[machine528]

I am abit confused about ATD and was hoping someone could clear up if ATD could be of use in PCT for light cycles of Hdrol or Epi. I am curious as to what you guys think is the best Anti Estrogen out there. I have heard alot of people saying to stay away from ATD and other saying if you take a light dose it isnt bad.

[MattMiller]

i have always heard to stay away from ATD in post cycle therapy...i read a reason why but i really cant remember what the person said or where i saw it. if i find something ill post it up for you but im sure someone else will chime in with an answer before then

[sundevil22]

I believe it is surpressive and so it wouldnt make a good pct

[Interlocutor]

Originally Posted by machine528

I am abit confused about ATD and was hoping someone could clear up if ATD could be of use in post cycle therapy for light cycles of Hdrol or Epi. I am curious as to what you guys think is the best Anti Estrogen out there. I have heard alot of people saying to stay away from ATD and other saying if you take a light dose it isnt bad.

best? "best" is a manifold question. maybe letrozole, which is extremely strong, also inhibits prolactin (IIRC) and does not depress IGF-1 (as do most/all other AIs). maybe adex, which may not be as "strong", but for which there are certain studies showing long (well, mid-) term efficacy and safety in males. maybe ATD, which is also pretty strong, but as it also binds to the androgen receptor, can be loaded with sides as compared to most other AIs, and has oral availability and half-life issues, but which is cheap as dirt and used for decades in science? maybe 6-OXO, which is DSHEA compliant (ATD and 6-bromo probably are not), but which may have estrogenic metabolites? maybe 6-bromo, with the issues about the different isomers? maybe formestane, which is great as stabndalone but which may also have slightly suppressive metabolites?

personally, i'd go with adex, if it were more easily available. for OTC i've gone with ATD as standalone in the past with good experience (aside from joint issues, lol), and in PCT as well.

Originally Posted by MattMiller

i have always heard to stay away from ATD in post cycle therapy...i read a reason why but i really cant remember what the person said or where i saw it. if i find something ill post it up for you but im sure someone else will chime in with an answer before then

many many people have used ATD successfuly in PCT in the "good old" days of Rebound XT etc.

Originally Posted by sundevil22

I believe it is surpressive and so it wouldnt make a good post cycle therapy

do you have any source on this info?

i can't remember anything on ATD being suppressive. however as opposed to most other AIs, ATD also apparently competitively binds to the androgen receptor, effectively making it not only an anti-estrogen, but - at least in theory - an anti-androgen as well. however, this effects of this are probably strongly dosage dependant.

ATD may act both as an androgen receptor blocker and as an aromatization inhibitor.

ATD was a moderately effective competitor for cytosol ARs particularly at higher concentrations, inhibiting almost 50% of AR binding at 10 (-6) M.

http://www.ncbi.nlm.nih.gov/pubmed/2...ubmed_RVDocSum

as on it being suppressive, the same study:

No agonistic properties of ATD were observed either behaviorally or biochemically.

to be suppressive, it must be an agonist of the HPTA, no? which it is apparently not. it is a mediocre AR antagonist, and a very strong aromatase antagonist, so that at a medium dosing (i.e. one where no loss of libido = possible competitive binding with T on the AR occurs) the strong benefits from the anti-aromatase activity far outweight the possible drawbacks from binding competitively to the AR.

also, other studies do NOT always seem to come to the same conclusion re AR binding.

anecdotal feedback seems to indicate that 50-75mg seems a dose which is comfortable for most males for a period of a few weeks, depending on bodyweight and individual factors.

IMHO the main point when using it in PCT is to taper it down to allow slow and steady reestablishment of normal estrogen levels and normalizing of possibly impaired aromatase and ER activity.

there has always been some discussion on ATD not being effective etc. etc., however, see the following studies which seem to indicate LH and test raise from ATD (which is what we want in PCT):

http://www.ncbi.nlm.nih.gov/pubmed/6...ubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/2...ubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/6...ubmed_RVDocSum

the issue on it being suppressive may stem from:

http://www.ncbi.nlm.nih.gov/pubmed/8...ubmed_RVDocSum

Animals treated with ATD had significantly reduced levels of aromatase activity in selected regions of the hypothalamus, preoptic area, and the amygdala (P < 0.05). Even though ATD inhibited brain aromatase activity, it did not prevent the negative feedback actions of T on LH secretion after Cx. In addition, ATD by itself inhibited LH secretion after Cx and activated brain androgen receptors.

however, that was for the castrated rats, for the uncastrated it was:

In sham-operated intact males, ATD produced variable surges of LH that were accompanied by elevations of T in the systemic circulation.

T.I.

[Hank Vangut]

use of ATD is debatable. this thread is a good read: Why ATD should never be used for post cycle therapy: new study