ok.. OTC for PCT such as novedex xt ,inhibit-e,reduce xt, ect.. alot of us dont like to use these because they are an ATD.. look at the ingredients on the bottle 3,17-keto-etiochol-triene is an ATD.
ATD is a type of AI that is known as a Suicide Inhibitor. Most that I know of don't like using ATD's due to the fact that it kills the aromitase enzyme. Another and more popular AI you should read up on is a Competitive Inhibitor. In a Comp Inhibitor the molecule just fills the active binding site of the aromatase enzyme and won't let it act on your free test. This means the body still sees the aromatase enzyme floating around and doesn't register to make more enzymes. On the other hand, with something like ATD a suicide inhibitor, the body sees the lack of enzymes (due to ATD killing them) and makes more aromatase enzymes for use. Both will work for PCT, but again most will recommend a competitive AI. Do some reseach on Advanced PCT by Anabolic Xtreme. It contains 6-Bromo which is a Comp AI.
i would just use a serm like nolva or clomid .. ATD is a suicide inhibitor ATD'S kill estrogen and you dont wanna do that..you just wanna regulate it. if you kill it then your body will have to reproduce it and it will at a higher rate and make you have a higher chance of having gyno-rebound when off cycle and pct.
ATD is not only a major libido killer, but it acts as an anti-androgen in the brain
ATD for Estrogen Control
ATD (3,17-dioxo-etiochol-1,4,6-triene) is a recent introduction to estrogen control. It is thought to stop estrogen production in a manner similar to steroidal AI???s such as exemestane. Brand name ATD???s are Rebound XT, Rebound Reloaded, Novedex XT, Ultra H.O.T and Ultra H.O.T.ter.
ATD is technically an
aromatase inhibitor, but with some interesting properties that make it a very useful addition to our estrogen control arsenals.
There are two negative feedback loops that we try to correct through post cycle therapy. The first is elevated estrogen levels from aromatase activity act on the hypothalamus to decrease GnRH production. The second is that elevated androgen levels stimulate androgen receptors in the hypothalamus causing decreased GnRH production. Decreased GnRH leads to reduced LH and FSH production, both of which are directly involved in testosterone production.
Typical PCT with SERM???s and AI???s address the estrogen component of this negative feedback, but do nothing for androgenic stimulation of the hypothalamus. ATD addresses the androgenic feedback loop. ATD has 90% androgenic activity in muscle tissue but only 10% androgenic activity in the hypothalamus.
ATD works for androgen activity the same way that tamoxifen works for estrogen. Tamoxifen blocks estrogen in breast tissue, but has positive effects in other tissue such as liver and bone. ATD blocks androgens in the hypothalamus, but allows it to be active in other tissue.
Because of this dual action estrogen levels are lowered while testosterone levels begin to rise. This is because ATD tricks your hypothalamus into thinking testosterone levels are low so it produces more. ATD provides benefits far beyond simply controlling estrogen in your body. Through its control over the androgen negative feedback loop testosterone production is restarted much faster. And the faster you recover your natural testosterone production the easier it is to keep muscular gains.
In addition to ATD???s benefits for post cycle therapy studies have shown that employing ATD during AAS use maintains significant HPTA function. This means reduced testicular atrophy and faster post-cycle recovery. This is something that you simply can???t get from estrogen control alone.
ATD can also be used by the natural athlete to increase testosterone production. In studies increases of up to 400% in testosterone have been seen. This is equivalent to injecting 400-600mg per week of testosterone enanthate or cypionate. This means continued growth for the natural athlete without the problems and
side effects usually associated with injecting testosterone.
While there should technically not be any difference between the ATD ptoducts I have personally seen the best results using Rebound XT by Designer Supplements. I believe it is also the most cost effective of the ATD products out there. Your mileage may vary.
I???ve found the following discussion on running SERM???s inverse to ATD???s which is both informative and by all accounts very effective. It has been posted on many forums and the credit for it goes to Dr. D. Thank you Dr. D!
???Discussion on running SERM inverse to ATD
Estrogen only ???rebounds??? based on the mechanism of suppression. SERM, for example, only masks estrogen expression by occupying receptors but estrogen production is left unchecked and actually increases as testosterone levels increase. AI???s like letro inhibit inducible enzymes and just like a leaky faucet, they body will eventually try to balance the equation with increased aromatase activity. Steroidal AI???s like Teslac, Exemestane, and ReboundXT will not result in ???rebound??? phenomena because the inhibition is non-competitive and irreversible. They act as false substrates, so aromatase is still happy to act on them (instead of
androstenedione) and the body keeps no record of an imbalance. There is no leaky faucet. In fact, after prolonged use, steroidal AI???s often produce a protracted anti-e benefit even after being discontinued. This is why I suggest an inverse taper with SERM and RXT for PCT with an abrupt stoppage of RXT at the end. As the SERM elevates androgen/estrogen production, the AI dose is increased to compensate while the SERM is phased out. It works quite well to use this approach and rebound is not encountered
ATD is similiar to Aromasin, they are both Type I steroidal AIs. It can actually be useful during and afterj a AAS cycle. I have also read that ATD actually can block testosterone from reaching the androgen receptors. Which is very bad. So I am not really sure about this compound. I have read that ATD also
POTENTIAL SIDE EFFECTS / INTERACTIONS:
AT/ATD are strong cytochrome P450 3A4 inhibitors (Ki values < 0.2 microM via in vitro human microsome studies). 3A4 is the workhorse of the P450 system. It accounts for 30% of P450 activity in the liver and 75% of the P450 activity in the small intestine (wait a minute ? this is where ATD-type supplements are absorbed). Because so much P450 activity is due to 3A4, it comes as no surprise that 3A4 performs the bulk of oxidative drug metabolism in humans. This makes 3A4 arguably the most important human P450 enzyme to understand. Until the mid-1990?s, the literature included references to 3A3or 3A3/4. It is now understood, however, that 3A3 is not a separate P450 enzyme but a transcript variant of 3A4. Subsequently, the list of drugs and supplements that are metabolized by 34A IS CONSTANTLY GROWING! 3A4 being a high-capacity/low-affinity enzyme if inhibited means you get spill-over of the drugs to the low-capacity/high-affinity subset [namely in the enterocytes of the gut (recalling the high percentage of 3A4 activity in the gut): 2D6, 2C9, and 2C19]. In English, this means you have the potential for immense toxicity in other drugs metabolized by this cytochrome enzyme.
I will center our discussion here on the supplements that have inhibited metabolism when concurrently used with AT/ATD preached about as classic adjuncts during PCT. In the late 1990s, several 3A4-related casualties occurred, and the drugs were removed from the US market by manufacturers. These cases are reminders of the potentially serious nature of 3A4 inhibition.
INTERACTION #1: Red Yeast Rice (RYR) ? a classically-described HMG Co-A reductase inhibitor and also anti-inflammatory and down-regulator of LDL receptors has the potential to cause Rhabdomyolysis (see my For the Love of Science and Medicine, Part II article for some clinical studies for evaluation) and extreme hepatotoxicity. I have already stated in Part II and previous articles/posts that RYR has absolutely NO business in a PCT regime following a C17 alkylated PH/PS/AAS. RYR coupled with either of the 3A4 inhibitors AT/ATD potentiates the aforementioned effects, so I amplify my response to the nth degree and ask with use of AT/ATD-containing products, you fully omit this item.
INTERACTION #2: Hawthorn Berry ? a classically-described blood pressure modifying agent and this is attributed to its calcium and beta-blockades as well as its ACE inhibition and diuretic action. This rather safe supplement on its own with a great track record becomes a different animal when combined with 3A4 inhibitors. It can actually drop your blood pressure to a level that would in itself be dangerous. The key here is that if you opt to throw this compound in solely at the time of cessation of PH/PS/AAS that may have elevated your blood pressure ? a decline of more than 25% at such a rapid rate can be deadly!
INTERACTION #3: Any sympathomimetic agent. While better avoided in the first place during PCT, people have considered certain agents that act through various andrenergic grounds and they too become MORE potent with AT/ATD.
CAUTION: Nolvadex, a commonly-puported ?must-have? by many authorities during PCT. This is an obvious display of their ignorance and blatant disregard for drug-drug interaction as Nolvadex (discussed at greater length in part IV) is metabolized through the 3A4. Now, in addition to people starting at dosing parameters as high as 40mg (which is a highly unnecessary dose even for the heaviest of cycles) with a 7-day half-life, you have increasing toxic levels in addition to what you have already put together. Retinopathy or liver toxicity anyone?
I am confused myself what do you guys think about all this. I can't tell if ATD is a good AI for on cycle or PCT use. I hear good things and bad thing. That part that I put in bold print I believe is very true and dangerous. When I first took novedex XT it was a new product a good many of years ago. Anyway I took it one night before I was going to sleep for the night. Well a good buddy of mine calls me and says he just got back from Iraq and wants me to go out to drink with him. So I decided to meet up with him I drank about 6 beers forgetting that I took the novedex and not thinking too much of it. My buddy drives us back to his place where I left my car. I tell him I got to piss and ask to use his bathroom. I go up stairs, piss, I am washing my hands one second and the next I wake up on the floor. He ran up stairs to see what the noise was banging on the door. I managed to get up opened the door told him I blacked out next second I am out again and he caught me before I fell. I ended up sleeping on his couch but my heart was palpitating real bad. I thought I was poisoned or something because 6 beers never did that to me this is when I used to drink quite often. I thought about it later that maybe the novedex had something to do with it. Well today I found this study which could explain what happened. I am not sure what to think of this supplement IS it GOOD or NOT? I know I will never drink while taking it again. I rarely drink anymore anyway. What do you guys think?