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Kacip fatimah raises libido by increasing testosterone levels in women
Portland, 23. July 2010
"Binding to estrogen receptors are being investigated. If they were phytoestrogens, the extract should also displace estradiol binding to the estrogen receptors. These phytoestrogens will then have certain effects on the animals depending on whether they are full estrogen agonists, or antagonists, or partial agonists like clomiphene. It is also possible that KF acts as estrogen receptor modulators (SERMS) like Tamoxifen or Raloxifene which is active at certain tissues only (4,5). For example, Reloxifene being active only at the bones and lipids and not the breasts and uterus, common target tissues for estrogen action.
"On the other hand, more is known about estrogen receptors and how it causes effects at the cellular level. There are two isoforms, alpha ( ERa) and beta (ERb) with 97% homology at the DNA binding site and 59% homology at the ligand binding site and more diverse at the or regions of the receptor molecule. Both isomers bind estradiol effectively and combine together or dimerized upon binding to estradiol at the DNA binding site called the estrogen response element ERE. The two isomers differ most at the so called Activation Function 1 and Activation Function 2 ( AF1 and AF2 ) in the N- and C- terminus respectively. When E2 binds to the receptor binding domain, the AF2 is exposed and interacts with cofactors which helps transmit the signal to the DNA (5,6,7). Other mechanism of action also exists in the tissues. Rather than dimerize, the ER may actually bind to DNA bound protein complexes such as Activating protein-1 and causes transrepression.
"In theory therefore, the phytoestrogen may have effects at the site of binding at both or one or other of the Estrogen receptor isomers, or act as an AF or as an activating Protein or like EGF act by modulating the receptor molecule, or as a peripheral enzyme modulator such as 11HSD. Recent studies at the IMR gave some clues to its mode of action. Given to normal female rats, the serum level of estradiol E2 were unchanged but the level of free testosterone wee significantly higher. In castrated rats, there were no significant effects on the levels of E2 or testosterone. These preliminary data suggest that Kacip Fatimah does not increase estrogen levels and but instead causes increase free testosterone from the ovaries a it does not work without ovaries. The increase in free testosterone may cause increase in libido and sexuality in women. This could be the effect that the women taking Kacip Fatimah are looking for!! It also means the Herb should not work in menopausal women if the effect is via increase production of testosterone ifrom the ovaries. On the other hand, if it were to work by peripheral enzymes converting E2 to testosterone, then it is independent of the ovaries but still needs adequate levels of estradiol. In women without pituitaries therefore, the herb should not work, unless the effect is like Clomiphene and causes increase in secretion of FSH from the pituitary, or by antagonizing the hormone, Inhibin produced by the ovaries at the pituitary level.
"Clearly the potential effect of Kacip Fatimah as a SERM and any possible increase risk for breast or uterine cancer has to be considered. The following pharmacological studies, in-vitro and in-vivo are being proposed to determine the possible mechanism of actions of KF, and the Clinical trials (Phase I, II, III) would evaluate the physiological effects of Kacip Fatimah in women and support the basic research being carried out in the IMR....
