Okay, so, I read through this entire thread. I have just one question: what form of white peony would one use? I did a quick search on Google and it is available as a tea, liquid extracts, and 'immune support' capsules.

Liquid extract would obviously work best as a topical treatment, but which of the other two is better for oral administration?

The tea isn't white peony, it's white tea, (credit Amber). The real WP exists in extract or capsule form, life extension has a capsule brand, extract blends are pretty popular. But, I'd spread the dosage over 3-4 times in a typical day, for instance.....15 minutes after each dose of E2, which is about the time it's metabolized. This way, the influence of aromatase is shifted away to form DHT, which as we all know DHT will ruin a perfectly good day of E2.

Btw, vitamin C improves the bioavailability of E2, so does egg whites.

Okay, so, liquid extract for topical, capsule for oral, grapefruit and vitamin d to spike E levels and further boost aromatase, continue working out to boost base T production for fuel...and find an endocrinologist to prescribe external E or win the lotto and buy a ton of Purafem.

Lol okay, extract is for liquid delivery too, I haven't tried making WP extract into a topical, a good carrier oil will be needed that includes Linolenic, (borage oil, evening primrose oil).

Be very careful with grapefruit juice, one needs to know exactly how their body responds to other meds before combining with grapefruit juice.

Good luck

That's good idea adding k2, how do you supplement it?, I tried grass fed butter in some coffee that Pom suggested, not bad. Egg yolks, gouda and brie cheese are other sources of k2 from what I've read.

Hi Lotus! I'm sorry I missed your reply before!

I get my K2 from Amazon in the UK of all places.

http://www.amazon.co.uk/gp/product/B00QQRQQH2

I believe the kind (MK-7) is important. This product comes from Natto (fermented soybeans). Importantly, is appears not possible to overdose on K2 (though you can on D3)

K2 is _very_ underrated. Without it, the Calcium that the D3 helps to move can get deposited in the arteries instead of the bones and teeth!

That study is a good find (thanks). A healthy immune system is a big priority in NBE for sure. Mine went haywire when I pushed too hard.

You're welcome!

...

Btw, I'm glad you came out of moth balls, welcome back.

Thanks! I'll stay longer this time. ("Oh no!" they wail...)

B.

Hey there B,

Hi Lotus! I'm sorry I missed your reply before!

No worries,

Thanks! I'll stay longer this time. ("Oh no!" they wail...)

Ha, They'll have to get over it


I saw one reference stating Vitamin K down-regulates E2 to E1, which is still ok because too much of E2 can find its way to proliferate breast cancer. But.....it was unclear whether that was just a female response, and tbh there's some distinct differences in stated research between the sexes.

Some other recent data suggests that hepatic drug metabolism may limit the availability of estrogens for binding to receptors, meaning an overworked liver from excess NBE/Hrt prevents proper synthesis for breast growth.

Oh, almost forgot, prolactin down regulates aromatase (estradiol and progesterone too), at what concentrations I'm not certain yet.

Lol okay, extract is for liquid delivery too, I haven't tried making WP extract into a topical, a good carrier oil will be needed that includes Linolenic, (borage oil, evening primrose oil).

Be very careful with grapefruit juice, one needs to know exactly how their body responds to other meds before combining with grapefruit juice.

Good luck

Not the juice, the whole fruit. More fiber.

So I've been looking into forskolin, cAMP and other aromatase ideas. When the afore mentioned items are exposed to E2 I think these levels mentioned below will see increased expression.

To further investigate the mechanism of induction of aromatase in H295R cells by the flavonoid quercetin and isoflavone genistein, their effect on intracellular cAMP production and the promoter-specific expression of mRNA coding for CYP19 was examined. Quercetin and genistein increased intracellular cAMP levels about 1.7-fold and 1.4-fold, respectively, after a 4 h exposure. In comparison, the positive control forskolin elevated cAMP levels over 5-fold. Initial RT-PCR experiments performed to detect cAMP promoter-specific transcript for CYP19 demonstrated that the cAMP analog 8Br-cAMP significantly increased pII and I.3 transcripts in a RNA concentration range between 0.1 and 100 ng (Fig. 4). The relative expression level of pII appeared to be greater than that of I.3, as did its inducibility by 8Br-cAMP, although we emphasize that the RT-PCR method was semiquantitative. Forskolin (data not shown), 8Br-cAMP, genistein and quercetin (Fig. 5) increased CYP19 mRNA levels that were specific for the aromatase promoters pII and I.3 after a 24 h exposure. Quercetin increased pII and I.3-specific transcript about 2.6-fold and 2-fold, respectively; genistein 2.3-fold and 1.8-fold, respectively (Fig. 5). The positive control 8Br-cAMP increased pII and I.3-specific transcript about 2.7-fold and 2.3-fold, respectively (Fig. 5).

Induction and Inhibition of Aromatase (CYP19) Activity by Natural and Synthetic Flavonoid Compounds in H295R Human Adrenocortical Carcinoma Cells
http://toxsci.oxfordjournals.org/content/82/1/70.long


Forskolin promotes aromatase 5 fold
Quercetin promotes aromatase 2-3 fold
White peony promotes aromatase 2 fold
Genistein increased intracellular cAMP levels about 1.7-fold and 1.4-fold,

Inhibition of 5α-reductase results in decreased conversion of testosterone to DHT, leading to increased testosterone and estradiol. Other enzymes compensate to a degree for the absent conversion, spec voifically with local expression at the skin of reductive 17b-hydroxysteroid dehydrogenase, oxidative 3a-hydroxysteroid dehydrogenase, and 3b-hydroxysteroid dehydrogenase enzymes. Inhibition of the enzyme can be classified into two categories: steroidal, which are irreversible, and nonsteroidal. 5-α reductase 2 is the one we're interested in.

Lotus, so is it beneficial to lower SHBG in aromatase based programs?

High SHBG will bind to free T and so there will be less T to be converted in E via aromatase, right? Adding Oats could be a possibility?

Lotus, so is it beneficial to lower SHBG in aromatase based programs?

High SHBG will bind to free T and so there will be less T to be converted in E via aromatase, right?

The higher the SHBG level, the lower the free testosterone level, and vice versa. A number of factors can affect SHBG concentrations in blood. They include obesity, menopause, insulin, and androgens, each of which decreases SHBG levels. In contrast, SHBG levels are increased by estrogens, thyroid hormone, liver cirrhosis, and prolonged stress.

Adding Oats could be a possibility?

Oats down-regulates SHBG and up-regulates free testosterone,


Binding distribution of principle endogenous steroid hormones in normal women during the menstrual cycle. ______________________________________________________
Of clinical importance is free testosterone, which is often elevated in hyperandrogenic women with clinical manifestations of hirsutism. The free testosterone is regulated by the concentration of SHBG in blood. The higher the SHBG level, the lower the free testosterone level, and vice versa. A number of factors can affect SHBG concentrations in blood. They include obesity, menopause, insulin, and androgens, each of which decreases SHBG levels. In contrast, SHBG levels are increased by estrogens, thyroid hormone, liver cirrhosis, and prolonged stress.






After menopause aromatase in adipose becomes the chief producer of estrogen, E1 estrone to be exact. But, as we know in adipose tissue estrone is weak, and it's produced from androstenedione of adrenal origin in relatively large quantities.



Although aromatase level per adipose tissue fibroblast may be small, the sum of estrogen arising from billions of adipose tissue fibroblasts in the entire body makes a physiologic impact. The principal product of the ovary is the potent estrogen estradiol. In adipose tissue, estrogenically weak estrone is produced from androstenedione of adrenal origin in relatively large quantities. However, at least half of this peripherally produced estrone is eventually converted to estradiol in extraovarian tissues.

Molecular Bases and Phenotypic Determinants of Aromatase
http://downloads.hindawi.com/journals/ije/2012/584807.pdf

IMO, promoter I.4 (skin and adipose) is the one we should focus on, (skin fibroblasts).



http://pharmrev.aspetjournals.org/content/57/3/359/F4.expansion

Physiological regulation of aromatase expression. FSH induces aromatase expression via a cAMP-dependent pathway in ovarian granulosa cells via promoter II. SF-1 mediates this action of FSH. On the other hand, a combination of a glucocorticoid and a member of the class I cytokine family induces aromatase expression in skin and adipose tissue fibroblasts via promoter I.4 located 73 kb upstream of the coding region. Binding of STAT-3 and glucocorticoid receptor (GR) upstream of promoter I.4 mediates regulation of aromatase expression in these fibroblasts.

Regulation of Aromatase Expression in Estrogen-Responsive Breast and Uterine Disease: From Bench to Treatment
http://pharmrev.aspetjournals.org/content/57/3/359.full.pdf

Attached Files

---

Vitamin D3 may indirectly affect cAMP production from PGE1 by 5x, in other words, this (D3) will help upregulate aromatase.

1,25DIHYDROXYCHOLECALCIFEROL INDUCES AN INCREASE IN PGE 1 - AND FORSKOLIN-STIMULATED CYCLICAMP PRODUCTION IN T47D HUMAN BREAST CANCER CELL LINE
ABSTRACT — The effect of 1, 25-dihydroxycholecalciferol [1, 25(OH)2 D3], the active form of vitamin D3, on cell growth, clonogenicity, and cyclic adenosine monophosphate (cAMP) production was examined in human breast cancer cell line T47D. 1,25(OH)2 D3 markedly inhibited proliferation of T47D cells in a time- and concentration-dependent manner. 1,25(OH)2 D3 5 times 10−7 reduced to 70% [3H]thymidine incorporation into DNA. Specific high affinity nuclear receptors for 1,25(OH)2 D3 were present in this cell line. The cAMP produced by T47D cells was measured during 10 min stimulation by effectors (prostaglandin E1 or forskolin). Without effector, T47D cells produced similar amounts of cAMP in control and 1,25(OH)2 D3-treated cells. After 3 days in the presence of 1,25(OH)2 D3, cAMP production was significantly increased compared to control cells when stimulated by 10−4 M prostaglandin E1 or 5 times 10−7 M forskolin (3.2- and 2.4-fold increase, respectively). This cAMP increase was concentration dependent within the same range that inhibited cell growth and clonogenicity. These results suggest that 1,25(OH)2 D3 may indirectly affect cAMP production by modulating the target cell response to stimulatory agents of cAMP production.

http://www.researchgate.net/publication/247668878_125DIHYDROXYCHOLECALCIFEROL_INDUCES_AN_INCREASE_IN_PGE_1_-_AND_FORSKOLIN-STIMULATED_CYCLICAMP_PRODUCTION_IN_T47D_HUMAN_BREAST_CANCER_CELL_LINE

vitamin D analogs significantly upregulated E2- and DHT-induced CK response. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs). An estrogenic response (from vitamin D) is seen in the intestinal tract. Vitamin D also helps with hair growth.
http://www.howtomakeyourhairgrowfast.net/does-vitamin-d-help-hair-growth.html


Interaction Between Estrogen and Vitamin D–Endocrine System: A Potential Addition to the Unitary Model of Osteoporosis
http://onlinelibrary.wiley.com/doi/10.1359/jbmr.1998.13.12.1954/full

Vitamin D modulation of the activity of estrogenic compounds in bone cells in vitro and in vivo.
Somjen D1.
Author information
Abstract
Vitamin D analogs modulate different organs, including modulation of energy metabolism, through the induction of creatine kinase (CK) activity. Skeletal organs from vitamin D-depleted rats showed lower constituent CK than those from vitamin D-replete rats. Moreover, estradiol-17beta (E2) or dihydrotestosterone (DHT), which increased CK in organs from intact female or male rats, respectively, stimulated much less CK in vitamin D-depleted rats. Treatment of intact female rats with noncalcemic vitamin D analogs significantly upregulated E2- and DHT-induced CKresponse. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs) in organs from intact or ovariectomized (Ovx) female rats but abolished SERMs' inhibitory effect on E2-induced CK. These analogs significantly increased estradiol receptor alpha (ERalpha) protein in skeletal organs as well as histomorphological and biochemical changes due to this treatment followed by E2 or DHT. The analogs alone markedly altered the growth plate and the trabeculae and increased trabecular bone volume (%TB V) and trabecular width. The addition of E2 or DHT to this treatment restored all parameters as well as increased %TBV and cell proliferation. Treatment of Ovx female rats with JK 1624 F2-2 (JKF) decreased growth-plate width and increased %TB V, whereas QW1624 F2-2 (QW) restored growth-plate width and %TB V. Treatment of E2 with JKF restored %TBV and growth-plate width, whereas E2 with QW restored all parameters, including cortical width. There was also upregulation of the response of CK to E2 in both combined treatments. Our human-derived osteoblast (hObs)-like cell cultures respond to estrogenic compounds, and pretreating them with JKF upregulated the CK response to E2, raloxifene (Ral), and some phytoestrogens. ERalpha and ERbeta proteins, as well as mRNA, were modulated by CB 1093 (CB) and JKF. JKF increased specific nuclear E2 binding in female hObs but inhibited specific membranal E2 binding. hObs express 25 hydroxyvitamin D3-1alpha hydroxylase (1-OHase)-mRNA and its biological activity, which are both modulated by parathyroid hormone (PTH) and estrogenic compounds. Our results demonstrate mutual interaction between vitamin D and estrogenic compounds. We therefore conclude that combined treatment with less-calcemic analogs of vitamin D and estrogenic compounds might be superior for treatment of bone damage caused by ovariectomy in female rats, with possible application for postmenopausal osteoporosis.
PMID: 17725484 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/pubmed/17725484

I just found another Aromatase alternative, (you'll never guess the name)

Icariin from Epimedium brevicornum Maxim promotes the biosynthesis of estrogen by aromatase (CYP19).
Yang L1, Lu D, Guo J, Meng X, Zhang G, Wang F.

Abstract
ETHNOPHARMACOLOGICAL RELEVANCE:
Epimedium brevicornum Maxim has long been used for the treatment of osteoporosis in China and other Asian countries. However, the mechanism behind the antiosteoporotic activity of this medicinal plant is not fully understood.
AIM OF THE STUDY:
The present study was designed to investigate the effects of five widely used antiosteoporotic medicinal plants (Epimedium brevicornum, Cuscuta chinensis, Rhizoma drynariae, Polygonum multiflorum, and Ligustrum lucidum) on the production of estrogen, and identify the bioactive compounds responsible for the estrogen biosynthesis-promoting effect.
MATERIALS AND METHODS:
Human ovarian granulosa-like KGN cells were used to evaluate estrogen biosynthesis, and the production of 17β-estradiol was quantified by a magnetic particle-based enzyme-linked immunosorbent assay (ELISA) kit. Further, the mRNA expression of aromatase was determined by a quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR), and the protein expression of aromatase was detected by western blotting. The activity of alkaline phosphatase (ALP) in rat osteoblastic UMR-106 cells was measured using p-nitrophenyl sodium phosphate assay.
RESULTS:
Among the 5 antiosteoporotic medicinal plants, the extract of Epimedium brevicornum was found to significantly promote estrogen biosynthesis in KGN cells. Icariin, the major compound in Epimedium brevicornum, was identified to be the active compound for the estrogen biosynthesis-promoting effect. Icariin promoted estrogen biosynthesis in KGN cells in a concentration- and time-dependant manner and enhanced the mRNA and protein expressions of aromatase, which is the only enzyme for the conversion of androgens to estrogens in vertebrates. Further study showed that icariin also promoted estrogen biosynthesis and ALP activity in osteoblastic UMR-106 cells.
CONCLUSIONS:
These results show that the promotion of estrogen biosynthesis is a novel effect of Epimedium brevicornum, and icariin could be utilized for the prevention and treatment of osteoporosis.

Give up?............

Aka-Horny Goat Weed.

Horny Goat Weed (likewise one of the members of the Epimidiumfamily) has on male libido are likely partly a result of the increased aromatase activity, as well. If it works for you, your estrogen levels are probably pretty low to begin with (this reasoning is based on the profound beneficial effects of estrogen on male libido in men expressing little to no aromatase enzyme; Carani. 1999).
http://suppversity.blogspot.de/2012/12/natural-sildenafil-testosterone.html




Horny Goat Weed (Epimedium)
Horny goat weed is an herb that has been a traditional remedy in China for centuries. It’s used for low libido, erectile dysfunction, fatigue, pain, and other conditions.

Why do people take horny goat weed?

Some men take horny goat weed in the belief that it’s a natural alternative to drugs for erectile dysfunction (ED). Although still preliminary, there’s new evidence to support the idea. A 2008 lab study found that a compound in the herb blocks the effects of an enzyme that restricts blood flow to the penis. Epimedium, the suspected active component of horny goat weed, appears to act as a phosphodiesterase inhibitor, similar to some drugs used for ED. What’s more, the study indicated that horny goat weed could theoretically work better -- and cause fewer side effects -- than current drugs for erectile dysfunction.
http://www.webmd.com/vitamins-and-supplements/lifestyle-guide-11/horny-goat-weed-epimedium