Just curious as to whether any of you have been able to control your PSA after recurrence? Since dutasteride is an inhibitor of all three 5a-reductase isoforms, it appears to be an effective suppressor of DHT which is a considerably more potent androgen than the testosterone it is derived from.
After RP and LN excision BCF I started applying tE2 gel which has been doing a great job of keeping my PSA down to levels below 0.01; however, I'm wondering if I had started taking dutasteride in place of Oestrogel, could I be experiencing similar results?
The well respected Dr. Snuffy Myers was prescribing dutasteride for many of his patients which I believe is a pretty good testimony for using the drug.
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E2-Guy
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My question would be, is this as effective at keeping the cancer from progressing, rather than merely effective at suppressing PSA? They are not the same, after all. While PSA is a proxy for cancer, it is not the cancer.
My impression has been that monotherapy with Avodart, and/or Proscar, might help PREVENT cancer by suppressing DHT. But while they also appear to keep PSA lower for those who already HAVE cancer, is the lower PSA level necessarily fully reflecting the death or senescence of cancer cells?
I guess intuitively I don't think taking dutasteride in place of Oestrogel would be as effective, if only just because it is a less drastic change to the "hormonal milieu" in which the cancer has already progressed. (In short, it packs less of a punch.)
PSA is a biomarker used by researchers and clinicians all over the world to measure extent of live active prostate cancer cells in regular,garden variety prostate cancer.
To think that PSA is going down for other reason than cancer cell dying only adds to confusion . And I am saying this for high PSA type plain acinar adenocarcinoma.
(In cases Neuro-endocrine, ductal or small cell PCa , this rule does not apply.)
Lectures by Bob Liebowitz stated that Proscar helps hide the "real" PSA level of a cancer. But I am not qualified to debate whether men without prostates could have higher or lower PSA expression for whatever reason.
PSA alone cannot be relied upon in men who still have prostates, however. Any researcher or clinician using PSA to measure extent of live active prostate cancer cells in men with prostates is making a mistake. They could be measuring BPH, etc.
I think you need to let go of everything Snuffy Myers said years ago - there is probably a lot better info now. He made a lot of very good guesses and a lot of very bad guesses.
5ARi's (like dutasteride) do NOT suppress testosterone, (T) they only suppress one of the metabolites of testosterone called DHT. DHT has high affinity for the androgen receptor (AR), which is what misled Snuffy and others. But suppressing DHT while allowing T to form will still activate the AR. And suppressing T formation down to castrate levels with estrogen or with GnRH agonists or antagonists (like Lupron or Firmagon) will not make appreciable amounts of T available to be metabolized into DHT anyway, so there is no need for a DHT blocker when using any of those medicines.
Eventually, there was an RCT that proved that dutasteride alone was not able to extend vacations in men on intermittent ADT. That put an end to any idea of using it in men on ADT (or should have).
Do you happen to have a citation for the study that proved that dutasteride alone was not able to extend vacations in men on intermittent ADT. I've been telling people that it can do so and that low dose bicaluatamide can also do so, both with lower side effects than ADT. My recommendations were based on claims from years ago and, if they're wrong, I'd like to see the RCT results that demonstrate that. In the meantime I'll stop recommending dutasteride until I learn more.
I agree with TA on DHT. Its a metabolite of T. T goes down...DHT goes down. I have seen this happen in my lab tests. Both T and DHT fall in tandem .
Many years ago ,a small study did show benefit of Finasteride in prolonging Off period of IADT but later on a larger study contradicted that finding.
So at present, the consensus seems that aromatase inhibitors like finasteride or dutasteride do not help when you have high T level during off period of IADT.
Beware of this drug. I was on Avadart to keep my numbers down and shrink my prostate. Problem is that it artificially kept the PSA numbers down to long as the cancer grew. Avadart masked my cancer until it was to late. When the numbers started climbing I already had stage 4 cancer with Mets. Due to the Avadart the doctor couldn’t figure out what was going on with my body changes. Avadart is a killer 😡😡
Thank you Larry for the 'heads-up'. Shortly prior to being diagnosed I had met two urologists at a conference who told me the things I was taking, e.g.. saw palmetto, vitamin E, lycopene and selenium could possibly mask symptoms of PCa. Due to a significant family history of PCa I was very proactive and was getting two exams/year; however, when I had my surgery (still TOTALLY asymptomatic) with a PSA of slightly over 5 it reveled a Gleason 8 score with T3a staging.
This exact same thing happened to me. I had no idea about Avodart artificially suppressing PSA. My PCP ordered yearly blood work but neglected to include PSA. I noted that and got it done and the PSA was 8. It was only when I went to a urologist with a PSA of around 8 that I found out that the true reading was actually around 16. By then, it was too late.
Told my urologist about it but he played dumb. Tried to get a lawyer but they blew me off. Just beware no one cares about your life but you and your loved ones. Keep fighting the monster
Read the drug labels, I took propecia and then 1/4 tablet of finisteride to prevent hair loss. Doctor didn't know what to watch for despite making proclamations of authority.
Either will reduce PSA, but then the rules change as on these drugs ANY rise I repeat again ANY rise what so ever in PSA has to be investigated. You can't wait until you hit 4 to take a look.
I totally agree with not waiting until you hit 4...my older brother was diagnosed when his PSA was at 2.2. Because of a significant family history I was extremely adamant about getting PSA's and DRE's for many years prior to being diagnosed at slightly over 4. After my surgery my urologist guessed that I had PCa years before my PSA had risen to 4 even though I was asymptomatic and DRE's indicated nothing abnormal. I never even had to make a pitstop during the night since I my prostate was of normal size.
I’ve been taking Avodart for over 6 years now per Snuffy but not as my only form of ADT, I’m also on Lupron and Xtandi. My PSA remains at undetectable levels despite my dx of stage 4 G9 PSA.
None of my current doctors including doctor Sartor have told me to make any changes in regards to Avodart or the “Snuffy protocol”, in fact they’ve been quite amazed at my status thus far.
IMO, Snuffy is an awesome doctor and I credit him with saving my life.
We need TA to jump back in and clarify questions raised by the above posts.
True or False
(1) 5Ari’s reduce PSA and reduce DHT .
(2) DHT is the derivative of Testosterone that most significantly activates the androgen receptor .
(3).Testosterone not converted to DHT can also activate the AR.
(4). 5ARi’s are good because as prostate cancer cells develop their development is attenuated by knocking down DHT which feeds the cancer.
(5). 5ARi’s are bad because by holding down PSA to levels considered “ normal “ on an age adjusted basis, they can mask the presence of prostate cancer since absent their use the PSA would be higher and reflect the possibility of cancer.
(6). On the “ off cycle” of intermittent ADT the 5ARi’s do not have the capacity to extend the off period because the cancer is at a developmental stage that the testosterone alone ( without the DHT effect) will fuel the cancer.
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How's your whiskers after ADT? 
What to do when in remission?
ADT + darolutamide + docetaxel (ARASENS trial) has anyone tried it?
Husband doesn’t want to continue ADT/treatments for stage 4. He is only 51. 
