Absolute BULLSHIT!!! Contagion.
Can you post even ONE citation from a peer reviewed journal that supports such GARBAGE,
How about an article which verifies the use of those "therapies" as a MEASURABLE means of altering E-2 levels, NOT!
No clown I'm NOT referring to a theoretical change from the use of DHT for instance (because of the differing DHT/E-2 SHBG affinities) but one that is demonstrable clinically, based on lab data.
Hey I've also heard; bulls ear wax, albino rat tails, frog urine, fingernail clippings of the "bull weasel beaver" (at least 6 months old) and "anal verge" witches pubic hair will have similar effects on E-2!
What utter nonsense!
I should have been more specific, those can be used to counter the bone loss associated with low E-2. Not to decrease E-2 levels, but yes, *some* of these can be used for that too!
Starting with
Osthole.
Osthole stimulates osteoblast differentiati... [J Bone Miner Res. 2010] - PubMed - NCBI
Osthole stimulates osteoblast differentiation and bone formation by activation of beta-catenin-BMP signaling.
Tang DZ1, Hou W, Zhou Q, Zhang M, Holz J, Sheu TJ, Li TF, Cheng SD, Shi Q, Harris SE, Chen D, Wang YJ.
Author information
Abstract
Osteoporosis is defined as reduced bone mineral density with a high risk of fragile fracture. Current available treatment regimens include antiresorptive drugs such as estrogen receptor analogues and bisphosphates and anabolic agents such as parathyroid hormone (PTH). However, neither option is completely satisfactory because of adverse effects. It is thus highly desirable to identify novel anabolic agents to improve future osteoporosis treatment. Osthole, a coumarin-like derivative extracted from Chinese herbs, has been shown to stimulate osteoblast proliferation and differentiation, but its effect on bone formation in vivo and underlying mechanism remain unknown. In this study, we found that local injection of Osthole significantly increased new bone formation on the surface of mouse calvaria. Ovariectomy caused evident bone loss in rats, whereas Osthole largely prevented such loss, as shown by improved bone microarchitecture, histomorphometric parameters, and biomechanical properties. In vitro studies demonstrated that Osthole activated Wnt/beta-catenin signaling, increased Bmp2 expression, and stimulated osteoblast differentiation. Targeted deletion of the beta-catenin and Bmp2 genes abolished the stimulatory effect of Osthole on osteoblast differentiation. Since deletion of the Bmp2 gene did not affect Osthole-induced beta-catenin expression and the deletion of the beta-catenin gene inhibited Osthole-regulated Bmp2 expression in osteoblasts, we propose that Osthole acts through beta-catenin-BMP signaling to promote osteoblast differentiation. Our findings demonstrate that Osthole could be a potential anabolic agent to stimulate bone formation and
prevent estrogen deficiency-induced bone loss.
And another -->
Osthole-mediated cell differentiation t... [J Pharmacol Exp Ther. 2005] - PubMed - NCBI
Next...Icariin.
Icariin protects against bone loss induced by oestrogen deficiency and activates oestrogen receptor-dependent osteoblastic functions in UMR 106 cells.
Icariin protects against bone loss induced by oestrogen deficiency and activates oestrogen receptor-dependent osteoblastic functions in UMR 106 cells
Cell Biochem Biophys. 2013 Sep;67(1):189-97. doi: 10.1007/s12013-013-9533-8.
Icariin protects against glucocorticoid-induced osteoporosis in vitro and prevents glucocorticoid-induced osteocyte apoptosis in vivo.
Feng R1, Feng L, Yuan Z, Wang D, Wang F, Tan B, Han S, Li T, Li D, Han Y.
Author information
Abstract
Icariin is the major active ingredient in Herba epimedii which is a commonly used Chinese herbal medicine for the treatment of osteoporosis. The present study aims to evaluate the osteoprotective effect of Icariin in glucocorticoid-induced osteoporosis in vivo and investigate the effect of Icariin on glucocorticoid-induced osteocyte apoptosis in vitro. A total of 48 female Sprague-Dawley rats were used. Glucocorticoid-induced osteoporosis was induced by daily injections of dexamethasone (0.1 mg/kg, daily, s.c.) for 60 days, whereas sham animals were injected daily with vehicle. At the end of the osteoporosis development period, osteoporotic rats were randomized to receive: vehicle (n = 8), Icariin (5,125 mg/kg, i.g.; n = 8), or alendronate (0.03 mg/kg, s.c.; n = 8) for 12 weeks. Sham animals were treated with vehicle for 12 weeks. At the beginning and at the end of treatments, animals were examined for bone mineral density. Serum bone-alkaline phosphatase and carboxy-terminal collagen cross links were measured. Primary osteocytes were isolated, and apoptosis was determined by trypan-blue assay. Interaction between Icariin and estrogen receptor and prosurvival signaling pathways activated by Icariin were also investigated. Icariin showed a comparable efficacy with alendronate in increasing bone mass. Icariin significantly increased bone-alkaline phosphatase (bone formation marker) and reduced carboxy-terminal collagen cross links (bone resorption marker). In vitro studies demonstrated that Icariin significantly prevented GC-induced apoptosis in osteocytes by activating ERK signaling via estrogen receptor. Our results suggest that Icariin might exert osteoprotective effect by maintaining osteocyte viability, thereby, regulating bone remodeling. Furthermore, our study provides preclinical evidence for the efficacy of Icariin for management of Glucocorticoid-induced osteoporosis.