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The present study investigated the effect of aldehyde dehydrogenase2 ( ALDH2 ) rs671 polymorphism and alcohol consumption on the severity of primary open-angle glaucoma (POAG). The questionnaire for alcohol consumption pattern and targeted genotyping for  ALDH2  rs671 polymorphism was performed from 445 Korean POAG patients. Retinal nerve fiber layer (RNFL) and ganglion cell-inner plexiform layer (GCIPL) thicknesses were measured and compared according to alcohol consumption and  ALDH2  rs671 genotype. Heavy drinking group eyes had thinner RNFL thickness than did abstinence group eyes (65.0 ± 10.9 vs. 70.9 ± 11.5 µm,  P  = 0.023). Both mild (65.8 ± 9.6 µm) and heavy (63.8 ± 8.4 µm) drinking group eyes had significantly thinner macular GCIPL thickness than did abstinence group eyes (68.1 ± 8.2 µm,  P  = 0.003). However,  ALDH2  rs671 polymorphism did not show any significant association with RNFL or GCIPL thickness. Alcohol consumption was significantly associated with GCIPL thinning (β = –0.446,  P  = 0.035) after adjustment for multiple confounding factors. As excessive alcohol consumption was significantly associated with thinner GCIPL thickness while  ALDH2  polymorphism had no significant effect on RNFL or GCIPL thickness, glaucoma patients should avoid excessive alcohol consumption regardless of  ALDH2  polymorphism.

Alcohol consumption is associated with glaucoma severity regardless of ALDH2 polymorphism