Conclusions to delayed gyno...?

[BHERTZ]

I am hoping that this thread is coming at just the right time.

At AM we all look out for each other. I feel that rather than having MANY ongoing threads which are slowly piecing together this delayed gyno jigsaw puzzle, I am hoping this thread can be used for people that wish to offer up their own personal opinions on the best way to combat this problem. This means...I want this thread to contain ONLY info about how to combat the idea of estrogen-rebound or a directly related issue.

Current knowledge, along with my own 2 cents:
~It appears that from this board (and others!) that delayed gyno is a severe problem with some new orals.
~It seems that delayed gyno is affecting people who PCT'ed both with AND without a SERM product, and is indepedent of cycle length.
~SD seems to be catching the brunt of this, however I feel that it's simply due to its popularlity. Let's face it, with more usage, more side effects should be expected to be reported (assumedly in quantity, not severity)

I wish to comment on the half life issue which has been beaten to death in other threads. I finally did the math, and based just on the numbers, there is only 1mcg (.001mg) of SD left in your system on the 25th day (120th hour into POST CYCLE) of a 21-day cycle. This assumes 20mg/day which seems to be commonplace around here.
[I did this simply by halfing all of the combined SD seen by your body on day 21.] Therefore, SD is not still floating around in your body 6 months after a cycle, so don't discuss it and clog this thread.

As already stated, I think we should discuss solely the idea of estrogen-rebound or any other mechanisms for delayed gyno.

andddd.....discuss!

 

[CDB]

Is there anyway upregulation of androgen receptors could matter in this? If I remember right when exogenous AAS are administered ARs upregulate, peak at 8-12 weeks and then dowregulate back to baseline. I have no idea if this is related to cycle length or whatever, but it did strike me that almost all the delayed gyno claims seem to be taking place in a similar timeframe.

Also, isn't Superdrol oxygen saturated DHT? DHT is one of the key hormones in regulation of the HPTA. It's my understanding that the main hormones that test gets converted to are estradiol through aromatization and DHT through the 5 alpha path, and that DHT is a crucial part of HPTA regulation especially when hormone levels are high, that it acts directly on the hypothalamus as a negative feedback loop. And while you want to discuss estrogen rebound, it's my understanding metabolites can have different half lives than their parent hormones.

So if you have some super long lived DHT metabolite in your system, and I would think more importantly if you used ATD as a PCT aid this could have the effect of blinding the hypothalamus through its SARM action to the high levels of this DHT metabolite. You could get a temporary semirecovery perhaps, and then once the ATD was discontinued you get suppressed again. So maybe it's not the PCT aids people don't use but what they did use that helps exacerbate the problem. Use of SERM would, I guess, produce a similar but less pronounced semi recovery. This delayed gyno problem seems to hit in the same way problems hit people when they start PCT on a long ester cycle too quickly before the hormones have cleared their system.

Or maybe I just need to pull my head out of my ass.

 

[BHERTZ]

no no no, your head is NOT in your ass. i followed as close as i could, and your logic seems right on par with the direction i was hoping this thread would take. :woohoo:

basically, as far as i can tell from my reading...
~SD is a saturated form of anadrol
~SD is reduced at C-5, therefore estrogen conversion is NOT an issue
~SD was expected to have very few metabolites.

from here i tried to dig up the metabolites. it appears that dromostanalone (aka drostanolon) is a metabolite of SD. it is a 2-methylated form of DHT.
the only websites i could find that listed half life data for this substance were not in english unfortunately.

so from here i started doing more searches, and some other people brought up good points - serms are extremely effective, but once off of them, you assumedly still have E to deal with, correct? a serm will block the receptor, but not bind to the actual enzyme and render it useless (as compared to ATD, etc.)...someone please correct me if i am wrong!

i am wondering if pct should be long (6+ weeks) with a possible ramping up OR pyramid of ATD products only? this may be a smoother transition regarding residual SD and/or present metabolites. all i know is that i plan on starting a methyl-drol/4AD cycle in a week, and i want to make sure the pct is where it needs to be.

any more ideas? i like where this is going so far...

 

[BHERTZ]

or is this totally off the mark? anyone?