2189 replies to this topic

[Phoebus]

great post ampaynz1! thanks for that, its always great to hear from somebody in the real world who actually took something as opposed to reading about test results.

these seem to be the things you noticed that may (or may not) have been a direct result of the A IV.

-not getting sick
-long term skin disorder healed
-nervousness

is that it? anything else you think could be related to the A IV? did you notice energy levels change? how severe was the nervousness and how long did it last?

also, where did you get your A IV from? did you use a specific product?

[Anthony_Loera]

As mentioned before, here are my initial Telomere results:

My August 2008 Telomere Results (PDF)

These measurements were done right after my 37th Birthday.
I have been on Resveratrol (2 grams daily) since October 2006, and recently started on Astral Fruit the week the blood was taken for this initial test.

If all goes well using Astral Fruit, my second test may show the same or longer telomere lengths.
I believe the real results should be on my 1 year anniversary.

Cheers
Anthony Loera

[Anthony_Loera]

Here's a tidbit from Life Extension regarding Telomerase:

http://www.lef.org/n...amp;l=0#article


Having said that, it maybe sooner than later, when you start seeing more supplements like Astral Fruit.

Cheers
A

[saxiephon]

Here's a tidbit from Life Extension regarding Telomerase:

http://www.lef.org/n...amp;l=0#article


Having said that, it maybe sooner than later, when you start seeing more supplements like Astral Fruit.

Cheers
A

That's interesting!

What do you think about studies that have shown an increase in bioavailability of astragaloside IV by adding chitosan.


SAX


Absorption enhancement study of astragaloside IV based on its transport mechanism in caco-2 cells.

Huang CR, Wang GJ, Wu XL, Li H, Xie HT, Lv H, Sun JG.

Drug Metabolism and Pharmacokinetic Research Center, China Pharmaceutical University, Nanjing, People's Republic of China.

The purpose of this study was to investigate the transport characteristics and mechanisms for discovering the possible causes of the low bioavailability of astragaloside IV and to develop an absorption enhancement strategy. Caco-2 cells used as the in vitro model. Results showed a low permeability coefficient (3.7 x 10(-8)cm/s for transport from the AP to BL direction), which remained unchanged throughout the concentration range studied, indicating that the transport of astragaloside IV was predominantly via a passive route. The AP to BL transport of astragaloside IV was found to be highly sensitive to the extracellular Ca2+ concentration, which suggested that its transport may be via a paracellular route. Both chitosan and sodium deoxycholate can increase the permeation efficiency of astragaloside IV. This study indicated that astragaloside IV having a low fraction dose absorbed in humans mainly due to its poor intestinal permeability, high molecular weight, low lipophilicity as well as its paracelluar transport may directly result in the low permeability through its passive transport. Meanwhile, chitosan and sodium deoxycholate can be used as absorption enhancers based on its transport mechanism.

[Anthony_Loera]

Yes, chitosan is interesting.

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

A

[saxiephon]

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

[Anthony_Loera]

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

Edited by Anthony_Loera, 19 September 2008 - 02:24 PM.

[zorba990]

I'm looking forward to trying this product.
I have a concern, though. Astragalus is a selenium accumulator.
Anthony, have you tested your product for selenium content?

ref: http://www.enotalone...ticle/9200.html

[Anthony_Loera]

I'm looking forward to trying this product.
I have a concern, though. Astragalus is a selenium accumulator.
Anthony, have you tested your product for selenium content?

ref: http://www.enotalone...ticle/9200.html

According to the fact sheet you linked to, Astragalus membranaceus (which we use, and is typically used in human astragalus supplement extracts...) does not have this issue, but other types mentioned in the sheet do.

Thanks
A

[ampaynz1]

I believe the nervousness might be more of a specific problem related to me and how my body reacts to it. Before I ordered 100grams of astragaloside IV I had bought a 2.5% bag of 500 grams astragalosides mixture. I reacted quite badly to this. My lymph node swelled up all over and the submandibular ones became quite noticeable. I got nervous with this one and also became dizzy too even after one dose. I emailed the company that sold it and the owner was taking a few grams of it each day without any side effects. With pure A-IV98% I am nervous for about 2 hours and it is tolerable. I gave some to my dad and he also gets nervous, but for a lot shorter time. I bought the 100grams of 98% astragaloside IV from company below. I simply wired them the money from my bank account to their bank account and received it in about 4-5 days via express mail. I was lucky because customs didn't open up the sealed gray bag. It came double bagged. I took some of it out and vacuumed sealed the bag and put in an airtight container and then in the freezer. To weigh it I bought a scale on ebay. The first one I bought worked great. It was gray in color 0-50grams down to 0.000grams and I tested it out down to 0.015 grams or 15mg. Anything below 15mg and the scale will read zero. After 15mg is added to the scale it will work great. The trick is to initially add more then 15mg to the scale all at once. Do it too slowly and it could be off a little. Sometimes it does reset itself to zero after 30seconds , but I just weigh it again and subtract container weight. I then bought a black colored scale on ebay and it was junk and broken on arrival. Probably just bad luck.

Shanghai Honghao Chemicals Co.Ltd
(Honghao Group Limited)
Tel:0862158708081-808
00862158739982-808
Fax:0862151069122 Mobile:008613482898874
Website:www.crudera.com
Msn:Honghao-marketing@hotmail.com
Email:marketing@eonwin.com.

[Phoebus]

I bought the 100grams of 98% astragaloside IV from company below. I simply wired them the money from my bank account to their bank account and received it in about 4-5 days via express mail.
Shanghai Honghao Chemicals Co.Ltd
(Honghao Group Limited)
Tel:0862158708081-808
00862158739982-808
Fax:0862151069122 Mobile:008613482898874
Website:www.crudera.com
Msn:Honghao-marketing@hotmail.com
Email:marketing@eonwin.com.

i went to that website and am unable to locate any astragaloside. i typed it in the search engine and go "sorry, there is no product" and also searched through the various listings. where exactly is it offered on that website? thanks.

[Anthony_Loera]

Ampaynz1,
You sure you got what you paid for?

A

Edited by Anthony_Loera, 22 September 2008 - 02:49 PM.

[100YearsToGo]

I would be carefull when increasing telomerase activity:

http://mcb.asm.org/c...ract/22/20/7291

"These observations suggest that high telomerase activity may cooperate with genetic alterations that occur with age to promote tumorigenesis"

But there is hope from same scientist:

http://www.dailymail...eat-cancer.html

"Top British geneticist Aubrey de Grey called it an ‘extraordinary breakthrough’ which scientists had been trying to achieve for years."

Edited by 100YearsToGo, 23 September 2008 - 12:28 AM.

[Phoebus]

http://mcb.asm.org/c...ract/22/20/7291

"These observations suggest that high telomerase activity may cooperate with genetic alterations that occur with age to promote tumorigenesis"

I dont think its that simple



http://www.nature.com/onc/journal/v21/n4/full/1205076a.html
Unfortunately, the strong link between telomerase and cancer has led some to confuse telomerase activation with cancer, and others to overstate the cancer risk of telomerase activation therapies for degenerative diseases. This review clarifies the difference between telomerase, which does not cause growth deregulation, and oncogenes, which do. It also addresses the concept of telomerase repression as a tumor suppressor mechanism early in life, with detrimental tissue degeneration and tumor-promoting consequences late in life. This extended view of the telomere hypothesis helps explain how telomerase inhibition can be therapeutic in cancer patients, while controlled telomerase activation for degenerative diseases may actually reduce, rather than increase, the frequency of age-related tumorigenesis.

[100YearsToGo]

http://mcb.asm.org/c...ract/22/20/7291

"These observations suggest that high telomerase activity may cooperate with genetic alterations that occur with age to promote tumorigenesis"

I dont think its that simple



http://www.nature.com/onc/journal/v21/n4/full/1205076a.html
Unfortunately, the strong link between telomerase and cancer has led some to confuse telomerase activation with cancer, and others to overstate the cancer risk of telomerase activation therapies for degenerative diseases. This review clarifies the difference between telomerase, which does not cause growth deregulation, and oncogenes, which do. It also addresses the concept of telomerase repression as a tumor suppressor mechanism early in life, with detrimental tissue degeneration and tumor-promoting consequences late in life. This extended view of the telomere hypothesis helps explain how telomerase inhibition can be therapeutic in cancer patients, while controlled telomerase activation for degenerative diseases may actually reduce, rather than increase, the frequency of age-related tumorigenesis.

Look at the wording "Others to overstate the cancer risk". It is clear even from this article that there is a cancer risk but Geron doesn't think it should be overstated. The study I posted tried to pinpoint exactly what this risk is. Because your article comes straight from Geron, it is understandable that they would want to understate the cancer risk. They have vested financial interest in telomerase repression/activation drugs. Other studies would be apreciated.

Don't get me wrong..I think telomerase activation is great for life extension when combined with some form of cancer supressing therapy. Check the second article I previously posted. It looks fantastic.

Edited by 100YearsToGo, 23 September 2008 - 01:42 PM.

[Anthony_Loera]

October 2002 Study:

We demonstrate here that increased cancer incidence and the reduced viability of K5-Tert mice are aggravated in a p53+/- genetic background, indicating that telomerase cooperates with loss of p53 function.
http://mcb.asm.org/c.../24/10/4275.pdf

While in the August 2008 Study:

The team of researchers achieved their results by inserting an extra copy of three genes - called telomerase, p53 and p16.

Inserting an extra copy improves their function in the body because they produce more protein, which makes them more active.

This in turn helps telomerase to protect chromosomes from shrinking, a process which normally happens naturally as all living creatures age. And it means p53 and p16 work to prevent cells mutating and dividing - and therefore preventing cancer - while producing a good balance of new and healthy cells.

Hmmm...
Having glanced at both... it appears it's not telomerase, but loss of p53 function that is the issue.

doing a quick google scholar search:
http://scholar.googl...amp;btnG=Search

we find that resveratrol helps p53 function.

A

Edited by Anthony_Loera, 23 September 2008 - 02:52 PM.

[100YearsToGo]

October 2002 Study:

We demonstrate here that increased cancer incidence and the reduced viability of K5-Tert mice are aggravated in a p53+/- genetic background, indicating that telomerase cooperates with loss of p53 function.
http://mcb.asm.org/c.../24/10/4275.pdf

While in the August 2008 Study:

The team of researchers achieved their results by inserting an extra copy of three genes - called telomerase, p53 and p16.

Inserting an extra copy improves their function in the body because they produce more protein, which makes them more active.

This in turn helps telomerase to protect chromosomes from shrinking, a process which normally happens naturally as all living creatures age. And it means p53 and p16 work to prevent cells mutating and dividing - and therefore preventing cancer - while producing a good balance of new and healthy cells.

Hmmm...
Having glanced at both... it appears it's not telomerase, but loss of p53 function that is the issue.

doing a quick google scholar search:
http://scholar.googl...amp;btnG=Search

we find that resveratrol helps p53 function.

A

I believe thats the right aproach. If you can find compounds that stimulate telomerase, p53 and p16 you may start aproaching same results as from inserting the genes. But wouldn't resveratrol inhibit telomerase? Appears that you can't have the cake and eat it too. Astragaloside with chitosan would cover telomerase, now we need potent stimulators for p53 and p16. Anyone done some research on this? I'll start looking.

[stephen_b]

The suggested dosing schedule is taking the two at different times though. I'm thinking of dosing astragaloside in the morning and resveratrol/curcumin later in the day.

Are there any implications for when to take that other cancer preventative, vitamin D?

Stephen

[Anthony_Loera]

Stephen is right,

folks need to take resveatrol and Astral Fruit at different times. I don't think there is an issue regarding Vitamin D and Astral Fruit.

Cheers
A

[100YearsToGo]

The suggested dosing schedule is taking the two at different times though. I'm thinking of dosing astragaloside in the morning and resveratrol/curcumin later in the day.

Are there any implications for when to take that other cancer preventative, vitamin D?

Stephen

Although Curcumin may prevent or combat cancer it seems not to activate p16.

http://clincancerres...ract/11/19/6994

"Whereas the expression of cyclin D1, an NF-ß–activated protein, was also reduced, there was no difference in the expression of p16 at the initial times after curcumin treatment."

It actually impairs p53 function.

http://carcin.oxford.../full/25/9/1611

Edited by 100YearsToGo, 23 September 2008 - 05:22 PM.

[Phoebus]

i think that we really dont understand the whole thing fully. we THEORIZE that p53 must be activated to suppress cancer, however the test show that not only does curcumin suppress p53 but it kill cancer cells left and right. so...how can that be? obviously something more is going on here.

as anthony pointed out, the one test which seemed to show that increase in telomerase activity was tumor promoting actually tested for multiple things so its impossible to make any firm conclusions based on that evidence.

my own theory is this. telomerase does not increase tumor activity, rather cancer cells exhibit high telomrase activity and so telomerase has been 'associated' with cancer cells, which is not the same as causing them or promoting them.

here is what i think happens.

1. telomerase activity drops as we age
2. this lead to shortening telomeres
3. eventually the telomeres shorten too much and cells replicate badly, apoptosis takes over but doesn't kill all the bad copies, so some turn immortal.
4. the immortal cells begin making their own telomerase in large amounts. thus telomerase is 'associated' with cancer cells.

however! its the LACK of telomerase that actually starts the process towards cancer, NOT the over activation. the run away telomerase activity of cancer cells happens only after a long period of being telomerase starved. thus if you actually had cancer, then telomerase activation might be a bad idea. but if you are a healthy middler aged or older person then telomerase activation would be a great thing.

again, this is my theory, and no i dont have absolute documentation to support it, its just what makes sense to me so far based on the evidence i have seen.

[100YearsToGo]

i think that we really dont understand the whole thing fully. we THEORIZE that p53 must be activated to suppress cancer, however the test show that not only does curcumin suppress p53 but it kill cancer cells left and right. so...how can that be? obviously something more is going on here.

as anthony pointed out, the one test which seemed to show that increase in telomerase activity was tumor promoting actually tested for multiple things so its impossible to make any firm conclusions based on that evidence.

my own theory is this. telomerase does not increase tumor activity, rather cancer cells exhibit high telomrase activity and so telomerase has been 'associated' with cancer cells, which is not the same as causing them or promoting them.

here is what i think happens.

1. telomerase activity drops as we age
2. this lead to shortening telomeres
3. eventually the telomeres shorten too much and cells replicate badly, apoptosis takes over but doesn't kill all the bad copies, so some turn immortal.
4. the immortal cells begin making their own telomerase in large amounts. thus telomerase is 'associated' with cancer cells.

however! its the LACK of telomerase that actually starts the process towards cancer, NOT the over activation. the run away telomerase activity of cancer cells happens only after a long period of being telomerase starved. thus if you actually had cancer, then telomerase activation might be a bad idea. but if you are a healthy middler aged or older person then telomerase activation would be a great thing.

again, this is my theory, and no i dont have absolute documentation to support it, its just what makes sense to me so far based on the evidence i have seen.

Yeah..cancer cells...It goes like this:

1) Most cancerous cells in humans have the P53 nocked out from them. P53 is not functioning in them
2) Some tumors still have P53

in case (1) you can not use p53 to target the cancer (curcumin might work here)
in case (2) you can use P53 to target the cancer. Some Chemo drugs use the availability of this gene

This is why improving expression of P53 will PREVENT cancer in people as it acts when a healthy cell turns defective, and is dividing for the first time. It will kill this cell before it continue division. If the defective cell is not detected by P53 because P53 is suppressed for whatever reason AND the DNA is boosted by telomerase you could have a problem. I think Anthony pointed this out.

If you allready have cancer, boosting P53 wont help as you would probably have a mass of tissue without P53. In that case curcumin etc. may help. But to avoid suppressing P53 in other healthy cells I don't think it is wise to supplement curcumin for too long. But thats my opinion.

We are talking life extension in a healthy individual here. We are trying to keep him healthy while extending life span. There are some chinese herb/vine that in clinical trials improved expression of P53 and/or target tumors without P53. I'm still checking them out. Drugs that affects pathways controlled by P53 could help control P53-deficient tumors. Metformin a widely used diabetes drug has shown this effect. But I need to find out more on possible side effects or effects on P16 and telomerase.

Edited by 100YearsToGo, 23 September 2008 - 08:14 PM.

[Phoebus]

We are talking life extension in a healthy individual here. We are trying to keep him healthy while extending life span. There are some chinese herb/vine that in clinical trials improved expression of P53 and/or target tumors without P53. I'm still checking them out. Drugs that affects pathways controlled by P53 could help control P53-deficient tumors. Metformin a widely used diabetes drug has shown this effect. But I need to find out more on possible side effects or effects on P16 and telomerase.

that great, and i am all for that. but this thread is about astragaloside and telomerase activity and whether or not they will promote health and extend life. i am just pointing out that just because telomerase activity is 'associated' with cancer does not mean it 'causes' cancer, two totally different things. in fact, I think that telomerase in a healthy individual is cancer preventive.

as for P53 activation, its a great subject, but perhaps a different thread is appropriate?

[100YearsToGo]

We are talking life extension in a healthy individual here. We are trying to keep him healthy while extending life span. There are some chinese herb/vine that in clinical trials improved expression of P53 and/or target tumors without P53. I'm still checking them out. Drugs that affects pathways controlled by P53 could help control P53-deficient tumors. Metformin a widely used diabetes drug has shown this effect. But I need to find out more on possible side effects or effects on P16 and telomerase.

that great, and i am all for that. but this thread is about astragaloside and telomerase activity and whether or not they will promote health and extend life. i am just pointing out that just because telomerase activity is 'associated' with cancer does not mean it 'causes' cancer, two totally different things. in fact, I think that telomerase in a healthy individual is cancer preventive.

as for P53 activation, its a great subject, but perhaps a different thread is appropriate?

Be patient. Astralogus and Telomerase activation has ramification..This thread is still about Astralogus and Telomerase. I think the following is good news. Anthony will be happy with this one:

http://carcin.oxford.../full/28/6/1347

"The successful promotion of apoptosis by AST in HT-29 colon cancer cells (with mutated p53 gene) and tumor xenograft has indeed proven that AST possesses strong anti-tumorigenic effects irrespective of the p53 status of the tumor."

Astro fruit is looking good.

[Obsidius]

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

I plan to order some Astral Fruit with my next order of resveratrol. Do you think the astral fruit should be cycled if used with chitosan, due to the increased absorption?

[Anthony_Loera]

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

I think if you are taking 2 capsules or more plus chitosan, then I have to agree that you may need a rest...

I was talking to a colleague and we think the rest may be smaller than the TA Sciences protocol (3 month on/ 3 Month off) if you are taking resveratrol. I am leaning toward a 2-3 week on / 1 week off at this point.

I will probably will take the first week of the month off once I introduce chitosan, just so I can easily remember when to rest. :D

Cheers
A

Edited by Anthony_Loera, 23 September 2008 - 09:55 PM.

[PWAIN]

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 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?

[Anthony_Loera]

I think I may have answered this earlier,

The issue is not resveratrol, as they aren't using it.
The issue is that it is possible, that over time, the cells may find a way to stop growth from telomerase.

As mentioned before, inserting a gene into a cell that permanently would have telomerase in the "on" position does not work. The healthy cell finds a way to stop it's growth... and the benefits in a healthy cell.

It's my understanding that the "cycleing" or "rest" from taking it, is to help avoid this issue.
We don't want Astral Fruit, at a high dose, to become less effective over time.

Cheers
A

Edited by Anthony_Loera, 24 September 2008 - 02:32 AM.

[niner]

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.

[niner]

i think that we really dont understand the whole thing fully. we THEORIZE that p53 must be activated to suppress cancer, however the test show that not only does curcumin suppress p53 but it kill cancer cells left and right. so...how can that be? obviously something more is going on here.

It either works through a different pathway, or its suppression of p53 is weak.

my own theory is this. telomerase does not increase tumor activity, rather cancer cells exhibit high telomrase activity and so telomerase has been 'associated' with cancer cells, which is not the same as causing them or promoting them.

here is what i think happens.

1. telomerase activity drops as we age
2. this lead to shortening telomeres
3. eventually the telomeres shorten too much and cells replicate badly, apoptosis takes over but doesn't kill all the bad copies, so some turn immortal.
4. the immortal cells begin making their own telomerase in large amounts. thus telomerase is 'associated' with cancer cells.

however! its the LACK of telomerase that actually starts the process towards cancer, NOT the over activation. the run away telomerase activity of cancer cells happens only after a long period of being telomerase starved. thus if you actually had cancer, then telomerase activation might be a bad idea. but if you are a healthy middler aged or older person then telomerase activation would be a great thing.

again, this is my theory, and no i dont have absolute documentation to support it, its just what makes sense to me so far based on the evidence i have seen.

Interesting concept. Short telomeres cause genetic instability resulting in transformation to a cancer cell, along with telomerase becoming constitutively active. I don't know if that's the kind of genetic instability that you get from short telomeres, though. There are plenty of other ways for mutations to happen, so if your hypothesis is correct, it's certainly not going to be the only way for a cell to become cancerous. BTW, this is not a theory, since it hasn't been tested. It's a hypothesis. Still interesting.