[Grunt76]

On July 20 I got into some pretty intense discussion on another board about IGF-1. I got so rattled with the misinformation that I decided to loose my 13 years of reading on IGF-1 onto that board. Here's the result.

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 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 R3 IGF-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? Clen/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 (and MGF too). 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.

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 50mcg 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.

What else?

All the talk about IGF-1's half-life is UTTER BULL****. 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 bull****. 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 localized effects. Period. You get them by pinning immediately postworkout. Period. End of argument.

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.

[Grunt76]

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 AAS 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 E3D igf-1 treatment is better than ED because ED downregulates the receptors too quick. It takes some time for receptors to be able to come back in full after a megadose of even 20mcg of IGF-1. 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, 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.

[Grunt76]

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 HGH?

Great questions. I'll start with some background on the peptides from back before IGF-1 was commonly used. GH 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 slin on its own doesn't do much for muscle. It does make you fat but not much bigger. With AAS 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 slin and GH are synergystic is that when levels of both are high, the liver turns the GH into IGF-1. That's right, when doing slin & GH, you are in fact using these because your body makes more IGF-1 with them. So it isn't the slin OR the GH 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 slin & GH 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 to IGF-1 receptor downregulation, 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 receptor downregulation is lesser with hIGF-1 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 receptors rest is extremely important to continued results. You get the same effect out of slin & gh 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 slin & gh are synergistic. Then the next question: what about slin & 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 that IGF-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 & IGF-1 at the same time. There is evidence that ED dosing of LR3 reduces GH release in the body, so it makes plenty of sense to use both at the same time.

Slin & 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 slin. The limit to the body's ability to release slin isn't easily reached. Even feeding 10,000 cals ED your body can produce the slin to store that. Easily.

Am I stating there is no use in pinning slin & IGF together? No. There is evidence that shows that pinning slin 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 slin, or slin reduced. I prefer the second option, although I am at a loss as to the amount of slin 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 slin. 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 releaser named GHB and combined that with a few ounces of sugar, the idea being of course a cheap version of GH & Slin. 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.

[Grunt76]

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.

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 AAS, the gains are "this many lbs of LBM". On clen/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 bodypart. 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.

[Grunt76]

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.

[Grunt76]

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 AAS? 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 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 AAS 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 & Slin are used by the liver to make IGF-1 which is then released into the bloodstream. AAS 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, a slightly different peptide than the systemic, for its own internal use. It is produced inside the cell, and acts on receptors within the cell. This is the pathway that AAS will greatly upregulate. This IGF-1 never leaves the cell.

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. So obviously when you know this it becomes obvious that the IGF-1 from AAS - the autocrine - will never give you the GH 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 causes organ growth *IS* systemic IGF-1. Most of the effects of GH are actually effects of IGF-1. GH 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. 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 AAS 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 bodybuilders IGF-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.

[Grunt76]

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.

IGF-1 is totally legal, so even if you get caught with some in a syringe, even if it comes to that, the police can only apologize politely for the trouble of questioning you and all that.

I still don't see how someone is going to find out what I do in my toilet stall though...

Never was a problem for me. I know a guy who tried in his car and was seen a few times, and got in some crazy situations with that. No police or anything, just zany adventures of a stressed guy.

[Grunt76]

Note: I use "Hyperplasia" in the above posts, knowing it isn't the exact word for growth of new myoblasts. Close enough I guess.

[Grunt76]

Great info Grunt....I always like reading your stuff. I am in the middle of a 16week AAS cycle, and I started it using IGF, by the end of this 16 weeker I should have not only larger cells from the AAS but new cells from the IGF that are now larger cause of the AAS correct.

Indeed my friend. It should be noted that the new cells are myoblasts, pre-muscle cells, that will fuse with your existing muscle cells and donate their nucleii which are in fact myonucleii.

A muscle's protein-repair engine is the myonucleii. The more of them in a cell, the bigger the cell and the greater the ability to regenerate protein. This explains the permanent gains from IGF-1 in that the number of myonucleii does not easily decrease, which gives a cell a new minimum size. Unless of course a person undergoes starvation, but that's not the case around these parts. When we take AAS, it's the myonucleii that get stimulated into overdrive.

[Grunt76]

i know nuttin about igf so dont take this wrong im just curious, was this info from research or someones theroy. the only reason i ask is cuzz you put a limit on the mcgs before it went to intestins. everyone is different where did the # come from? thanks for your time.

It's all Grunt76's work. 13 years of research and human trials.

You are right, the number is a guesstimate. From talking with other users, 40mcg is a dose at which, when injected immediately postworkout, good long-term gains are experienced with slowly diminishing effect.

The ideal dose would be the one that you can use forever. Remember, if you inject just the right amount immediately postworkout, there will be no spillover of the IGF-1 into other receptors and so these (local) receptors will have plenty of time to re-upregulate before next injection time, and so for every bodypart.

Sadly I must report that I have not yet found that "perfect dose" so 40mcg is a good place to go, where you get your results, no major gut effect and only slow desentitization.

No matter how you split it, the "perfect dose" would be variable depending on muscle worked, intensity of workout and about a zillion other factors, making it just a theoretical thing.

[curqleez]

May be too soon to ask this but any info on Peg mgf?

[jomi822]

Originally Posted by Grunt76

The other pathway, the one that is rarely discussed, is the autocrine pathway. This is where a cell will produce its own IGF-1, a slightly different peptide than the systemic, for its own internal use. It is produced inside the cell, and acts on receptors within the cell. This is the pathway that AAS will greatly upregulate. This IGF-1 never leaves the cell.

this seems to lend credibility to those who thing long term steroid use can initiate muscle cell hyperplasia.

[glenihan]

saw this on the other board .. what great info .. and even got almost pro's backing .. that's big in my book