Alcohol最新文献

Despite the considerable change in alcohol consumption during the COVID-19 pandemic, the impact of the pandemic on the suicide rate in terms of alcohol consumption was not studied. This study was performed to examine whether the change in the suicide rate during the COVID-19 pandemic was related to alcohol consumption and whether the relation was specific to suicides when compared to mortality due to other causes. We performed a comparative interrupted time series (CITS) analysis for the suicide rate of people aged 19 to 60 with three comparison groups (the suicide rate of people aged 19 and under, the cancer death rate of people aged 19 to 60, and alcohol-induced death rates). The suicide rate of people aged 19 to 60 and alcohol consumption per capita, along with alcohol-induced death rates, continued to decrease during the pandemic in 2020 and 2021, while the suicide rate of people aged 19 and under and the cancer death rate showed increases. In the comparative interrupted time series model, alcohol consumption had an increasing effect on the adult suicide rate compared to comparison groups when time trends and changes associated with COVID-19 were adjusted. This study shows that the decrease in the adult suicide rate in Korea during the pandemic was associated with the decrease in alcohol use among the adult population. Considering that means restriction is the most effective way of controlling suicide and that alcohol can be the most potent and final trigger for suicide, the decrease in suicides during the pandemic and its association with alcohol consumption should be understood as a call for further efforts to decrease alcohol consumption.

While past studies have provided evidence linking excessive alcohol consumption to increased risk for cardiovascular diseases (CVDs) and colorectal cancer (CRC), existing data on the effects of moderate alcohol use on these conditions have produced mixed results. The purpose of this study was to investigate the effects of moderate alcohol consumption on risk factors associated with the development of CVDs and CRC in adult rats. Twenty-four, 14-month-old, non-deprived male Wistar rats were randomly assigned to either an ethanol group, which consisted of voluntary access to a 20% (v/v) ethanol solution on alternate days, or a water control group (n = 12/group) for 13 weeks. Blood samples were collected to analyze levels of albumin, glucose, adiponectin, lipids, oxidized low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (apoA1), C-reactive protein (CRP), high-mobility group box 1 protein (HMGB-1), tumor necrosis factor-alpha (TNF-α), thyroxine, thyroid-stimulating hormone, 8-oxo-2′-deoxyguanosine (8-oxo-dG), liver function enzymes, and antioxidant capacity. Colonic gene expression related to colon carcinogenesis was also assessed. Ethanol-treated rats were found to have significantly higher HDL-C and apoA1 levels compared to controls. Moderate alcohol consumption led to significantly lower CRP levels and a trend for decrease in HMGB-1, TNF-α, and 8-oxo-dG levels. In the ethanol-exposed group, colonic gene expression of superoxide dismutase was upregulated while aldehyde dehydrogenase 2 showed a trend for increase compared to the control group. These results indicate that adopting a moderate approach to alcohol consumption could potentially improve health biomarkers related to CVD and CRC by increasing HDL-C levels and antioxidant activity and reducing DNA damage and inflammatory activity.

While DNA serves as the fundamental genetic blueprint for an organism, it is not a static entity. Gene expression, the process by which genetic information is utilized to create functional products like proteins, can be modulated by a diverse range of environmental factors. Epigenetic mechanisms, including DNA methylation, histone modification, and microRNAs, play a pivotal role in mediating the intricate interplay between the environment and gene expression. Intriguingly, alterations in the epigenome have the potential to be inherited across generations. Alcohol use disorder (AUD) poses significant health issues worldwide. Alcohol has the capability to induce changes in the epigenome, which can be inherited by offspring, thus impacting them even in the absence of direct alcohol exposure. This review delves into the impact of alcohol on the epigenome, examining how its effects vary based on factors such as the age of exposure (adolescence or adulthood), the duration of exposure (chronic or acute), and the specific sample collected (brain, blood, or sperm). The literature underscores that alcohol exposure can elicit diverse effects on the epigenome during different life stages. Furthermore, compelling evidence from human and animal studies demonstrates that alcohol induces alterations in epigenome content, affecting both the brain and blood. Notably, rodent studies suggest that these epigenetic changes can result in lasting phenotype alterations that extend across at least two generations. In conclusion, the comprehensive literature analysis supports the notion that alcohol exposure induces lasting epigenetic alterations, influencing the behavior and health of future generations. This knowledge emphasizes the significance of addressing the potential transgenerational effects of alcohol and highlights the importance of preventive measures to minimize the adverse impact on offspring.

Background

To understand why some individuals who develop alcohol use disorders (AUD) first begin to drink heavily, a number of scales have been developed that index aspects of alcohol craving and restraint from drinking. We developed a new measure called the Alcohol Consumption Questionnaire (ACQ), based in part on items modified from scales used to index binge eating, because there are data to suggest that binge eating and binge drinking may share common antecedents. We present an initial validity study using data from a sample of Mexican Americans.

Methods

Data were from 699 Mexican American young adults in San Diego County, CA. A subsample (n = 60) had short-term test-retest data. Factor analysis and reliability assessment guided item reduction. Item response theory (IRT) analyses quantified item severity and identified questions with differential item functioning (DIF). Logistic regression assessed associations of mean scale scores with AUD, adjusting for key demographics, alcohol expectancies and subjective response to alcohol. We also examined associations with a protective genetic variant downstream from the alcohol dehydrogenase 7 (ADH7) gene.

Results

The scale was reduced from 20 to 14 questions, which can be summarized by a single overall score (Cronbach's alpha = 0.896) or by two sub-scores (Consumption: 12 items, Cronbach's alpha = 0.896; Enjoyment: 2 items, Cronbach's alpha = 0.780). Test-retest reliability was very high (0.80–0.98) in this sample. The overall ACQ score and each subdomain score were strongly associated with AUD (ORs = 5.95 mild; 11.41 moderate; 48.56 severe) and family history of AUD. Respondents with the protective genetic variant had significantly lower overall ACQ scores (p < 0.001).

Conclusion

The ACQ is a novel measure of alcohol consumption with strong relationships with both the AUD phenotype and ADH7 gene variants in a sample of Mexican American young adults.

Introduction

Large population-based studies have suggested a link between increased alcohol use and reduced pain. In addition, these studies suggest that higher levels of pain intensity are associated with an increase in alcohol consumption and rates of hazardous drinking which potentiates the risk of developing alcohol use disorders (AUD). The mechanisms and determinants of the alcohol–pain interaction can be studied in preclinical studies.

Methods

The overall goal of this study is to use animal models to explore the impact of acute postoperative pain on alcohol intake. To achieve this, we characterized the timeline and levels of alcohol intake and preference in mice after laparotomy in the 2-bottle choice paradigm.

Results

Our results show that laparotomy surgery increased alcohol intake and preference in male mice but not females in the 2-bottle choice and 3-bottle choice assays. In addition, ketoprofen administration blocked the increase in alcohol consumption in male mice after laparotomy. We also found that changes in alcohol initial sensitivity and acute functional tolerance, using loss of righting reflex (LORR) response, occur after surgery in mice.

Conclusion

Taken together, these findings suggests that sex, pain and alcohol sensitivity-related factors may modulate the relationship between alcohol consumption and pain.

Background

Alcohol abuse (AA) has s high prevalence, affecting 10 to 15 million Americans. While AA was demonstrated to negatively impact cardiovascular health, limited evidence from existing studies presents conflicting findings regarding the effects of AA on coronary artery bypass grafting (CABG) outcomes. This study aimed to compare the in-hospital outcomes after CABG between AA and non-AA patients.

Methods

Patients who underwent CABG were identified in National Inpatient Sample from Q4 2015–2020. Exclusion criteria included age<18 years and concomitant procedures. A 1:3 propensity-score matching was used to address differences in demographics, socioeconomic status, primary payer status, hospital characteristics, comorbidities, and transfer/admission status between AA and non-AA patients. In-hospital outcomes after CABG were examined.

Results

There were 5694 (3.39%) AA patients who underwent CABG. After matching, 17,315 from 162,488 non-AA patients were matched to all AA patients. AA and non-AA patients had comparable mortality (1.64% vs 1.55%, p = 0.67) and MACE (2.46% vs 2.56%, p = 0.73). However, AA patients had higher cardiogenic shock (8.31% vs 7.43%, p = 0.03), mechanical ventilation (11.51% vs 7.96%, p < 0.01), hemorrhage/hematoma (57.49% vs 54.75%, p < 0.01), superficial (0.99% vs 0.61%, p < 0.01) and deep wound complications (0.37% vs 0.18%, p = 0.02), reopen surgery for bleeding control (0.92% vs 0.63%, p = 0.03), transfer out (21.00% vs 16.38%, p < 0.01), longer time from admission to operation (p < 0.01), longer length of stay (p < 0.01), and higher hospital charge (p < 0.01).

Conclusion

While AA was not found to be linked with in-hospital mortality or MACE after CABG, it was independently associated with postoperative complications. These findings could enhance preoperative risk stratification for AA patients and inform postoperative management following CABG.

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Recently, researchers have proposed an updated model of executive functions that includes relational integration, the mental ability to bind information into more complex structures. Hangover is known to disrupt other core components of executive functions, but little is known about how it influences relational integration. Therefore, this study aimed to investigate how hangover influences performance on a relational integration task. Twenty-seven participants completed an online relational integration task and mood- and emotion-regulation questionnaires during a hangover and no-hangover condition in this naturalistic design study. Results indicated that relational integration was impaired in hangover (p < 0.001, η_p² = 0.562) relative to the no-hangover condition. In addition, participants experienced greater difficulties in regulating emotions (p < 0.001, d = 0.85) and lower mood (p < 0.001, d = 0.88) during hangover. These results suggest that relational integration is impaired in hangover and add weight to the argument that cognitive impairments in hangover may be due to the hangover-related impact on domain-general processing resources.