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

DatBtrue · Oct 27, 2008

vast568 said:
Hey dat I read that study you posted (pg 10 AM) called:

"GHRP-2, a GHS-R agonist, directly acts on myocytes to attenuate the dexamethasone-induced expressions of muscle-specific ubiquitin ligases, Atrogin-1 and MuRF1, Daisuke Yamamoto, et al., Life Sciences 82 (2008) 460–466"

vast568; said:
Is there any way you could break this down into us simple people language? I really do not understand " Atrogin-1 and MuRF1 mRNA" but it seems like GHRP-2 and 6 may be more different than one just not causing hunger. Thanks.

The primary research in this area is focused on preventing muscle wasting due to age, inactivity, disease & medical states such as AIDS, cancer, sepsis & burn victims...

...so they explore the molecular mechanisms modulating muscle mass.

There are two ways to do that. One increase HYPERTROPHY, the other decrease ATROPHY.

These are not two sides of the same coin. A primary mode for hypertrophy is understanding the IGF-1 signaling. This is what takes place once an IGF-1 molecule binds to a IGF Receptor in target tissue. A decent mental image is a lock (receptor) accepts the key (IGF-1 molecule) which turns the switch and starts a cascade of signaling which results in blocking apoptosis (cell death), inducing protein synthesis, gene transcription and proliferation. All of this induces skeletal muscle hypertrophy.

All of us experience atrophy to some dgree but it is most pronounced if we are vastly underfed, have a severe hormonal imbalance or have an underlying medical condition. In those instances a process of muscle atrophy accelerates. Conditions that cause atrophy lead to a decrease in the size of pre-existing muscle fibers resulting from increases in the rate of ATP-dependent ubiquitin-mediated proteolysis.

Proteolysis is the degradation (digestion) of proteins. Ubiquitin is a regulatory protein whose primary function is labeling proteins for degradation. The labeling process is catalyzed by enzymes called ubiquitin ligases. Once this process is initiated other ligases attach additional ubiquitin molecules to create a polyubiquitin chain. This chain is easily bound by and eventually degraded by a proteasome.

That is how muscle fiber is digested.

Where do these highly destructive ubiquitin-protein ligases come from?

There are genes that encode these proteins. Normally a certain amount is created but under conditions of atrophy these genes may be very active and encode/create a lot of these destructive ligases.

Those genes were identified within the last 5 or so years and they are:

MAFbx/Atrogin-1, and MuRF1

In mice it was discovered that these two genes are required for muscle atrophy because muscle atrophy doesn't occur in mice if these genes are knocked out.

So some research focuses on ways to reduce these two genes expression during periods when naturally they would become most active.

Enter our friends the "Growth Hormone Releasing Peptides" and the studies you mention posted in my thread on AnabolicMinds.

Force245 · Oct 27, 2008

Thanks Dat, that was very helpful...

I think what will be reserached is first a IGF 30 day at 50mcg bilaterally PWO then a break then into the CJC/GHRP protocol. I guess during the research the monitoring of blood sugar will be watched as to monitor the need for exogenous insuling. Thanks

weltweite · Oct 27, 2008

If GHRP or CJC increases the GH pulse intensity and amount, would insulin prevent those GH pulses from even occuring in the first place? Would it be wise not to use insulin during GHRP and CJC administration?

DatBtrue · Oct 28, 2008

weltweite said:
If GHRP or CJC increases the GH pulse intensity and amount, would insulin prevent those GH pulses from even occuring in the first place?

NO.

weltweite said:
Would it be wise not to use insulin during GHRP and CJC administration?

No. GH is not anabolic w/o insulin. Here is an illustration and my response to this question on AM a while back.

xxxxx; said:
Dat, what is your opinion on using insulin while on CJC-1295 and GHRP-6?
I.E; Dosing CJC and GRHP pre-workout and taking insulin post-workout? Anything to be gained by this?

Yes.

I am tired of seeing the same wrong explanations on why insulin & growth hormone are anabolic so lets take a look. I don't feel like writing an article so I'll just borrow from a couple of sources.

Insulin physiology

It is often stated that the primary benefit of insulin in bodybuilding is that it increases the uptake of glucose into muscle and further that this movement of glucose is insulin dependent. But that is not exactly true. It may not be widely known but it is clearly established that insulin is NOT needed for glucose uptake and utilisation in man and therefore glucose uptake is NOT insulin dependent

There is a sufficient population of glucose transporters in all cell membranes at all times to ensure enough glucose uptake to satisfy the cell’s respiration, even in the absence of insulin. Insulin can and does increase the number of these transporters in some cells but glucose uptake is never truly insulin dependent.

Stimulatory & Inhibiting actions

Through stimulating the translocation or movement of 'Glut 4' glucose transporters from the cytoplasm of muscle and adipose tissue to the cell membrane insulin increases the rate of glucose uptake to values greater than the uptake that takes place in the basal state without insulin.

When insulin is administered to people with diabetes who are fasting, blood glucose concentration falls. It is generally assumed that this is because insulin increases glucose uptake into tissues, particularly muscle. In fact this is NOT the case and is another error arising from extrapolating from in vitro rat data. It has been shown quite unequivocally that insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production without stimulating peripheral glucose uptake. As hepatic glucose output is 'switched off' by the inhibiting action of insulin, glucose concentration falls and glucose uptake actually decreases. Contrary to most textbooks and previous teaching, glucose uptake is therefore actually increased in uncontrolled diabetes and decreased by insulin administration.

When insulin is given to patients with uncontrolled diabetes it switches off a number of metabolic processes (lipolysis, proteolysis, ketogenesis and gluconeogenesis) by a similar inhibiting action. The result is that free fatty acid (FFA) concentrations fall effectively to zero within minutes and ketogenesis inevitably stops through lack of substrate. It takes a while for the ketones to clear from the circulation, as the 'body load' is massive as they are water and fat soluble and distribute within body water and body fat. Since both ketones and FFA compete with glucose as energy substrate at the point of entry of substrates into the Krebs cycle, glucose metabolism increases inevitably as FFA and ketone levels fall (despite the concomitant fall in plasma glucose concentration).

Thus insulin increases glucose metabolism more through reducing FFA and ketone levels than it does through recruiting more glucose transporters into the muscle cell membrane.

NOTE: The above was taken from:

Mechanism of action of insulin in diabetic patients: a dose-related effect on glucose production and utilisation, Brown P, Tompkins C, Juul S & Sonksen PH, British Medical Journal 1978 1239–1242.

Anabolic effect

Through facilitating glucose entry into cells in amounts greater than needed for cellular respiration insulin will stimulate glycogen formation.

It is possible to increase muscle bulk and performance not only through increasing muscle glycogen stores on a "chronic" basis but also to increase muscle bulk through inhibition of muscle protein breakdown. Just as insulin has an inhibiting action in inhibiting glucose breakdown in muscle glycogen, it also has an equally important inhibiting action in inhibiting protein breakdown.

The evidence now indicates that insulin does NOT stimulate protein synthesis directly (this process is under the control of growth hormone (GH) and insulin-like growth factor-I (IGF-I)). It has long been known that insulin-treated patients with diabetes have an increase in lean body mass when compared with matched controls. This results from insulin's inhibition of protein breakdown in muscle tissue.

Growth Hormone Anabolic Actions

GH’s major action is to stimulate protein synthesis. It is at least as powerful as testosterone in this effect and, as they both operate through distinct pathways, their individual effects are additive or possibly even synergistic. In addition to stimulating protein synthesis, GH simultaneously mobilises fat by a direct lipolytic action. Together, these two effects are responsible for the 'partitioning' action of GH whereby it diverts nutritional calories to protein synthesis, possibly through using the energy derived from its lipolytic action. It most likely stimulates protein synthesis through mobilisation of amino acid transporters in a manner analogous to insulin and glucose transporters.

IGF-I also acts directly to stimulate protein synthesis but it has a weaker lipolytic action. GH, IGF-I and insulin thus act in concert to stimulate protein synthesis.

GH and IGF-I act in a promoting manner to stimulate protein synthesis while insulin acts in its characteristic inhibiting manner to inhibit protein breakdown. Thus they are synergistic in their powerful anabolic action.

Insulin is essential for the anabolic action of GH. GH administration in the absence of adequate insulin reserves (as during fasting or in Type 1 diabetes) is in fact catabolic and its lipolytic and ketogenic properties can induce diabetic ketoacidosis. Thus GH and insulin are closely linked in normal physiology and it is of great interest to see that athletes have discovered ways in which this normal physiological dependence can be exploited to enhance performance.

NOTE: The above was "lifted" with little change from parts of:

HORMONES AND SPORT: Insulin, growth hormone and sport, P H Sonksen, Journal of Endocrinology (2001) 170, 13–25

medium al · Oct 28, 2008

DatBtrue said:
I'd rather not do that. Instead I'll give you some thoughts:

The quality of synthetic GH & CJC-1295 being sold today (10/27/08):

CJC-1295 is being wholesaled by some Chinese facilities, but the actual peptide is not CJC-1295, it is a slightly modified GRF(1-29). A significant number of people are using a compound to induce GH release that has a half-life measured in minutes rather than true CJC-1295 which has a half-life measured in days. That will make a big difference in one's results.

This is very worrisome. Is there any way, for example, board sponsors here could look into this issue, or be prompted to do so? I have asked for COA's from one and were told they were not available for peptides. Not even sure a COA would tell me what I needed to know. I have also gotten some peptide material that was suspect (to say the least) from other companies (not a board sponsor here any longer). Another I broke out into weird boils-zits after using, threw it away.

Just looking for some way for the trusted vendors here to rule out fake CJC at the wholesale level. Messing around with mystery peptides is a bit scary. Not to mention expensive.

BTW DB, thanks for all the great info, I have been reading this thread and the sister version at AM since its inception.

edit: I suspect this applies to ALL peptides, not just CJC. I had problems with some GHRP6, and so did someone else on another board.

2bvajra · Oct 29, 2008

Dat somewhere in this forum I think you discuss storage of CJC and GHRP but there are 11 pages now and it would take a lot of reading to find it, so maybe a refresher: Shelf life? Freeze or just refrigerate? For short term (per vial use)it's refrigerate I know but long term? Thanks.

dragonfire101 · Oct 29, 2008

What if one would substitute IGF-1 instead of insulin. Would that still create the anabolic action of GH.

DatBtrue · Oct 29, 2008

2bvajra said:
Dat somewhere in this forum I think you discuss storage of CJC and GHRP but there are 11 pages now and it would take a lot of reading to find it, so maybe a refresher: Shelf life? Freeze or just refrigerate? For short term (per vial use)it's refrigerate I know but long term? Thanks.

datBtrue; said:
The reconstitution agent for both CJC-1295 & GHRP-6 is Bacteriostatic Water (BW).

Here are a few interesting snippets from studies on storage:

Storage

The following paragraph comes from a study that sent the peptide home with study participants for self-administration.

Vials were stored frozen until dispensed to the subjects, then kept at 4 C for 10 days at home. High performance liquid chromatographic analysis showed that the peptide was stable at 4 C for at least 2 weeks.

The following seems to indicate that GHRP-6 which is a simple peptide chain unlike IGF-1 which is more complex, is relatively resistant to degradation under the right circumstances at room temperature for almost five years.

The influence of the various buffer species (acetate, citrate, phosphate and borate) was shown to be different and the maximum stability of GHRP-6 was revealed to be in acetate buffer of pH 5.5-6.0. Degradation of GHRP-6 was greater in citrate-containing buffers than in acetate-containing ones. Furthermore, in the citrate-containing buffers, the higher buffer concentration caused greater degradation than the lower ones, but the concentration effect was negligible in acetate-containing buffers. Aqueous solution of GHRP-6 buffered with acetate (0.01 M, pH 5.5) showed a predicted t90% of 4.73 years at 20°C. - Degradation kinetics of growth hormone-releasing hexapeptide (GHRP-6) in aqueous solution, In Sik Ha… International Journal of Pharmaceutics Volume 144, Issue 1, 22 November 1996, Pages 91-97

It is worth noting the characteristics of the primary aqueous solution we use to reconstitute these peptides:

Bacteriostatic Water for injection, USP is a sterile, nonpyrogenic preparation of water for injection containing 0.9% (9 mg/mL) of benzyl alcohol added as a bacteriostatic preservative. It is supplied in a multiple-dose container from which repeated withdrawals may be made to dilute or dissolve drugs for injection. The pH is 5.7 (4.5 to 7.0)

Or for GHRH

datBtrue; said:
In general the following applies:

Therapeutic Peptides and Proteins:
Formulation, Processing, and Delivery
Systems, Second Edition
by Ajay K. Banga

5.5.4 Storage in solid state

Lyophilized powders can be quite stable as long as they are not reconstituted.
For example, Activase® lyophilized powder shows no significant loss of
bioactivity after storage for more than 4 years at controlled room temperature.

Degradation in the solid state often takes place by aggregation. The
stability of a protein in the solid state is dependent on the moisture content
of the solid, temperature, and composition of the formulation....

These degradation factors become more important the longer the chain of amino acids becomes & with the inclusion of amino acids sensitive to degradation.

Storage of unreconstituted peptides in frozen form (devoid of moisture) is always far more preferable for long-term storage then reconstituted peptides.

GHRP-6 is a simple chain with no extra-sensitive amino acids. But Growth Hormone Releasing Hormone (GHRH) is more sensitive because it is a longer chain composed of some sensitive amino acids. The added bioconjugation complex of CJC-1295 appears to be stable and shouldn't effect degradation/life of the peptide it is attached to...GHRH.

To answer stability questions the best way is to find studies that specifically examine the stability of the peptide you are interested in.

We have already looked to a very comprehensive study of GHRP-6 now lets look at a stability study for a slightly modified GHRH (and by undeclared assumption CJC-1295).

Investigation of the chemical stability of a new growth hormone-releasing hormone (GHRH) analogue by HPLC, M Idei, I Mezo, EZ Szabo, and G Keri, Biomed Chromatogr, March 1, 1996; 10(2): 89-91

The stability of a new active growth hormone-releasing hormone analogue (D-Ala2,Nle27,(gamma-amino-butyric acid)30-GHRH(1-30)-NH2) was investigated during storage at different temperatures in aqueous solution. Samples stored for various periods of time were analysed by HPLC.

It is concluded that in aqueous solution D-Ala2, Nle27,(gamma-amino-butyric acid)30-growth hormone-releasing hormone (1-30)-NH2 is stable: at least for 36 days at 4 degrees C; for 28 days at 25 degrees C; and for 10 days at 37 degrees C.

DatBtrue · Oct 29, 2008

dragonfire101 said:
What if one would substitute IGF-1 instead of insulin. Would that still create the anabolic action of GH.

Nope.

Force245 · Oct 30, 2008

DatBtrue said:
NO.

No. GH is not anabolic w/o insulin. Here is an illustration and my response to this question on AM a while back.

View attachment 22287

Yes.

I am tired of seeing the same wrong explanations on why insulin & growth hormone are anabolic so lets take a look. I don't feel like writing an article so I'll just borrow from a couple of sources.

Insulin physiology

It is often stated that the primary benefit of insulin in bodybuilding is that it increases the uptake of glucose into muscle and further that this movement of glucose is insulin dependent. But that is not exactly true. It may not be widely known but it is clearly established that insulin is NOT needed for glucose uptake and utilisation in man and therefore glucose uptake is NOT insulin dependent

There is a sufficient population of glucose transporters in all cell membranes at all times to ensure enough glucose uptake to satisfy the cell’s respiration, even in the absence of insulin. Insulin can and does increase the number of these transporters in some cells but glucose uptake is never truly insulin dependent.

Stimulatory & Inhibiting actions

Through stimulating the translocation or movement of 'Glut 4' glucose transporters from the cytoplasm of muscle and adipose tissue to the cell membrane insulin increases the rate of glucose uptake to values greater than the uptake that takes place in the basal state without insulin.

When insulin is administered to people with diabetes who are fasting, blood glucose concentration falls. It is generally assumed that this is because insulin increases glucose uptake into tissues, particularly muscle. In fact this is NOT the case and is another error arising from extrapolating from in vitro rat data. It has been shown quite unequivocally that insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production without stimulating peripheral glucose uptake. As hepatic glucose output is 'switched off' by the inhibiting action of insulin, glucose concentration falls and glucose uptake actually decreases. Contrary to most textbooks and previous teaching, glucose uptake is therefore actually increased in uncontrolled diabetes and decreased by insulin administration.

When insulin is given to patients with uncontrolled diabetes it switches off a number of metabolic processes (lipolysis, proteolysis, ketogenesis and gluconeogenesis) by a similar inhibiting action. The result is that free fatty acid (FFA) concentrations fall effectively to zero within minutes and ketogenesis inevitably stops through lack of substrate. It takes a while for the ketones to clear from the circulation, as the 'body load' is massive as they are water and fat soluble and distribute within body water and body fat. Since both ketones and FFA compete with glucose as energy substrate at the point of entry of substrates into the Krebs cycle, glucose metabolism increases inevitably as FFA and ketone levels fall (despite the concomitant fall in plasma glucose concentration).

Thus insulin increases glucose metabolism more through reducing FFA and ketone levels than it does through recruiting more glucose transporters into the muscle cell membrane.

NOTE: The above was taken from:

Mechanism of action of insulin in diabetic patients: a dose-related effect on glucose production and utilisation, Brown P, Tompkins C, Juul S & Sonksen PH, British Medical Journal 1978 1239–1242.

Anabolic effect

Through facilitating glucose entry into cells in amounts greater than needed for cellular respiration insulin will stimulate glycogen formation.

It is possible to increase muscle bulk and performance not only through increasing muscle glycogen stores on a "chronic" basis but also to increase muscle bulk through inhibition of muscle protein breakdown. Just as insulin has an inhibiting action in inhibiting glucose breakdown in muscle glycogen, it also has an equally important inhibiting action in inhibiting protein breakdown.

The evidence now indicates that insulin does NOT stimulate protein synthesis directly (this process is under the control of growth hormone (GH) and insulin-like growth factor-I (IGF-I)). It has long been known that insulin-treated patients with diabetes have an increase in lean body mass when compared with matched controls. This results from insulin's inhibition of protein breakdown in muscle tissue.

Growth Hormone Anabolic Actions

GH’s major action is to stimulate protein synthesis. It is at least as powerful as testosterone in this effect and, as they both operate through distinct pathways, their individual effects are additive or possibly even synergistic. In addition to stimulating protein synthesis, GH simultaneously mobilises fat by a direct lipolytic action. Together, these two effects are responsible for the 'partitioning' action of GH whereby it diverts nutritional calories to protein synthesis, possibly through using the energy derived from its lipolytic action. It most likely stimulates protein synthesis through mobilisation of amino acid transporters in a manner analogous to insulin and glucose transporters.

IGF-I also acts directly to stimulate protein synthesis but it has a weaker lipolytic action. GH, IGF-I and insulin thus act in concert to stimulate protein synthesis.

GH and IGF-I act in a promoting manner to stimulate protein synthesis while insulin acts in its characteristic inhibiting manner to inhibit protein breakdown. Thus they are synergistic in their powerful anabolic action.

Insulin is essential for the anabolic action of GH. GH administration in the absence of adequate insulin reserves (as during fasting or in Type 1 diabetes) is in fact catabolic and its lipolytic and ketogenic properties can induce diabetic ketoacidosis. Thus GH and insulin are closely linked in normal physiology and it is of great interest to see that athletes have discovered ways in which this normal physiological dependence can be exploited to enhance performance.

NOTE: The above was "lifted" with little change from parts of:

HORMONES AND SPORT: Insulin, growth hormone and sport, P H Sonksen, Journal of Endocrinology (2001) 170, 13–25

Thank You ver much Dat. I think this small portion of the article finally resolves question and unlocks an aspect of secret knowledge. You are truely an asset. Thanks You.

GoneForever · Oct 31, 2008

DatBtrue said:
Yes. Growth Hormone is a uni-sexual hormone. It is not specific to either sex and is present in both.

The primary difference appears to be the secretory release pattern. See the normal GH secretory pattern over 24 hours charted in my post #6 in this thread for both men & women.

Women have more pulses throughout the day and higher troughs. Men have a huge night-time pulse that results in most of their GH release for the day.

Dosages for children and women should probably be determined by weight. So 1mcg/kg is the saturation dose for either GHRH (CJC-1295) and also the GHRPs (GHRP-6, etc)

Unit Conversion:
1kg = 2.2lbs
50kgs = 110lbs
70kgs = 154lbs.

Also with women we are not overly concerned with supporting the night-time pulse...although it is probably a good idea to use the same dosing pattern as I laid out.

Wow I didnt realize women needed such a low dose. My wife used it in the past with good success at 200mcg before bed and she weights 135lbs. Very muscular, good genetics. She is 25yrs old. Dat, she is now taking 150mcg before bed but thats too high huh? Maybe drop it to 75mcg or 100mcg?

dicko53 · Oct 31, 2008

This is one of the most interesting and informative threads that I've enjoyed. Pity I'm not bright enough to follow it all

I'm 53 and at the end of my current AAS cycle I'm going to commence TRT. I'm going to use 125mg Test E and 250iu HCG E7D along with 25mg Proviron ED. Possibly an AI though not sure.

I'm also going to commence DATs protocol with 100mg CJC and 200mg GHRP before bed 5 times a week (gonna leave the weekends for late nights and beer

) I've got Hygetropin and was going to take 4iu along with the other peptides before bed but wondered if it would be better to take immediately pre-workout with my MRP straight after training??

I am looking to be taking the above for the long haul and also wondered if the were any contraindications to any of it?

Cheers.

Mr.Bill · Oct 31, 2008

"cjc 2 times a week at 250mcg monday and thurs

ghrp 1000mg a week at 200mcg per ed monday-friday"

"Change the GHRP-6 dosing to 140mcgs and take it pre-bed every night of the week. Your sleep and night-time pulse will thank you.

In fact, especially older guys, but most of us could benefit from just taking 100mcg of GHRP-6 pre-bed each night."

Amazing amount of information here, Thanks !!

As fitting into the older guy category, 49. And needing to lose body fat, yes about 25% here.
Dialing in my low carb diet.

Would the above protocol be good for my main goal of losing body fat and visceral fat. 250mcg 2X a week of cjc, and 140-200 mcg ed at bedtime of ghrp.

I train around 5-6:00 in the evenings, so the 2X a day protocols might not work as pinning after training and then at around 10:00 pm bedtime.

Thanks again

DatBtrue · Oct 31, 2008

fourthgen said:
Wow I didnt realize women needed such a low dose. My wife used it in the past with good success at 200mcg before bed and she weights 135lbs. Very muscular, good genetics. She is 25yrs old. Dat, she is now taking 150mcg before bed but thats too high huh? Maybe drop it to 75mcg or 100mcg?

When it comes to the hormone "growth hormone releasing hormone" there is variability among people. For instance some people resensitize to it more quickly after a saturation dose and thus can actually get a second pulse on the heels of the first with a subsequent dose. The majority of people need more time to resensitize (at least several hours).

Also while the response to GHRPs (such as GHRP-6) is fairly consistent and predictable (everyone experiences an amplified pulse) the response to GHRH between people of the same age, sex and weight can vary considerably.

All of this to say that while we can make fairly decent generalizations in regard to dosing, the exact dose is a bit subjective.

Now as far as your wife's dosing it is not "too high" in respect to doing harm. Her dose is fine where it is... however she may be wasting some amount in that she can achieve the same level of effect with a lower dose.

She is doing things properly by backing the dose down and seeing if it continues to work just as well. If that dosing level works then she can step it down a little more and see how that works.

DatBtrue · Oct 31, 2008

dicko53; said:
...I'm also going to commence DATs protocol with 100mg CJC and 200mg GHRP before bed 5 times a week (gonna leave the weekends for late nights and beer ) I've got Hygetropin and was going to take 4iu along with the other peptides before bed but wondered if it would be better to take immediately pre-workout with my MRP straight after training??

I would do one of two things. Either:

Take the synthetic GH (4iu) in the morning and the CJC/GHRP pre-bed, or
Take the synthetic GH (4iu) PWO and the CJC/GHRP pre-bed

If you can give yourself 12 hours between the synthetic GH (4iu) administration & the CJC/GHRP you will minimize the likelihood/extent of its inhibition on natural GH release at the pituitary.

dicko53; said:
I am looking to be taking the above for the long haul and also wondered if the were any contraindications to any of it?

If you are on medications it is always good to go to the book or ask a doctor about such things. As a general rule though if you are on blood thinners never take anything w/o a doctor signing off on it.

DatBtrue · Oct 31, 2008

Mr.Bill said:
...Would the above protocol be good for my main goal of losing body fat and visceral fat. 250mcg 2X a week of cjc, and 140-200 mcg ed at bedtime of ghrp.

I train around 5-6:00 in the evenings, so the 2X a day protocols might not work as pinning after training and then at around 10:00 pm bedtime.

Thanks again

Yes if you give yourself a sufficient amount of time on these peptides. Six months would be a good start.

Make sure your diet is dialed in...by that I mean set things up so with your diet you would have lost weight week to week even without the peptides. Don't make them do the heavy work ...that part is diet related.

Now at your age (by that I mean around the age of 42 there is a significant drop in the level of GH produced and a weakening of the pulsatile profile) restoring your GH levels to that of youth will contribute to a reduction in the weight you hold in your mid-section. But this takes time...having a youthful GH hormone profile for 3 months is better then one month and having such a profile for six months is better still.

As you lose weight don't specifically look at your belly. At 25% BF you will notice that you lose it around the periphery first. Your face and shoulders will lean out first but you may not lose much in the belly for while. The body feels that fat on the periphery is expendable and will let that go first. It holds on to the core fat the longest as that fat pad may be needed to draw on in times of famine. So sadly that is the last to go.

The upper, above the navel area will probably go before the rest of the mid-section leaving the below the navel and love handles still full of fat. This has a tendency to make things look worse than they are. Just don't give up and stick to the plan.

Now restoring your GH levels to that of youth will make it easier to lose those love handels and lower belly BUT that doesn't really happen until the body sheds fat everywhere else. Thus six months is needed before you can celebrate your return to "svelt".

muscledoc1 · Oct 31, 2008

Got a question about GH for you DAT(i know its off the cjc topic here-so i understand if you won't answer it)-i recently started doing 2iu's in the am(pre cardio)-and 2iu's in the pm(pre workout)-should i change that protocol if my goals are to lose body fat and get some of the other benefits of gh?

DatBtrue · Nov 1, 2008

muscledoc1 said:
Got a question about GH for you DAT(i know its off the cjc topic here-so i understand if you won't answer it)-i recently started doing 2iu's in the am(pre cardio)-and 2iu's in the pm(pre workout)-should i change that protocol if my goals are to lose body fat and get some of the other benefits of gh?

4ius of GH that has not undergone thermal shape change used over a decent period of time is fine for fat loss.

So you could take it all at once or split it the way you have.

The shape of the GH in plasma curve indictes that a single dose of GH will be active for about 12 hours before it basically flatlines. So your split will elevate GH throughout the entire 24 hour day. That means GH will exert an overall lipolytic effect all day & night.

If you dose the full 4iu at one time you will have have GH elevated in plasma for only half of the day. Now this isn't to bad if you dose in the morning and by the time you go to bed you can hope for at least a partial return of your own natural secretion in the form of the night-time pulse. You could even try to encourage with GHRP-6 and/or a litle gaba and /or attempt to reduce somatostatins negative influence through the use of something like L-Dopa or arginine.

In the end it is up to you. Not everyone can use 4iu in the morning and get a natural GH release in the evening...some will others might be supressed into the next day or so.

The key though no matter which way you use it is to run it for a long enough period of time to garner some results and that will require a minimum several months.

VictorZ06 · Nov 1, 2008

Dat, I'm curious as to what the proper protocol would be for a BB/mass gain dose for one using GH as well.

I just started using 5iu (will go up) of GH right now (2.5iu 6am, 2.5iu pre work out), and would like to know how to best work the CJC/GHRP-6 in there (dose sched). (been on your BB suggested dose for 5 weeks now) THANKS!!!

finny · Nov 1, 2008

Dat, to expand on this, what do you think about a single dose of say 20-30IUs once a week for bb purposes or 3x10IUs?

VictorZ06 said:
Dat, I'm curious as to what the proper protocol would be for a BB/mass gain dose for one using GH as well.

I just started using 5iu (will go up) of GH right now (2.5iu 6am, 2.5iu pre work out), and would like to know how to best work the CJC/GHRP-6 in there (dose sched). (been on your BB suggested dose for 5 weeks now) THANKS!!!