(28-03-2015, 06:08 AM)Dfleurs Wrote: Hmmmm so is reishi still good to take? i guess taking everything in moderation is always better but NBE is such a long journey thus everything will be kind of long term type
Absolutely, it benefits NBE by reducing DHT and up-regulates estrogen receptors. Here's some interesting info on how estrogens behave (mayo clinic), it's been stated before that PM
behave's like E1 (estrone). I've highlighted the points of interest. For example, E1 plays a role in peripheral aromatization of androstenedione (that's through the A4 pathway), IMO, it's a back door growth opportunity. But circulating E2 is the most bio-active (free) estrogen, in other words, the strongest estrogen. Phytoestrogens don't produce estrogens as we know, but they up-regulate estrogen receptors, that's where E2 (the body's own natural estrogen, not the pharma kind, that's a different topic altogether, interact with receptors and activate growth), Hopefully.
But.....if you don't reduce DHT (as we know) breast growth is very limited, that's the bottom line.....
Estrogens are involved in development and maintenance of the female phenotype, germ cell maturation, and pregnancy. They also are important for many other, nongender-specific processes, including growth, nervous system maturation, bone metabolism/remodeling, and endothelial responsiveness.
The 2 major biologically active estrogens in nonpregnant humans are estrone (E1) and estradiol (E2). A third bioactive estrogen, estriol (E3), is the main pregnancy estrogen, but plays no significant role in nonpregnant women or men.
E2 is produced primarily in ovaries and testes by aromatization of testosterone. Small amounts are produced in the adrenal glands and some peripheral tissues, most notably fat. By contrast, most of the circulating E1 is derived from peripheral aromatization of androstenedione (mainly adrenal).
E2 and E1 can be converted into each other, and both can be inactivated via hydroxylation and conjugation. E2 demonstrates 1.25-5 times the biological potency of E1. E2 circulates at 1.5-4 times the concentration of E1 in premenopausal, nonpregnant women. E2 levels in men and postmenopausal women are much lower than in nonpregnant women, while E1 levels differ less, resulting in a reversal of the premenopausal E2:E1 ratio.
E2 levels in premenopausal women fluctuate during the menstrual cycle. They are lowest during the early follicular phase. E2 levels then rise gradually until 2 to 3 days before ovulation, at which stage they start to increase much more rapidly and peak just before the ovulation-inducing luteinizing hormone/follicle stimulating hormone surge at 5 to 10 times the early follicular levels. This is followed by a modest decline during the ovulatory phase. E2 levels then increase again gradually until the midpoint of the luteal phase and thereafter decline to trough, early follicular levels.
Measurement of serum E2 forms an integral part of the assessment of reproductive function in females, including assessment of infertility, oligo-amenorrhea and menopausal status. In addition, it is widely used for monitoring ovulation induction, as well as during preparation for in vitro fertilization. For these applications E2 measurements with modestly sensitive assays suffice. However, extra sensitive E2 assays or simultaneous measurement of E1, or both are needed in a number of other clinical situations. These include inborn errors of sex steroid metabolism, disorders of puberty, estrogen deficiency in men, fracture risk assessment in menopausal women, and increasingly, therapeutic drug monitoring, either in the context of low-dose female hormone replacement therapy or antiestrogen treatment.
http://www.mayomedicallaboratories.com/t...tive/81418
Steroid Pathway
http://www.mayomedicallaboratories.com/i...thways.pdf
