ALDH2, ADH1B, and ADH1C genotypes in Asians: a literature review

Department of Psychiatry, University of California, San Diego, USA.
Alcohol research & health: the journal of the National Institute on Alcohol Abuse and Alcoholism (Impact Factor: 0.58). 02/2007; 30(1):22-7.
Source: PubMed

ABSTRACT Variants of three genes encoding alcohol-metabolizing enzymes, the aldehyde dehydrogenase gene ALDH2 and the alcohol dehydrogenase genes ADH1B and ADH1C, have been associated with reduced rates of alcohol dependence. The genotype prevalence of these genes varies in general samples of different Asian ethnic groups. The ALDH2*2 allele appears to be most prevalent in Chinese-American, Han Chinese and Taiwanese, Japanese, and Korean samples. Much lower rates have been reported in Thais, Filipinos, Indians, and Chinese and Taiwanese aborigines. ADH1B*2 is highly prevalent among Asians, with the exception of Indians. ADH1C*1 also is highly prevalent in Asians, but has only been examined in a few studies of Chinese and Korean samples.

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    • "La cause la plus fréquente de réactions d'intolérance est un déficit enzymatique en aldéhyde déshydrogénase, favorisant l'accumulation d'acétaldéhyde, un intermédiaire toxique du métabolisme de l'alcool qui provoque bouffées de chaleur (flush), tachycardie, céphalées, rhinorrhée et variations de la pression artérielle après consommation de boissons alcoolisées . Ce mécanisme d'intolérance concerne près de 50 % des individus d'origine asiatique [4]. Des réactions d'intolérance peuvent également être favorisées par la présence de sulfites. "
    La Presse Médicale 10/2014; 43(10). DOI:10.1016/j.lpm.2013.12.020 · 1.08 Impact Factor
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    • "Ethanol is mainly metabolized by the sequential dehydrogenation enzyme system: first, ADH catalyzes ethanol to acetaldehyde, and then ALDH2 catalyzes acetaldehyde to acetic acid30. Approximately 40% of the East Asian population carries one or two mutant ALDH2*2 alleles, which leads to significantly deficient enzymatic activity10,22. The present study showed that even low to moderate alcohol consumption may be harmful or at least have no benefit in ALDH2 mutant mice. "
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    ABSTRACT: Aim: To investigate the roles of acetaldehyde dehydrogenase 2 (ALDH2), the key enzyme of ethanol metabolism, in chronic low to moderate alcohol consumption-induced heart protective effects in mice. Methods: Twenty-one male wild-type (WT) or ALDH2-knockout (KO) mice were used in this study. In each genotype, 14 animals received alcohol (2.5%, 5% and 10% in week 1–3, respectively, and 18% in week 4–7), and 7 received water for 7 weeks. After the treatments, survival rate and general characteristics of the animals were evaluated. Serum ethanol and acetaldehyde levels and blood lipids were measured. Metabolomics was used to characterize the heart and serum metabolism profiles. Results: Chronic alcohol intake decreased the survival rate of KO mice by 50%, and significantly decreased their body weight, but did not affect those of WT mice. Chronic alcohol intake significantly increased the serum ethanol levels in both WT and KO mice, but KO mice had significantly higher serum acetaldehyde levels than WT mice. Chronic alcohol intake significantly increased the serum HDL cholesterol levels in WT mice, and did not change the serum HDL cholesterol levels in KO mice. After chronic alcohol intake, WT and KO mice showed differential heart and serum metabolism profiles, including the 3 main energy substrate types (lipids, glucose and amino acids) and three carboxylic acid cycles. Conclusion: Low to moderate alcohol consumption increases HDL cholesterol levels and improves heart energy metabolism profile in WT mice but not in ALDH2-KO mice. Thus, preserved ALDH2 function is essential for the protective effect of low to moderate alcohol on the cardiovascular system.
    Acta Pharmacologica Sinica 07/2014; 35(8). DOI:10.1038/aps.2014.46 · 2.91 Impact Factor
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    • "Studies in Asia and the United States have consistently found higher rates of alcohol dependence in individuals of South Korean heritage compared with Taiwanese and Chinese heritage (Helzer et al., 1990; Luczak et al., 2004). Different rates of alcohol dependence between Koreans and Chinese are partly explained by ALDH2*2 prevalence, with approximately 30% of Koreans and up to 50% of Chinese possessing ALDH2*2 (Eng et al., 2007), but data also suggest the strength of the ALDH2*2 effect may differ across these groups (Luczak et al., 2004, 2006). Furthermore , the prevalence of AUDs appears to be decreasing in the country of South Korea and increasing in China (Cochrane et al., 2003; Hahm and Cho, 2005; Helzer et al., 1990). "
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