OBJECTIVETo clarify the dose-response relationship between alcohol consumption and type 2 diabetes.RESEARCH DESIGN AND METHODSA systematic computer-assisted and hand search was conducted to identify relevant articles with longitudinal design and quantitative measurement of alcohol consumption. Adjustment was made for the sick-quitter effect. We used fractional polynomials in a meta-regression to determine the dose-response relationships by sex and end point using lifetime abstainers as the reference group.RESULTSThe search revealed 20 cohort studies that met our inclusion criteria. A U-shaped relationship was found for both sexes. Compared with lifetime abstainers, the relative risk (RR) for type 2 diabetes among men was most protective when consuming 22 g/day alcohol (RR 0.87 [95% CI 0.76–1.00]) and became deleterious at just over 60 g/day alcohol (1.01 [0.71–1.44]). Among women, consumption of 24 g/day alcohol was most protective (0.60 [0.52–0.69]) and became deleterious at about 50 g/day alcohol (1.02 [0.83–1.26]).CONCLUSIONSOur analysis confirms previous research findings that moderate alcohol consumption is protective for type 2 diabetes in men and women.

Overall, end-point was an important source of heterogeneity among study results. This result has important implications not only for studies in which the burden of disease attributable to alcohol consumption is estimated, but also for prevention.

BackgroundObservational studies have suggested a complex relationship between alcohol consumption and stroke, dependent on sex, type of stroke and outcome (morbidity vs. mortality). We undertook a systematic review and a meta-analysis of studies assessing the association between levels of average alcohol consumption and relative risks of ischemic and hemorrhagic strokes separately by sex and outcome. This meta-analysis is the first to explicitly separate morbidity and mortality of alcohol-attributable stroke and thus has implications for public health and prevention.MethodsUsing Medical Subject Headings (alcohol drinking, ethanol, cerebrovascular accident, cerebrovascular disorders, and intracranial embolism and thrombosis and the key word stroke), a literature search of MEDLINE, EMBASE, CINAHL, CABS, WHOlist, SIGLE, ETOH, and Web of Science databases between 1980 to June 2009 was performed followed by manual searches of bibliographies of key retrieved articles. From twenty-six observational studies (cohort or case-control) with ischemic or hemorrhagic strokes the relative risk or odds ratios or hazard ratios of stroke associated with alcohol consumption were reported; alcohol consumption was quantified; and life time abstention (manually estimated where data for current abstainers were given) was used as the reference group. Two reviewers independently extracted the information on study design, participant characteristics, level of alcohol consumption, stroke outcome, control for potential confounding factors, risk estimates and key criteria of study quality using a standardized protocol.ResultsThe dose-response relationship for hemorrhagic stroke had monotonically increasing risk for increasing consumption, whereas ischemic stroke showed a curvilinear relationship, with a protective effect of alcohol for low to moderate consumption, and increased risk for higher exposure. For more than 3 drinks on average/day, in general women had higher risks than men, and the risks for mortality were higher compared to the risks for morbidity.ConclusionsThese results indicate that heavy alcohol consumption increases the relative risk of any stroke while light or moderate alcohol consumption may be protective against ischemic stroke. Preventive measures that should be initiated are discussed.

The risk for hypertension increases linearly with alcohol consumption, so limiting alcohol intake should be advised for both men and women.

SUMMARYPurpose: The purpose of this research was to analyze and quantify the association between alcohol consumption and epilepsy as an independent disease, in part operationalized by the occurrence of unprovoked seizures, as well as to examine causality. Methods: Systematic review, meta-analysis. Results: A strong and consistent association between alcohol consumption and epilepsy/unprovoked seizures was found with an overall relative risk (RR) of 2.19 [95% % confidence interval (CI) 1.83-2.63]. There was a doseresponse relationship between the amount of alcohol consumed daily and the probability of the onset of epilepsy. Individuals consuming an average of four, six, and eight drinks daily had RRs of 1.81 (95% % CI 1.59-2.07), 2.44 (95% % CI 2.00-2.97), and 3.27 (95% % CI 2.52-4.26), respectively, compared to nondrinkers. Several pathogenic mechanisms for the development of epilepsy in alcohol users were identified. Most of the relevant studies found that a high percentage of alcohol users with epilepsy would qualify for the criteria of alcohol dependence. Data were inconclusive regarding a threshold for the effect of alcohol, but most studies suggest that the effect may only hold for heavy drinking (four and more drinks daily). Discussion: The relationship between alcohol consumption and epilepsy and unprovoked seizures was quantified and several pathogenic mechanisms were suggested, although none of them has been proven to be the unique causative pathway for epilepsy. Certain limitations underlying this study require further research to clarify the outstanding statistical issues and pathogenesis of epilepsy in heavy drinkers.