2189 replies to this topic

[hav]

Just suggests to me that telomerase activation and telomere length are not the only answer. Which I've been hearing round here quite a while. Suggests maybe antioxidants and telomere protecting supplements many also be important.

Howard

[romtm]

To antioxidants,telomere activators and telomere protecting supplements, I added stem cell activator ,HGH activator and hormone modulation therapy.Plus exercise-a proven telomere activator.

[AdamI]

Based on this, it seems clear that simply inducing telomerase is not the answer. Somehow we would have to both induce telomerase and increase the repair of these Telomerase Associated Foci (TAF) of DNA damage.

Any ideas?

Got an idea take AC-11 it repairs single and double stranded DNA damage. It has been proven in studies where mice were subjected to the same light as the study you wrote about.
With 1 month treatment of AC-11 most of the DNA damage had been repaired in the mice... sounds good right:)?

Solgar and Wellness sells it under patent. Think Solgar has the european market and Wellness has the North american market.

[Turnbuckle]

Based on this, it seems clear that simply inducing telomerase is not the answer. Somehow we would have to both induce telomerase and increase the repair of these Telomerase Associated Foci (TAF) of DNA damage.

Any ideas?

Got an idea take AC-11 it repairs single and double stranded DNA damage. It has been proven in studies where mice were subjected to the same light as the study you wrote about.
With 1 month treatment of AC-11 most of the DNA damage had been repaired in the mice... sounds good right:)?

Solgar and Wellness sells it under patent. Think Solgar has the european market and Wellness has the North american market.

Which is basically cat's claw extract, I believe.

[AdamI]

yeah it from Cats claw, only the bark and its also treated on some way. boiled in a certain amount of time and soo forth...

[smithx]

I looked around for AC-11, and found that LEF dropped their "Optimized Cats Claw" product, Solgar no longer sells AC-11, but only "Cat's Claw Inner Bark Extract", and the only companies which do sell it are ones I've never heard of.

I wonder if it was discovered that something is wrong with AC-11 and that's why everyone dropped it. I suspect lawsuits may have been to blame.

[AdamI]

here you go, AC-11 from Solgar. http://www.amazon.co...31536346&sr=8-1

From AC-11.com We create AC-11® using a patented “aqueous hot water extraction” and purification process standardized to a minimum of 8% Carboxy Alkyl Esters (CAE) concentration.

Also says it Optigenex that has the patent... as far as I know there is only 2 companies that is allowed to sell it, Solgar in europe and Wellness in America

[smithx]

It's no longer listed on Solgar's main site. Optigenex's site appears to be offering to sell it to whomever, so I'm curious that there are not more people selling it if it actually is safe and effective.

[AdamI]

I think they are looking for companies to sell it outside of europe and america. I doubt they will give another "player" license to sell it on europe or the american market. Looks like there tactic is to have one exclusive seller on each market. Guess you could email them?

[smithx]

This article implies that cell senescence (what we're trying to avoid) is caused by damages to telomeres. The shortening, according to them, may be due to oxidative damage, and when the telomeres are too short, the proteins which protect them and keep them looped don't attach properly.

But they also talk about telomerase having anti cell senescence properties independent of telomere extension, which is interesting. The fact that telomerase may increase survival of cancer cells irrespective of telomere length is potentially worrisome:

In recent years, indications for additional functions of telomerase independent of telomere maintenance are accumulating. If telomerase is inhibited in tumour cells, there is either a delayed response that depends on telomere shortening or a rapid effect on cell viability without any measurable effect on telomere length (106–110). These data suggest that telomerase promotes cell survival and stress resistance by mechanisms that appear to be largely independent on telomere length maintenance. Zhang et al. and Fu et al. (111,112) showed an increased resistance of hTERT overexpressing cells to apoptotic stimuli at an early, premitochondrial step. Sharma et al. (113) found an increased repair capacity of hTERT overexpressing cells. We and others demonstrated an enhanced sensitivity of tumour cells to certain DNA damaging agents when telomerase was impaired (107,113–117). We showed that overexpression of TERT conferred increased stress resistance, improved antioxidant defence and differentiation capacity to mouse embryonic stem cells (118).
Ectopic hTERT expression in normal cells as well as hTERT inhibition/depletion in telomerase positive cancer cells and even in yeast S. cerevisiae caused significant changes to the transcriptome and global gene expression patterns (106,108,119,120) that are largely unrelated to telomere maintenance. Interestingly, among a wide range of functional classes, large groups of genes with functions in metabolism, specifically mitochondrial metabolism, have repeatedly been reported to appear dependent of telomerase (106,119). Bagheri et al. (106) found that telomerase modulated glucose consumption and appeared to control the glycolytic pathway in tumour cells, thereby potentially altering the energy state. Recently, telomerase has been added to a growing list of proteins, such as p53, HMGA1, VHL, APP, prohibitins, Lon-protease, etc., that can shuttle between the nucleus and the different subcellular compartments including mitochondria. Importantly, it has been shown that telomerase that normally is located in the nucleus can shuttle to cytoplasm and/or mitochondria upon oxidative challenge (55,121–123).

[johnross47]

This article implies that cell senescence (what we're trying to avoid) is caused by damages to telomeres. The shortening, according to them, may be due to oxidative damage, and when the telomeres are too short, the proteins which protect them and keep them looped don't attach properly.

But they also talk about telomerase having anti cell senescence properties independent of telomere extension, which is interesting. The fact that telomerase may increase survival of cancer cells irrespective of telomere length is potentially worrisome:

In recent years, indications for additional functions of telomerase independent of telomere maintenance are accumulating. If telomerase is inhibited in tumour cells, there is either a delayed response that depends on telomere shortening or a rapid effect on cell viability without any measurable effect on telomere length (106–110). These data suggest that telomerase promotes cell survival and stress resistance by mechanisms that appear to be largely independent on telomere length maintenance. Zhang et al. and Fu et al. (111,112) showed an increased resistance of hTERT overexpressing cells to apoptotic stimuli at an early, premitochondrial step. Sharma et al. (113) found an increased repair capacity of hTERT overexpressing cells. We and others demonstrated an enhanced sensitivity of tumour cells to certain DNA damaging agents when telomerase was impaired (107,113–117). We showed that overexpression of TERT conferred increased stress resistance, improved antioxidant defence and differentiation capacity to mouse embryonic stem cells (118).
Ectopic hTERT expression in normal cells as well as hTERT inhibition/depletion in telomerase positive cancer cells and even in yeast S. cerevisiae caused significant changes to the transcriptome and global gene expression patterns (106,108,119,120) that are largely unrelated to telomere maintenance. Interestingly, among a wide range of functional classes, large groups of genes with functions in metabolism, specifically mitochondrial metabolism, have repeatedly been reported to appear dependent of telomerase (106,119). Bagheri et al. (106) found that telomerase modulated glucose consumption and appeared to control the glycolytic pathway in tumour cells, thereby potentially altering the energy state. Recently, telomerase has been added to a growing list of proteins, such as p53, HMGA1, VHL, APP, prohibitins, Lon-protease, etc., that can shuttle between the nucleus and the different subcellular compartments including mitochondria. Importantly, it has been shown that telomerase that normally is located in the nucleus can shuttle to cytoplasm and/or mitochondria upon oxidative challenge (55,121–123).

http://www.scienceda...20312152645.htm new way of treating mitochodrial problems?

[AdamI]

I am beta-tasting a new product ill call ... iceberg for now.

I do believe it increases telomere length in immune cells.

A

Is it easier to induce Telomerase in immune cells(since they have some already)? Or is that the only cells you tested the product on soo far?

[cytg]

Came across this video earlier today, learned a lot of useful info, thought I'd share it:

http://www.youtube.com/watch?v=hayIfgL3OYs

I may just be an ill informed civilian layman, non the less my bs-meter rises when I see and hear something like this
(attached

4 caps * 365 days * 5mg = 7300mg = 7,3 grams of TA65.
Apparantly that equates to 650 pounds of the raw product, Astragalus, if you should chew it in its original form.

Thats is alot of god damned product. If this is true, it is not 'found' somewhere,in china is it? I can only imagine It is massively farmed over alot of realestate ...

Attached Thumbnails

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[NefarioCall]

i spent a few hours scanning over this topic today. I have not read every post yet (although i'll look back across it some more).
i am a 27 year old male. I have not had so much as a cold since i was feverish for about 36 hours back in 2006.
The time before that i cannot really remember. It had to have been at least 2002.
Until 2009 however, my diet was heavy in crap such as McDonald's.
I have in the last three years slowly changed my diet and plan to continue doing so.
I have noticed tremendous changes in that time to my overall 'look of healthiness and feel'.
Others frequently comment on this change, although i as not 'sick' before hand, so i cannot comment on substantial changes there.

For reference, my current diet includes generally:
Pasta/Rice Grain / Bakery fresh breads
Tomatoes, Veggie hot dogs and burgers,
Lots of Lentils, some dairy, no meat,
Beans ... for the most part.
(its a work on progress but really much better than it used to be)

In supplementation of that, my daily regimen includes:
Astragalus Root (3 grams of 0.5% natures way)
Gotu Kola (2 grams natures way)
Fo-Ti (1 gram natures way)
Ginseng (1 gram 10:1 extract)
Glutathione (200mg snorted, reason for this is stomach acid destroys it and i have no means to inject it. Lungs are a proven method).
Red Reishi (500mg 5:1 extract)
Lecithin (10 grams)

I have done no tests and unfortunately cannot provide raw numbers.

I am curious however, after having read through this thread.
An earlier post quotes that a healthy 20 year old would have about 8,000 base pairs of Telomeres.
The margin of error in testing is +/- 500 base pairs, but the base pair loss is 50-100 pairs per year.
A bit of simple math suggests to me that the margin of error is thus 5-10 YEARS.
.... and this thread is only 4 years old.

i understand that there is hope that test results over a period of 2-4 years would show increased base pairs that exceed the margin of error.
Should this be discovered to a degree substantial enough, it would be a significant discovery,
and i would imagine also be very important for those who are older than i am.

However, if a treatment for example is able to exceed the base pair loss only slightly, by say, maybe 100 base pairs,
then over the entire length of this threads history, a person would have 400 more base pairs than in 2008,
which still falls into the margin of error and could read as 'no change', however, in reality, even a small increase
is self sustaining and to some degree every bit as significant as 1,000 base pairs per year with the exception that
for someone who is much older, they would not be able to turn back the already advanced clock as quickly.

For myself, being 27, 'No change' would be a complete victory, at least regarding this 'part' of immortality.

[AdamI]

Glutathione (200mg snorted, reason for this is stomach acid destroys it and i have no means to inject it. Lungs are a proven method).

I didn't know that stomach acid destorys it. Why are there no Glutathione with double casings that resist stomach acid. As far as I know it's quite cheap...
are there any?

Fo-Ti sounds interesting, with the old story of the man that became 130 years and got he's black hair back...

[NefarioCall]

I haven't searched online thoroughly enough to know how many varieties of Glutathione are out there.
(For those who don't know it, Glutathione is a substance found to be deficient in the vast majority of the sick and elderly. highest levels found in healthy youth ~ lowest levels in hospitalised elderly).
My nearest store only had one in stock which is a standard single casing.
My regimen is a work in progress, so if i can find something better i'll go with that on the next bottle.

i read somewhere in this thread that grey hair is an indication of chromosome damage?
That it is basically a visual guide to how far progressed you are to dying of 'old age'.
That seems accurate to me, and there is significant study to show that Fo-Ti reverses this.
...so i consider it important.

Edited by NefarioCall, 18 March 2012 - 04:28 PM.

[AdamI]

I see that you don't take Resveratrol, that could be something in your regime. Since it promotes production of Sirt 1 that helps production of telomerase.

[gamesguru]

That it is basically a visual guide to how far progressed you are to dying of 'old age'.
That seems accurate to me, and there is significant study to show that Fo-Ti reverses this.

Do you know which study you're talking about?
See this, about fo-ti root. It's very interesting.

Molecular Authentication of the Traditional Medicinal Plant Fallopia multiflora
The root of Fallopia multiflora is one of the most widely used traditional Chinese medicines. However, it is often confused and substituted with the roots of F. multiflora var. ciliinervis, Pteroxygonum giraldii, Cynanchum auriculatum, and Stephania cepharantha. To establish a DNA polymorphism-based assay for the identification of F. multiflora, the nuclear ribosomal DNA (nrDNA) internal transcribed spacer (ITS) regions of six Fallopia species were sequenced and analyzed. Based on the diversity of ITS regions among the species the diagnostic primers PMITS28 and PMITS545, which amplified an expected 517-bp DNA fragment from F. multiflora DNA, were designed. No amplified product was observed when DNA from other species was used. This method can be used for the authentication of F. multiflora. (https://www.thieme-c.../s-0029-1185382)

I see that you don't take Resveratrol, that could be something in your regime. Since it promotes production of Sirt 1 that helps production of telomerase.

It's not proven that resveratrol directly activates sirt1 (http://www.ncbi.nlm....pubmed/15684413). It probably does activate sirt1, among other helpful genes. It has some drawbacks, but it looks really promising.

See these two wiki articles:
http://en.wikipedia....and_resveratrol
http://en.wikipedia....nisms_of_action

[niner]

i read somewhere in this thread that grey hair is an indication of chromosome damage?
That it is basically a visual guide to how far progressed you are to dying of 'old age'.

I've not heard this. There are a lot of people who are otherwise healthy yet get grey hair at a relatively young age. I'm not aware of any studies comparing lifespan to hair color. There could be something to it, in that grey hair might be an indication of excess stress, but I think it's mostly due to a genetically determined level of catalase.

[zorba990]

I haven't searched online thoroughly enough to know how many varieties of Glutathione are out there.
(For those who don't know it, Glutathione is a substance found to be deficient in the vast majority of the sick and elderly. highest levels found in healthy youth ~ lowest levels in hospitalised elderly).
My nearest store only had one in stock which is a standard single casing.
My regimen is a work in progress, so if i can find something better i'll go with that on the next bottle.

i read somewhere in this thread that grey hair is an indication of chromosome damage?
That it is basically a visual guide to how far progressed you are to dying of 'old age'.
That seems accurate to me, and there is significant study to show that Fo-Ti reverses this.
...so i consider it important.

Liposomal Glutathione is out there and can also be made with DIY methods.

[Getm]

I found this info and please correct me if I'm wrong - does it says that l-arginine promotes telomerase activity in HeLa ?
http://www.tumorres....tasis/43162.htm
If so maybe there would be a chance to increase telomerase activity by combining l-arginine with TA-65 or other telomerase activators ?

[AdamI]

Sounds like it, but how big of a dose are they talking about in the study of l-arginine?
Seems like one need a very high dose too measure any difference, couldn't figure out what dose they used...

[Getm]

The article says the concentration should be 5 ~ 25 mM for the promotion of telomerase.
I found that l-arginine has molecular weight of 174.20
So the concentration should be 871mg/L ~ 4355mg/L
Human body is aprox. 80L so one must consume 70-350g l-arginine Huge

[AdamI]

hehe yeah, soo no point in pondering about that then. Take some extra TA-65 instead;)

[aaaaaaal]

In the harvard study, what happened to the mice who had their aging reversed, are they still alive???

"These mice were equivalent to 80-year-old humans and were about to pass away," says Ronald DePinho, co-author of the paper and a scientist at Dana-Farber Cancer Institute in Boston. After the experiment, "they were the physiological equivalent of young adults."

[aaaaaaal]

"These mice were equivalent to 80-year-old humans and were about to pass away," says Ronald DePinho, co-author of the paper and a scientist at Dana-Farber Cancer Institute in Boston. After the experiment, "they were the physiological equivalent of young adults."

Can someone tell me what happened to the mice? Thanks

[AdamI]

mice cemetary

[aaaaaaal]

mice cemetary

So, what did they die of seeing as they were "the physiological equivalent of young adults"?

Edited by jorgepl22, 05 May 2012 - 07:51 PM.

[hav]

So, what did they die of seeing as they were "the physiological equivalent of young adults"?

Here's the actual paper on the study:

http://www.ncbi.nlm....cles/PMC3057569

... which seems to have allot less information in it than the articles I've seen about it. It does indicate, however:

Correspondence and requests for materials should be addressed to ; Email: ron_depinho@dfci.harvard.edu

Howard

[niner]

So, what did they die of seeing as they were "the physiological equivalent of young adults"?

Once they actually became old adults, they probably died of the same stuff that any mouse dies of. It's important to keep in mind what was going on in this experiment. Mice were made artificially "old" before their time by causing their telomeres to become critically short. They were not actually "old", in that they didn't have all of the damage that an actual old mouse would have. They were "artificially old", and it was possible to rescue them from this condition by turning on their telomerase. Turning on telomerase in a mouse (or human) that was truly old would not have the same effects, though it does appear to help.