Estrogen rebound on cold turkey?

[barbelle]

So at the end of a reasonable cycle of test, your body has stopped producing testosterone and has increased aromatase levels (especially if you used an AI on cycle).

When you stop exogenous test, your body starts producing testosterone again (assuming you've managed to avoid testicular atrophy) but you have a raised level of aromatase, so the test will all be converted into estrogen and you get bitch tits.

If you use a suicidal AI in PCT, you will temporarily combat the estrogen, and will speed up testosterone recovery, but your body will also start increasing aromatase even further, so you will later get estrogen rebound, with bitch tits etc.

Instead, you want to block the estrogen receptors with Nolva, so that your HTPA can recover without the increased estrogen ratio causing trouble.

So, how much of an actual risk is rebound bitch tits if going cold turkey after 12 weeks of 500 mg / week? Is a SERM PCT only useful to maximize gains and not strictly necessary?

I'm trying to figure out a way to avoid using a SERM.

 

[caveman72]

can I ask why is it Just curiosity.
there is a compound called pride made from broccoli. look it up it may work I've read others use it

 

[caveman72]

prid. not pride damn cell.prid.

 

[barbelle]

Why I'd like to avoid SERMS? See my other thread, the SERMS don't look healthy, and they are pretty unresearched when it comes to high doses in men. Even Tamoxifen is avoided by many women with breast cancer because there is some indication it has teratogenic effects, as well as possibly directly reducing fertility in the user.

Don't get my wrong, I realize steroids aren't exactly health food, and I realize the value of PCT for reducing shutdown time.

I'm just trying to figure out the absolutely least risky way of doing them, instead of starting from a cycle tuned for maximum gains and then try to find ways of reducing sides.

Prid sounds interesting, but I couldn't find anything via google, any links?

 

[barbelle]

Uh huh did you mean an intravaginal device? Very funny...

 

[barbelle]

My original question is really if estrogen rebound is a major issue immediately after a testosterone cycle, or if the problem with shutdown is only from low testosterone.

 

[GigaloRob]

Estrogen rebound and Bigfoot have something in common, both are a myth. To my knowledge there is no studies, data ect... to prove this actually occurs.

 

[barbelle]

There are no studies on anything it seems. If the gubbamint had taken one percent of the money the spend on harassing chemical athletes, and instead used that money for androgen research, oh well...

 

[Docd187123]

Estrogen rebound won't happen. It's a bro science topic that stuck around.

 

[barbelle]

Just to be clear, when you say it's a myth, are you talking about estrogen rebound from Arimidex, or estrogen rebound from going cold turkey off a short ester testosterone? If it is the latter, then the only problems associated with cold turkeying are those directly caused by temporary hypogonadism, right? Meaning you will have low estrogen as well.

 

[barbelle]

Does that not imply that either A) aromatase production upregulates so slowly that a 12 week test cycle does not affect it much,
or B) aromatase production is so quickly and tightly regulated that it is able to adapt to sudden hypogonadism before problems arises.

I'm sorry if this is described in the literature or in well known internet postings, I have not been able to find it.

 

[Docd187123]

Just to be clear, when you say it's a myth, are you talking about estrogen rebound from Arimidex, or estrogen rebound from going cold turkey off a short ester testosterone? If it is the latter, then the only problems associated with cold turkeying are those directly caused by temporary hypogonadism, right? Meaning you will have low estrogen as well.

I'm talking about estrogen rebound period.

As Dr. Scally mentioned in a post on here a while ago, the "rebound" or whatever you want to call it of estrogen is dependent on the PK and PD of the aromatase inhibitor you take. But it's not a rebound as your body simply returns back to homeostasis. Again to paraphrase the good doctor, when testosterone levels return to baseline or increase from almost nothing post cycle, do you call that testosterone rebound? No, you call that recovery. Same concept with estrogen.

Coming off testosterone cold turkey means once the last of the exogenous testosterone is metabolized and excreted, there is very little test in the body for the aromatase enzyme to convert to estrogen. How could there even be any type of "estrogen rebound" in this case?

 

[Northern Nutrition]

Last cycle i experienced ferritin rebound. Wtf??

 

[barbelle]

Coming off testosterone cold turkey means once the last of the exogenous testosterone is metabolized and excreted, there is very little test in the body for the aromatase enzyme to convert to estrogen. How could there even be any type of "estrogen rebound" in this case?

I will look up the thread by Dr. Scally, but the mechanism would be a slower downregulation of aromatase than upregulation of testosterone. I was always under the impression that this was so. Thus when testosterone started bouncing back, there would still be too much aromatase present and all of it would turn into estrogen.

I can't really see how suicidal aromatase inhibitors can work if aromatase production is speedily regulated.

 

[Docd187123]

I will look up the thread by Dr. Scally, but the mechanism would be a slower downregulation of aromatase than upregulation of testosterone. I was always under the impression that this was so. Thus when testosterone started bouncing back, there would still be too much aromatase present and all of it would turn into estrogen.

Look at table 4 In this study.

http://www.breast-cancer-research.com/content/pdf/bcr1757.pdf

I can't really see how suicidal aromatase inhibitors can work if aromatase production is speedily regulated.

I think arimidex is superior to exemestane in almost every aspect.

 

[barbelle]

Look at table 4 In this study.
http://www.breast-cancer-research.com/content/pdf/bcr1757.pdf

Ok, so that says that 12 weeks after seizing AI use, estrogen is pretty much back to normal, in post-menopausal women. Is is interesting and promising, but what does it say about the levels during those 12 weeks, for steroid injecting men? I'd have to look at other studies to see if men's testosterone doesn't bounce back so much quicker than post-menopausal women's that increased aromatase might have negative effects, in men.

Would they worry about temporarily higher level of estrogen in these women that may be insignificant for them, but that could cause gyno in a man? I think not, and this might have happened without being notes in that study.

My biggest take-away from quickly skimming the article was that 3 months after 2.5 mg eod letro, bone resorption was still significantly elevated, and they speculate that letro might have additional negative impact on bone formation other than just lowering estrogen. Non-steroidal AI's scare me, the very molecules look like poisons.

I think arimidex is superior to exemestane in almost every aspect.

Why? Anyway, my point was that if aromatase regulation was much faster than testosterone regulation, suicidal inhibitors would not work very well, because the body would ramp up aromatase production. The same would obviously be true for non-suicidal inhibitors. I don't this is so, aromatase regulation is slower than testosterone regulation.

 

[Docd187123]

Ok, so that says that 12 weeks after seizing AI use, estrogen is pretty much back to normal, in post-menopausal women. Is is interesting and promising, but what does it say about the levels during those 12 weeks, for steroid injecting men? I'd have to look at other studies to see if men's testosterone doesn't bounce back so much quicker than post-menopausal women's that increased aromatase might have negative effects, in men.

It is evidence pointing towards there being no such thing as estrogen rebound. I've yet to see a single shred of objective evidence pointing to it's existence. You've only been speculating it exists but the burden of proof is on proving it's existence.

Taken from Anabolics 10th ed by William Llewellyn

Would they worry about temporarily higher level of estrogen in these women that may be insignificant for them, but that could cause gyno in a man? I think not, and this might have happened without being notes in that study.

My biggest take-away from quickly skimming the article was that 3 months after 2.5 mg eod letro, bone resorption was still significantly elevated, and they speculate that letro might have additional negative impact on bone formation other than just lowering estrogen. Non-steroidal AI's scare me, the very molecules look like poisons.

Why? Anyway, my point was that if aromatase regulation was much faster than testosterone regulation, suicidal inhibitors would not work very well, because the body would ramp up aromatase production. The same would obviously be true for non-suicidal inhibitors. I don't this is so, aromatase regulation is slower than testosterone regulation.

I'm not understanding what you're trying to get across here

 

[Docd187123]

I re-read some old threads, and perhaps "estrogen rebound" refers to a different phenomena than I have in mind.

Do you guys mean a long term or permanent increase in estrogen, establishing a new higher "baseline" so to speak, when you say estrogen rebound?

I only meant a temporary rebound in the sense that having a to high level of aromatase when stopping injections would lead to all your testosterone being converted into estrogen when endogenous T production ramps up, and this goes on for a while until aromatase production is reduced from the body sensing high E levels. But by then you'd already have tits. My impression is that this is what you're telling me does not happen.

Why would aromatase levels be too high after discontinuing injections? If you used an AI properly then your E2 levels will be right in range throughout the cycle and up until PCT started.

 

[barbelle]

Sorry I deleted that post because it seemed confusing.

I wasn't sure if the proper term was estrogen rebound or upregulation.

From what I understand, aromatase production is mainly influenced by estrogen/testosterone ratio. So if you have very high testosterone, you body produces more aromatase so that it can be converted into estrogen. The ramping up of aromatase production is quicker than the ramping down, and aromatase stays until it is eliminated by ubiquitination and it has a long half life.

The body thus has a fixed point of E/T that it will allow you to have, and it is even worse because if your T is too high then it might even decide to tilt that ratio in favor of estrogen.

This not correct? I guess since I've never read about people having to continuously up their AI dose while on TRT, I must be wrong somewhere.

 

[barbelle]

I think I had already read most of the threads on meso about rebound, but I suffer from information overload. Sorry if you guys think the issue has already been settled a long time ago.

Still, if estro rebound is a myth, why is a SERM better than Aromasin for PCT?