Target Breath Alcohol Concentration Research Articles

The impact of alcohol consumption on implicit racial bias.

Researchers and theorists studying intergroup relations have been interested in the impact of alcohol on interracial responding. Theories predict that alcohol will exacerbate expressions of racial bias by increasing reliance on stereotypes and/or by decreasing controlled processing and self-monitoring. Prior studies testing these theories have often examined alcohol's effects on implicit (i.e., indirect) measures of racial bias with inconsistent results. However, previous research in this area has suffered from several methodological limitations, including small sample sizes and doses of alcohol that may have been too low to induce substantial intoxication. Here, in more than triple the number of alcohol participants than the largest prior study, we tested whether an intoxicating dose of alcohol (target breath alcohol concentration of .08%) exacerbated implicit racial bias. Young adults who identified as races other than Black or African American (N = 207) were randomly assigned to consume an alcoholic or placebo beverage and completed the race-based Implicit Association Test (race IAT) testing implicit preference for White (vs. Black) individuals [or, conversely, bias against Black (vs. White) individuals]. All participants demonstrated an implicit racial bias (i.e., linking traditionally Black names with negative/unpleasant words), with no difference in this implicit racial bias across beverage conditions. Specifically, there were no differences between alcohol participants' race IAT D scores (M = 0.55, SD = 0.39), and placebo participants' race IAT D scores (M = 0.59, SD = 0.35), b = 0.05, 95%CI [-0.07, 0.18], p = .422. These findings challenge theories and prior studies suggesting that alcohol increases implicit racial bias. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Bicycling during alcohol intoxication

The number of bicycling fatalities was 19 450 between 2010 and 2018 in Europe. The number of bicyclists killed when intoxicated by alcohol is harder to establish given the lack of reliable data. In Sweden, drunk bicycling is socially acceptable and legal (unless reckless). This experiment aimed to investigate how alcohol intoxication affect bicycling stability performance, executive functions, and self-rated ability. The experiment was completed on a wide treadmill that allowed control of several influencing factors such as speed and physical effort. Intoxicated and sober participants bicycled on the treadmill for five 10 minute sessions. Alcohol as administered incrementally to reach a target breath alcohol concentration level of 0.8‰. Stability decreased with intoxication; especially roll rate measurements were identified as being adequate indicators of bicycling instability. Executive function was negatively affected, and ability ratings decreased due to intoxication. The intoxicated participants were aware of their reduced ability to bicycle in a safe manner on a group level but not on an individual level. However, this insight does not affect their intention to bicycle intoxicated.

The effects of oral and vaporized cannabis alone, and in combination with alcohol, on driving performance using the STISIM driving simulator: A two-part, double-blind, double-dummy, placebo-controlled, randomized crossover clinical laboratory protocol.

The legalization of cannabis for medicinal and non-medicinal purposes, and the corresponding increase in diversity of cannabis products, has resulted an urgent need for cannabis regulatory science. Among the most pressing needs is research related to impairment due to cannabis exposure, especially on driving performance. The present project was designed to evaluate the impact of oral and vaporized cannabis, when administered alone or in combination with alcohol, on simulated driving performance (STISIM driving simulator), cognitive/psychomotor ability, and field sobriety performance. Healthy adults will complete two, double-blind, double-dummy, placebo-controlled, randomized crossover clinical laboratory studies, one with oral cannabis (16 men/16 women) and the second with vaporized cannabis (16 men/16 women). In each study, participants will complete seven experimental sessions during which acute doses of placebo or high Δ9-THC cannabis containing 0, 10, or 25 mg Δ9-THC will be administered both alone and in combination with placebo or alcohol-containing beverages (target breath alcohol concentrations, BAC, of 0.0% or 0.05%). A positive control session (i.e., alcohol at target BAC of 0.08% with placebo cannabis) will also be completed. Simulated driving performance tests (available for download; see Methods), field sobriety assessments, subjective drug effect questionnaires, a mobile device impairment test (DRUID app), and collection of whole blood specimens will be completed repeatedly during each session. Linear mixed models will be used to test for differences across experimental conditions and a priori planned comparisons will be used to determine differences between conditions of interest (e.g., cannabis alone vs cannabis with alcohol). This research is designed to extend prior studies of cannabis and alcohol on driving performance by using oral and vaporized routes of cannabis administration. By increasing understanding of impairment associated with co-use of alcohol and these novel forms of cannabis, this research could inform impairment detection standards for cannabis and alcohol and have important implications for law enforcement, public policy decisions regarding accessibility of these substances, and education of the general population who may use cannabis and/or alcohol. Lastly, this manuscript provides interested researchers with access to the simulated driving scenarios and data extraction tools developed for this study as a means of facilitating future cross-study comparisons, which is important given the heterogeneity in methods used across laboratories in prior research.

Female drinkers are more sensitive than male drinkers to alcohol-induced heart rate increase.

The present study examined the acute effect of alcohol and its cues on autonomic and cardiovascular physiology, as indexed by changes in heart rate (HR), in a relatively large sample of healthy young adult men and women. Participants (27-31 years old, final N = 145) were administered an alcoholic beverage (n = 88; 52 women) or a placebo beverage (n = 57; 35 women) in a simulated bar. Target breath alcohol concentration (BrAC) was .08 g%. HR was recorded while participants were seated alone during an initial baseline assessment in a lab room; seated with others during preparation and administration of 2 beverages in a simulated bar; and seated alone in the lab room at ascending, peak, and descending BrAC. HR increased over time for participants in both beverage groups during beverage preparation. During beverage consumption, HR decreased over time in those who drank placebo whereas HR increased over time in those who drank alcohol, increasing at a faster rate in women compared to men. HR remained elevated at the ascending, peak, and descending limb assessments only in participants who drank alcohol with HR increasing over time at ascending BrAC in the women but not men. Sex differences in HR under alcohol were not explained by sex differences in body mass index, BrAC, recent alcohol use, or subjective stimulation. Our findings suggest that women may be more sensitive to alcohol-induced increases in HR, especially in environments where alcohol cues are abundant. This may have implications for cardiovascular risks associated with alcohol. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

The Interplay Between Subjective Response to Alcohol, Craving, and Alcohol Self-Administration in the Human Laboratory.

Despite a rich literature on human laboratory paradigms of subjective response (SR) to alcohol, craving for alcohol, and alcohol self-administration, few studies have examined the interplay across these 3 constructs. The present study addresses this gap in the literature by examining the interplay between SR, craving, and self-administration in the human laboratory. Data were culled from a medication study (NCT02026011) in which heavy drinking participants of East Asian ancestry completed 2 double-blinded and counterbalanced experimental sessions. In each experimental session, participants received a priming dose of intravenous (IV) alcohol to a target breath alcohol concentration (BrAC) of 0.06g/dl and measures of SR (stimulation and sedation) and alcohol craving were collected across rising BrACs. The IV alcohol challenge was immediately followed by a 1-hour alcohol self-administration period. Mixed model analyses found a positive and significant relationship between the slope of stimulation and the slope of craving during the alcohol challenge. The relationship between sedation and craving, however, was not significant. The slope of craving during the alcohol challenge significantly predicted a higher number of mini-drinks consumed and lower latency to first drink. Further, mediation analyses found that craving was a significant mediator of the relationship between stimulation and total number of mini-drinks consumed, but the same pattern was not found for sedation. Insofar as alcohol self-administration represents the end point of interest for a host of experimental and clinical research questions, the present study suggests that alcohol craving represents a more proximal predictor of self-administration than measures of alcohol-induced stimulation. It is recommended that human laboratory models interpret measures of SR and craving in light of their relative predictive utility for drinking outcomes.

Working Memory Performance Following Acute Alcohol: Replication and Extension of Dose by Age Interactions

Despite the substantial number of older adult drinkers, few studies have examined acute alcohol effects in aging samples. We have explored these interactions across a variety of neurobehavioral domains and modalities and have consistently observed age-contingent vulnerabilities to alcohol-associated decrements in neurobehavioral functions. However, these studies have not been sufficiently powered to address sex differences, and, thus far, no attempt has been made to replicate results. The current study addresses these gaps. The study used a double-blind, placebo-controlled, factorial design with two age groups (older, 55-70 years; younger, 25-35 years) and three doses (target breath alcohol concentrations: .00, .04, and .065 g/dl). Replication analyses used an independent sample (n = 90) to replicate age-contingent alcohol effects reported by Boissoneault (n = 90). Samples were combined (N = 180; 91 women) to enable sex analyses. The dependent measure was performance efficiency in a visual working memory task. A complex interaction between sex, age, and dose, F(2, 178) = 4.15, p = .02, appeared driven by age-contingent divergence in working memory performance, which was most pronounced between women at the .065 dose, t(28) = 4.61, p < .01, d = 1.68. Replication analyses revealed a pattern of age differences consistent with previous results, although the previously reported age by alcohol interaction failed to reach statistical significance. Results provide further support for the hypothesis that neurobehavioral effects of acute alcohol are age dependent and offer evidence that this interaction may be moderated by sex. Extensions of this work are needed to identify underlying processes and ascertain the functional impact of these effects on the health and well-being of aging adult drinkers.

Effects of Varenicline Alone and in Combination With Low-dose Naltrexone on Alcohol-primed Smoking in Heavy-drinking Tobacco Users: A Preliminary Laboratory Study.

Heavy-drinking tobacco users are less likely to successfully quit smoking than their moderate-drinking counterparts, even when they are prescribed smoking cessation medication. One strategy for improving treatment outcomes in this subgroup of tobacco users may be to combine medication therapies to target both alcohol and tobacco use simultaneously. Adding naltrexone to frontline smoking cessation treatments may improve treatment outcomes in this group. This double-blind, placebo-controlled human laboratory study examined the effects of varenicline (2 mg/d) and varenicline (2 mg/d), combined with a low dose of naltrexone (25 mg/d) on alcohol-primed smoking behavior in a laboratory model of smoking relapse in heavy-drinking tobacco users (n = 30). Participants attended a laboratory session and received an alcohol challenge (target breath alcohol concentration = 0.030 g/dL). They completed a smoking delay task that assessed their ability to resist smoking followed by an ad libitum smoking phase (primary outcomes). They also provided ratings of subjective drug effects and craving, and carbon monoxide levels were measured after smoking (secondary outcomes). Participants receiving varenicline monotherapy delayed smoking longer and smoked fewer cigarettes than those on placebo. Participants receiving varenicline + low-dose naltrexone did not delay smoking longer than those receiving varenicline alone. Participants in both active medication arms smoked fewer cigarettes ad libitum than those receiving placebo. Varenicline can improve smoking outcomes even after an alcohol prime, supporting its use in heavy drinkers who wish to quit smoking. Findings did not support increased efficacy of combined varenicline + low-dose naltrexone relative to varenicline monotherapy.

Effect of Intravenous Ethanol on Capsaicin-Induced Hyperalgesia in Human Subjects.

The objective of this study was to assess ethanol's (EtOH's) effects on capsaicin-induced hyperalgesia in healthy participants. Specifically, we investigated the change in area of capsaicin-induced hyperalgesia following 3 interventions: intravenous EtOH at 2 targeted breath alcohol concentrations (BrAC), or placebo. Eighteen participants participated in 3 test days in a randomized order. Each test day, participants received an intradermal capsaicin injection on the volar surface of the forearm, followed by either infusion of high concentration EtOH (targeted BrAC=0.100g/dl), low concentration EtOH (targeted BrAC=0.040g/dl), or placebo. The area of hyperalgesia was determined by von Frey technique at 2 time points, prior to EtOH infusion, and again when target BrAC was reached. The primary outcome was the percent change in the area of capsaicin-induced hyperalgesia. Additional outcome measures included the visual analogue scale of mood states (VAS), which was administered at each time point. There was a marked 30% reduction in the area of capsaicin-induced hyperalgesia with infusion of a high concentration of EtOH (p<0.05). Low concentration EtOH produced a 10% reduction in hyperalgesia area, although this finding did not reach significance. Further, participants reported significant feelings of euphoria and drowsiness at high concentrations of EtOH (p<0.05), as measured by the VAS. In a human model examining pain phenomena related to central sensitization, this study is the first to demonstrate that capsaicin-induced hyperalgesia is markedly attenuated by EtOH. The capsaicin experimental pain paradigm employed provides a novel approach to evaluate EtOH's effects on pain processing. The antihyperalgesic effects of EtOH observed have important clinical implications for the converging fields of substance abuse and pain medicine and may inform why patients with chronic pain often report alcohol use as a form of self-medication.

The Effect of Varenicline on the Neural Processing of Fearful Faces and the Subjective Effects of Alcohol in Heavy Drinkers.

Pharmacotherapies for alcohol use disorder have been shown to reduce hazardous drinking and improve overall health. The effect sizes for the effectiveness of these medications, however, are small, underscoring the need to expand the range of therapeutics and develop personalized treatment approaches. Recent studies have suggested that varenicline, an α4β2-nicotinic partial agonist widely used for smoking cessation, can help alcoholics reduce drinking, but the neurocognitive underpinnings of its effectiveness remain largely unexplored. In this double-blind study, 32 heavy drinkers were randomized to receive varenicline (2mg/d) or placebo. After 2weeks of dosing, participants underwent functional MRI scans, during which they viewed images of faces with either neutral or fearful expressions at baseline and following an intravenous alcohol infusion to a target breath alcohol concentration of 80mg%. Blood oxygen level-dependent (BOLD) response was analyzed with Analysis of Functional Neuroimaging software. Linear mixed-effects models were used to examine the effects of facial expression (fearful vs. neutral) and medication (placebo vs. varenicline) on BOLD response. The effect of medication on measures of subjective response to alcohol was also examined. Results indicated a significant facial expression-by-medication interaction in the left amygdala. The groups showed equivalent activation to neutral faces, but, whereas the placebo group showed increased activation to fearful faces, the varenicline group showed no change in activation. Amygdala activation to fearful faces correlated with number of drinks in the previous 90days and Obsessive Compulsive Drinking Scale scores. There was no effect of varenicline on subjective response to alcohol. Our results indicate that varenicline may disrupt amygdala response to fearful faces in heavy drinkers. Further, amygdala activation correlated with alcohol consumption, suggesting that the effects of varenicline may be related to aspects of drinking behavior. These results suggest that amygdala response to fearful faces may be developed as a biomarker of the effectiveness of medications being developed for the treatment of alcohol use disorder.

Differences in IV alcohol-induced dopamine release in the ventral striatum of social drinkers and nontreatment-seeking alcoholics

BackgroundStriatal dopamine (DA) has been implicated in alcohol use disorders, but it is still unclear whether or not alcohol can induce dopamine release in social drinkers. Furthermore, no data exist on dopamine responses to alcohol in dependent drinkers. We sought to characterize the DA responses to alcohol intoxication in moderately large samples of social drinkers (SD) and nontreatment-seeking alcoholics (NTS). MethodsTwenty-four SD and twenty-one NTS received two [11C]raclopride (RAC) PET scans; one at rest, and one during an intravenous alcohol infusion, with a prescribed ascent to a target breath alcohol concentration (BrAC), at which it was then “clamped.” The alcohol clamp was started 5min after scan start, with a linear increase in BrAC over 15min to the target of 80mg%, the legal threshold for intoxication. Target BrAC was maintained for 30min. Voxel-wise binding potential (BPND) was estimated with MRTM2. ResultsIV EtOH induced significant increases in DA in the right ventral striatum in NTS, but not SD. No decreases in DA were observed in either group. ConclusionsAlcohol intoxication results in distinct anatomic profiles of DA responses in SD and NTS, suggesting that in NTS, the striatal DA system may process effects of alcohol intoxication differently than in SD.

Functional significance of subjective response to alcohol across levels of alcohol exposure.

Pre-clinical neurobiological models of addiction etiology including both the allostatic model and incentive sensitization theory suggest that alcohol consumption among alcohol-dependent (AD) individuals will be dissociated from hedonic reward as positive reinforcement mechanisms wane in later stage dependence. The aims of this study are to test this claim in humans by examining the relationship between dimensions of subjective responses to alcohol (SR) and alcohol craving across levels of alcohol exposure. Non-treatment-seeking drinkers (n = 205) completed an i.v. alcohol challenge (final target breath alcohol concentration = 0.06 g/dl) and reported on SR and craving. Participants were classified as light-to-moderate drinkers (LMD), heavy drinkers (HD) or AD. Analyses examined group differences in SR and craving response magnitude, as well as concurrent and predictive associations between SR domains and craving. At baseline, LMD and AD reported greater stimulation than HD, which carried over post-alcohol administration. However, stimulation was dose-dependently associated with alcohol craving in HD only. Furthermore, lagged models found that stimulation preceded craving among HD only, whereas this hypothesized pattern of results was not observed for craving preceding stimulation. Sedation was also positively associated with craving, yet no group differences were observed. In agreement with the prediction of diminished positive reinforcement in alcohol dependence, this study showed that stimulation/hedonic reward from alcohol did not precede craving in AD, whereas stimulation was dose-dependently associated with and preceded craving among non-dependent HD.

Factor Structure of Subjective Responses to Alcohol in Light and Heavy Drinkers.

Subjective responses (SRs) to alcohol have been implicated in alcoholism etiology, yet less is known about the latent factor structure of alcohol responses. The aim of this study was to examine the factor structure of SR using a battery of self-report measures during a controlled alcohol challenge. Nontreatment seeking drinkers (N=242) completed an intravenous alcohol challenge including the following SR measures: Biphasic Alcohol Effects Scale, Subjective High Assessment Scale, Profile of Mood States, Alcohol Urge Questionnaire, and single items assessing alcohol "Liking" and "Wanting." Ascending limb target breath alcohol concentrations were 0.02, 0.04, and 0.06, and descending limb target was 0.04g/dl. Exploratory factor analyses were conducted separately on estimates of mean and dose responses on the ascending limb and on descending limb data. To examine the generalizability of this factor structure, these analyses were repeated in heavy drinkers (≥14 drinks/wk for men, ≥7 for women; n=132) and light drinkers (i.e., nonheavy drinkers; n=110). In the full sample, a 4-factor solution was supported for ascending limb mean and dose responses and descending limb data representing the following SR domains: Stimulation/Hedonia, Craving/Motivation, Sedation/Motor Intoxication, and Negative Affect. This 4-factor solution was replicated in heavy drinkers. In light drinkers, however, SR was better summarized by a 3-factor solution where ascending mean and descending limb responses consisted of Stimulation/Hedonia, Craving/Motivation, and a general negative valence factor, and dose responses consisted of a general positive valence factor, Sedation/Motor Intoxication, and Negative Affect. These findings suggest that SR represents a multifaceted construct with consistent factor structure across both ascending and descending limbs. Further, as drinking levels escalate, more defined Craving/Motivation and negative valence dimensions may emerge. Longitudinal studies examining these constructs are needed to further our understanding of SR as potentially sensitive to alcohol-induced neuroadaptation.

Cognitive impairment following consumption of alcohol with and without energy drinks.

The aim of this study was to assess the relative effects of alcohol mixed with energy drink (AmED) versus alcohol alone on cognitive performance across the ascending and descending breath alcohol concentration (BrAC) limb using doses similar to real-world intake. Using a single-blind, placebo-controlled, crossover design, 19 participants completed 4 sessions where they received: (i) placebo, (ii) alcohol, (iii) AmED 500ml energy drink (ED), and (iii) AmED 750ml ED. Performance on measures of psychomotor function (Compensatory Tracking Task [CTT]), information processing (Digit Symbol Substitution Task [DSST]; Inspection Time Task [ITT]), and response inhibition (Brief Stop-Signal Task [Brief SST]) was assessed at ~0.05% ascending BrAC, ~0.08% peak BrAC, and ~0.05% descending BrAC. The ITT and Brief SST showed no differential effect of AmED versus alcohol (gs<0.30 and gs<0.36, respectively). Moderate magnitude improvements in alcohol-induced impairment of CTT and DSST performance were observed after AmED versus alcohol on the descending BrAC limb (gs>0.45 and gs>0.37, respectively). A moderate magnitude decrease in DSST errors was also observed after AmED relative to alcohol at 0.050% ascending target BrAC (gs>0.43). Changes in cognitive function after AmED administration were dependent on the degree of intoxication, BrAC curve limb, and ED volume. Co-administration of ED doses which matched (500ml) and exceeded (500ml) maximum daily intake guidelines with alcohol decreased impairment of psychomotor function and global information processing after alcohol consumption. These results cannot be necessarily interpreted to suggest that people are less impaired after AmED, as behavior is the result of coordination of multiple cognitive functions, and reduced impairment on one aspect of cognition may not translate into global improvements.

Acute effects of moderate alcohol on psychomotor, set shifting, and working memory function in older and younger social drinkers.

ABSTRACT. Despite substantial attention being paid to the health benefits of moderate alcohol intake as a lifestyle, the acute effects of alcohol on psychomotor and working memory function in older adults are poorly understood. The effects of low to moderate doses of alcohol on neurobehavioral function were investigated in 39 older (55-70 years; 15 men) and 51 younger (25-35 years; 31 men) social drinkers. Subjects received one of three randomly assigned doses (placebo, .04 g/dl, or .065 g/dl target breath alcohol concentration). After beverage consumption, they completed the Trail Making Test Parts A and B and a working memory task requiring participants to determine whether probe stimuli were novel or had been presented in a preceding set of cue stimuli. Efficiency of working memory task performance was derived from accuracy and reaction time measures. Alcohol was associated with poorer Trail Making Test Part B performance for older subjects. Working memory task results suggested an Age × Dose interaction for performance efficiency, with older but not younger adults demonstrating alcohol-related change. Directionality of change and whether effects on accuracy or reaction time drove the change depended on the novelty of probe stimuli. This study replicates previous research indicating increased susceptibility of older adults to moderate alcohol-induced psychomotor and set-shifting impairment and suggests such susceptibility extends to working memory performance. Further research using additional tasks and assessing other neuropsychological domains is needed. (J. Stud. Alcohol Drugs, 75, 870-879, 2014).

Subjective response to alcohol and ADH polymorphisms in a select sample of young adult male East Indians and Africans in Trinidad and Tobago.

Level of response to alcohol has been associated with risk of alcohol dependence in a number of ethnic groups. In the present study, subjective and objective responses to alcohol were evaluated in Indo-Trinidadians (Indo-T) and Afro-Trinidadians (Afro-T). Associations of alcohol dehydrogenase polymorphisms with response to alcohol, using the Subjective High Assessment Scale (SHAS), and breath alcohol concentrations (BrAC) were tested. Regular male drinkers without alcohol dependence (n = 112) ages 18-25 years participated in alcohol challenge sessions consisting of placebo and two doses of alcohol (target BrAC: 0 g/dl for placebo, .04 g/dl low dose, and .08 g/dl high dose) and genotyped for variants in ADH1B*3 and ADH1C*2. Indo-T had significantly higher BrAC, pulse rates, and cortisol levels when compared with Afro-T but did not have significantly higher SHAS values. Higher responses on the SHAS items muddle/confused and nauseated were significantly associated with the presence of at least one ADH1B*3 allele following the high dose of alcohol in Afro-T. Indo-T with at least one ADH1C*2 allele displayed significantly different Drug × Time interactions for the SHAS item effects of alcohol at the low dose and for the SHAS items clumsy, muddle/confused, effects of alcohol, floating, drunk, and total at the high dose from Indo-T with two ADH1C*1 alleles. This is the first study that has investigated individual sensitivity to alcohol in a Caribbean population and in people of East Indian descent. Indo-T with at least one ADH1C*2 allele may be at higher risk for heavy drinking by feeling less of the effects of alcohol, including nausea. In Afro-T, having at least one ADH1B*3 allele appears to exert a protective effect by enhancing the unpleasant effects of alcohol, such as nausea and confusion.

Varenicline, low dose naltrexone, and their combination for heavy-drinking smokers: human laboratory findings.

Heavy-drinking smokers constitute a sizeable and hard-to-treat subgroup of smokers, for whom tailored smoking cessation therapies are not yet available. The present study used a double-blind, randomized, 2 × 2 medication design, testing varenicline alone (VAR; 1 mg twice daily), low dose naltrexone alone (L-NTX; 25 mg once daily), varenicline plus naltrexone, and placebo for effects on cigarette craving and subjective response to alcohol and cigarettes in a sample (n = 130) of heavy-drinking daily smokers (≥10 cigarettes/day). All participants were tested after a 9-day titration period designed to reach a steady state on the target medication. Testing was completed at 12 h of nicotine abstinence, after consuming a standard dose of alcohol (target breath alcohol concentration = 0.06 g/dl) and after smoking the first cigarette of the day. The combination of VAR + L-NTX was superior to placebo, and at times superior to monotherapy, in attenuating cigarette craving, cigarette and alcohol "high," and in reducing ad-lib consumption of both cigarettes and alcohol during the 9-day medication titration period. These preliminary findings indicate that clinical studies of the combination of VAR + L-NTX for heavy drinkers trying to quit smoking are warranted and may ultimately improve clinical care for this sizeable and treatment-resistant subgroup of smokers.

Influence of Sensation Seeking on Response to Alcohol Versus Placebo: Implications for the Acquired Preparedness Model

Previous research has identified several aspects of behavioral undercontrol that are associated with heavy drinking and problems. Further, research on the acquired preparedness model (Smith and Anderson, 2001) has identified biased learning as a potential mechanism of these effects. Traits like sensation seeking have been linked to stronger positive and weaker negative expectancies, which, in turn, contribute to increased risk for heavy drinking and problems. Although expectancies are thought to represent potentially biased expectations about drinking outcomes, they may also reflect individual differences in alcohol response. The present study examined the strength of associations between sensation seeking and both expectancies (response to placebo) and subjective response under alcohol. Using a between-subjects design, young adult social drinkers (N = 236) were randomly assigned to receive alcohol (target breath alcohol concentration of .08%) or placebo, after which they reported on subjective experiences of stimulation and sedation. Sensation seeking was significantly related to stimulant response, and the strength of this association did not differ by beverage condition (alcohol vs. placebo). The findings argue against a pharmacological explanation for results of prior studies of the acquired preparedness model and support a biased learning interpretation of relations between sensation seeking and positive expectancies. Results also extend the findings on the acquired preparedness model to an implicit measure of positive alcohol expectancies (subjective response to placebo). Future studies using additional measures of implicit expectancies (e.g., Implicit Association Test) would be helpful in determining the relative strength of implicit and explicit expectancies as mediators within the acquired preparedness model.

Interactions between age and moderate alcohol effects on simulated driving performance

There is a substantial body of literature documenting the deleterious effects of both alcohol consumption and age on driving performance. There is, however, limited work examining the interaction of age and acute alcohol consumption. The current study was conducted to determine if moderate alcohol doses differentially affect the driving performance of older and younger adults. Healthy older (55-70) and younger (25-35) adults were tested during a baseline session and again following consumption of one of three beverages [0.0% (placebo), 0.04% or 0.065% target breath alcohol concentration]. Measures of driving precision and average speed were recorded. Older adults performed more poorly on precision driving measures and drove more slowly than younger adults at baseline. After controlling for baseline performance, interactions between alcohol and age were observed following beverage consumption on two measures of driving precision with older adults exhibiting greater impairment as a result of alcohol consumption. These data provide evidence that older adults may be more susceptible to the effects of alcohol on certain measures of driving performance. An investigation of mechanisms accounting for alcohol's effects on driving in older and younger adults is required. Further evaluation using more complex driving environments is needed to assess the real-world implication of this interaction.

The Acute Effects of Alcohol on Sleep Architecture in Late Adolescence

Alcohol consumption is prevalent in late adolescence; however, little is known about its effect on sleep in this group. In mature adults, alcohol decreases sleep onset latency (SOL) and sleep efficiency (SE) and increases wake after sleep onset (WASO). It also increases slow wave sleep (SWS) and decreases rapid eye movement (REM) sleep in the first half of the night, with the inverse occurring in the second half. Alcohol's effect on sleep during late adolescence is of interest given that this age group shows both dramatic increases in alcohol consumption and significant developmental changes in the central nervous system. This study examined the effect of alcohol on sleep architecture in women and men aged 18 to 21 years and whether previously reported sleep architecture effects may have been as an artificial result of changes to sleep cycle length. Twenty-four (12 women) healthy 18- to 21-year-old light social drinkers (19.1 ± 1.0 years) underwent 2 conditions: presleep alcohol (target breath alcohol concentration [BAC] 0.10%) and placebo-administered under controlled conditions, followed by standard polysomnography. In the alcohol condition, mean BAC at lights out was 0.084 ± 0.016%. Time in bed, total sleep time, and SOL (all p > 0.05) did not differ between conditions. However, there was less REM (p = 0.011) and more stage-2 sleep (p = 0.035) in the alcohol condition. Further, alcohol increased SWS (p = 0.02) and decreased REM sleep (p < 0.001) in the first half of the night and disrupted sleep in the second half, with increased WASO (interaction: p = 0.034), and decreased SE (p = 0.04) and SWS (p = 0.01) and no REM sleep rebound in the second half of the night (p = 0.262). Additionally, alcohol had no effect on sleep cycle length (p = 0.598). The results were broadly consistent with the adult literature with the novel extension that half night sleep architecture effects could not be attributed to changes in sleep cycle length. However, alcohol did not reduce SOL, or result in a REM rebound following reduced REM in the first half of the night. The results suggest that the effects of alcohol on sleep are modified by sleep's prevailing developmental stage.

Subjective Response to Alcohol Among Alcohol‐Dependent Individuals: Effects of the Mu‐Opioid Receptor (OPRM1) Gene and Alcoholism Severity

Subjective response to alcohol has been examined as a marker of alcoholism risk. The A118G single-nucleotide polymorphism (SNP) of the mu-opioid receptor (OPRM1) gene has been previously associated with subjective response to alcohol in heavy drinkers. This study seeks to extend the literature by examining the effect of OPRM1 genotype on responses to alcohol in a sample of alcohol-dependent individuals. A secondary aim of this study is to examine alcoholism severity as a predictor of subjective responses to alcohol. Nontreatment seeking problem drinkers (n = 295) were assessed in the laboratory for clinical dimensions of alcohol dependence. Following prospective genotyping, 43 alcohol-dependent individuals across the 2 genotype conditions (AA, n = 23 and AG/GG, n = 20) were randomized to 2 intravenous infusion sessions: 1 of alcohol (target breath alcohol concentration = 0.06 g/dl) and 1 of saline. Measures of subjective responses to alcohol were administered in both infusion sessions. Alcohol-dependent G-allele carriers reported greater alcohol-induced stimulation, vigor, and positive mood, as compared to A-allele homozygotes. There was no genotype effect on alcohol-induced sedation or craving. There was a statistical trend-level severity × alcohol interaction such that individuals at higher levels of severity reported greater alcohol-induced tension reduction. These results support the hypothesis that OPRM1 genotype moderates the hedonic effects of alcohol, but not the sedative and unpleasant effects of alcohol, in a sample of alcohol-dependent patients. Results are discussed in light of a clinical neuroscience framework to alcoholism.