HGH vs IGF-1

Because IGF-1 is expensive compared to HGH.
Rare to find, often pharma increlex, a lot of fake.
I am not sure if some UGL offer lyophilised mecasermin, but as far as I know it's not stable and never saw a Jano report of it.

IGF-1 is different from the available cheap versions such as IGF LR3 and DES.
IGF LR3 won't raise your IGF-1 levels but it will make them lower.

And last thing, IGF-1 levels aren't the main benefit of HGH IMO, high IGF-1 levels stimulate lipogenese and make you store fat quicker, most of HGH users love HGH because it can keep you lean.

The 3D visual, good sleep, and all health benefits aren't necessary linked to igf-1 levels but more to HGH serum levels.

Igf-1 is like e2, e2 is results of test conversion, igf-1 is result of hgh conversion, levels are often random, e2 have a lot of benefits but it's not the main reason why we take test, so is igf-1.
 
So Igf-1 not ideal for fat burn?
No, not at all. I've never heard that as a benefit anywhere.

Pretty sure what QSC said is also what @Type-IIx has mentioned, at least in a few posts in the past. He would be the perfect guy to answer more in detail, if even needed.

I remember reading about cancer in children using increlex. Not sure how much of a risk that is for adults...
 
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No, not at all. I've never heard that as a benefit anywhere.

Pretty sure what QSC said is also what @Type-IIx has mentioned, at least in a few posts in the past. He would be the perfect guy to answer more in detail, if even needed.

I remember reading about cancer in children using increlex. Not sure how much of a risk that is for adults...
GH is lipolytic, whereas IGF-I opposes this effect somewhat (e.g., rhGH can stimulate local lipoatrophy vs. rhIGF-I local lipohypertrophy). GH & IGF-I act in a complementary fashion in many biological effects, e.g., the hyperglycemic effect of GH is opposed by the hypoglycemic effect of IGF-I, resulting in a middling-out of behavior. But IGF-I does enhance insulin sensitivity & fatty acid, glucose metabolism, thereby indirectly enhancing fat loss.

The primary reason that healthy adults generally use rhGH rather than rhIGF-I is because rhGH stimulates the complementary functions of GH/IGF-I, that in turn stimulate growth & metabolism. RhIGF-I (e.g., Increlex) is indicated for one very small clinical population, severe primary IGF-I deficiency; that is usually comorbid with absolute resistance to GH (such that rhGH cannot stimulate liver-secreted IGF-I).

Neither rhIGF-I nor rhGH have been shown to increase morbidity in long-term analyses of clinical populations due to neoplasms or cancers. While the two drugs can logically worsen prognosis of certain active neoplasms because of their mitogenic and proliferative effects, they have not been shown to initiate mutagenesis.
 
GH is lipolytic, whereas IGF-I opposes this effect somewhat (e.g., rhGH can stimulate local lipoatrophy vs. rhIGF-I local lipohypertrophy). GH & IGF-I act in a complementary fashion in many biological effects, e.g., the hyperglycemic effect of GH is opposed by the hypoglycemic effect of IGF-I, resulting in a middling-out of behavior. But IGF-I does enhance insulin sensitivity & fatty acid, glucose metabolism, thereby indirectly enhancing fat loss.

The primary reason that healthy adults generally use rhGH rather than rhIGF-I is because rhGH stimulates the complementary functions of GH/IGF-I, that in turn stimulate growth & metabolism. RhIGF-I (e.g., Increlex) is indicated for one very small clinical population, severe primary IGF-I deficiency; that is usually comorbid with absolute resistance to GH (such that rhGH cannot stimulate liver-secreted IGF-I).

Neither rhIGF-I nor rhGH have been shown to increase morbidity in long-term analyses of clinical populations due to neoplasms or cancers. While the two drugs can logically worsen prognosis of certain active neoplasms because of their mitogenic and proliferative effects, they have not been shown to initiate mutagenesis.
BUT, has there been a study that was NOT with folks with hypogonadism/low GH/inactive pituitary? so of course folks would not die of cancer on GH at a higher rate than those with placebo, as your not looking at a normal population ;). however if you have a long term study of HGH in normal(not deficient) population id love to see it! however have to be careful comparing people who need HGH for aids or esp pituitary issues vs normal population as far as cancer. HUGE difference. but maybe you have a study(but I HIGHLY doubt would get approved to be done). otherwise gotta be careful with drawing conclusions without background info.

what about the many mice studies that show increase hgh causes mice to die sooner and loose cognitive function faster than mice with a dificiency?

do smaller dogs/humans that live longer have less hgh or less binding capacity? (I actually dont know, but assume at least part of why they dont grow as tall) they may say oh there bigger so heart has to work harder... but what grows the heart, hgh..

anyway, on a rant. just wanted to make a point that morbidity/cancer as in the case of HGH studies is a little skewed as of course extends life of chronic wasting in adults. but likely won't do the same for normal population. UNLESS of course you can cite a study not done on deficient population.
 
Thank you @Type-IIx for your knowledge... so I guess if someone wanted to trim up, burn fat, build muscle, without the hyperglycemic effects - would IGF-1 be good to use, or is HGH really going to be superior in that aspect, and suggested to use, perhaps with metformin or berberine?

Thank you.
 
Thank you @Type-IIx for your knowledge... so I guess if someone wanted to trim up, burn fat, build muscle, without the hyperglycemic effects - would IGF-1 be good to use, or is HGH really going to be superior in that aspect, and suggested to use, perhaps with metformin or berberine?

Thank you.
Although this question was not addressed to me, I'll provide my thoughts (for whatever they're worth).

The short answer is: you're on the right track.

I like berberine with hGH a lot. Metformin, functionally, is similar... However, it seems to lead to GI-related issues for many users. This leads to issues eating, which, largely leaves a lot of progress on the table... Can't eat, can't grow.

I've taken IGF-1 LR3, Increlex, various generic hGH and pharma hGH over the years... The results from Increlex were the best (in terms of muscle gained), but, I also carried a lot of water and honestly the cost was too limiting to justify.

Your best bet would be quality hGH and berberine..

Then, MAYBE IGF-1 LR3 solely for its insulin sensitizing effects (if needed) if you want to really blast hGH (6iu+ daily) for a period...
 
GH is lipolytic, whereas IGF-I opposes this effect somewhat (e.g., rhGH can stimulate local lipoatrophy vs. rhIGF-I local lipohypertrophy). GH & IGF-I act in a complementary fashion in many biological effects, e.g., the hyperglycemic effect of GH is opposed by the hypoglycemic effect of IGF-I, resulting in a middling-out of behavior. But IGF-I does enhance insulin sensitivity & fatty acid, glucose metabolism, thereby indirectly enhancing fat loss.

The primary reason that healthy adults generally use rhGH rather than rhIGF-I is because rhGH stimulates the complementary functions of GH/IGF-I, that in turn stimulate growth & metabolism. RhIGF-I (e.g., Increlex) is indicated for one very small clinical population, severe primary IGF-I deficiency; that is usually comorbid with absolute resistance to GH (such that rhGH cannot stimulate liver-secreted IGF-I).

Neither rhIGF-I nor rhGH have been shown to increase morbidity in long-term analyses of clinical populations due to neoplasms or cancers. While the two drugs can logically worsen prognosis of certain active neoplasms because of their mitogenic and proliferative effects, they have not been shown to initiate mutagenesis.
^these are the types of posts we need. Nice write up!
 
Because IGF-1 is expensive compared to HGH.
Rare to find, often pharma increlex, a lot of fake.
I am not sure if some UGL offer lyophilised mecasermin, but as far as I know it's not stable and never saw a Jano report of it.

IGF-1 is different from the available cheap versions such as IGF LR3 and DES.
IGF LR3 won't raise your IGF-1 levels but it will make them lower.

And last thing, IGF-1 levels aren't the main benefit of HGH IMO, high IGF-1 levels stimulate lipogenese and make you store fat quicker, most of HGH users love HGH because it can keep you lean.

The 3D visual, good sleep, and all health benefits aren't necessary linked to igf-1 levels but more to HGH serum levels.

Igf-1 is like e2, e2 is results of test conversion, igf-1 is result of hgh conversion, levels are often random, e2 have a lot of benefits but it's not the main reason why we take test, so is igf-1.
so does igf1 lr3 work like endogenous igf1 or different/not? curious because you said it lowers the levels. and if it works differently, how?
 
BUT, has there been a study that was NOT with folks with hypogonadism/low GH/inactive pituitary? so of course folks would not die of cancer on GH at a higher rate than those with placebo, as your not looking at a normal population ;).
Fair point actually (I was going to breeze past this post at first). I've remarked about the long-term data on this population before; and when I did so I was careful to point out that since lifespan would be significantly reduced for this population without GH/IGF-I replacement, it's difficult to draw associations about qualitatively different uses in our population.

However, this data does not stand alone; it is supported by in vitro data that fails to show any causal effect of GH/IGF-I on mutagenesis.
however if you have a long term study of HGH in normal(not deficient) population id love to see it! however have to be careful comparing people who need HGH for aids or esp pituitary issues vs normal population as far as cancer. HUGE difference. but maybe you have a study(but I HIGHLY doubt would get approved to be done). otherwise gotta be careful with drawing conclusions without background info.

what about the many mice studies that show increase hgh causes mice to die sooner and loose cognitive function faster than mice with a dificiency?

do smaller dogs/humans that live longer have less hgh or less binding capacity? (I actually dont know, but assume at least part of why they dont grow as tall) they may say oh there bigger so heart has to work harder... but what grows the heart, hgh..

anyway, on a rant. just wanted to make a point that morbidity/cancer as in the case of HGH studies is a little skewed as of course extends life of chronic wasting in adults. but likely won't do the same for normal population. UNLESS of course you can cite a study not done on deficient population.
Long-term high dose GH/IGF-I increases body size, and epidemiological data does support an association in humans with increased body size & cancer risk, as well as morbidity. As in, very tall people tend to die younger than average, for example. A weakness with observational data like this is that it often leads to errors in associating cause/effect correctly, and misses tertiary variables and the like, or third factors that might be at play (e.g., perhaps taller people work in more dangerous professions or are placed in more risky conditions in their field of employ). This is not to say that I don't think there is some contribution of a high cell # on risk of mutagenesis over the lifespan, it seems fairly logical that larger people would be more susceptible to cancers and the like to me as a first impression.
 
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I got massive running cjc and ipamorelin stacked with igf-1 and ghrp-6 / ghrp-2, plus sermorlein. Also was running HGH frag.
2-4IU HGH at bed time as well.
 
I think it was a joke

EDIT: or maybe not lol mentioned "did a bunch of hgh peptides" in another thread. seems like a good way to get ALL the sides vs being selective and not 4 things that do the same thing, but to each there own!
 
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