Abstract
To learn the effects of alcohol and of the aldehyde dehydrogenase 2 (ALDH 2) genotype on diabetic neuropathy, 119 drinkers among 143 male NIDDM patients were studied. Subjects with different ALDH 2 genotypes were examined for a correlation of nerve conduction velocity (NCV) with clinical parameters. The results showed that 72 had an active ALDH 2 and 47 had an inactive ALDH 2 genotype. A positive correlation of NCV with current alcohol consumption was seen in the active ALDH 2 group (p <0.05). A negative correlation of NCV with past alcohol consumption was found in the inactive ALDH 2 group (p <0.01). These findings suggest a different association of the alcohol effect with neuropathy in the different ALDH 2 genotype groups. We speculate that, because alcohol intake in the absence of ALDH 2 activity facilitates acetaldehyde accumulation, acetaldehyde toxicity may precipitate peripheral neuropathy in the inactive ALDH 2 group. The positive correlation of current alcohol consumption with NCV in the active ALDH 2 group suggests that patients with less neuropathy in that group tend to drink more alcohol. We speculate that, in the artive ALDH 2 group, alcohol neither facilitates acetaldehyde accumulation nor injures nerves. Conversely, the vasodilative effect of alcohol may prevent progression of neuropathy. In conclusion, this is the first indication of a role of the ALDH 2 genotype in diabetic neuropathy. This gives new insight into the etiology of diabetic neuropathy.
