I take supplements for the prostate, hopefully that helps. I drink tons of water too.
MESO-Rx
Anabolic Steroids
Prostate ...
- Thread starter Michael Scally MD
- Start date
I don't know man. I know what a 22ga feels like after that pin cuts through a stopper twice first, or even I tried to RE-Pin one time in the same injection process. I could tell that pin was gonna fight on those occasions, but I did it anyway just to see. IT HURTS...!
So I am guessing the instrument they use to dissect and capture the prostate tissue is NEW for every sample...? And Probably a Round uniform cutting tip (as opposed to the angled tip for injections?? Maybe 15-17 ga..??
I wonder how often the Urologist fires the HARPOON thru that prostate and returns with NO CORE Sample
??? I am thinking it hurts more closer to the central CNS "core area", or am I off? DO THEY ANESTHETIZE the prostate in some way first...?
More SO to the point - I am wondering why they cant just take some kind of "sonogram" Instrument in the rectum and see with great certainty.?? It would seem like ANY UN-UNIFORM growth would just need to go...?!?
Finally, and A QUESTION. All respect and I have not looked at this thread in a while. What about physical sensation after. It seems like I recall they went in the get ALL OF YOURS..? Or was it just partial..? How are you doing right now for (1) Erections, (2) Sensation, (3) "Semen Production/expulsion"..? But is there any "orgasm sensation" coming from Penile nerves at this time? Or do you think the prostate is essential for good sex feeling/sensation? Do you still find any "Climax Point" at any time..?
*** The guy I know that had his prostate completely removed at age 40 was just miserable for the longest time, and cause he loved sex, jakin, whatever - it was literally his first passion in life... After his complete prostate removal he simply could not get it up even a year later. I was only communicating through grapevine, and I kept passing along "get the caverject" (cause nothing else would work). Finally he did, and was just raving the praise of successful workings..! He DID even try the erectile medication you insert in the urethra and with no good results first as well.... But the caverject seemed to get it..
On a personal note from my side. And Grandad died of PC at 75 (Diagnosed @70yrs never removed), DAD diagnosed at 52 and fully removed, ME early 40's and soon to see the uro for 2nd exam ever. Ironically, and while dad constantly has a PSA climbing as high as 0.08 (I think, but they never find any prostate remaining)... But Dad was recently diagnosed with Liver Cancer (a bile duct type). It was described as a good removal and the chemo was described by him as fairly light with the exception of shitting chemically induced smoking hot turds... Which included Pancreatic Cancer diagnosed a few weeks after removal of liver cancer. Then a couple months later they said in his lungs, and that Chemo is apparently ROUGH....! Still the formal long and short is that they do not indicate that any of this cancer is Prostate related. I have to wonder as I remember seeing grand dad's full body scans and everything just tore up bones and all.
In final defense of Dads PC really possibly NOT relating to all this other recent cancer - He spent his life on a golf course playing a lot. Knowing the correlation of Herbicide with Pancreatic cancer, I would suggest he had the Pancreatic many years after the PC at 52, but as the potential source of liver and lung now occurring. And thinking about handling golf tees, golf balls, picking up divots to reset and just having golf turf all over hands to wipe face and mouth with. I have also worked on a golf course when younger and remember them loading up the trailer pulled sprayer wearing space suits to handle just a cup of this concentrated herbicide to load the large prayer tank... But when you consider the patrons at a golf course have no idea WHEN the course is sprayed, and how much is present in grass and surface turf - it makes you think twice about playing golf...! Herbicides are stated to have "half-lives" in turf management/application which are similar to Injectable esterfied T -as to how long they are "effectively potent" in the ground they are applied....
It also makes me wonder if his Type II diabetes diuagnosed around 56-60yrs was primarily related to hidden/preliminary pancreatic cancer, only telling at early 70's. It would be interesting to see a study on the rate of avid golfers and Pancreatic cancer.. I am just thinking is WOULD NOT be good to be playing a round of golf and spitting on golf balls on the same day which herbicides were applied... i just dont think the modern medicine is actively checking pancreatic function and condition, and simply because its not an organ you can operate without... So I am guessing Pancreatic Cancer is only diagnosed once cancer has spread, or malfunctioning significantly..
So I am guessing the instrument they use to dissect and capture the prostate tissue is NEW for every sample...? And Probably a Round uniform cutting tip (as opposed to the angled tip for injections?? Maybe 15-17 ga..??
I wonder how often the Urologist fires the HARPOON thru that prostate and returns with NO CORE Sample
??? I am thinking it hurts more closer to the central CNS "core area", or am I off? DO THEY ANESTHETIZE the prostate in some way first...?More SO to the point - I am wondering why they cant just take some kind of "sonogram" Instrument in the rectum and see with great certainty.?? It would seem like ANY UN-UNIFORM growth would just need to go...?!?
Finally, and A QUESTION. All respect and I have not looked at this thread in a while. What about physical sensation after. It seems like I recall they went in the get ALL OF YOURS..? Or was it just partial..? How are you doing right now for (1) Erections, (2) Sensation, (3) "Semen Production/expulsion"..? But is there any "orgasm sensation" coming from Penile nerves at this time? Or do you think the prostate is essential for good sex feeling/sensation? Do you still find any "Climax Point" at any time..?
*** The guy I know that had his prostate completely removed at age 40 was just miserable for the longest time, and cause he loved sex, jakin, whatever - it was literally his first passion in life... After his complete prostate removal he simply could not get it up even a year later. I was only communicating through grapevine, and I kept passing along "get the caverject" (cause nothing else would work). Finally he did, and was just raving the praise of successful workings..! He DID even try the erectile medication you insert in the urethra and with no good results first as well.... But the caverject seemed to get it..
On a personal note from my side. And Grandad died of PC at 75 (Diagnosed @70yrs never removed), DAD diagnosed at 52 and fully removed, ME early 40's and soon to see the uro for 2nd exam ever. Ironically, and while dad constantly has a PSA climbing as high as 0.08 (I think, but they never find any prostate remaining)... But Dad was recently diagnosed with Liver Cancer (a bile duct type). It was described as a good removal and the chemo was described by him as fairly light with the exception of shitting chemically induced smoking hot turds..
. Which included Pancreatic Cancer diagnosed a few weeks after removal of liver cancer. Then a couple months later they said in his lungs, and that Chemo is apparently ROUGH....! Still the formal long and short is that they do not indicate that any of this cancer is Prostate related. I have to wonder as I remember seeing grand dad's full body scans and everything just tore up bones and all.In final defense of Dads PC really possibly NOT relating to all this other recent cancer - He spent his life on a golf course playing a lot. Knowing the correlation of Herbicide with Pancreatic cancer, I would suggest he had the Pancreatic many years after the PC at 52, but as the potential source of liver and lung now occurring. And thinking about handling golf tees, golf balls, picking up divots to reset and just having golf turf all over hands to wipe face and mouth with. I have also worked on a golf course when younger and remember them loading up the trailer pulled sprayer wearing space suits to handle just a cup of this concentrated herbicide to load the large prayer tank... But when you consider the patrons at a golf course have no idea WHEN the course is sprayed, and how much is present in grass and surface turf - it makes you think twice about playing golf...! Herbicides are stated to have "half-lives" in turf management/application which are similar to Injectable esterfied T -as to how long they are "effectively potent" in the ground they are applied....
It also makes me wonder if his Type II diabetes diuagnosed around 56-60yrs was primarily related to hidden/preliminary pancreatic cancer, only telling at early 70's. It would be interesting to see a study on the rate of avid golfers and Pancreatic cancer.. I am just thinking is WOULD NOT be good to be playing a round of golf and spitting on golf balls on the same day which herbicides were applied... i just dont think the modern medicine is actively checking pancreatic function and condition, and simply because its not an organ you can operate without... So I am guessing Pancreatic Cancer is only diagnosed once cancer has spread, or malfunctioning significantly..
They numbed it first,they used the sonogram to guide the needles to take samples. I dont know if they changed the needle ever time i couldnt see because i was on my side.They gave me a valium to take before the biopsy,but to tell you thruth i couldnt tell that it really did any good.I don't know man. I know what a 22ga feels like after that pin cuts through a stopper twice first, or even I tried to RE-Pin one time in the same injection process. I could tell that pin was gonna fight on those occasions, but I did it anyway just to see. IT HURTS...!
So I am guessing the instrument they use to dissect and capture the prostate tissue is NEW for every sample...? And Probably a Round uniform cutting tip (as opposed to the angled tip for injections?? Maybe 15-17 ga..??
I wonder how often the Urologist fires the HARPOON thru that prostate and returns with NO CORE Sample
More SO to the point - I am wondering why they cant just take some kind of "sonogram" Instrument in the rectum and see with great certainty.?? It would seem like ANY UN-UNIFORM growth would just need to go...?!?
Finally, and A QUESTION. All respect and I have not looked at this thread in a while. What about physical sensation after. It seems like I recall they went in the get ALL OF YOURS..? Or was it just partial..? How are you doing right now for (1) Erections, (2) Sensation, (3) "Semen Production/expulsion"..? But is there any "orgasm sensation" coming from Penile nerves at this time? Or do you think the prostate is essential for good sex feeling/sensation? Do you still find any "Climax Point" at any time..?
*** The guy I know that had his prostate completely removed at age 40 was just miserable for the longest time, and cause he loved sex, jakin, whatever - it was literally his first passion in life... After his complete prostate removal he simply could not get it up even a year later. I was only communicating through grapevine, and I kept passing along "get the caverject" (cause nothing else would work). Finally he did, and was just raving the praise of successful workings..! He DID even try the erectile medication you insert in the urethra and with no good results first as well.... But the caverject seemed to get it..
On a personal note from my side. And Grandad died of PC at 75 (Diagnosed @70yrs never removed), DAD diagnosed at 52 and fully removed, ME early 40's and soon to see the uro for 2nd exam ever. Ironically, and while dad constantly has a PSA climbing as high as 0.08 (I think, but they never find any prostate remaining)... But Dad was recently diagnosed with Liver Cancer (a bile duct type). It was described as a good removal and the chemo was described by him as fairly light with the exception of shitting chemically induced smoking hot turds..
In final defense of Dads PC really possibly NOT relating to all this other recent cancer - He spent his life on a golf course playing a lot. Knowing the correlation of Herbicide with Pancreatic cancer, I would suggest he had the Pancreatic many years after the PC at 52, but as the potential source of liver and lung now occurring. And thinking about handling golf tees, golf balls, picking up divots to reset and just having golf turf all over hands to wipe face and mouth with. I have also worked on a golf course when younger and remember them loading up the trailer pulled sprayer wearing space suits to handle just a cup of this concentrated herbicide to load the large prayer tank... But when you consider the patrons at a golf course have no idea WHEN the course is sprayed, and how much is present in grass and surface turf - it makes you think twice about playing golf...! Herbicides are stated to have "half-lives" in turf management/application which are similar to Injectable esterfied T -as to how long they are "effectively potent" in the ground they are applied....
It also makes me wonder if his Type II diabetes diuagnosed around 56-60yrs was primarily related to hidden/preliminary pancreatic cancer, only telling at early 70's. It would be interesting to see a study on the rate of avid golfers and Pancreatic cancer.. I am just thinking is WOULD NOT be good to be playing a round of golf and spitting on golf balls on the same day which herbicides were applied... i just dont think the modern medicine is actively checking pancreatic function and condition, and simply because its not an organ you can operate without... So I am guessing Pancreatic Cancer is only diagnosed once cancer has spread, or malfunctioning significantly..
I don't know maby i got lucky because there was no pain,even when he injected the novocaine to numb the prostrate.Im sure he changed the needle after each sample was pulled from the prostrate so it wouldn't contaminate the other samples.they record the location of each sample when they suck it out.It sounded like a bb gun going off each time they took a sample,it felt like a puff of air like you get when they do an eye exam.The doc asked what it felt like to me and i told him it tickeled,he said i was the only person that ever said that....I really never felt any sharp pain and it didnt hurt the next either but i did pee a little blood but nt much.....they use a sonogram to visually see if theres any signs of cancer and if there is they take samples,if theres no visual signs they dont.
Knudsen KE. Hormone Whodunit: clues for solving the case of intratumor androgen production. Clin Cancer Res. http://clincancerres.aacrjournals.org/content/early/2014/08/16/1078-0432.CCR-14-1188.abstract
One of the key mechanisms by which prostate cancer cells evade hormone therapy is through intatumor testosterone production.
New evidence points toward androstenedione as a potential precursor of intratumor androgen production, and furthers nomination of AKR1C3 as a therapeutic target in advanced disease.
One of the key mechanisms by which prostate cancer cells evade hormone therapy is through intatumor testosterone production.
New evidence points toward androstenedione as a potential precursor of intratumor androgen production, and furthers nomination of AKR1C3 as a therapeutic target in advanced disease.
Vis AN, van der Sluis TM, Al-Itejawi HHM, van Moorselaar RJA, Meuleman EJH. Risk of disease flare with LHRH agonist therapy in men with prostate cancer: Myth or fact? Urologic oncology. http://www.urologiconcology.org/article/S1078-1439(14)00158-6/abstract
Objectives - The traditional assumption of a linear relationship between serum testosterone and prostate cancer growth has been seriously challenged, as overwhelming evidence contradicts its basic principles.
Luteinizing hormone–releasing hormone (LHRH) agonists are known to cause a peak in serum testosterone level in the initial weeks of treatment, and prevention of the clinical sequelae of testosterone flare by concomitant use of antiandrogens is recommended.
Along the present biological concept that there appears to be a limit to the ability of androgens to stimulate prostate cancer growth, termed the saturation model, the use of antiandrogens to prevent this disease flare is questioned. The purpose of this review is to gain historical and modern evidence to provide an objective and up-to-date basis for clinical decision making.
Methods and Materials - We performed a comprehensive research of the electronic databases PubMed and Embase until April 1, 2014. Studies with the subject of disease flare in men with prostate cancer on LHRH agonist therapy were included, as were studies that assessed the efficacy of antiandrogens to prevent this flare. Case reports were included as well.
Results - Overall, 25 studies considering disease flare were included: 9 randomized clinical trials with an LHRH agonist and an LHRH agonist/antiandrogen arm, 14 observational studies evaluating LHRH agonists only, and 2 case reports. The incidence of disease flare was reported between 0% and 83% owing to a wide set of clinical, biochemical, and radiological factors evaluated. In some of the randomized clinical trials, a statistically significant reduction of the incidence of disease flare by concomitant use of antiandrogens was reported. Most of these historical studies report on subjective worsening of disease symptoms as outcome measure. More objective outcome measures such as the prostate-specific antigen level did not seem to increase to higher than the baseline values.
Conclusions - At present, there is a lack of compelling data showing definite disease progression during the short period of testosterone flare after initiation of LHRH agonist therapy. Based on the saturation model, presence of disease flare and the need to prevent this flare by concomitant use of antiandrogens might well be a misconception.
Objectives - The traditional assumption of a linear relationship between serum testosterone and prostate cancer growth has been seriously challenged, as overwhelming evidence contradicts its basic principles.
Luteinizing hormone–releasing hormone (LHRH) agonists are known to cause a peak in serum testosterone level in the initial weeks of treatment, and prevention of the clinical sequelae of testosterone flare by concomitant use of antiandrogens is recommended.
Along the present biological concept that there appears to be a limit to the ability of androgens to stimulate prostate cancer growth, termed the saturation model, the use of antiandrogens to prevent this disease flare is questioned. The purpose of this review is to gain historical and modern evidence to provide an objective and up-to-date basis for clinical decision making.
Methods and Materials - We performed a comprehensive research of the electronic databases PubMed and Embase until April 1, 2014. Studies with the subject of disease flare in men with prostate cancer on LHRH agonist therapy were included, as were studies that assessed the efficacy of antiandrogens to prevent this flare. Case reports were included as well.
Results - Overall, 25 studies considering disease flare were included: 9 randomized clinical trials with an LHRH agonist and an LHRH agonist/antiandrogen arm, 14 observational studies evaluating LHRH agonists only, and 2 case reports. The incidence of disease flare was reported between 0% and 83% owing to a wide set of clinical, biochemical, and radiological factors evaluated. In some of the randomized clinical trials, a statistically significant reduction of the incidence of disease flare by concomitant use of antiandrogens was reported. Most of these historical studies report on subjective worsening of disease symptoms as outcome measure. More objective outcome measures such as the prostate-specific antigen level did not seem to increase to higher than the baseline values.
Conclusions - At present, there is a lack of compelling data showing definite disease progression during the short period of testosterone flare after initiation of LHRH agonist therapy. Based on the saturation model, presence of disease flare and the need to prevent this flare by concomitant use of antiandrogens might well be a misconception.
They can do a sonogram before a biopsy to visually see any cancer before doing the biopsy..If there appears to be any suspicious areas then they would do a biopsy.Theres really no way to know if theres cancer unless they take samples and test them.Best to catch it early before it spreads or you will have some serious issues you dont want,a biopsy is well worth it....
Prasad V. It Is Time to Stop Screening for Prostate Cancer. JAMA Intern Med. Published online September 01, 2014. http://archinte.jamanetwork.com/article.aspx?articleID=1899553
Prostate-specific antigen (PSA) screening has been a disappointing public health strategy. The history of the PSA test will one day serve as a reminder that, although all of us in health care want to do everything possible to reduce the mortality of cancer, the early adoption of screening techniques on the basis of insufficient evidence can lead to more harm than good.
In this issue of JAMA Internal Medicine, Sammon and colleagues remind us that this day has not yet arrived. Contrary to the recommendations of the US Preventive Services Task Force (USPSTF) against routine screening, the use of prostate cancer screening continues at an alarming rate. More than one-third of men in America 80 years and older are screened, more than 40% of men aged 75 to 79 years, and nearly one-half of men between and 65 and 74 years. http://archinte.jamanetwork.com/article.aspx?articleid=1899555
The goal of cancer screening—like that of all interventions performed on healthy people—is to improve quantity or quality of life. Prostate-specific antigen screening has never shown an overall mortality benefit in any population.
We continue to screen for prostate cancer at too high a rate. This trend cannot and should not continue.
Prostate-specific antigen (PSA) screening has been a disappointing public health strategy. The history of the PSA test will one day serve as a reminder that, although all of us in health care want to do everything possible to reduce the mortality of cancer, the early adoption of screening techniques on the basis of insufficient evidence can lead to more harm than good.
In this issue of JAMA Internal Medicine, Sammon and colleagues remind us that this day has not yet arrived. Contrary to the recommendations of the US Preventive Services Task Force (USPSTF) against routine screening, the use of prostate cancer screening continues at an alarming rate. More than one-third of men in America 80 years and older are screened, more than 40% of men aged 75 to 79 years, and nearly one-half of men between and 65 and 74 years. http://archinte.jamanetwork.com/article.aspx?articleid=1899555
The goal of cancer screening—like that of all interventions performed on healthy people—is to improve quantity or quality of life. Prostate-specific antigen screening has never shown an overall mortality benefit in any population.
We continue to screen for prostate cancer at too high a rate. This trend cannot and should not continue.
When I hear expressions like "Improve the quality of life" I really just start to gleam mortality. Because really this expression is primarily associated with DEATH IN ROUTE... So how is a PSA going to improve? I don't know. Thought a nice long DRE from a smokin hot urologist chick might do a little something for me... Go ahead and toss me up in the stirrups for that one...
! (on a side note I DID observe stirrups in the Prostate docs office..
)
Well after all, why would we want to conduct a test which might imply a reason for a closer look and perhaps even a little digital fun - But MONEY... When after all, I hazard that most men shy away from a DRE almost a similarly as a colon scope. The funny part being that the colon cancer being very curable if EASILY detected on a scan.
THE TRUTH (one would think) is that men should be going to their docs and hiking their asses up insisting of a thorough look at every chance. THE IRONY being that the only real solution is a form of cannibalism to a critical area that essentially TAKES THE FUN OUT OF LIFE...
Is MONEY an I$$UE..? Hmmmm. Consider that the PSA test is the PSYCHOLOGICAL BRIDGE to get many guys to BEND OVER... But what the heck, we are ALL going to have it anyway right?? So just cut out the needless expense, WAIT to FIND it till we are 75, and then tell us how "pointless" it is to act on it be then anyway - "you lived a full life right..!!!?!" Where will the financial line be drawn. And where do MORALS & ETHICS Intersect. How long before internist don't mention an odd note in a DRE. How long before UROLOGIST are completely motivated to employ "Watchful Waiting", and based on WHAT CRITERIA.. How much $$ to save if we can just get em to 75...?! Right...
So it looks like a FLIP FLOP. Soon the PSA score only having relevance if a prostate physical irregularity is manually determined, or the patient has active issues complaining too. Still then, the PSA does not elevate in many cases where the cancer is already ensuing... At least until its a biological horror show. So again WHEN does the doc ring the action bell..?!
And all along, the information about things like Tumeric, which there is a lot of data that indicates a man may not even have to cross the bridge. The information about potential benefits of aspirin. How much cancer like this is simply POSSIBLY due to poor physical conditioning and prolonged blood supply deprivation?
What is the data on Erectile dysfunction saying? How does it correlate. Is the cardio related ED NOT a strict function of HEART-TO-PENIS, but more like HEART-TO-PROSTATE!?!?. You have to wonder. You could argue well it gets hard until I get my fat ass moving and what little muscle I have hogs what little blood I have - BUT TO WHERE...?! How is it that the prostate has become so "scientifically detached" from erectile disorders, and when the removal of the prostate appears to be the sure fire way to destroy erectile capacity?!!? Somebody tell me WHY THE FUCK Cocks are still being MAIMED like cannibals carving a steak to treat conditions like PRIAPISM. Has it even ever been challenged or tried that the REASON for a PRIAPISM could be related to a temporary prostate condition primarily?!?! I wonder has the condition of the prostate ever even been documented in a single priapism case? (really I don't know??). But I would be happy to take a one hour prostate massage over a 15 ga SHUNT in my cock head any day of the week..!!
Or consider a erection is not even possible for a spine with damage at that vertebra!! So hows about a simple temp spinal block to bring that bad boy down..? Turn things off "at the source" for shitz sake..! A rational LACK of LOGIC appears to continue to Ensue..
BACK ON TRACK & THE POINT - The Penile to Prostate relation is too intertwined to NOT be examining these avenues with regard to prostate cancer... I wonder what the percentage of men who are diagnosed with prostate cancer who can still get it up is?? Would they even say??
! (on a side note I DID observe stirrups in the Prostate docs office..)Well after all, why would we want to conduct a test which might imply a reason for a closer look and perhaps even a little digital fun - But MONEY... When after all, I hazard that most men shy away from a DRE almost a similarly as a colon scope. The funny part being that the colon cancer being very curable if EASILY detected on a scan.
THE TRUTH (one would think) is that men should be going to their docs and hiking their asses up insisting of a thorough look at every chance. THE IRONY being that the only real solution is a form of cannibalism to a critical area that essentially TAKES THE FUN OUT OF LIFE...
Is MONEY an I$$UE..? Hmmmm. Consider that the PSA test is the PSYCHOLOGICAL BRIDGE to get many guys to BEND OVER... But what the heck, we are ALL going to have it anyway right?? So just cut out the needless expense, WAIT to FIND it till we are 75, and then tell us how "pointless" it is to act on it be then anyway - "you lived a full life right..!!!?!" Where will the financial line be drawn. And where do MORALS & ETHICS Intersect. How long before internist don't mention an odd note in a DRE. How long before UROLOGIST are completely motivated to employ "Watchful Waiting", and based on WHAT CRITERIA.. How much $$ to save if we can just get em to 75...?! Right...
So it looks like a FLIP FLOP. Soon the PSA score only having relevance if a prostate physical irregularity is manually determined, or the patient has active issues complaining too. Still then, the PSA does not elevate in many cases where the cancer is already ensuing... At least until its a biological horror show. So again WHEN does the doc ring the action bell..?!
And all along, the information about things like Tumeric, which there is a lot of data that indicates a man may not even have to cross the bridge. The information about potential benefits of aspirin. How much cancer like this is simply POSSIBLY due to poor physical conditioning and prolonged blood supply deprivation?
What is the data on Erectile dysfunction saying? How does it correlate. Is the cardio related ED NOT a strict function of HEART-TO-PENIS, but more like HEART-TO-PROSTATE!?!?. You have to wonder. You could argue well it gets hard until I get my fat ass moving and what little muscle I have hogs what little blood I have - BUT TO WHERE...?! How is it that the prostate has become so "scientifically detached" from erectile disorders, and when the removal of the prostate appears to be the sure fire way to destroy erectile capacity?!!? Somebody tell me WHY THE FUCK Cocks are still being MAIMED like cannibals carving a steak to treat conditions like PRIAPISM. Has it even ever been challenged or tried that the REASON for a PRIAPISM could be related to a temporary prostate condition primarily?!?! I wonder has the condition of the prostate ever even been documented in a single priapism case? (really I don't know??). But I would be happy to take a one hour prostate massage over a 15 ga SHUNT in my cock head
any day of the week..!! Or consider a erection is not even possible for a spine with damage at that vertebra!! So hows about a simple temp spinal block to bring that bad boy down..? Turn things off "at the source" for shitz sake..! A rational LACK of LOGIC appears to continue to Ensue.. BACK ON TRACK & THE POINT - The Penile to Prostate relation is too intertwined to NOT be examining these avenues with regard to prostate cancer... I wonder what the percentage of men who are diagnosed with prostate cancer who can still get it up is?? Would they even say??
Nakano K, Kiuchi H, Miyagawa Y, Tsujimura A, Nonomura N. [Testosterone Replacement Therapy for Late-Onset Hypogonadism after Radical Prostatectomy : A Case Report.]. Hinyokika Kiyo 2014;60(8):397-400. http://www.ncbi.nlm.nih.gov/pubmed/25179991
A 53-year-old man presented to our hospital with a few-month history of fatigue and anorexia. His aging male's symptoms (AMS) score was 57, and the free testosterone value was low (6.5 pg/ml). He was diagnosed with severe late-onset hypogonadism indicative of androgen replacement therapy (ART). His serum prostate specific antigen was 8.7 ng/ml, and pelvic magnetic resonance imaging showed a low intensity area in the peripheral zone of the prostate.
A systematic 10-core prostate biopsy revealed one core of adenocarcinoma with a Gleason score of 33=6. Imaging examination revealed organ-confined prostate cancer that was cT2aN0M0. Given his desire for ART for the treatment of hypogonadism, the patient underwent open radical prostatectomy. Pathologic examination demonstrated prostate adenocarcinoma that was pT2aN0, and Gleason score of 33=6.
After confirming that the prostate specific antigen value was under 0.01 ng/ml for three years after prostatectomy, the patient received 125 mg methyltestosterone monthly. His hypogonadism-related symptoms diminished and AMS score dropped to 48.
During a three-year follow-up of ART, no biochemical recurrence was found.
A 53-year-old man presented to our hospital with a few-month history of fatigue and anorexia. His aging male's symptoms (AMS) score was 57, and the free testosterone value was low (6.5 pg/ml). He was diagnosed with severe late-onset hypogonadism indicative of androgen replacement therapy (ART). His serum prostate specific antigen was 8.7 ng/ml, and pelvic magnetic resonance imaging showed a low intensity area in the peripheral zone of the prostate.
A systematic 10-core prostate biopsy revealed one core of adenocarcinoma with a Gleason score of 33=6. Imaging examination revealed organ-confined prostate cancer that was cT2aN0M0. Given his desire for ART for the treatment of hypogonadism, the patient underwent open radical prostatectomy. Pathologic examination demonstrated prostate adenocarcinoma that was pT2aN0, and Gleason score of 33=6.
After confirming that the prostate specific antigen value was under 0.01 ng/ml for three years after prostatectomy, the patient received 125 mg methyltestosterone monthly. His hypogonadism-related symptoms diminished and AMS score dropped to 48.
During a three-year follow-up of ART, no biochemical recurrence was found.
Black A, Pinsky PF, Grubb RL, 3rd, et al. Sex steroid hormone metabolism in relation to risk of aggressive prostate cancer. Cancer Epidemiol Biomarkers Prev. http://cebp.aacrjournals.org/content/early/2014/08/30/1055-9965.EPI-14-0700.abstract
Background: The combined action of androgens and estrogens-specifically their balance-may play a role in prostate carcinogenesis but existing evidence is sparse and inconsistent. We investigated associations between serum sex steroid hormones, including estrogen metabolites, and risk of aggressive prostate cancer.
Methods: In a case-control study nested within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial cohort we measured serum estrone, estradiol and 13 estrogen metabolites, in the 2-, 4, or 16-hydroxylation pathways, using a liquid chromatography-tandem mass spectrometry assay.
Cases (n=195) were non-Hispanic white men aged 55-70 years when diagnosed with aggressive prostate cancer (stage III or IV and/or Gleason >/=7). Controls (n=195) were non-Hispanic white men without prostate cancer who were frequency-matched to cases by age and year at blood draw, time since baseline screen.
Only men with serum testosterone and sex hormone-binding globulin measured previously were eligible. Logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95%CI).
Results: Risk of aggressive prostate cancer was strongly inversely associated with estradiol:testosterone ratio (OR 4th quartile vs. 1st =0.27, 95% CI 0.12-0.59, p trend=0.003) and positively associated with 2:16alpha-hydroxyestrone ratio (OR 4th quartile vs. 1st =2.44, 95% CI 1.34-4.45, p trend=0.001). Estradiol, estrone and estrogen metabolites were unrelated to risk.
Conclusions: Our findings suggest that sex steroid hormones, specifically the estrogen-androgen balance, may be important in the development of aggressive prostate cancer.
Impact: Improved understanding of the hormonal etiology of prostate cancer is critical for prevention and therapeutic interventions.
Background: The combined action of androgens and estrogens-specifically their balance-may play a role in prostate carcinogenesis but existing evidence is sparse and inconsistent. We investigated associations between serum sex steroid hormones, including estrogen metabolites, and risk of aggressive prostate cancer.
Methods: In a case-control study nested within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial cohort we measured serum estrone, estradiol and 13 estrogen metabolites, in the 2-, 4, or 16-hydroxylation pathways, using a liquid chromatography-tandem mass spectrometry assay.
Cases (n=195) were non-Hispanic white men aged 55-70 years when diagnosed with aggressive prostate cancer (stage III or IV and/or Gleason >/=7). Controls (n=195) were non-Hispanic white men without prostate cancer who were frequency-matched to cases by age and year at blood draw, time since baseline screen.
Only men with serum testosterone and sex hormone-binding globulin measured previously were eligible. Logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95%CI).
Results: Risk of aggressive prostate cancer was strongly inversely associated with estradiol:testosterone ratio (OR 4th quartile vs. 1st =0.27, 95% CI 0.12-0.59, p trend=0.003) and positively associated with 2:16alpha-hydroxyestrone ratio (OR 4th quartile vs. 1st =2.44, 95% CI 1.34-4.45, p trend=0.001). Estradiol, estrone and estrogen metabolites were unrelated to risk.
Conclusions: Our findings suggest that sex steroid hormones, specifically the estrogen-androgen balance, may be important in the development of aggressive prostate cancer.
Impact: Improved understanding of the hormonal etiology of prostate cancer is critical for prevention and therapeutic interventions.
Last edited:
Linna123
New Member
Hi,
Regarding the issue of prevention of prostate cancer, there is still a lingering controversy about true prevention. Consequently, most physicians believe that there is no easy substitute for a healthy lifestyle involving eating a healthy diet, avoiding dietary excesses, eating plenty of fruits and vegetables, getting lots of exercise and being physically active, visiting the doctor on a regular basis, and most importantly achieving and maintaining a normal body weight.
Regarding the issue of prevention of prostate cancer, there is still a lingering controversy about true prevention. Consequently, most physicians believe that there is no easy substitute for a healthy lifestyle involving eating a healthy diet, avoiding dietary excesses, eating plenty of fruits and vegetables, getting lots of exercise and being physically active, visiting the doctor on a regular basis, and most importantly achieving and maintaining a normal body weight.
Edelman S, Butler J, Hershatter BW, Khan MK. The Effects of Androgen Deprivation Therapy on Cardiac Function and Heart Failure: Implications for Management of Prostate Cancer. Clin Genitourin Cancer. http://www.clinical-genitourinary-cancer.com/article/S1558-7673(14)00156-6/abstract
Conflicting clinical evidence regarding the possible association between androgen deprivation therapy (ADT) with heart failure in men with prostate cancer is reviewed, including 2 population-based registries showing such an association, and 1 showing no association.
Studies of the effects of androgens on cardiomyocyte contractility at the molecular level, the effects of testosterone on the cardiovascular system, particularly cardiac function, and the beneficial effects of testosterone therapy for patients with heart failure might help illuminate this controversy. Future studies are needed to evaluate the effect of ADT on end points of heart failure.
The authors weigh the possible adverse effects of ADT on cardiac function and heart failure against its known benefits to cancer outcomes, defined according to published, randomized trials, in a discussion of the implications of the preclinical and clinical literature on the management of prostate cancer in men at risk for heart failure.
In the absence of conclusive evidence that ADT causes heart failure, the authors discuss clinical situations in which ADT may be delayed, given on a short-term or intermittent basis, or withheld from treatment with the goal of reducing the risks of heart failure without compromising prostate cancer outcomes.
Conflicting clinical evidence regarding the possible association between androgen deprivation therapy (ADT) with heart failure in men with prostate cancer is reviewed, including 2 population-based registries showing such an association, and 1 showing no association.
Studies of the effects of androgens on cardiomyocyte contractility at the molecular level, the effects of testosterone on the cardiovascular system, particularly cardiac function, and the beneficial effects of testosterone therapy for patients with heart failure might help illuminate this controversy. Future studies are needed to evaluate the effect of ADT on end points of heart failure.
The authors weigh the possible adverse effects of ADT on cardiac function and heart failure against its known benefits to cancer outcomes, defined according to published, randomized trials, in a discussion of the implications of the preclinical and clinical literature on the management of prostate cancer in men at risk for heart failure.
In the absence of conclusive evidence that ADT causes heart failure, the authors discuss clinical situations in which ADT may be delayed, given on a short-term or intermittent basis, or withheld from treatment with the goal of reducing the risks of heart failure without compromising prostate cancer outcomes.
Basch E, Loblaw DA, Oliver TK, et al. Systemic Therapy in Men With Metastatic Castration-Resistant Prostate Cancer: American Society of Clinical Oncology and Cancer Care Ontario Clinical Practice Guideline. Journal of Clinical Oncology. http://jco.ascopubs.org/content/early/2014/09/03/JCO.2013.54.8404.abstract
Purpose To provide treatment recommendations for men with metastatic castration-resistant prostate cancer (CRPC).
Methods The American Society of Clinical Oncology and Cancer Care Ontario convened an expert panel to develop evidence-based recommendations informed by a systematic review of the literature.
Results When added to androgen deprivation, therapies demonstrating improved survival, improved quality of life (QOL), and favorable benefit-harm balance include abiraterone acetate/prednisone, enzalutamide, and radium-223 (223Ra; for men with predominantly bone metastases). Improved survival and QOL with moderate toxicity risk are associated with docetaxel/prednisone.
For asymptomatic/minimally symptomatic men, improved survival with unclear QOL impact and low toxicity are associated with sipuleucel-T.
For men who previously received docetaxel, improved survival, unclear QOL impact, and moderate to high toxicity risk are associated with cabazitaxel/prednisone.
Modest QOL benefit (without survival benefit) and high toxicity risk are associated with mitoxantrone/prednisone after docetaxel.
No benefit and excess toxicity are observed with bevacizumab, estramustine, and sunitinib.
Recommendations Continue androgen deprivation (pharmaceutical or surgical) indefinitely.
Abiraterone acetate/prednisone, enzalutamide, or 223Ra should be offered; docetaxel/prednisone should also be offered, accompanied by discussion of toxicity risk. Sipuleucel-T may be offered to asymptomatic/minimally symptomatic men.
For men who have experienced progression with docetaxel, cabazitaxel may be offered, accompanied by discussion of toxicity risk. Mitoxantrone may be offered, accompanied by discussion of limited clinical benefit and toxicity risk.
Ketoconazole or antiandrogens (eg, bicalutamide, flutamide, nilutamide) may be offered, accompanied by discussion of limited known clinical benefit. Bevacizumab, estramustine, and sunitinib should not be offered.
There is insufficient evidence to evaluate optimal sequences or combinations of therapies. Palliative care should be offered to all patients.
Purpose To provide treatment recommendations for men with metastatic castration-resistant prostate cancer (CRPC).
Methods The American Society of Clinical Oncology and Cancer Care Ontario convened an expert panel to develop evidence-based recommendations informed by a systematic review of the literature.
Results When added to androgen deprivation, therapies demonstrating improved survival, improved quality of life (QOL), and favorable benefit-harm balance include abiraterone acetate/prednisone, enzalutamide, and radium-223 (223Ra; for men with predominantly bone metastases). Improved survival and QOL with moderate toxicity risk are associated with docetaxel/prednisone.
For asymptomatic/minimally symptomatic men, improved survival with unclear QOL impact and low toxicity are associated with sipuleucel-T.
For men who previously received docetaxel, improved survival, unclear QOL impact, and moderate to high toxicity risk are associated with cabazitaxel/prednisone.
Modest QOL benefit (without survival benefit) and high toxicity risk are associated with mitoxantrone/prednisone after docetaxel.
No benefit and excess toxicity are observed with bevacizumab, estramustine, and sunitinib.
Recommendations Continue androgen deprivation (pharmaceutical or surgical) indefinitely.
Abiraterone acetate/prednisone, enzalutamide, or 223Ra should be offered; docetaxel/prednisone should also be offered, accompanied by discussion of toxicity risk. Sipuleucel-T may be offered to asymptomatic/minimally symptomatic men.
For men who have experienced progression with docetaxel, cabazitaxel may be offered, accompanied by discussion of toxicity risk. Mitoxantrone may be offered, accompanied by discussion of limited clinical benefit and toxicity risk.
Ketoconazole or antiandrogens (eg, bicalutamide, flutamide, nilutamide) may be offered, accompanied by discussion of limited known clinical benefit. Bevacizumab, estramustine, and sunitinib should not be offered.
There is insufficient evidence to evaluate optimal sequences or combinations of therapies. Palliative care should be offered to all patients.
Roediger J, Hessenkemper W, Bartsch S, et al. Supraphysiological androgen levels induce cellular senescence in human prostate cancer cells through the Src-Akt pathway. Mol Cancer 2014;13(1):214. http://www.molecular-cancer.com/content/13/1/214/abstract
BACKGROUND: Prostate cancer (PCa) is the second leading cause of cancer mortality of men in Western countries. The androgen receptor (AR) and AR-agonists (androgens) are required for the development and progression of the normal prostate as well as PCa.
However, it is discussed that in addition to their tumor promoting activity, androgens may also exhibit tumor suppressive effects. A biphasic growth response to androgens a growth-promoting and -inhibition has been observed that suggests that administration of supraphysiological androgen levels mediates growth reduction in AR expressing PCa cells.
METHODS: Detection of senescence markers, three dimensional interphase fluorescence in situ hybridization (3D-iFISH), qRT-PCR, Western blotting, detection of GFP fusions, prostatectomy, ex vivo culturing.
RESULTS: Here, we describe that supraphysiological levels of androgens induce cell cycle arrest and markers of cellular senescence in human PCa cells, which may in part explain the growth inhibitory role of androgens. The expression of the senescence associated beta galactosidase is observed by treatment with the natural androgen DHT or the less metabolized synthetic androgen R1881. The induction of senescence marker was detected in human PCa cell lines as well as in human primary PCa tissue derived from prostatectomy treated ex vivo.
Using interphase FISH (iFISH) suggests that the androgen-induced cellular senescence is associated with localizing the genomic E2F1 locus to senescence associated heterochromatic foci. Analysis of different signaling pathways in LNCaP cells suggest that the p16-Rb-E2F1 pathway is essential for the induction of cellular senescence since treatment with siRNA directed against p16 reduces the level of androgen-induced cellular senescence.
Based on the rapid induction of androgen-mediated cellular senescence we identified the Src-PI3K-Akt-signaling pathway and autophagy being in part involved in androgen regulation.
CONCLUSIONS: Taken together, our data suggest that AR-agonists at supraphysiological levels mediate induction of cellular senescence in human PCa cells, which may have a protective anti-cancer role. These results provide also new insights for understanding androgen-mediated regulation of PCa growth.
BACKGROUND: Prostate cancer (PCa) is the second leading cause of cancer mortality of men in Western countries. The androgen receptor (AR) and AR-agonists (androgens) are required for the development and progression of the normal prostate as well as PCa.
However, it is discussed that in addition to their tumor promoting activity, androgens may also exhibit tumor suppressive effects. A biphasic growth response to androgens a growth-promoting and -inhibition has been observed that suggests that administration of supraphysiological androgen levels mediates growth reduction in AR expressing PCa cells.
METHODS: Detection of senescence markers, three dimensional interphase fluorescence in situ hybridization (3D-iFISH), qRT-PCR, Western blotting, detection of GFP fusions, prostatectomy, ex vivo culturing.
RESULTS: Here, we describe that supraphysiological levels of androgens induce cell cycle arrest and markers of cellular senescence in human PCa cells, which may in part explain the growth inhibitory role of androgens. The expression of the senescence associated beta galactosidase is observed by treatment with the natural androgen DHT or the less metabolized synthetic androgen R1881. The induction of senescence marker was detected in human PCa cell lines as well as in human primary PCa tissue derived from prostatectomy treated ex vivo.
Using interphase FISH (iFISH) suggests that the androgen-induced cellular senescence is associated with localizing the genomic E2F1 locus to senescence associated heterochromatic foci. Analysis of different signaling pathways in LNCaP cells suggest that the p16-Rb-E2F1 pathway is essential for the induction of cellular senescence since treatment with siRNA directed against p16 reduces the level of androgen-induced cellular senescence.
Based on the rapid induction of androgen-mediated cellular senescence we identified the Src-PI3K-Akt-signaling pathway and autophagy being in part involved in androgen regulation.
CONCLUSIONS: Taken together, our data suggest that AR-agonists at supraphysiological levels mediate induction of cellular senescence in human PCa cells, which may have a protective anti-cancer role. These results provide also new insights for understanding androgen-mediated regulation of PCa growth.
Zhou CK, Pfeiffer RM, Cleary SD, et al. Relationship Between Male Pattern Baldness and the Risk of Aggressive Prostate Cancer: An Analysis of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Journal of Clinical Oncology. http://jco.ascopubs.org/content/early/2014/09/15/JCO.2014.55.4279.abstract
Purpose Male pattern baldness and prostate cancer appear to share common pathophysiologic mechanisms. However, results from previous studies that assess their relationship have been inconsistent. Therefore, we investigated the association of male pattern baldness at age 45 years with risks of overall and subtypes of prostate cancer in a large, prospective cohort—the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.
Methods We included 39,070 men from the usual care and screening arms of the trial cohort who had no cancer diagnosis (excluding nonmelanoma skin cancer) at the start of follow-up and recalled their hair-loss patterns at age 45 years. Hazard ratios (HRs) and 95% CIs were estimated by using Cox proportional hazards regression models with age as the time metric.
Results During follow-up (median, 2.78 years), 1,138 incident prostate cancer cases were diagnosed, 571 of which were aggressive (biopsy Gleason score ≥ 7, and/or clinical stage III or greater, and/or fatal). Compared with no baldness, frontal plus moderate vertex baldness at age 45 years was not significantly associated with overall (HR, 1.19; 95% CI, 0.98 to 1.45) or nonaggressive (HR, 0.97; 95% CI, 0.72 to 1.30) prostate cancer risk but was significantly associated with increased risk of aggressive prostate cancer (HR, 1.39; 95% CI, 1.07 to 1.80). Adjustment for covariates did not substantially alter these estimates. Other classes of baldness were not significantly associated with overall or subtypes of prostate cancer.
Conclusion Our analysis indicates that frontal plus moderate vertex baldness at age 45 years is associated with an increased risk of aggressive prostate cancer and supports the possibility of common pathophysiologic mechanisms.
Do you think it has to do with possibly higher DHT levels/
No.
Do Testosterone Levels Have Prognostic Significance in Patients with Metastatic Prostate Cancer (mPCa) Treated with Combined Androgen Blockade (CAB)? [NO]
In 1941, Huggins and Hodges reported the hormone dependence of prostate cancer, and ADT has since become the standard systemic therapy for patients with mPCa.
Historically, the castration level was considered to be <0.5 ng/mL. However, since 1996, a method using chemiluminescent technology for clinical use has resulted in more accurate serum testosterone measurements.
Oefelein et al. reported a median testosterone level of 0.15 ng/mL after surgical castration when testosterone levels were measured by current testing methods. Thus, they suggested that a castration level of <0.2 ng/mL should be the aim of ADT.
Morote et al. reported that the lowest testosterone castration level with a significant effect on survival free of PSA progression was 0.32 ng/mL.
Perachino et al. also suggested a direct correlation between the risk of death in mPCa patients and testosterone levels achieved during ADT. However, most of the patients in these studies received GnRH agonist monotherapy.
In the present study, we retrospectively investigated the relationship between serum testosterone levels in mPCa patients receiving CAB and their prognosis.
In our study, no threshold (0.15, 0.2 or 0.32 ng/mL) of the median testosterone levels showed a significant relation with Time To Progression (TTP), Cancer-Specific Survival (CSS), or Overall Survival (OS) in Japanese metastatic prostate cancer patients treated with CAB.
Yasuda Y, Fujii Y, Yuasa T, Yamamoto S, Yonese J, Fukui I. Do testosterone levels have prognostic significance in patients with metastatic prostate cancer treated with combined androgen blockade? International Journal of Urology. http://onlinelibrary.wiley.com/doi/10.1111/iju.12623/abstract
In 1941, Huggins and Hodges reported the hormone dependence of prostate cancer, and ADT has since become the standard systemic therapy for patients with mPCa.
Historically, the castration level was considered to be <0.5 ng/mL. However, since 1996, a method using chemiluminescent technology for clinical use has resulted in more accurate serum testosterone measurements.
Oefelein et al. reported a median testosterone level of 0.15 ng/mL after surgical castration when testosterone levels were measured by current testing methods. Thus, they suggested that a castration level of <0.2 ng/mL should be the aim of ADT.
Morote et al. reported that the lowest testosterone castration level with a significant effect on survival free of PSA progression was 0.32 ng/mL.
Perachino et al. also suggested a direct correlation between the risk of death in mPCa patients and testosterone levels achieved during ADT. However, most of the patients in these studies received GnRH agonist monotherapy.
In the present study, we retrospectively investigated the relationship between serum testosterone levels in mPCa patients receiving CAB and their prognosis.
In our study, no threshold (0.15, 0.2 or 0.32 ng/mL) of the median testosterone levels showed a significant relation with Time To Progression (TTP), Cancer-Specific Survival (CSS), or Overall Survival (OS) in Japanese metastatic prostate cancer patients treated with CAB.
Yasuda Y, Fujii Y, Yuasa T, Yamamoto S, Yonese J, Fukui I. Do testosterone levels have prognostic significance in patients with metastatic prostate cancer treated with combined androgen blockade? International Journal of Urology. http://onlinelibrary.wiley.com/doi/10.1111/iju.12623/abstract
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