Study Explores Impact of Antioxidants, Genetics on Age-Related Macular Degeneration

JANUARY 11, 2017
Ellen Kurek
A team of Polish investigators recently shed light on the interplay between antioxidant capacity and genes in the development of age-related macular degeneration (AMD) in a study that verified the importance of ensuring adequate antioxidant capacity to prevent AMD. The study also identified a subset of patients who may benefit especially from antioxidant supplementation because a genetic polymorphism reduces their retina’s ability to scavenge free radicals and thereby increases their risk of AMD.

Patients and practitioners alike have been turning toward antioxidant nutrients to prevent or forestall the progression of AMD since publication of the results of the Age-Related Eye Disease Study (AREDS) in 2001. Since then, AREDS 2 has established that the phytonutrients lutein and zeaxanthin, vitamins C and E, and the minerals copper and zinc can reduce the rate of progression of advanced AMD. Moreover, 10-year follow-up of patients assigned to receive the original AREDS formulation, which used beta carotene instead of phytonutrients, found that the reduction in the odds of developing advanced AMD was statistically significant for those with wet AMD but not for those with dry AMD.

The new study provides further evidence of the importance of sufficient antioxidant capacity in the prevention of AMD. To investigate antioxidative markers in the pathogenesis of AMD, the team studied 510 subjects, including 240 AMD patients and 270 controls. They measured the activity of the antioxidant enzymes superoxide dismutase (SOD), catalase, and glutathione peroxidase and examined their association with single nucleotide polymorphisms (SNPs) of the respective genes for these enzymes.

They used the restriction fragment length polymorphism technique to determine which genetic polymorphisms to select. They then chose 60 subjects (30 AMD patients and 30 controls) in whom to determine the activity of their antioxidant enzymes by using a spectrometric method.

This method showed a statistically significant decrease in all three antioxidant enzymes evaluated in AMD patients versus controls. Moreover, it indicated that the risk of AMD was statistically significantly greater in those with the Pro197Leu C/T genotype of the glutathione peroxidase gene than it was in those without this genotype (odds ratio (OR) = 2.78; 95% confidence interval (CI), 1.78–4.25). In contrast, it indicated that the A/C genotype and the C allele frequencies of the A/C polymorphism of the SOD1 gene reduced the risk of AMD to a statistically significant degree (OR = 0.48; CI, 0.27–0.85).

“Our data showed that insufficient antioxidant capacity may have an important role in age-related macular degeneration,” the Polish team concluded.

A report on the study, “Analysis of antioxidative factors related to AMD risk development in the polish patients,” was published online on December 9, 2016, in Acta Ophthalmologica.

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