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Igf-1 R3???
- Thread starter getbig27
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ultragainz
New member
4 weeks on 4 weeks off is good..you can take it for the first 4 weeks with gh and slin.....
ultragainz
New member
i never used it but yea i think the gainz are keepable...and yes you can use it in a cutting cycle....
From what I've read on IGF-1, it's a great product, if you can get it in a stable form. Too much shaking of the product renders it useless. But, if you get it stable, apparently the stuff is great for size. The more you eat the more you grow. Isn't that true for everything though? On the downside, it appears that IGF-1 can increase estrogen levels. I'm not sure of the pathway, but I believe that the IGF-1 can bind with estrogen receptors, but not in a good way like Nolvadex, or Clomid. There was a post somewhere, (not sure if on this site, sorry) about how this may be the pathway that Fina causes gyno, that is by increasing IGF-1 which increases estogen, not by increased progesterone levels, as is usually assumed.
Getbig27, all things being equal, I'd say that IGF-1 is better than HGH. The main reason for using HGH is to increase IGF-1 levels, so by using the IGF-1, you are in essence going "right to the source" But, I think more research needs to be done, as far as IGF's results for bodybuilding purposes, before conclusions can be made.
IGF-1 is a hormone and does not bind to the estrogen receptor in any way that I have seen. It is responsible for cell proliferation however and has been proven to cause gyno in some at high levels. I made many posts on this in the past and have heard of people making a correlation between igf-1 and estrogen yet no one is showing me any proof of this. IGF-1 levels are naturally higher when we are yournger and growing, if it bound to the estrogen receptor as some falsly believe juvinile gyno would be rampant.
Additionally, many of the abstracts I have posted show that tren and/or tren and estrogen increase IGF-1 levels, if igf-1 levels bound to the estrogen receptor they would fool the body into thinking there was more estrogen than there really is which may do one of a couple things, first it would likely lower output of fsh/lh which in turn would drop test levels. Also, since estrogen seems to increase igf-1, it would perhaps put the body into an infinite cycle of increasing igf-1 which in turn, as some may believe, attach to the estrogen receptor which in turn would cause more igf-1 which in turn....I think you see where I am going.
Now, as pointed out many times in the past nolva ( a well known anti-e) not only blocks estrogen BUT ALSO lowers igf-1 levels, which in part are likely due to the fact that estrogen levels are lower as well. Anastrozole also lowers estrogen levels but seems to effect IGF-1 levels much less than nolva. This all leads me to believe that estrogen is only partially responsible for increasing IGF-1.
Anyways, enough babling for now. But for those that think IGF-1 bind to the estrogen receptor, I for one would like some proof to back up these claims. I for one could probably use a bit more fiber in my diet, so find me the proof and I will print this thread and eat my words.
Now, as pointed out many times in the past nolva ( a well known anti-e) not only blocks estrogen BUT ALSO lowers igf-1 levels, which in part are likely due to the fact that estrogen levels are lower as well. Anastrozole also lowers estrogen levels but seems to effect IGF-1 levels much less than nolva. This all leads me to believe that estrogen is only partially responsible for increasing IGF-1.
Anyways, enough babling for now. But for those that think IGF-1 bind to the estrogen receptor, I for one would like some proof to back up these claims. I for one could probably use a bit more fiber in my diet, so find me the proof and I will print this thread and eat my words.
hard_core_jr
New member
If Fina raises IGF-1 levels would it be better to take IGF-1 R3long with Fina or something like Sust and Deca?
Well, as I mentioned above estrogen is one factor in raising IGF-1 levels so any drug that aromatizes and does not have the aromitization blocked with raise IGF-1 levels to an extent. Tren seems to be the king of raising IGF-1 levels and deca does as well. As with all hormone levels in our bodies they are monitored by multiple means and appropriate measures are taken with regard to adjucting thier output. Often times when on AAS that increases IGF-1 levels, GH output will decrease since to our bodies GH is the main factor in the release of IGF-1. Now, keep in mind, IGF-1 levels in conjunction with estrogen and prolactine and progesterone combine forces to increase the risk of gyno. I am still looking into specifics, But I bet if you couple IGF-1 r3 with tren you would greatly increase your risk of gyno. For that simple fact I think I would try it with test or another product that does not increase IGF-1 levels so dramatically.
On that same note however, I would honestly try it post cycle to help keep gains and get a better idea of what it can do by itself.
On that same note however, I would honestly try it post cycle to help keep gains and get a better idea of what it can do by itself.
The Iron Game
New member
A comparison of hGH and IGF-1 separately, in lean body mass on subjects of of sufficient age to not require it for actual medical purposes. ENJOY
Divisions of Endocrinology, Nemours Children's Clinic, Baptist Medical Center, Jacksonville, Florida 32207, USA.
Severe gonadal androgen deficiency can have profound catabolic effects in man. Hypogonadal men develop a loss of lean body mass, increased adiposity, and decreased muscle strength despite normal GH and insulin-like growth factor I (IGF-I) concentrations. We designed these studies to investigate whether GH or IGF-I administration to male subjects with profound hypogonadism can diminish or abolish the catabolic effects of testosterone deficiency. Moreover, we also examined the nature of the interactions among GH, IGF-I, and androgens in specific genes of the im system. A group of 13 healthy subjects (mean age, 22 +/- 1 yr) was studied at baseline (D1) and 10 weeks after being made hypogonadal using a GnRH analog (GnRHa; D2). At 6 weeks from baseline they were started on either recombinant human (rh) IGF-I (60 microg/kg, sc, twice daily) or rhGH (12.5 microg/kg, sc, daily) for 4 weeks. On each study day subjects had infusions of L-[(13)C]leucine; indirect calorimetry; isokinetic dynamometry of the knee extensors; determination of body composition (dual energy x-ray absortiometry) and hormone and growth factor concentrations, as well as percutaneous muscle biopsies. Their data were compared with those of previously studied male subjects who received only GNRHA: Administration of rhIGF-I and rhGH to the hypogonadal men had similar effects on whole body metabolism, with maintenance of protein synthesis rates, fat oxidation rates, and fat-free mass compared with the eugonadal state, preventing the decline observed with hypogonadism alone. This was further amplified by the molecular assessment of important genes in muscle function. During rhIGF-I treatment, im expression of IGF-I declined, and IGF-binding protein-4 increased, similar to the changes during GnRHa alone. However, rhGH administration was associated with a marked increase in IGF-I and androgen receptor messenger ribonucleic acid concentrations in skeletal muscle with a reciprocal decline in IGF-binding protein-4 expression in the hypogonadal men. The gene expression for myostatin did not change. These effects were accompanied by a much greater increase in plasma IGF-I concentrations after rhIGF-I (225 +/- 32 vs. 768 +/- 117 microg/L) compared with the concentrations achieved during rhGH (217 +/- 20 vs. 450 +/- 19 microg/L). We conclude that 1) rhGH and rhIGF-I both may be beneficial in preserving lean body mass and sustaining rates of protein synthesis during states of severe androgen deficiency in man; 2) GH may affect the im IGF system via an a paracrine, local production of IGF-I; 3) androgens may be necessary for the full anabolic effect of GH/IGF-I in man. These hormones, particularly GH, may play a role in the treatment of hypogonadal men rendered hypogonadal pharmacologically or those unable to take full testosterone replacement. The latter requires further study.
Divisions of Endocrinology, Nemours Children's Clinic, Baptist Medical Center, Jacksonville, Florida 32207, USA.
Severe gonadal androgen deficiency can have profound catabolic effects in man. Hypogonadal men develop a loss of lean body mass, increased adiposity, and decreased muscle strength despite normal GH and insulin-like growth factor I (IGF-I) concentrations. We designed these studies to investigate whether GH or IGF-I administration to male subjects with profound hypogonadism can diminish or abolish the catabolic effects of testosterone deficiency. Moreover, we also examined the nature of the interactions among GH, IGF-I, and androgens in specific genes of the im system. A group of 13 healthy subjects (mean age, 22 +/- 1 yr) was studied at baseline (D1) and 10 weeks after being made hypogonadal using a GnRH analog (GnRHa; D2). At 6 weeks from baseline they were started on either recombinant human (rh) IGF-I (60 microg/kg, sc, twice daily) or rhGH (12.5 microg/kg, sc, daily) for 4 weeks. On each study day subjects had infusions of L-[(13)C]leucine; indirect calorimetry; isokinetic dynamometry of the knee extensors; determination of body composition (dual energy x-ray absortiometry) and hormone and growth factor concentrations, as well as percutaneous muscle biopsies. Their data were compared with those of previously studied male subjects who received only GNRHA: Administration of rhIGF-I and rhGH to the hypogonadal men had similar effects on whole body metabolism, with maintenance of protein synthesis rates, fat oxidation rates, and fat-free mass compared with the eugonadal state, preventing the decline observed with hypogonadism alone. This was further amplified by the molecular assessment of important genes in muscle function. During rhIGF-I treatment, im expression of IGF-I declined, and IGF-binding protein-4 increased, similar to the changes during GnRHa alone. However, rhGH administration was associated with a marked increase in IGF-I and androgen receptor messenger ribonucleic acid concentrations in skeletal muscle with a reciprocal decline in IGF-binding protein-4 expression in the hypogonadal men. The gene expression for myostatin did not change. These effects were accompanied by a much greater increase in plasma IGF-I concentrations after rhIGF-I (225 +/- 32 vs. 768 +/- 117 microg/L) compared with the concentrations achieved during rhGH (217 +/- 20 vs. 450 +/- 19 microg/L). We conclude that 1) rhGH and rhIGF-I both may be beneficial in preserving lean body mass and sustaining rates of protein synthesis during states of severe androgen deficiency in man; 2) GH may affect the im IGF system via an a paracrine, local production of IGF-I; 3) androgens may be necessary for the full anabolic effect of GH/IGF-I in man. These hormones, particularly GH, may play a role in the treatment of hypogonadal men rendered hypogonadal pharmacologically or those unable to take full testosterone replacement. The latter requires further study.
The Iron Game
New member
Department of Medicine/Endocrinology, University of New Mexico School of Medicine, Albuquerque 87131-5271, USA.
OBJECTIVE: To increase lean body mass and improve health status in patients with wasting associated with the acquired immunodeficiency syndrome (AIDS) by treatment with recombinant human growth hormone (rhGH), recombinant human insulin-like growth factor 1 (rhIGF-1), or both. DESIGN: Randomized, double-blind, placebo-controlled clinical trial. SETTING: University of New Mexico Clinical Research Center and University of Texas Southwestern Medical Center. PATIENTS: 60 patients with AIDS and wasting as defined by the Centers for Disease Control and Prevention. Patients were divided into four groups of 15 patients each. INTERVENTION: Group 1 received 1.4 mg of rhGH once daily plus placebo twice daily; group 2 received 5 mg of rhIGF-1 twice daily plus placebo once daily; group 3 received 5 mg of rhIGF-1 twice daily plus 1.4 mg of rhGH once daily; and group 4 received placebo three times daily. MEASUREMENTS: Body weight, body composition, muscle strength, protein catabolism, quality of life, and immune status were assessed at baseline, and changes in these variables were measured at 6 and 12 weeks. RESULTS: At 6 weeks, lean body mass had increased and total fat mass had decreased in the groups receiving rhGH, rhIGF-1, or both. Group 3 had the greatest changes in lean body mass (mean +/- SE, 3.2 +/- 0.59 kg; P < 0.001); only in this group were changes in body mass maintained at 12 weeks. Only patients in group 1 had improvement in muscular strength of the knees and upper body (P = 0.04) and quality of life (P = 0.01). Immunologic function did not improve in any group. CONCLUSIONS: Growth factor therapy had significantly increased lean body mass and decreased fat mass by 6 weeks, but these improvements persisted for 12 weeks only in group 3. Growth factor therapy at the dosages used in this study is not recommended because the magnitude of weight gain was modest and improvements in quality-of-life measures varied.
Publication Types:
Clinical trial
Multicenter study
Randomized controlled trial
OBJECTIVE: To increase lean body mass and improve health status in patients with wasting associated with the acquired immunodeficiency syndrome (AIDS) by treatment with recombinant human growth hormone (rhGH), recombinant human insulin-like growth factor 1 (rhIGF-1), or both. DESIGN: Randomized, double-blind, placebo-controlled clinical trial. SETTING: University of New Mexico Clinical Research Center and University of Texas Southwestern Medical Center. PATIENTS: 60 patients with AIDS and wasting as defined by the Centers for Disease Control and Prevention. Patients were divided into four groups of 15 patients each. INTERVENTION: Group 1 received 1.4 mg of rhGH once daily plus placebo twice daily; group 2 received 5 mg of rhIGF-1 twice daily plus placebo once daily; group 3 received 5 mg of rhIGF-1 twice daily plus 1.4 mg of rhGH once daily; and group 4 received placebo three times daily. MEASUREMENTS: Body weight, body composition, muscle strength, protein catabolism, quality of life, and immune status were assessed at baseline, and changes in these variables were measured at 6 and 12 weeks. RESULTS: At 6 weeks, lean body mass had increased and total fat mass had decreased in the groups receiving rhGH, rhIGF-1, or both. Group 3 had the greatest changes in lean body mass (mean +/- SE, 3.2 +/- 0.59 kg; P < 0.001); only in this group were changes in body mass maintained at 12 weeks. Only patients in group 1 had improvement in muscular strength of the knees and upper body (P = 0.04) and quality of life (P = 0.01). Immunologic function did not improve in any group. CONCLUSIONS: Growth factor therapy had significantly increased lean body mass and decreased fat mass by 6 weeks, but these improvements persisted for 12 weeks only in group 3. Growth factor therapy at the dosages used in this study is not recommended because the magnitude of weight gain was modest and improvements in quality-of-life measures varied.
Publication Types:
Clinical trial
Multicenter study
Randomized controlled trial
The Iron Game
New member
Please note, this is a post from War Lobo:
IGF1 stands for insulin like growth factor. It mimics insulin in the human body and also at the same time makes the muscles more sensitive to insulin’s effects. It is a growth factor and is the most potent one in the human body at that. IGF causes muscle cell hyperplasia, which is an actual splitting and forming of new muscle cells. This was thought to only be possible during puberty. IGF is much more potent at this effect than growth hormone is, in fact almost all of the effects you see from growth hormone come from the increased amount of IGF that your liver produces when the GH is destroyed. So it would be very easy to say that IGF is a much more potent and cheaper alternative to GH use, although GH is more effective for fat loss than IGF due to some other effects that it causes such as metabolism increase and the ability to effectively use more insulin, T3, and anabolic steroids.
Another advantage that IGF has over GH is that it has much more of an affinity to attach to muscle cells instead of bone and organ cells. Growth hormone has been know to cause a lot of organ enlargement and bone elongation since it attaches to all types of receptor cells. IGF is much more likely to go where we want it, our muscle cells. IGF-1 attaches to myogenic stem cells which are only located in muscle and connective tissues. These myogenic stem cells are responsible for the production of myoblast cells which in turn are responsible for the buildup and repair of connective tissues (ligaments, tendons, cartilage, and joints to a certain extent).
So from this you can see that IGF-1 is great for increasing the strength of tendons and also for helping to heal existing injuries while at the same time helping to prevent them. IGF-1 is also responsible for increased protein synthesis and amino acid synthesis.
IGF does not have to be used along with anabolic steroids, GH, insulin, or thyroid hormones to be effective. It causes muscle growth on its own. In fact some people prefer to use it during their breaks from steroid cycles since IGF has no effect on natural test production. It could effectively be used along with ***, clomid, and PGF2a for a hell of an off cycle stack which would allow your body to return to normal and still allow you to grow!! On its own IGF will give an increase of around 2 lbs. of new solid lean muscle tissue every two weeks, and is also is know for its ability to strip off bodyfat and GREATLY increase vascularity, bodyfat decreases of 5-8% over a 50 day cycle are not uncommon. But, of course you will be much happier with the results if you use the IGF along with anabolic steroids, testosterone, and insulin.
The use of steroids along with the IGF allow you to quickly mature and strengthen the new muscle tissue that the IGF has formed, and may also speed the process of hyperplasia. If you need any help setting up a great stack to
use along with the IGF just let me know and I can help you out. I speak with lots of top bodybuilders and guru’s so I am very knowledgeable.
The dosage issue for IGF is where the most controversy lies. Dosages used by competitive athletes most commonly range anywhere between 60mcg/day to 100+mcg/day. The trick is finding the dosage that works best for YOU. For most the best results appear when you reach a dosage of 80mcg/day, while some do
receive good results from only 40mcg/day. I personally feel the best results begin to be noticed at a dosage of 100mcg/day. I personally am using 150mcg/day during my current cycle.
Also I should let you know that the form of IGF is the Long R3 analog. It has been chemically altered and has a longer half-life than regular IGF, which only lasts about 10 minutes in the human body once injected. The Long R3 IGF-1 has a half-life of 6-10 hours, so you will only need to inject once or twice per day. The best time to inject is after lifting and in the morning, so it would be best to use half the dosage in the morning and the other half after lifting. This will take maximal advantage of IGF’s insulin
mimicking effects.
IGF1 stands for insulin like growth factor. It mimics insulin in the human body and also at the same time makes the muscles more sensitive to insulin’s effects. It is a growth factor and is the most potent one in the human body at that. IGF causes muscle cell hyperplasia, which is an actual splitting and forming of new muscle cells. This was thought to only be possible during puberty. IGF is much more potent at this effect than growth hormone is, in fact almost all of the effects you see from growth hormone come from the increased amount of IGF that your liver produces when the GH is destroyed. So it would be very easy to say that IGF is a much more potent and cheaper alternative to GH use, although GH is more effective for fat loss than IGF due to some other effects that it causes such as metabolism increase and the ability to effectively use more insulin, T3, and anabolic steroids.
Another advantage that IGF has over GH is that it has much more of an affinity to attach to muscle cells instead of bone and organ cells. Growth hormone has been know to cause a lot of organ enlargement and bone elongation since it attaches to all types of receptor cells. IGF is much more likely to go where we want it, our muscle cells. IGF-1 attaches to myogenic stem cells which are only located in muscle and connective tissues. These myogenic stem cells are responsible for the production of myoblast cells which in turn are responsible for the buildup and repair of connective tissues (ligaments, tendons, cartilage, and joints to a certain extent).
So from this you can see that IGF-1 is great for increasing the strength of tendons and also for helping to heal existing injuries while at the same time helping to prevent them. IGF-1 is also responsible for increased protein synthesis and amino acid synthesis.
IGF does not have to be used along with anabolic steroids, GH, insulin, or thyroid hormones to be effective. It causes muscle growth on its own. In fact some people prefer to use it during their breaks from steroid cycles since IGF has no effect on natural test production. It could effectively be used along with ***, clomid, and PGF2a for a hell of an off cycle stack which would allow your body to return to normal and still allow you to grow!! On its own IGF will give an increase of around 2 lbs. of new solid lean muscle tissue every two weeks, and is also is know for its ability to strip off bodyfat and GREATLY increase vascularity, bodyfat decreases of 5-8% over a 50 day cycle are not uncommon. But, of course you will be much happier with the results if you use the IGF along with anabolic steroids, testosterone, and insulin.
The use of steroids along with the IGF allow you to quickly mature and strengthen the new muscle tissue that the IGF has formed, and may also speed the process of hyperplasia. If you need any help setting up a great stack to
use along with the IGF just let me know and I can help you out. I speak with lots of top bodybuilders and guru’s so I am very knowledgeable.
The dosage issue for IGF is where the most controversy lies. Dosages used by competitive athletes most commonly range anywhere between 60mcg/day to 100+mcg/day. The trick is finding the dosage that works best for YOU. For most the best results appear when you reach a dosage of 80mcg/day, while some do
receive good results from only 40mcg/day. I personally feel the best results begin to be noticed at a dosage of 100mcg/day. I personally am using 150mcg/day during my current cycle.
Also I should let you know that the form of IGF is the Long R3 analog. It has been chemically altered and has a longer half-life than regular IGF, which only lasts about 10 minutes in the human body once injected. The Long R3 IGF-1 has a half-life of 6-10 hours, so you will only need to inject once or twice per day. The best time to inject is after lifting and in the morning, so it would be best to use half the dosage in the morning and the other half after lifting. This will take maximal advantage of IGF’s insulin
mimicking effects.
The Iron Game
New member
it is suspended in BA to keep it more stable and make it easier to transport and use. Do not go over the 5 week mark.
The Iron Game
New member
Re: How do you inject it?
Yes
Saltee said:
Yes
The Iron Game
New member
notpuff said:
any muscle you gain will depend on nutrition
but igf is a little different, very similar to insulin in many ways.
The Iron Game
New member
notpuff said:
slin is only dangerous to those who have not researched it fully or to those who use a more is better approach
The Iron Game
New member
hard_core_jr said:
fina will not increase igf levels more than igf itself, on a side note testosterone also increases igf levels
notpuff, your welcome
In a way I think you are comparing apples and oranges here. Tren should give more mass gains per say. Igf-1 is more like GH in its effects at burning fat. As I mentioned in another thread muscle cells have so many satelite cells that lay dormant around them. The number of muscle cells we have is fixed and the number of satelite cells is limited by the number of muscle cells. When needed these satelite cells become full blown cells and add to our muscle mass but as we approach our genetic potential the number of these unused satelite cells diminish. IGF-1 can cause the creation of NEW cells and with them new satelite cells which can in essence take us beyond what nature has intended for us. AAS will allow us the best growth of what we have. IGF-1 will allow us to add muscle and grow beyond.
As TIG pointed out many AAS raise IGF-1, some better than others. Test raises IGF-1 but I believe its mostly due to the additional aromatization into estrogen, since estrogen is also a factor in igf-1 release. Tren has shown to greatly increase IGF-1 levels. Also as tig pointed out after so long at elevated levels our bodies feedback mechanism reduce the effectiveness of exogenous IGF-1 at the 4-6 week mark.
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