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Research based supplements for improving eyesight


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#1 Lufega

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Posted 26 July 2009 - 10:34 PM


These are just a collection of statements and studies I found while researching alpha-1-antitrypsin deficiency (A1AT) and it's relationship to decreased levels of glutathione. Doing this, I found there's also a relationship b/w A1AT, corneal problems and antioxidants. I've also been reading into improving conditions like myopia and astigmatism and found some studies that make important implications.

Supplements discussed: Magnesium, Zinc, NAC, Glisodin, Vitamin E, Pycnogenol, Taurine. I omitted vitamin A, Lutein and the "xathins" as these have already been discussed in this board but are just as important.

Zinc and Myopia

>Myopia is a refractive error where there is antero-posterior elongation of the orbit causing light to focus in front of the retina.

Prevention of axial elongation in myopia by the trace element zinc.

The effect of the trace element zinc on the change in the axial length and diopters and the variations of activities of superoxide dismutase (SOD) and nitric oxide synthase (NOS), and the content of NO in the retino pigmental epithelium choroid homogenate of the myopic eyes in form-sense-deprived chicks were studied. The results show that zinc can inhibit the elongation of axis oculi and increase the diopters in myopia. Meanwhile, the activities of SOD and NOS and the content of NO are significantly increased compared with the model group, indicating that zinc can be used to prevent and treat myopia to a certain extent.


>SOD is increased in myopia---> increased oxidative stress? Why??

Effects of zinc and copper metabolism in highly myopic patients.

There is considerable evidence supporting a link between abnormalities in zinc and copper metabolism and some disorders of the retinal pigment epithelium. Anatomical studies in highly myopic eyes show important changes in this retinal layer. We measured the blood concentrations of zinc and copper and the urine concentration of copper in different groups of highly myopic patients from Caucasian and African populations, and in highly myopic patients with retinal detachment. In the Caucasian myopic groups, many patients showed high levels of zinc and low levels of copper in serum. In the high myopic group with retinal detachment, serum zinc and copper concentrations were significantly elevated. The importance of our findings and their connection to the retinal pigment epithelium is discussed.


>Can anyone access this study? Is copper/zinc low or not being used by cells for connective tissue repair? Is it high, being pro-oxidant and activating metalloproteinases and destroying connective tissue?

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Keratoconus and Magnesium

The possible relationship between keratoconus and magnesium deficiency.

The cause of keratoconus is unknown. However, an earlier report demonstrated magnesium deficiency in keratoconus patients, and suggested that magnesium deficiency could pathologically affect the mechanisms of the cornea. Experimental and clinical papers concerning a possible relationship between keratoconus and magnesium deficiency were reviewed. These studies have demonstrated molecular and cellular alterations specific to the keratoconic cornea, including: thinning and fragmentation of membranes, degenerated cells and collagen fibres, swelling of the mitochondria, and biochemical abnormalities in protein synthesis. Similar alterations have reportedly been induced by magnesium deficiency. This review suggests a possible relationship between the specific keratoconic disorders and the alteration induced by magnesium deficiency at the intracellular and extracellular levels. Although the etiology of keratoconus is still unknown, this paper may give some new ideas for further experimental and clinical studies on the etiology of keratoconus.


>Astigmatism is considered the early beginnings of keratoconus since they both involve corneal changes. Magnesium has therapeutic implications here as well.

>The vitreous humor is composed of water and hyaluronic acid among other things. Hyaluronic acid formation is dependent, in part, on magnesium and zinc. Intraocular pressure is maintained between 10-20 mm Hg by a combination of Vitreous humor production and drainage. I am magnesium deficient. My intraocular pressure is 6 in the left eye and 10 in the right eye. Both are low.


Corneal changes in magnesium-deficient rats.

PURPOSE: The purpose of the current study is to investigate the cornea in magnesium (Mg) deficiency and elucidate the local function of trace elements. METHODS: After delivery, mother Wistar Kyoto rats were fed a low Mg diet containing 0.1 mg Mg/100 g diet with all other nutrients and distilled and deionized water. Infant rats were suckled by their mothers for 21 days and then fed the same Mg-deficient diet. Control mother rats were fed commercial rat pellets containing 24 mg Mg/100 g diet and all other nutrients. The corneas were examined by electron microscopy at 6 weeks of age. RESULTS: In the Mg-deficient rats, serum Mg levels were significantly lower and calcium (Ca) levels higher than in the control rats. The corneas of Mg-deficient rats showed decreased microvilli and microplicae in the epithelial cells of the most superficial layer, increased mitochondria with abnormal shapes in the basal cells in the epithelium, condensed chromatin in the nuclei of the basal cells, and high density deposits and macrophage-like cells in the subepithelium of the stroma. Mg-deficient rats had pentagonal and square endothelial cells. CONCLUSION: Since Mg2+ has biologic functions including structural stabilization of protein, nucleic acids, and cell membranes, Mg deficiency may induce changes in the corneal surface and nuclei of corneal epithelial and endothelial cells. These disturbances may interfere with protection from infections, foreign bodies, dryness, and direct exposure to air. Thus, Mg is essential for the cornea to maintain normal structure and function.



--------------------------

http://www.opticiano...spx?ItemID=2103 (Great site for anything eye-related)

"Keratocononus, is a degenerative, non-inflammatory disorder of the cornea. It is characterised by central and para-central corneal stromal thinning and subsequent conical ectasia. This conical distortion of the cornea results in irregular astigmatism with associated reduction in visual performance. It typically presents in adolescence and progresses in a variable manner."

"The occurrence of keratoconus is usually an isolated condition, but it has been reported to occur with increased frequency in a number of ocular and systemic disorders.. Ocular associations include vernal disease, retinitis pigmentosa, blue sclera, aniridia, ectopia lentis and Leber’s congenital amaurosis. Systemic associations include atopy, magnesium deficiency, Down’s syndrome, Turner syndrome, connective tissue disorders (such as Marfan’s, Ehlers-Danlos, osteogenesis imperfecta and pseuodoxanthoma elasticum), mitral valve prolapse, Laurence-Moon-Biedl syndrome, Rieger’s syndrome and neurofibromatosis."

"It is, therefore, likely that the development of keratoconus is the final common pathway for several different disorders."

>So, if you have keratoconus or even astigmatism, I would be searching hard for some kind of ocular or systemic problem. This also means, if you can find a way to stabilize or reverse the condition, it will also have a positive effect on the disease state.

>This is where it gets good..

"Laboratory studies have indicated that keratoconic corneas show signs of increased activity of proteinase enzymes and a reduced activity in the proteinase inhibitors found within the cornea. This imbalance between corneal metalloproteinases (MMP) and its inhibitors (tissue inhibitors of metalloproteinases or TIMPS) can reduce the various extracellular matrices and proteins within the cornea, resulting in stromal thinning and breaks in Bowman’s layer/epithelial basement membrane. Enzyme proteinase inhibitors found to be reduced in keratoconic corneas include α1-proteinase inhibitor (this is the same as alpha-1-antitypsin. A deficiency of this can be treated with NAC), α2-macroglobulin and TIMP-1.17-19 These deficits may lead to an increase in the degradative enzymes present, including cathepsins, trypsins, and MMPs, including MMP-1, MMP-2 and MMP-13.20-23 Levels of TIMP-1 are also reduced by the presence of peroxynitrate, a cytotoxic by-product from the nitric oxide pathway. As yet, the cause for this increased proteinase activity in keratoconic corneas is not known. It may be related to a state of increased oxidative stress found within the keratoconic cornea.

" It is known that as the cornea is responsible for absorbing most of the UVB light that enters the eye, it has to process the oxygen-free radicals produced. Oxygen-free radicals or reactive oxygen species (ROS) are high energy molecules that can build up and cause oxidative damage to cells by reacting with proteins, DNA and membrane phospholipids.26 In addition, ROS produce aldehydes via ROS-mediated lipid peroxidation. These aldehydes can be destructive to cells by interfering with proteins and DNA, altering signal transduction and gene expression. Normally the cornea eliminates ROS by various antioxidant enzymes, including superoxide dismutase, (SOD), catalase, glutathione reductase and glutathione peroxidise and protects itself from lipid peroxidation damage by glutathione S-transferase and aldehyde dehydrogenase enzymes (ALDH3). It has been shown that keratoconic corneas are deficient in SOD, catalase and ALDH3. These deficits may cause a significant build up in malondialdehyde (MDA) a cytotoxic aldehyde from both the lipid peroxidation and nitric oxide pathways."

>Part 2 of the article talks about treatment and it goes off in the typical profit-minded fashion using lasers and other costly, invasive procedures. It says nothing about restoring magnesium status or increasing glutathione, SOD and catalase defenses. So NAC and Glisodin have important implications here. There are more studies that support this.

Superoxide dismutase isoenzymes in the normal and diseased human cornea.

PURPOSE: The human cornea, a tissue much exposed to oxidative stress, is rich in extracellular superoxide dismutase (SOD). In this study, the contents and distributions of the SOD isoenzymes in the normal human cornea were compared with those in corneas affected by keratoconus and bullous keratopathy. METHODS: The central and peripheral parts of normal human corneas were analyzed separately. Central corneal buttons were obtained from patients with keratoconus and bullous keratopathy who were undergoing primary keratoplasty or retransplantation. SOD enzymatic activities were determined by a direct spectrophotometric method, and extracellular SOD and the cytosolic Cu- and Zn-containing SOD (CuZn-SOD) proteins were determined with ELISA and studied with immunohistochemistry. RESULTS: The total SOD content, and particularly the extracellular SOD content, was lower in the central than in the peripheral normal cornea. CuZn-SOD and extracellular SOD were demonstrated in all three corneal layers. CuZn-SOD was found in cells, whereas extracellular SOD appeared to be localized on cell surfaces, in basal membranes, and in the stroma. In keratoconus, corneal levels of extracellular SOD were half those in the control corneas, whereas CuZn-SOD and the mitochondrial Mn-containing SOD levels were normal. In bullous keratopathy, apart from edematous dilution, SOD isoenzyme levels were essentially normal. In a remarkable finding, the same pattern in SOD isoenzyme levels as in the original disease was also found at retransplantation. CONCLUSIONS: Extracellular SOD and CuZn-SOD show markedly different distribution patterns within the human cornea. Extracellular SOD activity in the central cornea is halved in keratoconus, compared with that in normal control corneas. The finding of a similar reduction at retransplantation in keratoconus suggests reduced corneal extracellular SOD synthesis in cells of the host as a cause of the low enzyme levels.


Increased levels of catalase and cathepsin V/L2 but decreased TIMP-1 in keratoconus corneas: evidence that oxidative stress plays a role in this disorder.
CONCLUSIONS: Keratoconus corneas have elevated levels of cathepsins V/L2, -B, and -G, which can stimulate hydrogen peroxide production, which, in turn, can upregulate catalase, an antioxidant enzyme. In addition, decreased TIMP-1 and increased cathepsin V/L2 levels may play a role in the matrix degradation that is a hallmark of keratoconus corneas. The findings support the hypothesis that keratoconus corneas undergo oxidative stress and tissue degradation.


Edited by Lufega, 26 July 2009 - 10:54 PM.

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#2 Lufega

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Posted 26 July 2009 - 10:34 PM

Vitamin E

Effect of vitamin E on the cornea in keratoconus


>There's no abstract for this study. But another study said this:

[New developments in the treatment of keratoconus]

The results of penetrating and lamellar keratoplasty in patients with keratoconus are communicated. In penetrating keratoplasty the graft healed clear in 93.5% of the cases treated (266 operations). A new method of surgical treatment of acute total keratoconus by "biological covering" with a lamellar corneal graft is proposed, which enables the process to stabilize, the eye to be saved, and in isolated cases a visual acuity of 0.5 or more to be achieved. The authors describe a new trend in studying the pathogenesis of keratoconus on the basis of biochemical investigations of the damaged areas of the cornea (lowering of the activity of enzymes of the antioxidant system and reduction in tocopherol content). A new method of conservative treatment for the initial forms of keratoconus using phonophoresis of Vitamin E (tocopherol) is proposed on the basis of the data gathered in the biochemical investigations.


>So vitamin E is implicated, I'm just not sure how.

Remarkable success of antioxidant treatment (selenomethionine and vitamin E) to a 34-year old patient with posterior subcapsular cataract, keratoconus, severe atopic eczema and asthma. PMID: 3389102 [PubMed - indexed for MEDLINE]


>This is another study with no abstract. Glutathione is again implicated, probably a decrease in function.

[Glutathione antioxidant system in keratoconus]

[Article in Russian]

Titarenko ZD, Levitskiĭ AP.


>Finally, this study tries to link everything together:

Everett Kinsey lecture. The elusive causes of keratoconus: a working hypothesis.

PURPOSE: Keratoconus is a diseasethat has been recognized clinically for many years. However, it is only more recently that a better understanding has been achieved in the area of keratoconus pathogenesis. The purpose of this paper is to summarize the completed research, review ongoing studies, and present a hypothesis for keratoconus pathology. METHODS: We used immunochemistry and molecular techniques to characterize keratoconus corneas. RESULTS AND CONCLUSIONS: Our hypothesis attempts to incorporate many of the recognized biochemical and molecular abnormalities found in the keratoconus corneas. Our hypothesis states: 1) there is abnormal processing of the free radicals and superoxides within the keratoconus corneas; 2) there is a build-up of destructive aldehydes or peroxynitrites within the corneas; 3) the cells that are damaged irreversibly undergo the process of apoptosis; and 4) the cells that are damaged reversibly undergo wound healing or repair. As part of the wound healing process, various degradative enzymes and wound healing factors are upregulated, which leads to focal areas of corneal thinning and fibrosis. Future studies will be directed to testthis working hypothesis and determine if these theories are valid.

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Taurine

Roles in vision and cataracts.

"A cataract is a clouding of the normally clear lens of the eye. It impairs vision, though today visual loss is often reversible by surgical measures. Cataract formation is speculated to be due largely to oxidation of protein and glycosylation of proteins in the lens of the eye. A lack of the antioxidant nutrients (taurine, Vitamin A, carotenoids, Vitamin C, and Vitamin E) is major factors for the development of cataracts. Taurine acts as an antioxidant by preventing changes in the levels of glutathione (a selenium-requiring substance), ATP, and insoluble proteins -- factors that predispose the formation of cataracts. It also prevents oxidative damage by scavenging hydroxyl radicals. Through a reaction with a sugar-based molecule, taurine and hypotaurine reduce the glycation and denaturation of lens protein "

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Pycnogenol

Recycles Vitamin C+E and endogenous antioxidant systems (such as SOD, catalase and glutathione)

Pycnogenol® increases anti-oxidative enzyme concentrations in the retina of rats, suggesting a lower risk for retinopathy and cataract formation.

Effects of Low-Carbohydrate Diet and Pycnogenol® Treatment on Retinal Antioxidant Enzymes in Normal and Diabetic Rats.

Pycnogenol® either alone or in combination with other antioxidants stimulates antioxidant enzyme activities in the retina of diabetic rats.

Effects of Antioxidant Treatment on Normal and Diabetic rat retinal enzyme activities.

Pycnogenol® protects retina of the eye against damage caused by oxidative stress. The effect is more pronounced when compared to other antioxidant bioflavonoids.

Pycnogenol® enhances the effects of other antioxidants like Coenzyme Q10 when combined together.

The anti-melanogenic effect of pycnogenol by its anti-oxidative actions.

Pycnogenol is a natural plant extract from pine bark that contains compounds that have anti-oxidative, free-radical scavenging properties. In this work, utilizing cultured B16 melanoma cells (B16 cells), pycnogenol was investigated for its ability to inhibit tyrosinase activity and melanin biosynthesis. We also examined the anti-oxidative power of pycnogenol by measuring its suppressive effect against peroxynitrite (ONOO-), superoxide (.O2), nitric oxide (NO.), and hydroxyl radical (.OH)-scavenging activities using an electron spin resonance spectrometer. Results show that pycnogenol had a strong anti-tyrosinase activity and suppressed melanin biosynthesis. Further, our results showed that through its anti-oxidative properties, pycnogenol suppressed .O2) NO., ONOO-, and .OH in in vitro assays, and reactive species, ONOO-, .O2, and NO., while up-regulating the reduced glutathione/oxidized glutathione ratio in B16 cells. Based on the findings, we propose that pycnogenol exerts anti-melanogenic activity via its anti-oxidative actions.


Edited by Lufega, 26 July 2009 - 10:34 PM.


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#3 Lufega

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Posted 27 July 2009 - 12:44 AM

Keratoconus involves increased oxidative stress, apoptosis and magnesium deficiency as well as deficiency of metalloproteinase inhibitors like A1At and a decrease in antioxidants. I found a study that linked magnesium with all the other factor. This is amazing.

Effects of long-term dietary intake of magnesium on oxidative stress, apoptosis and ageing in rat liver.

Martin H, Uring-Lambert B, Adrian M, Lahlou A, Bonet A, Demougeot C, Devaux S, Laurant P, Richert L, Berthelot A.
Laboratoire de Toxicologie Cellulaire, EA 2SBP, UFR des sciences médicales et pharmaceutiques, Besançon, France. helene.martin@univ-fcomte.fr
In the present study, we investigated the effect of long-term dietary Mg intake on the rate of oxidative stress, apoptosis and ageing in rat livers. To address this issue, rats were fed diets containing either a moderately deficient (0.15 g Mg/kg diet), a standard (0.8 g Mg/kg diet) or a high (3.2 g Mg/kg diet) Mg dose for two years. It is noteworthy that a higher percentage of animal mortality was observed in the lowest Mg diet, as compared to the other groups. Oxidative stress and antioxidant status were evaluated by measuring different enzyme activities, among which glutathione peroxidase activity was significantly reduced when Mg content was decreased in the diet. Moreover, we obtained an activation of caspase-3 and a higher lipid peroxidation in the Mg-deficient group, as compared to the Mg standard group, while no changes in Mg-supplemented group were observed, in accordance with our previously published data in primary cultures of rat hepatocytes (Martin et al., J Nutr 2003). Telomere shortening was measured in rat livers, as a marker of ageing. We found that telomere length was decreased in old animals, as compared to young animals confirming that telomere shortening correlated well with ageing events. Moreover, in old animals, we obtained a decrease of telomere length in the Mg-deficient group, as compared to the other groups. Taken together, our results show that a long-term chronic Mg deficiency led to oxidative stress, apoptosis and an acceleration of ageing in rat livers.



#4 PYER

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Posted 22 January 2010 - 05:26 PM

Keratoconus involves increased oxidative stress, apoptosis and magnesium deficiency as well as deficiency of metalloproteinase inhibitors like A1At and a decrease in antioxidants. I found a study that linked magnesium with all the other factor. This is amazing.

Effects of long-term dietary intake of magnesium on oxidative stress, apoptosis and ageing in rat liver.

Martin H, Uring-Lambert B, Adrian M, Lahlou A, Bonet A, Demougeot C, Devaux S, Laurant P, Richert L, Berthelot A.
Laboratoire de Toxicologie Cellulaire, EA 2SBP, UFR des sciences médicales et pharmaceutiques, Besançon, France. helene.martin@univ-fcomte.fr
In the present study, we investigated the effect of long-term dietary Mg intake on the rate of oxidative stress, apoptosis and ageing in rat livers. To address this issue, rats were fed diets containing either a moderately deficient (0.15 g Mg/kg diet), a standard (0.8 g Mg/kg diet) or a high (3.2 g Mg/kg diet) Mg dose for two years. It is noteworthy that a higher percentage of animal mortality was observed in the lowest Mg diet, as compared to the other groups. Oxidative stress and antioxidant status were evaluated by measuring different enzyme activities, among which glutathione peroxidase activity was significantly reduced when Mg content was decreased in the diet. Moreover, we obtained an activation of caspase-3 and a higher lipid peroxidation in the Mg-deficient group, as compared to the Mg standard group, while no changes in Mg-supplemented group were observed, in accordance with our previously published data in primary cultures of rat hepatocytes (Martin et al., J Nutr 2003). Telomere shortening was measured in rat livers, as a marker of ageing. We found that telomere length was decreased in old animals, as compared to young animals confirming that telomere shortening correlated well with ageing events. Moreover, in old animals, we obtained a decrease of telomere length in the Mg-deficient group, as compared to the other groups. Taken together, our results show that a long-term chronic Mg deficiency led to oxidative stress, apoptosis and an acceleration of ageing in rat livers.



******************************************************************************

PYER

Eyesite suplements can be helpful but only to a point.

Once again, I want to pin point a problem with relying entirely on a chemical basis to eyesite improvement or other physical ailments.

I know that the human psyche has the potential to cure eyesite through intensive therapy from within to the external character level in consciousness.
The reason for humans to encounter difficulty in eyesite cures is primarily due to natal disorders, and/or adult frustrations which humans think it's not important to have to deal with or balance. It takers facing the youth of oneself in tune with nature and in meditation for what it is like practice which can be boring to the average human. How do you change this? Through psychological adjusting.
I fear the future super-progress in drug therapy in the shoes of the less fortunate in self knowledge of what is illusion, and then what is delusion and what it can to the human body in the long run!

Antonio
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#5 Lufega

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Posted 25 May 2010 - 11:18 PM

Update: Studies found elevated levels of cathepsin G (a serine protease) in the eyes of patients with keratoconus. Searching for "keratoconus" and "cathepsin" pulls up 18 studies in PUBMED.


Cathepsin G is inhibited (very well, it seems) by boswellic acids.

Identification of human cathepsin G as a functional target of boswellic acids from the anti-inflammatory remedy frankincense.

Institute of Pharmaceutical Chemistry, Johann Wolfgang Goethe-University Frankfurt, Frankfurt, Germany.
Abstract

Frankincense preparations, used in folk medicine to cure inflammatory diseases, showed anti-inflammatory effectiveness in animal models and clinical trials. Boswellic acids (BAs) constitute major pharmacological principles of frankincense, but their targets and the underlying molecular modes of action are still unclear. Using a BA-affinity Sepharose matrix, a 26-kDa protein was selectively precipitated from human neutrophils and identified as the lysosomal protease cathepsin G (catG) by mass spectrometry (MALDI-TOF) and by immunological analysis. In rigid automated molecular docking experiments BAs tightly bound to the active center of catG, occupying the same part of the binding site as the synthetic catG inhibitor JNJ-10311795 (2-[3-[methyl[1-(2-naphthoyl)piperidin-4-yl]amino]carbonyl)-2-naphthyl]-1-(1-naphthyl)-2-oxoethylphosphonic acid). BAs potently suppressed the proteolytic activity of catG (IC(50) of approximately 600 nM) in a competitive and reversible manner. Related serine proteases were significantly less sensitive against BAs (leukocyte elastase, chymotrypsin, proteinase-3) or not affected (tryptase, chymase). BAs inhibited chemoinvasion but not chemotaxis of challenged neutrophils, and they suppressed Ca(2+) mobilization in human platelets induced by isolated catG or by catG released from activated neutrophils. Finally, oral administration of defined frankincense extracts significantly reduced catG activities in human blood ex vivo vs placebo. In conclusion, we show that catG is a functional and pharmacologically relevant target of BAs, and interference with catG could explain some of the anti-inflammatory properties of frankincense.



#6 Cless986

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Posted 26 May 2010 - 02:35 AM

Zinc and Myopia

>Myopia is a refractive error where there is antero-posterior elongation of the orbit causing light to focus in front of the retina.

QUOTE
Prevention of axial elongation in myopia by the trace element zinc.

The effect of the trace element zinc on the change in the axial length and diopters and the variations of activities of superoxide dismutase (SOD) and nitric oxide synthase (NOS), and the content of NO in the retino pigmental epithelium choroid homogenate of the myopic eyes in form-sense-deprived chicks were studied. The results show that zinc can inhibit the elongation of axis oculi and increase the diopters in myopia. Meanwhile, the activities of SOD and NOS and the content of NO are significantly increased compared with the model group, indicating that zinc can be used to prevent and treat myopia to a certain extent.


>SOD is increased in myopia---> increased oxidative stress? Why??

QUOTE
Effects of zinc and copper metabolism in highly myopic patients.

There is considerable evidence supporting a link between abnormalities in zinc and copper metabolism and some disorders of the retinal pigment epithelium. Anatomical studies in highly myopic eyes show important changes in this retinal layer. We measured the blood concentrations of zinc and copper and the urine concentration of copper in different groups of highly myopic patients from Caucasian and African populations, and in highly myopic patients with retinal detachment. In the Caucasian myopic groups, many patients showed high levels of zinc and low levels of copper in serum. In the high myopic group with retinal detachment, serum zinc and copper concentrations were significantly elevated. The importance of our findings and their connection to the retinal pigment epithelium is discussed.


>Can anyone access this study? Is copper/zinc low or not being used by cells for connective tissue repair? Is it high, being pro-oxidant and activating metalloproteinases and destroying connective tissue?


sorry if its a stupid question, but I dont get the article...so, are you saying that high levels of zinc can impair my eyes? I have myopia.
almost 4.0

#7 Lufega

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Posted 26 May 2010 - 05:07 AM

Cless,

I have those same questions. For that, I want to read the full study. Now we understand something about mineral status in the CNS. Just because serum levels of zinc are high, it doesn't mean the values are high in the CNS, where its needed by the eyes.

#8 GhostBuster

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Posted 26 May 2010 - 01:02 PM

Cless,

I have those same questions. For that, I want to read the full study. Now we understand something about mineral status in the CNS. Just because serum levels of zinc are high, it doesn't mean the values are high in the CNS, where its needed by the eyes.


Anecdote:

I am myopic and the last time I checked my sight, it had gone worse. But the curious thing was that with help of stronger lenses I was able to see all the letters that were shown to me. If I recall it right, I was tested upto 1.7. Before I was seeing barely normal even after corrections. Lately I have been taking lutein, blueberries, magnesium, zinc, vitamin E & K and others and so it makes me wonder if those have had an effect on my optimal visual capacity...

Edited by GhostBuster, 26 May 2010 - 01:06 PM.


#9 david ellis

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Posted 26 May 2010 - 03:30 PM

Cless,

I have those same questions. For that, I want to read the full study. Now we understand something about mineral status in the CNS. Just because serum levels of zinc are high, it doesn't mean the values are high in the CNS, where its needed by the eyes.


Anecdote:

I am myopic and the last time I checked my sight, it had gone worse. But the curious thing was that with help of stronger lenses I was able to see all the letters that were shown to me. If I recall it right, I was tested upto 1.7. Before I was seeing barely normal even after corrections. Lately I have been taking lutein, blueberries, magnesium, zinc, vitamin E & K and others and so it makes me wonder if those have had an effect on my optimal visual capacity...


It is very interesting that high zinc folks have some vision problems. The Age-Related Eye Disease study(AREDS) comes up with a recommendation to take 69.6 mg/day of zinc. This difference will not be reconciled soon.

#10 Mike Coza

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Posted 27 February 2012 - 08:15 AM

You can improve your eyesight vision through exercises if you do this regularly and it is more effective if you eat healthy foods that are rich in vitamin A, C, and E. I had also undergo in this natural vision correction, before I had a myopia but after this treatment my vision slowly become clear. At first I doubt the effectiveness of it but when I try it I was amazed. I can now see much clearly even in a distance. by the way, here is the link of the said natural vision correction

http://bit.ly/HowGetRidOfYourGlasses - Improve Vision
It will help you to get rid of your eyeglasses.
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#11 noos

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Posted 07 December 2012 - 05:50 AM

You can improve your eyesight vision through exercises if you do this regularly and it is more effective if you eat healthy foods that are rich in vitamin A, C, and E. I had also undergo in this natural vision correction, before I had a myopia but after this treatment my vision slowly become clear. At first I doubt the effectiveness of it but when I try it I was amazed. I can now see much clearly even in a distance. by the way, here is the link of the said natural vision correction

http://bit.ly/HowGetRidOfYourGlasses - Improve Vision
It will help you to get rid of your eyeglasses.

This looks as spam. User has only 2 posts on same subject.
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#12 meatwad_is_immortal

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Posted 03 January 2013 - 10:42 PM

I have extensive experience with improving eyesight.

When I was 19, my prescription was -2.75 which is bordering on unable to find your toothbrush if there is only a nightlight - unable to function :P.

3 years later, I was accepted to Air Force pilot training with a diopter prescription of -0.75 which put me at the minimum 20/50 visual accuity.

I also passed my driver's and private pilot tests with "no corrective lenses."

I'll be as brief as I can here: Bad eyesight is caused by bad diet and bad habits.

Western diet and "medicine" tend to ruin the small intestine and prevent nutrient uptake. As well, the diet is poor in bio-available minerals. This causes lack of proper function in areas of the body that rely on strong anti-oxidant action and involve complex constructions. The eye....

Second, studying or using a computer too close to the face causes the lense of the eye to spend too much time in the "football" shape. Within a few years, this shape becomes semi-permanent and the muscles can no longer pulll the lense flat enough to see in the distance without glasses. This is myopia.

Opthamologists will tell you ANYTHING other than the truth, which is that diet and habit are the cause. They sell you glasses or contacts and your fate is sealed because those two things will make your vision worse over time and recovery becomes difficult to impossible.

To improve myopia, you must first eliminate the habits you have and change to a 75% fresh vegetable diet with no wheat, little dairy and basically heath nut bent.

Next, you need to NEVER wear your (myopia) corrective lenses to read, use the computer or otherwise do anything within arm's length. Get a selection of reading glasses ($10 at wallmart) in 1.0, 2.0 and 3.0 and use them whenever you read. Use whichever strength makes it *just barely* possible to focus on what you are doing with bright overhead light.

Spend 1 hour (cummulative) per day staring outside at the horizon while relaxing your eyes and blinking - NEVER SQUINT - until you get an increase in focus. This will be fleeting at first but improve over time. Your eye muscles behave like other muscles and get sore, refuse to work right with overwork.. etc.

The more time you spend working them hard to focus, the more effect you will see.

Convince your evil Opthomologist to give you a prescription that is .5 diopters less strong than you need to see 20/20. Do this every 6 months (and keep up the exerises) and you will get better.

To do what I did and eventually get back to 20/20 takes MORE DEDICATION than most humans posses. Read that again.

Chances are that you will not succeed because you will not put in the effort for the roughly 3 years that it took me. BTW, I am back to -1.0 because I got lazy and ruined my small intestine, but I am BACK on the wagon now :P

Good luck.

Anecdotally, I went camping once and got to eat several POUNDS of wild blueberries for 3 straight days. My eyesight improved by a solid 0.5 diopters for REAL, but the improvement faded after 3 days being home. Drat.

Edited by meatwad_is_immortal, 03 January 2013 - 10:45 PM.

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#13 bariotako

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Posted 17 April 2018 - 09:45 AM

Astigmatism is considered the early beginnings of keratoconus since they both involve corneal changes. Magnesium has therapeutic implications here as well."

 

 

 

25% of the population  have  astigmatism 

 

The prevalence of keratoconus  is  betwenn 1/500  and 1 / 100 000 

 

 

You probably have keratoconus and you want other people to have your shity disease :)   sorry but you  have a RARE DISEASE, you are probably ALONE , now get out from this website :) 


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#14 bariotako

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Posted 23 April 2018 - 04:12 PM

"Pointless , timewasting" 

 

haha i was right, you  indeed have keratoconus :)


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#15 jroseland

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Posted 27 March 2022 - 11:02 AM

SKQ1-powered Visomitin is my favorite, alas it's become Unobtainium. In this interview, The Blind Biohacker makes the case that addressing trauma stimulates neuroplasticity which can address vision issues...

 

1*dMCyn3g_uncPrA7edRiT6w.jpeg

Listen: The Blindness-Beating Biohacker - Victor Mifsud Interview






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