Re: solitary bony metastasis treatment

I have just completed another cycle of my homegrown therapy: 3 months castrate followed by 3 months with testosterone [T] > 1,000 ng/dL. The difference this time is that I was receiving radiation on L5 during the castrate phase.

The PSA during these cycles follow a familiar patern to me. PSA is very close to zero when I begin the T phase. During the third month of T, it rises 50% to ~37.

I didn't do monthly tests in this cycle. I wasn't sure how the radiation would affect them. But at the end of the third month of T, on2/29, my PSA was only 13.6.

Seems that almost two-thirds of my PSA was due to the L5 lesion. That still leaves the one-third, of course.

I have never produced much PSA. It was only 0.8 when a nodule was found. So the numbers above are big numbers for me.

My aim with radiation was to (a) treat the lesion before it became a major problem; (b) debulk the cancer; (c) discover the L5 contribution to my PSA number.

I shall now resume monthy PSA testing & discover how the lesion was affecting PSA doubling time.

I'm posting this as it might be of interest to anyone with a solitary bony met.


10 Replies

  • What do you mean by "castrate?" Did you actually have an orchiectomy?

    I had a bilateral orchiectomy in November to try to lower the testosterone and to get off of the Lupron. My testosterone level still remains too high, though, well above the 20 or less therapeutic level. (I guess that I'm so much of a stud that my body still produces so much testosterone----even with testicles

    But I don't regret having the orchiectomy--- I got a nice new set of large fake balls, as my own testicles had shrunk so much from three years of hormone therapy.

    My own PSA has been climbing, though, I'm on Xtandi and was on a reduced dose, but we just increased the dose back to 120 mg, so I'm hoping that it will bring the PSA back down. It's currently up to 5.20 in Feb., from 3.61 in January.


  • By castrate, I meant <50 ng/dL. I suppose I should aim lower. I'm still intact, but with some atrophy, of course.

    Good luck with the higher Xtandi dose.



    Perhaps in future there might be a more scientific method in alternating castration therapy with testosterone therapy?

  • I must have read hundreds of study papers that open with a discussion of ADT; its initial success in most men, followed by failure in 18-24 months in most cases.  The first paragraph of such papers started to read like boilerplate text. 

    About 11 years ago, I read a paper where the author hypothesized that testosterone [T] might reverse ADT resistance.   His idea was that T would select for cells that would respond to ADT, & that a man might survive many years by cycling back & forth.  As I recall, it was published in a lesser known journal & I doubt that many noticed it.

    I was ~57 then, & trying to figure out how to survive the next 25 years (LOL), so found the idea intriguing.  A common response to ADT is for for PCa cells to create more copies of the androgen receptor [AR].  Another is for AR to gain function - essentially, multiple copies of transcription specs - aka AR amplification.  A third response involved AR mutations.

    I wondered what the optimal time would be to switch from ADT to T.  Seemed to me that AR mutations were to be avoided, & waiting for ADT failure might not be a good idea.

    In looking at intermittent ADT IADT], I came across statements indicating that the ADT phase had to be about 12 months.  Shorter periods lead to a rapid return of PSA.  Dr Myers has an interesting string of vblog posts on durable remission & he mentioned that one can only do IADT 2-3 times before CRPC occurs, so the idea is to make the off-phase as long as possible.  Two years?  Three?  

    I didn't like the idea of CRPC at all, so decided that 12 months of ADT was too long.

    Samuel Denmeade at Johns Hopkins has written about rapid cycling, which he now calls "bipolar androgen therapy" [BAT].  Instead of stepping through his papers, lets cut to the pilot study paper of last year [1].

    "16 asymptomatic CRPC patients with low to moderate metastatic burden were treated with testosterone cypionate (400 mg intramuscular; day 1 of 28) and etoposide (100 mg oral daily; days 1 to 14 of 28)."

    "No patient developed worsening pain due to prostate cancer, nor were there any other skeletal events or evidence of worsening urinary obstruction. Furthermore, with seven patients exhibiting PSA declines, the study met the primary endpoint of at least three subjects with PSA declines. The PSA declines observed in this study are particularly remarkable because PSA is an androgen-stimulated gene product. BAT also produced objective radiographic responses in 50% of patients with RECIST-evaluable disease. Finally, post hoc analysis showed that 10 of 10 (100%) of men treated with BAT responded to second-line therapies after BAT, with 3 subjects responding to an agent on which they had previously progressed. These data suggest that BAT may have the potential to reverse resistance to androgen-ablative therapies, potentially resensitizing men to drugs to which their cancer had become resistant."

    Frankly, I'm surprised that the results were that good, considering that these were CRPC men.

    I can envision some kind of 'restart' T intervention during ADT, where cells are resensitized, pushing CRPC further into the future.

    A note on the T dose: "testosterone cypionate (400 mg intramuscular; day 1 of 28)".

    I use 80 mg weekly when I am in my T phase.  My T was above 1,000 ng/dL on day 8 (just before the next shot), the one time I tested, so I know the stuff lingers.  The study:

    "dose and formulation produce supraphysiologic testosterone levels (>1500 ng/dl) within the first few days after injection, with a subsequent decline to high-normal testosterone levels after 2 weeks, and a return to near-castrate testosterone levels by 28 days"



  • I agree. Sounds right. Looks good. Are we nuts?

  • How did you get your doctor to go along and prescribe these medications?

  • Slowly, non-confrontational, & chatting about the studies over time.

  • Making friend huh.

    The old fashioned way.


  • I don't understand how or why you call these treatments you're receiving "homegrown" therapies. They seem like pretty standard, traditional treatments to me.

    Nothing alternative or natural? Hope you're doing well.

    I was diagnosed with metastatic prostate cancer in early March 2016, just a little over one month ago. I have refused any traditional procedures, including chemo, radiation, hormonal therapies. I am using, aggressively, several natural therapies now. Massive doses of liposomal Vitamin C (30 to 40 grams per day), cannabis oil ingested orally, frankincense essential oil, genikonoko, agaricus mushroom tea (from Japan), Protandim, Beta 1,3 Glucan, curcumin supplements, tumeric powder, cayenne pepper, no meat, no dairy (except cottage cheese, for its rich sulphuric protein), lots of greens and rainbow vegetables. Lots of purified water and green tea. No sugar, no wheat.

    Seems to me these regimens are more "homegrown" than your surgery and radiation treatments. I am 85 year old professional still working about 40 hours per week.

  • My father died of prostate cancer, but had few symptoms until shortly before his death. (He was being treated however.) How are you tracking the progress of your disease?

    I do agree that your regimen is more "homegrown" in that it requires no Rx from a physician.

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