[Lotus]

Hi Steve, (and thanks). 

Here's something interesting, the study and (follow up study below) track prolactin production in human breasts tissue indicating adipose (fat tissue) creates more prolactin than glandular tissue. Prolactin in adipose is described as a circulating hormone. Note the 10 fold increase by day 10. So, progesterone lowers PRL and estradiol had no effect in this study. 

In other words, having more fat in your breasts would indicate a higher presence of prolactin, conversely, more glandular would indicate higher progesterone.....in theory (lol, just an opinion). Higher prolactin in men turns off the pituitary signal to make more T, and although estradiol is unaffected (in this study) one should believe it's keeping estradiol low.....aka- no boob growth. So if indeed prolactin is cyclic in nature, (peaks on day 10) the other nine days are optimal growth cycles for breasts......feel free to chime in. 


Prolactin expression and secretion by human breast glandular and adipose tissue explants.
Zinger M1, McFarland M, Ben-Jonathan N.
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Abstract
Prolactin (PRL) is a 23-kDa hormone produced by the pituitary and extrapituitary sites. The main target of PRL is the breast, where it affects cellular growth, differentiation, and milk production. Recent evidence suggests that locally produced PRL plays a role in breast tumorigenesis. Our objective was to examine PRL synthesis/release in different tissues of the human breast and determine the effect of ovarian steroids. Breast tissue, obtained from women undergoing mastectomy or breast reduction, was separated into glandular (nonmalignant) and adipose explants and incubated for 10 d. Conditioned media were analyzed for PRL by a bioassay. PRL release from glandular explants decreased by 60% from d 1-3, followed by a 4-fold increase on d 10. PRL release from adipose explants was unchanged from d 1-3 and increased more than 10-fold by d 10. PRL gene expression, determined by RT-PCR, was low on d 0 and markedly increased on d 10 in both types of explants. De novo synthesis of PRL was confirmed by metabolic labeling. Progesterone suppressed PRL release from glandular explants without affecting adipose explants. Estradiol did not alter PRL release from either tissue. In conclusion, the human breast produces and releases bioactive PRL, with a higher release rate by adipose than glandular tissue. The time-dependent rise in PRL release suggests removal from inhibitory control. Progesterone may be one of the factors that suppresses PRL production in the glandular compartment, whereas the factor(s) that regulate adipose PRL are unknown. These data suggest an autocrine/paracrine role for PRL in human glandular and adipose breast tissue.

Adv Exp Med Biol. 2015;846:1-35. doi: 10.1007/978-3-319-12114-7_1.
Prolactin (PRL) in adipose tissue: regulation and functions.
Ben-Jonathan N1, Hugo E.
Author information


Abstract
New information concerning the effects of prolactin (PRL) on metabolic processes warrants reevaluation of its overall metabolic actions. PRL affects metabolic homeostasis by regulating key enzymes and transporters associated with glucose and lipid metabolism in several target organs. In the lactating mammary gland, PRL increases the production of milk proteins, lactose, and lipids. In adipose tissue, PRL generally suppresses lipid storage and adipokine release and affect adipogenesis. A specific case is made for PRL in the human breast and adipose tissues, where it acts as a circulating hormone and an autocrine/paracrine factor. Although its overall effects on body composition are both modest and species-specific, PRL may be involved in the manifestation of insulin resistance. 
PMID: 25472532  DOI: 10.1007/978-3-319-12114-7_1