Self‐Reported Alcohol‐Associated Symptoms and Drinking Behavior in Three ALDH2 Genotypes Among Japanese University Students

Abstract

We for the first time demonstrated clear associations between the ALDH2 genotype, self-reported alcohol-associated symptoms, and alcohol drinking behavior among Japanese university students.

ALDH2*2 and peer drinking in East Asian college students

“…Because ALDH2 *2/*2 carriers are more sensitive to alcohol (31,32), differences between ALDH2 *2/*2 and ALDH2 *1/*2 were also evaluated. The two genotypes were similar ( p > .05) on all study variables, including alcohol consumption, t ( 97 ) = − 1.04, p = .300, and number of friends who got drunk, χ 2 (4, 100) = 1.81, p = .771. …”

“…Subjects who carried the ALDH2 *2(+) allele drank less alcohol, t (281.28) = − 3.94, p < .001, than those who carried the ALDH2 *2(−) genotype. There was no relationship between ALDH2 *2 status and peer drunkenness, χ 2 (4, 313) = 6.65, p = .155. About 44% of subjects reported that most or all of their friends got drunk.…”

“…One hundred and ten subjects who did not meet criteria for lifetime drinking were excluded, recognizing that alcohol exposure is required to assess genetic risk or protection for alcohol use. Excluded and included subjects were not significantly different based on ALDH2 *2 status, χ 2 (1,428) = .172, p = .678, age, t (426) = −.406, p = .685, or gender, χ 2 (1, 428) = .239, p = .625, but excluded students did have fewer friends who got drunk χ 2 (4, 420) = 69.80, p < .001. For example, 42.1% of those excluded from the study reported none of their friends got drunk compared to 10.9% of lifetime drinkers.…”

“…This is due in part to an allele (i.e., ALDH2 *2 or A-allele at rs671) more commonly carried by northeast Asians (30–50%) and rare in non-Asians (3). The ALDH2 *2 allele is linked to alcohol-related flushing, an adverse reaction to the metabolism of alcohol that includes reddening of the face, headaches, nausea, drowsiness, and abnormal heart beats (4,5). Alcohol-related flushing occurs when a deficient enzyme, for metabolizing acetaldehyde, the primary metabolite of alcohol, to acetate, results in a buildup of acetaldehyde in the body (6).…”

The role of ALDH2 and ADH1B polymorphism in alcohol consumption and stroke in Han Chinese

“…To date, the ALDH2*2 variant allele has been shown to be the strongest genetic modifier of drinking behaviour and risk of alcoholism [28,37,38]. Previous genotype-phenotype correlation studies have demonstrated that non-alcoholic Asian individuals carrying the ALDH2*2 variant allele, regardless of their ADH1B genotype, responded to low-to-moderate doses of alcohol with markedly increased acetaldehyde levels, pronounced cardiovascular haemodynamic effects and unpleasant subjective feelings [25,39-41]. These adverse reactions to acetaldehyde may considerably reduce the frequency and quantity of alcohol consumption,[41,42] thereby providing protection against excessive drinking and the development of alcoholism [39,43].…”