I have responded to the Bouncers online journal with the same post but feel that this needs a more general airing. So here goes:
I have decided to change tack on the IGF1 Long 3. I have it but wont use it again. Here is my reasoning.
I have doubt's about the use of Long L3 (gro-pep et al). The modification to this analogue of human IGF-1 results in it not reacting to IGF-1 binding proteins (IGF bp) there are number of bp (seven or more) and they play a part in transport and regulation of the effects of IGF-1 in tissues. In serum IGF-1 is predominantly bound to bp-3. In order to cross into tissues from the blood it needs to then bind to bp-2, a cross membrane shuttle. No binding to bp-2 no movement of IGF-1 into tissues.
This is a fundemental flaw in using Long 3. By sub-cutaneous injection it will not get into the bloodstream period and even by intra muscular injection you would need many, many injections into the muscle to get usefull distribution! This lack of binding is not an issue in tissue culture (its actual use) because cultures are usually single cell layers where the IGF-1 receptors are exposed directly to the media containing the long 3.
Use of normal, receptor grade IGF-1 will be effective. However, the amounts produced naturally in the body are relatively high and to boost these levels you would need a prohibitively expensive amount of IGF-1. It has been demostrated that by using Growth Hormone at even 2 I.U. per day can lead to a threefold increase in IGF-1 lvels in elderly patients( who are often GH deficient) and so this is the most effective means of increasing IGF-1 levels.
I think that the pain of injections may be caused by the modification to the IGF-1 analogue. Whilst the bulk of the protien is human (and should not cause any adverse reaction when injected) i suspect that this modification is not a naturally occuring form and as such this is the cause of the pain (on injection), not the fact that the IGF-1 is reconstituted in ( a very mild) acid (proof of this is that mixed with say 4x it's volume of PBS which should neutralize the acid has no effect on the inflammatory response
I believe that the bouncer has given a usefull and true report on the use of IGF-1 long 3 and when you look at the science behind it we should give up on this product and move on!
My supply is staying in the freezer. I may use it tissue culture studies (its correct use) but that's it!
Cheers all,
Sootybaby
I have decided to change tack on the IGF1 Long 3. I have it but wont use it again. Here is my reasoning.
I have doubt's about the use of Long L3 (gro-pep et al). The modification to this analogue of human IGF-1 results in it not reacting to IGF-1 binding proteins (IGF bp) there are number of bp (seven or more) and they play a part in transport and regulation of the effects of IGF-1 in tissues. In serum IGF-1 is predominantly bound to bp-3. In order to cross into tissues from the blood it needs to then bind to bp-2, a cross membrane shuttle. No binding to bp-2 no movement of IGF-1 into tissues.
This is a fundemental flaw in using Long 3. By sub-cutaneous injection it will not get into the bloodstream period and even by intra muscular injection you would need many, many injections into the muscle to get usefull distribution! This lack of binding is not an issue in tissue culture (its actual use) because cultures are usually single cell layers where the IGF-1 receptors are exposed directly to the media containing the long 3.
Use of normal, receptor grade IGF-1 will be effective. However, the amounts produced naturally in the body are relatively high and to boost these levels you would need a prohibitively expensive amount of IGF-1. It has been demostrated that by using Growth Hormone at even 2 I.U. per day can lead to a threefold increase in IGF-1 lvels in elderly patients( who are often GH deficient) and so this is the most effective means of increasing IGF-1 levels.
I think that the pain of injections may be caused by the modification to the IGF-1 analogue. Whilst the bulk of the protien is human (and should not cause any adverse reaction when injected) i suspect that this modification is not a naturally occuring form and as such this is the cause of the pain (on injection), not the fact that the IGF-1 is reconstituted in ( a very mild) acid (proof of this is that mixed with say 4x it's volume of PBS which should neutralize the acid has no effect on the inflammatory response
I believe that the bouncer has given a usefull and true report on the use of IGF-1 long 3 and when you look at the science behind it we should give up on this product and move on!
My supply is staying in the freezer. I may use it tissue culture studies (its correct use) but that's it!
Cheers all,
Sootybaby

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