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Hi Dat.
Did that poster happen to mention just how much DHEA he was taking for this effect?
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Dat's - CJC-1295 & GHRP-6 (Basic Guides)
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Hi Dat.
Did that poster happen to mention just how much DHEA he was taking for this effect?
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Thank you for the reply. I must have missed it earlier
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Not Dat,
But from what I have read/seen is that 25mg BID of a good brand seems to do the trick an supply enough exogenous DHEA.
Enough to bring subjective levels up above mid range, yet still small enough of a dose to keep DHEA --> Estradiol conversion mild
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Dat: Minimal impact? What about the study in your post #492? Am I overemphasizing its relevance?
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Thanks for that info.!!
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Estrogen - Women & GHRH/GHRP-6
You're right! My mistake... I am glad you guys are on top of things.
Allow me to use your question to touch on estrogen & give out a little information that is important to woman concerning use of GHRH & GHRP-6.
ESTROGEN
Well DHEA conversion to estrogen has a pronounced positive effect on GH.
But I wonder...if you have a big fat pad & are an older guy or even a younger guy with a hormonal profile skewed toward "excess" estrogen already...whether DHEA will have a positive impact on GH production.
Conversely what happens when we reduce either estrogen or its ability to act...
AND which is more important in regard to negative impact on GH:
- the act of aromatization of testosterone to estradiol or
- absolute estrogen levels
Well that study I posted in post #492 found that the aromatization of testosterone to estradiol was important and that tamoxifen at 20 mg/day for 3 weeks reduced GH by about 50%, GH pulse by about 40% and IGF-1 by about 30%.
How about estrogen in general? ...lets look at estrogen supplementation (in females)
Well estrogen impairs the action of GH. Women are less responsive than men to GH treatment.
Oral estrogen especially inhibits GH's actions in dose-dependent fashion. However transdermal estrogen administration seems to bypass some of the increases in body fat and reductions in lean mass often seen in postmenopausal women given oral estrogen....so that mode of administration appears to minimize some of the negative impact of GH.
Oral estrogen administration leads to a reduction in IGF-I levels despite any increase in GH levels (from supplementation). The reason being that estrogen impairs the ability of GH to stimulate hepatic IGF-I production because of its negative impact on the growth hormone receptor and signalling.
So how does estrogen effect the use of GHRH and GHRP-6 to effect release of GH?
It seems that GHRP-6 (assume all GHRPs) induce a greater GH release response in the somatotrophs in the presence of estrogen then GHRH. Estrogen administration markedly decreases GH release in response to GHRH. *
So women should always include a GHRP (GHRP-6, GHRP-2, Hexarelin, Ipamorelin) in their therapy. GHRH (mod GRF(1-29), Sermorelin, CJC-1295) by itself will be inhibited in its action on GH release by the sex hormone estrogen.
* - Regulation of His-dTrp-Ala-Trp-dPhe-Lys-NH2 (GHRP-6)-lnduced GH Secretion in the Rat, Federico Malloa, Neuroendocrinology 1993;57:247-256
You're right! My mistake... I am glad you guys are on top of things.
Allow me to use your question to touch on estrogen & give out a little information that is important to woman concerning use of GHRH & GHRP-6.
ESTROGEN
Well DHEA conversion to estrogen has a pronounced positive effect on GH.
But I wonder...if you have a big fat pad & are an older guy or even a younger guy with a hormonal profile skewed toward "excess" estrogen already...whether DHEA will have a positive impact on GH production.
Conversely what happens when we reduce either estrogen or its ability to act...
AND which is more important in regard to negative impact on GH:
- the act of aromatization of testosterone to estradiol or
- absolute estrogen levels
Well that study I posted in post #492 found that the aromatization of testosterone to estradiol was important and that tamoxifen at 20 mg/day for 3 weeks reduced GH by about 50%, GH pulse by about 40% and IGF-1 by about 30%.
How about estrogen in general? ...lets look at estrogen supplementation (in females)
Well estrogen impairs the action of GH. Women are less responsive than men to GH treatment.
Oral estrogen especially inhibits GH's actions in dose-dependent fashion. However transdermal estrogen administration seems to bypass some of the increases in body fat and reductions in lean mass often seen in postmenopausal women given oral estrogen....so that mode of administration appears to minimize some of the negative impact of GH.
Oral estrogen administration leads to a reduction in IGF-I levels despite any increase in GH levels (from supplementation). The reason being that estrogen impairs the ability of GH to stimulate hepatic IGF-I production because of its negative impact on the growth hormone receptor and signalling.
Estrogen inhibits GH activation of the JAK/STAT pathway. The inhibition is dose-dependent and results from suppression of GH-induced JAK2 phosphorylation, leading to reduction in transcriptional activity. Estrogen does not affect phosphatase activity but stimulates expression of SOCS-2, which in turn inhibits JAK2 activation. Thus, esotrogen inhibits GH receptor signalling by stimulating SOCS-2 expression. - Growth hormone receptor modulators, Vita Birzniece & Akira Sata & Ken KY Ho, Rev Endocr Metab Disord
So how does estrogen effect the use of GHRH and GHRP-6 to effect release of GH?
It seems that GHRP-6 (assume all GHRPs) induce a greater GH release response in the somatotrophs in the presence of estrogen then GHRH. Estrogen administration markedly decreases GH release in response to GHRH. *
So women should always include a GHRP (GHRP-6, GHRP-2, Hexarelin, Ipamorelin) in their therapy. GHRH (mod GRF(1-29), Sermorelin, CJC-1295) by itself will be inhibited in its action on GH release by the sex hormone estrogen.
* - Regulation of His-dTrp-Ala-Trp-dPhe-Lys-NH2 (GHRP-6)-lnduced GH Secretion in the Rat, Federico Malloa, Neuroendocrinology 1993;57:247-256
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Local Actions of Estrogens in Males
This (to me) is a fascinating look at a topic few understand ...and that is the role of estrogen levels in males, the role of locally produced estrogen & its local use and the relationship between androgens & estrogen (two sides of the same coin?).
There are too many misconceptions about this topic.
Here are a few quotes from an article I am reading:
Oestradiol: an Endocrine or Paracrine Hormone?
Traditional endocrinology has assumed that, in the male, oestradiol synthesized by testicular Leydig cells and, to a lesser extent, by adipocytes and muscle, circulates in the bloodstream and acts throughout the body at sites where ERs are expressed (Fig. 2). Based on what we know now about the multiplicity of sites of ER expression, it seems somewhat incongruous that the relatively unchanging blood levels of oestrogens could regulate functions at this many different sites.
This raises the possibility that regulation is achieved predominantly by local production and action of oestradiol by conversion of the precursor, testosterone, which is produced by Leydig cells and which circulates at high levels in the bloodstream (Fig. 2). If this interpretation is correct, it would be expected that the enzyme aromatase would be expressed at many of the sites at which ERs are expressed.
...
...it is becoming increasingly clear that although oestradiol in blood emanates primarily from cells such as Leydig cells and adipocytes, these cells produce the oestradiol at least partly for local actions (Lafontan and Berlan 1995, Ge et al. 1996)
Androgens and Oestrogens:All a Question of Balance?
...
It is a remarkable coincidence that androgen receptors are expressed at the majority of sites at which ERs are expressed and, as aromatase is also expressed at many of the same sites (and possibly also 5-alpha-reductase), it can be envisaged that the local balance between oestrogen and androgen action could be finely regulated. We know already that androgens can regulate expression of aromatase at several sites. In this way, local modulation of the balance of androgen/oestrogen action could be envisaged to regulate target cell function.
There are some interesting pieces of evidence which suggest that it is the balance between androgen and oestrogen action that is important. The most dramatic example is ‘clover disease’ in sheep (Bennett et al. 1946), in which the ingestion of clover containing phytoestrogens (weak oestrogens) resulted in the deaths, owing to hypertrophy of the bulbo-urethral glands, of castrated rams (with low circulating testosterone levels) but had little effect on intact rams (with high circulating testosterone levels).
Another example is that quite similar developmental abnormalities of the male reproductive system can be induced by exposure to either an anti-androgen or an oestrogen (Toppari et al. 1996). Equally, gynaecomastia in males can be caused by either too much oestrogen or too little androgen (Bulun et al. 1997). - The Roles of Oestrogen in the Male, Richard M. Sharpe, TEM Vol. 9, No. 9, 1998
This (to me) is a fascinating look at a topic few understand ...and that is the role of estrogen levels in males, the role of locally produced estrogen & its local use and the relationship between androgens & estrogen (two sides of the same coin?).
There are too many misconceptions about this topic.
Here are a few quotes from an article I am reading:
Oestradiol: an Endocrine or Paracrine Hormone?
Traditional endocrinology has assumed that, in the male, oestradiol synthesized by testicular Leydig cells and, to a lesser extent, by adipocytes and muscle, circulates in the bloodstream and acts throughout the body at sites where ERs are expressed (Fig. 2). Based on what we know now about the multiplicity of sites of ER expression, it seems somewhat incongruous that the relatively unchanging blood levels of oestrogens could regulate functions at this many different sites.
This raises the possibility that regulation is achieved predominantly by local production and action of oestradiol by conversion of the precursor, testosterone, which is produced by Leydig cells and which circulates at high levels in the bloodstream (Fig. 2). If this interpretation is correct, it would be expected that the enzyme aromatase would be expressed at many of the sites at which ERs are expressed.
...
...it is becoming increasingly clear that although oestradiol in blood emanates primarily from cells such as Leydig cells and adipocytes, these cells produce the oestradiol at least partly for local actions (Lafontan and Berlan 1995, Ge et al. 1996)
Androgens and Oestrogens:All a Question of Balance?
...
It is a remarkable coincidence that androgen receptors are expressed at the majority of sites at which ERs are expressed and, as aromatase is also expressed at many of the same sites (and possibly also 5-alpha-reductase), it can be envisaged that the local balance between oestrogen and androgen action could be finely regulated. We know already that androgens can regulate expression of aromatase at several sites. In this way, local modulation of the balance of androgen/oestrogen action could be envisaged to regulate target cell function.
There are some interesting pieces of evidence which suggest that it is the balance between androgen and oestrogen action that is important. The most dramatic example is ‘clover disease’ in sheep (Bennett et al. 1946), in which the ingestion of clover containing phytoestrogens (weak oestrogens) resulted in the deaths, owing to hypertrophy of the bulbo-urethral glands, of castrated rams (with low circulating testosterone levels) but had little effect on intact rams (with high circulating testosterone levels).
Another example is that quite similar developmental abnormalities of the male reproductive system can be induced by exposure to either an anti-androgen or an oestrogen (Toppari et al. 1996). Equally, gynaecomastia in males can be caused by either too much oestrogen or too little androgen (Bulun et al. 1997). - The Roles of Oestrogen in the Male, Richard M. Sharpe, TEM Vol. 9, No. 9, 1998
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MGF Revisited
I was asked a very good question from WW so I thought I'd post it & my response here.
My position concerning MGF can be found at: http://www.professionalmuscle.com/forums/showthread.php?p=487161#post487161
Yes that 7 year old study screwed up my initial thinking as well.
I fell for the same language. Here is a post I made on AM last October asking Bob for his thoughts.
So I decided to actively research MGF. I read the 20 or so articles by Goldspink and I never again saw him postulate about a second distinct receptor. His research went forward to develop the understanding that I summarized in my post here on PM ...that is that MGF is expressed internally but is capable of interacting with the IGF-1 receptor IF it finds itself outside the cell.
The MGF experiments all show huge growth effect IF MGF expression is increased within the cell (inserted via a viral vector) and Goldspink made reference once or twice to pegylating MGF and injecting in vivo and they did get some positive results (but far less then when they expressed MGF internally).
So recently an MD magazine article wrote on peg MGF and quoted that study. So I again reexamined the topic and I tried to contact Mr. Goldspink for clarification. But he never got back to me.
This does piss me off a little because I contact scientists all the time and they all get back to me and love to talk about their work. But not Goldspink.
As it stands I hold the belief that his results with peg-MGF injected from without are a result of binding to an IGF-1 receptor. Goldspink has NEVER EVER EVER demonstrated how injected peg-MGF mediates its actions.
He has along with others specifically described how MGF is created and how it behaves all within the cell. In other words MGF acts within the cell of its birth.
This does not mean I have given up. Damaged brain cells seem to be able to make use of peg-MGF and I still have not taken the time to understand liposomal delivery of compounds through the cell-wall without receptor mediation.
So with the understanding I possess I prefer to look to strategies that increase the expression of Mechano Growth Factor inside muscle tissue because they have been demonstrated to work.
- Dat
I was asked a very good question from WW so I thought I'd post it & my response here.
My position concerning MGF can be found at: http://www.professionalmuscle.com/forums/showthread.php?p=487161#post487161
weltweite said:
Yes that 7 year old study screwed up my initial thinking as well.
I fell for the same language. Here is a post I made on AM last October asking Bob for his thoughts.
Hey Bob have you ever seen a study describing/mapping out the distinct MGF signaling pathway?
I know that studies * demonstrate that the signaling pathway is distinct from IGF-1Ea. Thats why you could inject both concurrently into muscle and they wouldn't interfere with one another...they don't share the same receptor/mechanism.
I know that studies * demonstrate that the signaling pathway is distinct from IGF-1Ea. Thats why you could inject both concurrently into muscle and they wouldn't interfere with one another...they don't share the same receptor/mechanism.
* "Also the selective blocking of the IGF-I receptor provides evidence that MGF increases myoblast proliferation via a different signalling pathway." - Different roles of the IGF-I Ec peptide (MGF) and mature IGF-I in myoblast proliferation and differentiation, Shi Yu Yang,Geo¡rey Goldspink, FEBS Letters 522 (2002) 156-160
So I decided to actively research MGF. I read the 20 or so articles by Goldspink and I never again saw him postulate about a second distinct receptor. His research went forward to develop the understanding that I summarized in my post here on PM ...that is that MGF is expressed internally but is capable of interacting with the IGF-1 receptor IF it finds itself outside the cell.
The MGF experiments all show huge growth effect IF MGF expression is increased within the cell (inserted via a viral vector) and Goldspink made reference once or twice to pegylating MGF and injecting in vivo and they did get some positive results (but far less then when they expressed MGF internally).
So recently an MD magazine article wrote on peg MGF and quoted that study. So I again reexamined the topic and I tried to contact Mr. Goldspink for clarification. But he never got back to me.
This does piss me off a little because I contact scientists all the time and they all get back to me and love to talk about their work. But not Goldspink.
As it stands I hold the belief that his results with peg-MGF injected from without are a result of binding to an IGF-1 receptor. Goldspink has NEVER EVER EVER demonstrated how injected peg-MGF mediates its actions.
He has along with others specifically described how MGF is created and how it behaves all within the cell. In other words MGF acts within the cell of its birth.
This does not mean I have given up. Damaged brain cells seem to be able to make use of peg-MGF and I still have not taken the time to understand liposomal delivery of compounds through the cell-wall without receptor mediation.
So with the understanding I possess I prefer to look to strategies that increase the expression of Mechano Growth Factor inside muscle tissue because they have been demonstrated to work.
- Dat
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Dat
The localized production of estradiol from fatty tissue is one of the reasons many experts are speculating why female pre-teens are beginning to go through puberty at alarming rates.
The rising obesity epidemic in children is the cause of the excess fatty tissue. Fat kids - Local, excessive estradiol production, which kicks in puberty.
So perhaps it's not just hormones in the meat(yea right! We all know how effective oral GH is
), bad water, or pesticides.
The localized production of estradiol from fatty tissue is one of the reasons many experts are speculating why female pre-teens are beginning to go through puberty at alarming rates.
The rising obesity epidemic in children is the cause of the excess fatty tissue. Fat kids - Local, excessive estradiol production, which kicks in puberty.
So perhaps it's not just hormones in the meat(yea right! We all know how effective oral GH is
), bad water, or pesticides.
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So would it be beneficial for a young male on a cycle of AAS and using only ghrp-6 to add in 25mg of dhea daily to further emplify the effect of ghrp-6?
Dat, it would be great if you could chime in on the effect of using dhea in conjunction ghrp-6. Cant seem to access the AM link you gave earlier in your thread.
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25mg BID is twice a day dosing
It certainly wouldn't hurt anything, and is cheap, and would only benefit.
My bigger concern would be to make sure you are
1. Running hcG the entire time your "on" to facilitate natural production and prevent any atrophy that might occur
2. Make sure estradiol is kept in check with a good AI such as arimidex or aromasin
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DHEA
In response to:
and
I no longer have a thread at AM.
The original DHEA posts and my response were as follows:
Initial Post -
My response
Nice speculation & accurate it seems.
In my old archive on GHS I found a folder I had labeled DHEA and an abstract that is directly on point.
It turned out that estrogen was the important factor so this dissertation is really a standalone but the following abstract explains what you may have experienced.
In response to:
and
I no longer have a thread at AM.
The original DHEA posts and my response were as follows:
Initial Post -
I just started taking 100 mgs. of DHEA the other day. I took my second dose today with fish oil, came home and took my 200 mcg dose of GHRP-6. I am experiencing a pronounced tingling in my hands and feet. DHEA MAY be called the "Mother Hormone" for good reason from what I'm experiencing.
I have experienced minor tingling before when taking GHRP-6 alone. I'm speculating that DHEA might boost GHRP-6 effects thus a (more pronounced feeling). This is only speculation. I have no studies to back it. I'd be interested to hear what others have to say about it.
My response
Nice speculation & accurate it seems.
In my old archive on GHS I found a folder I had labeled DHEA and an abstract that is directly on point.
It turned out that estrogen was the important factor so this dissertation is really a standalone but the following abstract explains what you may have experienced.
Restoration of aging growth hormone cells by dehydroepiandrosterone via estrogen receptors by Iruthayanathan, Mary, Ph.D., University of Arkansas for Medical Sciences, 2004, 136 pages; AAT 3165066
Abstract (Summary)
Dehydroepiandrosterone (DHEA) is the most abundant circulating steroid in humans. With progressive aging there is a decline in the levels of DHEA, growth hormone (GH) and sex steroids. DHEA levels seem to correlate inversely with morbidity and mortality associated with aging. Hence, it is widely used as an anti-aging supplement to counter these effects. DHEA is considered traditionally as a precursor hormone for estrogens and androgens and to have no function of its own, as it does not have a specific receptor. The decline in GH levels with aging is associated with a loss of GH cells (somatotropes) in the pituitary.
The objective of this study was to learn if the functions of somatotropes can be restored in aging female rats (12-14-months and 18-months) to levels seen in young, diestrous rats (3-4 months). Using in vitro and in vivo methods, the results indicate that DHEA acts directly at the level of the pituitary to restore GH gene expression to levels seen in young rats. The study employed cytochemical and molecular techniques (immunocytochemistry, in-situ hybridization, QRT-PCR) to assess the function and gene expression of somatotropes.
This is the first study to our knowledge, to show a loss of GH-releasing hormone-receptor (GHRH-R) binding cells in aging female rat pituitaries, which could also be a contributory factor in the decline of GH levels. Short-term DHEA treatment of 18-month-old rats, in vivo , increases the number of GHRH-binding cells in the pituitary resulting in a two-fold increase in serum GH. The study also addresses mechanisms behind DHEA's restoration of aging somatotropes in vitro using inhibitors (trilostane and aminoglutethemide) that block specific metabolic pathways of DHEA. The study shows that DHEA needs to be aromatized to estrogen to restore GH expression in aging somatotropes. ICI 182,780, an estrogen receptor (ER) antagonist, also blocked the restorative effects of DHEA, suggesting that ERs play a key role in DHEA's action on aging somatotropes. In summary, this study shows that DHEA has direct actions on the pituitary, possibly after aromatization to estrogen. The findings in aging rats suggest that DHEA replacement might benefit individuals with low GH levels.
Advisor: Childs, Gwen V.
School: University of Arkansas for Medical Sciences
School Location: United States -- Arkansas
Keyword(s): Restoration, Aging, Growth hormone, Dehydroepiandrosterone, Estrogen receptors
Source: DAI-B 66/02, p. 658, Aug 2005
Source type: Dissertation
Subjects: Cellular biology
Publication Number: AAT 3165066
ISBN: 9780542002564
Abstract (Summary)
Dehydroepiandrosterone (DHEA) is the most abundant circulating steroid in humans. With progressive aging there is a decline in the levels of DHEA, growth hormone (GH) and sex steroids. DHEA levels seem to correlate inversely with morbidity and mortality associated with aging. Hence, it is widely used as an anti-aging supplement to counter these effects. DHEA is considered traditionally as a precursor hormone for estrogens and androgens and to have no function of its own, as it does not have a specific receptor. The decline in GH levels with aging is associated with a loss of GH cells (somatotropes) in the pituitary.
The objective of this study was to learn if the functions of somatotropes can be restored in aging female rats (12-14-months and 18-months) to levels seen in young, diestrous rats (3-4 months). Using in vitro and in vivo methods, the results indicate that DHEA acts directly at the level of the pituitary to restore GH gene expression to levels seen in young rats. The study employed cytochemical and molecular techniques (immunocytochemistry, in-situ hybridization, QRT-PCR) to assess the function and gene expression of somatotropes.
This is the first study to our knowledge, to show a loss of GH-releasing hormone-receptor (GHRH-R) binding cells in aging female rat pituitaries, which could also be a contributory factor in the decline of GH levels. Short-term DHEA treatment of 18-month-old rats, in vivo , increases the number of GHRH-binding cells in the pituitary resulting in a two-fold increase in serum GH. The study also addresses mechanisms behind DHEA's restoration of aging somatotropes in vitro using inhibitors (trilostane and aminoglutethemide) that block specific metabolic pathways of DHEA. The study shows that DHEA needs to be aromatized to estrogen to restore GH expression in aging somatotropes. ICI 182,780, an estrogen receptor (ER) antagonist, also blocked the restorative effects of DHEA, suggesting that ERs play a key role in DHEA's action on aging somatotropes. In summary, this study shows that DHEA has direct actions on the pituitary, possibly after aromatization to estrogen. The findings in aging rats suggest that DHEA replacement might benefit individuals with low GH levels.
Advisor: Childs, Gwen V.
School: University of Arkansas for Medical Sciences
School Location: United States -- Arkansas
Keyword(s): Restoration, Aging, Growth hormone, Dehydroepiandrosterone, Estrogen receptors
Source: DAI-B 66/02, p. 658, Aug 2005
Source type: Dissertation
Subjects: Cellular biology
Publication Number: AAT 3165066
ISBN: 9780542002564
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"I still have not taken the time to understand liposomal delivery of compounds through the cell-wall without receptor mediation."
I was wondering about this! I'm going to do some research later tonight about it, and see what I can find. Thanks once again!
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16/6
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Hey WW here is some of my original musings on MGF making its way outside of the cell.
MGF has a short half-life in the extracellular compartment (outside the cell), due to proteolysis. MGF does not bind to the known IGF-I binding proteins that stabilize IGF-I in muscle as well as in the blood. It is produced as a pulse after exercise/damage and it does not survive in the extracellular compartment for any appreciable length of time.
But what if MGF does make it to the cell surface? Presumably it would bind to the IGF-Receptor and initiate the AKT signaling pathway which will stimulate cell growth signals. In other words MGF stops being MGF and behaves like IGF-1 in initiating anabolic events.
So how would MGF that is created inside the cell make its way to the surface?
I don't know. The following possibility was described on page 240 of "The Encyclopaedia of Sports Medicine, 2000 edition" but was dropped in later editions.
"The specific binding protein for MGF appears to be Creatine Kinase (MM) in muscle and (BB) in the central nervous system. Creatine Kinase is bound to the miofibrils but detaches when the ph falls below 7 and when the myofibrils are stretched. (Kraft et al 2000). MGF binds strongly to Creatine Kinase which when the muscle is damaged exits from the fibers through the damaged and leaky membrane. This indicates that MGF can be regarded as a repair factor and that it is overexpressed when a muscle is overloaded which then results in hypertrophy."
The half-life by-the-way of Creatine Kinase in plasma is just 48 minutes. - J. Biol. Chem., Vol. 262, Issue 27, 13020-13026, 09, 1987
I can find no other references to this concept so maybe it is incorrect.
Now this was before they understood that MGF is created in the cell and translocates to the nucleus where it mediates events without ever interacting w/ a receptor. But for our purposes in trying to see if injected MGF could get into the cell and behave as MGF it is interesting that post exercise the muscle cell membrane is described as "damaged and leaky".
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How much GH do we secrete in IUs?
You see people on boards making all sorts of silly claims concerning how many ius we normally secrete.
Did anyone catch the chart I posted in Post #558 which revealed that 24-hour GH secretion in males of ages 16 to 25 was just under 600mcg?
Nutropin reveals that 1 iu of their GH is equal to 333 mcg, so a normal young male secretes about 2iu of GH a day.
A normal male aged 26 to 35 secretes less than 1 iu of GH with the following age groups secreting less.
Now the comparison isn't entirely accurate (Nutropin weight to how much GH ends up in plasma) but even if we add 50% to the value we are still talking about a normal male aged mid-twenties to mid-thirties secreting less than 2iu of GH a day.
So do you think a middle aged male could benefit by a true (meaning accurate as opposed to Chinese generic product) 1-2iu increase in GH (such that can be created with just GHRP-6 alone)?
From the stand point of healthy restoration to youthful levels, the answer is yes.
For the lazy here is the chart from that post:
Anti-Aging
You see people on boards making all sorts of silly claims concerning how many ius we normally secrete.
Did anyone catch the chart I posted in Post #558 which revealed that 24-hour GH secretion in males of ages 16 to 25 was just under 600mcg?
Nutropin reveals that 1 iu of their GH is equal to 333 mcg, so a normal young male secretes about 2iu of GH a day.
A normal male aged 26 to 35 secretes less than 1 iu of GH with the following age groups secreting less.
Now the comparison isn't entirely accurate (Nutropin weight to how much GH ends up in plasma) but even if we add 50% to the value we are still talking about a normal male aged mid-twenties to mid-thirties secreting less than 2iu of GH a day.
So do you think a middle aged male could benefit by a true (meaning accurate as opposed to Chinese generic product) 1-2iu increase in GH (such that can be created with just GHRP-6 alone)?
From the stand point of healthy restoration to youthful levels, the answer is yes.
For the lazy here is the chart from that post:
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:c:eeky-sm
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Dat, another question if you dont mind.
Whats your opinion of a young male running GHRP-6 on a long term basis, say 6 to 12 mths? Will it cause suppression of natural GH production once we come off after this long period?
Would it also be beneficial to run it long term instead of cycling them (AAS style) as i read one of your posts mentioning that usage of peptides for a period of at least 6 months or more is reccommended.
It would be great if there are studies showing this with regards to young males(21years above).
Your input is greatly appreciated.
Whats your opinion of a young male running GHRP-6 on a long term basis, say 6 to 12 mths? Will it cause suppression of natural GH production once we come off after this long period?
Would it also be beneficial to run it long term instead of cycling them (AAS style) as i read one of your posts mentioning that usage of peptides for a period of at least 6 months or more is reccommended.
It would be great if there are studies showing this with regards to young males(21years above).
Your input is greatly appreciated.
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Thank you for the detailed response...very interesting. I also wonder if supps. like L-Dopa or 1 carboxy could amplify the effects of GHRP-6..hmmm
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