Samantha G. Skinner, Eliana G. Aleman, Julio Rivera, Nikhila Kalapatapu, Dhruv Kantilal, Daryl L. Davies, Liana Asatryan
{"title":"Alcohol-Induced Early-Stage Liver Injury Contributes to Increases in Voluntary Alcohol Intake and Cognitive Deficits in Mice","authors":"Samantha G. Skinner, Eliana G. Aleman, Julio Rivera, Nikhila Kalapatapu, Dhruv Kantilal, Daryl L. Davies, Liana Asatryan","doi":"10.1111/acer.70391","DOIUrl":"10.1111/acer.70391","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Liver–brain communication is increasingly recognized as a potential contributor to vulnerability to alcohol use disorder (AUD). However, the behavioral consequences of early alcohol-associated liver disease (ALD) remain underexplored. This study aimed to determine whether alcohol-induced hepatic injury influences subsequent alcohol consumption and cognitive outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Female C57BL/6J mice were fed a Lieber–DeCarli (LDC) ethanol diet to induce early-stage ALD-like pathology, followed by a voluntary two-bottle choice (TBC) paradigm measuring alcohol consumption. Behavioral assessments included novel object recognition, T-maze with spontaneous alternation, and elevated plus maze. Hepatic steatosis was measured by histology and triglyceride quantification; inflammatory gene expression was evaluated by RT-qPCR, and hippocampal BDNF/TrkB signaling was investigated by western blot.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>LDC mice on an ethanol diet developed hepatic steatosis and hepatomegaly compared with controls. These mice also consumed significantly more alcohol during initial TBC testing, with intake positively correlated with the degree of steatosis. Hepatic steatosis was transient, recovering by the end of TBC period with accompanied upregulation of inflammatory markers and evidence suggestive of neutrophilic infiltration in ethanol-exposed mice. These mice also exhibited impaired spatial working memory without significant differences in long-term recognition or anxiety-like behavior in the elevated plus maze. In addition, ethanol exposure was associated with reduced hippocampal expression of BDNF and its receptor TrkB.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that alcohol-induced early hepatic injury may contribute to increased alcohol consumption and impaired spatial working memory performance paralleling sustained hepatic inflammation and dysfunction in neurotrophic signaling. Further investigation is warranted to elucidate the mechanisms underlying liver–brain communication in the context of AUD and ALD progression.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674609","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}
Andrew M. Ballester, Felicia W. Chi, Stacy A. Sterling
{"title":"Association Between Alcohol Brief Intervention and Emergency Department and Inpatient Utilization Over 2 Years","authors":"Andrew M. Ballester, Felicia W. Chi, Stacy A. Sterling","doi":"10.1111/acer.70395","DOIUrl":"10.1111/acer.70395","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Brief Interventions (BIs) in primary care are an effective, evidence-based tool for reducing the cost and harm associated with unhealthy alcohol use. However, little is known about the impact of alcohol BIs on the utilization of acute healthcare services over time. This study aims to examine the association between receiving a BI in the outpatient setting and Emergency Department (ED) and inpatient utilization over 2 years among adults screening positive for unhealthy alcohol use.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This population-based, retrospective observational study utilized electronic health record (EHR) data collected between January 1, 2013 and June 30, 2019 of 254,190 adult primary care patients who screened positive for unhealthy alcohol use. Patients were grouped by whether or not they received a BI for unhealthy alcohol use from their primary physician at the index date. ED and inpatient utilization was assessed for each 6-month interval following the index screening up to 24 months. Separate generalized estimating equation (GEE) logistic models with inverse probability treatment weighting (IPTW) were fit to examine the associations between BI receipt and ED and inpatient utilization over the 2-year follow-up period.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>IPTW GEE models indicated that receiving BI was associated with significantly lower odds of ED (aOR [95% CI] = 0.96 [0.94–0.98]) and inpatient utilization (aOR [95% CI] = 0.96 [0.93–1.00]) over the 2-year follow-up period. However, the association between BI and ED utilization attenuated over time, and receiving a BI was only significantly associated with lower inpatient utilization in the first 6 months following index.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The observed reductions in ED and inpatient utilization contribute novel insight into the duration of BI's harm-reduction effects. Ultimately, our findings support widespread implementation of BI programs in primary care settings as a means of reducing acute healthcare utilization.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674642","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}
Tareq Al-Ahdal, Brenda Cabrera-Mendoza, Stefan Listl, Renato Polimanti
{"title":"Deciphering the Relationship Between Alcohol Consumption, Oropharyngeal Cancers, and Socioeconomic Determinants","authors":"Tareq Al-Ahdal, Brenda Cabrera-Mendoza, Stefan Listl, Renato Polimanti","doi":"10.1111/acer.70393","DOIUrl":"10.1111/acer.70393","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Alcohol drinking is a major risk factor for oropharyngeal cancer, yet the nature of risk differences across drinking patterns remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We leveraged data from large-scale genome-wide association studies to conduct Mendelian randomization analyses, assessing the effects of alcohol intake with meals, intake frequency, maximum habitual intake, and drinks per week on risks of oral cavity cancer, pharyngeal cancer, stomatitis, lichen planus, and oral leucoplakia. Multiple Mendelian randomization methods were applied to model pleiotropic effects, and multivariable analysis was performed to evaluate the interplay between alcohol consumption and household income.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Alcohol intake frequency was associated with increased risk of oral and pharyngeal cancer. In contrast, alcohol intake with meals showed an apparent protective association with these outcomes, which was nullified after adjusting for household income in the multivariable analysis—indicating that the observed benefit was explained by higher socioeconomic status. The frequency-risk relationship remained significant after adjustment, highlighting intake frequency as an independent risk factor under MR assumptions. The number of drinks per week was linked to increased stomatitis risk, and this association remained significant after accounting for household income, suggesting an independent effect of alcohol consumption on stomatitis risk under MR assumptions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Cancer prevention strategies should target harmful alcohol consumption patterns with attention to drinking frequency and socioeconomic context, rather than treating alcohol exposure as monolithic.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674591","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}
Eric Kan, Andrew T. Marshall, Deborah Jonker, Letitia Butler-Kruger, Weslin Charles, Asheeqa Petersen, Lucy T. Brink, Jonathan C. Ipser, Shantanu H. Joshi, Katherine L. Narr, Hein J. Odendaal, Freda Scheffler, Kirsten A. Donald, Dan J. Stein, Elizabeth R. Sowell
{"title":"Prenatal Alcohol and/or Tobacco Exposure, White-Matter Microstructure, and Cognition: Analyzing a South African Birth Cohort With Neurite Orientation and Dendrite Dispersion Imaging","authors":"Eric Kan, Andrew T. Marshall, Deborah Jonker, Letitia Butler-Kruger, Weslin Charles, Asheeqa Petersen, Lucy T. Brink, Jonathan C. Ipser, Shantanu H. Joshi, Katherine L. Narr, Hein J. Odendaal, Freda Scheffler, Kirsten A. Donald, Dan J. Stein, Elizabeth R. Sowell","doi":"10.1111/acer.70387","DOIUrl":"10.1111/acer.70387","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Prenatal exposure to alcohol (PAE) and/or tobacco (PTE) may impact neurobiological and cognitive development years after such exposures have occurred. While such effects on cortical gray matter and cognition are widely researched, there is less research on the effects of PAE and PTE on white-matter development and cognition, particularly in non-clinical, community samples.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed white-matter microstructure and its cognitive correlates in four hundred and sixty five 8–12-year-olds in the urban Cape Town region of South Africa: 192 were prenatally exposed to alcohol <i>and</i> tobacco (PAE + PTE), 73 to tobacco only (PTE), 102 to alcohol only (PAE), and 98 to neither tobacco nor alcohol (CON). White-matter microstructure was quantified via neurite orientation and dendrite dispersion imaging (NODDI). The outcome variables were fractional anisotropy (FA), the neurite density index (NDI), and neurite orientation dispersion index (ODI) for 52 white-matter tracts. Cognition was measured using the Wechsler Intelligence Scale for Children—Fifth Edition (WISC-V).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>PAE (but not PTE) was associated with NDI in 35 of 52 white-matter tracts analyzed. There were no false-discovery-rate (FDR) corrected main effects of PAE or PTE on FA or ODI. For 17 of the 35 tracts affected by PAE, the corresponding NDIs were positively associated with scores on the WISC-V Processing Speed Index.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our previous research of neuroanatomical structure in this cohort suggested that there are stronger effects of PTE on cortical gray matter. In contrast, the present data suggest that PAE may have stronger associations with white-matter microstructure, with such effects potentially manifesting as downstream deficits in processing speed.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674446","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}
Sundararajan Mahalingam, Ramesh Bellamkonda, Kusum K. Kharbanda, Ojeshvi Ethiraj, Carol A. Casey, Karuna Rasineni
{"title":"Alcohol Exposure Alters the Ghrelin System: In Vitro Mechanistic Insights Into Impaired Glucose Sensing and Enhanced Ghrelin Secretion","authors":"Sundararajan Mahalingam, Ramesh Bellamkonda, Kusum K. Kharbanda, Ojeshvi Ethiraj, Carol A. Casey, Karuna Rasineni","doi":"10.1111/acer.70392","DOIUrl":"10.1111/acer.70392","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Ghrelin, a stomach-derived orexigenic peptide, typically rises during fasting to stimulate food intake. Chronic alcohol consumption elevates circulating ghrelin, which induces alcohol craving and increases intake in clinical and preclinical models. By increasing alcohol drive, ghrelin contributes to alcohol use disorder (AUD) and accelerates alcohol-associated liver disease (ALD) by inhibiting insulin secretion and promoting adipose lipolysis. However, the cellular mechanisms by which ethanol dysregulates ghrelin secretion remain unclear. This study investigated how ethanol modulates ghrelin production and disrupts nutrient sensing in ghrelin-secreting cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Stomach (SG-1) and pancreatic (PG-1) ghrelinoma cells were treated with 25 mM or 50 mM ethanol for 48 h, after which ghrelin synthesis and secretion were measured. Further, the interaction between ethanol and other physiological regulators (glucose [10 mM], insulin [20 mM], and palmitic acid [400 μM]) of ghrelin secretion was evaluated. Intracellular glycolytic rate was characterized using Seahorse-XFe analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Chronic ethanol exposure (48 h) significantly increased ghrelin secretion and the mRNA encoding for ghrelin and ghrelin O-acyltransferase (GOAT), an enzyme that activates ghrelin. Under normal conditions, high glucose effectively suppressed ghrelin secretion; however, ethanol pretreatment blunted this inhibitory effect. While palmitic acid alone had no effect, its combination with ethanol synergistically enhanced ghrelin secretion. Mechanistically, ethanol-pretreated cells exhibited a metabolic impairment characterized by increased glucose uptake but significantly reduced basal glycolysis, proton efflux rate (PER), and compensatory glycolytic capacity. This metabolic failure was linked to the profound downregulation of the rate-limiting enzymes glucokinase, hexokinase, and pyruvate kinase.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Ethanol drives increased ghrelin by disrupting the glucose-sensing machinery within ghrelin-secreting cells. By suppressing key glycolytic enzymes, ethanol uncouples the cell from glucose, mimicking a state of starvation despite nutrient availability. Targeting these metabolic pathways may provide a novel therapeutic strategy for the interconnected pathologies of AUD and ALD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13438128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674611","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":"Youth Involvement in Family Drinking and Parental Permission to Sip/Taste Alcohol: A Test of an Early Risk Pathway to Perceived Parental Approval of Underage Alcohol Use","authors":"Bernard Pereda, Craig R. Colder","doi":"10.1111/acer.70354","DOIUrl":"10.1111/acer.70354","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Several alcohol-specific parenting behaviors are associated with adolescent alcohol use. An important next step in the literature is integrating these behaviors into unified risk pathways, which have the potential to inform preventive interventions and public health messaging. Youth involvement in family drinking (i.e., asking children to fetch, pour, and open drinks) reflects parental-approved contact with alcohol, which may present the opportunity for sipping/tasting alcohol with parental permission. In turn, sipping/tasting alcohol with parental permission may increase adolescents' perceived parental approval of underage drinking, a known risk factor for alcohol use later in adolescence and young adulthood. This indirect pathway was tested and sensation seeking was posited as a moderator of the association between youth involvement in family drinking and sipping/tasting alcohol with parental permission.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The community sample included 260 parent-teen dyads (adolescents aged 11–12 years; 60.85% White, 28.9% Black or African American, 2.33% Asian, 1.16% American Indian or Alaska Native, and 7.36% identified as “more than one race”). Hypotheses were tested using path modeling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Youth involvement in family drinking was positively associated with sipping/tasting with parental permission and perceived parental approval of underage alcohol use. Sipping/tasting with parental permission was not associated with perceived parental approval of underage alcohol use. Moderation was not supported.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Youth involvement in family drinking may be the start of an early risk pathway that facilitates sipping/tasting with parental permission and directly shapes adolescent perceptions of parental approval of underage alcohol use. Lack of moderation may suggest that progression to sipping/tasting is driven more strongly by a family environment that approves of alcohol exposure rather than adolescent temperament. Findings highlight the utility of considering different alcohol-specific parenting practices mechanistically in risk models.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671365","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":"Increased Prevalence of Rare Copy Number Variants in Australian Children With Fetal Alcohol Spectrum Disorder: Experience in a State-Wide Diagnostic Service","authors":"Suzy Byrnes, Felicity Collins, Elizabeth Elliott","doi":"10.1111/acer.70352","DOIUrl":"10.1111/acer.70352","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Prenatal alcohol exposure (PAE) can result in fetal alcohol spectrum disorder (FASD), a permanent, heterogeneous condition characterized by severe neurodevelopmental impairments with or without microcephaly, characteristic facial dysmorphology, and congenital anomalies. Clinical and pre-clinical studies suggest that genetic factors, in the mother or fetus, influence the phenotypic outcomes following PAE. The objectives of this study were to evaluate the prevalence and types of DNA copy number variants (CNVs) in children (0–18 years) diagnosed with FASD and to identify genes known to be associated with neurodevelopmental disorders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Chromosomal microarray (CMA) was performed in children diagnosed with FASD in the NSW CICADA FASD Service—a state-wide multidisciplinary diagnostic clinic in Australia. We performed a retrospective chart review of 175 patients diagnosed with FASD between 2015 and 2022 to obtain data on medical and family history, phenotype, and genotype. All CMA results were reviewed by a clinical geneticist.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A rare CNV was identified in 38 of 157 (24.2%) patients who had CMA testing and 40 unique CNVs were identified. In four patients, a neurodevelopmental susceptibility syndrome was identified including Xq28 microduplication syndrome, 16p12.2 microdeletion syndrome, 17q11.2 microduplication syndrome, and an atypical variant of 22q11.2 deletion syndrome. Two children had incidental pathogenic variants. In 32 of 38 (84.2%) cases with a rare CNV, 34 variants of unknown significance (VOUS) were identified, of which 13 encoded a total of 14 genes associated with common neurodevelopmental disorders. Three variants of uncertain significance (VOUS) encoded different subunits of the voltage-dependent calcium channel complex protein (CACNB2, CACNA1A, CACNA2D3).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These novel results suggest that approximately one in four children diagnosed with FASD may harbor a rare CNV, of which 85.0% are currently of uncertain clinical significance. Genetic testing can support the FASD diagnostic process and may reveal additional diagnoses or sources of genetic vulnerability to FASD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13431349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671386","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}
Celisse Bibr, Kelly D. Harding, Kathy Unsworth, Cherise Carlaw, Ben Balfour, Jacqueline Pei
{"title":"Building Toward Better Housing for Canadians With Fetal Alcohol Spectrum Disorder","authors":"Celisse Bibr, Kelly D. Harding, Kathy Unsworth, Cherise Carlaw, Ben Balfour, Jacqueline Pei","doi":"10.1111/acer.70351","DOIUrl":"10.1111/acer.70351","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Individuals with disabilities have a right to live independently, be included within their communities, and have adequate standards of living and social protections. However, individuals with fetal alcohol spectrum disorder (FASD) experience elevated obstacles to obtaining and maintaining housing. In addition to brain-based differences that can create barriers to successful navigation of daily demands, many individuals with FASD experience mental health concerns, substance use, or trauma, and the experience of being houseless is, in itself, traumatic. These factors often compound, leaving individuals with FASD disproportionately affected by the ongoing housing and cost of living crisis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study brought together 47 Canadian housing providers, youth with FASD, caregivers, researchers, and policy makers to understand the challenges and opportunities for housing options for individuals with FASD. Reflexive thematic analysis was conducted to explore the aim of the research: individuals' living experiences, perspectives, and recommendations on what safe and stable housing for individuals with FASD could look like.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Four themes were generated describing how housing experiences for individuals with FASD could be improved: (1) being able to access all that is needed for housing; (2) embracing individuality and the pitfalls of blanket approaches; (3) working as a team to foster interdependency; and (4) the need for greater understanding of FASD across all sectors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The results of this study provide vital insights on the needs of individuals with FASD in the context of housing and suggest ways forward to reduce the disproportionate impact of the Canadian housing crisis on individuals with FASD and their families.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671378","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}
Kyler S. Knapp, Braden K. Linn, Junru Zhao, Gregory E. Wilding, Scott F. Coffey, Suzy B. Gulliver, Clara M. Bradizza, Paul R. Stasiewicz
{"title":"Emotion Regulation Treatment for Alcohol Use Disorder: Results of a Stage II Randomized Clinical Efficacy Trial","authors":"Kyler S. Knapp, Braden K. Linn, Junru Zhao, Gregory E. Wilding, Scott F. Coffey, Suzy B. Gulliver, Clara M. Bradizza, Paul R. Stasiewicz","doi":"10.1111/acer.70350","DOIUrl":"10.1111/acer.70350","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Despite strong links between emotion regulation (ER) difficulties and problem drinking, few studies have directly addressed whether interventions that target ER positively impact drinking outcomes. In a prior Stage 1a/1b behavioral therapies development study, we developed an Emotion Regulation Treatment (ERT) for alcohol use disorder (AUD) that included strategies addressing prolonged direct experiencing of emotion, mindfulness, and coping and distress tolerance. Results demonstrated the feasibility and initial efficacy of ERT as a supplement to cognitive behavioral therapy (CBT) for AUD. Based on this initial success, the current study reports on a fully powered stage II randomized clinical efficacy trial to compare CBT plus ERT (CBT + ERT) to CBT plus an active health and lifestyles (HLS) control (CBT + HLS) and explore potential mechanisms of action.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Adults (<i>n</i> = 194) with moderate-to-severe AUD were enrolled in 12 week outpatient treatment and randomized to either the CBT + ERT or CBT + HLS treatment condition. Analyses evaluated (1) the impact of treatment condition on percent days abstinent (PDA) and percent heavy drinking days (PHDD) at end of treatment (EOT) and 3, 6, and 12 months posttreatment, and (2) whether change trajectories of negative affect, craving, mindfulness, cognitive reappraisal, or adaptive alcohol coping, assessed daily or weekly during treatment, partially accounted for associations between treatment condition and EOT alcohol outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The CBT + ERT group had greater PDA at all posttreatment follow-ups relative to the CBT + HLS group. There were no group differences in PHDD. Levels of PDA and PHDD did not change across posttreatment follow-ups for either group. The CBT + ERT group exhibited greater adaptive alcohol coping across the first week of treatment, which in turn was associated with higher PDA and lower PHDD at EOT. No other mediation effects were detected.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>CBT + ERT was associated with greater PDA at EOT relative to CBT + HLS, an association that was partially explained by greater adaptive coping early in treatment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671353","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}
Roberto Andrade, M. Windy McNerney, Eric P. Kraybill, Claudia B. Padula, Timothy C. Durazzo
{"title":"The OPRM1 A118G G Allele Is Associated With Poorer Auditory-Verbal Learning and Memory, Executive Functions, and Working Memory in Veterans Undergoing Residential Treatment for Alcohol Use Disorder","authors":"Roberto Andrade, M. Windy McNerney, Eric P. Kraybill, Claudia B. Padula, Timothy C. Durazzo","doi":"10.1111/acer.70385","DOIUrl":"10.1111/acer.70385","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The neurocognitive dysfunction observed in Alcohol Use Disorder (AUD) is related to a complex interplay between genetic, neurobiological, and environmental factors. The μ-opioid receptor (MOR), encoded by the <i>OPRM1</i> gene, modulates reward processing, stress responsivity, and excitatory–inhibitory activity within prefrontal–limbic and hippocampal circuits implicated in neurocognition. The common A118G (Asn40Asp, rs1799971) polymorphism alters MOR expression and signaling, but its contribution to domain-specific cognitive functioning in AUD, particularly among Veterans, has received limited investigation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Veterans (<i>n</i> = 127) in residential treatment for AUD completed a neurocognitive battery assessing the following domains of functioning: auditory-verbal and visuospatial learning and memory, executive function, and working memory. Participants were genotyped for <i>OPRM1</i> A118G, and A homozygotes and G-allele carriers (AG/GG) were compared on the above measures, using bootstrapped generalized linear models, adjusted for age, education, biological sex, race, pre-study alcohol consumption, and brain-derived neurotrophic factor (<i>BDNF</i>) (rs6265) and catechol-O-methyltransferase (<i>COMT</i>) (rs4680) genotypes, which have been previously shown to be associated with neurocognition.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>G-allele carriers demonstrated significantly worse performance than A homozygotes on measures of auditory-verbal learning and memory, cognitive flexibility/set shifting, auditory working memory, and on a composite average of all measures. <i>BDNF</i> or <i>COMT</i> genotypes were not associated with any measure, and there were no significant interactions among <i>OPRM1</i>, <i>BDNF</i>, and <i>COMT</i> genotypes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Findings suggest that altered MOR signaling in G-allele carriers may be associated with differences in prefrontal network efficiency, potentially justifying future studies investigating the relationship between <i>OPRM1</i> and glutamatergic plasticity. The results highlight a potential genetically influenced contributor to the neurocognitive heterogeneity in AUD and underscore the possible value of integrating MOR-related biological markers into neurocognitive assessment of individuals with AUD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"50 8","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148665237","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}