personally if they offer Du Zhong, I think it'd be a righteous addition to any natural test booster. Cortex extract that is.

why would you drop icariin? Every product has a 10% extract which is literally shit at trace amount. Smaller amounts of higher extract would be necessary, or a ridiculous amount of the shitty extract.

Just a litte reference, feel free to post your own ideas.

3,4-Divanillyltetrahydrofuran 400 MG
Horny Goat Weed Extract 400 MG N/A
Longjack 100:1 100 MG
Resveratrol 250 MG
Tribulus terrestris 400 MG
Avena Sativa Powder 400 MG
Coleus Forskohlii 60 MG

maybe if horny goat weed was dropped, every single product on the market has Icarrin.

Why don't you guys have I3C?

Benson - Have you gotten an opportunity to play with this at all or is the price still holding you back?

I guess I wasn't aware that something that presumably helps shift test => free test has estrogenic properties. Can you point mein a direction I can read up on this?

Benson - Have you gotten an opportunity to play with this at all or is the price still holding you back?

Not used it myself but the energetics of this herb are well known in TCM and would be useful in this instance I think.

I may just be a scaredy-cat (I'm the same guy who avoids kaempferol and arecoline) but I sent you a PM

Phytochemistry. 2007 May;68(10):1448-58. Epub 2007 Apr 16. Links
Taxonomic, genetic, chemical and estrogenic characteristics of Epimedium species.Shen P, Guo BL, Gong Y, Hong DY, Hong Y, Yong EL.
Department of Obstetrics and Gynecology, National University Hospital, Yong Loo Lin School of Medicine, Lower Kent Ridge Road, Singapore 119074, Republic of Singapore.

To understand the factors contributing to estrogenic properties of extracts from the genus Epimedium L. (Berberidaceae), we performed taxonomic, genetic and chemical characterization on 37 specimens from 18 species and related these to estrogen receptor (ERalpha and ERbeta) bioactivity, as measured by reporter genes in stable human cells. Boot strap values derived from amplified fragment length polymorphisms indicated that specimens of E. koreanum, E. brevicornum, E. myrianthum, E. leishanense, and E. membranaceum were genetically distinct and this was supported by their very similar ERalpha activities. In contrast, specimens from E. pubescens and E. sagittatum were diverse both genetically, chemically and in terms of ERalpha and ERbeta bioactivities. Strikingly, a genetic cluster comprising six rare Epimedium species exhibited strongest ERalpha and ERbeta activity, and this bioactivity was positively correlated with content of trace flavonoid aglycones (kaempferol, apigenin, quercetin, luteolin and breviflavone . In contrast, there was no association between estrogenic activity and the major flavonol glycoside constituents (icariin and epimedin A-C). Although they exhibited equally strong ERalpha and ERbeta activity, E. koreanum can be clearly differentiated from E. pubescens and E. brevicornum by genetic distance and its significantly lower content of epimedin C. Our morphologic, genetic, chemical and bioactivity profiling provide the basis for the production of extracts with reproducible estrogenic properties. Such reproducibility will be critical for the standardization of Epimedium-based products.

PMID: 17434191 [PubMed - indexed for MEDLINE]

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2005 Mar;34(2):131-6.Links
[Preparation of two derivatives from icariin and investigation of their estrogen-like effects.][Article in Chinese]


Ye HY, Liu J, Lou YJ.
College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310031, China.

OBJECTIVE: To investigate the estrogen-like activities of icariin (ICA), icaritin (ICT) and desmethylicaritin (DICT) and their structure/activity relationships. METHODS: ICT was hydrolyzed from ICA by cellulase and then DICT was demethylated from ICT in boron tribromide and dichloromethane system. Estrogen-sensitive MCF-7 cells and T47D cells were co-incubated with different concentrations of test compounds for 6 and 9 d respectively, and the cell proliferation was measured by MTT. RESULTS: ICT and DICT both markedly enhanced cell proliferation. Compared with estradiol (10.(-9) mol/L), the proliferative effects of 10.-6 mol/L ICT and DICT on MCF-7 cells were 90.0% and 94.0% (P<0.01), respectively, and those of T47D cells were 65.6% and 50.0%. (P<0.01). But this phenomenon was not observed with ICA. Cell proliferation induced by ICT and DICT was completely antagonized by 10.(-7 )mol/L pure estrogen receptor antagonist, ICI182,780. CONCLUSION: ICT and DICT possess estrogen-like activity of enhancing proliferation in MCF-7 and T47D cells. However, ICA appears to have no estrogenicity on MCF-7 and T47D cell lines in vitro.

PMID: 15812886 [PubMed - indexed for MEDLINE]

Pharmazie. 2005 Feb;60(2):120-5.Links
Determination of rat urinary metabolites of icariin in vivo and estrogenic activities of its metabolites on MCF-7 cells.Liu J, Ye H, Lou Y.
Department of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, PR China.

To confirm that the estrogenic activity of icariin is based on the close relationship between the structures of its metabolites and the effects of their binding to target hormone receptors, the metabolism of icariin in rat urine was analyzed in vivo, and the estrogenic activity of its metabolites was measured in cultured MCF-7 human breast cancer cells, respectively. By CZE analysis, peaks corresponding to the relative positions of desmethylicaritin and icaritin were observed in the urine sample. Structural analysis following LC-ESI-MS revealed molecular ions [M-H]- of 512.8, 353.3, and 367.0 for metabolites consistent with those of icariside II, desmethylicaritin, and icaritin. Icariin, icaritin, and desmethylicaritin were analyzed for their estrogenicity using MCF7-cell proliferation (E-screen test). MCF-7 cells were cultured in an estradiol free medium and then exposed to 10(-8) to 10(-5) mol/L icariin and its metabolites, icaritin and desmethylicaritin, for 6 days. Icaritin and desmethylicaritin significantly increased cell proliferation, and the cell number increased from 1.61 to 4.14 fold compared with the untreated control, but the parent compound icariin failed to exhibit this effect. These results indicate that icariin is converted to icariside II, desmethylicaritin, and icaritin in vivo, and that the latter two act as a weak xenoestrogen on MCF-7 cells.

PMID: 15739900 [PubMed - indexed for MEDLINE]

got it. I did some research. Apparently he is ignoring the different isoflavons. You can't group ALL icariin derivatives together. As seen here:
and again here
I would however, not close the book on this as of yet... one comment in this study makes me wonder for a second..
Is this saying that even if you are taking icariin it metabolizes into the lesser more estrogenic forms of itself?

breast cancer cells proliferate on estrogen. Not sure why they'd discount it like that. Unless I'm wrong about MCF-7 cells..

breast cancer cells proliferate on estrogen. Not sure why they'd discount it like that. Unless I'm wrong about MCF-7 cells..

I very well could be confused, I will look later have to hit the gym.

I am curious if you understand the types of cells that were used in these in vitro experiments?

1st study:
The overexpression of yhp23 limits the applicability of things studied in yeast cells, despite the connotation of estrogen agonism and/or anti-androgenic effects. Why? Because this overexpression increases ER transcriptional activation making them relatively a weak model at best.

2nd study:
MCF-7 cells and T47D cells are human breast cancer cell lines - essentially oncogenes already overexpressing estrogenic potential. Fortunately, breast cancer cell lines are found in only about 1% of human males. That said, these are NOT the same cells responsible for mammary overexpression leading to prototypical gyno.

Furthermore, I also addressed the WHY we chose the particular extract of choice, NOT citing more than a 20% icariin extract. You must keep in mind the limits of the model you are speaking of:

icariin --> icaritin + desmethylicaritin (which I thought I expressed clearly above...alas I digress...)


Can I ask why it is that people think that in vitro experiments truthfully define these agents? Is this part of the bb.com culture to rely on abstract posting for their "research" information? I am uncertain as I don't come here enough probably, but really...this is mildy distressing if so.

D_

Has anyone bothered having bloodwork done on these 'Natty Test Boosters'...?

Unless you are a rat, Trib isn't really going to do a great deal...

there is no trib in the formula Redsky posted.

I was about to say something to the effect of:
"That's why there's no trib in my formula. "