109
views
0
recommends
+1 Recommend
0 collections
    0
    shares
       
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      ALDH2, ADH1B, and ADH1C Genotypes in Asians: A Literature Review

      research-article
      Overview Bookmark

            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.

            Main article text

            People of Asian descent, as a whole, have lower rates of alcohol dependence compared with other ethnic groups (Grant et al. 2004). Within Asians, however, rates of alcohol dependence differ across ethnic subgroups. For example, relatively high rates of alcohol dependence have been found among Koreans and Korean Americans, whereas relatively low rates have been found in Chinese and Chinese Americans (Helzer et al. 1990; Luczak et al. 2004). Prevalence rates of alleles of genes encoding alcohol-metabolizing enzymes vary across Asian ethnicities (e.g., Goedde et al. 1992). This may in part account for some of the ethnic differences in rates of alcohol involvement. The purpose of this article is to review genotype1 prevalence rates of three genes, the aldehyde dehydrogenase gene ALDH2 and the alcohol dehydrogenase genes ADH1B and ADH1C.2

            These three genes code for isoenzymes that metabolize alcohol into acetaldehyde (ADH1B and ADH1C) and acetaldehyde into acetate (ALDH2). The common forms of these alleles are ADH1B*1, ADH1C*2, and ALDH2*1. The variant forms of the alleles (ADH1B*2, ADH1C*1, and ALDH2*2) are hypothesized to alter conversion rates during alcohol metabolism and lead to an excess buildup of acetaldehyde (see Eriksson 2001). The excess acetaldehyde is thought to lead to heightened responses to alcohol and thereby reduce heavy alcohol use, associated problems, and the development of alcohol use disorders (see Wall et al. 2005 for further details). A meta-analysis of 15 Asian (Chinese, Japanese, Korean, and Thai) studies with data from over 4,500 alcohol-dependent and control subjects collected between 1979 and 2004 found possession of one variant ALDH2*2 allele was associated with a fivefold reduction in alcohol is dependence and possession of two ALDH2*2 alleles was associated with a nine-fold reduction (Luczak et al. 2006).3 In Asians with no ALDH2*2 alleles, possession of one variant ADH1B*2 allele was associated with a four-fold reduction in alcohol dependence and possession of two ADH1B*2 alleles was associated with a five-fold reduction (Luczak et al. 2006). ADH1C*1 also has been related to protection against alcohol dependence, but this association has been attributed to the ADH1C gene being in close proximity to the ADH1B gene on the chromosome so that the genotypes are correlated (Osier et al. 1999).

            Determining how frequently certain genotypes occur in different populations is useful for behavioral genetics research. It is important to establish the prevalence rates of these genotypes in various ethnic groups to determine their unique contribution to alcohol involvement within each ethnicity. To achieve this goal for Asian populations, an extensive literature review of studies determining the prevalence of the ALDH2, ADH1B, and ADH1C genotypes in various Asian ethnic groups was performed, as described in the following sections.

            Prevalence of ALDH2,ADH1B, and ADH1C Genotypes in Asian Populations

            Study Design

            To identify studies eligible for this analysis, the authors of this article surveyed the Medline literature database using the National Library of Medicine’s PubMed (January 1966 to April 2006) online search engine. The search first was conducted using the keywords “(aldehyde dehydrogenase OR ALDH) AND Asian;” then, additional searches were conducted by replacing “Asian” with specific Asian ethnicities (i.e., Chinese, Filipino, Indian, Japanese, Korean, Malaysian, and Thai). The series of searches then was repeated using the keywords “(alcohol dehydrogenase OR ADH).” The retrieved abstracts were read to identify studies that reported prevalence rates of the various ALDH2, ADH1B, and ADH1C genotypes in general samples of the different ethnic groups. The studies thus identified were read in their entirety to assess whether they were appropriate for including in this analysis. Studies that reported only allele frequencies instead of genotypes, compared treatment samples with control groups, or selected samples based on specific alcohol-related medical conditions (e.g., cirrhosis or head and neck cancers) were excluded. All references cited in the appropriate articles also were reviewed to identify additional relevant publications.

            Despite the stringent criteria for the selection of studies to be included, the following caveats should be noted:

            • Some samples included in the analysis may not be entirely random because participants were screened for certain medical disorders (e.g., diabetes, heart conditions, and stroke) that have been related to alcohol in addition to other factors.

            • Samples with allele distributions that do not meet Hardy-Weinberg equilibrium4 (which are marked in the table summarizing the results) should be viewed with caution because the genotype distribution in these studies is not consistent with the expected distribution for a general sample.

            Results of the Analysis
            Distribution of ALDH2 Genotypes

            The ALDH2*2 allele is thought to occur exclusively in Asians; however, its prevalence varies across Asian ethnicities (see Table 1). Five studies determined the ALDH2 genotype in Han Chinese and Taiwanese people.5 In these studies, 20 to 47 percent of the participants were heterozygous and 1 to 8 percent were homozygous for ALDH2*2 (Goedde et al. 1992; Luo et al. 2001, 2005; Novoradovsky et al. 1995; Shen et al. 1997). Overall, approximately one-third of the Han Chinese possessed at least one ALDH2*2 allele. The prevalence of the ALDH2*2 allele was particularly high in one study of Han Taiwanese and two studies of Chinese Americans, with about half of these samples possessing at least one ALDH2*2 allele, including 7 to 8 percent who were homozygous for ALDH2*2 (Hendershot et al. 2005; Luczak et al. 2004; Novoradovsky et al. 1995). The large variation in prevalence rates found among Han Chinese and Taiwanese samples might be explained by the different geographic locations from which the samples were obtained. The sample with the highest prevalence was from Taiwan, where 55 percent of participants possessed at least one ALDH2 allele (Novoradovsky et al. 1995). Conversely, the samples with the lowest prevalence were from central and northern China, where 22 percent of participants possessed at least one ALDH2*2 allele (Luo et al. 2001; Shen et al. 1997). For the studies with intermediate prevalence rates (i.e., 30 to 32 percent), the samples were from southwest China (Luo et al. 2005) or their location was not reported (Goedde et al. 1992).

            The ALDH2*2 allele was less commonly found in aboriginal Chinese and Taiwanese samples (e.g., Ami, Atayal, Bunun, Elunchan, Mongolian, and Paiwan), with 2 to 12 percent of study participants being heterozygous and only 0.3 percent (i.e., 2 of 585 people analyzed) being homozygous for ALDH2*2 (Chen et al. 1997; Shen et al. 1997; Thomasson et al. 1994).

            Data from 10 Japanese studies indicated that 41 to 52 percent of Japanese possessed at least one ALDH2*2 allele, including 1 to 8 percent who were homozygous for ALDH2*2 (Amamoto et al. 2002; Goedde et al. 1992; Higuchi et al. 1996; Saito et al. 2003; Sun et al. 1999; Takeshita and Morimoto 1999: Takeshita et al. 1994; Tanaka et al. 1997; Yamada et al. 2002; Yokoyama et al. 2005). Somewhat higher rates were reported in one small Japanese study (N = 15), in which 66 percent of the participants possessed at least one ALDH2*2 allele, including 13 percent who were homozygous for ALDH2*2 (Shibuya et al. 1989).

            Five studies of Korean, Korean-American, and Korean-Chinese samples found that approximately one-third (29 to 37 percent) of Koreans had at least one ALDH2*2 allele, including 2 to 3 percent who were homozygous for ALDH2*2 (Goedde et al. 1992; Hendershot et al. 2005; Lee et al. 1997; Luczak et al. 2004; Shen et al. 1997). Finally, ALDH2*2 was much less common among other Asian ethnicities, including Filipinos, Indians, Malays, Siberian Yakuts, and Thais, than in Chinese, Japanese, and Korean samples, with 0 to 10 percent of study participants possessing at least one ALDH2*2 allele (Goedde et al. 1992; Novoradovsky et al. 1995). Taken together, all the studies reviewed here demonstrate great diversity among Asian ethnic groups in the prevalence of heterozy-gosity or homozygosity for ALDH2*2.

            Distribution of ADH1B Genotypes

            The ADH1B*2 allele was highly prevalent in Asian ethnic groups, particularly in northeast Asians (i.e., Chinese, Japanese, and Koreans) (see Table 1). Among the Han Chinese and Taiwanese and the Chinese Americans, 84 to 92 percent possessed at least one ADH1B*2 allele, including 40 to 60 percent who were homozygous for ADH1B*2 (Chao et al. 1987; Goedde et al. 1992; Lee et al. 1989; Luczak et al. 2004; Shen et al. 1997). Rates of having at least one ADH1B*2 allele were slightly lower in some Chinese and Taiwanese aborigine groups (e.g., 63 percent in Elunchan, 74 percent in Mongolian, and 78 percent in Ami) but were higher in others (e.g., 98 to 100 percent in Atayal, Bunun, and Paiwan) (Chen et al. 1997; Shen et al. 1997; Thomasson et al. 1994).

            The ADH1B*2 allele also was commonly found in Japanese people. In 10 studies of Japanese, 81 to 100 percent of participants possessed at least one ADH1B*2 allele, including 34 to 71 percent who were homozygous for the allele (Goedde et al. 1992; Higuchi et al. 1996; Saito et al. 2003; Shibuya et al. 1989; Sun et al. 1999; Suzuki et al. 2004; Takeshita et al. 1996; Tanaka et al. 1997; Yamada et al. 2002; Yin et al. 1984). The results of one of the studies (Yin et al. 1984), in which ADH1B*2 prevalence rates were among the lowest for Japanese and Japanese Americans, however, must be viewed with caution because the distributions were not in Hardy-Weinberg equilibrium.

            The prevalence of ADH1B*2 also was high in three Korean samples, with 88 to 96 percent of participants possessing at least one ADH1B*2 allele and 50 to 65 percent possessing two ADH1B*2 alleles (Goedde et al. 1992; Luczak et al. 2004; Shen et al. 1997). Among Filipinos and Malays, more than 80 percent of study participants carried at least one ADH1B*2 allele (Goedde et al. 1992) as well. Intermediate rates were found in Thais (54 percent), and ADH1B*2 was least common in Indians, where only 15 percent possessed at least one copy of the allele (Goedde et al. 1992).

            Distribution of ADH1C Genotypes

            ADH1C genotypes only have been examined in a few Chinese and Korean samples, but in these samples the ADH1C*1 allele was highly prevalent. In one study of Han Chinese, 97 percent of participants possessed at least one ADH1C*1 allele, including 83 percent who were homozygous (Shen et al. 1997). Comparably high proportions (97 to 100 percent) of seven Chinese aboriginal populations possessed at least one ADH1C*1 allele, although the rates of homozygosity for ADH1C*1 were more variable (59 to 99 percent) in these populations (Chen et al. 1997; Shen et al. 1997; Thomasson et al. 1994). Finally, the prevalence of ADH1C*1 in one Korean Chinese sample was similar to the rates reported in Chinese samples, with 99 percent of subjects possessing at least one ADH1C*1 allele, including 86 percent who were homozygous for the allele (Shen et al. 1997).

            Summary

            This literature review highlights the fact that the prevalence of ALDH2, ADH1B, and ADH1C alleles vary greatly across Asian ethnic groups. For example, whereas approximately half of Chinese-American and Japanese samples and approximately one-third of Korean and Han Chinese and Taiwanese studied carry at least one ALDH2*2 allele, the prevalence of this allele is much lower (10 percent) in Thais, and almost no Filipinos, Indians, or Chinese and Taiwanese aborigines carry the allele, with the exception of Mongolians (12 percent). Similarly, the ADH1B*2 allele is found in 80 percent or more of Han Chinese and Taiwanese, Filipino, Japanese, Korean, and some Chinese and Taiwanese aborigine people but only in about 15 percent of Indians. Finally, the ADH1C*1 allele was found in almost all Chinese and Korean people studied, but it has not been analyzed yet in other Asian ethnic groups. Such summaries of general-sample prevalence rates are important for understanding risk and protective factors for alcohol use disorders because they facilitate comparisons of the contribution of these alcohol-metabolizing enzymes and their variants to alcohol-related behaviors within and across ethnic groups.

            Acknowledgements

            This research was funded by National Institutes of Health grants K02–AA–00269, K08–AA–14265, R01–AA– 11257, and T32–AA–013525 and a grant from the Alcoholic Beverage Medical Research Foundation.

            Footnotes

            1

            Every person possesses two copies of each allele; these two alleles make up the genotype.

            2

            ADH1B and ADH1C were formerly called ADH2 and ADH3, respectively (for more information, see the accompanying article by Edenberg).

            3

            If a person has two copies of the same allele, the person is called homozygous for that allele; if the two copies are of different alleles, the person is called heterozygous.

            4

            Hardy-Weinberg equilibrium is the stable frequency distribution of genotypes, as measured by the proportion of the alleles that result as a consequence of random mating.

            5

            The Han are the main ethnic group found in the People’s Republic of China and Taiwan.

            Financial Disclosure

            The authors declare that they have no competing financial interest.

            References

            1. Amamoto K, Okamura T, Tamaki S, et al.. Epidemiologic study of the association of low-Km mitochondrial acetaldehyde dehydrogenase genotypes with blood pressure level and the prevalence of hypertension in a general population. Hypertension Research. Vol. 25:857–864. 2002. [PubMed]

            2. Chao T-J, Chang C-P, Chang M-C, et al.. Liver alcohol and aldehyde dehydrogenase isoenzymes in Chinese. Proceedings of the National Science Council, Republic of China Part B, Basic Science. Vol. 11:260–265. 1987. [PubMed]

            3. Chen WJ, Loh EW, Hsu Y-PP, Cheng ATA. Alcohol dehydrogenase and aldehyde dehydrogenase and alcoholism among Taiwanese aborigines. Biological Psychiatry. Vol. 41:703–709. 1997. [PubMed]

            4. Eriksson CJP. The role of acetaldehyde in actions of alcohol (Update 2000). Alcoholism: Clinical and Experimental Research. Vol. 25:15S–32S. 2001. [PubMed]

            5. Grant BF, Stinson FS, Dawson DA, et al.. Prevalence and co-occurrence of substance use disorders and independent mood and anxiety disorders: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. Archives of General Psychiatry. Vol. 61:807–816. 2004. [PubMed]

            6. Goedde HW, Agarwal DP, Fritze G, et al.. Distribution of ADH2 and ALDH2 genotypes in different populations. Human Genetics. Vol. 88:344–346. 1992. [PubMed]

            7. Helzer JE, Canino GJ, Yeh E-K, et al.. Alcoholism: North America and Asia. Archives of General Psychiatry. Vol. 47:313–319. 1990. [PubMed]

            8. Hendershot CS, MacPherson L, Myers MG, et al.. Psychosocial, cultural and genetic influences on alcohol use in Asian American youth. Journal of Studies on Alcohol. Vol. 66:185–195. 2005. [PubMed]

            9. Higuchi S, Matsushita S, Muramatsu T, et al.. Alcohol and aldehyde dehydrogenase genotypes and drinking behavior in Japanese. Alcoholism: Clinical and Experimental Research. Vol. 20:493–497. 1996. [PubMed]

            10. Lee K-H, Kwak B-Y, Kim J-H, et al.. Genetic polymorphism of cytochrome P-450E1 and mitochrondrial aldehyde dehydrogenase in a Korean population. Alcoholism: Clinical and Experimental Research. Vol. 21:953–956. 1997. [PubMed]

            11. Lee S-C, Lin J-S, Chou F-J, Yin S-J. Lung alcohol and aldehyde dehydrogenase isoenzymes in Chinese. Journal of the Formosan Medical Association. Vol. 88:437–442. 1989. [PubMed]

            12. Luczak SE, Wall TL, Cook TAR, et al.. ALDH2 status and conduct disorder mediate the relationship between ethnicity and alcohol dependence in Chinese-, Korean-, and White-American college students. Journal of Abnormal Psychology. Vol. 113:271–278. 2004. [PubMed]

            13. Luczak SE, Glatt SJ, Wall TL. Meta-analyses of ALDH2 and ADH1B with alcohol dependence in Asians. Psychological Bulletin. Vol. 132:607–612. 2006. [PubMed]

            14. Luo H-R, Tu G-C, Zhang Y-P. Detection of usual and atypical aldehyde dehydrogenase alleles by mismatch amplification mutation assay. Clinical Chemistry and Laboratory Medicine: CCLM/FESCC. Vol. 39:1195–1197. 2001. [PubMed]

            15. Luo H-R, Israel Y, Tu G-C, et al.. Genetic polymorphism of aldehyde dehydrogenase 2 (ALDH2) in a Chinese population: Gender, age, culture, and genotypes of ALDH2. Biochemical Genetics. Vol. 43:223–227. 2005. [PubMed]

            16. Novoradovsky A, Tsai S-JL, Goldfarb L, et al.. Mitochondrial aldehyde dehydrogenase polymorphism in Asian and American Indian Populations: Detection of new ALDH2 alleles. Alcoholism: Clinical and Experimental Research. Vol. 5:1105–1110. 1995. [PubMed]

            17. Osier M, Pakstis AJ, Kidd JR, et al.. Linkage disequilibrium at the ADH2 and ADH3 loci and risk for alcoholism. American Journal of Human Genetics. Vol. 64:1147–1157. 1999. [PubMed]

            18. Saito K, Yokoyama T, Yoshiike N, et al.. Do the ethanol metabolizing enzymes modify the relationship between alcohol consumption and blood pressure? Journal of Hypertension. Vol. 21:1097–1105. 2003. [PubMed]

            19. Shen Y-C, Fan J-H, Edenberg HJ, et al.. Polymorphism of ADH and ALDH genes among four ethnic groups in China and effects upon the risk for alcoholism. Alcoholism: Clinical and Experimental Research. Vol. 21:1272–1277. 1997. [PubMed]

            20. Shibuya A, Yasunami M, Yoshida A. Genotypes of alcohol dehydrogenase and aldehyde dehydrogenase loci in Japanese alcohol flushers and non-flushers. Human Genetics. Vol. 82:14–16. 1989. [PubMed]

            21. Sun F, Tsuritani I, Honda R, et al.. Association of genetic polymorphisms of alcohol metabolizing enzymes with excessive alcohol consumption in Japanese men. Human Genetics. Vol. 105:295–300. 1999. [PubMed]

            22. Suzuki Y, Fujisawa M, Ando F, et al.. Alcohol dehydrogenase 2 variant is associated with cerebral infarction and lacunae. Neurology. Vol. 63:1711–1713. 2004. [PubMed]

            23. Takeshita T, Morimoto K. Self-reported alcohol-associated symptoms and drinking behavior in three ALDH2 genotypes among Japanese university students. Alcoholism: Clinical and Experimental Research. Vol. 23:1065–1069. 1999. [PubMed]

            24. Takeshita T, Morimoto K, Mao XQ, et al.. Characterization of the three genotypes of low Km aldehyde dehydrogenase in a Japanese population. Human Genetics. Vol. 94:217–223. 1994. [PubMed]

            25. Takeshita T, Mao X-Q, Morimoto K. The contribution of polymorphism in the alcohol dehydrogenase β subunit to alcohol sensitivity in a Japanese population. Human Genetics. Vol. 97:409–413. 1996. [PubMed]

            26. Tanaka R, Shiratori Y, Yokosuka O, et al.. Polymorphism of alcohol-metabolizing genes affects drinking behavior and alcoholic liver disease in Japanese men. Alcoholism: Clinical and Experimental Research. Vol. 21:596–601. 1997. [PubMed]

            27. Thomasson HR, Crabb DW, Edenberg HJ, et al.. Low frequency of the ADH2*2 allele among Atayal natives of Taiwan with alcohol use disorders. Alcoholism: Clinical and Experimental Research. Vol. 18:640–643. 1994. [PubMed]

            28. Wall TL, Shea SH, Luczak SE, et al.. Genetic associations of alcohol dehydrogenase with alcohol use disorders and endophenotypes in White college students. Journal of Abnormal Psychology. Vol. 114:456–465. 2005. [PubMed]

            29. Yamada Y, Sun F, Tsuritani I, Honda R. Genetic differences in ethanol metabolizing enzymes and blood pressure in Japanese alcohol consumers. Journal of Human Hypertension. Vol. 16:479–486. 2002. [PubMed]

            30. Yin S-J, Bosron RF, Li T-K, et al.. Polymorphism of human liver alcohol dehydrogenase: Identification of ADH2 2-1 and ADH2 2-2 phenotypes in the Japanese by isoelectric focusing. Biochemical Genetics. Vol. 22:169–180. 1984. [PubMed]

            31. Yokoyama M, Yokoyama A, Yokoyama T, et al.. Hangover susceptibility in relation to aldehyde dehydrogenase-2 genotype, alcohol flushing, and mean corpuscular volume in Japanese workers. Alcoholism: Clinical and Experimental Research. Vol. 29:1165–1171. 2005. [PubMed]

            Floating objects

            Table 1

            Genotypes for Genes Encoding Aldehyde Dehydrogenase (ALDH2) and Alcohol Dehydrogenase (ADH1B and ADH1C)

            Study AuthorsSampleALDH2 Genotypes prevalence (%)ADH1B Genotypes prevalence (%)ADH1C Genotypes prevalence (%)

            *1/*1*1/*2*2/*2*1/*1*1/*2*2/*2*1/*1*1/*2*2/*2
            Han Chinese and Taiwanese
              Chao et al. 198760 male and 11 female liver specimens103159
              Goedde et al. 1992132 subjects*7029184844
              Lee et al. 198953 lung specimens93060
              Luo et al. 200150 subjects78202
              Luo et al. 2005444 males and 204 females68284
              Novoradovsky et al. 1995173 blood donors45478
              Shen et al. 1997c100 male7820216444083143
              Total6630411404983143
            Chinese American
              Hendershot et al. 2005110 male and 113 female college students51437
              Luczak et al. 200492 males and 98 females college students4844883358
              Total4943783358
            Chinese and Taiwanese Aborigine
              Chen et al. 1997
                Ami46 subjects*93702238409820
                Atayal67 subjects*9730021799640
                Bunun118 subjects*98201306988120
                Paiwan71 subjects*9550031699910
              Shen et al. 1997
                Elunchana68 males93613754959383
                Mongolian66 males8812026443073262
              Thomasson et al. 1994
                Atayala80 males and 80 females*9451324749730
              Total955010325888111
            Filipino
              Goedde et al. 199286 subjects*9910194040
            Indian
              Goedde et al. 1992a,b179 subjects*973185105
            Japanese
              Amamoto et al. 2002a749 males and 1,286 females48457
              Goedde et al. 199253 subjects*55432165034
              Higuchi et al. 1996230 male and 221 female hospital employees and relatives5935673558
              Saito et al. 2003335 males5341683557
              Shibuya et al. 198915 males*33531302971
              Sun et al. 1999643 male hospital and civil service employees5836643561
              Suzuki et al. 20041,126 males53461
              Takeshita & Morimoto 1999389 males and 34 females medical students54405
              Takeshita et al. 1994424 male and 100 females metal plant workers57377
              Takeshita et al. 1996424 male and 100 females metal plant workers63360
              Tanaka et al. 1997a189 males5148153857
              Yamada et al. 2002855 male factory workers5836643660
              Yin et al. 1984b97 liver samples132958
              Yokoyama et al. 2005139 male and 112 female workers59338
              Total5440663560
            Japanese American
              Yin et al. 1984b97 liver samples193447
            Korean
              Goedde et al. 1992218 subjects*7227243165
              Lee et al. 1997481 subjects71263
              Total7126343165
            Korean American
              Hendershot et al. 200597 male and 108 female college students67322
              Luczak et al. 2004107 male and 107 female college students66313103653
              Total66322103653
            Korean Chinese
              Shen et al. 1997105 males6334311385086131
            Malay
              Goedde et al. 199273 subjects*9370174835
            Thai
              Goedde et al. 1992111 subjects90100464113
            Siberian Yakut
              Novoradovsky et al. 1995209 subjects10000
            a

            not in Hardy-Weinberg equilibrium for ALDH2;

            b

            not in Hardy-Weinberg equilibrium for ADH1B;

            c

            not in Hardy-Weinberg equilibrium for ADH1C;

            df

            = 1, p < .05 for all.

            *

            Sample size varies by gene analyzed.

            Author and article information

            Journal
            Alcohol Res Health
            Alcohol Res Health
            ARH
            Alcohol Research & Health
            National Institute on Alcohol Abuse and Alcoholism
            1535-7414
            1930-0573
            2007
            : 30
            : 1
            : 22-27
            Author notes

            M imy Y. E ng, P h.D., is a postdoctoral fellow in the Department of Psychiatry, University of California, San Diego, and the Veterans Medical Research Foundation, San Diego, California.

            S usan E. L uczak, P h.D., is an assistant research professor in the Department of Psychology, University of Southern California, Los Angeles, California, and an assistant adjunct professor in the Department of Psychiatry, University of California, San Diego, California.

            T amara L. W all, P h.D., is a professor in the Department of Psychiatry, University of California, and associate chief of the Psychology Service, Veterans Affairs San Diego Healthcare System, San Diego, California, and a research scientist in the Veterans Medical Research Foundation, San Diego, California.

            Article
            arh-30-1-22
            3860439
            17718397
            927aaa57-b1bd-4392-9a6f-d74dc577c957
            Copyright @ 2007

            Unless otherwise noted in the text, all material appearing in this journal is in the public domain and may be reproduced without permission. Citation of the source is appreciated.

            History
            Categories
            Focus on Special Populations

            alcohol dependence,ethanol metabolism,ethanol-to-acetaldehyde metabolism,alcohol dehydrogenase (adh),aldehyde dehydrogenase (aldh),acetaldehyde,aldh2,adh1b,adh1c,risk factors,protective factors,genetic factors,ethnic groups,asians,chinese,filipino,indian,japanese,korean,malaysian,thai

            Comments

            Comment on this article