Effects Of Acute Alcohol Intoxication Research Articles

Effect of acute alcohol consumption on blunt bowel mesenteric injury: a retrospective analysis

BackgroundThe effect of alcohol consumption on trauma remains controversial. The effects of alcohol on hemorrhage and peritonitis after blunt abdominal trauma have rarely been discussed. This study aimed to explore the effects of acute alcohol intoxication on the clinical characteristics, injury patterns, and outcomes in a surgical blunt bowel mesenteric injury (BBMI) cohort.MethodsA retrospective data analysis was performed using trauma cases of patients who had been tested for alcohol and had surgically proven BBMI from a Trauma Registry System from 2009 to 2021. Patients were grouped according to their positive blood alcohol concentration (BAC; >0.5% vs. no BAC; less than 0.5% no BAC) upon arrival at the emergency department (ED). The injury characteristics, physiological parameters, and outcomes with respect to post-injury complications and mortality were assessed.ResultsIn total, 142 patients with surgical BBMI were included. Of these, 116 and 26 patients were assigned to the BAC-negative and BAC-positive groups, respectively. The overall injury severity, injury pattern, and age were comparable between the groups. The patients in the BAC-positive group had a significantly lower systolic blood pressure (99 mmHg vs. 119 mmHg; p = 0.046), worse shock index (0.96 vs. 0.82; p = 0.048), and lower percentage and number of packed red blood cells transfused (34.6% vs. 57.8%; p = 0.032 and 0 U vs. 2 U; p = 0.031) than those in the BAC-negative group. Additionally, although not statistically significant, patients in the BAC-positive group had lower leukocyte counts (9,700 cells/mm3 vs. 11,600 cells/mm3; p = 0.165 ) at the ED. However, significantly reduced percentages of leukocytes ≥ 12,000 cells/mm3 (26.9% vs. 48.3%; p = 0.048) and ≥ 12,000 or ≤ 4,000 cells/mm3 (26.9% vs. 50.9%; p = 0.027) were observed in the BAC-positive group at the ED. Furthermore, the 30-day mortality rate did not show statistically significant differences, and there was a higher incidence of bowel-related mortality in the BAC-positive group (11.5% vs. 1.7%, p = 0.043).ConclusionsFor patients with BBMI arriving alive to the hospital, acute alcohol consumption was associated with significantly worse hemodynamic parameters, interfered inflammation status, and higher bowel related mortality rate.

Binge drinking episode causes acute, specific alterations in systemic and hepatic inflammation-related markers.

Frequent binge drinking is a known contributor to alcohol-related harm, but its impact on systemic and hepatic inflammation is not fully understood. We hypothesize that changes in immune markers play a central role in adverse effects of acute alcohol intake, especially in patients with early liver disease. To investigate the effects of acute alcohol intoxication on inflammation-related markers in hepatic and systemic venous plasma in people with alcohol-related liver disease (ArLD), non-alcoholic fatty liver disease (NAFLD) and healthy controls. Thirty-eight participants (13 with ArLD, 15 with NAFLD and 10 healthy controls) received 2.5 mL of 40% ethanol per kg body weight via a nasogastric tube. Seventy-two inflammation-related markers were quantified in plasma from hepatic and systemic venous blood, at baseline, 60 and 180 min after intervention. Alcohol intervention altered the levels of 31 of 72 and 14 of 72 markers in the systemic and hepatic circulation. All changes observed in the hepatic circulation were also identified in the systemic circulation after 180 min. Only FGF21 and IL6 were increased after alcohol intervention, while the remaining 29 markers decreased. Differences in response to acute alcohol between the groups were observed for 8 markers, and FGF21 response was blunted in individuals with steatosis. Acute alcohol intoxication induced changes in multiple inflammation-related markers, implicated in alcohol metabolism and hepatocellular damage. Differences identified between marker response to binge drinking in ArLD, NAFLD and healthy controls may provide important clues to disease mechanisms and potential targets for treatment. NCT03018990.

Nerve Growth Factor in Psychiatric Disorders: A Scoping Review.

Neurotrophins have been implicated in multiple psychiatric disorders. Nerve Growth Factor (NGF) is one of the major neurotrophins that has attracted much research interest. Therefore, we undertook, to the best of our knowledge, the first scoping review encompassing all major psychiatric disorders and their relation to NGF. This review aimed to identify the current position of NGF in psychiatric research and to outline present gaps in knowledge, which can be answered with a more detailed systematic review in the future. Suitable studies were identified using PubMed. A total of 20 studies were included in the review: two on bipolar affective disorder (BPAD), three on schizophrenia, seven on depression, and eight on alcohol use disorder. NGF levels are definitively reduced in BPAD and depression, while NGF levels in schizophrenia decreased further after treatment than in the drug-naïve state. The effect of treatment on NGF levels in depression varied based on treatment modalities and severity of depression. In patients with depression, raised NGF was a predictor of conversion to bipolar disorder (BD). NGF levels were raised in acute alcohol intoxication and withdrawal but normalized slowly as abstinence was maintained. NGF may play a protective role in preventing the toxic ill effect of acute alcohol intoxication on the central nervous system. Based on current knowledge, NGF levels may be a useful biomarker of a chronic mental stress condition. However, further research is needed before it can be used to identify a specific psychiatric illness or predict treatment response.

Elevated creatinine kinase levels amongst Dutch adolescents with acute alcohol intoxication

This study aims to explore the prevalence of creatinine kinase elevation amongst a sample of Dutch adolescents admitted for acute alcohol intoxication. The data on all admitted adolescents < 18 years old with acute alcohol intoxication between 2008 and 2021 were collected from a Dutch major district general hospital, Reinier de Graaf Gasthuis, in Delft. Overall, 495 adolescents who were treated for symptoms of acute alcohol intoxication during this period were included in the study. When evaluating the blood samples of the included patients, elevated creatinine kinase levels were found in 60% of the cases, with a mean of 254 U/I (normal value ≤ 145 U/I). A confirmed diagnosis of rhabdomyolysis (increase in CK > fivefold the upper limit of normal) was present in 4.4% of cases. Moreover, using a linear regression this study found that a higher blood alcohol concentration was associated with higher creatinine kinase levels, when adjusted for positive drug screenings amongst the adolescents with acute alcohol intoxication (p = 0.027; β = 66.88; 95% CI 7.68 − 126.08). Conclusions: This is the first study focusing on how acute alcohol intoxication affects adolescents’ muscle tissue. The results could potentially help to prevent alcohol use within the sports world. It could also aid understanding of how acute alcohol intoxication influences the breakdown of adolescents’ muscle tissue.What is Known:• Alcohol, alongside pharmaceutical agents and illicit drugs, is a significant cause of rhabdomyolysis (increase in creatinine kinase > fivefold the upper limit of normal).• Creatinine kinase elevation in alcohol intoxicated patients may be as a result of direct “muscular” toxicity” (myotoxicity) or from prolonged immobilization and ischemic compression induced by coma.What is New:• Our retrospective cohort study is a pioneer in addressing the effect of acute alcohol intoxication amongst adolescents (< 18 years) upon muscle tissue (creatinine kinase level) within a large population. When evaluating the blood samples of the included population, elevated creatinine kinase levels were found in 60% of the cases, with a mean of 254 U/I (normal value ≤ 145 U/I).• There is an association between alcohol intoxication and elevated creatinine kinase levels amongst adolescents. Future research is needed to further understand the pathophysiology and causality of this interaction.

The effect of acute alcohol intoxication on alcohol cue salience: An event-related brain potential study.

Alcohol cue salience is considered core to the broader understanding of drinking behaviors. In the present research, we sought to build the knowledge of alcohol cue salience by exploring P3 responses to alcohol images among social drinkers within a large-scale alcohol-administration study. Participants (N = 246) were randomly assigned to receive either a moderate dose of alcohol (target BAC = .08%) or a nonalcoholic control beverage. Following beverage administration, participants engaged in image-viewing tasks while EEG was recorded. We examined the impact of alcohol on the amplitude of P3 responses to pictures of alcoholic versus nonalcoholic beverages, exploring both beverage-manipulation and individual-difference moderators of these effects. Results revealed a significant effect of acute alcohol intoxication on P3 responses across stimulus types, with the overall amplitude of P3 being significantly smaller among participants consuming alcohol versus a nonalcoholic beverage. In addition, results revealed a significant main effect of image type, such that P3 amplitude was larger for alcohol images compared to nonalcohol images. No interactions emerged between stimulus type and beverage condition or stimulus type and AUD risk level. With the aim of better understanding the potential influence of the broader context on responses to individual cues, the present study examined the perceived salience of alcohol cues within a drinking setting. Findings provide evidence for alcohol cue salience that is both robust and also widespread across drinkers. More generally, the present study's findings may offer new directions for understanding neurocognitive processes of alcohol cue salience across contexts. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Assessing driving-relevant attentional impairment after a multiday drinking session: A two-phase pilot study.

BackgroundThe possibility of residual impairment of cognitive performance after multiday drinking sessions is particularly important given the potential for the deleterious effects of fatigue and hangover. This pilot study aimed to devise a methodology to compare sober performance on driving‐relevant attentional tasks at the end of a 4‐day music festival with performance at varying levels of the breath–alcohol curve.MethodsFifty‐two participants completed selective and sustained attention tasks at a breath alcohol concentration (BrAC) of 0.00%, 0.05%, and 0.08% following acute dosing in a controlled laboratory setting. A subset of participants (n = 13) were then tested at the conclusion of a 4‐day music festival at 0.00% BrAC, with task performance compared with laboratory results.ResultsDuring the laboratory phase, sustained attention was poorer at the 0.05% ascending timepoint only (compared to 0.00% BrAC). During the festival phase, participants made a greater number of errors on the selective attention task predeparture than at 0.00% and 0.05% BrAC in the laboratory. Sustained attention performance was poorer while intoxicated in the laboratory.ConclusionsOur findings suggest that the absence of blood alcohol acutely may not be indicative of unimpaired cognitive performance and that other factors related to multiday drinking may produce driving‐related attentional deficits. The findings reinforce the need to measure attentional performance in real‐world drinking contexts despite the methodological complexities of doing so. A larger study is warranted to replicate the findings and should include attentional measures that either are more sensitive to the effects of acute alcohol intoxication than those in our study or are based on a driving simulator.

ДОФАМИНЕРГИЧЕСКАЯ СИСТЕМА ГИПОТАЛАМУСА И СТРИАТУМА ГОЛОВНОГО МОЗГА КРЫС ПРИ КОМПЛЕКСНОМ ВОЗДЕЙСТВИИ ГИПОДИНАМИИ И ОСТРОЙ АЛКОГОЛЬНОЙ ИНТОКСИКАЦИИ

Background. The growth of industrialization is accompanied by a decrease in human motor activity, and chronic stress increases the risk of alcoholism. The combination of these factors has a negative effect on the physiological and biochemical processes in the body. Purpose of work. To determine the state of the components of the dopaminergic system in the hypothalamus and striatum of rats during acute alcoholization against the background of hypodynamia. Material and methods. The experiment was carried out on male rats weighing 180-200 g, which, after hypodynamia for a period of 7, 14 and 28 days, were once injected with 25% alcohol at a dose of 3.5 g / kg. The content of the components of the dopaminergic system was determined by high performance liquid chromatography. Results. The striatum is characterized by a decrease in the activity of the dopaminergic system on the 7th day of hypodynamia, followed by its activation with an increase in the period of immobilization to 28 days. In the hypothalamus in the early stages of hypodynamia with subsequent OAI, the changes are poorly expressed, however, on the 28th day, dopamine turnover is activated. Conclusions. The combined effect of acute alcohol intoxication and hypodynamia leads to more pronounced changes in the dopaminergic system in the striatum than in the hypothalamus. Acute alcohol intoxication has a stimulating effect on the dopaminergic system of the hypothalamus and striatum only for long periods of hypodynamia (28 days).

Effect of acute alcohol intoxication on scale-free neural activity in the lateral septum in rats

Electrophysiological recordings of brain activity show both oscillatory dynamics that typically are analyzed in the time-frequency domain to describe brain oscillatory phenomena and scale-free arrhythmic activity defined as neural noise. Recent studies consider this arrhythmic fractal dynamics of neural noise as a sensitive biomarker of a number of cognitive processes, activity of neurotransmitter systems, changes that accompany neurodegenerative and psychiatric disorders including alcohol use disorder. We tested the changes in neural noise induced by acute alcohol intoxication in the lateral septum for the entire spectrum (1–200 Hz) of local field potential signal and for frequency specific ranges (delta, theta, beta, gamma and epsilon bands). Five male Wistar rats were implanted with intracranial electrodes and local field potential signal was measured for baseline activity and activity induced by acute ethanol intoxication (2 g/kg). Change in neural noise dynamics was assessed as a change in the slope of linear regression fit of power spectral density curves in double logarithmic scale. In our study alcohol resulted in lower incline of scale-free activity in the lateral septum for high frequency range and for the whole spectrum, which is interpreted generally as increase in neural noise and change in neuronal processing in a more stochastic way initiated by the acute alcohol intoxication. At the same time, we observed decrease in neural noise for low frequency range. The observed changes may be related to the shift of the excitatory-inhibitory balance towards inhibition and changes in neurotransmission mostly in the GABAergic system. Scale-free activity was sensitive in the conditions of acute alcohol intoxication, therefore to understand its role in alcohol use disorder we need more data and studies on the underlying processes. Future studies should include simultaneous recordings and analysis of arrhythmic dynamics with the oscillatory and multiunit spiking activity in the lateral septum. It can reveal the contribution of different-scale processes in changes driven by acute alcohol intoxication and clarify the specific electrophysiological mechanisms.

MRI Analysis Of the Water Content Change In the Brain During Acute Ethanol Consumption Via Quantitative Water Mapping.

Alcohol consumption influences the water balance in the brain. While the impact of chronic alcohol misuse on cerebral water content has been the subject of several studies, less is known about the effects of acute alcohol misuse, with contradictory results in the literature. Therefore, we investigated the effects of acute alcohol intoxication on cerebral water content using a precise quantitative magnetic resonance imaging (MRI) sequence. In a prospective study, we measured cerebral water content in 20 healthy volunteers before alcohol consumption and after reaching a breath alcohol concentration of 1 ‰. A quantitative MRI water mapping sequence was conducted on a clinical 3 T system. Non-alcoholic fluid input and output were documented and accounted for. Water content was assessed for whole brain, grey and white matter and more specifically for regions known to be affected by acute or chronic alcohol misuse (occipital and frontal lobes, thalamus and pons). Changes in the volume of grey and white matter as well as the whole brain were examined. Quantitative cerebral water content before and after acute alcohol consumption did not differ significantly (P≥0.07), with changes often being within the range of measurement accuracy. Whole brain, white and grey matter volume did not change significantly (P≥0.12). The results of our study show no significant water content or volume change in the brain after recent alcohol intake in healthy volunteers. This accounts for the whole brain, grey and white matter, occipital and frontal lobes, thalamus and pons.

Acute alcohol intoxication modulates the temporal dynamics of resting electroencephalography networks.

This study aimed to provide a currently missing link between general intoxication-induced changes in overall brain activity and the multiple cognitive control deficits typically observed during acute alcohol intoxication. For that purpose, we analyzed the effects of acute alcohol intoxication (1.1‰) on the four archetypal electroencephalography (EEG) resting networks (i.e., microstates A-D) and their temporal dynamics (e.g., coverage and transitions from one microstate to another), as well as on self-reported resting-state cognition in n = 22 healthy young males using a counterbalanced within-subject design. Our microstate analyses indicated that alcohol increased the coverage of the visual processing-related microstate B at the expense of the autonomic processing-related microstate C. Add-on exploratory analyses revealed that alcohol increased transitions from microstate C to microstate B and decreased bidirectional transitions between microstate C and the attention-related microstate D. In line with the observed alcohol-induced decrease of the autonomic processing-related microstate C, participants reported decreases of their somatic awareness during intoxication, which were positively associated with more transitions from microstate C to microstate B. In sum, the observed effects provide mechanistic insights into how alcohol might hamper cognitive processing by generally prioritizing the bottom-up processing of visual stimuli over top-down internal information processing. The fact that this was found during the resting state further proves that alcohol-induced changes in brain activity are continuously present and do not only emerge during demanding situations or tasks.

"Twenty-first birthday drinking: Extreme drinking episodes and white matter microstructural changes in the fornix and corpus callosum": Retraction of Boness et al. (2019).

Reports the retraction of "Twenty-first birthday drinking: Extreme-drinking episodes and white matter microstructural changes in the fornix and corpus callosum" by Cassandra L. Boness, Ozlem Korucuoglu, Jarrod M. Ellingson, Anne M. Merrill, Yoanna E. McDowell, Constantine J. Trela, Kenneth J. Sher, Thomas M. Piasecki and John G. Kerns (Experimental and Clinical Psychopharmacology, 2020[Oct], Vol 28[5], 553-566). The explanation for the retraction: In preparing to use the DTI images for secondary data analysis, it was discovered that multiple participants had the wrong DTI data included for Session 1 analyses. This was due to a file transfer error that incorrectly substituted another participant's DTI data for the correct DTI data. In correcting the error and reanalyzing the data, our findings changed in ways that were nontrivial and, thus, exceed what would be appropriate for a corrigendum. (The following abstract of the original article appeared in record 2019-72844-001.) The 21st birthday celebration is characterized by extreme alcohol consumption. Accumulating evidence suggests that high-dose bingeing is related to structural brain changes and cognitive deficits. This is particularly problematic in the transition from adolescence to adulthood when the brain is still maturing, elevating the brain's sensitivity to the acute effects of alcohol intoxication. Heavy drinking is associated with reduced structural integrity in the hippocampus and corpus callosum and is accompanied by cognitive deficits. However, there is little research examining changes in the human brain related to discrete heavy-drinking episodes. The present study investigated whether alcohol exposure during a 21st birthday celebration would result in changes to white matter microstructure by utilizing diffusion tensor imaging measures and a quasi-experimental design. By examining structural changes in the brain from pre- to postcelebration within subjects (N = 49) prospectively, we were able to more directly observe brain changes following an extreme-drinking episode. Region of interest analyses demonstrated increased fractional anisotropy in the posterior fornix (p < .0001) and in the body of the corpus callosum (p = .0029) from pre- to postbirthday celebration. These results suggest acute white matter damage to the fornix and corpus callosum following an extreme-drinking episode, which is especially problematic during continued neurodevelopment. Therefore, 21st birthday drinking may be considered an important target event for preventing acute brain injury in young adults. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Effect of acute alcohol intoxication on mortality, coagulation, and fibrinolysis in trauma patients.

The effect of alcohol on the outcome and fibrinolysis phenotype in trauma patients remains unclear. Hence, we performed this study to determine whether alcohol is a risk factor for mortality and fibrinolysis shutdown in trauma patients. A total of 686 patients who presented to our trauma center and underwent rotational thromboelastometry were included in the study. The primary outcome was in-hospital mortality. Logistic regression analysis was performed to determine whether alcohol was an independent risk factor for in-hospital mortality and fibrinolysis shutdown. The rate of in-hospital mortality was 13.8% and blood alcohol was detected in 27.7% of the patients among our study population. The patients in the alcohol-positive group had higher mortality rate, higher clotting time, and lower maximum lysis, more fibrinolysis shutdown, and hyperfibrinolysis than those in the alcohol-negative group. In logistic regression analysis, blood alcohol was independently associated with in-hospital mortality (odds ratio [OR] 2.578; 95% confidence interval [CI], 1.550-4.288) and fibrinolysis shutdown (OR 1.883 [95% CI, 1.286-2.758]). Within the fibrinolysis shutdown group, blood alcohol was an independent predictor of mortality (OR 2.168 [95% CI, 1.030-4.562]). Alcohol is an independent risk factor for mortality and fibrinolysis shutdown in trauma patients. Further, alcohol is an independent risk factor for mortality among patients who experienced fibrinolysis shutdown.

Twenty-first birthday drinking: Extreme-drinking episodes and white matter microstructural changes in the fornix and corpus callosum.

The 21st birthday celebration is characterized by extreme alcohol consumption. Accumulating evidence suggests that high-dose bingeing is related to structural brain changes and cognitive deficits. This is particularly problematic in the transition from adolescence to adulthood when the brain is still maturing, elevating the brain's sensitivity to the acute effects of alcohol intoxication. Heavy drinking is associated with reduced structural integrity in the hippocampus and corpus callosum and is accompanied by cognitive deficits. However, there is little research examining changes in the human brain related to discrete heavy-drinking episodes. The present study investigated whether alcohol exposure during a 21st birthday celebration would result in changes to white matter microstructure by utilizing diffusion tensor imaging measures and a quasi-experimental design. By examining structural changes in the brain from pre- to postcelebration within subjects (N = 49) prospectively, we were able to more directly observe brain changes following an extreme-drinking episode. Region of interest analyses demonstrated increased fractional anisotropy in the posterior fornix (p < .0001) and in the body of the corpus callosum (p = .0029) from pre- to postbirthday celebration. These results suggest acute white matter damage to the fornix and corpus callosum following an extreme-drinking episode, which is especially problematic during continued neurodevelopment. Therefore, 21st birthday drinking may be considered an important target event for preventing acute brain injury in young adults. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Spatio-temporal effects of acute alcohol intoxication on endocannabinoid system in rat brain and blood.

The endocannabinoid system (ECS) has been shown to play a critical role in the regulation of alcohol intake and alcohol-related behaviors. However, there are discrepancies between studies examining the interaction of the ECS and alcohol administration due to different experimental procedures. The present study aims at clarifying the time course effects of acute alcohol consumption on the ECS in the peripheral circulatory systems and central nervous systems of the same cohort of subjects. We have closely monitored the critical indicators reflecting changes of the ECS during the entire process from alcohol absorption to its metabolization, after acute alcohol (4.5g/kg) intake by intragastric administration, including two key endocannabinoids (arachidonoylethanolamide and 2-arachidonoylglycerol) and their hydrolytic enzymes (fatty acid amide hydrolase and monoacylglycerol lipase) in blood and three brain regions, as well as a crucial and abundant receptor (cannabinoid 1 receptor) of the ECS in the three brain regions. Our results indicate that acute alcohol consumption inhibits endocannabinoid (eCB) production in the blood and in the prefrontal cortex of the brain, whereas the reverse was observed in the brain regions of the hippocampus and striatum. The variation between levels of two hydrolytic enzymes in the blood and in the three brain regions failed to reach statistical significance. After acute alcohol consumption, CB1R levels in striatum, hippocampus, and prefrontal cortex showed a similar trend of increasing, while the significant changes occurred at different time points. The present findings reveal different ligand-receptor changing patterns in the blood and in different brain regions, supporting the notion that the ECS plays a vital role in acute alcohol intoxication. Additionally, the temporal effects of alcohol on key elements of the ECS of blood and different brain nuclei were different. Our investigation may lead to a deeper understanding of the effect of acute alcohol consumption on the ECS.

Acute Alcohol Effects on Response Inhibition Depend on Response Automatization, but not on GABA or Glutamate Levels in the ACC and Striatum.

Alcohol increases GABAergic signaling and decreases glutamatergic signaling in the brain. Variations in these neurotransmitter levels may modulate/predict executive functioning. Matching this, strong impairments of response inhibition are one of the most consistently reported cognitive/behavioral effects of acute alcohol intoxication. However, it has never been investigated whether baseline differences in these neurotransmitters allow to predict how much alcohol intoxication impairs response inhibition, and whether this is reflected in neurophysiological measures of cognitive control. We used MR spectroscopy to assess baseline (i.e., sober) GABA and glutamate levels in the anterior cingulate cortex (ACC) and striatum in n = 30 healthy young males, who were subsequently tested once sober and once intoxicated (1.01 permille). Inhibition was assessed with the sustained attention to response task (SART). This paradigm also allows to examine the effect of different degrees of response automatization, which is a known modulator for response inhibition, but does not seem to be substantially impaired during acute intoxication. As a neurophysiological correlate of response inhibition and control, we quantified EEG-derived theta band power and located its source using beamforming analyses. We found that alcohol-induced response inhibition deficits only occurred in the case of response automatization. This was reflected by decreased theta band activity in the left supplementary motor area (SMA), which may reflect modulations in the encoding of a surprise signal in response to inhibition cues. However, we did not find that differences in baseline (i.e., sober) GABA or glutamate levels significantly modulated differences in the size of alcohol-induced inhibition deficits.

The Interaction of Rape Myth Acceptance and Alcohol Intoxication on Bystander Intervention.

Bystander interventions for sexual assault promote third-party interference. People who endorse rape myths blame victims more and perpetrators less; consequently, rape myth acceptance (RMA) can impede helping behaviors toward sexual assault victims. Acute alcohol intoxication may exacerbate the effects of RMA on bystander intervention. In this study, we examined the influence of RMA-and potential moderating effect of acute alcohol intoxication-on predictors of bystander intervention. Young adults (N = 128) completed a survey in a lab setting, then consumed either an alcoholic or control beverage, read and listened to a fictional sexual assault scenario, and finally completed a semi-structured interview and postexperiment survey assessing their perceptions of the scenario. Using multivariate analysis of covariance (MANCOVA), we found people with higher RMA blamed the victim more and perpetrator less; they were also less likely to perceive responsibility to intervene for a sexual assault victim. Alcohol intoxication did not exacerbate these effects. That is, alcohol intoxication was not a context in which RMA was expressed more strongly. We recommend bystander programs continue to address RMA, specifically as a barrier to intervening.

A meta‐analysis of the effects of acute alcohol intoxication on witness recall

SummaryThere is widespread belief in the legal system that alcohol impairs witness testimony. Nevertheless, most laboratory studies examining the effects of alcohol on witness testimony suggest that alcohol may affect the number of correct but not incorrect details recalled. However, it is difficult to draw conclusions because sample sizes, testing paradigms, and recall measures vary between individual studies. We conducted a meta‐analysis to address this issue. We found alcohol intoxication had a significant and moderate sized effect on the number of correct details recalled (g = 0.40). The effect of alcohol on the number of incorrect details recalled was not significant. Further, the effect of alcohol on the recall of correct details was significantly moderated by multiple factors like intoxication level, the retention interval length between encoding and recall, and the types of questions asked (i.e., free recall vs. cued recall). We discuss the applied implications of the results.

Lack of sexual dimorphism on the inhibitory effect of alcohol on muscle protein synthesis in rats under basal conditions and after anabolic stimulation.

Previous studies indicate women have a higher blood alcohol (i.e., ethanol) and acetaldehyde concentration after consuming an equivalent amount of alcohol, and that women are more susceptible to the long‐term negative health effects of alcohol. However, there is a paucity of data pertaining to whether there is a sexual dimorphic response in skeletal muscle to alcohol. Adult male and female Sprague–Dawley rats were used and the primary endpoint was in vivo determined muscle (gastrocnemius) protein synthesis (MPS). The initial study indicated MPS did not differ in female rats during proestrus, estrus, metestrus, or diestrus; hence, subsequent studies used female rats irrespective of estrus cycle phase. There was no difference in MPS between male and female rats under basal fasted conditions, and the time‐ and dose‐responsiveness of both groups to the inhibitory effect of acute alcohol did not differ. The ability of alcohol to suppress MPS was comparable in male and female rats pretreated with alcohol dehydrogenase inhibitor 4‐methylpyrazol. Chronic alcohol feeding for 6 weeks decreased MPS in male but not in female rats; however, MPS was reduced in both sexes at 14 weeks. Finally, oral gavage of leucine increased MPS similarly in male and female rats and chronic alcohol feeding for 14 weeks prevented the anabolic effect in both sexes. These data suggest normal fluctuations in ovarian hormones do not significantly alter MPS in female rats, and that there is no sexual dimorphic response to the effects of acute alcohol intoxication on MPS. While chronic alcohol consumption appeared to decrease MPS at an early time point in male compared to female rats, there was no sex difference in the suppressive effect of alcohol at a later time point. Overall, these data do not support the prevailing belief that females are more susceptible than males to alcohol's catabolic effect on MPS.

Alcohol Hangover Increases Conflict Load via Faster Processing of Subliminal Information.

The detrimental effects of acute alcohol intoxication and long-term alcohol (ab)use on cognition are well-known. Yet, only little is known about the cognitive effects of an acute alcohol hangover, even though it might affect executive functions associated with workplace performance or driving skills. Given that alcohol hangover may increase the speed of information accumulation, we assessed the behavioral effects of conflict load (induced by a subliminal prime) on cognitive control, as assessed via the Flanker effect. We employed a counter-balanced within-subject design, where n = 25 healthy young males were tested once after a sober night and once after a night of experimentally induced heavy drinking of cheap brandy/red wine (2.6375 g alcohol per estimated liter of body water within 2–3 h). Alcohol hangover neither increased the cognitive conflicts induced by consciously processed distractors alone (i.e., the Flanker effect), nor modulated conflict adaptation (i.e., the Gratton effect). Instead, hangover potentiated the detrimental effects of conflicting subliminal primes on top-down cognitive conflicts. This effect was likely due to an increase in the speed of information accumulation from visual stimuli and the resulting increase in subliminal conflict load induced by incompatible primes. We further found the size of this effect to be positively correlated with age and subjective sleepiness during the hangover state, but the hangover effect remained significant even after correcting for those covariates. We further found no correlation of the behavioral effect with the subjective overall rating of hangover symptoms or the maximal breath alcohol concentration reached during prior intoxication. Taken together, our findings suggest that alcohol hangover may affect cognitive performance due to an increase in non-conscious processing of visual distractors. While the size of this effect might increase with age and sleepiness, it is not entirely dependent on those covariates and not necessarily related to subjective ratings of general hangover symptoms/impairment.

Effects of Acute Alcohol Intoxication on Empathic Neural Responses for Pain.

The questions whether and how empathy for pain can be modulated by acute alcohol intoxication in the non-dependent population remain unanswered. To address these questions, a double-blind, placebo-controlled, within-subject study design was adopted in this study, in which healthy social drinkers were asked to complete a pain-judgment task using pictures depicting others' body parts in painful or non-painful situations during fMRI scanning, either under the influence of alcohol intoxication or placebo conditions. Empathic neural activity for pain was reduced by alcohol intoxication only in the dorsal anterior cingulate cortex (dACC). More interestingly, we observed that empathic neural activity for pain in the right anterior insula (rAI) was significantly correlated with trait empathy only after alcohol intoxication, along with impaired functional connectivity between the rAI and the fronto-parietal attention network. Our results reveal that alcohol intoxication not only inhibits empathic neural responses for pain but also leads to trait empathy inflation, possibly via impaired top-down attentional control. These findings help to explain the neural mechanism underlying alcohol-related social problems.