Social and problem drinking : relationships with cognition, motivation and impulsivity

Background: A growing body of research suggests that phenomena typically observed in alcohol dependence syndrome (ADS), which are believed to reflect dysfunctional activity within the mesocorticolimbic (MCL) dopamine (DA) system – notably, heightened cue-reactivity (CR) and disturbances of inhibitory control/impulsiveness – are present in non-physically-dependent drinkers. Aims: The present thesis investigated these findings further via three empirical studies. The first developed and gathered preliminary validation data on a new self-report questionnaire measuring ‘recent’ impulsiveness – the Recent Impulsivity Scale (STIS). The second and third examined whether, and to what extent, CR and disturbances of inhibitory control were present in heavy social drinkers (HDs) and problem drinkers (PDs), respectively, compared to controls; and also whether these variables were related to SIS scores. Additionally, Study 3 also examined whether PDs demonstrated disturbed responsivity to non-alcohol-associated reward-related stimuli – another manifestation of dysfunction within MCL DA circuitry – compared to controls. A further aim of Study 3 was to explore whether in social drinkers (SDs) a small ‘priming’ dose of alcohol would increase impulsivity and CR. The possible contribution of familial predisposition to alcohol use disorders (AUDs) was also investigated. Principal findings: • The RIS comprised two factors: Cognitive Impulsivity (CI) and Motor Impulsivity (MI). The final version demonstrated good internal and test-retest reliability, and good construct validity. Across the three studies RIS scores correlated significantly with several – though not all – self-report measures of recent alcohol intake and behavioural indices of CR, non-alcohol-related reward responsiveness, impulsivity and decision-making. • HDs in Study 2 showed elevated electrophysiological (but not subjective) CR – reflected in heightened P3 amplitudes – compared to light drinking controls. • During acute abstinence, the PDs in Study 3 demonstrated evidence of (i) dysfunctional responsiveness to non-alcohol-associated reward-related stimuli and (ii) subjective CR, compared to socially drinking controls. • The PDs of Study 3, but not the HDs in Study 2, demonstrated evidence of heightened impulsiveness, compared to controls. • There was no indication that the respective abnormalities demonstrated by HDs and PDs reflected differential familial predisposition to AUDs. • SDs in Study 3 did not show effects of alcohol priming. Conclusions: There was considerable support for the thesis that cognitive and behavioural characteristics believed to reflect disturbances of brain reward pathways are manifest in non-dependent drinkers rather than being confined to those with alcohol dependence. They may develop as a consequence of cumulative alcohol consumption, though the cross-sectional nature of these studies cannot exclude the possibility that they precede and are possibly risk factors for heavy drinking. In general, the present data are consistent with contemporary neurobiological models of addiction and suggest a continuum along which abnormalities develop in parallel with cumulative alcohol consumption.