Moderate Dose Of Alcohol Research Articles

Moderate alcohol disrupts a mechanism for detection of rare events in human visual cortex

Moderate doses of alcohol (blood alcohol concentration [BAC] of about 0.05%) may result in acute impairments at various levels of information processing. A number of reports have documented detrimental effects of moderate alcohol on the mismatch negativity (MMN), the electrocortical manifestation of a rapid (100 ms poststimulus) mechanism dedicated to the detection of unexpected auditory change (e.g., Jääskeläinen, et al., 1995). Recently, we and others identified a partial visual counterpart of the MMN, sometimes called the rareness-related negativity (RRN). Analogous to the MMN, the RRN evolves at about 100 ms after the unexpected change and was localized in visual cortex (Kenemans, et al., 2003). Rapid detection of unexpected events is important for everyday-life conditions like driving, prompting the question whether the visual RRN shows sensitivity to moderate alcohol similar to the MMN. In all, 16 subjects were tested either under moderate alcohol or under placebo. Unexpected visual change was implemented by presenting 2.4 versus 0.6 c/d gratings in pseudorandom sequences according to a deviant (10%)/standard (90%) schedule. The alcohol effects on MMN reported before were replicated. Furthermore, the RRN, defined as the difference between deviant and standard event-related potentials between 120 and 170 ms at Oz, was present under placebo but not under alcohol. It is concluded that moderate alcohol does indeed impair the rapid detection in visual cortex of unexpected changes. In contrast, electrocortical correlates of lower level sensory processing were still significantly present under alcohol.

Individual differences in acute alcohol impairment of inhibitory control predict ad libitum alcohol consumption

Research has begun to examine how acute cognitive impairment from alcohol could contribute to alcohol abuse. Specifically, alcohol-induced impairment of inhibitory control could compromise the drinker's ability to stop the self-administration of alcohol, increasing the risk of binge drinking. The present study was designed to test this hypothesis by examining the relation between acute alcohol impairment of inhibitory control and alcohol consumption during a single drinking episode. Twenty-six healthy adults performed a cued go/no-go task that measured inhibitory control. The study tested the degree to which their inhibitory control was impaired by a moderate dose of alcohol (0.65 g/kg) versus a placebo and the extent to which individual differences in this impairment predicted levels of alcohol consumption as assessed by ad lib drinking in the laboratory. In accord with the hypothesis, greater impairment of inhibitory control from alcohol was associated with increased ad lib consumption. Acute impairment of inhibitory control might be an important cognitive effect that contributes to abuse in addition to the positive rewarding effects of the drug.

Effects of alcohol on inhibitory processes

Earlier work has shown that alcohol may have disinhibiting effects on behaviour. Two studies tested the effects of a moderate dose of alcohol (0.6 g/kg) versus placebo on tasks that evaluate inhibitory processes related to alcohol stimuli, in moderate-to-heavy social drinkers (student population). An inhibition of interference task, the Stroop task (ST; study 1), and an inhibition of a prepotent response task, the go/no-go task (GNG; study 2), were used. The effects of alcohol on working memory function were also examined. Participants preloaded with alcohol made more errors on the colour and alcohol ST than those preloaded with placebo. In the GNG task, responding to alcohol-related pictures was slower than responding to neutral pictures. When participants were required to switch responding from neutral to alcohol-related go stimuli, responding became slower; however, responding to alcohol go stimuli became faster as time progressed; no effect of alcohol was found. Alcohol had no effect, compared with placebo, on the working memory tasks. Therefore, a moderate dose of alcohol had restricted effects on inhibitory processes: only interference inhibition measured in the ST was affected. Although the data obtained with the GNG task did not show an effect of alcohol on response inhibition, increased latency of response in the presence of alcohol-related stimuli compared with neutral stimuli indicates that alcohol stimuli are more salient to social drinkers, attracting a greater amount of attention.

Effects of Alcohol on Simulated Driving and Perceived Driving Impairment in Binge Drinkers

Binge drinking (heavy episodic alcohol use) is associated with high rates of impaired driving and myriad alcohol-related accidents. However, the underlying reasons for the heightened accident risk in this demographic group are not known. This research examined acute alcohol effects on simulated driving performance and subjective ratings of intoxication and driving ability in binge and nonbinge drinkers. Young social drinking college students (24 binge drinkers and 16 nonbinge drinkers) participated in this study. Participants attended a session during which they received a moderate dose of alcohol (0.65 g/kg) and a session during which they received a placebo. A simulated driving task measured participants' driving performance in response to each dose. Subjective responses to each dose were also assessed, including ratings of sedation, stimulation, and driving ability. The acute dose of alcohol impaired multiple aspects of driving performance in both binge and nonbinge drinkers. Under alcohol, all participants had greater difficulty in maintaining their lane position, maintaining the appropriate speed and made multiple driving errors compared to placebo performance. By contrast, compared with nonbinge drinkers, binge drinkers reported feeling less sedated by the alcohol and reported having a greater ability to drive following the acute dose of alcohol. Reduced subjective intoxication and perceived driving impairment in binge drinkers may account for the greater accident risk in this demographic group. Binge drinkers may lack the internal sedation cue that helps them accurately assess that they are not able to effectively drive a vehicle after drinking.

Escalated Aggression after Alcohol Drinking in Male Mice: Dorsal Raphé and Prefrontal Cortex Serotonin and 5-HT1B Receptors

A significant minority of individuals engages in escalated levels of aggression after consuming moderate doses of alcohol (Alc). Neural modulation of escalated aggression involves altered levels of serotonin (5-HT) and the activity of 5-HT(1B) receptors. The aim of these studies was to determine whether 5-HT(1B) receptors in the dorsal raphé (DRN), orbitofrontal (OFC), and medial prefrontal (mPFC) cortex attenuate heightened aggression and regulate extracellular levels of 5-HT. Male mice were trained to self-administer Alc by performing an operant response that was reinforced with a delivery of 6% Alc. To identify Alc-heightened aggressors, each mouse was repeatedly tested for aggression after consuming either 1.0 g/kg Alc or H2O. Next, a cannula was implanted into either the DRN, OFC, or mPFC, and subsets of mice were tested for aggression after drinking either Alc or H(2)O prior to a microinjection of the 5-HT(1B) agonist, CP-94,253. Additional mice were implanted with a microdialysis probe into the mPFC, through which CP-94,253 was perfused and samples were collected for 5-HT measurement. Approximately 60% of the mice were more aggressive after drinking Alc, confirming the aggression-heightening effects of 1.0 g/kg Alc. Infusion of 1 microg CP-94,253 into the DRN reduced both aggressive and motor behaviors. However, infusion of 1 microg CP-94,253 into the mPFC, but not the OFC, after Alc drinking, increased aggressive behavior. In the mPFC, reverse microdialysis of CP-94,253 increased extracellular levels of 5-HT; levels decreased immediately after the perfusion. This 5-HT increase was attenuated in self-administering mice. These results suggest that 5-HT(1B) receptors in the mPFC may serve to selectively disinhibit aggressive behavior in mice with a history of Alc self-administration.

A controlled study of the time-course of breath alcohol concentration after moderate ingestion of ethanol following a social drinking session

This paper evaluates the breath alcohol concentration (BrAC), nausea (feeling of being slightly intoxicated) and subjective driving performance after ingesting a moderate dose of alcohol in the presence of a light meal, which intends to approach a social drinking setting. 119 healthy individuals (69 males and 50 females, aged 21.7 ± 3.0) ingested three glasses of wine (95 mL each) and their BrAC was determined by an Alcotest 7410 at 15, 30, 45, 60, 90 and 120 min post-drinking. 46% of females and no male subjects exceeded a BrAC of 0.25 mg/L, the legal limit for driving fixed by some Western countries. 53% of the study population felt nausea during the experimental session and 20% self-reported impairment of their driving skills. In both cases these subjective effects were more pronounced in females. The major determinants of mean BrAC were time post-drinking, gender (male) and body mass index (BMI), all these variables being inversely associated. Females and individuals with a BMI lower than 22.5 kg/m 2 were at an increased risk of exceeding the legal limit of BrAC. The feeling of nausea was significantly associated with gender (females), the ingestion of up to 2 drinks on weekdays, and having exceeded a BrAC of 0.25 mg/L during the experimental study. The main predictor of self-perception of impaired driving skills was the feeling of nausea, followed by a BrAC in excess of 0.25 mg/L. In conclusion, both females and subjects with lower BMI are at an increased risk of exceeding the legal limit of BrAC after moderate alcohol consumption resembling a social drinking setting.

Moderate doses of alcohol disrupt the functional organization of the human brain

Acute alcohol administration decreases overall brain glucose metabolism, which serves as a marker of brain activity. The behavioral effects of alcohol, however, are likely to reflect not only changes in regional brain activity but also the patterns of brain functional organization. Here we assessed the effects of a moderate dose of alcohol on the patterns of brain activity and cerebral differentiation. We measured brain glucose metabolism in 20 healthy controls with positron emission tomography and fluorodeoxyglucose during baseline and during alcohol intoxication (0.75 g/kg). We used the coefficient of variation (CV) to assess changes in brain metabolic homogeneity, which we used as a marker for cerebral differentiation. We found that alcohol decreased the CV in the brain and this effect was independent of the decrements in overall glucose metabolism. Our study revealed marked disruption in brain activity during alcohol intoxication including decreases in global and regional brain differentiation, a loss of right versus left brain metabolic laterality and a shift in the predominance of activity from cortical to limbic brain regions. The widespread nature of the changes induced by a moderate dose of alcohol is likely to contribute to the marked disruption of alcohol on behavior, mood, cognition and motor activity.

Effects of Topiramate on Urge to Drink and the Subjective Effects of Alcohol: A Preliminary Laboratory Study

Topiramate was recently reported to be efficacious in reducing drinking rates and craving among individuals with alcohol dependence in a randomized controlled trial, but dose effects could not be determined. This laboratory study systematically examined the dose-dependent effects of topiramate on cue-elicited craving and other putative mechanisms of its pharmacotherapeutic effects on drinking. Male and female heavy drinkers (n = 61) were randomized to 1 of 3 medication conditions (200 mg/d; 300 mg/d; placebo) in a double-blind study. Participants reached the target dose after a 32-day titration period, then were stabilized for approximately 1 week. All then participated in a laboratory assessment of alcohol cue reactivity and of the subjective effects of a moderate dose of alcohol. Both doses of topiramate reduced the frequency of heavy drinking during the titration period as compared to placebo. However, topiramate did not affect self-reported craving for alcohol during the titration period, during the cue reactivity protocol, or in response to the alcohol challenge procedure. Topiramate reduced the stimulating effects of alcohol ingestion compared to placebo, but only in the 200 mg group. The results of this study support previous findings that topiramate reduces drinking, but the behavioral mechanism underlying this effect does not appear to be attenuation of craving for alcohol as measured using the approaches employed in this study. Rather, the results tentatively suggest that topiramate may exert its beneficial effects by altering the subjective experiences of alcohol consumption. Limitations of the current study are discussed and complementary methods are recommended for future studies, such as the use of behavioral economic paradigms and ecological momentary assessment.

Direct effects of alcohol on hepatic fibrinolytic balance: Implications for alcoholic liver disease

The pathogenesis of alcoholic liver disease (ALD) remains uncertain. Fibrin production and degradation are altered in experimental liver injury. We have recently identified increased expression of a number of genes (annexin A2 (ANXA2), p11, tPA and PAI-1) that implicate fibrinolysis in ALD progression. Aim of our study was to study the direct effect of alcohol on fibrinolysis and plasmin activity in hepatic cell lines and in vivo. Expression of pro- and anti-fibrinolytic genes was determined in liver biopsies from patients with progressive ALD and in HepG2, Huh7 and LX-2 cells exposed to alcohol. The functional effects on fibrinolysis and plasmin activities were determined. C57BL6 female mice were given a single dose of alcohol and serum and liver triglyceride content and serum plasmin activity determined. Alcohol induced a significant up-regulation of ANXA2, PLG, PAI-1 and p11 in human ALD, cell lines and in mice exposed to alcohol. Up-regulation of ANXA2 and p11 was inhibited by the alcohol dehydrogenase inhibitor 4-methylpyrazole. Fibrinolysis and plasmin were increased in HepG2 and LX-2 cells by 10mM alcohol and was inhibited by ANXA2 blocking antibody. Plasmin also increased in mice given a moderate dose of alcohol. By contrast, there was striking up-regulation of PAI-1 in mice given a high dose of alcohol with associated decrease in plasmin. Alcohol directly alters hepatic expression of pro- and anti-fibrinolytic genes in a dose dependent manner with low dose promoting fibrinolysis and high dose inhibiting fibrinolysis. After a large dose of alcohol in vivo, the dominant effect was up-regulation of hepatic PAI-1 with suppression of plasmin. The effect of alcohol on fibrinolysis and plasmin is mediated in part by ANXA2. Alcohol directly influences hepatic pathways of fibrinolysis that may contribute to ALD.

Changed accumbal responsiveness to alcohol in rats pre-treated with nicotine or the cannabinoid receptor agonist WIN 55,212-2

Alcohol, nicotine, and cannabinoid acutely increase the activity of the mesolimbic dopamine (DA) pathway. Although polysubstance consumption is a common pattern of abuse in humans, little is known about dopamine release following pre-exposure to these drugs. The purpose of this study was to test whether alcohol-induced dopamine release into the nucleus accumbens (NAc) shell is modified by different pre-treatments: water (i.g.), alcohol (1 g/kg, i.g.), nicotine (0.4 mg/kg, s.c.), and WIN 55,212-2 (1 mg/kg, s.c.). Male Wistar rats were treated (i.g.) for 14 days with either water or alcohol. In the following 5 days rats were injected (s.c.) with vehicle, nicotine, or WIN 55,212-2. Finally, a cannula was surgically implanted into the NAc shell and alcohol-induced extracellular dopamine release was monitored in freely moving rats. Alcohol (1 g/kg; i.g.) only increased the release of dopamine when animals were previously treated with water. This DA increase was markedly inhibited by (subchronic) treatment (5 days) with nicotine or WIN 55-212-2 as well as by previous (chronic) exposure to alcohol (14 days). These data demonstrate that pre-treatment with nicotine and the cannabinoid agonist WIN 55,212-2 is able to change the sensitivity of the NAc shell in response to a moderate dose of alcohol. Therefore, cannabinoid and nicotine exposure may have important implications on the rewarding effects of alcohol, because these drugs lead to long-lasting changes in accumbal dopamine transmission.

Dose‐Dependent Deficits in Dual Interstimulus Interval Classical Eyeblink Conditioning Tasks Following Neonatal Binge Alcohol Exposure in Rats

Neonatal alcohol consumption in rats is widely used to model cerebellar injury arising from 3rd-trimester human fetal alcohol exposure. Binge alcohol exposure of 5 g/kg/day or more over postnatal days (PD) 4 to 9 in rats damages the cerebellum and consequently impairs classical eyeblink conditioning (EBC). The present study sought to identify deficits in EBC using doses lower than those that have been reported previously following alcohol exposure limited to PD4-9. Complex conditioned response (CR) timing tasks utilizing 2 interstimulus intervals (ISIs) were used to test the hypothesis that 3 g/kg/day of alcohol would produce early onset and early peaked CRs, whereas 4 and 5 g/kg/day would impair CR acquisition. Five neonatal treatment groups were used: (1) undisturbed controls, (2) sham intubation controls, (3) 3 g/kg/day of alcohol, (4) 4 g/kg/day of alcohol, or (5) 5 g/kg/day of alcohol. Intubations occurred over PD4-9. In adulthood, rats were trained using ISI discrimination (Experiment 1) or temporal uncertainty (Experiment 2) EBC tasks. In ISI discrimination, 2 distinct conditioned stimuli (CSs; tone and light) are reinforced with a periocular shock unconditioned stimulus (US) at 2 different CS-US intervals. Temporal uncertainty is identical in design with the exception that the same CS is presented at both CS-US intervals. Alcohol-exposed subjects were impaired in CR acquisition in a task- and dose-dependent fashion. CR deficits were most salient in the peak amplitude measure and occurred in both tasks following alcohol exposure at 4 and 5 g/kg/day. Alcohol at a dosage of 3 g/kg/day impaired CR acquisition only in ISI discrimination. All alcohol doses failed to produce short latency CRs in either task. Alcohol-exposed subjects displayed later-onset and later-peaked CRs to the long-ISI CS in ISI discrimination relative to controls. ISI discrimination training may be ideal to identify CR deficits resulting from neonatal exposure to moderate alcohol doses. Applications of this EBC task to humans may enable reliable early identification and diagnosis of individuals with fetal alcohol spectrum disorders.

Differential effects of alcohol on working memory: Distinguishing multiple processes.

The authors assessed effects of alcohol consumption on different types of working memory (WM) tasks in an attempt to characterize the nature of alcohol effects on cognition. The WM tasks varied in 2 properties of materials to be retained in a 2-stimulus comparison procedure. Conditions included (a) spatial arrays of colors, (b) temporal sequences of colors, (c) spatial arrays of spoken digits, and (d) temporal sequences of spoken digits. Alcohol consumption impaired memory for auditory and visual sequences but not memory for simultaneous arrays of auditory or visual stimuli. These results suggest that processes needed to encode and maintain stimulus sequences, such as rehearsal, are more sensitive to alcohol intoxication than other WM mechanisms needed to maintain multiple concurrent items, such as focusing attention on them. These findings help to resolve disparate findings from prior research on alcohol's effect on WM and on divided attention. The results suggest that moderate doses of alcohol impair WM by affecting certain mnemonic strategies and executive processes rather than by shrinking the basic holding capacity of WM.

Effects of THC on driving performance, physiological state and subjective feelings relative to alcohol

Background The effects of marijuana or THC on driving has been tested in several studies, but usually not in conjunction with physiological and subjective responses and not in comparison to alcohol effects on all three types of measures. Objective To assess the effects of two dosages of THC relative to alcohol on driving performance, physiological strain, and subjective feelings. Method We tested the subjective feelings and driving abilities after placebo, smoking two dosages of THC (13 mg and 17 mg), drinking (0.05% BAC) and 24 h after smoking the high dose THC cigarette, while monitoring physiological activity of the drugs by heart rate. Fourteen healthy students, all recreational marijuana users, participated in the study. Results Both levels of THC cigarettes significantly affected the subjects in a dose-dependent manner. The moderate dose of alcohol and the low THC dose were equally detrimental to some of the driving abilities, with some differences between the two drugs. THC primarily caused elevation in physical effort and physical discomfort during the drive while alcohol tended to affect sleepiness level. After THC administration, subjects drove significantly slower than in the control condition, while after alcohol ingestion, subjects drove significantly faster than in the control condition. No THC effects were observed after 24 h on any of the measures.

The influence of alcohol on basic motoric and cognitive disinhibition

It has been proposed that alcohol weakens control processes, which in turn supports the occurrence of disinhibited behaviours. Two studies were run, in parallel (both with 32 participants) using a between-subject design to investigate any disinhibiting effects of a moderate dose of alcohol (0.6 g/kg compared to placebo), previously found to trigger increased desire for alcohol. Disinhibiting effects were tested on basic motoric and cognitive control processes, using a go/no-go (GNG) and the Stroop task (ST) respectively. Although a higher proportion of participants wanted more alcohol under the alcohol preload (priming effect), this effect was not found to be significant. In the GNG task, correct response latency (RL) decreased from baseline [P = 0.008] while number of incorrect hits increased [P = 0.030] irrespective of treatment, indicating the formation of a habit-like response and motoric disinhibition. Although error rate did not differ between groups, an interaction occurred with regard to erroneous RL: participants under alcohol became quicker, while those under placebo became slower [P = 0.014]. In the ST, those preloaded with alcohol made significantly more errors [P = 0.021] and were quicker to complete the task [P = 0.044] compared with those preloaded with placebo, indicating a strong alcohol effect on cognitive disinhibition. The data suggest that a moderate dose of alcohol, which induces priming to want more alcohol, had disinhibiting effects both on a basic motoric and a cognitive inhibitory task. Thus the idea that priming may be mediated by the disinhibitory effects of alcohol is supported.

Effects of a Moderate Evening Alcohol Dose. II: Performance

This second of a pair of papers investigates the effects of a moderate dose of alcohol and staying up late on driving simulation performance and simple visual reaction time (RT) at a known circadian phase in well-rested young adults. Twenty-nine adults (9 males), ages 21 to 25 years, spent 1 week on an at-home stabilization schedule of 8.5 to 9 hours, followed by 3 nonconsecutive nights in-lab: adaptation, placebo, and alcohol. Performance task practice occurred on 3 occasions before the study. Alcohol (vodka; 0.54 g/kg men; 0.49 g/kg women mixed with tonic) was consumed over 30 minutes ending 1 hour before normal bedtime; the same quantity of beverage was given on placebo. Driving simulation (with drive-only and dual-task drive and subtract components) and psychomotor vigilance task (PVT) testing occurred before and after alcohol/placebo ingestion. Breath alcohol concentration (BrAC) readings were taken before all test sessions. Saliva samples were taken approximately every 30 minutes to determine circadian phase. Driving simulation and PVT variables significantly deteriorated with increasing time awake. Driving simulator lane variability was worse with alcohol compared with placebo at 15.5 hours awake. No PVT variable showed an effect of alcohol. Driving simulation performance deteriorated with extended waking and with alcohol; driving was most impaired at the peak alcohol level. The PVT, less complex than the driving simulation, did not show effects of alcohol, a finding consistent with previous literature that disruptive effects of low alcohol concentrations increase with task complexity. Overall, simulated driving performance is significantly impaired late at night when even a moderate dose of alcohol is consumed.

Effects of a Moderate Evening Alcohol Dose. I: Sleepiness

Few studies examining alcohol's effects consider prior sleep/wake history and circadian timing. We examined introspective and physiological sleepiness on nights with and without moderate alcohol consumption in well-rested young adults at a known circadian phase. Twenty-nine adults (males=9), ages 21 to 25 years (M=22.6, SD=1.2), spent 1 week on an at-home stabilized sleep schedule (8.5 or 9 hours), followed by 3 in-lab nights: adaptation, placebo, and alcohol. Alcohol (vodka; 0.54 g/kg for men; 0.49 g/kg for women) or placebo beverage was consumed over 30 minutes ending 1 hour before stabilized bedtime. In addition to baseline, 3 sleep latency tests (SLTs) occurred after alcohol/placebo ingestion (15, 16.5, and 18 hours after waking). Stanford Sleepiness Scales (SSS) and Visual Analog Scales (VAS) of sleepiness were completed before each SLT and approximately every 30 minutes. The Biphasic Alcohol Effects Scale (BAES) was administered a total of 4 times (baseline, 5, 60, and 90 minutes postalcohol/placebo). Subjects' circadian phase was determined from melatonin levels in saliva samples taken at approximately 30-minute intervals. All sleepiness and sedation measures increased with time awake. Only SSS and BAES sedation measures showed higher levels of sleepiness and sedation after alcohol compared with placebo. The mean circadian phase was the same for assessments at both conditions. Alcohol did not increase physiological sleepiness compared with placebo nor was residual sedation evident under these conditions. We conclude that the effects on sleepiness of a moderate dose of alcohol are masked when sleep-wake homeostatic and circadian timing influences promote high levels of sleepiness.

Alcohol Selectively Reduces Brain Activity During the Affective Processing of Negative Information

Although it has frequently been suggested that alcohol influences emotions such as anxiety and fear through the modulation of affective information processing, few studies addressed this topic using objective measures. The acute effects of alcohol on affective processing of pictorial stimuli were investigated using electrophysiological measures. Event-related brain potentials (ERP) resulting from watching pleasant, unpleasant, and neutral pictures were investigated in a group of participants receiving a beverage containing a moderate dose of alcohol (n=26) and a group of participants receiving a nonalcoholic placebo beverage (n=24). Both early [early posterior negativity (EPN)] and late [late positive potential (LPP)] ERP components were employed as index of emotional processing. The results show that alcohol reduced brain activity during watching unpleasant information in a late stage (700-1000 ms). This suggests that alcohol selectively influences the processing of unpleasant information. The findings are in concordance with theories linking alcohol administration to decreased processing of affective information. The results are discussed in the context of the role of the effect of alcohol on affective information processing, and its relevance to alcoholism.

The effects of alcohol on laboratory-measured impulsivity after l-Tryptophan depletion or loading

Indirect evidence supports a link between serotonergic activity and individual differences in the behavioral response to alcohol, but few studies have experimentally demonstrated that an individual's biological state can influence the sensitivity to alcohol-induced behaviors. Our purpose was to temporarily modify serotonin synthesis in healthy individuals to determine how altered biological states may interact with alcohol administration to affect impulsive behavior. In a repeated-measures design, 18 normal controls consumed a 50-g L: -tryptophan (Trp) depleting (ATD) or loading (ATL) amino-acid beverage that temporarily decreased or increased (respectively) serotonin synthesis before receiving either a moderate dose of alcohol (0.65 g/kg) or placebo. All participants completed three impulsivity testing sessions on each of the five experimental days. Session one was a baseline session. Session two included testing after ATD-only or ATL-only. Session three included: (1) placebo after ATL (ATL+PBO); (2) placebo after ATD (ATD+PBO); (3) alcohol after ATL (ATL+ALC); (4) alcohol after ATD (ATD+ALC); and (5) Alcohol-only conditions. Impulsivity was assessed using the Immediate Memory Task (Dougherty et al., Behav Res Methods Instrum Comput 34:391-398, 2002), a continuous performance test yielding commission errors that have been previously validated as a component of impulsive behavior. Primary findings were that ATD-only increased impulsive responding compared to ATL-only, and ATD+ALC increased commission errors to levels higher than either the ATL+ALC or Alcohol-only conditions. These findings demonstrate that reduced serotonin synthesis can produce increased impulsivity even among non-impulsive normal controls, and that the behavioral effects of alcohol are, in part, dependent on this biological state.

Evening Alcohol Suppresses Salivary Melatonin in Young Adults

The study objective was to determine the acute effects of a moderate evening dose of alcohol on salivary melatonin levels in humans with stable prior sleep‐wake histories and in a controlled environment. Twenty‐nine adults (nine males) ages 21 to 25 (M=22.6, SD=1.2) yrs adhered to a 10‐day at‐home stabilized sleep schedule followed by three in‐lab adaptation, placebo, and alcohol (order counterbalanced) study nights. Alcohol (vodka: 0.54 g/kg for men and 0.49 g/kg for women) or placebo beverage was consumed over 30 min, ending 1 h before stabilized bedtime. At 140 and 190 min after alcohol administration, melatonin level was reduced by 15% and 19%, respectively, in comparison to placebo. The findings indicate that a moderate dose of alcohol in the evening suppressed melatonin in young adults.

Men's likelihood of sexual aggression: the influence of alcohol, sexual arousal, and violent pornography

AbstractPrevious research findings have indicated that both alcohol intoxication and violent pornography exposure may contribute to increased sexual aggression by men. This study used an experimental paradigm to examine the effects of a moderate alcohol dose, alcohol‐related beliefs, and victim response on men's self‐reported likelihood of committing sexual aggression. A community sample of male social drinkers (N=84) participated in an experiment in which they read an eroticized rape depiction after completing an alcohol administration protocol. The stimulus story varied whether the victim, who initially expressed unwillingness to engage in sexual activity, expressed pleasure or distress in response to the man physically forcing her to perform several explicit sex acts. A path analytic model illustrated that participants' self‐reported likelihood of behaving like the sexual aggressor in the story was directly related to their own sexual arousal. Heightened sexual arousal was reported by participants who had consumed alcohol, those who read the victim‐pleasure story, and those who believed that drinking women are sexually vulnerable. Results suggest that sexual arousal to violent pornography, as influenced by acute alcohol intoxication and other factors, may be an important component of men's perceptions of their own sexual aggression likelihood. Aggr. Behav. 32:581–589, 2006. © 2006 Wiley‐Liss, Inc.