Published online before print August 22, 2009, doi: 10.1161/CIRCGENETICS.109.873604
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Original Articles |
Alcohol Intake, Myocardial Infarction, Biochemical Risk Factors, and Alcohol Dehydrogenase Genotypes
From the Center for Alcohol Research (J.S.T., M.G.), National Institute of Public Health, University of Southern Denmark, Copenhagen, Denmark; The Copenhagen City Heart Study (M.G., B.G.N.), Bispebjerg Hospital, Copenhagen University Hospital, Copenhagen, Denmark; and Department of Clinical Biochemistry (J.S.T., B.G.N.), Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark.
Correspondence to Janne S. Tolstrup, Center for Alcohol Research, National Institute of Public Health, Øster Farimagsgade 5a, DK-1399 Copenhagen, Denmark. E-mail jst{at}niph.dk
Received April 16, 2009; accepted July 27, 2009.
Background— The risk of myocardial infarction is lower among light-to-moderate alcohol drinkers compared with abstainers. We tested associations between alcohol intake and risk of myocardial infarction and risk factors and whether these associations are modified by variations in alcohol dehydrogenases.
Methods and Results— We used information on 9584 men and women from the Danish general population in the Copenhagen City Heart Study. During follow-up, from 1991 to 2007, 663 incident cases of myocardial infarction occurred. We observed that increasing alcohol intake was associated with decreasing risk of myocardial infarction, decreasing low-density lipoprotein cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and high-density lipoprotein cholesterol, and with U-shaped nonfasting triglycerides. In contrast, ADH1B and ADH1C genotypes were not associated with risk of myocardial infarction or with any of the cardiovascular biochemical risk factors, and there was no indication that associations between alcohol intake and myocardial infarction and between alcohol intake and risk factors were modified by genotypes.
Conclusions— Increasing alcohol intake is associated with decreasing risk of myocardial infarction, decreasing low-density lipoprotein cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and high-density lipoprotein cholesterol, and U-shaped nonfasting triglycerides. These associations were not modified by ADH1B and ADH1C are genotypes.
Key Words: blood pressure • genetics • cardiovascular diseases • myocardial infarction • epidemiology • alcohol • cardiovascular risk factors • alcohol dehydrogenase genes