Check this out
Originally posted by Bobo
http://www.anabolicminds.com/forum/showpost.php?p=124665&postcount=31
Originally Posted by Rogue Drone
Pat Arnold had this response at .bb
Pat, I am interested in knowing what you would recommend for pct after a 4 week m1t cycle, 6oxo or nolva?
"What i recommend in a more general sense is an aromatase inhibitor over an estrogen receptor antagonist like nolva
whether the aromatase inhibitor is arimidex, femara, or 6-OXO does not necessarily matter as long as an effective dose is taken
the reason I feel this way is because ERA's like nolva raise SHBG along with testosterone which means that your total test goes up but free bioavailable test really does not. So although your balls may recover you are not getting the actual hormone activity you need
With an aromatase inhibitor your test production increases but SHBG does not go up. You get your cake and can eat it too"
I say use them both
Here is the other side of the arguement w/ references:
""I would not use 6-oxo or any aromatase inhibitor post cycle. I have a theory based on numerous post cycle bloodwork data that people have sent me to comment on. Complete recovery of the HPA means both free and total test return to the normal range. Androgens dramatically lower SHBG. In fact, it can stay lowered for months after a cycle. As long as SHBG stays low, total test will be low, even if free test is normal. I have seen this phenomenon in quite a few bloodwork printouts. Aromatase inhibitors typically lower SHBG by blocking estrogen production. (Estrogen elevates SHBG). So taking an aromatase inhibitor post cycle just prolongs recovery.
The traditional post cycle ancillaries, clomid and nolvadex, raise SHBG, but block the suppressive effects of estrogen on the HPA at the hypothalamic/pituitary level. They allow total test to return to normal more quickly.
I have often heard the response "Well as long as free test is normal, what does it matter whether total test is low?" Test circulates in three fractions, free, SHBG bound, and "weakly bound" or albumin bound. The free+albumin bound is considered the bioavailable fraction. So you can have free test that is normal, but if total test is low, albumin bound test will be low as well, leading to low bioavailable test. This is why guys complain about low libido post cycle even if free test is normal. And the cases I have seen where this happens most often are those where guys have used an aromatase inhibitor post cycle.
One has to differentiate between aromatase inhibitors and SERMS like nolva and clomid. All are generally lumped together as antiandrogens. Only the aromatase inhibitors lower SHBG. The other two, being SERMs are estrogenic in this regard and raise SHBG. The more efficient the aromatase inhibitor is at blocking E2 production, the more impact it will have on SHBG. Exemestane, the most efficient aromatase inhibitor (a so called "suicide inhibitor since it permanently deactivates the enzyme) lowers SHBG the most.
As to how they lower total test, if test starts to increase during HPA recovery, and SHBG is low, the free fractions will increase disproportionally to total test, and then start to act directly on the hypothalamic GnRH pulse generator to dampen GnRH output, which inturn blunts LH secretion. So yes the free fractions are responsible for feedback inhibition
Bear in mind that there are elements of fact and elements of hypothesis in my comments. I'm hypothesizing that using post cycle aroamtase inhibitors impairs recovery by invoking the factual observations that amomatase inhibitors lower SHBG (fact), which increases the free test fraction (fact), which will then blunt GnRH release (fact). Unfortunately there are no studies of which I am aware where aromatase inhibitors were ever used to treat post cycle HPA suppression. I find it remarkable that in all the medical literature there are 2 studies where clomid was used for this, and 1 study where HCG was used.
There is another reason I would not use aromatase inhibitors post cycle. Animal studies have shown that blocking the conversion of test to estradiol locally, within the vascular endothelium, greatly accelerates the development of atherosclerotic plaques. During a cycle this is probably not going to be a problem, because there will still be plenty of aromatization going on (anastrazole and letrozole only block aroud 50% to 60% of aromatization). But post cycle, when test and estrogen are very low, blocking aromatization could, if it is valid to extrapolate the animal studies to people, accelerate atherosclerosis."
Here are links to a few of the animal studies:
http://www.pnas.org/cgi/content/full/98/6/3589
http://www.pnas.org/cgi/content/full/99/6/4055
http://circres.ahajournals.org/cgi/...y=BqyNB.4rGiPYQ