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Thread: Igf-1 r3

  1. #1
    ramacher's Avatar
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    Igf-1 r3

    One of my friends was telling me about this I am currently on 6IU ED blue tops. What is exactly is IGF-1 R3 and could I take both HGH and it at the same time? Benefits?

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    I'm no pro, but you probably don't want to take both at the same time. HGH does a bunch of stuff, but *probably* the most important thing it does is make your body release IGF (insulin like growth factor) and this is the main stuff that tells your cells to split and duplicate. If you're already on HGH, taking IGF-1 on top of it is just asking for side effects like HGH gut, organs getting too big, bone growth, etc. You'll have too much IGF-1 in your system if you're already on a healthy dose of HGH. So basically, HGH makes you big by producing IGF. Adding more IGF would be over doing it.

    Some neat info I copied and pasted from some google searches:

    IGF prevents insulin from transporting glucose across cell membranes. As a result the cells have to switch to burning off fat as a source of energy. This is why HGH and IGF-1 are so effective at burning fat.

    There is a lot of talk about the similarity between IGF and growth hormone . The most often asked question is simply which is more effective. GH doesn’t directly cause your muscles to grow, it works very indirectly by increasing Protein synthesis capabilities, increasing the amount of insulin a person can use effectively, and increasing the amount of anabolic steroids a person can use effectively. GH also indirectly causes muscle growth by stimulating the release of IGF when it (the GH) is destro in the human body. So one way you could look at it as GH being a precursor to IGF. So to put it simple IGF is more effective at directly causing muscle growth and density increases. IGF is also much more cost effective.

    IGF can also be effectively used by itself and gains will still be easily noticeable. With growth hormone you need to use high amounts of anabolics and often insulin to see any gains at all, this is not the case with IGF. IGF can be used by itself and is often used by bodybuilders who bridge between cycles, during this bridge is a good time to use IGF since it has no effect on natural testosterone production so it will therefore allow you to return to normal in terms of hormone levels.

    “Long R3 IGF-1 is significantly more potent than IGF-1. The enhanced potency is due to the decreased binding of Long R3 IGF-1 to all known IGF binding proteins. These binding proteins normally inhibit the biological actions of IGF’s.”

    And finally another difference from what I know (which is not much lol I'm a rookie reearching the stuff as we speak)... One neat thing about IGF over HGH is you can spot inject it. Right after you work out a muscle, you can IM inject IGF and this supposedly makes that specific muscle grow more.

    Hopefully somebody who knows more about this stuff can confirm or deny some of the stuff I posted here.... I only know enough to be dangerous lol

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    ramacher's Avatar
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    That makes sense. Thanks alot!

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    IGF R3 is a nothing more than an expensive GDA.

    Pinn said this years ago when it first started becoming more popular.

    Run some searches on here, and you'll get your answers.

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    ReBilly's Avatar
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    what's a GDA?

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    glucose disposal agent

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    Quote Originally Posted by D7M View Post
    IGF R3 is a nothing more than an expensive GDA.

    Pinn said this years ago when it first started becoming more popular.

    Run some searches on here, and you'll get your answers.
    Correct^^ agreed.

    LR3 is the biggest con on the market, its a waste of money if you want to run IGF go with IGF-1 if you can find it, or play it safe with GH

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    ramcher,

    Please look at this thread (post #2) explaining structures and differences in IGF-1 and IGF-1 LR3.

    Difference between IGF LR3 and IGF

    -Gear

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    Here is a clinical study I found which involves GH and IGF-1 (not LR3-IGF-1) infusion in healthy humans.

    Insulin -like Growth Factor I as an Anabolic Agent in Catabolic States
    Carolyn A. Bondy, MD; Louis E. Underwood, MD; David R. Clemmons, MD; Hans-Peter Guler, MD; Mark A. Bach, MD, PhD; and Monica Skarulis, MD

    Dr. David Clemmons (Division of Endocrinology, University of North Carolina): Growth hormone has been proposed as an anabolic therapy for patients with various catabolic conditions, including renal failure, corticosteroid therapy, protein wasting caused by malnutrition, burns, and recovery from surgery or acute illness [29]. Because growth hormone may cause suboptimal improvement in these catabolic states [30, 31], other therapeutic strategies have been proposed to improve or augment its anabolic effects. Studies conducted in nutritionally deprived rats and humans have provided some knowledge of the mechanisms that may contribute to suboptimal anabolic response. Fasting results in complete refractoriness to growth hormone, which appears to be mediated by down-regulation of growth hormone receptors [32]. In contrast, less severe insults, such as a protein restriction of 66% or a caloric restriction of 50%, induce various defects, including the inability to generate a normal IGF-I response, abnormal clearance of IGF-I, and refractoriness to IGF-I itself [33, 34]. It is not clear which of these mechanisms functions in severe catabolic states.
    Although precise strategies to overcome specific deficits in the growth hormone/IGF-I pathway have not been identified, alternative approaches, such as administering IGF-I, have been tested. Six healthy young adult volunteers were fed calorically restricted diets (20 kcal/kg per day) for 2 weeks. During the second week of caloric restriction, IGF-I (Genentech) was infused at a dosage of 12 µg/kg per hour for 16 hours daily for 6 days. When the IGF-I infusion was completed, participants were fed a normal diet for 2 weeks and then the caloric restriction was repeated for another 2-week period; they received a daily injection of growth hormone (50 µg/kg) during the second week. Nitrogen balance improved markedly during both IGF-I and growth hormone treatments [35]. Insulin-like growth factor I decreased blood glucose from 4.94 ± 0.91 mmol/L to 3.13 ± 0.44 mmol/L, whereas growth hormone increased blood glucose levels to 5.48 ± 1.0 mmol/L, despite the fact that IGF-I decreased serum C-peptide from 2.14 ± 0.89 mmol/L to 0.97 ± 0.14 mmol/L and growth hormone increased C-peptide to 3.12 ± 0.59 mmol/L. Thus, IGF-I induced substantial hypoglycemia even though C-peptide was suppressed, suggesting that IGF-I, rather than insulin, lowered blood glucose levels. The clinical utility of IGF-I may be limited to those catabolic patients in whom unacceptable degrees of hyperglycemia develop with growth hormone or who have type II diabetes mellitus before therapy is begun.
    To avoid the problem of hypoglycemia and possibly improve the anabolic response to IGF-I, we wanted to determine if a combination of growth hormone and IGF-I would be safer and more efficacious. The rationale for this approach was based on the view that growth hormone and IGF-I have unique anabolic actions and that they have opposite effects on glucose metabolism. Seven healthy adult volunteers were studied during caloric restriction in a protocol exactly parallel to that described previously, except that IGF-I alone (administered as in the previous study) was compared with IGF-I infusion plus growth hormone injections [36]. The diet restriction reduced nitrogen balance to +139 ± 48 mmol/L. The growth hormone and IGF-I combination caused substantially greater nitrogen retention (262 ± 43 mmol/L per day) than did IGF-I alone (108 ± 29 mmol/L per day). Combined growth hormone and IGF-I treatment also caused substantial urinary potassium conservation, which suggests that most of the protein accretion occurred in muscle and connective tissue. Furthermore, all participants who received the growth hormone and IGF-I combination had a positive nitrogen balance, whereas none had a positive balance with growth hormone or IGF-I alone. The mean capillary blood glucose level with growth hormone and IGF-I treatment was 4.3 ± 1.0 mmol/L compared with 3.8 ± 0.8 mmol/L with IGF-I alone.
    As in the previous study, IGF-I caused a marked decline in C-peptide, whereas no change was seen with the growth hormone and IGF-I combination, suggesting that the combination maintained a more normal carbohydrate metabolism. Peak serum IGF-I levels were substantially higher with the growth hormone and IGF-I combination (1854 ± 708 ng/mL compared with 1092 ± 503 ng/mL). Insulin-like growth factor-binding protein-3 associates with an acid-labile subunit [37], and levels of both decreased in the group receiving IGF-I alone but increased and remained stable in the group treated with growth hormone and IGF-I. Both groups had similar side effects, which were limited to edema and jaw pain, but only participants receiving IGF-I alone had symptomatic hypoglycemia.
    Several mechanisms might account for this enhanced response. 1) Higher serum IGF-I levels were achieved with combined growth hormone and IGF-I. 2) Growth hormone may have direct anabolic actions on muscle and skeletal tissues. 3) The growth hormone and IGF-I combination may be more effective in improving tissue IGF-I levels, and this change may be more important than increasing serum IGF-I concentrations. 4) Clearance of IGF-I may be markedly altered by the coadministration of growth hormone, which stabilizes the ternary IGF-binding complex, potentially providing sustained metabolic action. 5) Combined growth hormone and IGF-I results in substantially greater serum insulin concentrations, and maintaining insulin concentrations may augment the anabolic effect of IGF-I.
    The growth hormone and IGF-I combination offers hope for patients who are severely catabolic and refractory to either hormone alone or who are at risk for hypoglycemia with IGF-I alone. The results also suggest that chronic conditions such as short stature in children with relative growth hormone insensitivity may respond to combined growth hormone and IGF-I therapy, which is safe and more efficacious. Whether this degree of improvement can be achieved in multiple clinical situations must be determined.

    Here is the full article link:
    http://www.annals.org/content/120/7/593.full

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