1153 replies to this topic

[QuestforLife]

No I don't.

 

My point is that cells with damaged mitochondria, i.e., reduced capacity for oxidative phosphorylation, have the potential to become cancer cells. So restricting their access to free telomeres is probably a good idea.

 

Once cancer cells have immortalised, they have almost infinite ability to mutate and could probably learn to live off toxic waste, if that is what they needed to do to survive. 

 

 

[Advocatus Diaboli]

 

.

.

The following claim was made in post # 1139: 

 

"Cancer cells can’t burn fats."

 

In post # 1140 I asked if there were any references for that claim.

 

In post # 1141 a response, presumably to my query, was given: "No I don't." with "have any references" omitted, but understood.

 

The claim (cancer cells can't burn fats) in post #1139, when viewed as a gross assertion, is false. And, in violation of Hitchens's razor, I claim that certain cancer cells can, and do, burn fats. 

 

The fact that certain cancer cells (including the most prevalent types) can burn fats also makes the following claim (post # 1139) false:

 

"So those precious telomeres are only being handed over to trustworthy guardians."

[QuestforLife]

Perhaps so, but you are focusing on a minor supposition of mine not central to the main point of my post, which is restated here in case you are having trouble distinguishing it: an exciting new source of telomeres has been discovered in the body that does not require telomerase.

I also beleive - without full references though backed up my years of my own research - that only handing over such telomeres only to mitochondrially healthy cells IS a pretty good defence against cancer. Even though in some circumstances cancers cells can burn fats.

[dlewis1453]

This is very exciting news! Thank you for sharing it with us. I was wondering if you would have a big research or protocol breakthrough to share with us in 2026 and you have already delivered. 

 

I was intrigued to read, in the paper you shared titled "CD4⁺ T cells confer transplantable rejuvenation via Rivers of telomeres," that: "These Rivers were then transferred into aged recipients (20 months old). One year later (32 months), River-treated mice showed marked rejuvenation in brain, liver, lung, kidney, and heart; senescence-associated β-galactosidase activity 33,34 was reduced (Fig. 4c), sMAC (sestrin2+ p-p38+ ) formation diminished, and p16^INK4a and IL-6 expression decreased (ED Fig. 10)." The fact that the telomere sharing is not limited to the immune system but instead spills out to the other major organs of the body, including the brain, is very promising. It seems that the "Rivers" carry both telomere and stemness cargo at the same time, as the paper says: "The failure of APC telomere vesicles lacking stemness factors to rejuvenate recipients, compared with the robust systemic effects of Rivers, underscores stemness cargo as key determinant of rejuvenation."

 

The peptide sequence is very short, so it should not be prohibitively expensive (on a per mg basis) to have it synthesized in China. The fact that it is a cyclic peptide will add some to the cost, but with such a short sequence it should be economically feasible on a per mg basis. Have you estimated a human dose yet? The dose size will obviously have a big impact on the total cost.

 

I'm sure you are already thinking up a protocol. I'm very curious to hear your thoughts. Perhaps entering fusion with stearic acid + sulforaphane before administering the peptide could enhance results. The paper mentions that immune stimulation is necessary. The authors used a vaccine, but hopefully something more accessible would work for us. One possibility would be to consume large oral doses of a postbiotic, such as the product Immuse, which is a heat-killed version of the very immunogenic bacterium Lactococcus lactis. Research has shown that heat-killed Lactococcus lactis is one of the rare substances that is able to directly activate plasmacytoid dendritic cells, which in turn increases the number and activity of T-cells.

 

I am wondering if some of the benefits of Turnbucle's C60 +fusion stem cell  protocol were mediated via these Rivers of telomeres + stemness?

[QuestforLife]

I am wondering if some of the benefits of Turnbucle's C60 +fusion stem cell protocol were mediated via these Rivers of telomeres + stemness?

Exactly. From Baati 2012: "C60 concentration reached the limit of solubility in spleens."

So maybe we don't need to stimulate the immune system at all.

[Advocatus Diaboli]

.

.

 

Below, the "Perhaps so" is referring to certain elements of my post # 1142.

 

QuestforLife writes, in post # 1143: 

 

"Perhaps so, but you are focusing on a minor supposition of mine not central to the main point of my post, which is restated here in case you are having trouble distinguishing it: an exciting new source of telomeres has been discovered in the body that does not require telomerase."

 

"Cancer cells can’t burn fats." is a "minor supposition"? Supposition? Clearly, that claim was an unsubstantiated assertion, not a supposition. Later on you correctly amended your original claim by writing (as you do ex post facto my remarks in other posts): "Even though in some circumstances cancers cells can burn fats.". It seems as if you were trying to have your tergiversation cake and eat it too.

 

Assertions that appear to be presented as being "facts", but aren't, need to be exposed for what they are, i.e. "fake news", to use a phrase that has gained popularity in common parlance. It really doesn't matter if something is "not central to the main point of my post" or not. If  "fake news" isn't "nipped in the bud" it is possible that it could be cited by others as being fact, thus adding to the already too-full universe of misinformation. 

 

Your original assertion about cancer cells not being able to burn fats was presented without stipulation(s) and remains unequivocally and categorically wrong, and thus was in need of correction--and, to reiterate, regardless of whether the claim was central to your main point, or not.

 

"I also beleive - without full references though backed up my years of my own research - that only handing over such telomeres only to mitochondrially healthy cells IS a pretty good defence against cancer. Even though in some circumstances cancers cells can burn fats.". 

 

Sorry, but you need to provide citation to a reference which describes the mechanism by which that "handing over" is effectuated. A claim (that isn't obvious) without providing citation is worthless.

 

You write: "handing over such telomeres only to mitochondrially healthy cells" (my emphasis). If your use of "only" is meant to mean hand over just to the healthy, non-cancerous, cells, it would be problematical to effectuate such a selective handover. For example, a telomere handover to  cancer cells might result in adverse bodily effects--an observation which should be obvious to you (see below for a discussion on what is considered to be "healthy"). So, unless a way to enable a selective handover to only healthy non-cancerous cells is developed, the utility of such a proposed handover would be highly questionable, at best.

 

Also, be aware that "mitochondrially healthy" is a double edged sword--from the cancer's viewpoint the dysfunctional unhealthy mitochondria (as seen from the body's viewpoint) are seen as being mitochondrially healthy because any disruption of these "unhealthy mitochondria" could result in the death of the cancer cells, which is not a condition that cancer cells would consider to be "healthy".

 

For an in-depth discussion of part of the above, see this article review. Some of what you'll find in the review:

 

The central theme is that in cancer, "mitochondria orchestrate multiple cellular processes critical to tumor development" and undergo "metabolic reprogramming" . This is the essence of domestication—being repurposed for the cancer's needs.

 

It explicitly states that mitochondria are "essential for cellular energy generation" (functional) but also that "mitochondrial dysfunction in tumors is highly heterogeneous" and "genetic and epigenetic alterations... disrupt oxidative phosphorylation" (pathological) . It perfectly captures the dual nature.

 

The review is explicitly about "mitochondria-based cancer interventions" and "targeting mitochondrial function represents a promising therapeutic strategy" . It frames the disruption of this co-opted state as a key to stopping cancer, validating that true dysfunction is catastrophic.

 

The entire premise of the review is that mitochondria are co-opted to support "uncontrolled growth, survival, and treatment resistance" . This directly implies they are functioning optimally for the tumor's agenda which is the cancer's definition of "healthy".

 

Approximately 10-15% of cancers use the ALT pathway, which doesn't require telomerase at all.      

         

A defense mechanism based on regulating telomerase, would completely miss the ALT pathway cancers. Those cancers maintain their telomeres through homologous recombination, not enzyme activity, making them invisible to telomerase-based controls. 

 

I suspect that the "exciting new discovery" isn't actually as exciting as you apparently believe it to be.

[QuestforLife]

.

I suspect that the "exciting new discovery" isn't actually as exciting as you apparently believe it to be.

 

 

Thanks for the long and irrelevant post. 

 

Try to take a step back and see the wood through the trees. If you are able. 

[Advocatus Diaboli]

.

.

 

 

"Long and irrelevant"--from QuestforLife's post #1147 

 

I'm not sure why the length of my post is worthy of comment, considering the fact that some people, you for example, have made much longer posts in this thread. And, surely, the length of my post didn't tax the limits of your intellectual ability?

 

As far as "relevance" is concerned, I certainly can't guarantee that what I write will be compatible with any particular person's ability to establish a suitable nexus among the various constituent elements of the post, making things snap into focus for them. 

 

Furthermore, I would suggest that the "relevance" of my post is directly proportional to a person's comprehension aptitude as well as the extent and depth to which their metacognition is operant. From your comment it's apparent that you didn't experience a burst of gamma-band activity in your right hemisphere's anterior superior temporal gyrus, followed closely by a dopamine-mediated activation of your nucleus accumbens. Too bad.

 

So, try this redacted and condensed version of my post on for size, that is, assuming you're willing to put your money where your mouth "I also beleive [sic]..." is:

 

You wrote:

 

"I also beleive - without full references though backed up my years of my own research - that only handing over such telomeres only to mitochondrially healthy cells IS a pretty good defence against cancer. Even though in some circumstances cancers cells can burn fats.". 

 

Please describe the mechanism by which a "handing over", only to mitochondrially healthy cells, is effectuated. Supply citations of substantiation.

 

TIA ("thanks in advance")

[QuestforLife]

My long posts actually have something of value in them.

 

You are just a pedant.

 

If you bothered reading the paper we are discussing you’d understand how the telomere hand-over process works. Then you might be able to postulate some situation where a cancer cell could take advantage of that to the detriment of the body.  Then, if your argument had sufficient merit, it might warrant a rethink of whether the proposed treatment for aging in the paper is wise. 

 

But you have done none of that. You have just written sentences such as:

 

Furthermore, I would suggest that the "relevance" of my post is directly proportional to a person's comprehension aptitude as well as the extent and depth to which their metacognition is operant.

 

Don’t bother posting unless you have something constructive to contribute. 

 

Edited by QuestforLife, Yesterday, 04:29 PM.

[Advocatus Diaboli]

QuestforLife, how can I possibly assess the efficacy of a proposed telomere-hand-over mechanism that would selectively deliver benefit only to mitochondrially healthy cells (body perspective) when such a proposed mechanism isn't discussed in the paper?

 

It is you, not the paper, that has made a selective claim that "...handing over such telomeres only to mitochondrially healthy cells IS a pretty good defence against cancer.". 

 

The "you" in the following refers to me, AD (see my nick): "Then you might be able to postulate some situation where a cancer cell could take advantage of that to the detriment of the body."

 

QuestforLife, it is you that are making the selective-mechanism claim. Not me, and not the paper. So, in your explanation of how this selective mechanism works, you would have to explain why a cancer cell would not (remember, your mechanism is selective only to healthy non-cancer cells) be able to take advantage of the mechanism for its benefit.

 

QuestforLife writes: "If you bothered reading the paper..."

 

The following summarizes my understanding of the paper, in brief:

 

The paper does not contain explicit, detailed statements that directly address the receptor or molecular mechanism by which a "River" is taken up by a target cell.

 

The paper is significantly more detailed about the release mechanism than the uptake mechanism. And it is you that are inferring, by way of your claim, that the paper suggests that there could be a selective uptake mechanism that targets only mitochondrially healthy cells.

 

The paper uses the word "targeted" but does not define the targeting mechanism. The abstract states that Rivers enable "targeted rejuvenation of senescent tissues across multiple organs". It also claims that Rivers travel systemically, acting as a youth signal that reaches the brain, liver, heart, and lungs. However, the paper does not identify the specific receptor or ligand that allows a River to bind specifically to a senescent cell versus any other cell--such as a cancer cell, for example.

 

The paper demonstrates that after Rivers are injected, senescent cells in distant organs show rejuvenation . This proves that uptake occurs, but it does not explain the molecular "address label" that guides the River to a specific cell. And, knowing the address label would be crucial in determining whether a River can be beneficially used by a cancer cell or not.

 

The paper places an emphasis on cargo, not delivery. The proteomics analysis focuses heavily on what is inside the River (depletion of GAPDH, enrichment of stemness factors) . The paper does not contain a parallel analysis of the River's surface markers (the "keys") or the corresponding receptors on target tissues (the "locks").

 

There is no experimental data in the paper demonstrating that uptake is dependent on the metabolic state of the recipient. Dependence is an inference that can be drawn from targeting claims of an undefined targeting mechanism (see above), not a fact that the paper actually demonstrates.

 

The paper manipulates FAO in T cells (via CPT1A restoration, ceramide modulation, PE supplementation) and directly measures River release. As an aside, you now admit that cancer cells can burn fat.

 

Proteomics (DIA and DDA) compare Rivers to APC vesicles, showing GAPDH depletion and stemness factor enrichment.

 

The paper injects Rivers into aged mice and observes rejuvenation in brain, liver, heart, etc. However, the paper does not manipulate recipient metabolic states (e.g., blocking FAO in target tissues, inducing different metabolic profiles) to see if uptake is blocked or altered.

 

The paper shows that Rivers "target" senescent tissues but does not identify the receptor-ligand pair. There were no experiments blocking putative receptors, no knockout models, no competition assays.

 

The paper states that Rivers enable "targeted rejuvenation of senescent tissues across multiple organs". That is an outcome statement—it shows that after injection, senescent cells in various organs improve. But it does not establish the mechanism of that targeting.

 

If, upon reflection, you find that your claim was poorly worded, then fine. However, if you continue to maintain there could be an "only" mechanism then the burden is on you to present it along with any material that supports it.

[dylansin]

Fascinating discussion on the Rivers of telomeres paper. The connection between mitochondrial health and telomere maintenance really underscores how central metabolic fitness is to the whole aging equation.

One angle I find particularly interesting is the NAD+ dimension here. Given that NAD+ is a critical cofactor for sirtuins (especially SIRT1 and SIRT3) which regulate both mitochondrial biogenesis and telomere integrity, it seems plausible that maintaining robust NAD+ levels could support the very metabolic environment that makes cells "worthy recipients" of these telomere Rivers. SIRT3 specifically protects mitochondrial function under stress, and SIRT1 has been shown to modulate telomere attrition rates through its interaction with the shelterin complex.

The paper's finding that fatty acid oxidation capacity in T cells determines River release is also worth noting—this ties directly into the NAD+/NADH ratio as a gatekeeper of beta-oxidation efficiency. Cells with depleted NAD+ pools tend to have impaired FAO, which based on this research would mean reduced capacity for telomere sharing.

For anyone looking to dig deeper into the practical side of NAD+ supplementation and its effects on mitochondrial health, I came across a useful overview at glunovabio.com that covers the different precursors and delivery methods. Might be relevant context for thinking about how to optimize the cellular environment for these kinds of interventions.

Really looking forward to seeing QuestforLife's protocol thoughts on the cyclic peptide approach.

[QuestforLife]

 

The following summarizes my understanding of the paper, in brief:

 

The paper does not contain explicit, detailed statements that directly address the receptor or molecular mechanism by which a "River" is taken up by a target cell.

 

The paper is significantly more detailed about the release mechanism than the uptake mechanism. And it is you that are inferring, by way of your claim, that the paper suggests that there could be a selective uptake mechanism that targets only mitochondrially healthy cells.

 

The paper uses the word "targeted" but does not define the targeting mechanism. The abstract states that Rivers enable "targeted rejuvenation of senescent tissues across multiple organs". It also claims that Rivers travel systemically, acting as a youth signal that reaches the brain, liver, heart, and lungs. However, the paper does not identify the specific receptor or ligand that allows a River to bind specifically to a senescent cell versus any other cell--such as a cancer cell, for example.

 

The paper demonstrates that after Rivers are injected, senescent cells in distant organs show rejuvenation . This proves that uptake occurs, but it does not explain the molecular "address label" that guides the River to a specific cell. And, knowing the address label would be crucial in determining whether a River can be beneficially used by a cancer cell or not.

 

The paper places an emphasis on cargo, not delivery. The proteomics analysis focuses heavily on what is inside the River (depletion of GAPDH, enrichment of stemness factors) . The paper does not contain a parallel analysis of the River's surface markers (the "keys") or the corresponding receptors on target tissues (the "locks").

 

There is no experimental data in the paper demonstrating that uptake is dependent on the metabolic state of the recipient. Dependence is an inference that can be drawn from targeting claims of an undefined targeting mechanism (see above), not a fact that the paper actually demonstrates.

 

The paper manipulates FAO in T cells (via CPT1A restoration, ceramide modulation, PE supplementation) and directly measures River release. As an aside, you now admit that cancer cells can burn fat.

 

Proteomics (DIA and DDA) compare Rivers to APC vesicles, showing GAPDH depletion and stemness factor enrichment.

 

The paper injects Rivers into aged mice and observes rejuvenation in brain, liver, heart, etc. However, the paper does not manipulate recipient metabolic states (e.g., blocking FAO in target tissues, inducing different metabolic profiles) to see if uptake is blocked or altered.

 

The paper shows that Rivers "target" senescent tissues but does not identify the receptor-ligand pair. There were no experiments blocking putative receptors, no knockout models, no competition assays.

 

The paper states that Rivers enable "targeted rejuvenation of senescent tissues across multiple organs". That is an outcome statement—it shows that after injection, senescent cells in various organs improve. But it does not establish the mechanism of that targeting.

 

If, upon reflection, you find that your claim was poorly worded, then fine. However, if you continue to maintain there could be an "only" mechanism then the burden is on you to present it along with any material that supports it.

 

 

Thank you for reading the paper. I'd agree that further work remains to be done to fully elucidate the mechanism by which rivers of telomeres are passed on throughout the body and if this also requires the recipient cells to be capable of FAO, as with the APC-T cell link.  

 

It was never my intent to concentrate on a cancer angle, I only mentioned that in passing, and as you have repeatedly pointed out, it was not factually accurate because some cancer cells can burn fats. Further work will be required to determine whether such cancer cells, if present in the body, could be the recipient of rivers of telomers.

 

The way my mind works is to see potential connections, even tenuous ones, and then build a chain of evidence that can substantiate those chains. Or not. 

[QuestforLife]

Fascinating discussion on the Rivers of telomeres paper. The connection between mitochondrial health and telomere maintenance really underscores how central metabolic fitness is to the whole aging equation.

 

I agree it is a very interesting angle. Years ago I wrote a paper titled 'Have we moved past calorie Restriction yet?'

 

When I envisaged the paper, I was thinking in terms of this being a criticism of life extension research and lack of progress. But it quickly morphed into a realisation that metabolic health was central to health and ageing and that many approaches to extend life were often exercising this same central pathway.

 

Though the body has many incredibly intricate mechanisms, it also can be understood from a top-down, system-level view. And that is why, when I see a paper like the 'Rivers of Telomeres' one, it attracts my attention. 

 

I recall a paper some time ago finding telomere extension from NMN treatment. I note they saw increased guanine metabolites. The mice also had increased thermogenesis.

 

It would be interesting to find out if things such as fasting or increased reliance on fats at a body level, did trigger this release of rivers of telomeres, in addition to the other benefits already known. 

Edited by QuestforLife, Today, 09:12 AM.

[Advocatus Diaboli]

QuestforLife writes:  "The way my mind works is to see potential connections, even tenuous ones, and then build a chain of evidence that can substantiate those chains. Or not."

 

Your thought process sounds very similar to bisociation. But, from other posts of yours I have detected expression of ideas that to my mind are very likely generated by elements of lateral, divergent, and aleatory thinking, among others. And, I suspect that's how "unexpected" progress in a field can be made.

Edited by Advocatus Diaboli, Today, 09:35 AM.