13 replies to this topic

[Never_Ending]

I'm interested in seeing what people's views are on this poll. In my view I consider telomere length and telomerase to be necessary but not sufficient. I believe that if the length runs out deterioration will happen but if it does not run out there's still other factors contributing to the aging process.

 

Also there is the concern that telomerase activation in high levels might trigger other issues, perhaps.

 

How much are we able to really elevate telomerase safely in the body? I assume we can't keep raising the dose of things like astragalosides until it starts reversing telomere length, or is it possible.

 

If there are counterproductive effects of high doses of telomerase activators is there a way to separate the wanted effects from the unwanted?

 

Just some questions to consider and hopefully trigger some good discussion.

Edited by Never_Ending, 16 August 2016 - 01:05 PM.

[PeaceAndProsperity]

Why can't I quote OP posts anymore?

 

 

 I assume we can't keep raising the dose of things like astragalosides until it starts reversing telomere length,

What do you mean by this, does it really have the possibility of reducing telomerase activity or shortening telomeres?

[Never_Ending]

Why can't I quote OP posts anymore?

 

 

 I assume we can't keep raising the dose of things like astragalosides until it starts reversing telomere length,

What do you mean by this, does it really have the possibility of reducing telomerase activity or shortening telomeres?

 

Oh that's a misunderstanding,   I mean reversing(the length) from the typical way that the length moves(getting shorter). So reversing in length meaning that it helps lengthen. Reversal(make longer instead of shorter) would require a larger dose (a small dose would slow down the shortening).

 

My concern was about Potential unforeseen effects of larger doses.

Edited by Never_Ending, 17 August 2016 - 12:48 PM.

[Graviton]

At least, some studies(although they were funded by vendors) suggest that cycloastragenol increases telomerase activity in vitro.

As I think, telomere lengthening and increasing telomerase activity is/are important for both health span and life span, but solely increasing telomere length/ telomerase activity would not give a significant effect on either health span or life span. There should be some other factors necessarily(or required to be) improved or modified to shed light on telomere/telomerase life span effects . About 90% of cancer cells use telomerase for extending their telomere length while other cells go through different process for their continuous divisions. Somehow, those processes lengthen their telomeres, but it seems that they affect other molecular/genetic factors too. In this context, telomere lengthening/ telomerase activity appears to be necessary condition for life-extension, but not sufficient condition to treat, cure, or anything like that.

Edited by Graviton, 21 August 2016 - 06:25 AM.

[Never_Ending]

To me the fact that cancer cells use telomerase seems not too much of an issue. Cancer cells can potentially use anything at the availability of cells. It seems that telomeres are a limiting factor for life but as for other potential limiting factors, they have to be explored more.

[SearchHorizon]

To me the fact that cancer cells use telomerase seems not too much of an issue. Cancer cells can potentially use anything at the availability of cells. It seems that telomeres are a limiting factor for life but as for other potential limiting factors, they have to be explored more.

 

You are probably familiar with parabiosis. That not only tells you there is an aging signal in plasma, but also that it particular tissues are sending the age signals. If telomerase is expressed as a function of those signals, then we probably should look for the tissues sending those signals in the first place. And it is in those tissues that we need to evaluate the effects of telomerase.

[Never_Ending]

 

 

 

You are probably familiar with parabiosis. That not only tells you there is an aging signal in plasma, but also that it particular tissues are sending the age signals. If telomerase is expressed as a function of those signals, then we probably should look for the tissues sending those signals in the first place. And it is in those tissues that we need to evaluate the effects of telomerase.

 

Regarding parabiosis, I think we need to consider the many potential meanings of what it shows us, because it can be a bit misleading. When blood is connected it's very possible that  some vital resource(that young mouse's blood has more of) comes alongside signal.

If we focus on the signal end of things then we can try to discover similar substances maybe supplements that can activate those signals. Have they found any notable ones? (aside from telomerase aspects)

Edited by Never_Ending, 12 March 2017 - 01:51 PM.

[MikeDC]

Telemere length and telemerase activity are determined by longevity gene expressions such as sirt1. Decreasing NAD+ is a major cause of accelerated aging and age related diseases.
Supplementing NAD+ with Niagen will slow down aging, prevent age related diseases, and increase telemere length as well. We have been looking for something in our body that dicrease as we age and we turn younger if we supplement. We finally found the first one, NAD+.

[GreenPower]

I am still looking for studies showing any kind of substance increase the length of telomeres in vivo in otherwise healthy people. The ones I've seen have either lacked the necessary amount of test subjects, used test subjects with some kind of disease, drawn strange conclusions from studies where necessary data hasn't been properly presented or other stuff which makes it impossible to draw any kind of conclusions. If making claims to the contrary, please present us with the studies supporting these claims.

 

As a side note, there are anecdotes that some substances could actually shorten the mean telomere lengths rather than increase it. Examples are the tests that I and Anthony Loera did with Astragaloside IV a few years ago. You might therefore want to take some precautions with which substances you include in your regimen. The Astragalus plant also have a tendency to accumulate unwanted metals like Iron, Arsenic and Mercury, so you would want your supplier to test for these substances before you buy their products.

 

As for now my personal hypothesis is that Cycloastragenol might have a weak positive effect if taken for a long time on some types of immune cells, but no - I don't have any actual evidence for these claims other than personal n=1 studies.

 

 

[Never_Ending]

I am still looking for studies showing any kind of substance increase the length of telomeres in vivo in otherwise healthy people. The ones I've seen have either lacked the necessary amount of test subjects, used test subjects with some kind of disease, drawn strange conclusions from studies where necessary data hasn't been properly presented or other stuff which makes it impossible to draw any kind of conclusions. If making claims to the contrary, please present us with the studies supporting these claims.

 

As a side note, there are anecdotes that some substances could actually shorten the mean telomere lengths rather than increase it. Examples are the tests that I and Anthony Loera did with Astragaloside IV a few years ago. You might therefore want to take some precautions with which substances you include in your regimen. The Astragalus plant also have a tendency to accumulate unwanted metals like Iron, Arsenic and Mercury, so you would want your supplier to test for these substances before you buy their products.

 

As for now my personal hypothesis is that Cycloastragenol might have a weak positive effect if taken for a long time on some types of immune cells, but no - I don't have any actual evidence for these claims other than personal n=1 studies.

 

Well it's agreed we cannot take any studies at face value.

 

How many test subjects did you have in your tests? It's only consistent if we take the same skeptical stance regarding negative effects in the same way we take the positive ones. Even though you presented it with words such as "could" or "tendency", yet those are nonetheless still claims.
 

Edited by Never_Ending, 18 March 2017 - 12:25 AM.

[SearchHorizon]

Regarding parabiosis, I think we need to consider the many potential meanings of what it shows us, because it can be a bit misleading. When blood is connected it's very possible that  some vital resource(that young mouse's blood has more of) comes alongside signal.

 

 

If we focus on the signal end of things then we can try to discover similar substances maybe supplements that can activate those signals. Have they found any notable ones? (aside from telomerase aspects)

 

 

Isolating the signal is difficult, because there are so many things in plasma.

 

(1) With respect to parabiosis experiments, I'd like to note one biological event that reminds me of it: reproduction. I have heard of cases in which an older woman that bears a first child and gives birth appears to get younger. If the fetus and the mother share some bodily fluid, then the parabiosis experiment would explain the phenomenon.

 

(2) I'd like to return to the idea of tissue of specificity in our body's inability to "renew." The idea is that, in our body, some cells age due to downstream effects from other cells that generate aging signal (by either lack of some biochemical or by its presence).  I am saying that this is suggested at by the parabiosis experiment. This concept is also hinted at through experiments involving head transplants. 

 

(3) If such un-renewable cells exist, then it is natural to ask if telomerase could "renew" them. I think experiments tend to support the notion that there are cells that telomerase cannot help divide. If telomerase were the KEY to aging, we probably should have been able to extend the lifespan of mice multifold through manipulation of telomerase. This has not been the case.

Edited by SearchHorizon, 20 March 2017 - 07:25 AM.

[Never_Ending]

 

(1) With respect to parabiosis experiments, I'd like to note one biological event that reminds me of it: reproduction. I have heard of cases in which an older woman that bears a first child and gives birth appears to get younger. If the fetus and the mother share some bodily fluid, then the parabiosis experiment would explain the phenomenon.

 

(2) I'd like to return to the idea of tissue of specificity in our body's inability to "renew." The idea is that, in our body, some cells age due to downstream effects from other cells that generate aging signal (by either lack of some biochemical or by its presence).  I am saying that this is suggested at by the parabiosis experiment. This concept is also hinted at through experiments involving head transplants. 

 

(3) If such un-renewable cells exist, then it is natural to ask if telomerase could "renew" them. I think experiments tend to support the notion that there are cells that telomerase cannot help divide. If telomerase were the KEY to aging, we probably should have been able to extend the lifespan of mice multifold through manipulation of telomerase. This has not been the case.

 

 

Regarding   1)  I don't believe it's the same concept because usually the flow of substance is really just from mother to the offspring rather than both ways. This is quite similar to certain microorganisms where the new budding  has low damage because it doesn't get the damaged parts of the parent.

 

3) It's unclear to talk about  "key" to aging because come things are crucial but they are not enough on their own. So even if one thing itself cannot make lifespan multifold , it can still be a crucial part.
 

Edited by Never_Ending, 25 March 2017 - 07:43 PM.

[HaplogroupW]

Regarding   1)  I don't believe it's the same concept because usually the flow of substance is really just from mother to the offspring rather than both ways.

 

I think Amy Wagers' parabiosis experiment did not connect their circulatory systems; rather merely skin. It seems doubtful to me that we can be certain that that connection is any more or less unidirectional than that of a mother and foetus.
 

[hav]

Don't think the last poll question has enough choices. My personal opinion is that increasing or maintaining telomere length probably increases both quality of life and lifespan but that the lifespan effect is somewhat smaller.  I recall the death rate/telomere-length plots I've seen in studies showing a lower rate with a flatter curve in earlier years as length is maintained with a steeper and faster fall off towards the end pushing the life-span averages up a bit overall.  Suggesting a better quality of life over a longer period and perhaps a delayed but quicker demise.

 

Howard