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Posted By : Dreamerboy - 1/12/2014 7:42 AM
Someone recently posted a question about the link between testosterone and prostate cancer and one member (I think Tall Allen) posted some links showing that those with low testosterone are actually prone to get the diseases and he posted some studies to back that up. Some have also pointed out that most of us get prostate cancer at times in our lives when our testosterone is diminishing.

Now I'm confused - it has been proven that testosterone lowering drugs are successful in slowing aggressive prostate cancer. So why would those with low testosterone be more susceptible to the disease?

Is there a difference regarding testosterone with lower grade prostate cancers?

Just wondering if anyone has looked into this or done any research.
B-year: 1959 PSA ~7.4
-1Biopsy: 2011; 2/12 positive, G6(3+3), both 30% T1c
-2012 Tesla 3 MRI - no nodules or progression outside prostate.
-2nd biopsy 2 /10 positive, G6, 40 & 70%
-3rd Biopsy July 2013 3/13 positive, G6, 1%, 5%, 40%
Active surveillance; following Ornish/Michael Milken-style diet

Posted By : lapilot - 1/12/2014 8:22 AM
Simply stated testosterone and DHT (Dihydrotestosterone) fuels prostate cancer. Is testosterone or DHT implicated in the cause of prostate cancer, I do not know. Genetics, epigenetics, diet and possibly prostate inflammation and/or infections has been implicated in the cause prostate cancer.

It is well known that reducing testosterone levels to castration levels ( less than 20 ng/dL).

" Men who maintained a serum PSA level of lower than 20 ng/dL had a mean PSA progression-free survival of 106 months versus 90 months for those with levels between 20 and 50 ng/mL and only 72 months if the mean serum PSA level was higher than 50 ng/mL" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725306/
Age 60, Parametric MRI 8/18/13 negative findings
biopsy 9/5/13, PSA 6.2, 13 core of which 6 are postive
left laterial base 10% G6(3+3)
left laterial apex 10% G6(3+3)
right base 15% G7(3+4)
right laterial base 15% G6(3+3)
right laterial mid 60% G6(3+3)
right lateral apex 20% G6(3+3)
Robot Surgery scheduled 11/11/13
Post surgery path T2c N0

Posted By : PeterDisAbelard. - 1/12/2014 8:49 AM
Among other things, you said...
Now I'm confused - it has been proven that testosterone lowering drugs are successful in slowing aggressive prostate cancer. So why would those with low testosterone be more susceptible to the disease?

The honest answer is that nobody knows for sure. There are a number of theories that fit most of the data but none of them explain everything we see. My favorite is the "saturation" theory. It states that prostate cells (normal ones and cancers) have androgen receptor sites on their surface. These are spots where a testosterone molecule can attach to the cell and "activate" the receptor. There are a finite number of these receptors and thus a limit to the number of testosterone molecules that can attach. Once all the receptors are full adding more testosterone makes no difference. The cell is 'saturated'.

Androgen-sensitive cells need at least some of their sites activated to grow. For example, men and women have the same breast cells but those cells are sensitive to Estrogen not to Testosterone and so we guys grow different bits at puberty than do the ladies. The amount of testosterone that is needed to activate most of the activation sites is fairly low so you can have lower than normal testosterone and still have plenty for your cancer cells to grow. The analogy I use is that to a man drowning in the middle of the ocean low tide is no help: as long as the water is over his head it doesn't matter how deep it is.

So, actually, drugs that "lower" testosterone don't actually have much effect on prostate cancer (as you would expect). The drugs that really knock it back mostly eliminate testosterone. The process is called chemical castration in some of the literature but that term is seldom used by our doctors because some men react badly to the word "castration." I know I do.

That's the basics. You can go a bit further with the saturation theory. When androgen sensitive cells have to struggle to get their activation sites activated they tend to grow more activation sites to try to snag a few more testosterone molecules out of the rather thin soup. This might be where they get into trouble. Those extra activation sites have a chance of making trouble. Some of them may cause too much growth, or the wrong kind. They might cause the cell to become cancerous. That would be how the saturation model would explain low-testosterone causing an increased risk of cancer.

The same process, more or less, explains how cancer cells become castrate resistant with time. In the absence of testosterone the cancer cells grow more and more receptors and every now and then they grow a receptor that turns on even without activation, or is activated by something else. Once you have enough cells with these receptor sites that don't need testosterone then your cancer has turned "castrate resistant" and it may be time for another type of treatment in addition to the hormones.

There you go. Everything I know about your question and quite a bit more that I made up.

Posted By : Dreamerboy - 1/12/2014 10:01 AM
That was an excellent reply Peter and what you say makes sense even if some of it is theoretical - Thank you.
B-year: 1959 PSA ~7.4
-1Biopsy: 2011; 2/12 positive, G6(3+3), both 30% T1c
-2012 Tesla 3 MRI - no nodules or progression outside prostate.
-2nd biopsy 2 /10 positive, G6, 40 & 70%
-3rd Biopsy July 2013 3/13 positive, G6, 1%, 5%, 40%
Active surveillance; following Ornish/Michael Milken-style diet

Posted By : Tall Allen - 1/12/2014 2:42 PM
I like PDAs explanation and would add one more thing. Cells "communicate" with one another. Healthy prostate cells, which need T to stay healthy, send out signals that seem to suppress cancerous cells. Conversely, cancerous cells can put out growth factors that may turn healthy cells cancerous (this is called phenotype switching) - sort of like a zombie bite. So there is a dynamic equilibrium process going on. In advanced stages, the equilibrium tips in favor of the cancerous cells, but before cancerous cells emerge, normal levels of testosterone keep the healthy cells predominant.

Interestingly, there is a clinical trial now to alternate periods of complete T starvation with periods where T is supplemented. The T starvation will kill off the androgen-reliant cancer cells. The T supplementation will keep many of the cancer cells from becoming castration-resistant. It is hoped that this will maintain the equilibrium for a longer time.

- Allen

Posted By : Dreamerboy - 1/12/2014 3:10 PM
Thanks Tall Allen. Here is an interesting link I found on the topic.

http://www.lef.org/magazine/mag2008/dec2008_Destroying-the-Myth-about-Testosterone-Replacement-Prostate-Cancer_02.htm
B-year: 1959 PSA ~7.4
-1Biopsy: 2011; 2/12 positive, G6(3+3), both 30% T1c
-2012 Tesla 3 MRI - no nodules or progression outside prostate.
-2nd biopsy 2 /10 positive, G6, 40 & 70%
-3rd Biopsy July 2013 3/13 positive, G6, 1%, 5%, 40%
Active surveillance; following Ornish/Michael Milken-style diet

Posted By : PSA3DOT7 - 1/13/2014 9:00 AM
I have low testosterone and low PSA, and had a Gleason 9. I'm back on T supplementation after my RRP. Dr Mulhall makes a good case for T replacement therapy post RRP in men with low testosterone! I've been on T for a awhile post RRP and my latest PSA < .01 (see below)
Age 58
Gleason 9 (5+4) 1/16 +cores
PSA < 0.01 (11/2013, 01/2014)
pre-Op PSA 3.7 (08/13), 2.4(03/12), 1.9 (12/10), 1.6 (12/09) -- 0.8 (03/04)
RRP Oct2013, Nerve sparing one side
ED - PDE5i at 5-6am, 60% erections 2/week,
Incontinence - Dry nights, 1 pad/day 3-5grams
HRT Testogel 50mg/day
T2 Diabetic on Insulin
Hypertension on perindopril arginine

Posted By : PeterDisAbelard. - 1/13/2014 9:42 AM
Tall One,

I have read [ OK, tried to read ] the study on which I believe the clinical trial is based. Adaptive Auto-Regulation of Androgen Receptor Provides a Paradigm Shifting Rationale for Bipolar Androgen Therapy (BAT) for Castrate Resistant Human Prostate Cancer ( abstract: www.ncbi.nlm.nih.gov/pubmed/22396319) and if I read it right (which is by no means a certain thing) then the statement about the effect of the testosterone supplementation is stronger than you mentioned. The sudden increase in androgens tends to induce cell death in (some of) the castrate resistant cells.

I hope something comes of this since, while I would very much like to avoid castrate resistant prostate cancer altogether, should it happen to me then this is the only treatment regimen that sounds like any fun at all.

Posted By : gibson00 - 1/13/2014 11:52 AM
Regarding the 'those with low testosterone are diagnosed more often...'.
I brought this up with my father's oncologist, and what he said, and what I've since agreed with based on lots of reading, is that men with naturally low testosterone are NOT diagnosed more frequently with prostate cancer.
However, when they are, it tends to be a higher grade cancer.

Some studies actually showed higher PCa rates in control groups compared to those getting T-supplementation.
Cheers

Posted By : Tall Allen - 1/13/2014 12:14 PM
PDA,

I think you understood quite well. I think that this kind of T cycling may slow the beast down for at least a subset of men with PC, but I'm doubtful it can work for everyone. There is evidence that androgen-independent cancer cells are present even at early stages and cancer stem cells seem to be impervious to ADT. The strategy of keeping cells vulnerable to ADT will eventually fail unless we also attack the cancer from another direction.

I posted more info in an earlier thread, which I'll reprint here:

The Johns Hopkins researchers said...
To our great surprise we have learned in laboratory studies that hormone-resistant prostate cancer cells that make high amounts of the androgen receptor are killed when exposed to high levels of testosterone. This result is exactly opposite of what we expected. We think what is happening is that prostate cancer cells must first make and then remove the androgen receptor in order to produce more cancer cells. In the presence of high levels of testosterone, the androgen receptor does not get removed from the cell like it is supposed to and this cause the cells to die when they try to divide to make daughter cells.
These laboratory results led us to test this concept in a small clinical study in men with hormone-resistant prostate cancer. In this study we found that more than 50% of the men showed signs of prostate cancer response when treated with high doses of testosterone. In addition, all of the men reported remarkable improvement in quality of life. Many of the men were able to once again engage in sexual activity with their spouses. Muscle strength and energy level also markedly improved. Some men remained on treatment for a year or more.

These results suggest a new paradigm for treating prostate cancer that would involve sequentially lowering and then raising testosterone to high levels. This treatment is unique as far as cancer therapies go in that it has the potential to stop the growth of cancer while at the same time making the patients feel better, not worse.

(from their post on the Start-a-Cure website)

This group at Johns Hopkins established the theoretic basis for this testosterone therapy, which they call “Bipolar Androgen Therapy.”:
Combinatorial androgen receptor targeted therapy for prostate cancer
Adaptive auto-regulation of androgen receptor provides a paradigm shifting rationale for bipolar androgen therapy (BAT) for castrate resistant human prostate cancer.

And they also did a small clinical trial, which they are now seeking to expand:
Bipolar androgen therapy: the rationale for rapid cycling of supraphysiologic androgen/ablation in men with castration resistant prostate cancer.
A Phase II Study of Bipolar Androgen-based Therapy for Men with Androgen Ablation Naive Recurrent Prostate Cancer


There is other evidence to support their theory. Many studies show that naturally low levels of testosterone (hypogonadism) is associated with both incidence and aggressiveness of prostate cancer. For example:

Low testosterone levels are related to poor prognosis factors in men with prostate cancer prior to treatment.
Serum testosterone level as a predictor of biochemical failure after radical prostatectomy for localized prostate cancer.
Lower serum total testosterone is associated with lymph node metastases in a radical prostatectomy cohort study.
Low testosterone levels are related to poor prognosis factors in men with prostate cancer prior to treatment.
Low serum testosterone levels are predictive of prostate cancer.
Circulating free testosterone is an independent predictor of advanced disease in patients with clinically localizedprostate cancer.
Usefulness of Preoperative Serum Testosterone as a Predictor of Extraprostatic Extension and Biochemical Recurrence

Some have gone so far as to suggest that low testosterone is not just associated with PC but is in fact a cause of prostate cancer. In the following review of lab studies, the authors find that testosterone can bind with the membrane androgen receptor to trigger apoptosis (programmed cell death) in androgen-independent prostate cancer cells, which normally do not undergo apoptosis:
Could Testosterone Have a Therapeutic Role in Prostate Cancer?

Dr. Prehn at UW postulates that as we age and our testosterone levels decline, the cells of the healthy prostate attempt to compensate for the depleted androgen by producing a lot of extra cells (compensatory hyperplasia). And the quickly proliferating cells eventually exhibit cancerous characteristics like dysplasia (Gleason grade) and immortality. These cells are capable of surviving and proliferating in an androgen-poor environment and eventually adapt to the selective pressure of their low androgen environment by becoming entirely androgen independent. This process is exacerbated by ADT.

Prehn believes that supplementing testosterone up to normal levels at an early age may prevent PC. He also believes that giving very high doses of testosterone or DHT to men whose cancer has already progressed to androgen independence may reverse the selective pressure on the cancer cells and cause them to become androgen-dependent once again. Thus, a strategy of cycling ADT with high androgens may keep the cancer from reaching a tipping point beyond which it can’t be controlled.

On the Prevention and Therapy of Prostate Cancer by Androgen Administration

His hypothesis has so far been born out in animal studies in mice and dogs and in small pilot human studies.

A group at the U. of Chicago with CRPC and no or little metastases treated 15 men with testosterone. Three had decreased PSA while on treatment.
A Randomized Phase I Study of Testosterone Replacement for Patients with Low Risk Castrate Resistant Prostate Cancer


In a Memorial Sloan Kettering study on 12 men with metastatic castration-resistant prostate cancer (mCRPC) found such treatment was safe, but none achieved an objective response, but none achieved supraphysiological levels of testosterone either.
Phase 1 Trial of High-Dose Exogenous Testosterone in Patients with Castration-Resistant Metastatic Prostate Cancer

At Beth Israel Deaconess/ Harvard, 13 testosterone-deficient men with untreated prostate cancer on Active Surveillance were given testosterone for a median of 2.5 years. No cancer was found on 54% of f/u biopsies. There was no disease progression or distant mets.
Testosterone therapy in men with untreated prostate cancer


Drs. Leibowitz, Vogelzang et al. have taken the radical step of treating men with very high doses of testosterone and dutasteride, in some cases reaching serum levels of 3000 ng/dL.. They treated 96 men who were hypogonadal and had been treated for their PC, mostly with intermittent ADT alone (63%). After a median of 3 years, 57% did not experience PSA progression, suggesting that there is a subset on whom such therapy may be beneficial.

Testosterone replacement in prostate cancer survivors with hypogonadal symptoms

Here’s a good review article that discusses the research:
Androgens as therapy for androgen receptor-positive castration-resistant prostate cancer

Post Edited (Tall Allen) : 1/13/2014 11:20:12 AM (GMT-7)


Posted By : Nomar Lupron 4 Me - 1/13/2014 2:21 PM
As usual PeterDA and Tall Allen did an excellent job on the science that answers your question.

I cannot keep up with them but will offer the layman's view to your question: " So why would those with low testosterone be more susceptible to the disease?"

Age.

Testosterone tend to decrease as men age.

PCa tends to surface at higher ages, though some on this forum are now being diagnosed as early as age 40.

So even though drastically lowering the T impedes the growth of existing PCa, both lower T and higher incidence of PCA tend to happen as we age.

Some have even said that being diagnosed with PCa just means you lived long enough.

If Testosterone were the cause of PCa, all teenage males would have it.

Back on a serious note, thanks PeterDA and Tall Allen for your thorough analysis.

LupronJim
65 - DX 64 2/13 PSA 3.68 (6 mo doubling) Gleason 9 (4+5)

T1CN0M1B stage IV w. 7 of 12 cores worst ones 70% right PNI

oligometastatic 5 tumors 1 right sacroiliac, 2 thoracic vertebral bodies (spine), 2 right posterior ribs

1st Lupron 4 month 3-28-13, 2nd Aug 1
PSA down was 3.68, 0.68 on 08-08-13
PSA 0.20 on 11-12-13, T=5

UF & Shands treating w curative intent, not just palliative.

LupronJim

Posted By : Desertrat1 - 1/14/2014 8:07 AM
Dreamerboy's link www.lef.org/magazine/mag2008/dec2008_Destroying-the-Myth-about-Testosterone-Replacement-Prostate-Cancer_02.htm is a chapter out of Abraham Morgentalers book: Testosterone for Life: Recharge Your Sex Drive, Muscle Mass, Energy and Overall Health by Abraham Morgentaler.

The book is a very good read and I read it at the most opportune time. My PSA was always in the mid to high 300 range, and I was always told my T was ok. Right after my RALP I suffered from malaise something fierce. I was always tired yet couldn't sleep. My mind wasn't sharp at all. I read Abraham's book and approached my URO about HRT. My first total T count was 345 which was good according to my URO. My GP said he would treat me at the 345 level because I was on the low end and symptomatic but he would require approval from my URO which I wasn't going to get. During my GP's annual blood test he also ran another T test and this one came back 262 which did get my URO's attention. My URO ran another T test and my total T was 200. I was 18 months post RALP and he reluctantly agreed to start allowing me HRT. He usually likes to wait 24 months. It was Abraham's book that got me on track to start T and I'm glad I did. I feel much better today because of it. It is a real crock that T is a controlled substance. The pharmacies are real tight when you can pick up a refill.

As a side note, I get pissed anytime someone asks why I haven't castrated our little 20 pound mutt. I always tell them to go read Abraham Morgentaler's book Testosterone for Life. My dog eats as much as he wants, he is very slim, active and healthy. If T is good for me it is good for him and that I treat my dog just like I want to be treated.
FAV song "I'm still standing"www.youtube.com/watch?v=dq2uAUjkLIw
AGE 59, 9/2011 PSA 4.7 BIOPSY 4 cores 3X3 RALP 1-2012
Final PATH: 3X4 G7, 7% VOLUMN, LEFT SIDE, pT2a
perineural Invasion:Focally observed
MARGINS & EXTRAPROSTATIC EXT NEGATIVE
psa 4-12 thru 1-13 a zero
99%continent ED: injected 110 times 5-1-2012 thru 5-29-13
Able to switch to pills in june 2013 yippee

Posted By : Dreamerboy - 1/16/2014 9:44 PM
I've just ordered that book from the library - thanks for the suggestion Desertrat1.

On one hand, I'm happy that more is coming to light on this topic but on the other hand it makes me a little angry. You have to wonder how much research has been going on with prostate cancer, when so little attempt seems to have been made to test "conventional wisdom". It makes you wonder what other things are being taken for granted by the professionals that perhaps should be challenged. I tend to think that if prostate cancer was one of the emotionally-charged diseases that we would have far more answers than we do now.
B-year: 1959 PSA ~7.4
-1Biopsy: 2011; 2/12 positive, G6(3+3), both 30% T1c
-2012 Tesla 3 MRI - no nodules or progression outside prostate.
-2nd biopsy 2 /10 positive, G6, 40 & 70%
-3rd Biopsy July 2013 3/13 positive, G6, 1%, 5%, 40%
Active surveillance; following Ornish/Michael Milken-style diet

Posted By : clanda - 1/17/2014 5:21 AM
When I was Dx in September 2013, my total natural T level was 1250. Amongst a host of other factors, I just felt that the high T level was another no-no and I chose RALP in November. I am very pleased with my decision and consider myself very lucky.
Age: 63 at Dx 9/4/13
PSA 2/02 1.3, 8/13 1.6
2 of 12 cores positive (5% & 10%) Gleason 3 + 3, T2a
DRE hard area or nodule
Free Testosterone 139.9 pg/ml (13.99 ng/dl) (513.57 Pmol/L)
Father died of PCa age 66 in 1978
RALP with Dr A. Tewari Mt Sinai Hospital NY 11/12/13
Path: Gleason 7 3+4 T2c, 38g, Organ confined, PNI present, no EPE
PSA 12/30/13 <0.02 undetectable

Posted By : Tall Allen - 3/18/2014 12:11 PM
I noticed today that the researchers at Johns Hopkins, in collaboration with the National Cancer Institute, have apparently received funding for their Bipolar Androgen Therapy clinical trial and will begin enrollment soon. They will be giving supraphysiologic levels of testosterone to men with metastatic CRPC who have rising PSA following Zytiga or Xtandi use. The goal is to see if the testosterone restores sensitivity to those medicines. Here are details:

RE-sensitizing With Supraphysiologic Testosterone to Overcome REsistant (The RESTORE Study)

Posted By : BillyBob@388 - 3/20/2014 8:22 AM
PSA3DOT7 said...
I have low testosterone and low PSA, and had a Gleason 9. I'm back on T supplementation after my RRP. Dr Mulhall makes a good case for T replacement therapy post RRP in men with low testosterone! I've been on T for a awhile post RRP and my latest PSA < .01 (see below)


My total and free testosterone, at least in recent years, has run at very low normal levels, just above what would be considered below the normal range. In fact, it was while seeking possible testosterone therapy that I got the PSA done which ended up with me diagnosed with a G9 PC.

My friend here in town, who had his RALP a few years before me, had for many years before that suffered with way below normal T, although he had also been treated with injections for a couple of years. Although probably he had low T for many years before he got any T therapy. So that is 2 I know of, plus PSA3DOT7, or a rather small study. LOL! But, kind of makes me wonder. ( BTW, my friend who had the RALP: he has been back on T injections pretty much ever since his RALP. He insists that he can not make it otherwise, can't stand a low T. So far, so good)

Dreamerboy, according to Abraham Morgentaler MD, as has been pointed out, rather than it being like he was taught- i.e. T is like feeding a hungry tumor, it is more like a drink for a thirsty tumor. IOW, we can keep eating long past when we are no longer hungry, and then repeat again shortly with another piece of dessert or snacking in front of the TV, as our waist lines attest. But most of us will not normally drink more water than is needed to quench our thirst, no matter how much water is available. The body can only make use of so much water, unlike food calories which can be stored.

Ans it seems that it takes very little T to give PC cells all the "water" they need to grow. So being low won't do much good, rather you need to be close to zero, and very few low T men are anywhere near zero. And some are thinking once you get very much above zero heading for low normal, you are already passing the point where the PC cells can not use any additional T, and doubling it from that low point( whatever exactly that low point actually is) will make no difference.

Because his peers told him he better stop giving T because he was going to feed a hidden PC, Morgentaler started doing PBx on men before he would administer T. As the years went on and the numbers grew, he found that a higher % of men in his studies, who had low T, had PC than the groups who had normal or high T. Worse, the men with the lowest T had an increased risk of more aggressive PC than those with higher T. I guess if I had been one of his patients, I would have fit into that category. At least based on Morgentaler's studies and theories, which are probably still not accepted by most Uros. But maybe if I had got that T replacement therapy like I started to 10 or 15 years ago, I would be in a better condition now?

Because normal or slightly higher T levels are a positive in so many things related to men's health, I wish some big studies would be done to clear this up. Because it might be, maybe, that those of us trying to survive PC, who also run on the low T side, would do better if we got out T on up to 700 or so. IOW, maybe we would be better of, PC wise, either with zero T or a fairly high T, but not a low T. One extreme or another, maybe? I wish we could find out for sure like right now!
PSA 9.1 102813, 10.8 ~112013, drop to 8.1 on 021214 after VitC/VitK3 50 to 1 for about 2 months(coincidence?).
Bx on 112013 at age 64 yrs 11 months, with 5 of 12 pos with one G9, 1 PNI, T2B.
RALP with lymph nodes at Vanderbilt 021914. (nodes clear, but some seminal ves. involvement, still G9, thinks he got probably got it all by cutting wide )
Foley out 030314
JP drain out on 031014

Posted By : Tall Allen - 3/20/2014 10:57 AM
BillyBob,

My guess is that if you asked Uros at Vanderbilt, or other major tertiary care facilities, they would be amenable to TRT. They have seen the studies, and keep up with evidence-based medicine. The Uros in community practice - probably less so. There are many men post-treatment for PC who are on TRT these days, 5 guys in my PC support groups alone. There is a lot of suggestive evidence that low testosterone is associated with PC and may cause it, which is what led to the new clinical trial I posted above.

Your doctors will probably want to make sure that your PSA is undetectable and remains that way for awhile before they start you on TRT. There's no point supplementing T if there's any indication that they might have to start you on ADT anytime soon.

- Allen

Posted By : BillyBob@388 - 3/20/2014 12:51 PM
Tall Allen said...
BillyBob,

My guess is that if you asked Uros at Vanderbilt, or other major tertiary care facilities, they would be amenable to TRT. They have seen the studies, and keep up with evidence-based medicine. The Uros in community practice - probably less so. There are many men post-treatment for PC who are on TRT these days, 5 guys in my PC support groups alone. There is a lot of suggestive evidence that low testosterone is associated with PC and may cause it, which is what led to the new clinical trial I posted above.

Your doctors will probably want to make sure that your PSA is undetectable and remains that way for awhile before they start you on TRT. There's no point supplementing T if there's any indication that they might have to start you on ADT anytime soon.

- Allen


Thx, good points!
PSA 9.1 102813, 10.8 ~112013, drop to 8.1 on 021214 after VitC/VitK3 50 to 1 for about 2 months(coincidence?).
Bx on 112013 at age 64 yrs 11 months, with 5 of 12 pos with one G9, 1 PNI, T2B.
RALP with lymph nodes at Vanderbilt 021914. (nodes clear, but some seminal ves. involvement, still G9, thinks he got probably got it all by cutting wide )
Foley out 030314
JP drain out on 031014

Posted By : tarhoosier - 3/20/2014 1:57 PM
Perhaps relevant: I was diagnosed at age 58 a month after I asked for a T test at my GP. I had a period of reduced sexual energy. Result-T=370. I have no idea what it had been at any previous time. After diagnosis it was suggested to me that some of the native T is used by prostate cancer cells for growth, more so than healthy cells, thus leading to a lower T level in such men. I had large volume G9 cancer, 11/12+ at biopsy.
So perhaps the cancer causes the low(er) T, not t'other way round.

Post Edited (tarhoosier) : 3/20/2014 2:00:16 PM (GMT-6)


Posted By : BillyBob@388 - 3/20/2014 2:30 PM
tarhoosier said...
Perhaps relevant: I was diagnosed at age 58 a month after I asked for a T test at my GP. I had a period of reduced sexual energy. Result-T=370. I have no idea what it had been at any previous time. After diagnosis it was suggested to me that some of the native T is used by prostate cancer cells for growth, more so than healthy cells, thus leading to a lower T level in such men. I had large volume G9 cancer, 11/12+ at biopsy.
So perhaps the cancer causes the low(er) T, not t'other way round.


Could be. I posted a couple of links in another T thread here where that was the conclusion of the study: that the aggressive cancers caused the low T. I think they came to that conclusion because estrogen(estradiol) was decreased also, both only in the men with aggressive PC. Coincidentally or not, I am a G9 and always ran low normal for both total and free T as well as estrogen, low E even for a man. It just so happens that I had been checking mine 3 times over a decade, and it was always that result. I wish I had kept a closer watch on my PSAs while I was at it, or at least paid more attention to the rise!
PSA 9.1 102813, 10.8 ~112013, drop to 8.1 on 021214 after VitC/VitK3 50 to 1 for about 2 months(coincidence?).
Bx on 112013 at age 64 yrs 11 months, with 5 of 12 pos with one G9, 1 PNI, T2B.
RALP with lymph nodes at Vanderbilt 021914. (nodes clear, but some seminal ves. involvement, still G9, thinks he got probably got it all by cutting wide )
Foley out 030314
JP drain out on 031014

Posted By : redheadskier - 4/7/2014 8:24 AM
Tall Allen,
Do you have any thoughts on how this would apply to men with bone mets?

Thanks,
Lisa
Husband Frank, age 59
9/10/13 PSA 9.2 tested at GP, follow-up appt. w/urologist, his opinion retest 3-4 months
1/13/14 PSA 15.8
1/30/14 BX G4+4, changed to 4+5
2/3/14 CT Scan negative, relook 2/20/14 mets
2/12/14 Appt. with radiation oncologist, ordered a bone scan
2/20/14 Bone Scan 2/25/14 Bone Biopsy
2/27/14 T1cNXM1b or Stage IV D2
3/4/14PSA 17.4 Began bicalutamide 3/18/14 Eligard/Zometa

Posted By : Tall Allen - 4/7/2014 8:42 AM
Lisa,
When they say the trial is for men who have metastatic castration-resistant PC (mCRPC) they mean bone mets (M1). In this clinical trial, they're looking for men whose metastatic disease has progressed (either PSA continues to climb or there is radiological evidence of continued spread) while on Zytiga or Xtandi.

- Allen

Posted By : redheadskier - 4/7/2014 1:27 PM
Thanks, Lisa
Husband Frank, age 59
9/10/13 PSA 9.2 tested at GP, follow-up appt. w/urologist, his opinion retest 3-4 months
1/13/14 PSA 15.8
1/30/14 BX G4+4, changed to 4+5
2/3/14 CT Scan negative, relook 2/20/14 mets
2/12/14 Appt. with radiation oncologist, ordered a bone scan
2/20/14 Bone Scan 2/25/14 Bone Biopsy
2/27/14 T1cNXM1b or Stage IV D2
3/4/14PSA 17.4 Began bicalutamide 3/18/14 Eligard/Zometa

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