Chromium (As Chromium 454™ Bio-Organic Yeast Extract Matrix)
Cinnulin PF Cinnamon (Cinnamomum Cassia) Water Extract (Bark) [Std. To 0.95% (1.66 Mg) Trimeric
Quercetin (As Quercetin Dihydrate)
Green Tea (Camellia Sinensis) Extract (Dried Leaves)(Decaffeinated) [Std. To 95% Polyphenols, 45% Epigallocatechin-3-P-Gallate] **
GlucoHelp (Lagerstroemia Speciosa L.) (Leaf [Std. To 18% Corosolic Acid] **
CoffeeBerry FORTE Coffee (Coffea Arabica) Extract (Decaffeinated) (Fruit) [Std. To 50% Total Phenolic Acids And 15,000 µmole/gm ORAC
and vanadyl sulfate
background:
just switched to eq/test from deca/mast/test, was on test for months prior and also been using GHRH 100mcg, GHRP6 125mcg two times a day (in the morning and PWO)
4 iu slin PWO
during this transition i decided to cycle on/off slin from now on (slin only, aas and GHRH will keep going), 5 days on slin, 5 days off. During the off period from slin, i use supplements containing the above ingredients.
observation:
my ankles were swollen noticeably during deca/mast/test and also prior,,,during the transition to test/eq and slin to supplements, my ankle swelling has disappeared. I can see my ankle bone and veins. Also severe lethargy has subsided as well.
concern:
since GH effects are so subtle and cumulative I can not tell that if the supplements have stopped GH pulse from GHRH/GHRP6 or not, so I must go by side effects and if I do not see GH sides then I conclude that GH pulses have stopped. Or is this a new found remedy for edema and lethargy? I hope I am not wasting money here. It has been 4 days on the OTC supps, will jump back on slin on Thursday and will report back if edema occurs again.
your thoughts? or anybody...
forgot to add, was taking forslean 1 cap a day for past 5 days,,,now i have stopped. Was using forskolin to mimic TSH to combat lethargy as an experiment, didnt do much to help anything during those 5 days. Maybe its now helping?
Hey, I don't know if this helps but my wife stays away from deca because it blows her up with water. Definitely the test will cause water I always notice swelling in the ankles when I take it. Seeing that you didn't have this after the switch, it may have been the deca.
What is anyones opinion on waiting 3 hours after a fatty meal to take the GHRP6/CJC combo?
I'm trying to figure out timings, but usually right before bed I have a tablespoon of olive oil and a protein shake. Obviously that would blunt the release.
Maybe take the olive oil and protein shake 30 minutes AFTER the administeration? Would that be sufficient time?
i like that thought. It was my first time (not sure why i waited for so long cuz it was awesome) ever on Deca so I am not familiar with its sides....so it could very well be nandrolone and me.
well slin will start in a few days, i will report back if anythign changes, thank you for your input.
What is anyones opinion on waiting 3 hours after a fatty meal to take the GHRP6/CJC combo?
I'm trying to figure out timings, but usually right before bed I have a tablespoon of olive oil and a protein shake. Obviously that would blunt the release.
Maybe take the olive oil and protein shake 30 minutes AFTER the administeration? Would that be sufficient time?
forgot to add, was taking forslean 1 cap a day for past 5 days,,,now i have stopped. Was using forskolin to mimic TSH to combat lethargy as an experiment, didnt do much to help anything during those 5 days. Maybe its now helping?
Actually forskolin may increase GH additively w/ GHRPs.
"In this study, forskolin additively, not synergistically, stimulated GH release induced by GHRP-2." - Mechanisms of action of growth hormone-releasing peptide-2 in bovine pituitary cells, S. G. Roh , J Anim Sci 1997. 75:2744-2748
Actually forskolin may increase GH additively w/ GHRPs.
"In this study, forskolin additively, not synergistically, stimulated GH release induced by GHRP-2." - Mechanisms of action of growth hormone-releasing peptide-2 in bovine pituitary cells, S. G. Roh , J Anim Sci 1997. 75:2744-2748
I wonder if that is simply from the increased testosterone, and ultimately, estrogen, that forskolin brings to the table.
A good forskolin product is one of the better "herbal" testosterone boosters out there.
I have read literature that increased testosterone levels will enhance GH production by 10% or so.
This is usually based on someone previously hypogonadal and now receiving testosterone replacement, so obviously forskolin cannot replicate that big of a test increase.
not to get too carried away with forskolin but someone with endo background said forskolin is a dirty way to raise cAMP. I guess too many other things get affected along the way?
also I pointed some studies out at AM saying forskolin by itself or with HCG will only produce androstenedione, will not go further to make test. At least that was from the study i saw. But as always AM's supplement company reps defended forskolin as a great t booster.
just sharing that forskolin isn't that great, and use caution until further info i guess.
and then there are so many studies on TSH, and thyroid hormones with forskolin to make my head spin.
I have dropped forskolin and no difference in lethargy,,,,Dat not sure if you've seen mikewithbigpecs (LOL) thread, because him and i are suffering from GH induced lethargy that just won't go away. I've heard many things including blood sugar level and thyroid. Any thoughts? or did I miss your earlier discussion on this, sorry if so.
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.
* "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.
My test subject was administered PEG-MGF by itself (no other peptides, AAS, etc.) for one month cycles (2 x 500mg per week) on two separate occassions and received very pleasing results -- no noticeable water retention, fat loss, some body recomp.
Ideally, I would have liked to rotate my subject between CJC / GHRP-6 and PEG-MGF cycles but the combination of CJC / GHRP-6 results in too much water retention and a bloated gut in this subject.
Questions:
Any idea how long PEG-MGF can be safely administered without sides or receptor downregulation at 1mg per week?
Any benefit or disadvantages to combining GHRP-6 with PEG-MGF?
At least that was MY point. That doesn't necessarily mean I am correct.
However if your read my posts you would know that THAT is my current position so why do you ask your questions??
IF PEG-MGF behaves as MGF (i.e. causes myoblast proliferation but prevents differentiation) you want it to act as long as possible. I was looking at one of the fibroblast growth factors (there are many variants) and it also is a proliferating agent. But once proliferation stops and differentiation occurs thats it. That cell will not divide or proliferate.
...anyway so it seems that you would want to hold the proliferation "gas pedal" down for as long as possible while keeping differentiation factors from acting.
So, I don't know ...but when I was thinking about fibroblast growth factor (because it can do the same thing as MGF & there is a receptor for it) I was thinking maybe you just use it for a while. I think one study showed proliferation continued for at least 80 days straight in the same cell. So if you could do that or come close when you turn the cell into a muscle cell it will have the greatest potential to increase in size & strength.
I know none of this is what you were asking ...but go substitute the term IGF-1 for PEG-MGF in your question and see if you already have an understanding.
I know people like to megadose these peptides. RP tells people I am wrong when I talk about saturation doses of 1mcg/kg. He says dosing should be much higher than 3mcg/kg. Of course he sells the stuff & gets his information from
So here is some science for you on maximal effective dosing.
Growth Hormone-Releasing Activity of Hexarelin, a New Synthetic Hexapeptide, after Intravenous, Subcutaneous, Intranasal, and Oral Administration in Man, E. Ghigo, E. Arvat, L. Gianotti, B. P. Imbimbo, V. Lenaerts, R. Deghenghi, And F. Camanni,J. Clin. Endocrinol. Metab., Mar 1994; 78: 693 - 698
The greatest effect by the iv route was observed after 2 ug/kg hexarelin, as in a previous phase I study (26). In that study there was a 107% increase in AUC, moving from 0.5-1 ug/kg, and a further 27% augmentation with the 2 ug/kg dose. Thus, 2 ug/kg seems to approach the maximal effective dose.
...
We found a dose-related effect after SC hexarelin. The GH response with the dose of 1.5 ug/kg is similar to that recently reported after SC administration of GHRP-2, which is considered to be the most potent synthetic peptide (14). The biological bioavailability of hexarelin after SC administration was 86.1 +/- 12.0% and 67.9 +/- 17.6% in men and women, respectively. We found a trend toward a lower responsiveness in women, which is in accordance with previous data reported by Bowers using GHRP-6 (14).
26 - Imbimbo BP, Mant T, Edwards I’k, et al.Growth hormone releasing activity of hexarelin in humans: a dose-response study, Abstract 371. Int Symp on Growth Hormone II: Basic and Clinical Aspects. 1992.
So you double effectiveness when you go from .5mcg/kg to 1mcg/kg but just get a further 27% increase by going to 2mcg/kg and really no more effect beyond 2mcg/kg.
Of course you will increase your hunger but hunger ain't GH release.
At least that was MY point. That doesn't necessarily mean I am correct.
However if your read my posts you would know that THAT is my current position so why do you ask your questions??
IF PEG-MGF behaves as MGF (i.e. causes myoblast proliferation but prevents differentiation) you want it to act as long as possible. I was looking at one of the fibroblast growth factors (there are many variants) and it also is a proliferating agent. But once proliferation stops and differentiation occurs thats it. That cell will not divide or proliferate.
...anyway so it seems that you would want to hold the proliferation "gas pedal" down for as long as possible while keeping differentiation factors from acting.
So, I don't know ...but when I was thinking about fibroblast growth factor (because it can do the same thing as MGF & there is a receptor for it) I was thinking maybe you just use it for a while. I think one study showed proliferation continued for at least 80 days straight in the same cell. So if you could do that or come close when you turn the cell into a muscle cell it will have the greatest potential to increase in size & strength.
I know none of this is what you were asking ...but go substitute the term IGF-1 for PEG-MGF in your question and see if you already have an understanding.
I actually agree with your assertion that PEG-MGF acts just like IGF-1 and definitely appreciate your thoughts on this topic. The results I've seen seem to support your position.
So, with the assumption that the results I've seen are from the actions of PEG-MGF binding with IGF-1 receptors, I'm just trying to get an idea as to how long one can benefit from the IGF-binding actions of PEG-MGF without downregulation or sides, and also whether there is benefit to stacking with another peptide.
...So, with the assumption that the results I've seen are from the actions of PEG-MGF binding with IGF-1 receptors, I'm just trying to get an idea as to how long one can benefit from the IGF-binding actions of PEG-MGF without downregulation or sides, and also whether there is benefit to stacking with another peptide.
Well my guess is that if Peg-MGF is acting as IGF-1 it is doing so much better then IGF-1 LR3.
IGF-1 LR3 has the disadvantage of having a lower affinity for the IGF-1 receptor. Think weaker magnet... Now the supposed advantage of LR3 is that it stays around for a while. But that could be a disadvantage because it will probably cause negative feedback which inhibits GH release.
See IGF-1 naturally binds to IGF-1 receptors on the somatotrophs (somatotrophs, sometimes written as somatotropes are cells in the anterior pituitary which secrete hormones when instructed. In this case GH) and usually brings about an inhibition of GH release for a few hours. It is only a few hours because it is the concentrated synthesis from the liver brought on by the GH pulse which hits the somatotrophs in concentrated form.
Peg-MGF if it inhibits GH probably does so similar to what happens naturally (i.e. just a few hours).
Now IGF-1 LR3 because it is around a while might bring prolonged inhibition.
Now what about IGF-1 receptor downregulation?
This is not a concern with peg-MGF.
What are we talking about by this concept of "IGF-1 receptor downregulation"? In general receptors don't live for long periods of time. They are constantly made, translocated to cell surfaces and then part breaks off and becomes a binding protein circulating in plasma and part gets internalized into the cell.
What is important is what happens when an IGF-1 ligand binds to an IGF-1 receptor. Chronic exposure could mean those intracellular events desensitize. This doesn't happen really with natural IGF-1 and I don't think it will happen with peg-MGF (because it is medium-lived). Now with IGF-1 LR3 since it is long-lived it could do that.
Now if you want to use mod GRF(1-29)/GHRP-6 w/ peg-MGF you can do that. Just use the peg-MGF so as not to interfere with natural post-workout production of real MGF & so as not to interfere with GH release.
Now if you want to use mod GRF(1-29)/GHRP-6 w/ peg-MGF you can do that. Just use the peg-MGF so as not to interfere with natural post-workout production of real MGF & so as not to interfere with GH release.
Thanks DAT.....very useful. I'm thinking PEG-MGF 2 x 500mg per week and 100mg GHRP-6 at night. When you say "interfere with the GH release", since the PEG-MGF has a fairly long half-life due to the PEGylation, will it interfere with the nightly GH release which GHRP-6 promotes?
Dat, what do you think of the following study which in a round about way states old gents don't get effective long term results from GHRP-2
Sustained Elevation of Pulsatile Growth Hormone (GH)
Secretion and Insulin-Like Growth Factor I (IGF-I),
IGF-Binding Protein-3 (IGFBP-3), and IGFBP-5
Concentrations during 30-Day Continuous Subcutaneous
Infusion of GH-Releasing Peptide-2 in
Older Men and Women"
CYRIL Y. BOWERS, RAMONA GRANDA, SUBBURAMAN MOHAN, JONATHAN KUIPERS, DAVID BAYLINK, AND JOHANNES D. VELDHUIS
The Journal of Clinical Endocrinology & Metabolism 89(5):2290 –2300 (year 2004)
I've been buttin heads with my fellow moderator over at Dr J's site on the effectiveness of GHRH + GHRP versus straight GH injects.
He feels the new protocols are not effective for anyone over 60 and that older guys should use straight GH injects only.
You're wrong. That is not the conclusion of the study, Sustained Elevation of Pulsatile Growth Hormone (GH) Secretion and Insulin-Like Growth Factor I (IGF-I), IGF-Binding Protein-3 (IGFBP-3), and IGFBP-5 Concentrations during 30-Day Continuous Subcutaneous Infusion of GH-Releasing Peptide-2 in Older Men and Women, Cyril Y. Bowers, The Journal of Clinical Endocrinology & Metabolism 2004 89(5):2290–2300
This is one of those really good studies for the reason that it fully references and incorporates knowledge from other studies as well as its own findings and then gives the current state of our understanding. The primary author Cyril Bowers is the father of GHRPs...as he was the first to discover them.
This study underscores so many positive aspects of GHRPs+GHRH and reinforces much of what I have said that I am surprised anyone would attempt to use it to draw negative conclusions.
Not only that we can follow references from this study and add to our existing knowledge base. So lets begin.
Elderly women (post-menopausal) had a better response to GHRP & GHRP+GHRH then elderly men. Why?
Gender comparisons disclosed that acute bolus iv injection and 30-day continuous sc infusion of GHRP-2 stimulate about 2-fold greater GH secretion in hormonally replaced postmenopausal women than in elderly men. ...short-term supplementation of estradiol potentiates acute responses to synthetic GHRPs in prepubertal girls and postmenopausal women. An inferred molecular mechanism is the ability of estradiol to enhance transcriptional activity of the human GHRP receptor gene promoter in vitro (87). However, whether the latter mechanism operates in vivo or whether chronic vis-a-vis short-term estrogen replacement enhances hypothalamo-pituitary,responsiveness to GHRP receptor agonists has not been elucidated.
Okay...
So that must mean elderly men get no benefit? Hell no!
In short-term clinical studies in postmenopausal women, continuous iv infusion of GHRP-2 separately or combined with GHRH for 24 h amplifies pulsatile and total GH secretion by 30- to 120-fold and elevates fasting IGF-I concentrations (27–29). The present outcomes extend such inferences in older men and women by demonstrating that unvarying sc infusion of GHRP-2 for 1 month augments pulsatile, total, 24-h rhythmic, and entropic measures of GH secretion and IGF-I, IGFBP-3, and IGFBP-5 concentrations. From a qualitative viewpoint, the foregoing specific ensemble of neuroendocrine and systemic responses is identical to that observed at the time of maximal linear growth in healthy pubertal girls and boys (66). From a quantitative vantage, continuous GHRP-2 administration for 2 and 4 wk increased the 24-h GH secretion rate in elderly adults to approximately 0.5 mg (assuming a 7% distribution volume). The latter value is approximately 50% of that attained in adolescents at peak growth velocity (66–68).
Wow! So GHRP-2 administration restores GH levels to that of youth.
What about IGF-1?
Constant sc delivery of GHRP-2 for 30 d increased fasting concentrations of IGF-I, IGFBP-3, and IGFBP-5, but not those of non-GH-dependent proteins, IGFBP-4 and IGF-II (91).
How about young people. Does prolonged use of GHRP increase IGF-1 and is this sufficient to induce growth?
Interventional trials in children with idiopathic short stature indicate that once or repeated daily administration of a GHRP receptor agonist by intranasal, sc, or oral routes for 6 months can accelerate linear growth over the baseline rate (75–79). In these reports, fasting morning GH concentrations increased by 2- to 4-fold initially and then declined by about 50% to a plateau value that exceeded baseline by approximately 2-fold. In contradistinction, IGF-I concentrations rose promptly and remained equivalently elevated for at least 6 months of secretagogue delivery. We report comparable temporal dissociation between GH secretion and IGF-I concentrations during 30-d continuous GHRP-2 delivery in healthy elderly adults.
Okay enough with that...
Lets move on to learning a few other things from this & referenced studies.
Don't dose GHRPS too high!!!
How many times have I stated THAT?!.
From the discussion:
A key mechanistic insight of this investigation is that administration of GHRP-2 as an unvarying and submaximal stimulus will sustain physiological features of somatotropic axis activation for at least 1 month. In contrast, intermittent stimulation with a high dose of GHRP rapidly down-regulates GH secretion (see introduction). The present concept is adumbrated in short-term studies (0.5–4 d), wherein repeated or continuous submaximal GHRP administration appears to maintain elevated GH concentrations and drive pulsatile GH secretion (25–29, 62–64). The exact basis for the apparent resistance to down-regulation of secretagogue effects under uninterrupted and submaximal feedforward is not known.
From the introduction:
...Acute administration of a high dose of GHRP downregulates homologous responsiveness of the somatotropic axis in all mammalian species studied (20 –24). However, limited indirect data suggest that continuous delivery of or repeated exposure to a low dose of GHRP can maintain elevated GH secretion and IGF-I concentrations for 12 h to 4 d (25–31). We hypothesized that constant exposure to a submaximal concentration of GHRP may mimic the physiological pattern of relatively stable systemic ghrelin concentrations (32, 33).
As it turned it out they were correct. Thirty days of GHRP-2 use continue to be effective at low dose.
Here is the really cool stuff
But the really interesting part of the study was a reference to another study which tells us how the elderly can achieve a GH release equal to what youth can achieve. Lets take a look at, Age-related Variations in the Neuroendocrine Control, More Than Impaired Receptor Sensitivity, Cause The Reduction in the GH-releasing Activity of GHRPs in Human Aging, Emanuela Arvat, Pituitary 1998;1:51–58.
First they reiterated what is known and that is that "the pituitary GH releasable pool is preserved in aging". That "age-related variations in the neural control of GH secretion play a major role in the reduced activity of GH/IGF-I axis in aging. ...data support the existence, in this period of life, of concomitant somatostatinergic hyperactivity and hypoactivity of GHRH secreting neurons".
While GHRH+GHRPs do overcome some of this attenuated signaling it is not sufficient to evoke identical GH release response between young and elderly. Young people are more responsive to GHRH+GHRPs then the elderly.
Apparently GHRPs can reduce the negative inhibition of somatostatin but do not completely overcome the hyperactivity that comes with age.
BUT what they found was that if Arginine (an inhibitor of somatostatin) was added to GHRH+GHRP then the amount of GH released from this trilogy was identical to that achieved by young people when they used either GHRH+GHRP or the trilogy.
Young people have far less somatostatin inhibition. GHRPs are capable of restoration by themselves. Arginine is of no additional value to the young (who use GHRH+GHRP). But it is very valuable to the elderly.
The effect of arginine on the GH response to HEX and/or GHRH was of particular interest. In fact, in young we found that arginine, which strongly potentiates the GHRH-induced GH rise, does not modify the GH response to HEX either alone or combined with GHRH [36 and present study] Differently from in young, in elderly subjects we found that arginine potentiates not only the GH response to GHRH but even those to HEX and HEX plus GHRH, restoring them to levels recorded in young.
So how much Arginine?
They administered .5g/kg. So that would be 45 grams per 90 kilo person.
Does it have to be that high?
Well in Synergy of L-arginine and growth hormone (GH)-releasing peptide-2 on GH release: influence of genderLaurie Wideman, Judy Y. Weltman, James T. Patrie, C. Y. Bowers, Niki Shah, Shannon Story, Arthur Weltman, And Johannes D. Veldhuis, Am J Physiol Regulatory Integrative Comp Physiol 279: R1455–R1466, 2000 they use 30 grams of infused Arginine and found synergy between GHRP-2 & Arginine with a better response in woman.
Sounds good but how about an oral dose ..and can we get it lower?
Well in the following study they found 8 grams of oral Arginine to be effective with GHRP-6 in the elderly but as we would expect not the young.
Arginine enhances the growth hormone-releasing activity of a synthetic hexapeptide (GHRP-6) in elderly but not in young subjects after oral administration, Ghigo E, Arvat E, Rizzi G, Bellone J, Nicolosi M, Boffano GM, Mucci M, Boghen MF, Camanni F., J Endocrinol Invest. 1994 Mar;17(3):157-62.
So in conclusion if you are over 60 years of age and you want a GH release equal to what can be achieved by the youth add Arginine.
Perhaps we can extend this to other somatostatic inhibitors as well such as L-Dopa.
If you are a youth you will not benefit by adding Arginine & probably other somatostatin inhibitors such as Huperzine-A to a protocol involving GHRH+GHRPs.
Thanks DAT.....very useful. I'm thinking PEG-MGF 2 x 500mg per week and 100mg GHRP-6 at night. When you say "interfere with the GH release", since the PEG-MGF has a fairly long half-life due to the PEGylation, will it interfere with the nightly GH release which GHRP-6 promotes?
I apologize for not knowing the exact half-life of peg-MGF. To my knowledge no study has ever examined it. I read a lot from people on various forums who want to make the half-life of peg = peg-MGF.
This is not an accurate way to do it. Pegylation shelters some of the most susceptible amino acid bonds to quick enzymatic cleavage. But thats it. Breakdown will occur regardless of pegylation and the breakdown will occur on the MGF molecule itself.
Anyway I conjecture that the half-life of peg-MGF is no more than several hours...perhaps 4 hours...
So based on my conjecture you would want to keep administration of peg-MGF to at least 4 hours before bed.
Great posting DAT. This is of very much interest to us older folks. I have noticed that quite a few anti-aging clinics are using peptides and charging people out the butt for doing it.
Do you think that it is possible that older people see quicker and more dramatic results since GH, IGF-1 etc levels have declined?
Sleep, particularly the type of sleep that is restorative declines as we age. This is theorized to increase the body's susceptibility to stress and inflamation....the "repair & restoration" time period is decreased...
If you notice from my post Post #578 - How much GH do we secrete in IUs? that normal young males (age 16 - 25) secrete about 2iu of growth hormone a day with the majority of it occurring at night & that elderly people secrete as little as .25iu AND most of it occurs during the day NOT the night...
...well you'll start to understand that getting the pituitary to secrete just 1 extra iu can be a big deal AND oh how wonderful it is if we can get a lot of that to occur at night. That will bring deeper Slow Wave Sleep, more GH which will increase IGF-1 and just more restoration and better health.
You might think that is great for someone over 60 BUT if you look at those charts you'll see that GH drop off occurs earlier then most think and by the time you are in the 36 to 50 year old age bracket your nightime GH release has declined to less then your daytime GH release.
Its very empowering to know & understand these things. A man in his 30's doesn't think of himself as very old but changes are occurring in his body that could impact his health.
But really the stuff that excites me is that important immune related organs such as the Thymus which shrinks as we age regains size and vitality due to growth hormone, IGF-1 and possibly the GHRPs (Ghrelin-mimetics). The Thymus has receptors for Ghrelin-mimetics (GHS-receptor). GHRPs have healthy actions themselves.
Dr. Crisler who posts here as Swale has moved from using just Sermorelin (GHRH) to using Sermorelin + GHRP-6 in his practice following the protocol discussed in this thread. He is gathering clinical data...
So far the positive is that IGF-1 levels increased by a third over just Sermorelin.
Now Sermorelin is too short-lived in my opinion. Most of us are using a modified version which I call modified GRF(1-29) and this is probably superior to Sermorelin because it survives the initial degradation via enzymatic cleavage and thus has a longer half-life.
So to answer your question older people have bodies that miss what GH & IGF-1 did for their health. So for them a little goes an awfully long way...and as you can see it doesn't take a whole lot of aging to be considered endocrinologically old.
My absolute favorite post on anti-aging was made by a poster named DatBtrue... if he's reading this thread here's a shout out to you broheim. Anyway there is so much meat in posts #486-490 on Page 25 that it puts this little post to shame.
For instance an argument against restoring GH levels in humans as they age are the mice studies which show longer life-spans if their levels of GH & IGF-1 are low to nothing. But the flaw in the study is that those mice were kept in stress free environments. Those mice die quickly in stressed environments.
The point is that GH & IGF-1 plays a part in allowing our body's to deal positively with stress in our systems. As a consequence those studies have little practical value to understanding what is healthy for the aging human.
I recently looked at a study of centurions in a closed population (Iceland) which discovered among a great many things that these 100+ year old women (but not the 100+ year old men) had higher then expected IGF-1 levels. They had IGF-1 levels that were equal to women 30 years younger then them.
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