Bruce D. Bartholow

Automatic and Controlled Processes and the Development of Addictive Behaviors in Adolescents: A Review and a Model

This paper presents a review and a model of the development of addictive behaviors in (human) adolescents, with a focus on alcohol. The model proposes that addictive behaviors develop as the result of an imbalance between two systems: an appetitive, approach-oriented system that becomes sensitized with repeated alcohol use and a regulatory executive system that is not fully developed and that is compromised by exposure to alcohol. Self-regulation critically depends on two factors: ability and motivation to regulate the appetitive response tendency. The motivational aspect is often still weak in heavy drinking adolescents, who typically do not recognize their drinking as problematic. Motivation to regulate use often develops only years later, after the individual has encountered serious alcohol-related problems. Unfortunately, at that point behavioral change becomes harder due to several neurocognitive adaptations that result from heavy drinking. As we document, there is preliminary support for the central elements of the model (appetitive motivation vs. self-regulation), but there is a paucity of research directly addressing these mechanisms in human adolescents. Further, we emphasize that adolescent alcohol use primarily takes place in a social context, and that therefore studies should not solely focus on intra-individual factors predicting substance use and misuse but also on interpersonal social factors. Finally, we discuss implications of the model for interventions.

Personality and substance use disorders : A prospective study

The personality systems of Cloninger (as measured by the Tridimensional Personality Questionnaire [TPQ]) and Eysenck (as measured by the Eysenck Personality Questionnaire [EPQ]) both have been linked to substance use and abuse. The current study examined the predictive utility of both systems for substance use disorder (SUD) diagnoses, both cross-sectionally and prospectively. Participants (N = 489 at baseline) completed the EPQ and TPQ and were assessed via structured diagnostic interview at baseline and 6 years later (N = 457 at follow-up). Both the EPQ and TPQ scales demonstrated bivariate cross-sectional and prospective associations with SUDs. Within each system, those dimensions marking a broad impulsive sensation-seeking or behavioral disinhibition trait were the best predictors prospectively, although the 2 systems were differentially sensitive to specific diagnoses. These relations remained significant even with autoregressivity, other concurrent SUD diagnoses, and multiple personality dimensions statistically controlled.

Correlates and Consequences of Exposure to Video Game Violence: Hostile Personality, Empathy, and Aggressive Behavior

Research has shown that exposure to violent video games causes increases in aggression, but the mechanisms of this effect have remained elusive. Also, potential differences in short-term and long-term exposure are not well understood. An initial correlational study shows that video game violence exposure (VVE) is positively correlated with self-reports of aggressive behavior and that this relation is robust to controlling for multiple aspects of personality. A lab experiment showed that individuals low in VVE behave more aggressively after playing a violent video game than after a nonviolent game but that those high in VVE display relatively high levels of aggression regardless of game content. Mediational analyses show that trait hostility, empathy, and hostile perceptions partially account for the VVE effect on aggression. These findings suggest that repeated exposure to video game violence increases aggressive behavior in part via changes in cognitive and personality factors associated with desensitization.

Does the Gun Pull the Trigger? Automatic Priming Effects of Weapon Pictures and Weapon Names

More than 30 years ago, Berkowitz and LePage (1967) published the first study demonstrating that the mere presence of a weapon increases aggressive behavior. These results have been replicated in several contexts by several research teams. The standard explanation of this weapons effect on aggressive behavior involves priming; identification of a weapon is believed to automatically increase the accessibility of aggression-related thoughts. Two experiments using a word pronunciation task tested this hypothesis. Both experiments consisted of multiple trials in which a prime stimulus (weapon or nonweapon) was followed by a target word (aggressive or nonaggressive) that was to be read as quickly as possible. The prime stimuli were words in Experiment 1 and pictures in Experiment 2. Both experiments showed that the mere identification of a weapon primes aggression-related thoughts. A process model linking weapons as primes to aggressive behavior is discussed briefly.

Short- and Long-Term Effects of Fraternity and Sorority Membership on Heavy Drinking: A Social Norms Perspective

This study sought to determine whether the well-established relation between fraternity/sorority (Greek) membership and heavy alcohol use persists beyond the college years and whether some common third variables might account for the relation between Greek status and heavy drinking. During each of 4 years of college and 1 additional year, young adults (N = 319) completed measures of alcohol use, personality, alcohol expectancies, and environmental influences on drinking. Throughout the college years, Greeks consistently drank more heavily than non-Greeks. Statistically controlling for previous alcohol use did not eliminate this effect. However, Greek status did not predict postcollege heavy drinking levels. Also, perceived peer norms for heavy drinking mediated the relation between Greek affiliation and heavy alcohol use. Results are discussed in terms of situational determinants of heavy alcohol involvement in young adults.

The neural correlates of race

Behavioral analyses are a natural choice for understanding the wide-ranging behavioral consequences of racial stereotyping and prejudice. However, studies using neuroimaging and electrophysiological research have recently considered the neural mechanisms that underlie racial categorization and the activation and application of racial stereotypes and prejudice, revealing exciting new insights. Work that we review here points to the importance of neural structures previously associated with face processing, semantic knowledge activation, evaluation and self-regulatory behavioral control, enabling specification of a neural model of race processing. We show how research on the neural correlates of race can serve to link otherwise disparate lines of evidence on the neural underpinnings of a broad array of social-cognitive phenomena; we also consider the implications for effecting change in race relations.

Emotional foundations of cognitive control

Often seen as the paragon of higher cognition, here we suggest that cognitive control is dependent on emotion. Rather than asking whether control is influenced by emotion, we ask whether control itself can be understood as an emotional process. Reviewing converging evidence from cybernetics, animal research, cognitive neuroscience, and social and personality psychology, we suggest that cognitive control is initiated when goal conflicts evoke phasic changes to emotional primitives that both focus attention on the presence of goal conflicts and energize conflict resolution to support goal-directed behavior. Critically, we propose that emotion is not an inert byproduct of conflict but is instrumental in recruiting control. Appreciating the emotional foundations of control leads to testable predictions that can spur future research.

Stereotype activation and control of race bias: Cognitive control of inhibition and its impairment by alcohol.

Two experiments tested the hypothesis that alcohol increases race-biased responding via impairment of self-regulatory cognitive control. Participants consumed either a placebo or alcohol and then made speeded responses to stereotypic trait words presented after White and Black face primes while behavioral and event-related brain potential (ERP) data were recorded. Alcohol did not affect stereotype activation in either experiment. Experiment 2 showed that alcohol significantly impaired the ability to inhibit race-biased responses but did not reliably influence control of counterstereotypic responses. This disinhibition appears driven by impairment of regulative cognitive control, as indexed by amplitude of the negative slow wave ERP component. These findings suggest that controlling racial bias can be a function of effective implementation of basic self-regulatory processes in addition to the motivational processes identified in other research.

Alcohol effects on performance monitoring and adjustment: affect modulation and impairment of evaluative cognitive control.

Alcohol is known to impair self-regulatory control of behavior, though mechanisms for this effect remain unclear. Here, we tested the hypothesis that alcohols reduction of negative affect (NA) is a key mechanism for such impairment. This hypothesis was tested by measuring the amplitude of the error-related negativity (ERN), a component of the event-related brain potential (ERP) posited to reflect the extent to which behavioral control failures are experienced as distressing, while participants completed a laboratory task requiring self-regulatory control. Alcohol reduced both the ERN and error positivity (Pe) components of the ERP following errors and impaired typical posterror behavioral adjustment. Structural equation modeling indicated that effects of alcohol on both the ERN and posterror adjustment were significantly mediated by reductions in NA. Effects of alcohol on Pe amplitude were unrelated to posterror adjustment, however. These findings indicate a role for affect modulation in understanding alcohols effects on self-regulatory impairment and more generally support theories linking the ERN with a distress-related response to control failures.

Effects of alcohol consumption and alcohol susceptibility on cognition: A psychophysiological examination.

The present study sought to examine acute effects of alcohol on cognitive processing and performance within the context of two prominent theories of alcohols effects; namely, that alcohol restricts the focus of attention (e.g. Steele and Josephs, 1990. Journal of Abnormal Psychology, 97, 196-205) and that alcohol impairs response inhibition (e.g. Fillmore and Vogel-Sprott, 1999. Experimental and Clinical Psychopharmacology, 7, 49-55; Fillmore and Vogel-Sprott, 2000. Journal of Studies on Alcohol, 61, 239-246). Forty-five participants were randomly assigned to receive either a placebo level of alcohol (0.04 g/kg), a moderate dose (0.40 g/kg), or a higher dose (0.80 g/kg). Brain electrical activity (ERPs) and behavioral responses (reaction time and accuracy) were measured while participants performed a modified flanker task, in which a target letter was flanked by response-compatible or response-incompatible letters. Analyses of behavioral data showed that alcohol increased response competition in accuracy but not response times, suggesting that alcohol influences response selection more than attentional processes per se. This finding is in-line with predictions derived from the response inhibition model. ERP latency data provided mixed support for both models. ERP amplitude data showed that the high dose of alcohol primarily influenced a mostly frontal negativity in the ERP, present on both correct and incorrect response trials. Differences in self-reported susceptibility to alcohol were most evident in the amplitude of the P3 component. Findings are discussed in terms of the differential effects of acute dose and susceptibility on information processing.