This study was supported in part by National Health Research Institute Grant NHRI-EX91-8939SP (RBL), Tri-Service General Hospital Grant TSGH-C92-46 (RBL), National Science Council Grant NSC 90-2314-B-016-081 (RBL), NSC90-2314-B-409-001 (JFL) and NSC87-2418-H-006-008-Q11 (HCK), and by the Department of Health Grant DOH 88-TD-1107 (HCK). Aspects of this work were presented at the XXIII CINP Congress held June 23-27, 2002 in Montreal, Canada.
No Alcoholism-Protection Effects of ADH1B*2 Allele in Antisocial Alcoholics among Han Chinese in Taiwan
Article first published online: 3 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 29, Issue 12, pages 2101–2107, December 2005
How to Cite
Lu, R.-B., Ko, H.-C., Lee, J.-F., Lin, W.-W., Huang, S.-Y., Wang, T.-J., Wu, Y.-S., Lu, T.-E. and Chou, Y.-H. (2005), No Alcoholism-Protection Effects of ADH1B*2 Allele in Antisocial Alcoholics among Han Chinese in Taiwan. Alcoholism: Clinical and Experimental Research, 29: 2101–2107. doi: 10.1097/01.alc.0000191765.49737.55
Reprint requests: Ru-Band Lu, MD, Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, No. 1, University Road, 701, Tainan, Taiwan, R.O.C.; Fax: +886-6-302-8012; E-mail:
- Issue published online: 3 MAY 2006
- Article first published online: 3 MAY 2006
- Received for publication April 15, 2005; accepted September 1, 2005.
- Antisocial Personality Disorder
Abstract: Background: Thomasson et al., (1991) suggested that the genetic variation at ADH1B and ALDH2 influences the risk of alcoholism. The ADH1B*2 and ALDH2*2 alleles had been thought to be protective against alcoholism. Recent studies have suggested that either physiological tolerance of blood acetaldehyde, or innate insensitivity to it, or both may play a crucial role in keeping alcoholism from developing by protecting against adverse reactions. ALDH inactive form resulting from ALDH2*2, which slows the elimination of acetaldehyde and the more active isozymes produced by ADH1B*2, could generate higher acetaldehyde levels and thus deter heavy drinking (Thomasson et al., 1991). The genotype frequency of ADH1B*2/*2 and ALDH2*(1/*2 or 2/*2), which are regarded protective against drinking behavior, is about 70% and 50%, respectively, among the Han Chinese population in Taiwan (Chen et al., 1999a). Most previous studies, however, have failed to separate the effects of antisocial personality disorder from those of alcoholism because of their high comorbidity. To understand the relationship among alcoholism, antisocial personality disorder, and the protective effects of ADH and ALDH, it is necessary to recruit individuals with antisocial personality disorder but without alcoholism. This study was designed to stratify subjects by various ADH1B and ALDH2 genotypes for a more effective association study. The strata were: antisocial alcoholics, antisocial non-alcoholics, community alcoholics, and normal controls.
Methods: We recruited 579 Han Chinese individuals in Taiwan, intending to examine the alcoholism-protection effects of different ADH1B and ALDH2 genotypes with or without antisocial personality disorder.
Results: We found no difference of ADH1B*2 allele frequency between the subjects of antisocial alcoholism and subjects of antisocial non-alcoholism, but we found significant difference of ALDH2*2 allele between these two groups.
Conclusions: We concluded that there is no alcoholism-protection effect of ADH1B*2 allele in antisocial alcoholics among Han Chinese in Taiwan.