[Lotus]

So sorry lotus for making you keep on repeating the same thing, i am totally a noob when coming to [/align] scientific stuff so i might have overlooked it in the thread

But thanks a lot for explaining and answering it again. I have just added reishi in my program, hope it will works for me

No apologies necessary , honestly the tech stuff doesn't come with a manual that we all can understand, too bad huh?.

Ask away, if anything sharing info helps us to better our programs. For instance E1, (estrone) is derived from peripheral aromatization of androstenedione (mainly adrenal)".

E2 is produced primarily in ovaries and testes by aromatization of testosterone. Small amounts are produced in the adrenal glands and some peripheral tissues, most notably fat. By contrast, most of the circulating E1 is derived from peripheral aromatization of androstenedione (mainly adrenal). E2 and E1 can be converted into each other, and both can be inactivated via hydroxylation and conjugation. E2 demonstrates 1.25-5 times the biological potency of E1. E2 circulates at 1.5-4 times the concentration of E1 in premenopausal, nonpregnant women.

[Lotus]

Progesterone and estrogen E2 (together) in-quote-"induced proliferation that resulted in sidebranching and alveologenesis," but E+P treatment produced more proliferation sooner and extensive sidebranching and alveologenesis. The exact amounts of E2 (estradiol) and progesterone weren't given. In other words having progesterone combined with E2 produces side-branching of the breasts (outward growth),

function of progesterone receptor isoforms in normal adult mouse mammary gland.
Aupperlee MD1, Haslam SZ.
Author information
Abstract
In normal mouse mammary gland, the mitogenic action of progesterone (P) is mediated by two P receptor (PR) isoforms, PRA and PRB. PRA is predominantly expressed in the adult virgin, and PRB is predominantly expressed during pregnancy. To investigate hormonal regulation of PR isoform expression and isoform-specific functions in vivo, adult ovariectomized BALB/c mice were treated for 3, 5, or 10 d with estrogen (E), P, or estrogen plus progesterone (E+P). Using an immunohistochemical approach with isoform-specific antibodies, we investigated hormonal regulation of PRA and PRB and their functional roles in proliferation and morphogenesis. Significant E-induced proliferation was only observed after 5 d at the distal tips of ducts; there was no sidebranching or alveologenesis. P induced proliferation that resulted in sidebranching and alveologenesis, but E+P treatment produced more proliferation sooner and more extensive sidebranching and alveologenesis. PRA levels were increased by E and decreased by P. Increased PRB levels were induced by treatment with P or E+P and coincided with the formation of alveoli. PRA was the predominant PR isoform expressed during sidebranching, and colocalization of PRA with 5-bromo-2'-deoxyuridine revealed that proliferation of PRA-positive and -negative cells was responsible for P-induced sidebranching. PRB was the predominant PR isoform expressed during alveologenesis, and colocalization of PRB with 5-bromo-2'-deoxyuridine showed that both PRB-positive and -negative cells proliferated during alveolar expansion. These results demonstrate different hormonal regulation of PRA and PRB levels in vivo and suggest that P can induce proliferation through either PRA or PRB via direct and paracrine mechanisms.
http://www.ncbi.nlm.nih.gov/pubmed?filters=&orig_db=PubMed&cmd=Search&term=148%2A%5Bvolume%5D%20AND%202290%5Bpage%5D%20AND%202007%5Bpdat%5D%20AND%20Aupperlee%20MD%5Bauth%5D

[The First Aria]

No apologies necessary , honestly the tech stuff doesn't come with a manual that we all can understand, too bad huh?.

Ask away, if anything sharing info helps us to better our programs. For instance E1, (estrone) is derived from peripheral aromatization of androstenedione (mainly adrenal)".

E2 is produced primarily in ovaries and testes by aromatization of testosterone. Small amounts are produced in the adrenal glands and some peripheral tissues, most notably fat. By contrast, most of the circulating E1 is derived from peripheral aromatization of androstenedione (mainly adrenal). E2 and E1 can be converted into each other, and both can be inactivated via hydroxylation and conjugation. E2 demonstrates 1.25-5 times the biological potency of E1. E2 circulates at 1.5-4 times the concentration of E1 in premenopausal, nonpregnant women.

Hey Lotus, my tests came back and my androstenedione levels are like 14 mgl instead of 21. Could that mean the rest are getting converted to E???

[Lotus]

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.

[elainecd]

My God Lotus.....you just keep on finding new stuff!
Thank you and before I start searching......what's best common source(s) for these essential fatty acids?

I need some, seems like I saw some in your NBE foods post.

Tomorrow (4/27) I celebrate 8 full months on NBE. Yippee!
Really appreciate your help and advice.

[Lotus]

My God Lotus.....you just keep on finding new stuff!
Thank you and before I start searching......what's best common source(s) for these essential fatty acids?

I need some, seems like I saw some in your NBE foods post.

Tomorrow (4/27) I celebrate 8 full months on NBE. Yippee!
Really appreciate your help and advice.

Sure, my pleasure. Have you ever tried coconut oil as a supplement?, taking coconut oil 2000 mg (to start) along with 1200 to 1800 mg of fenugreek aids in building tissue and reduces DHT. The fatty acids in CO (lauric acid and capric acid) are found in human breast milk, the theory would be to induce prolactin type response in building milk supply, whether lactation is produced is lacking conformation, regardless of that, the health benefits alone are worth looking into. Also, these omega 6's would be a good addition too. (Organic only)

Borage or hemp oil
Krill oil
Cod liver oil
Chia seeds
Black currant oil
Evening primrose oil

[Lotus]

Welcome, I've decided to combine 3 threads into one, making it easier to reference for myself and anyone seeking specific info, unfortunately it will be a lengthy thread. Be my guest and read the whole thing (if you dare lol), you will find some of the lastest discoveries used at BN. I apologize for removing pics, we all have our reasons, sometimes I update them. Although I've attached these two as reference.

Good luck, give me a shout if you actually complete the read, you might be the First, if you do I'll give you a complete program overview (it's the least I could do, considering wasting your valuable time with the read lol.)



The following post is from page one, (the beginning lol).

---------------
I haven't shared a plan because I was still tweaking it, I had to see if it worked first, so here's what i used.Yeah I know, this should go in the program section, but feel I need to share in the guy section today. My goal was to prove that a guy could be bigger than B-cup*. In 12 months I never measured myself until a couple of weeks ago. I don't know why,but never felt the need until I found sfem's breast measuring guide. According to the table I'm a C-cup, 9 .75 on the right, 9.5 on the left. I've checked it several times just to make sure.


Starting Doses
----------------------
PM -500 mg tab,6 tabs,total=3000mg (am,noon,pm)
SP -450mg 4x a day (am,noon,pm)
PC -1/4 teaspoon (applied to chest and wrists) 2x a week
Massage -when ever you can,5 min ea. side
Calcium - 600mg 3x a day (am,noon,pm)
Revised Doses
-----------------------------
PM 500 mg tab,6 tabs,total= 3000 mg (am,noon,pm)
Spearmint caps -400 mg 3x(am,noon,pm)
PC - 1/4 teaspoon (applied to chest and wrists)3x a week
Calcium -600mg 3x a day (am,noon,pm)
Massage 5 min same as above

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

Currently on a break from the plan due to health reasons, so I'm trying to find a detox plan that's right for me. I've said this before, there are possible risks when you are experimenting with NBE. You can find that information here, so again, pay close attention to the side effects you might get.


I doubled checked the cup size again 5 days after starting the break, and I'm getting a 1/4 inch increase, I'll check it in a few days to see if it holds. Please note this is just my plan, I put this program together from researching other BN members plans.




Take care, Lotus

Thank you Eve.

[pom19]

Well Lotus, you know I like the one in black bra. POM

[Lotus]

Well Lotus, you know I like the one in black bra. POM

Thanks POM, sadly the bra wearing days evolved back to wearing T-shirts lol. I think I get mistaken as a transman with as many times I've heard ma'am. I'm ok with that, although I'll point "I'm a guy". I think I've figured out what gender binary straight men with breast are, basically they're genetic transman), or transman-man or even transgenticman (that one lol doesn't exist). So......call this a new gender fluid, which btw, I've asked Eve to include "Fluid" to our gender identity section, (and why not) I authored that section so why shouldn't be able to suggest adding an inclusion. Why not open the gender section to what it should be......any related gender, MtF, FtM, Bi, Pan, Metro, gay/lesbian etc. (although I do like the ring of transman-man, wouldn't that be MtFM..... I don't consider this new gender binary to be in a lesbian relationship with a spouse/girlfriend, you certainly don't refer a transman being in a lesbian relationship. Honestly .......it's still straight men being straight, except it?...... well, no offense but I don't care if some can't.

[Lotus]

The death of DHT,

dutasteride (the strongest anti-androgen) dual inhibition reduces median serum DHT levels by 90% at 2 weeks and 93% at 2 years.

This is why breast growth takes a while, include feminaztion in the statement. So, a little help from the studio audience please.


If males produce 3mg to 10mg of Testosterone daily and 4% gets converted to DHT, how much anti-androgens are needed to give DHT a proper burial?, (I think of it as the NBE therapeutic edge)


????..... Give it your best shot, no one answer is a wrong answer.