BACKGROUND: Epilepsy is one of the most common neurological disorders, affecting approximately 50 million people worldwide. Although a positive association between alcohol consumption and epilepsy has been demonstrated in previous meta-analyses of case-control studies, the results of several recently published large cohort studies are contradictory. Therefore, we conducted an updated meta-analysis that included more recent data to clarify the association between alcohol consumption and epilepsy.
METHODS: The search was performed on 25 January 2021 using the Embase and MEDLINE databases. Cohort or case-control studies were eligible for inclusion in this study. We used restricted cubic spline analysis to perform a dose-response meta-analysis.
RESULTS: A total of eight studies, including three cohort and five case-control studies, were included in our meta-analysis. The pooled risk of epilepsy was 1.70 (1.16-2.49) in alcohol users compared to non-drinkers. Subgroup analysis of 50 g units showed that the epilepsy risk increased as alcohol intake increased. The pooled risk of cohort studies was 1.00 (0.65-1.54), and the pooled risk of case-control studies was 2.61 (1.29-5.29). According to the dose-response analysis, the regression coefficient was 1.009 (1.004-1.014), indicating a significant positive dose-response relationship.
CONCLUSION: Unlike the case-control studies, the cohort studies did not reveal a significant association between alcohol consumption and epilepsy. Further large cohort studies for the general population are required to assert a definite causal relationship between alcohol consumption and epilepsy and to identify a potential threshold.
BACKGROUND: The dose-response association between alcohol consumption and the subsequent pancreatic cancer risk by individuals' glycaemic status is unclear.
RESEARCH DESIGN AND METHOD: This large-scale nationwide cohort study included 9,514,171 adults without cancer who underwent health examinations under the Korean National Health Insurance Service in 2009 and were followed-up until December 2017 for pancreatic cancer development. Multivariable Cox proportional hazards regression analysis was performed.
RESULTS: During a median follow-up period of 7.3 years, 12,818 patients were newly-diagnosed with pancreatic cancer. Among individuals with normoglycemia, a J-shaped association was observed between the frequency of alcohol consumption (1-2 and >/=5 days/week: hazards ratio [HR]; 95% CI, 0.91; 0.85-0.97 and 1.13; 1.002-1.27, respectively) and pancreatic cancer risk, after adjusting for potential confounders. However, in patients with impaired fasting glucose (IFG), pancreatic cancer risk increased with increased frequency and average daily amount of alcohol consumption (all P for trend <0.01). IFG combined with heavy alcohol consumption (30 g/day) was associated with 38% increased pancreatic cancer risk (HR, 1.38; 95% CI, 1.23-1.54). Diabetes was associated with an increased pancreatic cancer risk regardless of alcohol consumption and 70% increased risk even in non-drinkers (HR, 1.70; 95% CI, 1.61-1.80).
CONCLUSIONS: The J-shaped dose-response association between alcohol consumption and pancreatic cancer risk was observed only in individuals with normoglycemia, not in patients with IFG and diabetes. Complete alcohol abstinence may help reduce pancreatic cancer risk in patients with IFG and diabetes.
BACKGROUND:AIMS: Gallstone disease (GSD) is a common gastrointestinal disorder. Clinical epidemiological studies revealed that alcohol consumption has a preventive effect on the development of GSD. This study aimed to evaluate the relative risks of drinking for GSD development and investigate the dose-response relationships.
METHODS: A systematic search of the MEDLINE, EMBASE, and Cochrane Library databases for studies published up to 2018 was performed. All studies that satisfied the following eligibility criteria were included: patients with GSD with or without cholecystitis; and cohort or case-control studies investigating the association between alcohol consumption and GSD development.
RESULTS: Sixteen case-control studies including 24,401 gallstone cases and 76,185 controls, and eight cohort studies with 14,693 GSD cases among 2,432,471 person-years were enrolled. Alcohol consumption presented a decreased overall risk of GSD (pooled relative ratio [RR], 0.84; 95% confidence interval [CI], 0.79 to 0.89; p=0.02). Subgroup analyses according to drinking levels indicated a gradual risk reduction for GSD compared to nondrinkers (light: RR, 0.96; 95% CI, 0.94 to 0.99; p=0.75; moderate: RR, 0.80; 95% CI, 0.75 to 0.85; p=0.27; high: RR, 0.66; 95% CI, 0.56 to 0.79; p0.01). A nonlinear risk reduction was observed in a dose-response meta-analysis of all the studies (n=14, p0.01 for nonlinearity).
CONCLUSIONS: In this systematic review with meta-analysis, alcohol consumption could decrease the risk of GSD, and the dose-response analysis revealed a dose-dependent linear risk reduction and a weakened linear trend between alcohol consumption levels less than and greater than 28 g/day.
BACKGROUND: Studies on the relation between alcohol consumption and risk of colorectal adenoma (CRA), a precursor of colorectal cancer, have been inconsistent. AIM: A systematic review with meta-analysis was conducted to investigate the association and the dose-response of alcohol with CRA.
METHODS: A literature search was performed on PubMed to identify relevant studies published up to January 2014. A fixed or random effects model was used to estimate summarised relative risks (RRs) and 95% confidence intervals (CIs) for the association between alcohol intake and CRA risk. Statistical heterogeneity between studies was assessed with the chi(2) statistic and quantified by I(2).
RESULTS: Twenty-three case-control studies and two cohort studies were included in the meta-analysis. All drinkers were associated with 17% increased risk for CRA, compared with nondrinkers or occasional alcohol drinkers. The dose-response analysis demonstrated that for drinkers of 10, 25, 50 and 100 g/day alcohol consumption, the estimated RRs of CRA were 1.02 (95% CI 0.89-1.16), 1.06 (95% CI 0.92-1.20), 1.16 (95% CI 1.02-1.33) and 1.61 (95% CI 1.42-1.84) respectively, in comparison with non-/occasional drinkers. The risks were consistent in the subgroup analyses of gender and site of adenoma, while it was stronger in European studies than the studies in the US and Asia.
CONCLUSIONS: This study suggests that alcohol intake is related to a significant increase of risk for colrectal adenoma.