The impact of alcohol consumption on frontal asymmetry and risk-taking

Reinforcement sensitivity theory outlines three systems which guide our decision-making and risk-taking. The behavioral activation system (BAS) increases sensitivity to rewarding stimuli (i.e., approach motivation), while the flight-fright-freeze system (FFFS) increases sensitivity to threatening stimuli (i.e., avoidance motivation) and revised behavioral inhibition system (r-BIS) mediates competition between BAS and FFFS. Alcohol is established to diminish neural indices associated with FFFS and r-BIS; however, whether intoxication also influences neural correlates of BAS is unclear. The current experiment (N = 71) used electroencephalography (EEG) to assess frontal-cortical asymmetry associated with BAS versus r-BIS during the balloon analogue risk task (BART). Participants consumed alcoholic versus non-alcoholic (placebo) drinks. Intoxicated participants exhibited greater risk-taking compared to placebos. Yet, placebos exhibited greater relative left frontal-cortical asymmetry during the first half of BART trials (i.e., associated with approach motivation) followed by a shift toward relative right frontal-cortical asymmetry in the second half of trials (i.e., associated with inhibition). Relative left frontal-cortical asymmetry observed among placebos predicted poorer BART performance. Intoxicated participants did not exhibit these shifts in frontal asymmetry, likely indicating impaired or delayed engagement of inhibitory control. Despite greater risk-taking, intoxicated participants responded more conservatively during the second set of BART trials. However, unlike placebos, these shifts in performance were unrelated to frontal asymmetry, suggesting alternative mechanisms underlying their behavioral adjustments. Findings provide novel insights into neural correlates of approach motivation following actual versus perceived consumption of alcohol, supporting links between frontal-cortical asymmetry and risk-taking, in addition to suggesting unique pathways which promote impulsiveness.