I recently reported my experience with BAT (DIY BAT and DIY BAT-an interim report.) There was discussion of the risks of trying BAT as a management tool and my response was that my personal risk analysis indicated the danger period was the first 3 months where there was a possibility of a spike in PSA. My research suggested that the few cases where a large increase occurred were not cases of genuine BAT. I recently came across an interview with Sam Denmeade which seems to confirm that. Demeade says the worst case involves PSA continuing on its upward trajectory neither diminished nor accelerated and unaffected by testosterone,
Naturally, we all have to do our own risk analysis for all treatments at our stage and equally obviously do such experiments under medical supervision if at all possible. Unfortunately sometimes it is not possible.
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kaptank
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Denmeade said: "... the levels decline slowly over a month, without the sharp drop-off that we would prefer to see. The daily administration of testosterone gels effectively provides a normal physiologic or replacement level of testosterone, but it does not provide enough testosterone to produce a supraphysiologic level."
For most of the years that I alernated between 3 months castrate & 3 months T, I was using daily AndroDerm patches. For a couple of years I was at the 5mg dose (options were 2.5 mg & 5 mg), but the company reduced those doses to 4 mg & 2 mg. Even on 4 mg, my T was abover 1,000 ng/dL (but not much higher - never supraphysiological).
When, because insurance was objecting to the high cost of Androderm, I switched to T cypionate, injected weekly, my T on day 8, before another injection, was still above 1,000 ng/dL. It would be interesting to plot daily T for a month on BAT. For how many days is T above 350 ng/dL? How many days is T at castrate levels? & how many days in between? The latter is problematic IMO, because estrodiol can become dominant. With the patch I could quickly go from 1,000 ng/dL to castrate.
What I was always aiming for was dynamic equilibrium. Denmeade, with T above 2,000 ng/dL is expecting far greater cell death. I have never really understood his explanation for that. I wonder what Morgentaler thinks? Androgen receptors are "saturated" with T at fairly low levels (~250 ng/dL). How can one get more T into cells once they are saturated?
I think Demeade was aware that T can cause cancer cell death by a number of pathways. In the case of the androgen receptor route, apart from "saturation" there is the regulation/switch off of variant androgen receptors (ARV7 etc) and also the various signalling pathways by which the cancer reproduces. Its not so much getting T into the cell but altering the T environment around it. Another, independent route is double strand DNA breaking which is well demonstrated in vitro. Disabling DNA repair (PARP inhibitors) is a complementary line of approach and checkpoint inhibitors another. From the start, the Johns Hopkins mob were interested in combining BAT with means to inhibit DNA repair. Denmeade mentions a forthcoming trial COMBAT CRPC doing that.
Fact is: we really know bugger all.
Its an important point you make: that in going from castrate to supraT and back again, its essential to spend as little time as possible in the low-normal T range, where the cancer is happiest. To the best of my ADT raddled memory, for their first trial Johns Hopkins did some studies of the course of T levels over the month. Peak 36-48 hours after injection. At 1 week entering high-normal levels then a steady decline to near castrate. At least a few days in the danger zone. Great variablity among subjects.
Kap, was wondering, when you did BAT, did you stop taking any receptor blockers like Biclatudamide or Apalutamide and just do the Abirat or Lupron? Reason I ask is, it seems to me when cycling from Hi T to Lo T it might be possible to get to the low T state pretty quickly by taking intermittent Bicalutimde during the transition?
When starting BAT I waited a month after stopping bicalutamide to let the androgen blocker leave my system before I injected T. I kept the primary ADT throughout (zolodex, similar to Lupron). I haven't found any reference to this in the research but it seems obvious to me that if you want to temporarily saturate cancer cells with T there should be nothing in your system (like an antiandrogen) that blocks the cell's access to it. ADT does not block, it just stops production of T. I haven't used any of the second generation androgen blockers (eg Abi or Enza) yet. The problem with intermittent bicalutamide is it still takes that month to clear after the last dose. So in the "androgen phase" when I am injecting T I try to be as free of antiandrogens/androgen blockers as possible.
And of course the obvious reason. D'Oh. ADT brain. In Vitro experiments have shown for decades that supraphysiological levels of T are cyto-toxic to a degree at least equivalent to most chemo agents. (I don't know about docetaxel) Confirmed In Vivo with mice grafts.
So its interesting that BAT apart from its direct effect, has an effect on future treatment - reversal of ADT resistance. Denmeade hints at another such case of "(re-)setting the immunological scene": subsequent use of checkpoint inhibitor.
By the way, yours is a thoughtful direction of treatment.
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BAT and other update
Helping my Doctors Give Assent to BAT
