Modifiable Risk Factors for Age-related Macular Degeneration (AMD): Population-based Study Findings

Jie Jin Wang
Centre for Vision Research, Department of Ophthalmology, University of Sydney, Sydney, Australia

Purpose: Age-related macular degeneration (AMD) is now the leading cause of irreversible blindness and moderate visual impairment among older persons in many countries. Recent research on AMD risk factors has led to the identification of a few AMD-related gene loci and a few modifiable risk and protective factors. These provide insights into future research directions to reveal the aetiology of AMD. This presentation will summarise findings on a number of consistently documented, potentially modifiable, AMD risk factors and will draw mainly from recent population-based studies.

Methods: Literature search for population-based study reports on AMD risk factors. 
Results: To date, smoking is the most consistently found, modifiable AMD risk factor, across many different populations and ethnic groups. Longitudinal observations from general older populations have consistently documented a 2-3 fold increased risk of developing AMD associated with current smoking. Current smokers have also been shown to develop late AMD at an earlier age (by 5-10 years) than non-smokers. Among past smokers who had stopped smoking for nearly two decades, the excess risk of AMD appears to reduce to an insignificant level.
Higher dietary intake of omega-3 fatty acids, or frequent and regular consumption of fish, has been associated with a reduced risk of AMD in a number of studies.

The Rotterdam Study found that global diet quality that includes higher dietary intakes of zinc and antioxidants (beta carotene and vitamins C and E) provided a 35% reduced AMD incidence over 8 years. Direct evidence showing that high antioxidant nutrient intakes reduce AMD progression comes from a large randomised clinical trial, the Age Related Eye Disease Study (AREDS). In this study, use of high-dose zinc and antioxidant supplements led to a 25% reduction in progression to late AMD among persons with moderate to relatively advanced early AMD signs.
A recent report using pooled cross-sectional data from three population-based studies in the USA supported an association between cataract surgery that was performed before baseline examinations and an increased prevalence of late AMD. This link was stronger among persons who had cataract surgery performed at least 5 years earlier. Longitudinal data (over 5 and 10-year periods) from both the Beaver Dam and Blue Mountains Eye Studies have consistently indicated a link between cataract surgery and the subsequent incidence of AMD. The increased risk of AMD, particularly neovascular AMD, was around 3-4 fold higher in pseudophakic than in phakic eyes.
Finally, manifestations of chronic inflammatory processes (e.g. elevated levels of C-reactive protein, fibrinogen, white cell count and other factors) may also portend a higher risk of AMD progression that may be both potentially modifiable and subject to gene-environment interaction (via CFH gene variants). This mechanism could account, in part, for the link with cataract surgery.  

Conclusions: Based on current evidence, including animal data, smoking is likely to have a causal role (as trigger or promoter) in the development of both neovascular and atrophic late AMD. The ocular hazards from smoking deserve attention from health policy makers, public health and medical professionals. Regular intakes of fish and foods with high levels of zinc and antioxidant micro-nutrients are likely to benefit older persons at high risk of AMD. Interactions between genetic susceptibility and environmental triggers/ promoters are likely to provide keys that could increase our understanding of the pathogenesis of AMD. For persons at high risk of AMD, the timing of cataract surgery also needs to be investigated further, if the reported link with AMD is confirmed in future studies.

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