BOSTON -- (January 2, 2003) - Researchers have established for the first time that the dietary supplement zeaxanthin plays an essential role in protecting the retina of the eye from the damaging effects of light.
Working with quail as an animal model, research performed at Schepens Eye Research Institute and the Harvard Medical School Department of Ophthalmology and sponsored in part by Dennis Gierhart, Ph.D., founder and CEO of ZeaVision, L.L.C. (www.zeavision.com), provided the first direct experimental evidence that zeaxanthin and lutein, the only two carotenoids selectively accumulated by the human retina, play a protective role.
"Our studies demonstrated that light damage is strongly influenced by the amount of zeaxanthin in the retina, and that significantly greater retinal protection is provided at dietary levels higher than those normally occurring in the diet," said C. Kathleen Dorey, principal investigator formerly with Schepens and now with R&D Consulting. "Zeaxanthin is well suited to its role in maintaining retinal health, and may be an important strategy to prevent or intervene in macular degeneration. It preferentially accumulates in the macula where it absorbs harmful blue wavelength light, and it accumulates in the RPE and the most vulnerable portions of the photoreceptors where its potent anti-oxidant capacity can prevent oxidative damage, a problem that increases with aging."
Macular pigment has been implicated as a risk factor in age-related macular degeneration (AMD). Vision loss with AMD is due to the irreversible death of photoreceptors and/or the invasion of leaky, unwanted blood vessels into the retina. Some clinical studies have found evidence that people with higher dietary or serum levels of zeaxanthin and lutein had reduced risk for advanced stages of age-related macular degeneration.
Significantly lower macular pigment levels have been found in people with factors known to increase risk for AMD, in eyes with AMD, and in eyes at high risk for AMD. Epidemiologic studies have shown that people with higher dietary or plasma lutein/zeaxanthin have reduced risk for advanced stages of AMD. It is not yet clear whether the reduced risk for AMD is due to lutein/zeaxanthin or due to some other nutrient in the plants containing carotenoids. The Schepens work clearly shows that the carotenoids protect the retina from light damage in animals. Some studies have identified light damage as a risk factor in AMD.
To test their hypothesis, Dr. Dorey and her colleagues selected Japanese quail -- the retinas of which closely resembles the human macula in having more cone photoreceptors than rods and in the highly selective accumulation of zeaxanthin and lutein from their diet -- to examine the effect of manipulating dietary carotenoids on light damage to retinas. The quail were raised on diets that were normal, carotenoid-deficient, or carotenoid-deficient supplemented with high doses of zeaxanthin.
In the short-term study, reported in the November 2002 issue of Investigative Ophthalmology and Visual Science (IOVS), the team divided the carotenoid-deficient quail into two groups, and for one week preceding light damage, they fed one group zeaxanthin-supplemented diet. The study established that photoprotection was strongly correlated with the concentration of zeaxanthin in the retinas of the quail. Retinas with low concentrations of zeaxanthin had suffered severe light damage, as evidenced by a very high number of apoptotic photoreceptor cells, while the group with high zeaxanthin concentrations had minimal damage. Apoptosis is programmed cell death, the final common pathway for photoreceptor death in retinal degeneration.
In the long-term study, reported in the November 2002 issue of Experimental Eye Research, groups of quail were raised for six months on carotenoid-deficient, normal or zeaxanthin-supplemented diets before exposure to brighter light. The results showed extensive damage to the retina in the carotenoid-deficient animals, as evidenced by large numbers of both dying photoreceptors and gaps or "ghosts" marking sites where photoreceptors had died. The group of quail with normal dietary levels of zeaxanthin showed significantly less retinal damage than did the zeaxanthin-deprived group, while the quail group receiving high levels of zeaxanthin had few ghosts in their retinas.
These experiments showed protection of both rod and cone photoreceptors. The research further demonstrated that retinas were protected by both zeaxanthin and another antioxidant, vitamin E. Damage in these experiments was clearly reduced by zeaxanthin and tocopherol, but not lutein. Further experiments would be needed to determine whether elevated lutein would offer protection.
Dorey concluded: "Zeaxanthin has been extensively studied for safety and has been reviewed as a dietary ingredient by the FDA. We hope this work further stimulates interest in clinical trials, and believe that zeaxanthin has a potential to eventually complement other strategies to improve the treatment of this vision-robbing disease."
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The research team included:
** Lauren R. Thomson, M.D. Yoko Toyoda, M.D. Z-Y Wong, M.D., Francois C. Delori, Ph.D., and C. Kathleen Dorey, Ph.D. (now with R&D Consulting) at Schepens Eye Research Institute.
** Kevin M. Garnett, BS, MBA at Applied Food Biotechnology, Inc. (O'Fallon,
** Kimberly M. Cheng, Ph.D. and Cathleen R. Nichols at Department of Animal Sciences, University of British Columbia (Vancouver)
** Neal E. Craft, Craft Technologies, Inc. (Wilson, N.C.)