Estrogen rebound on cold turkey?

[Docd187123]

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?

1) There's not much studies done on PCTs. Dr. Scally's protocol which includes HCG, Clomid, and nolva is probably one of the most clinically effective and supported protocols in existence.

2) one possible difference is that clomid acts as an estrogen at the pituitary sensitizing it to the action of GnRH. Aromasin does not do this.

3) the major roadblock to recovery as stated by Llewellyn is not restoration of LH but Leydig cell sensitivity to LH. HCG would be used to help with this. HCG also increases intra-testicular E2 which cannot be treated with an AI meaning you'd want to use a SERM for this not aromasin.

 

[BirdieNumNum]

Estrogen rebound occurs definately. Regardless of what anyone says.

 

[GigaloRob]

Estrogen rebound occurs definately. Regardless of what anyone says.

Attention everyone Jay Monks has spoken. Forget that there is no studies,facts, or data to back up this claim. Bro science is not actual science.

 

[BirdieNumNum]

Who cares my friend. The fact it hasnt been looked into or studied enough, no data proving... It has happened to me and pretty much messed every effort at restoring my HPTA. Ive managed to increase my natty test and watch it diminish... Followed by extreme cardiac pains. Even blockages in my blood vessels - which im sure is down to too much e2. Currently on armidex first time ever and have seen my test level rise dramatically But e2 is still above range. I accept there is no "proof" but i know it occurs.

 

[GigaloRob]

Who cares my friend. The fact it hasnt been looked into or studied enough, no data proving... It has happened to me and pretty much messed every effort at restoring my HPTA. Ive managed to increase my natty test and watch it diminish... Followed by extreme cardiac pains. Even blockages in my blood vessels - which im sure is down to too much e2. Currently on armidex first time ever and have seen my test level rise dramatically But e2 is still above range. I accept there is no "proof" but i know it occurs.

Yeah i mean who cares about actual facts when you can provide anecdotal evidence that means nothing. Ask yourself, if you know it occurs then why is there not one single piece of evidence to prove your point? Is it because the intellect of Jay Monks surpasses every medical/professional mind in this area? The easy obvious answer is no. You are free to believe what you want but please stop trying to pass off your so called "experience" as absolute fact.

There are also people to this day claiming to have seen Elvis but that does not mean I should be checking stub hub for his comeback tour dates.

 

[BirdieNumNum]

Yes it is a shame that there is no evidence to back up what i am saying. The reason for this may be, that it has not actually been studied? Maybe i was predisposed to increased aromatize activity but i have not noticed or felt a single symptom until steroids were used. Again i know it to be true whether you do or not. I must add this is over a year since i taken any steroids.

 

[Northern Nutrition]

The endocrine system is not made of rubber.

 

[barbelle]

Taken from Anabolics 10th ed by William Llewellyn
View attachment 31348

That looks like cypionate/enanthate. With propionate, the curve would have a steeper slope from week one to two, and the levels would start rising from 2mg/ml from week 2 or 3. Those 2mg/ml would be overwhelmed by aromatase levels upregulated to cope with 4.5mg/ml or more, is my thinking.

If there is no estrogen rebound, and I accept your bro science saying that there isn't, where does the aromatase go? Something must be happening apart form just half lives doing their thing, or there would be rebound. So what is it?

In another thread, somebody said that non-aromatising steroids like tren does not cause aromatase upregulation (AU). Is this really true? That surprises me. I thought any androgenic activity would cause AU. Tren seems to have strong androgenic activity in the brain.

From what I remember, androgenic activity, testosterone levels, and estrogen/testosterone ratio all influence aromatase production, as the body tries to keep homeostasis, and high androgen levels are energy expensive (in an evolutionary sense). Your body is constantly trying to make you fat and lazy, and is expecting your surroundings to provide you with stimulus to require you to become masculine only if necessary.

Has Dr. Scally published any studies on hormone fluctuations post steroid use? I couldn't find any.

 

[Docd187123]

That looks like cypionate/enanthate. With propionate, the curve would have a steeper slope from week one to two, and the levels would start rising from 2mg/ml from week 2 or 3. Those 2mg/ml would be overwhelmed by aromatase levels upregulated to cope with 4.5mg/ml or more, is my thinking.

If there is no estrogen rebound, and I accept your bro science saying that there isn't, where does the aromatase go? Something must be happening apart form just half lives doing their thing, or there would be rebound. So what is it?

In another thread, somebody said that non-aromatising steroids like tren does not cause aromatase upregulation (AU). Is this really true? That surprises me. I thought any androgenic activity would cause AU. Tren seems to have strong androgenic activity in the brain.

From what I remember, androgenic activity, testosterone levels, and estrogen/testosterone ratio all influence aromatase production, as the body tries to keep homeostasis, and high androgen levels are energy expensive (in an evolutionary sense). Your body is constantly trying to make you fat and lazy, and is expecting your surroundings to provide you with stimulus to require you to become masculine only if necessary.

Has Dr. Scally published any studies on hormone fluctuations post steroid use? I couldn't find any.

Broscience? I was paraphrasing one of the most respected doctors in the field of endocrinology who, through my research on the topic, I found to be 100% correct.

You made the claim of estrogen rebound occurring. The burden of proof is on you to show this with more than theoretical speculation.

Yes compounds like tren don't aromatize. There are also some that do aromatize obviously and even ones that don't aromatize but they or their metabolites can bind to and activate the ER such as oxymetholone.

 

[BirdieNumNum]

How Would one cause aromatase downregulation? by taking aromasin?

 

[Dr JIM]

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...

There is plenty of data that PROVES the term dubbed "estrogen rebound" by PED forum "bros" is a concocted myth, that at best is the result of non-scientists erroneously extrapolating petri disk studies to humans.

Heck do you even know what a teratogen is, and if so why would post-menopausal females be concerned about it, lol!

 

[Dr JIM]

Estrogen rebound occurs definately. Regardless of what anyone says.

Yep and the sky is green with purple pokey dots, "regardless of what ANYONE says".

Now that's real science LMAO!

 

[Dr JIM]

That looks like cypionate/enanthate. With propionate, the curve would have a steeper slope from week one to two, and the levels would start rising from 2mg/ml from week 2 or 3. Those 2mg/ml would be overwhelmed by aromatase levels upregulated to cope with 4.5mg/ml or more, is my thinking.

If there is no estrogen rebound, and I accept your bro science saying that there isn't, where does the aromatase go? Something must be happening apart form just half lives doing their thing, or there would be rebound. So what is it?

In another thread, somebody said that non-aromatising steroids like tren does not cause aromatase upregulation (AU). Is this really true? That surprises me. I thought any androgenic activity would cause AU. Tren seems to have strong androgenic activity in the brain.

From what I remember, androgenic activity, testosterone levels, and estrogen/testosterone ratio all influence aromatase production, as the body tries to keep homeostasis, and high androgen levels are energy expensive (in an evolutionary sense). Your body is constantly trying to make you fat and lazy, and is expecting your surroundings to provide you with stimulus to require you to become masculine only if necessary.

Has Dr. Scally published any studies on hormone fluctuations post steroid use? I couldn't find any.

Aromatase activity is genetically FIXED and does NOT fluctuate based on the amount of substrate available in serum

There are multiple studies in both PMP females and in Hypogonadal males that show the TT:E-2 ratio remains relatively constant DURING and AFTER SERM therapy.

The presence of "E-2 rebound" would require an opposing effect such as either a E-2 level that EXCEEDS pretreatment values or a TT:E-2 ratio reversal!

 

[caveman72]

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?

I'm sorry it was not calked prid. its called d.I.m. but regardless if I got the initials correct. it might be d.e.m. but its made from broccoli I believe but its a natural way to battle estrogen. Google one eod those two they even use it in. some over the counter supplements

 

[Dr JIM]

I'm sorry it was not calked prid. its called d.I.m. but regardless if I got the initials correct. it might be d.e.m. but its made from broccoli I believe but its a natural way to battle estrogen. Google one eod those two they even use it in. some over the counter supplements

Unfortunately like most supps they fail to post any evidence that supports the efficacy of such "therapy".

 

[BirdieNumNum]

I myself have had a rebound like effect of e2. So please shoot me for believing it to be true.

 

[Docd187123]

I myself have had a rebound like effect of e2. So please shoot me for believing it to be true.

Please post up your pre and post bloodwork along with what protocol and compounds you were following.

 

[BirdieNumNum]

If Aromatase activity increases dramatically whilst on a heavy cycle, leading to a down regulation of 5 alpha reductase, leaving non if any DHT in the body.. wouldnt hyperestrogenism set in? ...estrogen rebound.

 

[Northern Nutrition]

I myself have had a rebound like effect of e2. So please shoot me for believing it to be true.

Bang!

 

[Dr JIM]

If Aromatase activity increases dramatically whilst on a heavy cycle, leading to a down regulation of 5 alpha reductase, leaving non if any DHT in the body.. wouldnt hyperestrogenism set in? ...estrogen rebound.

With comments of that nature it's clear your haven't the faintest idea about what in-vivo pharmacologic "rebound" actually is.

But give it your best shot or continue parroting "bro science" never knowing what the facts are.