Negative urgency as a risk factor for hazardous alcohol use: Dual influences of cognitive control and reinforcement processing

Abstract

Negative Urgency (NU) is a prominent risk factor for hazardous alcohol use. While research has helped elucidate how NU relates to neurobiological functioning with respect to alcohol use, no known work has contextualized such functioning within existing neurobiological theories in addiction. Therefore, we elucidated mechanisms contributing to the NU-hazardous alcohol use relationship by combining NU theories with neurobiological dual models of addiction, which posit addiction is related to cognitive control and reinforcement processing. Fifty-five undergraduates self-reported NU and hazardous alcohol use. We recorded EEG while participants performed a reinforced flanker task. We measured cognitive control using N2 activation time-locked to the incongruent flanker stimulus, and we measured reinforcement processing using the feedback-related negativity (FRN) time-locked to better-than-expected negative reinforcement feedback. We modeled hazardous drinking using hierarchical regression, with NU, N2, and FRN plus their interactions as predictors. The regression model significantly predicted hazardous alcohol use, and the three-way interaction (NU × N2 × FRN) significantly improved model fit. In the context of inefficient processing (i.e., larger N2s and FRNs), NU demonstrated a strong relationship with hazardous alcohol use. In the context of efficient processing (i.e., smaller N2s and FRNs), NU was unrelated to hazardous alcohol use. Control analyses ruled out the potential impact of other impulsivity subscales, individual differences in dimensional negative affect or anxiety, and use of substances other than alcohol, and post hoc specificity analyses showed that this effect was driven primarily by heavy drinking, rather than frequency of drinking. This analysis provides preliminary evidence that brain mechanisms of cognitive control and reinforcement processing influence the relationship between NU and hazardous alcohol use, and confirms a specific influence of negative reinforcement processing. Future clinical research could leverage these neurobiological moderators for substance misuse treatment.

Keywords: Alcohol; Cognitive control; Dual model; Event-related potential; Negative urgency; Reinforcement processing.

Figure 1.

Task diagram for the modified reinforcement flanker paradigm. Participants were cued as to whether the current trial was to be positive or negative reinforcement with a white square or a white circle, respectively. Negative reinforcement trials are of primary importance for the current manuscript. Participants then had to respond to a congruent or incongruent flanker arrow stimulus. Only correct trials were analyzed, and participants were shown the correct feedback image on every trial prior to the point feedback being shown. Finally, participants were given some amount of points (on average +0 for negative reinforcement). The crucial task manipulation was that for every trial, the amount of points given deviated slightly from the overall mean expectation, generating prediction errors in better-than-expecteds/worse-than-expected outcomes. ERP values were separately computed for better-than-expected outcomes (+11 to +30 points above expectation) and worse-than-expected outcomes (−30 to −11 points below expectation); outcomes that were roughly as-expected (−10 to +10 points from expectation) were not analyzed.

Figure 2.

Grand-average ERP waveforms derived from the modified reinforcement flanker task. Note that positive values are plotted upward on the y-axis. Left panel indicates the ERP time-locked to the flanker arrow stimulus and separated by stimulus congruency, and the topographic plot illustrates the scalp distribution of the incongruent – congruent difference waveform from 250 to 350 ms post-stimulus. Right panel indicates the ERP time-locked to negative reinforcement feedback presentation and separated into better-than-expected and worse-than-expected outcomes (outcomes that were roughly as expected were not analyzed), and the topographic plot illustrates the scalp distribution of the worse-than-expected – better-than-expected difference. The incongruent N2 was selected as a measure of cognitive control and the better-than-expected FRN was selected as a measure of reinforcement processing. Primary moderation analyses examined the raw condition ERPs as moderators, however, we also ran control analyses using residualized ERP amplitudes (incongruent N2 with congruent N2 regressed out, better-than-expected FRN with worse-than-expected FRN regressed out).

Figure 3.

Model diagram for the proposed moderated-moderation model. We suggest that neural indices of both impaired cognitive control and impaired reinforcement processing should moderate the relationship between individual differences in NU and problematic drinking behaviors. This effect is in line with dual models of addiction, which do not suggest that cognitive control causes reinforcement processing, or that reinforcement processing causes cognitive control (the assumption of causation is necessary for a mediation analysis). Instead, dual models suggest that the influence of cognitive control on eventual actions can be weakened or eliminated entirely by overly inefficient reinforcement processing. The appropriate test, when the relationship between variables changes as a function of another variable, is a test for moderation.

Figure 4.

These moderated moderation results suggest a theoretical interpretation where control over prepotent actions moderates the influence of NU on hazardous alcohol use, but the moderating effect of prepotent cognitive control is itself moderated by reinforcement processing. This result shows that the moderating role of cognitive control is most present when paired with efficient reinforcement processing and is most clearly seen when comparing image “A” on the left to image “C” on the right. Moderation effects were probed at −1 SD, the mean, and +1 SD. Image “A” illustrates at inefficient levels of salience processing (−1 SD), a strong, positive relationship between NU and hazardous alcohol is present regardless of the efficiency for cognitive control. In contrast, image “C” illustrates when efficient levels of salience processing (+1 SD) are paired with efficient levels of cognitive control (+1 SD), NU’s relationship with hazardous alcohol use is almost reversed (and is non-significant). Thus, our analyses revealed that moderating effects of inhibition were most prominent when reinforcement processing was also efficient. Further, our analyses indicated the relationship between NU and AUDIT sum was weakest, and therefore psychiatric outcomes best, when both inhibition and reinforcement processing were efficient.