OK Ill bite.
Lets start, for the sake of having viable, provable data and only that included in this let agree that to support your position you need to have at least some proof. Neither an audio interview nor an article with no references will work as such. I hope we can agree to that much.
I feel like all of your data and your opinion is formed by and relies 100% on this article you keep quoting. BUt the article itself is misleading and outdated at best. And its never good to use only one source especially again one with no valid references. So from now on if your going to put up some numbers or "facts" please reference an actual study or clinical trial. This way we dont have to argue the facts.
So, with regards to Follidrones ability to reduce myostatin. You state that this is why your here so Ill address that specifically. Follidrone has epicatechin yes and epicatechin lowers myostatin. Im hoping that at this point we dont need to argue that but for the sake of having the facts present lets support that statement that follistatin lowers myopstatin and that follistatin is also anabolic apart from its ability to lower myostatin.
Follistatin=
Oral Epicatechin safely increases follistatin 250%=
"Average day 5 follistatin AUC levels were ~2.5 fold higher vs. day 1 AUC levels in the b.i.d. group. (−)-EPI was safe with no observed adverse effects"
"Antagonists of myostatin, a blood-borne negative regulator of muscle growth produced in muscle cells, have shown considerable promise for enhancing muscle mass and strength in rodent studies and could serve as potential therapeutic agents for human muscle diseases. One of the most potent of these agents, follistatin, is both safe and effective"
"Of special concern was the heart, since it is also a muscle. Careful study showed there were no cardiac implications in the monkeys, nor did autopsies reveal any changes in other organs."
"Several myostatin-binding proteins capable of regulating myostatin activity have been discovered. Follistatin is an especially robust antagonist of myostatin and has even shown muscle-enhancing effects beyond those predicted by myostatin inhibition alone"
"We therefore extended our FS344 gene transfer technology to a non-human primate, the cynomolgus macaque (Macaca fascicularis), to establish a paradigm for strengthening the quadriceps muscle that could serve as the basis for testing in patients. We report here that injection of AAV1-FS344 was well tolerated by all macaques and led to increased muscle mass and strength."
"There are several ways to suppress myostatin, but careful studies with mice show that follistatin, also a protein, seems to be the most effective. Scientists have identified the gene controlling follistatin production, allowing research on the potential control of myostatin production to move forward. A 2008 trial showed that the systematic suppression of myostatin did not appear to pose any danger to a group of muscle disease patients"
"Significant increases in strength and individual muscle weight were seen in mice that the Mendell-Kaspar team treated with follistatin."
" It was clear from casual observation and also meticulous measuring that monkeys treated with follistatin had significant gains in quadriceps size over the nontreated monkeys, and that their gain in strength was functional."
Studies have shown that it does take a bit for increased follistatin to work. 8 weeks is the sweet spot. Which is why those taking Follidrone for longer periods mention the GDA and endurance and pump first and then muscle and strength sometime around the second bottle.
"Drs. Mendell and Kaspar:No, we used Follistatin to suppress the myostatin gene in our studies.
TMA member: How long did it take before muscle growth was realized?
Drs. Mendell and Kaspar:About 8 weeks following the injection, one could noticeably see that the muscles were getting bigger."
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Your debating if we are keeping myostatin inhibited long enough-
Again Follidrone 2 is not just epicatechin. EPI has a relatively short halflife and while it is extended a bit and its absorption is increased a ton by our absorption package we dont rely on it only.
Both ecklonia cava and Flos carthami are exceptional myostatin inhibitors. Ecklonia cava, being a marine plant is not water soluble so it takes much longer to be absorbed and has about a 12 hour halflife meaning its still working at 50% after 12 hours. This is why we do 2x daily doses. If proper dosing is followed myostatin is inhibited 24 hours a day. Also keep in mind that while epi alone increases follistatin 250% the combo of EPI, Flos and ecklonia increases it and lowers myostatin a TON more than epi alone. I wouldnt for a second doubt a 500% increase in follistatin knowing that epi alone gives 250%.
"ecklonia cava has a 12 hour half life
ECE is a unique polyphenol in that it has a very long half-life in the body. This is because ECE is a marine-based polyphenol which is 40% fat-soluble. Virtually all other polyphenols are derived from land-based plants and are water-soluble. The half-life of ECE is up to 12 hours, compared to 30 minutes for water-soluble, land-based polyphenols. ECE has the ability to cross the blood-brain barrier."
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You see part of the problem with your theory that Increased follistatin doesnt increase muscle or strenth and that it causes weakened muscles is that this theory is derived from ancient studies in knockout animals. Why is this a problem? You cant compare the effects in knockout animals who never had or have myostatin to short term reductions in fully developed adults. Look at it like this if you took a man and castrated him at birth so that he could never produce male hormones like testosterone or DHT he would never hit puberty, never function sexually and likely be sickly, feeble and weak. He would never fully develop and probably remain childlike forever. Im not sure exactly what would happen but I can imagine it wouldnt be pretty. This represents the myo knockout animals. Compare this to a man whos testosterone level was, for a short period abnormally low post cycle. Yes he may feel depressed, might lose some of his cycle gains etc but shortly thereafter, when his test levels return to normal he will be perfectly fine. This, represents the man whos myostatin is reduced by a supplement after he is fully grown and developed. Its not perfect but you see that there is a vast difference in the expected effects and side effects.
Short term suppression vs knockout. All of the negative things you might hear about reduced myostatin come generally from knockout studies not short term supplementation. Short term myostatin inhibition has been shown to be perfectly safe. This includes muscles, tendons, cardiac tissue and all organs. I posted several quotes above that support this.
I also posted plenty of supporting facts regarding myostatin inhibition, specifically from increased follistatin not only increases muscle mass but also increases functional strength.
Your primary arguments are=
We cant lower myostatin long enough. Follidrone 2 does.
Its not lowered enough. The combination of EPI, ECK and Flos will certainly lower it enough to cause increases in muscle mass and strength.
The muscle tissue disappears. I dont see any evidence of this. Again the studies supporting this are decades old and on knockout animals. This doesnt directly translate.
There is something wrong with the muscle tissue and as a result it doesnt make you stronger. I posted several quotes from recent studies that prove otherwise.
REF:
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Reference 1. Kota, J. et al. Sci. Transl. Med.; published online Nov.
11, 2009; doi:10.1126/scitranslmed.3000112 | Article Contact: Brian K.
Kaspar, The Ohio State University, Columbus, Ohio e-mail:
[email protected] Contact: Jerry R. Mendell, The
Research Institute at Nationwide Children's Hospital, Columbus, Ohio
e-mail: jerry.me
