HGH

[The Sundance Kid]

I've heard that the stuff is pretty easy to get a hold of these days. I know there are a couple of "youth Clinics" around here that specialize in losing weight, cosmetic surgery, ect.ect.ect.

I was just wondering how easy the stuff is to get? Has anyone ever used it? How much does it cost? Do you inject it or take in orally?


Any info on the subject would be greatly apprechated.

[DonFrye]

Very expensive. Very expensive. I doubt you would want to deal with the physical side effects, also. Lots of negatives involved from my experience. If you're going to go that route, you might as well just juice up for 2 short cycles, but I would never condone that. Ever.

[Ubermensch]

Originally Posted by The Sundance Kid

I've heard that the stuff is pretty easy to get a hold of these days. I know there are a couple of "youth Clinics" around here that specialize in losing weight, cosmetic surgery, ect.ect.ect.

I was just wondering how easy the stuff is to get? Has anyone ever used it? How much does it cost? Do you inject it or take in orally?


Any info on the subject would be greatly apprechated.

You can shoot HGH anyone who give you a pill is a bullshitter. Its pretty much the same formula that I wrote in the other thread if they are pills. Anyway you can Shoot HGH for about 3 weeks to a month then don't do it for a while and then you can do it again. The problem is that your pinal gland (if I remember right) can start to over produce HGH as a side effect and you will get Acromegalia then look like a freak and have all sorts of problems. See a doctor who knows his shit and use the plan he devises. It's fuckin expensive for the real deal my friend.

[DonFrye]

Originally Posted by Ubermensch

You can shoot HGH anyone who give you a pill is a bullshitter. Its pretty much the same formula that I wrote in the other thread if they are pills. Anyway you can Shoot HGH for about 3 weeks to a month then don't do it for a while and then you can do it again. The problem is that your pinal gland (if I remember right) can start to over produce HGH as a side effect and you will get Acromegalia then look like a freak and have all sorts of problems. See a doctor who knows his shit and use the plan he devises. It's fuckin expensive for the real deal my friend.

Definitely. Swollen knuckles and joints, protruding forehead, painful knees, diabetes, many side effects. Acromegaly is the primary and most noted one. The cost for true HGH is so expensive it should not even be mentioned. The cheapest I've seen is 375.00 for 100 i.u. and if you're taking 4-6 i.u. per day for 6-8 weeks, you can tell that it isn't going too far. Here's a product article from one of the "Places" that sells it:



"The use of exogenous sources of Growth Hormone has been popular in the United States for almost 8 years now. Originally, athletes used biologically active forms that were the actual extract of the pituitary glands of cadavers. While production was under way on the synthetic, recombinant DNA versions of this drug, it was discovered that the biologically active form was associated with the formation of a rare brain virus called Creutzveldt Jacob Disease. This was a fatal virus that afflicted a very small number of GH users, none of whom were athletes. In light of this discovery, the FDA removed all of these natural GH versions from the market in the United States. Luckily, the synthetic recombinant versions were approved by the FDA a short time afterwards. These versions were developed after years of experiments with amino acid chains. The first of these versions was patented and produced by Genentech Labs with the brand name Protropin. A short time later, another form of synthetic Growth Hormone gained FDA approval. It was produced by Eli Lilly Labs and brand named Humatrope. This product was allowed to be patented because it was shown to be unique in that it contained a slightly different amino acid chain than the Protropin. The difference was that Humatrope had 191 amino acid chains in sequence and Protropin had 192. For some very complicated reasons, the 191 amino acid configuration has been shown to be more effective. It had been speculated that these synthetic versions of GH would greatly improve the cost effectiveness of using GH, yet that has not been the case. It has been used extensively by athletes who are attempting to alter their body composition. Growth Hormone itself, is an endogenous hormone produced by the pituitary gland. It exists at especially high levels during the teen years when it promotes growth of almost all tissues. It also contributes to the deposition of protein and promotes the breakdown of fat for use as energy. As the body reaches full maturation, the endogenous levels of GH are substantially diminished. After this, GH is still present in the body but at a substantially lower level where it continues to aid in protein synthesis, RNA and DNA reactions and the conversion of body fat to energy. By introducing an exogenous source of this hormone, athletes are hoping to promote these effects, causing the body to deposit more muscle tissue while atthe same time reducing body fat stores. On paper, GH should work exceptionally well; however, it does not seem to be delivering up to its potential. Most athletes who have experimented with this product end up being disappointed. There is some evidence that exogenous sources of GH are being destroyed by antibodies which appear after the introduction of the synthetic compound. Although the 191 amino acid sequence versions have been shown to produce less of an antibody reaction, they are still not yielding consistent results. I have speculated as to whether the introduction of exogenous GH would yield an appreciable degree of efficacy simply due to the fact that the body does not have sufficient receptor affinity to GH in the post-teen years. A number of athletes claim that GH is not that effective on its own, but in a stack with steroids it can do remarkable things. Perhaps there is some type of actual synergism created by the concomitant use of these two agents. Empirical data suggests that the efficacy of GH is dose related and that the majority of users may not have been taking enough Although Growth Hormone is banned by athletic committees, there is no method for the detection of it which allows drug tested competitors to use this product freely without any ramifications. Adverse reactions to GH use are rare but technically could involveacromegaly (elongation of the feet, forehead and hands). Other possible side effects involve overgrowth of the elbows or jaw, thickening of the skin and a type of diabetes. Effective dosages seem to be in the area of 4 IU/day. Cycle length is usually determined by how long the athlete can afford it. Some take the product for 6 week cycles, others use it year round."



There you go. All you would need to know. Just remember, these guys are selling it.

[The Sundance Kid]

So how much $? per cycle?

[DonFrye]

750-1000. 42 days @ 4 i.u.= 168 i.u. 42 days @ 6 i.u. = 252 i.u. and at about 375-400 per 100 i.u. you can do the math. And that's only 6 week cycles. Most people do about 8.

[The Sundance Kid]

i.u.= international unit?


So what is the bottome line on a six week cycle?

[DonFrye]

750-1000 depending where you get it. IU is International Unit.

[adonis]

This was recently posted at my other board in the anabolics section.

Originally Posted by Bryan Haycock

by Bryan Haycock - There are primarily two theories as to how GH exerts its growth promoting effects. The first theory is called the Dual Effector theory (Green, 1985). The second theory is called the Somatomedin ("mediator of growth") Hypothesis (Daughaday, 1972). Both theories are fairly strait forward. Let?s start with the Dual Effector theory.

The Dual Effector theory states that GH itself has anabolic effects directly on body tissues. This theory has been supported by studies looking at the effects of injecting GH directly into growth plates. Genetically altered strains of mice have also help to support this theory. When comparing mice that genetically over express GH and mice that over express insulin-like growth factor-1 (IGF-1), GH mice are larger. Those who support the dual effector theory site this evidence. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished. Clearly IGF-1 has got to be involved somewhere between the pituitary and the target tissue (i.e. muscle). The Somatomedin hypothesis clears things up somewhat.

The Somatomedin hypothesis states that GH exerts its growth promoting effects through IGF-1. More specifically, GH is first released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs work as endocrine growth factors, meaning that they travel in the blood to the target tissues after being released from cells that produced it, specifically the liver in this case. Many studies have been performed showing that animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. Admittedly, the effects are similar to those observed after GH administration. In fact, additional studies have shown IGF-1 to be greatly inferior as an endocrine growth factor requiring almost 50 times the amount to exert that same effects of GH (Skottner, 1987). Recently rhIGF-1 has become widely more available and is currently approved form the treatment of HIV associated wasting. This increased availability allowed testing of this hypothesis in humans. Studies in human subjects with GH insensitivity (Laron syndrome) have consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993). These results indicate that although IGF-1 might be the mediator of GH effects, it's not as simple as just getting the liver to release IGF-1.

So the main difference between these two theories is that the Dual effector theory states that GH doesn?t necessarily need IGF-1 to work, the Somatomedin hypothesis insists it does. In reality both theories are correct. It?s just that the Somatomedin hypothesis focuses on "circulating" IGF-1, the Dual Effector theory recognizes that although IGF-1 is still the active hormone, it doesn't have to come from the blood (liver), it can be produced on location by the very cells that use it.

In summary, by combining the Dual Effector theory and the Somatomedin hypothesis there are three main mechanisms by which GH makes things grow (Spagnoli,1996). First, the effects of GH on bone formation and organ growth are mediated by the endocrine action of IGF-1. As stated in the Somatomedin hypothesis, GH, released from the pituitary, causes increased production and release of IGF-1 into the general circulation. IGF-1 then travels to target tissues such as bones, organs, and muscle to cause anabolic effects.

Second, GH regulates the activity of IGF-1 by increasing the production of binding proteins (specifically IGFBP-3 and another important protein called the acid-labile subunit) that increase the half-life of IGF-1 from minutes to hours. Circulating proteases then act to break up the binding protein/hormone complex thereby releasing the IGF-1 in a controlled fashion over time. GH may even cause target tissues to produce IGFBP-3 increasing its effectiveness locally.

Third, GH may influence the activity of IGF-1 on an autocrine/paracrine level. Autocrine means that a hormone has an effect on the cell that produced it, paracrine means to have an effect on the "cell(s)" next to it as well. This is a completely localized effect, not dependent on the blood stream to carry things where you want them. Muscle growth from weight training is the result of IGF-1 being produced by the muscle cells themselves, not the liver. In fact, IGF-1 form the liver is genetically different from IGF-1 produced in your muscles. This information should explain why using IGF-1 systemically (from the blood stream) has been a hit and miss proposition.

In order to sufficiently address the role of GH and IGF-1 in muscle growth, we need to explore the mechanism of not only IGF-1?s autocrine/paracrine actions, but also the mechanisms of muscle growth itself.

The ability of muscle tissue to constantly regenerate in response to activity makes it unique. Its ability to respond to physical/mechanical stimuli depends greatly on what are called satellite cells. Satellite cells are muscle precursor cells. You might think of them as "pro-muscle" cells. They are cells that reside on and around muscle cells. These cells sit dormant until called upon by growth factors such as IGF-1. Under the influence of IGF-1 these cells divide (proliferate) and genetically change (differentiation) into cells that have nuclei identical to those of muscle cells. These new satellite cells with muscle nuclei are critical if not mandatory to muscle growth.

Without the ability to increase the number of nuclei, a muscle cell will not grow larger and its ability to repair itself is limited. The explanation for this is quite simple. The nucleus of the cell is where all of the blue prints for new muscle proteins come from. The larger the muscle, the more nuclei you need to maintain protein synthesis. There is a "nuclear to volume" ratio that cannot be overridden. Whenever a muscle grows in response to mechanical overload (i.e. weight training) there is a positive correlation between the increase in the number of myonuclei and the increase in muscle cell's cross sectional area (CSA). When satellite cells are prohibited from donating new nuclei, overloaded muscle will not grow (Rosenblatt,1992 & 1994; Phelan,1997). So you see, one important key to exercise induced muscle growth is the activation of satellite cells by growth factors such as IGF-1.

Few people realize that you can inject a muscle with IGF-1 and it will grow! Studies have shown that, when injected locally, IGF-1 increases satellite cell activity, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area (Adams,1998). I'm not really sure why someone would choose to inject oil instead of IGF-1. Oil gives you lumps and causes your peers to make jokes about you behind your back. IGF-1 just makes the muscle grow and leaves people wondering how you brought up those lagging rear delts.

Scientists are now figuring out the signaling pathway by which mechanical stimulation and IGF-1 activity leads to all of the above changes in satellite cells, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area just outlined above. This research is stemming from studies done to explain cardiac hypertrophy. It involves a muscle enzyme called calcineurin which is a phosphatase enzyme activated by high intracellular calcium ion concentrations (Dunn, 1999). Note that overloaded muscle is characterized by chronically elevated intracellular calcium ion concentrations. Other recent research has demonstrated that IGF-1 increases intracellular calcium ion concentrations leading to the activation of the calcineurin signaling pathway, and subsequent muscle fiber hypertrophy (Semsarian, 1999; Musaro, 1999). I am by no means a geneticist so I hesitated even bringing this research up. To avoid confusion I will enlist the help of the people doing the research. The researchers involved in these studies have explained it this way, IGF-1 as well as activated calcineurin, induces expression of the transcription factor GATA-2, which accumulates in a subset of myocyte nuclei, where it associates with calcineurin and a specific dephosphorylated isoform of the transcription factor nuclear factor of activated T cells or NF-ATc1. Thus, IGF-1 induces calcineurin-mediated signaling and activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-ATc isoforms to activate gene expression programs leading to increased contractile protein synthesis and muscle hypertrophy. Simple huh?

Anybody really interested in how muscles grow is going to have to brush up on their genetics (including myself). Until then please don't send me a barrage of questions about GATA-2 or NF-Atc isoforms. These aren't things we know how to directly manipulate with supplements yet.

hGH Resources

Saizen Prescribing Information

References

Green H., Morikawa M., Nixon T. A dual effector theory of growth hormone action. Differentiation 29:195, 1985

Daughaday WH., Hall K., Raben MS., et al: Somatomedin: A proposed designation for the "sulfation factor" Nature 235:107, 1972

Skottner A., Clark RG., Robinson ICAF., et al: Recombinant human insulin-like growth factor: Testing the Somatomedin hypothesis in hypophysectomized rats. J Endocrinol 112:123 1987

Rank MB., Savage MO., Chatelain PG., et al: Insulin-like growth factor improves height in growth hormone insensitivity: Two year's result. Horm Res 44:253, 1995

Savage MO., Blum WF., Ranke MB., et al: Clinical features and endocrine status in patients with growth hormone insensitivity (Laron syndrome). J Clin Endocrinol Metab 77:1465, 1993

Spagnoli A, Rosenfeld RG. The mechanisms by which growth hormone brings about growth. The relative contributions of growth hormone and insulin-like growth factors. Endocrinol Metab Clin North Am 1996 Sep;25(3):615-31

Rosenblatt JD, Parry DJ., Gamma irradiation prevents compensatory hypertrophy of overloaded extensor digitorum longus muscle. J. Appl. Physiol. 73:2538-2543, 1992

Rosenblatt JD, Yong D, Parry DJ., Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Muscle Nerve 17:608-613, 1994

Phelan JN, Gonyea WJ. Effect of radiation on satellite cell activity and protein expression in overloaded mammalian skeletal muscle. Anat. Rec. 247:179-188, 1997

Adams GR, McCue SA., Local infusion of IGF-1 results in skeletal muscle hypertrophy in rats. J. Appl. Physiol. 84(5): 1716-1722, 1998

Dunn SE., Burns JL., & Michel RN. Calcineurin is required for skeletal muscle hypertrophy. J. Biol. Chem. 274(31):21908-21912, 1999

Semsarian C, Wu MJ, Ju YK, Marciniec T, et al. Skeletal muscle hypertrophy is mediated by a Ca2+-dependent calcineurin signaling pathway. Nature 1999 Aug 5;400 (6744) :576-81

Musaro A, McCullagh KJ, Naya FJ, Olson EN, Rosenthal N. IGF-1 induces skeletal myocyte hypertrophy through calcineurin in association with GATA-2 and NF-ATc1. Nature 1999 Aug 5;400(6744):581-5

If you need any more info feel free to PM me. It's best kept out of the forums (for safety and privacy).