Testosterone as fuel, let's think about it together ...

I'm an extremely active 68 year old and I've always had a problem with low testosterone.

@ginger38314

As I understand it, the older you get, the lower your testosterone production. The question is, does physical activity increase or decrease testosterone levels for those taking ADT and lutamide?

@denis76 Age 70 here and as active as I can be. Take care of a multi-acre homestead w/ associated livestock. Certainly not going to run a marathon but I walk an inclined tread mill 2-3 miles a day and do resistance band training 5 days per week. My last testosterone level was 9 ng/dl on 12/3/25. Prior to ADT, T measured at 450. That said, my short answer to your question is NO, exercise does not increase T levels for those taking ADT and/or ARSI (Orgovyx/Nubeqa in my case.)

1. When prostate cancer cells have been deprived of testosterone for a long time, they can adapt by producing necessary precursors like cholesterol, or by converting adrenal androgens into testosterone,

2. Having your balls amputated (an orchiectomy) has similar side-effects as being on androgen deprivation therapy (except for an orchiectomy being permanent).

Yes, exercise does cause a very slight increase in testosterone, but it’s not long-lasting (otherwise, bodybuilders wouldn’t have to regularly use testosterone or other performance-enhancing drugs).

3. Yes, there are a number of foods that inhibit testosterone synthesis. But, you’d have to ingest a lot of these to have the same effect as hormone therapy.

Also, note that there are two types of hormone therapy:
> androgen deprivation therapy (ADT), like Eligard, Lupron, etc, that result in the suppression of testosterone production, and
> androgen receptor pathway inhibitors (ARPI), like Zytiga (abiraterone), Xtandi (enzalutimide), etc., which inhibit the pathways for testosterone synthesis,

4a. Many assumptions being made. Requires much in-depth discussion.

4b. Yes, both excess weight and extreme thinness significantly affect testosterone production. Obesity lowers testosterone by increasing the conversion to estrogen via aromatase. Being severely underweight or experiencing rapid weight loss can also lower testosterone due to insufficient nutritional intake.

Again, exercise may cause s very brief, small increase in testosterone, but nothing to lose any sleep over. Remember that if it’s heart-healthy, it’s usually also prostate-healthy.

(I started getting PSA tests in 2000, was diagnosed with PCa in 2012, active surveillance for 9 years, and then treated with proton radiation + ADT in 2021; most recent PSA was 0.314. I lift weights 2-3 times/week and swim laps for a mile 2-3 times/week. Never have a second thought about too much exercise.)

@brianjarvis

Thanks, Brian for you sharing your knowledge and experience.

I'm interested in a group of patients (I've heard of them living with a black spider for 20-30 years) and why some don't have tumor growth (metastases), while others with the exact same diagnosis don't. Clearly, this depends on a number of factors (age, mutations, whether treatment works or doesn't, individual characteristics), but I'm specifically interested in testosterone.

Let's try to think logically.

Let's divide people into two groups: the first group are survivors, the second are non-survivors. The first and second groups share one common feature: testosterone is their fuel.

It follows, then, that testosterone isn't the only factor, but rather enters into complex relationships with other factors, yet it remains the dominant factor.

We understand that if we restrict the black spider's testosterone supply and its ability to metabolize it in both ways, resistance will develop, and the higher the Gleason score, the faster it does. But this begs the question: why does one group survive after resistance develops, while the other dies? The obvious conclusion is that testosterone acts as a precursor, and then biological mechanisms change so that something else becomes the cancer fuel instead of testosterone. What fuels cancer after resistance develops?

And what's better: maximally suppressing testosterone or, conversely, maintaining slightly elevated levels while periodically lowering them to prevent resistance from developing? In other words, feeding the black spider occasionally to prolong the period before resistance develops. I think that's what people who live 20-30 years with cancer do, right?

In other words, my hypothesis is that we need to vary the periods of physical activity. For example, sit for three months and not move a thing, and then move actively for three months, lifting weights, etc. Not moving for a long time is bad, but constantly moving is also bad. We need to constantly challenge the body to change the "rules of the game" for the black spider. I understand that this may seem naive, but biological processes must change in a way that radically impacts the pathology. Then, I could be wrong, the pathology will be constantly on the move and won't be able to adapt and accelerate for growth.

In other words, we're acting in much the same way as cancer itself. It adapts, and we adapt to it.

If the drug you were taking is not lowering your testosterone, then you need to switch to a different drug. One of the other people in this forum had a problem with Leuprolide Not dropping his testosterone down. Switched to Firmagon, Which works like Orgovyx And his testosterone came down. One is an agonist, and the other is an antagonist. They work a little differently and can drop the testosterone for a person that has a problem with one type, but not the other.

Another person had to switch just the other way in order to get the testosterone down.

You could also try estradiol patches, A third technique that will drop the testosterone just as low as ADT.

Testosterone isn't fuel; it's a trigger. It binds to a receptor in the prostate cancer cells, and that tells them "OK, it's time to start reproducing."

As others have mentioned, eventually prostate-cancer cells may become "castrate-resistant," evolving an ability to turn themselves "on" into reproduction mode by generating a bit of their own testosterone. That used to happen in 18–24 months on just ADT; now they know that for metastatic prostate cancer, if you combine ADT with an ARSI (like Abiraterone or one of the -lutamides) right from the start — what's called "doublet therapy" — it postpones castrate-resistance significantly, and sometimes indefinitely. ADT works by blocking testosterone production at source, while ARSIs work by blocking it at destination (the receptors in the cancer cells), so it's a one-two punch.

If you don't go on ADT or ARSIs, you won't develop castrate resistance, but the cancer will keep spreading anyway, which is what you're trying to prevent. If the cancer spreads further into bones and vital organs, it won't be much comfort thinking "at least I didn't develop castrate resistance." 😕

@denis76 I would first preface by saying that what might appear to be logical, might not be scientific. Any hypotheses not vetted (& controlled), might introduce unintended variables or confounders that make the results unpredictable. As a retired computer scientist, I’m cautious about defining scenarios that appear to be comparable (or at least similar), but may or may not be.

What we do know is that while testosterone may be the dominant factor early and through the prostate cancer diagnosis, there is evidence that it may not be such a primary factor later in the diagnosis (i.e., the non-survivors), when just like other cancers (brain, lung, lymphoma, etc.), glutamine (& possibly other factors) fuels cancer growth, metastasis, and disease progression.
—> that would be a partial answer to your question of “What fuels cancer after resistance develops?”
—> it’s also known that prostate cancers absorb amino acids at a much more rapid pace than do normal prostate cells. That is another possible fuel source.

This is a very complex mechanism and I would hesitate to synthesize it down to a (seemingly) simple scenario,

@jeffmarc

Ye Jeff, thanks for your advice. Now my testosterone is down on 1.5 times. I hope that Erleada+ ADT is working!

Hmmm...I dont see where you mentioned if you were on ADT right now....if yes, then sitting around in a chair, gaining 10 kilos, might not be the best thing to do. If you are on ADT I dont think you can exercise enough to raise your T. If you are not on ADT....well, sitting around in a chair for 3 months, gaining 22 lbs might not be the best thing to do. Laughing at my own BS....Im awful! Seriously, do what you think is best for you, you have all the information you need on this forum. I read here all the time.