Telomere structural research

Hi to all:

I am curious as to what current research pathway might lead to the most tangible/promising candidates for life extension? Would anyone be aware of any facet of research that is dealing specifically with the possible manipulation/replenishment of telomeric structures, or any efforts underway that are aimed at surpassing the Hayflick limit, without compromising cellular integrity?

I ask because I will be investigating/conceptualizing hypothetical (for now) strategies by which Nanomedical devices and procedures might intervene at the cellular level to potentially enhance their longevity.

Many Thanks

L-Carnosine reduces Telomere Damage.

Biochem Biophys Res Commun. 2004 Nov 12;324(2):931-6.
L-carnosine reduces telomere damage and shortening rate in cultured normal fibroblasts.

Shao L, Li QH, Tan Z. Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, PR China.

Telomere is the repetitive DNA sequence at the end of chromosomes, which shortens progressively with cell division and limits the replicative potential of normal human somatic cells. L-carnosine, a naturally occurring dipeptide, has been reported to delay the replicative senescence, and extend the lifespan of cultured human diploid fibroblasts. In this work, we studied the effect of carnosine on the telomeric DNA of cultured human fetal lung fibroblast cells. Cells continuously grown in 20 mM carnosine exhibited a slower telomere shortening rate and extended lifespan in population doublings. When kept in a long-term nonproliferating state, they accumulated much less damages in the telomeric DNA when cultured in the presence of carnosine. We suggest that the reduction in telomere shortening rate and damages in telomeric DNA made an important contribution to the life-extension effect of carnosine.

Are there any others where this is used in combination with other studies that would greater enhance this affect?
~John

How much does carnosine extend life?

In mice it would seem to extend lifespan by about 20%. I'm not certain how this would translate to human physiology.

Sounds like a hard problem... Extending the number of times a cell divides will neccessarily give it more potential to evolve into cancer. And this works just fine if you use telomerase (which already has telomere lengthening and mitogenic signaling properties, for the latter check recent work by Blasco group). There has been a problem extending telomeres in blood stem cells though (if you cant find it ask, and I will be happy to look up the ref for you) so that's what a "nano" might help doing.

Anyway, what your nanos would need to do simultaneously is enhance DNA repair and/or fix existing mutations using external info. Current pre- or low-end nanotech could help to do the latter by localizing replacement stem cells in the proper positions (so the number of times each individual clone has to divide would remain constant or actually shorten, see also WILT). To that end, your nanos might have one domain that binds high affinity to the replacement cell, and one that binds high affinity to the target niche. That together with a function to kill the native stem cell occupying the target niche and then disable the nanobot might do a lot. This type of surface recognition nanotech is reasonably advanced and has been used to selectively kill model cancer cells a couple of times. I hope this gave you some ideas on what to look for...

In mice it would seem to extend lifespan by about 20%. I'm not certain how this would translate to human physiology.

Im looking for a database of antiaging interventions, I know there is one becouse I have I have been there before.It includes all possible interventions such as carnosine feeding and CR etc. Could someone of you help me with the link?

Extending the number of times a cell divides will neccessarily give it more potential to evolve into cancer.

I would guess carnosine interferes with ROS generation somehow thereby preventing erosion of telomeres and need for cell divsion due to damage.

Geron is developing drug candidates to treat various degenerative diseases by the controlled activation of telomerase. Data published by the company and others has indicated that cellular aging caused by shortening telomeres, which occurs in numerous tissues throughout the human body, causes or contributes to chronic degenerative diseases and conditions including anemia, AIDS, macular degeneration (a chronic disease of the eyes often leading to vision loss), atherosclerosis (narrowing of arteries which reduces blood flow to internal organs) and impaired wound healing. Controlled activation of telomerase in normal cells can restore telomere length, improve functional capacity, and increase the proliferative lifespan of cells.

In 2005, Geron formed a new joint venture company, TA Therapeutics, Ltd. (TAT), with the Biotechnology Research Corporation (BRC) of Hong Kong. TAT will conduct research and commercially develop products that utilize telomerase activator drugs to restore the regenerative and functional capacity of cells in various organ systems that have been impacted by senescence, injury or chronic disease. TAT is owned 50% by Geron and 50% by BRC, a company established by the Hong Kong University of Science and Technology, Geron's research partner in the development of telomerase activator drugs.

There are no marketed products for telomerase activation at this time. But I'm sure many are watching and waiting for that day.

Cheers [lol]

Geron is developing drug candidates to treat various degenerative diseases by the controlled activation of telomerase.

Very interesting. I would be quite surprised if they succed. By which mechanism would they activate telomerase?

Telomerase activation is presently thought to improve the genetic stability of human cells against cancer.
The danger of cancer goes up in humans after cells become senescent, especially in epithelial tissue and
in lymphocytes. After the cell has become cancerous, then telomerase inhibition becomes attractive as therapy,
because cancer cells often activate telomerase as part of their growth strategy. This sometimes fails, however,
because cancer cells may use the ALT mechanism instead of activating hTERT to produce telomerase.
I note that germ cells such as sperm and egg have high continuous levels of telomerase,
and show no cancer problems. Similarly, stem cells intermittantly activate telomerase so that they
can have many more cellular divisions than the normal somatic 50 cellular divisions from the embyonic.
stage of human development, up to 1000 cell divisions. Furthermore, cultured human cells in vitro typically
become immortal without cancerous effect when exogenous telomerase is applied to the culture.
The good news is that hTERT is not thought to be an oncogene causing cancer. In my opinion, telomerase
activation as anti aging strategy is only worrisome when no guard band is included
to catch cancer cells activated by carcinogens in cases in which the cancer uses hTERT activation.
That is, it seems safe enough to use cyclic telomerase activation such as suggested by Noel Patton
at TA Sciences in connection with therapy using TA-65, a telomerase activator based on astragalus
extract and present as a minor component (cycloastragenol?), or chemically obtained from astragalus extracts
or constituents such as astragaloside iv, as described in Geron patent literature.
See http://greenwood.s5....gevity.html#(7) to study other small molecule telomerase activators and also see Michael Fossel's MD-PhD book Cells, Aging, and Human Disease.
I think cyclic telomerase activation will make our genes more stable against cancer, and that our
strategy in life extension should include cyclic telomerase activation as a matter of course, so that we do not
suffer much from the presence of senescent cells in our bodies. This also requires limiting cellular wastes
such as lipofuscin, and avoiding other mechanisms that can trigger senescence, such as high levels of
oxidative radicals that damage telomeric DNA in the absence of transcription, which tends to repair
transcribed DNA. It may also be required, as shown by Zs-Nagy, to keep the cell membrane permeability to
potassium in nerve cells within acceptable range by the use of DMAE, Centrophenoxine, or other drugs, if
we mean to obtain extremely long life spans approaching physical immortality with rejuvenation included. Similar
considerations may apply to chlorine in muscle cells. Improving DNA shielding with antioxidants and
antiglycating drugs such as carnosine should help ward off senescence effects due to telomeric DNA damage, and
DNA repair may be accelerated by other mechanisms such as application of Cat's Claw Extract or Pero's AC-11.
Incidentally, I still think extra vitamin C should be useful to 2500 mg/day. The aging of mitochondrial DNA
is better protected against when telomeres are long, as then the cell automatically generates higher
levels of endogenous antioxidants. I note that alpha lipoic acid plus acetyl L-carnitine has been effective
in mitochondrial recovery, and that treatment with NO using arginine supplements and endogenous nitric oxide synthetase
effectively promotes mitochondrial genesis. Otherwise, observe that membrane-damaging peroxynitrites generated by NO
are effectively countered with the gamma tocopherol form of vitamin E.

Edited by jamesagreen, 10 January 2008 - 10:36 PM.

Telomerase activation is presently thought to improve the genetic stability of human cells against cancer.
The danger of cancer goes up in humans after cells become senescent, especially in epithelial tissue and
in lymphocytes. After the cell has become cancerous, then telomerase inhibition becomes attractive as therapy,
because cancer cells often activate telomerase as part of their growth strategy. This sometimes fails, however,
because cancer cells may use the ALT mechanism instead of activating hTERT to produce telomerase.
I note that germ cells such as sperm and egg have high continuous levels of telomerase,
and show no cancer problems. Similarly, stem cells intermittantly activate telomerase so that they
can have many more cellular divisions than the normal somatic 50 cellular divisions from the embyonic.
stage of human development, up to 1000 cell divisions. Furthermore, cultured human cells in vitro typically
become immortal without cancerous effect when exogenous telomerase is applied to the culture.
The good news is that hTERT is not thought to be an oncogene causing cancer. In my opinion, telomerase
activation as anti aging strategy is only worrisome when no guard band is included
to catch cancer cells activated by carcinogens in cases in which the cancer uses hTERT activation.
That is, it seems safe enough to use cyclic telomerase activation such as suggested by Noel Patton
at TA Sciences in connection with therapy using TA-65, a telomerase activator based on astragalus
extract and present as a minor component (cycloastragenol?), or chemically obtained from astragalus extracts
or constituents such as astragaloside iv, as described in Geron patent literature.
See http://greenwood.s5....gevity.html#(7) to study other small molecule telomerase activators and also see Michael Fossel's MD-PhD book Cells, Aging, and Human Disease.
I think cyclic telomerase activation will make our genes more stable against cancer, and that our
strategy in life extension should include cyclic telomerase activation as a matter of course, so that we do not
suffer much from the presence of senescent cells in our bodies. This also requires limiting cellular wastes
such as lipofuscin, and avoiding other mechanisms that can trigger senescence, such as high levels of
oxidative radicals that damage telomeric DNA in the absence of transcription, which tends to repair
transcribed DNA. It may also be required, as shown by Zs-Nagy, to keep the cell membrane permeability to
potassium in nerve cells within acceptable range by the use of DMAE, Centrophenoxine, or other drugs, if
we mean to obtain extremely long life spans approaching physical immortality with rejuvenation included. Similar
considerations may apply to chlorine in muscle cells. Improving DNA shielding with antioxidants and
antiglycating drugs such as carnosine should help ward off senescence effects due to telomeric DNA damage, and
DNA repair may be accelerated by other mechanisms such as application of Cat's Claw Extract or Pero's AC-11.
Incidentally, I still think extra vitamin C should be useful to 2500 mg/day. The aging of mitochondrial DNA
is better protected against when telomeres are long, as then the cell automatically generates higher
levels of endogenous antioxidants. I note that alpha lipoic acid plus acetyl L-carnitine has been effective
in mitochondrial recovery, and that treatment with NO using arginine supplements and endogenous nitric oxide synthetase
effectively promotes mitochondrial genesis. Otherwise, observe that membrane-damaging peroxynitrites generated by NO
are effectively countered with the gamma tocopherol form of vitamin E.
Furthermore, separate papers by Vasa and Hayashi show that nitric oxide (NO) produces telomerase activation in the
endothelial cells of the vascular endothelium. 5 grams/day arginine with 1 gram of citrulline may be used
in combination with exercise to elevate NO levels, as described by Dr. Louis B. Ignarro in his book NO More Heart Disease.
As for telomerase activation using astragalosides, I am now experimenting with 6 x 200 mg/day Solaray Astragalus Root
Extract (1200 mg/day), which initial calculations show should approach 5 mg/day astragalosides, the dose I formerly
obtained from GAIA Herbs Astragalus Root Extract (1 mg astragalosides per 30 drops) before they changed their formula
to something I computed to be about 1/13th as strong. A weaker dose of astragalosides will still fight off viruses responsible
for the common cold by activating Interleukin 2. However, a stronger dose is desirable for telomerase activation, probably
5-10 mg/day astragalosides. Geron recommends up to 100 mg/day Astragaloside IV, and a related but different molecule
is used for TA-65, if I not mistaken, which is marketed by TA Sciences.

Otherwise, observe that membrane-damaging peroxynitrites generated by NO
are effectively countered with the gamma tocopherol form of vitamin E.

Interesting remark. This is a bit off-topic, but maybe this can help in avoiding the potentially damaging effects of arginine supplementation as suggested in:

L-Arginine Supplementation in Peripheral Arterial Disease

No Benefit and Possible Harm
Andrew M. Wilson, MBBS, PhD; Randall Harada, MD; Nandini Nair, MD, PhD; Naras Balasubramanian, PhD; John P. Cooke, MD, PhD From the Division of Cardiovascular Medicine (A.M.W., R.H., N.N., J.P.C.) and Department of Biostatistics (N.B.), Stanford University School of Medicine, Stanford, Calif.

Correspondence to John P. Cooke, MD, PhD, Division of Cardiovascular Medicine, Stanford University Medical Center, Falk Cardiovascular Research Institute, 300 Pasteur Dr, Stanford, CA 94305. E-mail john.cooke@stanford.edu

Received December 20, 2006; accepted May 3, 2007.

Background— L-Arginine is the precursor of endothelium-derived nitric oxide, an endogenous vasodilator. L-Arginine supplementation improves vascular reactivity and functional capacity in peripheral arterial disease (PAD) in small, short-term studies. We aimed to determine the effects of long-term administration of L-arginine on vascular reactivity and functional capacity in patients with PAD.

Methods and Results— The Nitric Oxide in Peripheral Arterial Insufficiency (NO-PAIN) study was a randomized clinical trial of oral L-arginine (3 g/d) versus placebo for 6 months in 133 subjects with intermittent claudication due to PAD in a single-center setting. The primary end point was the change at 6 months in the absolute claudication distance as assessed by the Skinner-Gardner treadmill protocol. L-Arginine supplementation significantly increased plasma L-arginine levels. However, measures of nitric oxide availability (including flow-mediated vasodilation, vascular compliance, plasma and urinary nitrogen oxides, and plasma citrulline formation) were reduced or not improved compared with placebo. Although absolute claudication distance improved in both L-arginine- and placebo-treated patients, the improvement in the L-arginine-treated group was significantly less than that in the placebo group (28.3% versus 11.5%; P=0.024).

Conclusions— In patients with PAD, long-term administration of L-arginine does not increase nitric oxide synthesis or improve vascular reactivity. Furthermore, the expected placebo effect observed in studies of functional capacity was attenuated in the L-arginine-treated group. As opposed to its short-term administration, long-term administration of L-arginine is not useful in patients with intermittent claudication and PAD.

However, too much gamma-toc does not appear to go well with exercise. It seems that one cannot win.

Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans
Christian P. Fischer,¹ Natalie J. Hiscock,² Samar Basu,³ Bengt Vessby,³ Anders Kallner,⁴ Lars-Börje Sjöberg,⁵ Mark A. Febbraio,² and Bente K. Pedersen¹

ABSTRACT

Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR--tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CE), RRR--tocopherol 290 IU/day + RRR--tocopherol 130 IU/day + AA 500 mg/day (CE), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, -tocopherol, -tocopherol, AA, and 8-iso-prostaglandin-F₂ (8-PGF₂). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF₂, increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CE. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CE, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CE. The results indicate that -tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.

Edited by andre, 24 March 2009 - 06:08 PM.

Telomerase activation is presently thought to improve the genetic stability of human cells against cancer.
The danger of cancer goes up in humans after cells become senescent, especially in epithelial tissue and
in lymphocytes. After the cell has become cancerous, then telomerase inhibition becomes attractive as therapy,
because cancer cells often activate telomerase as part of their growth strategy. This sometimes fails, however,
because cancer cells may use the ALT mechanism instead of activating hTERT to produce telomerase.
I note that germ cells such as sperm and egg have high continuous levels of telomerase,
and show no cancer problems. Similarly, stem cells intermittantly activate telomerase so that they
can have many more cellular divisions than the normal somatic 50 cellular divisions from the embyonic.
stage of human development, up to 1000 cell divisions. Furthermore, cultured human cells in vitro typically
become immortal without cancerous effect when exogenous telomerase is applied to the culture.
The good news is that hTERT is not thought to be an oncogene causing cancer. In my opinion, telomerase
activation as anti aging strategy is only worrisome when no guard band is included
to catch cancer cells activated by carcinogens in cases in which the cancer uses hTERT activation.
That is, it seems safe enough to use cyclic telomerase activation such as suggested by Noel Patton
at TA Sciences in connection with therapy using TA-65, a telomerase activator based on astragalus
extract and present as a minor component (cycloastragenol?), or chemically obtained from astragalus extracts
or constituents such as astragaloside iv, as described in Geron patent literature.
See http://greenwood.s5....gevity.html#(7) to study other small molecule telomerase activators and also see Michael Fossel's MD-PhD book Cells, Aging, and Human Disease.
I think cyclic telomerase activation will make our genes more stable against cancer, and that our
strategy in life extension should include cyclic telomerase activation as a matter of course, so that we do not
suffer much from the presence of senescent cells in our bodies. This also requires limiting cellular wastes
such as lipofuscin, and avoiding other mechanisms that can trigger senescence, such as high levels of
oxidative radicals that damage telomeric DNA in the absence of transcription, which tends to repair
transcribed DNA. It may also be required, as shown by Zs-Nagy, to keep the cell membrane permeability to
potassium in nerve cells within acceptable range by the use of DMAE, Centrophenoxine, or other drugs, if
we mean to obtain extremely long life spans approaching physical immortality with rejuvenation included. Similar
considerations may apply to chlorine in muscle cells. Improving DNA shielding with antioxidants and
antiglycating drugs such as carnosine should help ward off senescence effects due to telomeric DNA damage, and
DNA repair may be accelerated by other mechanisms such as application of Cat's Claw Extract or Pero's AC-11.
Incidentally, I still think extra vitamin C should be useful to 2500 mg/day. The aging of mitochondrial DNA
is better protected against when telomeres are long, as then the cell automatically generates higher
levels of endogenous antioxidants. I note that alpha lipoic acid plus acetyl L-carnitine has been effective
in mitochondrial recovery, and that treatment with NO using arginine supplements and endogenous nitric oxide synthetase
effectively promotes mitochondrial genesis. Otherwise, observe that membrane-damaging peroxynitrites generated by NO
are effectively countered with the gamma tocopherol form of vitamin E.
Furthermore, separate papers by Vasa and Hayashi show that nitric oxide (NO) produces telomerase activation in the
endothelial cells of the vascular endothelium. 5 grams/day arginine with 1 gram of citrulline may be used
in combination with exercise to elevate NO levels, as described by Dr. Louis B. Ignarro in his book NO More Heart Disease.
As for telomerase activation using astragalosides, I am now experimenting with 6 x 200 mg/day Solaray Astragalus Root
Extract (1200 mg/day), which initial calculations show should approach 5 mg/day astragalosides, the dose I formerly
obtained from GAIA Herbs Astragalus Root Extract (1 mg astragalosides per 30 drops) before they changed their formula
to something I computed to be about 1/13th as strong. A weaker dose of astragalosides will still fight off viruses responsible
for the common cold by activating interferon. However, a stronger dose is desirable for telomerase activation, probably
5-10 mg/day astragalosides. Geron recommends up to 100 mg/day Astragaloside IV, and a related but different molecule
is used for TA-65, if I not mistaken, which is marketed by TA Sciences. I might add that Nature's Way astragalus root
extract, featuring 1.25 mg of astragalosides per 250 mg capsule, may be useful at 4 capsules per day for 5 mg/day
of astragalosides. Geron recommended between 50 and 100 mg of astragaloside IV for telomere reconstruction,
so that larger doses of commercially available astragalosides from extracts might be used if 5 mg/day on a 15 day
on, 15-day off cycle provides inadequate telomerase activation to achieve 0.75 years per month rejuvenation rate,
about the best that TA Sciences has reported based on 460 base pairs of telomere growth per year using their
astragaloside TA-65.

Edited by jamesagreen, 30 March 2009 - 03:52 PM.

Telomerase activation is presently thought to improve the genetic stability of human cells against cancer.
The danger of cancer goes up in humans after cells become senescent, especially in epithelial tissue and
in lymphocytes. After the cell has become cancerous, then telomerase inhibition becomes attractive as therapy,
because cancer cells often activate telomerase as part of their growth strategy. This sometimes fails, however,
because cancer cells may use the ALT mechanism instead of activating hTERT to produce telomerase.
I note that germ cells such as sperm and egg have high continuous levels of telomerase,
and show no cancer problems. Similarly, stem cells intermittantly activate telomerase so that they
can have many more cellular divisions than the normal somatic 50 cellular divisions from the embyonic.
stage of human development, up to 1000 cell divisions. Furthermore, cultured human cells in vitro typically
become immortal without cancerous effect when exogenous telomerase is applied to the culture.
The good news is that hTERT is not thought to be an oncogene causing cancer. In my opinion, telomerase
activation as anti aging strategy is only worrisome when no guard band is included
to catch cancer cells activated by carcinogens in cases in which the cancer uses hTERT activation.
That is, it seems safe enough to use cyclic telomerase activation such as suggested by Noel Patton
at TA Sciences in connection with therapy using TA-65, a telomerase activator based on astragalus
extract and present as a minor component (cycloastragenol?), or chemically obtained from astragalus extracts
or constituents such as astragaloside iv, as described in Geron patent literature.
See http://greenwood.s5....gevity.html#(7) to study other small molecule telomerase activators and also see Michael Fossel's MD-PhD book Cells, Aging, and Human Disease.
I think cyclic telomerase activation will make our genes more stable against cancer, and that our
strategy in life extension should include cyclic telomerase activation as a matter of course, so that we do not
suffer much from the presence of senescent cells in our bodies. This also requires limiting cellular wastes
such as lipofuscin, and avoiding other mechanisms that can trigger senescence, such as high levels of
oxidative radicals that damage telomeric DNA in the absence of transcription, which tends to repair
transcribed DNA. It may also be required, as shown by Zs-Nagy, to keep the cell membrane permeability to
potassium in nerve cells within acceptable range by the use of DMAE, Centrophenoxine, or other drugs, if
we mean to obtain extremely long life spans approaching physical immortality with rejuvenation included. Similar
considerations may apply to chlorine in muscle cells. Improving DNA shielding with antioxidants and
antiglycating drugs such as carnosine should help ward off senescence effects due to telomeric DNA damage, and
DNA repair may be accelerated by other mechanisms such as application of Cat's Claw Extract or Pero's AC-11.
Incidentally, I still think extra vitamin C should be useful to 2500 mg/day. The aging of mitochondrial DNA
is better protected against when telomeres are long, as then the cell automatically generates higher
levels of endogenous antioxidants. I note that alpha lipoic acid plus acetyl L-carnitine has been effective
in mitochondrial recovery, and that treatment with NO using arginine supplements and endogenous nitric oxide synthetase
effectively promotes mitochondrial genesis. Otherwise, observe that membrane-damaging peroxynitrites generated by NO
are effectively countered with the gamma tocopherol form of vitamin E.
Furthermore, separate papers by Vasa and Hayashi show that nitric oxide (NO) produces telomerase activation in the
endothelial cells of the vascular endothelium. 5 grams/day arginine with 1 gram of citrulline may be used
in combination with exercise to elevate NO levels, as described by Dr. Louis B. Ignarro in his book NO More Heart Disease.
As for telomerase activation using astragalosides, I am now experimenting with 6 x 200 mg/day Solaray Astragalus Root
Extract (1200 mg/day), which initial calculations show should approach 5 mg/day astragalosides, the dose I formerly
obtained from GAIA Herbs Astragalus Root Extract (1 mg astragalosides per 30 drops) before they changed their formula
to something I computed to be about 1/13th as strong. A weaker dose of astragalosides will still fight off viruses responsible
for the common cold by activating interferon. However, a stronger dose is desirable for telomerase activation, probably
5-10 mg/day astragalosides. Geron recommends up to 100 mg/day Astragaloside IV, and a related but different molecule
is used for TA-65, if I not mistaken, which is marketed by TA Sciences. Still another way to get 5 mg/day astragalosides
is to take 4 capsules of Nature's Way astragalus root extract, available from Herbal Remedies astragalus. This corresponds
to the maximum dose of astragalus root used in Chinese medicine, 33 grams. However, since Geron recommends
50 to 100 mg astragaloside IV for maximum telomerase activation, higher doses of extract for higher astragaloside dosing
can be envisioned.

Edited by jamesagreen, 30 March 2009 - 04:16 PM.

Are you a bot or what? I mean - why do you keep repeating the same quote?

Are you a bot or what? I mean - why do you keep repeating the same quote?

I'm guessing you have never visited his longevity webpage... great stuff there... but very hard to look at without going cross-eyed due to the layout and backgroung image... easy enough to adjust with a few clicks of the mouse though.

Anyway on the posts in question here, he actually is changing it... problem is he is doing it within a quoted block with no clear indication of what is changing... You either have to read real close or diff it.

The changes (between his last two posts) are at the end. He went from:


is used for TA-65, if I not mistaken, which is marketed by TA Sciences. I might add that Nature's Way astragalus root extract, featuring 1.25 mg of astragalosides per 250 mg capsule, may be useful at 4 capsules per day for 5 mg/day of astragalosides. Geron recommended between 50 and 100 mg of astragaloside IV for telomere reconstruction, so that larger doses of commercially available astragalosides from extracts might be used if 5 mg/day on a 15 day on, 15-day off cycle provides inadequate telomerase activation to achieve 0.75 years per month rejuvenation rate, about the best that TA Sciences has reported based on 460 base pairs of telomere growth per year using their astragaloside TA-65.

to:

is used for TA-65, if I not mistaken, which is marketed by TA Sciences. Still another way to get 5 mg/day astragalosides is to take 4 capsules of Nature's Way astragalus root extract, available from Herbal Remedies astragalus. This corresponds to the maximum dose of astragalus root used in Chinese medicine, 33 grams. However, since Geron recommends 50 to 100 mg astragaloside IV for maximum telomerase activation, higher doses of extract for higher astragaloside dosing can be envisioned.

Edited by frankbuzin, 02 April 2009 - 01:26 AM.

Yeah, I haven't noticed that, thanks!