My prior pct post got hijacked by a bunch of muscleheads squabbling over the benefits of test taper and T-Nation etiquette so I didn't get as much info as I need.
As far as I can figure now that I am off my first cycle of test, I need to be concerned with controlling estrogen and encouraging my natural test production to ramp back up to normal. A number of people have advocated Nolva 40mg a day for 2 weeks then 20mg a day for 2 more weeks. Being a SERM rather than an AI it seems this will be great for preventing post cycle gyno but won't do much to keep estrogen low. Additionally it won't do much to raise my test production since I'll still have suppressive blood levels of test for a few more weeks.
Prisoner 22 on the other hand indicated continue with my adex reducing the dose over approx a 4 week period. This seems to make more sense as it will actually prevent estrogen levels from increasing. He also indicated that after that a SERM could be applied. I assume that NOLVA can assist in increasing my test levels once the blood levels of test come back down to non suppressive levels. Do I have this right? If so at what point would I add the Nolva in and would it be in addition to adex or after I am done with adex?
Thanks again for all the input from you vets that have helped make my first cycle a success.
Prisoner22, no you didn't. As previously discussed I'm not doing the test taper (any more than the half life will inherently provide) for a couple of reasons first I do not want to extend length of cycle, secondly I'm out of test, third gains stopped weeks ago. I like your advice on not doing mega doses of hcg at end of cycle (I think your view is more conservative than the traditional advice and I like that). Also, I like your advice re adex and consider it much better advice than the usual advice of nolva only. But in your other posts the only mention you made of nolva (or any other serm) is after the 4-6 weeks of decreasing adex then it would be time to introduce a serm. When and how much? I asked that before in the other thread but it got lost in all the other bull shit.
I would also like other vets to give their opinion on this but I think you scare the shit out of them. Pretty soon T-Nation will have to be renamed "Prisoner 22's test taper forum" you tend to jump on people who don't agree to your theory on this. I love the fact that you're passionate about your believe in the theory. And I love the fact that your willing to spend so much of your time shareing it with dick heads like me. But you could stand to lighten up a little when confronting people who don't agree with you on this. Yea I know from your avatar your twice the body builder I ever was and yea I know your education in these manners is far supperior to most on this forum but you could lighten up a bit. For what its worth I've read tons of your posts and you are winning over some converts you don't need to tell everyone they are complete dip shits for doing what's been working for them and the majority of users for a decade or so, and that you'll fly over to kick their ass if they don't agree your smarter. I may be exagerating a little but I think you get my meaning.
I would recomend that you stick with adex or femara while on cycle, but for pct, a test/ proviron mix would work well, simmilar to masteron and test. Obviously though if you were using a lightly aromatising cycle, such as equipoise, and winstrol or tbol... nolvadex and proviron would work just fine. But for a test, dbol type cycle, go with the AI if at all possible.
Equipoise is a testosterone-Drug. It is testosterone based, and in the testosterone family of derivatives, since it is simply testosterone with one added bond (c1-2) which slows aromatization and makes it a poor substrate for interaction with the 5a-reductase enzyme. Other than this one added bond, the steran nucleus of this steroid is testosterone- and is ergo a "testosterone drug."
There are three major (recognized) families of anabolic steroid derivatives (Testosterone/19-nor/DHT). Equipoise is squarely in the testosterone family of derivatives and although it isn't simply testosterone - it can hardly be considered a "non-testosterone drug" in any serious conversation about anabolics.
To be honest I haven't really considered any of the other steroids that convert to dht, nor tested.
The masteron/ test taper however, first off is the most practical combo as both drostanolone enathate, and propinate are available, as are the testosterone enanthate and propinate. Therefore, it gives you the choice whether you want to taper with an enathate ester or a propinate ester. You can then pick either the two propinates, or the two enanthate esterfied drugs, and inject them in a 50/50 ratio at the same time. Now of course masteron does have anti estrogen properties, as well as shbg affinity, so test, needs to be used to achieve the same effect, and concurrently, less estrogen aromatises, creating less suppression. This is an alternative to using just a plain test taper with a little bit of adex (which is the more practicle way as not everyone has the extra money or even the availability of masteron), and of course there has been some indication that adex/ AI/ SERM use can cause up-regulation of the ER, making your body hypersensitive to estrogen. This would explain part of the 'rebound' that many experience when they come off their AI or serms, and of course another reason why I recomend that AI's be tapered off gradually to avoid the rebound.
Well masteron can also blunt this problem as well, and then of course as the two drugs are slowly tapered down the body has time to adjust itself gradually.
Yes alot of 'loose' theory here, however, it works - as I have stated before when I am at about the 35mg/35mg per week phase of masteron and test taper, my balls are really sore and swollen - feeling like they are going to explode - and that's after a 9 month countinues cycle without any hcg use.
Neither Masteron nor Winstrol convert to DHT. Are you saying they do?
All DHT derived steroids (except for A50) share all of those properties. Are you saying to just taper with any DHT derivative?
WHy did you say you never considered any other steroid besides Masteron for a taper, since (following your reasoning on aromatization, SHBG, etc..) there are steroids that achieve the effects Masteron does at a much lower dose, and are cheaper.
Wouldn't an oral be MUCH more effective? I mean...once you considered Masteron, wouldn't Proviron be more sound, for obvious reasons?
Why would estrogen suppression by Masteron not cause a rebound, but estrogen suppression caused by a Type-II AI would? Couldn't it be the other way around?
(I am only talking about Type IIs because they are only type you are talking about, from what I see)?
Logically, wouldn't a type-I AI be a better choice, if one were to follow your reasoning? If not, then why not?
What mechanism of action does masteron inhibit estrogen by, and why wouldn't that cause as much potential for a rebound when compared to an AI? Type-I or Type-II?
AR and P22 are both very, very bright guys. I would like to see them discuss things instead of bashing each other. Between the two of them they could build the six million dollar man. This conversation does seem to be going better than usual. Congrats.
Yes, proviron would work as well, however for simplicities sake I prefer masteron, for reasons said above. Now the small amount of masteron you would need for a taper, and the fact that it is readilly available through most quality UG labs, means at least for myself price isn't an issue.
I don't believe that money should every be an issue in cycling anyways - the user should be able to afford all the neccessary drugs to have a successfull cycle and pct with minimal side effects, and maximal results, or he should not cycle untill he has obtained the required funds... but that is another topic..
the more complicated you make things the more difficult it will be for others to understand, and the easier it will be to error.
I have never tried the other dht steroids in a taper, however their properties are not the same as masteron and proviron, in for example their known binding afinity to SHBG, and their antiestrogen properties. That's not to say that they won't work, but I have not tested them personally nor do I know anyone who has in a taper.
Anyways what class of antiestrogen these drugs are is irrelevant to the bottom line. The bottom line is, when you slowly taper, your body has time to adjust, and compensate. It does not matter what 'class' of anti estrogen you do use provided that you slowly taper off it in then end to avoid the rebound. This is just an alternative method to using an AI with testosterone.
I came across this idea, from individuals on hrt who were complaining of gynocomastia, and needing to take a antiE concurently. This of course is not a long term option in my view, and the idea came to me that using a steroid concurently like masteron - or proviron, would solve the user's predicament, by allowing him to keep his libido, high, however, and still get all the benifits of testosterone, without the side effects of aromatisation, of estrogen to the extent where the problems were surfacing. I then realised this would also work well in a taper post cycle, and it does.
Logically, wouldn't an oral DHT derivative be FAR SUPERIOR? Explain why not, if not...
Wouldn't proviron, winstrol, etc...be a better choice? I mean...if they aren't, but still applying your reasoning on masteron....something doesn't fit.
Really? Which ones do not share the SHBG capabilities of Mast/Prov? In my research so far, they all do....that is to say 100% of them. Which don't?
I believe they all do, off the top of my head. And wouldn't orals typically be far superior to injectables, in this regard? I mean...shit...don't basically all steroids lower SHBG, including testosteone?
Why even mention it as one of the reasons to include Masteron, since the other drug in your taper has the same property (lowers SHBG).
What's the RBA of the various DHT derived steroids to SHBG (you logically would need to know it for all of them, to make the above statement that they all differ from masteron and proviron).
How is the class irrelevant? Wouldn't a type-I produce less rebound? Isn't it basically impossible for a type-I to provide a real rebound effect?
I understand all of your rational, but even if your reasoning were to be granted, wouldn't any dht derivative be at least as useful or maybe more useful for a taper than masteron? And preferentially an oral over Masteron?
I wasn't aware of the points you made. It is my understanding that masteron and proviron are known for their anti-estrogen properties - their ability to tie up the aromatase enzyme, and their SHBG affinity, however I see your reasoning.
Now of course my knowledge of winstrol is that there was an assumption that it quite possibly had anti-estrogen properties, but the proof of it was not confirmed and the mechanism of action unknown.
That is why I never even considered using this compound, and for that mater any of the compounds that aromatise, and any of the compounds that don't support libido on a near equal, footing as testosterone.
Now my knowledge is that proviron and masteron are pretty much pure DHT in the body, which is the hormone that supports libido. That was a major factor in choosing these compounds.
I looked for compounds that were going to support libido, in ratio to their binding affinity to the AR.
I didn't want to use a compound in a taper that would bind well to the AR - or even better than testosterone. A hormone such as that would cause suppression, but proportionately to to the steroids testosterone, proviron and masteron, not support libido equally.
Therefore, if the individual tapering was backing down his dose in relation to strength of libido, he may be unable to do so, as more testosteone would be needed to make up for the weekness of the other hormone in that area, which would result in continued suppression. That is why a compound like boldenone wasn't even considered as it is a weak 'testosterone' like molecule and I was not going to even bother tapering off on that, as my objective was full recovery, not first ruling out compounds that may not work as well, or at all.
That is why I have contended also that you must wait for all non testosterone hormones to fully clear your body before begining a taper, as they will just interfere in the process.
Of course as I have said, after the taper is fully completed, that is the time to use nolvadex if needed for a further boost.
and don't forget, I have stated a testosterone taper is also good using adex concurently, however, I do believe you could taper without an AI at all, as once hormone levels of testosterone fall below normal physiological levels, the body should begin to compensate, down regulate the ER, and begin producing testosterone to make up for the deficit. I do believe however the taper without arimidex would need to be more gradual to allow more time for all this to take place.
As for taking orals instead of injectables in a taper, sure it could be done, but the dosing would be more complicated, as such things as half lives, and absorption from the GI would have to be taken into account.
I personally prefer injectable, as at least I know - especially if the two drugs have the exact same ester attatched, exactly what is going into the body, and that the clearance times of the drugs will be simmilar. - Just easier in the long run, and as you know when helping others, the easier you make it to understand, the less explaining is needed and the more people are going to have success.
Although I don't agree with the idea of tapering at all, in any way, the substitution of Aromasin for both the Masteron and Arimidex would be a better idea.
Aromasin causes no rebound, lowers estrogen, and lowers SHBG.
Thats why I asked about why you hadn't thought to use a type-I AI.
Again, I think the whole protocol is flawedm but Aromasin in lieu of the Masteron and Armidex would be logical.
For SHBG RBA, winstrol is far superior to masteron. I would imagine it to be superior to masteron for estrogen suppression also, for obvious reasons...and it's mechanism of action would clearly be the same, unless the pyrazol group contributed some unknown property.
Again, I think the idea of a taper is flawed, since you really don't make any inroads (zero) towards recovery of endogenous hormone recovery while you have any amount of exogenous hormone in you, but wouldn't Aromasin be more logical, ultimately?