2189 replies to this topic

[mrkosh1]

This is important news!

If Sierra Sciences has found a neutraceutical that can produce a hit of 30 or 30% of what a Hela cell produces, this could be the most important breakthrough in the history of anti aging!

Can anyone else contact Sierra Sciences? We need to get them to confirm or deny this.

Can anyone here tell me where this seminar can be found on the internet?

[Anthony_Loera]

I will email them again, however I wouldn't keep my hopes up because of another recent email I got from TA Sciences which I may share (to put things in perspective...) if we get no comment from Sierra Sciences. However, I would much prefer Bill to help us out on the recent marketing, as it makes more sense to hear news from the horse's mouth.

Cheers
A

Edited by Anthony_Loera, 17 August 2011 - 06:10 PM.

[Anthony_Loera]

Ok,
I have received the email from Bill Andrews, and have posted it in the other thread.

Cheers
A

[mrak1979]

hi anthony, which other thread are you referring to? can u provide a link?

thanks

[niner]

hi anthony, which other thread are you referring to? can u provide a link?

Here it is, from the horse's mouth...

[niner]

Along with the conference call video above, Elle Magazine (what, you don't read Elle?) just published a really nice article about the history and future of the telomere story.

[missminni]

Along with the conference call video above, Elle Magazine (what, you don't read Elle?) just published a really nice article about the history and future of the telomere story.

I don't read Elle, but the link you give here doesn't work.

[rwac]

Along with the conference call video above, Elle Magazine (what, you don't read Elle?) just published a really nice article about the history and future of the telomere story.

I don't read Elle, but the link you give here doesn't work.

There you go, missminni.

Attached Files

•  elle_ta.pdf   1.97MB   327 downloads

[missminni]

Along with the conference call video above, Elle Magazine (what, you don't read Elle?) just published a really nice article about the history and future of the telomere story.

I don't read Elle, but the link you give here doesn't work.

There you go, missminni.

thanks!

[mrkosh1]

We need some specific clarification.

I listened to the first video. There were three calls in the video.

In the first call about the first batch of substances tested, I am absolutely certain the following was stated about the compound.

"This is the scale... if our control sample is about 6% percent of hela, this is more than 11% percent of hela."

In the second call about the second batch of substances tested (specifically number 38), the following is stated. It does not make sense, unless it is of greater potency than the first.

"This is the first time we have ever seen a strong hit from a natural product."

In the third call, he is very excited, and wants to tell the following results to Popular Science. I am not sure if he states 3.28 percent, or 30.28 percent.

"The new hit actually got a score of (3.28 or 30.28) which is more than twice as potent as product B......"

Ok.

This is my analysis.

In the first call, the hit was an 11. He was not too excited about it.

The second hit was the "first time we have ever seen a strong hit from a natural product." If the second hit was first time they had ever seen a strong hit from a natural product, it had to be stronger than the first hit, which was 11% of Hela.

In the final call, he is more excited than ever, and mentions that the last hit was actually 3.28 or 30.28. I could not tell which one he stated. However, I doubt he would be very excited about this if he had already found a hit of greater than 11%. Also, we know from the second call, that compound 38 was the first strong hit they had found in a natural product.

I think they have found a compound that has 30% of Hela.

We need to email Andrews again, and ask for some clarification.

At a minimum, we need to know what was the numbers he reported in this call.

I'm thinking he did report that the final one was 30%.

[niner]

Along with the conference call video above, Elle Magazine (what, you don't read Elle?) just published a really nice article about the history and future of the telomere story.

I don't read Elle, but the link you give here doesn't work.

That's weird, it works for me. Anyone else have trouble with that link?

We need some specific clarification.

I heard it very differently... My version is in the Product B thread.

[rwac]

That's weird, it works for me. Anyone else have trouble with that link?

For some reason firefox doesn't download it properly, but wget does.
Didn't check other browsers though.

[Suzudo]

From a little before my last comment in the forum wanted to expose this and subsequent comments have encouraged me to get time to expose it. I hope that my English this time is more decent.


Divide the possible solution of the target in 3 groups and each of these groups into two groups:

1 - Preventing and repairing cell damage

2 - Lengthening telomeres safely

3 - Facilitate cell differentiation by creating new tissue in damaged tissue without involving loss of telomeres. Rebuild damaged tissues

1, 2 and 3 is always involved TP53 (P53) as a regulator

in 1 TP53 orders senescence, apoptosis and repair if necessary

in 2 TP53 prevents the development of tumors due to excessive lengthening of telomeres in cells damaged


"hnRNP F" prevents TERRA (Tel-RNA) binds to telomeres. "hnRNP F" seems to be formed from the TP53 molecule as a regulator. View Maria Antonia Blasco work in Nature Marhuenda end of 2010 that "hnRNP F" prevents TERRA (Tel-RNA) binds to telomeres

in 3 TP53 deciding whether to produce tissue differentiation or not as the length of telomeres. View María Blasco's work published in February 2011





in 1:
To avoid damage by superoxide and chemicals, prevent damage to protein folding, prevent accumulation of damaged proteins, prevent damage to DNA (SOD, antioxidants -take very much antioxidant also gives many cases of cancer because the body also uses as oxidizing- experiment that worked María Blasco, good fats processing, activating genes control protein folding, activate SIRT1 and reduce peroxides)

b-damage repair (remove damaged proteins such as activating autophagy, activate SIRT1, activate TP53, chitosan nerves damage repaired)


in 2:
a-activate TP53 (p53)
b-activate TERT


in 3:
Cell differentiation to turn on if necessary: ​​long telomeres and actived TP53
b-curb stop before full differentiation instead of forming scar tissue of low quality and prevent automatic suicide of new neurons within two weeks of training. Help the body in the formation and improvement of tissue


The ways in which cancer cells become immortal seem linked to forms that counteract the types of apoptosis or cell suicide.

-A self-eating, autophagy, and disappear
-B replication. In each copy the telomeres get shorter until there a set of cells without telomeres. The chromosomes are attached and are destroyed and removed

in A: Immortalization is achieved by activating the autophagy of damaged parts as misfolded proteins by recycling the material consumption and costs by lowering the overall cell

in B: immortalization is achieved by activating telomerase in each copy so that the cell do not lose a significant amount of telomeres and growing group of cells (and can be dispersed). That does not imply that telomerase is carcinogenic but it is used by cancer cells and may help

Therefore autophagy and telomerase in a controlled manner are the main targets

Another form of immortalization appears to occur in cell differentiation and inflammation processes in the repair of damaged tissues in adult animals:

First. It de-differentiated fibroblasts and telomerase is activated preparing cells.
Second. Crashes telomerase and activate mechanisms to prevent tumor formation while differentiated cells
Third. Differentiation is completed before the perfect formation of new tissue in mammals (in animals like the salamander or the axolot completes formation of new tissue that until the end) except in the liver where it did complete such differentiation in mammals.

In animals with long telomeres but with the ability to regenerate, the life is much shorter (axolots, and so on) that in animals with shorter telomeres without that capability, but with greater amount of tissue damage support (whales). Limb regeneration involves billions of copies and therefore telomeres shortening per copy, end therefore has to accept or low quality tissue, but for cause incidental damages or disease and not regular aging, and this should be achieved a extreme telomere length

The Hydra is immortal but cells adults are germ cells, is also able to differentiate and repair damage to any tissue, hydras extend telomeres long and safe keeping in the same process of differentiation. I do not know the final end but who do not have cancer tumors for this activity.

The differentiation seems that skin cancers can be activated final differentiation genes allowing telomerase activity yet not differentiated cell and continue its spread and growth. That seems to occur in skin cancers and indications are that the TP53 can be sensitive and be damaged by excessive ultraviolet light






B: Experiments on mice conducted by Maria Antonia Blasco
Marhuenda inserting 3 copies of TP53 in the DNA rather than the normal two (one per parent) and 3 copies of TERT in place of 2, extends the lifespan of normal mice by 40% (not 50% but increased TERT (telomerase) is 50% but less of the increase), which itself was not extended aging time if not the youth . The time it took before aging. Also do not show any cancerous tumor

Three copies of TERT with only two copies of TP53 always ended in large amounts of cancerous tumors. So, although telomerase itself is not carcinogenic, it not can be activated without control of the TP53

Three copies of TP53 extends bit life and these mice did not show any cancerous tumor.

It was the union of TP53 and TERT which expanded youth safe and healthy.

Other:

Removing SCH9 encoding serine kinase teorina
SOD2 increases, resistance to stres, Active Msn2 and Msn4
SCH9 removing triples lifetime of an organism.

Also has lengthened life significantly in mice by giving melatonin. The same amount of lengthening life flies by giving them root Rhodiola Rosea

Has been achieved lengthening of life with an lithocholic acid equivalent to a low calorie diet in mice (prevents damage in protein folding and improved lipid transport, and so on)

And it has achieved lengthening of life in mice with rapamycin by mechanisms similar to low-calorie diet and autophagy of damaged proteins, but rapamycin eliminates the immune system

There are several known activators of autophagy:

Rapamycin eliminated the immune system and if not discovered a safe alternative is ruled out even if proven to work.

The clonidine is activator of autophagy but is antihypertensive is also anti insomnia is used in opioid detoxification in hiperhidrólisis sleep against the syndrome of attention deficit hyperactivity, reduce ICT, against menopausal symptoms, against syndrome Tourette, and so on. So it seems to have too many interactions. Although some positive look is extremely dangerous even for healthy people with diabetes can reduce insulin levels. Rule it out in round

Verapamil induces autophagy in waste celurales as misfolded proteins and therefore for this it is interesting to keep neurons, front with Alzheimer's or ALS. The case is that it is hypotensive and vasodilator. It may be appropriate but it is too low voltage is low or has high blood pressure medication that interferes hypotensive. It seems that root extracts of Rhodiola Rosea are hypertensive (which would rosavin) and could be compensated

for point 1 could serve as triggers of TP53: resveratrol, luteolin, apigenin and others. If the resveratrol result inhibitor TERT could use other that not they were in appropriate doses. But I would say that resveratrol is the first choice or to take into account.

All these substances have a structure and molecular radial position of some similar. The genistein low expression of TELO2 as estradiol but genistein prevents SIRT1 binds to TP53, genistein increases the expression of TP53. The genistein increases the expression of SOD1 mRNA and genistein increases the expression of MYO1D

In addition, the tocopherol increases the activity of TP53 special supplement to consider (and are antioxidants by phenolic hydrogen. React with reactive forms of oxygen. They protect the unsaturated fatty acids from oxidation which is a differentiator and activate MYO1D muscle tissue.

to point "1"
As a substance to protect proteins from misfolding of simulating low-calorie diet: acid lithocholic

As activators of protective of ROS (reactive forms of oxygen or superoxide plus toxic) avoiding damage to the folding of proteins and DNA damage: the need activating endogenous forms of SOD (super oxide dismutase, the three varieties SOD1, SOD2 and SOD2) and cancellation of peroxides

In this return to be eligible resveratrol, luteonina, apigenin, and so on.
Steric acid increases the expression of SOD1 but lowers the SOD2 although this is fixed by adding resveratrol (which prevents this from happening and therefore increases SOD1 and SOD2)

Pantothenic acid increases the production of glutathione to protect from damage caused by peroxides

Glutathione directly prevents the damage caused by peroxides

And the chitosan has good protection

For part "b" of point "1":

You can activate SIRT1 by resveratrol, luteonina, apigenin, and so on.

And you can eliminate misfolded proteins re-using them emulating a hypocaloric diet, eliminating cellular waste accumulation in neurons in ALS, and others with verapamil which would be very important at this point. Chitosan has been shown to repair damaged nerve cells.


For point "2":

TP53 Triggers: resveratrol, luteolin, apigenin, and so on. The issue is whether resveratrol has negative effects to the activation or action of TERT and if there is anything that will neutralize this effect in this case




They appear to be activators of TERT:

Raloxifene (low expression of hnRNP A2B1, hnRNP U, hnRNP H1-view articles on Maria Antonia Blasco Marhuenda about riboproteíns TERRA (telARN) and TERT- and increases activity of TERT expression and phosphorylation)

Tamoxifen (low expression of hnRNP A2B1

Cycloastragenol

Estradiol (increase TERT expression and activity, increases expression and activity of TERT mRNA, increasing expression of hnRNP A2B1 mRNA)

Cycloestragenol and estradiol have similar structures that are repeated in many molecules with some activity in TERT. The structure of saponin with a dual activity in soluble and a lipid or fat

Estradiol activates TERT but acts negatively with lipid mechanism
Estradiol causes maldistribution of fat, promotes heart attacks, thrombus formation

Substances such as estradiol, cycloestragenol, lithocholic acid or beta-sitosterol have a shared and one that differs. Purslane (Portulaca oleacea) appears in addition to beta-sitosterol and lithocholic acid has more unidentified saponins may be implicated in the activation of TERT.

Well this structure is repeated is a saponin with a water-soluble part must be related to the activation of TERT and other fat-soluble will be related to lipid transport or prevent damage to protein folding. Interestingly estradiol TERT activator is decent but the other functions are unwanted and would amount to a high calorie diet with fat accumulation in an inappropriate manner, the possibility of heart attacks, blood clots. The structure works well in these features is the lithocholic acid (acid of liver that also has purslane) comparing all these molecules might be possible to design one that had all the desired and no adverse.

Perhaps mixing estradiol and adding more acid lithocholic ring could get the negative effects of estradiol or not. Do not know


The TERT (telomerase) is not carcinogenic but may help in cases of damaged cells to become cancer as shown by María Blasco work with mice with overexpression of TERT

Estradiol can cause breast cancer and others.

It takes time to activate the TP53 and TERT in the cell, the same cell
Another trigger would ephitelion as discussed in the forum. This would form in the pineal gland. The pineal gland from tryptophan, form serotonin at day, and melatonin at night. Giving melatonin to mice is the long life and giving substances that triggers the production of serotonin in the pineal gland, such as are contained in the extract of Rhodiola rosea root in flies has also extended the life in the same proportion accurate than that of mice with melatonin suggests that melatonin and serotonin are indicators for the production of ephitelion. And surely equivalent

Serotonin is an antidepressant, increases mental activity (and helps physical activity) and the rosavin has capacities anti-anxiolytic. It appears that new neurons are formed routinely and increases at the training exercise, antidepressant and blueberries, new neurons which last about two weeks unless made a mental activity more than usual. Serotonin is formed whole in the gland epithelial but only part became ephitelión and melatonin, although more number more serotonin you have. And melatonin is formed in various parts of the body as I said, only a portion intake and the brain would not help the mental activity although daytime sleep. Since it appears that the hypertensive effects rosavin that can offset the hypotensive verapamil would choose above melatonin as first choice.

I not have come to analyze the point "3" except the recommendation of the chitosan at the moment.

with point "1" and "2" and chitosan formulation could be a first:

Lithocholic acid
Resveratrol
Verapamil
Cycloestragenol
Root extract of Rhodiola Rosea, or rosavin and salosindre
Chitosan

To consider adding luteolin, apigenin and resveratrol or replace these or similar substances in appropriate dosage to achieve the same result without adversely affecting the expression of TERT, if resveratrol result negative for TERT

also consider adding pantothelic acid and / or glutathione

and further, consider adding steraic acid when using resveratrol as an option
or tocopherol to increase the activity of TP53 (which in turn can go well in point 3 for cell differentiation and whether telomeres are long) as well as protection against oxidation

So another formulation may, for example:

Lithocholic acid
Luteolin
Verapamil
Cycloestragenol
Rosavin and Salosindre
Tocopherol
Pantothelic Acid (and/or Glutatión)
Chitosan


Then keep watching to see if or where purslane is an activator of TERT quite safe. And if you discover a way to lengthen telomeres by activating more TERT according TERRA safely and that TP53 should have plenty of cascade reactions with other proteins and / or peptides and may hnRNP F can be lowered safely, for example

The addition of estradiol or use of estradiol was instead of cycloestragenol, may work with more of lithocholic acid, but it seems too risky. Imagine a person over 40 years with a perfect complexion at age 12 but with a body with morbid obesity and heart problems in addition to a thrombus at any time.

to point "3":

It appears that new neurons are formed but are destroyed after two weeks of training, except mental exercise is more than usual. It can stimulate the formation of these neurons with exercise, it seems that some antidepressants, and also with simple things like blueberries. The death of neurons seems necessary for the formation of links but not excessive and there seems to be a chemical form that they can be kept in that case.

From adult stem cells can repair some tissues, and have substances of differentiation so much as stop the differentiation. The latter can determine a tissue or another depending on the amount of times.

but if cut and other events: fibroblasts approach the damaged area. Fibroblasts de-differentiatet. And the new tissue is differentiated or even extremity but the process is stopped before reaching the tissue regeneration giving a poor quality that makes of patch. This prevents the loss of telomere length too.

There are signaling molecules such as myostatin stop that avoids the formation of muscle tissue. When less is more is generated and vice versa. The MYO1D, however, is a molecule of cell differentiation. Small amounts of myostatin have more muscle mass means having more with less exercise and less likely to gain weight, also a more rapid aging of the tissue. Having more myostatin is having to make greater effort to achieve muscle mass, regeneration slower, more likely to get fat

Tretionin retinoic acid or used for cell differentiation: Increased expression of ESR1 mRNA of HDAC1 from MyoD, STAT1, STAT2 in from MSX1 mRNA, MSX2 mRNA, TP53 (although in some cases down), TP53 mRNA TP53 activity

but low activity of TERT, TERT mRNA, the expression of TERT and TERT mRNA

It is dangerous ingested and used topically. The fact is indicating that for and what not.



Mammals can regenerate the liver but no other organs or tissues in the same way. In contrast, other beings even regenerate members of the body. but do not live as long telomeres, have less amount of tissue and regeneration member of the body means in an infinite number of copies of cells

It is assumed that the complex activates the differentiation MSX1 in embryos and MSX2 in adult animals. The hydra would be part of their adult tissue cells in germinal stage without significant loss of telomeres and with full feedback and be immortal and strangely did not have cancer because of that? Why?

The MSX2 would the liver of mammals or animals such the axolotl in your body in general and nervous system problems, of course. The hydra has a nervous system simple also enough to regenerate nerves (more reason to need autophagy and others)

Well, there are assumptions in that tissue regeneration would prevent the molecules stop continuing the process would not occur or be disabled by the MSX2 in mammalian liver or the body of beings like the axolotl.

It has been speculated that they must be related to these signals the immune system or be produced by it. Because young children have regenerated fingertips and quickly lost that power while improving the immune system. But soon shortened telomeres and could directly connected though a guess. Do not know.

There are about 30 substances are tested for tissue regeneration in case of injury. One made headlines for a random accident. I mean http://www.physorg.c...ws90693701.html

many years a person fond of the model plane with a propeller cut a small piece of a finger and could not find the piece. A family physician who gave a dust and gave him the piece of finger regenerated including bone, nerves, arteries, muscles, and so on. in a few weeks getting a little every day in the wound. The resulting finger piece of what looked like the owner harder than the other fingers, something different (and I guess it's because he was older tissue, having made so many copies for a little over a cm)

The powder in question was obtained as follows:

Without knowing the specific molecules or to indicate that the differentiation continue to block or stop signs of differentiation but are surely part of the extracellular matrix, we chose to use those and they had together: the inside of gall bladders pig livers is scraped. Pig tissue for compatibility. The result is cells but also molecules including proteins of the extracellular matrix, may that microorganism. It is acid that destroys cell walls and DNA strands and whatever it takes to not have danger without so much as to destroy the molecules involved in what you want. Can be acetic acid or another? and then the result is freeze dried to preserve it to reduce as much as possible to what you want to use aseptic

And this dust what is used.

Perhaps with very long telomeres and a continued safe enlargement treatment you could use the powder to regenerate damaged tissues, and so on.

If so would solve point 3 and with the help of 1 and 2



If these substances are not enough by themselves or disregard them, if you could, without gene therapy occurred to me that:

Long ago a test failed HIV vaccine using a common cold virus as a vector for HIV molecules that do not change and remain the same in all viruses. So that any person has acquired immunity to HIV by having that person, specific antibodies against these substances as antigens, by chance, so that it could have happened that immunity by bone marrow transplantation cure AIDS and others.

The vaccine works in monkeys but not in humans probably because people had had contact with the virus antibody and had chosen for him

So he has proposed using plasmids containing the sequences of these molecules and adjuvants to generate antigens in epithelial cells out of the same molecules marked as antigens for the body to produce antibodies.

Plasmids be inserted through an injection of compressed air and electrically stimulate the skin to penetrate the cells and get the effect.

Should be able to generate antibodies against specific molecules without creating an auto-immune disease maybe just maybe some proteins could be chosen to insert their genetic sequences in plasmids with adjuvants and injection system using compressed air and electrical stimulation of the skin, which create antibodies against these specific proteins. do not know if it would work. But this outbreak seem prime candidates soon

SCH9
mdm2
Pinx1
Myostatin

Download SCH9 because SOD2 increases, resistance to stres, Active MSN2 MSN4,
and the elimination of SCH9, triples lifetime of some organisms.
mdm2, because it is the antagonist of TP53. Rhoche has a substance called nutlin (which seems to work best is the version nutlin 3a) that is used in chemotherapy down mdm2 and up the production and activity of TP53

PinX1 antagonist of TERT (of the telomerase). Perhaps telo2 or another, but PinX1 antagonist of TERT seems pretty clear, do not know if have other significant interactions

Pinx1 should not attempt download if you have not had success with SCH9 and mdm2

And Myostatin, already placed but should not be lowered also has had previous success with

would take more than whites and gave no problems exist and is unlikely and very difficult but could perhaps studying of these substances and their interactions

--------------
This suggests that if this will work on putting SCH9 and mdm2 and adjuvant plasmid injection of compressed air and electrical stimulation might be a cure for some cancers and especially for early cancer vaccine
--------------

And if it is not enough this or that mixtures of substances have little effect even many years taking them every day. Should it work, could take such substances or any specific treatments to rejuvenate effectively or lengthen telomeres and then repair tissues

This is curious.

Well I wanted to note that it has to be careful to read information on increases expression and activity of genes and / or unwanted proteins and down unwanted substances as determined by the value these

Paraquat is a herbicide used as a poison and have used people to commit suicide ingesting. It seems to be blocked in human SOD2 far as you can depending on the concentration and thus diluted was used with some confidence (now largely banned its use). But there is a mutated form of SOD2 that seems to block it is to some people. Near the site of my work there is a place where a boy that used to kill weeds in a farm I had and the solution with enough water to wet his skin solvent. In other case people do not go, in that case was found badly at night and went to sleep the next day was dead, poisoned.

If paraquat is inserted in some animals activated TERT, TP53, Varieties of SOD, including cell differentiation. Everything seems to not be achieved with a single substance at the moment and it seems that some override others, get this. But the fact is that it is a desperate response to the organism against massive destruction. It is not the elixir of youth quite the opposite and this is a side effect of response to a terrible attack. And this is relevant: The body has mechanisms to enable all this time in case of extreme necessity.


Another thing is, it was found recently that in the case of progeny cells (Hutchinson-Gilford syndrome) had decreased the amount of a protein to healthy cells (in addition to having high amounts of protein that lowers progerin Quantity rapamycin curiously). This is the BANF1 and is responsible to prevent damage to DNA in the processes of cell division. Which makes sense: their low level errors cause by creating large amounts of damage as progerin protein (a protein would be wrong to eliminate efficient autophagy) and need for more cells to obtain copies of the same number of correct cells in another person. With what besides accumulating damage telomere shortening and grow old prematurely before. The fact is that increasing amounts of BANF1 seems to rejuvenate cells. It is not clear but may be more mechanisms and some form of control over the entire recipe without mixtures of many substances.


<a name="result_box5">It seems that purslane contains linoleic acid and many things but among them:


Tryptophan
Tocopherol
Lithocholic acid
steraic ácid
sistosterol
Glutatión
Omega 3
Pantholenic Acid
Luteolin
Apigenin
Liquiritin
Genistein



But no one has remained young forever by eating large amounts of purslane (which also contains unwanted oxalates) yes that is eaten in some places. and assigning to a diet of vegetables in the same places there is less incidence of cancers, more centenarians if quality of life, less heart disease and older people with a good general physical age but also aging.

It would be interesting to use purslane as other plants as a source of these substances using using such a quantity of plant were necessary and not a small amount given that in some places is consumed quite a number of purslane. The amount of substance is much lower than necessary for these formulations, if the plant food directly. How must have substance in the capsules if it is a direct preparation of the plant without separate and concentrate the substances?


Shilima khemen

[unglued]

So are there ANY formal medical studies showing resveratrol having ANY actual beneficial health effects whatsoever when taken as a supplement by real live human beings?

Even ONE?

Not sure why that question is being asked in this topic, but...

A recent review paper available online concluded that not enough human studies have been completed yet to convince them.

The overall conclusion is that the published evidence is not sufficiently strong to justify a recommendation for the administration of resveratrol to humans, beyond the dose which can be obtained from dietary sources. On the other hand, animal data are promising in prevention of various cancer types, coronary heart diseases and diabetes which strongly indicate the need for human clinical trials.
...
Several clinical trials of oral Resv as a pure compound or using Resv-rich products (grapes and grape juice) are under way. In total, 24 clinical studies are listed at the homepage http://clinicaltrials.gov/ having Resv as the major experimental subject or as part of a clinical trial. Therefore, it is our recommendation that clinical trials should focus on biomarkers of cancers, diabetes and metabolic syndromes as well as neurological diseases (Table 7).

Based on the limited number of human studies, the working group has concluded that there is not at the moment enough available and scientifically valid data on the effect of Resv to conclusively state whether it could be a disease preventive substance in humans or could be used for human life extension (Table 1). It is therefore vital to perform such studies.

See Review article of resveratrol-based human clinical trials topic, which is in the actual Resveratrol forum. That would be a better place to ask that question

[unglued]

TA-65 is cycloastraganol which is not a novel compound. Even if it was made synthetically as a bio-identical compound it wouldn't be novel. If they made a telomerase activator that was novel it would require FDA approval.

They do, and they will. Not TAT2, but TAT153, renamed GRN510 now that the joint venture is finished.

We were able to show that administration of the small molecule telomerase
activator, GRN510, in an animal model of idiopathic pulmo-
nary fibrosis, resulted in increased telomerase activity in the
lung tissue, reduced inflammation, preserved functional
lung tissue, slowed disease progression and attenuated loss
of pulmonary function. We are not aware of any drugs that
reduce the fibrotic process in lung disease or other organs.
Our goal for 2011 is to complete the preclinical toxicology
and other studies that will better enable us to determine
whether GRN510 is a candidate to take forward to an IND
application.

-- From Geron Annual Report 2010, Letter to Stockholders.

As most of you know, an IND is a request to the FDA for permission to start testing in human clinical trials (in the U.S). The few drugs that make it past all three phases of clinical trials the require FDA permission to sell.

Edited by unglued, 04 September 2011 - 09:26 PM.

[boylan]

Anthony - any news on the new astral fruit product?

I second the question...

[Age50less]

Brand new to site; have been reading all of this information for about 5 days now; whew! I want to get started on the Astragalus or Cycloastragenol but really don't know what products are legit or not. Anyone have any experience with the "McKenzie Protocol"?
TA-65 is way too pricey!

[Anthony_Loera]

Anthony - any news on the new astral fruit product?

My apologies, it is taking longer than expected, although we have made some real progress on some formulations that are not ready for prime time.

As soon as we have some data I can talk about, I will let you know.

A

[brainerd]

I wonder if it would be possible to increase the uptake of astragalus extract by embedding it in liposomes?

I seems to work well with curcumin and some other substances.

http://www.longecity...made-liposomes/

[JChief]

Anyone know of any economical sources for telomerase activators? (not TA-65 which is not economical nor available that I know of without entering into their protocol paid lab rat situation) To me these have the potential to put Resveratrol to shame with regards to extending lifespan.

Currently I take Astragalus standardized to 4% isoflavones at about a gram a day (though I have no idea how much astragalosides are in this I take it because it is cost effective) Also I take 500 mg of another product Natures Way standardized to 0.5% astragalosides. Alternatively you could get Gaia's product also standardized to 0.5% astragalosides. But both of these have so little astragalosides in them that in order to get 40-50 mg which I read somewhere was effective one would have to take a lot. There are also products standardized to 70% polysaccharides, which from what I have read would include some astragalosides. The whole issue is kind of muddy to me, any clarity would be appreciated.

Ron Teeguarden has a new supplement containing Astragaloside IV called which you can find here. Anyone tried it?

[Anthony_Loera]

I don't have to. The formula contains a telomerase inhibitor which likely cancels out ay telomerase benefits.

Why do people miss the obvious inhibitors? Geez.

Cheers
A

[maxwatt]

There are conflicting studies on whether resveratrol (present in small amounts in the Teeguarten formula) actually inhibits telomerase or not. Possibly it is concentration dependent. But I would not recommend a combination formula like that unless it is backed up by some solid studies.

[niner]

The Teeguarden pill has more resveratrol than astrogalosides, for what it's worth. I was tempted to edit out the link to his site above, but I decided to leave it, in the event that anyone would like an object lesson in the concept of RIPOFF.

[Suzudo]

I wish to indicate possible extensions and errors in my previous post

By "ephitelion" meant "ephitalon" http://www.ncbi.nlm....pubmed/12937682
Forgiveness

Resveratrol seems to activate SIRT1 also activates autophagy mechanisms of damaged proteins and organelles. Autophagy is also activated by verapamil.

Also resveratrol activates the noch channel that creates new neurons
This is interesting in relation to neuronal degeneration diseases, Alzheimer's, Parkinson's, etc..
http://www.cell.com/...8674(10)00674-4
For example
But the resveratrol little crosses the blood brain barrier.
Recent studies suggest that the brain-barrier can be opened by adenosine

http://www.eurekaler...u-btb091311.php


In the mixture of compounds for the formulations of the article would go well an inhibitor of myostatin. And helping the regeneration of lost muscle mass. Though I suppose it depends on the kind of life we ​​take each and diet and exercise

Estradiol is harmful in many ways even if telomerase activator. The Grapefruit (citrus paradisi, pommelo, pummelo) juice helps to maintain higher than normal levels of estradiol in the body.
The fact is that many seem to have collateral damage does not appear to compensate and not get the effect you want. But lithocholic acid and resveratrol have effects contrary to those harmful effects of estradiol. It also appears that resveratrol blocks the expression of ESR1 but increase their activity. As grapefruit juice helps to maintain high levels of estradiol prevented the removal of existing, may serve mixed with resveratrol and lithocholic acid

On the "vaccine / cure":
Although you can synthesize design substances against antibodies against own substances (myo-29 as against myostatin already been done successfully) working perfectly. And it seems you can indicate substances as adjuvants to antigens for the body to make antibodies themselve either with marker substances (vaccines are being tested) or plasmids improved system that is more promising. It happens that a healthy body does not create antibodies to the substances to which you are accustomed and that does not make antibodies against own. That's why the vaccine did not work against the HIV virus because they were known cold the rest. So, at first, seems impossible to make that system permanent modification

But there was a curious advance the fight against Alzheimer's. I mean the vaccine

EE-AD-SP1 tested in mice




Contains a new Immunogen andadjuvant that allows the creation of antibodies and proteins recognized by the immune system. Against Alzheimer's proteins in this case

Does anyone know who made it or how it works? Is it designed from the molecule you want to use as antigen or what types of molecules it work?

If you could choose from a list of own substances then we could get the proposed change

In the list of targets for antibody
SCH9
mdm2
Pinx1
Myostatin

Lack a clear targeted inhibitor of autophagy damaged proteins and damaged organelles.

There is an article on aging
http://www.geriatria...descargas/7.pdf

Focused on autophagy proteins and damaged organelles and repair of damaged tissues

To activate the autophagy of damaged proteins and organelles indicates a target that seems clear:

mTOR serine / kinase theronine

It appears that activation of SIRT1, resveratrol or rapamycin lower the amount of this molecule (mTOR) activating the mechanism of autophagy of damaged proteins and organelles.
And there is evidence that lower PI3K/Akt/mTOR mediated signaling increases longevity in mice significantly


Thus, and as long as they could have an adjuvant to make the immune system to create antibodies against own substances and using the trick of plasmids improved. The target list would be:

SCH9
mdm2
mTOR serine / kinase theronine
Pinx1
Myostatin


And to make it perfect would be required to include in it a clear and resounding inhibitor of the differentiation of tissues, inhibitorof restoration and creation of members and others. But if any mammalian

In my previous post I commented extramolecular matrix powder from pig gallbladder as a trigger mechanism

By

http://www.geriatria...descargas/7.pdf

The set of Wnt glycoproteins which would activate the regeneration of tissue differentiation during embryonic development play an important role in cell proliferation, differentiation, orientation, adhesion, survival and
apoptosis (Li et al., 2006, Patapoutian and Reichardt, 2000).
In adults, the Wnt pathway has been linked to processes of tissue homeostasis or balance (MacDonald et al., 2009).
Activation of Wnt canonical pathway positively regulates the maintenance of adult stem cells, adult neurogenesis (Lie et al., 2005), hair regeneration (Ito
et al., 2009) and bone in adult mice

The fact is that activation of Wnt extends life like that sometimes life shortened in other cases. Which makes sense, if by creating new tissue lost many copies of telomeres in cells.
This would imply that could include an activator of Wnt in the above formulations or this activator keep apart until they are quite elongated telomeres in case of its age

If there is a clear inhibitor for Wnt body's own, putting the final target inhibitor. Complete the list of targets against which to raise antibodies, achieving the perfect and complete formulation

Not is good to have antibodies against PinX1 (inhibitor of telomerase itself) without possessing antibodies to mdm2 (own inhibitor of TP53) since it can trigger cancerous tumors as genetic manipulation experiments showed Maria Blasco

And it would be nice to have antibodies against an endogenous inhibitor of Wnt without possessing antibodies for PinX1

This suggests that perhaps should be done in several steps

So the target list for immunization by injection enhanced of plasmids by compressed air and electrical stimulation, is


Antigen - adjuvant promoter of antibody for body's own substances already known to exist and that there may be one of the experimental vaccine similar in EE-AD-SP1. Lack of information by if someone has

SCH9
mdm2
mTOR serine / kinase theronine
Pinx1
Myostatin

Wnt glycoproteins Inhibitor unknown

(Care that the target would be the inhibitor. The glycoproteins-Wnt should enlarge)

Shilima khemen

[Suzudo]

http://tesis.com.es/...guladora-senal/

http://jcs.biologist...1/1793.full.pdf

Uff

[boylan]

Anthony,

Is RevGen still going to be offering their own telomerase activator? I notice that you are offering TA-65 for $220.

[hamishm00]

C'mon dude, read the same page on the revgenetics website where it is selling the TA-65 - I thought it was pretty clear. Also, Anthony has already responded to this question on this page (i.e. see above).

[missminni]

Sorry to be the bearer of bad news, but I just met a veterinarian who is treating my dogs with prolotherapy.
She's 61 years old, in great shape physically, looks much younger, and is very conscious of diet and health
with no history of cancer.

She did the TA65 program with a doctor who is involved in the program that TA Sciences promotes and ended
up with cervical cancer and had to have a hysterectomy at 59 yrs old and post menopause.

Of course she totally attributes it to the TA65. She is so angry that it's not being reported.
Since this obviously is going to be considered anecdotal who knows how many other cases
are going unreported, I want to post it here so those interested can make an informed decision.
It certainly has halted my enthusiasm for it.

holy cow...I just checked and saw that revgenetics is now selling TA Sciences product.
They also offered their product to Harlan, the pharmacy that compounds LivLong.
I guess they are trying to unload the product because there have been some
very suspicious side effects they are neglecting to report, as with the lady I mentioned above.
Beware. This is really unethical.

Edited by missminni, 30 September 2011 - 04:33 PM.

[johnross47]

Obviously it is anecdotal. What we would all like to know (I assume) is whether the incidence of cancers in the TA65 using population (and the Astral Fruit using population too) is higher than for a matched sample of the general population. As an Astral Fruit user nearly 65 years old I have a definite interest in the answer.

[missminni]

Obviously it is anecdotal. What we would all like to know (I assume) is whether the incidence of cancers in the TA65 using population (and the Astral Fruit using population too) is higher than for a matched sample of the general population. As an Astral Fruit user nearly 65 years old I have a definite interest in the answer.

That will be difficult to do if TA Sciences is not reporting the incidences.