4 replies to this topic

[Rocket]

www.abc.net.au/news/2016-05-04/newcastle-scientist-discovering-healing-power-blood-protein/7383726

[alc]

You can invite to this discussion an individual from this forum ... he is a sens troll and small oracle at the same time ... lol ... he knows everything and anything before happens ... lol ... he created a discussion to convince that gdf11 gives up the throne of rejuvenation ... maybe right now he is hard editing his previous posts to cosmeticize them ... lol

 

 

and now seriously: there is a lot of evidence in this area of research, and we can pull a lot of meaningful data from parabiois for the groups like us that are interested (can I use the word "obsessed") in rejuvenation. Seems like there is a lot of good things coming out recently, indicating a lot of potential. For sure not the totally rejuvenation, we all dream about, but still will have a huge impact.

 

So the mini-Oracles and trolls should stop posting continuously same ss, and let the science move on. That way we can get to some results soon, instead of keep beating the bushes.

 

Thank you.

 

[corb]

You can invite to this discussion an individual from this forum ... he is a sens troll and small oracle at the same time ... lol ... he knows everything and anything before happens ... lol ... he created a discussion to convince that gdf11 gives up the throne of rejuvenation ... maybe right now he is hard editing his previous posts to cosmeticize them ... lol

 

 

and now seriously: there is a lot of evidence in this area of research, and we can pull a lot of meaningful data from parabiois for the groups like us that are interested (can I use the word "obsessed") in rejuvenation. Seems like there is a lot of good things coming out recently, indicating a lot of potential. For sure not the totally rejuvenation, we all dream about, but still will have a huge impact.

 

So the mini-Oracles and trolls should stop posting continuously same ss, and let the science move on. That way we can get to some results soon, instead of keep beating the bushes.

 

Thank you.

 

alc, the only troll is you.
What I posted was a paper penned by one of the most prominent scientists in the field. The titles was the one she had chosen for the paper.
If you want to call Irina Conboy a troll feel free to do it, her emails are public.

As for GDF11 I can post more than one paper questioning it's efficacy and most of them are not opinion pieces done by undergrads but papers done by whole teams with decades of accumulated work in the field. By the way, as the time goes on the more papers being published are ones questioning the original reports.

 

 

 

Here you go. Last 3 months.

 

 

This  “Controversies  in  Cardiovascular  Research”  article  evaluates  the  evidence  for  and  against  the 
hypothesis that the circulating blood level of growth differentiation factor 11 (GDF11) decreases in old age and
that  restoring  normal  GDF11  levels  in  old  animals  rejuvenates  their  skeletal  muscle  and  reverses  pathological 
cardiac hypertrophy and cardiac dysfunction. Studies supporting the original GDF11 hypothesis in skeletal and
cardiac muscle have not been validated by several independent groups. These new studies have either found no
effects of restoring normal GDF11 levels on cardiac structure and function or have shown that increasing GDF11
or its closely related family member growth differentiation factor 8 actually impairs skeletal muscle repair in old
animals.  One  possible  explanation  for  what  seems  to  be  mutually  exclusive  findings  is  that  the  original  reagent 
used to measure GDF11 levels also detected many other molecules so that age-dependent changes in GDF11 are
still not well known. The more important issue is whether increasing blood [GDF11] repairs old skeletal muscle
and reverses age-related cardiac pathologies. There are substantial new and existing data showing that GDF8/11
can exacerbate rather than rejuvenate skeletal muscle injury in old animals. There is also new evidence disputing
the idea that there is pathological hypertrophy in old C57bl6 mice and that GDF11 therapy can reverse cardiac
pathologies.  Finally,  high  [GDF11]  causes  reductions  in  body  and  heart  weight  in  both  young  and  old  animals, 
suggestive  of  a  cachexia  effect.  Our  conclusion  is  that  elevating  blood  levels  of  GDF11  in  the  aged  might  cause 
more harm than good.
(
Circ Res
. 2016;118:1143-1150. DOI: 10.1161/CIRCRESAHA.116.307962.)

 

Another one.

 

Summary

Recent high-profile studies report GDF11 to be a key circulating ‘anti-aging’ factor. However, a screen of extracellular proteins attempting to identify factors with ‘anti-aging’ phenotypes in aged murine skeletal muscle satellite cells did not identify GDF11 activity. We have been unable to confirm the reported activity of GDF11, similar to other laboratories offering conflicting data and describe our attempts to do so in this short take.

http://onlinelibrary... inconvenience.

 

The closest I've seen to a new paper saying GDF11 is in any way good or useful is the one done by the original Walker group and even they are not so blindly enthusiastic about it to say this is as clean cut a topic as you would like to think it is

 

Effect of GDF11 Supplementation on Cardiac
Hypertrophy
Our studies published in 2013
24
and 2015
111
reported an anti-
hypertrophic  effect  of  rGDF11  administration  by  comparing 
heart  weight/tibia  length  ratio  in  treated  and  control  aging 
mice, whereas the study by Smith et al
110
reported no effects
on  the  heart.  As  discussed  above,  this  disagreement  may  re-
late  to  dose-dependent  effects  of  rGDF11  on  cardiac  mass, 
but  it  is  also  important  to  emphasize  that  Smith  et  al
110
  did 
not observe changes in body weight in rGDF11 injected mice,
whereas we reported a significant decrease in body weight in

aging  mice  with  exogenous  rGDF11.
111
  Observations  from 
our  laboratories  indicate  that  exogenous  rGDF11  decreases 
body weight in old mice in a dose-dependent manner (unpub-
lished data and studies by Sinha et al,
24
and Poggioli et al
111
).
Although rGDF11 directly activates SMAD signaling in car
-
diomyocytes,
111
it is also possible that the reduction in cardiac
size  with  exogenous  rGDF11  in  vivo  is  because  of  an  indi-
rect  effect  of  rGDF11.  A  systemic  signal,  possibly  initiated 
by a reduction in body size or a change in a specific tissue, is
plausible. For example, there is a clear evidence for cross talk
between  adipose  tissue  and  cardiac
166,167
  and  skeletal
139,168,169
tissues. Thus, any interpretation of a direct effect of rGDF11
on  the  myocardium  must  be  considered  in  the  context  of  its 
systemic effects.
In conclusion, GDF11 has emerged as an intriguing can-
didate  in  the  regulation  of  vertebrate  aging  and  considerable 
progress has been made in the analysis of its role in the pro-
gression  of  age-associated  disease.  Future  investigation  of 
GDF11  and  myostatin  biology  and  biochemistry  will  clarify 
the similarities and differences in the functions of these pro-
teins and advance our understanding of organismal aging and
disease.

 

Strange how the "trolls" in the medical community got activated one by one, huh.
I guess they all want to troll you personally.

 

You're hilarious. And a bit pitiable.

I had decided not to involve myself with this topic but I guess it's better that I do than to let disinfo blossom on a forum which should have rational stances on medical science.

[alc]

(OT but funny] - thanks for turning yourself in ... lol ...you fell into the trap immediately, because the troll cannot resist the temptation for posting on every subject ... lol ... logic is what fails you first, then the troll attitude that result in weak understanding in many subjects ... keep trying though (meanwhile, science moves on).

[pleb]

Corbs not a troll he's simply applying an amount of scepticism just playing devils advocate based on other reports he's read.
Wagers original study may be correct and the second group may have misidentified the protein (gdf8 and another) as wagers has since stated. But the second group are still sticking by their testing results. But time will tell who's correct.

Edited by pleb, 02 June 2016 - 07:34 AM.