I was digging around some articles and came across this one:
Asensi, M.; et al. Free Radical Biology & Medicine, Vol. 33, No. 3, pp. 387â??398, 2002
The relationship between resveratrol (RES) bioavalability and its effect on tumor growth was investigated. Tissue levels of RES were studied after i.v. and oral administration of trans-resveratrol (t-RES) to rabbits, rats, and mice. Half-life of RES in plasma, after i.v. administration of 20 mg t-RES/kg b.wt., was very short (e.g., 14.4 min in rabbits). The highest concentration of RES in plasma, either after i.v. or oral administration (e.g., 2.6 Â± 1.0 Î¼M in mice 2.5 min after receiving 20 mg t-RES/kg orally), was reached within the first 5 min in all animals studied. Extravascular levels (brain, lung, liver, and kidney) of RES, which paralleled those in plasma, were always < 1 nmol/g fresh tissue. RES measured in plasma or tissues was in the trans form (at least 99%). Hepatocytes metabolized t-RES in a dose-dependent fashion (e.g., 43 nmol of t-RES/g Ã? min in the presence of 20 Î¼M tRES), which means that the liver can remove circulating RES very rapidly. In vitro B16 melanoma (B16M) cell proliferation and generation of reactive oxygen species (ROS) was inhibited by t-RES in a concentration-dependent fashion (100% inhibition of tumor growth was found in the presence of 5 Î¼M t-RES). Addition of 10 Î¼M H2O2 to B16M cells, cultured in the presence of 5 Î¼M t-RES, reactivated cell growth. Oral administration of t-RES (20 mg/kg twice per day; or included in the drinking water at 23 mg/l) did not inhibit growth of B16M inoculated into the footpad of mice (solid growth). However, oral administration of t-RES (as above) decreased hepatic metastatic invasion of B16M cells inoculated intrasplenically. The antimetastatic mechanism involves a t-RES (1 Î¼M)-induced inhibition of vascular adhesion molecule 1 (VCAM-1) expression in the hepatic sinusoidal endothelium (HSE), which consequently decreased in vitro B16M cell adhesion to the endothelium via very late activation antigen 4 (VLA-4).[/quote]
Basically, what I got out of the article was that resveratrol has decent oral bioavailability, but due to the 1st pass effect, will become metabolized very quickly. In the discussion, the authors stated that keeping an aqueous solution of resveratrol in the mouth for 1 min was quite effective in spiking blood serum levels of it. But they also stated that resveratrol has a very short half life in the blood stream (14 min).
So, for those who are knowledgeable about such things (such as Bill Roberts), my questions are:
-Since it has such a short half life, will it really be that effective at aromatase inhibition and acting as a SERM?
-If so, then if someone were to supplement with resveratrol such as Rez-V, should we instead keep the tab in our mouth for a bit to vastly enhance absorbtion (as gross as that sounds)? I suppose you can just suck on some peanut butter/grapes to get the resveratrol out of there…haha.