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Medical Forum / Diseases and Disorders / Prostate Cancer / December 2004Testosterone after surgery
RP surgery was last July. My 3 months post op PSA was .004. I went to my regular doctor this week. One of my complaints was severe lack of energy. Lab tests came back - testoterone level is at 98, which the doc said was very low. Doc said to check with my urologist about testosterone treatment. Any comments? Charlie Leo > RP surgery was last July. My 3 months post op PSA was .004. I went to > my regular doctor this week. One of my complaints was severe lack of > energy. Lab tests came back - testoterone level is at 98, which the > doc said was very low. Doc said to check with my urologist about > testosterone treatment. Any comments? Hi, Charlie. I had LRP two years ago. Before surgery, I was taking hormone replacement. Since surgery, I have had no supplements. My energy level is off. My depression is worse. I just feel like I'm dragging much of the time. But I know, too, that in some cases Testosterone can encourage the growth of PCa. I have had two separate urologists tell me that they would consider putting me back on TRT after a period of five years of PSAs that are undetectable. At that five year point, I still don't know if I would be willing to take the risk. I'd like to know what you find out in reply to this post.. and elsewhere... concering TRT after RP. Please share! Take care! MikeH Something's amiss here. Your doc says you should consider adding testosterone to your system after RRP. Mine says I should risk horrendous side effects to eliminate testosterone (my fingers and/or brain cells get lost typing that dang word) from my system after RRP. Assuming both docs are well-informed (I believe mine is), and presuming my first post-op PSA will be 0.0000000 or thereabouts, what's the difference in our cases? My PC was Gleason 8 (by definition, high-risk), my tumors involved both lobes, and although I had no mets even to any lymph nodes, one seminal vesicle was partially invaded, so my odds of recurrence are on the bad side of a coin toss. Maybe your PC was low-grade and smaller? And it's my understanding that testosteone isn't just "capable of encouraging PC growth in some cases", that in almost every case it is like pouring gasoline -- OK, maybe charcoal briquettes -- on the fire. I.P. > > RP surgery was last July. My 3 months post op PSA was .004. I went to > > my regular doctor this week. One of my complaints was severe lack of [quoted text clipped - 18 lines] > Take care! > MikeH I.P., I presume you were talking to me. I didn't do the DHEA under Doc's orders (although he knows I was taking it B4 the RRP). I've been taking DHEA for 7 years now. I know my TST level is abnormally low otherwise. I wouldn't be doing it if there was any indication that all the PCA wasn't removed 17 mos ago. I even had the nerve bundles removed. The Doc said he caught my PCA early. Only 15% of the cells, both lobes, were PCA, and no margins reached. Yea, I'm taking a bit of a risk, but I think it's a good gamble, and my quality of life is hugely better on 25 mg of DHEA. I would just drag, etc. without it. Hi, I.P. As I said, two *different* urologists told me this. One was the urologist who did my surgery. Another is a urologist in Atlanta who I am sure is well-informed. Both said *after 5 years of undetectable PSAs*. I had a Gleason of 3 + 3 = 6, stage T1C. My PSA was 8.1 at time of surgery, but some of that was due to prostatitis... I'll never know how much. I had nerve sparing procedure and margins were all negative. I have every reason to believe that all the cancer was contained. But there is always that chance that a rogue cell got out and is floating around inside me someplace. It is my understanding that there are *some* PCa cells that are stimulated by Testosterone and some that are not. But the problem seems to be that it is almost impossible to determine what kind of PCa cells one may have. I'm 3 years away from even *considering* this, so I'm certainly not promoting the idea. But it *is* something that some urologists obviously see as a quality of life issue. If I make it to five years, I'll have to do a lot of research... and a lot of soul searching. I guess the biggest quandery on my part is that if a guy has a normal range of Testosterone and has PCa.... and it is self-contained.... that man is not castrated, chemically or physically, to completely cut off his supply of *normal level* testosterone. I have a hard time understanding why it would be *more* dangerous for a guy who has low testosterone (like me) to take supplementation to bring him up to the *normal* level, where other guys already *are*. I mean... if one guy can have a testosterone level of 600... and be fine... why can't I add some to get my 380 up to 600 if it improves my quality of life? To be honest, my testerone replacement never seemed to have much effect on my libido. But it had a HUGE impact on my chronic depression and dysthmia. I felt better than I have ever felt in my life during that time. Take care... MikeH > Something's amiss here. Your doc says you should consider adding > testosterone to your system after RRP. Mine says I should risk horrendous [quoted text clipped - 45 lines] >> Take care! >> MikeH My God . . . I looked up "dysthmia". Not only is it frightening to consider such a problem, but it sounds very fortunate that you even realize you have it and want to eliminate it. It sounds like something out a science fiction movie: "Not only are you truly ill, but we've erased all your memories of ever feeling better so you won't WANT to get better". I doubt I'd wait out 5 years with zero PSA before seeking the fix . . .unless, of course, I didn't remember ever feeling any better, thus didn't really believe I was ill . . . NASTY "disease". Now the real question your case raises that pertains to MY dilemma is, "Can low testosterone cause dysthmia, or were you destined to get it anyway and the low T is just a coincidence?" I.UP. > Hi, I.P. > [quoted text clipped - 28 lines] > depression and dysthmia. I felt better than I have ever felt in my life > during that time. > My God . . . I looked up "dysthmia". Not only is it frightening to > consider [quoted text clipped - 15 lines] > > I.UP. Good question, IP... I just know that I felt 100% better when taking the T replacement. Never in my entire 53 years have I ever felt physically *better* than during that time. Anti-depressants help at times, but they, too, have their side effects. I read an article about how low T levels can contribute to depression... and talked with my therapist about it... and he said, "why don't we try it?" I saw an endocrinologist and found that the T levels were, indeed, low.... and so it went. BTW, depression in women can also be related to low T levels, as well. This is not to say that *all* depression is caused by hormone deficiency... far from it. But it *is* something to look at in trying to get a the root of depressive problems and find the best therapy for them. MikeH >Subject: Re: Testosterone after surgery >From: "MH" lkgmoiREMOVE@yahoo.com [quoted text clipped - 15 lines] >It is my understanding that there are *some* PCa cells that are stimulated >by Testosterone and some that are not. No, almost all PCa cells are stimulated by testosterone, while a few are not. During HT that large majority stop growing, but the tiny minority continue their merry way. After three years or so, the population of the insensitive fellows has grown enough that they become noticeable... > But the problem seems to be that it >is almost impossible to determine what kind of PCa cells one may have. I'm [quoted text clipped - 18 lines] >Take care... >MikeH > No, almost all PCa cells are stimulated by testosterone, while a few are not. > During HT that large majority stop growing, but the tiny minority continue > their merry way. After three years or so, the population of the insensitive > fellows has grown enough that they become noticeable... Danny, Do you have any references to any peer reviewed medical articles that show that PCa cells are stimulated by testosterone other than when nothing is done to stop the testosterone from being converted to DHT and E? Ed Friedman Every book, website, abstract, and study I've read that addresses T says it feeds PC cells. That's why we use ADT, and why ADT stops PC until it mutates to AIPC. Either we're misunderstanding your question or you're misunderstanding our answers. I.P. > > No, almost all PCa cells are stimulated by testosterone, while a few are not. > > During HT that large majority stop growing, but the tiny minority continue [quoted text clipped - 6 lines] > show that PCa cells are stimulated by testosterone other than when > nothing is done to stop the testosterone from being converted to DHT and E? > Every book, website, abstract, and study I've read that addresses T says it > feeds PC cells. That's why we use ADT, and why ADT stops PC until it mutates > to AIPC. Either we're misunderstanding your question or you're > misunderstanding our answers. > I.P. "Everybody knows" is not science. I won't bore you with a litany of "everybody knows" that have been shown to be totally false in the history of medicine. The following are scientific facts: 1. T will feed PC cells if nothing is done to prevent it from being converted to DHT and E. 2. PC cells contain the enzyme 5-alpha reductase which converts T to DHT. 3. PC cells contain the enzyme aromatase which converts T to E. The question I am asking is what scientific evidence exists to support the statement that T itself feeds PC cells? Ed Friedman You just answered your own question, in Scientific Fact #1, first five words. The rest of that sentence poses a different scenario, so apparently we do not understand your REAL question. I.P. > The following are scientific facts: > > 1. T will feed PC cells if nothing is done to prevent it from being > converted to DHT and E. > The question I am asking is what scientific evidence exists to support > the statement that T itself feeds PC cells? I.P...I think Ed is asking the following question: What effect, if any, would T have upon PCa cells, if aromatase and 5AR inhibitors were also administered to the patient?..Best wishes and good health, Ron It's beginning to sound that way. Thanks. I.P. > I.P...I think Ed is asking the following question: What effect, if any, > would T have upon PCa cells, if aromatase and 5AR inhibitors were also > administered to the patient?..Best wishes and good health, Ron > I.P...I think Ed is asking the following question: What effect, if any, > would T have upon PCa cells, if aromatase and 5AR inhibitors were also > administered to the patient?..Best wishes and good health, Ron Do you think he is asking the question because of intellectual curiosity or, more likely, because he plans to apply the answer to his own medical care. I've inveighed against that sort of thing repeatedly. It is fine to understand as much as you can about prostate cancer, but I believe it is a falacy that you can understand it all well enough to make scientific judgements about your own treatment. Even physicians are advised not to treat themselves, and that is even more true for laymen. It is very easy when evaluating evidence to selectively choose the bits of evidence that support what you would like to believe. That is why you go to an objective expert who will try to give an honest judgement. OTOH, the experts don't have the time (nor we the capacity in a half-hour consult) to download 6-8 books' worth and 50 websites' worth of information, and I want a good portion of that, as least the parts pertinent to my decisions. If I had read just one good magazine article, let alone a book chapter, on PSA three years ago, I'd probably have caught my PC before it escaped my prostate, conceivably even when it was a Gleason 7 or 6, if it ever was. Additionally, many studies and reputable authors claim that many doctors don't know and/or don't tell us many of the facts about QOL, because their oath, their statistics, their patient follow-up, and their reputation don't place a high priority on QOL. And, of course, every patient has a different SE mix he's willing to tolerate at different stages of his medical status. The docs don't know our preferences until we tell 'em, we can't tell 'em until we see the menu, we won't see the whole menu until we start reading, the menu will scare the hell out of us until we balance the odds of incurring each SE, the meds to combat SEs have their own SEs, we ain't getting all that in a consult or three, and there are SEs I ain't putting up with until I see some pretty distinct proof that my PC is raging again . . . if then. I suspect all that contributed to Scholz's statement in PRCI Insights, "The major difference between treatments today is likely to be quality of life, not length of life." And I believe it was he who added "thus we may as well choose treatments based on SEs". My doc came right and told me, "Here's my advice, and it's just that . . . advice. Go, read, hit the internet (carefully), think, discuss, decide, and get back to me." Every PC doc I've seen has said, at every decision point, "It's your call. It's far too personal for me to dictate." I.P. "Leonard Evens" <len@math.northwestern.edu> wrote > > Do you think he is asking the question because of intellectual curiosity > or, more likely, because he plans to apply the answer to his own medical [quoted text clipped - 7 lines] > of evidence that support what you would like to believe. That is why > you go to an objective expert who will try to give an honest judgement. > OTOH, the experts don't have the time (nor we the capacity in a half-hour > consult) to download 6-8 books' worth and 50 websites' worth of information, [quoted text clipped - 14 lines] > with until I see some pretty distinct proof that my PC is raging again . . . > if then. I don't disagree with anything you said. I certainly did lots of research of my own. In fact, my cancer was diagnosed as a result of a suspicious PSA velocity over a two year period, which I brought to the attention of my primary care physician. In principle, he was supposed to check previous values when my PSA went over 4, but in those days they still used paper records, and it was difficult to do on a busy day, so he didn't. But my point is that the purpose of all this research is to be in a position to ask your doctor questions. At that point he should have plausible answers or else you should get yourself another doctor. Maybe he will ahve to go do some research himself and get back to you. My primary care physician does that and is not reluctant to admit initial ignorance about some topic. What you shouldn't do, I feel, is to decide in advance, on the basis of your understanding of the medical literature, or, worse, what you find at random on the web, what the situation is. You can read all the books and articles you want, but in the end you have to choose a doctor on the basis of his qualifications and your ability to communicate with him, not his advocacy of controversial positions, and then do what the doctor says. > I suspect all that contributed to Scholz's statement in PRCI Insights, "The > major difference between treatments today is likely to be quality of life, [quoted text clipped - 5 lines] > get back to me." Every PC doc I've seen has said, at every decision point, > "It's your call. It's far too personal for me to dictate." About the internet, the crucial word is "carefully". I'm pretty knowledgeable and good at evaluating evidence, but when it concerns me personally I find I can be misled by what I find on the web. Almost all the doctors I've had have had the attitude you describe. That is part of my definition of a highly qualified physician. > I.P. > [quoted text clipped - 11 lines] >>of evidence that support what you would like to believe. That is why >>you go to an objective expert who will try to give an honest judgement. > You can read all the books > and articles you want, but in the end you have to choose a doctor on the > basis of his qualifications and your ability to communicate with him, > not his advocacy of controversial positions, and then do what the doctor > says. I'm not often willing to let a doctor make my decision for me. What I want, and what most docs have encouraged me to do over the decades, is to get sufficient authoritative facts and medical opinions about prognosis and treatments and risks -- including the docs' advice and second opinions on debatable cases -- and make my own decision. Some calls are no-brainers, others obviously not. I love it when the doc says of my decision, "You made the right call", but my strong bias towards QOL over heartbeat may not lead to the docs' blessings if my cancers progress . I'm not convinced yet that I want to even try out ADT, because it takes two months for T to hit bottom, weeks to many months more for some of the major SEs to kick in, more weeks to months for SEs to abate (if they do abate) after IAD stops . . . by which time it's nearing time for another round of ADT. That trial process could cost me a year with low QOL, which, if I were to have only 3-4-5 years of heartbeat anyway, is a year I may not want to throw away in the hopes of extending my life by a few months --- the best estimate I've seen for the median benefit of HT. I have a psychologist at the hospital inquiring among the staff about exactly these kinds of questions. She's consulting with oncologists, endocrinologists, urologists, other psychologists, and patients, because she was surprised to hear that some of the leading PC authors are accusing their peers of underassessing, underreporting, and undertreating HT SEs. Docs, both individually and institutionally, try to maximize lifespan first and foremost, then try to palliate the patient within that criterion. I have no intent of falling unwitting victim to that cruel (IMO) paradigm. I hope folks don't interpret my constant references to my own case as selfishness. Sure, I hope it will help me learn some relevant facts for my decisions, but I hope it will also make others further ponder their own cases, choices, and decisions, beyond what their doctors have the time to offer. I.P. Ed Friedman wrote...snip... > The following are scientific facts: > [quoted text clipped - 9 lines] > > Ed Friedman Hi Ed...Both Strum and Walsh say repeatedly in their books that T and DHT stimulate PCa cell growth, but no referencea were provided. I suspect that their statements are based upon the experimental observation that both T and DHT bind to the androgen receptor, albeit DHT more strongly. This binding of T or DHT then permits the AT-androgen complex to begin its signaling process. Having said that, let me quickly add that different PCa cell lines may respond differently. Nonetheless, the key fact to me is that both T and DHT bind to the AR...Best wishes and good health, Ron > Hi Ed...Both Strum and Walsh say repeatedly in their books that T and > DHT stimulate PCa cell growth, but no referencea were provided. I [quoted text clipped - 5 lines] > differently. Nonetheless, the key fact to me is that both T and DHT > bind to the AR...Best wishes and good health, Ron Ron, If you check out Urology. 1995 Feb;45(2):282-90, "Finasteride dose-dependently reduces the proliferation rate of the LnCap human prostatic cancer cell line in vitro", you will see that it is pretty clear that DHT is really what stimulates PCa growth, and not T (although it is always possible for a mutation to develop that behaves differently). Ed Ed...I will get the article and read it, but right off the bat I have two comments / questions. First, I'm leery of mouse model studies, in vitro studies are even further removed. More importantly, DHT has not been found in PCa cells, so I'm left wondering how it could bind to the AR within the PCa cell and thereby enhance its proliferation and survival. Interesting stuff!..Ron >Subject: Re: Testosterone after surgery >From: Ed Friedman ed@math.uchicago.edu >Date: 12/22/2004 4:42 PM Central Standard Time >Message-id: <yLmyd.1$25.1309@news.uchicago.edu> And it really doesn't matter. If there is no testosterone to convert to DHT, there will be no DHT. Whether the cancer eventually stops needing Testosterone or eventually stops needing DHT, it is the fact that a small percentage of the cancer continues to grow and becomes dominant eventually that is important. You have one to five years, median three years, before failure. >> Hi Ed...Both Strum and Walsh say repeatedly in their books that T and >> DHT stimulate PCa cell growth, but no referencea were provided. I [quoted text clipped - 15 lines] > >Ed Hi Danny...Leibowitz and others are trying to demonstrate that HT doesn't have to fail due to androgen independence. They are hopeful that if you keep changing the drug regimen you can "shock" the PCa cells back into an androgen dependent state. We need more work, more experiments, to see what the ultimate outcome will be, but there is hope...Best wishes and good health, Ron What about the shock and awe that regimen presents to our bodies and psyches? I.P. > Leibowitz and others . . . are hopeful > that if you keep changing the drug regimen you can "shock" the PCa > cells back into an androgen dependent state. I.P. wote, "What about the shock and awe that regimen presents to our bodies and psyches?" The regimens being discussed (Dr. Leibowitz') involve administering high levels of T after a course of HT. I suspect that is a lot more palatable to our bodies and psyches...Best wishes and good health, Ron Wouldn't that blast of T => DHT => cancer growth? And the "shock & awe" was attributed to frequent changes in ADT chemicals. I.P. > I.P. wote, "What about the shock and awe that regimen presents to our > bodies and [quoted text clipped - 3 lines] > high levels of T after a course of HT. I suspect that is a lot more > palatable to our bodies and psyches...Best wishes and good health, Ron I.P....I don't know enough about Dr. Bob's protocol to give a meaningful answer. Perhaps he administers something to shut that conversion down. The high T is supposed to kill the AIPc cells and / or "shock" them back to an androgen dependent state. The high T must feel good...right?...Best wishes and good health, Ron > I.P....I don't know enough about Dr. Bob's protocol to give a > meaningful answer. Perhaps he administers something to shut that > conversion down. The high T is supposed to kill the AIPc cells and / > or "shock" them back to an androgen dependent state. The high T must > feel good...right?...Best wishes and good health, Ron Ron, All of his patients get 5-alpha reductase II inhibitors to prevent T being converted to DHT - both during ADT and afterwards (for the rest of their lives) The high T does not kill the AIPC cells per se - it just stimulates the production of specific proteins (e.g. U19) which increase the rate of apoptosis. In fact, it appears that the AIPC cells are less susceptible to high T than ordinary PC cells - at least they produce less U19 when exposed to T than ordinary PC cells do. Ed Friedman >Subject: Re: Testosterone after surgery >From: "ron" oitbso@yahoo.com [quoted text clipped - 7 lines] >experiments, to see what the ultimate outcome will be, but there is >hope...Best wishes and good health, Ron Hope it works. Casodex and Proscar worked for me for a year, but leuprolid acetate(Lupron) never worked for me at all. My testosterone is 5 whats... with all this "ng/dl" units given here, I'm not sure what units are being reported by my lab anymore. ;-} Hi Danny...For T, ng/dL x 0.0347 = nmol/L During traditional HT, the goal is to get T below 20 ng/dL, or 0.69 nmol/L...Best wishes and good health, Ron At risk I will enter into the discussion...... Danny's Doctor (he's mine too) told me that his goal was to get T below 5.0) Mike > Hi Danny...For T, > > ng/dL x 0.0347 = nmol/L > > During traditional HT, the goal is to get T below 20 ng/dL, or 0.69 > nmol/L...Best wishes and good health, Ron Hi Mike...If the units on the "5.0" are ng/dl (nanograms / deciliter), then that is below 20 ng/dl, and I lower is better while on ADT..Best wishes and good health, Ron >Subject: Re: Testosterone after surgery >From: "gourd_dancer" mnospam@sbcnospamglobal.net [quoted text clipped - 5 lines] > >Mike yup. Mine sits around 5 to 7. Danny >> Hi Danny...For T, >> >> ng/dL x 0.0347 = nmol/L >> >> During traditional HT, the goal is to get T below 20 ng/dL, or 0.69 >> nmol/L...Best wishes and good health, Ron >Subject: Re: Testosterone after surgery >From: "I.P. Freely" fuhgeddaboutit@noway.not [quoted text clipped - 7 lines] >well-informed (I believe mine is), and presuming my first post-op PSA will >be 0.0000000 or thereabouts, what's the difference in our cases? I repeat my regular quibble here: no reputable lab will ever report your PSA as 0.00000000 The best will be " < 0.04 " or thereabouts. But the doc's advice certainly sounds odd. >My PC was Gleason 8 (by definition, high-risk), my tumors involved both >lobes, and although I had no mets even to any lymph nodes, one seminal [quoted text clipped - 34 lines] >> Take care! >> MikeH Not really. I think most sources, Walsh not included, recomend early, preemptive ADT after RP pathology verifies locally advanced PC (seminal vesicle involvement) and Gleason 8, regardless of post-op PSA. My post-op PSA was reported as 0.006 (the 0.000000 comment simply meant undetectable PSA, not a reported number), but the chance of micromets still warrants early HT, according to my docs. We gonna have a BIG discussion about that in January, wsith my discussion points appearing here in advance for comment. I.P. > >Subject: Re: Testosterone after surgery > >From: "I.P. Freely" fuhgeddaboutit@noway.not [quoted text clipped - 11 lines] > 0.00000000 The best will be " < 0.04 " or thereabouts. But the doc's advice > certainly sounds odd. >Subject: Re: Testosterone after surgery >From: "I.P. Freely" fuhgeddaboutit@noway.not [quoted text clipped - 10 lines] > >I.P. Wow- Seven Time More Precise now! I had the impression the doc had advised taking testosterone..., very odd. Laprolid acetate and Casodex, of course. >> >Subject: Re: Testosterone after surgery >> >From: "I.P. Freely" fuhgeddaboutit@noway.not [quoted text clipped - 15 lines] >advice >> certainly sounds odd. Not on my watch. I don't yet believe (still reading, but running out of new stuff to read) LHRH analogs are worth their SEs, by my criteria. I'm looking into the feasibility of Casodex monotherapy, plus trying to find ways to test my cancer's level of androgen dependence other than a course of ADT. Casodex shows real promise of nearing full-blown ADT's results w/o the SEs, in fact with ancillary benefits. I.P. > >Subject: Re: Testosterone after surgery > >From: "I.P. Freely" fuhgeddaboutit@noway.not [quoted text clipped - 13 lines] > Wow- Seven Time More Precise now! I had the impression the doc had advised > taking testosterone..., very odd. Laprolid acetate and Casodex, of course. I resumed 25 mg DHEA right after surgery, found I needed the energy. Am 18 months post RRP now. I decided I would take risk since my PCA was caught early. Have had no detectable PCA since. I have only become continent in the past week or so, and it was a real battle that I don't think I could have won without an adequate supply of DHEA (to increase Testosterone level) - it took a lot of effort and energy to get bladder/sphincter control back to normal. > RP surgery was last July. My 3 months post op PSA was .004. I went to > my regular doctor this week. One of my complaints was severe lack of [quoted text clipped - 3 lines] > > Charlie Leo > RP surgery was last July. My 3 months post op PSA was .004. I went to > my regular doctor this week. One of my complaints was severe lack of [quoted text clipped - 3 lines] > > Charlie Leo I did some research on Pubmed and now know even less than I did before. I searched on (DHEA "prostate cancer") and read several of the hits. Most said testosterone and DHEA are dangerous, but one "Prevention of prostate cancer by androgens: experimental paradox or clinical reality" said it might actually be protective (!) in men whose testosterone level is abnormally low to being with. As with so much in medicine, it sounds like the experts just don't have enough information to give definitive advice. My personal approach to this issue is that hormones are very powerful drugs that need to be approached with caution. Their effects are potentially very great and not very well understood. I remember, for example, when estrogen was touted as protective against heart disease and Alzheimer's disease - though possibly leading to breast cancer. Then later the doctors announced that the cancer danger was real and the heart disease protection was not so real. Then they announced that estrogen not only doesn't protect against Alzheimer's, it may actually promote it. Testosterone supplementation seems to me to involve an unknown amount of risk. Does that mean we shouldn't do it? I don't think so. But perhaps it means that we should try more conservative solutions first - diet, rest, exercise, talk therapy, even anti-depressants, and only consider testosterone supplementation if other approaches aren't helping and the condition that the testosterone treats is very difficult to live with. Balancing a known benefit against an unknown risk can't be done entirely rationally. There isn't enough information. So, as with the surgery vs. radiation decision and the continuous vs. intermittent HT decision, there seems to be room for personal choice based on subjective factors. Alan You nailed my "rationale" -- or lack thereof -- on the head. The two dominant themes I find in my post-RRP HT literature research so far, whether intermittent or indefinite, are: 1. It WILL degrade QOL, ranging from significantly to drastically. 2. It MIGHT even let our hearts beat longer. Uh, isn't that (arguably) two strikes? Your post suggests that similar contradictions may confuse the testosterone supplementation issue. I.P. "Alan Meyer" <ameyer2@yahoo.com> wrote > > I did some research on Pubmed and now know even less than I > did before. . . . [quoted text clipped - 6 lines] > vs. intermittent HT decision, there seems to be room for > personal choice based on subjective factors. > RP surgery was last July. My 3 months post op PSA was .004. I went to > my regular doctor this week. One of my complaints was severe lack of [quoted text clipped - 3 lines] > > Charlie Leo If you do get testosterone supplementation it is essential that you add a 5AR2 inhibitor, such as finasteride, just in case there are any cancer cells that survived the surgery (DHT fuels prostate cancer growth, but T does not). It would probably help to get an aromatase inhibitor as well. Ed Friedman > If you do get testosterone supplementation it is essential that you add a > 5AR2 inhibitor, such as finasteride, just in case there are any cancer > cells that survived the surgery (DHT fuels prostate cancer growth, but T > does not). It would probably help to get an aromatase inhibitor as well. Ed, What does the 5AR2 inhibitor do? And what is the difference between DHT and T? What is an aromatase inhibitor? DIM, for example? Thanks, MikeH > Ed, > What does the 5AR2 inhibitor do? And what is the difference between DHT and [quoted text clipped - 3 lines] > Thanks, > MikeH Mike, 5AR2 inhibitors prevent the conversion of T to DHT, finasteride being the most popular. The difference between DHT and T is that both stimulate the growth of prostate cancer in vitro, but if finasteride(F) is added to T, it stops this stimulation of growth in a dose-dependent manner, but F does nothing when added to DHT. This strongly implies that DHT and not T is what stimulates the growth of prostate cancer.Also, T has been shown to produce proteins that promote apoptosis (killing of defective cells, such as cancer), e.g., U19. Aromatase inhibitors are drugs such as arimedex, which recently made the news because of its benefits for breast cancer patients. There really is no effective aromatase inhibitor that is non-prescription, and when using one you want to be under a doctor's supervision because too much can be harmful to your health. DIM is good to use, but not effective enough, because it doesn't prevent estradiol(E) formation. Aromatase converts T into E, which can stimulate the growth of prostate cancer and which stimulates the production of a protein, bcl-2, that inhibits apoptosis. An alternative to an aromatase inhibitor would be an anti-estrogen, such as tamoxifen. Tamoxifen has been shown to kill prostate cancer cells in vitro and has been shown to reduce the production of bcl-2. I haven't located any published papers using it in prostate cancer patients yet, but several suggested that it should be looked into. In summary, if you just take T with no inhibitors, you will increase your levels of DHT and E which is extremely bad news for anyone who has prostate cancer. Ed Friedman On December 10, Ed Friedman wrote, in pertinent part: (snip) > Aromatase inhibitors are drugs such as arimedex, which recently made the > news because of its benefits for breast cancer patients. There really [quoted text clipped - 11 lines] > located any published papers using it in prostate cancer patients yet, > but several suggested that it should be looked into. Excellent. Thanks. This is the sort of post more of which I hope to see. One of the suggested anti-bcl-2 therapies makes use of what are called antisense oligonucleotides (or, easier to type, ASO's). It's outlined in Strum's excellent _A Primer on Prostate Cancer_ at pp 172-174. Evidently, ASO therapy against bcl-2 has been found to induce aptoptosis in PCa cells. References are: Miyake et al., Anstisense bca-2 oligodeoxynucleotides inhibit progression to androgen-independence after castration in the Shionogi tumor model. Cancer Res 59:4030-4, 1999. Miyake et al., Chemosensitization and delayed androgen-independence of prosate cancer with the use of antisense bcl-2 oligodeoxynucleotides. J Natl Cancer Inst 92:34-41, 2000. -- and two more that Strum cites. I'll provide the citations if desired. There were, at the time the book was published (2002) clinical trials in progress. Regards, Steve J |
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