Looks like a great deal for 30 bucks. I may have to grab one of those. Thanks for the tip.

Testofen is the best stuff I've used to raise libido, lessen refractory period, and increase "load." It boggles my mind why supp companies haven't rushed to put this into their 'natty test' formula's. This stuff is even backed by clinical research!

Instead, designer puts I3C in their test booster - an ingredient which is inherantly estrogenic and anti-androgenic!!!!!!! But that's off on a tangent.

Deisel:
when you used the Testofen, did you notice rise in estrogen? did you take an AI along with it?

thanks

Diesel
any idea what that AI component might be?

I wonder if this stuff is suppresive or can it be used PCT in place of Fennugreek/Tribulus?

Testofen is not suppressive. In my next post cycle therapy I will probably use FUSION ZEUS, bulk Testofen is horrid so I am going with a capped brand. ZEUS is the best price for what you get (mg's of Testofen) compared to other Testofen products.

Just cap it yourself. It's so much cheaper than paying for a pre capped namebrand. I capped mine w/ longjack 20:1 and 3% rhodiola. I've been on it for about a week.

My back has broken out more than normal and I've def. been hornier lately, so that's a good indication that it's doing something.
They say it takes about 12 days to really start seeing full effects, so I'm excited to see how good it gets.

Aside from capping this stuff, how else do you get it down? I just purchased some so I guess you just throw the 300 mg in then choke it down on some water? Also, should it be taken on an empty stomach? Thanks.

josh,Will you be using an AI with your Testofen/Long Jax?

also , what was your experience with Longjack? Good for test? libido? any estrogen concerns?
thanks

Testofen sounds real nice, I wonder why more companies are not making product with this in it.

well there was one product, if i recall correctly, made by scivation called fenotest and it proclaimed these type of results. but, sales were never particularly great and recently i think they have discontinued there sale.

on a side note, if the results are as such that the claims are true in elevating testosterone, lowering skin fold thickness, and increased nitrogen retention. my question is does it require pct, because in theory should almost double testosterone production?

That's probably as good as it gets with regards to its potential anti-estrogenic properties. There's a few mechanisms for MCF-7 cell induced apoptosis and one of them is decreasing the amount of estrogen available to the cell. In this case, the fenugreek probably has an anti-aromatase component (I don't have the full article), but also existing as an ER binding antagonist. I've seen similar results with resveratrol.

Mitochondria, calcium, and calpain are key mediators of resveratrol-induced apoptosis in breast cancer.

Sareen D, Darjatmoko SR, Albert DM, Polans AS.
Department of Biomolecular Chemistry, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA.

Resveratrol (RES), a natural plant polyphenol, has gained interest as a nontoxic chemopreventive agent capable of inducing tumor cell death in a variety of cancer types. However, the early molecular mechanisms of RES-induced apoptosis are not well defined. Using the human breast cancer cell lines MDA-MB-231 and MCF-7, we demonstrate that RES is antiproliferative and induces apoptosis in a concentration- and time-dependent manner. Preceding apoptosis, RES instigates a rapid dissipation of mitochondrial membrane potential by directly targeting mitochondria. This is followed by release of cytochrome c and second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI (Smac/DIABLO) into the cytoplasm and substantial increase in the activities of caspases-9 and -3 in MDA-MB-231 cells. In addition, live cell microscopy demonstrates that RES causes an early biphasic increase in the concentration of free intracellular calcium ([Ca2+]i), probably resulting from depletion of the endoplasmic reticulum stores in breast cancer cells. In caspase-3-deficient MCF-7 cells, apoptosis is mediated by the Ca2+-activated protease, calpain, leading to the degradation of plasma membrane Ca2+-ATPase isoform 1 and fodrin; the degradation is attenuated by buffering [Ca2+]i and blocked by calpain inhibitors. Mitochondrial permeability transition pore antagonists also blocked calpain activation. In vivo mouse xenograft studies demonstrate that RES treatment inhibits breast cancer growth with no systemic toxicities. Together, these results suggest a critical role for mitochondria not only in the intrinsic apoptotic pathway but also in the Ca2+ and calpain-dependent cell death initiated by RES. Thus, RES may prove useful as a nontoxic alternative for breast cancer treatment.