Get to know your estrogen receptors: “alpha vs beta”

Dr. Weeks’ Comment:  Estrogen is classified by the FDA as a “carcinogen” – estrogen predisposes to or causes cancer.  (Don’t worry guys, your lady’s estrogen is not contagious and your can’t catch it by kissing…)


But the picture is more complex:  estrogen is really a class of hormones. There are at least 8 types of estrogens:  E1 = estrone, E2 = estradiol,  E3 = estriol,  etc.  Furthermore, we now have learned that there are 2 major estrogen receptors:  estrogen receptor alpha (ERa)  and estrogen receptor beta (ERb)    – all you really need to know, Dear Reader, is that “Beta is Better”.

The ERb   PROTECTS  against cancer and the ERa  WORSENS cancer.

It is also helpful to know that soy interacts predominately with the health promoting ERb and NOT with the dangerous ERa.  (There is a lot of misinformation about soy which centers around cancer risk but now you know the reason why it is actually highly beneficial for treating people with cancer). That is why my patients drink whole, organic, non-GMO, fermented soy. Also, they eat cruciferous vegetables and supplement with BioDim.   All this get your more….. “3 beta adiol” !  (Wazzat?   read on!)



Cancer Res. 2005 Jun 15;65(12):5445-53.

The androgen derivative 5alpha-androstane-3beta,17beta-diol inhibits prostate cancer cell migration through activation of the estrogen receptor beta subtype.

Guerini V, Sau D, Scaccianoce E, Rusmini P, Ciana P, Maggi A, Martini PG, Katzenellenbogen BS, Martini L, Motta M, Poletti A.

Institute of Endocrinology, University of Milan, Italy.


Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5alpha-reduced testosterone derivative, dihydrotestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor-independent mechanism. We have shown that the dihydrotestosterone metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor beta (ERbeta), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERbeta signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERbeta activation in prostate cancer cells.

Moreover, 3beta-Adiol, through ERbeta, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells.

The inhibitory effects of 3beta-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that (a) circulating testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and (b) that the estrogenic effect of testosterone derivatives (ERbeta-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis.

These results also shed some light on clinical observations suggesting that alterations in genes coding for 3beta-hydroxysteroid dehydrogenases (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary prostate cancer.



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