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irongame427
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+ 6 Possibly a new way to pct?

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So this is something I've been thinking about alot lately and another post today made me wanna go ahead and start a discussion on the topic of pct and serms. So before I get into that I'm just gonna briefly explain the chain of events that lead our bodies into producing testosterone naturally, as this is what we all strive for during pct. Just so anyone who's not fimilar with it can still understand and join in the the discussion. And this is just a generalized version of the process, its a little more complicated then how I will explain it.

So this process is just not one step, its a chain of events that occur. The hypothalamic–pituitary–gonadal axis, is responsible for the production of testosterone. But like I said its a chain reaction that occurs and the end result is the production of testosterone, and some estrogen. So the first part of this process is the hypothalamus creates and releases gonadotropin-releasing hormone (GnRH). When the hypothalamus releases GnRH this signals the pituitary gland to release Luteinizing-hormone (LH), and follicle-stimulating hormone (FSH). After the pituitary gland releases LH it travels through he blood stream down and tells your leydeg cells in your testes to produce and release testosterone.

So what that being said we have these different pct drugs that basically cut out different steps in this process. The first ill talk about is human chorionic gonadotropin or HCG. HCG is basically a synthetic form of LH. When you inject it on cycle it mimics the effects of LH. Whether you actually release a tiny but of testosterone while your on cycle I don't know, but the benefits of using it on cycle n boosting testosterone. We have plenty of it with all the test were injecting lol. In my opinion the best way to use it is throughout your entire cycle. There have been a few studies on recovering test levels after discontinuing the administration of exogenous testosterone, and the problem with recovery was due to desensitization of leydeg cells. The studies showed that the LH levels returned to normal after about 3 weeks when they stopped testosterone injections but test levels took many more weeks to rise. This is due to the fact that when you're on cycle your entire HPTA is shutdown. So your leydeg cells (which are responsible for producing testosterone) lie dormant for many months. So as I stated before HCG mimics the effects of LH, so by using it on cycle your leydeg cells will still be getting that LH signal a few times a week and remain awake and active for the duration of the cycle. By doing so we should be able to avoid the desensitization that will occur and in turn make for a faster and easier recovery. The other method of using hcg is for the last few weeks of a cycle and attempt to "wake up" your lydeg cells and testes and reverse atrophy. That way when you start pct your testes are already at full size and the SERMS can help kickstart your natural test as fast as possible as opposed to waiting for your balls to plump back up during the first few weeks of pct. This is beneficial because you will not produce test at optimal rates with raisin size balls, I'm not sure if you'll produce any test until there close to full size. But like I said before I believe you should use hcg on cycle to prevent this from occurring in the first place. It's never easy to try to explain to a girl why she's able to fit both of your balls in her mouth at the same time. That is unless you wanna tell every girl you bag that you're on steroids. I don't know about you but I'm trying to avoid that conversation. So use hcg to prevent this from occurring. Just my opinion, but that's a discussion for another day.

The next drugs we use are the selective estrogen receptor modulators or SERMs. There are many different ones available but I'm just gonna talk about most commonly used ones and that's tamoxifen citrate or brand name nolvadex and clomiphene citrate or brand name Clomid. Clomids great for pct because it stimulates LH. So since you know understand the important role of LH in this processs you can see why clomid is a great pct drug. It stimulates the pitutary gland to produce LH which in turn will signal your testes to produce and release testosterone. And Nolva exerts it's test boosting effects in some of the same ways as well as through some other pathways through feed back loops with associated with estrogen, but I will not get into as that's not the point of this post.

And the last one is triptorelin. Think of triporelin as a synthetic form of GnRH. Its basically the same concept as HCG. It mimics the action of GnRH, so when you use it it stimulates the pituitary to release LH, and blah blah blah you should know what happens next by now.

So whats the problem here? Well lately I've been thinking and Ive realized we keep skipping one very important step in all this. And thats the most important step, the first one. This entire process is not gonna work once you come off the SERMs if the hypothalamus is not producing GnRH. The serms make it possible to skip the first step, the trip makes it possible to get the pituitary to release LH without the hypothalamus producing GnRH, and the hcg makes it possible to skip both the hypothalamus releasing GnRH, and the pituitary releasing LH
So thats why these are beneficial during pct, you come off gear and you have the clomid and nolva stimulating LH so you don't have to wait for the hypothalamus to start producing GnRH first. So the clomid and nolva will raise your test a bit so you're not spending a month with literally zero test in your body. Thats a great way to lose all your gains.

So now what Im thinking here is why don't we have a drug that stimulates GnRH? We have drugs in triptorelin that mimics the actions of GnRH, but it doesnt stimulate the hypothalamus into actually producing it, We have the serms that stimulate LH, FSH, and we have a drug in HCG that mimics the actions of LH. So I want to find a drug that stimulates GnRH, its the first step in this chain of events, and the most important if you want to naturally produce testosterone. Without the hypothalamus producing GnRH, the pituatiy will not release LH and FSH, which means the testes will not produce testosterone.

So I have been doing a little research about this lately and I have came across a class of drugs that actually stimulate the hypothalamus to produce GnRH. They are called GnRH agonists , and I'm sure you can guess what there used for, the same thing all of our pct drugs are used for and thats fertility. There are currently two of these drugs available, the first is called and Zoladex, which are injected sub q, and the second is Synarel, which is a nasal spray. I havent finished reading about these drugs enough at this point but i will continue to do so over the next few weeks. But if these really work like they are designed to it could be a big breakthrough in pct. Instead of just bypassing steps these drugs will actually start from the very first step of the process. They should stimulate the release of GnRH, which will signal the pituitary to release LH and FSh, which will trigger the testes to produce testosterone. Overtime pct protocols have evolved alot. Back in the early days they didnt even do pct, then the next belief was pyramiding the doses and tapering off. Then we got into the protocols and our current methods with the serms. But we need to continue to improve these methods. I don't know about you guys but I'm all about having the smoothest pct and having the highest chance of recovery possible.

Swoleosis's picture

Iron, did you ever follow up on your research of GnRH agonists? I'd be interested in seeing what you found out about them. This was a great read, thanks!

irongame427's picture

A little bit. I found these medications are not easy to find. At at the moment the doses are very undefined for what we would be using them for. Triptorlin is used in men with prostate cancer and we use 100mcg just enogh to stimulate the pituitary response we are after. In prostate cancer they use huge doses to basically dump all the LH out of the pituatary so after the initial surge of test there is no more left to fuel growth of cancer. So with these other meds I found the recommend doses are most likely much higher then what we would need. So it would take some time and experimentation to figure it out exactly. I still need to keep reading about it but I got alof on my plate right now.

GrowMore's picture

Completely agree, a smooth PCT is more wanted than anything else IMO. Great solid write up.

6 months old..

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cartman69's picture

Yep, basically these two drugs cause an efflux of LH(for testosterone production) and FSH(for sperm production) to be released from the anterior pituitary through dosages that are not nearly as defined as our other less superior mimicking counterparts...However, I, for one, would not see this as a deterrent but rather an opportunity, to look into further but cautioning on the side of not shutting down the axis all together....regardless, hmg, is yet another new player on the field that shows much promise by naturally elevating LH While also raising FSH which hcg does not do...leading to a more natural progression of increasing one's sperm and testosterone levels post cycle...and who knows, maybe these two other analogues, could further aid the process....regardless, good research...;)

UgtaBkdNme's picture

Nice write up Iron.

Sulo's picture

NMDA , d aspartic acid, naturally stimulates the release of gnrh and other hormones correct me if im wrong

irongame427's picture

The study done on a asparic acid was misleading. I believe it showed a 40% imcrase in testostrone in hypogonadal men in just a few days, but after I think it was 13 days levels had returned back to baseline.

crazymofo's picture

GnRH agonists are used to purposely cause hypogonadism in males to help treat prostate cancer.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1550783/

http://www.webmd.com/prostate-cancer/lh-rh-agonistsgnrh-agonists-for-pro...

The way I understand them is that they overstimulate the pituitary to the point it "dumps" all gonadotropin hormones and then is left empty and unable to stimulate the testes.

irongame427's picture

Thats the kinda info I'm looking for bro thanks for contributing. Like I said in my post I havent done a great deal of research on the actual GnRH agonists. The idea of a drug that stimulates GnRH was what I have been realy thinking about. I didnt even know they had those types of drugs that stimulate GnRH until I was writing this. Like i said my idea was just something that starts the process from the very beginning which is getting he hypothalamus to produce GnRH. Gonna start reading more about the agonists now and see what I'm come up with .

crazymofo's picture

Well they do work to stimulate test if used in the right dosage. Triptorelin is actually a GnRH agonist itself. BUT for medical purposes it is given in much higher dosages then the standard 100mcg one gets from a peptide source. They can work but they are so powerful they can cause the opposite of the desired effect. And to be honest I have a hard enough time trusting sources as is when it comes to dosage.

http://www.nlm.nih.gov/medlineplus/druginfo/meds/a611047.html

irongame427's picture

Thats what I was just about to say, If you use it in the proper dose you can stimulate just enough so you don't overstimulate the production of GnRH and cause the pituitary to release all of the LH. And ya i hear you on not trusting the sources. With sit like trip if you use to much you can chemically castrate yourself, so imagine if the peptide source have you 1000mcg by mistake instead of 100. Ive heard even using like 100 to many times without enough time between them can cause castration. So imagine if you got one big ass dose of it by mistake.