Genetic differences in ethanol metabolizing enzymes and blood pressure in Japanese alcohol consumers

Yamada, Yuichi; Sun, Fang; Tsuritani, Ikiko; Honda, Ryumon

doi:10.1038/sj.jhh.1001415

Cited by 34 publications

(24 citation statements)

References 26 publications

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“…From these results, it can be concluded that acetaldehyde accumulates even in moderate alcohol consumers irrespective of ALDH2 and CYP2E1 genotypes, and that neither those genotypes nor urinary acetaldehyde affects common health consequences related to moderate alcohol consumption. A possible etiological role of ALDH2 deficiency and consequent high blood acetaldehyde in alcohol-related hypertension has been suggested by Itoh et al (1997), but effects of ALDH2 genotypes on the alcohol-blood pressure relationship have been ruled out in many studies (Okayama et al 1994;Tsuritani et al 1995;Tanaka et al 1997;Takagi et al 2001;Amamoto et al 2002;Yamada et al 2002), similar to the present results. A high incidence of myocardial infarction in those having ALDH2 deficiency has been demonstrated to be a reflection of the low serum HDLc due to low alcohol consumption (Takagi et al 2002).…”

Section: Discussionsupporting

confidence: 87%

ALDH2 and CYP2E1 genotypes, urinary acetaldehyde excretion and the health consequences in moderate alcohol consumers

et al. 2005

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Deficiencies in mitochondrial low-Km aldehyde dehydrogenase (ALDH2) activity, and consequently high blood acetaldehyde levels, have been suggested to relate to various diseases in Japanese, including esophageal cancer. In the present study, 200 men aged 35-59 years randomly selected from an occupational population were analyzed for the association of ALDH2 genotypes and cytochrome P450-2E1 (CYP2E1) genotypes with the urinary excretion of acetaldehyde (which is bound to some chemicals in the urine) and with common alcohol-related health consequences. Urinary acetaldehyde excretion was increased, reflecting increased alcohol consumption even in this moderate alcohol-consuming population. Neither the ALDH2 nor the CYP2E1 genotypes showed significant influence on the elevation of urinary acetaldehyde excretion. Neither these genotypes nor urinary acetaldehyde concentration significantly affected blood pressure, serum aspartate aminotransferase and gamma-glutamyl transferase activities, or serum HDL-cholesterol and lipid peroxide concentrations. It was concluded that acetaldehyde accumulates in moderate alcohol consumers irrespective of ALDH2 and CYP2E1 genotype, and that the implications of these genotypes and acetaldehyde accumulation in terms of common alcohol-related health consequences were obscure. The results also suggest that the carcinogenicity of acetaldehyde on esophageal mucosa depends greatly upon repeated exposure to high blood acetaldehyde, even through transient rather than chronic exposure.

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Section: Discussionsupporting

confidence: 87%

ALDH2 and CYP2E1 genotypes, urinary acetaldehyde excretion and the health consequences in moderate alcohol consumers

et al. 2005

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“…In our study, the ALDH2 genetic polymorphism was also significantly associated with alcohol consumption and influenced the risk of CAD. Fourth, ALDH2 genetic polymorphism may increase blood pressure, influencing the risk of CAD (Yamada et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Aldehyde dehydrogenase 2 (ALDH2) polymorphism gene and coronary artery disease risk: a meta-analysis

Zhang¹,

Wang²,

Bao-quan³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We studied the association between aldehyde dehydrogenase 2 (ALDH2) polymorphism and coronary artery disease (CAD) and clarified the mechanisms underlying this association. We searched the ISI, Medline (Ovid), PubMed, CNKI, Wanfang, and Weipu Databases. Statistical analysis was performed using Revman 5.0 and Stata12.0 softwares. A total of 3305 cases and 5016 controls in 12 casecontrol studies were included in this meta-analysis. Variant A allele carriers showed a 48% increased risk of CAD compared with homozygote A allele [odds ratio (OR) = 1.48, 95% confidence interval (CI) = 1.18-1.87 for AA + AG vs GG]. In subgroup analysis by gender, significantly elevated risks were found in the mixed group (OR = 1.78, 95%CI = 1.42-2.22) but not in males (OR = 1.12, 95%CI = 0.79-1.57). In subgroup analysis by disease type, significant elevated risks were associated with A allele carriers in myocardial infarction [OR = 1.69, 95%CI = (1.05-2.71)], in coronary (2015) heart disease (OR = 1.36, 95%CI = 1.00-1.86), but not in coronary heart disease plus diabetes mellitus subjects (OR = 1.57, 95%CI = 0.58-4.29). Moreover, those with the GG genotype consumed significantly more alcohol than those with the AA/AG genotypes (standard mean deviation: 6.32 g, 95%CI = 2.09-10.55, P = 0.000). ALDH2 polymorphisms may be risk factors for CAD. Moreover, CAD patients with ALDH2 genotypes AG and AA consumed significantly less alcohol than those with GG. To further evaluate gene-gene and gene-environment interactions between ALDH2 polymorphisms and the risk of CAD, more studies with larger groups of patients are required.

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“…Several studies have investigated the influence of rs671 genotypes on blood pressure. 11,[15][16][17] Almost all earlier studies, except for the one by Itoh et al, have reported that ALDH2 rs671 cannot significantly influence the alcohol-blood pressure relationship. 18 The following reasons may account for discrepancies between the results of our study and those of others: (1) sample size is relatively small in other studies; (2) physiological, aging-related blood pressure elevation is not negligible when the average age of the participants is relatively high in some studies; (3) the confounding pressor effects of the amounts of alcohol consumption may not be sufficiently adjusted for by multivariate analysis alone using the entire study population; and (4) nondrinkers should be excluded from the analysis to evaluate 'gene-environment (that is, alcohol intake in this case) interaction.…”

Section: Alcohol Metabolizing Enzymes and Blood Pressure M Tsuchihashmentioning

confidence: 99%

Gene–environmental interaction regarding alcohol-metabolizing enzymes in the Japanese general population

et al. 2009

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Epidemiological studies have shown that excessive alcohol consumption is a potent risk factor to develop hypertension. In addition, some polymorphisms of the alcohol metabolism genes have been reported to exert significant impacts on the risk of alcoholism. We investigate the relevance of genetic susceptibility to drinking behavior and its influence on the sensitivity to pressor effects of alcohol in the Japanese general population. We initially screened SNPs in four candidate genes by resequencing. From 35 SNPs thus identified, 10 tag SNPs were selected and used for large-scale association analysis in a total of 5724 subjects. Among the SNPs tested, significant association (Po0.001) with drinking behavior was observed for ADH1B Arg47His (rs1229984) and ALDH2 Glu487Lys (rs671) polymorphisms. All subjects with Lys homozygote (AA genotype) of rs671 turned out to be nondrinkers and the combination of two SNP genotypes appeared to substantially influence people's drinking behavior in a synergistic manner. rs671 was significantly associated with blood pressure (P¼0.0001-0.0491) in subgroups of drinkers. In the context of gene-environment interaction, our data clearly show the genetic impacts of two SNPs on drinking behavior and of one SNP on the sensitivity to the pressor effects of alcohol in the Japanese general population.

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Genetic differences in ethanol metabolizing enzymes and blood pressure in Japanese alcohol consumers

Cited by 34 publications

References 26 publications

ALDH2 and CYP2E1 genotypes, urinary acetaldehyde excretion and the health consequences in moderate alcohol consumers

ALDH2 and CYP2E1 genotypes, urinary acetaldehyde excretion and the health consequences in moderate alcohol consumers

Aldehyde dehydrogenase 2 (ALDH2) polymorphism gene and coronary artery disease risk: a meta-analysis

Gene–environmental interaction regarding alcohol-metabolizing enzymes in the Japanese general population

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