[Lancer]

With my program, I've been using between 1000mg to 1500mg of WP. I use WP during the day, since 1500mg of RR still makes me drowsy. Most of the year I was using 1500mg, so I tried cutting back to 1000mg for a month. I don't know if it did "anything" since I recently had a growth spurt of my right breast while using 1000mg, compared to the 1500mg.

I know every body's different, but I was wondering if 1500mg might be too high or not, thanks.

[Lancer]

Okay. Let me rephrase the question...

Would taking "too much" WP not be good?

I know too much PM is, but what about WP?

I'm thinking on going back to 1500mg again next month.

Thanks

[AliceDydro]

Too much WP can raise E levels beyond what your body will tolerate for keeping a steady level of T. Over time, that will lower T and thus the potential for E as a result. Stick with 1000 while you are seeing growth.

[Lotus]

Too much WP can raise E levels beyond what your body will tolerate for keeping a steady level of T. Over time, that will lower T and thus the potential for E as a result. Stick with 1000 while you are seeing growth.

How much is too much when the manufacturer recommended dosage is between 1,000mg to 3,000 mg?... I used 2,000mg a day (for a period when I was doing NBE and never had a problem). You don't cite scientific literature to support your claim. The glycosides are low in WP, so at best WP increase aromatase production by 2-3 fold. 

Kit,

White peony inhibits (type I) 5 alpha reductase, upregulates aromatase (testosterone converted to estrogen) a 2-3 fold effect (30 percent increase), sufficient. I like it for its anti-oxidant and anti-inflammatory properties, which WP reduces the inflammatory response of IL-6 (interleukin 6) a direct mediator of inflammation, many other benefits (blood purifier) too.

The other things mentioned could fit well for you. Good luck

Effect of paeoniflorin, glycyrrhizin and glycyrrhetic acid on ovarian androgen production

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 (by 2 to 3 fold) activity to promote estradiol synthesis by the direct action on the rat proestrous ovary. 
paeoniflorin-affects the conversion between delta 4-androstenedione and testosterone to inhibit testosterone synthesis and stimulate the aromatase activity to promote estradiol synthesis
https://pubmed.ncbi.nlm.nih.gov/1897494/


Paeoniflorin (aka-white peony) regulates the conversion of 4-androstenedione and testosterone, thereby inhibiting testosterone synthesis which promotes the enzyme aromatase making more estradiol. 
However, it needs to be the right kind of white peony meaning the highest standerized amount available...preferably generic. 
When you raise estradiol it lowers prolactin, so you don't need vitex for this reason.
Inhibiting gastrin lowers dopamine, which then lowers prolactin.

[Lotus]

WP Info: 

Androgen modulators from the roots of Paeonia lactiflora (paeoniae radix) grown and processed in nara prefecture, Japan.
Washida K1, Itoh Y, Iwashita T, Nomoto K.
Author information


Abstract
The monoterpene glycoside, 3'-O-galloylpaeoniflorin (1), and four known compounds, 6'-O-galloylalbiflorin (2), pentagalloylglucose (3), 6'-O-benzoylpaeoniflorin (4) and 6'-O-galloylpaeoniflorin (5), were isolated from the roots of Paeonia lactiflora that had been grown and processed in Nara prefecture, Japan, as androgen modulators. Their structures were elucidated based on spectroscopic analysis. Compounds 2 and 3 showed strong androgen receptor (AR) binding activity (IC(50) values 33.7 and 4.1 microg/ml, respectively), 1, 4 and 5 showed weak activity (20, 31 and 12% at 120 microg/ml, respectively). However, paeoniflorin (6) and albiflorin (7), the structures of which are related to 1, 2, 4 and 5, showed no activity. These results suggested that both the structure of albiflorin and the galloyl moiety are important for 2 to show strong AR binding activity. Furthermore, compounds 1-5 inhibited growth of an androgen-dependent LNCaP-FGC (prostate cancer cell line), and were indicated to be AR antagonists. Compounds 2 and 3 might be candidates as safe, natural anti-androgens.

glycyrrhetic acid on ovarian androgen production.
Takeuchi T1, Nishii O, Okamura T, Yaginuma T.
Author information


Abstract
We have shown that traditional herbal medicine, Shakuyaku-Kanzo-To consisted of Shakuyaku and Kanzo decreased serum testosterone levels in woman and rat. Therefore, paeoniflorin and glycyrrhizin, a main component of Shakuyaku and Kanzo, respectively, and glycyrrhetic acid, a metabolite of glycyrrhizin in vivo, were investigated for the steroid production in the rat ovary on the morning of proestrus. The homogenized tissues of one ovary were incubated in the Dulbecco's modified Eagle medium (pH 7.5) with 100 micrograms/ml of paeoniflorin, glycyrrhetic acid and glycyrrhizin and the medium only (the control) at 37 degrees C for 270 min. After the centrifugation, the concentrations of delta 4-androstenedione, testosterone and estradiol in the supernatants were determined by RIA. The production of the hormones expressed by [concentration x supernatant volume/weight of the ovary] was compared to the control. 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.

* White Peony (Paeonia lactiflora): Also known as Chinese Peony, the ornamental plant has been shown to contain at least two compounds, 6'-O-galloylalbiflorin andpentagalloylglucos, which bind to the androgen receptor and thusly inhibit its activation by testosterone, DHT and weaker androgens (Washida. 2009).

Hi there BN, I don't expect everyone to follow where I'm going with this new research for BN, but basically a short explanation is that I've found addtiional info that White Peony inhibits prostate cancer (which mostly is androgen driven) along with treating many other illnesses. Though one particular find is that WP gives support for treating diabetes, though I find it to be from β-cells (or generation of β-cells) which is newer science (or on the horizon) for the treatment of diabetes (via stem cell technology). 

But.....by inhibiting cancer, WP inhibits androgens, though I think we'll see it (inhibiting androgens aka DHT) in a new light through the PI3K/Akt/mTOR signaling pathway. (more on that later).

I'll be posting additional info on β-cells and the pancreas......

Paeonilorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling
http://www.ncbi.nlm.nih.gov/pmc/articles...2-1471.pdf

PI3K/Akt/mTOR signaling is mediated by Paeoniflorin

mTOR signaling impacts most major cellular functions, e.g. PI3K mediates G1 cell cycle progression and cyclin expression through the activation of AKT/mTOR/p70S6K signaling pathway in the prostate cancer cells.
http://www.sciencedirect.com/science/art...1X03018734

Paeoniflorin (100mg/kg) and EGCG inhibit B lymphocyte (B cell) proliferation and induced B lymphocyte apoptosis. In conclusion, BAFF/BAFF receptor might regulate B cell anti-apoptosis through PI3K/Akt/mTOR pathway. 

BAFF/BAFF-R involved in antibodies production of rats with collagen-induced arthritis via PI3K-Akt-mTOR signaling and the regulation of paeoniflorin.
http://www.ncbi.nlm.nih.gov/pubmed/22760071


Rapid determination of paeoniflorin from Paeonia sinjiang K. Y. Pan. by rapid resolution liquid chromatography
A rapid, effective, binary reverse phase rapid resolution liquid chromatographic method has been developed for the determination of Paeoniflorin extracted from Paeonia sinjiang K. Y. Pan
http://www.ncbi.nlm.nih.gov/pmc/articles...rt=classic


Pro-apoptotic effect of epigallo-catechin-3-gallate on B lymphocytes through regulating BAFF/PI3K/Akt/mTOR signaling in rats with collagen-induced arthritis.
http://www.ncbi.nlm.nih.gov/pubmed/22760071


regeneration of pancreatic β-cells.
Minami K1, Seino S2.
Author information


Abstract
Newly generated insulin-secreting cells for use in cell therapy for insulin-deficient diabetes mellitus require properties similar to those of native pancreatic β-cells. Pancreatic β-cells are highly specialized cells that produce a large amount of insulin, and secrete insulin in a regulated manner in response to glucose and other stimuli. It is not yet explained how the β-cells acquire this complex function during normal differentiation. So far, in vitro generation of insulin-secreting cells from embryonic stem cells, induced-pluripotent stem cells and adult stem/progenitor-like cells has been reported. However, most of these cells are functionally immature and show poor glucose-responsive insulin secretion compared to that of native pancreatic β-cells (or islets). Strategies to generate functional β-cells or a whole organ in vivo have also recently been proposed. Establishing a protocol to generate fully functional insulin-secreting cells that closely resemble native β-cells is a critical matter in regenerative medicine for diabetes. Understanding the physiological processes of differentiation, proliferation and regeneration of pancreatic β-cells might open the path to cell therapy to cure patients with absolute insulin deficiency. 
KEYWORDS:


Brain Res. 2015 Aug 27;1618:149-58. doi: 10.1016/j.brainres.2015.05.035. Epub 2015 Jun 3.
Paeoniflorin attenuates Aβ1-42-induced inflammation and chemotaxis of microglia in vitro and inhibits NF-κB- and VEGF/Flt-1 signaling pathways.
Liu H1, Wang J2, Wang J3, Wang P4, Xue Y5.
Author information

Abstract
Alzheimer׳s disease (AD) is a neurodegenerative disease with elusive pathogenesis, which accounts for most cases of dementia in the aged population. It has been reported that persistent inflammatory responses and excessive chemotaxis of microglia stimulated by beta-amyloid (Aβ) oligomers in the brain may accelerate the progression of AD. The present study was conducted to explore whether paeoniflorin (PF), a water-soluble monoterpene glycoside isolated from the root of Paeonia lactiflora Pallas, could attenuate Aβ1-42-induced toxic effects on primary and BV-2 microglial cells in vitro. Our data showed that PF pretreatment inhibited Aβ1-42-induced production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in rodent microglia. Also, the nuclear translocation of nuclear factor kappa B (NF-κB) subunit p65 and the phosphorylation of NF-κB inhibitor alpha (IκBα) in Aβ1-42-stimulated microglial cells were suppressed by PF administration. Moreover, PF treatment reduced the release of chemokine (C-X-C motif) ligand 1 (CXCL1) and chemokine (C-C motif) ligand 2 (CCL-2) from Aβ1-42-stimulated microglia. Additionally, application of PF inhibited the increases in vascular endothelial growth factor (VEGF) and VEGF receptor 1 (Flt-1) triggered by Aβ1-42, and resulted in a concomitant reduction in microglial chemotaxis. Restoration of VEGF was noted to counteract the inhibitory effect of PF, suggesting that PF mitigated Aβ1-42-elicited microglial migration at least partly by suppressing the VEGF/Flt-1 axis. In summary, in presence of Aβ1-42, PF pretreatment inhibited the excessive microglial activation and chemotaxis.

peony root extract has helped my areolas both in size and color. At least I think they have. If I don't do it once a day they def go back smaller.

Cool, 

White peony inhibits the 5 alpha reductase enzyme (from the conversion to DHT) in the sebaceous glands, which produces sebum. 

Thanks Elaine, good to hear from you.

I think lemon and orange peel could work too, try it. the fact they inhibit DHT (CYP17 inhibitor) makes sense too. 

In conclusion, we suggest in the present study that the supplementation with lemon polyphenols suppressed body weight gain and body fat accumulation by increasing the peroxisomal β-oxidation, which was likely mediated via up-regulation of the mRNA levels of PPARα in the liver. In addition, the levels of serum insulin, glucose and leptin were significantly improved by lemon polyphenols, thereby improving the insulin resistance. We suggest that a supplementation with lemon polyphenols may prevent or improve obesity and insulin resistance by modulating lipid metabolism and preventing metabolic syndrome as a representative, lifestyle-related cluster of diseases caused by an excessively high fat diet. 

Lemon Polyphenols Suppress Diet-induced Obesity by Up-Regulation of mRNA Levels of the Enzymes Involved in β-Oxidation in Mouse White Adipose Tissue
http://www.ncbi.nlm.nih.gov/pmc/articles...43-201.pdf

Have you seen this study?

Androgen Modulators from the Roots of Paeonia lactiflora (Paeoniae
Radix) Grown and Processed in Nara Prefecture, Japan
Kazuto W ASHIDA ,* , a Yoshiyuki I TOH , b Takashi I WASHITA , b and Kyosuke N OMOTO a

https://www.jstage.jst.go.jp/article/cpb...9_971/_pdf

We have thus isolated the first hormone modulators from
the roots of P. lactiflora. This is the first report of paeoni-
florin and albiflorin derivatives such as 1, 2, 4 and 5 showing
AR binding activity. Interestingly, compounds 6 and 7
showed no AR binding activity. The AR binding activity of
6-O-galloylalbiflorin (2) was much stronger than that of the
galloylpaeoniflorin derivatives (1, 5). These results suggested
that both the structure of albiflorin and the galloyl moiety
were important for 2 to show strong AR binding activity. Ad-
ditionally, 6-O-galloylpaeoniflorin (5) displayed the weakest
AR binding activity of the paeoniflorin derivatives (1, 4, 5).
The only structural differences between 2 and 5 are at C-4
and C-9, so the galloyl moiety of 2 might interact with the
carbonyl group of C-9 and/or the hydroxyl group of C-4.
It has been reported that 3 can inhibit growth of prostate
cancer LNCaP cells by two aspects including inhibition of 5-
a -reductase activity and expression of AR protein levels;
however, the AR binding activity of 3 has not been re-
ported. 12) We propose that 3 inhibits prostate cancer cell
growth partly by acting as an AR antagonist.
The AR binding activity of compound 3 was equivalent to
flutamide (IC 50 5.0 m M ), 13) which is in clinical use, and the
activity of compound 2 was also relatively strong. Additon-
ally, because Paeoniae radix was taken in long time as a
crude drug, compounds 2 and 3 might be candidates as safe,
natural AR antagonists.

That's a great find Atom, (thanks)

It looks like  6 -O-galloylalbiflorin and pentagalloylglucose acts like flutamide (a strong non-steroidal anti-androgen), but flutamide carries hepatic risks (toxicity). Aside from the health benefits of WP, the fact it inhibits human prostate cancer cells is a major find. 



So, in ovaries WP promotes aromatase, (I believe in the breasts too), inhibits DHT in sebum, inhibits prostate cancer cells, (which means it inhibits C17 @ CYP17 P450 enzyme, a strong anti-androgen. The lab dosage was 2 grams (I'll have to double check). Roots be king.

paeoniflorin (white peony) enhances phosphorylation and acquisition of the (DNA)deoxyribonucleic acid–binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1. 

Paeoniflorin, a novel heat shock protein–inducing compound 
https://www.ncbi.nlm.nih.gov/pmc/article...-4-378.pdf


Heat-shock factor-1, steroid hormones, and regulation of heat-shock protein expression in the heart.
Knowlton AA1, Sun L.
Author information


Abstract
Heat-shock proteins (HSPs) are an important family of endogenous, protective proteins. Overexpression of HSPs is protective against cardiac injury. Previously, we observed that dexamethasone activated heat-shock factor-1 (HSF-1) and induced a 60% increase in HSP72 in adult cardiac myocytes. The mechanism responsible for this effect of dexamethasone is unknown. Because HSP90 is known to bind the intracellular hormone receptors, we postulated that the interaction between HSP90, the receptors, and HSF was an important element in activation of HSF-1 by hormones. We hypothesized that there is an equilibrium between HSP90 and the various receptors/enzymes that it binds and that alteration in levels of certain hormones will alter the intracellular distribution of HSP90 and activate HSF-1. We report that, in adult cardiac myocytes, HSF-1 coimmunoprecipitates with HSP90. HSP90 redistributes in cardiac myocytes after treatment with 17beta-estradiol or progesterone. Estrogen and progesterone activate HSF-1 in adult male isolated cardiac myocytes, and this is followed by an increase in HSP72 protein. Testosterone had no effect on HSP levels; however, no androgen receptor was found in cardiac myocytes; therefore, testosterone would not be expected to effect binding of HSP90 to HSF. Geldanamycin, which inactivates HSP90 and prevents it from binding to receptors, activates HSF-1 and stimulates HSP72 synthesis. Activation of HSF-1 by steroid hormones, resulting from a change in the interaction of HSP90 and HSF-1, represents a novel pathway for regulating expression of HSPs. These findings may explain some of the gender differences in cardiovascular disease.

Paeoniflorin, a novel heat shock protein–inducing compound 
Dai Yan,1 Kiyoto Saito,1,2 Yuri Ohmi,1 Noriyo Fujie,1 and Kenzo Ohtsuka1 
1Laboratory of Cell and Stress Biology, Department of Environmental Biology, Chubu University, 1200 Matsumoto-cho, Kasugai, Aichi 487-8501, Japan 2Department of Medical Imaging and Information, Graduate School, Suzuka University of Medical Science, 1001-1 Suzuka, Mie 510-0293, Japan 
Abstract Heat shock proteins (HSPs) are induced by various physical, chemical, and biological stresses. HSPs are known to function as molecular chaperones, and they not only regulate various processes of protein biogenesis but also function as lifeguards against proteotoxic stresses. Because it is very useful to discover nontoxic chaperone- inducing compounds, we searched for them in herbal medicines. Some herbal medicines had positive effects on the induction of HSPs (Hsp70, Hsp40, and Hsp27) in cultured mammalian cells. We next examined 2 major constituents of these herbal medicines, glycyrrhizin and paeoniflorin, with previously defined chemical structures. Glycyrrhizin had an enhancing effect on the HSP induction by heat shock but could not induce HSPs by itself. In contrast, paeoniflorin had not only an enhancing effect but also an inducing effect by itself on HSP expression. Thus, paeoniflorin might be termed a chaperone inducer and glycyrrhizin a chaperone coinducer. Treatment of cells with paeoniflorin but not glycyrrhizin resulted in enhanced phosphorylation and acquisition of the deoxyribonucleic acid–binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1. Also, thermotolerance was induced by treatment with paeoniflorin but not glycyrrhizin. Paeoniflorin had no toxic effect at concentrations as high as 80 g/ mL (166.4 M). To our knowledge, this is the first report on the induction of HSPs by herbal medicines.

[Lancer]

Thank you, Lotus, for supplying this information. It was through this information that I chose WP to be one of the 2 AAs that I use in my program. It's just that it seems no one gave me any info on how much to take.

All I know, when I used 1000mg, it seemed that it took 2 weeks to "feel" like the PM was working. When I used 1500mg for almost all year, I never really noticed that 2 weeks for it to "feel" like it's working. And, it felt like not too much T came back into my system during my week off of all pills.

But I didn't know if the potential "high" amounts of E would inhibit breast growth.

Thanks for everything, everybody. I'm considering 1500mg, unless it won't be a "good" thing.

[Lancer]

It's just I experimented with different programs over the years, and I don't really remember which plan produced much breast growth the best.

2023 is the first year I did a program the right way.

My first year I didn't take any breaks of 2000mg PM whatsoever, and I went over half the year before I had to stop because of signs of blood clot.

My second year, I tried to do it similar to a natural woman's period cycle. I went most of the year before stopping because of blood clot risk.

This was the first year I went 3 weeks solid of 2000mg PM before taking the last week off of pills. I never had to stop for clot risk, but I was also using 1500mg WP instead 1000mg from my 2 previous years...

Believe it or not. I may switch back to the 'cycle' method, but I've never been on the same plan for more than a year.

So I am wrestling whether to keep my current plan for a second year or to go back to the cycle plan.

[Lancer]

And on top of that. During the breaks during the 'cycle' method of PM, I double-dosed the amount of FG pills during the off week. My right breast was leaking, even had some white...

My left breast didn't do anything. And now during my 2023 method, I STILL leak sometimes (including yesterday, but not white) with my right breast and nothing with my left. I haven't taken any FG all year.

My right feels much more developed and firm compared to my left, even though the amount tissue of both breasts are similar in feel. I know this, because I have my sister and aunt check for me.

I'm still wondering if it's because my left breast experienced partial budding when I was a teenager, and have more volume due to fat, while my right breast didn't do anything when I was younger and had much less volume.