Acute Alcohol Consumption Research Articles

Abstract 12236: Population-Level Analyses of Alcohol Consumption as a Predictor of Acute Atrial Fibrillation Episodes

Introduction: We conducted an instrumental variable analysis to test whether acute alcohol consumption leads to increased emergency department (ED) visits for AF at the level of the general population. Methods: We analyzed blood alcohol concentration measurements obtained from individuals using commercially available Bluetooth-enabled breathalyzer devices (BACtrack, San Francisco, CA) collected between January 1, 2014 and December 31, 2016 to identify dates associated with heightened alcohol consumption that corresponded to recurrent, nationally-recognized events. Outcomes included ED visits with AF (main analysis) or supraventricular tachycardia (SVT; as a negative control) in California between January 1, 2005 to December 30, 2015 using Office of Statewide Health Planning and Development data. A secondary analysis examining rates of new-onset AF was conducted. We utilized population denominators for age, sex, and race/ ethnicity in California from the US Census. Multivariable adjusted Poisson regression models were utilized to compare rates of AF during and 6 days following instrumental events compared to all other days of the year. Results: Using 1,269,054 breath alcohol measurements obtained from 36,158 individuals, we identified 8 recurring events associated with heightened alcohol consumption. After multivariable adjustment, excess alcohol consumption inferred from our instrumental variables was associated with 719 additional AF visits per 100,000 person-years (95% CI 189-1249, p = 0.008; Table ). The association between these events and new-onset AF exhibited a stronger effect (1,757 additional visits, 95% CI 945-2,569, p < 0.001). A negative control analysis failed to exhibit significantly heightened rates of SVT during those same dates. Conclusion: These data suggest that acute alcohol consumption is associated with a higher risk for discrete AF episodes, as well as for new-onset (incident) AF, in the general population.

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.

Acute Consumption of Alcohol and Discrete Atrial Fibrillation Events.

Patients' self-reports suggest that acute alcohol consumption may trigger a discrete atrial fibrillation (AF) event. To objectively ascertain whether alcohol consumption heightens risk for an AF episode. A prospective, case-crossover analysis. Ambulatory persons in their natural environments. Consenting patients with paroxysmal AF. Participants were fitted with a continuous electrocardiogram (ECG) monitor and an ankle-worn transdermal ethanol sensor for 4 weeks. Real-time documentation of each alcoholic drink consumed was self-recorded using a button on the ECG recording device. Fingerstick blood tests for phosphatidylethanol (PEth) were used to corroborate ascertainments of drinking events. Of 100 participants (mean age, 64 years [SD, 15]; 79% male; 85% White), 56 had at least 1 episode of AF. Results of PEth testing correlated with the number of real-time recorded drinks and with events detected by the transdermal alcohol sensor. An AF episode was associated with 2-fold higher odds of 1 alcoholic drink (odds ratio [OR], 2.02 [95% CI, 1.38 to 3.17]) and greater than 3-fold higher odds of at least 2 drinks (OR, 3.58 [CI, 1.63 to 7.89]) in the preceding 4 hours. Episodes of AF were also associated with higher odds of peak blood alcohol concentration (OR, 1.38 [CI, 1.04 to 1.83] per 0.1% increase in blood alcohol concentration) and the total area under the curve of alcohol exposure (OR, 1.14 [CI, 1.06 to 1.22] per 4.7% increase in alcohol exposure) inferred from the transdermal ethanol sensor in the preceding 12 hours. Confounding by other time-varying exposures that may accompany alcohol consumption cannot be excluded, and the findings from the current study of patients with AF consuming alcohol may not apply to the general population. Individual AF episodes were associated with higher odds of recent alcohol consumption, providing objective evidence that a modifiable behavior may influence the probability that a discrete AF event will occur. National Institute on Alcohol Abuse and Alcoholism.

Quantifying risk of injury from usual alcohol consumption: An instrumental variable analysis.

Numerous studies of roadside accidents among emergency room patients show elevated risk of injury from acute alcohol consumption, i.e., recent drinking precedes the injury event. The observed effects are large and show a dose-response relationship. In contrast, studies quantifying the association between injury risk and chronic consumption, such as past-year average volume, show lower relative risk estimates than those from acute consumption. Combining data from 4 waves of US National Alcohol Surveys (NAS) for years 2000-2015 (N=29,571, 53% overall cooperation rate), we estimated the risk of any past-year injury from past-year volume using logistic regression. This was contrasted with an instrumental variable (IV) analysis utilizing a 2-stage residual inclusion (2SRI) approach to estimate injury risk from volume, which adjusted for unobserved confounders using state beer and spirits tax rates, zip code-level outlet and bar density, and control state status as instruments. Based on the combined US population surveys and controlling for sociodemographics, using conventional logistic regression, the odds ratios of injury from an average volume of 1, 2, and 5 drinks per day were 1.12 [95% confidence interval: 1.02, 1.24], 1.10 [1.00, 1.22], and 1.04 [0.88, 1.22], respectively. These compared with 1.67 [1.00, 2.78], 2.38 [0.87, 6.54], and 6.98 [0.57, 85.89] using the IV method. The proportion of injury attributed to alcohol also increased in magnitude, from 6.2% [0.3%, 11.9%] using the conventional approach to 17.9% [8.2%, 27.7%] using the IV method. The association between injury and chronic alcohol consumption may be confounded by unobserved factors, resulting in a possible downward bias of the risk estimate.

Impact of acute ethanol intake on cardiac autonomic regulation

Acute alcohol consumption may facilitate cardiac arrhythmias underlying the ‘Holiday Heart Syndrome’. Autonomic imbalance is promoting atrial arrhythmias. We analyzed the effects of alcohol on measures of the cardiac autonomic nervous system and their relation to arrhythmias. In 15 healthy individuals, alcohol was administered parenterally until a breath alcohol concentration of 0.50 mg/l. High-resolution digital 30-min ECGs were recorded at baseline, at the time of maximum alcohol concentration, and after alcohol concentration returned to near baseline. Using customized software, we assessed periodic repolarization dynamics (PRD), deceleration capacity (DC), standard measures of heart rate variability (SDNN; RMSSD; LF; HF), and standard ECG parameters (mean heart rate; PQ; QRS; QTc interval). At the maximum alcohol concentration, PRD levels were significantly increased compared to baseline [1.92 (IQR 1.14–3.33) deg2 vs. 0.85 (0.69–1.48) deg2; p = 0.001]. PRD levels remained slightly increased when alcohol concentrations returned to baseline. DC levels were significantly decreased at the maximum alcohol concentration compared to baseline [7.79 (5.89–9.62) ms vs. 9.97 (8.20–10.99) ms; p = 0.030], and returned to baseline levels upon reaching baseline levels of alcohol. Standard HRV measures were reduced at maximum alcohol concentration. The mean heart rate increased significantly during alcohol administration. QRS and QTc duration were significantly prolonged, whereas PQ interval showed no change. Our findings revealed an increase of sympathetic activity and a reduction of parasympathetic activity under the influence of alcohol administration, resulting in autonomic imbalance. This imbalance might ultimately trigger arrhythmias underlying the ‘Holiday Heart Syndrome’.

Reliability and validity of a 3-min psychomotor vigilance task in assessing sensitivity to sleep loss and alcohol: fitness for duty in aviation and transportation.

The psychomotor vigilance task (PVT) is a widely used objective method to measure sustained attention, but the standard 10-min version is often impractical in operational settings. We investigated the reliability and validity of a 3-min PVT administered on a portable handheld device assessing sensitivity to sleep loss and alcohol in relation to a 10-min PVT and to applied tasks. A total of 47 healthy volunteers underwent a 12 consecutive days sleep lab protocol. A cross-over design was adopted including total sleep deprivation (38 h awake), sleep restriction (SR, 4 h sleep opportunity), acute alcohol consumption, and SR after alcohol intake (SR/Alc 4 h sleep opportunity). Participants performed a 10-min and 3-min PVT and operationally relevant tasks related to demands in aviation and transportation. Sleep loss resulted in significant performance impairments compared with baseline measurements detected by both PVT versions-particularly for mean speed (both p < 0.001)-and the operationally relevant tasks. Similar effects were observed due to alcohol intake (speed: both p < 0.001). The 3-min and 10-min PVT results were highly correlated (speed: between r = 0.72 and r = 0.89). Three of four aviation-related tasks showed robust correlations with the 3-min PVT. Correlations with the parameters of the task related to transportation were lower, but mainly significant. The 3-min PVT showed a high reliability and validity in assessing sleep loss and alcohol-induced impairments in cognitive performance. Thus, our results underline its usefulness as potential fitness for duty self-monitoring tool in applied settings.

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.

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.

Drinking Off(s) the Clock: Chronic Alcohol Suppresses Skeletal Muscle Molecular Clock

Circadian rhythms generated both centrally in the suprachiasmatic nucleus (SCN) and peripherally at the tissue level assist in the maintenance of physiological homeostasis, while circadian disruption is a characteristic of several diseases. The intrinsic skeletal muscle core clock has emerged as a key feature of metabolic control and influences several aspects of muscle physiology including contractile strength and mitochondrial content. Alcoholic muscle disease or myopathy is characterized by skeletal muscle weakness and myofiber atrophy resulting from the prolonged consumption of alcohol. Despite alcoholic myopathy being more prevalent than alcoholic liver disease, the entirety of mechanisms leading to its onset remains unknown. Alcohol disrupts normal cyclic expression of several core clock genes within the brain and liver, and we previously reported that acute alcohol intoxication disrupts the skeletal muscle core clock. Thus, the goal of this work was to determine whether the chronic consumption of alcohol dysregulates the skeletal muscle core molecular clock and clock-controlled genes (CCGs) in concert with alcoholic myopathy. Methods: C57BL/6Hsd female mice (12wks old) were pair fed a control liquid diet (CON) or an isocaloric ethanol (EtOH) containing liquid diet of increasing concentration (up to 32% kcal EtOH) for 7 weeks. Gastrocnemius muscles were collected from CON (n=4) and EtOH (n=3-4) mice every 4-hours for 24-hours. RNA was isolated, cDNA synthesized, and RT-PCR was performed. Results: Body weight and fat mass between groups was similar at sacrifice while liver mass was increased by alcohol. Lean mass assessed by MRI tended to be decreased by alcohol (p=0.06). Chronic alcohol consumption disrupted genes of the core clock including suppressing the rhythmic peak in expression of brain muscle ARNT like-1 (Bmal1), period (Per) 1 and 2, and cryptochrome 2 (Cry2). Genes involved in the regulation of Bmal1 also exhibited lower rhythmic peaks including Rev-erb (NR1D1) and myoblast determination protein 1 (MyoD), with significant reductions apparent at several of the 4-hour time points. The CCG D-box binding PAR BZIP transcription factor (DBP) was also suppressed at the end of the light phase and beginning of the dark active phase (ZT8 and ZT12). Skeletal muscle atrophy related genes forkhead box O1 (Foxo1), regulated in development and DNA damage response 1 (Redd1) and muscle RING-finger protein 1 (Murf1) were also altered by alcohol at the start of the dark (active) cycle. These data contrasted our previously described acute model in which subtle rhythmic shifts and large changes in the expression of several genes were observed specifically when blood alcohol levels (~4-12hr) were elevated. Therefore, there is a differential response of the skeletal muscle to acute and chronic alcohol consumption with prolonged intake leading to a lower amplitude of change over the 24-hour cycle of several core clock related genes. Future work will focus on determining the contribution of these disruptions to metabolic and functional perturbations characteristic of chronic alcoholic myopathy and the impact of these disruptions on the development of alcoholic myopathy.

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.

Acute alcohol consumption increases systemic endotoxin bioactivity for days in healthy volunteers—with reduced intestinal barrier loss in female

ObjectiveTrauma is the most common cause of death among young adults. Alcohol intoxication plays a significant role as a cause of accidents and as a potent immunomodulator of the post-traumatic response to tissue injury. Polytraumatized patients are frequently at risk to developing infectious complications, which may be aggravated by alcohol-induced immunosuppression. Systemic levels of integral proteins of the gastrointestinal tract such as syndecan-1 or intestinal fatty acid binding proteins (FABP-I) reflect the intestinal barrier function. The exact impact of acute alcohol intoxication on the barrier function and endotoxin bioactivity have not been clarified yet.Methods22 healthy volunteers received a precisely defined amount of alcohol (whiskey–cola) every 20 min over a period of 4 h to reach the calculated blood alcohol concentration (BAC) of 1‰. Blood samples were taken before alcohol drinking as a control, and after 2, 4, 6, 24 and 48 h after beginning with alcohol consumption. In addition, urine samples were collected. Intestinal permeability was determined by serum and urine values of FABP-I, syndecan-1, and soluble (s)CD14 as a marker for the endotoxin translocation via the intestinal barrier by ELISA. BAC was determined.ResultsSystemic FABP-I was significantly reduced 2 h after the onset of alcohol drinking, and remained decreased after 4 h. However, at 6 h, FABP-I significantly elevated compared to previous measurements as well as to controls (p < 0.05). Systemic sCD14 was significantly elevated after 6, 24 and 48 h after the onset of alcohol consumption (p < 0.05). Systemic FABP-I at 2 h after drinking significantly correlated with the sCD14 concentration after 24 h indicating an enhanced systemic LPS bioactivity. Women showed significantly lower levels of syndecan-1 in serum and urine and urine for all time points until 6 h and lower FABP-I in the serum after 2 h.ConclusionsEven relative low amounts of alcohol affect the immune system of healthy volunteers, although these changes appear minor in women. A potential damage to the intestinal barrier and presumed enhanced systemic endotoxin bioactivity after acute alcohol consumption is proposed, which represents a continuous immunological challenge for the organism and should be considered for the following days after drinking.

The association between the time of alcohol drinking and injury risk in Thailand: a cross\u2010sectional emergency department study

BackgroundAlthough the relationship between acute alcohol consumption and injuries is well recognized, studies exploring how the time of day the drinking commences affects alcohol-related injuries have been scarce. This contribution examines the associations between the time at which the drinking began and the duration of the drinking, the volume of alcohol consumed, the injury type, and the blood alcohol concentration (BAC) level.MethodThis study employed a cross-sectional survey, which was conducted in two hospital emergency departments (ED) in Chiangmai Province, Thailand. The sample was composed of 519 injured patients aged 18 years and older. Outcome measures included the BAC and type of injury. Exposures included the quantity of alcohol consumed, the time the drinking commenced, and the pattern of drinking involved. ResultsThe injured patients who drank alcohol within six hours prior to sustaining their injury were more likely to get injured and present themselves at the ED at night (20:00–04:00) compared to those who sustained an injury but did not drink in the hours prior. However, this relationship was only true for unintentional injuries, not intentional ones. The majority of participants consumed their first drink between 16:00 and 20:00. On average, among the 104 patients who drank prior to sustaining an injury, the total amount of alcohol consumed was 6.9 drinks, the duration of drinking was 2.6 h, the rate of drinking was 6.0 drinks/hour, and the BAC was 0.119 gm%. Every drink increased the BAC by 0.012 gm% and each year of increasing age increased the BAC by 0.003 gm%. People who were older, less educated, and drank more frequently tended to have their first drink earlier than other drinkers. An earlier start to their drinking resulted in a faster pace of drinking and a higher BAC.ConclusionsBAC increased with the total amount of alcohol consumed and the age of the drinker. Different groups of people had their first drink at different times of the day, resulting in differences in the rate of drinking, the BAC, the time of injury, and the time they presented to the ED after injury.

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 effect of alcohol on food-related attentional bias, food reward and intake: Two experimental studies

Acute alcohol consumption has been shown to increase food intake, and long-term alcohol consumption may be a risk for weight gain. A potential, but under-studied, mechanism for this effect is alcohol's ability to enhance food reward. In two studies, participants consumed an alcoholic drink (Study 1: 0.3 grams of alcohol per kilogram of bodyweight (g/kg); Study 2: 0.6 g/kg) and a placebo-alcohol drink in a within-subjects design. In both studies, food-related appetitive and motivational states, and attentional bias (AB) towards food-related cues were measured. In Study 1 (N = 44), participants completed a visual probe task with concurrent recording of eye-movements which measured AB towards images of palatable foods, unpalatable foods, and non-food control items. Participants also completed measures of appetite and snack urge ratings, salivary response towards palatable foods and an ad libitum food taste test. In Study 2 (N = 84), participants completed a similar procedure, but completed a modified Stroop task which measured differences in food-related and alcohol-related AB across the two drink conditions. In Study 1, there was no difference in food-related AB between drink conditions, and no differences in snack urge, appetite ratings, salivary response, or food intake. In contrast, Study 2 showed an alcohol-induced increase in AB towards food, but not alcohol. Snack urge, alcohol urge ratings and ad libitum food intake were also higher after alcohol consumption, relative to the placebo. Collectively, these findings suggest that alcohol can increase food reward and food intake, but these effects may only occur at a higher dose.

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.

Effect of trauma-related stress after alcohol consumption on perceived likelihood of negative consequences and willingness to drive

BackgroundAlcohol-related motor vehicle crashes are a major preventable cause of death in the United States. One potential factor that may modulate the influence of alcohol on driving-related cognitions and decision-making is trauma-related stress. Indeed, in addition to compelling research indicating that both acute trauma-related stress and acute alcohol consumption may independently affect driving-related risky decision-making, there is reason to believe that the combination of these antecedents may have an exacerbating effect. MethodsThe current study evaluated the influence of induction of acute trauma-related stress (via script-driven imagery) after alcohol consumption (0.06% Breath Alcohol Concentration [BrAC]) on driving-related cognitions – perceived likelihood of negative consequences and willingness to drive – among 25 trauma-exposed (currently symptomatic) adult drinkers from the community (M = 24.08; 36.0% female). ResultsParticipants who were acutely exposed to trauma-related stress after alcohol consumption evidenced lower perceived likelihood of being pulled over by a police officer (ηp2 = 0.38, large effect size) and lower perceived likelihood of getting in an accident (ηp2 = 0.17, medium-to-large effect size) relative to participants exposed to a neutral cue; conversely, participants exposed to trauma-related stress after alcohol consumption evidenced greater willingness to drive (d = 1.16, large effect size) than participants exposed to a neutral cue. ConclusionsGenerally, findings suggest that individuals with a trauma history that are acutely exposed to trauma-related stressors (e.g., reminders of their traumatic experience) may be particularly vulnerable to poorer driving-related decision-making after alcohol consumption. Results provide a meaningful target for the development of intoxicated driving prevention and intervention efforts geared specifically for individuals with trauma history.

Alcohol-associated liver disease: A review on its pathophysiology, diagnosis and drug therapy.

One of the global burdens of health care is an alcohol-associated liver disease (ALD) and liver-related death which is caused due to acute or chronic consumption of alcohol. Chronic consumption of alcohol damage the normal defense mechanism of the liver and likely to disturb the gut barrier system, mucosal immune cells, which leads to decreased nutrient absorption. Therapy of ALD depends upon the spectrum of liver injury that causes fatty liver, hepatitis, and cirrhosis. The foundation of therapy starts with abstinence from alcohol. Corticosteroids are used for the treatment of ALD but due to poor acceptance, continuing mortality, and identification of tumor necrosis factor-alpha as an integral component in pathogenesis, recent studies focus on pentoxifylline and, antitumor necrosis factor antibody to neutralize cytokines in the therapy of severe alcoholic hepatitis. Antioxidants also play a significant role in the treatment but till today there is no universally accepted therapy available for any stage of ALD. The treatment aspects need to restore the gut functions and require nutrient-based treatments to regulate the functions of the gut system and prevent liver injury. The vital action of saturated fatty acids greatly controls the gut barrier. Overall, this review mainly focuses on the mechanism of alcohol-induced metabolic dysfunction, contribution to liver pathogenesis, the effect of pregnancy, and targeted therapy of ALD.

Biomarker Signatures to Monitor Alcohol Consumption and Induced Organ Damage

The difficulty to differentiate long duration alcoholic behaviours is a major obstacle in the diagnosis and its treatment. Biomarkers in alcoholism are indicative of recent alcohol consumption or alcohol-induced organ damage. They are broadly divided into two; state markers, which are tools indicative of acute or chronic alcohol consumption, and trait markers, which are markers indicative of a genetic predisposition responsible to develop alcohol dependence. This review aimed to sensitise the practitioners on different alcohol state markers available now-a-days. An electronic search in Google Scholar, MEDLINE, and PubMed was conducted by using following keywords: Alcohol biomarkers, State markers, Trait markers, Alcohol consumption test. Studies on alcohol biomarkers published in English language were included in this review. Reviews and studies with free access to only abstract have been excluded. The state markers mostly used to identify chronic alcohol exposure are the Gamma-Glutamyltransferase (GGT), Aspartate and Alanine Aminotransferase (AST and ALT) which are routine serum liver function panels and Mean Corpuscular Volume (MCV) which is a haematological marker. The available non-conventional state biomarkers are Phosphatidylethanol (PEth), Fatty Acid Ethyl Esters (FAEE) and 5-Hydroxytryptophol (5-HTOL). The novel state markers which have been developed in recent research context are still awaiting validation and possible introduction to commercial settings are Plasma Sialic Acid Index of Apolipoprotein J (SIJ), Total Serum Sialic Acid (TSA), Acetaldehyde, Acetaldehyde adducts, anti-adduct antibodies and β-Hexosaminidase. Conventional alcohol biomarkers are routinely used in clinical practice. Non-conventional biomarkers seem to be promising for its estimation. Novel biomarkers are at various stages of research and development.

К МОРФОЛОГИИ ИЗМЕНЕНИЙ В ЯИЧКАХ ЭКСПЕРИМЕНТАЛЬНЫХ ЖИВОТНЫХ ПРИ ХРОНИЧЕСКОМ ОТРАВЛЕНИИ АЛКОГОЛЕМ

The experiment with the chronic effects of alcohol on experimental animals reflects the picture of long-term use of alcoholic beverages by a person with alcoholism. It is impossible to fully study the ultrastructural changes in internal organs, including the reproductive system, in humans, both in acute and chronic alcohol consumption, but the results obtained in the experiment can be extrapolated to humans. The results obtained showed that changes in the parenchymal-stromal elements of the testicles during chronic alcoholization are reduced to dystrophic transformation of the spermatogenic epithelium. The testicular stroma is characterized by pronounced circulatory disorders with plethora and stasis in the postcapillaries and small veins, edema, phenomena of perivascular and interstitial sclerosis, with foci of pronounced hyalinosis, most expressed by 2-3 months of alcoholism. By 6 months of the model experiment, there was no dynamics of the growth of morphological changes, partial adaptation to constant intoxication with ethyl alcohol.

The role of alcohol consumption on acetaminophen induced liver injury: Implications from a mathematical model

Acetaminophen (APAP) overdose is one of the predominant causes of drug induced acute liver injury in the U.S and U.K. Clinical studies show that ingestion of alcohol may increase the risk of APAP induced liver injury. Chronic alcoholism may potentiate APAP hepatotoxicity and this increased risk of APAP toxicity is observed when APAP is ingested even shortly after alcohol is cleared from the body. However, clinical reports also suggest that acute alcohol consumption may have a protective effect against hepatotoxicity by inhibiting microsomal acetaminophen oxidation and thereby reducing N-acetyl-p-benzoquinone imine (NAPQI) production. The aim of this study is to model this dual role of alcohol to determine how the timing of alcohol ingestion affects APAP metabolism and resulting liver injury and identify mechanisms of APAP induced liver injury. The mathematical model is developed to capture condition of a patient of single time APAP overdose who may be an acute or chronic alcohol user. The analysis suggests that the risk of APAP-induced hepatotoxicity is increased if APAP is ingested shortly after alcohol is cleared from the body in chronic alcohol users. A protective effect of acute consumption of alcohol is also observed in patients with APAP overdose. For example, simultaneous ingestion of alcohol and APAP overdose or alcohol intake after or before few hours of APAP overdose may result in less APAP-induced hepatotoxicity when compared to a single time APAP overdose. The rate of hepatocyte damage in APAP overdose patients depends on trade-off between induction and inhibition of CYP enzyme.