IGF-1 Applied to Bodybuilding
Here I will post indepth articles I have found that are very informative and fairly accurate
The IGF1 Hype
There is a considerable amount of hype surrounding IGF1. Every one is blaming the distended bellies of modern Bodybuilders on it. Also the freaky proportions that old bodybuilders that have been around for years are starting to attain. Anti-aging proponents are touting it as the miracle cure for every thing from Parkinson's disease to Alzheimer's. And the medical community has published numerous articles on it for its ability to cause cancer, diabetes and gigantism. While at the same time performing documented experiments on thousands of patients of muscle wasting diseases. And reporting significant turnabouts in there conditions. So what is a guy to think about IGF1 as far as athletic enhancement is concerned? Well first of all you need to know that most experiments conducted with IGF1 do not list the type of IGF used. I have written Dr. Robert Saline of the Swedish rejuvenation institute on several occasions and we have had in-depth discussions on the subject of IGF1 for physical appearance enhancement. He feels it would be unethical to prescribe IGF1 to a bodybuilder to increase muscle mass simply due to the fact that IGF1 has valid applications in the medical community, (Like I could give a rats ass about "ethical"). He can not argue that it is extremely effective as a promoter of muscle growth far beyond what androgens (steroids) alone can offer. Well fortunately in America IGF1 is not a drug (yet) and the FDA has no control over it as of now. This will change in the very near future however, Im absolutely sure of it.
How to use IGF1
What users report
Users of IGF1 have reported various results but all along the same lines, It does not appear to be dramatically less effective in any one individual (at least not to the best of my knowledge). I have a good friend who had to stop taking IGF1 due to stomach illness that was completely unrelated But he to experienced good gains from it for the 2 weeks he was on it, his dosage was 120mcg per day. One hour after the first injection he went to the gym and immediately told me about the uncontrollable pump he got from just one set.
That would indicate to me that he was experiencing some form of cell volumization. The general consensus on IGF1 seems to be that its benefits are as fallow:
Increased Pump Pumps are reported to be so severe that workouts are often cut short due to lack of ability to the muscle through the full range of motion...ouch
Gains retention is increased if IGF is used in a cycle I am not sure why, but IGF1 seems to make gains on a cycle stick with virtually no post cycle loss. Every bodybuilder I've spoken with seems to think this for some reason. Most of them use drugs like Anadrol or Dianabol with it because of the amount of size attained with these drugs. The usual draw back to these drugs is that in most users there is a post cycle "crash" that occurs, so the reasoning is to toss IGF1 into the stack and grow larger faster with out the post cycle crash blues.
Reverses testicular atrophy
Testicles if shrunken will return to "full swing" so to speak even in the middle of a cycle. If not shrunken they will not shrink during the cycle. This may explain partially why gains are kept after the cycle.
Fatigue
Users report feeling drained and tired all day. This seems to be one of the negative side effects to IGF1, it will make you sleep longer and you will require more sleep at night to feel rested for the morning. This is common with high doses of human growth hormone - somatropin - and exhibited in children, whose IGF1 levels are extraordinarily high. A child needs 4 hours more sleep than an adult on average does. This may be directly or indirectly related to IGF1 levels.
Stiffness
An almost arthritic feeling is commonly associated with high levels of human growth hormone - somatropin - , well IGF1 has the exact same property. IGF1 will cause your hands, fingers and knuckles to ache this is one way you can be sure you got real IGF1.
IGF-1's Side effects
Every thing has a down side. To bake a cake ya gotta brake an egg. IGF1 is no exception. The drug used in larger quantity around the 100mcg+ range will cause headaches, occasional nausea and can contribute to low blood sugar or hypoglycemia in some users. Although I have never heard of this first hand I'm sure its true.
IGF1 will attach its self to the lining of the intestine and cause atrophy of the gut. Every thing IGF1 touches will grow and you have a lot of receptors on the lining of the large intestine and inner wall of the abdominal well. This is what causes the gh - growth hormone (somatropin) - gut look. You can easily avoid this by limiting your dosages and cycle lengths. IGF1 cycles should be kept to 4-6 weeks with 4-6 weeks off in-between. IGF-1 is considerably more powerful than human growth hormone - somatropin - and you need to think of it along those lines as far as dosing goes. We all know what to much HGH can do over prolonged periods of usage. The Neanderthal look is definitely not going to win any shows this year. I would recommend 80 mcg a day for 4 weeks at a time you should get good results from that for a while. I don't know if you will need to up the dosage at any point, but I would think in the case of IGF1 it wouldn't matter. If 80mcg doesn't do it for ya, then bump it up to 100 You should definitely feel it at this point If not suspect the IGF1 as being fake. Beyond 120 mcg per day your asking for trouble, This compound demands as much respect as its sister amino Insulin.
Clinical Facts about IGF-1
IGF-1 is a polypeptide of 70 amino acids (7650 daltons), and is one of a number of related insulin-like growth factors present in the circulation. The molecule shows approximately 50% sequence homology with proinsulin and has a number of biological activities similar to insulin. IGF-1 is a mediator of longitudinal growth in humans or how tall you are capable of becoming. Serum IGF-1 concentrations are altered by age, nutritional status, body composition, and growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For the diagnosis of acromegaly, a single IGF-1 concentration is more reliable than a random human growth hormone - somatropin - measurement (Oppizi, et al., 1986). IGF-1 can be used for the assessment of disease activity in acromegaly (Barkan, et al., 198.
Almost all (>95%) of serum IGF-1 circulates bound to specific IGF binding proteins (IGFBPs), of which six classes (IGFBPs 1-6) have been identified (Rudd, 1991). BP3 is thought to be the major binding protein of IGF-1.
Summary:
Although the mechanisms underlying age associated muscle loss are not entirely understood, researchers attempted to moderate the loss by increasing the regenerative capacity of muscle. This involved the injection of a recombinant adeno-associated virus directing overexpression of insulin-like growth factor I (IGF-I) in differentiated muscle fibers.
They demonstrated that the IGF-I expression promotes an average increase of 15% in muscle mass and a 14% increase in strength in young adult mice (Figure 1), and remarkably, prevents aging-related muscle changes in old adult mice, resulting in a 27% increase in strength as compared with uninjected old muscles (Figure 2). Muscle mass and fiber type distributions were maintained at levels similar to those in young adults. These results suggest that gene transfer of IGF-I into muscle could form the basis of a human gene therapy for preventing the loss of muscle function associated with aging and may be of benefit in diseases where the rate of damage to skeletal muscle is accelerated.
Discussion:
I’m not sure where to begin. This study has the potential to completely change the way we age.
In this experiment, a recombinant adeno-associated virus, directing overexpression of insulin-like growth factor I (IGF-I) in mature muscle fibers, was injected into the muscles of mice. The DNA that was originally in the virus was removed along with markers that stimulate immune response. DNA coding for IGF-1 was then put into the virus along with a promoter gene to ensure high rates of transcription. The results, as you can see by figures 1 & 2, were dramatic.
IGF-1 plays a crucial role in muscle regeneration. IGF-1 stimulates both proliferation and differentiation of stem cells in an autocrine-paracrine manner, although it induces differentiation to a much greater degree. IGF-1, when injected locally, increases satellite cell activity, muscle DNA, muscle protein content, muscle weight and muscle cross sectional area. The importance of IGF-1 lies in the fact that all of its apparent functions act to induce muscle growth with or without overload although it really shines as a growth promoter when combined with physical loading of the muscle.
IGF-1 also acts as an endocrine growth factor having an anabolic effect on distant tissues once released into the blood stream by the liver. IGF-1 possesses the insulin-like property of inhibiting degradation, but in addition can stimulate protein synthesis. The insulin-like effects are probably due to the similarity of the signaling pathways between insulin and IGF-1 following ligand binding at the receptors.
The ability of IGF-I to stimulate protein synthesis resembles the action of gh - growth hormone (somatropin) - , which was shown in separate studies on volunteers to stimulate protein synthesis without affecting protein degradation. Although it is often believed that the effects of GH are mediated through IGF-1, this cannot be the case entirely. First, the effects of the two hormones are different, in that GH does not change protein degradation. Second, the effect of GH is observed with little or no change in systemic IGF-1 concentrations. Age related muscle loss has been prevented with GH injections, however it is believed that this is accomplished through IGF-1.
The results of this study are similar to other studies where IGF-1 was injected directly into muscle tissue, resulting in increases in size and strength of experimental animals. Using a virus as a genetic vehicle has an advantage over simply injecting the growth factor. The effects of a single viral treatment last significantly longer (months if not years) because the muscle cell itself is constantly overproducing its own IGF-1 from injected DNA.
The fact that the IGF-1 produced by the muscle of these mice did not reach the blood stream is interesting. Systemic injections of IGF-1 have not been successful in inducing this kind of anabolic effect in humans. In addition, IGF-1 produced by the liver is genetically different than that produced by muscle tissue. It could be that providing additional DNA for the muscle to produce it’s own IGF-1 is the key to achieving anabolic and rejuvenative effects specifically in skeletal muscle.
In this study there was a preferential preservation of type IIb muscle fibers in aging mice. These are the fibers most sensitive to muscle hypertrophy from training and they are also the first fibers to disappear with aging. In the mice receiving the engineered virus, there was also a preservation of the motor neuron, leading to an increase in functional capacity. It is speculated that age related muscle loss is secondary to the loss of neuronal activation of type-II fibers. By preventing the degeneration of typ-II motor units, functional capacity could be maintained into old age. This technique may also serve useful in the prevention of osteoporosis. Further study is necessary to determine wether IGF-1 is having an effect only on muscle fibers or on nervous tissues as well.
Finally, it was also exciting to see muscle growth in the young mice who received the injection (15% increase in muscle mass). This means that the injection provided levels of IGF-1 far and above what the muscle normally has access to and not simply a preservation of normal levels. Remember that this was not combined with exercise. The growth of the injected muscles happened even without an extreme mechanical stimulus. The mice were simply allowed to run around as they usually do. Because of these dramatic results, the authors expressed concern about the use of this technique to enhance performance or cosmetic appearance. Research Update is not my personal soap box so I won’t go off on the gender centered hypocrisy of cosmetic enhancement in our society. All we can hope for is that this technique will be used to treat more important diseases such as muscular dystrophy and thereby become somewhat available for other uses as well.
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If you want to use IGF for localization growth get some rhIGF-1. It binds to the wound only and does not go into the bloodstream. This helps repair the injection wound and makes new cells in that area only. While Long R3 IGF binds somewhat to the would then makes its way to the blood stream causing growth throughout the body..
This is false.
The difference between rhIGF-1 and Long R3 is that the Long R3 does not get bound by binding protein and thus is 100% active whereas you do lose a great % of whatever amount of rhIGF-1 you inject to IGFBP3.
While technically it is true that if you inject a large amount of the rhIGF-1 it will have almost only localized effect, it is so because the "excess" that does not bind to cells in the muscle in which it is injected is rapidly bound up by IGFBP3 and thus rendered mostly unusable by cells elsewhere. It would be much much better in such a case to inject a smaller amount and not have ANY excess that gets bound up by IGFBP's.
And while technically it is true that if you inject a large amount of Long R3IGF-1 in a muscle, it will first bind to the nearest available receptor, and spread, binding to more and more receptors and not be bound up and neutralized by IGFBP's, meaning that it will travel all through your body and grow all kinds of tissue. This is called the systemic effect of IGF-1. Therein lies the only distinction in terms of BOTH half-life and localized/systemic effect between the Long and the human varieties.
What does all this mean?
It means that technically, for the part of the muscle in which you inject, THERE IS NO DIFFERENCE BETWEEN rhIGF-1 and Long R3 IGF-1. They both have the EXACT SAME LOCAL EFFECT. But rhIGF-1 gets neutralized quick, whereas Long R3 gets to float around until it finds a receptor.
What does all this tell us?
It tells us many things. Let's start with what we want, then see where that leads us. What do we want? Bigger muscles. More muscle cells that we will later grow with exercise and gear. A pump? Fatloss? Yeah, right. You can get a pump with a good "pump" product for a quarter of the price of IGF-1. Fatloss? Clenbuterol/Alb and T3/T4 will give it to you again at a fraction of the price of IGF-1. More muscle cells, you can ONLY get with IGF-1. Nothing else will give it to you and if you are using IGF-1 for anything else, you are misusing it. More muscle cells is CLEARLY the best use for IGF-1. It also has the very great benefit of fusing the myoblasts to the actual muscle cells as well as many other general cellular upkeep chores.
What does all this tell us?
It tells us that we should use IGF-1 to make more muscle cells. It's the only thing that can give it to us and more cells is more growth, which is our goal.
What does this tell us?
The localized effects are the best. Long R3 IGF-1 can float around your body and attach to anything that has IGF-1 receptors. The intestines is the place that has the MOST IGF-1 receptors and it also happens to have lots of blood flow. Injecting large amounts of Long R3 ENSURES that you are growing your intestines. Remember, more cells doesn't equal more size right away. Wait a bit, and see them grow.
What does this mean?
It means that if you are injecting upwards of a certain amount of IGF-1 you are growing your intestines. Yes you are also growing muscle and you may be getting leaner in the process. Your waistline looks trimmer. Nice. A few months down the line, your new intestinal cells will be of their full adult size and you will have acquired the perma-bloat look. Guaranteed. Maybe not Coleman-size perma-gut, but SOME perma-gut and it will keep growing. Guaranteed. Just as your new muscle cells can keep growing and growing IF you pin IGF-1 in a way to maximize new muscle cell creation.
HOW?
Heavy resistance exercise strongly upregulates the IGF-1 receptors on the stressed muscle. That means that after your workout, the muscles you trained are at their BEST STATE for receiving IGF-1 and growing many new cells. That's when you pin. This upregulation of IGF-1 receptor during exercise is short-lived. The science is not readily available so I am unable to quote a paper, but within 60 minutes of the last set, the receptors are back at baseline. This means, PIN IMMEDIATELY POSTWORKOUT and you will get your new muscle cells. PIN A LESSER AMOUNT and you will get only new MUSCLE cells out of your IGF-1. Pin more and you will grow other things, including stuff you wish you didn't grow.
HOW MUCH?
How much IGF-1 your muscle can take before you end up growing guts and stuff is wildly variable from person to person, from muscle to muscle. Myself at 220lbs for example, can go 40mcg in my biceps, 50mcg in most other muscles and 60mcg in my thighs, no problem. Dosed sporadically, 3-4 times a week, I can keep at this rate pretty much forever. This is immediately postworkout. If pinned at another time, you would have to reduce the amount a little, since your local receptors won't be any more receptive than the others.
What else?
All the talk about IGF-1's half-life is UTTER BULLSHIT. It is technicality without any real-world applicability. Yes rhIGF-1 has a "short half-life". But what does it mean? It means that it is either taken up by a cell receptor or bound up by a binding protein in short order. Does it mean that 20 minutes after the IGF-1 is pinned you should pin more because "blood levels are low"? Not by any means. Once it's activated a cell receptor, that's where it initiates a cellular response that will take about 72 hours to be complete and which will consume lots of energy. So the half-life of 20 minutes means NOTHING BECAUSE THE EFFECTS STILL LAST 72 HOURS ALL THE SAME.
What about Long R3 IGF-1?
Yes technically it has a longer half-life. Why? Because it either gets rapidly taken up by a cell receptor or... Just floats around. Until it can find a receptor or is destroyed by the immune system or some other metabolizing mechanism. BUT THIS MEANS ***NOTHING***!!! Why does it mean nothing? BECAUSE once it attaches to a cell receptor, it initiates a cellular response that will take about 72 hours to be complete. THIS CELLULAR RESPONSE IS ALL THAT INTERESTS US. Not "blood levels", that's utter bullshit. As a matter of fact, the one thing YOU DO NOT WANT IS FOR BLOOD LEVELS OF IGF-1 TO BE ELEVATED. Because that means you are growing everywhere and this means first and foremost your guts. Sure it feels like it's working while you're on. Just you wait 9 months and see that you look like Craig Kovacs. Bravo, you now have the biggest intestines in the world.
Half-life means nothing. Localized vs systemic = bad argument. You want mostly localized effects. Period. You get them by pinning immediately postworkout. Period. End of argument. You will get some degree of systemic effect no matter what you do. You can minimize it with my method.
OMFG I am so tired of all the misinformation floating around on IGF-1. Look at the length of this post. Did you read all of it? You should, you know.
Grunt, I am also interested in the amount your recommend shooting post workout?
40mcg is plenty. We have to realize that this is a huge amount compared to what the body naturally produces. Maybe we can ask TheGame46 who is working on his master's degree in endocrinology what the actual amount produced by a normal human, say even with exercise, but it's probably something less than 1mcg.
20mcg each side. 30 each side in the quads. That's plenty. Now, you won't see major, immediate LBM increases, but THAT IS NOT WHAT IGF-1 IS FOR. That's what anabolic steroids are for. 40-50mcg total will let you get plenty of hyperplasia, not grow your intestines too much, and save you plenty of $. The newly added muscle cells will take months to grow, but they will, and you will use IGF-1 again because it gets reasonably inexpensive with such a protocol.
Another thing: much of the newer research shows that EOD and even E3Digf-1 treatment is better than ED because ED makes the IGF-1 lose its effect too rapidly. It is still unknown wether this effect comes from receptor downregulation or depletion of myoblasts. More research will certainly provide a definitive answer. Either way, it takes some time for the effects to come back in full after a bout of ED IGF-1 treatment. So you may want to think about switching to EOD lifting and IGF-1 immediately postworkout every workout, or 2on/1off and pin the lagging muscle E3D. These dosing patterns won't give you pounds of immediate muscle, but they will give you hyperplasia and myoblast fusion, which means continued growth at very decent rates, and the ability to continue treatment for a long while until response diminishes.
And no Coleman guts.
I was thinking about trying IGF, very interesting info here. Thanks Grunt for posting this info. A couple of other questions that maybe you can answer, if you don't mind. How does IGF interact with insulin, i.e. can it be pinned with insulin post workout? Also, what are your thoughts on taking IGF durring a cycle of human growth hormone - somatropin - ?
Great questions. I'll start with some background on the peptides from back before IGF-1 was commonly used. gh - growth hormone (somatropin) - was the first peptide to be used in Bodybuilding. We pretty much know what GH does and doesn't do and all that, so I'll skip this part. Then came along insulin. It quickly became apparent that insulin on its own doesn't do much for muscle. It does make you fat but not much bigger. With anabolic steroids and tons of food, it's better. Later it became extremely clear that Slin & GH was the winner combo, the most synergistic combination around.
What few people realize even today - and it's been what, nearly 20 years of insulin usage in BBing, is that the very reason why insulin and gh - growth hormone (somatropin) - are synergystic is that when levels of both are high, the liver turns the GH into IGF-1. That's right, when doing insulin & gh - growth hormone (somatropin) - , you are in fact using these because your body makes more IGF-1 with them. So it isn't the insulin OR the gh - growth hormone (somatropin) - nor actually the compounding of the effects of each, but rather good old IGF-1. Even the name Insulinlike Growth Factor, has been made such because of the origin of the compound in Insulin and Growth Hormone.
Now, the IGF-1 from insulin & gh - growth hormone (somatropin) - is not long R3 IGF-1, it's hIGF-1. It's different and possibly the effects are somewhat different than when using Long R3, especially with regards toIGF-1 losing effectiveness, which is likely much lesser with the liver-synthesized IGF-1 than with the Long R3. No studies proving this, it is theory at this point and such a study will possibly never be made, for many good reasons. One reason why hIGF-1 loses effectiveness less quickly is its half-life, or its very limited ability to run around the body and saturate all receptors everywhere. And here we join up with the EOD and E3D protocols which state that letting the body rest is extremely important to continued results. You get the same effect out of insulin & gh - growth hormone (somatropin) - because of IGFBP3 that mops up the IGF-1 within minutes of synthesis, which makes it impossible to saturate the receptors and lets them rest. Similar effect, completely different way of achieving it.
So insulin & gh - growth hormone (somatropin) - are synergistic. Then the next question: what about insulin & IGF or Gh & IGF? IGF is synergistic with both. MOST of the effects of GH are mediated through IGF-1 but not ALL of them. Among the good effects of gh - growth hormone (somatropin) - thatIGF-1 does not exert is anabolism to ligaments, for example. This is just an example to show that there is a benefit to using gh - growth hormone (somatropin) - & IGF-1 at the same time. There is evidence that ED dosing of LR3 reduces gh - growth hormone (somatropin) - release in the body, so it makes plenty of sense to use both at the same time.
insulin & IGF is a different animal. Most of the benefits of insulin come from its ability to increase IGF-1. Unless you are diabetic, your body makes enough insulin. Eat more, it releases more insulin. More carbs? More insulin. The limit to the body's ability to release insulin isn't easily reached. Even feeding 10,000 cals ED your body can produce the insulin to store that. Easily. This is not to say that exogenous insulin supplementation is not useful. I have seen an account that multiple daily doses of just 3iu produces a body-wide pump that lasts all day. Look, I'm not diabetic but I have never achieved this effect with my own natural insulin. So obviously there's something going on there.
Am I stating there is no use in pinning insulin & IGF together? No. There is evidence that shows that pinning insulin with IGF-1 increases the length of the effects of IGF-1. Especially the hypoglycemic effects, obviously, but this has pretty far-ranging and beneficial implications, among which saturating the lean cells with nutrients and having a low blood sugar level are not the least. Obviously they are both hypoglycemic compounds so carbs have to be adjusted up when adding IGF-1 to insulin, or insulin reduced. I prefer the second option, although I am at a loss as to the amount of insulin you would have to remove for compensation with, say, 40mcg IGF-1.
Personally I have not done this. Both my grandfathers were diabetics, so I'm not playing with insulin. Especially that I have a natural tendency to go hypoglycemic easily. IGF-1 though is simply GREAT for me.
What I did do, over 10 years ago, is use an extremely potent gh - growth hormone (somatropin) - releaser named GHB - gamma hydroxybutyric - and combined that with a few ounces of sugar, the idea being of course a cheap version of GH & insulin. Obviously it worked great over a few months and it did produce hyperplasia, as made very obvious by the muscle size I retained when taking a 2 year layoff from lifting because of a non-training related injury.
Dont take this as me being a **** but do you have some experience with IGF Grunt? If so what were your gains? And have you tried rhIGF? What kind of gains from those? I would guess with as much knowledge you have on this you'd have to have run it before.
I have run LR3 at 20, 30, 40 and 50mcg ED as well as variations of only postworkout pinning. I suggested EOD and gapped dosing way before lab research showed that this would be a better dosing protocol.
In my experience, IMMEDIATELY-POSTWORKOUT dosing is all-important to hyperplasia. SOME benefit is had by pinning preworkout and at other times, but the vey best resutls from pinning immediately postworkout. I have experimented with 5-minutes postworkout and 20-30 minutes postworkout and have found the 5-minutes postworkout dosing to be VASTLY superior to any other dosing protocol. I know it isn't the most practical for most of us, but I'm saying what I have seen on myself. Others report only slightly better results from going immediately postworkout as compared to, say, 20-30 minutes post.
Gains out of IGF-1 are difficult to account for. Firstly, it is much more a recomposition compound than a mass or fatloss compound. On anabolic steroids, the gains are "this many lbs of LBM". On Clenbuterol/Thyroid, gains are "so many lbs of flab". On IGF-1 the gains are "some fatloss, some muscle gain/retention, and this many new cells that I will grow in the coming months".
But suffice it to say that my first experimentation protocol was 5 minutes postworkout in my biceps, delts and chest because my previous research had indicated that the postworkout window was limited, and because those were my lagging bodyparts. My biceps went from 17" to 17½" in the first 2 weeks along with some fatloss and another ½" in the 2 months afterward, my DB curls going from 55 x 10 to 65 x 10. That was after 12 years of natural training, with genetic potential pretty maxed out. Chest and delt results I did not even attempt to quantify but the difference was clearly visible.
On another board there was a log where the guy was shooting only his biceps because he read that local effects were little and his bis were lagging. A couple months after his log was done I asked about his biceps and he said they had now taken the lead in his muscular development.
WOW this thread is awesome. I am 100% with you on the conservitave part, why put your health and life and for alot of of us here LOOKS in jepordy? On the other hand I must be the devils advocate, even though I feel a bit overwhelmed by some of these knowledgable bros...
Could this change with large doses of anabolic steroids? I could be wrong. Completely so, but with verry large amounts of certain anabolics your IGF raises drasticaly. Why would this not result in some for of perma gut?
I beleive gh - growth hormone (somatropin) - can cause some organ growth correct? Maybe that has a different mechanism but it seams this only happens at verry high doses over verry long periods of time.
Why do we not see such organ growth with the use of extreme amounts of anabolic androgenic steroids over periods of years? And a more importantly, if you were to take large doses of AAS especialy those of the stronger breed do you think that the doses could increase, perhaps from increasing the rate of the receptors processing the IGF-1r3.
Also wouldn't it be verry usefull to use this chemical post cardio because of the blood pumping so drasticaly to the muscle sites, even pre or mid cardio work out?
I'm sorry if I'm being dense, I gotta ask the questions!!
Those are actually some very good questions. The answers are equally good.
There are two completely different ways in which IGF-1 is produced in the body. Even the IGF-1 molecule itself is slightly different in each case. The first, well known case, is where gh - growth hormone (somatropin) - & insulin are used by the liver to make IGF-1 which is then released into the bloodstream. anabolic androgenic steroids has little to no bearing on this systemic, or "paracrine" IGF-1. It just circulates in the bloodstream and eventually finds an IGF-1 receptor on the outside surface of a cell and attaches to it, activating it.
The other pathway, the one that is rarely discussed, is the autocrine pathway. This is where a cell will produce its own IGF-1, different peptides than the systemic, for its own internal use. These are called IGF-1Ea and IGF-1Ec or MGF. They are produced inside the cell, and act on receptors within the cell and just outside of the cell, on the myoblasts. These peptides don't go anywhere. When they leave the cell, they stay close to the surface. This is the pathway that anabolic androgenic steroids will greatly upregulate.
So on one hand you have the systemic with its effects on the surface receptor and you have the autocrine with its effects on the internal receptor, on the myoblasts and also perhaps on the surface receptor. So obviously when you know this it becomes obvious that the IGF-1 from anabolic androgenic steroids - the autocrine - will never give you the gh - growth hormone (somatropin) - gut because the IGF-1 that it makes your cells produce never leaves the cell itself, it doesn't circulate around to go attach to an intestinal wall receptor.
The pathway through which gh - growth hormone (somatropin) - causes organ growth *IS* systemic IGF-1. Most of the effects of gh - growth hormone (somatropin) - are actually effects of IGF-1. gh - growth hormone (somatropin) - is simply not very active on many cells but it is much converted by the liver into IGF-1 and this is what mediates the effects of gh - growth hormone (somatropin) - . As I posted above, there ARE some effects of GH that are not mediated through IGF-1 but most of them are.
As far as upregulating the surface receptors through anabolic androgenic steroids usage, I have seen no evidence that points that way, but that is not entirely impossible. Improbable, but not impossible.
As far as pinning post-cardio, I don't see it. In my opinion, for bodybuildersIGF-1 has two main purposes: firstly hyperplasia, its main use, and secondly general tissue repair, meaning healing and preventing injury. Ligaments aren't repaired by IGF-1 but they're a rare exception. It is too expensive and too good at better things IMO to be wasted on a simple pump.
How would one transport this to the gym for post wo injection? What's the best way to maintain integrity, avoid heat and not losse any?
Suggestions?
Diluted in AA, it is stable for a year at 98 degrees F. Of course, the insides of your car in the midst of a sunny summer day will be much hotter than that. Not the inside of your locker though.
What I always do is to load up a syringe with just the needed amount of IGF & AA, then use a small amount of aluminum foil to make a spacer between the end of the plunger and the cylinder to avoid discharging the syringe in transit, and put this and a couple alcohol pads and my BW inside a sunglass case in my gym bag.
I grab my bag after my workout, go change in the shower or toilet and pin at the same time. Then I get my shake.
Here I will post indepth articles I have found that are very informative and fairly accurate
The IGF1 Hype
There is a considerable amount of hype surrounding IGF1. Every one is blaming the distended bellies of modern Bodybuilders on it. Also the freaky proportions that old bodybuilders that have been around for years are starting to attain. Anti-aging proponents are touting it as the miracle cure for every thing from Parkinson's disease to Alzheimer's. And the medical community has published numerous articles on it for its ability to cause cancer, diabetes and gigantism. While at the same time performing documented experiments on thousands of patients of muscle wasting diseases. And reporting significant turnabouts in there conditions. So what is a guy to think about IGF1 as far as athletic enhancement is concerned? Well first of all you need to know that most experiments conducted with IGF1 do not list the type of IGF used. I have written Dr. Robert Saline of the Swedish rejuvenation institute on several occasions and we have had in-depth discussions on the subject of IGF1 for physical appearance enhancement. He feels it would be unethical to prescribe IGF1 to a bodybuilder to increase muscle mass simply due to the fact that IGF1 has valid applications in the medical community, (Like I could give a rats ass about "ethical"). He can not argue that it is extremely effective as a promoter of muscle growth far beyond what androgens (steroids) alone can offer. Well fortunately in America IGF1 is not a drug (yet) and the FDA has no control over it as of now. This will change in the very near future however, Im absolutely sure of it.
How to use IGF1
What users report
Users of IGF1 have reported various results but all along the same lines, It does not appear to be dramatically less effective in any one individual (at least not to the best of my knowledge). I have a good friend who had to stop taking IGF1 due to stomach illness that was completely unrelated But he to experienced good gains from it for the 2 weeks he was on it, his dosage was 120mcg per day. One hour after the first injection he went to the gym and immediately told me about the uncontrollable pump he got from just one set.
That would indicate to me that he was experiencing some form of cell volumization. The general consensus on IGF1 seems to be that its benefits are as fallow:
Increased Pump Pumps are reported to be so severe that workouts are often cut short due to lack of ability to the muscle through the full range of motion...ouch
Gains retention is increased if IGF is used in a cycle I am not sure why, but IGF1 seems to make gains on a cycle stick with virtually no post cycle loss. Every bodybuilder I've spoken with seems to think this for some reason. Most of them use drugs like Anadrol or Dianabol with it because of the amount of size attained with these drugs. The usual draw back to these drugs is that in most users there is a post cycle "crash" that occurs, so the reasoning is to toss IGF1 into the stack and grow larger faster with out the post cycle crash blues.
Reverses testicular atrophy
Testicles if shrunken will return to "full swing" so to speak even in the middle of a cycle. If not shrunken they will not shrink during the cycle. This may explain partially why gains are kept after the cycle.
Fatigue
Users report feeling drained and tired all day. This seems to be one of the negative side effects to IGF1, it will make you sleep longer and you will require more sleep at night to feel rested for the morning. This is common with high doses of human growth hormone - somatropin - and exhibited in children, whose IGF1 levels are extraordinarily high. A child needs 4 hours more sleep than an adult on average does. This may be directly or indirectly related to IGF1 levels.
Stiffness
An almost arthritic feeling is commonly associated with high levels of human growth hormone - somatropin - , well IGF1 has the exact same property. IGF1 will cause your hands, fingers and knuckles to ache this is one way you can be sure you got real IGF1.
IGF-1's Side effects
Every thing has a down side. To bake a cake ya gotta brake an egg. IGF1 is no exception. The drug used in larger quantity around the 100mcg+ range will cause headaches, occasional nausea and can contribute to low blood sugar or hypoglycemia in some users. Although I have never heard of this first hand I'm sure its true.
IGF1 will attach its self to the lining of the intestine and cause atrophy of the gut. Every thing IGF1 touches will grow and you have a lot of receptors on the lining of the large intestine and inner wall of the abdominal well. This is what causes the gh - growth hormone (somatropin) - gut look. You can easily avoid this by limiting your dosages and cycle lengths. IGF1 cycles should be kept to 4-6 weeks with 4-6 weeks off in-between. IGF-1 is considerably more powerful than human growth hormone - somatropin - and you need to think of it along those lines as far as dosing goes. We all know what to much HGH can do over prolonged periods of usage. The Neanderthal look is definitely not going to win any shows this year. I would recommend 80 mcg a day for 4 weeks at a time you should get good results from that for a while. I don't know if you will need to up the dosage at any point, but I would think in the case of IGF1 it wouldn't matter. If 80mcg doesn't do it for ya, then bump it up to 100 You should definitely feel it at this point If not suspect the IGF1 as being fake. Beyond 120 mcg per day your asking for trouble, This compound demands as much respect as its sister amino Insulin.
Clinical Facts about IGF-1
IGF-1 is a polypeptide of 70 amino acids (7650 daltons), and is one of a number of related insulin-like growth factors present in the circulation. The molecule shows approximately 50% sequence homology with proinsulin and has a number of biological activities similar to insulin. IGF-1 is a mediator of longitudinal growth in humans or how tall you are capable of becoming. Serum IGF-1 concentrations are altered by age, nutritional status, body composition, and growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For the diagnosis of acromegaly, a single IGF-1 concentration is more reliable than a random human growth hormone - somatropin - measurement (Oppizi, et al., 1986). IGF-1 can be used for the assessment of disease activity in acromegaly (Barkan, et al., 198.
Almost all (>95%) of serum IGF-1 circulates bound to specific IGF binding proteins (IGFBPs), of which six classes (IGFBPs 1-6) have been identified (Rudd, 1991). BP3 is thought to be the major binding protein of IGF-1.
Summary:
Although the mechanisms underlying age associated muscle loss are not entirely understood, researchers attempted to moderate the loss by increasing the regenerative capacity of muscle. This involved the injection of a recombinant adeno-associated virus directing overexpression of insulin-like growth factor I (IGF-I) in differentiated muscle fibers.
They demonstrated that the IGF-I expression promotes an average increase of 15% in muscle mass and a 14% increase in strength in young adult mice (Figure 1), and remarkably, prevents aging-related muscle changes in old adult mice, resulting in a 27% increase in strength as compared with uninjected old muscles (Figure 2). Muscle mass and fiber type distributions were maintained at levels similar to those in young adults. These results suggest that gene transfer of IGF-I into muscle could form the basis of a human gene therapy for preventing the loss of muscle function associated with aging and may be of benefit in diseases where the rate of damage to skeletal muscle is accelerated.
Discussion:
I’m not sure where to begin. This study has the potential to completely change the way we age.
In this experiment, a recombinant adeno-associated virus, directing overexpression of insulin-like growth factor I (IGF-I) in mature muscle fibers, was injected into the muscles of mice. The DNA that was originally in the virus was removed along with markers that stimulate immune response. DNA coding for IGF-1 was then put into the virus along with a promoter gene to ensure high rates of transcription. The results, as you can see by figures 1 & 2, were dramatic.
IGF-1 plays a crucial role in muscle regeneration. IGF-1 stimulates both proliferation and differentiation of stem cells in an autocrine-paracrine manner, although it induces differentiation to a much greater degree. IGF-1, when injected locally, increases satellite cell activity, muscle DNA, muscle protein content, muscle weight and muscle cross sectional area. The importance of IGF-1 lies in the fact that all of its apparent functions act to induce muscle growth with or without overload although it really shines as a growth promoter when combined with physical loading of the muscle.
IGF-1 also acts as an endocrine growth factor having an anabolic effect on distant tissues once released into the blood stream by the liver. IGF-1 possesses the insulin-like property of inhibiting degradation, but in addition can stimulate protein synthesis. The insulin-like effects are probably due to the similarity of the signaling pathways between insulin and IGF-1 following ligand binding at the receptors.
The ability of IGF-I to stimulate protein synthesis resembles the action of gh - growth hormone (somatropin) - , which was shown in separate studies on volunteers to stimulate protein synthesis without affecting protein degradation. Although it is often believed that the effects of GH are mediated through IGF-1, this cannot be the case entirely. First, the effects of the two hormones are different, in that GH does not change protein degradation. Second, the effect of GH is observed with little or no change in systemic IGF-1 concentrations. Age related muscle loss has been prevented with GH injections, however it is believed that this is accomplished through IGF-1.
The results of this study are similar to other studies where IGF-1 was injected directly into muscle tissue, resulting in increases in size and strength of experimental animals. Using a virus as a genetic vehicle has an advantage over simply injecting the growth factor. The effects of a single viral treatment last significantly longer (months if not years) because the muscle cell itself is constantly overproducing its own IGF-1 from injected DNA.
The fact that the IGF-1 produced by the muscle of these mice did not reach the blood stream is interesting. Systemic injections of IGF-1 have not been successful in inducing this kind of anabolic effect in humans. In addition, IGF-1 produced by the liver is genetically different than that produced by muscle tissue. It could be that providing additional DNA for the muscle to produce it’s own IGF-1 is the key to achieving anabolic and rejuvenative effects specifically in skeletal muscle.
In this study there was a preferential preservation of type IIb muscle fibers in aging mice. These are the fibers most sensitive to muscle hypertrophy from training and they are also the first fibers to disappear with aging. In the mice receiving the engineered virus, there was also a preservation of the motor neuron, leading to an increase in functional capacity. It is speculated that age related muscle loss is secondary to the loss of neuronal activation of type-II fibers. By preventing the degeneration of typ-II motor units, functional capacity could be maintained into old age. This technique may also serve useful in the prevention of osteoporosis. Further study is necessary to determine wether IGF-1 is having an effect only on muscle fibers or on nervous tissues as well.
Finally, it was also exciting to see muscle growth in the young mice who received the injection (15% increase in muscle mass). This means that the injection provided levels of IGF-1 far and above what the muscle normally has access to and not simply a preservation of normal levels. Remember that this was not combined with exercise. The growth of the injected muscles happened even without an extreme mechanical stimulus. The mice were simply allowed to run around as they usually do. Because of these dramatic results, the authors expressed concern about the use of this technique to enhance performance or cosmetic appearance. Research Update is not my personal soap box so I won’t go off on the gender centered hypocrisy of cosmetic enhancement in our society. All we can hope for is that this technique will be used to treat more important diseases such as muscular dystrophy and thereby become somewhat available for other uses as well.
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If you want to use IGF for localization growth get some rhIGF-1. It binds to the wound only and does not go into the bloodstream. This helps repair the injection wound and makes new cells in that area only. While Long R3 IGF binds somewhat to the would then makes its way to the blood stream causing growth throughout the body..
This is false.
The difference between rhIGF-1 and Long R3 is that the Long R3 does not get bound by binding protein and thus is 100% active whereas you do lose a great % of whatever amount of rhIGF-1 you inject to IGFBP3.
While technically it is true that if you inject a large amount of the rhIGF-1 it will have almost only localized effect, it is so because the "excess" that does not bind to cells in the muscle in which it is injected is rapidly bound up by IGFBP3 and thus rendered mostly unusable by cells elsewhere. It would be much much better in such a case to inject a smaller amount and not have ANY excess that gets bound up by IGFBP's.
And while technically it is true that if you inject a large amount of Long R3IGF-1 in a muscle, it will first bind to the nearest available receptor, and spread, binding to more and more receptors and not be bound up and neutralized by IGFBP's, meaning that it will travel all through your body and grow all kinds of tissue. This is called the systemic effect of IGF-1. Therein lies the only distinction in terms of BOTH half-life and localized/systemic effect between the Long and the human varieties.
What does all this mean?
It means that technically, for the part of the muscle in which you inject, THERE IS NO DIFFERENCE BETWEEN rhIGF-1 and Long R3 IGF-1. They both have the EXACT SAME LOCAL EFFECT. But rhIGF-1 gets neutralized quick, whereas Long R3 gets to float around until it finds a receptor.
What does all this tell us?
It tells us many things. Let's start with what we want, then see where that leads us. What do we want? Bigger muscles. More muscle cells that we will later grow with exercise and gear. A pump? Fatloss? Yeah, right. You can get a pump with a good "pump" product for a quarter of the price of IGF-1. Fatloss? Clenbuterol/Alb and T3/T4 will give it to you again at a fraction of the price of IGF-1. More muscle cells, you can ONLY get with IGF-1. Nothing else will give it to you and if you are using IGF-1 for anything else, you are misusing it. More muscle cells is CLEARLY the best use for IGF-1. It also has the very great benefit of fusing the myoblasts to the actual muscle cells as well as many other general cellular upkeep chores.
What does all this tell us?
It tells us that we should use IGF-1 to make more muscle cells. It's the only thing that can give it to us and more cells is more growth, which is our goal.
What does this tell us?
The localized effects are the best. Long R3 IGF-1 can float around your body and attach to anything that has IGF-1 receptors. The intestines is the place that has the MOST IGF-1 receptors and it also happens to have lots of blood flow. Injecting large amounts of Long R3 ENSURES that you are growing your intestines. Remember, more cells doesn't equal more size right away. Wait a bit, and see them grow.
What does this mean?
It means that if you are injecting upwards of a certain amount of IGF-1 you are growing your intestines. Yes you are also growing muscle and you may be getting leaner in the process. Your waistline looks trimmer. Nice. A few months down the line, your new intestinal cells will be of their full adult size and you will have acquired the perma-bloat look. Guaranteed. Maybe not Coleman-size perma-gut, but SOME perma-gut and it will keep growing. Guaranteed. Just as your new muscle cells can keep growing and growing IF you pin IGF-1 in a way to maximize new muscle cell creation.
HOW?
Heavy resistance exercise strongly upregulates the IGF-1 receptors on the stressed muscle. That means that after your workout, the muscles you trained are at their BEST STATE for receiving IGF-1 and growing many new cells. That's when you pin. This upregulation of IGF-1 receptor during exercise is short-lived. The science is not readily available so I am unable to quote a paper, but within 60 minutes of the last set, the receptors are back at baseline. This means, PIN IMMEDIATELY POSTWORKOUT and you will get your new muscle cells. PIN A LESSER AMOUNT and you will get only new MUSCLE cells out of your IGF-1. Pin more and you will grow other things, including stuff you wish you didn't grow.
HOW MUCH?
How much IGF-1 your muscle can take before you end up growing guts and stuff is wildly variable from person to person, from muscle to muscle. Myself at 220lbs for example, can go 40mcg in my biceps, 50mcg in most other muscles and 60mcg in my thighs, no problem. Dosed sporadically, 3-4 times a week, I can keep at this rate pretty much forever. This is immediately postworkout. If pinned at another time, you would have to reduce the amount a little, since your local receptors won't be any more receptive than the others.
What else?
All the talk about IGF-1's half-life is UTTER BULLSHIT. It is technicality without any real-world applicability. Yes rhIGF-1 has a "short half-life". But what does it mean? It means that it is either taken up by a cell receptor or bound up by a binding protein in short order. Does it mean that 20 minutes after the IGF-1 is pinned you should pin more because "blood levels are low"? Not by any means. Once it's activated a cell receptor, that's where it initiates a cellular response that will take about 72 hours to be complete and which will consume lots of energy. So the half-life of 20 minutes means NOTHING BECAUSE THE EFFECTS STILL LAST 72 HOURS ALL THE SAME.
What about Long R3 IGF-1?
Yes technically it has a longer half-life. Why? Because it either gets rapidly taken up by a cell receptor or... Just floats around. Until it can find a receptor or is destroyed by the immune system or some other metabolizing mechanism. BUT THIS MEANS ***NOTHING***!!! Why does it mean nothing? BECAUSE once it attaches to a cell receptor, it initiates a cellular response that will take about 72 hours to be complete. THIS CELLULAR RESPONSE IS ALL THAT INTERESTS US. Not "blood levels", that's utter bullshit. As a matter of fact, the one thing YOU DO NOT WANT IS FOR BLOOD LEVELS OF IGF-1 TO BE ELEVATED. Because that means you are growing everywhere and this means first and foremost your guts. Sure it feels like it's working while you're on. Just you wait 9 months and see that you look like Craig Kovacs. Bravo, you now have the biggest intestines in the world.
Half-life means nothing. Localized vs systemic = bad argument. You want mostly localized effects. Period. You get them by pinning immediately postworkout. Period. End of argument. You will get some degree of systemic effect no matter what you do. You can minimize it with my method.
OMFG I am so tired of all the misinformation floating around on IGF-1. Look at the length of this post. Did you read all of it? You should, you know.
Grunt, I am also interested in the amount your recommend shooting post workout?
40mcg is plenty. We have to realize that this is a huge amount compared to what the body naturally produces. Maybe we can ask TheGame46 who is working on his master's degree in endocrinology what the actual amount produced by a normal human, say even with exercise, but it's probably something less than 1mcg.
20mcg each side. 30 each side in the quads. That's plenty. Now, you won't see major, immediate LBM increases, but THAT IS NOT WHAT IGF-1 IS FOR. That's what anabolic steroids are for. 40-50mcg total will let you get plenty of hyperplasia, not grow your intestines too much, and save you plenty of $. The newly added muscle cells will take months to grow, but they will, and you will use IGF-1 again because it gets reasonably inexpensive with such a protocol.
Another thing: much of the newer research shows that EOD and even E3Digf-1 treatment is better than ED because ED makes the IGF-1 lose its effect too rapidly. It is still unknown wether this effect comes from receptor downregulation or depletion of myoblasts. More research will certainly provide a definitive answer. Either way, it takes some time for the effects to come back in full after a bout of ED IGF-1 treatment. So you may want to think about switching to EOD lifting and IGF-1 immediately postworkout every workout, or 2on/1off and pin the lagging muscle E3D. These dosing patterns won't give you pounds of immediate muscle, but they will give you hyperplasia and myoblast fusion, which means continued growth at very decent rates, and the ability to continue treatment for a long while until response diminishes.
And no Coleman guts.
I was thinking about trying IGF, very interesting info here. Thanks Grunt for posting this info. A couple of other questions that maybe you can answer, if you don't mind. How does IGF interact with insulin, i.e. can it be pinned with insulin post workout? Also, what are your thoughts on taking IGF durring a cycle of human growth hormone - somatropin - ?
Great questions. I'll start with some background on the peptides from back before IGF-1 was commonly used. gh - growth hormone (somatropin) - was the first peptide to be used in Bodybuilding. We pretty much know what GH does and doesn't do and all that, so I'll skip this part. Then came along insulin. It quickly became apparent that insulin on its own doesn't do much for muscle. It does make you fat but not much bigger. With anabolic steroids and tons of food, it's better. Later it became extremely clear that Slin & GH was the winner combo, the most synergistic combination around.
What few people realize even today - and it's been what, nearly 20 years of insulin usage in BBing, is that the very reason why insulin and gh - growth hormone (somatropin) - are synergystic is that when levels of both are high, the liver turns the GH into IGF-1. That's right, when doing insulin & gh - growth hormone (somatropin) - , you are in fact using these because your body makes more IGF-1 with them. So it isn't the insulin OR the gh - growth hormone (somatropin) - nor actually the compounding of the effects of each, but rather good old IGF-1. Even the name Insulinlike Growth Factor, has been made such because of the origin of the compound in Insulin and Growth Hormone.
Now, the IGF-1 from insulin & gh - growth hormone (somatropin) - is not long R3 IGF-1, it's hIGF-1. It's different and possibly the effects are somewhat different than when using Long R3, especially with regards toIGF-1 losing effectiveness, which is likely much lesser with the liver-synthesized IGF-1 than with the Long R3. No studies proving this, it is theory at this point and such a study will possibly never be made, for many good reasons. One reason why hIGF-1 loses effectiveness less quickly is its half-life, or its very limited ability to run around the body and saturate all receptors everywhere. And here we join up with the EOD and E3D protocols which state that letting the body rest is extremely important to continued results. You get the same effect out of insulin & gh - growth hormone (somatropin) - because of IGFBP3 that mops up the IGF-1 within minutes of synthesis, which makes it impossible to saturate the receptors and lets them rest. Similar effect, completely different way of achieving it.
So insulin & gh - growth hormone (somatropin) - are synergistic. Then the next question: what about insulin & IGF or Gh & IGF? IGF is synergistic with both. MOST of the effects of GH are mediated through IGF-1 but not ALL of them. Among the good effects of gh - growth hormone (somatropin) - thatIGF-1 does not exert is anabolism to ligaments, for example. This is just an example to show that there is a benefit to using gh - growth hormone (somatropin) - & IGF-1 at the same time. There is evidence that ED dosing of LR3 reduces gh - growth hormone (somatropin) - release in the body, so it makes plenty of sense to use both at the same time.
insulin & IGF is a different animal. Most of the benefits of insulin come from its ability to increase IGF-1. Unless you are diabetic, your body makes enough insulin. Eat more, it releases more insulin. More carbs? More insulin. The limit to the body's ability to release insulin isn't easily reached. Even feeding 10,000 cals ED your body can produce the insulin to store that. Easily. This is not to say that exogenous insulin supplementation is not useful. I have seen an account that multiple daily doses of just 3iu produces a body-wide pump that lasts all day. Look, I'm not diabetic but I have never achieved this effect with my own natural insulin. So obviously there's something going on there.
Am I stating there is no use in pinning insulin & IGF together? No. There is evidence that shows that pinning insulin with IGF-1 increases the length of the effects of IGF-1. Especially the hypoglycemic effects, obviously, but this has pretty far-ranging and beneficial implications, among which saturating the lean cells with nutrients and having a low blood sugar level are not the least. Obviously they are both hypoglycemic compounds so carbs have to be adjusted up when adding IGF-1 to insulin, or insulin reduced. I prefer the second option, although I am at a loss as to the amount of insulin you would have to remove for compensation with, say, 40mcg IGF-1.
Personally I have not done this. Both my grandfathers were diabetics, so I'm not playing with insulin. Especially that I have a natural tendency to go hypoglycemic easily. IGF-1 though is simply GREAT for me.
What I did do, over 10 years ago, is use an extremely potent gh - growth hormone (somatropin) - releaser named GHB - gamma hydroxybutyric - and combined that with a few ounces of sugar, the idea being of course a cheap version of GH & insulin. Obviously it worked great over a few months and it did produce hyperplasia, as made very obvious by the muscle size I retained when taking a 2 year layoff from lifting because of a non-training related injury.
Dont take this as me being a **** but do you have some experience with IGF Grunt? If so what were your gains? And have you tried rhIGF? What kind of gains from those? I would guess with as much knowledge you have on this you'd have to have run it before.
I have run LR3 at 20, 30, 40 and 50mcg ED as well as variations of only postworkout pinning. I suggested EOD and gapped dosing way before lab research showed that this would be a better dosing protocol.
In my experience, IMMEDIATELY-POSTWORKOUT dosing is all-important to hyperplasia. SOME benefit is had by pinning preworkout and at other times, but the vey best resutls from pinning immediately postworkout. I have experimented with 5-minutes postworkout and 20-30 minutes postworkout and have found the 5-minutes postworkout dosing to be VASTLY superior to any other dosing protocol. I know it isn't the most practical for most of us, but I'm saying what I have seen on myself. Others report only slightly better results from going immediately postworkout as compared to, say, 20-30 minutes post.
Gains out of IGF-1 are difficult to account for. Firstly, it is much more a recomposition compound than a mass or fatloss compound. On anabolic steroids, the gains are "this many lbs of LBM". On Clenbuterol/Thyroid, gains are "so many lbs of flab". On IGF-1 the gains are "some fatloss, some muscle gain/retention, and this many new cells that I will grow in the coming months".
But suffice it to say that my first experimentation protocol was 5 minutes postworkout in my biceps, delts and chest because my previous research had indicated that the postworkout window was limited, and because those were my lagging bodyparts. My biceps went from 17" to 17½" in the first 2 weeks along with some fatloss and another ½" in the 2 months afterward, my DB curls going from 55 x 10 to 65 x 10. That was after 12 years of natural training, with genetic potential pretty maxed out. Chest and delt results I did not even attempt to quantify but the difference was clearly visible.
On another board there was a log where the guy was shooting only his biceps because he read that local effects were little and his bis were lagging. A couple months after his log was done I asked about his biceps and he said they had now taken the lead in his muscular development.
WOW this thread is awesome. I am 100% with you on the conservitave part, why put your health and life and for alot of of us here LOOKS in jepordy? On the other hand I must be the devils advocate, even though I feel a bit overwhelmed by some of these knowledgable bros...
Could this change with large doses of anabolic steroids? I could be wrong. Completely so, but with verry large amounts of certain anabolics your IGF raises drasticaly. Why would this not result in some for of perma gut?
I beleive gh - growth hormone (somatropin) - can cause some organ growth correct? Maybe that has a different mechanism but it seams this only happens at verry high doses over verry long periods of time.
Why do we not see such organ growth with the use of extreme amounts of anabolic androgenic steroids over periods of years? And a more importantly, if you were to take large doses of AAS especialy those of the stronger breed do you think that the doses could increase, perhaps from increasing the rate of the receptors processing the IGF-1r3.
Also wouldn't it be verry usefull to use this chemical post cardio because of the blood pumping so drasticaly to the muscle sites, even pre or mid cardio work out?
I'm sorry if I'm being dense, I gotta ask the questions!!
Those are actually some very good questions. The answers are equally good.
There are two completely different ways in which IGF-1 is produced in the body. Even the IGF-1 molecule itself is slightly different in each case. The first, well known case, is where gh - growth hormone (somatropin) - & insulin are used by the liver to make IGF-1 which is then released into the bloodstream. anabolic androgenic steroids has little to no bearing on this systemic, or "paracrine" IGF-1. It just circulates in the bloodstream and eventually finds an IGF-1 receptor on the outside surface of a cell and attaches to it, activating it.
The other pathway, the one that is rarely discussed, is the autocrine pathway. This is where a cell will produce its own IGF-1, different peptides than the systemic, for its own internal use. These are called IGF-1Ea and IGF-1Ec or MGF. They are produced inside the cell, and act on receptors within the cell and just outside of the cell, on the myoblasts. These peptides don't go anywhere. When they leave the cell, they stay close to the surface. This is the pathway that anabolic androgenic steroids will greatly upregulate.
So on one hand you have the systemic with its effects on the surface receptor and you have the autocrine with its effects on the internal receptor, on the myoblasts and also perhaps on the surface receptor. So obviously when you know this it becomes obvious that the IGF-1 from anabolic androgenic steroids - the autocrine - will never give you the gh - growth hormone (somatropin) - gut because the IGF-1 that it makes your cells produce never leaves the cell itself, it doesn't circulate around to go attach to an intestinal wall receptor.
The pathway through which gh - growth hormone (somatropin) - causes organ growth *IS* systemic IGF-1. Most of the effects of gh - growth hormone (somatropin) - are actually effects of IGF-1. gh - growth hormone (somatropin) - is simply not very active on many cells but it is much converted by the liver into IGF-1 and this is what mediates the effects of gh - growth hormone (somatropin) - . As I posted above, there ARE some effects of GH that are not mediated through IGF-1 but most of them are.
As far as upregulating the surface receptors through anabolic androgenic steroids usage, I have seen no evidence that points that way, but that is not entirely impossible. Improbable, but not impossible.
As far as pinning post-cardio, I don't see it. In my opinion, for bodybuildersIGF-1 has two main purposes: firstly hyperplasia, its main use, and secondly general tissue repair, meaning healing and preventing injury. Ligaments aren't repaired by IGF-1 but they're a rare exception. It is too expensive and too good at better things IMO to be wasted on a simple pump.
How would one transport this to the gym for post wo injection? What's the best way to maintain integrity, avoid heat and not losse any?
Suggestions?
Diluted in AA, it is stable for a year at 98 degrees F. Of course, the insides of your car in the midst of a sunny summer day will be much hotter than that. Not the inside of your locker though.
What I always do is to load up a syringe with just the needed amount of IGF & AA, then use a small amount of aluminum foil to make a spacer between the end of the plunger and the cylinder to avoid discharging the syringe in transit, and put this and a couple alcohol pads and my BW inside a sunglass case in my gym bag.
I grab my bag after my workout, go change in the shower or toilet and pin at the same time. Then I get my shake.
