Almost a year ago I had radiation and started Lupron, Prednesone, and Abiraterone which immediately brought my PSA and T levels to undetectable.
I also enrolled in a clinical trial of an experimental immunotherapy drug SD-101 along with infusions of Keytruda (pembrolizumab). I became extremely depressed, suicidal, lost all sex drive, sleeping 18 hours a day and sometimes entire days. After 8 months of this I learned that Merck cancelled clinical trials of Keytruda for treating PCa after initial results showed it ineffective. So I confronted my oncologist and asked why we were continuing with therapy shown ineffective and making me miserable? She said the study protocol demanded it for 10 more months. Why 10? Just a number they made up she said.
I told her we were done, withdrew from the trial, and stopped all medications. My new doctor didn't want to speak ill of his colleague but pretty much said I made the right call. (And I later learned I was in the placebo group and never got the SD-101.)
Now a year later my PSA is still undetectable and T rose to 9 (normal range 251-1068). I'm feeling better but still depressed and I want my sex drive back.
So the plan now is to retest in Sept and if PSA is still undetectable then restart testosterone injections. I want my T levels on the high side of normal since the saturation models predict that low T fuels PCa and higher levels inhibit it.
I'm wondering about adding Arimidex and/or Finasteride to suppress E2 and DHT since there are some theories that they, not testosterone, are what fuels PCa.
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The E2 and DHT ideas are just theories in need of further research:
What is the medical evidence for and against The Estradiol-Dihydrotestosterone model of prostate cancer?
The Estradiol-Dihydrotestosterone (E2-DHT) model proposes that an imbalance in the levels of estradiol and dihydrotestosterone in the prostate can contribute to the development and progression of prostate cancer. However, the evidence for and against this model is mixed and controversial.
For the E2-DHT model:
• A number of studies have found that men with prostate cancer have higher levels of estrogen (which is converted from testosterone) and lower levels of androgens such as DHT, compared to men without prostate cancer (1,2). This suggests that an imbalance between estrogen and androgens may be involved in the development of prostate cancer.
• Experimental studies in animals have also shown that estrogens can promote the growth of prostate cancer cells, while androgens can inhibit their growth (3).
• Some clinical studies have suggested that drugs that block the conversion of testosterone to DHT (such as finasteride or dutasteride) may reduce the risk of prostate cancer, especially in men with high levels of DHT (4,5).
Against the E2-DHT model:
• Other studies have failed to find a consistent association between estrogen or androgen levels and prostate cancer risk or aggressiveness (6,7). Some studies have even found that higher levels of androgens may be protective against prostate cancer (8).
• Clinical trials of drugs that block the conversion of testosterone to DHT have shown mixed results, with some studies showing a reduction in prostate cancer risk, while others have shown no effect or even an increased risk of high-grade prostate cancer (9,10).
• Some studies have suggested that other factors, such as inflammation or genetics, may play a more important role in the development and progression of prostate cancer than the E2-DHT model (11).
In summary, while there is some evidence to support the E2-DHT model, the overall picture is mixed and the model is not widely accepted as a definitive explanation of prostate cancer development and progression. More research is needed to better understand the complex interactions between hormones, inflammation, genetics, and other factors in prostate cancer.
References:
1 Furuya Y, Akakura K, Ito H. Estradiol upregulates and DHT downregulates the expression of estrogen receptors a and ß in the human prostate cancer cell line LNCaP. Prostate. 2002;51(2):98-103. doi: 10.1002/pros.10091
2 Ho SM, Tang WY, Belmonte de Frausto J, Prins GS. Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4. Cancer Res. 2006;66(11):5624-32. doi: 10.1158/0008-5472.CAN-06-0516
3 Litvinov IV, Antony L, Dalrymple SL, Becker R, Cheng L, Isaacs JT. PC-3 prostate carcinoma cells produce and secrete estradiol-17beta and express estrogen receptor alpha. J Urol. 2003;170(2 Pt 1):548-55. doi: 10.1097/01.ju.0000076589.10744.99
4 Thompson IM, Goodman PJ, Tangen CM, et al. The influence of finasteride on the development of prostate cancer. N Engl J Med. 2003;349(3):215-24. doi: 10.1056/NEJMoa030660
5 Andriole GL, Bostwick DG, Brawley OW, et al. Effect of dutasteride on the risk of prostate cancer. N Engl J Med. 2010;362(13):1192-202. doi: 10.1056/NEJMoa0908127
6 Hsing AW, Stanczyk FZ, Bélanger A, et al. Reproducibility of serum sex steroid assays in men by RIA and mass spectrometry. Cancer Epidemiol Biomarkers Prev. 2007;16(5):1004-8. doi: 10.1158/1055-9965.EPI-06-0935
7 Ewing SK, Schmitz KH, Kurzer MS, et al. Serum sex hormones in men: associations with physical activity, aging, and obesity. Ann Epidemiol. 2010;20(4):317-25. doi: 10.1016/j.annepidem.2010.01.007
8 Platz EA, Leitzmann MF, Rifai N, Kantoff PW, Chen YC, Stampfer MJ. Sex steroid hormones and the androgen receptor gene CAG repeat and subsequent risk of prostate cancer in the prostate-specific antigen era. Cancer Epidemiol Biomarkers Prev. 2005;14(5):1262-9. doi: 10.1158/1055-9965.EPI-04-0738
9 Redman MW, Tangen CM, Goodman PJ, et al. Finasteride does not increase the risk of high-grade prostate cancer: a bias-adjusted modeling approach. Cancer Prev Res (Phila). 2008;1(3):174-81. doi: 10.1158/1940-6207.CAPR-08-0040
10 Thompson IM, Goodman PJ, Tangen CM, et al. Long-term survival of participants in the prostate cancer prevention trial. N Engl J Med. 2013;369(7):603-10. doi: 10.1056/NE
My RO explicitly not allowing me to add to the firmagon injection anything like Abiraterone because he wants to see how my PSA drops after the irradiation of my prostate with 38Gy in 5 fractions.
He said that the PSA will go down for 18 months after the sbrt or my prostate.
Believe me if you would not have Abiraterone you would also go down to the nadir PSA much longer. You should clarify this with your doctors.
I read your bio and am confused. It appears that you wrote that you were diagnosed as distant metastasis, thus RT could not provide a cure, and SOC would be ADT,etc.
You also say you accepted Firmagon, etc.....so at what time did your Docs decide to do RT...without ADT???
I have a terminal condition. RT is done to avoid local spread of the CRPC from my Prostate to rectum etc saving me from complications. It is not necessary to extend my life. I don't have any visible mets now.
Is Preventive RT now considered SOC......I see definite positives, as you mention...but also the potential for downsides? Congrats on the clean scans!! CRPC or not, I guess we all have a terminal condition or conditions.
I will tell you honestly. I irradiated my Prostate because I believed that it is a right thing to do considering that at PSA 1.25 the PSMA PET scan didn't find any visible mets and that my Prostate was 95% full of cancer SUV Max 14 on the PSMA PET scan. I had to choose between chemotherapy or radiation.
The cancer in the prostate usually stops responding to global treatments at some point in time.
With the RT of my CRPC Prostate we are saving more advanced treatments for the future. I believe it is more comfortable on Degarelix than on Abiraterone. We will see. At the moment I still reasonably fine, actually I feel excellent for a terminal illness with distant mets. Without mets with possibility of a cure I would be definitely on Abiraterone.
I have locally advanced prostate cancer finished treatment in 2016 and my testosterone has not recovered psa 0.03,but now I have been diagnosed with osteoporosis and I can't put any weight on I am only 8st a walking skeleton I have also just had a zoledronic acid infusion to strengthen my bones, I have just started to take creatine monohydrate to see if it will help me put any weight on,any help please.
I feel sorry for you and I am always thinking about you. Can you contact someone competent in Prostate cancer treatment? Ask for a referral to see a medical oncologist to discuss with him your options.
I wish I could help somehow, I suggest you start separate post and ask for help and hopefully some members here can provide you with appropriate suggestions.
I strongly suspect that most of the du jour wonder drugs that oncologists and urologists recommend - parroting the medical establishment's official wisdom - are minimally effective and maximally damaging. The evidence that these so-called wonder drugs do much besides enrich Big Pharma is scant (I came to this conclusion after maybe a hundred hours of research - it wasn't made lightly). I have a circle of male friiends and relatives that were diagnosed with PC about the same time I was (I was Gleason 9, they were Gleason 8s). They all took all the drugs and radiation their oncologists/urologists recommended - and endured years of pain, sickness, depression before the cancer metastasized and killed all of them. That was five years ago. I felt and continue to feel fine - jogging, weight-lifting, working around the house (did a new roof a couple years back). Doesn't prove anything, I know, but then who bears the burden of proof? They went through hell and thousands of dollars for what, exactly?
Thank you Claw. I know that we in very similar circumstances don't have the "evidence" to prove anything. But after 6 years of not having those "recommended" treatments while watching my closest friends suffer gives me a sense of peace. Yes, my QOL sucks but I still go out every morning to feed the ducks and chickens. I still give my wife a hug and kiss in the morning. Maybe our desire for living physically gets in the way of looking higher for life.
I also fired my oncologist (but for a different reason). I had undetectable PSA for 17 months. I talked to a Urologist who prescribed testosterone for me (self injection). My PSA has only increased by 0.03 in one year. FEEL BETTER SOON!!!
Good for you! Yes if your testosterone does not recover go for testosterone replacement. Arimidex is not necessarily unless you get gynecomastia. Estrogen is not the enemy for most of us. Neither is finasteride or dutasteride helpful unless using AR blockers without ADT. These also interfere with the benefit of BAT programs that work through DHT. That is not you at this time. Paul
First I do not like it when someone on this post uses the word Fire, that shows a lack of respect and ignorance on your part!!! Our docs are not gods, but each one does their best!!!
You need to get better informed of everything involved in our care before spouting off!!
I have a very good MO. Early on I talked about getting a 2nd opinion and/or someone else. She said, that is OK with me, its your body. Also it went almost without saying that she is very busy with a dance card booked out 2-3-4 months and anyone who thinks the grass is greener elsewhere is free to step in whatever lurks in green grass. Be careful of "firing" someone, as replacing them will entail lengthy times etc in getting a new accepting-patients provider. Its a form of bridge-burning.
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A new chapter
Why is Testosterone Increasing?
Low testosterone / PSA failure / risk of death.
Keytruda-viable option?
