Ask Michael Scally: Why Use Both Clomid and Nolvadex Together for PCT?

[Jeton]

oh, n b4 i ferget:

opcorn:

 

[LostTime]

You have quite the way with words, my friend.

 

[IronCore]

which side of ur "bright line" would u put me on? is it the same side that these researchers(Dorner, Docke et al.) would put me on?

The side with the rest of the ones wearing the Dirty Sanches...

I think your just an anomaly... Queer isn't it?
opcorn:

 

[Jeton]

The side with the rest of the ones wearing the Dirty Sanches...

I think your just an anomaly... Queer isn't it?
opcorn:

hush yo mouth, jeeziz freek...if u only knew how many of "yor kaahnd" ask for my cock-wrath..

there is in fact a spectrum of sexual orientations in men, and sexual-behavior/orientation research is still riven with incompetent n primitive control- n selection criteria.

 

[BBC3]

Mmmmhh. I am going to have to chime in.

We have had a similar argument on many days an in many ways. I would like to point one thing out. I all my research, I have seen where it is stated that Clomid has a direct action on the hypothalmus, and it seems like the restart action associated with Nolva is more perhipheral, site, and CNS related. At least that is the way it is generally discussed from a laymans' perspective. The one sure thing is that I have never seen it stated that Nolva's action is the result of the drugs direct activity to the hypthalmus, so a reading layman would have to assume its restart action comes as a result of a receptor site CNS type feedback to the brain, moreso than Clomid. Perhaps that is the difference, which is significant if so. This would also explain the reported effective synergy of the two drugs combined. However, I have also read it is only a slightly increase effect that results from simultaneous use. Come and get it!!!!!

This is one of the explanations that Dr. Scally has given:

I strongly disagree with Dr. Scally's reasoning behind the use of clomid. What he is describing here is "estrogen priming," the concept that estrogen makes the pituitary more sensitive to GnRH from the hyp[othalamus, 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. For starters, take a look at an authoritative reference work like Grossman's Clinical Endocrinology, which states (pg. 99):That states pretty clearly that there is no priming in males, only negative feedback. The last emboldened sentence in this quote directly contradicts Dr Scally's quote at the top. If clomid were to produce estrogenic action in the pituitary, it would only 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.

This older paper had a very interesting finding:In other words, estrogen levels during brain development are responsible for the sex-specific differences in gonadotrophin secretion and estrogen feedback at the pituitary. The important point of this research is that males (with the exception of homosexuals) were not found to have any positive feedback from estrogen. Those results that were "strongly confirmed."

Finally, there's this research, which couldn't have been any more relevant. It directly examined the effects of nolva and clomid on the pituitary of human males. 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 understand Dr. Scally's position for using clomid during PCT. It assumes estrogen priming in males, yet both 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.

I'd really like to hear Dr. Scally's response to this.

-Conciliator

 

[Conciliator]

I all my research...

You don't do research, remember? You come up with random, unsupported ideas that usually fly in the face of research. And then when I post references and studies that squarely contradict you, you attack me personally for "cutting and pasting" and for not thinking for myself, as though blind guesses give us insight into the true nature of reality. I can't remember you referencing a study for anything, ever. It's just your baseless claims and wild hunches in rapid succession.

I have seen where it is stated that Clomid has a direct action on the hypothalmus, and it seems like the restart action associated with Nolva is more perhipheral, site, and CNS related. At least that is the way it is generally discussed from a laymans' perspective.

No, that's not how nolva is generally discussed. You're projecting your eccentric ideas onto the bodybuilding community. When discussed in the context of PCT, nolva and clomid are both generally said to act by competitively blocking estrogen from receptors in the hypothalamus and pituitary.

The one sure thing is that I have never seen it stated that Nolva's action is the result of the drugs direct activity to the hypthalmus, so a reading layman would have to assume its restart action comes as a result of a receptor site CNS type feedback to the brain, moreso than Clomid.

First, what do you mean when you say "receptor site CNS type feedback to the brain"? You frequently invent technical sounding phrases that are vague or meaningless. Are you talking about estrogen receptors in the spinal cord (one part of the CNS) giving negative feedback to the hypothalamus in the brain (the other part of the CNS)? Your vague phrases aren't impressing or enlightening anyone. I don't think you even know what exactly you mean when you say things like this.

Second, do you not realize how illogical your line of reasoning is? You're making a fallacious [ame="http://en.wikipedia.org/wiki/Argument_from_ignorance"]Argument from ignorance - Wikipedia, the free encyclopedia@@AMEPARAM@@/wiki/File:Question_book-new.svg" class="image"><img alt="Question book-new.svg" src="http://upload.wikimedia.org/wikipedia/en/thumb/9/99/Question_book-new.svg/50px-Question_book-new.svg.png"@@AMEPARAM@@en/thumb/9/99/Question_book-new.svg/50px-Question_book-new.svg.png[/ame], claiming that since you've never seen any evidence for direct action, that you "would have to assume" an alternative view that's also unsupported. I'm sorry, but if you haven't seen evidence that something is true, it does not constitute evidence that it's false. A lack of evidence is neither evidence for or against. You then commit a [ame="http://en.wikipedia.org/wiki/Non_sequitur"]Non sequitur - Wikipedia, the free encyclopedia@@AMEPARAM@@/wiki/Fileisambig_gray.svg" class="image"><img alt="Disambiguation icon" src="http://upload.wikimedia.org/wikipedia/commons/thumb/5/5f/Disambig_gray.svg/30px-Disambig_gray.svg.png"@@AMEPARAM@@commons/thumb/5/5f/Disambig_gray.svg/30px-Disambig_gray.svg.png[/ame] to favor a particular alternative theory that has no supporting evidence either.

Third, you're incorrect in the first place to think that there's no evidence for direct action on estrogen receptors in the hypothalamus. For example, this study from 2008 explains that "Tamoxifen citrate inhibits hypothalamic estrogen receptors [4]; thus, gonadotropin-releasing hormone (GnRH) secretion is stimulated." And this older study from 1988 found that tamoxifen, like estradiol, binds to estrogen receptors in hypothalamic cell nuclei. The fact you haven't seen something hardly means anything in light of your thoroughgoing ignorance of basic topics.

 

[BBC3]

First of all I would like to give you a lovely TOUCH'e. Your first paragraph is the only one that contain any truth at all. I do love to attack you!!!!!

Secondly, What I find most amazing is that I have now fiured out that you dont even read or know what it is you are pasting!! You recently pasted an article on Deca in that last argument with Bill Roberts, and when I quoted the article, you did not even recognize it and further disputed the information from your own pasted article!!

I never said I dont research. I just never used to copy all the articles and studies for further reference. SO what I am referrning to is that if you go through all your studies, you will not find a single one that specifically states Nolve acts DIRECTLY on the brain. Clomid is the only SERM I have ever seen described that way, and not on every occasion. I looked below and I am guessing they are newer publications. HIstorically Nolva has not been stated working as such.

To enlighten you on my reference to CNS. I am describing a process I would not expect you to identify with as clearly, it is not understood by the medical community ( or anyone conclusively), so there are no studies out there for you to hang you hat on. I was referring to the possibility that ALL PARTS of the body may be linked to the brain via the CNS. This would mean that, by means of a nerve receptor working in conjection with a hormonal receptor, the body would be able to tell the brain that the receptor was not "on or off" by means of a direct site measurement and signalling back to the brain via CNS routes. Hence a gazillion tiny little hormonal thermostats.

AND BY THE BY, IT WAS I WHO FIRST ARGUED WITH YOU THAT THE SERM ACTION WAS DIRECT TO THE HYPOTHALMUS, AND YOU WHO AGRUED THAT IT WAS NOT. I would be happy to find the thread if you like. I think I was the one who forced you clear on this matter. Do you deny this??

I am growing most certain that you may indeed be schizophrenic!?!?!!!?! Arguing with you is worse than arguing with a wall. Its like arguing with an ever changing maze of walls that moves to suit its self. A maze that there is no way to the end.

I would like to disclaim. I do not intend to be insulting. I just cant figure out the communication problem. You talk about me not hearing, but I think its you I swear.... Regarding my posting style. It is caviated as anecdotal, which is fine, as it is ALWAYS designed to provoke thought. If you look at my writings objectively and as a point of question seaching for further clarity for all. So I appreciate your feedback.

So do you really believe that the brain does not get direct CNS feedback from every single area of the body?? The simple fact the feelings, like pain and pleasure, report directly to the brain, is proof enough.

There are clearly (3) routes of stimulating the Brain for hormonal restart.
(a) Direct action on brain receptors,
(b) Direct action on local & perhipheral receptors.
(c) And finally, a simple reaction to a drug by unknown, or inherent, design/intent. A potential "side effect" so to speak.

Now go swat some more....

You don't do research, remember? You come up with random, unsupported ideas that usually fly in the face of research. And then when I post references and studies that squarely contradict you, you attack me personally for "cutting and pasting" and for not thinking for myself, as though blind guesses give us insight into the true nature of reality. I can't remember you referencing a study for anything, ever. It's just your baseless claims and wild hunches in rapid succession.
No, that's not how nolva is generally discussed. You're projecting your eccentric ideas onto the bodybuilding community. When discussed in the context of PCT, nolva and clomid are both generally said to act by competitively blocking estrogen from receptors in the hypothalamus and pituitary.
First, what do you mean when you say "receptor site CNS type feedback to the brain"? You frequently invent technical sounding phrases that are vague or meaningless. Are you talking about estrogen receptors in the spinal cord (one part of the CNS) giving negative feedback to the hypothalamus in the brain (the other part of the CNS)? Your vague phrases aren't impressing or enlightening anyone. I don't think you even know what exactly you mean when you say things like this.

Second, do you not realize how illogical your line of reasoning is? You're making a fallacious argument from ignorance, claiming that since you've never seen any evidence for direct action, that you "would have to assume" an alternative view that's also unsupported. I'm sorry, but if you haven't seen evidence that something is true, it does not constitute evidence that it's false. A lack of evidence is neither evidence for or against. You then commit a non sequitur to favor a particular alternative theory that has no supporting evidence either.

Third, you're incorrect in the first place to think that there's no evidence for direct action on estrogen receptors in the hypothalamus. For example, this study from 2008 explains that "Tamoxifen citrate inhibits hypothalamic estrogen receptors [4]; thus, gonadotropin-releasing hormone (GnRH) secretion is stimulated." And this older study from 1988 found that tamoxifen, like estradiol, binds to estrogen receptors in hypothalamic cell nuclei. The fact you haven't seen something hardly means anything in light of your thoroughgoing ignorance of basic topics.

 

[Conciliator]

Secondly, What I find most amazing is that I have now fiured out that you dont even read or know what it is you are pasting!! You recently pasted an article on Deca in that last argument with Bill Roberts, and when I quoted the article, you did not even recognize it and further disputed the information from your own pasted article!

Since you like to just say things without any evidence or support, let me refresh your memory by doing the opposite: This is the study on deca. This is where I mentioned the half-life of deca based on that study (table 4). Here, you didn't understand the difference between half-life and time to peak, saying that I posted about time to peak when I didn't. Here I corrected you, saying "No, I didn't post that. I think you're confusing the absorption half-life with the time to peak, which are two different pharamacokinetic variables." Apparently that wasn't clear enough for you. You follow it up, here, by quoting the study. Ironically, you're the one who didn't even know what he was posting, as your excerpt simply confirms what I said about the half life (the t1/2). There was nothing for me to say in response to you as what you posted is what I said to begin with. Facts are a bitch, huh?

SO what I am referrning to is that if you go through all your studies, you will not find a single one that specifically states Nolve acts DIRECTLY on the brain.

Are you brain-dead? Do you just gloss over my posts without actually reading them. Look at the last two links in my last post to you. The second one is a study showing that nolva acts DIRECTLY on estrogen receptors in hypothalamic cells in the brain.

HIstorically Nolva has not been stated working as such.

WHERE? Where has nolva been stated not to work directly on the hypothalamus? I challenge you to cite even one article on PCT that claims nolva signals the hypothalamus indirectly.

To enlighten you on my reference to CNS. I am describing a process I would not expect you to identify with as clearly, it is not understood by the medical community ( or anyone conclusively), so there are no studies out there for you to hang you hat on.

So in other words, you're talking about pure conjecture with no supporting evidence whatsoever. OK.

 

[Conciliator]

AND BY THE BY, IT WAS I WHO FIRST ARGUED WITH YOU THAT THE SERM ACTION WAS DIRECT TO THE HYPOTHALMUS, AND YOU WHO AGRUED THAT IT WAS NOT. I would be happy to find the thread if you like. I think I was the one who forced you clear on this matter. Do you deny this??

Yes, I deny this. It doesn't even make any sense. You're arguing in this thread that "The one sure thing is that I have never seen it stated that Nolva's action is the result of the drugs direct activity to the hypthalmus." And then you follow it up with "IT WAS I WHO FIRST ARGUED WITH YOU THAT THE SERM ACTION WAS DIRECT TO THE HYPOTHALMUS." You're a delusional nut. I've always argued that Nolva and other SERMs work by blocking estrogen at the hypothalamus and pituitary, not some peripheral site.

Here's that thread you're referring to. What do you know... you argue "Regarding the action and location of receptors. I guess you are now in agreement with me that they are no where near the pituitary? At least 99.9% of them....?" and I respond to you "What the hell are you talking about? Of course there are estrogen receptors in the pituitary. They're also in the hypothalamus. When you take SERMS for PCT, you're taking them to block estrogen in the pituitary and in the hypothalamus. That's where estrogen exerts negative feedback on GnRH release and LH release." Also here: "It should be clear after reading that that there are androgen and estrogen receptors in the hypothalamus and the pituitary. The reason you take SERMs during PCT is to block estrogen in those tissues."

Note that it was that some thread where you demonstrate gross ignorance about SERMs, arguing that they don't act as estrogens in some tissues (the whole "selective" effect). It's a good thread for anyone to read. In fact, I referred to it as another example of the many ridiculous things you've argued: https://thinksteroids.com/community/posts/624740

Now who's the schizophrenic one? Try to find even one reference supporting your claims. And then look at all my references. WAKE UP and realize that what you're claiming happened is drastically different than what actually did happen. Question what's going on in your head...

So do you really believe that the brain does not get direct CNS feedback from every single area of the body?? The simple fact the feelings, like pain and pleasure, report directly to the brain, is proof enough.

Are you joking? The fact that some things are reported to the brain through the nervous system is proof that everything is? Please tell me that you can reason more logically than that, especially when you consider that we know hormones act directly on the brain for feedback control.

 

[Jeton]

Conciliator, if ur not going to respond to my post, i'm left assuming u have no answer to the questions regarding sexual orientation-based variation of effect of Clomid...and so the assertions about Clomid's variation of effect are the fruit of one study with as yet undescribed sample-size and selection criteria.

in other words, it's a prelimenary assertion at best.

 

[OhNoYo]

Con, it seems that you are arguably the most knowledge individual on this forum, especially regarding certain aspects of endocrinology. If I may ask, what is your education background + work experience, Sir?

 

[Conciliator]

Conciliator, if ur not going to respond to my post, i'm left assuming u have no answer to the questions regarding sexual orientation-based variation of effect of Clomid...and so the assertions about Clomid's variation of effect are the fruit of one study with as yet undescribed sample-size and selection criteria.

in other words, it's a prelimenary assertion at best.

I am going to respond. Tonight I should have a chance to go by my university's library and get the full text of the study in question. From all the other references I've posted, however, I think it's clear that men (at least those who identify as heterosexual) do NOT normally exhibit estrogen priming. And in those who do identify as homosexual, there very well may be estrogen priming, though it's stil totally unclear how clomid administration would impact on that.

 

[Stretch]

Con, it seems that you are arguably the most knowledge individual on this forum, especially regarding certain aspects of endocrinology. If I may ask, what is your education background + work experience, Sir?

I've pondered the same many times.

 

[OhNoYo]

I've pondered the same many times.

I'm sure we are indeed in a large boat regarding this, Stretch! Pertaining to endocrinology at the biochemical level, Con knows his shit to say the least!

 

[BBC3]

Thats it. Its just been too long a day. I am going to vomit now....

 

[BBC3]

He won't acknowledge you unless you kick him in his tiny little balls. And they are not shut down either!!!![)]

Conciliator, if ur not going to respond to my post, i'm left assuming u have no answer to the questions regarding sexual orientation-based variation of effect of Clomid...and so the assertions about Clomid's variation of effect are the fruit of one study with as yet undescribed sample-size and selection criteria.

in other words, it's a prelimenary assertion at best.

 

[Stretch]

I agree.

But I also believe that BR knows his shit. And conciliator and BR disagree on a number of issues.

Conciliator most powerful asset is his ability to communicate. He has a gift for organizing his thoughts in a very logical way. This can also allow him to APPEAR more knowledgeable about a topic than he actually is. For the record I am NOT saying that he isn't knowledgeable, or uses his communication skills to BS his way through arguments. It is possible, but I don't know my shit well enough to discern whether this is the case or not. It is merely perplexing to me that two individuals who are very educated, could disagree on so many things.

Con, likes to argue, would have made a hell of a lawyer.

It is my personal opinion that he is a professor of some sort.

 

[jackiebigmur]

this seems to be a never ending debate. My question is: since both clomid and nolva only occupy the receptors and don't actually reduce the levels of estrogen - where does it go? And is it possible that when you discontinue the use will the estrogen level still be the same?

 

[OhNoYo]

this seems to be a never ending debate. My question is: since both clomid and nolva only occupy the receptors and don't actually reduce the levels of estrogen - where does it go? And is it possible that when you discontinue the use will the estrogen level still be the same?

It all depends when you stop taking the SERM. Think of it this way to make it easy, the AAS you inject doesn't stay in your system forever right, so y wud estrogen stay in your system forever either? It wouldn't.

 

[jackiebigmur]

yeah, that makes sense. So the serm helps with the natural t- production helping the overall balance until the estrogen gets to a normal level? I guess it's all about trying to get everything back to normal. Thanks