28-01-2021, 04:42 AM
Thank you Drulactin, Stevenator, Steffy Anne and Bobbi for the Christmas comments. I apologize for not replying to queries (TroubleWithNibbles & Jamie Lee).
Here's a lower risk breast growth plan:
OTC Estriol/Estradiol cream. 1x per day.
Progesterone cream - w/the above.
Reishi 1-2× per day (600mg)
Vitamin D3 (in organic olive oil, 5,000 to 10,000 iu per day.)
Calcium-600mg per day (must take w/vit D3)
Other potential add-ons:
Forskolin
Resveratrol
Tuarine
Acetyl-L-Carnitine
Estriol (E3) is considered the safest of the 3 estrogens. Therefore, we add progesterone for a few reasons.
Estrogen and progesterone are synergistic when combined together for breast growth. Another reason for adding progesterone is to help alleviate poor breast growth outcomes. I'll list two studies regarding over stimulation of estrogen only that leads to breast bud fusion. When this happens the tips of breasts buds (called T.E.B. aka Terminal End Buds) fuse and prevent further growth. I believe there's still a chance that TEB's can recover from being fused. And when we say "fused" we mean the tip of the breast buds are fried.
I think this might also explain why people hit that wall of no further growth. This is where progesterone exerts some of its benefits, by including progesterone you can lower the prothrombotic side effects from straight use of estrogen only by 10-15%.
Listed Science:
I know transgender studies don't apply to all, however, the context of breast fusion and progesterone are relevant to this forum.
PHYTOESTROGENS NEARLY KILLED ME (DVT):
http://andiepasdedeux.com/phytoestrogens...ed-me-dvt/
Progesterone Is Important for Transgender Women’s Therapy—Applying Evidence for the Benefits of Progesterone in Ciswomen
https://academic.oup.com/jcem/article/104/4/1181/5270376
Predictive Markers for Mammoplasty and a Comparison of Side Effect Profiles in Transwomen Taking Various Hormonal Regimens
https://academic.oup.com/jcem/article/97...22/2536439
Inhibition of GPR30 by estriol prevents growth stimulation of triple-negative breast cancer cells by 17β-estradiol
https://pubmed.ncbi.nlm.nih.gov/25496649
Progesterone for the prevention and treatment of osteoporosis in women
https://pubmed.ncbi.nlm.nih.gov/29962257/
Chronic Stress Facilitates the Development of Deep Venous Thrombosis
https://www.hindawi.com/journals/omcl/2015/384535/
Progesterone metabolites rapidly stimulate calcium influx in human platelets by a src-dependent pathway
Peter F Blackmore. Steroids. 2008 Aug.
Abstract
The effects of several steroids and their metabolites were examined for their ability to rapidly alter intracellular free calcium ([Ca(2+)](i)) in the anucleate human platelet. Earlier studies suggested that steroids had direct and rapid non-genomic effects to alter platelet physiology. The rationale for performing this study was to investigate the signal transduction events being activated by steroids. Super-physiologic concentrations (1.0-10.0microM) of beta-estradiol and several estradiol metabolites and analogs potentiated (approximately twofold) the action of thrombin to elevate [Ca(2+)](i) in platelets, whereas 10.0microM progesterone inhibited the action of thrombin by 10-15%. Progesterone and beta-estradiol by themselves did not affect [Ca(2+)](i). Progesterone metabolites can achieve high blood concentrations. Some progesterone metabolites, particularly those in the beta-conformation, were potent stimulators of Ca(2+) influx and intracellular Ca(2+) mobilization in platelets. They activated phospholipase C because their ability to increase [Ca(2+)](i) was inhibited by the phospholipase C inhibitor U-73122. The ability of pregnanediol and collagen to increase [Ca(2+)](i) was inhibited by the src tyrosine kinase inhibitor PP1, whereas the actions of thrombin and thapsigargin to increase [Ca(2+)](i) were not affected by PP1. The effects of progesterone metabolites to increase [Ca(2+)](i) were observed with concentrations as low as 0.1microM. Pregnanolone synergized with thrombin to increase [Ca(2+)](i). It is hypothesized that human platelets possess receptors for progesterone metabolites. These receptors when stimulated will activate platelets by causing a rapid increase in [Ca(2+)](i). Pregnanolone, isopregnanediol and pregnanediol were the most effective stimulators of this newly identified src-dependent signal transduction system in platelets. Progesterone metabolites may regulate platelet aggregation and hence thrombosis in vivo.
Estriol: emerging clinical benefits
https://journals.lww.com/menopausejourna...ts.15.aspx
Here's a lower risk breast growth plan:
OTC Estriol/Estradiol cream. 1x per day.
Progesterone cream - w/the above.
Reishi 1-2× per day (600mg)
Vitamin D3 (in organic olive oil, 5,000 to 10,000 iu per day.)
Calcium-600mg per day (must take w/vit D3)
Other potential add-ons:
Forskolin
Resveratrol
Tuarine
Acetyl-L-Carnitine
Estriol (E3) is considered the safest of the 3 estrogens. Therefore, we add progesterone for a few reasons.
Estrogen and progesterone are synergistic when combined together for breast growth. Another reason for adding progesterone is to help alleviate poor breast growth outcomes. I'll list two studies regarding over stimulation of estrogen only that leads to breast bud fusion. When this happens the tips of breasts buds (called T.E.B. aka Terminal End Buds) fuse and prevent further growth. I believe there's still a chance that TEB's can recover from being fused. And when we say "fused" we mean the tip of the breast buds are fried.
I think this might also explain why people hit that wall of no further growth. This is where progesterone exerts some of its benefits, by including progesterone you can lower the prothrombotic side effects from straight use of estrogen only by 10-15%.
Listed Science:
I know transgender studies don't apply to all, however, the context of breast fusion and progesterone are relevant to this forum.
PHYTOESTROGENS NEARLY KILLED ME (DVT):
http://andiepasdedeux.com/phytoestrogens...ed-me-dvt/
Progesterone Is Important for Transgender Women’s Therapy—Applying Evidence for the Benefits of Progesterone in Ciswomen
https://academic.oup.com/jcem/article/104/4/1181/5270376
Predictive Markers for Mammoplasty and a Comparison of Side Effect Profiles in Transwomen Taking Various Hormonal Regimens
https://academic.oup.com/jcem/article/97...22/2536439
Inhibition of GPR30 by estriol prevents growth stimulation of triple-negative breast cancer cells by 17β-estradiol
https://pubmed.ncbi.nlm.nih.gov/25496649
Progesterone for the prevention and treatment of osteoporosis in women
https://pubmed.ncbi.nlm.nih.gov/29962257/
Chronic Stress Facilitates the Development of Deep Venous Thrombosis
https://www.hindawi.com/journals/omcl/2015/384535/
Progesterone metabolites rapidly stimulate calcium influx in human platelets by a src-dependent pathway
Peter F Blackmore. Steroids. 2008 Aug.
Abstract
The effects of several steroids and their metabolites were examined for their ability to rapidly alter intracellular free calcium ([Ca(2+)](i)) in the anucleate human platelet. Earlier studies suggested that steroids had direct and rapid non-genomic effects to alter platelet physiology. The rationale for performing this study was to investigate the signal transduction events being activated by steroids. Super-physiologic concentrations (1.0-10.0microM) of beta-estradiol and several estradiol metabolites and analogs potentiated (approximately twofold) the action of thrombin to elevate [Ca(2+)](i) in platelets, whereas 10.0microM progesterone inhibited the action of thrombin by 10-15%. Progesterone and beta-estradiol by themselves did not affect [Ca(2+)](i). Progesterone metabolites can achieve high blood concentrations. Some progesterone metabolites, particularly those in the beta-conformation, were potent stimulators of Ca(2+) influx and intracellular Ca(2+) mobilization in platelets. They activated phospholipase C because their ability to increase [Ca(2+)](i) was inhibited by the phospholipase C inhibitor U-73122. The ability of pregnanediol and collagen to increase [Ca(2+)](i) was inhibited by the src tyrosine kinase inhibitor PP1, whereas the actions of thrombin and thapsigargin to increase [Ca(2+)](i) were not affected by PP1. The effects of progesterone metabolites to increase [Ca(2+)](i) were observed with concentrations as low as 0.1microM. Pregnanolone synergized with thrombin to increase [Ca(2+)](i). It is hypothesized that human platelets possess receptors for progesterone metabolites. These receptors when stimulated will activate platelets by causing a rapid increase in [Ca(2+)](i). Pregnanolone, isopregnanediol and pregnanediol were the most effective stimulators of this newly identified src-dependent signal transduction system in platelets. Progesterone metabolites may regulate platelet aggregation and hence thrombosis in vivo.
Estriol: emerging clinical benefits
https://journals.lww.com/menopausejourna...ts.15.aspx