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


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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    • "Although there exists controversy about sample size requirements in behavioral genetics (Burmeister et al., 2008), there is a robust literature on these functional polymorphisms in alcohol-metabolizing genes, including their biobehavioral mechanism of action. As a result, ALDH2 and ADH are among the most widely studied and supported polymorphisms in alcoholism genetics (for review, see Eng et al., 2007; Wall, 2005), thus justifying their evaluation in this sample. As noted previously, the lack of genetic data for participants' parents limits our ability to dissociate genetic effects from FH and ethnicity. "
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    ABSTRACT: Objective: Among Asian American young adults, variations in alcohol-metabolizing genes (i.e., aldehyde dehydrogenase [ALDH2] and alcohol dehydrogenase [ADH1B]) are protective, whereas Korean ethnicity, family history of alcohol problems (FH), and acculturation represent risk factors for alcohol misuse. This study aims to integrate these genetic and environmental factors in a sample of Asian Americans expressing a wide range of alcohol use behaviors and problems. Method: Participants were 97 Asian American young adults (42% female) recruited as heavy and light drinkers (n = 49 and 48, respectively). Participants completed the Alcohol Use Disorders Identification Test, Timeline Followback, Vancouver Acculturation Index, and Family Tree Questionnaire. All participants provided buccal cell samples for DNA analysis. Results: Family history-positive (FH+) subjects reported greater alcohol use than family history-negative (FH-) subjects. A FH × ALDH2 interaction was observed such that FH- subjects demonstrated no ALDH2 effect, yet in FH+ subjects, the ALDH2*2 genotype was associated with increased alcohol use. A significant main effect of acculturation was also moderated by FH such that the positive association between acculturation and alcohol use was greater among FH+ subjects and, in particular, among FH+ men. Conclusions: Although preliminary, these results suggest that the potential protective effects conferred by ALDH2 and ADH1B are moderated by FH, such that a positive FH appeared to abolish the protective effect of these genes. Further, acculturation was associated with greater alcohol use in FH+ subjects only. If replicated in larger samples, these data suggest that alcohol-metabolism genes may not be protective in the context of high environmental risk.
    Full-text · Article · Sep 2015 · Journal of studies on alcohol and drugs
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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. "

    Full-text · Article · Oct 2014 · La Presse Médicale
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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.
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