[Candace]

Beta sitosterol does inhibit 5-AR, but the content in peony is too low for your reference to specify it, so the effective peony dose would be impractical, and perhaps dangerous if it caused an overdose of the major components.

Oh really, then prove it!

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.

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!

[Lotus]

Somebody else provided you with the answers and you never acknowledged it.

Thanks, Candace. How reliable are product claims that they are "standardized?"

FWIW, here is some research on reishi I assembled. the first link includes a detailed article.

Estrogenic effects and 5-alpha reductase inhibiting effects of reishi - Ganoderma lucidum

http://www.academia.edu/6924010/Ganoderm...acrofungus

http://link.springer.com/article/10.1007...008-0992-2

http://www.raysahelian.com/ganoderma.html

http://www.nuskin.com/global/library/pdf...tudies.pdf

http://functionalfoodscenter.net/files/63502376.pdf

http://www.livestrong.com/article/526240...ne-levels/

http://www.rawforestfoodsblog.com/is-rei...ndrogenic/

[Lotus]

You have not provided a legitimate answer, you're just blowing smoke in a desperate attempt to avoid having to admit that you were wrong about something.

More proof-(you blew this info off).

To evaluate the safety and efficacy of an extract of Ganoderma lucidum that shows the strongest 5alpha-reductase inhibitory activity among the extracts of 19 edible and medicinal mushrooms by a double-blind, placebo-controlled, randomized and dose-ranging study in men with lower urinary tract symptoms (LUTS).
-------------------------------------------------------

Ganoderma lucidum: A Potent Pharmacological Macrofungus
http://www.researchgate.net/profile/Prak...acological

Page 722, anti-androgen activity, page 724 estrogenic activity

5α-reductase inhibition, androgen receptor binding activity, prostate cancer cell lines.
_____________________________

Target proteins of ganoderic acid DM provides clues to various pharmacological mechanisms

While screening mushrooms, we discovered that ethanol extracts of G. lingzhi showed the strongest 5α-reductase inhibitory activity among 19 species of mushrooms. Furthermore, treatment with the fruit body of G. lingzhi itself, or its ethanol extracts, significantly inhibited testosterone induced growth of the ventral prostate in rats9, 10. Our group previously isolated a series of triterpenoids from G. lingzhi. These compounds suppressed the proliferation of androgen-dependent and androgen-independent prostate cancer cell lines11 and estrogen-dependent MCF-7 cells12, and inhibited osteoclastic differentiation13. Among these triterpenoids, we found that only ganoderic acid DM (1, Fig. 1) had multiple functions, such as 5α-reductase inhibition, androgen receptor binding activity, prostate cancer cell, and proliferation and osteoclast differentiation11, 12, 13, 14. Although 1 affects different signaling pathways in different cell lines and has multiple functions, we have identified its target proteins, which explain and clarify the universal mechanism of its medicinal efficacy.

http://www.nature.com/srep/2012/121130/s...00905.html

________________________________________

Ganoderma - a therapeutic fungal biofactory.
http://www.researchgate.net/profile/Russell_Paterson/publication/6882609_Ganoderma_-_a_therapeutic_fungal_biofactory/links/00b7d5225ef366b7c6000000?ev=pub_ext_doc_dl&origin=publication_detail&inViewer=true

_________________________________________

Ganoderma lucidum inhibits proliferation and induces apoptosis in human prostate cancer cells PC-3
http://www.reishiessence.com/images/int_...cology.pdf

[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.

[Lotus]

I'm not done with Reishi:

In the last few years, the use of herbal therapies in alternative medicine has increased. Although the number of cancer patients using herbal dietary supple- ments is not exactly known, the evidence of the increasing use of dietary supplements in cancer treatment is reported.

Most prostate cancers initially depend on androgens for their growth. Therefore, they can often be controlled by various therapies that block the synthesis of androgens, their conversion to the active form dihydrotestosterone (DHT) or the function of the AR.

Ganoderma lucidum (Reishi) is part of the herbal mixture PC-SPES, which showed activity against hormone refractory disease in prostate cancer patients. Extracts of PC-SPES demonstrated estrogenic effects and decreased growth of hormone sensitive as well hormone-insensitive prostate cancer cells. In light of the results, these effects might be related not only to anti-cancer effects of G. lucidum (Reishi) but also to anti-androgen effects. Since excessive 5 alpha-reductase activity has been proposed to be a possible contributing factor in prostate cancer development or progression, the development and progression of prostate cancer may also be affected by diets containing inhibitors of 5 alpha reductase. So to understand how Reishi benefits 5 ar, you have to look at cancer research.

However, the major barrier to therapy is the eventual progression of the disease to what appears to be an androgen-independent stage. Two mechanisms have been proposed for the development of androgen-independent prostate cancers. The first mechanism is based on increased androgen receptor signaling caused by mutations in the AR that allow it to be activated by ligands other than DHT or by signaling pathways induced by a tyrosine kinase receptor, such as Her/2neu . The second mechanism is based on activation of growth-enhancing pathways that function independent of the AR, thus overcoming the growth inhibition caused by anti-androgen therapies, e.g. Ganoderma lucidum (Reishi mushroom).

Ganoderma lucidum exerts its effect on cancer cells by multiple mechanisms and may have potential therapeutic use for the prevention and treatment of cancer.
Introduction

The popular edible mushroom Ganoderma lucidum (Reishi) has been widely used for the general promotion of health and longevity in Asian countries. The dried powder of Ganoderma lucidum was popular as a cancer chemotherapy agent in ancient China. Ganoderma lucidum inhibits constitutively active transcription factors nuclear factor kappa B (NF-kappaB) and AP-1, which resulted in the inhibition of expression of urokinase-type plasminogen activator (uPA) and its receptor uPAR. Ganoderma lucidum also suppressed cell adhesion and cell migration of highly invasive breast and prostate cancer cells, suggesting its potency to reduce tumor invasiveness. Thus, Ganoderma lucidum clearly demonstrates anticancer activity in experiments with cancer cells and has possible therapeutic potential as a dietary supplement for an alternative therapy for breast and prostate cancer. However, because of the availability of Ganoderma lucidum from different sources, it is advisable to test its biologic activity.


Abstract
In humans, 5 alpha-reductase is involved in the development of benign prostatic hyperplasia. Triterpenoids isolated from ethanol extracts of Ganoderma lucidum (Fr.) Krast (Ganodermataceae) inhibited 5 alpha-reductase activity. The presence of the C-3 carbonyl group and of the C-26-alpha, beta-unsaturated carbonyl group was characteristic of almost all inhibitors isolated from G. lucidum.

5alpha-reductase inhibitory effect of triterpenoids isolated from Ganoderma lucidum.
http://www.ncbi.nlm.nih.gov/pubmed/16462054


Structure-activity relationship for inhibition of 5alpha-reductase by triterpenoids isolated from Ganoderma lucidum.
http://www.ncbi.nlm.nih.gov/pubmed/16962782


Ganoderma lucidum inhibits proliferation and induces apoptosis in human prostate cancer cells PC-3
http://www.spandidos-publications.com/ij...3/abstract

Ganoderma lucidum (Reishi mushroom) for cancer treatment.
http://www.ncbi.nlm.nih.gov/pubmed/22696372

Ganoderma lucidum suppresses motility of highly invasive breast and prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/12408995

Ganoderma lucidum inhibits proliferation and induces apoptosis in human prostate cancer cells PC-3.
http://www.ncbi.nlm.nih.gov/pubmed/1506733

Androgen receptor-dependent and -independent mechanisms mediate Ganoderma lucidum activities in LNCaP prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/17786330

[Lotus]

I did not ask for the IC50 of 5-alpha reductase, I asked for "And for each of them ... what is the IC50 for 5-AR?

Uh, yeah!, you did!

what is the IC50 for 5-AR,

You've also been reported for your troll behavior to the site administrator regarding harassment of another member, clearly 95% of your posts are to my threads, which show the pattern of abuse and harassment, you also haven't authored any of your own threads, there's plenty of other threads out there to call into question, your obsession with mine borders on stalking.

[Lotus]

I'm not trying to sugar coat Reishi, there's some known interactions like with any herb/med that everyone should be aware of if you're currently on or will consider using Reishi. consider. As always consult with your healthcare professionals.

Here's some info concerning Reishi, some of which has been already provided, thank you to those who contributed:

Ganoderma Lucidum Side Effects
http://www.livestrong.com/article/112069...e-effects/

Ganoderma Lucidum-Drug Interactions
http://cordyceps-sinensis.org/ganoderma-...de-effects

Reishi mushroom (Ganoderma lucidum)
http://v1.naturalstandard.com/naturalsta...rsion=true

Oral doses of 150-300mg three to four times daily have been standardized to contain 10-12.5% polysaccharides and 4% triterpenes per dose.

Dosing:
Adult (age ≥18):
Oral:
General: Doses of 2-6g raw reishi or an equivalent dosage of concentrated extract has been taken daily with meals.
Cancer: Doses of 600-1,800mg reishi mushroom as Ganopoly® has been taken three times daily for up to 12 weeks (10; 11; 16).
Chronic hepatitis B: Ganopoly® has been taken three times daily (dose unavailable) for 12 weeks (17).
Coronary heart disease: Ganopoly® has been taken three times daily (dose unavailable) for 12 weeks (18).
Diabetes: A dose of 1,800mg Ganopoly® has been taken three times daily for 12 weeks (19).
Hypertension: A clinical trial reported using linzhi extract (reishi) in daily doses of 55mg for four weeks (20).
Poisoning (Russula subnigricans): A dose of 100g reishi mushroom has been boiled in 600mL water per dose (21).
Postherpetic neuralgia: In clinical reports of reishi used in pain management for herpes zoster (shingles), reishi has been administered in doses from 36-72g dry weight in three divided doses daily for up to 10 days (22).
Proteinuria: Doses of 500-1,125mg reishi mushroom has been taken daily for up to 26 months (12; 13; 14).


Adenosine: Reishi mushroom contains high levels of adenosine (34).
Analgesics: Theoretically, reishi mushroom may increase the effects of analgesics. Reishi mushroom plus the traditional Chinese medicine (TCM) herbal combination formula, San Miao San (SMS), was reported to reduce pain in patients with active rheumatoid arthritis when taken in combination with standard arthritis medications (35). However, these effects cannot be definitively attributed to reishi mushroom because other herbs were also taken.
Anesthetics: Based on secondary sources, reishi mushroom may interact with anesthetics.
Antibiotics: Based on in vitro evidence, reishi mushroom and cefazolin may have synergistic effects against Bacillus subtilis and Klebsiella oxytoca (36); the combination of Ganoderma lucidum with ampicillin, cefazolin, oxytetracycline and chloramphenical may also have additive, antasgonistic or synergistic interactions (36).
Anticoagulants and antiplatelets: Based on laboratory evidence, reishi may affect platelet aggregation (15). Reishi mushroom contains high levels of adenosine, which may be responsible for inhibition of platelet aggregation (34; 37), but there is controversy in this area. Concomitant therapy with reishi and anticoagulants or NSAIDs may theoretically lead to additive effects or increased risk of bleeding due to potential prolongation of prothrombin time.
Antidiabetic agents: Based on animal evidence, reishi may reduce blood sugar levels and increase insulin levels (31; 32).
Antihypertensive drugs: Based on animal study, mycelium isolated from reishi mushroom (28) and a peptidoglycan of reishi (38) may have hypotensive effects. In laboratory study, the 70% MeOH extract of Ganoderma lucidum demonstrated an inhibitory activity on angiotensin converting enzyme (39).
Antilipemic agents: In laboratory study, reishi can inhibit the rate-limiting enzyme HMG-CoA in cholesterol biosynthesis (40).
Antineoplastic agents: Based on in vitro and animal studies, reishi mushroom may theoretically increase the effects of antineoplastic agents (3; 4; 5; 8; 9; 10; 11; 24; 30; 41; 42; 43; 44; 45; 46; 46; 47; 48; 49; 50; 51; 52; 53; 54; 55; 56).
Antiretroviral agents, protease inhibitors: Based on laboratory evidence, triterpenes isolated from Ganoderma lucidum may inhibit HIV or HIV protease (2; 57).
Antiviral agents: Based on laboratory evidence, the acidic protein bound polysaccharide (APBP) isolated from capophores of Ganoderma lucidum may have synergistic effects when administered with acyclovir (58).
Aspirin/aspirin-containing drugs: Based on laboratory evidence, reishi may affect platelet aggregation (15); adjustments may be necessary if the patient is receiving therapy aspirin.
Cardiovascular agents: Based on animal study, mycelium isolated from reishi mushroom (28) and a peptidoglycan of reishi (38) may have hypotensive effects. In laboratory study, the 70% MeOH extract of Ganoderma lucidum demonstrated an inhibitory activity on angiotensin converting enzyme (39).
CNS stimulants: Theoretically, use of reishi and amphetamines may result in an antagonistic effect.
Hepatotoxic agents: Theoretically, the risk of liver damage may increase when reishi mushroom powder is taken with drugs that are known to damage the liver (23). However, another hepatoprotectant study performed in rats showed that extracts from reishi-reduced free radicals that harm the liver (33)
Immunomodulators: Based on in vitro animal evidence, Ling zhi-8 may be a potent immunosuppressive drug in vitro able to delay rejection in allogeneic pancreatic islet transplantation (59).
Neurologic agents: Ganoderma lucidum spore preparations have been used in patients with atrophic myotonia (7). Based on secondary sources, use of reishi and amphetamines may result in an antagonistic effect.
Thyroid hormones: Based on secondary sources, reishi mushroom may interact with thyroid agents.

[Candace]

(By the way, the term is "antagonists" or "inhibitors", not "chemical constituents".)

constituent
a part of the whole; component.

(an essential part : component, element)

You wrote "chemical constituents for 5 ar", which doesn't make sense. You should have written "chemical constituents that inhibit 5-AR", or more succinctly "5-AR inhibitors".

Whaaaaat? This chart and this paper say otherwise. You also used to believe that DHT could not be aromatized. What changed your mind?

Ha!, you actually caught that, I do have a sense of humor though. DHT can't be converted to estrogen.

Raise of hands: how many people reading this find deliberate misinformation funny? Grow up, Lotus.

You have not provided a legitimate answer, you're just blowing smoke in a desperate attempt to avoid having to admit that you were wrong about something.

Wrong about what?, I'll admit when I'm wrong, (which I have, and offered an apology to all, can you admit when you're wrong?).

45-25-45 asked about getting a strong 5-AR inhibitor. My reply as it pertained to peony stated "I'm not aware of any evidence that White Peony inhibits 5-AR. It seems to just lower testosterone synthesis and increase aromatase." You responded to my statement by citing this paper which says nothing about peony vs 5-AR. It appears as though you misinterpreted the abstract and believed that it said green tea and peony inhibit 5-AR. But rather than admitting you made a mistake, you desperately combed through peony's chemicals looking for something that inhibits 5-AR. However, the only 5-AR-inhibiting chemicals in peony are too dilute to make a difference. Look at these generic examples: low concentrations of an inhibiting chemical are as ineffective as a concentration of zero, so your logic in declaring peony a 5-AR inhibitor is faulty. And since this is an applied science forum, one should only call an extract a 5-AR inhibitor if it has clinically-relevant 5-AR inhibition effects in humans.

You've painted yourself into a corner here. The next time someone asks for a 5-AR inhibitor recommendation, you can either 1) not say peony and thus tacitly agree with me, or 2) say peony and be guilty of providing bad advice.

You've already provided an example of me admitting I'm wrong. When I first read your posts about reishi as a 5-AR inhibitor I was enthusiastic and jumped on the bandwagon. But when I discovered the disturbingly low half-life of the triterpenes I wrote about my misgivings.

You never did address this:

I got a Marcy Recumbent Mag Cycle from Amazon and souped up the resistance by pulling off the housing and placing Neodymium Magnets (1/2 x 1/4 inch Disc N48) on to the existing magnet. (Wearing work gloves to avoid pinched skin!) I then adjusted the resistance to the lowest level that I wasn't spinning on and worked my way up over time. My thighs are now so huge that Vaseline will not prevent me from chafing while running - I need compression shorts for that. I think my butt got bigger too. Pics below, no feminization treatments ever used.

I don't mean to sound rude but how do you go from light toned skin to very dark toned skin... Sorry I'm a moderator for another site and I feel suspicious.

http://www.breastnexus.com/showthread.php?tid=21138&page=3

This is off-topic, creepy, and misleading. Emma did not quote me, and was obviously asking Cassi the question. I did not address the question because I did not take Cassi's pictures.

More proof-(you blew this info off).

To evaluate the safety and efficacy of an extract of Ganoderma lucidum that shows the strongest 5alpha-reductase inhibitory activity among the extracts of 19 edible and medicinal mushrooms by a double-blind, placebo-controlled, randomized and dose-ranging study in men with lower urinary tract symptoms (LUTS).
-------------------------------------------------------

Ganoderma lucidum: A Potent Pharmacological Macrofungus
http://www.researchgate.net/profile/Prak...acological

Page 722, anti-androgen activity, page 724 estrogenic activity

5α-reductase inhibition, androgen receptor binding activity, prostate cancer cell lines.
_____________________________

Target proteins of ganoderic acid DM provides clues to various pharmacological mechanisms

While screening mushrooms, we discovered that ethanol extracts of G. lingzhi showed the strongest 5α-reductase inhibitory activity among 19 species of mushrooms. Furthermore, treatment with the fruit body of G. lingzhi itself, or its ethanol extracts, significantly inhibited testosterone induced growth of the ventral prostate in rats9, 10. Our group previously isolated a series of triterpenoids from G. lingzhi. These compounds suppressed the proliferation of androgen-dependent and androgen-independent prostate cancer cell lines11 and estrogen-dependent MCF-7 cells12, and inhibited osteoclastic differentiation13. Among these triterpenoids, we found that only ganoderic acid DM (1, Fig. 1) had multiple functions, such as 5α-reductase inhibition, androgen receptor binding activity, prostate cancer cell, and proliferation and osteoclast differentiation11, 12, 13, 14. Although 1 affects different signaling pathways in different cell lines and has multiple functions, we have identified its target proteins, which explain and clarify the universal mechanism of its medicinal efficacy.

http://www.nature.com/srep/2012/121130/s...00905.html

________________________________________

Ganoderma - a therapeutic fungal biofactory.
http://www.researchgate.net/profile/Russell_Paterson/publication/6882609_Ganoderma_-_a_therapeutic_fungal_biofactory/links/00b7d5225ef366b7c6000000?ev=pub_ext_doc_dl&origin=publication_detail&inViewer=true

_________________________________________

Ganoderma lucidum inhibits proliferation and induces apoptosis in human prostate cancer cells PC-3
http://www.reishiessence.com/images/int_...cology.pdf

The first passage has already been addressed: I thanked you for finding it and I then used it to show that reishi is significantly inferior to beta-sitosterol for 5-AR inhibition in humans. The other links you provided contain no human data regarding 5-AR so are irrelevant to my concerns about short half-life interfering with effectiveness. Quit attacking a straw man.

[Lotus]

keep digging that hole, your days are numbered here (@ BN) , just by the mere fact of your troll harrasment.


More eveidene that disproves your troll nonsense: (Note the date of posting)

Hops raises prolactin and IGF-1 (lacking source). It's good during follicular.
Massage raises prolactin, and short intense exercise is supposed to raise IGF-1

Chasteberry is supposed to raise progesterone (lacking source), but lower excessive prolactin.

Here are estrogenic herbs... http://www.ncbi.nlm.nih.gov/pmc/articles...objectonly

Red reishi reduces DHT
White peony increases estrogen while lowering androgens.

Pueraria M. I heard on threads is both estrogenic and progestogenic.

Paeonia has been shown to positively influence low progesterone, reduce elevated androgens (testosterone) and acts to modulate estrogen and prolactin. In vitro, the active constituent paeoniflorin has been shown to affect the ovarian follicle by its action on the aromatase enzyme. Aromatase is important for follicle maturation, ovulation and corpus luteum function, steroid hormone synthesis and the regulation of the conversion of androgens to estrogens. The biofeedback in the pituitary and hypothalamus rely on aromatase to regulate prolactin and GnRH. The daily dose for Paeonia is 4.5 to 9 mL of a 1:2 dried plant extract.

http://www.townsendletter.com/Nov2004/phyto1104.htm

5α-Reductase inhibitory activity-guided fractionation of the EtOH extract of the fruiting body of Ganoderma lucidum (LEYSS.:FR.) KARST. (Ganodermataceae), which is called Reishi, or Mannentake in Japan and Lingzhi in China, led to the isolation of two active compounds which were ganoderic acid DM and 5α-lanosta-7,9(11),24-triene-15α,26-dihydroxy-3-one with an IC50 of 10.6 μM and 41.9 μM respectively. A carboxyl group of side chain of ganoderic acid DM is essential to elicit the inhibitory activity because of much less activity of its methyl ester.
http://www.ncbi.nlm.nih.gov/pubmed/16462054

[Lotus]

Paeonia lactiflora (White peony)
Paeonia lactiflora has been used for gynecological conditions by both Chinese and Western herbalists, and is used by Western herbalists for PCOS, hyperprolactinemia, endometriosis, ovarian failure and androgen excess. Paeonia has been shown to positively influence low progesterone, reduce elevated androgens (testosterone) and acts to modulate estrogen and prolactin.7 In vitro, the active constituent paeoniflorin has been shown to affect the ovarian follicle by its action on the aromatase enzyme.8 Aromatase is important for follicle maturation, ovulation and corpus luteum function, steroid hormone synthesis and the regulation of the conversion of androgens to estrogens. The biofeedback in the pituitary and hypothalamus rely on aromatase to regulate prolactin and GnRH. The daily dose for Paeonia is 4.5 to 9 mL of a 1:2 dried plant extract.9

The traditional Chinese/Kanpo formula known as Shakuyaku-Kanzo-To or TJ-68, which is a decoction of Glycyrrhiza glabra and Paeonia lactiflora, has been the subject of a number of clinical trials, all of which demonstrate activity in the hormonal regulation of androgens. In one trial involving eight women with hyperandrogenism and oligomenorrhea, the formula was given for 2 to 8 weeks. This combination regulated the LH to FSH ratio. Over this period of time, serum testosterone levels decreased to less than 50 ng/dL and this resulted in seven of the eight women ovulating regularly.10

Another trial involved 20 women diagnosed with PCOS. The formula was successful in lowering testosterone in 90% of the women, of which 25% went on to conceive.11 It is suggested that it acts directly on the ovary, increasing the activity of aromatase, which promotes the synthesis of estradiol from testosterone, thus lowering serum testosterone levels. It also seems to regulate the LH to FSH ratio.12



Effect of TCM herbal TJ-68 (shakuyaku-kanzo-to) on polycystic ovarian disease

JANUARY 28, 2014 BY SOUL CYSTERLEAVE A COMMENT

Effect of TJ-68 (shakuyaku-kanzo-to) on polycystic ovarian disease.

Takahashi K, Kitao M. Department of Obstetrics and Gynecology, Shimane Medical University, Izumo, Japan. Int J Fertil Menopausal Stud. 1994 Mar-Apr;39(2):69-76

OBJECTIVE–To investigate the effect of an herbal medicine, Shakuyaku-Kanzo-To (TJ-68), on endocrine variables in patients with polycystic ovarian disease (PCOD).

SETTING–Medical university hospital.

PATIENTS AND INTERVENTIONS–Thirty-four Japanese women with PCOD were treated daily with 7.5 g of TJ-68 for 24 weeks. Testosterone (T), free-testosterone (free-T), sex hormone binding globulin (SHBG), LH, FSH, estrone, 17 beta-estradiol, 3,4-dihydroxyphenylglycol (DOPEG), and 3, 4-dihydroxyphenylacetic acid (DOPAC) were examined.

RESULTS–No side effects were observed in any cases. At 4 weeks after initiation of treatment, serum T and free-T levels significantly decreased, while SHBG was not significantly elevated. Meanwhile, after 12 weeks of treatment, the mean serum T level of the patients who became pregnant decreased to 35% of that before the treatment, but levels did not change in the patients who failed to conceive. There was no significant difference in estrone/estradiol ratio before and after treatment, but the estradiol/testosterone ratio increased significantly after 4 weeks of treatment. The LH/FSH ratio after 24 weeks of treatment was significantly lower than that before treatment. DOPEG and the DOPEG/DOPAC ratio significantly decreased after 4 weeks of treatment.

CONCLUSIONS–It is suggested that TJ-68 acts directly on the ovary first, increasing the activity of aromatase, which promotes the synthesis of estradiol from testosterone, thus lowering serum T levels. Furthermore, the effect on catecholamines results in gradually improving the dissociate phenomenon of LH/FSH ratio. Therefore, TJ-68 is an effective herbal medicine for decreasing serum free-T levels and achieving pregnancy in patients with PCOD.