Arimidex (Anastrozole) is a non-steroidal AI. I was under the impression that it is suppressive and should not be used in post cycle therapy.
Hmm... my impression was that adex, like formestane, is a 3rd gen AI, which means it's selective, and does not inhibit adrenocorticosteroid synthesis like 1st gen AIs (such as aminoglutethimide). i don't know about ATD and 6-OXO, though, maybe some sides attributed to those are because of that?
as on being suppressive... i wouldn't know about that, some studies i've seen do not seem to support this effect in vivo. see:
Effect of chronic administration of an aromatase i...[J Endocrinol. 2000] - PubMed Result (but see the comment on estrogen)
Estrogen suppression in males: metabolic effects. [J Clin Endocrinol Metab. 2000] - PubMed Result
E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T, sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change.
if it were suppressive, shouldn't LH/FSH decrease?
also:
The effect of aromatase inhibition on sex steroids...[J Clin Endocrinol Metab. 2001] - PubMed Result
After 9 weeks of treatment, there were significant decreases in estradiol, estrone, and sex hormone-binding globulin levels by 29%, 73%, and 16%, respectively, and total testosterone increased significantly by 56%.
Effects of aromatase inhibition in elderly men wit...[J Clin Endocrinol Metab. 2004] - PubMed Result
Mean bioavailable testosterone increased from 99 to 207 in group 1 and from 115 to 178 ng/dl in group 2. Total testosterone levels increased from 343 to 572 ng/dl in group 1 and from 397 to 520 ng/dl in group 2. Serum estradiol levels decreased from 26 to 17 pg/ml in group 1 and from 27 to 17 pg/ml in group 2. Serum LH levels increased from 5.1 to 7.9 U/liter and from 4.1 to 7.2 U/liter in groups 1 and 2, respectively. <...>. Serum estradiol levels decrease modestly but remain within the normal male range.
also pretty interesting:
Short-term aromatase-enzyme blockade unmasks impai...[J Clin Endocrinol Metab. 2005] - PubMed Result
Exposure to anastrozole reduced (24-h pooled) serum estradiol concentrations by 50% and elevated mean LH concentrations by 2.1-fold in both the young and older cohorts. <...> In summary, administration of a potent and selective aromatase antagonist reduces estradiol and elevates mean LH concentrations equivalently in young and older men.
in the light of those documented LH improvements even with short-term administration at recommended dose, do you have any link/study which shows in which way it would be suppressive? woudn't suppression indicate activity on the HPTA, which seems simple to imagine for a steroidal AI or its metabolites, but not that simple for a non-steroidal AI (how does that bind to the AR, for example?).
Also, I wonder if estrogen actually rebounds as intensely and quickly as it seems. I've seen AI philosophies with no serm where the AI is ramped down (ie 75,50,50,25 ATD). So this philosophy says estrogen rebounds HARD and FAST :think: Overkill on the AI?
maybe i can provide some input in this:
1. depending on the AI, this does not necessarily completely destroy/eliminate estrogen. if you look at many of the available studies (see above), one does find that estrogen is decresed by certain amount, depending on the actual AI applied and the dosing scheme used. if applied carefully, AIs can be helpful in actually controlling (not erasing) estrogen while helping to raise LH, FSH and Test.
2. the idea behind the tapered-down aproach (which was mainly intended for those who don't want or can't use a SERM)is as follows: after a cycle of a non-aromatizing compound, there is very little estrogen in the system. bot testh and e are low. however, aromatase and estrogen activity may (and this is the big question mark) be upgraded. i.e. what little test you produce initially is immediately/to a large amount converted to e (and DHT, obviously). with the short half-life of orals, this would indicate a phase where the anabolic effects of the oral is quickly vanishing, whereas the test is still to low (if its converted "away" to e) to excert an anabolic effect, thusly making it difficult to hang unto gains made on-cycle.
the AI is added to prevent/reduce conversion of test to e, to help the t to remain unconverted and to maintain gains. the ramp-down of the AI in the following phase is then intended to allow the body to slowly normalize aromatase and e levels over time, while minimizing the risk of rebound. i.e. the idea is not to recover from total shutdown as quickly as possible, but to help maintains gains and normalize aromatase and e levels in a controlled and consistent manner over time.
3. SERMs notoriousy have very long half-lifes (between 5 and 9 days, depending on the exact compound). while you have peak levels a few hours after ingestion, stable serum levels are only reached after prolonged ingestion. the idea to start high on the AI in AI/SERM combined PCT protocols is to allow the SERM a few days to build up to effective serum levels, while preventing conversion of test (little as it may be) to e, at a time when estrogen receptor activity may be upgraded and against which no sufficient protection may be initially available.
In the popular AI inverse to serm theory, I see a more intelligent plan. But it seems that mild gyno sometimes pops up AFTER even a seemingly solid post cycle plan... hence a delayed estrogen rebound. Some taper after the ramp to avoid the rebound. Looks good IMO.
i'm always a strong proponent for tapering down AIs, regardless if used standalone, starting from high-point, or after slow ramp-up. the issue i have with ramp-up/taper-down is that this makes for an excessively long AI phase - if you consider a 4 week cycle of a non-aromatizing anti-estrogenic compound such as SD or Havoc as being part of this. then you'll have cycle time + ramp up time + taper down time... possibly pretty long toi be low on e.
finally, if you ramp up the ai while tapering down the SERM, do you not delay the increase in estrogen (against which the serm is supposed to protect you, breast- and hpta-wise) into the phase where you already have low or no serum levels of the SERM left in the system? why then have a SERM in the first place, if you delay estrogen production until the SERM is gone?
personally, and i am in no way advocating this as the best solution, nor am i actually convinced that it is, i currently believe that if you want to combine SERM and AI it's best to start the AI moderately high (see above for the reasoning), and to taper it down such as to allow estrogen production to reoccur/increase while the SERM is still in full effect to protect the HPTA and breast tissue from its effects. one also has to take into consideration the long half-life of SERMs here, and the build-up of serum levels of the SERM over time.
T.I.