Download - What the Bleep We Know About Cataract & Nutrition!

What the Bleep We Know About Cataract & Nutrition!

By Dr. Glen Swartwout

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

Nutrition in the prevention and reversal of cataracts:

Antioxidants:

Free radical pathology is a major theme of cataract formation, as with most age-related anddegenerative processes. Oxidation of cell membrane lipids may play an important role incataractogenesis. Most of the nutritional components of cataract prevention and reversal are relatedto boosting antioxidant defenses. Taking a good optimum potency multivitamin is an importantfoundation for a cataract prevention program, since the use of multi-vitamin/mineral supplementshas been identified as a preventive factor in the medical and epidemiological literature. In the early1950's one doctor had already reported either improvement or little to no progression of cataracts inhis patients who followed a nutritional prevention program including water, beneficial foods andsupplements. 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 cataractby 36 to 44%. While a control group taking placebo tablets had their cataracts worsen from 20/30 to20/40 during a 6 month study, others taking beta carotene and vitamin E experienced an initialimprovement in vision, and never dropped below 20/30. Be aware of a variety of basic adjustmentsthat are able to be madeto a standard

centrifugal or positive displacement pump. Regarding pumps that have overhung impellers, movingto a solid shaft is a desirable refinement instead of the more common sleeved shafts. Mechanicalseals can be enhanced with tungsten carbide faces, and elastomers ought to be changed to Viton.Furthermore, magnetic bearing protectors will prove to be a vast improvement compared to the lipseals that the vast majority of commercial pumps use to keep bearing sump oil free fromcontaminants.

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. Correctingthese factors with such remedies as microwater, friendly bacterial flora, digestive enzymes andhomeopathics to stimulate nutrient utilization can also help us get the most out of our diet and oursupplements. When possible, a nutritional program should be maintained for at least 3 to 4 monthsbefore considering cataract surgery.

Vitamin-A and Carotenoids:

Low levels of beta carotene increase cataract risk 7 fold. Beta carotene may act as a filter, absorbinghigh 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 plasmalevels of beta carotene are linked to increased risk of both cortical and subcapsular cataracts. In onestudy, over 50,000 registered nurses who took in more vitamin A through both diet and supplementsthan 80% of the women in the group showed 39% less cataract risk than the women with intakes inthe lowest 20% of the group. Increased beta carotene intake is associated with decreased risk ofcataract and increased visual acuity with and without glasses (at 20 mg/day). A dosage range from10,000 to 25,000 and even 200,000 IU daily of beta carotene has been recommended. Vitamin A hasalso 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 beingrecommended for cataract prevention, as new research highlights their roles in protection againstfree radical damage, including that induced by exposure to UV radiation. Since beta carotenecompetes for absorption with other carotenoids, rotation of carotenoid foods or supplements hasbeen suggested, especially when high levels of beta carotene or carrots (e.g. carrot juice) are beingingested.

Lutein improves visual acuity in cataract (p < 0.005) compared to controls taking a placebo or a verylow dosage of vitamin E. Glare also decreases with lutein. There was no progression of the cataractsfor four of the five subjects in the lutein group, three of five in the vitamin E group and only one offive in the placebo group. Maximum serum concentrations of lutein and tocopherol were achievedafter 3 to 6 months of supplementation. (Olmedilla B, Granado F, Blanco I, Vaquero M. Lutein, butnot 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 caninduce a relative deficiency of another, as they work sequentially as coenzymes in the electrontransport chain. Some practitioners suggest up to 150 mg of a balanced B complex. Activated Bcomplex 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 aco-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, amajor source of chemical reducing power. Thiamine deprivation (TD) is considered a classic model ofsystemic oxidative stress and is linked with degenerative diseases. TD in mice and rats producesneurodegeneration similar to Alzheimer's disease. Cataract is linked to thiamine and oxidativestress. After 12 days on a thiamine-depleting protocol, posterior sub-capsular (PSC) lens fiber celldegeneration is seen in experimental animals. This area also showed increased levels of Alzheimerprecursor protein, Abeta peptides, and presenilin 1. Thiamine (TTFD) or Cocarboxylase forms ofVitamin B1 are recommended.

B2 (Riboflavin, FMN & Riboflavin 5Ã�-Phosphate):

Riboflavin is needed to make flavin adenine dinucleotide (FAD), a coenzyme for glutathionereductase which Ã�recyclesÃ� the antioxidant glutathione. Riboflavin deficiency probablycontributes to cataract formation in malnourished populations in the 3rd-World. Riboflavindeficiency 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 RDAof riboflavin, supplemenation of levels above the RDA increase glutathione reductase activity.Supplementation of 10 mg/day of riboflavin increases plasma glutathione by 83% resulting inimproved antioxidant protection.

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

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 patientsunder age 50, 20% are deficient in riboflavin, and thus may benefit from moderate levels ofsupplementation. Over age 50, 34% of cataract patients were found deficient in riboflavin, while in acontrol group with normal clear lenses, none were deficient in this vitamin. Another study showed81% 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 thatexcess may also have the potential to contribute to lens damage.

Can the same substance cause the same disease in both excess and deficiency, while potentiallytreating it in intermediate doses? Most definitely. In fact, this common fact is part of the basis of theentire science of pharmacology, known as the Arndt-Schultz Law. The pharmacological law ofdosage effects states that minute doses, as used in homeopathy and nutrition tend to stimulate bodyfunctions, yet moderate doses as used in drug and even nutritional megadose therapies suppressthese 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 5Ã�-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 thecrucial lens anti-oxidant glutathione (GSH). Cataract is associated with increased oxidative stress. Inlens tissue, movement of glucose through the polyol pathway is the major cause of hyperglycemicoxidative stress. The enzyme Aldose Reductase (AR) reduces glucose to sorbitol and contributes tooxidative stress by depleting its cofactor NADPH. Sorbitol dehydrogenase, the second enzyme in thepolyol pathway, converts sorbitol to fructose. This process contributes to oxidative stress becausedepletion of the cofactor NAD+ leads to more glucose entering the polyol pathway. Chronicoxidative stress generated by the polyol pathway contributes to diabetic cataract and other diabeticcomplications. Stable NADH (reduced beta-Nicotinamide Adenine Dinucleotide) supplements arenow commercially available.

B5 (Pantothene):

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

B6 (Pyridoxine, Pyridoxal-5Ã�-Phosphate):

Vitamin B6 is also important for slowing aging of the lens, especially in diabetics, as it inhibitsnonenzymatic glycosylation of lens proteins. Pyridoxine supplementation has been suggested atdosages of 100 mg taken 3 times a day. This vitamin, when indicated by magnesium deficiency orother means, may also be recommended in the activated form of pyridoxal-5Ã�-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 adeficiency 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 incataract.

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

B14 (TMG):

Trimethylglycine (TMG) is an even more powerful methyl donor than DMG. It reversesatherosclerosis by methylating homocysteine (a stronger predictor of cardiovascular disease than ischolesterol) to methionine, elevates mood and prevents cancer by providing a protective methylcoating on DNA. It is recommended at 500 mg 3 times a day sublingually in powder form. TMGderives a pleasant natural sweet taste from the amino acid glycine (which derives its name from itssweet taste). TMG is also strongly recommended for anyone taking SAMe, which converts tohomocysteine upon donating a methyl group. TMG recycles homocysteine back to SAMe throughmethylation, explaining its mood elevating property. After donating a methyl group, TMG becomesDMG (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 treatingcataracts 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 inthe production of aqueous humor, the fluid that feeds the lens, reaching 30 to 50 times the levelfound in the blood. The normal, healthy lens contains a higher level of vitamin C than any otherorgan except the adrenal glands, yet when cataracts are forming, the vitamin C level is either verylow 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 invitamin 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 dry pitwithout cataracts. Low levels of vitamin C in the diet as well as poor absorption due tohypochlorhydria increase the risk of cataract. Vitamin C supplementation in animals minimizesclumping of lens proteins due to UV exposure. Vitamin C has also been shown both in vitro and invivo to prevent the cataract forming effects of the sugar galactose. In one study, sugar cataractscould be triggered in 69% of animalsÃ� 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 reducesintracellular sorbitol accumulation. Since vitamin C and the enzyme SOD are partners in scavengingsuperoxide radicals, a lack of either one places greater demand on the other partner. Ascorbic acidprevents light-mediated damage to the cation pump in the lens. It also prevents light induced lipidperoxidation in the lens, acting as a UV filter in the aqueous humor and lens. This is why nocturnalanimals have much lower levels of vitamin C in their eyes than animals that are active in thesunlight. In guinea pigs, Vitamin C supplements helped prevent lens damage from UV as well asprotein damage from heat. Supplementation in guinea pigs resulted in a 345% increase in vitamin Cin 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 vitaminC into the blood or the aqueous humor results in improved vision in 70% of cataract patients. Onestudy showed that over 50,000 registered nurses who took vitamin C supplements for at least 10years experienced a 45% lower risk of forming cataracts. A study by Dr. James Robertson, anepidemiologist at the University of Western Ontario found that people over age 55 who took avitamin C supplement daily for at least five years reduced their risk by 70%. Supplementing 500mg/day reduces sorbitol levels in the blood by 12.6% in normal adults, and when combined withbioflavonoids, this improves to 27%. At 2,000 mg/day of vitamin C the reduction in sorbitol improvesto 56%. This effect is of particular importance for cataract patients with a diagnosed condition ofdiabetes, and also for the 35% of cataract patients who have undiagnosed diabetes that fails to showup on standard tests of blood sugar and urine sugar. Clinical studies have shown that vitamin C canstop the progression of cataracts, in many cases even with doses as low as 1 gram/day. Even at 350mg/day for 1 or 2 months, 60% of patients with low vitamin C levels show improved vision. Peoplewith higher blood levels of vitamin C, equivalent to supplementing more than 800 mg/day, showreduced risk of developing cataracts. Even at a supplemental dosage range of 300 to 600 mg perday, cataract risk is reduced by 70%. Additional research confirms protection against subcapsularand possibly cortical cataract with dosages between 300 mg and 1250 mg per day. Researchers atthe Human Nutrition Research Center on Aging at Tufts University recommend more than 500mg/day of vitamin C to help prevent cataracts, a dosage which can only by achieved in most casesthrough supplementation. A dosage of 1 gram 3 times a day has been suggested as part of a totalpreventive 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 pHbuffered mineral ascorbates, fat-soluble ascorbyl palmitate. The ester form of Vitamin C (composedof two Vitamin C molecules attached together) doubles intestinal absorption as well as cellularabsorption, reaching 4 times higher intracellular concentrations which stay twice as long in thebody, 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.

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

Vitamin P: Bioflavonoids:

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

Quercetin:

Quercetin, one of the most studied antioxidants, is recommended at a dosage of 500 mg 3 times aday. Another guideline that has been offered is to take about 100 mg of bioflavonoids for every 500mg of vitamin C. Bioflavonoids are especially important in diabetes, and quercetin can preventsubcapsular and possible other forms of diabetic cataract which form during prolonged periods ofelevated 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 wasdeveloped, but was not approved as a drug due to its toxic side effects. Even so, the aldosereductase inhibition proved to reverse cataracts in diabetic rats as well as various problems due todiabetes in humans, yet quercetin works better. Quercetin has been shown to decrease lens swellingexperienced by diabetics. Of 45 bioflavonoids tested, quercetin was the most effective for preventionof 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 clearlenses, compared to 10% that were not treated with quercetin. Even those that failed to totallyprevent lens clouding during quercetin treatment developed much less severe cataracts than thosewithout treatment. Quercetin is commercially obtained from red onions (Allium cepa).

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

OPCs (Pycnogenols, etc.):

Pycnogenol is also suggested, with potential sources from grape seed and skin (Vaccinium vitisidaea) 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 avery pleasant tasting sublingual tablet.

Rutin:

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

Vitamin-D:

A dosage of 1000 IU/ day of vitamin D has been suggested. Vitamin E Low vitamin E levels increasecataract 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 glycosylationof lens proteins, thus slowing aging of the lens.

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

Vitamin E supplementation has been associated with maintaining better visual acuity both with andwithout glasses at levels of just 50 IU/day. At a dosage of 400 IU/day, cataract risk is reduced by upto 56%.

Dosages of between 400 to 1200 IU/day of natural (d isomer) dry vitamin E are suggested, withincreasing dosages often being required with more advanced age. The dry form is better absorbedand 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 macularedema and other inflammatory side effects water impeller of cataract surgery when taken beforeand 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 thereforeremains stable (Unique E). Other oil form Vitamin E supplements must be refrigerated to preventrancidity (which may have occurred in processing, storage, shipment or on the shelf prior topurchase) which counteracts any potential benefits from supplementation.

Minerals:

Calcium:

Along with magnesium, moderate intake of calcium has been recommended. Animals fed a calciumdeficient diet produced cataracts. Calcification in the lens can cause 'snowy' cataracts. Anteriorpolar cataracts appear as calcium deposits early in life, often as a result of intolerance to dairyproducts. Calcium mishandling, with deposition in tissues such as the lens can be triggered bydeficient or excess calcium, but also by deficient magnesium or chromium, excess phosphorus orother acid forming substances, food allergies, or unstable blood sugar regulation. Often, moderatesupplementation of a bioavailable calcium such as microcrystalline hydroxyapatite (MCHA) canimprove 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 andmore 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 includinghypertension, hypercholesterolemia and diabetes. Glucose tolerance factor (GTF) chromium helpsregulate blood sugar and improve circulation. Chromium deficiency is a factor in adult-onsetdiabetes impairing the body's response to insulin, resulting in elevated blood sugar. Levels reducedfrom normal by 60% have been found in the lens in both diabetic and senile cataract. A dose of 200

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mcg/day has been recommended.

Copper:

Copper supplementation can stimulate the production of the antioxidant enzyme superoxidedismutase (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 with50 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 isknown to promote free radical pathology, so supplementation with moderate to large doses of ironshould be avoided unless a specific need has been determined. When indicated, an absorbable formof iron such as picolinate (e.g. Ferrasorb) is recommended both to optimize absorption and minimizethe constipation caused by many iron supplements.

Magnesium:

Magnesium should be supplemented when deficient. Magnesium affects sugar regulation and nervefunction as well as vitamin B6 metabolism. Magnesium glycinate is the best absorbed form of thisimportant 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 inpotassium. Sweet fruits should not be emphasized (e.g. banana and papaya), since sugar is a strongrisk factor for cataract formation.

Rare-Earth-Trace-Minerals:

Rare earth minerals found in trace amounts are capable of extending the life-span of laboratoryanimals 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. Theflexibility 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 coralin the life process of marine animals. Coral Calcium (EricssonÃ�s Alkamine Coral Calcium) isproduced at a low temperature to preserve biologically active mineral electron structure. Whenplaced in water, surface minerals are ionized, releasing free electrons which produce an anti-oxidanteffect in the water (-100 mV, compared to +500 mV typical oxidizing potential of tap water). In thisprocess, 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 alkalinityreaches approximately 9.5 pH, associated with significant reductions in cardiovascular disease inepidemiological 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, theOkinawans have the fewest cataracts despite their location 800 miles south of the southern tip of themain Japanese islands, thus receiving more UV sunlight than in any other part of Japan. Theremarkable health and longevity found in Okinawa has been attributed primarily to the distinctlydifferent drinking water found in those coral reefs, which is alkaline and anti-oxidant, compared tothe acidic, oxidizing water found in the volcanic islands of the rest of Japan. Okinawan Sango coral isavailable in sachets, like little tea bags, as well as in a finely ground powder, for treating water. Itconverts chlorine gas into chloride ions in seconds and eliminates most other toxins from water by acombination of electrolysis and adsorption. Alkalinity released, primarily due to the dominantCalcium and Magnesium carbonates found in coral, as well as the broad spectrum of 72 traceminerals including rare earth minerals are stable in the resulting water over long periods. Theelectron content providing anti-oxidant properties, however, reaches its maximum in 5-10 minutesand then dissipates over a period of about 24 hours. Corals from other parts of the world havesimilar effects, but not as potent as the Sango coral of Okinawa. This coral water is called Ã�milk ofthe oceanÃ� just as the milky high mineral content water in mountainous areas renowned for theirhigh longevity is known as Ã�glacial milk.Ã�

Selenium:

Selenium (Se) supplementation can stimulate production of the antioxidant enzyme glutathioneperoxidase (Gpx). Selenium is normally found at high levels in the lens. The selenium content oflenses with cataracts is only 15% of normal. In one study, animals fed a selenium deficient dietproduced cataracts. Selenium protects the lens against damage from methyl mercury. Selenium incombination with vitamin E, with which it is synergistic, is used by veterinarians to treat cataracts indogs, resulting in improved vision an in many cases clearing of the periphery of the lens. A dosage of200 to 400 mcg/day of selenium is recommended, and organically bound selenium, such asselenomethionine is much preferred. Selenium toxicity, found in certain areas of the country wherethe 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 foundin people with cataract. People over age 65 tend to get only 2/3 of the RDA for Zinc, while aging canincrease the need for zinc in order to maintain a positive zinc balance. Zinc deficiency may causecataracts 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 withadequate zinc supplementation. Zinc is needed for SOD activity as well. Zinc levels also drop to lessthan 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. Zincalso affects sugar regulation, immune function and healing. A highly absorbable form of zincsupplementation such as zinc picolinate, zinc monomethionine, or zinc aspartate should be used atlevels up to 50, 75, or 100 mg/day. Improvement in visual acuity in cataract patients has beenreported from 20/200 to 20/25 within as little as 6 months using a multiple nutrient supplementcontaining 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 thatform the lens proteins occurs in several ways. Photo-oxidation of aromatic amino acids, especiallytryptophan, is due to exposure to excess ultraviolet light. Swelling of the lens also increasessusceptibility 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 tofurther damage, while also interfering with its normal function. The rate of glycosylation is reducedwhen blood sugar regulation is improved. The percentage of insoluble protein is fairly stable atabout 3.3% up to about age 50, but then rises to about 9% in the 50's, 16% in the 60's, 17% in the70's, and 40% in the 80's on average. Glycosylation inhibitors include: Carnosine and CalciumPyruvate.

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

Cysteine:

Cysteine stimulates the body's production of glutathione. Supplementation of cysteine along with theother amino acid components of glutathione has been shown to benefit cataracts. Dosages of 400mg/day of cysteine, together with 200 mg/day each of L-glutamine and L-glycine have beenrecommended. Eggs are also rich in cysteine, and eggs increase cholesterol less than eating redmeats, while up to 3 eggs a week do not increase cholesterol. When poached or boiled, thecholesterol in eggs is not oxidized, and thus is not a stress to the body. Eggs from free-rangechickens are higher in antioxidants and contain about one third of the cholesterol. Commercial eggsare 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 ofcataract, 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 ofglutathione 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 highlevels in the lens. It protects the important sulfhydryl bonds in the lens' proteins against bothendogenous and exogenous toxins, as well as free radicals, and plays other important roles inmaintaining 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 superoxideradicals. At levels found in the normal lens, it inhibits glycation of proteins, preventing thedenaturation of lens structural elements and their exposure to thiol oxidation and protein-proteindisulfide formation. Glutathione also prevents lipid peroxidation. Glutathione levels in the lens dropsharply with cataract formation, especially of the posterior subcapsular type. Intravenous injectionsof glutathione improved lens clarity of 30% of patients, while none improved with a placebo. A dailydosage 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 supportincreased 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 dipeptideCarnosine.

L-Carnosine:

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

L-lysine:

Lysine supplementation has been suggested. In diabetic animals, blood sugar levels decreased fromabout 300 mg dL-1 to about 100 mg dL-1 with oral lysine supplementation. The levels of glycosylatedhemoglobin and glycated lens proteins increased in diabetic controls while they were normal withlysine supplementation. Untreated diabetic animals developed cataracts within 3 months, while fiveout 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 theUSDA 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, aswell as in the antioxidant enzyme methionine sulfoxide reductase. Cysteine and methionine are therate-limiting amino acids in the formation of glutathione.

N-acetyl cysteine:

A stable form of cysteine, N-acetyl-cysteine (NAC) supplementation provides antioxidant activity. Itincreases production of glutathione, one of the most important antioxidants in the eye (seeglutathione above). Researchers recommend using it in combination with a multi-vitamin. Dailydoses 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 thistime due to a contaminated batch of products made by a new biotechnology method by onemanufacturer in Japan. In Canada, where the product is back on the market but only under adoctorÃ�s prescription, the cost is nearly 10 times what it was as a nutritional supplement in Canadaor the U.S., not including the additional cost of the doctorÃ�s visit to get a prescription. Turkey meatis high in tryptophan.

Glandulars:

Thyroid glandular supplementation has been recommended. Eye tissue, adrenal, DHEA, humangrowth 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 ofthe 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 maculardegeneration. Wright/Gaby Nutrtion Institute, 1991.

Schoenfeld ER, et al. Recent epidemiological studies on nutrition and cataracts in India, Italy andthe 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 ThroatMonthly, Feb. 1952, 31:79-83.

Sperduto R.D., et al, Ã�The Linzian cataract studies,Ã� Archives of Opthalmology, 111: 1246-53,1993.

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

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


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

Jacues P.F., Chylack L.T., Ã�Epidemiologic evidence of a role for the antioxidant vitamins andcarotenoids in cataract prevention,Ã� 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 andwithout senile cataract. Arch Opthalmol 1988: 106:337-340.

Hankinson SH, et al. Nutrient intake and cataract extraction in women: a prospective study. BritishMedical Journal, 305:335-9, August 8, 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 CollegePublications, 1987.

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

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

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


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 celldegeneration 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 JClin 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 andriboflavin deficiency. Lancet 1:12-3, 1978.

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

Schendel H., Gordon A., Effect of riboflavin on plasma growth hormone and serum iron in man. Am JClin 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.





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 thewithdrawal 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. Withspecial 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.



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

Balch JF and Balch PA. Prescription for. Most installed pumps were not initially sourced for theirpresent use. Frequently, a line in a factory is relocated and the pump that once providedcooling fluidto an injection molding machine is now needed to move oil from a rail car to a tank. All too often,this causes a substantial number of problems for the pump and the facility. Pumps operate wherethe pump curve crosses the system curve. If you move a pump from one system to another, thismeans that the system curve is different. This new system may cause the pump to operate away fromits best efficiency point, leading to noise and other component failures that are merely symptoms of

a mis-matched pump and system.Nutritional Healing. Garden City Park, NY: Avery Publishing Group,1990. p173.


Clark J.I., Ã�Cataract inhibitor slated for clinical trials,Ã� Opthalmology Times, July 1, 1992, p.13.

Solomon L.R., Cohen K., Erythrocyte o@ transport and metabolism and effects of vitamin B6 therapyin 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 Bcomplex supplement.


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


Jacues P.F., et al, Ã�Nutritional status in persons with and without senile cataract:blood vitamin andmineral levels,Ã� 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 NatlAcad 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 MedRes 1978:67:161-164.

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

Taylor A., Ã�Associations between nutrition and cataract,Ã� Nutrition Reviews47: 225-34, 1989.

Chandra D.B., Varma R Ahmad S., Varma S.D., Vitamin C in the human aqueous humor andcataracts. 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 withsenile cataracts. Arch Opthalmol 1936:15:78-83.

Ringvold A., et al, Ã�Senile cataract and ascorbic acid loading,Ã� Acta Opthalmologica 63:277-80,1985.

Blondin J., et al, Ã�Delay of UV-induced eye lens protein damage in guinea pigs by dietaryascorbate,Ã� Journal of Free Radicals in Biology & Medicine 2:275-81, 1986.

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

VinsonJ.A., Ã�The effect of ascorbic acid on galactose-induced cataracts,Ã� Nutrition ReportsInternational 33:665-68, 1986.

Vinson J.A., Staretz M.E., Bose P., Kassm H.M., Basalyga B.S., In vitro and in vivo reduction oferthrocyte 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:preventionby 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 damageby 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 damagein 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 damageby dietary vitamin C. Fed Proc 1986:45:478.

Josephson EM. Science. September 6, 1935.

Bouton S.M., Ã�Vitamin C and the aging eye,Ã� 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. BritishMedical Journal, 305:335-9, August 8, 1992.

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

Vinson J.A., Ã�Research shows vitain C helps avert diabetes complications,Ã� Drug Topics, January22, 1990, P.35.

Dugmore W.N. Tun K., Ã�Glucose tolerance tests in 200 patients with senile cataracts,Ã� BritishJournal 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 ThroatMonthly 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 Practice44(11):475-6, 1990.


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, Ã�Nutritional status in persons with and without senile cataract:blood vitamin andmineral levels,Ã� American Journal of Clinical Nutrition, 48:152-8, 1988.


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

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

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


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 diabeticcomplications. In Cody V, Middleton E Jr, Harborne JB (Eds.). Plant Flavonoids in Biology andMedicine. Biochemical Pharmacological and Structure-Activity Relationships. Alan R. Liss, Inc. NewYork, 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 andcomplications of diabetes. Ann Intern Med 1984:101:82-91.

Chaudry P.S., et al, Ã�Inhibition of human lens aldose reductase by flavonoids, sulindac andindomethacin,Ã� Biochemical Pharmacology 32: 1995-98, 1983.

Varma S.D., et al, Ã�Refractive change in allozan diabetic rabbits control by flavonoids,Ã� ActaOpthalmologica 58:748-59, 1980.

Varma S.D., Ã�Inhibition of lens aldose reductase by flavonoids --their possible role in the preventionof diabetic cataracts,Ã� Biochemical Pharmacology 25:2505-13, 1976.


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


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





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


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

Bland J. Vitamin E and the accessory lipid antioxidants. In Worthington-Roberts B ed: ContemporaryDevelopments 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 EPhotochem Photobiol 1982:36:623-626.

Ross WM, et al. Modelling cortical cataractogenesis: III. In vivo effects of vitamin E oncataractogenesis 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. EyeRes. 36(5):645-53, 1983.

Creighton MO, et al. Modelling cortical cataractogenesis: V. Steroid cataracts induced by solumedrolpartially 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.


Robertson J. Cataract prevention: Time for a clinical trial? British Journal of Clinical Practice44(11):475-6, 1990.


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

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


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 ofNutrition 10(1):79-86, 1991.

Duncan G., Marcantonio J.M., Ã�Lens calcium and cataract,Ã� in PRESBYOPIA RESEARCH, GerardObrecht and Lawrence W. Stark, editors, Plenum Press, New York, 1991, pp. 33-40.

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


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Lane B.C., Ã�Fish methylmercury and human cataractogenesis,Ã� Presentation at the AmericanAcademy of Optometry meeting, December 13, 1992.

Brooksby L.O., A practitionerÃ�s esxperience with selenium-tocopherol in treatment of cataracts andnuclear sclerosis in th dog. Vet Med SAC 1979:74:301-301.




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

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

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Fosmire G.J., Manuel P.A., Smiciklas-Wright H., Dietary intakes and zinc status of an elderly ruralpopulation. 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. JGerontol 1981:36:558-563.

Racz P, et al. Bilateral cataract in acrodermatitis enteropathica. J. Pediatr. Ophthalmol. Strabismus16(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.

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

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



Cole H., Ã�Enzume activity may hold key to catarct prevention,Ã� J. American Medical Assn.,254:1008, 1985.

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


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

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Rathbun W.B., Holleschau A.M., Ã�The effects of age on glutathione synthesis enzymes in lenses ofOld World simians and prosimians,Ã� 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.Box5550, Huntington Beach, CA 92646. p.14.

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




Sulochana KN, Punitham R, Ramakrishnan S. Beneficial effect of lysine and amino acids oncataractogenesis in experimental diabetes through possible antiglycation of lens proteins. Exp EyeRes 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 Sci80:2044-8, 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 againstpulmonary O2 toxicity by N-acetylcysteine. Eur Respir J 1989:2:116-126.

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

Ferrer J.V., et al, Ã�S enile cataract: a review on free radical related pathogenesis and antioxidantprevention,Ã� Archives Gerontology 13:51-59, 1991.





Author's Bio:Â

Dr. Glen is a leader in the field of nutritional eye care, and is featured in Alternative Medicine: TheDefinitive Guide.

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