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ChemOne - Long r3 IGF-1
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ChemOne - Long r3 IGF-1 - 11-06-2006, 06:11 AM

I was recommanded to use this by pincrusher and I would like to know actually what will it do. My bodyfat is 10% was 11% when I started my cycle. My goal is to stay around 220 and lose about ten pounds which will be pushing it and replace it with 10 pounds of mass. Also does anybody recommand anything to bring my veins out more. I have until Dec 21 to do this.
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11-06-2006, 10:16 AM

from all accounts igf is a stronger gh. gh actually makes your body produce more igf which is what causes muscle growth.
for your short timeframe you want to make your progress, igf will help because it will not only keep off unwanted fat while eatting to grow but will help your veins come out some, will cause big pumps in the gym, will cause muscle growth by creating new muscle instead of just trying to increase the size of current muscle cells. here are some articles for ya to read:

here are a bunch of articles posted on intensemuscle about igf that simplifys it somewhat but provides great info for you to understand.

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IGF1, also known as somatomedin C, is polypeptide hormone about the same size as insulin. It is produced pre***inantly in the liver in response to growth hormone (GH) release from the pituitary gland. Many of the growth promoting effects of GH are due to its ability to release IGF1 from the liver. The conversion ratio of GH to IGF1 varies greatly in different individuals but most external sources of GH convert around 4-6mcg of IGF per one I.U. of GH. IGF-1 acts on several different tissues to enhance growth. IGF1 belongs in the 'superfamily' of substances known as 'growth factors,' along with epidermal (skin), transforming; platelet derived fibroblast, nerve, and ciliary neurotrophic growth factors. None of the other factors have any bearing on exoskeletal tissue incidentally however These agents all have in common the ability to stimulate cell division, known as mitogenesis, and cell differentiation. Meaning That In the case of IGF1 which does act on muscle tissue it will initiate the growth of new muscle fibers, and subsequently new receptors for testosterone. Users have unanimously concluded that it enhances cycles of steroids significantly. They also seem to be adamant about its ability to reduce fat and improve vascularity a great deal.

How to use IGF1

Assuming that you have acquired legitimate IGF1 (R3) long chain, That's IGF1 with the binding protein added. You should take dosages ranging from 60mcg up to 120mcg per day in divided doses. One injection in the morning and again at bed time. Never exceed 120mcg in one day. IGF1 can cause serious gastrointestinal problems such as tumors intestinal swelling diarrhea and vomiting. Most IGF1 comes in a concentration of 1000mcg per ML or CC so it makes it easy to measure in an insulin syringe. 10 IU on the syringe is 100mcg. Do the math.

IGF + Insulin

If you plan on doing IGF1 with Insulin, listen closely IGF1 is not that expensive, sure you can get away with using less by including insulin in the stack, but IGF1 and Insulin together have a pro-insulin effect on your blood sugar balance. It can enhance the chances of a hypoglycemic episode ten fold. I would recommend against it for any one not ABSOLUTLY comfortable with insulin or IGF1.

Here is how insulin and IGF1 work together. Igfbp3 is the binding protein, which allows IGF1 to remain active in the system for a long enough period of time to really work its magic. IGF1 by nature has a half-life of less than 10 minutes by its self. The molecule was so small it would escape the blood stream very rapidly. This was the reason IGF1 was so "underground". It took very frequent injections at high dosages to achieve even minimal results. Aside from this reconstituting the compound required a degree in biochemistry. This short acting version was the only IGF1 known until recently IGF1 would have been administered in 100 mcg dosages 4-6 times a day. That is a hell of a lot of IGF1. That explains a lot of the distended bellies. Now with R3 long chain IGF1 and the Binding protein IGFBP3 IGF1 will last up to 6 hours in the system. By binding IGF to the IGFBP3 you make the molecule larger and it gets trapped in the blood stream until the protein is broken down and the IGF molecule escapes. You can further its life by combining Insulin with it, although I here its very risky. Insulin prevents the breakdown of IGFBP3 and leaves the IGF1 molecule roaming free in the blood stream for longer periods of time up to 12 hours as insulin levels return to normal IGFBP3 will begin to break down and the IGF1 will escape from its bound protein IGFBP3 again having a half life of less than 10 minutes.

Insulin should be taken at the normal dosage it is usually administered at minus 10% about 45 minutes prior to the IGF1 infusion. Again let me remind you this can be deadly if you don't know what you are doing. And of course do not use Insulin for the nighttime injection of IGF1 by taking it in the morning you prolong the IGF1's half life to 12 hours and then take a 6 hour injection, you should be fine. Hell if you want to eat a big bowl of rice and drink another 100g of simple carbs 45 minutes before the bed time IGF1 infusion you could spike insulin for at least a few hours of extended IGF1 activity. If your not going to be using insulin in the stack then go ahead and do the same in the morning.

What users report

Users of IGF1 have reported various results but all along the same lines, It does not appear to be dramatically less effective in any one individual (at least not to the best of my knowledge). I have a good friend who had to stop taking IGF1 due to stomach illness that was completely unrelated But he to experienced good gains from it for the 2 weeks he was on it, his dosage was 120mcg per day. One hour after the first injection he went to the gym and immediately told me about the uncontrollable pump he got from just one set.

That would indicate to me that he was experiencing some form of cell volumization. The general consensus on IGF1 seems to be that its benefits are as fallow:

Increased Pumps are reported to be so severe that workouts are often cut short due to lack of ability to the muscle through the full range of motion...ouch

Gains retention is increased if IGF is used in a cycle I am not sure why, but IGF1 seems to make gains on a cycle stick with virtually no post cycle loss. Every bodybuilder I've spoken with seems to think this for some reason. Most of them use drugs like Anadrol or Dianabol with it because of the amount of size attained with these drugs. The usual draw back to these drugs is that in most users there is a post cycle "crash" that occurs, so the reasoning is to toss IGF1 into the stack and grow larger faster with out the post cycle crash blues.

Reverses testicular atrophy

Testicles if shrunken will return to "full swing" so to speak even in the middle of a cycle. If not shrunken they will not shrink during the cycle. This may explain partially why gains are kept after the cycle.

Fatigue

Users report feeling drained and tired all day. This seems to be one of the negative side effects to IGF1, it will make you sleep longer and you will require more sleep at night to feel rested for the morning. This is common with high doses of HGH and exhibited in children, whose IGF1 levels are extraordinarily high. A child needs 4 hours more sleep than an adult on average does. This may be directly or indirectly related to IGF1 levels.

Stiffness

An almost arthritic feeling is commonly associated with high levels of HGH, well IGF1 has the exact same property. IGF1 will cause your hands, fingers and knuckles to ache this is one way you can be sure you got real IGF1.

IGF-1's Side effects

Every thing has a down side. To bake a cake ya gotta brake an egg. IGF1 is no exception. The drug used in larger quantity around the 100mcg+ range will cause headaches, occasional nausea and can contribute to low blood sugar or hypoglycemia in some users. Although I have never heard of this first hand I'm sure its true.

IGF1 will attach its self to the lining of the intestine and cause atrophy of the gut. Every thing IGF1 touches will grow and you have a lot of receptors on the lining of the large intestine and inner wall of the ab***inal well. This is what causes the GH gut look. You can easily avoid this by limiting your dosages and cycle lengths. IGF1 cycles should be kept to 4-6 weeks with 4-6 weeks off in-between. IGF-1 is considerably more powerful than HGH and you need to think of it along those lines as far as dosing goes. We all know what to much HGH can do over prolonged periods of usage. The Neanderthal look is definitely not going to win any shows this year. I would recommend 80 mcg a day for 4 weeks at a time you should get good results from that for a while. I don't know if you will need to up the dosage at any point, but I would think in the case of IGF1 it wouldn't matter. If 80mcg doesn't do it for ya, then bump it up to 100 You should definitely feel it at this point If not suspect the IGF1 as being fake. Beyond 120 mcg per day your asking for trouble, This compound demands as much respect as its sister amino Insulin.

Clinical Facts about IGF-1

IGF-1 is a polypeptide of 70 amino acids (7650 daltons), and is one of a number of related insulin-like growth factors present in the circulation. The molecule shows approximately 50% sequence homology with proinsulin and has a number of biological activities similar to insulin. IGF-1 is a mediator of longitudinal growth in humans or how tall you are capable of becoming. Serum IGF-1 concentrations are altered by age, nutritional status, body composition, and growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For the diagnosis of acromegaly, a single IGF-1 concentration is more reliable than a ran*** hGH measurement (Oppizi, et al., 1986). IGF-1 can be used for the assessment of disease activity in acromegaly (Barkan, et al., 198.

Almost all (>95%) of serum IGF-1 circulates bound to specific IGF binding proteins (IGFBPs), of which six classes (IGFBPs 1-6) have been identified (Rudd, 1991). BP3 is thought to be the major binding protein

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The present study was undertaken to test the hypothesis that direct IGF-I infusion would result in an increase in muscle DNA as well as in various measurements of muscle size. Either 0.9% saline or nonsystemic doses of recombinant human IGF-I (rhIGF-1) were infused directly into a non-weight-bearing muscle of rats, the tibialis anterior (TA), via a fenestrated catheter attached to a subcutaneous miniosmotic pump. Saline infusion had no effect on the mass, protein content, or DNA content of TA muscles. Local IGF-I infusion had no effect on body or heart weight. The absolute weight of the infused TA muscles was ~9% greater (P < 0.05) than that of the contra-lateral TA muscles. IGF-I infusion resulted in significant increases in the total protein and DNA content of TA muscles (P < 0.05). As a result of these coordinated changes, the DNA-to-protein ratio of the hypertrophied TA was similar to that of the contra-lateral muscles. These results suggest that IGF-I may be acting to directly stimulate processes such as protein synthesis and satellite cell proliferation, which result in skeletal muscle hypertrophy.
Discussion: The details of the mechanisms and pathways by which mechanical stress stimulates localized muscle fiber hypertrophy are still being elucidated. It is clear however, that growth hormone (GH), fibroblast growth factors (FGF) and insulin-like growth factors (IGF) play a central role in this process. Insulin-like growth factor I (IGF-I) peptide levels have been shown to increase in overloaded skeletal muscles (G. R. Adams and F. Haddad. J. Appl. Physiol. 81: 2509-2516, 1996). In that study, there was an increase in IGF-1 content before measurable increases in muscle protein and was correlated with an increase in muscle DNA content. Several other studies have shown that muscle fibers undergoing hypertrophy, due to mechanical stress, express elevated levels of IGF-I prior to hypertrophy.
IGF-1 appears to be an important regulator of the nuclear to cytoplasmic ratio. Studies have show that a muscle will only undergo hypertrophy if it can maintain the ratio of the cell?s volume to the number of nuclei within a finite limit. In the study above, a relatively "unloaded" muscle, the anterior tibialis, was injection with 0.9 - 1.9 micrograms/kg/day of rhIGF-1 which then mimicked the effects of physically loading the muscle. There was an increase in protein content, cross sectional area and DNA content. The increase in muscle DNA is presumed to be a result of increased proliferation and differentiation of satellite cells which donate their nuclei upon fusion with damaged or hypertrophying muscle cells. Take note that the quantities of IGF-1 used in the injections were extremely small, much smaller than studies that have shown relatively poor results from administering IGF-1 systemically which range from 1.0 to 6.9 milligrams/kg/day.
All of the attention and discussion of half-hazzardly injecting fat into muscles to increase the girth of a limb is only a symptom of the obsessive nature of bodybuilding. I would imagine that locally injecting minute amounts (micrograms) of rhIGF-1 to actually increase the growth of individual muscles would be a far better alternative to injecting fat, Esiclene or even getting silicone implants. Those bodybuilders at the national or professional level with lagging calves would be wise to consider the results of this study should they stumble across a bottle of Genentech?s rhIGF-1!

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The GH/IGF-1 Axis

Your body?s GH levels are tightly regulated by numerous chemical messengers including macronutrients, neurotransmitters, and hormones. The signal to increase your body?s GH levels starts in the hypothalamus. There, two peptide hormones act in concert to increase or decrease GH output from the pituitary gland. These hormones are somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin acts at the pituitary to decrease GH output. GHRH acts at the pituitary to increase GH output. Together these hormones regulate, in pulsatile fashion, the level of GH you have floating around in your body (see Fig. 1).

Several factors can effect this delicate balance. First, GH is subject to negative feedback in response to its own release. GH, as well as IGF-1, circulate back to the hypothalamus and pituitary to increase SS release, thereby decreasing GH release. GH may also act in an autocrine and paracrine (i.e. Effecting the source cells and neighboring cells without having to enter the circulation) fashion within both the hypothalamus and pituitary.

Neurotransmitters also effect GH levels at the hypothalamus. This neuroendocrine control is still being elucidated but some factors are already clearly involved (see table 1).

Table 1.

Neurotransmitter system Effect on GH Neurotransmitter or drug
Adrenergic
a2 Increase
a1 Decrease
Decrease

Clonidine
Methoxamine
Clenbuterol

Cholinergic Increase Acetylcholine
Opioids Increase Morphine
Dopamine Increase L-Dopa
Gut-brain peptides Increase

Nutrition and metabolic factors also modulate GH levels. A fall in blood glucose such as during exercise or during sleep causes an increase in GH secretion. High protein feedings increase acute GH secretion. Some amino acids such as L-arginine seem to increase GH by decreasing SS release from the hypothalamus. Even the vitamin Niacin has been shown to increase exercise induced GH release by 300- 600%(Murray, 1995). In this particular study there were four separate trials where 10 subjects cycled at 68% VO2 max for 120 min followed by a timed 3.5-mile performance task. Every 15 min during exercise, subjects ingested 3.5 ml./kg lean body weight of one of four beverages: 1) water placebo (WP), 2) WP + 280 mg nicotinic acid.l-1 (WP + NA), 3) 6% carbohydrate-electrolyte beverage (CE), and 4) CE + NA. Ingestion of nicotinic acid (WP + NA and CE + NA) blunted the rise in free fatty acids (FFA) associated with WP and CE; in fact, nicotinic acid ingestion effectively prevented FFA from rising above rest values. The low FFA levels with nicotinic acid feeding were associated with a 3- to 6-fold increase in concentrations of human growth hormone throughout exercise. The question remains, does this dramatic, yet temporary, increase in GH lead to a greater training effect? It may lead to greater glycogen storage capacity but other than that, we really don?t know.

Caloric restriction dramatically reduces serum levels of IGF-1 yet at the same time increases GH release. This mechanism effectively helps the individual adapt metabolically without having anabolic actions which would potentially hasten death by starvation. It is important to understand that GH can either be anabolic or catabolic. When nutrient intake is high, GH secretion is increased leading also to increased levels of IGF-1, IGFBP3 and insulin. The main role of GH under these conditions is to increase anabolism through local growth factors like IGF-1 and insulin. Conversely, when nutrient intake is low, GH is again increased. But this time there is no concomitant increase in IGF-1, IGFBP3, or insulin. Under these circumstances GH is acting as a catabolic hormone increasing the utilization of fat for fuel thus sparing body glucose yet having no muscle building effects. This behavior of the GH/IGF-1 axis is part of what makes it so difficult to build muscle while dieting. It should be noted that locally produced IGF-1 in skeletal muscle responds normally to training while dieting. This makes heavy poundages a must when trying to get ready for a show without the use of drugs.

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Growth Hormone: How does it work?

It is always prudent to have a basic understanding of how a supplement, hormone or drug works to build and/or preserve muscle before considering its use. The knowledge of how a hormone acts in the body is necessary to make your own decisions and manage your own regimens if you plan on utilizing it. Without this understanding you will no doubt end up wasting a lot of money and perhaps put your health at risk.

It has been long believed that GH exerts its anabolic effects on peripheral tissues through IGFs, also known as somatomedins ("mediator of growth"). Binding proteins play an important role in moderating the anabolic effects of both GH and IGF-1. IGF-1 is controlled by at least 6 different binding proteins and there may others waiting to be elucidated. To date there are a couple theories as to just how GH causes growth in target tissues. The first theory is called the somatomedin hypothesis (Daughaday, 1972).

The Somatomedin hypothesis states that GH is released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs got there name because of there structural and functional similarity to proinsulin. This hypothesis dictates that 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. Indeed, many studies have followed showing that in animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. The effects were similar to those observed after GH administration. Interestingly, additional studies also followed that showed 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) has consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993).

The second theory as to how GH produces anabolic effects is called the Dual Effector theory (Green, 1985). This theory states that GH itself has anabolic effects on body tissues without the need of IGF-1. This theory has been supported by studies injecting GH directly into growth plates. Further evidence supporting this theory lies in genetically altered strains of mice. When comparing mice who genetically over express GH and mice who over express IGF-1, GH mice are larger. This evidence has been sited by some to support the dual effector theory. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished.

The Somatomedin theory and the Dual Effector theory are not all that different. One simply asserts that GH can produce growth without IGF-1. From the research I am inclined to believe in the Somatomedin theory. This only becomes an issue when one decides whether or not to use just GH or to combine it with IGF-1 or insulin.

From the evidence currently available you can count on three major mechanisms by which GH leads to growth (Spagnoli, 1996).

The effects of GH one 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.
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.
IGF-1 not only has endocrine actions, but also paracrine/autocrine actions in target tissues. This means that as GH travels to my muscles, the muscle cells increase there production of IGF-1. This IGF-1 may then travel to adjacent cells (especially satellite cells) leading to growth and enhanced rejuvenative ability of cells that didn?t see any GH. This is as suggested by the Dual Effector theory.

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IGF-1: How does it work?

To understand how IGF-1 works you have to understand how muscles grow. The ability of muscle tissue to constantly regenerate in response to activity makes it unique. It?s 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. Once this happens these cells divide and genetically change 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 come from. The larger the muscle, the more nuclei you need to maintain it. In fact there is a "nuclear to volume" ratio that cannot be overridden. Whenever a muscle grows in response to functional overload there is a positive correlation between the increase in the number of myonuclei and the increase in fiber 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 unnatural muscle growth is the activation of satellite cells by growth factors such as IGF-1.

IGF-1 stimulates both proliferation (an increase in cell number) and differentiation (a conversion to muscle specific nuclei) in an autocrine-paracrine manner, although it induces differentiation to a much greater degree. This is in agreement with the Dual Effector theory. In fact, 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).

On the very cutting edge of research scientists are now discovering 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 signaling pathway, and subsequent muscle fiber hypertrophy (Semsarian, 1999; Musaro, 1999). I am by no means a geneticist so I hesitated even bringing this new research up. In summary 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. Did you get all that?

In this the first part of "Growing beyond what nature intended" we have discussed the role, function and interaction of growth hormone and insulin-like growth factor-1 in tissue growth. This is referred to collectively as the GH/IGF-1 axis. We learned that this axis is controlled by negative feedback meaning that GH, after being released, circulates back to the hypothalamus and pituitary to effectively stop further GH release. We learned that circulating IGF-1 has the same inhibiting effect on GH release. We discussed very briefly the role of neurotransmitters in regulating GH release through growth hormone releasing hormone (GHRH) and somatostatin (SS). We even touched on the nitty gritty details of just how IGF-1 does its magic on muscle cells. I?m afraid I may have disappointed a few of you waiting for the "how to" section of this article. Never fear, in part II you will learn about the effects of these hormones as well as androgens, insulin and thyroid hormones when given, individually and combined, to previously healthy individuals. I will remind you that this article is not intended to encourage you put your health at risk, or to break the law by acquiring and using these substances illegally. As always, the goal Meso-Rx is not to condone the use of performance enhancing substances, but to educate by providing unbiased information about all aspects of high level sport performance and bodybuilding.

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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 HCG, 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 body fat and GREATLY increase vascularity, body fat 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.

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I was picking a very advanced Bro's brain and was able to collect this info from him:

Go with 40mcg ed for 25 days straight for your 1st time regardless of weight of your animal. I have yet to see anyone have better results with more than 40 who ran 40 the first time around. Let me clairfy. I have yet to see hear from someone who ran their second cycle yet.

Or try this:
weeks:
1gh
2gh
3gh
4gh
5gh + igf
6gh + igf
7gh + igf
8gh + igf



If you have to dilute your 1mg with 2ml of BA. This make it a little easier to measure. On a 1cc slin pin each click would be 2iu=10mcg. 10iu =50mcg.

This makes it alot easier. I always pull 90 units of BW then pull the IGF-1 to disired amount. Then you can shoot it first. Good Luck

DOSAGES

If you are just going to use it by itself, try 40 mcg ed. 1 bottle will last you about 1 month and you should see good results from that.

If you are experienced with AAS, and you are going to run some other things with it, you could probably get away with 30 mcg

I am starting to learn that it is a lot like test to a certain point, the more the better. Obviously there is a point of diminshing returns, but I haven't hit it yet. My understanding is that is probably about 150 mcg per day.

I started at 30 mcg per day, and have gradually moved it up to 80 mcg (40 am / 40 pm)




NOTE:
this IFBB pro stated that the standard dose is 0.8mcg/kg of bodyweight.
Email: [email protected]
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IGF FAQ
From Dr JMW @ AS

Long?R3IGF-I is an analog of human IGF-I.
? It is a superior alternative to insulin in serum-free media.
? It increases protein production by cells in culture medium.
? It increases cell viability by inhibiting apoptosis.
? It has a longer half-life in cell culture than insulin.
? It is readily available.
? There is secure and ample manufacturing capacity at GroPep Limited.
? No animal- or human- derived material is used in the manufacture or storage of Long?R3IGF-I.
? Long?R3IGF-I is already being used in the manufacture of three (3) biopharmaceuticals approved by FDA and EMEA.

Frequently Asked Questions

What cell types will respond to Long?R3IGF-I?
All cells that have a Type I IGF receptor will potentially respond. Most commercially used cells including CHO, fibroblasts and hybri***as have a type I IGF receptor. All cells which respond to pharmacological concentrations of insulin (>1 mg/liter) will respond to Long?R3IGF-I (10-50 mg/liter).

Is storage of the stock solution at 4C acceptable?
Yes

How long is the stock solution stable for under these storage conditions?
Liquid stability data shows that Long?R3IGF-I is stable for 3 years (-20C to 37C). Therefore, the stock solution should be stable at 4C for 3 years.

What type of preparation is available?
Liquid formulation, preferable for GMP production.
Freeze dried preparation.

Is Long?R3IGF-I stable?
Re-test date for freeze-dried peptide is 3 years. Liquid formulation stability studies have recently been completed. It is stable for 3 years (-20C to +37C). We have data indicating stability in media at 4C for 1 year.

Here is an article written by a self-experimenter.

December 15, 2000

Answer: What a perfect question! You actually have talked to just the right person. I have a business associate that worked for the company that produces this in Australia. Several years ago, I ordered 10mg of Long R3 IGF-1 and used it for several months. What I found out was truly amazing.

Before I tell you about my results, let me tell you that if you are going to use IGF-1 then make sure it is the Long R3 version! Let me explain. Regular IGF-1 like what is produced in your body is transported around connected to binding proteins. There are quite a few of these and their main purpose is to grab ahold of the IGF-1 peptide and keep it from being quickly degraded. Without these binding proteins, all of the IGF-1 would be metabolized in the body within a few minutes. The problem (at least it seems like a problem but might actually be a good thing) is that these binding proteins basically prevent the IGF-1 from performing its function. As long as IGF-1 is attached to the binding protein it cannot do the cool stuff that it wants to do. Regular IGF-1 must be released from its binding protein in order to accomplish its mission. Part of the problem is that much of the IGF-1 is degraded before it is released (seems like much is wasted doesn?t it?)

With Long R3 IGF-1 this problem doesn?t exist. Understand that the Long R3 version does not bind to the various binding proteins. It is free to move throughout your body and immediately start doing all the cool stuff that it wants to do. Again, understand that the Long R3 version is several orders of magnitude stronger than regular IGF-1.

If you would happen to use regular IGF-1, you would need several milligrams per day in order to get the desired effect. With the Long R3 version, you need only microgram quantities. Long R3 is also inherently MUCH cheaper to produce. What I am saying is that for the average person, regular IGF-1 is not practical-it is too expensive and you need to use too much. With Long R3 IGF-1, the price to results ratio is pretty good!

Something else I want to explain is how I went about preparing it for injection into my body. Unfortunately, this is not easy and the average person will have a hard time doing it. At the time, I worked in a sophisticated lab which had all of the necessary equipment. I ordered 10mg of Long R3 IGF-1 and it came in a single flip-top vial. 10mg might not seem like much but believe me, when it comes to Long R3 IGF-1, it is a ton! Some people might say to just add saline to the vial, keep it in the fridge and inject it when necessary. However, this will not work well because the IGF-1 is not highly stable and will degrade in an aqueous environment. 10mg was enough for many months and I needed a way that would allow the IGF-1 to remain potent during this entire time. I did my research and developed my method. I ordered what is known as microvials and sterilized them. I then diluted the IGF-1 with sterile water and added just a tad of acid to increase stability. Although it took quite a while, I then used a micropipette and alliquotted an amount of solution that contained 50mcg into one of my microvials. I closed the microvial and then froze it in a deep freezer. When I was ready to inject, I took out one or more of my microvials, thawed it out, combined it with saline and injected it.

When I first started taking Long R3 IGF-1, I used 50mcg every other day. Amazingly, within days, I started noticing some effects in my body. I felt super hungry all of the time and just felt ?anabolic?. I can?t describe this feeling except to say that it was very similar to being on anabolic steroids (I wasn?t on at the time). Within one month, I gained almost 17 pounds of fairly lean mass! After the first month, something happened though and I noticed that it didn?t seem to be working that well. I upped the dosage several times over the next month to keep up the desired effects. On the third month, I was using several hundred micrograms per day but wasn?t noticing any further gains. All in all, I gained about 20 pounds of pretty solid mass!

Please notice that almost all of my gains were within the first month of taking the Long R3 IGF-1. After this first month, my gains slowed down considerably and eventually stopped altogether even though I was taking high dosages. Why did this happen?

From all of my research, I suppose one of two things might have happened to prevent me from making further gains. What I truly suspect is that the Long R3 IGF-1 downregulated the amount of binding proteins being produced by my body (research confirms this). When I first started to inject the IGF-1, I was supplementing my own body?s IGF-1. I not only had my own IGF-1 working throughout the day but I had the potent surges of Long R3 IGF-1 that I would inject. Over time though, the binding proteins were downregulated. Of course my body continued to produce some (albeit less) IGF-1, however, because there were very little or no binding proteins it was quickly degraded. From what I can tell, I was in a state where 95% of the day my body did not have the benefits of IGF-1. Basically, it got what it got when I injected the Long R3 version.

The other possibility is that I built up antibodies to the Long R3 IGF-1 which basically sought out and destroyed what I injected. Although possible, I don?t believe this actually happened because it is not supported by research. I have seen no evidence which suggests that Long R3 IGF-1 causes antibody production.

To fix the above problem, one would have to cycle the Long R3 IGF-1. The best thing would probably be to take it every other month. This would allow your own body?s IGF-1 and binding proteins to return to normal.

Overall, I had a good experience with Long R3 IGF-1. The results were different than with steroids. I have noticed that steroids cause preferential growth of certain muscles, especially those that are stressed (as in lifting). The IGF-1 though seemed to cause my entire body to get a little thicker. I guess IGF-1 is less compensatory in nature and exerts a more whole-body anabolicity.

Would I recommend IGF-1? To the right person who is very careful and knows what he?s doing and has a good background in the sciences and has access to a good lab, YES! However, you can tell that I have listed many prerequisites to using it. For the average Joe, I believe is is just too complicated to be safe.
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pincrusher
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11-06-2006, 10:18 AM

from all accounts igf is a stronger gh. gh actually makes your body produce more igf which is what causes muscle growth.
for your short timeframe you want to make your progress, igf will help because it will not only keep off unwanted fat while eatting to grow but will help your veins come out some, will cause big pumps in the gym, will cause muscle growth by creating new muscle instead of just trying to increase the size of current muscle cells. here are some articles for ya to read:

here are a bunch of articles posted on intensemuscle about igf that simplifys it somewhat but provides great info for you to understand.

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IGF1, also known as somatomedin C, is polypeptide hormone about the same size as insulin. It is produced pre***inantly in the liver in response to growth hormone (GH) release from the pituitary gland. Many of the growth promoting effects of GH are due to its ability to release IGF1 from the liver. The conversion ratio of GH to IGF1 varies greatly in different individuals but most external sources of GH convert around 4-6mcg of IGF per one I.U. of GH. IGF-1 acts on several different tissues to enhance growth. IGF1 belongs in the 'superfamily' of substances known as 'growth factors,' along with epidermal (skin), transforming; platelet derived fibroblast, nerve, and ciliary neurotrophic growth factors. None of the other factors have any bearing on exoskeletal tissue incidentally however These agents all have in common the ability to stimulate cell division, known as mitogenesis, and cell differentiation. Meaning That In the case of IGF1 which does act on muscle tissue it will initiate the growth of new muscle fibers, and subsequently new receptors for testosterone. Users have unanimously concluded that it enhances cycles of steroids significantly. They also seem to be adamant about its ability to reduce fat and improve vascularity a great deal.

How to use IGF1

Assuming that you have acquired legitimate IGF1 (R3) long chain, That's IGF1 with the binding protein added. You should take dosages ranging from 60mcg up to 120mcg per day in divided doses. One injection in the morning and again at bed time. Never exceed 120mcg in one day. IGF1 can cause serious gastrointestinal problems such as tumors intestinal swelling diarrhea and vomiting. Most IGF1 comes in a concentration of 1000mcg per ML or CC so it makes it easy to measure in an insulin syringe. 10 IU on the syringe is 100mcg. Do the math.

IGF + Insulin

If you plan on doing IGF1 with Insulin, listen closely IGF1 is not that expensive, sure you can get away with using less by including insulin in the stack, but IGF1 and Insulin together have a pro-insulin effect on your blood sugar balance. It can enhance the chances of a hypoglycemic episode ten fold. I would recommend against it for any one not ABSOLUTLY comfortable with insulin or IGF1.

Here is how insulin and IGF1 work together. Igfbp3 is the binding protein, which allows IGF1 to remain active in the system for a long enough period of time to really work its magic. IGF1 by nature has a half-life of less than 10 minutes by its self. The molecule was so small it would escape the blood stream very rapidly. This was the reason IGF1 was so "underground". It took very frequent injections at high dosages to achieve even minimal results. Aside from this reconstituting the compound required a degree in biochemistry. This short acting version was the only IGF1 known until recently IGF1 would have been administered in 100 mcg dosages 4-6 times a day. That is a hell of a lot of IGF1. That explains a lot of the distended bellies. Now with R3 long chain IGF1 and the Binding protein IGFBP3 IGF1 will last up to 6 hours in the system. By binding IGF to the IGFBP3 you make the molecule larger and it gets trapped in the blood stream until the protein is broken down and the IGF molecule escapes. You can further its life by combining Insulin with it, although I here its very risky. Insulin prevents the breakdown of IGFBP3 and leaves the IGF1 molecule roaming free in the blood stream for longer periods of time up to 12 hours as insulin levels return to normal IGFBP3 will begin to break down and the IGF1 will escape from its bound protein IGFBP3 again having a half life of less than 10 minutes.

Insulin should be taken at the normal dosage it is usually administered at minus 10% about 45 minutes prior to the IGF1 infusion. Again let me remind you this can be deadly if you don't know what you are doing. And of course do not use Insulin for the nighttime injection of IGF1 by taking it in the morning you prolong the IGF1's half life to 12 hours and then take a 6 hour injection, you should be fine. Hell if you want to eat a big bowl of rice and drink another 100g of simple carbs 45 minutes before the bed time IGF1 infusion you could spike insulin for at least a few hours of extended IGF1 activity. If your not going to be using insulin in the stack then go ahead and do the same in the morning.

What users report

Users of IGF1 have reported various results but all along the same lines, It does not appear to be dramatically less effective in any one individual (at least not to the best of my knowledge). I have a good friend who had to stop taking IGF1 due to stomach illness that was completely unrelated But he to experienced good gains from it for the 2 weeks he was on it, his dosage was 120mcg per day. One hour after the first injection he went to the gym and immediately told me about the uncontrollable pump he got from just one set.

That would indicate to me that he was experiencing some form of cell volumization. The general consensus on IGF1 seems to be that its benefits are as fallow:

Increased Pumps are reported to be so severe that workouts are often cut short due to lack of ability to the muscle through the full range of motion...ouch

Gains retention is increased if IGF is used in a cycle I am not sure why, but IGF1 seems to make gains on a cycle stick with virtually no post cycle loss. Every bodybuilder I've spoken with seems to think this for some reason. Most of them use drugs like Anadrol or Dianabol with it because of the amount of size attained with these drugs. The usual draw back to these drugs is that in most users there is a post cycle "crash" that occurs, so the reasoning is to toss IGF1 into the stack and grow larger faster with out the post cycle crash blues.

Reverses testicular atrophy

Testicles if shrunken will return to "full swing" so to speak even in the middle of a cycle. If not shrunken they will not shrink during the cycle. This may explain partially why gains are kept after the cycle.

Fatigue

Users report feeling drained and tired all day. This seems to be one of the negative side effects to IGF1, it will make you sleep longer and you will require more sleep at night to feel rested for the morning. This is common with high doses of HGH and exhibited in children, whose IGF1 levels are extraordinarily high. A child needs 4 hours more sleep than an adult on average does. This may be directly or indirectly related to IGF1 levels.

Stiffness

An almost arthritic feeling is commonly associated with high levels of HGH, well IGF1 has the exact same property. IGF1 will cause your hands, fingers and knuckles to ache this is one way you can be sure you got real IGF1.

IGF-1's Side effects

Every thing has a down side. To bake a cake ya gotta brake an egg. IGF1 is no exception. The drug used in larger quantity around the 100mcg+ range will cause headaches, occasional nausea and can contribute to low blood sugar or hypoglycemia in some users. Although I have never heard of this first hand I'm sure its true.

IGF1 will attach its self to the lining of the intestine and cause atrophy of the gut. Every thing IGF1 touches will grow and you have a lot of receptors on the lining of the large intestine and inner wall of the ab***inal well. This is what causes the GH gut look. You can easily avoid this by limiting your dosages and cycle lengths. IGF1 cycles should be kept to 4-6 weeks with 4-6 weeks off in-between. IGF-1 is considerably more powerful than HGH and you need to think of it along those lines as far as dosing goes. We all know what to much HGH can do over prolonged periods of usage. The Neanderthal look is definitely not going to win any shows this year. I would recommend 80 mcg a day for 4 weeks at a time you should get good results from that for a while. I don't know if you will need to up the dosage at any point, but I would think in the case of IGF1 it wouldn't matter. If 80mcg doesn't do it for ya, then bump it up to 100 You should definitely feel it at this point If not suspect the IGF1 as being fake. Beyond 120 mcg per day your asking for trouble, This compound demands as much respect as its sister amino Insulin.

Clinical Facts about IGF-1

IGF-1 is a polypeptide of 70 amino acids (7650 daltons), and is one of a number of related insulin-like growth factors present in the circulation. The molecule shows approximately 50% sequence homology with proinsulin and has a number of biological activities similar to insulin. IGF-1 is a mediator of longitudinal growth in humans or how tall you are capable of becoming. Serum IGF-1 concentrations are altered by age, nutritional status, body composition, and growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For the diagnosis of acromegaly, a single IGF-1 concentration is more reliable than a ran*** hGH measurement (Oppizi, et al., 1986). IGF-1 can be used for the assessment of disease activity in acromegaly (Barkan, et al., 198.

Almost all (>95%) of serum IGF-1 circulates bound to specific IGF binding proteins (IGFBPs), of which six classes (IGFBPs 1-6) have been identified (Rudd, 1991). BP3 is thought to be the major binding protein

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The present study was undertaken to test the hypothesis that direct IGF-I infusion would result in an increase in muscle DNA as well as in various measurements of muscle size. Either 0.9% saline or nonsystemic doses of recombinant human IGF-I (rhIGF-1) were infused directly into a non-weight-bearing muscle of rats, the tibialis anterior (TA), via a fenestrated catheter attached to a subcutaneous miniosmotic pump. Saline infusion had no effect on the mass, protein content, or DNA content of TA muscles. Local IGF-I infusion had no effect on body or heart weight. The absolute weight of the infused TA muscles was ~9% greater (P < 0.05) than that of the contra-lateral TA muscles. IGF-I infusion resulted in significant increases in the total protein and DNA content of TA muscles (P < 0.05). As a result of these coordinated changes, the DNA-to-protein ratio of the hypertrophied TA was similar to that of the contra-lateral muscles. These results suggest that IGF-I may be acting to directly stimulate processes such as protein synthesis and satellite cell proliferation, which result in skeletal muscle hypertrophy.
Discussion: The details of the mechanisms and pathways by which mechanical stress stimulates localized muscle fiber hypertrophy are still being elucidated. It is clear however, that growth hormone (GH), fibroblast growth factors (FGF) and insulin-like growth factors (IGF) play a central role in this process. Insulin-like growth factor I (IGF-I) peptide levels have been shown to increase in overloaded skeletal muscles (G. R. Adams and F. Haddad. J. Appl. Physiol. 81: 2509-2516, 1996). In that study, there was an increase in IGF-1 content before measurable increases in muscle protein and was correlated with an increase in muscle DNA content. Several other studies have shown that muscle fibers undergoing hypertrophy, due to mechanical stress, express elevated levels of IGF-I prior to hypertrophy.
IGF-1 appears to be an important regulator of the nuclear to cytoplasmic ratio. Studies have show that a muscle will only undergo hypertrophy if it can maintain the ratio of the cell?s volume to the number of nuclei within a finite limit. In the study above, a relatively "unloaded" muscle, the anterior tibialis, was injection with 0.9 - 1.9 micrograms/kg/day of rhIGF-1 which then mimicked the effects of physically loading the muscle. There was an increase in protein content, cross sectional area and DNA content. The increase in muscle DNA is presumed to be a result of increased proliferation and differentiation of satellite cells which donate their nuclei upon fusion with damaged or hypertrophying muscle cells. Take note that the quantities of IGF-1 used in the injections were extremely small, much smaller than studies that have shown relatively poor results from administering IGF-1 systemically which range from 1.0 to 6.9 milligrams/kg/day.
All of the attention and discussion of half-hazzardly injecting fat into muscles to increase the girth of a limb is only a symptom of the obsessive nature of bodybuilding. I would imagine that locally injecting minute amounts (micrograms) of rhIGF-1 to actually increase the growth of individual muscles would be a far better alternative to injecting fat, Esiclene or even getting silicone implants. Those bodybuilders at the national or professional level with lagging calves would be wise to consider the results of this study should they stumble across a bottle of Genentech?s rhIGF-1!

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The GH/IGF-1 Axis

Your body?s GH levels are tightly regulated by numerous chemical messengers including macronutrients, neurotransmitters, and hormones. The signal to increase your body?s GH levels starts in the hypothalamus. There, two peptide hormones act in concert to increase or decrease GH output from the pituitary gland. These hormones are somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin acts at the pituitary to decrease GH output. GHRH acts at the pituitary to increase GH output. Together these hormones regulate, in pulsatile fashion, the level of GH you have floating around in your body (see Fig. 1).

Several factors can effect this delicate balance. First, GH is subject to negative feedback in response to its own release. GH, as well as IGF-1, circulate back to the hypothalamus and pituitary to increase SS release, thereby decreasing GH release. GH may also act in an autocrine and paracrine (i.e. Effecting the source cells and neighboring cells without having to enter the circulation) fashion within both the hypothalamus and pituitary.

Neurotransmitters also effect GH levels at the hypothalamus. This neuroendocrine control is still being elucidated but some factors are already clearly involved (see table 1).

Table 1.

Neurotransmitter system Effect on GH Neurotransmitter or drug
Adrenergic
a2 Increase
a1 Decrease
Decrease

Clonidine
Methoxamine
Clenbuterol

Cholinergic Increase Acetylcholine
Opioids Increase Morphine
Dopamine Increase L-Dopa
Gut-brain peptides Increase

Nutrition and metabolic factors also modulate GH levels. A fall in blood glucose such as during exercise or during sleep causes an increase in GH secretion. High protein feedings increase acute GH secretion. Some amino acids such as L-arginine seem to increase GH by decreasing SS release from the hypothalamus. Even the vitamin Niacin has been shown to increase exercise induced GH release by 300- 600%(Murray, 1995). In this particular study there were four separate trials where 10 subjects cycled at 68% VO2 max for 120 min followed by a timed 3.5-mile performance task. Every 15 min during exercise, subjects ingested 3.5 ml./kg lean body weight of one of four beverages: 1) water placebo (WP), 2) WP + 280 mg nicotinic acid.l-1 (WP + NA), 3) 6% carbohydrate-electrolyte beverage (CE), and 4) CE + NA. Ingestion of nicotinic acid (WP + NA and CE + NA) blunted the rise in free fatty acids (FFA) associated with WP and CE; in fact, nicotinic acid ingestion effectively prevented FFA from rising above rest values. The low FFA levels with nicotinic acid feeding were associated with a 3- to 6-fold increase in concentrations of human growth hormone throughout exercise. The question remains, does this dramatic, yet temporary, increase in GH lead to a greater training effect? It may lead to greater glycogen storage capacity but other than that, we really don?t know.

Caloric restriction dramatically reduces serum levels of IGF-1 yet at the same time increases GH release. This mechanism effectively helps the individual adapt metabolically without having anabolic actions which would potentially hasten death by starvation. It is important to understand that GH can either be anabolic or catabolic. When nutrient intake is high, GH secretion is increased leading also to increased levels of IGF-1, IGFBP3 and insulin. The main role of GH under these conditions is to increase anabolism through local growth factors like IGF-1 and insulin. Conversely, when nutrient intake is low, GH is again increased. But this time there is no concomitant increase in IGF-1, IGFBP3, or insulin. Under these circumstances GH is acting as a catabolic hormone increasing the utilization of fat for fuel thus sparing body glucose yet having no muscle building effects. This behavior of the GH/IGF-1 axis is part of what makes it so difficult to build muscle while dieting. It should be noted that locally produced IGF-1 in skeletal muscle responds normally to training while dieting. This makes heavy poundages a must when trying to get ready for a show without the use of drugs.

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Growth Hormone: How does it work?

It is always prudent to have a basic understanding of how a supplement, hormone or drug works to build and/or preserve muscle before considering its use. The knowledge of how a hormone acts in the body is necessary to make your own decisions and manage your own regimens if you plan on utilizing it. Without this understanding you will no doubt end up wasting a lot of money and perhaps put your health at risk.

It has been long believed that GH exerts its anabolic effects on peripheral tissues through IGFs, also known as somatomedins ("mediator of growth"). Binding proteins play an important role in moderating the anabolic effects of both GH and IGF-1. IGF-1 is controlled by at least 6 different binding proteins and there may others waiting to be elucidated. To date there are a couple theories as to just how GH causes growth in target tissues. The first theory is called the somatomedin hypothesis (Daughaday, 1972).

The Somatomedin hypothesis states that GH is released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs got there name because of there structural and functional similarity to proinsulin. This hypothesis dictates that 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. Indeed, many studies have followed showing that in animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. The effects were similar to those observed after GH administration. Interestingly, additional studies also followed that showed 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) has consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993).

The second theory as to how GH produces anabolic effects is called the Dual Effector theory (Green, 1985). This theory states that GH itself has anabolic effects on body tissues without the need of IGF-1. This theory has been supported by studies injecting GH directly into growth plates. Further evidence supporting this theory lies in genetically altered strains of mice. When comparing mice who genetically over express GH and mice who over express IGF-1, GH mice are larger. This evidence has been sited by some to support the dual effector theory. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished.

The Somatomedin theory and the Dual Effector theory are not all that different. One simply asserts that GH can produce growth without IGF-1. From the research I am inclined to believe in the Somatomedin theory. This only becomes an issue when one decides whether or not to use just GH or to combine it with IGF-1 or insulin.

From the evidence currently available you can count on three major mechanisms by which GH leads to growth (Spagnoli, 1996).

The effects of GH one 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.
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.
IGF-1 not only has endocrine actions, but also paracrine/autocrine actions in target tissues. This means that as GH travels to my muscles, the muscle cells increase there production of IGF-1. This IGF-1 may then travel to adjacent cells (especially satellite cells) leading to growth and enhanced rejuvenative ability of cells that didn?t see any GH. This is as suggested by the Dual Effector theory.

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IGF-1: How does it work?

To understand how IGF-1 works you have to understand how muscles grow. The ability of muscle tissue to constantly regenerate in response to activity makes it unique. It?s 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. Once this happens these cells divide and genetically change 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 come from. The larger the muscle, the more nuclei you need to maintain it. In fact there is a "nuclear to volume" ratio that cannot be overridden. Whenever a muscle grows in response to functional overload there is a positive correlation between the increase in the number of myonuclei and the increase in fiber 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 unnatural muscle growth is the activation of satellite cells by growth factors such as IGF-1.

IGF-1 stimulates both proliferation (an increase in cell number) and differentiation (a conversion to muscle specific nuclei) in an autocrine-paracrine manner, although it induces differentiation to a much greater degree. This is in agreement with the Dual Effector theory. In fact, 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).

On the very cutting edge of research scientists are now discovering 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 signaling pathway, and subsequent muscle fiber hypertrophy (Semsarian, 1999; Musaro, 1999). I am by no means a geneticist so I hesitated even bringing this new research up. In summary 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. Did you get all that?

In this the first part of "Growing beyond what nature intended" we have discussed the role, function and interaction of growth hormone and insulin-like growth factor-1 in tissue growth. This is referred to collectively as the GH/IGF-1 axis. We learned that this axis is controlled by negative feedback meaning that GH, after being released, circulates back to the hypothalamus and pituitary to effectively stop further GH release. We learned that circulating IGF-1 has the same inhibiting effect on GH release. We discussed very briefly the role of neurotransmitters in regulating GH release through growth hormone releasing hormone (GHRH) and somatostatin (SS). We even touched on the nitty gritty details of just how IGF-1 does its magic on muscle cells. I?m afraid I may have disappointed a few of you waiting for the "how to" section of this article. Never fear, in part II you will learn about the effects of these hormones as well as androgens, insulin and thyroid hormones when given, individually and combined, to previously healthy individuals. I will remind you that this article is not intended to encourage you put your health at risk, or to break the law by acquiring and using these substances illegally. As always, the goal Meso-Rx is not to condone the use of performance enhancing substances, but to educate by providing unbiased information about all aspects of high level sport performance and bodybuilding.

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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 HCG, 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 body fat and GREATLY increase vascularity, body fat 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.

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I was picking a very advanced Bro's brain and was able to collect this info from him:

Go with 40mcg ed for 25 days straight for your 1st time regardless of weight of your animal. I have yet to see anyone have better results with more than 40 who ran 40 the first time around. Let me clairfy. I have yet to see hear from someone who ran their second cycle yet.

Or try this:
weeks:
1gh
2gh
3gh
4gh
5gh + igf
6gh + igf
7gh + igf
8gh + igf



If you have to dilute your 1mg with 2ml of BA. This make it a little easier to measure. On a 1cc slin pin each click would be 2iu=10mcg. 10iu =50mcg.

This makes it alot easier. I always pull 90 units of BW then pull the IGF-1 to disired amount. Then you can shoot it first. Good Luck

DOSAGES

If you are just going to use it by itself, try 40 mcg ed. 1 bottle will last you about 1 month and you should see good results from that.

If you are experienced with AAS, and you are going to run some other things with it, you could probably get away with 30 mcg

I am starting to learn that it is a lot like test to a certain point, the more the better. Obviously there is a point of diminshing returns, but I haven't hit it yet. My understanding is that is probably about 150 mcg per day.

I started at 30 mcg per day, and have gradually moved it up to 80 mcg (40 am / 40 pm)




NOTE:
this IFBB pro stated that the standard dose is 0.8mcg/kg of bodyweight.
Email: [email protected]
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IGF FAQ
From Dr JMW @ AS

Long?R3IGF-I is an analog of human IGF-I.
? It is a superior alternative to insulin in serum-free media.
? It increases protein production by cells in culture medium.
? It increases cell viability by inhibiting apoptosis.
? It has a longer half-life in cell culture than insulin.
? It is readily available.
? There is secure and ample manufacturing capacity at GroPep Limited.
? No animal- or human- derived material is used in the manufacture or storage of Long?R3IGF-I.
? Long?R3IGF-I is already being used in the manufacture of three (3) biopharmaceuticals approved by FDA and EMEA.

Frequently Asked Questions

What cell types will respond to Long?R3IGF-I?
All cells that have a Type I IGF receptor will potentially respond. Most commercially used cells including CHO, fibroblasts and hybri***as have a type I IGF receptor. All cells which respond to pharmacological concentrations of insulin (>1 mg/liter) will respond to Long?R3IGF-I (10-50 mg/liter).

Is storage of the stock solution at 4C acceptable?
Yes

How long is the stock solution stable for under these storage conditions?
Liquid stability data shows that Long?R3IGF-I is stable for 3 years (-20C to 37C). Therefore, the stock solution should be stable at 4C for 3 years.

What type of preparation is available?
Liquid formulation, preferable for GMP production.
Freeze dried preparation.

Is Long?R3IGF-I stable?
Re-test date for freeze-dried peptide is 3 years. Liquid formulation stability studies have recently been completed. It is stable for 3 years (-20C to +37C). We have data indicating stability in media at 4C for 1 year.

Here is an article written by a self-experimenter.

December 15, 2000

Answer: What a perfect question! You actually have talked to just the right person. I have a business associate that worked for the company that produces this in Australia. Several years ago, I ordered 10mg of Long R3 IGF-1 and used it for several months. What I found out was truly amazing.

Before I tell you about my results, let me tell you that if you are going to use IGF-1 then make sure it is the Long R3 version! Let me explain. Regular IGF-1 like what is produced in your body is transported around connected to binding proteins. There are quite a few of these and their main purpose is to grab ahold of the IGF-1 peptide and keep it from being quickly degraded. Without these binding proteins, all of the IGF-1 would be metabolized in the body within a few minutes. The problem (at least it seems like a problem but might actually be a good thing) is that these binding proteins basically prevent the IGF-1 from performing its function. As long as IGF-1 is attached to the binding protein it cannot do the cool stuff that it wants to do. Regular IGF-1 must be released from its binding protein in order to accomplish its mission. Part of the problem is that much of the IGF-1 is degraded before it is released (seems like much is wasted doesn?t it?)

With Long R3 IGF-1 this problem doesn?t exist. Understand that the Long R3 version does not bind to the various binding proteins. It is free to move throughout your body and immediately start doing all the cool stuff that it wants to do. Again, understand that the Long R3 version is several orders of magnitude stronger than regular IGF-1.

If you would happen to use regular IGF-1, you would need several milligrams per day in order to get the desired effect. With the Long R3 version, you need only microgram quantities. Long R3 is also inherently MUCH cheaper to produce. What I am saying is that for the average person, regular IGF-1 is not practical-it is too expensive and you need to use too much. With Long R3 IGF-1, the price to results ratio is pretty good!

Something else I want to explain is how I went about preparing it for injection into my body. Unfortunately, this is not easy and the average person will have a hard time doing it. At the time, I worked in a sophisticated lab which had all of the necessary equipment. I ordered 10mg of Long R3 IGF-1 and it came in a single flip-top vial. 10mg might not seem like much but believe me, when it comes to Long R3 IGF-1, it is a ton! Some people might say to just add saline to the vial, keep it in the fridge and inject it when necessary. However, this will not work well because the IGF-1 is not highly stable and will degrade in an aqueous environment. 10mg was enough for many months and I needed a way that would allow the IGF-1 to remain potent during this entire time. I did my research and developed my method. I ordered what is known as microvials and sterilized them. I then diluted the IGF-1 with sterile water and added just a tad of acid to increase stability. Although it took quite a while, I then used a micropipette and alliquotted an amount of solution that contained 50mcg into one of my microvials. I closed the microvial and then froze it in a deep freezer. When I was ready to inject, I took out one or more of my microvials, thawed it out, combined it with saline and injected it.

When I first started taking Long R3 IGF-1, I used 50mcg every other day. Amazingly, within days, I started noticing some effects in my body. I felt super hungry all of the time and just felt ?anabolic?. I can?t describe this feeling except to say that it was very similar to being on anabolic steroids (I wasn?t on at the time). Within one month, I gained almost 17 pounds of fairly lean mass! After the first month, something happened though and I noticed that it didn?t seem to be working that well. I upped the dosage several times over the next month to keep up the desired effects. On the third month, I was using several hundred micrograms per day but wasn?t noticing any further gains. All in all, I gained about 20 pounds of pretty solid mass!

Please notice that almost all of my gains were within the first month of taking the Long R3 IGF-1. After this first month, my gains slowed down considerably and eventually stopped altogether even though I was taking high dosages. Why did this happen?

From all of my research, I suppose one of two things might have happened to prevent me from making further gains. What I truly suspect is that the Long R3 IGF-1 downregulated the amount of binding proteins being produced by my body (research confirms this). When I first started to inject the IGF-1, I was supplementing my own body?s IGF-1. I not only had my own IGF-1 working throughout the day but I had the potent surges of Long R3 IGF-1 that I would inject. Over time though, the binding proteins were downregulated. Of course my body continued to produce some (albeit less) IGF-1, however, because there were very little or no binding proteins it was quickly degraded. From what I can tell, I was in a state where 95% of the day my body did not have the benefits of IGF-1. Basically, it got what it got when I injected the Long R3 version.

The other possibility is that I built up antibodies to the Long R3 IGF-1 which basically sought out and destroyed what I injected. Although possible, I don?t believe this actually happened because it is not supported by research. I have seen no evidence which suggests that Long R3 IGF-1 causes antibody production.

To fix the above problem, one would have to cycle the Long R3 IGF-1. The best thing would probably be to take it every other month. This would allow your own body?s IGF-1 and binding proteins to return to normal.

Overall, I had a good experience with Long R3 IGF-1. The results were different than with steroids. I have noticed that steroids cause preferential growth of certain muscles, especially those that are stressed (as in lifting). The IGF-1 though seemed to cause my entire body to get a little thicker. I guess IGF-1 is less compensatory in nature and exerts a more whole-body anabolicity.

Would I recommend IGF-1? To the right person who is very careful and knows what he?s doing and has a good background in the sciences and has access to a good lab, YES! However, you can tell that I have listed many prerequisites to using it. For the average Joe, I believe is is just too complicated to be safe.
__________________
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pincrusher
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11-06-2006, 10:18 AM

from all accounts igf is a stronger gh. gh actually makes your body produce more igf which is what causes muscle growth.
for your short timeframe you want to make your progress, igf will help because it will not only keep off unwanted fat while eatting to grow but will help your veins come out some, will cause big pumps in the gym, will cause muscle growth by creating new muscle instead of just trying to increase the size of current muscle cells. here are some articles for ya to read:

here are a bunch of articles posted on intensemuscle about igf that simplifys it somewhat but provides great info for you to understand.

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IGF1, also known as somatomedin C, is polypeptide hormone about the same size as insulin. It is produced pre***inantly in the liver in response to growth hormone (GH) release from the pituitary gland. Many of the growth promoting effects of GH are due to its ability to release IGF1 from the liver. The conversion ratio of GH to IGF1 varies greatly in different individuals but most external sources of GH convert around 4-6mcg of IGF per one I.U. of GH. IGF-1 acts on several different tissues to enhance growth. IGF1 belongs in the 'superfamily' of substances known as 'growth factors,' along with epidermal (skin), transforming; platelet derived fibroblast, nerve, and ciliary neurotrophic growth factors. None of the other factors have any bearing on exoskeletal tissue incidentally however These agents all have in common the ability to stimulate cell division, known as mitogenesis, and cell differentiation. Meaning That In the case of IGF1 which does act on muscle tissue it will initiate the growth of new muscle fibers, and subsequently new receptors for testosterone. Users have unanimously concluded that it enhances cycles of steroids significantly. They also seem to be adamant about its ability to reduce fat and improve vascularity a great deal.

How to use IGF1

Assuming that you have acquired legitimate IGF1 (R3) long chain, That's IGF1 with the binding protein added. You should take dosages ranging from 60mcg up to 120mcg per day in divided doses. One injection in the morning and again at bed time. Never exceed 120mcg in one day. IGF1 can cause serious gastrointestinal problems such as tumors intestinal swelling diarrhea and vomiting. Most IGF1 comes in a concentration of 1000mcg per ML or CC so it makes it easy to measure in an insulin syringe. 10 IU on the syringe is 100mcg. Do the math.

IGF + Insulin

If you plan on doing IGF1 with Insulin, listen closely IGF1 is not that expensive, sure you can get away with using less by including insulin in the stack, but IGF1 and Insulin together have a pro-insulin effect on your blood sugar balance. It can enhance the chances of a hypoglycemic episode ten fold. I would recommend against it for any one not ABSOLUTLY comfortable with insulin or IGF1.

Here is how insulin and IGF1 work together. Igfbp3 is the binding protein, which allows IGF1 to remain active in the system for a long enough period of time to really work its magic. IGF1 by nature has a half-life of less than 10 minutes by its self. The molecule was so small it would escape the blood stream very rapidly. This was the reason IGF1 was so "underground". It took very frequent injections at high dosages to achieve even minimal results. Aside from this reconstituting the compound required a degree in biochemistry. This short acting version was the only IGF1 known until recently IGF1 would have been administered in 100 mcg dosages 4-6 times a day. That is a hell of a lot of IGF1. That explains a lot of the distended bellies. Now with R3 long chain IGF1 and the Binding protein IGFBP3 IGF1 will last up to 6 hours in the system. By binding IGF to the IGFBP3 you make the molecule larger and it gets trapped in the blood stream until the protein is broken down and the IGF molecule escapes. You can further its life by combining Insulin with it, although I here its very risky. Insulin prevents the breakdown of IGFBP3 and leaves the IGF1 molecule roaming free in the blood stream for longer periods of time up to 12 hours as insulin levels return to normal IGFBP3 will begin to break down and the IGF1 will escape from its bound protein IGFBP3 again having a half life of less than 10 minutes.

Insulin should be taken at the normal dosage it is usually administered at minus 10% about 45 minutes prior to the IGF1 infusion. Again let me remind you this can be deadly if you don't know what you are doing. And of course do not use Insulin for the nighttime injection of IGF1 by taking it in the morning you prolong the IGF1's half life to 12 hours and then take a 6 hour injection, you should be fine. Hell if you want to eat a big bowl of rice and drink another 100g of simple carbs 45 minutes before the bed time IGF1 infusion you could spike insulin for at least a few hours of extended IGF1 activity. If your not going to be using insulin in the stack then go ahead and do the same in the morning.

What users report

Users of IGF1 have reported various results but all along the same lines, It does not appear to be dramatically less effective in any one individual (at least not to the best of my knowledge). I have a good friend who had to stop taking IGF1 due to stomach illness that was completely unrelated But he to experienced good gains from it for the 2 weeks he was on it, his dosage was 120mcg per day. One hour after the first injection he went to the gym and immediately told me about the uncontrollable pump he got from just one set.

That would indicate to me that he was experiencing some form of cell volumization. The general consensus on IGF1 seems to be that its benefits are as fallow:

Increased Pumps are reported to be so severe that workouts are often cut short due to lack of ability to the muscle through the full range of motion...ouch

Gains retention is increased if IGF is used in a cycle I am not sure why, but IGF1 seems to make gains on a cycle stick with virtually no post cycle loss. Every bodybuilder I've spoken with seems to think this for some reason. Most of them use drugs like Anadrol or Dianabol with it because of the amount of size attained with these drugs. The usual draw back to these drugs is that in most users there is a post cycle "crash" that occurs, so the reasoning is to toss IGF1 into the stack and grow larger faster with out the post cycle crash blues.

Reverses testicular atrophy

Testicles if shrunken will return to "full swing" so to speak even in the middle of a cycle. If not shrunken they will not shrink during the cycle. This may explain partially why gains are kept after the cycle.

Fatigue

Users report feeling drained and tired all day. This seems to be one of the negative side effects to IGF1, it will make you sleep longer and you will require more sleep at night to feel rested for the morning. This is common with high doses of HGH and exhibited in children, whose IGF1 levels are extraordinarily high. A child needs 4 hours more sleep than an adult on average does. This may be directly or indirectly related to IGF1 levels.

Stiffness

An almost arthritic feeling is commonly associated with high levels of HGH, well IGF1 has the exact same property. IGF1 will cause your hands, fingers and knuckles to ache this is one way you can be sure you got real IGF1.

IGF-1's Side effects

Every thing has a down side. To bake a cake ya gotta brake an egg. IGF1 is no exception. The drug used in larger quantity around the 100mcg+ range will cause headaches, occasional nausea and can contribute to low blood sugar or hypoglycemia in some users. Although I have never heard of this first hand I'm sure its true.

IGF1 will attach its self to the lining of the intestine and cause atrophy of the gut. Every thing IGF1 touches will grow and you have a lot of receptors on the lining of the large intestine and inner wall of the ab***inal well. This is what causes the GH gut look. You can easily avoid this by limiting your dosages and cycle lengths. IGF1 cycles should be kept to 4-6 weeks with 4-6 weeks off in-between. IGF-1 is considerably more powerful than HGH and you need to think of it along those lines as far as dosing goes. We all know what to much HGH can do over prolonged periods of usage. The Neanderthal look is definitely not going to win any shows this year. I would recommend 80 mcg a day for 4 weeks at a time you should get good results from that for a while. I don't know if you will need to up the dosage at any point, but I would think in the case of IGF1 it wouldn't matter. If 80mcg doesn't do it for ya, then bump it up to 100 You should definitely feel it at this point If not suspect the IGF1 as being fake. Beyond 120 mcg per day your asking for trouble, This compound demands as much respect as its sister amino Insulin.

Clinical Facts about IGF-1

IGF-1 is a polypeptide of 70 amino acids (7650 daltons), and is one of a number of related insulin-like growth factors present in the circulation. The molecule shows approximately 50% sequence homology with proinsulin and has a number of biological activities similar to insulin. IGF-1 is a mediator of longitudinal growth in humans or how tall you are capable of becoming. Serum IGF-1 concentrations are altered by age, nutritional status, body composition, and growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For the diagnosis of acromegaly, a single IGF-1 concentration is more reliable than a ran*** hGH measurement (Oppizi, et al., 1986). IGF-1 can be used for the assessment of disease activity in acromegaly (Barkan, et al., 198.

Almost all (>95%) of serum IGF-1 circulates bound to specific IGF binding proteins (IGFBPs), of which six classes (IGFBPs 1-6) have been identified (Rudd, 1991). BP3 is thought to be the major binding protein

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The present study was undertaken to test the hypothesis that direct IGF-I infusion would result in an increase in muscle DNA as well as in various measurements of muscle size. Either 0.9% saline or nonsystemic doses of recombinant human IGF-I (rhIGF-1) were infused directly into a non-weight-bearing muscle of rats, the tibialis anterior (TA), via a fenestrated catheter attached to a subcutaneous miniosmotic pump. Saline infusion had no effect on the mass, protein content, or DNA content of TA muscles. Local IGF-I infusion had no effect on body or heart weight. The absolute weight of the infused TA muscles was ~9% greater (P < 0.05) than that of the contra-lateral TA muscles. IGF-I infusion resulted in significant increases in the total protein and DNA content of TA muscles (P < 0.05). As a result of these coordinated changes, the DNA-to-protein ratio of the hypertrophied TA was similar to that of the contra-lateral muscles. These results suggest that IGF-I may be acting to directly stimulate processes such as protein synthesis and satellite cell proliferation, which result in skeletal muscle hypertrophy.
Discussion: The details of the mechanisms and pathways by which mechanical stress stimulates localized muscle fiber hypertrophy are still being elucidated. It is clear however, that growth hormone (GH), fibroblast growth factors (FGF) and insulin-like growth factors (IGF) play a central role in this process. Insulin-like growth factor I (IGF-I) peptide levels have been shown to increase in overloaded skeletal muscles (G. R. Adams and F. Haddad. J. Appl. Physiol. 81: 2509-2516, 1996). In that study, there was an increase in IGF-1 content before measurable increases in muscle protein and was correlated with an increase in muscle DNA content. Several other studies have shown that muscle fibers undergoing hypertrophy, due to mechanical stress, express elevated levels of IGF-I prior to hypertrophy.
IGF-1 appears to be an important regulator of the nuclear to cytoplasmic ratio. Studies have show that a muscle will only undergo hypertrophy if it can maintain the ratio of the cell?s volume to the number of nuclei within a finite limit. In the study above, a relatively "unloaded" muscle, the anterior tibialis, was injection with 0.9 - 1.9 micrograms/kg/day of rhIGF-1 which then mimicked the effects of physically loading the muscle. There was an increase in protein content, cross sectional area and DNA content. The increase in muscle DNA is presumed to be a result of increased proliferation and differentiation of satellite cells which donate their nuclei upon fusion with damaged or hypertrophying muscle cells. Take note that the quantities of IGF-1 used in the injections were extremely small, much smaller than studies that have shown relatively poor results from administering IGF-1 systemically which range from 1.0 to 6.9 milligrams/kg/day.
All of the attention and discussion of half-hazzardly injecting fat into muscles to increase the girth of a limb is only a symptom of the obsessive nature of bodybuilding. I would imagine that locally injecting minute amounts (micrograms) of rhIGF-1 to actually increase the growth of individual muscles would be a far better alternative to injecting fat, Esiclene or even getting silicone implants. Those bodybuilders at the national or professional level with lagging calves would be wise to consider the results of this study should they stumble across a bottle of Genentech?s rhIGF-1!

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The GH/IGF-1 Axis

Your body?s GH levels are tightly regulated by numerous chemical messengers including macronutrients, neurotransmitters, and hormones. The signal to increase your body?s GH levels starts in the hypothalamus. There, two peptide hormones act in concert to increase or decrease GH output from the pituitary gland. These hormones are somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin acts at the pituitary to decrease GH output. GHRH acts at the pituitary to increase GH output. Together these hormones regulate, in pulsatile fashion, the level of GH you have floating around in your body (see Fig. 1).

Several factors can effect this delicate balance. First, GH is subject to negative feedback in response to its own release. GH, as well as IGF-1, circulate back to the hypothalamus and pituitary to increase SS release, thereby decreasing GH release. GH may also act in an autocrine and paracrine (i.e. Effecting the source cells and neighboring cells without having to enter the circulation) fashion within both the hypothalamus and pituitary.

Neurotransmitters also effect GH levels at the hypothalamus. This neuroendocrine control is still being elucidated but some factors are already clearly involved (see table 1).

Table 1.

Neurotransmitter system Effect on GH Neurotransmitter or drug
Adrenergic
a2 Increase
a1 Decrease
Decrease

Clonidine
Methoxamine
Clenbuterol

Cholinergic Increase Acetylcholine
Opioids Increase Morphine
Dopamine Increase L-Dopa
Gut-brain peptides Increase

Nutrition and metabolic factors also modulate GH levels. A fall in blood glucose such as during exercise or during sleep causes an increase in GH secretion. High protein feedings increase acute GH secretion. Some amino acids such as L-arginine seem to increase GH by decreasing SS release from the hypothalamus. Even the vitamin Niacin has been shown to increase exercise induced GH release by 300- 600%(Murray, 1995). In this particular study there were four separate trials where 10 subjects cycled at 68% VO2 max for 120 min followed by a timed 3.5-mile performance task. Every 15 min during exercise, subjects ingested 3.5 ml./kg lean body weight of one of four beverages: 1) water placebo (WP), 2) WP + 280 mg nicotinic acid.l-1 (WP + NA), 3) 6% carbohydrate-electrolyte beverage (CE), and 4) CE + NA. Ingestion of nicotinic acid (WP + NA and CE + NA) blunted the rise in free fatty acids (FFA) associated with WP and CE; in fact, nicotinic acid ingestion effectively prevented FFA from rising above rest values. The low FFA levels with nicotinic acid feeding were associated with a 3- to 6-fold increase in concentrations of human growth hormone throughout exercise. The question remains, does this dramatic, yet temporary, increase in GH lead to a greater training effect? It may lead to greater glycogen storage capacity but other than that, we really don?t know.

Caloric restriction dramatically reduces serum levels of IGF-1 yet at the same time increases GH release. This mechanism effectively helps the individual adapt metabolically without having anabolic actions which would potentially hasten death by starvation. It is important to understand that GH can either be anabolic or catabolic. When nutrient intake is high, GH secretion is increased leading also to increased levels of IGF-1, IGFBP3 and insulin. The main role of GH under these conditions is to increase anabolism through local growth factors like IGF-1 and insulin. Conversely, when nutrient intake is low, GH is again increased. But this time there is no concomitant increase in IGF-1, IGFBP3, or insulin. Under these circumstances GH is acting as a catabolic hormone increasing the utilization of fat for fuel thus sparing body glucose yet having no muscle building effects. This behavior of the GH/IGF-1 axis is part of what makes it so difficult to build muscle while dieting. It should be noted that locally produced IGF-1 in skeletal muscle responds normally to training while dieting. This makes heavy poundages a must when trying to get ready for a show without the use of drugs.

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Growth Hormone: How does it work?

It is always prudent to have a basic understanding of how a supplement, hormone or drug works to build and/or preserve muscle before considering its use. The knowledge of how a hormone acts in the body is necessary to make your own decisions and manage your own regimens if you plan on utilizing it. Without this understanding you will no doubt end up wasting a lot of money and perhaps put your health at risk.

It has been long believed that GH exerts its anabolic effects on peripheral tissues through IGFs, also known as somatomedins ("mediator of growth"). Binding proteins play an important role in moderating the anabolic effects of both GH and IGF-1. IGF-1 is controlled by at least 6 different binding proteins and there may others waiting to be elucidated. To date there are a couple theories as to just how GH causes growth in target tissues. The first theory is called the somatomedin hypothesis (Daughaday, 1972).

The Somatomedin hypothesis states that GH is released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs got there name because of there structural and functional similarity to proinsulin. This hypothesis dictates that 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. Indeed, many studies have followed showing that in animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. The effects were similar to those observed after GH administration. Interestingly, additional studies also followed that showed 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) has consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993).

The second theory as to how GH produces anabolic effects is called the Dual Effector theory (Green, 1985). This theory states that GH itself has anabolic effects on body tissues without the need of IGF-1. This theory has been supported by studies injecting GH directly into growth plates. Further evidence supporting this theory lies in genetically altered strains of mice. When comparing mice who genetically over express GH and mice who over express IGF-1, GH mice are larger. This evidence has been sited by some to support the dual effector theory. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished.

The Somatomedin theory and the Dual Effector theory are not all that different. One simply asserts that GH can produce growth without IGF-1. From the research I am inclined to believe in the Somatomedin theory. This only becomes an issue when one decides whether or not to use just GH or to combine it with IGF-1 or insulin.

From the evidence currently available you can count on three major mechanisms by which GH leads to growth (Spagnoli, 1996).

The effects of GH one 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.
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.
IGF-1 not only has endocrine actions, but also paracrine/autocrine actions in target tissues. This means that as GH travels to my muscles, the muscle cells increase there production of IGF-1. This IGF-1 may then travel to adjacent cells (especially satellite cells) leading to growth and enhanced rejuvenative ability of cells that didn?t see any GH. This is as suggested by the Dual Effector theory.

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IGF-1: How does it work?

To understand how IGF-1 works you have to understand how muscles grow. The ability of muscle tissue to constantly regenerate in response to activity makes it unique. It?s 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. Once this happens these cells divide and genetically change 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 come from. The larger the muscle, the more nuclei you need to maintain it. In fact there is a "nuclear to volume" ratio that cannot be overridden. Whenever a muscle grows in response to functional overload there is a positive correlation between the increase in the number of myonuclei and the increase in fiber 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 unnatural muscle growth is the activation of satellite cells by growth factors such as IGF-1.

IGF-1 stimulates both proliferation (an increase in cell number) and differentiation (a conversion to muscle specific nuclei) in an autocrine-paracrine manner, although it induces differentiation to a much greater degree. This is in agreement with the Dual Effector theory. In fact, 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).

On the very cutting edge of research scientists are now discovering 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 signaling pathway, and subsequent muscle fiber hypertrophy (Semsarian, 1999; Musaro, 1999). I am by no means a geneticist so I hesitated even bringing this new research up. In summary 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. Did you get all that?

In this the first part of "Growing beyond what nature intended" we have discussed the role, function and interaction of growth hormone and insulin-like growth factor-1 in tissue growth. This is referred to collectively as the GH/IGF-1 axis. We learned that this axis is controlled by negative feedback meaning that GH, after being released, circulates back to the hypothalamus and pituitary to effectively stop further GH release. We learned that circulating IGF-1 has the same inhibiting effect on GH release. We discussed very briefly the role of neurotransmitters in regulating GH release through growth hormone releasing hormone (GHRH) and somatostatin (SS). We even touched on the nitty gritty details of just how IGF-1 does its magic on muscle cells. I?m afraid I may have disappointed a few of you waiting for the "how to" section of this article. Never fear, in part II you will learn about the effects of these hormones as well as androgens, insulin and thyroid hormones when given, individually and combined, to previously healthy individuals. I will remind you that this article is not intended to encourage you put your health at risk, or to break the law by acquiring and using these substances illegally. As always, the goal Meso-Rx is not to condone the use of performance enhancing substances, but to educate by providing unbiased information about all aspects of high level sport performance and bodybuilding.

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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 HCG, 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 body fat and GREATLY increase vascularity, body fat 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.

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I was picking a very advanced Bro's brain and was able to collect this info from him:

Go with 40mcg ed for 25 days straight for your 1st time regardless of weight of your animal. I have yet to see anyone have better results with more than 40 who ran 40 the first time around. Let me clairfy. I have yet to see hear from someone who ran their second cycle yet.

Or try this:
weeks:
1gh
2gh
3gh
4gh
5gh + igf
6gh + igf
7gh + igf
8gh + igf



If you have to dilute your 1mg with 2ml of BA. This make it a little easier to measure. On a 1cc slin pin each click would be 2iu=10mcg. 10iu =50mcg.

This makes it alot easier. I always pull 90 units of BW then pull the IGF-1 to disired amount. Then you can shoot it first. Good Luck

DOSAGES

If you are just going to use it by itself, try 40 mcg ed. 1 bottle will last you about 1 month and you should see good results from that.

If you are experienced with AAS, and you are going to run some other things with it, you could probably get away with 30 mcg

I am starting to learn that it is a lot like test to a certain point, the more the better. Obviously there is a point of diminshing returns, but I haven't hit it yet. My understanding is that is probably about 150 mcg per day.

I started at 30 mcg per day, and have gradually moved it up to 80 mcg (40 am / 40 pm)




NOTE:
this IFBB pro stated that the standard dose is 0.8mcg/kg of bodyweight.
Email: [email protected]
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IGF FAQ
From Dr JMW @ AS

Long?R3IGF-I is an analog of human IGF-I.
? It is a superior alternative to insulin in serum-free media.
? It increases protein production by cells in culture medium.
? It increases cell viability by inhibiting apoptosis.
? It has a longer half-life in cell culture than insulin.
? It is readily available.
? There is secure and ample manufacturing capacity at GroPep Limited.
? No animal- or human- derived material is used in the manufacture or storage of Long?R3IGF-I.
? Long?R3IGF-I is already being used in the manufacture of three (3) biopharmaceuticals approved by FDA and EMEA.

Frequently Asked Questions

What cell types will respond to Long?R3IGF-I?
All cells that have a Type I IGF receptor will potentially respond. Most commercially used cells including CHO, fibroblasts and hybri***as have a type I IGF receptor. All cells which respond to pharmacological concentrations of insulin (>1 mg/liter) will respond to Long?R3IGF-I (10-50 mg/liter).

Is storage of the stock solution at 4C acceptable?
Yes

How long is the stock solution stable for under these storage conditions?
Liquid stability data shows that Long?R3IGF-I is stable for 3 years (-20C to 37C). Therefore, the stock solution should be stable at 4C for 3 years.

What type of preparation is available?
Liquid formulation, preferable for GMP production.
Freeze dried preparation.

Is Long?R3IGF-I stable?
Re-test date for freeze-dried peptide is 3 years. Liquid formulation stability studies have recently been completed. It is stable for 3 years (-20C to +37C). We have data indicating stability in media at 4C for 1 year.

Here is an article written by a self-experimenter.

December 15, 2000

Answer: What a perfect question! You actually have talked to just the right person. I have a business associate that worked for the company that produces this in Australia. Several years ago, I ordered 10mg of Long R3 IGF-1 and used it for several months. What I found out was truly amazing.

Before I tell you about my results, let me tell you that if you are going to use IGF-1 then make sure it is the Long R3 version! Let me explain. Regular IGF-1 like what is produced in your body is transported around connected to binding proteins. There are quite a few of these and their main purpose is to grab ahold of the IGF-1 peptide and keep it from being quickly degraded. Without these binding proteins, all of the IGF-1 would be metabolized in the body within a few minutes. The problem (at least it seems like a problem but might actually be a good thing) is that these binding proteins basically prevent the IGF-1 from performing its function. As long as IGF-1 is attached to the binding protein it cannot do the cool stuff that it wants to do. Regular IGF-1 must be released from its binding protein in order to accomplish its mission. Part of the problem is that much of the IGF-1 is degraded before it is released (seems like much is wasted doesn?t it?)

With Long R3 IGF-1 this problem doesn?t exist. Understand that the Long R3 version does not bind to the various binding proteins. It is free to move throughout your body and immediately start doing all the cool stuff that it wants to do. Again, understand that the Long R3 version is several orders of magnitude stronger than regular IGF-1.

If you would happen to use regular IGF-1, you would need several milligrams per day in order to get the desired effect. With the Long R3 version, you need only microgram quantities. Long R3 is also inherently MUCH cheaper to produce. What I am saying is that for the average person, regular IGF-1 is not practical-it is too expensive and you need to use too much. With Long R3 IGF-1, the price to results ratio is pretty good!

Something else I want to explain is how I went about preparing it for injection into my body. Unfortunately, this is not easy and the average person will have a hard time doing it. At the time, I worked in a sophisticated lab which had all of the necessary equipment. I ordered 10mg of Long R3 IGF-1 and it came in a single flip-top vial. 10mg might not seem like much but believe me, when it comes to Long R3 IGF-1, it is a ton! Some people might say to just add saline to the vial, keep it in the fridge and inject it when necessary. However, this will not work well because the IGF-1 is not highly stable and will degrade in an aqueous environment. 10mg was enough for many months and I needed a way that would allow the IGF-1 to remain potent during this entire time. I did my research and developed my method. I ordered what is known as microvials and sterilized them. I then diluted the IGF-1 with sterile water and added just a tad of acid to increase stability. Although it took quite a while, I then used a micropipette and alliquotted an amount of solution that contained 50mcg into one of my microvials. I closed the microvial and then froze it in a deep freezer. When I was ready to inject, I took out one or more of my microvials, thawed it out, combined it with saline and injected it.

When I first started taking Long R3 IGF-1, I used 50mcg every other day. Amazingly, within days, I started noticing some effects in my body. I felt super hungry all of the time and just felt ?anabolic?. I can?t describe this feeling except to say that it was very similar to being on anabolic steroids (I wasn?t on at the time). Within one month, I gained almost 17 pounds of fairly lean mass! After the first month, something happened though and I noticed that it didn?t seem to be working that well. I upped the dosage several times over the next month to keep up the desired effects. On the third month, I was using several hundred micrograms per day but wasn?t noticing any further gains. All in all, I gained about 20 pounds of pretty solid mass!

Please notice that almost all of my gains were within the first month of taking the Long R3 IGF-1. After this first month, my gains slowed down considerably and eventually stopped altogether even though I was taking high dosages. Why did this happen?

From all of my research, I suppose one of two things might have happened to prevent me from making further gains. What I truly suspect is that the Long R3 IGF-1 downregulated the amount of binding proteins being produced by my body (research confirms this). When I first started to inject the IGF-1, I was supplementing my own body?s IGF-1. I not only had my own IGF-1 working throughout the day but I had the potent surges of Long R3 IGF-1 that I would inject. Over time though, the binding proteins were downregulated. Of course my body continued to produce some (albeit less) IGF-1, however, because there were very little or no binding proteins it was quickly degraded. From what I can tell, I was in a state where 95% of the day my body did not have the benefits of IGF-1. Basically, it got what it got when I injected the Long R3 version.

The other possibility is that I built up antibodies to the Long R3 IGF-1 which basically sought out and destroyed what I injected. Although possible, I don?t believe this actually happened because it is not supported by research. I have seen no evidence which suggests that Long R3 IGF-1 causes antibody production.

To fix the above problem, one would have to cycle the Long R3 IGF-1. The best thing would probably be to take it every other month. This would allow your own body?s IGF-1 and binding proteins to return to normal.

Overall, I had a good experience with Long R3 IGF-1. The results were different than with steroids. I have noticed that steroids cause preferential growth of certain muscles, especially those that are stressed (as in lifting). The IGF-1 though seemed to cause my entire body to get a little thicker. I guess IGF-1 is less compensatory in nature and exerts a more whole-body anabolicity.

Would I recommend IGF-1? To the right person who is very careful and knows what he?s doing and has a good background in the sciences and has access to a good lab, YES! However, you can tell that I have listed many prerequisites to using it. For the average Joe, I believe is is just too complicated to be safe.
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