Clinical Study Breakthrough
By Carlon M. Colker, M.D., FACN
There has been a litany of drama and deception that has surrounded my attempts to come to market with Folstaxantm, the first legitimate natural myostatin inhibitor in the form of a dietary supplement. It is also the story of MYO-T12tm, which is the amazing product that came out of my continued perseverance on the project. This is my accounting as best and as honestly as I can write about it.
As far as a background understanding, in only the last approximate decade of scientific study has research finally unlocked the true key to muscle growth. It's not testosterone. It's not growth hormone. It's something much, much more powerful. The essence of massive muscle growth is not about hormonally stimulating the most muscle production. In fact, we've been wrong all along. It's about countering the force that gets in the way of uninhibited extreme muscle growth. The presence of myostatin (then called "growth and differentiation factor 8" or "GDF-8") has been identified as the force responsible for inhibiting the growth of extreme amounts of muscle. In other words it is the primary cause responsible for limiting muscle growth despite slaving away in the gym for years.
Myostatin is a protein produced by a specific gene sequence in the DNA of nearly every vertebrate animal. It works very early in the embryo and during later development to modulate muscle growth by inhibition. Animals and people that naturally lack the gene needed to produce myostatin are otherwise healthy yet are well muscled. Those same individuals with a little bit of training gain slabs of muscle. It has been theorized that this vestigial control over muscle gains was needed to prevent an organism from being overly muscled and thus fall more easily to predation either because they were too bulky to speed away or because they just looked more delicious. So through Darwinian selection, having little or no myostatin has become exceedingly rare among animals and humans. Nevertheless those rare survivors live normal, happy, albeit well-muscled lives. As an example, one needs to look no further than the Belgian Blue bull and the Piedmontese breeds which are born without the gene to produce myostatin. These animals do not seem adversely effected by the absence of myostatin. The same is true for humans.
The pharmaceutical industry is hard at work developing vaccines to knock out natural production of myostatin. While vaccines have been developed and preliminarily tested, a shroud of secrecy surrounds their progress. All we know for sure is that everything seems to have stalled. Preliminary research looks sketchy from a safety standpoint so already some early initiatives have been abandoned. Rumors are circulating regarding the safety of these vaccines linked to the possibility that, by completely blocking myostatin rather than just lowering it, they may pose health dangers. These drugs operate immunologically by having an actual antibody attack the body's own myostatin. Sound scary? Well, you may not be alone. If it didn't give those companies and the FDA pauses for thought, we might have seen one on the market by now.
So where does that leave us? Are there other myostatin inhibitors that don't operate like vaccines? The answer is, yes.
In 2005 I discovered a natural substance known to inhibit myostatin found in significant levels in standard store-bought fertilized chicken eggs (Journal of the American College of Nutrition, Volume 25, No. 5; Abstract 65; October 2006). This was astounding to me because it is right there in our food supply. Farmers eat fertile eggs all the time. In fact, I've been going to the organic market and buying them for years without fully realizing their hidden power. The beauty of these eggs is that they are 100% natural and believed by the USDA to be no better or worse for you than standard store-bought eggs! But what truly separate regular eggs from fertile eggs are about 20,000 cells barely visible to the naked eye. These cells produce at least one myostatin inhibitor that we know about. These inhibitors are released in steps from the membrane into the yolk to promote early embryo development and growth. These substances are consumed and disappear in a matter of days after incubation.
So while there was no question that the fertilized egg has within it a dietary source of natural myostatin inhibitors, the problem then became one of trying to figure out how to get enough. In other words, how many eggs can you stuff in without going to the poor house, living in the bathroom, and gaining too much fat from the calories? Trying to eat all those fertile eggs is not practical, either physiologically, economically, or gastronomically!
Shortly thereafter I contracted a biopharma company out of San Antonio, Texas called Celldyne Biopharma, LLC to help me develop the process and move closer to a commercially viable product. The joining of forces seemed logical because of their representations that they had relationships with hatcheries and extensive knowledge in their affiliate fields of vaccine production and FDA compliance. At the time, they also told me that they specialized in antibodies and recombinant proteins for metabolic diseases. With their assistance I was able to generate a desiccated fertile egg powder that maintained active myostatin inhibition (not an easy task by any measure).
So in the next step furthering this research, in 2006 I demonstrated that myostatin inhibition from fertile eggs is biologically active (Journal of the American College of Nutrition, Volume 25, No. 5; Abstract 66; October 2006). I undertook the study in an effort to identify whether this orally ingested source was actually absorbed and pharmaco-kinetically active in the human model. I set out to prove that, not only does one of the orally ingested active ingredients increase, but it also significantly reduces serum myostatin levels. Celldyne produced a first generation of fertile egg yolk powder properly processed to preserve activity. This first generation version was called Folstaxantm. After initial blood draw and subsequent oral Folstaxantm dosing, serum levels were qualitatively and quantitatively measured as an indicator of absorption and hormonal influence.
The results showed a baseline myostatin level of 46pg/ml. In the following 12 hours after Folstaxan™ administration myostatin declined with a 24 hour level of 31pg/ml.
These results clearly indicated that Folstaxantm, when orally ingested, significantly down-regulating myostatin. These results were peer reviewed and published (Colker C, Absorption profile and hormonal influences of fertile egg yolk ingestion in the human. 2006 Annual Meeting of the American College of Nutrition and abstract publication in Journal of the American College of Nutrition, Volume 25, No.5, Abstract 66; October 2006).
To be objective, the product intake was far too bulky and we did not have a precise measurement of the initial bolus. Add to that, it was only in one subject. So we needed to further refine the product and then go ahead and test it more precisely in a larger sample population. In August of 2008 we performed a study on a more refined and debulked version of the product. Using this product, at a significantly lower serving size of only 20 grams in a one-time serving, the study was undertaken in seven male subjects. In this case I was strictly interested in myostatin levels as an indicator of true pharmacokinetic activity. Serum myostatin levels were tested at baseline, 12 hours, and 24 hours. Results showed an average baseline myostatin level of 27pg/ml; 12 hours after ingestion, average serum myostatin declined to 24.43pg/ml; Average serum myostatin continued to decline with a 24 hour level of 23.86pg/ml. Though two out of the seven tested were non-responders, the mean change overall in myostatin among the subjects went down by -11.32% in 24 hours. These results were peer reviewed and published (Colker C, Effect of Debulked Fertile Egg Yolk Ingestion On Serum Myostatin Levels. Reviewed and accepted for poster presentation at the 2008 Conference on Post-Translational Modification: Detection and Physiological Evaluation for the American Society for Biochemistry and Molecular Biology; Category: Unusual Modifications; Abstract 10; October 2008).
The results were very exciting because it represented a major reduction in myostatin. In a 2001 published study from Johns Hopkins University, as little as a 20% reduction in serum myostatin results in a very significant increase in muscle mass. So while we were hoping for at least a 20% decrease in this larger group, we at least knew we were on the right track.
Saying that what came next took me by surprise is an understatement. My involvement with Celldyne would be a mistake I would live to regret. In dealing with Celldyne I counted on their representations that they were not a dietary supplement company and instead were purely pharmaceutical. I actually took solace in this. Their President and CEO, Rick Green III said they were a subdivision of "big-pharma" companies named TEKSA and INCELL. He said they were experienced in immune-hormonal medicine and had relationships with large hatcheries in Mexico. Looking back at the time I thought, since I have been criticized by some for having worked so closely with dietary supplement companies which was an industry that according to some was sketchy and untrustworthy, this new pharma relationship was supposed to be a step up. All this could not have been further from the truth. The fact is I never had a dietary supplement company try and steal one of my ideas, file a fraudulent patent application on my invention, and then try and squeeze me out completely!
Getting back to the story, while things were moving along beautifully with research and development, Celldyne started pulling back on the project crying poverty and being increasingly more difficult to communicate with. At one point they were completely non-responsive. It was total radio silence. This came as a shock at the time since research and development had been progressing. So what was their problem? Had they really given up on me and my invention? Hardly, it turned out they were actually quite busy secretly filing a bogus patent on my project with the USPTO claiming that Rick Green and his grandfather were the sole inventors and not me! In addition Celldyne put up a Folstaxantm website and attempted to sell their product to the public with no permission whatsoever from me. Again all this is going on without my direct knowledge or consent. The fact is that although we had good product for research purposes, we simply were not even near having a product ready for public consumption. The product they finally decided to shove in a canister and hawk to the public was vastly inferior in terms of quality and content. In fact I had verified the concentration by analysis and it came out worse than our data for whole yolk controls! Also it was clumpy and insoluble, smelled terrible, and tasted even worse (something Rick alluded to in a company email later brought out in discovery). Add to that this company, again without my knowledge or consent put the product out into the marketplace with no expiration date on the label and no bacterial testing that I ever saw! As far as I know it could have been a jar full of salmonella! To add insult to injury, they did this all while putting my name on the label!
So basically I had no choice but to file suit against them in Connecticut federal court. I think it took them by surprise because my guess is they were counting on me just disappearing. After two days of intense arguments in front of United States District Court Judge Alvin W. Thompson, in a huge decision that granted me a preliminary injunction against them, he ruled completely in my favor. They were forced to stop selling the product they were holding out as Folstaxantm and shut down their website. In fact the testimony was so convincing that the judge, without my team even asking, actually broadened the preliminary injunction to further protect my interests and further restrain Celldyne and the Greens. Eventually we settled the law suit before it went to trial, where I would have creamed them. They ended up making me a lump sum cash payment along with handing back over the patent control, Folstaxantm name and trademark, all notes and files, and a few other stipulations. All in all, truth prevailed in the end, but it was not an experience I would care to relive.
In the mean time I was determined to not waste anymore time so I was already busy on my own independently developing and producing a desiccated fertile egg yolk product that preserved the yolk membrane and accompanying blastodisc. Although this time I was focused other factors in the blastodisc that were working to reduce myostatin in a far greater way the active component originally thought to be the target. The idea was to preserve as much biologic activity as possible as I set out to create an even better product.
Equipped with the prerequisite knowledge that at least one biologically active factor hated heat and was inactivated by it, I found out that Celldyne's method of irradiating the eggs was a very poor idea for a number of reasons. It turned out that this method first and foremost was and is not accepted by the FDA as an adequate way of pasteurizing a dietary supplement. In particular, salmonella is a major concern among experts because irradiation may not eradicate it at all! Add to that, in our own experiments we found out that irradiation destabilizes the yolk membrane (the location of the blastodisc), thus creating a messy slurry of egg white and yolk. As a result a consistently clean separation between yolk and white was not possible, thus reducing the potential concentration of actives. This explained why the Folstaxantm product was yellow-white in color and not the bright yellow color of a yolk, which it should be if properly handled. Finally irradiation is still heat producing and may have inactivated much of the remaining active factors. Then there was the issue of centrifuging (another method chosen by Celldyne to debulk). This simply added more harshness to the handling of the product and thus created more of a mess, serving only to reduce the active levels even further.
After establishing a carefully selected group of procedures and proprietary sequence of steps, including a new way of pasteurizing not previously available to us, my new "high grade handling" method was set to be tested. Using one active as a barometer to measure the concentration of available cofactors, in February of 2009 our sample was 3rd party tested and found to have a potency 6.45 times Celldyne's version of Folstaxantm! Also we tested everything for pathogens including salmonella and it all checked out perfectly.
After some solubility work and light flavoring, it was time to put the product to the test and see if it really was inhibiting myostatin better than the old Folstaxantm product. The study took place in April of 2009. Recall that the results of a prior study on Folstaxantm produced an average reduction of serum myostatin at 24 hours of 11.32% in seven subjects ingesting 20 grams of product, with two non-responders. In contrast, my latest generation of product would be tested in ten healthy adult male human subjects while only administering only a single 10 gram serving size (half the amount given to subjects in the last study). This study was undertaken to test the hypothesis of whether my high-grade handling method eliminated the need for irradiation and centrifuging thus creating a more highly effective product at a much lower serving size. After baseline myostatin testing, subjects received a single serving bolus of only ten grams. Results showed an average baseline myostatin level of 27.5pg/ml, which was consistent with the last study since it seems that generally speaking men ages 20-55 have serum myostatin levels at or around 30pg/ml. But then in dramatic fashion something extraordinary happened at between 12-18 hours after dosing. The average serum myostatin declined to 12.6pg/ml with every subject responding positively! This was a staggering 46% drop in myostatin from baseline across all ten subjects! Add to that, unlike the previous study done on the old Folstaxantm where 2 out of the seven subjects were non-responders, here all ten subjects responded. Finally, at the 24-30 hour time point with a mean value of 28.1pg/ml, the average myostatin level completely normalized.
As a result of this study, I finally had the results that proved once and for all that my new method of high-grade handling was more effective than anything seen to date. It was so far beyond anything I ever did with Celldyne that I could not have been happier. Upon careful study of the data, it was the dramatic drop in myostatin at 12 hours that just bowled me over, and so was born the name MYO-T12tm (a name I chose to underscore the effectiveness at the 12 hour point). Of course I should point out that I was equally pleased with the complete normalization of myostatin levels in test subjects after 24 hours. In this way it's nice to know that, should you decide to not take a subsequent serving of the product, you can expect your levels to return to what they were within a matter of hours. Keep in mind that this was in sharp contrast to the pharmacokinetic drug action of the vaccines that were developed and abandoned by the pharmaceutical industry in part because of the effect of the drugs on completely and irreversibly shutting down myostatin production.
This study was and is landmark. Because it proved naturally occurring follistatin not only occurs in our food supply, but when properly handled in the form of MYO-T12tm, can in fact reduce myostatin levels. This is achieved without blocking it completely with potentially harmful vaccine antibodies that the drug companies are trying to develop. The most recent research also proved that levels in the subjects not having taken any subsequent servings of product completely normalized their myostatin levels within a maximum of 30 hours.
All this taken together, my hope is that MYO-T12tm emerges as the single most powerful approach to building massive muscles in otherwise healthy male subjects. In fact, I feel it's a more powerful approach than testosterone, growth hormone, or anything else I have seen.
For some time MYO-T12tm was made available through my dear friends at Prosource. But It seemed I'd bit off more than I could chew because the demand for the product way out-stripped the supply. As an understandable result, with people waiting patiently for product, Prosource elected to honorably refund money when appropriate and step away from future distribution, effectively handing the reigns back to me. They were wonderful through the entire process because I don't think anyone could have anticipated the enormity of the excitement around this product and the resultant onslaught of orders.
Fortunately, supply is catching up to demand as now all orders are being filled through the website www.myot12.com.
So that's my story. It's the truth as best as I can tell it. It's been about a decade of hard work, research, pain, disappointments, lawyers, lawsuits, lamenting, and ultimately success with vindication. In closing my deepest appreciation to those readers and consumers who have followed the story, shared in my aggravation and disappointments, waited patiently for product, and never stopped believing in me and my work. I love you all.
