Several decades of research from various laboratories, including our own, has demonstrated that this action is mediated by the estrogen receptor (ER) {alpha} subtype and involves a cascade of events that permanently and irreversibly alter gene expression patterns in the gland (PROSTATE).12 These data indicate that exposure to estrogen causes prostatic inflammation and directly links estrogen and prostatitis.
Quoted this just in case you people didnāt notice + not to advertise or convince but to confirm these. I speak with noniman (and solon) daily and iām preetty sure he doesnāt lie to me.
I would be interested too, actually I think it would even be possible to ask him via email directly (without being one of his patients) althoughā¦ Heās an urologist and I doubt that many non-endocrinologists doc know much about adiol-G (some endo even dont know crap about it).
EDIT
I know I havent posted my story and i should have, but although Ive never had any hormonal bloodwork done (dumb, i know) Iām pretty sure my adiol-G is low. About 2,5 years ago I did an experiment with VERY high dose DHEA (1000-1500mg per day) along with low dose tamoxifen (nolvadex, 5mg per day) for a month. Results : got leaner, packed muscle more easily, a lot of libido and sensitivity got back, and I could achieve quite good erections (still not 100% quality though) without any PDE5 inhibitor. Actually it worked much better for erection that the cycle of Hdrol that I did recently (didnt do anything on that front altough it made me feel AWESOME for the 1st three weeks). Oh, and by the end of the DHEA cycle I experienced an increase in urination frequency, sign of prostate enlargement but it subsided (also, kept using nolva solo for 3 weeks after DHEA cessation).
And later here I read this about DHEA increasing adiol-g viewtopic.php?f=9&t=3233
But there is a more recent study (a thesis!) about this āThe role of the prostate in androgen metabolismā diss.kib.ki.se/2009/978-91-7409-462-6/thesis.pdf
Im too lazy to read it all and get anything significant out of this
I think solonjk mentioned he is going to get his adiol-g tested again once he has finished his treatment. If his levels improve then it will be very interesting indeed.
Does anybody else ever experience pains in the stomach area? i have done frequently in the past, and today too. Apparently this is often caused by an infection from another area - my bet would be from the pelvis, i.e. prostatitis!
Right by the side of my bellybutton, if i press that area, i feel a sharp pain!?
i agree, it would be great to know exactly what the link was.
I just came across this study i thought was interesting:
Experimental Autoimmune Prostatitis: Dihydrotestosterone Influence Over the Immune Response
In experimental autoimmune prostatitis in a rat model of chronic prostatic inflammation of noninfectious origin the prostatic 5Ī±-dihydrotestosterone (DHT) concentration decreases because of depressed 5Ī±-reductase activity. This decrease in androgens in situ could favor the development of autoimmune status at the same time. We noted that a DHT increase could protect the gland from immune aggression and/or its consequences in regard to prostatic androgenic metabolism.
I like where this thread is going. This is exactly what we should do right now : review as much as possible of the scientific literrature to find the explanation of how 5AR inhibition can lead to prostatitis.
Even though prostatitis might be the cause of ALL of our symptoms (post-finasteride cessation), we need to find out and prove that finasteride was indeed the trigger that caused it to worsen/develop. Or else Merk will easily affirm that theyāve never had any responsability with the burden of PFS sufferers.
I think if you extrapolate from the information heās provided and people have posted, his name for āPFSā is āurogenital inflammation and infection.ā Which any male, 5ARI user or not, can contract in his view. And it sounds like he might be wondering aloud about a mechanism/theory in which finasteride plays a role in initiating or accelerating a pathogenic environment which leads to this inflammation. I donāt think heās necessarily preoccupied by exploring this (as much as we are or should be), because when prostatic inflammation presents itself, he treats; thatās his specialty. The concept of CP and this proposed mechanism, is a theory that the researchers ought to entertain and explore and contact him about, because theyāre all stuck thinking about it from their frame of reference (and weād be better-served by a multi-pronged approach). Additionally, I feel weāre a bit stuck on labels like PFS. Granted, we havenāt had dozens of āPFSersā come back all healed up, and I cannot speak for the doctor, all Iām doing is speculating and interpreting the info we have out there. But sift through the many pages in this thread, and youāll discern his stance on the matter, and maybe the definition of PFS will come to mean āimmuno-suppression and prostate irritation to the point of urogential infection and sexual and hormonal-related symptomsā or ISAPITTPOUIASAHRS for short.