2189 replies to this topic

[Ben K]

resveratrol appears to inhibit telomerase

I'm not sure I understand this reasoning. If having more telomerase is beneficial, and resveratrol inhibits it, wouldn't you want to take something that increases it at the same time?

[niner]

resveratrol appears to inhibit telomerase

I'm not sure I understand this reasoning. If having more telomerase is beneficial, and resveratrol inhibits it, wouldn't you want to take something that increases it at the same time?

There's more to it than that. This is my present understanding, which might be flawed: Normally, there is no (or an insignificant amount of) telomerase in the cell. The astragalosides purportedly cause telomerase to be "expressed"; that is, the DNA instructions are read and a new copy of the telomerase protein is assembled. The telomerase, once expressed, will be active until it is degraded, unless it is inhibited by something. The big question is how long does the telomerase remain active? I will only hazard a guess that it is a matter of days rather than hours. If that guess is right, then it would be better to cycle resveratrol and astragalosides over a longer period. On the other hand, if resveratrol is not a potent inhibitor of telomerase, then as soon as the level of resveratrol in the cell drops a bit below the IC50 for inhibition, you are mostly back in business. We know that resveratrol levels in blood fall off pretty quickly, and they don't get all that high in the first place. We don't know the concentration of resveratrol in the cellular compartment where the telomerase resides. Maybe it's a problem, maybe it's not. The three pieces of data that would help us figure this out are:

a) How long is telomerase active after it is expressed?
b) What is the IC50 for resveratrol inhibition of telomerase?
c) What is the intracellular concentration of resveratrol for a given plasma concentration? (probably varies by cell type and location)
d) (extra bonus question, relevant to (a)) Is there a mechanism to specifically degrade or deactivate telomerase on a schedule, or is it allowed to hang out until it is damage by some stochastic process?

[medievil]

resveratrol appears to inhibit telomerase

I'm not sure I understand this reasoning. If having more telomerase is beneficial, and resveratrol inhibits it, wouldn't you want to take something that increases it at the same time?

There's more to it than that. This is my present understanding, which might be flawed: Normally, there is no (or an insignificant amount of) telomerase in the cell. The astragalosides purportedly cause telomerase to be "expressed"; that is, the DNA instructions are read and a new copy of the telomerase protein is assembled. The telomerase, once expressed, will be active until it is degraded, unless it is inhibited by something. The big question is how long does the telomerase remain active? I will only hazard a guess that it is a matter of days rather than hours. If that guess is right, then it would be better to cycle resveratrol and astragalosides over a longer period. On the other hand, if resveratrol is not a potent inhibitor of telomerase, then as soon as the level of resveratrol in the cell drops a bit below the IC50 for inhibition, you are mostly back in business. We know that resveratrol levels in blood fall off pretty quickly, and they don't get all that high in the first place. We don't know the concentration of resveratrol in the cellular compartment where the telomerase resides. Maybe it's a problem, maybe it's not. The three pieces of data that would help us figure this out are:

a) How long is telomerase active after it is expressed?
b) What is the IC50 for resveratrol inhibition of telomerase?
c) What is the intracellular concentration of resveratrol for a given plasma concentration? (probably varies by cell type and location)
d) (extra bonus question, relevant to (a)) Is there a mechanism to specifically degrade or deactivate telomerase on a schedule, or is it allowed to hang out until it is damage by some stochastic process?

What if you take resveratrol first thing in the morning and astragalus before going alseep? This should atleast have some benefits i gues?

[sasha59]

This is from TAsciences instructions with regards to other supplements copied from page 30 of this thread:

1. How to take TA-65 daily:
We recommend taking TA-65 capsules on an empty stomach. You may take TA-65 either in the morning or in the evening before bedtime. If you take TA-65 in the morning, it should be taken before breakfast. Please wait approximately 1 hour after taking TA-65 before eating or taking any other nutritional supplements.
Please note: If you take resveratrol, curcumin (tumeric), quercetin, green tea extract, or silymarin (milk thistle); you should take those products approximately 12 hours before or 12 hours after taking TA-65. These supplements should not be taken at the same time as TA-65.

I'm no expert, but I'm confused as to why the recommendations of the people who produced the stuff in the first place are being second guessed. They seem to think that taking resveratrol and TA-65 on the same day isn't a problem.

I would think that taking one or another but not both on a given day would reduce the time that either of the supplements have to work by half, thereby reducing there effectiveness perhaps by half as well.

Is there something here I missed?

Sasha

Edited by sasha59, 12 January 2010 - 04:21 PM.

[Anthony_Loera]

Sasha,

0- As a friend of mine has posted... Biology is complex.
1- EOD resveratrol (from the studies) produced great results. No issue there...
2- In Vitro studies our scientist has done one healthy blood, Res and Cycloastragenol, leads me to say folks need to take these separately.
3- TA-65 is not Cycloastrgenol (no one has proved this)

Cheers
A

Edited by Anthony_Loera, 12 January 2010 - 05:37 PM.

[xtol]

Sasha,

0- As a friend of mine has posted... Biology is complex.
1- EOD resveratrol (from the studies) produced great results. No issue there...
2- In Vitro studies our scientist has done one healthy blood, Res and Cycloastragenol, leads me to say folks need to take these separately.
3- TA-65 is not Cycloastrgenol (no one has proved this)

Cheers
A

It seems telomerase activators (whether TA-65 or Cycloastragenol) should be taken separately, but the length of time separating them is unknown (unless the questions posted by niner are answered. Perhaps TA Sciences has done tests and that is why they recommend a 12-hour interval. That would seem about right, unless telomerase is activated for several days after CycloA dosing. So, given the state of our knowledge, it may depend on what process the individual values most at the time - activation or inhibition. In the absence of test results, the safe bet is to take no resveratrol, etc., all the while you are taking CycloA or other activator.

[mrak1979]

In one of the conference presentations by Sierra Sciences, CEO Dr. Bill Andrews says his lab has tested resveratrol with telomerase and they've found that it doesn't inhibit telomerase. He believes that the connection was trumped up by pro-resveratrol researchers who wanted to portray it as an anticancer substance, because telomerase activation has been linked to cancer in the popular view.

[xtol]

In one of the conference presentations by Sierra Sciences, CEO Dr. Bill Andrews says his lab has tested resveratrol with telomerase and they've found that it doesn't inhibit telomerase. He believes that the connection was trumped up by pro-resveratrol researchers who wanted to portray it as an anticancer substance, because telomerase activation has been linked to cancer in the popular view.

Right. Well, in support of that is this:
http://anti-agingfir...-of-telomerase/

And so far the program seems to be working for Vince. (see the link, 'how am i doing').

[full_circle]

hi, newbie here. i'm no biochemist (am physicist) but looking at the list of telomerase inhibitors,

Curcumin
Resveratrol
Quercetin
Melatonin
Green tea
Cacao
Alliicin (garlic)
Silymarin

they all seem to have one thing in common --> inhibitor of cytochrome P450.
can we infer that any foods/supplements that inhibit cytochrome P450 may also be telomerase inhibitors? (grapefruit juice anyone?)

i also remember that CYP3A family has to do with cholesterol synthesis... do you think telomerase activation requires high cholesterol(ldl) level?

very crude thought, nonetheless a thought

btw,
i personally take Berberine for ldl reduction. Anyone aware if Berberine inhibits telomerase? (Berberine does inhibit CYP3A4)
Also, does DHA/EPA in fishoil also inhibit telomerase? (if so, does this mean we need to give up vascular health for telomerase activation..?)

Edited by full_circle, 15 January 2010 - 09:55 PM.

[niner]

hi, newbie here. i'm no biochemist (am physicist) but looking at the list of telomerase inhibitors,

Curcumin
Resveratrol
Quercetin
Melatonin
Green tea
Cacao
Alliicin (garlic)
Silymarin

they all seem to have one thing in common --> inhibitor of cytochrome P450.
can we infer that any foods/supplements that inhibit cytochrome P450 may also be telomerase inhibitors? (grapefruit juice anyone?)

i also remember that CYP3A family has to do with cholesterol synthesis... do you think telomerase activation requires high cholesterol(ldl) level?

very crude thought, nonetheless a thought

btw,
i personally take Berberine for ldl reduction. Anyone aware if Berberine inhibits telomerase? (Berberine does inhibit CYP3A4)
Also, does EPA in fishoil also inhibit telomerase?

There are a lot of P450s, and they cover a diverse chemical binding space. While at least some of the compounds in the list are inhibitors of some P450s, I don't think that the relationship to telomerase inhibition would necessarily hold. Telomerase inhibition may have some overlap to one particular P450 or P450 subfamily; that is not unreasonable and has been seen in other cases; e.g. P4503A4 inhibitors are frequently p-glycoprotein inhibitors. I don't think that telomerase inhibition requires cholesterol, or that EPA is an inhibitor. Don't know about berberine but I kind of doubt it.

[full_circle]

i just google searched and all studies seem to indicate that PUFAs are potent telomerase inhibitors.
i have this hunch that there is a correlation between "bad" cholesterol and telomerase activation (more vldl/ldl, stronger activation) as well as between efficient clearence of xenobiotic substance and stronger activation.
does this mean maybe i should be more inclined to buy into the minority reports that bad cholesterols are actually good..? (i btw have always doubted that hypercholesterolemia is bad.)

also found that Berberine is a moderate telomerase inhibitor.
btw,

Curcumin
Resveratrol
Quercetin
Melatonin
Green tea
Cacao
Alliicin (garlic)
Silymarin

they all are inhibitor of cytochrome P450.

Edited by full_circle, 15 January 2010 - 10:32 PM.

[niner]

Curcumin
Resveratrol
Quercetin
Melatonin
Green tea
Cacao
Alliicin (garlic)
Silymarin

they all are inhibitor of cytochrome P450.

Which one or ones? There are a lot of P450s with very different substrate specificity.

[full_circle]

Which one or ones? There are a lot of P450s with very different substrate specificity.
there are plenty of inducers of cytochrome P450 as well but none of them in the list are
niner, i get it. but you need to be open to new ideas no matter how unlikely and unsubstantiated they may sound, especially when you are charting a newest territory such as this. for example, who would have thought that a coagulation vitamin, only found in "bad" food such as butter, egg yolk and animal fat turn out to be the artery-decalcifying / plaque-dissolving activator-x? (i'm talking vitamin k2 MK-4 which, i am positive, is the key to french paradox). making connections between seemingly irrelevant / intuitively repulsing ideas/things is what drives science forward.

i propose to see if food preservatives such as BHT may turn out to be potent telomerase activators. Animals (not flies, well.. maybe flies too but i'm talking dogs and monkeys here) fed good quantity of BHT consisitently live much longer life and i have always thought there is more to this than bht's strong ldl-antioxidant effect. despite its amazing life-extending effect, BHT paradoxically raise "bad cholesterol" level quite substantially. BHT is also an extremely potent P450, especially CYP3A, inducer (i wonder TA-65 and/or Cycloastrgenol has similar effect..) imho, a large chunk of clue to immortality may lie in understanding vldl/ldl better.

not much time for now to elaboarte on this.
ciao

Edited by full_circle, 16 January 2010 - 11:26 AM.

[Anthony_Loera]

In one of the conference presentations by Sierra Sciences, CEO Dr. Bill Andrews says his lab has tested resveratrol with telomerase and they've found that it doesn't inhibit telomerase. He believes that the connection was trumped up by pro-resveratrol researchers who wanted to portray it as an anticancer substance, because telomerase activation has been linked to cancer in the popular view.

Resveratrol has dose dependent benefits, and while low doses may not show much... higher doses tell another story. Of course the question then becomes at what dose does resveratrol start to inhibit telomerase. We ask you to avoid taking it together with Astral Fruit:

http://cat.inist.fr/...cpsidt=17980790

A number of studies performed in our laboratory and elsewhere, showed that resveratrol is able to prevent carcinogenesis and to impair tumor growth and progression. In order to provide additional information on the pleiotropic effects of resveratrol on malignant cells, the present study was performed to test the in vitro influence of the compound on the growth and TLMA of HT-29 and WiDr human colon cancer cell lines. The results confirmed that resveratrol has a direct, dose dependent, inhibitory effect on cell proliferation in both lines. In addition, for the first time, relatively high concentrations of this compound were found to be able to substantially down-regulate telomerase activity. These preliminary results further support the potential role of resveratrol in chemoprevention/chemotherapy of human colon tumor cells and provide the rational basis for novel strategies in cancer control.

http://www.ncbi.nlm....pubmed/16465368

A number of previous studies investigated the in vitro effects of resveratrol on malignant human breast epithelial cell replication. The aim of the present study was to evaluate the activity of resveratrol on human metastatic breast cancer cells. The study was performed on the MCF-7 tumor cell line. Cell growth, cell cycle perturbation and apoptosis were evaluated by trypan blue dye exclusion assay, flow cytometric analysis and confocal fluorescence microscopy. TRAP assay and Western blot analysis respectively detected levels of telomerase activity and levels of hTERT in intracellular compartments of MCF-7 cells treated with resveratrol. Resveratrol has a direct inhibitory effect on cell proliferation. The results demonstrate that the drug induces apoptosis in MCF-7 cells, in a time- and concentration-related manner. Our results also show that the growth-inhibitory effect of resveratrol on malignant cells is mainly due to its ability to induce S-phase arrest and apoptosis in association with reduced levels of telomerase activity. In particular, TRAP assay and Western blot analysis respectively showed that resveratrol treatment down-regulates the telomerase activity of target cells and the nuclear levels of hTERT, the reverse transcriptase subunit of the telomerase complex. In our experimental model of breast cancer, resveratrol shows direct antiproliferative and pro-apoptotic effects. Studies on telomerase function and intracellular hTERT distribution point out that this agent is endowed with additional suppressive functions on critical tumor biological properties. These results speak in favor of a potential role of resveratrol in chemoprevention/chemotherapy of breast cancer.

Edited by Anthony_Loera, 17 January 2010 - 02:21 PM.

[Suzudo]

http://www3.intersci...842375/abstract

*******************
Telomerase activity was significantly reduced in aged rats compared to young animals. Melatonin significantly *increased* the telomerase activity of both young and aged rats. The MDA levels of gastric mucosa in the aged rats were significantly higher than those of the younger rats.
*******************

http://www.citeulike...article/6370223


******************
Melatonin *inhibits* telomerase activity in the MCF-7 *tumor cell line*
******************


Shilima khemen

[jpauling]

Fullcircle, you may be on to something. I had my cholestrol checked two weeks ago and got borderline-high, which was a surprise since my reading has always been healthy and steady. I am a health conscious 45 year old, I check my level twice a year. For last 6 months I have been eating and living healthy as usual and did not add or subtract my supplements except the addition of Astragaloside, so I can only attribute this to the Astragaloside I started taking 4 months back.

Do any Astragaloside users here have the same problem?

[Suzudo]

http://www.cnio.es/e...cion.asp?pag=35

and


http://docs.google.c...StHhIQNZ9QRumDQ

or http://www.cnio.es/e...ic07-en-314.pdf


))

Shilima khemen

[medievil]

Fullcircle, you may be on to something. I had my cholestrol checked two weeks ago and got borderline-high, which was a surprise since my reading has always been healthy and steady. I am a health conscious 45 year old, I check my level twice a year. For last 6 months I have been eating and living healthy as usual and did not add or subtract my supplements except the addition of Astragaloside, so I can only attribute this to the Astragaloside I started taking 4 months back.

Do any Astragaloside users here have the same problem?

I hope you realise that high cholesterol does mean nothing, read duke's healt summary for more info.

[niner]

Fullcircle, you may be on to something. I had my cholestrol checked two weeks ago and got borderline-high, which was a surprise since my reading has always been healthy and steady. I am a health conscious 45 year old, I check my level twice a year. For last 6 months I have been eating and living healthy as usual and did not add or subtract my supplements except the addition of Astragaloside, so I can only attribute this to the Astragaloside I started taking 4 months back.

Do any Astragaloside users here have the same problem?

You might have been seeing cholesterol seasonality.

Seasonal variation of plasma lipids has been shown in a large longitudinal trial of 35-59-year-old men [1]. Peak levels of total cholesterol, low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol all occurred in winter. This confirmed the results of earlier studies which had generally shown highest levels of total cholesterol in winter [2-4], although some found peaks in spring [5] and autumn [6], and some found no seasonal variation of total cholesterol [7, 8]. Seasonal variation in triglycerides seems to be less consistent but peak levels may occur in the autumn [1]. Most of the subjects in these studies were middle-aged adults and little is known of seasonal variation of serum lipids in elderly people.

[full_circle]

To jpauling,

being a non-biochemist, as i am a mere mortal physicist from south korea, you and anyone here are free to take what i write never-seriously. i do not have much time so i'll be succinct and to the point.

you've been on twice-a-year checkup of your cholesterol profile. thus, provided that you've been doing this for a couple of years, i'll rule out seasonal fluctuation explanation.

as to "I hope you realise that high cholesterol does mean nothing", this is right and wrong.

it is right in a sense that high level of so called "bad cholesterol" turns out to be a lot less harmful than thought b4, if not not-at-all harmful.
the real culprit is oxidized ldl (think of it as a rancid oil circulating in your blood). it does tremendous damage to the endothlium (inner lining of artery).

thus, as long as you keep your ldl not-oxidized, high cholesterol (almost) doesn't matter. (now of course there is this "homocysteine" thing, i'll talk about it in a minute)

however, this only applies under one condition: that you got healthy endothelium with no or minimal micro-lesions, which in reality never is true for any ppl 20+ years of age.

once you have micro-lesion, ldl will build up on that lesion, regardless oxidized or not, nevertheless oxidized ldl will yield much speedier build up: sooner or later you will develop atherosclerosis.

so to sum up,
had you started taking ldl-oxidization suppression measure b4 you were 20 years old, high cholesterol does mean nothing. if not, high cholesterol does matter and you need to start ldl-oxidization suppression measure right away.

then what are the substances that curb ldl-oxidization?
vitamin C doesn't cut it because it is not lipophilic.
the most potent lipophilic antioxidant that i know are food preservatives such as BHT and BHA.

***** i am compiling list of strong lipophilic antioxidants, so anyone here, please share strong lipophilic antioxidants in your lists, natual or synthetic. (btw vitamin E is a weak lipophilic antioxidant)*****

am i taking food preservative supplement? yes i do. 500mg of daily BHT in divided dose, so does my collegue, who is in research team of another potent but relatively unknown telomerase activator, ginsenoside Rh family, found in korean ginseng.

omg i am out of time, i'll later continue on ginsenoside and on why telomerase activator shouldn't be taken alone w/o lipophilic antioxidants.

wish you a great day.

Edited by full_circle, 18 January 2010 - 12:20 PM.

[GreenPower]

To jpauling,

being a non-biochemist, as i am a mere mortal physicist from south korea, you and anyone here are free to take what i write never-seriously. i do not have much time so i'll be succinct and to the point.

you've been on twice-a-year checkup of your cholesterol profile. thus, provided that you've been doing this for a couple of years, i'll rule out seasonal fluctuation explanation.

as to "I hope you realise that high cholesterol does mean nothing", this is right and wrong.

it is right in a sense that high level of so called "bad cholesterol" turns out to be a lot less harmful than thought b4, if not not-at-all harmful.
the real culprit is oxidized ldl (think of it as a rancid oil circulating in your blood). it does tremendous damage to the endothlium (inner lining of artery).

thus, as long as you keep your ldl not-oxidized, high cholesterol (almost) doesn't matter. (now of course there is this "homocysteine" thing, i'll talk about it in a minute)

however, this only applies under one condition: that you got healthy endothelium with no or minimal micro-lesions, which in reality never is true for any ppl 20+ years of age.

once you have micro-lesion, ldl will build up on that lesion, regardless oxidized or not, nevertheless oxidized ldl will yield much speedier build up: sooner or later you will develop atherosclerosis.

so to sum up,
had you started taking ldl-oxidization suppression measure b4 you were 20 years old, high cholesterol does mean nothing. if not, high cholesterol does matter and you need to start ldl-oxidization suppression measure right away.

then what are the substances that curb ldl-oxidization?
vitamin C doesn't cut it because it is not lipophilic.
the most potent lipophilic antioxidant that i know are food preservatives such as BHT and BHA.

***** i am compiling list of strong lipophilic antioxidants, so anyone here, please share strong lipophilic antioxidants in your lists, natual or synthetic. (btw vitamin E is a weak lipophilic antioxidant)*****

am i taking food preservative supplement? yes i do. 500mg of daily BHT in divided dose, so does my collegue, who is in research team of another potent but relatively unknown telomerase activator, ginsenoside Rh family, found in korean ginseng.

omg i am out of time, i'll later continue on ginsenoside and on why telomerase activator shouldn't be taken alone w/o lipophilic antioxidants.

wish you a great day.

Interesting post. In my "6-month period on AIV/3-month on Orlistat" I also took the rather strong oxidant Ginkgo Biloba (100 mg, corresponding to 24 mg flavonoid glycosides and 6 mg terpenoids). After the six month period my Cholesterol levels had improved considerably (see previous posts). I'm not sure if it's lipophilic, but would you consider it possible to attribute this improvement to the Gingko Biloba rather than the AIV or Orlistat?

[mpe]

Bill Andrews presentation @Logevity summit 2009 on telomerase activators (November 2009)

One of the world's leading scientists in the field of telomere biology explains the role telomeres play in cellular aging and the extensive discoveries his company has made and continues to make related to "telomerase," the enzyme that activates telomerase expression

: Part1, Sierra Sciences CEO Bill Andrews, Ph.D.

: Part2, Sierra Sciences CEO Bill Andrews, Ph.D.

: Part3, Sierra Sciences CEO Bill Andrews, Ph.D.

They are testing 33 telomerase inducers + TA65, he states it will take 15 years to get a drug through the FDA.
(but he did not deny the fact that it would be possible to get it prior of FDA approval)
I wonder why nobody did ask him if his telomeres got longer in 2 years of ta-65.

What i find interesting is that at a certain point he says that ta65 is a mild activator of telomerase, and in his opinion it would be more effective a high activator.

I asked Bill Andrews about his Telomere Length and below is his reply


From: Bill Andrews

Sent: Thursday, January 14, 2010 3:00 PM

To: admin@epn.com.au

Cc: Jon Cornell

Subject: RE: William Andrews Telemore Lengths



Hello Michael,

Sorry I wasn’t available to reply to your email earlier. However, everything Jon says is 100% accurate.

Today’s methods of telomere length measurement are good for showing large increases in telomere lengths but it is very difficult to see small increases or decreases in the rate of telomere shortening.

By the way, I have been taking TA-65 for 2 years and 10 months now. And, I have no intention of stopping. I like what it is doing and everyone else that is taking it likes what it is doing. I haven’t heard a single bad comment about TA-65 from any of the people that I know that are taking it.

-Bill Andrews

William H. Andrews, Ph.D.
President & CEO
Sierra Sciences, LLC
“Cure Aging or Die Trying”

ph: 775-856-9500, ext. 108

fax: 775-856-9510

cell and text: 775-530-1516
e-mail: bandrews@sierrasci.com

web: http://www.sierrasci.com

Where’s Bill? http://www.sierrasci.com/Travel_Schedule.html



From: Jon Cornell
Sent: Tuesday, January 12, 2010 1:46 PM
To: admin@epn.com.au
Cc: Bill Andrews
Subject: FW: William Andrews Telemore Lengths



Michael –



This is Bill Andrews’ assistant, Jon Cornell. I’ve heard Bill answer these questions enough times that I can answer them for you, but I’m cc’ing Bill on this e-mail and he’ll correct me if I’m wrong about anything.



Yes, Bill has had his telomere lengths measured at regular intervals since taking TA-65, and yes, the data has shown a small increase in mean telomere length – but the increase was within the margin of error, meaning that his telomeres may or may not have actually lengthened. Measuring mean telomere length is a very imperfect science, although there are several labs throughout the world who are striving to perfect it.



However, TA-65 may not work by increasing mean telomeres length in humans. There is evidence that telomerase preferentially elongates the shortest telomeres in the body, as well as evidence that it is only the shortest telomeres in the body that really matter when it comes to causing aging.



And there is an experimental telomere measurement procedure that has been recently developed by

Edited by Mikee5, 19 January 2010 - 05:52 AM.

[medievil]

To jpauling,

being a non-biochemist, as i am a mere mortal physicist from south korea, you and anyone here are free to take what i write never-seriously. i do not have much time so i'll be succinct and to the point.

you've been on twice-a-year checkup of your cholesterol profile. thus, provided that you've been doing this for a couple of years, i'll rule out seasonal fluctuation explanation.

as to "I hope you realise that high cholesterol does mean nothing", this is right and wrong.

it is right in a sense that high level of so called "bad cholesterol" turns out to be a lot less harmful than thought b4, if not not-at-all harmful.
the real culprit is oxidized ldl (think of it as a rancid oil circulating in your blood). it does tremendous damage to the endothlium (inner lining of artery).

thus, as long as you keep your ldl not-oxidized, high cholesterol (almost) doesn't matter. (now of course there is this "homocysteine" thing, i'll talk about it in a minute)

however, this only applies under one condition: that you got healthy endothelium with no or minimal micro-lesions, which in reality never is true for any ppl 20+ years of age.

once you have micro-lesion, ldl will build up on that lesion, regardless oxidized or not, nevertheless oxidized ldl will yield much speedier build up: sooner or later you will develop atherosclerosis.

so to sum up,
had you started taking ldl-oxidization suppression measure b4 you were 20 years old, high cholesterol does mean nothing. if not, high cholesterol does matter and you need to start ldl-oxidization suppression measure right away.

then what are the substances that curb ldl-oxidization?
vitamin C doesn't cut it because it is not lipophilic.
the most potent lipophilic antioxidant that i know are food preservatives such as BHT and BHA.

***** i am compiling list of strong lipophilic antioxidants, so anyone here, please share strong lipophilic antioxidants in your lists, natual or synthetic. (btw vitamin E is a weak lipophilic antioxidant)*****

am i taking food preservative supplement? yes i do. 500mg of daily BHT in divided dose, so does my collegue, who is in research team of another potent but relatively unknown telomerase activator, ginsenoside Rh family, found in korean ginseng.

omg i am out of time, i'll later continue on ginsenoside and on why telomerase activator shouldn't be taken alone w/o lipophilic antioxidants.

wish you a great day.

Thats a very interesting post

[full_circle]

glycosides and terpenoids are low to moderate in lipophilicity and imo to get a decent ldl-oxidation lowering effect out of
these, one needs to take scores if not hundreds of grams a day, which will harm you.

now as to cholesterol profile, ginkgo biloba, to my knowledge, isn't so good in lowering cholesterol, so i would say it was AIV or Orlistat.

i would personally stay away from platelet function modifying agents such as aspirin or ginkgo biloba since evidence suggests that our body exhausts all means necessary to compensate it, in process of which arise plethora of side effects <-- only natural since platelet being such a crucial factor for survival. one should instead find the base cause of platelet aggregation. one should also stay away from agents that mess with vitamin K, since this will calcify the artery.
(Interestingly, vitamin k2 mk-4 de-calcifies artery)

hope you the best, GreenPower.

back to telomerase activator, Jpauling, my ginsenoside researcher friend confirms that yes, telomerase activators do tend to elevate cholesterol. i had dinner with him over the weekend and as usual when it comes to ginsenoside, he would only answer yes/no to my question so this time i drilled him with a ton of it.

are you taking ginsenoside Rh? no, and it is not exactly Rh, but i can't tell you what it is. smile.
is this because there are too many unknowns? yes
is cancer and atherosclerosis part of unknowns? yes
will it worsen mild atherosclerosis? most likely
is it because telomerase activators elevate cholesterol? yes
is it also because endothelium cells may start to grow? very likely
(growth of endothelium is bad for pre-existing atherosclerosis)
other reasons? smile
does fishoil suppress endothelial growth? is this one reason that it is beneficial for atherosclerosis? yes

why do telomerase activators elevate cholesterol? smile
i thought about it and came up with this explanation: telomerase activators induce formation/growth of new cells and for new cells to form and grow, more ldl is needed since it is ldl that is the vehicle which delivers the building blocks to the cells. am i on right track? yes
is ginsenoside strong CYP3A inducer? yes
are all telomerase activators strong CYP3A inducers? most likely
is this why telomerase activators elevate cholesterol? chicken or the egg
i get it. do telomerase activators behave like BHT? in many ways, yes.
why do you take BHT besides its ldl-oxidation quenching effect? a couple of reasons but you already know them all.
is BHT's lipid-coated virus inactivating effect part of your reasons? yes
do lipid-coated viruses shorten life? yes
i recently read a study suggesting 100% world population has hsv-1, true? very likely
does it cause atherosclerosis? yes
does it mess with telomeres? most likely
why not take antivirals? they don't work as well as BHT and they mess with your DNA as well.

would you take telomerase activator without BHT? no
is it because more ldl-oxidation quenching is needed due to elevated ldl level? yes
other reasons? a couple more but quite complicated.
will you ever take telomerase activator? (this guy is 35 years old) maybe in 10 years but never now.
does ginsenoside quench homocysteine? yes
does upregulated CYP3A quench homocysteine? yes
do you take Trimethylglycine? no. a number of side effects outweigh the benefit. i eat lots of tangerine and orange for folic acid and take vitamin B supplements. tangerine/orange is excellent for good cholesterol profile too. and BHT also is a strong homocysteine terminator. be careful with sam-e and a couple more popular supplements. they raise homocysteine level.

do you know a lot about TA65? smile
how do you compare ginsenoside to TA65? smile
how do you compare ginsenoside to Cycloastragenol? smile
why you are not doing human trial? too many unknowns
are you doing animal trial? yes
promising results? mixed results
why TA65 ppl and others don't do animal trails? smile
when do you think ginsenoside technology will get mature enough to be ready for human? ? not any time soon.
in 2 years? 10 years, hopefully

Edited by full_circle, 19 January 2010 - 04:57 PM.

[full_circle]

oh btw Jpauling, are you related to Linus Pauling? i have tremendous respect for his hypothesis on Primates' origin of vldl. i follow Pauling therapy: lysine and high dose of vitamin c, plus proline and copper. copper supplement btw, my friend says essential if you take telomerase activator (enhanced collagen synthesis).

Edited by full_circle, 19 January 2010 - 05:33 PM.

[DeadMeat]

It seems Astragalus compounds have competition: purslane herb aquenous extracts(PHAS). And for a change, with in vivo evidence for telomerase activation AND increase in telomere lengths in a nice and dose dependent manner.
http://www.ncbi.nlm....pubmed/17764668

In order to evaluate mechanisms of natural plant purslane herb aquenous extracts (PHAS) for neuroprotective, we assessed neuroprotective effects of PHAS at doses of 2.5, 5 and 10 mg/(kg day) on SD mice injected daily with D-gal (50 mg/(kg day)) by behavioral tests. PHAS-fed mice showed higher activity upon induction by new environmental stimuli, lower anxiety and higher novelty-seeking behavior in the open field tasks, and significantly improved learning and memory ability in step-through compared with D-gal-treated mice. We further examined the mechanisms involved in neuroprotective effects of PHAS on mouse brain. PHAS significantly increased superoxide dismutase (SOD) activity and decreased the malondialdehyde (MDA) level. Meanwhile, PHAS also could up-regulate telomere lengths and telomerase activity in PHAS-fed groups. Furthermore, we examined the expression of p21(waf1) and p53 mRNA and protein in mouse brain by western blot analysis and real-time RT-PCR. We found that p21(waf1)was down-regulated by PHAS without changing the expression of p53. The results of this study suggested that the PHAS might be a primary target of p21(waf1)and the neuroprotective effect of PHAS might be carried out through a p21(waf1)-dependent and p53-independent pathway.

From the full text version:

Purslane herb powder also extends the life span of drosophila by regulating telomere length [6].

TRF length was determined using pulse gel electrophoresis followed by Southern blot hybridization with telomere-specific probes.Average telomere lengths were shown in Fig. 3A. Telomere length assay revealed that PHAS-fed groups were longer than those in the controls and d-gal model groups. PHAS-fed group of different concentrations led to resulted in the significant increment of the mean telomere length (Fig. 3B, P < 0.05). We then again evaluated the effect of PHAS on telomerase activity. Our data suggested that PHAS could up-regulate telomerase activity in PHAS-fed groups. Telomerase activity were shown in Fig. 3C. It revealed that PHAS-fed groups had higher than those in the controls and d-gal model groups. PHAS-fed group of different concentrations led to resulted in the significant increment of the telomerase activity.

[bsm]

It seems Astragalus compounds have competition: purslane herb aquenous extracts(PHAS). And for a change, with in vivo evidence for telomerase activation AND increase in telomere lengths in a nice and dose dependent manner.
http://www.ncbi.nlm....pubmed/17764668

From the full text version:

Purslane herb powder also extends the life span of drosophila by regulating telomere length [6].

TRF length was determined using pulse gel electrophoresis followed by Southern blot hybridization with telomere-specific probes.Average telomere lengths were shown in Fig. 3A. Telomere length assay revealed that PHAS-fed groups were longer than those in the controls and d-gal model groups. PHAS-fed group of different concentrations led to resulted in the significant increment of the mean telomere length (Fig. 3B, P < 0.05). We then again evaluated the effect of PHAS on telomerase activity. Our data suggested that PHAS could up-regulate telomerase activity in PHAS-fed groups. Telomerase activity were shown in Fig. 3C. It revealed that PHAS-fed groups had higher than those in the controls and d-gal model groups. PHAS-fed group of different concentrations led to resulted in the significant increment of the telomerase activity.

Thanks for posting this. Can you provide the telomere lengths?

I found a newer article but I don't have access to the full text. Maybe someone can post the telomere lengths from this newer article?
"Retracted: Antiaging effect of purslane herb aqueous extracts and its mechanism of Action."
http://www.ncbi.nlm....pubmed/19367671

[rwac]

"Retracted: Antiaging effect of purslane herb aqueous extracts and its mechanism of Action."
http://www.ncbi.nlm....pubmed/19367671

The retraction has been agreed due to overlap with the following article: Zhang Hongxing, Yu Nancai, Huang Guofu, Shao Jianbo, Wu Yanxia, Huang Hanju, Liu Qian, Ma Wei, Yi Yandong and Huang Hao. Neuroprotective effects of purslane herb aquenous extracts against d-galactose induced neurotoxicity.

http://www.ncbi.nlm....pubmed/17764668

[niner]

"Retracted: Antiaging effect of purslane herb aqueous extracts and its mechanism of Action."
http://www.ncbi.nlm....pubmed/19367671

The retraction has been agreed due to overlap with the following article: Zhang Hongxing, Yu Nancai, Huang Guofu, Shao Jianbo, Wu Yanxia, Huang Hanju, Liu Qian, Ma Wei, Yi Yandong and Huang Hao. Neuroprotective effects of purslane herb aquenous extracts against d-galactose induced neurotoxicity.

http://www.ncbi.nlm....pubmed/17764668

Wow, that's weird. Tried to publish the same thing twice, got busted, and had to retract it! First time I've seen that. "aquenous"... You would think that at least the reviewers or the "editors" would catch that. I've never seen a paper that so much looked like it came straight out of Google Translate.

So. Is purslane the new TA65? Did Geron just miss that one? Or is this a mirage?

[full_circle]

aren't there (too) many species in purslane family? i wonder which one. btw i hear that finding telomerase activators are not that difficult and they are not as scarce as we think: just gather up as many herb substances you can think of and screen them through a few proprietary criteria then test them: a Thomas Edison approach if you will. ginsenoside camp that i have mentioned already identified 30+ and i am positive that small and big labs around the world, and even some private labs have identified hundreds. i reckon the relevant quest at this time is to find activators that can selectively turn on the right ones (and turn off the wrong ones, as we all know, activating all telomeres in body will surely shorten life) <--this, i would think, will be very very difficult to achieve, if not impossible to achieve.

Edited by full_circle, 27 January 2010 - 12:20 PM.