Myostatin mutant baby

[BajanBastard]

MGF actually is IGF-1...it's a splice variant of it, produced in muscle. There is also another IGF-1 splice variant expressed in muscle too. The IGF-1 that most people refer to is hepatic IGF-1 and may not have much effect on muscular growth when systemic. When injected or overexpressed in muscle though, it acts like the muscular form(s) of IGF-1. GH not only increases hepatic IGF-1, but also induces expresion of IM IGF-1. When people refer to nolva reducing serum IGF-1 levels, they fail to realize that this doesn't affect IGF-1 levels expressed within muscle.....at least from what I've seen.

when i grow up i want to be just like you..

[Pure Power]

Awesome. Sheerly amazing to me. Where do you pick up research studies on this type of information. I don't have the 10ns of thousands to go through and get my phd but I would love to read the books!
Einstein, have you yourself done any indepth research in this relm either on yourself or on another subject? Also this varient.... Have you heard anything as to how/if the tissue continues to grow even after administration. As if it became acustom to it so it just produces more? I apreciete your willingness to share the knowledge, its rare people take the time to educate others. U and all the mods/vets rock.

[ItalianMuscle]

I want to block or slow down my myostatin... I hope someone makes something to slow it down..

[einstein1905]

Awesome. Sheerly amazing to me. Where do you pick up research studies on this type of information. I don't have the 10ns of thousands to go through and get my phd but I would love to read the books!
Einstein, have you yourself done any indepth research in this relm either on yourself or on another subject? Also this varient.... Have you heard anything as to how/if the tissue continues to grow even after administration. As if it became acustom to it so it just produces more? I apreciete your willingness to share the knowledge, its rare people take the time to educate others. U and all the mods/vets rock.

Pubmed is a great site for reading up on things of this sort. The abstracts that you sift through can be kind of daunting, if you're not familiar with all the terminology, but if you actually read the full text of the papers, the introductions are usually more generalized and easy to read....and full of good info and the relevant background info.
I haven't done any physical research in the area of myostatin...just literature research.
growth won't continue without a continued source of IGF-1, and even then it's been shown that the gains plateau over time (assumedly due to limited satellite cell supply). This is yet another reason why cycling IGF-1 is a good idea. I wrote something on satellite cell regulation in the IGF-1 forum, if you're interested in that. This is all just very interesting and relevant stuff, so it's not really a chore to read about it.

[Pure Power]

I did read your stuff. That's why I value your opinion. Thanks for the tip on that website, I'm going to check it out. I wanted to swing something past you btw.
I have heard it would only take 2-3 mg of an androgen to saturate all your receptors. So in that sence taking a gram of test for ecample shouldn't show such a difference compaired to 300 mg. But they are finding when test is high growth goes up, and then so does igf and all its other counter parts. Could this be part of this phenominon? Is igf-1 the most acute anabolic substance in the body, or is there real founded research showing other even more specific growth factors or chemicals found? My ultimate goal and dream would be to be in a think lab and have info and a bank roll to supply the research, but even research done rarely goes public, so its hard to even just learn from the outside.

[einstein1905]

I did read your stuff. That's why I value your opinion. Thanks for the tip on that website, I'm going to check it out. I wanted to swing something past you btw.
I have heard it would only take 2-3 mg of an androgen to saturate all your receptors. So in that sence taking a gram of test for ecample shouldn't show such a difference compaired to 300 mg. But they are finding when test is high growth goes up, and then so does igf and all its other counter parts. Could this be part of this phenominon? Is igf-1 the most acute anabolic substance in the body, or is there real founded research showing other even more specific growth factors or chemicals found? My ultimate goal and dream would be to be in a think lab and have info and a bank roll to supply the research, but even research done rarely goes public, so its hard to even just learn from the outside.

There are so many indirect actions od AAS on anabolism, that saturating receptors (ARs) isn't the limiting factor. saturating receptors merely means that the rate of AR synthesis is slower than the rate of AAS:AR binding, due to AAS concentration, since ARs turn over at a rapid rate. By there are several nongenomic actions of AAS, not mediated by ARs. Also, conversion to estrogen potentiates several mechanisms contributing to anabolism. It's hard to say just what factors are at play that mediate growth.....we're limited by what's currently known. 10 years ago people said GH and estrogen were responsible for the majority of breast development, but now we know that it's EGF and IGF-1, acting in a paracrine manner, that are the responsible factors (or so we think). estrogen acts by increasing EGF, and GH by increasing IGF-1, depending on the tissues in question....potentially, we may find that EGF and IGF-1 work by some , yet unknown, intermediates.
It's exciting, challenging, and frustrating doing research.....you're usually wrong.....you usually fail, but when things do work out, it justifies it all, for the most part.

[BeefCakeStew]

Its all in July 2004 scientific America. The whole article is alot longer and a good read, id suggest buying it. Hopefully the post isn't too long.

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 AAVIGF- 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- 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.”

H. LEE SWEENEY is professor and chairman of physiology at the University of Pennsylvania
School of Medicine.

“Gene Doping” Scientific America, Volume 291 pg62

[bubbathegut]

stop the insanity

[einstein1905]

Its all in July 2004 scientific America. The whole article is alot longer and a good read, id suggest buying it. Hopefully the post isn't too long.

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 AAVIGF- 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- 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.”

H. LEE SWEENEY is professor and chairman of physiology at the University of Pennsylvania
School of Medicine.

“Gene Doping” Scientific America, Volume 291 pg62

Actually, the scientific american article is a summary of his recent paper. You can access all of his recent papers on pubmed....type in "sweeney" "igf-1", and that'll pull up most of them. Some may not have access to the full text articles....if you want them, email me, and I can email you pdfs.

[Pure Power]

Igf-1 also plays a huge roll in prostate cancer so I hear... Along with estrogen, actualy if u have cancer igf is just a bad idea in general from what I understand. It basicaly speeds up yhe doubling of cancer cells. Is this because cancer has satalite cells of its own? Or does cancer just divide?
Back to what I was thinking with blocking myostatin.... Would that just cause genisis skellital muscle or does it excite satalite cells and improve protein synthesis?
Have you heard anything on if blocking myostatin affects any other tissue in growth or performance? Sounds to me like it could hostipalize you with insane growth rates and likelyhood of cancer. This extra swull baby has potential for huge growth but sounds like he would burn out fast. JMO

[einstein1905]

Igf-1 also plays a huge roll in prostate cancer so I hear... Along with estrogen, actualy if u have cancer igf is just a bad idea in general from what I understand. It basicaly speeds up yhe doubling of cancer cells. Is this because cancer has satalite cells of its own? Or does cancer just divide?
Back to what I was thinking with blocking myostatin.... Would that just cause genisis skellital muscle or does it excite satalite cells and improve protein synthesis?
Have you heard anything on if blocking myostatin affects any other tissue in growth or performance? Sounds to me like it could hostipalize you with insane growth rates and likelyhood of cancer. This extra swull baby has potential for huge growth but sounds like he would burn out fast. JMO

Myostatin is a member of the TGF-beta family. TGF-beta members have all sorts of roles in the body at different developmental stages. They mainly control/inhibit growth, but they can also act as proangiogenic factors, which facilitate metastasis of cancers. It does look like myostatin is only expressed in skeletal muscle though, and the myostatin KO animals had no trend in health problems from what I've read.


IGF-1 both increases synthesis of contractile proteins within myocytes as well as causes satellite cells to fully differentiate into myocytes

IGF-1 is increased in a number of different cancers. There are many possible mechanisms for it. In breast cancer, mammary fat pads show increased expresion of IGF-1....this is likely due to interactions between actual carcinogenic cells and the neighboring stromal cells, especially since pituitary GH remains constant. IGF-1 increases the doubling rate of many different cell types, with various epithelial cells being most relevant. IGF-1 does not cause cancer....it merely is a player in the progression of an existing cancer.

[dan.19.]

does any one know if there are any pictures of this kid and where to see them

[einstein1905]

does any one know if there are any pictures of this kid and where to see them

PM Blown SC....he has pics