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There have been a few questions regarding MGF as of of late. I recently had a discussion w/ LakeMountD w/ regards to IGF & MGF. Thought I would share. Big A does not like links to other boards, so I will copy and paste. Also included is a link to a word doc written by LakeMountD. The info is fairly technical, but so is the subject matter. It may cause some to rethink the conventional IGF protocols as well. LakeMountD will be updating the word doc as new info, through personal experience & empirical evidence, becomes available. So if you are truly interested I recommend you perhaps bookmark the the word doc and check periodocally.
http://www.thefilehut.com/userfiles/lakemountd/MGF-IGF-1Compile.doc
LMD
Don't worry about injecting times. (IGF) For some reason people are freaking out about doing injections only post workout. With the active life of this stuff being anywhere from 8-12 hours (depending on which company you ask), you should split the injection into 2x per day. One more towards the morning, one more towards afternoon, just be sure to keep your carb intake up as insulin production will be cut somewhere on the level of 1/8th to 1/12th, this can cause hypoglycemia if you aren't careful. The 2x per day injection, however, will keep blood serum levels high all day.
Don't worry about injecting into the particular muscle either. You can inject anywhere, this is a systemic compound and the compound is distributed through the body quite fast, as seen by the rise of blood sugar and drop of insulin. Your body will use the LR3 where it is needed, for satellite cell differentiation. This stuff is much more anabolic than the natural IGF-1 that your body produces.
Rex
So its your opinion that maintaining a blood level translates to greater efficacy vs. the higher peak concentration obtained w/ once daily, or PWO only, dosing? Is this based on literature or personal experience? Does more frequent dosing not lead to quicker downregulation? I'm not disagreeing w/ you here as no one can truly answer this definitively of course, just want your thoughts.
LMD
Downregulation is going to take place either way. It is an unfortunate side effect to these large doses. Personally I believe that LR3 IGF-1 is a big cause of it because of it being much more anabolic than rhIGF-1 and because of its half life. The half and active lives of this compound are long enough it is going to happen either way unless you run very low dosage of this stuff. Personally I believe a combo of IGF + MGF is the way to go but only using the dosing scheme I outlined in an article I wrote. I will post it at the end of this post. Read the part that says "Written by LakeMountD", it is the third section down.
There is no real way to determine downregulation effect since all scientific evidence uses rhIGF-1. Sutdies done on dwarfism as well as a few other things involving some sort of GH or IGF-1 deficiencies all use it. The other problem is the fact that in these studies they are using dosages on the scale of 600mcg/kg of bodyweight in young children!!! That is an incredible dosage of rhIGF-1. The study I have found that it increased plasma levels by 2-3 fold while downregulating receptors 50%. The other problem? They were testing receptors on the intestine. There are naturally more there as it is but we can only assume similar downregulation is occurruing in muscle as well.
I have proposed before that a 3 day per week injecting of IGF-1 might be optimal to growth as well as allowing time for receptors to be brought back up. Lactosis actually increases receptor count, so those down days or not injecting LR3 IGF-1 (the 3-4 days of non use) when you are working out you are also increasing receptors.
This is all based off theory + scientific data using similar compounds.
Rex.
Very well written reference. Thank you for your time in putting that together.
You specifically addressed what I was getting at, both in the post above and in your article. Many people have been disappointed w/ IGF. There are those who label such people as "non-responders." Its always been my position that this is simply not possible due to its role in normal physiological development. In reality, I believe the problem lies in unrealistic expectations. This is many times coupled w/ a complete lack of understanding of the efficiency of physiolgical mechanisms employed by the body to maintain homeostasis when bombarded w/ massive amounts of an extremely anabolic hormone w/ pharmacokinetic action that extends considerably past that of "natural" IGF. You raise the point that GH's effects, many of which we attribute to IGF, are best obtained over time. It may be, as you suggest, that the typical bodybuilder mentality has failed us where the conventional IGF protocol is concerned.
Is it unreasonable to suggest that the best way to employ LR3 IGF-1 may be in smaller, less frequent doses over time? Such as 20mcg PWO only in the off season. Assuming 3-4 workouts/week. The co-employment of HumR or Humalog @ 6-10 IU w/ the IGF, and 2-4IU of GH one hour later would seem to have many synergistic actions. Injection of 100mg of T suspension would be adviseable as well.
I know people who use a year round post workout only protocol similar to the above (or exactly like) in the off season when training is limited to 4 days per week. It is difficult to evaluate efficacy as these people are already quite large, and it is merely one part of a much larger polypharmacologic regimen.
All of my thoughts on this and rationale for it are beyond the scope of this post. You understand what I'm saying however w/out me having to say it. Thoughts?
LMD
Wow, good post, finally someone who doesn't post off just what they think or off of what they heard, a well thought out response haha. I salute you .
Yes, you are right, there is no such thing as a non-responder unless you have Laron's Dwarfism or some other sort of GH deficiency. Even people with muscular dystrophy still produce IGF-1, their body just fails to splice towards the MGF variant.
Although I agree with the fact that HumR, GH, IGF-1, and test. susp. would be an outstanding stack, I tried to focus on more of just IGF-1 and MGF ran by themselves or as a combination mainly because I felt once we figured this out to an extent, you could always add other things for better results later on.
I do believe, though, that lower dosages with a longer period of time could be effective. Think of it this way, if GH passes through the liver and signals for IGF-1 production and only 1% of the IGF-1 that is produced is unbound you can imagine how much IGF-1 is present. Now lets add in a much larger amount of exogenous GH and we can increase serum plasma levels, lets say by twice as much. This number is still NOWHERE near what exogenous LR3 IGF-1 can provide. GH users, as stated, can use year around and produce results, telling me that it avoids significant IGF-1 downregulation. This is also due to the fact that hIGF-1 binds to the IGF-1 BP3 and your body can stil somewhat regulate serum levels.
One of the biggest mistakes people are making is they think that LR3 IGF-1 is sort of "bypassing" using GH and moving straight into the final product, much like a person would make the jump from 4-AD to an injectable test. variant. This is their downfall, however, they are leaving out a very important variable. To our advantage LR3 IGF-1 cannot be bound to IGF-1 BP3, however, it also CANNOT splice towards MGF. MGF plays an important role in proliferating satellite cells to the affected area. In fact, it plays a much more significant role than even IGF-1 in my opinion. MGF, although it has a binding protein (which helps act as a time released growth factor), does not bind to IGF-1 receptors so is not affected by the downregulation problem. With the amount of LR3 IGF-1 that people are injecting, I don't feel there is enough natural MGF being produced to proliferate enough satellite cells for great amounts of LR3 IGF-1 to be super effective. That is why I have been such a big advocate of mixing both. I am assuming you wrote my big section in that article that explains mgf inhibiting myotube production, these things need to be dosed right and they make a great combo.
Mainly what I am saying is I feel once we get a good idea of dosages on these things I believe we can make significant progress in a much shorter amount of time. And we haven't began to touch on the subject of hyperplasia yet.
I will be testing out my hypothesis VERY soon. Hopefully starting in the next month or so.
Rex
Precisely the type of mechanism I was speaking of that most people simply do not understand.
LMD
I actually came up with something new as of recently. I am going to directly quote it from the AM . c o m post that I made earlier today. This could provide insight as to why IGF isn't working its wonders after 3-4 weeks of continued use. Something to look at past down-regulation of receptors, which might not be to blame.
"Okay well after staring at study after study, pissed off at the fact I can't find much on downregulation of IGF-1 receptors I got to thinking. I am posting this here because I am only one person and although I spend hours on this stuff per day I can only see so many studies at once. If you see anything that goes with this subject please post it but I think I might be on to something here. Bear with me .
People are complaining that they aren't seeing results after 4 weeks. I don't believe this is TOTALLY due to downregulation. The main study I found on downregulation stated that in the intestines there was a 50% drop in IGF-1 receptors after rhIGF-1 was administered after time. But serum levels increased 2-3 fold, so this should be enough to cover most of the downregulation. Although you might not have read that study, you probably have read somewhere that supplemenation with LR3 IGF-1 suppresses nautral hGH output. hGH passes through the liver and signals the body to produce IGF-1, which in turn is spliced towards MGF following a workout. After 4 weeks I assumg your natural hGH levels would be quite suppressed compared to normal, especially at these crazy dosages like 80mcg/daily etc. This is your body's natural reaction, it can't just stop making IGF-1, it has to stop producing hGH to do this.
Okay now I am starting to get to my point. As time goes by your body stops producing MGF. MGF is what proliferates (brings in) massive amounts of satellite cells that are fused to muscle and activated (differentiated) by the LR3 IGF-1. HOWEVER, if you don't have much MGF being produced then your LR3 IGF-1 (at the 80mcg or whatever that you are injecting) doesn't have a significant amount of satellite cells to fuse and activate, it is working with a depleted pool of them, making it feel like the effects stop working.
How do I know that this is a good possibility? Well when I was taking it, I saw no difference in how hungry I was on that stuff from the day I started taking it till the 4 week mark. This means that it was still binding weakly to the insulin receptor and was still binding to the IGF-1 receptor. This hunger is different from normal hunger, I would have to get up in the middle of the night and eat a big tablespoon of peanut butter and have some milk or my stomach would be killing me.
Very interesting find here though guys, we might be able to run LR3 longer with MGF use (following my protocol of only injecting MGF on day 1 and day 2, however).
Let me know what you guys think."
Rex
Extremely plausible. I'll go further and say highly likely as much, possibly more, of a contributing factor as downregulation. Again, multiple mechanisms at play in the maintenance of homeostasis. This is a simple explanation. Its somewhat amazing that it has not been suggested, to my knowledge, until now. Good work.
There is so much emphasis placed on the pituitary axis with regards to testosterone. People seem to ignore pituitary lag as it relates to GH. While the mechanisms behind the efficacy of testosterone are more complex than most realize, it is nowhwere near as complex as the interactions of GH, insulin, and subsequent growth factors. While there has been a move as of late to address this issue where GH is concerned (with qod dosing, etc) due to the study presented on children comparing daily and qod admininstration and the subsequent effects on pituitary lag upon cessation, no one has addressed this issue w/ regards to IGF.
Again, this is fairly technical information. If you can weed through it you will invariably increase your knowledge w/ regards to the physiology of these hormones. Many of these thoughts have never been proposed anywhere to my knowledge. Feel free to post up questions and I will clear the muck as best I can.
Rex.
http://www.thefilehut.com/userfiles/lakemountd/MGF-IGF-1Compile.doc
LMD
Don't worry about injecting times. (IGF) For some reason people are freaking out about doing injections only post workout. With the active life of this stuff being anywhere from 8-12 hours (depending on which company you ask), you should split the injection into 2x per day. One more towards the morning, one more towards afternoon, just be sure to keep your carb intake up as insulin production will be cut somewhere on the level of 1/8th to 1/12th, this can cause hypoglycemia if you aren't careful. The 2x per day injection, however, will keep blood serum levels high all day.
Don't worry about injecting into the particular muscle either. You can inject anywhere, this is a systemic compound and the compound is distributed through the body quite fast, as seen by the rise of blood sugar and drop of insulin. Your body will use the LR3 where it is needed, for satellite cell differentiation. This stuff is much more anabolic than the natural IGF-1 that your body produces.
Rex
So its your opinion that maintaining a blood level translates to greater efficacy vs. the higher peak concentration obtained w/ once daily, or PWO only, dosing? Is this based on literature or personal experience? Does more frequent dosing not lead to quicker downregulation? I'm not disagreeing w/ you here as no one can truly answer this definitively of course, just want your thoughts.
LMD
Downregulation is going to take place either way. It is an unfortunate side effect to these large doses. Personally I believe that LR3 IGF-1 is a big cause of it because of it being much more anabolic than rhIGF-1 and because of its half life. The half and active lives of this compound are long enough it is going to happen either way unless you run very low dosage of this stuff. Personally I believe a combo of IGF + MGF is the way to go but only using the dosing scheme I outlined in an article I wrote. I will post it at the end of this post. Read the part that says "Written by LakeMountD", it is the third section down.
There is no real way to determine downregulation effect since all scientific evidence uses rhIGF-1. Sutdies done on dwarfism as well as a few other things involving some sort of GH or IGF-1 deficiencies all use it. The other problem is the fact that in these studies they are using dosages on the scale of 600mcg/kg of bodyweight in young children!!! That is an incredible dosage of rhIGF-1. The study I have found that it increased plasma levels by 2-3 fold while downregulating receptors 50%. The other problem? They were testing receptors on the intestine. There are naturally more there as it is but we can only assume similar downregulation is occurruing in muscle as well.
I have proposed before that a 3 day per week injecting of IGF-1 might be optimal to growth as well as allowing time for receptors to be brought back up. Lactosis actually increases receptor count, so those down days or not injecting LR3 IGF-1 (the 3-4 days of non use) when you are working out you are also increasing receptors.
This is all based off theory + scientific data using similar compounds.
Rex.
Very well written reference. Thank you for your time in putting that together.
You specifically addressed what I was getting at, both in the post above and in your article. Many people have been disappointed w/ IGF. There are those who label such people as "non-responders." Its always been my position that this is simply not possible due to its role in normal physiological development. In reality, I believe the problem lies in unrealistic expectations. This is many times coupled w/ a complete lack of understanding of the efficiency of physiolgical mechanisms employed by the body to maintain homeostasis when bombarded w/ massive amounts of an extremely anabolic hormone w/ pharmacokinetic action that extends considerably past that of "natural" IGF. You raise the point that GH's effects, many of which we attribute to IGF, are best obtained over time. It may be, as you suggest, that the typical bodybuilder mentality has failed us where the conventional IGF protocol is concerned.
Is it unreasonable to suggest that the best way to employ LR3 IGF-1 may be in smaller, less frequent doses over time? Such as 20mcg PWO only in the off season. Assuming 3-4 workouts/week. The co-employment of HumR or Humalog @ 6-10 IU w/ the IGF, and 2-4IU of GH one hour later would seem to have many synergistic actions. Injection of 100mg of T suspension would be adviseable as well.
I know people who use a year round post workout only protocol similar to the above (or exactly like) in the off season when training is limited to 4 days per week. It is difficult to evaluate efficacy as these people are already quite large, and it is merely one part of a much larger polypharmacologic regimen.
All of my thoughts on this and rationale for it are beyond the scope of this post. You understand what I'm saying however w/out me having to say it. Thoughts?
LMD
Wow, good post, finally someone who doesn't post off just what they think or off of what they heard, a well thought out response haha. I salute you .
Yes, you are right, there is no such thing as a non-responder unless you have Laron's Dwarfism or some other sort of GH deficiency. Even people with muscular dystrophy still produce IGF-1, their body just fails to splice towards the MGF variant.
Although I agree with the fact that HumR, GH, IGF-1, and test. susp. would be an outstanding stack, I tried to focus on more of just IGF-1 and MGF ran by themselves or as a combination mainly because I felt once we figured this out to an extent, you could always add other things for better results later on.
I do believe, though, that lower dosages with a longer period of time could be effective. Think of it this way, if GH passes through the liver and signals for IGF-1 production and only 1% of the IGF-1 that is produced is unbound you can imagine how much IGF-1 is present. Now lets add in a much larger amount of exogenous GH and we can increase serum plasma levels, lets say by twice as much. This number is still NOWHERE near what exogenous LR3 IGF-1 can provide. GH users, as stated, can use year around and produce results, telling me that it avoids significant IGF-1 downregulation. This is also due to the fact that hIGF-1 binds to the IGF-1 BP3 and your body can stil somewhat regulate serum levels.
One of the biggest mistakes people are making is they think that LR3 IGF-1 is sort of "bypassing" using GH and moving straight into the final product, much like a person would make the jump from 4-AD to an injectable test. variant. This is their downfall, however, they are leaving out a very important variable. To our advantage LR3 IGF-1 cannot be bound to IGF-1 BP3, however, it also CANNOT splice towards MGF. MGF plays an important role in proliferating satellite cells to the affected area. In fact, it plays a much more significant role than even IGF-1 in my opinion. MGF, although it has a binding protein (which helps act as a time released growth factor), does not bind to IGF-1 receptors so is not affected by the downregulation problem. With the amount of LR3 IGF-1 that people are injecting, I don't feel there is enough natural MGF being produced to proliferate enough satellite cells for great amounts of LR3 IGF-1 to be super effective. That is why I have been such a big advocate of mixing both. I am assuming you wrote my big section in that article that explains mgf inhibiting myotube production, these things need to be dosed right and they make a great combo.
Mainly what I am saying is I feel once we get a good idea of dosages on these things I believe we can make significant progress in a much shorter amount of time. And we haven't began to touch on the subject of hyperplasia yet.
I will be testing out my hypothesis VERY soon. Hopefully starting in the next month or so.
Rex
Precisely the type of mechanism I was speaking of that most people simply do not understand.
LMD
I actually came up with something new as of recently. I am going to directly quote it from the AM . c o m post that I made earlier today. This could provide insight as to why IGF isn't working its wonders after 3-4 weeks of continued use. Something to look at past down-regulation of receptors, which might not be to blame.
"Okay well after staring at study after study, pissed off at the fact I can't find much on downregulation of IGF-1 receptors I got to thinking. I am posting this here because I am only one person and although I spend hours on this stuff per day I can only see so many studies at once. If you see anything that goes with this subject please post it but I think I might be on to something here. Bear with me .
People are complaining that they aren't seeing results after 4 weeks. I don't believe this is TOTALLY due to downregulation. The main study I found on downregulation stated that in the intestines there was a 50% drop in IGF-1 receptors after rhIGF-1 was administered after time. But serum levels increased 2-3 fold, so this should be enough to cover most of the downregulation. Although you might not have read that study, you probably have read somewhere that supplemenation with LR3 IGF-1 suppresses nautral hGH output. hGH passes through the liver and signals the body to produce IGF-1, which in turn is spliced towards MGF following a workout. After 4 weeks I assumg your natural hGH levels would be quite suppressed compared to normal, especially at these crazy dosages like 80mcg/daily etc. This is your body's natural reaction, it can't just stop making IGF-1, it has to stop producing hGH to do this.
Okay now I am starting to get to my point. As time goes by your body stops producing MGF. MGF is what proliferates (brings in) massive amounts of satellite cells that are fused to muscle and activated (differentiated) by the LR3 IGF-1. HOWEVER, if you don't have much MGF being produced then your LR3 IGF-1 (at the 80mcg or whatever that you are injecting) doesn't have a significant amount of satellite cells to fuse and activate, it is working with a depleted pool of them, making it feel like the effects stop working.
How do I know that this is a good possibility? Well when I was taking it, I saw no difference in how hungry I was on that stuff from the day I started taking it till the 4 week mark. This means that it was still binding weakly to the insulin receptor and was still binding to the IGF-1 receptor. This hunger is different from normal hunger, I would have to get up in the middle of the night and eat a big tablespoon of peanut butter and have some milk or my stomach would be killing me.
Very interesting find here though guys, we might be able to run LR3 longer with MGF use (following my protocol of only injecting MGF on day 1 and day 2, however).
Let me know what you guys think."
Rex
Extremely plausible. I'll go further and say highly likely as much, possibly more, of a contributing factor as downregulation. Again, multiple mechanisms at play in the maintenance of homeostasis. This is a simple explanation. Its somewhat amazing that it has not been suggested, to my knowledge, until now. Good work.
There is so much emphasis placed on the pituitary axis with regards to testosterone. People seem to ignore pituitary lag as it relates to GH. While the mechanisms behind the efficacy of testosterone are more complex than most realize, it is nowhwere near as complex as the interactions of GH, insulin, and subsequent growth factors. While there has been a move as of late to address this issue where GH is concerned (with qod dosing, etc) due to the study presented on children comparing daily and qod admininstration and the subsequent effects on pituitary lag upon cessation, no one has addressed this issue w/ regards to IGF.
Again, this is fairly technical information. If you can weed through it you will invariably increase your knowledge w/ regards to the physiology of these hormones. Many of these thoughts have never been proposed anywhere to my knowledge. Feel free to post up questions and I will clear the muck as best I can.
Rex.
Last edited:
Cost is $100/mg.
