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Medical Forum / Diseases and Disorders / Prostate Cancer / August 2005End of PSA Era?
"My one wish with prostate cancer," says Dr. Thomas Stamey, a veteran researcher at Stanford University, "is that before a doctor does anything aggressive, he would tell his patient that all men will develop the disease eventually." He pauses to let the bad news sink in. "The good news," he wants doctors to add, "is that the rate of dying from prostate cancer is infinitesimal." Stamey has been in a reflective mood of late because of the growing realization, by him and others, that the screening test he helped discover is far less useful for detecting prostate cancer than many had once believed. In 1987, a team led by Stamey found that high levels of prostate-specific antigen (PSA) circulating in the blood were a strong indication of prostate tumors. Before then, the only way to detect prostate cancer was with a painful biopsy, and this is still used to confirm the disease. But with a simple PSA test , doctors thought they could weed out men who don't need the more invasive procedure, as well as spot tumors at an earlier, more treatable stage. The test has proven a powerful draw: about half of all men over the age of 50 get annual PSA tests. Now, Stamey hopes that men will be open to the older means of screening for prostate cancer. "I don't think PSA adds very much," he says. The End of the PSA Era? These second thoughts stem from a troubling variety of evidence that suggests widespread testing is possibly causing more harm than good. Although death rates from prostate cancer are lower than they were before PSA screening, these rates have also declined in countries where this type of testing is not commonly used. If one were to randomly biopsy men, as Dr. Wael Sakr of Wayne State University did on a group who were accidentally killed on the streets of Detroit, about 8 percent of those in their 20s would have prostate cancer, with the rates steadily increasing as men age. Indeed, about 80 percent will develop the disease by the age of 70. Some of these tumors are clearly dangerous. But most are slow moving, and many prostate cancer patients can go 20 years without any need for treatment, according to a recent study led by Dr. Peter Albertson. With widespread PSA screening picking up these relatively benign tumors, Stamey fears that the tests are leading to unnecessary treatment and worry. "I've been as guilty as anyone else," he says. Not everyone is willing to give up on PSA screening quite yet. "We know it's not a perfect test," says Jamie Bearse, a spokesperson for National Prostate Cancer Coalition, which advocates annual PSA screening for men 40 years and older. Bearse is hopeful that newer screening tests will prove more discerning. In the meantime, he says, the PSA test is the best early detection option men have. "They would rather know, than not know." Normal vs. Abnormal PSA Yet it is increasingly hard to determine even a broad risk prediction from PSA testing. Traditionally, doctors used a PSA measurement of 4 as a key cut off point: lower than 4 millimeters of PSA in the blood meant that men were considered cancer free, whereas higher or equal to 4 suggested the need for a biopsy to confirm the disease. But looking at nearly 5,500 men who had a PSA test and then at least one biopsy, researchers found this cutoff point often missed tumors or implied that men had cancers that weren't in fact really there, according to recent results published in the Journal of the American Medical Association. Indeed, a PSA level of 4.1 millimeters accurately predicts only 20 percent of prostate cancers and leads to false alarms about 6 percent of the time. Lowering the threshold will detect more cancers, but at the price of causing men to undergo biopsies for no reason or finding many benign tumors that only need to be monitored. A PSA cutoff of 2.1, for example, would yield false readings more than 85 percent of the time to catch only slightly more than half of all tumors. The authors of the study, led by Dr. Ian Thompson of the University of Texas Health Science Center in San Antonio, call for a substantial "reeducation" effort on the increasingly murky role of PSA. "It will be a challenge to the medical community to change the long held notion that there is a 'normal' PSA level," the authors write. Researchers still hold out hope for measuring PSA velocity, the rise of PSA over time that gives an indication if the tumor is growing. As an initial detection tool, Stamey says that doctors should return to looking at increasing age, along with a family history of the disease, as a way of determining who may be at greater risk for prostate cancer and in need of a biopsy to catch tumors early. Other than that, he adds, "We have as much a way of predicting who will need a biopsy based on looking at someone's eyes." Ongoing studies are continuing to look at whether PSA testing saves lives, and the American Cancer Society and other test supporters urge men to discuss the pros and cons of screening with their doctors. But the creator of the PSA test is calling for the end. "All men will develop a prostate cancer," says Stamey. "That's a given." > "My one wish with prostate cancer," says Dr. Thomas Stamey, a veteran > researcher at Stanford University, "is that before a doctor does anything > aggressive, he would tell his patient that all men will develop the disease > eventually." He pauses to let the bad news sink in. "The good news," he > wants doctors to add, "is that the rate of dying from prostate cancer is > infinitesimal." This is a strange use of the term "infinitesimal". The American Cancer Society estimates that this year 232,090 cases of prostate cancer will be diagnosed, and 30,350 men will die of prostate cancer. Thus the deaths ware estimated to be about 13 percent of the diagnosed cases. However, it should be kept in mind that prostate cancer has a long time horizon, so the men who die of the disease this year were diagnosed over the course of the last 15 to 20 years. In previous years, the number of diagnosed cases may have been somewhat less because the size of the vulnerable population of older men was smaller. So the 13 percent figure underestimates the death rate to some degree. Also, of course treatment during the intervening years has played some role in reducing the death rate. So the natural untreated death rate for prostate cancer is presumably higher than 13 percent. The term infinitesimal is a technical mathematical term which is often misused by lay people. But what it usually means is that the number being discussed is very small. People might differ about what might be considered infinitesimal, but 13 pwercent is certainly not in that category by any stretch of the imagination. Of course, Dr. Stamey, may not be talking about the ratio of deaths to diagnosed cases of prostate cancer. He may be talking about the conjectured prevalence of microscopic evidence of prostate cancer detected in autopsy studies. This incidence increases with age, and there are various studies with different estimates ranging over a fairly wide range but some go as high as 80 percent in older men. But it is very important to distinguish the kind of cancer which might be detected on autopsy with the kind which is detected clinically using current methods. The number of men diagnosed clinically at some time in life is about 15 percent and that figure has remained relatively stable for quite a long time. Let us imagine a doctor having this conversation with a man who has been diagnosed with prostate cancer who is considering treatment. Which base number should the doctor divide by? A presumed number which includes all men or the base number for men clinically diagnosed with prostate cancer? It would seem divideing by the first number would be highly misleading and totally irrelevant. > Stamey has been in a reflective mood of late because of the growing > realization, by him and others, that the screening test he helped discover [quoted text clipped - 21 lines] > PSA screening, these rates have also declined in countries where this type > of testing is not commonly used. I would like to see the evidence for that. It certainly hasn't in all such countries. > If one were to randomly biopsy men, as Dr. Wael Sakr of Wayne State > University did on a group who were accidentally killed on the streets of [quoted text clipped - 7 lines] > widespread PSA screening picking up these relatively benign tumors, Stamey > fears that the tests are leading to unnecessary treatment and worry. Stamey and Albertsen are well none critics of PSA testing. And--suprise, suprise!---they keep coming up with studies proving their point. I've looked at Stamey's last study and I didn't find it at all convincing. Albertsen's study was more interesting, but it also suffered from serious defects, which were noted by anothher article in the same issue of the JAMA. Even though, Albertsen's study did show that at least for Gleason 7 cases, the likelihood of death from prostate cancer within 5 to 10 years was pretty high. > "I've been as guilty as anyone else," he says. > [quoted text clipped - 46 lines] > > "All men will develop a prostate cancer," says Stamey. "That's a given." >> "My one wish with prostate cancer," says Dr. Thomas Stamey, a veteran >> researcher at Stanford University, "is that before a doctor does anything [quoted text clipped - 27 lines] > conjectured prevalence of microscopic evidence of prostate cancer detected > in autopsy studies. I can find no evidence that your assumption is true. The only real correlate of finding prostate cancer is looking for it. This incidence increases with age, and > there are various studies with different estimates ranging over a fairly > wide range but some go as high as 80 percent in older men. But it is very > important to distinguish the kind of cancer which might be detected on > autopsy with the kind which is detected clinically using current methods. Once again, you have made an assumption which may be comforting to you, but has no scientific basis. The number of men diagnosed clinically at some time in life > is about 15 percent and that figure has remained relatively stable for > quite a long time. Let us imagine a doctor having this conversation with > a man who has been diagnosed with prostate cancer who is considering > treatment. Which base number should the doctor divide by? This is not the issue either. If the man is 80, he has virtually 100% chance of having prostate cancer if anyone looked for it. > A presumed number which includes all men or the base number for men > clinically diagnosed with prostate cancer? It would seem divideing by the > first number would be highly misleading and totally irrelevant. And that is because the research has not been done. We are in the dark ages as far as prostate cancer is concerned. Those on-going studies are 10 years out now and except for that one you refer to so much, the main ones have kept quiet, even though on the radio at 8 years they said, 'no result.' >> Stamey has been in a reflective mood of late because of the growing >> realization, by him and others, that the screening test he helped [quoted text clipped - 24 lines] > I would like to see the evidence for that. It certainly hasn't in all > such countries. I stated this earlier that for such diseases as heart disease, declines started long before aggressive treatments. You don't like to hear that but why assume just because surgery is offered, it does some good? >> If one were to randomly biopsy men, as Dr. Wael Sakr of Wayne State >> University did on a group who were accidentally killed on the streets of [quoted text clipped - 12 lines] > suprise!---they keep coming up with studies proving their point. I've > looked at Stamey's last study and I didn't find it at all convincing. This is going to be your conclusion for any study that does not say, "Surgery must save lives because it must, because it must, because it must...." Albertsen's study was more interesting, but it also > suffered from serious defects, which were noted by anothher article in the > same issue of the JAMA. Even though, Albertsen's study did show that at > least for Gleason 7 cases, the likelihood of death from prostate cancer > within 5 to 10 years was pretty high. Once again, does surgery prolong life? No proof here. Just wishes. >> "I've been as guilty as anyone else," he says. >> [quoted text clipped - 49 lines] >> >> "All men will develop a prostate cancer," says Stamey. "That's a given." This last sentence is a simply FAct. The only issue is whether today's aggressive approaches lengthen life. >>>"My one wish with prostate cancer," says Dr. Thomas Stamey, a veteran >>>researcher at Stanford University, "is that before a doctor does anything [quoted text clipped - 179 lines] > This last sentence is a simply FAct. The only issue is whether today's > aggressive approaches lengthen life. George, I'm afraid that Leonard is correct. Prostate cancer will kill a little over 2% of men in this country, and around 1 in 6 men will be diagnosed with it, which ends up being around 13% of those diagnosed with it dying from it. Ed Friedman >>>>"My one wish with prostate cancer," says Dr. Thomas Stamey, a veteran >>>>researcher at Stanford University, "is that before a doctor does [quoted text clipped - 191 lines] > > Ed Friedman So the more you look, the more you diagnose is what Stamey states. At some point, it will be 100%. The issue is survival, which is where the research literature so far is worthless. > So the more you look, the more you diagnose is what Stamey states. At > some point, it will be 100%. The issue is survival, which is where the > research literature so far is worthless. George, I agree with you almost entirely. The number would not quite be 100% because men who eat lots of soy products all of their life would not get prostate cancer (which is why Japan has the world's lowest rate). Also, now that anti-aging doctors are gaining more popularity, men who make use of their services and maintain ideal levels of T, DHT, and E should never get prostate cancer nor BPH (and should eliminate any that may be within them). However, I believe that the reason that the rate of death from prostate cancer declines following localized treatment, whereas the overall mortality rate does not improve is due to an example of the Competitive Risk Model. In this case, low endogenous levels of T is correlated positively with many known risk factors in men. Men with the lowest levels of T are most likely to have more aggressive Gleason scores, higher cholesterol, higher blood pressure, higher triglycerides, and increased chance of Alzheimer's. They also have decreased cognitive functionality in their brain so in theory they may be more likely to die from accidents as well. Considering that cardiovascular ailments are the number one killer of men, and that low levels of T are associated with all known risk factors for that, then even if men avoid dying from prostate cancer, if they were going to die from prostate cancer then they would still die at about the same time from one of the other major killers if they don't correct their hormonal imbalance. Ed Friedman >> So the more you look, the more you diagnose is what Stamey states. >> At some point, it will be 100%. The issue is survival, which is where [quoted text clipped - 27 lines] > > Ed Friedman If the death rate from prostate cancer shows any decline in treated groups, that is still not proven because they studies are not yet in. Perhaps there will be very small differences after a long period of time. Maybe not. As for the Competitive Risk Model, you are mixing together about a half-dozen supposed risk factors for death overeall, and with prostate cancer only maybe. What you propose cannot be researched given any current level of knowledge of basic biology. Look at how homone replacment therapy for women doubled risk factors for cancers, but no one noticed. That was self-selection at work. The healthy self-selected treatments. So are the men with low risk factors self-selecting for PSA or other visits to doctors which will eventually end in about 100% chance of a biopsy? As for the 100% of us will get prostate cancer by 80, I think that is an accepted figure and not something recently throught up. > If the death rate from prostate cancer shows any decline in treated > groups, that is still not proven because they studies are not yet in. [quoted text clipped - 9 lines] > of us will get prostate cancer by 80, I think that is an accepted figure and > not something recently throught up. George, The figure that I have seen is ~80% of men who died in their 70's showing up with prostate cancer (PC) on autopsy. Having finished my model on prostate cancer (published at http://www.tbiomed.com/content/2/1/10), I am unable to find any published studies that do not fit my model perfectly. So I am making statements based on the assumption that my model is totally correct. The reason that men who eat lots of soy all of their adult life won't get PC is because soy binds preferentially to ER-beta, and both ER-alpha and ER-beta are needed for telomeres to form (which is one of the first steps needed for PC to grow). However, if a man has any PC cells within him and eats soy, especially in conjunction with a 5AR2 inhibitor, then the PC will have a shorter doubling time (appear to be more "aggressive"). So one prediction from my model is that all of the men in the recent PCPT trial who took F and showed up with high grade gleason scores either had remarkably low values of T, or more likely, consumed lots of soy products. I agree with you that most men over 50 are going to show PC if you do enough biopsies and that PSA is just the excuse needed by doctors to do lots of biopsies. I disagree with you that there is no way to test the Competitive Risk Model. It justs needs epidemiological studies to look for correlations between levels of T and causes of death. Those studies have already been done for most of the risk factors for death, as I stated before (see "Testosterone and other anabolic steroids as cardiovascular drugs." Am. J. Ther. 1999; 6 (3): 167-174 ). As to the relationship of endogenous levels of T and PC, let me quote the following from Dr. Leibowitz's web site: "An article appeared in the Journal of Urology, May 2002, Volume 167, pages 2025-2031. Some of the points from this article are that “previous investigators have suggested an association between low serum testosterone and high-grade disease in men diagnosed with prostate cancer.” Since PSA production is known to be under the control of androgen, PSA levels can be artificially lowered in an androgen deficient state. In this study, there were approximately 4% of 2,254 patients who presented with a Gleason score of 7-10 and a PSA of 4 or less. Their outcome was significantly worse than the patients with Gleason scores 7 to 10, but PSA’s higher than 4. The article states, “Our study provides evidence to support the previous hypothesis of other authors that low serum free testosterone may be a marker for more aggressive prostate cancer, particularly for patients with a PSA of 4 or less.”" Ed Friedman >> If the death rate from prostate cancer shows any decline in treated >> groups, that is still not proven because they studies are not yet in. [quoted text clipped - 57 lines] > > Ed Friedman As you say in your article, you cannot say what would be needed to lower PCa rates, right? Or, in reality, is a high soy diet the way to go based on cross-national comparisons? > >> If the death rate from prostate cancer shows any decline in treated > >> groups, that is still not proven because they studies are not yet in. [quoted text clipped - 61 lines] > lower PCa rates, right? Or, in reality, is a high soy diet the way to go > based on cross-national comparisons? I doubt that there is any solid evidence about soy products preventing cancer. More likely just a generic thing. For example Black men have a much higher incidence of prostate cancer than White men. >> >> If the death rate from prostate cancer shows any decline in >> >> treated [quoted text clipped - 92 lines] > cancer. More likely just a generic thing. For example Black men have a > much higher incidence of prostate cancer than White men. I wonder if Ed would agree with that. After all, disease patterns change when migrants enter the USA and give up high-soy diets. > >> >> If the death rate from prostate cancer shows any decline in > >> >> treated [quoted text clipped - 95 lines] > I wonder if Ed would agree with that. After all, disease patterns change > when migrants enter the USA and give up high-soy diets. Could well be. How about African men compared to American blacks? Or perhaps Ameican Blacks diet is different than the average White. > Could well be. How about African men compared to American blacks? Or > perhaps Ameican Blacks diet is different than the average White. All this is vastly more complicated than the categories we use to characterize people. First of all, there is an enormous amount of genetic diversity in sub-Sahara Africa, more so than on other continents. So there is no special reason to believe that all African men would fare the same way with respect to prostate cancer. Similarly, there is also quite a lot of genetic diversity among African American men. Many such men have a larger genetic contribution from their European ancestors than from their African ancestors. And it would make a difference which particular Africans were their ancestors. Skin color is not a very good indication of a man's genetic history. African American men as a group do in fact have a greater incidence of prostate cancer and also are more likely to die of it. My guess is that this is a consequence of a combination of genetic and environmental considerations and the mix may be entirely different for different men. But the most important risk factors in any case have nothing to do with such matters, they are (1) being a man and (2) growing older. > > Could well be. How about African men compared to American blacks? Or > > perhaps Ameican Blacks diet is different than the average White. [quoted text clipped - 16 lines] > But the most important risk factors in any case have nothing to do with > such matters, they are (1) being a man and (2) growing older. It does seem that diet does have effects on various cancers. I would point to the consumption of fish by the Japanese more than soy. Maybe adopting their whole diet is really necessary. > Could well be. How about African men compared to American blacks? Or > perhaps Ameican Blacks diet is different than the average White. This has been discussed before. Basically, the darker the skin color the less vitamin D is formed from sunlight. The farther away from the equator you go, the greater the adverse effect this has. Therefore, the simplest explanation for the increased rate of PCa (as well as for hypertension) in American blacks is vitamin D deficiency. E.g., here is an excerpt from http://www.nih.gov/news/pr/dec96/niehs-11.htm "Their study, in the journal Cancer Research, is the latest tantalizing suggestion of a possible role for vitamin D, from the sun or diet, in reducing prostate cancer risk, the second leading cancer killer of men. More than 40,000 men are expected to die of the disease this year.... This study follows one in which other investigators found that men living in northern latitudes with less total sunlight exposure (and therefore less production of vitamin D by the skin) seem to have a higher incidence of prostate cancer." Ed Friedman >> Could well be. How about African men compared to American blacks? Or >> perhaps Ameican Blacks diet is different than the average White. [quoted text clipped - 16 lines] > > Ed Friedman Skin color is a local adjustment to the amount of sunshine available. It is possible that such adjustments have secondary problems/benefits. >> >> >> If the death rate from prostate cancer shows any decline in >> >> >> treated [quoted text clipped - 130 lines] > Could well be. How about African men compared to American blacks? Or > perhaps Ameican Blacks diet is different than the average White. I suspect there are widespread food differences between ethnic groups in the USA. In fact, there ARE differences. > As you say in your article, you cannot say what would be needed to >lower PCa rates, right? Or, in reality, is a high soy diet the way to go >based on cross-national comparisons? George, I'm afraid that I didn't make myself clear. The cross-national comparisons does nothing to prove that soy prevents PCa. The proof is my model, which is based on scientific facts. The fact that Japan has the lowest rate of PCa is simply verification that my model is correct. Simlarly, the paper "Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation" Prostate 22 (4): 335-45, 1993 also supports the fact that soy prevents prostate cancer (genistein is one of the main proteins found in soy), but does not prove it. The proof is just logical deduction from facts presented in my paper: 1. PCa requires telomere formation in order to grow initially. 2. Estradiol(E2) binding to both ER-alpha and ER-beta are required to form telomeres in PCa. 3. Soy binds preferentially to ER-beta, preventing E2 from binding to it and therefore preventing telomere formation in PCa. 4. Therefore, if you ingest sufficient amounts of soy protein all of your life, you cannot generate telomeres in PCa and therefore it cannot grow. On the other hand, my model clearly shows that if you already have PCa, then soy will speed its growth because E2 binding to ER-beta downregulates bcl-2, the protein that protects PCa from apoptosis. Similarly, my model shows that it is fairly easy to prevent PCa without resorting to the use of soy. Basically, you just have to optimize the levels of T, DHT, and E2 in your body in order to eliminate all PCa and BPH. Again, this is scientific fact and holds unless there is a rare mutation present (something you would expect only in late stage PCa) which protects the PCa from apoptosis. To give you supporting evidence of this (which again, proves nothing), in my own case, my PSA was 3.5 in 9/2002, 4.5 in 9/2003, and 6.5 in 5/2004. Today my PSA is 2.1, following 4 months of trying to optimize my hormonal levels (my DHT is still a little high, but I'm working on it). Ed Friedman >> As you say in your article, you cannot say what would be needed to >>lower PCa rates, right? Or, in reality, is a high soy diet the way to go [quoted text clipped - 41 lines] > > Ed Friedman Ok, once again, could you tell us how you lowered your PSA? What exactly did you do? I afraid I don't remember what you posted previously on this subject. > "Ed Friedman" <ed@math.uchicago.edu> wrote in message > Ok, once again, could you tell us how you lowered your PSA? What exactly > did you do? I afraid I don't remember what you posted previously on this > subject. George, Basically, you have to adjust all of your hormones to their values in an optimal teenager - high T, low DHT, and low E2. This is not something you can do by yourself. You have to work in conjunction with a knowledgable physician. Ed Friedman > Basically, you have to adjust all of your hormones to their values in an > optimal teenager - high T, low DHT, and low E2. Ed..I've read that DHT levels decrease with age (which makes sense since it is derived from T via the 5AR1,2 pathways), so wouldn't a teenager have higher DHT levels than a man in his 50-70s?..Ron > Ed..I've read that DHT levels decrease with age (which makes sense > since it is derived from T via the 5AR1,2 pathways), so wouldn't a > teenager have higher DHT levels than a man in his 50-70s?..Ron Ron, You are correct. DHT is essential for good health, and there is an optimal range to shoot at for it. Before I started treatment, my DHT was right in the optimal range. However, because some of the added T gets converted to DHT, I have to take 5AR2 inhibitors to try to get my DHT back down into range again. So to correct what I said before, T should be at the high end of optimal range, DHT at the low end, and E2 in the middle of its optimal range. This will end up with DHT a bit lower than what it was as a teenager. Ed Friedman >> "Ed Friedman" <ed@math.uchicago.edu> wrote in message Ok, once again, >> could you tell us how you lowered your PSA? What exactly did you do? I [quoted text clipped - 8 lines] > > Ed Friedman Now how are you going to find such a person? >>>"Ed Friedman" <ed@math.uchicago.edu> wrote in message Ok, once again, >>>could you tell us how you lowered your PSA? What exactly did you do? I [quoted text clipped - 10 lines] > > Now how are you going to find such a person? George, Excellent point! One of the major shortcomings of the American medical system is that such people are very hard to find. Also, even if you find one, your insurance company probably won't pay for the visits nor the drugs and hormones used. In my own case, I looked for a specialist in anti-aging. I made sure that he understood the importance of all of the hormones being in balance (run away from any doctor who thinks that T is the only thing that matters). As a bonus, I found one who was capable of reading and understanding my published paper, and who agreed with my conclusions. Such doctors do exist, but it definitely takes work to find out who they are. Good luck, Ed Friedman >>>>"Ed Friedman" <ed@math.uchicago.edu> wrote in message Ok, once again, >>>>could you tell us how you lowered your PSA? What exactly did you do? I [quoted text clipped - 30 lines] > > Ed Friedman Actually I am not looking, but I was wondering what kind of drugs you need access to. Are you using prescription drugs? Why do you of all people need a physician to tell you what you need to do? >>>>>"Ed Friedman" <ed@math.uchicago.edu> wrote in message Ok, once again, >>>>>could you tell us how you lowered your PSA? What exactly did you do? I [quoted text clipped - 34 lines] > need access to. Are you using prescription drugs? Why do you of all people > need a physician to tell you what you need to do? George, Personally, I am taking testosterone (which requires a prescription), DHEA (doesn't require a prescription), finasteride (to keep DHT from getting too high - requires a prescription) and arimidex (to keep E2 from getting too high - requires a prescription). The exact amount changes in accordance with what the blood tests reveal. The goal is to optimize all values, and to keep them optimized. Ed Friedman >>>>>>"Ed Friedman" <ed@math.uchicago.edu> wrote in message Ok, once again, >>>>>>could you tell us how you lowered your PSA? What exactly did you do? [quoted text clipped - 45 lines] > > Ed Friedman Thanks. Are there any plans to do a long-term test with a wider group of people? Ed...If you don't mind sharing, what were your diagnostic stats (PSA, GS, TNM staging) and what is your treatment history and PSA and hormonal levels by date...Ron > Ed...If you don't mind sharing, what were your diagnostic stats (PSA, > GS, TNM staging) and what is your treatment history and PSA and > hormonal levels by date...Ron Ron, I decided never to get a biopsy (which really pissed off my urologist) in spite of increased PSA velocity (as I listed before) and a number (6.5) that mandated a biopsy. Like the recent post of the horror story following a biopsy, I was aware that there was a small, but real, chance of serious complications following a biopsy, and I saw no upside to doing it at that time. At that point, I started doing my research, and in a matter of weeks came to the following conclusions: 1. If I took a biopsy, PCa would almost certainly be detected if they kept doing it enough (as it would in all men my age unless they've eaten lots of soy products every day of their life). 2. Both surgery and radiation were ridiculous options. They guaranteed a poor quality of life and both had an extremely small chance of doing anything good. 3. Dr. Leibowitz and Dr. Tucker had a 100% success rate with early stage PCa (stages T1-T3, with average PSA of 13) using intermittent triple androgen blockade. Their high dose testosterone replacement option following blockade was especially effective. Knowing that, I started to research PCa as if my life depended on it. I figured I had plenty of time before my PSA would reach 13, and I had decided that if I needed to start treatment, it was insane to consider anything other than intermittent triple androgen blockade (e.g., a very recent post in this newsgroup showed that 9 year biological failure rates for surgery was 24% and for radiation was 30% - nowhere near the 0% of Dr. Leibowitz and Dr. Tucker). Having finished and published my paper, I am now extremely confident with my knowledge about PCa. I've read hundreds of articles, and my model explains every finding out there, no matter how trivial or how inexplicable the author found the results. Outside of what was printed in my paper, I now have a plausible model of how PCa starts, and can explain biochemically what happens to cause early stage PIN, late stage PIN, PCa and BPH. I understand the ways to prevent PCa and how to effectively treat it using systemic manipulation of hormone receptors. I even understand what mutations might make T harmful and what drugs can be used to counter it. In short, at this point, I feel that I have an almost complete understanding of PCa, and am starting to focus my attention to breast cancer, which I strongly suspect can be eliminated by the same manipulation of hormonal receptors that works on PCa. What I have set in motion for PCa will continue on its own momentum. I know that my model is correct, and there are some top doctors at top research centers in this country who have read my paper and are excited about it. In the upcoming years, I expect that experiments will be done that show my model correct in all of its aspects. Finally, to answer your question about treatment history - I did what I could without prescription drugs to slow down PCa's doubling rate. I took lycopene, vitamin E plus selenium, DIM, vitamin D3, plus some herbs to alter hormonal balances (I won't mention them here, because I don't want anyone messing with hormones unless under a doctor's supervision. I wouldn't have done that myself if I had known back then that there were doctors out there who knew what they were doing in balancing all of a body's hormone levels.) After all of this, my PSA was at 3.2 when I started real hormonal treatment in March, 2005. In May, my PSA went to 2.6 and in July to 2.1. Also, of course, I know enough to avoid all soy and flaxseed products while taking 5AR2 inhibitors. Before starting treatment, my T was too low, my DHEA was way too low, my E2 was way too high, and my DHT was about right. At this point, my T is about where it should be, my DHEA is still a little low, my E2 is where it should be, and my DHT is a bit high. I hope to move towards optimizing all values in the upcoming months. I'm not giving exact figures because I don't want anyone trying this themselves (e.g. by buying drugs illegally or in Mexico) without being under a doctor's supervision. Ed Friedman >> Ed...If you don't mind sharing, what were your diagnostic stats (PSA, >> GS, TNM staging) and what is your treatment history and PSA and [quoted text clipped - 74 lines] > this themselves (e.g. by buying drugs illegally or in Mexico) without > being under a doctor's supervision. So you are being treated for prostate cancer despite never having had what the urology profession, misguided as they may be, consider a definitive diagnosis of that disease? > Ed Friedman >>> Ed...If you don't mind sharing, what were your diagnostic stats (PSA, >>> GS, TNM staging) and what is your treatment history and PSA and [quoted text clipped - 80 lines] > >> Ed Friedman Now, now Len. Lighten up. We all own our own bodies and if he wants to keep his PSA down, he can do so even if he does or does NOT have a traditional diagnosis. > So you are being treated for prostate cancer despite never having had > what the urology profession, misguided as they may be, consider a > definitive diagnosis of that disease? Leonard, I never said I was being treated for PCa (although, like George, I believe that virtually all men over 50 have some PCa in them). I am simply optimizing my health by optimizing my hormonal levels. One of the results that my model predicts is that this treatment should minimize my PSA, whether the PSA is being generated from BPH (although my prostate size is normal) or from PCa. Also, my HDL cholesterol has increased by 25% in the 4 months since treatment started, and I'm expecting all of the other known effects to take effect in the upcoming months (increased muscle mass, decreased body fat, stronger bones, increased cognitive function, etc.). I apologize if I gave you the wrong impression. Ed Friedman > > So you are being treated for prostate cancer despite never having had > > what the urology profession, misguided as they may be, consider a [quoted text clipped - 16 lines] > > Ed Friedman Of course, low cholesterol is a good correlate of a cancer diagnosis too. >> So you are being treated for prostate cancer despite never having had >> what the urology profession, misguided as they may be, consider a [quoted text clipped - 14 lines] > > I apologize if I gave you the wrong impression. I understand your point, but perhaps in the future you might include the fact that you haven't been clinically diagnosed in your posts. I think many of the people reading your posts have assumed you have been diagnosed with prostate cancer. Otherwise, they might ask why you are posting in prostate cancer newsgroups. Since you do seem to be advocating a different approach to that disease, that might make sense. Perhaps others will differ with me, but that is my opinion. As to the point about men over 50 having "some" prostate cancer, I think it is important to distinguish between microscopic evidence of cancer which might be found on autopsy from cancer which has risen to the level where it can be detected in a clinical context. Estimates of prostate cancer in autopsy studies are very high, 50-80 percent, depending on age. On the other hand, only about one is six men in the US will ever be clincially diagnosed with prostate cancer in his lifetime. The argument that no one has been looking for prostate cancer in the other five sixths really doesn't hold water, given the emphasis on screening in the US. Even in the subpopulation being screened, when a PSA test leads to a biopsy, only something like between one in four biospies show the clinical existence of prostate cancer. On the other hand, I think the evidence shows that aggressive screening will detect many cancers that are basically innocuous along with those that require treatment. So under current practice, some cancers are being treated needlessly, and in some cases there are serious side effects. The trouble is that no one yet knows how to distinguish cearly and definitively those that need treatment from those that don't. We can hope that current research will lead to better tests. Meanwhile, each man has to decide for himself whether the threat of side effects of an unnecessary treatment are more scary than the threat of developing advanced metastatic prostate cancer. > Ed Friedman > As to the point about men over 50 having "some" prostate cancer, I think > it is important to distinguish between microscopic evidence of cancer > which might be found on autopsy from cancer which has risen to the level > where it can be detected in a clinical context. This distinction is of your invention only. >>As to the point about men over 50 having "some" prostate cancer, I think >>it is important to distinguish between microscopic evidence of cancer >>which might be found on autopsy from cancer which has risen to the level >>where it can be detected in a clinical context. > > This distinction is of your invention only. This is a primary example of argument by assertion. He completely ignores the arguments I made based on the frequency of prostate cancer detection in autopsy and the frequency of clinical detection of prostate cancer in practice. I didn't make up the numbers. I also didn't make up the idea that there was a distinction. For example, Peter Scardino, of Sloan Kettering, who is a world famous expert on prostate cancer, also explains the distinction in his new book. Dr. Scardino has an extensive list of publications on the subject in peer reviewed journals. As far as I can tell, George Conklin has not published anywhere on the subject in a peer reviewed forum or journal. (Of course, neither have I.) I think it is important to understand the science in all its complexity. There are in fact serious unresolved questions about prostate cancer, and some of the points made by critics of screening and early treatment need addressing. But some things you often see stated are oversimplifications which can lead people who have not studied the subject to be confused. The high prevalence of microscopic evidence of prostate cancer in older men is a fact. It has signficance, and undoubtedly there is much to be learned about it. But it is not the same as clincical evidence of prostate cancer, as a cursory look at the numbers shows. Identifying the two is sloppy reasoning which no serious scientist would engage in. For example, if you think the two are the same, then you lose interest in the question of what leads the great majority of those innocuous cancers never to rise to the level where they are detectable clinically. The argument that "all" men have prostate cancer and if you look hard enough you will find it is really a counsel of despair. It seems to take it as given that prostate cancer is either innocuous or essentially incurable. But, as best I can tell, the data are not consistent with that. Some clinically detected prostate cancers, particularly those of Gleason grade 6 or below would never bother the patient during his lifetime. Just how many is really unknown. One study suggested the percentage was 15-35 percent depending on ethnicity, but I think a lot more research has be done on this matter before taking any numbers seriously. On the other hand, the argument for treating Gleason 7 (and some Gleason 8) cancers aggresively, is, I think, pretty strong. Albertsen's study, which is sometimes quoted as evidence against early aggressive treatment, shows that Gleason 7 cancers have a high likelihood of metastasizing within 5-10 years. Recurrence rates for such cancers after treatment are much lower. By the way, the strongest argument supporting the belief that a lot of clinically diagnosed prostate cancer is innocuous is the fact that one study suggested that if you biopsied all man past a certain age, independent of PSA or DRE results, more than 15 percent of the biopsies would detect prostate cancer. Of course, some of those cancers, if untreated would metastasize, but it seems reasonable that a significant number of them would never bother the patient. No one knows how many there are of each. As a final remark, let me note that the high prevalence of evidence on autopsy of prostate cancer is most pronounced in older men. The standards of practice in urology today recommend against aggressive treatment through surgery or radiation of prostate cancer in older men. Many experts, including Patrick Walsh, the apostle of aggressive treatment, question the wisdom of screening in such men. It is in younger men that the more serious question arises. How many men in their 50s and 60s are being needlessly treated for prostate cancer. Such men may have surgery or radiation which may produce undersirable side effects in an attempt to prevent something that may not become a problem for 15 years or more, and in many of them may never be a problem at all. I think it is important for doctors to explain this to men considering such treatment, but they should also be aware of the possible consequences of not being treated. You make a best either way. It is always comforting to believe you know the truth and your decision was the correct one, but real life is not that simple. >>>As to the point about men over 50 having "some" prostate cancer, I think >>>it is important to distinguish between microscopic evidence of cancer [quoted text clipped - 7 lines] > in autopsy and the frequency of clinical detection of prostate cancer in > practice. No one is looking for prostate cancer if you are under 30. But when yhou look for it, you tend to find it. The only correlate is looking. I didn't make up the numbers. I also didn't make > up the idea that there was a distinction. For example, Peter Scardino, of > Sloan Kettering, who is a world famous expert on prostate cancer, also > explains the distinction in his new book. Dr. Scardino has an extensive > list of publications on the subject in peer reviewed journals. As far as I > can tell, George Conklin has not published anywhere on the subject in a > peer reviewed forum or journal. (Of course, neither have I.) How many men under go a biopsy year after year after year until something is found? > I think it is important to understand the science in all its complexity. > There are in fact serious unresolved questions about prostate cancer, and [quoted text clipped - 5 lines] > learned about it. But it is not the same as clincical evidence of > prostate cancer, Wrong. A biopsy finds microscopic evidence. The only difference is one is looking vs. autopsy. George wrote...snip...A biopsy finds microscopic evidence. The only difference is one is looking vs. autopsy The only difference between a biopsy and an autopsy examination of the prostate is that in the former case you are looking for PCa? I Don't think that is correct. In the publications were the prostate cancer incidence vs decade of life correlation emerged, they were looking for PCa in the autopsies. A key difference between biopsy and autopsy exploration of the prostate is the degree of thoroughness. The biopsy examines a very small portion of the prostate (in fact some regions cannot be examined by traditional trans-rectal biopsy), while the autopsy permits detailed examination of the entire organ...Ron > George wrote...snip...A biopsy finds microscopic evidence. The only > difference is one [quoted text clipped - 9 lines] > cannot be examined by traditional trans-rectal biopsy), while the > autopsy permits detailed examination of the entire organ...Ron So? The problem is that a biopsy is a very chancy thing because it depends on what is looked at. It is guesswork. If you look hard enough on a biopsy with a living man, you will find the same things, identically, that an autopsy would find. No difference. >>George wrote...snip...A biopsy finds microscopic evidence. The only >>difference is one [quoted text clipped - 14 lines] > a biopsy with a living man, you will find the same things, identically, that > an autopsy would find. No difference. Pay attention to what you just said. I think we all agree that if you removed a living man's prostate and examined it in the detail that the prostate is examined in an autopsy, that the results would be the same. That is not the issue. The question is whether the cancers found by biopsy differ in any signficant way from those found when a complete dissection of the prostate is possible. There are some obvious differences. If nothing else, very small cancers are not going to be found on biopsy or only rarely so. Larger cancers, which plausibly might be those more likely to develop aggressively, are more likely to be found on biopsy. In addition, biopsies are done usually because of some other indication such as high PSA, high rate of change of PSA, or an abnormal DRE. The results of the biopsy are not used in isolation from those additional facts. The real question then, whether a cancer too small to found on biopsy with no additional suggestions of anything unusual should be treated exactly the same as one large enough to be detected by biopsy and with those additional factors. In other words, you have to look at the conditional probability that the cancer is significant given all the other information available. Let's look at a similar situation. When men with BPH have transurethral surgery to open the urethra, the tissue removed is often examined by a pathologist. Sometimes that tissue if found to have cancer in it. Yet it is pretty well known that such cancers are more likely to be innocuous than cancers found by the usual biopsy procedure, and they are often treated as such. According to your reasoning, there should be no difference. >>>George wrote...snip...A biopsy finds microscopic evidence. The only >>>difference is one [quoted text clipped - 41 lines] > treated as such. According to your reasoning, there should be no > difference. Pretty well known? Such cancers are treated just like they were found with a biopsy. That's simply not true. These are the prostate tumors that are predominantly GS=4 or 5, and as such, WW, rather than invasive treatment, is a common practice...Ron > That's simply not true. These are the prostate tumors that are > predominantly GS=4 or 5, and as such, WW, rather than invasive > treatment, is a common practice...Ron Doing noting is an option no matter how the cancer is discovered. It is one of the standard options. You seem to habitually recast the discussion. This becomes tiresome after a while. Of course doing nothing (WW) is an option if cancer is found by either a biopsy or TURP. The point is, the ratio of WW to invasive treatment is markedly different between the two. Cancers found by these two methods are NOT treated the same, as you said...Ron > You seem to habitually recast the discussion. This becomes tiresome > after a while. Of course doing nothing (WW) is an option if cancer is > found by either a biopsy or TURP. The point is, the ratio of WW to > invasive treatment is markedly different between the two. Cancers > found by these two methods are NOT treated the same, as you said...Ron Well, my post on this is based on how a close relative was advised, and he got the same identical advice because he was told it did not matter how the cancer was found, it was all the same process after a TURP. If you wish to deny the idea that everyone will have PCa by age 80, and then say, "It does not matter if not discovered by a needle because I say so," then you can hide your head in the sand and preach. But where is the science here? You just hate research. > Well, my post on this is based on how a close relative was advised, and > he got the same identical advice because he was told it did not matter how > the cancer was found, it was all the same process after a TURP. It does not matter how the cancer is found, but statistically speaking, PCa found by TURP generally has a lower GS than PCa found by needle biopsy and it is the clinical parameters such as PSA, PSADT, PSAD, GS, stage, etc. that play into determining the treatment or "process" as you call it. > If you wish > to deny the idea that everyone will have PCa by age 80, and then say, "It > does not matter if not discovered by a needle because I say so," It does matter how the cancer is discovered (removing the double-negative), not because I say so, but rather because PCa first identified by TURP, needle biopsy, DRE, autopsy (statistically speaking) often have different clinical characteristics (disease volume is another good one) as outlined above...so say books and journals. > then you > can hide your head in the sand and preach. But where is the science here? > You just hate research. Insightful as usual, my research group will get a laugh out of that. >> Well, my post on this is based on how a close relative was advised, >> and [quoted text clipped - 24 lines] > > Insightful as usual, my research group will get a laugh out of that. >> Well, my post on this is based on how a close relative was advised, >> and [quoted text clipped - 7 lines] > stage, etc. that play into determining the treatment or "process" as > you call it. So are you willing to say that if a needle finds cancer, it is going to be more aggressive than if its found with a TURP? And why was it established here a long time ago that right now no one seems to be researching using a TURP as a possible cure for PCa, if it removes PCa? >> If you wish >> to deny the idea that everyone will have PCa by age 80, and then say, "It [quoted text clipped - 5 lines] > speaking) often have different clinical characteristics (disease volume > is another good one) as outlined above...so say books and journals. So, DRE finds more aggressive cancers? Maybe you ought to post some research articles since you claim that is your forte. Looking at a tumor so far visually has proven a poor predictor of the future. Until science moves on to looking at genetic material, current pathology is stone-age. And while you are at it, why are the results from massive surgeries over the past 20 years so slight? > So are you willing to say that if a needle finds cancer, it is going to > be more aggressive than if its found with a TURP? Statistically speaking, yes. TURPs probe the central zone of the prostate, TR needle biopsy the peripheral zone. It is well documented that peripheral zone tumors are, on average, more aggresive than central or transition zone tumors. See Walsh's book for starters. > And why was it established here a long time ago that right now no one > seems to be researching using a TURP as a possible cure for PCa, if it > removes PCa? 80% of all PCa tumors occur in the TZ, only 5% in the CZ. TURP can only affect tumors in the CZ. Hence it cannot treat the overwhelming majority of PCa tumors. > So, DRE finds more aggressive cancers? Maybe you ought to post some > research articles Men with cT2 tumors, those identifiable by DRE, have worse outcomes than those found by needle biopsy (cT1c). See the Hopkins nomograms (M. Han, A. W. Partin, M. Zahurak, S. Piantadosi, J. Epstein and P. C. Walsh; J. Urol., 169, 517-523, 2003). > since you claim that is your forte. I never claimed any special prowess, but thank you for the attribution. > Looking at a tumor so far visually has proven a poor predictor of the > future. Until science moves on to looking at genetic material, current > pathology is stone-age. I'm sure that current pathology will look "stone-age" somewhere in the future, but it is where things stand today. Note however that Ploidy analysis is commercially available today. Fascinating genetic experiments are being reported almost daily. > And while you are at it, why are the results from massive surgeries over > the past 20 years so slight? Results on thousands and thousands of men treated surgically at university affiliated hospitals have been published. However most men are treated at community practices, where the surgeons are less inclined / incented to publish. Until patients demand it be different, it will not change. >> So are you willing to say that if a needle finds cancer, it is going to >>be more aggressive than if its found with a TURP? [quoted text clipped - 41 lines] > inclined / incented to publish. Until patients demand it be different, > it will not change. Prostate cancer surgery is no different from treatment for any other disease in this respect. Physicians at university affiliated hospitals are often paid in part to do research. Community based physicians generally have neither the training nor the inclination to collect data and publish the results. However, we can hope that with greater use of computer based medical information systems it will be possible to do more statistical analysis of community based medicine. By the way, it is not clear from his wording whether he means that the results are not reported or that surgery is ineffective. I think the data from published studies shows that surgery is generally extremely effective for Gleason 6 cancers and moderately effective for Gleason 7 cancers. There is even at least one recent study that shows that it is reasonably effective for Gleason 8 cancers. By "effective" I mean that recurrence rates after 7-10 years appear to be relatively low. Of course those results will be biased upwards because the surgeons at university affiliated centers will generally be better qualified. Still, I don't think the issue is whether or not surgery can cure prostate cancer in appropriate cases. I think the issue is how many cancers treated by surgery (or for that matter radiation) are innocuous and would never bother the patient during his lifetime. That is particularly true for Gleason 6 and lower cancers. There is also the question of how aggressive treatment in an attempt to cure the cancer compares with watchful waiting followed by hormone therapy if and when necessary. While that question is related to the earlier one, it is not the same. You would have to isolate those cancers which would otherwise be likely to metastasize, and at present there is no way to do that. Also, on the basis of what we know about prostate cancer, we would expect the results to depend strongly on age. >>> So are you willing to say that if a needle finds cancer, it is going >>> to [quoted text clipped - 73 lines] > about prostate cancer, we would expect the results to depend strongly on > age. This is a correct the whole issue still awaits the PIVOT and other controlled studies. The results are still out and they seem to be approaching the point where some big differences should have happened but so far apparently not. >>You seem to habitually recast the discussion. This becomes tiresome >>after a while. Of course doing nothing (WW) is an option if cancer is [quoted text clipped - 9 lines] > can hide your head in the sand and preach. But where is the science here? > You just hate research. LOL! > You seem to habitually recast the discussion. This becomes tiresome > after a while. Of course doing nothing (WW) is an option if cancer is > found by either a biopsy or TURP. The point is, the ratio of WW to > invasive treatment is markedly different between the two. Cancers > found by these two methods are NOT treated the same, as you said...Ron I know you didn't write the above reply to me and sorry for butting in here. I am supposedly a great candidate for prostate cancer due to the size of my prostate and the fact that I have had prostate problems for at least 10 years and recently turned 50. I have seen a good friend die of bowel cancer which may or may not have come from his prostate. By the time they found it, finding where it started was really not the thing to worry about. I am often sad once more because he is gone and his wife alone in a new house though close to their kids, thank goodness. So I had given the whole thing a lot of thought. I decided that I will continue with what I am doing for my prostate right now but not bother about cancer. I know that sounds stupid and mind numbing to most in here but it seems unavoidable to me in any case, hard to find if I have it right now and when it is found, should that be the case, likely nothing can be done about it anyway due to the fact that I am not going to bother trying to find it. With all that said, I haven't made a real point so far so thought I would close with what made me send this posting. I am constantly wondering WHY people are so afraid of death. Sure, the manner of it is something to be concerned about but why not just attempt to enjoy life with whatever is left and deal with the consequences if/when they come? If, in my lifetime, cancer and prostate probs could be positively cured, I would sure be in that line-up to get that cure but until then, all I can say is that death, by whatever means, is inevitable. Just make it a good one. I risked blowing myself up rescuing someone from a car once and nearly had the car blow up in my face while pulling the guy out - a guy I didn't know and of course got no thanks from anyone (which wasn't what I was after, anyway but I sure wasn't after the threat of being put in gaol by the cops for doing it which came up after that actually FROM the cops) and had I died trying to rescue him, that would have been a good death. Dying in my sleep is also a good death (likely because of other health problems) but I really do enjoy certain TV shows which my wife also enjoys and we love making our own Pizza at home and eating it while watching them, laughing our guts silly, watching science fiction which we both love, tending to our dogs which we both love and also loving each other. There sure is a lot to worry about in the world but it doesn't have to rule your life - and that INCLUDES the problem discussed in here. I don't mean "don't try and find a way out" but just "don't let it rule your life to the detriment of everything and everyone around you". Sounds sorta "new age rubbish" to a lot of people most likely. It's just plain old "don't let the ones you love down while thinking about yourself and don't miss the point of life - which is to live, love and laugh!" >>You seem to habitually recast the discussion. This becomes tiresome >>after a while. Of course doing nothing (WW) is an option if cancer is [quoted text clipped - 7 lines] > prostate and the fact that I have had prostate problems for at least 10 > years and recently turned 50. I am not a physician, but I don't remember seeing any evidence that any of what you describe makes you specially prone to have prostate cancer. But if you are having problems with your prostate, you should definitely be under the care of a urologist. Cancer aside, such problems can lead to difficulty urinating, and if ignored can in some cases lead to kidney failure. A neighbor of mine had that happen to him and now has to have dialysis twice a week. These problems can be treated long before they become serious, so whatever else you do, please don't ignore them. > I have seen a good friend die of bowel cancer > which may or may not have come from his prostate. Or it could have arisen directly in the bowel or colon. If it started in the prostate, that should be pretty clear from routine tests. > By the time they found it, > finding where it started was really not the thing to worry about. That sounds doubtful. Knowing where the cancer originated could make a big difference in how it would be treated. Metastatic prostate cancer usually responds quite well to hormone therapy, while colon cancer would probably be treated another way. > I am often > sad once more because he is gone and his wife alone in a new house though [quoted text clipped - 6 lines] > when it is found, should that be the case, likely nothing can be done about > it anyway due to the fact that I am not going to bother trying to find it. You should definitely be seeing a urologist if you are having problems with your prostate for the reasons I gave above. A urologist would probably routinely examine your prostate with his finger, and he would probably recommend a PSA test. That might lead to a biopsy, which I suppose you could refuse. Or you could refuse to have a PSA test. If I were in your situation, I would want to know just what is wrong with my prostate, and I wouldn't try to tell my dcotor how to go about his business. Once I had all the knowledge I needed, I would then decide what to do. But if you would rather not know, that is up to you. Of course, if you do have prostate cancer and if it develops, eventually it will bring itself to your attention with unmistakeable symptoms, which you will have to have treated. On the other hand, that might never happen or not happen for many years. > With all that said, I haven't made a real point so far so thought I would > close with what made me send this posting. I am constantly wondering WHY [quoted text clipped - 18 lines] > here. I don't mean "don't try and find a way out" but just "don't let it > rule your life to the detriment of everything and everyone around you". You have a right to live your life the way you want. No one else can tell you what to do. But you should really try to be informed before you make important decisions like the above. As best I can tell, you are not yet knowledgeable about either ordinary routine prostate problems or prostate cancer. Benign prostate problems can be treated, and if untreated can lead to a significant amount of misery. The situation for prostate cancer is not so clearcut. Some skeptics about early treatment would argue agains screening which might result in an attempt to cure an early prostate cancer. They argue that it might never amount to anything and the treatment could be worse than the disease. On the other hand, if prostate cancer does advance and metastasize, it is a particularly unpleasant way to go. Before you make decisions like this, you should really try to find out what you can about the subject. Peter Scandino of Sloan Kettering has written a new book about the prostate. I strongly recommend it. I found it at my public library. > Sounds sorta "new age rubbish" to a lot of people most likely. It's just > plain old "don't let the ones you love down while thinking about yourself > and don't miss the point of life - which is to live, love and laugh!" >> Ed...If you don't mind sharing, what were your diagnostic stats (PSA, >> GS, TNM staging) and what is your treatment history and PSA and [quoted text clipped - 76 lines] > > Ed Friedman Actually what you seem to need is a good LAB in order to keep your chemistry the way you want it. Another data point falls into place...A study has just been published which examines the effect of PSA testing in Japan (Int J Urol. 2005 Jul;12(7):662-7; Clinical characteristics of prostate cancer in Japanese men in the eras before and after serum prostate-specific antigen testing; Okihara K, Nakanishi H, Nakamura T, Mizutani Y, Kawauchi A, Miki T.). In their conclusion the authors state "Migrations in the age of patients (toward younger patients), the stage of the cancer (towards earlier stages) and the histological findings (toward favorable findings), in addition to changes in treatment options, have contributed to the prolonged survival of Japanese men with prostate cancer after the PSA testing was introduced." This result serves to further strengthen similar conclusions reached in analogous studies performed in Olmstead, MI; the state of Iowa; Tyrol, Austria and Montreal, Canada...Best wishes and good health, Ron > Another data point falls into place...A study has just been published > which examines the effect of PSA testing in Japan (Int J Urol. 2005 [quoted text clipped - 11 lines] > analogous studies performed in Olmstead, MI; the state of Iowa; Tyrol, > Austria and Montreal, Canada...Best wishes and good health, Ron I tend to agree with you. Unfortunately, all such results may be questioned by confirmed skeptics. Migration towards younger patients and earlier stages would be considered evidence that the effect of testing is mainly to treat cases of men who would never be bothered by their (innocuous) cancers during their lifetimes. The problem is that it is hard to agree on a meaningful endpoint at which point testing can be compared to alternatives. Given the long time horizon for prostate cancer, I agree with you that overall mortality, which ignores a host of other issues, and which get contaminated after sufficeintly long time by other factors, is not a good choice. In my opinion, by the time any really large scale study of sufficent duration could come to any conclusion, newer methods of differentiating potentially aggressive prostate cancers from innocuous ones will become available, and the whole question of the effectivenss of PSA screening will become moot. In the meantime, PSA testing, combined with DRE is basically all we have, and if used intelligently can help many, but not all, men avoid some misery. > Another data point falls into place...A study has just been published > which examines the effect of PSA testing in Japan (Int J Urol. 2005 [quoted text clipped - 11 lines] > analogous studies performed in Olmstead, MI; the state of Iowa; Tyrol, > Austria and Montreal, Canada...Best wishes and good health, Ron Irrelevant. Of course if you test younger and younger men and tell them they have the disease earlier, surviorship will appear to increase. Nothing changes, but the apperance of survivorship increases. It is the totality of confirmatory signals that is not irrelevant. It is simple to reject any single data point, after all, these experiments were designed by humans and involve humans. Each individual experiment has its own flaws and vagueries. Yet the the results from this series of independent examinations taken as a whole cannot be dismissed. Some of the experiments, like the latest, involve comparing the same geographic region at two different times, other experiments compare neighboring regions in a parallel, contemporary fashion, still other experiments involve variations on these themes. Present a convincing set of arguments that explains how a series of independent and different experiments all reach the same, erroneous conclusion, namely that PSA testing saves lives, and I will listen...Ron > It is the totality of confirmatory signals that is not irrelevant. It > is simple to reject any single data point, after all, these experiments > were designed by humans and involve humans. Each individual experiment > has its own flaws and vagueries. Yet the the results from this series > of independent examinations taken as a whole cannot be dismissed. Some Sorry but yes they can. You see, if you go younger and younger, you will find less and less instance of cancer but if you check a control group you WILL definitely save more lives because PSA, digital exam, you are more likely to shoot a fish in a barrel - which is just what this is - than miss. What is more telling is just to have the normal stats of normal life reviewed. The fact that PSA testing is there makes it more likely that more people will be found simply because it makes them think more about it and they dont have to go through a digital exam. This doesnt make it more accurate and even the developer of PSA has since said he rushed in to his findings and believes it isnt all it was originally thought to be. Quite simply, if you give a school full of children the news that they can take a needle and avoid polio, you will get less taking the exam thus more chance of more there with polio than if you got another school with the same number of children and told them that if they take this strawberry tasting stuff THEY will avoid polio. Not only will it make the kids think of polio, they will all realise that there is no pain or discomfort in taking it. Those in the school taking the needle will have a percentage who will "take their chances" rather than the needle. You can only HONESTLY take data that wasnt meant to prove anything but is there in any case. If you get data from all doctors for whatever amount of years, you will also find more bowel cancer being found since PSA came out. Like the example above, you tell a male he can be tested with a finger up the bum or a blood test he will take the blood test. What would be more relative is to set up two doctors' surgeries where one gives only rectal exams and the other does only PSA and see which of them finds more. You will find, I believe, not a lot of difference percentage-wise but you will find more people taking up the PSA test rather than the digital one. Thus in total numbers you will find more cancer found at the PSA testing clinic for those reasons. I guess you could say that if you told people you could find cancer with a lollipop in the mouth and taking a reading of their spit on it, you would find more people going to that doctor than the PSA or digital rectal exam clinic, too. Would you find more cancer? Probably yes and not because the test is valid but you will have more patients. > of the experiments, like the latest, involve comparing the same > geographic region at two different times, other experiments compare [quoted text clipped - 3 lines] > different experiments all reach the same, erroneous conclusion, namely > that PSA testing saves lives, and I will listen...Ron I guess the most telling argument is the person who invented PSA testing saying it isn't really working is cogent enough for me. Alas Coilman, why do you believe him now? He's the same fellow who told you the PSA test was a good test 20 years ago. While the test does have its shortcomings (many of which can be removed by looking at PSA trends along with DRE, rather than a single PSA test), the fact that when one county screens its population with the PSA test and the neighboring county does not, then 10 years down the road PCa mortslity falls in the screened county, but does not in the neighboring county; and the divergent behavior continues over a period of years...this means something. We are each free to interpret the data as we see fit. My interpretation has lead me to ask my sons to start their PSA baseline at age 35...Best wishes and good health, Ron > Alas Coilman, why do you believe him now? He's the same fellow who > told you the PSA test was a good test 20 years ago. While the test [quoted text clipped - 3 lines] > neighboring county does not, then 10 years down the road PCa mortslity > falls in the screened county, but does not in the neighboring county; You must be able to give a good cite for this claim, right? Here are two: Screening for Prostate Cancer: Updated Experience from the Tyrol Study Wolfgang Horninger, MD*, Andreas Berger, MD, Alexandre Pelzer, MD, Helmut Klocker, MD, Wilhelm Oberaigner, MD, Dieter Schönitzer, MD, Gianluca Severi, MD, Chris Robertson, MD, Peter Boyle, MD, and Georg Bartsch, MD Department of Urology, University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria. E-mail: wolfgang.horninger@uibk.ac.at Current Urology Reports 2004, 5:220-225 Current Science Inc. ISSN 1527-2737 Links to the "Cancer in Iowa: 2005" report and reports from previous years are available in the "Publications" section at the registry's Web site, www.public-health.uiowa.edu/shri/. People may also request a copy of the re-port by calling the registry at (319) 335-8609. Between 1990-92 and 2000-02, the prostate cancer death rate in Iowa declined around 30 percent in men in the age groups less than 85 years of age, but de-clined only 10 percent in those 85 years and older. "This correlates with the stage shift information and supports the hypothesis that prostate cancer screening is saving lives," Lynch said. Here are two: Screening f |
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