I’m not on the patch, currently @ 6mg of E2 daily, but knowing the transdermal patch doesn’t impair GH/IGF-1 in the liver?...shoot girlfriend(s)

the patch is actually better suited for MTF hrt. Now, somatostatin inhibits hGH/IGF-1 in liver, there’s a supplement that inhibits somatostatin thereby stimulating GH/IGF-1....which is what we want in HRT/NBE...it’s actually what I consider is the missing ingredient for MTF HRT. We need youthful levels of GH/IGF-1..as we know puberty is a growth phase, so we can consider beginning HRT puts us smack dab back at a puberty stage, so let’s take advantage of it. Muscle wasting is not an ideal way to feminize, think lean tissue, I believe you’ll see that ever wanted hourglass take shape over the wasting of muscle a lot quicker, and healthier. Intermittent fasting will (12-24hrs) help improve receptor sensitivity...which is lost over time.
Estrogen regulation of growth hormone action.
Review article
Leung KC, et al. Endocr Rev. 2004.
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Abstract
GH plays a pivotal role in regulating body growth and development, which is modulated by sex steroids. A close interplay between estrogen and GH leads to attainment of gender-specific body composition during puberty. The physiological basis of the interaction is not well understood. Most previous studies have focused on the effects of estrogen on GH secretion. There is also strong evidence that estrogen modulates GH action independent of secretion.
Oral but not transdermal administration of estrogen impairs the metabolic action of GH in the liver, causing a fall in IGF-I production and fat oxidation. This results in a loss of lean tissue and a gain of body fat in postmenopausal women and an impairment of GH effect in hypopituitary women on GH replacement. The negative metabolic sequelae are potentially important because of the widespread use of oral estrogen and estrogen-related compounds. Estrogen affects GH action at the level of receptor expression and signaling. More recently, estrogen has been shown to inhibit Janus kinase/signal transducer and activator of transcription signaling by GH via the induction of suppressor of cytokine signaling-2, a protein inhibitor for cytokine signaling. This represents a novel paradigm of steroid regulation of cytokine receptors and is likely to have significance for a diverse range of cytokine function.
https://academic.oup.com/edrv/article-lo....2003-0035
(11-10-2017, 06:11 PM)Lotus Wrote: GH / IGF-1 (growth hormones) in combination with estradiol helps developed TEB's (terminal end buds)....the essential part of mammary ductal system, (terminal ends buds are likely the first stage of breast growth in puberty), though I believe you can still grow (or mature) TEB's in adulthood.
GH improves estrogen receptors, E2 also regulates ERβ/PI3-K pathway.
Somatostatin inhibits hGH/IGF-1, in other words, somatostatin sabotages meaningful growth of IGF-1. Choline inhibits somatostatin making way for GH to stimulate IGF-1, a dose of 500-600mg creates a 4 fold increase...see choline study.
http://www.breastnexus.org/showthread.php?tid=28232