Testosterone replacement after radiation and Orgovyx?

Posted by brownsf @brownsf, Dec 9 1:16am

I had an RP in 2008 and a recurrence last year. I was treated with 5 months of Orgovyx and 37 radiation sessions, both of which ended about 18 months ago. My PSA has been undetectible since then but my Testosterone seems stuck around 160-180. I'm considering testosterone replacement therapy. The main symptoms I'm having from low T are tiredness and weight gain. The doctors tell me they would monitor my PSA and testosterone monthly if I begin T therapy and stop it if my PSA increases---but there's a small chance that stopping the T therapy would not restore my PSA to undetectable. They would not quote any odds. So I'm torn--it would be nice to be less tired and reverse the weight gain but after surviving the cancer and recurrence, I really don't want to go through it again. Of course, I can always wait longer to make a decision since there's a small possibility my T could still come back on its own. I'm wondering about the experience/advice of others who have been through this.

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@seasuite

I had just four months of Orgovyx, completed end of January. My T recovery has been slow and only 50% recovered. My RO referred me to a specialist that he said I could see after one year, meaning January 2025. This guy is a testosterone expert and we can come to a consensus whether it's a good decision for me or not. My RO doesn't feel there's much risk in my particular case. While I'm mostly recovered, I still have some hot flashes, about 5 pounds of extra belly fat and can't seem to run the entire distance on a 5K race that I was able to do just before Orgovyx. I'm 72 and my PCa was 4+3.

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Wouldn’t sweat 5 lbs and the 5K. You have been thru male menopause and it takes a while to come back!
You might never come back all the way, but if you are a runner, you know how to train to reach a goal, right? Forget your past glory😁 and now train as if you’ve never completed a 5K. You’ll be surprised how fast you can achieve this without T supplements. Training and discipline will get you where you want to go without risking a recurrence of your cancer.
Let’s see: 5K in an hour…. vs. a lifetime of ADT and all that goes with it. I know what my decision would be.

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@northoftheborder

I think it's important to note that while there have been some interesting smaller studies, BAT isn't proven in bigger trials yet (those are underway now, one paired with Enzalutamide, and one paired with Xofigo).

Here's what Johns Hopkins says:

«"They called this alternating approach “Bipolar Androgen Therapy” (BAT) because it cycles between polar extremes of very high and very low male hormones. “The idea,” Denmeade explains, “is to mess up the cancer cell’s ability to adapt.” Paradoxically, although low levels of testosterone can make prostate cancer cells grow, “at high doses, the cancer cells don’t grow as well, or they die.”»

It seems they're testing it specifically on cancer that has already become castrate-resistant, *not* for castrate-sensitive prostate cancer — in other words, it is a potential next step once ADT stops working, not an alternative to ADT for nmCSPC or mCSPC.
https://www.hopkinsmedicine.org/news/articles/2023/12/bipolar-androgen-therapy-trials-under-way

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I agree, but have a question. I you’ve been on ADT and your T has been at castration level that long, isn’t any remaining cancer by definition castrate resistant?

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@ddl

I agree, but have a question. I you’ve been on ADT and your T has been at castration level that long, isn’t any remaining cancer by definition castrate resistant?

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@ddl wrote "I agree, but have a question. I you’ve been on ADT and your T has been at castration level that long, isn’t any remaining cancer by definition castrate resistant?"

Unfortunately, no. It might just be dormant, at least according to my oncology team, and exposure to testosterone might make it active again (ADT doesn't so much kill prostate cancer as hit the "Pause" button). Once the cancer starts growing again, it has more opportunity for mutation, including mutations that create castrate-resistant cells.

That said, future research could throw more light on this. Once they have a way to detect dormant cancer cells in our blood or elsewhere, they'll have a better idea of what's going on. And maybe they will even find situations where BAT makes sense for nmCSPC and mCSPC.

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