Alcohol Cue Exposure Research Articles

Effects of Alcohol Cue Reactivity on Subsequent Treatment Outcomes Among Treatment-Seeking Individuals with Alcohol Use Disorder: A Multisite Randomized, Double-Blind, Placebo-Controlled Clinical Trial of Varenicline.

The alcohol cue reactivity paradigm is increasingly used to screen medications for the treatment of alcohol use disorder (AUD) and other substance use disorders. Yet, its prospective association with craving and naturalistic drinking outcomes in clinical trials remains unknown. This study embedded repeated human laboratory assessments of alcohol cue reactivity within the context of a randomized controlled trial to examine the effects of varenicline tartrate (Chantix® ), a partial agonist of α4β2 nicotinic acetylcholine receptors, on alcohol craving among treatment-seeking heavy drinkers with AUD. Our main objectives were to test whether varenicline, as compared to placebo, blunts alcohol cue-elicited craving and test whether alcohol cue reactivity observed in the human laboratory predicts subsequent alcohol craving and use during the remainder of the trial. This double-blind, randomized, 2-site study compared the effects of varenicline (up to 2mg/d) and placebo on responses to in vivo alcohol cue and affective picture cue exposure in the human laboratory. Forty-seven volunteers (18 females, 29 males), ages 23 to 67years (M=43.7, SD=11.5), were recruited from the community via advertisements to participate in a clinical trial designed to study the effects of varenicline on alcohol use. Participants were randomized to either varenicline or placebo for 6weeks. Varenicline did not attenuate cue-induced alcohol craving relative to placebo, but craving captured during the cue reactivity paradigm significantly predicted subsequent alcohol use in real-world settings during the clinical trial. Higher craving predicted heavier alcohol use. Our results are among the first to show alcohol cue-induced craving captured during a human laboratory paradigm predicts drinking outcomes in the context of a clinical trial.

Heart Rate Variability, Cue-Evoked Ventromedial Prefrontal Cortical Response, and Problem Alcohol Use in Adult Drinkers

BackgroundMany studies employed cue exposure paradigms to investigate the neural processes underlying cue-elicited alcohol craving. Cue exposure elicits robust autonomic reactivity. However, whether or how cue-elicited autonomic response relates to the severity of alcohol misuse and the neural bases underlying the potential relationship remain unclear. MethodsWe examined cue-related brain activations in association with heart rate variability, as indexed by the root mean square of the successive differences (RMSSD), during alcohol versus neutral cue blocks in 50 adult alcohol drinkers (24 men). Imaging and heart rate variability data were collected and processed with published routines. Mediation analyses were conducted to examine the interrelationship between regional activities, cue-elicited changes in RMSSD, and the severity of problem alcohol use, as assessed with the Alcohol Use Disorders Identification Test (AUDIT). ResultsThe results showed higher RMSSD during alcohol than during neutral cue exposures, with alcohol (vs. neutral) cue-evoked RMSSD positively correlated with AUDIT score. Further, alcohol (vs. neutral) cue-elicited activity in the ventromedial prefrontal cortex was negatively correlated both with increases in RMSSD and with the AUDIT score. Mediation analyses suggested that the RMSSD mediated the relationship between ventromedial prefrontal cortex cue activity and the AUDIT score. ConclusionsThese findings substantiate the neural correlates of the presumably parasympathetic response during alcohol cue exposure and the interrelationship among ventromedial prefrontal cortex activity, autonomic response, and problem alcohol use.

The effect of cognitive distraction on the processing of alcohol cues

ABSTRACTA range of studies have demonstrated that regular drinkers respond to alcohol-related stimuli with increased self-reported craving for alcohol (cue-reactivity). Considerable individual differences have been found in terms of the magnitude of the craving response. However, less work has been conducted to assess the role of cognitive factors in influencing alcohol cue-elicited craving. This study assessed the effect of a cognitive distraction task and individual variability in trait-mindfulness on responses to alcohol cues using a standard cue reactivity paradigm. Sixty-nine regular social drinkers were randomly allocated to one of the two experimental conditions – no instructions vs cognitive distraction (asked to focus on milk) – and were presented with alcohol. Results indicated that positive craving (i.e., desire to drink for positive reinforcement) increased from neutral to alcohol-cue exposure, and that those in the cognitive distraction condition reported significantly lower positive urge to drink after alcohol-cue exposure. No relationship between alcohol craving and mindfulness was found. Implications of the findings are discussed with a particular focus on the role of cognitive distraction in cue-reactivity and the potential utility of using a cognitive distraction technique to reduce alcohol craving.

Impulsivity moderates the effect of social anxiety on in-lab alcohol craving

Social anxiety (SA) is thought to relate to alcohol misuse. However, current evidence is inconsistent – especially in young adulthood. Recent non-experimental data show that trait impulsivity moderates the effect of SA on alcohol misuse. Specifically, this work suggests that concurrently elevated impulsivity may draw attention to the immediate, anxiolytic effects of drinking – thus promoting alcohol misuse among those high in SA. Otherwise, without elevated impulsivity, a socially anxious person may not drink due to focusing on alcohol's possible negative outcomes (e.g., embarrassing behaviours). The next step in this research is to examine if impulsivity impacts in-the-moment subjective craving among socially anxious individuals. This was the goal of the present experiment. After baseline measures, undergraduate participants (N = 110) completed the Trier Social Stress Test followed by an alcohol (versus neutral) cue exposure. Subjective craving ratings were collected at both baseline and post-cue exposure. Moderation analyses revealed that socially anxious individuals endorsed strong cravings following an alcohol (but not a neutral) cue exposure, but only if they also had elevated impulsivity. In-lab craving was positively correlated with retrospective reports of alcohol misuse. Our findings demonstrate that impulsivity contributes to SA-related risk for alcohol misuse.

The effect of alcohol cue exposure and acute intoxication on inhibitory control processes and ad libitum alcohol consumption

RationaleAlcohol intoxication and alcohol cue exposure impair ‘reactive’ inhibitory control and increase motivation to drink. However, inhibitory control is a multi-component process that also comprises signal detection and proactive control. It is unknown whether intoxication and cue exposure selectively influence these subprocesses in heavy drinkers.ObjectivesIn two pre-registered studies, we investigated whether exposure to alcohol-related cues (study 1) and alcohol priming (study 2) impair each of these subprocesses of inhibitory control and increase motivation to drink.MethodsIn study 1, 64 heavy drinkers completed a modified stop-signal task in an alcohol context (with embedded alcohol cues) and a neutral context (with embedded neutral cues) followed by a subjective measure of craving and a bogus taste test to measure ad libitum alcohol consumption. In study 2, 36 heavy drinkers consumed an alcoholic beverage (0.6 g/kg body weight), an alcohol-placebo beverage, and water on a within-subjects basis, followed by the modified stop-signal task and a bogus taste test.ResultsIn study 1, alcohol cue exposure did not impair inhibitory control subprocesses. Reactive control was unexpectedly better following alcohol cue exposure (compared to neutral cue exposure). However, craving and ad libitum consumption increased as expected. In study 2, reactive control was significantly impaired following the alcohol and control primes, relative to the placebo, but there was no effect on proactive slowing or signal detection. As expected, intoxication increased motivation to drink and ad libitum consumption (compared to placebo and control).ConclusionsAlcohol intoxication and cue exposure increase motivation to drink in the absence of impairments in subcomponents of inhibitory control.

Elucidating the Effect of a Brief Drinking Intervention Using Neuroimaging: A Preliminary Study.

Brief interventions have empirical support for acutely reducing alcohol use among non-treatment-seeking heavy drinkers. Neuroimaging techniques allow for the examination of the neurobiological effect of behavioral interventions, probing brain systems putatively involved in clinical response to treatment. Few studies have prospectively evaluated whether psychosocial interventions attenuate neural cue reactivity that in turn reduces drinking in the same population. This study aimed to examine the effect of a brief intervention on drinking outcomes, neural alcohol cue reactivity, and the ability of neural alcohol cue reactivity to prospectively predict drinking outcomes. Non-treatment-seeking heavy drinking participants were randomized to receive a brief interview intervention (n=22) or an attention-matched control (n=24). Immediately following the intervention or control, participants underwent a functional magnetic resonance imaging scan comprised of the alcohol taste cues paradigm. Four weeks after the intervention (or control), participants completed a follow-up visit to report on their past-month drinking. Baseline and follow-up percent heavy drinking days (PHDD) were calculated for each participant. There was no significant effect of the brief intervention on PHDD at follow-up or on modulating neural activation to alcohol relative to water taste cues. There was a significant association between neural response to alcohol taste cues and PHDD across groups (Z>2.3, p<0.05), such that individuals who had greater neural reactivity to alcohol taste cues in the precuneus and prefrontal cortex (PFC) had fewer PHDD at follow-up. This study did not find an effect of the brief intervention on alcohol use in this sample, and the intervention was not associated with differential neural alcohol cue reactivity. Nevertheless, greater activation of the precuneus and PFC during alcohol cue exposure predicted less alcohol use prospectively suggesting that these neural substrates subserve the effects of alcohol cues on drinking behavior.

Effects of exposure to alcohol‐related cues on racial discrimination

AbstractPrior research has shown that exposure to alcohol‐related images exacerbates expression of implicit racial biases, and that brief exposure to alcohol‐related words increases aggressive responses. However, the potential for alcohol cue exposure to elicit differential aggression against a Black (outgroup) relative to a White (ingroup) target—that is, racial discrimination—has never been investigated. Here, we found that White participants (N = 92) exposed to alcohol‐related words made harsher judgments of a Black experimenter who had frustrated them than participants who were exposed to nonalcohol words. These findings suggest that exposure to alcohol cues increases discriminatory behaviors toward Blacks.

P.6.b.012 - A high working memory load preceding alcohol cue exposure, reduces the desire for alcohol in non-treatment seeking problem drinkers

This chapter sets the tone for the purpose of the book. It begins by creating an awareness of the importance of an initial piping design set-up and moves to introducing in summary the topics that are covered in more detail in the following chapters. Summarization begins with a review of the common aspects of piping design set-up known to all piping designers; these being standards, specifications, and procedures. The chapter moves to discussing the often overlooked project management documentation, such as the Design Basis Memorandum and Project Execution Plan, of which the piping lead must inform themselves due to there being information contained in this documentation that can impact set-up decisions. The chapter is concluded by emphasizing that the piping lead is accountable for the piping set-up on the project.

Drinking water to reduce alcohol craving? A randomized controlled study on the impact of ghrelin in mediating the effects of forced water intake in alcohol addiction

BackgroundRecent data suggest that ghrelin is involved in the pathophysiology of alcohol use disorders, affecting alcohol self-administration and craving. Gastric ghrelin secretion is reduced by stomach distension. We now tested the hypothesis whether the clinically well-known effects of high-volume water intake on craving reduction in alcoholism is mediated by acute changes in ghrelin secretion. MethodsIn this randomized human laboratory study, we included 23 alcohol-dependent male inpatient subjects who underwent alcohol cue exposure. Participants of the intervention group drank 1000ml of mineral water within 10min directly thereafter, compared to the participants of the control group who did not. Craving and plasma concentrations of acetylated ghrelin were measured ten times during the 120min following the alcohol cue exposure session. ResultsIn the intervention group, a significant decrease in acetylated ghrelin in plasma compared to the control group was observed. This decrease was correlated to a reduction in patients’ subjective level of craving. In the control group, no decrease of acetylated ghrelin in plasma and no association between alcohol craving and changes in plasma concentrations of acetylated ghrelin were observed. ConclusionsOur results present new evidence that the modulation in the ghrelin system by oral water intake mediates the effects of volume intake with craving reduction in alcohol use disorders. Hence, in addition to pharmacological interventions with ghrelin antagonists, the reduction of physiological ghrelin secretion might be a target for future interventions in the treatment of alcohol craving.

Elevated alcohol consumption following alcohol cue exposure is partially mediated by reduced inhibitory control and increased craving

RationaleExposure to alcohol-related cues leads to increased alcohol consumption, and this may be partially attributable to momentarily impaired impulse control.ObjectivesWe investigated if exposure to alcohol cues would impair inhibitory control and if the extent of this impairment would partially mediate the effect of alcohol cues on subsequent voluntary alcohol consumption.MethodsWe recruited 81 heavy drinkers (50 female) who completed baseline measures of inhibitory control (stop-signal task) and subjective craving before random allocation to an alcohol cue exposure or control group. The alcohol cue exposure group then completed a second stop-signal task (with embedded alcohol cues) with concurrent exposure to olfactory alcohol cues, in an alcohol context. The control group completed a second stop-signal task (with embedded water cues), accompanied by exposure to water cues, in a neutral context. Then, subjective craving and ad libitum alcohol consumption were measured in all participants.ResultsInhibitory control worsened (compared to baseline) to a greater extent in the alcohol cue exposure group compared to the control group. Craving and ad libitum alcohol consumption were elevated in the alcohol cue exposure group compared to the control group, although the group difference in alcohol consumption fell short of statistical significance. In support of our hypotheses, multiple mediation analyses demonstrated that elevated ad libitum alcohol consumption following alcohol cue exposure was partially mediated by both impaired inhibitory control and increased craving.ConclusionsThese findings suggest that state fluctuations in inhibitory control are a potential mechanism through which alcohol cues increase drinking behaviour.

Effects of varenicline on alcohol cue reactivity in heavy drinkers.

Clinical trials and human laboratory studies have established that varenicline can reduce rates of alcohol use among heavy drinkers. Less is known about the mechanisms by which varenicline has this effect on drinking behavior. Reactivity to alcohol cues is often cited as the primary cause of relapse among those being treated for alcohol use disorder, and several front-line treatments for alcohol use disorder work, at least in part, by minimizing cue-induced alcohol craving. The current double-blind, placebo-controlled human laboratory study tested the effects of varenicline on alcohol cue reactivity in a group of heavy-drinking adult smokers and nonsmokers. As part of a larger series of sequential human laboratory experiments testing the effects of varenicline on drinking outcomes, participants were assigned (between-participant) to receive either active varenicline (2mg/day) or placebo. Following a titration period, participants (n=77) attended a laboratory session during which they were exposed to alcohol and neutral cues using a standard cue reactivity paradigm. Alcohol cue exposure increased craving for alcohol in both medication groups. However, participants receiving varenicline showed a smaller increase in alcohol craving compared to participants receiving placebo. The medication effect did not differ between smokers and nonsmokers. Among smokers, alcohol cue exposure also increased tobacco craving. Varenicline did not attenuate this effect. Results support the use of varenicline for reducing alcohol use in heavy drinkers and identify a potential mechanism by which varenicline reduces drinking. Varenicline continues to show promise as a pharmacological treatment for alcohol use disorder.

Changes in the Relative Balance of Approach and Avoidance Inclinations to Use Alcohol Following Cue Exposure Vary in Low and High Risk Drinkers.

According to the ambivalence model of craving, alcohol craving involves the dynamic interplay of separate approach and avoidance inclinations. Cue-elicited increases in approach inclinations are posited to be more likely to result in alcohol consumption and risky drinking behaviors only if unimpeded by restraint inclinations. Current study aims were (1) to test if changes in the net balance between approach and avoidance inclinations following alcohol cue exposure differentiate between low and high risk drinkers, and (2) if this balance is associated with alcohol consumption on a subsequent taste test. In two experiments (N = 60; N = 79), low and high risk social drinkers were exposed to alcohol cues, and pre- and post- approach and avoidance inclinations measured. An ad libitum alcohol consumption paradigm and a non-alcohol exposure condition were also included in Study 2. Cue-elicited craving was characterized by a predominant approach inclination only in the high risk drinkers. Conversely, approach inclinations were adaptively balanced by equally strong avoidance inclinations when cue-elicited craving was induced in low risk drinkers. For these low risk drinkers with the balanced craving profile, neither approach or avoidance inclinations predicted subsequent alcohol consumption levels during the taste test. Conversely, for high risk drinkers, where the approach inclination predominated, each inclination synergistically predicted subsequent drinking levels during the taste test. In conclusion, results support the importance of assessing both approach and avoidance inclinations, and their relative balance following alcohol cue exposure. Specifically, this more comprehensive assessment reveals changes in craving profiles that are not apparent from examining changes in approach inclinations alone, and it is this shift in the net balance that distinguishes high from low risk drinkers.

Hope, coping skills, and the prefrontal cortex in alcohol use disorder recovery

ABSTRACTBackground: Alcohol use disorders adversely affect individual and societal health. These disorders are a chronic brain disease, and protective factors against relapse should be studied. Prefrontal cortex (PFC) dysfunction is evident in alcohol use disorders, and research that explores recovery of the PFC in alcohol use disorders is needed, specifically in regard to how psychological and behavioral factors can augment medicalized treatments and protect against relapse. For example, hope or a belief that recovery is possible is an important cognitive construct—thought to precede behavioral action—that has been associated with relapse. Objectives: In this study, associations between healthy coping skills and hope (psychological/behavioral factors) and PFC regional activation in response to alcohol cue exposure were examined. It was also examined whether such associations were unique to alcohol cues. Methods: Forty-two participants, 32 males and nine females in recovery from an alcohol use disorder (AUD), were administered a subjective hope and coping in recovery measure. They also viewed alcohol, positive, negative, and neutral cues during functional near-infrared spectroscopy (fNIR) PFC assessment. Results: Levels of healthy coping skills positively correlated with activation in the right dorsomedial prefrontal cortex (DMPFC) in response to alcohol cues. This finding was unique to alcohol cues. Conclusion: The association between coping skills and activation of the right DMPFC in response to alcohol cues may reflect greater action restraint and top-down PFC control processing that may protect against relapse.

Attentional bias to alcohol stimuli predicts elevated cue-induced craving in young adult social drinkers

Considerable evidence has identified biased cognitive processing of alcohol-related stimuli as an important factor in the maintenance of alcohol-seeking and relapse among individuals suffering from alcohol use-disorders (AUDs). In addition, a large body of research has demonstrated that exposure to alcohol cues can elicit powerful alcohol cravings. Little is known, however, about the possible relationship between attentional bias and cue-induced cravings, and even less is known about these processes in social drinkers without a personal history of AUDs. The goal of this study was to examine the possibility that attentional biases toward alcohol-related stimuli would predict elevated cue-induced alcohol craving in this population. Young adult social drinkers (N=30, Mean age=22.8±1.9, 61% female) recruited from an urban university population completed a visual dot probe task in which they were presented with alcohol and neutral stimulus pictures that were immediately followed by a visual probe replacing one of the pictures. Attentional bias was measured by calculating reaction times to probes that replaced alcohol stimuli vs. neutral stimuli. Participants then completed a classic alcohol cue-exposure task and reported cravings immediately before and after alcohol and neutral cue-exposures. Not surprisingly, exposure to alcohol cues elicited significant cravings. Consistent with the study hypothesis, larger attentional biases toward alcohol stimuli predicted higher levels of alcohol craving. Findings demonstrate that heightened attention to alcohol stimuli can significantly impact motivation to consume in healthy young adults, and suggest a possible pathway linking cognitive processes early in the drinking trajectory to the later development of AUDs.

Development of the Neuroimmune Modulator Ibudilast for the Treatment of Alcoholism: A Randomized, Placebo-Controlled, Human Laboratory Trial.

Current directions in medication development for alcohol use disorder (AUD) emphasize the need to identify novel molecular targets and efficiently screen new compounds aimed at those targets. Ibudilast (IBUD) is a neuroimmune modulator that inhibits phosphodiesterase-4 and -10 and macrophage migration inhibitory factor and was recently found to reduce alcohol intake in rats by ∼50%. To advance medication development for AUD, the present study consists of a randomized, crossover, double-blind, placebo-controlled laboratory study of IBUD in nontreatment-seeking individuals with current (ie, past month) mild-to-severe AUD. This study tested the safety, tolerability, and initial human laboratory efficacy of IBUD (50 mg b.i.d.) on primary measures of subjective response to alcohol as well as secondary measures of cue- and stress-induced changes in craving and mood. Participants (N=24) completed two separate 7-day intensive outpatient protocols that included daily visits for medication administration and testing. Upon reaching a stable target dose of IBUD (or matched placebo), participants completed a stress-exposure session (day 5; PM), an alcohol cue-exposure session (day 6; AM), and an i.v. alcohol administration session (day 6; PM). Participants stayed overnight after the alcohol administration, and discharge occurred on day 7 of the protocol. Medication conditions were separated by a washout period that was ⩾7 days. IBUD was well tolerated; however, there were no medication effects on primary measures of subjective response to alcohol. IBUD was associated with mood improvements on the secondary measures of stress exposure and alcohol cue exposure, as well as reductions in tonic levels of craving. Exploratory analyses revealed that among individuals with higher depressive symptomatology, IBUD attenuated the stimulant and mood-altering effects of alcohol as compared with placebo. Together, these findings extend preclinical demonstrations of the potential utility of IBUD for the treatment of AUD and suggest that depressive symptomatology should be considered as a potential moderator of efficacy for pharmacotherapies with neuroimmune effects, such as IBUD.

Alcohol-cue exposure decreases response inhibition towards alcohol-related stimuli in detoxified alcohol-dependent patients

The induction of alcohol craving and the cognitive processing of alcohol-related stimuli in alcohol-dependent patients have been reported to compete with inhibitory control and contribute to alcohol relapse. The aim of the present study is to investigate whether the induction of a craving state, using an alcohol cue exposure paradigm, influences response inhibition towards both neutral stimuli and alcohol-related stimuli in alcohol-dependent patients. Thirty-one detoxified alcohol-dependent patients were exposed to either their preferred alcoholic beverage or to a glass of water. They then performed a modified stop signal task, which used alcohol-related words, neutral words and non-words, and a lexical decision as the Go response. The alcohol-cue exposure group reported significantly higher alcohol craving and showed higher percentages of commission errors towards alcohol-related words than the control group. All participants, but especially those of the alcohol-cue exposure group, showed also shorter reaction times when alcohol words were used as targets in go trials. The induction of alcohol craving in detoxified alcohol-dependent patients increases the motivational salience value of alcohol stimuli, leading them to automatically approach alcohol-related cues and therefore impairing response inhibition towards those stimuli.

The CRF1 Antagonist Verucerfont in Anxious Alcohol-Dependent Women: Translation of Neuroendocrine, But not of Anti-Craving Effects.

Blockade of corticotropin-releasing factor receptor 1 (CRF1) suppresses stress-induced alcohol seeking in rodents, but clinical translation remains. Here, we first showed that the CRF1 antagonist verucerfont potently blocks hypothalamic-pituitary adrenal (HPA) axis activation in adrenalectomized rats. We then evaluated verucerfont for its ability to block HPA axis activation and reduce stress-induced alcohol craving in alcohol-dependent patients. Anxious, alcohol-dependent women (age 21-65 years, n=39) were admitted to the NIH Clinical Center and completed withdrawal treatment before enrollment if needed. One-week single-blind placebo was followed by randomized double-blind verucerfont (350 mg per day) or placebo for 3 weeks. Verucerfont effects on the HPA axis were evaluated using the dexamethasone-CRF test. Craving was evaluated using two established protocols, one that combines a social stressor with physical alcohol cue exposure, and one that uses guided imagery to present personalized stress, alcohol, or neutral stimuli. An fMRI session examined brain responses to negative affective stimuli and alcohol cues. In contrast to our recent observations with another CRF1 antagonist, pexacerfont, verucerfont potently blocked the HPA axis response to the dexamethasone-CRF test, but left alcohol craving unaffected. Right amygdala responses to negative affective stimuli were significantly attenuated by verucerfont, but responses to alcohol-associated stimuli were increased in some brain regions, including left insula. Discontinuation rates were significantly higher in the verucerfont group. Our findings provide the first translational evidence that CRF1 antagonists with slow receptor dissociation kinetics may have increased efficacy to dampen HPA axis responses. The findings do not support a clinical efficacy of CRF1 blockade in stress-induced alcohol craving and relapse.

Cue reactivity and its relation to craving and relapse in alcohol dependence: a combined laboratory and field study.

The present study investigated the nature of physiological cue reactivity and craving in response to alcohol cues among alcohol-dependent patients (N = 80) who were enrolled in detoxification treatment. Further, the predictive value with regard to future drinking of both the magnitude of the physiological and craving response to alcohol cues while in treatment and the degree of alcohol-cue exposure in patients’ natural environment was assessed. Physiological reactivity and craving in response to experimental exposure to alcohol and soft drink advertisements were measured during detoxification treatment using heart rate variability and subjective rating of craving. Following discharge, patients monitored exposure to alcohol advertisements for five consecutive weeks with a diary and were followed up with an assessment of relapse at 5 weeks and 3 months post-discharge. The results indicated that the presence of alcohol cues such as the portrayal of the drug and drinking behaviour induced physiological cue reactivity and craving. Additionally, cue reactivity and craving were positively correlated, and cue reactivity was larger for patients with shorter histories of alcohol dependence. Further, patients reported a substantial daily exposure to alcohol cues. The magnitude of cue reactivity and the craving response to alcohol cues at baseline and degree of exposure to alcohol cues in patients’ natural environment did not predict relapse. It is concluded that the presence of alcohol cues such as portrayal of alcoholic beverages and drinking behaviour induces cue reactivity and craving in alcohol dependence through a conditioned appetitive response.

Alcohol-cue exposure effects on craving and attentional bias in underage college-student drinkers.

The effect of alcohol-cue exposure on eliciting craving has been well documented, and numerous theoretical models assert that craving is a clinically significant construct central to the motivation and maintenance of alcohol-seeking behavior. Furthermore, some theories propose a relationship between craving and attention, such that cue-induced increases in craving bias attention toward alcohol cues, which, in turn, perpetuates craving. This study examined the extent to which alcohol cues induce craving and bias attention toward alcohol cues among underage college-student drinkers. We designed within-subject cue-reactivity and visual-probe tasks to assess in vivo alcohol-cue exposure effects on craving and attentional bias on 39 undergraduate college drinkers (ages 18-20). Participants expressed greater subjective craving to drink alcohol following in vivo cue exposure to a commonly consumed beer compared with water exposure. Furthermore, following alcohol-cue exposure, participants exhibited greater attentional biases toward alcohol cues as measured by a visual-probe task. In addition to the cue-exposure effects on craving and attentional bias, within-subject differences in craving across sessions marginally predicted within-subject differences in attentional bias. Implications for both theory and practice are discussed. (PsycINFO Database Record

Brief and extended alcohol-cue-exposure effects on craving and attentional bias.

Past research has shown that underage college-student drinkers (UCSDs) report increased subjective craving and exhibit stronger attentional biases to alcohol following alcohol-cue exposure. To date, less research has examined whether momentary decreases in alcohol craving are associated with reductions in attentional bias. One experimental manipulation that has been used to produce within-session decreases in alcohol craving is to extend the duration of laboratory-based alcohol-cue exposure protocols. The aim of this study was to examine the effects of both brief and extended alcohol-cue exposure on subjective craving and attentional bias among UCSDs. Eighty participants were randomized either to a group that received a short, in vivo, alcohol-cue-exposure period (short-exposure group [SE], 2 3-min blocks) or to a group that received a long-exposure period (long-exposure group [LE], 6 3-min blocks). Both groups completed a visual probe task before and after cue exposure to assess changes in attentional bias. Analyses revealed no group differences in mean craving or mean attentional bias before or after cue exposure. Further, exploratory analyses revealed no sex differences in our measures of craving or attentional bias. For Group LE, but not Group SE, within-session changes in craving positively predicted within-session changes in attentional bias. However, further analyses revealed that this relationship was significant only for women in the LE group. Implications for treatments that aim to reduce craving and/or attentional bias are discussed.