· Sports are enormously popular, and one striking pattern is that boys and men are typically much more involved than are girls and women. This sex difference has policy implications, and it raises. vehicle the subject normally uses This page was last edited on 17 May , at All structured data from the main, Property, Lexeme, and EntitySchema namespaces is available under the Creative Commons CC0 License; text in the other namespaces is available under the Creative Commons Attribution-ShareAlike License; additional terms may. · Observational 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 Cited by: Article Interspecies Chimerism with Mammalian Pluripotent Stem Cells Jun Wu, 1Aida Platero-Luengo, Masahiro Sakurai, 1Atsushi Sugawara, Maria Antonia Gil,2 Takayoshi Yamauchi. there is an association between passive smoking and a number of diseases, lung cancer in particular.” Not true, insis-t ed WHO. Smokers themselves are not the only ones who suf-.
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Observational studies have suggested a complex relationship between alcohol consumption and stroke, dependent on sex, type of stroke and outcome morbidity vs. 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. 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. The 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.
These 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.
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Stroke is an international health problem with high associated human and economic costs. Among adults, it is the second-leading cause of death worldwide, and ranks fourth in overall disease burden. Recent trend analysis showed that stroke incidence and associated deaths appears to be rising, particularly in economically emerging countries [ 1 , 2 ]. Recent projections suggest that, without intervention, the number of deaths from stroke will continue rising, to 6.
Risk factor identification and analysis is therefore a high priority in various fields of stroke research and will be important in containing and reducing this heavy disease burden. It is well accepted that heavy alcohol consumption has been linked to an increased risk of ischemic stroke [ 4 ] and hemorrhagic stroke [ 4 — 6 ]. However, some studies of moderate alcohol and stroke reported a protective effect of alcohol at these doses [ 4 , 7 — 9 ] while others have found that moderate consumption increases the overall risk [ 5 , 10 ].
This study will attempt to systematically estimate the impact of alcohol for stroke separately by event outcome and provide estimates by level of alcohol consumption via meta-analysis. No language restrictions were applied. Generally, studies were eligible for inclusion if they were original publications we excluded letters, editorials, conference abstracts, reviews, and comments of case-control and cohort studies reporting incidence, hazard ratio HR , relative risk RR or odds ratio OR of alcohol consumption in comparison to no alcohol consumption.
In addition, bibliographies of key retrieved articles, relevant reviews and meta-analyses were hand searched. To be included in our meta-analysis, a published study had to meet the following criteria: 1 had to be an original research study not a review ; 2 cohort or case-control study in which medically confirmed ischemic or hemorrhagic stroke were end points i. All data were independently abstracted by means of a standardized protocol.
RRs were abstracted by sex, subtype of stroke ischemic or hemorrhagic , end point incidence mortality, morbidity , and level of alcohol consumption. If studies only reported results for both sexes combined, the same results were applied to both female and male datasets.
Similarly, if combined results were reported for mortality and morbidity studies, the same results were applied to both mortality and morbidity datasets. To ensure accuracy in data abstraction, five included and five excluded studies were randomly chosen to be abstracted independently by a co-author HI. There was a For data abstraction the raters agreed on Where disagreements existed, both authors discussed the discrepancy until a consensus was reached.
Where consumption was reported in drinks and not grams, the gram pure alcohol equivalent described in the article was used as a conversion factor if stated, and if not, conversion from standard drinks was based on geography: for Canada For all other countries without clear standard drink specifications 12 grams pure alcohol was used.
For those studies [ 4 , 6 , 9 , 10 , 14 — 18 ] that did not report measures of association separately by sex, the estimates were used for men as well as women. Information on alcohol consumption was extracted. When ranges of alcohol consumption were given, the midpoint was taken.
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Studies reporting RR of ex-drinkers relative to lifetime abstainers [ 14 , 15 , 19 — 24 ] were grouped together by sex and a pooled RR for ex-drinkers was determined. In addition, the ratio of ex-drinkers relative to lifetime abstainers in this pooled estimate was calculated. For those studies only reporting current abstention, the proportion of lifetime abstainers and ex-drinkers was estimated based on the ratio of ex-drinkers previously calculated and the RRs in each article were adjusted based on the pooled RR.
The dose-response relationship between alcohol consumption and risk of strokes was assessed with random effects meta-regression models. Based on previously published research, the association between alcohol consumption and stroke was expected to be both linear and non-linear, depending on the subtype. Alcohol consumption was modeled as a continuous variable using the fractional polynomial method [ 26 ] to estimate the relationship between alcohol consumption and the logarithmized RR of stroke subtypes.
In order to be flexible in fitting the best model, we conducted the meta-regression using linear as well as first-order and second-order fractional polynomials with powers of -2, -1, Best-fit curves or lines were assessed using standard goodness-of-fit statistics with an emphasis on reduced deviance gain compared with the quadratic model. Comparisons of curves to determine the best fit were made using a Chi-square distribution, as recommended by Royston [ 27 ].
Statistical heterogeneity among studies was assessed using both the Cochrane Q test and the I 2 statistic. A value of zero indicates no observed heterogeneity, and larger values show increasing heterogeneity [ 28 , 29 ].
Results of systematic review of the relationship between alcohol and stroke subtypes. The characteristics of the study subjects and design of the studies are presented in Additional files 1 and 2. The number of subjects in the cohort studies ranged from in the study by Kiyohara et al [ 16 ] to , in the study by Klatsky et al [ 19 ]. Among all cohort studies, 13 studies [ 14 , 16 , 19 — 21 , 23 , 24 , 34 — 38 ] reported ischemic stroke, and 12 studies [ 5 , 15 , 16 , 19 , 22 — 24 , 33 , 34 , 36 , 38 , 39 ]; reported hemorrhagic stroke as the outcome.
Similarly, 15 studies [ 5 , 15 , 16 , 20 — 24 , 33 — 39 ] had mortality as the end point; whereas 11 studies [ 5 , 14 , 16 , 19 — 21 , 23 , 33 , 34 , 36 , 37 ] had morbidity as end point. The follow-up period ranged from 4 to 30 years.
Seven studies [ 4 , 8 — 10 , 18 , 40 , 41 ] collected data on ischemic stroke and 4 studies [ 4 , 6 , 9 , 17 ] collected data on hemorrhagic stroke. Three studies [ 6 , 17 , 18 ] had mortality as the end point and 9 studies [ 4 , 6 , 8 — 10 , 17 , 18 , 40 , 41 ] had morbidity as an end point. Forest plot of risk estimates for alcohol consumption related to haemorrhagic stroke of men by endpoint 15 studies.
Forest plot of risk estimates for alcohol consumption related to haemorrhagic stroke of women by endpoint 8 studies. Forest plot of risk estimates for alcohol consumption related to ischemic stroke of men by endpoint 18 studies. Forest plot of risk estimates for alcohol consumption related to ischemic stroke of women by endpoint 11 studies.
Meta-analysis showing the dose-response relationship between alcohol and hemorrhagic stroke by sex and by endpoint. Meta-analysis showing the dose-response relationship between alcohol and ischemic stroke by sex and by endpoint. The overall results indicated a positive association between heavy alcohol consumption and RR of hemorrhagic-stroke mortality, irrespective of sex Figure 6. Compared to the reference group of lifetime abstainers, at 96 grams 8 US standard drinks of pure alcohol per day, RRs of 1.
For women, the curve was J-shaped; there was a protective effect of moderate drinking up to 36 grams of pure alcohol or about 3 drinks a day. The nadir was reached at less than 1 drink per day RR: 0. On the other hand, an overall nonlinear association between alcohol consumption and RR of ischemic-stroke was observed. The association between alcohol consumption and RR of ischemic-stroke mortality had a J-shaped relationship irrespective of sex or end points Figure 7.
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Similarly, the risk of ischemic-stroke morbidity for both sexes resulted in a J-shaped curve as well. However, the interaction term was not significant among men. The findings from the sensitivity analyses based on different exclusion criteria are presented in Additional file 4. Risk estimates changed very little after the exclusion of: a studies without computed tomography CT scans or other imaging measures; b studies that did not adjust for important confounders age, smoking and hypertension ; c or studies fulfilling criteria a or b.
The curvilinear relationship for ischemic stroke resembles the dose-response relationship between alcohol and ischemic heart disease [ 52 ] with the same postulated underlying biological mechanisms [ 53 — 55 ]. For hemorrhagic stroke, hypertension plays a more prominent role in the etiology. Alcohol, already operant at low doses, has been identified as a major risk factor for hypertension [ 56 ], and might explain the different dose-response relationship [ 45 , 48 ].
One of the main results of this study is the difference between mortality and morbidity as an endpoint, especially for women. While higher effects of alcohol on mortality compared to morbidity have been demonstrated for other chronic disease e.
Both for questions of etiology and prevention, however, such a distinction is necessary. We conducted a meta-regression as a sensitivity analysis for each stroke type to measure the impact of study type case control vs.
This analysis is subject to general strengths and limitations of meta-analyses, in addition to some subject-specific issues. Of the former, a major limitation is that the quality of our study depends on data from original publications included in our analysis. Our study may thus inherit some problems of potential bias and confounding effects associated with observational studies.
However, a randomized controlled trial of alcohol consumption and stroke has not been performed and is highly unlikely to be conducted in the future for ethical reasons. Consequently, we must rely on data from observational studies to draw conclusions and make recommendations. Of the latter, a limitation is that CT scans and other imaging techniques were not available for some of the studies [ 5 , 14 , 19 , 22 , 35 , 36 , 38 , 58 ].
At present, a CT scan is the most reliable method of distinguishing between hemorrhagic and ischemic strokes [ 59 , 60 ], but unfortunately these studies primarily used autopsy report, death certificates, or death registry data to make diagnoses and determine the outcome of stroke subtypes.
However, given that the dose-response curve differed by type of stroke, any bias introduced would dilute such a difference. Additionally, our sensitivity analysis showed little difference as the shape of association remained unchanged. Second, the selection of the reference group may vary among studies [ 61 ].
For instance, some studies used the lowest consumption level as the reference group while others used abstainers. It has been suggested that the non-linear association of between alcohol consumption and mortality from cardiovascular diseases could be due to the inclusion of ex-drinkers in the referent group of abstainers [ 25 , 62 , 63 ]. To avoid combining studies that were not comparable, we chose to correct the RR from studies based on current abstention by introducing the effect for former drinkers based on a meta-analyses of the studies where former drinkers were separated from lifetime abstainers.
We calculated this correction for fatal and non-fatal outcomes combined to achieve more stable results, which may have biased the current results. Finally, assessment methods for alcohol consumption may vary among studies.
Alcohol consumption is usually measured by self-reported alcohol drinking habits. Such data are subject to recall bias. For example, heavy drinkers may be more likely to underreport their alcohol consumption or respondents simply forget about their consumption in retrospective recalls, which tends to result in an underestimation of alcohol consumption [ 64 — 66 ].
Overall, our study showed differential impact of alcohol consumption on both type and outcome of stroke. Clearly, to reduce the risk of stroke, any heavy consumption of alcohol should be avoided.
With respect to moderate consumption of up to 3 drinks, the results are mixed: moderate consumption seem to be protective for ischemic stroke only, but slightly detrimental or at best neutral for hemorrhagic stroke.
In line with the results on the cardio-protective effect of alcohol including the evidence on biological pathways [ 53 , 67 ], it seems reasonable that the protective effect on ischemic stroke is limited to people who not only on average drink moderately, but who also avoid heavy drinking occasions [ 55 ]. Finally, we would like to point out the implications of our findings for global public health.
Overall, we recognize that total abstention, while beneficial for some stroke subtype, is advocated to reduce total mortality and morbidity, including that from injury.