Aldehyde dehydrogenase genotypes and male alcohol use disorders: A case-control study in Khon Kaen, north-east Thailand

Citation
S. Nanakorn et al., Aldehyde dehydrogenase genotypes and male alcohol use disorders: A case-control study in Khon Kaen, north-east Thailand, PSY CLIN N, 53(3), 1999, pp. 397-405
Citations number
41
Categorie Soggetti
Clinical Psycology & Psychiatry
Journal title
PSYCHIATRY AND CLINICAL NEUROSCIENCES
ISSN journal
13231316 → ACNP
Volume
53
Issue
3
Year of publication
1999
Pages
397 - 405
Database
ISI
SICI code
1323-1316(199906)53:3<397:ADGAMA>2.0.ZU;2-1
Abstract
A genetic epidemiological case-control study on aldehyde dehydrogenase 2 (A LDH2) genotype and male probable alcohol use disorders (AUD) was performed in Khon Kaen province, northeast Thailand. One hundred and twenty-four of c ases (probable AUD) were obtained from male villagers aged 18-65 years usin g the modified Michigan Alcoholism Screening Test-Thai version. The same nu mber of controls were selected, being matched with the cases in terms of ag e (+/- 4 years) within the same village. Marital status, education history and past or present histories of physical illnesses were essentially the sa me for the cases and the controls. All of the cases and 85.5% of the contro ls were current drinkers, and the cases tended to drink significantly more often than the controls. Genomic DNA was extracted from fingernails and ALD H2 genotypes were determined by polymerase chain reaction technique and dig ested by Ksp 632I. The ALDH2 genotypes of the cases and the controls were n ot significantly different: 90.3% versus 91.1% normal homozygote; 8.1% vers us 8.9% heterozygote; and 1.6% versus 0.0% mutant homozygote, respectively. Among the normal homozygote, the daily amount of alcohol intakes of the ca ses were significantly larger than that of the controls (56.2 +/- 40.6g vs 8.1 +/- 14.1g), the same was found among the ALDH2 deficient (55.9 +/- 43.4 vs 2.2 +/-5.8 g). Multivariate analysis based on the conditional logistic regression model showed no significant association of AUD with ALDH2 genoty pe, marital status, education history, or past history of injury, however, occupation and daily amount of alcohol intake were found to be significantl y associated with AUD (OR = 10.72, 95% CI = 1.15 - 99.99, P = 0.037, and OR = 1.12, 95% CI = 1.06 - 1.18, P = 0.000, respectively). Non-farmers showed 10.7 times larger risk of developing AUD compared to farmers, and the subj ects had three times more chance of developing AUD for each increase of 10 g of the daily amount of alcohol intake.