Proof of igf saturation?

[Thebigone]

Is there actually any proof. I've been on 50-100mcg lr3 4x per week for about 6weeks and love it. I'd like to run it forever like with GH but is there any scientific proof?

 

[RamboStallone]

I have yet to see proof of saturation or "desensitization" in regards to Lr3. However, all the board "guru's" claim so...I've come to the conclusion it's made up bro science or something that must've been pulled out of context. GH or GH secretagogues seem to increase binding proteins so I doubt any saturation will occur there. Then there is the whole "lock and key" theory about the receptors becoming "desensitized" because of the Lr3 chain not being exact and causing the receptor to stop accepting it. Again, no proof but parrots like Dave Palumbo continue to repeat this.

I'm interested to see if anyone has come across some actual data.

I wonder if just using Lr3 alone would increase binding proteins? Maybe the key to keeping the Lr3 working is to use GH/GH secretagogues in conjunction to keep an environment of increased binding proteins. Not sure entirely.

 

[RamboStallone]

Looks like this Dutch researcher thought the same. His first argument for combining GH and IGF (not Lr3 but same theory should apply), is that IGF would work better because of the increased binding proteins from the GH administration.

http://www.ergo-log.com/ghigf1.html

 

[Thebigone]

I have yet to see proof of saturation or "desensitization" in regards to Lr3. However, all the board "guru's" claim so...I've come to the conclusion it's made up bro science or something that must've been pulled out of context. GH or GH secretagogues seem to increase binding proteins so I doubt any saturation will occur there. Then there is the whole "lock and key" theory about the receptors becoming "desensitized" because of the Lr3 chain not being exact and causing the receptor to stop accepting it. Again, no proof but parrots like Dave Palumbo continue to repeat this.

I'm interested to see if anyone has come across some actual data.

I wonder if just using Lr3 alone would increase binding proteins? Maybe the key to keeping the Lr3 working is to use GH/GH secretagogues in conjunction to keep an environment of increased binding proteins. Not sure entirely.

Yah I use peps and gh too. I think it's a myth just like AAS saturation as well.

 

[Thebigone]

I still can't believe there had been talk for decades about Igf saturation and not a single article ever proved it. This should be a staple like HGH.

 

[sciroxx-lab]

I have yet to see proof of saturation or "desensitization" in regards to Lr3. However, all the board "guru's" claim so...I've come to the conclusion it's made up bro science or something that must've been pulled out of context. GH or GH secretagogues seem to increase binding proteins so I doubt any saturation will occur there. Then there is the whole "lock and key" theory about the receptors becoming "desensitized" because of the Lr3 chain not being exact and causing the receptor to stop accepting it. Again, no proof but parrots like Dave Palumbo continue to repeat this.

I'm interested to see if anyone has come across some actual data.

I wonder if just using Lr3 alone would increase binding proteins? Maybe the key to keeping the Lr3 working is to use GH/GH secretagogues in conjunction to keep an environment of increased binding proteins. Not sure entirely.

The lr3 version travels relaively free in the serum without attaching to binding proteins, or at least to much more lower degree, this is the great advantage of it. You may find a breif explanation here - http://www.ncbi.nlm.nih.gov/pubmed/18567600
You'll also learn that it's found to be (at least in mice) to be more effective then regular IGF1 is recuperation of damaged or injured muscle

 

[RamboStallone]

The lr3 version travels relaively free in the serum without attaching to binding proteins, or at least to much more lower degree, this is the great advantage of it. You may find a breif explanation here - http://www.ncbi.nlm.nih.gov/pubmed/18567600
You'll also learn that it's found to be (at least in mice) to be more effective then regular IGF1 is recuperation of damaged or injured muscle

Interesting. I thought we wanted the igf to attach to the binding proteins?

So basically lr3 does not need a fatigued muscle to attach to. If this is true for the other analogue des, then site injections are meaningless and igf (lr3 & des) will work any time of the day.

 

[RamboStallone]

The lr3 version travels relaively free in the serum without attaching to binding proteins, or at least to much more lower degree, this is the great advantage of it. You may find a breif explanation here - http://www.ncbi.nlm.nih.gov/pubmed/18567600
You'll also learn that it's found to be (at least in mice) to be more effective then regular IGF1 is recuperation of damaged or injured muscle

I understand what you are getting at now, lr3 does not need the binding proteins to work like standard igf1. Is this also true for des?

That actually makes sense for lr3 since for igf1 the binding proteins lengthen it's half life and circulate the igf in muscles tissues. Lr3 is already altered to lengthen the half life, it's like an igf1 and igfbp in one!

This is probably not true for des. This may be why des is better used around training time.

 

[RamboStallone]

It seems both have a low binding affinity to the igfbps but still bind to the igf1 receptor. Thanks for this new info scrioxx! It means neither des nor lr3 need the igfbps to function.

des(1-3)IGF-1 is a naturally-occurring, endogenous protein, as well as drug, and truncated analogue of insulin-like growth factor 1 (IGF-1).[1][2][3][4] des(1-3)IGF-1 lacks the first three amino acids at the N-terminus of IGF-1 (for a total of 67 amino acids, relative to the 70 of IGF-1).[5] As a result of this difference, it has considerably reduced binding to the insulin-like growth factor-binding proteins (IGFBPs) and enhanced potency (about 10-fold in vivo) relative to IGF-1.[1][2][3][5]

The amino acid sequence of des(1-3)IGF-1 is TLCGAELVDA LQFVCGDRGF YFNKPTGYGS SSRRAPQTGI VDECCFRSCD LRRLEMYCAP LKPAKSA.[5]

Long arginine 3-IGF-1, abbreviated as IGF-1 LR3 or as LR3-IGF-1, is a synthetic protein and lengthened analogue of human insulin-like growth factor 1 (IGF-1).[1][2] It differs from native IGF-1 in that it possesses an arginine instead of a glutamic acid at the third position in its amino acid sequence ("arginine 3"), and also has an additional 13 amino acids at its N-terminus (MFPAMPLLSLFVN) ("long"), for a total of 83 amino acids (relative to the 70 of IGF-1).[2] The consequences of these modifications are that IGF-1 LR3 retains the pharmacological activity of IGF-1 as an agonist of the IGF-1 receptor, has very low affinity for the insulin-like growth factor-binding proteins (IGFBPs), and has improved metabolic stability.[1][2] As a result, it is approximately three times more potent than IGF-1,[3] and possesses a significantly longer half-life of about 20–30 hours (relative to IGF-1's half-life of about 12–15 hours).[4]

The amino acid sequence of IGF-1 LR3 is MFPAMPLSSL FVNGPRTLCG AELVDALQFV CGDRGFYFNK PTGYGSSSRR APQTGIVDEC CFRSCDLRRL EMYCAPLKPA KSA.[5]

 

[beastcoast95]

rambo, are you concluding that DES is good localized or no?

 

[RamboStallone]

rambo, are you concluding that DES is good localized or no?

Since both have the ability to bind to the igf1 receptor receptor without the need of binding proteins to regulate them then I would venture to say both lr3 and des have localized effects, des much greater then lr3 because of the amino acid sequence and it's half life.

 

[gh0st]

Looks like this Dutch researcher thought the same. His first argument for combining GH and IGF (not Lr3 but same theory should apply), is that IGF would work better because of the increased binding proteins from the GH administration.

http://www.ergo-log.com/ghigf1.html

Good LINK!

The lr3 version travels relaively free in the serum without attaching to binding proteins, or at least to much more lower degree, this is the great advantage of it. You may find a breif explanation here - http://www.ncbi.nlm.nih.gov/pubmed/18567600
You'll also learn that it's found to be (at least in mice) to be more effective then regular IGF1 is recuperation of damaged or injured muscle

Interesting. I thought we wanted the igf to attach to the binding proteins?

So basically lr3 does not need a fatigued muscle to attach to. If this is true for the other analogue des, then site injections are meaningless and igf (lr3 & des) will work any time of the day.

I do site injections with ALL IGF! des or lr3 and i use to feel the same way about des however in the past two years i have learned to just use lr3 and do multiply micro injections!
I have found that this is the best way to utiize igf and to do it imidiate pre wo. using peg the next day in the same manner actually! rotating from lr3 to peg every other day!

 

[BigTex]

I have yet to see proof of saturation or "desensitization" in regards to Lr3. However, all the board "guru's" claim so...I've come to the conclusion it's made up bro science or something that must've been pulled out of context. GH or GH secretagogues seem to increase binding proteins so I doubt any saturation will occur there. Then there is the whole "lock and key" theory about the receptors becoming "desensitized" because of the Lr3 chain not being exact and causing the receptor to stop accepting it. Again, no proof but parrots like Dave Palumbo continue to repeat this.

I'm interested to see if anyone has come across some actual data.

I wonder if just using Lr3 alone would increase binding proteins? Maybe the key to keeping the Lr3 working is to use GH/GH secretagogues in conjunction to keep an environment of increased binding proteins. Not sure entirely.

AMEN BRO! Never seen any evidence that there is a saturation level of that receptors are desensitized. I have no idea where Palumbo get this stuff either. Maybe he can come here and explain it?

 

[sbend140]

I am running 20mcg daily IGF-1lr3 through my HRT clinic. The doctors have told me you can run it year round. The only issue is $ as the stuff runs $600 for a two weeks supply.

 

[Late_Starter]

I am running 20mcg daily IGF-1lr3 through my HRT clinic. The doctors have told me you can run it year round. The only issue is $ as the stuff runs $600 for a two weeks supply.

20mcg.. my anti-aging clinic has me using 140mcg!

Not every day though, only workout days pinned pre-WO.
Maybe that's why I need so much carbs and get tired... might reduce it save some money

 

[sbend140]

20mcg.. my anti-aging clinic has me using 140mcg!

Not every day though, only workout days pinned pre-WO.
Maybe that's why I need so much carbs and get tired... might reduce it save some money

I'm getting really nice results from 20mcg day. 10 in the AM, 10 in the PM. The pumps I get in my arms are insane. I'm also running 3iu of HGH every day but Sunday.

My clinic also has me on 250mg test and 200mg Nandrolone per week.

It's pretty fucking expensive but well worth it for all pharma grade stuff, and all legal.

 

[Late_Starter]

I'm getting really nice results from 20mcg day. 10 in the AM, 10 in the PM. The pumps I get in my arms are insane. I'm also running 3iu of HGH every day but Sunday.

My clinic also has me on 250mg test and 200mg Nandrolone per week.

It's pretty fucking expensive but well worth it for all pharma grade stuff, and all legal.

Yeah the cost is high but for refrigerated Peptides I'd rather know the quality and not have to mess around with reconsitituting myself.

I don't know where mine get their doses from. Their ghrp dose recommendations are way high as well. Maybe they want to ensure visible results quickly..

I'll have to use my own judgment and use less, save some $ using less too

Sent from my E6653 using Professional Muscle mobile app

 

[RamboStallone]

Yeah the cost is high but for refrigerated Peptides I'd rather know the quality and not have to mess around with reconsitituting myself.

I don't know where mine get their doses from. Their ghrp dose recommendations are way high as well. Maybe they want to ensure visible results quickly..

I'll have to use my own judgment and use less, save some $ using less too

Sent from my E6653 using Professional Muscle mobile app

Igf1 and lgf1-lr3 are two different protein sequences with different half lives and dosage requirements. Maybe your clinic gave you igf1 not lr3? Lr3 is 3x more potent then standard igf1.

 

[BigTex]

Igf1 and lgf1-lr3 are two different protein sequences with different half lives and dosage requirements. Maybe your clinic gave you igf1 not lr3? Lr3 is 3x more potent then standard igf1.

I believe you are right Rambo, clinics do not prescribe IGF-1Lr3 or DES but do prescribe IGF-1 ( in the USA). Increlex and Somavert are 2 that come to mind.

Here is the recommended dosing for IGF-1 - 0.04 to 0.08 mg/kg (40 to 80 micrograms/kg) twice daily by subcutaneous injection. If well-tolerated for at least one week, the dose may be increased by 0.04 mg/kg per dose, to the maximum dose of 0.12 mg/kg given twice daily. So 140mcg/day would make sense.

 

[RamboStallone]

I believe you are right Rambo, clinics do not prescribe IGF-1Lr3 or DES but do prescribe IGF-1 ( in the USA). Increlex and Somavert are 2 that come to mind.

Here is the recommended dosing for IGF-1 - 0.04 to 0.08 mg/kg (40 to 80 micrograms/kg) twice daily by subcutaneous injection. If well-tolerated for at least one week, the dose may be increased by 0.04 mg/kg per dose, to the maximum dose of 0.12 mg/kg given twice daily. So 140mcg/day would make sense.

I don't know of any pharmacy lr3 or des ever being produced, both increlex and iplex (the only pharma igf I know of) are IGF1 as you indicated, which the dosage is higher since it has a shorter active life and needs binding proteins to be effective. Should be used with HGH or GH secretagogues since they increase igf binding proteins.