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Astragalus, Astragaloside IV


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#121 Anthony_Loera

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Posted 24 September 2008 - 04:00 AM

I am wondering why TA Sciences have the 3 month on 3 month off rather than say a simpler 1 week on 1 week off or even a 1 day on 1 day off. Could it be that it takes time to build up the teleromerase or for the additional telemerase to work? Quite a few medications take a month or more to really work. Taking resveratrol within 24 hours or more might cause this not to work or work very minimally because as soon as we start to get some effect, we dampen it with Resv. Could 3 months of only astragaloside and maybe a multi and 3 months full supps and double resv be a better way to go? Do we know what supps are taken by participants of the Patton protocol while taking astragaloside?

I think the idea behind the TA Sciences (Patton) protocol is that if there are any incipient cancers that do not have telomerase "switched on", then you want a significant amount of time without telomerase activation to give them a chance to "burn themselves out"; i.e., to divide until they have depleted their telomeres. If you use too short a cycle, you might risk activating any incipient tumors that have normal quiescent telomerase. If I start using this stuff, I will probably go with the long interval. What's the hurry?

I am concerend that we will see no result or a very minor result when taken within 24 hours of resv. Anyone else share this concern?

Is there some evidence that resveratrol will deactivate telomerase? I've not heard of that.



Resveratrol has been shown to inhibit or "down-regulate" telomerase activity in colon cancer. Regarding the Patton protocol, I have to disagree with you on that one. Immortal cells, usually never burn themselves out... otherwise they would not be immortal, the would not be cancerous.

The patton protocol doesn't use an inhibitor or other drug to stop telomerase. Geron never licensed that one out to TA Sciences... I also believe that drug from Geron, is not ready for primetime yet, as it is still in trials:

http://geron.com/pro...cancerdrug.aspx

I believe for folks considering a supplement, Astragaloside IV (astral fruit) is a good option. We know that Telomerase does not cause cancer, not an oncogene, and it appears that the issue may reside with p53 or p16 failing. We just need to know more about these 2 IMHO to see if we can add something to folks diet that might help cover the issues with the p16 gene...

100YearstoGo... thanks for those links, it sets our sights on something else that might be helpful to add as a supplement... I know this topic may have expanded a bit, but I do appreciate the new information. If you do find something that may be helpful to the p16, please post it for people to consider.

For now I think taking Astral Fruit and resveratrol are good choices. Let's see if I maybe able to find something for p16, then we maybe covering most of the issues and find some possible protection against developing immortal cells.

A

#122 acoli

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Posted 24 September 2008 - 07:10 AM

Anthony, when do you anticipate chitosan will be in astral fruit, and will the website state chitosan as an ingredient? Also, if chitosan increases absorption 60 fold, wuldn't this be way more effective then ta-65? Since it has been stated that the cyclo. molecule(basically ta-65) is perhaps 3 times effective as astralagus IV, wouldnt astralagus IV plus chitosan then be 20 times ta-65? If so, wouldn't that be an extreme amount? astralagus IV would have to be lowered to like 2 mg? This seems unreasonable and my logic is probably flawed, so I'll wait for your answer.

#123 Anthony_Loera

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Posted 24 September 2008 - 01:50 PM

Hi acoli,

we haven't decided the final formulation for the next batch. We will post chitosan on the label and website, so you can consider it when it comes out.

We don't know what TA-65 is, if it's simply one of the other extracts, then you are probably right.
However, if it's a formulation rather than a single ingredient, it may not be so.

Cheers
A

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#124 VinceG

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Posted 24 September 2008 - 06:10 PM

Yes, chitosan is interesting.

But it's my understanding that the astragaloside iv, needs to be in the chitosan, not just mixed in.

A




As may be indicated in the study I'll take 500MG chitosan followed by the your product from now on.


SAX


I just read the full document this morning, and again I stand corrected SAX.
It appears EDTA tken with Astragaloside IV increases absorption by 30 fold, while 0.1% chitosan increases absorption by over 60 fold.

To say the least, we will be adding chitosan to our next formulation, and will start adding chitosan to my regimen.

Thank you SAX for this info, I believe many here will benefit from it.

Anthony Loera


Anthony. I am interested in Revgenetic's plans for next-generation Astral Fruit, particularly when do you think you will have a product with chitosan and/or a more powerful product avaiable? If the bioavaioability data you cite is to be believed, I would think a chitosan-potentiated version of your present-dose pill would deliver more than enough astragaloside IV. At much greater effectiveness and at much lower cost than a 100mg pill without chitosan. Also, from the data you cite it seems that EDTA would do the job too.
Vince

#125 Guest_aidanpryde_*

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Posted 24 September 2008 - 06:26 PM

As I have already written in this thread, Resveratrol is not blocking telomerase action in non malignant cell, but more activating telomerase through an Akt dependent pathway. The highest telomerase activation reached with resveratrol was around 50 µM. (1)
This study was done on endothelial cells.

So once again:

"Key results:Resveratrol dose dependently prevented the onset of EPCs senescence and increased the proliferation and migration of EPCs. The effect of resveratrol on senescence could not be abolished by eNOS inhibitor or by an oestrogenic receptor antagonist. Resveratrol significantly increased telomerase activity and Akt phosphorylation. "

We know that Telomerase does not cause cancer, not an oncogene, and it appears that the issue may reside with p53 or p16 failing. We just need to know more about these 2 IMHO to see if we can add something to folks diet that might help cover the issues with the p16 gene


I do not know if the P16 is supressed through Astragaloside IV like it is by the HDTIC astragalus compounds. Perhaps the telomerase activating mechanism is the one supressing the P16. In cells which got inserted an extra chromosome for telomerase, the P16 sequence became methylated and the gene expression on this way epigenetically supressed. Also supressing P16 could activate telomerase, but in experiments this was achieved through complete disactivation of P16, which is not the case with a supplement like Astragaloside IV. P53 and P21 are not influenced by HDTIC.

Furthermore the antisenescence action is perhaps partially achieved through supression of P16. So doing something to avoid this could be wrong. You should also consider, that resveratrol is not only activating telomerase but is also supressing P16. (2) It is interesting, that a defect P16 tumorsupressor is associated with melanoma, but resveratrol (activates telomerase and dimnishes P16) is associated with protection from melanoma and other kind of cancer. Sounds strange eh?

You should also consider that P16 is not totaly deactivated through supps, but its expression limited.


(1)
Xia L, Wang XX, Hu XS, Guo XG, Shang YP, Chen HJ, Zeng CL, Zhang FR, Chen JZ.
Resveratrol reduces endothelial progenitor cells senescence through augmentation of telomerase activity by Akt-dependent mechanisms.
Br J Pharmacol. 2008 Jun 30.

(2)
Huang J, Gan Q, Han L, Li J, Zhang H, Sun Y, Zhang Z, Tong T.
SIRT1 Overexpression Antagonizes Cellular Senescence with Activated ERK/S6k1 Signaling in Human Diploid Fibroblasts.
PLoS ONE. 2008 Mar 5;3(3):e1710

Edited by aidanpryde, 24 September 2008 - 06:28 PM.


#126 100YearsToGo

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Posted 24 September 2008 - 06:56 PM

"100YearstoGo... thanks for those links, it sets our sights on something else that might be helpful to add as a supplement... I know this topic may have expanded a bit, but I do appreciate the new information. If you do find something that may be helpful to the p16, please post it for people to consider."

You're welcome.

My aim with the P53 and P16 stuff was to show people that you have to keep expression of those genes healthy if you are boosting telomeres to youthfull levels. As you age mutations starts affecting healthy cells. As you pointed out this is NOT caused by boosted telomerase activity. However if the mutated cells are not destroyed, telomerase may play a role in helping these mutated cells divide at a rate that would be higher than if you were a person with low levels of telomerase activity. I pointed this out by refering to a spanish study in my first post.

As some extra insurance you could add Saikosaponins ( derived from a herb extract) to the regimen. Studies show that it boost P53 and P16 and is strongly anti cancer. People may want to check it out.

#127 Guest_aidanpryde_*

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Posted 24 September 2008 - 07:52 PM

I am not sure if I can follow the string of this discussion for following reasons:

- Why do you think that the Astragaloside IV will deactivate P16 and P53? And especially why P53 too, which is independent from the P16 and was never mentioned even not in the HDTIC-paper?

- Where is the evidence for this kind of action for the compound we are speaking about?

- Why do you want suddenly to activate the senescence promoting P16 and P53 tumorsupressors although senescence is something you want to avoid?

-(for the sake of discussion let us assume that Astragaloside will supress P16 like HDTIC does) so why do you think that a supplement induced P16 supression will lead to cancer, when P16 supression through resveratrol is not doing this?

So please before you start even to prepare any formulations to "stimulate P53 and P16" hold on and think once again about it.

#128 100YearsToGo

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Posted 24 September 2008 - 08:12 PM

I am not sure if I can follow the string of this discussion for following reasons:

- Why do you think that the Astragaloside IV will deactivate P16 and P53? And especially why P53 too, which is independent from the P16 and was never mentioned even not in the HDTIC-paper?

- Where is the evidence for this kind of action for the compound we are speaking about?

- Why do you want suddenly to activate the senescence promoting P16 and P53 tumorsupressors although senescence is something you want to avoid?

-(for the sake of discussion let us assume that Astragaloside will supress P16 like HDTIC does) so why do you think that a supplement induced P16 supression will lead to cancer, when P16 supression through resveratrol is not doing this?

So please before you start even to prepare any formulations to "stimulate P53 and P16" hold on and think once again about it.


No I never said Astragaloside IV will de-activate P53 or P16. There is no beweis :) (evidence) for this.
But there is evidence in studies that P53 and P16 function will decline with age. Also probably because of this, unchecked mutation in cells and cancer risk will increase. My point is, you would not want P53 and P16 activity of an old guy of 50 with telomerase activity of an 18 year old person. Also if you are supplementing with stuff that suppress P53 and P16 you are in even greater danger. Did you read the two spanish studies of my first post? And no I'm not preparing any formulation yet in my Frankenstein laboratory. ;)

Edited by 100YearsToGo, 24 September 2008 - 08:56 PM.


#129 Guest_aidanpryde_*

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Posted 25 September 2008 - 11:25 AM

Beweis? Are you speaking german or using a translator? :) ;)

P53 and P16 are declining in age? I only know the opposite to be true, cells express higher levels of this tumorsupressors in age, and tumorsupressors being probably a part of the factors leading to senescence. Supplement activated telomerase is in my opinion not compareable with any kind of cancer related extreme telomerase expression, which is necessary to maintain the short telomeres of cancer cells. Further we should not forget the cancer supressive telomerase action and its other telomere independent actions like probably DNA repairing mechanisms. (1)

I have used Resveratrol as an example to show, that it probably also activates telomerase (and supresses P16) but is cancerprotective. Also the tetrapeptide Epithalon which shows telomerase activation and telomere lengthening in human cells, decreases in vivo the cancer incidence.
So it is not possible to state clearly that an enhanced telomeraseproduction+light supression of P16 will lead to tumorigenesis.

(1)
Cong Y, Shay JW.
Actions of human telomerase beyond telomeres.
Cell Res. 2008 Jul;18(7):725-32. Review.

#130 100YearsToGo

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Posted 25 September 2008 - 02:05 PM

Beweis? Are you speaking german or using a translator? ;) :)

P53 and P16 are declining in age? I only know the opposite to be true, cells express higher levels of this tumorsupressors in age, and tumorsupressors being probably a part of the factors leading to senescence. Supplement activated telomerase is in my opinion not compareable with any kind of cancer related extreme telomerase expression, which is necessary to maintain the short telomeres of cancer cells. Further we should not forget the cancer supressive telomerase action and its other telomere independent actions like probably DNA repairing mechanisms. (1)

I have used Resveratrol as an example to show, that it probably also activates telomerase (and supresses P16) but is cancerprotective. Also the tetrapeptide Epithalon which shows telomerase activation and telomere lengthening in human cells, decreases in vivo the cancer incidence.
So it is not possible to state clearly that an enhanced telomeraseproduction+light supression of P16 will lead to tumorigenesis.

(1)
Cong Y, Shay JW.
Actions of human telomerase beyond telomeres.
Cell Res. 2008 Jul;18(7):725-32. Review.



Do they have translators for German? :)

(1) Enhanced P53 function is important to have to live a healthy LONG life. We suppose Telomerase activation will help us with LONG life. The healthy or long part is unsure. Cancer kills.
(2) Function of P53 is diminished with age.


(1): http://www.nature.co...bs/415045a.html

The p53 tumour suppressor is activated by numerous stressors to induce apoptosis, cell cycle arrest, or senescence. To study the biological effects of altered p53 function, we generated mice with a deletion mutation in the first six exons of the p53 gene that express a truncated RNA capable of encoding a carboxy-terminal p53 fragment. This mutation confers phenotypes consistent with activated p53 rather than inactivated p53. Mutant (p53+/m) mice exhibit enhanced resistance to spontaneous tumours compared with wild-type (p53+/+) littermates. As p53+/m mice age, they display an early onset of phenotypes associated with ageing. These include reduced longevity, osteoporosis, generalized organ atrophy and a diminished stress tolerance

and check this

The super P53 mouse:

http://www.pubmedcen...gi?artid=137187

(2):

I should have said function not expression. Critically short telomeres may act as a mitotic clock to signal the cell cycle arrest at senescence. The cycle arest is executed through p53 pathways. That is one of the reasons why you see more P53 activity in old age. P53 is also responsable for detecting DNA damage due other reasons and initiate cell cycle arrest. We also see more damage the older you get. The development of human cancer is frequently associated with the inactivation of the pRb and p53 pathways. We see that cancer risk increases with age and we can conclude that the activation of p53 pathways throughout the body is not optimal. At least it is not preventing cancer occuring in some parts of the body. Healthy cells are of course..healthy. You are saying trying to help mantaining healthy P53 pathways is not necessary?

"When activating p53 and p16 in mice, the incidence of cancer is reduced to practically zero. We don’t think the mice lived longer because they had less cancer but because these genes also protected against aging,“ co-scientist Manuel Serrano said.
The mice are expected to live up to four-and-a-half years though their average lifespan is three years. “This is the equivalent of humans living to 125,“ said the scientists."

I didn't make that up. I don't think it's wise to just ignore these genes while boosting telomerase unless you think that telomerase is enough to boost life extension. The quote above suggest that, that is not enough.

#131 Anthony_Loera

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Posted 25 September 2008 - 09:42 PM

Anthony. I am interested in Revgenetic's plans for next-generation Astral Fruit, particularly when do you think you will have a product with chitosan and/or a more powerful product avaiable? If the bioavaioability data you cite is to be believed, I would think a chitosan-potentiated version of your present-dose pill would deliver more than enough astragaloside IV. At much greater effectiveness and at much lower cost than a 100mg pill without chitosan. Also, from the data you cite it seems that EDTA would do the job too.
Vince



Hi Vince,

we are currently testing Astragaloside 4 powder, as we are considering a 20% or better purity. With this new information, I believe we will need to test for clean chitosan, as my concern is mercury in chitosan. The product may take some time to show up at our website, maybe 3-4 months, but I believe it will be well worth it. For those that need something now, I suggest to go using SAX's route, and buy chitosan from a great source. (Yes, I just received my Chitosan package today from LEF, so Sax is not alone now...)

My other question regards folks being allergic to chitosan, because of the shellfish aspect.
I am not sure how prevalent this is, but may require us to continue having one product without it, I am not sure yet, as the alternative is EDTA for folks with allergies. Then there is the ongoing p16 debate, which is quite interesting. Although I am trying to keep it out of my mind, I can't say that it isn't coloring a consideration for a new formulation. For now, I will keep these two separate.

I have to say, the future looks quite busy. The formulation is being debated a bit, so I am not sure what the final formulation will look like right now.

A

#132 stephen_b

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Posted 25 September 2008 - 10:54 PM

I bought some 500mg/capsule chitosan after I read the study myself, although I think that maybe overkill.


LEF also sells 250 mg capsules on their site, but iHerb only carries LEF's 500 mg capsules.

Chitosan is fairly expensive. Did the study say how much was used to increase astragaloside absorption?

Stephen

Edit: LEF's site says "Ascorbic acid (vitamin C) helps activate chitosan in the stomach and intestine.125,126 It is important to take pure ascorbic acid to enhance the effects of chitosan." More variables ....

Edit2: Source naturals also makes a 250 mg product (iHerb), labeled "minimum 90% deacetylated chitin", which is cheaper.

Edited by stephen_b, 25 September 2008 - 10:59 PM.


#133 niner

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Posted 26 September 2008 - 03:32 AM

I am wondering why TA Sciences have the 3 month on 3 month off rather than say a simpler 1 week on 1 week off or even a 1 day on 1 day off. Could it be that it takes time to build up the teleromerase or for the additional telemerase to work? Quite a few medications take a month or more to really work. Taking resveratrol within 24 hours or more might cause this not to work or work very minimally because as soon as we start to get some effect, we dampen it with Resv. Could 3 months of only astragaloside and maybe a multi and 3 months full supps and double resv be a better way to go? Do we know what supps are taken by participants of the Patton protocol while taking astragaloside?

I think the idea behind the TA Sciences (Patton) protocol is that if there are any incipient cancers that do not have telomerase "switched on", then you want a significant amount of time without telomerase activation to give them a chance to "burn themselves out"; i.e., to divide until they have depleted their telomeres. If you use too short a cycle, you might risk activating any incipient tumors that have normal quiescent telomerase. If I start using this stuff, I will probably go with the long interval. What's the hurry?

Regarding the Patton protocol, I have to disagree with you on that one. Immortal cells, usually never burn themselves out... otherwise they would not be immortal, the would not be cancerous.

I'm not thinking about immortal cells. Those are already cancer cells, presumably with constitutively active (i.e. always "on") telomerase. I'm concerned about any cells that have already been transformed almost all the way to immortal, but still have inactive telomerase. If we lengthen the telomeres on these cells, they will at least stay around longer, and due to the genetic instability of cancer cells, would be more likely to mutate in such a way as to permanently activate the telomerase, which would make them truly immortal. As long as their telomerase is inactive, they will not be able to divide past the Hayflick limit. Using a long interval between courses of Astragaloside IV will provide time for any such cells to exhaust their telomeres and at least become senescent. Whether or not they would undergo apoptosis or otherwise die is another question.

#134 Anthony_Loera

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Posted 26 September 2008 - 03:17 PM

I am wondering why TA Sciences have the 3 month on 3 month off rather than say a simpler 1 week on 1 week off or even a 1 day on 1 day off. Could it be that it takes time to build up the teleromerase or for the additional telemerase to work? Quite a few medications take a month or more to really work. Taking resveratrol within 24 hours or more might cause this not to work or work very minimally because as soon as we start to get some effect, we dampen it with Resv. Could 3 months of only astragaloside and maybe a multi and 3 months full supps and double resv be a better way to go? Do we know what supps are taken by participants of the Patton protocol while taking astragaloside?

I think the idea behind the TA Sciences (Patton) protocol is that if there are any incipient cancers that do not have telomerase "switched on", then you want a significant amount of time without telomerase activation to give them a chance to "burn themselves out"; i.e., to divide until they have depleted their telomeres. If you use too short a cycle, you might risk activating any incipient tumors that have normal quiescent telomerase. If I start using this stuff, I will probably go with the long interval. What's the hurry?

Regarding the Patton protocol, I have to disagree with you on that one. Immortal cells, usually never burn themselves out... otherwise they would not be immortal, the would not be cancerous.

I'm not thinking about immortal cells. Those are already cancer cells, presumably with constitutively active (i.e. always "on") telomerase. I'm concerned about any cells that have already been transformed almost all the way to immortal, but still have inactive telomerase. If we lengthen the telomeres on these cells, they will at least stay around longer, and due to the genetic instability of cancer cells, would be more likely to mutate in such a way as to permanently activate the telomerase, which would make them truly immortal. As long as their telomerase is inactive, they will not be able to divide past the Hayflick limit. Using a long interval between courses of Astragaloside IV will provide time for any such cells to exhaust their telomeres and at least become senescent. Whether or not they would undergo apoptosis or otherwise die is another question.



Hmm... I believe it may not work that way. What you are suggesting telomerase will do (if I understand it correctly) is an act typically seen by an oncgene.

An oncogene and not telomerase, will change the cell and give it the ability to use telomerase for it's own evil purpose. The oncogene would change the cell regardless of whether telomerase was on or off at the time. Remember that telomerase happens naturally throughout life, specially when you body is getting ready to combat disease.

A

#135 100YearsToGo

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Posted 27 September 2008 - 01:54 AM

Niner, I understand your concern. Note that astragalus in itself has anti cancer activity:

http://carcin.oxfordjournals.org/cgi/content/full/28/6/1347


To be extra safe you could take a safe p53 activating herb with your Astral fruit. Among others I'm taking a good look at Ashwagandha because:

1) It has been widely used since acient times in Ayurvedic medecine. It is also called the indian Gingseng.
2) It selectively activates P53 in tumor cells, Causing cell death or arrest. It does not activate P53 in healthy cells

http://clincancerres...tract/13/7/2298

Point (2) is important because an abnormal activation of P53 may cause cell scenesence as some studies show. This would work against the aim of telomerase activation. Ashwaganda does not activate P53 in healthy cells, leaving telomerase to do it's life extension wonders in them.

Disclaimer: I'm not taking astral fruit and I'm not taking ashwagandha yet, Although the folowing information makes it extra attractive:

http://medicinehunte.../ashwaganda.htm :)

I'm don't expect any bad interaction between Astral Fruit and Ashwaganda. One is a root the other a herb. Maybe Anthony can chip in here. Does astral fruit diminish the above mentioned effect Anthony? :)

#136 niner

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Posted 27 September 2008 - 04:04 AM

Niner, I understand your concern. Note that astragalus in itself has anti cancer activity:

http://carcin.oxfordjournals.org/cgi/content/full/28/6/1347

Interesting paper. Astragalus has a lot of biological activities... They used a total extract rather than a purified astragaloside IV. However, the EC50 for growth inhibition of the HT-29 colon cancer cells was 39.8 and 31.6 mcg/ml after a 48 hour incubation. Using a MW of 785 (astragaloside IV) as a standin, this would work out to a 50 uM blood level, which is pretty high for a drug like this. However, in the same paper they also got significant results on implanted HT-29 tumors in mice using ORAL dosing! So that's pretty cool. There's apparently more going on than the in vitro work would suggest. I didn't see any mention of the dose, although I was just skimming.

#137 rimrockjim

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Posted 28 September 2008 - 06:26 PM

Niner, I understand your concern. Note that astragalus in itself has anti cancer activity:

http://carcin.oxfordjournals.org/cgi/content/full/28/6/1347


To be extra safe you could take a safe p53 activating herb with your Astral fruit. Among others I'm taking a good look at Ashwagandha because:

1) It has been widely used since acient times in Ayurvedic medecine. It is also called the indian Gingseng.
2) It selectively activates P53 in tumor cells, Causing cell death or arrest. It does not activate P53 in healthy cells

http://clincancerres...tract/13/7/2298

Point (2) is important because an abnormal activation of P53 may cause cell scenesence as some studies show. This would work against the aim of telomerase activation. Ashwaganda does not activate P53 in healthy cells, leaving telomerase to do it's life extension wonders in them.

Disclaimer: I'm not taking astral fruit and I'm not taking ashwagandha yet, Although the folowing information makes it extra attractive:

http://medicinehunte.../ashwaganda.htm :)

I'm don't expect any bad interaction between Astral Fruit and Ashwaganda. One is a root the other a herb. Maybe Anthony can chip in here. Does astral fruit diminish the above mentioned effect Anthony? ;)



New to this site and not the braniac I need to be to follow this thread, but the subject fascinates me. My own understanding of ageing is that telemere lenghthening may be the holy grail of anti ageing. Appears that science may getting close to solving the telemere problem. If so, what a social delemma it will cause. What with the current population stretching available resources. But, that is a political issue I suppose. As for me I have been on antioxidants (A, B, C and E) for 40 years and up to 5 years, for such as ALA, ALC, Res, tumeric, Carnosine ( an telomerase activator, or so Dr Ray Sahalien says), ashwa, and astrag and just about everything except Astral fruit. May start that after more results and testing are seen on this thread. Can not afford the TA-65, that's for rich folks. I don't undersatnd why they can not sell their product as just a supplement and let us decide it's effectiveness, just like all the other products out there. Is greed rearing it's ugly head here?

#138 malbecman

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Posted 29 September 2008 - 10:20 PM

Don't forget to take a look at this pilot study that just came out from Dean Ornish and shows an increase in telomerase from lifestyle changes, not just a supplement. It looks pretty promising.
They also had this cohort examined for prostate cancer and showed decreases in some of those markers as well.....


http://www.imminst.o...showtopic=24322

#139 100YearsToGo

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Posted 29 September 2008 - 11:49 PM

The following effect of astragaloside is less well known:

"The results showed that per cent viability, number of progressive motile spermatozoa, curvilinear velocity, average path velocity and amplitude of lateral head displacement were significantly enhanced by A. membranaceus (P < 0.05 or < 0.01)"

http://www.ncbi.nlm....pubmed/15084153

This could be important if you still want to have kids when you're 145. :)



#140 niner

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Posted 30 September 2008 - 02:38 AM

New to this site and not the braniac I need to be to follow this thread, but the subject fascinates me.

Welcome to ImmInst! Telomerase activation is pretty cool, I agree.

My own understanding of ageing is that telemere lenghthening may be the holy grail of anti ageing.

Well, it's a necessary but not sufficient condition for eternal youth. There are a lot of other things that will need to be fixed as well; in fact telomere lengthening is one of seven things that Aubrey de Grey discusses. Lengthening telomeres should definitely get us something, though I'm not exactly sure what it will turn out to be.

Is greed rearing it's ugly head here?

Well, sure, but it's a free market. Competition is developing, and it will be a hell of a lot less than $25K.

#141 Guest_aidanpryde_*

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Posted 30 September 2008 - 03:53 PM

This discussion is becoming interesting.
I don`t say, that we should not support the "healthy" function of tumor supressing proteins, in that way I am speaking of things like enhancing DNA repair in order to prevent deletion of P53 genes or any unwanted epigenetic changes, but not of boosting the level of P53 in cells, where it is functioning normally or is already overexpressed due to aging.
I have read a review in which the paper mentioning the "super 53mice", which develop less tumors and live to a normal age, was quoted. I have also read the paper now.

The authors of the super P53mice study have worked with other methods, not just implementing P53 cDNA or any modified "superversions" of this protein but a whole segment including introns and other regulating genes. It is indeed interesting, but we should not forget studies in which a stronger P53 function lead to fewer cancers and accelerated aging. So it is note worthy to say that P53 binds to MnSOD in mitochondria, disactivating its function and leading to apoptosis and cell damage, an action which could be a sideeffect of a higher P53 expression. (1) On the other side (mitochondria targeted) telomerase is doing something similar and is also enhancing mitochondrial stress.

I have used resveratrol several times as an example for this very strange behaviour.

Resveratrol is not only supressing P16 but also P53 through activation of SIRT-1 and deacetylation of P53. (2)
Inactivation of Sirt1 and 2 leads to activation of P53. (3)
Furthermore it is deacetylating the retinoblastoma (RB) factor and on this way contributing to the inactivation of RB. (4)
What is really irritating me, is that this compound, resveratrol, is lowering the level and effectivity of 3 important tumor supressor proteins (P53, P16, RB) and is plus activating telomerase and despite all of this facts it is: cancer protective.

I think this whole stuff is not so easy as it seems, and I would also need time to read more about it, right now I am learning for exams and have a lack of time but I will try to read more after that.


(1)
Zhao Y, Chaiswing L, Velez JM, Batinic-Haberle I, Colburn NH, Oberley TD, St Clair DK.
p53 translocation to mitochondria precedes its nuclear translocation and targets mitochondrial oxidative defense protein-manganese superoxide dismutase.
Cancer Res. 2005 May 1;65(9):3745-50.

(2)
Cao C, Lu S, Kivlin R, Wallin B, Card E, Bagdasarian A, Tamakloe T, Wang WJ, Song X, Chu WM, Kouttab N, Xu A, Wan Y.
SIRT1 confers protection against UVB- and H(2)O(2)-induced cell death via modulation of p53 and JNK in cultured skin keratinocytes.
J Cell Mol Med. 2008 Aug 4. [Epub ahead of print]

(3)
Brooks CL, Gu W.
p53 Activation: a case against Sir.
Cancer Cell. 2008 May;13(5):377-8.

(4)
Wong S, Weber JD.
Deacetylation of the retinoblastoma tumour suppressor protein by SIRT1.
Biochem J. 2007 Nov 1;407(3):451-60.

Edited by aidanpryde, 30 September 2008 - 04:04 PM.


#142 Anthony_Loera

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Posted 07 October 2008 - 05:33 PM

FYI on the P16 item you mentioned 100years...

I have a quote on it, but it is quite expensive at this time.

To produce 10% saikosaponin A, we could supply bulk as 20kgs.

Price is USD 885/kg


I still think it's an option, but I think I need more studies to consider it, specially at a 10% purity.

A

Edited by Anthony_Loera, 07 October 2008 - 05:35 PM.


#143 zorba990

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Posted 07 October 2008 - 05:42 PM

Re Chitosan, I wonder if N-Acetyl Glucosamine (NAG) would work as well?
It's something I already have from Beyond a century in powdered form.

(BTW I don't do well with seafood, but NAG doesn't bother me)

#144 100YearsToGo

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Posted 07 October 2008 - 09:05 PM

FYI on the P16 item you mentioned 100years...

I have a quote on it, but it is quite expensive at this time.

To produce 10% saikosaponin A, we could supply bulk as 20kgs.

Price is USD 885/kg


I still think it's an option, but I think I need more studies to consider it, specially at a 10% purity.

A


Maybe you can just grind in some Bupleurum root?
no, seriously...I suppose the few western studies concentrate on the liver because Bupleurum has been used by the chinese for a long time (over 2000 years they say) for liver ailments. This let to testing of its active saikosaponin ingredients on the liver. Of course the interesting thing is its activation of P53 and p16 to stop carcinoma. One study show this also happening in lung cancer.

Maybe you allready did but if not take a look at Sho-Saiko-To. It's a bupleurum decoction used in japan. Studies in japan show additionaly:

- Antiproliferative effects on ovarian cancer lines
- Antiproliferative effects on lung cancer (again)
- Antiproliferative effect on malignant melanoma (skin cancer)
- Some very interesting other stuff

Here is an (incomplete) list of japan studies:


Edited by 100YearsToGo, 07 October 2008 - 09:18 PM.


#145 stephen_b

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Posted 07 October 2008 - 09:46 PM

Astral fruit + 250 mg chitosan before bedtime proved too stimulating to me <yawn>. I think I'll switch to mornings.

StephenB

Edited by stephen_b, 07 October 2008 - 09:46 PM.


#146 stephen_b

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Posted 09 October 2008 - 05:53 PM

LEF magazine came in the mail today. It has an article that discusses therapies for telomere extension. I was waiting for them to announce a telomerase activation product but that didn't happen (:)).

StephenB

Edited by stephen_b, 09 October 2008 - 05:54 PM.


#147 Anthony_Loera

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Posted 09 October 2008 - 06:49 PM

LEF magazine came in the mail today. It has an article that discusses therapies for telomere extension. I was waiting for them to announce a telomerase activation product but that didn't happen (:)).

StephenB



Hey,
if anyone here works for LEF, let them know we don't mind wholesale orders.

Cheers!

A

#148 100YearsToGo

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Posted 10 October 2008 - 04:57 PM

LEF magazine came in the mail today. It has an article that discusses therapies for telomere extension. I was waiting for them to announce a telomerase activation product but that didn't happen ( :) ).

StephenB



The storm petrel. The only animal whose telomeres lengthen with age. Telomere lengthening will likely make you live longer but not forever. Take that lesson from the storm petrel:

http://www.ncbi.nlm....pubmed/18071200

These birds die of other causes. That means we need to tackle other issues as well.
On the other hand the increase in life span is nothing to sniff at. They live 4 times longer than what would be expected based on body mass.

Edited by 100YearsToGo, 10 October 2008 - 05:27 PM.


#149 stephen_b

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Posted 10 October 2008 - 06:11 PM

The storm petrel [...]

From wikipedia:

The Leach's Petrel is a small bird at 18-21 cm in length with a 43-48 cm wingspan ... Lifespan for this bird is unusually long for a bird of such rather small size, with an average of 20 years and a maximum recorded lifespan of 36 years

In comparison, pigeons are about 33 cm in size, so this is a fairly small bird.

StephenB

Edited by stephen_b, 10 October 2008 - 06:11 PM.


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#150 Anthony_Loera

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Posted 10 October 2008 - 09:33 PM

Hi 100YessToGo...

Maybe you can just grind in some Bupleurum root?


Yes, the extract for saikosaponin A (not "b" or "c", etc) is actually from the Bupleurum root.

I think it is expensive because I am singling out the purity for the one type of saikosaponin that I believe affects p16.
The others (b, c, etc) don't seem to.

A




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