Please Scroll Down to See Forums Below You guys are not paying attention. Prolactin does not, and will not, and has never mediated cellular mitosis. It is simply a chemical messenger. The estrogen receptor becomes up regulated in the presence of prolactin. Estrogen will cause and is the only hormone that causes cell differentiation of ductile tissue in the breast. The presence of prolactin will activate the estrogen receptor hence even a small fraction of estrogen will cause tissue growth. Too much test in the system causes gyno but that does not mean that the test itself is the actual culprit. This same logic applies to this situation. Open you fucking eyes and learn something so that you can give people the correct information rather than all the Hocus Pocus Witchcraft bullshit that is spread around here. Everything I have stated is medical fact. Not some bovine study or monkey study done with rectal suppositories. Or do we need to continue to perpetuate the myth of the dumb ignorant bodybuilder.
The Almighty
New member
LONE_AZ said:
Dont get me wrong, I totally understand this. I believe it was FONZ who wrote something a while back saying along the lines of the same thing. I am not arguing with the science...I simply say that it worked for me and for 99% of the other people I have spoken with about this. My understanding is that if 9 out of 10 people used vitex and say that it cleared up their gyno in less than a month then obviously something in it has to be working.
G
Golfer18--old
Guest
So your saying its estrogen right?
100% correct... But look more towards the estrogen receptor and receptor modulation. Because even with normal amounts of estrogen if the receptor is up regulated you can get gyno. Prolactin will accomplish this in some people rather quickly. So the trick with tren and deca is to keep your receptors in a normal state or down regualted this is a very tricky task.
LONE_AZ, you are partly correct. Estrogen seems to be a key ingredient in development of gyno, but progesterone is capable of inducing proliferation of epithelial cells in the alveoli of mammary tissue. (Mammary tissue contains two components: ducts and alveoli. Estrogen is thought to be the mediator of ductal proliferation, while progesterone controls alveolar proliferation.)
For those interested, the study whose abstract is reproduced below pretty well summarizes the current knowledge about mammary proliferation. A much more detailed, and highly recommended summary can be found at:
http://www.endotext.org/male/male14/male14.htm
Ann Med 1998 Dec;30(6):511-24
Effects of sex steroids on proliferation in normal mammary tissue.
Soderqvist G.
Department of Woman and Child Health, Karolinska Hospital, Stockholm, Sweden. [email protected]
Numerous women are treated with a combination of oestrogen and progestogen for contraception and hormone replacement therapy worldwide. A possible increased risk of cancer in target organs has been discussed vividly for many years. While oestrogens are clearly mitogenic for breast epithelial cells, there has been considerable uncertainty about the effects of progestogens. This article reviews current knowledge on this field, including our own data. Oestrogen receptors are down-regulated during the luteal phase, while progesterone receptors remain at a high level throughout the menstrual cycle. According to most studies, in vivo proliferation of normal breast epithelial cells is higher during the luteal phase in the vast majority of women. Normal breast tissue can convert oestrone sulphate to oestradiol. A negative correlation between the levels of circulating oestradiol and the enzyme converting oestrone into oestradiol suggests a local regulatory mechanism of tissue oestradiol formation. Serum progesterone levels correlate positively with sulphatase activity while 19-norsteroid progestogens may be inhibitory. We found that long-term continuous combined hormonal treatment with conjugated equine oestrogens and medroxyprogesterone acetate induced a proliferative response in the breasts of surgically postmenopausal macaques. The effect of combined treatment was more pronounced than that of oestrogen treatment alone. Both endogenous progesterone and exogenous progestogens increase proliferation of breast epithelial cells. Exogenous progestogens down-regulate both oestrogen and progesterone receptors. Oestrogen and progestogens may have both direct and indirect stimulating effects on proliferation. The finding of a positive correlation between insulin-like growth factor I messenger RNA and proliferation found in hormonally treated women with low receptor levels suggests the possibility of nonreceptor-mediated effects of sex steroids on proliferation, which needs to be investigated further.
For those interested, the study whose abstract is reproduced below pretty well summarizes the current knowledge about mammary proliferation. A much more detailed, and highly recommended summary can be found at:
http://www.endotext.org/male/male14/male14.htm
Ann Med 1998 Dec;30(6):511-24
Effects of sex steroids on proliferation in normal mammary tissue.
Soderqvist G.
Department of Woman and Child Health, Karolinska Hospital, Stockholm, Sweden. [email protected]
Numerous women are treated with a combination of oestrogen and progestogen for contraception and hormone replacement therapy worldwide. A possible increased risk of cancer in target organs has been discussed vividly for many years. While oestrogens are clearly mitogenic for breast epithelial cells, there has been considerable uncertainty about the effects of progestogens. This article reviews current knowledge on this field, including our own data. Oestrogen receptors are down-regulated during the luteal phase, while progesterone receptors remain at a high level throughout the menstrual cycle. According to most studies, in vivo proliferation of normal breast epithelial cells is higher during the luteal phase in the vast majority of women. Normal breast tissue can convert oestrone sulphate to oestradiol. A negative correlation between the levels of circulating oestradiol and the enzyme converting oestrone into oestradiol suggests a local regulatory mechanism of tissue oestradiol formation. Serum progesterone levels correlate positively with sulphatase activity while 19-norsteroid progestogens may be inhibitory. We found that long-term continuous combined hormonal treatment with conjugated equine oestrogens and medroxyprogesterone acetate induced a proliferative response in the breasts of surgically postmenopausal macaques. The effect of combined treatment was more pronounced than that of oestrogen treatment alone. Both endogenous progesterone and exogenous progestogens increase proliferation of breast epithelial cells. Exogenous progestogens down-regulate both oestrogen and progesterone receptors. Oestrogen and progestogens may have both direct and indirect stimulating effects on proliferation. The finding of a positive correlation between insulin-like growth factor I messenger RNA and proliferation found in hormonally treated women with low receptor levels suggests the possibility of nonreceptor-mediated effects of sex steroids on proliferation, which needs to be investigated further.
G
Golfer18--old
Guest
So this explains why liquidex and vitex cut my problems....
The relevant quote regarding prolactin from the article I linked to is this:
Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. (39, 23). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.
Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. (39, 23). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.
superchicken
New member
ok so the t3 i can vouch for does help fina gyno, im on 100 tren ed and was noticing a little soreness, i started my t3 and its gone quickly.
i planned to run the fina still after the t3 is finished, how bad is this gonna come back and hit me, as my t3 levels will likely be suppressed for a while.
would taking 12.5mcg t3 after ramping down until fina is finished be a good idea?
i can get bromo if thats the best solution.
i planned to run the fina still after the t3 is finished, how bad is this gonna come back and hit me, as my t3 levels will likely be suppressed for a while.
would taking 12.5mcg t3 after ramping down until fina is finished be a good idea?
i can get bromo if thats the best solution.
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