19-11-2014, 02:54 AM
(18-11-2014, 08:38 PM)iaboy Wrote: So..... Estriol is the best one to use then? Other than PM, is there any herbal way to get it?
well, some food sources are broccoli, cauliflower, cabbage,
ia, ok if I take the long way around this?,
It is now known that estrogens exert their end-organ effect by activating a complex intracellular mechanism. Tissues which respond to estrogen possess intracytoplasmic proteins (receptors) that preferentially bind specific steroids.
For instance, a cell from the uterus will possess 5000–15,000 estrogen receptors whereas a cell from the spleen will have none. These receptors recognize estrogens by their three dimensional and chemical characteristics and bind it with high affinity (KD =10-10), specificity, and saturability.
The estrogen molecules present in the circulation are relatively loosely bound to intravascular carrier proteins (sex-steroid-binding globulin [SBG]) (KD = 10-8) or to albumin. In excess of 95% of the estrogen in the circulation is found in the bound form. The estrogen readily diffuses across the cell membrane in its active free form due to a concentration and a binding gradient. The estrogen molecule is relatively small (molecular weight is 300) and lipophilic and probably passes through the cell membrane by simple diffusion.
Once in the cell, the estrogen is promptly bound to the intracellular (intracytoplasmic) receptor protein, which then undergoes a series of complex spatial changes prior to intranuclear transport. This nuclear transport occurs within 30–45 minutes after the target tissue is exposed to estrogen. The following system of nuclear interactions between receptor and DNA is a model that has been proposed by McCarty.3 The activated receptor–estrogen complex then nonspecifically binds to the DNA and protein of dispersed chromosomes (euchromatin) and stimulates acetylation of the histone protein.
This acetylation of the histones in nucleosomes causes the nucleosome to “open up” and expose specific DNA segments for transcription. The “estrogen message” is transcribed into new messenger RNA which then migrates back into the cytoplasm and activates various cellular processes including new protein synthesis. The now “freed” receptor protein is probably recycled back into the cytoplasm for further use.
The estrogen receptor recognizes a molecule as being “estrogen” if its size, three-dimensional configuration, and charge are similar to the parent molecule. Therefore, the nonsteroidal synthetic estrogens may not resemble the “prototype” estrogen (estradiol-17β) on paper diagrams but are very similar in shape and other properties as seen by the cellular receptor. Estrogen receptors are perhaps the determinants of potency for estrogenic substances.
The estrogen receptors preferentially bind estradiol over estriol (2x) and estrone (3x).5 This receptor also discriminates among the estrogens by binding estradiol within the cellular nucleus longer than the weaker estrogens estriol and estrone.
Therefore, estradiol is the most potent of the natural estrogens probably because of the greater affinity and duration of its receptor-binding compared with the other available estrogens. Receptors for estrogen and other steroid hormones can now be accurately quantified and studied. Estrogen in physiologic concentrations stimulates the synthesis of estrogen receptors and of progesterone and testosterone receptors.
Progesterone and testosterone, however, inhibit estrogen receptors. Progesterone inhibits its own receptor population in the secretory phase of human endometrium. Thus, it is apparent that for estrogen to bind and influence a tissue, the specific estrogen receptors must be present. The potency of a particular estrogen in a tissue roughly parallels and is probably dependent on the quantity of the estrogen receptor in the cells of that tissue. Studies with estrogen receptors in breast cancers are being successfully utilized to predict the responsiveness of these tumors to hormonal manipulation.
http://www.glowm.com/section_view/item/2.../value/237
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The adrenal gland is the primary source of estrogen in postmenopausal women, and estrone is the dominant estrogen, the E2:E1 ratio being reversed after menopause. In comparison to those of cycling women, estrone levels are reduced to low follicular phase levels. There is an insignificant contribution to the estrone pool from estradiol conversion, ovarian estrone secretion, and conversion of ovarian androstenedione
However, virtually all the total estrone production can be accounted for by peripheral conversion of androstenedione in adipose tissue and liver. There is a strong correlation with age and obesity in the conversion efficiency of androstenedione to El. The nonobese postmenopausal woman has an average androstenedione to E1 conversion rate of 2.7%, compared with 5.1% for the obese postmenopausal patient with uterine bleeding secondary to increased endogenous estrogen.
the beltway would never be the same. I'd even make it an open mic lasting till we the people had our say!. 
psa over, now back to nbe and your regular scheduled breast growth. 