Dr. Rosedale wrote a lot on MDA on telomere issues. I thinks he gives a pretty convincing argument that we need to wait for more accuracy, precision, and research before really using this in everyday practice.
An snippet of a very long and through article. http://www.marksdailyapple.com/the-tall-tail-of-telomeres/
"How about current laboratory testing for telomere length? It merely requires a tube of blood since one of the very few cell types that is easily accessible and where telomerase is present such that telomere length can increase are white blood cells. Is the test meaningful? Probably not very. The rate of telomere attrition, the rate of decrease in telomere length that may be more important than absolute length, will increase with increased cellular damage and turnover such as that caused by oxidation, free radical damage, glycation, and inflammation. In other words, all that a higher rate of telomere shortening of any kind might indicate is an increased rate of cellular damage, but it doesn???t tell you what is causing the damage. Glucose perhaps?
Many, including myself, believe that all shortening of WBC telomere length in particular reflects, is the state of inflammation. There are many other much simpler and less expensive, albeit less glamorous markers for this such as a C-reactive protein or even the sedimentation rate. Furthermore, both a healthy, though at the time less active immune system, and an overly stressed or suppressed immune system might, at least theoretically, lead to less telomere attrition due to less cellular proliferation.
Though the rate of white blood cell TL shortening has been shown to decrease and TL may even increase with certain changes in lifestyle such as exercise and diet (that might just reflect improved immune response), TL also has been shown to oscillate even if you don???t do anything; not change your diet, nor exercise, take antioxidants, or think positively about your TL.
However, the biggest problem in measuring TL in WBC???s is that there are many different telomeres of different lengths in many different kinds of cells with differing rates of attrition. An increase in white blood cell TL or reduced rate of shortening does not necessarily reflect a change in other telomeres, especially from other cell types. For instance, in cells that don???t divide, such as heart and nerve cells, TL is somewhat meaningless. Telomere length even varies depending on the kind of white blood cells.
Robust evidence also shows that it is not the length of telomeres, or even the rate of telomere reduction with age that matters, but rather that telomeres must get to a critically short length for adverse genetic repercussions to take place. Measuring WBC TL only measures average WBC telomere length and not the number of critically short telomeres....
Telomere length is correlated with rate of cellular replication, and cellular replication is increased with increasing mTOR, IGF-I and inflammation. Therefore, it very well could be that the correlation between telomere length and longevity is only just that, a correlation, and not a cause, and the underlying mechanism of aging has much more to do with levels of glucose, mTOR, IGF-I???and insulin and leptin. That is likely true. Indeed, telomere length, has been shown to be highly (negatively) correlated with leptin levels (see below).
As I was actually writing this article, one of the most significant studies to be published pertaining to telomeres in recent years came out of Maria Basco???s lab from Spain. I will discuss it more at length below. It shows just how important it is to orchestrate telomere length and telomerase. It must be turned on, or off, at a certain time and place for there to be any chance at significantly improved health without increasing cancer risk.
The telomere theory as a cause of aging was hotly debated over a decade ago in many biology of aging conferences where university researchers got together to discuss their latest findings. Now, this is barely discussed outside of pseudoscientific circles??? Perhaps the latest Basco study will reinvigorate this debate.
I believe that lengthening telomeres, most specifically in stem cells, and then only temporarily to mitigate against increasing cancer risk, may offer potential to increase health span and delay the onset and even treat certain chronic diseases of aging. However, this is not the same or as powerful as increasing maximal lifespan and stretching out youth that research into genetic pathways of aging regulated by nutrient sensors (insulin, leptin, and mTOR) offer, as illustrated by the increase in maximal lifespan of many species by 200% and more when insulin, IGF-I, and mTOR are genetically suppressed.
One must accurately define health before directions to be healthy are given and just like health is not low cholesterol, health is not defined or synonymous with long telomeres.
Life is dependent on the coordination of its constituent parts. This is especially true pertaining to the length of telomeres of the various cells and organs to maintain health but prevent a high risk of cancer."
asked byLady_Arwen (6259)
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on June 20, 2012
at 05:33 AM
I was intrigued by your post, thinking "well, you'd have to do some pretty gnarly genetic engineering to lengthen peoples' telomeres" and came across this quote by Stanford researchers in an article in PNAS:
"In order for a cell to become cancerous, one of the things it has to do is switch on the telomerase gene which makes the telomeres longer," he said. "The body has decided that the best way to keep an organism alive is to keep telomerase turned off, because otherwise you can get mutations and cancer too easily."
The quote was part of a larger article in futurepundit about anti-aging therapies which said this:
"Even if telomere lengthening makes adult stem cells more able to replicate and even if this results in better body repair that doesn't mean that telomere lengthening would become a generally good thing to do to all adult stem cells in a human body. It is possible that telomere lengthening will allow cells that have otherwise damaged DNA to survive and to become cancerous. It is theorized that telomere shortening is a safeguard mechanism to help prevent cells from turning into cancer cells.
Another part of the puzzle needed to make a safe and effective rejuvenation therapy is the ability to sort thru adult stem cells and separate out the ones that have the least amount of DNA damage. Then one could take the better less damaged cells and extend the telomeres and reimplant them into the body. These more carefully selected cells would present less risk of becoming cancerous. To further reduce the risk of cancer from stem cells that have had their telomeres lengthened it will some day be possible to apply gene therapies that would repair a small number of locations in the genome where mutations contribute to the conversion of cells into cancers."
Me, unless I had an incurable fatal disease and decided for some bizarre reason that I'd rather become a science experiment than die peacefully and naturally, I would never hack my own DNA artificially. Scientists love to mess around with stem cells (blood, hair, etc) and try to find ways to control them (see above) but they have not had much success with this so far without cancer cropping up. I find the idea almost freakishly Matrix-like and scary. IMHO (and I think we're in agreement here) it's better to maximize the life span we've been handed - and by maximize I mean quality and meaningfulness, not length.
Here's the futurepundit article: http://www.futurepundit.com/archives/000664.html
and here's the press release about the PNAS article: http://www.sciencedaily.com/releases/2002/11/021120064507.htm