I've seen a number of posters here and there who say they use one of the "mides" listed above with no ADT like Lupron, Eligard, Firmagan, or Orgovyx, etc.
If so, did you begin that regimen after being on first level ADT for a while along with the 'mide," or did you start on the "mide" alone at the start?
Interested in all answers, but I'm metastatic and have been on Lupron (only) for 5.5 years (and still have prostate), and thinking about adding one of the "mides."
I'm particularly interested if you transitioned to a "mide" only from first level ADT only, and are metastatic to bones/organs.
Thanks.
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yes im one like kal who it has really effected . it works but .......the weight gain .. the joint pain and the fn muscle loss....jealous of those whobcan run marathons, bike 20 miles and still sxrew like rabbits.....but im glad i did the living that wore my ass out.....death will be a breezrle....
I haven’t done it myself, but I know some who have with good result, particularly abiraterone and darolutamide. Some MO’s won’t go along with it, but others either endorse it or will honor requests.
Besides a better side effect profile (whether real or placebo effect), it is theorized that switching up therapies keeps the disease off balance, so to speak.
Again, daro and abi have the better reputation, but they all have potential issues of their own. Ask your doctor, if you’re willing to take the risk.
They may say yes, or they may that changing drugs to fix what isn’t broken, without proof of its efficacy, is insane. On the other hand, they don’t have to live through years of testosterone suppression.
A few testimonials from places like this can’t tell you much ,but if you are having a hard time with side effects and looking to try it, a few positive reports should be plenty enough to persuade you. This is why some will advise against it, which is understandable.
The real question is, how much can it hurt to try it? No one yet knows, but more are doing so nowadays regardless.
Good points. My side effects from Lupron haven't been awful, but if eventually I'll need to add something, I thought I'd explore the option of monotherapy ahead of CR.
We are on the same train of thought. Coming up on my 3rd anniversary of Eligard Monotherapy with excellent results. Original mets in pelvic lymph nodes were quickly reduced. PSA reduced from 1429 to .04 soon after start of Eligard and holding to this day. Cat scan and bone scan clean. Yes, Eligard has been very effective. But, side effects continue to be problematic. Started additional inclusion of Bicalutamide this very week with intent to stop the Eligard shots after next shot, with Oncologist's approval. No balking from her would indicate positive experience with Bicalutamide monotherapy. This should allow the rest of my body a delicious drink of testosterone. Yay!!! We will see how the PSA tests hold up. Do not intend to ever go back on the Eligard treatments, no matter what.
BTW - I have read somewhere that Bicalutamide Monotherapy is SOC in the UK. Why not here? Money/profits? Or just replaced by next generation of the 'mides' here in the USA?
I do not advise anyone to follow this avenue of treatment. I am only relaying my personal journey.
Before I started Eligard shots, I took Bicalutamide for a month to suppress any peaks caused by the Eligard. My psa went from 17 to 9. I continued with Eligard only for 5 years, which brought the psa down to .8, then slowly back up to 2.4. About 1-1/2 years ago I added darolutamide, which brought the psa down to "undetectable," where it remains.
I'm tolerating the se...but like you, a drink/bath of testosterone would be welcome! My question is: doesn't Bicalumide also suppress testosterone?
Hey Okay4now - 'My question is: doesn't Bicalumide also suppress testosterone?'
That is not my understanding of how it works. My understanding of Bicalutamide is that it interrupts the attachment processes by the prostate cancer cell's receptors of the circulating testosterone, thus the classification of it being an anti-androgen. Your body is then free to produce, and use, all the testosterone it can. Theoretically, this should work better than the use of the Hormone Drugs as they only work on the testes, allowing your adrenals and other testosterone producing organs to produce what little 'T' they do and then being available to the cancer cells. Any corrections to my understandings are more than welcome.
I do not advise anyone to follow this avenue of treatment. I am only relaying my personal journey.
After eleven years of on and off ADT plus surgery and radiation I began Xtandi (enzalutimide) seven years ago as a mono therapy. I remain on it still. I have used varying doses from 1 to 4 capsules perday. 4 is the standard dose. This is all with the supervision of my MO. My psa has stayed between 0.1-0.3 the entire time. Side effect was breast growth when I started this after an off ADT treatment period and return of testosterone. I am on 1/day now and follow that because an off period from all treatment with an inevitable return to some testosterone reducing treatment in the future more growth will occur and I wish to limit that. My 18th anniversary of diagnosis is in six weeks.
My treatment response is not "normal" and is anecdotal.
All of the following is based on my understanding from discussion with my MO about doing mono-therapy with darolutamide. I’d welcome anyone to correct my thinking, since I would love to be wrong:
My motivation for doing -mide mono was to get back the T and address muscle loss. She told me that, while it’s true that these drugs don’t shut down T production, their mechanism is to block the androgen receptor and prevent the T from getting into the cell.
So I can’t have it both ways. T is either getting into the cell, or it’s not. If T is getting into cell, you both support muscle growth (etc) and feed the PC.
That said, the androgen receptor is not the only receptor that engages with T, so one might see some improved ability to e.g. maintain muscle. But that would seem to imply there’s also some T available to keep the cancerous cells growing. Arrrrgggghhhh.
Loki you are right. The T blocking mechanism works against tumor cells and also all cells so serum T is unavailable anwhere except perhaps in tiny amounts. My MO question was if there is aromatisation of T to E2, as breast growth is a symptom, then does the new source of E2 enter bone and provide bone resorption as in normal untreated men. I have no definite answer for that. MO and a few amateur experts could speculate but no evidence/proof and I operate as if there is no benefit from E2.
OK I think you’re saying that you want normal amounts of bone resorption, but the tiny amounts of T may inhibit the conversion to E2…so your bone resorption would be decreased…and these lowered levels of bone resorption are not what you want.
While on Xtandi my T is not reduced but is blocked at the cellular level where the drug interferes with the androgen receptor on cell surface. (pardon my uneducated description of mechanism). Thus I have circulating T of about 500 ng/dl (normal range) continuously. This T is unavailable to any cells (as I understand it.) When I began this cycle seven years ago I was during an off ADT treatment period and my T was ~400 and then starting the Xtandi blocking forced the normal level of T to change to E2 with the side effects including breast growth. Fooling with the hormones is tricky stuff. Once a few months pass the endocrine system stabilizes and the conversion to E2 ceases. That is where I have been for some years. My testicles pump T and my serum circulating T is strong, higher even than it might have been in a normal man my age because the T is not metabolized in any organ thus is at an elevated level. My testicles are "normal" size and sensitivity. T is there but of very limited utility.
FYI bicalutamide (Casodex) is one of the prohibited drugs for physical competitions because it affects testosterone testing results among other unnatural effects.
My E2 question was that with the conversion of T to E2 would it provide the bone health E2 provides in all people, male and female? Or would Xtandi (or some other action) prohibit that effect. Note that for those with very low T due to drugs or surgery the low T provides little to no E2 for bone health. I have high T but still unlikely to have E2 effectiveness or at least that is how I am operating.
You mention normal size/sensitivity wrt testicles…makes me wonder, if one was doing monotherapy darolutamide (e.g.), is libido affected? i.e. do erections happen more easily, since there’s plenty of T … or is libido something that also calls for unblocked androgen receptors?
I know I’ve changed the subject on you. Forgive me, I’m just thinking out loud.
Metastasis to S 1 vertebra in 2012 during off period, psa 8-9, and RT to prostate bed, pelvic nodes and met. Resumed ADT and then on and off two times until starting Xtandi monotherapy in 2017. PSMA in 2023 showed met at L3 with psa at 0.3. Surprised me both the met and the low psa identification. RT in June 23 and continuing with Xtandi and psa down to 0.1 in Jan 24. I continue to respond to whatever T reducing or blocking medication is chosen.
I am sorry I don’t find the reference but a recent study had 3 arms. One was LUPRON only one LUPRON and one of amides and one with amides only. The duo did best then the amides only and last the LUPRON group. I remember the outcome but not sure which group they were treating. I think it was urology today in last month but maybe more mainstream later.
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