Even though I had just finished 1 year on Darolutamide, Orgovyx, and Non SOC 10mg Osterine and 10mg Cardarine every day with good results. The last quarter showed my E2 drop from normal levels to very low levels causing irritability, skin health was getting worse, and my desire to do things like think about any future projects was gone.
I was starting to feel it was time to delay CRPC while maintaining QOL.
My protocol is basic at this time. Stay on Orgovyx throughout. 7 day washout with darolutamide, then inj 100mg T-propionate first day and 75mg every other day for the two week high T cycle.
The next day after last T inj start back on daro again for 2 weeks then rinse and repeat.
Note: I am taking letrozol .625mg every 3 days during High T and a little into Daro cycle.
(I will adjust as needed to maintain E2 between 20-30pg/ml.
Note: I am not taking any SARMs during High T, but am during washout and daro cycle.
All the while testing T, PSA, ultra sen PSA, E2
My Numbers before BAT
uPSA <0.02
T 14
E2 <10
Testing During High T phase of the first cycle. (note: I tested this on last injection day a few hours after injection) I was expecting T to be higher so I will test on First 100mg T injection on the next cycle as well as an off T inj day.
(Addendum: Russ informed me my T will be its highest 6-8 hours after injection so my number was spot on for 3 hours after injection.)
PSA 0.33
T 1,800
Testing four days before end of Daro Cycle
uPSA 0.08
T 24
E2 <15
The reason I test 4 days before projected end of Daro cycle is that if my it takes 4 days to get results for uPSA.
if uPSA is to high (number undetermined) I will stay on Daro another week and retest.
Since my PSA did drop back down close to my nadir of (<0.02) I will begin daro washout for 7 days before starting High T cycle again.
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KocoPr
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Your T is inline with theory (spot on). If you want to measure the max, measure 6 to 8 hours after injection (Tmax varies by individual). 3 hours isn't enough time for full absorption and your prior levels drop almost 50% in a day.
Thanx for the post-cycle update. I always admire a man with a plan - especially when it is well-conceived, of his own making, and gives priority to QOL!
Have fun on the hormone roller coaster. Think of it as a ride at Coney Island.
Best of luck with continued good results. Stay S&W
PS. Your target of 20-30 on E2 is the same one I am using for bical mono +. I first remember that target (unrelated to BAT) coming from Nal and/or Patrick many years back.
Thanks. That's an interest perspective to consider. Along with a much-delayed post on PCa metabolism, I have started doing some digging into Friedman's favored membrane AR and will post what I find. Eventually. . .
Let me know what you think about it. I'm in the middle of a mAR/iAR experiment. First half of BAT/SPA I'm doing normal T. Should trigger iAR actions with some mAR. Next half of BAT/SPA I'm going to block iARs and attempt to lower intracellular DHT. That should hit mARs. I'll monitor PSA but regardless I plan to do 2 weeks of daro and 1 week of nothing (Lupron constantly throughout).
If it works, new therapy is born. However it goes I'll let Friedman know the results. If results are negative it doesn't prove anything unfortunately. Studies are wishy washy on blocking iARs and reducing DHT in cells.
Will do. My first scan was that the research specific to mAR is pretty skimpy, but it is a recognized element in AR, so maybe he is right that most docs and researchers are missing its role altogether?
Many texts don't even recognize that mARs exist. Rather new development. ZIP9 and some G proteins are mARs. Xtandi might inhibit iARs while leaving mARs relatively untouched. Some studies indicate Caso blocks iARs but leaves mARs open. One study shows that it blocks ZIP9 but leaves GPRC6A open.
The terminology used by Papakonstanti/Castanas was a bit different at the start. This link might not get all of their papers, but there are 23 hits, going back to 2002!
I should point out that I have never advocated normal T levels for men with PCa. My opinion is that either you go castrate levels of T or superphysiologic levels of T (with aromatase inhibitors and with or without 5AR inhibitors).
Thanks. Which way you think it is better to introduce 5 ARI (most likely finasteride, because of much shorter half life than dutasteride) into high testosterone part of the BAT cycle:
1. Do separate BAT cycles, one BAT cycle without finasteride on the background and then one with finasteride?
2. Do first half part on high testosterone of the same BAT cycle without finasteride and then second half on high testosterone of the same BAT cycle with finasteride?
I agree with you that finasteride makes more sense than dutasteride. I'm not a physician, but in theory I would prefer option 2. It is known that finasteride by itself amplifies intracellular androgen receptors (iAR) number. Nobody has checked whether or not it still amplifies when high T is present instead of normal T. If high T plus finasteride fails to amplify iAR, then normal T plus finasteride should do the trick, although the literature only reported that after 30 days. I have no idea how much amplification would be present after 15 days. Obviously, finasteride alone results in a better quality of life than ADT does.
Thank you! Option 2 is what Russ exactly intends to try.
Interesting suggestion to contemplate that if high testosterone with finasteride fails to amplify iAR...
then maybe let testosterone in one of the cycles to recover naturally (on Orgovyx it can be relatively fast) while taking finasteride and run it for 30+ days.
In one of the modified BAT cycles with orgovyx it might look like that:
- drop Orgovyx on the day of first testosterone injection;
- half way through high testosterone cycle introduce finasteride;
- continue finasteride without Orgovyx after testosterone injections are over and till natural testosterone rebounds and continue on natural levels of testosterone for 30+ days....
Or if on continuous Lupron or on continuous orgovyx (to be on the safer side):
- half way through high testosterone cycle introduce finasteride;
- after finishing high testosterone period, drop level of testosterone by injections or patches to normal level and continue with finasteride for 30+ days...
Of course period 30+ days on normal testosterone sounds risky... maybe weekly monitor PSA can reduce the risk.
I should point out that for many years Dr. Leibowitz had used high T plus finasteride following ADT on his PCa following patients and they were able to stay on this for years at a time before needing to undergo ADT again. See: web.archive.org/web/2021030...
Ed, While I think maybe you have commented on it previously, please remind me/us on your opinion about Morganthaler's Saturation Model? I.e., Has it changed any from that stated in your 2009 letter to EAU linked below?
Letter to the Editor:
Re: Abraham Morgentaler, Abdulmaged M. Traish, Shifting the Paradigm of Testosterone and Prostate Cancer: The Saturation Model and the Limits of Androgen-Dependent Growth. Eur Urol 2009;55:310–21
I stand by that letter to EAU, but let me explain how I view what actually happens when talking about varying levels of T alone. When T levels are low enough (castrate level) apoptosis occurs due to calcium ion overload. As T levels increase, PCa grows at its optimal rate, because there is a balance between iAR and mAR. Increased levels of T have little effect on PCa growth. However, there is not much mAR on normal prostate epithelial cells. As PCa occurs, mAR is now readily observable and increased mAR correlates with increased Gleason score. So a high enough level of T before PCa occurs will prevent it (think teenagers) and will kill it if administered at the very beginning of PCa formation, before it has a chance to increase mAR levels.
There is probably a saturation limit for both iAR and mAR, but I believe it is at much higher levels than Morgentaler thinks it is, otherwise Dr. Danmeade would not have to go to levels above 3000 ng/dL as part of his BAT protocol.
Research shows either very high or very low T. High = DNA DSBs, etc. etc. etc. Low = pressure on androgen-sensitive cells. DNA DSBs continue to increase as DHT goes to levels that correspond to T > 50,000 ng/dl. 1500 is rather low IMO. I went above 25k one time and PSA went out of control. Now I limit it to 2000-3500 ng/dl. That's what I was doing for the last couple of years and it seemed to work well.
I'm in the middle of high T w/o finasteride and then high T w/ finasteride and darolutamide (for safety I'm going to enter into typical ADT+daro state for 2-3 weeks after the SPT/Fina/Daro is done. I'll let you know how it goes.
If it does both, it won't work as intended. If daro works similar to Xtandi, and if Xtandi leaves mARs unblocked, daro might work. If not, Caso blocks ZIP9 but supposedly it doesn't block GPRC6A so I might try it next. Longer half-life though and that makes it less than optimal.
I find one study that says one thing and another that contradicts it. Might be cell line dependent or depend on mutations or... I'm not a researcher so the way I can prove it or disprove it (in me) is to try it and test it. Just takes a while to do this. Rapid pulses appear to work. Hours or days. Daro seems to work. Casodex supposedly does not block anabolism. I tested that and know that this is false. Maybe it leaves some anabolic processes open but, in my experience, not all.
So far the guys who started pBAT while they were HSPC are still HSPC. One of the HU members has used a modified BAT for 14 years and is still HSPC.
It was not but i was apprehensive but i did my homework and basically asked him to support my decision to do BAT. I also told him I would send my BAT protocol to him, and test results.
He said I know you and you are on top of your health so of course I will support you.
He asked if he needed to write prescriptions but i said it was not necessary. He wasn’t surprised. He asked about future appointments and i said of course we will keep our standard quarterly appointments and tests as I am still taking Orgo and Daro. I could tell he was relieved to here that.
KocoPr - That aligns with the support I've gotten from my MO. If one provides a sensible plan and the back-up research to support it, I would hope most MOs would do likewise. After all, it is our cancer and lives we are talking about - and not theirs.
Congrats for being on top of the game. How do you get T supply without dr's prescription? It's hard to find a MO in Southern CA who supports BAT and writes the Rx.
Your approach and response was similar to mine. Once I made the decision to go forward with BAT my MO went along. He has even gone so far to administer BAT to one of his patience in his practice. We can change the world, even if it is only one patient at a time!
Would be very interested to know PSA numbers on a day before or the same day of the next testosterone injection (of course prior to injection😅).
I think it would be great if you update this thread when tests become available to wrap up this first cycle.
Also if you don't mind please share how it felt to have testosterone back albeit temporary after one tear on castrate level (energy level, hot flashes, etc...) ... or it was to short to notice a difference as yet?
😅 yes, but it is highly unlikely in the nearest future... only if BAT become SOC🤐
Then maybe we can see some kind of rapid BAT patches XR or pills XR developed that raise you testosterone to suprophysiological level during the day and then bring it to castrate level during the night hours... or one pill in the morning to boost testosterone and one pill before sleep to bring it to castrate level both XR and with very short half life.😉
In short: T = subtract 40 years from my chronological age. No T = add 20 years to my chronological age. I don't have to say anything to my friends for them to know if I'm on low T or high T. And my wife is "pleased" when I'm high T.
To my surprise I didn’t feel like i was on top of the world but it did feel slightly better than being on ADT. BIG BUT here, i was also on a years worth of Osterine and Cardarine during my whole ADT year.
I expect to feel better and better as the cycle of T goes on.
It's very encouraging that we have interest from the mainstream treatment, diagnostic, and research communities for PCa. Multiple n=1 patients are now sending info to major research centers and interacting in realtime with them - fully outside of clinical trials. We also have a member here at FPC who is doing similar data sharing on dosing reduction with Moffitt's Gatenby. Seems a bit of confirmation for my oft-quoted Mukherjee's Rule #2: “Normals” teach us rules; “outliers” teach us laws.
The fact that those all-important elements of cancer treatment development recognize the importance of outliers seems to me to be a sign of better things to come. We may finally be helping to make Don Pescado's "Science is Coming" more real than ever.
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