Also I was speaking about the possibility that superdrol could effect the er, not m1t. So your take on anadrols estrogenic effects as well?
Anadrol is a mystery to me that I should look into when I have time. Might convert to an estrogenic metabolite. Or, it could be this:
neither convert to DHT. anadrol is a DHT derivative however. halo OTOH is not a DHT derivative, it is a testosterone derivative
Also, neither should aromatize to estrogens. However, anadrol may have intrinsic estrogenic activity (binds directly to the estrogen receptor). I say this because like estrogens, anadrol has an acidic proton on the outer side of the A-ring (and this property may be very important to estrogen's binding to estrogen receptor)
Source: forum.bodybuilding.com/showpost.php?p=7414027&postcount=20
That is an old quote (2005) from Patrick Arnold. He may have come across research indicating something else since then. Someone should ask.
As far as superdrol, some say it is more androgenic than Vida tests etc. would indicate. If so, it shouldn't cause estrogenic sides, as it wouldn't seem to be able to bind to the ER being 5-alpha reduced, and its androgenic activity would oppose estrogenic effects. If it is indeed as low on the androgenic potency as Vida says, that could be the cause, but I would still think the lengthy action (long half life from 17a-methylation) of it and decent androgenic potency, along with being taken in supraphysiological levels for an androgen would combat estrogenic sides. In that case, it could be from contamination with another steroid from the manufacturer.
Another question is this; when are the estrogenic sides experienced? Many 17a methyls lower SHBG. If the steroid is administered and SHBG is reduced in the first few days, the initial circulating T and E, much of it bound to SHBG and serum albumin produced before HPTA shutdown starts could be freed up to act at the ER. The freed estrogen could act directly, and the freed testosterone would be likely to convert via aromatase to estrogen and do the same. Circulating aromatase can't act on superdrol so it would be available to act on the freed T. So estrogenic sides at the cycle onset might be possibly reasonable. Also, estrogenic sides post cycle while T/E ratio is low and superdrol is no longer circulating to oppose estrogen makes sense as well. Estrogenic effects during the cycle would be the toughest to explain. I am just throwing out ideas here.