SOME GOOD NEWS - Improvement Without Knives or Rays

Howard J. Cohen, Ph.D.


Mountain View Prostate Cancer Support Group

Talk given 4 November 1999

Text written 10 March 2000 -- 25 May 2026

© Copyright 2000-2026 Howard J. Cohen, Ph.D., All Rights Reserved


http://www.cohensw.com/mvpcsg_nov99.html -- slides (a summary from 1999)

http://www.cohensw.com/mvpcsg_nov16_ppt.pdf -- slides (a summary from 2016)

http://www.cohensw.com/mvpcsg_nov99_text.html -- text (this document)

A work in Progress


Contents

Dedication

Introduction

Who am I?

A History of My Disease

What Did I Do?

Education

The Theory

Vitamins and Herbs

Diet and Exercise

Alternative Practitioners

Secret Weapons

Bottom Lines

Bibliography

Glossary

Appendix A: The Nature of the Beast - The Course of the Disease

Appendix B: Current Medical Treatment Options

Appendix C: Future Therapies

Appendix D: Change Log (What's New)


Prostate Cancer Site Map
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Dedication

This web paper is dedicated to the memory of my wife of 43 years, Barbara Cohen (24 August 1945 -- 11 July 2016).

It was Barbara's intuition that mothers' milk could fight cancer and her web research that turned up the first article for us in August 1999, that started my healing journey and which resulted in this web site. In addition, it was her way with people that led to my first receiving milk from a donor and to my later being able to purchase milk from a Milk Bank.

Some of this story will unfold as you read this paper.

It was her love and support, her intuition, insights and comfort with people, that led to the so far happy conclusion of my cancer story. Twenty four years after diagnosis (September 2023) I have no detectable cancer without any medical interventions beyond non-invasive diagnostics. She will be sorely missed.

Read on for more details.


Introduction

On 4 November 1999 I gave a talk based on the accompanying slides to the Silicon Valley (California) Prostate Cancer Support Group at one of their monthly meetings at El Camino Hospital in Mountain View. Since then I have been asked a number of times for the information in my talk. But, since it was not written down, I had to reinvent it, in abbreviated form, each time.

This is my attempt to flesh in the details and history "once and for all". That is, to write it down in a more complete and narrative style than the slides and also to have a base for keeping my story current, as time and my medical history evolve.

This is a living, evolving document, with continual minor changes, new references, new test results, and ocassional major revisions and additions, although it is based on that talk of hope in November 1999.

On 3 November 2016, almost 17 years later to the day, I gave an update talk to the same Silicon Valley Prostate Cancer Support Group at El Camino Hospital in Mountain View, California.

A link to both the original 1999 slides and the 2016 slides are noted above.

Here I seek to accomplish a number of things. This paper is

I put significant effort into researching and understanding prostate cancer and HAMLET in the first years after my diagnosis, including the bulk of the effort in putting this web page together. During the dot-com (and high tech and biotech) bust of 2003-2004, my focus changed to economic survival. And then as the economy improved and my cancer became undetectable, I have spent less effort in trying to keep up to date than I did initially. What I am doing seems to be working and, while I acknowledge prostate cancer and my need to be sure it remains undetectable, I do not want it to dominate my life.

I keep my personal story and test results up to date and add references and discussions as I come across them (either in my travels around the web or via prostate cancer newsletters or references kindly forwarded to me by friends, acquaintances or strangers). I suggest that the reader may use this as a starting point for his/her research but to bring your searches up through the current state of the art, as many of the references herein are, perforce, dated or obsolete, since this web site has been growing for over two decades and cruft accumulates (or events continue evolving).

And I wish you all good health, a positive attitude and much support.
 

[A Note to the Reader]

I would welcome feedback and dialog on the material presented here. This could range from typos to infelicities of expression to areas that are unclear or which you might desire a more detailed exposition. Also, corrections to factual or reference material or additional items or issues you think I should know about. And, as always, kudos are welcome as well.


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Who am I?

I was trained as a scientist, hence a skeptic to unfounded claims. I received a Ph.D. in theoretical physics when the job market for academics was rapidly disappearing in the mid-1970's, and switched into the nascent field of software engineering and computer programming early on after graduate school.

Most of the work I have done professionally has involved some sort of scientific or engineering applications (see my web pages for details), including the past several years (since late 1996) in biotechnology and genomics. With this all, I can claim scientific literacy and an analytical approach, a belief that I can master most areas of knowledge, and a sense of numeracy, an appreciation of numbers and statistics. While I have not had much training in biology and none in medicine, I was able to educate myself about prostate cancer and the available treatment modalities in a very intense couple of months immediately after my diagnosis.

I was diagnosed in July 1999, just before my 54'th birthday. I have always been quite healthy, in reasonably good physical condition, slim, and with a good diet.

And I have usually had a take-charge attitude with regard to my own well-being. I view doctors as partners, well trained technicians who should be working for me and with me. I have little regard for those who try to elevate themselves to god-like status or view their patients/clients as slabs of meat to be treated as objects rather than as people with whom they are collaborating. The ultimate responsibility for my health lies with me.

And finally, I have humility in the face of cancer. It is a very serious disease (or set of diseases) with extremely serious consequences and should not be denied, ignored, or trifled with. Being diagnosed was a great shock that was counter to the myth I have lived by, that of Good Health and Immortality (which really translates to a long and healthy life). And it took a little while to hear the diagnosis and its implications and to mobilize myself in the midst of the rest of my life.


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A History of My Disease

The following table describes the evolution of my PSA levels with time. This data is also graphed below. All PSA values have been determined at Stanford Hospital unless otherwise noted. In mid-2001, Stanford changed the test used to give an extra significant figure in the results.
 
PSA vs Time
Date 02/25/95 12/15/97 04/27/99 07/27/99 08/01/99 09/21/99 10/12/99 10/27/99 11/29/99
PSA 1.72 1.9 5.4 diagnosis 6.2 (est) 1.9 1.4*
finger prick
2.2 2.1
Date 01/04/00 02/07/00 03/16/00 04/17/00 06/02/00 07/10/00 08/10/00 09/08/00 09/21/00
PSA 2.4 2.0 1.8 2.0 2.2 2.3 2.2 3.8** 2.5
Date 10/05/00 11/10/00 12/11/00 01/11/01 02/15/01 03/01/01 04/05/01 05/09/01 05/11/01
PSA 2.2 2.2 2.1 2.2 2.8 2.5 2.6 19.6***
prosta-
14.0***
titis
Date 05/25/01 06/06/01 07/11/01 08/14/01 09/10/01 10/09/01 11/08/01 12/11/01 01/09/02
PSA 4.0 2.5 2.3 1.91 2.12 1.93 2.15 2.15 8.64*
pros-
Date 01/11/02* 01/15/02* 01/21/02* 01/29/02 02/05/02 02/13/02 02/22/02 03/28/02 04/29/02
PSA 6.70
tatit-
5.43
is
5.45 4.01 2.97 2.43 2.51 2.49 2.15
Date 05/28/02 06/24/02 07/22/02 07/22/02 08/20/02 09/26/02 11/04/02 12/10/02 01/27/03
PSA 2.08 2.07 2.16 1.63**
UCSF
2.08 1.96 2.37 2.08 2.59
Date 02/05/03 03/11/03 04/22/03 06/17/03 06/17/03 08/01/03 09/22/03 11/17/03 01/13/04
PSA 2.40 1.95 1.89 2.18 2.26
UCSF
2.15 2.25 1.88 2.08
Date 03/19/04 05/06/04 07/14/04 08/04/04 08/05/04 10/15/04 12/03/04
***
12/13/04 12/22/04
PSA 2.29 1.91 2.54 2.53 1.95
UCSF
2.17 6.45
prostatitis
3.37 3.29
Date 03/28/05
***
04/05/05
***
06/01/05
***
07/06/05
***
08/09/05 09/21/05 11/21/05 01/18/06 03/06/06
PSA 5.3 7.43 4.42 18.3 2.44 3.03 2.23 2.37 3.27
Free PSA 15 %                
Date 03/06/06
UCSF
04/18/06 08/14/06 01/22/07 03/05/07 05/07/07 08/22/07 09/28/07 12/18/07
PSA 3.65 4.33 4.78 3.61 4.34
UCSF
3.46 4.62 5.14 3.25
Free PSA   16 %              
Date 02/14/08 07/07/08 09/22/08 02/13/09 06/18/09 11/04/09 03/19/10 10/11/10 02/22/11
PSA 4.00 4.00 5.86 5.72 5.92 5.00 4.61 4.7 5.84
Free PSA                  
Date 06/10/11 11/02/11 03/14/12 07/27/12 10/11/12 12/17/12 03/04/13 03/25/14 02/17/15
PSA 5.4 5.2 4.7 6.1 7.22
Hunter Labs
6.8 7.3 7.40
Hunter Labs
8.1
Free PSA             21 %   17 %
Date 06/17/15 10/29/15 02/04/16 04/14/16 08/18/16 12/13/16 03/02/17 05/31/17 09/11/17
PSA 8.8 7.8 10.5 8.2 9.9 9.7 11.5 10.0 8.1
Free PSA 15.9 %                
Date 12/07/17 02/13/18 05/16/18 11/09/18 04/17/19 06/03/19 10/31/19 02/24/20 06/10/20
PSA 8.6 10.2 7.68
PAMF
8.2 10.4 9.0 11.1 14.5 13.1
Free PSA 20 %           19 %    
Date 12/03/20 03/15/21 06/04/21 12/09/21 03/09/22 06/02/22 08/02/22 11/30/22 03/07/23
PSA 12.4 12.5 9.9 6.3 9.3 8.2 7.0 8.0 7.7
Free PSA                  
Date 05/16/23 09/05/23 01/17/24 06/05/24 09/05/24 12/10/24 03/11/25 09/03/25 02/18/26
PSA 7.5 7.0 9.7 10.6 8.3 10.3 9.2 9.4 8.2
Free PSA                 26% = 2.1
[Graphical Image of PSA vs Time]

In about 1993, a friend of mine who was just 50 at the time, was diagnosed with prostate cancer. His PSA was about 142 when diagnosed (normal range is 0.0 to 4.0 ng/ml) and 180 when he received a radical prostatectomy at Stanford University Hospital by the fabled Dr. Freiha, who has since retired and then resumed practice at the Palo Alto Veterans' Administration hospital. Since then, my friend had been on and off hormone therapy and seemed to have his cancer under control. (In late 2005, after 12 years of intermittant hormonal blockade [which will be discussed in Appendix B], he developed hormone refractory prostate cancer and explored chemotherapy options. He tried mothers' milk briefly in 2007. He died of prostate cancer in June 2008, surviving 15 years, although he was only given one to two years to live at his initial diagnosis.)

I thought that his cancer might be correlated with his work and where he has been living for some time. My impression is that the synthetic estrogenergic chemicals used in pesticides and herbicides by agribusiness to increase their yields and profits at the expense of the health of farm workers and the rest of us is correlated with the sharp rise of breast and prostate cancer in the decades since the Second World War. (See reference, below). And my friend was involved in the food processing industry and lived in lovely rural areas where heavy industrial agriculture took place. I thought his exposure was probably higher than normal, hence a likely contributor to the cancer. I don't know if the epidemiology supports this or not, yet we are all, urban and rural, exposed to enormous amounts of toxic and teratogenic chemicals in our air, water and food, things to avoid, yet things impossible to avoid. I have also found out that he has a genetic predisposition, since his father and uncle have had prostate cancer. There have been no cases I know of in my family except an uncle who had a mild case in his mid-80's (he had brachytherapy and lived to 96).

But somehow, I thought I was immune. Even so, in my periodic physicals, I had to insist that my physician do a PSA test in addition to the usual DRE (digital rectal exam, where a gloved finger probes for irregularities on the back wall of the prostate gland).

The PSA's were normal. The last normal one was in December of 1997, when it was 1.9 ng/ml.

In late April 1999, I had another "annual" physical. The PSA came back as 5.4 ng/ml. This was alarming for two reasons. First, the absolute number was above the "normal" range of 0.0-4.0 ng/ml. And second, the rate of increase seemed rather steep. This is also a sign that there is a cancer that is beginning to grow rapidly. In fact, a conservative estimate of the growth rate is to assume that it was linear and started just after the last "normal" reading. In that case, in these 16 months it increased by 3.5 ng/ml, which is a rate of 0.21875 ng/ml/month. If it started increasing (linearly) after that time, its rate of increase must have been even higher.
 

[Aside about PSA]

I should probably say a few words about what PSA is and what it isn't. It stands for Prostate Specific Antigen, a particular chemical that seems only to be secreted by prostate cells. It is often a proxy for prostate cancer, but not always. Men can have prostate cancer with low or normal PSA levels. Conversely, a high level may not mean cancer but may be the result of an infection of the gland (prostatitis) or a benign enlargement of the gland (BPH, benign prostate hyperplasia), which often occurs in older men and frequently leads to urinary problems.

In addition, the PSA in normal men fluctuates naturally. It increases for two or three days after ejaculation (by roughly 10-15%, according to Professor Peter Carroll, UCSF, personal communication, 29 May 2001) or any disturbance of the gland. The medical literature indicates that you can expect PSA levels to fluctuate about 10-15% normally. And the lab results are also not that reproducible; different labs have their own biases. Even drawing blood and dividing it into two samples which are then sent to the same lab may produce results 10-15% apart. So what one looks for is long term trends, averaging out the fluctuations. And more frequent measurements allow the fluctuations to be seen and the trends to emerge from the data, as is true for any statistics.

It took until mid-June to get an appointment with a urologist at Stanford, one recommended by my physician, also at Stanford. We chatted and he recommended an ultrasound (TRUS, a trans-rectal ultasound), combined with a biopsy, which was scheduled for early July. With the TRUS, an ultrasound probe is inserted in the anus and moved around. It creates crude images of the interior of your pelvis, especially of the prostate gland. I couldn't see much there, but a trained radiologist (ultra-soundist?) can see abnormalities in the organ and surrounding tissues, if they are bigger than some minimum (and crude) resolution. The prostate volume can also be measured, which helps in determining whether there is enlargement due to BPH or other conditions.

My TRUS showed nothing out of the ordinary.

At the same time, the ultrasound probe can be used for taking biopsy samples. The ultrasound image can guide the doctor to point the tip to particular locations on the gland (for example, left upper, left mid, left lower, etc.). A spring loaded hollow needle can be fired through the rectal wall into the prostate to draw a cell sample about 1 mm in diameter and 10 to 15 mm long. These samples are stained, fixed, and sent to a pathology lab for examination under a microscope. The procedure takes maybe 15 minutes. It is uncomfortable and unpleasant but tolerable. In my case, 10 samples were taken.

A week and a half later, my wife and I went to meet the urologist at Stanford for the results. In my first two visits, he was punctual, pleasant, if drabbly efficient. This time, the bean counters at the hospital, in their increasing quest for milking money from both doctors and patients, had overbooked him, and he was over an hour late getting to see us. This was creating problems since my wife had clients of her own to see that afternoon, and I had business obligations. We were not pleased when he finally had time for us, with a couple of residents hanging out in the back of the room to observe.

The results were kind of ambiguous. The Pathology Department had seen nothing awry in the samples. The Urology Department pathologist (Dr. John McNeal, a world-class master of the art of reading and interpreting slides) had re-examined them and found that in one core from the left midsection, there was a 1 mm square region that seemed as if the cells might be cancerous. I was to come back for some additional sampling in that region.

As soon as he said that, I stopped being able to hear. I was stunned by the news and furious at our mistreatment. He must have talked for a while longer, but I did not remember what he said. I made an appointment for the next week, when 4 more cores were taken from the left-midsection. The results came via a phone call on 27 July: one of these also had a 1 mm square group of cancer cells. The Gleason score was 3+3, a value found in about 2/3 of new diagnoses, meaning a not very aggressive cancer. I had time to think and learn and make some decisions.
 

[Aside about Gleason scores]

The Gleason score is a subjective interpretation of how malignant the prostate cancer cells look under a microscope. The two values are the nature of the primary population of cancer cells and the nature of the secondary population of cancer cells. Each score may range from 1 to 5, one being "almost normal" and 5 being "very aggressively malignant". A score of 3 is about average, and in my two small samples both primary and secondary populations were 3.

The primary population is the dominant one, after "normal" cells are discounted. This is the bulk of the non-normal cells on the slide. There may be a smaller population of non-normal cells, and this is referred to as the secondary population and determines the second value in the Gleason score. If there is no such secondary population, both Gleason values are the same (e.g., 3+3).

The order of the two values in the score are of significance; that is, 4+3 is more aggressive and worrysome than 3+4, for example.

A good reference, with diagrams, is noted in the Bibliography.


[Note about estimated PSA]

The estimated value in the table of 6.2 at the time of my biopsies in late July 1999 was a conservative guess. It assumes the slowest possible growth of my PSA values consistent with the 1.9 in December 1997 and the 5.4 in April 1999, namely a linear growth that started exactly in December 1997. Over 16 months, the PSA score grew by 3.5, so I extrapolated the same growth out another 4 months to August, yielding a value of 6.2 about the time I started responding to my diagnosis.

If we assume that the PSA growth started later than December 1997, its linear growth rate would have had to be steeper, and the August 1999 value higher.

Likewise, a more realistic model is based on the fact that cancer cell growth, once started, is more or less exponential, and so constantly accelerating. This also yields an even higher estimated value by August 1999.

[I should point out that "conservative guess" as I used it in the first sentance of this note was meant as a mathematically conservative estimate, in the sense of not overestimating my PSA -- what was the smallest reasonable value it might have been? One might make a medically conservative guess, where "conservative" means to not underestimate the severity of the cancer, and this, of course, would be a somehat larger number, depending on the growth model assumed.]


[Notes on the subsequent values]

A prostate biopsy is a violent agitation of the gland and its natural healing mechanism elevates the PSA level for some considerable time, whether there is cancer present or not. The general consensus is to wait 2 months after a biopsy for follow on PSA measurements. And so I did.

In the meantime, I began to put a program together and follow it. More on this below. I should note that all tests except one were done at Stanford University Hospital, so I had tried to eliminate the variations due to laboratories. The first PSA, at the end of September 1999 was 1.9 ng/ml, exactly what it was in December 1997 when it was normal.

A couple of weeks later, a local Longs Drugstore offered a low-cost finger-prick version of the PSA test, which I decided to try. Instead of drawing blood, sending it to a lab and getting the results back in a day or two, they used a finger prick to draw a few drops of blood that were then impressed on some blotter paper. This was sent to a lab in the mid-west and results mailed back about two weeks later. Not all that much more convenient, in my book. But their value was 1.4 ng/ml, the lowest on the chart. Since it was a different lab, it is denoted by an asterisk (*) in the table above. [The test described is not an off-the-shelf kit; rather it was done by a lab tech who travelled from store to store, also doing cholesterol and other screenings.]

Subsequent values, at roughly one month intervals, have fluctuated about 2.2 +/- 0.2 ng/ml (that is plus or minus roughly 10%), as expected if it were really "constant".



[Notes on the 3.8 of 8 September 2000]

This is an interesting story, but to tell it here would be to get ahead of myself. The context would be missing. It is discussed below.


[Notes on the values of May 2001]

This is an interesting story, but to tell it here would be to get ahead of myself. The context would be missing. It is discussed below.


[Notes on the values of January 2002]

This is an interesting story, but to tell it here would be to get ahead of myself. The context would be missing. It is discussed below.


[Notes on the values of July 2002]

On 22 July 2002, I had my PSA taken at Stanford Univeristy Hospital, my usual site, about 9:30 am. It was 2.16 ng/ml, consistent with my "normal" and with the last couple of readings. About 11:00 am, I was scheduled for an MRIS at UCSF, and they also drew blood for a PSA. It was 1.63 ng/ml. The difference is beyond mere fluctuations and, I suppose, is a cautionary tale about using the same lab consistently.


[Notes on the values of Dec 2004 - Jul 2005]

In the winter of 2004-2005, through early summer of 2005, I had prostatitis again, which drove up my PSA values. A further discussion is below.


[Notes on the values of Feb 2020 - present]

Beginning in February 2020, my PSA values have been gradually decreasing. A further discussion is below.



Top

What Did I Do?

After the initial shock wore off a bit, and I gave myself a week or so to assimilate the bad news, I decided that I had to educate myself about the disease and about my options. My understanding, from a conversation with the Stanford urologist who delivered the news, was that my cancer was still rather small and not very aggressive. This gave me some time to learn, some time to collect my thoughts, some time to explore and find the best practitioners in the Bay Area.

My experience, explorations and evolving program of treatment will be discussed in greater detail in subsequent sections, but the major components should be mentioned here:


Top

Education

My initial approach was to buy and read a few books. I figured that by doing so, I would have in each a coherent picture of the authors' knowledge and points of view. This would bootstrap a basic understanding of the anatomy and physiology of the gland and lay out most of the treatment options as of the time of their writing, roughly a year or two before my diagnosis.
 

Books

These are the books I read in the approximate order that serendipity led me to them:

Web

I also went on the Web early in this process. Working at a high-tech company, I had fast web access, so frustration with the slowness of searching from home over a modem connection was not much of a factor. What was a consideration for me was the sheer volume of data, from reputable and solid, through first person accounts, to the somewhat fringe. Not only is there an enormous quantity to wade through, but, at every stage, one needs to judge the usefulness and veracity and relevance of what you are reading.

Early on in the process I came across Andy Grove's 1996 Fortune Magazine article on his experience with prostate cancer. And, for a while, his choices (high dose seed implants and removal followed by external beam conformal X-radiation) made a lot of sense to me. His is a very well written and important story.
 

MDs

I also talked with doctors. I wanted to find the best in the Bay Area. And since I live only a few miles from Stanford University Medical Center, I tried them first. I figured that the Bay Area was a world-class center of research in general and should have some world-class prostate cancer treatment centers and physicians. I did not want to have to go far from home, if I could avoid it, for consultation and treatment because of the additional strain it would put on my wife and myself.

I consulted at first with the Stanford urologist. I knew I did not want him to be my primary physician in treating my cancer, but he could recommend people. Naturally, the several top US institutions came up:

Poking a little further, UCSF also started coming up a lot. (http://ucsf.edu/)

My wife has a cousin who was a urologist in Southern California. We spoke with her a few times. She was supportive but rather traditional in her approach: being a surgeon, she believed surgery to be the most appropriate thing for me to do. But she was still supportive of my desire to try to avoid both surgery and radiation, if possible. Unfortunately, she was not familiar with Bay Area practitioners.

I called an old college friend who is now a Professor in the Medical School at the University of Virginia. When we had spoken about his research a year or two previous, it seemed as if he were onto something that could be very clinically useful in addressing all kinds of ailments, including cancer. Unfortunately, it still seemed 5 to 10 years out. However, he had a former colleague, an MD/PhD who did post doctoral research with him, who was now a urologist at the University of Chicago. And he was involved with surgery as well as other research. He had been trained at UCLA and did a residency in urology at Stanford, so he was familiar with the players in the Bay Area. And he was open to the possibilities of alternative treatments.

So I called Professor Mitchell Sokoloff in Chicago and he was gracious enough to spend a lot of time on the phone with me, and then kept up an email correspondence. He also recommended Professor Peter Carroll, chairman of the urology deparment at UCSF as a world class surgeon and good person. I felt good getting an independent, knowledgeable person with no axe to grind or self-interest to promote as a foil to my ideas and discoveries.

I spoke with Steven Hancock, MD, at the Stanford Radiological Oncology facility. We spoke of the different forms of radiation, of what they did there, and of survival rates, long term and short term, as well as the side effects of the treatment. When he finally showed up, an hour and a half late for our appointment, he was willing to spend as much time with us as we needed as well as to provide reprints of research he had been involved with on long-term survival rates.

I spoke with Dr. Gill, the Stanford urology surgeon who inherited Dr. Freiha's mantle as the most skillful surgeon there. But he was a rather closed individual, unwilling to even look at some research we had brought for his consideration. He may have been a skilled mechanic, but I wanted to be treated as a person rather than as a slab of meat.

I spoke with Professor Peter Carroll at UCSF, first a long telephone conversation and then in person. He is not only an expert on the nerve sparing forms of radical prostatecomy, but is involved in various kinds of research on prostate cancer, including some studies with colleagues on dietary approaches, including Dr. Dean Ornish's program at the  Preventive Medicine Research Institute in Sausalito, Calif. He was very open to following along with my program, although he also felt that, at best, I'd only be postponing the inevitable. My wife and I felt that we could work with him as a partner, whether I opted for surgery in the end, or if I could avoid it forever.
 

Talking

We talked with prostate cancer survivors, learned their stories, their lessons, their contacts. This includes my friend who is into 7 years post-op (as of Autumn 2000) and doing quite well. I also started attending the monthly meetings of a local prostate cancer support group where I could learn from others' experiences as well as help educate people about what I found or knew. This paper is based on a short talk I gave my third month there.
 

Radical Prostatectomy

This is the medical option we initially decided to pursue, if we had to pursue any medical option. Our reasoning was this. First off, by the medical criteria, I was a prime candidate for surgery: I am young, healthy, not overweight, with a small, early stage tumor. This means I'd be easy to operate on, would likely recover quickly from the surgery, and it would be very probable that the entire cancer would be removed in the procedure.

Side effects of incontinence and impotence, however, are significant, even with the best of nerve sparing surgeries and surgeons. (A recent study [Siegel, et al., Journal of Urology, vol 165, no 2, pp 430-435 (Feb 2001)] found that "Erectile dysfunction develops in greater than 80% of the patients treated for prostate cancer" whether by surgery or external beam radiation.)

Radiation therapies (seed implants of various types, external beam Xrays or proton beams) as well as cryotherapies are less invasive, but also lead to similar complications and side effects. They come on a bit more gradually, but in the end roughly 30-50% of men who have undergone either approach are impotent (depending on whose statistics you read) and 10% have some form of incontinence, whether mild and annoying or severe and limiting.

The downside of radiation is the long-term survival statistics relative to surgery. Both are comparable out to about 10 years for "best practice". (Reference) After that, folks who have had radiation do not, on the average, survive as long or have as a high a percentage who remain prostate cancer free. This may not be as great a consideration to, say, an 80 year old with heart problems, but to me, with my intent to live another 40 or more years, it is an important consideration.

Another consideration is that surgeons do not like to operate on someone who has had radiation, if their prostate cancer recurs. This is because the radiation has toughened the tissue of and surrounding the prostate, which makes the surgery a little more difficult. Such "salvage surgery", however, is done by some surgeons.

In the end, physical removal of the organ and the cancer seemed like it would be more effective than trying to kill the cancer cells via some other modality. With improved surgical and post-operative techniques, I had hoped that the negative consequences of the procedure could be minimized, if not eliminated. And having found Dr. Peter Carroll gave me some assurances that I had found a master craftsman with a lot of experience and who I could work with, if or when I chose that route.
 

Aggressive Monitoring/Active Surveillance

The question to be addressed here is, How do you know whether your approach is working or not, whether the cancer is disappearing, being held in check, or growing and merits a more radical approach?

The answer is, figure out what techniques and technologies allow one to "see" what is happening with the cancer and sample often enough to follow its course and fluctuations. And do so with a greater frequency than the physicians might recommend. Again, you must be your own best advocate.
 

PSA
There are a number of approaches. The first and most obvious is following my PSA levels. These I have taken roughly every month (versus the every 3 months that was suggested by my urologist). PSA, as discussed elsewhere here, is a proxy for the growth of cancer, in general. But not always. In some men, prostate cancer abounds with a low PSA level. In others, elevated PSA is a result of non-malignant causes. I suspect both these situations do not occur too often, but with a high enough frequency to have been noted. My PSA rise seems to have been an appropriate tip-off that something was awry.

Another consideration with PSA is that herbs such as saw palmetto, one of the things I started taking, tend to lower the levels. This is probably a good thing. But is it just masking the cancer or is it really fighting it? I haven't heard any answers to that question.

So, this is one easy step in following how things are going. By and large, since I started my program and PSA monitoring, it has been 2.0 ng/ml +/- 10%, the fluctuation range I was told to expect and within the "normal" reading I had pre-cancer.

It should be noted that as a man ages, his prostate gland starts growing. So a larger normal gland, putting out a roughly constant amount of PSA protein per unit volume, will, over the years result in higher PSA values overall. That is why the "normal" ranges are larger as men get older. The rise in my PSA with the years, especially after mid-2008 (9 years after diagnosis), is consistent with this and not alarming.
 

DRE
The DRE is a traditional way to find cancers that have grown to palpable size on the back wall of the prostate. But it is useless in detecting small cancers such as mine until they are quite a bit more advanced. Since I want to prevent mine from getting to that stage, the DRE would be a null test, basically a waste of time.
 
TRUS
Likewise, a Trans-Rectal UltraSound, while able to image more of the prostate, is also a rather crude imaging tool. Its resolution is poor and its sensistivity to growths in the gland is also not very good. It is better than the DRE for detecting physical abnormalities, but again, it is incapable of detecting cancers as small as mine. So, this, too, does not seem like a useful avenue to pursue.
 
MRI Spectroscopy
This is a technique pioneered at the University of California, San Francisco by Professor John Kurhanewicz and his colleagues, and recently (winter 2000?) begun on an experimental basis at Memorial Sloan-Kettering in New York City. It combines magnetic resonance imaging of the pelvic region with a superimposition of spectroscopic data that are very sensitive to prostate cancer cell metabolism. A coil is inserted in the rectum and a pickup is placed on the abdomen while one is in a strong field magnetic resonance imaging device. The closeness of the probe to the region being imaged allows the resolution of the MRI images to be 0.5mm x 0.5mm pixels, with slices about 3mm apart. The software transforms the geometries to be faithful representations in two dimensions, unlike the ultrasound images.

The spectroscopic part is done simultaneously. Here the returned radiofrequency radiation is analyzed and the energy in various frequency bands calculated. There are particular regions indicative of the amount of activity in the citrate cycle (one path of cellular energy utilization), of choline metabolism, creatine levels, and of some other distinct cellular metabolic processes. Combined, these are very sensitive to the nature of the cells in the voxel (volume element) being sampled. The sampling can distinguish among

The sensitivity is very high although the spatial resolution is much lower than the MRI imaging itself. The spectroscopic voxels are approximately 1/4 cc, which translates to cubic volumes of 6.25 mm on each side. The coarser resolution is due to the need to subtract out the higher (dominant) water background to be able to discern the other, weaker, peaks.

With the 3 Tesla machine, under development since 2003 (and still in test as of Aug 2004), the spatial and volumetric resolution is much better: voxels are now 0.16 cc, translating to a cube with sides roughly 5.5 mm.
 

September 1999 Imaging
I had my first MRIS done on 1 September 1999, roughly 6 weeks after my second set of biopsies. Biopsies are violent attacks on the gland and cause some amount of internal bleeding where the samples are taken. Blood accumulates in and near the prostate and it may take a couple of months for it to fully dissipate. And this blood confounds the imaging, making it more difficult to interpret whether there is some abnormality in the gland or whether what is being seen is merely an artifact. Such was the case on my first imaging. The imaging did confirm the presence of cancer, more on the right side (where the biopsies discovered it), with scattered evidence of possible cancer in the left side. It showed no penetration of the capsule (a thin membrane enclosing the prostate gland) or external evidence of cancer in lymph nodes, seminal vesicles, or bones. There was a question about whether some of what the images showed was cancer near the capsule (edge of the gland) or just blood.
 
April 2000 Imaging
My second MRIS was done on 3 April 2000, 7 months after the first. All bleeding-related artifacts were gone, although the cancer was still there. It was confined near the mid-line, a bit more on the right than left. It was difficult to compare the true extent with September's images due to the confounding effects of the earlier bleeding. Overall, there were no abnormalities noted in the high resolution images. At that resolution, my gland was both small and healthy looking.
 
November 2000 Imaging
My third MRIS was done on 3 November 2000, another 7 month interval. The state of my gland was essentially unchanged from April's imaging. The gland was small (34 cc) and healthy looking in the imaging part, with some color differences from "normal" from the midgland to the apex [bottom] near the midline; most of this was not supported by the spectroscopic component of the imaging. However, there was a small amount of malignant tissue metabolism still detected at the apex near the midline, unchanged from April.

And, there is no sign of any disease outside the prostate nor at the capsule (the boundary of the gland).
 

April 2001 Imaging
My fourth MRIS was done on 19 April 2001, 2 weeks after a PSA reading of 2.6. The imaging showed a gland of 39 cc (and a PSA density of 0.06). It showed some enlargement of the central gland, consistent with BPH, and some evidence of prostatitis, even though I was symptom-free. The gland was about 5 cc larger than 5 months previous.

There was one voxel of borderline cancer metabolism. In previous images, there were several voxels of borderline metabolism, all within the right mid gland. "The spectroscopic abnormalities are much less evident on the present study." And later, "The spectroscopic findings are much less apparent on the present scan, suggestive of positive treatment response."

And again, there was no sign of any disease outside the prostate nor at the capsule (the boundary of the gland). All good news, indeed.
 

January 2002 Imaging
My fifth MRIS was done on 9 January 2002, a few hours after a PSA reading of 8.64. (On 11 Jan, PSA was 6.70; on 15 Jan it was 5.43; on 21 Jan it was 5.45.)

This imaging showed a number of voxels in the right midgland with abnormality, changes in all 3 markers (decreased citrate, elevated choline, ...[?] polyamines). Prostate volume was 33 cc (smaller than previous images). The radiologist's report states "The focus at the right base is more apparent as compared with the prior examination....MR spectroscopy demonstrates interval development of a small focus of tumor metabolism at the right base."

Further discussions, informed by my experience with asymptomatic prostatitis in May 2001, led to my being told that an acute infection could lead to these signals. [Most men with prostatitis have chronic infections, which present differently in the MRIS. The primary researcher said he had seen acute prostatitis only 2 or 3 times out of the several thousand images he had looked over in his career. However, he declined the opportunity to reimage me immediately after my course of antibiotics, foregoing the possibility of developing a before and after to allow better discrimination between acute prostatitis and cancer.] In order to rule that out, or to deal with it, I started on a 2 week course of Cipro, a powerful antibiotic, on 23 January 2002, followed by a second 2-week course. As one can see from the graph and table in the beginning of this paper, my PSA came down to around 2.4 after 3 weeks, stayed there for a couple of months, and then returned to my "normal" levels of about 2.0 ng/ml. I conclude from this that the anomolous readings in this set were another episode of asymptomatic prostatitis.
 

July & September 2002 Imaging
My sixth MRIS was done on 22 July 2002. About an hour and a half before the test, I had blood drawn at Stanford Hospital; the PSA was 2.16 ng/ml. I also had blood drawn at UCSF; the PSA was 1.63 ng/ml. Go figure.

There was no evidence of any metabolic abnormality in the Spectroscopic analysis. That is, no evidence of any cancer. The radiologist concluded that all abnormalities seen in the previous image of 9 Jan 2002 were due to prostatitis rather than cancer, and that all had resolved themselves in the interval. The gland measured 36 cc; using the Stanford PSA of 2.16 ng/ml, my PSA density was 0.060 ng/ml/cc.

My previous images will hopefully be of some help in allowing the research team to come up with a scheme for differentiating prostatitis from cancer. Since they have few unambiguous images of acute infection, all the data they can get will help.

This finding does not necessarily mean all my cancer is eradicated. Rather, it has regressed to the point that this imaging technique is unable to see it amidst the surrounding healthy tissue. As a consequence, I do not plan of changing my regimen.

On 9 September 2002 I had a color doppler TRUS by Dr. Katsuto Shinohara at UCSF. Absolutely no abnormalities or suspect areas were seen. Dr. Shinohara said that "power doppler ultrasounds" that I had heard of were exactly the same as what he was using. It was a relief to have both imaging modalities confirm that any remnant cancer is too small and inactive to be picked up by these techniques. Prostate size was estimated to be about 40 cc; using the previous PSA of 2.08 ng/ml, my PSA density was 0.052 ng/ml/cc. He also noted "about 14 cc of transient hypoplasia", something I need to have clarified.
 

June 2003 Imaging
My seventh and eighth MRSIs were done on 16 June 2003. The first was a standard exam, done at UCSF on their 1.5 Tesla GE machine. The second was done that same afternoon at a 3 Tesla GE machine installed at SRI in Menlo Park, CA. The latter's magnetic field strength is twice that at UCSF, and so allows for higher resolution images, better spectroscopy and/or faster acquisition times. It is being calibrated and I volunteered for a side-by-side comparison study as the scientists and operators try to arrive at the best settings for the highest quality imaging.

The MRI images both showed no abnormalities. In the right midgland region, the images were a little darker than normal, but nothing notable. (Recall that previous imaging and the biopsies indicated cancer metabolism in the left midgland, where there is now no evidence of cancer.) The gland volume was estimated to be 38.0 cc; using the PSA value of 2.18 ng/ml, the PSA density was 0.057 ng/ml/cc.

Spectroscopically, in both images, in the right base to midgland, there was an alteration in the expected normal metabolism. Here, however, there was no elevation of the choline signal, there was a loss of some SNR [signal to noise ratio], and there was a loss of citrate levels. These are less a sign of cancer than a possible signal of chronic prostatitis, especially considering how these signatures come and go from image to image over the years.

I had another power doppler TRUS on 04 August 2003 with Dr. Shinohara at UCSF for an independent corroboration of the MRSI results. Again, no signs of cancer were apparent. The gland had grown some (see table below), but showed no signs of malignancy. The left midgland showed a persistant hypervascularity (increase above normal of amount of blood vessels). This is the same area that the June 2003 MRSIs showed signs of lingering possible prostatitis. Recall that the positive biopsies were originally in the right midgland, far from this region.

On 07 June 2004, I had my next power doppler TRUS with Dr. Shinohara at UCSF. The prostate volume was about 48 cc; the year before it was about 46 cc by TRUS. This was essentially the same size. Dr. Shinohara stated that the MRSI underestimates the size by about 20% relative to the TRUS. [The corresponding MRSI volume would thus be about 37 cc.]

He also saw a small protrusion of the prostate into the bladder on one side, indicative of mild BPH. There were a couple of small areas of hypervascularization [that is, increased blood flow], one on each side, but he did not feel that they were large enough or strong enough to be of concern. And he mildly suggested another biopsy, which I resisted and we discussed.
 

August 2004 Imaging
My ninth and tenth MRSI images were done on 5 August 2004. In the morning, I was imaged in the new 3 Tesla GE machine at UCSF's new China Basin facility in San Francisco. In the afternoon, the same protocols were used at their standard 1.5 Tesla machine at their original facility. As in the previous year, a side-by-side comparison allows both validation and improvement to the settings used in running the machine as well as in the software used for post-run analysis.

The 3 Tesla images provided a much higher spatial resolution than the 1.5 T images, and both sets were in concordance. The news again was good - no signs of cancer, no changes from the previous imaging, to the limits of the technique's resolution. Recall that my biopsy found some small amounts of cancer in the right midgland in July 1999. None of that has appeared in the images for quite some time, so is not growing, if still present at all.

Again, the radiologist noted "a small focus of decreased T2 signal within the right midgland with equivalent signal on MR spectroscopy." In this region of the gland there is a mix of stromal cells and glandular cells. The glandular cells create the prostatic fluid which flows down the local ducts, eventually accumulating in the seminal vesicles and the ejaculate. This fluid has lots of free water. The T2 imaging measures the morphology or anatomy by looking at water. Lots of free water implies a very long T2 relaxation time.

In prostate cancer, the glandular cells are the ones that become malignant, in general, and the ducts get filled with cancerous growth. This leads to less water being present and a darkening in the T2 weighted image. However, other things can cause this as well, and so spectroscopy is used to try to differentiate what is going on. In my case, this same area has "equivocal metabolism", the same as in previous images, though different from when I was imaged during a bout of prostatitis. So there is no obvious cancer signal and no changes over several years, all good news. Only a biopsy of that region could serve to differentiate histologically what is really going on there, but for me there is currently no incentive to do so -- the potential gain of knowledge would not inform any decision to do anything. If any cancer is still invisible to MRSI and TRUS and my PSA levels are relatively static, I should just keep on doing what I'm doing.
 

March 2006 Imaging
My eleventh MRSI was done in the 3 Tesla GE machine at UCSF's China Basin facility on 6 March 2006. Because of the prostatitis that seemed to be running in my system from December 2004 through around August of 2005, we decided to wait until my PSA returned to its "normal" levels and stabilized there before doing another set of images. This is because prostititis often looks like cancer in the spectroscopic images and we did not want to confound the interpretation process.

I received a CD-ROM of the non-spectroscopic images, along with WindowsXP software for looking at them, when I left the imaging session, and a more complete CD-ROM with all my images from all MRSIs by mail a week or so later. The CD-ROM now includes a Windows-based image viewing program, with an on disk manual for how to use the software. Still, interpreting the images is another issue altogether, and guidance should be provided there, too. The CD-ROM should also include the spectroscopic images, which take additional processing, but are now also available to the subject.

The radiologist report took about a week to be drafted. It contained very little information -- seemingly, less and less each time -- but the bottom line is that there have been essentially no changes since my previous images, in fact, almost no changes for several years. This is good, as there are also no signs of cancer. On the side opposite where my biopsy found a little cancer, there are some changes again, likely due to inflammation. ("A small band-like area of decreased T2 signal is seen in the left mid gland, which extends towards the apex. This may represent prostatitis.")

The rise in my PSA (at Stanford) to 3.27 ng/ml on the day of the exam is of concern. It may be the beginnings of another round of asymptomatic prostatitis. I doubt that it is an artifact of a URI (upper respiratory infection, a cold) I was just getting over at the time.
 

March 2007 Imaging
On 5 March 2007 I had my twelth MRSI using the 3 Tesla machine at UCSF's China Basin facility. The new aspect to this imaging session was the use of a Gadolinium contrast agent for the last set of images. Gadolinium is a common contrast agent used in MRIs and is administered intravenously. It makes cancerous tissue easier to see. This was also to be a baseline imaging session before I started taking Peenuts as a supplement to try to reduce or eliminate my background chronic (asymptomatic) prostatitis inflammation.

The results were the best yet. Essentially, there were still no signs of cancer, a small region of ambiguous signal previously seen in my images was even smaller and more difficult to discern. There were no detectable metabolic abnormalities.

February 2008 Imaging
On 29 February 2008 I had my thirteenth MRSI using the 3 Tesla machine at UCSF's China Basin facility, this time with no contrast agent. I reviewed preliminary images with a radiologist after the imaging session. (The spectroscopic images require additional processing and take an extra three days or so to be developed, according to him.) Everything looked "normal", with no significant changes from previous images (which are also available on their computer system for comparisons).

The written radiology report also noted that the "[p]reviously described focal area of low T2 signal within the right midgland is no longer seen in the current study... MR spectroscopy demonstrates no definite abnormality.... No definite MR or MRS evidence of tumor."

The biopsy I had in 1999 found tumor in the left midgland, which never showed up in the MRSI imaging I have had. However, there have been low level ambiguous signals in the right midgland in all images up until the February 2008 imaging. I take this to indicate some improvement in an undefined irregularity there.

After the imaging, I also was interviewed by a Product Manager from MedRad, a company that makes the transrectal probe used in the MRSI procedure. The videotape is to be used in educational videos on the process and technology from a patient's point of view.

March 2009 Imaging
On 31 March 2009 I had my fourteenth MRSI using the 3 Tesla machine at the new UCSF Mission Bay campus, at Byers Hall, also with no contrast agent. A new rigid endorectal probe was used as part of the qualification of the technology. In particular, in addition to looking at signals from hydrogen (mostly in water), it also was looking at signals from Carbon-13.

Again, the radiologist's report stated: "MR imaging and MR spectroscopy demonstrate no convincing evidence of tumor. There is no extracapsular extension or seminal vesicle invasion. No lymphadenopathy is seen in the pelvis.... No suspicious osseous lesions identified."

March 2010 Imaging
On 16 March 2010 I had my fifteenth MRSI using the 3 Tesla machine at the new UCSF Mission Bay campus, at Byers Hall, also with no contrast agent. A new rigid endorectal probe was used again as part of the qualification of the technology. In particular, in addition to looking at signals from hydrogen (mostly in water), it also was looking at signals from Carbon-13.

Again, the radiologist's report stated: "...no clear cut tumor metabolism is observed. No extracapsular extension, no seminal vesicle invasion, no lymphadenopathy, no suspicious bone lesions.... Compared to the study from 03/2009, no significant change. No tumor focus in either MR or MR spectroscopy."

March 2011 Imaging
On 28 March 2011 I had my sixteenth MRSI using the 3 Tesla machine at the UCSF China Basin facility. Again, no contrast agent was used. My reported prostate size was much larger than the previous year (67 cc versus 47.4), and will be recalculated. (See the note below.)

Signs of BPH were clear, both spectroscopically and morphologically (the shapes of elements in the regular imaging). Again, there was the "equivocal metabolism" in the right base to mid-gland. This is not a sign of cancer, but not normal cells either. For the most part, it has been present in my images from the beginning, growing and shrinking. It is likely a sign of an underlying inflammation or infection that never quite goes away. There were no significant changes from the last year's MRSI, which is a consistent motif in the radiologist reports over the years.

April 2012 Imaging
On 4 April 2012 I had my seventeenth MRSI using the 3 Tesla machine at the UCSF China Basin facility. Again, no contrast agent was used. My reported prostate size was larger than in previous years, and I am sure a recalculation would reduce this size somewhat.

Again, "extensive changes related to benign prostatic hypertrophy with associated nodules" were noted. These nodules were "unchanged compared to prior exams, and [do] not demonstrate any other diffusion or spectroscopic abnormality." And, "No change compared to prior exams."

March 2013 Imaging

On 20 March 2013 I had my eighteenth MRSI using the 3 Tesla machine at the UCSF China Basin facility. This time, a gadolinium contrast agent was used for the final set of images, after the spectroscopy.

Again, there were no signs of cancer (or prostatitis), but the radiologist noted "extensive changes related to benign prosthetic hypertrophy [BPH], with associated nodules." As can be seen from the table below, my gland continues to grow.

April 2014 Imaging

On 21 April 2014 I had my nineteenth MRSI using the 3 Tesla machine at the UCSF China Basin facility. This time, a gadolinium contrast agent was used for the final set of images, after the spectroscopy.

The radiology report noted that my gland continued to grow and that "the central gland (transitional zone) [signal intensity] is related to benign prostatic hyperplasia" or BPH. In addition, there was no evidence of extension beyond the prostate gland, seminal vesical, lymph node or bone involvement.

While there is "no clear abnormal spectroscopy" in the right apex region, a "decreased T2 signal" may be "suspicious for focus of prostate cancer". Again, an ambiguous signal, which may also be an artifact of the prostatitis I had from September to Decemeber of 2013.

In the subsequent imaging, April 2015, this signal from the right apex was absent, an indication that this was inflammation and not cancer.

April 2015 Imaging

On 23 April 2015 I had my twentieth MRSI using the 3 Tesla machine at UCSF's new Bakar Cancer Center in Mission Bay, San Francisco. Gadolinium contrast was again used for the final images in the sequence.

The radiology report discussed a 13 mm focal lesion in the left posterolateral peripheral zone and the midgland/apex, which had not been seen in previous images. On review of the 2014 images, a tiny amount of signal was seen in the diffusion images in this region, but it was unremarkable at the time (i.e., not significant enough to make remarks about). Four of the seven parameters that current imaging technology provides are consistent with cancer -- or inflammation. It is still difficult to differentiate prostatitis from cancer on the images. If cancer, the imaging is consistent with Gleason 3, a slow growing cancer. It was suggested that I continue active surveillance and wait another year for my next imaging.

The change in prostate volume, from 56 cc in 2014 to 75 cc in 2015 is also suspicious. The folks in radiology reexamined the images to derive better volume estimates for both years, which impact the PSA density calculations. Given the current numbers (PSA 8.1 in Feb 2015, volume of 75 cc), my PSA density is 0.108, well within the "safe" range of <0.15.

Note: because the jump in volume as measured by the radiologist from year to year was unreasonably large (56 cc to 75 cc), I asked the researchers to recalculate the 2014 and 2015 volumes more accurately. The 2014 volume was changed to 56.3 cc. The 2015 volume was changed to 60.72 cc. This leads to a PSA density in 2015 of 8.1/60.72 = 0.133.

June 2016 Imaging

On 03 June 2016 I had my twenty-first MRSI using the 3 Tesla machine at UCSF's new Bakar Cancer Center in Mission Bay, San Francisco. Gadolinium contrast was again used for the final images in the sequence.

The radiologist's report noted that the central gland is consistent with benign prostatic hyperplasia (BPH). It also noted again a lesion in the left anterior peripheral zone (1.1 cm x 0.57 cm x 0.8 cm) with a well defined focus of low signal intensity on T2-weighted imaging, marked restricted diffusion and suspicious enhancement (DCE positive). However, on spectroscopy, no suspicious metabolism is seen in the lesion.

On consultation with the researchers, the suspicious area from 2 years ago had vanished (the left peripheral zone), and the new one (left apex peripheral zone) appears with 4 weak signals, but no spectroscopic signal. This can be prostatitis and seems not something to worry about since PSA is steady and PSA density remains steady and within the safe range as well.

The radiology report stated the gland volume was 78.1 cc; on request for a remeasure from the images, a radiologist came up with 82.4 cc and a researcher who had recalculated my PSA volume in the past came up with 73.9 cc. All of these, of course, are estimates.

June 2017 Imaging

On 9 June 2017 I had my twenty-second MRSI using the 3 Tesla machine at UCSF's Bakar Cancer Center in Mission Bay, San Francisco. Gadolinium contrast was again used for the final images in the sequence.

Again, the radiologist's report noted that the central gland is consistent with benign prostatic hyperplasia (BPH). The 1.1 cm lesion seen last year in the left peripheral zone could not be seen at all this time in either T1, T2 or diffusion weighted imaging.

No suspicious metabolism (indicative of cancer) could be seen anywhere. There were no signs of extension outside the prostate capsule, into lymph nodes, seminal vesicles or bones.

The PI-RADS score was assigned a value of 3, indicating that something is suspicious but cannot be classified as cancer. This is consistent with low grade asymptomatic prostatitis which can look like prostate cancer in these images. The fact that lesions come and go and that my PSA density is consistently arount 0.10 enhances this interpretation.

The prostate volume estimated was 91.2 cc. This year I did not have a more accurate recalculation done.

June 2018 Imaging
On 12 June 2018 I had my twenty-third MRSI using the 3 Tesla machine at UCSF's China Basin facility in San Francisco. Gadolinium contrast was again used for the final image in the sequence.

The prostate volume was estimated to be 100.6 cc. With my most recent PSA of 7.68, that leads to a PSA density of 0.07 ng/ml/cc, indicating no cancer is present.

To quote the report:
  Heterogeneous appearance of the central gland is consistent with benign prostatic hyperplasia.
  No suspicious lesions identified on MRI.
  Capsular margin and neurovascular bundle: No evidence of macroscopic extracapsular extention.
  Seminal vesicles: No evidence of seminal vesical invasion.
  Lymph nodes: No lymphadenopathy in the field of view.
  Bones: No suspicious lesions in the field of view.
  ...
  IMPRESSION:
  -PI-RADS v2 score 2: clinically significant cancer is unlikely to be present.
  -The lesion identified previously is even less conspicuous and may have represented sequelae of prostatitis.

June 2019 Imaging
On 20 June 2019 I had my twenty-fourth MRSI using the 3 Tesla machine at UCSF's Mission Bay facility in San Francisco. Gadolinium contrast was again used for the final image in the sequence. This was the first image where an endorectal probe was not used. Rather, I lay on top of a probe plane and had another placed over my abdomen. (This later was the same as in all prevous images.) The technician explained that new hardware and software allowed faster and sharper images to be taken without needing to use the endorectal pickup device. In fact, the imaging session took about 40 minutes as opposed to previous ones which took an hour to an hour and twenty minutes, depending on which images were being taken.

The prostate volume was estimated to be 100 cc. With my most recent PSA of 9.0, that leads to a PSA density of 0.09 ng/ml/cc, indicating no cancer is present.

To quote the report:
  Heterogeneous appearance of the central gland is consistent with benign prostatic hyperplasia.
  Capsular margin and neurovascular bundle: No evidence of macroscopic extracapsular extension.
  Seminal vesicles: No evidence of seminal vesical invasion.
  Lymph nodes: 8 mm left pelvic sidewall node...
  Bones: No suspicious lesions in the field of view.
  ...
  IMPRESSION:
  -PI-RADS v2 score 2: clinically significant cancer is unlikely to be present.
  No evidence of macroscopic extracapsular extension. No evidence of seminal vesicle invasion.
  Nonspecific 8 mm left pelvic sidewall lymph node. No suspicious bone lesions.
  No change from 2018.

July 2020 Imaging
On 7 July 2020 I had my twenty-fifth MRSI using a 3 Tesla machine at UCSF's China Basin facility in San Francisco. This is a strictly radiology facility, so there was minimal liklihood of exposure to Covid-19. There were also few people at the facility, unlike in years past.

Again, there was no endorectal probe and the imaging session took only about 40 minutes. Aside from the prostate having grown slightly from last year (from 100 to 107.5 cc), consistent with its trend over the years (see the table below), results were essentially unchanged from those quoted from the 2019 report, above. Again, "No significant changes seen since the prior MRI."

July 2021 Imaging
On 08 July 2021 I had my twenty-sixth MRSI using a 3 Tesla machine at UCSF's China Basin facility in San Francisco, including, as usual, one set of images taken with Gadolinium contrast. There were still Covid precautions (mostly masking of staff and visitors) in effect.

Again, there was no endorectal probe and the imaging session took only about 40 minutes. Aside from the prostate having grown slightly from last year (from 107.5 to 115 cc), consistent with its trend over the years (see the table below), results were essentially unchanged from those quoted from the 2020 report (and previous reports), above. Again, "No significant changes seen since the prior MRI." And, "PI-RADS v2.1 score 2: clinically significant cancer is unlikely to be present."

August 2022 Imaging
On 07 August 2022 I had my twenty-seventh MRSI using a 3 Tesla machine at UCSF's Mission Bay campus in San Francisco, including, as usual, one set of images taken with Gadolinium contrast. There were still Covid precautions (mostly masking of staff and visitors) in effect.

Again, there was no endorectal probe and the imaging session took only about 40 minutes. Aside from the prostate having grown slightly from last year (from 115 to 117 cc), consistent with its trend over the years (see the table below), results were essentially unchanged from those quoted from the 2020 report (and previous reports), above. Again, "No significant changes seen since the prior MRI." And, "PI-RADS v2.1 score 2: clinically significant cancer is unlikely to be present."

September 2023 Imaging
On 14 September 2023 I had my twenty-eigth MRSI using a 3 Tesla machine at UCSF's China Basin facility in San Francisco, including, as usual, one set of images taken with Gadolinium contrast.

Again, there was no endorectal probe and the imaging session took only about 40 minutes. Aside from the prostate having grown slightly from last year (from 117 to 118 cc), consistent with its trend over the years (see the table below), results were essentially unchanged from those quoted from the 2020 report (and previous reports), above. Again, "No significant changes seen since the prior MRI." And, "PI-RADS v2.1 score 2: clinically significant cancer is unlikely to be present."

September 2024 Imaging
On 17 September 2024 I had my twenty-ninth MRSI using a 3 Tesla machine at UCSF's China Basin facility in San Francisco, including, as usual, one set of images taken with Gadolinium contrast.

Again, there was no endorectal probe and the imaging session took only about 30 minutes (a new and slightly faster machine). Aside from the prostate having grown a bit from last year (from 118 to 133 cc), consistent with its trend over the years (see the table below), results were essentially unchanged from those quoted from the 2020 report (and previous reports), above. Again, "No significant changes seen since the prior MRI." And, "PI-RADS v2.1 score 2: clinically significant cancer is unlikely to be present."

September 2025 Imaging
On 18 September 2025 I had my thirtieth MRSI using a 3 Tesla machine at UCSF's China Basin facility in San Francisco, including, as usual, one set of images taken with Gadolinium contrast.

Again, there was no endorectal probe and the imaging session took only about 30 minutes (a new and slightly faster machine). Aside from the prostate having grown a bit from last year (from 133 to 142 cc), consistent with its trend over the years (see the table below), results were essentially unchanged from those quoted from the 2020 report (and previous reports), above. Again, "No significant changes seen since the prior MRI." And, "PI-RADS v2.1 score 2: clinically significant cancer is unlikely to be present."

The next imaging, probably to be done around September 2026, should again be easy to compare with the current images and a progress/regress of the cancer should be discernible.
 

Prostate Size and PSA Density
Date 09/01/1999 04/03/2000 11/03/2000 04/19/2001 01/09/2002 07/22/2002 06/16/2003 08/04/2003 06/07/2004
Prostate Size
cc
?? ?? 34 39 33 40 38 46
TRUS
48
TRUS
PSA Density
ng/ml/cc
?? ?? 0.065 0.067 0.26
prostatitis
0.060 0.057 0.047 0.040
Date 08/05/04 03/06/06 03/05/07 02/29/08 03/31/09 03/16/10 03/28/11 04/04/12 03/20/13
Prostate Size
cc
46 49.2 42.3 45.0 37.0 41.5 39.9 50.4 54.1
PSA Density
ng/ml/cc
0.055 0.074 0.103 0.089 0.15 0.111 0.146 0.093 0.135
Date 04/21/14 04/23/15 06/03/16 06/09/17 06/12/18 06/20/19 07/07/20 07/08/21 08/07/22
Prostate Size
cc
56.3 60.72 73.9 91.2 100.6 100 107.5 115 117
PSA Density
ng/ml/cc
0.131 0.133 0.111 0.110 0.076 0.090 0.122 0.086 0.060
Date 09/14/23 09/17/24 09/18/25            
Prostate Size
cc
118 133 142            
PSA Density
ng/ml/cc
0.059 0.062 0.066            

[Notes on Prostate Volume and PSA Density]

On 7 September 2004, I received a phone call from one of the UCSF researchers. I was concerned about the apparent growth in size of my prostate over the previous five years and had discussed this issue with Professor John Kurhanewicz at UCSF. His team had reanalyzed my images from 1999 to the present and found, with a more detailed and precise analysis, that my gland volume was essentially unchanged, approximately 36 +/- 3 cc. In general, the radiologists apply a simple curve fitting algorithm to estimate the gland volume, and there are approximations and room for error in the process. This recalculation also has implications for estimated PSA density; the numbers in the table above have not been corrected for the "constant" gland volume.

In 2011 I again had my prostate volume recalculated by a more accurate technique. The 2010 original value of 47.4 cc was adjusted to 41.5, and the original 2011 value of 67.0 cc was adjusted to 39.9 cc. These are significant differences. I am sure the 2012 value of 50.4 would also be adjusted downward if more accurate techniques were used. But these take a little more human effort to perform.

In any event, the growth of my gland would explain the gradual rise in background PSA -- there is more healthy tissue (or BPH tissue) to generate PSA.

[Note added 3 April 2013 after a conversation with Nanette Perez, RN at UCSF Urologic Oncology Dept.] PSA density has come to be considered a more important indicator of prostate health in recent years. Any value less than 0.15 is indicative of a healthy prostate, one not excreting more PSA per unit volume than expected. Higher values may be indicative of cancer or of prostatitis. This calculation is obviously sensitive to the proper calculation of PSA volume. Consulting the above table, all my PSA density values have been "good" ones so far.


 
UCSF Protocol
The UCSF protocol for aggressive monitoring or Active Surveillance (as I remember it) is This involves a number of ways of tracking the existence and growth/regression of the cancer, using blood markers and physical imaging, as well as grabbing cell samples for histology. Each modality serves to corroborate the others, while providing somewhat independent means to avoid measurement errors or blind spots in any one method. Except for the repeat biopsies (as noted above), this seems reasonable to me. It may be contrasted with the PRIAS (Prostate cancer Research International: Active Surveillance) Project, a European approach using only PSA and biopsies.

The important point in this is not to remain passive and ignorant, but to keep track of how well life style and other changes are keeping the cancer in check, to buy time for better medical approaches to emerge, and to avoid, as long as possible, the side effects of any medical treatments, noting that many prostate cancers are overtreated and may likely remain indolent for the rest of your life.
 


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The Theory

The concept behind what I put together was to engage and enhance my immune system's response to the cancer by as wide a variety of methods as I could. The general approach is discussed in Dr. Andrew Weil's book, Spontaneous Healing, which I came across a couple of months into this process.

The basic idea is that cells are constantly undergoing division in the body. Statistically, it is likely that some small fraction of these divisions are incorrect, producing malignant cells. This can be due to a variety of factors, including

Many of these mutant cells are not viable and die. Many have benign or irrelevant changes. But some fraction become malignant, depending on the accumulated mutations in the cellular DNA.

In general, the immune system is capable of finding and killing all these cells since cancer is a rather rare disease compared to all the cell divisions that occur in a body over its lifetime. What I was seeking to do was augment and increase the functioning of my cellular immune system, since my malignant load was higher than the "normal" background and additional help was needed. But, if I could succeed at that, I could, at best, eradicate the cancer; at the middle, keep it at bay and treat it like a chronic, non-life threatening disease; and at worst, buy some time for medical techniques and options to improve, as they have been rapidly over the past few years.


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Vitamins and Herbs

The first pillar of my program is the use of vitamins and supplements. Over the course of the years I had gradually increased the variety and quantity of what I had taken, even though I am a firm believer of getting as much proper nutrition as you can from good, fresh, wholesome food.

As a background, this is what I had been taking for years:

Vitamins C and E are well known to be important anti-oxidants, helping repair cellular and nuclear damage due to free radicals. Linus Pauling, a great advocate of vitamin C, once noted that humans are the only primate species that does not produce vitamin C endogenously. And based on the production of our nearest species relatives in terms of milligrams/kilogram body weight, he advocated that we humans take between 2 and 17 grams per day. He stayed on the high side and lived a very productive life until the age of 93.

Vitamin C is one vitamin that you cannot overdose on. Any extra amount that your body cannot use is excreted, so it is useful to spread out the dosages over the day. It should also be noted that if you increase the amount you take too rapidly, a possible side effect is diarrhea, so a gradual increase is to be recommended, allowing one's body to adjust.

The vitamin A was suggested to me some years back by my dermatologist to clear up a minor skin problem. It also has good anti-oxidant effects. However, one can overdose on A, and so should be careful about the doses taken.

Gingko is noted as helping increase blood flow. This is why it is often referred to as a memory enhancer (blood flow in the brain). But any improvement in circulation should also help the body function more appropriately.

The "B-100" is a multi-B-vitamin pill with the following ingredients:
 

"B-100" contents
Ingredient Amount % RDA
B1 (Thiamine Hydochloride) 100 mg 6660
B2 (Riboflavin) 100 mg 5880
B6 (Pyridoxine Hydrochloride) 100 mg 5000
B12 (Cyanocobalamin) 100 mcg 1660
Niacinamide 100 mcg 500
Pantothenic Acid 100 mg 1000
Inositol 100 mg No Value Claimed
Choline (Bitartrate) 100 mg No Value Claimed
d-Biotin 100 mcg 33
PABA (Para Amino Benzoic Acid) 100 mg No Value Claimed
Folic Acid 0.2 mg 50
Nutritional Yeast 100 mg No Value Claimed

The Ca/Mg/Zi tablet was for general health. I don't remember when or why I started taking it. I had been taking one aspirin per day as a general prophyllactic for heart and circulatory problems; it is well-known that such a regimen decreases one's risk for heart attacks (combined, of course, with not smoking, eating properly and getting sufficient exercise) as well as colon cancer [studies that came out in 2002].
 

This is what I added to my regimen in the first month or so:

The grape seed extract was recommended as a potent anti-oxidant by my acupuncturist, who is also an MD. The CoEnzyme Q10 was recommended by my chiropracter. CoEnzyme Q10 is more noted as protecting the heart than anything specifically prostate oriented. [cf.] It also increases the effectiveness of other antioxidants, such as Vitamins C and E.

The Selenium amd the lycopenes were recommended by Dr. Carroll at UCSF. Lycopenes are a chemical found in cooked tomatoes (as well as some other foods, including strawberries and watermelon) that are thought to be especially helpful in fighting prostate cancer. I get most of mine in one 8 ounce glass per day of a V-8-like juice (Knudsen's Very Veggie is an organic product, Trader Joe's has Garden Patch, and there is always V-8 itself and lots of other variations. I don't know the lycopene content of these, since only Knudsen publishes it on their label.) [Research published in the May 2006 Journal of Nutrition (Vol. 136, pp. 1287-1293) indicates that lycopene is most effective when taken along with viitamin E. (See https://www.webmd.com/prostate-cancer/news/20040930/vitamin-e-lycopene-fights-prostate-cancer
At some point I switched to getting my lycopenes in pill form to cut back on the amount of liquids I was drinking.

Selenium is noted as helping the anti-oxidant activity of vitamin E and should be taken with it. To quote the Life Extension Foundation,

"As an essential cofactor of glutathione peroxidase, selenium is an important antioxidant. It is also involved with iodine metabolism, pancreatic function, DNA repair, immunity and the detoxification of heavy metals. Studies have shown that selenium can help prevent some cancers and cataracts."

The generic prostate health pill was suggested by my daughter, who is an advocate of alternative medicine. These are its ingredients
 

Generic Prostate Pill Contents
Ingredient Amount
Vitamin B6 5 mg
Zinc 15 mg
Copper 1 mg
Saw Palmetto Berry 600 mg
Active Aminos (L-Glutamic Acid, Glycine, L-Alanine) 170 mg
Pumpkin Seed 50 mg
Pygeum Bark Extract 10 mg
Burdock Root 5 mg
Cayenne Fruit 5 mg
Goldenseal Plant 5 mg
Gravel root 5 mg
Juniper Berry 5 mg
Marshmallow Root 5 mg
Parsley Leaf 5 mg
White Pond Lily Root 5 mg

In March 2001, I added the following items to my regimen:

Green tea is noted for its polyphenols, which are anti-oxidants and thought to contribute to the low incidence of prostate cancer in Japan, among people on traditional diets (which are low fat, with lots of vegetables and green tea). N-acteylcysteine is a source of cysteine, an essential part of the glutathione antioxidant system.

In March 2002 I added this to my regimen:

In February 2007 I added 400 IU Vitamin D twice daily to my regimen. While this is a small dose, there have been studies of high dose Vitamin D (as Calcitriol) with erstwhile positive effects on prostate cancer. However, high doses of Vitamin D can be toxic, so without further research into the matter, I decided to use a little safely rather than none at all. Later, I increased this to 1000 IU twice a day, based on research showing Vitamin D's anti-cancer effects.

In November 2009, I increased my dose of Vitamin D to 2000 IU, twice a day, based on discussions with an MD. My recent blood levels of D3 were 44 ng/ml (Oct 2009), whereas suggested values are in the range 50-65 ng/ml (and many lab tests actually overestimate the blood levels, so perhaps a value of 80 ng/ml may be a reasonble goal).

On 10 March 2007 I started using Peenuts, 2 pills daily, as part of a study at UCSF to investigate whether this herbal supplement can help alleviate prostatitis and its consequent underlying chronic (if asymptomatic) inflammation. Peenuts contains the following ingredients per capsule:
 

Peenuts Contents
Ingredient Amount
Vitamin C 20 mg
Vitamin E (d-α tocopherol) 50 IU
Vitamin B6 20 mg
Zinc 20 mg
Selenium 100 mcg
Proprietary Blend
  Glycine
  L-Alanine
  Glutamic Acid
  Saw Palmetto
  Pygeum Extract
  Pumpkin
  Stinging Nettle
  Echinacea Purpurea
  Garlic
  Gingko Biloba
600 mg

Peenuts was created by a Florida Urologist, Dr. Ronald Wheeler (see http://www.peenuts.com/), who claims significant success in reducing prostatic fluid inflammation in men taking this pill. He has at least one peer reviewed paper on these studies and is collaborating with UCSF on another study, where MRSI of both men and their expressed prostatic secretions (EPS) will be used as measuring modalities. That is, microscopic evaluations of the EPS as well as MRSI imaging and analysis of the EPS as well as the men it came from will look for indications of inflammation over time. (See the discussions below for my history of recurrent prostatitis and for current theories of how chronic inflammation may give rise to cancer.)
 

These are the things I stopped taking in September 1999:

I stopped the aspirin in case I might need surgery. Aspirin promotes bleeding (or slows clotting), good for the heart but not good in healing from surgery. Somehow, it had not felt right to resume taking it. Here I went along with my intuition. (Which reversed again in Nov 2000 after hearing a talk on nutrition and prostate cancer by Mark Moyad, PhD, MD at a Prostate Cancer Symposium at UCSF; so I'm back to one aspirin a day as a prophyllactic measure for my heart and circulation. I have also seen reports that aspirin, as an NSAID [non-steroidal anti-inflamatory drug] has some anti-cancer properties, another reason to continue taking low doses on a daily basis.)

Dr. Carroll noted that some cancers feed on Calcium and suggested I stop taking it as a supplement. I haven't changed the amount I do (or do not) get from my food, however. (See http://www.docguide.com/news/content.nsf/news/391BD0B73B4A876C85256ACE00516B45? OpenDocument&id=7ED78FC79E323C75852569CB00019463&c=Prostate%20Cancer&count=10
- "High Calcium Intake May Increase Risk Of Prostate Cancer", for example, which is no longer available as of June 2009.)
 

PollenAid
In late November 2009 I started taking PollenAid (1 capsule in the morning, 1 at night -- although the recommended dose is 3/day) on the suggestion of a urologist. He referred to peer reviewed studies (which I have yet to receive copies of) indicating this may be useful in dealing with my underlying prostatitis. See the references below.
 

statins
In the autumn of 2000, I also started taking Zocor (simvastatin), 10 mg per day, since I had mildly elevated cholesterol (starting about 230). http://www.merck.com/product/usa/pi_circulars/z/zocor.html

In June 2002, my MD switched me to Lipitor (ataorvastatin calcium) http://www.lipitor.com, since my liver enzyme tests had begun to creep up the to high normal boundary. Changing statins is a way to control these, frequently.

I stopped Lipitor after about 9 months, resumed 10 mg of Lipitor in December 2004, and stopped again in February 2005. Blood tests showed good lipid control with the 2 months on Lipitor, and rising levels in the following 2 months off (early April 2005). In mid-April I began taking Niacin (750 mg each evening, increased to 1000 mg per evening after 2 months, and then to 1500 mg each evening 8 months later [Feb 2006]; to 2000 mg each evening as of Feb 2007) to see if that would correct my lipid levels, which it has, for the most part.

I had stopped taking Lipitor in February 2005, when I experienced some serious side effects -- syncope (fainting) and banging my head in the fall. This is when I switched to Niacin for cholesterol control. Since January 2012 I have been taking 1500 mg of Niacin every evening. This has been sufficient for good lipid control.

The statin drugs, aside from affecting cholesterol and lipid and trigyceride levels, also seem to have some anti-cancer properties. I don't have references available.
 

Naturopath
In October 1999, I saw a Naturopath near Vancouver, British Columbia. I'll discuss him below, in the section on Alternative Practitioners. He also gave me a bunch of stuff to take that I added to my regimen after my PSA test of 27 Oct 1999.
 

Naturopath's Contributions
Pill Name & Dosage Ingredient Amount % RDA
Lycopenes (1 3x/day) Lycopenes 5 mg Not Known
Prostate Support (1 3x/day) Vitamin C 10 mg 16.6
Vitamin B6 10 mg 500
Vitamin E 5 i.u. 16.6
Zinc (chelate) 1 mg 6
L-Glycine 120 mg Not Known
L-Alanine 120 mg Not Known
L-Glutamic Acid 120 mg Not Known
Saw Palmetto 106 mg Not Known
Pygeum Africanus Extract, bark 10 mg Not Known
Pygeum Africanus Herb 20 mg Not Known
Pumpkin Seed 200 mg Not Known
Stinging Nettle 75 mg Not Known
Echinacea (Root) 25 mg Not Known
Gingko Biloba 20 mg Not Known
Wild yam 20 mg Not Known
Uva Ursi 10 mg Not Known
Inositol (1 3x/day) Inositol Nicotinate 300 mg Not Known
Chromiun (Proteinate) 100 mcg Not Known
Pyridoxal 5' Phosphate (Vitamin B6) (1 in am) Vitamin B6 50 mg Not Known
Zinc Citrate (1 in am) Zinc Citrate 30 mg Not Known
Thuya Occ. (3 pastels in pm) ?? ?? Not Known
Conium Mac. (3 pastels in am) ?? ?? Not Known
Liquid "gunk" (1/2 tsp in am and in pm) Mixture of lots of stuff ?? Not Known

  I saw him once more, in December 1999, but shortly thereafter stopped following his regimen.
 
 
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Diet and Exercise

Exercise keeps the blood flowing, the endorphins active, the immune system happy. I had been practicing yoga regularly for about 12 years and have tried to continue that. I also, for a while, added some aerobic activities. But I have found it hard, especially over the cold, dark winter, to continue this with any regularity. Mostly, now, my wife and I take our dogs out for some vigorous walks a couple of times a week. The frequency tracks the weather and daylight -- less in the winter, more otherwise.

My diet has gone through a couple of modifications. At first, the general tendency was to more vegetables and fruit and tofu and less meat. My lunches consist of a smoothie and some salad and sometimes a small amount of leftovers from the previous night's dinner. I cut back my coffee to one cup per day (from 2).

In December 1999, my wife saw Dr. Diana Schwarzbein, a Santa Barbara endocrinologist, for help with her diabetes. Dr. Schwarzbein has a dietary approach to dealing with diabetes that seems applicable to health in general. It is well described in her book, The Schwarzbein Principle. So for our meals at home, we began following this program, where I would eat more carbohydrates than my wife.

It was pretty consistent with our general approach although it involves eating more protein or meat than we were used to. The general principles are

Additional benefits of this diet are touted to be increase of muscle mass (if you exercise), decreasing total cholesterol and "bad" lipids (LDL), as well as a generally healthier body and disposition (see the chapter on serotonin).

By and large, we've always eaten pretty much this way except that we've increased the amount of organic food in our diet.


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Alternative Practitioners

In my opinion, Western medicine has a lot to offer the world by taking a mechanistic analytical approach to understanding how the body functions, from the cellular level on up. This has been incredibly important in informing public health measures as well as being able to treat a wide variety of diseases and conditions and return people to health, alleviate pain and suffering, and improve quality of life.

However, there are some things lost in its reductionist approach. One is the realization that the patient is a person rather than a bag of symptoms. Another is that the person comes from a complex web of history and social interactions and beliefs. And another is an appreciation of the ability of the body to heal itself given the stimulus and opportunity and help to do so. And another is a dismissal of things that do not fit into its mechanistic picture.

Acupuncture
So I sought to augment my care by seeing three kinds of alternative practitioners. The first is an acupuncturist. The one I chose was trained as an MD and came highly recommended. I saw him in order to enhance the functioning of my immune system, to enable it to fight off the cancer. At first I saw him weekly, but after a couple of months, I cut down to once a month. I continued with this practitioner until August 2004.

In February 2005 I started seeing a Japanese acupuncturist (a somewhat different style than Chinese acupuncture) for about a year.

Chiropractic
The second practitioner I saw was a chiropractor. The idea here was that if I had any structural issues, subtle or otherwise, that prevented proper innervation of my organs, that would subtract from my systems' optimum performance and health, including that of my immune system. The chiropractor I initially chose was a friend who had recently graduated Chiropractic College and been licensed. His practice was just starting out so he had a lot of time to work with me and explore various possibilities. I saw him about once a week or so for about 3 months and then stopped when he felt there was nothing more he could do for me structurally.

In July 2000 I started being treated by a Network Chiropractic practice. This is a more subtle form of manipulation, more frequent than standard chiropractic practice, also designed to fully and properly align the spine and permit proper flow of nerve energy, hence better health and healing, including enhanced immune system functioning. In March 2001, the practice moved to another city, which was inconvenient to get to, and I decided to stop going there and focus instead on more active pursuits, such as resuming my yoga practice.

Naturopathy
This is a more interesting story. At the first Prostate Cancer Support Group meeting I went to in September 1999, I replaced another fellow as the youngest in the group. We got to chatting after the meeting and he mentioned that he had a friend in Vancouver who is successfully controlling his prostate cancer through dietary and holistic means.

I contacted the friend via email and then in a long phone conversation. He had also been trained as a physicist and worked as one for some years before drifting into the field of government science and development policies. He was associated with Simon Fraser University in Vancouver and also did work for the Canadian government as well as consulted with other governments on these issues. Obviously a person coming from the same Western analytical approach as I did, at least originally, not one to be easily bamboozled by various forms of mumbo-jumbo. He had decided upon his diagnosis three years earlier (1996) that he too wished to avoid surgery and radiation and their attendant side effects, so sought alternative approaches. Among other things, he increased the amount of organic and healthy food in his diet. And he found a local Naturopath as one of his practitioners, an older Dutch physician who originally trained and practiced as a neurologist for many years. Eventually, Pieter became a psychiatrist and later on retrained again as a naturopath and homeopath.

On this recommendation, we booked a business/pleasure trip to Vancouver, one of our favorite cities, for mid-October 1999. The doctor took some medical history, and then used an interesting device attached to his PC to measure balances and imbalances in my body. There are references in the Bibliography. The technique used is popular in Europe, unknown in the US, and is called ElectroAcupuncture according to Voll (or EAV), after its inventor, a German physician named Voll. He then gave me this list of things noted above. He also gave me an injection of dead and diluted prostate cancer cells to boost my immune response, a homeopathic approach.

We saw him again over Christmas 1999. He said I was better but not cured yet and did more of the same, keeping the medications almost the same.

As I ran out of his supplements during the month of April 2000, I stopped taking them. We had noted that my PSA had gone down for 2 months before I started the naturopathic treatments, and so determined that whatever good they might be doing, they were not crucial to my good health. It was also expensive and inconvenient to travel to Canada, even a few times a year (he would have preferred every 2 months). So the next part of the experiment has been to omit the naturopathic treatments and supplements. I always have the option of resuming them.


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Secret Weapons

I refer to these next two items as "secret weapons" because they are not well known or used here in the U.S. for dealing with cancer. Nothing in the preceding melange of things to ingest or do is unusual or out of the ordinary. But not many people know about pau d'arco or the use of human mother's milk. And I will now discuss these elements of my regimen.

pau d'arco

Pau d'arco is a common remedy in South and Central America for a variety of ills. It is said to be used as an antibiotic, an anti-fungal, to treat diabetes and skin problems, and to treat cancer, among other things. It is derived from the inner bark of the taheebo tree, originally native to the Amazon rain forests, though now found from Argentina through Costa Rica. Most of the research I was able to come across about this plant has been done in Argentina and is in Spanish. Web references follow in the Bibliography.

My younger daughter spent the 1998-1999 academic year studying in Costa Rica, with an emphasis on alternative medicine techniques. Part of the time was spent doing an internship on a farm where medicinal plants are grown using organic, sustainable agriculture. And pau d'arco is one of the plants grown there. She brought some back to the U.S. and suggested I take it as a tea when I was diagnosed. Since then, we've bought a pound at a time directly from the source. It goes a long way. We've found the tea to be available in some health food stores in California and over the web, but we've also found that it is difficult to vouch for the quality of what you're getting. Since  pau d'arco comes from the inner, living, bark (the phloem) of the tree, often it is adulterated with other barks.

The mixture I get is mixed with some ginger and tumeric, spices also noted for their medicinal qualities as well as interesting tastes. I bring a quart of water with 1 teaspoon of the mix to a boil, them simmer 10 minutes and strain. The suggested dosage is 2 to 3 cups a day, although I seem to average one to two a day.

One can also buy the tea without the ginger and tumeric or use it to make an infusion. I don't mind the taste as it is and haven't experimented with it.

In October 2001 I sent in another order for pau d'arco to my source in Costa Rica. Six weeks later, my letter was returned for having an insufficient address, though it used the same address I had been successful with several times before. Email did not bounce nor did it receive a reply. And a fax also went through, again with no reply. I had no direct phone number to call. As I was running low, I decreased the amount I was drinking to a few cups a week, and gradually stopped taking pau d'arco as the year ended, with no apparent effect on PSA. I can only conclude that this tea is not crucial in my program. It may well have helped, but was not the "Secret Weapon" I originally hoped it might be. In early 2002, my Costa Rican contact resumed communications (new email address, more complete postal address) and I am again able to get an ongoing supply.

I stopped taking pau d'arco in July of 2003. I noticed no change in my condition or numbers without that tea and have come to believe that it was not an essential element of my regimen.
 

Mother's Milk

When I was diagnosed, my wife started doing some research of her own into cancers. She found on the Web a New York Times article from 19 July 1999 about research into the use of human mother's milk to fight cancer. This work was being done at Lund University in Sweden and had recently received a $250,000 grant from the American Cancer Society to continue. Later on, I found that this article was based on a feature in the June 1999 issue of Discover magazine which explored the discoveries in more detail. [This article is available on line, as noted in the Bibliography, or you can visit your local public library to read or photocopy it.]

In brief, about 1994 Anders Håkansson, then a graduate student in Catharina Svanborg's laboratory at Lund University, found by accident that adding human mother's milk to a cell culture of cancer cells caused them to all die. This was true for a wide variety of human cancer cell types. On the other hand, normal cells were unaffected.

So they injected human tumors into rats. When the tumors started growing, they started treating the tumors with mother's milk. In most cases the tumors shrank or died. What seems to be happening is that there is some combination of factors in the milk that causes "programmed cell death" or apoptosis in cancer cells and not in non-malignant cells.

Why would this work? One speculation is that the time of most rapid post-natal cell growth is the months and year just after birth, when the normal infant should be nursing. Since rapid cell growth is fraught with the dangers of bad replication and malignant transformations, a natural mechanism that would kill such new cancer cells is a reasonable thing to have developed evolutionarily. In fact, it should be common in all mammals, one might conjecture.

In fact, it is well known that nursed infants have 1/9 the probability of contracting any kind of childhood cancer as infants who are not nursed, as well as having fewer allergies, less asthma, and fewer childhood diseases.

The Swedes then turned the focus of their research into understanding the cellular and molecular basis of these observations, doing some good science in the process. It seemed as if the major factor is something called MAL, multimeric Alpha-Lactalbumin, along with some potentiating factors. They found that pastuerization destroys the multimeric character of this compound and also its cancer-killing abilities. Their focus, however, is to isolate and patent the factors, then to license them to drug companies and live well on the royalties.

My reasoning was quite the opposite. If the potent parts of mother's milk can get into the infant's body via his/her gut, it is very likely that the same is true for an adult who ingests it as well. True, with a much larger body weight and size than an infant, there would be a greater dilution, but any apoptosis than can be induced over as long a period of time as the milk is available would help keep the cancer under control or even, in the best of worlds, eliminate it.

I contacted Dr. Håkansson by email and received copies of three of their research papers (in English).

Shortly after we found the New York Times article, we reconnected with a colleague I had worked with some years previous. His wife was nursing an 8 month old and she herself was a cancer survivor. She agreed to pump her breasts for me. So from late August 1999 for almost a year, I had a supply of mother's milk, which ended when my donor weaned her child. I am endeavoring to continue having a supply from healthy, health-conscious women.

Almost every day (depending on the supply), I took about 2 ounces of mother's milk mixed into a smoothie (orange juice, yogurt, tofu, various fresh and frozen fruits) as part of my lunch. It is a simple, healthy, and palatable way to take this part of my regimen.

I believe that these two items, but mostly the mother's milk, have made the difference for me in keeping my cancer under control and my PSA scores down in the mid-normal range. Everything else has helped, to a greater or lesser degree, but this "secret weapon" has been the crux of it all.

While pau d'arco is mildly difficult to get, it is available. Mother's milk, on the other hand, requires some luck or connections. It is a hypothesis I made that the same positive anti-cancer effects can also be obtained from certain kinds of raw mammal milk, perhaps goat or cow, perhaps some more closely related species. The key word here is "raw", since pastuerization (heat) destroys the effect, and raw milk might come with its own health concerns. It would be interesting and quite useful if some academic, less motivated by greed, would pursue this line of inquiry.

In July 2000, my source of mother's milk told me she was planning on weaning her child, which was a perfectly reasonable thing to do. My wife found a possible source via a Milk Bank, but they needed a prescription from an MD to give me the milk, only because providing milk to adults was not a usual course of action. So, in mid-July I asked my urologist for one.

In the meantime, I had received the April 2000 PNAS paper from the Swedish researchers. In it, they had isolated the essential cofactor in human mother's milk that caused multimeric alpha-lactalbumin to undergo its shape changes into the form that kills cancer cells. This cofactor is oleic acid, which I then discovered was abundant in olive oil. While waiting for the prescription, I experimented using raw cow's milk from a health food store instead of the no longer available mother's milk, adding in about 1 cc or so of olive oil. I also increased the amount of cow's milk to 4 ounces a day, from the 1 to 2 ounces of milk that my donor had been pumping, on the average.

This did not work. After about 1 week of the new regimen, the PSA on 10 August was a consistent 2.2. About 4 weeks later, on 8 September, it had increased to 3.8! This is a doubling time of about 6 weeks.

Again, I requested a prescription from my urologist, but he wrote back

	"...I have no experience with prescribing mother's milk and do not 
	feel comfortable prescribing something I know little about...."
So I found two other MDs who would support me and who wrote me the prescription. The folks at the Milk Bank were wonderful and fully aware of the Swedish research. The director had spent a few hours the previous month (August 2000) talking with the discoverer of the effect and a key researcher on the Lund University team at a conference in Washington, DC and was already supplying the milk to a few small and successful pilot studies in other parts of the country (that is, individuals, such as myself, with various forms of cancer).

Within one week, my PSA had dropped to 2.5 ng/ml, and I was greatly relieved. Since nothing else had changed in my regimen, it became abundantly clear that the crucial factor in controlling my cancer was the milk. Everything else may help, but nothing else was sufficient unto itself to keep my PSA down and the cancer under control.

(According to their papers and personal communication, the oleic acid, in the warm, acid environment of the human gut, transforms the physical conformation (or shape of the molecule) of the multimeric alpha-lactalbumin molecules into another form they call HAMLET [for Human Alpha-lactalbumin Made LEthal to Tumors], which induces apoptosis in malignant cells.)

This experience leads to some additional questions:

The milk from the Milk Bank is pasteurized. According to Dr. Håkansson, the process they use, required by California state law, will degrade some, but not all, of the apoptotic activity of the milk. For that reason, I was using 7 ounces a day of the Milk Bank's pasteuerized mother's milk.
 
 

[Aside about another's experience]

One of the men in my prostate cancer support group has been using dietary means to keep his PSA about 3.5 ng/ml for some time. Based on my experience, he got a prescription for mother's milk from his physician and used about 7 ounces per day for 2 months. He was disappointed that he did not see any notable decrease in his PSA and so stopped the experiment.



 

Strange PSA values in May 2001

Three weeks after the MRI/MRIS of April 2001, before I had those results in hand (UCSF was understaffed in the Radiology Department and was quite behind in making timely interpretations of the images), I returned to Stanford University Hospital for my monthly PSA test. On 9 May 2001, the value was 19.6 ng/ml. This was an astounding jump from the 2.6 it had been 5 weeks previous. Did the lab make a big mistake? Had the Milk Bank changed how it processed milk? What else was going on? Had the cancer exploded?

I went back two days later, on 11 May 2001, to repeat the test. It came back as 14.0 ng/ml. Curiouser and curiouser. Is a drop of 5.6 ng/ml in two days reasonable? The numbers were frightening and did not make a lot of sense until I got the MRI report. As noted above, it showed (marginally) less cancer than in previous images, but also noted evidence of prostatitis, something which could account for these PSA values. My urologist suspected prostatitis as the cause of these readings and put me on antibiotics. After one week, the PSA went down to 4.0 ng/ml. We decided, after a week break, to do another week's worth of Cipro (500 mg), which brought the PSA back to 2.5 ng/ml, roughly where it had been before the infection. Apparently, prostatitis may be asymptomatic, though rarely. Reviewing the original biopsy report of July 1999, it stated that there was evidence for my having had prostatitis (apparently it permanently affects some noticeable characteristics of the prostate cells it infects) and I may well be harboring a latent infection which occasionally flares asymptomatically. There is some sense of relief, but also one of mystery.

By the way, the Milk Bank claimed no changes to its processing/pasteurization protocol.
 

Raw Milk Again

The anomalously high values of early May 2001, due to prostatitis, put a scare into me and also concerned the folks at the Mothers' Milk Bank. The Director began to investigate what it would take to get me raw milk. She attended a conference in Vancouver in June of all the North American milk banks and found that nothing in the organization's charter or by-laws prevented the distribution of raw milk, as long as appropriate releases were signed. She checked with the California Department of Health, which also had no objections, provided appropriate informed consent was available. She requested generic release forms from the local blood banks, modified them, and had the organization's attorney (a former milk donor) and medical director approve them. And finally, on 9 August 2001, almost 3 months after the first high PSA reading, I was able to get a batch of raw milk.

The Milk Bank routinely screens all donated samples for bacterial count. The biochemist had started sequestering samples with extremely low counts for me. The bacterial levels in these is equivalent (or almost) to those in pasteurized samples. Naturally, all donors are screened via blood tests, when they sign on, for an array of potentially transmissable diseases. So the milk, raw or processed, is likely quite clean. I have no need to fight off cancer to catch some other disease.

A week and a half later, a PSA test gave the value of 1.9 ng/ml, equivalent to my "normal" value of December 1997 and among the lowest values I have had, even though I halved the quantity of milk I was using (from 7 ounces/day of pasteurized to 3.5 ounces/day of raw milk). This is very encouraging.
 

Strange PSA values in January 2002

This seems to have been another case of asymptomatic prostatitis, since it responded to a course of Cipro I started on 23 January. On its own, my PSA came down rather quickly from 8.67 to 5.45 and stabilized there for a week. After less than a week on Cipro, it was down to 4.01. I got enough Cipro for a 2-week course, and renewed it for another 2 weeks.

It is apparent to me that cancer and BPH do not behave this way, spiking and dropping, as my PSA did in May 2001 and again in January 2002. Certainly, Dr. Carroll also seemed unable to explain this behavior. And Dr. Kurhanewicz pointed out that the increased activity in the MRIS of 9 January 2002 might be attributable to an acute stage of prostatitis rather than increased cancer metabolism. He mentioned that he had only seen this twice in the 4000 or so images he has looked at over the years, since most prostatitis he sees is chronic, and so has less metabolic activity. This seems to be the explanation.
 

Strange PSA values in the winter and spring of 2005

The spike in Dec 2004 (6 weeks after a 2.17, a value of 6.45, which fell on its own to 3.37 two weeks later and 3.29 a week and a half following) are again not typical of prostate cancer. Rather, they are signs of an infection. In consultation with my urologist, I started on a prophylactic 4 week course of Cipro on 31 Dec 2004. Our plan was to wait about 2 weeks after it was finished to do another PSA measurement.

About 10 days after I finished the Cipro, I had the symptoms of a prostatitis attack, including painful and frequent urination. Blood work showed a raging infection. So I started a 2 week course of Floxin, another antibiotic in the same family as Cipro. It took a few days for the symptoms to abate, but they did around mid-February.

On 28 March 2005, I went for another PSA and my first free PSA measurement. The result is expressed as a ratio of free (or unbound PSA) to total PSA (that is, to bound plus unbound PSA). Values below 10% are indicative of cancer (>40% probability of active PCa); values above 25% are indicative of no active cancer (<10% probability), for PSA values in the range of 4-10 ng/mL. Mine was 15%, in the ambiguous range. [A conversation with Nanette Perez, RN at UCSF Urologic Oncology on 3 April 2013 led to the rule of thumb that free PSA > 20% is considered to indicate no cancer present.]

Since Stanford sends the Free PSA to an outside lab to be processed, I figured the PSA value was not comparable to most of the others, so I redid my PSA on 05 April 2005. It was significantly elevated from the value of the previous week, indicating to me that I was still harboring an infection (which was thankfully asymptomatic). Further followup was due with a power doppler TRUS on 11 April and a consultation with my urlogist the following week.

The TRUS showed no changes from the previous year or the year before and no obvious signs of cancer, which was reassuring. My uroligist agreed that I still had prostatitis, that I was lucky to be symptom free, and that chronic infection was problematic for several reasons:

My PSA values continued to jump wildly about, 4.42 in June, 18.3 in July, and then settled back to normal at 2.44 in early August, for reasons that elude me. Somehow, the infection has (hopefully) run its course and is done.
 

Free PSA evolution

UCSF had not issued scrips for Free PSA measurements very often (see the table of PSA values above), but began again in 2026. As noted above, Free PSA values >20% are indicative of no cancer being present, while values <10% likely signify cancer is present. On 18 February 2026, my Free PSA was 26% (2.1/8.2 = 0.256), well within the "safe" zone.
 

PSA Decline since the COVID pandemic started

In February 2020 my PSA hit a peak of 14.5 mg/ml, but has been declining since pretty consistently. This is a good thing, but I have no idea why this is happening. The COVID pandemic started in mid-March 2020 with its attendant shelter-in-place regimen and I spent most of my time at my significant other's, which led me to decrease my ingestion of mothers' milk to once a week (from my usual twice a week -- see Dosage Summary below). The size of my prostate, as determined by my annual MRSIs, while continuing to increase, has done so much more gradually as well in this time frame. (See below). It is curious.
 

Dosage Summary

Here's a summary of what I had been taking over time:
 
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Bottom Lines

So, what conclusions can one draw from all of this? What might be applicable to you, another person diagnosed with prostate cancer, or a friend or relative of such a person? There are a few things I can say, but, as usual, your milage may vary -- that is, your results may not be the same as mine and you need to exercise your best judgement in the end.
 

PSA Improvement

Mine was much better and much faster than I had expected. As discussed above, a very conservative linear model would have put mine about 6.2 ng/ml at the time I was diagnosed. And I only started putting my regimen together over the following month. Hence, I expected my PSA, as measured at the end of September 1999, to be roughly where it was at the time of diagnosis or a little lower. I thought it would have continued increasing for a while and, at best, had a short period of time to start reversing, if what I was doing was really effective.

Instead, it came down to "normal" (1.9 ng/ml) right away and more or less has stayed at 2.0 +/- 10%. This was quick; I was suprised and pleased.

What is the "magic bullet"?

I don't know. I suspect it is the mothers' milk. But there is no way of really telling unless I start cutting things out. However, I have no desire to do that experiment on myself. In general, I subscribe to the philosophy of "If it ain't broke, don't fix it."

Since I started the Naturopathic remedies relatively late in the game (at the end of October 1999, when I already had 2 or so low PSA's), I know that these were not decisive. They may well have helped sustain the effects of everything else, but were not the crucial elements in controling my PSA levels.

My experience in August and September 2000, when I did not have access to human mother's milk but everything else in my regimen stayed constant, as discussed above, leads me to now believe that the mother's milk is the crucial aspect of my program, the "magic bullet". It seems insufficient, so far, to eliminate the disease, but capable of holding it at bay, as indicated by my monthly PSA results and validated by the semi-annual MRI/MRIS imaging. (Actually, according to the history of my MRSI images, discussed above, it seems that my cancer has been essentially undetectable since around 2002, only 3 years into my regimen. I write this aside in 2019, 20 years after diagnosis when it seems obvious to me that human mothers' milk is indeed the "magic bullet" for eliminating my cancer.)

I stopped taking the pau d'arco in July 2003, with no noticeable effect on my TRUS (Aug 2003) or subsequent PSAs. I currently don't think this is a "magic bullet", although it may well have some positive medicinal effects.
 

How General is This?

Again, I don't know. With a data set of one person, it is impossible to generalize on how well this would work for another person or, if so, how quickly it would work. In that sense, my experience is anecdotal. That means it is useful; it is, as we said in math classes, an existence proof. But it does not guarantee that the same will happen for every (or any) other man who tries this all. (Some small pilot studies by the Swedes -- with human glioblastomas, bladder cancers and colon cancers -- indicate possible potent effects of HAMLET in vivo. See the Bibliography for the peer reviewed articles.)

How Long Will it Last?

Again, time will tell. So far, we know that my PSA went way down very quickly and has stayed in mid-normal ranges for over 4 years (as of this writing). The results of all my MRI Spectroscopies are discussed above. (As I add this aside, it has been 20 years since my diagnosis and I am cancer free; or, more precisely, any cancer in my system is undetectable.)

What should you do?

Obviously, you should do what you think is right for you, is best for you, is most appropriate for you. One should not take cancer lightly. On the other hand, MDs have their own prejudices about what the most appropriate approaches are ("If the only tool you have is a hammer, everything looks like a nail") as well as a strong financial incentive to treat you with their technologies. On the other hand, wishful thinking is no substitute for action, usually.

You need to understand your own health, your own unique personal conditions and values, the stage and aggressiveness of your cancer, and what all the (rapidly changing) medical options that are available to you may be. And you may often have to fight an unresponsive medical bureaucracy or HMO or insurance company that has only its owners' bottom line at heart, not your well-being or even survival. A large and daunting task for anyone, no doubt, but do-able.

Another caveat is that if you have any Gleason 4 or above in your biopsy samples, you will need to do more than only lifestyle changes. According to a paper by Professor Thomas Stamey of Stanford University Hospital [ref needed!], the strongest negative indicator of survival time is the percent of Gleason 4 or higher in one's biopsy samples. In this case, informed medical action is appropriate along with lifestyle and dietary changes. Even in this case, give yourself enough time to get past your shock, to become informed enough about all alternatives, and to find the best practitioner of the approach you decide upon.

In any event, do not try my approaches instead of medical modalities if your cancer is spreading, growing, creating symptoms, or otherwise showing signs of aggressiveness. All of this can be used as an adjunct to more conventional therapies, if necessary. Remember, I am not practicing medicine, I am presenting my own personal story and discoveries and you are, in the end, the only one responsible for your own health, along with those experts you hire to inform and assist you.

Aggressive Monitoring (aka Active Surveillance)

One doesn't just set a course and assume it is working. I have taken an approach of aggressively monitoring my cancer, as best I can. This means having a monthly PSA blood test (versus once every three months, as proposed by my urologist). It also means having an MRI Spectoscopy every 6 months or so (versus the once a year suggested by my urologist).

Other tests are available. These include the DRE (digital rectal examination), the TRUS (trans-rectal ultrasound), biopsies and other blood work. In my case, I don't think these would tell me anything, mostly because they didn't before. That is, my cancer was so small and early stage, it was invisible to the DRE and TRUS I had in July 1999. And the biopsies are like poking into a haystack with a needle, looking for a pingpong ball. Or perhaps a marble. If the target is small enough, one has a very small likelihood of poking into it with a few at random stabs. Finally, the blood work (such as Free PSA and other enzymes) merely serve to indicate the likelihood of cancer; since we know that cancer exists, these also would not yield new information.

I have more confidence in the MRIS, in my case, because it can image everything (bigger than some minimum, of course) and differentiate cancer from non-malignant tissue. I also have a "before" for comparison, a "before" that showed the location and extent of cancer, so we will be able to see its progression or regression.

Simple Conclusion

The approaches I have outlined here cannot hurt as supplements to more traditional, medical, or conservative approaches or to "watchful waiting".
 
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Bibiography