Ethanol Metabolism Research Articles

Clinical Evaluation of Hovenia dulcis Extract Combinations for Effective Hangover Relief in Humans

Alcohol consumption is associated with both short- and long-term adverse effects, including hangover symptoms. The objective of this study was to examine the potential benefits of traditional beverages containing a combination of Hovenia dulcis extract (HD) with either Pueraria lobata extract (HDPB) or glutathione yeast extract (HDGB) in abbreviating alcohol intoxication and mitigating hangover symptoms. A total of 25 participants between the ages of 19 and 40 who had previously experienced a hangover were evaluated in a randomized, double-blind, crossover, placebo (PLA)-controlled clinical trial. Results showed that lower blood alcohol concentrations in the HDPB and HDGB groups were significantly lower than in the PLA group at 0.25 and 0.5 h, suggesting that HD aids in early alcohol metabolism (0 h, p < 0.05). Analysis of the hourly Acute Hangover Scale (AHS) showed that all treatment groups had significantly reduced gastrointestinal disorder symptoms compared to the PLA group (p < 0.05). It can be confirmed that hangover symptoms can be significantly improved by consuming HD combination drinks, apart from the effect of reducing blood alcohol and acetaldehyde concentrations. Therefore, it is predicted that the consumption of natural phytochemicals added to HD is safe for humans and may help accelerate recovery from hangover symptoms.

Glutathione's Role in Liver Metabolism and Hangover Symptom Relief: Dysregulation of Protein S-Glutathionylation and Antioxidant Enzymes.

Hangovers from alcohol consumption cause symptoms like headaches, nausea, and fatigue, disrupting daily activities and overall well-being. Over time, they can also lead to inflammation and oxidative stress. Effective hangover relief alleviates symptoms, prevents dehydration, and replenishes energy needed for daily tasks. Natural foods considered high in antioxidants and antiinflammatory properties may aid in the hepatic breakdown of alcohol. The study aims to investigate the impact of glutathione or its enriched yeast extract, which is recognized for its antioxidant characteristics, on alcohol metabolism and alleviating hangovers in a rat model exposed to binge drinking. In this study, glutathione and its enriched yeast extract controlled hangover behaviour patterns, including locomotor activity. Additionally, it enhanced the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) following ethanol ingestion (3 g/kg). Further, the incorporation of glutathione led to an increase in the expression of antioxidant enzymes, such as SOD and catalase, by activating the nuclear erythroid 2-related factor 2 (Nrf2) signaling pathway. This activation reduced the excessive production of reactive oxygen species (ROS) and malondialdehyde. Next, glutathione modulated the activity of cytochrome P450 2E1 (CYP2E1) and the protein expressions of Bax and Bcl2. Besides, in vitro and in vivo investigations with glutathione demonstrated a regulating effect on the pan-s-glutathionylation and its associated protein expression, glutaredoxin 1 (Grx1), glutathione-S-transferase Pi (GST-π), and glutathione reductase (GR). Together, these findings suggest that glutathione or its enriched yeast extract as a beneficial dietary supplement for alleviating hangover symptoms by enhancing alcohol metabolism and its associated Nrf2/Keap1 signalings.

Tandem Imaging of Breath Ethanol and Acetaldehyde Based on Multiwavelength Enzymatic Biofluorometry.

Highly sensitive and selective imaging of human-borne volatile organic compounds (VOCs) enables an intuitive understanding of their concentrations and release sites. While multi-VOC imaging methods have the potential to facilitate step-by-step metabolic tracking and improve disease screening accuracy, no such system currently exists. In this study, we achieved simultaneous imaging of ethanol (EtOH) and acetaldehyde (AcH), the starting molecule and an intermediate metabolite of alcohol metabolism, using a multiwavelength VOC imaging system. The system employed alcohol dehydrogenase-catalyzed substrate oxidation (ADHOX) and reduction (ADHRD) reactions. The oxidation of EtOH by ADHOX in the presence of NAD+ produced NADH, which was subsequently oxidized by diaphorase (DP) with resazurin, leading to the resorufin formation, characterized by red fluorescence (excitation at 560 nm and fluorescence at 590 nm). Reduction of AcH by ADHRD consumed NADH, leading to a decrease in blue fluorescence (ex. 340 nm, fl. 490 nm). Meshes incorporating ADHOX-DP or ADHRD were arranged in tandem in front of a camera. Fluorescence images were captured, while a mixture of gaseous EtOH and AcH was applied by switching between two bandpass filters at 1 Hz. Each mesh exhibited selective responses to the target VOCs, with no significant impact on the dynamic range observed in either the single or tandem configurations (EtOH 1-300 ppm, AcH 0.2-5 ppm). The 90% response time was close after time-domain image differential analysis (EtOH = 26 s and AcH = 15 s). Furthermore, the system enabled simultaneous and quantitative imaging of EtOH and AcH concentrations in the breath after alcohol consumption. It also distinguished differences in alcohol metabolism based on the alcohol dehydrogenase 2 (ALDH2) activity, as indicated by the EtOH/AcH ratio (ALDH2 active vs nonactive: 120.9/0.71 ppm vs 129.2/1.99 ppm).

Alcoholic Extracts from the Ganoderma Lucidum Fermentation Product Alleviated Ethanol-Induced Liver Injury, Gut Leakiness, and Gut Dysbiosis in Mice.

The hepatoprotective effect of the alcoholic extracts of Ganoderma lucidum fermentation products (GFE) was investigated. C57BL/6 mice were pretreated with GFE for 7 days and then subjected to the chronic-binge ethanol feeding model. GFE pretreatment significantly reduced the ethanol-induced elevated serum levels of aspartate aminotransferase (AST) and alanine transaminase (ALT), hepatic steatosis, and increased triglyceride content. GFE pretreatment also altered hepatic alcohol metabolism, suppressed oxidative stress by decreasing the expression of Cyp2e1, and increasing the level of GSH. Lipidmoic analysis revealed that GFE pretreatment effectively increased ratio of phosphatidylcholines /phosphatidylethanolamine (PC/PE) in the liver. Furthermore, mice pretreated with GFE demonstrated decreased hepatic inflammation and plasma lipopolysaccharide (LPS) levels. Additionally, the mRNA expression of gut tight junction proteins such as ZO-1, Occludin and Claudin-1, along with antimicrobial peptide (e.g., Reg3β and Reg3γ) were up-regulated by GFE pretreatment. 16s rRNA sequencing revealed that GFE increased Bacteroidales, Parabacteroides, and Dubosiella, which were associated with hepatic steatosis, inflammation and intestinal barrier function parameters. These results demonstrate that GFE can prevent ethanol-induced liver injury and inflammation, gut leakiness and restore gut microbiota dysbiosis.

Angelica sinensis polysaccharide could alleviate the gastrointestinal damage in alcoholic fatty liver disease mice: Regulation of alcohol metabolism and enhancement of short-chain fatty acids utilization

Ethnopharmacological relevanceDysfunction of the intestinal barrier was an important trigger for alcoholic liver damage and alcohol had brought about intestinal damage before causing liver damage. The root of Angelica sinensis (Oliv.) Diels, crucial traditional medicinal material, was widely utilized for its blood-invigorating, intestinal-lubricating and gynecological benefits. Angelica sinensis polysaccharide (ASP) was an essential natural active ingredient of Angelica sinensis and exhibited considerable potential for gastrointestinal protection. Nevertheless, the systematic research of ASP on the gastrointestinal tract remained insufficient. Aim of this studyTo systematically explore the protective effect and underlying mechanisms of ASP against alcohol-induced gastrointestinal injury, including the stomach, ileum and colon. Materials and methodsThe AFLD mice model was established via the intragastric administration of alcohol twice a day for one week. The protective effect of ASP on the representative segments of the gastrointestinal tract (stomach, ileum and colon) was subsequently studied after confirming its hepatoprotective activity. The impact of ASP on gastrointestinal alcohol metabolism was examined to explain its antioxidant and antiapoptotic activities. Furthermore, the effect of ASP on short-chain fatty acids (SCFA) in the colon and colonic contents was investigated to further enhance the understanding of the underlying mechanisms. ResultsASP could reduce oxidative stress and apoptosis in the gastrointestinal tract via regulating CYP2E1-mediated alcohol metabolism. Additionally, ASP could significantly increase the levels of FFAR2, FFAR3 and HCAR2 in colon, thereby promoting the utilization of SCFA. ConclusionASP was proven for the first time to improve gastrointestinal damage caused by alcohol, indicating its enormous potential as a candidate medicine for the treatment of alcohol related gastrointestinal injury.

Maternal alcohol consumption during pregnancy and child development: Role of ADH1B and ALDH2 gene polymorphisms-The Yamanashi Adjunct Study of the Japan Environment and Children's Study.

The role of polymorphisms in genes regulating alcohol metabolism, particularly those modulating the impact of prenatal alcohol exposure on the neurodevelopment of offspring, remains inconclusive. Herein, we aimed to determine the involvement of ADH1B and ALDH2 gene polymorphisms in maternal alcohol consumption during pregnancy and the risk of developmental delay in offspring in a Japanese population. We analyzed 1727 mother-child pairs from the Yamanashi Adjunct Study of the Japan Environment and Children's Study. Maternal alcohol consumption during pregnancy was determined through a mid-pregnancy questionnaire and categorized into three groups: never-drinkers, those who quit drinking in early pregnancy, and current drinkers. Developmental delays in children were assessed in five domains using the Japanese version of the Ages and Stages Questionnaire, Third Edition (J-ASQ-3) at 3 years of age. We conducted a logistic regression analysis to explore the relationship between maternal drinking status during pregnancy and developmental delays in offspring with respect to maternal ADH1B (rs1229984) or ALDH2 (rs671) gene polymorphisms. Children born to mothers who continued alcohol consumption during pregnancy had a higher risk of delayed communication skills at 3 years of age compared with children born to mothers who did not drink alcohol (adjusted odds ratio [OR], 5.82; 95% confidence interval, 1.84-18.38). Analysis by ALDH2 gene polymorphism revealed that alcohol consumption by mothers carrying the wild-type ALDH2 (*1/*1) increased the risk of delayed communication skills at 3 years of age, whereas alcohol consumption by mothers carrying a heterozygotic genotype of ALDH2 (*1/*2) enhanced the risk of developmental delay in all five domains of the J-ASQ-3. The impact of ADH1B gene polymorphism could not be clearly elucidated. Our results suggest that alcohol consumption by pregnant females carrying the deficient variant ALDH2*2 genotype may increase the risk of developmental delay in their offspring.

Relationship between moderate alcohol consumption, genetic polymorphisms and body weight in a population sample of Puerto Madryn, Argentina

Introduction. The relationship between obesity and alcohol consumption is a topic of significant interest to public health. Alcoholic beverages contribute additional calories to the diet, which could be a relevant factor to the overweight risk. However, its association with weight gain is controversial and influenced by multiple factors. Objective. To analyze the relationship between moderate alcohol intake and body mass index, considering the variables that may influence this relationship. Materials and methods. The sample consisted of 155 individuals from Puerto Madryn (Argentina). Each participant completed a questionnaire about health, lifestyle, demographic, and socioeconomic factors. Anthropometric measurements were taken, and polymorphisms of 18 genes related to alcohol metabolism were genotyped. Results. We found that moderate alcohol consumption is associated with a lower body mass index, particularly in females. An increase of 14 grams of alcohol was associated with a risk of 0.68 for obesity and 0.71 for overweight. The T variant of the marker rs4646543 (ALDH1A1), a gene involved in alcohol metabolism and adipogenesis, was associated with a higher frequency of alcohol consumption. Conclusion. The findings of this study suggest that moderate alcohol consumption does not significantly contribute to body weight in the sample studied. Furthermore, the association with genetic variants, such as those of the ALDH1A1 gene, may provide a biological explanation for the inverse relationship observed between weight and alcohol consumption.

Biased allosteric modulator of neurotensin receptor 1 reduces ethanol drinking and responses to ethanol administration in rodents

Alcohol use disorders (AUDs) impose an enormous societal and financial burden, and world-wide, alcohol misuse is the 7th leading cause of premature death [1]. Despite this, there are currently only 3 FDA approved pharmacological approaches for the treatment of AUDs in the United States. The neurotensin (Nts) system has long been implicated in modulating behaviors associated with alcohol misuse. Recently, a novel compound, SBI-553, that biases the action of Nts receptor 1 (NTSR1) activation, has shown promise in preclinical models of psychostimulant use. Here we investigate the efficacy of this compound to alter ethanol-mediated behaviors in a comprehensive battery of experiments assessing ethanol consumption, behavioral responses to ethanol, physiological sensitivity to ethanol, and ethanol metabolism. Additionally, we investigated behavior in avoidance and cognitive assays to monitor potential side effects of SBI-553. We find that SBI-553 reduces ethanol consumption in mice without altering avoidance behavior or novel object recognition. We also observe sex-dependent differences in physiological responses to sequential ethanol injections in mice. In rats, we show that SBI-553 attenuates sensitivity to the interoceptive effects of ethanol (using a Pavlovian drug discrimination task). Our data suggest that targeting NTSR1 signaling may be promising to attenuate alcohol misuse, and adds to a body of literature that suggests NTSR1 may be a common downstream target involved in the psychoactive effects of multiple reinforcing substances.

Mitochondrial quality control in alcohol-associated liver disease.

Excessive alcohol consumption is a leading cause of alcohol-associated liver disease (ALD), a significant global health concern with limited therapeutic options. Understanding the key factors contributing to ALD pathogenesis is crucial for identifying potential therapeutic targets. Central to ALD pathogenesis is the intricate interplay between alcohol metabolism and cellular processes, particularly involving mitochondria. Mitochondria are essential organelles in the liver, critical for energy production and metabolic functions. However, they are particularly vulnerable to alcohol-induced damage due to their involvement in alcohol metabolism. Alcohol disrupts mitochondrial function, impairing ATP production and triggering oxidative stress, which leads to cellular damage and inflammation. Mitochondrial quality control mechanisms, including biogenesis, dynamics, and mitophagy, are crucial for maintaining optimal mitochondrial function. Chronic alcohol consumption disrupts mitochondrial quality control checkpoints, leading to mitochondrial dysfunction that impairs fatty acid oxidation and contributes to hepatic steatosis in ALD. Moreover, alcohol promotes the accumulation of damaged mitochondria and the release of proinflammatory components, exacerbating liver damage and inflammation. Preserving mitochondrial health presents a promising therapeutic approach to mitigate ALD progression. In this review, we provide a comprehensive overview of the effects of alcohol on mitochondrial function and quality control mechanisms, highlighting their role in ALD pathogenesis. Understanding these mechanisms may pave the way for the development of novel therapeutic interventions for ALD.

Interaction between catalase metabolism of ethanol and peroxisomal fatty acid oxidation

Interaction between catalase metabolism of ethanol and peroxisomal fatty acid oxidation

Structural analysis of ExaC, an NAD+-dependent aldehyde dehydrogenase, from Pseudomonas aeruginosa

The opportunistic pathogen Pseudomonas aeruginosa (Pa) utilizes ethanol as an energy source, however, ethanol metabolism generates acetaldehyde, a toxic byproduct. To mitigate this toxicity, P. aeruginosa employs aldehyde dehydrogenases (ALDHs) to oxidize acetaldehyde into less harmful compounds. ExaC, an NAD+-dependent ALDH from P. aeruginosa (PaExaC) and a member of group X ALDHs, plays a critical role in this detoxification by oxidizing both aldehydes and hydrazones. In this study, we determined the crystal structures of PaExaC in its apo and NAD+-bound forms. PaExaC functions as a homodimer, with three distinct domains: an NAD+ binding domain, a catalytic domain, and an oligomerization domain. Structural analyses revealed that PaExaC’s substrate entry channel (SEC) is optimized for size-selective aldehyde metabolism, with Leu120, Tyr462, and Thr302. Comparative structural and docking analyses with other ALDHs further validated PaExaC’s preference for small aliphatic aldehydes and hydrazones. These findings highlight PaExaC’s role in aldehyde detoxification, facilitating P. aeruginosa survival in diverse environments, and provide structural insights for developing targeted inhibitors to help treat infections.

Protective Effect and Mechanism of L-Theanine on Acute Alcoholic Liver Injury in Mice.

Acute alcoholic liver injury (AALI), a global health concern, is exacerbated by excessive episodic drinking. L-theanine (LTA), a compound found in tea leaves, mitigates the AALI-induced liver oxidative stress and inflammation. However, its relationship with alcohol metabolism and its liver-protective mechanism remains unexplored. This study investigates the protective mechanisms of LTA against AALI in mice. The results demonstrate that LTA mitigates liver tissue damage and reduces the serum levels of aspartate aminotransferase and alanine aminotransferase, and liver levels of triglycerides, malondialdehyde, reactive oxygen species (ROS), tumor necrosis factor-α, interleukin-6, and interleukin-1β. However, LTA enhances the activity of ethanol-metabolizing enzymes and decreases ethanol and acetaldehyde serum levels. Mechanistically, LTA accelerates alcohol metabolism by upregulating the hepatic expression of ADH6, ALDH1B1, ALDH2, CAT, and ACSS1 mRNA and protein in AALI mice, LTA downregulates the expression of CYP2E1 mRNA and protein and promoting antioxidative activities thus reducing the accumulation of ROS. This attenuated inflammation by inhibiting the phosphorylation of nuclear factor-kappa B inhibitor alpha (IκBα) and downregulating the hepatic expression of NF-κB p65, TNF-α, IL-1β, IL-6 mRNA, and protein. LTA is a beneficial dietary supplement that protects against AALI by modulating alcohol metabolism and the TNF-α/NF-κB pathway.

Assessment of Quality of Life of Caregivers of Patient with Alcoholic Liberty Disease

Alcoholic liver disease (ALD) is a progressive condition resulting from chronic and excessive alcohol consumption, leading to liver cell damage. Although the liver is the primary site for alcohol oxidation, a small amount is also metabolized in the stomach. Ethanol metabolism primarily produces acetaldehyde, a toxic byproduct responsible for symptoms such as facial flushing, headaches, nausea, and increased heart rate, all of which contribute to the development of ALD. The risk of developing ALD varies among individuals, but it generally increases with alcohol intake beyond certain thresholds: more than two standard drinks per day for men and more than one standard drink per day for women. Alcoholic liver disease (ALD) can progress to fibrosis and cirrhosis, potentially leading to liver infection. The prevalence of ALD fluctuates over time and varies by region due to factors such as alcohol consumption patterns, healthcare accessibility, and public health initiatives. ALD poses a significant global health challenge, highlighting the need for increased awareness about the dangers of excessive alcohol consumption and the promotion of responsible drinking practices. Medical guidance and support are essential in educating individuals about the risks of overconsumption. According to the latest surveillance report from the National Institute on Alcohol Abuse and Alcoholism, liver cirrhosis ranked as the 12th leading cause of death in the United States in 2007, with 29,925 deaths, nearly 48% of which were alcohol-related.

Pueraria Extract Ameliorates Alcoholic Liver Disease via the Liver-Gut-Brain Axis: Focus on Restoring the Intestinal Barrier and Inhibiting Alcohol Metabolism.

Alcoholic liver disease (ALD) is one of the causes of hepatocellular carcinoma, accompanied by intestinal leakage and microbial changes. Pueraria has protective effects on liver injury. The aim of this study was to investigate the mechanism of pueraria in the treatment of ALD. UPLC-Q/TOF-MS was used to analyze the composition of the pueraria extract (PUE). Acute and chronic ALD models were established to evaluate the antialcoholic and hepatoprotective effects of PUE. As a result, PUE treatment reduced the serum levels of ALT, AST, TC, and TG and inflammatory factors and alleviated liver inflammation and drunk state. PUE decreased the gene expression of ADH1 and the serum level of acetaldehyde (ACH) to inhibit the generation of ACH from ethanol metabolism, increased the gene level of ALDH2 to accelerate the decomposition of ACH, and thereby alleviated liver inflammation and intestinal barrier damage. Meanwhile, 16 S rDNA revealed that PUE altered the microbiota composition, reduced the amount of Proteobacteria and Desulfobacterota, and thus inhibited the generation of lipopolysaccharide and its downstream-like TLR4/MyD88/NF-κB pathway. PUE also increased the abundance of Bacteroides, Ruminococcus, and Prevotella and producted short-chain fatty acids to protect the intestinal wall. Treatment with fecal microbiota transplantation further confirmed that PUE gut microbiota dependently alleviated ALD. Therefore, PUE regulated gut microbiota and inhibited ethanol metabolism to alleviate ALD through the liver-gut-brain axis. It has good prospects in the future.

Altered Expression of Neuroplasticity-Related Genes in Alcohol Addiction and Treatment.

Alcohol use disorder's complexity arises from genetic and environmental factors, with alcohol metabolism genes and neurotransmitter pathways being critical. This study aims to analyze synaptic plasticity gene expression changes in individuals with AUD in order to study their contribution to AUD development and to identify potential biomarkers of treatment response. RNA was extracted from whole peripheral blood (20 patients, 10 healthy controls), before and after treatment (Qiagen AllPrep RNA/DNA Mini Kit), and the gene expression of 84 genes related to neuroplasticity was studied using the RT2 Profiler for Human Synaptic Plasticity RT-PCR Array (PAHS-126ZA, Qiagen), comparing AUD patients to control and responders to non-responders. The potential prognostic/predictive biomarkers were searched using machine learning models. A total of 35 dysregulated genes were found in AUD patients. EPHB2, EGR, and AKT1 were increased, while TIMP1, NCAM1, and GRM2 were decreased. Responders showed distinct gene expression profiles at baseline. After treatment, the expression of 57 genes was normalized, while NCAM1, GRM2, and BDNF showed the most significant recovery. EGR4, INHBA, and NCAM1 emerged as potential biomarkers to predict treatment success. These results indicate that gene profiles in peripheral blood can serve as prognostic markers for the prognosis and treatment of AUD, although further validation is required.

Tolerance and efficient metabolization of extremely high ethanol concentrations by a social wasp

Ethanol, a natural by-product of sugar fermentation, can be found in various fruits and nectar. Although many animals routinely consume ethanol in low concentrations as part of their natural diets, its inherent toxicity can cause severe damage. Even species particularly well adapted to ethanol consumption face detrimental effects when exposed to concentrations above 4%. Here, we investigated the metabolism of ethanol and its impact on survival and behavior in the Oriental hornet (Vespa orientalis), a social wasp that naturally consumes ethanol. We show that chronic ethanol consumption, even at concentrations as high as 80%, had no impact on hornet mortality, construction behavior, or agonistic behavior. Using 13C1 labeled ethanol, we show that hornets efficiently metabolized ingested ethanol and at a much higher rate than honey bees. The presence of multiple copies of the alcohol dehydrogenase (NADP+) gene in the Vespa genera suggests a potential mechanism for ethanol tolerance. These findings support the hypothesis that the mutualistic relationship between ethanol-producing organisms and vespid hosts may be at the origin of their remarkable capacity to utilize and metabolize ethanol.

Mitochondria and Alcohol-Associated Liver Disease: Pathogenic Role and Target for Therapy.

Alcohol-associated liver disease (ALD) is one of the leading causes of chronic liver disease and a major cause of liver-related death. ALD is a multifactorial disease triggered by the oxidative metabolism of alcohol which leads to the activation of multiple factors that promote the progression from steatosis to more advanced stages like alcohol-associated steatohepatitis (AH) that culminate in alcohol-associated cirrhosis and hepatocellular carcinoma. Poor understanding of the complex heterogeneous pathology of ALD has limited drug development for this disease. Alterations in mitochondrial performance are considered a crucial event in paving the progression of ALD due to the crucial role of mitochondria in energy production, intermediate metabolism, calcium homeostasis, and cell fate decisions. Therefore, understanding the role of mitochondria in eliciting steatosis and progression toward AH may open the door to new opportunities for treatment. In this review, we will cover the physiological function of mitochondria, its contribution to ALD in experimental models and human disease, and explore whether targeting mitochondria may represent a game changer in the treatment of ALD.

Efficacy and Safety of Wilac L Probiotic Complex Isolated from Kimchi on the Regulation of Alcohol and Acetaldehyde Metabolism in Humans.

Alcohol-related hangovers impact both physical and mental wellness, largely due to acetaldehyde levels produced through alcohol metabolism. The present study investigated the efficacy and safety of the Wilac L probiotic complex (Levilactobacillus brevis WiKim0168 and Leuconostoc mesenteroides WiKim0172 isolated from kimchi) in improving hangovers post-alcohol consumption. This study was conducted as a randomized, double-blind, crossover placebo-controlled clinical trial from August 2023 to February 2024. Subjects (n = 26) were randomized into six test groups consuming three products, the Wilac L probiotic complex, Wilac L35 (Wilac L probiotic complex with Pyrus pyrifolia Nakai), or placebo, in different orders with crossover after a wash-out interval of 7-10 days. Blood alcohol and acetaldehyde concentrations were measured 0, 0.25, 0.5, 1, 2, 4, 6, and 15 h after alcohol consumption. The blood acetaldehyde levels measured with Wilac L probiotic complex supplementation were significantly lower than the control at 0.25 (p = 0.0381), 0.5 (p = 0.0498), and 1 h (p = 0.0260) post-consumption. The blood acetaldehyde levels after Wilac L35 consumption compared to the control are significant at 0.25 (p = 0.0115), 0.5 (p = 0.0054), 1 (p = 0.0285), 2 (p = 0.0113), and 6 h (p = 0.0287) post-consumption. No significant adverse events were reported. The Wilac L probiotic complex is associated with decreased blood acetaldehyde levels and improved subjective hangover symptoms.

To Drink or Not to Drink? Investigating Alcohol’s Impact on Prostate Cancer Risk

Background/Objectives: Prostate cancer (PCa) is a significant global health issue. The relationship between alcohol consumption and PCa risk has been the subject of extensive research, yet findings remain inconsistent. This review aims to clarify the association between alcohol intake and PCa risk, its aggressiveness, and the potential metabolic pathways involved in PCa onset. Methods: A comprehensive literature search was conducted across multiple databases, including PubMed and MEDLINE, focusing on epidemiological studies, meta-analyses, cohort studies, and case–control studies. Studies evaluating alcohol consumption, prostate-specific antigen (PSA) levels, and PCa risk were included. The review also explored the roles of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in alcohol metabolism. Results: The analysis reveals a complex relationship between alcohol consumption and PCa. Heavy alcohol intake is associated with an increased risk of PCa, particularly more aggressive forms, and higher mortality rates. However, studies also show weak or no association between moderate alcohol consumption and PCa. The variability in findings may be attributed to differences in alcohol types, regional factors, and study methodologies. Conclusions: The link between alcohol consumption and PCa risk is multifaceted. While heavy drinking appears to increase the risk of aggressive PCa, the overall relationship remains unclear. Further research is needed to better understand these associations and inform public health recommendations and cancer prevention strategies.

Protective mechanisms of Hovenia dulcis Thunb extracts on acute alcoholism and liver injury

As a traditional Chinese medicine for anti-alcoholism, Hovenia dulcis Thunb (HDT) is widely used in the treatment of alcoholism and alcohol-related liver diseases. However, the scientific evidence of its mechanism has not been clearly established. In this study, a mouse model of acute alcoholism was established to explore the protective mechanisms of three kinds of HDT extracts on acute alcoholism and liver injury from the perspectives of behavioral indicators, serum and liver biochemical indicators, alcohol metabolic enzyme activity, intestinal flora, and liver metabolomics. The results showed that the extracts of HDT shortened the time of sobering up, significantly increased the activity of alcohol metabolic enzymes and antioxidant capacity, promoted ethanol metabolism, and had a certain preventive effect on alcoholic liver injury while preventing adverse reactions caused by alcohol. Notably, HDT water extract (HDTs) demonstrated superior anti-alcohol and liver protective properties compared to polysaccharide and polyphenol extracts of HDTs. It may be through the regulation of intestinal flora imbalance, specifically Muribaculaceae and Dubosiella to modulate biosynthetic pathways of phenylalanine, tyrosine, and tryptophan, ultimately mitigating oxidative stress caused by ethanol consumption. This suggests that HDTs may have potential in preventing acute alcoholism and liver injury.