I believe I fianly found SOMETHING that speaks directly to this issue:
First, to summarize: They treated young growing rats with oral resveratrol, as well as estrodiol for comparison. They found that all of the changes produced by estrodiol were NOT mimicked by resveratrol, and that resveratrol even PREVENTED the effects of serum estrogen, one of which was lowered cholesterol (strangely, this might be seen as a benefit of estrogen by these researchers).
The last sentence in this abstract was certainly the most convincing:
These in vivo [using whole, living organisms] results suggest, in contrast to prior in vitro [using cells in a petri dish] studies, that resveratrol has little or no estrogen agonism on reproductive and nonreproductive estrogen target tissues and may be an estrogen antagonist.
In other words, when applied, it seems resveratrol may just be the estrogen antagonist [anti-estrogen] we all hoped it would be, including being an antogonist on REPRODUCTIVE as well as non reproductive tissue.
Of course, I think there is still more room for human studies.
For the full abstract:
Is Resveratrol an Estrogen Agonist in Growing Rats?1
Russell T. Turner, Glenda L. Evans, Minzhi Zhang, Avudaiappan Maran and Jean D. Sibonga
Departments of Orthopedics, Biochemistry, and Molecular Biology, Mayo Graduate School of Medicine, Rochester, Minnesota 55905
Address all correspondence and requests for reprints to: Russell T. Turner, Ph.D., Orthopedic Research, Room 3Ã¢??69 Medical Science Building, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905.
Trans-3,4,5-trihydroxystilbene (resveratrol), a polyphenolic compound found in juice and wine from dark-skinned grape cultivars, was recently shown to bind to estrogen receptors in vitro, where it activated transcription of estrogen-responsive reporter genes. The purpose of this 6-day study in weanling rats was to determine the dose response (1, 4, 10, 40, and 100 Ã?Âµg/day) effects of orally administered resveratrol on estrogen target tissues. The solvent (10% ethanol) had no significant effect on any measurement or derived value. 17Ã??-Estradiol treatment (100 Ã?Âµg/day) decreased the growth rate, final body weight, serum cholesterol, and radial bone growth (periosteal bone formation and mineral apposition rates) at the tibia-fibula synostosis. In the uterus, 17Ã??-estradiol treatment increased wet weight, epithelial cell height, and steady state messenger RNA levels for insulin-like growth factor I. In contrast, resveratrol treatment had no significant effect on body weight, serum cholesterol, radial bone growth, epithelial cell height, or messenger RNA levels for insulin-like growth factor I. Resveratrol treatment resulted in slight increases in uterine wet weight, but significance was achieved at the 10-Ã?Âµg dose only. A second experiment was performed to determine whether a high dose of resveratrol (1000 Ã?Âµg/day) antagonizes the ability of estrogen to lower serum cholesterol. As was shown for the lower doses, resveratrol had no effect on body weight, uterine wet weight, uterine epithelial cell height, cortical bone histomorphometry, or serum cholesterol. 17Ã??-Estradiol significantly lowered serum cholesterol, and this response was antagonized by cotreatment with resveratrol. These in vivo results suggest, in contrast to prior in vitro studies, that resveratrol has little or no estrogen agonism on reproductive and nonreproductive estrogen target tissues and may be an estrogen antagonist.