What does epiandro first convert to?

[netflixNchill]

Since its 2-step, what hormone is the first step. Wondering if there is a chance of that first hormone aromatizing

 

[Toren]

Epiandrosterone is first converted to either Androstanedione or Androstanediol. Both can be converted to Estrone in the human body. I have no idea of the percentage but I would guess that it is person-dependent (available enzymes in the body and current hormone levels/various feedback mechanisms).

 

[netflixNchill]

Finally someone with actual knowledge of this compound. So epiandro can infact convert to estrogen.. Great should have been running an AI this whole time for safe measure. Toren would 12.5mg eod of exemestane suffice?

 

[netflixNchill]

highlander31

 

[Toren]

I am by no means an expert on these compounds. I just do as much research (on as many things related to the field of steroids) as I can. I am definitely still learning myself. Honestly, people who specialize in these areas can stil learn everyday.

Here are the links (with more info) that I should have posted earlier for the isomers of Androstanediol.

Androstanediol (Alpha - Beta)

I would not normally suggest that people run an AI with a PH that ultimately converts to a known estrogen antagonist. Most people who run these PHs have no issue with excess estrogen binding. We all react differently though. Any time we disrupt the natural hormonal balance of our bodies, strange things can happen. We can have signs of high estrogen when our estrogen is within range or even below the normal range. The same thing can be attributed to prolactin as well. Our hormones work in unison. This is evident where we see people running massive amounts of powerful aromatase inhibitors (such as Letrozole) and yet are still having issues with estrogen binding to the receptors in breast tissue. At this point in time, we need something to block the receptor as E is probably already lower than it should be (under normal circumstances).

If peoplle are having issues with ER binding on a cycle that is not normally considered to be 'wet', their best bet is to get bloodwork to see what hormones are out of balance. Without bloodwork, personally, I would be tempted to lightly use Raloxifene or Tamoxifen. This of course can bring about it's own set of concerns but light, short duration usage should not be a concern for most people.

The balance of our hormones is what is most important as they work with eachother to maintain homeostasis through various checks and balances. Ultimately, some of us are just unlucky when these things get out of balance, while some of us seem to skate by without any noticeable issues at all.

 

[T-Bone]

I read elsewhere that it's doesn't convert to estrogen at all.

 

[Toren]

I read elsewhere that it's doesn't convert to estrogen at all.

I've read the same thing as well many times.

 

[T-Bone]

I've read the same thing as well many times.

WesleyInman I think was talking about it a while back.

 

[Toren]

5?-Androstane-3?,17?-diol (3?-diol), an estrogenic metabolite of 5?-dihydrotestosterone, is a potent modulator of estrogen receptor ER? expression in the ventral prostrate of adult rats

Androgen metabolite-dependent growth of hormone receptor-positive breast cancer as a possible aromatase inhibitor-resistance mechanism. - PubMed - NCBI

The androgen metabolite, 5

Interaction of Androst-5-ene-3

Edit:

The last link shows that there are many known androgens that can directly act as an agonist for the estrogen recpetor. Even if a hormone does not directly convert to one of the forms of estrogen, it can still act on the estrogen receptor. We also know that there are various hormones that act as agonists for both the androgen and estrogen receptor. These studies indicate that 5α-Androstane-3β,17β-diol (androstanediol), a known metabolite of, and precursor to DHT can act directly on the ER.

 

[StatePlan1425]

These links state that the metabolites themselves are estrogenic, not that they aromatize into estrogen (if I'm reading correctly) that would suggest an AI would be of little use.

Thanks for this thread. I have been procrastinating for some time asking about these metabolites.

 

[netflixNchill]

So if they're estrogenic but don't convert, what would be the course of action. I just popped half a pill of Exemstane (12.5mg) and trying to locate some local nolva. I may just drop the epiandro if the AI doesn't work

 

[Toren]

These links state that the metabolites themselves are estrogenic, not that they aromatize into estrogen (if I'm reading correctly) that would suggest an AI would be of little use.

Thanks for this thread. I have been procrastinating for some time asking about these metabolites.

Check my edit. I added some info while you posted. It seems to indicate that they can be considered an androgen or an estrogen as they can activate both receptors. The links do show that an AI would not be very hepful against these metabolites but they may be helpful to prevent other T to E conversion.

 

[Toren]

So if they're estrogenic but don't convert, what would be the course of action. I just popped half a pill of Exemstane (12.5mg) and trying to locate some local nolva. I may just drop the epiandro if the AI doesn't work

Nolva or Ralox seems to be the best bet if staying on cycle. It's certainly what I would do (short of going to a doctor) if having symptoms of over-stimulation of the breast ER.

 

[StatePlan1425]

Agree an AI will obviously help minimize aromatization of T and others to various estrogens. In terms of these DHT metabolites, what would be fascinating to know is what effects are being elicited when it is binding to the ER. Obviously, most of this research is being done in terms of BC and PC cell stimulation. Is it possible that the metabolites could actually be beneficial in terms of not allowing free E2 from attaching? Meaning, you take enough of this, you have more of these metabolites than free E2, less E2 attached on the ER and thus, a perceived "hardening" effect. Not really because of more DHT (though there would be conceivable more via the second conversion) but rather because E2 has no where to attach? I'm I way off base here??

 

[netflixNchill]

I have no clue lol I just want my right nipple to stop aching

 

[Toren]

Agree an AI will obviously help minimize aromatization of T and others to various estrogens. In terms of these DHT metabolites, what would be fascinating to know is what effects are being elicited when it is binding to the ER. Obviously, most of this research is being done in terms of BC and PC cell stimulation. Is it possible that the metabolites could actually be beneficial in terms of not allowing free E2 from attaching? Meaning, you take enough of this, you have more of these metabolites than free E2, less E2 attached on the ER and thus, a perceived "hardening" effect. Not really because of more DHT (though there would be conceivable more via the second conversion) but rather because E2 has no where to attach? I'm I way off base here??

Good questions. I'd love for someone a lot smarter and more knowledgeable than me to chime in here.

As far as what effects these metabolites might elicit, I guess that would depend on whether or not they would be considered partial or full agonists of the respective receptors in question. I would think binding affinity would also play a role in long-term effects of these metabolites as well. According to the last link I posted, E1 and E2 both have stronger binding affinity than 3b-diol so it seems that there would need to be a massive amount of the metabolite in order to show a stronger agonist action (on the ER) than E1 or E2. Having said that, I don't see how an ER agonist would elicit androgenic properties. The conversion or binding affinity of other androgenic hormones or metabolites in the body would be dominant in eliciting said effects.

I am basing this off of my interpretation of these studies and past research and not because I have some direct knowledge or degree in the area. Just wanted to put that out there. :]

 

[Toren]

I have no clue lol I just want my right nipple to stop aching

If it's aching. Nolva, 10mg for 3 days and I bet the ache goes away.

 

[netflixNchill]

Currently in the process of acquiring some

 

[hvactech]

i wouldnt worry too much about epiandro causing a rise in e2 levels or causing itching nips...

 

[netflixNchill]

When my arms are down it appears "fatty" but when I lift my arms it's flat as a door nail
I am about 14.5% BF

 

[netflixNchill]

i wouldnt worry too much about epiandro causing a rise in e2 levels or causing itching nips...

The only other thing I'm on is xosterone, and only at 350-450mg

 

[Toren]

i wouldnt worry too much about epiandro causing a rise in e2 levels or causing itching nips...

I defintiely agree with that statement. I hope people don't se this thread and freak out as most people will not have an issue with a prohormone to DHT. I do think that it hammers home why we always tell people to cover their bases and be prepared for anything when playing with hormones. We definitely all react in different ways.

 

[NoAddedHmones]

I defintiely agree with that statement. I hope people don't se this thread and freak out as most people will not have an issue with a prohormone to DHT. I do think that it hammers home why we always tell people to cover their bases and be prepared for anything when playing with hormones. We definitely all react in different ways.

Here is a chart showing Epiandrosterones pathways. It does not have potential to convert to any precursors of Estrogens or estrogen itself.

It is a two step conversion to DHT via conversion into A-dione then into DHT

or alternatively

into 3Beta-diol then into DHT

Neither intermediary compounds aromatize.

 

[StatePlan1425]

Thanks for the chart. Very helpful especially because it details the exact variants of enzymes (e.g. 17b HSD-1 vs 17b HSD-3)

I think we all agree, that there is no aromatization to E1,E2,E3. However, what we are wondering about are the intermediate metabolites. These appear to also attach and stimulate the ER to some degree.

Fascinating stuff here actually.

 

[Hastur]

Here is a chart showing Epiandrosterones pathways. It does not have potential to convert to any precursors of Estrogens or estrogen itself.

View attachment 132095

It is a two step conversion to DHT via conversion into A-dione then into DHT

or alternatively

into 3Beta-diol then into DHT

Neither intermediary compounds aromatize.

100% correct. Spot on. It is already "5-alpha reduced", it cannot convert or aromatize to Estrogen. And its intermediate metabolites do not convert or aromatize either for this reason. If you are concerned with the diones and diols of this particular compound interacting with the estrogen receptor, I have not seen evidence showing this to be the case, nor do anecdotal reports of EpiAndro use support this.

 

[StatePlan1425]

Thanks Hastur. What do you make of the studies posted by Toren?

 

[highlander31]

Both netflixNchill and myself have/are having nipple swelling /nipple issues with the Epiandro. I dropped it and after 2 days it completely cleared up. Stayed without it for another day or 2 and then added 1 cap in preworkout and 3-5 hours after my workout, boom, the swelling was back no mistake.

 

[YouBet33]

Both netflixNchill and myself have/are having nipple swelling /nipple issues with the Epiandro. I dropped it and after 2 days it completely cleared up. Stayed without it for another day or 2 and then added 1 cap in preworkout and 3-5 hours after my workout, boom, the swelling was back no mistake.

What brand are you using

 

[Toren]

Here is a chart showing Epiandrosterones pathways. It does not have potential to convert to any precursors of Estrogens or estrogen itself.

View attachment 132095

It is a two step conversion to DHT via conversion into A-dione then into DHT

or alternatively

into 3Beta-diol then into DHT

Neither intermediary compounds aromatize.

I've seen that graph (<-- including origin link in case anybody is interested) before as well as ones similar to it. It was always my understanding that DHT and it's metabolites could not aromatize nor exert any estrogenic effects or have any interaction with the ER. At the very least, the links and studies I posted indicate that the precursors/metabolites to DHT and Androsterone/Epiandrosterone (3-alpha and beta diol) can both interact with the ER to some degree and that the pathway does exist.

The wikipedia pages that I linked in my earlier post indicates that 5a-androstanedione is a metabolic precursor to both T and E, 5α-androstane-3α,17β-diol is a weak estrogen and that 5α-androstane-3β,17β-diol is a "potent estrogen". The references are at the bottom of the linked pages.

The book Molecular Mechanisms in Spermatogenesis states that "3b-diol binds ERb with higher affinity compared to E2, and must therfore be considered an estrogen". The book also states "Thirty years ago it was noted that 3b-diol is an estrogenic metabolite of DHT". [The source is not available for free]

This link also states that 3b-diol binds to the ER-beta.

I don't know what else to add. I'm just researching and reading and learning some stuff as I go about it. I've never seen anybody indicate that Epiandro or any of it's metabolites aromatize or are estrogenic in nature but I don't see anything here that disputes that either.

100% correct. Spot on. It is already "5-alpha reduced", it cannot convert or aromatize to Estrogen. And its intermediate metabolites do not convert or aromatize either for this reason. If you are concerned with the diones and diols of this particular compound interacting with the estrogen receptor, I have not seen evidence showing this to be the case, nor do anecdotal reports of EpiAndro use support this.

I haven't seen any anecdotal reports of EpiAndro causing issues either (other than in this thread) but I have seen many people run non-aromatizing compounds and even DHT-based compounds and have issues with gyno or pseudo-like gyno symptoms. Aching from over-activation of the ER also seems to happen at times with dry compounds. People just need to be prepared for ALL potential issues and make sure their bases are covered. I also hope kids read this and understand the potential pitfalls of playing with their hormones.

 

[Toren]

Let me just state that I am NOT suggesting that Epiandro is causing or will cause gyno!! I believe that some people are just prone to sides like these when they throw their hormonal state out of balance. I still believe that Epiandro will be a safe compound for most people and that these incidents are isolated in nature. DHT-based steroids do have an antagonistic effect on estrogen but to what degree that will avert issues is solely dependent on the individual. DHT has been shown to be a useful treatment or preventative agent against gynocomastia.

 

[Toren]

What brand are you using

I really hope this doesn't turn into a thread about specific brands. That just means it might eventually get locked or deleted as people get out of hand.

Just my two cents.

 

[netflixNchill]

It's settled, I'm dropping the epiandro and going to continue exemestane and hopefully acquire some nolva

 

[YouBet33]

I really hope this doesn't turn into a thread about specific brands. That just means it might eventually get locked or deleted as people get out of hand.

Just my two cents.

Valid point

 

[T-Bone]

Both netflixNchill and myself have/are having nipple swelling /nipple issues with the Epiandro. I dropped it and after 2 days it completely cleared up. Stayed without it for another day or 2 and then added 1 cap in preworkout and 3-5 hours after my workout, boom, the swelling was back no mistake.

 

[T-Bone]

You know stressing out so much about gyno can actually cause you to get gyno...Doesn't matter what you are taking. Don't believe me?. Look it up. Ask a doctor. Psychological problems can actually cause physical symptoms. Not calling you guys nuts or anything, I'm just letting you know that this is possible and I bet it happens more often than people think.

 

[netflixNchill]

I'm nuckin futs

 

[highlander31]

You know stressing out so much about gyno can actually cause you to get gyno...Doesn't matter what you are taking. Don't believe me?. Look it up. Ask a doctor. Psychological problems can actually cause physical symptoms. Not calling you guys nuts or anything, I'm just letting you know that this is possible and I bet it happens more often than people think.

True but this is not the case for me I was thinking it would do the opposite and harden me up especially the chest

 

[T-Bone]

http://www.webmd.com/mental-health/somatoform-disorders-symptoms-types-treatment

 

[Mister_T_]

Both netflixNchill and myself have/are having nipple swelling /nipple issues with the Epiandro. I dropped it and after 2 days it completely cleared up. Stayed without it for another day or 2 and then added 1 cap in preworkout and 3-5 hours after my workout, boom, the swelling was back no mistake.

did you find that by emptying the cap into pre workout that the effects were a little stronger during workout?

 

[brofessorx]

Toren you are confusing binding affinity (strength it binds with) with receptor interaction (signals being sent by compound)

Ideally serms like nolva bind with but have no interaction ( no communication) with the er.

The studies you posted ( I didn't read them all, first two an last one) that I read show the metabolite in question binds strongly with the er, but interaction is little to none.

It's the interaction with the estrogen receptor or progestin receptor that matter, when thinking of this subject.

Also, if it has 5a in the structure, it can not aromatize.

 

[StatePlan1425]

I think the term you're looking for is Intrinsic Activity. The higher the IA of a SERM, the more estrogenic the effects. Additionally, we have to remember the S in SERM. Both Tamoxifen and Raloxifene elicit an estrogenic effect in bone cells for example.

So what does all this have to do with the metabolites of EpiAndro? IMO, it means these guys are more complex than they're being marketed as. I think we may collectively be guilty of over simplifying the MOA. The very fact that BC and PC researchers are delving into trying to better understand what these guys are doing should clue us in to the complexity. I'm NOT saying EpiAndro is bad. It may turn out that they indeed have a "SERM like" effect in addition to some DHT conversion. But I, for one thought the AM family was about delving into the complex things as a collective...otherwise I could just go read FLEX... ;-)

All kidding aside, I realize that EpiAndro is one of the last legal PHs left, many guys anecdotally love it, and several companies have a financial interest in its continued popularity. All these things can still be true but wouldn't you like to know what it REALLY (or better, what it fully) does rather than "it's a two step conversion to DHT that cannot aromatize" ? If we don't know, we don't know but let's not be to quick to be dismissive.

 

[brofessorx]

Efficacy, intrinsic activity, interaction, no matter how you dress up a pig, it's still a pig.

Most users are happy with epiandro. I've only ran androsterone, but it didn't do anything for me.

Take home from this is results are user dependent an messing with your hormones can bring unwanted side effects.

Aromatizable or not, estrogenic sides are always a possibility.

 

[Toren]

Toren you are confusing binding affinity (strength it binds with) with receptor interaction (signals being sent by compound)

Ideally serms like nolva bind with but have no interaction ( no communication) with the er.

The studies you posted ( I didn't read them all, first two an last one) that I read show the metabolite in question binds strongly with the er, but interaction is little to none.

It's the interaction with the estrogen receptor or progestin receptor that matter, when thinking of this subject.

Also, if it has 5a in the structure, it can not aromatize.

I'm definitely not confusing binding affinity with receptor interaction; I do understand the difference. Receptor interaction also has a lot to do with hormone binding location on/in the cell.

Tamoxifen, as well as other SERMs, can be both an antagonist and an agonist, either binding and blocking regular cellular action or binding and stimulating regular cellular action. It depends on the location of the receptor interaction within the cell and within the body. This is why we know that it is both an anti-estrogen and can be estrogenic in nature as well.

If you have time, read the rest of the studies and links (I know I posted a lot). Some of them indicate that the precursors and metabolites of DHT (the ones I mentioned in this thread) not only bind to the ER (weakly) but are also full blown ER agonists and can signal gene transcription. That goes way above and beyond what most people (companies) would like us to believe. I'll admit that I'm not sure how involved this interaction is on a grand scale within our bodies but I do think it's interesting to know that these pathways do exist.

I think the term you're looking for is Intrinsic Activity. The higher the IA of a SERM, the more estrogenic the effects. Additionally, we have to remember the S in SERM. Both Tamoxifen and Raloxifene elicit an estrogenic effect in bone cells for example.

So what does all this have to do with the metabolites of EpiAndro? IMO, it means these guys are more complex than they're being marketed as. I think we may collectively be guilty of over simplifying the MOA. The very fact that BC and PC researchers are delving into trying to better understand what these guys are doing should clue us in to the complexity. I'm NOT saying EpiAndro is bad. It may turn out that they indeed have a "SERM like" effect in addition to some DHT conversion. But I, for one thought the AM family was about delving into the complex things as a collective...otherwise I could just go read FLEX... ;-)

All kidding aside, I realize that EpiAndro is one of the last legal PHs left, many guys anecdotally love it, and several companies have a financial interest in its continued popularity. All these things can still be true but wouldn't you like to know what it REALLY (or better, what it fully) does rather than "it's a two step conversion to DHT that cannot aromatize" ? If we don't know, we don't know but let's not be to quick to be dismissive.

Well said! I couldn't agree more.

Efficacy, intrinsic activity, interaction, no matter how you dress up a pig, it's still a pig.

Most users are happy with epiandro. I've only ran androsterone, but it didn't do anything for me.

Take home from this is results are user dependent an messing with your hormones can bring unwanted side effects.

Aromatizable or not, estrogenic sides are always a possibility.

I agree completely on your last three points. I made sure to mention all three in various posts in this thread. I'm definitely not bashing Epiandrosterone at all. I stumbled across some interesting info, and coupled with some stuff I read years ago and plenty of new information I was unaware of, I though it was a pretty intersting topic.

One thing I do know is that scientists 100 years from now will laugh at us. There is definitely so much we don't yet know.

 

[WesleyInman]

I see anti estro effects with myself and my clients with Randro and Epiandro. People who have gyno, or pegyno see shrinking of accumulations while on these products.

Of course we know that Nolva is the best option since it is a breast cancer drug that targets breast tissue at the cellular level..

With that being said, epiandro and androsterone are amazing DHT compounds. My personal favorites.

 

[brofessorx]

Of course

 

[chenk]

(old thread I know) i believe 400mg a day epi is shrinking the little bit of gyno that I had. My estrogen is low I can tell

I see anti estro effects with myself and my clients with Randro and Epiandro. People who have gyno, or pegyno see shrinking of accumulations while on these products.

Of course we know that Nolva is the best option since it is a breast cancer drug that targets breast tissue at the cellular level..

With that being said, epiandro and androsterone are amazing DHT compounds. My personal favorites.