The Atayal with alcohol use disorders also had a lower frequency of ALDH2*2 than the controls; this allele is known to be responsible for the alcohol-flush reaction among Asians, and thereby deters drinking.
Among the Atayal, the group with alcohol use disorders (alcohol dependence and alcohol abuse) had a significantly lower frequency of the ADH2*2 allele (0.82) than those without alcohol use disorders (0.91).
Our data do not support the hypothesis that the A1 allele of the TaqI A polymorphism of the DRD2 gene increases susceptibility to alcohol-use disorders in the Atayals of Taiwan.
On a group level, the rare frequencies of ALDH2*2, the inactive allele of ALDH2, among these aborigines may account partially for their vulnerability to alcohol use disorders.
The role of cholecystokinin (CCK), CCK-A or CCK-B receptor antagonists in the spontaneous preference for drugs of abuse (alcohol or cocaine) in naive rats.
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).
ADH2*2, however, was not related to alcohol use disorders, alcohol-induced flushing and associated symptoms, number of binge drinking episodes in the past 90 days, maximum number of drinks ever consumed, or self-reported levels of response to alcohol.
Because family history of alcoholism is one of the best predictors of the development of alcohol use disorders, this pilot study suggests that, in this sample of African American young adults, the ADH2*3 allele may be associated with a lowered risk for the development of alcoholism.
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.
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.
However, multivariate analyses under a hierarchically well-formulated model strategy with interaction and confounding assessment indicated that (i) heavy alcohol intake was a significant risk factor (odds ratio per 1.0 g of daily ethanol intake; 1.096, 95% confidence interval; 1.026-1.171) for developing AUD after adjusting for other confounders; and (ii) ADH2*1/1 genotype and ALDH2*1/1 genotype were not risk factors after adjusting for daily ethanol intake and other confounders.
However, multivariate analyses under a hierarchically well-formulated model strategy with interaction and confounding assessment indicated that (i) heavy alcohol intake was a significant risk factor (odds ratio per 1.0 g of daily ethanol intake; 1.096, 95% confidence interval; 1.026-1.171) for developing AUD after adjusting for other confounders; and (ii) ADH2*1/1 genotype and ALDH2*1/1 genotype were not risk factors after adjusting for daily ethanol intake and other confounders.
These findings are consistent with the hypothesis that enhanced sensitivity to alcohol and lower levels of alcohol use reflect the mechanism by which ADH1B*2 protects against developing an AUD.
Associations of alcohol dehydrogenase (ADH) gene polymorphisms (ADH1B*2 and ADH1C*1) with a lifetime alcohol use disorder (AUD) were examined in White college students.
Associations of alcohol dehydrogenase (ADH) gene polymorphisms (ADH1B*2 and ADH1C*1) with a lifetime alcohol use disorder (AUD) were examined in White college students.