Ever since Huggins discovered that castration offered palliation for men with PCa, albeit temporary, there has been a belief that testosterone [T[ acts like gasoline on a fire. A number of study papers have appeared over the past 15 years that have shown that low T is a risk factor for more serious PCa. However, that has had little impact on the gasoline hypothesis.
If T is gasoline, what is dihydrotestosterone [DHT] ten times more powerful than T?
When I was diagnosed 16 years ago, I quickly discovered that the androgen receptor [AR] was mutated after ADT, but was generally "wild type" at diagnosis.
At that time, there was great interest in the new estrogen receptor [ER], ERbeta. Most of the research had been done in breast cancer [BCa], but ERbeta had been found in prostatic epithelial cells. Interestingly, ERbeta was downregulated in PCa cells - an early event. Also, the classic ER - now renamed ERalpha, which was normally confined to the stroma, began to appear in PCa cells. BCa studies had concluded that ERalpha was growth-promoting & that ERbeta opposed growth & protected against proliferation.
I had immediately failed RP & salvage radiation, which left Lupron, Taxotere & an early death - so I thought I'd try T. My PSA remained steady for 6 months (until I injected B12).
I learned that when T bonded with AR, it did not mean that cell division would occur. There were AR coactivators & corepressors. The AR & the vitamin D receptor [VDR] had interactions & so on. A year or two later, I read about 3beta-adiol.
When 5alpha-reductase acts on T to produce DHT, this kicks off production of an enzyme to clear DHT from the cell. DHT has a very narrow window in which to promote growth. One of the metabolites of DHT, surprisingly, is an estrogen - 3beta-adiol - which happens to be the natural ligand for ERbeta. When 3beta-adiol binds to ERbeta there is resistance to further growth.
So, by allowing DHT production, I was also allowing ERbeta to prevent proliferation. DHT is an intrinsic factor in growth regulation.
This was good until presumably the cancer suppressed ERbeta completely & DHT was no longer my friend. At that point, I started to use Avodart to inhibit 5alpha-reductase.
So the above is my attempt to rehabilitate DHT as one of the good players.
***
In the new Swedish study:
"Contradictory to what one might assume given the androgenic potency of dihydrotestosterone (DHT) there are indications that high DHT levels protect from prostate cancer. We want to determine whether there is a long-term association between baseline levels of DHT and death from prostate cancer."
They followed 65 cases & 130 controls from 1988/9 for 30 years
"High DHT levels were positively correlated to a lower risk for prostate cancer death in the entire cohort: HR = 0.44 ..."
"DHT is negatively associated with long-term prostate cancer death regardless of clinical presentation at time of inclusion."
. 2020 May 5. doi: 10.1002/pros.23991. Online ahead of print.
Association Between Dihydrotestosterone and Long-Term Risk for Prostate Cancer Mortality: A Prospective Cohort Study
Per-Olof Lundgren 1 , Anders Kjellman 1 , Ulf Norming 2 , Ove Gustafsson 1
Affiliations collapse
Affiliations
1 Department of Clinical Science, Intervention, and Technology, Karolinska Institute and Karolinska University Hospital, Stockholm, Sweden.
2 Department of Clinical Science and Education, Södersjukhuset, Stockholm, Sweden.
PMID: 32368817 DOI: 10.1002/pros.23991
Abstract
Background: The androgen metabolism plays an important role in the progression of prostate cancer. Contradictory to what one might assume given the androgenic potency of dihydrotestosterone (DHT) there are indications that high DHT levels protect from prostate cancer. We want to determine whether there is a long-term association between baseline levels of DHT and death from prostate cancer.
Method: During the years 1988 and 1989, 1782 men out of 2400 invited were screened for prostate cancer. The invited men were randomly selected from a background population of more than 27 000 men. Serum levels of DHT were analyzed for all 65 men diagnosed in the trial and 130 controls from the same cohort without any signs of prostate cancer. In this study we evaluate outcomes for the whole cohort (n = 195), the men without clinical signs of prostate cancer at beginning of follow up (n = 130) and men with screening detected cancer (n = 65). The cohort was followed up after 30 years and data from the Swedish Cause of Death Registry and the Swedish Cancer Registry were extracted. Hazard ratios (HRs) were calculated using Cox regression models.
Result: High DHT levels were positively correlated to a lower risk for prostate cancer death in the entire cohort: HR = 0.44 (0.25-0.77 95% confidence interval [CI]). The positive correlation remained significant for the subgroup analysis. HR for the men enrolled in the study without any clinical signs of prostate cancer was 0.25 (0.07-0.88 95% CI) and for the men with a prostate cancer diagnosis at time of inclusion: HR = 0.50 (0.26-0.94 95% CI).
Conclusion: DHT is negatively associated with long-term prostate cancer death regardless of clinical presentation at time of inclusion.
How does one increase their levels of dihydrotestosterone?
I had RP 12/2018 and was diagnosed with G4+5, lymph node positive, seminal vessicle and bladder wall invasive PrC. A few months later I did ADT for 5 months (via estrogen patches). Then a month of casadex and dutasteride. Then started high t (400mg/wk of cyp). Along with an AI (estradiol is 18 pg/ml). Dutasteride and finasteride to lower DHT (last measured 12/2019 and it was 31.8 ng/dl). Cabergoline to lower prolactin (now 3.2 ng/ml).
If you were in my particular state, what would you do?
Thanks for the account of your own strategy. My own path has had some similarities and some differences. Dx 2002, adjuvenant RP 2002, watch and wait, intermittent zolodex to continuous, then bicalutamide, then BAT. Its clear we know bugger-all about the whole T, DHT, E2 (and who knows how many intermediaries) cycle. We are learning as we go but its clear to me that hiT therapies are part of the management toolbox.
I like that, but how to increase DHT? I am not on any form of hormone treatment at the moment, and deprivation has never been my preference.... Increasing DHT grabs my attention.... Cheers
Way above my pay grade and some clarification is needed.... but I think the study Patrick refers to is suggesting (indicating?) that higher DHT is protective against getting PCa and/or suggests lower mortality once you get it. That does not necessarily mean it is a good thing once you have PCa and a BCR after treatments. My understanding is that for most of us here who have/had PCa and multiple treatments, that it is better to suppress DHT rather than increase.
Yeah.... I'm confused by that too, but the study seems to show benefit with or without P cancer. Buggered if I know the answer... The infamous Snuffy Myers seems to be of the opposite view. So much for specialists knowing the answer... Cheers
I’ve used the Snuffy Myers regimen which includes dutasteride to prevent the production of DHT for the past 6 years. So far so good in the treatment of Stage 4, G9 PCa. Non of my current oncologists have had any issue with it including Dr. Sartor who picked up my care after Snuffys retirement. I’ll stay the course, if it works don’t fix it.
Patches help with Lupron side effects, I used to get severe hot flashes every hour, it’s almost eliminated them. They also promote bone health and probably have some anti cancer properties. Xtandi causes fatigue, cognitive issues, headaches, etc. and you have to keep an eye on BP if that’s an issue with you. That’s been my experience, some guys have an easier time, others worse. I reduced my dose on the advice of doctor Sartor to help with side effects which seem to be cumulative. I’ve been taking 80mg for a couple of years now and it helped make side effects more tolerable. Xtandi may be starting to lose its punch however after over 5 years, I’ve started getting flickers of PSA after being undetectable for a long time.
OK thanks for the info Ed. I hope it all keeps working for you. Keep praying, fishing and doing yoga type exercise and relaxation stuff.
I was just about to ask my family doctor to add Avodart to the works but now I'm puzzled. I'd read Snuffy Myers recommendation but this implies the opposite. I think I'll hold off adding anything to what I'm already taking.
Please note that this study was for DHT levels from a population before their diagnosis in the subsequent period. It was not a result of their therapies after diagnosis which is not described. So it does not address implications for raising or lowering DHT levels in the treatment of advanced PC.
Thanks for your analysis on this very complicated aspect and implications for the ERbeta and DHT. I Need to study this more.
I think that some clarification is needed, based on a few comments above.
The men who were diagnosed at the time that the DHT test was done had a 50% less chance of dying from PCa if they were in the high DHT group. This would have included men who subsequently had ADT & ~zero DHT. Having high DHT at diagnosis means that there is a significant lower risk of lethal disease.
For the men who did not have PCa 30 years earlier, some would go on to develop the disease. But there was a 75% less chance of death due to PCa if the DHT was high at the start of the study.
Overall, the best advice to young men would be to check DHT levels. I'm guessing that normal-high testosterone (>700 ng.dL, say) & normal estradiol (20-30 pg/mL) would ensure that.
For men with low DHT at diagnosis, who are treatment-naive, would it be worth raising DHT? I believe so. But for heavily treated men, the window for benefit has long closed & one should consider Avodart.
Well, I feel its way to late to worry about my initial dhT levels at diagnosis, but while taking Zytiga for the 8 months that it suppressed Psa, and slowed Pca growth, ( but not stop it ), I took avodart for awhile and there was no measurable effect at all.
Zytiga interferes with adrenal gland operation and hence predisonolone is taken at 10mg daily to replace what is made by adrenal gland, but I had heart rate problems with Zytiga, and it was distressing at times. Once at the start of a 85km cycle ride with a group men in mid 2017, I went up this long hill in first 10km of ride, and stopped at traffic lights. Heart kept pounding away and I had strange sensation like pulsating sciatica up my spine. it subsided after 20 seconds, and I completed the ride.
But the problem re-occurred again and more often as summer began, so I quit my group to cycle alone in early mornings. I also added more potassium from english spinach and button mushrooms to my diet, and problem lessened, despite normal potassium levels in blood tests. When I quit Zytiga these HR problems all went away after a few months.
Patrick, I recall a previous discussion on this site that mentioned something about a lower free-testosterone (post-treatment, on ADT) level being correlated with longer lifespan. Do you recall this? I just got my free testosterone result today for the first time so I want to interpret whether it might be encouraging or discouraging.
I also was a dr Myers patient and am continuing my avadort treatment for controlling DHT . Dr drake agreed to continuing , but once made the comment “ how do you know that hi DHT isn’t your friend?” — in the light of my staying in the supra T level with Xtandi and getting good results.
Is this dual nature of DHT due time to the time dependent changes in things like ERbeta vs ERalpha etc?
Thought this was an area of interest to Nalakrats; has he reacted to this report?
He does a pretty deep dive on the ERalpha and ERbeta. I still have trouble following it all, but Dr. Myers' approach seems to be consistent with Friedman - that controlling DHT once you have PCa - is advised.
Well, as I indicated, DHT was my friend until it wasn't. So I had to smile when I read Dr. Drake's comment.
{It was my friend when the PSADT was > 2 years, & decidedly not when the PSADT sank to 3 months.}
In my "clarification" post, above, I distinguish between treatment-naive PCa (when DHT is still a friend) & heavily-treated PCa (when DHT is no longer friendly). Somewhere in between, the DHT...3beta-adiol... ERbeta pathway no longer functions. Probably because the cancer has totally down-regulated ER-beta.
Somewhere in the literature there is info on upregulating ERbeta, but that's not likely to occur once we go down the ADT path, IMO.
Nalakrats is relaxing while the group is on a COVID holiday.
Dr Friedman’s book was interesting. One other thing he pointed out , I believe, is if you doing testosterone replacement to be sure to use bio identical human testosterone . A bit off the subject but potentially useful
There's mountain of incomprehensible info in your post, or else I am very dumb.
I was diagnosed Gleason 9, inoperable, Psa 6, 2009, age 62.
I think many mets were present, all too small to be seen in scans.
I always thought that ADT causes testosterone ( T ) production in testicles, but while on ADT with Luron, Lucrin etc, a small amount of di-hydrotestosterone ( dhT ) is still made by adrenal glands which is enough to keep Pca progressing slowly at first, and when ADT fails as it always does, the Pca is generating its own dhT so it rapidly grows, and drugs such as Cosadex ( bicalutamide ), Xtandi enzalutamide, Zytiga arbiterone, are given to add about a year to suppression of Pca growth speed, by means of interfering with dhT productions.
Plain ADT lasted 6 years but each of the 3 add-on drugs all worked for less than a year each. Chemo failed, and only Lu177 had any big effect at reducing the Pca and thus reducing Psa and prolonging QOL.
But its a year since last Lu177 shot, and Psa is rising again rapidly, and I may have to have repeat shots of Lu177, maybe with a little Ac225 added, depending on what next PsMa Ga68 scans tell the doctors.
Where does dhT fit into this history of Pca?
I am continuing with ADT, which I suspect is having zero effect now, and if stopped, my balls would not turn back on to make T so could I just stop ADT and take T pills to boost T levels to normal?
I know that would have me feel a lot better, and younger, even though I get older, for awhile longer.
T and dhT has always seemed to be my enemy, so I thought it best I maintained low levels of both, and so did all the doctors.
I did have two pauses in ADT during the 6 years of T suppression, and during on both pauses my Psa shot up like a rocket. I'd have died in 2014 had it not been for ADT. And if Lu177 had not worked, more chemo probably would have had no effect, and I'd be in palliative care now. Instead, I am cycling about 200km a week, and glad to be alive.
The study found that men with high levels of DHT at diagnosis had reduced risk of PCa-death over the following 30 years.
If you start out with high DHT you do better - even if you receive ADT (which lowers DHT to nothing).
In fact, there is another study where:
"Twenty-three patients were determined to have CRPC. These CRPC patients had a significantly high concentration of tissue T ... and low concentration of tissue 5α-dihydrotestosterone (DHT) .., resulting in a higher tissue T/DHT ratio" [1]
You say that "Plain ADT lasted 6 years", which suggests that your DHT might have been high at diagnosis.
I see. Well, not one doctor mentioned DHT during my time with Pca.
I did meet a man who did say he had a blood test to find out what his DHT level was and test took time and was expensive, but it yielded no useful info and his time on ADT after a failed RP lasted only 3 months before it failed, and salvation IMRT to RP site failed, and when Cosadex was added his Psa went from 7 to 40, so Cosadex seemed to feed his Pca growth. He began to want Lu177 after chemo failure seemed apparent after 4 shots, but instead soldiered on to have 10 chemo shots, and Psa just went up, and methinks some mutated. He died in hospital with un-treatable Pca mutated mets in his liver, despite having 10 chemo shots. After chemo, he had analysis to find he was Brca2 positive, and so he had PARP inhibitor, and Psa went from 40 to 432. Basically, nothing worked to stop his Pca. He lasted 3 years only after diagnosis, before he turned 60, with two teenage kids and a wife of 50.
When I saw what happened to my friend, I kind of lost confidence in much of the gee-wiz analysis and decision making by doctors based on expensive analysis.
I can only guess my DHT might have been high at diagnosis, but back in 2009, it was an entirely irrelevant factoid, and doctors were addicted to simple mainstream protocol for Pca treatment, and if a man failed all manner of ADT + add on drugs, then he went to chemo with Docetaxel with a high failure rate. As years went by, Cabazitaxel was next chemo invented that might be tried, but I read all about it and thought is hardly any better than Docetaxel. Carboplatin, a platinum based chemo was next rung on the ladder, and probably has The Worst side effects, but when I had my chemo, there was a 4th type of chemo I was not told about. All this is often quite useless against some Pca.
But Lu177 was not useless for me.
This only works well if there is high uptake of Ga68 in PsMa scans. Even then, 30% of men don't get a fix with Lu177 because they have a large % of Pca that does not uptake Ga68, and does not appear in PET part of PsMa scans.
The trouble with research findings and probabilities about Pca is that its so easy to find yourself in the 1 in 20 who are supposed to get Pca at 60, then quite remarkable that you find yourself in a smaller group where your Pca is found to be inoperable after docs open you up, and the prevention measures you have followed for previous 10 years of annual Psa tests have all been in vain.
What needs to happen is to have Medicare fund PG removal well before Psa gets to 3.0, when full examination should be compulsory. Even where no Pca has been found, a man should be able to insist on PG removal at Psa of 3, especially if there was a family history of cancers. The cost to Medicare of an early RP is maybe 1/20 of the costs of a 10 year long fight.
But my cousin of 75 has Psa of 1.0, and has some mild swelling of PG, and no sign of Pca, and Psa has been constant for years. It is possible the marriage of his father to his mother created DNA that didn't lead to Pca, wheras my father's marriage to my mother did not make DNA change that prevented Pca, Brca, Oa. My cousin is overweight and has other problems, and so if a man does not get cancer he has other things to contend with.
I have tired my best to successfully avoid the weight problem and "other things".
What would my survival time be had my DHT levels been found early? Its way too late to ever know.
I could be dead in a year. It depends on what my Pca does, and if I am lucky enough to get treatment that works for another year. Then in a year after that, I'll be saying I'll be lucky to last another year, and so on.
Our medical system in Australia can't be that bad it lets too many die too early.
While other countries have dreadful problems with C19, we have lost only 97 ppl to this virus. There has been a big lifestyle change by many ppl to being more alone for most of their time, something I mastered at 30, in 1979. Its unfortunate that many are now unemployed.
But most had jobs which were not essential for our species to exist.
Instead of buying lunch at a take-away cafe for$20, I make my own for $5 at home. Did I ever need the cafe habit? Well, when I was poor I sure never needed it. I can afford it now, but would save about$100 a week just by spending 10 minutes a day making my own lunch.
Meanwhile, its a beautiful fine autumn day here, and I'll be in my shed soon to test an electronics circuit I made yesterday. Very nice in my shed, nobody to annoy me and quiet, and I can concentrate without the unrelenting distractions of having to partake in a pile of modern life I never ever found very enjoyable, herded together to make a profit for a boss. I hope tomorrow is also a good day, and I'll go for long bike ride.
I found HU this past week, and I have been looking around, and learning. I’m 73 yrs old, and I began my PCa journey in 7/19 with the MRI guided biopsy followed by a RARP both at MGH in Boston, MA. I’m GS 9. Post surgical pathology revealed no LN nor SV PCa present, but two spots in the PH bed margins. Pré -op bone scan was negative as was blood tests. Post-op SEs have been minimal. My QOL is fine but no sexual function. I have been a vegan for the past 5 yrs. after diagnosis of coronary artery disease in 11/15. My post-op PSA was undetectable in 12/19, and in 6/20, I’ll get the ultra sensitive PSA test to assess my situation. I expect BCR eventually, so I’m trying to learn about future PCa maintenance. Any suggestions towards an educational path? Your guidance would be appreciated.
If your Psa tests give Psa below 0.01, and scans don't show any Pca, then there is not much to worry about for now, until Psa rises and scans show where Pca has appeared.
If all you had was PG removal operation, maybe you are doing well, but Gleason 9 very often means there is some Pca spread somewhere, and sooner or later it will grow big enough to be seen in scans and to make Psa rise.
There is not much that can prevent or eliminate this tiny amount of Pca post RP if it is present, and your situation does not mean you ought to start ADT which will probably suppress any mets you have, but not kill them. I have known men whose Psa went to below 0.01, so they were said to have "Pca undetectble" but never were considered to have remission, where ALL Pca in their body just was not present, and that after 10 years without any further treatment of any kind, Pca did not return. I did meant one who had Gleason 5, low Psa at diagnosis, has 70 grey EBRT, ans 2 years of ADT, and that was that, and 10 years later he told me that he had the same treatment that I had initially and he was fine, so therefore I would be fine, but I had Gleason 9, inoperable in 2010, and I bet very many microscopic size mets began in many places, and none of these began to show up in PsMa Ga68 scans until 2016.
But Psa after my initial treatment of ABRT + ADT never went below 0.08. When I stopped the ADT in late 2012, Psa went back up to 8.0 within 6 months in 2013, so I had to re-start ADT, thn get more RT and other drugs to suppress Pca. But it still grew during that time, and when all anti hormone drugs failed I had chemo which failed and only Lu177 was able to kill a big % of all Pca in countless mets I had in lymph nodes and bones.
I've never been worried by complete extermination of sexual function because I have lived alone for countless years and all possible women of the right age for me to date have all "dried up" with menopause, and most are quite allergic to anything male, except tradesmen who have to keep repairing things in their old houses, or doctors, who manage to keep them alive longer.
I'd like a partner, and have a sexless relationship, but it is just never going to happen. Nearest thing to being married for last 40 years was to rent out 2 rooms in my house to females who I found had very limited interest in sex for 101 reasons, but otherwise were responsible types of ppl I could get along with on day to day basis, without the silly expectations that sexual entanglement brings. The idea of being able to perform sexually at 72 is absurd; almost nobody can go near how they did things at 40 or younger; and I know there are exceptions, but often they are lying about what they say they are doing together. We get old, and sex is a thing for young ppl, and its a bit like riding a bicycle; you never forget how to, but at 42 I could ride 300km in a day, and average speed was 28kph, but now at 72 I would struggle to ride more than 100km, and my speed would be 21kph. But I can do a good 70km 3 times a week, and that's a much better achievement than having "Old Person sex" 3 times a week.
I can't find any females at all interested in cycling like I do. They would maybe do 20km max at such slow speed I would fall asleep if I rode with them. Once in a blue moon, a young woman overtakes me on my rides around my town, and its been years since any man over 65 has over taken me. I overtake quite a few ppl now riding E-bikes, with a 100W electric motor to assist them because they have long list of medical conditions that prevent them ever getting fit as may be possible.
My Psa is rising, and yesterday I had another test, before I see my oncologist next thursday, and I bet Psa > 5, and I will ask him to refer me again to the doc giving Lu177 to I can have more of that therapy because it probably will work to give me more time with good QOL without worry that I'll die in a year's time. I spent usd $27,000, to stay alive last year, with good QOL, so I may have to spend more to stay alive longer, and stop Pca growing in my bones. Once the bone mets become big enough, a man can have micro-fractures of bones, and that means pain, and his bones are starting to crumble to bits. Small mets in bones are quite tolerable, but once big enough, a man is in permanent trouble.
I've lasted more than 10 years since a "high risk Gleason-9 diagnosis" and QOL has been good. I want more years alive, and well.
If you are capable of reading genuinely scholarly articles posted online about Pca, then you will know how to better manage what may be a chronic disease that takes 20 years to kill you. I had two male cousins of mine, sons of my father's sister, and both had bad dementia by 70, and one got Pca, and his heroically enduring wife arranged for brachy therapy, BT, and that seemed to stop his Pca, but his dementia killed him.
He could not have easily coped to prolong his life much had he been alone after 70 but I seem to not have any impairment that stops me seeking and getting best treatment possible, so my luck is good. So you won't know how you will go in future because it just has not happened yet.
Thanks for the detailed and thoughtful reply. Your analysis of my present situation sounds correct. My post RARP pathology report staged me as pTa3NO with 4+5= G9 - High Risk. So, now, I wait and study. I split my time between New England and FL, so I see a urologist at both ends of the country.
My FL urologist's advice thus far was to avoid radiation and if necessary use ADT if my PSA begins to rise and BCR seems apparent. This urologist is a retired surgeon who performed RARP for twenty plus years at a larger medical center in FL and is now teaching in semi-retirement at UF Shands.
His comment concerning the SEs of radiation was that he'd never met a radiologist who would not radiate anything if it would stand still for a few moments, so he has always counseled his patients towards ADT. Interesting? His option is that with ADT one can stop the treatment, but with radiation, once the treatment is done, the SEs are with the patient forever.
Presently, in the states, obtaining a PSMA scan is difficult. Being 73, my care has thus far been paid by Medicare and by my secondary insurer that covers the 20% which Medicare will not pay. Since PSMA scans are still under review by the US FDA, and there are clinical studies occurring in several locations, I may be able to obtain a scan through a clinical study if I fit into their guidelines. There's a few cancer centers in the US where one can obtain a PSMA and pay for the service oneself. I'm willing to do this if it fits into my treatment plan.
The scan is not obtainable at MGH where my RARP was done in 9/19. When the BCR occurs, I'll need to seek some guidance from my MO and RO at MGH and decide what course of treatment to pursue. I've met both the MO and the RO just once during my initial PCa team gathering at MGH. I selected Dr. Douglas Dahl for the surgery option, so I have not had any further contact with either the RO or the MO who were part of the MGH evaluation team. Dahl did a great job, and I had no recovery issues.
I agree with your observations about the sexual activities of men in their seventies and beyond. I was diagnosed with coronary artery disease in 11/15 and recommended for quintuple coronary by-pass surgery. I cancelled the surgery two days before it was to be done and sought additional opinions. I felt extremely rushed by the cardiac team I was working with at the time. From a second and a third option, I learned that I could probably avoid the by-pass surgery if I chose to alter my diet and lifestyle.
My wife and I switched to a plant based diet, I dropped fifty pounds, reduced my cholesterol and blood pressure significantly and brought my cardiac functioning back to normal and stable functioning. What I learned was that when cardiac calcium build-up begins in one's vascular system, that plaque adheres to the vascular walls everywhere - not just in one's heart.
One of the first places for calcium plaque to clog the flow of blood is through one's plumbing is within one's penis. ED is an early indicator of coronary artery disease. It's the canary in the cardiac coal mine. Looking back now, when a man begins asking his primary care doc for meds to help relieve ED, that should be when the primary care doc sends his patient for a coronary calcium scan to see if there is plaque building up with the patient's vascular system. Unfortunately, this doesn't happen in many situations. If it did, they'd be fewer heart attacks and men would learn that they are clogging up their penis' vascular supply with the crap that they've been putting in their mouths.
I relate this to you in connection with my PCa because I was already a victim of ED when the PCa was diagnosed, so the decision not to spare the vascular bundle within my prostate gland during my surgery wasn't a difficult decision to make. I'd already been dealing with ED for about ten years. My wife had been suffering with virginal dryness because of menopause, so our sex life had been sporadic and difficult for several years. We talked about the PCa surgery decision, and we opted for QOL instead of a youthful macho fantasy.
Like you, I believe that most men in their seventies and beyond are reluctant to admit that their sexual activity has been reduced or is non-existent, and they cling to their macho image of themselves. When I've talked with close friends about this, most try to avoid the issue unless they are realists and have undergone PCa treatments.
So, this is where I am now, and I hope you're able to get some relief and additional QOL time with the Lupron 177. If I can manage to get fifteen to twenty years with the management of my PCa using whatever treatments are necessary that don't make my life miserable, I'll be a happy man. Enjoy your time while you can still get on your bike and enjoy the rides.
You are right about radiation side effects (SE), they can be dreadful, but in my case with a total of 101Grey of high power Xrays to PG, SE on bowels did not last long and I am still continent. To kill Pca in PG, sometimes 150Grey is needed, and that's when SE with Xrays become unfeasable. Brachtherapy, BT, is a good option, but the nerves in area will suffer. Much better now is Lu177, if your Pca makes a good image with PsMa Ga68 scan, because Lu177 is well targeted by a ligand chemical that makes Lu177 gather at met sites where it radiates with alpha or beta particles that travel only 2mm in flesh, so its more accurate than a surgeon.
I hear you loud and clear about change of lifestyle instead of op for bypass surgery.
At 62 I was cycling real fast, with Rodger functioning like he was 25, but finding a female partner who still worked OK was impossible.
My vascular system is just fine, but Rodger clogged up with fibroids after long term effects of ADT plus EBRT effects on nerves. ADT cause the most damage, and after a certain number of years having low testosterone damages Rodger so bad he does not recover. I don't care about being Macho Man, It is more about being Sir Vivor, and if anyone thinks I am weak, then they can see how they go cycling will me across town and round about for 3 hours at a time.
The Lu177 is a nuclide, and I suggest you read up about online, under "theranostic Pca treatments."
Thanks for the clear coherent response, and for the heads-up about the theranostic PCa treatments. I recall reading about nano-medicine, but I had no idea that PSMA-PET/CT with theranostic treatments were this far along.
It's doubtful that I'd fly west to your country for treatment, but the UK or Germany is possible, and it makes perfect sense to me that when the eventual BCR occurs for me that I get the PSMA-PET/CT scan followed by treatments of any identified micro mets rather than becoming involved in ADT or salvage radiation.
What will be interesting is how my UO, MO and RO react when I explain to them that I want to go in the theranostic PCa direction instead of the SOC that the NUUN defines. I need to investigate how long one waits for the PSA number to increase before exploring an initial PSMA-PET/CT scan.
Sorry to hear that Rodger went into retirement during your PCa treatments. Sounds like his retirement happened about the same time that Hobart retired due to my CAD (coronary artery disease). It happens to all guys, and only a few of us admit the end of that era. For me, it made the decision about not sparing the nerve bundle during RP surgery a quick decision. I sent Hobart for counseling to the HR department to explain his retirement options.
Next month I'll get the ultrasensitive PSA test, and I'll find out if my BCR journey is about to begin or if I have a reprieve for awhile. Take care of yourself, and keep me posted on how your treatments are progressing. Thanks for your guidance and knowledge sharing.
My Mr Rodger is a drain pipe only these daze. Not just retired, but any hopes for any relationship with any Ms Fanny have been exterminated. I like a bicycle ride - better than sex.
What is least said sentence in all languages of the World?
"Jus' you lie down 'ere luvvy, it won't cost yer anyfink"
your doc give you the referral for another Lu177 treatment?
I go in about two weeks for my nine month PSA and T test, so I’ll let you know how that turns out.
Looking around this forum and at the Inspire one definitely opens up the PCa treatment world so I’m acquiring a greater view of the wide universe of PCa treatment options. It does make one feel like being in a game show where the host keeps saying to the contestant, “Would you like door number one, two or three?” And the contestant has no idea what’s behind those doors until he has opened one of them and stepped through. Then the reaction may be, “Oh shit, this was a mistake”, but it is often too late.
I get my next Psa test tomorrow, and see my onco about options next Thursday.
I'll let everyone know.
Cancer doctors often try to tell patients something will work, so you have the treatment they say you need, but it does not work. But my onco said to me before I began chemo that it probably would not work. And when it didn't, he happily referred me to docs giving Lu177, who preferred to be less certain about an outcome, but just stated that 70% of men who get Lu177 after PsMa Ga68 scans show they should get a benefit, do get that benefit, ie, a year later their Psa is a lot lower than when they begin Lu177. They didn't promise any cure or remission, and said after 4 shots said I might need more Lu177.
PeterMac Hospital in Melbourne have said men who get a fairly good response with 4 shots of Lu177 may have two lots of repeat shots and get up to 40 months more life, ie, 3.3 years of life extension with few side effects. I don't have scan report yet and docs have not yet looked at it, but I'll know more later this week, and maybe I end up going to Peter Mac in Melbourne instead of to TA in Sydney.
Remember the 1960s pop song Green Door, where a male crooned the lyrics "What's behind the Green Door ?......" Maybe the song expected a nice ready for action blonde to be behind the green door.
Few have a green door on their houses now, and once you open a green door where there is one, you are likely to be greeted by a skinny vegan who is a green warrior trying to save the environment while most ppl completely ignore all such issues.
It wood be pointless for me to knock on a pink door, for I am pointless, due to ADT.
But today I will try to cycle 70km, no doors to open.
Sure I remember “I saw an eyeball peeking from a smoky cloud behind the green door. When I said Joe sent me someone laughed out loud behind the green door.....Green door what’s those secrets you’re keeping?”
Good luck with your test, doc inter-action and the next decisions. I’ll be
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