Finasteride & Dutasteride are 5-alpha reductase inhibitors (5-ARIs). They are used to treat benign prostatic hyperplasia (BPH). They do this by inhibiting the aromatization of testosterone [T] to the more potent dihydrotestosterone [DHT]. BPH-related PSA is reduced.
The Prostate Cancer Prevention Trial (PCPT) & the Reduction by Dutasteride of Prostate Cancer Events [REDUCE] study showed that Finasteride & Dutasteride, respectively could lower the incidence of lesser cancer. PCa-related PSA due to low-level PCa was therefore also reduced.
"Asked for his perspective, Ian Thompson, Jr., MD, of the University of Texas Health Science Center at San Antonio and principal investigator of the ... {PCPT}, pointed out that in his experience, the "vast majority" of physicians know that finasteride suppresses PSA levels by about 50%."
The traditional PSA cutoff for a biopsy is designed on the basis that 20% of the men will be diagnosed with PCa, and that a high % of men with PCa would be detected. Most men in the group who are not diagnosed presumably have high PSAs due to BPH. Screening is a compromise that balances excess biopsies against seious cases with low PSA.
Men using a 5ARI will produce less BPH PSA 'noise' & less low-level PCa PSA. It's obvious that a lower screening PSA cut-off for biopsy should be used for such men.
I never used a 5ARI before diagnosis. My PSA was only 0.8 when a nodule was discovered - well below the cutoff for a biopsy. The probability of PCa at lower PSAs is low, but that doesn't mean that the probability of serious disease is also lower - in this case, far from it. In the 5ARI population, PCa is more likely to be serious. By the time that PSA has risen to the conventional cutoff, the PCa will be more advanced than in the non-5ARI population. Hence:
"Men receiving a 5-alpha reductase inhibitor (5-ARI) for treatment of benign prostatic hypertrophy who developed prostate cancer were more likely to have a delay in diagnosis as well as worse outcomes than non-users, a population-based cohort study found."
I am sure that many doctors knew this 20 years ago.
"In marked contrast to the non-users, 35% of 5-ARI users had a delay in diagnostic biopsy of more than 5 years after the initial PSA elevation compared with 12% of non-users," the authors wrote in JAMA Internal Medicine."
"Furthermore, 5-ARI users had a 39% greater risk of dying from prostate cancer ... and a 10% greater risk of all-cause mortality ..."
Some in this group feel that lowering PSA can mask the presence of serious disease. This is a case where a drug (not a supplement) does exactly that.
My feeling is that all men on a 5ARI should have an annual PSA test and doctors should look at the PSA doubling time trend - not the absolute PSA, which could be quite small.
I suspect, due to media coverage, that some 5ARI users will conclude that Finasteride/Dutasteride increases their risk for fatal PCa. In a sense they would be correct, but that would be due to doctor incompetence IMO.
Thanks for posting. Yes this why my Dad had a delayed diagnosis and he was going to the “top” urologist in Atlanta. Yes, the psa should be doubled when on this drug. This IS NOT common knowledge. This needs to be on the nightly news because people will lose their lives over this.
And just a year after diagnosis, 2 top centers waited 6 months between scans with rising alk/phos but low psa.... they wanted to “save” second line treatment till needed. Now it’s end treatment options as it became Aggressive Variant Prostate Cancer. Just because your MO is Harvard educated and has 500 article credits and seems really kind/smart...they can screw up big time or hopefully save your life. Wow sorry to vent, but super frustrated. Don’t second guess yourself even if you seem annoying or don’t know all the proper lingo. Common sense and street smarts isn’t offered in medical school. Never give in.
When diagnosed, we rush into treatment without a PCa knowledge base to guide us. When primary (curative) therapy fails, I believe that patients need to quickly build such a base. A doctor may put you on a particular treatment because that's what he does for all patients.
My experience with doctors has been good. My advice is to be friendly, show that you are knowledgable but not pushy. Over time, a partnership may develop. Make it clear why you you'd prefer to avoid a certain treatment. Discuss alternatives but don't make any demands. & so on. Get the doctor to think outside of his usual protocol.
With PubMed, patients & care-givers have access to the same studies as the docs. Retired patients have a lot more time to get up to speed than doctors do.
& in a group such as this, someone is bound to post up-to-date info that might be useful.
It's a shame that your dad was a victim of the common 5ARI knowledge gap.
Thanks so much, great advice. I had these fantasies of showing up in the packed waiting room of his oncologist to ask for a moment of his time. And when the answer was no...telling everyone to be careful with Finasteride and what happened. Wasted energy though to be frustrated, certainly time better spent like you do with your research and educating others.
I have to make peace with it as my Dad has. And I thought I had. The reality is even if scans had been done sooner variant PC happens and maybe would be in same boat. I do think earlier tissue biopsy and a second more extensive round of genetic testing was warranted. Especially true to do this when you think all is good and “contained”! Now considering dual chemo trial and olaparib along with 2 more consults.
I’m sorry to hear about your Dad’s experience. Thanks for sharing. I am also in the Atlanta area and my Urologist immediate prescribed Dutasteride upon my diagnosis until the results of my OncotypeDX and MPMRI were received. My OncotypeDX was very low and I have my MRI in 3 weeks. After researching I stopped taking Dutasteride due to numerous concerns until My wife and I had further discussion with my Urologist. I resumed taking it but am still concerned and not fully sold on this path. I plan to get a 2nd Opinion through the Emory Multi Discipline program and/or Duke.
I was diagnosed in April 17, 2019 at age 51 with a Gleason 6 in 2 cores. PSA 5.4
Thank you Patrick for the useful information you have provided. I have no difficulty in understanding the essence of your explanation. But I would like to get my own situation clarified by you. Please do it for me.
Dxed in March 2015 @ PSA 9.50 asymptomatic, GS 5+4, T2c No Mx. Immediately treated with RP + IMRT + ADT. 2 years continuous ADT ended in April 2017. Two weeks after my initial treatment PSA went undetectable and I am in stable remission without any health problem and PSA remaining at 0.008ng/ml ( checked every 3 months ). I am 72 years now.
Although I stopped all treatments for PCa since April 2017 I am still continuing with the 5-ARI : Avodart. For a year I took 01 capsule for a day and now the dose reduced to 01 capsule every 3 days because of its very long half life ( I learned this fact later ).
Where do I stand now ? Is it better to continue taking Avodart or discontinue for the possibility of masking PSA and faking the progression of the disease? What is your opinion? I am using Avodart for whatever it is worth since majority of PCa patients who have received treatment from Dr. Charles Snuffy Myers believes that taking Avodart even during the period of remission is beneficial in managing the disease.
One reason for Dr. Myers interest in Avodart was no doubt due to the fact that he is an excessive DHT producer. He warned that T was "not the problem" in PCa, & that doctors should check DHT levels, since DHT was the true target of ADT. Castration therapy does not guarantee that DHT is low enough. PCa could find other pathways to produce DHT that did not rely on T as a starting point.
But it seems that he also favored DHT suppression in men with normal DHT production, when in remission.
In your situation, could Avodart give a false sense of comfort comparable to that seen for users with intact prostates? I don't see how that would occur with no BPH & no low-Gleason cells.
You had "2 years continuous ADT". Time enough for cells to have learned other ways of producing DHT. Blood tests wouldn't be useful IMO. It's prudent to inhibit production. I'd go further & say that it would also be prudent to use a statin (full dose).
Some will say that Avodart is not useful, but, as a long-time user, I side with Myers ... & Nalakrats. The percentage of cases where Avodart is useful may well be small - too small to show up in a study, but lacking a test, I prefer to continue with Avodart.
Yes, Avodart has a long half-life of about 5 weeks. It takes a long time to reach the steady-state serum Dutasteride concentration of ~40 ng/mL. And it may not require daily doses of 0.5 mg to maintain that plateau.
pjoshea13 Patrick, out of curiosity, do you happen to know how many doses of Avodart per week would provide a steady state? If it's less than daily intake, we may consider reducing the dosage for my Dad (not that he's every complained from Avodart side effects).
Incidentally, we just had our first meeting with Dr. Drake last month. Drake didn't make any changes to my dad's drug regiment, leaving the Avodart as part of the regimen (along with Metformin, simvastatin, Zytiga, Lurpon, aspirin, low-dosage estradiol patch, and Xgeva).
Dr. Myers found, in the few of his patients who had castrate T while on ADT, but substantial DHT, that as little as 0.5 mg / week was required to bring DHT down to an acceptable level.
With DHT production within PCa cells for internal use, we have no means to figure out the lowest effective dose. (Assuming that there is no leakage into blood.)
Incidentally, Myers wanted to avoid unnecessary daily dosing because the drug was on patent at that time. It is less expensive now.
Thank you very much Patrick for your prompt reply. I always respect your opinions very much and also appreciate your continuous supply of useful scientific information with your analyses to our PCa community.
On my specific question, since you are a long-time user of Avodart I have no hesitation to continue with same for it can do no harm. Besides, since I have less DHT or no DHT under my scalp, I have more hair on my head than before!
I guess I’m one of the victims. I had bph , took finasteride for many years and was dx with gl9 PCa , stage pt3b post RP. I still take avodart along with metformin , a statin, celecoxib and for three months now estradiol patches in lieu of an LHRH agonist. Doing well.
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