Confused on when to use DES IGF1

[123cctv]

4:30 am GHRP/cjc pre-workout
5:00 am Workout
6:45 am MGF shot in bodypart worked
4:00 pm IGF

Repeat the next day only on workout days Mon., Tues. Thurs. Fri.

This has become the quote DatBtrue thread. Here's another from the man:

"See your native MGF expression works post workout. You don't interfere with it by inducing differentiation w/ external admin of IGF-1 until later,"

The bottom line here is dose IGF after MGF, not prior to. Dose MGF after WO when proliferation occurs.

 

[123cctv]

For post-workout mgf use, I'll be sticking with regular mgf just to be on the safe side. It's kind of a quirky mental thing, but I want to get the purest form of the drug and as closely related to original, usable form as possible.

I understand you. Everyone has their preferences and I respect them all. By the way, I am unaware that there are multiple ways to manufacture PEG. What I have learned though is that the pegylated ver. is small enough to penetrate the vascular wall.

The other thing is, if mgf is working, in part, like igf-1, then wouldn't that be potentially putting a halt on the proliferation process even as it begins to occur? We're only going to see part of the mgf actually make it into the cells and the rest just bind to the igf-1 receptor. See what I'm saying?

I think I understand what you are saying. If MGF binds to the IGF receptor it will act as IGF = differentiation? Perhaps another misunderstanding is occurring? MGF does bind to the the IGF receptor, as there is no MGF receptor per se. When MGF expression exists, i.e. proliferation, it's doing this via a different pathway than IGF. However both uitlize the same receptor, thougjh not at the same time.

In the end, the suggested method of getting the injected MGF to properly express itself is to admin it when it's naturally occurring which has been established to be PWO.

Hope this helps!

 

[123cctv]

.What have you guys heard on DES in BW instead of AA?

Keep in mind even if degradation occurs at approx 3 weeks (comparable to IGF-1LR3 in BW), potency will not drop to 0.0 at 3 weeks one day. Degradation is a slow process. Even if you waited another 3 weeks, I couldn't imagine potency had dropped to 50%. This is however only a guess.

 

[123cctv]

What do you guys think about this? If there is any practical truth to this, then we'd want to somewhat time our injections of syntherol and run des igf-1 at a time that best took advantage of whenever we wanted to have differentiation occcur (after major discomfort had subsided possibly?)

Sorry, but I've never researched Syntherol so I'd rather not comment. Interesting thoughts though.

 

[chemicalwarrior]

I understand you. Everyone has their preferences and I respect them all. By the way, I am unaware that there are multiple ways to manufacture PEG. What I have learned though is that the pegylated ver. is small enough to penetrate the vascular wall.



I think I understand what you are saying. If MGF binds to the IGF receptor it will act as IGF = differentiation? Perhaps another misunderstanding is occurring? MGF does bind to the the IGF receptor, as there is no MGF receptor per se. When MGF expression exists, i.e. proliferation, it's doing this via a different pathway than IGF. However both uitlize the same receptor, thougjh not at the same time.

In the end, the suggested method of getting the injected MGF to properly express itself is to admin it when it's naturally occurring which has been established to be PWO.

Hope this helps!

Well, it just seemed that all over dat's thread he talks about how mgf, when it binds to the igf-1 receptor, "acts like igf-1" since all it can do at that receptor is basically activate it. It can't "act like mgf" at the igf-1 receptor because what it does (as far as properties being unique to mgf) has to be done within the cell.

Thanks for your thoughts on the size of the pegylated mgf though. I appreciate that and that clears some questions up. But, yeah, it can be pegylated at various points in the amino acid chain rendering somewhat different properties based on where the pegylation occurs. I'm not sure how universal a "standard" is across the board in the process among manufacturers or how much these differences affect the nature of the drug. That's why I'm somewhat hesitant to rely on peg-mgf for post workout proliferation purposes.

But, I am beginning to believe that it (peg-mgf) may make a much better igf-1 than igf1-lr3 for a number of reasons- that is if it truly is fully acting like igf-1 when it binds to igf-1 receptors. I recently read about a study that showed how gh and igf-1 decrease a specific chemical that relates to body fat regulation and how it is likely that that is their main method of fat loss. If we count on peg-mgf being a more bio-identical and effective igf-1 type of drug that only affects muscle cells and not other igf-1 receptors (as it is reputed to do) then we may unlock some new uses for it.

My problem with igf1-lr3 is that it has been altered so much- by adding on the 13 aminos to the sequence- that I really question whether or not it is still exhibiting characteristics specific to igf-1 rh or is it only acting as an insulin in this form? I tend to think the latter. That's why I'm excited lately about des igf-1. It's like igf-1 rh, but more effective- at least on paper and logically.

Thanks again for your input and thoughts! It's been good discussing this with you and I've learned quite a bit.

 

[tornpie]

IGF-1 des 1,3

It's the only form of IGF I've used and it was amazing that something had so profound an effect on my body in under an hour. I used roughly 50-100 mcg total split into 10-20 mcg injections into each muscle worked immediately post workout. I also consumed a couple of whey shakes loaded up with sucrose to combat the hypoglycemia I'd experience and to aid the protein synthesis. I was using it during pct after a 80 mg trenbolone acetate ed based cycle which I think may have had a lot to do with its efficacy. Trenbolone is supposed to drastically increase IGF-1 receptors. As far as mixing with MGF and other IGF, I wouldn't have any idea what to suggest other than HGH or CJC and GHRP should be used to counter IGF inhibition of endogenous GH. Furthermore, IGF-1 des 1,3 doesn't seem to even have an agreed upon dosing protocol. As with a lot of these things, it seems like when one decides to start playing with the body at such a low level, results can probably vary drastically from one body to the next. We may occasionally get stuck trying to get it perfect when it's damn near impossible to do. In any case, it's always helpful to have people post their experiences and ideas when running the various peptides.

 

[chemicalwarrior]

Tornpie, thanks for your input. Have you ran it very long at this point? What have been your results so far?

With all the talk about mgf, we kinda lost site of the fact that des was the main topic. I think that des alone should be effective post workout (maybe 1/2 hr-1 hr) since the training alone causes mgf to be expressed within muscle cells. What you are doing sounds like it is along these lines and I'm very curious to hear your results!!

 

[tornpie]

chemicalwarrior, I ran it for about two weeks post cycle in June. I only had 1 mg and it was the loss of my peptide virginity. I was amazed that I was still gaining strength and mass with no trenbolone and my boys being half the size lol. My feelings of what was going on during the post workout injections was this is some very potent stuff and a hell of a lot is going on. Intuitively, I think something like what you are saying is right. There seems to be a small window of time to inject it and to have the proper raw materials available for optimal functioning. It has a very small half life, but what I felt going on in a matter of 20-30 minutes seemed to be profound. I wish I could say something about the longer term effects, but I haven't been too consistent in my workouts and everything since June due to other life circumstances, but in the next few months I plan to run a much more intense and structured AAS and peptide cycle. I want to have a test, bold, mast, tbol cycle and maybe a little tren thrown in just to assist the IGF receptivity of my muscles. I haven't really looked too much yet into how test, bold, mast, and tbol affect the addition of exogenous IGF.

The more I am thinking about this now, the more I think that proper GH, IGF-1, and AAS manipulation (not necessarily sky high levels in any of the three) are the holy grail here. Kind of like what dat goes over with GH pulsing. There are probably a lot of advantages to IGF-1 des 1,3's short half life (at least in my current scant knowledge of the growth factors) such as less negative feedback to GH, working more local muscle than all over the body, etc.

One word of caution, I recently read that even minor perturbations to the insulin/IGF balance in rats has dramatic reductions in life expectancy. IGF just seems potent enough to possibly mess it up. As for me, I'm not all that worried since in my view having higher IGF levels and utilization is far better than the opposite. My friend's father just died of cirrhosis and it occurred to me that many of his problems were from a deficit of IGF such as wasting, bone fragility, etc. I can't believe there hasn't been any research studies done administering IGF to people with terminal liver problems. They find the GH keeps going up and up and the geniuses doing the research and treating these problems can't seem to figure out that the GH is being cranked out because it's trying to get more IGF in the system when then liver can't make it anymore. Sometimes they'll administer GH in a study, but I have yet to find one about IGF.

Sorry, it's a bit of a messy post but it's 2:55 am and I am exhausted. Anyhow, I definitely plan to use IGF-1 des 1,3 again and would like to be more systematic in administration, monitoring, and such to start doing my own little research into it. It's hard enough to dig up decent research on AAS let alone peptides. I guess that's why we take our balls out of our purses and step up to the plate. I recently thought that hell I've been playing with myself for over 20 years, might as well try to be as sophisticated and dramatic as possible about it as I get older!

 

[chemicalwarrior]

Tornpie, I appreciate the post. Thanks. I hear you on the disruptions in insulin and igf-1 balance etc. I think we're ok in that des is in and out of the system so quickly. That's one of the reasons I'm personally shying away from longer acting igf-1 drugs like peg mgf and lr3.

 

[tornpie]

Been really kicking this stuff around in my head the last few days about IGF-1. Just read "The Youth Pill" by David Stipp and he talks a little on how lower IGF-1 and insulin levels are correlated with longer life span. When I read the whole book and thought about it, I think that insulin may ultimately be the culprit. Going to research this more and going to invest in a glucose monitor. I am going to try to discipline myself to journal my eating and supplementation and start to get a baseline of what my blood sugar is doing. Crude for now, but when I get a little more disposable cash beyond my supplementation, I would like to start getting daily recordings of my insulin, igf-1, and gh levels. There is a mathematics going on here that if figured out would probably yield some hardcore results for not only optimal hormone use but much wider applications.

I need to think about this stuff more but got a initial idea of where to start. Anyhow, my first initial guess on how to mitigate the long term problems of insulin and igf probably lie in Na R-ALA supplementation. That stuff is pretty hardcore I believe in restoring insulin sensitivity and reducing the aging increases in insulin resistance.

 

[chemicalwarrior]

Been really kicking this stuff around in my head the last few days about IGF-1. Just read "The Youth Pill" by David Stipp and he talks a little on how lower IGF-1 and insulin levels are correlated with longer life span. When I read the whole book and thought about it, I think that insulin may ultimately be the culprit. Going to research this more and going to invest in a glucose monitor. I am going to try to discipline myself to journal my eating and supplementation and start to get a baseline of what my blood sugar is doing. Crude for now, but when I get a little more disposable cash beyond my supplementation, I would like to start getting daily recordings of my insulin, igf-1, and gh levels. There is a mathematics going on here that if figured out would probably yield some hardcore results for not only optimal hormone use but much wider applications.

I need to think about this stuff more but got a initial idea of where to start. Anyhow, my first initial guess on how to mitigate the long term problems of insulin and igf probably lie in Na R-ALA supplementation. That stuff is pretty hardcore I believe in restoring insulin sensitivity and reducing the aging increases in insulin resistance.

I like the way you think. Let me know how using the ala goes. Haven't researched that stuff in years, but still curious about it.

 

[tornpie]

chemicalwarrior, I just looked at your site. I like the way you think as well.

I haven't had much chance to research much more about the insulin/igf-1 receptors. They have a special mechanism that move in a interrelated fashion it seems.

On a related note, I'm coming to the opinion that one can supplement oneself thin on off-cycle beyond DNP and clen/t3. I don't think there's a magic bullet, but I've noticed success with a modified anarchy stack. Na-RALA and Acetyl L-Carnitine seem to do it and throwing in GTE, forskolin, TTA, and TMG seem to give me a nice steady weight loss. I'm not sure if each work according to the popular reasoning behind their mechanisms but in indirect ways like boosting energy, endurance, and motivation. Kind of like back in the day when I could lose a pound or so a week while drinking 10-20 beers virtually every night while not changing my diet or at least not conscious of restricted my food intake in anyway. I believe that it kept my NADH elevated to keep me constantly energetic. I believe that each supplement greases some part of the mechanism and not one by itself can do it. I believe that proper vitamin and mineral intake is also essential (not in the form of a super compressed cheap ass multi at walmart or GNC) but preferably using powders in the most bioavailable form. I think all of these have a part to play in insulin resistance, levels, so on and so forth.

I've been reading up on a lot of the anti-aging stuff and most of what it happens to be is war against glycation and insulin spikes beyond oxidative stress, hormone decline, and diminishing methylation. I'm trying carnosine right now and it seems to help but not in the way NARALA does. Benfotiamine and all the associated AGE inhibitors/breakers are often researched with diabetics, not only to prevent excessive AGEs but also they seem to help blood glucose and insulin. Wonder if anyone is looking at IGF-1 at the same time in any of this research?

Have you tried any dopamine agonists (cabergoline or bromocriptine) for fat loss? I'm intrigued by the research and findings how it seems to normalize GH, ghrelin, and leptin levels besides suppressing prolactin. I would like to add this to my intercycle cutting stack soon. Damn, I wish I could afford a cycle right now!!! It's so much easier with clen/t3 and not having to worry about catabolism.

 

[forklift28]

Nice site CW..interesting reads you got there..now all you gotta do is get some sources and make me a mod. and we are off..j/k ing..I like the ideas you present there..kepp up the good work bro..BTW you got P.M.