Genetic susceptibility, dietary antioxidants combine to reduce AMD risk

By Lucy Piper, Senior medwireNews Reporter

Dietary intake of antioxidants is associated with a reduced risk of developing early age-related macular degeneration (AMD) in people at high genetic risk of the condition, pooled analysis of two studies suggests.

“The interplay between nature and nurture may provide a better understanding of why some, but not all, persons with AMD-related genetic risk variants develop this condition”, comment researchers Jie Jin Wang (University of Sydney, New South Wales, Australia) and colleagues.

They investigated the possible interplay between genetic susceptibility and the intake of dietary antioxidants on the risk of developing AMD in 1854 participants from the Blue Mountains Eye Study (BMES) and 2778 from the Rotterdam Study (RS), who were followed up for 15 years.

Of the BMES participants, 723 did not develop AMD, 467 had incident early AMD and 88 had incident late AMD. The corresponding numbers for the RS participants were 2006, 657 and 115, respectively.

Pooled data analyses showed that individuals at high genetic risk of AMD, due to having at least two risk alleles of either or both of the CFH-rs1061170 and ARMS2-rs10490924 variants, had a significant 22% reduced risk of early AMD and a 25% reduced risk of any AMD if they consumed high levels of lutein/zeaxanthin (third tertile versus first and second).

This pattern was relatively consistent across both studies when assessed individually, the researchers note in Ophthalmology. By contrast, individual findings from the BMES and RS were less consistent for the modification effects of weekly fish consumption and high dietary vitamin C intake.

Pooled analysis showed that weekly fish consumption versus less than one serving a week was associated with a significant 46% reduction in the risk of late AMD among people at high genetic risk of the condition and a high vitamin C intake was associated with a nonsignificant 33% reduced risk of late AMD.

However, these two effects were largely driven by findings from the BMES, Wang and co-workers point out.

For individuals not genetically at risk of AMD, there was no association between antioxidant intake and the likelihood of developing the condition.

The researchers suggest that high intakes of antioxidants may counteract activation and amplification of the complement pathway, which is thought to play a role in the development of AMD.

They conclude: “The relatively consistent pattern of the effect modifications between [lutein/zeaxanthin] intake and AMD-related genetic risk levels in our 2 cohorts may have clinical implications in the management of patients with AMD.”

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