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Advanced Prostate Cancer
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Prostate Cancer and using Androgel to Re-activate Testosterone Levels

I've always heard that testosterone is not good if you have prostate cancer. But I've been reading on occasion that once prostate cancer is in remission testosterone can be used to gain back strength etc.

I'd be afraid to use testosterone even if my cancer is in remission because the prostate cancer might come back again.

Does anyone have any thoughts or experience with this?

Thanks very much,


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I have the same concern. There have been discussions here about 'BAT' therapy where the treatment alternates between androgen deprivation therapy (ADT) and testosterone supplementation to elevate testosterone levels. Supposedly confuses the cancer and prevents progression. Don't know if I, or more importantly my doctor/oncologist, would have the courage to pursue this.

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Been on Xtandi for 3-1/2 years with undetectable PSA. My T has risen to about 225. Docs will not consider ADT "holiday" or anything else for that matter as Xtandi seems to working so well in my case.


Many experts believe that testosterone replacement therapy (TRT) can lead to recurrence if you have PCa that is currently in remission. But not everyone—Morgentaler, for example, as discussed in this abstract, thinks this is a myth: ncbi.nlm.nih.gov/pubmed/168... See also Patrick’s thread from 2-3 weeks ago labeled "Testosterone Therapy & PCa Risk".

I asked Mark Scholz about TRT for me a few months ago and he was supportive, saying that if the cancer comes back we can always resume ADT. So I decided to try TRT, despite the risk.

My history:

PSA 8.6 in 2009; RALRP (positive margins/Gleason 9/PNI/SV involvement); PSA 1.08 two months post-surgery, followed by ADT + EBRT to prostate bed + pelvic nodes (all in 2009); PSA remained undetectable for two years, then biochemical recurrence (w/ 4-month PSADT). Began Leukine March 2014 which dropped PSA from 0.4 to 0.2 and sustained it there for 1.5 yrs when I began 10 months on Firmagon + Xtandi (Nov 2015). That dropped my PSA from 0.2 to undetectable where it remains today. After stopping ADT/Xtandi Sep 2016, T rose to 206 by Apr 2017, then fell steadily to 134 as of Aug 2017. Serum LH and FSH were high in this period, indicating primary testicular failure. Began TRT 9/6/17 using testosterone cypionate (injection, so different from Androgel skin patch) and T rose within 2 wks to 1079 (above my target of 600). PSA remains undetectable as of 11/20 at < .006. I am continuing with Leukine, 500 mcg qd, alternating two wks on then two wks off. Also working to limit DHT rise associated with TRT by using high-dose Avodart.

I don’t expect to stay in remission indefinitely, whether with or without TRT. My energy, ability to add muscle mass, and enthusiasm for taking on new pursuits are all much improved since starting TRT. Morgantaler thinks that PCa cells reach T-saturation at about 250 ng/dL. If that’s true, all I’m doing is pushing my T up modestly to reach this saturation level, but dramatically in terms of how much better I feel. So far I like how this experiment is going!


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Thanks for your reply.


Dave, Could you tell us the doctor who has been treating you during the course of your disease management, especially the use of Leukine. In my part of the world, doctors are not even aware or willing to go down this road. Appreciate any additional info. Thanks.


rassu, when it comes to my use of Leukine, the two docs who were most involved were Robert Robles (Pleasant Hill, CA) and Snuffy Myers (Earlysville, VA; retired last month). Robles recommended trying Leukine initially and continues as the prescribing doc. He’s used to Leukine because he’s mostly a blood cancer guy, where its often used, but he knew it also can have effectiveness with PCa. After a few weeks at a relatively low dose, Myers proposed stepping up the dose to what I documented above, and Robles readily agreed. I know that Bob Leibowitz (Los Angeles) also uses Leukine with many of his PCa patients. I’m sure there are others, but it will probably take an out-of-the-box thinker to get a prescription. Be aware that Leukine is also tricky when it comes to insurance coverage. CVS pulled it from their formulary effective 1/1/18. I would choose a drug plan that includes Leukine in their formulary unless you have a prior track record demonstrating that Leukine produced growth arrest in your situation. Cost is also an issue--$7000 for 4-week supply before insurance.

Leukine isn’t a panacea for everyone with PCa, but IMO if it were tried more often in those with low-volume disease, the average length of remission in this group of patients would be extended considerably. Eric Small’s 2006 study: “Seven of 29 evaluable patients (24%) remained free of disease progression at a median of 5.1 years (range 4.5 to 5.6 or greater) from the start of Leukine therapy.”

Eric Small's 2006 study: ncbi.nlm.nih.gov/pubmed/166...


How are you doing at this point?




The good news is that my PSA is currently undetectable (<0.006) and b-s ALP is within ref range at 17.8 (7.6-24.8). However, after 8 months on TRT my PSA became detectable for three successive months and PSADT was averaging 2.6 months in this period. So I D/C TRT 7/13/18. Surprisingly, as of 8/20/18 my PSA fell 60% to once again <0.006 where it has remained to present.

Without the TRT my T is running between about 100 ng/dL when on Leukine (which I am continuing) and 200 when off of Leukine. I feel the effects of low-T, but am thankful no further steps needed right now to lower androgen stimulus to the cancer. I am continuing Avodart as I have for years to maintain low serum DHT.

The T lowering effect of Leukine is a mystery, and I didn't observe this when my T was higher. Scholz acknowledged that the correlation is clear in my case between lower T after two weeks of daily Leukine vs two weeks off of Leukine. He said he had never seen this before.



That's great about your undetectable!

Would like a little more info on your experience "So I D/C TRT 7/13/18. Surprisingly, as of 8/20/18 my PSA fell 60% to once again <0.006 where it has remained to present."

After my 2012 RALP (GL 3+4, T2C+ due to one pos margin), I was psa undetectable for two yrs. But my T bounced around lower range, between 200's to low 400's untreated. In 2014, uro allowed Androgel--didn't absorb well (or something), so 2016 he switched me to T-cyp inj. By 2017, T was 750 but psa started creeping into the .020s, then Dec. 2018 I got a .052. I went off the T shots (my call, not uro's) and Jan. 2, 2019 psa was down to .041. Similarly, I went off T shots for 6 mths in 2017 (my call), and saw about 60% psa drop like you did before feeling good about restarting my T shots then. Have never been on AIs. I did self test (LabCorp) sensitive estradiol Aug 2016 at 46.1 (above range).

All this does not fit the "saturation theory", does it? You used the word "surprisingly". Yep! Did you ever get an explanation of why psa would drop with TRT DC'd? Any info would help me understand. Thanks, Robert


Robert, I asked Scholz what my PSA dropping so precipitously to undetectable (after D/C TRT) might suggest. He didn’t offer anything.

I reached the same conclusion that you did: for me (and now you), Morgentaler’s T saturation theory, with a saturation point of around 250 ng/dL, doesn’t fit at least some patients’ data.

My theory: when tumor burden is pretty low, cancer variant is favorable, and immune system is able to exert some tumor control, then reducing the androgen stimulus via lower circulating T can tip the balance and allow the immune system to keep the cancer in check or even drive it to complete remission. And this can occur, in some patients, with rather modest lowering of serum T.

In recent years Myers said (multiple times) “the goal should be a complete and durable remission.” To Myers that meant PSA was undetectable and no other evidence of tumor from scans/serum ALP/etc. I think that’s a worthy goal to consider for someone in your situation. It’s obviously not attainable for a lot of guys with advanced PCa.

My target for serum estradiol is 20-30. At estradiol of 46, I would use Arimidex to lower it. If you do that, try just 1/4 tab of Arimidex—very potent med!



On your “My theory...”.

Yes, probably exactly what you laid out. I believe you have nailed it, sir.

You know, I have feverishly been reading research reports on TRT, esp. when administered to PCa survivors, and finding unusual comments along the way like these:

Liebowicz, BJU, 2010, “While most men in this series had increasing PSA levels during TRT, stopping TRT typically resulted in PSA declines...”

Pastuszak, J. Uro., 2013, “...In hypogonadal men with a history of prostate cancer after RP, TRT results in increases in serum T levels, with a small but significant rise in PSA and a lower BCR rate in treated men compared with age matched reference men without symptomatic evidence of hypogonadism, even in men with a history of CaP bearing high risk features...”

Morales, BJU Int., 2011, “...The responses to testosterone supplementation were varied according to each individual and were unpredictable. While some men showed little change after years of treatment, others exhibited a rapid and significant increase in PSA levels. In others, the use of intermittent therapy resulted in synchronous changes in PSA levels. Interruption of TTh invariably translated into a decrease in PSA to pre-therapy levels...”

Unless same patients were at castrate level T, those PSA changes should not be happening, if Morganthaler’s saturation theory is right. He says prostate cells are exquisitely sensitive to T in castrate range, but not at all otherwise.

I supposedly have only a 3mm intraprostatic margin left in me (assuming no micro-mets or ctc), which 2nd path by Epstein determined to be a 3+3=6. Retired in 2015, have been watching diet and ramped up aerobic & weights, and have finally beaten my ten years of pre-diabetes down to where my A1C is now 5.2 (ref range 4.8 – 5.6). Rarely sick or even colds now. So my immune system is probably best in my life, though hitting age 70 this year.

Additionally, per Friedman’s “The New Testosterone Treatment”, early this month I started DIM tablets, increased cruciferous veggies, mushrooms, etc. Maybe this will help push estradiol down, even in absence of AI meds. So my (Feb) uPSA next Mon. and the one early March should, hopefully, show me the downward uPSA trend I want. Next uro appt. is June. He never mentioned AIs to me, but he would probably give me AI script if I justified it.

Guess I am done with TRT forever. My shot early last Dec. was my last. Too scared now. At my annual uro appt mid-Dec., he was thinking it might be recurrence, and was talking to me about maybe getting Axumin or PSMA scan down the road. I’ve been having bad thoughts about “what if saturation theory is wrong?” and “what if I’ve actually been screwing myself with five years of TRT?” I did feel a little better being on TRT. But, in my case at least, going off it for six months in 2017, and again for the last two months, has not been all that bad. I fully agree with Myers on striving for complete remission. No assurance I can get back there but gonna try. If ostopenia arrives down the road, there are meds to treat it.

Thank you so much for your assistance.



Have you reduced/eliminated your transdermal estradiol? That should be the main lever for managing serum E2. I only use AI infrequently for quick lowering if way too high (happened when I started TRT—dramatic E2 rise.

Getting you to complete remission will very likely require some form of ADT. I used Firmagon + Xtandi for 9 months (PSA fell to undetectable after one month) even though I wasn’t metastatic or CRPC. Myers said goal was to achieve as deep a remission as possible.

Low bone density may become an issue, but better to be proactive on that front. I monitor bone density annually via QCT, keep serum E2 in 20-30 range, keep serum bone resorption marker C-telopeptide towards low end of reference range w/ low-dose form of denosumab.



“Have you reduced/eliminated your transdermal estradiol? That should be the main lever for managing serum E2. I only use AI infrequently for quick lowering if way too high (happened when I started TRT—dramatic E2 rise.”

Over the last year, wife and I switched tableware/food storage (BPA or estrogenic) to glass/metal and use stainless steel bottles for biking/hiking. Otherwise, other than the food changes I mentioned before, have no other estrogen control in place. Uro will probably give me AI script when I see him again in June, if I need it. Have read elsewhere what you said about AIs being really powerful.

“Getting you to complete remission will very likely require some form of ADT. I used Firmagon + Xtandi for 9 months (PSA fell to undetectable after one month) even though I wasn’t metastatic or CRPC. Myers said goal was to achieve as deep a remission as possible.”

You had an amazing response! When I went off TRT for six months in 2017, I almost got down to undetectable again (.017 on LabCorp uPSA with .015 lower limit). Might have if I hadn’t “got brave” again and restarted my self T-cyp injections. Since I don’t feel in real danger at the moment, may just ride this out for awhile and see if I can get there with D/C TRT only. Problem is my PCP and Uro don’t seem to share my concern about rising uPSA. PCP says “Your not going to die of this, don’t worry”. Uro seems ambivalent. In 2013, after new joint ASTRO/AUA recommendations came out, I discussed ART with him. He was pretty much against it. We compromised by sending my slides off to Epstein for a 2nd path to get the Gleason at my one 3mm margin (first path did not so state). Epstein came back 3+3=6 margin, so I kinda relaxed a bit. Even in Dec. 2018 appt., Uro said he was not sure I was headed to BCR. He said Axumin is only good at .4 or above. PSMA is better, but not available in my mid-sized city in southwest U.S. and would be more accurate at higher uPSA. Can and will travel to UCLA and pay out-of-pocket if I need to. What I’m getting at is I’m not currently positioned to get top-notch expertise on this, like getting well administered ADT, without travel, like MDA in Houston. Which is feasible, if really needed. Agree with Myers about deep remission, but may take a little time to get it together. Assuming I can. I am very aware I am lucky to even have a shot at what Myers calls “deep remission”.

“Low bone density may become an issue, but better to be proactive on that front. I monitor bone density annually via QCT, keep serum E2 in 20-30 range, keep serum bone resorption marker C-telopeptide towards low end of reference range w/ low-dose form of denosumab.”

Excellent info. Was wondering how to monitor bones. Interestingly, Friedman’s book references JAMA study of optimal estradiol at 21.80 – 30.11 pg/mL. I see Medicare allows a DXA scan for men over 70 (August for me). I can get a CTx blood test for about $100 out-of-pocket or maybe Uro will script it when I see him again in June. Interesting the Quest writeup for CTx warns to avoid biotin (vitamin found in many multi-vits) for 72 hrs before. Same warning for the uPSA test. Guess it interferes with the test substrate or something.

All really good info to get me started. Am starting to see a “plan” for me, assuming I actually get a couple more monthly uPSAs trending down. If it trends up, I’m probably off to MDA or U.T. Southwestern for an initial sit-down.

Many, many thanks. Have not found anyone else with the knowledge to get me squared away!


I had 6 months of Lupron total, beginning 2 months prior to radiation with a .8 psa result. My doctor wanted me to wait 2 years before bringing my T level back up, but I am insisting on bring it up now 7 months after treatment and watching psa levels closely. Wish me luck and good luck to you!

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Thanks for your reply.


Good luck and please keep us posted this is of great interest for a lot of us.


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I am a sample of one. My PSA has been undetectable for the last 3 years. “T” has average 11ng/dL during that time, never going above 15. Sounds good. Castrate level seems to be keeping the PSA undetectable. However, my Oncologist suggested TRT in the form of Androgel, due to a nonexistent quality of life. He recognized it, but I didn’t. I began the TRT about 10 months ago. First month after T rose to 387 ng/dL. Next month it was around 800. But after the first month of TRT, PSA became .1. Second month, .2. Since the introduction of testosterone my PSA has been increasing by .1 each month. Scary, and I’m not sure how far to let it go. Will ADT slow the rising PSA again? No idea. A quandary to be sure. I didn’t realize how poor of a QOL I was living until I began having one.

But the empirical evidence of one (my case) does indicate a relationship between castrate levels of T and PSA.



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