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 -- 09 May 2014

© Copyright 2000-2014, Howard J. Cohen, Ph.D., All Rights Reserved -- slides (a summary) -- text (this document)

A work in Progress



Who am I?

A History of My Disease

What Did I Do?


The Theory

Vitamins and Herbs

Diet and Exercise

Alternative Practitioners

Secret Weapons

Bottom Lines



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


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.

The slide show's main page is noted above.

[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.


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 genetics. 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.


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***
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+
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
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++
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
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
2.17 6.45
3.37 3.29
Date 03/28/05
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
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
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  
PSA 5.4 5.2 4.7 6.1 7.22
Hunter Labs
6.8 7.3 7.40
Hunter Labs
Free PSA             21 %    
[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 has been on and off hormone therapy and seems to have his cancer under control. (In late 2005, after 12 years of intermittant hormonal blockade [which will be discussed in Appendix B], he seems to have developed hormone refractory prostate cancer and is exploring chemotherapy options. He tried mothers' milk briefly in 2007. He died of prostate cancer in June 2008.)

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.

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.


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:



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.


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


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.


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. (

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.


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.

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.

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.
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 t 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: " 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 reported 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 prostatititis I had from September to Decemeber of 2013.

The next imaging, probably to be done around April 2015, 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
?? ?? 34 39 33 40 38 46
PSA Density
?? ?? 0.065 0.067 0.26
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
46 49.2 42.3 45.0 37.0 41.5 39.9 50.4 54.1
PSA Density
0.055 0.074 0.103 0.089 0.15 0.111 0.146 0.093 0.135
Date 04/21/14                
Prostate Size
PSA Density

[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 become 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 (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.


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.


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]

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 Calictriol) 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
  Glutamic Acid
  Saw Palmetto
  Pygeum Extract
  Stinging Nettle
  Echinacea Purpurea
  Gingko Biloba
600 mg

Peenuts was created by a Florida Urologist, Dr. Ronald Wheeler (see, 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 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.)

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.

In the autumn of 2000, I also started taking Zocor (simvastatin), 10 mg per day, since I had mildly elevated cholesterol (starting about 230).

In June 2002, my MD switched me to Lipitor (ataorvastatin calcium), 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.

These 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, and I have been on low doses.

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


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.


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.

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 see 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 am 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).

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.

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.


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 seems 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 these "secret weapons" have 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.

Dosage Summary

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

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 or 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.

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.

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.

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

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".




I'll define a few terms used above that may not be obvious to a reader who is not conversant with prostate cancer. Please email me any others you think should be in this list.

[A more extensive prostate cancer glossary is available at, part of Robert Young's Phoenix5 site, referenced above.]


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

In which we give a brief overview of the possible course of prostate cancer.

Scope of the Issue

"The American Cancer Society estimates that 198,100 men in the United States will be diagnosed with prostate cancer during 2001. The group estimates prostate cancer will kill 31,500 men in the United States in 2001, making it the second-leading cause of cancer deaths in American men after lung cancer. More than 70% of all prostate cancers are diagnosed in men older than 65 years. Early diagnosis using the prostate-specific antigen (PSA) test and digital rectal exams means the 5-year survival rate for men with prostate cancer has increased from 67% 20 years ago to 93% today." (This paragraph is quoted from a news release on Medscape about the article Nature Genetics 2001;27(2):172-180 (6 Feb 2001)).

The corresponding 2003 figures are "more than 220,000" men being diagnosed with prostate cancer in the U.S, "nearly 30,000" dying from it. (From a Seatle Times story.) A New York Times article ( notes that the U.S. 2003 incidence will be 220,900 cases with 28,900 deaths and 1.8 million men living with the disease.

The American Cancer Society's 2004 estimates are 230,000 men diagnosed, almost 30,000 deaths (from, but this site seems to have removed all archives before 2008).

The American Cancer Society's 2005 estimates are 232,000 men diagnosed, and 30,000 deaths (from, 9 Jan 2006).

"The National Cancer Institute of Canada estimates that 17,800 Canadian men will be diagnosed with prostate cancer in 2001, making prostate cancer the leading cancer diagnosed in Canadian men." (From, a press release, 26 Nov 2001, no longer available on the web site as of June 2009.)

"Prostate cancer is on course to become the most common men's cancer in Britain in the next 3 years, health experts said on Monday. Cases of the disease have doubled in the past 20 years and scientists predict the numbers will continue to rise as the population ages and more men are tested for the illness. ... Around 22,000 cases of prostate cancer are diagnosed in Britain each year and 9,500 men die of the disease annually." (Originally from, which is no longer available. It was a summary of a press release from Reuters, 27 May 2002. -- June 2009.)

"As the Baby Boomers approach 60, there is an increased need to assist newly diagnosed and advanced disease patients and their families. The number of men diagnosed with prostate cancer is expected to increase by 40% from approximately 230,000 to more than 300,000 a year. Over the next 10 years, the number of prostate cancer deaths could rise from 30,000 to 50,000." (From an USToo email, 30 May 2006)

"Prostate cancer is one of the most common cancers in men. Each year 543,000 new cases are reported worldwide and the disease kills 200,000 mostly older men in developed countries." (From a Reuters news story, 5 Dec 2006, that had been located at
but is no longer there as of June 2009.)

"Among men, prostate cancer is the most common cancer (next to skin) and the second leading cause of cancer-related deaths in men in the United State. According to the American Cancer Society more than 218,890 men will be diagnosed with prostate cancer in 2007." (From an email from the National Prostate Cancer Coalition, 12 March 2007.)

"In 2007, approximately 1 of 6 men in the United States received a diagnosis of prostate cancer, and 1 in 34 died from it." (From Walsh, et al., NEJM, 357:26, p 2696, referring to A. Jemal , R. Siegel, E. Ward, T. Murray, J. Xu, M.J. Thun, Cancer Statistics, 2007, CA Cancer J Clin 2007;57:43-66.)

"In 2007, prostate cancer was diagnosed in an estimated 218,900 men in the United States, and approximately 27,050 men died of the disease." (From , Wilt, et al., Annals of Internal Medicine, Vol 0, Issue 2008, pages 000605-200803180-00209-E-209 (18 March 2008))

"More than 186,000 U.S. men will be diagnosed with prostate cancer [in 2009], and nearly 29,000 will die, according to cancer society estimates." (From, a New York Times article on over diagnosis of prostate cancer.)

"It is estimated [by the American Cancer Society that] 192,280 men will be diagnosed with prostate cancer in 2009 and 27,360 men will die from the disease." (From a Reuters press release, reproduced at, 27 May 2009.)

The American Cancer Society estimated that in 2009 192,280 men were diagnosed with prostate cancer and 27,360 died from prostate cancer. Alarmingly, their 2010 estimates (issued 15 June 2010) were of a significant increase: 217,730 men diagnosed and 32,050 deaths. (From )

In 2010, it was estimated that 217,730 men were diagnosed with prostate cancer and 32,050 men died of the disease in the U.S. U.S. medical costs linked to prostate cancer care were estimated at $9.9 billion in 2006. (From )

It is estimated that in 2011, approximately 240,000 men will be newly diagnosed with prostate cancer and 33,000 will die of the disease. (From

According to ASCO [the American Society of Clinical Oncology], more than 241,000 men in the United States will be diagnosed with prostate cancer in 2012, and 28,000 men will die from the disease. (From>)


In autopsies of men who have died from other causes, both in the United States and in other countries (e.g., Europe and Japan), microscopic amounts of prostate cancer are found in frequencies increasing with the deceased's age, sometimes even in their teens. It seems likely from this that there are natural processes that lead some prostate cells to undergo a transformation to a cancerous state and then to lay dormant, neither being killed by the host's cellular immune system nor moving on to the rapid cell growth typical of active and of metastatic cancers.

Thus, it is more and more likely, as one ages, that there is a small but real burden of prostate cancer cells that could become active. The relative frequency of this being the case seems to vary from society to society, which informs some of the thinking about the relationship between diet and nutrition and prostate cancer. For example, the death rates at all ages of prostate cancer in Japan is much lower than in the United States. However, it is likely not a genetic difference that is in play here, since second and subsequent generation Japanese-Americans have substantially similar incidence rates to Caucasian Americans. That is, acculturation to the typical U.S. diet or lifestyle (versus the typical traditional Japanese diet) increases the incidence of active prostate cancer and its resulting death rate.

The questions one must ask are, What causes the cancer to become activated? How can we reasonably alter lifestyle to decrease our probability of getting or activating our latent prostate cancer? How can we reasonably alter our lifestyle to deal with prostate cancer that has already become active? These issues were discussed briefly in the body of this paper from the point of view of my personal experience.

In the pre-detection phase, life is normal -- PSA remains in the normal range, the gland stays a normal size and does not cause urinary problems. The cancer cells, if any, remain microscopic or as very small inclusions within the gland. (It should be noted that unlike many other cancers which seem to arise from a single cell gone awry, prostate cancer, even in its pre-detection phase, seems to be multi-focal. That is, it arises in a number of locations within the gland. In that sense, too, it may be thought of as a systemic disease.)

The Possible Role of Infection and Inflammation

I mentioned earlier that I had suspected that an early bout of prostatitis, when I was in my mid-20's, may have led to a slow cascade of events which culminated in my prostate cancer. Since prostatitis is difficult to really eradicate, even with powerful antibiotics, and may flare up asymptomatically, doing cellular damage repeatedly, it could well be a culprit. After I wrote that, I came across a press release from Johns Hopkins University about such a hypothesis published in the 16 September 2002 issue of Nature Genetics. I will quote the release here.
BALTIMORE, Sept. 15 (AScribe Newswire) -- Researchers at Johns Hopkins, Wake Forest, and The National Human Genome Research Institute have implicated mutations in a "heart disease gene" in hereditary prostate cancer. The findings, which offer new evidence that at least some cases of prostate cancer may begin with an infection and inflammatory response, will be published online September 16, 2002, in Nature Genetics.

The gene, called macrophage scavenger receptor-1 (MSR1), was identified more than 20 years ago as a factor in plaque formation in arteries, a process that contributes to coronary artery disease, or so-called hardening of the arteries. MSR1 helps immune system cells called macrophages clean up cellular debris from bacterial infections and damaged fats or lipids. Macrophage activity has been known to increase in the early stages of prostate cancer, and the Hopkins investigators suspected that some MSR1 mutations might inhibit the ability of macrophages to clean up properly after prostate infections, producing inflammatory lesions that are often markers of prostate cancer.

This is the first time that MSR1 has been linked to cancer, and it may tie infections and similar environmental exposures to cancer of the prostate in a way that we haven't thought about before, says William B. Isaacs, Ph.D., professor of urology and oncology at the Brady Urological Institute and Kimmel Cancer Center at Johns Hopkins.

Hunting for gene mutations that increase one's risk for prostate cancer, researchers screened 159 families with hereditary prostate cancer and found seven different mutations in the MSR1 gene in 13 families or about eight percent of the hereditary prostate cancer families studied.

To compare the impact of this gene in men with non-hereditary sporadic prostate cancer, the researchers screened another 731 men, 365 with prostate cancer and 366 without. Overall, the research team found that MSR1 mutations were about seven times more common in men with prostate cancer than in those without. Mutations were found in 12.5 percent of African American men with prostate cancer as compared to 1.8 percent without the disease. In men of European descent, 4.4 percent of men with prostate cancer and less than one percent without prostate cancer had MSR1 mutations. "This genetic evidence suggests that MSR1 may play an important role in prostate cancer susceptibility in both African American men and men of European descent," says Jianfeng Xu, M.D., Dr. PH, of the Center for Human Genomics at Wake Forest.

Isaacs and colleagues will conduct additional studies to uncover the pathway that the MSR1 gene controls and confirm the prevalence of MSR1 mutations in larger studies.

The research was funded by the National Cancer Institute, the Department of Defense, CaPCURE, Fund for Research and Progress in Urology, and the William Thomas Gerrard, Mario Anthony Duhon, Jennifer and John Chalsty Professorship in Urology.

Participants in this research include Jianfeng Xu and S. Lilly Zheng of Wake Forest University, Akira Komiya of Johns Hopkins, Josyf Mychaleckyj of Wake Forest, Sarah Isaacs of Johns Hopkins, Jennifer Hu of Wake Forest, David Sterling of St. Louis University, Ethan Lange, Gregory Hawkins, and Aubrey Turner of Wake Forest, Charles Ewing, Dennis Faith, Jill Johnson, Hiroyoshi Suzuki, Piroska Bujnovszky, Kathleen Wiley, Angelo DeMarzo, and G. Steven Bova of Johns Hopkins, Baoli Chang, M. Craig Hall, and David McCullough of Wake Forest, Alan Partin of Johns Hopkins, Vahan Kassabian of Georgia Urology P.A., John Carpten, Joan Bailey-Wilson, and Jeffrey Trent of the National Human Genome Research Institute (NHGRI), NIH, Jill Ohar of St. Louis University, Eugene Bleecker of Wake Forest, Patrick C. Walsh of Johns Hopkins, and Deborah Meyers of Wake Forest.

Related Web Sites: Johns Hopkins Brady Urological Institute:

Johns Hopkins Kimmel Cancer Center:

AScribe - The Public Interest Newswire / 510-653-9400
(c)2002 AScribe News, Inc.

Another web site ( elaborates a bit:
Most cancers develop at the site of a chronic inflammation. During an inflammatory response, damaged cells and invading white blood cells release a large amount of highly damaging free radicals into the tissues spaces. These free radicals serve many different functions, including the destruction of microorganisms. Phagocytic white blood cells, such as neutrophils and macrophages, are not all that intelligent. They do not know if they are eating a microorganism or cleaning up debris, such as cigarette tar in the lungs. The free radicals they release can kill microorganisms in the tissues, as well as induce substantial tissue damage. If this inflammation becomes chronic, the free radicals can damage the DNA and repair proteins of cells resulting in the formation of cancer cells. [1 September 2005]

In March 2006, the possible involvement of a virus in the development of some prostate cancers was published (Identification of a Novel Gammaretrovirus in Prostate Tumors of Patients Homozygous for R462Q RNASEL Variant, Urusman, et al., Public Library of Science, Volume 2, Issue 3, MARCH 2006

The study on pomegranate juice (noted above) from 1 July 2006 Clinical Cancer Research has an interesting discussion of the role of inflammation on oncogenesis. To quote at length again

Chief, however, among the potentially explanatory hypotheses is the role of inflamation in cancer and the antioxidant and anti-inflammatory effects of pomegranate polyphenols. Chronic inflammation has been linked to the incidence of many cancers, including that of prostate (37). Studies investigating samples of human tissues have shown that epithelial cell proliferation is increased by inflammation (38). An increased risk of cancer is associated with inflammatory mechanisms, as ~15% of all cancers can be related to chronic inflammation (38). Epidemiologic studies have found an increased risk for prostate cancer in men who have a prior history of sexually transmitted disease or prostatitis (39). Inflammation in the microenvironment of the prostate cancer cell may stimulate the multistep process of carcinogenesis by up-regulating the production of pro-inflammatory cytokines and their signaling pathways. In fact, proliferative inflammatory atrophy has recently been proposed as a precursor to prostatic intraepithelial neoplasia and prostate cancer (40).

Inflammation can result in persistent oxidative stress in cancer cells and the reactive oxygen species may lend cancer cells a survival advantage (41-43). Mild levels of oxidative stress stimulate cancer cell proliferation (42) and increase mutation rates through DNA damage and/or epigenetic changes (44). De Marzo et al. (40) have shown the loss of glutathione S-transferase P1 as an early event in prostate tumors that sets the stage for stimulation of growth by oxygen radicals. Oxidative stress has also been shown to increase cancer cell proliferation by increasing the sensitivity of growth factor receptors and by altering transcription factor activity. Inflammatory cells, such as macrophages and mast cells, release angiogenic factors and cytokines like tumor necrosis factor-α, interleukin-1, and vascular endothelial growth factor, which signal cell growth and proliferation. Additionally, cytokines regulate signaling pathways that control proliferation, apoptosis, differentiation, and metastasis....

The role of antioxidants derived from the diet in protection against oxidative stress and the development or progression of cancer remains a topic of significant controversy.

Three of the references cited seem to me to be worth pursuing and are: Other references relate to the Nuclear Factor - kappa B pathway, which, when activated by inflammation may lead to cancer-generating or sustaining events. Two such reviews are: Another set of recent articles of interest are: The July 2007 edition of Scientific American has an article on the link between the immune system and inflammation and cancer. The URL is
for purchase or login (or go to your local library). It starts

A Malignant Flame
Understanding chronic inflammation, which contributes to heart disease, Alzheimer's and a variety of other ailments, may be a key to unlocking the mysteries of cancer
By Gary Stix
More than 500 million years ago a set of specialized enzymes and proteins evolved to defend our primitive ancestors against assaults from the outside world. If a microbe breached the shell of some Cambrian-era fauna, the members of this early vintage immune system would stage a savage but coordinated attack on these interlopers -- punching holes in cell walls, spitting out chemical toxins or simply swallowing and digesting the enemy whole. Once the invaders were dispatched, the immune battalion would start to heal damaged cells, or if the attacked cells were too badly damaged it would put them to rest....

An article published in April 2014 found another strong link between inflammation and prostate cancer. It is summarized in The original research can be found at
From the Abstract:
...Conclusion: Inflammation, most of which was chronic, was common in benign prostate tissue, and was positively associated with prostate cancer, especially high grade. The association did not seem to be due to detection bias.
Impact: This study supports an etiologic link between inflammation and prostate carcinogenesis, and suggests an avenue for prevention by mitigating intraprostatic inflammation.

Pesticide Links

Long-term study continues to document pesticide links to illness: Prostate cancer, lung cancer, diabetes, multiple myleoma, leukemia and other health effects occur more in people who are exposed to pesticides routinely than the general population, according to the Agricultural Health Study (, a collaborative effort between the National Cancer Institute (NCI) (, the National Institute of Environmental Health Sciences (NIEHS), and U.S. EPA. The AHS is tracking 90,000 participants over 14 years so far, with another ten years of expected study. All subjects are certified pesticide applicators and their spouses who also work on farms. "Those men with a family history of prostate cancer had increased risk from exposure to Sutan herbicide; the organophosphate insecticides chlorpyrifos, coumaphos, fonophos, and the pyrethroid insecticide permethrin for animal uses." For women with a family history of breast cancer, the scientists found an association with higher breast cancer rates among those whose husbands used the organophosphate diazinon. "Paraquat, EPTC (eptam), parathion, malathion, chlorpyrifos, atrazine and alachlor were [also] associated with wheeze... the sound produced by narrowed passages deep in the lungs."
Read the study's 2006 update ( The High Plains Journal reported on the update (

(From Pesticide Action Network Updates Service 10 May 2007-- See )

Early Stage

In the early stage of the disease, the blood levels of PSA may rise asymptomatically (as did mine). Or the cancer may grow, with low PSA, until it is palpable in a routine DRE or after causing some urinary difficulties.

In general, at this time, the cancer is still completely contained in the prostate gland (within the capsule, which is a membrane surrounding the gland) and is likely not to be too aggressive (say, Gleason score 3+3, which is what 2/3 of initial diagnoses are, according to my original urologist). The cancer is still relatively slow growing. One has time to become educated and make an informed decision about the appropriate course of action. Do not let anyone (including doctors) push you into doing anything irreversible before you understand what you are dealing with and what your options truly are.

Treatment options are discussed in Appendix B.

Post-Treatment Recurrence

In the best of all worlds, after treatment the cancer never recurs and you eventually recover from any negative effects of the treatment. Or, like me (so far), you find a way to keep your cancer under control with non-technological means, and you manage to continue doing so forever.

But that does not happen all the time. Or sometimes, the cancer is detected after it has escaped the gland. There are second line treatments, also discussed in Appendix B. These often help for a significant period of time. (I have met men in my support group who have been on hormone blockades of one sort or another for over 20 years.)

The likelihood of recurrence is a function of how soon the cancer was detected, what treatment modality was used, the skill of the practitioner, and luck. Also is age -- older men (70% of those first diagnosed are over 65 years old) may well die of something else before their prostate cancer recurs, which is considered a "cure".

Usually recurrence is detected via periodic PSA blood tests. Less frequently, PSA stays low but other symptoms indicate the cancer has come back. [Is this true??] Some of the originally available treatments may be used for recurrence - radiation and hormone blockade, primarily. Surgery is possible after radiation (called "salvage surgery"), though many surgeons do not want to put in the extra effort required, as noted above.

In general, the population of prostate cancer cells needs a form of testosterone, the male hormone produced 95% in the testes and 5% in the adrenal glands, in order to live and thrive and grow. This form is dihydrotestosterone, or DHT, and is produced in the prostate by an interaction with another hormone, 5-alpha-reductase. What hormone blockade therapies do is to deprive these cells of DHT and starve them. There are a number of different ways of doing this.

However, there is often a subpopulation of prostate cancer cells that are not dependent on DHT for survival. The longer DHT is missing, the more the sensitive cells will die and a subpopulation that "doesn't care" will be left and will grow to be the majority population. And there are no standard and effective treatments for dealing with them that are available yet. This is one of the reasons for using an intermittant hormone blockade regimen -- when the cancer has been knocked back "enough", it is given a rest (along with the rest of your system) so that the androgen-independent cells remain a minority population. If/when the cancer again recurs, the hormone blockade approach may well work again.


When the cancer spreads outside the organ of origin and takes root in one or more other parts of the body, this is called metastasis. In general, prostate cancer first colonizes the seminal vesicles and the abdominal lymph nodes, which is why they are removed and biopsied during a radical prostatectomy. Other common sites are the pelvic bones and the vertebrae of the lower spine. Later metastases may go to the lungs or brain.

There is no commonly effective treatment for metastatic prostate cancer except for hormonal blockade although other chemotherapies are used as well, especially for hormone refractory prostate cancer. Various new therapies are in development and in clinical trials now, so the situation may improve in the not too distant future. However, any new drug or treatment must undergo a significant gauntlet in terms of efficacy and safety testing in order to achieve FDA approval, so this process of staged trials can go on for years. One can search for clinical trials to participate in, if you and your cancer meet certain criteria.

Unfortunately, prostate cancer that has metastasized to the bone is often quite painful. Combine this with the fact that hormonal blockade often leads to decalcification of the bones (osteoporosis), which makes them irreversibly weaker and more subject to fracture, and the situation of end game is not very pleasant, even with good pain management techniques.


APPENDIX B: Medical Treatment Options

In which we give a brief summary of what medical treatment options there are, with some pros and cons for each.

Current Therapies


The summaries here have not yet been vetted against the reference books I read over the last couple of years nor with any MDs. What you get is my impressions, memories and opinions. Please research anything I say much further before acting upon it. At some point, I will try to tidy this up.


A nomogram is a chart or table or graph that summarizes complex statistical data. The Memorial Sloan Kettering Cancer Center provides prostate cancer nomograms (as well as nomograms for some other types of cancer) that relate Gleason score, PSA and other factors to probabilities of survival for various medical treatment options. These may be downloaded to your computer or used on their web page. Supporting references are also available at their site

Watchful Waiting/Active Surveillance

"Watchful waiting" is a sophisticated form of "doing nothing" and monitoring it. More recently it has been referred to as "active surveillance", to imply a less passive approach. It is often the tack taken for men whose cancer is not very large or aggressive and who either are in a state of health where many of the standard medical treatments are not feasible or it is likely they will die of something else before the prostate cancer will give them symptoms.

Watchful waiting should always be combined with frequent monitoring of the cancer, usually via PSA testing (most MDs would say every 3-4 months or so) or some other modality (DRE, TRUS or MRI/MRIS, for example). It should probably be combined with some of the lifestyle changes also recommended, an increase in exercise, improvement in nutrition and diet.

With watchful waiting, it is not likely that the cancer will go away. It can be a time of self-education, a breather between the shock of diagnosis and the point at which intelligent, informed decisions can be made about the next steps to be taken in dealing with the condition.

Radical Prostatectomy

A surgical procedure whereby the prostate gland, the seminal vesicles, and the abdominal lymph nodes are removed. There are three variations on the theme. In the usual case, incisions are made in the abdomen and the surgeon has a clear field of view, although the incisions are larger than with the other two techniques. With this approach, however, it is sometimes possible to preserve the nerves that run along the back wall of the prostate and control erectile function (the so-called "nerve sparing" prostatectomy). The nerves may be spared by a physician of great skill if the evidence of cancer is not adjacent to the region where they run.

A relatively new technique is nerve replacement in those cases where the original nerves need to be removed. Nerves are taken from the ankle and microsurgically attached after the prostate and the erectile nerves are excised. This adds about 2 hours to the surgery time and has had some success.

A second approach to removing the prostate is to go in through the perineum, the area between the scrotum and anus. The incision is smaller, but the ability of the physician to see is more limited and I do not think that a nerve sparing approach is taken here.

A third approach is being pioneered at one hospital in Virginia. (I read about it on the web in Jan 2001, but lost the reference.) They are doing laparoscopic prostatectomies, going in through a small incision in the abdomen. They claim some successes, though I do not know much about this. It is also being done by James Karol, MD at the San Ramon Regional Medical Center in northern California. Here they use a da Vinci Surgical System, a computer enhanced surgical system approved by the FDA in July 2000. (Reference was Associated Press Newswires, 11 May 2001, as paraphrased in the California Prostate Cancer Coalition News, vol 3, issue 4, July 2001).

The positive things to say about radical prostatectomies are that they often can remove the entire cancer burden, if caught early enough. The survival rates of best practice after 10 years is highest for RP. The operation also makes sense, in my personal opinion, even if the cancer has spread from the gland, although further treatments are necessary for follow on. The purpose in this case would be to physically remove as much of the cancer burden as possible, allowing the subsequent therapies to have a greater chance of success. My friend, spoken of above, is a case where this approach saved his life. However, most surgeons will not do this. The protocol is to open you up and remove the lymph glands and seminal vesicles and send them to a pathology lab. If the immediate biopsies of these organs indicates that the cancer has spread from the prostate gland, the surgery is aborted and the patient sewn back up with his prostate and his cancer.

If you want something different to occur with you in this case, you must be very clear and very firm with your physician before an operation, perhaps insist on a written agreement.

The downside of RP is the high rates of impotence and non-trivial rates of incontinence. Impotence results from nerve removal or nerve damage (as well as often having a psychological component). Incontinence results from the nature of the surgery. The urethra is a tube which starts at the bladder, passes through the prostate and out through the penis. There are two sphincter muscles controlling the flow of urine - one at the attachment to the bladder, and one at the place where the urethra passes out of the prostate. In the surgery, the upper sphincter is removed with the prostate and the lower surgically reattached to the bladder. So, one has half the muscles stopping the flow that one had pre-surgery; and the reattachment might not have the integrity that the original sphincter had.

Walsh and his colleagues note that "other estimates from studies in the United States have been less promising, with rates of incontinence as high as 74% and rates of impotence as high as 90%. Thus, patients considering surgery should be referred to surgeons with considerable experience in order to optimize the likelihood of effective cancer control and to minimize the likelihood of complications." (See Walsh article and references therein.)

Even if potency returns, one has no ejaculate. (The bulk of the ejaculatory fluid is created by the prostate gland and seminal vesicles; when these are removed, the fluid is no longer present.) However, even if one has erectile disfunction, the nerves controlling sexual pleasure and arousal are not affected, so orgasm is possible with an openness to sexual exploration.

External Beam Conformal Radiation

Also called 3D Conformal Radiation, External Beam Modulated Radiation, and Intensity Modulated Radiation Therapy (IMRT). This technique uses shaped beams of X-Rays. "Modulation" also implies that the shape of the beams varies in time as well as in space. The usual course is 5 days a week for about 8 weeks, where each X-Ray session lasts about 20 minutes, more or less. The idea is to deposit enough X-Ray energy into the prostate to kill the cancer (and healthy) cells there, while doing as little damage to surrounding tissue, urethra and rectum as possible.

Often, a man will be put on 3 months of hormone blockade therapy before undergoing X radiation. This is done in order to shrink the size of the prostate and weaken the cancer, both of which allow this technique to be more effective. (This is known as neo-adjuvant hormonal blockade.)

X-Rays (basically very high energy photons or light waves) start depositing their energy as soon as they encounter matter. In this case, the matter is the patient's flesh. If too much energy is deposited outside the prostate there will be severe side effects. So the technology uses a number of external beams conformed to the patient's physiology. Each beam alone is too weak to do much damage to the tissue it goes through. But when they all meet at the prostate, their combined energy in the gland is supposed to be high enough to be effective there in causing cellular damage and death.

The software and hardware for designing and shaping the beams is constantly improving, as are the imaging techniques used to inform this software.

Survival rates for best practice out to about 10 years are comparable with best practice radical prostatectomy, but after 10 years fall off in comparison. (These are age-adjusted survival rates; that is, all other things being equal.) Other positives are that this technique is not as traumatic as surgery and can be done again if cancer recurs.

The X radiation damages the tissue it passes through. It makes it tougher, among other things. Most surgeons will refuse to do a radical prostatectomy on a patient who has had external beam radiation because the job of cutting through the tissues and removing the prostate is a little more difficult and time consuming than if radiation had not been used. There are, however, surgeons willing to do such "salvage surgery" if indicated (that is, if, after radiation, localized prostate cancer returns).

The side effects during radiation treatment are usually fatigue and often bowel problems. The lower bowel passes right behind the prostate and is naturally subject to significant radiation. Also, since intestinal cells are naturally very rapidly dividing, the radiation will do more damage to their DNA than to that of more quiescent cells.

Longer term side effects do include damage to the rectal wall, incontinence and impotence. These latter two effects often come on slowly, say over the course of a year after treatment. In best practice they are comparable to the rates quoted for radical prostatectomy. (These rates of side effects seem to be somehat higher if patients are asked rather than their doctors. Also, the answers do depend quite sensitively on how the questions are posed and the degrees of effect that can be described. But this is true for all side effects of all the treatments discussed here, and, I would venture, all other medical interventions.)

Walsh and his colleagues note that "Dose-escalated radiation with the use of conformal techniques causes intermittent rectal bleeding of grade 2 or higher (requiring transfusions, interventional radiology, or endoscopic or operative intervention) in 1.5 to 18% of patients and causes impotence in 40 to 60% of patients." (See Walsh article and references therein.)

Brachytherapy (Seed Implants)

Radiation can be delivered to the prostate gland locally, with less probability of damage to external tissue, the theory goes, if a radioactive substance is emplanted within the prostate. In brachytherapy, that is exactly what is done.

There are two flavors of this treatment. In one, the radioactive substance is put into the prostate gland in carefully controlled locations for carefully controlled amounts of time. This uses high powered radioactive materials (I don't recall which isotopes) and was the form that Andy Grove had done (see the article in the references, above).

In the other approach, the radioactive material is permanently emplanted in the prostate. One substance used has a half-life of about 3 months; the other has a half-life of about 18 months.

In all cases, the radioactive material is encased in rice-grain sized metal (titanium) pellets. The emplantation is done using trans-rectal ultrasound imaging to guide the placement of the pellets; and the planning is done beforehand using the various available imaging techniques. The idea is to spread the placement of the seeds throughout the gland, but not too close to the urethra, its sphincters, the nerve bundles running along the back side of the prostate which control erections, or the rectal wall, to minimize damage to those structures. The point of entry is again the perineal region between the anus and the scrotum, with long hollow tubes used to guide the placement.

Iodine-125 is one isotope used. It has a half-life of 59.4 days, with predominant decay energies at 27 and 35 kev. In a titanium seed, there is also a peak about 22 kev. These energies imply that the radiation is most intensive within millimeters.

Another isotope used is Palladium-103, with a half-life of 17 days. It has predominant peaks at 20 and 22 kev, so also deposit energy within millimeters of the seed.

Other isotopes are also used.

Both types of brachytherapy can be done with local anesthetic on an outpatient basis, so are far less traumatic than surgery and far less time consuming than Three-D Conformal Radiation. Survival rates for best practice are probably comparable to external X-Rays out to 5 years (but I do not have any of the statistics and that last statement is just a guess for now).

Brachytherapy may be done in conjunction with hormonal blockade (beforehand, to shrink the gland and kill off some of the cancer), or with external beam X-radiation (afterward, to enhance the effects).

Side effects also include impotence and incontinence as well as bowel upset and sometimes bowel damage.

In my opinion, follow on imaging with MRI/MRIS after, say 1 year, would allow the effectiveness of the treatment to be assessed. Any remaining cancer metabolism would indicate that additional seeds are needed and that the original placement did not fully cover the appropriate parts of the gland.

Another approach to brachytherapy is to do real-time planning. This involves pre-operative MRI, perhaps CT scans and prostascint scans which are combined (via software and hardware) with high resolution ulltrasound images minutes before and during the seed implantation procedures. The software determines the best location for each seed, based on the gland location and geometry and based on image analysis of the cancer's locations. Each seed is monitored and deviations from a planned location lead to immediate modifications in the planned locations of seeds not yet implanted. This prevents both cold spots and hot spots, locations which would receive too little or too much radiation. Such dyanmic adjustment can decrease the incidence of side effects, such as impotence, incontinence and rectal wall damage. Not all practitioners follow this approach yet.

Proton Beams

Protons are the heavy charged particles in atomic nuclei and may also be used to deposit energy into the prostate with the goal of destroying the cells there, both malignant and healthy. Proton beam therapy was pioneered at Loma Linda University in southern California and is also being investigated at Harvard University, in Cambridge, Massachusetts. The Loma Linda web site is given in the Bibliography, above.

Particle beams behave differently than X-Rays, which is the attractive feature of this technique. The goal of both is to deposit enough energy in the target cells that their DNA is broken and their metabolic processes are interfered with, leading to cell death. X-Rays, as noted above, start depositing their energy as soon as they encounter matter, such as the patient's flesh and organs outside the prostate, on their way to the prostate. That is why using many simultaneous low power beams from many directions, and shaping each quite precisely is important in trying to minimize collateral damage.

Protons go right through matter until a certain depth, at which they deposit all their energy. This depth can be tuned by carefully calculating the matter the beam will go through (by imaging and computer modelling) and then precisely tuning the beam's energy. In this way, much less collateral damage may be done. The process is designed to be more efficient than X-Rays in that regard.

Still, one needs to undergo a series of treatments for some weeks, meaning that one needs to be able to spend that time at Loma Linda. In addition, Three-Dimensional Conformal X-Radiation is often used in conjunction with proton beam therapy, though obviously less than when it is used alone.

Because the technique is relatively new, I don't believe the survival statistics go out beyond 5 years or so.

A web site for men who have undergone proton beam therapy, and with a great deal of information about that technology, is the Brotherhood of the Balloon,

A summary of the state of proton beam therapy as of 26 March 2012 may be found at
There are around 10 centers providing this therapy in the U.S., with more being built. The cost is greater than that of standard X-ray treatments, but the article questions whether or not the side effects of treatment are less than those of other medical therapies.


The idea here is to use extreme cold (liquid nitogren) to kill off the prostate cells, especially the cancer cells, without damaging other areas of the anatomy. This is done by inserting tubes through the perineum into the prostate, as guided by trans-rectal ultrasound. These tubes are insulated in the areas outside the prostate. Also, a heating catheter is inserted into the urethra and up to the bladder to prevent damage to these structures.

Liquid nitrogen is introduced into the cooling tubes for enough time to freeze the areas that are desired to be killed. I believe this can be done on an outpatient basis, much like brachytherapy.

The positives of this technique are its ease (vis-a-vis surgery and radiation therapies). Best practice is said to give comparable survival rates out to 5 years [I think - check this out later]. Side effects include damage to areas not intended for treatment, and include impotence, incontinence and bowel damage, with the resulting infections.

I don't think that cryotherapy has been around long enough for 10 year survival statistics to be available.

Ultrasound/thermal therapy/Hyperthermia

I don't know much about this. I think another technique that may be used to kill prostate cancer tissue is localized tissue heating via the application of ultrasound, microwaves, or radiofrequency radiation. I don't know how effective this is, survival statistics, what damage there is to surrounding tissue both because of energy deposition from the source and from heat transfer from the affected tissue.

Side effects would come about from damage to surrounding tissue - incontinence, impotence, bowel damage are the possibilities.

Hormonal Blockade

As discussed above, prostate cells and prostate cancer cells need the male hormone dihydrotestosterone (DHT) to function and survive, for the most part. DHT is produced in the prostate by the action of an enzyme (5-alpha reductase) on the hormone testosterone. Ninety five percent of the body's testosterone is produced in the testes; 5% comes from the adrenal glands.

In order to starve the prostate cancer cells, one wishes to deprive them of the DHT they need. This can be done in a number of ways, since there are a variety of pathways in the body to the production of DHT.

Any one or a combination of these actions serves to blockade some or all of the DHT. Different drugs are used for each step.

Common side effects of hormonal therapy are

but these are reversible when the treatment is discontinued.

If hormonal blockade is used too long, the prostate cancer cells that are sensitive to the lack of DHT die off sometimes leaving behind a small subpopulation that can live and grow independent of the presence or absence of DHT. These are called hormone refractory cells and a recurrence of the cancer due to these cells is known as hormone refractory prostate cancer. It is a form of the disease for which hormonal blockade, in any of its manifestations, does not work.

Thus, a standard protocol for hormonal blockade therapy is to be on it for about a year (or until the PSA falls below some standard value, nominally 0.01 ng/ml) and then to go off of treatment until it rises to some nominal value (say 1.0 or 2.0 ng/ml), cycling through on and off periods. The logic of the off period is to both allow your body to recuperate from the effects of the hormonal blockade and to allow any hormone-dependent prostate cancer cells to become the dominant population. Too long on blockade and any refractory cells may become the dominant population.

Hormonal blockade may also be used as a preliminary therapy, before surgery or radiation, to weaken and shrink the cancer and make it more amenable to the other treatments. It is also a therapy of last resort, after surgery and/or radiation have been ineffective in eradicating the cancer and it has metastasized. In this case, it buys time and some quality of life, but generally does not "cure" the cancer or keep it in check forever.

Further, for men with large glands, whether due to BPH or normal aging, a course of hormonal blockade is usually required before other treatments in order to shrink the physical size of the gland and allow subsequent treatments to be more effective. This is known as neo-adjuvant hormonal therapy.

The standard agents of hormonal blockade are

brand name - drug name - method of action - how administered

Bob Leibowitz, MD, in Los Angeles, is an advocate of triple hormone blockade. His web pages may be found at

A recent paper of his on triple hormone blockade is Treatment of Localized Prostate Cancer With Intermittent Triple Androgen Blockade: Preliminary Results in 110 Consecutive Patients, Robert L. Leibowitz and Steven J. Tucker, The Oncologist, Vol. 6, No. 2, 177-182, April 2001 and is currently available on line at
(Free registration is required for access.)

If Lupron is given with no other treatments, a situation known as PSA flare occurs which can be quite dangerous. For the first week or so after the injection, one's PSA levels rise dramatically and the prostate cancer cells seem to have greater activity. In some men, this has led to the formation of metastases where there were none previously or to a sudden exacerbation of symptoms. Flare may be avoided by simply preceding the administration of the Lupron by a week or so of Casodex.

Recent research at Johns Hopkins (published 1 Oct 2007) indicates that ADT may, however, promote the production of a molecule, Nestin, which promotes metastasis. A summary may be found at ("STANDARD TREATMENT FOR PROSTATE CANCER MAY ENCOURAGE SPREAD OF DISEASE"). The full article is Roles for the Stem Cell-Associated Intermediate Filament Nestin in Prostate Cancer Migration and Metastasis, Wolfram Kleeberger, G. Steven Bova, Matthew E. Nielsen, Mehsati Herawi, Ai-Ying Chuang, Jonathan I. Epstein and David M. Berman, Cancer Res 2007; 67 (19): 9199-206 (1 October 2007). The abstract is available at; they charge for access to the full article.

Research presented at the 2009 ASCO (American Society of Clinical Oncology) meeting presented newer findings about the androgen dependence of prostate cancers -- rather than being totally dependent on the androgens produced by the testes and adrenal glands, some prostate cancers can produce their own testosterone and drive their own growth. This has implications for ADT. A summary of the meeting's news for prostate cancer may be found at, by Christopher J. Logothetis, MD (Published: 06/29/2009), which includes a video tutorial. The research paper is Increased expression of androgen receptor (AR) and enzymes involved in androgen synthesis in metastatic prostate cancer: Targets for novel personalized therapies, N. Mitsiades, N. Schultz, B. S. Taylor, H. Hieronymus, J. Satagopan, P. T. Scardino, V. E. Reuter, C. Sander, C. Sawyers, H. I. Scher and Prostate Cancer Genome Project Group,

One caveat about hormonal blockade appeared in a study published in the 26 August 2009 issue of the Journal of the American Medical Association: Hormonal Therapy Use for Prostate Cancer and Mortality in Men With Coronary Artery Disease–Induced Congestive Heart Failure or Myocardial Infarction, Akash Nanda, MD, PhD; Ming-Hui Chen, PhD; Michelle H. Braccioforte, BS; Brian J. Moran, MD; Anthony V. D’Amico, MD, PhD, JAMA. 2009;302(8):866-873 (See for the abstract; full text may be purchased). Hormonal blockade in conjunction with radiation therapy led to increased mortality for men with a history of Coronary Artery Disease (CAD) induced Congestive Heart Failure or Myocardial Infarction but not among men with no comorbidity or a single CAD risk factor.


cf the information in the Prostate Cancer chapter (pp 577-618) of Disease Prevention and Treatment, 3rd Edition, published by Life Extension Media

Diet, Nutrition, Holistic modalities

include PC-SPES discussion

ProstRcision practiced by Radiotherapy Clinics of Georgia (RCOG) RCOG practices a combination of brachytherapy followed by External Beam Conformal Radiation Therapy.



APPENDIX C: Future Therapies

In which a brief listing of possibilities is given with some references for each.

The simple message here is that there are many avenues under investigation for controling or curing prostate cancer, many more than I've listed below. Not all will be effective, in the end of clinical trials, but there is no doubt that some will be. In two years or five years or ten years.

If one can control one's cancer by mean of some non-irreversible treatment for however long it takes for these future therapies to come to market, then cancer will be a chronic disease or one that is indeed eradicable. My dietary approach, with mother's milk, has been quite successful for me. It is up to each man, in consultation with his trusted and knowledgeable advisors, to decide which approach is most appropriate for him, given what he knows about his particular disease, his health in general, and a whole panoply of philosophical and quality of life issues.

But here there lies even more hope for the future, if we can get from here to there.



"The Pharmaceutical Research & Manufacturers Association calculates that there are currently 170 U.S. drug and biotech companies developing more than 400 potential new compounds to fight cancer, roughly double the number of just six years ago. Indeed, so many new drugs are in the works that clinical researchers are swamped, and cancer experts note that crucial human trials have been delayed due to lack of volunteers." - From Barrons, ~18 May 2001.

...more to come...



APPENDIX D: Change Log

Change Log (What's New)
Date Revisions
03/10/00 Original version started
02/03/01 Incorporated Ted Chamberlain's comments; began this log
02/08/01 Added link to HMBANA, hyperthermia refs; PSA value of 2/15/01
02/19/01 More MRI/MRSI references; pygeum ref; magnetic rods ref; Prostate Cancer Answers
web ref; tumeric ref; JUrol 165(2) ref on ED; PSA of 2.5 on 1 Mar 2001
03/06/01 Added Feb2001 Eur J Biochem ref; angiogenesis refs; more general links;
link to Doug Thornton's story
04/10/01 Added PSA of 2.6 of 5 Apr 2001; refs for some "Future Therapies"; Added
ref; MRIS of Apr 2001; strange high values of May 2001
05/26/01 Fixed typos, added references on TRUS & Gleason; PSA of 4.0 on 5/25/01; 2.5 of 6/6/01;
refs to Ornish's program, more about prostatitis; refs to oncolink, hrpc and Leibowitz
sites; more future therapy refs
07/11/01 PSA 2.3 on 7/11/01; Fixed lots of typos; Added refs for radiation therapies and cryosurgery.
08/24/01 PSA 1.91 on 8/14/01 & notes on Raw Milk Again; notes on selenium, CO-Q10, cucumin;
fixed lots of typos; added refs to Bibliography, including Clinical Trials pages, notes on
laparoscopic surgery, Nilandron, PSA flare, etc.
09/11/01 Green Tea refs; PSA 2.12 on 09/10/01
09/12/01 Added info on 2 isotopes used in brachytherapy.
09/24/01 Added Biomira ref.
10/04/01 Added calcium ref.
10/05/01 Added
10/10/01 Added PSA of 1.93 on 10/09/01; refs to Myriad Genetics, "icon", Peregrine Pharmaceuticals;
Abram Hoffer ref; change info on Moyad Medical Journal (no longer publishing);
added another apoptosis ref, more refs on green tea, Pamidronate, PC-SPES, and gene therapy
11/02/01 Added EGFR inhibitors ref; ref to Medscape's PCa Resource Center; PSA of 2.15 on 11/08/01
11/16/01 Added refs to microwave/thermal therapy, mouse studies with antibody/radioactive atom combo;
Larry Clapp; COX-2 inhibitors as anti-angiogenesis drugs; Canadian statistics; Irofulven;
Phenoxodiol; OGX-011; Iressa; kahalalide; Bacterial Therapy
12/06/01 Added refs on artemisinin; Selenium; PSA of 2.15 on 12/11/01
01/02/02 Added ref to "one man's overview", some text modifications; brought pau d'arco story up to
date; ref to CapCure conference
01/07/02 Added ref to Stanford Phase I on dendritic cell therapy.
01/10/02 Added PSA 8.64 of 01/09/02, 6.70 on 01/11/02, 5.43 on 01/15/02, 5.45 on 01/21/02;
4.01 on 01/29/02
02/05/02 2.97 on 02/05/02
02/22/02 2.43 on 02/13/02; 2.51 on 02/22/02
02/27/02 Added refs to reviews of RP and chemotherapy, and to the Cancer Control Journal;
to p53 gene therapy
03/08/02 Added Oncolytics Biotech ref
03/20/02 Added 3 clinical trials refs from UsToo
03/29/02 Added PSA of 2.49 of 03/28/02; ref on Huggins Symposium
04/29/02 Added PSA of 2.15 0f 04/29/02
05/17/02 Added AVI BioPharm reference
05/28/02 Added PSA of 2.08 of 05/28/02
06/11/02 Added refs to vaccine overview, antivascular therapies, turning cancer into a chronic disease,
vitamin E suppressing androgen receptor, British statistics, more on COX-2 and GVAX and
conjugated linoleic acid (Cla), high intensity focused ultrasound
06/26/02 Added PSA 0f 2.07 of 06/24/02; USNews ref on genetic issues
06/30/02 Changed ref for Hormone Refractory PCa Org (old web site was pirated, it seems)
07/11/02 Fixed typos, lots of misc cleanup
07/24/02 Added 2 PSAs of 07/22/02, space for MRI discussion; another viral therapy ref
08/01/02 Added MRIS of 22 July 2002
08/20/02 Added PSA of 2.08 of 08/20/02
09/10/02 Added info on TRUS of 09/09/02; some refs
09/26/02 Added PSA of 1.96 of 09/26/02
11/04/02 Added PSA of 2.37 of 11/04/02
12/10/02 Added PSA of 2.08 of 12/10/02
12/31/02 Added reference to Phoenix5 PCa glossary
01/28/03 Added PSA of 2.59 0f 01/27/03
02/06/03 Added PSA of 2.40 of 02/05/03
02/08/03 Added summary of milk dosages; fixed bottle size to 3.5 oz (had been written as 4 oz)
02/25/03 Added info to Gleason score discussion; clarified my "conservative" PSA estimate of 7/1999;
added Free PSA to Glossary; added discussion of possible role of infection in PCa genesis.
(Thanks to Jerry L for these suggestions.)
03/11/03 Added PSA of 1.95 of 03/11/03
04/08/03 Added Hamosh ref on mother's milk; URL for Discover article on mother's milk
04/23/03 Added 2003 incidence numbers; 04/22/03 PSA of 1.89
06/07/03 Added list of biopsy readers, end of Bibliography
06/17/03 Added PSAs of 2.18 (Stanford) and 2.26 (UCSF) of 06/16/03
06/26/03 Added MRSI info for 6/16/03 and table of prostate size, PSA density
07/11/03 Added 2 books to Bibliography/Other References
08/04/03 Added PSA of 2.15 of 08/01/03
08/14/03 Added URL
09/22/03 Added PSA of 2.25 of 09/22/03; TRUS of 08/04/03 results
11/18/03 Added PSA of 1.88 of 11/17/03; milk changes in Oct
12/04/03 Fixed some typos, brought a couple of sentences up to date
12/07/03 Add GE Medical Systems MRSI reference URL
12/23/03 Add 2003 statistics for PCa incidence (NYTimes)
01/13/04 Added PSA of 2.08 0f 01/13/04; added info on Dendreon's phase 3 trial
01/25/04 Noted Discover article is available on line
02/03/04 Added refs to BioSeeker Group publications
02/09/04 Added ref to Sloan Kettering PCa nomograms
02/25/04 Added section on Better Diagnostics, ref to copy of original NYTimes mother's milk article
03/16/04 Added ref
03/22/04 Added PSA of 2.29 of 03/19/04
05/06/04 Added PSA of 1.91 of 05/06/04
05/14/04 Added ref to Buffalo Niagara Prostate Cancer Consortium
06/07/04 Added info on TRUS of 06/07/04
06/10/04 Added link to Mayo Clinic pages
07/08/04 Added ref to
07/12/04 Added PCRI alternative URL and Helpline phone
07/15/04 Added PSA of 2.54 of 07/14/04
08/04/04 Added NutraSanus URL; added PSA of 2.53 of 08/04/04
08/05/04 Added PSA of 1.95 0f 08/05/04 (at UCSF); some notes on today's MRSIs
08/17/04 More info on 08/05/02 MRSIs
09/07/04 Added box on prostate volume recalculations
09/30/04 Added ref to UCSF web site PCa publications
10/12/04 Added link to Svanborg's HAMLET Bibliography
10/15/04 Added PSA of 2.17 of 10/15/04
11/09/04 Added notes and link to Prostate Cancer Foundation
12/14/04 Added PSAs of 6.45, 3.37 of 12/03, 12/13/04
12/23/04 Added PSA of 3.29 of 12/22/04
12/28/04 Added link to original and copy of SJ Merc article
01/07/05 Added 2 links to The Cancer Cure Coalition in Bibliography
01/20/05 Added ref to (brachytherapy)
01/23/05 Added link to original and copy of BBC Health article. Added 6 more mother's milk journal
02/06/05 Added ref to UK Telegraph 16 Jan 2005 article
02/15/05 Added refs to American Academy of Pediatrics new breastfeeding recommendations (benefits
of nursing); copy of letter to BBC.
02/24/05 Added PSA of 1.72 from 02/22/95. Added another mother's milk paper to Bibliography
04/07/05 Added PSAs from 03/28/05 (5.3), 4/05/05 (7.3) & prostatitis discussion
04/19/05 Added short discussions of pau d'arco and acupuncture history
05/05/05 Added some notes on future apoptosis inducing research, a comment on BAMLET.
05/07/05 Added quote on inflammation and cancer genesis in App A
06/01/05 Added PSA 0f 4.42 0f 6/01/05
06/07/05 Added ref to
08/11/05 Added PSA of 18.3 of 7/06/05, 2.44 of 8/09/05
09/22/05 Added PSA of 3.03 0f 9/21/05
10/12/05 Added link to National Prostate Cancer Coalition in Bibliography
11/21/05 Added PSA of 2.23 of 11/21/05
01/09/06 Added ACS 2005 estimates in App A
01/18/06 Added PSA of 2.37 of 01/18/06; fixed typos & added a few misc notes
03/07/06 Added PSA of 3.27 of 03/06/06; some early discussion of MRSI of 03/06/06
03/17/06 Added UCSF PSA of 3.65 of 03/06/06; added UCSF MRSI refs from MRSI radiology report
04/03/06 Added more on 3/6/06 MRSI
04/21/06 Added more info on artemisinin
04/28/06 Added free/total PSA of 0.7/4.33 of 04/18/06
04/30/06 Added ACOR ref in Bibliography
05/11/06 Added PLoS ref on possible viral involvement
05/30/06 Added USToo ref to projected increase in PCa cases and deaths
06/03/06 Added link to
06/10/06 Brought this Change Log out from hidden HTML comments to a Table. Added more section
separators and links to the Top
06/29/06 Make some mothers' milk papers downloadable
07/15/06 Add ref to Target Discovery protein isoform diagnostics
07/22/06 Added pomegranate ref & more inflamation info
07/24/06 Allow ftp of Pomemgranate paper from my web site
08/15/06 Added PSA of 4.78 of 8/14/06
09/08/06 Added Aaron Katz book ref; Hallgren HAMLET paper ref
09/19/06 Added ref to CYT-500 mab IND
10/05/06 Added ref to AZGP1 gene expression future diagnostic
10/09/06 Cleaned up the HTML with Firefox/Tidy's help
10/16/06 Added ref to genetic tests in PharmaWeek
10/30/06 Added ref to taking lycopene with vitamin E
11/22/06 Added MRSI ref (UCSF Report 8.3)
12/06/06 Added Progenics PSMA ref
12/15/06 Added world-wide incidence statistics
01/06/07 Added ref to Dr Myers' new book, Dr Liebowitz' web site; also ManNAc and AAV2 refs added
01/17/07 Added Prostatitis refs to Bibliography
01/22/07 Added PSA of 3.61 of 01/22/07
02/02/07 Added NF-kB refs under Inflammation section
04/08/07 Added PSA of 4.34 of 03/05/07 (UCSF); MRSI of 03/05/07; use of Peenuts, Vit D; Nelson
articles on inflammation and PCa
04/19/07 Added PRIAS Project ref, notes on UCSF monitoring protocol, and some comments
05/08/07 Added PSA of 5/07/07 of 3.46
05/10/07 Added Pesticide-PCa link references
05/14/07 Added CBS story on me
06/04/07 Added HIFU Wikipedia ref to Bibliography
06/27/07 Added refs for TheCure and July 2007 SciAm article
08/21/07 Added ref; female prostatitis refs
08/23/07 Added PSA of 4.62 of 08/22/07
09/30/07 Added PSA of 09/28/07 of 5.14; ref to
11/09/07 Added FOX Chicago TV piece; ScienceNews Dec 2006 article; Mossberg bladder cancer article
11/16/07 Added KTVU-TV story on me; URL of San Jose Mothers' Milk Bank
12/19/07 Added PSA of 12/18/07 of 3.25
12/28/07 Added refs to Walsh NEJM article of 27 Dec 2007
02/03/08 Added <meta description> tag
02/06/08 Add ref to & discussion of Wilt, et al, AnnIntMed review of PCa treatments & side effects
02/12/08 Added ref on modified VitE with apoptotic properties (Apr 2006) and UCSF Nutrition web page
02/15/08 Added PSA of 02/14/08 of 4.00
02/16/08 Added to Bibliography
02/17/08 Added Business Week 29 May 2006 article to Bibliography
02/18/08 Added EETimes ref on electroporation; Dr. Gary Onik's site; article on flax seed study from
2001; PNAS selenium study from 2006
03/06/08 Added Bibliography ref to Bisphenol A and PCa
03/10/08 Added refs to T. Colin Campbell and "The China Study"
03/19/08 Added MRSI of 02/29/08
03/25/08 Added ref for Power Doppler Ultrasound; added Anders' research URL
03/31/08 Added refs for general milk properties & for lactoferrin; Nestin refs on ADT
04/13/08 Added ref to Jenny Pettersson's Ph.D. thesis, on HAMLET
05/01/08 Added ref to Kanzius Research & nanotech
07/07/08 Added PSA of 4.00 of 07/07/08, and notes on Jeff's death
07/12/08 Added info on PCK3145 for HRPC
07/24/08 Added link to A's story of mothers' milk helping cure Stage 4 colorectal cancer
08/16/08 Added ftp of Walt D'Ardenne's story
09/16/08 Added ref to Newsweek story on cancer (6 Sep 2008)
09/25/08 Added PSA of 5.86 of 09/22/08
11/25/08 Added refs to, on Provenge; to Dana Jennings' NYTimes PCa blog; Mark
Lichty videos
12/03/08 Added next Dana Jennings' blog
12/09/08 Added next Dana Jennings' blog
12/16/08 Added next Dana Jennings' blog
12/23/08 Added next Dana Jennings' blog; more on Kanzius
12/24/08 Added ref to Zero (
01/06/09 Added next Dana Jennings' blog
01/08/09 Added refs to Ed Weinsberg's Conquer Prostate Cancer Now book & web site
01/15/09 Added next Dana Jennings' blog
01/21/09 Added next Dana Jennings' blog
02/03/09 Added next 3 Dana Jennings' articles
02/10/09 Added next Dana Jennings' blog
02/11/09 Added ref to sarcosine paper in Nature
02/13/09 Added PSA of 5.72 of 02/13/09
02/17/09 Added next Dana Jennings' blog
02/20/09 Added ref to
02/24/09 Added next Dana Jennings' blog (by Dr.John Mulhall) & to the "New" Prostate Cancer Infolink
02/25/09 Added ref to Israeli mAb research under "Nanotechnology"
03/02/09 Added links for comments on sarcosine; UCSD vaccine approach; new catheterless surgical
technique (NY Presbyterian hospital)
03/04/09 Added next Dana Jennings' blog
03/09/09 Added next Dana Jennings' blog
03/15/09 Fixed link & info on Prof. Svanborg's HAMLET web site
03/18/09 Added blurb on Purdue use of dual nanoparticles in cancer probe;
PSA Controversy section and 3 refs added
03/19/09 Added Vitamin D ref section
03/23/09 Added ref to breast feeding and SIDS risk decrease
03/24/09 Added refs to 14 additional PCa sites; next Dana Jennings blog;
several articles on PSA screening controversy; 5 more HAMLET research papers
03/31/09 Added next Dana Jennings' blog
04/03/09 Added Fiona Giles' article on me
04/07/09 Added next Dana Jennings' blog
04/08/09 Added notes on MRSI of 3/31/09
04/14/09 Added more Dana Jennings' blog entries; added article on successful follow on trial
of Dendreon's Provenge vaccine
04/17/09 Added ref to Medivation's new androgen blockade drug
04/20/09 Added 2000 Breast Cancer Action article on HAMLET, etc.
Added next Dana Jennings' blog
04/22/09 Added NYTimes & Obstetrics & Gynecology articles on benefits of nursing to mothers
04/28/09 Added next Dana Jennings' blog
05/05/09 Added next Dana Jennings' blog
05/19/09 Added next Dana Jennings' blog
05/26/09 Added next Dana Jennings' blog; ftp of Obama letter
06/01/09 Added SiteMap for the Prostate Cancer pages; removed reference to NPCC site (recently renamed
to ZERO)
06/02/09 Added next Dana Jennings' blog
06/12/09 Cleaned up HTML errors & warnings using
06/15/09 Begin cleaning up broken/obsolete links using
06/17/09 Added next Dana Jennings' blog
06/18/09 Added ref to J Human Nutrition & Dietetics article on nutrition & PCa (1 Apr 2009);
PSA of 5.92 of 06/18/09
06/22/09 Added new Green Tea study; cleaned up some broken links
06/27/09 Added ref to Tichenor article on HAMLET discovery
06/28/09 Added 2 refs to Australian minicell research
06/30/09 Added next 2 Dana Jennings' blogs
07/01/09 Added Jessica Lee blog interview of me
07/03/09 Added Proteasome HAMLET article from PLOSOne
07/06/09 Added Suzanne Rough's article on Quality of Life and the use of breast milk in cancer
07/07/09 Added next Dana Jennings' blog
07/13/09 Added ref to Snuffy Myers' article on hormonal therapies
07/21/09 Added next Dana Jennings' blog
07/25/09 Added Johns Hopkins ref on VitD
08/04/09 Added next Dana Jennings' blog
08/06/09 Added link to all the USToo Hot Sheets (newsletters)
08/08/09 Added info from 2009 ASCO mtg on ADT, etc.
08/17/09 Added next Dana Jennings' blog
08/26/09 Added ref to JAMA article on increased risk of ADT for men with congestive heart failure
08/29/09 Added link to site
08/30/09 Added link to story of a monthly PSA variation experiment
08/31/09 Added 3 refs on PSA and how non-prostate tissue may create it
09/08/09 Added next Dana Jennings' blog
09/15/09 Added next Dana Jennings' blog
09/22/09 Added next Dana Jennings' blog
09/26/09 Added ref to Cancer Research article on a set of urine protein markers for PCa
09/29/09 Added next Dana Jennings' blog
10/20/09 Added next Dana Jennings' blog
11/10/09 Added PSA of 5.0 of 11/04/09
11/21/09 Added refs on PARP Inhibitors
11/27/09 Added change to my Vit D intake, a Vit D ref, and addition of PollenAid to my regimen
12/12/09 Added Goldstraw, et al ref on inflammation & PCa
12/13/09 Added refs to Gunderson, et al on long term health benefits of nursing for women; USNews article on
PCa vaccines
12/18/09 Added ref to Lenz review of Vit D and cancer
12/19/09 Added link to NIH press release about clinical trials matching registry
01/19/10 Added ref section on Research Sites: Medscape, Medline, Pubmed, BioMedSearch
01/20/10 Added 2 new Dana Jennings' blogs
01/21/10 Added Medscape news on Active Surveillance as recommended sole initial treatment for PCa
01/25/10 Added link to IPCSG (San Diego support group) site
02/02/10 Added next Dana Jennings blog
02/03/10 Added link on Prostvac-VF anti-PSA vaccine trials
02/13/10 Added link to NYTimes article on robotic surgery
02/15/10 Added next Dana Jennings blog
03/03/10 Added next Dana Jennings blog
03/10/10 Added ref to reovirus study
03/16/10 Added next Dana Jennings blog
03/19/10 Added PSA of 4.61 of 03/19/10
03/25/10 Added info on MRSI of 03/16/10
04/02/10 Added ref to USNews article on PSA and related tests and related medscape article
04/06/10 Added next Dana Jennings blog; added another talactoferrin ref
04/12/01 Added info on the Santa Cruz support group's web site, newsletter archive, and several interesting
articles in the March 2010 issue (aggressive monitoring; Gleason score revisions; recommended
pathologists for second opinions)
04/14/10 Added link to Walt D'Ardenne's web site and story
04/26/10 Updated URL for NPCC
04/27/10 Added next Dana Jennings blog
04/28/10 Add new info on Provenge (likely) approval
04/29/10 Add NYTimes ref on Provenge approval by FDA
05/11/10 Added next Dana Jennings blog
05/25/10 Added next Dana Jennings blog
06/20/10 Added ACS 2010 estimates for disease and death counts
06/23/10 Added next Dana Jennings blog
06/29/10 Added WSJ ref to article on new diagnostics for PCa; update for clinical trials available for PCa
07/10/10 Added link to resource page at ProstateCancerInfoLink; added ref on new nanoparticle based PSA
test research at Northwestern U
07/18/10 Added link to Mino Freund's cancer blog
08/16/10 Added links to AdMeTech Foundation & to NCCN
08/21/10 Added ref to Dr Katz post on diet and gene expression
08/23/10 Added ref to articles on nanosensor breath detectors for cancers
08/27/10 Added ref to Fang, et al overview of ADT
08/29/10 Added ref to OGX-011
09/07/10 Added more Dana Jennings refs
09/15/10 Added next Dana Jennings blog
10/13/10 Added PSA of 4.7 of 10/11/10
10/20/10 Added refs to USToo Wichita & to their Active Surveillance doc; also ACS paper on increased
secondary tumor risk from radiation therapy; increased heart & diabetes risk from ADT
10/29/10 Added ref to PLoSONE article on new urine test for PCa
11/30/10 Added ref to real-time MRI work at UCSF
02/22/11 Added PSA of 5.84 of 2/22/11
04/27/11 Added 5 new refs on HAMLET and Mothers' Milk; MRSI of 28 March 2011
05/06/11 Added 2 new refs on PSA controversy, infection & sepsis due to PSA testing
06/02/11 Added Bob Whitesel's blog
06/10/11 Added Quertle, a new search tool
06/17/11 Added PSA of 5.4 of 6/10/11
07/03/11 Added 2 diet refs; expanded Bibliography TOC
07/18/11 Changed prostate size of 3/2011 from 67.0 to 39.9 cc and 3/2010 from 47.4 to 41.5 - remeasured
07/19/11 Added ref to article on Prostate Mapping Biopsy
08/16/11 Added ref to discovery of 5 SNPs associated with PCa mortality
11/04/11 Added PSA of 5.2 of 11/02/11
11/13/11 Added articles on biopsy dangers
12/08/11 Added notes on 2011 PCa toll (from NIH article)
01/31/2011 Added ASCO estimates of 2012 U.S. PCa incidence and deaths
02/28/12 Added ref to NIH Active Surveillance Conf (Dec 2011)
03/16/12 Added PSA of 4.7 of 03/14/12
03/26/12 Added Business Week article on proton beam therapy
04/05/12 Changed Bob Whitesel's URL
04/12/12 Added MRSI of 04/04/2012
05/23/12 Added update on As_story
06/25/12 Added ref to Gateway for Cancer Research
08/03/3012 Added PSA of 6.1 of 07/27/2012
10/07/12 Added Clinical Oncology News article on VitD, etc
10/17/12 Added PSA of 7.22 of 10/11/12 (Hunter Labs)
11/10/12 Added ref to
12/19/12 Added PSA of 6.8 of 12/17/2012
02/08/13 Fixed broken link for AAP breast feeding policy; added ref to a breast feeding guide
03/06/13 Add PSA of 7.3, free PSA of 21% of 3/04/2013
03/29/13 Added MRSI of 3/20/2013
04/03/13 Added notes on PSA density & free PSA
08/13/13 Added ref to courseware
11/03/2013 Added 2nd BAMLET ref (2010 article)
03/31/2014 Added PSA of 7.4 of 03/25/2014; ref to throat cancer patient who used mothers' milk
05/02/2014 Added MRSI of 04/21/2014
05/09/2014 Added refs on Active Surveillance; inflammation as correlated with PCa; phi test

Prostate Cancer Site Map

© Copyright 2000-2014, Howard J. Cohen, Ph.D., All Rights Reserved

Created: 10 March 2000
Last updated: 09 May 2014
Author: Howard J. Cohen   (