Lower Blood Alcohol Levels Research Articles

Predictive Power of Interictal Epileptiform Discharges in Fitness-to-Drive Evaluation.

This study aimed to evaluate and predict the effects of interictal epileptiform discharges (IEDs) on driving ability using simple reaction tests and a driving simulator. Patients with various epilepsies were evaluated with simultaneous EEGs during their response to visual stimuli in a single-flash test, a car-driving video game, and a realistic driving simulator. Reaction times (RTs) and missed reactions or crashes (miss/crash) during normal EEG and IEDs were measured. IEDs, as considered in this study, were a series of epileptiform potentials (>1 potential) and were classified as generalized typical, generalized atypical, or focal. RT and miss/crash in relation to IED type, duration, and test type were analyzed. RT prolongation, miss/crash probability, and odds ratio (OR) of miss/crash due to IEDs were calculated. Generalized typical IEDs prolonged RT by 164 ms, compared with generalized atypical IEDs (77.0 ms) and focal IEDs (48.0 ms) (p < 0.01). Generalized typical IEDs had a session miss/crash probability of 14.7% compared with a zero median for focal and generalized atypical IEDs (p < 0.01). Long repetitive bursts of focal IEDs lasting >2 seconds had a 2.6% miss/crash probabilityIED. Cumulated miss/crash probability could be predicted from RT prolongation: 90.3 ms yielded a 20% miss/crash probability. All tests were nonsuperior to each other in detecting miss/crash probabilitiesIED (zero median for all 3 tests) or RT prolongations (flash test: 56.4 ms, car-driving video game: 75.5 ms, simulator 86.6 ms). IEDs increased the OR of miss/crash in the simulator by 4.9-fold compared with normal EEG. A table of expected RT prolongations and miss/crash probabilities for IEDs of a given type and duration was created. IED-associated miss/crash probability and RT prolongation were comparably well detected by all tests. Long focal IED bursts carry a low risk, while generalized typical IEDs are the primary cause of miss/crash. We propose a cumulative 20% miss/crash risk at an RT prolongation of 90.3 ms as a clinically relevant IED effect. The IED-associated OR in the simulator approximates the effects of sleepiness or low blood alcohol level while driving on real roads. A decision aid for fitness-to-drive evaluation was created by providing the expected RT prolongations and misses/crashes when IEDs of a certain type and duration are detected in routine EEG.

Self-Assembled Micelles Improve the Oral Bioavailability of Dihydromyricetin and Anti-Acute Alcoholism Activity.

Dihydromyricetin (DMY) is highly effective in counteracting acute alcohol intoxication. However, its poor aqueous solubility and permeability lead to the low oral bioavailability and limit its clinic application. The aim of this work is to use Solutol®HS15 (HS 15) as surfactant to develop novel micelle to enhance the oral bioavailability of DMY by improving its solubility and permeability. The DMY-loaded Solutol®HS15 micelles (DMY-Ms) were prepared by the thin-film hydration method. The particle size of DMY-Ms was 13.97 ± 0.82 nm with an acceptable polydispersity index of 0.197 ± 0.015. Upon entrapped in micelles, the solubility of DMY in water was increased more than 25-fold. The DMY-Ms had better sustained release property than that of pure DMY. In single-pass intestinal perfusion models, the absorption rate constant (Ka) and permeability coefficient (Papp) of DMY-Ms were 5.5-fold and 3.0-fold than that of pure DMY, respectively. The relative bioavailability of the DMY-Ms (AUC0-∞) was 205% compared with that of pure DMY (AUC0-∞), indicating potential for clinical application. After administering DMY-Ms, there was much lower blood alcohol level and shorter duration of the loss of righting relax (LORR) in drunk animals compared with that treated by pure DMY. In addition, the oral administration of DMY-Ms greatly reduced oxidative stress, and significantly defended liver and gastric mucosa from alcoholic damages in mice with alcohol-induced tissue injury. Taken together, HS 15-based micelle system greatly improves the bioavailability of DMY and represents a promising strategy for the management of acute alcoholism. Graphical abstract.

Novel Binge Drinking Model Causes Perturbations in Muscle Metabolism with Refeeding

IntroductionIt is well known that acute alcohol intoxication impairs metabolic signaling within skeletal muscle including suppression of protein synthesis which is at least partially due to inhibition of mTOR activity as assessed by phosphorylation of its downstream substrates p70 ribosomal protein S6 Kinase 1 (S6K1), ribosomal protein S6 (rpS6) and eukaryotic initiation factor 4E (4E‐BP1). The current mouse model used to mimic binge drinking employs either oral gavage or intraperitoneal (IP) injection, both of which are stressful to the animal and in the case of the injection, lack physiological relevance as it bathes all organs in a high dose of alcohol while bypassing normal intestinal metabolism. Therefore, we wanted to determine if an acute ‘dose’ of alcohol incorporated into the food would be sufficient to mimic the binge drinking effects previously reported.MethodsC57BL6 male (n=9) and female mice (n=10) were randomized to receive either control liquid diet food (# 710027, DYETS, Bethlehem, PA), or a calorie (kcal) matched liquid diet containing 32% kcal from alcohol (# 710260, DYETS, Bethlehem, PA). Following a 1 week acclimation period to the control liquid diet, mice were fasted for 16 hours during their light cycle and then, at the onset of the dark cycle, were provided with liquid diet (Con or EtOH) for 30 minutes. The gastrocnemius (GAS) and blood were collected 1.5 hour after the beginning of the refeeding period. Western blots were performed on GAS for protein expression. T‐tests (2 tailed, unpaired) for males (Con vs. EtOH), and females (Con vs. EtOH), or between sexes of the same dietary treatment group, were used for analysis (p&lt;0.05).ResultsDespite the high concentration of alcohol in the liquid diet and its novel introduction to the EtOH group, male mice consumed the same volume of food regardless of treatment group. Control females though, consumed significantly more food than EtOH females (4.5 mL vs. 3.6 mL). Alcohol intake per kg body weight was higher in females than males; however, total alcohol intake (g), and blood alcohol levels (213 vs. 187 mg/dL), were not different between males and females. Alcohol intake decreased AKT S473 phosphorylation in GAS, along with phosphorylation of mTOR S2448 in males and females. Downstream substrates of mTOR were also suppressed by alcohol, including phosphorylation of S6K1 T389 and rpS6 S240/244.ConclusionDespite lower blood alcohol levels (compared to injection), alcohol reversed or prevented the increase in mTOR signaling typically induced by an anabolic stimulus (i.e. nutrient intake). Further, novel findings included the consumption of a high percentage of alcohol in liquid diet form without any prior exposure to a lower dose or acclimation period to alcohol. Future work will continue to characterize this model and lead to optimization of models of alcohol intoxication that best mimic human practice.

Do not drink and lyse: alcohol intoxication increases fibrinolysis shutdown in injured patients

IntroductionHigh alcohol consumption has been associated with decreased fibrinolysis and enhanced thrombosis risk in cardiovascular disease. In trauma, alcohol has been associated with poor clot formation; however, its effect on fibrinolysis has not been fully investigated. We assessed the association of blood alcohol levels and fibrinolysis in trauma activation patients.MethodsWe queried our prospective registry of trauma activations from 2014 to 2016. Associations between viscoelastic measurements [rapid thrombelastography (rTEG)] and blood alcohol level (BAL) were determined and adjusted for confounders by a multinomial logistic regression. Lysis phenotypes were defined by the % lysis in 30 min (LY30) as follows: hyperfibrinolysis ≥ 3%, physiologic 0.9–2.9%, and fibrinolysis shutdown < 0.9%.ResultsOverall, 191 (43.8%) had BAL measured. There were 65 (34%) patients that had no detectable BAL, 32 (16.8%) had BAL of 10–150 mg/dL, and 94 (49.2%) patients had BAL > 150 mg/dL. BAL had a moderate, but significant inverse correlation with LY30 (Rho = − 0.315, p < 0.001), while there were no significant correlations between BAL and other TEG values. The distribution of fibrinolysis phenotypes varied significantly by BAL levels (p < 0.009, with high BAL having more shutdown and less hyperfibrinolysis than the other two BAL level groups. Multinomial logistic regression showed that after adjustment for confounders, BAL levels > 150 mg/dL were independently associated with a threefold increase in the odds of shutdown compared to undetectable BAL (OR 3.37, 95% CI 1.04–8.05, p = 0.006). High BAL was also significantly associated with higher odds of shutdown compared to low BAL (OR 2.63, 95% CI 1.15–6.06). Compared to physiologic fibrinolysis, fibrinolysis shutdown was associated with increased mortality (OR 2.87, 95% CI 1.41–5.83) and VFD < 28 (OR 2.54, 95% CI 1.47–4.39).ConclusionIn the injured patient, high blood alcohol levels are associated with increased incidence of fibrinolysis shutdown. This finding has implications for postinjury hemostatic resuscitation as these patients may be harmed by anti-fibrinolytics. Further research is needed to assess whether the association with fibrinolysis is modified by the chronicity and type of alcohol consumed and whether anti-fibrinolytic therapy in intoxicated patients produces adverse effects.

The association between alcohol metabolism and genetic variants of ADH1A, SRPRB, and PGM1 in Korea.

Excessive alcohol consumption is a major public health problem in East Asian countries. Alcohol use leads to a cascade of problems including increased chances of risky behavior and a wide range of negative health consequences, from alcoholic liver disease to upper gastric and liver cancer. These alcohol effects are known to be influenced by ethnic variability and genetics. In this study, subjects were administered a single dose of alcohol (0.6g/kg for men or 0.4g/kg for women), and blood alcohol and acetaldehyde concentrations were measured eight times over 5 hours. To investigate genetically susceptible factors to alcohol metabolism, we selected single-nucleotide polymorphisms (SNP) of genes identified by prior genetic association studies for alcohol metabolism, alcohol consumption, alcohol dependence, and related traits, and performed genotyping on all subjects (n=104). We identified variations in the ADH1A, SRPRB, and PGM1 genes, which are directly associated with blood alcohol or acetaldehyde concentrations. Namely, the T allele of SRPRB rs17376019 and the C allele of PGM1 rs4643 were associated with lower blood alcohol levels, while the ADH1 rs1229976C allele group exhibited markedly higher blood acetaldehyde levels than those of the ADH1 rs1229976T allele group. This study demonstrates that genetic variations in ADH1A, SRPRB, and PGM1 are associated with variations in blood alcohol and acetaldehyde concentration after alcohol intake.

Sub‐neurodegenerative Levels of Binge Alcohol Reduce Calcium‐independent Phospholipase A2 (iPLA2) Levels in Rat Brain: An Unrecognized Initial Sign of Neuroinflammation

Selective degeneration of dentate granule cells in hippocampus (HC), pyramidal cells in entorhinal cortex (EC), and olfactory bulb neurons occurs in adult male rats subjected to severe alcohol (ethanol) binges over 4 days that generate maximal blood alcohol levels of 350–450 mg/dl. Concurrent with brain damage specifically in these brain regions, significant alterations are elicited by alcohol in the levels of phospholipase A2 (PLA2) enzymes, i.e., (1) increases in Ca2+‐dependent cytosolic cPLA2 and secreted sPLA2, two membrane phospholipid‐metabolizing enzymes causing neuroinflammation via mobilization of omega‐6 arachidonic acid, a largely pro‐oxidative neurocellular mediator; and (2) reductions in Ca2+‐independent iPLA2, known to selectively regulate membrane release and turnover of anti‐inflammatory, anti‐oxidative omega‐3 docosahexaenoic acid (DHA). Furthermore, these neurodegenerative and neuroinflammatory changes are replicated in vitro, along with a loss in DHA content itself, in rat organotypic adult‐age HC‐EC slice cultures binge‐treated with 100 mM (~460 mg/dl) alcohol. Importantly, DHA pre‐supplementation of the slices prevents the neurodegeneration and PLA2 changes caused by alcohol (Tajuddin et al. 2014). The objective of this study was to determine if phospholipid‐mediated neuroinflammatory changes exist from alcohol in the absence of neurodegeneration. Here we report that rats subjected to less severe binges ‐ and thus lower blood alcohol levels of ~200 mg/dl, which are insufficient to cause detectable brain damage and/or neuroinflammatory cPLA2 and sPLA2 elevations ‐nevertheless cause significantly reduced iPLA2 levels that are largely reversed by DHA supplementation. The results imply that iPLA2 depletion and, we suspect, loss of cellular/membrane DHA (that iPLA2 regulates), are critical, previously unappreciated first indicators or markers of brain neuroinflammation due to binge alcohol. Similar changes in iPLA2, potentially due to its sensitivity, may have a bearing on other forms of brain insults causing neuroinflammation and ultimately neurodamage.Support or Funding InformationResearch support: NIH U01 AA018279 (MAC and HYK) and NIH T32 AA013527 (Loyola Medical Center Alcohol Research Program)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Sudden unexpected death in alcohol misuse: a case report

Alcohol is associated with a significant number of sudden deaths per year in the UK and deaths from alcohol-related causes are increasing at an alarming rate. These deaths are more common among white men who are over 50 years with fatty changes rather than the cirrhotic liver. The only findings at postmortem are fatty liver and a negative or low blood alcohol level. The mechanism of death is uncertain in most of the instances but there are some theories related to the suggested mechanism. Sometimes, pre-existing minor causes are incorrectly diagnosed as the cause of death. Therefore, forensic pathologist experiences major difficulties in ascertaining the cause of death. Awareness of the association between alcohol-related fatty change and sudden death is essential to give a correct cause of death at the autopsy examination. A 63-year-old man was found dead in his bathroom by his partner. There was no past medical history of diabetes mellitus, hypertension and alcohol withdrawal. He consumed 5-6 bottles of wine per day over the past 9 months. Postmortem examination revealed slight jaundice, pallor, mild atheromatous changes in coronary arteries, mild left ventricular hypertrophy and marked fatty changes in the liver. Microscopic examination of the liver revealed severe steatosis, predominantly macrovesicular. In addition to that, there was no evidence of chronic disease or pathology. Toxicology analysis revealed 113mg/dl of blood alcohol reset of investigations were unremarkable. Limited biochemical analyses were done. They did not show any evidence of significant electrolytes imbalances or hypo or hyperglycemia. Excluding all the possibilities and considering macroscopic and microscopic features, and toxicological investigations, the cause of death was ascertained as sudden unexpected death in alcohol misuse (SUDAM).

Suicidal ideation, suicide attempts, and psychological distress among intoxicated adolescents in the pediatric emergency department

Background: Studies have emphasized screening for psychiatric disorders, especially suicide risk in emergency departments. Psychiatric disorders and experimentation with alcohol increase in adolescence and intoxications among patients challenge the staff in emergency departments.Aims: This study examined the degree of suicidal ideation (SI) and suicidal behavior in adolescents, and the extent to which they differed from non-suicidal patients in terms of alcohol use, psychological distress, self-esteem, and perceived social support.Methods: The study comprised 120 adolescents, a mean age of 14.2 years. Of them 60% were females. We collected data on the clinical characteristics and assessed the patient’s psychiatric status using self-report scales and analyzed blood samples for alcohol. A consulting psychiatrist interviewed each patient before discharge to evaluate potential SI or suicide attempt (SA) using structured and semi-structured scales.Results: Of the 120 patients 20% had SI or had made a SA. High psychological distress in girls, low blood alcohol levels (BALs), as well as low scores on self-esteem, on social support and on familial support were associated with patients with SI/SA. Logistic regression showed that the most significant variables with suicidal patients included low BAL and low self-esteem and high alcohol consumption. Psychological distress had a direct and mediational role in the suicidal patients.Conclusions: Adolescents referred to the pediatric emergency department with intoxication displaying high psychological distress and low self-esteem represent a high-risk group of teens. In this group, careful assessment of mental health status, screening for suicidal ideation, and SAs seems warranted.

Impact of day-of-injury alcohol consumption on outcomes after traumatic brain injury: A meta-analysis

ABSTRACTAlthough a known risk factor for traumatic brain injury (TBI), alcohol has been found to both promote and protect against secondary brain damage. However, it is presently unclear whether the cognitive, psychological and medical/functional outcomes of adults who have consumed alcohol prior to sustaining a TBI differ from those who have not. This meta-analysis examined the outcomes of groups that differed in terms of their day-of-injury (DOI) blood alcohol levels (BALs) by comparing positive with zero BAL (BAL+/BAL-) and high with low BAL (BALhigh/BALlow) samples. The PubMed, PsycINFO, EMBASE, and Scopus databases were searched from inception until the end of March 2015. Hedge’s g effects (continuous data) and odds ratios (categorical data) were calculated for 27 studies that compared either the outcomes of BAL+ and BAL− groups or BALhigh and BALlow groups. BAL+ was associated with significantly poorer cognitive outcomes (overall and on general tests) and higher levels of disability, and BALhigh was associated with shorter stays in intensive care. More generally, however, most effect sizes were small to low-moderate in size, non-significant and inconsistent in their direction. Although DOI alcohol consumption increases the risk of sustaining a TBI, it is not consistently associated with better or worse outcomes, other than subtle cognitive deficits; the source of which remains to be determined.

Successful conviction of intoxicated drivers at a level I trauma center.

IntroductionConviction rates for drivers driving under the influence (DUI) and in motor vehicle collisions (MVC) presenting to trauma centers are based primarily on data from the 1990s. Our goal was to identify DUI conviction rates of intoxicated drivers in MVCs presenting to a trauma center and to identify factors associated with the failure to obtain a DUI conviction.MethodsRetrospective study of adults (>18 years) presenting to a trauma center emergency department (ED) in 2007. Eligible subjects were drivers involved in a MVC with an ED blood alcohol level (BAL) ≥ 80mg/dL. Subjects were matched to their Department of Motor Vehicle (DMV) records to identify DUI convictions from the collision, the legal blood alcohol concentration (BAC), and arresting officer’s impression of the driver’s sobriety. We entered potential variables predictive of failure to obtain a DUI conviction into a regression model.ResultsThe 241 included subjects had a mean age of 34.1 ± 12.8 years, and 185 (77%) were male. Successful DUI convictions occurred in 142/241 (58.9%, 95% CI 52.4, 65.2%) subjects. In a regression model, Injury Severity Score > 15 (odds ratio = 2.70 (95% CI 1.06, 6.85)) and a lower ED BAL from 80 to 200mg/dL (odds ratio = 5.03 (95% CI 1.69, 14.9) were independently associated with a failure to obtain a DUI conviction.ConclusionSlightly more than half of drivers who present to an ED after a MVC receive a DUI conviction. The most severely injured subjects and those with lower BALs are least likely to be convicted of a DUI.

SAMe treatment prevents the ethanol-induced epigenetic alterations of genes in the Toll-like receptor pathway

Prior studies showed that Toll-like receptor (TLR) signaling pathway genes were upregulated in the liver of rats fed ethanol, but not in rats fed ethanol plus S-adenosylmethionine (SAMe). These results were obtained using a PCR microplate array analysis for TLRs and associated proteins such as proinflammatory cytokines and chemokine mRNA levels. A large number of genes were upregulated by the ethanol diet, but not the ethanol plus SAMe diet. In the present study, using the same experimental rat livers, DNA methylation analysis was done by using an Epitect Methyl DNA Restriction Kit (Qiagen, 335451) (24 genes). The results of all the genes combined show a highly significant increase in methylation in the ethanol-fed group of rats, but not in the dextrose-fed, SAMe-fed or ethanol plus SAMe-fed groups of rats. There was also an increase in DNA methylation in rats with high blood alcohol levels compared to a rat with a low blood alcohol level. The individual genes that were upregulated as indicated by the increased mRNA measured by qPCR correlated positively with the increased methylation of the DNA of the corresponding genes as follows: Cd14, Hspa1a, Irf1, Irak1, Irak2, Map3k7, Myd88, Pparα, Ripk2, Tollip and Traf6.

Self-reported drunk driving among Finnish adolescents

BackgroundDrunk-driving compromises traffic safety as it impairs driving skills even at very low blood alcohol concentrations among young drivers. According to previous research, the drunk-driving arrest incidence rate of 18–19-year-olds...

Alcoholic ketoacidosis and reversible neurological complications due to hypophosphataemia

A 57-year-old man with chronic alcoholism was admitted to our hospital due to disturbance of consciousness and polyradiculitis. Laboratory examination revealed metabolic acidosis, hypokalemia and hypophosphataemia. Alcoholic ketoacidosis is a common disorder in alcoholic patients. All patients present with a history of heavy alcohol misuse, preceding a bout of particularly excesive intake, which had been terminated by nausea, vomiting and abdominal pain. The most important laboratory results are: normal or low glucose level, metabolic acidosis with a raised anion GAP, low or absent blood alcohol level and urinary ketones. The greatest threats to patients are: hypovolemia, hypokaliemia, hypoglucemia and acidosis. Alcohol abuse may result in a wide range of electrolyte and acid-base disorders including hypophosphataemia, hypomagnesemia, hypocalcemia, hypokalemia, metabolic acidosis and respiratory alkalosis. Disturbance of consciousness in alcoholic patients is observed in several disorders, such drunkenness, Wernicke encephalopathy, alcohol withdrawal syndrome, central pontine myelinolysis, hepatic encephalopathy, hypoglucemia and electrolyte disorders.

S-adenosylmethionine decreases the peak blood alcohol levels 3 h after an acute bolus of ethanol by inducing alcohol metabolizing enzymes in the liver

Introduction An alcohol bolus causes the blood alcohol level (BAL) to peak at 1–2 h post ingestion. The ethanol elimination rate is regulated by alcohol metabolizing enzymes, primarily alcohol dehydrogenase (ADH1), acetaldehyde dehydrogenase (ALDH), and cytochrome P450 (CYP2E1). Recently, S-adenosylmethionine (SAMe) was found to reduce acute BALs 3 h after an alcohol bolus. The question, then, was: what is the mechanism involved in this reduction of BAL by feeding SAMe? To answer this question, we investigated the changes in ethanol metabolizing enzymes and the epigenetic changes that regulate the expression of these enzymes during acute binge drinking and chronic drinking. Methods Rats were fed a bolus of ethanol with or without SAMe, and were sacrificed at 3 h or 12 h after the bolus. Results RT-PCR and Western blot analyses showed that SAMe significantly induced ADH1 levels in the 3 h liver samples. However, SAMe did not affect the changes in ADH1 protein levels 12 h post bolus. Since SAMe is a methyl donor, it was postulated that the ADH1 gene expression up regulation at 3 h was due to a histone modification induced by methylation from methyl transferases. Dimethylated histone 3 lysine 4 (H3K4me2), a modification responsible for gene expression activation, was found to be significantly increased by SAMe at 3 h post bolus. Conclusion These results correlated with the low BAL found at 3 h post bolus, and support the concept that SAMe increased the gene expression to increase the elimination rate of ethanol in binge drinking by increasing H3K4me2.

Risks of Alcoholic Energy Drinks for Youth

Ingesting alcohol and energy drinks together is associated with a decreased awareness of the physical and mental impairment caused by the alcohol without reducing the actual impairment. This is of particular concern for youth who have a baseline of less mature judgment. Adding energy drinks to alcohol tends to increase the rate of absorption through its carbonation and dilution of the alcohol, and keep a person awake longer allowing ingestion of a greater volume of alcohol. At low blood alcohol levels, caffeine appears to decrease some of the impairment from the alcohol, but at higher blood alcohol levels, caffeine does not appear to have a modifying effect on either the physical or mental impairment induced by the alcohol. Obtaining this combination is made easier and more affordable for under aged persons by manufacturers of premixed alcoholic energy drink combination beverages. Awareness by medical and educational personnel and parents of this activity and its potential for harm is unknown.

S‐adenosylmethionine Down Regulates Blood Alcohol Level

Alcohol consumption raises blood alcohol levels (BALs), and causes an increase in the enzymes that metabolize ethanol, primarily alcohol dehydrogenase (ADH), acetaldehyde dehydrogenase (ALDH), and cytochrome P450 (CYP2E1). Recently, s‐adenosylmethionine (SAMe) was observed to reduce acute BALs. The question is what is the mechanism involved in this reduction of BAL by SAMe feeding? To answer this question we investigated the changes in ethanol metabolizing enzymes and the epigenetic changes that regulate these changes in acute binge drinking and chronic drinking. In the chronic model, rats were fed ethanol and SAMe for 1 month using the intragastric tube feeding model. In the acute models, rats were fed a bolus containing ethanol with or without SAMe and were sacrificed at 3 or 12 hours after the bolus. Western blot analyses showed that SAMe significantly induced ADH levels in the 3h liver samples. However, SAMe did not affect the changes in ADH levels for the 12h acute experiment or in the chronic experiment. Since SAMe is a methyl donor, it was suspected that the ADH gene expression change was due to a histone modification. Dimethylated histone 3 lysine 4 (H3K4me2), a modification responsible for gene expression activation, was found to be significantly increased by SAMe in the acute experiments. These results correlate with the low BAL found in the acute experiment and support the concept that SAMe is a promising modulator of gene expression caused by high levels of ethanol. Supported by NIH/NIAAA 8116.

Low blood alcohol levels. Experimental study on attention and body sway control functions

Objective Attempting to prevent alcohol-related road accidents requires sensitive, reliable and easy-to-use methods and instruments for ascertaining drivers’ state of intoxication. This paper examines the scientific validity of a method for assessing psychomotor performance combining measurement of neurosensory functions with the effect of low blood alcohol levels: body sway control and attention functions. Methods A double-blind, placebo-controlled study, with cross-over and random distribution on the effects of low blood alcohol levels. Psychomotor performance and body sway control were studied in 16 healthy volunteers after they had drunk a small dose of ethyl alcohol (0.5 g/kg) or placebo. Neurosensory and psychomotor functions were assessed by a Divided Attention Test (DAT), composed of the association between one test exploring short-term memory (Memory Test) and one exploring attention (Response Competition Test). Alterations in body sway were recorded by stabilometry. Tests were administered at 30, 60, 120 and 180 min after intake of alcohol. After a wash-out period of at least one week, subjects repeated the test after taking a second dose of alcohol or placebo. Blood alcohol concentrations were monitored by analysis of concentrations in expired air. Results A BAC under 50 mg/dL did not reveal statistically significant impaired memory capacities or motor coordination. Instead, statistically significant oscillations of body sway were measured ( p-values = 0.0001), especially when stabilometry was associated with deviant stimuli like those of the DAT ( p-values = 0.0001). Conclusions This study showed: (1) impaired performance, at the limits of statistical significance, on a complex psychometric test like the DAT; (2) some cognitive, attentive and visual perceptive functions are not compromised or at least not in a statistically significant manner; (3) a considerable alteration in the capacity for control of body sway after intake of alcohol becomes further and massively impaired when deviant stimuli are given; (4) this impairment appeared early and was more marked 1 and 2 h after intake of alcohol.

Age-related differences in the blood alcohol levels of Wistar rats

Knowledge of blood alcohol levels (BALs) that are achieved following ethanol administration is critical for contemporary efforts to develop animal models of alcoholism. Adolescent and adult male Wistar rats were administered varying doses of ethanol (0.75, 1.5 and 3.0 g/kg) via gavage or intraperitoneal injection and BALs were measured over a two hour period. The results showed that adolescent animals had lower BALs across all time points in comparison to adults following administration of 0.75 g/kg ethanol and that 1 h after administration of 1.5 g/kg ethanol, adolescent animals showed an enhanced rate of elimination. The highest dose of ethanol (3.0 g/kg) produced comparable BALs for both adolescents and adults during the two-hour sampling period; however, the BALs for both ages were lower following administration of ethanol by gavage at this dose. Furthermore, an order effects analysis highlights that depending on the route of administration, initial dose size can influence the BALs produced by lower doses of ethanol. The current data identify the importance of measuring the level of alcohol in the blood to confirm that target BALs are achieved for adolescents and equivalent BALs are being reached for both adolescent and adult animals when such comparisons are made.

Traffic Accidents in Switzerland: How Hazardous Are “High Risk” Groups? An Analysis Based on Police Protocols

Summary On January 1, 2005, Switzerland reduced the legal level of blood-alcohol concentration while driving from 0.8‰ to 0.5‰. This happend on basis of the assumption that more restrictive per mil levels increase road safety. The benefit of lower blood-alcohol levels, however, depends on whether drinking drivers indeed pose a risk for themselves and other road users. Analyses using official data of all 84,437 two-car crashes during 2001–2005 indeed show a higher relative risk of drinking to sober drivers. And, we also find evidence that prejudices against drivers with an Eastern European citizenship, contrary to recent newspaper articles, are groundless.

Does expectancy affect alcohol absorption?

Many factors influence alcohol absorption, yet few studies have addressed the issue of whether or not experimental manipulations themselves may affect alcohol absorption. The current balanced placebo design study comparing the expectancy effects of root beer and non-alcoholic beer vehicles resulted in significantly lower blood alcohol levels in the root beer condition than in the beer condition even though alcohol doses were the same. Two possible explanations are discussed; differences in expectancy may have affected absorption, or fructose in the root beer may have slowed absorption of alcohol relative to the maltose in beer. The literature does not provide strong evidence for either of the hypotheses. The implication of this study's results is that alcohol absorption rate may be an important source of confounding effects in behavioral research in the laboratory, because it may be affected by beverages or other experimental conditions.