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

Posted by denis76 @denis76, Mar 7 7:10am

Friends, I'm curious about your thoughts on the best strategy to keep testosterone levels low.

I'll share what I've read and the conclusions I've reached (they may be wrong), and I invite your opinions!

1. It's clear that testosterone is fuel. I've read that malignant cells produce testosterone themselves. Do you think this is true?

2. For a year, I had a problem – my testosterone wasn't dropping, and I was ready to have my balls amputated. It's worth noting that during this period (after chemotherapy, for about a year and a half, it was slowly increasing), I was very active (running, exercising). I decided to test one hypothesis (the more you move, the more testosterone is produced because it's used by the muscles). I abruptly stopped moving, which led to a sharp drop in my testosterone levels.

3. By lowering testosterone levels, we inhibit the pathways for testosterone synthesis, right? There are also a number of foods that inhibit testosterone synthesis, such as licorice root and green tea. They should be consumed regularly.

4. Testosterone has competitors in the body – other hormones. I've read that elevated cortisol lowers testosterone, and the same applies to prolactin.

This raises several questions.

a) Should we believe that physical activity is good? During exercise, muscles require glycogen (produced by the liver) and testosterone. Now, consider this: if cancer cells themselves produce testosterone, aren't we shooting ourselves in the foot? Training to the point of exhaustion, when we're exhausted, is a different matter.

b) Does excess weight or thinness affect testosterone production? Many of you have attended meetings attended by guys who have successfully battled this disease for years, and I wonder what they're like? Fat or thin, do a lot of exercise, or sit in a chair.

I just want to find a pattern! I feel like I'm wasting my time in a chair (I've gained 10 kg) and I need to get back into active exercise, but I'm afraid my testosterone will start to spike again.

Jeff, I wanted to hear you talk about being a monster who's been successfully fighting the black spider for 16 years! Amazing!

And the rest of you guys, I'm really curious what you think about this.

Thank you all! I wish you all success!

Interested in more discussions like this? Go to the Prostate Cancer Support Group.

Profile picture for northoftheborder @northoftheborder

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." 😕

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@northoftheborder

The whole difficulty lies in identifying cancer cells from healthy ones. If they could be destroyed, then perhaps the trigger and fuel issues wouldn't matter.

I think cancer behaves aggressively only under certain conditions. If these conditions were known, it would be a breakthrough. But, unfortunately, cancer behaves like normal cells, only with a broken self-destruction mechanism. Some people are lucky and the cancer "goes away"—that's what interests me more. Cause and effect. The difficulty is that there are so many factors, and it's much more difficult than solving second-order differential equations.

It turns out that our best strategy would be to determine how the dual combination will prevent resistance from developing. What should be done besides taking medications? If the answer to this question is related not only to testosterone but also to other factors, we need to dig deeper, interviewing survivors and applying pattern detection. In other words, what unites them. For example, comorbidities or a weak immune system will immediately lead to resistance. Diabetes is another example.

With AI, why can't we analyze the blood and other factors of survivors and statistically identify similarities? There are simulation models and powerful mathematical tools. Why, until now (and I could be wrong), have I never heard of data from survivors being analyzed and similarities being found? Is it really more profitable to sell drugs at huge prices instead of going this route?

I graduated from university with a degree in IT, and I still can't understand why medicine isn't following this path.

Some might argue that just because something works for one person doesn't mean it will work for another. But that's not the point. The discussion is about the combination of body characteristics and changes that lead to resistance never developing with ADT and lutamides!

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Profile picture for brianjarvis @brianjarvis

@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,

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@brianjarvis

\\prostate cancers absorb amino acids

I don't think it matters. You can't stop eating. Even if you do, cancer will start eating away at your body. Much has been written about fasting.

I agree that we need to be cautious with hypotheses, but what else can we do?

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Profile picture for stage4lovolmetpc @stage4lovolmetpc

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.

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@stage4lovolmetpc

Let me repeat: I watched my testosterone rise over the course of a year. I had tests done every three months. My doctor was at a loss. I had already changed my ADT medication. But as soon as I reduced my physical activity, my testosterone began to decline. I did this intuitively, reading numerous scientific papers on how testosterone is used after it's produced in the body. I may be wrong, but after reading a ton of scientific literature, I concluded that testosterone production also declines with decreased physical activity.

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Profile picture for denis76 @denis76

@stage4lovolmetpc

Let me repeat: I watched my testosterone rise over the course of a year. I had tests done every three months. My doctor was at a loss. I had already changed my ADT medication. But as soon as I reduced my physical activity, my testosterone began to decline. I did this intuitively, reading numerous scientific papers on how testosterone is used after it's produced in the body. I may be wrong, but after reading a ton of scientific literature, I concluded that testosterone production also declines with decreased physical activity.

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@denis76 That makes sense, I didnt see in the body of your post that you were on ADT that was apparently was not working, just that your T was rising. So how much did it go down to when you quit exercising? And what did it rise to before you started? Im hoping mine will be zero in a few weeks...Im exercising all day long and eating light, I def dont want to gain 20 lbs...Orgovyx and Abi for me. And yes, I also believe exercise will increase T.

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Profile picture for stage4lovolmetpc @stage4lovolmetpc

@denis76 That makes sense, I didnt see in the body of your post that you were on ADT that was apparently was not working, just that your T was rising. So how much did it go down to when you quit exercising? And what did it rise to before you started? Im hoping mine will be zero in a few weeks...Im exercising all day long and eating light, I def dont want to gain 20 lbs...Orgovyx and Abi for me. And yes, I also believe exercise will increase T.

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@stage4lovolmetpc

mmm.

After Docitaxel, my doctor prescribed ADT—an injection every three months (Zolodex 10.8). After seven months, my testosterone levels began to rise, and I was prescribed a different drug and a more aggressive method—one every 28 days. My testosterone levels slowly plateaued, and it was at that point that I intuitively decided to reduce my physical activity, which led to a sharp drop in my testosterone levels by 1.5 times.

My doctor said the new ADT is cumulative. Furthermore, I should note that my PSA level, after chemotherapy and on my previous ADT, had plateaued at 6.2 and didn't drop until Erleada and the switch to the other ADT. Plus, almost in despair, I began reducing my physical activity and drinking green tea and licorice root in huge quantities. And finnally I lowered my cholesterol levels several times and my lipids (they returned to normal) by starting to take statins. In a panic, I did something else, I don’t remember what.

A month ago, I had my biochemistry tests done, and my doctor said the results were excellent (knock on wood).

Of course, I admit that the decrease in testosterone isn't related to physical activity and is a result of the more aggressive ADT, but testosterone levels fluctuate throughout the day. They peak early in the morning and begin to decline throughout the evening. My last testosterone test was at 9 a.m., and each time, I took it at the same lab.

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Profile picture for denis76 @denis76

@stage4lovolmetpc

mmm.

After Docitaxel, my doctor prescribed ADT—an injection every three months (Zolodex 10.8). After seven months, my testosterone levels began to rise, and I was prescribed a different drug and a more aggressive method—one every 28 days. My testosterone levels slowly plateaued, and it was at that point that I intuitively decided to reduce my physical activity, which led to a sharp drop in my testosterone levels by 1.5 times.

My doctor said the new ADT is cumulative. Furthermore, I should note that my PSA level, after chemotherapy and on my previous ADT, had plateaued at 6.2 and didn't drop until Erleada and the switch to the other ADT. Plus, almost in despair, I began reducing my physical activity and drinking green tea and licorice root in huge quantities. And finnally I lowered my cholesterol levels several times and my lipids (they returned to normal) by starting to take statins. In a panic, I did something else, I don’t remember what.

A month ago, I had my biochemistry tests done, and my doctor said the results were excellent (knock on wood).

Of course, I admit that the decrease in testosterone isn't related to physical activity and is a result of the more aggressive ADT, but testosterone levels fluctuate throughout the day. They peak early in the morning and begin to decline throughout the evening. My last testosterone test was at 9 a.m., and each time, I took it at the same lab.

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@denis76 Yes, the T decline is due to ADT and not due to not exercising. I asked my Dr about licorice and other T lowering natural methods. No, he said, you have to go on the ADT. It took me a couple months but here I am, trying to learn as much as I can. Im wondering what your plateau number was....if you decreased it by 1.5 what did it go to? Thanks for talking!

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Profile picture for northoftheborder @northoftheborder

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." 😕

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@northoftheborder "Testosterone isn't fuel; it's a trigger."

Agreed. Using the wrong (layman) term to describe something as complex as hormonal interactions ends up deceiving people into the wrong conclusions.

Just like saying that if you stop eating, "cancer eats at your body."

To me, the purpose of this forum is to discuss facts, treatments, & reactions, not to speculate on science.

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Profile picture for stage4lovolmetpc @stage4lovolmetpc

@denis76 Yes, the T decline is due to ADT and not due to not exercising. I asked my Dr about licorice and other T lowering natural methods. No, he said, you have to go on the ADT. It took me a couple months but here I am, trying to learn as much as I can. Im wondering what your plateau number was....if you decreased it by 1.5 what did it go to? Thanks for talking!

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@stage4lovolmetpc

testosterone was 1.61 and drop to 1.0

on 1.7 eggs away (

After almost a year (chemotherapy and ADT), my PSA level hadn't dropped to 0 and remained at 6.2. It didn't drop any further. ADT wasn't working. The primary tumor, according to a PET/CT scan (SUVMAX), had only shrunk by 10%. Doctors didn't want to prescribe Erleada, but I growled like a bear and got it. Slowly, very slowly (over the course of another year), my PSA dropped to almost 0. Initially, my PSA was 530. Some doctors told me it was time to look for a grave, but I didn't give up and moved like a tank.

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Profile picture for denis76 @denis76

@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?

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@denis76 Exercise increases testosterone but ADT/lutamides keep it low enough to affect PCa cells.
I understand your conundrum but there’s no way sitting on your butt is going to be beneficial.
FYI, a friend with leukemia opted for no conventional treatment after speaking with various oncologists. He took Green Tea Extract in pill form and really brought all his blood cell levels to within normal range; his docs were very impressed!
But he got prostate cancer anyway and had to have surgery…I guess one size does not fit all?
Phil

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....high blood pressure can be called primary or secondary (with a cause) One of the secondary causes is a chemical found in licorice (5-HIAA). I would avoid it.

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