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The paradox of testosterone and ADT
It’s a curious thing, really — this blind devotion to testosterone as the prime mover in prostate cancer’s twisted little drama. One might imagine that a tumor emerging in an environment already barren of testosterone — my personal endocrine wasteland — might, out of sheer metabolic necessity, learn to dine elsewhere. Glucose, glutamine, maybe even sheer spite. In other words, it may never have been dependent on testosterone in the first place, rendering castration-based therapies about as effective as removing the steering wheel from a horse.
And yet, when I dared to suggest this — that perhaps my tumor was an evolutionary overachiever, already adapted to scarcity and thus indifferent to the standard hormonal starvation diet — I was met not with curiosity, but catechism. The gold standard, they said. Tried and true. As if medicine were a medieval guild and I, an unruly apprentice questioning the sacred text.
Now, don’t get me wrong — gold standards exist for a reason. They work. Mostly. But I’m not "mostly." I’m me. And my concern is not the statistical majority. It’s whether this doctrinal adherence overlooked a tumor that, by virtue of its very origin, had already found a detour around the testosterone toll booth.
So here we are: therapy proceeding with grim determination, and me quietly wondering if we’re starving a tumor that was never hungry in that way to begin with. And if that’s true, what then? Will the outcome reflect biology’s stubborn individuality, or medicine’s one-size-fits-all optimism?
Either way, it seems I’m not just fighting cancer — I’m also in a polite but pointed disagreement with protocol.
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Interesting, I have never heard of someone getting a test like this.
The size of the metastasis frequently do reduce, That’s one reason the radiation oncologist like to do ADT first. I’ve seen people post actual before and asked numbers in this forum and they were noticeable size differences. The PSA always goes down With ADT, whether it stays down is another thing. If it doesn’t stay down, people are called castrate resistant.
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1 ReactionSo many people go from surgery to recurrence, It may happen in a few months or many years, but it almost every single case ADT will bring the cancer down to undetectable. We’re talking somebody that has had no cancer drugs for 17 years, His reoccurrence has occurred by having lots of testosterone right there, So taking the testosterone away, should stop the cancer.
I don’t know what you’re talking about when you say grow in a naturally low testosterone environment. The only way you get a low testosterone environment is you take a drug that cuts down the testosterone or you get an orichotomy. If the PSA rises with an ADT Drugs, then you have castrate resistance.
How is ADT counter productive If you become castrate resistant. I know in my case Lupron still kept my PSA low, After I became castrate resistant, So it did make sense to continue using it.
Maybe I have missed your point?
My testosterone levels were below minimum threshold for a few years before the cancer was detected. Given the scarcity of testosterone, it still managed to establish and grow itself. I am assuming it had to find other sources of nourishment, or the tumor made its own testosterone. That explains its high PSA count as well as cribriform cells. Cutting off testosterone would, arguably, make the tumor more aggressive. No?
Didn’t we talk about this once before? Your testosterone doesn’t need to be even a couple hundred for prostate cancer to be very happy. Yours was well within that range if remember the number you originally posted.
Yes, my PSA went from .18 to < .05 - And that was just one month. I would think that the PSA drop lags a bit behind the drop in T. Small numbers but the % change is dramatic.
The radiation you are currently receiving is completing the process and will bring your PSA much lower.
But even with ADT, prior to radiation you still have a prostate, and yours contains a more aggressive cancer, so it is STILL producing loads of PSA. Ergo, your single digit number.
So to me, your pre/radiation numbers look really good and nothing in them portends an “a priori” castrate resistance.
What @stew80 posted only makes sense. More aggressive cancers, evidenced by higher Gleason scores - especially those with metastasis - are simply stronger, faster and more resistant to conventional therapy; their tendency to become CR is yet another facet to their innate aggressiveness.
Once CR occurs, it’s a whole different ballgame and the drugs involved in treatment come with side effects as well - some much more serious than “simple” ADT. So it really is in your best interests to pursue “the gold standard” with fingers crossed before you pursue the “mine is different” route.
Phil
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3 ReactionsYou’re right. I’ll take a chill pill.
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2 ReactionsColleen, I couldn’t find the link to ZOOM in today at the 12pm Prostate monthly meeting.
I had no idea there was a monthly meeting. Wouldn’t mind participating