Just read this article called "Can you see the Light?" posted by Hveragathi (Truth in Medicine Forum)...

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Can You See the Light?


While James Taylor saw fire and rain and Peter Gabriel saw the red rain coming down, an increasing number of American adults are seeing only a touch of grey. In fact, the American Foundation for the Blind (AFB) estimated more than 25 million American adults have significant vision loss, including individuals who are blind and those who have trouble seeing even when wearing corrective lenses. A report from Prevent Blindness America, “Vision Problems in the U.S.”, further noted 20.5 million Americans older than 40 have cataract, 5.3 million have diabetic retinopathy, 2.2 million have glaucoma and 1.6 million have late-stage age-related macular degeneration (AMD).1

Add to this the fact that more than 90 percent of adults surveyed recently by Transitions Optical said sight is their most important sense and the one they feared losing the most, and it’s easy to see why more attention is focused on preserving vision. However, vision is a fine-tuned, complex process involving the eye, nerves and brain. Light first hits the corneal surface and is focused to pass through the pupil and lens; it travels through the vitreous humor to the retina, a light-sensitive layer covered with photoreceptor cells that absorb the light and turn it into nerve impulses that are fed through the optic nerve into the brain for interpretation. The peripheral retina distinguishes light from dark and permits peripheral vision, while the macula focuses on fine detail and colors.

The retina is an ideal environment for the generation of free radicals since it has high levels of blood (and thus oxygen) supply, high-light exposure and cell membranes rich in polyunsaturated fatty acids. Therefore, environmental factors and simple ultraviolet (UV) radiation lead to oxidative stress, while nutritional imbalance can exacerbate visual impairment.

Two degenerative conditions of the eye have been linked to nutritional factors: AMD and cataract. AMD is among the leading causes of blindness in Western countries, affecting about 20 percent of all people older than 65; it is believed to be the leading cause of irreversible blindness in the elderly in Western populations. AMD is characterized by irreversible progressive degeneration of the macula lutea, the site of the highest visual acuity of the retina. Dry AMD, the more common form, occurs when light-sensitive cells in the macula slowly break down, blurring central vision. Its most common early symptom is the presence of drusen, yellow deposits under the retina. Wet AMD occurs when abnormal blood vessels behind the retina start to grow under the macula, raising the macula from its normal position and causing rapid damage.

Cataract remains the leading cause of blindness in the world. The lens becomes cloudy or opaque due to damage caused by oxidative stress, exposure to UV light and genetics; aging and inflammation are also associated risk factors. The two most common types of age-related cataracts are nuclear (center of the lens) and cortical (in the lens periphery).

Glaucoma is the second leading cause of blindness globally. The term refers to a group of eye diseases that cause vision loss through damage to the optic nerve. The two primary types of glaucoma are open-angle glaucoma (also known as primary open-angle glaucoma—POAG) and angle-closure glaucoma. POAG is the most common form and occurs when the eye’s drainage canals become clogged, increasing intraocular pressure (IOP). While vision loss from glaucoma is irreversible, it can be managed with medication or surgery.

One additional cause of blindness is diabetic retinopathy, whereby the disease damages the blood vessels that nourish the retina, causing the vessels to leak or break. It affects more than 4 million Americans. Macular edema (swelling) in diabetic retinopathy can be treated with laser surgery to slow fluid leakage and reduce the fluid levels in the retina.


As mentioned earlier, the eye is quite susceptible to oxidative damage, which has put antioxidants on the front line of investigation, as researchers try to determine how various nutrients work to quench free radicals and prevent associated degeneration. The highest profile trial in this area has been the Age-Related Eye Disease Study (AREDS), supported by the National Eye Institute (NEI), part of the U.S. National Institutes of Health (NIH); the original results were reported in October 2001.2 The trial involved more than 4,700 older adults across the United States who received one of four daily treatments: zinc (80 mg) alone; antioxidants alone (500 mg of vitamin C, 400 IU of vitamin E, 15 mg of beta-carotene and 2 mg of copper); a combination of antioxidants and zinc; or placebo. The researchers found the intervention slowed disease progression in patients with advanced AMD, but did not appear to have preventive effects in subjects without signs of AMD. NEI researchers suggested patients with intermediate risk of AMD or advanced AMD take an AREDS-type dietary supplement, and added studies suggest increasing dietary intake of macular xanthophylls and omega-3 polyunsaturated fatty acids (PUFAs)—as are being evaluated in AREDS2—may also be beneficial.3 Further, providing AMD patients with an AREDS-type antioxidant formula makes good economic sense, as RTI International researchers using a computerized model reported providing 10 million simulated individuals with the supplement increased quality-adjusted life years and lowered the risk of disease progression.4

This is not to say everyone is convinced of the benefits. In fact, two Cochrane Database Reviewsconclude there is inadequate research that antioxidant supplements can prevent or delay onset of AMD, or slow its progression; instead, they said further clinical trials beyond AREDS are needed to provide evidence of efficacy and show no long-term safety concerns.5,6 Similarly, initial results from the Blue Mountains Eye Study in Australia found no connection between dietary intake of antioxidants and zinc and early AMD.7

One possibility is that there is a genetic connection to AMD development and the supporting role of antioxidants. A study out of Oregon Health & Science University, Portland, found in a cohort of 876 adults at high risk of progression to advanced AMD, those with particular complement factor H (CFH) genotype polymorphisms were more likely to find benefit from AREDS intervention.8 NEI researchers commented assessments of genetic interactions may allow for more targeted interventions in those at moderate risk of advanced AMD.9

Interestingly, the original AREDS results did not find a connection between intake of the antioxidant formula and risk of cataract.10 Researchers have found an inverse association between blood levels of antioxidants (vitamin C, zeaxanthin, lutein, beta-carotene) and incidence of cataract.11 And while the Blue Mountains Eye Study did not find a link between early AMD and antioxidants, they did find a link between antioxidants and cataractogenesis.12 In looking at 10-year incidence of age-related cataract in more than 2,400 adults, participants with the highest intake of vitamin C or combined intake of antioxidants (vitamins C and E, beta-carotene and zinc) had a significantly reduced risk of nuclear cataract. Similarly, researchers from the Nurses Health Study, Harvard Medical School, Boston, found higher dietary intakes of vitamin E and lutein/zeaxanthin from food and dietary supplements were associated with significantly reduced risk of cataract.13


The positive effects of the xanthophylls lutein and zeaxanthin are likely not surprising, given the critical role these carotenoids play in the eye. It was first suggested in 1945 that the yellow color of the macula lutea in the retina is due to the presence of xanthophylls. This has been termed macular pigment and is entirely of dietary origin; humans are not able to synthesize carotenoids, nor has conversion of other carotenoids such as alpha-carotene or beta-carotene to lutein and zeaxanthin been reported. The retinal carotenoids have two distinct effects: blue-light filtering and antioxidant activity. Photoreceptors are very susceptible to short wave length blue light. Lutein and zeaxanthin absorb blue light because of their physical properties, and are located in the retina between the incoming light and the photoreceptors, rather like internal sunglasses. The distribution of lutein and zeaxanthin differs within the macula, with a higher ratio of zeaxanthin to lutein in the central area, according to a review paper from OmniActive Health Technologies. Further, approximately half of the zeaxanthin present in the center of the macula is meso-zeaxanthin, produced enzymatically or photochemically from dietary lutein within retinal tissue.

A review from the University of Manitoba, Winnipeg, noted evidence is accumulating about how increasing consumption of lutein and zeaxanthin positively impacts macular pigment optical density (MPOD), and the potential role this has in preserving vision and supporting retinal function.14 It appears various carotenoids exert their effects in several ways. For example, lutein may not only fight oxidative stress, but also protect against retinal ischemic damage,15 while also preventing neuroinflammation.16Astaxanthin, another carotenoid, also has an inhibitory effect on neuroinflammation, preventing retinal damage in vitro and in vivo.17

The basis of scientific evidence for supplementation with carotenoids, particularly lutein and zeaxanthin, continues to grow. The Lutein Antioxidant Supplementation Trial (LAST), conducted out of the Department of Veterans’ Affairs, Chicago, included 90 patients with atrophic AMD who received 10 mg of purified lutein (as FloraGLO® Lutein, from Kemin Health), purified lutein plus a broad spectrum antioxidant (as OcuPower, from Vitacost.com), or placebo for 12 months.18 Visual parameters, including MPOD, visual acuity and contrast sensitivity were improved in both the lutein and lutein combination groups, suggesting lutein’s key role in treating AMD. Follow-up findings found individuals who did respond to lutein supplementation had continuing increases in MPOD, even at 12 months of supplementation, leading researchers to suggest such an intervention could effectively re-establish the beneficial macular barrier.19 Researchers from the University of Pennsylvania, Philadelphia, reported similar positive findings after they administered lutein for six months to patients with foveal fixation; supplementation significantly increased serum lutein levels in 91 percent of patients and augmented MPOD in almost two-thirds of subjects, although there was no change in central vision.20

Another human study, this one a pilot study conducted in the United Kingdom, examined plasma and macular responses to lutein supplementation.21 The researchers examined the effect of daily supplementation with 20 mg of lutein ester (as XANGOLD®, from Cognis Nutrition & Health), supplying 10 mg/d of free lutein, on seven early AMD sufferers and six age-matched controls over 20 weeks. Supplementation increased plasma lutein and mean MPOD significantly. The researchers noted the findings suggested AMD is not associated with intestinal malabsorption of macular carotenoids, and even a diseased macula can accumulate lutein and/or zeaxanthin; further, they suggested the beneficial effects of lutein supplementation could be extended to subjects with established age-related maculopathy (ARM). And a trial out of the University of Munster, Germany, investigated the impact of a combination supplement (Ocuvite, from Bausch & Lomb) containing 12 mg of lutein ester and 1 mg of zeaxanthin (from Cognis) plus vitamin E, zinc and selenium, for six months in older adults with signs of AMD.22 A majority of subjects taking the supplement had increases in MPOD, including those with AMD; however, a number of “non-responders” showed increases in serum concentrations of lutein and zeaxanthin, but no rise in MPOD, indicating intestinal malabsorption is not responsible for a lack of MPOD.


Studies on zeaxanthin alone have also shown tremendous benefits. Studies using quail retinas have found increased levels of retinal zeaxanthin dose-dependently reduce light-induced photoreceptor apoptosis.23 And like lutein, zeaxanthin may have an impact on apoptosis.24 Researchers from the University of Teramo, Italy, investigated the impact of zeaxanthin on neuroblastoma cells, and found the carotenoid could induce apoptosis in diseased cells without inhibiting activity of lipoxygenase, while preventing apoptosis in healthy cells.

Intervention trials have shown positive results for zeaxanthin. London researchers found zeaxanthin (as OPTISHARP™, from DSM Nutritional Products) improved human color vision, visual acuity and vision in low-light conditions in healthy adults.25 Participants were given regular supplementation of zeaxanthin, lutein, a combination of the two or placebo; participants taking lutein and zeaxanthin showed significant improvements in visual acuity and color vision. In another study, DSM researchers found the xanthophylls increased MPOD, but in different areas of the macula—lutein appears to be predominantly deposited in the fovea, while zeaxanthin covers a wider retinal area.26

As the research has expanded on the role of xanthophylls in eye health, NEI initiated AREDS2, which seeks to elucidate whether adding additional nutrients to the original antioxidant formula could augment the results. Recruitment of 4,000 AMD patients for the study was completed in June 2008; for five years, the patients will receive one of four possible treatments, in addition to the original AREDS formula: 10 mg/d of lutein (as FloraGLO) plus 2 mg/d of zeaxanthin; 1 g/d of omega-3 fatty acids; a combination of lutein, zeaxanthin and omega-3s; or a placebo.

Carotenoid intake may also fight cataract development. Researchers from the Women’s Health Initiative, Harvard, recruited 1,802 older women from the cohort into the Carotenoids in Age-Related Eye Disease Study (CAREDS), and found those with the highest dietary intake of lutein and zeaxanthin had a 23-percent lower prevalence of nuclear cataract.27 Similar findings were reported by researchers at the University of Melbourne, Australia, who found adults with the highest dietary intake of lutein and zeaxanthin reduced the incidence of nuclear cataract by 36 percent.28 Data from the French Pathologies Oculaires Liées à l’Age (POLA) study found the highest quintile of zeaxanthin intake was significantly associated with reduced risk of ARM, nuclear cataract and any cataract.29

Diabetic cataract and retinopathy are also connected to carotenoid intake, according to some researchers. A study in diabetic rats found a combination of lutein and insulin could prevent alterations in glutathione content linked to diabetic cataract onset and progression;30 another animal trial examined the impact of zeaxanthin supplementation in diabetic rats and found the intervention could significantly inhibit diabetes-induced retinal oxidative damage and other abnormalities associated with pathogenesis of diabetic retinopathy.31 Similarly, Australian researchers have found type 2 diabetics with retinopathy had significantly lower serum levels of lutein, zeaxanthin and lycopene compared to the non-retinopathy group.32 Lycopene individually was significantly associated with greater risk and progression of diabetic retinopathy in a study out of China.33

However, carotenoids have a role to play even beyond prevention of disease states such as AMD or retinopathy. Enhancing MPOD by increasing consumption of dietary lutein and zeaxanthin may also reduce glare disability and shorten the time it takes to recover from direct light exposure. In a preliminary trial, researchers from the University of Georgia, Athens, evaluated MPOD in 36 healthy adults as well as photostress recovery, finding a strong relationship between MPOD and both glare disability and photostress recovery.34 A positive difference of 0.16 in MPOD between subjects corresponded to the ability to tolerate glare, and decreased photostress recovery time by 3 seconds. In a follow-up trial, 40 healthy adults received a daily dose of 10 mg lutein (as FloraGLO) and 2 mg zeaxanthin (as OPTISHARP, from DSM) for six months; the ingredients were formulated into beadlets (using Actilease® technology, from DSM).35 The researchers measured MPOD, glare disability and photostress recovery at baseline and then one, two, four and six months after starting supplementation. Most subjects showed increases in MPOD starting after one month of supplementation, with an average increase of 12 percent at two months, 24 percent at four months and 39 percent at six months, in relation to baseline values. The increases were seen across the board, regardless of MPOD at the start of the trial. There was also a significant increase in veiling glare tolerance starting at the four-month point, as well as a significant improvement in photostress recovery times, with recovery times decreasing by 5 seconds after six months of supplementation.


Like glare tolerance, eye fatigue is an eye condition that affects many adults. Clinical trials in Japan have ascertained astaxanthin (as AstaREAL®, from Fuji Health Sciences) can improve retinal blood flow,36and modulate parameters of asthenopia, an eye overuse condition marked by fatigue, red eyes, eye strain, pain in or around the eyes, blurred vision, headache and occasional double vision.37 In a double blind study involving 40 healthy adults with asthenopia, ingestion of 6 mg/d of H. pluvialis astaxanthin (as AstaREAL) improved accommodation times and subjective degree of asthenopia.38 Follow-up work found the 6 mg/d dose to be optimal for addressing accommodation power and subjective symptoms related to asthenopia.39 Additional research investigated the effects of astaxanthin on visual function in 40 healthy volunteers.40 Researchers provided 0, 2, 4 or 12 mg/d of astaxanthin (as AstaREAL) for 28 consecutive days; at study’s end, subjects taking 4 or 12 mg/d had significantly improved uncorrected far visual acuity and shorter positive accommodation time.

Obviously, there is great potential for antioxidants and carotenoids in supporting eye health. In a backgrounder on nutrition and eye disease for Vitamin & Nutraceutical Information Service (VNIS), supported by DSM, Johanna M. Seddon, M.D., reviewed the state of the research on antioxidants and eye health.41 She commented: “The scientific evidence describing the roles of nutrients in age-related eye disease is rapidly evolving, particularly for vitamins C, E, lutein, zeaxanthin and long-chain omega-3 PUFA. Yet, even though much has been learned about antioxidants and carotenoids and eye health, many questions remain to be answered by current and future studies. … Epidemiological data involving larger study populations are needed to help ascertain a role in prevention as well as treatment, and to refine the direction of clinical trials.”

Seddon’s mention of omega-3 PUFAs is not without good cause. As noted earlier, the AREDS2 trial included omega-3 PUFAs in the formulation along with lutein and zeaxanthin. Researchers from Tufts University, Boston, noted among participants in the original AREDS trial, those with the highest intakes of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) had a significantly lower risk of early AMD, as well as reducing the risk of progression to advanced AMD.42,43 A review by NEI researchers noted DHA and EPA play a number of important roles in the eye, protecting against light- and oxygen-induced oxidative damage; bolstering the health of retinal photoreceptor cell membranes; fighting inflammation and endothelial cell dysfunction; and down-regulating genes associated with vascular instability.44 Omega-3s are essential in brain and retinal development during the fetal and postnatal period, with DHA required for optimum functional maturation of the retina and visual cortex; extra DHA may even enhance visual acuity.45 Preliminary studies even suggest DHA may fight the onset or progression of retinitis pigmentosa.46

EFAs may even play a role in more complex eye conditions, such as glaucoma. An animal trial from the INRA Eye and Nutrition Research Group, Dijon, France, examined how a combination of omega-3 and omega-6 EFAs affected rats that were then subjected to a substantial increase in intraocular pressure (IOP).47 The combination of EPA, DHA and gamma-linolenic acid (GLA) protected the animals’ retinal structures and decreased glial cell activation induced by elevated IOP. The researchers have also reported patients with primary open-angle glaucoma have lower levels of blood cells of phophatidyl-choline (PC) carrying DHA, the levels of which were linearly correlated to visual field loss.48

There may also be a connection between omega-3 levels and dry eye syndrome. A review from Mt. Sinai School of Medicine, New York, noted studies suggest a relationship between EFA supplementation and improvement in dry eye syndrome.49 One such study, from the INRA group in France, examined the efficacy of omega-3 and omega-6 PUFAs in a rat model of dry eye syndrome.50 The combination of EPA, DHA and GLA partially prevented the course of dry eye induced by scopolamine administration, impacting lipid homeostatis. Topical application of DHA following corneal surgery was also shown in an animal trial to increase corneal epithelial cell proliferation, while EPA may increase tear volume and decrease inflammation associated with dry eye syndrome.51


Botanical Bounty

There are also a host of botanically derived nutrients that may help support healthy eyes. For example,anthocyanins, one class of flavonoids, have an array of health benefits, including supporting the eyes. A review from The Horticulture and Food Research Institute of New Zealand Ltd., Auckland, specifically cited anthocyanins’ antioxidant and anti-inflammatory effects, as well as their ability to preserve capillary integrity and improve vision.52 Anthocyanins are found in a wide range of fruits, particularly berries.

Black currant (Ribis nigrum) contains more than 15 different anthocyanins with antioxidant activity. Researchers from the University of Helsinki, Finland, identified four dominant compounds in black currants that were quantified as highly active radical scavengers and antioxidants.53 Researchers at Meiji Seika Kaisha Ltd., Saitama, Japan, examined the ocular distribution of black currant anthocyanins (BCAs) in animals after oral, intravenous and intraperitoneal administration, and found intact forms of the anthocyanins could pass through the blood-aqueous barrier and blood-retinal barrier, and were found in the vitreous, lens and ocular tissues.54 In vitro work by the team further demonstrated the ability of BCAs to regenerate rhodopsin.55

The researchers have extended their work into clinical trials. In a double blind, placebo-controlled crossover study with healthy adults (n=12), researchers provided BCAs at three dose levels (12.5 mg, 20 mg, 50 mg); intervention significantly improved eye adaptation to darkness and subjective symptoms of visual fatigue in a dose-dependent manner.56 Another trial demonstrated BCAs were beneficial in the phototransduction transformation of rhodpsin in the eye upon and after light absorption.57

Another berry, bilberry (Vaccinium myrtillus), has been used as food for centuries with medicinal use dating back to the Middle Ages, according to a monograph in the Alternative Medicine Review.58 While more traditionally used for scurvy and inflammatory conditions, current research is focusing on the treatment of ocular disorders. The monograph noted bilberry extract was studied by French researchers on Royal Air Force pilots during World War II, who found bilberry extract improved nighttime visual acuity. Research in this area has been inconclusive, with two different studies in young adult men finding bilberry anthocyanosides at various dosages (24 mg, 48 mg, 160 mg) had no effect on night vision acuity or night contrast sensitivity.59,60 In fact, a systematic review on trials about bilberry anthocyanosides for effects on night vision reported mixed results, but noted negative outcomes were associated with more rigorous methodology, lower dose levels and extracts from berries with more varied anthocyanoside content; the researchers concluded further trials into the effects of bilberry anthocyanosides and night vision are warranted.61

Other research avenues are opening for bilberry extract. In vitro work out of Columbia University, New York, reported bilberry anthocyanins could protect retinal epithelial cells against photooxidation and membrane permeability.62 Japanese researchers determined bilberry anthocyanoside and its constituents (cyanidin, delphinidin and malvidin) protect retinal ganglion cells against retinal damage, exerting neuroprotective effects via antioxidant mechanisms.63 And oral administration of bilberry extract showed a dose-dependent ability to decrease oxidative stress and reduce ocular inflammation in a Chinese animal study of endotoxin-induced uveitis.64

Specific clinical work done on a standardized extract of bilberry anthocyanosides (as MirtoSelect®, from Indena) has shown beneficial activity. Pharmacological studies have shown this bilberry extract, which is standardized to 36-percent anthocyanosides, increases capillary resistance, reduces abnormal vascular permeability, and has antioxidant activity. In addition, the extract may promote resynthesis of retinal pigments, benefiting visual acuity. One clinical study showed MirtoSelect helped recover reduced visual function caused by overuse of the eyes, improving subjective symptoms such as vision with sparks, dimming of eyesight and ocular fatigue in computer operators, office workers and students compared to subjects treated with a placebo.65


As noted earlier, bilberry may help reduce intraocular inflammation, a significant risk factor in development of glaucoma. Researchers at the University of Chieti-Pescara in San Valentino, Italy, divided 38 individuals into two groups to determine the effect of an active botanical supplement (Mirtogenol, containing 80 mg MirtoSelect and 40 mg Pycnogenol, from Horphag Research) on intraocular pressure (IOP).66 At the end of the six-month intervention, Mirtogenol lowered IOP in 19 of 20 patients versus one of the 18 patients in the control group.

On its own, Pycnogenol, standardized French maritime pine bark extract (supplied in the United States by Natural Health Science), has been investigated in the eye health field primarily for its potential role in addressing diabetic retinopathy. A review on the subject reported Pycnogenol’s ability to increase capillary resistance retains progression of the condition and reduces leakages into the retina, helping with partial recovery of visual acuity.67 Animal trials have further shown the ability of Pycnogenol to increase activity of retinal glutathione reductase and normalize elevated activity of superoxide dismutase (SOD) in the retina of diabetic rats;68 and to fight both retinopathy and diabetic cataractogenesis, particularly in combination with a low-glycemic diet in diabetic rats.69 Researchers at the University of Chieti-Pescara moved into a clinical trial, in which 24 patients with early diabetic retinopathy were given Pycnogenol for three months; visual improvement was subjectively perceived by 18 patients, and testing of visual acuity confirmed significant improvement from baseline.70 The researchers concluded Pycnogenol taken at an early stage of retinopathy may enhance retinal blood circulation and reduce edema, improving vision.

Another botanical that may improve blood circulation is Ginkgo biloba. In a trial out of Taiwan, researchers provided Ginkgo biloba extract (as Egb 761) to type 2 diabetics with retinopathy (n=25) for three months and reviewed several haemorrheological parameters.71 Ginkgo administration significantly reduced blood viscosity and blood viscoelasticity, which could facilitate blood perfusion, and significantly improved retinal capillary blood flow rate. Such activity could also support the use of ginkgo as a treatment for glaucoma, according to a review from the New York Eye and Ear Infirmary, which also cited the ability of the extract to inhibit nitric oxide (NO), and exert antioxidant and neuroprotective activities as complementary functions in this area.72 In fact, Japanese researchers found in an animal study that ginkgo extract could reduce retinal ganglion cell loss in eye with chronic, moderately elevated IOP.73

The root of the Ayurvedic botanical Coleus forskohlii contains the active constituent forskolin; it works by increasing cyclic adenosine monophosphate (cAMP). By activating cAMP, forskolin appears to help lower elevated IOP as seen in glaucoma.74 In a clinical trial in healthy young adults, topical administration of forskolin drops significantly reduced IOP and aqueous flow rate.75 Another crossover, double blind, placebo-controlled trial in healthy men also found a forskolin suspension could decrease IOP.76

Green tea also yields a powerful weapon in the eye health fight, epigallocatechin gallate (EGCG), which has been the subject of several studies concerning vision. In looking at an in vitro model of glaucoma, EGCG has been shown to protect retinal ganglion cells against oxidative-stress injury and reduce apoptosis as well as intracellular radical oxygen species (ROS) generation;77 in animals, administration of EGCG before ischemia to induce oxidative inflammation prevented many of the effects, protecting the retina from injury.78 Italian researchers conducted a short-term study in patients with ocular hypertension and open-angle glaucoma, finding EGCG administration could favorably influence inner retinal function.79 EGCG’s powerful antioxidant activities also may help fight cataractogenesis,80 and AMD, by protecting the retinal pigment epithelium.81





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