These results confirm previous findings in binge drinkers and suggest that in a nondependent alcohol-drinking group, differences can be seen in mood and cognitive performance between those that binge drink and those that do not.

These data suggest that alcohol given acutely impairs executive-type cognitive functions and that binge drinking may be associated with impaired cognitive function in a working memory and a pattern recognition task.

The effects of attentional training show limited generalisation to different alcohol cues and methods of measuring cognitive bias. Experimentally increased attentional bias seems to increase subjective craving, but only among participants who are aware of the experimental contingencies that were in place during attentional training.

These data support ideas derived from the incentive learning theories of drug addiction. Furthermore, these data suggest that history of alcohol exposure may influence the priming effects of an alcohol pre-load on attentional bias.

Studies of alcohol use often depend on self-reported alcohol intake measured by quantity/frequency questionnaires. Previous research has shown that alcohol consumption may be underestimated by this type of retrospective questionnaire. The primary aim of this study was to compare the accuracy of an Alcohol Use Questionnaire (AUQ) with a 4-week diary account. A further aim was to explore patterns of drinking in young social drinkers, with particular attention to binge drinking, which has been suggested as a factor in increasing the risk of alcohol dependency. University students completed the AUQ in the laboratory. They were then asked to keep a record of their alcohol, nicotine and caffeine consumption over a 4-week period (diary). The questionnaire and the diaries were compared on factors of alcohol intake (units per week) and patterns of drinking behaviour (speed of drinking, number of times being drunk and percentage of times getting drunk when drinking). The two measures (AUQ and diary) were highly correlated on alcohol consumption and the other questions relating to drinking behaviour. However, differences were found between the two measures on alcohol intake, speed of drinking (drinks per hour) and number of times being drunk. Alcohol consumption was underestimated by approximately 12% on the questionnaire, and, when the accuracy of estimation of drinking habits was examined, it was found that high drinkers tended to underestimate their drinking behaviour, whereas lower drinkers tended to overestimate. The results suggest that the AUQ can be used with a reasonable degree of confidence, bearing in mind the tendency for high drinkers to underestimate consumption and drinking behaviour. Relationships between 'binge scores', beverage specificity and alcohol consumption support the idea that the criteria for binge drinkers should be based on patterns of drinking rather than alcohol consumption.

The study offers a novel and neuropsychologically informed theoretical framework, as well as a cogent step forward to test transdiagnostic concepts in addiction research, with direct implications for assessment, diagnosis, staging of disorder, and treatment.

No abstract

Binge drinking is an increasingly recognized problem within the UK. We have studied the relationship of binge drinking to cognitive and emotional functioning in young adults, and have found evidence for increased impulsivity, impairments in spatial working memory and impaired emotional learning. Since in human studies it is difficult to understand whether such behavioural changes predate or are a consequence of binge drinking, we have also studied parallel behaviours in a rodent model, in which rats are exposed to intermittent episodes of alcohol consumption and withdrawal. In this model, and in parallel with our findings in human binge drinkers, and alcoholic patients who have undergone multiple episodes of detoxification, we have found evidence for impairments in aversive conditioning as well as increased impulsivity. These behavioural changes are accompanied by facilitated excitatory neurotransmission and reduced plasticity (long-term potentiation (LTP)) in amygdala and hippocampus. The impaired LTP is accompanied by both impaired associative learning and inappropriate generalization of previously learned associations to irrelevant stimuli. We propose that repeated episodes of withdrawal from alcohol induce aberrant neuronal plasticity that results in altered cognitive and emotional competences.