CHANGE THE NAME!
I propose that we stop using the name "CATARACT", and replace it by the longer but more suitable name,
"CRYSTALLIN DEFICIENCY SYNDROME". This new name tells eye doctors the reason why we have cataracts, and also suggests that correcting the deficiency of active crystallins in the lens will potentially reverse cataracts without surgery, thus saving the natural lens. That is the goal of all cataract patients. If only it were their goal too - but it's not.

The Mechanism of Cataract
Before we can understand how to cure it, we must know what it is.
I have been in contact with the last few cataract researchers in the world who still believe it is better to save the natural lens than to replace it with a plastic lens by surgery.

I have been talking in previous posts about the need to restore
active alpha-crystallin in the lens. Previously I had been thinking mainly of supplying these factors exogenously (from outside the lens). But now I realize that our cataractous lenses already contain all the necessary factors to repair themselves. This is what I learned from the Net, and from talking to one of the researchers.

In an adult person, there are secondary lens fibers on the equator of the lens which produce all the crystallins, alpha, beta and gamma. They probably also produce the reducing enzymes MsrA, MsrB which activate those crystallins, TXNL-6 (thioredoxin-like)-6 which activates the MsrA, and Trx1, Trx2 (thioredoxins) together with TrxR (thioredoxin reductase) which activate the TXNL-6. This constitutes a chain of reducing enzymes, each standing behind the other, with the final purpose of activating the crystallins.

Normally, the secretion of this biochemical mixture by the secondary lens fibers keeps the lens crystal clear. But once a cataract forms in the nucleus of the lens, the cataract builds a wall around itself through which these fiber secretions cannot penetrate. So the cataract grows, and grows, protected by its shield, until it finally engulfs the entire lens. This is what makes cataract so resistant to all our efforts to get rid of it.

Now we can understand why the cataract phototherapy developed by Dr. William Luftig in 1930 was able to affect cataract reversal in many cases. It is likely that certain wavelengths were able to activate the secondary lens fibers on the equator of the lens to produce much more crystallins, and probably also their reducing enzymes, which vanquished the cataract in the nucleus.

We can also understand the role of castor oil, MSM (methylsulfonylmethane) and NACA (N-acetylcysteine amide) in eliminating cataracts. Castor oil, anecdotally reported to be an excellent cataract remedy, penetrates deep into the ocular tissues, breaching the wall around the cataract, and probably carrying the crystallins and enzymes together with it so that the cataract is eliminated. It also contains undecylenic acid which inhibits the pro-cataract enzyme, calpain. It is unfortunate that castor oil apparently kills off some corneal cells if used in 100% concentration, which makes its use much less attractive. MSM also penetrates all the ocular tissues, which explains why it too is also sometimes mentioned as an anticataract agent – it probably also breaches the wall. But MSM eyedrops are difficult to get, and we don’t often hear good results with it.

Finally we come to NACA. Previously, researchers at one university had reported that a 1% solution of NACA in phosphate buffer also penetrates all the ocular tissues, and did in fact reverse Stage IV nuclear cataracts to Stage II with a high degree of statistical significance, in a rat model. It also had some success with posterior cataracts, although with a lower level of statistical significance, probably due to the greater distance of the posterior pole from the secondary lens fibers. Although the biochemical repair enzymes are probably different between humans and rats, nevertheless there are still common factors - the crystallins which keep the lens clear, the secondary lens fibers which produce the repair systems, and the wall around the cataract. This suggests that NACA will work in humans too, by carrying the human repair enzymes across the wall. In addition, it is carrying a thiol-based amino acid, N-acetylcysteine (NAC), which may be expected to activate all the other factors, right to the core of the lens. Although the parent amino acid, NAC, which is itself sold as a supplement, can have severe side effects when consumed in large amounts, it is very unlikely that any problems would be encountered with a 1% eyedrop formulation. Still, researchers urge caution until clinical trials prove safety and effectiveness, and also stress that the NACA which is commercially available is not pure enough to use for this purpose.

And this is the problem. On the face of it, NACA may be able to safely allow our own crystallins and reducing enzymes to reach the cataract and destroy it, restoring our vision without surgery. But, when the eye profession doesn't even want to save the human eye lens, who is going to do the clinical trials that we desperately need, and when?