Our eyes are our window on the world. Tragically, there are 30 to 50 million cases of blindness worldwide, and a far greater number of people suffering from visual impairment of some kind (Jacques 1999). Two of the leading causes of visual impairment and blindness are age-related macular degeneration and age-related cataracts (Gerster 1991; Jacques 1999). Both diseases appear to be related to light-induced oxidative processes within the eye (Gerster 1989; Snodderly 1995; Christen 1999).

Within the eye, the lens focuses incoming light onto the photosensitive retina, which transmits visual signals to the brain. The lens is made mostly of water and protein; the proteins are normally arranged such that light may pass through unimpeded. Cataracts are areas of the eye's lens that have become cloudy, due to the clumping together of proteins. These cloudy portions may grow over time and reduce the amount of light reaching the retina, resulting in blurred vision, and potentially leading to blindness. Although cataracts may be congenital, or brought on by diabetes, steroid use, or trauma, most are related to aging. Vision loss due to cataract is usually treatable only by surgical removal of the cataract.

The central area of the retina is known as the macula lutea ("yellow spot"). In the middle of the macula lies the fovea, the part of the retina which has the highest density of photoreceptors, hence gives us the highest visual acuity. Although retinal damage can result from injury (such as from staring at the sun), the slow degradation with age of the macular area of the retina, a condition known as age-related macular degeneration or AMD, is a leading cause of blindness (Gerster 1991; Seddon et al. 1994; Snodderly 1995). No treatment is available for most patients (Hampton and Nelsen 1992).

Both cataracts and AMD appear to be linked to the cumulative effects of a lifetime of light-induced oxidation. Both the lens and the retina are exposed continually to light (particularly blue light) and oxygen, which can work together to produce oxygen free radicals. In cataract formation, free radicals appear to impair the lens crystalline proteins, causing them to clump, and also damage proteolytic enzymes that would normally remove the damaged proteins (Gerster 1989). In the retina, with its high levels of oxygen and polyunsaturated fatty acids, peroxidation of membranes likely leads to the death of photoreceptor cells (Gerster 1991). It is therefore not surprising that factors known to be related to oxidation (cigarette smoking, cardiovascular disease, exposure to sunlight, low ocular melanin content) have been shown in epidemiological studies to be related to an elevated risk for AMD (Snodderly 1995; Snow and Seddon 1999).

The human body uses natural defenses against oxidation of these eye tissues, including the antioxidant enzymes glutathione peroxidase, superoxide dismutase, and catalase, as well as the antioxidant vitamins E and C, and the pigment melanin (Gerster 1991). Of particular significance may be the carotenoid pigments lutein and zeaxanthin, which are concentrated in the macula and give it its yellow color (Bone et al. 1985). These pigments are known to absorb blue light and have the potential to quench singlet oxygen (Landrum et al. 1999). Epidemiological studies have shown that a high dietary intake of carotenoids, specifically lutein and zeaxanthin (from spinach, kale, and other leafy green vegetables), is associated with a reduced risk for both nuclear cataracts and AMD (Seddon et al. 1994; Lyle et al. 1999). It has also been shown experimentally that regular consumption of lutein supplements can increase the macular pigment density in the eye, which may potentially reduce the risk for later development of AMD (Landrum et al. 1997). However, little is known about the potential unwanted interactions of carotenoids in the eye when taken in high-dose supplemental form, thus supplementation should be approached with some caution (Snodderly 1995).

Christen, W.G. (1999) Antioxidant vitamins and age-related eye disease. Proc. Assoc. Am. Physicians, 111:16-21.

Gerster, H. (1989) Antioxidant vitamins in cataract prevention. Z. Ernahrungswiss., 28:56-75.

Gerster, H. (1991) Antioxidant protection of the ageing macula. Age Ageing, 20:60-69.

Hampton, G.R., and P.T. Nelsen [eds]. (1992) Age-related Macular Degeneration: Principles and Practice. New York: Raven Press. 300 pp.

Jacques, P.F. (1999) The potential preventive effects of vitamins for cataract and age-related macular degeneration. Int. J. Vitam. Nutr. Res., 69:198-205.

Landrum, J.T., R.A. Bone, H. Joa, M.D. Kilburn, L.L. Moore, and K.E. Sprague. (1997) A one year study of the macular pigment: the effect of 140 days of a lutein supplement. Exp. Eye Res., 65:57-62.

Landrum, J.T., R.A. Bone, L.L. Moore, and C.M. Gomez. (1999) Analysis of zeaxanthin distribution within individual human retinas. Meth. Enzymol., 299:457-467.

Lyle, B.J., J.A. Mares-Perlman, B.E. Klein, R. Klein, and J.L. Greger. (1999) Antioxidant intake and risk of incident age-related nuclear cataracts in the Beaver Dam Eye Study. Am. J. Epidemiol., 149:801-809.

Seddon, J.M., U.A. Ajani, R.D. Sperduto, R. Hiller, N. Blair, T.C. Burton, M.D. Farber, E.S. Gragoudas, J. Haller, D.T. Miller, L.A. Yannuzzi, and W. Willett. (1994) Dietary carotenoids, vitamins A, C, and E, and advanced age-related macular degeneration. J.Am. Med. Assoc., 272:1413-1420.

Snodderly, D.M. (1995) Evidence for protection against age-related macular degeneration by carotenoids and antioxidant vitamins. Am. J. Clin. Nutr., 62(suppl):1448S-1461S.

Snow, K.K., and J.M. Seddon. (1999) Do age-related macular degeneration and cardiovascular disease share common antecedents? Ophthalmic Epidemiol. 6:125-143.