Alcohol最新文献

{"title":"Alcohol use disorder-associated pain: clinical and preclinical evidence","authors":"Yuyang Dong,&nbsp;Matthew W. Buczynski,&nbsp;Ann M. Gregus","doi":"10.1016/j.alcohol.2025.08.005","DOIUrl":"10.1016/j.alcohol.2025.08.005","url":null,"abstract":"<div><div>Alcohol Use Disorder (AUD) affects millions of people globally and is characterized by cycles of intoxication, withdrawal, and relapse. Convergent clinical and preclinical evidence strongly support the conclusion that AUD precipitates chronic pain marked by mechanical and thermal hypersensitivity, yet currently available FDA-approved therapeutics do not effectively manage AUD-associated pain. This review synthesizes clinical and preclinical evidence on AUD-associated pain, highlighting known phenomena of allodynia and hyperalgesia as well as small and/or large fiber neuropathy in patient subpopulations along with preclinical acute and chronic alcohol exposure paradigm-specific nociceptive phenotypes in rodents. Herein, we provide detailed descriptions and interpretations of outcome measures for different sensory modalities typically utilized in clinical and/or preclinical studies of nociception. We examine how these endpoints vary in rodent models according to the type of alcohol exposure paradigm with regard to route of administration, chronicity, and contingency (forced, voluntary, or combined). Finally, we summarize the prominent molecular mechanisms that have been proposed to mediate alcohol withdrawal-induced pain-like behaviors. While major advances have been made in treatment of AUD, critical gaps in understanding of human pain phenotypes due to lack of quantitative endpoints in clinical trials impede further advancement in refining preclinical models to recapitulate these features. Patient phenotype-driven preclinical models will increase cross-species translational potential for interrogating mechanistic underpinnings and thereby inform future drug discovery campaigns for treatment of AUD-associated pain.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"129 ","pages":"Pages 14-40"},"PeriodicalIF":2.9,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144989833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Liver transplantation for end-stage alcoholic liver disease: a single-center experience from mainland China” [Alcohol 44 (2010) 217–221]","authors":"Gui-hua Chen,&nbsp;Yang Yang,&nbsp;Min-qiang Lu,&nbsp;Chang-jie Cai,&nbsp;Qi Zhang,&nbsp;Ying-cai Zhang,&nbsp;Chi Xu,&nbsp;Hua Li,&nbsp;Gen-shu Wang,&nbsp;Shu-hong Yi,&nbsp;Jian Zhang,&nbsp;Jun-feng Zhang,&nbsp;Hui-min Yi","doi":"10.1016/j.alcohol.2025.08.001","DOIUrl":"10.1016/j.alcohol.2025.08.001","url":null,"abstract":"","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"128 ","pages":"Page 51"},"PeriodicalIF":2.9,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144912364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A conceptual framework for the intersection of hyperalgesia and hyperkatifeia in alcohol addiction","authors":"George F. Koob ,&nbsp;Leandro F. Vendruscolo","doi":"10.1016/j.alcohol.2025.08.004","DOIUrl":"10.1016/j.alcohol.2025.08.004","url":null,"abstract":"<div><div>Alcohol use disorder is a chronically relapsing disorder that is characterized by compulsive drug seeking and is hypothesized to result from multiple sources of motivational dysregulation in a three-stage cycle of addiction (incentive salience/pathological habits, withdrawal/negative affect, and preoccupation/anticipation). One major source of motivation in the withdrawal/negative affect stage is the physical pain and emotional pain of withdrawal and protracted withdrawal that drive pronounced drug-seeking behavior via the process of negative reinforcement. The construct of negative reinforcement is defined as alcohol taking to alleviate both physical pain and emotional pain (hyperkatifeia) that are created by alcohol abstinence following excessive alcohol consumption. Hyperkatifeia (derived from the Greek “katifeia” for dejection or negative emotional state) is defined as an increase in intensity of the constellation of negative emotional or motivational signs and symptoms of withdrawal from drugs of addiction. In humans and animal models, the repeated misuse of alcohol results in hyperalgesia and hyperkatifeia and is reflected by elevations of reward thresholds, lower pain thresholds, and anxiety- and dysphoric-like responses during alcohol withdrawal. Such symptoms are hypothesized to derive from molecular and neurocircuitry neuroadaptations within the reward system and brain stress systems (e.g., corticotropin-releasing factor, dynorphin, norepinephrine, hypocretin, vasopressin, glucocorticoids, and neuroimmune factors) and brain anti-stress systems (e.g., neuropeptide Y, endocannabinoids, and oxytocin) in the extended amygdala. Thus, our hypothesis is that alcohol withdrawal-induced hyperalgesia and hyperkatifeia persist into protracted withdrawal and contribute to the development and persistence of compulsive alcohol seeking. A conceptual framework for the intersection of physical and emotional pain in addiction is elaborated in the Catastrophizing, Anxiety, Negative Urgency, and Expectancy (CANUE) model, and a significant overlap of brain circuits that mediate emotional pain and physical pain involves the extended amygdala. The intersection of emotional and physical pain reinforces even more dramatically the role of negative reinforcement in alcohol addiction and fits a framework of allostasis (defined as stability with change) where other allostatic loads (defined as the cost of breaks with homeostasis on the body), such as genetics/epigenetics, childhood trauma, and other stressors, exacerbate hyperalgesia/hyperkatifeia in driving alcohol use disorder. The focus on treating hyperalgesia/hyperkatifeia that is associated with acute and protracted withdrawal opens new and exciting avenues for understanding the etiology of alcohol use disorder.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"129 ","pages":"Pages 1-13"},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144932462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing orbitofrontal cortex volume as a predictor of subjective response to alcohol during early adolescence","authors":"L.S. Aguilar,&nbsp;A.L. Wallace,&nbsp;K.E. Courtney,&nbsp;N.E. Wade","doi":"10.1016/j.alcohol.2025.08.002","DOIUrl":"10.1016/j.alcohol.2025.08.002","url":null,"abstract":"<div><div>Adolescence marks a critical window wherein individual differences in brain structure may influence the emergence of alcohol use behaviors. The orbitofrontal cortex (OFC), a region involved in reward processing and behavioral regulation, may play a key role in shaping early responses to alcohol. This study examined whether smaller OFC volume at ages 9–10 predicted likelihood of experiencing subjective effects of alcohol by ages 13–14. Participants (N = 206; 57 % female) were drawn from the Adolescent Brain Cognitive Development Study. Baseline medial and lateral OFC volumes were used. Subjective response to alcohol was measured during follow-up using a binary outcome (1 = any effect, 0 = no effects). Mixed-effects logistic regression models tested the association between OFC and alcohol response, adjusting for sex, parental education, race/ethnicity, intracranial volume, and site. Smaller left medial OFC at Baseline was significantly associated with greater odds of reporting subjective effects (OR = 1.70, p = .026). Youth who reported subjective effects also consumed more alcohol in the past year (p &lt; .001), but did not differ in their alcohol expectancies. Among those reporting subjective effects, OFC volume was not significantly associated with the amount or frequency of alcohol use. These findings suggest that smaller OFC volume may not reflect pharmacological sensitivity per se, but instead relate to early drinking behavior sufficient to elicit noticeable effects. This may reflect underlying impulsivity-related traits or altered neurodevelopmental trajectories that predispose youth to early and potentially riskier patterns of alcohol use. Results underscore the potential value of identifying structural brain markers that contribute to individual vulnerability for alcohol use during adolescence.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"128 ","pages":"Pages 43-50"},"PeriodicalIF":2.9,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voluntary wheel-running reduces harmful drinking in a genetic risk model for drinking to intoxication","authors":"Kolter Grigsby ,&nbsp;Zaynah Usmani ,&nbsp;Amy E. Chan ,&nbsp;Luis Tzab ,&nbsp;Justin Anderson ,&nbsp;Angela R. Ozburn","doi":"10.1016/j.alcohol.2025.07.004","DOIUrl":"10.1016/j.alcohol.2025.07.004","url":null,"abstract":"<div><div>Physical activity (PA) may provide an effective and equitable treatment option for addressing the harm associated with Alcohol Use Disorders (AUDs). Wheel-running (WR) – a well characterized rodent model of PA – reduces intake and craving for many drugs of abuse; however, its effects on models of harmful ethanol intake are mixed. This may in part be due to critical differences in drinking paradigm, genetics background, chronicity of ethanol, and the modality and duration of PA being tested. To compliment and extend prior work, we evaluated whether key stages of PA development would differentially reduce binge-like ethanol drinking in inbred High Drinking in the Dark (iHDID-1) mice, a unique genetic risk model for drinking to intoxication. AUD is a chronic, relapsing disorder. To better reflect this condition, adult female and male iHDID-1 mice underwent a chronic (4-weeks) “Drinking in the Dark” (DID) protocol – a model of binge-like ethanol drinking - along with a locked running (to control for the effect of novelty). Early stages of PA evoke much higher signs of physiological and neurological stress than more chronic, habitual stages of PA. Therefore, we tested whether acute WR (1-week) altered ethanol intake differently than chronic WR (4-weeks). Here, we found that both acute and chronic WR reduced ethanol intake in female and male iHDID-1 mice. To evaluate whether the effect of PA was specific to ethanol, we further tested whether acute WR reduced water intake in the DID protocol. Analysis revealed that male WR iHDID-1 mice had greater water intake than wheel-locked controls. Moreover, WR during the time of DID was positively correlated with water intake, but not ethanol intake, suggesting WR and DID are not competing behaviors. Taken together, these findings offer support for the role of PA as a meaningful intervention strategy for reducing harmful drinking and emphasize the need to explore the underlying neurobiological mechanisms as a means of guiding PA as an adjunctive therapy for AUD.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"128 ","pages":"Pages 35-42"},"PeriodicalIF":2.9,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144805456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcohol consumption during binge-eating episodes and associations with drinking patterns and alcohol problems among adults with binge-spectrum eating disorders","authors":"Megan L. Wilkinson ,&nbsp;Emily K. Presseller ,&nbsp;Claire Trainor ,&nbsp;Elizabeth W. Lampe ,&nbsp;Laura E. Boyajian ,&nbsp;Adrienne S. Juarascio","doi":"10.1016/j.alcohol.2025.07.005","DOIUrl":"10.1016/j.alcohol.2025.07.005","url":null,"abstract":"<div><div>Individuals with binge-spectrum eating disorders (BSEDs) clinically report drinking alcohol during binge-eating episodes, but no empirical research has yet been conducted. Drinking alcohol during binge-eating episodes may exacerbate overconsumption of food and feelings of guilt or sadness in response to binge eating. Characterizing this co-occurring behavior is therefore an important first step and contribution to knowledge about a potential contributor to binge eating. The current study aimed to characterize alcohol use during binge-eating episodes among adults with BSEDs and determine the relationship between this co-occurrence and demographic characteristics or clinical symptoms. Participants (<em>N</em> = 203) reported the frequency and average number of drinks consumed during binge-eating episodes, demographic measures, eating disorder symptomology, general alcohol use and alcohol problems, and depression symptoms. One-third of participants endorsed drinking alcohol during binge-eating episodes in the past three months, with the most common frequency being “rarely” and the typical number of drinks ranging from 1 to 4 drinks. Higher frequency of alcohol consumption during binge-eating episodes was associated with more frequent drinking generally, greater number of drinks during typical drinking episodes, and greater number of alcohol problems. The study's findings indicate potential associations between alcohol use patterns and binge eating, which could be clinically relevant for providers treating patients who consume alcohol. More research is needed with validated measures of co-occurring alcohol and binge eating episodes and in samples with greater variability of clinical severity and demographics.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"128 ","pages":"Pages 28-34"},"PeriodicalIF":2.9,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent inflammation does not promote aversion-resistant binge-like alcohol drinking in rats","authors":"Jessica A. Cucinello-Ragland ,&nbsp;Yolanda Campos-Jurado ,&nbsp;Lila Hershfelt ,&nbsp;Mateo Pujol ,&nbsp;Youssef Saad ,&nbsp;Bilal Zahoor ,&nbsp;Alexandre Neptune ,&nbsp;Jose A. Morón","doi":"10.1016/j.alcohol.2025.07.003","DOIUrl":"10.1016/j.alcohol.2025.07.003","url":null,"abstract":"<div><h3>Background</h3><div>Chronic pain is a leading cause of disability, significantly decreases quality of life, and is highly co-morbid with substance use disorders, including alcohol use disorder (AUD). This is due, in part, to the pain-relieving effects of alcohol acting as a potential driving force for the progression and maintenance of AUD. Despite a substantial body of historic, anecdotal, clinical, and epidemiological evidence supporting the analgesic efficacy of alcohol, few preclinical studies have investigated the effects of pain on volitional alcohol drinking. Further, no studies to date have investigated aversion-resistant drinking in the context of persistent pain.</div></div><div><h3>Methods</h3><div>To address this gap in the literature, the current study combined quinine adulteration with the drinking in the dark (DID) model of binge-like alcohol drinking to assess the effects of complete Freund's adjuvant (CFA)-induced persistent inflammation on aversion-resistant binge-like alcohol drinking in female and male Long Evans rats.</div></div><div><h3>Results</h3><div>Consistent with previous findings from our laboratory, CFA did not affect binge-like alcohol drinking in either sex, although female rats did consume greater levels of alcohol during baseline and post-CFA DID sessions. Similarly, CFA did not affect quinine adulterated binge-like alcohol drinking in either sex.</div></div><div><h3>Conclusions</h3><div>This study is the first to investigate the impact of persistent inflammation on aversion-resistant alcohol drinking. Although we found no effects of CFA on quinine adulterated binge-like alcohol drinking, these findings provide the groundwork for future investigations into this otherwise unstudied aspect of the pain-alcohol relationship.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"128 ","pages":"Pages 21-27"},"PeriodicalIF":2.9,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pain and alcohol consumption among people living with HIV: examining the moderating roles of depression and social support","authors":"Nadine R. Taghian ,&nbsp;Tibor P. Palfai ,&nbsp;Michael R. Winter ,&nbsp;Theresa W. Kim ,&nbsp;Kara M. Magane ,&nbsp;Richard Saitz ,&nbsp;Michael D. Stein","doi":"10.1016/j.alcohol.2025.07.002","DOIUrl":"10.1016/j.alcohol.2025.07.002","url":null,"abstract":"<div><div>Pain and heavy alcohol use are common among people living with HIV (PLWH), and influence one another, potentially exacerbating these conditions over time. This study examines the prospective association between pain and alcohol use among PLWH with a history of unhealthy drinking behaviors and/or substance use and tests whether depression and social support are moderators. A sample of 233 participants from the Boston Alcohol Research Collaborative on HIV/AIDS cohort completed measures of pain intensity (i.e., average severity of pain in the past week) and pain interference (i.e., average interference of pain in everyday life), heavy episodic drinking, number of drinks, social support and depression at baseline and 6 months later. Negative binomial regression analyses assessed whether pain at baseline predicted alcohol use at 6 months, and examined baseline social support and depression as moderators. Pain intensity was significantly associated with number of drinks (IRR = 1.80, 95 % CI: 1.05, 3.08) but not number of heavy drinking days (IRR = 1.84, 95 % CI: 0.83, 4.07), while pain interference was not associated with number of drinks (IRR = 1.63, 95 % CI: 0.96, 2.75) nor heavy drinking days (IRR = 1.43, 95 % CI: 0.64, 3.17) at six months. Neither social support, nor depression were significant moderators of the association between pain and 6-month alcohol use outcomes. Pain intensity is prospectively associated with more alcohol use, but not with heavy drinking among PLWH. We conclude that pain is an important factor to address when considering interventions to reduce alcohol use among PLWH.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"128 ","pages":"Pages 13-20"},"PeriodicalIF":2.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcohol, aging, and the gut microbiome: Intersections of immunity, barrier dysfunction, and disease","authors":"Esther Melamed ,&nbsp;Wiramon Rungratanawanich ,&nbsp;Suthat Liangpunsakul ,&nbsp;Katherine A. Maki ,&nbsp;Rebecca L. McCullough ,&nbsp;Cristina Llorente","doi":"10.1016/j.alcohol.2025.07.001","DOIUrl":"10.1016/j.alcohol.2025.07.001","url":null,"abstract":"<div><div>Alcohol consumption exerts complex, dose- and context-dependent effects on human health, particularly by influencing the gut microbiome, intestinal barrier integrity, immune regulation, and aging processes. Genetic variation and advancing age are two major, and often interacting, factors that modify the risk of alcohol-related diseases. Among genetic factors, the prevalent aldehyde dehydrogenase 2 polymorphism (ALDH2∗2) compromises acetaldehyde clearance, driving toxic metabolite accumulation, oxidative stress, and increased intestinal permeability that disrupts gut microbial communities, even at low levels of alcohol consumption. Heavy and chronic alcohol use further disrupts gut microbial communities, erodes mucosal integrity, and drives systemic inflammation, contributing to alcohol-associated liver disease (ALD), neuroinflammation, and multi-organ injury. Aging independently worsens these effects by promoting chronic low-grade inflammation and impaired immune responses, heightening susceptibility to alcohol-induced pathology. In specific contexts, such as certain autoimmune diseases, low to moderate alcohol intake may exert immunomodulatory effects and influence the gut microbiome, potentially contributing to reduced inflammation and alterations in microbial composition. This review synthesizes current mechanistic insights into how alcohol, host genetics, the gut microbiome, immune regulatory pathways, and aging intersect to influence disease risk. As global populations age and the burden of alcohol-related health issues rises, there is an urgent need for integrated, systems-level approaches. Future research should prioritize precision-based, gut-targeted strategies aimed at restoring microbial balance, maintaining intestinal barrier integrity, and mitigating alcohol-related harm across the lifespan.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"128 ","pages":"Pages 1-12"},"PeriodicalIF":2.5,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Explaining increased efficacy of naltrexone in the treatment of alcohol dependent patients with a family history of alcohol use disorder: A systematic review on the role of reward sensitivity and sweet liking","authors":"Jan van Amsterdam ,&nbsp;Wim van den Brink","doi":"10.1016/j.alcohol.2025.06.004","DOIUrl":"10.1016/j.alcohol.2025.06.004","url":null,"abstract":"<div><div>A positive family history of alcohol use disorder (FHA+) is one of the strongest risk factors for developing alcohol use disorder (AUD) compared. Importantly, naltrexone (NTX) has shown higher efficacy in treating FHA + AUD patients than FHA− AUD patients. Possibly, this may be explained by the attenuation of high reward sensitivity and liking sweet substances (“sweet liking”; SL) in FHA + AUD patients. This systematic review explores whether attenuation by NTX of reward sensitivity and SL explains its higher efficacy in FHA + compared to FHA− AUD patients.</div><div>Separate systematic literature searches were performed on the effect of NTX in FHA + AUD patients, the effect of NTX on reward sensitivity, and the associations of FHA+ with reward sensitivity and SL.</div><div>In total, 36 eligible studies were included (6 for the effect of NTX in FHA + AUD patients, 18 for reward sensitivity, and 12 for sweet liking). In 5 out of 6 studies, a moderating effect of FHA + on NTX treatment efficacy in AUD was shown, with higher efficacy of NTX in FHA + AUD patients. In 6 out of 8 studies, reward sensitivity moderated the treatment effect of NTX in AUD, and in 9 of 10 studies, reward sensitivity was attenuated by NTX. In 3 studies, SL positively moderated the effect of NTX in AUD. Finally, in 9 of 9 studies, SL was attenuated by NTX and enhanced by (partial) opioid agonists.</div><div>Increased reward sensitivity (and sweet-liking as its possible indicator) appeared to be positively associated with FHA+ and was attenuated by NTX, which may (partly) explain the increased effect of NTX in FHA + AUD patients. These results may foster personalized pharmacotherapy in AUD patients.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 63-72"},"PeriodicalIF":2.5,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}