How many of you use IronPimper's PCT advice (ATD based instead of SERM)

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dmbwhiteguy

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I will be running a SD cycle here pretty soon. No pulsing, just straight up 4 wks @ 10/20/30/30 followed by 4 wks of PCT consiting of 5 days of Nolva and the rest of the PCT Novedex XT & supporting supps.

IronPimper had a great thread over at BB.com regarding how a SERM can be used for a few days (3-5days) lowering the dose each day, while simultaneously ramping up an ATD product and then continuing that ATD for the remainder of PCT.

Any thoughts on this method? I have used it with success, I am just interested in other's opinions. Thanks
 
thesinner

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I've heard of dosing Clomid for a couple of days, but never with tamoxifen.

.
 
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He's saying to run a SERM only for a few days though. I don't remember reading that in Dr. D's thread.
Eh, I thought I remembered somebody talking about that very thing since nolva is hepatoxic...I could be wrong and I'm not going to try and go back through that LONG thread.

After reading thesinners comment I was likely confusing the nolva with clomid...now that I think about it though, the discussion was about taking clomid the first few days and then changing over to nolva...you're right, that's a slightly different conversation from the original post. I would think that at least two to three weeks of nolva would needed, but likely more.
 
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here is a link to that thread

http://forum.bodybuilding.com/showthread.php?t=526986


While nolva and clomid are quite popular, they have several drawbacks. Firstly, both nolva and clomid show an affinity for increasing shbg. It should be noted that clomid raises levels of shbg more so than nolva. If you are not familiar with the effects of elevated shbg, let me help. When nolva and clomid increase lh and fsh, they stimulate more production of test in the testes. When shbg increases the test produced in the body tends to be bound test. As we know, this is detrimental to our goals. We want free test, which only occurs when levels of test are elevated, but shbg remains low.

Another drawback is that nolva and clomid are extremely hepatoxic. That makes them less than optimal for use as pct to a methyl compound. Combining a 3-5 week cycle of a methylated aas/ph/ps with a pct of 3-5 weeks of clomid and/or nolva would be very taxing on the liver.

Clomid also has another problem. It should only be used for a week at most. While it is superior at stimulating lh production, it also decreases sensitivity in the pituitary to Gnrh. This means that as use of clomid continues, the pituitary will produce less lh despite the increase in Gnrh.

Nolva's last drawback is due to its very nature. Since it only blocks estrogen receptors, it allows circulating estrogen to continue to exist. If used for pct of an aromatizing drug, levels of circulating estrogen would be greatly increased when nolva usage was discontinued. Again, this is a less than desirable characteristic, as one of our main goals was to limit estrogen induces sides.

So, let's talk atd. Atd offers several advantages over our more traditional pct drugs. Firstly, atd does not show any affinity for increasing shbg. That means that while test levels continue to increase, there will be an abundance of free test. This allows us to better maintain gains, as well as strength during pct.

Secondly, atd has been shown to be equally as productive as nolva and clomid in stimulating the release of gnrh, and therefore, lh and fsh. Since atd binds directly to the enzyme, there is a decrease in actual levels of circulating estrogen, this is akin to nolva and clomid's action of binding to the receptor, except that it will drastically reduce the chance of estrogen rebound.

Thirdly, atd has the ability to address the androgen feedback loop. This means that atd will block the pituitary from receiving the signals that tell it to stop producing gnrh. This occurs when levels of androgens begin to increase greatly. That means that the pituitary will continue to produce more and more gnrh, therefore more and more lh and fsh. That will allow the testes to more test, and do so more rapidly.

As you can see, atd would be the better option for almost all pct protocols. Where nolva supposedly "shines" is in its ability to allow for the production of new estrogen. This allows for improvement in lipid profiles. This is, however, and ill conceived advantage. A steroidal ai, like atd, also allows for production of new estrogen. The only product I know of that does not allow for any increase in circulating estrogen is arimidex.

So, what do we need? Well, ideally any cycle/pct would include hcg. Since it is the only true lh mimitek out there, and when used in the correct doses is unsurpassed in its ability to maintain testicular mass and function. However, since this isn't an option for everyone, we need something else. I would suggest the use of an ATD product in conjunction with a few other products. A sample might look like so:

75mg atd + 50mg dhea + 1.8g fenugreek + 600mg 6-oxo
50mg atd + 75mg dhea + 2.4g fenugreek + 600mg 6-oxo
25mg atd + 100mg dhea + 3g fenugreek + 400mg 6-oxo
25mg atd + 3.6g fenugreek + 200mg 6-oxo

The combination of 6-oxo and an atd allows the atd to focus on the destruction of estrogens. The 6-oxo is then free to aid in the stimulation of lh and fsh. As neither 6-oxo or atd increase sbgh, there is no concern for desensitization of the pituitary. Therefore, and overload of lh stimulation would be beneficial to our goals. If one so desired, they could also add a cortisol control product, most notably 7-oxo-dhea, as well as a natural test booster. Natural test boosters generally increase free test as well, and do not show any affinity for increasig sbgh. Therefore, even more free test.

On a last note, ALR has noted that studies show that atd can be used on cycle, at about 75mg per day in order to maintain healthy testicular mass and function. I am slightly leary of this hypothesis, but I have not tried it on my own. Since atd does address both feedback loops, it is possible that it could be used on cycle to maintain healthy levels of lh production, though I am not sure, and would not want someone on a strong cycle to try this out.


Originally Posted by ekilla2003
well its legal and from my eyes the best pct product to use so why not

You are entitled to your opinion, all I need is some science to back it up, and I'll change my mind. Everything I have read says otherwise. I'll put it this way, nolva has 2 real advantages: firstly, it acts faster. Since it binds to the receptor instead of the enzyme its effects are seen immediately. Secondly, it is very powerful in the liver, which is why it is so helpful in recovering healthy lipid values. If you love nolva, the best way to use it is for 3 days at the beginning of pct, 60/40/20 while increasing your atd dosage 25/50/75. Starting day 4 you would drop nolva and keep using the atd and taper it down slowly over a 3-4 week period.
 
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that is pretty much the meat of the post...the important parts anyway.

hopefully that can open this topic up for more discussion
 
TripDog

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...im waiting for jomi to come here and start a rukus about atd..... *waits patiently*
 
jomi822

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ill ask one very loaded question for starters (you faggoty fagot tripdog):

Why would you run atd if you already have tamoxifen?
 
pistonpump

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6oxo is a suicide inhibitor why would you run both doesnt make sense to me. Atd absolutely kills my penis so i dont really care what it does ill use something else...
 
thesinner

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As far as I'm concerned, there's absolutely no benefit to combining aromatase inhibitors. As aromatase decreases, selectivity decreases, and side effects start "popping up". In the case of ATD or Letro, "popping up" is a misleading way to word it ;)
 
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i appreciate the replies and imput.

i usually stick with what i know, but maybe this time i will veer of my path of a familiarity and try a different PCT route.

i'll prob run Nolva @ 20/20/20/20 ( i feel that Nolva does not need to be dosed any higher than this to get your test back up safely and efficiently)

appreciate it guys
 
wastedwhiteboy2

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too much atd dries me out. so I would want to run the nolva a little longer.
 
jomi822

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people associate their lack of libido with atd being a strong AI

thats just plain wrong. ATD binds to, and deactivates the androgen receptor. you arent not getting wood because you have low estrogen, you are not getting wood because you have turned off your androgen receptors using a dirty, useless compound called ATD.
 
TripDog

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Jomi is the official ATD hater of Anabolic Minds. I do agree with him after reading studies about it.
 
pistonpump

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Jomi is the official ATD hater of Anabolic Minds. I do agree with him after reading studies about it.
im his groupie. ATD can eat a big fat goat penis! oh...wait thats nyc's job...Atd and nyc should hook up and be the useless pieces of crap couple :lol:
 
atnartist

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so why would nt you run a natural test booster while running a cycle so that your boys might stay producing and healthy? I was running a ph that I loved but the libido was way low, started on axis ht at one week before ending the ph and within a day I could tell a big difference.
 
RenegadeRows

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I would not use ATD to replace a SERM.
 
jomi822

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Jomi is the official ATD hater of Anabolic Minds. I do agree with him after reading studies about it.
ATD is great if you hate your wang and sex life. if you ever need some help or counseling on giving up the banging of goats you tell me and ill put you on an ATD regiment to obliteratre your HPTA and shrink your nads.
 
thesinner

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ATD is great if you hate your wang and sex life. if you ever need some help or counseling on giving up the banging of goats you tell me and ill put you on an ATD regiment to obliteratre your HPTA and shrink your nads.
Selectivity varies greatly depending upon dosage.

The reason most people get ATD-**** is because they're taking 75mg.


Structurally, ATD is very similar to Aromasin. Only difference is that instead of a ketone, we have an double bond.
ATD:
http://upload.wikimedia.org/wikipedia/commons/e/eb/1,4,6-androstatrien-3,17-dione.png
Aromasin:
Image:Exemestane.svg - Wikipedia, the free encyclopedia

The trick with pretty much every steroidal aromatase inhibitor is a partial negative charge hanging off the #6 carbon. We see this is 6-oxo, 6-bromo, aromasin, ATD, and 3OHAT. What happens is this negative charge causes a steric strain with the androgenic receptor, greatly decreasing the odds of it binding.

With ATD, this partial charge hanging off carbon 6 comes from only one free electron; whereas, with a ketone there is 4 free electrons. ATD has a greater affinity for the aromatase; however, it also has a greater affinity for the AR. As we ramp up the dose, serum concentrations increase, affinity for the AR increases.

I'm guessing that ALRI (company to first market this as a supplement...as far as I know) found out about this compound from some old research leading up to the release of Aromasin.
 
TripDog

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Selectivity varies greatly depending upon dosage.

The reason most people get ATD-**** is because they're taking 75mg.


Structurally, ATD is very similar to Aromasin. Only difference is that instead of a ketone, we have an double bond.
ATD:
http://upload.wikimedia.org/wikipedia/commons/e/eb/1,4,6-androstatrien-3,17-dione.png
Aromasin:
Image:Exemestane.svg - Wikipedia, the free encyclopedia

The trick with pretty much every steroidal aromatase inhibitor is a partial negative charge hanging off the #6 carbon. We see this is 6-oxo, 6-bromo, aromasin, ATD, and 3OHAT. What happens is this negative charge causes a steric strain with the androgenic receptor, greatly decreasing the odds of it binding.

With ATD, this partial charge hanging off carbon 6 comes from only one free electron; whereas, with a ketone there is 4 free electrons. ATD has a greater affinity for the aromatase; however, it also has a greater affinity for the AR. As we ramp up the dose, serum concentrations increase, affinity for the AR increases.

I'm guessing that ALRI (company to first market this as a supplement...as far as I know) found out about this compound from some old research leading up to the release of Aromasin.
:goodpost:
 
jomi822

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Selectivity varies greatly depending upon dosage.

The reason most people get ATD-**** is because they're taking 75mg.


Structurally, ATD is very similar to Aromasin. Only difference is that instead of a ketone, we have an double bond.
ATD:
http://upload.wikimedia.org/wikipedia/commons/e/eb/1,4,6-androstatrien-3,17-dione.png
Aromasin:
Image:Exemestane.svg - Wikipedia, the free encyclopedia

The trick with pretty much every steroidal aromatase inhibitor is a partial negative charge hanging off the #6 carbon. We see this is 6-oxo, 6-bromo, aromasin, ATD, and 3OHAT. What happens is this negative charge causes a steric strain with the androgenic receptor, greatly decreasing the odds of it binding.

With ATD, this partial charge hanging off carbon 6 comes from only one free electron; whereas, with a ketone there is 4 free electrons. ATD has a greater affinity for the aromatase; however, it also has a greater affinity for the AR. As we ramp up the dose, serum concentrations increase, affinity for the AR increases.

I'm guessing that ALRI (company to first market this as a supplement...as far as I know) found out about this compound from some old research leading up to the release of Aromasin.
Im not sure if what you said is arguing for or against my criticism of ATD. Some people are going to look at "The reason most people get ATD-**** is because they're taking 75mg." and say "well i guess it ok if i take a low dose". Which is not necessarily true.

If there are studies, ON THE BOOKS, showing that ATD attaches to, and deactivates, the AR (which was measured by WEIGHING SEX ORGANS), why the hell would anyone take it?

you know what is better than measuring viability for PCT vs. AR binding affinity and selectivity? NOT TAKING ATD and taking an SERM instead, especially with enormous anecdotal evidence showing that ATD in some way shape or form seems to ruin almost every pct i have seen (with the exception of ONE).
 
thesinner

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Im not sure if what you said is arguing for or against my criticism of ATD. Some people are going to look at "The reason most people get ATD-**** is because they're taking 75mg." and say "well i guess it ok if i take a low dose". Which is not necessarily true.
I'm not trying to take sides, so much as add to the information being shared. I think ATD can be an effective testosterone boosting supplement if taken within it's effective realms.

For PCT, I agree there's better stuff out there, for sure. SERM's, better AI's, even proviron helps increase nut production. I think this Ironpimper protocol sounds a little.....well...I'm not a fan (and I don't suppose you are either).

If there are studies, ON THE BOOKS, showing that ATD attaches to, and deactivates, the AR (which was measured by WEIGHING SEX ORGANS), why the hell would anyone take it?
Do you have a link to those? I remember seeing one of these a while back. I doubt they have the info I'm looking for, but it'd be nice to see them.

The argument I make is that there will exist a point where the testosterone raising effects vs. the antiandrogenic effects will reach a maximum, and a limit on the curve where the antiandrogenic effects would approach zero.

If numerous studies have shown that alcohol hurts the liver, kills brain cells, negatively impacts estrogen:androgen ratios, and (if taken at a high enough dose) shuts down the autonomic nervous system.....why the hell would anyone drink?

you know what is better than measuring viability for post cycle therapy vs. AR binding affinity and selectivity? NOT TAKING ATD and taking an SERM instead, especially with enormous anecdotal evidence showing that ATD in some way shape or form seems to ruin almost every post cycle therapy i have seen (with the exception of ONE).
I will give ya that one because I agree with you ;)
 
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sinner, with the double bond on aromasin instead of the ketone on ATD.....how does that change the two. Specifically and laymans term sort of..?

i wouldnt think this would make aromasin weaker as doses are usually lower mg for mg...
 
thesinner

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sinner, with the double bond on aromasin instead of the ketone on ATD.....how does that change the two. Specifically and laymans term sort of..?

i wouldnt think this would make aromasin weaker as doses are usually lower mg for mg...
ATD has the double bond. And, my bad, Exemstane has an alkene on it (not a ketone, my computer cut off the structure last time). This means they both have the same charge hanging out at carbon 6, it is just adjusted a little bit with aromasin.

Basically, think of a magnet. Opposites attract, likes repel. Hold two magnets with the same poles 2 feet appart. You barely (if at all) feel them repel. Now move them 2 inches away. You feel them pushing each other away a little bit. Now try and touch them, they're really trying to push appart. What's been done with the structural changes from ATD to aromasin is that the negative charge has been moved so that it will be closer to the negative charge on the AR.

http://www.rxlist.com/cgi/generic/exemest.htm
 
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The best post cycle therapy I've ever had included a low dose of ATD, not to mention it really helped me get rid of Gyno. I love the stuff. At low doses, it seems very beneficial, and I never had a problem with ATD-d!ck, even at 100mg. To each his own. I will continue to use it in conjunction with a SERM if I ever do anabolics again.
 
pistonpump

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ATD has the double bond. And, my bad, Exemstane has an alkene on it (not a ketone, my computer cut off the structure last time). This means they both have the same charge hanging out at carbon 6, it is just adjusted a little bit with aromasin.

Basically, think of a magnet. Opposites attract, likes repel. Hold two magnets with the same poles 2 feet appart. You barely (if at all) feel them repel. Now move them 2 inches away. You feel them pushing each other away a little bit. Now try and touch them, they're really trying to push appart. What's been done with the structural changes from ATD to aromasin is that the negative charge has been moved so that it will be closer to the negative charge on the AR.

http://www.rxlist.com/cgi/generic/exemest.htm
...so aromasin does not bind to the AR as good as ATD.

It doesnt make sense to me i would think if ATDs charge was farther from the AR then it would bind more, correct? Then it should be stronger at estrogen suppression as well...so why are doses usually 3x that of aromasin?

damn chemistry.... haha
 
thesinner

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You're comparing them by oral doses, and assuming they have the same oral bioavailability and the same molecular weight.

Sticking a methyl on Carbon 6 might aid in absorption, as seen with the designer steroid M1P.

Aside from that, I think ATD is disgustingly overdosed. 25-30mg will give you plenty of estrogen suppression and testosterone boosting.
 
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I personally like dermabolics' ATD transdermal spray. It only has 25 mg. per 5 sprays which is enough in my opinion. I also buy 5 grams of androstenetrione powder(6-oxo) and add it to the ATD and shake it up and use them together. 5 sprays equal out to 25 mg. ATD and about 140 mgs. androstenetrione.This seems to be just about perfect for me. I hope this helps!!!
 

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