2189 replies to this topic

[johnross47]

http://ijp-online.co...ge=81;aulast=Li

full article here

[romtm]

I am currently using astragalus extract while waiting for Anthony's new product, and hoping it will be within budget, (Astral Fruit was only just within budget) but even on a one week on, one week off regime I have increasing insomnia through the on week, which gradually goes after two days off. In the on week I also have extremely vivid and complicated dreams, and those fade to normal in the off week. By the end of the on week the dreams have got to the point where my sleep has become extremely "noisy" with long periods of repetitive images and phrases instead of more coherent dreams. ( if any dream could be called coherent.....my usual dreams do at least feature a series of discreet events in some sort of sequential story) Has anyone else experienced this? I don't recall it happening on cycloastragenol to anything like this degree.

I just started to take a new Telomerase Activator called Revital-TA from Provita Nutrition Canada.Cost 60 USD/60 capsules,and each capsule contain 5 mg cycloastragenol, 50 mg astragaloside IV ,250 mg astragalus extract 20:1,colostrum and others(see my previous post).

Price is very good for me ,and I hope for results.

[AdamI]

It's only 25 mg AIV per capsule I beleave, not 50 mg?

[romtm]

It's only 25 mg AIV per capsule I beleave, not 50 mg?

In one capsule of Revital TA are 70-80 mg of Astragaloside IV-50 mg in pure form plus 20-30 mg from the 250 mg of Astragalus extract 20:1.
Also 5 mg of more absorbable form of Cycloastragenol.

[romtm]

I double checked.
In one capsule are 25 mg of Astragaloside IV and another 50 mg of Astragaloside IV are from Astragalus Extract 20:1 (is stated in a brochure that I received from manufacturer).Totally 70-80 mg.

[hav]

I think you'd get more of everything except the cycloastraganol from 500 mg of a good standardized extract. I was thinking of adding some cyclo to the 500 mg I take. Greenpower reported earlier in this thread of his own telomere mesurements that he got better test results back from taking a 500 mg extract than from cyclo or A4 alone. His A4 alone results were the lowest of the 3. Which is why I stopped adding A4 to the standardized extract I take. But I don't think anyone reported on taking a standardized extract + cyclo together.

Howard

[romtm]

I think you'd get more of everything except the cycloastraganol from 500 mg of a good standardized extract. I was thinking of adding some cyclo to the 500 mg I take. Greenpower reported earlier in this thread of his own telomere mesurements that he got better test results back from taking a 500 mg extract than from cyclo or A4 alone. His A4 alone results were the lowest of the 3. Which is why I stopped adding A4 to the standardized extract I take. But I don't think anyone reported on taking a standardized extract + cyclo together.

Howard

A4(and astragalus extract) work together with cyclo not direct to activate the enzyme telomerase,but to strengthen the immune system. Same colostrum.In this formula is included TA-100S-a proprietary sulphated cyclo derived small molecule.

I contacted the manufacturer and they reply that this form of cyclo have better absorbtion and contain a smaller molecule of cyclo-with 1-2 clusters(I don't know exactly what this means) -something similar like in TA-65-I believe.I think that normal molecule of cyclo has low absorbtion,and this can be a reason for the telomere results reported by Greenpower.

Astragalus extract is 20:1 concentration, 250 mg/capsule is equivalent with 5000 mg of astragalus.And I take 2 capsules/day.

I try to make a Telomere test next month,and six months later,and I will post it.I need to fly to Madrid-Spain-is the only clinic in Europe that make this test( for 500 Euros )

Andrei

[AdamI]

Better thing to do is maybe analyse those capsule and see if they contain what they say, instead of spending 500 euros on that test? Did they tell you how they make Cyclo with sulphated, I mean should that process be very complicated?
Do you know when König started selling it? The release date of Revial-TA?

[Robert89]

Surely if the capsules are made in Canada under supervision, you can expect the capsules to have what they say they have. The only people who weren't putting clearly the contents of their capsules were the makers of TA-65. Pretty much everyone else clearly marks the labels with the contents of such. If a maker of nutraceuticals has got the nuance to label according clearly, and manufacture in a country like Canada, the chances are they are bona fide.

[romtm]

Better thing to do is maybe analyse those capsule and see if they contain what they say, instead of spending 500 euros on that test? Did they tell you how they make Cyclo with sulphated, I mean should that process be very complicated?
Do you know when König started selling it? The release date of Revial-TA?

Because the regulations in Canada for supplements producttion are more severe compared with regulation in USA,I think that the capsules contain what they say. Are very professionaly sealed,labelled and lots of details.I was curious about how Cyclo is sulphated and make it smaller size molecules,and they told me that is an ultrasound technology and gave me more explanations but I don;t understand it..I don;t know if is complicated-but they won my trust.I sent them 3 emails and responded in maxim 24 hours,and first order I received in one working day(they have office and warehouse in my country,also doctors for evaluations and recomandations).I also spoke by phone with canadian director of Provita and gave me all the details that I asked.I bought from them also Stemulin (Stem Cell activator)and HGH activator-part of Gerontoversal protocol.It was my decision.

Releasing date for Revital TA was end of last year,so unfortunatelly not enough time to see results on any user of Revital TA.

I hope this help.

[Anthony_Loera]

I double checked.
In one capsule are 25 mg of Astragaloside IV and another 50 mg of Astragaloside IV are from Astragalus Extract 20:1 (is stated in a brochure that I received from manufacturer).Totally 70-80 mg.

I call BS on the statement above.

At the most 250mg of 20:1 extract will have about 1 to 1.5 mg of A4.
To get all the way up to 50mg would require taking 8.2 to 12.5 grams a day of 20:1 extract.

There is no way Astragalus 20:1 extract has as much Astragaloside IV, as stated by romtm.
See attached (25:1 and 50:1 lab COA's).

I would stay away from these folks because of claims made to romtm. I personally believe that If the manufacturer is stretching the truth about one ingredient, there is no reason the would not stretch the truth on other ingredients or things regarding the product.

Cheers

A

Attached Files

•  Astragalus-Cycloastragenol-50to1-04132011.pdf   15.77KB   224 downloads
•  Astragalus-Cycloastragenol-25to1-04132011.pdf   15.72KB   219 downloads

Edited by Anthony_Loera, 14 February 2012 - 04:29 PM.

[romtm]

I double checked.
In one capsule are 25 mg of Astragaloside IV and another 50 mg of Astragaloside IV are from Astragalus Extract 20:1 (is stated in a brochure that I received from manufacturer).Totally 70-80 mg.

I call BS on the statement above.

At the most 250mg of 20:1 extract will have about 1 to 1.5 mg of A4.
To get all the way up to 50mg would require taking 8.2 to 12.5 grams a day of 20:1 extract.

There is no way Astragalus 20:1 extract has as much Astragaloside IV, as stated by romtm.
See attached (25:1 and 50:1 lab COA's).

I would stay away from these folks because of claims made to romtm. I personally believe that If the manufacturer is stretching the truth about one ingredient, there is no reason the would not stretch the truth on other ingredients or things regarding the product.

Cheers

A

I just sent an email to manufacturer and ask to explain their claim and the contain of Astragaloside IV in the Astragalus extract

But only for informations. I bought last year 20% Astragaloside IV powder from a serious UK supplier . Also I bought with 50% concentration,later.This I am sure that is Astragalus extract with 20% Astragaloside,or 50%. Each Astragalus extract can have a different Astragaloside IV contain.Same is with Resveratrol.Can contain any procentaje of Trans Resveratrol-from 1% to 99%..I have capsules with 20% transresveratrol,and capsules with 98% transresveratrol.

Also I have Astragalus extract (1:1)capsules with 0,7% astragaloside IV.If same Astragalus source will be concentrated to 20:1,the contain of Astragaloside will be 14%.Theoretically!

But I will post the answer from manufacturer.I was suspicious too about this claim from Provita.

[Anthony_Loera]

Unless you have COA's for the items you previously purchased, I cannot agree with your statements.

A

[brokenportal]

http://www.longecity.org/forum/donate/goal-8-cryopreservation-research/ ' class='bbc_url' title='External link' rel='nofollow external'>

[hav]

Romtm ,

I think you may be misunderstanding the specs. They are probably talking about a standardized extract when they refer to .7% astragaloside. When I was pricing in bulk a while back with kalix, it was about the same price as a 35:1 extract. Same for an extract referenced to 70% polysacharides. A 20:1 extract was about half the price and 1:1 was way cheaper in comparison. Suggesting their 20:1 extract might be about .4 % a4.

Howard

[romtm]

Unless you have COA's for the items you previously purchased, I cannot agree with your statements.

A

1.I requested from my last UK supplier and from Provita Canada a report of analyses of their astragalus extract.I wait for the answers.

Provita Canada(manufacturer )responded to me that was a mistake only on their on-line romanian sales agent site . Astragalus extract used in Revital TA contain 3% Astragaloside IV,not 20% like was posted,and the mistake was corrected .The sales agent made a confusion between 20:1 and 20%.

2.In your post number 61 on this forum ,you posted Report of Analyses for your astragalus extract product with 13,3% A4.You explained that a 250 mg capsule of astragalus extract sold by Revgenetics contained 13,3% A4,more exactly- 33mg of A4 in one capsule.

3.You can see on Made-in-China.com that are many chinese manufacturer of Astragalus extract with 1-99% contain (at customer request)of Astragaloside IV -test by HPLC,with samples if needed for testing.

[Anthony_Loera]

Hi romtm,

Correction: The 250mg I mentioned was to match the reference to the post you made about your product against the Astragalus extract that was tested. RevGenetics does not sell any 250 mg astragalus capsules.


As far as the Made-in-china info:

===============================================================================================================
you are now trying to mix oranges with apples, and trying to confuse things:

1- You can't make me believe that because you found a Chinese source that says they can produce a material on the web somewhere. that it somehow translates to your product automatically having that amount when there is no COA available to back up the claim. Heck, forget the literature about the 50mg...What does the label actually say? It actually only says 25mg of A4 (see image attached).

That amount is also the only amount I expect to see in the COA. To sum up, according to the label.... the 50mg claim from the addition of 250mg of Astragalus is total baloney. At this point, it is obvious that the literature made by company re-selling you the product is incorrect, and cannot be trusted.


Now... let's beat a dead horse:

2- Again, you cannot assume that a 20:1 natural extract has such an enormous amount of A4, without spiking it. Even chinese standards of astragalus extraction have a tiny amount of A4 (see the end of the standards paper attached called 'Radix_Astragali"). This leads me to believe the product is spiked with a material of higher purity that infringes on Geron's patent. Heck even without the marketing baloney, I can read the label now... and know that this product infringes on the Geron patent.

3- Lastly...yes even 'Organic' Astraglus purchased from Starwest botanicals had a ridiculously low amount of A4 (see COA of Organic material attached)

===============================================================================================================

So at this point...

there is no way you are going to convince me that the product literature is correct regarding 50mg of A4 from a 20:1 extract. Again, I would personally avoid this... as it all seems pretty darn hokey to me... specially because I have spent the money testing Astragalus at varying concentrations... instead of relying on marketing from most companies.


A

Attached Thumbnails

• 

Attached Files

•  Radix_Astragali.pdf   503.92KB   187 downloads
•  040711-0215-Organic.pdf   65.5KB   231 downloads

[PWAIN]

Hi romtm,

Correction: The 250mg I mentioned was to match the reference to the post you made about your product against the Astragalus extract that was tested. RevGenetics does not sell any 250 mg astragalus capsules.

Maybe you mean does not CURRENTLY sell...

Post 61:

Hi Smithx,

I just added this to the free shipping section.

It is a 250mg capsule, of which 33mg is Astragaloside IV, COA is below:
http://revgenetics.c...OA_07072008.pdf

At this time we recommend only 1 capsule a day.

Cheers
A

[Anthony_Loera]

PWAIN,

that post was in 2008,

so yes... I stand corrected: We don't currently sell 250mg astragalus capsules.


A

[Robert89]

2- Again, you cannot assume that a 20:1 natural extract has such an enormous amount of A4, without spiking it. Even chinese standards of astragalus extraction have a tiny amount of A4 (see the end of the standards paper attached called 'Radix_Astragali"). This leads me to believe the product is spiked with a material of higher purity that infringes on Geron's patent. Heck even without the marketing baloney, I can read the label now... and know that this product infringes on the Geron patent.

You make some good points about the discrepancies with the product we are discussing. I agree you seem to have shown some problems in the ingredients. Maybe it's some misunderstanding on the part of the poster, since the product is made in Canada, I doubt it is unreliable. Surely the Canadian equivalent of the FDA supervises these things? If you are doubting this product's manufacture, then surely all products cannot be trusted. How do we know what's in each capsule anyway? It seems to be a question of regulation.

What I don't understand is this reference to Geron's patent. Are you saying that Geron own's the patent for all products on the market that have A4 or cycloastragenol, or astragalus with A4 or cycloastragenol or other ingredients combined together? Are you sure this is true? It seems remarkable you can patent a naturally occurring plant and it's derivatives. Does that mean Vitamin C is patented by someone as well, since it's derived from oranges? If that's the case, Geron's claim sounds a bit outlandish.

[romtm]

Anthony,

1). I never used the word "natural" extract.To be clear,I claim and I am convinced that a product simply called "Astragalus"(like you also named it simply "Astragalus"in your COA posted,with 13,3% A4-so can be extract,or standardized extract)in a special extraction process can be supplied with a specific component,in our case A4(so the other components of Astragalus are simply removed ).I attached COA for Astragalus with 50% A4,and COA for Astragalus with 90% A4,and your COA-for comparation -with 13,3% A4.Of course the main difference is the price,that can be between aprox 40 USD/kg (A4 less then 1%) to aprox 6000 USD/kg(90%A4).

2). Regarding Revital TA.They corrected the mistake of their sales agent with the contain of A4 in their Astragalus extract and they take apologised for this.So in one capsule of Revital TA are 25 mg of A4 .Also are more A4 from Astragalus extract, that are not mentioned in the label.They use Astragalus extract 20:1 with 3% Astragaloside.

Astragalus extract 50:1 have 6% Astragaloside.See attached the Canadian COA for Astragalus extract 20:1 with 3% Astragaloside(I removed the canadian name of the lab-because I don't know if I have the right to post it).I don't have the contain of A4 from total Astragaloside from Astragalus and I am not interested.

3). I personally chose to take Revital TA,because is much cheaper than TA 65,have money back quaranty,have exact label with the ingredients (and TA-65 not),and replay promptly to all my questions(the mistake was from their sales agent,and was not claimed by Provitanutrition and was immediately corrected ).

4). Because you(Revgenetics) are seller of TA-65 and Provitanutrition are seller of Revital TA and I don't sell any supplements,I have no interest to be involved in any claims or disputes .I buy what is suitable for me and for my budget.Anyway,is not sure and guaranted the results for any of this supplements.
 Astragauls PE_COA Canada.pdf   87.53KB   495 downloads
 coa(84687-43-4)-E 90%.pdf   135.24KB   594 downloads
 coa(84687-43-4)-E 50%.pdf   134.7KB   279 downloads
 Astral_Fruit_COA_07072008.pdf   16.34KB   268 downloads

[hav]

2- Again, you cannot assume that a 20:1 natural extract has such an enormous amount of A4, without spiking it. Even chinese standards of astragalus extraction have a tiny amount of A4 (see the end of the standards paper attached called 'Radix_Astragali"). This leads me to believe the product is spiked with a material of higher purity that infringes on Geron's patent. Heck even without the marketing baloney, I can read the label now... and know that this product infringes on the Geron patent.

...

What I don't understand is this reference to Geron's patent. Are you saying that Geron own's the patent for all products on the market that have A4 or cycloastragenol, or astragalus with A4 or cycloastragenol or other ingredients combined together? Are you sure this is true? It seems remarkable you can patent a naturally occurring plant and it's derivatives. Does that mean Vitamin C is patented by someone as well, since it's derived from oranges? If that's the case, Geron's claim sounds a bit outlandish.

Curious about that myself. Haven't read Geron's patent but generally under US law you can patent a synthetic molecule, a process, or a formulation. If its both new and not obvious. In the case of adding cycloastragenol and/or astragaloside IV to astragalus root, that sounds more like an astragalus extract standardized on its own naturally occurring components as opposed to a formulation. My own perception is that the concept of a standardized extract is so commonly employed these days that it wouldn't be a very defensible patent candidate. Even if it was considered a formulation, varying ratios a small amount would probably defeat the patent. My own sense is that formulation patents are so indefensible that most companies tend to rely more on keeping their formulations a secret. And try to stymie competition that way. I think a process patent would hold up better. But that's not something the product label would tell you.

Howard

Edited by hav, 17 February 2012 - 02:23 PM.

[Hebbeh]

http://www.scienceda...20220161233.htm

Telomere Failure, Telomerase Activation Drive Prostate Cancer Progression

ScienceDaily (Feb. 20, 2012) — Genomic instability caused by an erosion of the protective caps on chromosomes, followed by activation of an enzyme that reinforces those caps, allows malignant cells to evade destruction and acquire more deadly characteristics, researchers report in an Online Now article at the journal Cell.

In a strain of mice engineered to develop prostate cancer, all mice that went through this two-step process developed lethal cancer and 25 percent had the disease spread to the spine. Two groups of mice that avoided this cycle developed only precancerous lesions or localized prostate cancer.
A comparative analysis of genetic changes in the metastatic mouse tumors and those found in metastatic human prostate cancer identified the Smad4 gene as a driver in bone metastasis. Fourteen other genes were found to be associated with human prostate cancer prognosis.
The research focused on telomeres -- repeat nucleotide sequences at the tips of chromosomes that prevent genomic damage during cell division. Telomeres shorten with each cell division, eventually permitting genomic instability in the cells that normally causes these abnormal cells to die.
In cancer the enzyme telomerase becomes activated and lengthens telomeres, preserving damaged cells to survive and reproduce. Telomerase is inactive in normal cells.
Telomerase activation confers new strengths on tumors
"These in vivo mouse studies, together with human and mouse prostate cancer genomic data, provide evidence that telomere dysfunction plays a critical role in prostate cancer initiation and progression," said co-senior author Lynda Chin, M.D., professor and chair of The University of Texas MD Anderson Cancer Center's Department of Genomic Medicine.
"Our studies also show that telomerase activation after genomic instability caused by telomere dysfunction enables evolving cancers to progress and acquire new biological properties, including central features of advanced human prostate cancer," Chin said.
Chin, co-senior author and MD Anderson President Ronald DePinho, M.D., and colleagues conducted this research while at Dana-Farber Cancer Institute in Boston.
Telomere dysfunction, fired-up telomerase, cause bone metastasis
The team took a strain of mice with both the p53 and pten tumor-suppressing genes knocked out that normally develop nonmetastatic prostate cancer and engineered some to express telomerase. They were cross-bred for several generations.

• Control mice with intact telomeres (either wild-type mice or those with telomerase expressed) avoided the genomic instability caused by telomere shortening. All of these mice developed locally invasive, nonmetastatic prostate cancer.
• Mice without telomerase were subject to telomere dysfunction and genetic changes and developed precancerous high-grade prostate intraepithelial neoplasia (HPIN) but 60 percent of them did not progress to prostate cancer. Signs of programmed cell death triggered by genetic abnormalities abounded in this group.
• Mice subject to telomere dysfunction, genomic instability and telomerase activation also developed HPIN but then progressed to lethal bulky tumors, with 5 of 20 developing spinal metastases that were not seen in the genome-stable mice.

"Not only did telomerase reactivation bypass the cancer progression block that arises with telomere dysfunction, it also conferred a new property -- bone metastasis -- that was not seen in tumors that did not go through telomere dysfunction followed by telomerase reactivation," said first author Zhihu Ding, Ph.D., formerly of Dana-Farber and now with Sanofi-Aventis, Inc.
"This provides the first genetic evidence that telomerase reactivation and genome stabilization are necessary to drive full malignant progression in epithelial cancers," Ding said.
Aligning genetic alterations in mice and humans
Chin, Ding and colleagues analyzed gene copy number aberrations -- genes deleted or amplified -- in 18 advanced tumors from the mice and 194 human prostate tumors.
They found 22 of the 94 copy number alterations involving deletion or amplification of 741 genes identified in mice were similar to those found in humans. A series of analyses of changes found in bone metastases pointed to deletions of the Smad4 tumor-suppressor gene, which regulates the transforming growth factor beta (TGF-ß) pathway.
The team took this finding back to the mouse model with tumor suppressors p53 and pten knocked out. These mice don't develop bone metastasis, but when the researchers also knocked out Smad4, more aggressive tumors developed, including bone metastasis in three of 24 mice.
Genes prognostic for human prostate cancer
Next, they looked at 14 genes in nine molecular pathways found to be enriched in bone metastasis to see if they were prognostic for recurrence (as measured by PSA levels after surgery) among 140 prostate cancer patients.
The 14-gene set was significantly prognostic of biochemical recurrence, providing evidence of their biological relevance to human prostate cancer, but the researchers noted that their individual contributions and mechanisms of action will require further research.
"Overall, our findings validate the integrative approach of employing genotype-phenotype correlations found in the mouse model with the power of genomic and bioinformatic analyses to discover and explain molecular mechanisms that drive prostate cancer," said co-first author Chang-Jiun Wu, Ph.D., a postdoctoral fellow in MD Anderson's Department of Genomic Medicine.
This research was funded by grants from the National Cancer Institute, the Prostate Cancer Foundation, the U.S. Department of Defense, the Damon Runyon Cancer Research Foundation, the Multiple Myeloma Research Foundation, an American Cancer Society and the Robert A. and Renee E. Belfer Foundation.

[Hebbeh]

http://www.scienceda...20220161229.htm

Blocking Telomerase Kills Cancer Cells but Provokes Resistance, Progression


ScienceDaily (Feb. 20, 2012) — Inhibiting telomerase, an enzyme that rescues malignant cells from destruction by extending the protective caps on the ends of chromosomes, kills tumor cells but also triggers resistance pathways that allow cancer to survive and spread, scientists report in the Feb. 17 issue of Cell.

"Telomerase is overexpressed in many advanced cancers, but assessing its potential as a therapeutic target requires us to understand what it does and how it does it," said senior author Ronald DePinho, M.D., president of The University of Texas MD Anderson Cancer Center.
"We exploited the experimental merits of mice to model and study more precisely telomere crisis, telomerase reactivation and telomerase extinction in cancer development, progression and treatment," DePinho said. "This elegant model exposed two mechanisms, including one unexpected metabolic pathway, used by cancer cells to adapt to loss of telomerase.
"These findings allow us to anticipate how tumor cells might respond to telomerase inhibition and highlight the need to develop drug combinations that target telomerase and these adaptive resistance mechanisms," DePinho said.
Researchers evaluated telomerase as a therapeutic target in experiments that originated in DePinho's lab at the Dana-Farber Cancer Institute in Boston. He became MD Anderson's fourth full-time president in September.
Telomerase activity is low or absent in normal cells, which have segments of repeat nucleotides called telomeres at the ends of their chromosomes that protect DNA stability during cell division, said first author Jian Hu, Ph.D., an instructor in MD Anderson's Department of Cancer Biology.
With each division the telomeres shorten, leading eventually to genomic instability and cell death, a period termed "telomere crisis," Hu said. In cancer, telomerase becomes active during telomere crisis and rescues the genomically abnormal cells by lengthening telomeres.
In a series of experiments in a lymphoma mouse model, the team found:

• Telomerase reactivation in malignant cells after genomic instability causes cancer progression.
• Inhibiting telomerase caused tumor cell death but also led to alternative lengthening of telomeres (ALT) independent of telomerase.
• ALT-positive cells increase both the expression and copy number of a gene called PGC-1ß, a key regulator of mitochondrial function, to compensate for mitochondrial and reactive oxygen species defense deficiencies.
• Targeting PGC-1ß to weaken mitochondria function enhances anti-telomerase therapy.

To study the impact of reactivated telomerase, DePinho and colleagues genetically modified mice to develop T cell lymphomas and to have telomerase reactivated when the mice are treated with 4-hydroxytamoxifen (4-OHT). They crossed the mice for several generations, treating some with 4-OHT and others with a control vehicle that did not trigger TERT activation.
Telomerase reactivation causes aggressive cancer
Third- and fourth-generation mice with telomerase activated by 4-OHT had a median survival of 30 days and more frequent tumor infiltration to the spleen, kidney, liver, lung, bone marrow and brain than did control-treated mice, 70 percent of which lived beyond 50 days. Tumor cells in control-treated mice were more likely to be detected and destroyed by tumor-suppressing p53 signaling.
"These findings are consistent with telomere crisis leading to genomic instability during early stage cancer, with reactivated telomerase protecting malignant cells later to ensure tumor progression," Hu said.
Telomere dysfunction causes cancer-promoting genetic changes
Later-generation mice with activated telomerase had 4,928 amplified genes and 2,297 deletions. The team compared these changes to those in human lymphoma tumors and found 565 matching amplified genes and 300 deletions.
These cross-species copy number alterations included several known tumor-suppressing genes and oncogenes, suggesting that initial telomere dysfunction not only drives primary tumor development but also confers malignant traits such as invasiveness.
Telomerase extinction works -- at first
The team then took tumor cells from late-generation mice with activated telomerase -- the aggressive tumors -- and passaged them four times through groups of mice treated with either 4-OHT to trigger telomerase production or the control vehicle that leaves the enzyme off.
During the first two rounds, survival for the two groups was about the same. In the third round, the control mice had a major improvement in survival over the telomerase arm, indicating that telomere erosion had allowed cellular defense mechanisms to pick off genomically unstable cells.
However, in the fourth passage, survival of the control-treated mice fell back toward that of mice with active telomerase. The tumors had become resistant without relying on telomerase.
Alternative lengthening of telomeres rescues cancer cells
An analysis showed that telomere lengths of tumor cells with active telomerase remained largely unchanged across the four passages. Telomeres shortened in cells lacking telomerase through the first two passages followed by a sharp increase during the third and fourth passages.
Other molecular evidence pointed to alternative lengthening of telomeres in telomerase-absent cells.
They found that ALT-positive tumors had different gene expression patterns -- 891 genes with increased expression, 1,345 with decreased -- compared to telomerase-positive tumors.
Key gene in mitochondrial pathway active in ALT cells
Many genes were found in networks regulating mitochondrial biology and oxidative stress regulation. PGC-1ß was the only gene in both pathways with increased expression and copy number gain in the ALT-positive tumors.
PGC-1ß is a master regulator of both pathways, which turn out to be dysfunctional in ALT-positive tumors. When the researchers knocked down PGC-1ß, mice with ALT-positive tumors survived much longer than those with intact PGC-1ß and than those with activated telomerase in their tumors.
In normal cells, power-generating mitochondria process fatty acids to produce ATP, a molecule that serves as the major energy source for the cell. Cancer cells generally rely more on sugar processing to generate energy. However, DePinho and colleagues note their genetic evidence suggests that mitochondria play a role supporting cancer cells.
This research was funded by grants from the National Cancer Institute, the Leukemia and Lymphoma Society, the Fundación Ramón Areces, and Helen Hay Whitney Fellowship, the Ellison Foundation for Medical Research and the American Cancer Society.

[niner]

Genomic instability caused by an erosion of the protective caps on chromosomes, followed by activation of an enzyme that reinforces those caps, allows malignant cells to evade destruction and acquire more deadly characteristics, researchers report in an Online Now article at the journal Cell.

The key here seems to be that the malignant cells initially had telomeres that were dangerously short, which led to genomic instability, then telomerase was turned on, causing the cells to evade apoptosis. If the telomeres had been lengthened before they got dangerously short, there presumably would have been no genetic instability. The relevance of this to someone taking a telomerase activator has to do with the possible presence of sub-clinical tumor cells that have dangerously short telomeres. If they get extended enough to avoid apoptosis, then you may have a problem. The fact that telomerase seems to preferentially lengthen short telomeres is part of the problem here. If the telomeres are TOO short, it would be better to kill the cell, not give it a new lease on life. The current crop of telomerase activators seem to be mild enough that any tumor cells outrun the available telomerase. Either that or the odds of finding a cell in this state of dangerously short telomeres, but not yet dead is pretty low. There's a growing body of experience with humans taking telomerase activators, and I've not heard of any increase in cancer rates. I suppose another explanation is that the current crop of telomerase activators don't activate very well. This paper does point out what could go wrong, at least theoretically. It tends to reinforce the idea that telomerase activators probably ought to be cycled. It would be nice if we could dig up some data on the rate at which cancer cells use up telomeres, and the length of time it takes between final telomere shortening and apoptosis, so that we could decide on a sensible cycling rate.

[Hebbeh]

Genomic instability caused by an erosion of the protective caps on chromosomes, followed by activation of an enzyme that reinforces those caps, allows malignant cells to evade destruction and acquire more deadly characteristics, researchers report in an Online Now article at the journal Cell.

The key here seems to be that the malignant cells initially had telomeres that were dangerously short, which led to genomic instability, then telomerase was turned on, causing the cells to evade apoptosis. [...] The relevance of this to someone taking a telomerase activator has to do with the possible presence of sub-clinical tumor cells that have dangerously short telomeres. [...] It would be nice if we could dig up some data on the rate at which cancer cells use up telomeres, and the length of time it takes between final telomere shortening and apoptosis, so that we could decide on a sensible cycling rate.

I agree...the take home message for me also, was the potential importance for cycling a telomerase activator to allow any unstable cells to undergo the necessary apoptosis and avoid allowing the cell to become malignant. Then the question becomes...what is the ideal on and off cycle length?

Edited by Michael, 25 May 2012 - 01:43 PM.

[Anthony_Loera]

Anthony,

1). I never used the word "natural" extract.To be clear,I claim and I am convinced that a product simply called "Astragalus"(like you also named it simply "Astragalus"in your COA posted,with 13,3% A4-so can be extract,or standardized extract)in a special extraction process can be supplied with a specific component, in our case A4(so the other components of Astragalus are simply removed ).I attached COA for Astragalus with 50% A4,and COA for Astragalus with 90% A4,and your COA-for comparation -with 13,3% A4.Of course the main difference is the price,that can be between aprox 40 USD/kg (A4 less then 1%) to aprox 6000 USD/kg(90%A4).

The item in Bold lead me to believe you are a seller of the product you are talking about, and not just a bystander. maybe a Freudian slip? The COA from RevGenetics was a 2008 COA, and not the most recent one. You try to compare it with an August 2010 coa and try to explain pricing which has no relevance because of the differing years of the COAs.

2). Regarding Revital TA.They corrected the mistake of their sales agent with the contain of A4 in their Astragalus extract and they take apologised for this.So in one capsule of Revital TA are 25 mg of A4 .Also are more A4 from Astragalus extract, that are not mentioned in the label.They use Astragalus extract 20:1 with 3% Astragaloside.

Since you have no proof of how much, its probably less than 0.04%

Astragalus extract 50:1 have 6% Astragaloside.See attached the Canadian COA for Astragalus extract 20:1 with 3% Astragaloside(I removed the canadian name of the lab-because I don't know if I have the right to post it).I don't have the contain of A4 from total Astragaloside from Astragalus

Enough said...


A

[johnross47]

Genomic instability caused by an erosion of the protective caps on chromosomes, followed by activation of an enzyme that reinforces those caps, allows malignant cells to evade destruction and acquire more deadly characteristics, researchers report in an Online Now article at the journal Cell.

This paper does point out what could go wrong, at least theoretically. It tends to reinforce the idea that telomerase activators probably ought to be cycled. It would be nice if we could dig up some data on the rate at which cancer cells use up telomeres, and the length of time it takes between final telomere shortening and apoptosis, so that we could decide on a sensible cycling rate.

I agree...the take home message for me also ...

Somewhat concerning....I have an appointment with an urologist on Monday to examine as yet unexplained problems which could be prostate or other urological issues. I have been using Astragalus in various forms....always on/off but of course the periods are guess work.

Edited by Michael, 25 May 2012 - 01:41 PM.

[zorba990]

Genomic instability caused by an erosion of the protective caps on chromosomes, followed by activation of an enzyme that reinforces those caps, allows malignant cells to evade destruction and acquire more deadly characteristics, researchers report in an Online Now article at the journal Cell.

The key here seems to be that the malignant cells initially had telomeres that were dangerously short, which led to genomic instability, then telomerase was turned on, causing the cells to evade apoptosis. If the telomeres had been lengthened before they got dangerously short, there presumably would have been no genetic instability. The relevance of this to someone taking a telomerase activator has to do with the possible presence of sub-clinical tumor cells that have dangerously short telomeres. If they get extended enough to avoid apoptosis, then you may have a problem. The fact that telomerase seems to preferentially lengthen short telomeres is part of the problem here. If the telomeres are TOO short, it would be better to kill the cell, not give it a new lease on life. The current crop of telomerase activators seem to be mild enough that any tumor cells outrun the available telomerase. Either that or the odds of finding a cell in this state of dangerously short telomeres, but not yet dead is pretty low. There's a growing body of experience with humans taking telomerase activators, and I've not heard of any increase in cancer rates. I suppose another explanation is that the current crop of telomerase activators don't activate very well. This paper does point out what could go wrong, at least theoretically. It tends to reinforce the idea that telomerase activators probably ought to be cycled. It would be nice if we could dig up some data on the rate at which cancer cells use up telomeres, and the length of time it takes between final telomere shortening and apoptosis, so that we could decide on a sensible cycling rate.

I agree...the take home message for me also, was the potential importance for cycling a telomerase activator to allow any unstable cells to undergo the necessary apoptosis and avoid allowing the cell to become malignant. Then the question becomes...what is the ideal on and off cycle length?

Somewhat concerning....I have an appointment with an urologist on Monday to examine as yet unexplained problems which could be prostate or other urological issues. I have been using Astragalus in various forms....always on/off but of course the periods are guess work.

During the off periods are you using high dose resveratrol and/or curcurmin?
Looks like it is generally regarded as very safe (astragalus), but can be a mild diuretic.
http://www.umm.edu/a...alus-000223.htm

[Robert89]

Genomic instability caused by an erosion of the protective caps on chromosomes, followed by activation of an enzyme that reinforces those caps, allows malignant cells to evade destruction and acquire more deadly characteristics, researchers report in an Online Now article at the journal Cell.

The key here seems to be that the malignant cells initially had telomeres that were dangerously short, which led to genomic instability, then telomerase was turned on, causing the cells to evade apoptosis. If the telomeres had been lengthened before they got dangerously short, there presumably would have been no genetic instability. The relevance of this to someone taking a telomerase activator has to do with the possible presence of sub-clinical tumor cells that have dangerously short telomeres. If they get extended enough to avoid apoptosis, then you may have a problem. The fact that telomerase seems to preferentially lengthen short telomeres is part of the problem here. If the telomeres are TOO short, it would be better to kill the cell, not give it a new lease on life. The current crop of telomerase activators seem to be mild enough that any tumor cells outrun the available telomerase. Either that or the odds of finding a cell in this state of dangerously short telomeres, but not yet dead is pretty low. There's a growing body of experience with humans taking telomerase activators, and I've not heard of any increase in cancer rates. I suppose another explanation is that the current crop of telomerase activators don't activate very well. This paper does point out what could go wrong, at least theoretically. It tends to reinforce the idea that telomerase activators probably ought to be cycled. It would be nice if we could dig up some data on the rate at which cancer cells use up telomeres, and the length of time it takes between final telomere shortening and apoptosis, so that we could decide on a sensible cycling rate.

I agree...the take home message for me also, was the potential importance for cycling a telomerase activator to allow any unstable cells to undergo the necessary apoptosis and avoid allowing the cell to become malignant. Then the question becomes...what is the ideal on and off cycle length?

Somewhat concerning....I have an appointment with an urologist on Monday to examine as yet unexplained problems which could be prostate or other urological issues. I have been using Astragalus in various forms....always on/off but of course the periods are guess work.

I have now stopped all forms of astragalus, AG4 and won't be taking cycloastragenol either. This new research really is not a good sign.

I also contacted a friend of mine, who is a US registered Chinese medicine practitioner - specializing in herbs. He told me to STOP taking Astragalus (or any derivatives of) UNLESS it was for a short term specific use. (Such as a problem with the immune system). He said it would lead to internal pain (abdomen area) - and that this medicine was only prescribed for short term use in the Traditional Chinese use. My guess is that the Chinese knew something that the West doesn't. This stuff comes with a warning attached - when used in the traditional sense.

In terms of TA Sciences telling us that there was or wasn't an increase in cancer or illness - I wouldn't want to trust them with my life either. These people aren't even from a research background. Half the people in the 'clinical trial' they did for 3 years dropped out. Those people dropped out because they weren't happy with TA-65.