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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.

BackgroundOne of the most prominent theories of drug addiction is the incentive sensitization model. Individual differences in the tendency to ascribe motivational salience to cues that predict reward, and their ability to promote reward-seeking behaviour have been identified as potentially important in understanding vulnerability to addiction and relapse. However, to date this behaviour has not been assessed in a treatment-seeking clinical population, highlighting a significant gap in the literature pertaining to incentive sensitization and drug addiction.MethodsIndividuals accessing drug and alcohol services with alcohol as primary drug of concern were recruited to participate in an intervention study. At the baseline session, participants completed various self-report measures (including the Alcohol Use Disorders Identification Test; AUDIT) in addition to a visual search task measuring sign-tracking to cues predicting monetary reward. Self-reported abstinence at 3-month follow up was primary outcome measure. All analyses and hypotheses were pre-registered.ResultsAt baseline (49 participants), AUDIT scores correlated with sign-tracking to signals of monetary reward, a relationship that cannot be explained by overall response time in the task or demographic variables. Sign-tracking, gender and craving during the sessions predicted return to use at 3-month follow up (41 participants). ConclusionsOur work demonstrates that involuntary sign-tracking to cues signalling non-drug reward is associated with problematic alcohol use and return to use at 3-month FU, in a treatment-seeking sample. Whether this automatic prioritisation of cues signalling reward is a consequence or vulnerability for problematic drug use remains to be seen.

AbstractAimsFor the first time, to our knowledge, in a clinical sample with alcohol use disorder (AUD), this study compared the effects of two versions of alcohol‐specific inhibition training (Alc‐IT) on drinking outcomes and on experimental parameters assessing two possible working mechanisms: stimulus devaluation and inhibitory enhancement.DesignMulti‐centre, double‐blind, three‐arm clinical RCT with 3‐, 6‐ and 12‐month follow‐up comparing standard Alc‐IT, improved Alc‐IT and an active control condition.SettingThree specialized AUD treatment centres in Switzerland.ParticipantsA total of 242 detoxified, recently abstinent patients with severe AUD (18–60 years; 29.8% female).Intervention and ComparatorBoth interventions [standard Alc‐IT (n = 84) and improved Alc‐IT (n = 79)] and the comparator [unspecific inhibition training (n = 79)] consisted of six sessions of a modified inhibitory task (Go/NoGo task) with alcohol‐related and neutral stimuli. Both versions of Alc‐IT required response inhibition in alcohol‐related trials but differed in Go/NoGo ratios (standard: 50/50; improved: 75/25), with improved Alc‐IT posing higher inhibitory demands. The control condition, an unspecific inhibition training, featured alcohol‐related pictures in Go as well as NoGo trials.MeasurementsThe primary outcome, percentage of days abstinent, was assessed at 3‐month follow‐up with a time‐line follow‐back interview.FindingsThe group receiving improved Alc‐IT showed a significantly higher percentage of days abstinent at 3‐month follow‐up compared with the control group [γcontrol = 74.30; γimproved = 85.78; β = 11.48, 95% confidence interval (CI) = 2.57, 20.40, P = 0.012, adjusted r2 = 0.062], while for standard Alc‐IT no effect significantly different from zero was detected (γstandard = 70.95; β = −3.35, 95% CI = −12.20, 5.50, P = 0.457, adjusted r2 = −0.04).ConclusionsAlcohol‐specific inhibition training with high inhibitory demands increased days abstinent at 3‐month follow‐up in patients with severe alcohol use disorder. Such an improved, inhibitory‐demanding, alcohol‐specific inhibition training outperformed the standard version of alcohol‐specific inhibition training, suggesting an inhibitory working mechanism.

Neuroimaging studies have demonstrated gray matter (GM) volume abnormalities in substance users. While the majority of substance users are polysubstance users, very little is known about the relation between GM volume abnormalities and polysubstance use.In this study we assessed the relation between GM volume, and the use of alcohol, tobacco, cocaine and cannabis as well as the total number of substances used, in a sample of 169 males: 15 non-substance users, 89 moderate drinkers, 27 moderate drinkers who also smoke tobacco, 13 moderate drinkers who also smoke tobacco and use cocaine, 10 heavy drinkers who smoke tobacco and use cocaine and 15 heavy drinkers who smoke tobacco, cannabis and use cocaine.Regression analyses showed that there was a negative relation between the number of substances used and volume of the dorsal medial prefrontal cortex (mPFC) and the ventral mPFC. Without controlling for the use of other substances, the volume of the dorsal mPFC was negatively associated with the use of alcohol, tobacco, and cocaine. After controlling for the use of other substances, a negative relation was found between tobacco and cocaine and volume of the thalami and ventrolateral PFC, respectively.These findings indicate that mPFC alterations may not be substance-specific, but rather related to the number of substances used, whereas, thalamic and ventrolateral PFC pathology is specifically associated with tobacco and cocaine use, respectively. These findings are important, as the differential alterations in GM volume may underlie different cognitive deficits associated with substance use disorders.

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.