Day 4,820 – PSA Results

Okay. I got antsy and went for my PSA test on Friday instead of next week. As expected, my PSA increased from 0.33 ng/mL on 6 December 2023 to 0.37 ng/mL on 19 January 2024.

The silver lining in that cloud is that the rate of increase slowed a bit and it didn’t increase as much as I expected it would.

Sometimes, I get too nerdy for my own good. There was a 91% increase between the May and October readings, and there was a 57% increase between the October and December readings, so I averaged the two increases (74%) and projected that this increase would land me at just over 0.5 ng/mL. This increase ended up being just 12% over the previous December reading. Fickle PSA.

I ran the numbers through the Memorial Sloan-Kettering PSA Doubling Time calculator again, using the five values from March 2023 (0.13) on. My PSA doubling time dropped from 6.7 months to 6.2 months, and my PSA velocity increased from 0.2 ng/mL/yr to 0.3 ng/mL/yr since calculating it back in December.

I went for the test early because I really wanted to know the PSA value going into the PSMA PET scan that’s scheduled on 31 January 2024. Plus, if it dropped, I would have had time to ask the urologist if it was worth going ahead with the scan at a lower PSA level. (Remember, I went for a PSMA PET scan when my PSA was 0.22 ng/mL, and it didn’t show anything at that PSA level. Why subject myself to another dose of Gallium-68 if the outcome may not produce any useful information?)

My follow-up with the urologist to review the PSMA PET scan and PSA results is on 13 February, and we’ll map out what’s next from there.

So that’s the latest and greatest. More to come.

Header image: The famous Torrey Pines Golf Course, San Diego, California, home to the Farmers Insurance Open golf tournament

Androgen Deprivation Therapy and Prostate Cancer

With androgen deprivation therapy (ADT) a near certainty in my future, I’ve been trying to get smarter about it. In my research, I came across this video from Dr. Eric Small at the University of California San Francisco (UCSF), that gives an introductory overview of ADT.

If you’re not familiar with some of the lingo and drug names, it may be like taking a sip of water from a fire hose, but Dr. Small gets the concepts across pretty clearly.

After watching the video, my pea-sized brain came up with what may be an oversimplified, imperfect analogy that may make Dr. Small cringe. (I’m happy to be corrected if this analogy is out to lunch!)

We know that prostate cancer needs testosterone to survive and grow, and the testes and adrenal glands both produce testosterone. So how do we cut off the supply of testosterone from those two sources to the cancer cells?

Imagine that the cancer is your backyard swimming pool (even a kiddie pool). Pools (cancer cells) need water (testosterone) to do what they do best. Your testes are one hose that fills the pool, and your adrenal glands are the second hose that fills the pool.

If we don’t want water (testosterone) in the pool (cancer), we shut off the spigots on the hoses to stop the flow. To turn off the spigot from the testes, we use one set of drugs (Lupron, Eligard, Zoladex, Firmagon, or Orgovyx). To turn off the spigot from the adrenal glands, we use a different drug, Abiraterone.

But there’s another way to stop the pool from getting water, and that’s to place a watertight cover over the top of it. That’s what the antiandrogen drugs do—they cover the pool and stop the water from getting in. These drugs are Flutamide, Nilutamide, Bicalutamide, Enzalutamide, Apalutamide, or Darolutamide.

ADT blocks the production of testosterone and antiandrogen drugs prevent the cancer cells from receiving the testosterone.

I’m sure more research is in my future, and I’ll be certain to share what I learn. In the meantime, don’t giggle too much at my analogy.