IGF1-LR3

[FrancisK]

I’ve been using it the week of, hitting body parts bi-laterally each day pre workout, 20mcg per shot 40mcg a day total for usually 5 days leading up.

You guys have had good results from mega doses a couple days prior?

 

[johnjuanb1]

I’ve been using it the week of, hitting body parts bi-laterally each day pre workout, 20mcg per shot 40mcg a day total for usually 5 days leading up.

You guys have had good results from mega doses a couple days prior?

I notice this week I’ve been doing 10ius Meditrope HGH plus 20ius novalin R split dose daily and 25mg MK-677 before bed. I stopped HGH and insulin, kept MK-677 in before bed, and added 100mcg IGF1-LR3 twice a day. 1.5 days later all bloat from Meditrope is gone, and I’m super full all the time. I think this would be great before completing even 2 days out.

Today I’m trying Mutant’s Protocol:
10ius subQ HGH followed by 11ius Novalin R IM preworkout, then 100mcg IGF1-LR3 IM post workout. Sip a loaded intraworkout shake. I may add insulin post workout with the IGF1 for synergy.

 

[johnjuanb1]

I notice this week I’ve been doing 10ius Meditrope HGH plus 20ius novalin R split dose daily and 25mg MK-677 before bed. I stopped HGH and insulin, kept MK-677 in before bed, and added 100mcg IGF1-LR3 twice a day. 1.5 days later all bloat from Meditrope is gone, and I’m super full all the time. I think this would be great before completing even 2 days out.

Today I’m trying Mutant’s Protocol:
10ius subQ HGH followed by 11ius Novalin R IM preworkout, then 100mcg IGF1-LR3 IM post workout. Sip a loaded intraworkout shake. I may add insulin post workout with the IGF1 for synergy.

OMG the pump was overwhelming on chest with this protocol. I got home 15 minutes ago and injected 100mcg IGF1-LR3 in my chest split bilaterally. I feel it hitting my brain hard. Blood sugar is dropping. I need to cook my fat free turkey burgers on bagels but I’m so relaxed lying here on my bed.

 

[Elvia1023]

JJ you are looking great. I will post more in here 2moro as I have some interesting experiments planned. I have just started 100mcg igf-1 des pre and post workout with slin. I have 1 vial of LR3 left and will run that after the DES. I will need to stock up on IGF-1 as I plan to incorporate quite a lot at the start of next year.

 

[concreter]

OMG the pump was overwhelming on chest with this protocol. I got home 15 minutes ago and injected 100mcg IGF1-LR3 in my chest split bilaterally. I feel it hitting my brain hard. Blood sugar is dropping. I need to cook my fat free turkey burgers on bagels but I’m so relaxed lying here on my bed.

I would not think you Needed additional Slin on 100 mcgs LR3.
I usually wait till my pre Slin-r has cleared! post 3 hrs.
Did you say 100mcgs twice Daily!!!!

 

[johnjuanb1]

I would not think you Needed additional Slin on 100 mcgs LR3.
I usually wait till my pre Slin-r has cleared! post 3 hrs.
Did you say 100mcgs twice Daily!!!!

You’re right. I didn’t do post workout slin.
I did 10ius HGH and 11ius slin preworkout and 100mcg IGF1-LR3 post workout. That’s all the peptides i took today. I didn’t want to risk going hypo.

 

[Anabolic-Chicken]

Name of the brand or the sponsor?

Thanks

 

[johnjuanb1]

So i did 4 Days in a row of IGF1-LR3. Im going to give my IGF1 receptors a break now for 4 days and stick to HGH/insulin/MK-677 then go back to IGF1. Little mini blasts i love! I go very high dose, get very good results, then refresh receptors and repeat. Soon I’ll add melanotan II to help with insulin sensitivity.

 

[r0idb0y]

good thread, i am just new to peptides , been doing oils for a few years and im very interested to learn more as it seems very indepth with lr3 , des and mk677, ghrp6 .. its got me in a spin as i want to know what is the best to run with sus and eq over 16 weeks with some winny for the first 6 weeks.

 

[Thebigone]

I would not think you Needed additional Slin on 100 mcgs LR3.
I usually wait till my pre Slin-r has cleared! post 3 hrs.
Did you say 100mcgs twice Daily!!!!

Don’t you want insulin with any dosage of igf? I thought insulin drastically. amplifies igf’s like it does with hgh and pretty much anything?

 

[MyNameIsJeff]

Don’t you want insulin with any dosage of igf? I thought insulin drastically. amplifies igf’s like it does with hgh and pretty much anything?

As far as I know, insulin can amplify the increase in IGF1 production that comes from elevated GH levels. It probably does so by upregulating GH receptors as well as by activating signaling molecules of the GH receptor transcription pathway, such as STAT5b.

After parturition, increased growth hormone (GH) secretion is important to preserve the metabolic homeostasis of energy-deficient dairy cows. Elevated plasma GH promotes lipid mobilization from adipose tissue, but paradoxically, is associated with depressed concentration of insulin-like growth factor-I (IGF-I), a growth factor produced in a GH-dependent fashion in liver. Primary factors regulating GH responses of liver and adipose tissue are poorly understood in periparturient dairy cows. Consistent with insulin being such a factor, its plasma concentration declined concomitantly with net energy balance (EB) and with plasma IGF-I in a group of 9 periparturient dairy cows. To test the role of insulin in regulating cellular determinants of GH responsiveness, hyperinsulinemic-euglycemic clamps were performed on 6 dairy cows in late pregnancy (28 d prepartum) before the reductions in EB, insulin, and IGF-I were initiated, and when they were completed in early lactation (10 d postpartum). Infusion of insulin nearly doubled the plasma concentration of IGF-I (P < 0.001) and hepatic levels of IGF-I mRNA during both states (P < 0.05). In liver, these responses were associated with increased abundance of the GH receptor protein (GHR; P < 0.05), whereas the abundance of intracellular mediators of GH actions (JAK2, STAT5, or STAT3) remained unaffected. Insulin also doubled GHR abundance in adipose tissue (P < 0.01), indicating that this effect is not liver specific. These results raise the possibility that insulin regulates the efficiency of GH signaling in liver and adipose tissue of dairy cows by acting as a rheostat of GHR synthesis.
PMID: 15113939

https://www.ncbi.nlm.nih.gov/pubmed/15113939

In vivo insulin appears to be necessary for normal liver GH responsiveness, probably by maintaining liver GHR levels (14-17). In Type 1 diabetic patients and streptozotocin-treated rodents, insulin deficiency is correlated with hepatic GH resistance which, in most studies, is associated with reduced levels of circulating GHBP in patients or decreased liver GHR in rodents (14-24). In streptozotocin-treated rats, circulating insulin-like growth factor 1 (IGF-1), whose mRNA expression is regulated by GH, is reduced as is GH binding capacity. Insulin treatment restores IGF-1 levels and in some, but not all experiments, restores GH binding (14, 17, 25-27). In Type 1 diabetic patients intraperitoneal insulin administration restores GHBP levels better than subcutaneous insulin treatment (19,20, 23).

Insulin Inhibits Growth Hormone Signaling via the Growth Hormone Receptor/JAK2/STAT5B Pathway

The STAT multigene family of transcriptional regulators conveys signals from several cytokines and growth factors upon phosphorylation by janus kinases (JAK). Activation of STAT5 is typically mediated by JAK2, but more recent data indicate a direct activation by the insulin receptor kinase. STAT5 exists in two closely homologous isoforms, STAT5a and b. We here describe the selective tyrosine phosphorylation of STAT5b in Kym-1 cells in response to insulin. Blocking insulin signalling by HNMPA-(AM)3, an insulin receptor kinase inhibitor, resulted in the loss of insulin-induced STAT5b tyrosine phosphorylation, whereas the inhibition of JAK2 by the JAK selective inhibitor tyrphostin AG490 had no effect. By contrast, in the same cells, IFNγ-induced STAT5b activation was JAK2-dependent, indicating that this signal pathway is functional in Kym-1 cells. We conclude from this rhabdomyosarcoma model that STAT5b, but not STAT5a is a direct target of the insulin receptor kinase.

https://www.sciencedirect.com/science/article/pii/S0014579399016890

A bit off topic, but interesting nonetheless: There seem to be beneficial effects from acutely elevated insulin levels, but detrimental effects from chronically elevated levels. Another reason why Lantus is no good and why keeping insulin sensitivity in check is so important.

Insulin is important for maintaining the responsiveness of the liver to growth hormone (GH). Insulin deficiency results in a decrease in liver GH receptor (GHR) expression, which can be reversed by insulin administration. In osteoblasts, continuous insulin treatment decreases the fraction of cellular GHR localized to the plasma membrane. Thus, it is not clear whether hyperinsulinemia results in an enhancement or inhibition of GH action. We asked whether continuous insulin stimulation, similar to what occurs in hyperinsulinemic states, results in GH resistance. Our present studies suggest that insulin treatment of hepatoma cells results in a time-dependent inhibition of acute GH-induced phosphorylation of STAT5B. Whereas total protein levels of JAK2 were not reduced after insulin pretreatment for 16 h, GH-induced JAK2 phosphorylation was inhibited. There was a concomitant decrease in GH binding and a reduction in immunoreactive GHR levels following pretreatment with insulin for 8–24 h. In summary, continuous insulin treatment in rat H4 hepatoma cells reduces GH binding, immunoreactive GHR, GH-induced phosphorylation of JAK2, and GH-induced tyrosine phosphorylation of STAT5B. These findings suggest that hepatic GH resistance may develop when a patient exhibits chronic hyperinsulinemia, a condition often observed in patients with obesity and in the early stage of Type 2 diabetes.

Insulin Inhibits Growth Hormone Signaling via the Growth Hormone Receptor/JAK2/STAT5B Pathway

In any case, based on what we know about the mechanisms by which insulin amplifies GH's effectiveness, I don't see how it would amplify the effects of exogenous IGF1. That's not to say that IGF1 and insulin can;t be used together, but I don't see much synergy between the two.

 

[johnjuanb1]

As far as I know, insulin can amplify the increase in IGF1 production that comes from elevated GH levels. It probably does so by upregulating GH receptors as well as by activating signaling molecules of the GH receptor transcription pathway, such as STAT5b.


https://www.ncbi.nlm.nih.gov/pubmed/15113939


Insulin Inhibits Growth Hormone Signaling via the Growth Hormone Receptor/JAK2/STAT5B Pathway


https://www.sciencedirect.com/science/article/pii/S0014579399016890

A bit off topic, but interesting nonetheless: There seem to be beneficial effects from acutely elevated insulin levels, but detrimental effects from chronically elevated levels. Another reason why Lantus is no good and why keeping insulin sensitivity in check is so important.


Insulin Inhibits Growth Hormone Signaling via the Growth Hormone Receptor/JAK2/STAT5B Pathway

In any case, based on what we know about the mechanisms by which insulin amplifies GH's effectiveness, I don't see how it would amplify the effects of exogenous IGF1. That's not to say that IGF1 and insulin can;t be used together, but I don't see much synergy between the two.

Very good finds. This makes sense. I lowered my insulin to 6ius 15 minutes after my 5iu HGH shots twice a day. The insulin is taken intramuscularly for shorter half life. I think using just enough insulin to overcome the insulin resistance of the HGH is the way to go. IGF1-LR3 I’ll use on days that have no HGH or insulin.

 

[notorius]

Very good finds. This makes sense. I lowered my insulin to 6ius 15 minutes after my 5iu HGH shots twice a day. The insulin is taken intramuscularly for shorter half life. I think using just enough insulin to overcome the insulin resistance of the HGH is the way to go. IGF1-LR3 I’ll use on days that have no HGH or insulin.

You still talking about Norvalin R, correct?

 

[johnjuanb1]

You still talking about Norvalin R, correct?

Yes, novalin R

 

[Thebigone]

As far as I know, insulin can amplify the increase in IGF1 production that comes from elevated GH levels. It probably does so by upregulating GH receptors as well as by activating signaling molecules of the GH receptor transcription pathway, such as STAT5b.


https://www.ncbi.nlm.nih.gov/pubmed/15113939


Insulin Inhibits Growth Hormone Signaling via the Growth Hormone Receptor/JAK2/STAT5B Pathway


https://www.sciencedirect.com/science/article/pii/S0014579399016890

A bit off topic, but interesting nonetheless: There seem to be beneficial effects from acutely elevated insulin levels, but detrimental effects from chronically elevated levels. Another reason why Lantus is no good and why keeping insulin sensitivity in check is so important.


Insulin Inhibits Growth Hormone Signaling via the Growth Hormone Receptor/JAK2/STAT5B Pathway

In any case, based on what we know about the mechanisms by which insulin amplifies GH's effectiveness, I don't see how it would amplify the effects of exogenous IGF1. That's not to say that IGF1 and insulin can;t be used together, but I don't see much synergy between the two.

Interesting. So insulin will only amplify the conversion of igf from exogenous HGH but will not amplify the effect of exogenous igf?

 

[concreter]

Plus you get an insulin like response from IGF LR3.
My blood sugar drops quickly with any strenuous activity..

I've been taking 4-6 ius GH 1 hr prior, then 15ius R just prior to workout.
Should I worry about insulin sensitivity with my onslaught of Micros at that Time ?
Basically 3 days a week, once a day!

 

[RamboStallone]

Interesting. So insulin will only amplify the conversion of igf from exogenous HGH but will not amplify the effect of exogenous igf?

Insulin raises igf, so combined with gh effects are amplified. Exogenous igf is a different animal, there's no conversion or anything being raised. So it just goes in and does its job. So slin wouldn't technically amplify igf but combining them will amplify the effects. Plus we are learning the more is around the more receptors flourish so depending on how you define "amplify" you can say they all kind of amplify each other. Synergy is the proper term.

 

[concreter]

Your not implying taking Slin w- IGF are you ?

 

[Thebigone]

Insulin raises igf, so combined with gh effects are amplified. Exogenous igf is a different animal, there's no conversion or anything being raised. So it just goes in and does its job. So slin wouldn't technically amplify igf but combining them will amplify the effects. Plus we are learning the more is around the more receptors flourish so depending on how you define "amplify" you can say they all kind of amplify each other. Synergy is the proper term.

Interesting. So technically if dieting you would want lower doses of igf with little carbs as that could possibly act keto’ish in a way? But only doses like 20mcg or so. Or would you want carbs post igf?

Also what about peptides with igf? I’d assume slim is good as peptides will increase natural igf therefor slin would amplify the effects. So slin would basically amplify the effects of almost anything other than lr3 or des?

 

[RamboStallone]

Your not implying taking Slin w- IGF are you ?

No I'm implying gh and slin together to maximize igf production. For instance gh/slin pre and lr3 post. Depends on the preferred timing by the individual.

You can do slin and igf together but I don't see the need to use them together, it would be better to let each shuttle nutrients at different times. You can use them together but better up the carbs I guess.

Edit: I see how what I wrote is confusing. What I meant is if you take slin and igf, sure you will get the effects of both at the same time but I don't see a reason to combine two things that do similar at the same time. I'd use the slin first and then the lr3 later, since the lr3 will pull everything into the muscle and tighten you up. The slin is not as selective as the igf for where it shuttles the nutrients. So my theory to limit fat gain is to have the lr3 later so it can "pick up the leftovers" if that makes any sense.