View Full Version : Gyno: nuclear receptor intervention as a preventive?

09-06-2006, 01:06 PM
Gyno and vitamin E. Topically applied and *moderate* internal supplementation with E and carotene may block overactivation of specific tissue/growth.

Points: reduce liver lipid imbalances, reduce tendency towards gyno, possibly acne and prostate, plus water retention (indirect action on kidney thru brain).

Logic as follows:


Paper describes mechanism of estrogen receptor antagonism by tamoxifen.

Estrogen is a key regulator of growth, differentiation and function in a broad range of target tissues, including the male and female reproductive tracts, mammary gland, bone, brain and the cardiovascular system. The biological effects of estrogen are mediated through estrogen receptor α (ERα) and estrogen receptor β (ERβ), which belong to a large superfamily of nuclear receptors that act as ligand-activated transcription factors. These receptors share a well-conserved DNA-binding domain (DBD) and a structurally conserved ligand-binding domain (LBD). The N-terminal domains of these receptors, on the other hand, do not resemble each other [1,2]. The classical mechanism of activation of ERs depends on ligand binding to the receptors, after which the receptors dimerize and bind to estrogen response elements (EREs) located in the promoters of estrogen-responsive genes [3]. Ligand binding also induces a conformational change within the LBD of the receptors, and this conformational change allows co-activator proteins to be recruited [4].

ERs may also regulate gene expression in the absence of DNA-binding by modulating the activities of other transcription factors via protein-protein interactions on DNA. This mechanism is referred to as cross-talk and is common for several nuclear receptors [5]. For example, ligand-bound ERs upregulate and downregulate transcription from genes that contain AP-1 sites, binding sites for the Jun/Fos complex, in a manner that depends on the type of cells and the subtype of ER [6-9].

These results suggest that non-genomic signalling is involved in the mechanism by which ERα and ERβ influence AP-1-dependent transcription. We have previously shown that Stat3 and Stat5 are targeted by non-genomic actions of ERs, and the results presented here allow us to conclude that ERs bound to 17β-estradiol mediate the transcriptional activation of promoters regulated by AP-1 and by Stat proteins via different combinations of signal transduction pathways. Our observations thereby provide new insights into the mechanisms by which ERs act at alternate response elements, and suggest a mechanism by which tamoxifen exerts its action as a tissue-selective agonist.

Who dances with AP-1 (regulates its expression) and reduces cross talk among nuclear receptors --> unwanted tissue activation?

Vitamin E and vitamin A.

Topical use of vitamin E is benign; I would try it in small doses, applied locally, once or twice per day, on cycle.

Side note: a vitamin E based tanning product I use has always reliably reduced skin inflammation and normalized the appearance of skin texture (reduced pore size, normalized pigmentation).

Side note 2: Beta-carotene is a precursor form of vitamin A. Its conversion to active form of vitamin A is limited by an enzyme reaction that prevents toxicity associated with overuse of the active form.

Tough Old Man
09-06-2006, 01:12 PM
Good Info T

09-06-2006, 01:14 PM
Very interesting, I will have to get some E and carotene and see how it works.

09-06-2006, 01:25 PM
Toptical E, on- and post cycle. Vitamin E and beta carotene - used as regular dietary supplements. Point is to provide augment vitamin E concentrationfor site-specific protection against unusual activation of ER through use of the topic. Buy inexpensive E in gel caps, break one open per application.

Sounds stupidly simple (and inexpensive). It is. Pretty sure it will work; how well depends on skin penetration and amount of tissue to be protected (eg., local body fat also absorbs E). Nipple is a direct topical delivery route to ductal cells.