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Link made between genetics, aging

gdf11 genetics

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#1 Jay Jordan Hawke

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Posted 20 February 2016 - 01:15 PM


Scientists at the University of Georgia have shown that a hormone instrumental in the aging process is under genetic control, introducing a new pathway by which genetics regulates aging and disease.

Click here for full article at Science Daily.


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#2 johnross47

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Posted 20 February 2016 - 01:58 PM

has anyone tried taking it? With what effect?



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#3 Nuke

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Posted 20 February 2016 - 02:57 PM

Thanks for the new study. I have had my eye of GDF11 for a while now. Will likely start it within a year or 2, maybe combining it with GHK.

 

http://www.longecity...xogenous-gdf11/

 

 



#4 Florian Xavier

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Posted 21 February 2016 - 03:51 AM

my bullshit detector sing



#5 niner

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Posted 21 February 2016 - 04:13 AM

Florian, I think your bullshit detector might be broken.  They found that GDF11 is under genetic control.  Why does that sound like bullshit to you?



#6 corb

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Posted 21 February 2016 - 06:04 AM

Misleading title and misleading content not correlating to the actual paper in Science Daily yet again.

The actual paper talks about genetic variations in relation to GDF11 levels and lifespans. So Florian's bullshit detector was pretty much on point.

 

http://biomedgeronto...5/gerona.glv308

 

 

This study revealed high heritability of GDF11 levels. Furthermore, our correlative data suggest that GDF11 may serve as a novel predictor of mammalian life span.


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#7 niner

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Posted 21 February 2016 - 10:18 PM

Thanks corb.  Correlation with genetic background isn't exactly "control".  Science Daily made it sound like more than it was.



#8 alc

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Posted 22 February 2016 - 01:13 AM

The abstract is quite clear as their UG news release.

 

"Overall, interactions between age and genetic background determined GDF11 concentrations, which were unaffected by sex."

 

also

 

"This study revealed high heritability of GDF11 levels."

 

then states "Furthermore, ...", but the previous statements are quite clear.

 

 

 

 

http://medicalpartne...-genetics-aging

 

 

 

"Scientists in the UGA College of Family and Consumer Sciences have now discovered that levels of this hormone are determined by genetics, representing another potential mechanism by which aging is encoded in the genome."

 

"

“Finding that GDF11 levels are under genetic control is of significant interest. Since it is under genetic control, we can find the genes responsible for GDF11 levels and its changes with age,” said the study’s senior author Rob Pazdro, an assistant professor in the college’s department of foods and nutrition.

 

"

 

"

The study confirmed results from previous experiments showing that GDF11 levels decrease over time and also showed that most of the depletion occurs by middle age.

In addition, the study examined the relationship between GDF11 levels and markers of aging such as lifespan in 22 genetically diverse inbred mice strains. Of note, the strains with the highest GDF11 levels tended to live the longest. "

 

"

“Essentially, we found a missing piece of the aging/genetics puzzle,” Pazdro said. “Very generally, we’ve made an important step toward learning about aging and why we age and what are the pathways that drive it. It’s the first step down a long road, but it’s an important step.”

 

It is a simple and clear statement - nothing to interpret.

 

Down at the bottom of the page is a link to request the .pdf:

 

"A PDF of this study is available on request to schupska@uga.edu"

 

Would be nice if people will stop interpreting when there is nothing to interpret.

 

Though, I have a feeling why some people are bothered by this ... "aging is encoded in the genome" they say  ...

 

 

 

 


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#9 corb

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Posted 22 February 2016 - 04:25 AM

Would be nice if people will stop interpreting when there is nothing to interpret.

 

Considering 90% of the article was opinion rather than fact, I'd say there is much to interpret.

 


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#10 corb

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Posted 22 February 2016 - 06:35 AM

I'm just going to leave this quote from a recent Irina Conboy paper here.

 

 

GDF11 was reported to enhance old muscle repair by attenuating the accumulation of DNA damage in the aged satellite cells [36]; however, a year earlier it was published that old muscle satellite cells do not accumulate DNA damage with age and that DNA damage in muscle stem cells is uncoupled from efficiency of muscle repair and likely represents a physiologically required process of terminal myogenic lineage differentiation [15], [45]. Once again, a key paper in a lesser impact journal questioning main conclusions of a high impact paper was not cited or caught in peer or editorial review.

In apparent disagreement between two recent studies, GDF11 does [41] and does not [46] reduce hypertrophy of old mouse hearts. Even if there is no direct connection to aging, stem cells or heterochronic parabiosis, ectopic GDF11 may reduce the mass of both young and old hearts [47].

Age-specific levels of GDF11 are also not without controversy: initially, it was reported that GDF11, but not GDF8/myostatin, declines with age [41]; then more recently it was determined that GDF8/myostatin does decline with age [48], an observation which was also reconfirmed by the original Cell authors, who now combine the two protein names into one, called GFD11/8 [47].

These controversies may be caused by the fact that antibodies to GDF11 have cross-reactivity with GDF8/myostatin. GDF11 antibody might also simply cross-react with immunoglobulins, which become elevated with age [47, 49]. A very elegant recent paper using a clean myostatin knock-out system demonstrated that GDF11 levels are 500 times less than that of myostatin or activin, thus precluding any competitiveness for the same receptor complexes and arguing against physiological modulation of pSmad2/3 signaling by GDF11 when myostatin, activin or TGF-beta1 are present [48].

Muscle tissue produces myostatin, so the age-specific decline in myostatin protein may reflect the loss of muscle mass in the old. Consequentially people or mice with physiologically higher muscle mass (particularly in older age) are likely to be healthier, thus exhibiting an indirect link between the levels of myostatin and the health of the heart and other organs. Notably, GDF11 is associated with human colon cancers, which is likely due to the pro-angiogenic properties of GDF11 and most TGF-beta family ligands [50, 51]. Accordingly, Alk1 and Alk5 inhibitors are studied as anti-cancer anti-angiogenic blockers [52, 53].

 

Take it for what it is. Or don't.



#11 alc

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Posted 24 February 2016 - 03:00 AM

"Take it for what it is. Or don't."

 

As usual, you are confused.

 

Just revisit you other posts around this forum see how many time you were off target.

 

The study by UG refers to something else: "aging is encoded in the genome" (that is something that itches you, clearly).

 

Conboy's study/article is discussing something that is not contradicting the above mentioned thing.

 

When I have more time, I'll post more, but by then, you can go back and do your homework read and (try to) understand what is this about.

 

Not sure what you want: to solve aging and accept what studies says, or engage in a whishful thinking approach (just because you believe in something, and not in sonething else).

 

If you want first option, then you need to open up your mind. For second option, just stay the course.


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#12 niner

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Posted 24 February 2016 - 03:32 AM

The UG study didn't show that aging was "programmed".  It showed that GDF11 levels were correlated with lifespan and were different for animals with different genetic background.  They didn't show that aging or GDF11 levels were under direct genetic control as the article implied.  The article made too much of a correlation, and as we all know, correlation != causation.   If and when they manage to show causation, I don't think anyone here will have a problem accepting that.  They just haven't show it yet.



#13 xEva

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Posted 24 February 2016 - 05:03 AM

The UG study didn't show that aging was "programmed".  It showed that GDF11 levels were correlated with lifespan and were different for animals with different genetic background.  They didn't show that aging or GDF11 levels were under direct genetic control as the article implied.  The article made too much of a correlation, and as we all know, correlation != causation.   If and when they manage to show causation, I don't think anyone here will have a problem accepting that.  They just haven't show it yet.

 

 

I wish you held de Grey and Rae writings to the same high standard.


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#14 corb

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Posted 24 February 2016 - 05:25 AM

"Take it for what it is. Or don't."

 

As usual, you are confused.

 

Am I really the one confused?

 

 

 

The study by UG refers to something else: "aging is encoded in the genome" (that is something that itches you, clearly).

 

Yes because regardless of what you think, genetically programmed aging would be de facto irreversible. Sorry. I still have hope that life extension (in contrast to lifespan tuning which is what most genetic methods do) is doable. Maybe you don't. Maybe you lack the knowledge to comprehend how difficult it would be for our civilization at the point it is at to affect such a complex molecular program.

 

 

Conboy's study/article is discussing something that is not contradicting the above mentioned thing.

 

Conboy - which is on the forefront of parakrine rejuvenation research - is verbatim saying we have no idea how to measure GDF11 in vivo.

The scientists in this paper, they use the same technique of GDF11 measurement that everyone else uses. Otherwise the paper would have been - novel GDF11 antibody yada yada.

 

So what is it that they measured? Is it GDF11? Is it myostatin? Is it something else?

The whole notion GDF11 decreases with age comes from the observation GDF11 supplementation has some beneficial effects in old mice - which I just remembered is also questioned in the same paragraph in the Conboy paper

 

 

A very elegant recent paper using a clean myostatin knock-out system demonstrated that GDF11 levels are 500 times less than that of myostatin or activin, thus precluding any competitiveness for the same receptor complexes and arguing against physiological modulation of pSmad2/3 signaling by GDF11 when myostatin, activin or TGF-beta1 are present

But that doesn't automatically mean it decreases with age.

Myostatin inhibition has effects in both YOUNG AND OLD animals - again, beneficial. So that protein working on the same ligand doesn't seem to have an age specific effect, it's good for both young and old.

 

So now with that in mind what proof does this paper have that GDF11 decreases with age. UNDER A PROGRAM ON TOP IT OFF?

 

They looked at a couple mouse breeds. They measured "GDF11" or God knows what at this point and they made an observation. In the paper, as far as I can get out of the summary it's a tame, scientifically sound observation. Some animals have more of this stuff (THROUGHOUT LIFESPAN) - they live longer. It seems to be heritable (that observation is weaker I doubt they studied more than a single generation but whatever not important at the moment).

 

The article in science daily has much less to do with the sanity in the paper and much more in the way of hyping up potential research subsidiaries.

 

You have to learn to read these articles AND IGNORE them. You read it to get the paper. You read the paper. If the paper is good then you get hyped. In this case the paper is meh.


Edited by corb, 24 February 2016 - 05:28 AM.


#15 corb

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Posted 24 February 2016 - 05:31 AM

 

The UG study didn't show that aging was "programmed".  It showed that GDF11 levels were correlated with lifespan and were different for animals with different genetic background.  They didn't show that aging or GDF11 levels were under direct genetic control as the article implied.  The article made too much of a correlation, and as we all know, correlation != causation.   If and when they manage to show causation, I don't think anyone here will have a problem accepting that.  They just haven't show it yet.

 

 

I wish you held de Grey and Rae writings to the same high standard.

 

 

What makes you think we don't?
I definitely don't think damage repair is as easy as De Grey thinks it is.

 

The difference is, at the baseline, De Grey at least makes sure they have the technology TO MEASURE what it is they're supposed to fix. These clowns don't.

 


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#16 xEva

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Posted 24 February 2016 - 11:28 PM

 

 

The UG study didn't show that aging was "programmed".  It showed that GDF11 levels were correlated with lifespan and were different for animals with different genetic background.  They didn't show that aging or GDF11 levels were under direct genetic control as the article implied.  The article made too much of a correlation, and as we all know, correlation != causation.   If and when they manage to show causation, I don't think anyone here will have a problem accepting that.  They just haven't show it yet.

 

 

I wish you held de Grey and Rae writings to the same high standard.

 

 

What makes you think we don't?
I definitely don't think damage repair is as easy as De Grey thinks it is.

 

The difference is, at the baseline, De Grey at least makes sure they have the technology TO MEASURE what it is they're supposed to fix. These clowns don't.

 

 

Clowns? You mean the real PhDs doing real research are clowns while the "honorary PhD" and a generous sponsor to biology with his B.S. in computers engineering approach, who delivers his off the wall theoretical ideas in a funny accent and hellovah annoying intonation --on top of rather bad diction!-- all the while sporting a very eccentric beard, is not? Whatever  you say corb  :-D   


Edited by xEva, 24 February 2016 - 11:30 PM.

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#17 corb

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Posted 25 February 2016 - 12:22 AM

 

 

 

The UG study didn't show that aging was "programmed".  It showed that GDF11 levels were correlated with lifespan and were different for animals with different genetic background.  They didn't show that aging or GDF11 levels were under direct genetic control as the article implied.  The article made too much of a correlation, and as we all know, correlation != causation.   If and when they manage to show causation, I don't think anyone here will have a problem accepting that.  They just haven't show it yet.

 

 

I wish you held de Grey and Rae writings to the same high standard.

 

 

What makes you think we don't?
I definitely don't think damage repair is as easy as De Grey thinks it is.

 

The difference is, at the baseline, De Grey at least makes sure they have the technology TO MEASURE what it is they're supposed to fix. These clowns don't.

 

 

Clowns? You mean the real PhDs doing real research are clowns while the "honorary PhD" and a generous sponsor to biology with his B.S. in computers engineering approach, who delivers his off the wall theoretical ideas in a funny accent and hellovah annoying intonation --on top of rather bad diction!-- all the while sporting a very eccentric beard, is not? Whatever  you say corb  :-D   

 

 

Having a PhD doesn't stop you from being a bad scientist. And it doesn't stop you from going to the gossip magazines of the scientific community to promote how much of a bad scientist you are for all to see.

 

As for De Grey, he has enough people with PhDs in the life sciences working with him to have more than enough validity.


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#18 xEva

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Posted 25 February 2016 - 01:00 AM

 

 

 

 

I wish you held de Grey and Rae writings to the same high standard.

 

 

What makes you think we don't?
I definitely don't think damage repair is as easy as De Grey thinks it is.

 

The difference is, at the baseline, De Grey at least makes sure they have the technology TO MEASURE what it is they're supposed to fix. These clowns don't.

 

 

Clowns? You mean the real PhDs doing real research are clowns while the "honorary PhD" and a generous sponsor to biology with his B.S. in computers engineering approach, who delivers his off the wall theoretical ideas in a funny accent and hellovah annoying intonation --on top of rather bad diction!-- all the while sporting a very eccentric beard, is not? Whatever  you say corb  :-D   

 

 

Having a PhD doesn't stop you from being a bad scientist. And it doesn't stop you from going to the gossip magazines of the scientific community to promote how much of a bad scientist you are for all to see.

 

As for De Grey, he has enough people with PhDs in the life sciences working with him to have more than enough validity.

 

 

 

 I know what you mean corb!    Not having a PhD can't stop  you from buying it (though it can't buy you looove, loove  .♫ ..♪..)

 

and yeah, sure it's good that de Grey hires and supports prominent scientists. It shows he has good sense  :-D but validity -? He would have it if he positioned himself as an eccentric  mécénat that he is, not a scientist. 


Edited by xEva, 25 February 2016 - 01:01 AM.

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#19 corb

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Posted 25 February 2016 - 01:08 AM

 
I know what you mean corb!    Not having a PhD can't stop  you from buying it (though it can't buy you looove, loove  .♫ ..♪..)

and yeah, sure it's good that de Grey hires and supports prominent scientists. It shows he has good sense  [:-D]  but validity -? He would have it if he positioned himself as an eccentric  mécénat that he is, not a scientist.

 

 

 

 

De Grey has enough published articles on biogerontology which on top of it are cited by PhDs in their own papers. He does have validity.
Whether you will ever agree to that or not, that is your own problem if I have to be honest.


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#20 xEva

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Posted 25 February 2016 - 02:35 AM

 

 
I know what you mean corb!    Not having a PhD can't stop  you from buying it (though it can't buy you looove, loove  .♫ ..♪..)

and yeah, sure it's good that de Grey hires and supports prominent scientists. It shows he has good sense  [ :-D]  but validity -? He would have it if he positioned himself as an eccentric  mécénat that he is, not a scientist.

 

 

 

 

De Grey has enough published articles on biogerontology which on top of it are cited by PhDs in their own papers. He does have validity.
Whether you will ever agree to that or not, that is your own problem if I have to be honest.

 

 

 

A I take it those are non-clown PhDs?  :-D


Edited by xEva, 25 February 2016 - 02:35 AM.

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#21 corb

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Posted 25 February 2016 - 03:04 AM

 

 

 
I know what you mean corb!    Not having a PhD can't stop  you from buying it (though it can't buy you looove, loove  .♫ ..♪..)

and yeah, sure it's good that de Grey hires and supports prominent scientists. It shows he has good sense  [ :-D]  but validity -? He would have it if he positioned himself as an eccentric  mécénat that he is, not a scientist.

 

 

 

 

De Grey has enough published articles on biogerontology which on top of it are cited by PhDs in their own papers. He does have validity.
Whether you will ever agree to that or not, that is your own problem if I have to be honest.

 

 

 

A I take it those are non-clown PhDs?  :-D

 

 

If they did research, with a methodology, which is known to be erroneous, and regardless of that and to make matters more red nose worthy, ignore all the challenge that has been produced towards the original work - challenge which has remained without rebuttal for months & and furthermore (because wasting their own time was not enough) go on to make ridiculous claims in the press.

I'll give them the pointy hat myself.


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#22 alc

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Posted 29 February 2016 - 02:37 AM

"Am I really the one confused?"


 

Yes you are ... a lot ... read your (other) posts carefully ...

 

"Yes because regardless of what you think, genetically programmed aging would be de facto irreversible." ...  wow,  for this kind of "monumental" thoughts they give awards ... just do a google search and see what kind of awards they are ... lol

 

"You have to learn to read these articles AND IGNORE them. You read it to get the paper. You read the paper. If the paper is good then you get hyped. In this case the paper is meh."

 

... now, this explain why you are confused ... in your mind, the research done by labs is not to be taken in consideration, but a "question of the month" type of explanation has more clout ... lol ... when you wake up to reality, please let us know.

 

Please start a comic section here on longevity, and start posting. We'll have some (good) laughter.

 

As for these "clowns", you should ask yourself a simple question: why labs around the world (that btw, do not have any relationship to each other), keep coming up with studies that point out to something that itches (more like irritates) you (and couple other individuals) a lot?

 

As for me, I really do not care if aging is driven by a programmed or damage ... what I really care is that we make serious progress and have some real medical technology on the market, that we will all benefit ... otherwise we are all going to die ... before you post some (s----d) things, please meditate (serious) about this.

 

But at the same time, I cannot read scientific papers that point out at something, and ignore them (like you do). That is not the way we will solve aging. Comprendre?

 

Since you became very interested in Conboy's work (please note that by doing this you become a rebel, as your good friends are funding Conboy's work just to see "couple things here and there, that are not too relevant"), please look at the "intrinsic/extrinsic aging of tissue stem cell" ...

 

One more thing: Conboy's are neighbors to Thomas Rando's lab, and if you pay attention to what he said for past years, you might not like what he is suggest for aging ...

 

good luck with your posts ... meanwhile, science moves on ...

 

 

 

 


 



#23 alc

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Posted 29 February 2016 - 02:43 AM

The UG study didn't show that aging was "programmed". 

 

Where did you read this?

 

I'm just going to copy-and-paste (again) what the lead researcher said:

 

"Essentially, we found a missing piece of the aging/genetics puzzle,” Pazdro said. “Very generally, we’ve made an important step toward learning about aging and why we age and what are the pathways that drive it. It’s the first step down a long road, but it’s an important step.”

 

Please read again the last two sentences. Unless this is another a-la STAP fiasco (yes, it could be) I'll take a researcher word, versus a comment on a forum.



#24 alc

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Posted 29 February 2016 - 02:48 AM

[OT

 

One thing that I found funny, is that a group of individuals here (we kind of know who they are ... lol) put a lot of effort to vote comments that are contradicting them with "unfriendly", "disagree", "dislike", etc. ... good job guys! ... I don't even bother with those ... but the question here is: if you feel so sure about your affirmations, why you feel the pressure?]


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#25 corb

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Posted 29 February 2016 - 08:05 AM

 

"Am I really the one confused?"


 

Yes you are ... a lot ... read your (other) posts carefully ...

 

"Yes because regardless of what you think, genetically programmed aging would be de facto irreversible." ...  wow,  for this kind of "monumental" thoughts they give awards ... just do a google search and see what kind of awards they are ... lol

 

"You have to learn to read these articles AND IGNORE them. You read it to get the paper. You read the paper. If the paper is good then you get hyped. In this case the paper is meh."

 

... now, this explain why you are confused ... in your mind, the research done by labs is not to be taken in consideration, but a "question of the month" type of explanation has more clout ... lol ... when you wake up to reality, please let us know.

 

Please start a comic section here on longevity, and start posting. We'll have some (good) laughter.

 

As for these "clowns", you should ask yourself a simple question: why labs around the world (that btw, do not have any relationship to each other), keep coming up with studies that point out to something that itches (more like irritates) you (and couple other individuals) a lot?

 

As for me, I really do not care if aging is driven by a programmed or damage ... what I really care is that we make serious progress and have some real medical technology on the market, that we will all benefit ... otherwise we are all going to die ... before you post some (s----d) things, please meditate (serious) about this.

 

But at the same time, I cannot read scientific papers that point out at something, and ignore them (like you do). That is not the way we will solve aging. Comprendre?

 

Since you became very interested in Conboy's work (please note that by doing this you become a rebel, as your good friends are funding Conboy's work just to see "couple things here and there, that are not too relevant"), please look at the "intrinsic/extrinsic aging of tissue stem cell" ...

 

One more thing: Conboy's are neighbors to Thomas Rando's lab, and if you pay attention to what he said for past years, you might not like what he is suggest for aging ...

 

good luck with your posts ... meanwhile, science moves on ...

 

Science moves on .... Does it really move on?
GDF11 "research" has created a plethora of promises and zero results.

This isn't new research. It's been going on for almost as long as statins and metformin - the results for those will keep on coming out and I already have a suspicion the trend of lackluster effect on longevity will be preserved.
 

As for my interest in Conboy, it goes as far as to point out that even proponents of the idea of paracrine signaling for anti aging strongly and firmly speak against this protein and it's place in aging. Her group's research is looking at a pathway which has seen more than enough mainstream research and has produced results beyond anti-aging.

 

What I find the most amusing about this discussion is two days ago a group published a very nice paper - that they've tuned some of the assays to actually detect GDF11 to some degree - which again, makes me giggle thinking about the conclusions of the starting article that was posted here considering how incapable the assays were of detecting GDF11 when they were "moving science on".

It'd be great if you could at least comprehend exactly this is the reason why I posted the Conboy paper - to show you she's collected a good amount of papers which question the validity of any large claims about the place of GDF11 in aging and as a therapeutic option.

 

Oh yeah as for my ""monumental"" thought is not my own.

You ever wonder why Calico's staff doesn't share Aubrey's enthusiasm for short term advancement in the field? :-D

For them hard life extension is far future, and  they have one or two award winning geneticists on their staff as it happens.


Edited by corb, 29 February 2016 - 08:10 AM.

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#26 to age or not to age

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Posted 29 February 2016 - 05:23 PM

I have reviewed my filmed interview with Irina and Michael Conboy with regard to Amy Wagers' research and GDF 11.

Let me say a few things:

She and Michael are respectful.  Amy was a colleague at Stanford with regard to parabiosis techniques.

Both Michael and Irina explain - and I have heard very similar things from Brian Kennedy, Lenny Guarantee and David Sinclair in terms of

their disputes - that science keeps testing itself, and that the peer reviewing process is a good thing, Everyone believes that science rights

itself going forward.

GDF11 - Irina explains that the GDF family improves blood vessel formation and is might have a positive impact on this or that tissue.

As I said they were circumspect and at pains not to go after Amy.

However - and Irina Conboy stipulated "so far"- her research really seems to be passing the smell test (my words).  Her confidence

level is palpable.  I will publish an excerpt soon. And as an intellect, she is as impressive as anyone I have filmed and know, including Kenyon,

Guarente, Sinclair, Austad, Kennedy, you name them. She is unabashed - explaining that 'she is not a good PR type (her accent is very heavy) - that some scientists are, and that this is a very important component for turning lab advances into concrete human interventions. 

 


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#27 alc

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Posted 06 March 2016 - 01:25 AM



 

Science moves on .... Does it really move on?
GDF11 "research" has created a plethora of promises and zero results.

This isn't new research. It's been going on for almost as long as statins and metformin - the results for those will keep on coming out and I already have a suspicion the trend of lackluster effect on longevity will be preserved.
 

As for my interest in Conboy, it goes as far as to point out that even proponents of the idea of paracrine signaling for anti aging strongly and firmly speak against this protein and it's place in aging. Her group's research is looking at a pathway which has seen more than enough mainstream research and has produced results beyond anti-aging.

 

What I find the most amusing about this discussion is two days ago a group published a very nice paper - that they've tuned some of the assays to actually detect GDF11 to some degree - which again, makes me giggle thinking about the conclusions of the starting article that was posted here considering how incapable the assays were of detecting GDF11 when they were "moving science on".

It'd be great if you could at least comprehend exactly this is the reason why I posted the Conboy paper - to show you she's collected a good amount of papers which question the validity of any large claims about the place of GDF11 in aging and as a therapeutic option.

 

Oh yeah as for my ""monumental"" thought is not my own.

You ever wonder why Calico's staff doesn't share Aubrey's enthusiasm for short term advancement in the field? :-D

For them hard life extension is far future, and  they have one or two award winning geneticists on their staff as it happens.

 

 

 

 

 

 

What can we do when people are confused? ... not much ... "science moves on" on all fronts ... lol ... it's not just about  GDF 11 alone ... it is about all work around the planet on reverse aging field  (by a lot of groups) ... part of their work (I'm referring to Conboy's) is about how much and when GDF11 is anti or become pro aging ... you missed the point (again) ... and this recent study confirm that there is a genetic switch that tells when that happens ... keep being confused? ... is not about a "miracle molecure" (yes, it's not a typo, I called it molecure) that reverses aging per total  ...  do you homework before posting (a lot and all over the places).

 

We know why Calico are not enthusiast about sens' approach ... but I like you to go do some searches on the web and find out for yourself (hint: read read some of reddit discussions with cso of sens ... lol ... he himself answered things about this ) ...  I'll leave the pleasure to you to discover it ...
 


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#28 corb

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Posted 06 March 2016 - 09:06 AM

it is about all work around the planet on reverse aging field  (by a lot of groups)

 

A lot of groups are trying to slow down aging.
SENS is the only group trying to reverse it.
And that was very well displayed by the Church article you posted where he tries to redefine what the word "reversal" means and then goes on to preemptively excuse himself because he fully knows  his genetic approaches only produce impressive results in animals with lifespans lower than an year.



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#29 alc

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Posted 13 March 2016 - 02:47 PM

 

it is about all work around the planet on reverse aging field  (by a lot of groups)

 

A lot of groups are trying to slow down aging.
SENS is the only group trying to reverse it.
And that was very well displayed by the Church article you posted where he tries to redefine what the word "reversal" means and then goes on to preemptively excuse himself because he fully knows  his genetic approaches only produce impressive results in animals with lifespans lower than an year.

 

 

 ... confused again ... seems like trolling is what you do very good ... you keep repeating same mantra like your cheerleader from fa  ... by the speed you post back your comments it's clear that you do not read, neither do your homework trying to find out where things stand ... you did not bother to search the reddit archive did you? ... wake up, the world is large ... next step for you would be to open the window and look out   ... as for Church group, we will see in near future what they are doing and what the results are ... if you are sure that they are wrong, write them a letter and explain where the "truth" stands  ... lol 
 


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