GH dosage for maximum of normal range
- Thread starter Mr.50
- Start date
colkurtz_spf
The horror
1 IU puts me in the high range. 1.2 puts me in the upper end of high. You have to see how you respond. Evryone is different.
I don't think it's necessary to dose twice per day. I dose in the morning to avoid shutting down the pituitary at night.
Mr.50
Board Supporter
smitty4
New member
With GH, I really don't understand why folks would take any days off...other than trying to save money, that is...
colkurtz_spf
The horror
Sorry to take so long to get back to you. I didn't see your response. I dose 6 on/1 off. I will be going to 5 on/2 off and increasing the dose to compensate. I'll still be dosing over 7 ius per week.
Many chose to dose 7 straight days; I've done it that way myself. I like to take a day or two off. Dosing in the morning keeps you from shutting down your pituitary at night, but IGF levels maintain for a few days, and the higher levels make it produce less. For whatever reason I do better with a few days off. Not everyone may be the same.
plymouth city
Banned
Your not the only one my friend. Lots of guys from other boards are huge advocates for EOD dosing or 5/2 dosing for GH.
One might speculate that it would also keep receptors from down regulating.
Anyone on GH with insurance? I was curious to know what it costs you and how much insurance covers.
colkurtz_spf
The horror
My doctor prescribes daily injections, but I've seen my best results from the 5 on/2 off protocol.
colkurtz_spf
The horror
My insurance won't cover any of this. I pay $11/IU for a generic, but I've seen the same compound for $8.
KSman
Member
If one has normal age related reduced GH production, where the hypothalamus and pituitary are working ok, but at low levels, the feedback is still working, but at a lower baseline; read on. If the h&p are damaged, the story is very different and the feedback to a dead process is non-concern.
There is a feedback system for GH, which ages and lowers levels over time. There are three things that reduce HG in a feedback fashion, one is excessive fat, cortisol also reduces GH, but the main feedback element is IGF-1. (This indirect feedback is not unique, consider that E is the strong feedback element for T.)
GH in serum lasts only a few minutes, so measuring that is rather useless. The GH causes IGF-1 levels to rise, and IGF-1 has a rather long serum lifetime. That is why IGF-1 is measured.
When you inject GH, IGF-1 increases. As the IGF-1 is rather persistent, then the thought that by avoiding injections later in the day that you can avoid negative feedback may be wishful thinking. For those with higher doses who inject 5 days and rest for 2, the IGF-1 levels may still be high enough to inhibit GH. Remember that if your GH is low, then any levels of IGF-1 above where your IGF-1 levels were (baseline) will be triggering negative feedback. For body builders who are young and healthy, they have normal higher GH and IGF-1 baselines to start. For them, if they take a two day rest off of GH, then when their IGF-1 levels fall below their [higher] baseline, that might trigger natural GH release. But when you have very low baseline levels of IGF-1, with two days off, your IGF-1 may easily stay above your low baseline and that would still be creating negative feedback.
So that is the wider picture. I had a quick look in a book for the half-life of IGF-1, which I did not find. The actual merits of these effects depend on that half-life, the dose and how fast one clears these things from serum. And IGF-1 gets bound in IGF-1 binding protein IGFBP-3 which also increased with age to reduce the effects of ones diminishing HG production.
IGFBP-3 increases with age, but also with GH production. If GH levels are very low, then IGFBP-3 will reduce. So that is a BW marker of low GH. With GH therapy, IGFBP-3 will increase and is probably responsible for some non-linear dose response effects.
I found this:
"""
IGFBP-3, the most abundant IGFBP in human serum, is synthesized mainly by hepatic Kupffer cells and binds over 90% of circulating IGF, resulting in a prolonged half-life (6). IGFBP-3 is also produced locally by a variety of normal and tumor cells, suggesting that the cellular microenvironment may directly affect the action of IGF-1 (11). The biological functions of IGFBP-3, aside from being the major binding protein for IGF-1, are complex and remain poorly understood. However, IGFBP-3 is known to inhibit cell proliferation by interfering with the interaction of IGF-1 and its receptor (34, 37). Interestingly, IGFBP-3 can also modulate cell growth and survival independently of IGF (7), presumably via interactions with cellular proteins such as the Alzheimer's survival protein, humanin (31), and nuclear targets such as the retinoid X receptor alpha (7, 8, 36).
"""
As GH increases IGFBP-3 levels and it also increases total IGF-1 half-life, increased GH from therapy will tend to increase the half-life of IGF-1. So that also has implications for the thought that a two day rest will allow the h&p to get active.
Some of the action of IGFBP-3 seems to be store and release, acting as a transport medium. I have not found out the fate of IGFBP-3. As folks have age related HG&IGF-1 decline and age related increases in IGFBP-3, some of the negative effects of aging might be from the increased binding of IGF-1 or a reduction in the release of ICF-1 from IGFBP-3. I have not found any info on how IGFBP-[1-6] are cleared from the blood stream. It has to clear somewhere as it is continuously produced. With increased ICGBP-3 levels with age, that clearance mechanism might be an age related 'sink' for IGF-1 which will reduce the amounts that are available for IGF-1 receptors.
There is a feedback system for GH, which ages and lowers levels over time. There are three things that reduce HG in a feedback fashion, one is excessive fat, cortisol also reduces GH, but the main feedback element is IGF-1. (This indirect feedback is not unique, consider that E is the strong feedback element for T.)
GH in serum lasts only a few minutes, so measuring that is rather useless. The GH causes IGF-1 levels to rise, and IGF-1 has a rather long serum lifetime. That is why IGF-1 is measured.
When you inject GH, IGF-1 increases. As the IGF-1 is rather persistent, then the thought that by avoiding injections later in the day that you can avoid negative feedback may be wishful thinking. For those with higher doses who inject 5 days and rest for 2, the IGF-1 levels may still be high enough to inhibit GH. Remember that if your GH is low, then any levels of IGF-1 above where your IGF-1 levels were (baseline) will be triggering negative feedback. For body builders who are young and healthy, they have normal higher GH and IGF-1 baselines to start. For them, if they take a two day rest off of GH, then when their IGF-1 levels fall below their [higher] baseline, that might trigger natural GH release. But when you have very low baseline levels of IGF-1, with two days off, your IGF-1 may easily stay above your low baseline and that would still be creating negative feedback.
So that is the wider picture. I had a quick look in a book for the half-life of IGF-1, which I did not find. The actual merits of these effects depend on that half-life, the dose and how fast one clears these things from serum. And IGF-1 gets bound in IGF-1 binding protein IGFBP-3 which also increased with age to reduce the effects of ones diminishing HG production.
IGFBP-3 increases with age, but also with GH production. If GH levels are very low, then IGFBP-3 will reduce. So that is a BW marker of low GH. With GH therapy, IGFBP-3 will increase and is probably responsible for some non-linear dose response effects.
I found this:
"""
IGFBP-3, the most abundant IGFBP in human serum, is synthesized mainly by hepatic Kupffer cells and binds over 90% of circulating IGF, resulting in a prolonged half-life (6). IGFBP-3 is also produced locally by a variety of normal and tumor cells, suggesting that the cellular microenvironment may directly affect the action of IGF-1 (11). The biological functions of IGFBP-3, aside from being the major binding protein for IGF-1, are complex and remain poorly understood. However, IGFBP-3 is known to inhibit cell proliferation by interfering with the interaction of IGF-1 and its receptor (34, 37). Interestingly, IGFBP-3 can also modulate cell growth and survival independently of IGF (7), presumably via interactions with cellular proteins such as the Alzheimer's survival protein, humanin (31), and nuclear targets such as the retinoid X receptor alpha (7, 8, 36).
"""
As GH increases IGFBP-3 levels and it also increases total IGF-1 half-life, increased GH from therapy will tend to increase the half-life of IGF-1. So that also has implications for the thought that a two day rest will allow the h&p to get active.
Some of the action of IGFBP-3 seems to be store and release, acting as a transport medium. I have not found out the fate of IGFBP-3. As folks have age related HG&IGF-1 decline and age related increases in IGFBP-3, some of the negative effects of aging might be from the increased binding of IGF-1 or a reduction in the release of ICF-1 from IGFBP-3. I have not found any info on how IGFBP-[1-6] are cleared from the blood stream. It has to clear somewhere as it is continuously produced. With increased ICGBP-3 levels with age, that clearance mechanism might be an age related 'sink' for IGF-1 which will reduce the amounts that are available for IGF-1 receptors.
plymouth city
Banned
Very cool ksman, thanks, always informative as usual.
Now comes the tricky part - to dose EOD/5-2 or ED? Conflicting info both ways. :think:
KSman
Member
I have no idea. You can find various and conflicting opinions. You could do ED for a while until that feels level, then set out a program of 3 rotating 4 week cycles and keep some notes. Whatever feels the best for you is probably the best. Try to keep the amount per week constant for your trials. If you are doing weight resistance training, cycles that yield IGF-1 pulses during or just after your training might have some merit from muscle response point of view. What the BB guys say about timing of IGF-1 might be worth thinking about. One could do a baseline ED or EOD and layer greater amounts on training day. You might feel some advantages, but perhaps not. What will confound all of this is the ongoing changes that will be occurring for a few months.
colkurtz_spf
The horror
My doctor won't prescribe it - Cenegenics policy. I have to go to a different clinic. They ship from Signature and tack on an additional cost per IU to cover their fees.
For some reason I seem to carry less body fat when dosing the same amount per week 5 days on/2 off. I'm not sure why. My doctor wants me to inject 7 days without a break. I have a blood draw in 6 weeks. It will be intesting to see how it effects my IGF level.
KSman
Member
"If GH levels are very low, then IGFBP-3 will reduce. So that is a BW (what is "BW"?) marker of low GH. With GH therapy, IGFBP-3 will increase and is probably responsible for some non-linear dose response effects. (Such as?)"
Such as: I was thinking that higher doses would increase IGFBP-3 which would damped ICF-1 effects by blunting spikes and creating more of a time release, as slower chemical change processes are required to release the IGF-1 from the binding proteins. So there may be some diminishing responses to higher dosing.
Does that make any sense?
"
(The IGF-1 assay is actually "Free IGF-1". Think of the implications of this with respect to IGFBP-3 concentration and subsequent GH dosing titration)."
I did not know that. That would seem to complicate things. The amount of free IGF-1 might be changeable or inconsistant. Might explain why my IGF-1 lab work was lower after starting TRT.