I’m placing this question here as I figure it’s the best place to catch Cy.
Someone said that in MuscleMag there is an article by Nelson Montana claiming that Clomid down regulates LH receptors, whereas Nolvadex up regulates them. Therefore, Clomid becomes less effective (and, actually, counterproductive)the longer you use it. Nolvadex, on the other hand, becomes more effective the longer you use it.
Cy, do you think this is accurate information? What is your opinion of the various anti-estrogen and anti-aromatase drugs–that is, have you any new thoughts on the subject since you wrote “E-man VS. T-man”?
Lastly, should one take an anti-aromatase if taking Nolvadex (to prevent a “backlash” effect after cesation, from Nolvadex up regulating estrogen receptors)?
P.S. I’m skeptical of the Nelson Montana article, as many of the studies I’ve seen using Clomid have test subjects taking Clomid for months at a time with consistently elevated total and free T levels at the end.
Unless there’s data demonstrating such an effect at the testicular level, it obviously has no basis, as it’s certainly not what one would expect to happen. I pointed out long ago, that one of the isomers in clomiphene may behave as an estrogen agonist, so that may be where such an idea is stemming from, but as you’ve pointed out, if that were the case, you’d expect to see something reported clinically (i.e., less of an effect upon endogenous testosterone production) and I’ve yet to see anything of that nature.
As for using an aromatase inhibitor or estrogen antagonist to prevent some sort of proposed “backlash” well, the idea is a bit faulty simply because the cell doesn’t differentiate between having no estradiol available for binding and having estradiol, but the receptor being occupied with another ligand. In other words, you’ll get up-regulation (assuming that’s the case) in either case as the cell is viewing (not literally) a lack of estradiol in both cases.