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Telomerase Activator in humans


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#31 jamesagreen

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Posted 23 June 2010 - 07:08 PM

Astragalus extracts lenthen telomeres until the t-loops close at the ends of the telomere and cells return to the pre-senescent immortal phenotype, eventually resetting gene expression to youthful levels. I get the impression that the maximum benefit from this sort of thing is about 9 years backwards in time per year of astrogaloside treatment, until you obtain the immortal phenotype and seem to hang on looking about 28. That is about what my calculations based on TA Sciences data show can be done with TA-65. I expect I am getting worse results with simple astragalus extract, but it does seem to be impacting my hair coloration and be reducing the number of grey hairs by reviving senescent stem cells. More careful scientific studies of readily available astragalus extracts are definitely in order, both in vivo and on in vitro cell cultures.

James, thanks for all the information. I'm wondering about the quoted part here, because it seems to me that if a cell has become senescent due to telomere shortness, and it then gets its telomeres extended and (presumably) becomes un-senescent, isn't it still saddled with all the injuries that it sustained over its life? In other words, it may still have sagging, leaky old mitochondria... Likewise, the extracellular matrix will still have whatever glycoxidation it already had, and all the old lipofuscin bodies will still be there. I don't see how lengthening telomeres alone can take you back to 28, unless maybe you are 27 when you start. It does make sense to me that telomerase activation might make a 90-year-old feel 80 again, but not 27. Is the impact on you hair coloration very noticeable? You look fairly young from your picture; do young people have enough cells with depleted telomeres to make a program like this worthwhile? I figure that I'll wait until I'm 65 to try TA-65, but is that the wrong approach?

Dear Sir,
As a matter of fact, I have seen papers showing that hTERT activation improves mitochondrial DNA repair (10).
Furthermore, hTERT activation improves telomere repair in non-telomeric nuclear DNA, too! With some additional
measures to improve mitochondrial biogenesis, perhaps by taking more arginine to boost Nitric Oxide levels,
one might overcome most mitochondrial problems in an aging specimen. Acetyl L-Carnitine and Alpha Lipoic Acid are also recommended for mitochondrial recovery. So I think the answer is that we are really expecting to
see rejuvenation results that are credible, eventually. However, the process is glacially slow,
as it takes maybe $50-$75 worth of astragalus extract plus bioavailability-improving Chitosan and Radix
Astragali (Astragalus Membranaceus Root) to get a rejuvenation rate of B = -5 years per year. It might improve the
rate, however, to eliminate all telomerase inhibitors whatsoever during the activation portion of series of
telomerase activation/telomerase inhibition time cells. High Polyphenol diets generate telomerase inhibitors
as products of digestion, so that recently I have decided to pursue telomerase activation in connection with
low polyphenol diets, and telomerase inhibition simultaneously with high polyphenol diets.
Jim Green - http://greenwdks.hos.../longevity.html (most complete, with files > 256 Kb)
backup: http://greenwood.s5.com/longevity.html .

Edited by jamesagreen, 23 June 2010 - 07:25 PM.

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#32 jamesagreen

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Posted 24 June 2010 - 02:14 PM

Can anyone answer my following questions on telomerase:

1. By activating the telomerase in the senesecent cells which has undergone damage in Mitochondria, has lipofuscin, etc...the new cell formed by multiplication has all the damages reversed or removed to form young cells?
2. I have seen literature of Prof.Shay and Wright on extending the telomerase in animals..Do they live longer? Link to Shay and Wright lab is given below:

http://www4.utsouthw...ight/index.html


Activating hTERT in the cellular nucleus improves DNA repair (10) overall in the nucleus,
not just in the telomeres. Furthermore, it improves DNA repair in mitochondria,
according to reports, which was quite a surprise. With regard to lipofuscin,
hTERT activation lengthens telomeres that strengthen adult stem cells which
can replace defective cells and enable more cell divisions in mitotic cells, so it does
tend to oppose lipofuscin problems to some degree. However, lipofuscin is primarily a
problem in cells that are not mitotic and do not divide, and is otherwise fixed with
CoQ10, ubiquinol, alpha lipoic acid, piracetam, and other drugs.
- Jim Green http://greenwdks.hos.../longevity.html (best, includes files > 256 kb)
Backup: http://greenwood.s5.com/longevity.html .

Edited by jamesagreen, 24 June 2010 - 02:15 PM.


#33 Luna

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Posted 24 June 2010 - 02:36 PM

I'd imagine that even if there was repair happening or damaged cells dying and healthy one replacing them it might not be too useful at old ages or even over the middle ages because the body has mostly damaged cells by then?

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#34 erzebet

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Posted 10 August 2014 - 03:35 PM

 

Can anyone answer my following questions on telomerase:

1. By activating the telomerase in the senesecent cells which has undergone damage in Mitochondria, has lipofuscin, etc...the new cell formed by multiplication has all the damages reversed or removed to form young cells?
2. I have seen literature of Prof.Shay and Wright on extending the telomerase in animals..Do they live longer? Link to Shay and Wright lab is given below:

http://www4.utsouthw...ight/index.html


Activating hTERT in the cellular nucleus improves DNA repair (10) overall in the nucleus,
not just in the telomeres. Furthermore, it improves DNA repair in mitochondria,
according to reports, which was quite a surprise. With regard to lipofuscin,
hTERT activation lengthens telomeres that strengthen adult stem cells which
can replace defective cells and enable more cell divisions in mitotic cells, so it does
tend to oppose lipofuscin problems to some degree. However, lipofuscin is primarily a
problem in cells that are not mitotic and do not divide, and is otherwise fixed with
CoQ10, ubiquinol, alpha lipoic acid, piracetam, and other drugs.
- Jim Green http://greenwdks.hos.../longevity.html (best, includes files > 256 kb)
Backup: http://greenwood.s5.com/longevity.html .

 

 

Can you provide updated links? The ones you included don't work anymore.

 



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#35 erzebet

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Posted 10 August 2014 - 03:48 PM

 

 

Astragalus extracts lenthen telomeres until the t-loops close at the ends of the telomere and cells return to the pre-senescent immortal phenotype, eventually resetting gene expression to youthful levels. I get the impression that the maximum benefit from this sort of thing is about 9 years backwards in time per year of astrogaloside treatment, until you obtain the immortal phenotype and seem to hang on looking about 28. That is about what my calculations based on TA Sciences data show can be done with TA-65. I expect I am getting worse results with simple astragalus extract, but it does seem to be impacting my hair coloration and be reducing the number of grey hairs by reviving senescent stem cells. More careful scientific studies of readily available astragalus extracts are definitely in order, both in vivo and on in vitro cell cultures.

James, thanks for all the information. I'm wondering about the quoted part here, because it seems to me that if a cell has become senescent due to telomere shortness, and it then gets its telomeres extended and (presumably) becomes un-senescent, isn't it still saddled with all the injuries that it sustained over its life? In other words, it may still have sagging, leaky old mitochondria... Likewise, the extracellular matrix will still have whatever glycoxidation it already had, and all the old lipofuscin bodies will still be there. I don't see how lengthening telomeres alone can take you back to 28, unless maybe you are 27 when you start. It does make sense to me that telomerase activation might make a 90-year-old feel 80 again, but not 27. Is the impact on you hair coloration very noticeable? You look fairly young from your picture; do young people have enough cells with depleted telomeres to make a program like this worthwhile? I figure that I'll wait until I'm 65 to try TA-65, but is that the wrong approach?

 

(Reply, March 20, 2008)
Lengthening telomeres results in more youthful patterns of gene expression from nuclear DNA, resulting in higher expression
levels for endogenous antioxidants, collagen, elastin, and other factors promoting youthful cell function and resulting in the
display of the immortal phenotype. Furthermore, it confers genetic stability on the cell tending to protect it from cancer, because
cancer often occurs due to end-point fusions when telomeres get disasterously short. Keeping the telomeres long keeps the
cell from activating a DNA damage checkpoint. The result is that cells seem to be relatively immune to free radical and
glycation damage by comparison with senescent cells. This is why cells can be immoralized with telomerase activation
in vitro in many cases. In reality, the time to take TA-65 or ethanolic astragalus extracts (perhaps in glycerin) to
activate telomerase is right about the time hairs turn grey. The greying of hairs tracks the death rate curves very well,
and corresponds to the population of senescent cells in the body, reflecting the senescence of stem cells that rejuvenate
grey hairs. So take TA-65 or astragalus extract to minimize the senescent cell population leading to cancer, heart attack,
stroke, macular degeneration, and so forth just as soon as grey hairs show up. They mirror the senescent cell population
supporting diseases of old age. That way we can hug the baseline of the death rate chart way out to several hundred
years or more, perhaps. Of course, it is clear that lipofuscin or ceroid removal in old people had better proceed in
parallel with small molecule telomerase activator treatments. For this lipofuscin removal task alpha lipoic acid, Piracetam, ubiquinol CoQ10,
old-fashioned ubiquinone CoQ10, and other drugs have been identified
. Just lengthening the telomeres helps a lot more than
seems reasonable, however, as youthful patterns of gene expression include more collagen and elastin, which slowly
restore old tissue to its former youthful appearance. Bear in mind that restoration of the extracellular matrix by the
technique of telomerase activation takes a little longer than the restoration of hair color due to lengthening stem cell
telomeres. However, it works. You can see the difference in home movies after 9 months of 5 mg/day GAIA astragalosides
from GAIA astragalus extract, requiring about 150 drops per day during the two-week activation period in which you
avoid telomerase inhibitors such as curcumin (turmeric), silymarin, garlic (allicin), melatonin, vitamin E, fish oil EPA,
resveratrol, and quercetin. These telomerase inhibitors can be taken during the next two weeks, before starting
all over again. After 11 months, the results look like 9 years per year backwards in time, about like we expect for
TA-65 based on reports of 460 bp per year, about 77 TTAGGG sequences per year, or approximately 45 twists of
the Watson-Crick DNA-B helix. However, results should become more dramatic as time goes on, because
after a year, 59 looks like 50, then theoretically 60 looks like 41, after which 61 looks like 32, and so on.
The effect is you get a Time Machine feeling about like something out of HG Wells, because of the cumulative
effect on the cells. TA-65's advantage may be merely chemical purity, so that our knowledge becomes more
precise, eventually. Or perhaps it works a bit faster, because in regular astragalus extract, we use the slightly
larger molecule astragaloside IV, primarily. Anyway, while using such a program, it is important to go ahead
and continue to work against glycation and free radical damage using carnosine, antioxidants, and vitamin C.
As for mitochondria, NO activation using bodybuilding exercises with arginine-enriched whey protein should
help revive mitochondria, which anyway turn over pretty rapidly, approximately every 14 days, if memory
serves. NO activation via the action of nitric oxide synthase on arginine also has the effect of activating telomerase in the vascular endothelium, according to
Vasa, et al., 2000, and Hayashi, et al., 2006, and of promoting mitochondrial biogenesis. Saving hair samples and counting grey hairs seems to be a poor
substitute for actually measuring telomere growth, but it is definitely easier on your bank account. I would say
that the difference in my gray hair levels is striking, especially when I get of the shower in the morning with
a head of wet hair, which tends to make it look darker, anyway. Perhaps this is why baptism was so popular, in fact.
I recommend preparing hair clippings from the top, the sides, and the back of the head when doing this experiment,
and filing them in envelopes for counts later. Mine looks like a case of salt and pepper got darker, and I am optimistic
about the future course of this treatment. Incidentally, the little picture of me on this web page looks like I looked with my hair dyed in 2001.

 

 

Can you provide any references for the substances you mentioned in removing lipofuscin?

 






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