LGD/SARM and prohormone synergy?

[SwoleSubject]

Hey everyone,

So me and a guy at my gym got into a discussion recently about using sarms and prohormones together, particularly LgD and DMZ. He had enough for a 4 week cycle of each, and his reasoning was thus: if he took 10mg of LGD and 30mg of DMZ every day for 4 weeks, he would gain more weight than taking one followed by the other for 8 weeks. Being that neither converts to estrogen, at least in any significant manner, he figured the gains would be easy to keep since it wouldnt be much water weight, as with dbol or something.

Now, to me, this sounds like bro science. DMZ and LGD are both very potent compounds, and I cant imagine that all of each of these would be absorbed, due to receptor overload. I do not have a source for this line of reasoning, but if anyone does I would much appreciate a link to it. If i am not mistaken, this is the reason that side effects increase with dosage. If I take 100mg of dmz, im not going to build 3x the muscle, im going to build similar amounts to 40mg with a whole ton more side effects. My understanding is that this occurs because the receptor can only "hold" so much of the DMZ (for argument we will say 40mg). If i put 40mg in my body, bam its all absorbed into the desired receptor. Anything over this, and some of the compound floats around in the bloodstream until it finds another receptor, NOT in the muscles, and bam, side effects.

What do you guys think!? Im really looking for sources here, but I never mind "bro science" as long as there is some logic behind it haha! Post your thoughts and what you would reccomend.

 

[Alpha1a]

In for information ! Got both these compounds sitting in my cabinet lol

 

[SwoleSubject]

Same here man!! But im on another cycle so I gotta resist the urges lol!

 

[YoungBodyBuil]

Over saturation of receptors is a myth. Also dosing OF ONE COMPOUND to an extreme poses more sides and that's why it's not done, nothing to do with over saturation.Also the limiting factor to growth and why at a certain point it is slowed is myostatin, has nothing to do with over-saturation. The longer you're on cycle the more your body increases the protein called myostatin which prevents the body from rapidly growing. (people with lower levels of myostatin have been linked to have cancers and tumors aka over growth of cells.) So the idea of using 2 powerful compounds for a shorter period of time versus megadosing one compound and using longer is safer and can yield very impressive gains. Some people who run extensive cycles run myostatin inhibitors or raise follistatin which suppresses myostatin. There's a lot involved but it has nothing to do with over saturation. Mega dosing is never advised especially not with a methyl.

 

[YoungBodyBuil]

There will always be a limiting factor as our body is programmed to always try to reach homeostasis. That's why people who run non-aromatising compounds get estro sides/gyno. When your body sees excess androgen's it'll raise estrogen to try to balance the system. In the case of what we're talkign about, Myostatin is the limiting factor in terms of gains on cycle especially as the cycle goes on longer.

 

[YoungBodyBuil]

Can your body ADAPT to higher levels of androgens causing you to need higher dosing? Sure, but the receptors themselves are not over saturated your body has just adapted to higher androgen levels. However in terms of cycling and the limiting factor to growth on a cycle is myostatin especially on longer cycles which is why some people use a peptide form of follistatin. YK-11 the SARM(wrongly labeled if you look at its chemical structure it is clearly a steroid.) works via Follistatin pathways.

 

[SwoleSubject]

Awesome info man! I had heard of Myostayin before, but was unaware that its levels in the bodies increase with length of cycle... Is this because the cycle itself makes your body produce more Myostatin, or is it the body releasing Myostatin because it sees the excess muscle growth as a bad thing??

Interes Point about mega dosing vs multiple compunds as well!! Will have to keep that in mind. I will concede that Im a fan of shorter cycles to combat shutdown, so its good to know there are other reason to support that method of dosing

 

[YoungBodyBuil]

Awesome info man! I had heard of Myostayin before, but was unaware that its levels in the bodies increase with length of cycle... Is this because the cycle itself makes your body produce more Myostatin, or is it the body releasing Myostatin because it sees the excess muscle growth as a bad thing??

Interes Point about mega dosing vs multiple compunds as well!! Will have to keep that in mind. I will concede that Im a fan of shorter cycles to combat shutdown, so its good to know there are other reason to support that method of dosing

Our bodies do not see things as we do.. it's not that specific excess muscle growth is not a bad thing. However excess growth can be. Your body doesn't think "oh it's muscle growth that's fine, I wont increase myostatin"... It's not that cut and dry, your body sees growth as growth no matter what it is. So when your body realizes excess growth.. Especially in a short time span ( a steroid cycle) it will raise Myostatin.

 

[SwoleSubject]

Got you! Not to change the subject too much, but youre not saying yk11 is a myo. Inhibitor are you? Only that it works via similar pathways? Or is it an inhibitor? I was under the impression that myo inhibitors must be injected but again maybe just bro science/regurgitated info

 

[YoungBodyBuil]

Got you! Not to change the subject too much, but youre not saying yk11 is a myo. Inhibitor are you? Only that it works via similar pathways? Or is it an inhibitor? I was under the impression that myo inhibitors must be injected but again maybe just bro science/regurgitated info

In that study Kanno experimented with C2C12-muscle cells, and not with lab animals or humans. Nevertheless Biological and Pharmaceutical Bulletin deemed Kanno's article interesting enough to publish it as a 'Highlighted Paper selected by the Editor-in-Chief'. We're not surprised. Kanno discovered that muscle cells manufacture more anabolic factors if you expose them to 500 nanomoles YK11 than if you expose the same muscle cells to 500 nanomoles DHT.


Japanese researchers are doing experiments with a new SARM which, if the first publications are anything to go by, has a stronger anabolic effect than classic steroids such as DHT. YK11 attaches itself to the androgen receptor, causes few androgen effects and inhibits – the researchers haven't quite worked out how – the effect of myostatin.

When the researchers deactivated the androgen receptor, YK11 lost its anabolic effect. So YK11 works via the androgen receptor. When the researchers deactivated follistatin, the anabolic effect disappeared too. Ergo: YK11 is a SARM and a myostatin inhibitor.

By the way, good old testosterone also stimulates the synthesis of follistatin. [Endocrinology. 2009 Mar; 150(3): 1259-68.] So maybe YK11 is a substance that’s as good a muscle strengthener as testosterone, but without the side effects.

"YK11 was shown to be an appropriate anabolic SARM", the researchers write. "However, further investigation is required to elucidate the mechanisms of the differential activation of the follistatin pathway by YK11 and DHT.


Look at the evidence above: YK11 causes a larger increase in the synthesis of Myf5, MyoD and myogenin than DHT does. Myf5, MyoD and myogenin are signal proteins that induce muscles to grow.


The figure below shows how that happens: YK11 induces muscle cells to make more follistatin – much more than DHT does. Follistatin is a strong myostatin inhibitor.


Japanese researchers are doing experiments with a new SARM which, if the first publications are anything to go by, has a stronger anabolic effect than classic steroids such as DHT. YK11 attaches itself to the androgen receptor, causes few androgen effects and inhibits – the researchers haven't quite worked out how – the effect of myostatin.

 

[YoungBodyBuil]

Got you! Not to change the subject too much, but youre not saying yk11 is a myo. Inhibitor are you? Only that it works via similar pathways? Or is it an inhibitor? I was under the impression that myo inhibitors must be injected but again maybe just bro science/regurgitated info

Basically, it has a stronger binding affinity for the AR than DHT does, it also has a higher myostatin inhibitory effect than DHT itself. The pure form Follistatin must be injected for potency. One can conclude from this study that, YK-11 can be seen as a Follistatin pre-cursor or a pro-hormone to follistatin.

 

[YoungBodyBuil]

Source:
Biol Pharm Bull. 2013;36(9):1460-5.

 

[SwoleSubject]

Would yk11 thus be a viable form of an oral myo inhibitor or would it still be too weak to affect levels in the body?

 

[YoungBodyBuil]

Would yk11 thus be a viable form of an oral myo inhibitor or would it still be too weak to affect levels in the body?

Yes, but the question here is, is it a viable option? Here's an excerpt from IronMagazine.

However, this would all be a moot point if not for the development of YK11; a DHT derivative which has thus far been falsely marketed as a S.A.R.M. Originally created at Toho University in Japan, this is one of those straight to market drugs we know very little about, as the total absence of both human and animal testing has made it difficult, if not impossible to determine exactly how it functions from both a pharmacokinetic and pharmacodynamic standpoint. With such studies being critical for establishing a chemical’s ideal dosing range, potential toxicity, efficacy, bioavailability, etc, we are almost completely in the dark with YK11, being forced to rely on anecdotal evidence alone as a means of evaluating its overall character. However, with such a limited number of independent user reviews currently available, we have yet to come to a general consensus regarding the most basic information.

Here’s what we do know about YK11. 1.) It is a partial androgen receptor agonist. 2.) It functions as a myostatin inhibitor. Let’s address number one first. As most of you know, steroids/S.A.R.Ms stimulate muscle growth mainly by attaching to and activating the androgen receptor. In the vast majority of cases, steroids/S.A.R.Ms are what’s known as full androgen receptor agonists, as they elicit a maximal response of the AR upon occupation. On the other hand, partial agonists activate the androgen receptor with only partial efficacy and may even display some antagonistic activity (an effect common to partial agonists), which means it could potentially block or dull the effects of full agonists (other steroids/S.A.R.Ms) at the androgen receptor.

Because of this, some have proposed that using YK11 in concert with supraphysiological doses of AAS may lead to a reduction in muscle growth. However, this belief assumes that YK11 is unable, in all cases, to activate the AR with equal potency (note: partial agonists are not necessarily weaker from a myotrophic standpoint). It also assumes that the individual is in a state of androgen receptor saturation—because even if YK11 did knock some AAS off their receptor sites, they would just re-attach at the first available opening. Still, there are no benefits associated with being a partial agonist, at least not when it comes to steroids/S.A.R.Ms. Therefore, we must acknowledge the potential for a worst case scenario, which is that YK11 might have an adverse effect at the androgen receptor.

However, before you write YK11 off as another failed experiment in a long line of S.A.R.M failures, keep in mind that YK11’s ability to initiate growth via AR activation was never its primary selling point. What I find really cool about this stuff, and what sets it apart from all other steroids/S.A.R.Ms, is its ability to function as a myostatin inhibitor. More specifically, it reduces the effectiveness of myostatin by increasing production of Follistatin; an antagonistic protein that directly stops myostatin from executing it inhibitory effect on muscle growth.

This effect actually isn’t unique, as many steroids function as myostatin inhibitors to one degree or another. However, what is unique is the potency with which YK11 works to combat this muscle destroying molecule. In one study, YK11 was shown to increase Follistatin production several times higher than DHT, which is itself a potent inhibitor of myostatin. With myostatin playing such a prominent role in the regulation of skeletal muscle mass, any drug capable of elevating Follistatin to this extent should appropriately garner the attention of bodybuilders worldwide.

Over the next 1-2 years we should start seeing more user reviews in conjunction with verifiable US lab work (to confirm compound legitimacy). While this will allow us to draw more reliable conclusions regarding its effects in bodybuilders, current user experiences are encouraging. Although there are some inconsistencies among user reports (which is to be expected in the absence of confirmable mass spec testing), there are also some commonalities. One of the most frequently reported effects is an increase in muscle fullness/pumps, with many individuals claiming that YK11 exceeds even oral AAS in this regard. While I can’t vouch for the truthfulness of these claims, as a previous user of genuine Follistatin, I can say with absolute certainty that this is a primary feature of this particular myostatin inhibitor. Given YK11’s ability significantly increase Follistatin levels, I wouldn’t be surprised if there was a direct connection between the two.

 

[SwoleSubject]

Fantastic info sir!!! i wish I could put this info on every board and correct a few misconceptions that even I had. You obviously have experience with this area, so what is your opinion about the potentially deadly consequences of inhibiting myostatin (heart growth, etc)? Is your understand that Myostatin levels revert after the use of follistatin/an inhibitor is discontinued ?