posted Sat, 09/15/2012 - 16:36
6989
+ 1 MGF vs PEG-MGF / IGF-LR3 vs IGF-DES
ad
what your guys' preference, experience, opinion, protocol? ive read that regular MGF is much more potent than peg and binds to the receptor better than the PEGlayted version even though the half life is much shorter. thoughts? same with LR3 vs DES. the DES in 4x as potent but shorter half life. opinions? whats better and does using the DES version reduce the risk of contracting growth of the intesines (gh gut) vs lr3?
- Bookmark
- 1
- 0
skalpabump, hoping to get some more answers on this
LR3 is the shit!!! I have tried both pinning before and post workout. I did 50mcg pwo until I ran out (about a few weeks)
I started IGF-1 LR3 on about my 4th day of PCT. I had run Dianabol from weeks 15-20 of my test EQ cycle. Funny because I only lost 4 pounds by the 3rd day of PCT. So I did the IGF for the whole duration of PCT. I actually look bigger than I did on cycle (weird) and I actually put those 4 pounds back on. Which means since I gained almost 20 pounds from the cycle I have kept every single pound.
The point is IGF-1 LR3 has made me continue to make gains during pct which is awesome for me since clomid makes me feel like shit. In a usual pct I get very unmotivated to eat or workout and I only get 5hrs sleep a night.
With the addition of IGF-1 LR3, I continued to sleep like a baby for 10 hours every night and I am extremely motivated to workout!! I also recover pretty fast for not being on any AAS. My strength has not changed much but I still have the strength that dbol gave me which is great.
I was very impressed in the igf and hope the cells mature and get bigger because that will just make me even more happy. By the way IGF makes you feel hungry so it is easy to keep those calories high even during pct and after.
I cannot wait to run IGF again this time I am gonna run 60mcg Post workout about every other day. I think every day dosing is unnecessary since the half life is so long. This time I am going to do EOD 60mcg (30mcg per muscle) and will do as soon as I start my next cycle. I will let everyone know how my results are. I want to have huge triceps lol like kevin levrone
skalpai plan on incorporating igf into my pct after my 1st cycle. have you ever used des before?
skalpaany thoughts on this guys view from the IMForums?
I guess ill take a second to step in and answer this correctly because no one has lr3 IGF-1 is not a "IGF-1" with increased half life, thats bro science and retarded, throw that away. LR3 really should be L Argˆ3 IGF-1. Its simply IGF-1 where glutamate-3 is replaced by arg or arginine. This change makes IGF binding proteins or IGFBP "confused", or more simply it just makes it very difficult for them to bind to this altered form of IGF. This gives Lr3 its increased "potency", as it wont be bound by IGFBP1-6. But the big downside to this is IGFB's are what regulate binding to the gastrointestinal tract. With this, lr3 increases its binding affinity by 2-5 fold in the gut, making it the most potent and most effective when it comes to growth and proliferation on the GI tract.
Lr3 is the worst possible choice of IGF varient if you are worried about tract growth. Noticed or not, it will bind and cause some growth and certainly a degree of proliferation. Variance will happen depending on your body, dosing, ect.
-twist
You are right, the arginine helps keep the IGFBP from tagging it.
Technically LR3 does not have a "longer half life" because IGF does not work same as steroids with esters.
IGF binds to IGF receptors and then its duration could vary.
I think people just refer to IGF having a longer half life so the common person can understand it better. Not everyone has taken general chemistry in college and understands stuff like esters, receptors, amino acids etc...
So its ok to just say IGF-1 LR3 is longer acting than DES because it is. LR3 does not increase the half life but overall it helps it have a longer lasting effect in our bodies.
skalpado you think having the arginine attached making it longer lasting is worth it not being able to be regulated in the intestine, which in turn can cause hypertrophy of the intesine? ive read des is 4x as potent as lr3. do you think it might be a similar situation to mgf where serum levels are higher just for a shorter period with the regular mgf / igf-des than with the PEGlayted/lr3 version?
skalpai came across this protocol by mike a. a while back, hope i can get some feedback from the vets on this approach.
Advanced PEG-MGF & IGF-1 LR3 Program Application:
Proliferation and Differentiation. What do these two words mean, how do these processes promote muscle growth, and how do we optimize them through the use of PEG-MGF and IGF-1? Please allow me to break this down into its most simple form. MGF is the hormone responsible for expanding our pool of stem cells. The expansion of these cells is what’s known as proliferation. Proliferation is the 1st step in the process of forming new muscle cells. Once these stems cells have received the message to proliferate through the actions of MGF, what type of cells they become, whether muscle or otherwise, depends on the message they later receive from other hormones.
IGF-1 is what’s known as a differentiator. Differentiation is the process responsible for turning immature stem cells into a defined cell type. When a stem cell is exposed to the actions of IGF-1, the cell type created is a muscle cell. However, it is very important to note that each of these processes must take place at the correct time. If one process is begun before the other has finished its work, either the entire process is short-circuited, or partial results are achieved. When a muscle(s) is exposed to stress (such as weight training), its first response is to produce localized MGF. MGF is produced only in the muscle, not in the liver like GH mediated IGF-1 production. After training, It is vital that MGF be allowed to fully perform its function of proliferation before IGF-1 is introduced into the system. Otherwise, the inhibitory actions IGF1 will immediately halt the proliferation process and reduce the total number of stem cells available for differentiation into muscle cells. In other words, introducing IGF-1 at the wrong time will limit our rate of muscle growth.
In the past, the typical manner of administering PEG MGF and IGF-1 would be to use 200-300 mg of PEG-MGF immediately post-workout 2X weekly, followed by an injection of IGF-1 the other 5 days per week. In principle this theory is sound, as the PEG-MGF will expand the number of available stem cells, which can then subsequently be differentiated by IGF-1 the following day. However, there are 3 significant problems with this method of use. For one, since PEG-MGF is typically injected only 2 X per week, the BB’r is usually going to choose to inject it after training the body parts he most wants to improve, but what happens if he also trains a body part on the days he administers IGF-1? Being that IGF-1 is typically administered on the days PEG-MGF isn’t (which is usually 5 days per week), it is highly likely that the BB’r is going to be training on at least some of the days he administers IGF-1. That means that on those days, the growth process involving these growth factors will be short-circuited, due to the inhibitory actions of exogenous IGF-1, and the end result will be less than optimal muscle growth.
The second issue which arises due to the current pattern of use is that by using PEG-MGF on non-consecutive days 2X per week, the proliferation process will always be cut short due to the constant interloping of exogenous IGF-1. Because of this, the number of available stem cell will never grow very large and the potential for differentiation will remain limited. The 3rd issue is in regards to PEG-MGF dosing….it is too light. It is now proposed that using 2 mg per week is much closer to the ideal dosage than the commonly prescribed 400 mg per week. If we use prior research as a gauge for determining proper dosing, it would point to our current dosing guidelines as being inadequate. It is a certainty that higher dosages of PEG-MGF are necessary in order to maximize stem cell proliferation. Although user experiences in this dosing range are currently minimal, what has been witnessed does appear to confirm this. In addition, the proposal is scientifically sound.
Now that I have explained the logic for why the older methods of administration are believed to be flawed in their approach, I will go over how to implement the new method of administration. The PEG-MGF molecule is always used over standard MGF, as MGF has a very short active life, being only minutes in length, while PEG-MGF will stay active for days. This enables the PEG version to deliver a much more pronounced effect. It is also important to remember that the PEG attachment does not alter the effects of the MGF molecule. The PEG attachment acts purely to extend its duration of action. As for what form of IGF-1 should be chosen, I believe IGF-1 LR3 is the superior choice only because of its greatly extended active life, which is about 24 hours in length. DES IGF-1 is a very potent form of IGF-1, being about 4X as potent as IGF-1 LR3 on a mcg basis, but its active life is only about 20 minutes. So, unless one was willing and able to administer DES many times per day, LR3 remains the better option for whole-body growth. DES is superior for site enhancement and will also deliver systematic benefits, but when it comes to a single daily injection, DES cannot trump LR3 when it comes to its whole-body benefits.
In contrast to most other injectable drugs, PEG-MGF cannot be administered with a singular inject. Several micro-injects must be used because even though PEG-MGF is systematic in its effects, the injected muscle will still receive a greater amount of benefit. Why? While both steroid esters and the PEG attachment serve primarily to extend the active life of the steroid, there are critical differences between the two. With esterfied AAS, the ester must first be cleaved from the steroid before it is able to attach to the AR and cause muscle growth. This is why esterfied steroids do not cause site growth (although some users think they do due to the inflammation and subsequent swelling which occurs), as the steroid will already have entered circulation and become systematic prior to the ester being cleaved from the steroid molecule. However, unlike AAS, the PEG portion of the drug does not need to be cleaved off before it is able to attach to its receptor site and deliver its message. Also unlike AAS, the MGF molecule (whether it is MGF or PEG-MGF) communicates through cell to cell interaction. Once the PEG-MGF comes in contact with a muscle cell (such as during an injection), the affected muscle cell will relay the same signal to the adjoining muscle cells. More so, this signal will eventually stop being passed along to adjoining cells, making a single inject unsuitable for treating the entire muscle.
Another characteristic of PEG-MGF, which plays a role in the way it is administered, is the fact that it causes a disproportionate degree of muscle growth in the injected muscle, compared to the rest of the body. However, with PEG-MGF being systematic in nature, one might ask why this happens, being that the compound will eventually spread around to the entire body anyway. This is a question I would have to research, so I cannot answer it right now. Still, I speculate that there may be 3 reasons for this. For one, the injected muscle is directly exposed to the entire amount of the drug on a first come basis. Two, the compound will immediately begin attaching to receptor sites as soon as it is injected, likely using up a substantial portion of the drug before it has a chance to become systematic. Three, due to the micro-injection technique, which is explained below, the entire muscle is exposed to the actions of the drug in large quantities.
Below I will lay out the micro-injection technique. It is a pain in the ass to be sure, but due to the use of 30-31gauge insulin needles, this process is made much more tolerable. The micro-injection process involves injecting a small portion of the drug into multiple locations within the same muscle. In the case of smaller body parts, this can be as many as 14-16 injections, split bi-laterally. In larger body parts, 20 injections split bilaterally is more appropriate. Remember, MGF communicates its actions cell to cell, so this micro-injection technique must be incorporated into one’s protocol if optimal results are desired. Using a small amount of injections will drastically limit the amount of muscle cells which are exposed to the actions of the MGF…and a single injection will severely limit the drug’s ability to turn on stem cell proliferation. Now, before anyone is turned away by the sheer volume of injections, it should be noted that this only needs to be performed twice weekly. In addition, the use of a 30-31gauge 1/2 inch insulin pin reduces scar tissue build-up to less than what would be experienced with just a couple injections using a 22 g. needle. The pain factor is almost a non-issue, as it should be near painless. Lastly, this only needs to be performed for 4 weeks, after which point MGF injections cease and are then followed by a single sub-q IGF-1 LR3 injection per day for the next 4 weeks. It is up to the individual if they want to repeat the program after its completion.
Here is an example of how one might target their chest with this program:
Weeks 1-4
Day #1 (post-workout): Inject 1 mg of PEG-MGF into the pecs. Split this 1 mg up into twenty 50 mcg injections and place 10 injects on the right side of the chest, followed by 10 injects in the left side of the chest. Make sure each injection is placed fairly evenly apart. Use a 30-31gauge 1/2 inch syringe.
Day #2 (about 3-4 days after day 1): Same as above.
Weeks 5-8
Days 1-28: IGF-1 LR3 @ 100 mcg once daily.