[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/v6/n7/fig_tab/nchembio.394_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/PMC3404296/?report=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.