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dc.contributor.author | Kabagambe, Edmond K. | |
dc.contributor.author | Baylin, Ana | |
dc.contributor.author | Ruiz Narváez, Edward A. | |
dc.contributor.author | Rimm, Eric B. | |
dc.contributor.author | Campos, Hannia | |
dc.date.accessioned | 2016-07-13T16:38:04Z | |
dc.date.available | 2016-07-13T16:38:04Z | |
dc.date.issued | 2005 | |
dc.identifier.issn | 1938-3207 | |
dc.identifier.uri | http://biblioteca.ccp.ucr.ac.cr/handle/123456789/1157 | |
dc.description.abstract | Moderate consumption of alcohol in developed countries has been associated with a reduced risk of myocardial infarction (MI) (1–3). This evident protection is thought to be due to improved plasma lipid profiles, particularly an increase in HDL cholesterol (4–6), increased adiponectin (7), reduced plasma fibrinogen (8), viscosity (9), platelet activity (10, 11), C-reactive protein (8, 12), and improved insulin sensitivity (13). However, the protective effect of alcohol is not uniform across sex and populations or socioeconomic classes (14, 15), which raises doubts as to whether alcohol per se is truly protective or instead is a marker for another protective factor associated with alcohol consumption (4). Others have suggested that certain types of alcohol, eg, wine, may be more protective than others (16 –18). Growing evidence (2, 6, 14) suggests that the amount and pattern of intake, rather than the type of alcohol (19, 20), are more important in explaining the effects of alcohol in populations. Other studies suggest that sex (14) and genetic diversity of alcohol users (6, 21) may also play an important role in explaining the observed protection and differences across studies. For instance, in a recent prospective study, alcohol was inversely related to MI in white Americans but was hazardous for hypertension and MI in African Americans (14, 22). These disparities could be due to differences in alcohol intake patterns or the prevalence of functional genetic polymorphisms in genes encoding alcoholmetabolizing enzymes that have been reported across races (23–26). Polymorphisms in the alcohol dehydrogenase gene have been associated with changes in bothHDLcholesterol and risk of MI in moderate drinkers (6). Apart from one multicountry study (3) in which consumption of alcohol was marginally associated with a reduced risk of MI, to date, no large case-control studies have investigated the association between alcohol intake, patterns, and risk of MI in developing countries where diet and lifestyles differ from those in Western cultures. We conducted a large (n = 4548), matched, incident casecontrol study of residents of the Central Valley of Costa Rica, a country with low wine intake, to determine whether alcohol users, compared with self-reported lifelong abstainers, are less likely to have an MI. We also determined whether the pattern of alcohol drinking is associated with the risk of MI or intermediate phenotypes such as plasma lipid concentrations | en |
dc.language.iso | en | en |
dc.publisher | American Society for Clinical Nutrition | en |
dc.rights | Atribución-NoComercial-CompartirIgual 3.0 Costa Rica | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/3.0/cr/ | * |
dc.subject | Infarto de miocardio | es |
dc.subject | Enfermedades cardiovasculares | es |
dc.subject | Colesterol | es |
dc.title | Alcohol intake, drinking patterns and risk of nonfatal acute myocardial infarction in Costa Rica | es |
dc.title.alternative | The American Journal of Clinical Nutrition, 82(6) | es |
dc.type | Article | en |
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