Myostatin Peptide,Could DOUBLE your MUSCLE!!

getswole

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You have to check this out,I'm gonna type a page up on this but in the meantime read this link...its a peptide that renders your myostatin producing gene Inactive,which is the gene responsible for limiting muscle cells growth...basically it limits the number of mucle cells your body is allowed to produce/However this peptide rendering the gene inactive puts your body in a state or hypertrophyand could nearly DOUBLE your muscle cells(Lean tissue)Its already been proven efective on cattle,mice,etc...supposedly its gonna be tested on human genomes...?SIGN ME THE FvCK UP!!!!
I'm gonna be watching this like a hawk...I wouldn't doubt if this can be gotten hold of...

Also already nicknamed the "Schwarzenegger gene"
This is the biggest thing I've ever heard of,Just imagine...read this link below

Big Blue
 

ReaperX

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I've heard about this before, hopefully something that alters myostatin and SARMs will eventually replace all the gear that is out there and still deliver results.
 
getswole

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I've heard about this before, hopefully something that alters myostatin and SARMs will eventually replace all the gear that is out there and still deliver results.
Its amazing...just imagine...

Theres an actuall peptide in existence,its just outrageously priced and noone seems to know the effects of it on the heart,since the heart is a muscle also...but look at those genetically mutated animals,they're gene is rendered inactive and they're hearts have no problems?

heres a sheep:
Beltex - the double muscled sheep

heres the Bull and mice:
Big Blue

and heres the dog,another bro posted earlier today:
Big Wendy the muscular whippet

Its all right here in front of us,why the hell hasn't anybody pursued this...?makes me wanna go get a biopharm degree...you think Itt Tech does a 6 wk biopharm course?LOL
 
CDB

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It's way expensive is the problem. Plus while it seems to work, and according to PA in another thread cardio risks seem minimal, no one knows the long term effects. Is the muscle maintainable at all once you come off? Who knows. The one site I know that carries the polyclonal antibodies gets two grand for a gram, and who knows how long that will last as there's little to nothing to go on for designing a cycle of the stuff.

Its amazing...just imagine...

Theres an actuall peptide in existence,its just outrageously priced and noone seems to know the effects of it on the heart,since the heart is a muscle also...but look at those genetically mutated animals,they're gene is rendered inactive and they're hearts have no problems?

heres a sheep:
http://www.beltex.co.uk/breed/index.html

heres the Bull and mice:
http://http://www.theantiagingdoctor.com/bigblue.htm

and heres the dog,another bro posted earlier today:
http://www.canada.com/victoriatimescolonist/story.html?id=67f15c17-2717-4022-bb76-1b982456e793&k=94653

Its all right here in front of us,why the hell hasn't anybody pursued this...?makes me wanna go get a biopharm degree...you think Itt Tech does a 6 wk biopharm course?LOL
 
getswole

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Ok,heres a study that showed 60% increase in lean muscle tissue in 2 weeks...

MOUSE STUDY: NEW MUSCLE-BUILDING AGENT BEATS ALL PREVIOUS ONES

The Johns Hopkins scientists who first created "mighty mice" have developed, with pharmaceutical company Wyeth and the biotechnology firm MetaMorphix, an agent that's more effective at increasing muscle mass in mice than a related potential treatment for muscular dystrophy now in clinical trials.

The new agent is a version of a cellular docking point for the muscle-limiting protein myostatin. In mice, just two weekly injections of the new agent triggered a 60 percent increase in muscle size, the researchers report in the Proceedings of the National Academy of Sciences, published online Dec. 5 and available publicly through the journal's website.

The researchers' original mighty mice, created by knocking out the gene that codes for myostatin, grew muscles twice as big as normal mice. An antibody against myostatin now in clinical trials caused mice to develop muscles 25 percent larger than those of untreated mice after five weeks or more of treatment.

The researchers' expectation is that blocking myostatin might help maintain critical muscle strength in people whose muscles are wasting due to diseases like muscular dystrophy or side effects from cancer treatment or AIDS.

"This new inhibitor of myostatin, known as ACVR2B, is very potent and gives very dramatic effects in the mice," says Se-Jin Lee, M.D., Ph.D., a professor of molecular biology and genetics in Johns Hopkins' Institute for Basic Biomedical Sciences. "Its effects were larger and faster than we've seen with any other agent, and they were even larger than we expected."

ACVR2B is the business end of a cellular docking point for the myostatin protein, and it probably works in part by mopping up myostatin so it can't exert its muscle-inhibiting influence. But the researchers' experiments also show that the new agent's extra potency stems from its ability to block more than just myostatin, says Lee.

"We don't know how many other muscle-limiting proteins there may be or which ones they are," says Lee, "but these experiments clearly show that myostatin is not the whole story."

The evidence for other players came from experiments with mighty mice themselves. Because these mice don't have any myostatin, any effects of injecting the new agent would come from its effects on other proteins, explains Lee. After five injections over four weeks, mighty mice injected with the new agent had muscles 24 percent larger than their counterparts that didn't get the new agent.

"In some ways this was supposed to be a control experiment," says Lee. "We weren't really expecting to see an effect, let alone an effect that sizeable."

In other experiments with normal female mice, weekly injections of the new agent provided the biggest effect on muscle growth after just two weeks at the highest dose given (50 milligrams per kilogram mouse weight). Depending on the muscle group analyzed, the treated mice's muscles were bigger than untreated mice by 39 percent (the gastrocnemius [calf] muscle) to 61 percent (the triceps).

After just one week, mice given a fifth of that highest dose had muscles 16 percent to 25 percent bigger than untreated mice, depending on the muscle group analyzed, and mice treated with one injection a week for two, three or four weeks continued to gain muscle mass.

But although the new agent seems quite promising, its advantage in potency also requires extra caution. "We don't know what else the new agent is affecting or whether those effects will turn out to be entirely beneficial," says Lee.

Lee says they also are conducting experiments with the mice now to see whether the effect lasts after injections cease and whether it helps a mouse model of muscular dystrophy retain enough muscle strength to prolong life.

The research was funded by grants from the National Institute of Child Health and Human Development and the National Cancer Institute and by funds from Wyeth Research and MetaMorphix Inc. The new agent was produced and first tested at Wyeth, and the inhibitor used in the current mouse studies was produced at MetaMorphix. All of the mouse studies described in this article and in the PNAS paper were conducted in Lee's laboratory at Johns Hopkins.

Authors on the report are Se-Jin Lee and Suzanne Sebald of Johns Hopkins; Lori Reed of Wyeth Exploratory Drug Safety, and Monique Davies, Stefan Girgenrath, Mary Goad, Kathy Tomkinson, Jill Wright and Neil Wolfman of Wyeth Discovery Research; Christopher Barker, Gregory Ehrmantraut, James Holmstrom and Betty Trowell of MetaMorphix Canada; Barry Gertz, Man-Shiow Jiang, Li-fang Liang, Edwin Quattlebaum and Ronald Stotish of MetaMorphix, Beltsville, Md.; Martin Matzuk of Baylor College of Medicine; and En Li of Harvard Medical School.

Myostatin was licensed by The Johns Hopkins University to MetaMorphix and sublicensed to Wyeth. Lee is entitled to a share of sales royalty received by The Johns Hopkins University from sales of this factor. The Johns Hopkins University and Lee also own MetaMorphix stock, which is subject to certain restrictions under university policy. Lee is a paid consultant to MetaMorphix. The terms of these arrangements are being managed by the university in accordance with its conflict of interest policies.
 
getswole

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Myostatin is a potent regulator of skeletal muscle. Following Dr. Se-Jin Lee’s (the scientific founder of MetaMorphix®) discovery of the myostatin protein and the gene encoding its production in 1997, he conducted controlled studies to characterize myostatin. Dr. Lee deleted the myostatin gene in mice using a technique referred to as gene “knockout,” which generated mice lacking the capability to produce the myostatin protein. Compared with their otherwise identical littermates, the knockout mice exhibited:

• Increased Muscle Mass: Knockout mice exhibited a two - to threefold
· increase in skeletal muscle mass.
• Decreased Fat Tissue: Knockout mice have 33% less body fat.
• Tissue Specificity: The myostatin protein increases skeletal muscle,
· but has no impact on cardiac or smooth muscle.
• No Abnormalities: Lifespan studies in knockout mice showed they
· had no abnormalities other than increased skeletal muscle.
• No Effect on Reproduction: knockout mice reproduced normally and,
· when bred with control mice, produced offspring with an intermediate
· increase in skeletal muscle.
• Dual Mode of Action: Knockout mice had an increase in number of
· muscle fibers (hyperplasia) as well as size of fibers (hypertrophy).
· They also had fewer and smaller fat cells.
• Broad Application Across Species: The biologically active region of the
· Myostatin gene is identical in mice, pigs, chickens, turkeys, and humans.


Reference: (Nature, May 1997)
 
getswole

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HUMAN THERAPEUTIC PROOF OF CONCEPT
Muscular dystrophy: Studies conducted by Wyeth and University of Pennsylvania School of Medicine as well as those from JHU demonstrate that abolishing myostatin activity in a line of mice that have muscular dystrophy results in increased muscle mass, size, and strength, while limiting breakdown of muscle tissue. Importantly, the diaphragm muscle shows less replacement of muscle tissue with fibroid and fatty tissue. These exciting results suggest that in addition to increased growth of muscle tissue, inhibition of myostatin may provide a slowing of the muscle degradation typically seen in this disease.
Muscle Wasting Diseases: Studies conducted by JHU demonstrated that over-expression of myostatin induces profound muscle loss analogous to that seen in human cachexia. These observations are important because it identifies myostatin as a key pharmacologic target for treating chronic muscle wasting commonly associated with cancer and AIDS as well as age-related muscle wasting called sarcopenia.

Type II diabetes : Studies conducted by Wyeth, JHU, and others have demonstrated that elimination of myostatin provides for an improved glucose regulation in diabetic mice.

Obesity: Studies by JHU, Wyeth and others have also demonstrated that deletion of myostatin results in a significant and dramatic reduction in fat mass in obese mice.

McPherron, A.C., Lee, S-J. 2002. Suppression of body fat accumulation in myostatin-deficient mice. J Clin Invest. 109 (5): 595–601.
Abstract
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If this works, and lowers in price with the necessary long term testing showing no or limited ill effects, watch out
 
getswole

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"There has been a small human trial with 15 subjects , results were 28% lean muscle mass on average over 5 weeks with dose of 1000mcg ew. We now have a finished product inhibitor of myostatin ACVR2B kits have 10 2ml vials @ 500mg/ml $1200 per kit."

This is from a "distributor." I am looking for this study as we speak.

He says one 1gm inject/wk IM. So 1 vial @ $120 per week. It is supposedly active for 21-28 days. It is an oil based inject, supposedly good for 1 year. Obviously no need for reconstitution. He claims only one factory is making this for human use & that he is currently the only distributor. Says he has sold 7 kits so far.

Above info was from nearly 2 years ago...

I'm trying not to violate any rules in my postings,mods feel free to edit as needed,thanks
 
EasyEJL

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60% in 2 weeks would so screw up tendons and ligaments it wouldnt be funny
 

ReaperX

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60% in 2 weeks would so screw up tendons and ligaments it wouldnt be funny
The biggest thing for me about gear is the heart. Virtually all the other problems associated with it are either cosmetic or not necessarly life threatening and can be corrected with enough sustained professional medical intervention.

With the heart, when you use gear if it enlarges then your SOL. The high mortality trend with WWE wrestlers makes it a scary enough proposition for me.
 
getswole

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60% in 2 weeks would so screw up tendons and ligaments it wouldnt be funny
Not for certain...joints of course would get additional stress...but for the ligaments/tissue itself should be very healthy...its not just hypertrophy as your used to with gear(increasing currect tissue size..)Its actually producing new muscle cells,thats where the growth is coming from(hyperplasma)along with some usuall hypertrophy

So joints yes...tissue..would be like blossoming new tissue,just think about that,supposedly stronger muscle tissue
 
getswole

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The biggest thing for me about gear is the heart. Virtually all the other problems associated with it are either cosmetic or not necessarly life threatening and can be corrected with enough sustained professional medical intervention.

With the heart, when you use gear if it enlarges then your SOL. The high mortality trend with WWE wrestlers makes it a scary enough proposition for me.
Thats true...but supposedly there are studies to back it up that the heart stuff isnt an issue so much...I'm trying to link to that study right now...can't find it...I will though...

Couldn't be much worse on your heart that tons of gear and a dirty diet(WWE)
 
getswole

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I believe I have seen this somewhere...oh yeah,it was the glowing stuff the HULK injected before he blew the fvck up!
 

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Thats true...but supposedly there are studies to back it up that the heart stuff isnt an issue so much...I'm trying to link to that study right now...can't find it...I will though...

Couldn't be much worse on your heart that tons of gear and a dirty diet(WWE)

Yeah I agree that is true. The guys on WWE use gear in excess and abuse the hell out of it. I find it hard to believe that they are even within 10% of being responsible using it...esp. with Benoit's case..even though he killed himself it'd be interesting to see how big his heart is.

Anyways, that is just my 2 cents. I don't really care about the cost, or legalities behind it, etc...it is just solely for me health risks that are the most intimidating.

If you find that article go ahead and post it, I'd be interested to see their findings.
 
Hank Vangut

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i can't wait until this stuff gets more mainstream.

professional sports are going to get a lot more entertaining!
 
getswole

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Heres some info on a german kid that had a semi-mutated gene,not as full on as the animals,but still very prenounced.



The German Super Baby
Superman Lives
Why he is so strong



Superman Lives

In 1999, a former professional sprinter gave birth to a bouncing baby boy in Berlin, Germany. For the past 4 years the baby boy has had a somewhat normal life - that is until researchers found out about him.

Researchers are not releasing much information and the family wishes to remain private. What they will say is that the boy is able to hold weights weighing nearly 10 pounds out to his side with his arms completely extended. Most adults have trouble doing this with half that weight. At 4 years old, the boy is extremely muscular displaying bulging calves and biceps. His muscle mass is twice that of normal 4 year old children and his fat content one half as much. He is as near a perfect specimen of man as you can possibly get.

Why he is so strong

Researchers have explained that the superhuman strength is the result of a mutated gene that is intended to restrict the production of myostatin. Myostatin, in the human body, limits the growth of muscles. In rare cases, one copy may be mutated producing extremely powerfully built people. The boys mother, father, uncle, and 3 other close relatives all have mutated copies and are know to be very muscular and extremely strong. In the boys case, it is even stranger - he has both copies of the DNA segment mutated, something scientists have never seen before. The result - a human that may grow to enormous proportions with the ability to lift extreme amounts of weight and possibly run faster than any human to date.

Researchers had already known that myostatin restricts muscle growth and knew that drugs limiting its production would produce super mice. Such super mice had been created in early 1997. Researchers are happy to report that the boy is perfectly healthy right now but fear that he may suffer heart or other ailments as he grows older.






Sources

(1) USA Today 06/24/2004
(2) MSNBC 06/24/2004
(3) AP Wire 06/24/2004
 
EasyEJL

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I tend to think the heart itself would be fine, in reading this just effects skeletal muscles...
 

ReaperX

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I tend to think the heart itself would be fine, in reading this just effects skeletal muscles...

I was talking about the heart muscle when using juice in general...not the myostatin stuff.
 
getswole

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I tend to think the heart itself would be fine, in reading this just effects skeletal muscles...
Thats what I've read...only stress is typical of being overweight in general..(carrying more lean tissue)and stress on the joints(again,typical)
 
getswole

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Gene Doping


Gene therapy for restoring muscle lost to age or disease is poised to enter the clinic, but elite athletes are eyeing it to enhance performance Can it be long before gene doping changes the nature of sport?

ATHLETES BUILD MUSCLE through intensive training. This Olympic-class rower's back displays the result of his hard work. But gene therapy could allow athletes to build more muscle, faster, and to stay strong longer without further effort.

Athletes will be going to Athens next month to take part in a tradition begun in Greece more than 2,000 years ago. As the world's finest specimens of fitness test the extreme limits of human strength, speed and agility, some of them will probably also engage in a more recent, less inspiring Olympic tradition: using performance-enhancing drugs. Despite repeated scandals, doping has become irresistible to many athletes, if only to keep pace with competitors who are doing it. Where winning is paramount, athletes will seize any opportunity to gain an extra few split seconds of speed or a small boost in endurance.
Sports authorities fear that a new form of doping will be undetectable and thus much less preventable. Treatments that regenerate muscle, increase its strength, and protect it from degradation will soon be entering human clinical trials for muscle-wasting disorders. Among these are therapies that give patients a synthetic gene, which can last for years, producing high amounts of naturally occurring muscle-building chemicals.


ADVERTISEMENT (article continues below)


This kind of gene therapy could transform the lives of the elderly and people with muscular dystrophy. Unfortunately, it is also a dream come true for an athlete bent on doping. The chemicals are indistinguishable from their natural counterparts and are only generated locally in the muscle tissue. Nothing enters the bloodstream, so officials will have nothing to detect in a blood or urine test. The World Anti-Doping Agency (WADA) has already asked scientists to help find ways to prevent gene therapy from becoming the newest means of doping. But as these treatments enter clinical trials and, eventually, widespread use, preventing athletes from gaining access to them could become impossible.


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Raising IGF-I allows us to break the connection between muscle use and its size.
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Is gene therapy going to form the basis of high-tech cheating in athletics? It is certainly possible. Will there be a time when gene therapy becomes so commonplace for disease that manipulating genes to enhance performance will become universally accepted? Perhaps. Either way, the world may be about to watch one of its last Olympic Games without genetically enhanced athletes.


THE BODY'S POWERHOUSE
Loss Leads to Gain
Research toward genetically enhancing muscle size and strength did not start out to serve the elite athlete. My own work began with observing members of my family, many of whom lived well into their 80s and 90s. Although they enjoyed generally good health, their quality of life suffered because of the weakness associated with aging. Both muscle strength and mass can decrease by as much as a third between the ages of 30 and 80.

There are actually three types of muscle in the body: smooth muscle, lining internal cavities such as the digestive tract; cardiac muscle in the heart; and skeletal muscle, the type most of us think of when we think of muscle. Skeletal muscle constitutes the largest organ of the body, and it is this type--particularly the strongest so-called fast fibers--that declines with age. With this loss of strength, losing one's balance is more likely and catching oneself before falling becomes more difficult. Once a fall causes a hip fracture or other serious injury, mobility is gone completely.



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With gene therapy poised to become a viable medical treatment, gene doping cannot be far behind.
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Skeletal muscle loss occurs with age in all mammals and probably results from a cumulative failure to repair damage caused by normal use. Intriguingly, aging-related changes in skeletal muscle resemble the functional and physical changes seen in a suite of diseases collectively known as muscular dystrophy, albeit at a much slower rate.

In the most common and most severe version of MD--Duchenne muscular dystrophy--an inherited gene mutation results in the absence of a protein called dystrophin that protects muscle fibers from injury by the force they exert during regular movement. Muscles are good at repairing themselves, although their normal regenerative mechanisms cannot keep up with the excessive rate of damage in MD. In aging muscles the rate of damage may be normal, but the repair mechanisms become less responsive. As a result, in both aging and Duchenne MD, muscle fibers die and are replaced by infiltrating fibrous tissue and fat.

in contrast, the severe skeletal muscle loss experienced by astronauts in microgravity and by patients immobilized by disability appears to be caused by a total shutdown of muscles' repair and growth mechanism at the same time apoptosis, or programmed cell death, speeds up. This phenomenon, known as disuse atrophy, is still not fully understood but makes sense from an evolutionary perspective. Skeletal muscle is metabolically expensive to maintain, so keeping a tight relation between muscle size and its activity saves energy. Skeletal muscle is exquisitely tuned to changing functional demands. Just as it withers with disuse, it grows in size, or hypertrophies, in response to repeated exertions. The increased load triggers a number of signaling pathways that lead to the addition of new cellular components within individual muscle fibers, changes in fiber type and, in extreme conditions, addition of new muscle fibers.

To be able to influence muscle growth, scientists are piecing together the molecular details of how muscle is naturally built and lost. Unlike the typical cell whose membrane contains liquid cytoplasm and a single nucleus, muscle cells are actually long cylinders, with multiple nuclei, and cytoplasm consisting of still more long tiny fibers called myofibrils. These myofibrils, in turn, are made of stacks of contractile units called sarcomeres. Collectively, their shortening produces muscle contractions, but the force they generate can damage the muscle fiber unless it is channeled outward. Dystrophin, the protein missing in Duchenne muscular dystrophy patients, conducts this energy across the muscle cell's membrane, protecting the fiber.


Yet even with dystrophin's buffering, muscle fibers are still injured by normal use. In fact, that is believed to be one way that exercise builds muscle mass and strength. microscopic tears in the fibers caused by the exertion set off a chemical alarm that triggers tissue regeneration, which in muscle does not mean production of new muscle fibers but rather repairing the outer membrane of existing fibers and plumping their interior with new myofibrils. Manufacturing this new protein requires activation of the relevant genes within the muscle cell's nuclei, and when the demand for myofibrils is great, additional nuclei are needed to bolster the muscle cell's manufacturing capacity.

PUMPING UP WITH CELLS
Local satellite cells residing outside the muscle fibers answer this call. First these muscle-specific stem cells proliferate by normal cell division, then some of their progeny fuse with the muscle fiber, contributing their nuclei to the cell. Both progrowth and antigrowth factors are involved in regulating this process. Satellite cells respond to insulinlike growth factor I, or IGF-I, by undergoing a greater number of cell divisions, whereas a different growth-regulating factor, myostatin, inhibits their proliferation.

With these mechanisms in mind, about seven years ago my group at the University of Pennsylvania, in collaboration with Nadia Rosenthal and her colleagues at Harvard University, began to assess the possibility of using IGF-I to alter muscle function. We knew that if we injected the IGF-I protein alone, it would dissipate within hours. But once a gene enters a cell, it should keep functioning for the life of that cell, and muscle fibers are very long-lived. A single dose of the IGF-I gene in elderly humans would probably last for the rest of their lives. So we turned our attention to finding a way to deliver the IGF-I gene directly to muscle tissue.


Donning New Genes
Then as now, a major obstacle to successful gene therapy was the difficulty of getting a chosen gene into the desired tissue. Like many other researchers, we selected a virus as our delivery vehicle, or vector, because viruses are skilled at smuggling genes into cells. They survive and propagate by tricking the cells of a host organism into bringing the virus inside, rather like a biological Trojan horse. Once within the nucleus of a host cell, the virus uses the cellular machinery to replicate its genes and produce proteins. Gene therapists capitalize on this ability by loading a synthetic gene into the virus and removing any genes the virus could use to cause disease or to replicate itself. We selected a tiny virus called adeno-associated virus (AAV) as our vector, in part because it infects human muscle readily but does not cause any known disease.
We modified it with a synthetic gene that would produce IGF-I only in skeletal muscle and began by trying it out in normal mice. After injecting this AAV-IGF-I combination into young mice, we saw that the muscles' overall size and the rate at which they grew were 15 to 30 percent greater than normal, even though the mice were sedentary. Further, when we injected the gene into the muscles of middle-aged mice and then allowed them to reach old age, their muscles did not get any weaker.

To further evaluate this approach and its safety, Rosenthal created mice genetically engineered to overproduce IGF-I throughout their skeletal muscle. Encouragingly, they developed normally except for having skeletal muscles that ranged from 20 to 50 percent larger than those of regular mice. As these transgenic mice aged, their muscles retained a regenerative capacity typical of younger animals. Equally important, their IGF-I levels were elevated only in the muscles, not in the bloodstream, an important distinction because high circulating levels of IGF-I can cause cardiac problems and increase cancer risk. Subsequent experiments showed that IGF-I overproduction hastens muscle repair, even in mice with a severe form of muscular dystrophy.

Raising local IGF-I production allows us to achieve a central goal of gene therapy to combat muscle-wasting diseases: breaking the close connection between muscle use and its size. Simulating the results of muscle exercise in this manner also has obvious appeal to the elite athlete. Indeed, the rate of muscle growth in young sedentary animals suggested that this treatment could also be used to genetically enhance performance of healthy muscle. Recently my laboratory worked with an exercise physiology group headed by Roger P. Farrar of the University of Texas at Austin to test this theory.
We injected AAV-IGF-I into the muscle in just one leg of each of our lab rats and then subjected the animals to an eight-week weight-training protocol. At the end of the training, the AAV-IGF-I-injected muscles had gained nearly twice as much strength as the uninjected legs in the same animals. After training stopped, the injected muscles lost strength much more slowly than the unenhanced muscle. Even in sedentary rats, AAV-IGF-I provided a 15 percent strength increase, similar to what we saw in the earlier mouse experiments.

We plan to continue our studies of IGF-I gene therapy in dogs because the golden retriever breed is susceptible to a particularly severe form of muscular dystrophy. We will also do parallel studies in healthy dogs to further test the effects and safety of inducing IGF-I overproduction. It is a potent growth and signaling factor, to which tumors also respond.

Safety concerns as well as unresolved questions about whether it is better to deliver AAV in humans through the bloodstream or by direct injection into muscle mean that approved gene therapy treatments using AAV-IGF-I could be as much as a decade away. In the shorter term, human trials of gene transfer to replace the dystrophin gene are already in planning stages, and the Muscular Dystrophy Association will soon begin a clinical trial of IGF-I injections to treat myotonic dystrophy, a condition that causes prolonged muscle contraction and, hence, damage.

A still more immediate approach to driving muscle hypertrophy may come from drugs designed to block myostatin. Precisely how myostatin inhibition builds muscle is still unclear, but myostatin seems to limit muscle growth throughout embryonic development and adult life. It acts as a brake on normal muscle growth and possibly as a promoter of atrophy when functional demands on muscle decrease. Experiments on genetically engineered mice indicate that the absence of this antigrowth factor results in considerably larger muscles because of both muscle fiber hypertrophy and hyperplasia, an excessive number of muscle fibers.


Making Muscle and More
Pharmaceutical and biotechnology companies are working on a variety of myostatin inhibitors. Initially, the possibility of producing meatier food animals piqued commercial interest. Nature has already provided examples of the effects of myostatin blockade in the Belgian Blue and Piedmontese cattle breeds, both of which have an inherited genetic mutation that produces a truncated, ineffective version of myostatin. These cattle are often called double-muscled, and their exaggerated musculature is all the more impressive because an absence of myostatin also interferes with fat deposition, giving the animals a lean, sculpted appearance.
The first myostatin-blocking drugs to have been developed are antibodies against myostatin, one of which may soon undergo clinical testing in muscular dystrophy patients. A different approach mimics the cattle mutation by creating a smaller version of myostatin, which lacks the normal molecule's signaling ability while retaining the structures that dock near satellite cells. This smaller protein, or peptide, essentially caps those docking locations, preventing myostatin from attaching to them. Injecting the peptide into mice produces skeletal muscle hypertrophy, and my colleagues and I will be attempting to create the same effect in our dog models by transferring a synthetic gene for the peptide.

Myostatin-blocking therapies also have obvious appeal to healthy people seeking rapid muscle growth. Although systemic drugs cannot target specific muscles, as gene transfer can, drugs have the benefit of easy delivery, and they can immediately be discontinued if a problem arises. On the other hand, such drugs would be relatively easy for sport regulatory agencies to detect with a blood test.


But what if athletes were to use a gene therapy approach similar to our AAV-IGF-I strategy? The product of the gene would be found just in the muscle, not in the blood or urine, and would be identical to its natural counterpart. Only a muscle biopsy could test for the presence of a particular synthetic gene or of a vector. But in the case of AAV, many people may be naturally infected with this harmless virus, so the test would not be conclusive for doping. Moreover, because most athletes would be unwilling to undergo an invasive biopsy before a competition, this type of genetic enhancement would remain virtually invisible.
And what of the safety of rapidly increasing muscle mass by 20 to 40 percent? Could an athlete sporting genetically inflated musculature exert enough force to snap his or her own bones or tendons? Probably not. We worry more about building muscle in elderly patients with bones weakened by osteoporosis. In a healthy young person, muscle growth occurring over weeks or months would give supporting skeletal elements time to grow to meet their new demands.

This safety question, however, is just one of the many that need further study in animals before these treatments can even be considered for mere enhancement of healthy humans. Nevertheless, with gene therapy poised to finally become a viable medical treatment, gene doping cannot be far behind, and overall muscle enlargement is but one way that it could be used. In sports such as sprinting, tweaking genes to convert muscle fibers to the fast type might also be desirable. For a marathoner, boosting endurance might be paramount.

Muscle is most likely to be the first tissue subject to genetic enhancement, but others could eventually follow. For example, endurance is also affected by the amount of oxygen reaching muscles. Erythropoietin is a naturally occurring protein that spurs development of oxygen-carrying red blood cells. Its synthetic form, a drug called Epoietin, or simply EPO, was developed to treat anemia but has been widely abused by athletes--most publicly by cyclists in the 1998 Tour de France. An entire team was excluded from that race when their EPO use was uncovered, yet EPO abuse in sports continues.

Gene transfer to raise erythropoietin production has already been tried in animals, with results that illustrate the potential dangers of prematurely attempting such enhancements in humans. In 1997 and 1998 scientists tried transferring synthetic erythropoietin genes into monkeys and baboons. In both experiments, the animals' red blood cell counts nearly doubled within 10 weeks, producing blood so thick that it had to be regularly diluted to keep their hearts from failing.

The technology necessary to abuse gene transfer is certainly not yet within reach of the average athlete. Still, officials in the athletic community fear that just as technically skilled individuals have turned to the manufacture and sale of so-called designer steroids, someday soon a market in genetic enhancement may emerge. Policing such abuse will be much harder than monitoring drug use, because detection will be difficult.

It is also likely, however, that in the decades to come, some of these gene therapies will be proved safe and will become available to the general population. If the time does arrive when genetic enhancement is widely used to improve quality of life, society's ethical stance on manipulating our genes will probably be much different than it is today. Sports authorities already acknowledge that muscle-regenerating therapies may be useful in helping athletes to recover from injuries.

So will we one day be engineering superathletes or simply bettering the health of the entire population with gene transfer? Even in its infancy, this technology clearly has tremendous potential to change both sports and our society. The ethical issues surrounding genetic enhancement are many and complex. But for once, we have time to discuss and debate them before the ability to use this power is upon us.
 

idunk42

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"There has been a small human trial with 15 subjects , results were 28% lean muscle mass on average over 5 weeks with dose of 1000mcg ew. We now have a finished product inhibitor of myostatin ACVR2B kits have 10 2ml vials @ 500mg/ml $1200 per kit."

This is from a "distributor." I am looking for this study as we speak.

He says one 1gm inject/wk IM. So 1 vial @ $120 per week. It is supposedly active for 21-28 days. It is an oil based inject, supposedly good for 1 year. Obviously no need for reconstitution. He claims only one factory is making this for human use & that he is currently the only distributor. Says he has sold 7 kits so far.

Above info was from nearly 2 years ago...

I'm trying not to violate any rules in my postings,mods feel free to edit as needed,thanks
I dont think this is the right stuff that is being tested now.

The stuff now is measure in the microgram and is way more expensive.

The place that CDB mentioned, recommeded .2-.5mcg per kg of bodyweight per day. So at almost 2K per g, a 15-20 day supply is all your gonna get.
 
thesinner

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I dont think this is the right stuff that is being tested now.

The stuff now is measure in the microgram and is way more expensive.

The place that CDB mentioned, recommeded .2-.5mcg per kg of bodyweight per day. So at almost 2K per g, a 15-20 day supply is all your gonna get.
Yeah, I remember reading about these actual, pharmaceutical-grade myostatin inhibitors (you know, the one's that actually work). It's gonna cost you more than my net worth to run for a reputable amount of time. Not to mention there's really not enough research out there to say for sure how safe/effective it's gonna be at the moment.

I remember the baby who was born in germany without the myostatin gene.....I think he's dead now.
 
BigVrunga

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Yes, the hearts efficiency increases during steroid use. I've read this before. It leads me to believe that you should be ok if you do mild cycles and always cycle off for a long enough period of time.
Indeed, especially considering that the study shows the heart slowly returns to normal after when you're back to baseline for a while.

bv
 
CryingEmo

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Indeed, especially considering that the study shows the heart slowly returns to normal after when you're back to baseline for a while.

bv

True story bro. This study indicates, however, close to a year is needed between cycles to return fully to normal.
 
BigVrunga

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True story bro. This study indicates, however, close to a year is needed between cycles to return fully to normal.
Good point man - I've always made it a point to take at least a year off inbetween any steroid use. Moreso because I'm overly cautious but from reading this study it seems like that's actually the way to go.

BV
 

ItsHectic

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I tend to think the heart itself would be fine, in reading this just effects skeletal muscles...
Did anyone read that whole article on the whippet?
It had normal lung and heart size, but twice the LBM it should, therefore its going to die a premature death.
 
getswole

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Did anyone read that whole article on the whippet?
It had normal lung and heart size, but twice the LBM it should, therefore its going to die a premature death.
Same situation as any form of gaining LBM....if your packing twice your normal LBM then your putting a strain on your heart regardless....doesn't matter how it got there...But through "Gene Doping" you could just get there much faster,easier,and if you think about that kind of quick gain...think how much healthier it would have to be versus the years of gear use/abuse in some cases....

Point is if your Planning on packing on some serious muscle,yes its gonna put a strain on your heart which wasn't meant to carry around a 300lb human being with a ton of LBM,but on the other hand with all that muscle think of your metabolism...you would be a calorie burning machine...it would be near impossible to get fat...I would say it would give you more flexebilty as to how clean your diet was.

Its very safe to say with all the advances being made into genetic research/development we will be seeing some crazy things happen in our lifetime..the info is out there,and there is a reason that theres millions of people against genetic tinkering,but the fact is the technology is here and getting more abundant everyday,but its studies like these that are some of the ones to catch our' attention in the bodybuilding community..Pretty much all gear was developed for medical purposes completely unrelated to Bodybuilding,mostly for the debilitating diseases such as cancer,muscular distrophy,aids wasting,etc....So to turn your head to Advances such as these would be ignorance to say the least...

As far as production of myostatin in the body and its limiting your"natural process" of max muscle tissue,Think of it like the Factory installed "Governor" in your car's computer,the one that limits your maximum mph and lets say at 120mph it cuts your fuel off to prevent possible engine damage....And then look at any race car ever built...they all started out as a "stock" factory car...but its always been auto enthusiasts that have studies the engines/mechanics and Removed those governors off the vehicles which normally could allow engine damage,but they have found many ways around the "damage" by improving certain parts/areas of the motor to allow the increased performance...Just like putting Nitrous on a car...you don't just take a stock car and hook nitrous up to it,first you have to build the engine properly to be able to handle the extra power your going to be using...otherwise your gonna straight blow that car to hell and back...And even when you do it properly,the engine still is going to have a much shorter lifespan,but its those odds of lifespan/vs increased performance that you have to weigh in and decide what is acceptable as your end result...Well our bodies are the same way...and its people using gear to try to get "swole" without having a clue or proper knowledge of its use/abuse and mixing gear with an environment where their body is in no shape whatsoever that they should even be thinking about gear use...this is where abuse spans from...in the end its our choice to make the most educated decision we can knowing the information we have taken the time to educate ourselves with ,and to not consider to entertain all aspects of technological advances being made would be to denie yourself of a possible healthier lifestayle and more productive gains.

Get Strong,Stay Strong,Live Long....:bb3:
 

ItsHectic

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Thats ****, we have a gene specificly to fight anabolism, thats like turboing a car but glueing the handbrake up.
 
CDB

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Thats ****, we have a gene specificly to fight anabolism, thats like turboing a car but glueing the handbrake up.
It's necessary to live. When we're young we need fat to develop properly, and that's a problem kids with this mutation face. Plus when we're grown muscle uses more energy to maintain than fat, which isn't too handy when you don't know where you're next meal is coming from.
 
getswole

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I agree with that,it would defenitely not be for younger users,per say...but I think the fact that you can control the dosage to limit you myostatin inhibition is gonna be the key to limiting your gains to what you think is healthy for yourself...it is defenitely not something to abuse...
 
BigVrunga

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Thats ****, we have a gene specificly to fight anabolism, thats like turboing a car but glueing the handbrake up.
Speaking strictly from an evolutionary standpoint - a 300lb human with 5% bodyfat would definitely not be able to outrun predators, and would be using much more energy to stay warm in colder climates. Not to mention the enormous emount of food you'd need to maintain that level of muscle tissue.

Maybe if the earth's gravity was a bit stronger it would be a different story:)

Bv
 
jomi822

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been following this for quite some time now. i made a couple of posts a year back concerning the subject (studies, articles, drug types) but no one seemed to be too intriqued by it. kind of died down as a "awesome, but not obtainable" subject.

as far as i know this is what we have-
monoclonal antibodies
polyclonal antibodies
two drugs being studied by the FDA
multiple cases of myostain gene inactivation in animals and one human

CDB, i know the website you are talking about that has the polyclonal antibody, and i believe it was proven to be fake.

i also heard word that some of the elite bodybuilders have been trying to get their hands on some of the FDA tested drugs (ACB3r2?) but i am not sure if it succeeded.
 
getswole

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i also heard word that some of the elite bodybuilders have been trying to get their hands on some of the FDA tested drugs (ACB3r2?) .
ACVR2B...I won't discuss details at this point,but it can be gotten hold of,thats all I will say
 
jomi822

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if you know where to get it (and we wont mention it of course), then i am sure the pros are aware of where to get it, and have done so.
 
getswole

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if you know where to get it (and we wont mention it of course), then i am sure the pros are aware of where to get it, and have done so.
Your exactly right,and I think its coming down to being a well kept secret at this point...in a top competetive environment nobody is gonna share that type of info if you think about it,especially with the general public...but we all know its safe to say at that that high in the rankings it would be hard to ignore a study like this,and when you got cash like that,it would be ignorant to rule out that "Gene Doping" is already in play...Everybody is looking for the extra edge,especially when you a top competitor,It could mean the difference between 1st,and 3rd
 
getswole

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Rare condition gives toddler super strength
Updated Wed. May. 30 2007 9:44 AM ET




Associated Press

ROOSEVELT PARK, Mich. --


Liam Hoekstra was hanging upside down by his feet when he performed an inverted sit-up, his shirt falling away to expose rippled abdominal muscles.

It was a display of raw power one might expect to see from an Olympic gymnast.

Liam is 19 months old.

But this precocious, 22-pound boy with coffee-colored skin, curly hair and washboard abs is far from a typical toddler.

"He could do the iron cross when he was 5 months old," said his adoptive mother, Dana Hoekstra of Roosevelt Park. She was referring to a difficult gymnastics move in which a male athlete suspends himself by his arms between two hanging rings, forming the shape of a cross.

"I would hold him up by his hands and he would lift himself into an iron cross. That's when we were like, 'Whoa, this is weird,'" Hoekstra said.

Liam has a rare genetic condition called myostatin-related muscle hypertrophy, or muscle enlargement. The condition promotes above-normal growth of the skeletal muscles; it doesn't affect the heart and has no known negative side effects, according to experts.

Liam has the kind of physical attributes that bodybuilders and other athletes dream about: 40 percent more muscle mass than normal, jaw-dropping strength, breathtaking quickness, a speedy metabolism and almost no body fat.

In fitness buffs' terms, the kid is ripped.

"We call him The Hulk, Hercules, the Terminator," his mother said.

Liam can run like the wind, has the agility of a cat, lifts pieces of furniture that most children his age couldn't push across a slick floor and eats like there is no tomorrow -- without gaining weight.

"He's hungry for a full meal about every hour because of his rapid metabolism," Dana Hoekstra said. "He's already eating me out of house and home."

Liam's condition is more than a medical rarity: It could help scientists unlock the secrets of muscle growth and muscle deterioration. Research on adults who share Liam's condition could lead to new treatments for debilitating ailments such as muscular dystrophy and osteoporosis.

If researchers can control how the body produces and uses myostatin, the protein could become a powerful weapon in the pharmaceutical arsenal. It also could become a hot commodity among athletes looking to gain an edge, perhaps illegally, on the competition, experts said.

For Liam, the condition has one potential drawback: Infants and toddlers need some body fat to feed brain growth and the development of the central nervous system.

Without adequate body fat, a child's growth can be stunted and the central nervous system can be impaired, said Dr. Erlund Larson, an internist at Hackley Hospital who is familiar with Liam's condition.

That Liam appears to be thriving, physically and mentally, is almost as amazing as his feats of strength. The product of a troubled mother who gave him up for adoption at birth, Liam was born with a suite of medical problems.

The fact that Liam was adopted by a physician assistant's family hundreds of miles from his birthplace -- a stable family with the knowledge and means to give him all the food, nurturing, horseplay and love he needs to thrive -- might be the most miraculous part of his story.

"God works in mysterious ways," said Neil Hoekstra, Liam's adoptive father.

Myostatin-related muscle hypertrophy was first documented in beef cattle and mice in the late 1990s, according to scientific literature.

In 1997, researchers at Johns Hopkins University Hospital in Baltimore determined that Belgian Blue cattle, an unusually muscular breed, had mutations in the gene that produces myostatin. Those scientists also produced muscular mice by deactivating the rodent version of the myostatin gene, according to scientific journals.

The first human case was documented in 2000, in a German boy, but wasn't reported in medical literature until 2004. The condition is so rare in humans that scientists don't know how many people have it, said Dr. Kathryn R. Wagner, a genetics expert at Johns Hopkins.

A genetic mutation prevents some people from producing myostatin. Those individuals can have twice the normal amount of muscle mass, according to medical literature.

In Liam's case, the myostatin his body produces is rejected by muscle cells. He and others with his condition can have up to 50 per cent more muscle mass than the average person, experts said.

The result of both types of myostatin-related muscle hypertrophy generally are the same: above average growth of skeletal muscles, incredible strength, a warp-speed metabolism and minimal body fat.

"Liam's never had any body fat," his mother said. "The only fat he has is in his cheeks."

The so-called myostatin blockade has generated tremendous interest in the bodybuilding community. Some nutritional supplements claim to block myostatin, but researchers have said the claims are not scientifically valid.

"If the myostatin protein is knocked out, muscles grow and rejuvenate much more quickly," Dr. Larson said. "It has potential for great abuse in the future as the new steroid."

For Liam's parents, the most pressing challenge is feeding the boy enough protein every day to fuel his body's high-performance motor. The wiry but muscular toddler eats six full meals per day and still struggles to gain weight.

Dr. Larson, the first physician to suspect Liam had myostatin-related muscle hypertrophy, said he was amazed by the toddler's strength.

"He was able to grab both of my hands and nearly do an iron cross," Dr. Larson said. "This is not something that happens for most men, ever, and here is this kid with this kind of power."

Larson said Liam's strength gives him a huge edge over other children, physically and in terms of self-confidence.

"When you've got that kind of power and that kind of strength, the world is open to you," Larson said. "He's agile because he's so strong -- when you've got that incredible power as a kid you're going to try a lot more things."

Liam's father, a die-hard University of Michigan fan, already is dreaming big things for his adopted son.

"I want him to be a football player. He could be the next Michael Hart," Neil Hoekstra said, referring to U-M's star running back.

Liam was born four weeks early and had a small hole in his heart. He also had eczema, enlarged kidneys, was lactose intolerant and had severe stomach reflux that made him vomit several times each day, his mother said.

No one knew then that the baby was among the few people known to have myostatin-related muscle hypertrophy.

Dana Hoekstra said her suspicion that Liam was physically different quickly intensified. Two days after he was born, Liam could stand up and support his weight if someone held his hands to provide balance, she said.

His heart and kidneys healed within a few months, but it took 18 months before he stopped throwing up daily.

Liam's muscular thighs at 5 months of age gave him the appearance of a miniature Lance Armstrong. By 8 months, Liam was doing pull-ups and, a month later, climbing up and down stairs, his mother said.

What really amazed his parents was the way Liam fell.

"When he fell backward, he would land on his butt, but he never hit his head on the ground," Dana Hoekstra said. "His stomach would tense up and he would catch himself before his head hit the ground. You could see his stomach muscles. He had a little six-pack."

Liam has given his mother a black eye and once punched a hole in the plaster wall during a tantrum. "That's called attitude," his mother said.

After a series of stunning physical exploits, Dana Hoekstra's father -- retired Muskegon attorney Darryl Cochrane -- told Dr. Larson about the boy.

"Grandparents like to brag and Darryl was bragging about how powerful this kid was," Dr. Larson said. "I had to see for myself."

Dr. Larson said Liam exhibited phenomenal strength.

"When I saw him I knew he had some condition," said Dr. Larson, who considered it "a wild longshot" that Liam could have myostatin-related muscle hypertrophy.

After Dr. Larson observed Liam, the boy's pediatrician referred the toddler to the genetics clinic at Spectrum Health in Grand Rapids. Doctors there said Liam was well below average for height, weight and head circumference.

But they noted "significant hypertrophy (enlargement) by the Hoekstras. The diagnosis: Myostatin-related muscle hypertrophy.of his leg, calf and arm muscles as well as increased strength," according to medical records provided

The doctors at Spectrum said Liam likely inherited the condition from his biological father, who was reported to be unusually strong, according to medical records.

An ultrasound performed on Liam when he was 14 months old revealed he had 40 percent more muscle than average, Dana Hoekstra said.

Liam's condition also caught the attention of Johns Hopkins researchers who were studying myostatin-related muscle hypertrophy.

A blood test determined that Liam did not have the genetic mutation that blocks all production of myostatin. Rather, he has the myostatin blockade, his mother said. His is one of roughly 100 known cases in the world, according to experts and medical literature.

Researchers at Johns Hopkins wanted to include Liam in a study of people with the condition. When they found 100 adults to participate, Liam was no longer needed. That was a relief for his parents, who did not want to subject Liam to the painful muscle biopsy that would be required of everyone in the study.

Dana Hoekstra said she was prepared to allow Liam to be part of the Johns Hopkins study if it could have led to new treatments for muscular dystrophy patients.

For now, the Hoekstras are content to let Liam lead a normal life. They have no plans to take the advice of friends who have jokingly suggested they hire an agent for Liam to line up pro sports deals or modeling contracts.

"It's great that he's going to have some extra muscle mass, but I don't want him to be viewed as some kind of freak," his mother said.

Dr. Larson said Liam shouldn't be viewed or treated differently than other children.

"He's a normal kid. He's just got that lucky twist," Dr. Larson said. "It's going to be fun to watch him grow."
 
getswole

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So as far as ACVR2B goes according to the documented studies...according to the mice study at 50mg/per 1kg(2.2lbs) body wieght in mice it was documented to produce over 60% increase in LBM in just 2 weeks at a single dose each week....of course this would be an abundant amount to administer to a 240lb human ,that would equate to over 5grams per injection per week if one was to follow the study,to follow the HIGHEST dose in the the documented procedure.Which would probably cost more than most peoples mortgage...but I don't think most would even want to entertain a gain of 60% in LBM in 2 weeks,it wouldn't be healthy....So that cuts down the required amount of antibody needed for preferable results...which could still be very expensive but very realistic at the same time,but even at the 5g price,I can think of a few who could have possibly swing that already...hmm....ummmm...Jay,Ronnie,......hmmm.....And of course the fact that there is no known test to date for usage,and possibly never will be...I guess we'll never know,not quite yet anyways...I'm not suggesting anything,I'm just saying at this point you would be ignorant to rule it out..
After all,the best secrets in any competetive environment,is best Kept a secret....
 
getswole

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Myostatin pro-peptide used to accelerate musclehealing/repair
Researchers have successfully used gene therapy to accelerate muscle regeneration in experimental animals with muscle damage, suggesting this technique may be a novel and effective approach for improving skeletal muscle healing, particularly for serious sports-related injuries.
These findings were presented at the American Society of Gene Therapy annual meeting in Baltimore recently.

Skeletal muscle injuries are the most common injuries encountered in sports medicine. Although such injuries can heal spontaneously, scar tissue formation, or fibrosis, can significantly impede this process, resulting in incomplete functional recovery. Of particular concern are top athletes, who, when injured, need to recover fully as quickly as possible.

In this study, the Pitt researchers injected mice with a gene therapy vector containing myostatin propeptide--a protein that blocks the activity of the muscle-growth inhibitor myostatin--three weeks prior to experimentally damaging the mice's skeletal muscles. Four weeks after skeletal muscle injury, the investigators observed an enhancement of muscle regeneration in the gene-therapy treated mice compared to the non-gene-therapy treated control mice. There also was significantly less fibrous scar tissue in the skeletal muscle of the gene-therapy treated mice compared to the control mice.

According to corresponding author Johnny Huard, Ph.D., the Henry J. Mankin Endowed Chair and Professor in Orthopaedic Surgery, University of Pittsburgh School of Medicine, and Director of the Stem Cell Research Center of Children's Hospital of Pittsburgh, this approach offers a significant, long-lasting method for treating serious, sports-related muscle injuries.

"Based on our previous studies, we expect that gene-therapy treated cells will continue to overproduce myostatin propeptide for at least two years. Since the remodeling phase of skeletal muscle healing is a long-term process, we believe that prolonged expression of myostatin propeptide will continue to contribute to recovery of injured skeletal muscle by inducing an increase in muscle mass and minimizing fibrosis. This could significantly reduce the amount of time an athlete needs to recover and result in a more complete recovery," he explained.
 
getswole

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Belgian Blue Bull...result of mutated myostatin genetics through the process of selective breeding...

And here is some disected muscle from anti-myostatin enhancement...
 
CDB

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CDB, i know the website you are talking about that has the polyclonal antibody, and i believe it was proven to be fake.
No ****? Those guys were fairly reliable during the ph/ps era. They were also the only ones I know of who carried hydroxy nandrolone in the decanoate injectable form.
 
getswole

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There are 2 substances and personally I wouldn't trust getting either from any type research company...All I will say is I have both of these priced from quite few different places...And I know for a fact the quality would not be of any question with a few of those,Seriously ...who even buys from the Research sites anyways?Except for the board sponsors of course;)
 

ItsHectic

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This kid is gonna be a mr. olympia and he wont even need steroids.
 

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