Do we start pct too early?

[Atomini]

From what I read, and it was a long whole ago, so I may b mis-remembering lol but clomid works as gnrh right? And in the feedback loop. Gnrh (from the hypothalamus) is the signal on the pituitary to release lh and fsh.......and tsh? Now if nolva acts on the pituitary to secrete lh and fsh (similar to how gnrh acts), why both? I could have swore I read nolva acts as lh and fsh. But like I said, long time ago and memory may not b serving correctly. Maybe I should continue use of noopept! :P

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Neither Clomid nor Nolvadex work as GnRH at the pituitary gland. They stimulate LH and FSH release from the pituitary by other means. They do so through Estrogen antagonism. As you may or may not already know, Nolvadex and Clomid are both SERMs (Selective Estrogen Receptor Modulators), which means they act as Estrogen antagonists in some tissues (breast tissue) and as Estrogen agonists in other tissues (such as the liver). One of the other areas they work as Estrogen antagonists is at the pituitary gland, where they work to block the ability for Estrogen to bind to receptors at the hypothalamus and pituitary glands. Estrogen serves as one of the hormones that the hypothalamust will monitor through receptors, and if too much of it is detected, the hypothalamus will reduce its signals to output LH and FSH. If too little of Estrogen is detected, it will do the opposite and signal increases in LH and FSH so as to increase Testosterone levels so as to restore Estrogen balance via aromatization.

In layman terms, Nolvadex and Clomid basically trick the hypothalamus and pituitary into thinking that there is insufficient Estrogen in the body (because they act as Estrogen antagonists at the receptor sites there), and so the HPTA basically goes "holy shit, we need to restore Estrogen levels by increasing output of Testosterone so a bit of it can get aromatized, lets start cranking out the LH and FSH!".

That's it. Nolvadex is not an LH/FSH analogue... it cannot possibly work like one, it isn't even a protein! HCG is considered an analogue of LH, because it contains a subunit in its quaternary protein structure that is 100% identical to LH, so it can interact with LH receptors at the Leydig cells of the testes. Nolvadex never has done this, does not do this, and can never possibly do this.

Clomid and Nolvadex = Estrogen antagonists at the hypothalamus.
HCG = LH mimetic at the Leydig cells of the testes

Hope that clears things up for you.

I always enjoy reading your theories, even if i dont always agree. lol. But i like the fact that you always seem to provoke my own thoughts.

Well, I should expand upon the idea of this 'build-up' I mentioned, but i'm too busy at the moment. It just involves math.... if you know advanced functions and calculus, you just take the formula for half-lives and/or exponential decay, plug the numbers in in terms of dose and days, and watch how many mg of a substance you'll have left over in your system after a number of weeks. Remember that the half-life only indicates how long it takes for a substance to reduce to half the original dose you took. Most dosing protocols call for a re-dose long before that half-life is up so as to maintain steady and stable peak optimal blood plasma levels. Essentially, you're piling dose on top of dose on top of dose.

[MickeyKnox]

Neither Clomid nor Nolvadex work as GnRH at the pituitary gland. They stimulate LH and FSH release from the pituitary by other means. They do so through Estrogen antagonism. As you may or may not already know, Nolvadex and Clomid are both SERMs (Selective Estrogen Receptor Modulators), which means they act as Estrogen antagonists in some tissues (breast tissue) and as Estrogen agonists in other tissues (such as the liver). One of the other areas they work as Estrogen antagonists is at the pituitary gland, where they work to block the ability for Estrogen to bind to receptors at the hypothalamus and pituitary glands. Estrogen serves as one of the hormones that the hypothalamust will monitor through receptors, and if too much of it is detected, the hypothalamus will reduce its signals to output LH and FSH. If too little of Estrogen is detected, it will do the opposite and signal increases in LH and FSH so as to increase Testosterone levels so as to restore Estrogen balance via aromatization.

In layman terms, Nolvadex and Clomid basically trick the hypothalamus and pituitary into thinking that there is insufficient Estrogen in the body (because they act as Estrogen antagonists at the receptor sites there), and so the HPTA basically goes "holy shit, we need to restore Estrogen levels by increasing output of Testosterone so a bit of it can get aromatized, lets start cranking out the LH and FSH!".

That's it. Nolvadex is not an LH/FSH analogue... it cannot possibly work like one, it isn't even a protein! HCG is considered an analogue of LH, because it contains a subunit in its quaternary protein structure that is 100% identical to LH, so it can interact with LH receptors at the Leydig cells of the testes. Nolvadex never has done this, does not do this, and can never possibly do this.

Clomid and Nolvadex = Estrogen antagonists at the hypothalamus.
HCG = LH mimetic at the Leydig cells of the testes

Hope that clears things up for you.

Fantastic explanation once again Atomini. ^^

Well, I should expand upon the idea of this 'build-up' I mentioned, but i'm too busy at the moment. It just involves math.... if you know advanced functions and calculus, you just take the formula for half-lives and/or exponential decay, plug the numbers in in terms of dose and days, and watch how many mg of a substance you'll have left over in your system after a number of weeks. Remember that the half-life only indicates how long it takes for a substance to reduce to half the original dose you took. Most dosing protocols call for a re-dose long before that half-life is up so as to maintain steady and stable peak optimal blood plasma levels. Essentially, you're piling dose on top of dose on top of dose.

I completely understand exponential and serum levels on cycle. But if you look at the values on an average recreational users cycle, the serum levels will only reach a certain point. And i wouldn't rely on one of those on line PCT Calculators for this (not that you do). BUT, having said that, at some time when you're free, can you post an example of this using Enanthate or some other long ester? I would really like to take a closer look at this theory Atomini.

I appreciate any input you can provide. Thanks in advance.

EDIT: Just to be clear, i don't want anyone to think we are discussing the doubling effect as that doesn't apply to AAS because of the ester being cleaved off and the oil/steroid being absorbed at an undetermined rate (at least to me)

[Tron3219]

I completely understand exponential and serum levels on cycle. But if you look at the values on an average recreational users cycle, the serum levels will only reach a certain point. And i wouldn't rely on one of those on line PCT Calculators for this (not that you do). BUT, having said that, at some time when you're free, can you post an example of this using Enanthate or some other long ester? I would really like to take a closer look at this theory Atomini.

I appreciate any input you can provide. Thanks in advance.

Agree 110% with the explanation! That's the atomini we've all grown to love. Idk wtf that short answer was all about the other day! Had me floored!

I'd also b more interested in seeing the buildup theory.

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