2-on/4-off cycles...BR, Dr Scally

[Reymak]

What about Nolva, I hate Clomid, would Nolva alone (e.g., 20mg ED) suffice for PCT for a 2-on/4-off and an occasional 2-on/2-off?

With 30-50mg Dbol& 100mg Tren at 2 wks., how long should PCT run, one week or two?

 

[Bill Roberts]

Nolvadex doesn't have a proven track record -- largely out of just not having much of a track record -- in 2-week cycles that I have written for others or have done myself. I just don't have the basis to say that it works as well.

For that matter, while I've seen Nolvadex alone much more frequently on longer cycles, I'm not at all convinced that Nolvadex alone is as good as Clomid. I rather suspect that it is not, but I don't have a conclusive basis to say that that is necessarily a fact.

If you hate Clomid, would you be willing to try 50/50 Clomid/Nolvadex? That might suit you better. You would just use half as much of each as would ordinarily be the case.

The main pharmacological difference between Clomid and Nolvadex is that Clomid is estrogenic in the pituitary and perhaps other brain tissues where Nolvadex is antiestrogenic.

Having only antiestrogenic activity perhaps may not give optimum effect, as estrogen can actually result in better responsiveness to LHRH, but having only the estrogenic activity of full dose Clomid can indeed be unsuitable for some. Cutting that in half, and then adding half-antiestrogenic activity, may markedly reduce or eliminate your problems.

 

[Reymak]

Thanks for the response, really, it's very much appreciated.

I've got one more question (probably only one

I perceive the above regiment as fairly light, i.e., 30-50mg Dbol + 50-100mg Tren A ED; would the following work, and does it really need to be run for two weeks considering the light AAS use?

Front-load: Clomid: 100mg + Nolvadex 40mg
6 Days: Clomid: 50mg + Nolvadex 10mg
7 days: Clomid: 25mg + Nolvadex 5mg

Thanks again,
Rey

 

[Bill Roberts]

Thanks for the response, really, it's very much appreciated.

I've got one more question (probably only one

I perceive the above regiment as fairly light, i.e., 30-50mg Dbol + 50-100mg Tren A ED; would the following work, and does it really need to be run for two weeks considering the light AAS use?

Front-load: Clomid: 100mg + Nolvadex 40mg
6 Days: Clomid: 50mg + Nolvadex 10mg
7 days: Clomid: 25mg + Nolvadex 5mg

Thanks again,
Rey

]

If the perspective is one of whether omitting the PCT could be gotten away with or not, it could be gotten away with.

I did some personal experimentation with no-PCT 2 week cycles on account of developing prohormone products which were suppressive, and wanting to have reasonable confidence that over-the-counter customers weren't going to have recovery issues, keeping in mind that they could hardly be advised that they should purchase Clomid.

My finding was that allowing 4 weeks between cycles with no PCT was nonproblematic, but training in the week or two was not as good as when PCT was used.

Earlier than that I had also experimented with supplement-only PCT, as I was doing informal testing of whether Vitex extract would be a useful addition to tribulus extract, and found that 2 on / 2 off without pharmaceutical PCT led to quite slow testicular atrophy over time, less when Vitex was included and more when it was only tribulus. For me the tribulus alone gave the same result as using nothing.

Short answer: pharmaceutical PCT is better but with the 2 week cycles one can get away without it.

As to whether your cycle is light, if you tested your LH level around day 10 or perhaps sooner than that you would find it to be zero. The cycle is fully suppressive. However, the suppressive effect disappears quite promptly on the anabolic steroids clearing the system.

 

[Conciliator]

Having only antiestrogenic activity perhaps may not give optimum effect, as estrogen can actually result in better responsiveness to LHRH,

According to what?

You're talking about estrogen priming here: the concept that estrogen makes the pituitary more sensitive to LHRH (also called GnRH) from the hypothalamus, so that more LH is released for a given GnRH stimulus. This is well known to occur in females leading up to ovulation. Unlike females, however, men don't have a preovulatory period or spikes in LH. The research is fairly clear that estrogen priming does not occur in males. First, look an authoritative reference work like Grossman's [ame="http://www.amazon.com/Clinical-Endocrinology-Ashley-Grossman/dp/0865426295"]Clinical Endocrinology[/ame], which states (pg. 99):

Progesterone, acting synergistically with oestrogens, exerts negative feedback on the hypothalamus during the luteal phase, thus limiting GnRH pulsatility and slowing LH pulse frequency. The mechanism of positive oestrogen feedback at the time of the LH surge has been much debated. There is now evidence that enhancement of both hypothalamic GnRH pulse generator activity and pituitary responsiveness to GnRH are involved. All species so far studied have shown an increased 'self-priming' effect of GnRH on the pituitary during the preovulatory period...

In males, the situation is more straightforward. Since LH surges do not occur, only negative feedback effects are relevant. Testosterone (and its active metabolite dihydrotestosterone, DHT) exerts major suppressive effects on both LH and FSH secretion, largely by inhibiting the GnRH pulse frequency generator, but possibly also by direct pituitary actions. Oestrogens in the male reduce pituitary responsiveness to GnRH.

That states pretty clearly that in males, estrogen produces negative feedback, not priming. The last sentence in bold directly contradicts the notion. If clomid were to produce estrogenic action in the pituitary, it would serve to inhibit LH secretion.

Grossman's statement is corroborated by the most recent research on the specific effects of androgens and estrogen on the pituitary and hypothalamus of healthy men. Here, it was shown that estrogenic action at the pituitary has an inhibitory effect on LH output. In other words, estrogen decreases pituitary sensitivity to GnRH. Estrogen does not produce positive feedback as seen in estrogen priming in females. The paper stated in its conclusion that "These data confirm previous work from our group which ... showed [estrogen] has both hypothalamic and pituitary sites of negative feedback in the male." In fact, "negative feedback at the pituitary requires aromatization," as testosterone itself doesn't produce negative feedback at the pituitary.

Finally, there's this study, which couldn't have been any more relevant. There, the effect of nolva and clomid on the pituitary of human males was directly examined. They infused the men with 100 mcg of GnRH and then measured LH output from the pituitary. The men taking nolvadex at 20mg/day had a significantly increased LH response to GnRH. In contrast, the men taking clomid had reduced LH output, a decreased sensitivity to GnRH. The researchers stated that "a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation."

All in all, I don't see what basis Bill has for the claim that estrogenic activity from clomid "can actually result in better responsiveness to LHRH." This assumes estrogen priming in males, yet both direct research and experts in endocrinology seem to squarely contradict the notion. Clomid appears to produce an estrogenic effect at the pituitary, yes, but the evidence shows that in males this serves to inhibit LH output, in contrast to nolva. All else being equal, that would make the use of clomid inferior to nolva for purposes of PCT.

 

[OhNoYo]

According to what?

You're talking about estrogen priming here: the concept that estrogen makes the pituitary more sensitive to LHRH (also called GnRH) from the hypothalamus, so that more LH is released for a given GnRH stimulus. This is well known to occur in females leading up to ovulation. Unlike females, however, men don't have a preovulatory period or spikes in LH. The research is fairly clear that estrogen priming does not occur in males. First, look an authoritative reference work like Grossman's Clinical Endocrinology, which states (pg. 99):


That states pretty clearly that in males, estrogen produces negative feedback, not priming. The last sentence in bold directly contradicts the notion. If clomid were to produce estrogenic action in the pituitary, it would serve to inhibit LH secretion.

Grossman's statement is corroborated by the most recent research on the specific effects of androgens and estrogen on the pituitary and hypothalamus of healthy men. Here, it was shown that estrogenic action at the pituitary has an inhibitory effect on LH output. In other words, estrogen decreases pituitary sensitivity to GnRH. Estrogen does not produce positive feedback as seen in estrogen priming in females. The paper stated in its conclusion that "These data confirm previous work from our group which ... showed [estrogen] has both hypothalamic and pituitary sites of negative feedback in the male." In fact, "negative feedback at the pituitary requires aromatization," as testosterone itself doesn't produce negative feedback at the pituitary.

Finally, there's this study, which couldn't have been any more relevant. There, the effect of nolva and clomid on the pituitary of human males was directly examined. They infused the men with 100 mcg of GnRH and then measured LH output from the pituitary. The men taking nolvadex at 20mg/day had a significantly increased LH response to GnRH. In contrast, the men taking clomid had reduced LH output, a decreased sensitivity to GnRH. The researchers stated that "a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation."

All in all, I don't see what basis Bill has for the claim that estrogenic activity from clomid "can actually result in better responsiveness to LHRH." This assumes estrogen priming in males, yet both direct research and experts in endocrinology seem to squarely contradict the notion. Clomid appears to produce an estrogenic effect at the pituitary, yes, but the evidence shows that in males this serves to inhibit LH output, in contrast to nolva. All else being equal, that would make the use of clomid inferior to nolva for purposes of PCT.

Con > BR or Con < BR opcorn: opcorn: opcorn: opcorn: opcorn:

 

[Bill Roberts]

When I say "does result" or "must result" or "always results in" the meaning is different than when I say "can" result.

I did not say that estrogenic activity of Clomid must result in increased sensitivity of the pituitary to LHRH.

"Can result," as I use the term, means either that it is known that this outcome sometimes occurs or that there is a mechanism by which it plausibly can occur and there is no known reason why it can't occur.

I don't think that the studies you cite, or any studies, demonstrate that Clomid cannot give a better result, due to this pharmacological difference, than Nolvadex for male bb'ers. I actually rather suspect you'd agree they don't prove any such thing.

 

[Conciliator]

When I say "does result" or "must result" or "always results in" the meaning is different than when I say "can" result.

If what we know is that estrogen priming "does not" occur in males, then why would you suggest that it "can" occur in males? It couldn't be more misleading to say that "estrogen can actually result in better responsiveness to LHRH" when we're not talking about females and when the evidence in males shows the opposite effect occurs.

I don't think that the studies you cite, or any studies, demonstrate that Clomid cannot give a better result, due to this pharmacological difference, than Nolvadex for male bb'ers. I actually rather suspect you'd agree they don't prove any such thing.

The question of whether nolva or clomid is better for overall recovery is distinct from the question of which is better at the level of the pituitary. I've addressed nothing but your statement on the latter.

The fact is, it's unknown which is superior for overall recovery. Nolva and clomid have not been studied head to head with testosterone as the endpoint. The best we can do is make inferences and educated guesses. I think it's significant that clomid and nolva have been shown to have opposite effects at the level of the pituitary, with a beneficial effect from nolva, and a detrimental effect from clomid. But overall, we just don't know. It hasn't been studied.

But that doesn't provide any license to imply things at the level of the pituitary that research has shown "does not" occur in men (estrogen priming) and, further, that research squarely contradicts (clomid "results in better responsiveness to LHRH").

What "can" occur in females is pretty irrelevant.

 

[Bill Roberts]

I really don't know why you would ask the first question. Do you really think you have evidence, let alone conclusive reason, to say that the biochemistry/pharmacology cannot exist in males when it is known that the human pituitary is capable of this? What biochemical pathway -- be specific -- is do you think not present or is rendered inoperable, and how has it been shown that the pathway is not present or is rendered inoperable in all circumstances in males?

If you really think you have such evidence, please elucidate and try some actual evidence this time instead of citations such as the above that don't in fact even touch on the question. They don't even remotely touch on it. Were you really unaware of that?

Your question also asserts that you KNOW that the phenomenon does not occur. Really, you know that it does not occur in the context of steroid cycles? How do you know this?

Your first citation most certainly doesn't even begin to show it. Do you really think it does? If not then why are you presenting it as doing so?

And then as to your second study, which you claim could hardly be more relevant, it doesn't even try to look at recovery from suppression caused by steroid use. It's completely not examining that at all.

You're not aware that the normal condition does not necessarily have to give the same results as the suppressed condition? This hasn't occurred to you?

I know you are a smart guy but sometimes you engage in inane argumentation such as the above arguing over words which in some cases really makes me doubt your actual level of comprehension.

If you weren't just out to argue and/or if you had better comprehension -- and if for whatever reason you don't think it's the case that Clomid has a better track record for post-cycle recovery and attribute my observations to fluke chance, which I will agree cannot be ruled out because it would take a pretty vast number of cases and accurate statistical work to demonstrate a vanishing probability -- you might have replied "Well I have not seen proof that this occurs in man or in men recovering from steroid cycles" and I would have replied "I haven't seen a study showing that either: rather I was saying there is a mechanism in human biochemistry which can cause this and we have no evidence that this has been abolished in males in all circumstances. If it surfaces or sometimes surfaces when recovering from the suppressed condition then this would be the only explanation we have as to why Clomid has a better track record, if we grant that."

That would have been productive, and valid. But your above stuff is not.

 

[Conciliator]

I love how Bill makes claims without any support or references. And then when multiple references are given that all stand in opposition to his claims, instead of admitting that his implications are very likely NOT the case, he dismisses the studies with a facile flick of the wrist because they're "only in males" and not in "steroid recovering males". Of course, he offers zero references and zero evidence that his position has more merit (or even any merit) over that demonstrated by the most relevant and applicable research.

Which is more likely Bill?

1) that a feature of female physiology happens to appear in males who are recovering from a steroid cycle, despite zero evidence for such a phenomenon...

or 2) that what we know about male physiology continues to hold true when males take steroids, consistent with all the evidence for that physiology?

I don't see how you don't think it's incredibly misleading to suggest the former (i.e. a superior effect of clomid at the pituitary) in light of the best evidence we have, all of which contradicts it.

 

[Bill Roberts]

Reread the previous. If you continue in your lack of comprehension then there is nothing I can do for you.

I can also do nothing for your inability to comprehend that the research you cite is NOT relevant to the question at hand. It doesn't even make the first beginning at addressing the issue in question.

If you genuinely can't grasp that studies on non-suppressed individuals don't necessarily match up with results with suppressed individuals then nothing can be done to help you.

The alternative is that you do understand it but you are simply addicted to your behavior.

You are not interested in the fact that some who have very many cases to base a judgment on, not just myself but also for example Dr Scally, have seen differences in outcome with suppressed individuals between Nolvadex, Clomid, or combination of the two. You have no alternate explanation for how this can be, and wrongly claim you know that a mechanism that is known to exist in the human species just couldn't possibly be working here, based on studies that don't even look at that in the slightest and so frankly I don't know how even an idiot could arrive at the conclusion that the studies showed that.

If the actuality is that you are a sincere human being actually trying to understand something, you should re-read my next-to-last paragraph of the last post in particular.

But if it's as I am getting the impression is the case, you really have no interest in anything but your pretense and your posing, then why waste your time re-reading anything.

While posting references that in no way prove one's point, as you have done above, and then beating one's chest about having posted them may impress those who don't know better, it just exposes one as either a fraud, poseur, or non-comprehending person to those that do. You're exposed.

 

[Conciliator]

OK. So let me get this straight. The effects of clomid and nolva on the pituitary of normal males "doesn't even make the first beginning at addressing the issue" of the effects in recovering males? Not even the first beginning. Yet female physiology does? Please explain, how does normal female physiology begin to address the question any better than normal male physiology? Alternatively, if you want to argue that both are completely and utterly irrelevant, then why would you imply either or, in this case, estrogen priming (i.e. the female physiology)?

I think it's ridiculous to say that both are completely and utterly irrelevant. I also think it's ridiculous to take the position that normal male physiology is less relevant to the question than normal female physiology. Accordingly, why would you imply the female physiology and estrogen priming?

 

[Conciliator]

As for Dr Scally, I'm extremely interested in his experience and results. He stated in this article on PCT (in men) that "Clomid acts as an estrogen, rather than an antiestrogen, by sensitizing pituitary cells to the action of GnRH." When I challenged this assertion with the same references and research I've posted in this thread, he explicitly told me "I do not argue for the use of clomiphene due to an E2 priming effect." I asked him to clarify the inconsistency in these statements and he never responded, so I'm not sure what he believes about this.

I also asked Dr Scally specific questions about his clinical experience. I asked him if he actually colleced data on three different groups (clomid, nolva, and clomid+nolva). I asked him if he had baseline test levels and final LH/test levels after a given treatment period or if his observations concerning nolva and clomid were more casual than that. I told him I was quite curious as to how systematically the three different protocols were tested and compared to each other. Although we had been having a conversation prior to this, he didn't respond to any of these questions

Which is all to say, you are mistaken to think I am not interested in his experience. I am "a sincere human being actually trying to understand something." I've gotten no answers from Dr Scally. I truly value his clinical experience, but I suspect that his opinions on nolva vs. clomid are based on hunches and casual observation, not data collection and statistical analysis. The most formal work he has done, as far as I know, is http://www.medibolics.com/ScallyVergelAstractHPGA.pdf, in which hCG+nolva+clomid was used in a PCT setting and shown to be effective for recovery. But it was an uncontrolled study. No superiority claims can be drawn from it, since there were no comparisons.

 

[Conciliator]

OK. So let me get this straight. The effects of clomid and nolva on the pituitary of normal males "doesn't even make the first beginning at addressing the issue" of the effects in recovering males? Not even the first beginning. Yet female physiology does? Please explain, how does normal female physiology begin to address the question any better than normal male physiology? Alternatively, if you want to argue that both are completely and utterly irrelevant, then why would you imply either, or in this case, estrogen priming (i.e. the female physiology)?

I think it's ridiculous to say that both are completely and utterly irrelevant. I also think it's ridiculous to take the position that normal male physiology is less relevant to the question than normal female physiology. Accordingly, why would you imply the female physiology and estrogen priming?

No response Bill?

 

[Bill Roberts]

I explained these matters clearly to you already. If you didn't get them then you won't get them by my repeating myself yet again.

If you choose to believe that the studies you cite on men who were not recovering from steroid cycles prove your points with regard to steroid cycle recovery and disprove what I am saying, then that is your prerogative.

And at least you've made yourself clear that you actually do believe that rather than it simply being that you are being argumentative. So maybe this will help me better interpret your future posts, which is always a good thing.

 

[Conciliator]

You continue to ignore the questions I've asked over the last few posts. Why don't you try answering a couple of them?

You've pointed out that the studies I referenced are not in the exact population we're talking about. I recognize that. The studies I posted are in males, but not steroid-recovering males. But then you appeal to female physiology, which is undoubtedly an even less relevant population. Accordingly, why would you imply female physiology and estrogen priming when the more relevant research suggests the exact opposite? Are you seriously going to argue that the research in males is less relevant?

 

[Bill Roberts]

Repeatedly you ask the same questions; I've answered them at least twice; and repeatedly you claim I have ignored them. This is simply false.

I may have given you credit for sincerely believing your above posts rather than simply being argumentative, but this above nonsense of repeatedly claiming the above has to fall into the category of being a person who will say anything to be argumentative.

It's too repetitive and utterly pointless. If you genuinely believe that the studies you cite on men not recovering from steroid cycles prove that a human mechanism, a control pathway in the pituitary that is known to exist cannot be operative in men recovering from steroid cycles then that is your business.

If you are ever able to and want to provide evidence actually showing that it is not via estrogenic effect in the pituitary that there is an observed difference in effect between clomiphene and tamoxifen in recovery from steroid cycles,, though that is the only known HPTA-relevant difference in mechanism of action between clomiphene and tamoxifen, you're more than welcome to do so. There will be a high degree of interest from many, including myself, if you ever do so and I definitely invite actual work from you in that area, rather than citation of studies that don't even glance at one single individual recovering from a steroid cycle.

Until you do that, I've answered you fully and as much as I think is suitable. Enjoy your day and have a good week.

 

[NotHuman]

Bill, instead of the "off" weeks, would it be ok to cruise on test at a low dose instead of adding pct items on the off weeks? I know recovering hpta won't happen, but my goal is to make optimal muscle gains. Would a 6 week on/3 week cruise dose work similarly to the guidelines you presented? Short esters like prop would be used like you said

 

[Bill Roberts]

If the goal is optimum muscle gains and HPTA suppression is simply not an issue, then there is no particular advantage to selecting an exact 2 week value for cycle length.

Alternating short cycles can still be very efficient but I would arrange them according to the training plan rather than aim for what would, if HPTA recovery isn't an issue, be only an arbitrary calendar value.

 

[GeorgeWBush]

Nandrolone phenypropionate is unproven in this application and I think would be a poor choice as recovery problems are common with nandrolone.
.

Yes, I'm very well aware of how severely nandrolone shuts down the htpa, however as someone with interest in nadrolone, despite its problems with recovery, I'm wondering if you have any advice with regard to a pct protocol for nandrolone, especially a longer cycle with it attached to decanoate ester. I was thinking about a normal 4 week pct cycle of clomid alongside exemstane and 15k iu of hcg prior to pct, also a very small dosage of ostarine (~10mg/day) to help with strength loss and muscle retention. I know excessive levels of clomid can be suppressive, and I've read studies regarding the carcinogenic potential of serms so I don't particularly want to over-do it but at the same time nandrolone is extremely suppressive and wish to have a full recovery so any advice or input would be greatly appreciated!