Advanced Prostate Cancer
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Avodart - Arimidex - and PCa

The 2 papers below show why it makes sense to take Avodart and Arimidex as part of any ADT protocol. Turns out DES can inhibit Telomerase, which explains why it can even be effective in CRPC...17B-Estradiol turns on Telomerase....DHT prevented programmed cell death in PCa


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Gus, thanks for the papers and research, all I can say is that whenever a therapy such as ketoconazole or zytiga would fail or early on when I had high liver numbers due to casodex 150, I would add transdermal estradiol in the form of climera 6 times .1 mg patch per week and always get a response , after many times and probally 5 or 6 years of use returning to it, On the last time I got a 30% with drawl response from with holding it.


These papers deal a lot with primary tumors. The problem is that not only are their are different stages the pc goes through before becoming crpc the various medical sequencing and combination also needs to be considered. Its sill a work in progrees. How to sequence or coombine med treating chronically trying to cure.



Haven't yet read the papers, but taking them as given it would seem "easy" to compare guys on and those not on Avodart or Arimidex along with Lupron. We should be able to see a difference in longevity or time to recurrence. My understanding is that has not been the case with Avodart. In fact, my new urologist just suggested that avodart (and Casodex) was not needed nor helpful. I stay on them, anyway!




I'm actually in the middle of a post on estradiol, so thanks for the second link.

Does it "make sense to take Avodart and Arimidex as part of any ADT protocol" as you suggest?

a) Avodart blocks the conversion of T to DHT. The intent of ADT is to make T irrelevant. Oncologists therefore do not test for DHT, as a rule. Dr Myers says this is a mistake. Logically, it makes sense to test for the hormone that actually drives PCa growth, but there is another reason: there are alternative paths to DHT that do not involve T. Avodart blocks those too.

Rather than dose all his patients with the standard 0.5 mg dose, Myers doses his DHT producers with the minimum dose that does the job. Sometimes, that requires no more than a weekly cap.

Note that Avodart has a long half-life. It takes a long time before the drug reaches the optimal level in the body, so don't expect quick results. (One can double-dose to get started, though.)

b) Arimidex inhibits the conversion of T to E2 (estradiol). The optimal range for E2 according to LEF is 20-30 pg/mL. Bone health seems to suffer if E2 < 12 pg/mL.

I agree that someone not on ADT might benefit from Arimidex, but E2 should be tested first. For thost on ADT, E2 may well be < 12, & a low-dose E2 patch should be used. If E2 is > 30 pg/mL while T is very low, Arimidex might be useful. If E2 is being used for ADT, then Arimidex makes no sense.


A note on testing.

Dr Myers tests DHT on the basis that serum levels mirror levels in PCa cells. I just don't believe it. (Because I cycle quickly from castrate to high-T, I use Avodart continuously. It is prudent to use Avodart when using T.)

I'm not sure that serum E2 levels tell one what is happening in PCa cells, either. Those cells are often high in both, ERalpha & aromatase. Even if E2 is in the 20-30 range, Arimidex can be used - provided that E2 is not permitted to dip below 12 pg/mL.



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