PCT Products

[kilo g]

I am looking for an ultimate PCT stack. I cant decide between these products...Inhibit, Rebound XT, AE PCT,6-oxo, etc...I want to take Two products that will block estrogen very well, boost test. and block cortisol.
Also, when taking these products do I taper down. What is a good starting dose and time, a good ending dose. I'll also throw in a trib product along with my milk thistle and saw palmetto. Any thoughts would be helpful!!
Thanks

[BillyB]

Inhibit-E which is ATD is very effective. It will stack nicely with Reduce-XT which is a cortisol blocker.

Here is some good info on ATD

ATD (1,4,6-androstatriene-3,17-dione) has been used since the 80’s by the department of Endocrinoligy and hundreds of other medical groups to conduct studies. Please note it is not ATD that they are studying, they use ATD as a verified and proven estrogen control. It is still being widely used in this manner. A search on pubmed.gov can verify this (115+ studies using ATD).

Info from Designer Supplements

What is Aromatase?
Aromatase is an enzyme from the cytochrome P450 group. As noted, it sanctions the conversion of androgens to estrogens. It is quite a two-faced enzyme, as it can be viewed as both negative and positive depending upon your point of view. Because it converts androgens into estrogens, this can be viewed as beneficial because of estrogens ability to add bloat, and thus strength, while also helping to lubricate joints during the stress of heavy weight lifting. It is also involved with growth hormone (hGH) to convert IGF-1 – a “localised muscle builder”. Estrogens also play a role in maintaining healthy cholesterol in your body. Too much estrogen, however, can be a major stumbling block for perfecting your ideal body. You only have to ask those with annoying steroidal or pubertal-induced gynecomastia (“gyno”) to be aware of this. Nothing destroys a trophy-winning physique more than visible lumps beneath your nipples. Estrogen can also be the root cause of subcutaneous water retention, which can obscure your cuts and definition when you’re ripped, which can be damn annoying.

There are prescription drugs available called aromatase inhibitors (AI) that prevent the process of aromatisation. These drugs are anastrazole (Arimidex), letrozole (Femara) and exemestane (Aromasin). It is the latter, exemestane that ATD is based and improves upon. These AI work in different ways based on their structure. To understand how ATD works, it is worth understanding how various AI work.

Competitive & Suicidal Aromatase Inhibition
Before discussing aromatase inhibition, let’s briefly discuss how the process of aromatisation works. To make this explanation as simple and easy to understand as possible, consider testosterone, estradiol and aromatase as three separate “blocks”. The testosterone and aromatase blocks have what are known as “active sites”, which is where the two blocks connect. Upon doing so, a reaction occurs that changes the testosterone (androgen) into estradiol (estrogen). The two blocks then disconnect, and the aromatase is then free to find another testosterone block to convert to estradiol. If you add an AI to the environment, the active site of the aromatase enzyme gets taken up by the AI, rendering the aromatase enzyme inactive and leaving the blocks of testosterone unaffected. At this point, it is required that we distinguish between the various types of AI and their subsequent effects.

Steroidal vs. Non-Steroidal AI
There are two classes of AI agents available – non-steroidal, which are anastrazole (Arimidex) and letrozole (Femara), and steroidal, which are exemestane (Aromasin) and ATD. Both types of AI act directly upon the aromatase enzyme, but they do so by different mechanisms and have different effects on cellular aromatase activity. Non-steroidal AI inhibition of the aromatase enzyme is reversible, and is known as “competitive inhibition”. The AI binds to the aromatase, thereby rendering it inactive, but can later disconnect from the enzyme, re-allowing it the ability to convert testosterone to estradiol. Because this effect is not permanent, there is potential for an estrogenic rebound effect, as aromatase activity is unregulated after removal. This is why it is generally recommended to follow up use of a non-steroidal AI like Arimidex with an anti-estrogen like tamoxifen (Nolvadex) – a compound that blocks the estrogen at the estrogen receptor site. Steroidal AI inhibition of the aromatase enzyme is irreversible. Once the AI connects to the aromatase, it is lights out for the enzyme. Even if you remove the steroidal AI from the environment, any bound aromatase enzymes remain bound. This is known as “suicide inhibition” because it also means lights out for the AI. Generally speaking, non-steroidal AI are associated with increased aromatase enzyme content and steroidal agents are associated with decreased content 1. Over time resistance to non-steroidal AI can develop, which does not occur with AI such as exemestane and ATD 1, 2.

Effects on Blood Lipids
One of the major concerns with AI is their effect on healthy cholesterol formation and blood profiles in general. It is unfortunate that all AI have been deemed reckless when it comes to blood profiles because it is the non-steroidal AI that have invoked this effect 5, 6. The steroidal AI exemestane has actually been shown to improve lipid metabolism 3, prevent bone loss 3, 4 and help raise high density lipoprotein – the “healthy” cholesterol 1. These effects have not been shown to occur using non-steroidal AI (in fact, they may even worsen the condition). The reason for such an effect is still under scrutiny, however, it is generally theorised that the androgenicity of the parent compound and its principal metabolite 17-hydroexemestane may be responsible for offsetting any negative impact suppressed estrogen may generate 1. While preclinical data on the use of ATD is not as abundant as exemestane, because ATD is based on the structure of exemestane, similar effect is to be expected. This has been the case for other studies using ATD and appears to be the case based on user feedback.

AI and Testosterone
Estrogens are produced primarily by the ovaries of females (and in other body organs to a much lesser extent). Males do not have ovaries, and so, as noted above, the aromatase enzyme is released to convert androgens into estrogens. When using an AI such as ATD levels of estrogens are reduced, which is eventually detected by the body. In a bid to maintain homeostasis, testosterone production and release is increased in an effort to correct the imbalance. Of course using ATD, any conversion is significantly hindered, thereby meaning the imbalance isn’t corrected until use of the product is ceased, so testosterone production remains higher than usual and estrogen levels remain low and controlled. And since steroidal AI do not appear to lose potency with use like non-steroidal AI, this effect is maintained for as long as you use the product.

References
1. Goss P. Anti-aromatase agents in the trea™ent and prevention of breast cancer. Cancer Control. 2002 Mar-Apr;9(2 Suppl):2-8.
2. Lonning PE. Exemestane: a review of its clinical effi cacy and safety. Breast. 2001 Jun;10(3):198-208.
3. Goss PE, Qi S, Cheung AM, Hu H, Mendes M, Pritzker KP. Effects of the steroidal aromatase inhibitor exemestane and the nonsteroidal aromatase inhibitor letrozole on bone and lipid metabolism in ovariectomized rats. Clin Cancer Res. 2004 Sep 1;10(17):5717-23.
4. Goss PE, Qi S, Josse RG, Pritzker KP, Mendes M, Hu H, Waldman SD, Grynpas MD. The steroidal aromatase inhibitor exemestane prevents bone loss in ovariectomized rats. Bone. 2004 Mar;34(3):384-92.
5. Wickman S, Saukkonen T, Dunkel L. The role of sex steroids in the regulation of insulin sensitivity and serum lipid concentrations during male puberty: a prospective study with a P450-aromatase inhibitor. Eur J Endocrinol. 2002 Mar;146(3):339-46.
6. Elisaf MS, Bairaktari ET, Nicolaides C, Kakaidi B, Tzallas CS, Katsaraki A, Pavlidis NA. Effect of letrozole on the lipid profi le in pos™enopausal women with breast cancer. Eur J Cancer. 2001 Aug;37(12):1510-3. 7. Covey DF, Hood WF. Enzyme-generated intermediates derived from 4-androstene-3,6,17-trione and 1,4,6-androstatriene- 3,17-dione cause a time-dependent decrease in human placental aromatase activity. Endocrinology. 1981 Apr;108(4):1597-9.

[ripped218]

I agree with Billy,ATD(Inhibit-E)and reduce xt(for cortisol) are great additions to PCT.

[UNCfan1]

From my personal experience Inhibit-E is great, its about the same as Gaspari's Novedex Xt but $10 cheaper and u get 30 more pills.

[ripped218]

From my personal experience Inhibit-E is great, its about the same as Gaspari's Novedex Xt but $10 cheaper and u get 30 more pills.
Novedex is actually a proprietary mixture of ATD and 3OHAT,so no one but Gaspari know's how much ATD is in novedex.

[UNCfan1]

Novedex is actually a proprietary mixture of ATD and 3OHAT,so no one but Gaspari know's how much ATD is in novedex.

Really, I didn;t know that. I still loved it though.