLISM, Issue 3 2007L.M. Veatch Background: Alcohol abuse, especially when experienced in multiple cycles of chronic abuse and withdrawal, leads to a sensitization of central nervous system hyperexcitability that may culminate in overt expression of seizures. In spite of the growing prevalence of alcohol abuse and dependence in females shown in recent epidemiologic studies, evidence of sexual dimorphism in the expression of alcohol withdrawal-induced seizures and the development of seizure sensitization following multiple cycles of ethanol (EtOH) exposure and withdrawal has not been examined in either animal models or in clinical reports. Methods: Subjects in these experiments were male and female C3H/Hecr mice. The female mice were intact or ovariectomized, with ovariectomized mice receiving 17- , -estradiol or placebo pellets. All mice were exposed to 4 cycles of exposure to 16-hour EtOH vapor, separated by 8-hour withdrawal periods. During each 8-hour withdrawal, hourly assessment of seizure propensity was assessed as handling-induced convulsions. Additional assessments were taken up to 72 hours after the final EtOH withdrawal cycle. Results: Male and female mice showed similar seizure propensity during an initial withdrawal from chronic EtOH. Across subsequent withdrawal cycles, however, male mice exhibited a robust increase in seizure severity beginning with the third withdrawal cycle. In marked contrast, female mice failed to demonstrate sensitization of seizure severity. The lack of seizure sensitization following up to 4 cycles of alcohol exposure and withdrawal could not be explained by hormonal status (presence or absence of estrogen) or by sex differences in blood alcohol levels. Conclusions: Male and female mice exposed to the same number of cycles of EtOH withdrawal demonstrate differences in expression of seizures. Males show the typical sensitization of seizures, or kindling response, which has been reported clinically as well as in animal models, but females do not. The reason for the lack of seizure sensitization in female mice remains to be elucidated, but may be related to sex differences in alcohol effects on excitatory/inhibitory neurotransmission, rather than to hormonal or blood alcohol level differences. [source] Fatty Acid Ethyl Esters in Meconium: Are They Biomarkers of Fetal Alcohol Exposure and Effect?ALCOHOLISM, Issue 7 2006Enrique M. Ostrea Jr. Background: Biomarkers of fetal exposure to alcohol are important to establish so that early detection and intervention can be made on these infants to prevent undesirable outcomes. The aim of this study was to analyze long-chain fatty acid ethyl esters (FAEEs) in meconium as potential biomarkers of fetal alcohol exposure and effect. Methods: Fatty acid ethyl esters were analyzed in the meconium of 124 singleton infants by positive chemical ionization gas chromatography/mass spectrometry (GC/MS) and correlated to maternal ethanol use. Results: A total of 124 mother/infant dyads were enrolled in the study: 31 were in the control group and 93 were in the alcohol-exposed group. The incidence (28% vs 9.7%, p=0.037) of ethyl linoleate detected in meconium was significantly higher in the alcohol-exposed groups than the control groups. Similarly, when the concentrations of ethyl linoleate in meconium were grouped (trichotomized), there was a significant linear by linear association between alcohol exposure and group concentrations of ethyl linoleate (p=0.013). Furthermore, only alcohol-exposed infants were found in the group with the highest ethyl linoleate concentration. The sensitivity of ethyl linoleate in detecting prenatal alcohol exposure was only 26.9%, and its specificity and positive predictive value were 96.8 and 96.2%, respectively. There was no significant correlation between the concentration of ethyl linoleate in meconium and absolute alcohol consumed (oz) per drinking day across pregnancy, although a trend toward a positive correlation is seen at lower amounts of alcohol consumed. Among the polyunsaturated, long-chain FAEEs, there was weak evidence that the incidence (21.5% vs 6.5%, p=0.057) and concentration (p=0.064) of ethyl arachidonate (AA) were significantly higher in the alcohol-exposed groups than the control groups. Ethyl linolenate and ethyl docosahexanoate (DHA) in meconium were found only in the alcohol group, although not at statistically significant levels. Highly significant correlations were found among the concentrations of ethyl linoleate, ethyl linolenate, ethyl AA, and ethyl DHA in meconium (correlations ranged between rs=0.203, p=0.024; and rs=0.594, p<0.001). Conclusion: We conclude that FAEEs in meconium, particularly ethyl linoleate and ethyl AA, are biomarkers of high specificity for prenatal exposure to alcohol in newborn infants. We also propose that ethyl AA and DHA could be potential biomarkers of fetal alcohol effects on the developing fetal brain and should be investigated further. [source] Impact of Alcohol Exposure After Pregnancy Recognition on Ultrasonographic Fetal Growth MeasuresALCOHOLISM, Issue 5 2006Nancy S. Handmaker Background: More than 3 decades after Jones and Smith (1973) reported on the devastation caused by alcohol exposure on fetal development, the rates of heavy drinking during pregnancy remain relatively unchanged. Early identification of fetal alcohol exposure and maternal abstinence led to better infant outcomes. This study examined the utility of biometry for detecting alcohol-related fetal growth impairment. Methods: We obtained fetal ultrasound measures from routine ultrasound examinations for 167 pregnant hazardous drinkers who were enrolled in a brief alcohol intervention study. The fetal measures for women who quit after learning of their pregnancies were compared with measures for women who continued some drinking throughout the course of their pregnancies. Because intensity of alcohol consumption is associated with poorer fetal outcomes, separate analyses were conducted for the heavy (average of ,5 drinks per drinking day) alcohol consumers. Fetal measures from the heavy-exposed fetuses were also compared with measures from a nondrinking group that was representative of normal, uncomplicated pregnancies from our clinics. Analyses of covariance were used to determine whether there were differences between groups after controlling for influences of gestational age and drug abuse. Results: Nearly half of the pregnant drinkers abstained after learning of their pregnancies. When women reportedly quit drinking early in their pregnancies, fetal growth measures were not significantly different from a non,alcohol-exposed group, regardless of prior drinking patterns. Any alcohol consumption postpregnancy recognition among the heavy drinkers resulted in reduced cerebellar growth as well as decreased cranial to body growth in comparison with women who either quit drinking or who were nondrinkers. Amphetamine abuse was predictive of larger cranial to body growth ratios. Conclusions: Alterations in fetal biometric measurements were observed among the heavy drinkers only when they continued drinking after becoming aware of their pregnancies. Although the reliance on self-reported drinking is a limitation in this study, these findings support the benefits of early abstinence and the potential for ultrasound examinations in the detection of fetal alcohol effects. [source] Alcohol-Induced Lipid and Morphological Changes in Chick Retinal DevelopmentALCOHOLISM, Issue 5 2004Yolanda Aguilera Abstract: Background: Alcohol exposure causes alterations in the lipid content of different organs and a reduction of long-chain fatty acids. During embryo development, the central nervous system is extremely vulnerable to the teratogenic effects of alcohol, and the visual system is particularly sensitive. Methods: White Leghorn chick embryos were injected with 10- and 20-,l alcohol doses into the yolk sac at day 6 of incubation. The lipid composition of the retina was analyzed in embryos at day 7 of incubation (E7), E11, E15, and E18. The percentages of phospholipids, free cholesterol, esterified cholesterol, diacylglycerides, and free fatty acids were estimated by using an Iatroscan thin layer chromatography flame ionization detector. Gas chromatography and mass spectrometry were used to determine fatty acid composition. The morphological study was performed at E7, E11, and E19 by means of semithin and immunohistochemical techniques. Results: In the retina, alcohol causes the total lipid content to change, with a remarkable increase in free cholesterol and a dramatic decrease in esterified cholesterol. Diacylglycerides and free fatty acids tend to increase. Phosphatidylcholine and phosphatidylethanolamine decrease, whereas phosphatidylserine, sphingomyelin, and phosphatidylinositol increase. The main fatty acids of the retina also undergo changes. At E7, myriotic acid increases, and oleic acid and polyunsaturated fatty acids such as arachidonic acid and docosahexaenoic acid decrease. From E18 onward, there is some recovery, except for fatty acids, which recover earlier. From a morphological point of view, alcohol effects on retinal development are various: increase of intercellular spaces in all cell layers, pyknosis with loss of cellularity in the inner nuclear cell layer and ganglion cell layer, retarded or disorderly cell migration, early cell differentiation, and loss of immunoreactivity for myelin oligodendrocyte,specific protein. Conclusions: Acute alcohol exposure during embryo development causes the lipid composition of the retina to change, with a trend to recovery in the last stages. These alterations are in line with the changes observed at a morphological level. [source] Fast, but Error-Prone, Responses During Acute Alcohol Intoxication: Effects of Stimulus-Response Mapping ComplexityALCOHOLISM, Issue 4 2004Tom A. Schweizer Abstract: Background: Although moderate doses of alcohol can impair performance on tasks that require information processing, little is known about the locus of the alcohol effects within the processing stream. This study used a psychological refractory period paradigm to investigate the effect of alcohol on the central, cognitive stage of information processing when task complexity is manipulated by altering stimulus-response compatibility. Methods: Thirty-four healthy male social drinkers were assigned to one of two groups (n= 17) that performed two tasks. Each trial consisted of a task 1 stimulus (tone) followed by a task 2 stimulus (letter) that was presented after one of four stimulus onset asynchronies (50, 200, 500, or 1100 msec). A baseline test of performance was obtained before the groups received a beverage containing either 0.0 g/kg (placebo) or 0.65 g/kg alcohol. Both groups were retested when blood alcohol concentration (BAC) was increasing and was decreasing. Results: The alcohol group made significantly more errors in task 1 compared with their drug-free baseline measure during the ascending phase of the BAC curve, and error rates increased to a greater extent for the more complex arbitrary stimulus-response mapping condition. Moreover, this increase in errors continued unabated during the descending phase of the BAC curve. Increasing BACs also slowed performance (longer reaction time), but unlike errors, reaction time returned to drug-free baseline levels when BAC was decreasing. Conclusions: The results provide evidence that an acute dose of alcohol can impair one aspect of the central, cognitive stages of information processing. The possibility that errors in information processing remain during decreasing BACs even after processing speed has returned to drug-free levels has important practical implications relating to the detrimental consequences of acute alcohol intoxication. [source] Alcohol-Induced Up-Regulation of Fibrinolytic Activity and Plasminogen Activators in Human MonocytesALCOHOLISM, Issue 8 2002Edlue M. Tabengwa Background Moderate alcohol consumption is associated with reduced risk for coronary heart disease. This may due, in part to increased fibrinolysis. Monocytes synthesize fibrinolytic proteins, tissue plasminogen activator (t-PA), urokinase plasminogen activator (u-PA), and their receptors. These studies were carried out to determine the effect of low alcohol on monocyte fibrinolytic activity and PA messenger RNA (mRNA) synthesis. Methods Peripheral blood monocytes and U937 cells were incubated in absence/presence of low alcohol (0.1%, v/v) for various times (0,1 hr), followed by incubations in the absence of alcohol (0,24 hr) before measurement of fibrinolytic activity and PA mRNA levels (reverse transcriptase polymerase chain reaction). Results Brief exposure (15 min, 4°C) of U937 cells to low alcohol resulted in an approximately 2- to 3-fold increase (269.0 ± 5.6 fmol/1 × 106 cells versus 656.0 ± 94.0 fmol/1 × 106 cells) in fibrinolytic activity. Preincubation of U937 cells and peripheral blood monocytes in low alcohol (1 hr, 37°C) followed by incubation in the absence of alcohol (24 hr) resulted in a sustained approximately 4- to 5-fold increase (414.0 ± 174.7 vs. 965.33.0 ± 104.8 fmol/1 × 106 cells) and an approximately 3- to 4-fold (20.5 ± 2.14 vs. 74 ± 2.28 fmol/2 × 106 cells, respectively) increase in fibrinolytic activity. Preincubation of monocytes with low alcohol (1 hr, 37°C) followed by incubation in the absence of alcohol (6 hr) resulted in an approximately 5- to 6-fold (0.06 ± 0.02 vs. 0.42 ± 0.02) and an approximately 2- to 3-fold (0.89 ± 0.04 vs. 2.07 ± 0.29) increase in t-PA and u-PA mRNA (reverse transcriptase polymerase chain reaction; PA/glyceraldehyde-3-phosphate dehydrogenase ratio), respectively. Conclusions These data suggest that low alcohol exerts a rapid, direct, and sustained effect on monocyte fibrinolytic activity, which may be, due in part, to increased monocyte t-PA/u-PA expression. These data provide a feasible molecular mechanism by which alcohol effects on monocyte fibrinolysis may contribute to the cardioprotective benefit associated with moderate alcohol consumption. [source] Grape Polyphenols Inhibit Chronic Ethanol-Induced COX-2 mRNA Expression in Rat BrainALCOHOLISM, Issue 3 2002Agnes Simonyi Background: Chronic ethanol has been shown to increase oxidative stress leading to neurodegenerative changes in the brain. Oxidative stress may up-regulate extracellular signal regulated kinases (ERK1/2) and, subsequently, the arachidonic acid cascade mediated by phospholipase A2 (PLA2) and cyclooxygenase (COX-2). Our earlier study showed that grape polyphenols (GP) could ameliorate oxidative damage to synaptic membrane proteins due to chronic ethanol treatment. This study was aimed at examining the effects of GP on mRNA expression of ERK1/2, cytosolic PLA2 (cPLA2), and COX-2 in different brain regions after chronic ethanol treatment. Methods: Male Sprague-Dawley rats were fed a Lieber-DeCarli liquid diet with ethanol or isocaloric amount of maltose, with or without GP for 2 months. In situ hybridization was carried out using coronal brain sections through the hippocampus. Results: Quantitative in situ hybridization showed no changes in ERK1 and cPLA2 mRNA levels in cortical areas and hippocampus after ethanol and/or GP administration. However, a decrease in ERK2 and an increase in COX-2 mRNA level was found in the hippocampus of ethanol-treated animals. GP completely inhibited the increase in COX-2 due to ethanol treatment. Conclusion: Increase in COX-2 expression may be an underlying mechanism for the increase in oxidative stress induced by chronic ethanol administration. Dietary supplementation of GP may have a beneficial role in inhibiting certain alcohol effects. [source] Serum 6-Beta-Naltrexol Levels Are Related to Alcohol Responses in Heavy DrinkersALCOHOLISM, Issue 9 2000Mary E. McCaul Background: There is strong evidence for the role of the endogenous opioid system in alcohol reinforcement and consumption; however, recent human laboratory studies and clinical trials have reported mixed effects of naltrexone (a nonselective opioid antagonist) on alcohol-related behaviors. This paper reports a secondary data analysis of a human laboratory study that examines the relationship between serum levels of 6-beta-naltrexol, the major, biologically active metabolite of naltrexone, and subjective effects of alcohol. Methods: The study used a within-subjects design to examine the effects of naltrexone (0, 50, and 100 mg/day) on subjective responses to alcohol (none, moderate, and high dose) in heavy drinkers (n= 23). Each subject received three doses of naltrexone in random order; each naltrexone dose was administered over an 8 day period on an inpatient unit, with a 1 week outpatient washout between doses. After stabilization at each of the naltrexone doses, subjects participated in three alcohol challenge sessions (none, moderate, and high dose) in random order; thus, each subject participated in a total of nine alcohol administration sessions. Results: Doubling the naltrexone dose (50 vs. 100 mg/day) doubled the mean serum 6-beta-naltrexol levels. At each naltrexone dose, there was a 4-fold range in 6-beta-naltrexol levels across subjects. Before alcohol administration, higher 6-beta-naltrexol levels were associated with higher ratings of sedation. After high-dose alcohol administration, higher 6-beta-naltrexol levels were associated with significantly lower ratings of liking and best effects. Conclusions: These findings provide further evidence of the involvement of the opioid system in the modulation of alcohol effects and suggest that serum 6-beta-naltrexol concentrations may be important in predicting therapeutic response to naltrexone. [source] Geometric morphometrics of corpus callosum and subcortical structures in the fetal-alcohol-affected brainBIRTH DEFECTS RESEARCH, Issue 1 2001Fred L. Bookstein Background Although experienced clinicians have been diagnosing fetal alcohol syndrome (FAS) for nearly 30 years, the rest of the spectrum of fetal alcohol damage is not being classified effectively. This article describes a quantification of neuroanatomical structure that may supply a useful discriminator of prenatal brain damage from alcohol. It is demonstrated in a data set of adults of both sexes. Methods Ninety adults (45 males) were examined by magnetic resonance imaging (MRI). These subjects were group-matched for age and ethnicity across three diagnoses: FAS, fetal alcohol effects (FAE), and normals. All FAS and FAE were heavily alcohol-exposed in utero; normals were not. From T1 -weighted MR brain images, we extracted 3D morphometric representations of shape for 33-landmark point configurations and 40-point outlines of the corpus callosum along its midline (a slightly nonplanar structure). Results There are striking differences between exposed and unexposed in the statistical distributions of these two shapes. The differences are better characterized by excess variance in the exposed group than by any change in average landmark or outline shape. For each sex, combining the callosal outline data with the landmark data leads to a powerful quadratic discriminator of exposed from unexposed. The discriminating features include the relationship of brain stem to diencephalon, and localized variabilities of callosal outline shape, but not diagnosis (FAS vs. FAE). Conclusions Statistical analysis of brain shape is a powerful new source of information relevant to fetal alcohol spectrum nosology and etiology. Patients with FAS and FAE do not differ in these brain shape features, but both differ from the unexposed. The aspects of brain shape that are especially variable may be entailed in the underlying neuroteratogenetic mechanisms. Teratology 64:4,32, 2001. © 2001 Wiley-Liss, Inc. [source] Fetal alcohol syndrome through the eyes of parentsADDICTION BIOLOGY, Issue 2 2004Jocie DeVries Although fetal alcohol syndrome (FAS) was first identified by research scientists in the USA in 1973, it was not until 1989 when an adoptive parent, Michael Dorris, wrote The Broken Cord, that a practical description of the disability came into public awareness. Within the next 2 years, parents of children diagnosed with this disability teemed up with interested professionals to organize the FAS Family Resource Institute (FAS*FRI). This educational non-profit organization has now devoted over a decade to their mission to identify, understand and care for individuals with fetal alcohol syndrome/effects (FAS/E) and to prevent this disability from occurring in future generations. Their mission has necessitated the identification of a behavioral phenotype for FAS/E, the development of a professional training curriculum, and operation of a national family advocacy and mentoring network. By adding their own families' experiences to the information gathered from thousands of other families with diagnosed children, they have accumulated enough experiential, frontline reports which are similar enough to serve as their research science base. [source] Pre-operative screening for excessive alcohol consumption among patients scheduled for elective surgeryDRUG AND ALCOHOL REVIEW, Issue 2 2007SWATI SHOURIE Abstract Pre-operative intervention for excessive alcohol consumption among patients scheduled for elective surgery has been shown to reduce complications of surgery. However, successful intervention depends upon an effective and practical screening procedure. This study examines current screening practices for excessive alcohol consumption amongst patients scheduled for elective surgery in general hospitals. It also examines the appropriateness of potential sites and staff for pre-operative screening. Forms used routinely to assess alcohol consumption in the pre-admission clinics (PAC) of eight Sydney hospitals were examined. In addition, the appropriateness of six staff categories (surgeons, surgeons' secretaries, junior medical officer, anaesthetists, nurses and a research assistant) and of two sites (surgeons' office and PAC) in conducting additional screening was assessed at two hospitals. Outcomes included observed advantages and disadvantages of sites and personnel, and number of cases with excessive drinking identified. There was duplication in information collected routinely on alcohol use in the PACs in eight Sydney Hospitals. Questions on alcohol consumption in patient self-completion forms were not validated. The PAC provided for efficient screening but time to surgery was typically too short for successful intervention in many cases. A validated tool and efficient screening procedure is required to detect excessive drinking before elective surgery. Patients often present to the PAC too close to the time of surgery for any change in drinking to reverse alcohol's effects. The role of the referring general practitioner and of printed advice from the surgeon in preparing patients for surgery needs further investigation. [source] Individual vulnerability to escalated aggressive behavior by a low dose of alcohol: decreased serotonin receptor mRNA in the prefrontal cortex of male miceGENES, BRAIN AND BEHAVIOR, Issue 1 2010S. Chiavegatto Low to moderate doses of alcohol consumption induce heightened aggressive behavior in some, but not all individuals. Individual vulnerability for this nonadaptive behavior may be determined by an interaction of genetic and environmental factors with the sensitivity of alcohol's effects on brain and behavior. We used a previously established protocol for alcohol oral self-administration and characterized alcohol-heightened aggressive (AHA) mice as compared with alcohol non-heightened (ANA) counterparts. A week later, we quantified mRNA steady state levels of several candidate genes in the serotonin [5-hydroxytryptamine (5-HT)] system in different brain areas. We report a regionally selective and significant reduction of all 5-HT receptor subtype transcripts, except for 5-HT3, in the prefrontal cortex of AHA mice. Comparable gene expression profile was previously observed in aggressive mice induced by social isolation or by an anabolic androgenic steroid. Additional change in the 5-HT1B receptor transcripts was seen in the amygdala and hypothalamus of AHA mice. In both these areas, 5-HT1B mRNA was elevated when compared with ANA mice. In the hypothalamus, AHA mice also showed increased transcripts for 5-HT2A receptor. In the midbrain, 5-HT synthetic enzyme, 5-HT transporter and 5-HT receptors mRNA levels were similar between groups. Our results emphasize a role for postsynaptic over presynaptic 5-HT receptors in mice which showed escalated aggression after the consumption of a moderate dose of alcohol. This gene expression profile of 5-HT neurotransmission components in the brain of mice may suggest a vulnerability trait for alcohol-heightened aggression. [source] Acute Alcohol Effects on Inhibitory Control and Implicit Cognition: Implications for Loss of Control Over DrinkingALCOHOLISM, Issue 8 2010Matt Field Alcohol impairs inhibitory control, and it alters implicit alcohol cognitions including attentional bias and implicit associations. These effects are seen after doses of alcohol which do not lead to global impairments in cognitive performance. We review studies which demonstrate that the effects of alcohol on inhibitory control are associated with the ability of alcohol to prime alcohol-seeking behavior. We also hypothesize that alcohol-induced changes in implicit alcohol cognitions may partially mediate alcohol-induced priming of the motivation to drink. Based on contemporary theoretical models and conceptualizations of executive function, impulsivity, and the motivational salience of alcohol-related cues, we speculate on other aspects of cognition that may underlie alcohol's effects on alcohol seeking. Inconsistencies in existing research and priorities for future research are highlighted, including dose effects and the potential interactions between chronic heavy drinking and the acute effects of alcohol on these cognitive processes. [source] Human Variation in Alcohol Response Is Influenced by Variation in Neuronal Signaling GenesALCOHOLISM, Issue 5 2010Geoff Joslyn Background:, Alcohol use disorders (AUD) exhibit the properties shared by common conditions and diseases classified as genetically complex. The etiology of AUDs is heterogeneous involving mostly unknown interactions of environmental and heritable factors. A person's level of response (LR) to alcohol is inversely correlated with a family history and the development of AUDs. As an AUD endophenotype, alcohol LR is hypothesized to be less genetically complex and closer to the primary etiology of AUDs. Methods:, A genome wide association study (GWAS) was performed on subjects characterized for alcohol LR phenotypes. Gene Set Enrichment Analysis (GSEA) of the GWAS data was performed to determine whether, as a group, genes that participate in a common biological function (a gene set) demonstrate greater genetic association than would be randomly expected. Results:, The GSEA analysis implicated variation in neuronal signaling genes, especially glutamate signaling, as being involved in alcohol LR variability in the human population. Conclusions:, These data, coupled with cell and animal model data implicating neuronal signaling in alcohol response, support the conclusion that neuronal signaling is mechanistically involved in alcohol's cellular and behavioral effects. Further, these data suggest that genetic variation in these signaling pathways contribute to human variation in alcohol response. Finally, this concordance of the cell, animal, and human findings supports neuronal signaling, particularly glutamate signaling, as a prime target for translational studies to understand and eventually modulate alcohol's effects. [source] Effects of a Moderate Evening Alcohol Dose.ALCOHOLISM, Issue 8 2007I: Sleepiness Background: Few studies examining alcohol's effects consider prior sleep/wake history and circadian timing. We examined introspective and physiological sleepiness on nights with and without moderate alcohol consumption in well-rested young adults at a known circadian phase. Methods: Twenty-nine adults (males=9), ages 21 to 25 years (M=22.6, SD=1.2), spent 1 week on an at-home stabilized sleep schedule (8.5 or 9 hours), followed by 3 in-lab nights: adaptation, placebo, and alcohol. Alcohol (vodka; 0.54 g/kg for men; 0.49 g/kg for women) or placebo beverage was consumed over 30 minutes ending 1 hour before stabilized bedtime. In addition to baseline, 3 sleep latency tests (SLTs) occurred after alcohol/placebo ingestion (15, 16.5, and 18 hours after waking). Stanford Sleepiness Scales (SSS) and Visual Analog Scales (VAS) of sleepiness were completed before each SLT and approximately every 30 minutes. The Biphasic Alcohol Effects Scale (BAES) was administered a total of 4 times (baseline, 5, 60, and 90 minutes postalcohol/placebo). Subjects' circadian phase was determined from melatonin levels in saliva samples taken at approximately 30-minute intervals. Results: All sleepiness and sedation measures increased with time awake. Only SSS and BAES sedation measures showed higher levels of sleepiness and sedation after alcohol compared with placebo. The mean circadian phase was the same for assessments at both conditions. Conclusions: Alcohol did not increase physiological sleepiness compared with placebo nor was residual sedation evident under these conditions. We conclude that the effects on sleepiness of a moderate dose of alcohol are masked when sleep,wake homeostatic and circadian timing influences promote high levels of sleepiness. [source] Effects of Variation at the ALDH2 Locus on Alcohol Metabolism, Sensitivity, Consumption, and Dependence in EuropeansALCOHOLISM, Issue 7 2006Peter A. Dickson 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. [source] Use of Genetic Analyses to Refine Phenotypes Related to Alcohol Tolerance and DependenceALCOHOLISM, Issue 2 2001John C. Crabbe Various explanations for the dependence on alcohol are attributed to the development of tolerance to some of alcohol's effects, alterations in sensitivity to its rewarding effects, and unknown pathologic consequences of repeated exposure. All these aspects of dependence have been modeled in laboratory rodents, and these studies have consistently shown a significant influence of genetics. Genetic mapping studies have identified the genomic location of the specific genes for some of these contributing phenotypes. In addition, studies have shown that some genes in mice seem to affect both alcohol self-administration and alcohol withdrawal severity: genetic predisposition to high levels of drinking covaries with genetic predisposition to low withdrawal severity, and vice versa. Finally, the role of genetic background on which genes are expressed is important, as are the specifics of the environment in which genetically defined animals are tested. Understanding dependence will require disentangling the multiple interactions of many contributing phenotypes, and genetic analyses are proving very helpful. However, rigorous understanding of both gene-gene and gene-environment interactions will be required to interpret genetic experiments clearly. [source] | ||||||||||||||||