My husband will soon be starting Formula 509 and will begin ADT and Salvage Radiation. Only recently has he gotten his first baseline Testosterone counts. Depending upon what chart you look at he is either lower or low normal at 189.
I find this to be curious in that I’ve often heard that Testosterone feeds Pca. Why would his PSA rise if his numbers are low?
At last check he was at .42 so he is barely recurrent but I truly expected his Testosterone numbers to be higher than they were.
Does this low T signal any other concerns?
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JosephineS
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His PSA will go down when his testosterone is less than 50 (ideally less than 20). People with progressing PC may have low testosterone values. Low testosterone is a factor associate with PC.
I had a testosterone of 120 to 180 when my cancer was progressing. My PSA when from 10 to 0.8 in less than 2 months when the testosterone was below 20.
One interpretation of the facts that Tall_Allen and tango65 cited is that there is a certain amount of testosterone that will stimulate all the cell division (cancer growth in this case) that is going to occur. Adding more T doesn't do any more and may actually tend to retard cancer growth - which is one reason why some researchers are experimenting with testosterone supplementation, or alternating deprivation and supplementation.
You have "often heard that Testosterone feeds Pca".
It's a common misconception, since castration is a treatment (althoigh never a cure).
Your husband & most in this group probably had dangerous levels of T in our 20's (LOL), yet none of us had PCa back then. It is usually the case that we lose 1-2% T every year, starting in our early 30's, & we are diagnosed when our T has perhaps been cut in half.
Anyway, there are now plenty of studies that suggest that normal-high T is protective.
I think that many have a simplistic view of T binding to the androgen receptor [AR] & automatically initiating cell division (proliferation). In fact, there are many cofactors involved. I have my own simplistic view that estradiol [E2] becomes the prime force behind proliferation, & that low T is merely permissive. When T is normal-high, it has a regulatory role. Estrogen-dominance is to be avoided, but doctors are not interested in E2 levels in men.
For men not on ADT, E2 should be in the 20-30 pg/mL range. Arimidex can be used to lower E2 levels. For T <350 ng/dL, I think that supplementation should be used. Personally, I would shoot for T>650 ng/dL.
I too have considerable reservations about the current theoretical basis for CaP (Ca Prostate) treatment and use of castration levels of T. As many readers will know this is also associated with emergence of therapy resistant neuroendocrine tumours in late stage CaP.
A very interesting study in Nature comms Sep 2024; “Androgen receptor monomers and diners regulate opposing biological processes in prostate cancer cells”, showed high T inhibits replication and promotes PSA synthesis while at lower levels T promotes cell proliferation. The mechanism relates to conversion of the monomeric androgen receptor being converted to dimeric and oligomeric forms at higher T levels which inhibit proliferation pathways at the nuclear level. This was in vitro work but it does partly reflect the beneficial effect of high dose T (BAT - Bipolar androgen therapy) in both castration sensitive and resistant CaP.
There is also a large international collaborative prospective analysis from Oxford looking at relation of T and IGF-1 levels as risk predictors of CaP. There is a clear dose relation between IGF- 1 level and development of CaP. For T , above a low threshold level there is increased risk but no dose relationship (which is consistent with a receptor saturation model).
Int J Epidemiology 2023,71-86,
These studies point to our current model of T driving CaP being too simplistic.
All thank you so much for your replies. I think you echoed what I had thought too. I’m glad he is finally starting treatment. I think we are still early in the disease progression to hope for a cure.
I’ve read that there could be a temporary ‘flare at the onset of hormone therapy. With low T do you think this is even likely?
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