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Introduction: Implicit drinking identity (i.e., cognitive associations between the self and drinking) is a reliable predictor of drinking. However, whether implicit drinking identity might mediate the relationship between other robust predictors of drinking and drinking outcomes is unknown. We hypothesized that implicit drinking would mediate the relationship between drinking motives and alcohol consumption and craving., Method: We assessed drinking motives at Time 1, implicit drinking identity at Time 2 (on average, 11 days later) and self-reported alcohol consumption and craving at Time 3 (on average, 6 days later) in a sample of 194 US undergraduates (54% women) who reported at least one heavy drinking episode (4 drinks for women, 5 for men) in the past month. Participants completed self-report measures of drinking motives, daily alcohol consumption, and current craving., Results: Implicit drinking identity uniquely mediated the relationship between social motives and alcohol consumption. It did not, however, mediate the relationship between motives and craving. Time 2 implicit drinking identity was positively associated with greater alcohol consumption and craving at Time 3, even after controlling for drinking motives. Subsequent analyses indicated significant indirect effects between social, enhancement, and coping motives (but not conformity) and consumption and craving when each motive was evaluated individually., Conclusions: Implicit drinking identity continues to have promise as a predictor of drinking outcomes and as a target for interventions. Future experimental and prospective studies will be critical to establish the circumstances under which implicit drinking identity is strengthened and/or activated and the resulting effects on hazardous drinking., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

The aim of the article was to assess how the perception of alcohol craving, which is one of the symptoms of alcohol dependence, evolved, as well as how it was reflected in the diagnostic classifications. The purpose of this article was also a discussion of the models of the origins of craving, explaining the etiology of this phenomenon and the tools for measuring this concept. The concept of craving, defined as a strong need or compulsion to drink alcohol, functioned for many years, not only in the clinical practice but also as a concept inherently associated with alcohol dependence. However, among experts and researchers, there was no consensus about the etiology of this phenomenon and its development. Some emphasize the emotional - motivational aspect of it, while in the literature also its cognitive - behavioral nature is highlighted. Craving as a symptom has been recognized as a diagnostic criterion of alcohol dependence in the International Statistical Classification of Diseases and Related Health Problems - ICD 10. In the year 2013, it was also indicated as a symptom of disorder resulting from alcohol abuse in the Diagnostic and Statistical Manual of Mental Disorders - DSM 5. It seems to be significant also to discuss the tools used to measure craving, both in clinical trials and therapeutic practice, among them: the Alcohol Specific Role Play Test, Obsessive Compulsive Drinking Scale (OCDS) Lubeck Craving Scale (LCRR) and Alcohol Urge Questionnaire (AUQ).

Background: Inflammation might play a role in the development of several psychiatric diseases. However, the origins of processes that mediate inflammation are unknown. We previously reported increased intestinal permeability, elevated blood lipopolysaccharide levels, and low-grade systemic inflammation associated with psychological symptoms of alcohol dependence in alcohol-dependent subjects. In this study, we tested inflammatory responses of peripheral blood mononuclear cells (PBMCs) to gut-derived bacterial products during detoxification and the relationship to alcohol craving., Methods: In 63 actively drinking noncirrhotic alcohol-dependent subjects, testing was performed at the beginning (day 2) and end (day 18) of alcohol detoxification and compared with testing in 14 healthy subjects. Activation of various intracellular signaling pathways by gut-derived bacterial products was analyzed by quantitative polymerase chain reaction, Western blotting, and DNA binding assays (for transcription factors). Toll-like receptor activation was assessed by cell cultures., Results: In addition to lipopolysaccharides, we showed that peptidoglycans may also cross the gut barrier to reach the systemic circulation. Both activate their respective Toll-like receptors in peripheral blood mononuclear cells. Chronic alcohol consumption inhibited the nuclear factor kappa B proinflammatory cytokine pathway but activated the mitogen-activated protein kinase/activator protein 1 pathway, together with the inflammasome complex. This activity resulted in increased messenger RNA and plasma levels of interleukin (IL)-8, IL-1β, and IL-18. Activated proinflammatory pathways, in particular, IL-8 and IL-1β, were positively correlated with alcohol consumption and alcohol-craving scores. Short-term alcohol withdrawal was associated with the recovery of lipopolysaccharide-dependent receptors but not peptidoglycan-dependent receptors., Conclusions: Lipopolysaccharides and peptidoglycans from the gut microbiota stimulate specific inflammatory pathways in peripheral blood mononuclear cells that are correlated with alcohol craving., (Copyright © 2014 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

A major block to recovery from alcoholism is substantial alcohol craving and the chronic relapsing nature of the illness. This chapter reviews relevant structural and functional neuroimaging studies and discusses neural mechanisms underlying alcohol craving and relapse in the context of influential risk factors (i.e., alcohol, alcohol cue, and stress). Review of neuroimaging studies suggests that neuroadaptations in the cortico-striatal-limbic circuit encompassing the medial prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex, striatum, and amygdala significantly contribute to overwhelming alcohol craving and early relapse after a period of abstinence. The cortico-striatal-limbic circuit plays an important role in the modulation of emotion, reward, and decision making. As functional and structural chronic alcohol-related neuroadaptations are consistently reported in this circuit, it is likely that sensitization of this circuit from continued alcohol abuse may contribute to high alcohol craving and early relapse via impairments in the prefrontal executive function related to emotion regulation and decision making. This vulnerable neurobiologic state may be manifested as compulsive craving and intense urge to resume alcohol drinking in the face of environmental risk factors, including alcohol, alcohol cue, or stressful live events., (© 2014 Elsevier B.V. All rights reserved.)