Alcohol (Hanover, York County, Pa.)最新文献

{"title":"Socioeconomic Status, Alcohol Use, and Mortality: Results From a Prospective Cohort Study","authors":"Ida Butovetsky,&nbsp;Sophie Baumann,&nbsp;Hans J. Grabe,&nbsp;Carsten Oliver Schmidt,&nbsp;Astrid Petersmann,&nbsp;Matthias Nauck,&nbsp;Lars Schwettmann","doi":"10.1111/acer.70402","DOIUrl":"10.1111/acer.70402","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Both all-cause and alcohol mortality follow a social gradient. Studies have provided evidence of interaction between socioeconomic status (SES) and alcohol use in predicting alcohol-attributable mortality. It is unclear whether this holds true for all-cause mortality. This study examines interaction effects and investigates the role of biomarkers in all-cause mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We included data from 4307 participants of the baseline survey (1997–2001) of SHIP (Study of Health in Pomerania)-START and a mortality follow-up from baseline until January 2023. All-cause mortality was the outcome; exposure variables were income or education as SES proxies, alcohol use, and biomarkers related to chronic alcohol consumption. Confounders were age, sex, marital status, smoking, and Body Mass Index (BMI). We used Cox proportional hazards regression (CPHR) in main analyses and CPHR and Aalen additive hazards regression (AAHR) in interaction analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our final samples (either with income or education) consisted of 3771/3939 individuals of whom 981 (26.0%) and 1047 (28.6%) died during the follow-up period. Adjusting for confounders, individuals with low income (HR = 1.31, CI = 1.11, 1.56; compared to high income) and both current abstainers that formerly consumed alcohol (HR = 1.56, CI = 1.27, 1.92) and individuals with high alcohol intake (HR = 1.31, CI = 1.03, 1.66; compared to individuals with low alcohol intake) showed increased mortality. Biomarkers were positively associated with mortality. There was evidence of statistical interaction effects, for example, increased risks in low-income current abstainers as well as individuals with moderate or high alcohol use.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We found a social gradient in all-cause mortality that was attenuated, but not fully explained, by risk factors. There was some evidence of statistical interaction effects between alcohol use and SES, but small subgroup counts limit the certainty of related conclusions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13545546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FASD Science and Policy Depend on Deeply Phenotyped Prospective Birth Cohorts","authors":"Emilie Bruzelius,&nbsp;R. Colin Carter","doi":"10.1111/acer.70404","DOIUrl":"10.1111/acer.70404","url":null,"abstract":"","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Articles of Public Interest","authors":"","doi":"10.1111/acer.70401","DOIUrl":"10.1111/acer.70401","url":null,"abstract":"","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148814979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling Concurrent Hedonic Disruption During Excessive Drinking and Abstinence-Related Negative Affect in a Novel Selectively Bred Mouse Line: The Crossed High Alcohol Preferring X High Drinking in the Dark (cHAPxHDID) Mice","authors":"Garrett A. Winkler,&nbsp;Nicholas J. Grahame","doi":"10.1111/acer.70400","DOIUrl":"https://doi.org/10.1111/acer.70400","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Alcohol use disorder (AUD) is often comorbid with depressive disorders such as major depressive disorder (MDD). These comorbidities are often modeled by allowing C57BL/6 (B6) mice to drink alcohol and testing for depressive- and anxiety-like phenotypes 2–3 weeks into abstinence; however, it should be noted that B6 mice are both inbred, which may limit external validity, and show modest intakes compared to humans with AUD. We have created a new selectively bred line of high alcohol-preferring mice, the crossed High Alcohol Preferring X High Drinking-in-the-Dark mice (cHAPxHDIDs). The cHAPxHDID mice have not been explored as a model of AUD + MDD comorbidity, nor has their drinking propensity been characterized in any publication to date.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used male and female cHAPxHDID mice and a home cage 2-bottle choice (2BC) paradigm (water/water v. 10% ethanol/water) for 5 weeks across three experiments. We characterized the cHAPxHDIDs' 2BC drinking by measuring intake over a day, along with blood ethanol concentrations (BECs). Additionally, we ran behavioral tests for negative affect at different timepoints in abstinence. Finally, we also probed for the emergence and sustenance of anhedonia during the drinking period with a modified 1% sucrose preference test (SPT).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We found that cHAPxHDID mice drink excessively, especially at the onset of the dark cycle, and achieve average BECs higher than 300 mg/dL. Ethanol drinkers showed increased latency in the novelty-suppressed feeding test (NSFT) at 6 days into abstinence. Alcohol-drinking mice reduced their sucrose intake during the drinking period beginning in Week 2, which normalizes at 48 h into abstinence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The cHAPxHDIDs show some evidence of depressive symptomatology after and during drinking. They drink excessive amounts of alcohol voluntarily, reaching high and sustained BECs. Taken together, our data suggest that the cHAPxHDIDs may be a promising model for excessive drinking and its mood-related comorbidities.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acer.70400","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Influence of Spousal Genotype on Alcohol Problems in Marriage","authors":"Sally I-Chun Kuo,&nbsp;Vivia V. McCutcheon,&nbsp;Fazil Aliev,&nbsp;Kathleen K. Bucholz,&nbsp;Danielle M. Dick,&nbsp;Howard J. Edenberg,&nbsp;Victor Hesselbrock,&nbsp;John R. Kramer,&nbsp;Dongbing Lai,&nbsp;Martin H. Plawecki,&nbsp;Marc A. Schuckit,&nbsp;Jessica E. Salvatore","doi":"10.1111/acer.70399","DOIUrl":"https://doi.org/10.1111/acer.70399","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The field's conventional understanding of how genetic factors impact risk for alcohol use disorder (AUD) typically focuses on direct genetic effects, or how an individual's own genetic predispositions are associated with the likelihood of experiencing clinically significant alcohol problems. More recently, studies of behavioral health outcomes in preclinical and human studies have demonstrated the potential importance of social genetic effects or the influence of a social partner's genotype on substance use and related outcomes. In this study, we sought to characterize social genetic effects for AUD, specifically in the context of marriage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The sample included 660 opposite-sex spousal dyads from the Collaborative Study on the Genetics of Alcoholism, restricted to individuals who were genetically similar to European reference panels. Measured and latent indicators of genetic risk included polygenic scores of problematic alcohol use (PGS_PAU) and parental history of AUD (PH_AUD), respectively. The outcome was Diaganostic and Statistical Manual (DSM)-5 alcohol use disorder criterion count (AUDcrit) during marriage. Multilevel models accounted for the non-independence of partners' data, including correlations between partners' genetic risk and residual covariance in AUDcrit.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After accounting for direct genetic effects (i.e., the influence of one's own genetic predispositions) and the correlations between partners' genetic predispositions, we found that having a spouse with higher PGS_PAU was associated with higher AUDcrit (B = 0.084, 95% CI [0.035, 0.132]). This social genetic effect was robust after adjusting for both partners' educational attainment. Spousal PH_AUD was not associated with AUDcrit. Exploratory analyses indicated that the social genetic effect of spousal PGS_PAU was stronger among male target individuals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Findings highlight the potential importance of social genetic effects for understanding the pathways from genotype to alcohol use disorder and the need for further investigation of latent measures of genetic predispositions in studies of social genetic effects.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acer.70399","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological Inhibition of HDAC6 Transiently Reduces Voluntary Ethanol Consumption in Male Mice","authors":"Kiera Fleck,&nbsp;Jeffery L. Dunning,&nbsp;Max Kreifeldt,&nbsp;Catherine Lopez,&nbsp;Seokjun Jo,&nbsp;Edward Roberts,&nbsp;Candice Contet","doi":"10.1111/acer.70380","DOIUrl":"https://doi.org/10.1111/acer.70380","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Histone deacetylase 6 (HDAC6) inhibition can alleviate depression- and anxiety-like behaviors. Accordingly, HDAC6 may be a promising target to mitigate negative reinforcement in alcohol use disorder (AUD). We previously reported reduced α-tubulin acetylation in mice withdrawn from chronic intermittent ethanol (CIE) vapor inhalation, suggesting potential HDAC6 hyperactivity in this mouse model of AUD. The present study aimed to probe the behavioral significance of this acetylation deficit by testing whether HDAC6 inhibition can reverse ethanol drinking escalation in CIE-exposed mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Male C57BL/6J mice were subjected to limited-access ethanol drinking sessions (two-bottle choice, 2BC) combined with CIE to escalate voluntary ethanol intake relative to air-exposed counterparts (Air). Ethanol and saccharin intake during 2BC was measured after acute and subchronic administration of bavarostat, a brain-penetrant HDAC6 inhibitor. Acetyl-lysine and acetyl-α-tubulin levels were quantified via immunoblotting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Acute administration of bavarostat at 100 mg/kg, but not lower doses, significantly reduced ethanol intake in both Air and CIE mice. Ethanol intake during subchronic administration of 100 mg/kg bavarostat was reduced on the first day in both Air and CIE mice compared to vehicle-treated counterparts, but this effect was lost on subsequent days. CIE mice also consumed more saccharin than Air controls. Bavarostat did not impact saccharin intake in either group. When saccharin was offered along with ethanol, CIE mice consumed significantly more ethanol and less saccharin than Air counterparts, indicating intact taste discrimination. Bavarostat administered prior to brain collection significantly increased acetyl-lysine and acetyl-α-tubulin levels in the frontal cortex, confirming reduced HDAC6 activity. These levels did not differ between Air and CIE mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Systemic administration of bavarostat reduces voluntary ethanol drinking in mice. This effect is dose-dependent, selective for ethanol, independent of ethanol dependence, and transient. These findings support HDAC6 as a viable target to acutely reduce the drive to consume ethanol.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acer.70380","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging Exacerbates Binge Ethanol-Mediated Bone Toxicity in Mice","authors":"Kim B. Pedersen,&nbsp;Mary Bordelon,&nbsp;Epiphany Baker,&nbsp;Meng Luo,&nbsp;Christopher M. Taylor,&nbsp;Jin-Ran Chen,&nbsp;Martin J. Ronis","doi":"10.1111/acer.70384","DOIUrl":"10.1111/acer.70384","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Alcohol consumption and aging are factors promoting osteopenia and osteoporosis. How these factors interact is poorly understood. To investigate this relationship, a binge ethanol exposure model in mice was used to determine how aging affects skeletal responses to binge ethanol.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Dmp1-Cre TdTomato mice with the fluorescent marker TdTomato expressed in osteoblasts and osteocytes, and control mice without Cre expression were used. Mice of both sexes at 12 weeks and 78 weeks of age were gavaged for four consecutive days with 3, 3, 4, and 4.5 g of ethanol/kg of body weight or with PBS (control). Skeletal responses were determined by serum bone turnover markers using ELISA and by gene expression and protein measurement in the femoral shaft and lumbar vertebrae using qRT-PCR and western blots.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Ethanol and aging both significantly decreased serum levels of Procollagen Type I (P1NP) and osteocalcin, indicating reduced bone formation. Serum levels of C-terminal telopeptide of type I collagen (CTX-1) increased significantly with ethanol exposure in the aging mice, reflecting enhanced bone resorption. In the femoral shaft, ethanol and aging increased the expression of genes involved in osteoclast activation, Calcitonin receptor (Calcr) and RANKL, with a significantly larger induction of receptor activator of nuclear factor-κB ligand (RANKL) mRNA in 78-week-old than 12-week-old mice. Expression of osteoblast-associated genes, Collagen Type I Alpha 1 Chain (Col1a1), Collagen Type I Alpha 2 Chain (Col1a2), and Sphingomyelin phosphodiesterase 3 (Smpd3), was downregulated by ethanol, with stronger ethanol-mediated reduction in the 78-week-old than 12-week-old mice. Aging did not decrease the expression of TdTomato mRNA or TdTomato protein, indicating no overall loss of osteoblasts and osteocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Binge ethanol exposure and aging independently and synergistically disrupt bone remodeling by inhibiting bone formation and enhancing bone resorption.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-Term Risk Stratification in Alcohol-Associated Hepatitis: Small HDL Particles and Inflammation Vulnerability Index Values Improve Model for End-Stage Liver Disease","authors":"Eduardo Vilar-Gomez,&nbsp;Margery A. Connelly,&nbsp;Vijay H. Shah,&nbsp;Irina Shalaurova,&nbsp;Jill M. Rafalko,&nbsp;Arun J. Sanyal,&nbsp;Naga P. Chalasani,&nbsp;Samer Gawrieh,&nbsp;TREAT Consortium","doi":"10.1111/acer.70388","DOIUrl":"10.1111/acer.70388","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Alcohol-associated hepatitis (AH) has high short-term mortality, whereas current prognostic models mainly reflect liver and renal dysfunction. The Metabolic Vulnerability Index (MVX) is a nuclear magnetic resonance-derived score comprising the Inflammation Vulnerability Index (IVX; small high-density lipoprotein particles [S-HDL-P] and GlycA) and the Metabolic Malnutrition Index (MMX). We evaluated whether MVX, IVX, and IVX components improve 90-day mortality prediction beyond Model for End-Stage Liver Disease (MELD) in AH.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Serum samples from 196 patients with AH, 169 heavy-drinking controls, and 351 healthy controls were analyzed by nuclear magnetic resonance spectroscopy. The primary outcome was 90-day AH-related mortality. Biomarkers were modeled continuously after standardization within the AH cohort; S-HDL-P was modeled per 1 SD decrease. Cox models were adjusted for MELD, age, sex, white blood cell count, and baseline antibiotic or corticosteroid use. Model performance was assessed using Akaike information criterion (AIC), likelihood-ratio testing, and Harrell's <i>C</i>-statistic.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among patients with AH, 30 AH-related deaths occurred within 90 days (15.3%). IVX and MVX were highest in AH cases and increased with AH severity, whereas MMX did not consistently differentiate severity. Lower S-HDL-P was independently associated with 90-day mortality in fully adjusted models (HR, 1.84; 95% CI, 1.01–3.35; <i>p</i> = 0.045), whereas GlycA was not (HR, 0.86; 95% CI, 0.54–1.37; <i>p</i> = 0.527). Adding S-HDL-P improved fully adjusted MELD-based model fit (AIC, 298.97 vs. 301.46; LR <i>p</i> = 0.034; <i>C</i>-statistic, 0.741 vs. 0.729). IVX showed supportive improvement in model fit and discrimination (AIC, 299.81; LR <i>p</i> = 0.056; <i>C</i>-statistic, 0.749). Continuous MELD interaction analyses supported risk separation for S-HDL-P (LR <i>χ</i>² = 6.20; <i>p</i> = 0.045) and IVX (LR <i>χ</i>² = 6.64; <i>p</i> = 0.036).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Lower S-HDL-P appears to be the principal short-term prognostic component within the IVX domain in AH. S-HDL-P and IVX may refine MELD-based 90-day risk stratification, pending external validation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148703005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative Three-Dimensional Characterization of Facial Dysmorphism in Self-Identified African-American Individuals With Prenatal Alcohol Exposure","authors":"Qing Li,&nbsp;Zahra Mozaffarian,&nbsp;Hanie Moghaddasi,&nbsp;Claire D. Coles,&nbsp;Julie A. Kable,&nbsp;Sarah N. Mattson,&nbsp;Jeffrey R. Wozniak,&nbsp;Kenneth Lyons Jones,&nbsp;Miguel del Campo,&nbsp;Leah Wetherill,&nbsp;Michael Suttie,&nbsp;the CIFASD Consortium","doi":"10.1111/acer.70396","DOIUrl":"10.1111/acer.70396","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The objective of this study was to characterize facial dysmorphology in a self-identified African-American cohort of children with prenatal alcohol exposure (PAE) and to evaluate the utility of computer vision-based methods for quantitative assessment and screening of facial form.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 307 self-identified African-American individuals were evaluated by expert dysmorphologists and classified according to PAE status as unexposed controls (controls), individuals with prenatal alcohol exposed without fetal alcohol syndrome (FAS)-associated physical features (AE), or individuals with prenatal alcohol exposed with FAS-associated physical features (AE-FAS). Three-dimensional (3D) facial images were analyzed using volumetric and measurement-based approaches. Statistical shape modeling was applied to support surface-based analysis, cluster identification, and group discrimination testing.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>(i) Facial growth in the AE-FAS group was significantly reduced. (ii) We observed a subgroup of AE clinically without FAS-associated physical features who displayed an affinity to the AE-FAS group in the unscaled models. (iii) Sex-stratified analyses revealed alcohol-associated alterations in sexual dimorphism of facial morphology, with a substantially stronger association between PAE and reduced facial growth in females than in males. (iv) Unique patterns of facial dysmorphology were exhibited in the AE group, showing underdevelopment of the zygomatic arch. (v) Using closest mean, support vector machine, and linear discriminant analysis, discrimination between AE-FAS and controls was moderate.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>3D facial analysis facilitates recognition of potential sex-related differences in facial morphology associated with PAE in African-American children, a population underrepresented in the clinical literature. The distinct patterns of dysmorphology observed may contribute to improved phenotypic characterization and diagnostic support.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13451575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148690345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Digital Cognitive Behavioral Therapy Reduces Heavy Drinking Among a Non-Treatment Sample of People With Alcohol Use Disorder: A Feasibility Trial With CBT4CBT","authors":"Anna Beth Parlier-Ahmad,&nbsp;Nicole Boss,&nbsp;Amber R. Green,&nbsp;Michelle Eglovitch,&nbsp;Ren Huang,&nbsp;Caitlin E. Martin,&nbsp;Lori Keyser-Marcus,&nbsp;Dace S. Svikis","doi":"10.1111/acer.70383","DOIUrl":"10.1111/acer.70383","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Most people with alcohol use disorder (AUD) do not receive treatment. Few digital evidence-based treatments have been tested among community-based samples of people with AUD. The present trial of Computer-Based Training for Cognitive Behavioral Therapy (CBT4CBT) (1) assessed CBT4CBT usability and acceptability and (2) explored alcohol-related outcomes by study condition in a non-treatment sample of people with AUD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>For the current two-arm clinical trial, a non-treatment sample of people with lifetime AUD and current heavy drinking was recruited using ResearchMatch.org and randomized (3:1) to the CBT4CBT program or an assessment-only control, stratified by sex (<i>N</i> = 160 total; CBT: <i>n</i> = 109; Co: <i>n</i> = 51). Study assessments included post-intervention acceptability ratings and self-reported alcohol-related measures administered at baseline, post-intervention, and 1-month follow-up.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Participants were 68.1% female and 31.9% male, in their early forties (<i>M</i> = 42.6, SD = 15.7, range 19–76 years). Most participants identified as white (65.0%) or Black (27.5%) and non-Latinx (89.4%). Acceptability ratings and usability measures for CBT4CBT were favorable and comparable to studies among clinical treatment samples. Participants in the CBT4CBT group demonstrated faster reductions in the percentage of drinking days and were significantly less likely to report any heavy drinking days than those in the control condition at 1-month follow-up. The CBT4CBT group reported higher recovery scores than the control group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The present study provides benchmark data on the use of CBT4CBT in a sample of people with AUD not receiving treatment. Findings have important clinical and research implications for expanding the reach of evidence-based addiction treatment beyond traditional treatment settings.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148681403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}