Alcohol最新文献

{"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}

{"title":"Associations of physical pain, alcohol use, and related factors in the daily lives of patients with chronic low back pain","authors":"Ian A. McNamara ,&nbsp;Jeff Boissoneault ,&nbsp;Jarrod M. Ellingson ,&nbsp;Jake Sauer ,&nbsp;Ryan W. Carpenter","doi":"10.1016/j.alcohol.2025.06.002","DOIUrl":"10.1016/j.alcohol.2025.06.002","url":null,"abstract":"<div><h3>Background</h3><div>Alcohol use and chronic pain are highly prevalent, costly, and have a bidirectional relationship. This may occur, in part, because of the analgesic effects of alcohol. Specifically, individuals may drink alcohol to address both physical pain and the subsequent increases in negative affect that may be brought on by painful experiences. The current project examined the Catastrophizing, Anxiety, Negative Urgency, and Expectancy (CANUE) model in daily life to better understand the association between alcohol use and pain.</div></div><div><h3>Methods</h3><div>Hypothesized paths of the CANUE model were examined using intensive longitudinal data (n = 34; total n_observations = 2960) collected using ecological momentary assessment over fourteen days from patients with chronic lower back pain who reported drinking alcohol (n_{drinking episodes} = 5.88). Multilevel models examined associations of pain, negative affect, and alcohol use, as well as potential moderators (pain-related cognitions, alcohol expectancies, and impulsivity) of these associations.</div></div><div><h3>Results</h3><div>Previous-occasion physical pain, but not cumulative-average pain, and pain-related alcohol expectancies, were associated with a greater likelihood of alcohol use. Though there was no main effect of cumulative-average negative affect on alcohol use, negative affect interacted with impulsivity, such that participants were more likely to continue drinking when experiencing increased negative affect and impulsivity. Results did not find a hypothesized indirect effect of pain on alcohol use via negative affect. Alcohol use was associated with reduced next-occasion pain and increased perceptions of alcohol-related pain relief.</div></div><div><h3>Discussion</h3><div>While cumulative-average pain was not associated with an increased likelihood of drinking, individuals were more likely to drink after occasions of elevated pain. This may indicate that participants drank to reduce pain, as was also suggested by the association between pain-related alcohol expectancies and drinking. This is one of the first studies to examine associations of alcohol use and chronic pain in daily life. The results provide evidence for the importance of pain as an antecedent to alcohol use. Findings supported some components of the CANUE model but also highlight the need for further investigation to inform potential revision of the mode.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 73-83"},"PeriodicalIF":2.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328083","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 use disorder exacerbates clinical and vascular risks differentially in psychiatric disorders","authors":"Eva Christina Meyer ,&nbsp;Younes Adam Tabi","doi":"10.1016/j.alcohol.2025.06.003","DOIUrl":"10.1016/j.alcohol.2025.06.003","url":null,"abstract":"<div><div>Alcohol Use Disorder (AUD) is a major public health concern with detrimental effects on cognitive and neurological function, yet its impact on psychiatric populations remains incompletely defined. In this global propensity score–matched cohort study, we examined the clinical and vascular consequences of comorbid alcohol abuse across diverse psychiatric disorders. Data from the TriNetX network, encompassing electronic medical records from 143 healthcare organizations, were analyzed. For each disorder—anxiety, depression, bipolar disorder, schizophrenia, reaction to severe stress, eating disorders, personality disorders, psychoactive substance dependence, developmental disorders, and obsessive-compulsive disorder—patients with alcohol abuse were matched 1:1 to those without, controlling for demographic and clinical factors. Over a 1095-day follow-up, outcomes evaluated included emergency department visits, pain prevalence, mortality, and cerebrovascular events (transient ischemic attacks and strokes). Alcohol abuse was consistently associated with significantly higher emergency care utilization, increased somatic pain, and elevated mortality across all groups. For instance, anxiety and depression cohorts exhibited 8.1% and 7.3% higher emergency visits and increased mortality by 2.7% and 2.4%, respectively, while schizophrenia showed a twofold increase in stroke risk and markedly higher pain (risk ratio 2.21). These results underscore that AUD exacerbates clinical and vascular risks in psychiatric patients, highlighting the urgent need for targeted interventions.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 85-92"},"PeriodicalIF":2.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328082","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":"Examining the moderating role of intolerance of uncertainty on pain tolerance and craving in patients with chronic pain and alcohol use disorder","authors":"Milena Radoman ,&nbsp;Emily Heilner ,&nbsp;Colleen McGowan ,&nbsp;Benazir Neree-Thompson ,&nbsp;Elcin Sakmar ,&nbsp;Rajita Sinha","doi":"10.1016/j.alcohol.2025.06.001","DOIUrl":"10.1016/j.alcohol.2025.06.001","url":null,"abstract":"<div><div>Chronic pain (CP) and alcohol use disorder (AUD) frequently co-occur, yet the psychological factors underlying their interaction remain unclear. Intolerance of uncertainty (IU) – a cognitive trait linked to distress in unpredictable situations – may influence pain management and coping behaviors in these populations. This study examined whether IU moderates pain and alcohol craving responses to a pain-related stressor in individuals with CP and AUD. Fifty-five adults aged 18–65 years were enrolled, including individuals with CP only (n = 20), AUD only (n = 14), CP + AUD (n = 8), and healthy controls (n = 13). Participants completed a self-report measure of IU and the Yale Pain Stress Test (YPST), an adaptation of the Cold Pressor Test, designed to elicit pain-related stress. Behavioral pain tolerance, subjective pain and alcohol craving were assessed across two experimental sessions, one with exposure to an ice-cold water stressor and the second with a warm-water control condition. Exposure to the pain-related stressor significantly reduced behavioral pain tolerance and increased subjective pain across all groups, and also heightened alcohol craving, particularly in individuals with AUD. IU moderated the pain experience during pain-related stress: in the CP + AUD group, higher IU was associated with lower pain tolerance, whereas in the AUD group, higher IU was correlated with greater pain tolerance. IU also moderated craving responses, with higher IU predicting increased craving in individuals with both CP and AUD. These preliminary findings highlight IU as a potential treatment target, suggesting that interventions aimed at improving uncertainty tolerance may enhance pain coping and reduce stress-driven alcohol-seeking behaviors in vulnerable populations.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 55-61"},"PeriodicalIF":2.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144295485","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":"Integrating TWAS and GWAS identifies gut microbiota–immune interactions to alcohol dependence genetics in European sample","authors":"Haohao Xu ,&nbsp;Peng Shen ,&nbsp;Zhenglin Zhao ,&nbsp;Yushuang Xing ,&nbsp;Tonghui Yi ,&nbsp;Chao Yang ,&nbsp;Han Gao ,&nbsp;Hongyan Guo ,&nbsp;Mingqian Zhao ,&nbsp;Shanbo Zhang ,&nbsp;Di Jia ,&nbsp;Weiming Zhao","doi":"10.1016/j.alcohol.2025.05.006","DOIUrl":"10.1016/j.alcohol.2025.05.006","url":null,"abstract":"<div><h3>Objective</h3><div>Alcohol dependence (AD) is a global public health concern with strong genetic characteristics. The purpose of this study was to explore the underlying pathogenic genes and mechanisms associated with AD.</div></div><div><h3>Methods</h3><div>This study employed a multi-omics Mendelian randomization approach to identify potential disease-causing genes for AD. Specifically, we integrated transcriptome-wide association studies (TWAS) with summary-data-based Mendelian randomization (SMR) to pinpoint candidate genes associated with AD. Additionally, mediating Mendelian randomization was utilized to investigate the mediating role of the gut microbiota in the relationship between immune cell phenotypes and AD.</div></div><div><h3>Results</h3><div>Two susceptibility genes associated with AD, ADH1C and POLI, were identified a joint analysis of SMR and integrated cross-tissue and single tissue TWAS in European population. A new genetic locus associated with AD, rs62307318, was uncovered through cross-organism TWAS. This finding was further validated using Mendelian randomization and Phenome-wide association analysis. Additionally, Mendelian randomization identified Paceibacteria as a possible mediator between Myeloid DC AC and AD.</div></div><div><h3>Conclusion</h3><div>This study identified two genes closely related to AD and explored the possible pathogenesis of AD, which provides a new insight into the treatment and pathogenesis of AD.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 11-20"},"PeriodicalIF":2.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227931","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 effects on associative and sensorimotor cortico-thalamo-basal ganglia circuits alter decision making and alcohol intake","authors":"David M. Lovinger","doi":"10.1016/j.alcohol.2025.05.005","DOIUrl":"10.1016/j.alcohol.2025.05.005","url":null,"abstract":"<div><div>Much of the behavioral repertoire of humans and other vertebrates is learned and controlled through the function of brain circuits involving the cortex, thalamus and Basal Ganglia (for simplicity we will refer to this as the Cortico-Thalamo-Basal Ganglia, or CTBG, circuitry). As the name implies, these circuits include the different regions of cortex and thalamus, as well as BG subregions including the striatum, globus pallidus (GP), substantia nigra (SN)/ventral tegmental area (VTA), and the subthalamic nucleus (STN). This circuitry has developed evolutionarily to provide overarching control of actions following discrete environmental events as well as self-initiated actions. Several parallel CTBG circuits have been identified and linked to different aspects of action control under different circumstances. Research in experimental psychology and Neuroscience has established how different CTBG circuits contribute to control of actions based on environmental circumstances and past learning history. There is also a large and growing body of evidence that misused substances, including alcohol, act on cells within these circuits. These actions promote acute intoxication and drug seeking and contribute to changes in behavior induced by chronic alcohol exposure, withdrawal and relapse. Alcohol exposure also influences which of the different CTBG circuits has the strongest influence on behavior. This review will cover the relevant circuitry and describe the current state of knowledge as to how alcohol alters CTBG circuit function and control of behavior. Studies in rodents, non-human primates and humans will be discussed. Finally, ideas for future research directions in this area will be considered.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 21-46"},"PeriodicalIF":2.5,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144210462","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 in comorbid alcohol use disorder and HIV: A network meta-analysis study","authors":"Muhammed Bishir,&nbsp;Mohamed Sheik Tharik Abdul Azeeze,&nbsp;Sulie L. Chang","doi":"10.1016/j.alcohol.2025.05.003","DOIUrl":"10.1016/j.alcohol.2025.05.003","url":null,"abstract":"<div><div>Alcohol use is prevalent among people with HIV (PWH). PWH often experience pain (said discomfort) and use alcohol to combat pain. We reported that short-term alcohol exposure exerts analgesic effect. Prolonged exposure is known to result in chronic pain. We hypothesize that alcohol exposure, either <em>in-vivo</em> for <em>macaques</em> or <em>in-silico</em> simulation exposure onto differentially expressed genes (DEGs) from HIV-1Tg rats and HIV patients, exacerbates discomfort in PWH. To substantiate this hypothesis, we analyzed genomic data collected from three brain datasets including the hippocampus of alcohol-exposed <em>Macaca mulatta</em> (GSE69685), HIV-1Tg rats (GSE47474), and post-mortem brain tissue of HIV-positive patients (GSE28160). Ingenuity Pathway Analysis (IPA)-Core Analysis revealed activation of neuroinflammation, neuropathic pain signaling pathways, and the inhibition of opioid signaling as well as in the increase of neuromuscular disease with neuropathy in <em>Macaca mulatta</em> exposed to binge EtOH and SIV infection. IPA-Core Analysis of the DEGs from HIV-1Tg rats, a rat model that mimics HIV patients on cART, possessing 7 of 9 HIV viral proteins, showed activation of neuroinflammation, neuropathic pain signaling pathways. IPA-Core Analysis of the DEGs from HIV patients showed activation of neuroinflammation and inhibition of neuropathic pain and increase in neuromuscular disease with neuropathy. To study the impact of alcohol exposure in HIV-1Tg rats and HIV patients, <em>in-silico</em> simulation of ethanol (EtOH) treatment mimicking exposure of alcohol onto the DEGs in response to HIV viral proteins in HIV-1Tg rats and HIV infection in HIV patients enhanced discomfort and increased neuromuscular diseases. These molecules showed significant modulation by simulated alcohol exposure, further supporting the link between alcohol use and heightened pain in PWH. Taking together, our findings suggest that alcohol consumption and HIV promote pain via modulating signaling pathways including neuroinflammation, and neuropathic pain signaling pathways and by disease like neuromuscular disease with neuropathy.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 43-53"},"PeriodicalIF":2.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183144","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 early adulthood increases the vulnerability of locus coeruleus neurons and amyloid beta pathology in female APP/PS1 mice","authors":"Shaydel Engel,&nbsp;Madison Dillerud,&nbsp;Matthew Scalf,&nbsp;Ruth Dobbelmann,&nbsp;Yijuan Du,&nbsp;Anna M. Lee,&nbsp;Steven M. Graves","doi":"10.1016/j.alcohol.2025.05.004","DOIUrl":"10.1016/j.alcohol.2025.05.004","url":null,"abstract":"<div><div>Alcohol use disorder is the most common substance misuse disorder and Alzheimer's disease (AD) is the most common neurodegenerative disease. Evidence suggests that alcohol consumption may increase the risk for developing dementia and AD. The locus coeruleus (LC) is a region wherein the impact of alcohol and AD may converge. The LC is a noradrenergic nucleus that is highly vulnerable to degeneration in AD, and loss of LC neurons is associated with increased amyloid beta (Abeta) pathology. The present study examined whether alcohol consumption during early adulthood impacts LC degeneration and Abeta using the APP/PS1 mouse model. Female APP/PS1 mice underwent an eight-week chronic intermittent access (IA) alcohol consumption paradigm followed by twenty-three weeks of abstinence; water-consuming control subjects were run in parallel. APP/PS1 mice that had IA to alcohol showed a 21.9% decrease in the number of LC neurons and a decrease in the length of noradrenergic axons innervating the primary motor cortex. Furthermore, this alcohol induced LC deficit was associated with an increase in Abeta pathology in the primary motor cortex. In contrast to results from female APP/PS1 mice, there were no deficits in axon length and only a 9.4% decrease in the number of LC neurons in non-transgenic female subjects after abstinence from IA to alcohol. Our results demonstrate that alcohol consumption during early adulthood increases the vulnerability of LC neurons to degeneration and exacerbates Abeta pathology in female APP/PS1 mice, providing evidence that a history of alcohol abuse may impact the trajectory and severity of AD.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 1-9"},"PeriodicalIF":2.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132153","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":"Ethanol exposure promotes tumor cell migration and angiogenesis in a mouse model of glioblastoma","authors":"Bianca L. Myers ,&nbsp;C. Fernando Valenzuela ,&nbsp;Tou Yia Vue","doi":"10.1016/j.alcohol.2025.05.002","DOIUrl":"10.1016/j.alcohol.2025.05.002","url":null,"abstract":"<div><div>Rapid progression of high-grade gliomas contributes to the poor survival rates of patients, particularly those with aggressive and heterogeneous brain tumors such as glioblastomas (GBMs). Before the onset of tumor symptoms, there exists a vulnerable period during which exposure to environmental factors could exacerbate glioma tumorigenicity. Alcohol (EtOH) is one such factor that has been shown to increase tumor size and vascularization of melanomas in xenograft mouse models and invasion of breast cancer cells in vitro. Currently, whether EtOH exposure promotes glioma progression in vivo is unknown. Here, we induced fluorescently labeled gliomas in immune-competent mice by injecting and electroporating <em>Cre</em> + CRISPR plasmids to delete tumor suppressor genes in neural progenitors lining the right lateral ventricle. Asymptomatic tumor mice were exposed to EtOH or Air vapors via inhalation chambers for five days, followed by two days of rest, then another five days of exposure. This paradigm produced blood ethanol concentrations (BECs) similar to episodic binge drinking, averaging ∼200 mg/dL on the final day of exposure. We found that EtOH exposure acutely increased tumor vascularization and invasion to the contralateral hemisphere. Notably, EtOH-exposed male mice exhibited a significant decrease in survival compared to Air-exposed controls and EtOH-exposed female mice. Overall, our study is the first to demonstrate that developing primary gliomas are susceptible to the tumorigenic effects of EtOH, with males being more vulnerable to increased mortality.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 11-21"},"PeriodicalIF":2.5,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144048658","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":"An exploratory study of cytokine and inflammatory profiles between young adult low-risk and at-risk drinkers","authors":"Mariann R. Piano ,&nbsp;Shane A. Phillips ,&nbsp;Chueh-Lung Hwang ,&nbsp;Keng-Yu Chang ,&nbsp;Kevin M. Najarro ,&nbsp;Rachel H. McMahan ,&nbsp;Elizabeth J. Kovacs","doi":"10.1016/j.alcohol.2025.05.001","DOIUrl":"10.1016/j.alcohol.2025.05.001","url":null,"abstract":"<div><h3>Background</h3><div>This exploratory study examined plasma levels of pro-inflammatory cytokines, chemokines and growth factors as well as intestinal fatty acid-binding protein (iFABP) and zonulin levels between young adult male and female low-risk and at-risk drinkers.</div></div><div><h3>Methods</h3><div>A total of 33 low-risk (phosphatidylethanol levels &lt;20 ng/ml; 19 female) and 44 at-risk drinkers (phosphatidylethanol levels ≥20 ng/ml; 30 female) were included in this study. Fasting blood samples were obtained in all participants. A multiplex assay was used to measure 48 chemokines and growth factors. An enzyme-linked immunoassay was used to measure plasma levels of human iFABP and zonulin.</div></div><div><h3>Results</h3><div>We found that in young female, at-risk drinkers had a lower level of granulocyte-macrophage colony-stimulating factor (p = 0.04) and platelet-derived growth factor BB (P = 0.04) than low-risk drinkers, while in males, an elevated level of interferon-gamma was found in at-risk drinkers compared to low-risk drinkers (P = 0.04). Intestinal fatty acid-binding protein levels were significantly higher and zonulin levels were significantly lower in at-risk-risk drinkers compared to low-risk drinkers (P = 0.001 and P = 0.02, respectively).</div></div><div><h3>Conclusions</h3><div>These findings suggest that at-risk drinking in young adults is associated with alterations in specific cytokines and proteins involved in intestinal barrier function.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 23-29"},"PeriodicalIF":2.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002028","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}