1) Agree and maybe through another mode of action also...many have said.... its not a drug that is fully understood
Its primary MOA is through estrogen antagoinism and there have been other studies done on its effects directly at the pituitary. So I'd say its a fairly understood compound in the way of raising endogenous testosterone.
2)I think thats exactly the point I stated above
3) I cannot, there are no studies on that, and Im not stating its going to raise testosterone on 500mg of E a week....my "theory" is more on "pulse signaling" and "prevention of dormancy" front....thats it....I feel and have for the last 13 years (in my opinion) its very important to send a "signaling" for lack of a better word at 4-8 week intervals than blast for 16 weeks to 24 weeks nonstop and hope on a wing and prayer that you will recover quickly after a half a year on (or continuously on)
How exactly does this "signalling" work. Because, to my knowledge, Clomid or any other SERM cannot override the negative feedback loop and thats what your claiming.
How can Clomid "signal" the HPTA when its shutdown using androgens when we know its primary MOA?
If it doesnt raise endo T when using steroids, whats the point in using it again...?
4) Why not? Im a much bigger fan of "well lets throw everything and the kitchen sink at it" than be picky or choosy when it comes to the HPTA (as I feel one of the main problems in bodybuilders careers are they concentrate too much about "how much am i going to gain when I am on" instead of concentrating on something just as important ..."how am i going to get myself back to square one hormonally as quickly as possible (to the best of my ability)
Because there is no evidence Clomid will override the negative feedback loop and raise GnRH, LH and FSH when shutdown using androgens, thats why its pointless using it for that reason.
Clomid is notorious for side effects, so its a bad choice anyway comparable to other SERMs, even if this phenomenom you speak of works. Which I dont believe it does.
5) Where am i saying that? My statement and only statement was that Ive soured on tamoxifen....as it relates to PCT...Im not comparing it to anything else...I just stated I personally have soured on it.
Tamoxifen is better than Clomid in comparable studies, so why wouldnt Tamoxifen also cause this "signalling" you speak of?
6) Damn you sure read something and then run with it to the tune of your own observations instead of reading the statement as it is typed. I said SERMS
MAINTAIN testosterone output? I did? Or you did? Again Im talking about signaling over dormancy. Nobody is going to have a 750ng/dl testosterone level pre cycle...and a 750ng/dl post cycle testosterone (cleared out) shortley thereafter with PCT. As far as Swale you might want to check into that again because he is starting to use clomid with TRT which goes directly against your argument.
**broken link removed**
and he has been thinking about it for awhile now
Bypass the HPTA
HRT with Clomid instead of hcg - Page 2
If the question was "hey Dante what would you rather have someone use during a cycle clomid or HCG?"....my answer would be HCG 100 times out of 100.....Im not championing for clomid here...its brutal on alot of people.
No, because they are the same.
If this "signalling" happens, why can it not be maintained?
You've offered no data to back even this "signalling" claim at all.
One can make assumptions on your theory's. Such as Clomid limiting HPTA inhibition on cycle and other SERMs would be able to repeat this "signalling" using basic logic and looking at other data available.
Suggesting SERMs to prevent "dormancy" on cycle is outdated information and its confirmed by your links dated 2005.
Scally suggests an "off peroid" every 12-16 months and introducing SERMs+HCG during this off time when HRT is stopped. That is not the same as staying on HRT or steroids and introducing SERMs at all.