BACKGROUND: Data on the association between alcohol consumption and ischemic stroke have been inconsistent. It is not known whether allele epsilon(4) of the apolipoprotein E (apoE) gene modifies the alcohol-stroke association. We sought to examine whether epsilon(4) allele of the apoE gene influences the association between alcohol consumption and ischemic stroke or high-density lipoprotein (HDL) cholesterol. METHODS: We examined a cohort of 7676 person-observations of the Framingham Heart Study. Incident stroke was ascertained by standardized methods. We used Cox proportional hazard model to estimate hazard ratios of ischemic stroke. RESULTS: The average age at baseline was 63 years and 55% of the participants were women. During a mean follow-up of 7.4 years, 222 new cases of ischemic stroke occurred (56 embolic and 166 atherothrombotic events). Comparing current drinkers with nondrinkers, multivariable adjusted hazard ratio (95% confidence interval) for ischemic stroke was 0.50 (0.24-1.07) in the absence of epsilon(4) allele and 0.70 (0.24-2.05) in the presence of epsilon(4) allele (P for interaction = .64) for those younger than 65 years. Similarly, we did not observe a statistically significant interaction between epsilon(4) allele and alcohol consumption on the risk of stroke among people aged 65 years and older (P for interaction = .17). Alcohol consumption was positively associated with HDL cholesterol independent of epsilon(4) allele and age. CONCLUSIONS: Our data do not provide evidence for an interaction between epsilon(4) allele and alcohol consumption on the risk of ischemic stroke in this population. Furthermore, apoE polymorphism did not influence the alcohol-HDL relation.
BACKGROUND: Data on the association between alcohol consumption and ischemic stroke have been inconsistent. It is not known whether allele epsilon(4) of the apolipoprotein E (apoE) gene modifies the alcohol-stroke association. We sought to examine whether epsilon(4) allele of the apoE gene influences the association between alcohol consumption and ischemic stroke or high-density lipoprotein (HDL) cholesterol. METHODS: We examined a cohort of 7676 person-observations of the Framingham Heart Study. Incident stroke was ascertained by standardized methods. We used Cox proportional hazard model to estimate hazard ratios of ischemic stroke. RESULTS: The average age at baseline was 63 years and 55% of the participants were women. During a mean follow-up of 7.4 years, 222 new cases of ischemic stroke occurred (56 embolic and 166 atherothrombotic events). Comparing current drinkers with nondrinkers, multivariable adjusted hazard ratio (95% confidence interval) for ischemic stroke was 0.50 (0.24-1.07) in the absence of epsilon(4) allele and 0.70 (0.24-2.05) in the presence of epsilon(4) allele (P for interaction = .64) for those younger than 65 years. Similarly, we did not observe a statistically significant interaction between epsilon(4) allele and alcohol consumption on the risk of stroke among people aged 65 years and older (P for interaction = .17). Alcohol consumption was positively associated with HDL cholesterol independent of epsilon(4) allele and age. CONCLUSIONS: Our data do not provide evidence for an interaction between epsilon(4) allele and alcohol consumption on the risk of ischemic stroke in this population. Furthermore, apoE polymorphism did not influence the alcohol-HDL relation.
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