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Cruelly ignored, but NOT forgotten
The whole world believes the eye profession treats all eye diseases. But although they had the means, they never wanted to treat cataract and still do not want to. Despite the fact that effective eyedrops had been developed by biochemists around the world since 1980, eye doctors still only want to perform cataract surgery, and destroy the natural lens even though cataracts could have been treated.
Few people are aware that the eyedrops in the list below were ever developed. But don't take my word for it, please look them all up on the Internet. They each clear the lens by different mechanisms. Each of them was a bright ray of hope for humanity. Most of them could have put an end to cataract surgery for good, but one after another, all of them were cruelly ignored. Despite their success in the lab, in animal models or even human trials, none of them were ever offered to cataract patients by the eye profession, as they should have been. Consequently, the only option available today continues to be surgery.
I often wondered whether any of the ophthalmologists appearing in the glowing advertisements for cataract surgery on the Net have had cataract surgery themselves. At least, one rarely hears about it. Probably, they are more reluctant than we are, since they know that a plastic IOL is inferior to their natural eye lens, and they know the risks.
Of course, everybody who is facing cataract surgery would rather avoid it, and clear their vision by treating their cataracts with eyedrops which do not destroy the integrity of their eye. Since many such eyedrops already existed, this means that cataract surgery is an unnecessary operation.
Even if the surgery is successful, all remaining power of accommodation is lost, so if a monofocal IOL is implanted, several pairs of eyeglasses will be needed to cope with near and distance vision. Also, due to the loss of accommodation, multifocal eyeglasses can no longer be used, so there may be trouble going up or down stairways. All this could have been avoided by the eyedrops in the list, which preserve the power of accommodation. As if that weren't enough, surgery carries risks of inferior outcomes and secondary complications.
Yet in the world today, many people with cataracts (around 35 million) do not have access even to surgery. The prior existence of these non-surgical eyedrops therefore also means that 35 million people are needlessly blind. Here is the list:
1. Reduced glutathione - a S=S bond breaker (Japan, 1960)
2. Esters that restore optical clarity (Benedek at al., MIT, 1980)
3. Bifunctional molecules that restore optical clarity "in lieu" of the natural chaperone, alpha-crystallin (Muthukumar, University of Massachusetts, 2017)
4. N-acetylcarnosine (NAC) (Babizhayev, Russia, 1996)
5. Organic germanium (G-132, G-385, etc.) - an AGE solubilizer (Nakamura et al., Kitasato University, Japan, 2000)
6. Lutein - a "surrogate" carotenoid (previously available on the Internet, but no longer)
7. Aldose reductase inhibitors (Kinoshita, 2010, USA)
8. C-KAD - a glycation inhibitor plus chelating agent (Chakshu Pharmaceuticals, 2002, USA)
9. NACA (N-acetylcysteine amide) - a reduced glutathione precursor (Ercal, University of Missouri, 2016)
10. Lanosterol and 25-hydroxycholesterol - "chaperone" stabilizers (Kang Zhang, USA, 2015)
11. Rosmarinic acid - an AGE crosslink breaker (Glikman et al, University of Tel Aviv, Israel, 2018)
This list is not exhaustive.
There are some limitations. Firstly, reduced glutathione works only in about 50% of cases. Next, although NAC can still be bought on the Internet, it is not likely to improve cataract unless combined with a chelating agent such as EDTA, as it was in C-KAD. Finally, lanosterol or other sterols are not likely to work unless some unmodified alpha-crystallin remains in the lens, as there would be in early cataract. But the other agents on this list do not have any such limitations. They reversed advanced cataracts too, and are desperately needed today. Anybody who reads this post and can do something about this tragic situation, please reply.
ALMOST TWO YEARS LATER, AND STILL NOTHING HAS BEEN DONE!!!
Rosmarinic Acid Restores Complete Transparency of Sonicated Human Cataract Ex Vivo and Delays Cataract Formation In Vivo Chemerovski-Glikman, M., Mimouni, M., Dagan, Y. et al.
This article appeared in the June, 2018 edition of the scientific journal, Nature.
Quote from this article:
Taken together, our results support the concept that aggregation inhibition may provide a pharmacological treatment strategy for cataract, and highlight rosmarinic acid as a promising potential for palliative treatment of cataract, the leading cause of blindness worldwide. Data obtained from carefully designed and conducted future clinical studies may provide a strong foundation for design of the proper treatment regimen, dosage and duration. We hope that in the near future this promising pharmacological treatment will provide a safe, inexpensive and easily-accessible therapy for cataract.
As my cataracts continue to worsen with no hope of treatment in sight, I called a professor in the university department where this work had been carried out. I asked him whether there had been any move towards an eyedrop based on this momentous discovery.
Q: What is the status of your application for an anticataract eyedrop based on rosmarinic acid?
A: Why don't you have surgery?
Q: Why do you ask me that question?
Silence of several seconds
A: You know, I'm not an eye doctor.
Q: Then why did you bother to do this research?
Silence of several seconds
A: I'm a scientist. It was for the sake of scientific knowledge. If you need treatment, ask your eye doctor.
Q: I told you, the eye profession won't help us.
A: You know, if people want to use our discovery, there's nothing to stop them.
Q: But cataract patients have no lab facilities to make sterile eye drops. What do you expect us to do?
A: Silence. No answer.
This concluded our conversation, which ended up going nowhere. Of course, I had not really expected anything else. He more or less admitted that this discovery, like all the anticataract agents before it, would be consigned to the annals of scientific knowledge without ever being used to help the 20 million+ human beings who are blind from cataract, and have to spend all their days fumbling around in eternal darkness. As I said before, mint contains rosmarinic acid, and mint is already a component of Ayurvedic (Indian) eye drops such as Isotine, where it is included at a concentration of 0.015%. The problem is, those eye drops also contain metal salts which would make the cataracts even worse. We need an eye drop with the mint, but without the metals.
As my cataracts continue to worsen, I felt the desire to once again call the local ophthalmology association and make my dissatisfaction known. I wanted to once more let them know that in the past, there were alternatives to cataract surgery which had successful clinical trials or were used successfully on large numbers of patients, such as certain eyedrops.
I regret that I cannot discuss these methods in this forum at this time for fear that the eye profession will attempt to block them. The fact that they are willing to block them, and to ensure that cataract surgery outlasts the human race, is clear from the details of our telephone conversation which went like this. My questions and comments are labeled "A", and their response is "B":
A: "According to statistics, most persons who undergo cataract surgery die within 5 years after the operation. Since there were successful alternatives to surgery in the past, why do you force people to have the operation today?"
B: "Most people with cataracts are elderly, and don't have long to live anyway. So if they do die soon after a cataract operation, it doesn't matter".
A: "I see.
Of course eyedrops for example take several months to work, whereas cataract surgery is very fast and therefore very profitable. But since there are alternatives which would enable me to keep my own eye lens, and avoid an incision as well as secondary complications, I strongly object to letting your surgeons cut on me just for the sake of your big profits".
B: "Do you really find that so objectionable?"
A: "Damn right I do".
I was so taken aback by this frank admission, that I decided there was no point in continuing the discussion. But, I felt that CureZone readers should know the other side's responses, so I have posted them here.
Today, a friend who came over disputed my title to SaintHood.
If I see halos around streetlamps, she says, it is the streetlamps which should be sanctified, not me, because they have the halos. Good point. But, since it is me who has the faulty nucleus, and since the streetlamps don't care whether we cure cataract or not (and I do), I still consider that I can call myself "Saint Nucleus", and all those of you with this type of cataract who want to cure it without ripping out the natural lens, are entitled to call themselves "Brothers of the Order of Saint Nucleus". Brothers, let us pray for a nonsurgical cure of nuclear cataract, and for good to triumph over evil.
THREE-STEP PLAN TO REVERSE NUCLEAR CATARACT WITH EYEDROPS
(1) EV06 eyedrops to break lens disulfide bonds and soften the lens.
This would allow (2) and (3) below to penetrate the lens.
Contain lipoic acid choline ester.
Bought by Novartis Pharma (which also has a huge surgical lens business) as an eyedrop to cure presbyopia for $465 million. Has already passed Phase II clinical trials in the US, but Novartis says it hasn't. Novartis has no plans to release this eyedrop which is therefore unavailable.
(2) AGE-crystallin crosslink breaker. Would contain phenacyl thiazolium bromide (PTB, synthetic) or chebula (Ayurveda, natural), or any other crosslink breaker. PTB was shown, at the University of Arkansas in 2008, to break crosslinks of AGEs with alpha-crystallin, and thereby reverse loss of chaperone function of alpha-crystallin. This discovery is the key to curing cataract blindness in 90 million people worldwide and alone is worth a Nobel Prize. The eye profession has no plans to use this discovery, therefore no intention to cure world blindness, and it is therefore unavailable.
(3) Alpha-crystallin stabilizers (sterols)
This means lanosterol and other sterols. They have the ability to refold and stabilize alpha-crystallin liberated by (2) from its shackles to AGEs. Once stabilized, alpha-crystallin will then interfere with the electrostatic attraction between beta- and gamma- crystallin protein molecules by masking the electrical charges on their surfaces, thereby separating the molecules, and breaking up large molecular aggregates into smaller ones. This will restore optical transparency to the lens, curing the cataract.
Lanosterol eyedrops are available, but cannot work on alpha-crystallin until the lens is firstly softened, and the alpha-crystallin is secondly released from its bonds to AGEs (Steps (1) and (2)) above.
My cataracts are yellow nuclear cataracts. I excerpted the following from an article which appeared in 2011:
"The ageing lens and cataract: A model of normal and pathological ageing"
"(b) Nuclear cataract
Strictly defined, a nuclear cataract is a lens opacity confined to the true nucleus of the lens whose shape is determined by the concentric arrangement of the fibres that compose it. Since the light-scattering properties of the lens nucleus increase progressively after the fourth decade, the point at which an increase in light-scatter may be designated a nuclear cataract becomes a matter of clinical judgement. While in some respects the molecular basis of nuclear cataract may be seen as an extension of those age-related events responsible for increased stiffness, light-scattering and coloration of the lens nucleus, it is the oxidative events discussed above, facilitated by the lack of nuclear GSH, that are the hallmark of nuclear cataract [63]. These are responsible for the formation of mixed disulphides and PSSPs, high molecular weight aggregates and increasing protein insolubility, which lead to lens opacity and the augmented accumulation of chromophores. These changes occur within the fibres of the lens nucleus with limited structural effect, which explains the gross morphology of the cataract".
In the same article, we find:
"With increasing levels of oxidative stress, proteins become thiolated by GSSG, cysteine and to a lesser extent γ-glutamyl cysteine, to form the mixed disulphides, PSSG, PSSC and PSSγGC [5]. These mixed disulphides may be further oxidized to form protein–protein disulphides (PSSPs), which are found increasingly in the high-molecular-weight, water-insoluble (WIS) fraction of the lens proteins, containing large, light-scattering, protein aggregates [18]".
First we remark that "disulfide bonds" can be broken by sulfites (the preservatives found in wine), and by a "sugar alcohol" known as "erythritol" (which is used as an artificial sweetener). There are even eye drops for dry eye which contain erythritol. Such eyedrops also contain electrolytes like potassium citrate that would interfere with the electrical attraction between proteins. It is this electrical attraction that causes the proteins to aggregate and form a cataract (so electrolytes are a very good idea), but sometimes also calcium chloride (I don't like the idea of dosing the eye with calcium salts, especially since calcium salt microspheres trigger macular degeneration). This more or less disqualifies these eye drops. But the next paragraph gets more interesting:
"Mixed disulphides and protein disulphides of this kind can be partially restored to their native state by two key redox repair systems. The GSH-dependent enzyme system, TTase, also known as glutaredoxin, exists in cytosolic and mitochondrial forms and catalyses the dethiolation of PSSG. The GSSG formed is recycled to GSH. Lens epithelial glyceraldehyde-3-phosphate dehydrogenase (G3PD) activity can be restored by TTase after H2O2 challenge, as may other SH-sensitive glycolytic enzymes such as hexokinase and pyruvate kinase [19].
The NAPDH-dependent enzyme TRx, present in both cytosolic and mitochondrial forms, reduces intra- and inter-molecular protein disulphides (PSSP). TRx is restored to its reduced state by TRx reductase (TR), with NADPH acting as a hydrogen donor. TRx works cooperatively with TTase to restore protein structure, conformation and function. Like TTase, TRx activity is also upregulated in response to oxidative stress. Both TTase and TRx systems can reactivate G3PD oxidized during the exposure of human epithelial cells to H2O2. Their activity, together with that of GR, falls with age [15]."
Therefore, apart from sulfites and erythritol, we see that the two enzymes TTase and TRx can at least "partially restore the protein disulfides to their native state". As noted in other posts, those two enzymes are found in brewer's yeast, which explains why brewer's yeast supplements are used to treat cataract.
When it boils down to it, this 40-page article is a thorough, in-depth evaluation of nearly all aspects of our problem - although the fact that cataract aggregations are largely the result of electrostatic interactions between lens proteins (Murugappan, 2010) is not mentioned. What is frustrating, as usual, is that the authors, despite having a complete understanding of cataract and the tools to reverse it at their disposal, MAKE NO ATTEMPT TO DO SO.
What is even more amazing: This article is published in the "Royal Society - Philosophical Transactions". But our lives depend on this information - there is nothing 'philosophical' about it.
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