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.
"Unchecked cell growth" & "hyperproliferation" are meaningless phrases.
Of course you find it hard to believe. You're a guy that can't even figure out how to reconstitute IGF-1. You come at me as if I owe you something which would be forgiveable if you pointed to some studies or something objective rather than "I find it hard to believe".
Do you know how fucking boring it is to read the book "Diagnosis and Management of Pituitary Disorders"? I do because I read it. Why did I read it? Because I want to know.
I've been using 2mgs/week of either CJC-1295 or modified GRF(1-29) and GHRP-6 for more than 6 months straight now. I have a vested interest in knowing. My life is valuable to me.
BadGenCD; said:
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.
What viewpoint? I presented a rather objective analysis. You are free to go read any science or medical tract you want. It does you absolutely no good to pester me.
You fail to distinguish between GHRH & CJC-1295. One has a half-life measured in minutes the other provides chronic GHRH. I have always been concerned about CJC-1295. You can read my more extensive thread at AM.
You also fail to understand that despite GHRH continously being available it does not, thanks to certain negative feeback like Somatostatin influence, provide constant stimulation.
Also my friend Bobaslaw pointed out to me that IGF-1 levels w/ CJC-1295 don't get jacked. He did so by pointing me to IGF-1 reference ranges.
My viewpoint has actually evolved from being concerned to not being concerned about CJC-1295. In addition for myself I prefer modified GRF(1-29) which eliminates (in my opionion) any such potentiality.
BadGenCD; said:
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.
Who cares what you "think". John F. Kennedy loved to talk with people about what they were experts in. If it was an ironsmith he enjoyed listening to him talk about his craft. He enjoyed it because he learned something. He didn't want to waste one single minute listening to what the ironsmith thought about Soviet-Sino relations because the ironsmith wasn't in a position to know.
You have demonstrated to me that on this topic you are not in a position to know. So I don't want to waste one single minute listening to the song playing inside your head.
Regardless, you are using a compound that is quite new and has undergone relatively very little clinical testing, notably on humans. If you want to be a guinea pig, be my guest. I'll stick with things that are tried and true.
Actually Ghrelin-mimetics and Growth Hormone Releasing Hormone are very well studied in humans. In fact Growth Hormone Releasing Hormone is an FDA approved drug called Sermorelin.
The compound with the modification of the amino-acid at the second position has also been well studied and the other modifications are not new and are safe.
So both Sermorelin and the modified version are safe in humans.
As far as albumin bioconjugates in particular the drug-affinity complex used in CJC-1295 it is fairly well studied especially in relation to an HIV drug and an insulin drug.
Yep I did...sorry about that. It looks like you have put some thought into it.
You spaced the GH & peptides properly. Low insulin in the morning w/ GH will be great if you use Hum-R and workout maybe 4 - 6 hours later. It will reduce protein degradation while you work out and your muscle bellies will be full of glycogen, plus if you are older it will help you recover.
The GH will still be in the system when you workout so the glucose disposal properties of IGF-1 will be of benefit.
The CJC or modified GRF(1-29) & GHRP-6 will help generate a bigger night pulse and deepen slow wave sleep which will help with recovery.
Dat
Sorry to dig up an old part of this topic which you have already replied to but would like your thoughts on this ?
I am using insulin along with GH at breakfast, above you advise Humulin-R 4-6 hours before workout, how with humulin-R its peak is quoted from 2-5 hours after injection.
So do you advise training on insulins peak or do you prefer to let it peak before training ?
Dat
Sorry to dig up an old part of this topic which you have already replied to but would like your thoughts on this ?
I am using insulin along with GH at breakfast, above you advise Humulin-R 4-6 hours before workout, how with humulin-R its peak is quoted from 2-5 hours after injection.
So do you advise training on insulins peak or do you prefer to let it peak before training ?
There are two peaks with Hum R. Both are over within 2.5 hours post injection. These peaks should be met with food in your system.
Insulin will still stay elevated above baseline for the next few hours. I like to eat at the 3 hour mark as well.
By the 4th hour I like to be in the gym. I keep a bottle of glucose tabs with me at all times as a precaution and may pop one every once in a while. The point is I am in no danger at this point.
I am an older guy, I like to put pressure on my fascia to try to get it more pliable and so having muscle bellies full helps that as well as helps with the lifts, but most importantly recovery is helped.
The downside though can be lower back muscle pumps. As a taller guy this can become bothersome if I squat heavy. So on those day I might wait till after 5 hours passes to let the insulin return to baseline. Sure my muscle bellies are full but not as much.
PWO I take in another administration of Hum-R.
A Phil Hernon style training routine really benefits from this protocol. I can lift 5 days straight, hitting body parts 2 to 3 times during that time period. With the insulin protocol and limiting my volume to a few exercises & sets of genuine intensity my muscles recover within 48 hours and are ready for a little more work.
So I get 2 to 3 growth events in per week...there is no time & with the compounds & food very little opportunity for catabolism...it is just about accreting muscle.
The CNS is not overly taxed by a single workout but the 2 days off for the weekened (which also includes zero insulin use) is sufficient for it to recover and start the week again.
DatBtrue your pm box if full bro. Im researching hum r and was wondering how long after the inject im not sub q can you consume protein fat meals again?
DatBtrue your pm box if full bro. Im researching hum r and was wondering how long after the inject im not sub q can you consume protein fat meals again?
First off you should always consume protein. That is a primary purpose of using GH & Insulin...to reduce protein degradation and increase protein synthesis. A sufficient pool of amino acids needs to be present.
People often refrain from eating fats in the presence of insulin. The conventional view would be no or limited fats during the time frame that involes the two peaks and limited fats during the duration of insulin elevation.
However I don't overly worry about some fat gain when I am trying to gain some size. I found for myself that it is better for muscle gain if I take in some fats right from the start. So I don't hesitate to use what someone would call shit food such as a Snickers Bar along with say tuna and oatmeal immediately PWO. For the next few hours my fat may be a bit limited and after the insulin clears my later meals include a lot of fat (primarily eggs).
Most people need to have at least 20% of their calories from fats with 25% being better when they are attempting to gain substantial muscle size.
Now if you need to really watch the bodyfat then you should consider not using Hum-R in favor of no or just Humalog in lower dose.
Nothing is EXACTLY cookie cutter. A lot has to do with knowing your body and that comes from experimentation, taking notes on how things went & why and not ever being in a hurry. What you learn this 6 months you can apply to your advantage in the next 6 months...
Humulin ? not sure of what insulin that is as always thought the prefix after humulin defined the type ! hence humulin-r like above and humulin-s (short acting) humulin-n (long acting) so wondered which type you were referring to ?
Which leads into my next question Humulin-r is not as easy for me to obtain yet i have loads of humalog, can humalog be used instead of humulin-r ?
If so how long before training would it best be used ?
I've only used humalog in the past. Too afraid to have long acting slin in me. I only did 10iu's humalog about 20min after my GH shot 3x per week. I followed the 10carbs per slin iu rule and immediately had around 100g waxy maize and then 70g whey(bcaa's,glutamine,creatine) Then 1hr-1.5hr later would follow the 5carbs per iu rule and I had 50carbs from something starchy like pasta or rice and had another 70g protien from a fast digesting meat like chicken. I would avoid fat with my pwo meal #1 and 2 and then 2.5hrs after my chicken/rice I was advised to just go back to normal eating and usually had something like 8oz steak,rice and olive oil. At that time I never had any hypo feelings and my glucose levels were pretty normal. That was usually around 4hrs after the slin shot.
ive been reading your stuff about these peptides all over the place and i cant wait to try them out. i know you have said it a few times i just wanted to double check, i want to use the cjc and ghrp6 during my pct in a few weeks but im more concerned with fat loss. would you recommend 50mcg cjc/100mcg ghrp6 at waking, pwo, prebed for fat loss.
thanks for your time and keep up the good work with the research its very much appreciated.
Humulin ? not sure of what insulin that is as always thought the prefix after humulin defined the type ! hence humulin-r like above and humulin-s (short acting) humulin-n (long acting) so wondered which type you were referring to ?
Which leads into my next question Humulin-r is not as easy for me to obtain yet i have loads of humalog, can humalog be used instead of humulin-r ?
If so how long before training would it best be used ?
I don't really like humalog for the purpose of gaining muscle mass. Most people think insulin is insulin no matter how long it acts. But that is not exactly true.
Insulin analogs have different characteristics because changing the shape of the molecule by changing amino acids can effect the degree to which it not only binds with its native insulin receptor but also determine if and to what degree it will bind to the IGF-1 receptor.
In addition at times the insulin ligand can also activate an intracellular pathway normally activated by IGF-1 WITHOUT actually binding to that receptor.
Humulin-Regular is as close as you can get to native insulin. While Humalog is an analog designed for speed of action.
Here is a quote from a journal article Novel insulin analogues and its mitogenic potential, Ivana Zib and Philip Raskin, Diabetes, Obesity and Metabolism, 8, 2006, 611–620 that will help us understand a little bit:
The effect of insulin on cells has been traditionally divided into two categories: metabolic and mitogenic. While the metabolic effects of insulin such as glucose transport and glycogen synthesis are mainly mediated through the insulin receptor, the mechanism of insulin’s mitogenic effect is not clear. It is thought that the mitogenic effect of insulin is mediated through insulin-like growth factor 1 (IGF-1) receptor stimulation and, unlike the metabolic effects, requires long-term insulin exposure.
It has been shown that overexpression of IGF-1 receptor causes mitogenic and neoplastic transformation in multiple cell lines, and elevated IGF-1 levels can cause progression of diabetic retinopathy. Therapy with IGF-1 induces proliferation in human breast cancer cells in vivo and in vitro. On the other hand, insulin receptor stimulation has also shown a ligand-induced mitogenic effect on cultured human breast cancer cells.
Because changing the structure of the insulin molecule may significantly alter both its metabolic and mitogenic activity, major concerns were raised about the safety of the insulin analogues.
Now this journal article addressed the safety aspects of several analogs being investigated which is not of concern to us. I say this because the quote is taken out of context and does not speak directly to Humulin-R nor Humalog. Rather I wanted to underscore that the sustained presence of insulin has mitogenic effects because of its engagement of the IGF-1 receptor (and pathways).
Mitogenic effects in muscle are good if you are trying to build mass. Obviously mitogenesis is not desirable in cancer cells.
This is one of the reasons why I prefer low to moderate elevations in insulin for prolonged periods of time WHEN I am in a highly anabolic state. I don't want fast acting insulin nor do I want huge insulin spikes at these times.
At other times this [long periods of elevated insulin levels] is not desirable and in fact can hinder what you are trying to accomplish.
I suppose that Humalog could be made to behave more like Humulin-R if you were to administer a second dose at the time when the first begins to wear off. If someone were to do this they really need to pay attention to their blood glucose by monitoring it through a glucose meter and be aware of the peaks and make sure to have the food in their system to meet those peaks.
I don't really like humalog for the purpose of gaining muscle mass. Most people think insulin is insulin no matter how long it acts. But that is not exactly true.
Insulin analogs have different characteristics because changing the shape of the molecule by changing amino acids can effect the degree to which it not only binds with its native insulin receptor but also determine if and to what degree it will bind to the IGF-1 receptor.
In addition at times the insulin ligand can also activate an intracellular pathway normally activated by IGF-1 WITHOUT actually binding to that receptor.
Humulin-Regular is as close as you can get to native insulin. While Humalog is an analog designed for speed of action.
Here is a quote from a journal article Novel insulin analogues and its mitogenic potential, Ivana Zib and Philip Raskin, Diabetes, Obesity and Metabolism, 8, 2006, 611–620 that will help us understand a little bit:
The effect of insulin on cells has been traditionally divided into two categories: metabolic and mitogenic. While the metabolic effects of insulin such as glucose transport and glycogen synthesis are mainly mediated through the insulin receptor, the mechanism of insulin’s mitogenic effect is not clear. It is thought that the mitogenic effect of insulin is mediated through insulin-like growth factor 1 (IGF-1) receptor stimulation and, unlike the metabolic effects, requires long-term insulin exposure.
It has been shown that overexpression of IGF-1 receptor causes mitogenic and neoplastic transformation in multiple cell lines, and elevated IGF-1 levels can cause progression of diabetic retinopathy. Therapy with IGF-1 induces proliferation in human breast cancer cells in vivo and in vitro. On the other hand, insulin receptor stimulation has also shown a ligand-induced mitogenic effect on cultured human breast cancer cells.
Because changing the structure of the insulin molecule may significantly alter both its metabolic and mitogenic activity, major concerns were raised about the safety of the insulin analogues.
Now this journal article addressed the safety aspects of several analogs being investigated which is not of concern to us. I say this because the quote is taken out of context and does not speak directly to Humulin-R nor Humalog. Rather I wanted to underscore that the sustained presence of insulin has mitogenic effects because of its engagement of the IGF-1 receptor (and pathways).
Mitogenic effects in muscle are good if you are trying to build mass. Obviously mitogenesis is not desirable in cancer cells.
This is one of the reasons why I prefer low to moderate elevations in insulin for prolonged periods of time WHEN I am in a highly anabolic state. I don't want fast acting insulin nor do I want huge insulin spikes at these times.
At other times this [long periods of elevated insulin levels] is not desirable and in fact can hinder what you are trying to accomplish.
I suppose that Humalog could be made to behave more like Humulin-R if you were to administer a second dose at the time when the first begins to wear off. If someone were to do this they really need to pay attention to their blood glucose by monitoring it through a glucose meter and be aware of the peaks and make sure to have the food in their system to meet those peaks.
So from your opinion the most effective use would be a moderate rise in insulin level 4-5 hours before a WO and then 4-5 hours post !
You can accomplish this with 2 shots of Humulin-R or at a push multi Humalog dosages (using gluco meter to get it spot on).
I know a few advocating long acting slin use (levemir etc) you posted that long periods of elevated insulin levels can hinder what we are trying to accomplish, in what way ?
Hi, hope DAT can help me (again) with this one. I have asked this before but I have had a few negative comments which have made me think again.
I am currently doing a TRT which I want to use long term. It is 100 mg Test, along with 250 iu HCG, and .25 mg Arimidex all E3D. (I was using Toremifene but have been advised against so switching to AI).
I am also using peptides which I have based on DAT's guidelines. I am taking 100 mg CJC and 250 mg GHRP6 Pre-bed and 3 iu Hygetropin PWO all on a 5/2 split.
I understand nothing works in isolation in the human body and wondered if these two separate long term cycles may interact in a negative way. I'm sure that each on there own is safe but together?? Is it possible that long term CJC can cause problems and if so, are there any warning signs to look out for? I am fairly sensitive to changes in my body so think I can pick up on most problems.
This thread is a credit to DAT and other bros who have contributed some excellent information. I am more than happy to be a guinea pig and offer my own experiences and anecdotal info but some of the proper scientific research here shows the incredible level of dedication which goes into maintaining this fantastic lifestyle we lead.
...
I know a few advocating long acting slin use (levemir etc) you posted that long periods of elevated insulin levels can hinder what we are trying to accomplish, in what way ?
On the one hand insulin at physiological levels activates the Insulin Receptor but not the IGF-1 Receptor nor the Insulin/IGF-1 Hybrid Receptor. That requires pharmacological dosing that is sustained as we talked about.
In addition insulin increases both GH production & the biosynthesis of growth hormone receptors.
Perhaps of most importance insulin presence during times of GH absence is capable of resensitizing some intracellular signaling pathways. What this means is simply this:
GH just by binding to a GH-receptor on a cell activates several signaling pathways in the cell which are responsible for growth. However when GH does this it turns on the mechanism which will eventually desensitize these pathways. These pathways need a break to resensitize.
Its kinda like they are factory workers and they get commands from GH. But after a while they get tired of hearing the "company line to increase production" so they stop working. If GH would just shutup for a while they can get their break from th GH "noise" and come back to the production line ready to produce again.
Now for some of these signalling pathways...yes they need that break BUT they need something else during that break or else when they are put back to work by the next wave of GH they still can't do much work. What they need is "coffee" and they take that coffee in the form of insulin. So the presence of high physiological to low/mod pharmalogical insulin levels is REQUIRED to fully resensitize some of these pathways.
This holds true for both the GH-GHR pathways, one of which (Stat5b) will end up signaling the creation of IGF-1 but also for an important pathway that IGF-1-IGF-1-receptor intiates that is NECESSARY for hypertrophy. That pathway is the phosphatidylinositol 3-kinase/Akt pathway
Take a glance at the following:
Signalling pathways that mediate skeletal muscle hypertrophy and atrophy, David J. Glass, NATURE CELL BIOLOGY VOL 5 FEBRUARY 2003
Here we have IGF-1 binding to a receptor and the green elements represent a positive pathway to hypertrophy. But look PI3k/Akt is crucial to carry the hypertrophy signal that IGF-1 initiated. But it is subject to desensitization like all pathways and NEEDS the presence of insulin to remain active.
On the other hand (and directly addressing your question) too much insulin for too long has negative consequences. The state of hyperinsulimia reduces the movement of those newly created GH- receptors to the cell membrane. In other words insulin helps create a lot of GH-receptors but too much insulin will hold them back from ever going to the cell membrane and being activated.
Sometimes it is not clear whether hyperinsulinemia results in an enhancement or inhibition of GH action. But if we go to various studies (most are animal models) it is clear that there is a level of insulin exposure that will actually reduce the activation of those intra-cellular signaling pathways.
Continuous insulin treatment in rat liver cells in vitro (i.e. out of the body) reduces GH binding, the number of GH-Receptors, GH-GH-Receptor induced phosphorylation of JAK2 which effects the tyrosine phosphorylation of the very important signaling pathway STAT5b.
I've never been able to exactly translate the message of these studies into a level of use in humans that would be below the threshold of hyperinsulimia. I just feel that spending the majority of the hours of the the day in a state where insulin levels are elevated with exogenic insulin administration moves you in that direction.
I do know that very large amounts of insulin IS SUFFICIENT to reduce GH-Receptor translocation during the period when insulin is spiked (which may be a short period of time) and that defeats the purpose for which I would use insulin in a bodybuilding way.
Also the concern is that tissue will become insulin resistant with chronic use and that will eventually creep one up to what could be characterised as being in a a state of hyperinsulimia even if previously those same doses did not. So breaks are probably important in that regard.
* - if we want we could just simplify everything and say "GH, IGF-I and insulin act in concert to stimulate protein synthesis. GH and IGF-I act to stimulate protein synthesis while insulin acts to inhibit protein breakdown. Thus they are synergistic in their powerful anabolic action." - Insulin, growth hormone and sport, P H Sonksen, Journal of Endocrinology (2001) 170, 13–25
So any advice for the fat loss, or should i just read the whole thing.
even though i have read it man times and still cant seem to find a straight forward answer. I would appreciate the help. any advice from anyone.
So any advice for the fat loss, or should i just read the whole thing.
even though i have read it man times and still cant seem to find a straight forward answer. I would appreciate the help. any advice from anyone.
Even if "they" call your peptide CJC-1295, they probably sold you GRF(1-29) period.
So dose it like GRF(1-29) and hit it three times a day with GHRP-6.
"Straight forward answer" okay sure.
Why can't you lose weight without growth hormone?
How old are you?
Fatloss is simple. You need to maximize the time period during the day when your body will burn fat. It won't do so in the presence of insulin or elevated blood glucose.
So buy a blood glucose monitor, prick your finger and figure out how to minimize the blood glucose spike post meal and how to lessen its duration.
Here is a hint. Use low GI foods. Construct meals with low Glycemic Load. Add fiber. Keep meals smaller and spaced out by 3 hours. Speed up the metabolism with cardio. Do cardio when blood glucose is not elevated. Don't be in a hurry and recognize that fat comes off the periphery before it comes off the core.
Growth Hormone does not melt fat off.
As my friend vadim_b1 just pointed out it is great for contest prep when you are striving for lower single digits in bodyfat...it helps keep muscle in those states.
But for a non-competitor who desires to get to 10% bodyfat GH is most definately not needed.
If you are say 40+ years of age having a youthful restoration of GH levels year around will help keep your core tighter if you have everything else in check.
But for young guys who really are just fat asses and lazy as well to think that GH will do all or even most of the work is just ridiculous. They think that they aren't lazy because they go to the gym and push a piece of iron for 30 seconds and then put it down several times. As my friend Razor Ripped has repeatedly pointed out you don't burn many calories that way.
Then all these young guy fat asses and lazy fucks to boot never ever seem to understand the use and misuse of food. So they spend way to much time looking for the magic compound that will overcome their laziness and help them get rid of their fat asses so they use Clenbuterol, T3, steroids, Growth Hormone, etc. and still they never accomplish what they want and if they do they never hold it for very long.
bmoney I'm not saying you are one of these guys but I'm asking. Are you one of these fat ass lazy fucks?
I'm sure that each on there own is safe but together?? Is it possible that long term CJC can cause problems and if so, are there any warning signs to look out for? I am fairly sensitive to changes in my body so think I can pick up on most problems.
Don't use CJC-1295 use modified GRF(1-29) and you won't need to worry about any potential pituitary problems as more fully described in my pituitary article.
Beyond the pituitary the potential problems are simply the same as those that would occur with synthetic GH, with perhaps less of a risk of prolactin fed carcinoma or other prolactin instigated/exacerbated problem. This "positive" aspect results from the 10% or so 20kDa GH. 20kDa GH is also responsible for lowering slighty the diabetogenic effect from straight 22kDA.
Nobody can insure your risks. Nor do I feel like explaining to you why mixing synthetic GH and GRF(1-29)/GHRP-6 may be less effective then running either one or the other.
Don't use CJC-1295 use modified GRF(1-29) and you won't need to worry about any potential pituitary problems as more fully described in my pituitary article.
Beyond the pituitary the potential problems are simply the same as those that would occur with synthetic GH, with perhaps less of a risk of prolactin fed carcinoma or other prolactin instigated/exacerbated problem. This "positive" aspect results from the 10% or so 20kDa GH. 20kDa GH is also responsible for lowering slighty the diabetogenic effect from straight 22kDA.
Nobody can insure your risks. Nor do I feel like explaining to you why mixing synthetic GH and GRF(1-29)/GHRP-6 may be less effective then running either one or the other.
So i guess it was a good thing that most cjc floating around was really grf. Hey dat, how do you feel about the theroy that the slowing of the natty t3 levels and rise in prolactin is less of a problem if you shoot your gh in one dose 3x per week opposed to daily mulitple times. Gavin Kane wrote this, and im just wondering if there is any science behind it, and when I think of science, I think of DAT. I ask b/c its probably not safe to run cabergoline year round if you use gh year round and thats pretty much all u can do to control prolactin.
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