two stage SD PCT?

jonny21

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I dunno bro.
I read it further up the thread. I guess it was someone talking nonsense.

So the Lewellyn article clearly says that both clomid and nolva both increase testosterone production in normal men. In this respect, nolva is a better PCT treatment than clomid for the "normal", aromatizing cycle. Now my question is geared towards a PCT that starts with very low estrogen and testosterone levels. Since the estrogen levels are low, an anti-estrogenic effect isn't needed.

A suppressive hormone that does not aromatize will leave very little estrogen in the body at the end of the cycle, from my reasoning. And very little testosterone. Am I missing something?
These 2 chemicals can increase testosterone levels. It doesn't matter what the cycle was. I do not even think it matters if you cycled. Don't get hung up on the whether or not the cycle contained aromatizable AAS or not. Shutdown is shutdown. The fact is that both of them will increase testosterone. And they also act as estrogens.

Edit: BTW, aromatization is not the only way estrogen is synthesized.
 
B5150

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I can read real good, Brian. Where are you going with this, man? Sorry, I feel like there is a hole in my knowledge, maybe someone wants to fill me in?
Basically what jonny said. Plus, is leaving our bodies with low/compromised estrogen levels a good idea? The SERM seams to Selectively manipluate Estrogen Receptors in an agonistic and antagonistic manner. It stimulates and reduces. And I believe that this synergistic duel action restores a balance in the process of restoring the HPTA. I am not an expert, but this is my take on it. Reduced estrogen levels seem to be no better than increased levels when it comes to restoring a balance needed for my system to be restored to normal and balanced.
 

doggzj

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BTW, who has bloodwork that shows that SD acts as an anti-estrogen?
It's piled in the information when SD was released by DS. I remember specifially Sledge telling people not to worry about weight loss in the first few days due to drop in estrogen and water. This is also why SD is considered a very dry compound.
 
jonny21

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It's piled in the information when SD was released by DS. I remember specifially Sledge telling people not to worry about weight loss in the first few days due to drop in estrogen and water. This is also why SD is considered a very dry compound.
There is a huge difference between non-aromatizing and anti-estrogen.

EDIT: Here us an excerpt from Superdrol for dummies.

Is 6oxo and Rebound XT good enough by itself for a superdrol PCT, most people say it is enough
No! By no means is 6oxo or Rebound standalone strong enough to restart the test production in your body. You need a SERM! Period!

Nolvadex is therefore ABSOLUTELY NECESSARY for an superdrolcycle. Please note its Nolvadex not novedex or nolvedex. Please look for Tamoxifen Citrate.
 
Mass_69

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Mass, while I'm not an expert in this field at all, I thought I'd add my input.

It just seems that people are destroying their estrogen levels. We already know SD works as a mild anti-estrogen. Then, people work into PCT and use Nolva and ATD. ATD is a lot more powerful at removing estrogen then most people know. Expecially after an SD only cycle, your estrogen levels should be low anyway! So libido remains low because your body has no estrogen to function properly.

Then you stop PCT, you have your body flowing with very high test levels. This leads to a very fast rise in estrogen levels, and thus, gyno symptoms. From what I do know, SDs anti-estrogen properties are just causing these cases to be more frequent then with other orals.

Also, we know that ATD is very effective at boosting test levels, so we have a situation where the body has no estrogen at all, and extremely high levels of test... Take it for what it's worth.

Respectfully submitted
doggzj,

While you are correct, I kind of already said that:

My guess would be either having estrogen levels too low, or AR binding by the ATD, or the combination. It's tough to tell, since E2 levels were not tested.

MDHT & SD are both slightly anti-E, so lowering estrogens even further with ATD probably didn't help. I'll save my ATD for non 5a-androstanes and stand-alone use.
 
Mass_69

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Great post, doggzj.

What's with all that "Nolva PCT" talk? Nolva blocks estrogen.
What Jonny & B said.

From now on, I am running a SERM after any androgen. Like I previously stated, I'll save my ATD/AIs for non-5a-reduced/aromatizing compounds & standalone use.
 
Mass_69

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BTW, who has bloodwork that shows that SD acts as an anti-estrogen?
It's piled in the information when SD was released by DS. I remember specifially Sledge telling people not to worry about weight loss in the first few days due to drop in estrogen and water. This is also why SD is considered a very dry compound.
I do recall reading at some point that 5a-reduced compounds are anti-estrogenic (DHT, Winny, Primo, etc.), hence the "hardening" effects of them. Don't know how that applies to anadrol, though...:think: Nevermind...
 
Grunt76

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What Jonny & B said.

From now on, I am running a SERM after any androgen. Like I previously stated, I'll save my ATD/AIs for non-5a-reduced/aromatizing compounds & standalone use.
I think my question is still unanswered: what usefulness is a SERM in a very low estrogen environment? Obviously the "healthy men" research is worthless in such a situation because healthy men have "normal" estrogen levels, not "very low" as when they are at the end of a non-aromatizing, suppressive cycle. I'm not saying Clomid or Nolva aren't useful, or questioning their role in PCT, I'm just trying to ascertain in exactly what capacity they would help, as the estrogen-blocking argument is moot.

Now I understand perfectly well that SERMs are somewhat estrogenic to some tissues and anti-estrogenic to others. In a normal PCT that begins with high estrogen, the role of nolva is very obvious to me: blocking estrogen from registering at the HPTA level stimulates FSH & LH, that's obvious and clear.

What about when there is close to no estrogen? Big Cat has stated that nolva after a winny cycle is useless for this very reason. And while I do not by any means agree with everything he says, he is a knowledgeable person and from my own research I agree with him on this point. A lot of the new designer steroids produce a hormonal profile that is equivalent to the end of a winny-only cycle.

And since Clomid and Nolva have very different profiles in terms of estrogenic effects to specific tissue, then there ensues that one is probably better than the other in a high estrogen situation OR a low estrogen situation. Perhaps one is better in both cases, but science on the topic would be important.

While you may all argue "Nolva is BEST", "SERMs are necessary" and so on, I will not disagree completely, but only try to understand why you would need Nolva after Winny or many of the new designers. If you do not understand Big Cat's (and my) point, then additional research is needed. If you understand it but have additional information that complements what that point asserts, then please share, for therein lies the hole in my knowledge. I like filling these holes! :)

Thanks for your patience!!! :thumbsup:
 

doggzj

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There is a huge difference between non-aromatizing and anti-estrogen.
Here's a bit from the Superdrol writeup. If this means Superdrol itself is anti-estrogen, it doesn't say. I know there is more information similar to this, but there's 100's of threads on SD, and I don't have the time to search them all for you.

EFFECTS

Anabolic effects & dosing requirements
As fascinating as all this chemistry might be, you are probably much more interested in how well Superdrol is going to work. What you are going to gain, and how much it will take you to make these gains? The gains from Superdrol are very dry and lean, so numbers do not tell the whole story, but let us look at them nonetheless. According to the book values, Superdrol should be 20% as androgenic as the reference standard methyl-test, and 400-800% as anabolic, while M1T is 910-1600%, and Anadrol closer to 300%, while being twice as androgenic as Superdrol, mg for mg. So in theory, Superdrol should be half as anabolic as the same dosage of M1T, and 10-20% as androgenic. This would mean that it should take twice the dosage of Superdrol to match the anabolic effects of M1T, at which dosage its androgenic side-effects would be 20-40% of those from M1T. Fortunately in the case of Superdrol it exceeds in practice its theoretical promise. All testers – who were selected in part because of their experience with M1T – found that the muscle gains produced from Superdrol were no less than 2/3 of what a comparable dose of M1T would have given them. Moreover, they found very few side-effects to complain about.
What this means for you is that you will need somewhere between 10 and 40mg of Superdrol per day. Period. There was, certainly, a desire to get this product to market before the ban, but because we were able to keep its chemistry secret, competition did not force it to be rushed, as was the case with M-Dien. Accordingly, proper testing was carried out, allowing us to determine real world dosing recommendations, not ballpark theoretical numbers. The following recommendations are honest and accurate: 10-15mg will be sufficient for beginners under 200lbs; 20-25mg for those advanced lifters under 200lbs, or for those above 200lbs but untrained; 30-35mg for men who have seriously trained themselves but are under 240lbs. For men who think they need to run a dose which falls between the use of whole capsules, one extra 10mg capsule can be taken before workouts, such that the weekly average is appropriate. as a rule of thumb, Superdrol will require 50% more of a dose than M1T to give you comparable gains in muscle. Any women who are entertaining the possibility of using Superdrol should reduce the weight to accord with their sex and their height, and then divide these dosages by a factor of no less than ten. Capsules will then have to be diluted in liquid to be measured accurately. For men, 40mg is a dose only for the very large or the true non-responders, by which I mean people who do not see results on less than 30mg of M1T. Very few people will need 40mg of Superdrol, and no one will need above 50mg. If used in a stack reduce the daily dose by 5-10mg, which would be very prudent given how well Superdrol will stack, and if not its expense, then your very limited supply.
The testers whose dosing fit the above guidelines gained, on average, five pounds of muscle in under three weeks, while losing water and gaining no fat on hyper caloric bulking diets. The quality of the gains from Superdrol comes from its likeness to Masteron while the quantity comes from its similarity to Anadrol. Masteron, expensive and very rare, is almost a perfect cutting steroid, being highly androgenic and anti-estrogenic. If you must have a rough comparison to something already out there, one tester described the quality of gains as being akin to those from fina or a test/halo combo, but such comparisons are bound to be inexact. Gains are very dry, and it makes muscles noticeably more hard and dense. The explosive gains from Anadrol are accompanied by a great deal of water retention and fat. M1T, as you surely well know, produces explosive gains not unlike those of Anadrol, but this comes at a cost. More on this later. As to how difficult it is to retain the gains from Superdrol, you are invited to follow the testers’ post-cycle results. To date, the results are promising, with no loss of mass or vascularity. The gains from Superdrol will be impressive, and they will not take long to start, but they will be more gradual to be recognized than those which come from aromatizing steroids. Your numbers in the gym and on the tape measure will go up, not explosively, but they will go up surely and steadily. The diuretic effect of Superdrol will at first mask the gains as you lose water and gain muscle. When mass begins to increase, it should do so disproportionately compared to tape-measurements. So if you are only checking the scale, or if you are not lean enough to notice the loss of water, persist and be rewarded.
 

doggzj

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I think my question is still unanswered: what usefulness is a SERM in a very low estrogen environment? Obviously the "healthy men" research is worthless in such a situation because healthy men have "normal" estrogen levels, not "very low" as when they are at the end of a non-aromatizing, suppressive cycle. I'm not saying Clomid or Nolva aren't useful, or questioning their role in PCT, I'm just trying to ascertain in exactly what capacity they would help, as the estrogen-blocking argument is moot.
Good point. We know that lowering estrogen from normal levels makes the body produce more test to compensate. It's possible that this is not the case in men with low estrogen levels, as the study posted doesn't apply to these men (aka men after superdrol usage).
 
jonny21

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Here's a bit from the Superdrol writeup. If this means Superdrol itself is anti-estrogen, it doesn't say. I know there is more information similar to this, but there's 100's of threads on SD, and I don't have the time to search them all for you.
Thanks, but you do not have to do any searching for SD threads for me. I think I have a fairly decent grasp of the process. I was attempting to convey some of this knowledge but obviously you seem to know it all already.

EDIT:

BTW, It would be prudent to remember that you are dealing with Superdrol not Masteron.
 
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Mass_69

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I think my question is still unanswered: what usefulness is a SERM in a very low estrogen environment? Obviously the "healthy men" research is worthless in such a situation because healthy men have "normal" estrogen levels, not "very low" as when they are at the end of a non-aromatizing, suppressive cycle. I'm not saying Clomid or Nolva aren't useful, or questioning their role in PCT, I'm just trying to ascertain in exactly what capacity they would help, as the estrogen-blocking argument is moot.
If you are coming off using SD, you may have lowered E levels, but not necessarily very low E (don't have blood work, only going by the write-ups/literature on SD). Adding ATD or another AI to the mix is what will cause the very low E levels.

As far as the SERM, I don't know the exact means or the specific actions on certain tissues, but I know it works (according to PubMed;)) to raise LH & FSH when the T levels are supressed. You make valid points, and I don't know that I can answer them correctly.

I do have this study here involving a low dose clomid (for 8 weeks), in which T, bioavailable T, and estradiol levels all increased. Unfortunately, I don't know what the baseline for E2 was, but it's not implied that it was low (assuming normal). That said, it appears that clomid could stimulate HPTA regardless of the E2 levels (as it increased but did not trigger a negative feedback).

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1917692&query_hl=10&itool=pubmed_docsum

In a normal PCT that begins with high estrogen, the role of nolva is very obvious to me: blocking estrogen from registering at the HPTA level stimulates FSH & LH, that's obvious and clear.
Nolva is usually the choice (or at least part of the equation) when E levels are high, because it has a high binding affinity to the E receptors in breast tissue, preventing gyno.

What about when there is close to no estrogen? Big Cat has stated that nolva after a winny cycle is useless for this very reason. And while I do not by any means agree with everything he says, he is a knowledgeable person and from my own research I agree with him on this point. A lot of the new designer steroids produce a hormonal profile that is equivalent to the end of a winny-only cycle.

And since Clomid and Nolva have very different profiles in terms of estrogenic effects to specific tissue, then there ensues that one is probably better than the other in a high estrogen situation OR a low estrogen situation. Perhaps one is better in both cases, but science on the topic would be important.

While you may all argue "Nolva is BEST", "SERMs are necessary" and so on, I will not disagree completely, but only try to understand why you would need Nolva after Winny or many of the new designers. If you do not understand Big Cat's (and my) point, then additional research is needed. If you understand it but have additional information that complements what that point asserts, then please share, for therein lies the hole in my knowledge. I like filling these holes! :)

Thanks for your patience!!! :thumbsup:
"And while I do not by any means agree with everything he says (Big Cat)" - I find myself in this same boat. I too am trying to fill in the holes. I've had the theory myself about why a PCT ancillary (for HPTA) is even necessary after using an androgen that can possibly lower both T & E2?? You would think that with both lowered, when the androgen left the body/ceased use, your HPTA would be humming on its own! But I chickened out and played it safe :D

Some more good info on Clomid & Nolva: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10796497&query_hl=7&itool=pubmed_docsum
 

doggzj

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Jonny> I'm just trying to help out here, and it seems like you aren't reading what we're posting.

I realize it is not Masteron, but in the context of the writeup that seems to be what it's saying. Also, I'm telling you directly, I have read some other posts back in 2004 that dealt with it's anti-estrogenic properties.

On top of that, I had a PM discussion with Dr.D about this topic way back before Bobo closed PMs down. I no longer have those to referance for this thread, but the jist of the discussion was dealing with running an AI with superdrol and that causing estrogen to be driven too low (because of SD already lowering estrogen).
 
jonny21

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Jonny> I'm just trying to help out here, and it seems like you aren't reading what we're posting.
As am I. I can follow along a thread. If you would look back to see why I originally posted recently you would see the fallacy of the statement made to which I was responding.

It's great that you are discussing the possibilites. But please do not confirm them as facts because you have found someone to agree with you. That is not the way. There are other considerations/possibilites also but without studies on multiple individiuals with bloodwork it is all conjecture.
 
Grunt76

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I want one.


I think jonny21 has been polite and doggjz a little hard about the searching for threads comment. Besides that, I don't think I'm actually agreeing to anything other than the questionability of universal nolva in PCT, especially in regards to the great difference in hormonal profile between someone who just ran a test cycle and these new estrogen-lowering substances.

A lot of PCT-thinking comes from the times when test/tren/winny or so was the bread and butter of hormonal supplementation. The new products leave you with a hormonal profile that is VASTLY DIFFERENT from what most "dark side" cycles do to you.

Doggjz sees this point, whereas you jonny21 seem to not see it, since none of your comments seem to reflect that. IMO.
 
jonny21

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I will direct you to my initial post in this thread: http://anabolicminds.com/forum/481704-post93.html

I was only commenting on the ability of Nolva to stimulate Testosterone. As for anything else there is not sufficient bloodwork or evidence to prove anything, assumptions/theories/ideas are not facts.

From the bloodwork shown earlier in this thread I could also assume a couple of things:
1-SD doesn't shut down HPTA hence the excellent Test Levels and decrease libido some experience while on cycle is due to low Estrogen
2-ATD is extremely efficient at stimulating testosterone

Whether these are facts would need to be determined by trials and bloodwork.
 

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Just thought I would throw this in.

My only experience with PH/PS or anything else was a short 15 day 1-T/4AD transdermal which I did pre-ban. It was only 15 days because of a rash even though I was rotating sites.

My PCT was 6OXO which I ended up taking for 4.5 weeks because it seemed to be helping me gain??

The following six months went fine when all of the sudden out of nowhere I developed a very small and painfull lump in/under my right nipple. At the time I wasn't sure what it was since it was so small and it had been so long since I had used the 1-T/4AD (this was my first and only try at PH/PS).

I decided to do nothing and within a couple of days the pain went away and within a few weeks there was no sign that it had ever happened.

I am almost convinced that my experience was a "delayed gyno".

1-T/4AD or anything like this might cause these symptoms.

:wtf:
 

Curious123

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i got puffy nips off of both m1t and superdrol...its odd i must say
Just wondering if anyone here worries about the possible effect this could have on your ability to father children?
 

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