Studiendatenbank

<h4>Background</h4>While alcohol consumption appears to influence the incidence of breast cancer (BC), its association with prognosis after a BC diagnosis remains less established. This meta-analysis aimed to explore the association between alcohol consumption on both BC incidence and outcomes.<h4>Methods</h4>A systematic literature search was conducted up to May 1st, 2025 (CRD42025593784). Retrospective and prospective studies reporting BC incidence, recurrences, and survival outcomes in women with history of alcohol consumption were included. Analyses according to alcohol intake levels (light, intermediate, heavy consumption) were performed. Main outcomes were BC incidence, BC recurrences, BC-specific survival (BCSS), and overall survival (OS). Pooled relative risk (RR) and hazard ratio (HR) with 95% confidence interval (CI) were calculated.<h4>Results</h4>Out of 5208 screened records, 37 studies including 2,565,920 women were included. Among 17 studies reporting on BC incidence, any alcohol consumption was associated with an increased BC incidence (RR 1.17, 95%CI 1.09-1.26; p < 0.001). BC incidence increased proportionally with higher levels of alcohol consumption: light RR 1.13 (95%CI 1.05-1.23; p = 0.002), intermediate RR 1.28 (95%CI 1.18-1.39; p < 0.001)​, and heavy consumption RR 1.52 (95%CI 1.38-1.67; p < 0.001). Among 20 studies assessing BC outcomes, no associations were found between alcohol consumption and BC recurrences (RR 1.02, 95%CI 0.93-1.11) nor BCSS (HR 0.9

With the increasing prevalence of alcohol-related diseases, expanding our understanding of the toxic effects of excessive alcohol consumption is critical for prevention and treatment of metabolic and inflammatory pathology. This review summarizes current knowledge on the metabolic dysfunction and inflammation caused by alcohol and their impact on the pathogenesis of alcohol-related liver disease (ALD), type 2 diabetes, cardiovascular disease, and obesity, and neurological damage. It highlights recent evidence that alcohol induces a cascade of reactive oxygen species (ROS)-mediated lipid peroxidation and nicotinamide adenine dinucleotide (NAD⁺) depletion, triggering mitochondrial dysfunction and metabolic imbalances in the liver, heart, pancreas, and brain. By integrating these mechanistic insights with emerging data on how disrupted lipid and glucose metabolism amplify immune dysregulation, the review underscores the interplay between metabolic and inflammatory pathways in exacerbating tissue injury across these organs. A deep understanding of these metabolic and inflammatory disruptions is therefore essential for developing novel therapeutic strategies, including metabolic and nutritional interventions, aimed at mitigating the health risks of excessive alcohol consumption.

Metabolic dysfunction-associated fatty liver disease (MASLD) is associated with severe forms of liver injury, including fibrosis and cirrhosis. The main risk factors for MASLD-obesity, type 2 diabetes mellitus (T2DM), dyslipidemia, and insulin resistance (IR)-contribute to metabolic disturbances that initiate hepatic steatosis. Metabolic and alcohol-related liver disease (MetALD) describes patients with MASLD who also present alcohol-associated hepatic injury. Chronic oxidative and inflammatory stress promotes the progression of steatosis in both conditions. T2DM and chronic alcohol consumption are independent lifestyle-related risk factors for cirrhosis within the spectrum of metabolic dysfunction-related liver disease (MASLD and MetALD). The coexistence of both conditions may exacerbate hepatic pathological alterations. IR, which is frequently observed in patients with cirrhosis, can lead to the development of a condition known as hepatogenic diabetes (HD). HD is characterized by hyperinsulinemia, IR, and β-cell dysfunction occurring during the onset of cirrhosis and is associated with hepatic inflammation even in the absence of traditional metabolic risk factors such as obesity or a prior history of T2DM. In this context, alcohol intake enhances lipolysis in peripheral tissues, promotes hepatic steatosis, and aggravates metabolic dysfunction, ultimately contributing to excessive mitochondrial production of reactive oxygen species (ROS). Therefore, the present review examin

<h4>Background/objectives</h4>Evidence suggests a J-shaped association between alcohol consumption and depression, but it remains unclear whether this reflects a true causal effect, reverse causation, or methodological bias. This uncertainty is particularly relevant in older adults, who are at increased risk for both depression and alcohol-related harms. This study aimed to examine the association between varying levels of alcohol consumption and depression risk in community-dwelling older adults.<h4>Methods</h4>We analyzed 16,563 community-dwelling older adults (mean age 75.1 ± 4.6 years) from the ASPirin in Reducing Events in the Elderly (ASPREE) trial. Alcohol intake, reported at baseline and follow-up, was categorized as abstinent, occasional, moderate, or above-guideline. Both intention-to-treat (classified by baseline alcohol consumption, regardless of later changes) and per-protocol (using annual time-updated alcohol consumption ) analyses were performed. To address confounding, informative censoring, and selection bias, we applied marginal structural models with inverse probability weighting.<h4>Results</h4>In per-protocol analyses, abstainers (OR 1.17), occasional drinkers (OR 1.11), and above-guideline drinkers (OR 1.15) were significantly associated with a higher risk of depression compared with moderate drinkers, consistent with a J-shaped association. Sensitivity analyses excluding former drinkers and those with baseline depressive symptoms showed similar results

<h4>Background</h4>Alcohol consumption has been linked to cancer risk. Evidence is strongest for seven cancer types: breast, colorectum, oesophagus, liver, mouth, pharynx, and larynx. However, evidence supporting a causal effect from Mendelian randomization is inconsistent.<h4>Methods</h4>We perform a comprehensive Mendelian randomization analysis to assess whether genetically-predicted alcohol consumption associates with risk of 20 cancers. Such associations would provide supportive evidence for a causal effect of alcohol consumption on cancer risk. We used 95 genetic variants associated with alcohol consumption at genome-wide significance. Primary analyses were conducted in European ancestry participants from UK Biobank (367,643 individuals), FinnGen (500,348 individuals), All of US (169,312 individuals), and Million Veteran Program (451,206 individuals). We also estimated associations in cancer-specific consortia.<h4>Results</h4>No association was observed between genetically-predicted alcohol consumption and overall cancer (odds ratio (OR) per 1 standard deviation increase in alcohol consumption 0.96, p = 0.45). Among the seven highlighted cancer types, we saw a multiply-corrected significant positive estimate for combined head/neck cancer (OR 1.51, p = 0.001), and nominally significant positive estimates for colorectal (OR 1.21, p = 0.035) and oesophageal (OR 1.42 p = 0.033) cancer. For liver cancer, there was a null estimate overall (OR 1.40, p = 0.10), but a nominally

Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, with alcohol consumption implicated in its etiology. However, alcohol's prognostic impact on CRC survival is unclear, and self-reported intake is limited by bias. This population-based cohort study evaluated blood DNA methylation-based alcohol scores as objective prognostic tools in 2,129 CRC patients from Germany's DACHS study (2003-2021; median follow-up: 10 years). Participants were recruited from 22 hospitals in Southwest Germany, including non-metastatic (n = 1757) and metastatic (n = 372) patients with complete methylation and alcohol data. All three assessed methylation scores (3-CpG, 450-CpG, 144-CpG) correlated with self-reported lifetime/recent alcohol intake (Spearman's r: 0.29-0.36; p < 0.0001), particularly recent consumption. In non-metastatic patients, self-reported alcohol consumption showed a J-shaped mortality risk, with elevated risks in heavy drinkers and abstainers. A similar dose-response pattern was observed for the 3-CpG methylation score, which showed consistent and robust associations with increased overall mortality (adjusted hazard ratio [aHR] per standard deviation increase: 1.18, 95% CI: 1.11-1.25), non-CRC-related mortality (1.22, 1.13-1.32), and CRC-specific mortality (1.12, 1.00-1.25). The 450-CpG score was associated with overall mortality (1.07, 1.00-1.15), non-CRC-related mortality (1.14, 1.05-1.23), and alcohol consumption-related mortality (1.59, 1.17-2.16). Thes

Alcohol consumption is a globally prevalent lifestyle factor with complex and sometimes paradoxical effects on cardiovascular health, particularly regarding acute coronary syndrome (ACS). Earlier epidemiological studies described a J-shaped relationship between alcohol consumption and ACS risk; however, emerging evidence has increasingly challenged the validity of this concept. Mendelian randomization studies, genetic data, and recent pooled analyses suggest that the apparent cardioprotective effects of light-to-moderate drinking are largely attributable to residual confounding, including abstainer bias and socioeconomic factors, rather than true causal mechanisms. In contrast, excessive alcohol intake is linked to increased oxidative stress, inflammation, hypertension, and prothrombotic states, all of which contribute to plaque instability and the precipitation of ACS. Additionally, acute heavy drinking episodes may induce coronary vasospasm and arrhythmias, further elevating ACS risk. Genetic factors, drinking patterns, and beverage types may also modulate the relationship between alcohol and ACS, indicating the need for personalized risk assessment. Understanding these complex interactions is essential for clinicians when counseling patients on alcohol consumption within the context of cardiovascular prevention. This review aims to delve into current evidence on the epidemiology and pathophysiology linking alcohol consumption with ACS, providing a nuanced perspective that

The relationship between alcohol and health is complex, and the evidence relating alcohol consumption to various cardiovascular diseases, cancers and other conditions is evolving. Moreover, alcohol drinking guidelines vary widely. Here we conducted 16 systematic reviews across four databases and conservatively re-evaluated dose-response relationships between alcohol consumption and 20 health outcomes, analysing 843 cohort and case-control studies using the Burden of Proof meta-analytic framework. We found that levels of current alcohol consumption are associated with increased risks for cancers of the breast, colorectum, oesophagus, larynx, lip and oral cavities, pharynx, liver, stomach, pancreas and prostate, as well as pancreatitis, cirrhosis and other chronic liver diseases, lower respiratory infections, tuberculosis, and atrial fibrillation and flutter. We found J- or U-shaped relationships between alcohol consumption and type 2 diabetes, Alzheimer's disease and other dementias, ischaemic heart disease, ischaemic stroke and haemorrhagic stroke. While potential health impacts at low-to-moderate levels varied by outcome, high levels of alcohol consumption were associated with increased risk across all outcomes.

Alcohol-related liver disease (ALD) and metabolic dysfunction-associated steatotic liver disease (MASLD) are the leading causes of advanced liver disease worldwide. The introduction of the steatotic liver disease (SLD) nomenclature, including MASLD, MetALD, and ALD, has increased the need for accurate assessment of alcohol consumption, as disease classification, prognosis, and management depend partly on alcohol exposure. Although structured interviews and validated questionnaires such as AUDIT and AUDIT-C remain standard tools, self-reported alcohol intake is limited by recall bias, underreporting, and variability in drinking patterns. This has led to growing interest in direct alcohol biomarkers that objectively reflect recent alcohol exposure. In this review, we summarise current knowledge on direct alcohol biomarkers, with particular focus on phosphatidylethanol (PEth), the most widely used alcohol marker in hepatology. We conclude that PEth provides a robust and clinically useful measure of recent alcohol consumption, but that its interpretation is influenced by biological variability and context. Importantly, currently used cut-offs are not firmly anchored to clinical outcomes and should not be applied mechanically to classify SLD subtypes. Instead, biomarker-derived measures and self-reported alcohol use should be regarded as complementary tools, best integrated in a longitudinal and clinically contextualised assessment of alcohol exposure.

<b>Background</b>: Alcohol use patterns influence health outcomes. This study examined sex-specific drinking trajectories and their associations with all-cause mortality and coronary heart disease (CHD) in the US-based Framingham Heart Study. <b>Method</b>: Among 6570 participants (mean age: 55 ± 13; 55% women) followed for 15 years, a growth mixture model identified four sex-specific alcohol consumption trajectories. Cox models examined associations of alcohol trajectories with CHD and mortality over 10 years of follow-up, adjusting for covariates. <b>Results</b>: This study identified four distinct, sex-specific alcohol consumption trajectories: the Moderate-Decreasing group (1179 women, 0-14 g/day; 1534 men, 0-28 g/day) showed a declining moderate intake, The Low-to-None group included light or non-drinkers (992 women, 826 men), the Inverse-U group (606 women, 199 men) showed variable intake over time, while the High-Decreasing group (858 women, 376 men) had high initial consumption (women > 14 and men > 28 g/day) that declined over time. Compared with the Moderate-Decreasing group, women in other groups had higher CHD risks (HRs 1.58-1.61) and greater mortality risk in the Low-to-None (HR 1.25) and Inverse-U (HR 1.28) groups. Men in Low-to-None had higher mortality (HR 1.17) and CHD (HR 1.60), while High-Decreasing showed the highest mortality (HR 1.27). Low-to-moderate drinking was associated with lower mortality and CHD risks; however, these findings do not confirm the

<h4>Background</h4>Long-term alcohol use is a recognised risk factor for liver, upper aerodigestive tract (UADT), colorectal, and female breast cancers, yet aggregate-level evidence linking alcohol consumption to mortality from these cancers remains limited. This study examined the potential preventive impact of reducing population drinking on cancer mortality in Australia, accounting for tobacco use and health expenditure.<h4>Methods</h4>Annual per capita alcohol and tobacco consumption data (aged 15+) from 1910-2018, and mortality data for UADT, liver, breast, and colorectal cancers from the 1950s-2018, were collected from national registries. Time series models were used to estimate sex- and age-specific associations and long-term lagged effects of alcohol and tobacco consumption.<h4>Results</h4>A one-litre per capita annual reduction in alcohol consumption was significantly associated with decreases in mortality: 3.6% (95% CI: 1.0-6.2%) in male and 3.4% (1.8-4.9%) in female UADT cancer; 3.9% (0.2-7.7%) in male liver cancer; 1.2% (0.7-1.7%) in male and 0.7% (0.2-1.4%) in female colorectal cancer; and 2.3% (1.7-3.0%) in female breast cancer over a 20-year period.<h4>Conclusion</h4>Reducing population-level alcohol consumption in Australia could substantially lower mortality from UADT, colorectal, male liver, and female breast cancers, particularly among older adults.

<h4>Background & aims</h4>Recent reclassification of steatotic liver disease (SLD) distinguishes metabolic dysfunction-associated steatotic liver disease (MASLD) from MetALD, a newly defined entity combining MASLD with alcohol consumption. Since the mechanisms linking alcohol consumption in the context of SLD to cardiovascular disease (CVD) - the leading cause of SLD mortality - remain elusive, we investigated how metabolic dysregulation and alcohol intake synergistically promote atherosclerosis.<h4>Methods</h4>Low-density lipoprotein receptor-deficient (Ldlr^-/-) mice were fed a high-fat, high-cholesterol (HFC) diet with regular or ethanol-containing drinking water (10-20% v/v). Germ-free and antibiotic-treated Ldlr^-/- mice were used to assess the contribution of ethanol-induced dysbiosis. Associations between alcohol consumption and cardiometabolic risk were assessed in two human cohorts (n = 5,115, n = 2,515).<h4>Results</h4>Ethanol intake in HFC diet-fed Ldlr^-/- mice exacerbated hepatic steatosis and systemic dyslipidemia, despite only modest elevations in systemic ethanol levels (p values ≤0.05). Liver transcriptomic profiling revealed ethanol-induced alterations in lipid metabolism and enhanced proinflammatory signatures, accompanied by increased recruitment of Ly6C^high monocytes to the liver (p = 0.0121) and elevated levels in the circulation (p = 0.0043). Correspondingly, ethanol-consuming HFC diet-fed Ldlr^-/- mice

<h4>Introduction</h4>The relationship between alcohol consumption and the incidence of myocardial infarction (MI), stroke and all-cause mortality exhibits significant regional variation.<h4>Objective</h4>This prospective study aimed to investigate this association analyzing data from a cohort of Swedish men aged 45-50 years at baseline, evaluating subgroups over various time intervals, and compiling data on cardiovascular endpoints.<h4>Methods</h4>The Coeur study, conducted between 1993 and 1995, included 973 middle-aged male employees out of a randomly selected sample of 1144 individuals from a Swedish automotive company. Participants were followed for 30 years using national health registers. The accumulated incidence of first-time stroke, first-time MI and all-cause mortality was calculated and adjusted for cardiovascular risk factors. Data analysis employed time-to-event methods (Kaplan-Meier's estimates and hazard ratios) and measures of association (odds ratios and correlation analysis).<h4>Results</h4>No statistically significant association was observed between alcohol consumption and stroke (<i>p</i> > 0.05). However, alcohol consumption was associated with lower odds of MI (OR = 0.57, 95% CI: 0.41-0.79) and a slight increase in survival time (HR = 0.997, 95% CI: 0.995-1.000). Alcohol consumers had a median survival advantage of 1.3 years compared to non-consumers. All beverage types showed a negative association with all-cause mortality (total alcohol: OR = 0.57; be

Dementia and cognitive decline among older adults are increasingly considered as a significant health burden with a high level of personal, societal, and economic implications. Understanding the influence of lifestyle factors and potential lifestyle modifications on the risk and progression of dementia may aid in offering a non-pharmacological approach to reducing this public health challenge. This study explores the impact of key lifestyle factors - diet, physical activity, smoking, and alcohol consumption - on both the risk and progression of dementia. A systematic literature review was conducted using a predefined search strategy. Studies were identified through searches of the databases PubMed, Scopus, Web of Science, Embase, Medline, and CINAHL. Studies published between 2014 and 2024 were included to capture recent evidence. The quality of the selected studies was assessed using the Newcastle-Ottawa Scale (NOS) for cohort studies and the Joanna Briggs Institute (JBI) Critical Appraisal Checklist for cross-sectional studies. A total of 1,135 studies were initially identified; 12 met the inclusion criteria and were critically reviewed. The findings suggest that each lifestyle factor exerts an influence on the risk and progression of dementia, albeit to varying degrees. Further research is needed to deepen the understanding of these relationships and inform targeted preventive strategies.

<h4>Background</h4>Stomach cancer presents complex etiological heterogeneity. Ethanol in alcoholic beverages and its metabolite acetaldehyde are carcinogens causally linked to several cancers, but their role in gastric carcinogenesis has not been established. We analyzed harmonized, individual-level prospective data to examine associations between alcohol intake and risk of stomach cancer and its subtypes.<h4>Methods</h4>In total, 2 009 951 participants in 20 cohorts (mean follow-up = 9 to 29 years) within the Pooling Project of Prospective Studies of Diet and Cancer (n = 8357 incident invasive gastric adenocarcinomas) were included. We used Cox regression to assess associations between alcohol intake and risk of stomach cancer overall and by anatomical and histological subtype and population subgroup, adjusting for confounders.<h4>Results</h4>Evidence for an association between alcohol intake and overall stomach cancer risk was weak (hazard ratio, HR, for ≥30 vs 0.1-<5 g/day: 1.06 [95% confidence interval, CI = 0.96 to 1.16], Pbetween-studies heterogeneity = .43). Positive associations with stomach cancer risk were observed in never smokers (HR, for ≥30 vs 0.1-<5 g/day: 1.20 [95% CI = 1.02 to 1.42]; Pinteraction = .02) and for Asian studies (HR, 1.21 [95% CI = 1.02 to 1.42]; Pinteraction = .01). Modest increased risks were observed for noncardia cancers such as those of the fundus, body, and greater curvature, but not distally located noncardia cancers. HRs did not differ ma

<h4>Background</h4>Atrial fibrillation (AF) is a leading cause of mortality and disability globally. While trends in AF-related deaths are well-documented, the influence of alcohol consumption and regional disparities, particularly across different Socio-Demographic Index (SDI) regions, remains underexplored.<h4>Objective</h4>To analyze global and regional trends in AF-related mortality from 1990 to 2021, focusing on age, sex, and the impact of alcohol consumption across regions and SDI.<h4>Methods</h4>Data from the Global Burden of Disease (GBD) Study 2021 were used to assess age- and sex-specific AF mortality rates in 204 countries. Mortality trends were analyzed from 1990 to 2021, with attention to age group (30-44, 45-64, 65-84, 85-94, 95 + years) and sex. The impact of alcohol on AF-related mortality was examined by WHO regional classifications.<h4>Results</h4>AF-related mortality increased globally in both men and women, with a higher rate in women. Female mortality increased notably in the 90-94 and 95 + age groups, while male mortality surged in the 30-44 and 85+ age groups. Regionally, Greenland showed a decline in male mortality, while Sweden's rates rose. In China, both male and female mortality rates decreased. Alcohol consumption had a significant impact on AF mortality in Europe and the Americas, with smaller effects in Africa, Southeast Asia, and the Eastern Mediterranean.<h4>Conclusion</h4>The global burden of AF-related mortality is rising, with significant a