heres a study which I as well as others duplicated several times on IGF-1 saturation time on HGH.
Systemic IGF-1 levels
Simply stated the synthetic Growth Hormone when administered intramuscularly or subcutaneously in high enough dose results in a release profile that is not pulsatile. The release profile is an elevation and this elevation results in higher levels of systemic IGF-1 in circulation then either an intravenous administration of GH or administration of the pulsatile https://spartanperformances.com/ (peptides).
While multiple daily dosings of GHRH/GHRP result in a significant rise in systemic IGF-1 (not graphed out here) they do not over time result in as substantial an elevation of circulating IGF-1 as synthetic GH administered non-intravenously.
To understand the difference in GH in plasma profile of synthetic GH administered by intravenous I provide a copy of the GH study graph identical to the clinical study graph posted above with the addition of the intravenous dosing of GH. As you can see intravenous dosing of GH results in what could be described as a pulse because GH is elevated very high and then clears quickly.
http://www.professionalmuscle.com/forums/attachments/peptides-growth-factors/28034d1245320711-dats-cjc-1295-ghrp-6-basic-guides-139.jpg
So what does a high dose of synthetic GH administered subcutaneously or intramuscularly (but not by IV) do to systemic levels of IGF-1?
To find out we must switch to a Japanese study which undertook such study.
In Pharmacokinetics and Metabolic Effects of High-Dose Growth Hormone Administration in Healthy Adult Men, Toshiaki Tanaka, et al., Endocrine Journal 1999, 46 (4), 605-612, fifteen healthy normal Japanese adult males aged from 20 to 27 years were administered various doses of recombinant GH (Norditropin). The GH was administered in a single dose at 9:00 a.m. after overnight fasting. Blood samples were collected at 0, 1, 2, 3, 4, 5, 6, 9, 12 and 24 hours after the single injection.
The doses administered were: .075iu/kg; .15iu/kg and .30iu/kg
When the average weight of each test subject is accounted for the doses administered approximated: 5iu; 10iu and 20iu
In the higher dose category the study dosed every day for a week and collected blood samples each day.
IGF-1 levels were measured and can be graphed as follows:
http://www.professionalmuscle.com/forums/attachments/peptides-growth-factors/28035d1245320716-dats-cjc-1295-ghrp-6-basic-guides-clipboard01.jpg
From this graph a few quick things can clearly be understood:
What none of this tells us
This does not tell us what is happening locally. By locally I mean IGF-1 that is not made in the liver and circulated systemically. Local IGFs are made in small amounts and used exclusively in the tissue of their birth.
Local IGF-1 in muscle has been demonstrated to be responsible for muscle growth and only if muscle-made IGF-1 is lacking does systemic IGF-1 play a significant (although incomplete) role.
Local IGFs in muscle are increased by growth hormone and testosterone. It is conjectured that pulsatile GH (such as IV dosing) or the use of GHRH/GHRPs results in high levels of muscle IGFs w/o creating high levels of systemic circulating IGFs.
If this proves to be true then that would be an advantage because high systemic levels of IGF-1 are positively correlated w/ cancer and mortality.
More detailed discussions about these sorts of things take place deeper in this thread.
Systemic IGF-1 levels
Simply stated the synthetic Growth Hormone when administered intramuscularly or subcutaneously in high enough dose results in a release profile that is not pulsatile. The release profile is an elevation and this elevation results in higher levels of systemic IGF-1 in circulation then either an intravenous administration of GH or administration of the pulsatile https://spartanperformances.com/ (peptides).
While multiple daily dosings of GHRH/GHRP result in a significant rise in systemic IGF-1 (not graphed out here) they do not over time result in as substantial an elevation of circulating IGF-1 as synthetic GH administered non-intravenously.
To understand the difference in GH in plasma profile of synthetic GH administered by intravenous I provide a copy of the GH study graph identical to the clinical study graph posted above with the addition of the intravenous dosing of GH. As you can see intravenous dosing of GH results in what could be described as a pulse because GH is elevated very high and then clears quickly.
http://www.professionalmuscle.com/forums/attachments/peptides-growth-factors/28034d1245320711-dats-cjc-1295-ghrp-6-basic-guides-139.jpg
So what does a high dose of synthetic GH administered subcutaneously or intramuscularly (but not by IV) do to systemic levels of IGF-1?
To find out we must switch to a Japanese study which undertook such study.
In Pharmacokinetics and Metabolic Effects of High-Dose Growth Hormone Administration in Healthy Adult Men, Toshiaki Tanaka, et al., Endocrine Journal 1999, 46 (4), 605-612, fifteen healthy normal Japanese adult males aged from 20 to 27 years were administered various doses of recombinant GH (Norditropin). The GH was administered in a single dose at 9:00 a.m. after overnight fasting. Blood samples were collected at 0, 1, 2, 3, 4, 5, 6, 9, 12 and 24 hours after the single injection.
The doses administered were: .075iu/kg; .15iu/kg and .30iu/kg
When the average weight of each test subject is accounted for the doses administered approximated: 5iu; 10iu and 20iu
In the higher dose category the study dosed every day for a week and collected blood samples each day.
IGF-1 levels were measured and can be graphed as follows:
http://www.professionalmuscle.com/forums/attachments/peptides-growth-factors/28035d1245320716-dats-cjc-1295-ghrp-6-basic-guides-clipboard01.jpg
From this graph a few quick things can clearly be understood:
- IGF-1 creation is a slow ongoing process that increases every day that you administer GH until it plateaus after a week. This should tell you that there is no fear that anything will specifically interfere with GH's ability to instigate IGF-1 creation. All of the timing protocols which fear that insulin or "this and that" will interfere with IGF-1 creation are baseless and such "write-ups" that call for timing are flawed.
- It is constant GH elevations that result in ever higher levels of systemic IGF-1 creation
What none of this tells us
This does not tell us what is happening locally. By locally I mean IGF-1 that is not made in the liver and circulated systemically. Local IGFs are made in small amounts and used exclusively in the tissue of their birth.
Local IGF-1 in muscle has been demonstrated to be responsible for muscle growth and only if muscle-made IGF-1 is lacking does systemic IGF-1 play a significant (although incomplete) role.
Local IGFs in muscle are increased by growth hormone and testosterone. It is conjectured that pulsatile GH (such as IV dosing) or the use of GHRH/GHRPs results in high levels of muscle IGFs w/o creating high levels of systemic circulating IGFs.
If this proves to be true then that would be an advantage because high systemic levels of IGF-1 are positively correlated w/ cancer and mortality.
More detailed discussions about these sorts of things take place deeper in this thread.