[Lotus]

I can imagine you as a pharma rep demanding that the FDA prove that your company's drug isn't safe and effective. I'll play along, though.

Oh ok, now we're on Peony, throw in towel for Reishi?

Since no concentration is given, we can assume that it's lower than the concentrations that are listed. Let's be generous and call it 0.03% beta sitosterol. Paeoniflorin is 3.3-9.4%. One 600 mg capsule of LEF's extract contains 252 mg paeoniflorin. Assuming that both chemicals are concentrated to the same degree in the extraction process, we would expect to see 0.8-2.3 mg of beta sitosterol in each capsule. The effective dose in the study I cited was 60 mg/day, so 26-75 capsules of peony per day would be required. Impractical!

So first Peony didn't have a 5 ar, and now it's not enough?, I'm just playing along too. You're still missing at least 2 more....., you're also assuming (or at least overlooking) WP is strictly taken for a 5ar, when it's for boosting aromatase

(Peony extract blocks DHT through inhibiting the 5 alpha reductase enzyme as well as increasing aromatase) Personally speaking I have a bachelors degree in chemistry so I can understand the research that is *there* .

(which obviously you don't )

The mere fact it has 5ar properties needs to be stated, and it will be more than your simple (un-qualified calculations) you're still missing 2 more 5ar's its chemical composition.

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.

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.

Be *very* careful with licorice. Seriously. As nuts as you think it might sound you can DIE.