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Circulation: Cardiovascular Genetics
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Published Online
on August 22, 2009

Circulation: Cardiovascular Genetics. 2009
Published online before print August 22, 2009, doi: 10.1161/CIRCGENETICS.109.873604
A more recent version of this article appeared on October 1, 2009
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Original Article

Alcohol Intake, Myocardial Infarction, Biochemical Risk Factors and Alcohol Dehydrogenase Genotypes

Janne S. Tolstrup1,4; Morten Grønbæk2 and Børge G. Nordestgaard3

1 Nat. Inst. of Public Health, Univ. of S. Denmark, Copenhagen, Denmark;
2 Nat. Inst. of Public Health, Univ. of S. Denmark & Copenhagen Univ. Hosp., Copenhagen, Denmark;
3 Copenhagen Univ. Hosp., Copenhagen & Herlev Hospital, Herlev, Denmark

* Corresponding author; email: jst{at}niph.dk

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 (ADHs).

Methods and Results—We used information on 9584 men and women from the Danish general population, the Copenhagen City Heart Study. During follow up, from 1991 through 2007, 663 incident cases of myocardial infarction occurred. We observed that increasing alcohol intake was associated with decreasing risk of myocardial infarction, decreasing LDL cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and HDL cholesterol, and with U-shaped non-fasting 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 and myocardial infarction or alcohol and risk factors were modified by genotypes.

Conclusions—Increasing alcohol intake associate with decreasing risk of myocardial infarction, decreasing LDL cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and HDL cholesterol, and with U-shaped non-fasting triglycerides. These associations were not modified by ADH1B and ADH1C genotypes.

Key Words: alcohol • blood pressure • cardiovascular diseases • epidemiology • genetics • myocardial infarction • epidemiology • cardiovascular risk factors • alcohol dehydrogenase genes