NO NO NO....!!!! We need some circulating estrogen to bind ER-beta.... I'll explain.....!!!
The Estrogen alpha receptor causes proliferation of cells, the beta receptor inhibits proliferation and increases differentiation, or the maturing process into a fully functioning cell. So when estrogen increases proliferation starts, and when it reaches a certain threshold more binds to the more abundant beta receptor slowing proliferation and increasing differentiation. This is relevant because though tamoxifen also binds the beta receptor it does so with less affinity than estradiol and its unclear as to whether it activates or blocks the beta receptor. The net result is that proliferation is halted by tamoxifen’s negative effect on the alpha receptor, but estradiol is left in circulation to activate the beta receptor. The beta receptor offers us several benefits, but here specifically it will further inhibit proliferation (tissue growth) and increase differentiation. Terminal differentiation aborts the proliferative capacity of a cell. So each cell that terminally differentiates is one more cell that won’t be replicating. These cells now await apoptosis (cell death) at the hand of androgen-mediated action..
One thing I do want to impart on people is that tamoxifen treatment must continue for some time to be effective. Too often tamoxifen is reported to be ineffective for acute treatment because it isn’t used sufficiently long. tamoxifen inhibits the growth of breast tissue, but does not reduce it on its own. This is mediated by your androgen levels as a male and an AAS user. These cells do not dissolve, they are ultimately destroyed by genomic signals. This takes some time. On top of that early cessation risks rebound effects. tamoxifen does not address circulating estradiol so early cessation will only lead to estradiol immediately binding ERalpha again, and barring any changes, starting problems all over again. Longer treatment with tamoxifen reduces ERalpha density (2), which only further promotes the beta-receptor mediated positive effects. It’s perfectly possible for tamoxifens effect to become visible after cessation, no doubt this is one primary reasons why treatments prescribed by quacks are sometimes deemed effective : they are administered at the time the cells are being destroyed, so that to a lay person it may seem that the medication is actually reducing his gyno. If ACTUAL tissue shrinks within days, its probably not what you are on right now, so if you took something because you thought tamoxifen did not work, and “it cleared up in three days” (I’m not kidding, I hear this stuff every day) its likely it was the tamoxifen and not the other drug.
If it turns out you are prone to gyno (early onset of gyno with testosterone only at moderate doses) you can always opt to make the needed changes in the future (preventive treatment with an AI or a SERM)....
Once nolva has stopped the gyno, you can use an AI to avoid a estrogen rebound... Tapering off the AI over a few weeks...!!
