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IGF-1 Levels Increases with Testosterone. Is GH Really Needed?

jrs

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IGF-1 Levels Increase with Testosterone. Is GH Really Needed?

Taken from this study http://ajpendo.physiology.org/cgi/reprint/281/6/E1172

This table shows the average of the before and after levels of IGF-1 following 16 weeks of Test E injections at the dosages listed in the first column.

IGF-I (ng/ml) (overall ANOVA P 5 0.0001)

25 mg 268 261
50 mg 246 225
125 mg 299 282
300 mg 314 388
600 mg 227 304


Now I don't know enough to know if these are significant changes are not. Only the 300mg weekly and 600mg weekly doses showed an increase and it was dose dependent.

Now, is this increase comparable to IGF-1 levels after GH supplementation? I have no idea what bloodwork looks like after such a thing.
 
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machola

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at least someone read the study i posted...

i don't think its comparable to hgh

300mg test increases igf-1 by 23%
600mg test 34%
 

jrs

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as a comparison, how much would say 2iu GH raise igf1 levels?

I wonder, if the study went above 600, 1000, 1500mg, if we would keep seeing a rise in igf1. I would assume so, up to a point.

Perhaps the higher igf1 the better, and even though test increases igf, even more must build more muscle and burn more fat. I guess in the end, the more stuff you take, the better in terms of progress. I thought this may mean that GH is pointless if you're on a high dose of test, but perhaps it just shows that those who do both have insanely high levels of hormones, etc that work wonders with proper diet, rest, and training.
 

machola

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as a comparison, how much would say 2iu GH raise igf1 levels?i don't know. datbrute might know this.

I wonder, if the study went above 600, 1000, 1500mg, if we would keep seeing a rise in igf1. I would assume so, up to a point.

Perhaps the higher igf1 the better, and even though test increases igf, even more must build more muscle and burn more fat. I guess in the end, the more stuff you take, the better in terms of progress. I thought this may mean that GH is pointless if you're on a high dose of test, but perhaps it just shows that those who do both have insanely high levels of hormones, etc that work wonders with proper diet, rest, and training.
wow. lots of good thoughts here. hopefully Dat will see this and post some info about hgh effects on igf-1
 

DatBtrue

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YOU ARE SAYING PROBABLY........AS IN YOU ARE GUESSING? WHAT BRINGS YOU TO THAT CONCLUSION? CAN YOU SHOW US THE RESEARCH?
:rolleyes:

Cut & paste from my thread: Post #360

I just started researching a little bit about "fibroblast growth factor" as an agent for myoblast proliferation perhaps to be used in place of MGF.

Anyway I came across this abstract on Trenbolone that was of interest in relation to proliferation and differentiation of satellite cells. Kinda makes me wish I could tolerate Trenbolone.


Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor I

SH Thompson, LK Boxhorn, WY Kong and RE Allen
Department of Animal Sciences, University of Arizona, Tucson 85721.


Endocrinology, Vol 124, 2110-2117, 1989


The potential role of satellite cells in mediating the effect of trenbolone [17 beta-hydroxyestra-4,9-11-trien-3-one (TBOH)] on skeletal muscle hypertrophy was examined.

Young female Sprague-Dawley rats received TBOH injections daily for 2 weeks; growth, body composition, and the composition of selected muscles were assessed. Treated rats grew more rapidly and deposited less body lipid and more protein. The semimembranosus muscle from treated rats was larger and had approximately 60% more DNA per muscle than muscles from control rats.

The addition of trenbolone directly to the medium of cultured satellite cells did not stimulate cell proliferation, nor did it augment the stimulatory response of these cells to fibroblast growth factor (FGF) or insulin-like growth factor I (IGF-I). In contrast, satellite cells cultured from TBOH-treated rats exhibited greater proliferative responses to FGF and IGF-I than satellite cells from control rats. In addition, serum from TBOH-treated rats stimulated greater cell proliferation in satellite cell cultures than serum from control rats.

These experiments suggest that one possible mechanism responsible for the ability of TBOH to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satellite cells as a result of the increased sensitivity of these cells to IGF-I and FGF.
 

DatBtrue

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PM sent. hope he responds
From the chart in post #7 of my thread on page 1 in the study "Pharmacokinetics and Metabolic Effects of High-Dose Growth Hormone Administration in Healthy Adult Men", Toshiaki Tanaka, et al., Endocrine Journal 1999, 46 (4), 605-612, where fifteen healthy normal Japanese adult males aged from 20 to 27 years were administered various doses of recombinant GH (Norditropin) we find that:

.075iu/kg (7.5iu in a 100kg man) generated about 300ng/ml by the end of the day.

.15iu/kg (15iu in a 100kg man) generated about 380ng/ml by the end of the day.

.30iu/kg (30iu in a 100kg man) generated about 420ng/ml by the end of the day.

Note that these were normal Japanese men in their 20's. They probably weighed on average 75 kilos so those GH dosing amounts would have in actuality been about 25% less... between about 5iu & 22iu.

This should give you an idea.

Psst... locally produced (i.e. autocrine/paracrine muscle produced as opposed to liver-produced systemic) IGF-1 is more important then absolute levels of systemic IGF-1.

How does testosterone & GH effect these levels? :)
 
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PHIL HERNON

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YES

From the chart in post #7 of my thread on page 1 in the study "Pharmacokinetics and Metabolic Effects of High-Dose Growth Hormone Administration in Healthy Adult Men", Toshiaki Tanaka, et al., Endocrine Journal 1999, 46 (4), 605-612, where fifteen healthy normal Japanese adult males aged from 20 to 27 years were administered various doses of recombinant GH (Norditropin) we find that:

.075iu/kg (7.5iu in a 100kg man) generated about 300ng/ml by the end of the day.

.15iu/kg (15iu in a 100kg man) generated about 380ng/ml by the end of the day.

.30iu/kg (30iu in a 100kg man) generated about 420ng/ml by the end of the day.

Note that these were normal Japanese men in their 20's. They probably weighed on average 75 kilos so those GH dosing amounts would have in actuality been about 25% less... between about 5iu & 22iu.

This should give you an idea.

Psst... locally produced (i.e. autocrine/paracrine muscle produced as opposed to liver-produced systemic) IGF-1 is more important then absolute levels of systemic IGF-1.

How does testosterone & GH effect these levels? :)
THATS WHAT I WANT TO KNOW!
 

machola

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Young female Sprague-Dawley rats received TBOH injections daily for 2 weeks
animal studies are unreliable predicting drug effects on humans. look at the rat igf-1 studies and myostatin inhibitor studies and compare to the human trials. i remember a study showing proviron(mesterolone) has a decent anabolic effect on rabbits but not humans
 

DatBtrue

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animal studies are unreliable predicting drug effects on humans. look at the rat igf-1 studies and myostatin inhibitor studies and compare to the human trials. i remember a study showing proviron(mesterolone) has a decent anabolic effect on rabbits but not humans
I hear what you are saying and your statement "...animal studies are unreliable predicting drug effects on humans" in general terms is correct.

But the reality is that your statement is meaningless because when you look at things at a systemic level in many cases they are almost indistguishable from humans...the mouse in particular.

When a topic is examined/studied no one scientific groups simply injects an animal, takes notes and then walks away. They have examined & studied the topic in vitro and 95% of their study is based on peer-reviewed science that has occurred elsewhere. In this instance the enhanced proliferation and differentiation of satellite cells via trenbolone incubation or as an adjunct in culture was established. They then used specifically designed rats as an in vivo model to advance the state of knowledge.

You machola & other bodybuilders take things one step further...

However if there is a correlation between certain biomarkers that is already established between the animal model & human then pushing forward with an experiment that is merely one step forward from what is known generates results that have various possibilities/probabilities in humans that are reliable parameters.

But machola you have a valid point when we attempt to extrapolate dosing & even effect from animal models to humans.

I saw a detailed article on how to use CJC-1295 one time by someone on a bodybuilding forum. They used the rat study of CJC-1295 and concluded that since CJC clears within a day or so in the study all bodybuilders need to dose daily. The problem was that they didn't understand that albumin in rats (to which CJC clings for life) has a short half-life of a day or so while human albumin has a half-life beyond 2 weeks.

Huge difference! But the unreliability came from the layman failing to fully read the study and understand the animal model & then misapplying what he thought he knew. :)
 

para

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From the chart in post #7 of my thread on page 1 in the study "Pharmacokinetics and Metabolic Effects of High-Dose Growth Hormone Administration in Healthy Adult Men", Toshiaki Tanaka, et al., Endocrine Journal 1999, 46 (4), 605-612, where fifteen healthy normal Japanese adult males aged from 20 to 27 years were administered various doses of recombinant GH (Norditropin) we find that:

.075iu/kg (7.5iu in a 100kg man) generated about 300ng/ml by the end of the day.

.15iu/kg (15iu in a 100kg man) generated about 380ng/ml by the end of the day.

.30iu/kg (30iu in a 100kg man) generated about 420ng/ml by the end of the day.

Note that these were normal Japanese men in their 20's. They probably weighed on average 75 kilos so those GH dosing amounts would have in actuality been about 25% less... between about 5iu & 22iu.

This should give you an idea.

Psst... locally produced (i.e. autocrine/paracrine muscle produced as opposed to liver-produced systemic) IGF-1 is more important then absolute levels of systemic IGF-1.

How does testosterone & GH effect these levels? :)
Those numbers for the patients IGF-1 level seem very low considering how much they were given. Look at the last guy 30ius a day only raised it to 420. I hit that at 36 years old and 3ius a day.
 

machola

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However if there is a correlation between certain biomarkers that is already established between the animal model & human then pushing forward with an experiment that is merely one step forward from what is known generates results that have various possibilities/probabilities in humans that are reliable parameters.
you're right. i should have been more clear... i think we can generally predict drug effects by testing on animals but not the extent of the effect
 

DatBtrue

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Those numbers for the patients IGF-1 level seem very low considering how much they were given. Look at the last guy 30ius a day only raised it to 420. I hit that at 36 years old and 3ius a day.
Yep. But that was the level 24 hours post administration. All groups except the highest received the one injection. "The subjects assigned to receive .30 IU/kg were administered for additional 6 days."

IGF-1 levels slowly build. From the same study:

"IGF-I concentrations almost reached a plateau at a significantly high level four days after the start of administration and remained at a high level (786-405.4 ng/ml) until day 8."​

igf-1.jpg
 

jrs

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Hard to tell from the chart.. what would you say are the average IGF1 levels at their highest point after 3 iu per day? the smallest amount on that chart i believe is ~7.5iu for a 100kg person. What would those levels top out at?

Also, to ask you directly, what do you think comparisons would be like between GH and testosterone alone? I'm sure using both would be optimal but is there theoretically a dose of test that would be equal to a small amount of gh rendering gh supplementation pointless?
 

DatBtrue

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Hard to tell from the chart.. what would you say are the average IGF1 levels at their highest point after 3 iu per day? the smallest amount on that chart i believe is ~7.5iu for a 100kg person. What would those levels top out at?

Also, to ask you directly, what do you think comparisons would be like between GH and testosterone alone? I'm sure using both would be optimal but is there theoretically a dose of test that would be equal to a small amount of gh rendering gh supplementation pointless?
You'll have to either extrapolate... or find another study that used normal young people at those lower dosing levels & measure IGF-1 levels. I'm sure they are in my database as well as pubmed so I'll keep an eye out...But past a certain level I don't much care about systemic IGF-1 levels.

Systemic IGF-1 levels are interesting because they can serve as markers for autocrine/paracrine IGFs. In other words if systemic IGF-1 is high then it is likely so is the local production/use. But other than that they are not important for muscle growth.

Do you understand what I am saying?

IGF-1 is predominantly synthesized in the liver where it then goes out and circulates. That is systemic (endocrine) IGF-1 and is what is measured in tests.

But IGF-1 (identical to the liver IGF-1) is produced in muscle cells as well. It is produced there and comes to the surface of a cell where it will bind to a receptor on the vary same cell. This is very powerful IGF-1 because unlike systemic a little goes a long way.

So what is important is the extent to which GH or testosterone increase this muscle made/used IGF-1. This is often referred to as autocrine/paracrine meaning made locally & used either in the same cell or a neighbor.

In mice who are engineered to not make muscle IGF-1 but plenty of systemic they fail to reach normal growth. They grow so systemic IGF-1 from the liver works but but not that effectively.

In mice with the reverse, i.e. engineered to make muscle IGF-1 but not systemic IGF-1 growth is normal.

The conclusion from many studies is that circulating IGF-1 is not sufficient for full growth but muscle IGF-1 is sufficient.

The other important IGF in muscle cells is mechano growth factor (MGF). This is a splice variant of IGF-1 meaning that the stimulus, mechanical load/weight training, alters gene transcription to alter IGF-1 to produce a variant. This variant never leaves the muscle cell and translocates to the nucleus of the cell where it mediates proliferative events.

IGF-1 on the other hand when it is produced moves to the cells cytoplasm and pools there until called to the surface where it finds its way to bind to an IGF-1 receptor.

Got it?
 

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