Dat's "best" way to use IGF-1 LR3

[DatBtrue]

I have mentioned micro-dosing IGF-1 LR3 over an area with more frequency and entry points for healing...

But people don't realize that it is also a way you create more IGF-1 in local tissue for growth. Why do 99% of the people want to do one big injection of IGF-1 LR3? It will go systemic meaning the molecule is so small and it is water loving so it is actually pulled toward the nearest capillary where it is small enough to penetrate the vascular wall and enter the blood stream. The larger the dose the more circulating IGF-1.

If you take a tiny insulin needle and micro dose a bunch of tiny doses over the muscle more will be taken up locally. Only a little bit will bind to a nearby receptor anyway before being sucked away to circulate. So why waste it? Why not go for a wider area of coverage?

If you take your 50mcg daily dose and administer 1.25mcg in 10 areas covering a square inch or two on the muscle on one side and then the other side and come back later that day and do the same thing in the same muscles YOU WILL BENEFIT far more then the all at once protocols.

By-the-way I am not recommending IGF-1 LR3. I am just saying if people are determined to use it they might as well try to get the most out of it.

 

[MrCyp]

I didnt think you were a big fan of IGF dat. Im curious to see if anyone gets some localized growth this way. Sounds interesting.

 

[chavo]

IGF-1 causes localized growth via MGF if I am not mistaken.

MGF is a variant splice off IGF-1.

 

[weltweite]

Just to add to this thread, I'm going to be starting this later this month to attempt a recovery on a torn bicep

 

[PsyT]

DAT,

would you change anything to the protocol if a person was using it in conjunction with PCT (to speed recovery)? I'm definitely going to try to scrape enough money together to grab a milligram of IGF...I was thinking everyday injections like you are mentioning...now I'll think about this micro injecting thing if you think that will still give me the PCT benefits...?

 

[DatBtrue]

I didnt think you were a big fan of IGF dat. Im curious to see if anyone gets some localized growth this way. Sounds interesting.

I'm not a big fan. But one of the things I have circled to do eventually is determine how much IGF-1 will cause proliferation and how much will cause differentiation.

Low dose causes differentiation. So if a bunch of IGF-1 is circulating from a IGF-1 LR3 administration it is likely to end up being a low dose ( a few drops in a big pond) and thus be a differentiator in local tissue where it will be taken up some.

The trick is to try to get it to proliferate. So if you can make more of it stay local, that tiny bit will probably be a high dose to local tissue. Thats all.

 

[DatBtrue]

DAT,

would you change anything to the protocol if a person was using it in conjunction with PCT (to speed recovery)? I'm definitely going to try to scrape enough money together to grab a milligram of IGF...I was thinking everyday injections like you are mentioning...now I'll think about this micro injecting thing if you think that will still give me the PCT benefits...?

Keep in mind insulin works well in PCT as a poor man's IGF-1. I recommended this to EDED last year and he can attest that it works.

If you use IGF-1 LR3 in PCT all you want to do is take it everyday for 3 weeks. How you take it doesn't matter because no matter what most will go systemic and work to help recovery.

So the trick is IF you are going to take it you might as well try to take it in a way that can help you with potential muscle building.

 

[PsyT]

THANKS! One more question...would you recommend mixing IGF and insulin at the same time? I'm thinking insulin humulin R 3IU 1 hour before working out followed 10 minutes later by sipping on a high carb(75g dextrose)/creatine/beta alanine drink. Then after workout some fruit juice and whey protein and a shot of IGF (25ug split bilaterally). Then an hour after that a complete meal with rice/meat/veggies.

Then before bedtime to round things out, 200ug GHRP6 and 100ug CJC1295.

Am I thinking safely here?

 

[Agent]

THANKS! One more question...would you recommend mixing IGF and insulin at the same time? I'm thinking insulin humulin R 3IU 1 hour before working out followed 10 minutes later by sipping on a high carb(75g dextrose)/creatine/beta alanine drink. Then after workout some fruit juice and whey protein and a shot of IGF (25ug split bilaterally). Then an hour after that a complete meal with rice/meat/veggies.

Then before bedtime to round things out, 200ug GHRP6 and 100ug CJC1295.

Am I thinking safely here?

That's about what I do. 5iu/50ug/200ug/200ug humulin R/LR3 IGF-1/GHRP-6/CJC-1295 in one syringe, shake and inject bilateral delt. I think I'll start injecting a 1/6 in each anterior, posterior, and regular delt.

 

[EDED]

Keep in mind insulin works well in PCT as a poor man's IGF-1. I recommended this to EDED last year and he can attest that it works.

If you use IGF-1 LR3 in PCT all you want to do is take it everyday for 3 weeks. How you take it doesn't matter because no matter what most will go systemic and work to help recovery.

So the trick is IF you are going to take it you might as well try to take it in a way that can help you with potential muscle building.

oops, just saw this

YES, thats correct sir! aahhahha

not alot either,

as for this pin cushion igf lr3 method,,,talk about pin cushion! i wonder if i can dose it like that eod since lr3 is longer acting?

 

[DatBtrue]

..

as for this pin cushion igf lr3 method,,,talk about pin cushion! i wonder if i can dose it like that eod since lr3 is longer acting?

No, no, no....

Attempts to Localize IGF-1 in Muscle

Remember a year a ago I wanted someone to carry the ternary complex?

The ternary complex is composed of IGF-I or IGF-II, IGF-binding protein-3, and the acid-labile subunit. IGF-1 alone or unlike binary complexes of IGFBP-3 and IGF-I can leave/or go into the circulation across the endothelium (surface of blood vessels) because they are small enough.

However ternary complexes because of their size are restricted to the circulation. They act as a relatively stable reservoir of circulating IGFs. Under certain circumstances IGFs are liberated from the ternary complex to exert their biological actions in tissues.

BUT if you remember I wanted to administer the premade ternary complex into muscle tissue. There it would not be trapped in circulation but trapped locally in muscle tissue. Now IGF-1 has a stronger attraction (affinity) for its receptor. If it is hanging around via the ternary complex i will disassociate and bind to a receptor when one is available.

If you recall we talked about how a drug company makes the ternary complex and how it is more effect for certain illnesses then exogenous IGF-1.

The problem is I could not get anyone to make and offer it. I even went so far as say make the IGF-1 bound to the binding protein and the GHRPs via GH will make plenty of acid-labile subunit which will bind immediately on injection.

But it never happened.

Second Best

So IGF-1 LR3 is a modification of native IGF-1. When you make the modification it loses most of its attraction to the binding proteins but it also has a reduced attraction to its own receptor. Think "weaker magnet".

We also know that upon injection it will circulated systemically. This means it won't stay local and what it will do is float around and bind where there are the highest concentration of receptors. This is the intestines.

If you recall this was a very good thing for me. It saved my life. A lot of the IGF-1 LR3 that I administered many years ago bound to receptors in my intestines and regrew the lining and greatly repaired it ability to absorb.

That was great for me but not so great if you want it to be taken up in muscle. I healed but the IGF-1 LR3 had no effect on increasing my muscle weight or mass.

So if people are administering IGF-1 LR3 it will circulate and bind everywhere but the concentration won't be high when some of it is taken up in muscle.

How Much IGF-1 is needed?

IGF-1 is made in the liver and circulates and it is made in local tissue. From the liver the amount is larger and measurable. From the muscle (or local tissue such as brain & bone) the amount that is made is super-tiny. It is not measurable w/o an expensive experiment. But that little bit is very powerful.

Experiments have demonstrated that mice can grow to full length w/ that tiny local made IGF-1 in muscle and bone, but if that is shutoff the liver-made circulating IGF-1 is never enough to make them grow to full size.

So the trick is to either increase local expression of IGF-1 in muscle. That is done w/ the GHRHs and GHRPs and GH and testosterone ...but ironically IGF-1 LR3 given at the wrong time hinders this local expression.

Now if you want to use IGF-1 exogenously you need to try to make it stay local and you don't need a lot. But you want wider coverage because you are doing all of this from outside looking in.

Micro-dosing IGF-1

So this protocol is an attempt to do what was originally hoped for... that is to make some of the IGF-1 bind to available receptors locally BEFORE traveling into the blood stream.

Anything more then a small amount is a waste because only the cells it will come in contact w/ and neighboring cells who can "pass on" the IGF-1 will be effected.

The method requires you the administrator to seed a wider area w/ tiny amounts of IGF-1 LR3 which will have the result of more cells positively benefiting.

The reason this is done twice a day is to hit more cells. It may seem like a lot of work but people who have used this approach to heal a local injury have found it effective.

 

[DatBtrue]

THANKS! One more question...would you recommend mixing IGF and insulin at the same time? I'm thinking insulin humulin R 3IU 1 hour before working out followed 10 minutes later by sipping on a high carb(75g dextrose)/creatine/beta alanine drink. Then after workout some fruit juice and whey protein and a shot of IGF (25ug split bilaterally). Then an hour after that a complete meal with rice/meat/veggies.

Then before bedtime to round things out, 200ug GHRP6 and 100ug CJC1295.

Am I thinking safely here?

Blood Glucose monitors give you the answer. I have administered both at the exact same time and taking BG readings and then the next day just one of them and taking readings (keeping everything else constant). The IGF-1 LR3 when added to insulin made the blood glucose readings a little more erratic but did not pull glucose levels down a lot over insulin alone.

IGF-1 PWO?

If you can make IGF-1 proliferate then okay but normally if differentiates. When you introduce a differentiator suddenly all of the proliferation stops and the differentiator goes about turning satellite cells into end product cells (myotubes).

For an elaboration and thorough understanding see my thread "Fibroblast Growth Factor (Secrets!!!)" in the Body Transformation > Muscle Acquisition section of my private forum.

 

[123cctv]

...but ironically IGF-1 LR3 given at the wrong time hinders this local expression.

Dat, at twice a day -- do you have any suggested times that you'd consider to be the *lessor* evil? Morning, eve, meals, PWO, etc?

Further, there's people who pin GHRP's/GHRH/GH together with IGF to which I believe is a complete waste as IGF-1 destroys GH. In other words, would you separate the pinning of each (if taking both GH and IGF) by several hours?

Thanks!

 

[PsyT]

Blood Glucose monitors give you the answer. I have administered both at the exact same time and taking BG readings and then the next day just one of them and taking readings (keeping everything else constant). The IGF-1 LR3 when added to insulin made the blood glucose readings a little more erratic but did not pull glucose levels down a lot over insulin alone.

IGF-1 PWO?

If you can make IGF-1 proliferate then okay but normally if differentiates. When you introduce a differentiator suddenly all of the proliferation stops and the differentiator goes about turning satellite cells into end product cells (myotubes).

For an elaboration and thorough understanding see my thread "Fibroblast Growth Factor (Secrets!!!)" in the Body Transformation > Muscle Acquisition section of my private forum.

THIS WENT OVER MY HEAD. I'll have to get crackin' at some research at your forum.

SIGNING OUT FOR NOW CAPTAIN (til further research)

 

[DatBtrue]

Dat, at twice a day -- do you have any suggested times that you'd consider to be the *lessor* evil? Morning, eve, meals, PWO, etc?

I've thought for a long while now that PWO was the wrong time to take IGF-1. The reason is simple. Resistance exercise is THE event that causes the body to make MGF. That is all that is meant when you see the language "MGF is a splice variant of IGF... there is a frame shift in the gene transcription...)

Inside a muscle cell after resistance exercise the body makes a variation of IGF-1 and does not make IGF-1. The variant it makes is called MGF. MGF stays in the cell and moves to the nucleus where it acts to proliferate.

IGF-1 is usually a differentiator. This means it takes all those proliferated "cells" and defines them. Tells them go be a "muscle cell". However IF MGF is busy proliferating and IGF-1 is introduced, MGF stops and IGF-1 then defines those newly created cells... but the creation has stopped.

Specific evidence for this behavior is IGF-1 doing that to Fibroblast Growth Factors proliferating action.

So post-exercise why do you want to stop your native MGF from proliferating? Let it work! Support it by using GH or GHRH/GHRPs or testosterone. If you are an older bodybuilder THIS is where you have a muscle building failure naturally. Aging people have a harder time engaging MGF after exercise. Thats why the GH, GHRH/GHRPs and testosterone have genuine value to them.

So post exercise MGF is proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> THEN you introduce IGF-1 which will define the newly proliferated "cells".

The PWO protocol which everyone seems to do(i.e. the Grunt protocol or even the Lakemount protocol) results in MGF breifly proliferating-> THEN IGF-1 stops it and defines those few new cells.

A better way to use IGF-1 would be away from the end of the exercise event.

Oops sorry EDED YOU were right.... my bad. ...yes you may be better off not to take IGF-1 every day. In the morning before a workout or the night before would give native MGF time to operate.

Further, there's people who pin GHRP's/GHRH/GH together with IGF to which I believe is a complete waste as IGF-1 destroys GH. In other words, would you separate the pinning of each (if taking both GH and IGF) by several hours?

PWO is an interesting time with some trade-offs. GHRH/GHRH/GH helps increase the MGF as noted. It also contributes to protein metabolism as I described in my protein metabolism article.... see the pretty little table at the end of that article (preventing oxidation of Leucine and increasing amino acid transport for example). But an argument can be made that GHRH/GHRH/GH increase FFAs and this will increase insulin resistance during a time when that isn't desirable...PWO yo don't want a decrease in insulin sensitivity.

...its a good argument, but it is overcome in large part by my carbless PWO w/ 1iu of insulin. See the subforum on my private forum for more detail.

So PWO IMHO is a time when you want GH as part of the protocol. IGF-1's glucose disposal is not needed because if you are familiar w/ my carbless PWO you do not want to refill glycogen stores right away unless you have a track meet the next day. You want to keep insulin sensitivity high and prolonged and this will have a positive effect on net protein synthesis and obviously keep your core tighter.

IGF-1 can also negatively feedback in several ways. One way is that it actually promotes somatostatin. Somatostatin is the hormone that shuts down GH release.

Now if you are not an insulin user you will be using Leucine PWO for two reasons one of which is to increase insulin. But somatostatin inhibits this effect!!! So you do not want IGF-1 present immediately PWO...

...note that circulating IGF-1 is different then newly introduced IGF-1. Newly introduced causes the body to react immediately.

I get the feeling I am rambling on so I will just stop and say seperate the IGF-1 from he GHRH/GHRP/GH administration.

 

[dragonfire101]

So post-exercise why do you want to stop your native MGF from proliferating? Let it work! Support it by using GH or GHRH/GHRPs or testosterone. If you are an older bodybuilder THIS is where you have a muscle building failure naturally. Aging people have a harder time engaging MGF after exercise. Thats why the GH, GHRH/GHRPs and testosterone have genuine value to them.

So post exercise MGF is proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> THEN you introduce IGF-1 which will define the newly proliferated "cells".

So post exercise MGF is proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> THEN you introduce IGF-1 which will define the newly proliferated "cells".

The PWO protocol which everyone seems to do(i.e. the Grunt protocol or even the Lakemount protocol) results in MGF breifly proliferating-> THEN IGF-1 stops it and defines those few new cells.

A better way to use IGF-1 would be away from the end of the exercise event.

So would exogenous MGF administration PWO amplify the already native MGF affects of proliferation or would one want to administer exogenous MGF at other times as well to get more chances to(duplicate) proliferation besides PWO.

BOTH

 

[PsyT]

DAT, you said IGF promotes somatostatin...would it be wise to take HUPERZINE every day that you will be injecting IGF?

Huperzine is an acetylcholine esterase inhibitor (the enzyme responsible for tearing up ACH). So inhibiting this enzyme will increase brain levels of ACH...increased ACH will DECREASE somatostatin.

 

[DatBtrue]

So would exogenous MGF administration PWO amplify the already native MGF affects of proliferation or would one want to administer exogenous MGF at other times as well to get more chances to(duplicate) proliferation besides PWO.

BOTH

MGF is capable of binding in order of preference, to the IGF-1 receptor, the IGF-1/insulin hybrid receptor and the insulin receptor. There is no MGF receptor and MGF normally never leaves the cell of its birth.

So how does exogenous MGF behave? That is a HUGE unclarified question. Recent studies block the IGF-1 receptor and administer MGF. They discover proliferative events.

Thats it. Noone has yet blocked the IGF-1/insulin hybrid receptor and the insulin receptor to see how MGF behaves when it binds to the IGF-1 receptor.

When we administer exogenous MGF all our receptors are unblocked and MGF like IGF-1 has a much stronger affinity for the IGF-1 receptor. Thats probably where it will bind. So when it does so how will it behave?

Will it acts as IGF-1 or will it act as MGF?

That is the state of the knowledge.

I know that some people like Big Bapper dosed it away from the post-workout event and had good success. He dosed Peg-MGF the night before a workout. Several others have described success to me w/ this type of dosing.

Believe me I want to know the answers but the scientist who discover MGF himself doesn't know.

 

[DatBtrue]

DAT, you said IGF promotes somatostatin...would it be wise to take HUPERZINE every day that you will be injecting IGF?

Huperzine is an acetylcholine esterase inhibitor (the enzyme responsible for tearing up ACH). So inhibiting this enzyme will increase brain levels of ACH...increased ACH will DECREASE somatostatin.

You don't want to keep somatostitin suppressed. There is nothing wrong with somatostatin and it serves many positive purposes. GHRPs do all that needs to be done to turn down somatostatin at the appropriate time.

However if you didn't use a GHRP and you needed somatostatin to be inactive during a period of time, for example if you want Leucine to increase insulin, then yes Hup would be a good choice.

But even if you block Somatostatin (w/ GHRP-6, etc.) then IGF-1 itself will still act directly on those pituitary cells and inhibit GH-release. It has a direct effect as well. It is just that its biggest inhibitory effect comes from increasing somatostatin.

But the real answer to solve the problem is to use testosterone. Testosterone blunts IGF-1 inhibition of GH. Here is a graph that demonstrates this from Testosterone Supplementation in Older Men Restrains Insulin-Like Growth Factor’s Dose-Dependent Feedback Inhibition of Pulsatile Growth Hormone Secretion, Johannes D. Veldhuis, Daniel M. Keenan, Joy N. Bailey, Adenborduin Adeniji, John M. Miles, Remberto Paulo, Mihaela Cosma and Cacia Soares-Welch,The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 1 246-254, 2009

​

 

[123cctv]

I get the feeling I am rambling on so I will just stop

No Dat, you're just being thorough, as always. Much appreciated.