Protective Effect Of Moderate Intake Research Articles

Relationship between Alcohol Intake and Stroke Severity in Japanese Patients: a Sex- and Subtype-Stratified Analysis

ObjectivesThis study aims to clarify the association between alcohol intake and stroke severity at admission and discharge according to sex and stroke subtype in Japanese patients with acute stroke. Materials and MethodsWe analyzed the data of 199,599 patients registered in the Japan Stroke Data Bank from 1999 to 2018, including sex, age, stroke subtypes (cardioembolic ischemic, noncardioembolic ischemic, hypertensive hemorrhagic, nonhypertensive hemorrhagic, and subarachnoid hemorrhagic), dates of onset and admission, National Institutes of Health Stroke Scale score at admission, modified Rankin Scale score at discharge, and alcohol intake. Multivariable logistic regression analysis adjusted for stroke-related factors was performed to estimate the odds ratios of alcohol intake for stroke severity. ResultsIn cardioembolic ischemic stroke, a significant protective effect of moderate intake on severity at admission was observed in both sexes. In noncardioembolic ischemic stroke, a significant protective effect on stroke severity at admission was found for each sex. At discharge, the results also showed a significant protective effect for each sex with moderate intake. For both subtypes of ischemic stroke, a J-shaped relationship between alcohol intake and stroke severity at admission and discharge was observed in women and men. In hypertensive hemorrhagic stroke, a significant protective effect was found in men at both admission and discharge. In women, heavy drinking had a significant harmful effect on stroke severity at admission. ConclusionsHabitual alcohol intake is associated with stroke severity at admission and discharge regardless of sex.

Wine, alcohol and cardiovascular risk: open issue

Wine, alcohol and cardiovascular risk: open issue

Alcohol and coronary heart disease: the evidence for a protective effect

There is a considerable body of evidence indicating that moderate alcohol intake is associated with a reduced incidence of, and mortality from, coronary heart disease (CHD). There is also substantial evidence that problem drinking (well beyond two drinks per day) is associated with increased cardiovascular mortality. However, the frequently reported harmful effect of alcohol abuse on CHD mortality rates could be a result of mislabeling as CHD conditions such as alcohol-ibduced dilated cardiomyopathy, dysrhythmias, and hypertensive cardiovascular disease. The combination of protective and harmful influences of alcohol consumption results in a U-shaped mortality curve. A true protective effect of moderate intake of alcohol is likely, because of consistent findings in many large, well-conducted studies of diverse population samples and the apparent specificity of the protective effect for CHD and possibly atherosclerotic-thrombotic brain infarction. There are also biologically plausible mechanisms whereby the protection might be conferred. Alcohol has been shown convincingly to raise HDL subfractions which have been found to be protective against CHD, and it may also provide protection by an antithrombotic effect. There is a suggestion that wine, and red wine in particular, may be more protective than other alcoholic beverages. However, it is difficult to control adequately for confounding factors, since persons who prefer wine have been found to have a more advantageous lifestyle, a better cardiovascular risk profile, are better educated, and smoke less. The evidence for a protective effect of moderate alcohol intake includes population studies of alcohol and CHD mortality in 20 countries, case-control studies, prospective cohort studies, arteriographic studies, and animal experiments. Nevertheless, because there are no controlled trial data, it is possible that some other factor may be responsible for the apparent protective effect of alcohol. The inclusion of former drinkers or sick individuals in the non-drinker category, and lack of control for cigarette smoking and other risk factors, have been excluded as reasons for higher CHD rates among individuals who do not consume alcohol. No alternative explanation for the protective effect has surfaced after two decades of investigation of the alcohol-CHD relationship, yet, the penalties of heavy alcohol consumption are too large to ignore. Until we can be sure that advice that encourages the public to drink to avoid coronary heart disease does not increase abuse, we must be cautious in making general recommendations.