Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of hypertension in the increased rate of heart attack reported in vigorously active subjects was examined in a large prospective study of 7735 middle-aged men drawn from general practices in 24 British towns (The British Regional Heart Study). Analyses were restricted to 5694 men with no evidence of pre-existing ischaemic heart disease or stroke at screening, in whom there were 311 major ischaemic heart disease events after 9.5 years follow-up. Risk of major ischaemic heart disease events decreased significantly with increasing physical activity to levels of moderate/moderately vigorous activity, with a 50% reduction in risk compared with inactive men after adjustment for age, body mass index, smoking, heavy drinking, social class and blood cholesterol. However, at the highest level of physical activity (vigorous group) risk of major ischaemic heart disease events was increased above that seen in the moderate/moderately vigorous group (rr = 1.68, P = 0.05). When separated into normotensives (n = 3888) and hypertensives (n = 1806; SBP > or = 160 mmHg or DBP > or = 90 mmHg or on regular antihypertensive treatment), the increased risk of major ischaemic heart disease events in the vigorous group was only evident in hypertensive men. They showed more than a twofold increase in risk compared with the moderate and moderately vigorous group (rr = 2.7, P < 0.05). In normotensive men, risk was significantly lowered in those engaged in moderate activity with no further decline in rate of heart attack at increasing levels of physical activity.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Physical activity, hypertension and risk of heart attack in men without evidence of ischaemic heart disease. 815 4

We have reviewed 156 papers which provided sufficient information to relate individual alcohol consumption to risk for a variety of physical damage. Overall, there was evidence for a dose-response relationship between level of alcohol consumption and risk of harm for liver cirrhosis, cancers of the oropharynx, larynx, oesophagus, rectum (beer only), liver and breast, and blood pressure and stroke. An increased risk of cardiac arrhythmias, cardiomyopathy and sudden coronary death was associated with heavy drinking. There was evidence for a protective effect of alcohol consumption against risk of coronary heart disease, which could be achieved at consumption levels of less than 10 g alcohol a day. The mortality of non-drinkers was higher than that of moderate drinkers in some studies. Level of alcohol consumption and total mortality were dose-related when non-drinkers were excluded. The finding of a dose-relationship between alcohol and harm suggested causality. It was not possible to define individual risk for all harms at a given level of alcohol consumption because of variations in methodology, but some idea of the order of magnitude of the increased risk can be obtained from calculating trends of pooled log-odds ratios. At levels of alcohol consumption of more than 20-30 g a day, all individuals are likely to accumulate risk of harm. Current guidelines on upper limits of lower risk drinking in different countries (168-280 g of alcohol a week for men and 84-140 g a week for women) reflect levels at which the risk of total mortality is not greatly increased above one.
 ...
PMID:The risk of alcohol. 806 77

Overwhelming evidence indicates that the Western diet plays a major role in atherogenesis. Clinicians are only now beginning to tease out the precise components of the diet that are harmful or beneficial. With respect to fat intake, it remains unclear whether it is the amount or type of fat that promotes atherosclerotic disease. There appears to be a consistent positive association of cholesterol, saturated fat, and possibly trans-fatty acid intake and atherosclerotic disease. Although there is general agreement that reducing intake of these dietary components would be beneficial, controversy remains on what should replace these harmful fats. Some researchers advocate massive reductions in total fat consumption with replacement with carbohydrates for everyone, whereas others recommend a Mediterranean-style diet, which replaces saturated animal fats with vegetable fats. Very low-fat diets have been shown to lower the chance of a heart attack among those with severe coronary artery disease, but for the majority of Americans who do not have obvious artery disease, there is no convincing evidence that a very low-fat diet is optimal. There may be other adverse health effects of this Asian diet, such as increased rates of hemorrhagic stroke. Further research is required to refine thinking on the optimal composition of fats in diet. The effects of alcohol consumption on chronic diseases are complex. The strength and consistency of the observational and experimental evidence strongly suggests a causal link between light to moderate alcoholic beverage consumption and reduced risks of CHD. These reductions in risk of CHD appear to be mediated largely by raising HDL cholesterol levels, although additional mechanisms remain possible and do not appear to be beverage specific. Maximal benefit in terms of CHD appears to be at the level of one drink per day. From a public policy standpoint, whether the benefits for CHD persist at heavy drinking levels or are attenuated is moot because clear harm of heavy drinking in terms of overall mortality outweighs any benefits in the reduction of heart disease. Although the association of alcohol and CHD is likely to be causal, any individual or public health recommendations must consider the complexity of alcohol's metabolic, physiologic, and psychological effects. With alcohol, the differences between daily intake of small to moderate and large quantities may be the difference between preventing and causing disease. A discussion of alcohol intake should be a part of routine preventive counseling. Given the complex nature of alcohol disease relationships, alcohol consumption should not be viewed as a primary preventive strategy; also, it should not necessarily be viewed as an unhealthy behavior. Based on the totality of available evidence, antioxidants represent a possible but as yet unproven means to reduce risks of cardiovascular disease. Although it remains unclear whether supplementation of diet with antioxidant vitamins will reduce risks of atherosclerotic disease, most researchers agree that consumption of fruits and vegetables is an important part of a healthy diet. The U.S. Department of Agriculture recommends two to four servings of fruit and three to five servings of vegetables per day.
 ...
PMID:Diet and heart disease. The role of fat, alcohol, and antioxidants. 907 92

Epidemiological evidence indicates that recent heavy alcohol consumption increases the risk for all major types of stroke, whereas light-to-moderate alcohol intake is associated with a decreased risk of ischemic stroke. Although heavy drinking elevates blood pressure, there is no firm evidence to indicate that alcohol consumption causes the formation of aneurysms, microaneurysms or other lesions in human arteries. Alcohol has been reported to precipitate vasoconstriction and rupture of small cerebral arteries in experimental animals. Alcohol-induced neck trauma has been shown to precipitate traumatic strokes, and alcohol-induced cardiac arrhythmias have been observed in patients with embolic brain infarction. The effects of alcohol on hemostasis, fibrinolysis and blood clotting are variable and could either prevent or promote the occurrence of strokes. The antiatherogenic effects of regular light-to-moderate alcohol consumption could be mediated by inhibition of low-density lipoprotein oxidation, and by elevated estrogen levels.
 ...
PMID:Alcohol and stroke: pathophysiologic mechanisms. 977 94

The complex relationship between alcohol consumption and stroke includes both benefits and risks. Regular light-to-moderate consumption of alcohol seems to decrease the risk for ischemic stroke by reducing atherothrombotic events, but the underlying mechanism is still unclear. Recent and current (but not previous) heavy drinking increases the risk for both hemorrhagic and ischemic strokes. Young and middle-aged men are stricken more often than women or elderly persons, probably because they are more often current heavy drinkers. Alcoholic cardiomyopathy is a cause of cardioembolic brain infarction. Cardiac arrhythmias caused by regular heavy drinking or binge drinking can precipitate thrombus formation and propagate already existing thrombi from the heart. The maintenance of high blood pressure by heavy drinking may promote cerebral arterial degeneration, but the effect of drinking habits on aneurysm formation is not known. Acute increases in systolic blood pressure and/or alterations in cerebral arterial tone could serve as mechanisms triggering hemorrhagic strokes during alcoholic intoxication. We lack studies to show that prevention of heavy drinking can efficiently influence the occurrence of strokes.
 ...
PMID:Alcohol consumption and stroke: benefits and risks. 979 60

Evident disparities in relationships make it desirable to consider several disorders separately. (1) Alcoholic cardiomyopathy was perceived 150 years ago, but understanding was clouded by recognition of beriberi and of synergistic toxicity from alcohol with arsenic or cobalt. (2) A report of a link between heavy drinking and hypertension in WWI French soldiers was apparently ignored for > 50 years. Epidemiological and intervention studies have now firmly established this association, but a mechanism remains elusive. (3) The 'holiday heart syndrome', an increased risk of supraventricular tachyarrhythmias in alcoholics, has been widely known to clinicians for 25 years; data remain sparse about the total role of heavier drinking in cardiac rhythm disturbances. (4) Failure of earlier studies to distinguish types of stroke impeded understanding; it now seems probable that alcohol drinking increases risk of haemorrhagic stroke but lowers risk of ischaemic stroke. (5) Heberden reported angina relief by alcohol in 1786, and an inverse alcohol-atherosclerosis association was observed by pathologists early in this century. Recent population studies and plausible mechanisms support a protective effect of alcohol against coronary disease. International comparisons dating back to 1819 suggest beverage choice as a factor, but this issue (the 'French Paradox') remains unresolved.
 ...
PMID:Alcohol and cardiovascular diseases: a historical overview. 994 84

The health effects of alcohol consumption remain complex for several reasons: the risks and benefits accrue over many years, assessment of drinking is generally based on self-report, drinking habits change over time and studies estimate average daily drinking disregarding how or when the beverage was consumed. In addition, alcohol consumption is associated with lifestyle factors which may confound relationship with disease. Despite these methodological difficulties, epidemiological studies are surprisingly consistent, showing that light to moderate intake is associated with a lower risk of total mortality compared with those who drink heavily or do not drink at all. Thus there is a J-shaped association of alcohol intake with risk of total mortality whose basis is likely to be the effect of summing the cause-specific effects at the various drinking levels. Studies using a diversity of methods and populations have consistently reported an inverse relationship between coronary heart disease and light to moderate drinking, with the depth and width of the J-shaped mortality curve depending on the underlying risk of coronary heart disease for that population. The higher risk of death at heavy drinking levels is due to increased risk of cancer, liver diseases, cardiomyopathy and stroke. The precise mechanisms behind these effects of alcohol are only now beginning to be understood. The most plausible mechanism by which alcohol reduces the risk of coronary heart disease is by its effects on blood lipids, particularly increases in high density lipoprotein (HDL) cholesterol: about 50% of the risk reduction attributable to alcohol is explained by changes in total HDL. Further support for the HDL hypothesis comes from the lack of a differential effect of alcohol by beverage type. While the association of alcohol and cardiovascular disease is likely to be causal, any public health recommendations must consider the complexity of alcohol's metabolic, physiological and psychological effects.
 ...
PMID:Alcohol intake, lipids and risks of myocardial infarction. 994 89

Epidemiological investigations have shown a linear positive correlation between the risk of haemorrhagic stroke and level of alcohol consumption. Ischaemic stroke shows a weaker relationship, which is J-shaped, suggesting that regular light-to-moderate alcohol consumption may carry a decreased risk. Case reports and case-control studies indicate that heavy recent drinking, but not heavy former drinking, increases the risk for both types of stroke. Larger amounts of alcohol are needed to trigger aneurysmal subarachnoid haemorrhage than spontaneous intracerebral haemorrhage. The increased risk caused by recent heavy drinking may be partly due to elevated systolic blood pressure, but alcohol may also provoke cerebral arterial vasospasm, as observed in animal experiments. Alcohol-induced fluctuation in haemostatic and fibrinolytic factors has not been proved to precipitate alcohol-related strokes, but may contribute to both an increase and a decrease of the risk. Subtypes of ischaemic stroke associate differently with alcohol consumption. A recent series of patients with ischaemic brain infarction showed that of the victims having a high and medium risk for cardiogenic embolism, 50% and 45% were intoxicated, respectively. This suggests that cardiogenic embolism is a significant mechanism leading to ischaemic stroke during heavy drinking of alcohol.
 ...
PMID:Mechanisms of alcohol-related strokes. 994 94

The relationship between alcohol consumption and stroke is uncertain. Heavy alcohol consumption has been associated with an increased risk of stroke, while light drinking appears to be protective. However, the evidence is not uniform. We sought to examine the relationship between alcohol consumption and stroke, according to stroke type. We performed a population-based case-control study from September 1990 to December 1991. The study comprised 467 incident cases of stroke and 477 controls aged between 40 and 85. Case was defined following WHO criteria and control was randomly selected from the study base population. Alcohol exposure was obtained by medical interview. We found that consumption of less than 30 g/day of alcohol was protective against all stroke types combined, the multivariated adjusted odds ratio (OR) was 0.58 (95% confidence interval [CI], 0.41-0.83). Moderate alcohol drinking is also protective against all cerebral infarction combined (OR = 0.53; 95% CI, 0.35-0.80) and cortical infarction (OR = 0.40; 95% CI, 0.18-0.86). Drinking up to 30 g/day of alcohol has a borderline protective effect on deep cerebral infarction (OR = 0.40; 95% CI, 0.16-1.02) and has no effect on intracerebral hemorrhage (OR = 0.88; 95% CI, 0.44-1.74). Heavy alcohol drinking, over 140 g/day, is a risk factor for all stroke types combined (OR = 3.2; 95% CI, 1.1-9.7), all cerebral infarction combined (OR = 5.0; 95% CI, 1.5-16.3), small deep cerebral infarction (OR = 9.7; 95% CI, 2.6-36.7), intracerebral hemorrhage (OR = 6.2; 95% CI, 1.3-24.0), and is marginally associated with superficial cerebral infarction (OR = 4.6; 95% CI, 1.0-20.6). The relationship between alcohol and stroke depends on the alcohol dose and the pathology of the disease. Atherosclerosis of the large and medium cerebral arteries is found mainly in superficial cerebral infarction, and this type of stroke shows a J-shaped relationship with alcohol similar to that found in coronary heart disease, suggesting that they are similar diseases. On the other hand, arteriosclerosis of the penetrating arteries has been found in deep cerebral infarction and intracerebral hemorrhage, while atherosclerosis is not prominent. This may explain why alcohol does not have a protective effect on cerebral hemorrhage whereas heavy drinking is a strong risk factor in these two types of stroke.
 ...
PMID:Alcohol and stroke: a community case-control study in Asturias, Spain. 1039 61

Free radicals are involved in the formation of both atherosclerosis and thrombosis. Therefore, considerable interest has recently been aroused by their role in the development of ischemic cerebral injury. Experimental observations suggest that antioxidants could reduce cerebral arterial vasospasm, reduce infarct size and prevent the development of both atherosclerosis and thrombosis. However, clinical evidence for these beneficial effects is still lacking. Alcohol can act as an antioxidant and an oxidant, and its intake seems to exert both beneficial and untoward effects on stroke, depending on drinking habits. Light-to-moderate regular alcohol intake has been suggested to protect against internal carotid artery atherosclerosis, a major cause of ischemic stroke. Ethanol metabolism in human blood vessel walls could antagonize the oxidation of LDL and thereby prevent the development of atherosclerosis. In addition, ethanol and the phenolic compounds of wine could decrease platelet aggregation and thromboxane formation and also prevent thrombus formation. Whether the effects are clinically significant remains to be proved. On the other hand, recent heavy drinking has been observed to worsen vasospastic ischemia caused by subarachnoid bleeding. Whether a lack of antioxidants is responsible for this effect also remains to be proved. Future stroke research should focus on solving these problems.
 ...
PMID:Oxidants, antioxidants, alcohol and stroke. 1047 72


<< Previous 1 2 3 4 5 6 Next >>