Moderate alcohol consumption appears to confer some protection against coronary heart
disease, which is related to changes in serum levels of lipoproteins, especially high-density
lipoprotein cholesterol (HDL-C) [
1
,
2
]. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) metabolizes acetaldehyde produced
from ethanol into acetate and plays a crucial role in the oxidation of acetaldehyde
in vivo [
[3]
]. A sequence variant (rs671) on chromosome 12q24.2 was found associated with inactive
ALDH2. A mutant allele, ALDH2*2, has a single point mutation (G to A transition in
exon 12) at position 1510 of the active ALDH2*1 gene, which results in a substitution
of glutamic acid 504 to lysine and produces inactive ALDH2 [
4
,
5
,
6
]. The Glu504Lys variant is almost exclusively present in East Asians, and Wada et
al. [
[7]
] found no variants of rs671 in a Caucasian population. The ALDH2 genotypes are closely
related to alcohol metabolism [
[3]
] and were recently found to be associated with atherosclerosis [
[8]
], hypertension [
9
,
10
,
11
], and myocardial infarction [
12
,
13
] in Asians. The risks have been attributed primarily to an increase in serum HDL-C
level. Recently, we reported an association of ALDH2 deficiency and increased risk
of type II diabetes mellitus in female patients with coronary artery disease but not
levels of serum lipids and/or lipoproteins or coronary atherosclerosis severity [
14
,
15
]. The reason for the discrepancy is unclear but may be related to low statistical
power or to differences among the ethnic groups studied.Keywords
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Article info
Publication history
Published online: June 14, 2010
Received:
January 23,
2010
Identification
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© 2010 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.