Effects Of Acute Alcohol Consumption 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.

Elevated Blood Alcohol Concentration Is Associated with Improved Clinical Outcomes of Intravenous Thrombolysis Treatment in Acute Ischemic Stroke Patients—A Retrospective Study

Intravenous thrombolysis (IVT) improves acute ischemic stroke (AIS) outcomes, but with limited success. In addition, ethanol potentiates the effect of r-tPA in ischemia models. The effect of acute alcohol consumption on IVT outcomes was investigated in a retrospective cohort study. AIS patients with detectable blood alcohol concentration (BAC) during IVT were included (alcohol group; n = 60). For each case, 3 control subjects who underwent IVT but denied alcohol consumption were matched in terms of age, sex, affected brain area, and stroke severity. Outcomes were determined using the NIHSS at 7 days and the modified Rankin scale (mRS) at 90 days. Patients were younger and had a less severe stroke than in a standard stroke study. Favorable long-term outcomes (mRS 0-2) occurred significantly more frequently in the alcohol group compared to controls (90% vs. 63%, p < 0.001). However, the rates of hemorrhagic transformation were similar. Multiple logistic regression models identified elevated BAC as a significant protective factor against unfavorable short-term (OR: 0.091, 95% CI: 0.036-0.227, p < 0.001) and long-term outcomes (OR: 0.187, 95% CI: 0.066-0.535, p = 0.002). In patients with BAC > 0.2%, significantly lower NIHSS was observed at 3 and 7 days after IVT vs. in those with 0.01-0.2% ethanol levels. Elevated BAC is associated with improved outcomes in IVT-treated AIS without affecting safety.

The Influence of Alcohol Consumption on Gambling: Do the Laboratory Study Findings Generalize to Natural Environments?

A recent meta-analysis of laboratory studies on the effects of acute alcohol consumption on risk-taking did not support that acute alcohol consumption increased risk-taking. Questions about whether this finding generalizes to those gambling in naturalistic settings remain. Therefore, we examined the gambling behavior of frequent gamblers who did and did not consume alcohol while gambling. Participants were 769 weekly gamblers (66% male) who were U.S. residents and at least 18years old. Participantsrecruited via MTurk completed measures through theQualtrics survey platform. Significant predictors of gambling under the influence of alcohol were drinking days per month and PGSI score. A linear regression model predicting percentage of time spent gambling under the influence of alcohol revealed that gambling days per week, gambling hours per day, PGSI score, and drinking days per month were significant predictors. Finally, significant predictors of spending at least 50% of gambling time gambling under the influence of alcohol included: gambling hours per day, PGSI score, and drinking days per month. These findings were consistent with the recent meta-analysis of laboratory studies. However, finding that gambling disorder symptoms and overall rates of alcohol consumption were related to gambling under the influence of alcohol replicated the frequently found relation of alcohol problems among those who also exhibit gambling problems.

Does acute alcohol consumption increase risk-taking while gambling? A systematic review and meta-analysis.

To estimate the effect of acute alcohol consumption on risk-taking while gambling, examine blood alcohol concentration as a moderator and explore possible moderators of this effect. A systematic review and meta-analysis was completed. A Boolean search strategy was used to identify studies that included (a) alcohol consumption as an independent variable; (b) a gambling or risk-taking task; (c) a control or placebo comparison; (d) human participants; and (e) English publications. Descriptive information, sample characteristics and experimental data were extracted from each study. Searched databases included: PsycINFO, Web of Science, Medline, Cochrane Library and ProQuest Dissertations and Theses. Included as participants were experiments that compared the effects of alcohol and non-alcoholic or placebo beverages on risk-taking while gambling. Comprehensive Meta-Analysis version 3.3.070 was used. Standardized mean differences of risk-taking while gambling between the experimental and control conditions were calculated when studies did not report effect sizes. Random-effects models were used for overall effect and meta-regressions while mixed-effects models were used for subgroup analyses. Twenty articles containing 47 alcohol versus control comparisons met inclusion criteria. The overall Hedges'g for the difference between groups consuming alcohol and groups consuming a placebo or non-alcoholic drink control was 0.03, 95% confidence interval (CI) = -0.07, 0.12, p = 0.60, indicating no significant difference. Larger effect sizes were found for studies using non-alcoholic control drinks (Hedges' g = 0.30, 95% CI = 0.01, 0.58) compared to placebo beverages (Hedges' g = -0.03, 95% CI = -0.13, 0.06), Cochran's Q= 4.67, p = 0.03. Finding that acute alcohol consumption had no reliable effect on risk-taking while gambling was consistent with existing animal research. No support was found for the relation between alcohol dose and risk-taking. The significantly larger effect size for experiments using non-alcoholic versus placebo beverages suggests the potential role of expectancy effects.

Deficits in episodic future thinking following acute alcohol consumption

RationaleAcute alcohol consumption adversely affects many cognitive abilities, including episodic memory and executive functioning. However, no study to date has tested whether these acute effects of alcohol also extend to episodic future thinking (EFT). This is a surprising omission given that EFT refers to the ability to imagine oneself experiencing the future, a highly adaptive ability that has been implicated in many important functional behaviours. EFT is also thought to impose demands on episodic memory and executive control.ObjectivesThe current study was designed to provide the first test of whether a moderate dose of alcohol influences EFT and whether any observed EFT difficulties are secondary to broader problems in episodic memory and executive functioning. Sex differences in EFT following acute alcohol consumption were also examined.MethodsOne hundred and twenty-four healthy adult social drinkers were recruited and randomly assigned to either the alcohol (n = 61) or placebo (n = 63) condition. Participants were administered a dose of 0.6 g/kg alcohol or a matched placebo drink.ResultsRelative to the placebo condition, EFT was impaired by acute alcohol consumption. This impairment was underpinned by broader difficulties with episodic memory, but not executive functioning. There were no sex differences in EFT performance following acute alcohol use.ConclusionThese data provide novel insights into the effects of acute alcohol consumption on EFT and the broader cognitive mechanisms that contribute to these difficulties. The results are discussed in relation to their implications for understanding many of the maladaptive behaviours commonly associated with acute alcohol use.

Prospective memory deficits following acute alcohol consumption.

Prospective memory is a critical neurocognitive capacity that refers to the ability to execute delayed intentions. To date, few studies have investigated the effects of acute alcohol consumption on prospective memory, and important questions remain about the mechanisms that might underpin acute alcohol-induced prospective memory impairment. The current study sought to clarify the nature and magnitude of prospective memory difficulties following acute alcohol consumption and to test the degree to which any problems with prospective remembering might be a secondary consequence of broader cognitive impairment. This study also investigated whether there were potential sex differences. In all, 124 healthy adult social drinkers were assigned to either the alcohol (n = 61) or placebo (n = 63) condition. Participants were administered a dose of 0.6 g/kg alcohol or a matched placebo drink and then asked to complete a measure of prospective memory. A broader neurocognitive test battery was also administered. Relative to the placebo condition, acute alcohol intoxication led to significant impairment on all prospective memory tasks, with effects mostly large in magnitude. These difficulties could not be explained by broader problems in retrospective memory, executive function or episodic future thinking. In addition, females recorded a higher blood alcohol concentration than males; however, no sex differences in prospective memory performance were identified following acute alcohol use. The results show that acutely, even a moderate dose of alcohol substantially impairs prospective memory function. These findings have potentially important implications for understanding many of the maladaptive behaviours associated with acute alcohol consumption.

Alcohol‐related suicide across Australia: a geospatial analysis

BackgroundThe acute effects of alcohol consumption are a major risk factor for suicide. Positive blood alcohol concentrations are present in almost one‐third of all suicides at time of death. These suicides are defined as alcohol‐related suicides. This cross‐sectional study examines the geospatial distribution/clustering of high proportions of alcohol‐related suicides and reports on socioeconomic and demographic risk factors. MethodsNational Coronial Information System (NCIS) data were used to calculate proportions of suicides with alcohol present at the time of death for each level 3 statistical areas (SA3) in Australia. A density analysis and hotspot cluster analysis were used to visualise and establish statistically significant clustering of areas with higher (hotspots) and lower (coldspots) proportions. Subsequently, socioeconomic and demographic risk factors for alcohol use and suicide were reported on for hot and cold spots. ResultsSignificant clustering of areas with higher proportions of alcohol‐related suicide occurred in northern Western Australia, the Northern Territory and Queensland, as well as inland New South Wales and inland Queensland. Clustering of SA3s with significantly lower proportions occurred in major city and inner regional Sydney and Melbourne. Conclusion and implications for public healthResults from this study identify areas in which prevention strategies should target alcohol use and can be used to inform prevention strategy design. Additionally, hotspots and coldspots identified in this study can be used for further analysis to better understand contextual risk factors for alcohol‐related suicide.

Effect of oral alcohol administration on plasma cytokine concentrations in heavy drinking individuals

BackgroundAlcohol is known to modulate the immune system, including cytokines, under conditions of both acute consumption and chronic use. The specific pro- and anti-inflammatory effects and mechanisms whereby alcohol consumption modulates circulating cytokine concentrations are not well understood. Few studies in humans have investigated the effect of acute alcohol consumption on plasma cytokine concentrations in individuals who are heavy drinkers. MethodsData were pooled from two studies involving a total of 25 non-treatment seeking, heavy drinking individuals who undertook an oral alcohol administration procedure. Plasma cytokine [Interleukin-10 (IL-10), Interleukin-6 (IL-6), Interleukin-18 (IL-18) and Tumor Necrosis Factor-alpha (TNF-α)] concentrations were measured at two baseline timepoints, then three hours after alcohol administration, and finally when breath alcohol concentrations returned to zero. Linear mixed models were conducted to determine whether there was a significant effect of time on cytokine concentrations. ResultsThere was a significant reduction in TNF-α concentration (F [3, 20.42] = 4.96, p = 0.01, η2p = 0.42) post alcohol administration, compared to baseline concentrations, and a significant increase in IL-6 concentrations (F [3, 27.81] = 9.06, p < 0.001, η2p = 0.49) post alcohol administration, compared to baseline. There were no significant changes in IL-18 or IL-10 concentrations. ConclusionsTo our knowledge, this is the first study to examine the acute effect of oral alcohol consumption on peripheral inflammatory markers in individuals with alcohol use disorder. Results indicate a clinically relevant increase in proinflammatory cytokines approximately 3 h after initial alcohol ingestion. Further research should be done to elucidate the complex interaction between alcohol and the immune system.

Effects of acute alcohol consumption on neuronal activity and cerebral vasomotor response

IntroductionIn the majority of European countries, driving after drinking small-moderate amount of alcohol is legal. Motivated by our previous studies on cerebral hemodynamics, we aimed to study whether a small-moderate blood alcohol content (BAC), at which driving is legal in some countries (0.8 g/L), influences the neuronal activity, neurovascular coupling, and cerebral vasoreactivity.MethodsAnalyses of pattern-reversal visual evoked potential (VEP) and transcranial Doppler (TCD) examinations were performed in thirty young healthy adults before and 30 min after alcohol consumption. Cerebral vasoreactivity was evaluated by breath holding test in both middle cerebral arteries. By using a visual cortex stimulation paradigm, visually evoked flow velocity response during reading was measured in both posterior cerebral arteries (PCA).ResultsThe BAC was 0.82 g/L and 0.94 g/L 30 and 60 min after drinking alcohol, respectively. Latency of the VEP P100 wave increased after alcohol consumption. Resting absolute flow velocity values increased, whereas pulsatility indices in the PCA decreased after alcohol ingestion, indicating vasodilation of cerebral microvessels. Breath holding index and the visually evoked maximum relative flow velocity increase in the PCA and steepness of rise of the flow velocity curve were smaller after than before alcohol consumption.ConclusionBAC close to a legal value at which driving is allowed in some European countries inhibited the neuronal activity and resulted in dilation of cerebral arterioles. Cerebral vasodilation may explain the decrease of cerebral vasoreactivity and might contribute to the disturbance of visually evoked flow response after alcohol consumption.

The effect of acute alcohol consumption on meal memory and subsequent food intake: Two laboratory experiments

Altering the quality of episodic meal memories has been shown to affect subsequent food intake. Acute alcohol consumption disrupts memory formation and produces short-term overeating. In two studies, we investigated whether alcohol consumption can affect meal-related memories and later food intake. Study 1 (N = 60, 50% male) investigated how consumption of an alcoholic drink (0.5 g/kg) prior to consumption of a lunch meal affected meal memory of that lunch, and later food intake, compared with a placebo-alcohol. Findings revealed that alcohol consumption did not impair meal memory, and did not affect subsequent food intake. Study 2 (N = 72, 50% male) investigated whether, due to alcohol's retrograde facilitation effect (the enhancement of recall due to reduced interference at the point of exposure) consuming alcohol after consumption of a lunch meal could enhance meal memory, compared with when consumed before a lunch meal (both a dosage of 0.6 g/kg), and compared with consumption of a soft drink. Contrary to prediction, alcohol consumed after a lunch meal did not significantly increase meal memory. But, certain types of meal memory were impaired when alcohol was consumed before the meal, compared with consumption of a soft drink. Subsequent food intake did not differ between conditions. Taken together, findings suggest that alcohol intoxication can impair some forms of meal memory recall, likely due to disruption of memory formation during the encoding phase. However, there was no evidence that this impairment contributes towards alcohol-induced overeating.

The acute effects of alcohol on state rumination in the laboratory

RationaleRumination is a repetitive, negative, self-focused thinking style associated with various forms of psychopathology. Recent studies suggest that rumination increases craving for alcohol and predicts harmful drinking and alcohol-related problems. However, the acute effects of alcohol on rumination have not been previously studied. It is proposed that alcohol may reduce ruminative thinking through decreasing negative mood.ObjectivesIn the present study, we aimed to test the previously unexplored effects of acute alcohol consumption on rumination in a hazardous drinking population.MethodsWe conducted a randomised placebo-controlled laboratory study to examine the effect of low (0.4 g kg−1) and high doses (0.8 g kg−1) of alcohol on state rumination compared to placebo. Participants completed a rumination induction task prior to receiving drinks. We then measured state rumination and mood at repeated time points; 30 min, 60 min and 90 min post-drinks consumption.ResultsWe found a significant decrease in state rumination in the low-dose alcohol group compared to placebo at 30 min post-alcohol consumption, but no difference was observed between the high-dose alcohol and placebo groups. Mediation analysis provided evidence for an indirect effect of alcohol on state rumination through concurrent changes in negative mood.ConclusionsThese findings suggest that acute alcohol consumption can regulate negative mood and concurrently rumination, providing preliminary evidence for the role of rumination in alcohol use disorders. Rumination may be a treatment target in alcohol use disorders.

Effects of Acute Alcohol Consumption on Cycling Anaerobic Exercise Performance: A Randomized Crossover Study

PURPOSE: Some athletes consume alcohol prior to training and sports events, possibly because they believe that alcohol may aid in reducing pain and anxiety, increasing confidence, and promoting aggressiveness. While previous studies have shown that alcohol consumption acutely impairs endurance exercise performance, its effects on anaerobic exercise performance have not been well established. Therefore, this study investigated the effect of a small dose of alcohol on anaerobic exercise performance.METHODS: In a randomized crossover design, nine healthy and recreationally active males (n=6) and females (n=3) participated in the study. Subjects consumed 0.7 g of alcohol per kg of lean body mass or a calorie/volume-matched sucrose beverage. Reaction time tests were performed before and 25 minutes after beverage consumption. Following the second reaction time test, subjects performed the 20-second Wingate anaerobic test (WAnT).RESULTS: Compared to the sucrose drink, alcohol showed no significant effects on peak power (p=.903), average power (p=.970), percentage power drop during WAnT (p=.593), or total energy produced during WAnT (p=.923). Moreover, alcohol did not affect the time course of power output during a 20s WAnT (p=.999 for all time points). In addition, reaction time was not significantly different when comparing alcoholic with sucrose drinks at different timepoint (Before; p=.999, After; p=.364).CONCLUSIONS: Although some athletes consume alcohol prior to engaging in sports events, assuming that it may improve anaerobic exercise performance, the results of the present study show that acute consumption of alcohol does not have effects on anaerobic exercise performance when compared to the control beverage.

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.

Effects of Acute Alcohol Consumption on Food Intake and Pictorial Stroop Response to High-Calorie Food Cues.

We examined (a) the effect of an acute dose of alcohol on the consumption of energy-dense food and (b) on cognitive bias towards high-energy-dense food cues and (3) whether the effect of an acute dose of alcohol on the consumption of energy-dense food would be mediated by cognitive bias towards high-energy-dense food cues. Heavy social drinkers (n=40) abstained from drinking for 12 hours before testing. On the test day, participants completed pre-challenge measures of alcohol and food craving, and cognitive bias towards alcohol in a placebo-controlled, double-blind design. Participants performed post-challenge measures of alcohol and food craving, ad lib energy-dense food consumption and cognitive bias. We did not observe any of the hypothesized interactions between challenge condition, consumption of energy-dense food and cognitive bias towards high-energy-dense food cues. Our data suggest that acute alcohol consumption does not influence the consumption of energy-dense food or cognitive bias towards high-energy-dense food cues. These findings may reflect that alcohol does not increase the appetitive value of food and food-related cues or that the measures used in this study were not sensitive to detect an effect. Further research is required to determine whether alcohol at higher doses and/or food cues that are frequently paired with alcohol intake stimulates changes in food intake and the reward value of food cues.

Acute Alcohol Intake Produces Widespread Decreases in Cortical Resting Signal Variability in Healthy Social Drinkers.

Acute alcohol intoxication has wide-ranging neurobehavioral effects on psychomotor, attentional, inhibitory, and memory-related cognitive processes. These effects are mirrored in disruption of neural metabolism, functional activation, and functional network coherence. Metrics of intraregional neural dynamics such as regional signal variability (RSV) and brain entropy (BEN) may capture unique aspects of neural functional capacity in healthy and clinical populations; however, alcohol's influence on these metrics is unclear. The present study aimed to elucidate the influence of acute alcohol intoxication on RSV and to clarify these effects with subsequent BEN analyses. 26 healthy adults between 25 and 45years of age (65.4% women) participated in 2 counterbalanced sessions. In one, participants consumed a beverage containing alcohol sufficient to produce a breath alcohol concentration of 0.08g/dl. In the other, they consumed a placebo beverage. Approximately 35minutes after beverage consumption, participants completed a 9-minute resting-state fMRI scan. Whole-brain, voxel-wise standard deviation was used to assess RSV, which was compared between sessions. Within clusters displaying alterations in RSV, sample entropy was calculated to assess BEN. Compared to the placebo, alcohol intake resulted in widespread reductions in RSV in the bilateral middle frontal, right inferior frontal, right superior frontal, bilateral posterior cingulate, bilateral middle temporal, right supramarginal gyri, and bilateral inferior parietal lobule. Within these clusters, significant reductions in BEN were found in the bilateral middle frontal and right superior frontal gyri. No effects were noted in subcortical or cerebellar areas. Findings indicate that alcohol intake produces diffuse reductions in RSV among structures associated with attentional processes. Within these structures, signal complexity was also reduced in a subset of frontal regions. Neurobehavioral effects of acute alcohol consumption may be partially driven by disruption of intraregional neural dynamics among regions involved in higher-order cognitive and attentional processes.

Effects of acute alcohol consumption on emotion recognition in high and low trait aggressive drinkers.

Background:Research suggests that acute alcohol consumption impairs processing of emotional faces. As emotion processing plays a key role in effective social interaction, these impairments may be one mechanism by which alcohol changes social behaviour. This study investigated the effect of individual differences on this relationship by comparing emotion recognition performance after acute alcohol consumption in individuals with high and low trait aggression.Methods:Regular non-dependent drinkers, either high or low in trait aggression participated in a double-blind placebo-controlled experiment (N = 88, 50% high trait aggressive). Participants attended two sessions. In one they consumed an alcoholic drink (0.4 g/kg) and in the other they consumed a matched placebo. They then completed two computer-based tasks: one measured global and emotion-specific recognition performance across six primary emotions (anger, sadness, happiness, disgust, fear, surprise), the other measured processing bias of two ambiguously expressive faces (happy–angry/happy–sad).Results:There was evidence of poorer global emotion recognition after alcohol. In addition, there was evidence of poorer sensitivity to sadness and fear after alcohol. There was also evidence for a reduced bias towards happiness following alcohol and weak evidence for an increased bias towards sadness.Conclusions:These findings suggest that alcohol impairs global emotion recognition. They also highlight a reduced ability to detect sadness and fearful facial expressions. As sadness and fear are cues of submission and distress (i.e. function to curtail aggression), failure to successfully detect these emotions when intoxicated may increase the likelihood of aggressive responding. This coupled with a reduced bias towards seeing happiness may collectively contribute to aggressive behaviour.

Corrigendum to Effects of acute alcohol consumption on emotion recognition in social alcohol drinkers.

Corrigendum to Effects of acute alcohol consumption on emotion recognition in social alcohol drinkers.

Alcohol, empathy, and morality: acute effects of alcohol consumption on affective empathy and moral decision-making

RationaleHypothetical moral dilemmas, pitting characteristically utilitarian and non-utilitarian outcomes against each other, have played a central role in investigations of moral decision-making. Preferences for utilitarian over non-utilitarian responses have been explained by two contrasting hypotheses; one implicating increased deliberative reasoning, and the other implicating diminished harm aversion. In recent field experiments, these hypotheses have been investigated using alcohol intoxication to impair both social and cognitive functioning. These studies have found increased utilitarian responding, arguably as a result of alcohol impairing affective empathy.ObjectivesThe present research expands existing investigations by examining the acute effects of alcohol on affective empathy and subsequent moral judgments in traditional vignettes and moral actions in virtual reality, as well as physiological responses in moral dilemmas.MethodsParticipants (N = 48) were administered either a placebo or alcohol in one of two dosages; low or moderate. Both pre- and post intervention, participants completed a moral action and moral judgment task alongside behavioural measures of affective empathy.ResultsHigher dosages of alcohol consumption resulted in inappropriate empathic responses to facial displays of emotion, mirroring responses of individuals high in trait psychopathy, but empathy for pain was unaffected. Whilst affective empathy was influenced by alcohol consumption in a facial responding task, both moral judgments and moral actions were unaffected.ConclusionsThese results suggest that facets, beyond or in addition to deficits in affective empathy, might influence the relationship between alcohol consumption and utilitarian endorsements.

Effects of Acute Alcohol Consumption on the Human Brain: Diffusional Kurtosis Imaging and Arterial Spin-Labeling Study.

Brain function and microstructure are affected by alcohol consumption. Until recently, the effect of alcohol on neural mechanisms has not been fully elucidated. Our aim was to explore the acute effects of alcohol on healthy human brains by diffusional kurtosis imaging and 3D arterial spin-labeling and elucidate structural and functional changes in the brain on acute alcohol intake. Conventional MR imaging, diffusional kurtosis imaging, and 3D arterial spin-labeling were performed on 24 healthy volunteers before and 0.5 and 1 hour after drinking alcohol. Participants were divided into 2 groups according to the response to alcohol: blushing (n = 12) and unblushing (n = 12) groups. Twenty brain regions were analyzed. Diffusional kurtosis imaging revealed an increase in mean kurtosis and fractional anisotropy at 0.5 hour post-alcohol intake in most brain regions, whereas mean diffusion was decreased in several brain regions at 1 hour after drinking. 3D arterial spin-labeling showed increased cerebral blood flow in most brain regions, particularly in the frontal regions. However, perfusion in the anterior commissure decreased. Regional changes in the brain correlated with various behavioral performances with respect to blush response and sex. In general, blushing individuals and men are more sensitive to alcohol with acute effects. Physiologic and microstructural alterations in the brain on alcohol consumption were examined. Brain areas with blood flow alteration detected by 3D arterial spin-labeling were highly consistent with susceptible areas detected by diffusional kurtosis imaging. The current study provides new insight into the effects of alcohol on the brain and behavioral performance in different blush response and sex populations.

Effects of acute alcohol consumption on emotion recognition in social alcohol drinkers.

Background:Research suggests that acute alcohol consumption alters recognition of emotional expressions. Extending this work, we investigated the effects of alcohol on recognition of six primary expressions of emotion.Methods:We conducted two studies using a 2 × 6 experimental design with a between-subjects factor of drink (alcohol, placebo) and a within-subjects factor of emotion (anger, disgust, sadness, surprise, happiness, fear). Study one (n = 110) was followed by a direct replication study (n = 192). Participants completed a six alternative forced choice emotion recognition task following consumption of 0.4 g/kg alcohol or placebo. Dependent variables were recognition accuracy (i.e. hits) and false alarms.Results:There was no clear evidence of differences in recognition accuracy between groups (ps > .58). In study one, there were more false alarms for anger in the alcohol compared to placebo group (n = 52 and 56, respectively; t(94.6) = 2.26, p = .024, d = .44) and fewer false alarms for happiness (t(106) = –2.42, p = .017, d = –.47). However, no clear evidence for these effects was found in study two (alcohol group n = 96, placebo group n = 93, ps > .22). When the data were combined we observed weak evidence of an effect of alcohol on false alarms of anger (t(295) = 2.25, p = .025, d = .26).Conclusions:These studies find weak support for biased anger perception following acute alcohol consumption in social consumers, which could have implications for alcohol-related aggression. Future research should investigate the robustness of this effect, particularly in individuals high in trait aggression.