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Curiously, I asked my highly respected urologist surgeon last summer at the 5 year follow up of my prostate removal if I could take testosterone to increase my libido which was ok but not as good as younger days....( those were the days ). He looked startled and said that that would be like throwing gasoline on a fire. He said that currently I had no measureable PSA but there could be some microscopic cells floating around in my blood stream causing no trouble that could become activated by testosterone. Not sure if that is of any help to your question as it's perhaps not 100 % related.
After surgery, salvage radiation and 6 months of Lupron I have been wondering about taking something to boost my testosterone. My PSA is undetectable and my testosterone went from 400 three months ago down to 305. Still getting hot flashes, albeit mild, and waking every 2 hours. I can live with it, if it means no cancer but it sure would be nice to be back to normal.
If you want to be REALLY confused about Testosterone, go along to Ask Dr Myers .
Although the piece is about Xtandi and other options, Dr Myers does expand on the courrent theories about how and when Testosterone does and doesn't fuel prostate cancer growth. Here is an extract to whet your appetitite:
When drugs like Lupron and Casodex have failed, the cancer is not in fact hormone resistant. In fact, the cancer has adapted by becoming even more sensitive to testosterone. This cancer can change to grow at testosterone levels 1/100 to 1/1,000 of that found in a normal adult male.
Lupron and Casodex fail because they are not powerful enough.Prostate cancer accomplishes this by several different mechanisms. Prostate cancer cells can make their own testosterone, making them independent of outside sources. The cells can increase the amount of androgen receptor so that it traps enough testosterone to continue to grow, like using a larger sail in a light wind. The cancer cells can also change the androgen receptor so that it treats Casodex or Eulexin as if it were testosterone, so that drugs that are used to block testosterone now act as if they were testosterone! This is why some patients respond when Casodex is stopped.
Finally, the androgen receptor can be altered so that it is activated with little or no testosterone. The end result of all of this research is that we now know that it is quite uncommon for prostate cancer to become androgen independent. This led to a blossoming in research to find drugs able to restore hormone-responsiveness in men with advanced prostate cancer.
Good explanations Terry, just want to show examples (done by patients, real world and not theories) as to what could happen or show results. I have been on drug therapies covering 11 years now in my high risk case. Done various protocols and some with great results and others rendering zero results, since I have done some experimenting or outside the typical norm of what our experts claim as your only options (supposedly), realize how wild and crazy PCa therapies and results can be.
Shorter story I did ADT3 in 2002-2004 and starting failing control, switched to DES 1 mg (8 yrs. of great control and outperformed ADT3), for additional laughs ADT3 around $13,000 per year and lousy side effects too, DES 1mg for $130 per year (about no side effects). Within the last year the DES was failing me, so tried various protocols (some of my own ideas), in a rising psa scenario found that although I failed on DES and estradiol patches and failed on casodex and eulexin useages. When combining casodex+DES did get a lowered psa result within a hrpca scenario, however it didn't last but maybe up to 2 months. Then tried other concepts and no results, tried the expensive protocol of Leukine+Keto+estradiol patches and psa rose on me, so no results (usually this is a highly effective protocol 70-80% response in Hrpca patients).
This is interesting, I recently decided to try a new protocol in a rapidly rising psa scenario and it is showing signs of usefulness and lowered psa. My onco-doc did present a Journal article found at our local support group, that combining an anti-androgen+estrogenic drug can get a new response in even hrpca patients, even though you failed those drugs prior in mono therapies. I tried it last year and it worked for 1-2 months, well I just this last month or so tried it again with a faster rising scenario but also doubled the doseages and it lowered my psa, again. So, the receptor thing is very complex as to how and why does this work, when the mono therapy on the same drugs fail???
I mentioned Doug's protocol unique pioneering protocol, he has very early known hrpca scenario and psa was around 2.0+ and failed many drug therapies early on and switched to others to keep psa this low, this long. His protocol to lower T level and especially DHT level (in other words cut off all the fuel to PCa that you can) rendered him fabulous results. His psa within weeks went from 2.0+ to .007 (which is uncommon in hrpca scenarios, and a number of years of drug therapies). His protocol did nothing for my case, but in 3 out 5 trying it, it did work or show good psa lowerings. He used: Lupron (just to lower his T level)+Dexamethasone+estradiol patch. His T level was <2.5 and his measured DHT level was <5.0 (119-719 is normal ranges), thus the fuel cut off and new psa of .007 (Dexamethasone he believes has 2 unknown pathways to effect DHT levels, Prednisone does not and he tried switching those and proved the point as to rising psa level while on Prednisone....very interesting stuff).
Bob, Fascinating stuff. I came across the following on Joel Nowak's Malecare web site:
"Apr 19, 2013: Why Prostate Cancer that is Hormone Resistant Still Responds to Hormone Manipulation
I don’t understand why if I have hormone resistant advanced prostate cancer why the new drugs, Zytiga and Xtandi work. These drugs are still hormone therapies, is my prostate cancer hormone resistant? I recently received an email asking me this question and I thought it might be a question many people have, so I am going to answer this on the blog.
First, I want to be clear, yes Zytiga and Xtandi are both hormonal therapies that do work for many men when their cancer has been classified as hormone resistant.
The failure of Lupron etc. and Casodex does not mean that our cancer no longer is dependent upon testosterone. What it really means is that our cancer now has adapted itself and become more sensitive to lower levels of testosterone and is able to find alternative sources of testosterone. Simply put, the Lupron and Casodex are no longer powerful enough to do the job.
This change is the result of three different mechanisms. We have now found out that prostate cancer cells themselves are capable of making their own testosterone, making them independent of outside sources; the cancer cells often are able to modify their androgen receptor so that Casodex encourages the cancer growth by treating the drug as if it were testosterone. (This is why in many men stopping Casodex will initiate a positive response) and the androgen receptor becomes more sensitive so that it needs much lower levels of testosterone to continue growing.
To be accurate it is quite uncommon for prostate cancer to become androgen independent. This understanding of the progression of prostate has led us to the new forms of hormone therapy using Zytiga and Xtandi.
Zytiga (given along with prednisone) was the first FDA-approved drug to respond to this understanding. Zytiga ‘s mechanism of operation is simple, it is much more efficient at blocking testosterone production then Lupron. Its most important difference is that it blocks testosterone production throughout the body; including the adrenal glands and the cancer cell itself. Zytiga is more efficient at lowering the levels of testosterone production in the entire body (not just from the testis).
The other new hormone therapy drug is known as Xtandi and it has a different mechanism of action from Zytiga and the other hormone therapy drugs. Xtandi has been called a “Super Casodex” because like Casodex, it binds to the androgen receptor, however Xtandi is five fold better at competing with testosterone for the androgen receptor than is Casodex. Xtandi uses different pathways that are used by Lupron and Casodex and is able to work even while Lupron and Casodex have failed.
The bottom line is that it is a misnomer to call prostate cancer that has begun to progress in the face of Lupron (etc.) and Casodex hormone resistant. In fact prostate cancer at this stage is still dependent on the androgens, but the cancer has actually developed additional pathways around these first stage treatments so that it can continue to progress. Zytiga and Xtandi respond to these new pathways, but they too only respond for a limited time as this cancer is able to develop even more new pathways.
Joel T. Nowak, M.A., M.S.W"
I found this veryu thoughtful and think it deserves a wide audience.
Yeah Ed agree with your information and knew that and understand that awhile ago, it can make its own fuel at some juncture without T levels happening. Xtandi(MDV3100) is an invention found to bind to the AR receptor when others like casodex, eulexin and nilandron have failed to be useful, the other drug Dr. Sawyers co-invented is ARN-509 it is like MDV3100 but might bind even better is the idea.
Zytiga as far as my simplistic boiled down thinking is re-engineered Ketoconazole and should hopefully work better than Keto, however Keto is dirt cheap in comparison, so for budget or cash buyers a huge consideration. What I really like seeing is combo drugs and cheap stuff that actually works or render results, we seldom see endorsements for the cheap drugs (estrogenics, keto, even casodex and some others). Whatever works for a patient is the main goal (regardless of pricing-in theory anyway), we want results and don't care about the details.
If you get chance read about the HedgeHog pathway (it is for real on cancers) and they are finding drugs that can render successes right now, they have not tried that much on combo drugs just yet and there might be some big future promise in doing such protocols. There are various pathways to effect PCa and that is why types of drugs out there are so darn similar. They have found we have estrogen receptors and it is even wilder than the AR receptor, it appears there is an alpha, a beta and maybe 3 other junk pathways for estrogens to effect PCa or our biologies....they cannot figure out how all of them interact and work, thus far. Seen some Journal article on such not long ago. We are for the most part given the dart board approach or playbook approach to patients for HT related therapies, they are not usualy custom tailored, at this time, but that is likely coming some day.
current thought tends to hold that LOW testosterone is one of the possible causes of PCa. I am on TRT, and Active Surveillance.
the linkage of testosterone to PCa is old school, and based upon flawed research and samplings.
it's an exhaustive topic, and I just don't have time now to write it all. do your own research. Abraham Morgentaler, M.D. was the one who broke it open in the mid 2000s, by actually going back and looking a the early studies, that were taken as gospel for 5 decades or more.
he found serious statistical, and modeling errors in the old research and thought. it's a real eye opener!!
I'll close with this bit of logic: if PCa was caused by high testosterone levels, why are there no cases from young men? where are the cases seen? IN OLDER men. what's going on in older men? LOWERED testosterone levels.
You can believe what you like but please don't encourage the users of this forum to think that if they let their testosterone rip their PCa will go away. That would be dangerous advice.
Young men don't get PCa (usually) because the cell reproduction system goes awry with age. Things go wrong in our bodies as we age and PCa is just one of those things that result. Our testosterone does decrease with age but remains a source of strength to the cancer.
If I were not on treatment suppressing my testosterone (successfully) and hence my DHT also, after nearly six years with a Gleason 9 PSA 62 at the outset, I'd be six feet under.
I can certainly live with the insignificant testosterone in my body. Perhaps a young man could not but, knocking 70, I'm very glad to be beating the PCa odds .