My experience 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 potentially is one of the pitfalls. If you don’t play by their rules you will not be invited to the party.
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.
God bless groups like these
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No_stone_unturned
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Patient summary: This study found that prostate cancer patients treated with transdermal oestradiol for hormonal therapy did not experience the loss in bone mineral density seen with luteinising hormone-releasing hormone agonists.
“This is a very good question. Yes you need zometa. The primary reason for zometa is to prevent skeletal-related events (pathological fractures, need for radiotherapy, cord compression), not merely to increase the bone density. This study is basically reporting that estrogen is better than LHRH agonist (eligard) in terms of their negative effects on bone density. Let's talk about this during our next visit. “ From my oncologist
I hate to say it, but I can only surmise that money is the core reason that high-dose transdermal estradiol isn't broadly accepted as ADT. If my PSA continues to rise, it's definitely the direction I'm taking.
Yes and No. My understanding is that estrogen pills were used as the primary Standard of care treatments for PCa before the discovery of our current line of adt. Although estrogen was superior to lupron/eligard/firmagon for side effects and seemingly as effective in keeping T levels castrate, it was inferior for blood clot risk. Therefore, estrogen was abandoned and these new treatments were funded and targeted as the future SOC. However it was later hypothesized and backed up by the PATCH trial and others, that estrogen, prescribed transdermally { (is that a word?) through the skin} significantly reduced clot risk.
Fast forward to today. Billions have been invested in our current therapies so the logical conclusion is what incentives are there to re-purpose an old cheap drug and lose billions in profits? Zero. And if I were them, I’d feel the same way.
Sometimes things are just because they are. Luckily, there’s so many amazing, smart, driven, resourceful, curious and relentless people in the world that don’t have to operate from a place of “earnings” to find the BEST solutions, NOT just the most profitable. We are blessed to have both cohorts.
Hi my father is getting estrogen therapy for crpc when 2nd gen ( abi ) failed. It seem to have stemmed his PSA growth for now.
Only problem is that he is taking it in pill form. So blood clot risk. I am trying to find an equivalent dose via gel or patch but unable to do so here in India. Curious, what dosage are you currently on?
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