Jacob
Senior Member
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The point I'm making is that if this stuff at least halts or slows down my loss, I am not going to be too concerned over 10 or 20 bucks either way...in the long run, sure, maybe, but its not like there is a huge difference in price...for a 6 month trial, it's all in the same ballpark for me
Ok..that's fine..but previously you said there was quite a difference in price. About $50 per 4 months. There was a major difference in price when Folexen was cheaper :doh: That's still assuming I did the calculations right.
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Is this s-equol or whatever it's called? It's also important that you guys understand that anything sold locally in Australia is expensive. The minimum 18+ year old wage in Aus is something like $15 an hour, on top of that you have Super contributions so it pushes it up even further.
I've emailed around to confirm what equol is being used. The ingredients on this page http://chiroevolution.com/prostizine.pdf say:
(R,S) Equol (patented & patent-pending) 6mg
But then under the "Study: Equol’s Other Positive Eects in the Body" they mention Phyto-600. A search for that talks about a soy-based feed or supplement etc. I'm assuming they're just using those studies for the "equol" benefits.
So it looks to be a mixture of both- R and S Equol. Will post if I get any responses. Maybe how much S-equol is in it..etc.
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Equol has recently caught the interest of many researchers due to its rich antioxidant activity and implications in cancer research [4,5]. The chemical structure of equol contains a stereocenter at carbon number 3 which gives it two possible enantiomers and it has since been proven that the production of equol by microflora in mammals or other animals is selective for the S - enantiomer only [5]. S-equol has unique chemical properties compared to its R - enantiomer. S-equol has been shown to have a modest affinity for binding to and mimicking estrogen's effects on estrogen beta receptors (ERβ) due to its similar structure to natural estrogens [5,7]. However, S-equol shows little affinity for estrogen alpha receptors (ERα). Furthermore, equol (i.e., the R- and/or S-isomer) can act as an anti-androgen [7]. Equol's anti-androgen activity is unique as equol does not bind the androgen receptor (AR) but specifically binds 5α-dihydrotestosterone (5α-DHT) with high affinity, and thereby prevents DHT from binding the AR [7], see Figure 1. This finding is reconfirmed and extended here. Additionally, equol's mechanism of action, namely, its ability to specifically bind 5α-DHT and prevent 5α-DHT's biological actions in physiological processes, was studied.
For example, it is known that prostate cancer cells are supported in their growth by androgen stimulation and the androgen-regulated expression of the prostate specific antigen (PSA) is a biological marker of such stimulation [8]. Logically, any treatment that could decrease PSA levels in prostate cancer cells, or antagonize specific androgen hormone action, would have great potential in addressing prostate disorders, such as benign prostatic hyperplasia (BPH) or prostate cancer. With this in mind, we sought, in the following experiments, to determine equol's effect on 5α-DHT levels in cultured human prostate cancer (LNCap) cells. We also examined equol's effect on both prostate weight and circulating hormone levels in vivo using Long-Evans rats. In brief, the present results demonstrate that equol: a) (R- and/or S-isomeric mixtures) has high binding affinity for 5α-DHT making it a potent selective androgen modulator (SAM), b) blocks the stimulatory androgen action of 5α-DHT in increasing prostate specific antigen (PSA) levels in human cancer (LNCap) cell cultures and, c) significantly decreases serum 5α-DHT and subsequently prostate weight without altering, testosterone, 17β-estradiol or LH levels. Applications for equol to improve prostate disorders and other androgen-mediated conditions is also discussed.
This is an example of equol preventing the stimulatory effects of 5α-DHT in vivo. Rats were injected with 1 mg of non-racemic equol (52% S-isomer, 48% R-isomer) for 25 consecutive days, and serum 5α-DHT levels and prostate weights were measured. Adult (50 day-old) males (n = 16), purchased from Charles River Laboratories (CRL; Wilmington, MA, USA), were caged individually and housed in the Brigham Young University Vivarium and maintained on an 11-dark, 13-hour light schedule (lights on 0600-1900). Before purchase, the male animals were fed a diet containing approximately 200 ppm of isoflavones at the supplier (CRL). At 50 days of age, upon arrival, the male rats were placed on a diet containing approximately 10 ppm of isoflavones; referred to hereafter as the low isoflavone diet (Zeigler Bros., Gardnes, PA, USA; Phytoestrogen Reduced Rodent Diet II). All animals remained on the low isoflavone diet until 216 days of age to exclude the influence of dietary isoflavones on the measured parameters. At 150 days of age the rats were divided into two groups (control or equol treatments) that were matched by age and body weight. Starting at 190 days of age the male rats received a daily subcutaneous 0.1cc injection at the nape of the neck of vehicle (n = 8) (dimethyl sulfoxide; DMSO) or equol (n = 8) at a dose of approximately 1.0 mg/kg for 25 consecutive days.
The body weights for each group were recorded weekly starting at 150 days of age before the treatments were initiated, with weights obtained immediately before and after the treatments were administered (there were no significant differences in body weights between the control and equol groups at the start of this experiment). At 216 days of age the animals were weighed [grams (g) ± 0.1 g], then anesthestized with Ketamine/acepromazine and blood was collected from the heart. Next the ventral prostate organ was dissected and weighed [milligrams (mg) ± 0.001 mg]. The collected blood samples were centrifuged and serum was stored at -20˚ C until assayed. All collection procedures were performed blind to the treatments. This animal protocol was approved by the Institutional Animal Care and Use Committee at Brigham Young University.
Serum testosterone, 5α-DHT, and 17β-estradiol were quantified by radioimmunoassay (RIA) kits purchased from Diagnostic System Laboratories (Webster, TX, USA). Luteininzing hormone (LH) was quantified by an assay utilizing standards from the National Institutes of Health (NIH) USA pituitary hormone program. The samples were run in duplicate for each RIA, with internal control samples. In all RIAs, the control values were within normal ranges. The intra-assay coefficients of variance for the assays were: testosterone = 6.0%; for 5α-dihydrotestosterone = 8%, 17β-estradiol = 5% and LH = 9%.
http://www.rbej.com/content/9/1/4/