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IEET > Life > Enablement > Innovation > Health > Staff > Kyle Munkittrick

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Another Tiny, Exciting Step Toward Life Extension


Kyle Munkittrick
By Kyle Munkittrick
Science Not Fiction

Posted: Dec 5, 2010

With the headlines screaming “age-reversing” possibilities regarding the Dana-Farber Cancer Institute at Harvard University’s results with mice telomerase manipulation, I felt a bit of cold water was in order.

I am as excited as can be about serious evidence for how important telomeres and telomerase is for anti-aging medicine, don’t get me wrong. But that evidence doesn’t mean there is going to be a longevity pill in our hands this year, this decade, or even this century. And more than a few folks with a grasp of science better than mine agree.

Thankfully, I’m not the only one. My fellow Discover blogger Jennifer Welsh has a great post on 80 Beats about why the discovery, though exciting, is far from a genuine anti-aging solution.
lab rats
The Harvard team showed the following: Mice engineered to lack telomerase aged prematurely. When given telomerase treatments, the mice rejuvenated to age-appropriate health without adverse side-effects. That’s it. That’s the extent of the discovery.

It still remains to be seen if telomerase treatments can delay normal aging, reverse normal aging, or extend life in any way in mice. From there scientists have to then figure out what side effects there are, why those side effects occur, and then somehow translate the results to human beings.

In short, the Harvard team only confirmed the hypothesis that telomerase in mice impacts the aging process and that it may have potential uses in treating premature aging. Hypotheses beget hypotheses. And not all our hypotheses hinge on mice…

READ THE REST


Kyle Munkittrick, IEET Program Director: Envisioning the Future, is a recent graduate of New York University, where he received his Master's in bioethics and critical theory.
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COMMENTS


This theory below was developed by Dr. Sigwin Raska, Phd Chem., assistant to Nobel prise winner Ruzicka in 1939, MA Physiology in Canada, MD from Chicago.

The following is based on a discussion I had with Sigwin in the early 1980’s regarding cellular senescence regarding an experiment that myself and Prof. John Armstrong at U of Ottawa developed and sent to David Suzuki; the results of the experiment disproved the pervailing crossover theory as the cells method of eliminating aging in germ-line cells.

Sigwin’s theory on cellular senescence:

The cell is a biochemical-electromagnetic machine. This machine manufactures complex molecular structures. It is not a perfect system, occasionally a malformed protein is produced. Early on in a cells life these mal-formed proteins, due to their small numbers have minimal effect on the cells normal functions. But as the cell grows older these malformed proteins accumulate; their collective accumulation effects the ability of the cell to function, the cell starts slowing down in its ability to complete its normal functions.

In the Harvard research, on the use of telemase to eliminate cellular senescence in mice, it was noted in the article by Harvard Science that there was a potential for cancer to develop in humans if telemase was employed. Raska’s hypothesis suggests that the accumulation of malformed proteins may act in a similar manner to the oncogenes that also produce malformed proteins, which inhibit cellular senescence and trigger a tissue repair mode [cancer]. By eliminating these malformed proteins in human cells, the successful Harvard experiment on mice could well work on humans. 

Certain cells don’t age they are embryonic cells prior to the formation of the next germ line/reproductive cells. These cells produce a large number of protolytic enzymes that re-metabolize the malformed proteins. This is an essential function: if their was aging in the reproductive cells it would accumulate in each successive generation.

After the reproductive cells are produced this function [cleaning the cell factory] becomes a disadvantage in the need to speedily fabricate the biggest, strongest, fastest, smartest animal. Once the animal reaches or nears its maximum potential it can reproduce off-spring, as such there is no need to clean the cells. Recycling the mal-formed proteins has not evolved, yet.

[Cancer cells, due to an internal malfunction that inhibit inter-cellular communication [Lowenstein] enter a tissue repair mode and produce protolytic enzymes, these enzymes, originally designed to break down the surrounding dead tissue, also break down the malformed proteins, and turn an aging cell into a super invasive cell.]

Reduction of telemeres may limit a cells reproductive capacity but they do not seem to reduce the cells capacity to do all of its other functions.

Experimentation

Find those sections of the DNA in early embryonic cell that produce protoytic enzymes. Compare these sites and actions of the protolytic enzymes produced by cancer cells and those produced by early embryonic cells.

Find a way of stimulating the DNA in differentiated cells to produce protolytic enzymes. Study the effect of these enzymes at different saturation levels..





I am always amazed when discussing the concept of stopping and reversing the aging process in people, how disinterested they seem.  I believe it is similar to how people treated the concept of space travel and going to the moon in the 1950’s and 1960’s. 

In the 1950’s the young and imaginative minds were busy reading science fiction comics of flying to the moon.  Then these unencumbered young men and women went on to study and work with NASA and other organizations which led to Neil Armstrong’s moon landing in 1969.

Now we are at the beginning of a new age, one where we may be able to stop and reverse aging, and I believe that this will be a far more significant achievement for our species than landing on the moon. 

Naturally there are great social ramifications and questions for this achievement, and there are excellent answers to these questions from the friends and leaders of the Methuselah Foundation.





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