We know what Ray cataract and Nutrition!

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90-furniture-30The clarity of the lens in the eye is one of the most important indicators of longevity. The man who undergoes cataract formation average live only 5 years after cataract surgery, the most common operation in Medicare. What the hell do we know about nutrition and cataract?
Nutrition in the prevention and reversal of cataracts:
antioxidant:
Pathology of free radicals is an important issue of cataract formation, as with most processes associated with aging and degenerative. The oxidation of lipids of the cell membrane can play an important role in cataractogenesis. Most food components of the prevention of cataracts and investment are related stimulate antioxidant defense. Take a good multivitamin optimum performance is an important prevention program cataract base, since the use of dietary / multivitamin mineral supplement was identified as a preventive factor in medical and epidemiological literature. In the early 1950s, the doctor had already reported an improvement or little or no progression of cataracts in patients who took a prevention program of diet, including water, food and beneficial dietary supplements. chlorophyll (45 mg / day), vitamin C (1000 mg / day) and vitamin A (200,000 IU / day) is recommended. A recent study with 26 vitamins and minerals, the risk of nuclear cataract reduced from 36 to 44%. While a control group on placebo pills had their cataracts 20 / 30-20 / 40 for a 6-month study they deteriorates, others take beta-carotene and vitamin E have improved the initial vision, and never allowed for 20 / 30 fall. Cataracts animals were reversed with dietary supplements.
As we age, we must absorb operating is typically a decline in our ability and nutrients. increasing the correction of these factors such as bacterial flora, the firmware to use, digestive enzymes and homeopathic use of nutrients can help make the most of our food and our supplements. If possible, a feeding program should be maintained considering at least three to four months before cataract surgery.
Vitamin A and carotenoids:
Increase low beta-carotene cataract risk levels 7 times. Beta-carotene can act as a filter, the high photon energy, protection against photooxidation of absorbed lens. Beta-carotene is the primary free radical scavenging of singlet oxygen and is used to treat photosensitivity. decreased levels of beta-carotene plasma with an increased risk of both cortical cataracts and subcapsular connected. In one study, more than 50,000 nurses, both in the diet to take vitamin A and adds that 80% of women in the group has the risk of cataracts 39% of women screened with income in the 20% group. assigned increased intake of beta-carotene with a lower risk of cataracts and increased visual acuity with or without glasses (20 mg / day). A dosage range from 10,000 to 25,000 or even 200,000 IU of beta-carotene has been recommended. Vitamin A has also proposed at an altitude of up to 50 000 (or 200 000) IU per day.
Carotenoids other than beta-carotene (in carrots), including lutein (found in green leafy vegetables), zeaxanthin, lycopene (in tomatoes) and astaxanthin (in salmon) are longer for the prevention of recommended Falls , as new research that highlights its role against the damage caused by free radicals to protect that were caused by exposure to UV radiation, including. Because beta-carotene is competing for the absorption of other carotenoids, food supplements or carotenoids rotation has been proposed, especially if (for example, carrot juice) can have high concentrations of beta-carotene or carrots.
Lutein improves visual acuity of cataract (p Nutrition 2003; 19: 21-4.)
B complex:
B vitamins are usually both synergistic and safer together. Too much vitamin B can have a relative deficiency of another sequentially induce how they work as coenzymes in the electron transport chain. Some professionals suggest up to 150 mg of a balanced B-complex tablets activated B complex for sublingual absorption formulated optimally are proposed.
B1 (thiamine and cocarboxylase):
thiamine supplementation of 50 mg / day is recommended in building B. Thiamine is a cofactor for enzymes that span the aerobic and anaerobic metabolism. This enzyme catalyzes the transketolase two out of three responses to the entry into the pentose phosphate, an important source for the chemical reduction of power. Removal of thiamine (TD) a classic model of systemic oxidative stress is pulled into consideration, and is associated with degenerative diseases. TD produced neurodegeneration in mice and rats similar to AD. Cataract is thiamine and oxidative stress. They were observed after 12 days in posterior subcapsular thiamine protocol one (PSC) degrading the lens fiber cell degeneration in experimental animals. Also it showed a higher level of protein and presenilin peptides precursor Alzheimer Abeta 1. thiamine (TTFD) or recommended cocarboxylase form of vitamin B1.
B2 (riboflavin, FMN and riboflavin 5 Otilde; phosphate)
Riboflavin is needed to flavin adenine dinucleotide (FAD), a coenzyme for glutathione reductase and ocirc; Recycle and Otilde; antioxidant glutathione. Riboflavin deficiency is likely to contribute to cataract formation in the population of the world suffer malnutrition in third. Riboflavin deficiency is also found in 33% of the geriatric population, although studies with cataract were mixed in terms of their relationship. Even more riboflavin RDA healthy people already consume supplemenation on the increase in glutathione reductase activity RDA levels. Supplementation of 10 mg / day of riboflavin plasma glutathione increases of 83% in enhancing antioxidant defenses leads.
Some researchers suggest that patients with cataracts should not take more than 10 mg / day of vitamin B, which can be combined with light to form free radicals that may contribute to cataract formation at higher concentrations. According to other sources to 50 and even as high as 300 mg / day, vitamin riboflavin, when added B to full complex (100 to 150 mg / day) with 50 mg of thiamine, and up to 500 mg / day every niacinamide and pantothenic acid. Some professionals suggest doses up to 100 mg 3 times daily in combination with a complex additional B In fact, one study found that six patients had cataracts in a study on vitamin B2 your cataract. Located within 9 months Cataracts have also started when they eliminated supplement.
in cataract Riboflavin is a good example of the importance of individual optimal diet. Animal studies show that rats, cats and pigs fed a diet deficient riboflavin products cataract. Low levels in rats cataract effects increased so galactose in the diet. Among cataract patients are under 50 years 20% lack of riboflavin, and therefore can benefit from moderate levels of supplementation. More than 50 years have 34% of patients with cataracts have been found deficient in riboflavin, whereas in a control group with normal clear lenses, I not been deficient in this vitamin. Another study showed 81% of patients with cataract deficiency, while only 12.5% ​​of people without cataracts were deficient. Therefore, a number of studies show that lack can cause cataracts, while there is evidence that excess also have the opportunity to contribute to damage to the lens.
the substance can cause the same disease, both the excess and deficiency, while potentially mean doses of treatment? Definitely. In fact, this city is part of the foundation of all science of pharmacology, said the law of Arndt-Schultz. dose drug law shows that smaller doses effects, such as used in homeopathy and nutrition tend to stimulate the body’s functions, even in moderate doses, as used in the drug and even nutritional therapies suppress megadoses of these features and an even higher level, the body works very to destroy.
Active coenzyme forms of vitamin B2, as flavin mononucleotide (FMN) or riboflavin Otilde 5; Phosphate recommended.
B3 (niacin, niacinamide (B4) and NADH):
niacinamide supplement has been proposed in an amount of 500 mg / day with a complex B
A form of active vitamin B3 NADPH coenzyme is necessary to regenerate sufficient amounts of essential lens antioxidant glutathione (GSH). The cataract is associated with increased oxidative stress. In the target tissue, the movement of glucose through the polyol pathway is the main cause of oxidative stress hyperglycemic. The enzyme aldose reductase (AR) reduces glucose to sorbitol and contributes to oxidative stress by its cofactor NADPH degrading. Sorbitol dehydrogenase, the second enzyme of polyol pathway converts sorbitol into fructose. This process contributes to oxidative stress, exhaustion due to cofactor NAD + more glucose in your driveway polyol. produces chronic oxidative stress through the polyol pathway contributes to diabetic cataract and other complications of diabetes. Stable NADH (nicotinamide adenine dinucleotide beta) are now commercially available supplements.
B5 (Pantothene):
proposal pantothenic acid supplements tested at 500 mg / day in combination with a complex full spectrum B. pantethinesulphonic lower the eyes of animals, aggregation of lens proteins involved in early inhibit cataract formation.
B6 (pyridoxine, pyridoxal-5 & Otilde; phosphate):
Vitamin B6 is also important to slow the aging of the lens, particularly in diabetics, because inhibits nonenzymatic glycation of the lens proteins. supplementation of pyridoxine at doses of 100 mg three times a day proposed. This vitamin, as indicated by a magnesium deficiency or other means may be advisable in the activated form of pyridoxal-5 and Otilde; Phosphate (P5P).
B7 (folic acid and folinic acid):
Low folate levels increase the risk of cataracts more than 8 times. Folic acid can help reduce shortages pteridine staggered, normally protect the damage of UV light optical agains. These compounds and enzymes that produce, found decreases in cataract.
Folic acid is the most common nutritional deficiency in modern culture. To be used, folic acid and tetrahydrofolate must first L-5-methyl-tetra-hydrofolate be converted. sublingual complement the active form of folic acid, folinic acid (L-5-methyl-tetra-hydrofolate) under the supervision of a physician is recommended.
B14 (TMG):
Trimethylglycine (TMG) is an even more potent than methyl donor DMG. atherosclerosis is reversed by methylation of homocysteine ​​(a predictor of cardiovascular disease than cholesterol) to methionine, elevates mood and prevents cancer by providing a protective layer of methyl DNA. It is recommended that 500 mg 3 times a day sublingually in powder form. TMG holds a pleasant sweet taste of the natural amino acid glycine (sweet taste of its name). TMG is also highly recommended for everyone takes, the SAM, which converts homocysteine ​​donating a methyl group. TMG recycled back through methylation of homocysteine ​​SAM, the confidence survey to explain the property. After donates a methyl group, is TMG DMG (see above). TMG is derived from sugarbeet.
B15 (DMG or pangamic acid):
Pangamic (dimethylglycine, DMG or vitamin B15) has proven very useful in the treatment of cataracts in a study of Russia, when combined with vitamins A and E. trimethylglycine (TMG), up 50% provides more functional as a group methyl, with all the advantages of DMG.
Vitamin C:
Low levels of vitamin C, the risk of cataracts to increase to 11 times. Vitamin C, in particular in the production of aqueous concentrates, which feeds the liquid lens, up to 30 to 50 times the level in the blood. The camera lens, healthy contains a level of vitamin C than any other organ except the adrenal glands, but when forming cataracts, vitamin C content is very low or nonexistent in the lens and low in the aqueous humor, the power the target provided. Because the inner core of the lens is denser, it is difficult for nutrients to reach, in an amount of vitamin C resulting about 25% smaller than the outer crust. The total reduction of vitamin C is both due Cataractogenesis impaired ability to secrete vitamin C in the aqueous humor and systemic deficiency of 40% of the same age without cataracts. Low levels of vitamin C in diet and malabsorption due to hypochlorhydria increase the risk of cataracts. Vitamin C supplementation in animals minimizes clumping of lens proteins by UV exposure. Vitamin C has also been demonstrated in vitro and in vivo to study the effects of the form of cataracts to prevent sugar galactose. In one study, sugar cataract could be activated in 69% of animals and Otilde; Eyes, but as they were given supplements of vitamin C, only 6% of the formed cataracts. For people with diabetes, and people in normal health, reduced vitamin C intracellular accumulation of sorbitol. Like vitamin C and SOD enzyme are partners in the production of superoxide radicals, lack of space, increased demand for the other pair. Ascorbic acid prevents damage when changing light by the cation of the pump in the lens. It also prevents lipid peroxidation induced in the lens, photo acts as a UV filter in the aqueous humor and the lens. For this reason, nocturnal animals in their eyes significantly lower levels of vitamin C have that animals that are active in the sun. In guinea pigs, vitamin C supplements helped lens damage by UV radiation and heat damage to the protein to avoid. Supplementation in guinea pigs resulted in an increase of 345% of vitamin C in the lens with a 25-fold increase in food intake.
In 1935, it was reported a measurable improvement within 2 weeks in most advanced cataract (20/70 or worse) with supplementation of vitamin C in Science. Direct injection of vitamin C in the blood or aqueous humor results in improved vision in 70% of patients with cataracts. One study showed that more than 50,000 nurses who took dietary supplements of vitamin C for at least 10 years had a 45% lower risk of cataract formation. A study by Dr. James Robertson, an epidemiologist at the University of Western Ontario found that people over 55 years, the extra day of vitamin C taken for five years reduced their risk by 70%. Filling 500 mg / day reduced sorbitol levels in the blood of normal adults 12.6%, and when combined with bioflavonoids, which improved to 27%. 2000 mg / day of vitamin C, the reduction to 56% sorbitol improved. This effect is particularly important for cataract patients with a diagnosed disease, diabetes, as well as 35% of cataract patients who have undiagnosed diabetes, which does not appear on the sugar in blood and the level of sugar in the urine. Clinical studies have shown that vitamin C, progression of cataract, in many cases, even as low as 1 to stop g / day dose. Even at 350 mg / day for 1 to 2 months 60% of patients with low levels of vitamin C show improved vision. People with high blood levels of vitamin C, which corresponds to complete more than 800 mg / day showed a lower risk of developing cataracts. Even in an interval of the additional dose of 300 to 600 mg daily, the risk of cataracts is reduced by 70%. Other research confirms the protection subcapsular cataract and cortical dose of between 300 mg and 1250 mg per day. Researchers at the Research Center for Human Nutrition at Tufts University on Aging suggested to help more than 500 mg / day of vitamin C prevent cataracts, a dose that achieved in most cases, supplementing it. A dose of 1 g to 3 times a day preventive diet was suggested as part of a general protocol. Topical application may also have pharmacological advantages.
Therapeutic considerations:
Vitamin C is provided in the form of an (ascorbic acid) acid, an ester of a neutral pH (polyascorbate) or mineral ascorbate buffer pH alkaline, soluble in fat ascorbyl available. The form of vitamin C ester (compound of two molecules of vitamin C together) intestinal absorption bed and cellular uptake and intracellular concentrations reached 4 times greater than, gram for gram are twice as long in the body.

Vitamin C is also affected by the regenerator antioxidant, alpha-lipoic acid and other antioxidants, in particular bioflavonoids (vitamin P). Ultimately, it is an antioxidant system is a subsystem of the whole physiology.
If vitamin C (a glucose derivative) is oxidized, glycosylation contributes to the protein as well as glucose. We have vitamin C promotes the oxidation of tryptophan, which. In crosslinks fluorescence peptide and protein insolubility This is another reason why it is important to have a strong antioxidant defense system, including factors such as alpha lipoic reducing (or composition recylce) to keep other antioxidants when oxidized.
Vitamin P: bioflavonoids:
Bioflavonoids are important antioxidants in preventing cataracts are synergistic with Vitamin C, and other body parts. Many herbal remedies contain bioflavonoids assets (the section below in herbal medicine to see).
Quercetin:
Quercetin, one of the most studied antioxidants, it is recommended that the dose of 500 mg three times a day. Another policy that has been offered is 100 mg bioflavonoids are up to 500 mg of vitamin C. Bioflavonoids is particularly important in diabetes and quercetin can and can prevent the capsule other forms of diabetic cataract, form over an extended period blood sugar, converting the sugar to avoid adhering to the lens. The nontoxic quercetin as an inhibitor of aldose reductase. An inhibitor of aldose reductase developed synthetic, but not yet approved as a drug because of its toxic side effects. However, aldose reductase inhibition demonstrated cataract in diabetic rats reversed, and various problems due to diabetes in humans, but works best quercetin. Quercetin has been shown by diabetics decreased swelling lens suffered. 45 test bioflavonoid quercetin was effective in preventing cataract in diabetic animals. A daily dose of 1000 to 3000 mg quercetin recommended. Quercetin has advantages in the form of eye drops and was treated with 50% of the lenses of the now clear animals compared with 10% who are not treated with quercetin. Even those who could not completely avoid clouding of the lens during cataract treatment quercetin have developed much less severe than those untreated. Quercetin is commercially red onions (Allium cepa) obtained.
A water-soluble form quercetin (quercetin dihydrate, the brand name: Garde pain Forte) is available in high power, efficiency significantly increased 100-fold increase in absorption compared to other forms of quercetin,
OPC (pycnogenols, etc.):
Pycnogenol also, with the possible sources of grape seeds and skin (Vaccinium vitis idaea) and extract of maritime pine bark (Pinus maritima) is suggested.
Maxogenol is a non-solvent extract OPC American white pine, grapes and other antioxidants in a great tasting sublingual tablet.
routine:
The routine is recommended for cataract. The routine has been proposed a dose of 250 mg / day. The routine is often derived from buckwheat.
Vitamin D:
90-furniture-30A proposed dose of 1000 IU / day of vitamin-D. Vitamin E low levels of vitamin E increase the risk of cataracts up to 3 times. Vitamin E deficiency can cause cataracts in animals. Vitamin E deficiency can result in diabetes, cataracts reversible. Vitamin E can prevent nonenzymatic glycation of the proteins of the lens, which slows the aging of the lens.

Vitamin E acts in synergy with selenium for antioxidant protection of the lens by preventing formation of lipid peroxides. One study showed that vitamin E reduces oxidative damage in vitro rat photo lens 80%. In vivo, vitamin E has been compared to most of the effects of diabetes in cataract formation shown to protect rat lenses. Vitamin E helps prevent damage and other causes, such as radiation and steroids. Blood levels of vitamin E almost double the risk of cataracts compared with a high level of development below.
Vitamin E has both maintain better visual acuity with and without glasses at concentrations of 50 IU / day. At a dose of 400 IU / day, the risk of cataracts is reduced to 56%.
Doses 400-1200 IU / day are offered by natural (isomer d) Vitamin E dry, they are with increasing doses required often with the elderly. The dry form is better absorbed and directed easier for the liver to a study by Dr. Jeffrey Bland process.
Doses at the upper end of the therapeutic range can help prevent cystoid macular edema and the control and other inflammatory side effects of cataract surgery, when taken before and after surgery. Topical application can have pharmacological advantages, too.
A form of vitamin E oil that is available is not diluted with other vegetable oils and is stable (Unique E), therefore. Other supplements of vitamin E with the oil must be refrigerated to prevent rancidity (which could occur in the processing, storage, transport or on the shelf before purchase) that meet the potential benefits of supplementation.
minerals:
calcium:
state with magnesium, calcium recommended moderate consumption. Animals fed a low-calcium diet cataract products. Calcifications in the lens may cause cataracts “snow”. Previous polar cataracts appear early as calcium deposits in life, often as a result of intolerance to dairy products. mishandling of calcium, with deposition in tissues such as the lens on the chromium deficient in calcium or excess, but also magnesium deficient or excess phosphorus or other forming substances acids are activated, food allergies or unstable regulation of blood sugar. Often supplementation of bioavailable calcium moderate as microcrystalline hydroxyapatite (MCHA) can improve the management of calcium and reduce calcium deposits.
calcium pyruvate acts as an inhibitor of glycation (eg, pyruvate-Plus).

chrome:
Chromium is found in whole grain products is lost in the refining of processed foods. Americans are increasingly spent time in this trace element, as they age, because it is “enriched” in processed foods usually find. This is an increased rate of cardiovascular diseases such as hypertension, high cholesterol and diabetes. Factor Glucose Tolerance (GTF) Chromium helps regulate and improve blood sugar levels in the blood of circulation. chromium deficiency is a factor in adult-onset diabetes, compromises the body’s response to insulin, resulting in elevated blood sugar. Smaller amounts than normal 60% were in the lens is both diabetic and senile cataract. a dose of 200 mcg / day is recommended.
copper:
supplementation copper can stimulate the production of superoxide dismutase antioxidant enzyme (SOD), such as zinc levels they are sufficient. Copper concentrations in the lens falling within 10% of normal in cataract formation. Supplementation of 3 mg / day in total nutrition program 50 mg / day of zinc is recommended until no copper toxicity.
iron:
High levels of iron are associated with a lower risk of cortical cataract. excess iron is known, however, to promote free radical pathology, so supplementation moderate to high doses of iron should be avoided, unless a specific need is determined. Where you indicate in absorbable form of iron in the form of chromium picolinate (z Ferrasorb) it is recommended to optimize both absorption and constipation caused by many iron supplements to minimize.
magnesium:
Magnesium must be completed when deficient. Magnesium affects sugar regulation and nerve function and metabolism of vitamin B6. magnesium glycinate is best absorbed form of this mineral macro important and often poor, and thus occur as diarrhea not less well absorbed forms are often at therapeutic doses.
manganese:
Manganese is involved in the third mineral SOD. Its level is reduced to half the normal amount of cataracts. A dose of 20 mg / day, are recommended.
potassium:
to increase potassium intake has also been proposed. Almost all vegetables and fruits are rich in potassium. sweet fruit should not be highlighted (eg, banana and papaya) because sugar is an important risk factor for cataract development risk.
Rare Earth Trace Minerals:

Rare earths are found in small amounts in a position to extend the life of laboratory animals to double. rare earth minerals are associated with longevity in parts of China, where they are on earth, and radiant energy ovens offer local brick. The flexibility of the eye lens is much two physiological associated with longevity.
rare earth minerals are also in the sea, and are concentrated and deposited in shells and coral found in the process of life of marine animals. Le Corail calcium (Ericsson and Otilde; alcamine coral calcium) produit est à basse température pour mineral préserver biologiquement structure électronique actif. Lorsqu’il est placé dans l’eau, minéraux sont les ionizes surface is libérant free electrons produisent qui un effet anti-oxidant dans l’eau (-100 mV to 500 mV relative pair of potentiel d’oxidation typique l’eau du robinet). Dans ce processus, le chlore gazeux dissous (Mortel poison des) est au ionize chlorure (un composant table salt). Les métaux lourds et d’autres sont adsorbées toxins to the surface du Corail ainsi que l’eau de l’mutatis alcalinité atteint environ pH 9.5, associé à une significant reduction cardiovasculaires diseases dans les études dans les wiggle épidémiologiques initialement au Japon, et plus tard reproduits in Europe.

Les Japonais ont the highest longévité de toute nation dans le monde. De tous les Japonais, Okinawa them ONT moins les Cataractes him Dépit de leur site 800 miles south of La Pointe sud des îles Main japonaises, ainsi plus recevant lumière dans toute autre UV-partie du Japon. The Santé et trouve à la remarquable longévité Okinawa a été très attribuée principalement to différente de l’eau dans les liens Récifs trouvée drinking coral, et qui est alcalin anti-oxidant, par à l’eau acide relationship oxidant trouvé dans les Îles du volcaniques reste du Japon. Okinawa Sango Corail is available in sachets, Comme des petits thé bags, ainsi que dans une poudre broyée confinement, pour le Traitement de l’eau. Elle ConvertIt le chlore ions gazeux in chlorure quelques secondes et Eliminate toxins plupart de l’eau par une combinaison de l’electrolysis et l’adsorption. Alcalinité publié, principalement because of calcium carbonates and dominants of magnésium présents dans le Corail, ainsi que le large specter of 72 trace elements, y compris les Terres Rares sont dans l’eau minéraux stables résultant southern chaise periods. The teneur in fournissant Propriétés electron anti-oxydantes, cependant, maximum son atteint in 5-10 minutes, puis une période south dissipe d’environ 24 heures. Coraux d’autres parties du monde ONT the similaires effets, pas mais aussi le Corail puissant That Sango d’Okinawa. Cette eau de Corail est appelé and Ograve, Le lait de l’Océan et oacute; tout comme l’eau laiteuse reputes de haute en teneur minéraux dans les régions Lunes Neuses verter leur est comme connu longévité élevée y Ograve; lait et glaciaire oacute.
selenio:
Le selenio (Se), la suplementación peut stimuler la production de l’antioxidante enzimas glutatión peroxidasa (GPx). El selenio se trouve à la gestión normal de niveaux élèves dans la lentille. La teneur en selenio de lentilles avec des Cataractes est à seulement 15% de la normal. Dans une étude, les animaux nourris avec alimentaire régimen de la ONU en deficiencia de selenio produit Cataractes. El selenio protège la lentille contre les dommages Causas par le Mercurio de méthyle. Le sélénium en combinaison avec la vitamine E, avec laquelle elle est synergique est utilisé par les vétérinaires pour traiter la cataracte chez les chiens, ce qui améliore une vision dans de nombreux cas, la compensation de la périphérie de la lentille. Une dose de 200 à 400 mcg / jour de sélénium est recommandée, et lié organiquement du sélénium, tels que la sélénométhionine est largement préférée. Toxicité Sélénium, a trouvé dans certaines régions du pays où le sol contient du sélénium excessive, peut également augmenter le risque de formation de la cataracte.
Zinc:
Le zinc a une activité antioxydante et stabilise également les membranes cellulaires. les niveaux de zinc plasmatique bas se trouvent chez les personnes atteintes de la cataracte. Les personnes de plus de 65 ans ont tendance à obtenir seulement 2/3 de la RDA pour le zinc, tandis que le vieillissement peut augmenter le besoin de zinc afin de maintenir un équilibre de zinc positif. La carence en zinc peut causer des cataractes chez les humains et les animaux, et est utilisé dans le traitement des deux. Dans une étude sur la truite, plus de la moitié des poissons développés cataractes sur un régime alimentaire déficient en zinc, alors qu’aucune cataractes formées avec la supplémentation en zinc adéquate. Le zinc est nécessaire pour l’activité de la SOD ainsi. Les niveaux de zinc baissent également à moins de 10% des niveaux normaux avec la formation de la cataracte. Le zinc est aussi importante pour le métabolisme de la vitamine A, la santé de l’épithélium de la lentille, et pour le métabolisme du sucre dans le tissu de la lentille. Zinc affecte également la régulation du sucre, la fonction immunitaire et la guérison. Une forme hautement absorbable de la supplémentation en zinc tels que le picolinate de zinc, monomethionine de zinc, ou de l’aspartate de zinc doit être utilisé à des niveaux allant jusqu’à 50, 75 ou 100 mg / jour. L’amélioration de l’acuité visuelle chez les patients de la cataracte a été rapporté de 20/200-20/25 dans aussi peu que 6 mois en utilisant un supplément nutriments multiples contenant du zinc.
Protéines: Les acides aminés, des polypeptides, des enzymes, des extraits glandulaires:
La lentille de l’œil est la protéine la plus concentrée dans le corps. Les dommages causés aux acides aminés formant les protéines du cristallin se produit de plusieurs façons. Photo-oxydation des acides aminés aromatiques, en particulier le tryptophane, est due à l’exposition à la lumière ultraviolette en excès. Gonflement de la lentille augmente également la sensibilité aux dommages. glycosylation non enzymatique des acides aminés est une troisième source importante de dommages. Dans ce processus, le glucose est lié de façon irréversible aux protéines rendant plus sensibles à d’autres dommages, tout en interférant avec sa fonction normale. Le taux de glycosylation est réduite lorsque la régulation du sucre dans le sang est améliorée. Le pourcentage de protéine insoluble est relativement stable à environ 3,3% jusqu’à environ 50 ans, mais monte à environ 9% dans les années 50, 16% dans les années 60, 17% dans les années 70, et 40% dans les années 80 en moyenne. Les inhibiteurs de glycosylation comprennent: carnosine et de pyruvate de calcium.
En général, l’apport ou la digestion des protéines insuffisante peut causer des cataractes. La plupart des Américains, à l’exception des végétariens, mais manger 2 à 3 fois trop de protéines. Enzyme supplémentation peut aider à la digestion des protéines, l’amélioration de la disponibilité des acides aminés, ainsi que l’aide de désintoxication et de réduire les processus inflammatoires. Supplémentation de bromélaïne a été recommandé.
cystéine:
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. Dog. 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.

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