[chrishoney]

Thank you for this explanation!

You can ignore my other query in your other thread if you wish, though even the links to your general searches would be fantastic to have.

While it may be very slightly over my head as endocrinology is not part of my scope of practice, I am obviously interested in it and can do the reading to get up to speed as necessary.

Also, from my reading of research literature, PM has been looked at to see how similar its estrogenic action was 17beta-estradiol in post menopausal women. So, while they were not specifically looking at how well it feminizes males, some research HAS looked at its estrogenic action as compared to estradiol in humans. For me, that's a strong pointer to it's potential for action in males since the biochemistry is basically the same.

Nice researching! This information will come in handy on another board I frequent on which the dominant opinion is that "natural products" are a waste of time and money and at best have a placebo effect.

Welcome to our little corner of breastnexus.

On a slightly different matter, you keep going on about PM being a testosterone down regulator & DHT blocker and slightly blocks aromatase, none of which I've ever read before ( not arguing just saying) but you seem to completely ignore the fact that it is a proven phyto-estrogen, which is its main ( and I thought, only) function in NBE - or have I missed something?

I'm sure there *are* studies that go on about the relative potency of particular estrogens vs their natural counterparts but the problem with leaving it at that is that not all phytoestrogens are made equal.

Some of them are still called phytoestrogens and yet they block the activity of estrogen in the body by competitively inhibiting the natural stuff, more strongly bind the receptor sites and then having much weaker action at the receptor sites.

What you want are herbs that have estrogenic effects that *don't* inhibit existing estrogens much and *also* add to the existing effects.


The problem you are asking is "how good is x herb compared to the natural estrogens in the body for doing exactly the same thing" but none of the researchers are asking that question!

There's an even worse problem. Asking the question "how good is x herb compared to natural estrogen in the body for doing exactly the same thing" is really asking 20 questions instead of just one.

Which means in addition to only being able to find the research that is being done it's also far easier to search for references on e.g. pureraria mirifica 5 alpha reductase or pureraria mirifica aromatase or pureraria 17 beta hydroxysteroid dehydrogenase than it is to look for pureraria mirifica competitive inhibitor estradiol/estriol/estrone, pureraria mirifica agonist estradiol/estriol/estone, pureraria mirifica binding receptor estradiol/estriol/estrone, pueraria relative stength estradiol/estriol/estrone or the other myriad combinations of things the three main estrogens do in the body (there are actually at least one more important one <17-alpha hydroxyestriol> and several lesser ones so the problem compounds even worse).

So to recap are far too many combinations of how the phytoestrogens could work as estrogens and the research *isn't* looking at that. The researchers definitely aren't searching for a better way to feminize someone using herbs. Instead they are looking for their effect on e.g. downregulating breast cancer by means of blocking aromatase or downregulating 5 alpha reductase to block prostate cancer etc etc

So i've sifted through the research looking for something *we* are not looking for and tying the scientific results back to my understanding of the steroid/enzyme tree in order to cut through the bullshit of what should work and what shouldn't work.

Which is not to say there' no value in knowing the many questions you're really asking because what you really want to know is "will this herb feminize me or will it not" but unfortunately as in everything that's not really a single question and the answer is often "yes but..."

Personally speaking I have a bachelors degree in chemistry so I can understand the research that is *there*.

For example gamma linoleneic acid and beta sitosterol are allegedly feminizing according to those who haven't read the research papers and just say they are phytoestrogens. Well yes they are phytoestrogens but while they partially block DHT like estradiol would they also block aromatase strongly and bind to the estradiol site more strongly than estradiol but then have much weaker action than estradiol would.

On the other hand there are other phytoestrognes like PM that doesn't seem to competitively block existing estrogens and also shift's the balance of the overall hormone system of the body towards estrogen dominance which is *good* from our perspective.

Likewise there are chemicals like spironolactone which are *not* phytoestrogens at all but they do things like block DHT strongly, do not inhibit aromatase at all and also downregulate testosterone back to andreneniostine.

Interestingly enough I looked at that this morning after I discovered what PM does to 17B-HSD type 2.

It looks to me that PM's mode of action includes being a slightly weaker version of spiro.

And there are people who feminize by taking only spiro with *no* phytoestrogens.

Anyways I hope your head is not spinning from this. I really enjoy this kind of thing.

[blomst]

Welcome, and thanks for making this great chart and bringing this research. I think these important details are ignored too much. It seems like it's assumed that if something has 'estrogenic activity' that it is beneficial for NBE, but there's so much to take into consideration. How does a certain phytoestrogen compare to estradiol? How does it affect the body's production or function of testosterone, or estradiol, or DHT, or aromatase, or 5ar? What other compounds are in the herb that could have different effects on these hormones and enzymes?

If all of this information was available I think NBE would have much better success rates. I suspect that many NBE programs are counterproductive. The main reason I'm not on PM now is that I've been worried that it would cause my already high T to shoot through the roof. I am mainly concerned with getting that T to turn into E.

[xxd]

Welcome, and thanks for making this great chart and bringing this research. I think these important details are ignored too much. It seems like it's assumed that if something has 'estrogenic activity' that it is beneficial for NBE, but there's so much to take into consideration. How does a certain phytoestrogen compare to estradiol? How does it affect the body's production or function of testosterone, or estradiol, or DHT, or aromatase, or 5ar? What other compounds are in the herb that could have different effects on these hormones and enzymes?

If all of this information was available I think NBE would have much better success rates. I suspect that many NBE programs are counterproductive. The main reason I'm not on PM now is that I've been worried that it would cause my already high T to shoot through the roof. I am mainly concerned with getting that T to turn into E.

I could only find three herbs that specifically raise aromatase which is the enzyme that converts T to E without blocking the estradiol receptors competitively:
licorice (which is the best at doing it but is dangerous) - multiplies aromatase production by 4.5 times
white peony (which is about half as potent as licorice) - multiplies aromatase production by 2 times
genistein (soy extract) - increases aromatase production by 40%.

D-aspartic-acid increases aromatase by 2X and estradiol by 80% but also increases T & DHT by 2x. With d-aspartic-acid you'd also need a DHT blocker.

That said, I don't know if increasing aromatase by this much would be enough by itself. It looks to me like PM doesn't increase T at all, quite the opposite. In fact I think if you take PM combined with one of the herbs above you're basically on a low dose sex change regime almost equivalent to taking hormones.

[Odile]

Hi xxd,

I'm a genetic female and since i've made some blood tests and found that i have low estrogen, low dhea and high delta-4-androstenedione, i've been thinking that the way to go for me is increase dhea, transforme testosterone and androstendione into estrogen via aromatase and at the same time blocking 5-alpha reductase.

So i've made some research trying to find out which herbs can help me and i actually can't find any dht blocker that doesn't inhibit aromatase at the same time.

So, as aromatase booster herbs i only can find white peony and licorice. But i've found now these two studies saying that licorice is actually an aromatase inhibitor.
http://www.greenmedinfo.com/article/lico...tive-agent
http://www.greenmedinfo.com/article/lico...ore-potent

And i've found that all the well-known dht blockers as saw palmetto, pumpkin seeds, pygeum, red reishi mushroom, reduce aromatase.

So it would be counter-productive taking white peony with some of these dht blockers, right?!
The only herb that seems not to be counter-productive taking with white peony as a dht blocker is actually white peony that seems to work as 5-alpha reductase blocker as well.

In the next study they talk again about licorice beeing a aromatase booster, that contradicts those two studies above. And the first sentence seems to contradict the the rest of the conclusions of the study. if someone can enlighten me!?

"Paeoniflorin, glycyrrhetic acid and glycyrrhizin decreased significantly the testosterone production but did not change that of delta 4-androstenedione and estradiol. Testosterone/delta 4-androstenedione production ratio was lowered significantly by paeoniflorin, glycyrrhetic acid and glycyrrhizin. Estradiol/testosterone production ratio was increased significantly by glycyrrhetic acid and not changed by paeoniflorin and glycyrrhizin. These results suggest that paeoniflorin, glycyrrhetic acid and glycyrrhizin affect the conversion between delta 4-androstenedione and testosterone to inhibit testosterone synthesis and stimulate the aromatase activity to promote estradiol synthesis by the direct action on the rat proestrous ovary.

[Scotti]

Anyways I hope your head is not spinning from this. I really enjoy this kind of thing.

Mine is...

Regardless, great post, thanks for sharing!

[Outsider]

...
And i've found that all the well-known dht blockers as saw palmetto, pumpkin seeds, pygeum, red reishi mushroom, reduce aromatase.

So it would be counter-productive taking white peony with some of these dht blockers, right?!
The only herb that seems not to be counter-productive taking with white peony as a dht blocker is actually white peony that seems to work as 5-alpha reductase blocker as well.
...

Those AA's you listed don't reduce aromatase, I'm not sure where you got that info from.
-edit- I was wrong, so disregard what I said about none of them reducing aromatase -edit-

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BO isn't an herb, but it causes aromatization, so d-aspartic-acid might potentiate the effects since the free T is converted to E. Though that might be too aggressive a combination.

[Odile]

well you can find several studies or articles refering that.

[Outsider]

well you can find several studies or articles refering that.

I apologize Odile, it appears I was indeed wrong, my fault for not looking harder.

I just found a study(Paul Stamets) that says red reishi reduces aromatase by 40%. With a little more digging I just found references to Pygeum and Pumpkin seed oil also being anti-aromatase.

Guess I need to drop the reishi from my BO program if that's the case. The Reishi extract powder was kind of nasty tasting anyways.

At least I still have WP.

Is there any other AA I can use that doesn't decrease aromatase?

[Odile]

The only dht blocker that i cannot find expressive information till now refering that also reduces aromatase is spearmint.
So maybe spearmint is the way to go with WP.

[Outsider]

I started out with spearmint leaf extract, but had to drop it from my program.

Spearmint decreases free T levels( free T is needed for aromatization), which is counter productive for BO or any other program built around aromatization.