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

rwxl · Apr 21, 2009

Add Insulin@5-6IU's

Hi Dat! Thanks for all the info on modified GRF(1-29) and GHRP-6. My peptides are from China and as several suppliers the "CJC-1295" was actually modified GRF(1-29) -but my supplier was honest enough to clarify this when I asked him about it. I'm on a moderate test/deca cycle since two months and just starting on week three with GRF(1-29) and GHRP-6. I'm thinking of adding Humalog@5-6IU's -I know that it's best used PWO, but if adding muscle is the primary goal would it also be beneficial to use it in the morning? I have peptides for 6 months and if you don't think that it's a very bad idea I'm planning on using them till I run out. Then switch to GH -when I've used this earlier I've injected 5IU's in the morning and 5IU's PWO ED. Would using 15-30IU's EOD be a better dosagescheme for musclebuilding?

Thanks and sorry for my english.

DatBtrue · Apr 21, 2009

anhuka said:
i have read Lyle macdonald book on bromo, there is any way you think that should be possible to restart our setpoint bodyfat wise?

it seems the pros do that ... does gh can do that ?

and what about killing fat cells ?

after reading the book on bromo it seems a good option to keep bf at aceptable levels and gain muscle but there would be other options ? maybe better options to keep hormonal levels stable on dieting or growing so one can put as mutch muscle as possible avoiding as mutch bf as possible ? with good nutrition of course

Well Lyles' book is not very scientific. But the rest of your questions go to the heart of the subject.

Is there such a thing as "set point"? YES
How is it induced? Through periods of drastic drops in negative energy balance coupled with body fat loss.

For example of how this works, the following abstract:

Estradiol has been implicated in the regulation of food intake; however, its effect seems to be exerted in a bimodal fashion. We examined whether a single im injection of estradiol valerate (E2V), lastingly effective, could induce changes in parametrial fat function that further induce a new set point of leptin sensitivity in the female rat. E2V induced severe anorexia and loss of body weight between d 4 and 12 posttreatment. E2V rats recovered normal food intake and departing body weights on wk 2 and 3 posttreatment, respectively; however, they did not reach body weights of control rats. On d 61 posttreatment, we found that unfasting E2V, vs control, rats displayed increased E2 and leptin circulating levels; reduced plasma tumor necrosis factor-alpha(TNF-alpha) concentrations; similar circulating levels of glucose, insulin, and triglyceride; and lower parametrial fat mass containing a higher number of adipocytes that, although normal in size, in vitro released more leptin.

...Our data strongly support a potent acute anorectic effect of E2 and that, after several weeks, E2 modified parametrial fat function and insulin sensitivity, protecting the organism against future unfavorable metabolic conditions. - Impact of estradiol on parametrial adipose tissue function: evidence for establishment of a new set point of leptin sensitivity in control of energy metabolism in female rat, J Piermaria, Endocrine, April 1, 2003; 20(3): 239-45.

In another study that measured Leptin & Ghrelin in Pro Bodybuilders as they dieted for a competition, Increases in ghrelin and decreases in leptin without altering adiponectin during extreme weight loss in male competitive bodybuilders, Jarek Maestu, Metabolism Clinical and Experimental 57 (2008) 221–225 they concluded,

There is also some evidence that ghrelin antagonizes leptin action at the hypothalamic level [28].

In conclusion, ghrelin concentrations significantly increase in the condition of negative energy balance that is accompanied by significant body mass loss in male subjects with initial low body fat values. However, despite continual negative energy balance and significant body mass loss, ghrelin concentrations reached a plateau beyond which there is no further increase in ghrelin.

28 - Shintani M, Ogawa Y, Ebihara K, et al. Ghrelin, an endogenous growth hormone secretagogue, is a novel orexigenic peptide that antagonizes leptin action through the activation of hypothalamic neuropeptide Y/ Y1 receptor pathway, Diabetes 2001;50:227-32

I was looking for a study that I have somewhere that measured hormonal levels and examined biological set-points in older people who went through several years of mass starvation when they were young. It was fascinating but damn it... I can't find it at the moment.

The point is that there can be set-points that change not only for the quantity of fat cells but in how they behave. Fatcells as a mass, or as a group basically act as an organism. They send out factors that communicate with peripheral tissue that effect peripheral tissue metabolism. That is why I consume macadamia oil.

The interplay between Leptin & Ghrelin or the balance between those two hormones if energy balance & fat mass is driven to extremes probably is the tip of the iceberg. There comes a point as seen in the bodybuilder study where Leptin does not decrease & Ghrelin does not increase and yet fat cells continue to shrink, fatmass decrease and perhaps fat cells die ** .

If this state is held for a period of time when energy balance is resumed and the Leptin/Ghrelin system begins functioning again we may have a new setpoint.

Please don't rely on this scientifically because is either an over-simplification or just straight-up Dat bullshit

...but seriously this is where the mind has to go to try to explain why when I, you and others drive our bodyfat down to say 7% (in men) and single digits (in women) we have a new "perceived" set point.

** - Energy deficit stimulates free fatty acid release from adipocytes (lipolysis), generating smaller adipocytes. Adipose tissue mass can also shrink due to loss of cells via apoptosis, a regulated cell death program. - Adipose cell apoptosis: death in the energy depot, A Sorisky, International Journal of Obesity (2000) 24, Suppl 4, S3-S7

NOTE to self: Go back and research adipose cell apoptosis.

DatBtrue · Apr 21, 2009

Wise Guy said:
...I wasn't specifically addressing the GH booster combo like GHRP + GHRH, but I was talking about GH levels all around.

...

This brings up a question I have for you - The GH booster combo of GHRH + GHRP, we know this stimulates pituitary output of GH......

But what else does it do? Does it boost pituitary output of other hormones possibly? Can it potentially strengthen LH pulses?

This is a big topic. I am going to mention something, side step and post on one or two things in (follow up posts) somewhat tangential for now.

First lets note a huge deficiency of this thread. We have talked about the Hypothalamus to the Pituitary (here we have lingered) and then on to GH-Receptors in the liver (where we went deep into understanding GH-Receptor birth), we have mentioned some intracellular signaling as a result of activating a receptor which leads to Stat5b pathway engendering the production of IGF-1. We have talked about levels & autocrine/paracrine growth factors and what they can do in the aged, for muscle building, for health and negative consequences as well.

But we never (except for a brief mention in my original article) talk about the neurons that are activated in the brain to induce the Hypothalamus to release GHRH & Somatostatin and all of the other precursor hormones.

Why does GHRP-6 differ from GHRP-2, differ from Ipamorelin, differ from Hexarelin, differ from the small non-peptide mimetics such as MK-677 and those developed from Ipamorelin? After-all they all belong to the same class known as GH Secretagogues or modulators of GH release. They all are capable of binding to the primary GH-Receptor (there is at least another sub-type).

They differ in regard to the neurons that they stimulate in the CNS. For instance GHRP-6's action in the Hypothalamus (not the pituitary ...these are two different actions) is not all about stimulating neurons that will increase GHRH. Nope... only 25% of GHRP-6's actions do that.

Now the small molecules such as MK-677 are more highly specific in the neurons they stimulate.

So you can say that the peptides are sloppier. But in being sloppier they are more closely related to Ghrelin and can exert a whole host of positive effects, or effects that in some circumstances are negative I suppose, or just neutral effects ...all depending on how we look at it.

For instance Dat? Well did you know that milligram doses of GHRP-6 as opposed to microgram doses actually exhibit an opposite effect in regard to GH release? Because GHRP-6 also stimulates other neurons at high dose somatostatin (the inhibiting hormone) can rise and overcome the concurrent stimulated rise in GHRH.

Anyway I am leaving off for now because I intend to now more sharply focus on this area and also deleve into the latest research on oral secretagogues.

Now the two follow up posts below will be a bit unrelated:

- One, GHRP-6's non-GH releasing effect of increasing GH synthesis and reload of stores in the somatotrophs (i.e. GH releasing cells in the pituitary).

- Two, GHRH's demonstrated positive effect on memory in the aged.

DatBtrue · Apr 21, 2009

GHRP-6 Releases & Reloads GH (i.e. synthesizes it)

I was reading a very important study * that is so technical it isn't worth quoting from.

Basically GHRP-6 and Ghrelin stimulate voltage changes within Somatotrophs (GH releasing cells in the pituitary). Ghrelin and GHRP-6 increase the firing frequency of spontaneous action potentials (SAP) in those cells and stimulate High Voltage Activated Ca2+ current density.

This has the effect of increasing the synthesis and release of GH. This is very important because we are talking about GHRP-6 not just adding to GH release but causing the synthesis or making of GH to be stored in the somatotrophs for further release. GHRP-6 acts to reload the GH chamber so-to-speak.

GHRP-6's effect on these voltage changes probably remain for a period of time...a week or two...after chronic exposure (or constant use) is stopped. This is probably one of the reasons why we continue to have optimal GH release for a few weeks post GHRP-6.

Anyway I just wanted to post this because I get tired of people thinking GHRP-6 because it is less expensive (or isn't as sexy) is something that you can forgo in favor of CJC-1295. Or just as bad people looking at other things to suppress somatostatin when GHRP-6 does that properly and so much more...such as synthesizing GH. Let me see you do that Huperzine A!

* Up-regulation of High Voltage-activated Ca2+ Channels in GC Somatotropes After Long-term Exposure to Ghrelin and Growth Hormone Releasing Peptide-6, Belisario Dominguez, Cell Mol Neurobiol (2008) 28:819–831

DatBtrue · Apr 21, 2009

ANTI-AGING: GHRH - Memory

Anti-aging

GHRH - Memory

Growth Hormone supplementation has been shown to improve the age-related decline in certain memory function. Bennett et al, in a study the full text of which is not readily available to me, have demonstrated the effectiveness of GHRH (modified at the 2nd amino acid position) in this regard. An effectiveness identical to those GH memory studies reviewed by Nyberg. This is exciting because it involves an analog of GRF(1-29) which moves us from Sermorelin toward the analog we use modified GRF(1-29) which is modified at the 2nd position as the one used in this study (w/ 3 other additional amino acid modifications)

The Bennett study is described in Handbook of The Biology of Aging, Sixth Edition, Editors Edward J. Masoro and Steven N. Austad, Academic Press 2006:

[P]revention of the age-related decline in growth hormone pulse amplitude and plasma IGF-1 by daily injections of [D-Ala2]GHRH for 18 months ameliorated the age-related decline in reference memory. In this latter study, performance of old animals treated with [D-Ala2]GHRH to raise growth hormone and IGF-1 levels was indistinguishable from that of young animals on the reference memory task. The improved performance in older animals appears to be associated with increased hippocampal glucose metabolism and NMDA receptor density (specifically NMDAR2a-c) (Bennett et al., 1997), an effect that can be mimicked by peripheral injections of growth hormone (Nyberg, 1997).

Bennett, S. A., Xu, X., Lynch, C. D., & Sonntag, W. E. (1997). Insulin-like growth factor-1 (IGF-1) regulates NMDAR1 in the hippocampus of aged animals, Society for Neuroscience Abstracts, 23, 349.

Nyberg, F. (1997). Aging effects on growth hormone receptor binding in the brain, Experimental Gerontology, 32, 521–528.

For those interested in this decade old Nyberg review here is the section which maintains relevance today:

...The possible function of GH receptors in other brain areas such as hippocampus, amygdala, and putamen is poorly understood. However, with regard to the GH binding sites present in, for example, hippocampus, it has been speculated that they may mediate effects on cognitive functions and memory, on motivational, and attentional mechanism. Previous studies have shown that all these dimensions may be affected during GH therapy leading to improvement in life quality (Mc Gauley, 1989; Bengtsson et al., 1993; Burman et al., 1995).

AGING EFFECTS ON GROWTH HORMONE RECEPTORS IN THE CNS

During the past decade a number of studies suggesting that aging may affect the content of neurotransmitter or neurohormone receptors in the brain. For instance, an age-related decrease in the binding to dopamine D1 receptors in frontal cortex and striatum was reported (Suhara et al., 1991). A similar observation was earlier reported for the dopamine D2 receptors (Creese et al., 1981). Also with regard to the content of opioid (Messing et al., 1981; Ueno et al., 1988) and adrenergic (Cimino et al., 1984) receptors an age-dependent reduction has been found.

We have recently observed an effect of aging on GH binding in the human and rat brain (Lai et al., 1993; Zhai et al., 1994; Nyberg and Burman, 1996). In the human brain we found a significant negative correlation between the density of hGH-binding and increasing age. This observeration was confirmed in several distinct brain areas including the choroid plexus, the hippocampus, the hypothalamus, the pituitary, and the putamen. The study was done with brain tissues collected from deceased subjects of both sexes with age between 40 and 90. The decline in GH binding with increasing age was evident both in male and female tissues. In most brain regions the decrease in binding density became obvious between 60 and 70. Between 40 and 60 years of age the level of GH binding remains unaltered (Lai et al., 1993). No data about GH binding before an age of 40 or in younger subjects are yet available.

In the rat brain (Zhai et al., 1994), however, it was possible to observe an increase in GH binding during the first weeks of life. The level of GH binding reaches a maximum around week 12 in most rat brain regions, after which it declines (Zhai et al., 1994). In certain CNS tissues, i.e., the spinal cord, the maximum of GH binding was observed earlier in the rat life.

The molecular mechanism behind the reduction in GH binding sites in the brain is still not clear. It is likely that this decline accounts for a general neuronal degeneration. For instance, data obtained in a previou study on age-related decrease in dopamine receptor density suggested that at least half of the receptor decrease could be explained by neuronal loss (Roth and Joseph, 1994). The remaining part of dopamine receptor loss was found to account for a reduced rate of receptor biosynthesis at the gene expression level (Mesco et al., 1991). We recently confirmed an age-related reduction in the expression of GH receptor mRNA in the human choroid plexus (Lai et al., unpublished). This decline, which was observed in both sexes, may also be explained by a decrease in the receptor biosynthesis and contribute to the observed reduction in GH binding.

The physiological consequences of the GH receptor downregulation in the CNS may be related to several of the impaired functions seen during aging. For instance, in GH-deficient adults common complaints before hormone therapy have been related to tiredness, low energy, lack of concentration, memory difficulties, and irritability (Bengtsson et al., 1993; Nyberg and Burman, 1996). As mentioned in the introduction, during GH treatment improvements have been observed in certain cognitive functions, in emotional reactions, in energy level, mood, and vitality (Mc Gauley, 1989; Bengtsson et al., 1993; Burman et al., 1995). The involvement of GH and its CNS receptors in learning processes and memory functions have been supported by studies where the hormone has been given to rats. It was thus shown that GH modulates both the long-term memory and the extinction response as recorded in a behavioral animal test (Schneider-Rivas et al., 1995). The hormone was found to facilitate long-term memory in young but not in old rats. Regarding the extinction response, the hormone was found to retard the extinction in young rats as well as in aged rats (Schneider-Rivas et al., 1995). It was further suggested that GH may induce its effects on memory and other cognitive functions by affecting the levels of somatostatin (Schneider-Rivas et al., 1995). This peptide was earlier found to influence modulatory processes of learning and memory (Alvarez and Cacabelos, 1990).

CONCLUSION

It appears evident from studies reviewed in this article that a previously observed decline in plasma concentration of GH with increased age is accompanied or paralleled by decreased density of GH binding sites in the brain. The consequences of this decrease may be related to impairments in many CNS functions suggested to be connected to the hormone and its receptor, i.e., functions associated with quality of life. The mechanism behind the observed downregulation in GH binding is still unclear, and further studies necessary to carry out for its clarification will be a challenge for future research.

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WC114 · Apr 22, 2009

Dat in previous post you talked about MGF enhancing longevity, I assume that would only apply to what the body can produce, would there be any benifit longevity wise to add MGF?

anhuka · Apr 22, 2009

thanks dat.

since i started the cjc and ghrp 1 week after ive done some blood work an my prolatin and cortisol are a little over the normal range , i dont really know if it was like that before since my T is way to the down side, can it be from the pepetides? i know that you all ready mention on this thread that the pepetides can make prolactin and cortisol to go a little up but still in the normal range , so i wonder...

any ideia on how to lower it and keep in the normal range while on the pepetides? l dopa? b6?

DatBtrue · Apr 22, 2009

WC114 said:
Dat in previous post you talked about MGF enhancing longevity, I assume that would only apply to what the body can produce, would there be any benifit longevity wise to add MGF?

On the first page, in the second post is a rough draft of an index for pages 1-26 of this thread.

One of the headings is Mechano Growth Factor (MGF)

Under that heading is a link to post # 349 - MGF will not behave as MGF when injected

Now what happens in the aged is that resistance exercise does not increase the expression of MGF the way it does for the young. The elderly are especially vulnerable because weight training does not have as much muscle building effect as it could & should, but for the lack of MGF expression.

MGF will not specifically benefit longevity (i.e. an increase in lifespan). Rather it contributes to the maintainence/acquisition of muscle mass which for example contributes to the speed of being able to extend your leg after you trip to prevent a fall.

One point that I have tried to drive home in this thread on this subject is that GH levels contribute to increasing MGF expression. Testosterone contribute to MGF expression. GH + testosterone contribute to MGF expression. IGF-1 administration inhibits GH & testosterone in their quest to increase MGF expression.

See the chart at: http://www.professionalmuscle.com/forums/showthread.php?p=458404

But the element of time is important! In the post that preceded the chart post I just gave you, you can see that 2 weeks was not enough BUT from the following link we can see that 12 weeks DID increase MGF mRNA levels (that means MGF is being synthesized).

http://www.professionalmuscle.com/forums/showthread.php?p=458400

Now in specific regard to expanding lifespan. Insulin & circulating IGF-1 levels need to be low, because certain elements of the intracellular pathway are activated and they can accumulate cellular damage over time...

So my hope is that somehow we can activate autocrine/paracrine growth factors for neuronal health & muscle maintainence for example selectively, when needed. This would include MGF or in the alternative maybe FGF-2.

So far we see that increasing GH increases both circulating IGF-1 and autocrine/paracrine actions so what we have with GHRH/GHRPs doesn't get us what we seek for lifespan extension.

BUT guess what? GHRH/GHRP pulsation is far better then the chronic use of synthetic GH because it has the same or better impact on autocrine/paracrine factors but less on systemic circulating IGF-1 levels. Better how? Better for health & maybe longevity... if being a mass monster is your goal then all bets are off.

Anyway WC I don't mind answering your questions and pointing to links in this thread because you have made an effort to read some of my posts. ...and I ENJOY interacting w/ such people in part BECAUSE you educate me with your intelligent questions ...seriously. So thank you.

But when I post a comment on the main forum I sometimes get a PM saying "you seem to know what you are talking about. So tell me how much GH do I need to take and for how long before my 50+ year old body can grow arms again."

Actually that was a PM from ToughOldMan yesterday and for some reason I resent PMs like that. But pleasantly I pointed him to my thread and I will be happy to interact with him after he has read something.

But boy do I resent that... I had even posted a link to this thread in his thread on how can I at my age get my arms to grow again and told him he needed to increase MGF expression and 3 grams of Leucine post-exercise.

Anyway whatever? His answer is so conveniently given in this post right here.

If he reads this then I will erase this part of the post.

DatBtrue · Apr 22, 2009

anhuka said:
thanks dat.

since i started the cjc and ghrp 1 week after ive done some blood work an my prolatin and cortisol are a little over the normal range , i dont really know if it was like that before since my T is way to the down side, can it be from the pepetides? i know that you all ready mention on this thread that the pepetides can make prolactin and cortisol to go a little up but still in the normal range , so i wonder...

any ideia on how to lower it and keep in the normal range while on the pepetides? l dopa? b6?

Yes it can come from the peptides.

Some people are sensitive to even small increases. Most are not...

But that is why I am going to pull the research on Ipamorelin and see if I can't get a wholesaler to synthesize it. The cost should be about the same as GHRP-6. Ipamorelin has no impact on prolactin & cortisol.

Countering it?

I use 250 mg of Mucuna pruriens, 40% L-Dopa every other day. L-dopa isn't safe to use for longer periods but Mucuna pruriens have constituents that metabolize L-Dopa in peripheral tissue and so it does not accumulate there...

It is inexpensive. I get it from here Beyondacentury for less then $15 for a year supply.

DatBtrue · Apr 23, 2009

rwxl said:
...I'm thinking of adding Humalog@5-6IU's -I know that it's best used PWO, but if adding muscle is the primary goal would it also be beneficial to use it in the morning? I have peptides for 6 months and if you don't think that it's a very bad idea I'm planning on using them till I run out. Then switch to GH -when I've used this earlier I've injected 5IU's in the morning and 5IU's PWO ED. Would using 15-30IU's EOD be a better dosagescheme for musclebuilding?

Probably information that can be helpful to you has been discussed and indexed in post #2 of this thread.

On page 1 I wrote the following as an intro. It doesn't mean that I will not be helpful. But it does does mean that I won't answer such questions. I think there is enough material here to answer your own questions ...and if you think I am unfair because it appears I have answered such questions in the past, I apologize.

From post 1 posted today:

The author of this thread is DatBtrue. He is an independent unaffiliated researcher. His posts and answers to questions are based on research of full text scientific and medical journal articles, reviews, studies as well as other relevant source material.

He has no economic interest in anything he writes about. He is just a gentleman whose curiosity & inquisitiveness has happened to spill over into this thread.

Although this site centers on bodybuilding, that is the least of his interests. He is primarily interested in the following and so the thread reflects these interests:

Anti-aging - which means if you are near 40 years of age or older a youthful restoration in the form, function, health & well-being of the vessel you inhabit.
Longevity - which means alternate-day fasting as a means to trigger those intracellular events that reduce the rate with which we age, incidence of disease and protection from things gone awry.
Skeletal Muscle - Maintaining it, acquiring it and displaying it in a manner that is healthy.
Health, health & health.

*** Although much inquiry pulls this discussion toward bodybuilding, and I believe that in order to understand we must explore and discuss without limit, I DO NOT advocate NOR do I advise the use of substances and protocols that can be harmful.

For instance pharmacological doses of most things can be harmful in the long-run. As an example this thread may discuss the science of insulin & anabolism but insulin use triggers intracellular events that can add to aging and reduce longevity.

This is not some bullshit disclaimer. If you are under the age of 21 I will not interact with you (other then to tell you if you are endangering yourself). If you are an adult I will only discuss the science. To the extent that a reply appears as advise, please understand that THAT is not my intent.

I am not a doctor of medicine and everything discussed herein is meant solely to share science and explore ideas and really cool stuff that nobody gives a damn about sharing with those beyond the cloister. - DatBtrue

Latest News

4/22/09 - We are discovering that synthetic GH can be used together with GHRP/GHRH in a protocol
4/22/09 - Thread is slowly being indexed a rough draft can be found below
4/22/09 - The GH comparison article needs to be rewritten to take into account GH's increasing impact on IGF-1 beyond 24 hours. The article as is provides a good comparison for GH in plasma between GH & CJC-1295 administration however the article fails to demonstrate that GH is a superior elevator of systemic IGF-1 levels (although autocrine/paracrine IGF effects are probably superior with GHRH/GHRPs)

WC114 · Apr 23, 2009

I remember about MGF acting as a superior IGF as far as growing muscle goes, I just wondered if it ever acted as MGF maybe through another pathway, or on different tissue,and how much of an impact it has on longevity. Anyway Dat thanks for posting and clearing that up, I think I need to go back and read the whole thread again.

anhuka · Apr 23, 2009

thank you so mutch dat very helpfull like always

Quad-smack · Apr 23, 2009

DatBtrue,
In your opinion, what would be a good metabolic enhancer for someone experimenting with GHRP-6 & GHRH mod-(1-29)? From what I understand, caffeine inhibits mTOR and increases plasma FFA. Both of which would be counter-productive, am I correct?
It's hard to find a caffeine-free metabolic enhancer that actually works. What about Ephedra?
Thank you in advance.

DatBtrue · Apr 24, 2009

Quad-smack said:
DatBtrue,
In your opinion, what would be a good metabolic enhancer for someone experimenting with GHRP-6 & GHRH mod-(1-29)? From what I understand, caffeine inhibits mTOR and increases plasma FFA. Both of which would be counter-productive, am I correct?
It's hard to find a caffeine-free metabolic enhancer that actually works. What about Ephedra?
Thank you in advance.

Metabolic enhancers....hmmmmm. Please don't tell me I need to give up my coffee... "you can take my coffee away from me only when you can pry it from my cold dead hands"

Well my friend if you are trying to lose bodyfat then you want to take advantage of GH's increase in lipolysis. What is lipolysis?

According to Wikipedia it "is the breakdown of fat stored in fat cells. During this process, free fatty acids are released into the bloodstream and circulate throughout the body."

According to Dat it "is the breakdown of fat stored in fat cells. During this process, free fatty acids are released into the bloodstream and circulate throughout the body."

So circulating free fatty acids are occuring and it is your job to maximize beta oxidation (or the extent to which they will penetrate the cell and be broken down in the mitochondria ...to generate acetyl-coa which enters the Krebs cycle). "Burn off" the fatty acids so to speak.

So you do that by being active during this time period & by not eating (or taking huge amounts of caffeine/stimulants/ephedra) which can raise blood glucose and thus insulin. Anything from not just sitting at a desk to actively performing cardio will fulfill your responsibilities.

If you have plenty of money you can load up on L-carnitine to help in the transport...

But better yet is to maximize FFA mobilization and couple that with cardio.

You can maximize FFA mobilization or lipolysis by increasing GH.

One thing I am experimenting with is administering GHRH/GHRP to create a GH pulse. Twenty minutes or twenty-five minutes later adding 1iu of synthetic GH. This so far (limited experience so far) seems to greatly amplify that GH pulse...which increase the FFAs in my blood stream...

...which then makes me go do some steady state cardio for 1 hour or more while listening to my Assimil French lessons...

...followed by not eating immediately after words during the remaining time that GH is active.

The cost of administering just 1iu of synthetic GH once a day on top of the GHRH/GHRP pulse is really low... but I am conjecturing gives you more bang for the buck then trying to find the "metabolic enhancer" which as I pointed out can also interfere with lipolysis.

EasyEJL · Apr 24, 2009

DatBtrue said:
If you have plenty of money you can load up on L-carnitine to help in the transport...

Since you mention it... what sort of dose of IM l-carnitine would you think it would take? 400-600mg/day? all at once or spread?

DatBtrue · Apr 24, 2009

Apology accepted Beefy.

TripDog · Apr 24, 2009

cjc flush

Dat whats up bro, amazing stuff here. I just shot the cjc I have and got a wicked flush. Is that common with modified, or could that actually be long acting cjc? Dude says in bold letters on his site THIS IS LONG ACTING .

DatBtrue · Apr 24, 2009

TripDog said:
Dat whats up bro, amazing stuff here. I just shot the cjc I have and got a wicked flush. Is that common with modified, or could that actually be long acting cjc? Dude says in bold letters on his site THIS IS LONG ACTING .

I think from that particular retailer you have the modified GRF(1-29).

You caught that retailer at a period of time when he has solid GHRP-6 and GRF(1-29). You're lucky.

His previous batch was poor quality ...even by his own admission. But that didn't stop him from then selling the remainder in 50mg batches w/o disclosing what he admitted to me & a few others. He said he needed to raise money and the next batch would be top quality. He acquired that from someone who had a batch leftover from before he went out of the peptide business.

That is the batch you probably have now. What about the next batch & god forbid if he relapsed into his previous substance abuse problems. I hope not.

BigTex · Apr 24, 2009

DatBtrue said:
His previous batch was poor quality ...even by his own admission. But that didn't stop him from then selling the remainder in 50mg batches w/o disclosing what he admitted to me & a few others. He said he needed to raise money and the next batch would be top quality. He acquired that from someone who had a batch leftover from before he went out of the peptide business.

DAT, this story sounds very familiar. If this is the same person, he mentioned this same story to me. I guess he didn't realize I had just made a purchase from him after we talked. More than likely got some of the bad batch without being told. Exactly why I have gone elsewhere. Nice guy but........

DatBtrue · Apr 25, 2009

GH + GHRH/GHRP

This is a response to Myosin's post in another thread but I thought it best posted here.

Although the first 90% of my thread doesn't reflect it ...my current thinking is that both the GHRP/GHRH can be run with synthetic GH at low dose.

Experiments so far with 100mcg GHRP-6 + 100mcg GHRH wait 20 minutes and administer 1iu of GH has demonstrated that GH used this way does not hinder a later pulse created with just the GHRP-6/GHRH alone.

Current experiments are identical to the above w/ 2iu instead of 1iu.

I suspect that will be okay as well.

I suspect also that this can be done multiple times a day if one chose, maybe even every 3 hours around the clock.

It is the beginning of something I feel could be a beneficial option for bodybuilders & bodysculpters but also an adjunct therapy for the GH deficient (who respond to the GHRH/GHRPs) and also for those that want higher GH levels w/ some of a blend of natural GH.

Remember natural GH release is made up of about 10% of a variety known as 20kda. This GH is just as anabolic w/o the ability to interact w/ the prolactin receptor. In some reports natural GH has less of a negative impact on fasted morning blood glucose readings then does the synthetic 22kda form.

So for some they may desire a blend.

Lucian reported last year that using 2iu of GH per day w/ two 250mcg dosings of GHRP-6 per day and 1mg of CJC-1295 (split into 2 dosings) felt like around 8 to 12iu of GH.

See: http://www.professionalmuscle.com/forums/showthread.php?t=39014

So it may be possible to do more by expending less financial resources across the trilogy.