I don't think I'd limit progesterone and estrogen together anymore, this is possibly why we don't see a balanced growth. Expand the possibilities beyond conventional science, that's when see a whole new dimension of NBE. Controlling androgens first, there are precursor hormones after all.
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?filte...%5Bauth%5
Estrogen's concentration in a particular tissue depends on many things,
including its affinity or binding strength for components of that tissue, relative to its affinity for the blood; the activity in that tissue of the aromatase enzyme, which converts androgens to estrogen activity of glucuronidase enzyme, that converts water-soluble estrogen glucuronides into the oil soluble active forms of estrogen; and the sulfatases and several other enzymes that modify the activity and solubility of the estrogens. The "
estrogen receptors," proteins which bind estrogens in cells, are inactivated by progesterone, and activated by many physical and chemical conditions.
Recently I've been reading articles from a PhD of biology named Ray Peat, here's a few paragraphs from his articles.
Quote:polyunsaturated fats and prostaglandins stimulate the expression of aromatase, the enzyme that synthesizes estrogen, aspirin decreases the production of estrogen.
Quote: The amount of estrogen in tissue is decreased when progesterone is abundant. In the absence of progesterone, tissues retain estrogen even when there is little estrogen circulating in the blood.
Quote:Estrogen is produced in many tissues by the enzyme aromatase, even in the breast and endometrium, although these are considered "target tissues" rather than endocrine glands. Aromatase increases with aging.
Quote:Estrogen is inactivated, mainly in the liver and brain, by being made water soluble by the attachment of glucuronic acid and/or sulfuric acid.