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RATIONALE: Alcohol administration and cue-reactivity paradigms are frequently used to screen for the initial efficacy of medications for alcohol use disorder (AUD). While medication effects on the primary outcomes for these paradigms are assumed to be qualitatively related, there is a critical lack of quantitative evidence to support this hypothesis. OBJECTIVES: The study aims to test the relationship between medication effect sizes on subjective response to alcohol administration and medication effect sizes for cue-induced craving to cue exposure, using meta-analysis. METHODS: Systematic literature searches were conducted to identify randomized trials, wherein AUD medications were tested using the alcohol administration and/or cue-reactivity paradigms. From these studies, descriptive statistics were collected to compute medication effect sizes on the primary outcomes for each respective paradigm. With medication as the unit of analysis, medication effect sizes in alcohol administration studies were compared with medication effect sizes in cue-reactivity studies using the Williamson-York regression which allows for meta-regression across independent samples. RESULTS: Medication effect sizes on alcohol-induced stimulation and alcohol-induced craving were not significantly associated with medication effect sizes on cue-induced alcohol craving (k stimulation = 10 medications, [Formula: see text] and k craving = 11 medications, [Formula: see text] (SE = 0.237), [Formula: see text]), respectively. Medication effect sizes on alcohol-induced sedation were significantly associated with medication effects on cue-induced craving (k = 10 medications, [Formula: see text] (SE = 0.258), [Formula: see text]), such that medications that increased alcohol-induced sedation were more likely to reduce cue-induced alcohol craving. CONCLUSIONS: With the exception of alcohol-induced sedation, there is little quantitative evidence of medication effects on subjective response domains measured during alcohol administration parallel medication effects on cue-induced alcohol craving. To provide additional context to the current study, future work should examine whether cue-reactivity findings predict clinical trial outcomes.

AimsThe current study examined the association between pain catastrophizing and alcohol cue-elicited brain activation in individuals with alcohol use disorder (AUD).MethodsNon-treatment seeking heavy drinkers with AUD (n = 45; 28 males) completed self-report measures of pain catastrophizing and alcohol use/problems as part of a clinical trial of the neuroimmune modulator ibudilast. Participants were randomized to either placebo (n = 25) or ibudilast (n = 20) and completed an functional magnetic resonance imaging (fMRI) scan to assess neural activation to alcohol cues 1 week into the medication trial. Multiple linear regression examined whether pain catastrophizing predicted cue-induced activation in a priori regions of interest, namely the dorsal and ventral striatum (VS). An exploratory whole-brain analysis was conducted to assess the relationship between pain catastrophizing and neural alcohol cue reactivity.ResultsPain catastrophizing predicted greater cue-induced activation in the dorsal (b = 0.006; P = 0.03) but not VS controlling for medication. Pain catastrophizing was positively associated with neural activation to alcohol cues in regions including the bilateral thalamus, left precuneus and left frontal pole.ConclusionGreater pain catastrophizing is associated with greater cue-induced neural activation in brain regions sub-serving habits and compulsive alcohol use. These findings provide initial support for a neural mechanism by which pain catastrophizing may drive alcohol craving among individuals with AUD.

BackgroundChronic pain and alcohol use disorder (AUD) are often co-occurring conditions. Pain catastrophizing, an emotional component of pain, and pain intensity are related to alcohol use as a coping mechanism; however, how pain interacts with tonic alcohol craving is an understudied area. This study sought to determine the unique and independent effects of pain intensity and pain catastrophizing on alcohol craving in heavy drinkers.MethodNon-treatment seeking heavy drinkers (n = 128) completed self-report measures of pain (both intensity and catastrophizing), depression, alcohol use and problems, and reasons for heavy drinking. A hierarchical regression examined the unique contribution of pain intensity to alcohol craving. Depression, pain catastrophizing, and alcohol use measures were added to the hierarchical model in sequential blocks.ResultsThe final model of the hierarchical regression demonstrated that pain catastrophizing has an independent effect on alcohol craving over and above demographic, pain intensity, depression, and alcohol measures. Exploratory analyses suggest that individuals in the high intensity pain grade have higher levels of depression symptomology, pain catastrophizing, alcohol use and problems, as well as engaging in heavy drinking to "feel normal" compared to the no pain and low intensity pain grades.ConclusionsThese results demonstrate that pain catastrophizing predicts alcohol craving independent of self-reported chronic pain intensity. Individuals with high intensity chronic pain have more severe alcohol use and mood-related symptomology. Upon replication in clinical samples, these findings can inform clinical care for pain management.

Alexithymia is a vulnerability factor for physical and mental illness that can significantly influence the daily function of alcohol-dependent patients. The aim of this study was to examine the indirect effect of obsessive thoughts and compulsive behaviors involving alcohol craving on the relationship between alexithymia, quality of life (QoL) of psychological well-being and health status. Three hundred and eighty-one outpatients (263 males and 118 females) in treatment for alcohol dependence completed self-report measures of alexithymia, alcohol craving, GHQ-28 (QoL-psychological well-being) and SF-36 (QoL-health status). Males scored significantly higher than females on aspects of alexithymia, and females reported significantly higher levels of alcohol craving. Path analysis showed an indirect effect of alcohol craving on the relationship between alexithymia, QoL-psychological well-being and self-reported QoL-health status for males only. The current study provides important new information about impaired self-reported health status and well-being among male alcohol-dependent treatment seekers with alexithymia.

Background: Alexithymia is a personality trait associated with emotion regulation difficulties. Up to 67% of alcohol-dependent patients in treatment have alexithymia. Objectives: The objective of this study was to investigate the direct and indirect effects of alexithymia, negative mood (stress, anxiety, and depression) and alcohol craving on alcohol dependence severity. Methods: Three hundred and fifty-five outpatients (mean age = 38.70, SD = 11.00, 244 males, range 18-71 years) undergoing Cognitive-Behavioral Therapy for alcohol dependence completed the Toronto Alexithymia Scale (TAS-20), Depression Anxiety Stress Scales (DASS-21), Obsessive Compulsive Drinking Scale (OCDS), and Alcohol Use Disorders Identification Test (AUDIT) prior to the first treatment session. Results: Alexithymia had an indirect effect on alcohol dependence severity, via both negative mood and alcohol craving (b = 0.03, seb = 0.008, 95% CI: 0.02-0.05). An indirect effect of negative mood on alcohol dependence via alcohol craving was also observed (b = 0.12, seb = 0.03, 95% CI: 0.07-0.16). Conclusions/importance: Alexithymia worked through negative mood and alcohol craving leading to increased alcohol dependence severity, indicating that craving had an indirect effect on the relationship between alexithymia and alcohol dependence severity. Targeting alcohol craving and negative mood for alcohol-dependent patients with alexithymia seems warranted.

BackgroundAlcoholics report persistent alcohol craving that is heightened by cognitive cues, stressful situations, and abstinence. The role of endogenous cannabinoids in human alcohol craving--though long suspected--remains elusive.Materials and methodsWe employed laboratory exposure to stress, alcohol cue, and neutral relaxed situations through guided imagery procedures to evoke alcohol desire and craving in healthy social drinkers (n = 11) and in treatment-engaged, recently abstinent alcoholic subjects (n = 12) and assessed alcohol craving, heart rate, and changes in circulating endocannabinoid levels. Subjective anxiety was also measured as a manipulation check for the procedures.ResultsIn healthy social drinkers, alcohol cue imagery increased circulating levels of the endocannabinoid anandamide, whereas neutral and stress-related imagery had no such effect. Notably, baseline and response anandamide levels in these subjects were negatively and positively correlated with self-reported alcohol craving scores, respectively. Cue-induced increases in heart rate were also correlated with anandamide responses. By contrast, no imagery-induced anandamide mobilization was observed in alcoholics, whose baseline anandamide levels were markedly reduced compared to healthy drinkers and were uncorrelated to either alcohol craving or heart rate.ConclusionsThe results suggest that plasma anandamide levels provide a marker of the desire for alcohol in social drinkers, which is suppressed in recently abstinent alcoholics.