Low-Km aldehyde dehydrogenase deficiency does not influence the elevation of blood pressure by alcohol

Increased alcohol consumption causes hypertension and leads to higher death rates by hemorrhagic strokes. About half of the Japanese population have inactive low Km aldehyde dehydrogenase (ALDH2), which metabolizes acetaldehyde to acetic acid at very low concentrations, leading to severe pharmacological effects of aldehyde when drinking alcohol. We determined persons with inactive ALDH2 using a ethanol patch test. All male workers (n + 163), aged from 21 to 62 years in one factory in Japan took part. They were divided into two groups by alcohol consumption (nondrinkers, light drinkers of < 32 ml/l ethanol per day and moderate to heavy drinkers of > or = 32 ml ethanol per day). The prevalence of persons with inactive ALDH2 was 52.1%. The prevalence of moderate to heavy drinkers among persons with inactive ALDH2 was significantly lower than that among those with active ALDH2 (23% and 41%, respectively: P < 0.05). No significant differences of BP were observed between ALDH2 inactive and active groups at the same consumption of alcohol. This study showed a significant relationship between categories of alcohol use and SBP and DBP (P < 0.05, respectively) controlled for age and body mass index. The mechanism by which alcohol use elevates BP is unlikely to be related to the inactive ALDH2. However, inactive ALDH2 may act as a protective factor against hypertension by reducing alcohol consumption.