[Lotus]

I'll just ask the obvious question, what do think is stonger DHT or aromatase?


If you remove DHT (or limit) what's left?

You got it, aromatase, which DHT is non-aromatizable!!!!

Even if you use this statement which lacks a research paper, what does it say?

Paul Stamets lists Red Reishi Mushroom extract - in the form of his own proprietary formulation, which is what we sell - as decreasing levels of 5-alpha-reductase by over 75%. Inhibition of 5-alpha-reductase is considered important to limiting prostate cancer growth. Stamets also lists Red Reishi Mushroom extract as decreasing Aromatase by over 40%. Aromatase is a breast cancer causative agent. 134

[Lotus]

free Testoserone not "total testosterone" will get converted through aromatase to E2, DHEA and DHEAS will convert to E1 through the androstenedione pathway, and E1 will fluctuate back and forth from E3 to E1, weak production to say the least, which one do you think benefits Breast growth?. But that adressses the other option for aromatase, in both sexes.

Focusing entirely on aromatase will leave you short in breast growth, and pressing the aromatase pedal will favor breast cancer if not careful, that's where detoxing comes into play in getting rid of the bad metabolites 4OH and 16OH.

_______________________

Spearmint affects FREE TESTOSTERONE, why would you take that to influence aromatase?

[Outsider]

I'll just ask the obvious question, what do think is stonger DHT or aromatase?


If you remove DHT (or limit) what's left?

You got it, aromatase, which DHT non-aromatizable!!!!

Even if you use this statement which lacks a research paper, what does it say?

Paul Stamets lists Red Reishi Mushroom extract - in the form of his own proprietary formulation, which is what we sell - as decreasing levels of 5-alpha-reductase by over 75%. Inhibition of 5-alpha-reductase is considered important to limiting prostate cancer growth. Stamets also lists Red Reishi Mushroom extract as decreasing Aromatase by over 40%. Aromatase is a breast cancer causative agent. 134

Lotus, in your opinion is it better to continue taking reishi or drop it from my BO program?

Though I guess the WP might help cancel out the decrease in aromatase somewhat.

[Lotus]

xxd was dialed in on NBE, which steered me into looking outside the box. We are finding new weapons to use towards NBE and even HRT imo, GnRH's is one approach as we've heard, ALA's, GLA's (MUFA's and PUFA's) mono and polyunsaturated fats, reducing inflammation are new tools just to say a few.

Outsider, we should change that name to insider lol, Personally I would stick to reishi, it also has strong aspects not mentioned, such as helping with oxidatitive stress, and reishi is another anti-inflammory which is huge, and that alone makes a powerful aromatase.

[Lotus]

Now here's something to try, and more info is posted here, but take a look at this.

So I see a possible correlation with inflammation (systemic, chronic) and phytoestrogens (maybe more so in PM). Now this could vary according to your inflammatory response, meaning what's in your daily diet.

“Acute inflammation normally resolves by mechanisms that have remained somewhat elusive. Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins. After entering tissues, granulocytes promote the switch of arachidonic acid–derived prostaglandins and leukotrienes to lipoxins, which initiate the termination sequence. Neutrophilrecruitment thus ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids, of resolvins and protectins, which critically shorten the period of neutrophil infiltration by initiating apoptosis. As a consequence, apoptotic neutrophils undergo phagocytosis by macrophages, leading to neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming growth factor-β1. The anti-inflammatory program ends with the departure of macrophages through the lymphatics.”
—Charles Serhan

So inflammation may also reduce the biosynthesis of albumin, the part of blood plasma that carries the more bio-active hormones that can be influenced to become active, unlike SHBG-sex hormone binding globulin.

Sorry if this is out there, I don't think this has been addressed yet, when you get time try and look over this link from Wikipedia, it's very informative. There's a ton of other info out there about this so other sites might explain it better. And seriously look into the ratio of omega 3's to omega 6's, it should favor more 3's, that should help in reducing immflamation. You might see some better gains once inflammation is reduced.



http://wikipedia.org/wiki/Inflammation#S...nd_obesity

[Outsider]

xxd was dialed in on NBE, which steered me into looking outside the box. We are finding new weapons to use towards NBE and even HRT imo, GnRH's are one approach, ALA's, GLA's (MUFA's and PUFA's) mono and polyunsaturated fats, reducing inflammation are new tools just to say a few.

Outsider, we should change that name to insider lol, Personally I would stick to reishi, it also has strong aspects not mentioned, such as helping with oxidatitive stress, and reishi is another anti-inflammory which is huge, and that alone makes a powerful aromatase.

Thank you Lotus, I guess the reishi can stay in my program after all.

[Lotus]

Here's another thing to consider:

In estrogen dominance the actual estrogen receptors become less responsive or sensitive, which is called desensitization.

So that's why taking too much E will slow a program, then you should consider a detox, "not a break" a real detox.

Last point about the stronger DHT pathway:

[Lotus]

Sorry I have one other point, lol a few. And we might be able to catch DHT going out hitting ERß , some new prospects.

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.

We have another tool in the tool shed for NBE, or in other words the prostrate and male reproductive organs has more estrogenic pathways (& production) than previously thought. I'm just in the process of connecting the dots and how these metabolites can help us. (Some theorized other metabolites had no value and dismissed them, here we clearly this that's not the case).


This next paragraph explains the process and is a step in the right direction.


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.

And this might help too.





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

Wow I forgot about this, but it's another potential tool for fighting DHT. (Fat men rejoice lol)


Human type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2) and androgen metabolism in prostate cells.
In prostate cells AKR1C2 acts as a 3-ketosteroid reductase to eliminate 5alpha-DHT and prevents activation of the androgen receptor. AKR1C2 does not act as an oxidase due to either potent product inhibition by NADPH or because it cannot surmount the oxidative 17beta-HSD present. Neither AKR1C2, retinol dehydrogenase/3alpha-HSD nor 11-cis-retinol dehydrogenase is a source of 5alpha-DHT in PC-3 cells.
http://www.ncbi.nlm.nih.gov/pubmed/12810547

Androgen inactivation and steroid-converting enzyme expression in abdominal adipose tissue in men.
In conclusion, androgen inactivation was detected in abdominal adipose tissue in men, with higher 3alpha/beta-HSD activity in the s.c. versus Om depot. Higher Om 5alpha-DHT inactivation rates were found in obese compared with lean men. Further studies are required to elucidate whether local androgen inactivation in abdominal adipose tissue is involved in the modulation of adipocyte metabolism and regional fat distribution in men.
http://www.ncbi.nlm.nih.gov/pubmed/17170221

Androgen metabolism in adipose tissue: recent advances.
We speculate that glucocorticoid-induced androgen inactivation could locally decrease the exposure of adipose cells to active androgens and partially remove their inhibitory effect on adipogenesis. We hypothesize that body fat distribution patterns likely emerge from the local adipose tissue balance between active androgens and glucocorticoids in each fat compartment.
http://www.ncbi.nlm.nih.gov/pubmed/19022338

[Lotus]

Listed in the Anti-Androgen thread and is often overlooked is that Reishi "has" estrogenic properties and at the same time addresses DHT, which makes it a Win-Win.

^^^^^^^^^^^^^^^^^

The ability to bind to human estrogen receptors (hERs) α and β of the ethanol extract of G. lucidum was confirmed by using the coactivator-bacterial alkaline phosphatase system.

Estrogen-like activity of ethanol extract of Ganoderma lucidum
http://link.springer.com/article/10.1007...008-0992-2

[Lotus]

Lastly:

The unique composition of human breast milk fat includes the fatty acids, lauric acid and capric acid, which have potent antimicrobial properties. These fatty acids offer the nursing infant protection from viruses such as herpes and HIV, protozoa such as giardia lamblia, and bacteria such as chlamydia and heliocobater.

Any lauric acid and capric acid in the diet becomes part of the adipose stores.

So taking along with a prolactin inducing herb such as Alfalfa/Fenugreek, coconut when taken internally will increase lauric acid reserves which then become apart of the fat tissues in the breasts which enlarges them... so adding coconut oil would be helpful, no telling by how much though