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

laskerja · Jan 31, 2009

Dat whats up bro? its laskerja from RR.

Thanks for all your help thus far. Just want you to check out this plan for me if you could.

So heres what I'm thinking

5AM: 3 IU of thanktropin
8:30:100mcg GHRP-6
9AM:meal 1
1pm:meal 2
6PM:meal 3
9pm:just finished working out, 500mg metaformin
930PM:meal 4
11:30pm:200mcg GHRP-6
12am:meal 5

a few questions about this protocol if you dont mind.
1) would 100mcg GHRP-6 be beneficial in the morning like I have it lied out, or should I just take more once daily (pre-bed)?
2) should I take more pre-bed anyways?
3)I am taking HGH 6 days a week, should I take GHRP every day?
4)will the metaformin interfere with where I am taking the GHRP?
5) should I cycle GHRP?
6) how many additional IU of GH will my body see with the amount of GHRP I am taking?

Thanks for the Help !!!!

DatBtrue · Feb 1, 2009

Well i don't know what jurisdiction you reside in, so in conformance with Big A's new policy I can talk about the science and in general terms but I can not give you advise.

So:

3iu of GH will be active for 3.5-4 hours after which you need another 3 or so hours of off time before a GH pulse will be effective (no matter whether it is natural or from synthetic GH). So GHRP-6 can be used effectively aprox. 7 hours after 3iu of GH has been administered. So if GH is administered at 5AM then GHRP-6 can be used at noon.

A 100mcg dose of GHRP-6 is the saturation dose. 200mcg could be used as well with diminished benefit.

GHRP-6 can be taken everyday (even 3 times a day) at saturation dose w/o worrying about desensitization. There does not need to be a break. Higher doses of GHRP-6 and moderate dosed Hexarelin will probably require a break.

Metaformin...I don't know how long it is active in the body. But I would be surprised if it interfered w/ IGF-1's intracellular pathways 3.5 hours post use.

Three spots of GHRP-6 at saturation dose per day probably gives the equivalent of 2 to 2.5iu of GH per day (guesstimation).

laskerja said:
Dat whats up bro? its laskerja from RR.

Thanks for all your help thus far. Just want you to check out this plan for me if you could.

So heres what I'm thinking

5AM: 3 IU of thanktropin
8:30:100mcg GHRP-6
9AM:meal 1
1pm:meal 2
6PM:meal 3
9pm:just finished working out, 500mg metaformin
930PM:meal 4
11:30pm:200mcg GHRP-6
12am:meal 5

a few questions about this protocol if you dont mind.
1) would 100mcg GHRP-6 be beneficial in the morning like I have it lied out, or should I just take more once daily (pre-bed)?
2) should I take more pre-bed anyways?
3)I am taking HGH 6 days a week, should I take GHRP every day?
4)will the metaformin interfere with where I am taking the GHRP?
5) should I cycle GHRP?
6) how many additional IU of GH will my body see with the amount of GHRP I am taking?

Thanks for the Help !!!!

hemipower · Feb 1, 2009

Joint health

Edit

laskerja · Feb 1, 2009

DatBtrue said:
3iu of GH will be active for 3.5-4 hours after which you need another 3 or so hours of off time before a GH pulse will be effective (no matter whether it is natural or from synthetic GH). So GHRP-6 can be used effectively aprox. 7 hours after 3iu of GH has been administered.

Thanks so much. just one more question about the above statement. So how long would a test subject need to wait between GHRP-6 shots for them to be effective? 7 hours? so if GH is givin at 5am, then 100mcg of GHRP-6 at noon, then the next dose of GHRP-6 would not be effective until 7pm? is this correct of am i missing something? sorry if this question seems ignorant, but thanks for all of your help.

DatBtrue · Feb 1, 2009

hemipower said:
Would 100mcg GHRP-6 in the AM and 100mcg CJC-1295 plus 100mcg GHRP-6 before bed be enough to see better sleep, better recovery, leaner, but MOST importantly - joint healing?

A test animal weighing about 100kgs is currently using IGF-1 at 50mcg/day as PCT and it may be helping to hold onto some muscle BUT joints are in excessive pain and getting worse by the day.

Would GHRP-6 and CJC taken at the dosage indicated be superior to IGF-1 admin for this experiment and the indicated needs??

Thanks!

Joint healing?

Most people report quicker connective tissue healing from direct IGF-1 injection into the ailing connective tissue. Getting your GH levels up should help but it takes time. Maybe three months down the line you will realize you feel better...but it isn't a matter of heal up in just a couple of weaks.

DatBtrue · Feb 1, 2009

You've mixed two concepts.

Synthetic GH or GH is different then Growth Hormone Releasing Peptide 6.

The former is the end product hormone, while the latter is a precursor hormone which induces natural pulsatile GH release.

GHRP-6 initiates a pulse of GH from the somatotroph stores in the pituitary. It takes time between pulses for these stores to be refilled BUT most importantly it takes time for these release mechanisms to be ready to act again. Almost everyone is capable of taking GHRP-6 every 3 hours post-pulse and generating a pulse of GH and some even sooner (within 1 hour of initial dosing even).

None of that has ANYTHING to do with the end product hormone GH binding to a GH-receptor on a cell in tissue (usually the liver) and activating the intra-cellular machinery to synthesize proteins, etc.

That machinery needs to have a break of 3 or so hours between GH-GH-R activations.

So if you mega-dose GH and it is active for 7 straight years you need to wait to take the next dose of GH. That wait is the 7 years that the first dose was active + 3 hours.

Thats all. In your case 3iu will probably keep GH in plasma elevated for 4 hours. It does no good to take another dose of GH or use GHRP-6 to induce GH release at hour 5, at hour six, etc. because the intracellular machinery won't be able to make effective use of it.

BUT if you wait for the initial GH dose to clear AND wait till the intracellular machinery is ready to act again, you can dose again to good effect.

laskerja said:
Thanks so much. just one more question about the above statement. So how long would a test subject need to wait between GHRP-6 shots for them to be effective? 7 hours? so if GH is givin at 5am, then 100mcg of GHRP-6 at noon, then the next dose of GHRP-6 would not be effective until 7pm? is this correct of am i missing something? sorry if this question seems ignorant, but thanks for all of your help.

hemipower · Feb 1, 2009

DatBtrue said:
Joint healing?

Most people report quicker connective tissue healing from direct IGF-1 injection into the ailing connective tissue. Getting your GH levels up should help but it takes time. Maybe three months down the line you will realize you feel better...but it isn't a matter of heal up in just a couple of weaks.

OK thanks Dat!

longrob · Feb 2, 2009

I Have Joined PM

Dat,
Nice to see you again. Am looking forward to following this thread, and I appreciate all the sponsors here at PM. Thanks!
Rob

EDED · Feb 2, 2009

I have joined here as well, coming from AM, OLM, IMA and anabolex....

thanks for the invite papapumpsd

question;

does anybody shoot GRF/GHRP6 in the same pin?

for awhile ive been separating them from fear of unknown unseen reaction that could take place due to their conformation or whatever..but its a pain in the ass and im eating up the syringes.

they shouldnt really affect each other when mixed right?

papapumpsd · Feb 2, 2009

Def. administer using the same pin.

If you think about it, having those two peps in the same pin is nothing compared to the environment they're in when injected into the human body. THAT is a complicated matrix.

EDED said:
I have joined here as well, coming from AM, OLM, IMA and anabolex....

thanks for the invite papapumpsd

question;

does anybody shoot GRF/GHRP6 in the same pin?

for awhile ive been separating them from fear of unknown unseen reaction that could take place due to their conformation or whatever..but its a pain in the ass and im eating up the syringes.

they shouldnt really affect each other when mixed right?

Wise Guy · Feb 2, 2009

This thread is so badass on so many levels. Perhaps the best thread on anti-aging being circulated throughout the net today.

Thank You.

And Swale, I'd love to see the results you have had. Post em up

Wise Guy · Feb 2, 2009

DatBtrue said:
Three spots of GHRP-6 at saturation dose per day probably gives the equivalent of 2 to 2.5iu of GH per day (guesstimation).

I take it that is irrespective of GHRH use?

DatBtrue · Feb 2, 2009

weltweite said:
Any advice would be appreciated on the downsides to doing a long acting insulin (levemir) with actual (the actual cjc-1295 peptide/ghrp-6) ?

Okay Welt... I'm sorry I haven't gotten back to you on your question on the pharmacokinetics of long-acting insulin. I don't have an answer for you.

But I do question the wisdom of having chronically elevated insulin levels.

The more I research...the more I discover rhythms and rhythms that relate to other types of rhythms. What we are talking about could simply be thought of as communication between & among cell groupings and activation, deactivation and modulation of intracellular mechanisms.

Anecdotally we can look to BigKiwi who posted that he used insulin to great effect in place of GH because he could not get GH in his part of the world. He grew...

Scientifically, we can attempt to explain BigKiwi's results by understanding that insulin as does GH, directly activates STAT5 via its own receptor in vivo. - Insulin selectively activates STAT5b, but not STAT5a, via a JAK2-independent signalling pathway in Kym-1 rhabdomyosarcoma cells, Peter Storz, FEBS Letters 464 (1999) 159-163

But that doesn't tell a bodybuilder how best to optimize insulin use.

There is a lot of evidence that periods of repression lead to periods of excess and vice versa. This is true on so many levels of human life. If you are flush with money and spend a lot if you become poor you cut spending back to the bare essentials. If you are poor and suddenly have a lot of money you buy more things and probably accumulate a lot of things you don't need. Your lifestyle grows.

This general rule seems to apply to our basic biology as well. For example, Catch-Up Growth after Glucocorticoid Excess: A Mechanism Intrinsic to the Growth Plate, Jeffrey Baron, Endocrinology 136: 1367-1371,1994

In humans and other mammals, the release from growth-inhibiting conditions, such as glucocorticoid excess, leads to supranormal linear growth....Here we show that suppression of growth within a single growth plate by locally administered glucocorticoid is followed by local catch-up growth that is restricted to the affected growth plate....To explain this finding, we propose that the normal senescent decline in growth plate function depends not on age per se, but on the cumulative number of stem cell divisions, and that glucocorticoid administration, by suppressing stem cell proliferation, delays senescence, resulting in catch-up growth after the growth-inhibiting agent is removed.

As a further but distinct example, we often find that greater amounts of potential muscle growth come from a growth factor (such as a fibroblast growth factor (FGF-2)) acting to repress skeletal muscle differentiation. It is the repression of differentiation that allows proliferation to continue unimpeded. When that repression is removed all of the proliferated myoblasts undergo differentiation.

It is the repression of differentiation by the growth factor FGF-2 that allows many more potential muscle cells to be created. When that inhibiting factor is removed and the growth factor FGF-4 is allowed to act via differentiation of those newly created cells noticeable skeletal muscle cells develop.

So repression leads to excess or substantial growth.

What happens if myoblast proliferation is drastically reduced because we are constantly allowing factors which differentiate to act? We lose potential muscle that we will never regain... and we have no or reduced growth.

Rhythms are important.

Rat studies don't correlate with humans but it is interesting to observe the interplay between GH pulses and insulin pulses in the troughs.

From, Pulsatile secretion of growth hormone and insulin in relation to feeding in rats, Patrick Even, Am J Physiol Regulatory Integrative Comp Physiol 253:772-778, 1987

The existence of 3-h pulsatile cycles of GH secretion was confirmed. In addition, short bursts of insulin secretion were observed in the middle of every second GH peak-to-peak interval.

In humans we find that, "insulin-regulated resensitization of GH signaling may be necessary to reset the complete response to GH after a normal, physiologic pulse of GH."

We further find that, "Insulin restored the ability of a second GH exposure to induce phosphorylation of MEK1/2 and ERK1/2 without altering GH receptor levels or GH-induced phosphorylation/activation of JAK2 and Raf-1. GH and insulin synergized in promoting cell proliferation." - Insulin Reverses Growth Hormone-induced Homologous Desensitization, Jie Xu, Zhongyu Liu, Thomas L. Clemens, and Joseph L. Messina, THE JOURNAL OF BIOLOGICAL CHEMISTRY VOL. 281, NO. 31, pp. 21594–21606, August 4, 2006

See also: Insulin Enhances Growth Hormone Induction of the MEK/ERK Signaling Pathway by the same authors in the same journal published earlier that year.

I don't want to ramble on...but I do want to emphasize that yes insulin (even physiological levels) are important to promote growth with growth hormone, but that chronic always on levels of insulin are not what is desirable.

pitbulladams · Feb 2, 2009

DatBtrue said:
You asked a very good question.

From: Insulin Regulation of Human Hepatic Growth Hormone Receptors: Divergent Effects on Biosynthesis and Surface Translocation, Kin-Chuen Leung, Nathan Doyle, Mercedes Ballesteros, Michael J. Waters, And Ken K. Y. Ho, The Journal of Clinical Endocrinology & Metabolism 2000 Vol. 85 No. 12 4712-4720

In the study they recognized the importance of insulin and how it interacts with growth hormone, specifically highlighting that "insulin is essential for GH stimulation of IGF-I production and growth."

They then focused on the results of their study. They found that:

- Insulin up-regulated total and intracellular GH-receptors in a concentration-dependent manner.

- The abundance of GHR messenger ribonucleic acid and protein, ... respectively, markedly increased with insulin treatment.

[So the more insulin that was used the more biosynthesis or creation of GH-receptors that occurred. Now these receptors while abundant were not necessarily moved to the surface of the cell nor where they activated. Just a pool of GHRs was created.]

CAVEAT: Parts of the GH-Receptor can move to the nucleus and mediate gene expression. See the wonderful post that follows on "Growth Hormone Receptor structure, post-biogenesis behavior and degradation"

- It increased surface GHRs in a biphasic manner, with a peak response at 10 nmol/L, and modulated GH-induced Janus kinase-2 phosphorylation in parallel with expression of surface GHRs.

[So insulin increases the number of GH-receptors that make it to the cell surface AND increase the "intensity" of activation...but up to a point. After that point is reached insulin begins to hinder both the number of GH-receptors and "intensity" of activation"]

To quote from the study on this point:

Insulin induced a concentration-dependent increase in GHR biosynthesis, but simultaneously inhibited surface translocation. However, the net effect of reducing receptor surface availability only occurred at concentrations greater than 10 nmol/L, a concentration causing 70% inhibition of surface translocation. These data suggest that up-regulation of surface GHRs can occur with as little as 30% of intracellular receptors available for translocation to the cell surface. At concentrations above 10 nmol/L, the inhibitory effect of insulin on surface translocation overrides the compensatory effect of a 4- to 5-fold increase in receptor biosynthesis.

[So this means that insulin increases GH-receptors by 400-500% but that as insulin rises it reduces the number of those GH-receptors that make it to the surface and are active. There is a point at which insulin begins to reduce the benefit of this GH-receptor creation. That point is 10 nmol/L of insulin. Just prior to that point insulin has inhibited substantially the translocation of GH-Receptors but the increased quantity made up for it and created an overall net benefit.]

So the problem becomes how to translate that pivot point (10 nmol/L) into a number we can use.

From: Correspondence Letter Regarding Article by von Lewinski et al, "Insulin Causes [Ca2+]i-Dependent and [Ca2+]i-Independent Positive Inotropic Effects in Failing Human Myocardium", Chih-Hsueng Hsu, MD; Cheng-I Lin, PhD; Jeng Wei, MD, Circulation. 2005;112:e367

...we find that "3 IU/L, equivalent to 20 nmol/L" ...so 10 nmol/L is equivalent to 1.5 IU/L

From Wiki Answers **broken link removed**

...we find that humans have 5-6 litres of blood in general.

So 5 x 1.5 = 7.5IU
So 6 x 1.5 = 9IU

Therefore the point at which the amount of insulin in plasma becomes a negative rather then a positive is approximately 7.5 to 9 IUs.

So to arrive at a net benefit an insulin amount below that threshold point such as 5-6 ius is desirable.

Dat
Ok so stay with me on this one..

I take it this info is pointing towards the use of say 5-6iu is better then the higher amounts i see guys using PWO like in the region 10-20iu's ?

What time duration is this amount of insulin over ?

As you know i have been dosing my GH first thing in the morning and was using 6iu humalog with it, then a second dose of 12iu Humalog PWO which is about 4 hours after my am GH/insulin shot.

Now based on this am i better dropping my insulin first thing and just use GH on its own followed by 6iu insulin PWO ?

Or would a smaller dosage at both AM and PWO be better ?

Cheers
PB

DatBtrue · Feb 2, 2009

Here is the Insulin Cheat Sheet I put together in September

The following was a nice little concise summation of the effect insulin has on GH, GHRs and intracellular events, put together about 6 months back. It was designed to be a pointer to the primary studies that demonstrate each point.

It might be of use to someone so I post it here today:

INSULIN CODEX - I

Many factors are known to regulate the responsiveness of the growth hormone receptor (GHR) to growth hormone (GH). The most important are insulin, thyroid [SEE: THYROID HORMONES CODEX] and sex hormones [SEE: ESTROGEN CODEX & TESTOSTEONE CODEX].

The growth-promoting action of GH is mediated by IGF-I which is produced mainly in the liver, but also in extrahepatic tissues. There is strong evidence that the anabolic action of GH requires the presence of insulin and adequate nutrition. This is exemplified in type 1 diabetes where IGF-I levels are low and longitudinal growth is impaired despite high serum levels of GH [1, 2]. These abnormalities are corrected by insulin treatment [3, 4].

Insulin's effect on GHR expression

The effects of insulin on GHR expression and function are tissue specific.

In cultures of rat hepatoma cells, insulin increases GHRs [5]. In animal studies, insulin deficiency results in a decrease of GH binding and GHR expression in liver [6, 7], which can be reversed by insulin administration [6, 8]. In extra-hepatic tissues such as bone and kidney, there is evidence that insulin down-regulates GHRs [9, 6–8].

It is well established that surface membrane receptors are dynamically regulated, with cell surface abundance representing the net balance of "recycling of internalised receptors" and translocation of newly synthesized receptors to the cell membrane.

There is recent evidence that the surface translocation of GH receptors is inhibited by insulin.

Insulin dose-dependently stimulates liver GHR synthesis and GH binding, however increasing insulin concentrations reduce GHR surface translocation, which overcomes the effect on receptor synthesis [5].

These findings show that the mechanism by which insulin regulates tissue responsiveness to GH is complex and in part mediated by effects on GHR expression and surface translocation.

Decrease in receptor surface availability with high dose insulin may represent rapid mechanism for insulin regulation of the GHR function.

In human studies, there is also evidence that insulin modulates the expression of GHRs. This is based on measurement of circulatory levels of GHBP. As GHBP is derived from proteolytic cleavage of the extracellular domain of the GH receptor, change in GHBP levels may reflect GH receptor status [10].

Thus when insulin levels are low, high levels of GH does not translate into a rise in circulating IGF-I [11-17]. In type I diabetes, GHBP levels are low and associates with low IGF-I levels [18]. These investigations have also observed a significant positive correlation between levels of GHBP and total insulin dose, suggesting that GHR status in humans is dependent on adequate insulinisation [18].

Insulin's effect on GH receptor signaling

There is strong evidence that insulin modulates GHR signaling in addition to the effects on receptor expression and surface translocation.

In rat hepatoma cells, low dose insulin administration results in GH-induced stimulation of JAK2 phosphorylation however high dose insulin treatment results in inhibitory effect [5, 19].

The effect of insulin on GHR function appears to be mediated by the PI-3 kinase and MAPK/ERK pathways [5, 20, 21]. It has been shown that insulin increases GH signaling by enhancing GH-induced activation of MAPK/ERK pathway through post signalling cross-talk [21].

In human muscle, in vivo, ERK1/2 phosphorylation was increased by insulin, but insulin per se did not induce phosphorylation of Stat5. [22]

Overall Summation

Insulin regulates GHR expression, translocation and GHR function. The regulation of GH receptor expression is complex and tissue dependent. Insulin stimulates hepatic GHR synthesis and GH binding but down-regulates GHR expression in kidney and bone tissue.

In liver, high concentrations of insulin reduce GHR surface translocation, in such a way as to regulate receptor surface availability.

The effects of insulin on GHR function are mediated by stimulation of GH-induced JAK2 phosphorylation, PI-3 kinase and MAPK/ERK pathways.

SOURCES:

1 - Horner JM, Kemp SF, Hintz RL. Growth hormone and somatomedin in insulin-dependent diabetes mellitus. J Clin Endocrinol Metab. 1981;53:1148–53.

2 - Tan K, Baxter RC. Serum insulin-like growth factor I levels in adult diabetic patients: the effect of age. J Clin Endocrinol Metab. 1986;63:651–5.

3 - Vigneri R, Squatrito S, Pezzino V, Filetti S, Branca S, Polosa P. Growth hormone levels in diabetes. Correlation with the clinical control of the disease. Diabetes. 1976;25:167–72.

4 - Amiel SA, Sherwin RS, Hintz RL, Gertner JM, Press CM, Tamborlane WV. Effect of diabetes and its control on insulin-like growth factors in the young subject with type I diabetes. Diabetes. 1984;33:1175–9.

5 - Leung KC, Doyle N, Ballesteros M, Waters MJ, Ho KK. Insulin regulation of human hepatic growth hormone receptors: divergent effects on biosynthesis and surface translocation. J Clin Endocrinol Metab. 2000;85:4712–20.

6 - Baxter RC, Bryson JM, Turtle JR. Somatogenic receptors of rat liver: regulation by insulin. Endocrinology. 1980;107:1176– 81.

7 - Menon RK, Stephan DA, Rao RH, Shen-Orr Z, Downs LS Jr, Roberts CT Jr, et al. Tissue-specific regulation of the growth hormone receptor gene in streptozocin-induced diabetes in the rat. J Endocrinol. 1994;142:453–62.

8 - Maes M, Ketelslegers JM, Underwood LE. Low plasma somatomedin-C in streptozotocin-induced diabetes mellitus. Correlation with changes in somatogenic and lactogenic liver binding sites. Diabetes. 1983;32:1060–9.

9 - Flyvbjerg A, Bennett WF, Rasch R, Kopchick JJ, Scarlett JA. Inhibitory effect of a growth hormone receptor antagonist (G120K-PEG) on renal enlargement, glomerular hypertrophy, and urinary albumin excretion in experimental diabetes in mice. Diabetes. 1999;48:377–82.

10 - Baumann G. Growth hormone binding protein 2001. J Pediatr Endocrinol Metab. 2001;14:355–75.

11 - Ho KY, Veldhuis JD, Johnson ML, Furlanetto R, Evans WS, Alberti KG, et al. Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man. J Clin Invest. 1988;81:968–75.

12 - Hartman ML, Veldhuis JD, Johnson ML, Lee MM, Alberti KG, Samojlik E, et al. Augmented growth hormone (GH) secretory burst frequency and amplitude mediate enhanced GH secretion during a two-day fast in normal men. J Clin Endocrinol Metab. 1992;74:757–65.

13 - Baxter RC, Bryson JM, Turtle JR. The effect of fasting on liver receptors for prolactin and growth hormone. Metabolism. 1981;30:1086–90.

14 - Maes M, Underwood LE, Ketelslegers JM. Low serum somatomedin-C in protein deficiency: relationship with changes in liver somatogenic and lactogenic binding sites. Mol Cell Endocrinol. 1984;37:301–9.

15 - Thissen JP, Triest S, Maes M, Underwood LE, Ketelslegers JM. The decreased plasma concentration of insulin-like growth factor-I in protein-restricted rats is not due to decreased numbers of growth hormone receptors on isolated hepatocytes. J Endocrinol. 1990;124:159–65.

16 - Ohashi S, Kaji H, Abe H, Chihara K. Effect of fasting and growth hormone (GH) administration on GH receptor (GHR) messenger ribonucleic acid (mRNA) and GH-binding protein (GHBP) mRNA levels in male rats. Life Sci. 1995;57:1655–66.

17 - Maccario M, Aimaretti G, Grottoli S, Gauna C, Tassone F, Corneli G, et al. Effects of 36 hour fasting on GH/IGF-I axis and metabolic parameters in patients with simple obesity. Comparison with normal subjects and hypopituitary patients with severe GH deficiency. Int J Obes Relat Metab Disord. 2001;25:1233–9.

18 - Kratzsch J, Keliner K, Zilkens T, Schmidt-Gayk H, Selisko T, Scholz GH. Growth hormone-binding protein related immunoreactivity is regulated by the degree of insulinopenia in diabetes mellitus. Clin Endocrinol (Oxf). 1996;44:673–8.

19 - Ji S, Guan R, Frank SJ, Messina JL. Insulin inhibits growth hormone signaling via the growth hormone receptor/JAK2/ STAT5B pathway. J Biol Chem. 1999;274:13434–42.

20 - Bennett WL, Keeton AB, Ji S, Xu J, Messina JL. Insulin regulation of growth hormone receptor gene expression: involvement of both the PI-3 kinase and MEK/ERK signaling pathways. Endocrine. 2007;32:219–26.

21 - Xu J, Keeton AB, Franklin JL, Li X, Venable DY, Frank SJ, et al. Insulin enhances growth hormone induction of the MEK/ERK signaling pathway. J Biol Chem. 2006;281:982–92.

22 - Growth Hormone Signaling in Vivo in Human Muscle and Adipose Tissue: Impact of Insulin, Substrate Background, and Growth Hormone Receptor Blockade, Charlotte Nielsen, et al., The Journal of Clinical Endocrinology & Metabolism July 2008 Vol. 93, No. 7 2842-2850

DatBtrue · Feb 2, 2009

First off when we translated the insulin concentration into "ius" the number we arrived at referred to circulating insulin in plasma. So that would mean any insulin the body creates and the amount that was released into the blood stream from the artificial insulin injected into tissue.

Does 5iu of insulin in a syringe equate to 5iu of insulin in plasma? Probably not and a lot depends on the type of insulin and its release profile. The best we can do is look at levels.

Is the 20iu level of Humalog injected going to negatively impact GH-receptors, erase the positive effects of insulin on GH? Yes.

Will 20iu of Humalog have better overall effect then 10iu on higher levels of protein synthesis and lower levels of protein degradation? Maybe.

Of course if all of that insulin is working to make tissue (especially muscle) more resistant to insulin... then you are altering muscle metabolism over the long run negatively. So perhaps you can counter that with macadamia oil...or not...who knows.

In my opinion 5-6ius is better then ridiculous high amounts of insulin.

In part because accreting muscle mass is a longer process then 3 months..it is a multi-year process. IMHO guys that swear by such high levels are confusing glycogen pumps for tissue accrual.

So you want to know which is better two helpings of insulin a day or one?

Probably the only things I can say are absolutely better are to take periodic breaks from insulin use, stay away from insulin when you are fat and make use of it when you are lean and growing.

What I can say is probably better is consistent use of moderate dosed insulin instead of high short-term use.

What I can say is very good especially in the early part of growth cycles is two sessions of insulin, morning & PWO.

I can also say though that just PWO is effective as well and as your growth cycle gets longer and you get bigger & fatter as well moving to PWO only might be a good idea.

Pit with your new experiments coming I'd drop that morning dose of slin. It is not going to contribute much in comparison to the compounds/protocol you are adding.

I'd say keep it simple and just do the insulin PWO.

pitbulladams said:
Dat
Ok so stay with me on this one..

I take it this info is pointing towards the use of say 5-6iu is better then the higher amounts i see guys using PWO like in the region 10-20iu's ?

What time duration is this amount of insulin over ?

As you know i have been dosing my GH first thing in the morning and was using 6iu humalog with it, then a second dose of 12iu Humalog PWO which is about 4 hours after my am GH/insulin shot.

Now based on this am i better dropping my insulin first thing and just use GH on its own followed by 6iu insulin PWO ?

Or would a smaller dosage at both AM and PWO be better ?

Cheers
PB

pitbulladams · Feb 2, 2009

Dat
Thank you again.

Right as with my up coming experiment, and my increase of Test to go with it, I will continue GH use split 4iu AM (with carbs) and 4iu PM (after carb cut-off) and should i stick with my 12iu humalog PWO or drop down to say 6iu ?

I will say even at my highest Insulin dosing AM and PWO with my split use of GH AM & PM and with the carb cut-off i have kept my body fat levels under control.

Cheers
PB

DatBtrue said:
First off when we translated the insulin concentration into "ius" the number we arrived at referred to circulating insulin in plasma. So that would mean any insulin the body creates and the amount that was released into the blood stream from the artificial insulin injected into tissue.

Does 5iu of insulin in a syringe equate to 5iu of insulin in plasma? Probably not and a lot depends on the type of insulin and its release profile. The best we can do is look at levels.

Is the 20iu level of Humalog injected going to negatively impact GH-receptors, erase the positive effects of insulin on GH? Yes.

Will 20iu of Humalog have better overall effect then 10iu on higher levels of protein synthesis and lower levels of protein degradation? Maybe.

Of course if all of that insulin is working to make tissue (especially muscle) more resistant to insulin... then you are altering muscle metabolism over the long run negatively. So perhaps you can counter that with walnut oil...or not...who knows.

In my opinion 5-6ius is better then ridiculous high amounts of insulin.

In part because accreting muscle mass is a longer process then 3 months..it is a multi-year process. IMHO guys that swear by such high levels are confusing glycogen pumps for tissue accrual.

So you want to know which is better two helpings of insulin a day or one?

Probably the only things I can say are absolutely better are to take periodic breaks from insulin use, stay away from insulin when you are fat and make use of it when you are lean and growing.

What I can say is probably better is consistent use of moderate dosed insulin instead of high short-term use.

What I can say is very good especially in the early part of growth cycles is two sessions of insulin, morning & PWO.

I can also say though that just PWO is effective as well and as your growth cycle gets longer and you get bigger & fatter as well moving to PWO only might be a good idea.

Pit with your new experiments coming I'd drop that morning dose of slin. It is not going to contribute much in comparison to the compounds/protocol you are adding.

I'd say keep it simple and just do the insulin PWO.

DatBtrue · Feb 3, 2009

I'd drop the Humalog down to 6iu.

One of the things that happens with the protocol that you are about to follow is that your body will absorb some of [...] and use it as an energy substrate.

I told you I was experimenting with that protocol some...and during that time I used the Hum-R PWO at 6-8iu w/ the mod GRF(1-29) & GHRP-6 as well as having a base low level of test.

I gained visceral fat as well as nice muscle mass.

See androgen receptors AND estrogen receptors are regulated upward as a result of [...] Its not a problem though but having insulin around during the 5 hours when I take in 50% of my calories plus having that extra energy substrate going unused meant a little fat gain.

pitbulladams said:
Dat
Thank you again.

Right as with my up coming experiment, and my increase of Test to go with it, I will continue GH use split 4iu AM (with carbs) and 4iu PM (after carb cut-off) and should i stick with my 12iu humalog PWO or drop down to say 6iu ?

I will say even at my highest Insulin dosing AM and PWO with my split use of GH AM & PM and with the carb cut-off i have kept my body fat levels under control.

Cheers
PB

GoneForever · Feb 3, 2009

So Dat in a month or so I plan on doing a bulker. Im over trying to stay lean but this round im not gonna be sloppy. Simple dose of test/deca but gonna up the Gh this time and add slin. I was thinkin about doing the 3x per week method pwo only since I train 3x per week. Was thinkin about 15iu's pwo with 10iu slin(humalog) 3x per week both shot IM at same time. Hows that sound?

DatBtrue · Feb 3, 2009

fourthgen said:
So Dat in a month or so I plan on doing a bulker. Im over trying to stay lean but this round im not gonna be sloppy. Simple dose of test/deca but gonna up the Gh this time and add slin. I was thinkin about doing the 3x per week method pwo only since I train 3x per week. Was thinkin about 15iu's pwo with 10iu slin(humalog) 3x per week both shot IM at same time. Hows that sound?

Give it a try bro and you tell me.

There is a lot of wiggle room in precisely how to do things. Some of it is a little subjective.

The high dose of GH with a day off will be sufficient to resensitize everything...so that looks good. The insulin PWO will give the GH anabolic meaning on top of a base of testosterone which will do so many things.

Looks good.