[Lotus]

Don't feel lonesome Hannah. I did as well.. But now started to do the Dr. Lotus approved method. LOL...

You're humor is so wicked lol, I dont know if I get it actually..

Lol, oh he IS wicked, lmao. Iaboy's humor is satirical at times, but he's straight forward (tells it like is and spoken from wisdom.......old fart).

[Lotus]

Sorry about this bump, here's some of the important things we need to keep in mind while grow boobs, and a few other things,

In other words, this confirms GID symptoms can be elevated by a suppression of T. So what are the things that inhibit the CYP17 enzyme, (plenty), the Pharma anti-fungal ketoconazole inhibits (strongly I might add) CYP17 enzyme. And guess what?, green tea, lemons inhibit CYP17.........amazing.

Thanks POM, sorry Ella.

Here's an example of what how interactions can happen, multiplying its effects. Say you drink green tea (a CYP17 inhibitor of testosterone). Now because you add piperine (in certain supplements, or added by supplementing) it increases the EGCG (polyphenols) in green tea by 1.3 fold.



J Nutr. 2004 Aug;134(8):1948-52.
Piperine enhances the bioavailability of the tea polyphenol (-)-epigallocatechin-3-gallate in mice.
Lambert JD1, Hong J, Kim DH, Mishin VM, Yang CS.
Author information
Abstract
(-)-Epigallocatechin-3-gallate (EGCG), from green tea (Camellia sinensis), has demonstrated chemopreventive activity in animal models of carcinogenesis. Previously, we reported the bioavailability of EGCG in rats (1.6%) and mice (26.5%). Here, we report that cotreatment with a second dietary component, piperine (from black pepper), enhanced the bioavailability of EGCG in mice. Intragastric coadministration of 163.8 micromol/kg EGCG and 70.2 micromol/kg piperine to male CF-1 mice increased the plasma C(max) and area under the curve (AUC) by 1.3-fold compared to mice treated with EGCG only. Piperine appeared to increase EGCG bioavailability by inhibiting glucuronidation and gastrointestinal transit. Piperine (100 micromol/L) inhibited EGCG glucuronidation in mouse small intestine (by 40%) but not in hepatic microsomes. Piperine (20 micromol/L) also inhibited production of EGCG-3"-glucuronide in human HT-29 colon adenocarcinoma cells. Small intestinal EGCG levels in CF-1 mice following treatment with EGCG alone had a C(max) = 37.50 +/- 22.50 nmol/g at 60 min that then decreased to 5.14 +/- 1.65 nmol/g at 90 min; however, cotreatment with piperine resulted in a C(max) = 31.60 +/- 15.08 nmol/g at 90 min, and levels were maintained above 20 nmol/g until 180 min. This resulted in a significant increase in the small intestine EGCG AUC (4621.80 +/- 1958.72 vs. 1686.50 +/- 757.07 (nmol/g.min)). EGCG appearance in the colon and the feces of piperine-cotreated mice was slower than in mice treated with EGCG alone. The present study demonstrates the modulation of the EGCG bioavailablity by a second dietary component and illustrates a mechanism for interactions between dietary chemicals.

http://www.ncbi.nlm.nih.gov/pubmed?filters=&orig_db=PubMed&cmd=Search&term=134%2A%5Bvolume%5D%20AND%201948%5Bpage%5D%20AND%202004%5Bpdat%5D%20AND%20Lambert%20JD%5Bauth%5D

Hi BN,

Here's a new idea to try...........citrus for breast growth (I'll explain). Three key enzymes (cyp 17, cyp 19, cyp 3A4) have direct pathways to breast/androgen synthesis. Cyp 3A4 controls more than 50% of how drugs are metabolized (I'd say that's a major regulator to piggy back off of), the only only issue there is mapping out all these key regulators, (it's like mapping out the genome).


Example: star fruit inhibits CY3A, more potent than grapefruit, ((which if you didn't notice, inhibiting CY3A4 will help with breast growth)).


Potent inhibition by star fruit of human cytochrome P450 3A (CYP3A) activity.
Hidaka M1, Fujita K, Ogikubo T, Yamasaki K, Iwakiri T, Okumura M, Kodama H, Arimori K.
Author information
Abstract
There has been very limited information on the capacities of tropical fruits to inhibit human cytochrome P450 3A (CYP3A) activity. Thus, the inhibitory effects of tropical fruits on midazolam 1'-hydroxylase activity of CYP3A in human liver microsomes were evaluated. Eight tropical fruits such as common papaw, dragon fruit, kiwi fruit, mango, passion fruit, pomegranate, rambutan, and star fruit were tested. We also examined the inhibition of CYP3A activity by grapefruit (white) and Valencia orange as controls. The juice of star fruit showed the most potent inhibition of CYP3A. The addition of a star fruit juice (5.0%, v/v) resulted in the almost complete inhibition of midazolam 1'-hydroxylase activity (residual activity of 0.1%). In the case of grape-fruit, the residual activity was 14.7%. The inhibition depended on the amount of fruit juice added to the incubation mixture (0.2-6.0%, v/v). The elongation of the preincubation period of a juice from star fruit (1.25 or 2.5%, v/v) with the microsomal fraction did not alter the CYP3A inhibition, suggesting that the star fruit did not contain a mechanism-based inhibitor. Thus, we discovered filtered extracts of star fruit juice to be inhibitors of human CYP3A activity in vitro.
PMID: 15155547 [PubMed - indexed for MEDLINE] Free full text

Here's what I'm thinking, tropicial fruits blocks the androgen pathway, like the enzyme CYP 17 does (inhibit androgen)........and, cyp 19 (is an aromatase promoter).

Inhibit CYP3A4
Inhibit CYP17
induce CYP19

In think incorporating a tropical fruit (call it a lotion?) massage, also adding a polyphenol (green tea extract, androgen inhibitor for max potential). Oral intake will still be the biggest bang though.

Anyways, with help from the one fella, I've got a head start on some of the enzymes (call them coregulators) mapped out. I'll post asap.

This is exciting stuff no? Who knew fruits would prove to be pro breast growth, and a healthy approach too.

This dumb fuffer's brain stopped working after reading one paragraph [/i]

Muther fluffin fuff myboobs ........j/k how about this?.

The DHT in ur nut sac can be made into estrogen without a big fuss. We can also reduce DHT in the prostate, reduce BPH and cancer by this second (newer estrogen) made from a side effect of DHT in the prostate and testes. Hopefully, this new process eliminates some of the supplements and lessens the strain on the liver, by all the NBE products. Not convinced?..........that crazy science mumbo jumbo I just listed says otherwise.

Could you summarize the supplements or procedure as to actually get your "DHT in ur nut sac [to be] made into estrogen" ? It looked like you first mentioned cortisol, so basically stress yourself out? Thanks!

If thats the case....no wonder transgender women are beautiful.....we stress over alot...thats alot of free flowing E in our veins.

Yes, stress makes you beautiful lol, wait what?. Isn't that typical though, one hormone gain means dealing with it's side effect and might impact the benefits of other hormones. However in this case cortisol has a direct effect on ER-b (estrogen receptor beta) in the prostrate and testes, HSD 11 beta type 1 reduces cortisone to the active hormone cortisol that activates glucocorticoid receptors, in that instance it (glucocorticoid receptors) helps with boob growth, which we have in boobs, about 20% (glucocorticoid receptors). Licorice and green tea reduce 11 beta HSD type 1. I believe Leptin does the same though. Soooo....following the science I colored highlighted the two key points of interest. As you read this process could go either way, imo if you suppress DHT it will upregulate estrogen to activate E1 to E2 the active form of estrogen (Estradiol), which is what feminizes. I do suggest (even with Hrt) you at least normalize the androgen production in the testes 1-2 times a month. The amino acids L-arginine, Tuarine, Tyrosine all helps in this new process, I will explain about those too.


Sex steroids and leptin regulate 11β-hydroxysteroid dehydrogenase I and P450 aromatase expressions in human preadipocytes: Sex specificities
Service de Biochimie et de Biologie Moléculaire, UPRES EA 2493, Faculté de Médecine Paris-Ile de France-Ouest, Université Versailles St Quentin, Centre Hospitalier de Poissy, 78303 Poissy Cedex, France.
The Journal of Steroid Biochemistry and Molecular Biology (Impact Factor: 3.63). 07/2006; 99(4-5):189-96. DOI: 10.1016/j.jsbmb.2006.01.007
Source: PubMed
ABSTRACT
Adipose tissue is an important site of steroid hormone biosynthesis, as type I 11beta-hydroxysteroid dehydrogenase (HSD1), the enzyme responsible for the conversion of cortisone into cortisol and the P450 aromatase, the enzyme catalysing androgens aromatization into estrogens, are both expressed in human adipose tissue. In the present report, we have investigated the possibility that sex steroids and leptin could regulate these two enzymes in cultured preadipocytes from men and women intra-abdominal fat depots. In women preadipocytes, human recombinant leptin down-regulates HSD1 mRNA expression (-58%) and P450 aromatase activity (-26%). Conversely, leptin up-regulates the HSD1 (2.4-fold) and the P450 aromatase (1.6-fold) mRNA expression in men preadipocytes. In women preadipocytes, 17beta-estradiol strongly stimulates HSD1 mRNA expression (10-fold) and, in contrast, decreases by half the P450 aromatase expression. In men, 17beta-estradiol has no influence on HSD1 expression but up-regulates P450 aromatase mRNA expression (2.4-fold). Finally, androgens increase by a factor of 2.5-5 the mRNA expression of both enzymes in men. These findings suggest that sex steroids and leptin either increase or decrease local cortisol and estrogens productions in men or in women preadipocytes, respectively. They also indicate that steroid metabolism in adipose tissue is controlled by a coordinated regulation of P450 aromatase and HSD1 expressions. Finally, the important sex-specific differences described herein may also contribute to explain the sexual dimorphism of body fat distribution in humans.

I'll post more info tomorrow (hopefully) have a good night.

Hi Lotuss, I was reading this:

Available research suggests that doses of more than 25 milligrams of lycopene daily may lower levels of low-density lipoprotein (LDL, or "bad") cholesterol and total cholesterol. Although this is promising, more high-quality research is needed in this area.

And I thought about the 'fat in fat out' sentence in the big post up here, could this be of help?.... Lowering ldl helps fat storage? Or is this totally off route..bc im already on green tea and coconutoil etc. Im searching for something new..

Hi Hannah,

This fat in/fat out is what I think that FAT Flux does for our fat cells, meaning that energy from new fat is used within that hour, in others words fuel for breasts cells to synthesize new growth. This is just a theory (lol, mine), but, I see the science, now extrapolating into NBE is the tough part. Emulsification in the intestines (or should I say, better Emulsification) is tied to progesterone and testosterone, (through a network of enzymes), I know, more complexity. however, insulin is the master control here, imo. Green tea helps in burning fat, (I think other fat supps can be helpful too), which can help fight LDL. Exercising can also benefit getting rid of storing the new fat. However, stored fats house estrogen, isn't that a huge potential to burn that stored estrogen?, I would think so considering we continue to add more and more phytoestrogens/estradiol. Studies show that the half life in E2 (Pharma) is present for days, so we may not think its (E2) there working (so I take more) but it's still working). TTYL


It is also possible for fat cells to take up glucose and amino acids, which have been absorbed into the bloodstream after a meal, and convert those into fat molecules. The conversion of carbohydrates or protein into fat is 10 times less efficient than simply storing fat in a fat cell, but the body can do it. If you have 100 extra calories in fat (about 11 grams) floating in your bloodstream, fat cells can store it using only 2.5 calories of energy. On the other hand, if you have 100 extra calories in glucose (about 25 grams) floating in your bloodstream, it takes 23 calories of energy to convert the glucose into fat and then store it. Given a choice, a fat cell will grab the fat and store it rather than the carbohydrates because fat is so much easier to store.

How Fat Cells Work
http://science.howstuffworks.com/life/ce...-cell2.htm

http://www.breastnexus.com/showthread.php?tid=17436&pid=163166&highlight=Green+tea#pid163166

[Lotus]

Don't feel lonesome Hannah. I did as well.. But now started to do the Dr. Lotus approved method. LOL...

You're humor is so wicked lol, I dont know if I get it actually..

Lol, oh he IS wicked, lmao. Iaboy's humor is satirical at times, but he's straight forward (tells it like is and spoken from wisdom.......old fart).

[Lotus]

Sheesh, seriously long post. Btw, Clelia is a scientist.

If you didn't catch this post from the research section I'd like to list here and give it a bit more text. The research posted below shows how I got to this theory (hypothesis) about Fatty Acids being a link to quote "that a third signalling pathway, involving cytoplasmic proteins and rapid membrane-initiated responses, serves largely for mitogenic E2-induced effects. " Most of the research is listed, although there's about a dozen more pages of related info in the NBE Strategies thread, Anti-Androgen thread for that matter too. The bottom line from putting all this together is that staight PM or even Hrt doesn't get it done without some other key links, e.g. EFA's essential fatty acids, certain carrier proteins, common links between 17 beta HSD's, aromatase, estrogen receptors, IGF-1, MAPK, PPP, and many others. But you can believe (or not).......your choice, but when I say it all makes a huge difference, it does, even our scientist Clelia states the existence (see page 142 listed below).

See yeah soon.

Ok, I'm gonna give this a shot at defining why essential fatty acids (EFA's) are important for NBE, any car buffs Lol?.

EFA's are like lubricants for car parts (e.g. molecules, steroids, DNA synthesis etc). They help help carry hormones to receptors, in other words, once they arrive at the cell membranes they (EFA's) make them more bioavailable. Soooo.....using these fat solubles supplements keep us squeaky, get it.



Figure 1: Bioactive lipid synthesis, metabolism and signaling pathways.
http://www.nature.com/nchembio/journal/v...94_F1.html

It is now known that estrogens exert their end-organ effect by activating a complex intracellular mechanism. Tissues which respond to estrogen possess intracytoplasmic proteins (receptors) that preferentially bind specific steroids.

For instance, a cell from the uterus will possess 5000–15,000 estrogen receptors whereas a cell from the spleen will have none. These receptors recognize estrogens by their three dimensional and chemical characteristics and bind it with high affinity (KD =10-10), specificity, and saturability.

NBE Strategies (receptor)
http://www.breastnexus.com/showthread.php?tid=22119&page=14&highlight=Receptors


Genomic and non-genomic effects of estrogens on endothelial cells.
http://www.ncbi.nlm.nih.gov/pubmed/15288766#

Palmitoylation-dependent estrogen receptor alpha membrane localization: regulation by 17beta-estradiol.
http://www.ncbi.nlm.nih.gov/pubmed/15496458

Role of ERbeta palmitoylation in the inhibition of human colon cancer cell proliferation.
http://www.ncbi.nlm.nih.gov/pubmed/17395984

S-palmitoylation modulates estrogen receptor alpha localization and functions.
http://www.ncbi.nlm.nih.gov/pubmed/16274718

Estrogen receptor signalling: bases for drug actions.
http://www.ncbi.nlm.nih.gov/pubmed/16178790

Starting off at page #137 to #147 is some very interesting research (page 142, is IMO one of the best inside the program lotus thread).
http://www.breastnexus.com/showthread.php?tid=17436&page=141

Minireview: The Androgen Receptor in Breast Tissues: Growth Inhibitor, Tumor Suppressor, Oncogene?
http://www.ncbi.nlm.nih.gov/pmc/articles...rt=classic
Credit Clelia for this research article (thanks)

Estrogen receptor signalling: bases for drug actions.

Abstract
Estrogen receptors (ERalpha and ERbeta) mediate the effects of 17beta-estradiol (E2) and account for E2 role on growth, development, and homeostasis maintenance in different tissues and organs. ERalpha and ERbeta function as ligand-dependent transcription factors which directly bind to specific estrogen responsive element (ERE) present into DNA and, in turn, regulate the transcription of E2-sensitive genes. In addition, ERalpha and ERbeta, without direct binding to DNA, regulate transcription indirectly by binding to other transcription factors activating or inactivating the transcription of E2-dependent-ERE-devoid genes. Along with these two E2 mechanisms, it has been recently uncovered that a third signalling pathway, involving cytoplasmic proteins and rapid membrane-initiated responses, serves largely for mitogenic E2-induced effects. The commitment of ERbeta in these rapid E2-induced effects is openly debated. This review will focus and summarize the latest findings regarding the multiple E2 molecular mechanisms and underlines the development of our understanding of anti-cancer drugs acting as ER signalling modulators.

Ok, I'll give it a shot, let's use women's androgens as an example , the major androgen in women is androstenedione, and it takes a pathway to testosterone through the androstenedione pathway to estrogen, with a slight detour (and I mean slight, hard to detect) DHT. The scale tips this pathway towards estrogen, part of what keeps females female. This pathway in males is consider a backdoor pathway, but because DHT is so much stronger it dominates through the standard pathway of testosterone and then enzyme 5 alpha reductase gives it a pass to DHT, unless we intercept it through another enzyme called aromatase, which will then convert to estrogen. But the odds are stacked against us unless preventive actions (anti-androgens) aren't out in place. I like to think of this 3 alpha-hydroxysteroid dehydrogenase" or 3b-Adoil for short, as booby trap (pun) for DHT to find along its pathway (downstream if you will).

In between the androgen pathway sits these booby traps (like light switches), that can block DHT. And so far the only thing I saw to prevent this was cortisteriods, (this action is more complicated I'm afraid too) to prevent this, but I don't think that's the end of the story yet, there's always new research coming out, and by this I mean in the way of cancer treatments, e.g. androgen blockade therapies, new trails etc. just a matter of time before its figured out.......hopefully I'll turn something up soon.

List of Corticosteroid Medications
http://www.livestrong.com/article/27014-...dications/

Here's the techinical version, and I'm sorry if here's where I lose yah.

Four human aldo-keto reductases (AKRs) that belong to the AKR1C subfamily function in vitro as 3-keto-, 17-keto- and 20-ketosteroid reductases or as 3alpha-, 17beta- and 20alpha- hydroxysteroid oxidases to varying degrees. By acting as ketosteroid reductases or hydroxysteroid oxidases these AKRs can either convert potent sex hormones (androgens, estrogens and progestins) into their inactive metabolites or they can form potent hormones by catalyzing the reverse reaction. In this manner they may regulate occupancy and trans-activation of steroid hormone receptors.

From an earlier post,


DHT has an estrogenic action,

The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events.


Recent data have shown that DHT may be converted into 5α-androstane- 3β-17β-diol (3β-diol) in a virtually irreversible reaction. Once considered inactive, 3β-diol is present in high concentrations in the male and indeed has biological activity. However, 3β-diol does not bind to the androgen receptor (AR), but rather to ERα and ERβ, with higher affinity for ERβ. Based upon these findings, we hypothesized that the modulation of AQP9 by DHT could be indirectly mediated by 3β-diol.

---------------------------

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615873/


Effects of 3-beta-diol, an androgen metabolite with intrinsic estrogen-like effects,

Abstract

Background: Fluid homeostasis is critical for normal function of the male reproductive tract and aquaporins (AQP) play an important role in maintenance of this water and ion balance. Several AQPs have been identified in the male, but their regulation is not fully comprehended. Hormonal regulation of AQPs appears to be dependent on the steroid in the reproductive tract region. AQP9 displays unique hormonal regulation in the efferent ductules and epididymis, as it is regulated by both estrogen and dihydrotestosterone (DHT) in the efferent ductules, but only by DHT in the initial segment epididymis. Recent data have shown that a metabolite of DHT, 5-alpha- androstane-3-beta-17-beta-diol (3-beta-diol), once considered inactive, is also present in high concentrations in the male and indeed has biological activity. 3-beta-diol does not bind to the androgen receptor, but rather to estrogen receptors ER-alpha and ER-beta, with higher affinity for ER-beta. The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the only estrogen to play a major role in the male reproductive system. Considering that both ER-alpha and ER-beta are highly expressed in efferent ductules, we hypothesized that the DHT regulation of AQP9 could be due to the 3-beta-diol metabolite.

Methods: To test this hypothesis, adult male rats were submitted to surgical castration followed by estradiol, DHT or 3-beta-diol replacement. Changes in AQP9 expression in the efferent ductules were investigated by using immunohistochemistry and Western blotting assay.

Results: Data show that, after castration, AQP9 expression was significantly reduced in the efferent ductules. 3- beta-diol injections restored AQP9 expression, similar to DHT and estradiol. The results were confirmed by Western blotting assay.

Conclusion: This is the first evidence that 3-beta-diol has biological activity in the male reproductive tract and that this androgen metabolite has estrogen-like activity in the efferent ductules, whose major function is the reabsorption of luminal fluids.





a) It has been shown that 3β-diol may have hormonal activity, not acting through the AR, but rather as a ligand for both ERα and ERβ.

b) 3β-diol has higher affinity for ERβ [31], which is abundant in the efferent ductule epithelium [40].

c) In human testis, the 3β-diol concentration is higher than DHT and estradiol [44,45]. It is reasonable to postulate that high concentrations of this metabolite may enter the lumen of efferent ductules.

d) The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events [26,28,32,46].

Also noteworthy is the fact that 3β-diol stimulates ERβ induced transcriptional activity equal to the cognate ligand estradiol, and the transcriptional selectivity of 3β-diol for ERβ is much greater than its binding selectivity [30,46]

-----------------------------


Concentrations of aromatase and estradiol in the prostate are low, indicating that estradiol may not be the only estrogenic molecule to play a role in the prostate. It is known that DHT can be metabolized to 5alpha-androstane-3beta,17beta-diol (3beta-diol), a hormone that binds to ERbeta but not to AR. The concentration of 3beta-diol in prostate is much higher than that of estradiol. Based on the high concentration of 3beta-diol and since this metabolite is a physiological ERbeta ligand, we hypothesized that 3beta-diol would be involved in the regulation of ERbeta expression.





An endocrine pathway in the prostate, ERbeta, AR, 5alpha-androstane-3beta,17beta-diol, and CYP7B1, regulates prostate growth.
http://www.ncbi.nlm.nih.gov/pubmed/12370428

I've spent more time researching on this backdoor estrogenic action of DHT, aka estrogen receptor beta. From what I see when DHT is metabolized in the liver we can force it to this ER-b back door, thereby lessening (or inactivating) it's potential. And imo cortisteriods inactivates DHT.

Hmmmm so is reishi still good to take? i guess taking everything in moderation is always better but NBE is such a long journey thus everything will be kind of long term type

I forget to include these studies, although somewhat technical it's still some solid info on reishi:


Ganoderma lucidum: A Potent Pharmacological Macrofungus
http://www.researchgate.net/profile/Prakash_Bisen/publication/40032434_Ganoderma_lucidum_a_potent_pharmacological_macrofungus/links/0fcfd505b4749c887f000000.pdf?ev=pub_ext_doc_dl&origin=publication_detail&inViewer=true


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


Target proteins of ganoderic acid DM provides clues to various pharmacological mechanisms:
http://www.nature.com/srep/2012/121130/s...p00905.pdf

______________________________

Other info:

Effect of epidermal growth factor and prostaglandin on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells
http://joe.endocrinology-journals.org/co...9.full.pdf

Comparative effects of DHEA vs. testosterone, dihydrotestosterone, and estradiol on proliferation and gene expression in human LNCaP prostate cancer cells
http://ajpendo.physiology.org/content/aj...3.full.pdf

Nutritional Influences on Estrogen Metabolism
http://www.afmcp-sa.com/ansr/MET451%20En...20ANSR.pdf

yep, maybe in men the estrogenic activity of soy is more effective than in women, but also it depends on individual genetics. You'll see in the link below, a very good article that summarize a lot of papers about phytoestrogens. After reading that, you can just say: yes, it could wbe helpful as it could be harmful... and maybe it's wise stay in the middle, not exceed:
http://foodforbreastcancer.com/foods/gen...d-daidzein

an extract of the article: (here it is something in english about equol and its conversion

Equol has been shown to have the strongest binding affinities and estrogenic activities (especially for ERβ) among the daidzin metabolites and has been hypothesized to be largely responsible for the estrogen-like activities of soy and its isoflavones. However, there is a great deal of variation among individuals in the metabolism of genistin and daidzin, which appears to be dependent partly on environmental factors, including other components of the diet, and partly on genetic factors.

Only 25% to 35% of the U.S. Caucasian population is capable of converting daidzein to equol, whereas people in high soy consumption areas of Asia have rates closer to 40% to 60%. There is some evidence that Hispanic or Latino women are also more likely to be equol producers. Approximately 80% to 90% of people harbor the bacteria required to produce ODMA. The frequency of equol producers in one study of vegetarians was found to be 59%, similar to the reported frequency in Japanese adults consuming soy, and much higher than for nonvegetarian adults (25%). One Japanese study found that consumption of dairy products was significantly higher in those who did not excrete equol than in those who did.



other papers that i looked at today:

http://www.ncbi.nlm.nih.gov/pubmed/25789108

http://www.ncbi.nlm.nih.gov/pubmed/25673549

http://www.ncbi.nlm.nih.gov/pubmed/25338271

http://www.ncbi.nlm.nih.gov/pubmed/25302172

http://www.ncbi.nlm.nih.gov/pubmed/25263312

http://www.ncbi.nlm.nih.gov/pubmed/25236805

isoflavones in the brain: http://www.ncbi.nlm.nih.gov/pubmed/25232349

http://www.ncbi.nlm.nih.gov/pubmed/22510793

http://www.ncbi.nlm.nih.gov/pubmed/25592466

http://www.ncbi.nlm.nih.gov/pubmed/24504368

http://www.ncbi.nlm.nih.gov/pubmed/24531783

http://www.ncbi.nlm.nih.gov/pubmed/24053483

Oh yeah ......you know I'll want to talk about this research studies , their just screaming "hey I'm here, read me" ......solve me......

Structure, function and tissue-specific gene expression of 3β-hydroxysteroid dehydrogenase/5-ene-4-ene isomerase enzymes in classical and peripheral intracrine steroidogenic tissues.
________________________________________
data indicate that the presence of multiple 3β-HSD isoenzymes offers the possibility of tissue-specific expression and regulation of this enzymatic activity that plays an essential role in the biosynthesis of all hormonal steroids in classical as well as peripheral intracrine steroidogenic tissues.

http://www.ncbi.nlm.nih.gov/pubmed/22217825

Bovine adrenal 3beta-hydroxysteroid dehydrogenase (E.C. 1.1.1. 145)/5-ene-4-ene isomerase (E.C. 5.3.3.1): characterization and its inhibition by isoflavones.
____________________________________________
The isoflavones daidzein, genistein, biochanin A and formononetin inhibit potently and preferentially the gamma-isozymes of mammalian alcohol dehydrogenase (gammagamma-ADH), the only ADH isozyme that catalyzes the oxidation of 3beta-hydroxysteroids. Based on these results, we proposed that these isoflavones might also act on other enzymes involved in 3beta-hydroxysteroid metabolism. Recently, we showed that they indeed are potent inhibitors of a bacterial beta-hydroxysteroid dehydrogenase (beta-HSD). To extend this finding to the mammalian systems, we hereby purified, characterized and studied the effects of isoflavones and structurally related compounds on, a bovine adrenal 3beta-hydroxysteroid dehydrogenase (3beta-HSD). This enzyme catalyzes the oxidation of 3beta-hydroxysteroids but not 3alpha-, 11beta- or 17beta-hydroxysteroids. The same enzyme also catalyzes 5-ene-4-ene isomerization, converting 5-pregnen 3, 20-dione to progesterone. The K(m) values of its dehydrogenase activity determined for a list of 3beta-hydroxysteroid substrates are similar (1 to 2 microM) and that of its isomerase activity, determined with 5-pregnen 3, 20-dione as a substrate, is 10 microM. The k(cat) value determined for its isomerase activity (18.2 min(-1)) is also higher than that for its dehydrogenase activity (1.4-2.4 min(-1)). A survey of more than 30 isoflavones and structurally related compounds revealed that daidzein, genistein, biochanin A and formononetin inhibit both the dehydrogenase and isomerase activity of this enzyme. Inhibition is potent and concentration dependent. IC(50) values determined for these compounds range from 0.4 to 11 microM, within the plasma and urine concentration ranges of daidzein and genistein of individuals on vegetarian diet or semi-vegetarian diet. These results suggest that dietary isoflavones may exert their biological effects by inhibiting the action of 3beta-HSD, a key enzyme of neurosteroid and/or steroid hormone biosynthesis.
http://www.ncbi.nlm.nih.gov/pubmed/10704908

estrogenic isoflavones are potent inhibitors of beta-hydroxysteroid dehydrogenase of P. testosteronii.
___________________________________________
The isoflavones daidzein, genistein, biochanin A and formononetin selectively inhibit the gamma-isozymes of mammalian alcohol dehydrogenase (ADH). Since gamma-ADH is the only ADH isoform that catalyzes 3 beta-hydroxysteroid oxidation, it was conjectured that these isoflavones might also inhibit other enzymes involved in 3 beta-hydroxysteroid metabolism. P. testosteronii beta-hydroxysteroid dehydrogenase (beta-HSD) was used to evaluate this hypothesis. Indeed, all isoflavones that inhibit gamma-ADH were found to be potent inhibitors of beta-HSD. Both the 3 beta- and 17 beta-HSD activities of the enzyme are inhibited. Kinetic analyses with pregnenolone (3-beta-OH) and testosterone (17-beta-OH) as substrates reveal that daidzein and genistein inhibit beta-HSD competitively with respect to the sterol substrates. Their Ki values are very similar and range from 0.013 to 0.02 microM. These results suggest that isoflavones may exert some of their biological effects by modulating activities of enzymes that metabolize steroids critical to hormonal and/or neuronal functions.
http://www.ncbi.nlm.nih.gov/pubmed/7488041#

What i do not understand up there underlined is:
why addiction of DHT didn't decrease gland morphology in adult mammary gland?
why affected just the midpuberty, retarding development?
maybe in the adult mammary gland, DHT in extra amount, is it converted in 3-diol? so it can neutralize is own androgenic effect? I don't know...maybe it's that back-door effect, but result is not estrogenic, otherwise mammary gland should have developed..

I could understand just flutamide action... in midpuberty should work less because of less presence of AR receptor. When AR receptors increase in post-puberty, the antagonism of them promote growing.

If we low DHT, we should mimic a bit flutamide action. And also, more testosterone will be converted in estradiol, as mentioned in your sign

Hi Clelia,

Hope you had a good weekend,

Sorry I jumped ahead a few spots, getting back to your question. 3b-diol does explain the back door response. I'm just wondering if there's a re-absorption response before being excreted?, (e.g. re-activate DHT, one more time) as seen with estrogen metabolites. I dunno?,

But in males it does seem that 3-diol has estrogen action (ER-b) in epithelia of efferent ductules and the epididymis. I'm going to post about 4-5 posts regarding this process (male ER-b) that I posted a few months ago if that's ok. If rather focus on mammary DHT's fine too, either way, there's much to solve with your help.

So what if there was way to influence an estrogen action in the Leydig cells since they already include estrogen receptors. Well, a pathway needs to be established. Here is one possible source, or could be a possible action.

Sperm, a source of estrogen
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1518866/
Environ Health Perspect. Oct 1995; 103(Suppl 7): 59–62.
PMCID: PMC1518866
Research Article
Sperm, a source of estrogen.

Other info: it's being researched already.

Estrogen signaling in testicular cells.

Aromatase transforms irreversibly androgens into estrogens and is present in the endoplasmic reticulum of various tissues including the mammalian testis. In rat all testicular cells except peritubular cells express aromatase. Indeed in adult rat germ cells (pachytene spermatocytes and round spermatids) we have demonstrated the presence of a functional aromatase (transcript, protein and biological activity) and the estrogen output is equivalent to that of Leydig cells. In addition in the adult rat, transcripts of aromatase vary according to the germ cell type and to the stages of seminiferous epithelium. By contrast with the androgen receptors mainly localized in somatic cells, estrogen receptors (ERs) are described in most of the testicular cells including germ cells. Moreover, besides the presence of high affinity ERα and/or ERβ, a rapid membrane effect has been recently reported and we demonstrated that GPR30 (a transmembrane intracellular estrogen receptor) is expressed in adult rat pachytene spermatocytes. Therefore estrogens through both GPR30 and ERα are able to activate the rapid EGFR/ERK/c-jun signaling cascade, which in turn triggers an apoptotic mitochondrial pathway involving an increase in Bax expression and a concomitant reduction of cyclin A1 and B1 gene levels. In another study in round spermatids of adult rat we have shown that the rapid membrane effect of estradiol is also efficient in controlling apoptosis and maturation / differentiation of these haploid germ cells. In man the presence of a biologically active aromatase and of estrogen receptors has been reported in Leydig cells, but also in immature germ cells and ejaculated spermatozoa. Thus the role of estrogen (intracrine, autocrine and / or paracrine) in spermatogenesis (proliferation, apoptosis, survival and maturation) and more generally, in male reproduction is now evidenced taking into account the simultaneous presence of a biologically active aromatase and the widespread distribution of estrogen receptors especially in haploid germ cells.

oK then I just have to ask...
Would men's sperm be a significant source of aromatase?

I think so, the study concluded that Leydig cells, germ cells, and seminiferous tubules all showed positive stains for aromatase. But it has to do more with the head (tip) of sperm.

I take that back, it's the tail that has the most aromatase and the head of the epididymis displays estrogen receptors where estrogen synthesis occurs.

Summary diagram of potential estrogen action in epithelia of efferent ductules and the epididymis. At least 4 potential pathways are considered. 1) testosterone (T) can enter the cell or be converted to E2 by aromatase (Arom) found in luminal sperm [54]. Testosterone binds AR and translocates into the nucleus, where it binds to AREs, on the promoter regions of genes with or without EREs. 2) E2 will either enter the cell, as did testosterone or bind the membrane ESR (mESR1). It remains controversial whether E2 binds GPR30 in the membrane [144] or collaborates with mESR1 to mediate epidermal growth factor receptor (EGFR) activation (nonclassical) of kinases and phosphorylation [180]. It is well known that E2 binds ESR1 and translocates into the nucleus for classical mediation of transcription through EREs and recruitment of numerous cofactor proteins (C1–3). It is unknown how AR and ESR1 compete for these cofactors, or what happens when the steroid balance is altered in a cell expressing both receptors. 3) The ESR1 can also be activated through phosphorylation and mediate transcription through the ERE. 4) It is well documented in other tissues that mESR1 binds E2, resulting in very rapid cell signaling [84, 175, 178]. This rapid steroid activity through the membrane receptor involves caveolin-1, G proteins, and the phosphorylation/dephosphorylation cascades, which mediate transcription either through the ESR1/ERE or other transcription factors (TF).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3071263/


I think we made an important step in solving the Estrogen action in Genetic Males and NBE.

Or a 67 yard field goal.

Clelia,
The part of the re-absorption might come from Aldo-keto reductases (AKRs), what do you think?.
Example:

Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR acts solely as a reductase to convert 5alpha-dihydrotestosterone (DHT), a potent ligand for the AR

_____________________________________________

It's like deconstructing a model (call it a airplane model) that someone else built, only you're working in reverse to deconstruct right. Same applies here, you see a study that states 5 alpha reductase is reduced in the liver, now maybe this study was for cancer research or something similar. Let's take one of these studies,

Role of human type 3 3alpha-hydroxysteroid dehydrogenase (AKR1C2) in androgen metabolism of prostate cancer cells.

Aldo-keto reductases (AKRs) is another superfamily class of enzymes like the Cytochrome P450 enzyme super family, which are present in most tissues of the body, and play important roles in hormone synthesis and breakdown (including estrogen and testosterone synthesis and metabolism), cholesterol synthesis, and vitamin D metabolism. Cytochrome P450 enzymes also function to metabolize potentially toxic compounds, including drugs and products of endogenous metabolism such as bilirubin, principally in the liver.

AKRs are involved in the development and progression of many cancers, as well as chemotherapeutic drug resistance. AKR1B1 and AKR1B10 are overexpressed in tumors, such as liver, breast, and lung cancer. Several AKRs (AKR1A1, AKR1B10, and AKR1C1-3) are involved in tobacco-carcinogenesis, but they also catalyze the detoxication of nicotine derived nitrosamino ketones. In addition, AKR1C1-3 enzymes play a key role in the regulation of proliferative signaling in hormone dependent cancers.

So what they did in this study was to cut off the androgen synthesis to the receptors using another steroid , Four human aldo-keto reductases (AKRs) that belong to the AKR1C subfamily function in vitro as 3-keto-, 17-keto- and 20-ketosteroid reductases or as 3alpha-, 17beta- and 20alpha- hydroxysteroid oxidases to varying degrees. By acting as ketosteroid reductases or hydroxysteroid oxidases these AKRs can either convert potent sex hormones (androgens, estrogens and progestins) into their inactive metabolites or they can form potent hormones by catalyzing the reverse reaction. In this manner they may regulate occupancy and trans-activation of steroid hormone receptors.

In English, I want to find the link to activate AKR1c in the liver to shut off the androgen receptors therefore DHT never gets activated, simple right?.

Regulates access of 5alpha-DHT to the androgen receptor.

Abstract
Pairs of hydroxysteroid dehydrogenases (HSDs) govern ligand access to steroid receptors in target tissues and act as molecular switches. By acting as reductases or oxidases, HSDs convert potent ligands into their cognate inactive metabolites or vice versa. This pre-receptor regulation of steroid hormone action may have profound effects on hormonal response. We have identified the HSDs responsible for regulating ligand access to the androgen receptor (AR) in human prostate. Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR acts solely as a reductase to convert 5alpha-dihydrotestosterone (DHT), a potent ligand for the AR (K(d)=10(-11)M for the AR), to the inactive androgen 3alpha-androstanediol (K(d)=10(-6)M for the AR); while RoDH like 3alpha-HSD (a short-chain dehydrogenase/reductase (SDR)) acts solely as an oxidase to convert 3alpha-androstanediol back to 5alpha-DHT. Our studies suggest that aldo-keto reductase (AKRs) and SDRs function as reductases and oxidases, respectively, to control ligand access to nuclear receptors.
http://www.ncbi.nlm.nih.gov/pubmed/17223255

Notice how Aldo-keto reductases (AKRs) position themselves between DHT and 3-diols, this is where the estrogenic action takes place. These actions of AKR1C's takes place in androgen metabolism of the prostate.

Aldo-keto reductases (AKRs) is another superfamily class of enzymes like the Cytochrome P450 enzyme super family.






Estrogen receptor β and 17β-hydroxysteroid dehydrogenase type 6, a growth regulatory pathway that is lost in prostate cancer

Estrogen receptor β (ERβ) is activated in the prostate by 5α-andros- tane-3β,17β-diol (3β-Adiol) where it exerts antiproliferative activity. The proliferative action of the androgen receptor is activated by 5α- dihydrotestosterone (DHT). Thus, prostate growth is governed by the balance between androgen receptor and ERβ activation. 3β- Adiol is a high-affinity ligand and agonist of ERβ and is derived from DHT by 3-keto reductase/3β-hydroxysteroid dehydrogenase en- zymes. Here, we demonstrate that, when it is expressed in living cells containing an estrogen response element-luciferase reporter, 17β-hydroxysteroid dehydrogenase type 6 (17βHSD6) converts the androgen DHT to the estrogen 3β-Adiol, and this leads to activation of the ERβ reporter. This conversion of DHT occurs at concentrations that are in the physiological range of this hormone in the prostate. Immunohistochemical analysis revealed that 17βHSD6 is expressed in ERβ-positive epithelial cells of the human prostate and that, in prostate cancers of Gleason grade higher than 3, both ERβ and 17βHSD6 are undetectable. Both proteins were present in benign prostatic hyperplasia samples. These observations reveal that for- mation of 3β-Adiol via 17βHSD6 from DHT is an important growth regulatory pathway that is lost in prostate cancer.

http://www.ncbi.nlm.nih.gov/pmc/articles...117772.pdf

_________________________________________________

As you can see the pathway for Testosterone, Approximately 7% of testosterone is reduced to 5α-dihydrotestosterone (DHT) by the cytochrome P450 enzyme 5α-reductase, an enzyme highly expressed in male sex organs and hair follicles. Approximately 0.3% of testosterone is converted into estradiol by aromatase (CYP19A1) an enzyme expressed in the brain, liver, and adipose tissues. Note-the percentages are slightly off, (multiple sources).

By inhibiting the enzyme 5-alpha reductase and promoting the enzyme aromatase along with your choice phytoestrogens or pharma E is key for breast growth in bio-males.

Herbs that convert aromatase-White Peony, Liorice root, Genistein (PM), BO.

Herbs that help block 5 ar, Licorice root, WP, Reishi, SP, pygeum, nettle root (NR is tricky though), BO (not an herb), chinese skullcap, linolenic acid, green tea, progesterone cream is a strong 5 ar, pumpkin seed oil, linolenic acid.

(Pharma-Dutasteride and Finasteride). Both finasteride and dutasteride undergo extensive hepatic metabolism primarily via the cytochrome P450 3A4 (CYP 3A4) isoenzyme system.

Bruno deLignieres, an impeccable French researcher and Thiery Hertoghe, MD, fourth generation in the most distinguished family of endocrinologists in Belgium, have put forth the notion that rising estrogen levels are more likely to be the initiator of the process and that testosterone and DHT may then be a secondary player (promoter). In fact, phytotherapy (large doses of phytoestrogens - soy) is commonly used in European medical practices to treat BPH.

(Jonathan Wright and Eugene Shippen have written excellent, and popular books, discussing these more far-sighted notions all too commonly overlooked and even rejected in current conventional American Medical thinking.)

Testosterone is reduced by the enzyme 5-a-reductase to DHT which is then thought to be the real culprit. The argument between the use of Saw Palmetto, Pygeum and Pumpkin seeds vs Proscar are both directed at blocking this enzyme. Strangely, DHT is most important for sexual vigor, so blocking this step may have some unintended consequences!

On the other hand, Testosterone is also converted into estradiol by aromatase (producing the aromatic ring). This occurs increasingly with age in the liver but most importantly ... in the fat stores.

http://www.antiaging.com/andropause/andropause2.html

Its been stated here before that the Androgen to Estrogen pathway is easier than the Testosterone to Estrogen pathway, and once again aromatase continues to demonstrate the factual evidence.

A couple of French researchers recently reported this:

Testosterone is reduced by the enzyme 5-a-reductase to DHT which is then thought to be the real culprit. The argument between the use of Saw Palmetto, Pygeum and Pumpkin seeds vs Proscar are both directed at blocking this enzyme. Strangely, DHT is most important for sexual vigor, so blocking this step may have some unintended consequences!

On the other hand, Testosterone is also converted into estradiol by aromatase (producing the aromatic ring). This occurs increasingly with age in the liver but most importantly ... in the fat stores.
Now you see the connection. As we age, and frequently gain increasing fat stores, we are feeding the aromatase connection, increasing our estradiol levels and if this theory holds, increasing the promotion of prostate disease.

Also that rising estrogen levels are more likely to be the initiator of the process and that testosterone and DHT may then be a secondary player (promoter). In fact, phytotherapy (large doses of phytoestrogens - soy) is commonly used in European medical practices to treat BPH.

Another example of the androgen/estrogen pathway:



http://www.antiaging.com/andropause/andropause2.html

That's a good find, Clelia. Thanks!

happy you appreciate, you're welcome

what's your opinion?, sorry.... I've listed like 10 issues lol.

yep, lot of stuff to read here ... i'm reading everything you reported.
I will answer later on.

The first thing that I want to say is...
I spent an afternoon trying to understand this:

In this study, we investigated whether development of the murine mammary gland could be altered by stimulating or suppressing androgen receptor (AR) signaling in vivo. Intact virgin female mice aged 5 wk (midpuberty) or 12 wk (postpuberty) were implanted with slow-release pellets containing either placebo, 5α-dihydrotestosterone (1.5 mg) or the AR antagonist flutamide (60 mg). Treatment with 5α-dihydrotestosterone from midpuberty to 12 wk of age-retarded ductal extension by 40% (P = 0.007), but treatment from 12-21 wk had no significant effect on gland morphology. In contrast, inhibition of AR signaling with flutamide from midpuberty had no effect on the mammary gland, but flutamide treatment from 12-21 wk increased ductal branching (P = 0.004) and proliferation (P = 0.03) of breast epithelial cells. The increased proliferation in flutamide-treated mice was not correlated with serum estradiol levels or estrogen receptor-α (ERα) expression.

http://www.ncbi.nlm.nih.gov/pubmed/21846805

moreover: In control mice, the frequency and intensity of AR immunostaining in mammary epithelial cells was significantly increased in the 12- to 21-wk treatment group compared with the 5- to 12-wk group (P < 0.001). In contrast, no change in ERα occurred, resulting in a marked increase in the AR to ERα ratio from 0.56 (±0.12) to 1.47 (±0.10).
--> this means that receptor ERalfa is in the same quantity, in midpuberty and postpuberty. In contrast, AR receptor triple from middlepuberty to post-puberty, and that's why breast stop to grow in female (because AR receptors increase a lot).

Also we see from your favourite article that male rats depleted of AR receptors, develop full mammary gland.

So we see how important is AR signals in breast size (despite everything else).

What i do not understand up there underlined is:
why addiction of DHT didn't decrease gland morphology in adult mammary gland?
why affected just the midpuberty, retarding development?
maybe in the adult mammary gland, DHT in extra amount, is it converted in 3-diol? so it can neutralize is own androgenic effect? I don't know...maybe it's that back-door effect, but result is not estrogenic, otherwise mammary gland should have developed..

I could understand just flutamide action... in midpuberty should work less because of less presence of AR receptor. When AR receptors increase in post-puberty, the antagonism of them promote growing.

If we low DHT, we should mimic a bit flutamide action. And also, more testosterone will be converted in estradiol, as mentioned in your sign

Circulating 2-hydroxy and 16-α hydroxy estrone levels and risk of breast cancer among postmenopausal women

Thank you about this information, i read the abstract but i didn't get it... it talks about a ratio between two components, but i don't see what ratio. I will open the pdf... but not now... (no time left), btw, do you know if there is something that low this risk?

On another note....I've seen that EPA and DHA reduces the risk of breast cancer by as much as a 32% reduction, I don't know the dosage.

the article you posted says:
"The purpose of the WHEL Study was to assess whether a major increase in vegetable, fruit, and fiber intake and a decrease in dietary fat intake reduces the risk of recurrent and new primary breast cancer and all-cause mortality among women with previously treated early-stage breast cancer.
Women with higher intakes of EPA and DHA from food had an approximate 25% reduced risk of additional breast cancer events, compared with the lowest tertile of intake. Women with higher intakes of EPA and DHA from food had a dose-dependent reduced risk of all-cause mortality. EPA and DHA intake from fish oil supplements was not associated with breast cancer outcomes. The investigation indicates that marine fatty acids from food are associated with reduced risk of additional breast cancer events and all-cause mortality. J. Nutr. 141: 201–206, 2011."
maybe you can find the answer at your question in this table:

" Anti-androgenic activity of fatty acids." http://www.ncbi.nlm.nih.gov/pubmed/19353546 (2009)

Great link, thank you so much, I can only think of two supplements that cam meet that demand........coconut oil and EPO-evening primrose oil.

and hemp seed oil

I've got to go now. I know that i still miss something, i'll come back next week, i'm off for the weekend. see you!

Hi Lotus, i like reading your posts, now I have no much time to answer, but I can tell you something

Thanks Clelia, , I appreciate your time.

Research is often controversial, because maybe in different studies there are differences that could affect results (for example, in vivo and in vitro can change final results).

Great point, I noticed limitations in some studies (e.g. available test samples w/regards to country's ban or limitations) could affect results, but I understand what you mean.

Also, we should take account of the target of the subject: different tissues can respond in different ways, with same inizial conditions. This is due to the variability of the receptor expressed in every tissue, which often are not the same and in same amount (understandably).

Ok, Like multiple response, or unintended consequence.

So, your research about the "estrogen DHT metabolite", is based on prostate, not breast tissue or skin. That's why men become bald: there is androgen dominance in their skin, and fighting DHT is proved good to grow hair.
Also, the DHT metabolite, interacts with ERb, and we know that alfa is better for breast growth, isnt it?

BPH/prostate research does seemed skewed towards 5-ar inhibitors/ anti DHT. Since the prostate is pro ER-a it seems likely estrogen could be a mediator of cancers too.

Its good to try to convert DHT in estrogen metabolite, but i think its better to shut it down, at least for breast growth.

I've seen some promising research that includes androgen blockade therapy, 17beta -HSD, even using prolactin molecules to box out DHT because of their larger size, suggesting to me PRL is DHT inhibitor. But I think COX is also an aromatase at PGE.

And if you do this, what about your prostate risk? Since the metabolite help prevent prostate cancer, what if you low it? I think you should read this also, maybe there are other mechanisms involved, in prostate cancer:

Yes, elimaniting androgen/DHT ip even in Mtf has long term consequence. The biological affects of androgens are are still needed. The assumptation of testosterone being poison is often misinterpreted. Testosterone is the sex hormone that converts to all estrogens, without T Mtf wouldn't make the necessary conversion to transition. I think it's a mistake to reduce testosterone, the reduction is needed at DHT...... and the reason is quite obvious.

" Anti-androgenic activity of fatty acids." www.ncbi.nlm.nih.gov/pubmed/19353546 (2009)

Great link, thank you so much, I can only think of two supplements that cam meet that demand........coconut oil and EPO-evening primrose oil.

The question we should be asking is how much......

As in how much Testosterone (DHT) do I need to overcome daily, or how much estradiol besides my .3 mg I produce daily is needed.

Here's what I mean--

According to the National Institutes of Health, the normal range of testosterone is 30 to 95 nanograms per deciliter (ng/dL) for women and 300 to 1,200 ng/dL for men, but individual laboratories might have a slightly different range that they consider normal. Also keep in mind that the levels vary with age. In women, the level of testosterone in the blood is lowest during puberty and adolescence, and is highest in pre- and post-menopausal women. For men, the levels increase during puberty and stay steady for much of their young adult life. They then slowly begin to decline during middle and older age.
http://www.livestrong.com/article/239396...r-a-woman/


Men and women produce exactly the same hormones, but in different amounts: as a rule, men produce 20 times more testosterone than women, while women produce more estrogen and progesterone. As with most things in nature, this "norm" can become imbalanced, and some women may have higher levels of testosterone, causing a unique set of symptoms.

Daily averages-

Endogenous avg. produced daily (males)

MEN
-Hormone ( FSH): 2 - 18 mIU/ml
-Testosterone 3mg to 10mg (daily)
-Prolactin 7 - 18 ng/ml
-FT-Free T is about 2% (this is the functional T)
-BT-Bound T or 98%
-Albumin 38% (bloodstream)
-SHBG is 60% (sex-hormone-binding-globulin)
-DHT approximately 7% of T is reduced by 5 ar
-Estradiol approximately 0.3% of testosterone is converted into E2 by aromatase (CYP19A1) of that 0.3%, 20% is directly produced by the testes. Roughly 60% of circulating estradiol is derived from direct testicular secretion or from conversion of testicular androgens. The remaining fraction is derived from peripheral conversion of adrenal androgens. The serum levels of estradiol in males (14 - 55 pg/mL) are roughly comparable to those of postmenopausal women (< 35 pg/mL).

Endogenous avg. produced daily (females)

WOMEN
-Testosterone 0.05 mg (produced daily)
-FT-Free T normal calculated free testosterone is 0.4 – 0.8 ng/dl (or 40 – 80 pg/dl).
-Albumin 34% bloodstream)
-SHBG is 66% (sex-hormone-binding-globulin)
-Estradiol 70 to 500 mg of estradiol daily, (depending on the phase of the menstrual cycle. This is converted primarily to estrone, which circulates in roughly equal proportion to estradiol, and to small amounts of estriol.)
-Estradiol in postmenopausal women (< 35 pg/mL).
-Progesterone levels tend to be < 2 ng/ml prior to ovulation, and > 5 ng/ml after ovulation. If pregnancy occurs, human chorionic gonadotropin is released maintaining the corpus leuteum allowing it to maintain levels of progesterone.

Avg tests

Hormone Follicular Day of LH Surge Mid-luteal
-Follicle Stimulating (FSH) < 10 mIU/ml > 15 mIU/ml -
-Luteinizing Hormone-(LH) < 7 mIU/ml > 15 mIU/ml -
-Prolactin < 25 ng/ml
-Thyroid Stimulating Hormone 0.4 - 3.8 uIU/ml (TSH)
-Estradiol ( E2) < 50 pg/ml ( Day 3) > 100 pg/ml
-Progesterone < 1.5 ng/ml > 15 ng/ml




Reference Values
Free Estradiol, Percent
Reference Ranges (%)

Adult Males 1.7 - 5.4
Adult Females 1.6 - 3.6

Free Estradiol, Serum
Reference Ranges (pg/mL)

Adult Males 0.2 - 1.5
Adult Females 0.6 - 7.1

Sex Hormone Binding Globulin (SHBG), Serum
Reference Ranges
Adult Males 20 - 60
Adult Female
Premenopausal 40 - 120
Postmenopausal 28 - 112

the most complete list here:
http://wikipedia.org/wiki/Reference_rang...lood_tests

This is very interesting:

Normal Hormone Proportions
http://georgiahormones.com/pdf/Brochure_...rtions.pdf

[/quote]

[Lotus]

Hi exceptional people,

In this study (animal) aromatase expression increased in the AT (318.5 +/- 60.6% of control in scAT, P n< 0.05, and 285.5 +/- 82.9% of control in vAT,

That's 60.6% in subcutaneous fat and 82.9% in visceral fat.

Chronic green tea consumption decreases body mass, induces aromatase expression, and changes proliferation and apoptosis in adult male rat adipose tissue.

Abstract
Green tea (GT) and its components have been shown to possess antiobesity properties and the corresponding mechanisms of action are being investigated, given the epidemic proportions of obesity incidence. In the current work, we used 12-mo-old male Wistar rats to test the effect of 6 mo of treatment with GT as the sole drinking beverage (52.8 +/- 6.4 mL/d) on adipose tissue (AT). AT aromatase expression was determined by Western blotting, plasma concentrations of 17beta-estradiol and testosterone were determined by RIA, and adipocyte size determined by measuring diameter in tissue sections. Proliferation and apoptosis were also assessed by Ki67 immunostaining and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling, respectively. Evaluations were made in subcutaneous (sc) AT and visceral (v) AT. Body weight increased over time in both groups (P < 0.001), but the increase was more pronounced in controls (P < 0.001) and food and fluid intake did not influence that effect. At the end of the experiment, aromatase expression increased in the AT (318.5 +/- 60.6% of control in scAT, P < 0.05, and 285.5 +/- 82.9% of control in vAT, P < 0.01). AT of GT-treated rats had a higher percentage of proliferating cells (204.1 +/- 19.5% of control in scAT, P < 0.01, and 246.6 +/- 50.2% of control in vAT, P < 0.01) and smaller adipocytes (78.3 +/- 1.7% of control in scAT, P < 0.001, and 87.9 +/- 3.2% of control in vAT, P < 0.05). GT also increased the number of apoptotic cells in vAT (320.4 +/- 21.9% of control; P < 0.001). These results suggest new mechanisms for GT on body weight and highlight its potential benefit to prevent or treat obesity and the metabolic syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/18936213#

[hannah]

So about the piperine you'd say add black pepper to or in a meal in-around your green tea?
Interesting stuff, wonder if there's a specific reason why pepper and polyphenols
bc its a growse combination when it comes to taste..lol..I mostly tend to go out from the ''nature takes care off it''
setpoint..
And I love the cp17-cyp34 enzyme research stuff:p Thanks a lot for all this,I"m am almostly cross-eyed now..time for a green tea

Oh I almostly forgot I got the full research link bout the enzymes for anyone who's interested: http://www.tandfonline.com/doi/pdf/10.1271/bbb.70511

And what about ''blocking'' LH?

[Lotus]

So about the piperine you'd say add black pepper to or in a meal in-around your green tea?
Interesting stuff, wonder if there's a specific reason why pepper and polyphenols
bc its a growse combination when it comes to taste..lol..I mostly tend to go out from the ''nature takes care off it''
setpoint..
And I love the cp17-cyp34 enzyme research stuff:p Thanks a lot for all this,I"m am almostly cross-eyed now..time for a green tea

Oh I almostly forgot I got the full research link bout the enzymes for anyone who's interested: http://www.tandfonline.com/doi/pdf/10.1271/bbb.70511

And what about ''blocking'' LH?

Awesome, (boobie points to Hannah)

Seriously , mapping these CYP enzymes can help us track drug interactions (i.e drug-drug interactions too). Another find is linking cell penetrating peptides (a pro boob carrier proteins) to boob growth. (more on that later, lol)

something interesting is seeing how a diet high in sugars and starch inhibit NBE. High blood sugars is no good for many reasons (diabetes, etc), but also looks to be the same. The way fatty acids stick like sludge in our blood is no good either, in other words , time to displace hormones from SHBG and fats in the blood.

Push for a plan that includes a major (multiples) anti-oxidant. I like the way astaxanthin looks for this, I think it's stronger than CoQ-10. But, the way coenzymes interact and react to boob growth is key new new growth, when used correctly.

Sooooo, reduce the inflammation in our bodies to free up new boob growth. Fruits and vegetables (in red pigment colors) are an easy fix, certainly a better (healthier) approach towards NBE imo.

@ Hannah, absolutely, by inhibiting LH it suppresses T, which as I stasted before, this would upreglaues FSH to synthesize (make more) estradiol. Piperine mixed in with_____ fill in the blank lol, red veggies would be my choice.


I look at this way, if my boobs ain't aching, dey ain't growing .

[Marcy]

Have you seen this article?

http://www.altmedrev.com/issues/81-volum...staxanthin

Seems this astaxanthin you've uncovered is some interesting stuff indeed!

[Lotus]

Have you seen this article?

http://www.altmedrev.com/issues/81-volum...staxanthin

Seems this astaxanthin you've uncovered is some interesting stuff indeed!

Great find on the review Marcy, thanks.

I like what astaxanthin does, and the small dose (up to 12 mgs) makes it an attractive option. But the other huge plus is its ability to inhibit DHT, coupled with the other antioxidant, weight management, pain relief, I'm like why the F*** haven't we seen this earlier. In the study below, I see astaxanthin kicking SP's butt when they where combined together, see for yourself. (That's just my opinion though).

I'm seeing red,

Chinese Red Yeast Rice Inhibition of Prostate Tumor Growth in SCID mice
http://www.ncbi.nlm.nih.gov/pmc/articles...320100.pdf

Gene expression of androgen synthesizing enzymes and androgen receptor (AR)
In RYR-fed animals, HSD3B2, AKR1C3 and SRD5A1 gene expression was downregulated more than threefold in LNCaP tumors, and more than twofold in LNCaP-AR tumors (P<0.05) (Figure 8A, 8B and 8C). The RYR diet also decreased AR expression more than twofold in androgen-independent SCID tumors (P<0.05) (Figure 9). The transcription levels of HSD3B2, AKR1C3 and SRD5A1 and AR were higher in androgen-independent tumors than androgen-dependent tumors (P<0.05) (Figures 8 and 9).

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A preliminary investigation of the enzymatic inhibition of 5alpha-reduction and growth of prostatic carcinoma cell line LNCap-FGC by natural astaxanthin and Saw Palmetto lipid extract in vitro.

J Herb Pharmacother. 2005;5(1):17-26.
Abstract
Inhibition of 5alpha-reductase has been reported to decrease the symptoms of benign prostate hyperplasia (BPH) and possibly inhibit or help treat prostate cancer. Saw Palmetto berry lipid extract (SPLE) is reported to inhibit 5alpha-reductase and decrease the clinical symptoms of BPH. Epidemiologic studies report that carotenoids such as lycopene may inhibit prostate cancer. In this investigation the effect of the carotenoid astaxanthin, and SPLE were examined for their effect on 5alpha-reductase inhibition as well as the growth of prostatic carcinoma cells in vitro. These studies support patent #6,277,417 B1. The results show astaxanthin demonstrated 98% inhibition of 5alpha-reductase at 300 microg/mL in vitro. Alphastat, the combination of astaxanthin and SPLE, showed a 20% greater inhibition of 5alpha-reductase than SPLE alone n vitro. A nine day treatment of prostatic carcinoma cells with astaxanthin in vitro produced a 24% decrease in growth at 0.1 mcg/mL and a 38% decrease at 0.01 mcg/mL. SPLE showed a 34% decrease at 0.1 mcg/mL.
CONCLUSIONS: Low levels of carotenoid astaxanthin inhibit 5alpha-reductase and decrease the growth of human prostatic cancer cells in vitro. Astaxanthin added to SPLE shows greater inhibition of 5alpha-reductase than SPLE alone in vitro.

PMID 16093232 [PubMed - indexed for MEDLINE]

Anti-cancer potential of flavonoids: recent trends and future perspectives
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3824783/

[Marcy]

WoW MoM! That is impressive. I've been thinking about putting SP back in my program and this might be worth a trial month or two. SP extract and low dose andastaxanthin. Hmmmm?

I think we might need a two letter designation for astaxanthin!