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Poster #17 - The effects of binge-drinking and depression on cognitive-control processes

Sat, March 23, 9:45 to 11:00am, Baltimore Convention Center, Floor: Level 1, Exhibit Hall B

Integrative Statement

Binge-drinking and depression are highly prevalent in late adolescence and young adulthood, particularly among the college-aged population. There are emerging literatures focused on delineating the neurobiological underpinnings of both binge-drinking and depression during adolescence. Psychophysiological evidence supports the hypothesis that depression interferes with neural systems involved in unconscious emotional processing, as dysregulated emotional processing is a core feature of depression (Bruder et al., 2012; Schupp et al., 2007; Cuthbert et al., 2000). In addition, emerging psychophysiological research suggests that binge-drinking appears to predict impairments that mimic those long observed in relation to chronic alcoholism, including a common finding of attenuated early attentional processes. The research findings on the trajectories from binge-drinking in adolescence to chronic alcoholism are mixed (Petit et al., 2013), however, it is crucial to identify risk and contextual factors among adolescents that contribute to the mechanisms behind pathological alcohol use and depression trajectories in this population.

The aim of the current study was to examine differences in neurocognitive processing of emotional stimuli via the assessment of Event Related Potentials (ERP) measured via electroencephalograph (EEG) recordings in relation to binge-drinking and symptoms of depression in college students. We hypothesized that binge-drinking/depressed participants will exhibit specific processing alterations for sad/angry stimuli, consistent with models of alcohol abuse being reinforced by facilitating reduced attention specifically to negative stimuli. Specifically, we hypothesized that binge-drinking/depressed participants will exhibit enhanced early N2 (F3/Fz/F4) responses and attenuated P3 (P3/Pz/P4) amplitudes in response to sad/angry stimuli relative to depressed-only participants.

Participants (n = 655; 54% female; 52.2% Caucasian) were recruited from undergraduate introductory psychology courses based on self-reported symptoms of depression and alcohol use, and completed questionnaires assessing symptoms of depression and alcohol use, including the CES-D and AUDIT. EEG data was obtained from participants (n = 100; 65% female; 68% Caucasian) during an Emotional Go/No-go task with happy, sad, angry, and calm faces. Repeated measures ANOVAs were conducted to examine the joint effects of depression and binge-drinking on attention to emotional stimuli.

A 4-way (emotion: happy, neutral, sad, angry) repeated measures ANOVA for response bias yielded a significant main effect of emotion in the depressed/nonbinge-drink group (F (3,65) = 9.18, p < .01). Follow up analyses indicated that d-prime scores differed across all emotions, with response bias the highest for angry (M = .270, SE = .09), then sad (M = .154, SE = .11), then happy (M = .066, SE = .11), and then neutral faces (M = .064, SE = .13; Figure 1). In the binge-drinking group, there were no significant differences in response bias across emotions. These results suggest that the attention biases for emotions are different depending upon the co-occurrence of binge-drinking and depression. Further analyses will focus on ERPs. Mean amplitudes of the components will be examined with 2 (Group: Depressed/Nondepressed) X 2 (Group: Binge/Nonbinge-drinkers) X 4 (Valence: Happy/Sad/Angry/Calm) X 2 (Cue type: Go/No-go) repeated measures ANOVAs. This work may ultimately point to specific neurocognitive risk processes that could be targeted in prevention and intervention programs for at-risk adolescents.

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