Breast Growth For Genetic Males

I'm taking WP per the bottle instruction, 1 capsule twice daily. I'm not sure that's enough AA. In addition, I drink Spearmint Tea daily. What's the NBE recommended dose? Thx

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).

(14-09-2016, 11:10 PM)Lotus Wrote: [ -> ]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.

(26-01-2016, 10:25 PM)Lotus Wrote: [ -> ]

(26-01-2016, 07:28 PM)Lotus Wrote: [ -> ]

(26-01-2016, 03:09 PM)elainecd Wrote: [ -> ]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. 

(22-01-2016, 05:31 AM)Lotus Wrote: [ -> ]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

(26-01-2016, 08:58 PM)Atom Wrote: [ -> ]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

Quote: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.

(26-01-2016, 09:26 PM)Lotus Wrote: [ -> ]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.

(13-12-2016, 07:34 AM)BeautifulBambi Wrote: [ -> ]So I'm not very bright on all this stuff but from what I collect by this is that White Peony does just fine by it's self? Big words confuse me

Sorry about the big words, lol it could considerd gibberish sometimes....... WP is a companion herb for NBE in my opinion, in other words, pair it with a phytoestrogens and some healthy fats (walnuts, olive oil etc) and it fits in nice.

(13-12-2016, 10:30 AM)Stevenator Wrote: [ -> ]I'm taking WP per the bottle instruction, 1 capsule twice daily. I'm not sure that's enough AA. In addition, I drink Spearmint Tea daily. What's the NBE recommended dose? Thx

Depends on the WP product, if it's not standardized, up to 3 grams might be needed.

It's Swanson's capsules. 
I'll have to check the label.

(15-12-2016, 10:57 PM)Stevenator Wrote: [ -> ]It's Swanson's capsules. 
I'll have to check the label.

I believe it's not standerized (lol, I have a bottle sitting on the shelf too). Here's a few things about WP, or where I think the rubber needs to meet the road, or more to the point finding a suitable WP supplement that contains two compounds: 6'-O-galloylalbiflorin and pentagalloylglucos, they bind androgen receptors and inhibit DHT. Let's let science solve this puzzle of what WP does for NBE.....which I think we just did. The dose could be less than I calculated earlier if these compound and the main glycoside 3'-O-galloylpaeoniflorin are present would be estimated at 1 gram.

Additionally, testosterone/delta 4-androstenedione production ratio is also reduced (significantly) by paeoniflorin (white peony). 

(26-01-2016, 09:26 PM)Lotus Wrote: [ -> ]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.

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.


Testosterone/delta 4-androstenedione production ratio was lowered significantly by paeoniflorin, and two compounds, 6'-O-galloylalbiflorin and pentagalloylglucos bind androgen receptors and inhibit DHT.

That's so odd, because I got Swanson's (2-Pack) based on their reputation, etc., thinking it *would be* standardized.

(09-12-2013, 10:05 PM)Lotus Wrote: [ -> ]Can feminizing go too far?,

 Honestly I'm not one to do much primping before the mirror, but I notice there's a difference in my appearance the other day. Cheek bones has softened, chin narrowed, face thinned, hair won't sit as usual (even with gel), it's like boing, bounces right back up

 Forgot to say that my cheek bones where hurting for awhile and didn't put it together!

 But if you start to notice that if you pinch yourself and get a little EXTRA!!, perhaps that's the subtle changes we're looking for!...it's just the feel, or the texture of it, not the manhide we all know,lol

 But about feminizing, how far is too far?

L.

People say I've lost weight, which I haven't, I've gained. But they see it in my face, I'm guessing, as the whole fat transfer might be happening. But reading this post made me think of cheek pain I've been experiencing lately. I wonder where it will lead. Gotta laugh about the hair quote. It's totally true.

(18-12-2016, 04:54 AM)Stevenator Wrote: [ -> ]

(09-12-2013, 10:05 PM)Lotus Wrote: [ -> ]Can feminizing go too far?,

 Honestly I'm not one to do much primping before the mirror, but I notice there's a difference in my appearance the other day. Cheek bones has softened, chin narrowed, face thinned, hair won't sit as usual (even with gel), it's like boing, bounces right back up

 Forgot to say that my cheek bones where hurting for awhile and didn't put it together!

 But if you start to notice that if you pinch yourself and get a little EXTRA!!, perhaps that's the subtle changes we're looking for!...it's just the feel, or the texture of it, not the manhide we all know,lol

 But about feminizing, how far is too far?

L.

People say I've lost weight, which I haven't, I've gained. But they see it in my face, I'm guessing, as the whole fat transfer might be happening. But reading this post made me think of cheek pain I've been experiencing lately. I wonder where it will lead. Gotta laugh about the hair quote. It's totally true.

That's awesome Stevenator, it'll change more lol. A misconception is estrogen doesn't change bone structure, science says otherwise. That cheek bone pain was so bizarre, I couldn't figure out how E was affecting my cheek bones, sure enough estrogen receptors are in bone, and E has a part in bone growth and deterioration.......that's structural changes. 

Estrogen and bone metabolism.
Väänänen HK1, Härkönen PL.
Author information

Abstract
Estrogen plays an important role in the growth and maturation of bone as well as in the regulation of bone turnover in adult bone. During bone growth estrogen is needed for proper closure of epiphyseal growth plates both in females and in males. Also in young skeleton estrogen deficiency leads to increased osteoclast formation and enhanced bone resorption. In menopause estrogen deficiency induces cancellous as well as cortical bone loss. Highly increased bone resorption in cancellous bone leads to general bone loss and destruction of local architecture because of penetrative resorption and microfractures. In cortical bone the first response of estrogen withdrawal is enhanced endocortical resorption. Later, also intracortical porosity increases. These lead to decreased bone mass, disturbed architecture and reduced bone strength. At cellular level in bone estrogen inhibits differentiation of osteoclasts thus decreasing their number and reducing the amount of active remodeling units. This effect is probably mediated through some cytokines, IL-1 and IL-6 being strongest candidates. Estrogen regulates the expression of IL-6 in bone marrow cells by a so far unknown mechanism. It is still uncertain if the effects of estrogen on osteoblasts is direct or is due to coupling phenomenon between bone formation to resorption.
https://www.ncbi.nlm.nih.gov/pubmed/8865143
 

The hair sitting tight I assumed was because of DHT being more present, that's the nearest I could figure anyways, now it's wavey and curly at times if that makes any sense. 

I'm curious just how much it will change (?)
I dig PM's calming effects & breast growth.  
I've yet to see any long term before/after facial changes. 
Pharma changes are very obvious. I do get confused about
fat/muscle changes vs. bone, though 
That link/info you just posted sounds a bit on the scary side.