I had a very spirited meeting with my MO in Thursday and as usual he was resistant to everything, but especially defensive when it came to estrogen. We discussed about five topics coming out of the large clinical trials of the last decade or more. I'll limit this post to low dose estrogen use.
I bought the ultra sensitive test for estradiol on a Black Friday sale from Ulta Labs (first time user). The results arrived today: less than 2.
For those who have or are using low dose estrogen:
Are you now or were you on denosumab or similar when starting (MO kept bringing up that he had me on denosumab)? If so, did you make an instant switch or continue on both for any period of time (how long)?
What dose did you start with, and if you increased upward or downward, when and how much?
In addition to those topics, any feedback regarding the experience of actual users of low dose estrogen will be welcomed.
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I'm still learning about the whole issue. No, I've wondered if others are substituting low dose estrogen for one of the bone strengtheners. Still very much on the front end, but low dose estrogen is often mentioned here without any mention of denosumab or similar.
Denosumab IS more powerful than estrogen, but has more powerful side effects, too.
Estradiol (E2) addresses the primary cause of bone density loss (low E2 levels, the same as in post-menopausal women, and in the same way) without denosumab's side effects, (back pain, muscle or bone pain, skin irritation, bloody or cloudy urine, painful urination, frequent urge to urinate, dizziness, and rash
I ever used desosumab. The information I posted about it was from the web site.
I was on high-dose estradiol (E2) for one week (April 15-22) and my PSA went from 4.67 to 3.31. Then my supply ran out and I started Orgovyx. Orgovyx matched the PSA reduction rate of E2 until I obtained a prescription for E2 again and switched.
Orgovyx brought my PSA down to 0.48 on August 12. E2 alone brought my PSA to 0.014 by the end of October where it has remained since.
My serum E2 levels are 500-600 pg/ml, which is higher than necessary, so I am titrating down to a level that is still effective, but closer to what the PATCH clinical trial (and other clinical trials) was achieving with four 100 mg/day patches.
The PATCH study targeted 50 pg/ml. Current oncological thinking is that 20 is better (longer time to develop castrate resistance). I would like to get to single digits if possible. I want to avoid having to take radiation.
(Edited to clear up confusion between the E2 level and dosing an Testosterone level. When I referred to 50 ng/ml and 20 ng/ml, I was writing about Testosterone. All other statistics were E2 (estradiol) or PSA)
"Current oncological thinking is that 20 is better (longer time to develop castrate resistance" I would like to see any evidence (peer-reviewed journal articles) of this if you have it.
The first evidence I found supporting the idea that 20 ng/mL rather than 50 ng/ml testosterone extends the likely time to developing castrate resistance (almost double) came from this article:
while it has only been cited 17 times, it does seem compelling.
Perhaps my use of the phrase "current oncological thinking" is premature, but it does make a little bit of sense since the clinical evidence (even if not massive) is enough to convince me to try.
You are welcome, Tall Allen. I have edited my post to clear up confusion about which hormone I was referring to. Sorry about that.
I do seek to lower my E2 dosing to the lowest level that is still effective. I recognize that there is danger with any "tinkering" with our bodies' endocrine systems and seek to minimize that risk while maximzing the benefits.
Men with bone metastases and CRPC should not take estrogen and need Zometa or Xgeva to prevent fractures. It's not just bone density loss that is the problem.
It's only been tested for mHSPC, not mCRPC. We know that estrogen alpha receptors (ERα) proliferate on castration-resistant PCa cells and they cause cancer cells to grow.
"Not just bone density loss that is the problem." Would you please tell us the other problems? I read what you answered to janebob9 about estrogen alpha receptors, but have seen little evidence myself in the literature (though admit to not having searched diligently yet). Could you help me out a bit in searching for cautions?
"Not just bone density loss that is the problem." refers to the fact that bone metastases cause bone overgrowth which makes bones brittle and more likely to fracture.
There is no clinical evidence that high-dose estrogen patches are helpful or even innocuous in mCRPC. High levels of estrogen in men suppresses endogenous testosterone production, just as high levels of testosterone does (by negative feedback) Castration level of testosterone slows PCa progression because there is no cancer cell replication without activation of the Androgen Receptor (AR). This much was known since the 1940s.
But estrogen also activates the Estrogen Receptors on prostate cancer cells. And there are many subtypes of ERs, some proliferative (ERα), some suppressive (ERß -and several conflicting isoforms). Some of the subtypes appear early, some later. Some are upregulated with castration resistance, some downregulated. This is less well understood, but the full results of the PATCH trial, when published, will provide important learning.
Until we know more, it is important to not go beyond the data just because one "reasons" that the biochemistry should work. Biochemistry, and especially steroid biochemistry is tremendously complex in humans. My guess is that eventually estrogens will be tailored to the ER subtypes of each patient. But we're not there yet.
So far, all we know is that high-dose estrogen patches as given in the PATCH trial is non-inferior to GnRH agonists and are safe.
Just what I need in the next phases of my research. I studied hard after my diagnosis, concentrating on hormone-sensitive PCa, but with a weather eye on the warnings I had received from my advisor at Fred Hutchinson Cancer Center, my support groups and local oncologists about the progression to castrate resistance.
I will study them in more detail when I can. Right now, I am recovering from a follow-up surgery. Four hours in the operating room and two hours coming out of anesthesia (I am told). And I just ate, so probably will nap now.
My local support group thinks of me as an expert, but in reality, I have a VERY narrow knowledge base at this point, having concentrated (lightly) on external beam radiation and ADT almost exclusively. I REALLY appreciate your wide breadth of knowledge.
I am confused now. I started Xgeva about a year and a half ago. At the same time I convinced the bone specialist to prescribe Estrogel. I thought that adding back some Estrogen would help with the bone loss. I get the Xgeva shot monthly and use the estradiol gel daily rubbed on inner thighs. I have noticed that my hot flashes are gone when using the gel.
So is it not a good idea to use the low dose Estrogel for these reasons. Am I feeding the cancer once again?
I have stopped all supplements and stopped trying to cure this disease with diet. I have been following SOC here in BC Canada and I am at the end of treatment options other than upcoming trials.
It seems like anything you try feeds cancer cells. Very frustrating for guys like myself that understand the science.
The low dose probably will have no effect on the cancer, but I can't guarantee that. As the cancer progresses to castration resistance, there are genomic changes in the receptors, both the androgen and the estrogen receptors, both in number per cell, and in kind.
Xgeva is much more powerful at preventing fractures - you don't need estrogen if you are taking it.
For your hot flashes, try Megace, venlafaxine, oxybutynin, or aural acupuncture instead.
Thanks for the reply. I don’t really need to specifically take anything for my hot flashes. I have had the hot flashes for years before the starting the Estrogen.
Why would anyone want to take an expensive drug that has a black box warning, and has some risks of serious side effects, when they could take an inexpensive, all-natural hormone that is supposed to be in your body? The normal range of estradiol in healthy men is greater than that of post-menopausal women, which is why they have worse osteoporosis than men, on average.
The less common, but serious side effects of Prolia (Denosumab) include:
Severe Hypocalcemia:
Symptoms: Muscle spasms, twitching, numbness, or tingling in the fingers, toes, or around the mouth.
Higher risk in individuals with kidney disease or low calcium levels before treatment.
Infections:
Serious infections such as cellulitis, ear infections, or skin infections may develop in rare cases.
Patients with a weakened immune system are more susceptible.
Osteonecrosis of the Jaw (ONJ):
Rare but severe complication where the jawbone doesn’t heal properly after an injury or dental procedure.
Risk factors: Poor dental hygiene, invasive dental procedures, cancer treatments, or long-term use of antiresorptive therapies.
Atypical Femur Fractures:
Unusual fractures of the thigh bone can occur after long-term use, though this is rare.
Allergic Reactions:
Symptoms: Severe itching, swelling, dizziness, or difficulty breathing may indicate an allergic response to Prolia.
New or Worsened Skin Conditions:
Severe rashes or dermatitis may develop in some individuals.
Spinal Fractures After Stopping Prolia:
Rapid bone loss and increased risk of fractures can occur when Prolia is discontinued without transitioning to another osteoporosis treatment."
None of these side effects are present with transdermal estradiol patch or gel therapy.
"Why would anyone want to take an expensive drug that has a black box warning, and has some risks of serious side effects, when they could take an inexpensive, all-natural hormone that is supposed to be in your body?"
For the same reason you would take opiates for bone met pain instead of aspirin.
With bone mets from skull to ankles and the damage done I needed bone strengthening Zometa (also no firm trials on it but apparently Zometa can at times prevent bone mets from having free reign at a tumor site).. Leaning on the couch armrest could be enough to crack a rib.
If your bones were crumbling would you ask for estrogen only?
I've said it before I wish these estrogen discussions could be tabbed as for those with low grade PC on continuous adt. Or to minimize other symptoms while staying on a bone strengthener.
I am curious why a smart guy like you decides to put up every possible side effect for the drug. You know well that will easily scare away any laymen anyone who hasn't grasped the serious state of there diagnosis and hopes they can avoid the treatment they need. Or a cheap shot to try to bolster you view. Seems you could do better.
I am so sorry to hear of your serious state of bone mets.
Thank you for the compliment, by the way.
You are correct that most men on I've been responding to are interested in the tradeoffs between Lupron ADT and transdermal Estradiol ADT.
Based on what I've learned from the PATCH trials, which included M1 men (results to be published in 2025) with "advanced prostate cancer", I would chose estradiol for osteoporosis first and then Xometa or Forteo second if the estradiol wasn't sufficient.
Low estradiol is a primary factor causing osteoporosis in men and post-menopausal women. It would likely help to prevent osteoporosis in your husband, at any stage of his disease. Data on CRPC men taking high-dose estradiol in place of Lupron ADT hasn't yet been published, but probably will be in the next year or so from the PATCH study.
I have been on Aledronic Acid for almost 4 years with some breaks in between. I was on ADT for almost 3 years and then Orchidectomy followed by Nubeqa. I explored low does estrogen/estrodiol extensively. My study shows that it is a reasonably simple and low cost method to achieve bone health. Aledronic Acid can cause necrosis in the gums so that remains a constant worry.
My MO was very reluctant and after a long struggle I was able to convince him that we should try. My study showed that the normal level of Estrogen in males is around 30 pgm/ml. To reach this level one needs either patches or gel.
Unfortunately, I found that the normal estrogen test using chemi-luminescence is not sensitive enough and one needs tests based on Liquid Chromatography/Mass Spectroscopy etc. Unfortunately, no one in India is conducting this test commercially. So I am stumped. I was very keen to try it out and see the impact on BMD.
It was interesting to read that Estrogen testing is possible at home! Would this replace ultrasensitive estrogen testing by the LAB? Would be interested to get more information on this.
Thanks very much! No, the Ulta Labs issues a blood test order, which I took to Quest Labs, it takes about 10 days to get the results, but Quest surprisingly put them on my portal. Very nice. You pay Ultra directly for the test (mine was $25 with taxes and fees) and bring the order in to Quest.
I’ve been on low dose estrogen (estradiol) for about 10 years now per Snuffy Myers for ADT SE’s and bone health and it may even have some benefit in the cancer battle. Snuffy has videos on YouTube about its use.
Personally if I have a doc resistant to everything I fire him/her. I’ve found it best to seek out an oncologist who specializes in prostate cancer, your average MO doesn’t have the expertise or experience since they are dealing with many forms of cancer and don’t necessarily keep up with the current treatments.
Ed, I always look forward to your comments. You done or are doing so many things, including out-of-box things.
I spoke to my RO last week about helping me find a different doctor, either at the same clinic or around town. I don't know if we have an oncologist in this county of 500K people, next to Orlando's NW major suburbs of Sanford. A little baffling, considering Florida must have more aging, diseased prostates than any state except maybe CA. There must be someone who knows more than my current MO, even if they don't deal exclusively with PCa.
I've been to both Mayo JAX and Moffett for second opinions, but would prefer not to make either my go-to place if at all possible. My urologist, whom I found as a Provenge provider, says MOs in this area are very weak on PCa treatment. However, our large scan facility has had the PSMA scan for several years now, my clinic has modern radiation machines, so it's not like anyone needs new equipment. They just need to turn the pages on some medical articles.
If I do BAT, I'll journey to JH, but I'll still need a local provider. If I need to go to MAYO MN, I can do that. I just haven't decided to yet.
I see Sartor ay Mayo in MN, I used to just drive to Tulane to see him for a few years since I live in the ATL area, however you might be able to connect with him through Mayo JAX. I’ve been to Mayo MN once and it was very impressive but I dread going through the hassle and expense of airports and flying. Fortunately I’ve been able to communicate with Sartor in other ways since things have been pretty stable, he coordinates with my local MO who views him as the expert.
Most of the out of the box treatments I’ve had are at the direction of Snuffy, he was way ahead of his time. And I’m still using most of them.
Yes, from everything I've heard he's very impressive. I emailed with him in Summer 2023 and told him I was in Daytona and asked him if he worked with anyone in the area. He didn't but he may not have realized how close I was to MAYO JAX. It's 100 mile fairly easy drive one way, and their parking/campus is far less hassle-free than Moffett. I may write him again.
He doesn’t work with anyone in JAX but if you become an established patient there you may be able to work through the system and tap into his expertise. If not it’ll probably be worth the trip to MN if you can swing it. You might want to wait until the weather warms up though, lol.
I wasn't sure if you were asking about high doses of E2 in place of ADT (as in the PATCH trial) or transdermal E2 patches in low dosages to combat the side effects of ADT. I have been doing the latter. I was already on Prolia, Lupron and Abiraterone when I started the E2 patches. I continued taking all of them. At the moment, I'm only using the E2 patches.
I was asking only about low-dose estrogen, not high dose in place of ADT.
You simply added low dose on top of Prolia? Then later discontinued everything except low-dose estrogen? Even the ADT? Because you weren't on ADT permanently? Have you drawn any conclusions from your personal usage of it?
No, I started the E2 when I was still on ADT, Zytiga, and Prolia. I eventually stopped the first two after taking them for the recommended length of time and while we wait to see what happens with PSA; otherwise, I would have continued the same routine. The E2 was purely an add-on, not a replacement for anything. I continue on the Prolia and E2. I've managed to get my E2 into a low normal range, while my T is still at rock bottom. I can't say I notice a big difference yet, but I am dealing with some other complications that might cloud that picture. I assume that it is an overall good thing that I have at least one thing that is normal again.
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