About Me

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Deep South, United States
Consultant, inventor, mentor, chess coach,. Current projects involve No Till Farming and staving off blindness due to cataracts among other projects. I also do confidential ghost writing (without taking any published credit. My current blindness makes me put this on hold for a while. I should have one eye working again in about four months. Fact, fiction, all subjects considered. I have heard My daughter Jennifer is alive. I would love it if she were to contact me here. I understand she would like to know me. I have sent a message by circuitous route. I can only hope. My posted Email works as well. We have four decades to catch up on.

This blog has been up for more than a year. The intent was to generate dialogues about serious problems and ideas. It has been almost exclusively a monologue. I have not been looking for large numbers of participants.

I would be quite happy with a few dozen imaginative, creative, thoughtful and inventive people who wish to address serious problems and issues. If anyone has any ideas about how to attract such a talented group I will certainly pay attention. I am not as computer conversant as I would wish. Anyone who could help in this regard would find me receptive to sharing my skills in other areas.

Tuesday, September 18, 2007

Cataract Correction Part Two

The goal is to rehabilitate the lens of the eye and recover visual acuity and the accommodative function of earlier years.Whatever the substances are that are producing the cloudy lens, there needs to be some sort of circulation going on within it, exchange of fluids in both directions across cellular membranes.

Those cells in the nucleus of the lens may be reacting to ionic transport pumping. I have a theory that a persons first and more advanced cataract is generally in the eye which was the weaker of the two even prior to the cataract. I have not seen any data on this. The idea may have no merit at all.

But back to fluid exchange. Can cataracts be forming due to a failure or diminution of the normal circulatory process? Due to a change in viscosity of the fluids? From dehydration due to failure to drink sufficient water? What other kinds of fluidic transfer could be playing a part? What about the flexure of the lens itself? Could there be a relationship between the reduction of the ability to flex the lens and a reduction of fluid exchange? Are the inclusions causing the reductions of clarity of vision within the cells of the lens or between them? The answers to these questions will bear on how to solve the problem.

Thursday, September 13, 2007

Cataract Correction Part one.

We ought to take a look at the various things that contribute to the loss of vision in age-related nuclear cataracts. At the top of the list, and most obvious, is a reduction of the transparency of the lens. The prevailing medical opinion is that this is an inevitable consequence of ageing, that once the opacity has developed, little can be done except the eventual removal of the offending lens, and replacement with a prosthetic lens of one variety or another.

We commonly refer to these cataracts as "senile." The currently prevailing view is that only surgery is a reasonable course of action. I am not at all confident that this is the case. Opposition to this perspective is not strong and is also suspect because of the potential for profits generated by sales of nutritional products, vitamins and minerals. There are several large pharmaceutical companies selling vitamin-mineral products based on the results of the ARREDS study. The pills are high in price, and the claims made for them are vague and insubstantial, referring to general eye health rather than stabilization or reversal of cataracts.

One smaller company uses the audio presentation of a maverick ophthalmologist (now dead) who makes some plausible claims that give cataract sufferers enough hope to try a product with some additional ingredients to the ones indicated in the ARREDS study, but the owner of the company is not inclined to actually discuss his product in detail and deal with the actual mechanisms of action. It never impresses me when a CEO does not respond to specific questions about his product or services.

But returning to cataracts, what are some of the elements of the formation of cataracts, and which of those contributing causative factors can be reduced or reversed? Current treatment of choice is surgical. Worldwide, there is probably no more commonly performed surgery. Odds of success are high. But there are risks as well, and some of them are substantial. This is reason enough to return to the subject of prevention and delay.

From my perspective, "senile" cataracts involve more than the developing cloudiness of the lens. The ability of the lens itself to be flexed into focus is also reduced with aging. The main contributor to this is probably the ongoing thickening of the lens. The actively replicating cells of the lens are in the cortex (outermost) layer. I have, as yet, been able to find little information about the metabolic activities of the nuclear (interior) layers of the lens. Certainly those deeper lens tissues are still metabolically supported in some ways. That implies that defects in the support process play a part in the development of the loss of clarity.

We also know that these deeper cells have no direct vascular support, and that they have no nuclei and no mitochondria. But certainly there is some sort of ongoing passive fluid exchange. These lenses are quite flexible and deformable. If some sort of fluid exchange were not going on, this sort of stasis would be unlikely to go on for decades.

So assuming a certain fluid exchange, understanding that mechanism might well provide a means of altering the fluid environment of the interior of the cell in such a way as to increase the transparency of those interior cells.

Going back to the flexibility of the lens, the musculature which accomplishes the focusing of the lens is attached to the outer edge. These strands of muscle are collectively known as "Zonules of Zinn." I would like to have a deeper understanding of the interface of these muscle cells and the cells of the lens cortex.

I'm feeling my way along with this, but at the moment my emphasis is on anti-oxidants and phytochemicals, as well as various means for increasing fluid transfer in the nuclear portion of the lens. Bear in mind that these lens cells are not vascularized and contain no mitochondria, so only passive and ionic circulation of fluids can be involved.

So to sum up, I believe that it is significant that in nuclear cataracts, these characteristics are most often present; there is a direct relationship with age, there is a thickening of the lens and a corresponding reduction of efficiency of accommodation (the ability to flex the lens to resolve images), there may also be some reduction of moisture content of the lens as well. This would certainly make the lens less pliable and make it far more likely that opaque substances accumulate in the tissues.
I suspect that there is also an age-related reduction in the strength of the zonule musculature. The efficient flexure of the lens is certainly an element affecting the passive movement of fluids through the lens.

So without regard to the exact nature of the opaque inclusions in the lens, it seems reasonable to pay close attention to the level of hydration (old people have a tendency to sometimes drink too little water), to increase the intake of anti-oxidants and phytochemicals, to review the nature of the lipids in the diet, and to do a variety of lens calisthenics (changing focal distance with increased frequency).

In my particular case, I suspect that my low intake of vegetables, particularly the dark leafy ones and the yellow and orange ones, has played a role in the cataract development. This is very difficult for me to correct. I buy enough vegetables, and have all kinds of good intentions, but then often forget to eat them before they spoil. I try to make up for it by eating more fresh fruits, but I do not know how effective this substitution is.

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