Does Vitex bind to the ER or inhibit aromatase? (It would be easy to test which if you don’t already know.)
It binds to the ER.
Great! This means Vitex will be effective against gyno (to some unknown degree).
Yep, and I’m currently experimenting to see to what degree.
No it doesn’t, Cy. I can’t find any evidence
that it binds to the ER (if you can, please
send it to me). Vitex is purely gonadotrophic.
This is why we have three other ingredients
in “M”. One will work as an antiaromatic to
a degree, one will work to help clear estrogen
from the blood, the last will work post
Not trying to be a dick, just trying to be
Vitex may reduce endogenous estrogen a little by other means but it is not a competitive ER agonist like tamoxifen, raloxifene or clomiphene.
I’m just trying to be factual as well. Thanks for not trying to make me look stupid. Here’s the study.
J Agric Food Chem 2001 May;49(5):2472-2479 Related Articles, Books, LinkOut
Evaluation of estrogenic activity of plant extracts for the potential treatment of menopausal symptoms.
Liu J, Burdette JE, Xu H, Gu C, van Breemen RB, Bhat KP, Booth N, Constantinou AI, Pezzuto JM, Fong HH, Farnsworth NR, Bolton JL.
Department of Medicinal Chemistry and Pharmacognosy, UIC/NIH Center for Botanical Dietary Supplements Research, College of Pharmacy, M/C 781, University of Illinois at Chicago, 833 South Wood Street, Chicago, Illinois 60612, USA.
Eight botanical preparations that are commonly used for the treatment of menopausal symptoms were tested for estrogenic activity. Methanol extracts of red clover (Trifolium pratense L.), chasteberry (Vitex agnus-castus L.), and hops (Humulus lupulus L.) showed significant competitive binding to estrogen receptors alpha (ER alpha) and beta (ER beta). With cultured Ishikawa (endometrial) cells, red clover and hops exhibited estrogenic activity as indicated by induction of alkaline phosphatase (AP) activity and up-regulation of progesterone receptor (PR) mRNA. Chasteberry also stimulated PR expression, but no induction of AP activity was observed. In S30 breast cancer cells, pS2 (presenelin-2), another estrogen-inducible gene, was up-regulated in the presence of red clover, hops, and chasteberry. Interestingly, extracts of Asian ginseng (Panax ginseng C.A. Meyer) and North American ginseng (Panax quinquefolius L.) induced pS2 mRNA expression in S30 cells, but no significant ER binding affinity, AP induction, or PR expression was noted in Ishikawa cells. Dong quai [Angelica sinensis (Oliv.) Diels] and licorice (Glycyrrhiza glabra L.) showed only weak ER binding and PR and pS2 mRNA induction. Black cohosh [Cimicifuga racemosa (L.) Nutt.] showed no activity in any of the above in vitro assays. Bioassay-guided isolation utilizing ER competitive binding as a monitor and screening using ultrafiltration LC-MS revealed that genistein was the most active component of red clover. Consistent with this observation, genistein was found to be the most effective of four red clover isoflavones tested in the above in vitro assays. Therefore, estrogenic components of plant extracts can be identified using assays for estrogenic activity along with screening and identification of the active components using ultrafiltration LC-MS. These data suggest a potential use for some dietary supplements, ingested by human beings, in the treatment of menopausal symptoms.
PMID: 11368622 [PubMed - in process]
The study says Vitex upregulates PR mRNA. That’s not enough info – there are two different PR receptors. One “functions as a transcriptional activator of progesterone-responsive genes, whereas …[the other] functions as a transcriptional inhibitor of all steroid hormone receptors.”
I stand corrected. Thanks for the abstract
Cy. I had glanced over it before and
ignored it (it is with the 50+ other abstracts
I have) as I was more interested in V’s effects
on the HPTA, LH, FSH and the Leydig Cells.
But you have managed to bring it to my attention and I am grateful for that.
Obviously, Cy was correct and I was incorrect. V has some ER binding capability and most likely works as a competitive agonist (like the Nolva). How much it works is a big question because E levels decrease in women who take V and you tend to see an increase in E when people take competitive agonists (before all of you freak out, if the E has nowhere to bind to, and in the case of a comp aggie it won't, the E can't impart an effect). -
No problem Brock. If anything I think this evidence makes “M” an even better product overall. Allow me to be one of the first to try “M” and we’ll be even.