[Lotus]

Back to the science:  

Methylsulfonylmethane (MSM) is a small molecule @ 94 daltons, which penetrates through skin layers. So following this idea of co-administration of prolactin plus progesterone to realize this 400% increase over E2 only, MSM (cream/lotion) seems like a great carrier. Now it's finding a prolactin cream idea to complete the sequence.....research drugs?....FG (fenugreek) is an herbal option (increases PRL), I'd use it as an oil followed by PC then MSM, (how I'd do it). 



http://press.endocrine.org/doi/10.1210/en.2003-0752?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&

Following PRL and PRLR interaction, signal transducers and activators of transcription (STATs) and Methylsulfonylmethane (MSM) 


Na+/taurocholate cotransporting polypeptide (ntcp) mediates the uptake of bile salts from plasma across the basolateral domain of the hepatocyte. We have demonstrated that ntcp expression can be induced by prolactin (PRL) and placental lactogen via the PRL receptor and signal transducers and activators of transcription (Stat)5a pathway. However, elevated levels of placental lactogen do not increase the expression of ntcp in pregnant rats. Because plasma estradiol (E2) levels are also elevated in pregnancy, we investigated the inhibitory effects of E2 on PRL-induced ntcp activation. E2 treatment inhibited the PRL-induced increase in liver ntcp mRNA to the same levels as in rats treated with E2 alone. Estrogen receptor-α (ERα) mRNA and protein expression in liver were increased 2.6-fold and 2.2-fold, respectively, in pregnancy relative to controls. In HepG2 cells, E2 repressed PRL-induced ntcp reporter gene expression in a dose-dependent manner in the presence of cotransfected ERα. The ERα antagonist ICI 182,780 reversed E2-induced repression, indicating specificity of inhibition by E2. Overexpression of coactivator p300 did not reverse the inhibitory effects of E2 and ERα. Western and gel shift analysis revealed that E2-bound ERα decreased the tyrosine phosphorylation and DNA-binding activity of Stat5a, indicating that the inhibitory effect of E2was mediated, at least in part, by interfering with PRL-mediated signal transduction. The present studies demonstrate the physiological significance of cross-talk between ERα and Stat5a in liver, in which both proteins are expressed. These data also establish a novel mechanism by which expression of ntcp, an important hepatic bile acid transporter, can be regulated by multiple hormones.

Growth hormone (GH) is regulator of bone growth and bone metabolism. GH activates several signaling pathways such as the Janus kinase (Jak)/signal transducers and activators of transcription (STAT) pathway, thereby regulating expression of genes including insulin-like growth factor (IGF)-1. GH exerts effects both directly and via IGF-1, which signals by activating the IGF-1 receptor (IGF-1R). In this study, we investigated the effects of MSM on the GH signaling via the Jak/STAT pathway in osteoblasts and the differentiation of primary bone marrow mesenchymal stem cells 
https://www.ncbi.nlm.nih.gov/pubmed/23071812

Transcription of the genes encoding both ERα (Esr1) and ERβ (Esr2) is stimulated by PRL through the Jak2–Stat5 pathway and Stat5-response elements that are located in each of the Esr promoters. 
http://www.cell.com/trends/endocrinology...0030-4.pdf

MSM stimulates the stat5 pathway, thus estrogen receptors are being stimulated by MSM.....(awesome huh?).