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PubMed2025

Association of alcohol and different types of alcoholic beverages on the risk of buccal mucosa cancer in Indian men: a multicentre case-control study.

INTRODUCTION: While a large proportion of buccal mucosa cancer (BMC) is attributed to tobacco use, the contribution of alcohol is little-known. In India, alcohols include internationally-recognised (IRL) and locally-brewed liquor (LBL) types, which might contribute differently to the risk of BMC. We conducted an observational study to evaluate the association of local and foreign alcoholic beverage use on the risk of developing BMC. METHODS: Data from 1803 BMC cases and 1903 visitor controls from a multicentric case-control study was analysed for 11 IRLs and 30 LBLs. Healthy visitor controls were randomly sampled from the source population of the study centres which enrolled the cases. Quantitative data on the amount, the number of times consumed per day or week, and the lifetime duration of consumption for each of the alcoholic beverages were collected using an interviewer administered standardised questionnaire, which was then used to estimate the grams per day consumption of alcohol. Odds ratios (OR) and 95% CI were estimated after adjustment for potential confounders, including tobacco use. The joint effect of tobacco and alcohol on BMC risk, the attributable fraction (AF) of cases and state-wise population attributable fraction (PAF) were estimated. RESULTS: An increased risk of 1.68 (95% CI=1.44-1.97), 1.72 (95% CI=1.46-2.04), and 1.87 (95% CI=1.46-2.39) was observed for ever-users of any alcohol, IRLs and LBLs, respectively for BMC. The findings show 9 grams/day of alcohol increased the risk of BMC by approximately 50%, and 62% of cases could be attributed to alcohol drinking and chewing tobacco, with an overall PAF of 11.3% for India. CONCLUSION: This study shows that alcohol, even in low quantities, increases the risk for BMC. Prevention of consumption of tobacco and alcohol together could substantially reduce the incidence of BMC.

Humans↗

PubMed2026

The effectiveness of protective behavioral strategies for reducing alcohol use and alcohol-related harms among adults: A systematic review and meta-analysis of randomized controlled trials.

OBJECTIVES: Excessive alcohol consumption is a major public health concern. Protective behavioral strategies (PBS) are widely incorporated into alcohol interventions, but their effectiveness and role as mechanisms of behavior change remain unclear. This systematic review and meta-analysis evaluated the effects of PBS-based interventions on alcohol consumption, alcohol-related harms, and PBS use. METHODS: PubMed, Embase, Scopus, CINAHL, and ProQuest were searched from inception to December 2025 for randomized controlled trials (RCTs) of adults (≥18 years) delivering PBS as an active intervention component. Random-effects meta-analyses using Hedges' g examined alcohol quantity, drinking frequency, alcohol-related problems, and PBS use. RESULTS: Fifteen RCTs were included, predominantly involving young adults attending U.S. universities. PBS interventions increased protective strategy use (g=0.23, p=0.005 after outlier removal), but alcohol effects were modest: no change in quantity (g=-0.05, p=0.162), small reduction in frequency (g=-0.09, p=0.014), and marginal reduction in problems (g=-0.07, p=0.052; significant in sensitivity analysis). Subgroup findings suggested greater effects at longer follow-up and when PBS was incorporated into multi-component interventions. Evidence supporting PBS as a mechanism of change was limited and inconsistent. CONCLUSIONS: PBS-based interventions produce modest, context-dependent effects on alcohol outcomes. Most evidence comes from young U.S. university students, underscoring the need for studies in more diverse adult populations and further mechanistic research.

Humans↗

PubMed2026

No association between alcohol consumption and hip osteoarthritis: a diverse national analysis of 87,585 adults from the "All of Us" research program.

INTRODUCTION: Hip osteoarthritis (OA) is estimated to affect 62.6 million individuals by 2050. A probable link exists between alcohol use and hip OA. However, the results are inconsistent, and the relationship between alcohol and hip OA remains speculative. To address these gaps, this study aimed to utilize the diverse, nationally representative All of Us Research Program dataset to explore the association between alcohol consumption and hip OA. METHODS: This retrospective case-control study utilized data from the All of Us Research Program Controlled Tier Dataset v8. 17,517 hip OA cases and 70,068 controls were identified. A 1:4 case-to-control matching ratio was applied based on age and sex. Alcohol use frequency was categorized into five levels: Never, Monthly or Less, Two to Four Times per Month, Two to Three Times per Week, and Four or More Times per Week. Multivariable logistic regression models evaluated the association between alcohol use frequency and hip OA after adjusting for demographic and clinical variables. RESULTS: Multivariable analysis found that alcohol use frequency was not significantly associated with hip OA. Compared to never users, participants with low (OR 0.98, 95% CI 0.93-1.04, P = 0.583), moderate (OR 0.99-1.01, all P > 0.05), and high (OR 1.02, 95% CI 0.95-1.09, P = 0.599) levels of alcohol consumption had no statistically significant differences in odds of hip OA. Female sex, Asian race, diabetes, hypertension, hyperlipidemia, and nicotine dependence increased the odds of hip OA. CONCLUSION: Any level of alcohol consumption was not significantly associated with the odds of hip OA. This study adds valuable insight to the current body of conflicting evidence. Further prospective studies appear warranted to shed light on the long-term effects of different alcoholic beverages on different joints. Key Points • This study found no significant association between any degree of alcohol consumption and the odds of developing hip osteoarthritis. • Utilizing data from 87,585 adults in the NIH "All of Us" Research Program, this is the first study to analyze this relationship in a large, nationally representative population. • The research provides clarity to previously conflicting literature by demonstrating that alcohol lacks a clear harmful or protective effect on the clinical course of the disease. • The analysis highlights that independent risk factors such as Asian race, nicotine dependence, and components of metabolic syndrome increase the odds of hip osteoarthritis.

Humans↗

PubMed2022

FGF21 suppresses alcohol consumption through an amygdalo-striatal circuit.

Excessive alcohol consumption is a major health and social issue in our society. Pharmacologic administration of the endocrine hormone fibroblast growth factor 21 (FGF21) suppresses alcohol consumption through actions in the brain in rodents, and genome-wide association studies have identified single nucleotide polymorphisms in genes involved with FGF21 signaling as being associated with increased alcohol consumption in humans. However, the neural circuit(s) through which FGF21 signals to suppress alcohol consumption are unknown, as are its effects on alcohol consumption in higher organisms. Here, we demonstrate that administration of an FGF21 analog to alcohol-preferring non-human primates reduces alcohol intake by 50%. Further, we reveal that FGF21 suppresses alcohol consumption through a projection-specific subpopulation of KLB-expressing neurons in the basolateral amygdala. Our results illustrate how FGF21 suppresses alcohol consumption through a specific population of neurons in the brain and demonstrate its therapeutic potential in non-human primate models of excessive alcohol consumption.

Alcohol Drinking↗

PubMed2025

Global Changes in Gene Expression and Splicing in Alcoholic Liver Disease.

Alcohol use disorder is a widespread illness commonly leading to alcoholic liver disease (ALD) and cirrhosis with an increased incidence of hepatocellular carcinoma (HCC), but the mechanisms of alcohol-related oncogenesis in the liver are incompletely understood. We tested the hypothesis that ALD predisposes to HCC via dysregulation of splicing. RNA sequencing was performed on liver biopsies from patients with different stages of ALD: early alcoholic steatohepatitis (eASH), non-severe alcoholic hepatitis (nsAH), and severe alcoholic hepatitis (sAH); furthermore, explants were collected from patients who underwent liver transplantation due to sAH (exAH). We found that alcohol caused widespread changes in transcriptome in all stages of ALD: among ~ 58,000 analyzed genomic features, ~ 4,900 were altered in eASH, ~ 9,100 - in nsAH, 14,100 - in sAH, and ~ 14,300 - in exAH. We observed thousands of missplicing events in all hepatic conditions, with mutually exclusive exons (MEE) being the most common event and exon skipping (ES) - second most common event. Analysis of ~ 600,000 exons revealed that ALD is associated with a genome-wide effect on exon expression, with ~ 50,000 exons being differentially expressed in eASH, ~ 130,000 - in nsAH, ~ 150,000 - in sAH, and ~ 120,000 - in exAH. To determine whether alcohol directly perturbs splicing, we subjected rats to alcohol vapor for 7 weeks and found that the expression of multiple snRNAs was drastically decreased, while expression of splicing factors was not affected. Screening of oncogenes and tumor suppressors, commonly involved in HCC pathogenesis, revealed that ALD affected the hepatic expression and/or splicing of most of these cancer-related genes. In summary, it appears that alcohol causes profound genome-wide changes in gene expression and splicing in the liver, likely via affecting the spliceosome. This results in altered expression and missplicing of key oncogenes and tumor suppressors involved in HCC, suggesting a novel mechanism of oncogenesis in the liver of patients with ALD.

alcohol use disorder↗

PubMed2026

Perceived partner substance use, genetic predispositions, and their associations with problematic alcohol use, emotional well-being, and relationship quality.

BACKGROUND: Romantic relationships are important contexts for substance use and emotional well-being. We tested the hypotheses that (i) genetic predispositions for alcohol consumption would be positively associated with partner substance use, (ii) partner substance use would moderate genetic influences on one's own alcohol outcomes, and (iii) partner discordance in substance use would be associated with lower emotional well-being and relationship quality. METHODS: Analyses included 2,357 participants (Mage = 51.4, 58.2% female) from the Collaborative Studies on the Genetics of Alcoholism. Focal measures included participants' reports of their own and their current partner's past-year substance use (frequencies of alcohol use, heavy drinking, drunkenness, cannabis use, and nicotine use), emotional well-being, and relationship quality. Participants' genetic predispositions were indexed with genome-wide polygenic scores for alcohol consumption (PGSAlc). Participant-partner substance use discordance was calculated as the difference between the participant's and their partner's use for each substance use measure, separately. RESULTS: Participant PGSAlc was not significantly associated with partners' perceived substance use. Frequent perceived partner alcohol use and heavy drinking significantly amplified the association between PGSAlc and alcohol use or drunkenness. Frequent perceived partner drunkenness and cannabis use significantly attenuated the association between PGSAlc and heavy drinking or frequency of alcohol use. Participant-partner discordance for several substance use measures was significantly associated with lower emotional well-being and relationship quality, controlling for participant and partner substance use main effects. CONCLUSIONS: The results highlight the importance of partner substance use in etiological models of alcohol use, emotional health outcomes, and relationship quality.

Humans↗

PubMed2026

Genetic regulation of AIF1 shapes immune and liver injury profiles in chronic alcohol use.

BACKGROUNDIn chronic alcohol consumers, immune cells may drive the progression from mild liver injury to more severe alcohol-associated liver disease (ALD), including alcohol-associated hepatitis (AAH) and cancer. Liver macrophages, both resident and infiltrating, express allograft inflammatory factor 1 (AIF1), which is upregulated during inflammation and enhances immune activation.METHODSUsing serum and urine samples from 868 individuals classified as having alcohol use disorder or not, based on DSM-IV/V criteria, along with serum and liver biopsy tissue from a second cohort of 27 patients diagnosed with AAH, we evaluated the impact of the AIF1 promoter single-nucleotide polymorphism (SNP) (rs3132451; C/C, C/G, G/G) on liver function markers and immune cell profiles.RESULTSAIF1 transcript levels were genotype dependent: C/C homozygotes expressed 5.2% of the levels observed in G/G individuals, while C/G heterozygotes expressed 46%. Unlike most SNPs associated with harmful effects, the G/G genotype is highly prevalent, present in about 70% of patients. Among chronic alcohol users, G/G individuals exhibited elevated markers of liver injury and a more than 3-fold increase in hepatic immune cells, including infiltrating AIF1+ macrophages and neutrophils. Despite similar durations of alcohol misuse, G/G individuals had higher Model for End-Stage Liver Disease scores compared with C/G individuals, indicating a significantly greater 90-day mortality risk. Notably, some immune abnormalities, such as elevated neutrophils, persisted in G/G males even after alcohol abstinence.CONCLUSIONThese findings suggest that functional genetic variation in AIF1 may contribute to the severity and persistence of ALD.TRIAL REGISTRATIONClinicalTrials.gov NCT02231840.FUNDINGResearch support was provided from the National Institute on Alcohol Abuse and Alcoholism of the NIH under grants 1ZIAAA000440-02 and R24AA025017.

Humans↗

PubMed2026

Prediction of alcohol consumption: The role of genetics, impulsivity, and sensation seeking from adolescence to adulthood.

BACKGROUND: There are well-known phenotypic and genetic associations among impulsivity, sensation seeking (SS), and alcohol consumption, but whether they vary between adolescence and early adulthood remains unclear. PURPOSE/HYPOTHESES: We hypothesized that adolescent alcohol consumption would be better predicted by polygenic indices (PGIs) of impulsivity and SS than PGIs of adult alcohol consumption (drinks per week; DPW), but that the reverse would be observed in young adulthood (i.e., stronger associations for DPW PGIs). METHODS: N = 733-754 twins of European genetic ancestry from the Colorado Longitudinal Twin Study were assessed at age 17 and/or 23 years using structural equation modeling. RESULTS: The SS PGIs were associated with alcohol consumption in adolescence (β=0.16), whereas DPW PGIs were associated with alcohol consumption in early adulthood (β=0.15). Additionally, phenotypic measures of impulsivity and SS are associated with alcohol consumption at both ages (β=.13-.21) and mediated some PGI-alcohol associations. DISCUSSION: These findings suggest that genetic influences on alcohol consumption change from adolescence to early adulthood, with genetic influences on sensation seeking most relevant to alcohol consumption in adolescence.

Humans↗

PubMed2026

Simulating the effects of an alcohol minimum unit price policy on distilled spirits sales in 28 states of the USA.

BACKGROUND AND AIMS: Excessive alcohol use is a leading preventable chronic disease risk factor. Alcohol minimum unit pricing (MUP) policies are not used in the United States despite evidence of associations with reduced drinking and alcohol-related harms. To inform potential population-level chronic disease prevention strategies, we estimated effects of various hypothetical MUPs on alcohol sales. METHOD: Simulation based on observational time-series data. We used weekly off-premises product-specific alcohol retail sales and prices in 28 states of the United States for November 2022-November 2023 from NielsenIQ to estimate the own-price elasticity of spirits and cross-price elasticities of wine, beer and ready-to-drinks with respect to spirits. Using estimated elasticities, we simulated changes in total alcohol sales associated with hypothetical spirits MUPs ranging from $0.10 to $1.10 per standard drink (0.6 fluid ounces of alcohol). RESULTS: A hypothetical MUP of $0.80 per standard drink on spirits yielded the largest estimated decrease in alcohol sales (-1.7%) and would affect 5374 of 26 249 spirits products. To reach the $0.80 MUP, the sales-weighted average price increase among affected products was $0.24 per drink. CONCLUSIONS: Minimum unit pricing policies on distilled spirits in the United States could shift purchasing behavior and help reduce alcohol-related harms.

alcohol policy↗

PubMed2026

Elevated intron retention implicates neuroinflammation in brains of individuals with alcohol use disorder.

Intron retention, a form of alternative RNA splicing, can occur as part of normal gene regulation or result from disruption of the splicing machinery. Retained introns can potentially form double-stranded RNA, activating innate immune sensors and inflammation. This mechanism has been implicated in cancer but has not been studied in neuropsychiatric diseases like alcohol use disorder. We systematically analysed transcriptome-wide intron retention events in post-mortem brain tissue from 142 individuals (66 with alcohol use disorder and 76 controls), encompassing 320 region-specific samples from the superior frontal cortex, nucleus accumbens, central nucleus and basolateral amygdala. Analyses were adjusted for demographic, technical and biological covariates. Validation was performed in alcohol-preferring (P) rats using long-read sequencing. In complementary experiments, immunofluorescent staining was used to detect double-stranded RNA in rat brain tissue, while single-cell RNA-sequencing was performed to test activation of double-stranded RNA-sensing pathways in human brains. Brains from individuals with alcohol use disorder showed significantly higher total intron retention compared with controls, independent of age, with females showing greater increases than males. A total of 368 introns were positively associated with alcohol use disorder, and these introns were significantly longer and had weaker splice acceptor sites compared with non-associated introns. Genes harbouring these intron retention events were enriched in Purkinje neurons, visual cortex neurons and oligodendrocytes. Computational predictions indicated these long introns could form duplex RNA structures. Increased double-stranded RNA was confirmed experimentally in multiple brain regions of alcohol-consuming rats, where it co-localized primarily with neuronal nuclei and dendrites. In individuals with alcohol use disorder, we found that multiple pathways including double-stranded RNA responses, neuroinflammation, interferon and NF-κB signalling, adaptive immunity and apoptosis were activated. In addition, NeuN-positive neuronal counts significantly decreased in both the prefrontal and visual cortices. Furthermore, single-cell analysis demonstrated upregulation of TICAM1, the target of double-stranded RNA sensor TLR3, in oligodendrocytes, as well as widespread activation of downstream inflammatory pathways across glial and neuronal cell types. These findings provide the first evidence that chronic alcohol consumption promotes an overall increase of intron retention in the brain and is associated with the presence of double-stranded RNA. Furthermore, the double-stranded RNA may contribute to neuronal loss and brain pathology by activating a neuroinflammatory response.

alcohol use disorder↗

PubMed2026

Effects of Acute Low- and Moderate-Dose Alcohol on Chronic Disease-Related Biomarkers in Healthy Light and Heavy Drinkers.

BACKGROUND: Alcohol consumption is a major contributor to global chronic disease, with growing evidence indicating health risks even at low levels of intake. However, mechanistic understanding of these risks relies heavily on preclinical models and observational data, leaving a critical gap in controlled experimental evidence regarding how alcohol perturbs human biological systems in vivo. METHODS: The present study utilized plasma samples from a randomized, placebo-controlled trial to evaluate the effects of low-dose (0.35 g/kg) and moderate-dose (0.60 g/kg) alcohol on disease-relevant biomarkers in 32 healthy adults (mean age = 25.0 ± 3.8 years; 21 female/11 male), characterized by light (n = 15) or heavy (n = 17) drinking. This design enabled evaluation of effects across dose, timescale, and drinking history, as well as assessment of their interactions. Plasma was collected at prebeverage baseline and hourly for 4 h afterward. Immunoassays quantified 10 disease-related biomarkers: adiponectin, angiogenin, D-dimer, high-sensitivity C-reactive protein (hsCRP), Intercellular Adhesion Molecule-1 (ICAM-1), Lipocalin-2 (LCN2), Matrix Metalloproteinase-7 (MMP-7), Matrix Metalloproteinase-9 (MMP-9), soluble Receptor for Advanced Glycation End-products (sRAGE), and Triggering Receptor Expressed on Myeloid cells 2 (TREM2). RESULTS: Main effects of group indicated that even in this young healthy sample, heavy drinking status was associated with higher levels of adiponectin, angiogenin, ICAM-1, LCN2, and sRAGE, a profile suggesting altered vascular and metabolic activity. Acute alcohol administration induced changes in sRAGE and hsCRP. Specifically, moderate-dose alcohol triggered an increase in the immunoglobulin sRAGE, which may reflect an acute compensatory response to inflammation and/or oxidative stress. Compared to placebo, hsCRP was lower in the low-dose alcohol condition; however, this finding should be interpreted in light of CRP biology. MMP-7, MMP-9, and LCN2 showed time-dependent fluctuations that were independent of experimental condition, highlighting the critical importance of placebo-controlled designs to account for diurnal/postprandial variation in immune biomarkers. CONCLUSION: Findings provide translational evidence that alcohol is associated with multisystem biomarker changes relevant to chronic disease and that alcohol-related biomarker perturbations vary by dose and chronicity.

Humans↗

PubMed2025

Dissecting metabolic dysfunction- and alcohol-associated liver disease (MetALD) using proteomic and metabolomic profiles.

BACKGROUND & AIMS: Metabolic dysfunction- and alcohol-associated liver disease (MetALD) is a poorly understood condition that bridges cardiometabolic and alcohol-related pathological characteristics. We aimed to differentiate patients with MetALD whose molecular signatures more closely resemble either alcohol-related liver disease (ALD) or metabolic dysfunction-associated steatotic liver disease (MASLD), and to assess their relative risks of complications and mortality. METHODS: We analysed data from 443,453 European participants in the UK Biobank, including 34,147 with MetALD, 11,220 with ALD, and 124,034 with MASLD. Elastic net regression was used to classify ALD and MASLD based on 249 plasma metabolites and/or 2,941 plasma proteins, with multiple sensitivity analyses. We then applied the resulting concise model to patients with MetALD to identify an alcohol-predominant group (classified as ALD) and a cardiometabolic-predominant group (classified as MASLD). Finally, we evaluated their 15-year risk of major outcomes (heart failure, myocardial infarction, stroke, cirrhosis, hepatocellular carcinoma, and mortality) using Cox regression. RESULTS: The metabolome alone discriminated ALD from MASLD with an AUC of 0.86, while the proteome alone achieved an AUC of 0.96. Adding age, sex, BMI, liver enzymes, or metabolome information did not enhance the AUC of the proteome model. A 10-protein model differentiated ALD from MASLD with an AUC of 0.93. This model identified that patients with alcohol-predominant MetALD had significantly higher risks of mortality, and cirrhosis, along with elevated fibrosis scores and higher fibrosis stages, compared to patients with cardiometabolic-predominant MetALD. CONCLUSIONS: This study highlights the value of proteomic subtyping in MetALD, enabling more personalized treatment strategies and improved prognostic assessment. IMPACT AND IMPLICATIONS: This study underscores the critical importance of distinguishing subtypes of metabolic dysfunction- and alcohol-associated liver disease (MetALD) using proteomic data, providing a foundation for personalized treatment strategies. The findings hold significant relevance for healthcare providers, researchers, and policymakers by highlighting the differing risks associated with alcohol-predominant vs. cardiometabolic-predominant MetALD. Clinicians can apply the classification model developed in this study to more accurately assess patients and guide targeted therapies and preventive measures based on individual profiles. However, limitations of the study, such as reliance on self-reported alcohol consumption and the specificity of diagnostic criteria, necessitate further validation in diverse cohorts.

Humans↗

PubMed2026

The impact of alcohol sale restrictions on unnatural deaths during the COVID-19 pandemic in Johannesburg, South Africa.

The COVID-19-related restrictions on the sale of alcohol in South Africa presented a unique opportunity to examine the association between alcohol availability and the prevalence of unnatural deaths. The study sample included all unnatural deaths investigated by the Johannesburg Forensic Pathology Services Medico-Legal Laboratory during the four COVID-19 alcohol restriction periods compared to the same time periods in the previous year when there were no restrictions. When alcohol sales were initially prohibited, there was a 54.2% decrease in cases of unnatural deaths (p < 0.05), suggesting a link between alcohol use and the occurrence of such deaths. Over all four periods of alcohol sale bans, there was a total reduction of unnatural deaths by 26.4% with declining frequencies in all demographics. There were significant decreases (p < 0.05) in the frequency of deaths in males, Black and Coloured individuals, and the 21-40 years age group. Deaths whose circumstances were a result of motor vehicle accidents, pedestrian vehicle accidents, and firearm discharges decreased significantly (p < 0.05). The cause of death due to blunt forces trauma and gunshot wounds also significantly decreased (p < 0.05). This study highlights the significant impact alcohol consumption has on mortality in South Africa.

Humans↗

PubMed2025

Alcohol-induced KDM5B activation in hepatocytes drives pathogenic cell-cell communication, leading to loss of liver function.

BACKGROUND: Alcohol-associated liver disease (ALD) is a major cause of alcohol-associated mortality. Previously, we identified KDM5B as a sex-specific mediator of ALD development; however, the mechanism behind KDM5B-induced pathological changes is not established. METHODS: Kdm5b flox/flox female mice were fed a western diet and 20% alcohol in the drinking water for 8-16 weeks (WDA). To induce KO, mice received 2×1011 genome copies of AAV8-CMV-Cre, AAV8-TBG-Cre, or AAV8-control. To test the role of myeloid C/EBPβ, Cebpbfl/fl, or Cebpbfl/fl Lyz2-Cre mice were fed WDA for 16 weeks. RESULTS: We found that Kdm5b KO prevented alcohol-induced liver fibrosis and liver inflammation in female mice. These changes were in part mediated by hepatocyte-to-non-parenchymal cell communication changes. KDM5B in hepatocytes promoted pro-inflammatory and pro-fibrotic changes in liver macrophages, endothelial cells, and stellate cells. Moreover, KDM5B promoted alcohol-induced early increase in EpCAM-positive liver progenitors and loss of liver function at later time points of alcohol feeding. We found that loss of liver function was dependent on a hepatocyte-to-macrophage communication feedback loop. KDM5B in hepatocytes inhibited macrophage C/EBPβ expression, which in turn resulted in loss of the mature KCs phenotype and prevented the ability of KCs to support hepatocyte differentiation, ultimately leading to loss of liver synthetic function. CONCLUSIONS: KDM5B activation in hepatocytes drives pathogenic cell-cell communication, leading to alcohol-induced loss of liver function in ALD.

Animals↗

PubMed2026

Moderate alcohol intake and heart rate variability adaptations to high-intensity interval training in healthy young adults: the BEER-HIIT study.

BACKGROUND: It is unknown whether daily alcohol consumption influences training effects on heart rate variability (HRV). This study investigated: (i) the effects of a 10-week high-intensity interval training (HIIT) on HRV in healthy young adults; and (ii) the effects of daily alcohol consumption on HRV responses to exercise. METHODS: 71 healthy young adults (18-40 years old; 52.1% women) participated in the BEER-HIIT study. We conducted a 10-week (2 days/week) controlled trial (ClinicalTrials.gov ID: NCT03660579). Participants were allocated to 5 groups: a non-training group (N-T) and four HIIT groups. Participants in the training groups chose whether to consume alcohol. Those choosing alcohol were randomly allocated to receive beer (5.4%; T-Beer) or an equivalent amount of alcohol (vodka; T-Ethanol) in sparkling water. Those choosing no alcohol were randomly allocated to receive alcohol-free beer (0.0%; T-Zero) or sparkling water (T-Water). Training comprised eight weight-bearing exercises performed in circuit form. HRV was measured before and after the intervention. RESULTS: No statistically significant between-group differences in HRV outcomes were detected after the intervention (all p > 0.05). CONCLUSIONS: Our findings indicate that: (i) no statistically significant differences in HRV responses were detected following a 10-week HIIT program using weight-bearing exercises performed twice per week; and (ii) no statistically significant differences in HRV responses were observed among the assigned beverage intervention groups. These findings should be interpreted cautiously because HRV was a secondary outcome and the study was not specifically powered to detect differences in these parameters.

alcohol↗

PubMed2026

Cobalt starvation affects multiple cellular processes in Desulfofundulus kuznetsovii TPOSR during alcohol oxidation.

Cobalt influences the methanol metabolism of Desulfofundulus kuznetsovii TPOSR, specifically by modulating the activity of one of its alcohol dehydrogenases (ADH), Adh1. However, the effects of cobalt on the broader proteome of strain TPOSR, as well as the utilization of alcohols besides methanol, remain unexplored. Here, proteomic analyses of strain TPOSR grown with and without cobalt on different alcohol substrates show that cobalt starvation impacts multiple cellular processes, including cobalamin biosynthesis, iron-sulphur cluster assembly and, most prominently, energy metabolism as indicated by altered abundances of hydrogenases and NAD(P)-dependent oxidoreductases. Despite the presence of six ADH-encoding genes in the genome, Adh1 is the dominant ADH during growth not only on methanol but also on several primary alcohols and diols (ethanol, 1-propanol, 1,2-propanediol, 1,3-propanediol, butanol, pentanol and heptanol). Enzymatic assays with purified Adh1 confirm activity with these substrates, except 1,3-propanediol, and show no activity toward secondary alcohols (2-propanol and 2-butanol). Comparative proteomics analyses of other sulphate-reducing microorganisms (SRMs), namely Desulfofundulus australicum and Solidesulfovibrio carbinolicus, further indicate that methanol and ethanol oxidation in SRMs is mediated by a single ADH/AOR pair. Together, these findings highlight the central role of cobalt in alcohol metabolism in strain TPOSR and identify conserved ADH/AOR enzymes as promising candidates for biotechnological applications.

Cobalt↗

PubMed2026

Frequent readmissions after hospitalization for alcohol withdrawal: a systematic review and meta-analysis.

BACKGROUND: Alcohol use disorder and alcohol withdrawal syndrome impose substantial clinical and economic burdens, with repeated hospitalizations being common. We aimed to systematically review readmission rates following inpatient detoxification, assess variation across study designs and hospital settings, and identify key risk and protective factors. METHODS: We performed a literature search in Embase and Pubmed on 10/04/2026 focusing on studies assessing in hospital alcohol detoxification. Exclusion criteria included studies on substance use other than alcohol and outpatient or residential treatment. Main outcome was rehospitalization, and meta-analysis was performed to estimate pooled readmission proportions. Secondary outcomes were risk factors and protective factors influencing the rate of rehospitalization. RESULTS: Twenty-five studies were included. The pooled proportion of readmissions following alcohol detoxification was estimated at 17% (95% CI: 14%-21%; 13 studies, n = 287,896) within 1 month, increasing to 44% (95% CI: 36%-52%; 8 studies, n = 2,877) at 1 year. Substantial between-study heterogeneity was observed. Subgroup analyses found no significant differences by hospital setting or time period. Findings for study aim and study design were mixed and based on limited data A small number of studies suggested associations with housing stability, employment, and treatment engagement. CONCLUSIONS: This meta-analysis suggests that approximately one in six patients are readmitted within 1 month and nearly half within 1 year after inpatient alcohol detoxification. However, readmission rates varied considerably across settings and populations. Future research should evaluate targeted interventions to reduce readmissions among high-risk patient groups.

Humans↗

PubMed2026

PCSK9 inhibition attenuates alcohol-induced cardiovascular dysfunction and links hepatic lipid accumulation to impaired myocardial contractile reserve.

Excessive alcohol consumption accelerates cardiovascular aging by promoting oxidative stress, inflammation, lipid dysregulation, fibrotic remodeling, and loss of ventricular-vascular reserve. PCSK9, a key regulator of cholesterol metabolism, has emerged as a mediator of age-related cardiovascular dysfunction and alcohol-associated liver and neurovascular injury. We investigated whether PCSK9 inhibition protects against alcohol-induced cardiovascular dysfunction and associated cardiac-hepatic injury in rats. Male Sprague-Dawley rats were assigned to pair-fed control or 35% ethanol liquid diet groups and treated weekly with subcutaneous alirocumab, 50 mg/kg, or vehicle for 6 weeks. Blood alcohol and cholesterol levels were measured; cardiac function was assessed by echocardiography and invasive pressure-volume analysis; and myocardial, vascular, and hepatic injury markers were quantified. Alirocumab reduced total cholesterol in both pair-fed and ethanol-fed rats without altering blood alcohol levels. Chronic ethanol exposure impaired systolic performance, myocardial contractile reserve, diastolic relaxation, and ventricular-arterial coupling, as reflected by reduced stroke volume, cardiac output, ejection fraction, fractional area change, dP/dtmax, stroke work, ESPVR slope, PRSW, and dP/dtmax-EDV, together with abnormalities in TauWeiss and dP/dtmin. PCSK9 inhibition markedly attenuated these functional deficits. Alirocumab also reduced ethanol-induced myocardial and vascular malondialdehyde accumulation and suppressed myocardial induction of NOX4, LOX1, iNOS, TNF-α, ANP, and profibrotic markers. Ethanol increased myocardial fibrosis, hepatic triglyceride accumulation, perilipin-2 staining, and mild hepatic fibrotic remodeling, all of which were attenuated by alirocumab. Liver triglyceride content correlated inversely with ESPVR slope and PRSW. These findings identify PCSK9 as a potential therapeutic target for alcohol-related cardiovascular dysfunction and associated cardiac-hepatic injury.

Accelerated aging↗