AbstractRationale: Theoretical accounts of substance use posit that changes in cognitive processes, particularly inhibitory control and attentional bias, are key determinants of consumption behaviour. However, existing research has lacked the nuance to examine (i) the relative contributions of alcohol’s pharmacological and anticipated effects in causing said changes in cognition and (ii) the ability to isolate cognitions from one another and the wider neuropsychopharmacological effects of alcohol. Aims: The current body of research therefore aimed to engage novel methods to more closely examine the extent to which transient changes in inhibitory control, attentional bias and craving govern the maintenance of alcohol consumption. Methods Study 1: In a counterbalanced, within participants design, measures of inhibitory control, attentional bias, craving, alcohol expectancies and ad libitum consumption were taken following alcohol pre-load (.6g/kg), placebo and control. Study 2: In a vertex-controlled within participants design, continuous theta burst (cTBS) transcranial magnetic stimulation (TMS) was deployed to the right-dorsolateral prefrontal cortex (DLPFC) with measures of inhibitory control taken pre- and post-stimulation, followed by a bogus taste task. Study 3: cTBS was utilised to stimulate the right- and left-DLPFC, medial orbital frontal cortex (mOFC) and vertex (control), combined with measures of inhibitory control, attentional bias, attentional inhibition and craving, followed by ad libitum consumption. Study 4: A novel naïve alcohol administration (.4g/kg) method was developed in order to remove anticipatory effects. Naïve, alcohol pre-load, placebo and pure controls alcohol pre-loads were applied in a between participants design. Measures of inhibitory control, attentional bias, craving and ad libitum consumption were taken following beverage administration. Results Study 1: Alcohol pre-load and placebo impaired inhibitory control and elevated craving, but heightened alcohol-related attentional bias was only observed following placebo. Increased ad libitum consumption was only evident following alcohol pre-load, with some tentative evidence to suggest that craving, but not inhibitory control, may play a mediatory role. Study 2: Stimulation to the rDLPFC impaired inhibitory control and was associated with increases in consumption ad libitum. There was, however, no apparent direct association between transient inhibitory control impairments and successive consumption. Study 3: cTBS to the right- and left-DLPFC impaired inhibitory control and cTBS to the mOFC reduced alcohol-related attentional bias. These changes, however, were not associated with one another. Craving increased following lDLPFC stimulation, but this was not associated with a heightening of attentional bias. Finally, elevated ad libitum consumption was observed following lDLPFC cTBS only and was mediated by changes in craving. Study 4: Both pharmacological (alcohol pre-load, naïve alcohol) and anticipation conditions (placebo alcohol) resulted in significant changes in inhibitory control and craving, however, heightened ad libitum consumption was observed only after pharmacological conditions. Furthermore, the association between initial beverage and subsequent consumption was partially mediated by craving, but not inhibitory control impairments.
Overall conclusions: The current body of research is the first to explore and systematically unpick alcohol’s pharmacology and anticipation on one hand and employ neuromodulation techniques to isolate cognitive changes and their respective roles in consumption behaviour on the other. It implicates craving as a potentially central motivational mechanism involved in driving and maintaining drinking episodes. Critically, transient fluctuations in craving appear to elevate consumption. It is also suggested that apparent losses of control are primarily driven by alcohol’s pharmacological, not anticipated effects. It is therefore recommended that rather than focussing on improving inhibitory control, as has been hitherto more common, interventions targeting explicit cognitions such as craving may be beneficial in reducing alcohol-related harms. Original contribution: The current thesis offers two distinct original contributions to knowledge, methodologically and theoretically. First, research within employed a novel alcohol naïve administration protocol to extricate alcohol pharmacology from anticipation. Second, TMS was utilised to isolate neural and cognitive changes from wider effects of alcohol pharmacology, to examine their respective contributions and interactions to drinking patterns. Theoretically moreover, the thesis findings implicate explicit (e.g., craving) rather than implicit (inhibitory control, attentional bias) cognitions as central mechanisms in the maintenance of consumption.
|Date of Award||25 Nov 2020|
|Supervisor||REBECCA MONK (Director of Studies), ADAM QURESHI (Supervisor) & Derek Heim (Supervisor)|
- alcohol consumption
- binge drinking
- inhibitory control
- attentional bias