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.
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.
Interesting. I thought we wanted the igf to attach to the binding proteins?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?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
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.rambo, are you concluding that DES is good localized or no?
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
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 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.
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
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'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.
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.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
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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.