217 replies to this topic

[PWAIN]

Came across this NewScientis article....Look REALLY exciting.

 

http://www.newscient...ml#.U_WIgaNXynl

 

GDF-11 is looking increasingly like it is the answer to our prayers. Not sure why there is not a LOT more excitement about GDF-11 and why we don't have a synthesis/group buy going.

[free10]

Came across this NewScientis article....Look REALLY exciting.

 

http://www.newscient...ml#.U_WIgaNXynl

 

GDF-11 is looking increasingly like it is the answer to our prayers. Not sure why there is not a LOT more excitement about GDF-11 and why we don't have a synthesis/group buy going.

 

A few more stories on it

 

http://www.gizmodo.c...f-young-people/

 

http://alzheimersnew...es-in-old-mice/

 

If started in October we might have some answers sneak out by Christmas on how well it is working. They are using blood though and not just GDF11, and blood may contain many more helpful substances in young blood. That is another thing you would think they would want to use the youngest blood they can get their hands on and not someone as old as 30.

[gt35r]

I hope GDF-11 is as even 1/8 as good as we have heard but don't assume it will be even remotely close to a fix to aging. I doubt GDF11 will address AGE formation or lipofuscin aggregation; this is one of the few situation where I would do anything to be wrong. 

[free10]

I hope GDF-11 is as even 1/8 as good as we have heard but don't assume it will be even remotely close to a fix to aging. I doubt GDF11 will address AGE formation or lipofuscin aggregation; this is one of the few situation where I would do anything to be wrong. 

 

If the young blood works, then I doubt anyone will be let down and it probably will work in humans as well as it does in mice. I am pretty sure if you rewire the brain and body back up to specs the body will know what to do with things like lipofuscin in cells. If that was about the only problem we had left it probably wouldn't take long to know just knock that one out. The only thing I wonder about is telomere length with it, since it needs to be addressed in humans, though it is not a problem in mice. But once again, if that is the only problem left then it would not probably be that hard to solve it fairly fast. Just a guess on my part.

 

October will be here before we will know it and news on what they see shouldn't take that long. If the news is really really good the things like GDF11 should be fairly easy to find cheaply. Or vacation rejuvenation facilities in other countries fairly cheap. I just don't see the FDA wiping out all the money medical makes here off of aging, by approving it.

[gt35r]

I seriously doubt that the cells are all of a sudden going to be able to take care of lipofuscin deposits. A lot of lipofuscins deposits exists because the cell does not have the mechanism to dissolve them;same goes from AGEs, ECM cross linking, and protein aggregations. 

[free10]

I seriously doubt that the cells are all of a sudden going to be able to take care of lipofuscin deposits. A lot of lipofuscins deposits exists because the cell does not have the mechanism to dissolve them;same goes from AGEs, ECM cross linking, and protein aggregations. 

 

Its a debate on wear and tear, or..... LOL

 

Maybe he can explain it better

 

http://www.programme...ma_exchange.pdf

 

From what I have seen through a number of recent studies reversing aging using different methods, I would have to say it looks like wear and tear has had its day. When build and repair fails/ends, then it just appears wear and tear has happened and is the cause. Just a guess on my part and some others.

[niner]

 

I seriously doubt that the cells are all of a sudden going to be able to take care of lipofuscin deposits. A lot of lipofuscins deposits exists because the cell does not have the mechanism to dissolve them;same goes from AGEs, ECM cross linking, and protein aggregations. 

 

Its a debate on wear and tear, or..... LOL

 

Maybe he can explain it better

 

http://www.programme...ma_exchange.pdf

 

From what I have seen through a number of recent studies reversing aging using different methods, I would have to say it looks like wear and tear has had its day. When build and repair fails/ends, then it just appears wear and tear has happened and is the cause. Just a guess on my part and some others.

 

I think you'll have a hard sell with this one.  The proponents of programmed aging point out that some degree of rejuvenation occurs when you put an old cell into a young environment, but I don't think they are addressing a couple things.  The first is how does the young environment get "old"?  Is it caused by damage?  The second relates to the cells they are looking at.  If the mitochondria are shot, the telomeres are gone, or the lysosomes are bloated, then all the youth signals in the world aren't going to help that cell.  How does programmed aging explain that?

[free10]

 

 

I seriously doubt that the cells are all of a sudden going to be able to take care of lipofuscin deposits. A lot of lipofuscins deposits exists because the cell does not have the mechanism to dissolve them;same goes from AGEs, ECM cross linking, and protein aggregations. 

 

Its a debate on wear and tear, or..... LOL

 

Maybe he can explain it better

 

http://www.programme...ma_exchange.pdf

 

From what I have seen through a number of recent studies reversing aging using different methods, I would have to say it looks like wear and tear has had its day. When build and repair fails/ends, then it just appears wear and tear has happened and is the cause. Just a guess on my part and some others.

 

I think you'll have a hard sell with this one.  The proponents of programmed aging point out that some degree of rejuvenation occurs when you put an old cell into a young environment, but I don't think they are addressing a couple things.  The first is how does the young environment get "old"?  Is it caused by damage?  The second relates to the cells they are looking at.  If the mitochondria are shot, the telomeres are gone, or the lysosomes are bloated, then all the youth signals in the world aren't going to help that cell.  How does programmed aging explain that?

 

 

Remember the young rapidly age when exposed to old blood, which is the reverse condition. How a cell acts seems to be guided in part by the shortening or lengthening of the telomeres, and the genetics change, so does the way the cell behaves changes and looks. Old cells with relengthen telomeres of humans cells start acting or functioning like they are young again and look under the microscope almost like a newborns, instead of the cells of an 80 year old. I suspect when the young signals come out this happens to the cells. I also suspect that our bodies are damaged by the bad cells with the short telomeres spewing the poisons (senescent cells), and when they stop they are repaired or replaced as needed if too badly damaged.

 

In other words you have several different processes going on at the same time, to change the way the cells act and look, and another process of tear down and replacement of too badly damaged cells. Now, no one has spoken about, or perhaps looked at yet what is going on with the telomere length in the younger environment, but I suspect it is changing to a longer version and that will change how those cells look and behave. They mainly focus on the stem cells being produced and going to different areas of the body for repair, which is great but I don't think it explains fully what they are seeing rapidly in the old mice, in days or a in few weeks. The enlarged heart shrinks back and they are able to run again almost with the speed and stamina of the young, and all the rest they are seeing in a fairly short period. I don't think this is simple repair by the new stem cells now being produced, but reminds me of another age reversals, also at Harvard, using a simple 30 day boost of telomerase in them.

 

The cells in us seem to go through an almost constant two step process of destroying cells and then replacing them throughout our lifetime. But what happens on the spine for example if the destruction process continues and the repair and replacement part falls behind or stops?? It is known, with smokers for example, the repair replacement is hindered by smoking. Ageing itself may be little more then  about that balance failing further down the road but more slowly.

 

In October the first human trials will start in Australia and more research and answers should be out though I am not real crazy about how they set it up giving them only some younger blood one time, and then asking for observations of a change. This, to my understanding, is not how any of the mice trials were done either with young blood, or GDF11 alone. It almost sounds like it is set up to fail.

 

In the end, if with have age reversal then the signs of damage can not and will not exist anymore because of the change by telomere, or by the tear down replacement cycle normal in the body, which is a longer process that takes sometimes decades one cell at a time. By the day or month, we learn what we did not about the whole subject, and find out a lot more yes we cans, then no we can not.

 

Just my view, as always, and reduced or condensed way  down because of the slowness of my typing LOL

[Rocket]

I think GT is correct about wear and tear having had its day and aging being the failure of build and repair. Why do muscles shrink with age? Because the build and repair mechamsms slow down... you cant build new muscle and the muscle you have isnt repaired. Progeria should have put and end to the accumulated wear and tear hypothesis decades ago.... a 9 year old kid is going to accumulate 80 years of wear and tear? No way. Unless an 80 year old looks 80 because the body slowly stopped repairing itself. Likewise, look at how rapidly a young child will age once their body stops repairing itself. Why does build abd repair fail? Probably telomeres.

Edited by Rocket, 28 August 2014 - 12:55 PM.

[Phoenicis]

it could be explained by epigenetic regulation, a sort of pre-programmed self destruct.

http://protein.bio.m...l/78091354.html

 

 

I seriously doubt that the cells are all of a sudden going to be able to take care of lipofuscin deposits. A lot of lipofuscins deposits exists because the cell does not have the mechanism to dissolve them;same goes from AGEs, ECM cross linking, and protein aggregations. 

 

Its a debate on wear and tear, or..... LOL

 

Maybe he can explain it better

 

http://www.programme...ma_exchange.pdf

 

From what I have seen through a number of recent studies reversing aging using different methods, I would have to say it looks like wear and tear has had its day. When build and repair fails/ends, then it just appears wear and tear has happened and is the cause. Just a guess on my part and some others.

 

I think you'll have a hard sell with this one.  The proponents of programmed aging point out that some degree of rejuvenation occurs when you put an old cell into a young environment, but I don't think they are addressing a couple things.  The first is how does the young environment get "old"?  Is it caused by damage?  The second relates to the cells they are looking at.  If the mitochondria are shot, the telomeres are gone, or the lysosomes are bloated, then all the youth signals in the world aren't going to help that cell.  How does programmed aging explain that?

 

 

[corb]

That's actually an interesting article.
I searched for mainstream research that can serve as proof and I found this

 

 

Donor age was not associated with the risk of PGD. In summary, the use of lungs from donors age 56 to 64 years may be safe for adult candidates without a high LAS and the use of lungs from pediatric donors is associated with a small increase in early graft failure.

*PGD - primary graft dysfunction.

http://www.ncbi.nlm....pubmed/24034167

 

Unfortunately it's not free but the abstract is interesting enough.

Doesn't say anything about how the lungs worked afterwards, but if they're safe for transplantation I'm thinking about as good as lungs from a younger donor.

 

I'll look for more articles with similar research matter. This does raise some questions, that is for sure.

[gt35r]

The wear and tear model applies to things outside the cell as well.

 

Even with good healthy cells, lets say fibroblast, a degenerating extracellular matrix is prohibitive for youthful function. For example, even in young people, the turnover rate for most types o collagen and elastin is too slow and ineffective to offset the damage done by glycation; and this is in the most optimistic circumstance.  So even if the fibroblast are in good health, they are jut unable to turnover the already damage collagen much less collagen that is heavily damaged from year of glycation. 

 

Just look of the half life of collagen and elastin in the aorta, we are talking about around 70 years. 

[Bryan_S]

Young blood to be used in ultimate rejuvenation trial

 

The first human trials are about to begin in early October, a team at Stanford School of Medicine will give a transfusion of blood plasma donated by people under 30 to older volunteers with mild to moderate Alzheimer's. See URL Link At this point researchers like Wyss-Coray at Stanford believes we could identify several factors that we could boost in older people, he says. "Then we might be able to make a drug that does the same thing. We also want to know what organ in the body produces these factors. If we knew that, maybe we could stimulate that tissue in older people." So the research on GDF-11 is in the human starting gate. Of course transfusions of blood plasma is not a path about to go mainstream. There are likely a number of signaling blood factors at work and it will take some time to isolate the proper combinations and synthesize them. 

 

Here is a funny twist because just this morning I was reading Josh Mitteldorf's notes from the recent Rejuvenation Biotech Conference. See URL link He says; "I found it ironic that Aubrey de Grey, whose SENS Foundation sponsoted the conference, expressed skepticism about this whole approach to aging.  He sees aging as a matter of accumulated damage rather than perverse signaling, and he imagines that epigenetic changes that happen with age are actually evolved for the body’s benefit.  He distinguished systematic epigenetic shifts with age, which he thinks are beneficial, from random epigenetic drift, which he thinks is detrimental."

 

I dont think any one thing will be the key and I'm not taking sides. Almost every day I see something someones turned up that adds to our knowledge of aging. At this point I see a group working on enhancing Mitochondrial function by stimulating NAD+ production, another working on Mitochondrial repair, Stanford and Harvard groups working on cell signaling blood factors and a host of others we haven't the time or space to include. Will one approach win out? I think eventually we'll have a convergence of understanding and at that point we will be able to direct our tissues to mediate disease and this will lead to the Longevity we seek.

Edited by Bryan_S, 31 August 2014 - 05:48 PM.

[corb]

Here is a funny twist because just this morning I was reading Josh Mitteldorf's notes from the recent Rejuvenation Biotech Conference. See URL link He says; "I found it ironic that Aubrey de Grey, whose SENS Foundation sponsoted the conference, expressed skepticism about this whole approach to aging.  He sees aging as a matter of accumulated damage rather than perverse signaling, and he imagines that epigenetic changes that happen with age are actually evolved for the body’s benefit.  He distinguished systematic epigenetic shifts with age, which he thinks are beneficial, from random epigenetic drift, which he thinks is detrimental."

 

Not surprising, if the young blood therapy proves to be as effective as it is in mice, we have to throw SENS out the door.

Well, not really but it goes from being the end all to another quick fix going for the symptom and not the cause.

Anyone would be miffed if their life's work was at stake.

 

The wear and tear model applies to things outside the cell as well.

 

Even with good healthy cells, lets say fibroblast, a degenerating extracellular matrix is prohibitive for youthful function. For example, even in young people, the turnover rate for most types o collagen and elastin is too slow and ineffective to offset the damage done by glycation; and this is in the most optimistic circumstance.  So even if the fibroblast are in good health, they are jut unable to turnover the already damage collagen much less collagen that is heavily damaged from year of glycation. 

 

Just look of the half life of collagen and elastin in the aorta, we are talking about around 70 years.

 

Well this is more of a debate for the aging theory forum I guess, and I do agree with you...
BUT, here comes the big but, what if we're looking at a "hybrid" model of aging. It's not impossible that some mechanisms could be lackluster while others are down regulated by a genetic factor. It could be as De Grey says and some of the down regulation might be beneficial, but if you look at the mouse studies for gdf11 it actually caused bone muscle and neuron regeneration, it basically makes stem cell therapies ... well, less significant at the least, depending on how well it performed. Or it could be used IN conjunction with stem cells. In fact it could make somatic stem cells a viable therapy.

 

This is all what if of course, I'm quite interested in what the human study will show. If they do it properly. I'm not sure they will at this point.

Edited by corb, 31 August 2014 - 08:46 PM.

[niner]

Any time something is presented as the one and only true cause of aging or the miracle that's going to make us all young, it's probably wrong.  The simpler and more singular the thing is, the more likely is is to NOT be the only cause of aging.  SENS covers a lot of territory with its seven forms of damage.  I think those things capture a large part of the difference between young and old organisms, but not all of it.   We've been hearing a lot of "programmed aging" talk lately.  I'd be more inclined to accept parts of it if someone could tell me what the "clock" was.   Telomeres?  I kind of doubt it, but if that's it, we know how to lengthen them.  I think the best candidate for the "clock", or the trigger for so-called "programmed" aging is simply some form or forms of damage of the sort that SENS addresses.  Maybe I'm just hung up on the term "programmed".  It sounds like it comes out of the "Intelligent Design" world.  If we call it something like aberrant signaling, then it seems more plausible.  Not as the sole cause of aging, of course, but as a minor, perhaps non-trivial component.

[corb]

I think the best candidate for the "clock", or the trigger for so-called "programmed" aging is simply some form or forms of damage of the sort that SENS addresses.  Maybe I'm just hung up on the term "programmed"

 

It's probably just damage done to the ribosomal dna, which results in damaged ribosomes, which are probably incapable of synthesizing proteins, which in turn makes for bad cell communication. I wouldn't say that's a minor cause of aging, if simply having the proteins at a nominal "youthful" level is enough to kick start regeneration in tissues.

I'm quite skeptical about programmed aging myself, which is why I'm not so much interested in this study per se, I'm more interested someone to do some in vitro studies and to get an idea what's happening precisely.

Edited by corb, 31 August 2014 - 11:06 PM.

[Avatar of Horus]

... Now, no one has spoken about, or perhaps looked at yet what is going on with the telomere length in the younger environment, but I suspect it is changing to a longer version and that will change how those cells look and behave. ...

Some work has been done:
post #31 from the topic: http://www.longecity...ndpost&p=633704

on aged fibroblasts and young ECM:

Restoration of senescent human diploid fibroblasts by modulation of the extracellular matrix
Choi et al., Aging Cell. 2011
http://www.ncbi.nlm....pubmed/21108727
free full: http://onlinelibrary...10.00654.x/full

Abstract
Human diploid fibroblasts have the capacity to complete a finite number of cell divisions before entering a state of replicative senescence characterized by growth arrest, changes in morphology, and altered gene expression. Herein, we report that interaction with extracellular matrix (ECM) from young cells is sufficient to restore aged, senescent cells to an apparently youthful state. The identity of the restored cells as having been derived from senescent cells has been confirmed by a variety of methods, including time lapse live cell imaging and DNA finger print analysis. In addition to cell morphology, phenotypic restoration was assessed by resumption of proliferative potential, growth factor responsiveness, reduction of intracellular reactive oxygen species levels, recovery of mitochondrial membrane potential, and increased telomere length. Mechanistically, we find that both Ku and SIRT1 are induced during restoration and are required for senescent cells to return to a youthful phenotype. These observations demonstrate that human cellular senescence is profoundly influenced by cues from the ECM, and that senescent cell plasticity is much greater than that was previously believed to be the case.

[niner]

Wow Avatar, that's pretty cool. I had no idea that senescent cells were that plastic. Do they have any idea what factors in young ECM cause this reversion to an apparently youthful state? Any idea how long the cells could maintain their new-found youth? Would sufficient damage to the cell prevent the reversion?

[Hebbeh]

 

Mechanistically, we find that both Ku and SIRT1 are induced during restoration and are required for senescent cells to return to a youthful phenotype.

 

This.  Resveratrol anyone?

[Avatar of Horus]

Wow Avatar, that's pretty cool. I had no idea that senescent cells were that plastic. Do they have any idea what factors in young ECM cause this reversion to an apparently youthful state? Any idea how long the cells could maintain their new-found youth? Would sufficient damage to the cell prevent the reversion?

 
These are good questions. I don't know exactly, as the cited paper not speaks much about this, only the induction of Ku70 and the SIRT1. But considering the hTERT, a possible candidate would be the involvement of the c-Myc transcription factor. Also reported as responsible in the case of the liver regeneration in parabiosis.
 
Regarding the cellular damage and rejuvenation levels, what can be considered here is the matter of the induced pluripotent stem cells (IPSC). The original Yamanaka IPSC reprogramming efficacy was extremely low, but later studies reported increased efficiency. Some details about these: http://en.wikipedia....otent_stem_cell
All the way to a deterministic level, with the NuRD complex, but this latter was questioned recently. Some infos about this: http://en.wikipedia....oldid=615340256
So possibly some additional testing would be good. After all that's what the experiments are for in the biomed research. (This applies to the following too.)
 
The original GDF11 paper was the cardiac hypertrophy one: http://www.ncbi.nlm....pubmed/23663781, which reported as a part of the possible relevant mechanism of action that Gdf11 suppresses the phosphorylation of Forkhead transcription factors, like the Foxo3a: Figure 7C:

And also was mentioned downstream of this the possible role of the induction of the proteasome, a mechanism of the removing of the damaged proteins, thus reducing proteotoxicity, i.e. a cellular detoxification process.
About this latter and the immortality of the germ line and embryonic stem cells, I suggest for reading the topic of 'Reproduction vs aging damage', from the #32 post:
http://www.longecity...ndpost&p=659213
May be worth noting that: this Foxo is the same that was implicated in the Insulin/DAF-16 pathway related life extension in C. elegans. And also related the life extension in the Igf signaling deficient dwarf mice. One type of them currently holds - if I am not mistaken - the record of the Methuselah Mouse prize.

Here is a recent study that may be relevant to the above:

FOXO3a potentiates hTERT gene expression by activating c-MYC and extends the replicative life-span of human fibroblast
Yamashita et al., PLoS One. 2014 Jul 7
http://www.ncbi.nlm....pubmed/25000517
full: http://dx.plos.org/1...al.pone.0101864

Abstract
In our previous studies, we reported that SIRT1 prevents cellular senescence in human fibroblast, and that SIRT1-induced inhibition of cellular senescence is due to enhanced hTERT gene expression. In this study, we investigate the molecular mechanisms behind SIRT1-induced potentiation of hTERT transcription and show that FOXO3a functions downstream of SIRT1 and prevents the induction of cellular senescence by enhancing hTERT gene expression. Furthermore, we found that FOXO3a-induced potentiation of hTERT gene expression is regulated in a c-MYC/E-box dependent manner. In addition, we found that FOXO3a binds to the novel binding element in the c-MYC promoter, and this interaction activates the transcription of the c-MYC gene. The resulting increase in c-MYC leads to higher levels of c-MYC recruited to the hTERT promoter and, in turn, activates hTERT gene expression. Taken together, this pathway might constitute the molecular basis for the anti-senescence effects of SIRT1 and FOXO3a.

Another paper can be mentioned here. About the Ku proteins, which may be involved in the immortality of the germ line cells:

Ku70 and non-homologous end joining protect testicular cells from DNA damage
Ahmed et al. 2013, http://www.ncbi.nlm....pubmed/23857907

 

[Bryan_S]

Not surprising, if the young blood therapy proves to be as effective as it is in mice, we have to throw SENS out the door.

Well, not really but it goes from being the end all to another quick fix going for the symptom and not the cause.

Anyone would be miffed if their life's work was at stake.

 

 

As far as SENS they are doing good work and I don't disrespect that. Aubrey de Grey has helped change the mindset of countless researchers and bring together research and ideas that never would have influenced each other.

 

One of the things I was intrigued by was a comment by Amy Wagers on GDF-11 and DNA repair. http://www.bioscienc...hit-clinic-year

If this proves to be true this might suggest that rejuvenated stem cells may not carry the cancer risk we fear. It would be interesting to see what activates the mini-chromosome maintenance helicase repair mechanism. As we grow older this process becomes sluggish to our detriment. Why, . . . is it the diminished loss of a signaling factor such as GDF-11 or are falling levels of NAD+ and reduced cellular energy levels for maintenance operations responsible? Maybe a combination of both.

 

If we can stimulate our own cellular maintenance protocols maybe we already have the toolkit within us already for self repair. It's early speculation but this would be an entirely divergent path than the SENS approach.

 

It's amazing how odd insights arise from the research. Now someone needs to prove or disprove the influence of these maintenance mechanisms. 

 

I dont think anyone will be miffed its all complementary science.

[Volcanic]

Like so many seemingly beneficial things, it's associated with cancer:

 

http://www.ncbi.nlm....pubmed/17912435

 

Unfortunately, the SENS approach to cancer is to deprive it of one of these otherwise beneficial effects, i.e., telomere lengthening. What we need, if at all possible, is something to break the link between robust growth/repair and cancer. 

 

FightAging! recently posted an article about the hydra:

 

https://www.fightagi...n-do-for-us.php

 

It seems that hydra can sexually reproduce and die, or asexually reproduce via budding while not aging so much... I can't help but wonder whether the hydra's "budding" is on par with more complex organisms' cancer.

 

 

The wear and tear model applies to things outside the cell as well.

 

Even with good healthy cells, lets say fibroblast, a degenerating extracellular matrix is prohibitive for youthful function. For example, even in young people, the turnover rate for most types o collagen and elastin is too slow and ineffective to offset the damage done by glycation; and this is in the most optimistic circumstance.  So even if the fibroblast are in good health, they are jut unable to turnover the already damage collagen much less collagen that is heavily damaged from year of glycation. 

 

Just look of the half life of collagen and elastin in the aorta, we are talking about around 70 years. 

 

Cancer may not be the only problem with robust repair; vascular and cardiac remodeling are also potentially detrimental. But the cardiac changes noted with GDF11 were positive, so maybe that's less of a concern.

[corb]

 

Unfortunately, the SENS approach to cancer is to deprive it of one of these otherwise beneficial effects, i.e., telomere lengthening. What we need, if at all possible, is something to break the link between robust growth/repair and cancer.

 

 

Cancers "hijack" most functions which typically keep us healthy. Their process of growth and repair is the same as ours just regulated differently. If the method that is used to stop their growth and repair is one that targets their growth and repair directly, it will also target our own repair mechanisms.

 

The philosophy of removing telomerase to fight cancer is basically the same as chemo, I've always felt like targeted and imunogenic treatments hold more promise, they build upon our mechanisms instead of going against them.

[Bryan_S]

Cellular RNA can template DNA repair in yeast

 

Here are 2 recent headlines in this area of aging. Research is already bearing fruit. 

 

http://phys.org/news...-dna-yeast.html

 

Key to Aging Immune System Is Discovered

http://www.ucsf.edu/...stem-discovered

 

As one person has pointed out it wont be a single thing that rejuvenates us. GDF-11 is only one prong on a multi-pronged fork, Dr. Amy Wagers at Harvard University has suggested there may be other growth differentiation factors at work. Dr. Wyss-Coray at the Stanford School of Medicine will give transfusions of blood plasma to his human subjects this October, this will throw a full array of young blood factors at their Alzheimer's subjects. Eventually "if" the animal studies are confirmed they will need to whittle down that blood factor list into something manageable that can be synthesized or work on developing drugs that promote our bodies to produce what we need.

 

So in any case we are not currently talking about whole body rejuvenation for those who have read the studies. Some of this seems to be tissue specific and in the case of some tissues there is very slow cell turnover so the accumulated damage will be difficult if not impossible to alleviate.

 

As far as cancers who at this early stage can envision a total solution. I will say from a broad general standpoint if we bolster the health, metabolism and immune system of an aging individual his or her system will be better prepared to recognize and deal with any abnormal cell development just as a younger individual does. So from this standpoint its possible we wont be significantly increasing our cancer risk. If you want to be totally sure you wont increase your cancer risk with a rejuvenation treatment the alternative is to do nothing but this may eventually lead to a naturally weakened immune system and increase your risk.

 

Damned if you do damned if you don't

 

Edited by Bryan_S, 04 September 2014 - 02:13 PM.

[pone11]

 

Like so many seemingly beneficial things, it's associated with cancer:

 

http://www.ncbi.nlm....pubmed/17912435

 

Unfortunately, the SENS approach to cancer is to deprive it of one of these otherwise beneficial effects, i.e., telomere lengthening. What we need, if at all possible, is something to break the link between robust growth/repair and cancer. 

 

 

That study says that GDF11 is found in the tumor.  The study does NOT say that GDF11 started the tumor.  The study does NOT say that introducing more GDF11 into the body would fuel the tumor.  

 

Tumors are basically immortal cells that use the body's best tools in a perverse way.  Aggressive tumors apparently use GDF11 for growth, but it remains to be seen if you inject GDF11 into a cancer patient will the tumor grow faster or not.   Italian researchers want to start human cancer trials with GDF11 soon.   See the bottom of this article in "chemotherapy aid" section:

http://www.newscient....html?full=true

 

It's important to note that the Harvard GDF11 studies showed repair to DNA, not corruption of DNA.   That strongly suggests an anti-cancer effect.   They are watching for tumor development in the animals they studied, and so far they have not seen it.

 

One outcome could be that GDF11 will be anti-cancer if you take it when you do not have cancer yet, but pro cancerous if you take it after you have cancer.    But we just don't know yet.

[pone11]

Given how remarkable some of these GDF11 studies have been, and how many research groups around the world are starting to notice the results and planning new research, I would like to know what is the legal status of GDF11 and the ability to sell it after safety is proven.

 

Is GDF11 in a similar status to a nutritional supplement because it is a naturally occurring chemical?  

 

Is it correct that no one can patent GDF11?

 

I know at least one company sells a recombinant form of it for some enormous amount of money.   But I presume that once safety is shown and sales become legal, that many labs will try to manufacture it and then it will just be pure capitalism, manufacturing efficiency, and price competition?   

 

It's worth nothing that in some of these studies Myostatin appears to perform almost equally well.   So reviewing its legal and commercial status would be worthwhile too.

 

In the Harvard studies, they are injecting GDF11 into the old mice every day, so it is at least possible that this would be something you would need to buy and inject in large quantities.  

 

But it would be oh so sweet if Big Pharma and FDA could do nothing to regulate or stop this, and the price ended up coming down to a dollar a day.   And equally sweet would be that the $1/day cure might single handedly wipe out about 1/4 of Big Pharma's market opportunity by lowering the incidence of disease significantly.

 

Edited by pone11, 13 January 2015 - 12:26 PM.

[Bryan_S]

pone11,

 

That is the dream.

 

As has been pointed out before, we have huge reserves of stem cells that we essentially leave on the table unused at death. It's believed our bodies do this in a strategy to prevent cancers.

 

Substances like GDF-11 are believed to be one arm of a treatment to increase health, countering the detrimental effects of aging. GDF-11 is a blood circulating, cell signaling protein factor. It is one of a number of cell signaling factors circulating within your body. Research is ongoing to better understand what drives these signaling protein factors. The fear is if we awaken our sleeping stem cells, will this also increase our potential for cancer? 

 

Increasing the cells ability to check for DNA errors and strengthen the immune system will be 2 other avenues for researchers to contend with. Advances in both have been made. That is why many of us are watching the NAD boosting research going on. It has the potential to increase cellular maintenance and produce a more youthful cellular environment.

 

Welcome to the LongeCity forums.

Edited by Bryan_S, 13 January 2015 - 07:39 PM.

[pone11]

That is the dream.

 

As has been pointed out before, we have huge reserves of stem cells that we essentially leave on the table unused at death. It's believed our bodies do this in a strategy to prevent cancers.

 

Substances like GDF-11 are believed to be one arm of a treatment to increase health, countering the detrimental effects of aging. GDF-11 is a blood circulating, cell signaling protein factor. It is one of a number of cell signaling factors circulating within your body. Research is ongoing to better understand what drives these signaling protein factors. The fear is if we awaken our sleeping stem cells, will this also increase our potential for cancer? 

 

Increasing the cells ability to check for DNA errors and strengthen the immune system will be 2 other avenues for researchers to contend with. Advances in both have been made. That is why many of us are watching the NAD boosting research going on. It has the potential to increase cellular maintenance and produce a more youthful cellular environment.

 

Welcome to the LongeCity forums.

 

 

This is all clear, but my question was about the legal status of GDF11.  And I'm asking what is the ability for multiple firms to manufacture it and compete on price.

 

In the end, if GDF11 by itself doubles lifespan and increases healthspan by 30% for people over 40, then we won't need to understand any other issue for it to be beneficial.   If we evaluate safety and cannot measure any increase in cancer or other diseases, understanding that bottom line is sufficient.  It would be nice to understand the mechanism, but understanding the mechanism isn't required to realize a benefit.

Edited by pone11, 13 January 2015 - 10:18 PM.

[niner]

In the end, if GDF11 by itself doubles lifespan and increases healthspan by 30% for people over 40, then we won't need to understand any other issue for it to be beneficial.   If we evaluate safety and cannot measure any increase in cancer or other diseases, understanding that bottom line is sufficient.  It would be nice to understand the mechanism, but understanding the mechanism isn't required to realize a benefit.

 

If it doubles lifespan but only increases healthspan by 30%, wouldn't that mean that people would be frail and debilitated for decades?  It doesn't matter, really, because there's no way that human lifespan is going to be doubled without dealing with a lot of other problems, like the systemic amyloidosis that kills most people over the age of 110.    I agree that the current fetish regarding mechanistic understanding is maddening when it results in good drugs languishing on the shelf.

[pone11]

 

In the end, if GDF11 by itself doubles lifespan and increases healthspan by 30% for people over 40, then we won't need to understand any other issue for it to be beneficial.   If we evaluate safety and cannot measure any increase in cancer or other diseases, understanding that bottom line is sufficient.  It would be nice to understand the mechanism, but understanding the mechanism isn't required to realize a benefit.

 

If it doubles lifespan but only increases healthspan by 30%, wouldn't that mean that people would be frail and debilitated for decades?  It doesn't matter, really, because there's no way that human lifespan is going to be doubled without dealing with a lot of other problems, like the systemic amyloidosis that kills most people over the age of 110.    I agree that the current fetish regarding mechanistic understanding is maddening when it results in good drugs languishing on the shelf.

 

 

It means that people would be 30% less debilitated and at some price point that would be a very cost effective thing for people to do.

 

It is extreme "glass half empty" thinking to demand comprehensive solutions to every health problem and social issue in order to justify taking a supplement or drug.   Why would anyone deny themselves being healthier at low cost, versus being 30% less healthy and paying just as much - or more - money to drug companies?

Edited by pone11, 14 January 2015 - 06:15 AM.