Dat's - CJC-1295 & GHRP-6 (Basic Guides)

EDED · Feb 12, 2009

DBT,

if someone (young or old) is taking HCG, he wouldnt have to think about taking extra DHEA right? since HCG will cause steroidogenesis and im sure it will follow all the process starting from cholesterol, at one point it will make DHEA too...

i guess DHEA supplementation with GHRH will be more beneficial for older folks

EDED · Feb 12, 2009

JohnnieFreeze said:
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

dopamine like arginine will lower somatostatins

also it will lower prolactin too but i hear chornic use of dopamine can be bad, i wouldnt use it all the time.

2bvajra · Feb 13, 2009

The present data demonstrate that the amount of REM sleep is reduced by approximately 50% in late life vs young adulthood. However, reduced amounts of REM sleep and significant sleep fragmentation do not occur until after age 50 years. The impact of aging on cortisol levels followed the same chronology. Aging was associated with an elevation of evening cortisol levels, reflecting an impaired ability to achieve evening quiescence following morning stimulation. Studies in both animals and humans have indicated that deleterious effects of HPA hyperactivity are more pronounced at the time of the trough of the rhythm than at the time of the peak.25, 54 Thus, modest elevations in evening cortisol levels could facilitate the development of central and peripheral disturbances associated with glucocorticoid excess, such as memory deficits and insulin resistance,24-25 and further promote sleep fragmentation. Indeed, elevated cortisol levels may promote awakenings.

I'm curious as to whether GH/GP has any inhibitory effect on cortisol production.

2bvajra · Feb 13, 2009

Opps. Missed the IMG code on that one.

EDED · Feb 13, 2009

i've read that GH inhibits 11bHSD (i forget if it was 11bHSD1 or 2) anyways, much like how 7-oxo-DHEA or glycyrrhetinic acid (licorice) affects cortisol methabolism through inhibition of 11bHSD enzyme,,,,which can cause lower Test and/or edema from increased aldosterone (GH gives you edema, probably tahts whyk, ibuprofen will help with taht though) and fat loss in adipose tissue is one benefit out of all those.

BUT, i know GH increases cortisol as well as prolactin too, so i dont get taht, its like stepping on gas and brake pads at the same time.

DatBtrue · Feb 13, 2009

MaTrlx said:
Whats your opinion of a young male running GHRP-6 on a long term basis, say 6 to 12 mths?

It can be run forever. I have been using it nonstop for the last 9 months. I'll use it everyday (or some form of a GHRP) for the rest of my life. Especially when I get my peptide synthesizer running and HPLC in place.

MaTrlx said:
Will it cause suppression of natural GH production once we come off after this long period?

It instigates natural secretion of GH. When you stop using GHRP-6 you will continue to experience a declining portion of the benefit for at least the next few weeks (study subjects: older adults). Eventually you will resume your age-appropriate "natural" GH release pattern.

There will be no suppression induced by GHRP-6.

MaTrlx said:
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.

The only time I would consider cycling would be if I were using high doses of CJC-1295. So 4mgs to 6mgs of CJC-1295 would be a level where my previous concerns for harm to the pituitary would come into play.

The parameters I would look for that could indicate danger would be the amount of systemic IGF-1 in plasma. With CJC-1295 I have a genuine concern of it raising base levels of GH chronically. What would happen if we elevated GH bases levels (irrespective of troughs) in someone for three straight years?

I don't really have these concerns with modified GRF(1-29) and GHRP-6 at saturation doses up to 3 times a day.

With GHRPs such as GHRP-6 the body has its own way of regulating things. If you use high doses of GHRP-6 the somatotropes will just desensitize to further GHRP-6 administrations. This is remedied by taking a break.

Desensitization won't occur at 100mcg per administration for GHRP-6. It may occur at 250+ mcg per administration.

MaTrlx said:
It would be great if there are studies showing this with regards to young males(21years above).

Studies in young men demonstrate that they respond very well to GHRP-6 (or any of the GHRPs)...in terms of creating a GH pulse of high amplitude.

Now at such a young age do their bodies really miss GH? No. So prolonged use will just serve as a base upon which they can do other things such as diet or attempt to grow muscle with anabolics, insulin or just doing things naturally.

GH as a base is anti-catabolic ...so even without adding compounds to make it anabolic it can provide benefits because if you reduce the break down and loss of muscle between bouts of growth you will slowly accrete more growth.

But for a young person to expect GH or peptides that release it to do all of the body-reconfiguring work is expecting the impossible.

MaTrlx · Feb 13, 2009

Thank you very much Dat for the detailed reply as usual. Cleared most of my doubts.

However, would i be losing out in terms of fully maximizing gh pulses and muscle growth by just running ghrp-6 at 200mcg split into 2 times a day with AAS cycles?

Been doing calculations and it is kinda costly to use both ghrp-6 and a modified GRF with AAS cycles throughout the offseason and come contest time.

I only intend to use both ghrp and a modified grf using your protocol closer to the contest date later in the year, say maybe 12 weeks out to maximise growth and conditioning as costs are high these days, while running just ghrp-6 @ 200mcg for now.

Would running just ghrp-6 with AAS at my current dose be a waste of time?

DatBtrue said:
It can be run forever. I have been using it nonstop for the last 9 months. I'll use it everyday (or some form of a GHRP) for the rest of my life. Especially when I get my peptide synthesizer running and HPLC in place.

It instigates natural secretion of GH. When you stop using GHRP-6 you will continue to experience a declining portion of the benefit for at least the next few weeks (study subjects: older adults). Eventually you will resume your age-appropriate "natural" GH release pattern.

There will be no suppression induced by GHRP-6.

The only time I would consider cycling would be if I were using high doses of CJC-1295. So 4mgs to 6mgs of CJC-1295 would be a level where my previous concerns for harm to the pituitary would come into play.

The parameters I would look for that could indicate danger would be the amount of systemic IGF-1 in plasma. With CJC-1295 I have a genuine concern of it raising base levels of GH chronically. What would happen if we elevated GH bases levels (irrespective of troughs) in someone for three straight years?

I don't really have these concerns with modified GRF(1-29) and GHRP-6 at saturation doses up to 3 times a day.

With GHRPs such as GHRP-6 the body has its own way of regulating things. If you use high doses of GHRP-6 the somatotropes will just desensitize to further GHRP-6 administrations. This is remedied by taking a break.

Desensitization won't occur at 100mcg per administration for GHRP-6. It may occur at 250+ mcg per administration.

Studies in young men demonstrate that they respond very well to GHRP-6 (or any of the GHRPs)...in terms of creating a GH pulse of high amplitude.

Now at such a young age do their bodies really miss GH? No. So prolonged use will just serve as a base upon which they can do other things such as diet or attempt to grow muscle with anabolics, insulin or just doing things naturally.

GH as a base is anti-catabolic ...so even without adding compounds to make it anabolic it can provide benefits because if you reduce the break down and loss of muscle between bouts of growth you will slowly accrete more growth.

But for a young person to expect GH or peptides that release it to do all of the body-reconfiguring work is expecting the impossible.

JohnnieFreeze · Feb 14, 2009

EDED said:
dopamine like arginine will lower somatostatins

also it will lower prolactin too but i hear chornic use of dopamine can be bad, i wouldnt use it all the time.

Thx for your input.

DatBtrue · Feb 15, 2009

JohnnieFreeze said:
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

Probably.

I took 250mgs of 40% L-Dopa last night in addition to my usual 100mcg of GHRP-6/mod GRF(1-29) and have some deeply crazy dreams.

DatBtrue · Feb 15, 2009

Here is another way to compare GHRPs & GH dosing vs effect

This study * caught my attention because it examined the pharmacokinetics of GHRP-2 and in so doing compared it to synthetic GH administration.

Basically they found 1mcg/kg of GHRP-2 half as effective as 43mcg/kg of synthetic GH...they found a linear relationship and therefore they conjectured that 2mcg/kg of GHRP-2 would be as effective as 43mcg/kg of synthetic GH.

However the studies participants were prepubescent children of short stature so we should use their weights. Googling revealed that 40lbs would be a decent approximation of such a young undersized male child. That converts to about 18 kilograms.

For synthetic GH that would mean the children received 43mcg * 18kg = 774mcg of GH.

Nutropin reveals that 1 iu of their GH is equal to 333 mcg so that equates to aproximately 2.3iu of GH.

For GHRP-2 that would mean the children received 1mcg * 18kg = 18mcg of GHRP-2.

Using the studies statement that 2mcg/kg of GHRP-2 equalled the synthetic GH dose we arrive at 2mcg * 18kg = 36mcg of GHRP-2 equally 2.3iu of synthetic GH...or further extrapolation 100mcg of GHRP-2 approximately = 6iu of synthetic GH.

I think the above extrapolation is too liberal for adults & thus flawed. So lets be real conservative in our approach and recognize that the studies used saturation doses (1mcg/kg). For adults I would like to stick with the definition of saturation dose of 1mcg/kg... and use that for adults so for a 100kg man that equals 100mcg of GHRP-2. That would mean a single 100mcg dose of GHRP-2 would equal 1.15iu of synthtic GH.

All this approach assumes is that the saturation dose for children produced the equivalent of 1.15iu of synthetic GH therefore the saturation dose for adults will do the same.

So 3 100mcg doses of GHRP-2 per day will conservatively equate to (1.15 x 3) about 3.5iu of synthetic GH. Note that if the average weight of the study children were really 50 pounds then this 3.5iu estimate becomes 4.2ius of synthetic GH.

So it is probably not unrealistic to figure that 100mcg of GHRP-6 dosed three times a day will yield the approximate equivalent of 3.5 to 4 ius of synthetic GH per day in a young adult male.

* Pharmacokinetics and Pharmacodynamics of Growth Hormone-Releasing Peptide-2: A Phase I Study in Children Catherine Pihoker, Gregory L. Kearns, Daniel French and Cyril Y. Bowers, The Journal of Clinical Endocrinology & Metabolism 1998 Vol. 83, No. 4 1168-1172

Abstract

Administration of GH-releasing peptide-2 (GHRP-2) represents a potential mode of therapy for children of short stature with inadequate secretion of GH. Requisite information to determine the dosing route and frequency for GHRP-2 consists of the pharmacokinetics (PK) and pharmacodynamics (PD) for this compound, neither of which have been previously evaluated in children. The purpose of this study was to characterize the PK and PD of GHRP-2 in children with short stature. Ten prepubertal children (nine boys and one girl; 7.7 ± 2.4 yr old) received a single 1 µg/kg iv dose of GHRP-2 over 1 min, followed by repeated (n = 9) blood sampling over 2 h. GHRP-2 and GH were quantitated by specific RIA methods. PK parameters were calculated from curve fitting of GHRP-2 and GH vs. time data. Posttreatment plasma GH concentrations (normalized for pretreatment values) were used as the effect measurement....

Discussion

The pharmacokinetics of GHRP-2 found in our cohort of pediatric patients are similar to those previously reported in healthy adult volunteers after iv administration of the peptide (3). A comparison of the maximum GH response observed after GHRP-2 administration between these two studies revealed similarities in both the magnitude (i.e. mean values = 44 µg/L in children vs. 55 µg/L in adults) and time of maximal response (i.e. average values = 45–60 min for both). The GH responses observed after iv or sc GHRP-2 are also similar to those previously reported after the parenteral administration of GHRP-6, GHRP-1, or GHRH (3, 4, 23, 24).

To our knowledge, our data represent not only the first report of GHRP-2 pharmacokinetics in pediatric patients, but also the first pharmacodynamic assessment of this peptide. Comparison of the serum concentration vs. time profiles for both GHRP-2 and GH in our subjects reveals an equilibration delay in the attainment of peak GH response, a period that we believe corresponds to the time course of GHRP-2 action. This assertion is supported in part by the consistent observation of an equilibration delay between the serum concentrations of GHRP-2 vs. effect (i.e. change GHt) curves, reflected by the production of a counterclockwise hysteresis and our success in using the sigmoid Emax model to effectively determine the pharmacodynamic parameters for GHRP-2. As previously reported by Holdford and Sheiner (22), the successful application of this pharmacodynamic model suggests both linearity and predictability in the drug concentration vs. effect relationship. Given the fact that GH is a proximate biological marker of GHRP (and presumably, GHRP-2) activity (23, 24), our assumptions entailed in the pharmacodynamic analysis of our data appear valid and reflective of the expected pharmacological response of GHRP-2.

Despite the apparent differences in serum GH pharmacokinetics reported after exogenous administration of the hormone (25) as opposed to the administration of GH secretagogues (26, 27, 28, 29, 30), both the pharmacokinetic and pharmacodynamic data from our study can be used to address the potential therapeutic efficacy of GHRP-2 in pediatric patients with GH insufficiency. First, the mean AUC for GH after the iv administration of a single 1 µg/kg dose of GHRP-2 (i.e. 50.7 ng/mL·h) was approximately 50% of the AUC at steady state (i.e. 114.2 ± 32.7 ng/mL·h) previously reported in a study of pediatric patients who received daily sc doses of 43 µg/kg methionyl GH (25). If one assumes linearity in the dose-response relationship for iv GHRP-2, administration of a single 2 µg/kg iv dose would be expected to produce an AUC for GH that would be virtually identical to that observed under steady state conditions after sc administration of the currently recommended daily doses of recombinant human GH (25), doses that have been shown to produce acceptable rates of linear growth in children who are GH deficient (30). Second, both the Cmax (mean, 50.7 ng/mL) and Emax values for GHRP-2 in our patient cohort (mean GH, 67.5 ng/mL) actually exceeded the average Cmax values for GH (37.6 ± 11.6 ng/mL; range, 17.6–49.5 ng/mL) after a single sc dose of 0.1 mg/kg methionyl GH to GH-deficient children (25). Finally, the EC50 for GHRP-2 in our study cohort (1.1 ± 0.6 ng/mL) was substantially less than the Cmax value (7.4 ± 3.8 ng/mL). This particular finding not only supports the adequacy of the 1 µg/kg iv dose of GHRP-2 in producing a desirable biological effect, but also suggests that extravascular administration of this peptide by a route that could be associated with up to a 50% reduction in bioavailability may still produce an acceptable increase in the serum GH concentration sufficient to initiate and sustain a desired growth response. This hypothesis is being tested by our group in dose-ranging studies of oral and intranasal GHRP-2 that are currently underway.

In conclusion, both the pharmacokinetics and pharmacodynamics of iv administered GHRP-2 in short children are predictable and reflective of the potential for therapeutic application of this peptide. The data produced in this investigation will enable the selection of GHRP-2 doses for future evaluation of their bioavailability, safety, tolerance, and efficacy in children.

Wise Guy · Feb 15, 2009

EDED said:
DBT,

if someone (young or old) is taking HCG, he wouldnt have to think about taking extra DHEA right? since HCG will cause steroidogenesis and im sure it will follow all the process starting from cholesterol, at one point it will make DHEA too...

i guess DHEA supplementation with GHRH will be more beneficial for older folks

Thatis just simply not true. Taking hcG will prevent testicular atrophy, and atrophy of the Leydig cells. This will help keep pregnenolone levels up, and natural production of many androgenic hormones, such as T and many of the andro steroids too.

However, most of the DHEA in the body is actually made in the adrenal glands, around 90%.

So hcG has little to do with DHEA levels.

It is a good rule of thumb that if someone has experienced enough of a decline in testosterone levels that it illicits some form of HRT, such as hcG or T supplementation, that their respective DHEA levels are also compromised.

A DHEA test, preferably by urinary analysis, would clear up any speculations.

DatBtrue · Feb 15, 2009

Wise Guy said:
Thatis just simply not true. Taking hcG will prevent testicular atrophy, and atrophy of the Leydig cells. This will help keep pregnenolone levels up, and natural production of many androgenic hormones, such as T and many of the andro steroids too.

However, most of the DHEA in the body is actually made in the adrenal glands, around 90%.

So hcG has little to do with DHEA levels.

It is a good rule of thumb that if someone has experienced enough of a decline in testosterone levels that it illicits some form of HRT, such as hcG or T supplementation, that their respective DHEA levels are also compromised.

A DHEA test, preferably by urinary analysis, would clear up any speculations.

That is a much more learned response then I was capable of giving. WG knows better then most in this area... so pay attention.

DatBtrue · Feb 15, 2009

BigTex said:
...So saying I trust him and he knows his business when buying this product and I have CJC 1295, is it better to stick with small doses (50-100mcg) of CJC 1295 2-3 x day or it is better to do with larger doses (250mcg) and go twice a week?

Why dose CJC-1295 3x a day?

Pulsation is paramount for growth because it is the pulses that act as communication signals to the Growth Hormone receptors in tissue. Naturally our hypothalamus releases a concentrated amount of GHRH during a period when somatostatin is not very active. This concentration of GHRH acts to communicate to somatotroph cells in the anterior pituitary to coordinate amongst themselves a network (see post #487) which will act together in concert to "squirt" out GH in the blood stream.

This concentrated GH makes its way to receptors in tissue and they (many many GH ligands) bind in mass to growth hormone receptors. An analogy would be if one Alien landed on Earth a few people would notice and run away screaming. BUT if a whole bunch of aliens landed in mass on the Earth the entire population would hear about, panic, run and scream.

What happens if Aliens dribble in from the sky here and there over time in an unconcentrated & uncoordinated fashion?

Some towns might be in an uproar but by and large the invasion effect would be diluted and although many would hear rumors about these things it probably wouldn't motivate them to action.

CJC-1295 enters the bloodstream and binds to albumin in plasma. When you inject it, it is concentrated and acts on the somatotrophs similar to natural GHRH release. BUT that is the ONLY time CJC-1295 amplifies a pulse. If you take it twice a week only because the half-life is long you rarely will amplify a pulse.

Instead CJC-1295 circulates and when the somatrophs are ready to act again some of the CJC-1295 binds to the somatrophs and they secrete growth hormone. However the measured result of CJC-1295 is that although it increases the total amount of GH, it does so only by raising base levels. It doesn't amplify a pulse.

However it doesn't interfere with pulsation. This means that the hypothalamus continues to release GHRH in response to neurological events that communicate concentrated release in a coordinated fashion with somatostatin withdrawal. It is the body's natural biorhythm that maintains natural pulsation.

CJC-1295 just makes the somatotrophs "leak" GH between the natural "squirts" therefore causing a rise in base levels (or troughs (i.e. between the waves/pulses)) ONLY.

Now GHRP-6 (or GHRP-2 or Hexarelin or Ipamorelin or the oral GHS such as MK-0677 & Ipamrelin derivatives) ALWAYS (almost without fail) initiates an amplified GH pulse. These GHRPs cause those natural events that inhibit somatostatin, that promote GHRH release and initiate their own amplifying effects directly on the somatrophs (probably even increasing coordination among somatroph populations) to occur within 5 minutes of injection.

The result of a GHRP-6 (i.e. all the GHS) injection is an amplified GH pulse.

So if there is added GHRH around GHRP-6 (all GHS) will synergistically create a much greater wave of GH release. It doesn't matter whether GHRH is in the form of Sermorelin (unmodified GRF(1-29) or modified GRF(1-29) or CJC-1295 (modified GRF(1-29) + the complex that permits binding to albumin))... GHRP-6 (all GHS) will synergize with it.

So IF you have CJC-1295 and you will use it with GHRP-6 (or any GHS) you don't need to coordinate CJC-1295 injections with GHRP-6 (GHS) because some GHRH will be floating around.

However if you use the shorter acting versions of GHRH then you do need to coordinate injection with GHRP-6 (GHS).

Although we don't need to, is there any benefit to coordinating an injection of CJC-1295 w/ GHRP-6?

Yes.

For the simple reason that injecting CJC-1295 creates a concentrated amount of GHRH that is available at the somatroph network in the pituitary AT THE SAME TIME as GHRP-6 (GHS) and in SUFFICIENT AMOUNT/CONCENTRATED FORM such that there is a greater contribution to that single GHRP-6 initiated pulse.

How much of an extra contribution?

I don't know. I do know that there is a likely contribution simply from the GH release profile of CJC-1295 as exhibited in the studies. A guesstimate without any real data would be 10% contribution...

WC114 · Feb 16, 2009

I was wondering if you could use syntherol to stretch the cells further to make it easier for MGF to get inside the cells since there may be a possibility for MGF to get inside the cell due to cell leakage after workout? I"m probably missing the concept here or somebody would have already done it, anyway just a thought.

BigTex · Feb 16, 2009

DatBtrue said:
Although we don't need to, is there any benefit to coordinating an injection of CJC-1295 w/ GHRP-6?

Yes.

For the simple reason that injecting CJC-1295 creates a concentrated amount of GHRH that is available at the somatroph network in the pituitary AT THE SAME TIME as GHRP-6 (GHS) and in SUFFICIENT AMOUNT/CONCENTRATED FORM such that there is a greater contribution to that single GHRP-6 initiated pulse.

Thanks DAT! This makes too much sense.

DatBtrue · Feb 16, 2009

Boosting Insulin Naturally

xxxx said:
...Would I benefit more from 3 iu Humulin-R mixed in with the GHRP-6 (with appropriate nutrient intake, of course) or just a mix of 25g hydrolyzed whey isolate + 5g BCAA's + 30g Dextrose about 15-20 min. post administration? Test & T3 available for optimizing outcome.

I understand not wanting to use exogenously administered insulin. Does this mean you would lose out on insulin's contribution to GH induced anabolism?

No...you can achieve what would amount to a couple iu of Hum-R by using glucose & leucine. The two work synergistically to spike insulin.

About 3.5 grams of Leucine was sufficient to double the insulin response to 25grams of glucose. See below:

Leucine, when ingested with glucose, synergistically stimulates insulin secretion and lowers blood glucose, Dionysia Kalogeropoulou, Metabolism Clinical and Experimental 57 (2008) 1747–1752

Thereafter, they received 25 g glucose or 1 mmol/kg lean body mass leucine or 1 mmol/kg lean body mass leucine plus 25 g glucose in random order. Serum leucine, glucose, insulin, glucagon, and alpha-amino nitrogen concentrations were measured at various times during a 2.5-hour period after ingestion of the test meal. The amount of leucine provided was equivalent to that present in a high-protein meal, that is, that approximately present in a 350-g steak. After leucine ingestion, the leucine concentration increased 7-fold; and the alpha-amino nitrogen concentration increased by 16%. Ingested leucine did not affect the serum glucose concentration. When leucine was ingested with glucose, it reduced the 2.5-hour glucose area response by 50%. Leucine, when ingested alone, increased the serum insulin area response modestly. However, it increased the insulin area response to glucose by an additional 66%; that is, it almost doubled the response. Ingested leucine stimulated an increase in glucagon. Ingested glucose decreased it. When ingested together, the net effect was essentially no change in glucagon area. In summary, leucine at a dose equivalent to that present in a high protein meal, had little effect on serum glucose or insulin concentrations but did increase the glucagon concentration. When leucine was ingested with glucose, it attenuated the serum glucose response and strongly stimulated additional insulin secretion. Leucine also attenuated the decrease in glucagon expected when glucose alone is ingested. The data suggest that a rise in glucose concentration is necessary for leucine to stimulate significant insulin secretion. This in turn reduces the glucose response to ingested glucose.

DatBtrue · Feb 16, 2009

Hey I like this board because a lot of guys are always thinking.

Injected MCT oil will disperse 25% along fascia lining and the remainder mostly will stretch fiber bundles. There are really two types of fascia and then penetrating offshoots called septa. The most pliable is generally the outer sheath which is kinda like a wrap that covers the area of several muscle groups. For instance the chest has this fascia covering it and then extending down to cover the abdominal area. The deep usually tougher fascia actually penetrates muscle. It is thought that fascia & penetrating septa help coordinate muscle movement by transmitting tension signals from one area to another.

Thickness of fascia varies greatly among individuals & within muscular areas in a single individual. In general the fascia covering the lower pectoral area is thicker then the upper pectoral area. This type of information is important to surgeons who do breast augmentation, particularly those that do so beneath the muscle... so autopsies & cadaver examinations are written up in certain specialty journals.

Take a look at how variable pec fascia thickness is between people (women). There is a whopping 400% variability between thinnest & thickest fascia in the lower pec region. It is not difficult to understand why there is such variability between guys when it comes to visual chest pop/appearance.

From: Anatomy and Clinical Significance of Pectoral Fascia, Lin Jinde, M.D., American Society of Plastic Surgeons Volume 118, Number 7 Pectoral Fascia

Back to your specific question. It is not likely that MCT oil will rupture individual cellular membranes. The MCT is a lipid & so is the make-up of cellular membranes so there should be no irritation/damage.

WC114 said:
I was wondering if you could use syntherol to stretch the cells further to make it easier for MGF to get inside the cells since there may be a possibility for MGF to get inside the cell due to cell leakage after workout? I"m probably missing the concept here or somebody would have already done it, anyway just a thought.

kutch · Feb 16, 2009

DatBtrue said:
No...you can achieve what would amount to a couple iu of Hum-R by using glucose & leucine. The two work synergistically to spike insulin.

About 3.5 grams of Leucine was sufficient to double the insulin response to 25grams of glucose. See below:

I was under the impression, from previous posts, that consuming carbs(and fats) within 30 minutes after injecting cjc/ghrp6 would diminish the returns.

Would the insulin spike from consuming some waxy maize and some BCAAs be beneficial to do within 15 minutes from administering cjc/ghrp6 knowing that carbs have been shown to reduce the effect?

DatBtrue · Feb 17, 2009

kutch said:
I was under the impression, from previous posts, that consuming carbs(and fats) within 30 minutes after injecting cjc/ghrp6 would diminish the returns.

Would the insulin spike from consuming some waxy maize and some BCAAs be beneficial to do within 15 minutes from administering cjc/ghrp6 knowing that carbs have been shown to reduce the effect?

I myself wait 30 minutes. The peak is around 25 - 30 minutes but w/ GHRP-6 which very readily crosses the blood brain barrier the GH release begins w/in 5 minutes.

EDED · Feb 17, 2009

Dat,

do you see any ingredients listed here that may affect GH pulse negatively from secretagogues?

Phosphocreatine, Creatine Monohydrate
Banaba Extract (Lagerstroemia Speciosa 1% Corosolic Acid)*, Gymnema Sylvestra (75% Extract), D-Pinitol*, Bioperine (95%-98% Piperine)* Registered Trademark of Sabinsa Corp. and holds patent #5, 536, 506).

and

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?