What is the difference betweem 191aa and 192aa? (other than one more extra amino acid)...and is there a 190? And which brands of HGH are considered to be 192aa which, if I am correct, are not as good as 191aa brands.......thanks!
~Knowledgeable Female Extraordinaire~
What is the difference betweem 191aa and 192aa? (other than one more extra amino acid)...and is there a 190? And which brands of HGH are considered to be 192aa which, if I am correct, are not as good as 191aa brands.......thanks!
Knowledgeable Member
191aa is identical to what your body produces, 192aa is not. That is why people get sides like redness and swelling with 192aa because the body is rejecting it because it doesn't recognize it.
I've never heard of 190aa.
VET
192aa is easier to make a lot of it was coming out of China several years ago.
~Knowledgeable Female Extraordinaire~
are there any pharmaceutical brands which are 192aa? for example, could Omnitrope ever be considered to be 192?
Banned
Hi SlimmerMe....
This is going to be a little random... but anyways, I joined this site because I saw a post you once made a couple of weeks ago about having your IGF-1 levels only increase by like 25 points or something after being on HGH for some time correct? I just wanted to say that you should be reporting that anti-aging doctor to the FDA, or to the authorities.
lol... to be honest, I practically only joined this forum to tell you that. But alas, I couldn't find the thread once I joined! I even looked through your post history with no luck. I'm pretty sure there is something wrong with the entire site though. I'm having a very difficult time navigating anything, so I'm glad I found this new thread of yours.
Either the anti-aging clinic, or their distributor is scamming you, or supplying you with fake or severely under-dosed HGH. I looked through your dosing protocol, and for a woman, 1.5iu/ed should yield substantially better results....
I would definitely not be buying anymore HGH from this doctor without demanding a free batch and subsequent free blood-work as proof of the authenticity of his products! If he denied this, I would simply just switch clinics, and inform him that you will be reporting him, and submitting the blood-work to whatever authorities review it.
Also.... To answer this threads question.... No, there are currently no pharmaceutical-brands of 192aa. Side-effects outweigh the benefits for most users (although some can tolerate it..)
Last edited by muscle_dysmorphia; 10-18-2010 at 11:49 AM.
~Knowledgeable Female Extraordinaire~
^^^ THANKS! I am wondering myself...and trying to figure out the best way to go about this...want to line all my ducks up in a row first...so this post of yours gives me a lot to think about...I appreciate it!
I was about to pick up the phone to call the pharmacist a minute ago...so..this post came in handy..perfect timing
ps: glad I inspired you to hang around a bit! LOL!!! and as far as finding post, with the new upgrade threads are hard to find....all of my earlier threads are not on my profile...as with many members...
Last edited by SlimmerMe; 10-18-2010 at 01:33 PM.
Banned
I'm glad! What I want you to know is that here in the USA it is completely possible that either:Originally Posted by SlimmerMe
a.) you're being scammed by your anti-aging doctor
b.) your doctor is being scammed by his pharmaceutical supplier.
The only reason I would be so upset is because of the total cost of HGH. Getting valid insurance coverage for HGH prescriptions occurs once in a blue moon, so I sympathize with the amount of capital that you have probably already (at this point) invested into this supposed Rx Growth Hormone.
Like I said in my original post, rather then calling in and switching brands, I believe that you should go in to your clinic in person and discuss some sort of compromise with your doctor. Explain to him that if he is not willing to come to some sort of deal that you're going to be forced to take legal proceedings.
Demand a new kit of whatever he considers this "best brand on pharmaceutical HGH" and demand free blood-work in a month to show that your liver is responding to the dose.
SlimmerMe, could you do me one more favor if possible? could you please add a link to this thread (to your other thread about the doctor's HGH...) i still can't find it...
~Knowledgeable Female Extraordinaire~
My threads are now there. I just checked.I am not sure which one you are talking about. The "Pathetic HGH results" thread? perhaps? http://forums.steroid.com/showthread...ths&highlight=
THANKS so much for your concern and input. I did call the pharmacist yesterday. He implied that women need to take much more than men to raise their IGF-1 level...he also said that with all of the other hormones..test.DHEA , E2,E3...that something could have really affected my results. I let him talk in the beginning to hear what all he was going to say...before I chimed in with my thoughts.. including did I have 191 or 192?...he said I did in fact have the 191. And that my Omnitrope is the same exact as all the other 191aa HGH. He then suggested I try GHRP-6. SO....I am now back to square one unless I pull a hissy fit with both the doc and the pharmacist who, by the way, I did get a good vibe from him actually. I talked to him for over an hour. So.....now I have to figure out what to do. I did get a script for Nutropin...lowest amount...to compare....so we shall see! THANKS AGAIN!!! I hope I do not have to go down the route of pinning them to the wall! PUN!
Last edited by SlimmerMe; 10-19-2010 at 12:03 PM.
Banned
Yes mame! the thread was "pathetic HGH results" thank you!
All US pharmaceutical grade HGH is 191aa.
The issue is that women's IGF-1 levels will elevate in a typical and predictable pattern. I can't be 100% predicted, but there is definitely a set of applicable ranges.
Note: Indeed there are certain things that will impact one's IGF-1 levels, but thyroid medication, with DHEA and testosterone surely SHOULDN'T decrease it that much.
What I'm wondering is what was your dosing protocol of ALL the hormones you're taking prior to the blood-test. (what dose and how many hours from getting your blood-work drawn.)
I wouldn't really be complaining to the pharmacist about the issue; I would head directly to the doctor.
Call me paranoid, but if the doctor is trying to get you to supplement peptides like GHRP-6 with your current HGH protocol I would seriously be starting to think that he is using the cheaper peptide to try and mimic HGH results.
Something seems very fishy here to me! (sorry if this is a bit of a rant, haha. just writing as I think!)
~Knowledgeable Female Extraordinaire~
The pharmacist suggested GHRP-6 to help my pituitary fire GH. The doctor does not even know this recommendation. I took my HGH around 1am and then bloodwork around 10:30 am if this makes a difference...hmmmm....maybe so.
I have been on 6mgs of test cream ED and 35 mgs of DHEA ED along with E2/3 4 mgs ED and Progesterone 25mgs and 50 more at night... and Armour. Hope this helps. The pharmacist also told me 35mgs of DHEA ED was way too high for a female and was surprised to hear this. It is not the same place where I get the other stuff.
VET
Hi slim, just a thought for you. When I researched on natural GH pulses throughout the day for females it was all over the place. On any given hour there was a dramatic difference in the level of GH in the woman's body. GH once secreted only lasts in the body for a very short time. Thus the frequent pulsing of the GH throughout the day. I wonder if that's what's happening to your IGF level? You pulse or take HGH. Your IGF level goes up. Then by the time you drive over to the doc, wait, fill out the forms, go in the examination room, wait again, etc. I wonder if the standard method of IGF testing for HGH is very accurate since the HGH life in the body is so short.
Banned
9 1/2 hours after administration would be the most likely key-contributor to the low levels IMO slimmerMe.
I would highly suggest re-testing with the HGH shot administered 45 minutes or less prior to the testing. (this would dictate if the HGH is having any supplemental effect on your liver! because if these tests came back with low levels you could slap your doctor with a class action lawsuit!haha.)
GHRP-6 is a quality compound. Although, I'm not too sure if it would be worth the price to pay for Rx GHRP-6, when one can get generics for so cheap...
Banned
Good thoughts here!
I agree, and also postulate about this often, as it is a concern of my own.
I currently am using both: prescribed HGH, and supplementing it with generic HGH. And I've been experimenting with my injecting protocol prior to blood-work. It's been a journey to say the least this far! haha.
I couldn't imagine how any of those so called IGF-1 or HGH blood-spot tests (that you send in through the mail.) would register anything accurate.... they seem like garbage to me.
~Knowledgeable Female Extraordinaire~
interesting as to timing of BW...so thanks to you both
GHRP-6 generics? what would be some of those names? for now, I am simply in the research stage...so anything I can find out helps! All I know is that he mentioned: Sormelin Acetate....thanks!
s
Banned
I believe you mean...Sermorelin.... he's a little write up that I copied and pasted for you. It's a useful peptide; although, one thing you've got to keep in mind is do you really want to be forking out tons of money for these GH releasing peptides, when you could just buy the real deal, HGH for probably about the same price??? (considering that you're getting it all Rx.. meaning it will all be pricy.)
Sermorelin is a synthetic version of the peptide hormone GHRH and can be considered interchangeable where acute effects of either are studied. Sermorelin is also referred to as GHRH (1-29) or GRF 1-29 because the peptide chain contains 29 aminos as opposed to the 44 in native GHRH. Native GHRH is produced in and released from the hypothalamus. GHRH causes the anterior pituitary’s somatotropes to release growth hormone, and also directly (by other mechanisms) promoted slow-wave sleep.[1] GHRH is released in pulses in the body that alternate with corresponding pulses of somatostatin or growth-hormone inhibiting-hormone. Somatostatin causes the pituitary to cease release of growth hormone. Ghrelin, released from the gut which circulates and acts as a hunger hormone, has synergistic activity in the body with GHRH and also suppresses somatostatin to make way for the GHRH pulse. If exogenous GHRH (sermorelin) is administered when somatostatin is active, it has no effect. Another difference between GHRH and sermorelin is that while an acute dose of either has the same effect, the pulse pattern of native GHRH – longitudinal release or release over time – is different from a single administration of sermorelin. To compensate for this difference in studies and in clinical uses, multiple injections of sermorelin are used, or sometimes sermorelin is administered from an intravenous pump device.
The effectiveness of peptides such as sermorelin for GH replacement therapy is generally greater than that of exogenous synthetic 22kDa growth hormone, attributable primarily to the pulsatility of the GH release induced (3 hour duration as opposed to 8 hour duration), or “spontaneity” as Lebl’s Czech study refers to it:
BACKGROUND: Treatment with growth hormone (GH) restores the natural growth rate in children with growth hormone deficiency (GHD). This is, however, achieved only after daily injections extending over many years and therefore daily short-term hypersomatotropinaemia. Stimulation of endogenous secretion of GH e.g. by oral administration of growth hormone-releasing peptide (GHRP) may help in future to eliminate these adverse aspects. This treatment could be beneficial in patients with a stimulable endogenous GH secretion. METHODS AND RESULTS: In order to find potential candidates for spontaneous secretion of GH the authors examined, using a test with sermoreline (GHRH1-29NH2), 31 children (21 boys) aged 5.8-16.5 years suffering from idiopathic (GHD), previously treated by daily GH injections. GH rose after stimulation with sermoreline to more than 14 mIU/l in 18/31 children (responders). The ratio of "responders" was higher in the sub-group of children with isolated GHD, as compared with multiple pituitary deficiency (p = 0.05) and insignificantly higher in the sub-group of children born by breech delivery (p = 0.13). CONCLUSIONS: More than half the children treated nowadays with GH could profit in future from the method of spontaneous GH secretions. The success of this procedure is more likely in children with isolated GHD and in breech delivered children.[2]
Because GH release varies greatly from person to person and in different life stages, and because different persons have different levels of cellular sensitivity to GH, one test used by practitioners to test for GH deficiency in short-stature children is to measure plasma blood levels and then administer GHRH and retest, in order to compare the “baseline” to an optimized release pattern for that particular individual:
Sermorelin is a well tolerated analogue of GHRH which is suitable for use as a provocative test of growth hormone deficiency when given as a single intravenous 1 microg/kg bodyweight dose in conjunction with conventional tests. Limited data suggest that once daily subcutaneous sermorelin 30 microg/kg bodyweight is effective in promoting growth in some prepubertal children with idiopathic growth hormone deficiency.[3]
Future therapies will likely include combined use of one of several GHRPs as well as sermorelin or a similar analog due to the necessity of inhibiting somatostatin for GHRH to work, as well as due to the overall synergy and efficacy as demonstrated in the following study by Pandya et al (note that endogenous GHRH is somewhat interchangeable with exogenous, if one adjusts to mimic release patterns in regards to administration of the synthetic version):
GH-releasing peptide-6 (GHRP-6) is a potent GH secretagogue that releases GH by uncertain mechanisms. To assess whether GHRH is required for GH release by GHRP-6 in humans, we used the specific antagonist to GHRH (N-Ac-Tyr1,D-Arg2)GHRH(1-29)NH2 (GHRH Ant). We have previously shown that GHRH-Ant (400 microg/kg) blocked the GH response to 0.33 and 3.3 microg/kg boluses of GHRH by 95% and 81%, respectively. Nine healthy men between the ages of 20 and 30 yr were studied on two occasions. They received either saline or GHRH-Ant (400 microg/kg, i.v.) at 0840 h, followed by GHRP-6 (1 microg/kg, i.v. bolus) at 0900 h. Blood was sampled every 10 min from 0800-1100 h. GH responses were measured as the maximal increase over the baseline GH concentration and as the area under the curve. GHRH-Ant eliminated most of the GH response to GHRP-6 [maximal increase over the baseline GH concentration, 33.8 +/- 4.8 vs. 6.2 +/- 1.8 microg/L (mean +/- SEM; P < 0.0001); area under the curve, 1701 +/- 278 vs. 376 +/- 113 microg/min x L (P < 0.001)]. These data show that endogenous GHRH is necessary for most of the GH response to GHRP-6 in humans.[4]
GHRP-6 is a peptide that is sold throughout the states from research chem websites. Usually you can buy them for like 15 - 20$ per 5mg/vial... cheaper in bulk... I don't know how much it would cost from an AA doc, but I would assume it would be a lot more! lool... just a hunch though.
Good conversation thus far guys and gals'
~Knowledgeable Female Extraordinaire~
MAN sakes alive! THANKS! I need to read and re-read again and again to absorb this!
Banned
No problem....
Here's some additional reading in case you have issues sleeping tonight! haha...
A profile of GHRP-6.... I've included the citations and references below in case you want to bring it with you to the doctor or something...
GHRP-6, a polypeptide hormone, is a growth hormone secretagogue and ghrelin mimetic and analog. GHRP-6 is from the first generation of GHRPs and causes significant release of growth hormone by itself, due both to its suppression of somatostatin (an antagonist to GHRH) and stimulation of release of GH from the anterior pituitary.[1] The cells that produce and release GH are known as somatotropes.[2] Like GHRP-2, GHRP-6 does not have ghrelin’s lipogenic properties. Unlike GHRP-2, GHRP-6 induces hunger consistently in mammals. GHRP-6 acts synergistically when applied during a native GHRH (growth-hormone releasing hormone) pulse or when coadministered with GHRH or a GHRH analog such as Sermorelin or GRF 1-29 (growth releasing factor, aminos 1-29).[1] The synergy comes both due to the suppression of somatostatin and the fact that GHRP-6 increases GH release per-somatotrope, while GHRH increases the number of somatotropes releasing GH.[1,2] There is also a secondary effect of neuronal excitation in the hypothalamus caused by GHRP-6, which lasts for approximately 3 hours after application, similar to GHRP-2.
Because they increase GH release to a degree dependent on their application, any GH secretagogue used at an effective dose offers the benefits of GH. Increased collagen production, better cellular repair of internal organs, increased healing capability, increased energy, improved sleep, increased lean body mass, and reduced body fat are all documented effects of GH. However, unlike the exogenous synthetic e. coli-derived 22kDa growth hormone in application, the resultant GH pulse from GHRP-6 lasts about three hours instead of eight. Overexposure to GH – that is, GH release that does not adhere to normal pulsatile rhythms of the body (a steeper curve, with a sharp peak and rapid decline) but instead lasts longer and does not reach the same amplitude (a shallow curve, with a slow rise and descent over eight hours) – results in cellular desensitization to the effects of GH. GH secretagogues do not result in cellular desensitization to GH in any quantity; the pituitary may stop responding to the signal the compounds indicate if they are used in extreme quantities, but when administered up to every three hours GHRP-6 can result in supraphysiological levels of GH that are nonetheless reasonably safe, unlike exogenous GH.
Each GH secretagogue – GHRP-2, GHRP-6, ipamorelin, hexarelin, etc – has unique properties beyond release of GH. As demonstrated in the rat, GHRP-6 does have some lipogenic properties that are additive but are dependent on insulin/glucose states. Granado et al find that “GHRP-6 and insulin exert an additive effect on weight gain and visceral fat mass accrual in diabetic rats, indicating that some of GHRP-6's metabolic effects depend on the insulin/glucose status.” [3] The rats who were administered GHRP-6 when insulin was quiet did not experience the same effects on adiposity and weight gain when compared to either group (insulin or insulin with GHRP-6).
Delagado et al document that the most important unique effect of GHRP-6 could be a neuroprotective effect that is independent of the established IGF-1 pathway:
Treatment of the fetal hypothalamic neuronal cell line RCA-6 with growth hormone-releasing peptide 6, an agonist of the ghrelin receptor, or insulin-like growth factor I activates intracellular signalling cascades associated with anti-apoptotic actions. Abnormally high concentrations of glutamate provoke over-excitation of neurons leading to cell damage and apoptosis. Thus, the aim of this study was to investigate whether the administration of growth hormone-releasing peptide 6 and insulin-like growth factor I attenuates monosodium glutamate-induced apoptosis in RCA-6 neurons and the mechanisms involved. Two different mechanisms are involved in glutamate-induced cell death, one by means of caspase activation and the second through activation of a caspase-independent pathway of apoptosis mediated by the translocation of apoptosis-inducing factor. Growth hormone-releasing peptide 6 partially reversed glutamate-induced cell death but not the activation of caspases, suggesting blockage of the caspase-independent cell death pathway, which included interference with the translocation of apoptosis-inducing factor to the nucleus associated with the induction of Bcl-2. In contrast, the addition of insulin-like growth factor I to RCA-6 neurons abolished glutamate-induced caspase activation and cell death. These data demonstrate for the first time a neuroprotective role for growth hormone secretagogues in the caspase-independent cell death pathway and indicate that these peptides have neuroprotective effects independent of its induction of insulin-like growth factor I.[4]
Citations:
[1] Bowers CY, Momany F, Reynolds GA. In vitro and in vivo activity of a small synthetic peptide with potent GH releasing activity. 64th Annual Meeting of the Endocrine Society, San Francisco, 1982, p. 205.
[2]Bowers CY, Momany F, Reynolds GA, Sartor O. Multiple receptors mediate GH release. 7th International Congress of Endocrinology, Quebec, Canada, 1984, p. 464.
[3]Granado M, García-Cáceres C, Frago LM, Argente J, Chowen JA. The positive effects of growth hormone-releasing peptide-6 on weight gain and fat mass accrual depend on the insulin/glucose status. Endocrinology. 2010 May;151(5):2008-18.
[4] Delgado-Rubín A, Chowen JA, Argente J, Frago LM. Growth hormone-releasing peptide 6 protection of hypothalamic neurons from glutamate excitotoxicity is caspase independent and not mediated by insulin-like growth factor I. Eur J Neurosci. 2009 Jun;29(11):2115-24.
Banned
Sorry SlimmerMe, I don't want to overwhelm you with material... but here is some additional reading as well into other Growth Hormone Releasing Peptides...
the CJC family is a very good group of GHRHs..... and I have been supplementing with it for some time now.
CJC-1293 Modified GRF (1-29)
In the healthy human body, large amounts of growth hormone are stored in the pituitary. The cells within the pituitary release growth hormone in response to signaling by GHRH (Growth Hormone Releasing Hormone), Ghrelin (of which GHRPs - Growth Hormone Releasing Peptides - are mimetics), and are inhibited from releasing these stores by Somatostatin. GHRH and Ghrelin act on different populations of somatotropes (GH releasing cells). GHRP/Ghrelin increases the number of somatotropes releasing GH but not the amount released by each cell; GHRH affects both the number of secreting cells and - more so - the amount they each secrete. [1] GHRH and Ghrelin are released in specific patterns that vary depending on event and environment: post-exercise, in response to slow wave sleep, in certain stages of life and physical development, and so on.
Most people (even the diseased) continue to possess the ability to make GH in the pituitary. The problem is in the signalling of the pituitary to release it and make more. Even most people with diseases that affect growth hormone secretion retain the ability to continue to make GH in their pituitaries. The disease states and symptoms result, most typically, in altered (dysfunctional) GH release signaling and this also affects the ability of the pituitary to continue to make more GH. [2]
Endogenous-type GHRH, which has a forty-four amino acid long chain (and a specific shape - thus making it a peptide as well as a hormone), has been marketed for the longest as Sermorelin in comparison to the other GHRH-type peptides. However, Sermorelin has been demonstrated to be degraded rapidly in the body and is cost-inefficient. But because most patients in need of GH therapy do retain the ability to produce and secrete their own GH, treatment with a GHRH-type analog remained hypothetically preferable to exogenous GH treatment. GH itself when administered exogenously results not only in "unnatural" release patterns, it results universally in down regulation of endogenous GH production - as do many hormones when applied exogenously.[3]
Sermorelin's limitations naturally resulted in a variety of formulations of GHRH analogs for therapeutic usage. CJC-1295, discussed in another article, is a GHRH analogue with attached MPA (aka DAC), binds to albumin in the bloodstream and circulates for a week or longer. Modified GRF 1-29, which is also called D-Ala2-GHRH-(1-29), [Nle27]-hGHRH(1-29)-NH2, GHRH (1-29)NH2, or ModGRF1-29, is the bioactive portion of GHRH(1-44) with fifteen amino acids subtracted and four amino acids replaced at the weakest points in the peptide structure.
Soule et al write that "D-Ala2 substitution contributes to the enhancement of biological activity by reducing metabolic clearance." [3] In a comparison study with synthetic exogenous GH for treating prepubertal GH deficiency, Lanes and Carillo concluded that "GHRH (1-29) at the dose and schedule used is generally effective in the treatment of GH deficiency." [4]
Campbell et al explain both GHRH(1-44)'s shortcomings in treatment as well as advantages offered by Modified GRF (1-29) and specific structural differences:
Native human GRF(1-44)-NH2(hGRF44) is subject to biological inactivation by both enzymatic and chemical routes. In plasma, hGRF44 is rapidly degraded via dipeptidylpeptidase IV (DPP-IV) cleavage between residues Ala2 and Asp3. The hGRF44 is also subject to chemical rearrangement (Asn8-->Asp8, beta-Asp8 via aminosuccinimide formation) and oxidation [Met27-->Met(O)27] in aqueous environments, greatly reducing its bioactivity. It is therefore advantageous to develop long-acting GRF analogues using specific amino acid replacements at the amino-terminus (to prevent enzymatic degradation): residue 8 (to reduce isomerization) and residue 27 (to prevent oxidation). Inclusion of Ala15 substitution (for Gly15), previously demonstrated to enhance receptor binding affinity, would be predicted to improve GRF analogue potency. Substitution of [His1,Val2]-(from the mouse GRF sequence) for [Tyr1,Ala2]-(human sequence) in [Ala15,Leu27]hGRF(1-32)-OH analogues completely inhibited (24-h incubation) DPP-IV cleavage and greatly increased plasma stability in vitro. Additional substitution of Thr8 (mouse GRF sequence), Ser8 (rat GRF sequence), or Gln8 (not naturally occurring) for Asn8 (human GRF sequence) resulted in analogues with enhanced aqueous stability in vitro (i.e., decreased rate of isomerization). These three highly stable and enzymatically resistant hGRF(1-32)-OH analogues, containing His1, Val2, Thr/Gln8, Ala15, and Leu27 replacements, were then bioassay for growth hormone (GH)-releasing activity in vitro (rat pituitary cell culture) and in vivo (SC injection into pigs). Enhanced bioactivity was observed with all three hGRF(1-32)-OH analogues. In vitro, these analogues were approximately threefold more potent than hGRF44, whereas in vivo they were eleven- to thirteen fold more potent.[5]
Just as GHRH and Ghrelin work in conjunction through different means for maximal GH release within the body, exogenous GHRH such as Modified GRF (1-29) results in a synergistic effect when used with a Ghrelin mimetic, such as the hexapeptide known as GHRP-6. [6] Pandya et al also conclude that "GHRH is necessary for most of the GH response to GHRP-6 in humans." [6] Massoud et al conclude that "Hexarelin and GHRH-(1-29)-NH2 are synergistic" [7] (Ed note: Hexarelin is another Ghrelin mimetic).
Sawada writes that "findings suggest that the KP-102-induced GH secretion largely depends on GRF and the secretagogue potentiates the GRF effect by antagonizing the SS action at the level of somatotropes. It is concluded that KP-102 alone or in combination with GRF provides a means of stimulating GH secretion in the face of elevated inhibitory tone mediated by SS." [8] (Ed note: KP-102 is the Ghrelin mimetic GHRP-2)
An abstract of a review by Hamilton touches on the main advantage of GRF(1-29) over, for example, CJC-1295 or synthetic GH:
...growth hormone secretion occurs in a rhythmic pattern regulated by intricate interactions between two neurohormones: growth hormone-releasing hormone (GHRH) and somatotropin release-inhibiting factor (SRIF).[...] research also indicates that there are sexual differences in the pattern of growth hormone release and that growth hormone regulates its own secretion by means of a negative feedback system. [9]
By mimicking natural release patterns with properly dosed and timed GHRPs (Ghrelin mimetics) and GHRH-analogues, negative feedback and undesirable side effects that are typically seen in synthetic GH therapy or even with past forms of GHRH administration (such as constant low-dose administration via pump) can be avoided.
For achieving ends other than restoring natural GH release in diseased patients, optimized rhythmic or pulsatile dosing of GHRH with or without a GHRP may be useful, as Vittone et al write about their findings on GHRH applied to healthy elderly men:
...data suggest that single nightly doses of GHRH are less effective than multiple daily doses of GHRH in eliciting GH- and/or IGF-I-mediated effects. GHRH treatment may increase muscle strength, and it alters baseline relationships between muscle strength and muscle bioenergetics in a manner consistent with a reduced need for anaerobic metabolism during exercise. Thus, an optimized regimen of GHRH administration might attenuate some of the effects of aging on skeletal muscle function in older persons.[10]
Cititations:
[1] Lewis UJ. Growth hormone: what is it and what does it do? Trends Endocrinol Metab 1992;3:117–121
[2] J Izdebski, J Pinski, JE Horvath, G Halmos, K Groot and AV Schally. Synthesis and Biological Evaluation of Superactive Agonists of Growth Hormone-Releasing Hormone. Proceedings of the National Academy of Sciences, Vol 92, 4872-4876.
[3] Soule S, King JA, Millar RP. Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men. J Clin Endocrinol Metab. 1994 Oct;79(4):1208-11.
[4]Lanes R, Carrillo E. Long-term therapy with a single daily subcutaneous dose of growth hormone releasing hormone (1-29) in prepubertal growth hormone deficient children. J Pediatr Endocrinol. 1994 Oct-Dec;7(4):303-8.
[5] Campbell RM, Stricker P, Miller R, Bongers J, Liu W, Lambros T, Ahmad M, Felix AM, Heimer EP. Enhanced stability and potency of novel growth hormone-releasing factor (GRF) analogues derived from rodent and human GRF sequences. Peptides. 1994;15(3):489-95.
[6]Pandya N, DeMott-Friberg R, Bowers CY, Barkan AL, Jaffe CA. Growth hormone (GH)-releasing peptide-6 requires endogenous hypothalamic GH-releasing hormone for maximal GH stimulation. J Clin Endocrinol Metab. 1998 Apr;83(4):1186-9.
[7]Massoud AF, Hindmarsh PC, Matthews DR, Brook. The effect of repeated administration of hexarelin, a growth hormone releasing peptide, and growth hormone releasing hormone on growth hormone responsivity. Clin Endocrinol (Oxf). 1996 May;44(5):555-62.
[8] Sawada H. Effect of newly developed analogue of growth hormone releasing peptide [D-Ala-D-beta Nal-Ala-Trp-D-Phe-Lys-NH2 (KP-102)] on growth hormone secretion in adult male rats (Trans. from Japanese). Nippon Ika Daigaku Zasshi. 1995 Apr;62(2):142-9.
[9] Hamilton J. A question of rhythm: recent advances in growth hormone research. CMAJ. 1995 Sep 1;153(5):585-8.
[10] Vittone J, Blackman MR, Busby-Whitehead J, Tsiao C, Stewart KJ, Tobin J, Stevens T, Bellantoni MF, Rogers MA, Baumann G, Roth J, Harman SM, Spencer RG. Effects of single nightly injections of growth hormone-releasing hormone (GHRH 1-29) in healthy elderly men. Metabolism. 1997 Jan;46(1):89-96.
~Knowledgeable Female Extraordinaire~
GOODNESS GRACIOUS! !!! BOY OH BOY! I have some reading to do! Thanks for your TIME in doing this., Muscle Dys... I appreciate it and will try to understand this. I have a lot to learn! I DO !!! Gotta put on my thinking cap now.
Banned
No problem!
HGH and peptides are a fascinating topic of discussion. I have spent countless days researching both (albeit a couple of years ago now!), and have drawn my own conclusions, but I would love to hear your opinion once you have taken the time to read through these profiles/studies, and deliberate on them. Pathways for these hormones are just so interesting in my eyes!
Have a good night, and we'll be in touch..
Banned
Perhaps helpful with the administration timing of your HGH shot, and the subsequent IGF-1 level....??
~Knowledgeable Female Extraordinaire~
THANKS!..I need to concentrate on all of the above to absorb all of this. I too love all of this research...to the point of obsession. And this forum sure adds to it...precisely why I got hooked...
~Knowledgeable Female Extraordinaire~
Wondering about the BOLD....any comments? cellular sensitivity? possible?
Last edited by SlimmerMe; 10-21-2010 at 01:58 PM.
~Knowledgeable Female Extraordinaire~
weight gain? if I am reading this correctly? yes...overwhelming..indeed!
Banned
Ghrelin-Hunger is a side effect that is associated with some peptide use. I find GHRP (growth hormone releasing peptides) to have the largest increase in the ghrelin. It's an odd feeling, but it's unmistakable. All you want to do is just eat carbs, ONLY CARBS. haha..
GHRP-6 is notorious for this
Cellular sensitivity just refers to the way in which individual bodies are able to essentially metabolize or utilize the hormone. All the article was trying to establish there, from my understanding, is that at every demographic one will see a variety of results, due to individual absorption rates.
Yes weight gain does occur. Keep in mind that the study was focused around diabetic rats though. lol.
From personal experience though, I will say that peptides can add quite a bit of sheer mass to an individual. (GHRP-6) If you're concerned about that, and are still considering going down the peptide route, then I would discuss with your doc/pharmacist about GHRP-2, which does not cause as prolific issues with grehlin hunger, and weight gain. (I know some people who consider GHRP-2 to be the far better of the two peptides; however, GHRP-6 is used far more often IMO.
-- Ask if you would like anymore/extra studies on peptides.
~Knowledgeable Female Extraordinaire~
Since HGH is a peptide, mass? or not. I ask this because if HGH is supposed to be good for lean mass then is this lean mass considered to be the mass you are speaking of...or mass in general. I hope this makes sense...
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