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.
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.
|Free PSA||15 %|
|Free PSA||16 %|
|Free PSA||21 %||17 %|
|Free PSA||15.9 %|
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.
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.
It should be noted that as a man ages, his prostate gland starts growing. So
a larger normal gland, puuting out a roughly constant amount of PSA protein
per unit volume, will, over the years result in higher PSA values overall.
That is why the "normal" ranges are larger as men get older. The rise in my PSA
with the years, especially after mid-2008 (9 years after diagnosis), is consistent
with this and not alarming.
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
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
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.
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."
Again, the radiologist's report stated: "...no clear cut tumor metabolism is observed. No extracapsular extension, no seminal vesicle invasion, no lymphadenopathy, no suspicious bone lesions.... Compared to the study from 03/2009, no significant change. No tumor focus in either MR or MR spectroscopy."
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.
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."
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.
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 prostatitis I had from September to Decemeber of 2013.
In the subsequent imaging, April 2015, this signal from the right apex was absent, an indication that this was inflammation and not cancer.
On 23 April 2015 I had my twentieth MRSI using the 3 Tesla machine at UCSF's new Bakar Cancer Center in Mission Bay, San Francisco. Gadolinium contrast was again used for the final images in the sequence.
The radiology report discussed a 13 mm focal lesion in the left posterolateral peripheral zone and the midgland/apex, which had not been seen in previous images. On review of the 2014 images, a tiny amount of signal was seen in the diffusion images in this region, but it was unremarkable at the time (i.e., not significant enough to make remarks about). Four of the seven parameters that current imaging technology provides are consistent with cancer -- or inflammation. It is still difficult to differentiate prostatitis from cancer on the images. If cancer, the imaging is consistent with Gleason 3, a slow growing cancer. It was suggested that I continue active surveillance and wait another year for my next imaging.
The change in prostate volume, from 56 cc in 2014 to 75 cc in 2015 is also suspicious. The folks in radiology with reexamine the images to derive better volume estimates for both years, which impact the PSA density calculations. Given the current numbers (PSA 8.1 in Feb 2015, volume of 75 cc), my PSA density is 0.108, well within the "safe" range of <0.15.
Note: because the jump in volume as measured by the radiologist from year to year was unreasonably large (56 cc to 75 cc), I asked the researchers to recalculate the 2014 and 2015 volumes more accurately. The 2014 volume was changed to 56.3 cc. The 2015 volume was changed to 60.72 cc. This leads to a PSA density in 2015 of 8.1/60.72 = 0.133.
The next imaging, probably to be done around April 2016, should again be easy
to compare with the current images and a progress/regress of the cancer
should be discernible.
[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.
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:
|B1 (Thiamine Hydochloride)||100 mg||6660|
|B2 (Riboflavin)||100 mg||5880/td>|
|B6 (Pyridoxine Hydrochloride)||100 mg||5000|
|B12 (Cyanocobalamin)||100 mcg||1660|
|Pantothenic Acid||100 mg||1000|
|Inositol||100 mg||No Value Claimed|
|Choline (Bitartrate)||100 mg||No Value Claimed|
|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
|Vitamin B6||5 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:
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:
|Vitamin C||20 mg|
|Vitamin E (d-α tocopherol)||50 IU|
|Vitamin B6||20 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
- "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). http://www.merck.com/product/usa/pi_circulars/z/zocor.html
In June 2002, my MD switched me to Lipitor (ataorvastatin calcium) http://www.lipitor.com, since my liver enzyme tests had begun to creep up the to high normal boundary. Changing statins is a way to control these, frequently.
I stopped Lipitor after about 9 months, resumed 10 mg of Lipitor in December 2004, and stopped again in February 2005. Blood tests showed good lipid control with the 2 months on Lipitor, and rising levels in the following 2 months off (early April 2005). In mid-April I began taking Niacin (750 mg each evening, increased to 1000 mg per evening after 2 months, and then to 1500 mg each evening 8 months later [Feb 2006]; to 2000 mg each evening as of Feb 2007) to see if that would correct my lipid levels, which it has, for the most part.
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.
|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.
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.
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 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.
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
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
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.
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
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/
From their FAQ page: "Quertle goes beyond simple term matching to identify the most salient information in the literature. Using a combination of linguistic methods, Quertle finds facts defined within documents, creating its own database of about 250 million relationships, and is able to report the ones that are relevant to your query. Quertle's approach is based on a thorough understanding of biology and chemistry and was built from the ground up to address the unique needs of this technical literature."
The following references are provided (as of March 2006) in an
MRSI Radiology Report:
The article also contains a good, though short, description of the
relationship between inflammation and oncogenesis. (See
It is interesting to note that the embryonic tissue that gives rise to the
prostate gland in male children gives rise to two small glands that
surround the female urethra -- the Skene glands and the paraurethral
glands. These glands also stain positive for PSA. It is thought that
their inflammation, a kind of female prostatitis, is one of the causes
of female urethral syndrome. Females with these disorders suffer the
same symptoms of urinary frequency, pain with urination, and pelvic
pain, that men with prostatitis have. See
These are books that I have not yet read but that came highly recommended.
These books were referred to me by a leader of The Prostate Forum of
Fullerton, California, the last of which is used in their classes for the
"newly diagnosed". Again, I have not read them.
A web link is http://clincancerres.aacrjournals.org/content/vol12/issue13/
which requires payment or a subscription. It may also be downloaded from ftp://www.cohensw.com/pub/pca/PomegranatesProstateCa_ClinCancRes_2006_12_13_4018.pdf
They claim this product
New Pilot Study Suggests Flaxseed And Low-Fat Diet Can Be Protective Against Prostate Cancer, ScienceDaily (Jul. 12, 2001)
(Download the June 2002 issue as a PDF and see page 2, top of middle column.)
The 28 March 2002 issue of Cancer Letters (vol 177, pp 163-172) had an article by Harvard Medical School researchers, indicating that CLA, an omega-6 fatty acid, can inhibit tumor growth and proliferation of human cancer cells. CLA also helps maintain a healthy heart and veins, maintain healthy cholesterol and triglyceride levels, act as an anti-oxidant and possesses anti-atherogenic properties. Recent human studies appear to indicate positive effects in helping to control plasma lipids, blood glucose and body weight when used in conjunction with diet and exercise.
More about CLA from a company selling it.
Transrectal Ultrasound and Biopsy in the Early Diagnosis of Prostate Cancer, Jefferey C. Applewhite, MD, Brian R. Matlaga, MD, MPH, David L. McCullough, MD, and M. Craig Hall, MD, in Cancer Control, JMCC 8(2) 141-150 (2001)
A good review of the history of TRUS as well as a thorough discussion of biopsy strategy for most efficient detection of prostate cancer. The standard 6-core approach is noted to be significantly inferior to 10-core and related strategies. The full text is downloadable as a PDF from this URL.
A good introduction and review article. Also available on the web as a downloadable PDF file, along with all previous issues, at http://www.prostatepointers.org/a27dsk329.html.
The article AN UPDATE OF THE GLEASON GRADING SYSTEM contains information (as of December 2009) on modifications to the Gleason scoring system, based on J Urol. 2010 Feb;183(2):433-40. Epub 2009 Dec 14. ( http://www.jurology.com/article/S0022-5347(09)02704-9/abstract -- full article is available for purchase.)
A very visual description of the surgery by its inventor, Dr. Patrick Walsh and his colleagues Arthur L. Brunett, MD and Alan W. Partin, MD, PhD. The presentation was originally written in 1993.
See also additional resources at http://urology.jhu.edu/prostate/cancer.php
Radical Prostatectomy in the Management of Clinically Localized Prostate Cancer, Raviender Bukkapatnam, MD, and Julio M. Pow-Sang, MD, Cancer Control 8(6):496-502, 2001.
A more modern summary of the procedure, including a discussion of laparoscopic techniques.
Had been at http://www.washingtonpost.com/wp-dyn/articles/A25443-2002Oct14.html
A Washington Post article from 15 October 2002 on laparoscopic prostate surgery, with pros, cons and a graphic. Abstract is available for free, full article is now for sale.
New Catheter-less Technique May Ease the Pain and Discomfort of Prostate Cancer Recovery when used with robotic laparoscopic surgery. This is a press release from NewYork-Presbyterian/Weill Cornell Medical Center (2 Oct 2008)
Results Unproven, Robotic Surgery Wins Converts, Gina Kolata (13 February 2010) -- A status report on robotic radical prostatectomies versus laparoscopic and open surgeries.
An overview of the history, technology and statistics of various approaches to external beam radiation therapies.
This link allows the free download of a PDF of the article.
Cancer Associated With a Greater Risk of Local Second Malignancy: Presented at ACS (8 October 2010). "Patients who receive radiation therapy for prostate cancer have a 3.5-times greater risk of developing a second malignancy, according to a study presented here at the 96th Annual Clinical Congress of the American College of Surgeons (ACS)...."
The American Brachytherapy Society web site
Stephen W. Doggett MD's site. Dr. Doggett practices in southern California an advanced approach to brachytherapy, involving real-time imaging and plan modification. His site contains a good tutorial on his techniques, with images.
Life Extension Foundation's overview on Prostate Cancer
Their overview on Early Stage Prostate Cancer
They are selling products, but have an interesting and accessible discussion of nutritionally oriented information.
Current Issues in the Management of Prostate Cancer: Charles Huggins Symposium. This CME (Continuing Medical Education) activity is based on transcripts and slides of presentations as delivered by the faculty at "Current Issues in the Management of Prostate Cancer: Charles Huggins Symposium" held just prior to AUA's 96th Annual Meeting at the Hilton Anaheim, Anaheim, California, on June 1, 2001, published 28 September 2001.
The web site of Doctor Bob Liebowitz and Steven Tucker's Compassionate Oncology Medical Group in Los Angeles. They have been on the forefront of the application of triple hormonal blockade therapies in prostate cancer.
Beating Prostate Cancer with Hormonal Therapy, Charles E. (Snuffy) Myers, M.D, Reprinted from PCRI Insights May, 2007 v 10.2
Dr. Myers, a urologic oncologist, was himself diagnosed with aggressive prostate cancer at age 55 in 1999. In this article he talks about myths about hormonal blockade, about the positive effects of attitude, and how hormonal blockade can be an effective therapy, even for many advanced cases of PCa.
Androgen Deprivation Therapy: A Survival Benefit or Detriment in Men With High-Risk Prostate Cancer?, L. Christine Fang, MD, Gregory S. Merrick, MD, Kent E. Wallner, MD, ONCOLOGY. Vol. 24 No. 9 (August 24, 2010)
An overview of the positive and negative aspects of ADT, both as a mono-therapy and as an adjuvant therapy.
"The FDA has asked manufacturers of gonadotropin-releasing hormone (GnRH) agonists -- a class of drugs used primarily to treat prostate cancer -- to add new warnings about the potential risk for heart disease and diabetes....Earlier this year, the American Heart Association, the American Urological Association, and the American Cancer Society issued a joint advisory warning of the increased risks of diabetes, myocardial infarction, stroke, and sudden death among men who use androgen deprivation therapy (ADT) to treat prostate cancer. GnRH is the most common form of ADT..." (20 Oct 2010)
Prostate Cancer Management and Cryosurgery in Older Adults, Ronald M. Benoit, M.D., Jeffrey K. Cohen, M.D., and Ralph J. Miller Jr., M.D., Geriatric Times, May/June 2001, Vol. II, Issue 3
An overview of treatment options for older men with an emphasis on cryosurgery.
Not available as of June 2009.
The website of Dr. Gary Onik and Florida Hospital/Celebration Health. Dr. Onik is the inventor and pioneer of ultrasound guided cryosurgery for both the prostate and the liver, and an advocate of prostate lumpectomy as well as 3D Prostate Mapping Biopsy. These are discussed on this site.
The Treatment Challenge of Hormone-Refractory Prostate Cancer, Julie A. Kish, MD, Raviender Bukkapatnam, MD, and Felipe Palazzo, MD, Cancer Care 8(6):487-495, 2001.
A summary of current and experimental chemotherapy approaches, with an emphasis on HPRC.
New cancer drug will prolong lives, Vancouver scientists say, Tiffany Crawford, Vancouver Sun August 27, 2010
OncoGenex Technologies, a University of British Columbia spinoff company, has licensed the drug OGX-011. In Phase 2 clinical trials, scientists discovered that the drug OGX-011 will extend a patient's life by about seven months, roughly double the life expectancy of chemotherapy alone in hormone resistant prostate cancer. The drug is given in conjunction with docetaxel and prednisone, and serves to inhibit the production of a gene protein called clusterin that protects cancer cells from cancer treatments, such as radiation and chemotherapy.
Prostate Cancer Test Found to Save Few Lives
An article summarizing two large studies on this subject (the next two references)
Mortality Results from a Randomized Prostate-Cancer Screening Trial , Gerald L. Andriole, M.D., et alia, New England Journal of Medicine (18 March 2009)
Screening and Prostate-Cancer Mortality in a Randomized European Study, Fritz H. Schröder, M.D., et alia, New England Journal of Medicine (18 March 2009)
Screen or Not? What Those Prostate Studies Mean -- A discussion of the ambiguities of the two previous studies.
Us TOO and 13 of America's prostate cancer organizations issue reaction to the PSA screening studies (23 March 2009)
What to Make of the Prostate Cancer Screening Studies, Bernadine Healy, M.D (March 23, 2009)
Commentary by the former head of the National Institutes of Health, the American Red Cross, and the College of Medicine and Public Health at Ohio State University.
A First-Generation Multiplex Biomarker Analysis of Urine for the Early Detection of Prostate Cancer, Bharathi Laxman, David S. Morris, Jianjun Yu, Javed Siddiqui, Jie Cao1, Rohit Mehra, Robert J. Lonigro, Alex Tsodikov, John T. Wei, Scott A. Tomlins, and Arul M. Chinnaiyan, Cancer Research 68, 645, February 1, 2008. doi: 10.1158/0008-5472.CAN-07-3224
A study of a set of proteins found in men's urine has identified a suite of 4 that together seem to have a greater selectivity and specificity for identifying the presence or absence of prostate cancer than the PSA test.
Can This Test Be Saved? Improving on PSA for Prostate Cancer Screening, Katherine Hobson, US News and World Report, Posted: March 29, 2010
Discussion of the PSA testing controversy and some additional related tests that may help differentiate indolent from aggressive cancers. One of these tests is noted in the next reference.
New PSA Test Improves Detection of Prostate Cancer, from Reuters Health Information, 24 Mar 2010 (See also J Urol 2010;183:1355-1359)
"Testing for the (-2)-isoform of proenzyme prostate specific antigen (p2PSA) is more accurate than PSA testing in differentiating prostate cancer from benign disease, according to a report in the April issue of The Journal of Urology...."
An article (5 May 2011) discussing infection and sepsis risk from PSA testing, adding to the controversy of whether the test may pose more harm than risk. (Further information may be gleaned from an abstract from the 2010 American Urological Association Meeting, May 29–June 3, 2010, San Francisco, CA -- see the first abstract at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931291/, Infectious Complications of Prostate Biopsies, and the references therein).
Two major PSA test kits were used to evaluate samples from over 200 men. Significant differences were found in the results of the kits versus each other and within each manufacturer's assay, depending on the lot of test chemicals used. The variations were in the 10% range overall.
Men without prostate cancer who had initial PSA in the 4.0-10.0 range were tested twice within 2 to 3 weeks. The variation from first to second sample was 23.5%; when the first sample was retested at the time of the second test, the variation found was 10.5%.
PSA was followed in 49 men with prostate cancer who used "watchful waiting". PSA was measured roughly every 6 months. No correlation was found with rate of increase and any other factor (age, stage, etc.). Significant variability was found in the rate of change. The most interesting result, of which there was no followup or further investigation, was that in 22% of the men in the study, the PSA levels decreased during the study with no medical intervention.
A sample of 949 men from a prostate cancer screening program who had no signs of cancer were studied with 2 or 3 PSA measurements taken 2 to 3 years apart. They found significant variation within individuals over time, but all within normal ranges. Overall, the values were fairly constant (PSA velocity approximately 0.0 ng/ml/year).
An interesting one man study of PSA variations as well as a discussion of his history and treatment decisions. As an experiment, for one month, he had his PSA measured at the same time every day, trying to keep his diet and routines fairly constant. Significant variation was seen.
Cancer: looking outside the genome, Judah Folkman, Philip Hahnfeldt & Lynn Hlatky, Nature Reviews Molecular Cell Biology 1, 76-79 (2000)
An overview of why taking a non-genomic point of view can be useful in synthesizing an approach to all cancers.
The full text is for sale; the abstract is available for free at http://www.nature.com/nrm/journal/v1/n1/abs/nrm1000_076a.html
A bibliography of research articles; free group membership required for access.
Center Watch Clinical Trials Listing Service
State by state listing of current clinic trials for prostate cancer.
Clinical trials site, etc
Clinical trials search engine
U.S. Oncology organizes & finds patients for trials
National Institutes of Health / National Library of Medicine pages on clinical trials - what they are and search capabilities. As of June 2001, over 5000 current trials were listed. As of June 2010, this search
( http://www.clinicaltrials.gov/ct2/results?cond="Prostate+Cancer") led to 1655 listed trials.
The National Comprehensive Cancer Network Also suggested by UsToo
The UsToo clinical trials page
NIH Announces First National Research Study Recruitment Registry
Nationwide Registry to "Match" Volunteers with Researchers
Individuals who want to participate in research studies now can connect online with researchers nationwide through the first disease-neutral, volunteer recruitment registry....
The Gateway for Cancer Research
An independent organization that funds cancer clinical trials. As of June 2012, they have 9 PCa trials ongoing (see http://www.demandcurestoday.org/cancer-research/cancer-type?cancertype=Prostate+Cancer)
Prostatitis -- Old Questions, New Answers: An Update for Clinicians CME/CE
Author: J. Curtis Nickel (Free registration required)
An overview of the current state (9 Jan 2007) of diagnosis and treatment of the several kinds of prostatitis.
The Wikipedia entry, with diagrams & references.
The Prostatitis Foundation, A patient oriented site dedicated to information on the cure and treatment of this disease.
Prostatitis Center, Tucson, Arizona
A medical practice centering around the treatment of prostatitis using a combination of prostatic massage and appropriate antibiotics (based on a pathologist's examination of expressed prostatic secretions). The approach of using deep prostate massage to empty the sacs and make them accessible to antibiotics or other medications seems to be more used in Europe and Asia than in North America.
The Prostatitis Clinic at the MacLeod Laboratory, New York City
Attila Toth, MD, Director
Their approach is a detailed examination of urine and seminal fluid for Chlamydia trachomatis (from the urethral swab), Mycoplasma group, complete screening for aerobic and anaerobic bacteria and yeast. This is followed by direct ultrasound guided transrectal injection of antibiotics and/or anti-fungals into the prostate.
Lou Surette's site on how to cheaply and easiy "clean out the plumbing" of your prostate using Sitz baths, an intriguing idea. He argues that this simple procedure can decrease the chances of prostatitis, BPH symptoms, and the possibility of prostate cancer. He's also an advocate of appropriate diet and supplementation. He seems to have created this site in early 2003. In May 2003, he was diagnosed with Chronic Lymphatic Leukemia (CLL) and began a separate web site to blog his experiences (http://radio.weblogs.com/0135129/ ). His last entry there is 12 May 2006 where he talks of palliative care.
Chemical in Plastics Is Tied to Prostate Cancer
(Originally published in the Los Angeles Times, 01 June 2006). "Bisphenol A, found in baby bottles and microwave cookware, permanently altered genes in newborn lab rats, a study finds."
An enthusiastic review and more information is at http://www.mycancerplace.com/forum/?action=view_topic&id=53&fid=15
The book is available from http://www.prostateforum.com
Reveiews on Amazon are either very positive or very negative.
An M.D. diagnosed with prostate cancer, Cohen researched the current and forthcoming diagnostics and treatments to avoid overtreatment and its side effects. Said to be pithy and highly readable.
There are several world-class experts in reading prostate cancer biospsy slides in addition to Dr. John McNeal, mentioned above. It might be prudent to have your slides sent to one of these folks to get their readings. A correct Gleason score, number of positive cores, and percentage of the cores that are positive are important factors in helping to decide the extent and aggressiveness of one's cancer and hence the appropriate course of action.
2807 N. Parham Road, Suite 114
Richmond, VA 23294, USA
Phone: 800 214-6628, Fax: 804 288-6568
Web Site: http://www.bostwicklaboratories.com
Johns Hopkins Hospital
401 North Broadway
Baltimore, MD. 21231-2410
Stanford University Hospital, Department of Urology
300 Pasteur Drive
Stanford, CA 94305
Phone: 650-723-6024 (Urology Dept.)
1854 Bearlane Drive Suite 17a Nashville, TN 37210
Phone: 615-847-0410 or 1-888-8OURLAB
Web Site: http://www.prostatelab.com
One danger of not having a biopsy, when called for, is not knowing the histology of one's prostate cancer, if present. However, there are dangers as well, which one should be aware of.
This is the October 2011 Veterans' Resources newsletter. Go to the bottom of the page and click on "Download Bulletin 111001". The article of note starts on page 12 of the Word file you'll get.
Men who underwent prostate biopsy were more than twice as likely to be hospitalized within 30 days compared with men who did not undergo the procedure, a study of Medicare beneficiaries showed. Procedural complications, such as infection and bleeding, as well as exacerbations of comorbid conditions contributed to a hospitalization rate of 6.9% following prostate biopsy versus a 2.9% hospitalization rate for controls....
the 22 September 2011 issue of MedPage Today.
Complications After Prostate Biopsy: Data From SEER-Medicare Presented at annual meeting of American Urological Association, San Francisco, California, May 29–June 3, 2010, Stacy Loeb, H. Ballentine Carter, Sonja I. Berndt, Winnie Ricker, Edward M. Schaeffer, The Journal of Urology, Volume 186, Issue 5 , Pages 1830-1834, November 2011.
The article also contains a good, though short, description of the relationship between inflammation and oncogenesis. (See below)
It is interesting to note that the embryonic tissue that gives rise to the prostate gland in male children gives rise to two small glands that surround the female urethra -- the Skene glands and the paraurethral glands. These glands also stain positive for PSA. It is thought that their inflammation, a kind of female prostatitis, is one of the causes of female urethral syndrome. Females with these disorders suffer the same symptoms of urinary frequency, pain with urination, and pelvic pain, that men with prostatitis have. See
These are books that I have not yet read but that came highly recommended.
These books were referred to me by a leader of The Prostate Forum of Fullerton, California, the last of which is used in their classes for the "newly diagnosed". Again, I have not read them.
[A more extensive prostate cancer glossary is available at
http://www.phoenix5.org/glossary/glossary.html, part of
Robert Young's Phoenix5 site, referenced above.]
It should be noted that other chemicals and drugs may also induce tumor cell apoptosis. To my (limited) knowledge, some of these are in various experimental or pre-clinical stages, but all have side effects of one sort or another. I do not believe that mother's milk has known side effects and it is currently available, whereas alternatives are not.
Necrosis is non-programmed cell death, usually due to outside
factors, such as radiation or attack by toxins. In the case of
necrosis the cell does not have time to orderly shut down. It
appears differently than an apoptotic cell.
A monomer in chemistry is a single unit. When a number of these single units are bound together, this is called a multimer. Just noting that something is multimeric does not say what the fraction is that is 2-meric, 3-meric, etc.
MAL in human mother's milk has been found to cause cancer cell death
(apoptosis) in vitro (in the test tube). The researchers at Lund
University also found that certain cofactors in the mother's milk
(oleic acid) are also required for MAL to be effective as a cancer
The spectroscopy component, done at the same time as the imaging,
has a coarser resolution, roughly cubes about 6mm on a side.
The spectral results
can be overlaid on the image to correlate cancer, BPH, necrotic
(dead) cells, and normal cells with the image.
Healthy prostate cells also produce PSA. A rule of thumb for what
one's "background" PSA should be if all cells are healthy is to
multiply the gland volume in cc by 0.066. For example, my gland's
volume on 22 July 2002 was 36 cc, as measured in an MRI. The
background PSA level should have been about 2.38 ng/ml; my
measured PSA was 2.16. [This value of 0.066 ng/ml/cc comes from
the PCRI (
newsletter PCRInsights, vol 5, no 1, July 2002,
page 7. All isues may be downloaded in PDF format from
TRUS is often done in conjunction with a prostate biopsy and is used to guide the biopsy sampling. It can also measure the prostate volume, that is the size of the gland.
A good review of TRUS, both historically and in guiding biopsies, can be found in the Bibliography.
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 ( http://www.nytimes.com/2003/12/23/health/23CANC.htm) 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 http://www.hon.ch/News/HSN/518884.html, 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 http://www.nytimes.com/aponline/AP-FIT-Prostate-Cancer-Obesity.html, 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 http://www.isip.com/press/press01/112601-Oncogenex.htm, a press release, 26 Nov 2001, no longer available on the www.isippharm.com 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 http://www.medscape.com/viewarticle/434192, 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 http://www.nytimes.com/aponline/2009/03/10/health/AP-MED-ProstateCancer.html, 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 http://www.zerocancer.org/site/News2?page=NewsArticle&id=10772, 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 http://www.zerocancer.org/site/News2?page=NewsArticle&id=11611&news_iv_ctrl=1001 )
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 http://www.bloomberg.com/news/2011-05-05/prostate-exam-deaths-tied-to-superbug-ills-spur-cancer-test-inquiries.html )
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 http://www.nih.gov/news/health/dec2011/od-07.htm)
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
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 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: http://www.hopkinskimmelcancercenter.org/
AScribe - The Public Interest Newswire / 510-653-9400
(c)2002 AScribe News, Inc.
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 http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.0020025)
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
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.
(From Pesticide Action Network Updates Service 10 May 2007-- See
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.
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.
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.
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.
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.
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.)
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
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, http://www.protonbob.com/proton-treatment-homepage.asp
A summary of the state of proton beam therapy as of 26 March 2012 may be
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.
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.
Side effects would come about from damage to surrounding tissue - incontinence,
impotence, bowel damage are the possibilities.
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.
Common side effects of hormonal therapy are
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
Bob Leibowitz, MD, in Los Angeles, is an advocate of triple hormone blockade. His web pages may be found at http://www.compassionateoncology.org/
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 http://www.hopkinsmedicine.org/Press_releases/2007/10_01_07.html ("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 http://cancerres.aacrjournals.org/cgi/content/abstract/67/19/9199; 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
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
http://jama.ama-assn.org/cgi/content/short/302/8/866 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.
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 BioSeeker Group had three interesting but prohibitively expensive publications which are no longer available on their web site as of June 2009. They would be out of date at this point. These are examples of other research reports available there:
"We Fought Cancer...And Cancer Won", from Newsweek, 6 September 2008.
"After billions spent on research and decades of hit-or-miss treatments, it's time to rethink the war on cancer." Not specifically about prostate cancer, but cancers in general.
(No longer available as of June 2009) A review of 4 emerging technologies in oncology: antibodies, anti-angiogenesis, signal transduction inhibition, and epidermal growth factor receptors (EGFR). (Dated 2 Jan 2002)
The 27 May 2002 issue of The Scientist had a cover story ("Reining in a Killer Disease") on work to control cancer, turning it into a chronic disease.
The five major targets in apoptosis, p53, Bcl-2, TRAIL, IAP and
Caspases, are the corner stones for further analysis in study to
address whether they are successful cancer therapeutic targets or
not and what level of competition is present. Only p53 and Bcl-2 are
apoptotic targets with drug candidates that have reached Phase III
clinical testing, although death receptors "TRAIL" are closing the gap.
... [There are currently] 5 drug candidates targeting the cell death
pathway, apoptosis. Additionally, more early stage candidates are
also under investigation, which brings the total number of companies
interested in this field to around 40.
Additional commentary may be found at
Cancer cells are often able to 'hide' from the immune system. However, certain type of cancers have a weakness in their cellular armor: an 'activated' Ras pathway, a sort of genetic soft spot found in perhaps more than two-thirds of all latent and actual tumors. Happily, healthy cells don't have this 'oncogene' or 'cancer gene' in their makeup. However, the Ras-activated cells are unable to manufacture the cellular protein PKR. In healthy normal cells, PKR prevents reoviruses from replicating. In Ras cells, this protection doesn't exist. Which means the reovirus can slip aboard, multiply and burst the infected cancer cell from within. Kill the killer.
"The big bonus is that the 'infection' is a true one; the reovirus spreads from cancer cell to cancer cell, clearing away the invader but leaving normal cells alone. This cycle of infection, replication and cell death is believed to roll on until there are no more 'victims' - cancer cells unwittingly burdened with an activated Ras pathway - left to kill." (From the press release quoted. 8 Mar 2002)
A more recent (29 April 2003) stock newsletter talking up Reolysin may
be found at
Published in the Elsevier journal Chemistry & Biology (Targeting Glycosylation Pathways and the Cell Cycle: Sugar-Dependent Activity of Butyrate-Carbohydrate Cancer Prodrugs, Srinivasa-Gopalan Sampathkumar, Mark B. Jones, M. Adam Meledeo, Christopher T. Campbell, Sean S. Choi, Kaoru Hida, Prasra Gomutputra, Anthony Sheh, Tim Gilmartin, Steven R. Head and Kevin J. Yarema, Chemistry & Biology 13, 1265-1275, December 2006). PDF is available for download from http://download.cell.com/chemistry-biology/pdf/PIIS1074552106003760.pdf
Two research abstracts on COX-2 inhibition and the suppression of prostate cancer. Quoted from the American Urological Association annual meeting, May 2002.
In March 2007, the FDA overruled its own scientific panel which had recommended approval of the drug, and sent it back for another clinical trial, with results due in 2009. This story may be found at http://caretolive.com/. This is of interest and concern since Provenge seemed effective with many fewer side effects than other medical treatments for prostate cancer.
(no longer available) discusses Phase II trial results of Cell Genesys' GVAX prostate cancer vaccine, with encouraging long term survival data. (19 May 2002)
notes that on 16 October 2008 the GVAX prostate cancer vaccine program was terminated during its phase 3 trials. A discussion of the program can be found in this article.
(Article no longer available at Reuter web site.) Research at UCSF by Prof Elizabeth Blackburn (2 July 2001)
(Article no longer available on the Reuters web site.) Work by British Scientists to block telomerase and restore mortality to cancer cells (28 September 2001)
(Article no longer available.) Scottish scientists turn cancer cell's signal to turn on telomerase gene into one to turn on nitroreductase gene, which activates a cell-killing drug. (21 November 2001)
Another summary, last updated 28 May 2007 (but may be newer when you read it)
(Page no longer available on Medscape.) Microwave Therapy Shows Promise as Treatment for Prostate Cancer
Press releases discusses J Urol 2001;166:1707-1714, a report on Phase I/II clinical trials using heat generated via microwaves from 5 antennas implanted in the prostate, with no major and few short term minor side effects. (16 Nov 2001)
http://ir.isispharm.com/releasedetail.cfm?ReleaseID=386855 Isis Pharmaceuticals and Oncogenex Technologies are developing antisense drugs for prostate cancer, OGX-011. (Original article was dated 26 Nov 2001, but is no longer available. This is a press release from 1 June 2009.)
From a press release (14 May 2002): "...announced the publication of two studies in Current Opinion in Molecular Therapeutics (2002) 4(2). These preclinical studies demonstrated potential for use of AVI's third-generation antisense drug platform, NEUGENE(R), in treating prostate cancer and viral infections caused by the Caliciviridae, a family of RNA viruses. 'AVI continues to build strong scientific support for its antisense technology,' said Patrick L. Iversen, Ph.D., AVI's senior vice president of research and development. 'These studies confirm our belief that NEUGENE compounds are capable of addressing a broad range of health problems for which there are no known cures.' Antisense as a Treatment for Prostate Cancer[:] Prostate cancer is the most frequently diagnosed malignancy and is the most common cause of mortality among men. In 'Prostate cancer: Status of current treatments and emerging antisense-based therapies,' Gayathri Devi, Ph.D., senior scientist at AVI, compared current prostate cancer treatment strategies with preclinical and clinical prostate cancer antisense studies conducted in the past year. Dr. Devi reviewed stages and treatment options for prostate cancer, which were linked to the antisense approach. Her research showed that AVI's antisense technology is an attractive alternative to traditional cancer therapies."
An up-to-date summary with references. Artemisinin is still primarily used as an anti-malarial agent, but work on cancer is continuing.
A bibliography of some scientific journal publications relating to research on using artemisinin to treat cancer. Also contains a link to a more extensive biobliography (> 350 articles as of Feb 2005).
Summarizes some of this information in more lay terms.
A summary from Memorial Sloan Kettering with a short bibliography.
A reasonable sounding alternative medicine site with more information about artemisinin.
"Satraplatin (BMS-182751 or JM-216) or bis (acetato) ammine dichloro (cyclohexylamine) platinum is a member of a novel class of platinum (IV) compounds developed by Johnson Matthey which are absorbed by the oral route. In preclinical studies, Satraplatin had shown cytotoxic and antitumor activities that are comparable to that of cisplatin or carboplatin."
"Clinical studies were conducted and had shown activity on platinum sensitive tumors, small cell lung cancer, and ovarian cancer. It has also shown activity in hormone-refractory prostate cancer. Dose-limiting toxicities are myelosuppression (neutropenia and thrombocytopenia) and gastrointestinal toxicity (diarrhea)."
"NeoOncoRx will explore this drug for prostate cancer. Prostate cancer is now the second leading cause of cancer death in men. It is estimated that in 2001, approximately 198,100 new cases and 31,500 prostate cancer-related deaths will occur in the United States. Treatment in prostate cancer provides prolonged disease-free survival for many with localized disease, but is rarely curative on patients with locally extensive tumor. Metastatic tumor is currently not curable. A continuing unmet medical need for new effective drugs still exist."
"The advantages expected from this novel oral platinum compound rely upon its oral route of administration. These include patient convenience and health cost containment, meaning outpatient therapy."
Additional work reported on in December 2008 in the Journal of Experimental and Therapeutic Oncology ( http://www.oldcitypublishing.com/JETO/JETO.html) has been summarized in several news articles
A new drug by Medivation, Inc. offers a radically different way of attacking prostate cancer, showing promising results in an initial trial and is set for larger-scale testing. A study report in the journal Science looked at this drug, MDV3100, and its ability to block the receptors for androgens which drive tumor growth on cells. After treatment with the drug, there were "sustained declines" in PSA levels in 43 percent of the participants, which the report called a "promising" result. The researchers now have data on 114 men given the drug.
"It showed not only declines in PSA but also regression of the tumor on scans and also that circulating tumor cell counts, another measure of treatment, converted from unfavorable to favorable in a considerable percentage of patients," said Dr. Howard I. Scher, chief of the genitourinary oncology service at Memorial Sloan-Kettering Cancer Center in New York City and co-author of the study.
Based on those results, an application for a large-scale trial has been submitted to the U.S. Food and Drug Administration.
"A parp also known as a Poly (ADP-ribose) polymerase is an enzyme which repairs damage done to our DNA. In basic terms a parp enzyme regulates our body repairing damaged DNA. In normal cells this is useful and stops cell death however Doctor de Bono and his colleagues have suggested that cancer cells may used the PARP repair method to their advantage. A parp-1 inhibitor is a new drug which causes inhibition of parp function. Studies recently conducted have shown that this new parp drug is an inhibitor of cancer as it disrupts the chemotherapy resistance in cancer cells." (From http://www.parp-inhibitors.com/
|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";
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,
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.|
|10/10/01||Added PSA of 1.93 on 10/09/01; refs to Myriad Genetics, "icon",
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
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 http://www.squarf.com/cancer.htm|
|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 http://gday-mate.com/prostate_cancer/ 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 www.malecare.com|
|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 http://www.nocancer.com/ (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
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 http://www.prostateforum.com/|
|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 http://dittany.googlepages.com/|
|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 http://www.prostate-usa.com/ 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 www.prostatitisclinic.com|
|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 beatcancer.org 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 caretolive.com, on Provenge; to Dana Jennings'
NYTimes PCa blog; Mark
|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 (zerocancer.org)|
|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 cleanprostate.com|
|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
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
|06/02/09||Added next Dana Jennings' blog|
|06/12/09||Cleaned up HTML errors & warnings using http://validator.w3.org|
|06/15/09||Begin cleaning up broken/obsolete links using http://www.dead-links.com|
|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 yananow.net 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
|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 myprostatecancerroadmap.com|
|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 OEDb.org 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|
|11/20/2014||Added link to list of MRSI sites|
|01/13/2015||Added Jay Cohen "Prostate Cancer Breakthroughs 2014" ref|
|02/20/2015||Added PSA of 8.1, free PSA of 17% of 02/17/2015|
|04/24/2015||Added MRSI of 04/23/2015|
|05/03/2015||Added "mobile friendly" meta tags for Google|
|05/08/2015||Added more on MRSIs of 04/23/2015 & 04/21/2014|
|05/28/2015||Added revised prostate volumes for 2014, 2015|
|06/02/2015||Added Scientific Computing PCa overview article|
|06/22/2015||Added PSA of 8.8 of 06/17/2015|
|06/27/2015||Added JRoyalSoc article on dangers of internet purchasing milk|
|07/30/2015||Added ref to WaPo article on PCa tumor genetic analysis &
biomarker discovery; also
EBioMedicine journal article
|08/02/2015||Added ref to Gut paper on HAMLET preventing mouse colon cancers|
|08/06/2015||Added ref to JAMA Pediatrics article on reduction of childhood cancers|
|08/11/2015||Added refs to WHO study on long term effects of breastfeeding, and to PAACT
article on MRSI
and PCa diagnostics
|10/07/2015||Added link to NCCN Guidelines for Prostate Cancer Patients|
|11/03/2015||Added PSA of 7.8 of 10/29/2015|
|11/14/2015||Added ref to mothers' milk bibliography at hamletpharma.com|
|11/20/2105||Added ref to Rath, et al review article on HAMLET|
|02/09/2016||Added PSA of 10.5 of 02/04/2016|
|02/18/2016||Added ref to Harvard 2016 Annual Report on Prostate Diseases|
|04/19/2016||Added PSA of 8.2 of 04/14/2016|