Acute Alcohol Consumption Research Articles

A case-crossover study of alcohol consumption, meals and the risk of road traffic crashes

BackgroundThe case-crossover (CC) design has proved effective to investigate the association between alcohol use and injuries in general, but has never been applied to study alcohol use and road traffic crashes (RTCs) specifically. This study aims at investigating the association between alcohol and meal consumption and the risk of RTCs using intrapersonal comparisons of subjects while driving.MethodsDrivers admitted to an Italian emergency room (ER) after RTCs in 2007 were interviewed about personal, vehicle, and crash characteristics as well as hourly patterns of driving, and alcohol and food intake in the 24 hours before the crash. The odds ratio (OR) of a RTC was estimated through a CC, matched pair interval approach. Alcohol and meal consumption 6 and 2 hours before the RTC (case exposure window) were compared with exposures in earlier control windows of analogous length.ResultsOf 574 patients enrolled, 326 (56.8%) reported previous driving from 6 to 18 hours before the RTC and were eligible for analysis. The ORs (mutually adjusted) were 2.25 (95%CI 1.11-4.57) for alcohol and 0.94 (0.47-1.88) for meals. OR for alcohol was already increased at low (1-2 units) doses - 2.17 (1.03-4.57) and the trend of increase for each unit was significant - 1.64 (95%CI 1.05-2.57). In drivers at fault the OR for alcohol was 21.22 (2.31-194.79). The OR estimate for meal consumption seemed to increase in case of previous sleep deprivation, 2.06 (0.25-17.00).ConclusionEach single unit of acute alcohol consumption increases the risk of RTCs, in contrast with the 'legal' threshold allowed in some countries. Meal consumption is not associated with RTCs, but its combined effects with sleepiness need further elucidation.

Short‐term Administration of Ethanol in Mice Deviates Antigen Presentation Activity Towards B Cells

Alcohol has a variety of short- and long-term effects on cell-mediated and humoral immune response. Herein, we have characterized the impact of high-dose EtOH administration on phenotypic and functional features of murine APC subsets, including dendritic cell (DC), macrophages and B cells. Impaired cytokine synthesis and Leishmania-phagocytosis was observed in peritoneal macrophages following EtOH administration. Moreover, EtOH exposure led to decreased levels of splenic myeloid DC and increased percentage of macrophages with no changes in splenic lymphoid DC and B cells. Adverse effects of short-term EtOH administration also resulted in impaired OVA-endocytosis by DC and macrophages. In contrast, EtOH consumption upregulates OVA-internalization by B cells. These changes on APC hierarchy may play a role shifting the fate of the immune response after EtOH ingestion. In addition to an overall downregulation of Toll-like receptor-TLR-4 expression by splenic APC, a downregulation of TLR-2 expression in macrophages was observed. Moreover, EtOH exposure altered the expression of co-signalling molecules on splenic APC, downregulating CD40 on macrophages and upregulating CD80 on B cells, with no impact on DC subsets. The net result of changes in TLR-mediated and co-stimulatory signals may determine the altered immunological status induced by acute consumption of alcohol. A direct impact of high-dose EtOH administration in the activation status of splenic CD4(+) T cells was observed. Together, our results demonstrated that short-term high-dose EtOH administration has differential impact on APC populations, downregulating splenic macrophages and DC activity but up-regulating B lymphocyte function as APC, and ultimately yielding a micro-environment that led to increased activation of CD4(+) T cells.

Acute and usual drinking among emergency trauma patients: a study on alcohol consumption and injury patterns

Objective:To investigate the relationship between usual and acute alcohol consumption among injured patients and, when combined, how they covary with other injury attributes.Methods:Data from a randomised sample of 486 injured...

Acute effects of intravenously administered ethanol on retinal vessel diameters and flicker induced vasodilatation in healthy volunteers

There is evidence from several vascular beds that acute alcohol consumption causes ocular hypotension and peripheral vasodilatation. The current study investigated the effects of intravenously administered ethanol on retinal vessel diameters and on flicker induced retinal vasodilatation. For this purpose, ethanol (0.35 g/kg) or placebo (physiologic saline solution) was administered intravenously for 40 min in a randomized, double masked, two way cross-over design to 12 healthy male volunteers. Retinal vessel diameters and flicker induced vasodilatation were measured before administration of ethanol as well as 30, 50, 90 and 130 min after the start of infusion with a retinal vessel analyzer. Intraocular pressure, systemic blood pressure and blood ethanol concentration were determined at the same time points. Intravenous administration of ethanol increased blood ethanol concentration from 0.0 g/l to 0.56 ± 0.10 g/l. Ethanol reduced IOP, but did not change ocular perfusion pressure. After cessation of the infusion blood ethanol concentration started to drop reaching a blood ethanol concentration of 0.22 ± 0.06 g/l 130 min after the start of infusion. Retinal arterial diameters increased significantly after administration of ethanol by a maximum of + 4.2 ± 4.0%, whereas no change was observed in retinal veins. Neither arterial nor venous diameters were influenced by administration of placebo. Flicker stimulation induced a significant dilatation in both arterial and venous diameters. Ethanol did not change flicker responses in arteries or in retinal veins. In conclusion, intravenous administration of ethanol increases retinal arterial diameters, whereas venous diameters remained unchanged. Whether this is related to a direct vasodilator effect or to a hitherto unidentified mechanism remains to be clarified.

Abstract: 556 TRIACYLGLYCEROL-RICH LIPOPROTEINS INFLUENCE THE INACTIVATION OF LIPOPROTEIN LIPASE BY ANGPTL 3 AND ANGPTL 4

Acute alcohol consumption can induce hypertriglyceridemia. Such an effect could be explained in part by the influence of alcohol on lipoprotein lipase (LPL) – the key enzyme responsible for triglyceride hydrolysis in circulation. Therefore, we have studied the effects of acute moderate alcohol consumption on LPL activity and on the concentrations of angiopoietin-like proteins 3 and 4 (ANGPTL3 and ANGPTL4), which are known to inhibit LPL.Two experiments were carried out in 8 healthy volunteers. They received 25 g of alcohol (vodka) in one experiment and water in the other (control). The in vivo function of LPL was estimated using intravenous fat tolerance tests (IVFTT) carried out before, 2 and 4 hours after alcohol administration. At the end of each experiment, LPL activity and mass were measured in post-heparin plasma (PHP). The concentrations of ANGPTL3 and ANGPTL4 in blood were measured before alcohol consumption and at the end of the experiments.LPL activity, as estimated using the IVFTT, was reduced by 25% and 24% two and four hours after the administration of alcohol, respectively, and was not affected in the control experiment. At the end of the experiment, LPL activity in PHP was 23% lower after alcohol consumption than in the controls. The concentrations of ANGPTL3 and ANGPTL4 had dropped to 67% and 86% of baseline values, respectively, at 280 min after alcohol consumption. These levels were not affected in the control experiment. The levels of ANGPTL4 but not those of ANGPTL3 were increased in PHP compared to both baseline values and values at 280 min.The capacity for triglyceride clearance seemed to be acutely reduced by alcohol consumption and the effect persisted for several hours. The levels of LPL activity in PHP were reduced to a similar extent. This reduction in LPL activity could not be explained by the changes in the levels of ANGPTL3 or ANGPTL4, which both decreased.

Associação entre o polimorfismo funcional do promotor ligado ao transportador da serotonina (5-HTTLPR): agressividade externalizada e internalizada e abuso do álcool.

Genetic factors of alcoholism influence the phenotypic heterogeneity of alcohol dependence, allowing the higher or lower expression of related aggressive behaviours. The pathogenesis of alcoholism and anti-social behaviour has been connected to serotonergic system dysfunction, given support to examine the association with 44-basepair insertion/deletion polymorphism of serotonin gene transporter (5-HTT). The study aims to assess the relationship between 5-HHTLPR polymorphism, aggressive behaviour and alcohol consumption pattern. There were recruited 97 alcohol dependent patients from the alcoholism unit (Etilo-Risco) of the Psychiatric Service of Santa Maria Hospital. Blood for DNA extraction and clinical and behavioural information was collected during the therapeutic program. Regarding 5-HTTLPR polymorphism prevalence in alcoholic population, 30.7% were homozygotic to l allele, 19.8% were homozygotic to s allele and 49.5% were heterozygotic l/s. Alcoholic patients carrying the l allele from 5-HTTLPR genotype showed significant lower scores of aggressivity during acute alcohol consumption, and alcoholic patients carrying the s allele showed significant higher scores of aggressivity (during acute alcohol consumption and abstinence), however, the results were not significant. The association between the functional nature of the s allele of 5-HTTLPR polymorphism with aggressive behaviour is in agreement with the general models of aggressivity that report low levels of central serotonergic activity related to impulsive and anti-social behaviours. The results demonstrate an association between 5-HTTLPR polymorphism and the auto and heteroaggressive behaviour in alcohol dependent population, particularly when aggressivity appears under acute alcohol consumption. During acute alcohol consumption stage, the presence of the l allele may act as a protective factor of aggressive behaviour risk, whereas the results tendency showed the s allele as susceptibility factor. Data suggests that the presence of s allele may confer a genetic vulnerability factor to the development of aggressive behaviour in alcohol dependent subjects, specially, in interaction with acute alcohol consumption stage.

Cinnamon Extract Protects against Acute Alcohol-Induced Liver Steatosis in Mice

Acute and chronic consumption of alcohol can cause increased intestinal permeability and bacterial overgrowth, thereby increasing portal endotoxin levels. This barrier impairment subsequently leads to an activation of hepatic Kupffer cells and increased release of reactive oxygen species as well as of tumor necrosis factor-α (TNFα). Recent studies have suggested that cinnamon extract may have antiinflammatory effects. In the present study, the protective effects of an alcoholic extract of cinnamon bark was assessed in a mouse model of acute alcohol-induced steatosis and in RAW 264.7 macrophages, used here as a model of Kupffer cells. Acute alcohol ingestion caused a >20-fold increase in hepatic lipid accumulation. Pretreatment with cinnamon extract significantly reduced the hepatic lipid accumulation. This protective effect of cinnamon extract was associated with an inhibition of the induction of the myeloid differentiation primary response gene (MyD) 88, inducible nitric oxide (NO) synthase (iNOS), and plasminogen activator inhibitor 1 mRNA expression found in livers of alcohol-treated animals. In vitro prechallenge with cinnamon extract suppressed lipopolysaccharide (LPS)-induced MyD88, iNOS, and TNFα expression as well as NO formation almost completely. Furthermore, LPS treatment of RAW 264.7 macrophages further resulted in degradation of inhibitor κB; this effect was almost completely blocked by cinnamon extract. Taken together, our data show that an alcohol extract of cinnamon bark may protect the liver from acute alcohol-induced steatosis through mechanisms involving the inhibition of MyD88 expression.

Effects of Acute Alcohol Consumption in Older and Younger Adults: Perceived Impairment Versus Psychomotor Performance

Perceived impairment and psychomotor performance following acute alcohol administration in older (ages 50-74, n=42; 22 male) and younger (ages 25-35, n=26; 12 male) adults were investigated in this study. Double-blind, placebo-controlled alcohol administration techniques were designed to produce peak levels of breath alcohol concentration consistent with an episode of social drinking (40 mg/100 ml). Behavioral measures (Trail Making Test, Forms A and B), as well as measures of self-reported perceived intoxication and impairment, were administered on the ascending and descending limbs at common time points after beverage ingestion. Results indicated that psychomotor performance differences did not parallel self-reported levels of perceived impairment. Relative to younger adults, older adults exhibited performance deficits on the ascending limb while simultaneously reporting less perceived impairment. Conversely, on the descending limb, older adults who received alcohol reported more perceived impairment than did those who received placebo, although psychomotor performance between these two groups of older drinkers did not differ. For younger participants, a moderate dose of alcohol facilitated performance on the ascending limb; however, these differences were not reflected on the descending limb. These results reinforce the common knowledge that self-reported measures may not provide an accurate reflection of performance outcomes and, importantly, that older adults may be impaired even under a moderate dose of alcohol, although they may not be aware (i.e., report) of this impairment.

P.2.01 Effects of acute alcohol consumption on attentional bias: a stimuli orientation effect

P.2.01 Effects of acute alcohol consumption on attentional bias: a stimuli orientation effect

Activation of Liver Tryptophan Pyrrolase Mediates the Decrease in Tryptophan Availability to the Brain after Acute Alcohol Consumption by Normal Subjects

We have previously suggested that acute ethanol consumption by normal subjects decreases the availability of circulating tryptophan (Trp) to the brain by activating liver Trp pyrrolase, the first and rate-limiting enzyme of the (major) kynurenine pathway of Trp degradation. The aim of the present study was to examine this hypothesis further by measuring plasma levels of kynurenine metabolites following alcohol consumption. After an overnight fast and a light breakfast, each of 10 healthy subjects received one of five drinks (placebo and doses of ethanol of 0.2, 0.4, 0.6 and 0.8 g/kg body weight in tonic water) on five different occasions. Blood samples were withdrawn 2 h later and plasma was analysed for concentrations Trp, competing amino acids (CAA) and kynurenine metabolites. Along with the depletion of plasma Trp and the decrease in its availability to the brain, as expressed by the ratio of [Trp]/[CAA], plasma kynurenine was elevated by doses of ethanol of 0.2-0.8 g/kg body weight. The ratio% of [kynurenine]/[Trp], an index of the expression of Trp pyrrolase activity, was also increased by all doses of ethanol. We conclude that activation of liver Trp pyrrolase mediates the depletion of plasma Trp and the decrease in its availability to the brain induced by acute ethanol consumption.

Alcohol Portrayal on Television Affects Actual Drinking Behaviour

Alcohol portrayal in movies and commercials is generally positive and might stimulate young people to drink. We tested experimentally whether portrayal of alcohol images in movies and commercials on television promotes actual drinking. In a naturalistic setting (a bar lab), young adult male pairs watched a movie clip for 1 h with two commercial breaks and were allowed to drink non-alcohol and alcoholic beverages. These participants were randomly assigned to one of four conditions varying on the type of movie (many versus few alcohol portrayals) and commercials (alcohol commercials present or not). Participants assigned to the conditions with substantial alcohol exposure in either movies or commercials consume more alcohol than other participants. Those in the condition with alcohol portrayal in movie and commercials drank on average 1.5 glasses more than those in the condition with no alcohol portrayal, within a period of 1 h. This study-for the first time-shows a causal link between exposure to drinking models and alcohol commercials on acute alcohol consumption.

Acute alcohol consumption aggravates the decline in muscle performance following strenuous eccentric exercise

This study investigated the effects of acute moderate alcohol intake on muscular performance during recovery from eccentric exercise-induced muscle damage. Eleven healthy males performed 300 maximal eccentric contractions of the quadriceps muscles of one leg on an isokinetic dynamometer. They then consumed a beverage containing 1 g/kg bodyweight ethanol (as vodka and orange juice) (ALC). On another occasion they performed an equivalent bout of eccentric exercise on the contralateral leg after which they consumed an isocaloric quantity of orange juice (OJ). Measurement of maximal isokinetic (concentric and eccentric) and isometric torque produced across the knee, plasma creatine kinase (CK) concentrations and muscle soreness were made before and at 36 and 60 h following each exercise bout. All measures of muscle performance were significantly reduced at 36 and 60 h post-exercise compared to pre-exercise measures (all p < 0.05). The greatest decreases in peak strength were observed at 36 h with losses of 12%, 28% and 19% occurring for OJ isometric, concentric, and eccentric contractions, respectively. However, peak strength loss was significantly greater in ALC with the same performance measures decreasing by 34%, 40% and 34%, respectively. Post-exercise plasma creatine kinase activity and ratings of muscle soreness were not different between conditions (both p > 0.05). These results indicate that consumption of even moderate amounts of alcohol following eccentric-based exercise magnifies the normally observed losses in dynamic and static strength. Therefore, to minimise exercise related losses in muscle function and expedite recovery, participants in sports involving eccentric muscle work should avoid alcohol-containing beverages in the post-event period.

Effects of acute alcohol consumption and vitamin E co-treatment on oxidative stress parameters in rats tongue

The aim of this study was to evaluate the effects of acute alcohol consumption and vitamin E co-treatment upon oxidative stress parameters in rats tongue. Thirty-eight, Wistar rats were separated into five groups (alcohol, alcohol/vitamin E, control, Tween, vitamin E). Alcohol and alcohol vitamin E groups had the standard diet, and 40% alcohol on drinking water. Other groups were fed with the same standard diet and water ad libitum. Vitamin E was given by gavage to vitamin E and alcohol/vitamin E rats twice a week. Alcohol and control groups were subjected to saline gavage and Tween group to 5% Tween 80 solution, the vitamin E vehicle. At day 14, the animals were anesthetized and specimens were obtained from tongue. Lipid peroxidation (TBARS), protein oxidative damage, catalase (CAT) and superoxide dismutase (SOD) activities were quantified. Alcohol group decreased TBARS in relation to control group and alcohol vitamin-treated animals decreased TBARS when compared to Tween and vitamin E groups. SOD activity was lower and CAT activity was higher in animals treated with both alcohol and vitamin E. These results suggest that short-term alcohol consumption decreases lipid peroxidation levels. Alternatively, alcohol/vitamin E group increased CAT, showing the toxicity of this association.

Effects of alcohol consumption and alcohol expectancy on the categorisation of perceptual cues of emotional expression

Evidence that alcohol leads to increased aggressive behaviour is equivocal and confounded by evidence that such effects may operate indirectly via expectancy. One mechanism by which alcohol consumption may increase aggressive behaviour is via alterations in the processing of emotional facial cues. We investigated whether acute alcohol consumption or the expectancy of consuming alcohol (or both) induces differences in the categorisation of ambiguous emotional expressions. We also explored differences between male and female participants, using male and female facial cues of emotional expression. Following consumption of a drink, participants completed a categorisation task in which they had to identify the emotional expression of a facial stimulus. Stimuli were morphed facial images ranging between unambiguously angry and happy expressions (condition 1) or between unambiguously angry and disgusted expressions (condition 2). Participants (N = 96) were randomised to receive an alcoholic or non-alcoholic drink and to be told that they would receive an alcoholic or non-alcoholic drink. Significant effects of alcohol were obtained in the angry-disgusted task condition, but only when the target facial stimulus was male. Participants tended to categorise male disgusted faces as angry after alcohol, but not after placebo. Our data indicate that alcohol consumption may increase the likelihood of an ambiguous but negative facial expression being judged as angry. However, these effects were only observed for male faces and therefore may have been influenced by the greater expectation of aggression in males compared to females. Implications for alcohol-associated aggressive behaviour are discussed.

In vitroandin vivomodels of acute alcohol exposure

Alcohol abuse is a global problem due to the financial burden on society and the healthcare system. While the harmful health effects of chronic alcohol abuse are well established, more recent data suggest that acute alcohol consumption also affects human wellbeing. Thus, there is a need for research models in order to fully understand the effect of acute alcohol abuse on different body systems and organs. The present manuscript summarizes the interdisciplinary advantages and disadvantages of currently available human and non-human models of acute alcohol abuse, and identifies their suitability for biomedical research.

Alcohol's Role in Men's Use of Coercion to Obtain Unprotected Sex

Past sexual victimization has been identified as a predictor of women's sexual risk-taking. In order to develop effective prevention and treatment programs, research is needed that examines perpetrators' characteristics. Thus, the goal of this study was to examine predictors of men's willingness to use coercive strategies to obtain sex without a condom. Male college students (n = 72) completed a survey that assessed past sexual assault perpetration, hostility, past misperception of women's sexual cues, usual alcohol consumption, and usual condom use. One month later, they participated in an alcohol administration study and watched a video about a couple in a consensual sexual situation. Participants were asked to evaluate how justified they would be in using a variety of coercive strategies to make the woman have unprotected sex. In hierarchical multiple regression analyses, there was a significant main effect of past perpetration such that men who had previously committed sexual assault felt more justified using coercive strategies to obtain unprotected sex than did nonperpetrators. Acute alcohol consumption did not have a main effect; however, it interacted with hostility and misperception. Among participants who consumed alcohol prior to watching the video, the greater their preexisting hostility, the more justified they felt in using coercion. Similarly, the more frequently drinkers had misperceived women's sexual intentions in the past, the more justified they felt in using coercion. Based on these findings, several specific suggestions are made for prevention and treatment programs, including targeted communication skills and normative feedback interventions.

A Blocker of N- and T-type Voltage-Gated Calcium Channels Attenuates Ethanol-Induced Intoxication, Place Preference, Self-Administration, and Reinstatement

There is a clear need for new therapeutics to treat alcoholism. Here, we test our hypothesis that selective inhibitors of neuronal calcium channels will reduce ethanol consumption and intoxication, based on our previous studies using knock-out mice and cell culture systems. We demonstrate that pretreatment with the novel mixed N-type and T-type calcium channel antagonist 1-(6,6-bis(4-fluorophenyl)hexyl)-4-(3,4,5-trimethoxybenzyl)piperazine (NP078585) reduced ethanol intoxication. NP078585 also attenuated the reinforcing and rewarding properties of ethanol, measured by operant self-administration and the expression of an ethanol conditioned place preference, and abolished stress-induced reinstatement of ethanol seeking. NP078585 did not affect alcohol responses in mice lacking N-type calcium channels. These results suggest that selective calcium channel inhibitors may be useful in reducing acute ethanol intoxication and alcohol consumption by human alcoholics.

Alcohol Impairs Long-Term Depression at the Cerebellar Parallel Fiber–Purkinje Cell Synapse

Acute alcohol consumption causes deficits in motor coordination and gait, suggesting an involvement of cerebellar circuits, which play a role in the fine adjustment of movements and in motor learning. It has previously been shown that ethanol modulates inhibitory transmission in the cerebellum and affects synaptic transmission and plasticity at excitatory climbing fiber (CF) to Purkinje cell synapses. However, it has not been examined thus far how acute ethanol application affects long-term depression (LTD) and long-term potentiation (LTP) at excitatory parallel fiber (PF) to Purkinje cell synapses, which are assumed to mediate forms of cerebellar motor learning. To examine ethanol effects on PF synaptic transmission and plasticity, we performed whole cell patch-clamp recordings from Purkinje cells in rat cerebellar slices. We found that ethanol (50 mM) selectively blocked PF-LTD induction, whereas it did not change the amplitude of excitatory postsynaptic currents at PF synapses. In contrast, ethanol application reduced voltage-gated calcium currents and type 1 metabotropic glutamate receptor (mGluR1)-dependent responses in Purkinje cells, both of which are involved in PF-LTD induction. The selectivity of these effects is emphasized by the observation that ethanol did not impair PF-LTP and that PF-LTP could readily be induced in the presence of the group I mGluR antagonist AIDA or the mGluR1a antagonist LY367385. Taken together, these findings identify calcium currents and mGluR1-dependent signaling pathways as potential ethanol targets and suggest that an ethanol-induced blockade of PF-LTD could contribute to the motor coordination deficits resulting from alcohol consumption.

Acute Alcohol Intake Induces SOCS1 and SOCS3 and Inhibits Cytokine‐Induced STAT1 and STAT3 Signaling in Human Monocytes

Acute alcohol consumption is associated with induction of immuno-inhibitory cytokines and down-regulation of pro-inflammatory responses to various pathogens. We previously reported that alcohol activates janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling leading to IL-10 induction. The JAK-STAT pathway also activates its own negative regulators, suppressors of cytokine signaling (SOCS) 1 and SOCS3. SOCS proteins are inducible inhibitors that negatively regulate STAT3/STAT1 signaling pathways induced by cytokines, IL-6 or IFNs. Here we aimed to explore the effect of acute alcohol on induction of SOCS1/SOCS3 and regulation of STAT3/STAT1 pathways induced by IL-6 or IFNs in human monocytes. Blood samples from normal volunteers were collected before and 24 hours after consumption of 2 ml vodka/kg body weight. For in vitro experiments human monocytes were pretreated with ethanol (EtOH) followed by stimulation with cytokines; proteins were analyzed by Western blot, nuclear protein binding to DNA by EMSA, and RNA by real time PCR. Acute in vivo or in vitro alcohol treatment increased both SOCS1 and SOCS3 RNA expression in monocytes. Alcohol treatment resulted in increased STAT3 and STAT1 DNA binding capacity. Activation of both STAT1 and STAT3 has been shown to induce SOCS1/3. We hypothesized that induction of SOCS proteins by alcohol in turn may lead to modulation of cytokine signaling through STAT1 and STAT3. Indeed, we observed significant down-regulation of IL-6-, IFNalpha- and IFNgamma-induced STAT1 DNA binding as well as inhibition of IL-6- and IFNgamma-induced STAT3 when alcohol was added to monocytes 3 hours prior to the cytokine stimulation. Consistent with inhibition of IL-6-induced STAT3 DNA binding in alcohol-pretreated cells, the levels of IL-6-dependent genes, MCP-1 and ICAM-1, was reduced after IL-6 stimulation. Similar to EtOH alone, combined EtOH+IL-6 simulation resulted in increased expression of both SOCS3 and SOCS1 genes. While acute alcohol treatment alone activates STAT1/3 signaling pathways and induces SOCS3 and SOCS1 levels in monocytes, alcohol also leads to down-regulation of IL-6-, IFNalpha-, and IFNgamma-induced signaling via STAT1/STAT3 pathways, likely through excessive SOCS activation.

Alcohol and Nonlethal Injuries: A Swiss Emergency Department Study on the Risk Relationship Between Acute Alcohol Consumption and Type of Injury

Acute alcohol consumption has been reported to be an important risk factor for injury, but clear scientific evidence on issues such as injury type is not available. The present study aims to improve the knowledge of the importance of alcohol consumption as an injury determinant with regards to two dimensions of the type of injury, namely the nature and the body region involved. Risk relationships between two injury type components and acute alcohol use were estimated through multinomial and logistic regression models based on data from 7,529 patients-among whom 3,682 had injury diagnoses-gathered in a Swiss emergency department. Depending on the type of injury, between 31.1% and 48.7% of casualties report alcohol use before emergency department attendance. The multinomial regression models show that even low alcohol levels are consistently associated with nearly all natures of injury and body regions. A persistent dose-response effect between alcohol levels and risk associations was observed for almost all injury types. The results highlight the importance and consistency of the risk association between low and moderate levels of acute alcohol consumption and all types of injury. None of the body regions and natures of injury could pride on absence of association between alcohol and injury. Public health, prevention, and care implications are considered.