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My take on IGF-1

Growth hormone treatment induces mammary gland hyperplasia in aging primates.

Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892-1770, USA.

The decline of growth hormone ( GH) and insulin-like growth factor I ( IGF-I) production during aging has been likened to the decrease in gonadal steroids in menopause. The repletion of GH/ IGF-I levels in aging individuals is suggested to restore the lean tissue anabolism characteristic of youth. In addition to anabolic effects on musculo-skeletal tissues, GH also stimulates mammary glandular growth in some species, although its effects on primate mammary growth remain unclear.

Some clinical observations implicate GH in human mammary growth, for example, gynecomastia occurs in some children treated with GH (ref. 6), and tall stature and acromegaly are associated with an increased incidence of breast cancer. To investigate the effects of GH/ IGF-I augmentation on mammary tissue in a model relevant to aging humans, we treated aged female rhesus monkeys with GH, IGF-I, GH + IGF-I or saline diluent for 7 weeks. IGF-I treatment was associated with a twofold increase, GH with a three- to fourfold increase, and GH + IGF-I with a four'-to fivefold increase in mammary glandular size and epithelial proliferation index. These mitogenic effects were directly correlated with circulating GH and IGF-I levels, suggesting that either GH or its downstream effector IGF-I stimulates primate mammary epithelial proliferation.
PMID: 9334728 [PubMed - indexed for MEDLINE]
 
and the DR. D recommend protocol to fix it.

The protocol is quite simple:
200mg Ibuprofren 3x/day (or 220mg Naproxen 2x/day - AM/PM)
60-120mg Raloxifene - PM

not sure on how long to take...
 
Grunt, have you seen this article in Newsweek:

Invalid Link Removed

It briefly mentions IGF-1 and the brain. Thought you and everybody else might find it interesting.
 
I just finished reading the entire thing myself.

Wait till you get near the end, third paragrap from the end. It starts off: "That gives rise to the question:..."

None of you will believe the irony of the paragraph! I just could not believe they wrote that.

That paragraph has nothing to do with IGF-1, just society as a whole.
 
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CRUNCH said:
I just finished reading the entire thing myself.

Wait till you get near the end, third paragrap from the end. It starts off: "That gives rise to the question:..."

None of you will believe the irony of the paragraph! I just could not believe they wrote that.
Click to expand...

I am only taking this "workout-in-a-pill" if it can also reproduce (1) the post-workout endorphin rush, and (2) all the fine ladies on the ellipticals... Somehow I don't think the latter will ever be possible.
 
I can just see it. They make a pill that provides all the positive aspects of exercise, but quadruples your liver values in less than a week.
 
TeamSavage said:
I am only taking this "workout-in-a-pill" if it can also reproduce (1) the post-workout endorphin rush, and (2) all the fine ladies on the ellipticals... Somehow I don't think the latter will ever be possible.
Click to expand...

ROFL!!! :rofl:

CRUNCH said:
I can just see it. They make a pill that provides all the positive aspects of exercise, but quadruples your liver values in less than a week.
Click to expand...

LMAO!! :rofl:

You guys are too funny! Reps! :)
 
Grunt76 said:
On July 20 I got into some pretty intense discussion on another board about IGF-1. I got so rattled with the misinformation that I decided to loose my 13 years of reading on IGF-1 onto that board. Here's the result.

This is false.

The difference between rhIGF-1 and Long R3 is that the Long R3 does not get bound by binding protein and thus is 100% active whereas you do lose a great % of whatever amount of rhIGF-1 you inject to IGFBP3.

While technically it is true that if you inject a large amount of the rhIGF-1 it will have almost only localized effect, it is so because the "excess" that does not bind to cells in the muscle in which it is injected is rapidly bound up by IGFBP3 and thus rendered unusable by cells elsewhere. It would be much much better in such a case to inject a smaller amount and not have ANY excess that gets bound up by IGFBP's.

And while technically it is true that if you inject a large amount of Long R3 IGF-1 in a muscle, it will first bind to the nearest available receptor, and spread, binding to more and more receptors and not be bound up and neutralized by IGFBP's, meaning that it will travel all through your body and grow all kinds of tissue. This is called the systemic effect of IGF-1. Therein lies the only distinction in terms of BOTH half-life and localized/systemic effect between the Long and the human varieties.

What does all this mean?

It means that technically, for the part of the muscle in which you inject, THERE IS NO DIFFERENCE BETWEEN rhIGF-1 and Long R3 IGF-1. They both have the EXACT SAME LOCAL EFFECT. But rhIGF-1 gets neutralized quick, whereas Long R3 gets to float around until it finds a receptor.

What does all this tell us?

It tells us many things. Let's start with what we want, then see where that leads us. What do we want? Bigger muscles. More muscle cells that we will later grow with exercise and gear. A pump? Fatloss? Yeah, right. You can get a pump with a good "pump" product for a quarter of the price of IGF-1. Fatloss? Clen/Alb and T3/T4 will give it to you again at a fraction of the price of IGF-1. More muscle cells, you can ONLY get with IGF-1 (and MGF too). Nothing else will give it to you and if you are using IGF-1 for anything else, you are misusing it. More muscle cells is CLEARLY the best use for IGF-1.

What does all this tell us?

It tells us that we should use IGF-1 to make more muscle cells. It's the only thing that can give it to us and more cells is more growth, which is our goal.

What does this tell us?

The localized effects are the best. Long R3 IGF-1 can float around your body and attach to anything that has IGF-1 receptors. The intestines is the place that has the MOST IGF-1 receptors and it also happens to have lots of blood flow. Injecting large amounts of Long R3 ENSURES that you are growing your intestines. Remember, more cells doesn't equal more size right away. Wait a bit, and see them grow.

What does this mean?

It means that if you are injecting upwards of 50mcg of IGF-1 you are growing your intestines. Yes you are also growing muscle and you may be getting leaner in the process. Your waistline looks trimmer. Nice. A few months down the line, your new intestinal cells will be of their full adult size and you will have acquired the perma-bloat look. Guaranteed. Maybe not Coleman-size perma-gut, but SOME perma-gut and it will keep growing. Guaranteed. Just as your new muscle cells can keep growing and growing IF you pin IGF-1 in a way to maximize new muscle cell creation.

HOW?

Heavy resistance exercise strongly upregulates the IGF-1 receptors on the stressed muscle. That means that after your workout, the muscles you trained are at their BEST STATE for receiving IGF-1 and growing many new cells. That's when you pin. This upregulation of IGF-1 receptor during exercise is short-lived. The science is not readily available so I am unable to quote a paper, but within 60 minutes of the last set, the receptors are back at baseline. This means, PIN IMMEDIATELY POSTWORKOUT and you will get your new muscle cells. PIN A LESSER AMOUNT and you will get only new MUSCLE cells out of your IGF-1. Pin more and you will grow other things, including stuff you wish you didn't grow.

What else?

All the talk about IGF-1's half-life is UTTER BULL****. It is technicality without any real-world applicability. Yes rhIGF-1 has a "short half-life". But what does it mean? It means that it is either taken up by a cell receptor or bound up by a binding protein in short order. Does it mean that 20 minutes after the IGF-1 is pinned you should pin more because "blood levels are low"? Not by any means. Once it's activated a cell receptor, that's where it initiates a cellular response that will take about 72 hours to be complete and which will consume lots of energy. So the half-life of 20 minutes means NOTHING BECAUSE THE EFFECTS STILL LAST 72 HOURS ALL THE SAME.

What about Long R3 IGF-1?

Yes technically it has a longer half-life. Why? Because it either gets rapidly taken up by a cell receptor or... Just floats around. Until it can find a receptor or is destroyed by the immune system or some other metabolizing mechanism. BUT THIS MEANS ***NOTHING***!!! Why does it mean nothing? BECAUSE once it attaches to a cell receptor, it initiates a cellular response that will take about 72 hours to be complete. THIS CELLULAR RESPONSE IS ALL THAT INTERESTS US. Not "blood levels", that's utter bull****. As a matter of fact, the one thing YOU DO NOT WANT IS FOR BLOOD LEVELS OF IGF-1 TO BE ELEVATED. Because that means you are growing everywhere and this means first and foremost your guts. Sure it feels like it's working while you're on. Just you wait 9 months and see that you look like Craig Kovacs. Bravo, you now have the biggest intestines in the world.

Half-life means nothing. Localized vs systemic = bad argument. You want localized effects. Period. You get them by pinning immediately postworkout. Period. End of argument.

OMFG I am so tired of all the misinformation floating around on IGF-1. Look at the length of this post. Did you read all of it? You should, you know.
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THATS REALLY GOOD INFO HERE,BUT I HEAR SO MANY OPINIONS BUT YOU REALLY SOUND LIKE YOU KNOW WHAT YOU ARE TALKING ABOUT,SO IF I ALREADY STARTED USING LR3 ABOUT A WEEK AND HALF AGO AT 80mcg. ED(I SPLIT TO 40mcgs. IN THE AM, AND 40mcgs. BEFORE I WORKOUT(I GOT THIS INFO FROM A DIFFERENT BOARD)-I LIKE YOUR WAY BETTER,IT MAKES MORE SENSE,SO WILL IT BE TOO LATE TO CHANGE TO 50mcgs. ONLY POST WORKOUT AND ALSO DOES BODY SIZE MATTERS WITH EACH INDIVIDUAL(IM 240 LBS.)AND WHATS THE LONGEST PERIOD I CAN USE IT FOR?
THANKS,muscledoc.
 
Grunt - When you talk about the glycogen hypersaturation (is that the right terminology?) caused by IGF-1, about how long after injection does that period last?

In other words, for about how many hours after injecting is the IGF-1 shuttling carbs into the injected muscle?
 
Grunt, I know you answered this before but I cant find it anywhwere..Im wondering what would be a good amount of NaCl to add to my reconstituted IGF..Im using 1mg with 2ml aa..with 1cc slin pins..Lets say im 6 ticks on that pin- can i load it to 20, 30 ticks??? I wanna get a good amount so it spreads out nicely..
 
slick said:
Grunt, I know you answered this before but I cant find it anywhwere..Im wondering what would be a good amount of NaCl to add to my reconstituted IGF..Im using 1mg with 2ml aa..with 1cc slin pins..Lets say im 6 ticks on that pin- can i load it to 20, 30 ticks??? I wanna get a good amount so it spreads out nicely..
Click to expand...

Yeah, fill to 30 or 50 or so, it works out nicely.

Sorry for not fieldiing all the questions, I am in vacation in Australia. And I have been cutting. :)

Expect pics :)
 
TeamSavage said:
Grunt - When you talk about the glycogen hypersaturation (is that the right terminology?) caused by IGF-1, about how long after injection does that period last?

In other words, for about how many hours after injecting is the IGF-1 shuttling carbs into the injected muscle?
Click to expand...

Bump to this question.
 
bump for that too, i think i remember reading on here that insulin response is different for roughly three days but i dont remember
 
Grunt76 said:

The difference between rhIGF-1 and Long R3 is that the Long R3 does not get bound by binding protein and thus is 100% active whereas you do lose a great % of whatever amount of rhIGF-1 you inject to IGFBP3.

While technically it is true that if you inject a large amount of the rhIGF-1 it will have almost only localized effect, it is so because the "excess" that does not bind to cells in the muscle in which it is injected is rapidly bound up by IGFBP3 and thus rendered unusable by cells elsewhere. .
Click to expand...


jeezus man, do some research. this is totally wrong

BioDrugs. 2003;17(5):375-9. Links
Somatomedin-1 binding protein-3: insulin-like growth factor-1 binding protein-3, insulin-like growth factor-1 carrier protein.[No authors listed]
Somatomedin-1 binding protein-3 [insulin-like growth factor-1 binding protein-3, SomatoKine] is a recombinant complex of insulin-like growth factor-1 (rhIGF-1) and binding protein-3 (IGFBP-3), which is the major circulating somatomedin (insulin-like growth factor) binding protein; binding protein-3 regulates the delivery of somatomedin-1 to target tissues. Somatomedin-1 binding protein-3 has potential as replacement therapy for somatomedin-1 which may become depleted in indications such as major surgery, organ damage/failure and traumatic injury, resulting in catabolism. It also has potential for the treatment of osteoporosis; diseases associated with protein wasting including chronic renal failure, cachexia and severe trauma; and to attenuate cardiac dysfunction in a variety of disease states, including after severe burn trauma. Combined therapy with somatomedin-1 and somatomedin-1 binding protein-3 would prolong the duration of action of somatomedin-1 and would reduce or eliminate some of the undesirable effects associated with somatomedin-1 monotherapy. Somatomedin-1 is usually linked to binding protein-3 in the normal state of the body, and particular proteases clip them apart in response to stresses and release somatomedin-1 as needed. Therefore, somatomedin-1 binding protein-3 is a self-dosing system and SomatoKine would augment the natural supply of these linked compounds. Somatomedin-1 binding protein-3 was developed by Celtrix using its proprietary recombinant protein production technology. Subsequently, Celtrix was acquired by Insmed Pharmaceuticals on June 1 2000.Insmed and Avecia, UK, have signed an agreement for the manufacturing of SomatoKine and its components, IGF-1 and binding protein-3.

Drugs R D. 2005;6(2):120-7. Links
Mecasermin rinfabate: insulin-like growth factor-I/insulin-like growth factor binding protein-3, mecaserimin rinfibate, rhIGF-I/rhIGFBP-3.[No authors listed]
Insmed is developing mecasermin rinfabate, a recombinant complex of insulin-like growth factor-I (rhIGF-I) and binding protein-3 (rhIGFBP-3) [insulin-like growth factor-I/insulin-like growth factor binding protein-3, rhIGF-I/rhIGFBP-3, SomatoKine], for a number of metabolic and endocrine indications.In the human body, IGF-I circulates in the blood bound to a binding protein-3 (IGFBP-3), which regulates the delivery of IGF-I to target tissues, and particular proteases clip them apart in response to stresses and release IGF-I as needed. IGF-I, a naturally occurring hormone, is necessary for normal growth and metabolism. For the treatment of IGF-I deficiency, it is desirable to administer IGF-I bound to IGFBP-3 to maintain the normal equilibrium of these proteins in the blood. Mecasermin rinfabate (rhIGF-I/rhIGFBP-3) mimics the effects of the natural protein complex in the bloodstream and would augment the natural supply of these linked compounds.The most advanced indication in development of mecasermin rinfabate is the treatment of severe growth disorders due to growth hormone insensitivity syndrome (GHIS), also called Laron syndrome. GHIS is a genetic condition in which patients do not produce adequate quantities of IGF because of a failure to respond to the growth hormone signal. This results in a slower growth rate and short stature. Mecasermin rinfabate also has potential as replacement therapy for IGF-I, which may become depleted in indications such as major surgery, organ damage/failure, traumatic injury, cachexia and severe burn trauma. It also has potential for the treatment of osteoporosis. Mecasermin rinfabate was developed by Celtrix using its proprietary recombinant protein production technology.


Exp Biol Med (Maywood). 2003 Sep;228(8):891-7. Links
Effects of insulin-like growth factor-1/binding protein-3 complex on muscle atrophy in rats.Zdanowicz MM, Teichberg S.
Department of Pharmaceutical Sciences, Massachusetts College of Pharmacy and Health Sciences, Boston, Massachusetts 02115, USA. [email protected]

Muscle atrophy and wasting is a serious problem that occurs in patients with prolonged debilitating illness, burn injury, spinal injury, as well as with space flight. Current treatment for such atrophy, which often relies on nutritional supplementation and physical therapy, is of limited value in preventing the muscle wasting that occurs. Considerable recent attention has focused on the use of anabolic growth factors such as insulin-like growth factor (IGF-1) in preventing muscle atrophy during limb disuse or with various catabolic conditions. However, potential side effects such as hypoglycemia appear to be limiting factors in the usefulness of IGF-1 for clinical treatment of muscle wasting conditions. The formulation of IGF-1 used in this study (IGF-1/BP3) is already bound to its endogenous-binding protein (BP3) and, as a result, has a greater specificity of action and significantly less hypoglycemic effect. Using a rat model of hind limb suspension (HLS) for 10 days, we induced marked muscle atrophy that was accompanied by enhanced muscle proteolysis and reduced muscle protein content. When HLS rats were treated with IGF-1/BP3 (50 mg/kg, b.i.d.), they retained greater body and muscle mass. Muscle protein degradation was significantly reduced and muscle protein content was preserved. The rate of protein synthesis, although somewhat reduced in HLS muscle, was not significantly elevated by IGF-1/BP3 treatment. Volume density of HLS-treated muscles were increased compared to untreated HLS rats and the actual number of fibers per area of muscle was likewise increased. The results of the current study suggest that IGF-1/BP3 might be useful for inhibiting muscle proteolysis in catabolic conditions and thus preserving muscle protein content and mass.

PMID: 12968060 [PubMed - indexed for MEDLINE]

J Trauma. 1999 Nov;47(5):904-10; discussion 910-1. Links
Anabolic effects of insulin-like growth factor in combination with insulin-like growth factor binding protein-3 in severely burned adults.Debroy MA, Wolf SE, Zhang XJ, Chinkes DL, Ferrando AA, Wolfe RR, Herndon DN.
Shriners Hospitals for Children, Galveston, Texas 77550, USA.

BACKGROUND: The purpose of this study was to determine the anabolic effects of recombinant human insulin-like growth factor-I (rhIGF-1) complexed with its principal binding protein IGF-1 binding protein-3 (IGFBP-3) in severely burned adults. METHODS: Ten burned adults were studied consecutively after receiving saline (pretreatment), then rhIGF-1/IGFBP-3 (treatment) for 5 days. Doses were 1, 2, and 4 mg/kg per day. Glucose, electrolytes, hormones, and leg muscle protein metabolism were determined. Nine other studies were performed on similarly injured adults at comparable times to the treatment studies to control for time effects. RESULTS: Serum IGF-1 and IGFBP-3 levels increased with all doses, but no incremental increases were found. Leg protein balance improved with rhIGF-1/IGFBP-3, which was associated with an increase in muscle protein fractional synthetic rate. These effects were independent of time. All patients were euglycemic without electrolyte imbalances. CONCLUSION: Net protein synthesis in the isolated leg of severely burned adults improved with rhIGF-1/IGFBP-3 without development of glucose abnormalities.

PMID: 10568720 [PubMed - indexed for MEDLINE]
 
I wondered how long it would take PA to find this thread after reading his IGF article in MD this month.


Welcome.
 
What are you trying to say, Patrick? I am explaining how things WORK for bodybuilders here, not doing theory. So while technically it can be argued that what I say is "not right", in practical application it is right.
 
Grunt76 said:
What are you trying to say, Patrick? I am explaining how things WORK for bodybuilders here, not doing theory. So while technically it can be argued that what I say is "not right", in practical application it is right.
Click to expand...


The bottom line for me is that IGF-1 and IGF-1LR3 are pretty poor muscle anabolic agents. they have some potent glucose disposal and water retention activity that gives one the sense of growth in the short term but the science is pretty convincing that any true growth from these agents (when administered systemically) is on non muscular tissues (visceral organs).

Not until adeno-associated virus delivered IGF-1 gene therapy is available will we see the true potential of IGF-1 made available.

Until then, people will be using a poorly selective anabolic agent with significant side effects (hypoglycemia, increased intracranial pressure, electrolyte disturbances, and organ growth). I occasionally have used LongR3 to try to heal connective tissue injuries and many of these side effects were, for me, more than just theory
 
Patrick Arnold said:
The bottom line for me is that IGF-1 and IGF-1LR3 are pretty poor muscle anabolic agents. they have some potent glucose disposal and water retention activity that gives one the sense of growth in the short term but the science is pretty convincing that any true growth from these agents (when administered systemically) is on non muscular tissues (visceral organs).

Not until adeno-associated virus delivered IGF-1 gene therapy is available will we see the true potential of IGF-1 made available.

Until then, people will be using a poorly selective anabolic agent with significant side effects (hypoglycemia, increased intracranial pressure, electrolyte disturbances, and organ growth). I occasionally have used LongR3 to try to heal connective tissue injuries and many of these side effects were, for me, more than just theory
Click to expand...

Ah, yes, I see. And mostly, I agree, actually. BUT when used IMMEDIATELY postworkout, when the IGF-1 receptors in the muscle just trained are fully upregulated, LR3 is able to exert a unique action on muscle cells that nothing else can achieve: hyperplasia. I think we will have to agree on that, and Antonio makes a pretty convincing argument that over time hyperplasia can be a very significant factor.

This is what "My take on IGF-1" is about, how to achieve maximum hyperplasia (even if little) AND minimize side effects such as organ growth, build it up over time and eventually you have physique-transforming effects.

Cheers Patrick,

Grunt
 
Grunt76 said:
Ah, yes, I see. And mostly, I agree, actually. BUT when used IMMEDIATELY postworkout, when the IGF-1 receptors in the muscle just trained are fully upregulated, LR3 is able to exert a unique action on muscle cells that nothing else can achieve: hyperplasia. I think we will have to agree on that, and Antonio makes a pretty convincing argument that over time hyperplasia can be a very significant factor.
Click to expand...


I have heard people theorize about this but i never heard any solid evidence supporting it. I think this might be more wishful thinking then science right now
 
Well wouldn't that blow HGH out of the water for anabolism? After all, HGH's "anabolism" is directly from IGF, right?
 
Patrick Arnold said:
I have heard people theorize about this but i never heard any solid evidence supporting it. I think this might be more wishful thinking then science right now
Click to expand...

Supporting what? The upregulation of IGF-1 receptors by exercise? If so, I have some good reading for you somewhere. If you mean the short-livedness of that effect, this is true, it has not been officially documented but that is because the receptor upregulation is inferred from genomic expression and of course there is no genomic expression for its downregulation...

Still, if you are willing to admit validity of anecdotal evidence, many experimenters report significantly better results by adding LR3 immediately postworkout as compared to 20, 30, 40, 60 minutes after.
 
Ubiquitous said:
Well wouldn't that blow HGH out of the water for anabolism? After all, HGH's "anabolism" is directly from IGF, right?
Click to expand...

but HGH has negligible muscle anabolism in adults with normal GH. the research is pretty clear on this

its cosmetic benefits are not from muscle protein accretion
 
Grunt76 said:
Supporting what? The upregulation of IGF-1 receptors by exercise?
Click to expand...

no , i am not looking for evidence supporting that. I am looking for evidence supporting the tremendous leap of faith you make after that

the bodybuilding community is a group of very motivated athletes. this motivation unfortunately leads to overly wishful thinking and self fullfilling prophecies.

i offer objectivism. reason. in the end, you will reach your goals more quickly and go down less dead traveling my road
 
Grunt76 said:
Still, if you are willing to admit validity of anecdotal evidence, many experimenters report significantly better results by adding LR3 immediately postworkout as compared to 20, 30, 40, 60 minutes after.
Click to expand...

i don't know these people you speak of and i have no idea what guidelines they followed. to make any conclusions based on such third hand hearsay would be foolish on my part

i am not closing my mind to the possibility of a viable method of IGF-1 usage for muscle anabolism. but after being in this industry for a long time i have learned the value of objectivism and skepticism
 
Ubiquitous said:
Well crap... I'm dealing with carpal sides for nothing? Curses.
Click to expand...

bottom line is, until we do a real analysis of body composition using this stuff we will not know the answer. It is very difficult to ascertain muscle mass gains when water retention is a factor in the equation

you need to determine LBM while taking into consideration water, and where mass gain is localized (muscles versus viscera)

this takes sophisticated testing

until then, the scientific literature strongly suggests that you are not experiencing substantial muscle anabolism
 
Patrick,

If the increase in local muscle mass is mostly water, how long after quitting IGF would this swelling come down? If -anectodally- people are experiencing lasting mass gains beyond this period, we have some anectodal evidence... Again, this will not be scientific of course...
 
Patrick Arnold said:
but HGH has negligible muscle anabolism in adults with normal GH. the research is pretty clear on this

its cosmetic benefits are not from muscle protein accretion
Click to expand...

I have to agree. GH is great stuff but it doesn't add that much muscle per se.


Patrick Arnold said:
no , i am not looking for evidence supporting that. I am looking for evidence supporting the tremendous leap of faith you make after that

the bodybuilding community is a group of very motivated athletes. this motivation unfortunately leads to overly wishful thinking and self fullfilling prophecies.

i offer objectivism. reason. in the end, you will reach your goals more quickly and go down less dead traveling my road
Click to expand...

Hm, you state that you do not know for sure and then that your way is better. Sounds like you are hyping yourself bro. I know for sure and my way is better, so that's that.


Patrick Arnold said:
i don't know these people you speak of and i have no idea what guidelines they followed. to make any conclusions based on such third hand hearsay would be foolish on my part

i am not closing my mind to the possibility of a viable method of IGF-1 usage for muscle anabolism. but after being in this industry for a long time i have learned the value of objectivism and skepticism
Click to expand...

I agree. I only admit validity of the observations because they are first-hand and that the situation was managed by myself to begin with, which allows me to know most of the parameters in the experiments, which were/are numerous enough to be statistically significant.
 
Is there any solid evidence for the hyperplasia claims made for LR3 IGF-1? I suppose muscle biopsies would be needed.
 
This is what i know. i took igf for two months my calves grew more in that period than the previous 4 months. i stopped igf for almost two months and my calves remained the same size.
When you stop you lose the pump but site specific growth does work. fatloss from igf is real.
as far as science is concerned let them play catchup.. igf works just like grunt says it does...
 
jonesboy said:
This is what i know. i took igf for two months my calves grew more in that period than the previous 4 months. i stopped igf for almost two months and my calves remained the same size.
When you stop you lose the pump but site specific growth does work. fatloss from igf is real.
as far as science is concerned let them play catchup.. igf works just like grunt says it does...
Click to expand...

Did you only site inject your calves during this period? Any systemic growth effects?
 
I am on a very low dose of anabolics and uing the igf with a diet that I have used for years. The only things that are different is the low doses ofaas & the addition of igf & pmgf.

I will be tracking my progress with bf% using a BodPod which is as accurate as hydrostatic weighing.

Seeing what can be achived with lower doses off aas months after I get all compounds out of my system and the water goes awy, will be a good indication as to how well these new compounds work.

If I wasn't so greedy for muscle growth now I would go with a "pepetides only" cycle and see what my results are. I am even half way contemplating the aas now and try it.

I'll think about that for another day or 2 since I am only 2 weeks into my cycle.
 
jenab123 said:
Did you only site inject your calves during this period? Any systemic growth effects?
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nope did calves, legs, shoulders and traps.. rotated the traps and shoulders.


saw growth in all areas of the body. But i am impressed. I have natural little legs, always have. They are real hard to grow. IGF has really helped in the legs,calves and trap area.. my shoulders have no problems growing. Currently using receptor grade at 30mcg bi lat..
 
jenab123 said:
Is there any solid evidence for the hyperplasia claims made for LR3 IGF-1? I suppose muscle biopsies would be needed.
Click to expand...

There is real evidence of hyperplasia without administering IGF-1. Read Jose Antonio's paper "Hyperplasia vs Hypertrophy: has the debate been settled?" I am sure I posted it on here and linked already from this thread. Here: Invalid Link Removed

IGF-1 is the one growth factor known to trigger hyperplasia. So... Between these two known facts and anecdotal evidence as reported by many such as jonesboy, it takes a very hard-headed skeptic to state that the evidence is unconvincing...
 
Grunt76 said:
There is real evidence of hyperplasia without administering IGF-1. Read Jose Antonio's paper "Hyperplasia vs Hypertrophy: has the debate been settled?" I am sure I posted it on here and linked already from this thread. Here: Invalid Link Removed

IGF-1 is the one growth factor known to trigger hyperplasia. So... Between these two known facts and anecdotal evidence as reported by many such as jonesboy, it takes a very hard-headed skeptic to state that the evidence is unconvincing...
Click to expand...

Thanks for the paper. Of course, the real standard of proof is to give it to a stray cat and see if it gets hyooge.

[to those of you that weren't around in the 90's, Andro Cat was the test subject.]
 
Grunt76 said:
There is real evidence of hyperplasia without administering IGF-1. Read Jose Antonio's paper "Hyperplasia vs Hypertrophy: has the debate been settled?" I am sure I posted it on here and linked already from this thread. Here: Invalid Link Removed

IGF-1 is the one growth factor known to trigger hyperplasia. So... Between these two known facts and anecdotal evidence as reported by many such as jonesboy, it takes a very hard-headed skeptic to state that the evidence is unconvincing...
Click to expand...

Well I am not saying it is unconvincing I was just asking what is the true state of peer-reviewed scientific knowledge on this subject, specifically the relationship between say media grade LR3IGF-1 and hyperplasia in humans.

My lab rat is using your protocol and is quite happy. Just wondering how much of his new gains he will keep, and whether to expect further gains after going off, as would be implied by there being any measurable hyperplasia.

I have concerns about staying on indefinitely. There are things you don't want to have growing which might under those circumstances, no matter how low the dose. Then there are impurities and who knows what else going on here.
 
I would have concerns about staying on indefinitely as well. Moreover, I lead a lifestyle that could be considered about the LOWEST risk level for cancer, and I do take my grape seed extract daily.

There is no research on LR3 in humans and no plans on there ever being any, it is a cell-culture product. Yes.
 
I had read that Lr3IGF-1 and HGH concurrently renders the risk of rapid growth of pre-existing cancer obselete. I'll try to find where I read that.
 
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