15-05-2019, 03:44 AM
I've also written about that by reducing DHT it up-regulates estrogen receptors in the past. E1 plays a role in peripheral aromatization of androstenedione (that's through the A4 pathway), but...E2 is the strongest form of estrogen. I read Dr. Powers stated he thinks more E1 is needed in the intial phase of breast growth, and as we know PM acts more E1, perhaps why some see results on just using PM to begin with. Now to further breast growth through tanner 3 to 5 you need a combination of progesterone, prolactin, IGF-1, glucocorticoid, free fatty acids, collagen, thermogenic repsone of hormone receptors, and a few other things.
From experience I've found that hyperinsulinaemia (too much glucose) has negative impact on breast growth. Evidence suggests this is the case in women with PCOS, which PCOS is hyperandrogenism....(a negative impact for breast growth) amongst stress and inflammation too a driving of PCOS, and stress decreases aromatase in ovarian cells, so...what does that tell yah.
E2 and E1 can be converted into each other, and both can be inactivated via hydroxylation and conjugation. E2 demonstrates 1.25 to 5 times the biological potency of E1. E2 circulates at 1.5 to 4 times the concentration of E1 in premenopausal, nonpregnant women.
(Mayo clinic).
Glucocorticoids increase androgen inactivation, I see resihi increases glucocorticoids to a degree thereby inactivatating androgens. Also, androgens, but not estrogens, increase beta adrenergic receptors while decreasing alpha adrenergic receptors- which results in increased levels of epinephrine/ norepinephrine due to lack of alpha-2 receptor negative feedback and decreased fat accumulation. In other words, epinephrine/ norepinephrine then act on lipolysis-inducing beta receptors.
So, one can say that by using beta blockers help with breast growth (by the above pathway) to liberate lipolysis for a thermogenic response. And from my experience this creates fullness in breast tissue (lol, mine).
And here's how:.
β 2 AR activation increases the intracellular cyclic AMP levels that activate protein kinase A, which in turn promotes activation of hormone-sensitive lipase that catalyses the ratelimiting step in lipolysis.
Metformin, blood pressure meds, ACE inhibitors come to mind.
Hi Stevenator...
From experience I've found that hyperinsulinaemia (too much glucose) has negative impact on breast growth. Evidence suggests this is the case in women with PCOS, which PCOS is hyperandrogenism....(a negative impact for breast growth) amongst stress and inflammation too a driving of PCOS, and stress decreases aromatase in ovarian cells, so...what does that tell yah.
E2 and E1 can be converted into each other, and both can be inactivated via hydroxylation and conjugation. E2 demonstrates 1.25 to 5 times the biological potency of E1. E2 circulates at 1.5 to 4 times the concentration of E1 in premenopausal, nonpregnant women.
(Mayo clinic).
Glucocorticoids increase androgen inactivation, I see resihi increases glucocorticoids to a degree thereby inactivatating androgens. Also, androgens, but not estrogens, increase beta adrenergic receptors while decreasing alpha adrenergic receptors- which results in increased levels of epinephrine/ norepinephrine due to lack of alpha-2 receptor negative feedback and decreased fat accumulation. In other words, epinephrine/ norepinephrine then act on lipolysis-inducing beta receptors.
So, one can say that by using beta blockers help with breast growth (by the above pathway) to liberate lipolysis for a thermogenic response. And from my experience this creates fullness in breast tissue (lol, mine).
And here's how:.
β 2 AR activation increases the intracellular cyclic AMP levels that activate protein kinase A, which in turn promotes activation of hormone-sensitive lipase that catalyses the ratelimiting step in lipolysis.
Metformin, blood pressure meds, ACE inhibitors come to mind.
Hi Stevenator...