Super Supps...the next wave..

S

seemore

Member
There has been much buzz about myostatin blockers since we discoverred what myostatin does a few years back.

Myostatin Blocker Information

Now the pharma companies are working on a drug (FDA approval) that inhibits myostatin and this will be out on the next couple of years, but obviously this will require a script and sides might be an issue.

Then some supp companies tried to sell a seaweed extract that does bind to myostatin in vitro, but there were no in vivo studies and it didn't seem to make it through absoprtion properly.

Now there is a new approach by a biotech supp company that seems to have some scientific backing. They were able to reduce blood concentrations of myostatin by 37% and they are now doing studies to see if this translates into lean muscle mass.

It looks like it has potential at least.
 
Hmmm...I wonder if they'll be needing any volunteers...???  
rock.gif



Heck, they shoot those bulls early due to health problems? Forget that! I'd just like to feel good again.
 
Well we aren't disabling the myostatin gene completely, in fact far from it, there was a 37% reduction in plasma mysostatin. So we won't get the effects of the bull. They are now testing to see if this translates into significant muscle gains and it just might you know.
 
From what I gather, this has little if any potential to "bodybuilders"

A person from BR was involved in the trials.
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">A person from BR was involved in the trials.</div>
What is BR?
 
This thing is being developed in order to help with disorders, so I doubt there will be much carryover into bodybuilding. But... you never know.
 
bodyrecomposition.com

Doesnt appear to do much in adults,

steroids are cheaper, better and actually have 50+ years of safety information behind them.
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">This thing is being developed in order to help with disorders, so I doubt there will be much carryover into bodybuilding.  But... you never know. </div>

Steroids today are manufactured under the guise of treating medical conditions. That is their real use and then they cross over to the black world. It will be no different with these. Gene doping is already happening after crossing over from treating leigitmate diseases.

what was the deal with the bodycomposition website I didn't find anything on myostatin blockers.

<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">steroids are cheaper, better and actually have 50+ years of safety information behind them.</div>

Erythropoietin (EPO), human growth hormone (hGH),
insulin-like growth factor-1 (IGF-1), peroxisome proliferatoractivated
receptor-delta (PPAR &amp;#948;), and myostatin inhibitor
genes have been identified as primary targets for doping

The article continues....

Is there an urgent need to detect gene doping?
The fact that detection of gene doping represents a top
priority for sport organizations is justified by a number of
factors: (1) potential to tremendously enhance athletic
performance, (2) successful gene doping of animals, and (3)
potential health risks. The extreme appeal of gene doping as
the ultimate performance enhancement method so far is
practically undisputed. The documented effectiveness of
gene doping is evident by several animal trials

So it would seem there is potential there.

Their potency also has the potential to be far greater. The early animal trials have been out of this world, incredible lean gains with no special diet or any resistance training, simply by reducing plasma mysostatin concentrations.
 
<div>
(seemore @ Aug. 01 2007,21:16)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">So it would seem there is potential there.

Their potency also has the potential to be far greater. The early animal trials have been out of this world, incredible lean gains with no special diet or any resistance training, simply by reducing plasma mysostatin concentrations.</div>
Unfortunately not all humans are rats


The animal stuff is cool, but to quote one guy who has trialed it


<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">It is very weak. Lacks potency, must be taken at around the gram mark, intravenously for practical purposes due to volume, and is still not particularly effective in people who don't suffer from dystrophic problems.

Any other effective compound of any relevant class is stronger.

Except for a perhaps a few other avenues of attacking the issue (which some companies are exploring), it is basically a dead end.</div>
 
Where's that from and which drug/supp?

I think we are talking about different things...WADA (world doping) have indentified myostatin gene doping as an ideal performance target. It is hoped that myostatin suppressors will have a similar effect seeing as they'll reduce plasma myostatin.
 
<div>
(seemore @ Aug. 03 2007,01:18)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Where's that from and which drug/supp?

I think we are talking about different things...WADA (world doping) have indentified myostatin gene doping as an ideal performance target. It is hoped that myostatin suppressors will have a similar effect seeing as they'll reduce plasma myostatin.</div>
Just becuase they have identified it does not make the ability to do so viable.

The drug in question is a myostatin inhibitor/binder.



<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Splinter is.</div>

Splinter was the pet rat of Hamato Yoshi.

Wooot!!! TMNT
 
<div>
(seemore @ Jul. 31 2007,08:38)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Well we aren't disabling the myostatin gene completely, in fact far from it, there was a 37% reduction in plasma mysostatin. So we won't get the effects of the bull. They are now testing to see if this translates into significant muscle gains and it just might you know.</div>
1. What's with the &quot;WE&quot; statement are you a promoter or primary researcher involved in the supplement? NOt to discredit you or anything like that but was just curious if you are directly involved.

2. A recent study shows that chronic training already reduced myostatin mRNA by some 70% (contrary to ealrier reports by Willoughby), so it's known that myostatin production reductions are part of the resistance training response do you believe this supplement would be additive too the already observed response?

3. What other possible effects are seen with any of the other MRF's ie. MyoD, Myogenin, Activin Receptors, FLRG among others?
 
If the plasma blood binders class doesn't work then the gene doping will certianly inactivate the myostatin gene, and this can already be setup quite easily. In fact gene doping has probably already happened according to WADA.

1. Well I am also a scientist in training so I use the term &quot;we&quot; as in: the world of journal articles that &quot;we&quot; see...

2. Yes it would most likely  have an additive effect, as follistatin is an endogenous chemical (our body makes it during development) and it binds to myostatin with a high affinity, so it will grab whatever myostatin is left in our plasma.

MRF regulation


Here's some of the initial research...there are 9 other papers in the process fo being published and a mass training one in the pipeline also (the make or break study). So far everything looks positive at least.

ABSORPTION PROFILE AND HORMONAL INFLUENCES OF FERTILIZED EGG YOLK INGESTION IN THE HUMAN

Journal of the American College of Nutrition
Volume 25, Number 5, October 2006
Colker, C. Peak Wellness, Inc. Greenwich, CT
Fertile egg yolks contain significant concentrations of follistatin. In an effort to identify whether this orally ingested source of naturally occurring follistatin is actually absorbed and pharmacokinetically active in the human model, this study was undertaken.

A male subject was chosen because the normal baseline male physiology does not regularly contain any measurable concentration of follistatin. Follistatin-rich fertile egg yolk powder properly processed to preserve active follistatin (Folstaxan) was obtained (Celldyne Biopharma, San Antonio, TX). After initial blood draw and subsequential oral Folstaxan dosing, serum follistatin levels were qualitatively and quantitatively measured as an indicator of absorption. In addition, since we know follistatin is a negative modulator of myostatin, serum myostatin levels were qualitatively and quantitatively measured as an indication of hormonal influence and thus true pharmacokinetic activity. Testing utilized purchased follistatin and myostatin standardized for verification. Confirmations were run by ELISA and quantitations by Liquid Chromatography Tandem Mass Spectrometer with third degree fragmentation (Expertox, Deer Park, TX).

Results showed as predicted, a zero level of follistatin at baseline with a myostatin level of 46 pg/ml, 12 hours after Folstaxan dosing. Serum follistatin measured 57.1 pg/ml with a decline of myostatin to 34 pg/m1, 24 hours after the initial dosing, follistatin levels began to predictably drop from the time of initial dosing to 11.4 pg/ml. Yet myostatin continued to decline slightly with a 24-hour level of 31 pg/ml. These results clearly indicate that a fertile egg yolk powder properly processed to preserve active follistatin, when orally ingested, results in detectable serum follistatin. Furthermore, this resultant follistatin presence has significant pharmacokinetic activity is shown by the hormonal down regulation of serum follistatin.

Follistatin complexes Myostatin and antagonises Myostatin-mediated inhibition of myogenesis.

Amthor H, Nicholas G, McKinnell I, Kemp CF, Sharma M, Kambadur R, Patel K
Department of Veterinary Basic Sciences, Royal Veterinary College, London NW1 OTU, UK.


Follistatin is known to antagonise the function of several members of the TGF-beta family of secreted signalling factors, including Myostatin, the most powerful inhibitor of muscle growth characterised to date. In this study, we compare the expression of Myostatin and Follistatin during chick development and show that they are expressed in the vicinity or in overlapping domains to suggest possible interaction during muscle development. We performed yeast and mammalian two-hybrid studies and show that Myostatin and Follistatin interact directly. We further show that single modules of the Follistatin protein cannot associate with Myostatin suggesting that the entire protein is required for the interaction. We analysed the interaction kinetics of the two proteins and found that Follistatin binds Myostatin with a high affinity of 5.84 x 10(-10) M. We next tested whether Follistatin suppresses Myostatin activity during muscle development. We confirmed our previous observation that treatment of chick limb buds with Myostatin results in a severe decrease in the expression of two key myogenic regulatory genes Pax-3 and MyoD. However, in the presence of Follistatin, the Myostatin-mediated inhibition of Pax-3 and MyoD expression is blocked. We additionally show that Myostatin inhibits terminal differentiation of muscle cells in high-density cell cultures of limb mesenchyme (micromass) and that Follistatin rescues muscle differentiation in a concentration-dependent manner. In summary, our data suggest that Follistatin antagonises Myostatin by direct protein interaction, which prevents Myostatin from executing its inhibitory effect on muscle development.

Dev. Biol. (2004)
PMID: 15136138

3. As far as side-effects, it looks like playing around with these growth regulators would be far less damaging than roids....no sultana nuts, erection problems, over stressed kidneys (blood, even if you have never seen a red tint there still be traces of blood in there). It wouldn't be a silver bullet but it has potential.

They thought cancer might be a problem as there is less regulation of cell division, but there was a study that quashed those concerns.
 
3. I wasn't specifically asking about sides, I am wondering what the implications are with normal endogenous production, binding, of other MRFs.

Even in the abstract you posted they note a drop in endogenous serum follistatin via downregulation of production. This could have specific effects and has this been measured to see what happens to production once supplementation stops.

Lastly it still isn't shown that this increase in serum binding has any significant impact on muscle growth in healthy populations. See Bamman MM, Petrella JK, Kim JS, Mayhew DL and Cross JM. Cluster Analysis Tests the Importance of Myogenic Gene Expression During Myofiber Hypertrophy in Humans. J Appl Physiol, 2007 and their follow up LOAD-MEDIATED DOWN-REGULATION OF MYOSTATIN mRNA IS NOT SUFFICIENT TO PROMOTE MYOFIBER HYPERTROPHY IN HUMANS: A CLUSTER ANALYSIS Jeong-su Kim, John K Petrella, James M Cross, and Marcas M Bamman, Articles in PresS. J Appl Physiol (August 2, 2007).
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Lastly it still isn't shown that this increase in serum binding has any significant impact on muscle growth in healthy populations.</div>

Yes this is true, I was just posting this as a new possiblity...we'll see in the next few years what happens...there was one study that found top bodybuilders were overrepresented in myostatin gene deficiencies (some more deficient than others). So myostatin gene doping will be a certified winner if the binders come up short.

http://www.superhumanradio.com/press/promo04282007qt.htm

here's an interview with the company, I'll stop posting now as things are probably going to go downhill from here. Remember nothing gained nothing lost, discussion is a good thing.

Dan you seem like a knowledgable guy, what was your opinion of humanafcort-a?
 
Do you mean humanofort? The stuff from chicken egg whites?

If so I don't know much about it except it's derived from the egg white and supposedly helps reduce cholesterol but I'm not really a supplement kinda guy. Unless it's T, Protein, Creatine or EFA I find most of them useless. Although I'm still holding promise in SARMs, but we'll see.
 
<div>
(seemore @ Aug. 07 2007,02:45)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">there was one study that found top bodybuilders were overrepresented in myostatin gene deficiencies (some more deficient than others).</div>
I cannot say I care to keep track of this stuff, do you have a link to the actual paper

<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">
http://www.superhumanradio.com/press/promo04282007qt.htm

here's an interview with the company</div>

the article talks about a publication, that you also mention above, in the Journal of the American College of Nutrition, Volume 25, Number 5, October 2006

However, when I go to the JACN and look at Volume 25, issue 5, october 2006, I cant see the reference in question.
Doing a google search for the exact title comes up with the manufacturers webpage as the only hit, and if I spread out the search a bit more I get more bbing site hits, but nothing of interest.

A pubmed search on the title gets me nothing, and opening that to &quot;follistatin egg&quot; strategy with limits around humans gets me nothing of interest.

Do you have a link to the actual paper/conference presentation?
 
You must log in or register to reply here.
Back
Top