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Abstract A case–control study on the relationship between alcohol dehydrogenase-2 (ADH2), aldehyde dehydrogenase-2 (ALDH2) and male probable alcohol use disorders (AUD) was performed in Khon Kaen, north-east Thailand. One hundred and fifty-three paired cases (probable AUD) and controls (non-probable AUD) were sampled from villagers aged 18–65 years using the modified Michigan Alcoholism Screening Test - Thai version, controls being matched for gender, age (± 4 years) and village. All of the cases and 86.9% of the controls were current drinkers. The percentage of ADH2*1/1 among cases was 47.1%, being significantly larger than the 29.4% among controls, and yielding a univariate odds ratio (OR) of 2.421* (95% confidence interval (CI) = 1.419–4.132) for developing probable AUD. The ALDH2*1/1 proportion among cases, 92.8%, was comparable to the 92.2% among controls, yielding a univariate OR of 1.100 (95%CI = 0.757–1.599). Multivariate analysis based on a conditional logistic regression model and a hierarchically well-formulated model strategy revealed that: (i) the OR of developing probable AUD due to 1 g increment of daily ethanol drinking was 1.110* among farmers (95%CI = 1.054–1.170); (ii) OR due to 1 g increment of daily ethanol drinking was 1.329* among non-farmers (95%CI = 1.109–1.593); (iii) OR due to either ADH2*1/1 or ALDH2*1/1 was insignificant; and (iv) the daily amount of smoking is independently associated with probable AUD. The present findings suggest that one of the genetic factors that may be related to probable AUD among Thai males living in the north-east is the ADH2 gene. [ABSTRACT FROM AUTHOR]

AbstractA genetic epidemiological case-control study on aldehyde dehydrogenase 2 (ALDH2) genotype and male probable alcohol use disorders (AUD) was performed in Khon Kaen province, north-east Thailand. One hundred and twenty-four of cases (probable AUD) were obtained from male villagers aged 18–65 years using the modified Michigan Alcoholism Screening Test-Thai version. The same number of controls were selected, being matched with the cases in terms of age (±4 years) within the same village. Marital status, education history and past or present histories of physical illnesses were essentially the same for the cases and the controls. All of the cases and 85.5% of the controls were current drinkers, and the cases tended to drink significantly more often than the controls. Genomic DNA was extracted from fingernails and ALDH2 genotypes were determined by polymerase chain reaction technique and digested by Ksp 632I. The ALDH2 genotypes of the cases and the controls were not significantly different: 90.3% versus 91.1% normal homozygote; 8.1% versus 8.9% heterozygote; and 1.6% versus 0.0% mutant homozygote, respectively. Among the normal homozygote, the daily amount of alcohol intakes of the cases were significantly larger than that of the controls (56.2 ± 40.6 g vs 8.1 ± 14.1 g), 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 genotype, marital status, education history, or past history of injury, however, occupation and daily amount of alcohol intake were found to be significantly 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 subjects had three times more chance of developing AUD for each increase of 10 g of the daily amount of alcohol intake. [ABSTRACT FROM AUTHOR]