Des (13) Igf1
 10112008, 01:36 PM
 Stats
 5'11" 240 lbs.
 Join Date
 Mar 2008
 Posts
 520
 Rep Power
 341
 Level
 19
 Lv. Percent
 21.66%
for me hyperplasia can be see if one has to take extended layoffs from training. you retain way more muscle than previous times when you have used igf for a few months in between. ive experienced this personally, Grunt has too and many others. its a debate but as that refernece says to me theres no debate.
Im happy I get hyperplasia and if you dont want any of that then dont take it.
edit: I should close by saying I ahve no reason to try to publicly defend my beliefs. im happy if nobody else was to use igflr3, all the more for me to use.lol.  10142008, 04:21 AM
 Stats
 5'9" 272 lbs.
 Join Date
 Oct 2005
 Age
 47
 Posts
 3,131
 Rep Power
 1784
 Level
 39
 Lv. Percent
 22.08%
It would be more appropriate to state that in sedentary people, GH results in IGF1 release whereas in athletes GH results mostly in MGF release (which is admittedly another form of IGF1 but still bears clarifying due to our needs and uses).
The GH releasers would most certainly be exactly BECAUSE there is a negative feedback loop. If I remember correctly, that negative feedback loop is mediated through somatostatin, and the releasers work through diminishing somatostatin effects. Which is perfect.
Actually LR3 has a SHORTER halflife in the body than normal human hepatic IGF1. And that's a GOOD thing.
Actually LR3 is considered to be roughly 10x as potent as hIGF1 and so is the DES[13] form, making them possibly equal. Then again, for our needs, only lab work (i.e. human trials, LMAO) will tell us which one is better.  10152008, 02:10 AM
 Stats
 5'5" 150 lbs.
 Join Date
 Dec 2006
 Posts
 6,897
 Rep Power
 365462
 Level
 58
 Lv. Percent
 2.61%
I have seen research however that suggests the half life of DES1,3 is so short yet powerful that there were some very interesting research articles a person found that showed research with LR 3, and DES. The DES is very powerful from what I have read, but yes the half life is extremely quick. I am not a researcher though. I would think looking at government websites such as National Institutes of Health, or NIST, or anything from some student researchers that post in there University blogs would allow us to better see how DES can or can not benefit us.

 10152008, 10:03 AM
 10152008, 12:16 PM
 Stats
 5'5" 150 lbs.
 Join Date
 Dec 2006
 Posts
 6,897
 Rep Power
 365462
 Level
 58
 Lv. Percent
 2.61%
I know. I want to see lab work too. If I can get it for a reasonable price I may do half des and the other half of the cycle lr3.
 10212008, 06:12 AM
lol Its the same information going around over and over...
IGF1=hyperplasia. Thats how your body does it.
LR3= bound IGF1. IS usefull in bb'ing, as it activates the slin receptors. So if your arguing that slin is ineffective then..
HOWEVER; LR3 CAN be broken dow by the body's normal processes just like IGH1. You theoreticly CAN produce more desigf this way then you normally might.
LR3 is modified at the beginning of the peptide chain I beleive, so if broken/cleaved in the middle, then the second half would be identical to a portion of the original IGF chain (in regards to desigf)
Its pricy; again. it has a short half life, again. You would need to use it in a manner simular to regular igf (not LR3)
for a few hundread dollars, you are better off going with LR3. If you want the novilty of being one of the privilaged who uses desigf, then by all means, do so. I totally understand. Ive spent the money right when mgf came out (and was one of the first to use/log it here)
My spelling DOES suck, and sucks more at 6am  10212008, 08:07 AM
 Stats
 5'9" 272 lbs.
 Join Date
 Oct 2005
 Age
 47
 Posts
 3,131
 Rep Power
 1784
 Level
 39
 Lv. Percent
 22.08%
What is it with you guys and long halflives?
First step is UNDERSTANDING HOW IT WORKS.
Second step is NOT WONDERING ABOUT halflife because it's NOT A POINT.
IGF1 binds to a receptor and activates intracellular pathways. WHY ON EARTH would you want it floating in your blood for a long time? It starts doing its job when it activates a receptor. The form of IGF1 that has the longest halflife is the hIGF1 which gets bound by IGFBP's. It floats around for hours. Instead, we inject stuff that binds to receptors right away and gets to work instead of floating around uselessly.
I can't believe this. Why am I always retyping the same stuff over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over and over again?  10212008, 09:00 AM
 Stats
 5'8" 216 lbs.
 Join Date
 Feb 2007
 Age
 37
 Posts
 1,733
 Rep Power
 1071
 Level
 31
 Lv. Percent
 12.39%
LOL grunt! Hey, if people want a long halflife for no good reason, go nuts! They're just repeating a fancy term they heard used for other compounds and think it fits for all compounds. These individuals would be known as simpletons. They refuse to attempt to understand the basics. I'm willing to bet they'd like an IGF compound w/a halflife of 10 years.....hey, why not?! That sh!t will be floating around "active" for 10 years....isn't that the point?! NOPE! The point is, as you have stated, to BIND to its appropriate receptor and "gets to work".
It really is as simple as you make it. IGF is a chemical messenger. It floats around and binds to a receptor and "tells" the cell to do something (aka, "sends the message"). Why someone would want this messenger bumbling around for a long time, who knows. Again, people are just regurgitating "hear say" in a way that makes no sense.  10212008, 09:12 PM
lol Im going to try and get you to repeat it one more time
almost anyways..
LR3, is a bound form of igf1; activates to a large degree the slin receptors, which is a immediate effect.
igf1 (what we would use) is not atached to a binding protein. which gives it an immediate effect.
So; as far as halflives go, are they the same in terms of effectiveness or is there some other measurement by which this is measured within the body?  10212008, 11:09 PM
 Stats
 5'9" 272 lbs.
 Join Date
 Oct 2005
 Age
 47
 Posts
 3,131
 Rep Power
 1784
 Level
 39
 Lv. Percent
 22.08%
LR3 is NOT a bound form of IGF1. It is an UNBINDABLE form of IGF1. Not to be confused with the hIGF1/IGFBP3 complex which is expensive but available also. hIGF1 binds to IGFBP's whether you like it or not. In other words, when you inject hIGF1, some of it will go to work on your target cells just like the LR3 and some of it will get bound by the various IGFBP's. Your liver may well start pumping out additional IGFBP's as well, sensing the amount of unbound IGF1 being out of whack.
I also want to know if LR3 will also trigger the release of IGFBP's which would be a FANTASTIC thing.
That it would bind more to the insulin receptor than hIGF1 contradicts pretty much everything I have seen on cell culture data. It activates the IGF1 receptor which shuttles in aminos and sugars. Whether or not the SAME intracellular pathways get activated as with hIGF1 I do not know, and in terms of efficacy, it is way up in the air. How would we compare???
I cannot for the life of me begin to think up an experiment that would do this in a "fair" manner.
I do know quite a few users of good IGF1 LR3 and none are conclusive that there is no NEW CELL EFFECT, i.e. permanent, delayed, longterm growth as well as other effects.  10222008, 04:40 PM
Alright I kinda inferred the answer to my question, in a way.
LR3 half life is SHORTER then igf1 simply because none of it gets bound or absorbed. It circulates until it activates. compared to igf1 which...will activate JUST as fast, but some will be bound.
assuming = doses of each,
you will activate more receptors with LR3 simply because binding proteins don't interfere, using = doses
That being said; compared to LR3, the des variant would simply have a stronger binding affinity (If I remember correctly, this is the case)????
So the only limiting factor here is the response the body can produce in response to site activation? (but I thought it was a off or on switch, not a "dimming" light with different degrees of activation)
I'm just thinking through things here would almost seem to me that if there is only one degree of activation on our body, it simply becomes a matter of activating X number of sites, which would make the des version just a more expensive option, and no better...
Thoughts?  10222008, 05:14 PM
 Stats
 5'9" 272 lbs.
 Join Date
 Oct 2005
 Age
 47
 Posts
 3,131
 Rep Power
 1784
 Level
 39
 Lv. Percent
 22.08%
Ah well this is where things get very complicated.
hIGF1 will not activate "as fast" as LR3 because it is bound to, say, IGFBP3, which "stores" IGF1 until receptors are "hungry enough" to warrant freeing the IGF1 molecule from the IGFBP and then activating the receptor. When is "hungry enough"? That is the allimportant question. Whereas LR3 will activate no matter if the receptor is all alone on the cell surface or part of a justworked muscle, very hungry for it.
That's why we inject the LR3 directly in the muscle just worked, the receptors are mightily upregulated, and you just hope that more of your LR3 goes to this specific muscle than other places. Which it would anyway if you went IV with it, since that muscle temporarily has a lot more receptors, comparatively. Still, putting it IN THERE simply CANNOT HURT. How much benefit is obtained by doing this? It cannot be easily quantified, but "some" would be appropriate.
When you state equal doses, do you mean in terms of molecule numbers or by weight? LR3 is heavier than hIGF1, meaning fewer molecules. LR3 is known to be about 10x more potent than hIGF1 at activating receptors, SPECIFICALLY BECAUSE the binding proteins need "hungry enough" receptors.
The body offers a number of responses to the various forms of IGF1 activating surface receptors. On a myotube, shuttling of aminos and carbs seems to be the main effect. On a myoblast, differentiation and fusion, thus increasing the neighboring myotube's myonuclear number, is another effect. If a sufficient concentration of myoblasts exists and a sufficient number of them get to the "fusion" part at a close enough time, a new myobtube is formed, and that is possibly the holy grail of bodybuilding: a new muscle cell. But no matter if you think of it as an on/off switch or different degrees of activation on a cell basis, on an organ basis, it is very much a dark/bright continuous spectrum.
Now does LR3 exert every single one of the actions of hIGF1 with equal efficacy? Unknown. Whereas DES IGF1 is naturallyoccuring, making it a potentially better option.
It's up in the air, really, and only people who have experience using LR3 and then DES will be able to testify. As you know, there is no human research on LR3 (except by us) and the same is true of DES.  10222008, 05:25 PM
Great class. This just keeps getting better.
 10222008, 05:39 PM
So it would seem binding affinity has no correlation then which would imply that the receptor is either activated or it is not.
Wouldn't that imply that it wouldn't matter weather our recepters were activated by a hit from LR3 or des the effect would be the same?
(which would mean spending more on the des would offer no benefit over LR3)
I beleive (and this isn't something new I thought of, but more a general statement) would be that the holy grail would be understanding by which mechanics the myoblast reaches or decides to fuse to a new cell over another action.
I would look into research done on bacteria and the chemical messages they give off to identify themselves to other same bacteria (I've seen something on this recentlyI think it was a simple amino acid) and the messages other bacterium give off to "intercept" this signal".. and since bacteria act simular in function to the body (single cells acting in concert..) ...I just think the operating level is simular between single cells and sourouning cells..
lol I'm going off the deep end here most likely  10222008, 05:46 PM
 Stats
 5'9" 272 lbs.
 Join Date
 Oct 2005
 Age
 47
 Posts
 3,131
 Rep Power
 1784
 Level
 39
 Lv. Percent
 22.08%
Certainly hyperplasia research is absolutely fascinating.
 05292011, 01:19 AM
 Stats
 5'9" 260 lbs.
 Join Date
 Jan 2010
 Posts
 540
 Rep Power
 362
 Level
 18
 Lv. Percent
 67.18%
This thread's been around a long time. Any results worth posting?
 06132011, 02:52 PM
 Stats
 5'10" 225 lbs.
 Join Date
 Oct 2009
 Posts
 1,494
 Rep Power
 27976
 Level
 30
 Lv. Percent
 39.71%
Bumpity