[hannah]

Progesterone restores estrogen receptor sensitivity to its original state. Progesterone also protects against the proliferate side of breast cancer in estrogen receptors. It also down regulates DHT through 5 alpha reductase. It has no feminzing effect. Progesterone in the presence of estrogen up-regulates side branching, and estrogen promotes the elongation of breasts. But......an odd spin is that progesterone down regulates it's own receptor.

Very interesting and helpful, Thank you very much Lotus. But I dont get the last part:
''But......an odd spin is that progesterone down regulates it's own receptor. ''
I dont know If I'm right but what I get from this is that if you take Progesterone-''cream,other stimulants'' your own natural progesterone will be down regulated, so create less progesterone?

Enzymes are definitely proteins. We know hormones can readily diffuse across cell membranes, but I think it's more beneficial for synthesis to have a carrier protein accompany it, in other words essential fatty acids. My first choice is coconut oil. We had a lengthy discussion about receptor up/down regulation, it's a good thread with attached research, take a look if you get time. Hannah, to answer your question, progesterone down regulation of its own receptor comes from the study below, as you can see PR also down-regulates estrogen receptor alpha and beta (ER-a & ER-b), sorry, but lol it's the techy stuff.


RECEPTOR REGULATION
http://www.breastnexus.com/showthread.php?tid=20747

REGULATION OF RECEPTOR NUMBERS


The half-life of steroid hormone receptors ranges from 2 to 4 hours for ERα 4 hours for AR, 7 to 10 hours for PR, and 19 hours for GR. The relatively long half-life of the steroid hormone receptors strongly suggests that the receptor proteins are recycled before eventual degradation.


Estrogen synthesis and signaling pathways during ageing: from periphery to brain
Steroid hormones generally autoregulate their receptor levels. Desensitization or downregulation of receptor numbers, measured by decreased ligand binding capacity, occurs in response to exposure to high levels of ligand and involves the reduction in receptor mRNA levels, decreasing the number of available receptors. The receptor gene may be negatively regulated by the hormonal ligand itself through its receptor protein interacting with specific HREs in the gene. Upregulation or self-priming may occur in an analogous fashion. Steroid hormones can regulate receptor levels for other hormones (e.g. E2 increases PR levels in estrogen-responsive tissues). Progesterone can downregulate its own receptors, as well as ERα and ERβ. This increase or decrease in receptor levels in homologous or heterologous regulation can be caused by alterations in receptor gene transcription or decay rates for receptor mRNA or protein. Binding of the cytosolic GR complex to very long 3'-untranslated regions of its receptor mRNA has been reported to cause premature degradation.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3595330/pdf/nihms-425860.pdf

Okay, I dont want to be rude, But I'm outta time now. So I'll read this techy stuff tomorrow, ha ha. Maybe during daytime I'm a bit more fresh to understand this and read this over and over and over again.LOL. Thanks Loots!