Understanding Clinical Trials

The Brain Can Produce Estrogen In Gushes!

Unbeknownst, to me, I was not aware of all the places in the body that can produce Estrogen. I got some interesting bloodwork back from my monthly PSA/hormone tests. Every month I get a PSA and I alternate each month with T and E2. So this month was PSA and E2, last month it was PSA and T. Last month I remained undetectable as to PSA, and T was at 10, after receiving a new Vantas Implant, which should be good for the next 15 months. So this month I wanted to know my E2. My last Check was 19. Now I take Proscar and Avodart, both anti-aromatase inhibitors, as well as DIM[Di-Indole Methane]. So wanting to get my E2 closer to 15, than 20, I increased my dose of DIM 25%. Yes I remain undetectable as to PSA, but got a big surprise when my E2 went up to 27. A 30% increase.

So I delved into research. Come to find that tissue, near the Testes, but not part of the sex glands can produce Estrogen. Well that made me scratch my head. OK. Where else. Well in further study the Lymph Node Fluid, can also produce Estrogen.

Well that made me scratch my head again. Because it is well known that the Adrenals produce some T, and the Leutenizing agents only affect the Testes, and not the Adrenals. So whatever T is produced by the Adrenals, in my drug/supplemental program, this should not allow the production of E2, via the process of aromatization, and the breakdown of DHT to E2, via the use of DIM.

Low and behold, I find thru more study that the Hypothalamus in the Brain can and does produce Estrogen sometimes in giant spurts. So the brain can produce Estrogen, and put it right into your blood.

So I do not have an answer yet, but my guess is that my E2 increase occurred when I tried to lower my E2 with more DIM, and some mechanism, or signal went to the Hypothalamus, and it reacted and dumped Estrogen into my blood to compensate for me trying to lower my E2 below some equilibrium point. The tissue near the Testes, the Lymph fluid, and Adrenals cannot by themselves account for such an increase. So it has to be from the Hypothalamus. Is Arimidex in my future. Will discuss with my Endo. Doc. and my oncologist. As if you follow my writings, I try very hard as do others here to keep my E2 low, as our PSA Sensitive Pca, cells enjoy E2 as food, as they have receptors for this Hormone. There would be no affect to Neuroendocrine Pca, or what some folks refer to as Hormone insensitive Pca cells.

Anybody, have a better scientific explanation, other than a botched up test. Hope this little dissertation adds some knowledge, as I know, and researchers know that as your body starts increasing Estrogen, your T goes down, And 20% of all men with low T get Prostate Cancer.

Nalakrats

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Hi Nalakrats,

I have Papillary Cribriform, is that the same as yours? My PSA was 8.1 at time of surgery and has risen to 0.7 since surgery 0n 4/19/2016 about 16 months ago. Haven't started any treatment yet, am I doomed?

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George--Papillary Cribriform, is just another term that can be used to describe Ductal Cribriform. More often women with Breast Cancer Cribriform, usually, Pathologists will use the term Papillary. So IMO, your Pca, sits in the same pew as mine. Ductal Cribriforms usually co-exist with every day Adeno carcinoma. If you get your Pathology report and read the whole report, you will probably find 2 pathologies Identified. Critical, is to know what your PSA was---the first one taken after surgery. And what was your nadir---the lowest your PSA got to. It appears your only treatment was Surgery and Active Surveillance. Is that correct===respond please. We are in a small club.

Nalakrats

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