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The Myth of LR3 IGF-I ("IGF1-LR3")'s Long Half-Life

I use it for advanced guys, with good results, but very differently from how it's used commonly. My protocol is proprietary. I edited this, because I would not actually apply LR3 IGF-I in your case.
I will get in touch! I really appreciate it sir! Sean
 
LR3, yes. It adds up at the doses & frequencies you need to use for any significant effects. It's WAY more expensive than a moderately-high pharma rhGH dose, that is going to give you severalfold the results of LR3 if you're healthy (i.e., GH responsive).
I see a lot of people saying 4 weeks on 4 weeks off lr3, do you find this neccesary? Or is this another 'give the AR a chance to resensitize"
 
I see a lot of people saying 4 weeks on 4 weeks off lr3, do you find this neccesary? Or is this another 'give the AR a chance to resensitize"
I don't see this as necessary because there's no known reason why its tachyphylactic effects would be any more profound than IGF-I's, for which yearslong treatment at a constant or relative dose is given to primary IGF-I deficient children with short stature.

RhGH sees substantial diminished potency at a constant dose that begins a trend decrement in ΔIGF-I between 4 & 5 mo. of continuous use and reaches a substantial decrement in GH response by month 9 (-42.73%) and yet guys still run rhGH year-round, and the same comment as for rhIGF-I's clinical use applies to rhGH with respect to short stature children.

I have all the horseshit saved that was written about LR3 IGF-I on BassKillerOnline, and it's just made up bro. That's where I think all of this bad information originated.
 
I don't see this as necessary because there's no known reason why its tachyphylactic effects would be any more profound than IGF-I's, for which yearslong treatment at a constant or relative dose is given to primary IGF-I deficient children with short stature.

RhGH sees substantial diminished potency at a constant dose that begins a trend decrement in ΔIGF-I between 4 & 5 mo. of continuous use and reaches a substantial decrement in GH response by month 9 (-42.73%) and yet guys still run rhGH year-round, and the same comment as for rhIGF-I's clinical use applies to rhGH with respect to short stature children.

I have all the horseshit saved that was written about LR3 IGF-I on BassKillerOnline, and it's just made up bro. That's where I think all of this bad information originated.
Fantastic - thanks!!
 
That's right, but I'd use rhIGF-I not LR3 in those cases, and in instances where GH response is low due to amenable health (e.g., liver, kidney disorders, prediabetes, obesity) or drug (e.g., trenbolone, estrogens) factors, try to ameliorate that first.

Does lower estrogen level increase or decrease liver hgh conversion to igf-1? So far what ive found is that lower estrogen levels are better (but not crashed levels)
 
Does lower estrogen level increase or decrease liver hgh conversion to igf-1? So far what ive found is that lower estrogen levels are better (but not crashed levels)
Well, high estrogens lower IGF-I, but it does not follow that low estrogen levels increase it.

I'll describe the process by which T=[Aromatase]=>E2 negatively feeds back on IGF-I bioavailability:

E2 is a negative factor for IGF-I bioavailability. That is, once aromatization is very high, E2 feeds back negatively on IGF-I levels because of IGFBP-1, an IGF-I binding protein that is increased by estrogens and inactivates IGF-I in its active form.

E2, then, is not a positive factor for enhancing IGF-I. Rather, aromatization as a process is.

Estrogens increase IGFBP-1, reducing IGF-I bioavailability and unleashing GH secretion by feedback withdrawal. It's why women have higher GH levels than men by body surface area and are less sensitive per-mg to rhGH, and require dose increase (titrating up) when using exogenous estrogens: oral estradiol dramatically decreases IGF-I activity, and transdermal less so.

The result of increasing E2 by T dose is a sort of asymptotic shape to the curve of T/IGF-I in men. That is, at low levels of E2 (because low T & therefore aromatization), IGF-I activity is also low. As the E2 levels (because moderate/moderately-high T and therefore aromatization) increase, IGF-I does as well. Up to a point where E2 effects begin to inhibit (negatively feed-back on) IGF-I. Then the curve starts to taper off, increasing at a decreasing rate initially, and then negatively accelerating.

So, the task of maximizing IGF-I requires both the use of aromatizing androgen (e.g., T) and if using moderately-high/high/very-high T doses, then also using an aromatase inhibitor (AI) at a dose that doesn't totally abrogate (block) aromatase but rather shifts the inflection point (asymptote) to the right on the T/IGF-I curve. Moreover, AI compound selection is paramount. Exemestane does not directly decrease IGF-I (because its primary active metabolite is an androgen & it possesses a steroidal core), so it is a good choice for this task.
 
Was wanting to run some peptides but I hear such hit and miss stuff about them it makes me not want to now.
 
Growth & Slin are peptides. Good ones.
Those are the only ones I've ran.
Green top hygetropins and humalin r from CVS.
This was 8 years or so ago.
Was say more towards, cjc, ghrp, lr3, tb500 all those new ones. Well i feel they are new. New to me lol
 
I know if you have good gh and use the slin right it's fucking crazy what it does.
 
By the law of large numbers, probably. It does have its uses in some cases, but it's less anabolic in human skeletal muscle (where it is equipotent to IGF-I) than slin or GH and the doses & frequencies at which they must be administered for any biologically relevant effect (typified by hypoglycemia) are tremendously expensive.
So which dose is effective? 1mg spread over the day? Higher then that?
 

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