IGF-2 causes small intenstinal growth?

I'm going by memory from what I've read over the past month or so. Now the main reason why people get "roid gut" is from the liver producing IGF-2 (or it's converted from IGF-1?)? Since the small intestines have many IGF-2 receptors, it grows larger? Is this correct? So how would a high amounts of l3 IGF-1 cause this undesirable side effect, if it all?

I'm a few weeks away from starting a month run of l3 IGF-1 with test prop. I'm thinking 60mcgs PWO (split morn/eve on off days). I just want to cover everything and get stuff settled in my mind.

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Originally Posted by Seattle Junk

I'm going by memory from what I've read over the past month or so. Now the main reason why people get "roid gut" is from the liver producing IGF-2 (or it's converted from IGF-1?)? Since the small intestines have many IGF-2 receptors, it grows larger? Is this correct? So how would a high amounts of l3 IGF-1 cause this undesirable side effect, if it all?

I'm a few weeks away from starting a month run of l3 IGF-1 with test prop. I'm thinking 60mcgs PWO (split morn/eve on off days). I just want to cover everything and get stuff settled in my mind.

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I would try only 30 on my first run if I were you. I did 60 and i had problems. Did 30 the 2nd time and sides are manageable. see how your body responds, there's plenty of time to increase the dosage on your next cycle, should you choose :wg:

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Originally Posted by Captain Fantastic

I would try only 30 on my first run if I were you. I did 60 and i had problems. Did 30 the 2nd time and sides are manageable. see how your body responds, there's plenty of time to increase the dosage on your next cycle, should you choose :wg:

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Do you recommend 30mcgs PWO or split, 15mcgs morn - 15mcgs PWO? I've read anything less that 50mcgs doesn't do much. What kind of sides did you notice at 60mcgs on your first run? What AAS do you usually run with your l3 IGF-1?

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Originally Posted by Seattle Junk

Do you recommend 30mcgs PWO or split, 15mcgs morn - 15mcgs PWO? I've read anything less that 50mcgs doesn't do much. What kind of sides did you notice at 60mcgs on your first run? What AAS do you usually run with your l3 IGF-1?

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I got results worthwhile with 30. whatever extra I might have gotten with 60 wasn't worth it. but I was on the AAS with the 60 so it could have influenced the whole deal. Maybe go ahead and try 50 since your not AAS. I'd just keep a steady food intake espicially before or right before you get the roid gut feeling.
I do 15 per muscle side per day. either PWO or in the PM about the same time. I got the roid gut. lasted at least a month PC before I started 30/day on 2nd cycle and it has subsided. I throw a shake in bed with me so in the AM I can take a drink and go back to sleep. The first run was with european AAS-primobolan-300 mg/wk, equipose 200 mg/wk, sustanon 200 mg/wk. Going to throw in some tren. on the next one and will be on HGH which I just started, 1st time. I see limited use of the Long R. once per cycle, once PC, max. :?: Do you know what to do about the roid gut? how permanent is it? is it a sympton of hypo :scratch: ? thankx

I wouldn't split doses until I was using 80mcg and as most of you already know, injecting into the worked muscles bilaterally, is not needed with LR3 IGF-1.

JohnnyB

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Originally Posted by JohnnyB

I wouldn't split doses until I was using 80mcg and as most of you already know, injecting into the worked muscles bilaterally, is not needed with LR3 IGF-1.

JohnnyB

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Johnny, do you think Cap F really got roid gut from l3? That's a perm change in organ growth.

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Originally Posted by Seattle Junk

Johnny, do you think Cap F really got roid gut from l3? That's a perm change in organ growth.

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The study I read says it doesn't happen, but another one said it does it you are using anti-inflamitories with it. So if he was use an anti-inflamitory, it can happen, but with streight LR3, I'm going to say no, with the info I have

JohnnyB

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Originally Posted by Seattle Junk

Johnny, do you think Cap F really got roid gut from l3? That's a perm change in organ growth.

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I don't know if I got true "roid gut" whatever that is. I'm sorry, I just copped that term off your post.
The best way I can describe it is it feels like hunger panes. No anti-inflamatories, just finesteride and some herbs and vitamins - milk thistle, aritichoke, mult. vitamin-no iron, vit. e, cranberry extract, calcium, zinc, chrom pic., mult. amino acid, and saw pawmetto. I come off the finesteride while taking a nandrolene derivative: ie: tren.

Does anyone see anything incompatible with the above?

Does anyone know the symptoms of hypo? what it is?

All response's kindly appreciated. :wg:

Cap. F.

oops, i did it again :lol:

I bet roid gut puts a few extra pounds on your squat?

use insulin with that shit and you'll see,

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Originally Posted by seatle junk

I'm going by memory from what I've read over the past month or so. Now the main reason why people get "roid gut" is from the liver producing IGF-2 (or it's converted from IGF-1?)? Since the small intestines have many IGF-2 receptors, it grows larger? Is this correct? So how would a high amounts of l3 IGF-1 cause this undesirable side effect, if it all?

I'm a few weeks away from starting a month run of l3 IGF-1 with test prop. I'm thinking 60mcgs PWO (split morn/eve on off days). I just want to cover everything and get stuff settled in my mind.

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again.....
the liver does not produce igf 2
nor is transformed from igf 1.
IGF-1 is secreted by the liver
IGF-2 is secreted by the brain, kidney, pancreas and muscle.
The IGF-2 receptor only binds IGF-2 and acts as a "clearance receptor" - it activates no intracellular signalling pathways, functioning only as an IGF-2 sequestering agent and preventing IGF-2 signalling.

see:

"Insulin-like growth factor (IGF)-2 is overexpressed in hepatocellular carcinoma and accompanying dysplastic lesions. IGF-2 signalling is mediated through IGF-1 receptor (IGF-1R), while mannose 6-phosphate/insulin-like growth factor-2 receptor (M6P/IGF-2R) controls pericellular levels of free IGF-2"
British Journal of Cancer (2003) 88, 733-739.
doi:10.1038/sj.bjc.6600777
focal overexpression of insulin-like growth factor 2.

N Sedlaczek1,2, A Hasilik3, P Neuhaus4, D Schuppan5 and H Herbst1

1.-Institute of Pathology, University of Muenster, Muenster, D-48129, Germany
2.-Department of Gastroenterology and Hepatology, Klinikum Benjamin Franklin, Free University of Berlin, Berlin, Germany
3.-Institute of Physiological Chemistry, Philipps-University, Marburg, Germany
4.-Department of Surgery, Charitè, Campus Virchow-Klinikum, Humboldt-University, Berlin, Germany
5.-Department of Gastroenterology and Hepatology, Friedrich-Alexander-University, Erlangen, Germany
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see:
Cohen, Pinchas, et al. "Insulin-like growth factors (IGFs), IGF receptors, and IGF-binding proteins in primary cultures of prostate epithelial". Journal of Clinical Endocrinology and Metabolism, Vol. 73, No. 2, 1991, pp. 401-07

There’s a trainer at my gym(says he’s going for his pro card) that has the biggest GH/IGF Gut.
This freak is about 5’8” 275 lbs and about 6% but he looks pregnant. It’s horrible. This guy is a mess. He wears tank tops and you can see the lumps where he just injected his biceps, Delts and triceps. To top it off, the big bicep vein on both arms are completely scarred up. I mean fresh red scares. He must be injecting
something into his veins. Don’t get me wrong, this guy is a monster but the dude need to clean his act up…
I bet this nut never cycles IGF.

Yo Freak, You Cycle? No, I don’t own a bike man….ha!

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Originally Posted by oswaldosalcedo

again.....
the liver does not produce igf 2
nor is transformed from igf 1.
IGF-1 is secreted by the liver
IGF-2 is secreted by the brain, kidney, pancreas and muscle.
The IGF-2 receptor only binds IGF-2 and acts as a "clearance receptor" - it activates no intracellular signalling pathways, functioning only as an IGF-2 sequestering agent and preventing IGF-2 signalling.

see:

"Insulin-like growth factor (IGF)-2 is overexpressed in hepatocellular carcinoma and accompanying dysplastic lesions. IGF-2 signalling is mediated through IGF-1 receptor (IGF-1R), while mannose 6-phosphate/insulin-like growth factor-2 receptor (M6P/IGF-2R) controls pericellular levels of free IGF-2"
British Journal of Cancer (2003) 88, 733-739.
doi:10.1038/sj.bjc.6600777
focal overexpression of insulin-like growth factor 2.

N Sedlaczek1,2, A Hasilik3, P Neuhaus4, D Schuppan5 and H Herbst1

1.-Institute of Pathology, University of Muenster, Muenster, D-48129, Germany
2.-Department of Gastroenterology and Hepatology, Klinikum Benjamin Franklin, Free University of Berlin, Berlin, Germany
3.-Institute of Physiological Chemistry, Philipps-University, Marburg, Germany
4.-Department of Surgery, Charitè, Campus Virchow-Klinikum, Humboldt-University, Berlin, Germany
5.-Department of Gastroenterology and Hepatology, Friedrich-Alexander-University, Erlangen, Germany
---------------------
see:
Cohen, Pinchas, et al. "Insulin-like growth factors (IGFs), IGF receptors, and IGF-binding proteins in primary cultures of prostate epithelial". Journal of Clinical Endocrinology and Metabolism, Vol. 73, No. 2, 1991, pp. 401-07

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Thanks, you're right. I did read about the brain, kidneys & pancreas excreting IGF-2. I'm just learning about all of this so it's good stuff. I really don't want roid gut, it looks terrible. I want to do lr3 safely, thanks.

thank you seattle.