Aldehyde dehydrogenase genotypes In Japanese alcoholics

Higuchi, Susumu; Matsushita, Satoru; Imazeki, Hiromi; Kinoshita, Tadao; Takagi, Satoshi; Kōno, Hiroshi

doi:10.1016/s0140-6736(94)91629-2

Cited by 233 publications

(178 citation statements)

References 3 publications

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“…A case-control study in a Thai population, where only 18% of the controls have inactive ALDH2, also showed a marginally significant modest positive association (38). The inhibitory effect of inactive heterozygous ALDH2 on alcohol drinking is influenced by sociocultural factors; thus, only 3% of Japanese alcoholics had the inactive heterozygous ALDH2 in 1979 as opposed to 8% in 1986 and 13% in 1992 (39).…”

Section: Discussionmentioning

confidence: 97%

Health Risk Appraisal Models for Mass Screening of Esophageal Cancer in Japanese Men

Yokoyama

Kumagai³

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Because early squamous cell carcinoma (SCC) of the esophagus is detectable by endoscopic esophageal iodine staining with high accuracy and is easily treated by endoscopic mucosectomy, it is important to develop efficient methods for screening candidates for the endoscopic examination. Inactive aldehyde dehydrogenase-2 (ALDH2) is a very strong risk factor for esophageal SCC in alcohol drinkers and thus may be suitable as a screening tool. Purpose: To assess the performance of health risk appraisal (HRA) models in screening for esophageal SCC in the Japanese male population. Methods: Two types of HRA models were developed based on our previous case-control study, which included assessment of ALDH2 activity and selected risk factors (HRA-G and HRA-F: activities of ALDH2 assessed by genotype and questionnaire for alcohol flushing, respectively). Each individual's risk of

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Section: Discussionmentioning

confidence: 97%

Health Risk Appraisal Models for Mass Screening of Esophageal Cancer in Japanese Men

Yokoyama

Kumagai³

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…There is one exception: the "flushing syndrome" variants at the aldehyde (ALDH) and alcohol (ADH) dehydrogenase loci in Asian individuals do provide genes of major effect in this population. Individuals with these gene variants are at much lower risk for becoming dependent on alcohol than individuals with other genotypes [13] in Chinese [14,15], Korean [16], Japanese [17][18][19][20][21][22] and other populations [23,24]. Homozygous ALDH2*2 individuals are strongly protected from alcohol dependence [17,18].…”

Section: Complex Genetic Influences On Human Addiction Vulnerabilimentioning

confidence: 99%

“…Individuals with these gene variants are at much lower risk for becoming dependent on alcohol than individuals with other genotypes [13] in Chinese [14,15], Korean [16], Japanese [17][18][19][20][21][22] and other populations [23,24]. Homozygous ALDH2*2 individuals are strongly protected from alcohol dependence [17,18].Linkage-based analyses for addiction vulnerabilities would be expected to reproducibly identify any gene whose variants exerted a major influence on human addiction vulnerability (see below). Linkage-based genome scans ask how markers and genes move together through families.…”

mentioning

confidence: 99%

“Higher order” addiction molecular genetics: Convergent data from genome-wide association in humans and mice

Uhl

Drgon

Johnson

et al. 2008

Biochemical Pharmacology

127

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Family, adoption and twin data each support substantial heritability for addictions. Most of this heritable influence is not substance-specific. The overlapping genetic vulnerability for developing dependence on a variety of addictive substances suggests large roles for "higher order" pharamacogenomics in addiction molecular genetics. We and others have now completed genomewide association (GWA) studies of DNAs from individuals with dependence on a variety of addictive substances vs appropriate controls. Recently reported replicated GWA observations identify a number of genes based on comparisons between controls and European-American and African-American polysubstance abusers. Here we review the convergence between these results and data that compares control samples and a) alcohol dependent European Americans, b) methamphetamine dependent Asians and c) nicotine dependent samples from European backgrounds. We also compare these human data to quantitative trait locus (QTL) results from studies of addiction-related phenotypes in mice that focus on alcohol, methamphetamine and barbiturates. These comparisons support a genetic architecture built from largely-polygenic contributions of common allelic variants to dependence on a variety of legal and illegal substances. Many of the gene variants identified in this way are likely to alter specification and maintenance of neuronal connections. KeywordsAssociation genome scanning; substance dependence; microarray; pooled; neuronal connections * To whom correspondence should be addressed at: Molecular Neurobiology, Box 5180, Baltimore, MD 21224 phone: (410) 550-2843 x 146, fax: (410) 550-1535, guhl@intra.nida.nih.gov. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access A. Studies of human addiction vulnerabilitiesVulnerability to addictions is a complex trait with strong genetic influences that are largely shared by abusers of different legal and illegal addictive substances [1][2][3][4]. This conclusion comes from family, adoption and twin studies. Family studies clearly document that first degree relative (eg sibs) of addicts display greater risk for developing substance dependence than more distant relatives [1,5]. Adoption studies consistently find greater similarities between substance abuse phenotypes with biological relatives than with adoptive family members [1]. In twin studies, differences in concordance between genetically identical and fraternal twins also support heritability for vulnerability to addictions [3,[6][7][8][9][10][11][12]. Twin data allows quantitation of the amount, about 50%, of ad...

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“…Alcoholism in Japanese (or other Asians) has provided a notable exception, where a major genetic effect of the ALDH2 locus is observed. In a comparison of Japanese alcoholic patient series accumulated at three different time points, Higuchi et al, (1994) have documented an apparent genotype x environment interaction effect, with the protective effect associated with the heterozygous genotype becoming less pronounced in more recent patient series, a diminished protective effect that is attributed by the authors to increased social pressures for drinking after work experienced by Japanese males. (Unusually, for a psychiatric disorder, the low-risk homozygous genotype is almost completely protective, with very few alcoholics with that genotype identified in the world's literature: e.g.…”

Section: Gxe Interaction With Measured Genotypesmentioning

confidence: 95%

Gene–Environment Interaction Effects on Behavioral Variation and Risk of Complex Disorders: The Example of Alcoholism and Other Psychiatric Disorders

Heath¹,

Todorov

Nelson

et al. 2002

Twin res.

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There have been few replicated examples of genotype x environment interaction effects on behavioral variation or risk of psychiatric disorder. We review some of the factors that have made detection of genotype x environment interaction effects difficult, and show how genotype x shared environment interaction (GxSE) effects are commonly confounded with genetic parameters in data from twin pairs reared together. Historic data on twin pairs reared apart can in principle be used to estimate such GxSE effects, but have rarely been used for this purpose. We illustrate this using previously published data from the Swedish Adoption Twin Study of Aging (SATSA), which suggest that GxSE effects could account for as much as 25% of the total variance in risk of becoming a regular smoker. Since few separated twin pairs will be available for study in the future, we also consider methods for modifying variance components linkage analysis to allow for environmental interactions with linked loci.

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Aldehyde dehydrogenase genotypes In Japanese alcoholics

Cited by 233 publications

References 3 publications

Health Risk Appraisal Models for Mass Screening of Esophageal Cancer in Japanese Men

Health Risk Appraisal Models for Mass Screening of Esophageal Cancer in Japanese Men

“Higher order” addiction molecular genetics: Convergent data from genome-wide association in humans and mice

Gene–Environment Interaction Effects on Behavioral Variation and Risk of Complex Disorders: The Example of Alcoholism and Other Psychiatric Disorders

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