Analyses of AREDS2 data on natural history of GA provide representative data on GA evolution and enlargement. GA enlargement, which was influenced by lesion features, was relentless, resulting in rapid central vision loss. The genetic variants associated with faster enlargement were partially distinct from those associated with risk of incident GA. These findings are relevant to further investigations of GA pathogenesis and clinical trial planning.

We have described a benign syndrome of isolated PSH in crowded and tilted optic discs in myopic eyes of white women. The PSHs do not cause visual symptoms and resolve spontaneously. We propose that an interplay of ocular motor forces, scleral thinning, and vitreopapillary traction acting on a morphologically vulnerable optic disc explains these hemorrhages.

This study replicates the results of previous natural history studies of eyes with DPED including the high rates of progression to late AMD and vision loss (regardless of progression to late AMD). The genetic associations are consistent with genes associated with AMD progression.

IMPORTANCEAfter the Age-Related Eye Disease Study 2 (AREDS2) study, the beta carotene component was replaced by lutein/zeaxanthin for the development of the revised AREDS supplement. However, it is unknown if the increased risk of lung cancer observed in those assigned beta carotene persists beyond the conclusion of the AREDS2 trial and if there is a benefit of adding lutein/zeaxanthin to the original AREDS supplement that can be observed with long-term follow-up.OBJECTIVE To assess 10-year risk of developing lung cancer and late age-related macular degeneration (AMD).