MESO-Rx
Anabolic Steroids
Hgh injection site
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ironwill1951
New Member
go to the websites of the pharma grade companies that produce HGH and see what they suggest.
I really wish you had just said forehead
@ironwill1951
But instead you gave the best advice OP could receive. Damit!
@ironwill1951
But instead you gave the best advice OP could receive. Damit!
Sub Q in the abdomen or hip area is fine. Rotate sites frequently. IM is also fine and can go anywhere you can get an insulin needle to hit muscle.
Oh shit too late
Per Serostim's manual
I think around the belly area is easiest.
I think around the belly area is easiest.
Per Serostim's manual
I think around the belly area is easiest.
The belly is the only place I've tried so I think I'll stick with that. I was reading some people saying IM is the way to go but after more research and the answers on here I wouldn't think so
savage lifter
New Member
Honestly this probably WOULD work HAHA! As long as you miss the testes, it'd just be like pinning somewhere behind the skin with very little fat.
my favorite spot is im in either quadricep with a 1/2 inch 30g syringe
I am currently "off" cycle right now which is 300mg of test which I run year round. But I will be bumping that up to 500mg test e and adding in deca primarily for joint pain.
iv injections are superior to sq and im. 1 iu done iv equals 2 iu done sq or Im because iv has near 100% absorption. Also iv creates a natural pulse and spike where sq and Im stays in your system too long causing a negative feedback and shutdown. Best way to dose hgh alone is 2iu 5x a day done iv every 3 hours for a total of 10 iu E3D i recommend going to Datbtrue forum for a more detailed explanation since he is the leading expert on hgh and peptides.
Define "superior", bc total absorption IS essentially equivalent when IDENTICAL drugs are being compared, with a few exceptions.
What can and often does change is the RATE and/or DURATION of absorption.
Before you suggest anyone is an "expert" cite a resume that reinforces such an assertion.
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Do you disagree or are you just asking an open ended question?
You need to define "superior" and cite evidence one route of parenteral
GH administration is "superior" to the other.
Based on what criteria?
And which moderator, admin or member on Datbtube is an "expert".
If they were experts, would such individuals be posting threads on a PEPTIDE forum, NOT!
GH administration is "superior" to the other.
Based on what criteria?
And which moderator, admin or member on Datbtube is an "expert".
If they were experts, would such individuals be posting threads on a PEPTIDE forum, NOT!
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Bradly
Member
Dat has been around for a long time and when people had questions about peptides, he had answers. His answers were accurate at a time when not alot of people knew much about peptides.
here is a random post from his forum:
Note: If you post on the open forum I will quote you, if you PM a question I will xxxxx out your name.
Please explain blood work from CJC-1295/CJC MPA... why you would use it
Hi, I had read long time ago about CJC 1295 with DAC, first that it was bad to take because of the continuous pulse, then that we could benefit from it with a very low dose while on top pulsing with ModGRF... Where can I find this info? been looking for about 30min and still cant find it. And CJC 1295 with DAC is not the same as CJC MPA correct?
A lot of other questions from members in this area...
Preamble
As you have learned from the Beginner material there are two classes of peptides that work together to increase growth hormone output. They are the native Growth Hormone Releasing Hormone (GHRH) and the Growth Hormone Releasing Peptides (GHRPs). Natively GHRH is released from cells in the hypothalamus into the median eminence where they find their way to cells in the anterior pituitary. They bind to GHRH receptors on "Growth Hormone making/storage cells" there and cause growth hormone (GH) release. The native hormone somatostatin in youth functions as a pulse generator by inhibiting GHRH induced GH release. As we age the hypothalamic neuronal system that releases GH begins to lose function from ROS (oxidative) damage, However the neuronal system that releases somatostatin is not damaged with age. As a consequence somatostatin begins to behave less and less like a pulse generator and more and more like an overly inhibiting hormone.
Ghrelin is a hormone made in the gut. It is a pro-hormone and one of the cleaved products from this large hormone is the acyl form. Acyl-Ghrelin is capable of binding to receptors on GH making/storing cells in the pituitary... the same ones that GHRH binds to, and in so doing it increases GH release. This activity is fairly limited in a natural state. Acyl-Ghrelin however is powerful as a GH releaser because it is capable of making somatostatin behave. This results in somatostatin acting like a pulse generator once again.GHRPs are by far the best Acyl-Ghrelin mimetics. They bind to the same receptor on the making/storing cells in the pituitary and synergize with GHRH to increase GH release. However they lack some of the effects of Acyl-Ghrelin related to surviving starvation such as fat storage.
GHRPs also have a significant group of positive effects that are unrelated to GH release which include reducing catabolism, supporting the immune system and in some instances hindering cancer. They can do this because they are able t bind to other types of receptors.
Analogs
An analog that extends the duration of Acyl-Ghelin is not a good thing for long term health. Acute or short term (pulsed) Acyl-Ghrelin (GHRPs) are anti-depressive, anti-anxiety, protective of stress and potentially neurologically protective. Chronic (non-pulsed) Ghrelin agonists (ibutamoren mesylate (MK-0677) increase stresses on the brain which may be depression producing, anxiety producing, fear conditioning, producing effects of chronic stress and potentially neurologically damaging.
On the other hand and analog that extends the duration of GHRH is a good thing for pulsation IF it only extends the life long enough to survive enzymatic degradation. Taking GHRH, chopping off the the 15 amino acid tale to eliminate amino acids that do anything creates a peptide with the same activity. This is called Growth hormone Releasing Factor amino acids 1 through 29 (GRF (1-29)). If you swap out 4 of the amino acids with amino acids that will be more structurally sound you end up with a peptide that will survive the 30 minutes + needed to find & bind to the GHRH receptor. This I call Modified GRF (1-29) (Mod GRF (1-29)
If you create an analog that lasts into what would be the next pulse (i.e. 3 hours) you create an an analog that is no longer contributing to physiology. Taking a drug affinity complex called maleimidopropionic acid which has some affinity for albumin in blood and attaching it to Mod GRF (1-29) via an added 29th amino acid - lysine created Mod GRF (1-29) + the reactive moiety maleimidopropionic acid [aka CJC-1295]
To be clear on nomenclature the phrase CJC-1295 was a code used by a science-based company no longer in business. It isn't descriptive of the peptide nor the drug affinity complex. There are many types of drug affinity complexes (abbreviated as DAC). Maleimidopropionic acid is but one. CJC-1295 should refer to Mod GRF (1-29) + the reactive moiety maleimidopropionic acid.
The with DAC (CJC-1295 w/ DAC) or without DAC(CJC-1295 no DAC) is meaningless but could be taken mean CJC-1295 and Mod GRF (1-29) respectively. CJC-1293 is a code name from the same defunct company which refers to GRF (1-29) with only one amino acid swap at the 2nd position, a D-alanine for alanine plus the lysine linker plus the eactive moiety maleimidopropionic acid. In broker speak CJC-1293 would be GRF(1-29){2nd D-AL} + DAC. I don't think the nomenclature especially as it pertains to CJC-1293 can be relied upon.
As an analog Mod GRF (1-29) + the reactive moiety maleimidopropionic acid [aka CJC-1295] confers a longer half-life to the compound. It raise the troughs of GH meaning there is GH bleed. This phrase simply means that GH base levels are elevated.
Is this Mod GRF (1-29) + the reactive moiety maleimidopropionic acid [aka CJC-1295] good or bad?
This analog does not create detriment to the brain. The concern with this analog centers on something that is a double edged sword - systemic IGF-1. Do you want systemic IGF-1 & to some extent local IGFs to be elevated OR do you want systemic IGF-1 to be physiological with local IGFs transiently elevated?
Lifespan, health and lower incidence of cancer come from low levels of IGF-1. Reciprocally higher levels of IGF-1 correlate with higher incidence of cancer and less longevity. If you are attempting to live a long life with intermittent fasting and such higher chronic IGF-1 will hinder you.
Without going into a lot of detail muscle-making relies on its own local IGF-1 primarily so increasing local IGFs is a good thing. However it will draw on systemic IGF-1 to create pools for use if needed. Worked muscle can become greedy for IGF-1.
Things can get a little more involved do before I discuss that let me say that in order to increase systemic IGF-1 there requires several things one of which is a prolonged period of time where GH binds to its receptor.
The other in part may explain why blood work varies.
Blood work for IGF-1 while using CJC MPA or CJC-1295
From the preamble you can see that a GHRP will increase GH pulsation and the amount identified in a plasma test in part by reducing somatostatin. It is not possible to measure increases in local IGFs but part of the real power of GHRH/GHRPs is that they do increase this local activity... although much to the chagrin of those that raise farm animals not in a prolonged way... which is good for health.
If you take away the GHRPs the GHRH analog will be left to fend for itself against somatostatin. Since somatostatin waxes and wanes you have not control over if/when the GHRH will be effective. This concept is more fully described here -> Post #2 Purpose for using GHRP/GHRH 10-15min prior to rHGH? [Actually evolved into a good discussion so moved here] - Dat and the chart which shows that GHRH will contribute to alot more added GH if administered into a rising natural GH wave then when administered when the wave is falling.
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The analog CJC MPA or CJC-1295 although long lasting still is beholden to whether somatostatin is waxing and waning. As a result blood work for IGF-1 will be variable.
Example of blood work from a user of AVs Proteins posted on another forum
Although examples of blood work from AVs CJC MPA may be found on the forum I am choosing to reference a thread on another forum.
From a recent thread on Meso-RX by Roastdawg<<BLOODWORK>> Tom's CJC-DAC
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"Ran 4mg of CJC-Dac from Tom for 5 weeks (two injections of 2mg each per week). My baseline igf-1 is 120, this test gave me a 345. So the increase over baseline was about 225ng."
So what variable in addition to all the aforementioned likely came into play? We have a highly purified peptide as described in journals (HPLC & MassSpec available to long-standing members w/o ill repute) which will be present for binding at the GHRH receptor for a prolonged period which will rise the GH troughs and create a GH/GH-receptor binding event that is long enough to sustain systemic IGF-1 creation. I'll detail the science a few paragraphs below.
What else? ...insulin
We do not know the nutritional state... we do know that insulin stimulates IGF-1, is synergistic w/ GH & increases liver insulin sensitivity as well as increases GH-receptor expression.
At this point in the discussion what I am posting is not so much about blood work as it is about using nutrition/absence of nutrition, insulin/absence of insulin, GH/absence of GH to lever secondary hormones such as IGF-1 local and systemic which will in turn feedback and interact with the initiating hormones (if they are present... often it will be a second dosing of GHRH/GHRP that interacts with IGF-1 local or systemic brought about in an earlier dosing).
Insulin stimulates IGF-1 but is synergistic w/ GH. As I've written many times a reasonable amount of insulin and GH are compatible w/ positive effects. Synergy in IGF-1 creation is one of them.
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Insulin by itself stimulates IGF-I synthesis in hepatocytes, but a synergistic effect is seen when insulin is administered in combination with GH, and even pretreatment with insulin increases the sensitivity of hepatocytes to GH (44). Likewise, administration of GH alone and administration by way of ip, but not sc, partly restore the reduced hepatic IGF-I mRNA expression in diabetic rats, whereas only coadministration of GH and insulin restores IGF-I mRNAlevels to those in control animals (45).
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44. Houston B, O’Neill IE 1991 Insulin and growth hormone act synergistically to stimulate insulin-like growth factor-I production by cultured chicken hepatocytes. J Endocrinol 128:389–393
45. Russell-Jones DL, Rattray M, Wilson VJ, Jones RH, Sonksen PH, Thomas CR 1992 Intraperitoneal insulin is more potent than subcutaneous insulin at restoring hepatic insulin-like growth factor-I mRNA levels in the diabetic rat: a functional role for the portal vascular link. J Mol Endocrinol 9:257–263
Diabetes (and highly insulin resistant states such as is often found in body building) = high GH but low IGF-1 - Why? = low insulin concentrations thus down-regulation of GH-receptors
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It is well known that patients with insulin-dependent diabetes have elevated GH levels, but inappropriately low levels of total and particularly free IGF-I (46, 47), suggesting a state of GH resistance. It seems plausible that this hepatic GH-resistance could be a consequence of low portal insulin concentrations with subsequent down-regulation of liver GHR expression.
So GH retainment and GH pulse strength correlate w/ IGFBP-1 in different ways (negative or positive) depending on whether GH is a raised trough, a strong pulse coming from a troug or a mass of GH coming from an elevation (IGF-1 binding protein reduces free IGF-1 so reducing it increases free IGF-1). In addition increased liver insulin sensitivity increases GH-receptor expression.
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We found that the baseline level of IGFBP-1 was a major negative predictor of GH clearance. IGFBP-1 is down-regulated by insulin (48–50) and GH (51, 52), and recent data suggest that serum IGFBP-1 reflects insulin sensitivity in humans (53–56). It could be hypothesized that the association between IGFBP-1 and GH clearance is secondary to the correlation between IGFBP-1 and insulin, with changes in portal delivery of and hepatic sensitivity to insulin being reflected in both changed IGFBP-1 levels and altered expression of liver GHRs. However, in GH-deficient adults serum levels of both IGFBP-1 and insulin are elevated, but still closely correlated (57), which suggests that GH contributes to the regulation of IGFBP-1 independently of the effect of insulin, and it seems possible that IGFBP-1 levels can be used as an independent predictor of GH clearance and sensitivity. Interestingly, IGFBP-1 has been reported to show strong positive correlations to the basal GH secretion rate and to the mass of GH secreted per burst, as assessed by deconvolution analysis of 24-h serum GH concentration profiles (6). One could speculate about whether the close negative correlation between IGFBP-1 and clearance influences the observed positive correlation between IGFBP-1 and deconvoluted GH secretion.
So one has to be careful with GH in that it can lead not only to an increase in IGF-1 but also to an increase in the binding proteins. Some binding proteins might be good in that they hold IGF-1 a t site but others like IGFBP-1 will increase clearance and decreasing it will increase free IGF-1. GH elevations and trough raises will increase measurable IGF-1 in plasma but much of it will be bound. So a high IGF-1 reading may include much IGF-1 that will not be "usable". Often a lower total serum IGF-1 will be made up of more free IGF-1.
Insulin and GH absence then GH & insulin presence versus Insulin always around and then GH & insulin
I like this study and will use the charts here Insulin and growth hormone act synergistically to stimulate insulin-like growth factor-I production by cultured chicken hepatocytes
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Fig. 1 Effect of insulin, GH and insulin plus GH on IGFI production by insulin-deprived chicken hepatocytes.... After 6 h in hormone-free medium, insulin (100 pg/1), GH (100 pg/1) or insulin plus GH (each at 100 pg/1) were added... the IGF-1 that accumulated was measured after 24 hours and reported on the chart.
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Fig. 3 Effect of insulin, GH and insulin plus GH on IGFI production on previously exposed chicken hepatocytes.... After 9 h in insulin medium cells were moved to a hormone free medium and insulin (100 pg/1), GH (100 pg/1) or insulin plus GH (each at 100 pg/1) were added immediately... the IGF-1 that accumulated was measured after 24 hours and reported on the chart
Finally from Cheat Sheet Overlay 1 for the Book of Growth [How to induce IGF-1 expression] in the Intermediate/Advanced forum.
There's a great study there called Defining the epigenetic actions of growth hormone: acute chromatin changes accompany GH-activated gene transcription, Chia DJ, Mol Endocrinol. 2010 Oct; 24(10):2038-49 which should clue you in to what it is we are discussing when we discuss pulsation vs elevations. Everything takes place at the level of the gene... access or blocking genes determines which will get activated and when. Although the study may seem confusing here is what the study is meant to do... it is meant to make you wonder.
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A large single does of GH creates gene access changes. From a physiological perspective, it is unknown whether the patterns of chromatin changes defined here in the liver after a single injection of a large dose of GH resemble the epigenetic effects after exposure to physiological GH levels. It is also unknown whether the histone modifications observed at each GH-activated gene are reset after every hormone pulse under normal physiological conditions, or whether the patterns of chromatin changes are unique to the liver, or are found in other GH-responsive tissues and cell types.
In other words GH does some interesting things when administered in a single dose. It is likely that these interesting things continue to come about if GH is pulsed and there is a reset. The differences that we discuss between pulsation and elevations manifest themselves at the level of epigenetic change.
So GH induced the expression of genes that result in systemic IGF-1 via prolonged activation of Stat5b... here is the cheat sheet.
120 minutes was insufficient where as 240 was sufficient to raise IGF-1 mRNA. So somewhere between 2 hours and 4 hours of stat5b activation brought on by GH binding to its receptor will be needed to increase IGF-1 systemically which will show up on a blood test. But here is the interesting thing... if you read that link in the Intermediate thread, the relevant portion of which I include below you'll see that the measure was in tissue. They measured IGF-1 levels in fat cells and in muscle cells. At the 2 hour mark both IGF-1 and the GH break down the suppressor of further stat5b signaling were present. In fact IGF-1 had increased by a factor of 17x in muscle.
Notice that Stat5b signaling which would result in IGF-1 was increased in adipose tissue and IGF-1 was not. Whereas in muscle it is likely that we are topping out IGF-1 creation because the product which will inhibit it was also high indicating that the feedback was in full force.
At the 240 minute mark (infusion in vivo healthy humans)
In muscle tissue, significant increase in SOCS3
In muscle tissue, significant increase in IGF-1 (17x increase)
In adipose tissue, increased SOCS3 mRNA.
In adipose tissue non-significant increase in IGF-1 mRNA
Anyway I hope this helps...
Note: I didn't proof read, just a free flow of thought so let me know if there are typos.
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