ok here are some quotes to point you in the right direction. You obviously do know some, and maybe even alot, about what you are talking about, but seem to get some things confused. You had much good things to say and got me thinking about some of it, but again some issues are confused. It’s random and not put together, but I do not have the desire right now to write an article.
Few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up.
Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody’s best interest to bring back natural test as soon as humanly possible.
Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That’s basically how the mechanism works, nothing more, nothing less.
Nolvadex and Clomid - Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall endogenous estrogen (not completely true as endogenous estrogen actually stays the same - neither lowered or RAISED)
Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it
blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to, ultimately leading to the destruction of estrogen and less produced as the hypothalamus senses the SERM as an estrogen and lowers production
Estrogen helps determine sexual aggression - too high and too low effects sexual aggression and libido.
Some clinicians expressed preference for an estradiol of around 32 pg/ml for optimal libido in men. However, this will depend on all the factors that determine libido. Some need more. Some need less.
An added risk of using an AI is of driving estrogen levels too low, with deleterious consequences for the lipid profile, calcium deposition, libido, etc
male patients who suffer E2 elevations above the top of normal range are placed on 0.25mg of Arimidex every third day
It is important to not lower estrogen too far, which is easy to do with an AI, as doing so has disastrous effects on the Lipid Profile, bone deposition, libido, etc. I prefer to maintain E in mid-range.
These results may indicate that the negative effects of estrogen deprivation in men only become manifest when the concentration falls below the levels induced by our intervention with anastrozole (77 pmol/l). This assumption is supported by the observation in the anastrozole group that, although effects of the reduction of serum E(2) on vascular parameters could not be demonstrated in subjects as a group, there was a correlation between individual serum E(2) and several vascular parameters.
a significant decrease in flow-mediated dilation was observed in subjects taking anastrozole [median, 6.1% (range, 5.2 to 13.4) to 3.5% (2.0 to 5.7), P=0.034] but not in the placebo group
Here is a place where you can see real-life experiences with Arimidex, most are women, but you will see that empiricaly it can cause estrogen to get too low and effect libido among other things - askapatient.com/viewrating.asp?drug=20541&name=ARIMIDEX
IF YOU CAN FIND SOME INFO ON ARIMIDEX BEING SELF-LIMITING TO THE POINT OF NOT LOWERING ESTROGEN TOO MUCH I WOULD LOVE IT! I’ve been using bunk stuff and would love to get my hands on this wonder drug - Arimidex!!!
References and research areas:
Circ Res. 2003 Nov 28;93(11):1127-33. Epub 2003 Oct 30
Eur J Endocrinol. 2006 Apr;154(4):569-75
Exp Physiol. 2006 Mar;91(2):445-56. Epub 2005 Dec 19.
John Crisler, DO
1: Cancer Res. 2002 May 1;62(9):2474-7
Fertil Steril. 1978 Mar;29(3):320-7.
J Clin Endocrinol Metab. 2000 Sep;85(9):3027-35
I am very happy you posted this