there are all these new variations out right now...all trying to fill the shoes of the longer standing peptide used in the BB community IGF-1 LR3..i guarentee that given enough time people will start contemplating are these a waste..right now there new so many people are on the bandwagon after breaking their ankles jumping off the igf1 lr3 bandwagon. how do you get 3 years of threads where people claim to have gotten good gains from lr3 when it doesn't work? it had to do something people will have their experiences and that just can't be ignored...
i get good gains on-cycle and during pct..i will continue to use it
how many othersw will continue to use LR3?
Hey Norman I thought about suggesting that to you when we talked privately. You are a nice guy and I can see you are bothered so let me give you some science that supports your position.
First though my advise is that if you gained from it then use it. Who cares what others think. There is no science that says LR3 will not bind to an IGF-1 receptor. It will... whether it is sufficient or not is an open unresolved question.
I am looking at a study right now that used high amounts of continually infused IGF-1 in three forms.
One group of diabetic rats got the truncated form, des(I-3)IGF-I and another group got the form with arginine at residue 3 and an N-terminal extension, termed LR3 IGF-I while another got straight IGF-1.
Another group was given insulin (30iu per day).
"All peptides increased muscle protein-synthesis rates and RNA levels by up to 50 %, with IGF-I the least potent."
"The highest dose rates used here were about 2.5 times those of the previous report [6] and induced growth rates almost equal to that observed for the insulin-treated rats. In fact, in terms of somatic growth the highest doses of des(l- 3)IGF-I and LR3-IGF-I were equipotent with the insulin treatment used here (1.25 mg/day per kg body wt.) and stimulated lean growth to the normal range for these rats.
Unlike insulin, the growth factors did not stimulate fat deposition, and in fact fat mass did not increase in proportion to the body mass. This difference could be explained by the paucity of type 1 IGF receptors in adipose tissue [19] and also argues against the IGF peptides acting via the insulin receptor to stimulate glucose uptake or other processes in this study. " - Insulin-like growth factor-I and more potent variants restore growth of diabetic rats without inducing all characteristic insulin effects, Frank M. TOMAS et al, Biochem. J. (1993) 291, 781-786
As far as which form is better: native IGF-1, Des or LR3:
"The variants were 2.5-3-fold more potent than was IGF-I (P < 0.001), with LR3-IGF-I consistently more potent than des(1-3)IGF-I (P = 0.1, NS)."
You can not use a study like this at all to figure out anything related to an effective human dosing schedule but it is one of several studies that refute the position of some that "IGF-1 LR3 is not capable of promoting growth".
It most certainly is capable.
It also refutes in part the people that say "LR3 is a good GDA but nothing more." You see LR3 does not bind to an insulin receptor to mediate these events. It binds to an IGF-1 receptor and through that becomes a good Glucose Disposal Agent. But if it is effective through that pathway to promote glucose disposal then it will also be mediating "hypertrophic" events as well.
So Norman you might wonder why I posted this since my opinion is that IGF-1 LR3 isn't an effective muscle builder unless it can be made to stay local perhaps by administering the ternary complex (IGF-1+IGFBinding Protein+Acid Labile Subunit). The reason is simple...there is no definitive resolution in the science and I like to learn and find all sorts of science that undermines or contradicts my opinions.
Plus I like to throw things up in my own face sometimes and say "take dat!"
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