I saw you said in another thread something about igf lr3 inhibiting muscle igf-1 creation by gh and slin. I don't remember exactly what you said, but would this mean you do not recommend using igf-1 lr3 with a slin+gh cycle? Or at least do not take your LR3 post workout with GH + slin? How about rH-IGF1 PWO? For example, take GH immediately PWO, then 20 mins later take rH-IGF1, then 10 mins later slin + carbs?
Also, what is everyone's opinion on GH + SLIN protocols for mass gains? I have heard so many different ones and issues with timing, etc. How would you include IGF in here and would you use LR3 or rH?
Gavin's protocol implements IGF LR3 correct? He basically says 10-15 IU GH PWO 3x weekly, wait 20 mins, do 30 mcg igflr3, then wait 10 mins and do your slin humalog...all IM right?
I like that idea, but I have always been really nervous about LR3 and it promoting cancer development. The fact that it decreases apoptosis and allows / promotes cells living longer than they should or cells living that shouldn't be living (b/c they should be killed by apoptosis b/c of mutations) makes me really nervous. How much do you guys think the LR3 helps? What about using rH-IGF?
also, didn't datbrue say that using LR3 around the same time as slin and GH was bad or something?
I think you are referring to the post where I said:
Also as a general note, rhIGF-1 (according to the studies) inhibits natural GH for a couple of hours post administration. Thats it. But IGF-1 LR3 has a different set of behavioral characteristics that probably mean it will inhibit GH release for a longer period of time.
I also said:
GH leads to creation of IGF-1 in muscle cells & MGF in muscle cells. That autocrine production and use is really the only thing that matters.
Then I posted a link to the following post I made in September (keep in mind IGF-IEa is the muscle form of IGF-1 & MGF is an IGF variant that is only expressed in muscle):
Cultured muscle cells as a system for the analysis of IGF-I splicing regulation by factors present in the circulation, Velloso,Cristiana P, The Physiological Society (2004) J Physiol 558P, C5
It has recently been shown that muscle cells grown in 3-D collagen matrixes upregulate IGF-I transcript expression in response to stretching of the matrix (Cheema et al., 2004). In the present work we have studied muscle cells in culture with the aim of determining if either or both of the two splice variants of IGF-I would be upregulated when treated with GH and/or IGF-I, in the absence of mechanical signals C2C12 myoblasts were grown to 50% confluency in medium containing 10% foetal calf serum (FCS). The cells were transferred to medium containing i) 1%FCS only, ii) 100 ng/ml rhGH iii) 100 pg/ml IGF or iv) both. In the untreated cells (i) both isoforms (IGF-IEa and MGF) were present. Treatment with rhGH alone lead to an increase in IGF-IEa and MGF of about 3 fold over control (Table 1). However, treatment with IGF-I abolished expression of both isoforms. When used in combination, the inhibitory effect of IGF-I overode the GH stimulation of IGF-IEa and MGF transcription. We conclude that muscle tissue can upregulate IGF-I isoform expression as a direct result of hormonal stimulation or stretch stimuli. The isoforms of IGF-I seem equally sensitive to GH stimulation in vitro. In vivo, a negative feedback mechanism may modulate the action of GH on IGF-I transcription in muscle tissue in by circulating or local IGF-I expression.
Table 1. IGFIa and MGF transcript levels (x 10-8 ng mRNA / µg RNA) in C2C12 cells following GH and IGF-I treatment.
Data are Means ± S.D. of three separate experiments. * Significant difference (P<0.5) relative to control (unpaired t-test).
I saw you said in another thread something about igf lr3 inhibiting muscle igf-1 creation by gh and slin. I don't remember exactly what you said, but would this mean you do not recommend using igf-1 lr3 with a slin+gh cycle? Or at least do not take your LR3 post workout with GH + slin? How about rH-IGF1 PWO? For example, take GH immediately PWO, then 20 mins later take rH-IGF1, then 10 mins later slin + carbs?
Also, what is everyone's opinion on GH + SLIN protocols for mass gains? I have heard so many different ones and issues with timing, etc. How would you include IGF in here and would you use LR3 or rH?
But while you were over at AnabolicMinds did you see the two studies I posted that indicate that administration of testosterone blunts IGF-1's inhibition of GH?
Rexanator gets credit for prompting me on this one.
There are so many reasons to have a base of testosterone in you when one runs a cycle. It doesn't even have to be a lot of testosterone.
I'll post it below and in my thread here.
Rexanator led me to Testosterone Blunts Feedback Inhibition of Growth Hormone Secretion by Experimentally Elevated Insulin-Like Growth Factor-I Concentration, Johannes D. Veldhuis, Stacey M. Anderson, Ali Iranmanesh and Cyril Y. Bowers, The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 3 1613-1617, 2005, where they found:
"...supplementation of a high dose of Te in middle-aged and older men attenuates IGF-I feedback-dependent inhibition of nadir and peak GH secretion."
The results of this study were confirmed in a recent study published this month:
Testosterone Supplementation in Older Men Restrains Insulin-Like Growth Factor’s Dose-Dependent Feedback Inhibition of Pulsatile Growth Hormone Secretion,Johannes D. Veldhuis, Daniel M. Keenan, Joy N. Bailey, Adenborduin Adeniji, John M. Miles, Remberto Paulo, Mihaela Cosma and Cacia Soares-Welch,The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 1 246-254, 2009
Background: Pulsatile GH secretion declines in older men. The causal mechanisms are unknown. Candidates include deficient feedforward (stimulation) by endogenous secretagogues and excessive feedback (inhibition) by GH or IGF-I due to age and/or relative hypoandrogenemia.
Hypothesis: Testosterone (T) supplementation in healthy older men will restrain negative feedback by systemic concentrations of IGF-I.
Subjects: Twenty-four healthy men (ages, 50 to 75 yr; body mass index, 24 to 30 kg/m2) participated in the study.
Methods: We performed a prospectively randomized, double-blind, placebo-controlled assessment of the impact of pharmacological T supplementation on GH responses to randomly ordered separate-day injections of recombinant human IGF-I doses of 0, 1.0, 1.5, and 2.0 mg/m2.
Analysis: Deconvolution and approximate entropy analyses of pulsatile, basal, and entropic (pattern-sensitive) modes of GH secretion were conducted.
Results: Recombinant human IGF-I injections 1) elevated mean and peak serum IGF-I concentrations dose-dependently (both P < 0.001); 2) suppressed pulsatile GH secretion (P = 0.003), burst mass (P = 0.025), burst number (P = 0.005), interpulse variability (P = 0.032), and basal GH secretion (P = 0.009); and 3) increased secretory pattern regularity (P = 0.020). T administration did not alter experimentally controlled IGF-I concentrations, but it elevated mean GH concentrations (P = 0.015) and stimulated pulsatile GH secretion (frequency P = 0.037, mass per burst P = 0.038). Compared with placebo, T attenuated exogenous IGF-I’s inhibition of GH secretory-burst mass (P < 0.038) without restoring pulse number, basal secretion, or pattern regularity.
Conclusion:The capability of systemic T to mute IGF-I feedback on pulsatile GH secretion suggests a novel mechanism for augmenting GH production.
Okay well, let's say I'm not taking testosterone datbrue. I'm still confused. So do you NOT recommend stacking GH/SLIN with IGF? And if so, does this apply to both LR3 and exogenous rHIGF-1? I think i've heard you say you don't like LR3 and that it is too risky in promoting cancer development (via repressing apoptosis, etc). I see the studies, but can you answer me your opinion without studies? =]
And what's the deal with a lot of IGF from china (almost all IGF we see) being derived from rat sources or being dangerous in some way or another? What would taking rat derived IGF do to a person? Would it just create antibodies to your own igf? (this would be really bad)
I've stopped taking lr3 awhile back. I just stick to An aas stack with hgh and slin and it works great. From my experience, test/hgh/slin stacked together work great synergistically without lr3 to promote lean muscle gains provided that your diet is in check. I didn't really see any difference in stacking lr3 along with the other stuff but maybe that's because I didn't use a high enough dose. I was doing 100mcgs ED.
IGF-1 in what ever form rhIGF-1 or IGF-1 LR3 or several Des forms will inhibit Growth Hormone's ability to increase IGF-1 & MGF in muscle.
Do you understand what I mean?
In the muscle cell IGF-1 & MGF are created. MGF never leaves the cell it just moves to the nucleus and acts.
IGF-1 pools in the cytoplasm and eventually may move to the surface of the cell and bind to a receptor on that same cell.
That action is WAY WAY WAY more productive then injecting IGF-1 in any form OR having the liver synthesize IGF-1 and sending it to circulate throughout the body.
BadGenCD said:
I'm still confused. So do you NOT recommend stacking GH/SLIN with IGF? And if so, does this apply to both LR3 and exogenous rHIGF-1?
Why would you want to administer IGF-1 with GH if it just fucks things up? I posted a study so you'd have something objective to consider rather than just a blanket statement from me.
Could you use IGF-1 with GH? Sure...but it doesn't make sense to do it without testosterone.
Could you use IGF-1 with GH w/o testosterone? Sure ...but it would be better if you spaced out the usage...
BadGenCD said:
I see the studies, but can you answer me your opinion without studies? =]
thank you for your answer...more questions and food for thought
Okay, so when you say space out the usage, you mean what exactly? Do IGF and GH on different days or a few hours apart or what?
And what is your opinion of LR3 IGF? I read so much bad info about it...it's quite scary tbh. The cancer stuff alone is terrifying, but then the letter from one of the doctors at gropep about how it can cause your immune system to attack its own IGF forever by antibodies building up (autoimmune disorder?). It's funny how people here say IGF doesn't cause cancer, it just "accelerates" existing cancer. That is such bs it's hilarious. The specific mechanism of action of IGF inhibiting apoptosis and causing more than normal mitotic growth of cells would be enough to grow cells that should otherwise self terminate or be destroyed by the immune system. Pretty scary IMO. Autoimmunity against your own igf is insane as well, tho im not sure how to check if you actually develop that.
That being said, there are a few sources for rH IGF, but i am now so skeptical of the quality and if it is even what they say it is. Would it even be beneficial to add and how would you?
but then the letter from one of the doctors at gropep about how it can cause your immune system to attack its own IGF forever by antibodies building up (autoimmune disorder?).
That's a bit over drawn. Sure you can develop anti-bodies to any drug or compound including synthetic GH. Just because this happens does not mean the body will attack its own tissue...could happen...doesn't mean it will.
It happened with some versions of the anthrax vaccine given to soldiers and U.S. armed forces personnel prior to the first Gulf War and continuing on...
They used squalene as an immunologic adjuvant or booster to attempt to make effective what they knew was an inadequate vaccine. They didn't see the danger because squalene is very common naturally though out the body. But for some reason in many people the body saw the injected squalene as an invader and developed killer cells to to destroy the injected squalene.
For some people this machinery turned on natural squalene in the body and attacked that as well. So they developed autoimmune diseases. Some people were overwhelmed and died within months. Most just developed debilitating symptoms that either led to slow death or incapacity.
A lot of people have some problems but are able to manage. They have no clue as to what is going on.
The majority of people were pretty much okay.
Anyway Gropep is not really reliable as they are merely attempting to dissuade human use. IGF-1 LR3 is just IGF-1 with a few modifications. It has been used in many studies on animals and I have never seen reference to antibodies developing.
I don't believe it is a probability only a general possibility.
BadGenCD said:
It's funny how people here say IGF doesn't cause cancer, it just "accelerates" existing cancer. That is such bs it's hilarious. The specific mechanism of action of IGF inhibiting apoptosis and causing more than normal mitotic growth of cells would be enough to grow cells that should otherwise self terminate or be destroyed by the immune system. Pretty scary IMO. Autoimmunity against your own igf is insane as well, tho im not sure how to check if you actually develop that.
No the real problem is that IGF-1 LR3 isn't checked/controlled by the binding proteins.
When GHRP-6 or GH increases IGF-1 it also increases binding proteins that check and control IGF-1. IGF-1 Binding Protein is synthesized as well as IGF-1 so the body has control over how it will be used.
Many types of cancer have the ability to produce growth factors such as GHRH, & IGF-1 within the local tissue the tumor controls. It is not dependent on systemic IGF-1...it makes its own...and uses the growth factors to metastasize (i.e. bust through boundaries and invade neighboring tissue).
Thats why the GHRH antagonists that are designed to act in specific tissue are effective at stopping many cancers from growing and in fact often shrink the tumors such that chemotherapy can become effective at eliminating the tumor.
BadGenCD said:
That being said, there are a few sources for rH IGF, but i am now so skeptical of the quality and if it is even what they say it is. Would it even be beneficial to add and how would you?
I wouldn't. I would use GHRH+GHRP or synthetic GH.
If I ever decided to use IGF-1 for local tissue growth I would combine rhIGF-1 w/ IGF-1 Binding Protein 5 and inject that locally into a muscle I wanted to grow. Once injected it would bind with Acid Labile Subunit and exert local effects (no systemic effects).
When RP asked me if I had any peptides I thought he should carry I mentioned this complex. But he just checked with his facility and they just talked nonsense to him which meant I had to suffer through a bunch of nonsense.
Then I asked C if he would be interested but he has a lot on his plate at the moment so can not do it.
I would consider using Peg-MGF as I have told you in this thread. It is likely a better form of IGF-1 then IGF-1 LR3 and/or native rhIGF-1.
I would elaborate but I just know that you will ignore what I say yet again and ask me something about IGF-1.
What we’ve got here is failure to communicate. Some men you just can't reach. So you get what we had here last week. Which is the way he wants it. Well, he gets it. And I don't like it any more than you men.
.gif "IP Gear")
BG you are making me laugh. Thats like saying Dat can you ride the bike without training wheels.
