The Paradox of Testosterone and Prostate Cancer

[Wilson6]

Very interesting read. I've always thought the worst place to be T wise is low to low normal (200 - 450 ng/dl) relative to the development of PCa and high Gleason score cancers.

Study Solves Testosterone’s Paradoxical Effects in Prostate Cancer

DURHAM, N.C. – A treatment paradox has recently come to light in prostate cancer: Blocking testosterone production halts tumor growth in early disease, while elevating the hormone can delay disease progression in patients whose disease has advanced.The inability to understand how different...

corporate.dukehealth.org

 

[rawdeal]

Interesting indeed. By the end of that they seem to think they may have identified a solution via a monthly high-dose injection of testosterone. To my semi-educated self that suggests Test U a helluva lot more than Prop, but their choice was not identified.

They go on to say they "have already developed new drugs . . . . " What could those be? If not Test U, would it be a new Sust-like blend designed for even more of a time-release effect?

And ... will any of us prostate owners live long enough to see this readily available to doctors and drug stores, or will we be able to approximate diy therapy using what is already available IF we ever get that diagnosis.

 

[Wilson6]

This aligns with the recent Danish longitudinal study comparing AAS vs non-AAS users and cancer dx over time. The incidence of overall cancer was the same, but there were no prostate cancers reported in the AAS users, whereas there were in the non-AAS group. IMO, keep your T in the upper end or low supraphysiologic range for life. Every guy if they live long enough will have PCa, perhaps microscopic but if you look for it on autopsy, you'll find it. The key is to limit proliferation and push the differentiation and that takes T and to keep a lid on it throughout life, not try to stop it once it begins to proliferate uncontrollably. If one looks at this from a global perspective, why is PCa a disease of aging that parallels the decline in T?

 

[myosin]

More evidence is that estrogen is the cause:.. more T, more E Conversion, keep it in check and admittedly speculation, maybe keep E on the lower end of Normal as we get older

 

[Wilson6]

More evidence is that estrogen is the cause:.. more T, more E Conversion, keep it in check and admittedly speculation, maybe keep E on the lower end of Normal as we get older

Then one would think that MTF trans would have a greater risk of PCa esp among older subjects than cis-men, but they are at least a 2x decr risk. However, their PSA at time of dx is pretty high (suggesting higher Gleason scores) so it might be that in the absence of T, proliferation is accelerated when PCa is present, but in the absence of PCa the low T environment is not favorable for the development of PCa, but when it develops look out below.

 

[Glycomann]

The answer to prostate cancer is a strong immune system, a clean lifestyle... and no more than 3 women at a time.

 

[myosin]

Then one would think that MTF trans would have a greater risk of PCa esp among older subjects than cis-men, but they are at least a 2x decr risk. However, their PSA at time of dx is pretty high (suggesting higher Gleason scores) so it might be that in the absence of T, proliferation is accelerated when PCa is present, but in the absence of PCa the low T environment is not favorable for the development of PCa, but when it develops look out below.

That’s really interesting actually, never looked at MTF data in that regard… honestly never crossed my mind , but a good aspect to look into more… As a last ditch effort they actually castrated bill bixby

The Role of Estrogens in Prostate Carcinogenesis: A Rationale for Chemoprevention

Estrogens as hormonal therapy, particularly diethylstilbestrol, are effective against androgen-dependent prostate cancer, but paradoxically estrogens might also be involved in the causation of this malignancy. Therefore, antiestrogens have been suggested ...

www.ncbi.nlm.nih.gov

• Observations from several studies led to the hypothesis that increased circulating estrogens might elevate prostate cancer risk and act through the estrogen receptor; this idea is strongly supported by the finding that estrogens enhance androgen-induced prostate cancer in an animal model.
• https://www.jci.org/articles/view/170809

 

[Wilson6]

The answer to prostate cancer is a strong immune system, a clean lifestyle... and no more than 3 women at a time.

At my age just trying to handle one at a time is enough.

 

[Wilson6]

That’s really interesting actually, never looked at MTF data in that regard… honestly never crossed my mind , but a good aspect to look into more… As a last ditch effort they actually castrated bill bixby

The Role of Estrogens in Prostate Carcinogenesis: A Rationale for Chemoprevention

Estrogens as hormonal therapy, particularly diethylstilbestrol, are effective against androgen-dependent prostate cancer, but paradoxically estrogens might also be involved in the causation of this malignancy. Therefore, antiestrogens have been suggested ...

www.ncbi.nlm.nih.gov

• Observations from several studies led to the hypothesis that increased circulating estrogens might elevate prostate cancer risk and act through the estrogen receptor; this idea is strongly supported by the finding that estrogens enhance androgen-induced prostate cancer in an animal model.
• https://www.jci.org/articles/view/170809

Will give these a read later today. The other thing that came to mind yesterday were the studies on 5ARIs showing a decreased risk of PCa but the degree of malignancy was increased. Same thing you see in MTF, less PCa but higher Gleason Scores. Why, both decrease intraprostatic androgen levels shifting the balance away from differentiation and toward proliferation, so when PCa is induced there are no brakes on the proliferation and differentiation is suppressed so it blows up. Thus only the guys that actually get to the point where it is induced are in trouble with low androgens. IMO, we have to be careful with suppressing E2 too much bc of all the other benefits, and the key is keeping the E2 to T and DHT ratio in check. Letting E2 rise in a decreasing T and DHT environment (older guys) is just asking for trouble. High T and high E2 is fine, low T and high E2 is not.

 

[DocOxRedox]

My doc

More evidence is that estrogen is the cause:.. more T, more E Conversion, keep it in check and admittedly speculation, maybe keep E on the lower end of Normal as we get older

I found a research study that covered this as a side note, but were focusing on other causes. I told my doc about my findings and he confirmed that high levels of E are direct contributors to prostate cancer.

 

[Glycomann]

I think it is interesting that PC emerges later in life when immune function is dropping as are cell cycle check points. Hormone levels shift and dominant ones might be more estrogenic. But, AAS users, whose hormones are all over the place and typically younger, don't seem to have a massive spike in PC compared to general population. I would guess that the major driver is a drop in immune function such as that of natural killer T-cells and others, along with their cytokines, that surveil the body for early cancer cells.

 

[Glycomann]

duplicate post