Excessive Alcohol Intake Research Articles

Transforming steatotic liver disease management: The emerging role of GLP-1 receptor agonists.

Chronic liver disease is a major cause of mortality, with approximately 2 million deaths worldwide each year, and it poses a significant economic burden. The most common cause of chronic liver disease in the United States and Europe is steatotic liver disease (SLD), which includes metabolic dysfunction-associated SLD, metabolic dysfunction and alcohol-associated SLD, and alcohol-associated liver disease (ALD). Effective treatment of these conditions is essential to reduce the liver disease burden, with promising approaches including treating cardiometabolic risk factors and excessive alcohol intake. Glucagon-like peptide 1 receptor agonists, both as monotherapy and in combination with other drugs, are gaining attention for their beneficial impact on cardiometabolic risk factors and excessive alcohol intake. In this review, we examine the molecular and clinical effects of glucagon-like peptide 1 receptor agonists, focusing on their direct hepatic steatohepatitis and liver fibrosis but also the indirect influence on cardiometabolic risk factors and excessive alcohol intake as key features of SLD. We also explore the future implications of glucagon-like peptide 1 receptor agonists for treating metabolic dysfunction-associated SLD, metabolic dysfunction and alcohol-associated SLD, alcohol-associated liver disease, and the potential challenges.

Excessive alcohol intake produces persistent mechanical allodynia and dysregulates the endocannabinoid system in the lumbar dorsal root ganglia of genetically-selected Marchigian Sardinian alcohol-preferring rats

Epidemiological data indicate a strong association between alcohol use disorder (AUD) and neuropathic pain. Genetically-selected Marchigian Sardinian alcohol-preferring (msP) rats exhibit a high preference for alcohol compared with their background strain (Wistar rats), but their sensitivity to mechanical allodynia after chronic alcohol exposure is unknown. The present study compared the development of mechanical allodynia between “low, non-pathological drinker” Wistar rats and “high drinker” msP rats using the two-bottle choice (2BC) free-access procedure. Several studies reported the involvement of endocannabinoids (eCBs) in modulating mechanical allodynia, but there are no data on their role in alcohol-related allodynia. Thus, the present study assessed eCBs and their related lipid species in lumbar dorsal root ganglia (DRG) and correlated them with mechanical allodynia in our model. We found that male and female msP rats developed persistent mechanical allodynia during protracted abstinence from alcohol, presenting no sign of recovery, as opposed to Wistar rats. This effect directly correlated with their total alcohol intake. Notably, we found a correlation between lower lumbar DRG 2-arachidonoylglycerol (2-AG) levels and the development of higher mechanical allodynia during abstinence in msP rats of both sexes but not in Wistar rats. Moreover, alcohol-exposed and abstinent msP and Wistar females but not males exhibited significant alterations of thromboxane B2 and prostaglandin E2/prostaglandin D2 compared with naive rats. These findings demonstrate that DRG 2-AG metabolism is altered in msP rats during prolonged abstinence and represents a potentially interesting pharmacological target for the treatment of mechanical allodynia during alcohol abstinence.

Acute Alcohol Consumption and Arrhythmias in Young Adults: The MunichBREW II Study.

and aims: Acute excessive alcohol intake may cause the holiday heart syndrome, characterized by cardiac arrhythmias including atrial fibrillation. Since underlying data are scarce, the study aimed to prospectively investigate the temporal course of occurring cardiac arrhythmias following binge drinking in young adults. A total of 202 volunteers planning acute alcohol consumption with expected peak breath alcohol concentrations (BAC) of ≥1.2 g/kg were enrolled. The study comprised 48-hour electrocardiogram (ECG) monitoring covering baseline (hour 0), 'drinking period' (hours 1-5), 'recovery period' (hours 6-19), and two control periods corresponding to 24 hours after the 'drinking' and 'recovery periods', respectively. Acute alcohol intake was monitored by BAC measurements during the 'drinking period'. ECGs were analyzed for mean heart rate, atrial tachycardia, premature atrial complexes (PAC), premature ventricular complexes (PVC), and heart rate variability (HRV) measures. Data revealed an increase in heart rate and an excess of atrial tachycardias with increasing alcohol intake. HRV analysis indicated an autonomic modulation with sympathetic activation during alcohol consumption and the subsequent 'recovery period', followed by parasympathetic predominance thereafter. PACs occurred significantly more frequently in the 'control periods', whereas PVCs were more frequent in the 'drinking period'. Ten participants experienced notable arrhythmic episodes, including atrial fibrillation and ventricular tachycardias, primarily during the 'recovery period'. The study demonstrates the impact of binge drinking on heart rate alterations and increased atrial tachycardias during 'drinking period', and the occurrence of clinically relevant arrythmias during the 'recovery period', emphasizing the holiday heart syndrome as a health concern.

Galangin Alleviates Alcohol-Provoked Liver Injury Associated with Gut Microbiota Disorder and Intestinal Barrier Dysfunction in Mice.

Prolonged and excessive intake of alcohol results in the onset of alcoholic liver disease, which is marked by oxidative stress, intestinal barrier dysfunction, and disturbance in the intestinal microbiome. Galangin, a potent flavonoid from Alpinia officinarum Hance, has been recognized for its diverse biological properties; however, its ability for protecting against alcohol-stimulated hepatotoxicity remains unexplored in prior research. In the current study, a Gao-Binge mouse model was established to assess the positive role and mechanisms of galangin upon alcohol-induced liver injury. The administration of galangin relieved liver pathological damage, oxidative stress, and NLRP3-mediated inflammation induced by alcohol. In addition, galangin significantly reversed abnormal intestinal histopathological manifestations and damaged the intestinal barrier function. Furthermore, microbiota composition revealed that galangin improved intestinal imbalance by improving the gut microbiota dysbiosis and short-chain fatty acid level. Collectively, this study explored the interactions between phytochemical factors and virulence factors and discovered that galangin powerfully improved alcohol-induced liver disease by repressing the inflammatory cascade via the gut microbiota-mediated gut-liver axis. These results suggested that alcohol-targeted natural products could have potential applications in promoting food safety and human health and offer valuable insights into the possible use of these substances in these important areas.

Transcriptional Patterns in Stages of Alzheimer's Disease Are Cell-Type-Specific and Partially Converge with the Effects of Alcohol Use Disorder in Humans.

Advances in single-cell technologies have led to the discovery and characterization of new brain cell types, which in turn lead to a better understanding of the pathogenesis of Alzheimer's disease (AD). Here, we present a detailed analysis of single-nucleus (sn)RNA-seq data for three stages of AD from middle temporal gyrus and compare it with snRNA-seq data from the prefrontal cortices from individuals with alcohol use disorder (AUD). We observed a significant decrease in both inhibitory and excitatory neurons, in general agreement with previous reports. We observed several cell-type-specific gene expressions and pathway dysregulations that delineate AD stages. Endothelial and vascular leptomeningeal cells showed the greatest degree of gene expression changes. Cell-type-specific evidence of neurodegeneration was seen in multiple neuronal cell types particularly in somatostatin and Layer 5 extratelencephalic neurons, among others. Evidence of inflammatory responses was seen in non-neuronal cells, particularly in intermediate and advanced AD. We observed common perturbations in AD and AUD, particularly in pathways, like transcription, translation, apoptosis, autophagy, calcium signaling, neuroinflammation, and phosphorylation, that imply shared transcriptional pathogenic mechanisms and support the role of excessive alcohol intake in AD progression. Major AUD gene markers form and perturb a network of genes significantly associated with intermediate and advanced AD. Master regulator analysis from AUD gene markers revealed significant correlation with advanced AD of transcription factors that have implications in intellectual disability, neuroinflammation, and other neurodegenerative conditions, further suggesting a shared nexus of transcriptional changes between AD and AUD.

Bergenin inhibits hepatic fat deposition by activating the AMPK signaling pathway, thereby attenuating alcoholic liver disease

Alcoholic liver disease (ALD) is a prevalent liver condition that arises from prolonged and excessive alcohol intake. Bergenin (BER) is an effective phytotherapeutic agent that exhibits pharmacological properties, including anti-inflammatory and anti-oxidative effects. To establish an in vivo model of ALD, C57BL/6 mice were continuously fed a high-fat diet (HFD) and administered alcohol gavage for 8 weeks, while concurrently administering BER and evaluated for therapeutic effects. After modeling, the therapeutic effects of BER were evaluated by observing histopathological changes and the detection of relevant biochemical indicators in mice. In addition, RNA sequencing of liver tissues was performed to analyze differentially expressed genes and to investigate the associated signaling pathways in order to elucidate the protective mechanisms of BER. These differentially expressed genes were mainly enriched in lipid metabolism pathways and the cytochrome P450 metabolism of exogenous substances. Subsequently, HepG2 was co-treated with sodium oleate (NaOA) and ethanol to establish an in vitro model, and the specific mechanism by which BER ameliorates ALD was further analyzed in depth. AMPK inhibitor, Compound C (CC), was demonstrated to significantly inhibit the regulation of lipid metabolism by BER in vitro. Finally, the differentially expressed genes selected were validated through qRT-PCR and Western blot analysis. Collectively, our findings revealed that BER effectively alleviated liver injury caused by alcohol and HFD in mice, significantly suppressing lipid deposition in ALD, enhancing alcohol metabolism, and mitigating oxidative stress.

Risk Factors and Prevention of Stomach Cancer, Excluding Helicobacter pylori

Gastric cancer is a significant health problem owing to its high incidence and mortality rate. The risk factors for gastric cancer include both uncontrollable (e.g., age, sex, and genetic predisposition) and controllable factors (e.g., <i>Helicobacter pylori</i> infection, smoking, alcohol consumption, obesity, and high-salt diets). Although treatment of <i>H. pylori</i> infections has been implemented as a primary preventive measure, the risk of gastric cancer may persist, highlighting the need for additional preventive measures. This review discusses various risks and protective factors associated with gastric cancer, studies conducted on these factors, and chemoprevention. Smoking is a risk factor for this disease; thus, is not recommended and current smokers are encouraged to quit because cessation can reduce the risk of gastric cancer. Excessive alcohol intake has been reported to increase the risk of gastric cancer as has the consumption of high-salt foods that can damage the gastric mucosa. Additionally, increasing the intake of fruits and vegetables, known for their protective effects against gastric cancer, can aid in its prevention. Studies on chemopreventive agents, including nonsteroidal anti-inflammatory drugs (e.g., aspirin), statins, and metformin, have been reported; however, evidence of their effectiveness remains insufficient to recommend these agents as preventive treatments. Additional well-planned studies on preventive medications and dietary approaches are necessary.

Alcohol-associated liver disease - a current overview.

Alcohol-associated liver disease (ALD) remains a major and increasingly pressing concern in hepatology. ALD includes spectrum of conditions, each with unique diagnostic and therapeutic challenges. Excessive alcohol intake is a leading preventable cause of physical harm, including ALD. The pathogenesis of ALD involves oxidative stress, inflammation, and lipid metabolism disruptions, with genetic predispositions playing a major role. ALD progresses from hepatic steatosis to steatohepatitis, and finally liver cirrhosis, which is marked by severe fibrosis and impaired liver function. Advanced ALD stages, particularly alcoholic hepatitis and liver cirrhosis, are characterized by high mortality rates. Management of ALD primarily involves strict abstinence from alcohol, which can reverse early-stage disease or halt progression. Nutritional support, vitamin supplementation, and symptomatic treatment are also essential. Liver transplantation is the only definitive treatment for alcoholic liver cirrhosis, but it is difficult for patients with a history of alcohol abuse to qualify for the procedure. Epidemiological data indicate a growing burden of ALD, especially among younger populations, exacerbated by increased alcohol consumption trends and the COVID-19 pandemic's influence on drinking behaviors. Despite ALD's significant impact, current therapies are limited, highlight- ing the need for innovative treatments and comprehensive patient management strategies. Individualized care, enhanced epidemiological research, and new therapeutic approaches are crucial to improving outcomes for ALD patients.

From risk to reward: Japan’s potential for health and economic improvements

This study examines the relationship between risky consumption behaviors, non-communicable diseases (NCDs), and socioeconomic costs in Japan using the Preventable Risk Integrated ModEl (PRIME). We assess the potential impact of healthier lifestyle choices on NCD incidences and costs in 2019. Japan's rising healthcare expenditures threaten its economic future. Excessive intake of salt, tobacco, and alcohol, along with insufficient fiber and fruit consumption, significantly contribute to high NCD rates. Our analysis shows that healthier behaviors could have prevented 564,000 NCD cases, potentially saving $35 billion in health costs and economic losses in 2019. We consider scenarios where smokers switch to heated tobacco products (HTPs), applying conservative risk reduction estimates. Higher risk reduction levels could triple smoking-attributable savings. Projecting these savings over ten years would increase economic benefits tenfold. The study emphasizes the need for comprehensive public health strategies promoting healthier lifestyles. Targeted interventions, such as stricter regulation of high-risk products and incentives for healthier alternatives, could reduce NCD incidences and healthcare costs. While PRIME provides valuable insights, further research is needed to refine our understanding of risk factor-disease relationships.

Alcohol Consumption and Cardiovascular Disease: A Narrative Review of Evolving Perspectives and Long-Term Implications.

Cardiovascular illnesses remain the primary cause of death, accounting for at least 17.9 million fatalities per year and posing a significant public health problem because of its extensive predominance and effect on healthcare systems. The etiology of cardiovascular disease is complex and involves several environmental and lifestyle factors. Alcohol use is a highly important determinant because of its dual-edged effect on cardiovascular health. Multiple studies indicate that moderate alcohol consumption may have certain advantages, such as slight enhancements in lipid profiles. Conversely, excessive alcohol intake is associated with serious negative consequences, including cardiomyopathy, hypertension, arrhythmias, and even mortality. The aim of this study is to provide a comprehensive analysis of the several effects of alcohol on cardiovascular health and their understanding within the medical field over time. It uses an interpretative narrative review methodology and analyzes studies that focus on genetic risk factors, gender differences, and shifts in paradigms in recent years. This article highlights the need for obtaining a thorough understanding of the effects of alcohol on cardiovascular health to support public health guidelines and clinical practice, and it underscores the significance of including alcohol consumption into the broader context of cardiovascular risk management and identifies important subjects for further study.

Hepatologists' Awareness and Knowledge of NAFLD and the Familiarity with Renaming NAFLD to MAFLD.

Non-alcoholic fatty liver disease (NAFLD) is an emerging epidemic; it is a negative diagnosis that depends mainly on the presence of hepatic steatosis with or without inflammation after the exclusion of other chronic liver diseases and excess alcohol intake. However, the new definition of MAFLD is a shift towards a diagnosis of inclusion based on the presence of metabolic dysfunction, regardless of alcohol consumption or other concomitant liver diseases. Given the growing relevance of the disease, data on hepatologists' views and understanding of NAFLD are limited, we aimed to determine hepatologists' awareness and expertise of NAFLD screening, diagnosis, and therapeutic options as well as the influence of changing the NAFLD name to MAFLD on awareness of the fatty liver disease (FLD). Most of the hepatologists agreed that NAFLD can cause serious hepatic illness and may be linked to metabolic risk factors, necessitating a multidisciplinary approach to treatment. Hepatologists have a poor understanding of NAFLD care. The shift in terminology from NAFLD to MAFLD will be more known to hepatologists, and it may offer better awareness of FLD. A multicenter online questionnaire of 655 hepatologists was carried out, giving a sample of 207 respondents. A survey composed of 36 questions was used to assess the level of hepatologists' awareness and practices in the screening, diagnosis, and management of NAFLD/MAFLD, as well as their familiarity with the nomenclature change from NAFLD to MAFLD. A total of 207 hepatologists were included, of which 107 (51.4%) were males, with a mean age was 36.4 years. 50.2% (n = 104) of the hepatologists were oriented with NAFLD. Only 41 (19.8%) realized that NAFLD may frequently result in severe hepatic disease. NAFLD is rarely screened by the majority of the participating hepatologists (118, 57%), and (135, 65.2%) of them use liver biopsy for diagnosis of NAFLD. In (104, 50.2%) hepatologists, changing the nomenclature of NAFLD was relatively familiar. Furthermore, 71.9% of hepatologists thought that the new nomenclature offers a better awareness of FLD. A small percentage of hepatologists agreed that NAFLD can cause serious hepatic illness and may be linked to metabolic risk factors, and around half of them realize that NAFLD necessitates a multidisciplinary approach to treatment. Hepatologists have a poor understanding of NAFLD care. The shift in terminology from NAFLD to MAFLD will be more known to hepatologists, and it may offer better awareness of FLD.

Quantification of alcohol intake in patients with steatotic liver disease and excessive alcohol intake

Quantification of alcohol intake in patients with steatotic liver disease and excessive alcohol intake

Exploring the interplay between kidney function and urinary metabolites in young adults: the African-PREDICT study

The exposure to modifiable risk factors at young ages have been linked to premature fatal and non-fatal cardiovascular and kidney outcomes. The use of urinary metabolomics has shown strong predictability of kidney function and cardiovascular disease (CVD). We therefore determined the associations between estimated glomerular filtration rate (eGFR) and urinary metabolites in young adults with and without CVD risk factors. Apparently healthy Black and White sexes were included (aged 20–30 years) and categorised by the presence or absence of risk factors, i.e., obesity, physical inactivity, smoking, excessive alcohol intake, masked hypertension, hyperglycemia, dyslipidemia and low socio-economic status, forming the CVD risk group (N = 1036), CVD risk clusters (i.e. presenting with 1 CVD risk factor (N = 344), 2 CVD risk factors (N = 360) and 3 + CVD risk factors (N = 332)) and the control group (N = 166). eGFR was calculated with CKD-EPI equations. A targeted metabolomics approach using liquid chromatography-tandem mass spectrometry was used to measure amino acids and acylcarnitines. Lower cystatin C-based eGFR were indicated in the CVD risk group, 2 and 3 + CVD risk clusters compared to the control group (all P ≤ 0.033). In the CVD risk group, eGFR associated positively with histidine, lysine, asparagine, glycine, serine, glutamine, dimethylglycine, threonine, alanine, creatine, cystine, methionine, tyrosine, pyroglutamic acid, leucine/isoleucine, aspartic acid, tryptophan, glutamic acid, free carnitine, acetylcarnitine, propionylcarnitine, isovalerylcarnitine, octanoylcarnitine and decanoylcarnitine (all P ≤ 0.044), with similar results found in the CVD risk clusters, particularly the 2 CVD risk cluster. eGFR was positively associated with metabolites linked to aromatic amino acid and branched-chain amino acid metabolism, energy metabolism and oxidative stress. These findings may indicate altered reabsorption of these metabolites or altered metabolic regulation to preserve renal health in the setting of CVD risk factors at this young age without established CVD.

Abstract Mo065: An Anti-arrhythmic Action and Novel Molecular Mechanisms of Alda-1 in Holiday Heart Syndrome

Introduction: Holiday Heart Syndrome (HHS) is caused by excessive binge alcohol intake. Atrial fibrillation (AF) is the most common arrhythmia in HHS patients. With a worldwide rising trend in heavy alcohol consumption despite significant prevention efforts, effective drugs against alcohol-evoked AF are in urgent need. Methods: We assessed the effect of Alda-1, a cardiac protective agent, on mitigating binge alcohol-evoked AF and alcohol-activated stress kinase JNK2 in 50mM alcohol-exposed (24hr) H9c2 differentiated myocytes and in a well-characterized HHS mouse model (2g/kg ethanol i.p., 4 injections, every other day). Alda-1’s effect on alcohol-evoked RyR2 channel-mediated Ca 2+ waves/sparks & tachycardia/fibrillation (AT/AF) incidence were measured in intact mouse atria. RyR2 channel open probability was assessed in human RyR2 single-channel recordings. Results: We found that Alda-1 significantly reduced atrial arrhythmia inducibility in HHS mouse atria, as evidenced by a decreased incidence of alcohol-evoked AT/AF (0 vs. 0.21 incidences/pacing attempts/animal; n=6, 8). Alda-1 is an agonist of aldehyde dehydrogenase 2 (ALDH2; a key enzyme in alcohol detoxification), which inhibits cellular apoptosis. We found that ALDH2 was increased by 42%±6 in HHS mice compared to controls, and which remained elevated upon Alda-1 treatment (n=6,7,7; p<0.05). HHS hearts showed unchanged apoptotic signaling pathways, suggesting alternative mechanisms in AF genesis. Our lab recently revealed a critical role of activated cardiac stress kinase JNK2 in AF risk. Intriguingly, Alda-1 suppressed alcohol-activated JNK2 by 70%±13 (immunoprecipitated JNK2-specific activity; n=9,9, p<0.001) (but not JNK1, the other cardiac JNK isoform) in cells, while JNK2 inhibition alleviated alcohol-evoked RyR2 channel dysfunction in human RyR2 channels as well as Ca 2+ -triggered atrial arrhythmic activities and AT/AF (0 out of 8; p<0.05) in intact mouse hearts. Conclusion: Alda-1 effectively mitigates binge alcohol-evoked atrial arrhythmogenesis by suppressing JNK2 activity independently of an ALDH2-mediated anti-apoptosis effect. Our findings highlight the potential of Alda-1 as a therapeutic agent for the increasing incidence of alcohol-evoked AF.

AYURVEDIC MANAGEMENT OF AVASCULAR NECROSIS WITH CHANDAN BALA LAKSHADI TAIL AND LAKSHADI GUGGUL

Avascular Necrosis (AVN) is a progressive degenerative condition of bone that mainly affects the bone of the lower region. It is more common in the hip joint. Avascular necrosis of the femoral head refers to the death of osteocytes with subsequent structural changes due to impaired blood supply. People between 30 and 50 years of age are usually affected. It is associated with excessive alcohol intake and long-term use of high-dose steroidal medications. On the contrary, Ayurvedic treatment provides long-term relief and prevents disease progression without drawbacks. it is Vata Pradhana Tridoshaja Vyadhi with Vikruti of Asthi-Majja Dhatu. In modern medicine, no specific treatment other than surgery is available. The present case study is upon a 45year male patient, diagnosed with avascular necrosis involving nearly 50 percent of the femoral head with moderate marrow oedema (stage 3rd) femoral head with complaints of pain in the bilateral hip region since one and half years, which was associated with difficulty in doing normal daily activities such as walking, sitting, squatting along with a change in the gate.

The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD)-related advanced fibrosis and cirrhosis in the United States population utilizing AGILE 3 + and AGILE 4 scores: analysis of the NHANES 2017–2018 cycle

BackgroundStudies attempted to estimate MASLD-related advanced fibrosis (AF) and cirrhosis (MC) prevalence utilized tests with low positive predictive value (PPV) which overestimates prevalence. AGILE3 + and 4 scores were developed to increase the PPV of both; respectively. In this study, we used these scores to assess the prevalence of AF and MC.MethodsParticipants aged ≥ 18 years with VCTE exam in the NHANES 2017–2018 cycle were included. We excluded pregnant women, patients with excessive alcohol intake, hepatitis B/C, and ALT or AST > 500 IU/L. MASLD was defined with CAP score > 248 dB/m. MASLD subjects with AGILE 3 + score of ≥ 0.68 and AGILE 4 score of ≥ 0.57 were considered to have advanced fibrosis and cirrhosis; respectively. AGILE 3 + of 0.45–0.67 and AGILE 4 of 0.25–0.57 were grey zone, whereas AGILE 3 + < 0.45 and AGILE 4 < 0.25 were considered a rule-out.Results1244 subjects were included in the final analysis. The Median age was 53 (51.4–54.6) years, 55.6% were male, median BMI was 33.8 kg/m2 and 41.1% had T2DM. Based on AGILE 3+, 80.3% of the MASLD population were at low risk for AF and 11.5% were in grey zone. The prevalence of AF due to MASLD was 8.1% corresponding to 4.5 million Americans. Based on AGILE 4 score, 96.5% of the MASLD population were at low risk for cirrhosis and 2.4% were in the grey zone. The prevalence of MASLD-cirrhosis was 1.1% corresponding to 610,000 Americans.ConclusionOur results suggest that approximately 4.5 million people in the U.S. have AF and 0.6 million have cirrhosis due to MASLD.

Hepatoprotective Effects of Aqueous Extract of Perilla fructescens against Alcohol-Induced Liver Injury in Mice

Excessive alcohol intake leads to significant physiological complications, particularly alcoholic liver diseases (ALD). The extent of liver damage caused by ethanol correlates with increased oxidative stress and accumulation of lipids in the hepatic tissue. In this study, we investigated the defense properties of the aqueous extract of Perilla frutescens Briton Var. acuta Kudo (PF) on hepatic injury in chronically ethanol-treated mice. The mice were orally administered the water extract from PF for 4 weeks with ethanol treatment (3 g/kg. P.O.). The level of malondialdehyde (MDA) in the liver tissues was determined. A substantial increase in MDA generation was detected in the livers of mice subjected to ethanol exposure, whereas the administration of PF markedly reduced MDA levels in hepatic tissues. Additionally, histological analysis of the liver tissue was performed. Histopathological investigation revealed a significant reduction in hepatocellular necrosis in the PF-treated group. This study demonstrated that the aqueous extract of Perilla frutescens Briton Var. acuta Kudo (PF) attenuated chronic ethanol-induced liver injury by augmenting the antioxidant capacity of mice. These results can be utilized for the development of high-value-added products using PF.

Liver Cancer Risk Across Metabolic Dysfunction-Associated Steatotic Liver Disease and/or Alcohol: A Nationwide Study.

New terminologies of metabolic dysfunction-associated steatotic liver disease (MASLD) have been developed. We assessed hepatocellular carcinoma (HCC) risk across MASLD and/or alcohol intake. We included participants aged 40-79 years receiving a national health checkup from 2009 to 2010 in the Republic of Korea, classified as follows: non-MASLD, MASLD, MASLD with increased alcohol intake (MetALD; weekly alcohol 210-420 g for male and 140-350 g for female individuals), and alcohol-associated liver disease (ALD; excessive alcohol intake with weekly alcohol ≥420 g for male or ≥350 g for female individuals). The primary outcome was HCC incidence. HCC risk was estimated using multivariable Cox proportional hazard models. Among 6,412,209 participants, proportions of non-MASLD, MASLD, MetALD, and ALD cases were 59.5%, 32.4%, 4.8%, and 3.4%, respectively. During follow-up (median 13.3 years), 27,118 had newly developed HCC. Compared with non-MASLD, the HCC risk increased from MASLD (adjusted hazard ratio [aHR] 1.66, 95% confidence interval [CI] 1.62-1.71) and MetALD (aHR 2.17, 95% CI 2.08-2.27) to ALD (aHR 2.34, 95% CI 2.24-2.45) in a stepwise manner. Furthermore, the older and non-cirrhosis subgroups were more vulnerable to detrimental effects of MASLD and/or alcohol intake, concerning HCC risk. Among the older, female, and cirrhosis subgroups, MetALD poses similar HCC risks as ALD. HCC risk increased from MASLD and MetALD to ALD in a stepwise manner, compared with non-MASLD. For an effective primary prevention of HCC, a comprehensive approach should be required to modify both metabolic dysfunction and alcohol intake habit.

Beneficial effects of Dendrobium officinale National Herbal Drink on metabolic immune crosstalk via regulate SCFAs-Th17/Treg

The development of gut-liver axis metabolic immune crosstalk is intimately associated with intestinal barrier disorder, intestinal SCFAs-Th17/Treg immunological imbalance, and disorders of the gut microbiota. Prior research has discovered that Dendrobium officinale National Herbal Drink (NHD), a traditional Chinese medicine drink with enhanced immunity, may enhance the immunological response in animals with impaired immune systems brought on by cyclophosphamide by repairing intestinal barrier function and controlling turbulence in the gut microbiota. However, whether NHD can further improve the gut-liver axis metabolic immune crosstalk and its related mechanisms need to be systematically studied. The purpose of this study is to clarify the function and mechanism of NHD in enhancing the gut-liver axis metabolic immunological crosstalk brought on by excessive alcohol intake. In this work, we set up a mouse model to analyze the metabolic and immunological crosstalk involving the gut-liver axis across 7 weeks of continuous, excessive drinking. At the same time, high and low doses (20,10 ml/kg) of NHD were given by gavage. The effect of NHD on improving the metabolism of gut-liver axis was evaluated by blood lipid, liver lipid deposition, liver function and intestinal pathophysiology. By measuring serum immunological indices, intestinal barrier, and intestinal immune barrier, the impact of NHD on enhancing immune and intestinal barrier function was assessed. Furthermore, immunohistochemistry, immunofluorescence, 16S rRNA, Western blot, q-PCR and other methods were used to detect gut microbiota, SCFAs-GPR41/43 pathway, intestinal Th17/Treg immune cells and PPAR-α-NPC1L1/SREBP1 pathway to elucidate the mechanism by which NHD enhances the gut-liver axis' metabolic immune crosstalk. Our study demonstrated that NHD has the potential to improve the pathophysiological damage caused by gut-liver axis in model mice. NHD also ameliorated the disorder of lipid metabolism. In addition, it regulated the levels of peripheral blood T cell immunity and serum immune factors. And NHD can restore intestinal mechanical and immune barrier damage. NHD has a favorable impact on the quantity of beneficial bacteria, including uncultured_bacterium_g__norank_f__muribaculacea and uncultured_bacterium_g__Turicibacter. Additionally, it raised the model mice's levels of SCFAs (n-butyric acid, isovaleric acid, etc.). This resulted in the promotion of intestinal GPR41/43-ERK1/2 expression and the reshaping of intestinal CD4+T cell Th17/Treg homeostasis. As a consequence, colon IL-22 and IL-10 levels increased, while colon IL-17A levels decreased. Lastly, NHD raised the amount of intestinal IAP/LPS, regulated the development of PPAR-α-NPC1L1/SREBP1 pathway in gut-liver axis, and improve lipid metabolism disorder. Our study found that NHD can improve the gut-liver axis metabolic immune crosstalk in model mice caused by excessive drinking. The mechanism might be connected to how NHD controls gut microbiota disorders in model mice, the activation of intestinal SCFAs-GPR41/43 pathway, the remodeling of Th17/Treg immune homeostasis of intestinal CD4+T cells, the improvement of IAP/LPS abnormality, and further mediating the PPAR-α-NPC1L1/SREBP1 pathway of lipid metabolism in gut-liver axis.

Emotional eating, internet overuse, and alcohol intake among college students: a pilot study with virtual reality.

The term emotional eating (EE) describes the tendency to eat as an automatic response to negative emotions and has been linked to anxiety and depression, common symptoms among the university population. The EE tendencies have also been associated with excessive internet use and an increase in alcohol intake among young university students. The aim of this study is to examine the relationship between the tendency towards EE and other health-compromising behaviors, such as excessive internet use or high alcohol intake. Additionally, it aims to investigate the association of these risky behaviors with the participants' performance level in a virtual reality (VR) task that assesses their executive functioning, and to assess impulsivity and levels of anxiety and depression. The results associate EE with excessive internet (r = 0.332; p < 0.01). use but not with alcohol consumption. Alcohol consumption was not associated with anxiety, depression, or impulsivity, but it was related to altered executive functions in the VR task: flexibility and working memory explained 24.5% of the variance. By contrast, EE and internet overuse were not related to executive function but were associated with impulsivity, depression, and anxiety. Impulsivity and depressive symptoms accounted for 45% of the variance in EE. Depression, trait anxiety and impulsivity explained 40.6% of the variance in internet overuse. The results reveal distinct patterns of psychological and neuropsychological alterations associated with alcohol consumption compared to emotional eating (EE) and excessive internet use. These findings underscore significant differences in the contributing factors between addictions and other substance-free addictive behaviors. For a deeper understanding of the various contributing factors to EE in college students, further research is recommended.