Alcohol最新文献

{"title":"Alcohol use and pain: Novel insights and emerging questions","authors":"Jeff Boissoneault","doi":"10.1016/j.alcohol.2025.12.001","DOIUrl":"10.1016/j.alcohol.2025.12.001","url":null,"abstract":"","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"130 ","pages":"Pages 73-75"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145727702","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":"Lateral hypothalamus CRFR1 regulation of binge drinking: Divergence along anterior-posterior axis","authors":"J.L. Ritchie , M.R. Eberle , J.A. Wojick , M.R. Campeau , L.S. Kooyman , T.E. Thiele , T.L. Kash","doi":"10.1016/j.alcohol.2025.11.002","DOIUrl":"10.1016/j.alcohol.2025.11.002","url":null,"abstract":"","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"130 ","pages":"Pages 6-13"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145514787","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":"Argument for the pharmacokinetically-informed preclinical researcher: A commentary for Alcohol","authors":"Nicholas J. Grahame","doi":"10.1016/j.alcohol.2025.11.003","DOIUrl":"10.1016/j.alcohol.2025.11.003","url":null,"abstract":"<div><div>The purpose of this commentary is to advocate for the importance of carefully considering ethanol pharmacokinetics when conducting preclinical studies involving alcohol consumption. Researchers working in this field commonly use alcohol drinking as a principle or ancillary measurement. However, the amount of alcohol consumed cannot substitute for an understanding of dose, which is an essential referent in any study involving pharmacology, especially in studies using 24-h, two-bottle choice access to alcohol. Dose is the critical variable for understanding potency and efficacy, for translating both across species (including to humans) and for accurately building on preclinical work using <em>in vitro</em> methodologies. Nonetheless, there is a wide variety of practices when it comes to consideration of the pharmacological relevance of alcohol intake measures. Notably, there are numerous published studies reporting intake rates for which blood ethanol concentrations (BECs) would either be zero or negligible, or would be so high as to be physiologically impossible. To combat these issues, the gold standard for understanding dose should be measurement of BEC. Where this is impractical or impossible, researchers must at a minimum carefully analyze rates of alcohol intake in their population against well-understood and easily modeled pharmacokinetic factors, such as rate of intake as it compares to rate of metabolism. Similar methods are increasingly apparent in clinical studies that use pharmacological modeling (so-called “eBAC”) along with measuring the rate of alcohol intake to estimate human BECs. In short, to make useful contributions to the study of alcohol drinking, authors should ensure that they are pharmacokinetically informed.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"130 ","pages":"Pages 1-5"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145537362","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":"Acute ethanol enhances septohippocampal coordination but disrupts intrinsic hippocampal theta dynamics during foraging","authors":"Caleb B. Darden ,&nbsp;Meagan D. Marks ,&nbsp;Andrew J. Kesner","doi":"10.1016/j.alcohol.2025.11.001","DOIUrl":"10.1016/j.alcohol.2025.11.001","url":null,"abstract":"<div><div>Theta oscillations – rhythmic patterns of synchronous activity within discrete brain regions – are known to support memory, navigation, and behavioral coordination, and are sensitive to pharmacological manipulation. Acute ethanol (EtOH) exposure has been shown to alter theta oscillations, but its effects on transient theta bursts and cross-regional coordination during naturalistic behavior remain unclear. We recorded local field potentials (LFPs) from the medial septum (MS), hippocampal <em>Cornu Ammonis 1</em> (CA1), and medial prefrontal cortex (mPFC) in freely foraging mice following intraperitoneal injection of EtOH (1.5 g/kg) or saline. We analyzed spectral power, theta burst dynamics, phase, and lag timing. Burst features from CA1 were used to train a machine learning classifier to predict session condition. EtOH impaired locomotion and reduced goal-directed behaviors, particularly early in the session. In CA1, theta power shifted toward lower frequencies and lagged coherence declined. EtOH increased the frequency but reduced the duration of theta bursts in CA1, and in MS, only burst count increased. EtOH enhanced the temporal alignment of MS–CA1 burst pairs. Phase-locking between CA1 and MS during coupled bursts remained present but showed altered structure. Our classifier achieved robust performance using burst features such as skew and entropy, and reliably distinguished treatment conditions. EtOH modulates septohippocampal dynamics by altering the timing and structure of theta bursts. These results suggest that burst-level features are sensitive markers of EtOH's circuit-level effects during naturalistic behavior.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"130 ","pages":"Pages 14-27"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145616102","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":"The impact of maternal separation stress on the CRFergic system in the extended amygdala and its relevance to acute stress-induced ethanol consumption in mice","authors":"Natalia Bonetti Bertagna ,&nbsp;Cristiane Aparecida Favoretto ,&nbsp;Ben Tagami Rodolpho ,&nbsp;Thamires Righi ,&nbsp;Cássio Morais Loss ,&nbsp;Ingrid B.M. Morais ,&nbsp;Talita A.M. Vrechi ,&nbsp;Adolfo Garcia Erustes ,&nbsp;Gustavo J.S. Pereira ,&nbsp;Tarciso Tadeu Miguel ,&nbsp;Fábio Cardoso Cruz","doi":"10.1016/j.alcohol.2025.11.004","DOIUrl":"10.1016/j.alcohol.2025.11.004","url":null,"abstract":"<div><div>Maternal separation (MS) is an early-life stressor associated with increased vulnerability to alcohol use disorders (AUD) later in life, potentially through alterations in corticotropin-releasing factor (CRF) signaling in the extended amygdala—comprising the bed nucleus of the stria terminalis (BNST) and amygdala (AMY). This study investigated the long-term effects of MS on ethanol consumption and CRFergic signaling following acute stress, considering possible sex-dependent differences. C57BL/6J pups were subjected to the MS paradigm from postnatal days (PND) 1–14; controls remained undisturbed. On PND 45, mice underwent an Drinking in the Dark (DID) protocol for three weeks, followed by operant alcohol self-administration under a fixed ratio schedule. They were then tested under a progressive ratio (PR) reinforcement schedule. After PR, a subset of mice was randomly assigned to the Rat Exposure Test (RET), while a second subset of mice was kept naïve for it. Finally, a 4h-binge session was allowed for all the animals. Results showed that female groups, independent of MS stress, consumed more ethanol than male groups during DID. Male MS mice spent more time in the home chamber during RET, which was associated with increased number of reinforcements and active nose pokes during binge protocol. MS mice not exposed to RET showed increased CRF-binding protein in the AMY and reduced CRFR1 receptor in the BNST; RET exposure led to increased CRFR2 receptor expression in the AMY of MS mice. These findings suggest that MS alters alcohol consumption, particularly in response to acute stress, in a sex-dependent manner, and the CRFergic system of mice exposed chronically to this substance.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"130 ","pages":"Pages 40-56"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145590130","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 induces neuroimmune dysregulation and soluble TREM2 generation in a human iPSC neuron, astrocyte, microglia triculture model","authors":"Andrew J. Boreland ,&nbsp;Yara Abbo ,&nbsp;Xindi Li ,&nbsp;Alessandro C. Stillitano ,&nbsp;Siwei Zhang ,&nbsp;Jubao Duan ,&nbsp;Zhiping P. Pang ,&nbsp;Ronald P. Hart","doi":"10.1016/j.alcohol.2025.10.006","DOIUrl":"10.1016/j.alcohol.2025.10.006","url":null,"abstract":"<div><div>Alcohol use disorders (AUDs) affect substantial populations worldwide and increase the risk of developing cognitive impairments and alcohol-associated dementia. While chronic inflammatory signaling likely plays an important role in alcohol-associated neurological sequalae, the precise mechanisms underlying alcohol-associated neuropathology remain enigmatic. We hypothesize that alcohol leads to neuroimmune dysregulation among neurons, astrocytes, and microglia; and is perpetuated by innate immune signaling pathways involving cell-cell signaling. To investigate how alcohol dysregulates neuroimmune interactions in a human context, we constructed a triculture model comprising neurons, astrocytes, and microglia derived from human induced pluripotent stem cells. After exposure to ethanol, we observed significant differential gene expression relating to innate immune pathways, inflammation, and microglial activation. Microglial activation was confirmed with morphological analysis and expression of CD68, a lysosomal-associated membrane protein and marker for phagocytic microglial activation. A striking finding in our study was the elevation of <em>TREM2</em> expression and, specifically, <em>TREM2</em> alternatively spliced isoforms that are predicted to give rise to soluble TREM2. <em>TREM2</em> loss-of-function variants have been reported to be a risk factor for Alzheimer's disease. These results suggest that ethanol exposure in the brain may lead to increased microglial activation and production of soluble isoform named <em>TREM2</em>^<em>219</em> through alternate splicing. Deciphering the molecular and cellular mechanisms underpinning ethanol-related neuroimmune dysregulation within a human context promises to shed light on the etiology of AUD-related disorders, potentially contributing to the development of effective therapeutic strategies.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"130 ","pages":"Pages 57-72"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145477380","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":"2025-12-01","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":"The impact of alcohol addiction on the quality of life, mental condition, clinical condition and nutritional status of patients with head and neck cancer","authors":"Karolina Dorobisz ,&nbsp;Tadeusz Dorobisz ,&nbsp;Katarzyna Pazdro-Zastawny ,&nbsp;Marzena Janczak ,&nbsp;Katarzyna Czyż","doi":"10.1016/j.alcohol.2025.10.005","DOIUrl":"10.1016/j.alcohol.2025.10.005","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;div&gt;Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide, with over 880,000 new cases reported worldwide each year. Tobacco smoking and alcohol drinking are the main risk factors for HNSCC, accounting for 30 % of HNSCC cases worldwide. Alcohol is a particularly important risk factor not only for HNSCC and was recognized in 1988 by the International Agency for Research on Cancer (IARC) as a very important risk factor for the incidence of oral cavity, oropharyngeal, hypopharyngeal and laryngeal cancers, and was classified as group 1 cancer risk factors. The aim of the study was to assess the impact of alcohol on the quality of life, mental state, clinical state and nutritional status in patients with HNSCC.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Material and method&lt;/h3&gt;&lt;div&gt;The single-center, prospective study included a group of 123 patients aged 42 to 89, treated for laryngeal cancer, pharyngeal cancer and cancer of unknown primary site HNSCC. Socio-demographic data and the presence of risk factors were assessed in each patient. The performance status of the patients was assessed using the Eastern Cooperative Oncology Group (ECOG) scale. The nutritional status of patients was assessed via a Body Mass Index (BMI) assessment and Mini Nutritional Assessment Short FORM (MNA-SF). Each patient was also assessed using the Nutrition Risk Screening 2002 (NRS2002). The level of depression and anxiety was assessed using the Hospital Anxiety and Depression Scale (HADS). Patients were also assessed for sleep problems using the Insomnia Severity Index. Quality of life was assessed using the Polish version of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Head and Neck Cancer 35 (EORTC QLQ-H&amp;N35). In each patient, the results of laboratory tests were also analyzed - morphology, nutritional parameters - total protein, total cholesterol and CRP protein level.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Patients who regularly drank alcohol more often suffered from throat cancer (91.2 %) and larynx cancer (59.2 %), while CUP was more often diagnosed in patients without a history of regular alcohol consumption. Patients who drank alcohol were diagnosed at a significantly higher stage compared to the group of non-drinkers. In the study group of patients regularly drinking alcohol with diagnosed HSCC, a significantly worse clinical condition, risk of malnutrition or malnutrition was demonstrated compared to patients with diagnosed HNSCC who did not drink alcohol. In laboratory tests, patients drinking alcohol had a lower hemoglobin level before treatment (11.7 vs 12.8 g/dl, p &lt; 0.001), a higher leukocyte level (10.3 vs 7.5 × 10 &lt;sup&gt;9&lt;/sup&gt;/l, p &lt; 0.001), a lower total protein level (6.3 vs 6.8 g/dl, p &lt; 0.001), a higher mean CRP level (8.0 vs 5.0 mg/l) and a lower total cholesterol level (134 vs 187 mg/dl, p &lt; 0.001). Those who drank alcohol more often had significan","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"129 ","pages":"Pages 150-156"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145358143","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":"Molecular mechanism underlying alcohol's residual effects: The role of acetaldehyde in mitochondrial dysfunction at synapses in mouse brain cortex","authors":"Analía G. Karadayian ,&nbsp;Lautaro Carrere ,&nbsp;Analia Czerniczyniec ,&nbsp;Silvia Lores-Arnaiz","doi":"10.1016/j.alcohol.2025.09.004","DOIUrl":"10.1016/j.alcohol.2025.09.004","url":null,"abstract":"<div><div>Alcohol residual effects impose significant physiological and cognitive burdens due to acute ethanol exposure; however, its underlying mechanisms remain poorly understood. This study investigates the role of acetaldehyde, the main ethanol metabolite, in driving mitochondrial dysfunction and synaptic impairment during hangover onset. Using a mice model, we evaluated the effects of ethanol (3.8 g/kg) and the alcohol dehydrogenase inhibitor 4-methylpyrazole (4-MP) on brain cortex synaptosomes.</div><div>Ethanol exposure significantly elevated serum acetaldehyde compared with control (p &lt; 0.05), and induced mitochondrial dysfunction, as evidenced by impaired respiration (30 % decrease in basal O₂ uptake vs. control), mitochondrial membrane depolarization and reduced ATP production (50 % decrease vs. control). These effects were mitigated by pre-treatment with 4-MP, which normalized acetaldehyde levels and partially restored mitochondrial function. Notably, ethanol downregulated synaptic proteins (nNOS, GluN2B, PSD-95; p &lt; 0.05), but 4-MP failed to prevent this reduction, suggesting that acetaldehyde would not be involved in synaptic proteins alterations. Further, ethanol disrupted calcium homeostasis and nitric oxide (NO) content. Interestingly, 4-MP alone also reduced calcium uptake and NO content (p &lt; 0.05), indicating potential off-target effects on neuronal signaling.</div><div>While the reduction in acetaldehyde levels preserved mitochondrial integrity, its inability to rescue synaptic protein loss highlights the complexity of hangover pathology, involving both acetaldehyde-dependent and -independent mechanisms. Our findings underscore acetaldehyde's pivotal role in hangover-associated mitochondrial dysfunction but reveal divergent pathways in synaptic impairment. These insights advance the search for targeted hangover therapies by delineating acetaldehyde-dependent toxicity.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"129 ","pages":"Pages 79-91"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092869","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":"Bidirectional relationships between daily sleep and alcohol use","authors":"Emma J. Tussey,&nbsp;Maria M. Wong","doi":"10.1016/j.alcohol.2025.09.002","DOIUrl":"10.1016/j.alcohol.2025.09.002","url":null,"abstract":"<div><h3>Background</h3><div>Prior longitudinal studies demonstrate that sleep disturbance is a risk factor for alcohol misuse. Experimental research also shows that alcohol intake negatively impacts sleep. The present study evaluated temporal bidirectional relationships between sleep and alcohol intake using intensive longitudinal methods.</div></div><div><h3>Methods</h3><div>57 college students (71 % female, Mage 24.1) participated in a two-week study assessing their daily sleep and alcohol use. Participants wore an actiwatch and completed daily diaries about their sleep and alcohol intake. Multi-level zero-inflated negative binomial models assessed whether prior sleep predicted next-day alcohol use. Linear multi-level models assessed whether alcohol use predicted daily sleep. All models assessed both within- (daily) and between-subject (average) effects because daily variations in sleep could influence alcohol use separately from average patterns and vice versa. Race, age, and sex were controlled in the analyses.</div></div><div><h3>Results</h3><div>Greater average wake after sleep onset (WASO) and sleep onset latency (SOL) and shorter daily total sleep time (TST) predicted greater next-day alcohol intake (WASO IR: 1.009; SOL IR: 1.011; TST IR: 0.998; p &lt; .05). Higher average alcohol intake predicted increased daily WASO (B = 8.944, SE = 4.551, p &lt; .05), TST (B = 12.717, SE = 5.877, p &lt; .05), and decreased daily restedness (B = −0.158, SE = 0.064, p &lt; .05).</div></div><div><h3>Conclusions</h3><div>These results highlight a dynamic bidirectional relationship between sleep and alcohol use. Findings suggest that average sleep and alcohol use patterns may be more meaningful to target than a single instance of poor sleep or excessive alcohol use.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"129 ","pages":"Pages 50-57"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008669","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}