(30-12-2011, 12:54 AM)mochaccino Wrote: I just found out that the xanthohumol in hops binds to testosterone receptors. Apparently thats what was meant by "inhibit". To me that seems to imply that hops should actually be androgenic at low doses, but Ive never heard of such a thing. Does "binding" to a receptor always mean that the receptor is "activated", so to speak, or can a receptor really be simply blocked? Is hops ever androgenic? What does this all mean? Im so confused, lol. To add to my confusion, I recently heard that beer lowers testosterone in men, but raises it in women. Beer contains vanishingly small amounts of xanthohumol, and hops is not the only (or possibly even the primary) reason why beer effects horomone levels. In other words, the whole beer issue might not even have anything to do with hops, but it is confusing. *sigh*
Isabella has a much better idea of the effects of hops than I but I can address the receptor binding question.
All, and I mean literally all, cells in the body have receptors embedded in the cell membrane. This is how the cell communicates with it's environment and how cell processes are affected by the environment. There is a new branch of biological sciences called epigenetics that is exploring the seemingly heretical idea that the real "brain" of the cell is the cell membrane studded with myriad receptor molecules, not the nucleus with it's DNA.
Molecules that trigger activity within the cell (called a ligand) have very specific receptors they bind with, and any molecule that closely matches the shape and molecular configuration of the real hormone can trigger the receptor as well. It is also possible for 'antagonist' molecules to bind to a receptor without triggering any activity within the cell.
Locks and keys are a good analogy. For any lock, only keys of a certain shape will even fit in the keyhole. If a key doesn't have the correct shape, it won't go in and therefore has no effect. Testosterone doesn't affect estrogen receptor molecules and vice versa.
However, keys of the correct shape will slide in, but if the number and size of the 'teeth' on the key aren't exactly right it still won't turn the lock, or have an effect. But now there is something already in the keyhole, and even though it's not creating an effect, it prevents the real key from doing it's job. Thus, we say that it is 'antagonistic' to the real key in that it prevents the real key from having it's usual effect.
This analogy breaks down a bit since some receptors are not so specific in what will trigger them, while others are highly specific in that only one molecule can ever trigger the receptor. Estrogen receptors apparently accept a class of molecules with varying degrees of effectiveness; for instance phytoestrogens have a weak estrogenic effect compared to estradiol but they do have an effect. The strength of an antagonist is thought to be dependent on the affinity of the antagonistic ligand to bind with and occupy the receptor preventing the real ligand from doing its job. Some antagonists bind very strongly and don't release very readily and others bind only weakly and release easily. It all depends on the molecular configuration and conformation of the receptors and ligands.
This part of biochemistry is fascinating, cutting edge stuff. I hope this wasn't overly technical and helps you understand how this all works.
) Im a female trying to avoid accidentally lowering my estradiol. Maybe Im imagining things, but I thought my first post implied otherwise. Oops 
