I received an email inquiring about the drug finastride that was prescribed to me after I was first diagnosed with class IV prostate cancer that metastacised to the bones. Here it is:

“Hi Vernon,

I am Arrow Durfee from www.HealthSalon.org

I suppose you won’t be too surprised to find out that you are being
discussed on a forum regarding PH and cancer treatment. The poster I
am discussing your treatment with posted this and I was kind of
stunned, wondering if it is true as I had not seen any mention of you
taking finasteride or casodex on your website. He said the following
about your treatment but I cannot find it on your blog. Could he have
found this information somewhere else? If so where?

“Pre-treatment PSA was 22 but has decreased to 5.88 after institution
of Finasteride and Casodex. So it was already at 5.88 when he started
the bicarb? Did it continue to fall after the Finasteride and Casodex?
He did not measure the PSA prior to the bicarb protocol. Apparently
not. That would be good to know. Since the doctors waited from March
to June to test, I assume they thought it would take that long for
those 2 drugs to work. Meaning the PSA was probably still falling by

Don’t get me wrong here. I’m very glad he got his PSA to 0.1.”

this is the forum page we are discussing this on:


I see now where you do mention that you were on these meds.. were you
on them when you did the bicarb thing also? At what point did you stop

I hope you can clarify this information. Many people think that you
did not do any type of chemo therapy what so ever.


This is me talking now. As you can see, Arrow did find where I spoke of finasteride. The doctor who prescribed finastride told me that the reason he is having me take finasteride is to sloooooooow the growth of the cancer. He also mentioned that its prostate specific antigen affects would also only be temporary. Its use was only for a limited time. He told me it would not fix the bone cancer or the prostate. Remember now that I am a human and not a doctor. I did not have a tape recorder with me recording this conversation with the doctors. Also, bear in mind (and those of you who have been to doctors know this) that the conversations that we as patients have with our doctors do not get written in their reports of the event word for word. Usually the will shorten it and say something like, “Mr so and so has these symptoms and I prescribed this for this reason.”

Here is an article that helps describe for me the drug finasteride and how it applied to me and to my treatment:

August 12, 2010
Chemoprevention in Prostate Cancer – do 5alpha-reductase inhibitors make things worse?
There’s a lot of media coverage today surrounding use of 5alpha-reductase inhibitors such as finasteride (Merck) and dutasteride (GSK) and their generic equivalents for chemoprevention of prostate cancer following publication of a study on finasteride by the American Association of Cancer Research (AACR) and one earlier this year on dutasteride in the New England Journal of Medicine (see references below for sources and the journal articles).

So what do these drugs do?

The drugs in the 5alpha-reductase class were developed for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to:

•Improve symptoms
•Reduce the risk of acute urinary retention
•Reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy.
Fair enough, but how does this relate to prostate cancer?

Well, testosterone is the major circulating androgen in men and is converted to the major intracellular androgen, dihydrotestosterone, by steroid 5alpha-reductase isoenzymes, designated as type 1 and type 2.  Finasteride inhibits the type 2 isoenzyme, whereas dutasteride inhibits both.

Many of you will be aware that in early stage prostate cancer, most men are hormone sensitive and respond to androgen deprivation therapy (ADT), which effectively acts as chemical castration to suppress the growth of the tumour of the prostate.  Later, when castration resistance sets in (CRPC), the disease is more advanced.  These days, if they are asymptomatic or mildly symptomatic, then a vaccine called sipuleucel-T (Provenge) can be considered or if metastatic and symptomatic, then chemotherapy with docetaxel (Taxotere) can be considered as a first-line option or cabazitaxel (Jevtana) after docetaxel has failed.

The goal of using the 5alpha-reductase inhibitors early was therefore to prevent or at the very least delay the development of malignant prostate cancer, essentially reducing the risk of developing the disease later.  Several studies have been published over the last decade to answer this question.

The big question is does this approach actually work?

My thinking was if it was that obvious, then surely urologists and primary care physicians would be rushing to prescribe either therapy?  Trouble is, they’re not, as this succinct AACR press release shows.

One of the problems is that the original Prostate Cancer Prevention Trial (PCPT) study back in 2003, a large randomized controlled trial consisting of 18,000 men, appeared to have conflicting results, since it showed:

•a 25 percent reduced risk of prostate cancer.
•a 27% increased risk in high-grade tumours, which was highlighted in the accompanying editorial.
This fact seems to have created doubt and concern amongst urologists and PCP’s.

Subsequently, there have been other reported studies with finasteride in 2008 (reanalysis of the 2003 data) and with dutasteride in the NEJM earlier this year, suggesting in both cases that the risk did not exist.  The doubt, however, still lingers as the AACR press release highlighted:

“64 percent of urologists and 80 percent of primary care physicians never prescribe finasteride for chemoprevention.

When asked for reasons for their decision, 55 percent said they were concerned about the risk of high-grade tumors and 52 percent said they did not know it could be used for chemoprevention.”

Another issue is the conflicting consequence of PSA suppression, which is still used by many urologists as the main biomarker for diagnosis and ADT treatment.  The NEJM editorial earlier this year noted the challenge:

“Among men without cancer, both finasteride and dutasteride treat lower urinary tract symptoms, produce dramatic prostate shrinkage, and reduce serum levels of PSA by 50% or more.

However, for the patient who believes that he is taking a drug to prevent prostate cancer, this decline in PSA level can lead to a false sense of security.”

Why is this?  The editorial went on to explain:

“Data from the PCPT indicate that finasteride produces a progressive suppression of PSA for the duration of treatment. To estimate what the “true” PSA level would be if finasteride were not taken, it is necessary to multiply the PSA level by 2.0 for the first 2 years, by 2.3 for years 2 through 7, and thereafter by 2.5.

However, if the PSA level ever begins to rise at all, a biopsy should be performed, because with an increase in PSA level, the risk of cancer is increased by a factor of 3 and the risk of high-grade disease is increased by a factor of 6.

In the Finnish study, men who received finasteride for more than 4 years had a risk of high-grade disease that was increased by a factor of 2.6.”

After reading all of the evidence in the various studies (cited below), I can see why physicians might be:

It’s hard to make solid sense of the real impact of all the research, even as an unbiased scientist given the data that has emerged.  My overall takeaway from all the articles was as follows:

•Dutasteride and finasteride do not prevent prostate cancer.
•They do shrink tumours that have a low potential for being lethal.
•They do not reduce the risk of a positive biopsy in patients who have an elevated PSA level or an abnormal digital rectal examination.
•Use of these drugs for prevention may be controversial because PSA levels are suppressed, giving a false sense of security.
•If prostate cancer develops, the diagnosis may be thus delayed (by artificially low PSA levels) until they have high-grade aggressive disease that may be more difficult to cure.
My final observation is that perhaps we should be monitoring other markers of disease such as circulating tumour cells (CTCs) in the blood rather than PSA. Whether this would be a better measure of disease or not remains to be elucidated, but would certainly be worth looking at in future studies to see if it is a more accurate biomarker in early prostate cancer.”
See the entire article including references here.

This is me speaking again. It seems that finasteride can be a little bit tricky. And speaking of tricky, I am under the impression that statins have a tendency to lower the PSA reading. At the time I was also on the cholestrol statin drugs. I suppose one would have to take into account this info also. Atorvastatin was one, as well as lovastatin and lipitor. Go here to see the drugs I was prescribed.

Allopurinol is also on that list, and there are some indications that that drug affects the PSA. I have no clue about the other drugs. And how do you factor in that I was not always on Allopurinol. It is too much for me to call. The bottom line for me is not only when the nurse said,  “First it was there, and then it was gone.” But more importantly and what had the most emotional and physical impact on me were the words in the letter from the hospital and the doctor that said, “NO CONVINCING EVIDENCE OF AN OSSEOUS METASTATIC PROCESS”! And this was after I was diagnosed with class 4 prostate cancer that metastacised to the bones from two different oncologists. The second opinion verified the first opinion, and also said there was more bone cancer in the pelvic area than was originally reported. You can imagine I felt relief.

And by the way. . . when my prostate specific antigen reading was at 0.1, the doctors were shocked that it was that low – even with finasteride and casodex. Of course, they did not write “We are shocked that the PSA dropped so dramatically” in the report. Those are words that they expressed to me. I will talk about casodex another time.

I hope that answers some of the questions about my adventure with finasteride. Also. . . I never did do chemotherapy, nor did I do radiation. The doctors insisted that because of the bone cancer, that in my case, surgery, chemo, and radiation were out of the question.

For another cancer metastacised to the bones baking soda success story go here.

Good night! Vernon “Vito” Johnston

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2 Responses to “Bone cancer: “First it was there, and then it was gone” the nurse said. Finasteride”

  1. […] I did correspond with him regarding this issue and I just got a reply. he wrote it up in his blog. http://phkillscancer.com/emails-from…id-finasteride __________________ "The nurse should be cheerful, orderly, punctual, patient, full of […]

  2. […] PSA went to 0.1 and your bone lesions regressed temporarily as a result of your cassodex treatment. Unfortunately, you will eventually become refractory to hormone […]

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