Des (1-3) Igf-1

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    i guess i misunderstood what was being said about this compound. i thought the half life was extended due to the lack of binding to IGFBP. if that is the case then the fact that it is 1000 percent more anabolic is negated right? it doesnt make sense to me right now from what i have read. maybe i should reread this ****. also i read on another board that lr3 igf1 is just a glucose disposal agent only and that the hyperslasia thing is more of a myth than fact. anyone care to comment.

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    i agree luda 100 percent something not adding up either way its seems to be working
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    200 bucks is not bad again that is buying just once. Think buying in bulk. It may drop it by few dollars.
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    I am getting a price this week for a 30 day supply to see how much I can get it for. If its reasonable I will think about it for the future.
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    Quote Originally Posted by djbombsquad View Post
    I am getting a price this week for a 30 day supply to see how much I can get it for. If its reasonable I will think about it for the future.

    DJ, I think you suffer from peptide ADD syndrome.
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    I have a friend that will do a cycle with me. I am currently logging cre 02 so I can't do any thing but once I am done I may do cre 02 and some peptides.
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    Quote Originally Posted by Bobaslaw View Post
    DJ, I think you suffer from peptide ADD syndrome.
    i was thinking more of 'pipe dreams' syndrome.
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    Quote Originally Posted by ludacris007 View Post
    i guess i misunderstood what was being said about this compound. i thought the half life was extended due to the lack of binding to IGFBP. if that is the case then the fact that it is 1000 percent more anabolic is negated right? it doesnt make sense to me right now from what i have read. maybe i should reread this ****. also i read on another board that lr3 igf1 is just a glucose disposal agent only and that the hyperslasia thing is more of a myth than fact. anyone care to comment.
    its not a myth, the research literature proves that igf causes hyperplasia and there is anecdotal evidence that lr3 can to a lesser degree mimic the body's own igf.
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    Quote Originally Posted by pumbertot View Post
    its not a myth, the research literature proves that igf causes hyperplasia and there is anecdotal evidence that lr3 can to a lesser degree mimic the body's own igf.

    I'm not saying you're wrong however theres a debate going on about that very question on another forum I belong to. I'm not sure it was who first wrote it but they are saying once you alter the protein chain that makes it the Lr3 version it's not the exacvt same compound and it's no longer useful as a bb'ing supplement. What heres the post I found on my other forum not saying I believe it or not. I'm willing to give anything a try once. I may react differently.

    After many years of making countless posts on LR3 IGF-1, I've finally tired of the topic.
    This will be my last post ever on LR3 IGF-1.

    1) Gropep,who invented LR3 IGF-1, altered the protein chain for prolonged lab experiments. Once the protein chain was altered, IGF-1 lost it's muscle building properties once converted to LR3 IGF-1

    2)Yes, some legit research has shown that IGF can multiply muscle fiber, but there is ZERO research on LR3 IGF-1, nor will there ever be. It was meant for lab cultures only

    3) Should you get IGF-1, it is rendered useless by using acetic acid, since you need the correct pH and ionic environment for the peptide chains to unwind. HCL is what's needed.

    4)The bulk of the response to IGF comes from it's ability to act as a sensational glucose disposal agent. This is the part where IGF's name, "Insulinlike", comes to the fore.

    5) I'm convinced any weight gain on LR3 IGF-1 is an uptick in glycogen/ water retention.

    6) Myself, along with several friends ,conducted studies on ourselves running LR3 IGF-1 at 3 different doses. Since LR3 IGF-1 is touted as some miracle mass builder, we never used steroids in our experiments. At 100 mcg, 150 mcg, and 200 mcg no one experienced muscle gains after 4 weeks on. Yes, we had hydrostatic testing done before during and after each experiment.

    I think you get my point ....no more LR3 IGF-1 debate for me. You want to piss your money away, go for it.


    ~RR
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    Also if they pegylated the (des) wouldn't that give it a longer half-life as well. I'd like to see that. B/c if it's just astronomically expensive and has a half life of a few minutes. That wouldn't have me buying it any time soon.
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    Quote Originally Posted by kbtoy31 View Post
    I'm not saying you're wrong however theres a debate going on about that very question on another forum I belong to. I'm not sure it was who first wrote it but they are saying once you alter the protein chain that makes it the Lr3 version it's not the exacvt same compound and it's no longer useful as a bb'ing supplement. What heres the post I found on my other forum not saying I believe it or not. I'm willing to give anything a try once. I may react differently.
    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.
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    Quote Originally Posted by papapumpsd View Post
    With all of Dat's data and convo on GH releasers, why would you run GHRP-6 w/o CJC-1295? And why would you run IGF-1 along with GH releasers? I may be mistaken, but Dat's thread has info saying there could be negative feedback at hand if administering exog. IGF-1.

    Remember, GH results in IGF-1 release.
    It would be more appropriate to state that in sedentary people, GH results in IGF-1 release whereas in athletes GH results mostly in MGF release (which is admittedly another form of IGF-1 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.


    Quote Originally Posted by xtraflossy View Post
    Well you have to do the math on this one..

    We use LR3 becasue it has a longer half-life then IGF1.
    We used MGF and the half life was too short so we used peg-mgf (as opposed to viral administration of course).

    Why?? Because while at $200 a gram, how many shots would you have to use daily to elicit the desired effect? (lol- you do know that you make this compound naturally right? ,..its cleaved via lactic acid if I recall correctly)

    Anyways, 30-100mcg shots a few times a day,.. you will go through it

    Then when you look at possible gains vs. price (and ease of use) LR3 looks much better.

    Now, should it become bound to something to preserve the halflife, then it will be a different story. But right now, it doesn't look like you can compare it to LR3, simply because the playing field isn't on even ground.
    Actually LR3 has a SHORTER half-life in the body than normal human hepatic IGF-1. And that's a GOOD thing.

    Actually LR3 is considered to be roughly 10x as potent as hIGF-1 and so is the DES[1-3] 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.
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    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.
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    Quote Originally Posted by djbombsquad View Post
    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.
    I'm ready for the lab work part of it...
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    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.
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    Quote Originally Posted by kbtoy31 View Post
    I'm not saying you're wrong however theres a debate going on about that very question on another forum I belong to. I'm not sure it was who first wrote it but they are saying once you alter the protein chain that makes it the Lr3 version it's not the exacvt same compound and it's no longer useful as a bb'ing supplement. What heres the post I found on my other forum not saying I believe it or not. I'm willing to give anything a try once. I may react differently.
    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 des-igf 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 des-igf)

    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 des-igf, 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
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    Quote Originally Posted by kbtoy31 View Post
    Also if they pegylated the (des) wouldn't that give it a longer half-life as well. I'd like to see that. B/c if it's just astronomically expensive and has a half life of a few minutes. That wouldn't have me buying it any time soon.
    What is it with you guys and long half-lives?

    First step is UNDERSTANDING HOW IT WORKS.

    Second step is NOT WONDERING ABOUT half-life because it's NOT A POINT.

    IGF-1 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 IGF-1 that has the longest half-life is the hIGF-1 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 re-typing 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?
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    Quote Originally Posted by Grunt76 View Post
    What is it with you guys and long half-lives?

    First step is UNDERSTANDING HOW IT WORKS.

    Second step is NOT WONDERING ABOUT half-life because it's NOT A POINT.

    IGF-1 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 IGF-1 that has the longest half-life is the hIGF-1 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 re-typing 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 again?
    LOL grunt! Hey, if people want a long half-life 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 half-life 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.
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    Quote Originally Posted by Grunt76 View Post
    It would be more appropriate to state that in sedentary people, GH results in IGF-1 release whereas in athletes GH results mostly in MGF release (which is admittedly another form of IGF-1 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 half-life in the body than normal human hepatic IGF-1. And that's a GOOD thing.

    Actually LR3 is considered to be roughly 10x as potent as hIGF-1 and so is the DES[1-3] 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.

    lol- Im going to try and get you to repeat it one more time
    almost anyways..

    LR3, is a bound form of igf-1; activates to a large degree the slin receptors, which is a immediate effect.
    igf-1 (what we would use) is not atached to a binding protein. which gives it an immediate effect.

    So; as far as half-lives go, are they the same in terms of effectiveness or is there some other measurement by which this is measured within the body?
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    Quote Originally Posted by xtraflossy View Post
    lol- Im going to try and get you to repeat it one more time
    almost anyways..

    LR3, is a bound form of igf-1; activates to a large degree the slin receptors, which is a immediate effect.
    igf-1 (what we would use) is not atached to a binding protein. which gives it an immediate effect.

    So; as far as half-lives go, are they the same in terms of effectiveness or is there some other measurement by which this is measured within the body?
    LR3 is NOT a bound form of IGF-1. It is an UNBINDABLE form of IGF-1. Not to be confused with the hIGF-1/IGFBP3 complex which is expensive but available also. hIGF-1 binds to IGFBP's whether you like it or not. In other words, when you inject hIGF-1, 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 IGF-1 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 hIGF-1 contradicts pretty much everything I have seen on cell culture data. It activates the IGF-1 receptor which shuttles in aminos and sugars. Whether or not the SAME intracellular pathways get activated as with hIGF-1 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 IGF-1 LR3 and none are conclusive that there is no NEW CELL EFFECT, i.e. permanent, delayed, long-term growth as well as other effects.
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    Alright- I kinda inferred the answer to my question, in a way.

    LR3 half life is SHORTER then igf-1 simply because none of it gets bound or absorbed. It circulates until it activates. compared to igf-1 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?
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    Quote Originally Posted by xtraflossy View Post
    Alright- I kinda inferred the answer to my question, in a way.

    LR3 half life is SHORTER then igf-1 simply because none of it gets bound or absorbed. It circulates until it activates. compared to igf-1 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?
    Ah well this is where things get very complicated.

    hIGF-1 will not activate "as fast" as LR3 because it is bound to, say, IGFBP3, which "stores" IGF-1 until receptors are "hungry enough" to warrant freeing the IGF-1 molecule from the IGFBP and then activating the receptor. When is "hungry enough"? That is the all-important question. Whereas LR3 will activate no matter if the receptor is all alone on the cell surface or part of a just-worked 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 hIGF-1, meaning fewer molecules. LR3 is known to be about 10x more potent than hIGF-1 at activating receptors, SPECIFICALLY BECAUSE the binding proteins need "hungry enough" receptors.

    The body offers a number of responses to the various forms of IGF-1 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 hIGF-1 with equal efficacy? Unknown. Whereas DES IGF-1 is naturally-occuring, 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.
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    Great class. This just keeps getting better.
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    Quote Originally Posted by Grunt76 View Post
    Ah well this is where things get very complicated.

    hIGF-1 will not activate "as fast" as LR3 because it is bound to, say, IGFBP3, which "stores" IGF-1 until receptors are "hungry enough" to warrant freeing the IGF-1 molecule from the IGFBP and then activating the receptor. When is "hungry enough"? That is the all-important question. Whereas LR3 will activate no matter if the receptor is all alone on the cell surface or part of a just-worked 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 hIGF-1, meaning fewer molecules. LR3 is known to be about 10x more potent than hIGF-1 at activating receptors, SPECIFICALLY BECAUSE the binding proteins need "hungry enough" receptors.

    The body offers a number of responses to the various forms of IGF-1 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 hIGF-1 with equal efficacy? Unknown. Whereas DES IGF-1 is naturally-occuring, 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.

    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 recently-I 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
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    Certainly hyperplasia research is absolutely fascinating.
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    This thread's been around a long time. Any results worth posting?
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    Bumpity
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