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What if this prevents cancer from becoming resistant?
I saw a thread about half-dose medications.
Guys, what do you think about whether resistance can be avoided? Read below.
Another option is to use different combinations of ADT and lutamide. For example, one month is ADT without lutamide, the second month is ADT with lutamide, the third month is lutamide without ADT, the fourth month is neither ADT nor lutamide, and then the cycle starts over again, so as not to repeat the previous cycle (the combinations would be reversed).
I had this thought, perhaps it's naive, but for some reason my intuition told me exactly this. What do you think?
In other words, varying the medications is necessary to avoid resistance. I've heard of guys who are still alive for 30 years; maybe they did exactly this?
I voiced this thought to my oncologist, and he said it wouldn't work with high Glyson levels.
At that moment, I thought about resistance as cancer adapting to low testosterone levels. The cells change and no longer respond to low testosterone.
And if you really want to "let the cancer swing," you can try to keep testosterone levels fluctuating rather than staying steady, and change the ADT + Lutamide combination depending on PSA growth. For example, if PSA growth is significant, ADT + Lutamide is taken for a month; if PSA growth is moderate, Lutamide alone is taken; if PSA growth is low, ADT alone is taken; and if PSA growth is not observed, the duration of Lutamide-only treatment is extended (2 months instead of 1 month). In any case, the method is based on the fact that we don't "create" a wall for the cancer, but rather a swing when it doesn't have time to adapt (testosterone levels fluctuate, but we don't allow it to fully utilize them with the help of lutamide).
I want to try this on myself, but fear holds me back. But who knows, maybe this method works.
Why do I think this method might work for those with a PSA level of almost 0 and whose cells have not yet become resistant to cancer?
Argument 1: If cells are still dependent on testosterone, they will respond to ADT and lutamide when drug therapy is resumed.
Argument 2: By changing combinations and increasing testosterone levels, we prevent cancer from becoming resistant because we are changing the "rules of the game" and not dealing with cells that are no longer responsive to ADT and lutamide.
Argument 3: By repeating combinations in a cycle (ADT and lutamide, ADT only, lutamide only), we maintain a basic level of protection by closely monitoring PSA levels, which is an indicator that resistance is not developing.
Argument 4: Cancer has little time to "start firing." A new combination will either lower testosterone (ADT) or dampen the ignition.
Argument 5: It's no secret that they're making money off us, and the higher the stage, the more money they make. But they can make much more money if resistance develops (medicine is a business), and perhaps that's why ADT and lutamide inevitably lead to the development of resistance! What if we take our luck by the balls and say no to a society in which someone profits by keeping silent about the easy way out (when registration doesn't occur)
And finally, if the cancer becomes resistant, then we're done for, and we need to avoid it at all costs to keep the cells sensitive to hormones.
What do you think, guys? Is it risky?
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@denis76 https://connect.mayoclinic.org/discussion/a-note-from-richard-wassersug-phd-about-the-use-of-estradiol-over-adt/
LIKE THIS!!
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2 Reactions@heavyphil Denis, let me know if you were able to open…
Phil
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1 ReactionHi,
It sounds like a good idea for a study/clinical trial but I would not try it on my own. Clinical trials usually have experienced doctors in their field plus a well versed statistician to set up the test properly.
Dave 3+4
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2 ReactionsTo expand the topic a bit, one of the biggest breakthroughs for metastatic prostate cancer this decade was the simple realisation that if a certain percentage of prostate cancer cells will eventually try to turn castrate resistant, wiping out as many of them as possible at the start — and keeping most of the rest dormant — means there will be many fewer cells that are candidates for mutation (n% of small number vs n% of big number: maybe so few that they can't build enough of a tumour to survive the body's immune system??).
That's why for metastatic prostate cancer, we've seen the big shift from sequential therapy — start gentle and escalate to a new treatment each time the current one falters — to full-on, attack mode, shock-and-awe, hitting the cancer with everything we have right at the start. This brings us to approaches like doublet therapy (ADT + ARSI for oligometastatic) or triplet therapy (ADT + ARSI + chemo for polymetastatic), metastasis-directed therapy (MDT), primary/pelvis-directed radiotherapy (PDRT), and so on.
It's also possible that they'll add surgical debulking of large lesions to the list before too long, because anything that decreases the number of cancer cells is a good thing. I did have debulking surgery in 2021, but only to save my spine and mobility; it's just a happy coincidence that it's being researched now as a primary path for cancer treatment, and may have helped me achieve an unexpectedly good outcome (so far 🤞) from what started out as a really desperate situation.
The lesson is that with metastatic prostate cancer, STOP BEING POLITE! (yes, I know it's a Canadian writing this). We have to fight dirty: slap it in the face, throw sand in its eyes, pull its hair, knee it in the groin, and don't give it a chance to catch its breath, figuratively speaking.
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8 Reactions@northoftheborder
So the main question is: can the PSA level tell us how many bad cells there are or not? These cells seem to be hiding/going dormant.
I've seen guys whose PSA levels dropped to 0 and then progressed. I've seen guys who had prostatectomy and died within a year. Of course, I'm talking about stage 4 and advanced cases.
I don't think there are other factors, if you will—an individual cancer profile and the body's individuality.
And I'll be honest, I'm scared. Erleada and ADT suppress the cancer, but I'm shaking like a slender aspen.
@denis76 No, PSA tells whether (non neuroendocrine) prostate cancer cells are active/awake.
MDT, PDRT, chemotherapy, radioligands, etc, kill prostate cancer cells. ADT encourages any survivors to go dormant. And ARSIs like the lutamides delay or prevent dormant cells from waking up by essentially pulling the blackout curtain shut.
In the recent past, when they'd treat metastasic prostate cancer with just ADT, there were a lot more cells still available to "wake up," and without ARSIs, the curtain was wide open for the sun to shine in, so it's not surprising that the old conventional wisdom was that hormone treatment would usually fail within 18 to 24 months (as they told me in 2021).
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