Anti aromatase for non-aromatising steriods?

[Problem]

For compounds that does not aromatize like epi, why some people use an AI for PCT?

Isn't useless when there's no estrogen when you come off cycle?

Enlighten me!

 

[bigpapa]

even though it does not aromatize there is still the risk of estrogen rebound. The AI helps to restore the natural balance of your hormones instead of just coming off cold turkey. it increases your level of free testosterone and keeps your estrogen under control so there s no big spike or rebound. it can also help restore you body's natural level of GH as well.

 

[Problem]

If there's no estrogen coming off cycle, how would the AI control the estrogen?

 

[bigpapa]

If there's no estrogen coming off cycle, how would the AI control the estrogen?

there is no guarantee there will be no estrogen

 

[monsterbox]

correct me guys.

if theres no estrogen when you come off, chances are there no test either.

As the test comes back, aromatizing occurs and you are left with above normal estrogen levels floating around while you reach normal levels. Using an AI/SERM blocks receptors and kills the enzyme.

 

[Problem]

correct me guys.

if theres no estrogen when you come off, chances are there no test either.

As the test comes back, aromatizing occurs and you are left with above normal estrogen levels floating around while you reach normal levels. Using an AI/SERM blocks receptors and kills the enzyme.

Kills the enzyme? blocks what receptor?

Test levels doesn't come back that quick after the cycle.

we need some clear info here. :think:

 

[corsaking]

The product description of Epi refers to it as "anti -estrogen with long lasting effect that is organ specific.So if it works by decreasing estrogen thereby creating an anabolic state (greater ratio between e and test -test being produced naturally by the body)i am not clear either why pct is required. Theres no pct for 6-oxo . nolvedex xt so its not clear to me either why pct is necessary

 

[dg806]

From Understanding Post Cycle T Recovery
by William Llewellyn



The Role of Anti-estrogens


It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.

 

[corsaking]

From Understanding Post Cycle T Recovery
by William Llewellyn



The Role of Anti-estrogens


It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.

So can i take from this that AIs only have a place whilest ON cycle

 

[dg806]

I think AI are better used on cycle while the Anti e like nolva is better for pct

 

[Problem]

From Understanding Post Cycle T Recovery
by William Llewellyn



The Role of Anti-estrogens


It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.

Great stuff.

do you have a link to the whole thing? it's an interesting read.

Thanx bro.

 

[dude123]

Anti-e's

I also was curious as to why people would want to use a anti-e post cycle, after using a product like Havoc/epistane? As both are anti-e's themselves. I understand the estrogen rebound thing, but they are all similar in action as estrogen receptor blockers...from what I have read. Both Epistane/Havoc compare their products in their advertisements as similar in action to Nolvadex which blocks the same estrogen receptor as Havoc/Epistane does. All three have been used as breast cancer medications. If Nolvadex/Havoc/Epistane all block the same estrogen receptor and you stop taking it, I presume all the estrogen that was building up in your body while taking these estrogen blockers would create a flood of excess estrogen[rebound effect] and would most likely lower your LH levels, which would in turn lower your production of testosterone to some degree. So I guess the reason for maybe taking a aromatase inhibitor[AI] post cycle after using a product like Havoc/Epistane. I have used Havoc before, but don't recall feeling like I needed a A.I. post cycle, felt no after effects/estrogen rebound from what I recall? So I'm not to sure why one would be to concerned about post cycle therapy using either Havoc/epistane? Taking Nolvadex post cycle after using a product like Havoc/Epistane, is like taking Havoc/Epistane after using Nolvadex...? Same difference, you would be just be continuing your cycle of anti-e's...all three work by the same similar mechanism from what I have read. Maybe taking a aromatase inhibitor like Gaspari's Novadex might help reduce the aromatase enzyme that converts testosterone to estrogen. Like maybe the last week of Havoc add the Novedex. I can understand taking Nolvadex as part of P.C.T. after a steroid cycle, but not after using a product like Havoc/Epistane.

 

[monsterbox]

i thought that when you come off a non-aromatizing cycle, test will be low and so will be estrogen.

Test will come back on its own and aromatize into estrogen at the same time. An AI is to control the estrogen that occurs as the testosterone comes back?

Isn't this why we use a SERM and then start an AI after the SERM.

 

[ironparson]

bump

 

[lennoxchi]

http://anabolicminds.com/forum/steroids/77359-neoborn-s-epistane.html this should answer any questions you might have. remember that epi IS a steroid, if you want to restart you HPTA after shutdown (which epi does have the potential to do) you might want a SERM

 

[Gutterpump]

So if it works by decreasing estrogen thereby creating an anabolic state (greater ratio between e and test -test being produced naturally by the body)i am not clear either why pct is required. Theres no pct for 6-oxo . nolvedex xt so its not clear to me either why pct is necessary

That's not how it works. It is an anabolic oral steroid which also happens to block aromatase. It's main effects are through it's anabolic actions. It will surpress your natural test. In the beginning of a cycle it may give you a boost though which is why many people report an initial boost in libido.

I think a small amount (10mg) over time may not be suppressive..and may boost natural test, but it will not be noticebly anabolic at that level.

 

[crazilyfter42]

The only time I include an AI in pct is when Im using clomid. I learned the hard way the first time when I did not do this. With nolva I have never found a need to do this.