Maybe people should cycle HRT, with testosterone for 3 months, and SERMs for the next three months, and repeat.
[quote]egnatiosj wrote:
okay no offense by this is terribly wrong.
First, I certainly do not believe that prostate cancer is linked to low testosterone levels. This can first be demonsrated by the fact that castrated boys, have never been noted to have suffered from any type of prostate cancer or benign hyperplasia (the source is a medical textbook). Another fact that causes me to disagree with this idea is that prostate cancer/growth has greater association with the western civilizations. Implying a cultural or diet factor. Studies of twins in Scandinavia suggest that forty percent of prostate cancer risk can be explained by inherited factors. Also, There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Daily use of anti-inflammatory medicines such as aspirin, ibuprofen, or naproxen may decrease prostate cancer risk.[20] Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk.
I have a problem with puttin such uninformed speculation on the internet for others to see, and perhaps believe. (God knows there are ignorant people who believe everything they read).
Lichtenstein, P; Holm NV; Verkasalo PK; Iliadou A; Kaprio J; Koskenvuo M; Pukkala E; Skytthe A; Hemminki K (July 13 2000). “Environmental and heritable factors in the causation of cancer?analyses of cohorts of twins from Sweden, Denmark, and Finland”. N Engl J Med 343 (2): 78?85. doi:10.1056/NEJM200007133430201. PMID 10891514.
Shannon, J; Tewoderos S, Garzotto M, Beer TM, Derenick R, Palma A, Farris PE (August 15 2005). “Statins and prostate cancer risk: a case-control study”. Am J Epidemiol 162 (4): 318?25. doi:10.1093/aje/kwi203. PMID 16014776. Epub 2005 July 13 [/quote]
Here’s a thought. Maybe since those castrated boys couldn’t produce Testoserone, the Testosterone could not be converted to Estrogen since it isn’t there. Maybe the Estrogen/Testosterone relationship has something to do with prostate cancer…
[quote]xXDevilDogXx wrote:
egnatiosj wrote:
okay no offense by this is terribly wrong.
First, I certainly do not believe that prostate cancer is linked to low testosterone levels. This can first be demonsrated by the fact that castrated boys, have never been noted to have suffered from any type of prostate cancer or benign hyperplasia (the source is a medical textbook). Another fact that causes me to disagree with this idea is that prostate cancer/growth has greater association with the western civilizations. Implying a cultural or diet factor. Studies of twins in Scandinavia suggest that forty percent of prostate cancer risk can be explained by inherited factors. Also, There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Daily use of anti-inflammatory medicines such as aspirin, ibuprofen, or naproxen may decrease prostate cancer risk.[20] Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk.
I have a problem with puttin such uninformed speculation on the internet for others to see, and perhaps believe. (God knows there are ignorant people who believe everything they read).
Lichtenstein, P; Holm NV; Verkasalo PK; Iliadou A; Kaprio J; Koskenvuo M; Pukkala E; Skytthe A; Hemminki K (July 13 2000). “Environmental and heritable factors in the causation of cancer?analyses of cohorts of twins from Sweden, Denmark, and Finland”. N Engl J Med 343 (2): 78?85. doi:10.1056/NEJM200007133430201. PMID 10891514.
Shannon, J; Tewoderos S, Garzotto M, Beer TM, Derenick R, Palma A, Farris PE (August 15 2005). “Statins and prostate cancer risk: a case-control study”. Am J Epidemiol 162 (4): 318?25. doi:10.1093/aje/kwi203. PMID 16014776. Epub 2005 July 13
Here’s a thought. Maybe since those castrated boys couldn’t produce Testoserone, the Testosterone could not be converted to Estrogen since it isn’t there. Maybe the Estrogen/Testosterone relationship has something to do with prostate cancer…[/quote]
Impressive; do you have an inside man at nellmed?
Estrogen-linked signaling helps drive a discrete and aggressive form of the disease caused by a chromosomal translocation, which in turn results in the fusion of two genes.
“Fifty percent of prostate cancers harbor a common recurrent gene fusion, and we believe that this confers a more aggressive nature to these tumors,” explains study senior author Dr. Mark A. Rubin, professor of pathology and laboratory medicine, and vice chair for experimental pathology at Weill Cornell Medical College. Dr. Rubin is also attending pathologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
“Interfering with this gene fusion ? or its downstream molecular pathways ? will be crucial in the search for drugs that fight the disease. Based on our new data, we now believe that inhibiting estrogen may be one way of doing so,” he says.
The findings are published in the May 27 online edition of the Journal of the National Cancer Institute. Dr. Rubin conducted the study while at the Brigham and Women’s Hospital and in collaboration with Dr. Todd Golub and other members of the Broad Institute of MIT and Harvard, in Cambridge, Mass. His team is now continuing this line of research at Weill Cornell.
Dr. Rubin, along with researchers at the University of Michigan, first discovered and described the common fusions between the TMPRSS2 and ETS family member genes subset of prostate cancer in the journal Science in 2005. “The discovery showed that these malignancies occur after an androgen (male hormone)-dependent gene fuses with an oncogene ? a type of gene that causes cancer,” he explains.
Experts have long understood that male hormones help spur prostate cancer ? in fact, androgen-deprivation therapy is a first-line treatment against the disease. And yet the disease can progress despite androgen reduction, suggesting that other pathways might be at work.
“So, we wanted to learn more ? what is the genetic and molecular ‘fingerprint’ of this aggressive subset of prostate tumor?” Dr. Rubin says.
Answering that question required the analysis of 455 prostate cancer samples from trials in Sweden and the United States that were conducted as far back as the mid-1970s.
“These samples were placed in fixative and not frozen, so we needed new methods of retrieving the genetic information,” Dr. Rubin says. To do so, his team led by co-lead authors Dr. Sunita Setlur and Dr. Kirsten Mertz developed an innovative technology for effectively “reading” the gene transcription profiles hidden in the samples.
“That led us to perform the largest gene-expression microarray analysis yet conducted in prostate cancer research, amassing information on more than 6,000 genes,” Dr. Rubin says. “This allowed us to obtain a robust, 87-gene expression ‘signature’ that distinguishes fusion-positive TMPRSS2-ERG cancers from other prostate malignancies.”
A close analysis of the signature yielded a surprise: that estrogen-dependent molecular pathways appear to play a crucial role in regulating (and encouraging) this aggressive subset of prostate cancer.
While estrogen is typically thought of as a “female” hormone, men produce it as well.
“Now, we show for the first time that this natural estrogen can stimulate the production of the cancer-linked TMPRSS2-ERG transcript, via the estrogen receptor (ER)-alpha and ER-beta. These receptors are found on the surface of some prostate cancer cells,” Dr. Rubin explains.
The finding could have implications for prostate cancer research, including drug development. According to Dr. Rubin, “We now believe that agents that dampen estrogen activity (ER-alpha antagonists) could inhibit fusion-positive prostate cancers. Alternatively, any intervention that boosts estrogen activity (ER-alpha) might also give a boost to these aggressive malignancies.”
Research into just why fusion-positive prostate cancers are so aggressive ? and potential molecular drug targets to help curb that aggression ? will continue under Dr. Rubin’s direction at Weill Cornell, in collaboration with members of his group and with computational biologist Dr. Francesca Demichelis.
“The technological achievement of using fixed samples that were up to 30 years old is significant,” Dr. Rubin says. “In the future, we hope to explore banked tissues from clinical trials to help understand why they failed. This should lead to insight for designing the next trial.”
This work was funded by the U.S. National Institutes of Health, a Prostate SPORE grant at the Dana-Farber/Harvard Cancer Center, Swiss Foundation for Medical-Biological Grants SSMBS, U.S. Department of Defense and the Prostate Cancer Foundation.
Co-researchers include study co-lead authors Dr. Sunita Setlur and Dr. Kirsten Mertz of Brigham and Women’s Hospital and Harvard Medical School, Boston; Dr. Yujin Hoshida and Dr. Todd Golub of the Broad Institute and the Dana-Farber Cancer Institute, Boston; Dr. Francesca Demichelis of Weill Cornell Medical College and Harvard Medical School, Boston; Dr. Mathieu Lupien of the Dana-Farber Cancer Institute; Dr. Sven Perner and Jeff Tang of Weill Cornell Medical College; Andrea Sboner of Yale University, New Haven; Dr. Yudi Pawitan and Dr. Katja Fall of the Karolinska Institutet, Stockholm, Sweden; Dr. Ove Andren, Dr. Jan-Erik Johansson and Dr. Swen-Olof Andersson, of Orebro University Hospital, Orebro, Sweden; Laura A. Johnson of Brigham and Women’s Hospital, Boston; Dr. Hans-Olov Adami, of Karolinska Institutet, Sweden, and Harvard School of Public Health, Boston; Dr. Stefano Calza, of the Karolinska Institutet, Sweden, and the University of Brescia, Italy; Dr. Arul M. Chinnaiyan, Dr. Daniel Rhodes and Scott Tomlins, of the University of Michigan Medical School, Ann Arbor; Dr. Lorelei Mucci and Dr. Meir Stampfer of Harvard Medical School, Harvard School of Public Health and Brigham and Women’s Hospital, Boston; Dr. Philip Kantoff of Dana-Farber Cancer Institute and Harvard Medical School; Dr. Eberhard Varenhorst, of University Hospital Linkoping, Sweden; and Dr. Myles Brown of the Dana-Farber Cancer Institute.
Dr. Mark A. Rubin, Dr. Francesca Demichelis, Dr. Sven Perner, Dr. Arul M. Chinnaiyan and Scott Tomlins are co-inventors on a patent filed by the University of Michigan and the Brigham and Women’s Hospital, covering the diagnostic and therapeutic fields for ETS fusions in prostate cancer.
XXXDD
impressive, do you have an inside man at nellmed?
Estrogen-linked signaling helps drive a discrete and aggressive form of the disease caused by a chromosomal translocation, which in turn results in the fusion of two genes.
“Fifty percent of prostate cancers harbor a common recurrent gene fusion, and we believe that this confers a more aggressive nature to these tumors,” explains study senior author Dr. Mark A. Rubin, professor of pathology and laboratory medicine, and vice chair for experimental pathology at Weill Cornell Medical College. Dr. Rubin is also attending pathologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
“Interfering with this gene fusion ? or its downstream molecular pathways ? will be crucial in the search for drugs that fight the disease. Based on our new data, we now believe that inhibiting estrogen may be one way of doing so,” he says.
The findings are published in the May 27 online edition of the Journal of the National Cancer Institute. Dr. Rubin conducted the study while at the Brigham and Women’s Hospital and in collaboration with Dr. Todd Golub and other members of the Broad Institute of MIT and Harvard, in Cambridge, Mass. His team is now continuing this line of research at Weill Cornell.
Dr. Rubin, along with researchers at the University of Michigan, first discovered and described the common fusions between the TMPRSS2 and ETS family member genes subset of prostate cancer in the journal Science in 2005. “The discovery showed that these malignancies occur after an androgen (male hormone)-dependent gene fuses with an oncogene ? a type of gene that causes cancer,” he explains.
Experts have long understood that male hormones help spur prostate cancer ? in fact, androgen-deprivation therapy is a first-line treatment against the disease. And yet the disease can progress despite androgen reduction, suggesting that other pathways might be at work.
“So, we wanted to learn more ? what is the genetic and molecular ‘fingerprint’ of this aggressive subset of prostate tumor?” Dr. Rubin says.
Answering that question required the analysis of 455 prostate cancer samples from trials in Sweden and the United States that were conducted as far back as the mid-1970s.
“These samples were placed in fixative and not frozen, so we needed new methods of retrieving the genetic information,” Dr. Rubin says. To do so, his team led by co-lead authors Dr. Sunita Setlur and Dr. Kirsten Mertz developed an innovative technology for effectively “reading” the gene transcription profiles hidden in the samples.
“That led us to perform the largest gene-expression microarray analysis yet conducted in prostate cancer research, amassing information on more than 6,000 genes,” Dr. Rubin says. “This allowed us to obtain a robust, 87-gene expression ‘signature’ that distinguishes fusion-positive TMPRSS2-ERG cancers from other prostate malignancies.”
A close analysis of the signature yielded a surprise: that estrogen-dependent molecular pathways appear to play a crucial role in regulating (and encouraging) this aggressive subset of prostate cancer.
While estrogen is typically thought of as a “female” hormone, men produce it as well.
“Now, we show for the first time that this natural estrogen can stimulate the production of the cancer-linked TMPRSS2-ERG transcript, via the estrogen receptor (ER)-alpha and ER-beta. These receptors are found on the surface of some prostate cancer cells,” Dr. Rubin explains.
The finding could have implications for prostate cancer research, including drug development. According to Dr. Rubin, “We now believe that agents that dampen estrogen activity (ER-alpha antagonists) could inhibit fusion-positive prostate cancers. Alternatively, any intervention that boosts estrogen activity (ER-alpha) might also give a boost to these aggressive malignancies.”
Research into just why fusion-positive prostate cancers are so aggressive ? and potential molecular drug targets to help curb that aggression ? will continue under Dr. Rubin’s direction at Weill Cornell, in collaboration with members of his group and with computational biologist Dr. Francesca Demichelis.
“The technological achievement of using fixed samples that were up to 30 years old is significant,” Dr. Rubin says. “In the future, we hope to explore banked tissues from clinical trials to help understand why they failed. This should lead to insight for designing the next trial.”
This work was funded by the U.S. National Institutes of Health, a Prostate SPORE grant at the Dana-Farber/Harvard Cancer Center, Swiss Foundation for Medical-Biological Grants SSMBS, U.S. Department of Defense and the Prostate Cancer Foundation.
Co-researchers include study co-lead authors Dr. Sunita Setlur and Dr. Kirsten Mertz of Brigham and Women’s Hospital and Harvard Medical School, Boston; Dr. Yujin Hoshida and Dr. Todd Golub of the Broad Institute and the Dana-Farber Cancer Institute, Boston; Dr. Francesca Demichelis of Weill Cornell Medical College and Harvard Medical School, Boston; Dr. Mathieu Lupien of the Dana-Farber Cancer Institute; Dr. Sven Perner and Jeff Tang of Weill Cornell Medical College; Andrea Sboner of Yale University, New Haven; Dr. Yudi Pawitan and Dr. Katja Fall of the Karolinska Institutet, Stockholm, Sweden; Dr. Ove Andren, Dr. Jan-Erik Johansson and Dr. Swen-Olof Andersson, of Orebro University Hospital, Orebro, Sweden; Laura A. Johnson of Brigham and Women’s Hospital, Boston; Dr. Hans-Olov Adami, of Karolinska Institutet, Sweden, and Harvard School of Public Health, Boston; Dr. Stefano Calza, of the Karolinska Institutet, Sweden, and the University of Brescia, Italy; Dr. Arul M. Chinnaiyan, Dr. Daniel Rhodes and Scott Tomlins, of the University of Michigan Medical School, Ann Arbor; Dr. Lorelei Mucci and Dr. Meir Stampfer of Harvard Medical School, Harvard School of Public Health and Brigham and Women’s Hospital, Boston; Dr. Philip Kantoff of Dana-Farber Cancer Institute and Harvard Medical School; Dr. Eberhard Varenhorst, of University Hospital Linkoping, Sweden; and Dr. Myles Brown of the Dana-Farber Cancer Institute.
Dr. Mark A. Rubin, Dr. Francesca Demichelis, Dr. Sven Perner, Dr. Arul M. Chinnaiyan and Scott Tomlins are co-inventors on a patent filed by the University of Michigan and the Brigham and Women’s Hospital, covering the diagnostic and therapeutic fields for ETS fusions in prostate cancer.
The older a man gets the more likely he is to be diagnosed with prostate cancer. It doesn’t really tend to be a problem until after the age of 55.
The older a man is, generally the lower his testosterone level.
If high testosterone was the cause of prostate cancer then teenagers would be dropping like flies from it.
Testosterone deprivation therapy works temporarily as a treatment for prostate cancer (approx 2 years) before it starts getting aggressive again. Androgen independent cancer cells proliferate afterwards.
The two year remittance of prostate cancer most likely is due to less estrogen substrate from the lower testosterone levels.
Testosterone protects against prostate cancer while estrogen feeds it.
Older men generally have a low testosterone/estrogen ratio resulting in a greater chance of developing prostate cancer.
The best treatment would be to increase testosterone through TRT while keeping estrogen levels low with an AI. You get the protective effects of testosterone while minimizing the cancer causing effects of estrogen.
1 thing my DR. taught me…is ‘we’ all settle for what ‘THEY’ call normal…he told me DO NOT,the range is so big…what 300-1000…
so I went to my endo and said hey…I do not want normal…I want optimal…so when he told me,well ya at 327,I said…and? I want 700+,he switched me to inject…
I got my TSH test yrs ago…it was noraml…but just above min…I said.no,I want higher.test me all you want…Im happy with being within range…but near the higher end…to many people think DR’s are Gods…not all are smart…and not all care…they just plug along…unless you speak up…you get no where… just my 2 cents.
[quote]fightu35 wrote:
1 thing my DR. taught me…is ‘we’ all settle for what ‘THEY’ call normal…he told me DO NOT,the range is so big…what 300-1000…
so I went to my endo and said hey…I do not want normal…I want optimal…so when he told me,well ya at 327,I said…and? I want 700+,he switched me to inject…
I got my TSH test yrs ago…it was noraml…but just above min…I said.no,I want higher.test me all you want…Im happy with being within range…but near the higher end…to many people think DR’s are Gods…not all are smart…and not all care…they just plug along…unless you speak up…you get no where… just my 2 cents.[/quote]
Wow, that was kind of tough to read.
So your levels are 700+ now? How old were you when you diagnosed at 327? I’m having issues as well, 27 years old this year.
sorry…I get hit in head alot…lol
I was 34 when 1st told my test was low,but I knew it was a prob for yrs…but to thick headed to get it checked…it was 198 at that time…androl brought it to the 300’s… the inject got me to 700’s
Ranges aren’t typically dictated by clinical symptoms but a sampling of the population. The “normal range” constitutes 95% of the population. The lower 2.5% and upper 2.5% are outside the range.
Many doctors wrongly assume symptoms are only expressed outside the range and 95% of the population is perfectly healthy.
If you get a good doctor they will prescribe based on symptoms not numbers.
It’s a shame most doctors don’t have the simple foresight to recognize this. Many doctors are great at memorizing facts but poor at understanding how systems work.
That’s how many of them got through med school unfortunately. They can memorize something and regurgitate it, without understanding it.
[quote]Headhunter wrote:
I’ve been thinking a lot about this.
Been injecting for a while and doing so made my hematocrit and hemaglobin shoot throught the roof.
I think young guys should have enough testosterone to make you competitive for females. Young guys have high test for that reason. Thus your ‘level’ is whatever makes you mildly aggressive, to the point where you are extroverted and competitive. Don’t exceed this or you’ll become too aggressive and kill someone. Keep increasing your dose until it feels right.
Old guys like me require lower Test. We’re done in the baby making game. For us, we just want to feel good.[/quote]
So what level should young guys have? I’m 31 and my level was tested at 427. I think my libido’s pretty low, but I’m not sure if it’s due to the test levels.
Deese…this si kinda what I ment.most all dr’s will say hey…ya normal…so tell them…well so is 800,so I want 800,and just keep saying ya sleep bad…no libio…etc… it worked for me…
[quote]bushidobadboy wrote:
Testosterone replacement therapy is still a relatively new concept. For years, the medical community didn’t believe that male hormones had any significant part to play in a mans health. There are still some physicians who believe this to be the case.
Further, there is the old stigma attached to people who want to better themselves through the use of ‘steeeroids’ and since test is the original and best steroid, many physicians are loth to prescribe it.
So what they do, IMO is provide a massive range of possible ‘acceptible’ blood levels, to give the poor physician planty of scope to duck out of his responsibility to patient care.
“Doctor, I feel like shit with all the symptoms of low T”. “Hmmm, OK but you are still within range, therefore I don’t feel comfortable treating you, even though it is clear that you would benfit from extra T.”
Though to give them some leeway and not to be too judgmental, DRs do have to justify their prescriptions. So in this day of ever-watchful authorities, coupled with the ‘fear’ of steroids amongst the general american populace, leaves may DRs extremely unwilling to ‘risk their careers’, by prescribing T to a dude who is ‘in range’, even though he genuinely has the need for T.
It’s a phucked up world we live in. Fortunately there are many DRs who are prepared to give the patient what they need for their health, despite the posible risks to their own careers.
Consider this: In the UK, it’s a lot harder to get T replacement. Go to your doc with a list of symptoms that are associate with low T and I suspect that blood levels of T would be the last thing he checks for.
Even if he does check for it, there will be an interminable waiting period before he does so. “Get more exercise, get more sleep, lets wait a few months and see if it goes away by itself, I don’t really know the first thing about male hormones, etc, etc” Will probably be the war-cry of most familly GPs.
As ever though, there are exceptions; Drs who genuinely seek to improve their own knowledge and the health of their patients. God bless 'em.
BBB[/quote]
Hi Bushy,
Long time. Just wanted to pop in and check out the goings on. I’ve been goofing off on other boards and it was refreshing to see your intelligent post. BTW, I’m in the process of going on TRT now.
Later,
Peck
[quote]Dopa wrote:
The older a man gets the more likely he is to be diagnosed with prostate cancer. It doesn’t really tend to be a problem until after the age of 55.
[/quote]
Hmm…true.
True
False. False reasoning and false science. Read about lead time, conditioning, epigenetics.
Generally a true observation.
Not true. Do you have proof of this? I doubt this. AIs do not work (see below) and DHT inhibition alone works a little, even in vitro, without altering estrogen levels.
Not true. Estrogen at low doses also had been used successfully in–for decades after failure of castration. Why it worked to any degree is a matter of discussion.
True and not true. Not false either: it is not at all established, and the reasoning is not true.
[quote]
The best treatment would be to increase testosterone through TRT while keeping estrogen levels low with an AI. You get the protective effects of testosterone while minimizing the cancer causing effects of estrogen.[/quote]
False. False. And False.
Charles Huggins won the Nobel Prize in 1966 by disagreeing with you and proving it. I presume that you will not be in Stockholm this year.
Further, recall that it is inhibiton of DHT, and inhibition of DHT synthesis from T, which reduces the risk of prostate cancer. (These maneuvers may typically raise estrogen levels slightly in the intact man.)
And using selective AIs has been tried, and failed repeatedly over the last 10 years. (One study, using aminoglutethimide may have worked because they also got hydrocortisone, which has independent benefit.) But other AIs fail to be effective.
There is a new one, abaratirone–again used with hydrocortisone–which may be useful, but watch–the data will be muddied by the use of HC.
so you do not feel AI’S work ? or are needed?
[quote]DrSkeptix wrote:
Dopa wrote:
The older a man gets the more likely he is to be diagnosed with prostate cancer. It doesn’t really tend to be a problem until after the age of 55.
Hmm…true.
The older a man is, generally the lower his testosterone level.
True
If high testosterone was the cause of prostate cancer then teenagers would be dropping like flies from it.
False. False reasoning and false science. Read about lead time, conditioning, epigenetics.
Testosterone deprivation therapy works temporarily as a treatment for prostate cancer (approx 2 years) before it starts getting aggressive again. Androgen independent cancer cells proliferate afterwards.
Generally a true observation.
The two year remittance of prostate cancer most likely is due to less estrogen substrate from the lower testosterone levels.
Not true. Do you have proof of this? I doubt this. AIs do not work (see below) and DHT inhibition alone works a little, even in vitro, without altering estrogen levels.
Testosterone protects against prostate cancer while estrogen feeds it.
Not true. Estrogen at low doses also had been used successfully in–for decades after failure of castration. Why it worked to any degree is a matter of discussion.
Older men generally have a low testosterone/estrogen ratio resulting in a greater chance of developing prostate cancer.
True and not true. Not false either: it is not at all established, and the reasoning is not true.
The best treatment would be to increase testosterone through TRT while keeping estrogen levels low with an AI. You get the protective effects of testosterone while minimizing the cancer causing effects of estrogen.
False. False. And False.
Charles Huggins won the Nobel Prize in 1966 by disagreeing with you and proving it. I presume that you will not be in Stockholm this year.
Further, recall that it is inhibiton of DHT, and inhibition of DHT synthesis from T, which reduces the risk of prostate cancer. (These maneuvers may typically raise estrogen levels slightly in the intact man.)
And using selective AIs has been tried, and failed repeatedly over the last 10 years. (One study, using aminoglutethimide may have worked because they also got hydrocortisone, which has independent benefit.) But other AIs fail to be effective.
There is a new one, abaratirone–again used with hydrocortisone–which may be useful, but watch–the data will be muddied by the use of HC.
[/quote]
Can you describe the epigenetic factors that influence BPH later in life?
[quote]pickapeck wrote:
DrSkeptix wrote:
Dopa wrote:
The older a man gets the more likely he is to be diagnosed with prostate cancer. It doesn’t really tend to be a problem until after the age of 55.
Hmm…true.
The older a man is, generally the lower his testosterone level.
True
If high testosterone was the cause of prostate cancer then teenagers would be dropping like flies from it.
False. False reasoning and false science. Read about lead time, conditioning, epigenetics.
Testosterone deprivation therapy works temporarily as a treatment for prostate cancer (approx 2 years) before it starts getting aggressive again. Androgen independent cancer cells proliferate afterwards.
Generally a true observation.
The two year remittance of prostate cancer most likely is due to less estrogen substrate from the lower testosterone levels.
Not true. Do you have proof of this? I doubt this. AIs do not work (see below) and DHT inhibition alone works a little, even in vitro, without altering estrogen levels.
Testosterone protects against prostate cancer while estrogen feeds it.
Not true. Estrogen at low doses also had been used successfully in–for decades after failure of castration. Why it worked to any degree is a matter of discussion.
Older men generally have a low testosterone/estrogen ratio resulting in a greater chance of developing prostate cancer.
True and not true. Not false either: it is not at all established, and the reasoning is not true.
The best treatment would be to increase testosterone through TRT while keeping estrogen levels low with an AI. You get the protective effects of testosterone while minimizing the cancer causing effects of estrogen.
False. False. And False.
Charles Huggins won the Nobel Prize in 1966 by disagreeing with you and proving it. I presume that you will not be in Stockholm this year.
Further, recall that it is inhibiton of DHT, and inhibition of DHT synthesis from T, which reduces the risk of prostate cancer. (These maneuvers may typically raise estrogen levels slightly in the intact man.)
And using selective AIs has been tried, and failed repeatedly over the last 10 years. (One study, using aminoglutethimide may have worked because they also got hydrocortisone, which has independent benefit.) But other AIs fail to be effective.
There is a new one, abaratirone–again used with hydrocortisone–which may be useful, but watch–the data will be muddied by the use of HC.
Can you describe the epigenetic factors that influence BPH later in life?[/quote]
Wish I could. Then I would be packing the tux for Stockholm.
There are 400 current studies on epigenetic control of cancers which include prostate cancer–all lab data. No human trials.
People in the field have a better understanding of this in other tumors; but you would think that breast and prostate cancer would be an ideal cell to study, since transcription events are so clearly tied to hormone exposure.
[quote]DrSkeptix wrote:
pickapeck wrote:
DrSkeptix wrote:
Dopa wrote:
The older a man gets the more likely he is to be diagnosed with prostate cancer. It doesn’t really tend to be a problem until after the age of 55.
Hmm…true.
The older a man is, generally the lower his testosterone level.
True
If high testosterone was the cause of prostate cancer then teenagers would be dropping like flies from it.
False. False reasoning and false science. Read about lead time, conditioning, epigenetics.
Testosterone deprivation therapy works temporarily as a treatment for prostate cancer (approx 2 years) before it starts getting aggressive again. Androgen independent cancer cells proliferate afterwards.
Generally a true observation.
The two year remittance of prostate cancer most likely is due to less estrogen substrate from the lower testosterone levels.
Not true. Do you have proof of this? I doubt this. AIs do not work (see below) and DHT inhibition alone works a little, even in vitro, without altering estrogen levels.
Testosterone protects against prostate cancer while estrogen feeds it.
Not true. Estrogen at low doses also had been used successfully in–for decades after failure of castration. Why it worked to any degree is a matter of discussion.
Older men generally have a low testosterone/estrogen ratio resulting in a greater chance of developing prostate cancer.
True and not true. Not false either: it is not at all established, and the reasoning is not true.
The best treatment would be to increase testosterone through TRT while keeping estrogen levels low with an AI. You get the protective effects of testosterone while minimizing the cancer causing effects of estrogen.
False. False. And False.
Charles Huggins won the Nobel Prize in 1966 by disagreeing with you and proving it. I presume that you will not be in Stockholm this year.
Further, recall that it is inhibiton of DHT, and inhibition of DHT synthesis from T, which reduces the risk of prostate cancer. (These maneuvers may typically raise estrogen levels slightly in the intact man.)
And using selective AIs has been tried, and failed repeatedly over the last 10 years. (One study, using aminoglutethimide may have worked because they also got hydrocortisone, which has independent benefit.) But other AIs fail to be effective.
There is a new one, abaratirone–again used with hydrocortisone–which may be useful, but watch–the data will be muddied by the use of HC.
Can you describe the epigenetic factors that influence BPH later in life?
Wish I could. Then I would be packing the tux for Stockholm.
There are 400 current studies on epigenetic control of cancers which include prostate cancer–all lab data. No human trials.
People in the field have a better understanding of this in other tumors; but you would think that breast and prostate cancer would be an ideal cell to study, since transcription events are so clearly tied to hormone exposure.
[/quote]
But here is an abstract, before publication, to appear in Biophysica et Biochimica Acta, a Swedish journal.
“There are numerous diseases associated with abnormal hormonal regulation and these include cancers of the
breast and prostate. There is substantial evidence that early hormonal perturbations (in utero or during early
development) are associated with increased disease susceptibility later in life. These perturbations may arise
from exposure to environmental agents or endocrine disruptors which mimic hormones and disrupt normal
hormonal signaling. Epigenetic alterations have often been proposed as the underlying mechanism by which
early hormonal perturbations may give rise to disease in adulthood. Currently, there is minimal evidence to
support a direct link between early hormonal perturbations and epigenetic modifications; or between
epigenetic alterations and subsequent onset of cancer. Given that epigenetic modifications may play an
important role in hormone-dependent cancers, it is essential to better understand the relationship between
the hormonal environment and epigenetic modifications in both normal and disease states. In this review,
we highlight several important studies which support the hypothesis that: hormonal perturbations early in
life may result in epigenetic changes that may modify hormone receptor function, thereby contributing to an
increased risk of developing hormone-related cancers.”
This reference was kindly provided to me by The Immortal One, Cy Willson.