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Astragalus, Astragaloside IV


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#2101 DorianGrey

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Posted 17 September 2013 - 04:34 PM

Bill Andrews announced that Sierra Sciences has discovered 39 telomerase activators that at up to 100 times more potent than TA65 and Product B. Trials to begin in 3 years.


No, he says 39 families were identified, so far more compounds have some effect and 100 would be 60% vs Hela? That's high.

Is the PK for those new substances linear or does it take less substance to get to about 1% activation compared to Hela (like Cyclo)? I am not sure what 100 times more potent really is supposed to mean.

It's exciting to see the progress Sierra seems to make, but I'd caution everyone based on the knowledge that about 1 in hundred lead substances become meaningful in pharmacology.
Once again, how many of these in-vitro compounds are absorbed well in the GI tract, have a good half-life time (e.g. Resveratrol has only minutes), don't degradate to early or react with proteins or glycans (think PQQ, a SIRT3 activator but very reactive), are cheap to extract (still an issue with Cyclo) and most important, come without adverse side effects (just think of Estrogen related substances).

#2102 marcobjj

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Posted 17 September 2013 - 09:14 PM

when we over exfoliate, nutrients from the dermis are sent up to the epidermis, an act that starves our precious dermis of nutrition.


One tissue causing another to starve by stealing nutrients? I mean, even if nutrients are "stolen" temporarily we have a circulatory system delivery nutrients. not that I advise over exfoliation but that notion seems far fetched.

It's also more or less a myth that differentiated cells wouldn't divide (although there are some that don't):


it's not a myth, come on now this is hardcore science. Post-mitotic cells/non-proliferative cells/G0/Terminally differentiated or whatever you wanna call it - has never been proven to be a myth, one post in a blog's comment section won't do it.
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#2103 GreenPower

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Posted 20 September 2013 - 01:49 PM

laser scar exfoliation is in fact a much more intense process.

Terminally differentiated cells such as skin do not get shorter on telomeres as they don't undergo mitosis or replicative senescence for that matter. Rather they inherit the amount of telomeres from the stem cells that give them origin.


If skin cells don't undergo mitosis and do not age from a telomere perspective, how would you explain that skin gets older?

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#2104 DorianGrey

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Posted 20 September 2013 - 08:47 PM

G0 cells are differentiated and can undergo mitosis when there are growth factors. I think Glia cells are a good example.

ut the reason skin is aging has also a lot to do with loss of collagen, built up of lipofuscin etc., for sure telomers are only a piece of puzzle. But how come old skin has about a third senescent cells and young skin doesn't? Shortened telomer length would explain that nicely.

#2105 marcobjj

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Posted 20 September 2013 - 11:21 PM

laser scar exfoliation is in fact a much more intense process.

Terminally differentiated cells such as skin do not get shorter on telomeres as they don't undergo mitosis or replicative senescence for that matter. Rather they inherit the amount of telomeres from the stem cells that give them origin.


If skin cells don't undergo mitosis and do not age from a telomere perspective, how would you explain that skin gets older?


Terminally differentiated cells such as skin fibroblasts don't undergo mitosis, they are as old or slightly older than their progenitor Stem cells that do divide and thus suffer telomere shortening and replicative senescence.

Edited by marcobjj, 20 September 2013 - 11:23 PM.


#2106 DorianGrey

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Posted 20 September 2013 - 11:48 PM

laser scar exfoliation is in fact a much more intense process.

Terminally differentiated cells such as skin do not get shorter on telomeres as they don't undergo mitosis or replicative senescence for that matter. Rather they inherit the amount of telomeres from the stem cells that give them origin.


If skin cells don't undergo mitosis and do not age from a telomere perspective, how would you explain that skin gets older?


Terminally differentiated cells such as skin fibroblasts don't undergo mitosis, they are as old or slightly older than their progenitor Stem cells that do divide and thus suffer telomere shortening and replicative senescence.

But didn't that funny YouTube doctor say stem cells have plenty of telomerase and therefore can't go senescent after a little bit of mitosis? Please, even Wikipedia states
"Fibroblasts make collagens, glycosaminoglycans, reticular and elastic fibers, glycoproteins found in the extracellular matrix and cytokineTSLP. Growing individuals' fibroblasts are dividing and synthesizing ground substance. Tissue damage stimulates fibrocytes and induces the mitosis of fibroblasts."
I've recently even watched a movie showing a fibroblast undergoing mitosis. Nobody doubts stem cells play a role in skin rejuvenation, but the aging is not primarily caused by that role.

#2107 hav

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Posted 21 September 2013 - 02:49 AM

laser scar exfoliation is in fact a much more intense process.

Terminally differentiated cells such as skin do not get shorter on telomeres as they don't undergo mitosis or replicative senescence for that matter. Rather they inherit the amount of telomeres from the stem cells that give them origin.


If skin cells don't undergo mitosis and do not age from a telomere perspective, how would you explain that skin gets older?


I think the only way skin cells can avoid cell division would be if you remove or kill them before they get a chance to divide. Stem cells may play a role in replacing lost skin cells but mitoses does too. The fact that many skin cells usually do undergo cell division is the basis of nevus counting and analysis and relating that to overall telomere length of skin and other cells in the body. Because apparently moles and freckles cannot form until after a sufficient number of skin cell divisions have taken place following a skin cell being replaced by stem-cell action. And longer telomere lengths throughout the body seem to relate to higher mole and freckle counts on the skin. And nevus counts and sizes decrease with age as shortened telomeres start limiting the ability of skin cells to achieve the needed number of cell divisions required to form replacement nevus cells. Here's a study all about it:

Nevus Size and Number Are Associated with Telomere Length

They used subjects who were identical twins to remove any genetic variables relating to mole propensity. An interesting consequence being that comparative telomere length differences as measured in their white blood cells were also totally dependent on environmental factors.

Howard

#2108 marcobjj

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Posted 21 September 2013 - 05:21 AM

But didn't that funny YouTube doctor say stem cells have plenty of telomerase and therefore can't go senescent after a little bit of mitosis? Please, even Wikipedia states
"Fibroblasts make collagens, glycosaminoglycans, reticular and elastic fibers, glycoproteins found in the extracellular matrix and cytokineTSLP. Growing individuals' fibroblasts are dividing and synthesizing ground substance. Tissue damage stimulates fibrocytes and induces the mitosis of fibroblasts."
I've recently even watched a movie showing a fibroblast undergoing mitosis. Nobody doubts stem cells play a role in skin rejuvenation, but the aging is not primarily caused by that role.


the problem is it's unsourced. Taken from that same wiki article (and also unsourced): " The suffix "blast" is used in cellular biology to denote a stem cell or a cell in an activated state of metabolism." So from a Wiki perspective skin fibroblast isn't a terminally differentiated cell afterall.

#2109 DorianGrey

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Posted 26 September 2013 - 05:00 PM

But didn't that funny YouTube doctor say stem cells have plenty of telomerase and therefore can't go senescent after a little bit of mitosis? Please, even Wikipedia states
"Fibroblasts make collagens, glycosaminoglycans, reticular and elastic fibers, glycoproteins found in the extracellular matrix and cytokineTSLP. Growing individuals' fibroblasts are dividing and synthesizing ground substance. Tissue damage stimulates fibrocytes and induces the mitosis of fibroblasts."
I've recently even watched a movie showing a fibroblast undergoing mitosis. Nobody doubts stem cells play a role in skin rejuvenation, but the aging is not primarily caused by that role.


the problem is it's unsourced. Taken from that same wiki article (and also unsourced): " The suffix "blast" is used in cellular biology to denote a stem cell or a cell in an activated state of metabolism." So from a Wiki perspective skin fibroblast isn't a terminally differentiated cell afterall.

http://en.wikipedia..../Hayflick_limit - the Hayflick limit is pretty much based on experiments with fibroblasts. I don't want to convince you, but based on all I know at this point I don't think stimulating mitosis is a great idea when you cannot preserve or extend the telomers, except there is a good reason to replace the existing tissue.

#2110 marcobjj

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Posted 29 September 2013 - 05:27 PM

Bill Andrews at 36 min mark says that microdermabrasion does in fact cause telomere shortening. So that must be also true with other peeling processes like exfoliation, retin a.



#2111 DorianGrey

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Posted 30 September 2013 - 02:12 PM

Thanks for the link, very interesting talk he gives. Some of the correlations of telomer length are too straight-forward (no error bars), but I like that he admits that there are very scattered results as well. The most interesting to me is when he says that the might be an unidentified suppressor protein for telomerase expression that is off in germ cells but on in most other cells, so no or very little telomerase is expressed.

Isn't there any proteome or gene activity study that could identify a protein that suppresses hTERT? Maybe hPOT1?

His HTS approach has at least given him 57 compound families so far and in next step they could do chemical design on lead substances.

Edited by DorianGrey, 30 September 2013 - 02:25 PM.


#2112 GreenPower

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Posted 02 October 2013 - 05:07 AM

I see that Calvin Harley and Dr H. Valenzuela have tested TA-65 with some test subjects for 2.5 years.

Some comments on the article describing the results:

Cholesterol
They have tested the "total amount" of cholesterol of the test subjects and states that the subjects total cholesterol decreased with an amount corrsponding to eleven years of age, Unfortunately this measurement doesn't say anything if you don't separate the measurement of the good HDL from the bad LDL. The best would have been if they had measured the relation between themand I don't see how this would be connected with reversing aging. Eating less carbs and more fat (so called LCHF) will give you the same results.

Lower blood pressure
The subjects systolic blood pressure (the higher of the two values) decreased with an amount corresponding to about 30 years, which is quite interesting. This would indicate a relative increase of HDL and a relative decrease of LDL. The actual numbers are however not shown.

Increase of bone density by 2%
Quite interesting.

My conclusion
The article concludes by saying that TA-65 "has a positive effect on our body's health by reversing years of damage due to aging". Please note that it doesn't say it actually reversed aging - only some damage associated with it. They could as well have accelarated aging by stimulating the division of certain types of cells, with "short term gain and long term pain" as a result.

Because Calvin Harley is the president and Chief Scientific Officer of "Telome Health Inc", which has the sole business idea to measures telomere lengths, I would expect the study to also include the measurement of telomere lengths. Because the arcticle doesn't even mention any measurements for telomeres I draw the conclusion that they couldn't detect any actual rejuvenation for any measured cell types.

I've been trying to find the actual study but haven't found it. Anyone having better luck?

Edited by GreenPower, 02 October 2013 - 05:17 AM.

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#2113 marcobjj

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Posted 02 October 2013 - 06:23 PM

They could as well have accelarated aging by stimulating the division of certain types of cells, with "short term gain and long term pain" as a result.



that is a very strange conclusion to make.

#2114 marcobjj

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Posted 03 October 2013 - 12:16 AM

Because the arcticle doesn't even mention any measurements for telomeres I draw the conclusion that they couldn't detect any actual rejuvenation for any measured cell types.


you are not drawing, you are jumping to conclusions here. How can you be in any position to draw a conclusion of a study you haven't read, based only on a 1 page article.

Edited by marcobjj, 03 October 2013 - 12:19 AM.

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#2115 hav

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Posted 03 October 2013 - 06:31 AM

Because the arcticle doesn't even mention any measurements for telomeres I draw the conclusion that they couldn't detect any actual rejuvenation for any measured cell types.


you are not drawing, you are jumping to conclusions here. How can you be in any position to draw a conclusion of a study you haven't read, based only on a 1 page article.


It's the same paper we discussed back in July:
http://www.ncbi.nlm....les/PMC3045570/

Howard

Edited by hav, 03 October 2013 - 06:37 AM.


#2116 marcobjj

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Posted 03 October 2013 - 07:07 AM

that study is from February 2011. The Revgenetics article published on 09/26/2013 keeps referring to it as "new TA65 study". In any case if it's the same study they did in fact measure telomere length.

#2117 GreenPower

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Posted 03 October 2013 - 07:11 AM

Because the arcticle doesn't even mention any measurements for telomeres I draw the conclusion that they couldn't detect any actual rejuvenation for any measured cell types.


you are not drawing, you are jumping to conclusions here. How can you be in any position to draw a conclusion of a study you haven't read, based only on a 1 page article.


It's the same paper we discussed back in July:
http://www.ncbi.nlm....les/PMC3045570/

Howard



No wonder I couldn't find this "New TA-65 Study" when I only searched for recent articles. Thanks for correcting my mistake, believing this was actually a "New TA-65 Study"..

Edited by GreenPower, 03 October 2013 - 07:12 AM.


#2118 GreenPower

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Posted 03 October 2013 - 07:32 AM

Because the arcticle doesn't even mention any measurements for telomeres I draw the conclusion that they couldn't detect any actual rejuvenation for any measured cell types.


you are not drawing, you are jumping to conclusions here. How can you be in any position to draw a conclusion of a study you haven't read, based only on a 1 page article.


I commented on the article, not the study which the article did not identify, didn't link to and which I couldn't find. The article didn't mention an increase in telomere length and now when the study have been identified, neither did the study. If you don't count the small subset of only 11% of the actual test subjects shown in "fig 3", where more than half of the subjects showed a decrease in mean telomere length after 12 months.

I therefore think my conclusion based on the limited amount of data provided by the article actually was correct.
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#2119 GreenPower

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Posted 03 October 2013 - 07:51 AM

They could as well have accelarated aging by stimulating the division of certain types of cells, with "short term gain and long term pain" as a result.


that is a very strange conclusion to make.


Please note that I didn't draw any conclusion regarding this matter, I only questioned the conclusions drawn by the article and presented an alternate theory fitting the data given.

In my view, presenting this old study as "new" doesn't exactly improve on my confidence in Revgenetics. First we have an old study which was actually an "hypothesis-generating exercise" where only selective data was published, which is then presented as "new" more than half a year after it's been published - and with so much of the original information left out that I didn't recognize which study they actually referred to.

This might indicate there's a certain lack of data supporting the theory that TA-65 might increase mean telomere length.

I will however continue to use up the Cycloastragenol I have in order to see if there's been a change in my own telomere lengths. My next telomere test will be in the beginning of next year.

I might need to buy an extra month of Cycloastragenol to make it a six months test. Beacuse Revgenetics doesn't sell it any longer I need to buy it from another source, though.

#2120 marcobjj

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Posted 03 October 2013 - 07:52 AM

you suggested that the Harley study could be hiding the telomere length data because the 1 page Revgenetics article made no mention of it. As it turns out, not only do they mention it but over 80% of subjects showed a reduction in critically short telomeres, and half showed an increase in mean telomere length.

you also said that TA65 "could as well have accelarated aging by stimulating the division of certain types of cells" - acting as a growth hormone essentially. You think that based on what exactly?

#2121 GreenPower

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Posted 03 October 2013 - 10:53 AM

you suggested that the Harley study could be hiding the telomere length data because the 1 page Revgenetics article made no mention of it. As it turns out, not only do they mention it but over 80% of subjects showed a reduction in critically short telomeres, and half showed an increase in mean telomere length.

you also said that TA65 "could as well have accelarated aging by stimulating the division of certain types of cells" - acting as a growth hormone essentially. You think that based on what exactly?


I think we have gone through the study in this thread like half a year ago. Anyway, regarding item one. In the baseline measurements you will note that the study first show the mean telomere length for all N=114 test subjects (table 2). When they later show the results after twelve months on TA-65, they only show the mean telomere length for n=13 test subjects (fig 3). For reasons not specified they have selected not to show the results for the other n=101 test subjects.

Regarding item 2. Let's say that a regimen accelerates the cell divisions of a certain type of cells (lymphocytes for example). If the same regimen does not also extend the telomeres of the chromosomes in this type of cell, ithis will result in the shortening of the mean telomere length in that type of cell.

In the latter scenario TA-65 doesn't necessarily need to act like a growth hormone, even if this might be suggested by the increase in bone density that the test subjects showed. Rapid division of a certain type of cell may also be associated with a large loss of this same type of cell. Because this was a "hypothesis-generating exercise" and not a controlled study where they suppy all of the relevant data, I deem the study to be of rather low relevance.

#2122 hav

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Posted 03 October 2013 - 02:53 PM

... As it turns out, not only do they mention it but over 80% of subjects showed a reduction in critically short telomeres, and half showed an increase in mean telomere length.

you also said that TA65 "could as well have accelarated aging by stimulating the division of certain types of cells" - acting as a growth hormone essentially. You think that based on what exactly?


... Regarding item 2. Let's say that a regimen accelerates the cell divisions of a certain type of cells (lymphocytes for example). If the same regimen does not also extend the telomeres of the chromosomes in this type of cell, ithis will result in the shortening of the mean telomere length in that type of cell.

In the latter scenario TA-65 doesn't necessarily need to act like a growth hormone, even if this might be suggested by the increase in bone density that the test subjects showed. Rapid division of a certain type of cell may also be associated with a large loss of this same type of cell. Because this was a "hypothesis-generating exercise" and not a controlled study where they suppy all of the relevant data, I deem the study to be of rather low relevance.


I may be mistaken but I think that paper may be based on data collected from Sierra Sciences owners and managers as well as employees who are required to take TA65 as a condition of employment. There's a lawsuit in progress that alleges that employment practice.

Dr Andrews mentioned that he takes TA65 himself and that his telomeres are among the 12 or 13 he talked about when he displayed the chart from the paper in his video. As employees come and go, maybe the 12 or 13 are his favorite friends and/or those longest involved with Sierra Sciences. Maybe they represent the only people involved in the data collection from beginning to end. The paper would certainly be more credible if he revealed that critical piece of information.

I hardly hear talk anymore of telomerase activators actually increasing mean or average telomere length. The focus is more on decreasing the relative number of critically short telomeres over time. I think the only logical way to account for observations of a decrease in the relative number critically short telomeres without an increase in overall average telomere length is to postulate a simultaneous decrease in the number of cells with both the longest and shortest telomeres.

A growth factor that affected cells proportionally to their telomere length would be consistent with that. And studies that show that telomerase is expressed during a phase of cell division. And also consistent with telomerase activation not increasing cancer incidence.

Consider that substances like ta65 may be a growth factor that causes cells with longer telomeres to divide more quickly. Thereby decreasing their average telomere length over time. While either having little effect or maybe even slowing down cell division in cells with the shorter telomeres. This would make the average telomere length for the short telomere group appear to increase over time relative to the long telomere group. While not necessarily increasing the overall average telomere length. Or impacting overall cell replacement needs.

I got the idea, btw, when I was trying to imagine how both average telomere length and the percentage of critically short telomeres could decline together and I got this image of a shrinking brontosaurus in my head. Thank you Dr. Anne Elk.

Howard

Edited by hav, 03 October 2013 - 02:55 PM.

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#2123 DorianGrey

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Posted 03 October 2013 - 04:34 PM

Looks like there is no downside in having long telomers (up to 100kB!). This study used telomerase immortalized human fibroblasts (cen3tel).

http://www.ncbi.nlm....pubmed/23570868

Interesting is the finding of a lack of a clear-cut relationship between telomere length, subtelomeric DNA methylation and expression in human cells. The cellular levels of the telomeric proteins hTERT, TRF1, TRF2 and Hsp90 rose with transformation and were independent of telomere length.
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#2124 DorianGrey

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Posted 03 October 2013 - 04:50 PM

Isn't there any proteome or gene activity study that could identify a protein that suppresses hTERT? Maybe hPOT1?



Interesting find regarding telomerase suppression (not hTERT suppression!):
http://www.nature.co...c_id=nature-2..

CST, composed of Cdc13, Stn1 and Ten1 plays a crucial role, so inhibition of one of these proteins could be a good target, probably Ten1 https://www.ideals.i....pdf?sequence=1 (yeast model)

"To determine whether Cdc13 can function with Stn1 and Ten1, I
purified the proteins, and tested the effects of the proteins on telomerase
activity. Ten1 alone caused inhibition of telomerase DNA-extension, while Stn1 alone
activated telomerase DNA-extension on a 23-base 3’-overhang template.
Cdc13 and Stn1 displayed a synergistic effect on telomerase DNA-extension, giving an
increased activation state in comparison to either protein alone. In the
presence of Cdc13 I observed a striking reduction in DNA extension with increasing
Stn1/Ten1 levels using the 23-base 3’-overhang. "

#2125 marcobjj

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Posted 03 October 2013 - 06:53 PM

I got the idea, btw, when I was trying to imagine how both average telomere length and the percentage of critically short telomeres could decline together and I got this image of a shrinking brontosaurus in my head. Thank you Dr. Anne Elk.


ha!

#2126 marcobjj

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Posted 03 October 2013 - 06:58 PM

Looks like there is no downside in having long telomers (up to 100kB!). This study used telomerase immortalized human fibroblasts (cen3tel).

http://www.ncbi.nlm....pubmed/23570868

Interesting is the finding of a lack of a clear-cut relationship between telomere length, subtelomeric DNA methylation and expression in human cells. The cellular levels of the telomeric proteins hTERT, TRF1, TRF2 and Hsp90 rose with transformation and were independent of telomere length.


interesting, that length would be roughly 1000 years of human lifespan.

#2127 blood

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Posted 04 October 2013 - 09:08 AM

New cycloastrogenol product (VItaSpin is run by Anthony from RevGenetics?):
http://www.vitaspin....ings-min-4.aspx

#2128 GreenPower

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Posted 05 October 2013 - 12:29 PM

New cycloastrogenol product (VItaSpin is run by Anthony from RevGenetics?):
http://www.vitaspin....ings-min-4.aspx


Cheap Then again they don't publish any accompanying lab reports which tells you about the amount of led, mercury, iron or other stuff which might be included.

#2129 GreenPower

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Posted 05 October 2013 - 01:37 PM

Consider that substances like ta65 may be a growth factor that causes cells with longer telomeres to divide more quickly. Thereby decreasing their average telomere length over time. While either having little effect or maybe even slowing down cell division in cells with the shorter telomeres. This would make the average telomere length for the short telomere group appear to increase over time relative to the long telomere group. While not necessarily increasing the overall average telomere length. Or impacting overall cell replacement needs.

I got the idea, btw, when I was trying to imagine how both average telomere length and the percentage of critically short telomeres could decline together and I got this image of a shrinking brontosaurus in my head. Thank you Dr. Anne Elk.

Howard


The idea seem logical enough. I suppose the theory to some extent could be substantiated by measuring the Standard Deviation of the Median Telomere Lengths, which together with the MTL would be lower than before. Or am I thinking in the wrong way here?

Something like this actually happened in a rather extreme fashion when I tried using AIV in my regimen. For reference I've included an extract from the excel chart which contain all my measurements.

I seem to remember a lab report published by Anthony, which stated that TA-65 at one time contained a measurable amount of AIV. This could possible mean TA-65 to some extent might have properties similar to taking AIV.

Attached Thumbnails

  • AIV.png

Edited by GreenPower, 05 October 2013 - 01:58 PM.


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#2130 hav

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Posted 06 October 2013 - 03:55 PM

Looks like there is no downside in having long telomers (up to 100kB!). This study used telomerase immortalized human fibroblasts (cen3tel).

http://www.ncbi.nlm....pubmed/23570868

Interesting is the finding of a lack of a clear-cut relationship between telomere length, subtelomeric DNA methylation and expression in human cells. The cellular levels of the telomeric proteins hTERT, TRF1, TRF2 and Hsp90 rose with transformation and were independent of telomere length.


interesting, that length would be roughly 1000 years of human lifespan.


The cells they are talking about gradually turn into malignant tumors:

In this paper, we exploited telomerase immortalized human fibroblasts (cen3tel) that gradually underwent neoplastic transformation during culture propagation to study telomere composition and length regulation during the transformation process.


I think what the paper is about is trying to understand what causes these cells with super long telomeres to eventually become cancerous by analyzing related gene and protein activity. The observed protein rise during cen3tel tumorigenesis suggests a p53 maintenance issue. And that maybe a danshen extract like tanshinone-I might complement cycloastraganol.

Howard




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