Differences between R-DHEA and Super Epi DHEA

[TubZy]

There isn't much info on 5b-DHT but I also found this. It seems to be the easiest to understand.

5b or not 5b? - Total Flex BlogTotal Flex Blog

"The conformational change involved in 5b-reduction makes the steroid anything but flat, and an extremely poor fit for the receptor. By way of an example, 5a-DHT has 173 times stronger binding affinity than 5b-DHT. [3] 5b-reduced steroids are effectively inactive."

"The upshot being, if any superdrol clone was using a 5b-isomer of the methasteron molecule, it wouldn’t be “weaker”, it quite simply wouldn’t work."

"A few years ago people began to notice that certain brands of superdrol clones list the active ingredient as 2a,17a-dimethyl-etiocholan-3-one-17b-ol, believing this to indicate that the steroid inside is 5-b reduced version, or a “b-isomer” of superdrol. Many even go so far as to use this as an explanation for cycles with these drugs that do not meet the expectations of the user, citing the “weaker b-isomer” as the excuse for the poor results."

[TubZy]

Yup....you're right....doesn't answer my question....lol

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I don't want to give you the wrong answer haha. My guess is that since 5b-DHT is the "inactive androgen form" it could bind to the estrogen receptor beta much easier. I don't think he is saying "estrogenic" like gyno etc. (even though it is an agonist of ERb) just saying it is a much weaker version compared to androsterone. My post above mentions how much stronger 5a-DHT is compared to 5b-DHT in terms of binding (way way stronger). So 5b-DHT could just be a "by product" of the during the production of DHT which is why it is considered inactive, with weaker traits. It basically just assists in the conversion and deactivates afterwards.

[Cdsnuts]

I don't want to give you the wrong answer haha. My guess is that since 5b-DHT is the "inactive androgen form" it could bind to the estrogen receptor beta much easier. I don't think he is saying "estrogenic" like gyno etc. (even though it is an agonist of ERb) just saying it is a much weaker version compared to androsterone. My post above mentions how much stronger 5a-DHT is compared to 5b-DHT in terms of binding (way way stronger). So 5b-DHT could just be a "by product" of the during the production of DHT which is why it is considered inactive, with weaker traits. It basically just assists in the conversion and deactivates afterwards.

I find it interesting that it would bind to the estrogen receptor at all.

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[TubZy]

I find it interesting that it would bind to the estrogen receptor at all.

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It is not that uncommon really. DHEA can also bind to ERb as well yet is androgenic (and a precursor to DHT as well) and stimulates 5AR. A lot of variables are in play like how strongly it binds, dosage etc.

DHEA metabolites activate estrogen receptors alpha and beta


One of your herbs does as well (schizandra)

Extracts from Schizandra chinensis fruit activate estrogen receptors: a possible clue to its effects on nitric oxide-mediated vasorelaxation. - PubMed - NCBI

[Cdsnuts]

It is not that uncommon really. DHEA can also bind to ERb as well yet is androgenic (and a precursor to DHT as well) and stimulates 5AR. A lot of variables are in play like how strongly it binds, dosage etc.

DHEA metabolites activate estrogen receptors alpha and beta


One of your herbs does as well (schizandra)

Extracts from Schizandra chinensis fruit activate estrogen receptors: a possible clue to its effects on nitric oxide-mediated vasorelaxation. - PubMed - NCBI

Hopefully Nostrum chimes in here soon. This has been a great discussion.

I guess when I think estrogen receptor, I think that only estrogen or estrogen like hormones/substances would bind to and activate it. It seems counter intuitive that an androgen would bind to an estrogen receptor. I wonder what the biological purpose of this would be?

But, back to my original question, which is do the DHT precusor's actually get "used" prior to becoming DHT? If the differences in isomers are "felt" prior to becoming DHT, this would lead one to believe that they are actually being utilized in some way before becoming the target hormone. Otherwise we would just strictly feel the action of DHT, not the isomers.

[Nostrum420]

Well damn...aren't you handy to have around....lol.

It seems have you been extremely under utilized over here?

Okay, so then regardless of the isomer, the end result is DHT, but differences in the isomer account for the different feel of the hormone. So then actually does that mean that the hormone is being utilized before it turns into DHT because of the feelings given by the different isomers? Because if we would just feel the end result, or the target hormone, then we would just be feeling DHT, not the differences caused by the alpha or beta isomer, correct?

Essentially, yes, there is some binding to androgen receptors in the brain by the unconverted hormones.

[Cdsnuts]

Essentially, yes, there is some binding to androgen receptors in the brain by the unconverted hormones.

Okay....that makes perfect sense as there would be no other way for those difference to be felt otherwise.

I'm now curious as to what happens to them after they bind and illicit their effects in the cells? Do they then get used again as they continue on the chain of transformation? Or once it's bound, it's used as is and then that's it?

[delsolrob]

good thread here! Thanks Nos and CD!

[Cdsnuts]

good thread here! Thanks Nos and CD!

Wow....you're alive Rob.

Would still love to know the answer to this question here.

Edit: The answer is simply that the prohormones (pre DHT metabolites) are used by the body as a standalone which means SOME of the precursors bind to the AR before conversion eliciting their response which is slightly different then the response of the target hormone, DHT.

This is why the different isomers have different "feels" to them.