89 replies to this topic

[Never_Ending]

Hello, many are familiar with the fact that there's two major theories of aging which is..

 

1. That there is an evolutionarily adaptive "death program(s)" that somehow determines the optimum lifespan of an organism and due to selective pressures that has developed over our evolutionary history.  (Suggested by people such as August Weismann)

 

2. That it is caused by slow wear and tear of internal and external usage of  human's bodies. And that our own bodies tries to compensate and export the damage but it isn't enough on its own (Like the view held by SENS and Aubrey De Grey)

 

 

However I concluded upon this possibility (that converges upon both the theories):

 

That after reaching a certain adult age the "wear and tear" process could simply be a passive mechanism in which evolution exerts it's selective pressures (specifically upon sexually reproducing species) (And passive because the body no longer implements the robust repair mechanisms to the same extent as it once did)

 

Since these selective pressures are mild (but possibly existent) in sexually reproductive organisms,  and likely negligible in asexual organisms. This also explains why the asexual organisms show much less if not negligible senescence.   An example being:  http://www.devbio.bi...du/?page_id=491

 

Since the forces towards decay and degeneration are ever present in organisms,   seems unlikely evolution would use an ACTIVE program to limit the lifespan. Why "invest" in such an active program if all it needs to do is only ensure the body's repair mechanisms robustness to a certain point but less and less after that point. (which naturally leads to decay and faltering of the body) (despite being passive it's still an adaptation because evolutionarily it's purposeful neglect)

 

Although this is a different Theory , the way to treat or reverse aging would be a very similar approach as that of SENS and other maintenance approaches.

 

However this Theory does address why asexual organisms with less selective pressures on lifespan(debatable) such as the Hydra show presumably negligible senescence.  And also it doesn't conflict with the logic behind the evolutionary adaptation theory.

 

What do others think about this? Any feedback is appreciated.

Edited by Never_Ending, 12 January 2016 - 05:36 PM.

[corb]

I really don't have anything to say beside that it is a good simple argument.

[Antonio2014]

That after reaching a certain adult age the "wear and tear" process could simply be a passive mechanism in which evolution exerts it's selective pressures (specifically upon sexually reproducing species) (And passive because the body no longer implements the robust repair mechanisms to the same extent as it once did)

 

I don't understand what you are trying to say.

 

Since these selective pressures are mild (but possibly existent) in sexually reproductive organisms,  and likely negligible in asexual organisms.

 

It's just the opposite. For asexual organisms in which progenitor and child are more or less equal (the same size, for example, instead of reproducing by budding), selective presure for damage repair mechanisms is always strong, and these organisms often show negligible senescence, whereas for sexual organisms like us, selective presure for damage repair mechanisms is strong in youth, weakens after the first breeding and becomes weaker and weaker after that. In this case, only the germ line shows immortality, and the somatic part of the organism ages (disposable soma theory).

[Never_Ending]

 

That after reaching a certain adult age the "wear and tear" process could simply be a passive mechanism in which evolution exerts it's selective pressures (specifically upon sexually reproducing species) (And passive because the body no longer implements the robust repair mechanisms to the same extent as it once did)

 

I don't understand what you are trying to say.

 

 

Since these selective pressures are mild (but possibly existent) in sexually reproductive organisms,  and likely negligible in asexual organisms.

 

It's just the opposite. For asexual organisms in which progenitor and child are more or less equal (the same size, for example, instead of reproducing by budding), selective presure for damage repair mechanisms is always strong, and these organisms often show negligible senescence, whereas for sexual organisms like us, selective presure for damage repair mechanisms is strong in youth, weakens after the first breeding and becomes weaker and weaker after that. In this case, only the germ line shows immortality, and the somatic part of the organism ages (disposable soma theory).

 

 

It's not the opposite you simply miss-understood what I meant. I mean't the selective pressure on limiting lifespan.  You are referring to the selective pressure to survive onwards. So what you say is true , what we said are basically two halves of the same coin

 

Edited by Never_Ending, 13 January 2016 - 04:05 AM.

[Kalliste]

Aging is probably a mix of different things. The best way to attack it is the engineering approach that Aubrey defends.

[Antonio2014]

It's not the opposite you simply miss-understood what I meant. I mean't the selective pressure on limiting lifespan.

 

Ah, ok, I misunderstood you.

 

Any evidence that such a pressure exists? What adaptive advantage can an organism have by dying younger?

[Rocket]

I have always thought that is what aging (mostly) is: not an active program to kill the organism, but rather a "turning off" of the program that builds and maintains the body, at which point chemistry takes over and does the rest.  That's why the anecdotal results of anti-aging when people manually turn on what the programming turned off as with HRT (test and growth), telomerase, and now apparently GDF11 may be important.

 

I also think the build and maintain program is only active through the early 20s because when humans were developing, they mostly simply dropped dead not soon thereafter their early 20s.  There was no adaptive reason keep things going when the organism was simply going to drop dead from a virus or infection. 

[Never_Ending]

It's likely true that the build and maintain program you mention starts tapering of after the 20s or 30s. And since it starts to taper the wear and tear becomes more and more evident. If there's very minor wear and tear then the result of the failing repair mechanisms are less obvious and the effects of aging are less pronounced.

[Never_Ending]

 

It's not the opposite you simply miss-understood what I meant. I mean't the selective pressure on limiting lifespan.

 

Ah, ok, I misunderstood you.

 

Any evidence that such a pressure exists? What adaptive advantage can an organism have by dying younger?

 

 

Well that's the point that has been controversial as whether or not it exists there have been reputable scientists on both sides of the fence.  The advantage isn't from dying younger it's a potential(unsure) advantage regarding generation turnover among sexually reproductive organisms , since the major advantage of sexual vs asexual is the change and diversity between generations that makes it flexible to environmental obstacles.     I said potential  advantage because I'm still on the fence about it and we have to keep in mind that even if such an adaptive thing exists it is a very very mild pressure and likely passive.

 

Maintenance would likely still be a primary approach for aging intervention

Edited by Never_Ending, 14 January 2016 - 05:12 PM.

[Antonio2014]

But where is the proof? There is good evidence of the failing-of-maintenance approach, and evolutive arguments to explain its existence. Where are the ones for the death-advantage approach?

 

As for the change of generations, in most sexual species, the parents force their children to live alone and far away from them when they can take care of themselves. So parents and children don't compete as adults. There is no need that the parents die young. The same can be said for most vegetables and fungi: their seeds or gametes are transported far away by the wind, insects, etc.

Edited by Antonio2014, 15 January 2016 - 09:39 AM.

[niner]

The "death program" hypothesis doesn't agree with what we actually observe in nature.  Animals that experience a lot of predation die young.  Animals that are safe from predation, like birds, bats, whales, clams, etc have unusually long lifespans for their size.  Why doesn't nature create a "death program" for them?  What's actually happening is that evolution has given better repair systems to the animals that can actually benefit from them, while there's not much point in good repair systems for insects and mice.  There is simply no need for a death program when animals die so often from predation and infection.  This "death program" idea might have occurred to a 19th century evolutionary biologist, but we've learned a lot in the intervening century+.   There is a belief afoot that if aging is programmed, then it will be simple to "reprogram" it, but if aging is due to accumulated damage, it will be impossible to fix.  Consequently, if you support programmed aging, then you are a positive thinker who supports ending aging, while if you support damage theory, then you are a deathist stick-in-the-mud.  Of course, since the premises are wrong, the conclusion is as well.   There are various kinds of paracrine signals, like hormones or GDF11, that have an appearance of "programming" to them.  Perhaps they are part of a developmental program that never quite shuts off, or more likely are an evolved defense against neoplasm, but their existence is not evidence for an evolved "death program".  Telomeres shorten with each cell division, and from oxidative damage, but these are a defense against cancer and form of damage, respectively, not an evolved death program.   We should definitely look at restoring paracrine signals to more youthful levels and repairing short telomeres, but I think that the idea of an evolved death program is an unhelpful distraction.

[Never_Ending]

The "death program" hypothesis doesn't agree with what we actually observe in nature.  Animals that experience a lot of predation die young.  Animals that are safe from predation, like birds, bats, whales, clams, etc have unusually long lifespans for their size.  Why doesn't nature create a "death program" for them?  What's actually happening is that evolution has given better repair systems to the animals that can actually benefit from them, while there's not much point in good repair systems for insects and mice.  There is simply no need for a death program when animals die so often from predation and infection.  This "death program" idea might have occurred to a 19th century evolutionary biologist, but we've learned a lot in the intervening century+.   There is a belief afoot that if aging is programmed, then it will be simple to "reprogram" it, but if aging is due to accumulated damage, it will be impossible to fix.  Consequently, if you support programmed aging, then you are a positive thinker who supports ending aging, while if you support damage theory, then you are a deathist stick-in-the-mud.  Of course, since the premises are wrong, the conclusion is as well.   There are various kinds of paracrine signals, like hormones or GDF11, that have an appearance of "programming" to them.  Perhaps they are part of a developmental program that never quite shuts off, or more likely are an evolved defense against neoplasm, but their existence is not evidence for an evolved "death program".  Telomeres shorten with each cell division, and from oxidative damage, but these are a defense against cancer and form of damage, respectively, not an evolved death program.   We should definitely look at restoring paracrine signals to more youthful levels and repairing short telomeres, but I think that the idea of an evolved death program is an unhelpful distraction.

 

Right I mostly hold the view that it's a matter of repair and maintenance. However although it's true animals get eaten and destroyed far more often than would deem necessary for any death mechanism, as long as some percentage survive the destructive forces... even such a case over countless years would be enough for any restrictive selective pressures to take place. Also humans(sexually reproductive) already have telomerase active in our germ cells(which basically don't age) it's actually turned off in soma cells by a blocker...  The hydra family(asexual) exemplified by the immortal jelly fish can activate telomerase without the blockage.  

If it was merely a race for survival by all means the pressure would be massive for an organism to leave telomerase active in all areas once such a valuable pathway is present.  (even after whichever percentage of them are eaten or destroyed by other means)

The "death program" theories are needless to say a big blunder. But the potential for the existence of Passive pressures that draw upon that concept could be there. If there were passive forces these could be relatively easy to overcome through various ways of signaling

Also repair and maintenance would still be the major approach

Edited by Never_Ending, 16 January 2016 - 09:59 PM.

[Antonio2014]

If it was merely a race for survival by all means the pressure would be massive for an organism to leave telomerase active in all areas once such a valuable pathway is present.

 

Nope. Telomerase is inactive in most human cells for good reasons: to prevent cancer. Hydras don't inactivate it because basically all their cells are stem cells. If you cut a hydra into pieces, each piece grows to form a full hydra. With our big number of cells and long lifespan, having all our cells being stem cells would kill us by cancer too soon.
 

[Never_Ending]

 

Nope. Telomerase is inactive in most human cells for good reasons: to prevent cancer.

 

 

Such decisiveness yet completely false......that belief is referring back to when they first discovered telomerase and saw that cancer cells express it to promote their never ending division. As of now there's more support that short telomeres promote cancer (in line with the fact that age is the biggest factor for cancer).  In light of the current understanding what you said is akin to saying putting on bandages will cause cuts.  Also I mentioned the sex/germ cells expressing telomerase shouldn't they be getting more cancer? And the telomerase studies on mice all extend their life, as a net result, even if we took a step back and took your claim as a given the net effect still won out, and no apparent mention of tumorgenesis.

 

http://www.nature.co...s.2010.635.html

 

Read the part where it says cancer link, that sufficiently addresses the concern

Edited by Never_Ending, 17 January 2016 - 03:11 AM.

[niner]

 

Nope. Telomerase is inactive in most human cells for good reasons: to prevent cancer.

 

No this belief is referring back to when they first discovered telomerase and saw that cancer cells express it to promote their never ending division. As of now there's more support that short telomeres promote cancer (in line with the fact that age is the biggest factor for cancer).  In light of the current understanding what you said is akin to saying putting on bandages will cause cuts.  Also I mentioned the sex/germ cells expressing telomerase shouldn't they be getting more cancer? And the telomerase studies on mice all extend their life, as a net result, even if we took a step back and took your claim as a given the net effect still won out, and no apparent mention of tumorgenesis.

 

But the cancer that we see is what has escaped the telomere limit, either through a mutation that makes telomerase constitutively active or through alternative telomere lengthening.  If it weren't for the limit imposed by telomeres, I think you'd see a lot more cancer, and you'd see it earlier in life, perhaps a lot earlier.

[Never_Ending]

 

But the cancer that we see is what has escaped the telomere limit, either through a mutation that makes telomerase constitutively active or through alternative telomere lengthening.  If it weren't for the limit imposed by telomeres, I think you'd see a lot more cancer, and you'd see it earlier in life, perhaps a lot earlier.

 

Here can you please clarify "the limit" ie the limit of lengthening or the short telomere limit? I just want to make sure I don't missunderstand.

[Antonio2014]

It's not clear that short telomeres promote cancer. Short telomeres are correlated with aging, and aging is correlated with cancer. Correlation doesn't imply causation. Anyway, even if short telomeres promote cancer, that doesn't contradict the fact that always-enlarging telomeres also promote cancer, and even more, cancerous cells absolutly need to enlarge their telomeres. A precancerous cell absolutly needs to mutate its telomerase controlling machinery. If you switch telomerase always on, the cell has one step less in the way to becoming cancerous. And, for abnormally short telomeres, the human body has already two responses: apoptosis and senescence.

 

Yes, germ/stem cells are prone to cancer, but they are too few compared to the rest of cells, so cancer risk is somewhat compensated.

 

As for telomerase as a rejuvenation therapy, it's unclear whether it extends lifespan in mice, and it probably reduces lifespan in humans. See: http://www.sens.org/...ate-life-launch
 

Edited by Antonio2014, 17 January 2016 - 09:33 AM.

[Never_Ending]

It's not clear that short telomeres promote cancer. Short telomeres are correlated with aging, and aging is correlated with cancer. Correlation doesn't imply causation. Anyway, even if short telomeres promote cancer, that doesn't contradict the fact that always-enlarging telomeres also promote cancer, and even more, cancerous cells absolutly need to enlarge their telomeres. A precancerous cell absolutly needs to mutate its telomerase controlling machinery. If you switch telomerase always on, the cell has one step less in the way to becoming cancerous. And, for abnormally short telomeres, the human body has already two responses: apoptosis and senescence.

 

Yes, germ/stem cells are prone to cancer, but they are too few compared to the rest of cells, so cancer risk is somewhat compensated.

 

As for telomerase as a rejuvenation therapy, it's unclear whether it extends lifespan in mice, and it probably reduces lifespan in humans. See: http://www.sens.org/...ate-life-launch
 

 

You quoting SENS is akin to me quoting someone that supports telomere activation (Since Aubrey De Grey view is against it).....Thats why I quoted from nature , make sense? Aubrey De Grey's   whole perspective is to stop cancer at all costs(and then worry about the consequences) and obviously blocking telomerase would help block the spread of cancer.

  Its reasonably clear it promotes lifespan in mice, and the mechanism that people think it to reduce lifespan in humans is due to a misunderstood correlation/causation relationship that started from the beginning of telomerase discovery.

[Antonio2014]

You quoting SENS is akin to me quoting someone that supports telomere activation (Since Aubrey De Grey view is against it).....Thats why I quoted from nature , make sense? Aubrey De Grey's   whole perspective is to stop cancer at all costs(and then worry about the consequences) and obviously blocking telomerase would help block the spread of cancer.

  Its reasonably clear it promotes lifespan in mice, and the mechanism that people think it to reduce lifespan in humans is due to a misunderstood correlation/causation relationship that started from the beginning of telomerase discovery.

 

Wow, I didn't expect an ad hominem from you.

 

Nothing to discuss, then.

Edited by Antonio2014, 17 January 2016 - 04:33 PM.

[Never_Ending]

 

You quoting SENS is akin to me quoting someone that supports telomere activation (Since Aubrey De Grey view is against it).....Thats why I quoted from nature , make sense? Aubrey De Grey's   whole perspective is to stop cancer at all costs(and then worry about the consequences) and obviously blocking telomerase would help block the spread of cancer.

  Its reasonably clear it promotes lifespan in mice, and the mechanism that people think it to reduce lifespan in humans is due to a misunderstood correlation/causation relationship that started from the beginning of telomerase discovery.

 

Wow, I didn't expect an ad hominem from you.

 

Nothing to discuss, then.

 

 

And where is the ad hominem ? Not sure what you're referring to, as all I did was point out that if you quote from a source like that I would have to quote from someone that supports telomerase for it to be a fair debate.  That's why I purposely chose to quote from nature. How is that an ad hominem attack, seriously?    If you're going to accuse me of things like that I don't think it would be a productive discussion anyways.

Edited by Never_Ending, 17 January 2016 - 07:44 PM.

[niner]

 

But the cancer that we see is what has escaped the telomere limit, either through a mutation that makes telomerase constitutively active or through alternative telomere lengthening.  If it weren't for the limit imposed by telomeres, I think you'd see a lot more cancer, and you'd see it earlier in life, perhaps a lot earlier.

 

Here can you please clarify "the limit" ie the limit of lengthening or the short telomere limit? I just want to make sure I don't missunderstand.

 

The Hayflick Limit.
 

[Never_Ending]

 

 

But the cancer that we see is what has escaped the telomere limit, either through a mutation that makes telomerase constitutively active or through alternative telomere lengthening.  If it weren't for the limit imposed by telomeres, I think you'd see a lot more cancer, and you'd see it earlier in life, perhaps a lot earlier.

 

Here can you please clarify "the limit" ie the limit of lengthening or the short telomere limit? I just want to make sure I don't missunderstand.

 

The Hayflick Limit.
 

 

 

The thing is cancerous cells are not normal cells, even if we turned off telomerase in cancerous cells it looks different from a normal cell and it IS different from a normal cell. The emphasis should be to not get normal cells turning cancerous. It's not as if a healthy human is getting cancerous cells left and right and the Hayflick limit being the only limiting factor. People shouldn't have cancerous cells at all.   And if other cells were already expressing telomerase there's no indication that it would promote cancerous cells to form.

 

If we took your viewpoint as a given(for discussion purposes) now there's 2 forces.  1 is telomerase and cancer the other is telomerase and the limit on lifespan. Since telomerase acts as a wall (hayflick limit) for our max lifespan these 2 forces are different types. 1 is where some might survive past the 125 mark onwards and manage to avoid cancer while some might be triggered to have cancer (uncertain). 2 is where despite some unknown amount of cancer resistance All will die before the 125 mark or around it.

 

For any hope of unlimited lifespans they likely should take the 2nd evil and work with it because the 2nd one opens up the wall at the ~125 mark

Edited by Never_Ending, 18 January 2016 - 12:09 AM.

[HighDesertWizard]

I find it useful to reference studies whenever possible... And to talk about Telomerase and Cancer without reference to NF-kB is a useless discussion...

 

Telomerase directly regulates NF-B-dependent transcription

 

Although elongation of telomeres is thought to be the prime function of reactivated telomerase in cancers, this activity alone does not account for all of the properties that telomerase reactivation attributes to human cancer cells. Here, we uncover a link between telomerase and NF-κB, a master regulator of inflammation. We observe that while blocking NF-κB signalling can inhibit effects of telomerase overexpression on processes relevant to transformation, increasing NF-κB activity can functionally substitute for reduced telomerase activity. Telomerase directly regulates NF-κB-dependent gene expression by binding to the NF-κB p65 subunit and recruitment to a subset of NF-κB promoters such as those of IL-6 and TNF-α, cytokines that are critical for inflammation and cancer progression. As NF-κB can transcriptionally upregulate telomerase levels, our findings suggest that a feed-forward regulation between them could be the key mechanistic basis for the coexistence of chronic inflammation and sustained telomerase activity in human cancers.

 

I got a copy of the full text PDF of this study by requesting it at ResearchGate.net... Here's Figure 7 from the study illustrating the authors' conception of the feed-forward loop. Both the abstract and the graphic figure make the point... To talk about Telomerase and Cancer without bringing NF-kB into the discussion is useless...

 

NF-kB inhibition is what makes for the difference vis-a-vis cancer prevention... See the survival curves here...

 

 

Edited by HighDesertWizard, 18 January 2016 - 12:39 AM.

[HighDesertWizard]

The NF-kB p50 and p65 Subunits become transformed within the nucleus into becoming a part of the Telomerase HoloEnzyme...

 

The graphic figure below shows another view of the feed forward loop reference in the last post. The graphic figure below is from Noncanonical Functions of Telomerase: Implications in Telomerase-Targeted Cancer Therapies

 

Edited by HighDesertWizard, 18 January 2016 - 12:42 AM.

[Rocket]

If it was merely a race for survival by all means the pressure would be massive for an organism to leave telomerase active in all areas once such a valuable pathway is present.

Nope. Telomerase is inactive in most human cells for good reasons: to prevent cancer. Hydras don't inactivate it because basically all their cells are stem cells. If you cut a hydra into pieces, each piece grows to form a full hydra. With our big number of cells and long lifespan, having all our cells being stem cells would kill us by cancer too soon.

Huh!?!?!? Not so!!!!!!!

Oh I forgot, cancer expresses telomerase and therefore telomerase causes cancer. How silly of me to forget that.

[niner]

 

 

 

But the cancer that we see is what has escaped the telomere limit, either through a mutation that makes telomerase constitutively active or through alternative telomere lengthening.  If it weren't for the limit imposed by telomeres, I think you'd see a lot more cancer, and you'd see it earlier in life, perhaps a lot earlier.

 

Here can you please clarify "the limit" ie the limit of lengthening or the short telomere limit? I just want to make sure I don't missunderstand.

 

The Hayflick Limit.

 

The thing is cancerous cells are not normal cells, even if we turned off telomerase in cancerous cells it looks different from a normal cell and it IS different from a normal cell. The emphasis should be to not get normal cells turning cancerous. It's not as if a healthy human is getting cancerous cells left and right and the Hayflick limit being the only limiting factor. People shouldn't have cancerous cells at all.   And if other cells were already expressing telomerase there's no indication that it would promote cancerous cells to form.

 

If we took your viewpoint as a given(for discussion purposes) now there's 2 forces.  1 is telomerase and cancer the other is telomerase and the limit on lifespan. Since telomerase acts as a wall (hayflick limit) for our max lifespan these 2 forces are different types. 1 is where some might survive past the 125 mark onwards and manage to avoid cancer while some might be triggered to have cancer (uncertain). 2 is where despite some unknown amount of cancer resistance All will die before the 125 mark or around it.

 

For any hope of unlimited lifespans they likely should take the 2nd evil and work with it because the 2nd one opens up the wall at the ~125 mark

 

Actually, healthy humans might get more cancerous cells than you'd think, but they are stopped by the immune system and/or the Hayflick Limit.  When mechanisms such as these fail, that's when you get a clinically relevant tumor.  I don't think that it's a given that the Hayflick Limit plays a big role in our maximum lifespan.  Most healthy cells don't divide all that often.  We have seen from Maria Blasco's lab that expressing extra telomerase in mice is good for a 13% increase in lifespan when started in old age, and 24% when started at one year.  This suggests that it's doing something good in a mammal, but I don't think we can extrapolate from these relatively small increases in lifespan to say that humans will live beyond 125.  Even though these mice lived somewhat longer, there are still other factors that are killing them, and there are a lot of other non telomere-related things that kill humans.  (like systemic amyloidosis, for example)  It's worth noting that it's pretty easy to increase the lifespan of short-lived species, but harder to increase the lifespan of long-lived species like us.

[Antonio2014]

 

 

You quoting SENS is akin to me quoting someone that supports telomere activation (Since Aubrey De Grey view is against it).....Thats why I quoted from nature , make sense? Aubrey De Grey's   whole perspective is to stop cancer at all costs(and then worry about the consequences) and obviously blocking telomerase would help block the spread of cancer.

  Its reasonably clear it promotes lifespan in mice, and the mechanism that people think it to reduce lifespan in humans is due to a misunderstood correlation/causation relationship that started from the beginning of telomerase discovery.

 

Wow, I didn't expect an ad hominem from you.

 

Nothing to discuss, then.

 

 

And where is the ad hominem ? Not sure what you're referring to, as all I did was point out that if you quote from a source like that I would have to quote from someone that supports telomerase for it to be a fair debate.  That's why I purposely chose to quote from nature. How is that an ad hominem attack, seriously?    If you're going to accuse me of things like that I don't think it would be a productive discussion anyways.

 

You dismissed the article only by who is his author, not even reading it, nor discussing any of its points. In the article, your de Pinho's article and others are discussed and put in context. It demonstrates that the rejuvenation claims of de Pinho and Blasco are unfounded. And if you had read it, you would know that the author is Michael Rae, not Aubrey de Grey.
 

Edited by Antonio2014, 18 January 2016 - 08:26 AM.

[Antonio2014]

We have seen from Maria Blasco's lab that expressing extra telomerase in mice is good for a 13% increase in lifespan when started in old age, and 24% when started at one year.

 

No, that is unproven. Read the link I posted above.
 

[Never_Ending]

 

I find it useful to reference studies whenever possible... And to talk about Telomerase and Cancer without reference to NF-kB is a useless discussion...

 

Telomerase directly regulates NF-B-dependent transcription

 

Although elongation of telomeres is thought to be the prime function of reactivated telomerase in cancers, this activity alone does not account for all of the properties that telomerase reactivation attributes to human cancer cells. Here, we uncover a link between telomerase and NF-κB, a master regulator of inflammation. We observe that while blocking NF-κB signalling can inhibit effects of telomerase overexpression on processes relevant to transformation, increasing NF-κB activity can functionally substitute for reduced telomerase activity. Telomerase directly regulates NF-κB-dependent gene expression by binding to the NF-κB p65 subunit and recruitment to a subset of NF-κB promoters such as those of IL-6 and TNF-α, cytokines that are critical for inflammation and cancer progression. As NF-κB can transcriptionally upregulate telomerase levels, our findings suggest that a feed-forward regulation between them could be the key mechanistic basis for the coexistence of chronic inflammation and sustained telomerase activity in human cancers.

 

 

Do you think it's possible that since NF-kB is proinflamatory that telomerase is upregulated as a homeostatic mechanism to ensure that the organism does not loose too much in terms of lifespan as well as healthspan?   Anyhow very interesting and productive to bring that up, there is probably even more that we've yet to discover.
 

[Never_Ending]

 

 You dismissed the article only by who is his author, not even reading it, nor discussing any of its points. In the article, your de Pinho's article and others are discussed and put in context. It demonstrates that the rejuvenation claims of de Pinho and Blasco are unfounded. And if you had read it, you would know that the author is Michael Rae, not Aubrey de Grey.

 

 

 

 

 

That's not what my point was,  regardless of the author SENS is against telomerase lengthening and that has been Aubrey De Grey's view it and effects which articles they choose to feature.  I never said that your article is disregarded I simply said I would have to quote a source with an orientation of pro telomerase (which their are many) for it to be an even field. I was merely noting this.
 

Also I very much like and respect SENS as well as their views on most areas of aging I simply disagree when it regards telomeres.

Edited by Never_Ending, 18 January 2016 - 02:16 PM.