Students' Drinker Prototypes and Alcohol Use in a Naturalistic Setting

Background:  Perceptions about the type of people who drink, also referred to as drinker prototypes, may strengthen young people's motivation to engage in alcohol use. Previous research has shown that drinker prototypes are related to alcohol consumption in both adolescents and young adults. However, the evidence for the strength of these relationships remains inconclusive. One of the caveats in former studies is that all insights about prototype relations are based on self-reported data from youngsters themselves, mostly gathered in a class situation, which may contain bias due to memory distortions and self-presentation concerns.
Methods:  The present study examined the impact of drinker prototypes on young adults' drinking patterns by using a less obtrusive measure to assess alcohol consumption, i.e. ad lib drinking among friend groups in the naturalistic setting of a bar lab. Drinker prototypes, self-reported alcohol use in the past, and observed alcohol intake in the bar lab were assessed among 200 college students. Relations between participants' drinker prototypes and their self-reported and observed drinking behavior were examined by computing correlations and conducting multilevel analyses.
Results:  Drinker prototypes were related to both self-reported and observed alcohol use. However, the drinking patterns of friend group members had a strong impact on participants' individual drinking rates in the bar lab. After these group effects had been controlled for, only heavy drinker prototypes showed relations with observed alcohol intake in the bar lab.
Conclusions:  These findings further establish the value of drinker prototypes in predicting young adults' drinking behavior and suggest that people's motivation to drink alcohol in real-life drinking situations is related to their perceptions about heavy drinkers.     

Blood Ethanol Concentrations in Rats Drinking Sucrose/Ethanol Solutions

BACKGROUND: The addition of sucrose to ethanol solutions results in a substantial increase in ethanol self-administration by rats that are deprived of neither food nor water. However, if sucrose alters ethanol absorption or metabolism, resulting in blood ethanol concentrations (BECs) not different from those resulting from lower intakes of ethanol/water solutions, then the usefulness of sucrose/ethanol mixtures in increasing ethanol consumption is questionable. The present study was conducted to determine whether the addition of sucrose to ethanol solutions altered BECs in an operant self-administration paradigm. METHODS: Tail blood (from male Long-Evans rats) was collected 30 min after the intake of four different solutions, i.e., 5% sucrose/20% ethanol, 5% sucrose/10% ethanol, 2% sucrose/10% ethanol, and 10% ethanol. RESULTS: Ethanol intakes (mean, 1.57+/-0.21 g/kg) and BECs (mean, 78.4+/-9.3 mg/100 ml) were highest when 5% sucrose was added to the ethanol solution. Moreover, the ratios between ethanol intakes and resulting BECs were approximately the same for all solutions. CONCLUSIONS: These findings indicate that, under the conditions of this procedure, the BEC reached is dependent on the amount of ethanol consumed and is not influenced by the addition of sucrose to the solution.     

Dopamine Release During Ethanol Drinking in AA Rats

The dopamine overflow in the nucleus accumbens of rats from the high alcohol drinking AA line was measured by microdialysis before, during, and after one-half hour sessions of cued drinking of ethanol flavored with saccharin and peppermint or, as a control, saccharinpeppermint drinking. The animals had had extensive previous experience with ethanol drinking. Self-administration of the ethanol solution did not raise the dopamine level substantially: there was a small (17%) but significant increase only during the first 10 min after the onset of drinking. Giving the rats a cue for ethanol, which was part of their daily routine drinking regime, did not raise the dopamine level before ethanol was presented to the rats (i.e., during "anticipation"). The results are consistent with our previous studies showing a lack of a large ethanol-induced dopamine response in rats with previous experience of drinking ethanol and with the idea that although dopamine may play some role in alcohol drinking, it is not the central substrate producing the reinforcement from ethanol in AA rats.     

Effects of Naloxone on Limited-Access Ethanol Drinking in Rats

The hypothesis that naloxone (NAL) decreases oral ethanol intake in rats by inducing a conditioned taste aversion (CTA) to ethanol was investigated. Rats were trained to drink 8% ethanol (v/v) on a 1-hr limited-access schedule. They received 4 days of intraperitoneal injections of 10 mg/kg of NAL, 10 min before limited-access (–10MIN group), immediately after limited-access (1HR group), or 3 hr after limited-access (3HR). Ethanol intake decreased in the -10MIN and 1HR groups during the injection period and on the postinjection day. In experiment 2, rats received 4 days of NAL injections when ethanol was not available (pre-exposure), and then the paradigm was repeated. In this experiment, there was no suppression of ethanol intake for any group on the postinjection day. The decrease in ethanol intake during injections observed for the 1HR in experiment 1 and the sustained suppression postinjection was interpreted as a CTA. Pre-exposure in experiment 2 abolished the CTA. Differences in the pattern ethanol intake for the -10MIN and 3HR groups during the experiments, however, suggest that a CTA is not the sole mechanism underlying NAL's suppressant effects on ethanol intake. In conclusion, in rats both the dose of NAL and the relative timing of NAL injections and ethanol drinking effect subsequent NAL suppression of ethanol intake.     

A Naturalistic Evaluation of a Group Intervention for Parents of Youth with Substance Use Disorders

ABSTRACT

Parents of youth with substance use disorders (SUDs) often play a vital role in successful treatment, yet little is known about interventions designed to help them cope with the stress of this role, especially as delivered in real-world settings. Evaluations of such interventions could potentially inform adaptations to enhance their clinical utility. Parents of youth with SUDs attending a clinician-led group based on the CRAFT model completed measures at intake, 4- and 8-weeks. Parents (n = 545) attended an average of 3.7 sessions; 12% completed all 8 weeks. Analysis of demographic predictors of retention indicated that older parents attended more sessions on average. Overall stress did not change across time points (p > .05). However, parents reported improvement in parent empowerment as measured by the Parent Empowerment Scale, a novel measure of parent empowerment in coping with their child’s SUD (p < .001). Clinician led evidence-informed group services may improve parents’ perceived ability to help their child with their SUD. Low retention rates highlight the need to better understand the factors contributing to retention, and the potential value of adaptations to shorten the intervention. Programs serving youth with SUDs may wish to consider integrating such group services to support parents.     

Intensity and Duration of Chronic Ethanol Exposure Is Critical for Subsequent Escalation of Voluntary Ethanol Drinking in Mice

Background: Excessive alcohol drinking continues to be an important health problem. Recent studies from our laboratory and others have demonstrated that animal models of ethanol dependence and relapse can contribute to understanding factors that contribute to excessive drinking. In this study, we tested the hypothesis that the amount and duration of ethanol exposure is critical for promoting the escalation in drinking by mice given access to ethanol in a limited access paradigm. Methods: We used several methods of chronic intermittent ethanol exposure in male C57BL/6J mice that would vary in the amount and duration of exposure to ethanol as indicated by blood ethanol concentrations (BEC). After establishing baseline drinking in the mice using a 2 hours, 2 bottle choice drinking paradigm, each study involved alternating between periods of ethanol exposure and periods of limited access to ethanol (1 cycle) for a total of 3 cycles. In Study 1, mice were allowed extended access (16 hours) to ethanol for oral consumption or remained in the home cage. In Study 2, the ethanol exposure consisted of intragastric gavage of increasing doses of ethanol or isocaloric sucrose as the control. Study 3 compared intragastric gavage combined with pyrazole, an alcohol dehydrogenase inhibitor, with vapor inhalation of ethanol using procedures known to lead to increased drinking in mice. Finally, Study 4 was a retrospective review of several studies conducted in our laboratory using inhalation procedures. The retrospective review encompassed a range of postvapor chamber BEC values and ethanol intakes that would allow a relationship between increased drinking and BEC to be examined. Results: Allowing mice to drink for longer periods of time did not cause increased drinking in subsequent limited access sessions. Likewise, gastric intubation of ethanol which produced high BEC (>300 mg/dl) with or without pyrazole did not increase drinking. Only the vapor inhalation procedure, which was associated with sustained BEC above 175 mg/dl for the entire exposure period resulted in increased drinking. The retrospective study provided further evidence that sustained BEC levels above 175 mg/dl was critical to the escalation in drinking. Conclusions: We found that the intensity (amount) and duration of ethanol exposure, indexed by BEC, is critical to produce increased drinking in mice. Specifically, BEC must regularly exceed 175 mg/dl for the escalation in drinking to occur. Future studies will examine neurobiological adaptations that may underlie the increased drinking behavior caused by chronic intermittent ethanol exposure.     

Naltrexone Effects on Ethanol Drinking Acquisition and on Established Ethanol Consumption in C57BL/6J Mice

Naltrexone's success as a treatment agent for alcoholism seems to be due to its ability to reduce craving in abstinent, dependent individuals and to reduce the pleasure associated with subsequent intake. However, more study is needed to establish the optimal amount of time that naltrexone treatment should be continued. Little information seems to have been collected regarding the most effective dosing regimen for reducing alcohol craving and consumption, and the usefulness of opiate antagonists in the prevention of alcohol dependence in nonaddicts, rather than just as a treatment agent in addicted individuals, also deserves further study. The alcohol-preferring C57BL/6J (B6) mice were used to: (1) study naltrexone effects on consumption in established drinkers using an increasing dosing regimen, (2) study naltrexone effects on the acquisition of ethanol drinking, and (3) study the effects of chronic naltrexone from timed-release pellets on drinking in alcohol-naive mice. Naltrexone reduced ethanol preference in established drinkers, but its effects waned at increasing doses. Naltrexone slowed the acquisition of ethanol drinking, but was ineffective when readministered after a phase when ethanol was offered in the absence of naltrexone. Mice with chronic naltrexone pellets consumed greater amounts of ethanol and showed higher ethanol preference than did placebo-pelleted animals. The observed reduced efficacy of naltrexone with increasing dosage and chronic treatment may have been due to naltrexone-induced opiate receptor changes. Such changes are presumably more likely to occur when naltrexone doses remain high or perhaps accumulate. Thus, dose and frequency of administration may be important factors in determining naltrexone's effectiveness in treating alcohol dependence.     

N-Acetylcysteine Improves Group B Streptococcus Clearance in a Rat Model of Chronic Ethanol Ingestion

Background: Sepsis is the most common risk factor associated with acute respiratory distress syndrome (ARDS) and results in a 40–60% mortality rate due to respiratory failure. Furthermore, recent epidemiological studies have demonstrated that a history of alcohol abuse increases the risk of ARDS by 3.6‐fold. More recently, group B streptococcus (GBS) infections in nonpregnant adults have been increasing, particularly in alcoholics where there is an increased risk of lobular invasion and mortality. We have shown in an established rat model that chronic ethanol ingestion impaired macrophage internalization of inactivated infectious particles in vitro and enhanced bidirectional protein flux across the alveolar epithelial‐endothelial barriers, both of which were attenuated when glutathione precursors were added to the diet. We hypothesized that chronic ethanol ingestion would increase the risk of infection even though GBS is less pathogenic but that dietary N‐acetylcysteine (NAC), a glutathione precursor, would improve in vivo clearance of infectious particles and reduce systemic infection. Methods: After 6 weeks of ethanol feeding, rats were given GBS intratracheally and sacrificed 24 hours later. GBS colony‐forming units were counted in the lung, liver, spleen, and bronchoalveolar lavage fluid. Acute lung injury in response to GBS was also assessed. Results: Chronic ethanol exposure decreased GBS clearance from the lung indicating an active lung infection. In addition, increased colonies formed within the liver and spleen indicated that ethanol increased the risk of systemic infection. Ethanol also exacerbated the acute lung injury induced by GBS. NAC supplementation normalized GBS clearance by the lung, prevented the appearance of GBS systemically, and attenuated acute lung injury. Conclusions: These data suggested that chronic alcohol ingestion increased the susceptibility of the lung to bacterial infections from GBS as well as systemic infections. Furthermore, dietary NAC improved in vivo clearance of GBS particles, attenuated acute lung injury, and disseminated infection.     

Development and Characterization of a Binge Drinking Model in Mice for Evaluation of the Immunological Effects of Ethanol

This study describes the development and characterization of a binge drinking model in which a single dose of ethanol (EtOH) is administered by gavage to B6C3F1 mice. Blood EtOH levels were monitored over time after administration of EtOH at doses of 3.0–7.0 g/kg. Peak levels were in the range of 0.2–0.5%, and clearance was complete within 2–12 hr. Substantial increases in blood corticosterone levels were noted. Behavioral changes in EtOH-treated mice aged 8 weeks ranged from no effect (3–4 g/kg) to severe ataxia (6–7 g/kg). In mice aged 16 weeks, a dosage of 7 g/kg caused loss of the righting reflex in some animals and severe ataxia in most of the others. Clinical chemistry results did not indicate biologically important changes in general physiological/homeostatic systems in EtOH-treated mice, but there were indications of minor liver damage at the 7 g/kg dosage. Thus, administration of EtOH to B6C3F1 mice by gavage produces behavioral changes, changes in blood EtOH levels, and probably glucocorticoid levels representative of at least some human binge drinkers. The model was used to evaluate the effects of binge drinking on antibody responses, and the results indicate the model will be useful for such studies.     

Psychological Correlates of Drinking Behavior in Social Drinker College Students

Psychological adjustment, cognitive functioning, and drinking behaviors have been shown to discriminate between alcoholic and control populations. Few data exist on the discriminatory power of such measures among social drinkers differing on alcohol intake level. The purpose of this study was to assess the relationship between alcohol consumption and psychological/cognitive functioning in a group of social drinker college students made up of equal numbers of males and females, matched on age and education, and varying on amount of alcohol consumed per drinking episode. Results indicate no relationship between alcohol consumption and cognitive functioning in this group of social drinkers. Drinking and psychological profiles of heavy social drinkers were very similar to those of diagnosed alcoholics and very dissimilar to light social drinkers. Such a finding suggests that these types of profiles may have predictive value for identifying at-risk social drinkers in the general population.     

Monitoring Ethanol Exposure in a Clinical Setting by Analysis of Blood, Breath, Saliva, and Urine

BACKGROUND: Several new technologies have been developed for estimating blood alcohol concentration (BAC), among others, by the analysis of alcohol in saliva specimens. The Q.E.D. is a new quantitative test designed for measuring ethanol in saliva and promising results have been obtained in various experimental settings. METHODS: In the present study, venous BAC was determined in 28 patients on arrival and when they were discharged from a detoxification unit. The results were compared with breath, saliva, and urine alcohol concentrations. Headspace gas chromatography was used for analysis of ethanol in blood and urine, and breath alcohol was determined with an Alcolmeter S-D2 instrument. RESULTS: The concentration of alcohol in urine was always higher than the BAC (mean difference, 0.62 mg/ml) and individual values were highly correlated (n=42; r=0.92). The handheld breath-alcohol instrument (Alcolmeter S-D2) showed good agreement with venous BAC (n=52; r=0.97; mean difference, 0.04 mg/ml). The saliva-alcohol test failed to perform well in our tests (n=36; r=0.75; mean difference, 0.55 mg/ml) mainly because of problems encountered in obtaining a sufficient sample for analysis in highly intoxicated patients. CONCLUSIONS: Because of the relatively low cost of the Q.E.D. ' saliva test, in comparison with a breath alcohol analyzer, the saliva test could be a cost-effective alternative in public health settings where mildly to moderately intoxicated persons are encountered.     

Psychophysiological Effects of Oral Ethanol in Alcoholics and Social Drinkers

The acute and extended effects of ethanol ingestion were examined in five alcoholic subjects, and five "social" drinkers. Six physiological and four subjective report measures were taken before, during and up to 90 min after the ingestion of ethanol in three doses and placebo. Findings showed that alcohol exerted significant dose-related physiological effects in the initial minutes of ingestion, and in extended analyses of physiological and subjective measures in both groups of drinkers. Alcoholics and social drinkers generally did not differ in their physiological responses to alcohol doses and placebo, while some evidence for tolerance to reported euphoric effects of alcohol in the alcoholic subjects was found. The possibility is raised that early physiological responses observed during ethanol ingestion may arise not only from pharmacological effects of the drink, but may also be evidence for conditional predrink responses.     

Patterns of Outcome: Drinking Histories over Ten Years Among a Group of Alcoholics

In a long-term follow-up study extending over 10 years of a cohort of 99 male alcoholics, interviews were achieved with 68 of them. Data obtained by personal recall are presented to illustrate the pattern of the men's drinking over the follow-up period. The changes over time and the difference between individuals are discussed.     

Effect of Pentylenetetrazole on Ethanol Intake, Ethanol Kinetics, and Social Behavior in Male Wistar Rats

Stress and anxiety are often implicated in excessive alcohol use. The nature of this interaction, however, is not understood. The aim of this study was to examine the effect of the anxiogenic agent, pentylenetetrazole (PTZ), on the acquisition and maintenance of ethanol drinking behavior in male Wistar rats. In rats maintained on a limited access procedure, with a choice between a 12% w/v ethanol (ETOH) solution and water available for 30 min each day, acute PTZ administration (1.5 to 15.0 mg/kg) did not modify ETOH intake. Chronic PTZ administration elicited a significant suppression in ETOH intake; however, this effect developed gradually over time. During the acquisition phase, chronic PTZ treatment also suppressed ETOH consumption. Chronic, but not acute, treatment with PTZ seemed to enhance water consumption. To assess whether the effect of PTZ on ETOH intake was due to either alterations in ETOH kinetics or behavior, blood ETOH levels and social interaction behaviour were examined. PTZ (15.0 mg/kg) produced a significant suppression in social interaction behavior, although tolerance developed to this effect on chronic PTZ administration. Both acute and chronic PTZ treatment (15 mg/kg) resulted in lower blood ETOH levels achieved after administration of 1.0 g/kg po of ETOH. Because the anxiogenic effect of PTZ was not maintained on repeated administration, yet the suppression of ETOH intake was only observed after chronic treatment, this suggests a dissociation between the processes regulating these behaviors.