Purpose. To review the proposed pathogenic mechanisms of age macular degeneration (AMD), as well as the role of antioxidants (AOX) and omega-3 fatty acids (ω-3) supplements in AMD prevention. Materials and Methods. Current knowledge on the cellular/molecular mechanisms of AMD and the epidemiologic/experimental studies on the effects of AOX and ω-3 were addressed all together with the scientific evidence and the personal opinion of professionals involved in the Retina Group of the OFTARED (Spain). Results. High dietary intakes of ω-3 and macular pigments lutein/zeaxanthin are associated with lower risk of prevalence and incidence in AMD. The Age-Related Eye Disease study (AREDS) showed a beneficial effect of high doses of vitamins C, E, beta-carotene, and zinc/copper in reducing the rate of progression to advanced AMD in patients with intermediate AMD or with one-sided late AMD. The AREDS-2 study has shown that lutein and zeaxanthin may substitute beta-carotene because of its potential relationship with increased lung cancer incidence. Conclusion. Research has proved that elder people with poor diets, especially with low AOX and ω-3 micronutrients intake and subsequently having low plasmatic levels, are more prone to developing AMD. Micronutrient supplementation enhances antioxidant defense and healthy eyes and might prevent/retard/modify AMD. 1. Introduction Age-related macular degeneration (AMD) is the most common cause of blindness in the Western world. AMD has a chronic progressive course and may require lifelong observation and therapy, becoming a socioeconomic problem as the proportion of the aged population is continuously increasing [1]. The evidence of extensive decline in quality of life and increased need of daily living assistance after long follow-up of patients with AMD substantiates the need to prevent vision loss and progression to blindness. Important advances in the understanding of AMD pathogenesis have been focused on the role of oxidative damage into the retina [2]. It is clearly established that reactive oxygen species (ROS) and oxidized lipoproteins are pivotal sources of cell and tissue stress constructing adequate background for parainflammation in the aging retina. This chronic situation contributes to the development and/or progression of AMD [3]. Angiogenesis and its downstream effects are important milestones in AMD [4, 5]. Furthermore, increasing evidence supports the fact that OS and apoptosis are closely linked processes and that both are implicated in the pathophysiologic mechanisms of AMD [2, 4, 5]. All these were
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