• Energy Research

AbstractGenetic variations in the mu‐opioid receptor (OPRM1) gene have been related to high sensitivity to rewarding effects of alcohol. The current study focuses on the neural circuitry underlying this phenomenon using an alcohol versus water taste‐cue reactivity paradigm in a young sample at relatively early stages of alcohol use, thus limiting the confound of variations in duration of alcohol use. Drinkers (17–21 years old) were selected on genotype carrying the AA—(n = 20) or the AG—(n = 16) variant of the A118G single nucleotide polymorphism (SNP) of the OPRM1 gene (rs1799971), and underwent functional magnetic resonance imaging (fMRI). Magnitude of the neural activity and frontostriatal functional connectivity in response to alcohol versus water were investigated. The AG‐group demonstrated reduced activation in prefrontal and parietal regions, including the inferior and middle frontal gyrus, superior and inferior parietal lobule, compared with the AA‐group. No activation differences were observed in the mesolimbic pathway. Connectivity from the ventral‐striatum to frontal regions for alcohol > water trials was higher in the AG than the AA group. For the dorsal‐striatum seed region, the AG group showed increased connectivity to non‐PFC regions. These results indicate that adolescents carrying the G‐allele may be more vulnerable for the alcohol to hijack the reward system in the absence of frontal control to regulate craving. This implies that findings of hyperactivation in the mesolimbic structures of G‐allele carriers in earlier studies might result from both genetic susceptibility and heavy drinking.

Background: Baclofen has shown promise in the treatment of alcohol dependence. However, its precise (neuro-) psychological working mechanism is still under debate. Aims: This study aimed to get a better understanding of baclofen’s working mechanism by examining the effect of baclofen on cognitive biases. It was hypothesized that baclofen, compared to placebo, would lead to weaker cognitive biases. Furthermore, given a suggested anxiolytic effect of baclofen, we expected that anxiety would moderate this effect. Methods: From a larger randomized clinical trial (RCT) with 151 participants, a subset of 143 detoxified alcohol-dependent patients, either taking baclofen or placebo, was examined. Attentional bias for alcohol (500 and 1500 ms), alcohol approach tendencies, implicit alcohol-relaxation associations and trait anxiety were assessed before the administration of baclofen or placebo. Four weeks later, 94 patients were still abstinent (53 in the baclofen and 41 in the placebo condition) and cognitive biases were assessed again. Results: At baseline, patients showed a vigilance-avoidance pattern for the attentional bias (at 500 and 1500 ms, respectively) and alcohol-negative associations. After 4 weeks, an indication for an attentional bias away from alcohol at 500 ms was found only in the baclofen group; however, cognitive biases did not differ significantly between treatment groups. No moderating role of anxiety on cognitive biases was found. Conclusions: Baclofen did not lead to a differential change in cognitive biases compared with placebo, and trait anxiety levels did not moderate this. A better understanding of the working mechanism of baclofen and predictors of treatment success would allow prescribing of baclofen in a more targeted manner.

Given the potential advantages of online assessment of implicit alcohol-related cognitive processes, the goal of this study was to empirically validate the online administration of the implicit association test (IAT). First, we examined whether an Internet-delivered IAT programmed in Flash can be as effectively used to assess implicit alcohol-related associations as equivalent IAT versions that are programmed in local lab software, such as Inquisit. Second, participants performed the IAT versions once in the controlled laboratory setting and once on their home computers via the Internet. Findings with the alcohol IAT versions were robust and did not vary systematically with respect to setting (home or lab) or assessment software (Flash or Inquisit). Importantly, there were also indications that IAT versions performed at home were more strongly related to explicit measures and drinking behavior than were lab-based IAT versions. Together, these findings demonstrate that the alcohol IAT can be validly administered online via participants' home computers.

Heavy alcohol drinking increases the incentive salience of alcohol-related cues. This leads to increased appetitive motivation to drink alcohol as measured by subjective craving and cognitive biases such as attentional bias and approach bias. Although these measures relate to the same construct, correlations between these variables are often very low. Alcohol consumption might not only increase different aspects of appetitive motivation, but also correlations between those aspects.To investigate the effect of a low alcohol dose on changes in various measures of appetitive motivation.Twenty-three heavy social drinkers were tested in 2 sessions, once after receiving an alcohol prime dose and once after receiving a placebo drink. After drink administration, attentional bias was measured with a visual-probe task using concurrent eye movement monitoring. Furthermore, we measured the approach bias with a stimulus response compatibility task and subjective craving with the Desires for Alcohol Questionnaire.After the alcohol prime dose, participants had higher levels of craving and more pronounced attentional bias (faster reaction times to probes that replaced alcohol rather than control pictures, increased maintenance of gaze on alcohol pictures, and a higher percentage of first eye movements directed toward alcohol pictures). Approach bias was not influenced by the alcohol prime dose. The correlation between attentional bias and approach bias was significantly higher after the alcohol than after the placebo drink.A low alcohol dose increased most measures of appetitive motivation for alcohol and increased the interrelation between cognitive measures of this construct.

Alcohol abuse is associated with a cluster of long-term changes in cognitive processes, as predicted by contemporary models of addiction. In this paper we review evidence which suggests that similar changes may occur during an alcohol binge, and as such they may play an important role in explaining the loss of control over alcohol consumption that occurs during alcohol binges. As a consequence of both acute alcohol intoxication (alcohol 'priming' effects) and exposure to environmental alcohol-related cues, we suggest that a number of changes in cognitive processes are likely. These include increased subjective craving for alcohol, increased positive and arousing outcome expectancies and implicit associations for alcohol use, increased attentional bias for alcohol-related cues, increased action tendencies to approach alcohol, increased impulsive decision-making, and impaired inhibitory control over drives and behaviour. Potential reciprocal relationships between these different aspects of cognition during an alcohol binge are discussed. Finally, we discuss the relationship between the current model and existing models of cognitive processes in substance abuse, and we speculate on the implications of the model for the reduction binge drinking and its consequences.

Alcohol impairs inhibitory control, and it alters implicit alcohol cognitions including attentional bias and implicit associations. These effects are seen after doses of alcohol which do not lead to global impairments in cognitive performance. We review studies which demonstrate that the effects of alcohol on inhibitory control are associated with the ability of alcohol to prime alcohol‐seeking behavior. We also hypothesize that alcohol‐induced changes in implicit alcohol cognitions may partially mediate alcohol‐induced priming of the motivation to drink. Based on contemporary theoretical models and conceptualizations of executive function, impulsivity, and the motivational salience of alcohol‐related cues, we speculate on other aspects of cognition that may underlie alcohol’s effects on alcohol seeking. Inconsistencies in existing research and priorities for future research are highlighted, including dose effects and the potential interactions between chronic heavy drinking and the acute effects of alcohol on these cognitive processes.

Background:  The use of alcohol is associated with various forms of automatic processing, such as approach tendencies and attentional biases, which may play a role in addictive behavior. The development of such automaticity has generally occurred well before subjects perform tasks designed to detect them. Although it seems plausible that this development involves some form of alcohol‐related conditioning, this process is not usually included in the experimental procedure.Methods:  The development of automaticity involving alcoholic or nonalcoholic stimuli was experimentally manipulated via a conditioning task. Subjects were presented with pairs of stimuli from a set of 4 stimuli: 2 pictures of alcoholic beverages, and 2 pictures of nonalcoholic beverages. One of the alcoholic and 1 of the nonalcoholic beverages was associated with reward, the other stimuli with punishment. Subjects had to learn to select the rewarded stimuli from pairs of 1 rewarded and 1 punished stimulus. The task, thus experimentally established reward versus punishment stimulus–response–outcome associations, for alcoholic and for nonalcoholic stimuli. Subsequently, a cued reversal task was used to test automaticity involving alcoholic versus nonalcoholic, and rewarded versus punished stimuli.Results:  An association was found between heavier drinking and an alcohol‐related conditioning bias: heavier drinkers had more difficulty overcoming a conditioned response when it involved selecting a previously punished nonalcoholic stimulus over a previously rewarded alcoholic stimulus.Conclusions:  The study provided novel information on secondary reinforcement involving alcoholic stimuli: heavier drinkers may more easily develop automaticity related to alcohol‐reward contingencies. This may have implications for interventions and the interpretation of findings concerning alcohol‐related automatic processing.