Msten and these orals you have mentioned are these Pro-hormones ? Just that I've never heard of em and I've got a quality source and never came across em,
I am desperate to run some test right now just on it's own because the lumps aren't quite away, it's like 1 biggish lump has broken up into smaller pieces so I defoe think the Letro is working, tho I only have 5 tabs left out of 30 so gna run at least another 2 boxes for sure,
would it be silly to run 500mgs Test in my circumstances ? I'm thinking yes ...
Just desperate to get back on, Letro will be in my diet forever, really.
When the lump has completely gone don't forget to taper off the Letro slowly or jump on Adex to avoid rebound...
I wouldn't automatically assume staying on Letro for life is your best course of action for the future, managing estrogen better, careful selection of compounds, regular blood tests might be your best course... IMO..
Remember estrogen isn't inherently bad, just too much of it is..!! (I've a post somewhere dedicated to the beneficial effects of estrogen on muscle growth, GH, IGF-1 etc)...
I've just re-read your post on gyno.. Apparently you may have issues with Deca.. I have a paper showing its about 60% as estrogenic as estrogen, but its effect is mediated through AR (androgen receptor), not aromatization or ER (estrogen receptor) binding... You may have to abstain from Deca, and carefully choose what future compounds better work for you without gyno issues...
Personally I'd be inclined to stay away from some of the newer powerful orals without a proper evaluation on how they may effect you.. Guido is very well versed and may best advise when the time is right...
Stick with what has been tried and tested for years... Test + Boldernone may be an excellent combo for you..
Regards what Neo just said on 200mg low dose:
It may be a sensible option in the near future as low dose androgen therapy may help your gyno issue...
Androgens are capable of inhibiting the estrogen-induced proliferation of mammary epithelial cells and abolish estrogen-induced augmentation of ER- expression. They also further promote pro-apoptotic (cell-killing) effects in a wide variety of breast cancer cell lines.
Zhou J, Ng S, Adesanya-Famuiya O, Anderson K, Bondy CA. Testosterone inhibits estrogen-induced mammary epithelial proliferation and suppresses estrogen receptor expression. FASEB J. 2000 Sep;14(12):1725-30.
Kandouz M, Lombet A, Perrot JY, Jacob D, Carvajal S, Kazem A, Rostene W, Therwath A, Gompel A. Proapoptotic effects of antiestrogens, progestins and androgen in breast cancer cells. J Steroid Biochem Mol Biol. 1999 Apr-Jun;69(1-6):463-71.
Selective estrogen receptor-β activation stimulates skeletal muscle growth and regeneration.
Velders M, Schleipen B, Fritzemeier KH, Zierau O, Diel P.
Source
Department Molecular and Cellular Sports Medicine, Deutsche Sporthochschule Köln, Am Sportpark Müngersdorf 6, 50933 Köln, Germany.
Abstract
There is increasing evidence suggesting that estrogens augment skeletal muscle regeneration processes after injury. To study the contribution of estrogen receptors α and β (ERα and ERβ) during muscle regeneration, skeletal muscles of ovariectomized (OVX) rats, as well as ERα- and ERβ-knockout (αErko and βErko) mice, were injured with a myotoxin (notexin). OVX rats were simultaneously treated with the ER-selective ligands genistein, ERα agonist 16α-LE2 (alpha), ERβ agonist 8β-VE2 (beta), or 17β-estradiol (E(2)). OVX rats showed significantly elevated serum creatine kinase (CK) activity after muscle injury compared to intact sham-treated animals. Treatment with ER ligands significantly reduced CK activity. TNF-α, IL-10, and MCP-1 expression served to characterize immune responses. Treatment with all ER ligands, but particularly E(2) and beta, reduced TNF-α, but elevated MCP-1 and IL-10 expression. PCNA and MyoD expression served to define satellite cell activation and proliferation and were found to be up-regulated by beta and E(2). To further study muscle regeneration responses, expression of the embryonic myosin heavy chain (MHC) was analyzed. Beta and E(2) but not alpha increased embryonic MHC expression compared to OVX. The absence of ERβ in βErko mice negatively affected CK activity levels and expression of satellite cell and muscle regeneration markers (MHC embryonic, MyoD, Pax7) compared with αErko and wild-type mice. In a classic Hershberger assay using male rats,
beta stimulated muscle growth, accompanied by a strong induction of IGF-1 expression. Our data provide evidence that ERβ signaling is involved in the regulation of skeletal muscle growth and regeneration by stimulating anabolic pathways, activating satellite cells and modulating immune responses.
http://www.ncbi.nlm.nih.gov/pubmed/22278942