What to take for as a anti Progesterone?

[buckwheat1]

Bromo/Dostinex are used to lower prolactin levels not progesterone. My questions are:

1. Has anyone seen studies or results showing that prolactin levels increase dramatically during a deca or fina cycle? I would like to see this info.

2. Does prolactin have a synergistic effect when combined with progesterone and possibly estrogen to induce gyno?


High prolactin levels can reduce libidio. After a male has a orgasm prolactin levels increase. This is why Dostinex allowed people to have multiple orgasms when they took Dostinex.

So, if prolactin is indeed raised with Deca then it may be one reason for the decrease in libido. In this case Bromo/Dostinex would probably help the situation.

Again, I have not seen info on how there is link with lower prolactin and how it helps prevent progestorone gyno.

 

[Spidey]

Bromo/Dostinex are used to lower prolactin levels not progesterone. My questions are:

1. Has anyone seen studies or results showing that prolactin levels increase dramatically during a deca or fina cycle? I would like to see this info.

2. Does prolactin have a synergistic effect when combined with progesterone and possibly estrogen to induce gyno?


High prolactin levels can reduce libidio. After a male has a orgasm prolactin levels increase. This is why Dostinex allowed people to have multiple orgasms when they took Dostinex.

So, if prolactin is indeed raised with Deca then it may be one reason for the decrease in libido. In this case Bromo/Dostinex would probably help the situation.

Again, I have not seen info on how there is link with lower prolactin and how it helps prevent progestorone gyno.

Yes, prolactin along with progesterone, estrogen, and IGF-1 can induce gyno. In fact, gyno can only happen if all of those hormones are present. If you block any of them (estrogen for example) gyno can not happen. All of those hormones have neccessary roles in the maturation of breast tissue.

 

[Deleted member 33117]

Yes, prolactin along with progesterone, estrogen, and IGF-1 can induce gyno. In fact, gyno can only happen if all of those hormones are present. If you block any of them (estrogen for example) gyno can not happen. All of those hormones have neccessary roles in the maturation of breast tissue.

Thank you. I get very annoyed by post on progesterone gyno. Its impossible for progesterone to cause gyno by itself, nor is it possible to get gyno without progesterone present at signifigant levels. You are correct, if any of those hormones drops to a very low level one does not develop gyno.

 

[variation]

Though I've read cases where too high of progesterone levels can prevent prolactin from causing mammary glands from producing lactate...

Now, two progesterone antagonists that come to mind are...

RU486

and

CDB-2914 (which I think is still quite experimental at this time..)

And personally, to be honest, I have no idea where to get either heh.. so if anyone else has any input on progesterone antagonists please post.

Now as far as difference between progesterone and estrogenic-induced gyno.. estrogen(s) cause the ductile systems of mammary glands to develop, as well as increased fat deposites on chest..

Progesterone causes the glands themselves to develop.

Now, let's take a look at this study in regards to estrogen receptor competition between the weak synthetic estrogen drugs and flavanoids.. As I've been saying for quite some time the phytoestrogens in soy are actually anti-estrogen at ER receptors, and this is just another study to back that statement up. Yet some people Want to cause controversy by arguing this point into the dirt and think they'll seem more manly if they don't consume soy products, while others just go with the hype..

Relationship between estrogen receptor-binding and estrogenic activities of environmental estrogens and suppression by flavonoids.

Han DH, Denison MS, Tachibana H, Yamada K.

Department of Environmental Toxicology, University of California, Davis 95616-8588, USA. [email protected]

In this study, we investigated the estrogenic activity of environmental estrogens by a competition binding assay using a human recombinant estrogens receptor (hERbeta) and by a proliferation assay using MCF-7 cells and a sulforhodamine-B assay. In the binding assay, pharmaceuticals had a stronger binding activity to hERbeta than that of some phytoestrogens (coumestrol, daidzein, genistein, luteolin, chrysin, flavone, and naringenin) or industrial chemicals, but phytoestrogens such as coumestrol had a binding activity as strong as pharmaceuticals such as 17alpha-ethynylestradiol (EE), tamoxifen (Tam), and mestranol. In the proliferation assay, pharmaceuticals such as diethylstilbestrol, EE, Tam, and clomiphene, and industrial chemicals such as 4-nonylphenol, bisphenol A, and 4-dihydroxybiphenyl had a proliferation-stimulating activity as strong as 17beta-estradiol (ES). In addition, we found that phytoestrogens such as coumestrol, daidzein, luteolin, and quercetin exerted a proliferation stimulating activity as strong as ES. Furthermore, we examined the suppression of proliferation-stimulating activity, induced by environmental estrogen, by flavonoids, such as daidzein, genistein, quercetin, and luteolin, and found that these flavonoids suppressed the induction of the proliferation-stimulating activity of environmental estrogens. The suppressive effect of flavonoids suggests that these compounds have anti-estrogenic and anti-cancer activities.

PMID: 12224631 [PubMed - indexed for MEDLINE]

daidzein, genistein are the primary flavanoids found in soy beans/products.