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

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

You just partially fueled some thoughts that I had after posting in your private forum

I was wondering in that thread why Gh increases MGF expression over time, yet the increases in IGF levels over time seems to play no role in inhibiting MGF expression.

I was trying to figure out why that didn't become a vicious circle

Then I thought if the liver produced IGF was a different isoform than the synthetic IGF, and is already circulating non-stop, perhaps it doesn't keep the MGF switched off from doing its work because we simply aren't using the multiple isoforms or the liver produced IGF isoform.

I was thinking it could be many reasons, from it simply being different isoforms that doesnt inhibit MGF expression, to the IGF circulating in large enough amounts/constantly to desensitize or overcome whatever the switch is that inhibits MGF expression....

I was thinking that something must desensitize over time, or something must increase "enough" over time to increase expression of the MGF. (wasn't it something like 12 weeks for MGF to elevate?)

Now I'm the one thats rambling (Its 2:40 in the morning :D so please excuse me if I didn't make much sense)
 
mgf

Hi Dat,

Long time how you still doing?

I just read in the new Muscular Development that Dan Gwartney reports that some Anecdotal reports on MGF suggest that a moderate dose injected under the skin , twice weekly, offers the best return. Advocates suggest it offers the best of GH's anabolic effects, with less associated water retention.

Whats your take on this because MGF for me works optimal when I take 60 mcg's before and 60 mcg's after training directly into the working muscle for that session.:)
 
Hi Dat,

Long time how you still doing?

I just read in the new Muscular Development that Dan Gwartney reports that some Anecdotal reports on MGF suggest that a moderate dose injected under the skin , twice weekly, offers the best return. Advocates suggest it offers the best of GH's anabolic effects, with less associated water retention.

Whats your take on this because MGF for me works optimal when I take 60 mcg's before and 60 mcg's after training directly into the working muscle for that session.:)

My take?

My take is that when someone talks about an MGF receptor I tune out. In the past I discovered people blasted me with the words of the abstract from the following study but it told me that they never read the full study.

Different roles of the IGF-I Ec peptide (MGF) and mature IGF-I in myoblast proliferation and differentiation, Shi Yu Yang,Geoffrey Goldspink, FEBS Letters 522 (2002) 156-160

ABSTRACT Blocking the IGF-I receptor with a specific antibody indicated that the function of MGF E domain is mediated via a different receptor.

When the actual study said:

FULL STUDY Also the selective blocking of the IGF-I receptor provides evidence that MGF increases myoblast proliferation via a different signalling pathway.

If you look around you'll see every once in a while someone who thinks they are handing my ass to me on this topic.

Whats your take on this because MGF for me works optimal when I take 60 mcg's before and 60 mcg's after training directly into the working muscle for that session.:)

So you have doubled your muscle mass in a few weeks! Thats impressive. Just like the studies where they use a viral vector to engender an increase in the expression of native MGF within muscle cells.

Good for you!

Advocates suggest it offers the best of GH's anabolic effects, with less associated water retention.

So it decreases oxidation of leucine. It increases the transport of BCCAs. It increases transport of other aminos. It increases whole body protein synthesis. It decreases whole body protein degradation through the IGF-1 it creates and decreases muscle protein degradation through the IGFBPs it creates.

It creates liver enzymes to metabolize sex steroids and by its release profile skews it to the appropriate gender which contributes to bone growth and anabolism.

Good to know. I have read just about everything that was published on Mechano Growth Factor but somewhere along the line I must have missed the suggestions of the Advocates, MD magazine and the reporting of Dan Gwartney.
 
Hi Dat,

Thanks again for all the info you are remarkable on your research.
 
Dat, I gotta tell ya, you really seem to know your shit.
So here is a question I am struggling with....my MD prescribed Gentopin for me after I failed a stimulation test. My insurance company refuses to cover the medication. I am looking for a viable alternative...and have been considering GHRP-6/CJC to run in conjuction with my regular HRT (test cypionate) and other "unprescribed" cycle items. If I run

test 500mg/week
GHRP 200mcg 3xdaily
CJC 100MCG twice weekly
Humulin R 5units daily

Do I need to concern myself with any of this IGF-1 longR3. Is there any advice you could give a "hypothetical person" in a situation similar to mine...since this stuff is for research only
 
Dat you crack me up....I love that I can sit here and learn and research, and just like that bust out hysterically laughing on one of your posts...lmfao

But it would be nice one day if we researchers have access to mgf w/ a mechanism to get that sucker into the cell....

Just an aside; I've researched lr3 and mgf a couple years back before the peps were readily avilable/known to us; the lr3 provided significantly better results vs the mgf; I know many people praise mgf and that you hypothesize perhaps it competes more efficiently than igf for igf cell receptors...Certainly not in my case...Just my 2 cents, though I understand the enormous variables involved, ie: product quality, genetic differences, dosing protocol, etc.

And I see that this microdosing lr3 in various surrounding sites is gaining some popularity here and appears to be breaking out of being just for healing tissue, but for muscle growth. The goal of course, trying to maximize the amount of igf which remains locally, as most will go systemic. Be interesting if this becomes the next cult practice with lr3 as opposed to the majority opinion thus far of more is better. BUT I remember who came up with the microdosing multiple sites YEARS ago...
 
dat, please tell me if this is completely retarded or if could yeild good/normal IGF-1 results. im thinking about trying it out.

u say use IGF-1 in tiny doses, multiple doses in the same area, twice a day.

would there be any benefit to just pinning bilaterally 2 times per day? first pins in the morning before breakfast pinning the muscles worked the previous day....and then the next bi-lat pins would be post workout into the muscle just worked that day.

waste of time?
 
dat, please tell me if this is completely retarded or if could yeild good/normal IGF-1 results. im thinking about trying it out.

u say use IGF-1 in tiny doses, multiple doses in the same area, twice a day.

would there be any benefit to just pinning bilaterally 2 times per day? first pins in the morning before breakfast pinning the muscles worked the previous day....and then the next bi-lat pins would be post workout into the muscle just worked that day.

waste of time?
my understanding is that pinning IGF immediately PWO is not a good idea. Wait a few hours so that endogenous MGF has a chance to work. *I THINK THIS IS CORRECT*

I like your idea of morning and PM pinning though. I'm going to do that I think...pin 40ug spread bilaterally with multiple tiny shots in upper. And then 40ug spread bilat multiple shots lower.
 
Dat, I have been reading your forums for a long time now, thanks for all the great info. I recall reading one of your threads where insulin was discussed, it is non-discriminatory in the sense that it lets glucose into both muscle and adipose cells, however post workout, and or while on AAS, or GH, it is more likely that insulin will store glucose in muscle cells.

My question is, could injecting glucagon post workout, while on AAS, or GH, lead to releasing glycogen and storing that in muscle cells and in that process could fat cells be broken down to replenish glycogen, which would then be released and let into muscle cells. It would be a way to literally turn fat into muscle if it worked. I am diabetic so I already take insulin daily, and have access to glucagon. It was just a thought that popped into my head as i was reading some of your threads. I would love to hear any thoughts you have on the subject.
 
would there be any benefit in using the same protocol for mgf/peg mgf?
 
You just partially fueled some thoughts that I had after posting in your private forum

I was wondering in that thread why Gh increases MGF expression over time, yet the increases in IGF levels over time seems to play no role in inhibiting MGF expression.

I was trying to figure out why that didn't become a vicious circle

Then I thought if the liver produced IGF was a different isoform than the synthetic IGF, and is already circulating non-stop, perhaps it doesn't keep the MGF switched off from doing its work because we simply aren't using the multiple isoforms or the liver produced IGF isoform.

I was thinking it could be many reasons, from it simply being different isoforms that doesnt inhibit MGF expression, to the IGF circulating in large enough amounts/constantly to desensitize or overcome whatever the switch is that inhibits MGF expression....

I was thinking that something must desensitize over time, or something must increase "enough" over time to increase expression of the MGF. (wasn't it something like 12 weeks for MGF to elevate?)

Now I'm the one thats rambling (Its 2:40 in the morning :D so please excuse me if I didn't make much sense)

Wow you have an active mind.

The feedback and inhibition doesn't last for long periods of time.

The literature describes many feedback mechanisms. But one is that local IGF-1 creation in the brain can cause inhibition of GHRH release.

Injected IGF-1 or even circulating IGF-1 from the liver will not readily cross the blood brain barrier. What happens though is certain pulses or levels of hormones (notably GH) will cause the local production of IGF-1 in brain cells.
 
Dat, I gotta tell ya, you really seem to know your shit.
So here is a question I am struggling with....my MD prescribed Gentopin for me after I failed a stimulation test. My insurance company refuses to cover the medication. I am looking for a viable alternative...and have been considering GHRP-6/CJC to run in conjuction with my regular HRT (test cypionate) and other "unprescribed" cycle items. If I run

test 500mg/week
GHRP 200mcg 3xdaily
CJC 100MCG twice weekly
Humulin R 5units daily

Do I need to concern myself with any of this IGF-1 longR3. Is there any advice you could give a "hypothetical person" in a situation similar to mine...since this stuff is for research only

Sure. I tried to PM you but it said you won't take PMs. If you like you can join my forum link below and PM me and I will help you.
 
dat, please tell me if this is completely retarded or if could yeild good/normal IGF-1 results. im thinking about trying it out.

u say use IGF-1 in tiny doses, multiple doses in the same area, twice a day.

would there be any benefit to just pinning bilaterally 2 times per day? first pins in the morning before breakfast pinning the muscles worked the previous day....and then the next bi-lat pins would be post workout into the muscle just worked that day.

waste of time?

You see what you are doing? You are twisting and turning to make it into something you want to do. I'm on to you my man. :)
 
Dat, I have been reading your forums for a long time now, thanks for all the great info. I recall reading one of your threads where insulin was discussed, it is non-discriminatory in the sense that it lets glucose into both muscle and adipose cells, however post workout, and or while on AAS, or GH, it is more likely that insulin will store glucose in muscle cells.

My question is, could injecting glucagon post workout, while on AAS, or GH, lead to releasing glycogen and storing that in muscle cells and in that process could fat cells be broken down to replenish glycogen, which would then be released and let into muscle cells. It would be a way to literally turn fat into muscle if it worked. I am diabetic so I already take insulin daily, and have access to glucagon. It was just a thought that popped into my head as i was reading some of your threads. I would love to hear any thoughts you have on the subject.

The answer is probably not... especially the way you described.

But my carbless PWO protocol is perfect for diabetic and normal people as well. You will gain muscle and lose fat. It increases both insulin sensitivity and insulin responsiveness. You don't want to replete, compensate, super-compensate PWO. You want that window to stay open, It is discussed in detail and logged on my forum.
 
would there be any benefit in using the same protocol for mgf/peg mgf?

Yes. It would. Whether you believe exogenous MGF will behave as MGF or IGF-1 doesn't matter. Which ever way it will act micro-dosing will be of benefit.

Micro dose because the cells that the needle inject will come in contact with are few so don't waste the MGF/IGF-1. 95% will probably be drawn quickly into the capillaries and travel systemically. So you use a microdose.

You want to come in contact with as many muscle cells as as possible so that is why you inject in many places over a given area.

If you could stand the trauma I'd love to see someone micro inject in 50 places over several square inches. Come back later and do it again.

But that isn't realistic so we choose a number we can handle.

Why are we doing this micro-inject thing? Because we have to come up with some way to increase the amount that will act locally. If we just inject once the peptide travels everywhere and we hope some will float by and bond to receptors in the muscle we want to activate.

So moderate doses won't have much effect. Big single doses will have more of an effect but it will also act on the heart, the gut, throughout the entire body. It seems silly to flood the body with IGF-1 which is anti-apoptosis (prevents cell death) just to effect a small muscle. Preventing cell death in some tissue creates the potential precursor cancer events to take shape.

As I said before with IGF-1 or MGF in either LR3 form or PEG the molecule is still small and it will move right through a blood vessel wall into the blood stream. Nobody is using a molecule that is too large to penetrate the vascular wall... so this is one "far from perfect" method to try to get the small molecule to bind to receptors on cells near the injection site.
 

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