[peggy]

Bottom line- low dose esstential fatty acids (eg-EPO) 2000 mg and 2000 mg omega 3's, coconut oil 2000 mg will have a big effect on ER-a bioavailability over straight use of phytoestrogens. And for more depth, RC, Vitex, Hops all have an ER-alpha affinity. Balance with turmeric, green tea, progesterone, WP, reishi and boobie friendly foods that's been shared and its a solid program.

So would you actually recommend RC? It does contain genistein, right? If yes which dosage?

[ellacraig]

Once you have answered Peggy Curious to hear of RC too . As a blood cleanser alone id like to try one day let alone the other benefits.


I think the obvious choice is to balance herbs that are PRO-ER-a with ER-b (protective receptor). Turmeric, green tea, essential fatty acids, and certain phtyoestrogens. 5 ar inhibitors are still a viable choice, reishi binds to ER's, not sure which one yet. WP is still a good choice. New weapons are things like 17 beta HSD's, type 1 & 4, plus CYP19 is still a viable option considering the andro to estro pathway,(that backdoor pathway is yet to be tapped).

[u]Im going to do a BWB lol "What phytoestrogens" -jokes on the BWB part but yes what are these phytos you speak of? Txs[/u]


Bottom line- low dose esstential fatty acids (eg-EPO) 2000 mg and 2000 mg omega 3's, coconut oil 2000 mg will have a big effect on ER-a bioavailability over straight use of phytoestrogens. And for more depth, RC, Vitex, Hops all have an ER-alpha affinity. Balance with turmeric, green tea, progesterone, WP, reishi and boobie friendly foods that's been shared and its a solid program.

Ok how many tablespoons of coconut oil would add up to 2000mg?

And what could be used in place of progesterone and at what point would you utilize that in your cycle if applicable?

Txs

[pom19]

1 Tablespoon of coconut oil = 13.05 grams.

[ellacraig]

1 Tablespoon of coconut oil = 13.05 grams.

YIKES so I only need as much as to LOOK at a tablespoon of coconut oil and I'l have my 2000mgs

[pom19]

1 Tablespoon of coconut oil = 13.05 grams.

YIKES so I only need as much as to LOOK at a tablespoon of coconut oil and I'l have my 2000mgs

-------------------------------------------
Way more than that. I suggest one tea spoon (Not table) 2 to 3 times/day.
When you spread it your body likes it more to absorb it properly.

[Lotus]

Botanicals and specifically their phytoestrogens, such as genistein and daidzein, preferentially bind and activate ERβ, thus may exert a safe estrogenic activity [15], [30]. However, the use of botanicals with only plant-derived estrogens in the absence of progestins might increase the risk of developing endometrial hyperplasia and cancer similar to conventional estrogen-alone HT

https://www.thieme-connect.com/products/...32-1328187

Red clover
http://www.ars-grin.gov/cgi-bin/duke/farmacy2.pl?1022

From what it looks RC shows weak progestrogenic activity, the dosage is sketchy for RC to achieve an ER-a affinity. Genistein in RC is reported at .45%, the main phyto's in RC are Biochanin A @ 14.26% Formononetin @ 14.47%

What does look promising is linoleic acid (EPO, evening primrose oil) in Vitex strongly stimulated ER-a.

1 Tablespoon of coconut oil = 13.05 grams.

YIKES so I only need as much as to LOOK at a tablespoon of coconut oil and I'l have my 2000mgs

-------------------------------------------
Way more than that. I suggest one tea spoon (Not table) 2 to 3 times/day.
When you spread it your body likes it more to absorb it properly.

Actually ingesting CO benefits breast growth more, you'll still get benefits from skin absorption. They have CO in a capsule form, (not a fan of the taste).

[peggy]

Thanks for your reply Lotus. So would you say that Vitex might be more safe to take than RC since Vitex will typically raise progesterone?

[Lotus]

Thanks for your reply Lotus. So would you say that Vitex might be more safe to take than RC since Vitex will typically raise progesterone?

They both have their issues, also each has different M/F reactions. Between the two it's like peeling an onion, so I'll need to spread this out over a few posts, cause peeling the layers there's so many other NBE possibilities. From what I've seen vitex has more safe guards. You'll literally find dozens if not 100's more studies of contradictory evidence (as usual). Imo, vitex has more safe guards, one positive is it's a COX2 inhibitor, which lowers PGE2 (prostaglandin 2 can stimulate cancer progression). Green tea is a COX 2 inhibitor.


Vitex agnus-castus extracts for female reproductive disorders: a systematic review of clinical trials.

one trial reported it to be superior to placebo for reducing TRH-stimulated prolactin secretion, normalising a shortened luteal phase, increasing mid-luteal progesterone and 17β-oestradiol levels, while the other found Vitex comparable to bromocriptine for reducing serum prolactin levels and ameliorating cyclic mastalgia.

http://www.ncbi.nlm.nih.gov/pubmed/23136064

Eight botanical preparations that are commonly used for the treatment of menopausal symptoms were tested for estrogenic activity. Methanol extracts of red clover (Trifolium pratense L.), chasteberry (Vitex agnus-castus L.), and hops (Humulus lupulus L.) showed significant competitive binding to estrogen receptors alpha (ER alpha) and beta (ER beta). With cultured Ishikawa (endometrial) cells, red clover and hops exhibited estrogenic activity as indicated by induction of alkaline phosphatase (AP) activity and up-regulation of progesterone receptor (PR) mRNA.

Bioassay-guided isolation, utilizing ER binding as a monitor, resulted in the isolation of linoleic acid as one possible estrogenic component of the extract. The use of pulsed ultrafiltration liquid chromatography-mass spectrometry, which is an affinity-based screening technique, also identified linoleic acid as an ER ligand based on its selective affinity, molecular weight, and retention time. Linoleic acid also stimulated mRNA ERbeta expression in T47D:A18 cells, PR


___________________________

COX is involved in the regulation of day-to-day cellular and metabolic activities such as maintaining stomach lining integrity, regulating blood flow within the kidneys, and balancing platelet function, [19] whereas COX-2 triggers by response to a variety of pro-inflammatory stimulation. [20] COX-2 regulates prostaglandin production by regulating arachidonic acid pathway in inflammatory cells for healing and repairing. [21] Therefore, inhibition of COX, and inhibiting the release of prostaglandins, is an important way to suppress inflammatory response (PGE2).

[Lotus]

Before I forget I wanted to share this tidbit, it's called Leucine. Leucine-rich proteins (amino-acids) are human co-regulators of estrogen receptor alpha (ER-a, the growth gene). (like I said, an onion).


Leucine works with the amino acids isoleucine and valine to repair muscles, regulate blood sugar, and provide the body with energy. It also increases production of growth hormones, and helps burn visceral fat, which is located in the deepest layers of the body and the least responsive to dieting and exercise.
http://www.vitaminstuff.com/amino-acid-leucine.html

Foods highest in Leucine
(based on levels per 200-Calorie serving)
http://nutritiondata.self.com/foods-0000...00000.html
Eggs whites, Soy, Tuna, etc.


J Biol Chem. 2001 Oct 12;276(41):38272-9. Epub 2001 Jul 31.
Molecular cloning and characterization of PELP1, a novel human coregulator of estrogen receptor alpha.
Vadlamudi RK1, Wang RA, Mazumdar A, Kim Y, Shin J, Sahin A, Kumar R.
Author information
Abstract
Nuclear hormone receptors (NRs) are transcription factors whose activity is regulated by ligands and by coactivators or corepressors. We report the characterization of a new NR coregulator: proline-, glutamic acid-, leucine-rich protein 1 (PELP1), a novel human protein that comprises 1,282 amino acids and is localized on chromosome 17. The primary structure of PELP1 consists of several motifs present in most transcriptional regulators including nine NR-interacting boxes (LXXLL motifs), a zinc finger, and glutamic acid- and proline-rich regions. We demonstrate that PELP1 is a coactivator of estrogen receptor alpha (ERalpha). PELP1 enhances 17beta-estradiol-dependent transcriptional activation from the estrogen response element in a dose-dependent manner. PELP1 interacts with ERalpha and also with general transcriptional coactivators p300 and cAMP response element-binding protein-binding protein. PELP1 was differentially expressed in various human and murine tissues with the highest expression levels in the testes, mammary glands, and brain. We also provide evidence supporting the developmental regulation of PELP1 expression in murine mammary glands, the detectable expression of PELP1 in human mammary cancer cell lines, and the enhanced expression of PELP1 in human breast tumors. These findings suggest that PELP1 is a novel coregulator of ERalpha and may have a role in breast cancer tumorigenesis.




http://www.endocrine-abstracts.org/ea/00...03p134.htm

[Lotus]

Red Clover,

It can go either way, I wouldn't take RC with a history of blood clots, although it's an anti-inflammatory. Here again you'll find contradictory evidence, some obvious ones are on ER-a & ER-b. My opinion?, it's a pro ER-a.......and an aromatase. You'll notice this quote " low dose affects vs. high dose affects" repeat itself.




Genistein, daidzein (Dixon-Shanies & Shaikh 1999), and biochanin A, a precursor of genistein (Dixon-Shanies & Shaikh 1999; Hsu et al. 2000), all inhibit the growth of the human ER positive breast cancer cells MCF-7. However, genistein (Twaddle et al. 1999), enterolactone and equol (Welshons et al. 1987), a derivative of daidzein, have also been shown to stimulate the growth of MCF-7 cells. The effect of many plant-derived estrogens on the DNA synthesis of MCF-7 cells is biphasic; at low concentrations (0.1-10 μM), genistein, biochanin A and enterolactone stimulate the DNA synthesis, whereas at high concentrations (20-80 μM) their effects are inhibitory (Wang & Kurzer 1997). This suggests that the low concentrations of plant-derived estrogens cause an estrogenic effect on MCF- 7 cells, but at high concentrations other mechanisms begin to have an influence. For more references see review by Tham et al. (1998).



biochanin A, shown to stimulate the growth of MCF-7 cells. The effect of many plant-derived estrogens on the DNA synthesis of MCF-7 cells is biphasic; at low concentrations (0.1-10 μM), genistein, biochanin A and enterolactone stimulate the DNA synthesis, whereas at high concentrations (20-80 μM) their effects are inhibitory (Wang & Kurzer 1997)
http://www.sciencedirect.com/science/art...0327100529
---------------------------------

Biochanin A (5, 7-dihydroxy-4’-methoxyisoflavone) is an isoflavone extracted from red clover (Trifolium pretense) by Pope et al. [92]. The first evidence that red clover has estrogenic activity were reported by Bennets et al. [93] after observing breeding problems of sheep grazing on red clover pastures which have been attributed to the isoflavone and coumestrol content of red clover. Serious fertility disturbances indicating estrogenic stimulation of cattle fed with red clover silage were reported [94-96]. Although biochanin A was moderately active in inhibiting microsomal aromatase activity (IC50: 5-10 μM) but was strongly active when tested in JEG-3 cells (human placental choriocarci- noma cell line). However, it did not inhibit aromatase activity in granulosa-luteal cells, and human preadipocyte cells and was also inactive in trout ovarian aromatase assay [61]. Interestingly, in MCF-7 cells (ER-positive breast cancer cells) biochanin A exhibited a dual action. It inhibited aromatase activity at low concentrations, but was estrogenic at high concentrations [97]. Furthermore, in SK-BR3 cells (ER-negative breast cancer cells) biochanin A was reported to inhibit aromatase enzyme activity and reduce mRNA expression. By using a luciferase reporter.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142499/