I'm back again for further research about the bone density medications, and now wondering about the use of bisphosphonates, denosumab and teriparatide? My PCP is suggesting these, but he's not current with the research about estrogen and testosterone use for PCa care.
My backstory is that I'm suffering from osteoprosis that has caused four compression fractures at L1, L2, L3 & L4 and at T11 in my spine. These were discovered following SRT during an MRI because of spinal pain. The MRI was used to determine if there was PCa in my spine or was it an orthopedic cause. The conclusion has been made that this is still orthopedic in nature. No evidence of PCa yet.
Further, I am not on any form of HT yet. I've had the gland removed in '19 and SRT using proton beam following BCR in '22 when my PSA reached .21. Now, I have a stable PSA at .15. I'm assuming that when the PSA begins to drift up and I can no longer use radiation to control the PCA, I'll be moving into the HT phase. I'm assuming that it is only when, not if.
If I begin using any of these suggested bone density enhancing drugs as suggested by my PCP for the osteoporois bone density, will the S/Es be unnecessary and will the drugs conflict with the future HT drugs?
I keep leaning towards using low dose tE2 now for bone density enhancement and increasing the dosage later for ADT if and when my PSA begins to rise. Do you veterans think this approach is wishful thinking? What would you do or have you done already to mitigate your own bone density problems?
Finally, it is doubtful that my MO nor my PCP will endorse the use of tE2 for either the bone density enhancement or the eventual ADT, so I'll most likely be on my own.
Thanks in advance for whatever you can suggest.
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On 9/24/20, my Estradiol was 34.7 pg/mL. I've asked my MO at a COE to put in an order for E with my PSA and other blood work, and my request is continually ignored. I'm assuming this is intentional, so I'll need to go to LabCorp or elsewhere. Thanks for your continued input.
A concern I have had from the beginning is "estrogen dominance" - the E2:T ratio. So, for a man not on ADT, if T is low E2 should be low too (closer to 12 pg/mL. Otherwise, 20 is a good target. I see no reason to aim for 30 pg/mL, even if T is very high.. I know that Nalakrats has similar concerns. The experts tend to ignore E2. The best way to eliminate estrogen dominance is by restoring healthy T levele - somewhere in the upper third of the reference range. (The 'feel good' region.)
So, now I'll research "estrogen dominance," Shit! something else to learn about. Does this put a damper on my thoughts about using tE2 for BMD treatment in preparation for expanded use when ADT is needed? Sounds like it might be when I learn what estrogen dominance can do to PCa progression. I know that Nal has resurfaced. I have not communicated with him since his departure from HU and learning he resurfaced on the FPC portal. Maybe he'll read our interactions and message me. Hope so. I've always enjoyed learning from him. Thanks again.
You already have the multiple spine compression fractures indicating that bone strength is compromised. You need a baseline DEXA scan to quantify it. ( Get it done at a facility that also reports Muscle Mass Indexes and Fat/ non lean Mass indexes as well as BMD scores.)
You do not yet have bone metastasis from PC. Congratulations. Important to try and keep it that way. A bone protective regimen such as Prolia appears to make bone matrix less susceptible to accepting metastasis. Though the evidence is soft. For me, the risk of mone mets is much higher (90%) than the risk of ONJ (2-5%). So I started Alendronate when BCR. Later switched to Prolia when osteopenia confirmed. About 12 years altogether and still no bone mets.
The estradiol patch strategy you describe is a good option for you. Low dose now and high dose as a form of ADT when needed. You could also combine that with a couple of years of Prolia if your dentition are in good shape. If you decide on E2 as long term strategy you could go have breast tissue irradiated to prevent future gynecomasty.
Thanks for your previous advice. I obtained the DXA scan and posted my results earlier in my response to Russ. Following your suggestion, I have an appointment with a spinal orthopedic specialist at the MGB Spinal Center in Boston next month> This doc specializes in spinal compression fractures, pain reduction, failed spinal surgeries etc. So, my belief is that he'll offer some sound recommendations. He has me getting an x-ray a half hour prior to our in office consult.
My PCP diagnosed my CFs as chronic and not acute meaning that since the fractures are older than six weeks, He explained to me that certain treatments of acute CFs are not successful when used with older chronic fractures. He suggested a list of BMD drugs used for osteoporosis. He pushed back immediately when I asked him if during his eighteen years practicing had he ever used estrogen therapy for treatment of BMD. He told me that he has never used estrogen. His belief was that estrogen and testosterone are linked within the body, and since testosterone is thought to be the cause of PCa, and the SOC for BMD as derived from endocrinologists is the drugs that he suggested. I'll be on my own with estrogen for BMD care.
Any suggestions of where to find the best mail order facilities to obtain .1 or .2% Estrogen patches? Is a prescription necessary for mail order? My Mexican friends can purchase tE2 gel 5% OTC for the equivalent of $18/tube. I haven't asked them about .1 or .2% patches yet?
Thanks for all your help with this maze of information.
From my experience with using estrogen as my only form of ADT, has been positive. However, when my psa started rising and I began to feel pain in my spine and pelvis my MO put me on Zometa (bone drug IV every 3 mo). Was it necessary? I have no idea. I now get mildly sick for about 36 hours after the infusion, nothing too crazy, but you’ll probably want to take the day after off if you can.
I was also accepted into a phase 1 trial and later told that I must go back on an ADT treatment for 6mo before they would accept me. The reason I was given was this: Although my T remains castrate with estrogen therapy “the sponsor requires the patient to be on a Standard of Care protocol for 6mo..”.
So HEADS UP for anyone on or considering Estrogen as your only form of ADT, this is one of the pitfalls. If you don’t play by their rules you will not be invited to the party. (I will start a new post about this so yours does not get hi-jacked by this subject .)
The good news is the establishment was willing to accept estrogen as a drug used to counteract the side effects from ADT. What that means is, I’m allowed to stay on it while on Lupron/firmagon ect.
IMO this is a paradigm shift in the cancer world suggesting that estrogen ADT as a SOC option may be reintroduced in the future. But in the meantime, they are atleast willing to respect it as a safe side effect solution. Albeit seemingly redundant in keeping T levels castrate, This is huge news for those of us who suffer the extreme end of hot flashes like myself. If you are thinking about estrogen, this is your way in.
I think you’re going to be hard pressed finding an answer to your question since estrogen is not necessarily studied for its prevention of bone loss in men. I’m sure you can find some papers and draw some conclusions, but once you leave the box it becomes even more challenging. God bless groups like these.
First, let me thanks all of the warriors for your responses. Without this core group of men, I'd be operating my medical practice with its single patient of one - just like many of us without any help. Now, some further background.
I had a DXA scan on 3/1/23. The results put me in the osteoprosis category. These were my results:
Lumbar spine from L1 through L4 BMD of 0.741 g/cm2, with T-score of -3.2. z score --2.1.
Right hip-total = BMD 0.605 g/cm2, with T-score of -2.8. z-score -2.0.
Right hip-neck = BMD of 0.527 g/cm2 with T-score of -3.0. z-score -1.6.
Left hip-total = BMD for T-score of 0.576 g/cm2 . z-score -2.2.
Left ip-neck = BMD of 0.474 g/cm2 with a T-score of -3.4. z-score -2.0.
On 9-24-20 my Estradiol blood test was 34.7 pg/mL. I have not had it tested again, but I plan to do so soon.
My total testosterone has been falling from 710 on 3/09, to 643.0 on 9/20, to 475.0 on 8/22 to 356 on 1/23. My free T has always been below the low range number of 6.6.
I read the S/Ls of Zytiga and because I have CAD (CABG5 on 7/29/21) and CHF, I'm reluctant to take this drug. My cardiac underlying complications are always shadowing my PCa care.
I have gynecomastia in my left breast. I have no idea why, but pain caused me concern, so I had a mammogram, and no presence of cancer was detected. Since I have gone to UPenn's Roberts Proton Center for my SRT in 8/22 thru 10/22 following BCR with a PSA of .21 at that time, I'm inclined to discuss radiating my breast tissue before beginning tE2 use. It seems to me that the limited invasion of the proton beam treatment immediately over my heart area would make sense if my RO at UPenn agrees. UPenn's radiology department offers all forms of radiation besides PBT, so I'm sure they do radiation for gynecomastia.
Reading and understanding the various information and S/Es of the drugs for BMD care can be daunting. I've been told that oncologists and endoconologists have each developed BMD drugs. So to whom you go for BMD care can determine which formation of the BMD drugs you will be offered. SOC varies between the two disciplines, and if your insurance may or maynot pay for one drug or another. Best to check first. I have dental implants, and I have had root canals. Thus some BMD drugs have dental S/Es that need to be considered. Mix the cardiac issues and the PCa disease into the mix and it is complicated.
My PCP suggested that I worry about S/Es too much and I should just deal with the immediate problem at present and worry about S/Es later. Sorry, but this seems just dumb to me.
As No-Stone-Unturned points out, if we choose to use estrogen for BMD mitigation and then expand its use for ADT primary treatment, we're moving out into our own territory. I tried to apply for a RCT with Novartis for their LU-177 infusions and because I had not had any ADT SOC drug treatments yet, I was rejected.
There are a few men sharing their experiences on this forum like Mateo and others who have decided to leave the US health care system and seek LU-177 infusions overseas. These are entrepreneurial medical pioneers and I applaud their courage and spirit. They would have been at the California gold rush towns early, and many of us would have joined them later. Think about the characters in the HBO series "Deadwood."
Thanks again Russ and the rest of you for the time you have taken to respond to me.
I'm dealing with gynecomatia myself and am now on tamoxifen 10 mg daily awaiting a decision in several week about doing RT. As you likely know, no treatment once gynecomatia has started will do much to reduce the "development". That said, in my case the 3 weeks or so of Tamoxifen has nearly eliminated the breast pain that suddenly arose.
My treatment situation is opposite yours, as I was using bicalutamide and adding dutasteride as part of a short-term treatment trial, so Tamoxifen's actions on estrogen components may be contraindicated in your case. Since you are using E2 as a your main treatment approach, you are in touch with the right people here, as they are ones who have also used E2.
Very Best to you as your try to sort you treatment/QOL issues out. Keep it Safe & Well while you do!
Thanks for your perspective on our breast issues. I have not begun any E2 use for BMD or ADT yet, but I think one or both will be on my treatment horizon soon. So, I’m exploring the pre-use radiation options before I introduce E2 into the party. I’ll post what I’m recommended and then what I decide to do eventually.
Thank you for your reply and thoughtful input. I replied to some of the previous posters adding comments I mulled over after reading your reply posting. A PCa survivor friends of mine and I talked about the oncologists endocrinologists conflict of research and medicine development. He was prescribed Xgena aka Prolia by his orthopedic affiliated endocrinologist. It was a long time reaching his pharmacy, and they notified him that Medicare does not cover its use so it was a $300 per injection cost. And, he learned that if he got the drug prescribed by his oncologist instead of his endocrinologist, the cost and availability and administration might be different. Turf wars among developing researchers and pattern holders I'm assuming.
It does not strike me as unusual that no one in our American capitalistic medical system wants to go near estrogen. It is cheap to obtain - sweet potatoes - and manufacture and it cannot be patterned. It makes sense that countries with national health care use estrogen extensively for care of PCa - Sweden almost exclusively and the UK, France, Israel and Canada. Those countries are stretching their drug budgets and will use the least expensive and most effective options that have a history of working well.
In the USA, the drug companies tweak a chemical formulas, file and receive a pattern and then advertise their new wonder concoction on cable television four times every hour. Send the lobbyists to DC and the salesmen into the doc's waiting rooms with free samples and invites to Vegas for the conventions as speakers. Bring the family. We get handed free samples without anyone really know what the SEs will be. We're told that these meds are SOC as vetted by the medical societies and the FDA. Take 'em and shut-up! Rant over. Sorry.
One of my PCa pals calls it his “I have cancer so I’m entitled to be pissed off” rants. It no longer works on our wives who reply, “We’re all dying of something, so take out the trash.” After I research my latest ailment, I mistakenly relax a bit, and then something else usually is introduced to complicate things.
I feel ok using 10mg megesterone a day. Was given 20mg for hot flashes, but 10 has worked for HF. I also take alondronate once a week. Last DEXA was ok.
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