[Lotus]

I think only IGF-1, prolactin, progesterone, and estrogens are the hormones that matter.

IGF-1 and prolactin are supposed to be high during follicular
Progestogens are supposed to be highest during luteal. Estrogens were also supposed to be higher than normal during luteal, but less as high as progestogens.

Perhaps other combinations of IGF-1, prolactin, estrogen, and progestogens are possible for different times. Prolactin did have effects at other times too for BCP users.

Perhaps LH and FSH are just indicators of other hormones, but may not be the ones effective. The only time that LH and FSH have a correlation, if I have this correct, is during days 5-10 for BCP users. LH does help start luteal, and it also might (hypothesis) be responsible for how much estrogen is present during luteal. White peony and red reishi can increase estrogens too (it is uncertain if these two herbs influence LH and FSH).

GH also has an influence (possibly indirectly), but this influence includes total body height (at least during puberty) and body weight.

I believe we have missing information of the Receptors and hormones that activate the receptors that are in connective breast tissue, if they are different than other connective tissue receptors.

Prolactin can be problematic with aromatase,

Aromatase activity is decreased by prolactin, anti-Müllerian hormone and the common herbicide glyphosate. Aromatase activity appears to be enhanced in certain estrogen-dependent local tissue next to breast tissue, endometrial cancer, endometriosis, and uterine fibroids.
http://wikipedia.org/wiki/Aromatase


Prolactin synthesis in primary cultures of pituitary cells: Regulation by estradiol
Abstract
Pituitary cells cultured with estradiol respond by a specific increase in prolactin synthesis. Extensive inhibition of DNA synthesis (61–78%) with hydroxyurea or cytosine arabinoside resulted in only 28–33% decrease in estrogen-induced prolactin synthesis. To assess the role of prolactin cell proliferation in the estrogen-induced response, mammotrophs were identified by immunocytochemistry. Cultures treated with estradiol for 1, 2 or 5 days contained 101 ± 1, 113 ± 2 and 132 ± 1% of the number of mammotrophs in controls. Estradiol treatment for corresponding periods resulted in prolactin synthesis representing 94 ± 5,144 ± 11 and 270 ± 22% of controls and prolactin mRNA levels representing 115 ± 7, 160 ± 7 and 322 ± 22% of controls. Thus estrogen caused a considerable increase in prolactin synthesis which paralleled the increase in prolactin mRNA levels and a much smaller relative increase in the number of mammotrophs. We conclude that regulation of prolactin synthesis by estrogen is mediated predominantly but not exclusively through stimulation of gene expression in existing pituitary cells.
http://www.sciencedirect.com/science/article/pii/0303720782900843

Evidence That Autoregulation of Prolactin Production Does Not Occur at the Pituitary Level
http://press.endocrine.org/doi/abs/10.1210/endo-110-3-722