My PSA lows tend to be around 3.3, and it occurs to me that some might think it odd that I don't drive it lower.
I think it is very common for men on ADT to draw too much comfort from a significant PSA reduction, if not a near-zero PSA. I have witnessed men misinterpret a dramatic drop in PSA as a possibility that ADT might actually be curative. In a paper from 2019:
"A large proportion of patients with metastatic prostate cancer reported beliefs inconsistent with understanding that treatment was not curative." [1]
Following my failed prostatectomy in March 2004, it seemed inevitable that Lupron would be in my near future. I had read dozens of papers with boilerplate introductions where ADT was described as a therapy that was usually effective at first, but for only 18-24 months in most men. So why rush into it? I decided to ignore the advice to "hit it hard and hit it early" and save palliative therapy for when palliation was required.
I started out with continuous testosterone on the basis that untreated men have 'wild type' androgen receptors. They also already have a decline in the beta estrogen receptor [ER] and an increase in the alpha ER.
While testosterone will convert to dihydrotestosterone [DHT] in the absence of Avodart, say, DHT is one's friend - until it isn't, imo. As with the vitamin D conversion of 25-D to 1,25-D, the presence of the strong hormone triggers its decay in prostatic cells. A metabolite of DHT - 3beta-diol - is the natural ligand of ERbeta (a growth inhibitor.) [2] As long as there is ERbeta, the narrow window of opportunity that DHT has, is followed by a sustained period of growth inhibition.
When my PSA doubling time began to shorten, I knew that I was losing ERbeta, so I switched to 3 months of ADT followed by 3 months of high-normal testosterone.
PCa begins to adapt to therapy from day one. What do those cells look like after 3 months of ADT - versus 6 months, 12 or 24?
For whatever reason, 3 months of ADT worked for me. Enough cells able to return to their "normal" pre-ADT state to crowd out the advanced cells that are suddenly at a disadvatage with restored testosterone levels.
Of note: I began ADT & the testosterone reset at the same time. Rapid androgen cycling, however defined, is not something one saves for later imo.
Incidentally, that phrase - rapid androgen cycling - brings to mind the work of Howard Scher [3] (2006)
When Abiraterone and Enzalutamide were approved, I was briefly tempted. But however efficient they were at controlling PSA, the effects were transient for most men.
In addition, I was wary of the new adaptations to Abi & Enza. Would testosterone be as effective after 3 months?
In the end, I decided to skip Abi, Enza & Lupron and go back in time to DES (diethylstilbestrol). It's a synthetic estrogen that maintains bone health even while estradiol falls to zero. And it has anti-PCa properties.
The reason why DES was phased out is that oral estrogens increase the risk of life-threatening blood clots. I take a very high dose of nattokinase to keep D-dimer low.
My approach is quite simple: as long as there is no upward PSA trend at the end of each 3 months, I am content. I don't worry that the PSA is not driven down to zero. I don't believe that a near-zero PSA is necessarily a good thing?
My approach is sometimes confused with BAT, but I originally used daily transdermal testosterone patches. Enough of a dose to create high-normal levels - not supraphysiological levels. With Denmeade's BAT, testosterone levels are modulated - and there is no castration-only phase. In my original protocol, there was an abrupt shift from high-normal to castrate testosterone.
More recently, I moved to something closer to BAT, with a single dose of testosterone cypionate at the start of the cycle (as with BAT) and two months of pure ADT at the end of the 28-day BAT phase. This is basically because insurance would no longer pay for the expensive testosterone patches. (I do not use daily DES during the first week of the 3 month cycle.)
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I don't make any changes to my supplement usage before a PSA test.
For men with intact prostates, the advice is to avoid stimulation of the prostate before a test. The aim is to avoid a "false positive", i.e. a result higher than the arbitrary cut-off for biopsy.
An example of a "false-negative", is failure to use a lower cut-off when taking a drug that targets BPH but not PCa. The old 4.0 PSA cut-off for biopsy takes into account the fact that BPH is common in screened populations. Take away BPH noise and a significantly lower cut-off must be used.
For men diagnosed with PCa who have had their prostates removed (as I have), PSA results are compared to historic results, rather than an external number. This is what the PSA was intended to be used for - a post-treatment tool. Importantly, the conditions should be similar during each test. The actual PSA number lacks significance imo.
During my 3-month cycle, my PSA might be 7.5 at the end of month-1 and 3.5 at the end of month-3. I don't usually check the former. All that concerns me is that there is no upward trend for month-3 results.
For curcumin, I use Longvida - sold by NOW Foods as CurcuBrain. It has been shown to cross the brain barrier, which is a good (if not scary) indicator of bioavailability.
I use curcumin because of the >150 PubMed hits for , not to mention the >250 hits for or ~500 for .
Within those papers there is ample evidence that curcumin has properties that are helpful against PCa. For example, as with a wide range of polyphenols, it can inhibit NF-kB activation and reduce pro-growth inflammation triggered by the cancer. If I am keeping markers of inflammation in check, why would I stop using any polyphenol or other anti-inflammatory agent before a PSA test?
To those who claim that curcumin, say, is masking the "real" PSA number, I would say that there is no "real" number. All that we have are numbers for comparison. For those who stop taking some or all of their supplements before a test, the important thing is consistency - but I doubt that there is any benefit.
-Patrick
[1] ncbi.nlm.nih.gov/pmc/articl...
51 yr old Gleason 9 with PSA 5.9 anyone with similar results?
Nitric Oxide -- slows prostate cancer progression and PSA doubling time.
