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.
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[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. |
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.
| Date | 02/25/95 | 12/15/97 | 04/27/99 | 07/27/99 | 08/01/99 | 09/21/99 | 10/12/99 | 10/27/99 | 11/29/99 |
|---|---|---|---|---|---|---|---|---|---|
| PSA | 1.72 | 1.9 | 5.4 | diagnosis | 6.2 (est) | 1.9 | 1.4* finger prick |
2.2 | 2.1 |
| Date | 01/04/00 | 02/07/00 | 03/16/00 | 04/17/00 | 06/02/00 | 07/10/00 | 08/10/00 | 09/08/00 | 09/21/00 |
| PSA | 2.4 | 2.0 | 1.8 | 2.0 | 2.2 | 2.3 | 2.2 | 3.8** | 2.5 |
| Date | 10/05/00 | 11/10/00 | 12/11/00 | 01/11/01 | 02/15/01 | 03/01/01 | 04/05/01 | 05/09/01 | 05/11/01 |
| PSA | 2.2 | 2.2 | 2.1 | 2.2 | 2.8 | 2.5 | 2.6 | 19.6*** prosta- |
14.0*** titis |
| Date | 05/25/01 | 06/06/01 | 07/11/01 | 08/14/01 | 09/10/01 | 10/09/01 | 11/08/01 | 12/11/01 | 01/09/02 |
| PSA | 4.0 | 2.5 | 2.3 | 1.91 | 2.12 | 1.93 | 2.15 | 2.15 | 8.64+ pros- |
| Date | 01/11/02+ | 01/15/02+ | 01/21/02+ | 01/29/02 | 02/05/02 | 02/13/02 | 02/22/02 | 03/28/02 | 04/29/02 |
| PSA | 6.70 tatit- |
5.43 is |
5.45 | 4.01 | 2.97 | 2.43 | 2.51 | 2.49 | 2.15 |
| Date | 05/28/02 | 06/24/02 | 07/22/02 | 07/22/02 | 08/20/02 | 09/26/02 | 11/04/02 | 12/10/02 | 01/27/03 |
| PSA | 2.08 | 2.07 | 2.16 | 1.63++ UCSF |
2.08 | 1.96 | 2.37 | 2.08 | 2.59 |
| Date | 02/05/03 | 03/11/03 | 04/22/03 | 06/17/03 | 06/17/03 | 08/01/03 | 09/22/03 | 11/17/03 | 01/13/04 |
| PSA | 2.40 | 1.95 | 1.89 | 2.18 | 2.26 UCSF |
2.15 | 2.25 | 1.88 | 2.08 |
| Date | 03/19/04 | 05/06/04 | 07/14/04 | 08/04/04 | 08/05/04 | 10/15/04 | 12/03/04 +++ |
12/13/04 | 12/22/04 |
| PSA | 2.29 | 1.91 | 2.54 | 2.53 | 1.95 UCSF |
2.17 | 6.45 prostatitis |
3.37 | 3.29 |
| Date | 03/28/05 +++ |
04/05/05 +++ |
06/01/05 +++ |
07/06/05 +++ |
08/09/05 | 09/21/05 | 11/21/05 | 01/18/06 | 03/06/06 |
| PSA | 5.3 | 7.43 | 4.42 | 18.3 | 2.44 | 3.03 | 2.23 | 2.37 | 3.27 |
| Free PSA | 15 % | ||||||||
| Date | 03/06/06 UCSF |
04/18/06 | 08/14/06 | 01/22/07 | 03/05/07 | 05/07/07 | 08/22/07 | 09/28/07 | 12/18/07 |
| PSA | 3.65 | 4.33 | 4.78 | 3.61 | 4.34 UCSF |
3.46 | 4.62 | 5.14 | 3.25 |
| Free PSA | 16 % | Date | 02/14/08 | ||||||
| PSA | 4.00 | ||||||||
| Free PSA |
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.)
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.
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[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.
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[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. |
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[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.] |
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[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". |
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[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. |
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[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. |
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[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. |
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[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. |
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[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. |
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:
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 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:
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.
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.
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.
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 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
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.
And, there is no sign of any disease outside the prostate nor at the
capsule (the boundary of the gland).
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.
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.
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.
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.
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.
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.
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.
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.
The next imaging, probably to be done around March 2009, should again be easy
to compare with the current images and a progress/regress of the cancer
should be discernible.
| Date | 09/01/1999 | 04/03/2000 | 11/03/2000 | 04/19/2001 | 01/09/2002 | 07/22/2002 | 06/16/2003 | 08/04/2003 | 06/07/2004 |
|---|---|---|---|---|---|---|---|---|---|
| Prostate Size cc |
?? | ?? | 34 | 39 | 33 | 40 | 38 | 46 TRUS |
48 TRUS |
| PSA Density ng/ml/cc |
?? | ?? | 0.065 | 0.067 | 0.26 prostatitis |
0.060 | 0.057 | 0.047 | 0.040 |
| Date | 08/05/04 | 03/06/06 | 03/05/07 | 02/29/08 | |||||
| Prostate Size cc |
46 | 49.2 | 42.3 | 45.0 | |||||
| PSA Density ng/ml/cc |
0.055 | 0.074 | 0.103 | 0.089 |
|
[Notes on Prostate Volume] 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. |
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 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
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.
As a background, this is what I had been taking for years:
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:
| Ingredient | Amount | % RDA |
|---|---|---|
| B1 (Thiamine Hydochloride) | 100 mg | 6660 |
| B2 (Riboflavin) | 100 mg | 5880/td> |
| 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 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 http://www.biospace.com/news_story.aspx?StoryID=15426.)]
Selenium is noted as helping the anti-oxidant activity of vitamin E and should be taken with it. To quote the Life Extension Foundation,
The generic prostate health pill was suggested by my daughter, who is an
advocate of alternative medicine. These are its ingredients
| 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:
In March 2002 I added this to my regimen:
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:
| Ingredient | Amount |
|---|---|
| Vitamin C | 20 mg |
| Vitamin E (d-α tocopherol) | 50 IU |
| Bitamin B6 | 20 mg |
| Zinc | 20 mg |
| Selenium | 100 mcg |
| Proprietary Blend
Glycine L-Alanine Glutamic Acid Saw Palmetto Pygeum Extract Pumpkin Stinging Nettle Echinacea Puprpurea Garlic Gingko Biloba |
600 mg |
Peenuts was created by a Florida Urologist, Dr. Ronald Wheeler (see
http://www.peenuts.com), who claims
significant success in reducing prostatic fluid inflammation in men
taking this pill. He has at least one peer reviewed paper on these
studies and is collaborating with UCSF on another study, where MRSI
of both men and their expressed prostatic secretions (EPS) will be
used as measuring modalities. That is, microscopic evaluations of the
EPS as well as MRSI imaging and analysis of the EPS as well as the men
it came from will look for indications of inflammation over time. (See
the discussions below for my history of recurrent prostatitis and for
current theories of how chronic inflammation may give rise to cancer.)
These are the things I stopped taking in September 1999:
Dr. Carroll noted that some cancers feed on Calcium and suggested I stop
taking it as a supplement. I haven't changed the amount I do (or do not)
get from my food, however. (See
http://www.docguide.com/news/content.nsf/news/391BD0B73B4A876C85256ACE00516B45?
OpenDocument&id=7ED78FC79E323C75852569CB00019463&c=Prostate%20Cancer&count=10
- "High Calcium Intake May Increase Risk Of Prostate Cancer", for example.)
statins
In the autumn of 2000, I also started taking Zocor (simvastatin), 10 mg
per day, since I had mildly elevated cholesterol (starting about 230).
http://www.zocor.com
In June 2002, my MD switched me to Lipitor (ataorvastatin calcium) http://www.lipitor.com, since my liver enzyme tests had begun to creep up the to high normal boundary. Changing statins is a way to control these, frequently.
I stopped Lipitor after about 9 months, resumed 10 mg of Lipitor in Decemeber 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 e 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.
Naturopath
In October 1999, I saw a Naturopath near Vancouver, British Columbia. I'll
discuss him below, in the section on Alternative
Practitioners. He also gave me a bunch of stuff to take that I added
to my regimen after my PSA test of 27 Oct 1999.
| 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 |
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
By and large, we've always eaten pretty much this way except that we've increased the amount of organic food in our diet.
However, there are some things lost in its reductionist approach. One is the realization that the patient is a person rather than a bag of symptoms. Another is that the person comes from a complex web of history and social interactions and beliefs. And another is an appreciation of the ability of the body to heal itself given the stimulus and opportunity and help to do so. And another is a dismissal of things that do not fit into its mechanistic picture.
Acupuncture
So I sought to augment my care by seeing three kinds of alternative
practitioners. The first is an acupuncturist. The one I chose was trained
as an MD and came highly recommended. I 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).
Chiropractic
The second practitioner I saw was a chiropractor. The idea here was that
if I had any structural issues, subtle or otherwise, that prevented proper
innervation of my organs, that would subtract from my systems' optimum
performance and health, including that of my immune system. The chiropractor
I initially chose was a friend who had recently graduated Chiropractic
College and been
licensed. His practice was just starting out so he had a lot of time to
work with me and explore various possibilities. I saw him about once a week
or so for about 3 months and then stopped when he felt there was nothing more
he could do for me structurally.
In July 2000 I started being treated by a Network Chiropractic practice. This is a more subtle form of manipulation, more frequent than standard chiropractic practice, also designed to fully and properly align the spine and permit proper flow of nerve energy, hence better health and healing, including enhanced immune system functioning. In March 2001, the practice moved to another city, which was inconvenient to get to, and I decided to stop going there and focus instead on more active pursuits, such as resuming my yoga practice.
Naturopathy
This is a more interesting story. At the first Prostate Cancer Support Group
meeting I went to in September 1999, I replaced another fellow as the
youngest in the group. We got to chatting after the meeting and he mentioned
that he had a friend in Vancouver who is successfully controlling his
prostate cancer through dietary and holistic means.
I contacted the friend via email and then in a long phone conversation. He had also been trained as a physicist and worked as one for some years before drifting into the field of government science and development policies. He was associated with Simon Fraser University in Vancouver and also did work for the Canadian government as well as consulted with other governments on these issues. Obviously a person coming from the same Western analytical approach as I did, at least originally, not one to be easily bamboozled by various forms of mumbo-jumbo. He had decided upon his diagnosis three years earlier (1996) that he too wished to avoid surgery and radiation and their attendant side effects, so sought alternative approaches. Among other things, he increased the amount of organic and healthy food in his diet. And he found a local Naturopath as one of his practitioners, an older Dutch physician who originally trained and practiced as a neurologist for many years. Eventually, Pieter became a psychiatrist and later on retrained again as a naturopath and homeopath.
On this recommendation, we booked a business/pleasure trip to Vancouver, one of our favorite cities, for mid-October 1999. The doctor took some medical history, and then used an interesting device attached to his PC to measure balances and imbalances in my body. There are references in the Bibliography. The technique used is popular in Europe, unknown in the US, and is called ElectroAcupuncture according to Voll (or EAV), after its inventor, a German physician named Voll. He then gave me this list of things noted above. He also gave me an injection of dead and diluted prostate cancer cells to boost my immune response, a homeopathic approach.
We saw him again over Christmas 1999. He said I was better but not cured yet and did more of the same, keeping the medications almost the same.
As I ran out of his supplements during the month of April 2000, I stopped taking them. We had noted that my PSA had gone down for 2 months before I started the naturopathic treatments, and so determined that whatever good they might be doing, they were not crucial to my good health. It was also expensive and inconvenient to travel to Canada, even a few times a year (he would have preferred every 2 months). So the next part of the experiment has been to omit the naturopathic treatments and supplements. I always have the option of resuming them.
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.
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 Washinton, 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. |
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.
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.
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.
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.
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.
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.
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.
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.
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.
An excellent summary of this study may be found in a New York Times Health blog: htpp://well.blogs.nytimes.com/2008/02/05/no-answers-for-men-with-prostate-cancer