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

smc252 · Nov 28, 2008

machola said:
same as ephedra. they work through the same mechanism. its bad for your heart

I've been on thyroid hormones for several years now. Don't kid yourselves T3 CAN be damaging to the heart at higher levels.

I'd never, ever, go over 100mcg/day of T3. I personally like ~50mcg/day split into 2 or 3 doses with meals.

machola · Nov 28, 2008

smc252 said:
I've been on thyroid hormones for several years now. Don't kid yourselves T3 CAN be damaging to the heart at higher levels.

I'd never, ever, go over 100mcg/day of T3. I personally like ~50mcg/day split into 2 or 3 doses with meals.

very true smc. the used to use it(they may still) at high doses for treatment of obesity and some people had heart problems.

GoneForever · Nov 28, 2008

I dont think clen v.s. ephedra is a fair comparison. Ephedra can be very safe if taken in lower doses and cycled properly. Clen is much worse on the heart muscle.

Dat, interesting you dont feel t3 is necassary on GH. I heard its a great additon to use either 25mcg t3 or 100mcg t4 longterm(3-5months) while on Gh and you get more outta the GH. I wonder if doing gh eod will prevent the lowering of natty t3 levels.

DatBtrue · Nov 29, 2008

fourthgen said:
...Dat, interesting you dont feel t3 is necassary on GH. I heard its a great additon to use either 25mcg t3 or 100mcg t4 longterm(3-5months) while on Gh and you get more outta the GH.

I am not going to directly address T3.

The approach many people have is that they take a survey across the boards and then ask me the same question and always preface it by "a lot of people say" or follow up by saying "that is not what I heard."

I don't mean to be a dick but I won't participate in penis or genitalia surveys.

Instead I'm going to explain to you why your use of Metformin with CJC-1295/GHRP-6 produced less than stellar results. From this explanation hopefully you'll understand that the proper answer to the types of questions you raise are far deeper then the gaggle of penises you survey would ever believe possible. Knowledge resides deeper then surface level...so lets take a look.

By now everyone should understand how we end up with more IGF-1 as a result of administering GHRH (CJC-1295, modified GRF(1-29) & Sermorelin) and a Ghrelin mimetic (GHRP-6, GHRP-2, Hexarelin, Ipamorelin & the nonmpeptide molecules) but I'll quickly recap.

Growth hormone (GH) is produced in the anterior pituitary, and is modulated by two hypothalamic hormones, growth hormone-releasing hormone (GHRH), which stimulates both the synthesis and secretion of GH; and somatostatin (SS), which inhibits GH release in response to GHRH.

GHRPs further modulate GH release by acting at both the hypothalamus and the anterior pituitary to enhance both the release and effect of GHRH and inhibit both the release and effect of somatostatin.

Administering GHRH (in the form of CJC-1295, modified GRF(1-29) or Sermorelin) together with a Ghrelin-mimetic (GHRP-6, GHRP-2, Hexarelin, Ipamorelin & the nonmpeptide molecules) both creates and amplifies a GH pulse in synergistic fashion.

GH is naturally secreted in pulsatile bursts from the anterior pituitary gland, a pattern that is necessary to achieve full biological activity. Basal concentrations (between pulses) of GH in blood are very low. GH also feeds back to inhibit GHRH secretion and probably has a direct inhibitory effect on secretion from the somatotroph (GH-producing cells).

GH binds with high affinity to its receptor, found in tissues throughout the body, and activation of this receptor stimulates the synthesis and secretion of insulin-like growth factor 1 (IGF-1). Although 90% of circulating IGF-1 is synthesized and secreted by the liver, many types of cells, including some found in the brain, muscle and vasculature, are capable of IGF-1 production.

Binding of the hormone IGF-1 to the IGF-1 receptor (IGFR) causes potent mitogenic effects, including increases in DNA, RNA and protein synthesis.

IGF-1 binding activates the IGF-1 receptor (IGFR), a receptor tyrosine kinase (which in essence means subsequent pathway activation will be by phosphorylation symbolized below by red p). The IGFR subsequently recruits the insulin receptor substrate (IRS-1), which results in the activation of two signaling pathways: the Ras–Raf– MEK–ERK pathway and the PI3K–Akt pathway. The Ras–Raf–MEK–ERK pathway is crucial in mitosis-competent cells for cell proliferation and cell survival. However, in adult skeletal muscle, the function of the Ras–Raf–MEK–ERK pathway is less clear.

The PI3K–Akt pathway has been shown to be both necessary and sufficient to induce skeletal muscle hypertrophy.

Moving down that pathway it has been demonstrated that Akt1 activity is required for IGF-1- mediated hypertrophy, and expression of activated Akt1 is sufficient to induce muscle hypertrophy.

Moving further down the pathway we find mTOR has been shown to have an important and central function in integrating a variety of growth signals, from simple nutritional stimulation to activation by protein growth factors, resulting in protein synthesis. Akt phosphorylates (or activates) mTOR and both Akt phosphorylation and mTOR phosphorylation are increased during muscle hypertrophy.

Metformin

Metformin chronically activates AMP-activated kinase (AMPK). AMPK slows liver glucose output by down-regulating expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase; in skeletal muscle, it boosts the efficiency of insulin-stimulated glucose uptake by increasing expression of GLUT-4. These effects mandate a down-regulation of insulin secretion.

The resulting reduction of liver insulin activity will suppress liver production of IGF-I while boosting that of IGFBP-1, thereby decreasing plasma free IGF-I.

Stimulation of AMPK with Metformin also interferes with the Ras–Raf–MEK–ERK pathway of IGF-I signaling by inhibiting the ability of IGF-I to activate ras and its downstream targets.

Stimulation of AMPK with Metformin also blocks the ability of the PI3K-Akt pathway to activate mTOR.

Since the Ras–Raf–MEK–ERK cascade, as well as mTOR and its downstream targets, are key mediators of IGF-I’s ability to increase hypertrophy a systemic increase in AMPK activity as brought about by Metformin will hinder the potential for hypertrophy not only by diminishing plasma levels of insulin and free IGF-I, but also by intervening in the post-receptor intracellular pathways mediated events which bring about these bodybuilding effects.

GoneForever · Nov 30, 2008

Wow, so metaformin would be a bad choice even if using real HGH. Using it will keep igf levels lower? Thats def not worth it.

As for the t3 I asked only b/c I heard the use of it helps aid in protein absorbtion. I dont know the science of it, just always used it b/c it was always recommened when on GH, but then again, anyone can recommened anything, without the science behind it nothing can be proved.

DatBtrue said:
I am not going to directly address T3.

The approach many people have is that they take a survey across the boards and then ask me the same question and always preface it by "a lot of people say" or follow up by saying "that is not what I heard."

I don't mean to be a dick but I won't participate in penis or genitalia surveys.

Instead I'm going to explain to you why your use of Metformin with CJC-1295/GHRP-6 produced less than stellar results. From this explanation hopefully you'll understand that the proper answer to the types of questions you raise are far deeper then the gaggle of penises you survey would ever believe possible. Knowledge resides deeper then surface level...so lets take a look.

By now everyone should understand how we end up with more IGF-1 as a result of administering GHRH (CJC-1295, modified GRF(1-29) & Sermorelin) and a Ghrelin mimetic (GHRP-6, GHRP-2, Hexarelin, Ipamorelin & the nonmpeptide molecules) but I'll quickly recap.

Growth hormone (GH) is produced in the anterior pituitary, and is modulated by two hypothalamic hormones, growth hormone-releasing hormone (GHRH), which stimulates both the synthesis and secretion of GH; and somatostatin (SS), which inhibits GH release in response to GHRH.

GHRPs further modulate GH release by acting at both the hypothalamus and the anterior pituitary to enhance both the release and effect of GHRH and inhibit both the release and effect of somatostatin.

Administering GHRH (in the form of CJC-1295, modified GRF(1-29) or Sermorelin) together with a Ghrelin-mimetic (GHRP-6, GHRP-2, Hexarelin, Ipamorelin & the nonmpeptide molecules) both creates and amplifies a GH pulse in synergistic fashion.

GH is naturally secreted in pulsatile bursts from the anterior pituitary gland, a pattern that is necessary to achieve full biological activity. Basal concentrations (between pulses) of GH in blood are very low. GH also feeds back to inhibit GHRH secretion and probably has a direct inhibitory effect on secretion from the somatotroph (GH-producing cells).

GH binds with high affinity to its receptor, found in tissues throughout the body, and activation of this receptor stimulates the synthesis and secretion of insulin-like growth factor 1 (IGF-1). Although 90% of circulating IGF-1 is synthesized and secreted by the liver, many types of cells, including some found in the brain, muscle and vasculature, are capable of IGF-1 production.

Binding of the hormone IGF-1 to the IGF-1 receptor (IGFR) causes potent mitogenic effects, including increases in DNA, RNA and protein synthesis.

IGF-1 binding activates the IGF-1 receptor (IGFR), a receptor tyrosine kinase (which in essence means subsequent pathway activation will be by phosphorylation symbolized below by red p). The IGFR subsequently recruits the insulin receptor substrate (IRS-1), which results in the activation of two signaling pathways: the Ras–Raf– MEK–ERK pathway and the PI3K–Akt pathway. The Ras–Raf–MEK–ERK pathway is crucial in mitosis-competent cells for cell proliferation and cell survival. However, in adult skeletal muscle, the function of the Ras–Raf–MEK–ERK pathway is less clear.

The PI3K–Akt pathway has been shown to be both necessary and sufficient to induce skeletal muscle hypertrophy.

Moving down that pathway it has been demonstrated that Akt1 activity is required for IGF-1- mediated hypertrophy, and expression of activated Akt1 is sufficient to induce muscle hypertrophy.

Moving further down the pathway we find mTOR has been shown to have an important and central function in integrating a variety of growth signals, from simple nutritional stimulation to activation by protein growth factors, resulting in protein synthesis. Akt phosphorylates (or activates) mTOR and both Akt phosphorylation and mTOR phosphorylation are increased during muscle hypertrophy.

View attachment 22880

Metformin

Metformin chronically activates AMP-activated kinase (AMPK). AMPK slows liver glucose output by down-regulating expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase; in skeletal muscle, it boosts the efficiency of insulin-stimulated glucose uptake by increasing expression of GLUT-4. These effects mandate a down-regulation of insulin secretion.

The resulting reduction of liver insulin activity will suppress liver production of IGF-I while boosting that of IGFBP-1, thereby decreasing plasma free IGF-I.

Stimulation of AMPK with Metformin also interferes with the Ras–Raf–MEK–ERK pathway of IGF-I signaling by inhibiting the ability of IGF-I to activate ras and its downstream targets.

Stimulation of AMPK with Metformin also blocks the ability of the PI3K-Akt pathway to activate mTOR.

Since the Ras–Raf–MEK–ERK cascade, as well as mTOR and its downstream targets, are key mediators of IGF-I’s ability to increase hypertrophy a systemic increase in AMPK activity as brought about by Metformin will hinder the potential for hypertrophy not only by diminishing plasma levels of insulin and free IGF-I, but also by intervening in the post-receptor intracellular pathways mediated events which bring about these bodybuilding effects.

DatBtrue · Nov 30, 2008

fourthgen said:
As for the t3 I asked only b/c I heard the use of it helps aid in protein absorbtion. I dont know the science of it, just always used it b/c it was always recommened when on GH, but then again, anyone can recommened anything, without the science behind it nothing can be proved.

T3 is in a different category. It may be used, but it is not necessary.

Thats all I'm saying. No need for science because you produce enought thyroid hormone to synthesize GH-receptors, synthesize GH and the like. Use it because you want the increase in metabolism as an adjunct to what you are doing and realize that 25mcg is sufficient to give you that metabolic bump...this may be more beneficial as the cycle goes forward.

Keep in mind what you want to accomplish on cycle as well. Running 75mcg+ may seem great to you but if you are trying to gain muscle (even on muscle building hormones) you may find yourself running in place.

Lower amounts with proper diet may help contribute to keeping fat off the mid-section while you gain muscle.

All in all sane doses of T3 can contribute to your cycle for sure. But its not going to make or break your overall results one way or the other.

Thats all there really is to it.

By-the-way the intracellular pathway blockage of IGF-1's mediated events by Metformin is a very good potential way to increase life-span (and reduce cancer-incidence). Unfortunately because Metformin acts in all tissue (including muscle) you will be greatly limiting IGF-1's positive effects.

likkayouth · Nov 30, 2008

DatBtrue said:
Keep in mind what you want to accomplish on cycle as well. Running 75mcg+ may seem great to you but if you are trying to gain muscle (even on muscle building hormones) you may find yourself running in place.

What if one only wants the accelerated recovery and fatloss benefits from elevated GH levels and/or AAS. For example, the perfect result from those would be:

subject's food intake meets the appetite increase from the peptides+/AAS
muscle mass stays the same
fat mass preferably decreases, or at least doesn't increase
strength when employing the muscles increases because of all the higher quality training sessions and the intermediate accelerated recovery.

Would adding 50-75 mcg T3 shift the results-curve to the above scenario? Would it have other, undesired, effects, like loss of strength, sleep, higher risk of injury, etc?
Would T4 be safer at dosage that compensate for the conversion rate?

Thanks

DatBtrue · Nov 30, 2008

likkayouth said:
Would adding 50-75 mcg T3 shift the results-curve to the above scenario? Would it have other, undesired, effects, like loss of strength, sleep, higher risk of injury, etc?
Would T4 be safer at dosage that compensate for the conversion rate?

25mcg of T3 is fine to help you on cycle add muscle mass. You do not need nor is it beneficial IMHO to use 75mcgs of T3 when you are attempting to build muscle.

Have you ever used T3? 75mcg will probably leave you breathy...you'll huff and puff more due to the increased metabolism...25mcg probably won't do that.

T4...what conversion rate? Tell me how you can predict exactly how much T4 will convert to T3 at any given point in time. T4 isn't safer then T3 and it is up to the body to decide how much of the T4 you provide will be converted to T3 so you lose control & predictability.

By-the-way the reason I was willing to even discuss T3 is to reiterate that it is not needed with GH or w/ GRF(1-29)/GHRP-6. Can it be used? Sure but again only to effect metabolism... Low dose to aid protein synthesis/utilization when attempting to gain muscle on cycle and higher dose if one wants to help lose fat.

likkayouth · Nov 30, 2008

DatBtrue said:
By-the-way the reason I was willing to even discuss T3 is to reiterate that it is not needed with GH or w/ GRF(1-29)/GHRP-6. Can it be used? Sure but again only to effect metabolism... Low dose to aid protein synthesis/utilization when attempting to gain muscle on cycle and higher dose if one wants to help lose fat.

I understand it is not needed. But since I have a little different goals from most, I had to ask

I'll probably experiment with 25mcg T3 per day for 2-3 weeks and evaluate how it affects the research.

GoneForever · Nov 30, 2008

Dat I read an article in LifeExtension about how Metaformin can help increase life span. Sucks that it effects IGF in muscle. So all this time people thought it was great for staying lean while on GH, really that was true to an extent b/c it blocks carb absorption but at the same time it also will slow down muscle growth. I'd much rather keep my IGF high. Looks like only time i'll be using metaformin is on those crazy days where cheat meals are just massive.

DatBtrue · Dec 1, 2008

fourthgen; said:
Looks like only time i'll be using metaformin is on those crazy days where cheat meals are just massive.

Or taking it to get back into ketosis. Or using it when you diet to reestablish "quiet periods" (i.e. periods where the insulin rise post meal is brought down so that the hormone glucagon can do its thing). There is no need to have IGF-1 jacked 24-7 when you diet.

My point which I am just not doing a very good job of conveying is that all these things are tools. Think about what you want to achieve and how best to use a particular tool such as Metformin or T3.

fourthgen; said:
Dat I read an article in LifeExtension about how Metaformin can help increase life span.

I am very disappointed in LifeExtension Magazine. They just had an issue that trumpeted an herb for weightloss. They relied heavily on unpublished research out of Cameroon that was submitted for consideration in a non-peer reviewed tertiary journal. So it is unavailable for review.

But the worst part was that they were misleading in referencing a study from the same Cameroon group that is actually available in a lesser publication. LEF when they trumpet 12+ pounds of weightloss in 30 days fail to tell you that the subjects were obese and that they were also put on 1800 calorie a day diets which were primarily fats (no/low carbs). Not only that, LEF talks about using 300mcg of the herb a day and sell their own LEF supplement based on 300mcg a day BUT this one available study used more than 3 grams per day.

Based on the way LEF presented selective facts and omitted important ones in this article (which was actually the entire magazine + their catalogue of supplements) I would be hesitant to ever rely on their presentations.

GoneForever · Dec 1, 2008

DatBtrue said:
Or taking it to get back into ketosis. Or using it when you diet to reestablish "quiet periods" (i.e. periods where the insulin rise post meal is brought down so that the hormone glucagon can do its thing). There is no need to have IGF-1 jacked 24-7 when you diet.

My point which I am just not doing a very good job of conveying is that all these things are tools. Think about what you want to achieve and how best to use a particular tool such as Metformin or T3.

Makes sense brother. I guess I have a hard on for IGF and want mine jacked all day and if dieting I could try to just keep carbs not too high on meals and use some ala to help with glucoagon but its nice that metaformin will help on those days where you just gotta eat a whole pizza. And at least metaformin is outta yah in 4hrs so, 4hrs of lower igf wont be that aweful. Dat do you ever use metaformin? Other than using it to get into ketosis if thats what you do(not my thing) what other times would you use it if you were dieting? Or even bulking?

DatBtrue · Dec 1, 2008

fourthgen; said:
And at least metaformin is outta yah in 4hrs so, 4hrs of lower igf wont be that aweful.

...and 4 hours won't hinder IGF-1. Remember we don't care about circulating IGF-1 levels too much. We only care about autocrine/paracrine IGF-1 & MGF.

These are made in the muscle cells. In fact MGF never leaves the muscle cell but acts internally. There is no MGF receptor.

As for muscle IGF-1 it is made inside the cell along with the receptor. It could (like locally produced GH) prebind w/ the receptor inside the cell and then translocate to the surface or simply make its way to the membrane and bond with a naked receptor.

This local action is way way way better and more effective then hoping some externally injected or liver synthesized IGF-1 comes floating by and binds.

So if IGF-1 & MGF are acting within muscle mediating events within the nucleus on a continual basis will it matter if for a few hours some of its intracellular action is inhibited? Probably not.

Keep in mind it is chronic or a lot of use of Metaformin or use at the wrong times that can become a problem.

On a diet THE most important thing is to keep insulin spikes from being too high (that will create fat spillover) and too prolonged. That is why you use low GI food such as Ezekial sprouted grain products, the type of barley that is low GI, sweet potatoes, lentils, strawberries, blueberries, etc. [hats off to Razor Ripped], keep feedings smaller and use fiber to slow digestion & reduce Glycemic Load to reduce the amount of blood glucose created by the meal.

In addition you add vanadyl sulfate & any GDA that you have proven (by taking blood sugar readings on your glucometer) to help remove blood glucose so as to lessen the secretion of insulin.

You space those meals three hours apart so that a lot of that time you are under the influence of glucagon and you keep total calories below what you need for the day and you will burn fat.

Use Psyllium husk powder to quiet the stomach. You can even munch on carrots w/o much impacting blood sugar during these quiet times. Coffee works as an appetite supressant but highly caffeinated stuff like espresso will actually increase blood sugar too much.

External IGF-1 is just a GDA on a diet. There is no real need for it. Expensive and a waste.

fourthgen; said:
Dat do you ever use metaformin?

Not too much. I use Vanadyl Sulfate and fiber. I manage carbs I don't usually eliminate them when I diet.

fourthgen; said:
Other than using it to get into ketosis if thats what you do(not my thing) what other times would you use it if you were dieting? Or even bulking?

It can be used after prolonged insulin use to help restore tissue sensitivity to insulin or reduce tissue insulin resistance. I don't need to do that but some might.

On a bulk I use Hum-R. (insulin).

GoneForever · Dec 1, 2008

I forgot all about vandyl. What dose do you use it at and how many times per day? Only with carb meals? I only use 300mg ala with carb meals but im gonna throw in some vanadly and up my fiber intake. Only gonna save metaformin for cheat meals or maybe high high carb up days and use it maybe in the morning ad evening but avoid it pwo area when I want IGF high.

pitbulladams · Dec 2, 2008

Dat
Quick question

Have searched but can't find details on it but know you said if using GHRP/slin then to split intake by 30mins to let GH rise.

I'm using just GH/insulin dosed AM now I can shoot these both at the same time can't I ?

Also do i need to leave any amount of time before I eat breakfast as i know some say you must wait 30mins after GH before eating ?

Cheer bro

PB

DatBtrue · Dec 2, 2008

pitbulladams; said:
I'm using just GH/insulin dosed AM now I can shoot these both at the same time can't I ?

Yes.

pitbulladams; said:
Also do i need to leave any amount of time before I eat breakfast as i know some say you must wait 30mins after GH before eating ?

Nope. GH is active straight away. GH-receptor expression will be increased immediately and the insulin is not high enough and chronic enough to effect GH-receptor translocation (i.e. movement to the cell surface). Insulin does however aid the synthesis of GH-Receptors.

GH will instigate synthesis of IGF-1 but this is not a one off. IGF-1 should already be elevated from continued GH use. Its like keeping an inflated balloon in the air by pushing it up every time if falls down to shoulder level. Each GH dose is like swating IGF-1 back up. As long as you dose GH regularly IGF-1 won't (like the balloon) hit the floor. So IMHO forum-logic concerning GH timing & IGF-1 creation is flawed.

Food won't interfere with GH's actions of binding to a receptor and mediating growth events such as IGF-1 synthesis in the liver & synthesis in muscle. But even if for some reason it were by the time you get the meal made and ingested the GH will have already binded to the receptors and initiated the first wave of events.

So you're fine doing it the way you propose.

pitbulladams · Dec 2, 2008

DatBtrue said:
25mcg of T3 is fine to help you on cycle add muscle mass. You do not need nor is it beneficial IMHO to use 75mcgs of T3 when you are attempting to build muscle.

Have you ever used T3? 75mcg will probably leave you breathy...you'll huff and puff more due to the increased metabolism...25mcg probably won't do that.

T4...what conversion rate? Tell me how you can predict exactly how much T4 will convert to T3 at any given point in time. T4 isn't safer then T3 and it is up to the body to decide how much of the T4 you provide will be converted to T3 so you lose control & predictability.

By-the-way the reason I was willing to even discuss T3 is to reiterate that it is not needed with GH or w/ GRF(1-29)/GHRP-6. Can it be used? Sure but again only to effect metabolism... Low dose to aid protein synthesis/utilization when attempting to gain muscle on cycle and higher dose if one wants to help lose fat.

Dat
Cheers for reply on Q in post above..

I know you are not going to much into thyroid meds but intrested in your post qouted here ^ i know many are not fans of T4 yet it is the preferred med for prescription !

Also seen articles on combined T3/T4 use being better the one alone, i know Armour thyroid and Thyrolar are dosed in 1 to 4 ratios.

So was considering a T3/T4 mix during my peptide use of 12.5mcg T3/50mcg T4 or 25mcg T3/100mcg T4 both being a 1 to 4 ratio.

And do know guys who measure the waking body temp (Oral or Anal) to access there core temp to sustain a normal body temp of i believe 37c or run it slightly higher for optimum weight loss !

Whats your opinion ?

Cheers again
PB

DatBtrue · Dec 3, 2008

pitbulladams said:
i know many are not fans of T4 yet it is the preferred med for prescription !

What you have to do is distinguish between physiological & pharmacological dosing and returning abnormal to normal versus taking steps to push normal to abnormal.

The medical profession is concerned with getting people healthy and as close to normal as possible. They NEVER want to dramatically elevate thyroid in a patient so that he/she can achieve cosmetic and body shape changes.

In my opinion what is best for the body is to take an approach of modifying parameters as far upstream as you can and then let the body make the adjustments downstream. The body is pretty smart and in general it knows how best to use end product hormones. Usually there is a rhythm to it often subtle that can have huge impacts on what happens after homones bind to receptors and mediate events within the cell.

I know this is far away from your original question but lets take a look at an intracellular signalling pathway that is fairly common (it is present in both GH/GHR binding as well as IGF-1/IGF-Receptor binding). I just want to quickly demonstrate to you that subtle variations in how hormones are released, in what concentrations, in the timing and in their interaction with other elements can have various impacts within different cells. Why? Because hormones and their rhythm of release provide in large part the instruction set to the cell on how it is to activate various pathways.

So as a quick prelude GHRH is not an end product hormone it is further upstream. It initiates GH release in pulsatile fashion. GH as a wave simultaneously finds GH receptors primarily in the liver where it binds (always in the same manner) and because of its 3-dimensional shape causes a slight twist in the GH-receptor root that goes into the cell, This twist brings certain molecules that make up signaling proteins into alignment, bringing these molecules into alignment triggers basic atomic interaction/covalent forces of attraction and movement of sub atomic particles such that they are "activated". Energy is transferred such that these signalling proteins can carry through cascades with other elements that collectively make up an intracellular pathway.

One such pathway is ERK MAP kinase. "ERK MAP kinase signaling plays a pivotal role in diverse cellular functions, including cell proliferation, differentiation, migration and survival." The method by which ERK is activated elicits distinct cellular outcomes. These graphs tell the story:

Here the length of time that this pathway stays active (sustained or transient) creates various & distinct cellular responses.

Here the strength of the activity that this pathway engenders (weak or strong) creates various & distinct cellular responses.

Here the location of the signaling protein, whether it stays in cytoplasm or moves to the nucleus creates various & distinct cellular responses. *

All of this to say that when you inject end-product hormones to some extent you take away the body's ability or rather its decision making power over how best to regulate tissue.

So from a medical point of view it is better to try to effect change further upstream and the let the body govern itself.

But you aren't talking about a healthful restoration or optimization when you talk about how you want the thyroid to behave. Bodybuilders want the thyroid to be overactive for periods of time to effect change within their own bodies. Overactive thyroid & increased metabolism is their sole goal and so to insure that this happens they use an end product hormone. The end product hormone is T3. It is a direct approach with a direct and predictable outcome. That is elevation of metabolism.

Now that does not mean that taking control away from the body won't have cellular outcomes that may be unhealthy. Bodybuilders seem to only focus on the question of will they "mess up" their thyroid. The answer for the most part is that the thyroid is resilient so bodybuilders call T3 usage safe.

Knowing guys that measure their body temperature to insure optimal results is an example of bodybuilders taking charge of their hormonal outcome with the sole goal being cosmetic results. The body in that instance steps aside as it has lost some of the decision making power over how it will best respond.

That is as close to an opinion as I can give on this topic.

It also may help those that are interested to visualize just what I am speaking to when I talk about "optimizing the signaling pathways" engendered by growth hormone and IGF-1.

It is not the absolute amount of hormone that is always important. Rather how that end product hormone is made to behave seems to be of most import. That is why a given level of naturally induced GH release which may result in lower GH in plasma as well as IGF-1 levels then a given level of administered synthetic GH, still might result in more growth.

* Reference - The duration, magnitude and compartmentalization of ERK MAP kinase activity: mechanisms for providing signaling specificity, Miki Ebisuya, Kunio Kondoh and Eisuke Nishida, Journal of Cell Science 2005 118 (14)

GoneForever · Dec 4, 2008

Anothy Roberts wrote some article about how t4, not t3 is crucial when using GH. Many called bs on it. I used both t4 at 100mcg and t3 at 25mcg when I was on GH in the past and didnt notice a diff at all. It was my understanding that 100mcg of T4 will just convert over to 25mcg of T3, the only diff is the t4 will stay in your system longer than t3 will, thats why I opted for t4 but I never really knew the real anwser behind it.

BadGenCD · Dec 4, 2008

Despite your studies that show that GHRH may not lead to tumor/adenoma formation, or at least can't directly link it to excess growth, I find it hard to believe that excess stimulation of the pituitary would not increase the risk of unchecked cell growth and hyperproliferation. This is like people arguing that IGF LR3 is not that risky. You have very minimal studies here that midly support your viewpoint...but this is hardly evidence definitively showing that CJC is not dangerous. It does look promising, I agree, but there are certainly major risks. I think CJC is probably best used in moderate dosages as a sort of rhGH PCT, not as a replacement for bodybuilding type GH gains.