BPC human trials so far have shown many positive results in treating several conditions that can affect the body. But, in general, BPC ligament healing is the main end result. But, with continued testing over time other results have been found. In this article, we look at what evidence has been confirmed from animal and human testing. This peptide also known as PLPL 10 and PLD is different from most research peptides because it extracted from the gastrointestinal protective protein.
BPC is classed as a Pentadecapeptide and is made up of 15 amino acids which come from the human gastric juice. This substance has the capability to heal wounds suffered in the human body. The fact that it has a positive effect on Angiogenesis means it can form new blood vessels and treat damaged tissues in the body.
From BPC human trials, new evidence has discovered it can help with problems associated with inflammatory bowel disease IBS and gastric ulcers. In addition data in laboratory tests and in-vivo research in humans and rodents has suggested BPC has the ability to repair bones, damaged teeth, gut, and tendons.
The testing was carried out using the peptide BPC dosage by injection subcutaneously under the skin and intramuscularly into the muscle. Experts in the medical industry have recognized BPC has the aptitude to give balance to the human gastric juice. It has shown it is effective in curing ulcers, IBS, upper and lower gut tract with no serious side effects.
To date, BPC has been shown to be safe and even beneficial at the cellular level. It is at present in testing to help treat multiple sclerosis. Due to the fact that it is proangiogenic or it promotes angiogenesis, it can increase the growth of cancer. Yet, other studies have found BPC helpful in lowering muscle wasting in cancer.
As with all new compounds BPC peptide has undergone several experimental stages and has revealed many results. Below is a list of some of the positive BPC benefits that have been logged by scientists :. As far as BPC side effects are concerned there have been no major problems reported from trials on rodents. But, some patients have experienced; dizziness, headaches, nausea, and redness from the injection. Many of these subside with use, but if symptoms persist then it is recommended to seek medical attention.The story of follistatin really began in although inadvertently with the discovery of a breed of cattle in Belgium that had excessive amounts of lean muscle tissue in conjunction with minimal levels of body fat.
For many years almost in fact nothing of note took place in regards to the development or understanding of follistatin — discovering, highlighting the effects of and understanding the myostatin molecule were to be the breakthrough elements we needed to fully appreciate precisely what follistatin was and how it functioned.
This discovery was to take even longer — not occurring until A further breakthrough discovery came in when Schuelke and colleagues documented a case of extreme myostatin deficiency occurring in a human infant.
Follistatin Gene Therapy
This case allowed us to fully appreciate precisely what physiological changes can occur in a human when myostatin presence within the system is negated. Similarly to the cattle variety previously discovered, she too was born with a severe myostatin deficiency. These tests yielded remarkable results in regards to precisely what follistatin may be capable of in a human host when used to suppress myostatin levels. History of Follistatin. The Story of Follistatin The story of follistatin really began in although inadvertently with the discovery of a breed of cattle in Belgium that had excessive amounts of lean muscle tissue in conjunction with minimal levels of body fat.
Where To Buy Follistatin. Authorized Reseller.Myostatin is a natural protein active in multiple species of animal, including us humans.
It does this to keep muscle growth in check. Most bio-chemical processes in the body have countering processes which form cycles to ensure there are no runaway reactions.
Obviously, anyone looking to build muscle would be interested in a safe way to inhibit the myostatin protein, even just a little, to allow for greater muscle growth gains. Even more advantageous to some people are the potential medical applications for treating some muscle-wasting diseases or conditions where retaining muscle mass is problematic.
Myostatin obviously has a necessary function with respect to muscle growth and regulation thereof. Myostatin inhibition in the case of the adult mice involves injection of natural or synthetic myostatin inhibitors such as Follistatin. The different methods show there are two specific periods of muscle growth development that myostatin regulates heavily.
Muscle Fiber Number has long been known to be set at the early stages of pre and post-natal development. In a very real sense, you are born with a large factor of your muscular potential already dialled in.
The contractile force generation of those fibers on the other hand is open for improvement. But before you run off and find some Follistatin — or other Myostatin inhibitor — to inject yourself with, there are some things you should know. Knocking out the myostatin gene at birth or inhibiting the protein it encodes later in life appears to positively affect muscle growth, in mice at least.
There has also been cases of human children who have been born with abnormally low myostatin activity that have highly developed muscle tissue. Basically, as toddlers, they look like miniature bodybuilders. Muscle protein synthesis is the process of building proteins which will ultimately make up the protein content of muscle fibers.
In fact, some research implies that myostatin actively triggers muscle atrophy muscle wasting when growth triggers are abnormally reduced such as during periods of extended inactivity like hospital bed rest, and chronic muscle disuse atrophy. Age-related muscle loss, aka Sarcopenia, might also be attributed to myostatin activity. The full cycle has been shown in studies by injecting mice with myostatinseeing them enter advanced muscle wastage, and then reversing it by administering one of the myostatin inhibitors e.
However, yet more research indicates that myostatin might simply be an anti-hypertrophy agent rather than the main muscle atrophy trigger. The difference is discrete but likely important. Studies investigating the effects of myostatin inhibition have shown that there is most likely a resultant increase in muscle mass, and probably through multiple biological pathways.
However, muscular development is not solely defined by size, but also strength and function. Some research highlights this in the context of myostatin by showing that knockout mice have significantly increased muscle mass but no strength increase compared to wild mice.FREAKY Results/Side Effects With YK11 HIGH DOSAGE Inject - Sarms Review
Not only were they no stronger than their wild, less massive counterparts, but when specific force was measured i. More recent research investigating myostatin inhibition following a stroke in mice contradicts the above knockout study and shows an increase in muscle mass and strength. Perhaps a more enlightening piece of scientific literature is found in the Gerontology mini-review of Myostatin and Sarcopenia age-related muscle wastage.
It appears to me that if the muscle weakness is a function of muscle mass wastage then there is a correlation between myostatin inhibition and improvements in muscle strength, largely because of the rehabilitation of muscle tissue.Although the authors are to be congratulated for performing a long and difficult study, its design could not possibly support this claim. Additionally, the publication reports a different primary outcome measure than the ClinicalTrials. Three IBM patients received unilateral quadriceps dosing and are not discussed.
Analysis of 6 patients with BMD participating in the trial was previously published in Molecular Therapy. B Hypothetical design in which 3 of the 4 interventions are controlled through blinding and use of a comparator group.
However, it is impossible for the authors to make that conclusion. Furthermore, the study did not control for placebo and related effects. Participants patients and investigators in this clinical trial were aware of the use of an intended therapeutic candidate based on cutting-edge science in an otherwise relentless progressive disease. Empirically, placebo responses in IBM are readily apparent in several published IBM double-blind randomized clinical trials, and their magnitiude may exceed that seen in the current study A.
Additionally, the analysis of the annualized 6MWT compared data from 6 patients with IBM with a post hoc chosen comparator group of 8 patients from a neuromuscular clinic and reported a p value of 0. A smaller comparator group would generally result in a larger, less significant p value. The frequency of adverse outcomes AEs data presented in the text and Table S2 is misleading.
These rates appear to be the frequency of a particular adverse event among all adverse events. This is an unprecedented method for reporting frequencies of safety data and highly misleading.
Follistatin closer to human trials
The published analysis is an unstated interim analysis at a post hoc chosen time-point. The trial is stated to have safety and efficacy endpoints at 2 years, but only 2 subjects have 6MWT data presented at 2 years in this publication.
The publication presents biomarker data comparing pre- and post-AAV-FS injection muscle biopsies interpreted as demonstrating that AAV-FS reduces muscle fibrosis and related molecular markers.
First, attribution of biomarker efficacy to AAV-FS is impossible because of trial design for reasons indicated above. Second, the injection sites, and hence the post-treatment biopsy sites located at injection sites, were purposefully selected based on magnetic resonance imaging MRI guidance as areas of reduced fibrosis.
The data simply confirm that there was less fibrosis in post-treatment muscle that was selected ahead of time to have less fibrosis. The supplemental methods indicate that, in the analysis of follistatin copy number in post-treatment muscle biopsies, subject 2 had no detectable FS DNA present.
National Center for Biotechnology InformationU. Journal List Mol Ther v. Mol Ther. Published online Sep 8. Steven A. Author information Copyright and License information Disclaimer. Greenberg: ude. This article has been cited by other articles in PMC. Open in a separate window. Acknowledgments S.
References 1.Also, Catechin is proven to have the body produce more follistatin. Tiger Fitness Inc. This product is not intended to diagnose, treat, cure, or prevent any disease. View cart. What is Follistatin and Does it Build Muscle? Follistatin is a fascinating protein that can increase muscle mass beyond natural potential by suppressing myostatin.
Scientists first identified follistatin while examining porcine re: pig follicular fluid in the ovaries. Follistatin is high in the non-essential amino acid cystine but unlike most proteins discussed in the fitness world, follistatin has carbohydrates attached to it. Another protein, follistatin-related gene FLRG acts on similar pathways as FS regarding its muscle building properties.
Increased lean tissue mass could give a bodybuilder an advantage in a competitive setting and be the differentiating factor between first and second place.
Whereas some myostatin inhibitors like Trichostatin A TSA require daily administration, increased levels of FS were observed up to 15 months after initial injection. The recent increase in attention in the science community on follistatin and other myostatin inhibitors is primarily due to the desire to find an alternative means to treat muscle disorders; the most popular current option is androgen steroids which pose a number of side-effects and long-term health risks.
At this point you might be wondering why follistatin use isn't more widespread in bodybuilders and other athletes. In the next section we will examine the current research on follistatin and whether it builds muscle mass. Does Follistatin Build Muscle? In short, follistatin does build muscle but not necessarily in humans. A number of studies support the muscle-building and anti-degenerative effects follistatin in rodents.
Unfortunately there is no formal research examining follistatin usage in human subjects but a quick Google search will yield countless amateur follistatin logs on bodybuilding and fitness forums.
Mice with suppressed myostatin had twice the muscle mass but mice with the follistatin transgene and suppressed myostatin had four times as much muscle mass compared to the control group. However, this doesn't stop bodybuilders from experimenting with this product; amateur logs online typically dose FS at one injection of micrograms mcg per day for anywhere from 10 to 30 days.
In fact, most users found the product did nothing at all. A handful of users claimed injections of FS to have miraculous effects on mass gain but if you examine their logs, FS appears to increase their appetite; some users increasing their caloric intake from to more than calories.
Any time you dramatically increase your caloric intake above your daily caloric requirement, you're going to gain weight. The users logging FS while undergoing a fat loss phase found that it didn't help to maximize fat loss or preserve muscle mass any more effectively than without using FS In conclusion, follistatin is a protein that can play a powerful role in reversing muscle loss and building new muscle mass, but given the cost and lack of research in human subjects, it's not recommended for the average or even the advanced athlete.
References 1 Rodino-Klapac, Louise R.Do you want to live a longer life in good health? Simple practices can make some difference, such as exercise or calorie restriction. But over the long haul all that really matters is progress in medicine: building new classes of therapy to repair and reverse the known root causes of aging. The sooner these treatments arrive, the more lives will be saved. Bioviva didn't succeed as originally envisaged, as a vehicle to bring human telomerase and follistatin gene therapy to the clinic; a recent article gave an outline of this history.
At the moment I think few people are working on follistatin delivery, more is the pity, and the telomerase gene therapy banner has been taken up by another group. The original volunteer test subject, Liz Parrishcontinues to perform a public service by publishing data on the outcome of her gene therapy - though I have to say that average telomere length as presently measured in sample of white blood cells is just about the least interesting of any measure one might propose to take following gene therapy with telomerase and follistatin.
Telomerase acts to lengthen telomeres, but average telomere length in immune cells is a terrible metric for age and tissue status.
Average telomere length is an outcome of the pace at which cells are created from their stem cell populations, fresh with long telomeres, and the pace at which they divide, losing a little telomere length each time. In immune cells these behaviors are highly variable, greatly influenced by many transient health and environmental circumstances that have little to do with aging.
Study after study shows immune cell telomere length to have a very poor correlation with age and age-related disease. So instead, how about metrics of stem cell activity, or immune function, for example? The rationale for telomerase gene therapy is largely that it increases stem cell activity in tissue maintenance, and since it also reduces cancer risk in miceone might suspect it is improving the ability of the immune system to destroy cancerous cells.
Average telomere length on its own is interesting, but it cannot be used to claim rejuvenation, as is done here. It is too disconnected from meaningful metrics of aging, those that are actually closely tied to function and damage. Before I underwent the therapy procedure, my white blood cell telomeres were measured in September, by SpectraCell's Texas laboratoryusing a blood sample. They were determined to be unusually short, meaning that I was aging much faster than others my age.
According to my telomeres, I was supposed to be in my mid-sixties. In Marchmy telomeres were again measured by SpectraCell. I had already started at a disadvantage, which multiplied the anticipation anxiety. Thankfully, the results exceeded all my expectations. They showed that my telomeres had been extended from an initial 6.
The gene therapies had restored my telomeres in these cells to my normal age. I hardly dared to hope there was room for improvement still.
History of Follistatin
In I went again for testing at SpectraCell. My telomeres further increased from 7. This outcome has exceeded all my expectations. First, because there have so far been no negative effects of my therapy. That is, no cancer, the alleged danger with activating the telomerase enzyme. But second, because my telomeres have continued to get longer without any additional treatment.
The same improvement was obtained following the muscle deterioration treatments: not only did my muscle mass increase after the myostatin inhibitor therapy, but continues to be robust 3 years after it took place. From pre-treatment to post treatment a growth in overall muscle mass and a reduction of intramuscular fat content was observed over a period of three years. This loss of intramuscular fat, also known as 'marbling', is associated with beneficial metabolic changes and improved musculature.
My overall body weight did not decrease during this period. As my personal experience shows, a single treatment stimulated the telomerase and the myostatin inhibitor enzymes for at least 3 years after being administered, with no adverse effect.
This can be a proof of concept that these two therapies, amply tested in animal models, are safe and efficient in humans. While telomeres extension therapy will be very useful in the future, for the moment I see it bringing only marginal improvement. Especially with Liz. What is a good news is that neither of the therapies had any adverse effects.Remember me This is not recommended for shared computers.
Sign in anonymously Don't add me to the active users list. Posted 09 December - AM. As published in the journal Science Translational Medicine, researchers at the National Children's Hospital NCH and Ohio State University have proven that blocking myostatin in monkeys will lead to skeletal muscle growth with few or no discernible negative side effects.
Myostatin is the protein that helps mammals regulate muscle building, acting as a signal for muscles to stop consuming resources and stop growing. Blocking myostatin leads to enhanced muscle strength and continuous muscle growth. You may remember Liam Hoekstra, the baby apparently born without the myostatin gene, and similarly enabled animals that have absurd strength. Using gene therapy, NCH scientists were able to get follistatin a myostatin blocker to promote phenomenal muscle growth in the quadriceps of macaque monkeys.
NCH is now working with the FDA to perform the preliminary steps necessary for a human clinical trial. We could see a superman gene therapy available in the next decade. Follistatin Gene Delivery Enhances Muscle Growth and Strength in Nonhuman Primates Abstract 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 in mice, but similar tests have not been performed in nonhuman primates.
To assess this important criterion for clinical translation, we tested an alternatively spliced form of human follistatin that affects skeletal muscle but that has only minimal effects on nonmuscle cells. When injected into the quadriceps of cynomolgus macaque monkeys, a follistatin isoform expressed from an adeno-associated virus serotype 1 vector, AAV1-FS, induced pronounced and durable increases in muscle size and strength.
Long-term expression of the transgene did not produce any abnormal changes in the morphology or function of key organs, indicating the safety of gene delivery by intramuscular injection of an AAV1 vector. Our results, together with the findings in mice, suggest that therapy with AAV1-FS may improve muscle mass and function in patients with certain degenerative muscle disorders. Community Forum Software by IP. Board Licensed to: ImmInst.
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