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tke Views: 9,476
Published: 4 years ago
 
This is a reply to # 2,187,504

Re: Challenge!


The Floater-Cataract Connection

It may seem surprising, but cataracts indirectly begin in the vitreous, not in the lens.
Until the year 2000, the eye profession denied the vitreous had any function in the human eye at all. University textbooks taught it had no function. Yet the vitreous is the most important part of the eye, because without it, the whole eye would collapse, the retina would detach. and we'd go blind.
So how, and why, did the eye profession refuse to admit that the vitreous had a function, to the point that although it occupies about 80% of the eye, eye charts did not even mark it, and its very existence was inexplicably surrounded by a wall of silence.
The vitreous is a "jelly" (gel) in which water is held "bound" by hyaluronic acid (HA). One molecule of HA binds up to 60 molecules of water in fixed positions, making its hydration factor of 60 the highest known in chemistry. So it is a "gel", but this gel is so flimsy that it needs extra support and body from superfine collagen fibrils running through it, from front to back.
The fibrils are like the strands of a spider's web, so fine (only a few nanometers in diameter) that they are invisible to us. But as the eye ages, the HA starts to leave the eye, and so the water can no longer be bound, and runs around free.
Two things happen as a consequence of this:
1) The fibrils clump together so that they become visible as "floaters" which cast shadows on the retina.
2) Oxygen from the retina at the back of the eye dissolves in the free water, and is carried to the lens at the front. This oxygen oxidizes transparent proteins, forming opaque, light-scattering proteins called "cataracts". Initially, the chaperone protein in the lens, "alpha-crystallin", reverses this oxidative damage, but eventually all the reserves of "alpha-crystallin" are used up, and the cataracts are then permanent. There are cells in the cortex of the lens which supply a very small amount of fresh "alpha-crystallin", but this is not enough to go round when oxygen is still being passed up front.

Theoretically, the cataracts could be reversed by supplying more 'alpha-crystallin" to the lens, perhaps as peptides (protein fragments) in eye drops, together with some agent that would carry them through the cornea, lens apsule and into the lens, and together with a reducing enzyme like methionine reductase to keep the "alpha-crystallin" active.

And theoretically, the "floaters" could be stopped from moving if the vitreous were stabilized (without the collagen fibrils however) by re-supplying HA to it. Again, a carrier would be required to get the HA into the vitreous, perhaps something that temporarily increases the permeability of the outer eye structures (like castor oil).

So we see, that far from having "no function in the human eye", the vitreous is key to preventing much of its pathology, including retinal detachment (before it separates from the retina due to loss of HA and shrinking), and "floaters", and cataracts. The eye profession denied it had any function at all right up to the year 2000. This could have been a matter of convenience, rather than ignorance - after all, you don't have to repair something with no function, do you?
 

 
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