04-02-2016, 03:30 AM
(03-02-2016, 01:30 PM)hannah Wrote: Wow this is so interesting, wish we could live in a BN house-clinic for awhile to talk things over in real life..that would be much fun, we exceptional people understand how much fun our body is and it would be great to share and talk bout this in real life(lol)..
I like it, sign me up, sounds like fun.
(03-02-2016, 01:30 PM)hannah Wrote: Anyhow back to the subject..How does nature activate estrogen receptors?
And how long does it take to activate estrogen receptors with for example PM?
A few ways actually. You see, lol, I know some crazy shit about estrogen receptors, for instance, androgens can enhance the sensitivity of receptors, in fact DHT is an anti-cancer in breast tissue, (gives way to why androgens in breasts tissue kills NBE lol). However, I'm thinking the best scenario of how to utilize androgens in the breasts, e.g. utilizing androgens that upregulate receptors (aka-co-regultors) and then flip those suckers back to synthesize as estrogens before they degrade, cool huh?.
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.
Same study:
In the event that estrogen action is reduced or nullified, either via loss of ERα or under conditions of long-term estrogen deprivation, AR levels increase, coregulatory interactions change, and AR becomes a surrogate ERα to sustain tumor growth. At a certain level of AR expression
PM needs the liver to activate ER's (for the most part), however, much of PM is lost this way. Sublingual delivery offers a higher bioavailability to target tissues, (breasts, are one of those target tissues. Sublingual E2 is rapid activation, like within minutes].
(03-02-2016, 01:30 PM)hannah Wrote: And where do we find all these thousands receptors? In the skin?
If so can applying PM on the body be helpful in activating these receptors?
Thanks for your answers hun! Youre a golden guy!
Those estrogen receptors are all throughout the body, bone, brain, eyes, boobs, testes, etc. just some aren't as responsive as others might be. DHT in the skin is a big problem. This is where aromatase can be tissue specific and makes its influence. However, I'd apply progesterone cream (strong DHT inhibitor) first, then wait about 10min (half life of PC is 5 min) and then apply PM cream.