What the Bleep We Know About Cataract & Nutrition!

The clarity of the crystalline lens in the eye is one of the most important predictors of longevity. The average person suffering cataract formation only lives 5 years after cataract surgery, the most common surgical procedure in Medicare. What the bleep do we know about nutrition and cataractogenesis?

Nutrition in the prevention and reversal of cataracts:

Antioxidants:

Free radical pathology is a major theme of cataract formation, as with most age-related and degenerative processes. Oxidation of cell membrane lipids may play an important role in cataractogenesis. Most of the nutritional components of cataract prevention and reversal are related to boosting antioxidant defenses. Taking a good optimum potency multivitamin is an important foundation for a cataract prevention program, since the use of multi-vitamin/mineral supplements has been identified as a preventive factor in the medical and epidemiological literature. In the early 1950's one doctor had already reported either improvement or little to no progression of cataracts in his patients who followed a nutritional prevention program including water, beneficial foods and supplements. He recommended chlorophyll (45 mg/day), vitamin C (1000 mg/day) and vitamin A (200,000 IU/day). A recent study using 26 vitamins and minerals reduced the risk of nuclear cataract by 36 to 44%. While a control group taking placebo tablets had their cataracts worsen from 20/30 to 20/40 during a 6 month study, others taking beta carotene and vitamin E experienced an initial improvement in vision, and never dropped below 20/30. Animal cataracts have also been reversed with nutritional supplements.

As we get older, there is typically a decrease in our ability to absorb and utilize nutrients. Correcting these factors with such remedies as microwater, friendly bacterial flora, digestive enzymes and homeopathics to stimulate nutrient utilization can also help us get the most out of our diet and our supplements. When possible, a nutritional program should be maintained for at least 3 to 4 months before considering cataract surgery.

Vitamin-A and Carotenoids:

Low levels of beta carotene increase cataract risk 7 fold. Beta carotene may act as a filter, absorbing high energy photons, protecting against photo-oxidation of the lens. Beta carotene is the primary scavenger of singlet oxygen free radicals and is used to treat photosensitivities. Decreased plasma levels of beta carotene are linked to increased risk of both cortical and subcapsular cataracts. In one study, over 50,000 registered nurses who took in more vitamin A through both diet and supplements than 80% of the women in the group showed 39% less cataract risk than the women with intakes in the lowest 20% of the group. Increased beta carotene intake is associated with decreased risk of cataract and increased visual acuity with and without glasses (at 20 mg/day). A dosage range from 10,000 to 25,000 and even 200,000 IU daily of beta carotene has been recommended. Vitamin A has also been suggested at a level of up to 50,000 (or even 200,000) IU per day.

Carotenoids other than beta carotene (in carrots), including Lutein (in green leafy vegetables), Zeaxanthin, Lycopene (in tomatoes) and Astaxanthin (found in salmon) are increasingly being recommended for cataract prevention, as new research highlights their roles in protection against free radical damage, including that induced by exposure to UV radiation. Since beta carotene competes for absorption with other carotenoids, rotation of carotenoid foods or supplements has been suggested, especially when high levels of beta carotene or carrots (e.g. carrot juice) are being ingested.

Lutein improves visual acuity in cataract (p < 0.005) compared to controls taking a placebo or a very low dosage of vitamin E. Glare also decreases with lutein. There was no progression of the cataracts for four of the five subjects in the lutein group, three of five in the vitamin E group and only one of five in the placebo group. Maximum serum concentrations of lutein and tocopherol were achieved after 3 to 6 months of supplementation. (Olmedilla B, Granado F, Blanco I, Vaquero M. Lutein, but not tocopherol, supplementation improves visual function in patients with age-related cataracts: a 2-y double-blind, placebo-controlled pilot study. Nutrition 2003;19:21-4.)

B-complex:

B vitamins in general are both synergistic and safer taken together. Excesses of one B vitamin can induce a relative deficiency of another, as they work sequentially as coenzymes in the electron transport chain. Some practitioners suggest up to 150 mg of a balanced B complex. Activated B complex tablets formulated for optimal sublingual absorption are suggested.

B1 (Thiamine and Cocarboxylase):

Supplementation of thiamine up to 50 mg/day in a B complex has been recommended. Thiamine is a co-factor for enzymes that bridge aerobic and anaerobic metabolism. One such enzyme, transketolase, catalyzes two of three reactions for entry into the pentose-phosphate pathway, a major source of chemical reducing power. Thiamine deprivation (TD) is considered a classic model of systemic oxidative stress and is linked with degenerative diseases. TD in mice and rats produces neurodegeneration similar to Alzheimer's disease. Cataract is linked to thiamine and oxidative stress. After 12 days on a thiamine-depleting protocol, posterior sub-capsular (PSC) lens fiber cell degeneration is seen in experimental animals. This area also showed increased levels of Alzheimer precursor protein, Abeta peptides, and presenilin 1. Thiamine (TTFD) or Cocarboxylase forms of Vitamin B1 are recommended.

B2 (Riboflavin, FMN & Riboflavin 5Õ-Phosphate):

Riboflavin is needed to make flavin adenine dinucleotide (FAD), a coenzyme for glutathione reductase which ÔrecyclesÕ the antioxidant glutathione. Riboflavin deficiency probably contributes to cataract formation in malnourished populations in the 3rd-World. Riboflavin deficiency is also found in 33% of the geriatric population, although studies have been mixed regarding its link to cataract. Even in healthy individuals who already consume more than the RDA of riboflavin, supplemenation of levels above the RDA increase glutathione reductase activity. Supplementation of 10 mg/day of riboflavin increases plasma glutathione by 83% resulting in improved antioxidant protection.

Some researchers recommend that cataract patients should not take more than 10 mg/day of this B vitamin as in higher concentrations it can combine with light to form free radicals which can contribute to cataract formation. Other sources suggest up to 50 and even as high as 300 mg/day of vitamin riboflavin when taken with the full B complex (100 to 150 mg/day), including 50 mg of thiamine, and up to 500 mg/day each of niacinamide and pantothenic acid. Some practitioners suggest dosages up to 100 mg taken 3 times a day in conjunction with a B complex supplement. In fact, one study found that all six of the cataract patients in a study on vitamin B2 had their cataracts eliminated within 9 months. The cataracts also started coming back when they eliminated the supplement.

Riboflavin in cataracts is a good example of the importance of individualized optimal nutrition. Studies in animals show that rats, cats and pigs fed a riboflavin-deficient diet produce cataracts. Low levels in rats increase the cataract forming effects of dietary galactose. Among cataract patients under age 50, 20% are deficient in riboflavin, and thus may benefit from moderate levels of supplementation. Over age 50, 34% of cataract patients were found deficient in riboflavin, while in a control group with normal clear lenses, none were deficient in this vitamin. Another study showed 81% of cataract patients to be deficient, while only 12.5% of people without cataract were deficient. Thus a number of studies show that deficiency may cause cataracts, while there is evidence that excess may also have the potential to contribute to lens damage.

Can the same substance cause the same disease in both excess and deficiency, while potentially treating it in intermediate doses? Most definitely. In fact, this common fact is part of the basis of the entire science of pharmacology, known as the Arndt-Schultz Law. The pharmacological law of dosage effects states that minute doses, as used in homeopathy and nutrition tend to stimulate body functions, yet moderate doses as used in drug and even nutritional megadose therapies suppress these functions, and still higher levels can destroy the very same body functions.

Active coenzyme forms of Vitamin B2, such as Flavin Mononucleotide (FMN) or Riboflavin 5Õ-Phosphate are recommended.

B3 (Niacin, Niacinamide (B4) & NADH):

Niacinamide supplementation has been suggested at a level of 500 mg/day with a full B complex.

An active coenzyme form of Vitamin B3, NADPH, is needed to regenerate adequate levels of the crucial lens anti-oxidant glutathione (GSH). Cataract is associated with increased oxidative stress. In lens tissue, movement of glucose through the polyol pathway is the major cause of hyperglycemic oxidative stress. The enzyme Aldose Reductase (AR) reduces glucose to sorbitol and contributes to oxidative stress by depleting its cofactor NADPH. Sorbitol dehydrogenase, the second enzyme in the polyol pathway, converts sorbitol to fructose. This process contributes to oxidative stress because depletion of the cofactor NAD+ leads to more glucose entering the polyol pathway. Chronic oxidative stress generated by the polyol pathway contributes to diabetic cataract and other diabetic complications. Stable NADH (reduced beta-Nicotinamide Adenine Dinucleotide) supplements are now commercially available.

B5 (Pantothene):

Pantothenic acid supplementation at the level of 500 mg/day has been suggested in combination with a full spectrum B complex. A pantetheine eye drop tested on animals inhibits the clumping of lens proteins involved in early cataract formation.

B6 (Pyridoxine, Pyridoxal-5Õ-Phosphate):

Vitamin B6 is also important for slowing aging of the lens, especially in diabetics, as it inhibits nonenzymatic glycosylation of lens proteins. Pyridoxine supplementation has been suggested at dosages of 100 mg taken 3 times a day. This vitamin, when indicated by magnesium deficiency or other means, may also be recommended in the activated form of pyridoxal-5Õ-phosphate (P5P).

B7 (Folic acid & Folinic acid):

Low levels of folic acid increase cataract risk by over 8 fold. Folic acid may help to compensate for a deficiency in pteridine compounds that normally protect the lens agains damage from UV light. These compounds and the enzymes which produce them have been found to be decreased in cataract.

Folic acid is the most common nutritional deficiency in modern culture. In order to be utilized, folic acid must be converted first to tetrahydrofolate and then to L-5-methyl-tetra-hydrofolate. Sublingual supplementation of the most active form of folate, folinic acid (L-5-methyl-tetra-hydrofolate) is recommended, under the guidance of a health practitioner.

B14 (TMG):

Trimethylglycine (TMG) is an even more powerful methyl donor than DMG. It reverses atherosclerosis by methylating homocysteine (a stronger predictor of cardiovascular disease than is cholesterol) to methionine, elevates mood and prevents cancer by providing a protective methyl coating on DNA. It is recommended at 500 mg 3 times a day sublingually in powder form. TMG derives a pleasant natural sweet taste from the amino acid glycine (which derives its name from its sweet taste). TMG is also strongly recommended for anyone taking SAMe, which converts to homocysteine upon donating a methyl group. TMG recycles homocysteine back to SAMe through methylation, explaining its mood elevating property. After donating a methyl group, TMG becomes DMG (see above). TMG is derived from beets.

B15 (DMG or Pangamic acid):

Pangamic acid (Dimethylglycine, DMG, or vitamin B15) was found to be very helpful in treating cataracts in a Russian study, when it was combined with vitamins A and E. Trimethylglycine (TMG) provides 50% more functional capacity as a methyl donor, with all the benefits of DMG.

Vitamin-C:

Low vitamin C levels increase cataract risk up to 11 times. Vitamin C is specifically concentrated in the production of aqueous humor, the fluid that feeds the lens, reaching 30 to 50 times the level found in the blood. The normal, healthy lens contains a higher level of vitamin C than any other organ except the adrenal glands, yet when cataracts are forming, the vitamin C level is either very low or non-existent in the lens and low in the aqueous humor which supplies nutrition to the lens. Because the inner nucleus of the lens is more dense it is more difficult for nutrients to reach it, resulting in a vitamin C level about 25% lower than the outer cortex. The overall reduction in vitamin C found in cataractogenesis is due both to impaired ability to secrete vitamin C into the aqueous humor, as well as systemic deficiency of 40% compared to people the same age without cataracts. Low levels of vitamin C in the diet as well as poor absorption due to hypochlorhydria increase the risk of cataract. Vitamin C supplementation in animals minimizes clumping of lens proteins due to UV exposure. Vitamin C has also been shown both in vitro and in vivo to prevent the cataract forming effects of the sugar galactose. In one study, sugar cataracts could be triggered in 69% of animalsÕ eyes, but when vitamin C supplements were given, only 6% formed cataracts. For those with diabetes as well as individuals in normal health, vitamin C reduces intracellular sorbitol accumulation. Since vitamin C and the enzyme SOD are partners in scavenging superoxide radicals, a lack of either one places greater demand on the other partner. Ascorbic acid prevents light-mediated damage to the cation pump in the lens. It also prevents light induced lipid peroxidation in the lens, acting as a UV filter in the aqueous humor and lens. This is why nocturnal animals have much lower levels of vitamin C in their eyes than animals that are active in the sunlight. In guinea pigs, Vitamin C supplements helped prevent lens damage from UV as well as protein damage from heat. Supplementation in guinea pigs resulted in a 345% increase in vitamin C in the lens with a 25 fold increase in dietary intake.

As early as 1935, improvement measurable within 2 weeks in the majority of advanced cataracts (20/70 or worse) with vitamin C supplementation was reported in Science. Direct injection of vitamin C into the blood or the aqueous humor results in improved vision in 70% of cataract patients. One study showed that over 50,000 registered nurses who took vitamin C supplements for at least 10 years experienced a 45% lower risk of forming cataracts. A study by Dr. James Robertson, an epidemiologist at the University of Western Ontario found that people over age 55 who took a vitamin C supplement daily for at least five years reduced their risk by 70%. Supplementing 500 mg/day reduces sorbitol levels in the blood by 12.6% in normal adults, and when combined with bioflavonoids, this improves to 27%. At 2,000 mg/day of vitamin C the reduction in sorbitol improves to 56%. This effect is of particular importance for cataract patients with a diagnosed condition of diabetes, and also for the 35% of cataract patients who have undiagnosed diabetes that fails to show up on standard tests of blood sugar and urine sugar. Clinical studies have shown that vitamin C can stop the progression of cataracts, in many cases even with doses as low as 1 gram/day. Even at 350 mg/day for 1 or 2 months, 60% of patients with low vitamin C levels show improved vision. People with higher blood levels of vitamin C, equivalent to supplementing more than 800 mg/day, show reduced risk of developing cataracts. Even at a supplemental dosage range of 300 to 600 mg per day, cataract risk is reduced by 70%. Additional research confirms protection against subcapsular and possibly cortical cataract with dosages between 300 mg and 1250 mg per day. Researchers at the Human Nutrition Research Center on Aging at Tufts University recommend more than 500 mg/day of vitamin C to help prevent cataracts, a dosage which can only by achieved in most cases through supplementation. A dosage of 1 gram 3 times a day has been suggested as part of a total preventive nutrition protocol. Topical application may have pharmacological benefits as well.

Therapeutic-considerations:

Vitamin C is available as an acid (ascorbic acid), a neutral pH ester (polyascorbate), alkaline or pH buffered mineral ascorbates, fat-soluble ascorbyl palmitate. The ester form of Vitamin C (composed of two Vitamin C molecules attached together) doubles intestinal absorption as well as cellular absorption, reaching 4 times higher intracellular concentrations which stay twice as long in the body, gram for gram.

Vitamin C is also affected by the anti-oxidant regenerator, alpha lipoic acid, and other anti-oxidants, especially the bioflavonoids (Vitamin P). Ultimately, we are dealing with an anti-oxidant system, which is a sub-system of the entire physiology.

When vitamin C (a derivative of glucose) becomes oxidized, it contributes to protein glycation, along with glucose. Spent vitamin C also favors tryptophan oxidation, resulting in fluorescent peptide cross-links and protein insolubilisation. This is another reason why it is important to maintain a strong anti-oxidant defense system, including factors such as alpha-lipoic acid which reduce (recylce or regenerate) other anti-oxidants when they become oxidized.

Vitamin P: Bioflavonoids:

Bioflavonoids are important antioxidants that are synergistic with vitamin C in cataract prevention as they are in other parts of the body. Many herbal remedies also contain active bioflavonoids (see section below on phytotherapy).

Quercetin:

Quercetin, one of the most studied antioxidants, is recommended at a dosage of 500 mg 3 times a day. Another guideline that has been offered is to take about 100 mg of bioflavonoids for every 500 mg of vitamin C. Bioflavonoids are especially important in diabetes, and quercetin can prevent subcapsular and possible other forms of diabetic cataract which form during prolonged periods of elevated blood sugar by preventing the conversion of sugar which would keep it stuck in the lens. Quercetin acts as a non-toxic aldose reductase inhibitor. A synthetic aldose reductase inhibitor was developed, but was not approved as a drug due to its toxic side effects. Even so, the aldose reductase inhibition proved to reverse cataracts in diabetic rats as well as various problems due to diabetes in humans, yet quercetin works better. Quercetin has been shown to decrease lens swelling experienced by diabetics. Of 45 bioflavonoids tested, quercetin was the most effective for prevention of cataracts in diabetic animals. A daily dosage of 1000 to 3000 mg of quercetin is recommended. Quercetin has benefits in eye drop form as well, with 50% of treated animals maintaining clear lenses, compared to 10% that were not treated with quercetin. Even those that failed to totally prevent lens clouding during quercetin treatment developed much less severe cataracts than those without treatment. Quercetin is commercially obtained from red onions (Allium cepa).

A water soluble form of quercetin (quercetin dihydrate; brand name: Pain Guard Forte) is now available in high potency, greatly increasing effectiveness through up to a 100-fold increase in the absorption compared to other forms of quercetin.

OPCs (Pycnogenols, etc.):

Pycnogenol is also suggested, with potential sources from grape seed and skin (Vaccinium vitis idaea) as well as maritime pine (Pinus maritima) bark extract.

Maxogenol is a non-solvent OPC extract of American white pine, grape and other antioxidants in a very pleasant tasting sublingual tablet.

Rutin:

Rutin has been recommended for cataract. A rutin dosage of 250 mg/day has been suggested. Rutin is frequently derived from buckwheat.

Vitamin-D:

A dosage of 1000 IU/ day of vitamin D has been suggested. Vitamin E Low vitamin E levels increase cataract risk up to 3 fold. Vitamin E deficiency can cause cataracts in animals. Vitamin E deficiency can cause reversible cataracts in diabetics, too. Vitamin E may prevent non-enzymatic glycosylation of lens proteins, thus slowing aging of the lens.

Vitamin E acts synergistically with selenium for antioxidant protection of the lens by preventing the formation of lipoperoxides. One study showed that vitamin E reduced photo-oxidative damage to rat lenses in-vitro by 80%. In-vivo, vitamin E has been shown to protect against most of the effects of diabetes on cataract formation in rat lenses. Vitamin E also helps to prevent damage from other etiologies, such as radiation and steroids. Low blood levels of vitamin E nearly double the risk of cataract compared to high levels.

Vitamin E supplementation has been associated with maintaining better visual acuity both with and without glasses at levels of just 50 IU/day. At a dosage of 400 IU/day, cataract risk is reduced by up to 56%.

Dosages of between 400 to 1200 IU/day of natural (d isomer) dry vitamin E are suggested, with increasing dosages often being required with more advanced age. The dry form is better absorbed and easier for the liver to process according to research by Dr. Jeffrey Bland.

Dosages at the high end of the therapeutic range can help to prevent and control cystoid macular edema and other inflammatory side effects of cataract surgery when taken before and after surgery as well. Topical application may have pharmacological benefits, too.

One oil form Vitamin E is available which is not diluted with other vegetable oils and therefore remains stable (Unique E). Other oil form Vitamin E supplements must be refrigerated to prevent rancidity (which may have occurred in processing, storage, shipment or on the shelf prior to purchase) which counteracts any potential benefits from supplementation.

Minerals:

Calcium:

Along with magnesium, moderate intake of calcium has been recommended. Animals fed a calcium deficient diet produced cataracts. Calcification in the lens can cause 'snowy' cataracts. Anterior polar cataracts appear as calcium deposits early in life, often as a result of intolerance to dairy products. Calcium mishandling, with deposition in tissues such as the lens can be triggered by deficient or excess calcium, but also by deficient magnesium or chromium, excess phosphorus or other acid forming substances, food allergies, or unstable blood sugar regulation. Often, moderate supplementation of a bioavailable calcium such as microcrystalline hydroxyapatite (MCHA) can improve calcium handling and reduce calcium deposition.

Calcium pyruvate acts as a glycation inhibitor (e.g. Pyruvate Plus).

Chromium:

Chromium, found in whole grains, is lost in refining of processed foods. Americans become more and more depleted in this trace mineral as they get older, since it is not generally found in 'enriched' processed foods. This is associated with increasing rates of cardiovascular disease including hypertension, hypercholesterolemia and diabetes. Glucose tolerance factor (GTF) chromium helps regulate blood sugar and improve circulation. Chromium deficiency is a factor in adult-onset diabetes impairing the body's response to insulin, resulting in elevated blood sugar. Levels reduced from normal by 60% have been found in the lens in both diabetic and senile cataract. A dose of 200 mcg/day has been recommended.

Copper:

Copper supplementation can stimulate the production of the antioxidant enzyme superoxide dismutase (SOD), as long as zinc levels are adequate. Copper levels in the lens drop to less than 10% of normal with cataract formation. Supplementation of 3 mg/day has been recommended along with 50 mg/day of zinc in a total nutritional program as long as there is no copper toxicity.

Iron:

High iron levels are associated with a decreased risk of cortical cataracts. Excessive iron however is known to promote free radical pathology, so supplementation with moderate to large doses of iron should be avoided unless a specific need has been determined. When indicated, an absorbable form of iron such as picolinate (e.g. Ferrasorb) is recommended both to optimize absorption and minimize the constipation caused by many iron supplements.

Magnesium:

Magnesium should be supplemented when deficient. Magnesium affects sugar regulation and nerve function as well as vitamin B6 metabolism. Magnesium glycinate is the best absorbed form of this important and often deficient macro-mineral, and this form does not produce diarrhea as less well-absorbed forms often do in therapeutic dosages.

Manganese:

Manganese is a third mineral involved in SOD. Its level drops to half of the normal level in cataract. A dosage of 20 mg/day has been recommended.

Potassium:

Increased potassium intake has also been suggested. Virtually all vegetables and fruits are high in potassium. Sweet fruits should not be emphasized (e.g. banana and papaya), since sugar is a strong risk factor for cataract formation.

Rare-Earth-Trace-Minerals:

Rare earth minerals found in trace amounts are capable of extending the life-span of laboratory animals by up to double. Rare earth minerals are associated with longevity in certain areas of China, where they are found in the soil and they provide radiant energy from communal brick ovens. The flexibility of the crystalline lens of the eye is the #2 physiological measure associated with longevity.

Rare earth minerals are also found in the sea, and are concentrated and deposited in shells and coral in the life process of marine animals. Coral Calcium (EricssonÕs Alkamine Coral Calcium) is produced at a low temperature to preserve biologically active mineral electron structure. When placed in water, surface minerals are ionized, releasing free electrons which produce an anti-oxidant effect in the water (-100 mV, compared to +500 mV typical oxidizing potential of tap water). In this process, dissolved chlorine gas (a deadly poison) is ionized to chloride (a component of table salt). Heavy metals and other toxins are adsorbed to the surface of the coral as well, while water alkalinity reaches approximately 9.5 pH, associated with significant reductions in cardiovascular disease in epidemiological studies carried out initially in Japan, and later replicated in Europe.

The Japanese have the highest longevity of any nation in the world. Of all the Japanese, the Okinawans have the fewest cataracts despite their location 800 miles south of the southern tip of the main Japanese islands, thus receiving more UV sunlight than in any other part of Japan. The remarkable health and longevity found in Okinawa has been attributed primarily to the distinctly different drinking water found in those coral reefs, which is alkaline and anti-oxidant, compared to the acidic, oxidizing water found in the volcanic islands of the rest of Japan. Okinawan Sango coral is available in sachets, like little tea bags, as well as in a finely ground powder, for treating water. It converts chlorine gas into chloride ions in seconds and eliminates most other toxins from water by a combination of electrolysis and adsorption. Alkalinity released, primarily due to the dominant Calcium and Magnesium carbonates found in coral, as well as the broad spectrum of 72 trace minerals including rare earth minerals are stable in the resulting water over long periods. The electron content providing anti-oxidant properties, however, reaches its maximum in 5-10 minutes and then dissipates over a period of about 24 hours. Corals from other parts of the world have similar effects, but not as potent as the Sango coral of Okinawa. This coral water is called Òmilk of the oceanÓ just as the milky high mineral content water in mountainous areas renowned for their high longevity is known as Òglacial milk.Ó

Selenium:

Selenium (Se) supplementation can stimulate production of the antioxidant enzyme glutathione peroxidase (Gpx). Selenium is normally found at high levels in the lens. The selenium content of lenses with cataracts is only 15% of normal. In one study, animals fed a selenium deficient diet produced cataracts. Selenium protects the lens against damage from methyl mercury. Selenium in combination with vitamin E, with which it is synergistic, is used by veterinarians to treat cataracts in dogs, resulting in improved vision an in many cases clearing of the periphery of the lens. A dosage of 200 to 400 mcg/day of selenium is recommended, and organically bound selenium, such as selenomethionine is much preferred. Selenium toxicity, found in certain areas of the country where the soil contains excessive selenium, can also increase risk of cataract formation.

Zinc:

Zinc has antioxidant activity and also stabilizes cell membranes. Low plasma levels of zinc are found in people with cataract. People over age 65 tend to get only 2/3 of the RDA for Zinc, while aging can increase the need for zinc in order to maintain a positive zinc balance. Zinc deficiency may cause cataracts in both humans and animals, and is used in the treatment of both. In one study on trout, over half the fish developed cataracts on a zinc deficient diet, while no cataracts formed with adequate zinc supplementation. Zinc is needed for SOD activity as well. Zinc levels also drop to less than 10% of normal levels with cataract formation. Zinc is also important for vitamin A metabolism, the health of the epithelium of the lens, and for the metabolism of sugar within the lens tissue. Zinc also affects sugar regulation, immune function and healing. A highly absorbable form of zinc supplementation such as zinc picolinate, zinc monomethionine, or zinc aspartate should be used at levels up to 50, 75, or 100 mg/day. Improvement in visual acuity in cataract patients has been reported from 20/200 to 20/25 within as little as 6 months using a multiple nutrient supplement containing zinc.

Protein: Amino-acids, polypeptides, enzymes, glandulars:

The lens of the eye is the most concentrated protein in the body. Damage to the amino acids that form the lens proteins occurs in several ways. Photo-oxidation of aromatic amino acids, especially tryptophan, is due to exposure to excess ultraviolet light. Swelling of the lens also increases susceptibility to damage. Nonenzymatic glycosylation of amino acids is a third major source of damage. In this process glucose is bound irreversibly to protein making it more susceptible to further damage, while also interfering with its normal function. The rate of glycosylation is reduced when blood sugar regulation is improved. The percentage of insoluble protein is fairly stable at about 3.3% up to about age 50, but then rises to about 9% in the 50's, 16% in the 60's, 17% in the 70's, and 40% in the 80's on average. Glycosylation inhibitors include: Carnosine and Calcium Pyruvate.

In general, insufficient intake or digestion of proteins can cause cataracts. Most Americans, with the exception of vegetarians, however eat 2 to 3 times too much protein. Enzyme supplementation can assist in protein digestion, improving amino acid availability, as well as aiding detoxification and reducing inflammatory processes. Supplementation of bromelain has been recommended.

Cysteine:

Cysteine stimulates the body's production of glutathione. Supplementation of cysteine along with the other amino acid components of glutathione has been shown to benefit cataracts. Dosages of 400 mg/day of cysteine, together with 200 mg/day each of L-glutamine and L-glycine have been recommended. Eggs are also rich in cysteine, and eggs increase cholesterol less than eating red meats, while up to 3 eggs a week do not increase cholesterol. When poached or boiled, the cholesterol in eggs is not oxidized, and thus is not a stress to the body. Eggs from free-range chickens are higher in antioxidants and contain about one third of the cholesterol. Commercial eggs are also frequently treated with arsenic and can carry salmonella bacteria or its toxins.

Glutathione:

Ever since 1912, it has been know that low glutathione in the lens is linked with 18 different types of cataract, including those caused by sugar such as in diabetes, cyanate from smoking, x-ray, inflammation such as in uveitis, and those simply associated with aging. The average level of glutathione drops anywhere from 4 to 14-fold as we get older.

Glutathione (GSH) is a tripeptide of glycine, glutamic acid and cysteine which is found in very high levels in the lens. It protects the important sulfhydryl bonds in the lens' proteins against both endogenous and exogenous toxins, as well as free radicals, and plays other important roles in maintaining a healthy lens as a coenzyme, and in the transport of both amino acids and cations. Glutathione functions to regenerate vitamin C when it has been oxidized by light or superoxide radicals. At levels found in the normal lens, it inhibits glycation of proteins, preventing the denaturation of lens structural elements and their exposure to thiol oxidation and protein-protein disulfide formation. Glutathione also prevents lipid peroxidation. Glutathione levels in the lens drop sharply with cataract formation, especially of the posterior subcapsular type. Intravenous injections of glutathione improved lens clarity of 30% of patients, while none improved with a placebo. A daily dosage of 50 mg has been suggested. Glutathione production is also stimulated by cysteine or NAC (see below), as well as riboflavin, selenium and NADPH (see Vitamin B3). Foods that support increased glutathione levels include those high in sulfur-bearing amino acids such as garlic, onions, beans, eggs and asparagus, as well as avocado.

Histidine:

Histidine deficiency can produce cataracts in animals. Histidine is needed to make the dipeptide Carnosine.

L-Carnosine:

Glycation inhibitors, like Carnosine and calcium pyruvate protect against Advanced Glycation Endproducts (AGE) damage. Because carnosine structurally resembles the sites that glycating agents attack, it sacrifices itself to spare the target. Carnosine also stimulates proteolytic pathways for the disposal of damaged and leaking proteins.

L-lysine:

Lysine supplementation has been suggested. In diabetic animals, blood sugar levels decreased from about 300 mg dL-1 to about 100 mg dL-1 with oral lysine supplementation. The levels of glycosylated hemoglobin and glycated lens proteins increased in diabetic controls while they were normal with lysine supplementation. Untreated diabetic animals developed cataracts within 3 months, while five out of six supplemented with lysine did not develop cataract.

L-phenylalanine:

Phenylalanine deficiency can produce cataracts in animals.

L-taurine:

Taurine has been reported as potentially related to cataract prevention based on research at the USDA Human Nutrition Research Center on Aging at Tufts University.

Methionine:

Methionine can also be beneficial, both as a precusor of cysteine in the production of glutathione, as well as in the antioxidant enzyme methionine sulfoxide reductase. Cysteine and methionine are the rate-limiting amino acids in the formation of glutathione.

N-acetyl cysteine:

A stable form of cysteine, N-acetyl-cysteine (NAC) supplementation provides antioxidant activity. It increases production of glutathione, one of the most important antioxidants in the eye (see glutathione above). Researchers recommend using it in combination with a multi-vitamin. Daily doses of either cysteine or NAC of 100 mg/day are recommended by one author.

Tryptophan:

Tryptophan deficiency is a risk factor for cataracts. Supplements are not available in the U.S. at this time due to a contaminated batch of products made by a new biotechnology method by one manufacturer in Japan. In Canada, where the product is back on the market but only under a doctorÕs prescription, the cost is nearly 10 times what it was as a nutritional supplement in Canada or the U.S., not including the additional cost of the doctorÕs visit to get a prescription. Turkey meat is high in tryptophan.

Glandulars:

Thyroid glandular supplementation has been recommended. Eye tissue, adrenal, DHEA, human growth hormone (hGH), IGF1 and cartilage supplements may also be beneficial.

Fats and Oils:

Avoid high levels of polyunsaturated fats (PUFA) found in vegetable oils, since these use up more of the fat soluble antioxidant vitamin E, since they are easily oxidized.

Avoid excess vitamin A, since it competes with vitamin E.

The next section will deal with light and radiation.

Endnotes (see print version for placement):

Gaby AR and Wright JV. Nutrtitional factors in degenerative eye disorders: cataract and macular degeneration. Wright/Gaby Nutrtion Institute, 1991.

Schoenfeld ER, et al. Recent epidemiological studies on nutrition and cataracts in India, Italy and the United States. Journal of the American College of Nutrition 10(5):540/Abstract 22, 1991.

Antioxidants prevent cataracts. The Nutrition Report, 10(8):59, August 1992.

Seddon, et al. Vitamin supplementation and the risk of cataract. Inv. Ophth. Visual Sci. 33:1097, 1992.

Teikari J. Prevention of cataract with alpha-tocopherol and beta carotene. Inv. Ophth. Visual Sci. 33:1307, 1992.

Atkinson DT. Malnutrition as an etiological factor in senile cataract. Eye, Ear, Nose and Throat Monthly, Feb. 1952, 31:79-83.

Sperduto R.D., et al, ÒThe Linzian cataract studies,Ó Archives of Opthalmology, 111: 1246-53, 1993.

Teikari J.M., ÒPrevention of cataract with alpha tocopherol (vitamin E) and beta carotene,Ó Investigative Opthalmolgy 33: ARVO Abstracts 3072, March 15, 1992.

Heffley J.D., Williams R.J., The nutritional teamwork approach: prevention and regression of cataracts. Proc National Academy of Science 1974:71:4161-4168.

Gaby AR and Wright JV. Nutrtitional factors in degenerative eye disorders: cataract and macular degeneration. Wright/Gaby Nutrtion Institute, 1991.

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p. 48.

Jacues P.F., Chylack L.T., ÒEpidemiologic evidence of a role for the antioxidant vitamins and carotenoids in cataract prevention,Ó American Journal of Clinical Nutrition, 53:352-55S, 1991.

Burton G and Ingold K. Beta-carotene: An unusual type of lipid antioxidant. Science 224:569-73, 1984.

Jacques et al. American Journal of Clinical Nutrition, July 1988; 48(1):152-8.

Jacques P.F., Chylack L.T. Jr., McGandy R.B., Hartz S.C. Antioxidant status in persons with and without senile cataract. Arch Opthalmol 1988: 106:337-340.

Hankinson SH, et al. Nutrient intake and cataract extraction in women: a prospective study. British Medical Journal, 305:335-9, August 8, 1992.

Schoenfeld ER, et al. Recent epidemiological studies on nutrition and cataracts in India, Italy and the United States. Journal of the American College of Nutrition 10(5):540/Abstract 22, 1991.

Teikari J. Prevention of cataract with alpha-tocopherol and beta carotene. Inv. Ophth. Visual Sci. 33:1307, 1992.

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p.50.

Pizzorno JE and Murray MT. A Textbook of Natural Medicine. Seattle, WA: John Bastyr College Publications, 1987.

Atkinson DT. Malnutrition as an etiological factor in senile cataract. Eye, Ear, Nose and Throat Monthly, Feb. 1952.

Balch JF and Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group, 1990. p173.

Duarte A. Cataract Breakthrough. Int Inst Nat Health Sci, Huntington Beach, Calif. 1982. p.149.

Balch JF and Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group, 1990. p173.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989

Frederikse PH, Farnsworth P, Zigler JS Jr. Thiamine deficiency in vivo produces fiber cell degeneration in mouse lenses. Biochem Biophys Res Commun 1999;258:703-707.

Levy Y., Dutta P., Pinto J., Rivlin R., Erythocyte lipid peroxidation during riboflavin deficiency. am J Clin Nutr 1986:43:656.

Bhat KS. Nutr Rep Int, 1987; 36:685.

Skalka H and Prchal J. Cataracts and riboflavin deficiency. Am J Clin Nutr 34:861-3, 1981.

Prchal J, et al. Association of pre-senile cataracts with heterozygousity for galactosemic states and riboflavin deficiency. Lancet 1:12-3, 1978.

Beutler E., Effect of flavin compounds on glutathione reductase activity: in vivo and in vitro studies. J Clin Invest 1969:48:1957-1966.

Schendel H., Gordon A., Effect of riboflavin on plasma growth hormone and serum iron in man. Am J Clin Nutr 1975:28:569-570.

Varma S, et al. Light-induced damage to ocular lens cation pump: Prevention by vitamin C. Proc Natl Acad Sci 76:3504-6, 1979.

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p.51.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989

Balch JF and Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group, 1990. p173.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Kavner RS, Dusky L. Total Vision. New York: A&W Visual Library, 1978. p.142.

Day P.L., Langston W.C., Further experiments with cataract in albino rats resulting from the withdrawal of vitamin G (B2) from the diet. J Nutr 1934:7:97-106.

Gershoff SN, et al. J. Nutr. 68:75-88, 1959.

Miller ER, et al. J. Nutr. 52:405-13, 1954.

Wintrobe M.M, Buschke W., Folis R.H. Jr., Humphreys S., Riboflavin deficiency in swine. With special reference to the occurrence of cataracts. Johns Hoopkins Hosp Bull 1944:75:102-114.

Srivastava S.K., Beutler E., Galactose cataract in riboflavin deficinet rats. Biochem ed 1972:6:372-379.

Skalka HW, et al. Riboflavin deficiency and cataract formation. Metabol. & Ped. Ophthalmol. 5(1):17-20, 1981.

Skalka H.W., Prchal J.T., Cataracts and riboflavin deficiency. Am J Clin Nutr 1981:34:861-863.

Skalka H.W., Prchal J.T., Cataracts and riboflavin deficiency. Am J Clin Nutr 1981:34:861-863.

Balch JF and Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group, 1990. p173.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989

Lee, A. Y. W., Chung, S. S. M. Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB J. 13, 23-30 (1999).

Balch JF and Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group, 1990. p173.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989

Clark J.I., ÒCataract inhibitor slated for clinical trials,Ó Opthalmology Times, July 1, 1992, p.13.

Solomon L.R., Cohen K., Erythrocyte o@ transport and metabolism and effects of vitamin B6 therapy in type II diabetes mellitus. Diabetes 1989:38:881-886.

Some practitioners suggest dosages up to 100 mg taken 3 times a day in conjunction with a B complex supplement.

Jacues P.F., Chylack L.T., ÒEpidemiologic evidence of a role for the antioxidant vitamins and carotenoids in cataract prevention,Ó American Journal of Clinical Nutrition, 53:352-55S, 1991.

Rao GN and Cotlier: The enzymatic activities of GTP cyclohydrolase, sepiapterin reductase, dihydropteridine reductase and dihydrofolate reductase; and tetrahydrobiopterin content in mammalian ocular tissues and in human senile cataracts. Comp Biochem Physiol 80B:61-6, 1985.

Kavner RS, Dusky L. Total Vision. New York: A&W Visual Library, 1978. p.143.

Jacues P.F., et al, ÒNutritional status in persons with and without senile cataract:blood vitamin and mineral levels,Ó American Journal of Clinical Nutrition, 48:152-8, 1988.

Duarte A. Cataract Breakthrough. Int Inst Nat Health Sci, Huntington Beach, Calif. 1982.

Varma S, et al. Light-induced damage to ocular lens cation pump: Prevention by vitamin C. Proc Natl Acad Sci 76:3504-6, 1979.

Bellows J. Biochemistry of the lens: Some studies on vitamin C and lens. Arch Ophthal 16:58, 1936.

Rawal U.M., Patel U.S., Desai R.J. Biochemical studies on cataractous human lenses. Indian J Med Res 1978:67:161-164.

Ringvold A., Johnsen H., Bilka A., Senile cataract and ascorbic acid loading. Acta Ophthalmol 1985: 63:277-280.

Taylor A., ÒAssociations between nutrition and cataract,Ó Nutrition Reviews47: 225-34, 1989.

Chandra D.B., Varma R Ahmad S., Varma S.D., Vitamin C in the human aqueous humor and cataracts. Int J Vitam Nutr Res 1986:56:165-168.

Bellows J. Biochemistry of the lens. V. Cevitamic acid content of the blood and urine of subjects with senile cataracts. Arch Opthalmol 1936:15:78-83.

Ringvold A., et al, ÒSenile cataract and ascorbic acid loading,Ó Acta Opthalmologica 63:277-80, 1985.

Blondin J., et al, ÒDelay of UV-induced eye lens protein damage in guinea pigs by dietary ascorbate,Ó Journal of Free Radicals in Biology & Medicine 2:275-81, 1986.

Vinson, et al. Nutrition Research (12):915-922, 1992.

VinsonJ.A., ÒThe effect of ascorbic acid on galactose-induced cataracts,Ó Nutrition Reports International 33:665-68, 1986.

Vinson J.A., Staretz M.E., Bose P., Kassm H.M., Basalyga B.S., In vitro and in vivo reduction of erthrocyte sorbitol by ascorbic acid. Diabetes 1989:38:1036-1041.

Varma S, et al. Protection against superoxide radicals in rat lens. Ophthalmol Res 9:421-31, 1977.

Varma S.D. Kumar S., Richards R.D., Light-induced damage to ocular lens cation pump:prevention by vitamin C. Proc Natl Acad Sci 1979:763504-3506.

Varma S.D., Srivastava V.K., Richards R.D., Photoperoxidation in the lensand cataract formation: preventive role of superoxide dismutase, catalase and vitamin C. Opthalmic Res 1982:14:167-172.

Blondin J., Baragi V.K., Schwartz E.R., Sadowski J., Taylor A., Prevention of eye lens protein damage by dietary vitamin C. Fed Proc 1986:45:478.

Tsao C.S., Xu L.F., Your M., Effect of dietary ascorbic acid on heat-induced eye lens protein damage in guinea pigs. Opthalmic Res 1990:22:106-110.

Blondin J., Baragi V.K., Schwartz E.R., Sadowski J., Taylor A., Prevention of eye lens protein damage by dietary vitamin C. Fed Proc 1986:45:478.

Josephson EM. Science. September 6, 1935.

Bouton S.M., ÒVitamin C and the aging eye,Ó Archives of Internal Medicine, 63: 930-45, 1939.

Bouton S.M. Jr., Vitamin C and the aging eye. Arch Intern Med 1939:63:930-945.

Hankinson SH, et al. Nutrient intake and cataract extraction in women: a prospective study. British Medical Journal, 305:335-9, August 8, 1992.

Robertson JM. A possible role for vitamins C and E in cataract prevention. American Journal of Clinical Nutrition 53:346S-351S, 1991.

Vinson J.A., ÒResearch shows vitain C helps avert diabetes complications,Ó Drug Topics, January 22, 1990, P.35.

Dugmore W.N. Tun K., ÒGlucose tolerance tests in 200 patients with senile cataracts,Ó British Journal of Opthalmology 64: 689-92, 1980.

Bouton S. Vitamin C and the aging eye. Arch Int Med 63:930-45, 1939.

Atkinson D. Malnutrition as an etiological factor in senile cataract. Eye, Ear, Nose and Throat Monthly 31:79-83, 1952.

Bouton S.M. Jr., Vitamin C and the aging eye. Arch Intern Med 1939:63:930-945

Friend, T. Vitamin C could cut cataract risk. USA Today, Life Section, Sept. 18, 1990.

Robertson J. Cataract prevention: Time for a clinical trial? British Journal of Clinical Practice 44(11):475-6, 1990.

Robertson JM. A possible role for vitamins C and E in cataract prevention. American Journal of Clinical Nutrition 53:346S-351S, 1991.

Varma SD. Annals of the New York Academy of Sciences. 1987; 498:280-306.

Blondin J, et al. J Free Radical Biol Med 1986;2(4):275-81.

Jacues P.F., et al, ÒNutritional status in persons with and without senile cataract:blood vitamin and mineral levels,Ó American Journal of Clinical Nutrition, 48:152-8, 1988.

Pizzorno JE and Murray MT. A Textbook of Natural Medicine. Seattle, WA: John Bastyr College Publications, 1987.

Varma SD, et al. Scientific basis for medical therapy of cataracts by antioxidants. American Journal of Clinical Nutrition 53:335S-345S, 1991.

Tessier F, Moreaux V, Birlouez-Aragon I, Junes P, Mondon H. Decrease in vitamin C concentration in human lenses during cataract progression. Int J Vitam Nutr Res 1998;68(5):309-15

Vinson, et al. Nutrition Research (12):915-922, 1992.

Pizzorno JE and Murray MT. A Textbook of Natural Medicine. Seattle, WA: John Bastyr College Publications, 1987.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989.

Todd GP. Nutrition, Health & Disease. Norfolk, Virginia: Donning Co., 1985. p.124.

Sharma S.D. Inhibition of aldose reductase by flavonoids: possible attenuation of diabetic complications. In Cody V, Middleton E Jr, Harborne JB (Eds.). Plant Flavonoids in Biology and Medicine. Biochemical Pharmacological and Structure-Activity Relationships. Alan R. Liss, Inc. New York, 1986, pp. 343-358.

Beyer-Mears A., Cruz E. Reversal of diabetic cataract by sorbinil, an aldose reductase inhibitor. diabetes 1985:34:15-21.

Kinoshita J.H. Kador P.F. Robison W.G. Datilis M.B. Cobo L.M., et al, Aldose reductase and complications of diabetes. Ann Intern Med 1984:101:82-91.

Chaudry P.S., et al, ÒInhibition of human lens aldose reductase by flavonoids, sulindac and indomethacin,Ó Biochemical Pharmacology 32: 1995-98, 1983.

Varma S.D., et al, ÒRefractive change in allozan diabetic rabbits control by flavonoids,Ó Acta Opthalmologica 58:748-59, 1980.

Varma S.D., ÒInhibition of lens aldose reductase by flavonoids --their possible role in the prevention of diabetic cataracts,Ó Biochemical Pharmacology 25:2505-13, 1976.

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p.50.

Mohan M, et al, ÒAnti-cataract effect of topical quercetin and myricetin in glactosemic rats,Ó Medical Science Research 16: 685-86, 1988.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Jackson M and Teague T. The Handbook of Alternatives to Chemical Medicine. (Oakland, California: Teague and Jackson, 1985) p. 65.

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p.50.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Jacues P.F., Chylack L.T., ÒEpidemiologic evidence of a role for the antioxidant vitamins and carotenoids in cataract prevention,Ó American Journal of Clinical Nutrition, 53:352-55S, 1991.

Kavner RS, Dusky L. Total Vision. New York: A&W Visual Library, 1978. p.152.

Devi A. Raina Pl, Singh A., Abnormal protein and nucleic acid metabolism as a couse of cataract formation induced by nutritional deficiency in rabbits. Br J Opthalmol 1965:49:271-275.

Todd GP. Nutrition, Health & Disease. Norfolk, Virginia: Donning Co., 1985. p.65.

Ceriello A., Giugliano D. Quataro A. donzella C. Dipalo G., et al, Vitamin E reductionof protein glycosylation in diabetes. Diabetes Care 1991:14:68-72.

Bland J. Vitamin E and the accessory lipid antioxidants. In Worthington-Roberts B ed: Contemporary Developments in Nutrition. CV Mosby, St. Louis, Mo, 1981. p135-60.

Varma SD, Richards RD. Photochem. & Photobiol. 36(6), 1982.

Varma S.D., Beachy N.A., Richards R.D., Photoperoxidation of lens lipids: prevention by vitamin E Photochem Photobiol 1982:36:623-626.

Ross WM, et al. Modelling cortical cataractogenesis: III. In vivo effects of vitamin E on cataractogenesis in diabetic rats. Can. J. Ophthalmol. 17(2):61-6, 1982.

Ross WM, et al. Radiation cataract formation diminished by vitamin E in rat lenses in vitro. Exp. Eye Res. 36(5):645-53, 1983.

Creighton MO, et al. Modelling cortical cataractogenesis: V. Steroid cataracts induced by solumedrol partially prevented by vitamin E in vitro. Exp. Eye Res. 37(1):65-76, 1983.

Vitale S, West S, Hallfrisch J, et al. Plasma antioxidants and risk of cortical and nuclear cataract. Epidemiology 1993: 4(3)195-203.

Teikari J. Prevention of cataract with alpha-tocopherol and beta carotene. Inv. Ophth. Visual Sci. 33:1307, 1992.

Robertson J. Cataract prevention: Time for a clinical trial? British Journal of Clinical Practice 44(11):475-6, 1990.

Robertson JM. A possible role for vitamins C and E in cataract prevention. American Journal of Clinical Nutrition 53:346S-351S, 1991.

Osilesi O, Trout DL, Ogunwole JO, et al. Blood pressure and plasma lipids during ascorbic acid supplementation in borderline hypertensive and normotensive adults. Nutr Res 1991; 11:405-12.

Robertson J., donner A.P., Trevithick J.R., ÒVitamin E intake and risk of cataracts in humans,Ó Annals New York Academy Sciences 570:372-82, 1989.

Pizzorno JE and Murray MT. A Textbook of Natural Medicine. Seattle, WA: John Bastyr College Publications, 1987.

Duarte A. Cataract Breakthrough. Int Inst Nat Health Sci, Huntington Beach, Calif. 1982. p. 55.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p.50.

Todd GP. Nutrition, Health & Disease. Norfolk, Virginia: Donning Co., 1985. p.16.

Varma SD, et al. Scientific basis for medical therapy of cataracts by antioxidants. American Journal of Clinical Nutrition 53:335S-345S, 1991.

Duarte A. Cataract Breakthrough. Int Inst Nat Health Sci, Huntington Beach, Calif. 1982. p. 55.

Couet C, et al. Lactose and cataract in humans: A review. Journal of the American College of Nutrition 10(1):79-86, 1991.

Duncan G., Marcantonio J.M., ÒLens calcium and cataract,Ó in PRESBYOPIA RESEARCH, Gerard Obrecht and Lawrence W. Stark, editors, Plenum Press, New York, 1991, pp. 33-40.

Christian Janet L., Greger J.L., NUTRITION FOR LIVING, 2nd edition, Benjamin Cummings, Menlo Park, Ca., 1988.

Whitney E.N., Hamilton E.M.N., Rolfes S.R., UNDERSTANDING NUTRITION, 5th edition, West Publishing, New York, 1990.

Pineau A, et al. A study of chromium and human cataractous lenses and whole blood of diabetics, senile and normal populations. Biological Trace Element Research 32:133-8, 1992.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Lane B, Nutrition and Vision, 274, in Bland J, Ed. 1984-85 Yearbook of Nutritional Medicine (New Canaan, Connecticut: Keats, 1985).

Swanson A and Truesdale A. Elemental analysis in normal and cataractous human lens tissue. Biochem Biophys Res Comm 45:1488-96, 1971.

Balch JF and Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group, 1990. p173.

Schoenfeld ER, et al. Recent epidemiological studies on nutrition and cataracts in India, Italy and the United States. Journal of the American College of Nutrition 10(5):540/Abstract 22, 1991.

Heinitz M. [Clinical and biochemical aspects of the prophylaxis and therapy of senile cataract with zinc aspartate.] Klin. Monatsbl. Augenheilkd. 172(5):778-83, 1978.

Swanson A and Truesdale A. Elemental analysis in normal and cataractous human lens tissue. Biochem Biophys Res Comm 45:1488-96, 1971.

Zarrow S. Keeping your eyes young and sharp. Prevention.

Lockie A. The Family Guide to Homeopathy, Symptoms and Natural Solutions. Simon & Schuster, 1989. p158.

Sasaki K, Ono M, Aoki K. Cataract epidemiology survey in the three climatically different areas in Japan--prevalence of cataracts and types of lens opacifications. Nippon Ganka Gakkai Zasshi 1995;99:204-11.

Lane B, Nutrition and Vision, 274, in Bland J, Ed. 1984-85 Yearbook of Nutritional Medicine (New Canaan, Connecticut: Keats, 1985).

Whanger P, Weswig P. Effects of selenium, chromium and antioxidants on growth, eye cataracts, plasma cholesterol and blood glucose in selenium deficient, vitamin E supplemented rats. Nutr. Rep. Int. 12:345-58, 1975.

Taussky H.H., Washington A., Zubillaga E., Milhorat A.T., Distribution of selenium on the tissues of the eye. Nature 1966:210:949-950.

Swanson A and Truesdale A. Elemental analysis in normal and cataractous human lens tissue. Biochem Biophys Res Comm 45:1488-96, 1971.

Couet C, et al. Lactose and cataract in humans: A review. Journal of the American College of Nutrition 10(1):79-86, 1991.

Lane B.C., ÒFish methylmercury and human cataractogenesis,Ó Presentation at the American Academy of Optometry meeting, December 13, 1992.

Brooksby L.O., A practitionerÕs esxperience with selenium-tocopherol in treatment of cataracts and nuclear sclerosis in th dog. Vet Med SAC 1979:74:301-301.

Pizzorno JE and Murray MT. A Textbook of Natural Medicine. Seattle, WA: John Bastyr College Publications, 1987.

Long RY. Cataracts may respond to nutrients. Health News & Review, p. 6, March/April, 1989

Duarte A. Cataract Breakthrough. Int Inst Nat Health Sci, Huntington Beach, Calif. 1982. p. 149.

Taylor A. Various nutrients studied for cataract prevention. Geriatrics 46(1):24, 1991

Anonymous. A radical approach to zinc. Lancet 1978:1:191-192.

Girotti A.W., Thomas J.P., Jordan J.E., Inhibitory effect of zinc (II) of free radical lipid peroxidation in erythrocyte membranes. J Free Radicals Biol Med 1985:1:395-401.

Bhat K.S., Plasma calcium and trace metals in human subjects with mar=ture cataract. Nutr Rep Int 1988:37:157-163.

Fosmire G.J., Manuel P.A., Smiciklas-Wright H., Dietary intakes and zinc status of an elderly rural population. J Nutr Elderly 1984:4(1):19-30.

Burke D.M., DeMicco F.J., Taper LJ., Ritchey S.J., Copper and zinc utilization in elderly adults. J Gerontol 1981:36:558-563.

Racz P, et al. Bilateral cataract in acrodermatitis enteropathica. J. Pediatr. Ophthalmol. Strabismus 16(3):180-2, 1979.

Cataract as an outcome of zinc deficiency in salmon. Nutr. Rev. 44(3):118-20, 1986.

Chuistova IP, et al. (Experimental morphological basis for using zinc in treating senile cataract.) Oftalmol Zh. (7):394-6, 1985.

Tiekert CG. More on the medical ÒcureÓ for cataracts. Letter to the Editor. J. Am. Vet. Med. Assoc. 188(12):1364, 1986.

Ketola HG. J. Nutr. 109:965-69, 1979.

Swanson A and Truesdale A. Elemental analysis in normal and cataractous human lens tissue. Biochem Biophys Res Comm 45:1488-96, 1971.

Heinitz M. (Clinical and biochemical aspects of the prophylaxis and therapy of senile cataract with zinc aspartate.) Klin. Monatsbl. Augenheilkd. 172(5):778-83, 1978.

Duarte A. Cataract Breakthrough. Int Inst Nat Health Sci, Huntington Beach, Calif. 1982. p. 54.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p.51.

Todd GP. Nutrition, Health & Disease. Norfolk, Virginia: Donning Co., 1985. p.15.

Gaby AR and Wright JV. Nutrtitional factors in degenerative eye disorders: cataract and macular degeneration. Wright/Gaby Nutrtion Institute, 1991.

Brownlee M., Vlassara H., Cerami A., Nonenzymatic glycosylation and the pathogenesis of diabetic complications. Ann Intern Med 1984:38:881-886.

Lerman S. Radiant Energy and the Eye. Macmillan, New York, 1980.

Schoenfeld ER, et al. Recent epidemiological studies on nutrition and cataracts in India, Italy and the United States. Journal of the American College of Nutrition 10(5):540/Abstract 22, 1991.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Cole H., ÒEnzume activity may hold key to catarct prevention,Ó J. American Medical Assn., 254:1008, 1985.

Hockwin O. Treatment of senile lens opacities, analysis of possible ways and means from the aging lens. Elsevier/North-Holland Biomedical Press, 1980. p281

Pizzorno JE and Murray MT. A Textbook of Natural Medicine. Seattle, WA: John Bastyr College Publications, 1987.

Vorster H.H., et al, ÒEgg intake does no change plasma lipoprotein and coagulation profiles,Ó American Journal of Clincial Nutrition 55:400-10, 1992.

Harding J.J., Crabbe M.J.C., ÒThe lens:development, proteins,metabolism and cataract,Ó in The Eye, Hugh Davson, editor, Volume 1B 3rd edition, Academic Press, Orlando, 1984.

Rathbun W.B., Holleschau A.M., ÒThe effects of age on glutathione synthesis enzymes in lenses of Old World simians and prosimians,Õ Current Eye Research 11:601-07, 1992.

Rathbun W and Hanson S. Glutathione metabolic pathway as a scavenging system in the lens. Ophthal Res 11:172-6, 1979.

Spector A. The lens and oxidative stress. Oxidative Stress: Oxidants and Antioxidants, Chapter 19. 529-558, 1991.

Duarte A. Cataract Breakthrough, International Institute of Natural Health Sciences, Inc., P.O.Box 5550, Huntington Beach, CA 92646. p.14.

Costagliola C., et al, ÒEffect of reduced gluathione parenteral administration on cataractogenesis,Ó Presentation at the 2nd International Congresss on Amino Acids and Analogues, Vienna, Austria, August 5-9, 1991.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.

Couet C, et al. Lactose and cataract in humans: A review. Journal of the American College of Nutrition 10(1):79-86, 1991.

Balch JF and Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group, 1990. p173.

Sulochana KN, Punitham R, Ramakrishnan S. Beneficial effect of lysine and amino acids on cataractogenesis in experimental diabetes through possible antiglycation of lens proteins. Exp Eye Res 1998;67:597-601

Couet C, et al. Lactose and cataract in humans: A review. Journal of the American College of Nutrition 10(1):79-86, 1991.

Taylor A. Various nutrients studied for cataract prevention. Geriatrics 46(1):24, 1991.

Garner W, et al. H2O2-induced uncoupling of bovine lens Na+, K+ -ATPase. Proc Natl Acad Sci 80:2044-8, 1983.

Cole H. Enzyme activity may hold the key to cataract activity. JAMA 254(8):1008, 1985.

Wagner P.D., Mathieu-Costello O., Debout D.E., Gray A.T., Natterson P.D., et al, Protection against pulmonary O2 toxicity by N-acetylcysteine. Eur Respir J 1989:2:116-126.

Corcoran G.B., Wong B.K., Role of glutathione in prevention of acetaminophen-induced hepatotoxicity by N-acetyl-L-cysteine in vivo:studies with N-acetyl-D-cysteine in mice. J Pharmacol Exp Ther 1986:238:54-61.

Veutler E., Nutritional and metabolic aspects of glutathione. Ann Rev Nutr 1989:9:287-302.

Ferrer J.V., et al, ÒS enile cataract: a review on free radical related pathogenesis and antioxidant prevention,Ó Archives Gerontology 13:51-59, 1991.

Sardi B. Nutrition and the Eyes. Vol. 1. (Montclair, California: Health Spectrum Publishers, 1994) p.50.

Varma SD, et al. Scientific basis for medical therapy of cataracts by antioxidants. American Journal of Clinical Nutrition 53:335S-345S, 1991.

Couet C, et al. Lactose and cataract in humans: A review. Journal of the American College of Nutrition 10(1):79-86, 1991.

Page LR. Healthy Healing. (Sacramento, California: Spilman Printing, 1990) p. 138.