AI's have their place in cycles. However, for PCT and _RECOVERY_ a SERM such as nolvadex is a much wiser choice. Most of this "AI for PCT" is due to supplement companies wanting to sell products. You will not see any educated person/trainer/doctor prescribe or promote an AI alone for PCT.
Do some research if you dont believe me. Many such as BigCat have already spoken out on this whole "push" towards AI's. It's not the smartest move for PCT. Dont take my word for it, research it for yourself.....
Quote:
-BigCat-
The reason not to use AI's during PCT is first of all because of the risk of rebound gyno, but more importantly because not only does it not contribute to recovery, it actually hinders it. In contrast to nolva for instance, it lowers instead of increases SHBG. Lower SHBG (and keep in mind that after androgen use SHBG is already seriously depressed) leads to slower recovery at more than one point in the HPTA.
Originally Posted by skelooth
wow I'm kind of in shock. Before this thread everyone and their brother recommended that proper PCT = SERM + AI. Now I have two bottles of ATD and I'm scared to ever touch them ever again.
I wouldn't know, since before this seems to refer to a few off months prior to this, when I wasn't following the supplement scene however.
Before this for me has been extensive experience in the steroid community where this subject has only popped up once or twice, rather unsupported, and was quickly disproven by the more scientific-minded members of the community. In that community, for quite some time, proper PCT has been described as HCG + SERM. So I don't understand this commotion. No one who actually knew what they were talking about ever said you should use an AI.
I doubt the tail end of this worthless thread will get much view. Not many will notice this post or care. Business as usual will continue.
A real PCT
http://www.medibolics.com/ScallyVergelAstractHPGA.pdf
More bad news for AI's and PCT
Quote:
Brain Res. 1994 Sep 19;657(1-2):105-23. Related Articles, Links
Effects of steroidal and non steroidal aromatase inhibitors on sexual behavior and aromatase-immunoreactive cells and fibers in the quail brain.
Foidart A, Harada N, Balthazart J.
Laboratory of Biochemistry, University of Liege, Belgium.
Castrated quail were treated with Silastic implants filled with testosterone (T) in association with injections of the aromatase inhibitors, R76713 (racemic vorozole; 1 mg/kg twice a day) or 4-hydroxyandrostenedione (OHA; 5 mg/bird twice a day). Control birds received no treatment (CX group) or were implanted with T capsules only (CX + T group). Both R76713 and OHA strongly inhibited the T-activated male copulatory behavior. This inhibition had the same magnitude in both groups. The growth of the cloacal gland, a strictly androgen-dependent process was not affected by these compounds. The treatments significantly affected the number of aromatase-immunoreactive (ARO-ir) cells in each of the six brain areas that were studied: the anterior and posterior parts of the sexually dimorphic medial preoptic nucleus (POM), the septal region, the bed nucleus of the stria terminalis (BNST) and the anterior and posterior parts of the tuber. This number was significantly increased in all areas by T. In agreement with our previous study, R76713 significantly inhibited this effect of T in the tuberal hypothalamus but not in the anterior POM nor in the BNST. By contrast the effect of T on the number of ARO-ir cells was completely blocked by OHA in all brain nuclei. The two inhibitors had statistically different effects in all brain regions.
Like in a previous study, R76713 increased the intensity of the staining of all ARO-ir cells. This effect took several days to develop suggesting a progressive build-up of the enzyme concentration. This was also suggested by the fact that a rebound in aromatase activity was observed 16 to 24 h after a single injection of R76713. The increased immunoreactivity was not observed in OHA-treated birds. The denser immunoreactivity in R76713-treated birds and the better tissue preservation due to the aldehyde fixative that had been used provided here a clearer picture of the cellular and subcellular localization of ARO-ir material. This allowed to identify new groups of immunoreactive cells, namely in the nucleus accumbens, in the area of the paleostriatum ventrale, in the nucleus taeniae, in the medial and caudal hypothalamus and in the medial part of the mesencephalon and of the pons. Most of the immunoreactive material was located in perikarya but some of these cells were also surrounded by dense networks of ARO-ir fibers often associated with immunopositive punctate structures.(ABSTRACT TRUNCATED AT 400 WORDS)
1: J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60. Related Articles, Links
Use of ultrasensitive recombinant cell bioassay to measure estrogen levels in women with breast cancer receiving the aromatase inhibitor, letrozole.
Klein KO, Demers LM, Santner SJ, Baron J, Cutler GB Jr, Santen RJ.
Children's Hospital of Orange County, California 92668, USA.
The development of well tolerated, potent, specific, and nontoxic aromatase inhibitors for the treatment of postmenopausal women with estrogen-dependent breast cancer has been a major goal of recent studies. The third generation inhibitors now under investigation are nearly 10,000-fold more potent than first generation compounds. Currently available RIAs for plasma estradiol lack sufficient sensitivity to measure levels during aromatase inhibition and, thus, to assess drug potency precisely. The availability of an ultrasensitive bioassay for estradiol provided the opportunity to accurately assess the potency of a new third generation triazole aromatase inhibitor, letrozole (CGS 20267). We used this assay to measure estradiol levels in 14 women with metastatic breast cancer given letrozole at doses of 100 micrograms to 5.0 mg/day over a 12-week period. The lack of differences between doses and sampling times allowed pooling of data. Basal estradiol levels of 7.2 +/- 1.9 pmol/L (mean +/- SEM, 1.95 +/- 0.52 pg/mL) fell to 0.26 +/- 0.11 pmol/L (0.07 +/- 0.03 pg/mL) during the first 6 weeks of therapy and to 0.48 +/- 0.18 pmol/L (0.13 +/- 0.05 pg/mL) during the second 6 weeks of therapy. Although plasma estradiol levels measured by RIA were significantly correlated with levels measured by bioassay (r = 0.79; P < 0.01), the degree of suppression assessed by the bioassay (95 +/- 2% after 6 weeks) was greater than that determined by the RIA (81 +/- 4%), presumably due to improved ability to measure very low estradiol levels.
We conclude that plasma estradiol is suppressed by letrozole to lower levels than previously observed, with equivalent suppression at all doses studied. A slight, although not statistically significant, rebound in estradiol levels occurs during the second 6 weeks of therapy compared to the first 6 weeks. Maximum inhibition of aromatase is achieved at letrozole doses as low as 100 micrograms.
Publication Types:
Clinical Trial
PMID: 7673408 [PubMed - indexed for MEDLINE]