 |
 | Home | Contact Us | FAQ | Search & Site Map | Link to Us |
 | Sign In | Join | Other 45 Sites in Network |
Medical Forum / Diseases and Disorders / Prostate Cancer / September 2007Walsh. Different,crucial Casodex excerpt. Help please clarifying
Here is another excerpt from Walsh's latest book paged 458/9- it seems crucial to deciding its use- but creates confusion for me for which I would be glad for any clarification. I have been recommended Casodex 150-mg against metastasis but decided not to take it before I'd read any of Walsh, having already decided on the QQL side. EXCERPT FROM WALSH Second edition page 458 More recently, however, doctors have become interested in using antiandrogens, especially bicalutamide, as monotherapy - that is, as a single agent, without any other form of treatment. The main goal here is to attempt to preserve sexual function. When bicalutamide is given in doses of 50 mg, three times a day, sexual interest is maintained in many men; however, beyond one year, only about 20 percent of men remain potent. This 150-mg daily dose of bicalutamide has been used in men with various stages of prostate cancer. For men with metastatic disease, it is less effective than an LHRH agonist. In men who don't have metastatic disease, there is a major red flag. Although bicautamide at this dose was never approved for use in the United States, it was in other countries. However, in England and Canada, the license for this use was withdrawn. This was based on the findings of a study in which men with localized disease were randomly assigned either to receive a placebo or to receive 150 mg of bicalutamide a day. More men in the bicalutamide group died-25 percent versus 20 percent of the men taking the placebo. The reason for this is unclear, but (as we will discuss later), this study's results are similar to the long-term findings of the Medical Research Council study. In this study, of men who received early hormonal therapy, the improvements in overall survival disappeared. Over time, because it is so tough on the rest of the body, prolonged hormonal therapy may do more harm than good. Thus, men with metastatic disease should not be treated with antiandrogen monotherapy. However, for men who start taking anti androgens when they have locally advanced disease, the survival rate appears to be about the same. Thus, there is real interest in using these drugs in men with advanced cancer that has not yet metastized_to_bone. Note: As we will discuss below no form of early hormonal therapy really prevents prostate cancer from progressing. The only thing it really delays is your knowledge of this progression. The fact that men can retain sexual interest makes antiandrogens the focus of intense research-particularly, scientists are investigating combining these drugs with others in hopes of improving quality of life in men undergoing hormonal therapy. However, the use of high dose antiandrogens as the only form of hormonal therapy for prostate cancer has not yet been approved in the United States. We need to understand the reason for the higher risk of death in men who receive 150 mg a day of bicalutamide before patients can safely consider this option. ________________- For me the most significant of Walsh's statements about Casodex: .. no form of early hormonal therapy really prevents prostate cancer from progressing. The only thing it really delays is your knowledge of this progression. Combined with: Over time, because it is so tough on the rest of the body, prolonged hormonal therapy may do more harm than good. The most important aspect of the whole excerpt above however I find confusing, and I can't work it out. It's almost certainly just me and no doubt my age. I am generally fatigued and find it increasingly difficult to concentrate and analyse. Can anybody clarify for me please? These are the key sentences for my confusion: 1. In men who don't have metastatic disease, there is a major red flag .. More men in the bicalutamide group died-25 percent versus 20 percent of the men taking the placebo .. . 2. Thus, men with metastatic disease should not be treated with antiandrogen monotherapy. (Didn't Walsh write in 1. above it was men 'who don't have'.? 3. Thus, there is real interest in using these drugs in men with advanced cancer that has not yet metastized_to_bone. (1. above - should not be used when men 'do not have'..? ) Thanks, and apologies if I'm simply being stupid. Postscript. For me Alan Meyer in one of his posts summarised the Casodex (and Pca) dilemma perfectly: If I may quote him: I would guess that a conclusion from that is that, like so much in prostate cancer, the patient must make choices based on insufficient information. The patient who wants the best chance of survival regardless of the side effects of ADT should request ADT. It might not increase his lifespan. But then again it might. On the other hand the patient who hates ADT and is willing to take his chances might choose to wait until symptoms are very close to developing. He might reduce his lifespan by doing that, but then again he might not. Thanks Alan and all the previous posters. > Here is another excerpt from Walsh's latest book paged 458/9- it seems > crucial to deciding its use- but creates confusion for me for which I > would be glad for any clarification. I have been recommended Casodex > 150-mg against metastasis but decided not to take it before I'd read > any of Walsh, having already decided on the QQL side. You will get plenty of information on this topic in responses from others. The best I saw was in an exchange between RalphV and Alan last week. I will include it below and apologize in advance to those with WebTV. I would only remind you that Casodex is a pill. If the QOL becomes an issue, you can always stop eating the pill. I have been on Lupron for four years and Casodex for one year. I work full time in a non-sedentary job, I walk 3-5 miles a day, 3-5 days a week (in 100 degree weather of late), and still have enough energy to work install a shelving unit in my utility room, pack it with stuff from my work room, run electricity to my work room, and strip a wood piece of furniture in the last several days. In the last week, I've played with all five of my grandchildren, watched Tiger golf and the Bengals win (for a change), and generally enjoy the hell out of life. Don't let the naysayers scare you into shortening your life. Here it is: Hi Steve, Not to worry! In his "new and improved" updated version Dr. Walsh used most of the old text fron the original version plus he added a couple of comments about studies (not referenced) supporting his views. Left intact are his comments about the randomized, control study done by Dr. Messing. He conveniently ignored the latest results of the study's update published before his book was updated (maybe because it showed the flaws of his views). Here are those results: Patients were accrued onto this trial from 1988-1993, and the median follow-up of the population entered into this study is currently 11.9 years (range, 9.7-14.5 years). Table 1. Immediate (n = 47) vs delayed (n = 51) androgen deprivation following radical prostatectomy: Total number of deaths Immediate therapy: 17 (36.2%) Total number of deaths Delayed Therapy: 28 (54.9%) Deaths from prostate cancer Immediate therapy: 7 (14.9%) Deaths from prostate cancer Delayed Therapy: 25 (49.0%) Messing EM, Manola J, Yao J, et al. Immediate versus deferred androgen deprivation treatment in patients with node-positive prostate cancer after radical prostatectomy and pelvic lymphadenectomy. Lancet Oncol 2006;7:472-479. Now, which group would you prefer to be in? Why would he ignore these results? Why does he go out of his way to say that these results have never been duplicated when there is ample evidence, including the VACOUR data to support a survival benefit of early versus delayed suppression. How is the data cited in his book (Pound C et al) that surgery alone is all is needed to control disease progression when so many men have biochemical progression after surgery? He mentions that on average it takes 8 years for men to develop metastasis after surgery (actually the study said the median was 8 years, which is a different thing). How do surgically treated men compare to those treated with other therapies? It is well supported by clinical studies that RT with adjuvant HT provides a survival benefit. The Messing study as well as Mayo studies support the survival benefit to early HT. Still Dr. Walsh continues to ignore the potential benefit of early systemic treatment with hormone suppression to fit his views... Not to worry Steve! "Non Illegitimi Carborundum" RalphV www.pcainaz.org/phpvv Ø If you were depressed by Dr. Walsh's views read on... As more men are diagnosed with earlier stages of prostate cancer including earlier stages of advanced prostate cancer, less men present with multiple lymph node or bone mets at diagnosis. This implies significantly less tumor burden and an opportunity for early hormone suppression to induce massive cell death in the androgen dependent portion of the tumor load. For many years, the medical profession had evidence that demonstrate that the lower the tumor burden the better the response to hormone suppression. This was clearly demonstrated by Crawford ED et al(7). In this study, men were stratified by the degree of their cancer progression. The response to combined hormone suppression was as follows: 1. Advanced with major symptoms such bone pain, weight loss etc. responded for 8.5 months. 2. Advanced with minor symptoms, responded for 15.4 months. 3. Advanced with disease limited to lymph nodes, response was 4 years. In this study, done more than a dozen years ago, even a significant number of the patients in the first group were responding after 4 years (about 10%). About 30% to 40% of the patients with disease limited to lymph nodes were still responding after 10 years. This is a clear indication that deprivation response is directly proportional to the degree of disease progression at the time of diagnosis and the tumor volume ratio of androgen dependent/androgen independent cells. More evidence of this is supported by Labrie et al (9) in a study in which response to androgen deprivation was correlated to the number of bone lesions at the initiation of therapy. Men with 5 or less bone mets had the longest response. These are known biological facts. Androgen dependent tumor cells die when deprived of androgens while androgen independent cells survive. Why would anyone allow androgen dependent cells to become androgen independent when they could be killed by androgen deprivation applied early on in the first place? Hormone suppression is known to prolong time to progression, but is it possible that it could also extend survival? There are a number of studies in which results indicate that early disease detection and early hormone suppression not only postpone disease progression but also improves survival. This is something that *fits* in the overall picture of explaining the 32.5% reduction in mortality experienced in the U.S.A. since the mid nineties. The old myth that patients diagnosed with advanced prostate cancer only respond to hormone suppression for a year or two is simply a myth. In this age of early detection and of earlier stages of advanced prostate cancer at diagnosis this myth is no longer supported by the current medical literature. This myth perseveres because of doctors that believe that saving hormone suppression for later when bone mets develop is perfectly fine. This IS NOT supported by current medical evidence. The real question then is the value of early versus delayed hormone suppression. In the original VACURG study, DES at 5 mg caused many vascular events causing death. This study did not demonstrate a survival advantage and in retrospect caused many clinicians to abandon the use of estrogen for the treatment of prostate cancer. In another VACURG (STUDY II) study of men with locally advanced and metastatic disease, 1 mg of diethylstilbestrol (DES) was slightly more effective than a toxic dose of 5 mg or a dose of 0.2 mg or a placebo. In a reanalysis of the VACURG data, a subset of younger men with earlier stages of prostate cancer when hormonally suppressed experienced a survival advantage(1). Similarly, The Medical Research Council Prostate Cancer Working Party Investigators Group study(2) revealed a survival advantage to early hormone suppression for locally advanced disease. The effects of immediate vs deferred therapy was evaluated in 987 asymptomatic patients in either Stage D2 or Stage C (T3) prostate cancer. Patients treated early exhibited a marked decrease in comorbid events, such as pathologic fractures, spinal cord compression, ureteral obstruction and extraskeletal metastases. Those on delayed therapy had twice the incidence of these events. The reduction in these disease related events is enough evidence to justify the use of early therapy. However, additional support for early therapy comes from survival data. Patients treated with early therapy exhibited a small but significant increase in rates of both overall survival and prostate cancer-specific survival. In patients with locally advanced non metastatic disease, the benefit was even more pronounced. The survival benefit increased over time; the survival rate at 10 years of patients receiving early therapy was almost twice that of patients receiving delayed therapy. This study clearly demonstrates that the earlier the stage of the disease, the less tumor burden at the initiation of therapy the better the results. This was a controlled randomized clinical trial. Another example of the potential benefit of early hormone suppression versus delayed we have the Messing EM et al study(3) in which immediate androgen deprivation after RP with positive lymph nodes resulted in a survival advantage for those treated early. At last follow up (median of 7.1 years) 77% of those treated early were alive as compared to 18% in the delayed group. As far as cause of death, 6.4% (3/47) patients died of PCa. In the delayed group, 31% (16/51) died of PCa. These are significant numbers that support early versus delayed suppression. The recent update published in 2006 and ignored by Dr Walsh is still very supportive of early suppression. Bolla M et al,(4) provided documentation that the combination of hormonal therapy and radiation therapy is superior to radiation alone in the management of T3 prostate cancer. In the Bolla study, 3 years of hormonal therapy in combination with 6-7 weeks of external beam radiation therapy (EBRT) resulted in a significant therapeutic benefit over radiation therapy alone. Estimates of survival after 5 years were greater following combined therapy vs EBRT (79% vs 62%). Furthermore, 85% of patients receiving combined therapy remained disease free, compared with 48% of patients receiving EBRT alone. Some have questioned whether radiation therapy contributed significantly to the outcome and whether it is clinically necessary. There is nevertheless a study done at M.D. Anderson that seems to answer this question. Sagars GK et al (5), showed that therapy with androgen deprivation treated patients had 58% failure rate at 5 years while those on combined therapy (RT + HT) had a 10% failure rate. This is not a randomized trial but it nevertheless supports the synergistic value of hormone suppression with radiation therapy. Recently D'Amico and coworkers (8) confirmed the synergistic value of androgen deprivation added to radiation treatment. This study reduced the deprivation period to six months and still obtained an overall survival benefit . Another randomized control trial that supports the benefit of adjuvant hormone suppression with RT is the Phase III RTOG Protocol 85-31(6). In this trial there was 84% of the combined arm showing no evidence of recurrence versus 71% in the RT arm at 5 years. More significant, the real benefit was in patients with more aggressive disease (Gleason 8 to 10) in which at the 5-year mark, 66% on the combined arm survived versus 55% in the RT arm. In 1998, Granfors et al., reported the results of a controlled trial in which 91 patients with surgically confirmed lymph node staged disease were randomized to orchiectomy plus radiotherapy and radiotherapy alone. Those patients on the RT alone arm that progressed were then treated with androgen deprivation. Clinical progression was observed in 61% of those treated with RT alone and in 31% in those on combined treatment. Mortality was 61% and 38% respectively. Disease-specific mortality was 44% with RT and 27% in the combined therapy group. Negative lymph node patients showed no significant difference in survival. These results suggests that early androgen suppression is better than delayed hormone suppression treatment for these patients The value of early hormone suppression is not clear-cut, absolute or proven case by these randomized clinical trials mentioned above, but the existing evidence should not be ignored and physicians that project a pessimistic stance to their patients need to revisit the latest medical literature and get back on track for the benefit of their patients. Why is then Dr. Walsh ignoring these results? Why would anyone advise men with advanced disease to postpone hormone suppression until they become less responsive is hard to understand, but this is what happens in many instances. Men need to realize that the there is a new paradigm for prostate cancer in the PSA era. Men should not allow a physician or layman confuse them on this issue. Don't allow an old myth to detract from your quality and extension of life if YOU DECIDE to be treated as early as possible. RalphV www.pcainaz.org/phpbb Sources: (1) Byar DP, et al. NCI Monograph 7. 1988;165-170. (2) Immediate versus deferred treatment for advanced prostatic cancer: initial results of the Medical Research Council Trial. The Medical Research Council Prostate Cancer Working Party Investigators Group. Br J Urol 1997 Feb;79(2):235-46 (3) Messing EM, Manola J, Sarosdy M, Wilding G, Crawford ED, Trump D. Immediate hormonal therapy compared with observation after radical prostatectomy and pelvic lymphadenectomy in men with node-positive prostate cancer. N Engl J Med. 1999;341(24):1781-1788. (4) Bolla M, Gonzalez D, Warde P, et al. Improved survival in patients with locally advanced prostate cancer treated with radiotherapy and goserelin. N Engl J Med. 1997;337:295-300. (5) Zagars GK et al., Management of unfavorable locoregional prostate carcinoma with radiation and androgen ablation. Cancer 1997 Aug 15;80(4):764-775 (6) Pilepich MV et al., Phase III trial of androgen suppression using goserelin in unfavorable-prognosis carcinoma of the prostate treated with definitive radiotherapy: report of Radiation Therapy Oncology Group Protocol 85-31. J Clin Oncol. 1997; 15: 1013 1021. (7) 1: Crawford ED, Eisenberger MA, McLeod DG, Spaulding JT, Benson R, Dorr FA, Blumenstein BA, Davis MA, Goodman PJ. A controlled trial of leuprolide with and without flutamide in prostatic carcinoma. N Engl J Med. 1989 Aug 17;321(7):419-24. PMID: 2503724 [PubMed - indexed for MEDLINE] (8) D'Amico AV, Manola J, Loffredo M, Renshaw AA, DellaCroce A, Kantoff PW. 6-month androgen suppression plus radiation therapy vs radiation therapy alone for patients with clinically localized prostate cancer: a randomized controlled trial. JAMA. 2004 Aug 18;292(7):821-7. (9)Labrie F, Dupont A, Cusan L, Gomez JL, Diamond P. Major advantages of "early" administration of endocrine combination therapy in advanced prostate cancer. Clin Invest Med. 1993 Dec;16(6):493-8. (10) AARON J. MILBANK, ROBERT DREICER, AND ERIC A. KLEIN. HORMONAL THERAPY FOR PROSTATE CANCER: PRIMUM NON NOCERE UROLOGY 60: 738-741, 2002 Other supportive references: Kozlowski JM, Ellis WJ, Grayhack JT Advanced prostatic carcinoma. Early versus late endocrine therapy. Urol Clin North Am 1991 Feb;18(1): 15-24 Mazeman E, Bertrand P. Early versus delayed hormonal therapy in advanced prostate cancer. Eur Urol. 1996;30 Suppl 1:40-3; discussion 49. Review. PMID: 9072496 [PubMed - indexed for MEDLINE] Anderson JB. Early versus deferred hormone therapy. Eur Urol. 1999;36 Suppl 2:9-13. PMID: 10529560 [PubMed - indexed for MEDLI Dr. Walsh wrote: "... Again, the cancer cells that ultimately prove fatal in prostate cancer are the hormone-insensitive cells. They keep right on growing, unaffected by hormonal therapy. To these cells, whether hormonal therapy comes earlier or later does not matter...." If I understand his position, he is implying that a man with prostate cancer has some number of androgen independent cells at the time of failure of primary treatment. This number will grow at a predetermined rate, regardless of whether ADT is applied or not. The other, androgen dependent cells, also grow, but they are irrelevant because their growth can be stopped at any time that they might cause, or be about to cause, symptoms. Once we apply androgen deprivation therapy, the androgen dependent cells cease to be a factor in the disease. In the passage quoted by Just, Walsh makes no biological argument for this view, but he does support it with some empirical research that appears to show that time of death is the same for most men receiving early or late ADT, thus implying that they must have had the same rate of growth of androgen independent cells. Does anyone know what the current molecular biological theory is regarding this view? Do our androgen independent cancer cells only come from other androgen independent cells? Or is it possible that cells with androgen dependence will sometimes give rise to daughter cells that are independent, or less dependent, on androgens? Is there any scientific consensus regarding this? If Dr. Walsh is right, a man with 1000n dependent cells and 1n independent cells will have the same life expectancy as a man with 0n dependent cells and 1n independent cells - assuming the characteristics of those independent cells are the same in the two men, and assuming that ADT is eventually used to keep the dependent cells from killing the man who has them. There is another issue that also clouds this. I had thought that androgen dependence was not a "yes" or "no" characteristic of cancer cells, but rather a "more" or "less" characteristic. I had thought that some cells are highly dependent and die without androgens; some are highly independent and are completely unaffected by the presence or absence of androgens; and some are in between. If that were true, then wouldn't early application of ADT slow the growth of cancer cells that will become dangerous? But of course, whatever the theory, if Dr. Walsh is right about the facts of survival - an issue which appears to be in dispute - then there wouldn't be much point to early ADT. Alan Alan, You hit the nail in the head! If androgen-dependent cells in time turn androgen- independent, why not kill them before they do? It seems that this process happens with accumulated cell mutations even before diagnosis and is one of the reasons why advanced PCa is more resistant to treatments. The presence of androgen-independent stem cells in the prostate gland at birth is the main reason androgen deprivation is not considered curative for prostate cancer. In simple words, prostate epithelium is made up of three different types of cells. The largest portion is made of secretory epithelial cells. There are also basal epithelial cells and endocrine-paracrine cells. Not much is known about the endocrine-paracrine cells, their function and androgen sensitivity. The normal secretory epithelial cells are sensitive to androgens while the basal cells do not require androgens to grow and can survive without it. Basal cells are believed to be the stem cells of the prostate or cells that generate secretory epithelial cells. Bruchovsky and others believes that androgen independence is related to a shift in the ratio of androgen-dependent cells to androgen-independent cells in the tumor load. This, happens as cell mutations accumulate and dedifferentiation proceeds to an endpoint. This would explain why very advanced PCa is already androgen-independent at diagnosis and does not respond to hormonal suppression. Arnold and Issacs describe the relationship between cell of origin for prostate cancer and androgen responsiveness. "Based on stem cell organization, it is possible for prostate cancer to have three distinct cells of origin. The first alternative is that the prostate cancer is monoclonally derived from an androgen-independent stem cell. Even if the cell of origin is an androgen-independent stem cell, it is still possible for the resulting cancer to be responsive to androgen ablation. The malignant stem cell could retain the ability to progress down the hierarchical pathway, giving rise to larger subsets of androgen-sensitive amplifying and even larger numbers of androgen-dependent transit malignant cells. Such a heterogeneous cancer composed of these three cell types would respond to androgen ablation with the elimination of the largest subset of cancer cells (i.e. the androgen dependent malignant transit cells) and a reduction in the growth rate of the next largest subset of cancer cells (i.e. the androgen- sensitive malignant amplifying cells). Such a response would not be curative because neither the malignant androgen-independent stem cell nor the androgen-sensitive malignant amplifying cells would be eliminated." "A second alternative is that the original prostate cancer is monoclonally derived from an androgen-sensitive amplifying basal cell. If this occurs, the cancer would again be androgen responsive because it is composed of androgen-sensitive malignant amplifying cells that retain the ability of differentiating into androgen-dependent transit cell progeny. Again, owing to clonal expansion, the major type of cancer cells present would be the androgen-dependent malignant transit cells. Such a heterogeneous cancer would be responsive to androgen ablation because of the elimination of the major subset of malignant transit cells; however, the cancer would not be cured by such therapy because the androgen-sensitive amplifying cells would not be eliminated." A third alternative is that the original cancer is monoclonally derived from an androgen-dependent transit (glandular) cell. If this occurs, the cancer would initially be highly androgen responsive to androgen ablation. If no further malignant progression occurred, the cancer theoretically could be cured by such therapy; however, even if this third possibility occurs and the initial prostate cancer is homogeneously composed of androgen-dependent cancer cells, as these cells undergo sufficient cellular proliferation to produce clinically detectable prostate cancer (i.e. more than 39 population doublings), a series of mechanisms would eventually lead to the heterogeneous development of malignant clones of androgen-sensitive or androgen-insensitive prostate cancer cells, or both." Then they further say: "Development of androgen-independent prostate cancer cells. As subpopulations of malignant prostate epithelial cells begin to grow independent of androgen, basic genetic changes likely occur in the cancer cell genome. The tumor cells become increasingly genetically unstable, developing clones that can proliferate without the requirement for androgenic stimulation (Isaacs et al. 1982, Wake et al. 1982). Once these androgen-independent clones develop, they have a growth advantage following androgen ablation over all other newly developed tumor clones that retain androgen dependence. Other genetic changes may contribute to the progression to androgen independence. The frequency of expression of the apoptosis inhibitor, bcl-2, has been correlated with the progression from androgen dependence to the androgen independent metastatic phenotype (Furuya et al. 1996). If cells over-express bcl-2 and are thereby protected from apoptotic stimuli, their resistance to androgen depletion is augmented, along with their ability to progress towards hormone-refractory tumors (Raffo et al. 1995)." I really believe that Dr. Walsh ignores much of the existing evidence because it doesn't fit the Hopkins mold where reliance is on surgery. RalphV www.pcainaz.org/phpbb Source: J T Arnold1 and J T Isaacs Mechanisms involved in the progression of androgen-independent prostate cancers: it is not only the cancer cell's fault. Endocrine-Related Cancer (2002) 9 61-73 Ralph, Thanks for the explanation. I have studied enough molecular biology that I could follow it to some degree. It appears that the bottom line for patients, if the theory is correct, is that early ADT might or might not be of significant help, depending on the specific characteristics of their cancer. For some patients it could be of great help, for others no help at all, and for others it might be of some help. Judging from the nature of the issues involved, it also sounds like a typical pathology lab would not be able to distinguish these cases and even a research institution would probably not be able to. It sounds like it would be necessary not only to biopsy the patient's cancer cells, but also to culture them and then subject them to various tests for androgen independence, and even then a patient couldn't know how representative the cells were of his total cancer. I would guess that a conclusion from that is that, like so much in prostate cancer, the patient must make choices based on insufficient information. The patient who wants the best chance of survival regardless of the side effects of ADT should request ADT. It might not increase his lifespan. But then again it might. On the other hand the patient who hates ADT and is willing to take his chances might choose to wait until symptoms are very close to developing. He might reduce his lifespan by doing that, but then again he might not. Life is full of tough choices isn't it? Alan  SignaturePSA 16 10/17/2000 @ 46 Biopsy 11/01/2000 G7 (3+4), T2c RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins PSA <.1 <.1 <.1 .27 .37 .75 PSAD 0.19 years EBRT 05-07/2002 @ 47 PSA .34 .22 .15 .21 .32 PSAD .056 years Lupron 07/03 (1 mo) 8/03 and every 4 months there after PSA .07 .05 .06 .09 .08 .132 .145 PSAD 1.4 years Casodex added daily 07/06 PSA <0.04, <0.05, <0.04 (06/12/2007) Non Illegitimi Carborundum >> Here is another excerpt from Walsh's latest book paged 458/9- it seems >> crucial to deciding its use- but creates confusion for me for which I [quoted text clipped - 21 lines] > >Steve thanks, and sorry to trouble you - but here comes my lack of net savvy.I sent it as an email but it bounced-?? I am not familiar with some of the abbreviaions used in these discussions. It would be helpful to occasionally spell out the terms. For example...I had to finally come to the conclusion...by luck...that "QOL" means "quality of life."....which may not be completely understood in every case. I'm not being critical...just very concerned in learning more about my options. Thanks Ralph >I am not familiar with some of the abbreviaions used in these > discussions. It would be helpful to occasionally spell out the terms. [quoted text clipped - 6 lines] > Thanks > Ralph This coming from a guy known only as "R L" :-) You are, of course, correct, Ralph. We do tend to over abbreviate and anagram. I will watch it until I have forgotten again. SignaturePSA 16 10/17/2000 @ 46 Biopsy 11/01/2000 G7 (3+4), T2c RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins PSA <.1 <.1 <.1 .27 .37 .75 PSAD 0.19 years EBRT 05-07/2002 @ 47 PSA .34 .22 .15 .21 .32 PSAD .056 years Lupron 07/03 (1 mo) 8/03 and every 4 months there after PSA .07 .05 .06 .09 .08 .132 .145 PSAD 1.4 years Casodex added daily 07/06 PSA <0.04, <0.05, <0.04 (06/12/2007) Non Illegitimi Carborundum I don't know exactly what you're asking, Mike, but I sent email to the email address I had listed for you. I hope it's still good. >>> Here is another excerpt from Walsh's latest book paged 458/9- it seems >>> crucial to deciding its use- but creates confusion for me for which I [quoted text clipped - 27 lines] >>Steve thanks, and sorry to trouble you - but here comes my lack of net >>savvy.I sent it as an email but it bounced-?? On Thu, 6 Sep 2007 13:34:41 -0400, "Steve Kramer" <skramer@cinci.rr.com> wrote:/ >I don't know exactly what you're asking, Mike, but I sent email to the email >address I had listed for you. I hope it's still good. [quoted text clipped - 27 lines] >>> >>>Here it is: RL. I really do appreciate your point re abbreviations. I often feel the same. I did in fact start to write QQL in full -but then thought it might appear patronising there are so many with a depth of knowledge in this group. One thing I do is always open the ng together with the list of abbreviations at: http://www.prostate-cancer.org/resource/acronyms.html and of course it hasn't got QQL! -in which case go to http://www.cancer.gov/templates/db_alpha.aspx?expand=Q. I often have to refer to one or other. Hope this helps. For STEVE Very many thanks for sending RalphV's post which shows Walsh has ignored a piece of research - does that destroy his whole argument? (I remain confused about what seems to me to be the contradictions in the excerpt I quoted.) Your physical activities Steve are tremendous -even for a totally fit man- and speak well for both pills' side effects - and your own will. You're also a knowledgeable analyst. Are you typical? May I however introduce another excerpt? (OK then I will!) Is this right, or wrong? If it's right, then it's almost a case of QED, is it not? I don't make any judgements. This is a very live question for me. I'd just like to try and get as clear as possible some further guidance as to whether I should take 150mg Casodex daily or not. HIFU definitely knocked off my prostate cells. It may well have given the old-one-two to my seminal vesicle cells as well (MRI in three weeks) (Hope you're UK 'RL'. If not 'the old one-two' is the knock out punch!) So, I'm sitting here, happily typing, with no pain and (at the moment) no side effects. And my bone scan recently was negative. But I know micrometastasis (Pca cells lurking in bones currently too few to be detectable) may well be lurking to have the last laugh. They might take 8 years (a median - in RalphV's post) to show themselves. So do I risk sitting here less cheerfully, with possible/probable? Casodex side-effects according to some users, for say, even four years (when anyway I'd be 84) for some gain which might be only illusory -according to the next excerpt from Walsh? EXCERPT WALSH PAGE 478 But doesn't receiving early hormonal therapy delay the progression of cancer? The answer is yes and no. It delays your knowledge of progression, but it doesn't stop the clock. Another way to look at it is "pay me now, or pay me later." Eventually, the result is the same. Hormonal therapy does two things: it stops cells from making PSA and shrinks the hormone-sensitive cell population. Say a man begins hormonal therapy when his PSA level is elevated, but his bone scan is negative. His PSA level will drop dramatically, and he may feel that his cancer is gone. But it's not; it has just slipped below the radar screen. Those hormone-insensitive cells continue to grow silently. There is a euphemism for this called a delay in progression. What it really is, unfortunately, is a silent progression. Over time (and this may take years), these hormone-insensitive cells will reappear on the medical radar the PSA level will begin to rise again, the bone scan will become positive, and the tumor will begin to attack bone, producing the signs and symptoms of advanced, hormone-refractory disease. Actually, this delay is just a time shift. Say the man waited to start hormonal therapy until his bone scan was positive. Right away, his tumor would shrink, his PSA level would fall, and the man would experience a remission of indefinite duration-until, just as in the first scenario, his hormone-insensitive cells reached a critical mass. Eventually-whether the man started hormonal therapy early or late-the result would be the same. If the man had begun hormonal therapy early, his cancer would have progressed, but he wouldn't have been aware of it. The trade-off is that he would have endured the side effects of hormonal therapy for a much longer time. If the man had begun hormonal treatment later, he would have had fewer side effects. What about peace of mind? Well, in both cases, the cancer is growing. The man who begins treatment early has a false peace of mind based on the idea that what he can't see won't hurt him /end excerpt Good luck to all. MikeHi Mike, The decision to initiate hormone suppression after recurrence is a patient's choice. The reason for that is because each patient has its own preferences and in the decision making process they could apply more weight to certain part of the treatment risk/benefit analysis points over others. Some personal preferences have more influence than others, but the bottom line it is the patient who needs to decide what is best for themselves at this point in their lives. I added some comments to the book's excerpt you introduced: (Excerpt starts) But doesn't receiving early hormonal therapy delay the progression of cancer? The answer is yes and no. It delays your knowledge of progression, but it doesn't stop the clock. Another way to look at it is "pay me now, or pay me later." Eventually, the result is the same. Hormonal therapy does two things: it stops cells from making PSA and shrinks the hormone-sensitive cell population. RV>+++++++> This is a rather simplistic view. When deprived, the androgen- dependent cells of the tumor load slow down proliferation and in time cells undergo programmed cell death. Dead cancer cells do not produce PSA or mutate further to acquire aggressive characteristics that in time become more difficult to treat. Say a man begins hormonal therapy when his PSA level is elevated, but his bone scan is negative. His PSA level will drop dramatically, and he may feel that his cancer is gone. But it's not; it has just slipped below the radar screen. Those hormone-insensitive cells continue to grow silently. RV>+++++++++++> Hormone insensitive cells can also respond to deprivation by slowing down their proliferating rate. This has been demonstrated by the fact that androgen deprived men experience reduced disease progression and metastasis. There is nothing "under the radar" in this. These are facts he ignored. There is a euphemism for this called a delay in progression. What it really is, unfortunately, is a silent progression. Over time (and this may take years), these hormone-insensitive cells will reappear on the medical radar the PSA level will begin to rise again, the bone scan will become positive, and the tumor will begin to attack bone, producing the signs and symptoms of advanced, hormone-refractory disease. RV>++++++++> What he described above ignored that when not deprived these cells can progress faster and continue to mutate and become more aggressive. This results in more treatment resistance. Actually, this delay is just a time shift. Say the man waited to start hormonal therapy until his bone scan was positive. Right away, his tumor would shrink, his PSA level would fall, and the man would experience a remission of indefinite duration-until, just as in the first scenario, his hormone-insensitive cells reached a critical mass. Eventually-whether the man started hormonal therapy early or late-the result would be the same. RV>+++++> Here he ignored the multiple studies in which early treatment has ended in disease-specific survival and overall survival. These studies also demonstrated a slower progression rate and metastasis. If the man had begun hormonal therapy early, his cancer would have progressed, but he wouldn't have been aware of it. The trade-off is that he would have endured the side effects of hormonal therapy for a much longer time. If the man had begun hormonal treatment later, he would have had fewer side effects. What about peace of mind? Well, in both cases, the cancer is growing. The man who begins treatment early has a false peace of mind based on the idea that what he can't see won't hurt him.....(end excerpt) RV>+++++++> Like many others opposed to hormone suppression, Dr. Walsh ignores the symptoms of disease progression while pointing to side effects of treatment. Can disease progress w/o side effects? Yes it can, but eventually the progression affects quality of life (QOL). This is well documented by the higher incidence of bone pain, ureteral obstruction and skeletal lesions in delayed treatment. This he purposely ignored to prove his point. RalphV www.pcainaz.org/phpbb > On Thu, 6 Sep 2007 13:34:41 -0400, "Steve Kramer" > [quoted text clipped - 105 lines] > > MikeHi > RL. I really do appreciate your point re abbreviations ... I don't feel a PCa pt is sufficiently educated in his disease to make sound major treatment choices until he is familiar with most common abbreviations. That applies especially with HT (aka ADT) because its *potential* for dramatic or even devastating SEs is so high. PCa = PC = prostate cancer. pt = patient. HT = hormone therapy = ADT = androgen derivation therapy. SE = side effects = any undesirable unintended effect > For STEVE Very many thanks for sending RalphV's post which shows > Walsh has ignored a piece of research - does that destroy his whole > argument? ... Has Walsh *ignored* a piece of research, or did he consider and dismiss it for some valid reason? I'd vote for the latter simply because Walsh has a whole medical staff at his disposal if I didn't have so much respect for Jordan's and RalphV's and Evens' and a few others' technical acumen. Either way, even an abbreviated, almost shorthand, list of pros and cons runs into multiple pages, so that issue is just one among very many in the ADT decision. > [Kramer's] physical activities are tremendous -even for a totally > fit man- and speak well for both pills' side effects > Are you typical? Not according to the hundreds of hours of research I did when considering ADT, nor to the university teaching hospital oncology board which reviewed my research, nor to this forum's review of my research, nor to m poll of this forum for its ADT SEs, nor to a geriatric men's psychologist I consulted, nor to virtually all studies and websites I found. If you're athletic, you can virtually count on losing that, according to many authorities. YMMV (your mileage may vary), and our individual priorities *do* vary very significantly. > I don't make any judgements. Ultimately, we have to make judgments, based on some preponderance of the evidence and opinions available and our own criteria. We should be very careful to bias that judgment towards large scale statistics rather than anecdotal stories. > So do I risk sitting here less cheerfully, with possible/probable? > Casodex side-effects according to some users, for say, even four years > (when anyway I'd be 84) for some gain which might be only illusory > -according to the next excerpt from Walsh? The risks of ADT SEs include a double-edged sword: We can always quit if its SEs are unacceptable, but the older we are, the more likely quitting may not end the SEs [because our T (testosterone) production may not resume]. And there's one other tidbit underscoring all the SE concerns: the therapeutic index -- the ratio of benefits to side effects. Although the range of life extension added by ADT is huge -- from zero to years -- the average runs something like 6-8 months, up to 13 months in limited specific classes of PC cases. Thus the benefit, the SEs, and obviously the therapeutic index are hugely variable among pts. Researching the severity, likelihoods, potential mitigation meds, and impacts on my life of the various ADT SEs, then balancing those vs its quantity and likelihood of benefit, was invaluable in my decision process. Then, of course, most of that goes in the dumpster if and when my cancer returns with significant symptoms. I.P. Many thanks to Steve Kramer and RalphV and to IP Freely for pithy, forthright analyses. And to Alan Meyer. RalphV begins: The decision to initiate hormone suppression after recurrence is a patient's choice. Ralph do I read this right? HT is for use 'after recurrence'? If I find in a few weeks my Seminal Vesicle cells have been destroyed (can't assume that yet) then I assume my 'recurrence' would be metastsasis. At the moment I don't have any such 'recurrence'. So anyway I'm not ready for HT? I wrote > I don't make any judgements. IPFreely commented: Ultimately, we have to make judgments, based on some preponderance of the evidence and opinions available and our own criteria. We should be very careful to bias that judgment towards large scale statistics rather than anecdotal stories. I didn't mean I don't want to judge on the evidence presented (that would mean I'm not trying to arrive at a decision). I meant the argument which ran through Just's original threads, as to whether Walsh was qualified or not to arrive at conclusions about hormonal treatment when his speciality is as a surgeon. This seems to me to be irrelevant. What he can be judged for only is on the evidence he puts forward. Which is statistics - I would never make any decision based on anecdote. But it's clear that - as in this whole complex web of PCA treatment - it's not as simple as that. Steve, Ralph and IPF's arguments are based on statistics. And they are diametrically opposed. Steve Kramer and RalphV attack Walsh with highly detailed statistical evidence; and IPFreely defends with equally intense feelings backed by further statistical evidence. All three are proven and deeply respected contributors to this invaluable ng . IPF, I do note, has personally done his own long, detailed research on the very subject. Another dilemma for me in reading both sides of the argument: Steve: If the QOL becomes an issue, you can always stop eating the pill. Versus (apologies, can't find origin): We can always quit if its SEs are unacceptable, but the older we are, the more likely quitting may not end the SEs [because our T (testosterone) production may not resume]. In two months I'm an octogenerian - albeit not necessarily venerable. I am no microbiologist, scientist or statistician and I could not follow so many of the learned details put forward. But I note another noted contributor can, Alan Meyer. He replied to a detailed scientific post by Ralph: >It appears that the bottom line for patients, if the theory is correct, is that early ADT might or might not be of significant help, depending on the specific characteristics of their cancer. For some patients it could be of great help, for others no help at all, and for others it might be of some help. Judging from the nature of the issues involved, it also sounds like a typical pathology lab would not be able to distinguish these cases and even a research institution would probably not be able to. It sounds like it would be necessary not only to biopsy the patient's cancer cells, but also to culture them and then subject them to various tests for androgen independence, and even then a patient couldn't know how representative the cells were of his total cancer. I would guess that a conclusion from that is that, like so much in prostate cancer, the patient must make choices based on insufficient information. The patient who wants the best chance of survival regardless of the side effects of ADT should request ADT. It might not increase his lifespan. But then again it might. On the other hand the patient who hates ADT and is willing to take his chances might choose to wait until symptoms are very close to developing. He might reduce his lifespan by doing that, but then again he might not./....end Alan quote I have to read all this information over again, But for me that seems, at the moment to be an answer. But there can be more to consider than statistic.I am getting rather desperate about getting my wife of 55 years home with me, from her nursing home. She is in good hands, I see her every day, but she knows we're not together and I believe even in her confusion she is aware of it and pines. I feel I have abandoned her. I'm waiting first for the MRI to be sure about my seminal vesicle.While there's some evidence it may help, my wife may be as good an argument as any for taking the pill, and throw it overboard if I feel the ship drifting. Thanks and best wishes to all. MikeHi Never more did I feel the need to quote my wise old mate Omar, as I did in my very first post: Myself when young did eagerly frequent Doctor and Saint, and heard great Argument About it and about, but evermore Came out by the same Door as in I went Hi MikeHI, Recurrence defined as detection of disease after a primary treatment. The implication here is that the primary treatment did not control the disease and there is established evidence of that. Recurrence could be established by a PSA elevation, biopsy or imaging tests. Your original treatment (HIFU) could have missed the seminal vesicle involvement and in your case treating the SV again with HIFU could resolve your condition. The treatment outcome should be monitored by frequent PSA measurement. At present, you do not need HT as you want to be able to observe the result of the second HIFU treatment without interference from hormonal suppression. The treatment of patients at high risk of recurrence BEFORE recurrence is established after a primary treatment is experimental. Some men are now being treated with combination treatments such as RT(or RP) + HT + Chemo when the diagnostic parameters point to high risk. Still this is experimental and follows what has been done in clinical studies for other cancers (such as BCa). Even when recurrence is established, patients should decide based on their personal preferences. Even when it seems reasonable to apply hormonal suppression as early as possible to prevent disease progression, it is still the patient's choice given the fact that HT can have side effects and these need to be compared to the symptoms of untreated disease pogression. Again a patient's choice. Be well and wish you be very best outcome from your recent treatment, RalphV www.pcainaz.org/phpbb > Many thanks to Steve Kramer and RalphV and to IP Freely for pithy, > forthright analyses. And to Alan Meyer. [quoted text clipped - 7 lines] > metastsasis. At the moment I don't have any such 'recurrence'. So > anyway I'm not ready for HT? > Steve: If the QOL becomes an issue, you can always stop eating the > pill. [quoted text clipped - 4 lines] > resume]. In two months I'm an octogenerian - albeit not necessarily > venerable. Mike, I may have slightly mislead you. If you start taking the pill and find, in the short term, that QOL becomes an issue, you can discontinue Casodex and your SEs will subside. If you take them for a couple of years, they may not subside. I believe you will find out quickly if you can handle the SEs. If you can handle the SEs, you will probably be taking the pill for the rest of your life and, therefore, have the SEs for the same duration. SignaturePSA 16 10/17/2000 @ 46 Biopsy 11/01/2000 G7 (3+4), T2c RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins PSA <.1 <.1 <.1 .27 .37 .75 PSAD 0.19 years EBRT 05-07/2002 @ 47 PSA .34 .22 .15 .21 .32 PSAD .056 years Lupron 07/03 (1 mo) 8/03 and every 4 months there after PSA .07 .05 .06 .09 .08 .132 .145 PSAD 1.4 years Casodex added daily 07/06 PSA <0.04, <0.05, <0.04 (06/12/2007) Non Illegitimi Carborundum > Versus (apologies, can't find origin): We can always quit if its SEs > are unacceptable, but the older we are, the more likely quitting may > not end the SEs [because our T (testosterone) production may not > resume]. In two months I'm an octogenerian Thus my comment about the possibility of irreversible SEs. > But there can be more to consider than statistic.I am getting rather > desperate about getting my wife of 55 years home with me, from her [quoted text clipped - 4 lines] > may help, my wife may be as good an argument as any for taking the > pill, and throw it overboard if I feel the ship drifting. I'm sorry to further confuse the issue, but ADT is still a dilemma for you, IMO. If you bring your wife home under your care, you'll need stamina, mental acumen, and an even disposition ... all threatened by ADT. I suggest that if maximizing your lifespan for her sake trumps your QOL -- a very admirable goal -- you spend some time in ADT's spell, with professional and close-friend evaluation as reality checks, before bringing her home. She may not be well served by the easily tired, slightly addled, and/or near-bipolar man *some* ADT pts become. OTOH, maybe a project would invigorate and motivate *her*. ;-) I.P. Mike, I'd like to respond to two aspects of your posting. > ... > Ralph do I read this right? HT is for use 'after recurrence'? > ... Ralph already answered this one, but I'd like to reinforce what I think he said. Unless you have evidence of recurrent disease, there is no established reason for taking HT. There are cases of younger men who have aggressive cancers for which their doctors are prescribing very aggressive treatment - including HT or even chemotherapy along with primary treatment - in hopes of destroying every vestige of cancer. But as Ralph says, this is not the common practice. In your case I would think it would be unnecessary. You don't know yet that you need HT at all and it seems to me to be a mistake to take a treatment that you don't know you need. It would be better to wait and see if you need it. At your age, even a recurrence may not be enough to establish that you need HT. If the cancer is growing slowly enough you might choose just to "watch and wait" before treating it since something else might get you first anyway. > ... > But there can be more to consider than statistic.I am getting rather [quoted text clipped - 6 lines] > pill, and throw it overboard if I feel the ship drifting. > ... It sounds from this paragraph as if your wife has Alzheimer's Disease. Is that correct? If so, then I have some more to say to you. My mother and mother-in-law both had it and my father had some sort of dementia in his last few years as well. Taking care of an Alzheimer's patient is a full-time job, and it gets harder and harder and harder and harder as time goes by. However confused your wife is now, if she has AD then three months from now she will be more confused, and in six months, twelve months, or at some time, she will need to be watched and looked after continuously, and I really mean continuously - no breaks. You can go to the bathroom and come out to find her in trouble in the kitchen, or vice versa. Also, it can be very difficult to place an AD patient in a good Alzheimer's residence. You can very suddenly find yourself in an emergency care situation. You could have a heart attack, or a fall, or some other serious problem. Suddenly you can't care for your wife. What do you do? You call the home where they were taking care of her and they tell you they're full up at the moment and have a waiting list, but hope to get your wife in in three months. So now what? Do you start making the rounds of homes, trying to find another good one that has an opening? It's not an easy task. You may not be up to it. And you may not find such a good place again. A typical AD patient will implore her husband or son or daughter to take her home. It will break your heart to see her like that. So you take her home and then, guess what, she's still miserable and she still asks to go home. You say, "But dear, you are home." And she says, "I don't remember this place. This isn't my home." You go out to the supermarket and come home to find your wife is gone. Or you find the police there and discover that your wife called them and told them that her husband has disappeared (my mother did that). Life can become very difficult. Unremitting effort is required. You become tired and worried and more tired, but there is no break. You may be able to give more support to your wife by visiting her every day in her current residence than by taking her home and having to do all the housework and care for her as well as spending time with her. This is NOT a disservice to her. It is NOT abandoning her. On the contrary, it may be doing for her what she most needs. I strongly suggest you make a posting to alt.support.alzheimers and consult with the folks there. They have some very experienced caregivers that can help you a lot to think through the problems and come up with good solutions. You're a good man Mike. You're facing the tough problems of old age that so many of us face, and you're trying to do it with intelligence and compassion. My hat is off to you. Best of luck. Alan >> [Kramer's] physical activities are tremendous -even for a totally fit >> man- and speak well for both pills' side effects [quoted text clipped - 7 lines] > athletic, you can virtually count on losing that, according to many > authorities. MikeHi -- I completely misunderstood your question. Thanks to IP for correcting my misimpression. I would say that I am not the typical ADT patient. I was always an active person in my career and life, but not one who exercised a lot. When I found I had cancer and would have it excised, I started walking and could barely make it one mile in 20 minutes. By the time I had surgery, six weeks later, I was doing 2 miles in 17 minutes, including on the ship during the cruise before my surgery. After surgery, I went right back to the healthplex and worked up to 3 miles and decided I was bored out of my mind. I've been walking in local parks ever since. It has made such a big difference on my life, my chronic back pain, my ADT SEs, etc., I just never stopped. In that, I believe I am probably very non-typical. So, my SEs are also non-typical. But then, I don't think there is a "typical" for ADT SEs. > On Thu, 6 Sep 2007 13:34:41 -0400, "Steve Kramer" > For STEVE Very many thanks for sending RalphV's post which shows > Walsh has ignored a piece of research - does that destroy his whole > argument? Dr. Walsh was there for me (well, his book was) during my first foray into this disease. I cannot say enough about how well he explained to me the disease, the options circa 2000, and the prospects of living to see my great grandchildren. I thought it a brilliant work and it was, without debate, the Bible of prostate cancer at the time. I recommended it to all. I recently heard of a 2nd Edition which I have been anxiously awaiting so that I could have updated information from him. As best as I can tell, there is little or no up-to-date information. Strum's A Primer on Prostate Cancer is a good book and Scardino's Prostate Book is probably the most up-to-date book on the market. Sadly, I think that Walsh got lazy and, while I think his information is still very good, you have to take it in the context of more modern literature. Based on that, I would say it does not destroy his whole argument, but I will say that it fails to support the argument substantively. > (I remain confused about what seems to me to be the > contradictions in the excerpt I quoted.) I do not think the confusion is in you. I think there is more research data than Walsh inculcated before writing his book. > Your physical activities > Steve are tremendous -even for a totally fit man- and speak well for > both pills' side effects - and your own will. You're also a > knowledgeable analyst. Are you typical? Analyst? Typical? LOL. I guess I do a pretty fair job at analysis, but I have no professional training in such. However, that which I am, I would say I'm fairly atypical. > I don't make any judgements. This is a very live question for me. I'd > just like to try and get as clear as possible some further guidance as > to whether I should take 150mg Casodex daily or not. I am sorry, but I cannot answer that for you. I can tell you that my answer when I was asked was, "yeah, let's go with the Casodex." Am I happy about it? Yes. I am alive, my QOL has not diminished much, and my PSA is in the sub-basement. I would rather not be on any ADT at all, but that, to me, is a decision made four years ago and I got results better than I anticipated. > So do I risk sitting here less cheerfully, with possible/probable? > Casodex side-effects according to some users, for say, even four years > (when anyway I'd be 84) for some gain which might be only illusory > -according to the next excerpt from Walsh? > > EXCERPT WALSH PAGE 478 [redacted] Like I said, I think it is pretty clear that Walsh made the 'observation' during the last millennium and has failed to change his mind in the face of countervailing data. In social circles, that kind of thought process would make him a bigot. > I > recently heard of a 2nd Edition which I have been anxiously awaiting so that [quoted text clipped - 6 lines] > whole argument, but I will say that it fails to support the argument > substantively. Walsh's new book adds about 100 pages, interwoven into his previous book at the word and sentence level to reflect his latest re-evaluations of PC and its treatments. I.P. >Walsh's new book adds about 100 pages, interwoven into his previous book >at the word and sentence level to reflect his latest re-evaluations of >PC and its treatments. > >I.P. Hi I.P.! What is your view on "Dr. Peter Scardino's Prostate Book" (latest edition: June 2006)? Would you recommend it? Just > Hi I.P.! > > What is your view on "Dr. Peter Scardino's Prostate Book" (latest > edition: June 2006)? > > Would you recommend it? Easily among the best of the crop. But even the least of the crop still added useful decision fodder. Each book emphasizes different aspects of PC, with some authors writing a page on a given topic while others devoted a chapter to that topic. Even the two-volume, 1500-page cancer treatment treatises written for physicians are solid, well-referenced sources of data and insight for us laymen, as long as we don't try to understand every sentence or medical term. Their very detailed Tables of Contents focus our reading on a few dozen pages of solid, useful meat with thorough references to sources. Current books of this type are found in bigger bookstores (our local Barnes & Noble has a section for health professionals) and probably bigger libraries. My VA hospital lets patients use its extensive medical library of hard copy, searchable electronic media, and online links; I'd guess many hospitals may do so at their physician's request. Don't overlook discount and used book stores; my new hardback copy of Scardino cost me a few bucks just months after its release and the used book stores reveal many PC books -- such as Strum -- I've not seen on strictly-new bookstore shelves. The free PC book available from the ACS offers unique treatment decision trees, and many major hospitals will sell us annual and/or quarterly publications discussing the latest and greatest ... and not so great ... findings and studies of PC research, written for patients. And yet I STILL find stuff right here in this forum I hadn't seen anywhere else, partly and lately because now that I'm cured*, my research has been curtailed by at least 95%. * i.e., an optimistic euphemism for no sign of recurrence coupled with the realization that if and when it recurs, I'll have plenty of time to resume the research without losing measurable ground. I.P. I am so very, very grateful to Steve, Ralph V, IP Freely, and Alan Meyer for your posts. They have merged in my mind as one harmonious message which I never had before. I do not need to take Casodex at this time. When I do need to take it, your posts will stand there for me as permanent signposts. You all made thoughtful comments about my wife for which I offer again many thanks. I am a bit choked up frankly by Alan's very feeling and instructive comments about Alzheimer's. They come from his own experiences, for which I am truly sorry. He has come face to face with it in triplicate. My wife in fact has multi- infarct dementia - the state, and downhill projections are the same -indeed I think there is some delay-help drugs for Alzheimer's, but not for dementia. The awful thing is that it was precipitated from handlable, to unhandleable in three weeks, following her being allowed to walk unaided in hospital -and falling and breaking her leg. So little time to adjust. Thank you Alan I know I have to consider everything you say. Your words, so paralleling what I hear from a very much loved partner -we met 55 years ago in College - give me so much support, and perhaps give me better insight into how is really best to be of help for her. I do see her every day -I miss a day sometimes when I'm a bit knocked out and then think of her pining. Thanks for Alzheimer support group ng and wilco. I am sending your post about my wife also to my sons and know how much they too will appreciate it. I have been going round in tight circles, and starting to lead them with me. You guys are a pillar of support for this newsgroup and in an important way for me. Thank you. > I am so very, very grateful to Steve, Ralph V, IP Freely, and Alan > Meyer for your posts. They have merged in my mind as one harmonious [quoted text clipped - 23 lines] > You guys are a pillar of support for this newsgroup and in an > important way for me. Thank you. Mike, it's stories and appreciation like yours that keep me here despite my unfavorable reception by so many people who have problems dealing with the harsh facts and blunt opinions I express when necessary. Your self-professed enlightenment will be *my* signpost next time I ask myself, "Why bother?". I.P. >> I am so very, very grateful to Steve, Ralph V, IP Freely, and Alan >> Meyer for your posts./snip .... >> You guys are a pillar of support for this newsgroup and in an >> important way for me. Thank you. IPFreely wrote: >Mike, it's stories and appreciation like yours that keep me here despite >my unfavorable reception by so many people who have problems dealing [quoted text clipped - 3 lines] > >I.P. A bit late, but, I.P. Never stop "bothering" Every piece of advice here is from people who care enough about others to summon up the time and energy to write and post. I have never quite understood the adjectives and adverbs therefore which accompany some disputes over facts. Each one of you posting is as valuable as the person posting the opposing conclusion about treatment, to an audience desperate for facts which directly affect their quality and length of life. And also we know there are probably countless score "lurkers" (as I have sometimes been) who read 'the stalwarts' who are the pillars of this group and are silently indebted to them. we know there are probably countless score "lurkers" yes there is.....or are....or .... Please don't stop posting. > A bit late, but, I.P. Never stop "bothering" A positive stroke is seldom too late and always welcome. > Every piece of advice > here is from people who care enough about others to summon up the time > and energy to write and post. I'm constantly impressed -- sometimes amazed -- by the level of effort some of these people go to to dig up, digest, analyze, and post such thorough summaries of the literature. Evens, Jordan, RalphV, Rosbif, Meyer, and Palmer come to mind, but there are many more who go way beyond the call of duty in that regard. THAT, I don't have the motivation to do, at least until I have a dog -- or a met -- in the fight again. > Each one of you posting is as valuable as the person posting > the opposing conclusion about treatment, to an audience desperate for > facts which directly affect their quality and length of life. Right on! The only scenario in which substantive debate is not educational is one in which all the facts are known and accepted ... definitely not the case with PC. Taking offense at debate or slinging mud at debaters obscures the value of such debate. I.P. the knowledge in walshs' book has been advanced.i recommend getting copies of "pcri insights"may 2007 vol 10:n0 2/1-800-641-7274 www.pcri.org/free/also/paact vol.23,num#3 september 2007/www.paactusa.org/616-453-1477/free i've been on horm.therapy twice.1st.time for 13 mos.don't do it mono.(casadex alone)it should be done in combination with(lhrh angonist)lupron 7.5mg+casodex(antiandogen)casodex 50 mg daily 2 weeks prior to lupron.if your dr.says no.find a new dr.p/c feeds on testosterone.in 2 ways/testis and androgen glands + others.p/c reponds to comb.horm.therapy. see www.leibowitz.com/org?this is not a cure.don't wait for symptoms.it will be too late.this will slow/stop the tumor growth while you safely decide what to do.but do something.don't let the doctors scare you.most don't really know p/c fully though they act as they do. |
Reply to this Message |
 Sign In
 Join
 My Latest Posts My Monitored Threads My Blog My Photo Gallery My Profile My Homepage Start New Thread Enable EMail Alerts Rate this Thread
|
©2008 Advenet LLC Privacy Policy - Terms of Use
This website includes both content owned or controlled by Advenet as well as content owned or controlled by third parties.